AIRP Vol 2

Radiologic
Pathology
)LUVW(GLWLRQ
VOLUME 2
Breast, Musculoskeletal, Nuclear, and Neuroradiology
Radiologic Pathology Correlations
2011
Editors
Ellen M. Chung, MD, COL, MC, USA
Chief, Pediatric Radiology
Jeffrey R. Galvin, MD
2012
Chief, Chest Radiology
Leonard M. Glassman, MD, FACR, FAIUM

Chief, Breast Radiology
ACR Breast Imaging Scientist
Grant E. Lattin Jr., MD, Maj, MC, USAF

Chief, Genitourinary Radiology
Rachel B. Lewis, LCDR, MC, USN

Chief, Gastrointestinal Radiology
Mark D. Murphey, MD Illustrators

Physician in Chief Aletta A. Frazier, MD
Chief, Musculoskeletal Radiology Dianne D. Engelby, MAMS, RDMS
International Course Director Heike Blum, MFA
Alice B. Smith, Lt. Col., MC, USAF

Chief, Neuroradiology
Production Team
Melanie J. De Boer, Senior Editor
Janice Danqing Liu, Administrative Assistant
i i
American Institute for Radiologic Pathology
American College of Radiology
Reston, VA 20191
© Copyright 2011 by the American Institute for Radiologic Pathology.
All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means:
electronic, mechanical, photocopy, recording, or any other information storage and retrieval system without
written permission of the publisher.
Made in the United States of America
Great care has been taken to guarantee the accuracy of the information contained in this volume. However,
neither the American Institute for Radiologic Pathology, American College of Radiology, nor the editors and
contributors can be held responsible for errors or for any consequences arising from the use of the information
contained herein.
987654321
Library of Congress Cataloging-in-Publication Data [in process]
Volume 1
ISBN – 10 1-559030-01-1
ISBN – 13 978-1-559030-01-4
Volume 2
ISBN – 10 1-559030-02-X
ISBN – 13 978-1-559030-02-1
ii
Preface
The American College of Radiology’s (ACR) American Institute for Radiologic Pathology
(AIRP) Radiologic Pathology Correlation Course enters its 63rd year of educating radiology
residents worldwide. This year, our staff and visiting lecturers have contributed their lecture
material and images to compile Radiologic Pathology 2011–2012, continuing the tradition of
presenting richly illustrated material that teaches the pathologic basis of disease to improve
our understanding of the imaging appearance of disease.
Acknowledgements
The annual production of the Radiologic Pathology Correlation Course and syllabus is made
!"##$%&'()*+",-*()*'()+'.'/0",#(#,!!"+)1(0'0$23)$"/1(3/0(#'&4'##(#'+5$2'("6(2",/)&'##(
individuals who work at the AIRP and the various institutions and organizations throughout
the world that believe in the importance of teaching the principles of disease through
radiologic pathologic correlation. The AIRP and the ACR express our deepest appreciation
and sincerest gratitude to:
– The members of the ACR who have, through their commitment to excellence and their
support of College activities, made it possible for the ACR to support the founding of
the AIRP,
– All radiologists and radiology residents who have contributed case material to the
Thompson Radiologic Pathologic Archive at the Armed Forces Institute of Pathology,
– All of our outstanding authors, illustrators, and department staff members who make
the course and the syllabus happen effortlessly year after year,
– And the extraordinary efforts of our in-house production team who have worked
diligently on the production of this syllabus.
Melanie J. De Boer, Senior Editor
Janice Danqing Liu, Administrative Assistant
iii
Faculty - VOLUME 2
Breast Radiology Mark J. Kransdorf, MD, FACR

Professor of Radiology
Mayo Clinic College of Medicine
Rochester, MN
Chief, Breast Radiology
and
American College of Radiology Breast Imaging
Consultant, Musculoskeletal Radiology
Department of Radiology
Silver Spring, MD
Mayo Clinic
and
Jacksonville, FL
Radiologist
Washington Radiology Associates, PC
Washington, DC
William B. Morrison, MD
and
Director, Division of Musculoskeletal
Clinical Professor
and General Diagnostic Radiology
Thomas Jefferson University Hospital
George Washington University Medical Center
Philadelphia, PA
Washington, DC
Angela M. Pansera, DO, Maj, USAF, MC Michael E. Mulligan, MD

Professor of Diagnostic Radiology
Chief of Mammography and Diagnostic Imaging
University of Maryland School of Medicine
Medical Director
Baltimore, MD
Malcolm Grow Medical Center
Andrews AFB, MD
and
Thomas Lee Pope Jr., MD, FACR
Professor of Radiology, Radiologic Science and
Assistant Professor of Radiology
Orthopedics
Uniformed Services University of the Health Sciences
Medical University of South Carolina
Bethesda, MD
Charleston, SC
and
Jennifer A. Harvey, MD, FACR
Consulting Radiologist
Medical Advisory Board
Director, Division of Breast Imaging
Radisphere National Radiology Group
University of Virginia Health System
Beachwood, OH
Charlottesville, VA
and
Former Distinguished Scientist
Musculoskeletal Radiology Former ARRS Visiting Scientist
Department of Radiologic Pathology
Armed Forces Institute of Pathology
Mark D. Murphey, MD
Washington, DC
Physician in Chief
Silver Spring, MD
Charles S. Resnik, MD
Professor of Diagnostic Radiology
and
University of Maryland School of Medicine
Baltimore, MD
Department of Radiology and Nuclear Medicine
and
Director, Section of Musculoskeletal Radiology
Bethesda, MD
Director, Residency Program
and
University of Maryland Medical Center
Staff Radiologist, Musculoskeletal Section
Baltimore, MD
Walter Reed Army Medical Center
Washington, DC
Timothy G. Sanders, MD
Director of Research and Education
NationalRad
Mark W. Anderson, MD
7''+8'&0(9'32*1(:;
Professor of Radiology and Orthopedic Surgery
and
Harrison Distinguished Teaching
Chief, Division of Musculoskeletal Radiology
University of Kentucky
University of Virginia Health System
Lexington, KY
Charlottesville, VA
Donald J. Flemming, MD Mark E. Schweitzer MD

G. Victor Rohrer Professor of Radiology Education
Chairman of Radiology
Professor of Radiology and Orthopedics
University of Ottawa
Penn State Hershey Medical Center
Ottawa, ON
Hershey, PA
and
Chief of Diagnostic Imaging
The Ottawa Hospital
Ottawa, ON
iv
Neuroradiology Radiology
Alice Boyd Smith, MD, Lt. Col., MC, USAF
Chief, Neuroradiology
Silver Spring, MD
and
Assistant Professor of Radiology
Bethesda, MD
Patricia A. Hudgins, MD, FACR

Professor, Department of Radiology
Neuroradiology
Emory University School of Medicine
Atlanta, GA
Kelly K. Koeller, MD, FACR

Associate Professor of Radiology
Neuroradiology
Mayo Clinic
Rochester, MN
Erin Simon Schwartz, MD

Associate Professor of Radiology
University of Pennsylvania School of Medicine
Pediatric Neuroradiologist
The Children’s Hospital of Philadelphia
Philadelphia, PA
James G. Smirniotopoulos, MD
Program Director, Diagnostic Imaging Program Center
for Neuroscience and Regenerative Medicine (CNRM)
Professor of Radiology, Neurology, and Biomedical
Informatics
Bethesda, MD
Wendy R. K. Smoker, MS, MD, FACR

Professor of Radiology, Neuroradiology and
Neurosurgery
Director of Neuroradiology
University of Iowa Hospitals and Clinics
Iowa City, IA
Nuclear Radiology
Darlene M. Fink-Bennett, MD
Assistant Clinical Professor of Radiology
Michigan State University
East Lansing, MI
and
Chief, Department of Nuclear Medicine-Royal Oak
William Beaumont Hospital
Royal Oak, MI
and
Clinical Professor of Nuclear Medicine
Oakland University William Beaumont School of
Medicine
Rochester, MI
v
Table of Contents - VOLUME 2
BREAST RADIOLOGY

Pathologic Basis of Breast Imaging ................................................................................................. 745
Breast Disease in Men and Young Women ...................................................................................... 753
Interpretation of Breast MRI ............................................................................................................765

! "#$%&'!(%)*+,*%'+-.&!////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////!001
Unusual Breast Cancers: Expanding the Differential ...................................................................... 777
Angela M. Pansera, DO, Maj, MC, USAF

Breast Masses, Benign and Malignant .............................................................................................783
Classic Breast Lesions ......................................................................................................................793
MUSCULOSKELETAL RADIOLOGY
Mark D. Murphey, MD
Radiologic Assessment of Joint Replacement and Imaging of Bone Grafts ................................... 805
! 23&*3)-&4$)$'%)!2%.+5$&'%'+-.&!-5!(6#-.+*!7$.%)!8.&35,*+$.*9!////////////////////////////////////////////////////!:;<
Fundamental Concepts of Musculoskeletal Neoplasms: Radiographs ............................................ 829
Fundamental Concepts of Musculoskeletal Neoplasms: CT and MRI ............................................ 839
Osteoid Lesions of Bone .................................................................................................................. 849
Cartilaginous Lesions of Bone ........................................................................................................ 865
! =+>#-3&!?$&+-.&!-5!'6$!23&*3)-&4$)$'%)!@9&'$A!/////////////////////////////////////////////////////////////////////////////!::B
! C)D6%>$'!@-3D!%.E!(9&'+*!?$&+-.&!-5!"-.$!////////////////////////////////////////////////////////////////////////////////////!<F1
! G3H'%%#'+*3)%#!@-5'!I+&&3$!2%&&$&!////////////////////////////////////////////////////////////////////////////////////////////////////!<;1
Musculoskeletal Angiomatous Lesions ........................................................................................... 929
Paget Disease ................................................................................................................................... 937
Musculoskeletal Infection I ............................................................................................................. 945
Musculoskeletal Infection II ............................................................................................................ 955
Imaging of Cervical Spine Trauma .................................................................................................. 967
Musculoskeletal Seminar I .............................................................................................................. 979
Musculoskeletal Seminar II ............................................................................................................. 985
! 23&*3)-&4$)$'%)!@$A+.%#!888!////////////////////////////////////////////////////////////////////////////////////////////////////////////!<<;
Musculoskeletal Seminar IV ............................................................................................................ 997
! 23&*3)-&4$)$'%)!@$A+.%#!J!/////////////////////////////////////////////////////////////////////////////////////////////////////////////!;FF0
! 278!-5!'6$!K.$$L!M%#'!;!///////////////////////////////////////////////////////////////////////////////////////////////////////////////////!;F;B
! 278!-5!'6$!K.$$L!M%#'!N!///////////////////////////////////////////////////////////////////////////////////////////////////////////////////!;FN;
! 278!-5!'6$!O#+&'!//////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////!;FN0
! 278!-5!'6$!C.4)$!%.E!=--'!//////////////////////////////////////////////////////////////////////////////////////////////////////////////!;F11
Donald J. Flemming, MD
! CDD#-%*6!'-!8.P%AA%'-#9!C#'6#-D%'6+$&!////////////////////////////////////////////////////////////////////////////////////////!;FQ;
! 278!-5!'6$!7-'%'-#!(355!///////////////////////////////////////////////////////////////////////////////////////////////////////////////////;FBB
Mark J. Kransdorf, MD, FACR

! ?$&+-.&!-5!R.4.-S.!T+&'-U$.$&+&L!VS+.U!@%#*-A%!%.E!?%.U$#6%.&!($))!T+&'+-*9'-&+&!///////////////!;FW;
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vi
Michael E. Mulligan, MD
! @4$)$'%)!2$'%&'%&$&Z!29$)-A%Z!?9AD6-A%!/////////////////////////////////////////////////////////////////////////////////////;F:<

! 8A%U+.U!-5!T$A%'-)-U+*!X+&-#E$#&!//////////////////////////////////////////////////////////////////////////////////////////////////;F<0
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! 27!C#'6#-U#%D69!-5![)$.-63A$#%)!8.&'%>+)+'9!////////////////////////////////////////////////////////////////////////////////;;N;
Mark E. Schweitzer, MD/William B. Morrison, MD

! 278!-5!'6$!V)>-S!/////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////;;1;
NEURORADIOLOGY

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! 8A%U+.U!-5!'6$!8.5#%69-+E!]$*4!///////////////////////////////////////////////////////////////////////////////////////////////////////;NFB
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! ?9AD6-A%!%.E!R.*-AA-.!]$3#-$D+'6$)+%)!I3A-#&!//////////////////////////////////////////////////////////////////////;NN<
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! (-.U$.+'%)!@D+.%)!C.-A%)+$&!///////////////////////////////////////////////////////////////////////////////////////////////////////////!;N:B
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vii
! 8A%U+.U!-5!'6$!@3D#%69-+E!]$*4!8L!@3D$#,*+%)Z!M%#%D6%#9.U$%)!%.E!(%#-'+E!@D%*$&!////////////////////!;1W<
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! @D+.$!88L!X$U$.$#%'+^$!X+&$%&$!%.E!8.5$*'+-.!/////////////////////////////////////////////////////////////////////////////////!;QF<
! @D+.$!888L!J%&*3)%#!%.E!2+&*$))%.$-3&!?$&+-.&!///////////////////////////////////////////////////////////////////////////////!;Q;0
NUCLEAR RADIOLOGY
! T$D%'->+)+%#9!8A%U+.U!/////////////////////////////////////////////////////////////////////////////////////////////////////////////////////!;QN0
! I69#-+E!(%.*$#!////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////!;Q10
! I69#-+E!8A%U+.U!//////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////!;QQ1
! ]3*)$%#!7%E+-)-U9!@$A+.%#!;!//////////////////////////////////////////////////////////////////////////////////////////////////////////!;QB;
INDEX!/////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////////!;QW<
viii
ix
Breast Radiology
743
744
Pathologic Basis of Breast Imaging
Leonard M. Glassman, MD, FACR

There are Two Diseases
!" Cancer and no cancer
Cancer has Two Predominant Signs

Figure 1 A & B
!" <3##(3/0(23&2$823)$"/
Top Image:
You Have the Opposite Side for Normal
Comparison ducts with
!" Anatomy is simple openings on
!" Physiology is almost irrelevant the nipple.
What You Need to Remember

!" =>?("6(23/2'+#(!+'#'/)(3#(23&2$823)$"/1(
mass, or both
!" 10% present as
!"@#A..')+$2(8/0$/-
!"Asymmetric tubular structure
!"Thickened skin pattern
!"Architectural distortion
!"Paget disease
!"Nipple/skin retraction
Rad Path Correlation – What You Need

to Remember Bottom
!" The mass edge interface with the Image:
#,++",/0$/-()$##,'(+'4'2)#()*'( Normal
aggressiveness of the underlying lesion ducts.
!" Benign masses tend to be less aggressive
than malignant masses
Rad Path Correlation – What You Need

to Remember
!" B*'(#*3!'("6()*'(23&2$823)$"/(+'!+'#'/)#(
a cast of an underlying anatomic or
pathologic space
!" Benign processes often cause smooth
spaces
!" Necrosis (benign or malignant) causes
irregular spaces Terminal Duct Lobular Unit (TDLU)
[Figure 2]
Normal Anatomy !" Short segment of terminal duct and a
!" Skin cluster of ductules (acini)
!" Nipple and areola !" Functional unit of the breast
!" Subcutaneous fat !" Ductal and lobular cancers begin here
!" Premammary fascia !" Explains mixed ductal and lobular features
!" Glandular cone in the same neoplastic lesion
!"Breast disease occurs here
!" Retromammary fascia
!" Retromammary fat
!" Muscle Figure 2
!" Ribs
Low power
photo-
Normal Ducts [Figure 1] micrograph
of a TDLU.
Pathologic Basis of Breast Imaging Breast Radiology

745
Embryology Mastitis [Figure 4]
!" Milk ridges !" Acute mastitis
!"Ventral ectodermal thickenings from !"Usually in lactating women with a
the axillary to the inguinal region cracked nipple
!"Usually limited to the pectoral regions !"Can go on to abscess
by the ninth week of embryonic life !" Chronic mastitis
Congenital Anomalies
!" Athelia
!"Rarest anomaly of the breast
!"Absence of the nipple
!" Amastia Figure 4
!"Agenesis of breast, areola, and nipple
!"Associated with hypoplasia of the Asymmetry
in the upper
ipsilateral pectoral muscles in 90% MLO which
!" Amazia disappeared
!"Absence of breast tissue only on antibiotic
therapy.
Congenital Anomalies [Figure 3]
!" Polythelia
!"Accessory nipple
!" Polymastia
!"Accessory breast tissue
Abscess [Figure 5]
Figure 3
Axillary
breast
tissue.
Figure 5
Pregnancy Changes Abcess.
!" Increased estrogen and progesterone
!"Estrogen promotes ductal growth
!"Progesterone promotes lobular growth
and breast secretion
!" Hyperplasia and hypertrophy Chronic Mastitis
!" Extremely dense breast pattern !" Chronic infection
!" C3/(#)$&&(#''(23&2$823)$"/#("/( !"TB
mammography !"Fungus
!" Can see masses on sonography !" Immunologic
!"Diabetes
Mastitis !"Amyloid
!" 3% of primary diagnoses at biopsy !"Wegener granulomatosis
!" Many different types !"Sarcoid
!"Infection !"Churg-Strauss
!"Systemic !" Idiopathic
!"Antigen-antibody reaction !"Necrobiotic xanthogranulomatosis
!"Idiopathic !"Granulomatous mastitis

746
Most Common Benign Neoplasms
!" Fibroadenoma
!" Intraductal papilloma
!" Hamartoma Figure 7
Fibroepithelial Lesions Horizontally

!" Epithelial and stromal elements oriented, oval
circumscribed
!"Fibroadenoma
homogeneous
#" Benign epithelial and stromal solid mass is a
elements &*+,"('-,."/
!"Phyllodes tumor
#" Benign epithelial and hyperplastic
or sarcomatous stroma
!"Carcinosarcoma
#" Both elements malignant
Fibroadenoma [Figures 6 to 9]
!" Begins in TDLU
!" Response to unopposed estrogen in young
women
!" Oval or round circumscribed nodule
!" <3A(*35'(2"3+#'(23&2$823)$"/1('#!'2$3&&A(
in periphery Figure 8
!" Growth pushes surrounding tissue without
Fibroadenoma.
invasion
!" 7%-16% of patients have multiple tumors
!" Polyclonal cell population
!" Stages of development
!"Proliferation of epithelial and stromal
elements in multiple lobules
!"C"/4,'/2'("6()*'(*A!'+!&3#)$2(&"%,&'#
!":"+.3)$"/("6(8%+"30'/".3)"$0(
nodules
!"Nodules coalesce to form FA
Figure 6 A & B
Top Image:
Fibroadenoma
with “push”
border
separating the
mass from the
surrounding
tissue.
Figure 9
Bottom !"#$%&'()&*+,"('-,."/
Image: Small
carcinoma
with invasive Carcinoma Arising in a Fibroadenoma
border. !" Rare
!" Most often lobular neoplasia (LCIS) or
DCIS
!" Invasive carcinoma very rare
!"Usually grows in from outside

747
Fibroadenoma with Phyllodes Papilloma [Figure 12]
Characteristics !" Papillary growth pattern supported by a
8%+"53#2,&3+(#)3&D
Phyllodes Tumor [Figure 10] !"Arises centrally
!" Benign epithelial elements and cellular !"Usually solitary
spindle cell stroma !" Papillomatosis
!" Can act malignant !"Arises peripherally in the TDLU
!"Local recurrence !"Usually multiple
!"Distant blood-borne metastases
!"Lymph node enlargement reactive
usually
!" Well-circumscribed lobulated mass
!" Similar appearance on sonography Figure 12
!"May have cystic spaces A&B
Top Image;
Solid
papilloma
inside dilated
01%(2&##'()
duct.
Figure 10 A & B
Left Image: Benign phyllodes tumor.

Right Image: Gross specimen of benign phyllodes
tumor.
Bottom Image:
Correlating
gross specimen
Carcinosarcoma [Figure 11]
of intraductal
papilloma.
Invasive Ductal Cancer [Figures 13 & 14]

!" EFG(H/")(")*'+I$#'(#!'2$8'0J
Figure 11 !"50%-75% of invasive cancers
!" Medullary
Irregular
!" Papillary
subareolar
mass is !" Colloid (Mucinous)
carcinosarcoma. !" Tubular
!" Metaplastic
!" Cribriform
!" Adenoid cystic
!" Paget disease
!" K/43..3)"+A

748
Medullary Carcinoma [Figure 15]
Figure 15
A&B
Top Image:
Round
carcinoma on
mammography,
a medullary
carcinoma.
Figure 13 A & B
Left Image: Spiculated invasive ductal carcinoma.
Right Image: Correlating gross specimen.
Figure 14
A&B Bottom
Image: Round
Top Image: medullary
Coarse carcinoma on
heterogeneous ultrasound.
"-()&-')
linear and
pleomorphic
$"#$%&$"3%,-4)
of invasive
ductal
carcinoma.
Papillary Carcinoma [Figure 16]
Bottom Image:
!"#$%&$"3%,-4)
caused by
tissue necrosis
and ductal
secretions. Figure 16
Round
encysted
papillary
carcinoma.
Types of Invasive Ductal Carcinoma

with Rounded Expansile Periphery
!" Medullary
!" Papillary
!" Cribriform
!" Colloid
!" Metaplastic (some)
Types of Invasive Ductal Carcinoma

with Improved Prognosis
!" Medullary
!" Papillary
!" Cribriform
!" Colloid
!" Tubular
!" Adenoid cystic Colloid Carcinoma

749
Tubular Carcinoma [Figures 17 & 18]
!" Typically spiculated
!" Must have 75%-100% tubular formation
!" Less than 75% acts like usual invasive
carcinoma
Figure 17
Spiculated
mass, a
typical tubular
carcinoma.
Figure 19 A & B
)5,6)7."8'9)7-:"4%:')#,*1#"+/);%-8#')&#'),+%'-3"3%,-),<)
invasive lobular carcinoma cells.
Bottom Image: Invasive ductal carcinoma cells form
thickened duct walls that in aggregate become a
palpable mass.
Figure 18
Low-power view of the spiculations of a tubular
carcinoma.
Figure 20
The typical
Adenoid Cystic invasive
carcinoma is
Adenoid Cystic Carcinoma a spiculated
mass.
Invasive Lobular Cancer [Figures 19 to 21]
!" Prognosis similar to invasive ductal cancer
!" Most commonly a spiculated mass
!" G".'(3+'(."+'(0$682,&)()"(#''(3#()*'A(3+'(
0$66,#'&A($/8&)+3)$/-
!"Present as asymmetric density

750
Figure 21
Asymmetry
is also a Figure 22
presentation
for invasive =,-46'$%&$)
lobular indistinct
carcinoma. mass is a
spindle cell
sarcoma.
Sarcoma
!" 1% of malignant breast tumors
!" 9+'3#)(2"/)3$/#(63)1(8%+",#()$##,'1(%&""0(
vessels, etc
!"@/-$"#3+2".31(.3&$-/3/)(8%+",#(
histiocytoma, chondrosarcoma,
rhabdomyosarcoma etc
!" Metaplasia can occur
!" Malignant transformation can occur
!" Often after chest or breast irradiation
Fibrosarcoma
Spindle Cell Sarcoma [Figure 22]
Figure 23 A & B
Angiosarcoma [Figure 23]
Left Image: Small angiosarcoma.
Right Image: Big angiosarcoma with wildly irregular
What You Need to Remember enhancemant.
!" The mass edge represents the
aggressiveness of the underlying
abnormality
!" B*'(#*3!'("6()*'(23&2$823)$"/(+'!+'#'/)#(3(
cast of an underlying space
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752
Breast Disease in Men and Young Women

Imaging of the Male Breast Benign Disease
!" No lactating adenomas
Development !"No pregnancy
!" Birth to puberty same as female !" Rare lobular tumors
!"No lobules without progesterone
Anatomy [Figure 1] !"Rare invasive lobular carcinomas
!" Major ducts with little branching reported
!" Connective tissue and fat !" V3+'(8%+"'!$)*'&$3&(&'#$"/#
!" Almost no lobules !"Fibroadenoma, phyllodes,
carcinosarcoma
!"Lesions begin in TDLU (lobules)
#" Lobular development rare in men
Gynecomastia
!" Potentially reversible enlargement of the
Figure 1 male breast
!" Presents as soft mobile tender subareolar
Normal mass
male !" Simultaneous proliferation of ducts and
breast
showing stroma without encapsulation
fat and !"Florid (early; nodular glandular) phase
&*+,14) #" Begins as increased number of
stranding. ducts and epithelial proliferation
I$)*('0'.3(3/0(2'&&,&3+(8%+"%&3#)$2(
stroma
#" Reversible phase
!"Fibrotic (late; dendritic) stage
#" Progresses to dilated ducts,
moderate epithelial proliferation
3/0(8%+"#$#
!"Diffuse glandular
Gynecomastia
!" Absolute increase in estrogen HCG or
Male Breast Disease estrogen precursors
!" Presents as mass, swelling, or pain !"Secretion by tumors
!" Presents as nipple discharge #" Leydig cell tumor
!" Can be benign or malignant #" Germ cell tumors
#" Hepatoma
Benign Disease #" Adrenal cortical tumors
!" Gynecomastia #" Pituitary tumors
!" Pseudogynecomastia !"Estrogen therapy
!" Papilloma #" Prostate carcinoma
!" Adenoma #" Topical estradiol to scalp
!" <A"8%+"%&3#)".3 !"Increase in estrogen precursors
!"More common in men than women #" Cirrhosis
!" Granular cell tumor #" Hyperthyroidism
!" Fibrocystic change
!" Diabetic mastopathy
!" Epithelial inclusion cyst
!" Cystic lymphangioma
!" Pleomorphic hyalinizing angiectatic tumor
of soft parts
!" Varix
!" Leiomyoma
!" Lipoma
Breast Disease in Men and Young Women 753 Breast Radiology

Gynecomastia
!" Relative increase in estrogen
!"Testicular failure or atrophy
#" Idiopathic
#" Cytotoxic chemotherapy
!"Puberty and senescence
#" Transient in puberty (1-2 years)
!"Klinefelter’s syndrome (XXY) Figure 3
!"Testicular feminization syndrome Smaller, more
!" Hyperthyroidism contracted
!"Reverses when the patient is euthyroid irregular
!" Refeeding after malnutrition or starvation subareolar
density
!" Onset of hemodialysis of chronic
gynecomastia.
Gynecomastia
!" Drugs (partial list)
!"Spironolactone
!"Reserpine
!"Digitalis Diffuse Glandular Pattern
!"Ergot !" Small heterogeneously dense breast
!"Thyroid extract
!"Dilantin Pseudogynecomastia [Figure 4]
!"Thiazide diuretics !" Usually bilateral
!"Cimetadine !" No palpable mass
!"Marijuana !" Excessive fat deposition in breast area
!"Normal variant
Gynecomastia !"Obesity
!" Mammographic patterns !"E',+"8%+".3)"#$#
!"E"0,&3+(-&3/0,&3+(H32,)'("+(4"+$0(
phase)
!"7'/0+$)$2(H2*+"/$2("+(8%+")$2(!*3#'J
!"Diffuse glandular (very high estrogen
levels)
Nodular Glandular Pattern [Figure 2]

!" Fan-shaped density radiating from the
nipple
Figure 4
!"May be more prominent in UOQ
!"Blends into surrounding fat Increased fat
deposition of
pseudogyne-
comastia.
M!"#$%"$&'()"*'++
Figure 2 A & B
!" G"&$)3+A(!3&!3%&'(8+.(.3##
Left Image: Flame-shaped subareolar nonencapsulated !"Rarely bilateral
density of acute gynecomastia.
Right Image: Typical ultrasound appearance of acute !"E"(23&2$823)$"/#
gynecomastia. !" Freely moveable
!" More common in men than women
Dendritic Pattern [Figure 3] !" Mean age late 50s
!" Subareolar density with prominent !" Circumscribed lobulated mass without
extensions into fat 23&2$823)$"/
!"Density smaller than nodular pattern !" Treated with local excision

M!"#$%"$&'()"*'++++++++[Figure 5] Male Breast Cancer
!" Frequently located subareolar
!"Most common presentation is a
painless subareolar mass
#" Mass usually eccentric to the
nipple
Figure 5
!"Mass round, oval, or irregular
!"C3&2$823)$"/#(+3+'(3/0(2"3+#'+()*3/($/(
Nonsubareolar
encapsulated women
circumscribed
mass requires Male Breast Cancer
biopsy, in !" Paget’s disease and skin ulceration more
this case a common than in women
.>,&*+,*#"43,."/
!" Axillary metastases similar to women at
same stage
!" Found at later stage than women
Male Breast Cancer

!" DCIS
!"10% of cases
!"Usually papillary type
!"Comedo type very rare
Granular Cell Tumor [Figure 6] !" Liposarcoma
!" Benign tumor of neural origin !" Lymphoblastic lymphoma
!" 6% in breast !" Metastasis
!" Typical age is 30s
!" Bimodal appearance Carcinoma Risk Factors
!"Spiculated or circumscribed !" Advanced age
#" Usually circumscribed in men !" Family history
!" Jewish heritage
!" Chest wall irradiation
!" Hyperestrogenism
!" Hyperthyroidism
!" Exposure to hepatotoxins
!" Occupational exposure to high heat
Figure 6
Carcinoma Risk Factors
!" BRCA 2 in 4-16% of cancer patients
=,-46'$%&$)
solid breast
!"40% in Iceland
mass, a !" Undescended testes
granular !" Orchiectomy and orchitis
cell tumor. !" Klinefelter’s syndrome
!"47, XXY
!"6% of male breast cancer
!"3% lifetime risk
Malignant Disease
!" Carcinoma
!" Metastasis
!" Lymphoma
!" Sarcoma
Male Breast Cancer

!" 1,690 new cases estimated in 2005 in US
!"460 men will die of disease in 2005
!" 1% of all invasive mammary cancers
!"Higher incidence in China and Africa
#" High incidence of
hyperestrogenism secondary to
parasitic liver disease

Invasive Ductal Carcinoma [Figures 7 & 8] Conclusion
!" Disease presents as mass pain or nipple
discharge
!" Gynecomastia and invasive ductal cancer
are the most common lesions in the male
breast
!"There are other rarer benign and
malignant lesions
!" Gynecomastia and carcinoma can look
similar
!"Biopsy is sometimes necessary
Figure 7 to separate gynecomastia from
carcinoma
Subareolar
!" All lesions eccentric to the nipple need
but
encapsulated biopsy unless they are characteristically
mass, benign
invasive !"Contain fat
ductal !"Lymph node
carcinoma.
Imaging in Young Women
Lesions in Young Women are Rare
!" Women 21 years of age and younger
!"Fibroadenoma (up to 95%)
!"Juvenile hypertrophy
!"Abscess and mastitis
!"Phyllodes tumor
!"Malignancy
#" Primary
#" Metastatic
!"Cysts are rare
!" Women over 21 years of age
!"Fibroadenoma
!"Abscess and mastitis
!"Phyllodes tumor
!"Cysts
#" More common as age approaches
35
!"Malignancy
Presenting Signs and Symptoms

!" Mass
!" Pain
!" Nipple discharge
!" Screening
!"Gene positive
!"Strong family history
Diagnosis in Young Women

!" Ultrasound is primary modality
Figure 8 !"Breasts are dense after puberty
Nonsubareolar irregular mass, invasive ductal !" Mammography is used in select older
carcinoma. patients
!"High risk screening
Gynecomastia Carcinoma !"Solid masses in patients over 30
!"Malignant-looking lesions

More Common Benign Lesions Giant Fibroadenoma [Figure 10]
!" Fibroadenoma
!"Juvenile
!"Giant
!" Phyllodes benign
!" Granular cell tumor
!" Lactating adenoma
!" Hamartoma Figure 10
!" Normal breast
!" Fibrocystic change Large
!" Intraductal papilloma circumscribed
!" Juvenile papillomatosis mass is a giant
&*+,"('-,."/
!" Mastitis
!" Juvenile hypertrophy
!" Diabetic mastopathy
Less Common Benign Lesions

!" Pseudoangiomatous stromal hyperplasia
(PASH)
!" Granulomatous mastitis
!" Fibromatosis
!" Adenosis
!" Fibroadenomatoid hyperplasia or nodule
!" Fibrosis
!" Mondor disease Juvenile Fibroadenoma
!" Varix
Phyllodes Tumor
!" Rosai Dorman disease (sinus histiocytosis
!" Benign epithelial elements and cellular
with lymphadenopathy)
spindle cell stroma
Fibroadenoma !" Can act malignant
!"Youngest patient age 5 in our series !"Local recurrence
!" Multiple in 16%-25% of patients clinically !"Distant blood-borne metastases
!"Do complete bilateral ultrasound? !"Lymph node enlargement reactive
!" Found in 25% of breasts examined usually
!" Well-circumscribed lobulated mass
microscopically
!" Similar appearance on sonography to
Fibroadenoma [Figure 9] 8%+"30'/".3
!"May have cystic spaces
Phyllodes Tumor
!" Benign (15% recurrence)
!"Pushing margins
!"Mild atypia
!"May recur locally
Figure 9 !"Rare metastases
!" Borderline (25% recurrence)
Circumscribed !" Malignant (30% recurrence)
horizontally
oriented !"Invasive margin
solid mass, a !"Moderate to severe atypia
&*+,"('-,."/ !"Common local recurrence
!"Hematogenous metastases
Phyllodes Tumor
!" Treatment
!"Wide local excision
Giant Fibroadenoma vs Juvenile !" You get 2 tries to get it right
Fibroadenoma !"Each recurrence may show grade
!" \$3/)(8%+"30'/".3(( deterioration
!"Large lesion > 10 cm
!" X,5'/$&'(8%+"30'/".3( Benign Phyllodes
!"Age 20 years or younger !" Can occur in girls under 10 years
!"Typically rapid growth and large size !"Usually older than 10 years
!"Usually pericanicular type with cellular !" Tendency to recur but not metastasize
stroma !" Pushing margins without invasion

Benign Phyllodes [Figure 11] Lactating Adenoma [Figures 13]
!" Young women
!" Pregnant or lactating women
!" Circumscribed lobulated masses
Figure 13
Lactating
adenomas.
Figure 11
Small slit-like nonvascular clefts are characteristic of a
phyllodes tumor.
Granular Cell Tumor [Figure 12]

!" Neural cell origin
!" Wide age range (17–75 years)
!"Average age 30s Juvenile Papillomatosis
!" Discrete round mass or spiculated mass !" Firm discrete mass
!"Push or invasive margin !"Localized, cystically dilated ducts with
!" Rare metastasis to axillary nodes intraductal proliferation
!"One case in literature of lung !" 2/3 less than 20 years old
metastases !" Association with family history of breast
carcinoma
!"10% develop carcinoma within 10
years
!" Treat with excisional biopsy
Juvenile Papillomatosis [Figure 14]

!" Age 14
Figure 14
A&B
Top Image:
Typical
multicystic
appearance
of juvenile
papillomatosis.
Figure 12 A & B
Top Image: Circumscribed granular cell tumor.

Bottom Image: Granular cell tumor gross specimen
showing an indistinct border with the surrounding fat. Bottom Image: Correlating gross specimen of juvenile
papillomatosis.

Juvenile Hypertrophy [Figure 15] PASH [Figure 17]
!" Usually age 11–14
!" M#,3&&A(2"$/2$0'#(I$)*(8+#)(.'/#'#
!" Usually lasts 3–6 months
!" Unilateral or bilateral palpable mass
!" Iatrogenic amastia if removed Figure 17
A&B
Top Image:
Tumoral type
of PASH.
Figure 15
11-year-
old girl with
juvenile
hypertrophy.
Bottom
Image:
Correlating
gross
specimen of
PASH.
Diabetic Mastopathy [Figure 16]
!" :"23&(8%+"#$#($/()*'(%+'3#)
!" Diabetes mellitus type 1 since childhood
!"Poorly controlled
!"Complications from vasculitis
elsewhere Granulomatous Mastitis [Figure 18]
!" Occurs in young to middle age !" Usually in reproductive age
!" Often within 3 years of pregnancy
!" Idiopathic
!" G!'2$82(23,#'#(.,#)(%'('L2&,0'0
!"TB or other bacteria
!"Sarcoid
!"Fat necrosis
!"Foreign body
Figure 18
Figure 16
Spiculated
Diabetic mastopathy.
high-density
mass is
granulo-
matous
PASH (Pseudoangiomatous Stromal mastitis.
Hyperplasia)
!" Wide age range
!" Focal lesion usually
!" Histologically shows slit-like separation of
stromal cells
!" Exaggerated stromal response to
hormone stimulation

Malignant Secretory Carcinoma
!" Youngest patient 5 years old in our series !" Previously called juvenile carcinoma
!"Secretory carcinoma !" Variant of invasive ductal carcinoma
!" Invasive ductal carcinoma !" Initial report age 3–15
!" DCIS !"Oldest patient 87 years old
!" Sarcoma !" Limited aggressiveness in younger
!"Angiosarcoma most common patients
!" Malignant phyllodes !"Nearly 100% curable in young patients
!" Lymphoma
!" Metastasis DCIS
!" Screening mammography in high risk
Invasive Ductal Carcinoma patients
!" Most common carcinoma !" Mass or nipple discharge
!" Youngest patient 6 years (not in this
series) Sarcoma
!" Signs similar to older patients !" Malignant mesenchymal tumors
!" 1% of malignant tumors in all ages
Medullary Carcinoma [Figure 19] !"Higher % in young women
!" After radiation therapy, 2–15 years
!" Many histological subtypes
Sarcoma
!" Angiosarcoma
!" Granulocytic sarcoma
!" Myosarcoma

!" 14–82 years
Figure 19 A, !"Mean of 35
B&C !" Lobulated mass
Top Image: !" Highly aggressive lesion
Medullary
!"Axillary metastasis rare
carcinoma.
!"Hematogenous metastasis usual
Middle
Image: 18
year old
woman with
a palpable
mass, a
medullary
carcinoma.
Bottom Image: Figure 20

Gross specimen Highly vascular small angiosarcoma.
with fairly well
('&-'()*,+('+4)
explains the Phyllodes Malignant
“benign” !" Usually older than 10 years
appearance !" Tendency to recur and metastasize
of medullary
!" Invasive margins
carcinoma.
!" Axillary adenopathy usually reactive
!" Metastases hematogenous

Phyllodes Malignant [Figure 21] Metastatic Disease
!" E',+"8%+"#3+2".3
!" In adults
!"Melanoma
!"Lung
!"Prostate
!"Lymphoma
Conclusions
!" Ultrasound is the primary modality in this
Figure 21
age group
Malignant !" Mammography is reserved for screening,
phyllodes likely malignant lesions and the older
tumor. patients in this group
!" MR indications are the same as for adults
!" Cysts are rare especially in the younger
age groups
!" Most solid lesions are benign
!"Fibroadenoma most common
!" Juvenile hypertrophy and juvenile
papillomatosis are unique to this age
-+",!(3/0(*35'(#!'2$82(3!!'3+3/2'#("/(
imaging
!" Malignant lesions occur and look like
Lymphoma malignant lesions in older women
!" Primary or secondary !"Invasive ductal carcinoma most
!" Focal mass or diffuse process common
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consecutive cases. Postgrad Med J 1985; 61:977-978.
42. Rogers DA, Lobe TE, Rao BN, et al. Breast malignancy in children. J Pediatr Surg 1994; 29:48-51.

43. Rosen PP, Holmes G, Lesser ML, Kinne DW, Beattie EJ. Juvenile papillomatosis and breast carcinoma.
Cancer 1985; 55:1345-1352.
44. Senocak ME, Gogus S, Hicsonmez A, Buyukpamukcu N. Cystosarcoma phylloides in an adolescent female.
Z Kinderchir 1989; 44:253-254.
45. G*$(@@1(\'"+-$3/WG.$)*(71(C"+/'&&(;71(')(3&T(V30$"&"-$23&(+'3#"/$/-N(.3&'(%+'3#)(.3##(I$)*(23&2$823)$"/#T(
Am J Roentgenol 2005; 185:S205-210.
46. Simmons PS. Diagnostic considerations in breast disorders of children and adolescents. Obstet Gynecol
Clin North Am 1992; 19:91-102.
47. Simmons PS. Breast disorders in adolescent females. Curr Opin Obstet Gynecol 2001; 13:459-461.
48. Squire R, Bianchi A, Jakate SM. Radiation-induced sarcoma of the breast in a female adolescent. Case
report with histologic and therapeutic considerations. Cancer 1988; 61:2444-2447.
49. Templeman C, Hertweck SP. Breast disorders in the pediatric and adolescent patient. Obstet Gynecol Clin
North Am 2000; 27:19-34.
50. b'$/#)'$/(G`1(C"/3/)(U:1(F+'&(G\1(c,2D'+.3/(X@1(9'&&3*(VT(G!'2)+,.("6(MG(8/0$/-#($/(!'0$3)+$2(3/0(
adolescent patients with palpable breast masses. RadioGraphics 2000; 20:1613-1621.
51. Wilson M, Cranor ML, Rosen PP. Papillary duct hyperplasia of the breast in children and young women.
Mod Pathol 1993; 6:570-574.
52. Sabate J, Clotet M, Torrubia S, Gomez A, Guerrero R, de Las Heras P, and Lerma E. Radiologic Evaluation
of Breast Disorders Related to Pregnancy and Lactation RadioGraphics, 2007; 27: S101 - S124

764
Interpretation of Breast MRI
Why MRI? Pretreatment Staging

!" Mammography is imperfect !" MRI changes treatment in 15%-30%
!" Ultrasound is limited !"Multifocal/multicentric disease
!" New technologies have limited data #" 20% of additional foci are benign
!"Positron emission mammography #" Lumpectomy to mastectomy in
!"Breast scintigraphy 15%
!"Laser mammography !"Larger area for lumpectomy than
!"Etc indicated by mammography or
sonography
Indications !"Chest wall involvement
!" Implant integrity !"2%-3% have cancer in the opposite
!" Problem solving breast
!" Screening
Preoperative – Multiple Sites
Breast Implants [Figure 1]
Preoperative – Larger Lumpectomy
[Figure 2]
Figure 2
Index lesion
with smaller
second focus
connected
by abnormal
linear
Figure 1 enhancement.
Bilateral “linguini sign” of intracapsular rupture.
Problem Solving – Good Indications

!" Metastatic disease with unknown primary
!"Usually for enlarged axillary or
supraclavicular nodes
!"MRI positive in 50%
!" Pretreatment staging Preoperative – Both Breasts [Figure 3]
!" Residual disease
!" Recurrence after breast conservation
!" Response to chemotherapy
Problem Solving – Bad Indications
!" Symptomatic patient with negative
mammogram/sonogram
!" Asymmetries
!"Global or focal
!"Abnormality in 1 view
!" Multiple, rounded, solid masses
Problem Solving – Weak Indications
!" Pathologic nipple discharge Figure 3
!"MR ductogram
!" C3&2$823)$"/# 4-mm enhancing mass left subareolar region is index
!"85% or less negative predictive value invasive ductal carcinoma lesion. Bilateral clumped
enhancement is bilateral diffuse ductal carcinoma in
!"Not good enough
situ (DCIS).
Interpretation of Breast MRI Breast Radiology

765
Residual Disease [Figure 4] Screening
!" Postoperative residual disease !" High-risk women
!"Postlumpectomy preradiation !" Average-risk women??
!"Used if margins positive or close
!"Negative MRI not perfect High Risk Screening
!"Positive MRI not perfect !" American Cancer Society Guidelines
#" Try to wait 1 month after surgery !"MRI and annual mammograms
beginning at age 30
!"20% or more lifetime risk (double the
general risk)
#" BRCA 1 or 2
#" Parent, sibling, or child with BRCA
1 or 2
#" Radiation treatment to chest
between ages 10 and 30
#" Begin 10 years after treatment
#" G$-/$823/)(!"#$)$5'(63.$&A(*$#)"+A
S,-.,#/'.)+Positive Family History

!" 5%-10% are genetically linked
!" 15%-20 % occur in women with a family
history
Figure 4
!" F/'(8+#)(0'-+''(+'&3)$5'(I$)*(%+'3#)(
Nodule on lateral capsule of seroma.
cancer before age 50 doubles risk (to
20%)
!"Mother, sister, daughter
Recurrence After Breast Conservation
[Figure 5] High Risk Syndromes
!" 10% recurrence at 10 years !" Li-Fraumeni
!" MRI usually positive for at least 2 years !"Multiple cancers
after completion of treatment !" Cowden (Multiple Hamartoma Syndrome)
!" @%/"+.3&(8/0$/-#(36)'+(O(A'3+#(3+'( !"Multiple cancers (breast and thyroid)
suspicious !" Bannayan-Riley-Ruvalcaba
!"Similar to Cowden Syndrome
Minimum Technical S01/,#/'),".(

!" 1.5T or greater
!"3T is not better
Figure 5
!" Bilateral breast coil
Spiculated !" Prone position
enhancing !" Voxel size 2.5 mm or less in any direction
mass in
surgical bed. !" Resolution 1 mm or less in plane
!" Contrast enhancement
!" Active fat suppression or subtraction on
contrast sequences
!" Biopsy availability
!" Computer-aided detection (CAD)?
Recurrence After Breast Conservation
!" Recurrence CAD
!" No recurrence !" Motion registration
!" Multiplanar reconstruction
Response to Chemotherapy !" Subtraction
!" Effectiveness of treatment (metabolic !" Automated kinetics
response to treatment) !"Curves
!"Change in size !"Peak enhancement
!"Routine contrast (change in kinetic !" Measurement package
curve) !" Kinetics only
!"Diffusion-weighted (free interstitial
water diffusion rate) Temporal vs Spatial Resolution
!"MR spectroscopy (choline peak !" Good spatial resolution more important
change) !" B'.!"+3&(+'#"&,)$"/(23/(%'(#32+$82'0(6"+(
!"Can predict response after days or better spatial resolution
weeks of treatment, not months
Interpretation of Breast MRI 766 Breast Radiology

Temporal Resolution - Kinetic Analysis
(Curves)
!" Threshold
!"% enhancement over baseline
!"50% minimum
!" Timing
!"Initial upslope
#" First 1-2 minutes usually
#" Slow, medium, or rapid
#" G!'2$82$)A(][?
#" Positive predictive value 60%
!"Delayed portion (> 2 minutes or after
curve changes) Figure 7
#" Increase, plateau, or washout A&B
!"Total time 6-7 minutes Kinetic
!"Need 3 points minimum to generate curve shows
curve rapid initial
!" 3 Curve types enhancement
and decrease
Type I [Figure 6]
(washout) on
delayed portion
!" Continued enhancement in delayed part – Type III.
of slope
!" 6% malignant
Type II [Figure 8]
!" Plateau in delayed part of slope
!"10% variance allowed from horizontal
Figure 6
A&B
Kinetic
curve shows
slow initial
enhancement
and persistent
enhancement
on delayed
portion – Type Figure 8
I. A&B
Kinetic
curve shows
slow initial
enhancement
and plateau
on delayed
portion –
Type II. 10%
enhancement
or washout
allowed on
delayed
portion on
Type II.
Type III [Figure 7]

!" Rapid or medium initial phase
!" Washout delayed phase
!" 29%-77% malignant

Sequences T2 Fat Suppressed – High Signal
!" T1-weighted precontrast and not fat !" Fibroadenoma
suppressed !" Colloid carcinoma
!" T2-weighted fat suppressed
T2 Fat Suppressed
!" T1-weighted dynamic contrast enhanced
!" Moderate signal
!" Active fat suppression and/or subtraction
!"Invasive lobular carcinoma
!"+/- multiplanar reconstruction
!"DCIS
T1 [Figure 9]
!"Fibrocystic change
!" Precontrast !" Low signal
!" Not fat suppressed !"Invasive ductal carcinoma
!" Central high signal !"G2&'+")$2(8%+"30'/".3
!"Lymph node !"Scar
!"Fat necrosis
T1-Weighted Dynamic Contrast
#" Fresh and chronic
!" Hamartoma
Enhanced
!" 3D T1-weighted fat suppressed spoiled
gradient-echo sequence typically
!" Multiple runs over 5-8 minutes
!"Each run < 2 minutes for kinetics
!" Gadolinium
!"0.1 mmol/kg bolus
Subtraction/Fat Suppression
!" Must use active fat suppression or
Figure 9 subtraction
!"Patient motion limits usefulness of
Mass with
internal
subtraction
fat is !"CAD software can help with motion
hamartoma. !" Both are best
Multiplanar Reconstruction
!" Useful to see around masses
!" Often done on late submillimeter
sequences
!"Isotropic
!"Less enhancement
Sensitivity and S01/,#/,)!

T2 Fat Suppressed [Figure 10]
!" Sensitivity 83%-100% for invasive
!" High signal disease
!"Cysts !" G!'2$82$)A(O=?WZ>>?(6"+($/53#$5'(0$#'3#'
!"Colloid carcinoma
!"<AL"$0(8%+"30'/".3 False Negatives
!"Lymph node !" Poor enhancement pattern
!"Fat necrosis !"16% DCIS and 3% invasive carcinoma
#" Fresh and chronic !" Invasive lobular carcinoma
!" Cysts !" Metastatic breast carcinoma
!" Low-grade DCIS
!" Well-differentiated invasive breast cancer
!"Colloid carcinoma
!" MRI dense breast
!"High background enhancement
!" Colloid carcinoma
Normal Examination
!" Background enhancement
!"Usually progressive over time
#" Diffuse
!"Hormonal enhancement
!" Image between day 5 and 12
!" Many false positives if imaged at other
Figure 10 times in premenopausal women
Multiple high-signal cysts on T2.

Hormonal Effects
!" Luteal phase day 22 (subtraction)
!" Follicular phase day 10 (subtraction)
Figure 12
Focus and Foci
!" Enhancements < 5 mm Nonenhancing
!"Too small to characterize septations
are well
!" Stable on follow-up usually seen in this
!" Chance of malignancy extremely low &*+,"('-,."/
Benign Lesions [Figure 11]

!" Fibroadenoma
!" Cysts
!" Lymph nodes
!" Fat necrosis Mass Shape
!" Hamartoma !" Round
!" Cysts (Post gadolinium) !" Oval
!" Lobulated
!" Irregular
!"32% cancer
!"Irregular (angiosarcoma)
Mass Margins
!" Smooth
Figure 11 !" Spiculated
!"80% cancer
Cysts can show
some mild !" Irregular
enhancement !" Smooth (Epidermal inclusion cyst)
of the walls
but no internal Mass Margins [Figure 13]
enhancement. !" Spiculated (Invasive ductal carcinoma)
Is MRI D1#.,),21+3"%+Benign Lesions?

!" Cyst
!" Fibroadenoma
!"Benign spatial characteristics
!"Nonenhancing septations
!"Type 1 curve Figure 13 A & B
!" Fatty lesions Left Image: Enhancing spiculated mass was invasive
!"Hamartoma ductal carcinoma.
!"Lipoma Right Image: Gross specimen of lesion shows
!"Fat necrosis corresponding mass with spiculations.
!" Lymph node
!"Benign spatial characteristics
!"Fatty hilum Mass Internal Enhancement Pattern
!" Benign lesions often hyperintense on T2 !" Homogeneous
!" Heterogeneous
Fibroadenoma [Figure 12] !" Rim
!" Benign spatial characteristics !"Cancer, fat necrosis, cyst with
!" Nonenhancing septations [Figure 10] $/43..3)$"/
!" Type 1 curve !"40% cancer
!" Dark internal septations
Fatty Lesions !" Enhancing septations
!" Hamartoma !" Central enhanced nidus
!" Homogeneous (invasive ductal carcinoma)
Mass
!" 3D lesion
!" Evaluate shape, margins, and internal
enhancement

Mass Internal Enhancement Pattern Distribution - Non-Mass
[Figure 14] !" Segmental (DCIS)
!" Heterogeneous (invasive lobular !" Regional (DCIS)
carcinoma)
!" Rim enhancement (invasive ductal Internal Enhancement Pattern - Non-
carcinoma) [Figure 13] Mass
!" Dark septations (8%+"30'/".3J !" Homogeneous
!" Enhancing septations (invasive ductal !" Heterogeneous
carcinoma) !" Punctate
!"Foci
!"25% cancer
!" Clumped
Figure 14 !"60% cancer
!" Reticular
Rim
!" Homogeneous (DCIS)
enhancement
characteristic
for Associated Findings
carcinoma. !" Skin or nipple involvement
!" Signal void
!" Muscle or chest wall invasion
!" Dilated ducts
!" Adenopathy
Non-Mass Enhancement DCIS [Figure 16]

!" Enhancement without 3D characteristics !" Curves not useful
!" Distribution !"Many cases of DCIS show no washout
!" Internal enhancement pattern #" Usually cases with slow initial
!" Symmetry or asymmetry enhancement
!" Non-mass enhancement
Distribution – Non-Mass !"Clumped, ductal, linear, segmental
!" Focal
!"< 25% of a quadrant
!" Ductal
!"60% cancer
!" Linear
!"Not ductal orientation
!"31% cancer
!" Segmental
!"Multiple ducts
!"78% cancer
!" Regional
!"Not ductal or segmental
!"21% cancer
Figure 16
!" Diffuse
!" Focal (DCIS) Diffuse non-mass enhancement lateral left breast was
DCIS.
Distribution – Non-Mass [Figure 15]
!" Ductal (DCIS)
!" ;$/'3+(H#)+".3&(8%+"#$#J(
Invasive Carcinoma [Figure 17]
!" Ductal
!" Lobular
!" Special types
Figure 15 !" Irregular mass
Linear !" Irregular or spiculated margins
enhancement !" Rim or heterogeneous enhancement
does not
follow the
course of the
ducts, stromal
&*+,4%4)%-)3?%4)
case.

Figure 17
Irregular
mass
posterior
lateral
right breast
touches but Figure 18
does not
enhance the
chest wall, Irregular
therefore no enhancing
chest wall mass was
involvement. invasive
lobular
carcinoma.
Special Types
!" Colloid carcinoma
!" K/43..3)"+A(23+2$/".3
!" Adenoid cystic carcinoma
!" Metaplastic carcinoma
Invasive Lobular Carcinoma [Figure 18]
Sarcoma Conclusion
!" Angiosarcoma
!" Changes treatment plan in 15%-30% of
!" Sarcoma with osseous differentiation
cases
Conclusion !"Larger lumpectomy or prelumpectomy
!" MRI is a powerful tool in cancer diagnosis chemotherapy
!" C3/(8/0(23/2'+(/")(#''/("/(")*'+($.3-$/- !"Mastectomy
!"Problem solving #" But rate of change to mastectomy
!"High risk screening is greater than recurrence rate if
!" Can monitor chemotherapy better than MRI is not done
other imaging !" We are still learning
References
1. Bartella L, Liberman L, Morris EA, Dershaw DD. Nonpalpable Mammographically Occult Invasive Breast
Cancers Detected by MRI. Am J Roentgenol 2006;186:865-70.
2. Jie Li, Dershaw DD, Lee CH, Kaplan J, and Morris E. MRI Follow-Up After Concordant, Histologically Benign
Diagnosis of Breast Lesions Sampled by MRI-Guided Biopsy. Am J Roentgenol 2009;193:850-55.
3. Kuhl CK, Schild HH, Morakkabati N. Dynamic Bilateral Contrast-enhanced MR Imaging of the Breast:
Trade-off between Spatial and Temporal Resolution. Radiology 2005;236:789-800.
4. Lehman CD, DeMartini W, Anderson BO, Edge SB, and Robinson KG.MRI-Detected Suspicious Breast
Lesions: Predictive Values of Kinetic Features Measured by Computer-Aided Evaluation. J Natl Compr Canc
Netw 2009;7:193-201.
5. Liberman L, Morris EA, et al. Breast Lesions Detected on MR Imaging: Features and Positive Predictative
Value. Am J Roentgenol 2002;179:171-8.
6. Loo, CE, Jelle Teertstra H, et. al. Dynamic Contrast-Enhanced MRI for Prediction of Breast Cancer
Response to Neoadjuvant Chemotherapy: Initial Results. Am J Roentgenol 2008;191:1331-38.
7. Mann RM, Kuhl CK et.al. Breast MRI: Guidelines from the European Society of Breast Imaging. Eur.
Radiol. 2008;18:1307-1318.
8. Rush Port E, Park A, Borgen PI, et al. Results of MRI Screening for Breast Cancer in High-Risk Patients
with LCIS and Atypical Hyperplasia. An Surg Oncol 2007;14:7.1051-7.
9. Saslow D, Boetes C, et al. for the American Cancer Society Breast Cancer Advisory Group. American
Cancer Society Guidelines for Breast Screening with MRI as an Adjunct to Mammography. CA Cancer J
Clin, Mar 2007;57:75-89.
10. Schnall MD, Blume J, et.al. Diagnostic Architectural and Dynamic Features at breast MR Imaging:
Multicenter Study. Radiology 2006; 238:42-53.
11. Wang LC, DeMartini WB, Partridge SC, Peacock S, and Lehman CD. MRI-Detected Suspicious Breast
Lesions: Predictive Values of Kinetic Features Measured by Computer-Aided Evaluation Am J Roentgenol
2009;193: 826-31.
772
Breast 4'&/,#/'),".(
Getting Great Mags [Figure 1]

!" C"/$/-()*'(8'&0("6(5$'I()"()*'(3+'3("6(
interest reduces scatter
!" Spot compression reduces breast
thickness reducing scatter and decreases
exposure time Figure 2
Metallic
artifact from
electrocautery
Figure 1 can also mimic
$"#$%&$"3%,-4/)
Cone to reduce
scatter and
spot to reduce
thickness,
thereby reducing
scatter and
exposure time.
Dermal C'&/,#/'),".(++++++++[Figure 3]
!" Cause: Ca++ in sebaceous
glands
!" Location: Think folds! Cleavage,
inframammary fold, axilla
BI-RADS Morphology !" Appearance: Grouped (bear paw or foot
!" Typically benign print), polygonal shape
!"Dermal Figure 3
!"Vascular
!"Milk of calcium The “tattoo” sign
!"Lucent centered (fat necrosis) in characteristic
!"Dystrophic of dermal
!"Popcorn-like calcs. They do
not change
!"Large rod-like (secretory) relationship
!"Suture to each other
!"Round in different
!"Punctate projections.
!" Intermediate
!"Amorphous or indistinct
!"Coarse heterogeneous Tangential View [Figure 4]
!" Suspicious
!"Fine, linear branching
!"Fine pleomorphic
Breast C'&/,#/'),".(++++++[Figure 2]
!" @+)$632)#(.$.$2D$/-(23&2$823)$"/#
!"Deodorant
!"Powder (Talc)
Figure 4
!"Ointment (zinc oxide)
!"Debris (sand/dirt)
!"Absence of emulsion Stromal C'&/,#/'),".(
!" Sutural
!" Vascular
!" Fat
!"Lucent centered (fat necrosis)
!" Fibroadenomas
!"Coarse heterogeneous
!"Coarse (popcorn-like)
Breast !"#$%&$"3%,-4 Breast Radiology

773
Vascular C'&/,#/'),".(++++++[Figure 5] Ductal C'&/,#/'),".(
!" Cause: Atherosclerosis !" Linear in morphology or distribution
!" Location: Arterial walls because lining up along a duct
!" Appearance: Parallel, linear !" Either:
!"Large rod-like (secretory)
#" Pathognomonically benign
appearance
!"High-grade DCIS
#" Often pathognomonic appearance
Large Rod-Like C'&/,#/'),".(++++++[Figure 7]

Figure 5 !" (Secretory or plasma cell mastitis)
!"Cause:
Early #" Probably due to involution. Do not
vascular see in premenopausal.
calcs can
mimic !"Location:
&-'@)#%-'"+) #" Periductal or intraductal
$"#$%&$"3%,-4/ !"Appearance:
#" Bilateral, needle-like, oriented
toward the nipple
Fat Necrosis/Oil Cyst [Figure 6]
Figure 6 A, B & C
Due to trauma- Figure 7

A, B & C
surgery- lumpectomy,
5ABC)0"64@)+'(1$3%,-D) Dashes- NO
radiation, seat belt DOTS.
injury. Fat necrosis
calcs can resolve
over time since they
represent a healing
process.
Ductal Carcinoma in Situ (DCIS) [Figure 8]

!" C"/8/'0()"()*'(.$&D(0,2)
!" BA!$23&&A(!+'#'/)#(3#(23&2$823)$"/#
!"Ductal = high grade
!"Lobular = low/intermediate grade
Epithelial C'&/,#/'),".(
!" Ductal
!"Linear in either morphology or Figure 8
distribution
Ductal
!"High-grade DCIS or secretory Carcinoma in
!" Lobular Situ (DCIS).
!"Variable morphology and distribution
!"Fibrocystic, sclerosing adenosis, low-
or intermediate-grade DCIS

774
Atypical Ductal Hyperplasia (ADH) Milk of Calcium [Figure 11]
[Figure 9]
!" Cellular atypia incomplete for diagnosis of
DCIS by either extent or morphology
!" Core biopsy with ADH
!"18%-50% upgraded to DCIS and/or
IDC at surgical biopsy
!"Excision always indicated
Figure 11 A, B & C
Cause: Dilated lobules (FCC)
Figure 9 Appearance: CC= round (pearls)
MLO= linear (teacups)
Atypical
Ductal
Hyperplasia
(ADH). Coarse Heterogeneous Calcs
!"Fibroadenoma
!"Papilloma
!"FCC
!"DCIS, often high grade
Lobular C'&/,#/'),".(
!" 7,'()"(23&2$823)$"/("6(0'%+$#d2'&&,&3+( C'&/,#15+Fibroadenoma [Figure 12]
material !" Cause:
!" Round, punctate, amorphous !"Degeneration
!" May be due to: !" Location:
!"Fibrocystic change, including milk of !"Anywhere
calcium !" Appearance:
!"Sclerosing adenosis !"Early - peripheral in nodule
!"Intermediate or low-grade DCIS !"Late - coarse, lobulated
!"@!!'3+3/2'($#(/")(#!'2$82W(``_(Z>?W
20%
Round C'&/,#/'),".(++++++[Figure 10]

!" Typically benign Figure 12
!" Baseline mammo
!"Probable benign (BI-RADS 3)
!"6/12/24 month follow up
!" NEW?
!"Not BI-RADS 3! High-Grade DCIS [Figure 13]
!" Fine linear branching
!" Fine pleomorphic
!" Coarse, heterogeneous
Figure 13
A&B
Two common
patterns
with high/
intermediate-
grade DCIS.
Figure 10
A,1-()$"#$%&$"3%,-4/

775
When is US Helpful in the Evaluation of Frequency of CA by Calc Descriptors
C'&/,#/'),".(6
!" `3&!3%&'(8/0$/-("/(2&$/$23&('L3.
!" Focal asymmetry or mass associated with
)*'(23&2$823)$"/#
!" Goal – identify invasive carcinoma
DDx Coarse Heterogeneous [Figure 14]

C'&/,#/'),".(
!" DCIS, often high-grade
!" Fibroadenoma
!" Papilloma
!" Fibrocystic change
!" Does stability help? Yes!
Breast C'&/,#/'),".(7+Conclusion
!" Most undergoing biopsy are intermediate
risk
!" Worst distributions: segmental or linear
!" b"+#)(."+!*"&"-AN(8/'1(&$/'3+(%+3/2*$/-
!" M#'("&0(8&.#(6"+(2"3+#'(*')'+"-'/'",#(
calcs
!" F&0(8&.#(&'##($.!"+)3/)(I$)*(3."+!*",#(
calcs
!" US helpful to identify invasive component
when DCIS is suspected
!" Judge by worst features!
Figure 14
C"-"8'.'-39)E4'),#()&#.4)"-()(%43+%*13%,-/
F'&-'()"-()$?"-8%-8)4#,G#>),:'+)3%.'HI72ABF;)J@)
New/increasing or segmental/linear distribution---
Biopsy.
DDx Amorphous C'&/,#/'),".(++++[Figure 15]

!" :$%+"2A#)$2(2*3/-'(H:CCJd8%+"#$#(]R?(
!" DCIS 20%
!"Low grade 60%
!"Intermediate grade 28%
!"High grade 12%
!" Sclerosing adenosis 7%
!" Does stability help? Yes!
Berg WA. Radiology. 2001.
Figure 15
Management: Use distribution.

K+,16'(),+)4'8.'-3"#)222I%,64>)L,#()&#.4)#'44)
important), Regional- Consider biopsy, Diffuse---BI-
RADS 2.

776
8.9(9'&+:%1'()+4'./1%(7+;"<+)"+=>0'.5+)?1+@@>

Unusual Types of Breast Cancer
!" Invasive lobular carcinoma (8%)
!" Subtypes of ductal carcinoma
!" Stromal tumors
!" Metastatic neoplasms
Invasive Lobular Carcinoma [Figure 1]

!" 6%-9% of breast cancers
!" Grows in single-layer sheets of cells
HK/0$3/(8&$/-J
Figure 2 B & C
Figure 1 A & B
Invasive Lobular Carcinoma. FNA lower sensitivity than for IDC, more commonly
associated with positive margins at excision, more
frequently treated with mastectomy.
Peritoneal metastasis is common. Can present on
Compared to Invasive Ductal Carcinoma imaging with the “shrinking breast.”
!" Invasive lobular carcinoma is:
!"<"+'(0$682,&)()"(0$3-/"#'("/(
mammography or clinical exam
!"Typically larger at diagnosis MR to Evaluate Extent of DZ [Figure 3]
!"Usually grade I, sometimes grade II !" MRI shows more extensive disease than
!"Lymph node metastasis less common mammography in 39% of ILC cases
for same size lesion
48-Year-old Woman With Palp Lump

Left Breast [Figure 2]
Figure 3 A & B
MRI sensitivity 93.9% for ILC.
Path correlation of size 0.81 to 0.97.
Washout pattern less common than for IDC.
Radial Sclerosing Lesion [Figure 4]

!" aka “radial scar”
!" 10%-30% associated with ADH, DCIS,
Figure 2A
Tubular CA
FNA lower sensitivity than for IDC, more commonly !" 29% of lesions suspected of being a radial
associated with positive margins at excision, more sclerosing lesion based on imaging are
frequently treated with mastectomy.
actually invasive carcinomas
Peritoneal metastasis is common. Can present on
imaging with the “shrinking breast.” !" Management controversial
Unusual Breast Cancers Breast Radiology

777
Figure 6
Figure 4 Tubular
can mimic
radial scar
Radial
at histology.
Sclerosing
Radial
Lesion.
scar has a
basement
membrane
with
myoepithelial
cells while
tubular CA
does not.
Architectural Distortion Without a
Central Mass (The “Dark Star”) [Figure 5]
!" Invasive lobular carcinoma Mucinous Carcinoma [Figure 7]
!" Radial sclerosing lesion !" 2% of breast cancers
!" Surgical scar !" Soft if palpable
!" Low-density, round, well-circumscribed, or
lobulated margins
Figure 7
Mucinous is
hyperintense
on T2. This
is also seen
with IDC
especially
if tumor
necrosis.
Medullary Carcinoma
!" < 2% of breast cancers
Figure 5 A & B !" Younger women
!" F6)'/(+",/01(I$)*($&&W0'8/'0(.3+-$/#
Architectural distortion without a central mass. !" Fast growth, but good outlook
!"Often present as palpable masses
!" Histology mimics poorly-diff IDC, but
Breast Cancer Types better prognosis than IDC-NOS
!" Ductal (85%)
!"Ductal Carcinoma In Situ (DCIS) Papillary Carcinoma [Figure 8]
!"Invasive ductal carcinoma !" 1%-2% of breast cancers
(IDC) !" Presentation
#" E")(F)*'+I$#'(G!'2$8'0(HEFGJ !"Nipple discharge
#" Tubular !"Palpable large subareolar mass
#" Medullary !"Intracystic cancer
#" Mucinous
#" Papillary
Tubular Carcinoma [Figure 6]

!" 1% of breast cancers Figure 8
!" Very low grade
!" Usually present as small spiculated Papillary
masses; spicules often longer than the Carcinoma.
central mass
!" Often multifocal
!" Excellent prognosis
!"=P?(23,#'(#!'2$82(H#,+5$53&(3)(Z>(
years)

778
Upgrade Rate with High-Risk Histologies
on CNB
Phyllodes Tumor [Figures 9 & 10]

!" Typical presentation: Figure 10
!"Rapidly growing palpable mass in
Grading (no longer malignant or benign)- low,
middle-aged to older women intermediate, or high grade.
!" Circumscribed, large, round, or oval mass Treated with wide excision. Hematogenous spread
!" <3A(.$.$2(8%+"30'/".31(%,)(+3!$0( (behaves like sarcoma).
growth and wrong age group
Juvenile (Giant) Fibroadenoma

[Figure 11]
!" Rapid growth
!" Typically occur during puberty or early
adulthood
!" Histologically same as pericanalicular
8%+"30'/".3#
Figure 9 A, B, C & D
Phyllodes can undergo sarcomatous degeneration.
An 18-year-old adult with rapidly enlarging mass.

779
!" More commonly seen postradiation
therapy
!" Risk increases 5 years posttherapy
!" `""+&A(0'8/'0(*$-*&A(53#2,&3+(.3##1(/")(
at lumpectomy bed
!" May be cutaneous
Figure 12
Metastasize
hematogenously.
Poor prognosis.
57-year-old
woman, s/p Figure 13 E & F
lumpectomy and
radiation therapy Rhabdomyosarcoma and leukemia.
7 years earlier.
Metastatic Lesions in the Breasts

Rhabdomyosarcoma and Leukemia
[Figure 14]
[Figure 13]
!" 1.2% of cancers in the breast
!" Rare
!" 9+'3#)(%'2".'#(8+.'+T(<3A("+(.3A(/")(
!" K/8&)+3)$5'(0'!"#$)#("6(),."+
have discrete palpable mass.
!" Primary rhabdo or leukemia of the breast
!" In order of frequency
extremely rare
!"Lymphoma
!" Typically advanced disease, but may be
!"Melanoma
8+#)(#$-/("6(+'2,++'/)(0$#'3#'
!"Rhabdomyosarcoma
!" K&&W0'8/'0(3+'3#("6(#*30"I$/-(I$)*(
!"Lung
hyperechoic regions on ultrasound
!"Ovarian
!"Renal
!"Cervical
!"Leukemia
Figure 14 A & B
Metastatic lesions in the breasts.
Rhabdomyosarcoma and leukemia.

780
Unusual Breast L1(,".(7+Summary
!" Invasive lobular carcinoma is highly
$/8&)+3)$5'1(&$D'(3(#!$0'+I'%(
!" Subtypes of invasive ductal carcinoma
(tubular, mucinous, medullary, papillary)
3+'()A!$23&&A(-+30'(K1(I'&&W0'8/'0(H'L2'!)(
tubular), and slow-growing (except
medullary)
!" `*A&&"0'#(3/0(8%+"30'/".3(+'!+'#'/)(
ends of a spectrum of disease
!" Primary breast cancer must be excluded
with unilateral axillary adenopathy
Figure 14 C & D
Metastatic lesions in the breasts.
Axillary Adenopathy
!" Bilateral
!"Non-Hodgkin lymphoma
!"Leukemia
!"Metastasis
!"HIV
!"Reactive
!"Histoplasmosis
!" Unilateral
!"Ipsilateral invasive breast carcinoma
!"Metastasis
!"Local dermatologic process
!"Potentially all bilateral processes
Paget Disease
!" Nipple eczema – moist, scaling. Leads to
ulceration and erosion.
!" 1%-5% of breast cancers
!" 95% have underlying breast cancer,
usually high-grade DCIS
!" Intraductal papilloma can cause similar
2&$/$23&(8/0$/-#1(%,)(/")(*$#)"&"-$2(8/0$/-#
PASH
!" PseudoAngiomatous Stromal Hyperplasia
!" Spaces that look like vessels
!" May be concordant with biopsy for focal
asymmetry
Granular Cell Tumor

!" Benign
!" Usually in tongue or SQ. 5% in breast
!" F6)'/(8+.(!3&!3%&'(&,.!(
!" K&&W0'8/'0(.3##($/(#,%2,)3/'",#(+'-$"/("6(
breast on mammography
!" Must be excised as may be locally
aggressive
Tobin CE. RadioGraphics. 1996.
Balzan SM. Eur J Surg. 2001.

781
782
Breast Masses, Benign and Malignant
Angela M. Pansera, DO, Maj, USAF, MC

Outline
!" Breast imaging lexicon
!"Mass vs asymmetry
!"Mammographic criteria for masses
!"Sonographic criteria for masses
!" Associated Findings
!"Skin thickening, nipple retraction,
Adenopathy
!"Additional features of masses to
consider
Breast Imaging Lexicon

!" Mass = space occupying lesion seen in
two projections
!"Seen on 2 views mammographically
!"Volumetric on ultrasound and MRI
!" Asymmetry = seen on a single projection
!"Global asymmetry = involves large Figure 1 C & D
portion of the breast (at least one
Global asymmetry is seen on only a single projection
quadrant) and involves at least one breast quadrant.
!"Focal asymmetry ocupa menos de 1 cuadrante
Global Asymmetry [Figure 1] Mass [Figure 2]
Figure 1 A & B
Global asymmetry is seen on only a single projection
and involves at least one breast quadrant.
Mass is a space-occupying lesion seen in two different
projections. IDC.
Breast Masses, Benign and Malignant 783 Breast Radiology
Mammographic Criteria for Masses
!" Shape
!" Margin
!" Radiographic density
Shape
!" Regular
!"Round
!"Oval
!"Lobular
!" Irregular
Regular Shape [Figure 3]

!" Round or oval
!" Cyst
!" Intracystic papilloma
!" Papillary carcinoma
!" Invasive ductal carcinoma
Figure 4 A, B & C
Undulating contour - IDC, IDC, and FA.
Circumscribed Margins [Figure 5]

!" Sharply bordered
!"e(PR?("6(.3+-$/(.,#)(%'(I'&&(0'8/'0
!" Abrupt transition between lesion and
surrounding tissue
!" “Always” benign
!"< 2% malignant
!"Highest NPV of all characteristics
!" Lymph node
!" Papilloma
!"Intraductal mass near nipple, most
Figure 3 A, B, C & D common
Regular shape includes spherical, ball-shaped, circular, !"May see internal vascularity in stalk
,+)#,*1#"+/);%.6#')*+'"43)$>43@)&*+,"('-,."@)"-() !"Most common cause for bloody
intraductal papilloma. discharge
!"Excision recommended: Can be focally
involved by ADH or DCIS
!"DCIS
Regular Shape – Lobular [Figure 4]
Irregular
!" Often malignant
!"Invasive ductal carcinoma
!"Benign papilloma
!"Fibroadenomatoid nodule
Margin son la descripción más importante

!" Circumscribed
!" Lobulated
!" K/0$#)$/2)(H$&&W0'8/'0J
!" Obscured
!" Spiculated Figure 5A
Classic US appearance of a lymph node.

Echogenic hilum containing normal hilar vessels.

I.5,(),./)+A,&&B51#.15C+Margins
!" Raises concern that there may be
$/8&)+3)$"/
!" 9'#)(#''/(I$)*(.3-/$823)$"/
!" M#,3&&A(#$-/$8'#(3(.3&$-/3/2A
!"50% malignant
Obscured [Figure 7]
!" Margin can not be seen adequately
because of overlying tissue
!" Term typically reserved for screening
mammograms
Figure 5B !" Spot compression usually resolves issue
Classic US appearance of a lymph node. !" Must differentiate
Echogenic hilum containing normal hilar vessels. !" Adenoid cystic carcinoma
!" Rare
!"Best diagnostic clue: circumscribed,
Lobulated Margins lobular mass
!" Macrolobulated !"Excellent prognosis
!"A few long, gentle lobulations
!" Microlobulated
!"Many short lobulations
Macrolobulated Margins
!" Large lobulations Figure 7 A,
B, C & D
!" Almost always benign
!" Fibroadenoma Margin that
is hidden by
Microlobulated Margins [Figure 6] superimposed
!" Small lobulations or adjacent
normal tissue.
!" Often malignant
Used when
!"25% malignant the physician
!" 67% microlobulated masses on US are believes
malignant the mass is
circumscribed
but the
margin is
hidden.
IDC.
Spiculated [Figure 8]
!" Radiating strands from the margin of the
mass
!" Spiculated margins almost always
malignant
!" 90% malignant
!" Highest PPV of all imaging characteristics
!" Occasional exceptions: radial scar and fat
Figure 6 A & B necrosis
Microlobulated.
Multiple small undulations. IDC and IDC.

Figure 8 A & B
Lines radiating
from margin
of mass.
Almost always
malignant
(90%).
Exceptions
include radial
scar and fat
necrosis. IDC.
Figure 9 A & B
Hematoma and IDC.
Most breast cancers are high or isodense to
&*+,8#"-(1#"+)3%441'/
Low Density [Figure 10]
Shape and Margin Related

!" <3+-$/(0'8/'#()*'(-+"I)*(!3))'+/
!" \+"I)*(!3))'+/(0'8/'#()*'(#*3!'
Describe Shape and Margins? Figure 10 A & B

All lesions containing fat, oil cyst, lipoma, galactocele,
Radiographic Density Densidad en relación al lymph node, mixed lesions such as hamartoma or
!" High tejido fibroglandular &*+,"('-,#%6,."@).,43)#%M'#>)+'6+'4'-3)")*'-%8-)
!" Equal (isodense) mass.
!" Low
!" Fat-containing BIRADS 2
Fat Containing
Density !" Lymph node Hamartoma: apariencia de mama
!" High is often malignant or hematoma !" Hamartoma dentro de la mama
!" Intermediate is often malignant
!" Low is almost always benign Same Descriptors Different Modality…
!" Lesions containing fat are benign Shape, Margins, and Density?
!"Biopsy if rapidly growing
Usefulness of Density
High Density [Figure 9] !" Margins and shape much more useful
!" Colloid carcinoma !" Fat-containing category very useful
!" Schwannoma
!" Hematoma Sonographic Characteristics
!" IDC !" Shape
!" Orientation
Intermediate Density !" Margin
!" Spindle cell carcinoma !" Lesion boundary
!" Invasive ductal carcinoma !" Echo pattern
!" Posterior acoustic features

Shape
!" Benign
!"Regular – round or oval (includes
two or three undulations ie
macrolobulated)
#" 10% malignant (usually round)
!" Malignant
!"Irregular
#" Not round or oval
Shape – Regular Figure 12 A & B

!" Cyst Left Image: US reveals a cystic and solid mass with
!" Fibroadenoma indistinct margins. Bx proven IDC.
Right Image: Oil cyst after reduction mammoplasty
in a 28-year-old woman with a palpable mass in the
Shape - Irregular region of postoperative scarring. Tangential spot
!" Invasive ductal carcinoma ."8-%&$"3%,-)."..,8+".@),*3"%-'()"<3'+)6#"$'.'-3)
!" Invasive lobular carcinoma of an external marker, shows a well-circumscribed
fat-density mass with a characteristically benign
Orientation – Parallel appearance. Bx proven fat necrosis.
!" Fibroadenoma
!" Carcinoma
!" Benign criteria = width to AP ratio greater
than 1.4
Orientation – Nonparallel (Taller Than Margin – Angular [Figure 13]
Wide) [Figure 11]

!" Invasive ductal
Figure 13 A & B
Angle between mass and surrounding tissue may be

Figure 11 A & B
obtuse or acute. Angulated margins are associated
Mass grows preferentially in AP dimensions, which is with malignancy in 60% of cases.
across normal tissue planes, indicating an aggressive Two cases of Bx proven IDC.
process such as breast carcinoma.
Margin tb en us es el criterio mas importante.

!" Circumscribed Margin – Macrolobulation
!" Not circumscribed !" Fibroadenoma
!"Indistinct
!"Angular
Margin – Microlobulation [Figure 14]
!" Fibroadenoma
!"Microlobulation
!" Metastatic melanoma
!"Spiculated
!"Metastases to the breast: incidence
Margin – Circumscribed 1%
!" Smooth outline !" Primaries
!" Thin capsule !"Leukemia/lymhoma > melanoma >
ovarian CA > lung CA, sarcoma
Margin – Indistinct [Figure 12] !"In up to 40%, no history of primary
!" Granular cell tumor CA
!" Invasive ductal !"Invasive ductal
!" Fat necrosis
!" Benign
!"Usual ductal hyperplasia, apocrine
metaplasia, and adenonosis

Describe Shape, Orientation, and Echo
Pattern? [Figures 16 & 17]
Figure 16
Abscess.
Ultrasound
reveals a
complex
cystic-solid
mass with
Figure 14 A & B thick wall or
septations.
Microlobulation have short-cycle undulation (more Hyperemia
than three) with a scalloped appearance. 67% of is commonly
microlobulated masses on US are malignant. Internal seen in
:"4$1#"+)0,G)%4)"#4,)-,3'(),-)$,#,+)0,G)%."8'4/) surrounding
Biopsy-proven IDC. tissue. Tx:
systemic
and local
Margin – Spiculated antibiotics.
!" Invasive ductal Percutaneous drainage for cavities < 3 cm; cavities 3-4
cm may require a catheter drainage.
Describe Shape, Orientation and Margin
Lesion Boundary
Figure 17
!" Transition zone between mass and tissue
!"Abrupt Subacute
!"Echogenic halo (commonly seen in Hematoma.
carcinomas and abscesses) Irregular
margins
Lesion Boundary – Abrupt with thick
hyperechoic
!" Cyst walls and
!" Complicated cyst mural
nodules and
Echogenic Halo [Figure 15] avascular
!" Invasive ductal septations.
No internal
vascular
0,G/)C,43)
hematoma
resolves
rapidly and
decreases
in size with
time.
Figure 15 A & B Posterior Acoustic Features [Figure 18]

Echogenic halo or wide transition zone at the boundary !" Enhancement
is associated with higher rate of malignancy (70%). !" Shadowing
Biopsy-proven IDC.
Echo Pattern
!" Anechoic
!" Hyperechoic
!" Mixed
!" Complex (complex cystic breast mass)
!"Complex cystic breast masses have a
substantial chance of being malignant;
malignancy was reported in 23%-
31%*
!" Complicated cyst
!" Isoechoic Figure 18 A & B
!"Contains calcs
Posterior acoustic enhancement is an indeterminate
!" Hypoechoic &-(%-8/)N,43'+%,+)"$,143%$)4?"(,G%-8)%4)4146%$%,14)"-()
*Doshi, Devang et al, “Complex Cystic Breast Masses: Diagnostic often seen with invasive carcinoma. Both lesions are
Approach and Imaging Pathologic Correlation,” RadioGraphics 2007; biopsy-proven IDC.
27:S53-S64.

Posterior Shadowing Negative and Positive Predictive Values
!" Invasive ductal carcinoma of US Features
!" Granular cell tumor
Describe Shape, Orientation, Margin,

Lesion Boundary, Echo Pattern, Doppler
Ultrasound, and Posterior Acoustic
Features [Figures 19 & 20]
!" U53&,3)'#(%&""0(4"I()"()*'(),."+
!"C3/2'+#(*35'(."+'(4"I(I$)*(&'##(
resistance
!" Many false negatives and false positives
!" Not useful
Raza, et al. US of Breast Mass Categorized as

BI-RADS 3, 4, 5: pictorial review of factors in-
01'-$%-8)$#%-%$"#)."nagement. RadioGraphics.
2010;30:1199-1213.
Associated Findings on Mammography

!" Skin thickening
!" Nipple retraction
Figure 19 A & B
!" Adenopathy
!" Paget disease of the nipple
62-year-old woman with abnormal mammorgram.
7-&#3+"3%-8)#,*1#"+)$"+$%-,."/ Skin Thickening [Figure 21]
Figure 20 A & B
Invasive duct
Invasive lob.
BI-RADS US Descriptors
Figure 21 A & B
Do not forget to notice the adjacent skin thickening.
IDC.
Associated Findings on Ultrasound

Raza, et al. US of Breast Mass Categorized as !" Axillary adenopathy
BI-RADS 3, 4, 5: pictorial review of factors in-
!" Multiple lesions
01'-$%-8)$#%-%$"#)."nagement. RadioGraphics.
!" Skin thickening
2010;30:1199-1213.
!" K&&W0'8/'0(I$)*($/)'/#'(!"#)'+$"+(32",#)$2(
shadowing without discrete mass

Associated Findings on Ultrasound Malignant US Characteristics
[Figure 22] !" Marked hypoechogenicity
!" Metastatic disease to the axilla !" Spiculation
!" Angular margins
!" Taller than wide
!" Posterior shadowing
!" Branch pattern
!" Duct extension
Well-Circumscribed Mass
!" Cysts
!" Fibroadenoma
!" Papilloma
!" Hematoma
!" Lymph node
Figure 22 A & B
!" Malignancy (primary or mets)
Abnormal morphology of the lymph node with !" Phyllodes tumor
':%('-$'),<)$,+3%$"#):"4$1#"+)0,G/)I%,64>)6+,:'-) !" Skin lesion
metastatic breast cancer to ipsilateral axillary lymph
node.
Fat-Containing Masses
!" Oil cyst
!" Galactocele
Bilateral Lymphadenopathy !" Lipoma
!" Lymphoid hyperplasia !" Lymph node
!" Collage vascular disorders !" Hamartoma
!"Rheumatoid arthritis (RA)
!"Systemic lupus erythematosus (SLE) Multiple Masses
!" Granulomatous disease (sarcoid, TB) !" Cysts
!" HIV !" Fibroadenomata
!" Silicone adenopathy !" Papillomatosis
!" If unilateral adenopathy $ must exclude !" K/8&)+3)$/-(23+2$/".3
occult breast CA !" Lymph nodes
!" Silicone granulomas
Additional Features of Masses to !" Hamartomas
Consider on Mammography !" Skin lesions
!" @##"2$3)'0(23&2$823)$"/# !" Phyllodes tumors
!" Effects on surrounding tissue !" Mets/lymphoma
!" “Halo” sign on mammography – a 1
mm sharp lucency surrounding the Spiculated Mass
mass, related to benign masses actively !" Carcinoma
changing shape, ie breast cyst !" Radial scar
!" Satellite lesions !" Fat necrosis
!" Multiple lesions !" Sclerosing adenosis
!" G)3%$&$)A(H6+".(!+'5$",#(8&.#J !" Postoperative scar or hematoma
Benign Characteristics Conclusions

!" Well-circumscribed !" BI-RADS assessment based on analysis of
!" Round or oval multiple descriptors with most suspicious
!" Round or oval calcs in tight clusters feature dictating assessment and
!" US recommendation
!"Hyperechoic !" For a lesion with benign feature, short-
!"Ellipsoid term follow-up is a reasonable option
!"Gentle bi- or trilobed (BIRADS 3)
!"Thin echogenic pseudocapsule !" For an older patient, the threshold to
biopsy should be lowered
Malignant Charateristics !" Masses that are characteristically benign
!" Spiculation can be left alone
!" K&&W0'8/'01(.$2+"&"%,&3)$"/ !"Lymph nodes
!" Malignant-type calcs !"Cysts
!" Skin thickening and retraction !"Hamartoma
!" Architectural distortion !"Epidermoid

References
1. Rahbar, Guitar et al. Benign versus malignant solid breast masses: US differentiation. Radiology 1999.
2. V3f31(')(3&T(MG("6(9+'3#)(<3##(C3)'-"+$f'0(3#(9KWV@7G(^1(]1(RN(!$2)"+$3&(+'5$'I("6(632)"+#($/4,'/2$/-(
clinical management. RadioGraphics Sep 2010;30:1199-213.
3. Shin Jung, et al. Probably benign breast masses diagnosed by sonography: Is there a difference in cancer
rate according to palpability? Am J Roentgenol April 2009:192.
4. Vade, Aruna, et al. Role of breast sonography in imaging palpable solid breast masses. Am J Roentgenol
191, Sep 2008.
5. Yang, Weis, et al. Benign and malignant breast masses and axillary nodes: evaluation with echo-
enhanced color power doppler US. Radiology 201;220:795-802.
6. The Breast Imaging Reporting and Data System® (BI-RADS®) Atlas. 4th Edition, ACR 2004.
7. Berg, et al. Diagnostic imaging breast. First Edition, Amirsys, Inc. 2006.
8. Doshi, Devang, et al. Complex cystic breast masses: diagnostic approach and imaging pathologic
correlation RadioGraphics 2007;27:S53-S64.
9. Majid, Aneesa, et al. Missed breast carcinoma: pitfalls and pearls. RadioGraphics 2003;23:881-95.
10. <3+#)'&&'+1(;,$#31(')(3&T(b'&&(0'8/'0(.3##'#($/()*'(%+'3#)T(V30$"\+3!*$2#(_"&(=1(E,.%'+(Z1(X3/(Z=Q=1(Z^W
37.

792
Classic Breast Lesions
Angela M. Pansera, DO, Maj, USAF, MC

Most Lesions Are Not S01/,#/ Sternalis [Figure 2]
!" Differentials can be given !" Anatomic variant, occurs in 8% of women
!" High likelihood that diagnoses can be and usually unilateral
made !" G,!'+82$3&()"()*'(`<
!" Is this a cyst or a solid mass? !" Sternal end of the PM and parallel to the
sternum
Aunt Minnie Does Exist !" May mimic a mass in the medial breast on
!" Who is Aunt Minnie and why do we care? CC mammogram
!" No differential is needed
!" Short interval follow-up unnecessary
The Aunt Minnies

!" Normal variants
!" Congenital anomalies
!" Fat-containing lesions
Figure 2 A & B
!" “Classic” breast masses
!" Foreign body
Another medial
!" 9'/$-/(23&2$823)$"/# “mass” on the CC
!" Uncommon entities view is the sternalis
muscle. Only seen
Normal Variants with certainty on the
!" Pectoralis major CC view, when the
!" Sternalis muscle is relaxed.
F'4$+%*'()"4)O0".'2
!" Lymph nodes shaped”. Cleavage
!"Intramammary view or ultrasound
!"Axillary may be helpful to
exclude a true mass.
Pectoralis Major [Figure 1]
Benign Axillary Lymph Nodes

!" Mass low to moderate density
Figure 1 A, B & C
!" G*3+!&A(0'8/'0
!" Round to oval
CC view !" Radiolucent hilus (visible in 78%)
showing the
pectoralis !" < 1.5 cm in the axilla
major as an
incompletely Axillary Adenopathy
seen “mass” !" But, be careful…
medially. !" Consider axillary adenopathy, > 2 cm,
non-fatty replaced
!" If unilateral adenopathy, suspect breast
CA until proven otherwise. Primary breast
CA may not be found in 33% of cases.
!" Watch for microCa++
Classic Breast Lesions Breast Radiology

793
Intramammary Lymph Nodes [Figures 3 & 4]
!" E"+.3&(8/0$/-
!" 28% of breasts
!" May enlarge and shrink in size
!" Circumscribed with hilar notch or fatty
hilum
!" Usually less than 10 mm in size
!" Not related to the usual lymphatic
drainage patterns
!" Usually upper outer quadrant
!" Hypoechoic smooth cortex with echogenic
hilium. Hilar vessels also visualized on Figure 4 E & F
color doppler images.
Classic ultrasound appearance of a benign lymph
!" Watch out for enlarged lymph nodes node. Hypoechoic reniform cortex with prominent
I$)*(3%/"+.3&(2"+)$23&(53#2,&3+(4"I(3/0( echogenic (fatty) hilum. On color dopper images, hilar
decreased echogenic hilium. vessels can also be seen.
Intramammary Lymph Nodes [Figures 5 & 6]

!" Consider metastatic ovarian Ca, breast
Ca, or gold injections
!" But, watch out for axillary and
intramammary lymph nodes with Ca++
Figure 3 A & B
Well-circumscribed sub cm reniform nodule with hilar

notch or fatty hilum. Intramammary lymph node.
Figure 5 A, B & C
Axillary Nodal
!"#$%&$"3%,-4/))
DDx:
Granulomatous
disease:
Tb, sarcoid,
histoplasmosis.
Metastatic
Disease: breast
CA, ovarian
Ca, thryoid Ca.
Figure 4 A, B, C & D Gold deposits
in patients with
Classic ultrasound appearance of a benign lymph intramuscular
node. Hypoechoic reniform cortex with prominent gold injections
echogenic (fatty) hilum. On color dopper images, hilar for RA; clumped
vessels can also be seen. deodorant.

794
Figure 6 A & B
Ultrasound reveals an abnormally enlarged hypoechoic

#>.6?)-,(')G%3?)$,+3%$"#@)"4)G'##)"4)?%#"+@)*#,,()0,G/))
Biopsy proved metastatic breast cancer to ipsilateral
axillary lymph node.
Figure 8 A & B
MLO mammography shows the typical appearance of

Congenital Anomalies ectopic breast tissue in the left axilla. The woman was
!" Polythelia asymptomatic and no further work-up is required.
!"Accessory nipples Aberrant breast tissue more common in the left axilla.
!"2.4% of neonates
!" Polymastia
!"2%-3% of women
!"Axillary breast tissue most common All Lesions That Contain Fat Are Benign
!"Inframammary fold and labia next E>/10)7
most common !" Very rare hamartomas
!" Phyllodes with liposarcoma
Polythelia [Figure 7]
!" Biopsy rapidly enlarging fatty lesions
Hamartoma [Figures 9 & 10]

!" U/23!#,&3)'0(63)(3/0(8%+"-&3/0,&3+()$##,'(
g(8%+"30'/"&$!".3
!" “Breast within a breast”
!" Usu asymptomatic
Figure 7
!" Extremely rare, malignancy may arise in
Accessory contained tissue elements
nipple in
the in-
framammary
crease.
Polymastia [Figure 8]
!" Congenital, but typically becomes Figure 9 A & B
apparent in puberty or lactation
Best diagnostic clue “breast within a breast.”
!" Can be palpable or visible Pseudocapsule, a rim of compressed parenchyma often
!" Can even lactate visible.
Fatty Lesions
!" Hamartoma
!" Lipoma
!" Fat necrosis
!" Galactocele
!" Epidermoid cyst

795
Oil Cyst [Figure 12]
!" Oil cyst after reduction mammoplasty in a
23-year-old woman
!" B3/-'/)$3&(#!")(.3-/$823)$"/(
mammogram, obtained after placement
of an external marker, shows a well-
circumscribed fat-density mass with a
characteristically benign appearance.
Figure 10 A & B
Figure 12
Mixture of sonolucent fat and echogenic glandular
elements on US. Usually oval-shaped and well- Spot
circumscribed. ."8-%&$"3%,-)
view reveals
an oval
Malignant Phyllodes With Liposarcoma radiolucent
mass with
curvilinear
Lipoma [Figure 11]
rim Ca++
!" Benign tumor typical of
!" Radiolucent, circumscribed oval, or round fat necrosis
mass in the left
!" Most common soft tissue tumor in adults; breast s/p
b/l reduction
solitary in women and multiple in men mammoplasty
!" No treatment necessary; may remove 8 years ago.
electively
Fat Necrosis - Progression
Galactocele [Figures 13 & 14]

!" Retention cyst from occulsion of a
lactiferous duct
!" `3)*"-/"."/$2(8/0$/-N(63)W4,$0(&'5'&("/(
upright horizontal beam
!" Palpable, generally painless, freely
mobile mass, in pregnant, lactating, or
early postlactation patient
!" 7L('#)3%&$#*'0(I*'/(.$&DA(4,$0($#(
3#!$+3)'0("+(.3##(I$)*(63)W4,$0(&'5'&(
present on 90 degree lateral
!" “Snowstorm” appearance with mobile
echogenic debris
!" Layering debris
Figure 11 A & B
MLO and CC views shows circumscribed fatty massà

lipoma. Pseudocapsule due to compressed normal
tissue.
Liposarcoma
Fat Necrosis
!" 50% have history of trauma
!" Including surgery and XRT
!" Develop 1.5-5 years posttrauma
!" Oil cyst
!" Develop peripheral rim Ca++
!" C3/(%'(#!$2,&3)'01(0,'()"(8%+"#$#d
desmoplastic rxn
!" Fat necrosis mass(es) decrease over time Figure 13 A & B
!" K.3-$/-(8/0$/-#("5'+&3!(I$)*(.3&$-/3/2A PQ)('8+'')#"3'+"#):%'G)+':'"#4)")<"3201%()#':'#)
!" Ca++ at lumpectomy site within 1.5 years in this 30-year-old lactating woman with a new,
painless mass classic for a glactocele. Aspiration for
more likely residual CA
symptomatic relief or when diagnosis is uncertain.
B46%+"3%,-),<)8#"$3,$'#')>%'#(4).%#M>)01%(/
796
Figure 14
Transverse
ultrasound
images of
a 38-year-
old lactating
woman shows
")01%(2&##'()
mass with
debris seen
to be mobile
with real-time
imaging.
Figure 16 A & B
Ultrasound reveals clusters of microcysts in a
Epidermal Inclusion Cyst [Figure 15] background of echogenic stroma due to increased
!" Benign cutaneous or subcutaneous &*+,4%4/)N'+<,+.)CA)%-)(">4)R2ST)"<3'+),-4'3),<)
menses to diminish false positives.
epithelial cyst arising from obstructed hair
follicle
!" Avoid FNA or core biopsy - contents
"6)'/($++$)3)$/-()"()*'(#D$/1($/43..3)"+A(
response and even abscess may occur
Figure 17 A & B
Figure 15 A & B Mammogram and ultrasound reveals a well-

circumscribed, round, or oval anechoic mass with
Ultrasound reveals a heterogeneously hypoechoic, imperceptible wall and posterior enhancement -
circumscribed mass with posterior acoustic &-(%-84)$,-4%43'-3)G%3?)")4%.6#')*+'"43)$>43)
enhancement corresponding to palpable lump in the (BI-RADS 2). Can aspiration if painful or equivocal on
subcutaneous tissue, classic for an epidermal inclusion imaging.
cyst. If suspected, do not biopsy as there is a high risk
of infection and skin irritation.
Complicated Cyst vs Complex Mass

Fibrocystic Changes (FCC) [Figure 16]
!" Mammographically dense breast with Pneumocystography [Figure 18]
scattered punctate Ca++ in adenosis and
4,2),3)$/-(2A#)#
!" B'+.(h8%+"2A#)$2(0$#'3#'i(#*",&0(%'(
avoided as FCC is considered a spectrum
of normal variation
!" True lateral helpful in depicting benign
milk of calcium
Simple Cyst [Figure 17]

!" :&,$0W8&&'0(+",/01("+("53&(#)+,2),+'(&$/'0(
by epithelium
!" Circumscribed, round or oval anechoic
mass with imperceptible wall and
posterior enhancement
!" G$f'(.3A(4,2),3)'(I$)*(.'/#)+,3&(2A2&'Y(
max size in premenstrual phase Figure 18 A & B
!" Aspiration if painful or equivocal on
imaging N-'.,$>43,8+"6?>@)+'6#"$%-8)3?')01%()G%3?)"%+)%-)
a cyst is one way of decreasing recurrence after
!" Postaspiration instillation of air decreases aspiration.
recurrence
797
Radial Scar
!" Complex sclerosing lesions, not truly scars
!" “Black star”
!" Proposed casus –(&"23&$f'0($/43..3)"+A(
rxn and chronic ischemia with subsequent
slow infarct
!" Prevalence: 0.1-2 per 1,0000
!" Associated with ADH and CA in up to 50% Figure 20
of cases
!" Excisional Biopsy Multiple
high density
masses is
Foreign Body another
!" G$&$2"/'("+(!3+368/ presentation
!"Free injection for free
!"Leakage from implants silicone
!" Surgical drain injection.
!" Wire fragments
!" Extracapsular implant rupture or extrusion
!" Silicone in an intact implant is anechoic
on US
!" Extruded silicone is hyperechoic on US -
“snowstorm”
Caskey CI. et al. RadioGraphics 1999;19:S39-
S51. Sutural C'&/,#/'),".(++++++[Figure 21]
!" Looks like sutures
Free Silicone (Implant Rupture)
!" Usually postradiation therapy
Free Silicone or P'%'3#.+++++[Figure 19]
Figure 21 A & B
;131+"#)$"#$%&$"3%,-4)
typically occur in postXRT
patients.
Surgical Drain
Figure 19 A & B
Wire Fragment
F'-4')&*+,4%4)"-()'U3'-4%:').%$+,$"#$%&$"3%,-4)%-)<+'') Benign C'&/,#/'),".(++
6"+"<&-),+)4%#%$,-')%-V'$3%,-)<,+)"18.'-3"3%,-/ !" Lobular
!" Sutural
!" Coarse or “popcorn-like”
!" Skin
!" Vascular
!" Secretory
Free Silicone [Figure 20]
!" Milk of calcium
!" Egg shell
Lobular C'&/,#/'),".(+
!" Tightly clustered
!" Round
!" Fit together like a jigsaw puzzle

798
Coarse or “Popcorn-Like” [Figure 22]
!" C3&2$8'01($/5"&,)$/-(8%+"30'/".3
!" C3&2$823)$"/(-'/'+3&&A(!'+$!*'+3&
!" Ca++ typically starts in the periphery
Figure 24 A & B
Mammogram shows typical serpiginous parallel-walled

,+)O3+".)3+"$MW)('-4'):"4$1#"+)$"#$%&$"3%,-4/))C">)?":')
O(,32("4?W)%-3'++163'()#%-'"+)$,-&81+"3%,-/
Figure 22 A & B
N,6$,+-2#%M')$"#$%&$"3%,-4)%-)&*+,"('-,."/)
!"#$%&$"3%,-)43"+34)%-)3?')6'+%6?'+>/
Figure 25
Mammogram
Skin C'&/,#/'),".(+++++++++[Figure 23] demonstrates
!" `"&A-"/3&(23&2$8'0(+$/-#(I$)*(&,2'/)( dense rod-like
centers $"#$%&$"3%,-4)
with some
!" B3/-'/)$3&(5$'I(I$&&(2"/8+.(0$3-/"#$# branching
forms seen
in a ductal
distribution
directed to
the nipple.
Milk of Calcium
Figure 23 A & B !" 9'/$-/(#'0$.'/)N(23&2$823)$"/#($/(.32+"W(
;M%-)L('+."#X)$"#$%&$"3%,-4)$"-)*')$,-&+.'()G%3?) or microcysts
tangential view. !" CC view: smudgy or fuzzy round
23&2$823)$"/#
!" LM or ML view: Ca++ are seen as sharply
Vascular C'&/,#/'),".(+++++++[Figure 24] 0'8/'01(2+'#'/)W#*3!'0(#'.$&,/3+1(
!" Parallel tracks associated with blood curvilinear (concave up), “tea cups”
vessels
Egg Shell C'&/,#/'),".
!" C3&2$823)$"/#(3+'("/()*'(",)#$0'("6()*'(
!" Thin benign Ca++ deposits found on the
tube
surface of a sphere
!" Vascular Ca++ in women < 50 years old
!" Unusually under 1 mm in thickness
suggest potential risk of CAD
!" <"#)(2".."/&A(h+$.i(23&2$823)$"/#($/()*'(
Secretory C'&/,#/'),".(++++++[Figure 25] wall of cysts and fat necrosis
!"Plasma cell mastitis
SVC Syndrome
!"Large rod-like
!" Dilated veins due to SVC obstruction
!";,.$/3&(23&2$823)$"/#(6"+.'0(I$)*$/(
!" SVC due thrombophebitis related to
ectactic ducts
indwelling catheters, mediastinal tumors
!"Ductal distribution, radiating to the
#,2*(3#(&A.!*".31(&,/-(23/2'+1(8%+")$2(
nipple
mediastinitis
!"> 1 mm in diameter
!" If venous dilation is unilateral, more
!"Relatively smooth
common on the right
!"May branch
!"Typically older women > 60 years old Chest. 2002;121:1361–1363.

799
Mondor Disease Steatocystoma Mutiplex
!" B*+".%"!*&'%$)$#("6(#,!'+82$3&(5'$/#("6( !" Steatocystoma multiplex is manifest by
chest wall multiple clinically palpable skin-colored
!" Present with a palpable cord-like or yellow nodules scattered on the axillae
structure, which is often painful and the anterior chest wall
!" Self-limiting, Rx with NSAIDs !" Included in the differential diagnoses
!" Association with breast Ca? of lipoma, fat necrosis, galactocele,
!" Risk Factors: surgery, biopsy, epidermal cyst, etc.
K/43..3)"+A(!+"2'##1(%+'3#)(23/2'+1( !" Findings of a well-circumscribed, round,
trauma fat-density nodule on mammography
!" Incidence: 0.5%-0.8% or an intradermal hypoechoic nodule
Shetty, Mahesh, Alfred Watson. Mondor’s disease on sonography, combined with a family
of the breast: sonopgraphic and mammographic history of steatocystoma multiplex
&-(%-84/)BYA/)JQQSDSRR9ZP[2ZP\/ (40%) and an extensive bilateral spatial
0$#)+$%,)$"/("6(/"0,&'#1(2"/8+.()*'(
Loa Loa diagnosis of steatocystoma multiplex
!" Also called the eye worm !" Nodules have internal radiolucency and
!" Found in rain forest and swamps of West peripheral continuous rim
Africa, especially Cameroon !" Sonogram shows well-circumscribed
!" B+3/#.$))'0(%A(03AW%$)$/-(2*+A#"!#(4$'# homogeneous hypoechoic cyst with
posterior enhancement. Cyst is located
Primary Osteosarcoma in dermis and expands to subcutaneous
!" Rarely presents as primary in the breast fat layer of left axilla, mimicking
!" Elevated AP levels subcutaneous lesion.
!" 27 to 89 years old
!" Median 64.5 years Some Diagnoses Can Be Made With
!" Highly aggressive tumors C".#51./1D
!" Poor prognosis due to local recurrence !" Make them when you can to guide
and hematogenous metastases management
!" @&&($/0')'+.$/3)'(8/0$/-#(#*",&0(%'(
followed (BI-RADS 3) or biopsied (BI-
RADS 4 or 5)
References
1. Breast Imaging Reporting and Data System® (BI-RADS®) Atlas The Breast Imaging Reporting and Data
System® (BI-RADS®) Atlas is a quality assurance guide to standardize breast-imaging reporting and to
facilitate outcome monitoring.
2. Alleva, D. Quentin et al. Radial Scar of the Breast: Radiologic Pathologic Correlation in 22 Cases.
RadioGraphics Oct 1999;19:S27-S35.
3. Berg, et al. Diagnostic Imaging Breast, First Edition, Amirsys, Inc. 2006.
4. 9+30&'A1(:+3/2$'#(')(3&T(B*'(G)'+/3&$#(<,#2&'N(@/(,/,#,3&(/"+.3&(8/0$/-("/(.3.."-+3!*AT(@.(X(
Roentgenol 166, Jan 1996.
5. Doshi, Devang et al. Complex Cystic Breast Masses: Diagnostic Approach and Imaging Pathologic
Correlation. RadioGraphics 2007;27:S53-S64 .
6. Padmanabhan, et al. A Clue to Superior Vena Cava Obstruction. Chest 2002;121:1361–3.
7. Park, Kae et al. Steatocystoma Multiplex: Mammographic and Sonographic Manifestations. Am J
Roentgenol:180, Jan 2003.
8. Majid, Aneesa et al. Missed Breast Carcinoma: Pitfalls and Pearls. RadioGraphics 2003;23:881-95.
9. <3+#)'&&'+1(;,$#3(')(3&T(b'&&(7'8/'0(<3##'#($/()*'(9+'3#)T(V30$"\+3!*$2#(_"&(=1(E,.%'+(Z1(X3/(Z=Q=1(Z^W
37.
10. Sabate Josep, et al. Osteosarcoma of the Breast. Am J Roentgenol 179, July 2002;277-8.
11. Shetty, Mahesh and Watson, Alfred. Mondor’s disease of the breast: sonopgraphic and mammographic
Findings. Am J Roentgenol 2001;177:893-6 .
12. G$/-'+1(C"+A(')(3&T(<3.."-+3!*$2(@!!'3+3/2'("6(@L$&&3+A(;A.!*(E"0'(C3&2$823)$"/($/(`3)$'/)#(I$)*(
Metastatic Ovarian Carcinoma. Am J Roentgenol 2001;176:1437-40.

800
801
802
Musculoskeletal
Radiology
803
804
Radiologic Assessment of Joint Replacement and Bone Grafts
Mark D. Murphey, MD
Current Joint Replacement
!" 800,000 total hip replacements annually
worldwide (200,000 in US)
!" 500,000 total knee replacements annually
worldwide
!" Metal components
!" Ultra high molecular weight polyethylene
Metallic Components
!" Cobalt-chromium-molybdenum alloy
!" Cobalt-chromium-tungsten alloy
!" Titanium-aluminum-vanadium alloy
Ultra-High Molecular Weight

Polyethylene Component
!" Allows articulation of metallic components
!" Lowers friction and prolongs wear Figure 1 A & B
!" Allows some plastic deformity improving
joint congruity Aseptic loosening of both acetabular and femoral
components of a total hip arthroplasty with bone
!" Radiolucent cement (arrows) and cement-metal lucency
(arrowheads) that progresses over several years
Complications of Joint Arthroplasty (right image). Cement fracture (open arrow) and
!" I. Loosening and/or infection lateral migration of the femoral stem (curved arrow)
!" II. Small particle disease (osteolysis) are also apparent.
!" III. Dislocation and abnormal alignment
!" IV. Fractures and nonunion
!" V. Heterotopic bone formation Bone Ingrowth (Porous Coated)
!" VI. Cement extrusion
Joint Arthroplasty
!" VII. Polyethylene liner displacement and
!" Improved longevity
metal arthropathy
!" Beads sintered onto metal surface
Loosening and/or Infection !" Bone ingrowth into irregular surface
!" Most common complication historically 01"*'*2"%)$3/("*.4
!" !"#$%&'()(*)+"##,-,.("/(, !" Technically demanding
!" 4%-13% hip replacement !" No motion to promote bone ingrowth
!" 7%-10% knee arthroplasty
Normal Radiographic Appearance
!" Approximately 5% failure rate or 95%
survival rate at 15 years
Ingrowth Arthroplasty [Figure 2]
!" Resorption of medial femoral cortex
Radiographic Signs: Loosening- !"Stress shielding/cancellization of the
Infection Cemented Arthroplasty cortex
!" Thin lucent rim with sclerotic margin
[Figure 1]
about metal (< 2 mm)
!" Cement-bone lucency or cement metal
!" Endosteal sclerosis
lucency > 2 mm
!" Prosthetic subsidence (< 10 mm)
!" Progressive widening of interfaces postop
!" Periosteal reaction and cortical thickening
!" Component migration
!" Not progress after 9-12 months postop
!" Fracture of metal or cement
!" Periosteal reaction
!" Smooth endosteal scalloping with cement
lucency
!" Air in soft tissues or joint
Joint Replacement and Bone Grafts 805 Musculoskeletal Radiology

Infection of Total Joint Arthroplasty
!" The major long-term complication
(1%-4%)
!"556)$-7()5)8*.(97):*7(*:
!"33% 3-12 months postop
!"33% > 12 months postop
!" Usually associated with loosening
!" !"#$%&'()(*)+"##,-,.("/(,)#-*8)/7,:("%)
loosening
Radiographic Signs Most Suspicious for

Infection [Figure 5]
!" Extensive bone destruction
!" Air in soft tissue and/or joint
!" Extensive or aggressive periosteal
reaction
!" Wide or irregular lucent zone
Figure 2 A & B
Normal appearance of ingrowth hip arthroplasty with
superolateral lucency (arrowheads) (< 2 mm) and
surrounding sclerosis and resorption of medial cortex
(arrow).
Loosening/Infection Radiographic
Findings with Ingrowth Arthroplasty
[Figures 3 & 4]
!" Prominent prosthetic subsidence
(> 8 mm)
!" Bone destruction
!" Component migration or motion
!" Prominent lucent zone about metal Figure 5 A & B
(> 2 mm) Infection of total knee arthroplasty with early
!" Increasing number of displaced beads prominent development of lucency and bone
destruction (arrows) about both the femoral and tibial
Figure 3 A & B components soon following surgery (two months-
previous normal postoperative radiograph not shown).
Aseptic
loosening
of femoral
component Radionuclide Evaluation of Total Joint
ingrowth hip Arthroplasty
replacement
with prominent !" Bone scintigraphy
lucency, lateral !" Gallium scan
migration of !" Indium WBC scan
femoral stem !" PET
(arrow), and
subsidence
medially
Bone Scintigraphy
(arrowhead). !" Normal increased activity postop
(6-9 months)
!" Increased activity subsequently suspicious
Figure 4 A, for loosening/infection
B&C
!" ;*.7:,%"$%
Aseptic !" Overall accuracy 50%-70%
loosening of
acetabular Gallium (GA-67) Scanning
component
ingrowth hip !" In conjunction with bone scan
replacement !" Incongruence with increased gallium
with prominent uptake vs bone scan suspicious for
lucency infection
(arrows) and
bead sheading
!" Not as accurate as bone scan WBC
(circles). combination

Indium-111 WBC Scanning
!" Increased sensitivity (50%-100%) and
7:,%"$%"(<)0=>6?@AA64)#*-)".#,%("*.)*#) Figure 6
TJR
!" Increased activity at tip of metal Digital
components can be normal for up to 2 subtraction
arthrogram
years postop with contrast
!" Used in conjunction with bone and bone in the bone
marrow scans incongruity with more remnant
uptake on WBC scan > 90% accuracy interface of
the acetabular
!" Sensitivity and the ability to correctly
component
localize infection decreases (zone II-
!"Infection becomes more chronic arrowhead)
!"Anatomic location more central and below
the inter-
Arthrography of Joint Arthroplasty trochanteric
line (arrows)
!" Purpose representing aseptic loosening of both components.
!"B1(/".)C&"+)#*-)%&'(&-,D7,.7"("E"(<
!"Document intraarticular location Arthrography and Bursa [Figure 7]
!"F*.$-8)'**7,.".2 !" Greater trochanteric 50%
!"Detect other causes of pain !" Supraacetabular 33%
!" Iliopsoas 17%
Hip Arthrography Technique
!" Can reduce accuracy of arthrography
!" G-,'"8"./-<)C&*-*7%*:<)/.+)-/+"*2-/:97
!" Anterolateral approach to metal at head Figure 7
neck junction 20 gauge spinal needle
!" Aspiration for culture Septic loosening
!" If no aspirate inject saline reaspirate of the femoral
component on
!" Contrast injection with subtraction arthrography
technique of a total hip
!" Radionuclide injection replacement
!" Pre- and postexercise radiographs with synovial
nodularity
in the joint
Arthrographic Criteria for Loosening/ (arrows) and
Infection [Figure 6] supraacetabular
!" Acetabular component bursa formation
!"Contrast in bone: cement or metal- (arrowhead).
cement interface all zones (90%) Contrast
extends below
!"Contrast in bone: cement or metal- intertrochanteric
cement interface zones I and II or line.
zones II and III (90%)
!"Contrast in zones I and III with
medium or large pseudocapsule bursa Small Particle Disease Osteolysis
(57%) [Figures 8 & 9]
!"Rim of contrast > 2 mm thick any !" Granulomatous pseudotumor/histiocytic
zone (95%) reaction/osteolysis (cytokine release)
!"H<8:9/("%)$''".2)0I4 !" Previously unusual arthroplasty late
!" Femoral component sequelae
!"Contrast in cement-bone interface !" Now may be most common cause failure
distal to intertrochanteric line (98%) !" Large lobulated lucencies and cortical
!"Contrast in bone-metal interface below thinning
intertrochanteric line (98%) !" Prosthesis loosening (5.3% THA)
!"Contrast at or below mid component-
long stemmed prosthesis (98%) Dislocation/Abnormal Alignment
Normal Alignment
Knee Arthrography Technique !" Hip
!" G-,'"8"./-<)C&*-*7%*:<)/.+)-/+"*2-/:97 !"Acetabular angle: about 40 degrees
!" Lateral patellofemoral or anterior (+/- 10 degrees) – AP view
intercondylar approach 20 gauge spinal !"Acetabular anteversion
needle 0-30 degrees – lateral view
!" Aspirate for culture !" Knee:
!" If no aspirate inject saline reaspirate !"Tibial plateau component parallel to
!" Contrast injection-subtraction technique C**-
!" Pre- and postexercise radiographs !"Tibia 5-7 degrees valgus
Greater Trochanteric Nonunion After
Figure 8 Total Hip Arthroplasty [Figure 11]
!" Improves exposure at surgery
Small particle
disease as a cause !" Osseous union normally 6-12 weeks
for loosening !" Nonunion results in lack of abductor
of femoral and support
acetabular !" Bursitis predisposes to dislocation
components
of a total hip
replacement with
Figure 11
multiple largely
A&B
intracortical areas
of radiolucency
Fracture
(arrowheads).
of greater
trochanteric
Figure 9 wire mesh
on follow-up
radiograph
Small particle
(right image)
disease
with retraction
(osteolysis or
due to the
granulomatous
pull of the abductors (arrow) about the total hip
psuedotumor)
replacement.
as a cause
for loosening
of the tibial
component of
a total knee
replacement
with large
mass-like Figure 12
radiolucency/low attenuation in the proximal tibia
(arrowheads) with associated fracture (arrow). Ingrowth total
hip replacement
Abnormal Alignment with fracture
Predisposing to Subluxation [Figure 10] (arrow) at the tip
!" Varus position of knee is unacceptable of the femoral
component
!" Acetabular angle > 50/55 degrees – AP !"#$%&'()*+,*
view cerclage wires.
!" Acetabular anteversion < 0 degrees or
> 30 degrees lateral view
!" Exceeding extremes of motion
!" Interposed material
!" Greater trochanteric separation
!" Joint effusion
Heterotopic Bone Formation After Total
!" Loss of soft tissue support or imbalance
(knee) Joint Arthroplasty [Figure 13]
!" Not infrequent – 3 weeks postop, 2 years
Figure 10
to mature
!" Hip: 21%-40%; knee:
Dislocated 10% anterior to femur
noncemented !" Predisposing conditions: ankylosing
total hip
replacement, spondylitis, DISH, prior occurrence
both femoral !" Treatment: radiation, steroids,
(arrowhead) diphosphanates, surgery, indocin
and acetabular
components Figure 13
(arrows), with
increased Prominent
inclination of heterotopic
the acetabular component as a predisposition to this bone formation
complication. (arrowheads)
about both
hips following
Fracture and Nonunion Associated with THR causing
Arthroplasty [Figures 11 & 12] reduced
abduction
!" Bone capability on
!" Metal the left leading
!" Cement to resection.
!" Polyethylene
Brooker C Heterotopic Bone History and Importance:
After hip replacement Bone Graft Procedures
Class I: small islands of bone First performed in 1688
Class II: bone projection from Second most frequently transplanted
acetabulum or femur with > 1 cm tissue
between osseous surfaces Vital for orthopedic management
Class III: < 1 cm between opposing
bridge surfaces Radiologic Assessment:
Class IV: osseous ankylosis bridging Important for Patient Management
joint Normal bone graft incorporation
Abnormal alterations
Cement Extrusion
Imaging Modalities
Vein or lymphatic Radiographs
Rarely nerve, vascular, bowel, or bladder Conventional tomography
injury Scintigraphy
Computed tomography (CT)
Polyethylene Liner Displacement and Magnetic resonance imaging (MRI)
Metal Arthropathy [Figure 14]
Allows metal-metal friction Bone Grafts Indications
Delayed and nonunion
Abnormal component position Pseudoarthrosis
Visualize radiolucent polyethylene Fill osseous defects or cavities
Metal: line sign and debris (metallosis) Arthrodesis
Prevented by early recognition Stabilize spinal segments
Bone stock in arthroplasty
Restore function in diseased articulations
C Bone Graft by Origin

Autograft
Allograft (homograft)
Xenograft (heterograft)
Bone graft substitute
C Bone Graft by Structure

Cancellous
Cortical
Combination
C Bone Graft by
Technique [Figure 15]
Figure 14 A & B Onlay
Displacement of polyethylene liner on follow-up Inlay
radiograph of total hip replacement (right image). Dowel
Note widened medial joint space compared to initial Muscle pedicle
postop radiograph (left image), “metal-line” sign Strut
(arrowhead), and radiolucent rotated polyethylene
liner (*). Vascularized
Clothespin (H)
Silicone Arthroplasty
Complications Figure 15
Fracture
Dislocation Pictorial
representation
Infection of onlay (A)
Silicone arthropathy and inlay (B
and insert)
bone graft
procedures.

Radiographic Evaluation of the Donor
Site [Figures 16 & 17]
Iliac
Fibula
Rib Figure 17
Distal radius
Calvarium CT of normal
Femoral head iliac bone
graft donor
Tibia site with
Greater trochanter outer shell
Posterior spine elements of bone
retrieved (arrowheads) and no violation of the SI joint
Normal Radiographic Appearance of (arrow).
Donor Site [Figure 18]
Wedge or oval defect Donor Site Complications
Irregular margins after surgery Pain
Failure to recognize (radiologists)
Subsequent marginal sclerosis Infection
Complete regeneration Muscle herniation
Involvement of sacroliac joint
Fracture
Normal Bone Graft:

Repair/Incorporation [Figures 19 & 20]
Cancellous autograph
donante Cortical autograft
de Vascularized autograft
injerto
Allograft
Figure 16 A & B
Dowel graft placed across a scaphoid nonunion
(arrows) with progressive healing at both the bone
grafted site (arrows) and bone graft donor site
(arrowheads) on radiographs three months apart. Figure 19 A,
B, C & D
Progressive
normal
incorporation
of cancellous
autograft
(arrows) about
posttraumatic
site in the
lower leg on
radiographs
with individual
osseous
fragments
coalescing into
mass.
Figure 18 A, B & C
Fibula resection for use as bone graft with
regeneration over time on three sequential
radiographs.

Important Terminology: Bone Graft
Healing
Osteoconduction: tissue ingrowth with
prominent vascular and mesenchymal
components
Figure 20 Osteoinduction: mesenchymal tissue
A, B & C differentiation into tissue capable of
Normal
osteogenesis
incorporation Osteogenesis: bone formation
(arrows) of
Vascularized Bone Autograft
graft replacing Rib
a humeral Iliac
resection for
Ewing sarcoma Fibula
reconstruction.
Three Indications: Vascularized Autograft
sequential Intercalary defects
radiographs Composite defects
show
progressive
Mandible reconstruction
Tumor resection
humerus (arrowhead). Conventional failure
Congenital pseudarthrosis

Vascularized Bone Autograft Allograft
Advantages Particulate
Graft remains viable Intercalary
Promotes healing Osteoarticular
Participates in osteogenesis
Improved strength Allograft Healing Depends on the
Disadvantages Recognized Immunologic Disparity
Microvascular surgery expertise
required Allograft Source and Pretreatment
Increased time for surgery Trauma 15-45 years of age
Two surgical sites No history neoplasm or infection
No steroids or respirator
Autograft Limitations Freeze or freeze-drying
Postoperative morbidity risk

Inability to mod for function

Osteoarticular Allograft
Osteochondral shell
Half joint
Whole joint
Osteoarticular Allograft
Low ratio bone: cartilage requires less
pretreatment
Cartilage immunoprivileged tissue
Success depends on osseous component
Bone Graft Complications

Infection
Nonunion or pseudarthrosis
Fracture
Graft resorption
Joint instability
Infection of Bone Graft

Persistent tissue swelling Figure 21 A, B & C
Periosteal reaction Allograft infection with progressive lack of osseous
Progressive bone destruction bridging (arrowheads) and ultimately fracture of
radiographs.
Infection of Bone Graft [Figure 21]

Autograft
Clinical evidence usually present Nonunion and Pseudarthrosis
Vascularized autograft Autograft
5% Failure to heal by 12 months
Allograft 14% in segmental cortical bone grafts
5%-13% soft tissue swelling (beyond 6 Vascularized autograft
months postop) 7% questionable graft viability
Increasing bone resorption (beyond 10 Bone scan – 1 week
weeks postop) Allograft
11% preventable with adequate
Nonunion and Pseudarthrosis osseous contact at host/graft junction
Persistent lucency graft/host junction
Sclerosis at margins change
Rounded osseous margins
Stress views helpful

Fracture Porous Ceramics
!" Linear lucency through graft !" Goniopora-cancellous bone
!" Callus !" Porites-cortical bone
!" Stress views helpful !" Approved human studies 1982
!" Initially weak mechanically
Fracture !" Strength increases after incorporation
!" Autograft !" More dense than native bone
!"Not infrequent !" Lucent peripheral band obliterated with
!"Often after healing with stress ingrowth
(6-8 months) !" Complications: fractures, implant failure,
!"More common in longer grafts infection
!" Vascularized autograft
!"Decreased incidence 3.5% due to Spinal Bone Graft Assessment
improved strength !" Causes of failed back surgery syndrome
!" Allograft (FBSS)
!"16.5% most at weak points !"Recurrent disk
!"Affected by pretreatment method !"Arachnoiditis
!"Epidural scar
Bone Graft Resorption !"Infection
!" Progressive graft loss !"Facet subluxation
!" Graft decreases in size !"Spinal stenosis
!" Graft decreases in density !"Pseudarthrosis
!" !"#$%&'()(*)+"7(".2&"79)#-*8)".#,%("*. !"Spine bone autograft: normal healing/
incorporation
Bone Graft Resorption !"Cervical: 3-4 months
!" Autograft !"Lumbar: by 9 months
!"Unopposed osteoblastic activity
!" Vascularized autograft Spine Bone Autografts:
!"Same as autograft Normal Healing/Incorporation
!" Allograft !" Cervical: 3-4 months
!"Acute or chronic rejection !" Lumbar: by 9 months
!"J-/#()-,:'/%,+)1<)$1-*&7)("77&,
Anterior Vertebral Interbody Fusion
Osteochondral Allograft: Joint Instability !" Cervical and lumbar spine
!" 2.9%-5.5% incidence !" L"1M)"'"/%M)*-)$1&'/-)2-/#(
!" Causes: articular incongruity; lack of !" Initial discrete graft-host junction
innervation and cartilage viability obliterated
!" AVN, neuropathic joint or rejection
!" F/.)1,)+"#$%&'()(*)+"7(".2&"79)#-*8) Radiologic Evaluation:
infection or rejection Spine Pseudarthosis [Figures 22 & 23]
!" Radiographs
Joint Instability: Radiographic Findings !"Oblique views best; radiolucent defect;
!" Joint narrowing and sclerosis motion with bending increase spine
!" Osteophytes and subchondral cysts curve
!" Fragmentation with debris !" Bone scintigraphy
!" K-/%(&-,)/.+)8"2-/("*.)*#)$3/("*. !"N"+,)-/.2,)7:,%"$%"(<)/.+)7,.7"("E"(<)
!" Weight-bearing views helpful Norman uptake < 6 months postop
!"Abnormal if increased uptake beyond 6
Xenograft
months postop
!" Supply-demand limitations of other graft
!"Abnormal if increased uptake beyond 6
!" Calf and ox-bone
months postop; improved with SPECT
!" Treated to prevent rejection
imaging; asymptomatic patients may
!" Used as spacer prevents soft tissue
have focal uptake
ingrowth
!" Conventional tomography
!" Other graft material in combination
!"AP optimal plane (2-5 mm) best
Bone Graft Substitutes reported method – 96% polydirectional
!" Hydroxyapatite (Ca 10 [PO4] 6 [(OH) 2]) best; limited availability and technically
!" Tricalcium phosphate (Ca3 [Po4] 2) demanding
!" Dense or porous ceramics
!" Osteoconductive but not osteoinductive

Figure 22
Pseudoarthrosis
of
posterolateral
lumbar spine
graft with
horizontal
radiolucent
clefts
(arrows) and
surrounding
sclerosis on
conventional
tomography.
Figure 23 A & B
Sagittal T1- (left image) and T2-weighted (right

image) MR images showing horizontal clefts
(arrowheads) in posterolateral lumbar bone graft with
Interbody Fusion Complications high signal on long TR image representing two sites of
!" Nonunion pseudoarthrosis.
!" Graft fracture
!" Extrusion of graft fragments
!" Infection
References
Joint Replacements
1. O/&,-)PNM)Q%9"'7)RS)P9,):/(9*'*2<)*#)(*(/')T*".()/-(9-*:'/7(<S)US)V,%9/."787)*#)"8:'/.()$3/("*.S)QW,',(/')
Radiol 1999;28(8):423-32. Review.
2. Chang JD, Lee SS, Hur M, Seo EM, Chung YK, Lee CJ. Revision total hip arthroplasty in hip joints with
metallosis: a single-center experience with 31 cases. J Arthroplasty 2005;20:568-73.
3. Heffernan EJ, Alkubaidan FO, Nielsen TO, Munk PL. The imaging appearances of metallosis. Skeletal
Radiol 2008;37:59-62.
4. Keogh CF, Munk PL, Gee R, Chan LP, Marchinkow LO. Imaging of the painful hip arthroplasty. AJR Am J
Roentgenol 2003 Jan;180(1):115-20.
5. Manaster BJ. From the RSNA refresher courses. Total hip arthroplasty: radiographic evaluation.
Radiographics 1996;16(3):645-60. Review.
6. Murphey MD, Sartoris DJ, Bramble JM. Radiographic Assessment of Bone Grafts. In: Bone Grafts from
Basic Science to Clinical Application, Habal MB, Reddi AH, Editors. Philadelphia: W. B. Saunders, 1992,
p.9-36.
7. Oswald SG, Van Nostrand D, Savory CG, Callaghan JJ. Three-phase bone scan and indium white blood
cell scintigraphy following porous coated hip arthroplasty: a prospective study of the prosthetic tip. J Nucl
Med 1989 Aug;30(8):1321-31.
8. Taljanovic MS, Jones MD, Hunter TB, et al. Joint arthroplasties and prostheses. RadioGraphics
2003;23:1295-314.
9. Weissman BN. Imaging of total hip replacement. Radiology 1997 Mar;202(3):611-23. Review.
Bone Graft
10. Ishii S, Shishido F, Miyajima M, Sakuma K, Shigihara T, Tameta T, Miyazaki M, Hashimoto N. Imaging
$.+".27)/()(9,)+*.*-)7"(,)/#(,-)"'"/%)%-,7()1*.,)9/-E,7(".2S)QW,',(/')L/+"*')XA@AY5Z[@A@\?X5S)
11. ]"+)^QM)R,*.)!JM)F9*)N_S)F/.)1*.,)7%".("2-/:9<):-,+"%()(9,)$./')*&(%*8,)*#):/7(,&-"`,+)/&(*2-/#(7I)
Skeletal Radiol 2010;39:1009-16.
12. Poffyn B, Sys G, Van Maele G, Van Hoorebeke L, Forsyth R, Verstraete K, Uyttendaele D. Radiographic
analysis of extracorporeally irradiated autografts. Skeletal Radiol 2010;39:999-1008

816
817
818
!"#$"%&#'(%()*%+!*,-.(#)*)-&,#+&.+/01&,-$+2(,*%+3,#".4$-(,$5
Mark D. Murphey, MD
Hyperparathyroidism Bone Resorption in Chronic Renal

!" Primary I,#".4$-(,$5+6/237+
!" Secondary !" Caused by osteoclastic activity
!" Tertiary !" 10% early stages; 50%-70% long-
standing disease
Primary HPT: Etiology !" Subperiosteal
!" Adenoma 80%-90% !" Cortical
!" Hyperplasia 10%-15% !" Subchondral
!" Carcinoma 2%-4% !" Trabecular
!" Nonparathyroid tumor !" Endosteal
!" MEN syndromes (1 and 2a) !" Subligamentous/subtendinous
!" Common: 1/500 women, 1/2000 men,
$#(9?7,E,.(9)+,%/+,7 Subperiosteal Resorption [Figures 1 to 4]
!" Initially described by Camp and Ochsner
Tertiary HPT: Etiology !" Pathognomonic hyperparathyroidism
!" Autonomous gland function !" Lace-like irregularity of cortical margin
progress to scalloping and spiculation
End-Stage Renal Disease: !" Earliest involvement middle phalanges/
Secondary Hyperparathyroidism terminal tufts-hands
!" Multiple causes !" Additional sites: upper medial tibia, femur
!" Most common cause glomerulonephritis and humerus, ribs, lamina dura
!" 0.01% US population
!" 85,000 hemodialysis patients/year
!" 8,000 renal transplantations/year
!" Involves all organ systems
!" Musculoskeletal manifestations common
and increasingly recognized
Secondary Hyperparathyroidism:
Etiology
!" Inability of renal excretion of phosphate
!" Resultant hyperphosphatemia
!" Hyperplasia of parathyroid chief cells and
increased parathormone (PTH)
!" Reduced degradation of PTH Figure 1 A & B
Subperiosteal resorption involving the middle,
Effects of PTH on Bone proximal, and terminal phalanges (arrows) resulting
!" Development of osteoclasts, osteoblasts, from secondary hyperparathyroidism and renal failure.
osteocytes Similar features are noted on the clinical photograph
!" Osseous resorption as well as clubbing.
!" Brown tumors
Renal Osteodystrophy Figure 2

!" Secondary hyperparathyroidism
!" Osteosclerosis Subperiosteal
!" Osteoporosis resorption involving
!" Osteomalacia the middle and
terminal phalanges
!" Q*#()("77&,)/.+)E/7%&'/-)%/'%"$%/("*. (solid arrows) resulting
from secondary
hyperparathyroidism
and renal failure.
The terminal phalanx
also shows band-like
acroosteolysis (open
arrow) resulting
from subperiosteal
resorption.
-.%/.01%2(0(!#0*-#$34(%!#!31$%*14*56"1$3/*7($#0*8$%.4&/3($/, 819 Musculoskeletal Radiology

Endosteal Resorption [Figure 6]
!" Causes scalloping of endosteum - hands
!" Osteopenia with loss of trabecular
Figure 3 sharpness
!" Calvarium – ”salt and pepper” appearance
Subperiosteal
with loss of distinction of tables
resorption
involving the Figure 6
lamina dura
(arrows) Endosteal
caused by resorption in
secondary the skull on CT
hyper- causing loss of
parathyroidism distinction of
and renal inner and outer
failure. table cortices
(salt and pepper
appearance-
arrowheads)
in secondary
hyperpara-
thyroidism.
Subchondral Resorption
[Figures 7 to 9]
!" Common in appendicular and axial
skeleton
!" Often in hands, single DIP joint (4th or 5th)
also MCP and PIP joints
!" More recently polyarticular involvement
Figure 4 A & B 40% of patients on long-term
9,8*+"/'<7"7)UG)/.+)$-7()FVF)T*".(7)a"(9)
Rib scalloping (arrowheads) due to superiosteal
resorption in a patient with chronic renal failure. symmetry
!" Simulates erosions, often progress, 50%
symptomatic
!" Other frequent sites: distal clavicle, AC
Cortical Resorption [Figure 5] joint (20%), SI joint, SC joint, symphysis
!" Caused by osteoclastic activity within pubis, posterior patella
haversian canal !" Pathologically collapsed cortical bone and
!" Radiographs: intracortical tunneling with overlying cartilage
increased lucent striations in cortex !" Initiates an osteogenic synovitis
!" ;*.7:,%"$%)$.+".2 !" Accentuated by mechanical stress, joint
incongruity, and intraarticular debris
Figure 7
Subchondral
resorption of
the metacarpal
heads (arrows)
from secondary
hyperpara-
thyroidism on
radiography
simulating
an erosive
arthropathy.
Figure 8
Subchondral
resorption of the
distal clavicle and
Figure 5 A & B acromion (arrows
Intracortical resorption with areas of and arrowhead)
intracortical tunneling (arrows) resulting from from secondary
hyperparathyroidism on radiography and matched hyperpara-
histologic macrosection showing resorption along thyroidism on
preexisting Haversian canals (arrowheads). radiography.

Figure 9
Brown tumor (*),

diffuse sclerosis
and subchondral
resorption
(arrows) about
the SI joints are
seen on this CT
of the pelvis in
a patient with
chronic renal
failure.
Subligamentous/Subtendinous
Resorption [Figure 10]
!" Patients usually asymptomatic
!" Radiographs: smooth and scalloped or Figure 11 A & B
irregular
Brown tumor of hyperparathyroidism involving the
!" Common sites tibia with pathologic fracture (arrows) on radiography
!"Inferior calcaneus and coronal macrosection. Cyst formation (*) is seen
!"Greater and lesser trochanters on the macrosection.
!"Anterior inferior iliac spine
!"Humeral greater tuberosity Periosteal New Bone: Formation
!"Ischial tuberosity !" Caused by osteoblastic activity
!"Elbow !" Prevalence 8%-25% often with
severe disease
!" Linear often with radiolucent zone
Figure 10 separating it from cortex
!" Can be laminated and chronically
Subligamentous/ thicken cortex
subtendinosis
resorption in !" Most common: humeri, femora, tibiae,
the pelvis on radii, ulnae, metacarpals, metatarsals,
radiography and phalanges
at the ischial
tuberosity and Osteosclerosis [Figures 12 & 13]
anterior inferior
iliac spine
!" Cause unknown 9%-34%
(arrowheads) !" Predilection for axial skeleton
resulting from !" “Rugger jersey” spine
secondary hyperparathyroidism and renal failure. !" Other sites: pelvis, ribs, and clavicles
!" Metaphyses and epiphyses can be
Brown Tumor (Osteoclastomas) involved
!" Caused by localized bone replacement by !" After renal transplant, osteosclerosis may
E/7%&'/-"`,+)$1-*&7)("77&, regress but more common to further
!" May become cystic after necrosis increase
/.+)'"b&,#/%("*.)0*7(,"("7)$1-*7/)
cystica) higher incidence in primary
hyperparathyroidism; 1.5%-1.7% in
secondary
Brown Tumor: Radiographic Findings

Figure 12
[Figures 9 & 11]
!" Often solitary; may be multiple Rugger
!" N,''?+,$.,+)'<("%)',7"*.7 jersey spine
!" Frequently eccentric or cortical with bands
(long bones) of sclerosis
!" May cause scalloping and bone expansion (arrows)
about the
!" VL)7"8"'/-)(*)JFP)8/<)9/E,)C&"+)',E,'7 endplates
!" Sites: rib, pelvis, facial bones and femora, superiorly and
axial skeleton can be involved inferiorly.
!" May heal after treatment with
%/'%"$%/("*.M)7%',-*7"7M)/.+)',7"*.)
disappearance

Figure 13
Diffuse
sclerosis of the
cervical spine
on radiography
in a patient
with secondary
Figure 14 A & B
hyperpara-
thyroidism. Rickets in the distal femur resulting from renal
failure on radiography and coronal macrosection with
metaphyseal widening and cupping (arrows) caused by
growth plate disorganization (arrowheads).
Osteopenia
!" Accumulated effect of osteomalacia, bone
resorption, and osteoporosis Slipped Epiphyses in CRI Induced
!" Contributory factors acidosis, Rickets
poor nutrition, azotemia, steroids, !" Not uncommon 10%
hyperparathyroidism, and !" Proximal femur and humerus, distal femur
reduced vitamin D and radius, metacarpal and metatarsal
!" After renal transplant, osteopenia may heads
worsen or bone mineral content may !" Greatest risk; adolescent boys,
increase uremia > 2 years, treatment close to
!" Predisposed to fractures (5%-25%): onset of puberty
vertebral body, pubic rami, and ribs !" Usually bilateral in chronic renal
!" Fracture healing. Normal but delayed ".7&#$%",.%<)0FLU4)/.+)*#(,.)
asymptomatic initially
Osteomalacia
!" Decreased active form of vitamin D Radiographic Findings: SCFE in CRI
!" Renal tissue hydroxylates vitamin D to [Figure 15]
active form !" Medial femur subperiosteal resorption
!" Additional factors; hypocalcemia, !" Increase epiphyseal plate width
".9"1"(*-7)(*)%/'%"$%/("*.)".)&-,8"/M) !" Decrease neck-shaft angle
aluminum toxicity, hepatic dysfunction !" P<:"%/')$.+".27)*#)7'"::,+)%/:"(/')#,8*-/')
epiphysis (SCFE)
Rickets
!" Common in children with chronic renal
".7&#$%",.%<
!" Normal vessels that invade zone of
:-*E"7"*./')%/'%"$%/("*.)#/"')(*)+,E,'*:
!" Result: disorganized cartilage zone
columns
Radiographic Findings in Rickets

[Figure 14]
!" Widened growth plate
!" Epiphyseal irregularity; metaphyseal
fraying and cupping
!" Delayed bone age and osteopenia
!" Bowed long bones and scoliosis
!" Concave vertebral endplates
!" Basilar invagination Figure 15
!" Triradiate pelvis and acetabuli protrusio Rickets of the proximal femora and bilateral SCFE
!" Rachitic rosary (arrowheads) in a renal failure patient on pelvic
!" Slipped epiphyses radiograph with hips abducted.

Radiographic Findings:
Osteomalacia in Adults
!" B7(,*:,."/)a"(9)"''?+,$.,+)(-/1,%&'/,)
unlike osteoporosis
!" Looser zones: pseudofractures
!"Uncommon: 1% CRI patients
!"Pubic rami, medial femoral neck,
scapulae, ribs, long bones, lesser
trochanters, ischial tuberosity
Soft Tissue and Vascular C*%$-4$*)-&,

!" Increases calcium: phosphate product
> 75 mg/dL
!" Contributory factor: local tissue damage
and alkalosis (calcium salt precipitation)
!" Common sites: ocular tissue, arteries,
subcutaneous, periarticular, and visceral
Periarticular C*%$-4$*)-&,+++++[Figures 16 & 17]

!" Asymptomatic or pain and joint limitation
!" Prevalence
!"7% after 1 year of hemodialysis
!"55% after more than 4 years of Figure 16 A to E
hemodialysis
Heterogeneous
!"Periarticular soft tissue mass large soft
(0.5%-1.2%) tissue mass
!" Often regresses with treatment (*) about the
!" Often multifocal and symmetric right shoulder
!" Secondary tumoral calcinosis on coronal STIR
MR images in
!" Dense and cloud-like on radiographs a patient with
!" Hydroxyapatite: chalky paste-like material renal failure
!" Can extend into tenosynovial tissue and initially sent
joints to radiology
for biopsy of
!" Sites: phalangeal joints, wrists, elbows, suspected sarcoma. Subsequent radiograph shows
shoulders, hips, knees, ankles %.+!0(*/#0/3&/#!31$*#$)*=#%/.0#"*/#!6(!("%*3$*!6(*/($!"#0*
vessels for hemodialysis. Diagnosis of periarticular
Arterial C*%$-4$*)-&, /#0/3&/#!31$*"(0#!()*!1*"($#0*4#30."(*<#%*>#)(*#$)*$1*
!" Occur in media and intimal tissue biopsy was necessary.
!" Pipestem appearance radiographically
!" F/.)8/W,)79&.(7)*-)$7(&'/)#*-)
9,8*+"/'<7"7)+"#$%&'(
!" Initially dorsalis pedis artery also leg,
hand, and forearm
!" Prevalence: 27% < 1 year therapy
!"83% with 8 years or more of therapy
!"Rare in children
!" Second type: nodular with luminal
encroachment, obstruction with
ulceration, gangrene, and cardiac failure
!" F/'%"$%/("*.)".)79&.()/.,&-<787
Figure 17
Visceral C*%$-4$*)-&,
9("3#"!3/.0#"*/#0/3&/#!31$*#+1.!*!6(*0(4!*63:*1$*5;*<3!6*
!" Usually not apparent on radiographs %(=("#0*/#0/3.>*?.3)*0(=(0%*@#""1<%A*3$*#*:#!3($!*<3!6*
!" May detect on bone scintigraphy (poor renal failure.
looking bone scan)
!" Sites: heart, lungs, stomach, kidneys Musculoskeletal Abnormalities More
!" Prevalence 79% Common After Treatment
!" In myocardial tissue important, can cause !" Aluminum toxicity
conduction defects and death !" Amyloidosis
!" Tendon rupture
!" Crystal deposition
!" Infection
!" Avascular necrosis (AVN)

Aluminum Toxicity Amyloidosis
!" Cause: ingestion of aluminum salts in !" Musculoskeletal involvement
phosphate – binding antacids to control !"Carpal tunnel syndrome
hyperphosphatemia !"Osseous and intraarticular deposition
!" Cannot excrete alumina !"Destructive spondyloarthropathy
!" Toxic effects
!"Cerebral (encephalopathy) Carpal Tunnel Syndrome in CRI
!"Osseous system !" Long-term hemodialysis prevalence
!" Prevalence 1%-30% (rare today) 2%-31%
!" Results in osteomalacia previously !" Equal sex distribution
responsible for most osseous !" No prevalence for dominant hand
abnormalities in patients on long-term !" Amyloid primary cause of median nerve
hemodialysis compression
!" Unknown mechanism !" Other causes: venous stasis and edema
!" Clinically: low PTH, serum aluminum -,'/(,+)(*)(-,/(8,.()$7(&'/
> 100 ng/mL
Osseous and Intraarticular Involvement
Aluminum Toxicity: in CRI [Figures 19 & 20]
Radiographic Findings [Figure 18] !" K*%/')'<("%)/-,/7)*-)',77)a,''?+,$.,+)
!" Osteomalacia: osteopenia, looser zones, intramedullary lytic lesions
fractures, rickets !" Most common: carpus – scaphoid, lunate
!" More than 3 atraumatic fractures (86%): and capitate – can enlarge
ribs, vertebrae, hips, pelvis, sternum, !" Other sites: humeral head, knee (patella),
clavicles, extremities and about hip
!" AVN !" Endosteal scalloping, fractures,
!" Lack of osteosclerosis extrinsic erosion from soft tissue mass,
!" Limited subperiosteal resorption neuropathic appearance
!" Bone biopsy - histochemical stain for !" Intraarticular deposition: common in hip,
aluminum knee, shoulder-low intensity on T2-W
images
Figure 18
Osteomalacia due to aluminum toxicity in a renal

failure patient with radiograph showing multiple Figure 19 A & B
nontraumatic fractures (arrows) and acetabulae
protrusio (curved arrows). Amyloidosis in a patient with /6"1$3/*"($#0*3$%.4&/3($/,*
causing multiple punched out lytic lesions in the wrist
(arrowheads).
Amyloidosis
!" Secondary due to chronic disease
!" B2: microglobulin
!" Areas of deposition: bone, tenosynovium,
intervertebral disk, cartilage, capsule,
ligament, muscle
!" Stains with Congo red, characteristic
under polarized microscopy and
immunoperoxidase methods

Figure 21
Destructive
spondyloarthropathy
at L5-S1 caused by
amyloid deposition
related to renal
failure with disc
narrowing and
destruction (arrows)
on radiograph
simulating infectious
spondylodiscitis.
Figure 20 A & B
Amyloid deposition in the hip joint of a renal failure Distinction of Infection Versus
patient on hemodialysis on coronal T1- and T2-
W MR images showing low signal intensity material in
Destructive Spondyloarthropathy
the joint (*) with extrinsic bone erosion (arrow). [Figure 22]
!" Clinical symptoms/laboratory evidence
lacking
!" Multilevel involvement unusual for
bacterial infection
!" Limited uptake on scintigraphy
Spontaneous Hemorrhage Associated !" CT: lack of paravertebral soft tissue mass
with CRI (also MRI)
!" In hemodialysis, patients likely related to !" MRI: disc/endplate marrow replaced T1-W
heparin !"No prominent increased intensity on
!" Most frequent in thigh T2-W
!" MRI best for evaluation; appearance
varies with hemorrhage age
Destructive Spondyloarthropathy
!" Described 1984 by Kuntz and colleagues
!" Usually in patients on long-term
hemodialysis (2-19 years)
!" Prevalence:15%; symptoms: pain
!" Cervical and lumbar spine
!" Multiple levels > 50% of patients
!" Rapid progression 33%;
simulates infection
!" Initial postulated etiology: crystal and
noncrystal deposition, neuropathic and
hyperparathyroidism Figure 22 A & B
!" Amyloid now considered offending agent
Destructive spondyloarthropathy related to amyloid
deposition (same patient as previous radiograph)
Destructive Spondyloarthropathy: with marrow and disk replacement remaining
Radiographic Findings [Figure 21] predominantly low signal intensity on all pulse
!" Discovertebral erosions with sclerosis sequences (*).
!" Vertebral body compression
!" Disk space narrowing with Schmorl nodes Tendon Rupture or Avulsion in CRI
!" Lack of osteophytes !" Spontaneous; in patients on long-term
!" Facet involvement with subluxation dialysis
!" Solitary or multiple
!" Tendon sites: quadriceps, patellar, triceps,
C,3*-7)/.+),3(,.7*-7)*#)$.2,-7
!" Cause: PTH excess – increased joint laxity
!"P,.+*.)%/'%"$%/("*.
!"Chronic acidosis
!" Result: decrease tendon tensile strength
and accelerated degeneration

Radiologic Findings Bone Scintigraphy in CRI [Figure 24]
in Tendon Rupture in CRI [Figure 23] !" Diffuse increased activity “super bone
!" Before rupture – may see subtendonous scan”
bone resorption !" May use as index of severity
!" After rupture – focal soft tissue swelling, !" Cause of increased activity is
effusion, subluxation %*81"./("*.)*#)E"(/8".)!)+,$%",.%<)/.+)
!" CT, MRI, or sonography to evaluate hyperparathyroidism
tendon integrity and disruption site !"Increase rate bone turnover and
collagen metabolism
!"Excess immature collagen
!"High enzyme activity
!"Increased osseous surface area for
Figure 23 binding
!" Increased focal or diffuse soft tissue
Spontaneous uptake
rupture
of the
quadriceps
tendon
(arrows) in a
renal failure
patient on
sagittal T2-W
MR image.
Crystal Deposition Disease in CRI

!" Calcium hydroxyapatite, CPPD,
monosodium urate, calcium oxalate
!" Hemodialysis elbow – olecranon bursitis
!" Calcium hydroxyapatite – EM or X-ray
diffraction
!" CPPD: chondrocalcinosis not common -
knee, wrist, hip, shoulders and symphysis
!" CPPD arthropathy rare in CRI
!" Gout: infrequent in CRI, radiographic
$.+".27)7/8,)/7)(9*7,)".):-"8/-<)
podagra except distribution
!" B3/'*7"7[)%9*.+-*%/'%".*7"7M)%/'%"$,+) Figure 24 A, B, C & D
joints, disks and periarticular, diffuse
osseous sclerosis Super scan on bone scintigraphy in chronic renal
failure.
Predisposition to Infection in CRI
!" Depressed host responsiveness
!" Steroids and immunosuppressive
treatment
!" ].(-<)7"(,)E"/)/-(,-"*E,.*&7)$7(&'/)#*-) Avascular Necrosis in CRI
hemodialysis !" Up to 40% of CRI patients after renal
!" Secondary infection in osteonecrosis transplantation
!" Additional factors: structural weakening,
Infection Associated with CRI fracture and collapse, excess PTH, graft-
!" Osteomyelitis and septic arthritis host reaction
!" Bacterial or fungal !" Most common site: femoral head
!" L/+"*2-/:9"%)$.+".27[)+,,:)7*#()("77&,) !" Other sites: humeral head, about knee,
swelling, periosteal reaction, bone talar dome, humeral condyles, cuboid,
destruction, and joint space narrowing – carpal bones, long bone diaphyses
same as other situations
!" Unusual syndrome – progressive
peripheral ischemic ulcers usually after
treatment and secondary infection

Avascular Necrosis in CRI Hyperparathyroidism:
!" Radiologic appearance identical to other Primary vs Secondary
causes AVN
1 2
!" MRI most sensitive however only 50%
!" Brown tumors +++ ++
show early changes
!" Osteosclerosis Rare +++
!" Osseous malignancy can complicate
!" Chondrocalcinosis + Rare
osteonecrosis and general increased
!" Periostitis Rare +
malignancy rate after renal transplant
References
1. Camacho CR, Talegon Melendez A, Valenzuela A, Gonzalez Guirao MA, Gomez Benitez S, Gil L, palma
^'E/-,`)^M)V/(,*7)^2&"'/-)RS)L/+"*'*2"%/')$.+".27)*#)/8<'*"+)/-(9-*:/(9<)".)'*.2?(,-8)9/,8*+"/'<7"7S)
European Radiology 1992;2:305-9.
2. Leone A, Sundaram M, Cerase A, Magnavita N, Tazza L, Marano P. Destructive spondyloarthropathy of
(9,)%,-E"%/')7:".,)".)'*.2?(,-8)9,8*+"/'<`,+):/(",.(7[)/)$E,?<,/-)%'"."%/')-/+"*'*2"%/'):-*7:,%("E,)7(&+<S)
Skeletal Radiol 2001 Aug;30(8):431-41.
3. Murphey MD, Sartoris DJ, Quale JL, Pathria MN, Martin NL. Musculoskeletal manifestations of chronic renal
".7&#$%",.%<S)L/+"*J-/:9"%7)@ZZ5)V/-Y@50X4[5>\?\ZS
4. Slavotinek JP, Coates PT, McDonald SP, Disney AP, Sage MR. Shoulder appearances at MR imaging in long-
term dialysis recipients. Radiology 2000 Nov;217(2):539-43.
5. Kovatcheva RD, Vlahov JD, Shinkov AD, Borissova AM, Hwang JH, Arnaud F, Hegedus L. High-intensity
focused ultrasound to treat primary hyperparathyroidism: a feasibility study in four patients. AJR Am J
Roentgenol 2010;195:830-6.

828
Fundamental Concepts of Musculoskeletal Neoplasm: Radiographs
Mark D. Murphey, MD
Introduction of the Players
Bone Tumors
T"8&1#+*1(+$%*##-4(9+:5+)0(-1+;*))(1,+&.+
differentiation. Tumors are graded on
their degree of anaplasia.
Skeletal Components Derived From

Embryonal Mesenchyme
!" Bone and cartilage progenitor cells
!" Periosteal cells
!" Hematopoietic cells
!" Lipocytes
!" Nerve and schwann cells
!" Fibroblasts
!" Osteoclasts and osteoclast-like cells
!" Endothelial cells
!" Perithelial cells
!" Notochordal cells (rests)
!" Histiocytic cells
!" Epithelial cells (rests)
Fundamental Concepts of MSK Neoplasm: Radiographs 829 Musculoskeletal Radiology

Incidence of Bone Tumors [Figure 1] Primary Benign Bone Tumors [Figure
!" Approximately one individual in 75,000 3]
develops a primary bone tumor that leads
to biopsy
!" About 4,000 new cases per year
Figure 3
Figure 1
Incidence of Bone Tumors Primary Malignant Bone Tumors

[Figures 2 to 4] [Figure 4]
!" Of biopsied primary bone tumors:
malignant tumors are three times more
common as benign lesions
!" Metastatic lesions are biopsied about
35 times more frequently than primary
tumors
Figure 4
Important Factors in Diagnosis of Bone

Figure 2 Tumors
!" Patient age and sex
!" Bone involved
!" Location of bone
!" Lesion margin
!" Matrix formation
T0(#(+1*9-&%&<-$+$0*1*$)(1-#)-$#+1(=($)+
the pathologic process and its biologic
activity.

Primary Benign Bone Tumors:
Age Distribution by Decade [Figures 5 & 6]
Figure 8 A, B & C
Ewing sarcoma involving the femoral diaphysis on

radiograph, T1-W MR and gross specimen.
Dahlin DC. Data on 8542 Cases. 1986

Figure 5
Location in Bone: Axial [Figures 9 & 10]
!" Central
!" Eccentric
!" Cortical
!" Juxtacortical
!" Soft tissue
Figure 6 Dahlin DC. Data on 8542 Cases. 1986 Figure 9
“The site frequency, peak age of

incidence, and numerical frequency
of bone tumor indicate that they are
not completely autonomous, but are
#":>($)+)&+)0(+%*?#+&.+4(%9+:(0*@-&1+
and developmental anatomy of normal
bone...”
Johnson L. 1953.
Location in Bone: Longitudinal

[Figures 7 to 10]
!" Epiphysis
!" Metaphysis
!" Diaphysis
Figure 7
Chondro-
blastoma
with lytic
lesion in the
epiphysis.
Figure 10

Pattern of Bone Destruction and
Lesion Margin [Figure 11]
Type I: geographic
Type II: motheaten

Type III: permeative
Transition zone
Figure 13 A, B & C
IA margin on radiograph, gross specimen, and

Figure 11 macrosection.
Margin R Biologic Activity
Aggressive vs Nonaggressive
Biologic Activity
Margin G Rate
Geographic IA Slow
Geographic IB Slow to intermediate
Geographic IC Intermediate
Motheaten Intermediate
Permeative Fast
Figure 14 A & B
IA Margin [Figure 12]
Brodie abscess with geographic IA margin. Note the
Geographic
Sclerosis
IB Margin [Figures 15 & 16]

Geographic
Figure 12
No sclerosis
Geographic
IA.
Geographic IA: Differential Diagnosis Figure 15

[Figures 13 & 14]
Bone cyst Geographic
Brodie abscess IB.
Cartilage lesions
Chondroblastoma
Enchondroma
Fibroxanthoma
Fibrous dysplasia

Geographic IB: Differential Diagnosis
Giant cell tumor [Figure 16]
Bone cyst
Cartilage lesions
Chondroblastoma
Enchondroma
Fibrous dysplasia
Myeloma/metastasis
Figure 18 A & B
Fibrosarcoma with geographic IC margins, particularly
macrosection.
Tumor Margin [Figures 19 to 22]

Motheaten
Permeative
Figure 16 A & B
Giant cell tumor of the distal radius with geographic IB
subchondral bone.
IC MARGIN [Figures 17 & 18]

Geographic
Figure 19 A & B
Left Image: Motheaten.
Right Image: Permeative.
Figure 17
Geographic
IC.
Geographic IC: Differential Diagnosis

Chondrosarcoma
Enchondroma (active) Figure 20
MFH/Fibrosarcoma [Figure 18]
Giant cell tumor/ABC/CMF Permeative.
Osteosarcoma
Metastasis/myeloma
Lytic Bone Lesion Margin

Type I: geographic
Type II: motheaten

Type III: permeative

Motheaten: Differential Diagnosis Lytic Patterns [Figure 23]
[Figures 21 & 22]
Ewing sarcoma
Round cell tumors
Osteomyelitis
Osteosarcoma
Langerhans cell histiocytosis (LCH)
Metastasis/myeloma
Permeative Differential Diagnosis

[Figures 21 & 22]
Ewing sarcoma
Round cell tumors
Fibrosarcoma
Metabolic disorders
Osteomyelitis Figure 23
Osteosarcoma
LCH I Margin [Figure 24]
Myeloma/metastasis
Figure 24 A, B & C
Figure 21 A, B & C
Multifocal acute bacterial osteomyelitis with
motheaten to permeative destructive pattern of bone
lysis on radiographs involving the tibia and femur.
Changing Margin [Figures 25 to 28]

Increased biologic activity
Figure 25
Changing
margin.
Figure 22 A & B
Hyperparathyroidism with variation of the permeative

Matrix Formation
I. Mineralized
Chondroid: rings, arcs, honeycomb
[Figures 29 & 30]
Figure 26 Osteoid: ivory or cloud-like [Figures 31 & 32]
II. Nonmineralized
Osteonecrosis Fluid
Soft tissue
malignant
transformation Fat
to malignant
histiocytoma
new lysis
periphery
on specimen
radiograph
representing
the changing
margin.
Figure 29 A, B & C
Figure 30
Chondrosarcoma
Figure 27 A & B
on specimen
radiograph and
gross specimen
new cortical destruction laterally and soft tissue mass show “ring and
mineralization
Figure 31
A&B
Pictorial
representation
of ivory or
cloud-like
Figure 28 A & B
Coronally sectioned gross specimen and macrosection

Periosteal Reaction: Aggressive
[Figures 34 & 35]
Codman triangle (A)
Sunburst (B)
Hair-on-end (C)
Laminated (D)
Figure 32 A & B
Periosteal Reaction: Nonaggressive

[Figure 33]
Solid (A)
Buttressing (B)
Expansion (C)
Septation (D)
Figure 34
A, B, C & D
Figure 33
A, B, C & D
Figure 35
Osteosarcoma
with
aggressive
“hair-on-end”
periosteal
reaction

Polyostotic vs Monostotic Holes in Bone Polyostotic Lesions: Malignant
Metastasis
Polyostotic Lesions: Benign Multiple myeloma [Figure 37]
Langerhans cell histiocytosis (LCH) [Figure Hemangioendothelioma
36]
Enchondromatosis
Fibrous dysplasia
Hereditary multiple exostoses (HME)
Osteomyelitis
Paget disease
Angiomatous lesions
Figure 37
Multiple myeloma on lateral skull radiograph with

Figure 36 multiple areas of bone lysis.
Langerhans cell histiocytosis with areas of calvarial
References
2.
3. Lodwick GS, Wilson AJ, Farrell C, Virtama P, Dittrich F. Determining growth rates of focal lesions of bone
4. Madewell JE, Ragsdale BD, Sweet DE. Radiologic and pathologic analysis of solitary bone lesions. Part I:
5. Ragsdale BD, Madewell JE, Sweet DE. Radiologic and pathologic analysis of solitary bone lesions. Part II:
6. Sweet DE, Madewell JE, Ragsdale BD. Radiologic and pathologic analysis of solitary bone lesions. Part III:
7. Miller TT. Bone tumors and tumorlike conditions: analysis with conventional radiography. Radiology

838
Fundamental Concepts of Musculoskeletal Neoplasm: CT and MRI
Mark D. Murphey, MD
Important Features in Evaluation of Soft Tissue Neoplasm

Musculoskeletal Masses !" Radiographs only occasionally helpful
!" Differential diagnosis !" CT and more often MRI can be tissue
!" Preoperative assessment and staging 7:,%"$%
But..
Osseous Neoplasm [Figure 1] !" VLU)/.+D*-)FP)/-,)/2/".)E"(/')#*-)+,$.".2)
!" Differential diagnosis of primary skeletal extent, staging, and preoperative
neoplasms is best determined by evaluation. Clinical and radiologic
radiographs characteristic often limit differential
But... diagnosis.
!" MRI and/or CT are vital for delineating
and staging osseous neoplasms prior to
Causes of Tissue S;($-4$+Diagnosis
surgery on CT/MRI in Evaluating Soft Tissue
Masses
!" 20%-50% cases
(My opinion will rise to 70%-90%)
!" Contrast resolution, MRI > CT
!" Multiplanar imaging, MRI > CT
!" Location of mass
Figure 1
!" Growth pattern and history
Enchondroma
vs
Soft Tissue Masses Diagnosed with
chondrosarcoma Imaging Alone [Figures 3 & 4]
on radiograph !" Lipomatous lesions
due to chondroid !" Angiomatous lesions
mineralization
(arrow).
!" Neurogenic tumors
!" ]'/7(*$1-*8/)/.+)$1-*8/(*7"7
!" PVNS and ganglion
Figure 3 A & B
Figure 2 A, B & C
Lipoma (coronal T1-W and T2-WIs) isointense to fat
Chondrosarcoma (same patient on all pulse sequences (*) with single thin septation
as previous radiograph) on (arrows).
MR due to associated cortical
destruction and soft tissue
mass (arrows) also seen in
gross specimen.
Fundamental Concepts MSK Neoplasm: CT and MRI 839 Musculoskeletal Radiology

Staging of Musculoskeletal Tumors:
Malignant
!" Stage 1 (G1): low grade, well
differentiated, few mitoses; tend to recur
locally [Figure 6]
!"1A – intraosseous/ intracompartmental
!"1B – extraosseous/
extracompartmental
!" Stage 2 (G2): High grade, poorly
differentiated, many mitoses; high
incidence of metastases [Figure 7]
!"2A – intraosseous/ intracompartmental
!"2B – extraosseous/
extracompartmental
!" Stage 3: metastases; regional or
remote (visceral, lymphatic, or osseous)
Figure 4 A & B [Figure 8]
Malignant peripheral nerve sheath tumor (arrow) in
patient with $(."1&+"1>#!1%3%*!,:(*B*@$1!(*%(/1$)* American Joint Commission Staging
small subcutaneous $(."1&+"1>#*C*/."=()*#""1<AD
Staging of Musculoskeletal Tumors:

Benign (G0) [Figure 5]
!" Stage 1 – unchanged or healing lesion;
well-encapsulated; indolent clinical course
!" Stage 2 – active growth; symptomatic,
remains intracapsular but may be
deforming
!" Stage 3 – aggressive local growth; may
penetrate cortex or compartment; higher
recurrence rate
Figure 5 A to F Figure 7 A, B, C & D

Enneking staging system (benign). Enneking staging system (malignant).
Fundamental Concepts MSK Neoplasm: CT and MRI 840

Musculoskeletal Radiology
American Joint Committee on Cancer
Staging for Primary Malignant Tumors
of Bone
Figure 8
Stage III.
metastases;
regional
or remote
(visceral,
lymphatic, or Staging for Primary Malignant Tumors
osseous). of Bone - Key
!" Tx = primary tumor cannot be assessed
CT chest
PET/CT. !" T0 = no evidence of primary tumor
!" T1 = tumor 8 cm or less in greatest
dimension
!" T2 = tumor more than 8 cm in greatest
dimension
!" T3 = discontinuous tumors in the primary
bone
Protocol for Sarcoma of Soft Tissue !" Nx = regional lymph nodes not assessed
!" N0 = no regional lymph node metastases
American Joint Commission Staging !" N1 = regional lymph node metastasis
!" Mx = distant metastasis cannot be
assessed
!" M0 = no distant metastasis
!" M1 = distant metastasis
!"M1a = lung
!"M1b = other distant sites
!" Gx = grade cannot be assessed
!" G1 = well-differentiated (low grade)
!" G2 = moderately differentiated (low
grade)
!" G3 = poorly differentiated (high grade)
!" G4 = undifferentiated (high grade)
Protocol for Sarcoma of Soft Tissue
!" Histologic grade (G)
!"G1: well-differentiated
!"G2: moderately well differentiated
!"G3-4 poorly differentiated,
undifferentiated
!" Primary tumor (T)
!"T1: tumor 5 cm or less in greatest
dimension
!"T2: tumor more than 5 cm in greatest
dimension
!" Regional lymph nodes (N)
!"N0: no regional lymph node
Figure 9
metastasis
!"N1: regional lymph node metastasis
!" Distant metastasis (M) Staging of Musculoskeletal Neoplasm
!"M0: no distant metastasis has Implication on Surgical Treatment
!"M1: distant metastasis
[Figures 9 & 10]
!" Intracapsular excision
!" Marginal excision
!" Wide excision
!" Radical resection
!" Amputation

Figure 10
Limb salvage procedures.
Figure 12 A & B
Ewing sarcoma following chemotherapy with

prominent reactive zone (*) around the low signal
Important Factors on Imaging for intensity pseudocapsule (arrows).
Staging Musculoskeletal Neoplasm
!" Intramedullary extent
!" Extent of soft tissue component
MRI May Overestimate Musculoskeletal
!" Lesion matrix
Neoplasm Extent Because of
!" Cortical involvement
!" Neurovascular involvement Surrounding Edema (Reactive Zone)
!" Joint involvement
Musculoskeletal Neoplasm Lesion Matrix
Intramedullary/Soft Tissue Evaluation
Extent Musculoskeletal Neoplasm !" I. Mineralized: CT > MRI
!"A. Chondroid - rings and arcs
[Figures 11 & 12]
[Figure 13]
!" MRI superior to CT
!"B. Osteoid – cloud-like, “ivory-like”
!"Superior contrast resolution
!"FS)B(9,-)%/'%"$%/("*.)?):9',1*'"(9M)
!"Multiplanar imaging capability
synovial sarcoma
!" Regional metastases-osseous/lymph node
!" II. Nonmineralized: MRI > CT
!" Can be helpful to direct biopsy
!"A. Fluid, necrosis, hemorrhage
!"Always perform in consultation with
[Figure 14]
orthopod
!"B. Fat
!"!*.,)".)".7("(&("*.)*#)+,$."("E,)
!"FS)Q*#()("77&,)c).*.7:,%"$%
procedure
!" Give orthopod anatomic landmarks
Figure 11 A, B & C
Osteosarcoma with spread across physeal plate Figure 13 A & B

(arrows) not seen on radiograph. Chondrosarcoma with chondroid matrix mineralization
not seen on radiographs or MRI.
Musculoskeletal Neoplasm:
Neurovascular Involvement
[Figures 16 to 20]
Vital information for surgical resection
MRI > CT (postcontrast if use CT-CTA)
Improved contrast resolution
of stenosis
9% in soft tissue sarcomas; 3.3% of
primary bone tumors
Axial plane usually best
Look for intact fat plane
Best on T1-W images
If fat plane lost cannot exclude
Figure 14 A & B involvement
involvement
(right image).
Cortical Involvement [Figure 15]
CT > MRI (my opinion)
MRI = CT (literature)
CT better spatial resolution
Important in differential diagnosis of
osseous lesions Figure 16 A & B
Important for surgical resection/staging
Figure 17
Pictorial
representation
without
neurovascular
tumor.
Figure 15 A & B
detect on MRI (right image) compared to CT (left

image).
Figure 18
Pictorial
representation
neurovascular
tumor.

Figure 19
Pictorial
representation
with
neurovascular
Figure 21
encasement by
tumor.
Pictorial
representation
without joint
involvement by
tumor.
Figure 20 A & B
Osteosarcoma with encased neurovascular bundle

(arrows) illustrated by the tumor replacing normal fat
seen about vessels on proton density MR images (left
image) and gross specimen (right image).
Ligament and Tendon Involvement Figure 22 A & B
!" Important for surgical reconstruction
!" MRI > CT; best on T2-W image Pictorial representation with joint involvement by
!" Tendons/ligaments low intensity vs tumor tumor.
high signal
!" On CT tendon/ligament similar to tumor
attenuation
!" Also multiplanar imaging of MR helpful
Musculoskeletal Neoplasm: Joint

Involvement [Figures 21 to 24]
!" Dramatically changes surgery from:
!"Limb salvage; intraarticular resection
!"Extraarticular limb salvage/amputation
!" MRI superior to CT - multiplanar imaging
!"Coronal or sagittal plane best
!" Three routes of spread into joint
!"Through bone/cartilage (transarticular)
!"Around joint margin (periarticular)
!"Along ligaments/tendons, or
hematogenous Figure 23 A & B
!" Presence of joint effusion – suggestive
!" Absence of joint effusion – excludes Pictorial representation with joint involvement by
tumor.

Imaging Characteristics Suggesting
Benign Soft Tissue Mass
!" Small size
!" Well marginated
!" Homogeneous signal intensity
!" No neurovascular encasement
!" Enhancement pattern dynamic MRI (late,
slow, diffuse/none)
Imaging Characteristics Suggesting

Malignant Soft Tissue Mass
!" Large size
!" G**-)8/-2".)+,$."("*.)a"(9),+,8/
!" Heterogeneous signal intensity
!" Neurovascular encasement
!" Enhancement pattern dynamic MRI (early,
rapid, peripheral)
Figure 24 A & B Distinction of Benign vs Malignant

Soft Tissue by MRI
Osteosarcoma invading the knee joint with effusion !" Totty – Radiology. 1986;160:135-141
(arrows) and tumor (*) along ACL (arrowheads) on (n=32)
sagittal T2-W MR and gross specimen.
!" Sundaram – MRI. 1988;6:237-248
(n=53)
!" Kransdorf – AJR. 1989;153:541-547
(n=112)
Overall Delineation of Musculoskeletal
!" Berquist – AJR. 1990;155:1251-1255
Masses: All Features (56 Cases, N=189) (n=95)
!" MRI > CT - 60%
!" Crim – Radiology. 1992;185:581-586
!" MRI = CT - 16%
(n=83)
!" CT > MRI - 24%
MRI (N=56) CT (N=56) Soft Tissue Masses Misinterpreted
Intramedullary extent 81% 5% on MRI: Benign vs Malignant
Soft Tissue Mass 89% 0% [Figures 25 to 27]
Mineralized Matrix 0% 92% !" Diabetic muscle ischemia
Cortical Involvement 7% 72% !" Hematoma
Neurovascular Involv. 78% 0% !" Fibromatosis
Joint Involvement 73% 3% !" Reactive lymph node, abscess, bursitis
!" V<*7"("7)*77"$%/.7
CT Indications
!" Synovial sarcoma
!" Cannot perform MRI
!" Myxoid liposarcoma
!" Matrix producing neoplasm not adequately
evaluated on radiographs
!" Unusual location
!"Ribs, sternoclavicular region, scapula
!"Abdominal/chest wall
!"Fibula
Figure 25
-,1%3!3%*1%%3&/#$%*<3!6*#EE"(%%3=(*#::(#"#$/(*1$*
coronal T2-weighted MRI.
Postoperative Imaging MRI/CT: Normal
!" MRI > CT – improved contrast resolution
!" Comparison to baseline study
Figure 26 0$-7()X?5)8*.(974
!" Recognize normal changes
Myositis !"Postop edema/myositis
1%%3&/#$%* !"Radiation necrosis
with early !"V&7%',)C/:
rim of
1%%3&/#!31$* !"Fluid collections – subfascial,
(arrow) on lymphocele/seroma
CT (same
patient as Postoperative Imaging MRI/CT:
previous Abnormal [Figures 28 & 29]
MRI).
!" New bone destruction/marrow
replacement
!" Any recurrent or residual nodular region
!"Tumor until proven otherwise
!"Texture sign
!"Regardless of signal characteristics
unless low all sequences representing
$1-*7"7)*-)C&"+)%*'',%("*.)09*8*2S)'*a)
T1/high T2)
!" Contrast studies can be helpful
Figure 27 A & B
Synovial sarcoma with homogeneous appearance

#$)*)(&$()*>#"E3$%*%.EE(%!3$E*#$*3$)10($!*0(%31$D*
8$!"3$%3/#00,*!6(*0(%31$*6#%*$1$%:(/3&/*4(#!."(%*14*#*
solid mass.
The general consensus is that in an

individual case, MRI is not accurate
(,&"<0+)&+;1(9-$)+?0()0(1+*+,&,#;($-4$+
solid soft tissue mass is benign or
malignant.
Musculoskeletal Neoplasm Follow-Up

!" Preoperative – posttherapy
!" Postoperative – recurrence
!" MRI superior to CT
Posttherapy Imaging
!" U.%-,/7".2)*77"$%/("*.)c)osteosarcoma, Postoperative lymphocoele/seroma (*) in patient with
Ewing sarcoma – radiographs/CT previous MFH resection with homogeneous low (T1)
!" Change in size and extent – MRI #$)*63E6*@;FA*%3E$#0*3$!($%3!,*#%*(':(/!()*41"*#*?.3)*
collection.
!" Increasing peritumoral edema
!" Tumor necrosis and hemorrhage
!"> 90% required for pathologic good
response
!"Dynamic MR, sonography, PET/CT
Post-Operative Imaging: Radiographs

!" Comparison to previous studies
!" Findings of recurrence
!"New bone destruction
!"New areas matrix formation

Figure 30 A,
B&C
Myxoid
MFH with
enhancing
peripheral
solid nodular
tissue
(arrows).
These
Figure 29 A to E
enhancing
Recurrent MFH (arrows) adjacent to residual areas
lymphocoele/seroma (*) (same patient as previous represent
MRI but 2 years later). Note the tumor staining on viable tumor regions and biopsy should be directed
angiogram (far right image - arrowhead) versus toward these regions as they harbor diagnostic tissue
=(%%(0%*)"#:()*#+1.!*?.3)*/100(/!31$*@/."=()*#""1<AD and were only detected after contrast administration.
Musculoskeletal Neoplasm use of MRI Musculoskeletal Masses Imaging Goals

with Gadolinium [Figure 30] !" Delineate precise extent of lesion
!" Increase lesion conspicuity (usually not !" Diagnosis/exclude metastases
needed) !" Give most likely tissue type and
!" P&8*-M),+,8/M)".C/88/("*.M)/.+)$1-*7"7) differential diagnosis
all enhance
!" Help differentiate cyst/hemorrhage
!" Helpful in postop cases to show nodular
enhancement with recurrence
!" Vanel/Bloem – dynamic subtraction MRI
early enhancement of recurrent tumor
and response to therapy
References
1. Berquist TH. Magnetic resonance imaging of musculoskeletal neoplasms. Clin Orthop Relat Res 1989
Jul;(244):101-18. Review.
2. Sundaram M, McGuire MH. Computed tomography or magnetic resonance for evaluating the solitary
(&8*-)*-)(&8*-?'"W,)',7"*.)*#)1*.,I)QW,',(/')L/+"*')@ZddY@\0e4[5Z5?=A@S
3. Enneking WF. A system of staging musculoskeletal neoplasms. Clin Orthop Relat Res 1986 Mar;(204):9-
24.
4. Enneking WF, Spanier SS, Goodman MA. A system for the surgical staging of musculoskeletal sarcoma.
Clin Orthop Relat Res 1980 Nov-Dec;(153):106-20.
5. Stacy SG, Mahal RS, Peabody TD. Staging of Bone Tumors: A Review with Illustrative Examples. Am J
Roentgenol Apr 2006;186:967-76.
6. Murphy WA Jr. Imaging bone tumors in the 1990s. Cancer 1991 Feb 15;67(4 Suppl):1169-76. Review.
7. Tateishi U, Yamaguchi U, Seki K, Terauchi T, Arai Y, Kim EE. Bone and soft-tissue sarcoma: preoperative
7(/2".2)a"(9)C&*-".,)@d)C&*-*+,*3<2'&%*7,)G]PDFP)/.+)%*.E,.("*./')"8/2".2S)L/+"*'*2<)XAA\YX=>[d5Z?
47.
8. Gartner L, Pearce CJ, Saifuddin A. The role of the plain radiograph in the characterization of soft tissue
tumours. Skeletal Radiol 2009;38:549-58.
9. Wu JS, Hochman MG. Soft-tissue tumors and tumorlike lesions: A systematic imaging approach.
Radiology. 2009;253(2):297-316.

848
Osteoid Lesions of Bone
Mark D. Murphey, MD
Osteoid Lesions of Bone Enostosis (Bone Island): Radiology
!" Enostosis and associated conditions [Figures 2 & 3]
!" Osteoma !" Round to oval (0.2-2.0 cm) osteoblastic
!" Osteoid osteoma area
!" Osteoblastoma !" Often epiphyseal or metaphyseal
!" Osteosarcoma !" Thorny, radiating spicules at margin but
a,''?+,$.,+
Enostosis (Bone Island): !" Vast majority (> 95%) no need for further
Clinical Characteristics radiologic evaluation following radiograph
!" Stieda 1905 – “Kompakten Knochenkerne” !" Bone scan usually normal (may show
!" f7&/''<)".%"+,.(/')$.+".2 minimal activity)
!" Patient asymptomatic !" May slowly increase or decrease in size
!" Common lesions – unknown frequency !" Differential diagnosis: osteoblastic
(0.43%-14% rib, pelvis, and spine) metastasis, osteoma, osteoid osteoma,
!" Rare in children low grade osteosarcoma
!" Bone scan (if needed to differentiate) in
Enostosis (Bone Island): Histology bone island usually normal (may show
[Figure 1] minimal activity)
!" Intramedullary location !" Follow-up in 1, 3, 6 and 12 months
!" Composed of normal appearing compact !" Biopsy if increase in size too rapidly
lamellar bone with haversian canals !"> 25% over 6 months
!" Blends with surrounding trabecular bone
creating irregular margin
!" Likely developmental – can be considered
a hamartoma
Figure 2 A to E
Enostoses with thorn-like margins (arrows) about the

Figure 1 A & B elbow and ankle in several patients on radiograph, CT
and T1-W MR.
Enostosis histologically with pink cortical bone (*) and
irregular thorn-like medullary margins (arrows).
Figure 3
Enostosis
with thorn-
like margins
(arrow).
Osteoid Lesions of Bone 849 Musculoskeletal Radiology

Giant Bone Island [Figure 4]
!" > 2-3 cm in size
!" Most often in pelvis
!" More likely to have increased activity
(25%) on bone scan (but usually mild;
< ant. iliac crest)
!" V*7()+"#$%&'()(*)+"##,-,.("/(,)#-*8)
sclerosing low grade intramedullary
osteosarcoma (on histology look for
entrapped host lamellar bone)
!" Identical on histology to other bone
islands
Figure 5 A & B
Left Image: Mixture of osteopoikilosis (circular areas

of sclerosis - arrow) and osteopathia striata (linear
areas of sclerosis - arrowhead).
Right Image: Mixture of osteopoikilosis (arrowhead)

and osteopathia striata (arrow) showing low signal
intensity on MRI.
Osteopathia Striata (Voorhoeve

Disease): Clinical Characteristics
!" Osteopoikilosis variant – 1924
!" ^&(*7*8/')+*8"./.(I
!" Usually asymptomatic or mild arthralgia’s
!" Associated syndromes – Goltz syndrome,
cranial sclerosis
Osteopathia Striata: Radiology
Giant bone island in the proximal femur on radiograph [Figures 5 & 6]
(arrowhead), bone scan (with only mild radionuclide !" Linear bands of sclerosis from metaphysis
uptake - circle) mildly with irregular thorn-like
margins, on CT (arrow) and low signal intensity on in long bones
axial T1-W MR (curved arrow). !" K/.?'"W,)1/.+7)*#)7%',-*7"7)".)C/()1*.,7)
(iliac)
!"Could simulate heavy metal poisoning
!" Sometimes associated with osteopoikilosis
Possible Diseases Related to Enostosis !" Bone scan - normal
!" Osteopoikilosis
!" Osteopathia striata
!" Melorheostosis
!" LEM D3 mutation Figure 6
Osteopoikilosis (Osteopathia Osteopathia

Disseminata): Clinical Characteristics striata with
!" Autosomal dominant inheritance; linear bands
asymptomatic of sclerosis
!"6/100,000 radiographs in the pelvis
and proximal
!" !,-8/(*$1-*7"7)',.("%&'/-"7)+"77,8"./(/))) femora.
!"Buschke Ollendorff syndrome
!" Keloid formation
!" May have mild arthralgias (15%-20%)
Osteopoikilosis: Melorheostosis: Clinical Data

Radiology and Pathology [Figure 5] !" Described 1922: Leri and Joanny
!" Numerous circular or ovoid radiodensities !" Only 50% evident before 20 years old
!" Often symmetric – no increased activity !" Equal sex distribution
on bone scan !" Often symptomatic – pain, decreased
!" Predilection epiphyses and metaphyses range of motion (ROM), contractures;
!" Also carpus, tarsus, pelvis limb swelling/length discrepancy and
!" May increase or decrease in size bowing
!" Pathology: same as solitary enostosis !" Scleroderma-like skin lesions over
osseous changes

Melorheostosis: Pathology Osteoma: Clinical Characterisitics
!" Thickened and enlarged cortical bone !" A benign, slow growing tumor, composed
!" Haversian canals normal with irregular of osteoid tissue
arrangement !" Found in cranial vault, sinuses, mandible
!" Marrow space may show increased and (rarely) long bones
cellularity !" Represent protruding mass of dense
!" Q*#()("77&,)8/<)%*.(/".)8/77)*#)$1-*&7) periosteal intramembranous bone on
("77&,)a"(9)*-)a"(9*&()*77"$%/("*. surface of host bone
!" Signs/symptoms depend on size/location
Melorheostosis: Radiology [Figures 7 & 8] !" Sinus lesions may lead to sinusitis,
!" Distribution - single limb - more common headache, or can grow into cranial vault
lower extremity !" Orbital lesion may cause exophthalmos,
!" One or more bones – sclerotome displacement of globe, diploplia
(skeleton supplied by spinal sensory !" 0.42% patients with sinus radiographs
nerves) pattern
!" Osseous excrescences often exuberant Osteoma: Pathology
and lobulated along bone surface - !" Nodules of dense osseous tissue
“candle wax” !" Differences from bone island:
!" Also endosteal involvement may extend !"Often a mix of woven and lamellar
into marrow space bone
!" Can extend into soft tissue with !"May/may not contain haversian
*77"$%/("*.M)*#(,.):,-"/-("%&'/- system
!" May lead to joint ankylosis !"Arises from cortex rather than
!" Intense activity on bone scan intramedullary
!"Do not blend with trabecular bone
!"Most frequent in the skull
!" In craniofacial area often in spectrum of
$1-*77,*&7)',7"*.7
Osteoma: Radiology [Figures 9 to 11]

!" Q9/-:'<)+,$.,+M)9*8*2,.,*&7M)1*.,)
mass arising from surface of bone
!" Most frequently diagnosed incidentally on
radiographs
!" Frontoethmoid sinus region 75%
!" Sphenoid 1%-4%
Figure 7 A, B & C
Left Image: Melorheostosis with mineralized inguinal
soft tissue mass (arrowhead).
Middle and Right Images: Melorheostosis classic
“dripping candle wax” appearance (arrow).
Figure 9 A & B
Large frontal sinus osteoma (*) on CT causing clinical
symptoms due to obstruction.
Figure 10
Gross specimen
calvarial
osteoma (*)
on surface of
Figure 8 A & B outer table
(arrow) but not
Melorheostosis involving foot with increased uptake on extending into
bone scan (same patient as previous two images). the diploic space
(DS).

Osteoid Osteoma Distribution [Figure 12]
!" Femur/tibia: 50%-60% of lesion
!" Most frequent in long bone diaphysis
(70%-80%)
!" Spine: 10%-20% (90% posterior
elements), 10% vertebral body, lumbar
59%
!" Hand/foot: 10%-20% – proximal phalanx,
Figure 11 metacarpal, scaphoid, navicular, calcaneus
!" Epiphyseal lesions are rare
Calvarial
osteoma (*).
Figure 12
Osteoma: Gardner Syndrome
!" Multiple osteomas are almost always Osteoid
associated with Gardner syndrome osteoma
distribution.
!"Familial autosomal dominant
(APC gene 5q22)
!"Intestinal polyposis
!"Multiple osteomas
!"Dental lesions
!"Fibromatosis in 10% typically
intraabdominal
!"Skin lesions
!"Q,1/%,*&7)%<7(7)/.+)$1-*8/7
Osteoid Osteoma: History

!" Described in 1935 by Jaffe as an
osteoblastic tumor composed of osteoid
and atypical bone
!" Established by Jaffe as a distinct clinical
and pathologic entity
!" Controversy remains as to true nature: Osteoid Osteoma: Pathology
".C/88/(*-<M)(-/&8/("%M)E/7%&'/-M)E"-/' !" The “nidus” is the lesion – yellowish to
red pea
Osteoid Osteoma: !" Composed of osteoid and woven bone
Clinical Characterisitics with interconnected trabeculae
!" 11% of all bone lesions that come to !" Background and rim of highly vascularized
biopsy (3% of primary bone tumors) $1-*&7)%*..,%("E,)("77&,
!" 13.5% of all benign biopsied bone tumors !" Extensive reactive bone may surround the
!" Spinal lesions commonly present with lesion
painful scoliosis, without neurologic !" No malignant potential
dysfunction
Osteoid Osteoma: C%*##-4$*)-&,
!" Intraarticular lesions often present with
!" Cortical (70%-75%): long bone shaft;
.*.7:,%"$%)E/2&,)T*".():/".
intense fusiform sclerosis; central nidus
!" Young patients usually 10-25 years (50%
!" Cancellous (25%) intermediate frequency;
second decade)
usually femoral neck, hand/foot; often
!" M:F approximately 2-4:1
limited surrounding sclerosis
!" Rare in African Americans
!" Intraarticular lesions (cortical/cancellous)
!" Pain almost invariably presenting
may have limited sclerosis/periosteal
complaint (1.6% painless – 50% of these
reaction and can be distant from nidus
in the hand)
!" Subperiosteal; rare, arises adjacent to
!" Night pain relieved by aspirin/
bone; usually femoral neck, talar neck,
nonsteroidals (31%-75%)
hand, foot; bone may show pressure
!"Inhibit prostaglandin E2, aggravated
erosion
by ETOH

Osteoid Osteoma
Radiology: Cortical Lesions [Figures 13 to 19]
!" Dense fusiform sclerosis
!" Periosteal bone solid, rarely lamilated
!" Nidus usually central, rarely > 1.5-2 cm
!" “Hot” on scintigraphy – double density
sign
!" ;"+&7)a,''?+,$.,+)*.)FP)a"(9)/)
smooth peripheral margin, +/- central
mineralization (50%)
Osteoid Osteoma: MR Imaging

!" Low to intermediate intensity T1-WI
!" Intermediate to high intensity T2WI
!" Low intensity all pulse sequences if totally
mineralized nidus (may variably enhance,
sometimes intensely)
!" May detect synovitis/joint effusion/soft
tissue edema that can be very prominent/
confusing imaging feature (86%)
!" Reactive marrow edema may obscure
lesion (77%)
!" CT more helpful in majority (can miss in
35% by MR alone); however, MRI may be Figure 14
E,-<)9,':#&')".)+"#$%&'()%/7,7S
CT of osteoid osteoma with central focus of
/#0/3&/#!31$D
Figure 15 A & B
MR imaging of osteoid osteoma with intermediate
signal intensity on T1- and T2-W (arrows). The
surrounding marrow edema is prominent (*) and can
obscure the nidus.
Figure 13 A & B
Humeral osteoid osteoma in the cortex with bone scan

showing “double uptake sign”.
Figure 16 A & B
Osteoid osteoma specimen radiograph shows central
/#0/3&/#!31$*#$)*($!3"(*nidus within the bivalved gross
specimen.

Cortical Osteoid Osteoma: Differential
Diagnosis
!" Brodie abcess
!" Stress fracture (linear not circular)
!" Langerhans cell histiocytosis
Osteoid Osteoma Radiology:

Intraarticular/Cancellous Lesions
Figure 17 A & B !" Reactive osteosclerosis/periosteal reaction
CT and postcontrast MR of an acetabular osteoid often mild/absent and may be distant
osteoma (arrows) with marked enhancement. from lesion
!" Associated joint effusion/lymphofollicular
synovitis
!" Regional osteoporosis-disuse
!" May have associated periostitis
!" May be diffusely “hot” on scintigraphy
!" Subperiosteal lesions present as
juxtacortical masses
Intraarticular Osteoid Osteoma:

Differential Diagnosis [Figures 20 & 21]
!" Rheumatoid arthritis, JRA
!" Tuberculous arthritis
!" ;*.7:,%"$%)7<.*E"("7
!" Septic arthritis
!" Osteoblastoma (particularly spine)
Figure 18 A & B
Radiograph and bone scan of spinal osteoid osteoma

in facet with a sclerotic pedicle (arrow) and increased
uptake on the radionuclide bone scan (arrowhead).
Figure 19
CT of spinal
osteoid
osteoma in
facet with
central Figure 20 A & B
/#0/3&/#!31$D
Subtle intraarticular osteoid osteoma (arrow) with
/($!"#0*/#0/3&/#!31$*/#.%3$E*(44.%31$*#$)*63:*G13$!*
widening simulating septic arthritis.
Figure 21A
Differential Diagnosis of Osseous Subtle

intraarticular
Lesions with Sequestra-Like osteoid
Appearance osteoma
!" Osteomyelitis – pyogenic (arrow)
!" Subacute osteomyelitis or unusual with central
/#0/3&/#!31$*
organism
causing
!" Osteoid osteoma/osteoblastoma effusion and hip joint widening simulating septic
!" Langerhans cell histiocytosis arthritis on CT and MR. The CT shows typical nidus
!" Metastases <3!6*/($!"#0*/#0/3&/#!31$*@#""1<A*!6#!*3%*)34&/.0!*!1*
!" Fibrosarcoma/MFH perceive on the MR.
!" Lymphoma

Osteoblastoma: Clinical Features
!" Patients are young, median age 18, 80%
are between 10-30 years old
!" M:F; 2-3:1
!" Pain is most common symptom, less
Figure 21 severe than osteoid osteoma
B&C
!" Less often at night and may or may not
be relieved by aspirin
Subtle
intraarticular Osteoblastoma: Skeletal Distribution
osteoid
[Figure 22]
osteoma
(arrow) !" Spine (40%) equally distributed cervical
with central through sacrum
/#0/3&/#!31$* !" About 30% occur in long bones (femur
causing and tibia most common)
effusion and
hip joint !" Skull, mandible, maxilla (15%)
widening !" Small bones of hand and feet (10%) and
simulating pelvis (5%)
septic arthritis
on CT and MR.
The CT shows
typical nidus
with central
/#0/3&/#!31$*
(arrow) that
3%*)34&/.0!*!1*
perceive on
the MR.
Figure 22
Osteoblastoma
skeletal
Osteoid Osteoma: Classic Treatment distribution.
!" Surgical excision: curative (88%-
97%) with complete nidus removal –
postintraoperative radiographs
!" Dramatic relief of symptoms
!" Recurrence due to incomplete excision
can then have multiple nidi
!" Problems
!"Locating lesion at surgery
!"Tetracycline and radionuclide labeling
Osteoid Osteoma:
Other Treatment Methods
!" Medical – spontaneous healing (may take
2-4 years) Osteoblastoma: Pathology
!" Percutaneous removal !" Micro: large number of osteoblasts
!" Percutaneous ablation (89%-95% producing trabeculae, osteoid or bone
success) !" Virtually indistinguishable from osteoid
!"Thermal radiofrequency osteoma on high-power histologic
!"Interstitial laser examination
!" Embolization single feeding artery !" At times minor microscopic differences
0:*(,.("/''<4I from osteoid osteoma but may rely on
radiology
Osteoblastoma
!" Rare benign osteoid producing tumor Osteoblastoma Radiology: General
characterized by osteoid and woven bone !" Described as having 3 radiologic patterns
production !"Similar to but larger than osteoid
!" Synonyms include: giant osteoid osteoma, osteoma (> 2 cm)
/.+)*7(,*2,."%)$1-*8/ !"Expansile lytic lesion with
!" About 1% of excised primary osseous mineralization
tumors !"More aggressive appearance -
!" Osteosarcoma 20x more common, osteoid marked bone destruction, scattered
osteoma 4x more frequent %/'%"$%/("*.M)/.+)7*#()("77&,)8/77

Osteoblastoma Radiology: S;($-4$ Osteoid Osteoma/Osteoblastoma
!" Radiologic features are not always Differential Diagnosis: Spine
distinctive !" Osteoblastoma
!" Lytic lesion with varying bone production !"Size > 1.5-2.0 cm
!" Cortex thinned with expanded contour, !"Growth and soft tissue mass
may be destroyed (62%), and have a soft !"Matrix – multifocal – noncentral
tissue mass !"Scoliosis (31%) and classic symptoms
!" Mineralization (55%-72%) may appear absent
like chondroid tissue, “arcs and rings,” but !" Pedicle sclerosis; lymphoma, mets,
no chondroid tissue pathologically spondylolysis, congenital abscence/
!" May have surrounding edema but less hypoplasia posterior elements, malaligned
common than osteoid osteoma apophyseal joints, unusual infection
!" Up to 16% secondary ABC component
!" Solid elements often low/intermediate Osteoblastoma Radiology; Long Bones
signal T2 MR [Figure 24]
!" Usually eccentric, metaphyseal (25%), or
Osteoblastoma Radiology: Spine diaphyseal (75%)
[Figures 22 & 23] !" Intramedullary or cortical, rarely
!" Posterior elements alone subperiosteal
most common (> 60%) !" Solid periostitis (50%)
!" Posterior elements extending into !" May appear as a blister lesion in hand or
vertebral body (25%) foot, may also have osteoporosis
!" Vertebral body alone (3%-15%) !" Correct diagnosis usually not suggested
!" V*-,)'"W,'<)(*)%*.(/".)*77"$%/("*.)/.+)7*#() prospectively
tissue mass
!" Less likely to elicit sclerosis
!" Scoliosis variably present (31%); less
characteristic than osteoid osteoma
Figure 22
Osteoblastoma Figure 24 A & B

of C3 spinous
process and H%!(1+0#%!1>#*14*:"1'3>#0*4(>."*<3!6*/#0/3&/#!31$*1$*
lamina. CT (arrow).
Osteoblastoma: Natural History

!" The lesion usually grows slowly
!" Treatment is curettage or excision
!" Recurrence rate is 10%-15%
Aggressive “Malignant” Osteoblastoma

!" Initially described in 1967 by Mayer
!" F*.7"+,-/1',)%*.(-*E,-7<)/.+)+,$."("*.)
not clearly established
!" Problems in distinction from
osteoblastoma like osteosarcoma and rare
reports of osteoblastoma recurring as
osteosarcoma
Aggressive Osteoblastoma: Pathology

!" Similar to conventional osteoblastoma
!" Wider, more irregular trabeculae
Figure 23 A & B
!" Lace-like osteoid
CT of C3 osteoblastoma with extensive mineralization. !" g/-"/1',)8"(*7,7)1&().*)/(<:"%/')$2&-,7
!" Epithelioid osteoblast

Aggressive Osteoblastoma: Osteosarcoma: Histologic Pattern
Clinical/Radiologic Characterisitcs Types %
[Figure 25] O
Fibroblastic (
Similar locations Chondroblastic 5%
examination with soft tissue mass Small cell 1%

Local recurrence rate up to 50% Other 2%
Usually no metastases
Primary Osteosarcoma: C
Types %
I
Gnathic 6%
Soft tissue 4%
Osteosarcomatosis-multifocal 1%-2%
Intracortical 0.2%
Secondary Osteosarcoma: C
Radiation induced (6%-22%)

Osteonecrosis
Figure 25 A & B
Aggressive osteoblastoma with large soft tissue mass
chronic
(arrow) and multilevel involvement. osteomyelitis, retinoblastoma
Osteosarcoma (OS) D
Osteosarcoma
differentiates to produce osteoid Primary, High-Grade, Intramedullary
“...If only 1% of a tumor manifests osteoid
Also termed central or conventional
Most patients are 15-25 years old, rare in
osteosarcoma”
component”
Only true for intraosseous neoplasm than 50% about the bones of the knee
90% are metaphyseal, 5%-10%
Mirra JM. “Bone Tumors.” Lee & Febiger, 1989. diaphyseal
Osteosarcoma is the second most Osteosarcoma Intramedullary:
common primary malignant bone tumor Radiology [Figures 26 to 29]
- 15% of all biopsied primary bone Usually mixed sclerosis and lysis
tumors.
Codman
Osteosarcoma:
Additional D (sunburst, hair on end)
precursor lesion or treatment Extend across epiphyseal plate
precursor or is metastatic from primary OS
6 months of each other
than 6 months apart
Osteosarcoma: General Pathology

Osteoid and/or immature bone production
by tumor cells

Figure 26 A & B
Figure 29 A & B
Intramedullary osteosarcoma with osteoid matrix
(arrows) and aggressive bone lysis (arrowheads). Intramedullary osteosarcoma with skip metastases (*)
on coronal STIR MR image and gross specimen with
distal primary lesion (arrow) and intervening normal
marrow (M).
Osteosarcoma Telangiectatic
Figure 27 !" Tumor largely composed of cystic cavities
containing necrosis and hemorrhage
Bone scan of (> 90 %)
intramedullary
osteosarcoma of !" 2.5%-12% of osteosarcomas
tibia with intense !" ABC-like - misdiagnosed on radiographs
radionuclide !" Distribution similar to other intramedullary
uptake. The osteosarcomas
femur and !"Femur, tibia, humerus
ankle also show
increased uptake !"Metaphyseal (90%), diaphyseal (10%)
(arrowheads) from
hypermia and Osteosarcoma Telangiectatic
disuse. [Figures 30 to 33]
!" Largely osteolytic and expansile
!" Look for small areas of osteoid
!"58% X-rays; 85% CT
!" Fluid-levels
(CT 48%/MRI 74% T1W/89% T2W)
!" Pathologic fracture (25%-61%)
!" Donut sign on bone scan (65%)
!" Previously worse prognosis, now
may actually be better than other
intramedullary osteosarcomas
(58%-67% 5-year survival)
Figure 30
Telangiectatic
osteosarcoma
of scapula with
thick peripheral
mineralization
(arrow).
Figure 28 A & B
Coronal STIR MR image and gross specimen of tibial
intramedullary osteosarcoma show identical lesion
extent (*).

Figure 31 Parosteal Osteosarcoma: Clinical and
Pathology
Telangiectatic !" Arise from outer layer of periosteum
osteosarcoma !" f7&/''<)/)'*a)2-/+,)(&8*-)c)$1-*1'/7("%)
of scapula with
thick enhancing stroma and streamers of woven bone
nodular wall !" Patients about a decade older than
containing intramedullary osteosarcoma; F > M
/#0/3&/#!31$* !" Location: femur (65%), humerus (15%)
(arrowheads)
and central
("1"/)0@A64M)$1&'/)0564M)#*-,/-8)0564
hemorrhage/ !" Most common posterior distal femur
necrosis (*) on metaphysis
CT.
Parosteal Osteosarcoma: Radiology
Figure 32 [Figures 34 to 36]
!" Initially an exophytic sclerotic mass
Gross !" F/&'"C*a,-?'"W,)a"(9)'&%,.()%',/E/2,):'/.,)
specimen between lesion and cortex
of scapular !" Radiodense centrally with growth can
telangiectatic reattach to cortex and obliterate cleavage
osteosarcoma
with cystic plane
spaces (*) !" MRI/CT to evaluate intramedullary
surrounded invasion important for surgical resection
by solid !" Long term survival 80%-90% (5-10
viable tissue
years)
(arrowheads).
Figure 33 A & B
Telangiectatic osteosarcoma of distal femur on

sagittal T1-weighted postcontrast MR image and
gross specimen showing thick nodular enhancement
peripherally in viable tumor (arrowheads) correlating
to gross specimen with central nonenhancing cystic/
necrotic regions (*).
Figure 34 A & B
Parosteal osteosarcoma with specimen radiograph and

gross specimen showing surface mass with central
dense stalk of attachment to the cortex (*) and lucent
cleavage plane (arrows).
Juxtacortical Osteosarcoma
!" Parosteal (65%)
!" Periosteal (25%)
!" High grade surface (10%)
!" Prognosis varies with grade and extent

Periosteal Osteosarcoma:
Clinical and Pathology
!" Periosteal osteosarcoma is usually
chondroblastic (> 90% of tumor) and
intermediate grade
!" Arise from inner layer of periosteum
Figure 35 !" More than 85% are in the diaphysis of the
A&B
femur and tibia; ulna and humerus (10%)
Parosteal !" Similar age to conventional osteosarcoma
osteosarcoma and sex distribution (M > F)
of the distal
femoral
!" Better prognosis but 15% rate of
metaphysis with metastasis
radiograph,
CT and gross Periosteal Osteosarcoma: Radiology
specimen and [Figure 37]
specimen
radiograph
!" Saucerized cortex with chondroblastic soft
showing surface tissue mass on imaging in area of erosion
mass (*), !" Cortical thickening at margins of erosion
lucent cleavage (40%)
plane (arrows) !" May have Codman triangle
and medullary
backgrowth !" Spiculated periosteal reaction
(arrowhead). !" Only rarely intramedullary invasion
reported
Figure 37 A & B
Periosteal osteosarcoma on radiograph and coronal CT

reconstruction with diaphyseal broad-based soft tissue
mass causing erosion of underlying thickened cortex
and “hair-on-end” periosteal reaction.
Osteosarcoma: High-Grade Surface

[Figures 38 & 39]
!" Histology high-grade similar to a
conventional osteosarcoma as is prognosis
with same potential for metastasis
!" Sites: femur (45%), humerus (26%),
Figure 36 A & B
$1&'/)0@A64M)&'./)0e64)
Parosteal osteosarcoma of the distal femoral !" Radiologic changes: broad-based lesion
metaphysis with radiograph, CT and gross specimen with osteoid arising on osseous surface
and specimen radiograph showing surface mass !" Similar appearance to periosteal
(*), lucent cleavage plane (arrows) and medullary
osteosarcoma but often more aggressive
backgrowth (arrowhead).

Figure 40
Gnathic
osteosarcoma
with an
aggressive
mixed lytic
and sclerotic
(arrows) lesion
destroying the
alveolar ridge
(arrowhead).
Osteosarcoma:
Low-Grade Intramedullary
frequency
than conventional osteosarcoma
(50%), NOF (25%), chondroblastoma

(15%), CMF (10%)
Figure 38 A & B
Osteosarcoma Low-Grade
High-grade surface osteosarcoma. Intramedullary [Figures 41 & 42]
Not uncommonly metapiphyseal
Location same as intramedullary
conventional
Central sclerosis with expansile
within
initial reports
ISS 2003 (Skel Rad
mass
metastatic rate
Figure 39 A & B
High-grade surface osteosarcoma (*) on sagittal T1-
weighted MR and sagittally sectioned gross specimen.
canal (M).
Gnathic Osteosarcoma [Figure 40]

About 6% of all osteosarcoma
Patients are usually older
Figure 41 A & B
About half are chondroblastic
Low-grade intramedullary osteosarcoma simulating
metastasize but invade locally) extension is suggested medially (*).

Osteosarcoma: Intracortical
Figure 42
[Figures 44 & 45]
Low-grade Very rare, only a handful of cases
intramedullary Almost all in the femur and tibia diaphysis
osteosarcoma The lesion is dominantly or exclusively
simulating intracortical with no (or only minimal)
intramedullary involvement
on radiographs.
CT reveals
a soft tissue
mass medially
(*) that would
not be seen in
Figure 44
Osteosarcoma: Intracortical
Soft Tissue (Extraskeletal) osteosarcoma
with matrix
mineralization
and location
years) within the
cortex (arrow)
on radiograph
Not uncommonly history of trauma (10%- and CT.
15%)
Relationship to
Osteosarcomatosis:
Multifocal Osteosarcoma [Figure 43] Figure 45
Rare
Intracortical
osteosarcoma
years old with matrix
mineralization
and location
within the
Type 3 likely represents metastatic cortex (arrow).
disease
Types 1 and 2 usually demonstrate a
Amstutz Cancer. 1969;24:923.
Osteosarcoma: Treatment and

Prognosis
Complete removal of the primary tumor –
Preoperative chemotherapy – look for >

90% tumor necrosis - most important
survival; 14% < 90% necrosis)

Postoperative chemotherapy
Overall 5-year survival 41%-64%
resection
Figure 43 A & B
Osteosarcomatosis with multifocal areas of
metaphyseal sclerosis (*) with primary dominant
sclerotic focus in the tibia (*) in the right image.

References
Enostosis and associated conditions
1. J-,,.7:/.)^M)Q(/+/'."W)LFSS)O*.,)"7'/.+[)7%".("2-/:9"%)$.+".27)/.+)(9,"-)%'"."%/')/::'"%/("*.S)F/.)^77*%)
Radiol J 1995 Oct;46(5):368-79.
2. Judkiewicz AM, Murphey MD, Resnik CS, Newberg AH, Temple HT, Smith WS. Advanced imaging of
melorheostosis with emphasis on MRI. Skeletal Radiol 2001 Aug; 30(8):447-53.
Osteoma
3. Sundaram M, Falbo S, McDonald D, Janney C. Surface osteomas of the appendicular skeleton. AJR Am J
Roentgenol 1996 Dec;167(6):1529-33.
Osteoid Osteoma
4. Klein MH, Shankman S. Osteoid osteoma: radiologic and pathologic correlation. Skeletal Radiol. 1992;
21(1):23-31. Review.
5. Davies M, Cassar-Pullicino VN, Davies AM, McCall IW, Tyrrell PN. The diagnostic accuracy of MR imaging in
osteoid osteoma. Skeletal Radiol 2002;31:559-69.
6. Kransdorf MJ, Stull MA, Gilkey FW, Moser RP, Jr. Osteoid osteoma. RadioGraphics 1991;11:671-96.
7. Davies A, Saifudding A. Imaging of painful scoliosis. Skeletal Radiol 2009;38:207-23.
8. Motamedi D, Learch TJ, Ishimitsu DN, Motamedi K, Katz MD, Brien EW, Menedez L. Thermal ablation of
osteoid osteoma: overview and step-by-step guide. Radiographics 2009;29:2127-41.
9. Mylona S, Patsoura S, Galani P, Karapostolkis G, Pomoni A, Thanos L. Osteoid osteomas in common and in
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10. Chai JW, Hong SH, Choi JY, Koh YH, Lee JW, Choi JA, Kang HS. Radiologic diagnosis of osteoid osteoma:
#-*8)7"8:',)(*)%9/'',.2".2)$.+7S)L/+"*J-/:9"%7)XA@AY5A[\5\?=ZS)
Osteoblastoma
11. h-**.)_VM)Q%9&-8/.7)RS))B7(,*1'/7(*8/[)%'"."%/')/.+)-/+"*'*2"%)$.+".27)".)Zd).,a)%/7,7S)L/+"*'*2<S)@ZZA)
Jun;175(3):783-90.
Osteosarcoma
12. Murphey MD, Robbin MR, McRae GA, Flemming DJ, Temple HT, Kransdorf MJ. The many faces of
osteosarcoma. RadioGraphics 1997 Sep-Oct; 17(5):1205-31.
13. !"7%,:*'/)KM)G*a,'')PUM);/9/')^S)P,'/.2",%(/("%)B7(,*7/-%*8/[)-/+"*'*2"%)/.+):/(9*'*2"%)$.+".27S)
RadioGraphics 2009;29:380-3.
Alphabet Soup and Cystic Lesions of Bone 863 Musculoskeletal Radiology

864
Cartilaginous Lesions of Bone
Mark D. Murphey, MD
Cartilaginous Lesions Osteochondroma: Pathology

!" Osteochondroma !" Medullary and cortical continuity with
!" Enchondroma underlying bone
!" Juxtacortical chondroma !" Hyaline cartilage cap
!" F9*.+-*8<3*"+)$1-*8/)0FVK4) !" Cartilage cap involutes after growth
!" Chondroblastoma (skeletal maturity)
!" Chondrosarcoma !" Only benign skeletal neoplasm associated
with radiation
Osteochondroma !" Can be induced by implanting epiphyseal
!" The most common benign neoplasm of tissue
bone that leads to biopsy !" Traumatic osteochondroma
Osteochondroma: Types Osteochondroma: Imaging

!" Solitary osteocartilaginous exostosis [Figure 2]
!" Hereditary multiple exostoses (HME) !" Mature bone: cortex and marrow
!"Diaphyseal aclasis !" _</'".,)%/-("'/2,)%/:[)%/'%"$%/("*.
!"Multiple osteochondromas !" Cortical and marrow continuity with
!"Osteochondromatosis underlying bone
!" Long bones: radiographs to diagnose
Osteochondroma: Clinical Data !"Metaphyseal
[Figure 1] !"Grows away from epiphysis
!" No sex predilection !"May be associated with failure of
!" Young patients (75% < 20 years old tubulation (particularly HME)
!" Present as a mass: responsible for !" Flat bones: often need CT/MR to diagnose
symptoms !"Tend to be larger and sessile
!" Location: femur (30%), tibia (20%), !"More variable appearance
humerus (20%), hand and foot (10%),
pelvis (5%), scapula (4%)
!" Treatment Individualized Resection
!"Dependent on symptoms/size/location
Figure 1 Figure 2 A & B
Osteochondroma Osteochondromas with marrow (*) and cortical

skeletal (arrows) continuity on radiography and histology.
distribution. Note undertubulation on macrosection in patent with
hereditary multiple exostoses (HME) with other small
0(%31$%*3)($!3&()*+,*6,#03$(*/#"!30#E(*/#:%
(arrowheads).
Cartilaginous Lesions of Bone 865 Musculoskeletal Radiology

Osteochondroma: Osteochondroma: Cartilage Cap
Radiographic Subtypes [Figures 3 & 4] [Figures 4 to 10]
!" Pedunculated !" L/+"*2-/:97[)%9*.+-*"+)%/'%"$%/("*.
!" Sessile !"Increasing destruction or change in
appearance
!"Worrisome for malignancy
!" Ultrasound: good for cap and bursae
!" FP[)7*#()("77&,)a"(9)%/'%"$%/("*.
!"F/.)1,)+"#$%&'()(*)+"7(".2&"79)#-*8)
muscle
!" BS: increased uptake
!" MRI: intermediate signal T1-WIs
!"High signal T2-WIs
!" Cap thickness: benign vs malignant
!"Benign < 2.0 cm
(0.1-2.2 cm; 79% < 10 mm)
!"Malignant > 2.0 cm
(2.0-17 cm; 74% > 4 cm)
!"!,:,.+7)*.)7W,',(/')8/(&-"(<I
Figure 3 A & B
Sessile and pedunculated osteochondromas with

marrow (*) and cortical (arrows) continuity.
Figure 5 A & B
Osteochondroma on CT with marrow and cortical

continuity.
Figure 4 A, B & C
9"1'3>#0*4(>."*1%!(1/61$)"1>#*<3!6*)34&/.0!,*3$*
identifying cortical and medullary continuity on the CT
scout views (arrows). Cortical and medullary continuity
are optimally revealed on CT (arrowheads).
Osteochondroma: Complications
!" Deformity
!"Cosmetic
!"Osseous and mechanical
!" Fracture
Figure 6 A, B & C
!" Vascular compromise
!" Neurologic sequelae Osteochondroma on radiograph and sagittal T1-W and
!" Bursa formation axial T2-W MR images with thin cartilage cap showing
!" Malignant transformation high signal on long TR MR (arrowhead).
Osteochondroma
!" The cartilage cap deserves the most
consideration in radiologic interpretation

Figure 7 A & B
Gross specimen and macrosection of resected

osteochondroma with thin bluish cartilage cap (*)
correlating with the imaging (same case as previous
images).
Figure 10 A & B
Sagittal STIR MR and gross specimen of resected

osteochondroma with high signal, thick cartilage cap
(15-year-old boy with thick cartilage cap simulating
malignancy but only represented growth due to young
age; same case as previous radiographs and axial
T1-W MR).
Subungual Exostosis:
Dupuytren Exostosis [Figure 11]
!" Osteochondroma variant
!" F > M (2:1); young 20-40 years old
!" Often painful; associated trauma/infection
(reactive)
!" ;,*:'/7("%)%<(*2,.,("%)/1,--/("*.)(0iYe4I
Figure 8 A & B !" J-,/()(*,)0\\6?dA64Y)$.2,-7)0@A6?
Lateral ankle radiographs at 3-year interval shows 14%)
growth of the osteochondroma in this 15-year-old boy. !" Fibrocartilage cap
The same radiographic appearance would represent !" Located away from physis
malignant transformation in an adult.
Figure 11 A & B
Subungual exostosis (arrow) with clinical photograph.

Figure 9 A & B
Axial T1-W MR images show cortical and marrow

(arrowheads) continuity and thick cartilage cap (*) (15
-year-old boy, same case as previous radiographs).

Dysplasia Epiphysealis Hemimelica:
Trevor Disease [Figures 12 to 14]
!" Male predominance (3:1) Figure 14
!" Rare
!" Swelling, pain, and deformity Dysplasia
epiphysealis
!" Usually lower extremity, unilateral hemimelica
!" 65% multiple bone involvement talus, (Trevor
distal femur, tibia disease) with
!" Ankle and knee most common the epiphyseal
!" Medial joint 2x lateral osteochondroma
(*) arising from
!" Lobular epiphyseal mass the posterior
!" Histologically identical to an femur on
osteochondroma coronal 3D CT
!" May produce deformity and secondary reconstruction
(same case
osteoarthritis as previous
images).
Figure 12
Hereditary Multiple Exostoses: Clinical
Dysplasia Data [Figures 15 to 17]
epiphysealis !" Male predominance (3:1)
hemimelica !" Autosomal dominant inheritance
(Trevor disease)
with early genu !" Variability in size and number
varus deformity !" Any portion of the skeleton preformed in
caused by the cartilage may be involved
epiphyseal !" Present in childhood
osteochondroma !" May be bilaterally symmetric
(arrow).
!" One side may predominate
!" Increased incidence of malignant
transformation (10%-20%)
!" Newer literature (3%-5%)
Figure 15 A & B
Hereditary multiple exostoses (HME) with associated
Figure 13 A & B
.$)("!.+.0#!31$*14*+1$(*@I"0($>(,("*?#%2*)(41">3!,AD
Dysplasia epiphysealis hemimelica (Trevor disease)
with the epiphyseal osteochondroma (*) arising from
the posterior femur on lateral radiograph and sagittal
T2-W MR. Figure 16
HME with
typical
pelvic and
proximal
femoral
deformity.

Figure 18
Osteochondroma
with malignant
transformation
skeletal
distribution.
Figure 17 A to F
HME with typical pelvic and proximal femoral

deformity. Bone scan shows a left pelvic lesion to
reveal more intense radionuclide uptake (*) and
this area demonstrates a very thick hyaline cartilage
cap (> 3 cm) and soft tissue mass with chondroid
mineralization (rings and arcs) (arrows) on CT
and T1-/T2-W MR images (arrows) resulting from Enchondroma: Distribution [Figure 19]
malignant transformation to chondrosarcoma. This is
also shown on the gross specimen.
Osteochondroma with Malignant

Transformation Distribution
[Figure 18]
Enchondroma: The Most Common Tumor

Encountered in the Phalanx.
Enchondroma: Types
!" Solitary enchondroma
!" Multiple enchondromatosis Figure 19
!" Ollier disease
Enchondroma
!" Maffucci syndrome skeletal
distribution.
Enchondroma: Clinical Data
!" 3%-5% all biopsied primary bone lesions;
1% all in bone tumors
!" No sex predilection
!" Peak incidence third decade
(10-30 years old)
!" Hands and feet (40%-65%), long tubular
bones (25%)
!" Phalanges and metacarpals most common
locations
!" V/<)1,)".%"+,.(/')$.+".2)*-):-,7,.()a"(9)
pathologic fracture

Enchondroma: Pathology
!" Rests of hyaline cartilage
!" Hyaline cartilage often with myxoid areas
!" g/-"/1',)/8*-:9*&7)%/'%"$%/("*.)/.+)
,.%9*.+-/')*77"$%/("*.
!" May cause expansile remodeling and
cortical thinning
Enchondroma: Imaging [Figures 20 to 22]

!" Geographic lytic lesion IA-IB
!" Central often metaphyseal
!" Expansile remodeling with prominent
thinned cortex (short tubular bones only) Figure 22 A,
!" Chondroid matrix in majority; 17% limited B&C
or none (radiographs); all by CT Enchondroma
!" MRI: lobulated margin of the distal
!"Marked increase intensity T2-WIs femur on
radiograph,
!"F/'%"$,+)%9*.+-*"+)'*a)".(,.7"(<) sagittal T1-W
and T2-W MR
images and
histology.
Note lobular
margin
(arrows), ring
and arc mineralization (arrowhead), no endosteal
scalloping, and high signal on long TR image
resulting from high water content of nonmineralized
hyaline cartilage. Mineralized hyaline cartilage stays
low signal intensity on T2 causing heterogeneous
appearance.
Multiple Enchondromatosis:
Clinical Data
!" Variable severity
!" May be predominantly unilateral
Figure 20 A & B
(Ollier disease – 1899)
Enchondroma of the phalanx with typical ring and !" May become stable at puberty
arc chondroid mineralization and deep endosteal
!" Increase malignant transformation to
scalloping.
chondrosarcoma (5%-50%)
!" Marked skeletal deformity
!" Not hereditary
!" Mild male predilection
!" Presents in childhood
Maffucci Syndrome
!" Described in 1881 by Maffucci as
enchondromatosis with hemangiomas
Maffucci Syndrome: Clinical Data

!" Multiple enchondromas
!" Cavernous hemangiomas
!" Very rare; nonhereditary
!" Mild male predilection
!" Hands and feet greatest involvement
!" Complications of hemangiomas
!" Malignant transformation
Figure 21 A & B !"Chondrosarcoma (15%-20%)
!"Vascular sarcoma (3%-5%)
Enchondroma of tibia on coronal T1-W and T2-W
MR images. Note lobular margin and no endosteal
!"Ovarian and pancreatic malignancy
scalloping and high signal on long TR image resulting !"Glioma and carcinoma
from high water content of nonmineralized hyaline
cartilage. Mineralized hyaline cartilage stays low signal
intensity on T2.

Maffucci and Ollier Syndromes:
Imaging Characteristics [Figures 23 & 24]
!" Lesions seen in infancy
!" Lytic columns from epiphyseal plate
extending into the metaphysis
!" Later typical enchondromata
!"Geographic IA-IB with expansion
!" F9*.+-*"+)8/(-"3)%/'%"$%/("*.
!" Growth disturbance and bowing
!" Enchondroma growth slows after plate
closure
!" Soft tissue masses with phleboliths
!" Chondrosarcomatous transformation
!"New bone destruction with ST mass
!"New periosteal reaction
!"Disorganized or destroyed matrix
%/'%"$%/("*.
Figure 24 C, D, E & F
Enchondromatosis on bone scan and extensive
deformity of the upper extremity on radiograph.
Note predominance on one side of the body on bone
scan. MR, CT, and gross specimen reveal malignant
transformation to chondrosarcoma with small
associated soft tissue mass laterally (arrows).
Juxtacortical Chondroma [Figure 25]

!" Arise adjacent to cortex beneath
Figure 23 A & B
periosteum
Enchondromatosis on radiograph and coronal T2* !" Metaphyseal
(GRE) MR image which show diagnostic columns of !" Proximal humerus (50%), femur and tibia
cartilage extending into metaphysis from epiphyseal also hands and feet (25%)
plate (arrows).
!" < 30 years old, M > F = 2:1
!" Often more cellular than enchondroma
Figure 25
Juxtacortical
chondroma
skeletal
distribution.
Figure 24 A & B
Enchondromatosis on bone scan and extensive
deformity of the upper extremity on radiograph. Note
predominance on one side of the body on bone scan.
MR, CT, and gross specimen (next images) reveal
malignant transformation to chondrosarcoma with
small associated soft tissue mass laterally (arrow).

Juxtacortical Chondroma: Imaging CMF: Pathology
[Figure 26] !" V<3*"+M)$1-*&7M)/.+)%9*.+-*"+)("77&,)".)
!" Cortical saucerization (1-3 cm) various proportions
!" Variable sclerosis/periosteal reaction !" Myxoid areas: central in lobules
!" Soft tissue mass with chondroid !" Cellular areas peripheral in lobules
%/'%"$%/("*.)0>A64 !" K*%")*#)%/'%"$%/("*.)>6?X\6
!" High intensity T2-W MR images !" Lobulated tumor mass
!" !"#$%&'()(*)+"##,-,.("/(,)%9*.+-*7/-%*8/
CMF: Radiology [Figure 28]
!" Geographic lesion IA-IC
!" Eccentric metaphyseal location; often
cortical (long bone lesions)
!" Expansile remodeling simulate cortical
permeation
!" Flat/short tubular bone lesions central
!" Rare matrix mineralization (CT)
!" MRI: similar to slightly lower intensity
than muscle T1-WIs
!"Very high signal intensity T2-WIs
Figure 26 A & B
Juxtacortical chondroma with extrinsic erosion or

saucerization (arrowheads) of metacarpal.
Chondromyxoid Fibroma (CMF):

Fibromyxoid Chondroma [Figure 27]
!" Rare, least common benign cartilage
tumor
!" Usually lower extremity
!"55% around knee, 20%-25% foot
!" Young adults, 60% < 30 years old
!" Rarely malignant transformation Figure 28 A & B
*561$)"1>,'13)*&+"1>#*<3!6*3$!"#/1"!3/#0*01/#!31$*
in the tibia and outer margin appearing aggressive
on radiograph (arrowhead) but intact on CT (arrow)
and low attenuation (*) resulting from high water
content hyaline cartilage (note the lack of matrix
mineralization).
Chondroblastoma: Codman Tumor -

Figure 27 History
!" Cartilage containing GCT
Chondromyxoid !"Kolodney 1927
&+"1>#*%2(0(!#0* !" Calcifying GCT
distribution. !"Ewing 1928
!" Epiphyseal chondromatous GCT
!"Codman 1931
Chondroblastoma: Clinical Data

!" Uncommon; 1%-2% all bone tumors
!" M > F = 2:1
!" Children and young adults; 90% 5-25
years old

Chondroblastoma: Location Chondroblastoma: Imaging
!" Epiphysis/apophysis only 40% [Figures 30 to 35]
!" Epiphysis and metaphysis 55% !" Geographic lytic lesion IA/IB
!" Metaphysis only 4% !" Eccentric > central; rarely expansile
!" F/'%"$,+)%9*.+-*"+)8/(-"3)))
Epiphyseal/Apophyseal Lesions: !"Radiographs (30%-55%); CT (90%-
Differential Diagnosis 95%)
!" Chondroblastoma !" Periosteal reaction 30%-62%
!" GCT !"Adjacent diaphysis/metaphysis
!" Subchondral cyst/intraosseous ganglion !" FPDVLU?C&"+)',E,'7DÔF)%*8:*.,.(7)
!" Infection common (21%-77%)
!" Langerhans cell histiocytosis !" MRI: not typical chondroid characteristics
!" Osteoid osteoma/osteoblastoma !"Beware! – low/intermediate T2-W
!" Clear cell chondrosarcoma (92%)
!"Extensive surrounding edema (69%)
Chondroblastoma: Location [Figure 29] !"Joint effusion (30%-77%)
!" Proximal femur 23%
!"Head and neck 16%
!"Trochanter 7%
!" Distal femur 20%
!" Proximal tibia 17%
!" Proximal humerus 17%
!" Hands and feet 10%
Figure 30 A & B
Chondroblastoma centered in the epiphysis but
Figure 29 extending into the metaphysis, matrix mineralization
and periosteal reaction extending into the diaphysis
Chondroblastoma (arrowhead) is also seen.
skeletal
distribution.
Chondroblastoma: Histology
!" Chondroblasts can be confused with
chondro/osteosarcoma Figure 31 A & B
!" Multinucleated giant cells
!" Chondroid 1%-15% Chondroblastoma on coronal T1-W and T2-W MR
images with the lesion showing low to intermediate
!" ABC component 5%-15% signal intensity on long TR image (arrowheads) and
!" U."("/''<)%,''&'/-Y)'/(,-).,%-*7"7M)$1-*7"7M) extensive surrounding marrow edema (*) (same
maturation patient as previous image).

Figure 35 A, B & C
Chondroblastoma with ABC component in the greater

trochanter. Multiple MR images show the lesion
Figure 32 largely composed of cystic areas (*) and small solid
component of chondroblastoma medially (arrows).
Chondroblastoma of greater trochanter
(apophysis = epiphyseal equivalent) on coronal T2-W
MR image with typical low signal intensity lesion
(arrow) and surrounding edema (*).
Chondroblastoma: Treatment
!" Curettage and cryosurgery or en bloc
resection and bone graft
!" Radiofrequency ablation
!" Local recurrence 5%-10%
!" Malignant chondroblastoma very rare
Chondrosarcoma Types: Primary

!" Intramedullary
!" Periosteal/Juxtacortical
!" Clear cell
!" Mesenchymal
!" Myxoid
!" Extraskeletal
!" Dedifferentiated
Chondrosarcoma Types: Secondary

Figure 33 A & B !" Enchondroma
!" Osteochondroma
!" Paget disease
!" Radiation induced
!" Miscellaneous
Chondrosarcoma: Pathology
!" Malignant tumor of cartilage often with
myxoid changes
!" Grades I (30%), II (40%), III (30%)
!" J-/+,)U)+"#$%&'()(*)+"##,-,.("/(,)#-*8)
benign
!" Diagnosis based on histologic and growth
features, symptoms, and tumor size/
location
Figure 34 A & B
Chondroblastoma with ABC component in the patella

presenting as a pathologic fracture. Radiograph and
sagitally sectioned gross specimen and macrosection
show the lytic expansile lesion with fracture, largely
composed of cystic (ABC) areas (*) and small solid
component of chondroblastoma inferiorly (arrow).

Intramedullary Chondrosarcoma:
Clinical Data [Figure 36]
!" Symptoms: pain (95%-99%)
and mass (82%)
!" M > F = 3:2
!" Average age 40-45 years; metaphysis
!" Location: femur (25%), pelvis (30%),
shoulder (15%), ribs/sternum (10%),
vertebrae (7%), scapula (5%)
!" 8%-17% all biopsied primary bone
tumors
Figure 37 A & B
Low-grade chondrosarcoma of the humerus with
typical features on multiple imaging modalities.
Radiograph shows typical ring and arc mineralization
of a chondroid lesion (white arrows) with deep
endosteal scallop (black arrow). Bone scan reveals
marked increased radionuclide uptake.
Figure 36
Intramedullary
chondrosarcoma
skeletal
distribution.
Figure 38 A & B
Low-grade chondrosarcoma of the humerus with
typical features on multiple imaging modalities. CT and
axial MR images show matrix mineralization on the
CT (white arrows) and typical septal and peripheral
enhancement of cartilage lesions on the postcontrast
MR (white arrows) (same patient as previous images).
Intramedullary Chondrosarcoma:
Imaging [Figures 37 to 45]
!" Geographic IA-IC to permeative
!"Often predominantly sclerotic
!" Deep endosteal scalloping
!" Cortical thickening/periosteal reaction
!" Expansile remodeling
!" Soft tissue mass (20%-76%)
!" Chondroid matrix (78% by X-ray;
94% by CT)
!" CT/conventional tomography
if matrix subtle Figure 39 A & B
!" MRI: similar to muscle T1-WIs Low-grade chondrosarcoma of the humerus with
!"Lobulated high intensity T2-WIs typical features on multiple imaging modalities.
Coronal T2-W MR and coronally sectioned gross
!"V/(-"3)%/'%"$%/("*.)'*a)".(,.7"(<
specimen reveal marrow replacement (large white
!"Peripheral/septal contrast arrows) and deep scalloping with early extension into
enhancement the soft tissues (small white arrows).

Figure 40
Intramedullary
chondrosarcoma
of femur with
chondroid
mineralization
superiorly
(arrow) and Figure 43
deep area CT of acetabular intramedullary chondrosarcoma
of scalloping shows matrix mineralization (arrowhead) and large
laterally associated soft tissue mass (*) (same patient as
(arrowhead). previous radiograph).
Figure 44
Coronal T2-W MR image of acetabular intramedullary

chondrosarcoma shows large high-signal intensity soft
tissue mass (*) (same patient as previous CT).
Axial proton density MR images show cortical
breakthrough and soft tissue mass (arrowheads) in
this femoral intramedullary chondrosarcoma (same
patient as previous radiograph).
Figure 42 Figure 45
Acetabular Intramedullary chondrosarcoma of anterior rib on CT

intramedullary with low-attenuation mass and matrix mineralization
chondrosarcoma (arrow).
shows subtle
bone destruction Juxtacortical/Periosteal:
(arrow) Chondrosarcoma [Figure 46]
and matrix
mineralization in
!" Second-fourth decades; male predilection
this complex area !" Metaphyseal particularly femur and
of anatomy. humerus
!" Similar to juxtacortical chondroma
!" Periosteal lesion – cortical erosion
!" F9*.+-*"+)8/(-"3)%/'%"$%/("*.
!" Larger size than juxtacortical chondroma
(> 3-4 cm)

Juxtacortical/Periosteal:
Chondrosarcoma [Figures 46 to 48]
!" Similar appearance to periosteal OGS (but
no hair-on-end periosteal reaction)
!" Intramedullary canal usually spared
!" Most lesions low grade
!" Treatment of wide surgical resection
!" Good prognosis: 83% 5-year survival
(low-grade lesions
Figure 48 A & B
Juxtacortical chondrosarcoma seen on multiple

imaging modalities. Sagittal T2-W MR shows high-
signal intensity of the mass (arrows and black M).
Figure 46 The coronally sectioned gross specimen reveals the
lobular chondroid growth (C), extrinsic erosion of the
Juxtacortical cortex (arrows), normal marrow space (white M) and
chondrosarcoma the periosteal elevation (P) (same patient as previous
skeletal &E."(AD
distribution.
Clear Cell Chondrosarcoma:
Clinical Data [Figure 49]
!" 2% of chondrosarcomas
!" 0.2% of all primary bone tumors
!" Slightly younger age
!" 75%-80% lesions proximal femur or
humerus
!" Flat bones involved, 10%
!" Propensity for epiphysis > 90%
!" Better prognosis
Figure 49
Clear cell
chondrosarcoma
skeletal
distribution.
Figure 47 A, B & C
Juxtacortical chondrosarcoma seen on multiple
imaging modalities. Radiograph, CT, and axial T1-W
MR show the juxtacortical mass (M) with chondroid
matrix mineralization (rings and arcs). There is
('!"3$%3/*("1%31$*14*!6(*&+.0#"*/1"!('*@+0#/2*#""1<%*
on radiograph/CT and curved arrow on MR) and low
attenuation of the nonmineralized components on CT
(*).

Clear Cell Chondrosarcoma: Pathology Extraskeletal Chondrosarcoma:
!" Clear cell chondrocytes Mesenchymal Type
!" Osteoblastoma like osseous metaplasia !" Young patients 23-44 years old
!" Areas of conventional chondrosarcoma !" 20%-30% soft tissue
50% !" Location: meninges and thigh
!" Chondroblastoma-like areas !" High-grade malignancy
!" Osteoclastic giant cells !" Mesenchymal cells with islands of
cartilage
Clear Cell Chondrosarcoma: Imaging !" Large soft tissue masses - may have
[Figure 50] %9*.+-*"+)8/(-"3)%/'%"$%/("*.
!" Geographic lysis IA to IC !" Metastases: lymph node, lung
!" P*(/''<)'<("%)0>A64Y)%/'%"$,+)%9*.+-*"+)
matrix 33% Mesenchymal Chondrosarcoma:
!" Rind of sclerosis (20%) simulates Pathology
nonaggressive lesion !" Undifferentiated mesenchymal cells
!" Soft tissue mass less common 10% !" Multifocal islands of malignant cartilage
!" MRI: often high signal T2-WIs images but !" Hemangiopericytoma-like areas
may have areas of low signal as well !" Aggressive high-grade lesions
!" Poor prognosis
Mesenchymal Chondrosarcoma:
Imaging [Figures 51 & 52]
!" Aggressive osseous destruction
motheaten to permeative
!" F9*.+-*"+)8/(-"3)%/'%"$%/("*.)',77)
prominent – small foci (60%-70%)
!" Soft tissue mass (near 100%)
!" Masses show lower water content (CT/
MR) and enhance diffusely; may see high
C*a)E,77,'7)0VL4
Clear cell chondrosarcoma of the proximal femoral

epiphysis with sclerotic margins simulating a
nonaggressive lesion on the radiograph (arrow),
/1$!#3$3$E*/61$)"13)*/#0/3&/#!31$*1$*5;*@#""1<6(#)%A*
simulating a chondroblastoma (but the patient is 40
years old) and revealing marrow replacement on MR
with high signal intensity on the STIR image (curved
arrows).
Figure 51 A & B
Mesenchymal chondrosarcoma showing very

aggressive bone destruction with large soft tissue
mass and chondroid matrix mineralization (arrows) on
Mesenchymal Chondrosarcoma: radiograph and CT.
Clinical Data
!" Less than 10% of chondrosarcomas
!" Younger age: averages 25 years
!" M=F
!" Osseous location: femur (15%), ribs
(15%), spine (10%), craniofacial (20%),
pelvis (10%)

Figure 54
Axial T2-weighted MR image reveals marked high
Figure 52 A & B signal intensity resulting from very high water content
of myxoid chondrosarcoma (same patient as previous
Mesenchymal chondrosarcoma on MR images
image).
show marrow replacement (M), diffuse contrast
enhancement, as well as small serpentine vessels
(arrows). This is not the enhancement pattern of
conventional chondrosarcoma (peripheral/septal)
@%#>(*:#!3($!*#%*:"(=31.%*&E."(AD
Dedifferentiated Chondrosarcoma:
Clinical Data
!" Older patients; average 60 years
!" 10%-20% chondrosarcomas
Myxoid Chondrosarcoma !" Often associated with secondary
!" Rare in bone: 12% chondrosarcomas chondrosarcoma (> 50%)
!" More aggressive radiologic appearance !" Location: femur (20%), humerus (15%),
!" Worse prognosis pelvis (30%), ribs and scapula (12%)
!" Look for myxoid areas
!"Low attenuation or signal intensity T1-
WIs; may show areas of hemorrhage Pathology
!"Very high signal intensity T2-WIs !" Low-grade chondrosarcoma
!"Contrast enhancement – peripheral/ !" Small foci higher-grade chondrosarcoma
diffuse !" Spindle cell component – MFH/
$1-*7/-%*8/M)*7(,*7/-%*8/M)
Extraskeletal Chondrosarcoma: rhabdomyosarcoma, GCT
Myxoid Type (Chordotic) [Figures 53 & 54]
!" Collision of two tumors
!" Middle-aged patients; average 50 years
!" Deep musculature tissue extremities
!" Thigh/popliteal fossa (70%) Imaging [Figures 55 & 56]
!" Low-grade malignancy; may recur late !" Radiology emulates pathology: beware
!" Hemorrhage and myxoid areas can be the dual characteristic
seen with imaging !"One region chondrosarcoma
!" Typical chondroid regions – radiographs !"Second area aggressive bone
!" Metastases: lymph node, lung destruction
!"Cortical permeation and soft tissue
mass (70%)
!" Biopsy of anaplastic region – confusing
!" Dedifferentiated component compared to
chondroid component
!"Different intrinsic characteristics
!"Different contrast enhancement
(diffuse)
Figure 53
Myxoid chondrosarcoma of proximal femur shows
bone destruction with intramedullary chondroid
mineralization (arrowhead) and large posterior soft
tissue mass with marked low attenuation (*) .

Low-Grade Chondroid Lesion:
Differential Diagnosis
!" Enchondroma
!" Low-grade chondrosarcoma
!" Bone infarct
Bone Infarct: Osteonecrosis

[Figures 57 & 58]
!" Ischemic area may undergo mineralization
!" Can have chondroid-like matrix
!" H**W)#*-):,-":9,-/')-"8)*#)%/'%"$%/("*.
!" No cortical thickening
!" Prominent areas of endosteal scalloping or
mass exclude osteonecrosis
!"Except malignant degeneration
Figure 55 A & B
Dedifferentiated chondrosarcoma with radiographs
showing typical chondroid mineralization (rings and
arcs) (arrow). There is anterior cortical destruction
with a small soft tissue mass (arrowheads).
Figure 57
Multiple
areas of
osteonecrosis
with serpentine
peripheral
/#0/3&/#!31$*
(arrows) and
simulating
chondroid
(ring and arc)
mineralization.
Figure 56 A & B
Dedifferentiated chondrosarcoma with postcontrast

fat- suppressed T1-W MR image showing typical
peripheral and septal enhancement in the cartilaginous
portion of the lesion (arrows) and diffuse enhancement
in the dedifferentiated anterior soft tissue component
(*) correlating with the sagitally sectioned gross
%:(/3>($*@%#>(*:#!3($!*#%*:"(=31.%*&E."(AD
Radiologic Differential of
Chondrosarcomatous Lesions
!" Aggressive chondroid lesion with soft
tissue mass
!"Higher grade conventional
chondrosarcoma
!"Dedifferentiated chondrosarcoma
!"Mesenchymal chondrosarcoma
!" H/-2,)C&"+)%*8:*.,.()1*.,)*-)7*#()("77&, Figure 58 A & B
!"Myxoid chondrosarcoma CT of osteonecrosis shows peripheral rim of serpentine
!" Change in appearance or foci of more /#0/3&/#!31$D*J3>.0#!31$*14*/61$)"13)*>3$("#03K#!31$*3%*
aggressive nature an artifact of radiographs in looking at a 3D structure
with a 1D image.

Diagnostic Dilemma Long Bone:
Enchondroma vs Chondrosarcoma
!" Enchondroma
!"Common in hand/foot
!"Rare in axial skeleton
!"Common in long bones
!"2% distal femur, 2.9% about the knee
!" Chondrosarcoma
!"Common in axial skeleton
!"Common in long bones
!"Rare in hand/foot
Enchondroma vs Low-Grade
Chondrosaroma: Clinical Data
!" Pain (95%-99%) and mass (20%-76%)
favor chondrosarcoma
!" Pain in enchondroma (40%)
!"Often related to activity
!"Stress microfracture
!"Vague longer duration
!" U7):/".)-,#,-/1',)(*)',7"*.I
!" Radiologic consultation
Enchondroma vs Low-Grade
Chondrosarcoma: Pathology
!" Permeation of chondroid tissue
!" Permeation of cortex
!" Soft tissue mass
!" Fibrous bands separating cartilage
!" Invasion of marrow fat
Long Bone Enchondroma: Imaging

!" Size < 6-7 cm (X-ray), < 5 cm (CT/MRI)
!" Bone scan =/< AIC* 79% (70%
homogeneous)
!" Majority in diaphysis
!" Endosteal scalloping depth
< 2/3 cortex (90%-95%)
!" No cortical thickening (17%)
!" Periosteal reaction (3%)
!" No cortical destruction/soft tissue mass
!" VLU):,-":9,-/'),.9/.%,8,.(I)))))))
Murphey. RadioGraphics. 98;18:1213.
*AIC = Anterior Iliac Crest
Long Bone Chondrosarcoma: Imaging

!" Majority in the metaphysis
!" Size > 6-7 cm (X-ray); > 5 cm (CT/MRI)
!" Bone scan =/> AIC* 82% (63%
heterogeneous)
!" Endosteal scalloping depth
> 2/3 cortex (75%-90%)
!" Cortical thickening (47%); periosteal
reaction (51%)
!" VLU):,-":9,-/')/.+)7,:(/'),.9/.%,8,.(I))))))
Murphey. RadioGraphics. 98;18:1213.
*AIC = Anterior Iliac Crest

References
Osteochondroma
1. Murphey MD, Choi JJ, Kransdorf MJ, Flemming DJ, Gannon FH. Imaging of osteochondroma: variants and
complications with radiologic-pathologic correlation. RadioGraphics 2000 Sep-Oct;20(5):1407-34. Review.
2. Bahk WJ, Lee HY, Kang YK, Park JM, Chun KA, Chung YG. Dysplasia epiphysealis hemimelica: radiographic
and magnetic resonance imaging features and clinical outcome of the complete and incomplete resection.
Skeletal Radiol 2010;39:85-90.
3. Bernard SA, Murphey MD, Flemming DJ, Kransdorf MJ. Improved differentiation of benign
osteochondromas from secondary chondrosarcoms with standardized measurement of cartilage cap at CT
and MR Imaging. Radiology 2010;255:3, 857-66.
Enchondroma
4. Murphey MD, Flemming DJ, Boyea SR, Bojescul JA, Sweet DE, Temple HT. Enchondroma versus
chondrosarcoma in the appendicular skeleton: differentiating features. RadioGraphics 1998 Sep-
Oct;18(5):1213-37; quiz 1244-5.
Juxtacortical chondroma
5. Robinson P, White LM, Sundaram M, Kandel R, Wunder J, McDonald DJ, Janney C, Bell RS. Periosteal
chondroid tumors: radiologic evaluation with pathologic correlation. AJR Am J Roentgenol 2001
Nov;177(5):1183-8.
F9*.+-*8<3*"+)$1-*8/)0FVK4)
6. N"'7*.)^RM)h<-"/W*7)VM)^%W,-8/.)HgS))F9*.+-*8<3*"+)$1-*8/[)-/+"*2-/:9"%)/::,/-/.%,)".)5d)%/7,7)/.+)
in a review of the literature. Radiology 1991 May;179(2):513-8. Review. Erratum in: Radiology 1991
Aug;180(2):586.
7. N&)FPM)U.a/-+7)FjM)BkH/&29'".2)QM)L*%W)VJM)O,/1*&()RNM)f..")hhS)F9*.+-*8<3*"+)$1-*8/)*#)1*.,Y)/)
clinicopathologic review of 278 cases. Hum Pathol 1998;29(5):438-46.
Chondroblastoma
8. Bloem JL, Mulder JD. Chondroblastoma: a clinical and radiological study of 104 cases. Skeletal Radiol
1985;14(1):1-9.
9. Nomikos GC, Murphey MD, Jelinek JS, Gannon FH. Advanced Imaging of Chondroblastoma. Radiology
2001;221(P):232. Abstract.
10. Rybak LD, Rosenthal DI, Wittig JC. Chondroblastoma: radiofrequency ablation-alternative to surgical
resection in selected cases. Radiology 2009;251:599-604.
11. Christie-Large M, Evans N, Davies AM, James SLJ. Radiofrequency ablation of chondroblastoma:
procedure technique, clinical and MR imaging follow up of four cases. Skeletal Radiol 2008;37:1011-7.
Chondrosarcoma
12. Murphey MD, Walker EA, Wilson AJ, Kransdorf MJ, Temple HT, Gannon FH. From the archives of the
AFIP: imaging of primary chondrosarcoma: radiologic-pathologic correlation. RadioGraphics. 2003 Sep-
Oct;23(5):1245-78. Review.
13. Unni KK, Dahlin DC, Beabout JW, Sim FH. Chondrosarcoma: clear-cell variant. A report of sixteen cases. J
Bone Joint Surg Am 1976;58:676-83.
14. Chaabane S, Bouaziz MC, Drissi C, Abid L, Ladeb MF. Periosteal Chondrosarcoma. AJR Am J Roentgenol
2009;192:W1-W6.

883
884
Fibrous Lesions of the Musculoskeletal System
Mark D. Murphey, MD
Fibrous Lesions Fibroxanthoma: Pathology
!" Fibroxanthoma (.*.*77"#<".2)$1-*8/4 !" N9*-'7D1&.+',7)*#)$1-*&7)("77&,
!" Fibrous dysplasia !" Variable cellularity
!" B7(,*$1-*&7)+<7:'/7"/Dadamantinoma !" Giant cells
!" !,78*:'/7("%)$1-*8/ !" Foam or xanthoma cells
!" Fibromatosis !" Areas hemorrhage/hemosiderin
!" V/'"2./.()$1-*&7)
histiocytoma/$1-*7/-%*8/)0VK_4 Fibroxanthoma: Skeletal Location
!" !,-8/(*$1-*7/-%*8/):-*(&1,-/.7)0!KQG4 [Figure 2]
!" Metaphyseal origin can migrate to
Fibroxanthoma: Other Terms diaphysis
!" Fibrous cortical defect !" Long tubular bones (90%)
!" ;*.*77"#<".2)$1-*8/)0;BK4 !" Lesions around knee (55%)
!" Fibrous medullary defect !" Tibia – 43%, femur (38%) (distal),
!" ;*.*7(,*2,."%)$1-*8/ Fibula (8%)
!" Upper extremity uncommon (8%);
Fibroxanthoma [Figure 1] Humerus (5%)
!" “...if the lesion has attained a fairly
large size and has penetrated into and
continues to grow in the medullary
%/E"(<M)"()%,/7,7)(*)1,)/)8,-,)$1-*&7)
cortical defect and is then known as a
.*.*77"#<".2)$1-*8/Sl
Jaffe, 1958.
Figure 2
Fibroxanthoma/
nonossifying
&+"1>#*%2(0(!#0*
distribution.
Figure 1 A & B
L(4!*8>#E(M*;,:3/#0*$1$1%%34,3$E*&+"1>#N
&+"1'#$!61>#*3$*!6(*!3+3#*@#""1<AD Fibroxanthoma: Radiology [Figures 3 to 5]
Right Image: O1$1%%34,3$E*&+"1>#N&+"1'#$!61>#*<3!6* !" Eccentric cortically-based lesion
6(#03$E*+,*('!($%3=(*1%%3&/#!31$*@#""1<AD !" Longitudinal growth pattern
!" Can extend or primarily involve
medullary cavity
!" Lobulated contour
Fibroxanthoma !" Expansile remodeling with trabeculation
!" Very common 20% F, 50% M, older than !" Cortex may appear permeated focally but
2 years old no soft tissue mass
!" Children and adolescents; M>F !" Usually a rim of sclerosis
!" Usually asymptomatic: only 2% of !" Bone scan: minimal to mild uptake
biopsied primary bone tumors !" PET: may show high SUV (0.7-18.8)
!" Heal spontaneously with average “life- (33% > 2)
span” of 29 months !" MR: can be low or high intensity on T2-
WIs
Fibrous Lesions of the Musculoskeletal System 885 Musculoskeletal Radiology
Fibroxanthoma: Natural History
[Figures 6 & 7]
!" Often heal with residual sclerosis start
from diaphyseal side
!" May persist or grow
!" Pathologic fracture: greater likelihood in
lesions > 3 cm, with > 50% bone width
involved and weight bearing bones
Figure 3 A, B & C
O1$1%%34,3$E*&+"1>#N&+"1'#$!61>#*3$*!6(*
distal femur on radiograph, gross specimen, and
macrosection.
Figure 6 A & B
8$!("=#0*E"1<!6*14*$1$1%%34,3$E*&+"1>#%N
&+"1'#$!61>#*#$)*>.0!3:0(*0(%31$%*@#""1<%A*3$*!6(*
time interval between two radiographs.
Figure 4 A to E
O1$1%%34,3$E*&+"1>#N
&+"1'#$!61>#*3$*!6(*)3%!#0*
femur on radiograph and
multiple MR images. Note
intracortical location,
heterogeneous signal
intensity on T2 with
areas of high signal and
enhancement.
Figure 7 A, B & C
P"#/!."(%*!6"1.E6*!6"((*$1$1%%34,3$E*&+"1>#%N
&+"1'#$!61>#%D
Figure 5
Left Image: Fibroxanthoma: Types and Associations

O1$1%%34,3$E*&+"1>#N [Figure 8]
&+"1'#$!61>#*3$*!6(*
&+.0#*<3!6*>().00#",*
!" Solitary or multiple
location (arrow) as is !" Multiple with .,&-*$1-*8/(*7"7)(<:,)@)
typical for lesions in !" Multiple with café au lait spots Jaffe-
this location. Campanacci syndrome
!" Oncogenic osteomalacia

Figure 8 A & B
-.0!3:0(*$1$1%%34,3$E*&+"1>#%N&+"1'#$!61>#%*
associated with $(."1&+"1>#!1%3%*BD
Figure 9 C, D, E & F
Benign Fibrous Histiocytoma Q($3E$*&+"1.%*63%!31/,!1>#*3$*!6(*)3%!#0*4(>."*3$*#*

25-year-old man. Radiographs show a multiseptated
[Figure 9]
metaphyseal lesion with sclerotic margins and mild
!" Use of this terminology controversial expansile remodeling of bone (arrows). Multiple MR
!" Patient often symptomatic images reveal a predominantly low-signal intensity
!" Radiographic appearance-larger lesions, lesion with mild enhancement (arrowheads). This
more expansion, medullary involvement, lesion is identical pathologically to nonossifying
&+"1>#N&+"1'#$!61>#*+.!*:#!3($!%*#"(*%,>:!1>#!3/*
older patient and older at presentation.
!" G/(9*'*2<)"+,.("%/')(*)$1-*3/.(9*8/
Fibrous Dysplasia:
Clinical Characteristics
!" Developmental anomaly of bone formation
!" Osteoblasts fail to develop
!" V/--*a)-,:'/%,+)1<)$1-*77,*&7)("77&,
!" Usually diagnosed between 2-30 years old
!" Males and females equally affected
!" Monostotic (70%-80%)
!" Polyostotic (15%-30%)
!" Café au lait spots: irregular serrated
borders (coast of Maine)
!" 1% of biopsied primary bone tumors
!" 7% benign bone tumors;
Figure 9 A & B
2.5% all bone lesions
Q($3E$*&+"1.%*63%!31/,!1>#*3$*!6(*)3%!#0*4(>."*3$*#*
25-year-old man. Radiographs show a multiseptated Fibrous Dysplasia: Monostotic
metaphyseal lesion with sclerotic margins and mild [Figure 10A]
expansile remodeling of bone (arrows). Multiple MR !" Smaller-sized lesions
images reveal a predominantly low signal intensity
lesion with mild enhancement (arrowheads). This !" Often asymptomatic
lesion is identical pathologically to nonossifying !" Café au lait spots less common
&+"1>#N&+"1'#$!61>#*+.!*:#!3($!%*#"(*%,>:!1>#!3/* !" Distribution: femur (35%-40%), tibia
and older age at presentation. (20%), skull and facial bones (10%-
25%), ribs (10%)
!" Uncommon sites: hands and feet, spine,
clavicle

Fibrous Dysplasia Radiology:
Appendicular Skeleton
[Figures 11 to 13]
!" Medullary diaphyseal lesions
!" Radiolucent with woven bone in marrow
creating “ground-glass” appearance
Figure 10 !" Expansile remodeling
A&B !" f7&/''<)a,''?+,$.,+)/.+)8/<)9/E,)
Left Image:
sclerotic rind (monostotic lesions)
Monostotic !" May have “multiloculated appearance”
&+"1.%* caused by subperiosteal reinforcement
dysplasia !" Areas of sclerosis (most common in skull)
skeletal !" Skeletal deformity: fracture, bowing
distribution.
(shepherd’s crook), growth disturbance
Right Image: (more common polyostotic disease)
Polyostotic
&+"1.%*
dysplasia
skeletal
distribution.
Fibrous Dysplasia: Polyostotic [Figure 10B]

!" Larger lesions, symptomatic earlier age
!" 70% present before age 10: limp, pain,
fracture or deformity
!" Cafe-au-lait spots > 50% patients
!" Involvement variable: 2 to > 75% of
skeleton, propensity to involve one side of Figure 11 A, B & C
body more extensively
Typical “ground-glass” appearance in several patients
!" Common sites: skull and facial bone <3!6*&+"1.%*),%:0#%3#D
(> 50%), long bones, ribs, pelvis
Fibrous Dysplasia Polyostotic:

Associations
!" Endocrinopathies: 2%-3% patients
!" McCune-Albright syndrome: bone lesions
cutaneous pigmentation, precocious
puberty – 20%-50% of females (only 1 in
30-40 have complete triad)
!" Others: hyperthyroidism,
hyperparathyroidism, acromegaly,
diabetes mellitus (DM), Cushing syndrome
!" Soft tissue myxoma – Mazabraud
syndrome
Fibrous Dysplasia:
Pathologic Characteristics
!" Fibrosseous metaplasia
!" Stroma may have cystic or myxoid
elements
!" Trabeculae are pure woven bone with
“alphabet soup” appearance
!" Occasional osteoblastic rimming and
chondroid foci
!" May have ABC/cystic component Figure 12
;,:3/#0*>1$1%!1!3/*&+"1.%*),%:0#%3#*3$*3$!("!"1/6#$!("3/*
femur with thick rind of sclerosis (arrow).

Figure 16
Fibrous
dysplasia on
T2-W MR with
prominent
low-signal
intensity in
the frontal
bone with
expansile
remodeling
(*).
Fibrous Dysplasia Radiology:

Figure 13 A & B Other Studies [Figures 17 to 19]
Fibrous dysplasia of rib on radiograph and !" Bone scan: usually increased activity
macrosection showing elongated involvement (*) of a probably more variable than recognized
prominent osseous extent. !" PET: may be markedly increased
(SUV 3-19)
!" CT: especially helpful in skull
Fibrous Dysplasia Radiology: !" MRI
Craniofacial Skeleton !"20% low-intensity T2-WIs
[Figures 14 to 16] !"20% same as fat T2-WIs
!" Commonly involved: frontal, sphenoid, !"60% high-intensity T2-Ws
ethmoid, maxilla, zygoma, parietal,
occipital, and temporal
!" Often mixed lucency and sclerosis
!" Sclerosis often marked at skull base – can
impinge on cranial nerves
!" Calvarium expanded with greater
involvement outer table
Figure 14
Fibrous
dysplasia of
the calvarium
with skull base
sclerosis (*)
and expansion Figure 17 A & B
of the occipital
outer table Fibrous dysplasia of the humerus with typical intense
(arrow). uptake of radionuclide on bone scan.
Figure 15
Coronal CT
reconstruction
14*&+"1.%*
dysplasia
shows mixed
lysis and
sclerosis and
outer table
expansion.
Figure 18
P3+"1.%*),%:0#%3#*14*4(>1"#0*)3#:6,%3%*<3!6*$1$%:(/3&/*
marrow replacement (*) on coronal T1-W MR image.

Fibrous Dysplasia:
!" Bone cyst
!" Fibroxanthoma (medullary)
!" Meningioma
!" Osteoblastoma (long bone)
!" Enchondromatosis
!" Paget disease
!" ;,&-*$1-*8/(*7"7
O#)(&4:1&"#+Dysplasia: Previous Terms

!" F*-("%/')$1-*&7)+<7:'/7"/
!" U.(-/%*-("%/')$1-*&7)+<7:'/7"/
!" B77"#<".2)$1-*8/))
!"Do not confuse with facial lesion
!" Juvenile adamantinoma
!" Differentiated adamantinoma
Figure 19
P3+"1.%*),%:0#%3#*14*4(>1"#0*)3#:6,%3%*<3!6*$1$%:(/3&/* O#)(&4:1&"#+Dysplasia:
marrow replacement and high signal intensity on Clinical Characteristics [Figure 21]
coronal T2-W MR image (*) (same patient as previous
MR). !" Unusual lesions: 0.2% of biopsied primary
bone tumors
!" Patients < 10 years; rare after 16 years
old
!" P"1"/)/'*.,)0\>6?dA64)*-)/'7*)$1&'/)
Fibrous Dysplasia: Complications 0@X64Y)$1&'/)*.'<)0\64M)1*(9)("1"/,)
[Figure 20]
(3%), rarely radius/ulna
!" Malignant transformation (0.5%) es raro
!" Osteosarcoma most frequently but also
MFH/$1-*7/-%*8/)/.+)chondrosarcoma
!" Both polyostotic and monostotic
!" Prior radiation in 30%
Figure 21
H%!(1&+"1.%*
dysplasia
skeletal
distribution.
Figure 20 A & B
-1$1%!1!3/*&+"1.%*),%:0#%3#*14*!6(*:"1'3>#0*4(>."*
with malignant transformation to MFH on radiograph
and gross specimen. Note ground-glass appearance
distally (*) and more aggressive bone destruction O#)(&4:1&"#+Dysplasia Pathology
proximal with extension through lesser trochanter !" g/7%&'/-"`,+)$1-*&7)7(-*8/)'"W,)$1-*&7)
proximally (arrows). dysplasia
MFH: HISTIOCITOMA FIBROSO MALIGNO !" Prominent osteoblastic rimming
!" No “alphabet soup” of woven bone
!" Can be weakly keratin positive but no
epithelial nests

O#)(&4:1&"#+Dysplasia: Radiology Adamantinoma: Clinical Characteristics
[Figures 22 & 23] !" Present with pain/swelling; often history
!" Lytic lesion anterior cortex mid tibial of trauma
diaphysis !" Do not confuse with mandibular
!" Often mixed with sclerosis and ameloblastoma
multifocal/extensive !" Rare low-grade malignancy (0.1%)
!" No soft tissue mass; may involve biopsied primary bone tumors
medullary canal !" Also previously called angioblastoma
!" Expansile remodeling and sclerotic !" M:F = 1.3:1; average 35 years old
component
!" Causes bowing, fracture, pseudarthrosis Adamantinoma: Pathology and Location
and may progress to involve entire tibia [Figure 24]
!" Homogeneous intermediate on T1 and !" Epithelial nests/prominent keratin staining
high on T2 !" O/%W2-*&.+)*#)1'/.+)$1-*&7)7(-*8/
!"Homogeneous mild to moderate !" May have foci of Ewing-like areas –
enhancement worse prognosis
!" P"1"/)0dA6?d>64M)("1"/)/.+)$1&'/)0>64M)
femur (5%), humerus (4%), ulna (3%),
$1&'/)0@64
Figure 24
Adamantinoma
skeletal
distribution.
Figure 22 A & B
;,:3/#0*1%!(1&+"1.%*),%:0#%3#*<3!6*(01$E#!()N
multifocal intracortical tibial involvement on
radiograph and matched macrosection (*).
Adamantinoma: Radiology
!" Diaphyseal to metadiaphysis – anterior
tibial cortex
Figure 23 A to F
!" Mixed lytic/sclerotic and extensive
;,:3/#0*1%!(1&+"1.%*),%:0#%3#*1$*-7*3>#E3$E* !" May be multifocal with medullary
with elongated intracortical tibial involvement and involvement and soft tissue mass
homogeneous intermediate signal intensity on T1-W
!" Expansile remodeling with cortical
and high signal on T2-W (arrows).
thickening

Adamantinoma:
Radiology and Prognosis [Figures 25 to 28]
!" MRI
!"Very heterogeneous high-intensity T2-
WI
!"Vascularity with prominent
enhancement
!" Locally aggressive
!" 10-year survival: 10%-65%
!" 15% patients die with metastases
Figure 28
Intraoperative photograph of adamantinoma of the

tibia with intracortical curretage (same patient as
previous radiograph, MR, and CT) with elongated
lesion centered in the cortex.
O#)(&4:1&"#+Dysplasia:
Relationship to Adamantinoma
Figure 25 A & B
!" Differentiation – patient age
!"Multiple recurrence
Adamantinoma of the tibia on radiograph with mixed
lytic and sclerotic lesion centered in the cortex and an !"MR (heterogeneous, prominent
elongated lesion. vascularity/enhancement)
!" Epithelial nests; both can be keratin
positive
!" Several cases reported of foci of
/+/8/.(".*8/)".)*7(,*$1-*&7)+<7:'/7"/)
and progression to adamantinoma
Desmoplastic Fibroma:
!" L/-,)$1-*&7)',7"*.)*#)1*.,
!" 0.2%-0.3% biopsied primary bone
neoplasms
Figure 26 A & B !" M=F or slight female predilection
Adamantinoma of the tibia on several CT images !" 70% 15-40 years old
(same patient as previous radiograph) with mixed lytic !" Desmoid tumor of bone (5-10 times less
and sclerotic lesion centered in the cortex (arrows). common than soft tissue lesion)
!" Location: femur, tibia, humerus, radius,
mandible, pelvis
!" Metaphyseal – central
!" Pain and swelling (90%)
!" Pathologic fracture (15%)
Pathology
!" Histology similar to soft tissue desmoid
!" J-*77)c)'*1&'/-)$-8)a9"(,)(*)2-/<)8/77
!" Fibroblasts producing well-formed
Figure 27 A, B & C
collagen
Adamantinoma of the tibia on multiple MR images !" Nuclear monotony, variable cellularity,
(same patient as previous radiograph and CT) with rare mitosis
elongated lesion centered in the cortex (arrows). !" L/-,'<)/77*%"/(,+)a"(9)$1-*&7)+<7:'/7"/
There is prominent heterogeneity on STIR.

Desmoplastic Fibroma: Radiology Bubbly Lesion of Bone: Fegnomashic
[Figures 29 to 31] F ibrous dysplasia
!" Lytic lesion with expansile remodeling E nchondroma/eosinophilic granuloma
!" May have sclerotic margin G iant cell tumor
!" Prominent internal trabeculation (75%) N)*.*77"#<".2)$1-*8/)0*-)+,78*:'/7("%)
!" May have aggressive appearance $1-*8/4
!" Intermediate intensity T2-W MR images O steoblastoma
!"Intermixed collagenized bands (64%) M etastases/myeloma
A neursymal bone cyst
S imple bone cyst
Figure 29
H yperparathyroidism (brown tumor)
Desmoplastic I nfection
&+"1>#*14*!6(* C)9*.+-*1'/7(*8/D%9*.+-*8<3*"+)$1-*8/
iliac bone with
prominent
multilocular Bubbly Lesion of Bone: Fog Machines
appearance F ibrous dysplasia
caused by O steoblastoma
internal G iant cell tumor
trabeculation.
M etastases/myeloma
A neursymal bone cyst
C)9*.+-*1'/7(*8/D%9*.+-*8<3*"+)$1-*8/
H yperparathyroidism (brown tumor)
I nfection
N)*.*77"#<".2)$1-*8/)0*-)+,78*:'/7("%)) )
) $1-*8/4
E nchondroma/eosinophilic granuloma
S imple bone cyst
Cortical Desmoid [Figures 32 & 33]

!" Avulsive cortical injury (chronic)
!" Posteromedial distal femur metaphysis
!" Stress related at attachment
!"Adductor magnus
!"Medial head gastrocnemius
!" Pathology simulates aggressive lesion
!" F9"'+-,.)$-7()+,%/+,)05>64
Figure 30 A & B !" More frequent in boys, often bilateral
Knee radiographs demonstrate the typical appearance !" Surface irregularity/lucency
14*#*)(%>1:0#%!3/*&+"1>#*/($!("()*3$*!6(*>().00#",* !" CT: looks like NOF – no soft tissue mass
canal metaphysis with geographic lysis, a narrow, but !" VLU[)8/<)7,,)7&--*&.+".2)".C/88/("*.
not entirely sclerotic margin and prominent septations
!" PET: may show high SUV (1-2.3)
(arrows).
Figure 32 A & B
Figure 31 A & B
Two patients with cortical desmoids (chronic avulsive
The gradient echo MR images show intermediate- injury) of the distal femur (arrows).
signal intensity and low-signal intensity collagenized
bands/cords (arrows).

Fibromatosis: Extraabdominal Desmoid
[Figures 34 to 36]
!" Painless slow-growing deep mass (25-35
years; F > M)
!" 2-4 people/million (700-900 people/year
US); rarely familial
!" Shoulder (20%), chest wall/back (15%),
thigh (12%), mesentery (10%), neck
(8%), knee (7%), buttock (6%)
!" Intermuscular along fascia/aponeurosis,
".$'(-/("E,
Figure 34
Figure 33 A & B
Sagittal CT reconstruction showing medial head of Postcontrast

gastrocnemius muscle extending into cortical desmoid axial T1-W
(arrow) and macrosection of reparative tissue (*) in a MR image
different patient. showing
('!"##+)1>3$#0*)(%>13)*@&+"1>#!1%3%A*<3!6*#$*
($6#$/3$E*:#"#%:3$#0*>#%%*@RA*#$)*300C)(&$()*
margins.
Fibromatosis
!" Deep: grow rapidly, larger more
aggressive
!"Intraabdominal, abdominal,
extraabdominal Figure 35
A&B
!"Trisomies chromosomes 8/20
!" Q&:,-$%"/'[)7'*a?2-*a".2M)78/''M)/-"7,) Axial STIR
from fascia/aponeurosis MR image
showing
!" Can be multifocal 5%-20% extra-
abdominal
Fibromatosis: Types desmoid
!" Extraabdominal desmoid (deep) @&+"1>#!1%3%A*
!" ^22-,77"E,)".#/.("',)$1-*8/(*7"7)0+,,:4 with a soft
tissue mass
!" R&E,."',)/:*.,&-*("%)$1-*8/)07&:S4
@RA*#$)*300C)(&$()*>#"E3$%*#$)*03$(#"*('!($%31$*
!" U.#/.("',)+,-8/'D+"2"(/')$1-*8/(*7"7)07&:S4 (fascial tail sign) laterally (arrow). These features
!" Adult palmar and plantar (sup.) are also shown on a gross specimen from a different
!" U.#/.("',)8<*$1-*8/(*7"7)01*(94 patient.
Fibromatosis: Pathology
!" Gross – glistening white, variable
cellularity
!" Q:".+',?79/:,+)$1-*&7)%,''7
!" Abundant collagen, can see mitoses
!" U.$'(-/("E,)2-*a(9)%*88*.
!" No malignant potential
Fibromatosis: Radiology
!" Soft tissue mass, unusual to calcify
!" Can erode adjacent bone
!" CT: soft tissue mass – may show
attenuation greater than muscle
!" MRI
!"T1-WI low/intermediate signal
!"T2-WI variable signal
!"Fascial tail sign (up to 80% cases)
!"Low signal bands (up to 86% cases)
!" Enhance with contrast

Figure 36 A to E
Extraabdominal desmoid in a 30-year-old woman with
multiple MR images showing an intermuscular soft
tissue mass (arrows) with inferior extension along
!6(*%.:("&/3#0*4#%/3#*@/."=()*#""1<A*#$)*01<C%3E$#0*
intensity collagenized bands (arrowheads).
Fibromatosis: Aggressive Infantile

Figure 38 A, B & C
[Figures 37 to 39]
!" Painless soft tissue mass, M > F Same patient as previous image showing multicentric
!" !"7%*E,-,+)$-7()(a*)<,/-7)*#)'"#, involvement with second site (*) in lower calf
!" Intermuscular: head/neck, shoulder, demonstrating high-signal intensity on axial T2-W MR
thigh, foot image. The patient ultimately required amputation as
shown on the gross specimen with the large recurrent
!" Can erode bone mass (*) .
!" Multifocal (10%-15%)
!" No metastasis; locally aggressive
and recurrence very common
(up to 80%-90%)
Figure 37 Figure 39
SEE"(%%3=(*3$4#$!30(*&+"1>#!1%3%*1$*%#E3!!#0*;BCT*
MR image with large mass eroding bone (*) which Axial T2-W MR image in patient with aggressive
ultimately led to amputation following multiple 3$4#$!30(*&+"1>#!1%3%*#4!("*"#)3#!31$*%61<%*>#"2()*01<*
recurrences. Note low-intensity bands (arrowheads). signal (arrows) resulting from collagenization following
successful nonoperative treatment.

Fibromatosis: Malignant Fibrous Histiocytoma (MFH)
Juvenile Aponeurotic Fibroma and Fibrosarcoma
!" Children/adolescents; M > F !" Osseous
!" Hands (77%), feet (13%) – palms and !" Soft tissue (ST)
soles
!" Painless, slow-growing mass Malignant Fibrous Histiocytoma:
!" F/'%"$%/("*.)/.+)'*%/')-,%&--,.%,)0>A64) Pathology
common !" Described 1964 - Stout and coworkers
!" Attached to tendon/aponeurosis !" Three cell types present
!"Fibroblastic spindle cells
Fibromatosis: Infantile Dermal/Digital !"Plump histiocytic cell (from marrow
!" Birth to 2 years old; F > M 8*.*%<(,7I4
!" Fingers > toes; dorsum; spare thumb/ !"Giant cells benign and malignant
great toe !" Histologic types: storioform (pleomorphic
!" Bone erosion rare, can have contractures 50%-60%), myxoid (25%),
!" Pathology: intracellular inclusion bodies 2"/.()%,'')0@A64M)".C/88/(*-<)0@A64M))
!" Recurrence local (60%) angiomatoid (5%)
!" No malignant matrix; diagnosis of
Adult Palmar Fibromatosis exclusion
!" Palmar (Dupuytren contracture) 1%-2% !" WHO 2002: undifferentiated high-grade
population (1/5 people older than 65) pleomorphic sarcoma (soft tissue lesions
!" M > F = 4-5:1; ulnar side, thumb and only)
".+,3)$.2,-)7:/-,+
!" Fibrous nodules - cords (40%-60% Fibrosarcoma: Pathology
bilateral) !" Malignant collagen-producing spindle cells
!" B(9,-)$1-*8/(*7"7)>6?XA6 !" “Herringbone” pattern – lower grade
!" Contractures/recurrence common lesions (I-II)
!" Higher grade (III-IV) lesions –
Adult Plantar Fibromatosis more anaplasia
!" Ledderhose disease !" No matrix or malignant giant cells
!" Less common than palmar; bilateral 20%-
50% Osseous MFH and Fibrosarcoma:
!" M > F (2:1); wider age range 55% < age Clinical Features
30 !" =A?\A)<,/-7)*'+M):,/W)".)$#(9)+,%/+,
!" Starts as single nodule middle to !" MFH 2%-5% of primary bone
medial sole malignancies
!" Often leads to early excision; !" Pain, swelling, and pathologic fracture
contractures rare (30%-50%)
!" Associated with palmar disease (10%- !" Slight male predilection (3:2)
65%) !" Metaphyseal – around knee (40%-80%),
femur (32%-50%), humerus (10%),
Infantile M5&4:1&8*)&#-# pelvis (10%)
!" Discovered at birth or within weeks (88% !" Secondary lesions (22%-28%, older
< 2 years of age) patients and worse prognosis) – Paget
!" Solitary form (good prognosis): multifocal +"7,/7,M)*7(,*.,%-*7"7M)$1-*&7)+<7:'/7"/M))))))
(poor prognosis) - soft tissue, muscle, chronic osteomyelitis
viscera
!" Bone lesions common but involute Osseous MFH and Fibrosarcoma:
!" Lesions grow in perinatal period Radiology [Figures 40 to 45]
!" V<*1'/7("%)/.+)$1-*1'/7("%)',7"*. !" Lytic lesions – from geographic IB to
8*(9,/(,.D:,-8,/("E,)c)-,C,%(7)(&8*-)
Fibromatosis: Treatment and Prognosis grade
!" Surgical excision – can ultimately require
!" With geographic IB-IC lesions -GCT
amputation
like; look for diaphyseal > epiphyseal
!" Interferon, hormonal, chemo/radiation
extension
therapy
!" Mild periosteal reaction (26%) or sclerosis
!" Radiofrequency ablation/cryoablation –
!" Soft tissue mass on MR 100%; joint
new therapy
involvement in 40%
!" Recurrence common (50%-87%) and
!" Variable but often only mild increased
increased if neurovascular involvement
intensity on T2-W MR images
!" High signal on T2 corresponds to more
cellular regions increasing recurrence
!" Reexcision may use radiation therapy
!"Can follow with MRI
Figure 44
Figure 40 Osseous MFH

(same patient
Osseous MFH as previous
with radiograph image) with
showing intraosseous
solitary lesion
geographic and large
lytic lesion associated soft
with wide zone tissue mass (*)
of transition but no matrix
(arrows). mineralization.
Figure 41 Figure 45
CT of osseous Axial T1-W

MFH shows MR image
no matrix of osseous
mineralization MFH (same
and cortical patient as
penetration previous
anteriorly with two images)
soft tissue mass shows
(*) (same patient marrow
as previous replacement and associated soft tissue
image). mass (*).
Osseous MFH and Fibrosarcoma:

Therapy and Prognosis
!" Treatment – wide local resection/
amputation
!" 5-year survival 34%-53%
!" Local recurrence common
!" Metastasis common – hematogenous –
lung (32%-53%) and bone (7%-15%)
Soft Tissue MFH: Clinical Features

!" Most common adult soft tissue (ST)
sarcoma
!" Accounting for 15%-30% of all ST
sarcomas
!" Incidence 1-2 cases/100,000 patients
Figure 42 A & B !" Age 50-70 years: M > F = 2:1
Coronal T1-W MR image and coronal gross specimen !" Location: deep soft tissue - lower
shows distal femoral MFH (same patent as previous extremity (50%), upper extremity
two images) not extending to subchondral bone (25%), retroperitoneum (15%),
(arrowhead) (as would be seen with giant cell tumor). head and neck (5%)
Musculoskeletal Soft Tissue Sarcoma

Figure 43 Incidence
Osseous !" V/'"2./.()$1-*&7)9"7("*%<(*8/)/.+)
MFH showing $1-*7/-%*8/)XA6?5A6
aggressive !" Liposarcoma 16%-19%
solitary !" Rhabdomyosarcoma 10%-19%
lytic lesion !" ;*.7:,%"$%)7:".+',)%,'')7/-%*8/))))))))))
(arrows) in
supraacetabular 5%-15%
region with !" Leiomyosarcoma 5%-10%
lateral cortical !" !,-8/(*$1-*7/-%*8/):-*(&1,-/.7)0!KQG4)
destruction 5%-10%
)34&/.0!*!1*
!" Synovial sarcoma 5%-10%
detect.

Soft Tissue Fibrosarcoma:
Clinical Features Figure 48
!" Palpable mass – deep soft tissues
!" Lower extremity – knee and thigh (45%), Largely
upper extremity (28%), trunk (17%), hemorrhagic
(*) soft tissue
head and neck (10%) MFH in the
!" Age: 30-55 years, no sex predilection anterior thigh
on CT with
Soft Tissue MFH and Fibrosarcoma: the only solid
Radiology [Figures 46 to 51] component
adjacent to the
!" Deep soft tissue mass – MRI > CT for anteromedial
evaluating extent prior to surgery femur
!" MRI: usually similar to muscle T1-W (arrowhead).
!"High intensity T2-W
!"May not show increased intensity on
T2-WIs
!" Pseudocapsule – low intensity all
sequences
!" F/'%"$%/("*.D*77"$%/("*.[)>6?XA6)VK_
!" May involve underlying bone
!" MFH: hemorrhage – high intensity T1-WIs
!" Can differentiate myxoid lesions look like
C&"+)a"(9).*+&'/-):,-":9,-/')%*.(-/7()
enhancement
Figure 49 A & B
Sagittal T1-W MR images before and after contrast
show enhancement of the solid component
(arrowheads) of the MFH and nonenhancing
hemorrhagic areas (*).
Figure 46 A & B
Soft tissue MFH with mass replacing vastus lateralis

muscle (*) on axial T1-W MR image.
Figure 50 A & B
Soft tissue MFH with soft tissue mass (*) causing

extrinsic erosion of adjacent femur (arrowheads) on
Figure 47 A & B
radiograph and gross specimen.
Soft tissue MFH with high-signal intensity mass (*) on

axial T2-W MR image (same patient as previous MR).

Soft Tissue MFH/Fibrosarcoma:
Therapy and Prognosis
!" Treatment – wide local resection/
amputation
!" Local recurrence common (10%-50%) -
follow-up imaging
!" Metastasis (40%) common –
hematogenous – lung, lymph nodes, liver,
and bone
D(18*)&4:1&#*1$&8*+Protuberans
(DFSP): Clinical Features
!" 6% all soft tissue tissue sarcomas
!" P9"-+)(*)$#(9)+,%/+,7)*#)'"#,
!" L,++"79)1-*a.)(*)1'&"79)7&:,-$%"/').*+&',)
!" May be multiple
!" Most common to affect trunk (50%)
!"Remainder head/neck, upper/lower
extremities
DFSP: Pathology
!" f."#*-8)$1-*1'/7(7
!" Storiform pattern (may be myxoid)
!" May have areas of higher-grade sarcoma
!"Usually $1-*7/-%*8/)0@\6?X\64
DFSP: Radiologic Characteristics

[Figure 51]
!" Q&1%&(/.,*&7)8/77)c).*)%/'%"$%/("*.7
!" Usually centered on skin and protuberant
!" ;*.7:,%"$%)7*'"+)".(-".7"%)#,/(&-,7)FPDVLU
!"Enhance with contrast, ST attenuation
!"Intermediate signal on T1;
high signal on T2
!" May have hemorrhage
!" Look for linear extension (skin/fascial tail
sign)
!"Satellite nodules
DFSP: Treatment and Prognosis

!" Surgical excision (wide with 3-cm margin)
!" Local recurrence 20%-55%
(within 3 years)
!"Higher with head/neck lesions Figure 51 A, B & C
(50%-75%)
DFSP on sagittal T1, axial STIR, and gross specimen
!" Metastases showing protuberant subcutaneous mass (*) involving
!"Lungs (5%-6%) the skin with linear extensions along the skin surface
!"Lymph nodes up to 25% of metastases (arrows).
!"Higher incidence with high-grade
component (21%)

References
K"1-*3/.(9*8/)0;*.*77"#<".2)$1-*8/4
1. Jee WH, Choe BY, Kang HS, Suh KJ, Suh JS, Ryu KN, Lee YS, Ok IY, Kim JM, Choi KH, Shinn KS.
;*.*77"#<".2)$1-*8/[)%9/-/%(,-"7("%7)/()VL)"8/2".2)a"(9):/(9*'*2"%)%*--,'/("*.S)L/+"*'*2<)@ZZd)
Oct;209(1):197-202.
2. Ritschl P, Karnel F, Hajek P. Fibrous metaphyseal defects--determination of their origin and natural history
using a radiomorphological study. Skeletal Radiol 1988;17(1):8-15.
Fibrous Dysplasia
3. Fitzpatrick KA, Taljanovic MS, Speer DP, Graham AR, Jacobson JA, Barnes GR, Hunter TB. Imaging
$.+".27)*#)$1-*&7)+<7:'/7"/)a"(9)9"7(*:/(9*'*2"%)/.+)".(-/*:,-/("E,)%*--,'/("*.S)^RL)^8)R)L*,.(2,.*'S)
2004 Jun;182(6):1389-98. No abstract available.
4. Jee WH, Choi KH, Choe BY, Park JM, Shinn KS. Fibrous dysplasia: MR imaging characteristics with
radiopathologic correlation. AJR Am J Roentgenol 1996 Dec;167(6):1523-7.
5. Singnurkar A, Phancao JP, Chatha DS, Stern J. The appearance of Mazabraud’s syndrome on 18F-FDG
PET/CT. Skeletal Radiol 2007;36:1085-9.
B7(,*$1-*&7)+<7:'/7"/D^+/8/.(".*8/
6. Van der Woude HJ, Hazelbag HM, Bloem JL, Taminiau AH, Hogendoorn PC. MRI of adamantinoma of long
bones in correlation with histopathology. AJR Am J Roentgenol 2004 Dec;183(6):1737-44.
Fibromatosis
7. Robbin MR, Murphey MD, Temple HT, Kransdorf MJ, Choi JJ. Imaging of Musculoskeletal Fibromatosis.
8. Kujak JL, Liu PT, Johnson GB, Callstrom MR. Early experience with percutaneous cryoablation of extra-
abdominal desmoid tumors. Skeletal Radiol 2010;39:175-82.
9. Ilaslan H, Schils J, Joyce M, Marks K, Sundaram M. Radiofrequency ablation: another treatment option for
local control of desmoid tumors. Skeletal Radiol 2010;39:169-73.
Malignant Fibrous Histiocytoma/Fibrosarcoma
10. V&-:9,<)V!M)J-*77)PVM)L*7,.(9/')_JS))V&7%&'*7W,',(/')8/'"2./.()$1-*&7)9"7("*%<(*8/[))-/+"*'*2"%?
pathologic correlation. RadioGraphics 1994;14:807-26.
11. h*:'/7)VFM)H,#W*a"(`)L^M)O/&,-)PNM)R*<%,)VRM)U'/7'/.)_M)H/.+/)RM)Q&.+/-/8)VS)U8/2".2)$.+".27M)
:-,E/',.%,)/.+)*&(%*8,)*#)+,).*E*)/.+)7,%*.+/-<)8/'"2./.()$1-*&7)9"7("*%<(*8/)*#)1*.,S)QW,',(/')
Radiol 2010;39:791-8.
!,-8/(*$1-*7/-%*8/)G-*(&1,-/.7)0!KQG4
12. P*--,22"/.")NFM)^'?U78/"')hM)V&.W)GHM);"%*'/*&)QM)BkF*..,'')RiM)h.*a'".2)V^S))!,-8/(*$1-*7/-%*8/)
protuberans: MR imaging features. AJR Am J Roentgenol 2002 Apr;178(4):989-93.
13. J**+".)JQM)Q9&'W".)OHM)h/&#8/.)L^M)V%F/-E"'',)VOS)G]PDFP)%9/-/%(,-"`/("*.)*#)$1-**77,*&7)+,#,%(7)".)
children: 18F-FDG uptake can mimic metastatic disease. AJR Am J Roentgenol 2006;187:1124-8.
14. Dinauer PA, Brixey CJ, Moncur JT, Fanburg-Smith JC, Murphey MD. Pathologic and MR imaging features of
1,."2.)$1-*&7)7*#(?("77&,)(&8*-7)".)/+&'(7S)L/+"*J-/:9"%7)XAA\YX\[@\5?d\S

901
902
Alphabet Soup and Cystic Lesions of Bone
Mark D. Murphey, MD
Alphabet Soup and Cystic Lesions of the

Bone
!" Giant cell tumor (GCT)
!" Unicameral bone cyst (UBC)
!" Aneurysmal bone cyst (ABC)
!" Epidermoid inclusion cyst
!" Subchondral cyst
!" Intraosseous ganglion
!" Posttraumatic cyst
Giant Cell Tumor (GCT): Clinical Featues

!" Approximately 5%-10% of all biopsied
primary bone tumors; 18%-23% of
benign bone neoplasms
!" Symptoms: pain and swelling often
Figure 1
relieved by decreased activity
!" Pathologic fracture 10%-35% GCT skeletal
!" Adults: 80% between 20-50 years old distribution.
!" Rare in children 1%-3% (< 14 years)
!" Sex distribution
!"F :M = 1.1-1.5:1 benign GCT
!"M:F = 3:1 malignant GCT
GCT: Location [Figure 1]

!" Originate metaphyseal side of growth
plate and grow to subchondral bone
(84%-99%)
!" Long tubular bones (75%-90%)
!" About knee (50%-65%) distal femur
(23%-30%), proximal tibia (20%-25%)
!" Radius (10%-12%); humerus (4%-8%)
!" Spine (7%-15%) – vertebral body –
sacrum-thoracic-cervical-lumbar
!" Pelvis (4%) hands/feet (5%)
!" Multifocal (.5%-1%) – skull and face
(Paget disease), Goltz syndrome GCT: Radiology [Figures 2 to 10]
!" Solitary eccentric geographic lytic lesion
GCT: Pathology extending into subchondral bone
!" Osteoclast-like giant cells (90%) !" Center of lesion-metaepiphysis
!" Mononuclear spindle cell stromal !" Margin IB (80%-85%), IC (10%-20%), IA
component (1%-2% but up to 20% by CT)
!" Hemorrhage, necrosis and hemosiderin !" No mineralized matrix
!" ABC-like areas 10%-15% !" Expansile remodeling (47%-60%)
with apparent cortical permeation
Osseous Lesions Containing Giant Cells (33%-50%)
!" GCT/ABC/UBC !"Septations-subperiosteal new bone
!" NOF/CMF/OGS !"Periosteal reaction unusual 10%-30%
!" Brown tumor HPT/chondroblastoma !" L/+"*'*2"%)%9/-/%(,-"7("%)+*).*()-,C,%()
!" Fibrous dysplasia and variants clinical behavior of GCT
!" Osteoblastoma !" Bone scan – doughnut sign (57%)
!" Giant cell reparative granuloma !" Usually a vascular lesion (75%-90%)
!" MRI > CT for evaluation of extent
!" Fluid levels in cystic (ABC) components
!" Low to intermediate intensity usually
predominates on T2-WIs (90%-95%) in
solid components

Figure 4 A & B
U5;*14*)3%!#0*4(>."*%61<%*<(00C)(&$()*E(1E"#:63/*@BQ*
margin) (arrow) lysis extending to subchondral bone.
Bone scan reveals marked increased uptake in femoral
GCT but also in the adjacent tibia and patella. The
Figure 2 A & B increased uptake in the tibia and patella are due to
GCT of the proximal tibia with geographic lytic lesion hyperemia and disuse, not tumor involvement.
with a mild rim of partial sclerosis (unusual in GCT)
(arrows), mild expansile remodeling and increased
radionuclide uptake on bone scan (right image).
Figure 5
Axial T1-W MR image shows marrow replacement and
small anterior soft tissue mass (*) resulting from this
benign GCT (same patient as previous radiograph and
bone scan).
CT of GCT shows no mineralized matrix (*) (same

patient as previous radiograph).

Figure 9
GCT of the
sacrum with
predominantly
Figure 6 low- to
intermediate-
U5;*14*!6(*&+.0#*<3!6* signal
marked expansile intensity (*)
remodeling of bone. on the axial
T2-W MR
image.
Figure 10 A & B
GCT of the sacrum with predominantly intermediate
signal intensity (*) on the sagittal T1-W MR image
and large associated soft tissue mass (*) correlating
identically with the sagittally sectioned gross specimen
(same as previous patient).
GCT:
Treatment and Prognosis
!" Curettage and cryosurgery or en bloc
resection and bone graft
!" Local recurrence rate 40%-60%
historically
Figure 7 A & B !" Current recurrence rate 2%-25%
Coronal T2-W MR image shows intermediate to low !" Denosumab medical therapy (86%
(*) signal intensity tissue typical of GCT. response)
!" Recurrence does not correspond to
radiologic or microscopic appearance
!" Osseous recurrence – new bone
destruction
!" Soft tissue recurrence-mass and may
calcify/ossify about periphery
!" May metastasize (2%-5%) (50% benign
histology)
Figure 8 !" Malignant GCT (5%-19%) (much < 5%
in our experience) (more common with
GCT of the patella radiation)
(sesamoids
and apophysis Giant Cell (Reparative) Granuloma
are epiphyseal
equivalents for !" Rare benign lesion described in 1953 by
the differential Jaffe
diagnosis of lytic !" Mandible/maxilla (3:1) (7% benign jaw
lesions). lesions; incidence 1.1/million) and hands/
feet
!" Phalanges > metacarpal > metatarsal >
carpus > tarsus
!" Women > men (jaw), 10-50 years old
(74% < 30 years old)
!" May have history of trauma

Giant Cell (Reparative) Granuloma: Simple Bone Cyst: Location/Etiology
Pathology [Figure 12]
!" Granuloma-like arrangement of !" Under age 20: humerus (55%-65%),
$1-*1'/7("%)7(-*8/)/.+)*7(,*"+)*.)8"%-* #,8&-)0X>6?5A64M)("1"/M)$1&'/M)-/+"&7M)
!" Metadiaphyseal lytic lesion and ulna rare
!" Expansile remodeling and trabeculation !" Over age 20: iliac bone/calcaneus
!" Recurrence only if incompletely excised !" Cause: lymphatic or venous obstruction
vs synovial origin
Giant Cell (Reparative) Granuloma:
Radiology [Figure 11]
!" Similar to GCT
!" May not extend to subchondral bone
(hand)
!" Expansile remodeling and trabeculation
!" May detect small amount of mineralization
Figure 11 Figure 12
Unicameral/
Giant cell Simple bone
(reparative) cyst skeletal
granuloma in distribution.
the second
metacarpal.
Unicameral Bone Cyst: Simple Bone Cyst

!" ^)C&"+?%*.(/".".2)',7"*.)'".,+)1<)
mesothelial (epithelial-like) cells usually
arising in metaphysis of long bone
adjacent to physis
Simple Bone Cyst: Clinical Features Simple Bone Cyst: Radiology

!" 3% of all biopsied primary osseous
[Figures 13 to 15]
neoplasms
!" Geographic IA lesion – originate in central
!" Young patients 85% < 20 years
metaphysis (active)
!" M > F = 2:1
!" Can migrate into the diaphysis (latent)
!" Pathologic fracture (50%)
!" Mild expansile remodeling
Simple Bone Cyst Pathology !" Not infrequently multilocular
!" F',/-M)7(-/a?%*'*-,+M)C&"+?$'',+)%<7( !" Pathologic fracture
!" F<7()'".".2[)(9".)C/(),:"(9,'"/'?'"W,)%,''7? !"“Fallen fragment” sign (5%)
mesothelial origin !" FPDVLU[).*.%*8:'"%/(,+)7,,)7"8:',)C&"+))
!" F*8:'"%/(,+)%<7(7?9,8*--9/2,M)$1-*? !"Thin wall and septal enhancement;
osseous repair tissue beware delayed MR imaging with
diffusion of contrast
!" CT/MRI: complicated cases with fracture
!"Q*'"+)%*8:*.,.(7M)(9"%W)a/''7M)C&"+)
level

Simple Bone Cysts: Treatment and
Course
!" Spontaneous regression or heal after
fracture
!" Curettage and bone grafting
Figure 13 !" Intralesional steroids (70%-95%
effective)
Simple bone !" Recurrence (20%-40%)
cyst with !"Increases with younger age and larger
fracture size
(arrow)
and “fallen
!" Extremely rare malignant transformation
fragment”
sign (curved Aneurysmal Bone Cyst (ABC) D(4,-)-&,
arrow). !" “The so-called aneurysmal bone cyst
is neither a cyst nor a neoplasm;
rather it is probably a periosteal to
intraosseous arteriovenous malformation
not uncommonly seen in association
with other well-known benign and even
malignant lesions”
Mirra JM. Bone Tumors. Lea & Febiger. 1989.
ABC: Clinical Features

!" 1%-6% of all biopsied primary osseous
neoplasms
!" 80%-85% 5-20 years old
!" Patients present with pain, swelling, and
pathologic fracture (10%-20%)
!" May be associated with trauma
!" Slightly more common in women
(1.5-2:1)
ABC: Secondary Lesion

!" 1%-32% of cases
!" Benign lesions chondroblastoma, CMF,
;BKM)JFPM)$1-*&7)+<7:'/7"/M)fOFM)Brown
tumor, hemangioma, giant cell reparative
granuloma
!" Malignant lesions hemangioendothelioma,
Figure 14 telangiectatic osteosarcoma,
Simple bone cyst in the calcaneus (arrow). chondrosarcoma
Osseous Lesions with Prominent Fluid

Levels Differential Diagnosis
!" ^.,&-<78/')1*.,)%<7()0*.'<)C&"+)',E,'74
!" Giant cell tumor (to bone end,
metaphyseal center)
!" Chondroblastoma (epiphyseal center)
!" Osteoblastoma (posterior elements spine)
Figure 15 !" Telangiectatic osteosarcoma (thick walls,
osteoid on CT)
Simple bone !" Fibrous dysplasia (diaphysis, “ground
cyst in the glass”)
calcaneous
on CT with
septation ABC: Pathology
(arrowheads). !" J-*77[)m1'**+?$'',+)7:*.2,l
!" F/E,-.*&7)1'**+?$'',+)7:/%,7)'".,)1<)
$1-*&7)a/''7
!" May see chondrosseous tissue indicating
repair

ABC: Location [Figure 16]
!" Long tubular bone (70%-80%)
!" Spine posterior elements: 15% (thoracic,
lumbar, cervical, sacral)
!" Pelvis (5%-10%)
!" Hands (10%-15%)
Figure 17 A & B
ABC (primary) with more prominent expansile
remodeling of bone posteriorly (more aggressive
appearance) (arrow) versus rim of sclerosis in other
areas (indolent appearance) (arrowheads).
Figure 16
ABC skeletal
distribution.
Figure 18 A & B
ABC (primary) with “donut” sign (increased uptake

peripherally and photopenia centrally) on bone
scintigraphy (same patient as previous radiographs).
ABC: Radiology [Figures 17 to 23]
!" Only osseous neoplasm named for its
radiologic appearance
!" Metaphysis (80%-90%), eccentric
medullary geographic lytic lesion
!" Can appear central with expansion
!" Diaphysis (10%-20%), often surface
lesions
!" Expansile remodeling uneven in
distribution creating one aggressive
margin
!" Spine: expansion can lead to neurologic
+,$%"(7
!" Periosteal membrane intact on CT/MRI
!" Bone scan: peripheral activity (65%)
!" K'&"+)',E,'7)0FPDVLU4[).*.7:,%"$%) Figure 19 A & B
representing sedimentation of blood SQ5*@:"3>#",A*1$*#'3#0*;FCT*-7*3>#E(*%61<%*?.3)*
!" Angiography: hypovascular lesion with levels (arrows) from hemorrhage in all parts of the
localized areas of increased vascularity lesion (same patient as previous bone scan).

Figure 20
ABC (primary)
with sagittal
gross specimen
showing blood-
&00()*%:#/(%*@RA*
lined by thin
septae (arrows)
(same patient as
previous MRI).
GCT with ABC component on various MR pulse
sequences with diffuse enhancement and
intermediate signal intensity of the solid component
@RA*#$)*"3>*($6#$/(>($!V*63E6*%3E$#0*#$)*?.3)*0(=(0*
in the cystic component (arrows).
ABC: Treatment and Prognosis

!" Rarely spontaneous regression
!" Curettage, cryosurgery, and bone grafting
!" Recurrence (10%-20%)
!" Radiation therapy
Figure 21 A & B !" Ablation (radiofrequency/
Coronal pre- and postcontrast T1-W MR images pharmaceutical or other methods) with
showing thin enhancing periphery and septae (arrows) methylmethacrylate placement
typical of a primary ABC. !" Radiofrequency ablation with
methylmethacrylate placement
!" Embolotherapy
Cory DA, et al. AJR. 1989;153:369.
ABC: Solid Variant?

!" Recently described (1983); controversial
!" Radiography: similar to other ABCs but
more often aggressive and axial location
!" _"7(*'*2<[)$1-*&7)("77&,):-*'"#,-/("*.M)
osteoid production, osteoclastic giant
cells, sinusoids
Epidermoid Inclusion Cyst [Figure 24]

!" Two types
!" Hand: distal phalanx-traumatic origin
!" Radiographs: punched out lesion with
surrounding sclerosis, dorsal cortex often
Figure 22 A & B absent
Coronal T1-W and sagittal T2-W MR images of a !" Skull: ntraosseous-frontal and temporal
secondary (chondroblastoma) ABC with cystic areas bone-congenital origin
/1$!#3$3$E*?.3)*0(=(0%*@#""1<%A*#$)*#$!("31"*%103)* !" L/+"*2-/:97[)a,''?+,$.,+)'<("%)',7"*.)
component (*).
sclerotic margin and can cause expansile
remodeling of bone
!" G/(9*'*2<[)7(-/("$,+)7b&/8*&7),:"(9,'"&8

Figure 24
Epidermoid
inclusion
cyst with
<(00C)(&$()*
Figure 26 A & B
terminal
phalangeal Intraosseous ganglion in the subchondral region of the
lytic lesion medial malleolus with intermediate-signal intensity
(arrows). on T1-W and high-signal intensity on T2-W (*) and
septation.
Posttraumatic Cyst [Figure 27]

!" Occurs as complication of fracture in
Subchondral Cyst children
!" Other terms: geodes and synovial cyst; !" Usually forearm-radius/ulna
no true epithelial or synovial lining !" F/&7,+)1<)9,8*--9/2,)(9,.)$1-*7"7
!" Middle- to older- aged patients !" L/+"*'&%,.()',7"*.)a,''?+,$.,+M)8/<)9,/')
!" Around joints and associated with other or persist
arthritic changes
!" ]("*'*2<[)7<.*E"/')C&"+)".(-&7"*.)E7)
osseous contusion
!" Can be large/solitary, articular damage
subtle simulating neoplasm (GCT)
Intraosseous Ganglion [Figures 25 & 26]

!" Uncommon lesion; middle-aged adults
!" Pain increases with activity
!" Periarticular, eccentric, geographic IA-IB
lytic lesion, high signal T2, rim enhance
!" > 80% of lesions: tibia (medial
malleolus), knee (posterior tibia), femur,
about wrist
!" Pathology: same as soft tissue ganglion
Posttraumatic cyst in the radius subsequent to a

fracture (arrows) three months earlier.
Figure 25 A & B
Intraosseous ganglion in the medial malleolus with

geographic lysis (arrows) and thin sclerotic margin
(IA).

References
General
1. Parman LM, Murphey MD. Alphabet Soup: Cystic Lesions of Bone. Seminars in Musculoskeletal Radiology
2000;4(1):89-101.
Giant Cell Tumor
2. Murphey MD, Nomikos GC, Flemming DJ, Gannon FH, Temple HT, Kransdorf MJ. From the archives of
AFIP. Imaging of giant cell tumor and giant cell reparative granuloma of bone: radiologic-pathologic
correlation. RadioGraphics 2001 Sep-Oct;21(5):1283-309. Review.
3. J*'+,.1,-2)LLM)F/8:1,'')FRM)O*.$2'"*)V[)J"/.(?%,'')(&8*-)*#)1*.,S)^.)/./'<7"7)*#)(a*)9&.+-,+)/.+)
eighteen cases. J Bone Joint Surg Am 1970;52:619.
4. V%J-/(9)GR[)J"/.(?%,'')(&8*&-)*#)1*.,[)/.)/./'<7"7)*#)$#(<?(a*)%/7,7S)R)O*.,)R*".()Q&-2)O-)@Z\XY>=[X@eS
5. Dahlin DC, Cupps RF, Johnson EW Jr: Giant Cell Tumor: a study of 195 cases. Cancer 1970;25:1061-70.
6. Sun, ZJ, Cai, Y, Zwahlen, RA, Zheng YF, Wang, SP, Zhao, YF. Central giant granuloma of the jaws: clinical
and radiological evaluation of 22 cases. Skeletal Radiol 2009;38:903-9.
7. Abdelrahman M, Bassiony AA, Shalaby H, Assal MK. Cryosurgery and impaction subchondral bone graft
for the treatment of giant cell tumor around the knee. Health Soc Serv J 2009;5:123-8.
8. Thomas D, Chawla SP, Skubitz K, Staddon AP, Henshaw R, Blay JY, Smith J, Ye Z, Roudier M, Jun S.
Denosumab treatment of giant cell tumor of bone: interim analysis of an open-label phase II study. J Clin
Oncol 26:2008 (May 20 suppl; abstr 10500).
Unicameral Bone Cyst
9. Glowacki M, Ignys-O’Byrne A, Ingys I, Mankowski P, Melzer P. Evaluation of volume and solitary bone cyst
remodeling using conventional radiological examination. Skeletal Radiol 2010;39;251-9.
Aneurysmal Bone Cyst
10. Martinez V, Sissons HA. Aneurysmal bone cyst. A review of 123 cases including primary lesions and those
secondary to other bone pathology. Cancer 1988 Jun 1;61(11):2291-304.
11. Kransdorf MJ, Sweet DE. Aneurysmal bone cyst: concept, controversy, clinical presentation, and imaging.
AJR Am J Roentgenol 1995 Mar;164(3):573-80. Review.
12. Bush CH, Adler Z, Drane WE, Tamurian R, Scarborough MT, Gibbs CP. Percutaneous radionuclide ablation
of axial aneurysmal bone cysts. AJR Am J Roentgenol 2010;194:W84-W90.
13. Maiya S, Davies AM, Evans N, Grimer RJ. Surface aneurysmal bone cysts: a pictorial review. Eur Radiol
2010;12:99-108.
14. Rossi G, Rimondi E, Bartalena T, Gerardi A, Alberghini M, Staals LE, Errani C, Bianchi G, Toscano A,
Mercuri M, Vanel D. Selective arterial embolization of 36 aneurysmal bone cysts of the skeleton with N-2-
butyl cyanoacrylate. Skeletal Radiol 2010;39:161-7.

912
Juxtaarticular Soft Tissue Masses
Mark D. Murphey, MD
Soft Tissue Masses In and About Joints
!" Tumor-like: tumoral calcinosis, pigmented
villonodular synovitis (PVNS), ganglion,
synovial cyst, 8<*7"("7)*77"$%/.7
Figure 1
!" Benign: synovial lipoma, myxoma,
synovial chondromatosis/chondroma,
Tumoral
nodular fasciitis calcinosis about
!" Malignant: synovial sarcoma, clear cell the shoulder with
sarcoma 0#"E(*/#0/3&()*
periarticular
Tumoral Calcinosis: Clinical Features mass (*) and
!" Usually children/young adults radiolucent
septations
!" Increased incidence in African Americans (arrowheads).
!" Familiar tendency (33% of cases)
!" Autosomal dominant with variable
expression
!" H/-2,)%/'%"$,+):/-//-("%&'/-)8/77[)9":M)
elbow, shoulder, foot, wrist
!" Can be associated with calcium
pyrophosphate dihydrate (CPPD)
arthropathy, pseudoxanthoma elasticum-
like syndrome
!" Also skin ulceration, marrow and dental
changes
!" Etiology: metabolic (few
hyperphosphatemia, normal calcium and
increased Vitamin D) trauma, idiopathic
Tumoral Calcinosis: Pathology

!" Gross-encapsulated multilocular mass,
$'',+)a"(9)E"7%*&7)%/'%"&8)9<+-*3</:/("(,
!" Fibrous septations
!" V/<)9/E,)".C/88/(*-<),',8,.(7
Tumoral Calcinosis: Radiology Figure 2 A & B

[Figures 1 to 7]
!" F/'%"$,+):/-//-("%&'/-)8/77 Tumoral calcinosis about the knee.
!" Extensor surface
!" Radiolucent septations (“chicken wire”)
!" Extraarticular (bursae); no loss ROM
!" Average 3 lesions/individual Figure 3
!" FPDVLU[)%/'%"&8)C&"+)',E,'7)0'"b&,$,+)
calcium “sedimentation” sign) Clinical
!"More active disease photograph
!" Bone scan: best for detection and in patient
localization with tumoral
calcinosis
!" MRI: low-signal T1-WIs about the knee
!"Variable low- to high- signal T2-WIs (same patent
!" Pseudoxanthoma elasticum-skin/vascular as previous
%/'%"$%/("*.M)-,("./)/.2"*"+)7(-,/W7 radiograph)
!" CPPD arthropathy showing
cosmetic
!" Dental abnormalities: root enlargement, deformity but
".(-/:&':)%/'%"$%/("*. no decreased
!" V/--*a)".E*'E,8,.([)%/'%"$%)8<,'"("7 range of
motion.
Martinez. Radiology. 1990;1974:225.
Juxtaarticular Soft Tissue Masses 913 Musculoskeletal Radiology

Figure 4
A&B
Tumoral
calcinosis
about the
elbow
extensor
surface.
Contralateral
elbow
revealed
identical
&$)3$E%*@$1!*
shown).
Figure 7 A & B
Radiograph of tumoral calcinosis about the shoulder

and intense radionuclide uptake on bone scintigraphy.
Tumoral Calcinosis: Treatment

!" Phosphate depletion therapy
!"Aluminum hydroxide
!"Acetazolamide
!" Surgical excision
(PVNS): Clinical Features

!" Proliferative disorder of synovium of joint,
tendon, or bursa
!" Young adults third and fourth decades
Figure 5 A, B, C & D !" Two types: diffuse (15%-25%) and
;.>1"#0*/#0/3$1%3%*#+1.!*!6(*63:*<3!6*/#0/3.>*?.3)* localized/focal (75%-85%)
levels (arrowheads) on CT. !" Symptoms: pain, swelling, ROM loss
PVNS: Pathology
!" ]("*'*2<)&.W.*a.[)".C/88/(*-<D
neoplasm/trauma
!" Variable degree of villous/nodular
synovial proliferation, and pigmentation
09,8*7"+,-".4M)/.+)".C/88/("*.)
components
!" J"/.()%,''7M)$1-*&7)("77&,M)3/.(9*8/)%,''7
PVNS: Location
!" Localized form: usually extraarticular
!"Giant cell tumor tendon sheath
(GCT - TS)
!"Hand (80%), feet, knee (12%)
!" Diffuse form (monoarticular) – knee
Figure 6 A & B
(60%-80%), hip, ankle, shoulder, elbow
Tumoral calcinosis about the shoulder with large PVNS Localized (GCT – TS): Radiology
/#0/3&()*:("3#"!3/.0#"*>#%%*@RA*%61<3$E*:("3:6("#0*#$)* !" Second most common mass hand/wrist
septal enhancement after contrast (arrowheads). !" Lobulated soft tissue mass < 2 cm
!" More common volar surface
!" Osseous erosion uncommon 10%-15%
Periarticular C*%$-4$*)-&,A+Differential PVNS: Diffuse Form: Radiology
Diagnosis !" Erosive bone lesion (50%): hip (93%),
!" Scleroderma shoulder (75%), knee (26%)
!" Other collagen vascular diseases !" Geographic IA lytic lesion: extrinsic
!" Chronic renal failure (secondary tumoral erosion
calcinosis) !" Joint effusion
!" Milk-alkali syndrome !" ^-(9-*2-/:9<[)1-*a."79)*-)%9*%*'/(,)C&"+M)
!" Synovial sarcoma 8&'(".*+&'/-)$''".2)+,#,%(7

PVNS: Radiology [Figures 8 to 14]
!" Bone scan: mild increase activity (statics)
!" Angiography: can show impressive
vascularity
!" CT: soft tissue mass, increased
attenuation
!" MRI: T1-WI – low-intenity mass T2-WI –
variable - usually prominent low intensity
regions
Figure 8
Figure 11 A & B
Localized form of
PVNS (GCT) of Localized form of PVNS with underlying bone erosion
tendon sheath) (arrows) as seen on the radiograph and intraoperative
with volar thumb photograph.
mass (*) on
sagittal T1-W MR
image.
Figure 12
Typical villonodular morphology (arrows) and brown

appearance resulting from hemosiderin deposition (*)
in diffuse intraarticular PVNS.
Figure 9 A & B
Same patient as previous MR image with intermediate

signal intensity in the GCT of tendon sheath (*) of the
thumb on axial
T2-W MR.
Figure 10 A & B
Left Image: PVNS of the hip (diffuse type) with

radiograph showing erosions on both sides of the joint Figure 13 A & B
(arrows) and maintained joint space. Diffuse intraarticular PVNS of the ankle with extensive
Right Image: PVNS hip (same patient as previous involvement of the anterior and posterior recesses (*)
radiograph) with marked low-signal intensity tissue on with contrast enhancement and low-signal intensity
coronal T2-W MR image (*). on T2-W and “blooming” artifact on the gradient echo
sequence.

Soft Tissue Ganglion: Radiology
[Figures 16 to 21]
!" Soft tissue mass (1.5-2.5 cm) – dorsum
hand/wrist
!" Attached to tendon sheaths usually no
communication with joint
!" Intraarticular lesions (0.2%-1.9% at
knee)
!" Rarely cause adjacent bone erosion;
:,-"*7(,/')-,/%("*.M)a/'')%/'%"$%/("*.
!" CT/SONO (US)/MRI: cystic mass
!" US: Complex appearance 57% these are
larger, wrist location, 15% internal echoes
/.+)@X6)1'**+)C*a
!" May have higher attenuation on CT or
signal T1-W MR image – high protein
Figure 14 A & B mucin
!" V/<)$'')a"(9)%*.(-/7()#*''*a".2)T*".()
Diffuse intraarticular PVNS of the ankle with extensive
involvement of the anterior and posterior recesses (*)
injection on delayed CT/MRI
with contrast enhancement and low-signal intensity !" Wall/septae may show mild enhancement
on T2-W and “blooming” artifact on the gradient echo
sequence (GRE).
Synovial-Based Lesion:
Differential Diagnosis [Figure 15]
!" PVNS/synovial chondromatosis
!" ^-(9-"("7[)".C/88/(*-<
!" Infection: unusual low-grade
!" Amyloid
Figure 16 A & B
!" Synovial sarcoma
Large ganglion in the most frequent location dorsal
to the proximal carpal row with low to intermediate-
Figure 15 signal intensity mass (*) on axial T1-W MR image and
homogeneous high signal intensity on T2-W.
PVNS knee
(diffuse type)
with large
amount of low Figure 17
signal intensity
intraarticular Large
hemosiderin ganglion in
laden tissue (*). the most
frequent
location
PVNS: Treatment and Results dorsal to
the proximal
!" Surgical resection/synovectomy carpal row
!" Recurrence rate with anechoic
!"GCT – TS (10%-20%) appearance
!"Diffuse form (40%-50%) on
!" Radiation – internal synovectomy – sonography
(*).
yttrium 90 and dysprosium 165 para recurrencias
Soft Tissue Ganglion: Clinical Features
!" Young adults (25-45 years old)
!" Most common mass hand/wrist (60% of
masses) No son quistes verdaderos. No tienen cubierta epitelial
!" Pain, tenderness, or functional impairment
(50%), rarely nerve palsy
Soft Tissue Ganglion: Pathology

!" Etiology: unknown – neoplasm,
".C/88/("*.M)(-/&8/
!" Thick-walled unilocular/multilocular cystic
spaces Figure 18
!" J,'/(".*&7)c)8&%".*&7)C&"+)-"%9)".) Ganglion in Guyon canal with intermediate-signal
hyaluronic acid and mucopolysaccharides intensity mass (*) on axial T1-W MR image.
Myxoma: Radiology [Figures 22 to 24]
!" Soft tissue mass; location: thigh,
shoulder, buttock, upper arm
!" Fluid characteristics CT/MRI
!" Sonography: hypoechoic with internal
echoes
!" High protein material may increase CT
attenuation or signal on T1-W MR image
!" Enhancement: peripheral rim/septae
(thick 43%) or mild diffuse pattern (57%)
!" Septations (43%) thick and mildly nodular
Figure 19 regions
Guyon canal ganglion (same patient as previous MR) !" Small rim of fat-like tissue CT (25%),
with marked high-signal intensity on axial T2-W MR MR (71%)
image (*) causing ulnar nerve entrapment symptoms. !" Edema surrounding mass MR (79%)
!" Rare to recur after removal
(partial or complete)
!" PET mild increase SUV (1.3-2.6)
Figure 20
In the
knee on CT
with low
attenuation
and multiple
septations
(*).
Figure 21
Figure 22
Intraarticular
ganglion (*) Intramuscular myxoma in paraspinal location on CT
in the knee on with low-attenuation mass (*) simulating a cyst.
sagittal T2-W
MR image with
septations
and marked
high-signal
intensity
(same patient
as previous
CT).
Myxoma: Clinical Features

!" Location: heart, subcutaneous,
intramuscular, juxtaarticular
!" Adults 40-70 years old
!" Slightly more common in women
!" Painless palpable mass
Myxoma: Pathology
!" Ovoid/globular whitish appearance
!" Contain gelatinous material
!" Unusual to have cystic spaces Figure 23
!" ;*)$1-*&7)%/:7&',M)1&(),+,8/)/.+)8&7%',)
atrophy surround mass Paraspinal intramuscular myxoma (same patient as
previous CT) with low echogenicity mass but some
internal echoes (*) are present suggesting that the
lesion is not cystic.

Popliteal Cyst (Baker Cyst)
!" Results from communication between
knee joint and gastrocnemius –
semimembranosus bursa
!" Increase incidence with age – 50%
autopsy series
!" Incidence varies - arthrography (7%-
42%), sonography (15%), MRI (5%)
!" Often asymptomatic or pain from other
causes
!" Uncommon to present as mass
!" May dissect in calf simulate DVT
!" U8/2".2)79*a7)".$'(-/("*.)*#)%/'#)0'*.2)
fusiform lesion) caused by extension
of cyst with dissection and surrounding
edema
Figure 24
Intramuscular myxoma in the forearm on sagittal Synovial Cyst: Radiology
MR imaging with low-signal intensity on T1-W and [Figures 25 to 30]
high-signal intensity on T2-W (*) simulating a cyst.
However, the intramuscular location, subtle rim of fat !" K'&"+?$'',+)8/77)c)QB;BDFPDVLU
(arrowheads on T1) and surrounding edema (arrows !" May have septations
on T2) exclude a cyst as a reasonable diagnostic !" Arthrography can show joint
consideration. communication
!" Can have solid components if complicated
(rupture) with hemorrhage, dissection, or
superimposed infection
!" Contrast enhancement of rim/septae
Myxoma: Differential Diagnosis !"Noncomplicated – thin walls
!" Abscess !" Contrast enhancement more complex in
!" Chronic hematoma complicated/ruptured popliteal cysts
!" Ganglion/synovial cyst/bursa !" F*8:'"%/(,+)%<7(7)+"#$%&'()(*),3%'&+,)
!" Other myxomatous neoplasms MFH/ other causes of mass; must look at
liposarcoma/neural tumors morphology
Synovial Cyst: D(4,-)-&,

!" A herniation or continuation of the
synovial membrane through the joint
capsule
Synovial Cyst: Location and Etiology

!" Most commonly recognized: popliteal
!" Shoulder, elbow, hip, hand, foot and ankle
!" Types
!"Primary: unknown cause - children
!"Secondary: any cause joint distention
!"Rheumatoid arthritis and juvenile
idiopathic arthritis (60%-70%)
Synovial Cyst: Pathology

!" K'&"+)$'',+)8/<)1,)8&'("'*%&'/- Figure 25 A & B
!" !,.7,)$1-*&7)a/'' Synovial cyst (popliteal) on CT with low attenuation
!" Lined by synovium (*) and single septation (arrowhead) in typical
location with neck between the semimembranosus and
gastrocnemius tendons.
Tb son comunes en las apófisis de las vértebras.

Figure 26
Synovial cyst
(popliteal -
same patient as
previous MR)
on axial T1-W
postcontrast
MR image with
peripheral/
septal but
nonnodular
enhancement
(arrowheads).
Figure 27
Figure 30 A & B
Synovial
Ruptured popliteal cyst on sagittal T1-W and T2-W MR
cyst
image with evidence of hemorrhage (*) and extensive
(popliteal
surrounding edema both superiorly and inferiorly
- same
(arrowheads).
patient as
previous
MR) on
axial T1-W
postcontrast MR image with peripheral/septal but
nonnodular enhancement (arrowheads).
Meniscal Cyst: Clinical Features

!" Adults (20-40 years); M > F = 2:1
!" Cystic masses related to meniscal tears
Figure 28 (1%-2% incidence)
!" Fluid accumulates from joint through tear
Synovial cyst !" Pain at night or after exercise
(popliteal -
same patient Meniscal Cyst: Radiology
as previous !" Radiographs: soft tissue mass
two MR’s) on
axial T2-W !" FPDQB;BDVLU[)C&"+)%*'',%("*.)/+T/%,.()(*)
postcontrast meniscus
MR image !" Lateral > medial 3-10:1 now more equal
with diffuse !" Medial: small cystic mass within or
high-signal intensity (*) and neck extending into joint
adjacent to meniscus
(arrowhead).
!" H/(,-/'[)'/-2,-)C&"+)%*'',%("*.)$''".2)
potential space between meniscus and
collateral ligament
!" MRI: best to evaluate meniscal tear and
extension into cyst
Figure 29 !" Must repair tear and resect cyst
Arthrogram showing Synovial Lipoma

the morphology of !" Two types
a ruptured popliteal !"Localized form
cyst with long !"Diffuse form: lipoma arborescens
fusiform shape and
irregular margins
/#.%()*+,*3$&0!"#!31$*
Synovial Lipoma: Localized
into surrounding !" Rare: knee most frequent
muscle. !" Solid fatty intraarticular mass
!" Filling defect on arthrogram
!" CT/MRI: lipomatous tissue

Lipoma Arborescens: Clinical Features Synovial Chondromatosis:
!" !"##&7,)".$'(-/("*.)*#)7<.*E"&8)1<)#/( Clinical Features
!" Monoarticular – knee (0.3% incidence on !" Formerly synovial osteochondromatosis
MRI) most common and due to cartilage metaplasia in
!" Often secondary (but can be primary) synovium
to chronic arthritis from trauma or !" Knee (50%-65%), hip, elbow, any joint
".C/88/(*-<)+"7,/7, can be involved
!" M > F = 2-4:1; third to sixth decade
Lipoma Arborescens: Radiology !" Joint pain (85%-100%), swelling (42%-
[Figures 31 & 32] 58%), decrease range of motion (38%-
!" Radiographs: soft tissue swelling 55%)
!" ^-(9-*2-/:9<[)8&'(":',)$''".2)+,#,%(7
!" FP)#/((<)".$'(-/("*. Synovial Chondromatosis: Pathology
!" MRI best to identify frond – like fatty !" Hyaline cartilage neoplasia in synovium
projections !" Cartilage nodules (2-3 cm) can break
away into joint, grow, reattach to
synovium
!" Cytogenetics – chromosome 6
abnormalities
!" Osteoid absent in up to 45% of cases
!" Hypercellularity and nuclear atypia
simulate cartilage malignancy
Synovial Chondromatosis Pathology:

Milgram Stages
!" Stage 1 (27%): active chondroid
neoplasia in synovium but no
intraarticular bodies
!" Stage 2 (33%): active synovial chondroid
Figure 31 neoplasia and intraarticular bodies
Lipoma arborescens with villonodular fronds of fatty !" Stage 3 (40%): no active synovial
tissue (arrows) extending into the knee joint on chondroid neoplasia but intraarticular
sagittal T1-W MR image. bodies (inactive)
!" Poor documentation of disease
progression
Synovial Chondromatosis: Radiology

[Figures 33 to 37]
!" L/+"*2-/:97[)%/'%"$,+)1*+",7)0\A6?Z>64M)
may ossify, extrinsic erosions (30%), joint
widened, OA changes
!" Radiographs normal (5%-30%)
!" Bone scan: mild increased activity
!" ^-(9-*2-/:9<[)$''".2)+,#,%(7
!" Ultrasound: heterogeneous mass with
hyperechoic foci that may show posterior
acoustic shadowing
!" CT low-attenuation thickening about
joint, effusion often small if present,
%/'%"$%/("*.D*77"$%/("*.
!" MRI: variable depending on degree of
mineralization, some hyperintensity T2-
Figure 32 WIs
Lipoma arborescens (same patient as previous MR) !" Can also involve tendons and bursa
%61<3$E*63E6C%3E$#0*3$!($%3!,*?.3)*%.""1.$)3$E*4#!!,* !" Secondary chondromatosis: trauma, OA,
nodules (arrows) on sagittal T2-W MR image. RA, AVN, osteochondritis dissecans

Figure 33
Synovial
chondromatosis
with multiple
"1.$)*&003$E*
defects on hip
arthrography.
O1*/#0/3&/#!31$*
was seen on pre-
arthrography
radiographs (not
shown).
Figure 37
Figure 34
Synovial chondromatosis of right hip (same patient as
Synovial previous radiograph and CT) with extensive high signal
chondro- intensity intraarticular tissue (*) about the femur (F)
matosis of the +.!*/#0/3&/#!31$*3%*$1!*#::#"($!*1$*;FCT*-7*3>#E(D
shoulder with
innumerable
/#0/3&()*
intraarticular
osteochondral
bodies all Synovial Chondromatosis:
similar in size RICE BODIES
and shape on Treatment and Prognosis
radiograph. !" Surgical synovectomy removal of
fragments
!" Recurrence common (3%-23%)
Figure 35
!" External radiation therapy
Synovial !" Internal RT: nuclear medicine
chondromatosis 7<.*E,%(*8<I
of right hip
with subtle !" Rare degeneration (5%) into
/#0/3&/#!31$%* chondrosarcoma
(arrowhead) !"Look for marrow invasion
)34&/.0!*!1*
detect on Soft Tissue Chondroma:
radiograph,
although joint Clinical Features
is widened !" Less common than synovial
(arrow). chondromatosis
!" Third and fourth decades, M > F
!" Slow-growing masses, painless
!" Fingers (80%), hands, toes, feet, trunk
Soft Tissue Chondroma: Pathology

!" Usually < 3 cm, often attached to tendon
!" Mature hyaline cartilage lobular pattern
!" F/.)79*a)*77"$%/("*.
!" Fibrous capsule not tenosynovium unlike
synovial chondromatosis
Soft Tissue Chondroma: Radiology

[Figures 38 to 41]
!" ;*.7:,%"$%)7*#()("77&,)8/77)-,'/(,+)(*)UG)
joint
Figure 36
!" Also common in infrapatellar fat
Synovial chondromatosis of right hip (same patient !" Chondroid matrix can ossify
#%*:"(=31.%*"#)31E"#:6A*<3!6*>.0!3:0(*/#0/3&/#!31$%* !" Unusual to erode underlying bone
(arrowheads) about hip on CT.

Figure 41
Soft tissue
chondroma in
Hoffa fat pad
on radiograph
with large
/#0/3&()*>#%%D
Figure 38 A & B
Soft tissue /61$)"1>#*14*!6(*&$E("*1$*"#)31E"#:6%* Heterotopic Bone Formation:
<3!6*0#"E(*/#0/3&()*>#%%*@#""1<6(#)%AD Myositis O##-4$*,#
!" Young adults, M > F, usually trauma
Figure 39 history
!" No history trauma 25%-50%; also
Soft tissue
chondroma of paraplegics
!6(*&$E("*1$* !" Can involve muscles, fascia, tendons,
CT with large subcutaneous fat
/#0/3&()*>#%%* !" Initially pain/tenderness and localized
(arrowheads). mass; pain decreases with time
O1$/#0/3&()*
portion is low
attenuation, Heterotopic Bone Formation: Location
consistent with !" Extremities: 80%, anterior compartments
a chondroid !" Lower extremity: quadriceps muscle
lesion (same !" Upper extremity: brachialis muscle
patient as
previous
!" Subcutaneous fat: 30% of cases
radiograph).
Heterotopic Bone Formation: Pathology
!" Zonal pattern of maturation
!"F,.(-/')"88/(&-,)*7(,*"+D$1-*1'/7("%)
tissue
!"Periphery calcifying osteoid to mature
lamellar bone
!" Cortical bone with further maturation
Heterotopic Bone Formation: Radiology

!" Early soft tissue mass and edema
!" F/'%"$%/("*.)X?=)a,,W7)(9,.)8/(&-,7)
(zonal phenomena) to central trabecular
and peripheral cortical bone
!" Usually separable from cortex but may be
attached
Heterotopic Bone Formation Radiology

[Figures 42 & 43]
Figure 40 A, B & C
!" Bone scan marked increased activity
Soft tissue /61$)"1>#*14*!6(*&$E("*1$*-7*3>#E3$E*
!" Angiography: staining and neovascularity
with high water content soft tissue mass (arrowheads)
consistent with a chondroid lesion (same patient as early
previous CT and radiograph). Note that the mass !" FP[)1,7()(*)7,,),/-'<)*77"$%/("*.):/((,-.)
3%*#)G#/($!*!1*!6(*?('1"*!($)1$*@;A*+.!*)1(%*$1!* with peripheral rim – enhances with
extend along as it would be expected in tenosynovial contrast
chondromatosis.

Heterotopic Bone Formation: Heterotopic Bone Formation:
MR Imaging [Figures 42 to 44] Treatment and Prognosis
!" Early to intermediate !" May resorb or be asymptomatic
!" Normal with displaced fascial planes (T1- !" Resect after maturation (12-18 months)
W) !" Premature resection – recurrence with
!" Increased intensity mass with prominent vengeance
edema (T2-WI) !" Rare report malignant transformation
!" H/(,[)9,(,-*2,.,*&7)a,'')+,$.,+)8/77) !" Malignant myositis (mucinous carcinoma)
marrow fat on T1-W/T2-W MR images, no
edema, low intensity rim Nodular Fasciitis: Clinical Features
!" Often misinterpreted as malignant tumor !" Very common; most frequent tumor-like
',7"*.)$1-*&7)("77&,
!" Most common benign mesenchymal lesion
misdiagnosed as sarcoma
!" Rapidly growing mass 1-2 weeks duration
Figure 42
!" Young adults (20-40 years old), M < F
!" History of trauma (10%-15%)
Heterotopic
bone formation Nodular Fasciitis: Location
(myositis !" Upper extremity (50%): volar forearm
1%%3&/#$%A*<3!6* !" Trunk (20%): chest wall and back
peripheral rim
14*/#0/3&/#!31$* !" Head and neck (18%) in children
on radiograph !" Rare hand/feet/lower extremity (16%)
(arrow).
Nodular Fasciitis: Pathology
!" Subcutaneous type (70%): soft tissue
Separada del hueso nodule
!" Intramuscular type (15%): not
circumscribed multinodular
!" U88/(&-,)$1-*1'/7(7)".)"--,2&'/-)#/7"%',7
!" Reticulin meshwork, collagen minimal,
".C/88/(*-<)/.+)8&%*"+)%*8:*.,.()
Nodular Fasciitis:
Radiology and Treatment [Figure 45]
!" ;*.7:,%"$%)78/'')7*#()("77&,)8/77))))))))))
(< 4 cm); may show fascial extensions
!" CT/MRI: mass with irregular margins and
hetergeneous on MRI, surrounding edema
!" May suggest malignancy on imaging and
pathology
Figure 43 A & B !" Surgical resection: recurrence rare
Heterotopic bone formation (same patent as previous (1%-2%) even if incomplete
"#)31E"#:6A*<3!6*:("3:6("#0*"3>*14*/#0/3&/#!31$*@#""1<A*
separated from femoral cortex on CT.
Figure 45
Nodular
fasciitis of
the forearm
on coronal
STIR MR
image with a
high-signal
intensity
Figure 44 A & B subcutaneous
mass (*) with
Heterotopic bone formation (same patient as previous linear fascial
radiograph and CT) on axial T2-W MR image with extensions
heterogeneous mass (arrow) suggesting a more (“fascial tail”
#EE"(%%3=(*$(1:0#%!3/*:"1/(%%*#%*:("3:6("#0*/#0/3&/#!31$* sign) (arrows) both superiorly and inferiorly.
is less apparent.
Synovial Sarcoma: Clinical Features
!" Malignant mesenchymal tumor
!" Young adults 15-40 years old
(30% < 20 years old)
!" Fourth to sixth most common soft tissue
sarcoma
!" Painful deep soft tissue mass
!" Often indolent slow-growing mass
(average 2-4 years to diagnosis)
Musculoskeletal Soft Tissue Sarcoma:

Incidence
!" MFH/Fibrosarcoma (20%-30%)
!" Liposarcoma (16%-19%)
!" Rhabdomyosarcoma (10%-19%)
!" ;*.7:,%"$%)7:".+',)%,'')7/-%*8/)0>6?
15%) Figure 46 A & B
!" Leiomyosarcoma (5%-10%) Synovial sarcoma of the foot with indolent appearing
!" !,-8/(*$1-*7/-%*8/):-*(&1,-/.7)0!KQG4) extrinsic bone erosion on radiograph (arrow).
(5%-10%)
!" Synovial sarcoma (2%-10%)
Synovial Sarcoma: Location

!" Extraarticular adjacent to tendons bursa,
ligaments > 90%
!" Intraarticular < 10%
!" Lower extremity (60%-71%) around knee
Figure 47
!" Upper extremity (16%-25%) around wrist
Synovial
Synovial Sarcoma: Pathology sarcoma about
!" Two cell lines elbow with
!"Epithelial (keratin positive) /#0/3&/#!31$*
!"Spindle cells (arrowhead) in
!" Monophasic (50%-60%)/biphasic (20%- mass near but
not in the joint
30%)/ poorly differentiated (15%-25%) on radiograph.
!" g/-"/1',[)%/'%"$%/("*.M)9,8*--9/2,
!" Cytogenetic abnormality t(X;18)
(p11;q11) 90%
Synovial Sarcoma: Radiology

[Figures 46 to 50]
!" L/+"*2-/:97[).*-8/')0>A64)*-).*.7:,%"$%)
soft tissue mass near joint
!" Bone erosion or periosteal reaction
(11%-20%), bone invasion (5%)
!" Q*#()("77&,)%/'%"$%/("*.)&:)(*)5A6)c)1,7()
by CT
!" Bone scan: increased activity
!" MRI
!"T1-WI: similar to muscle
!"T2-WI: usually high intensity
!"Triple sign on T2-W MR (35%-57%;
.*.7:,%"$%4
!"Very heterogeneous (“bowl of grapes”
sign)
!" ;*()&.%*88*.'<)a,''?+,$.,+)a"(9)
pseudocapsule – “benign characteristics”
(small lesions < 5 cm) Figure 48 A to E
!" Fluid levels 10%-25% (hemorrhage 47%)
Multiple MR images reveal the large soft tissue mass
worse prognosis in highly vascular lesions (curved arrows) with heterogeneity and areas of
necrosis/hemorrhage (arrows).

Figure 49
Synovial
sarcoma about
the ankle on
coronal T1-W
MR image with
heterogeneous
hemorrhagic Figure 51
mass (*) A&B
invading bone
(arrowhead). Clear cell
sarcoma on
MR imaging
with origin in
the quadriceps
Figure 50 tendon as
evidenced on
Synovial
the axial image
sarcoma about
with low signal
the ankle (same
intensity tendon
patient as
both anterior
previous MR)
and posterior
on axial T2 -W
to the mass
MR image with
(arrowheads).
heterogeneous
Sagittal T2-W
multicom-
MR shows
partment mass.
$1$%:(/3&/*
The lesion
intermediate
demonstrates
signal intensity.
the “triple” and
“bowl of grapes”
signs.
Synovial Sarcoma:
Treatment and Prognosis
!" Surgical resection/amputation
!" Radiation therapy/chemotherapy
!" Local recurrence (30%-50%) Clear Cell Sarcoma:
!" 5-year survival 36%-76%; 10-year Treatment and Prognosis
survival 20%-63% !" Surgical resection/radiation/chemotherapy
!" Metastases (16%-25%) – lung (94%), !" Poor prognosis
lymph node (10%), marrow (8%-11%) !" Local recurrence and metastases
!" Mets: lungs, lymph nodes, bone
Clear Cell Sarcoma: Clinical Features
!" Malignant melanoma of soft parts N&,$*%$-4(9+Juxta/Intraarticular Soft
!" Arise in tendons/aponeurosis Tissue Masses Differential Diagnosis
!" Deep tissue without skin involvement !" Synovial/meniscal cyst
!" Foot/ankle (43%), knee, thigh, hand !" Ganglion/myxoma
!" Adults 20-40 years old; F > M !" Gouty tophus
!" Hemangioma/PVNS
Clear Cell Sarcoma: Pathology !" Lipoma
!" Cells with clear cytoplasm !" Synovial sarcoma
!" K-/8,a*-W)*#)$1-*%*''/2,.*&7)("77&,
!" Intracellular melanin (60%-75%) C*%$-4(9+Juxta/Intraarticular Soft
!" Hemosiderin also present Tissue Masses Differential Diagnosis
!" V<*7"("7)*77"$%/.7
Clear Cell Sarcoma: Radiology [Figure 51]
!" Aneurysm
!" Soft tissue mass at/in tendon/aponeurosis !" Gouty tophus
!" Bone erosion/destruction !" Hyperparathyroidism/hemangioma
!" FPDVLU[)".$'(-/("E,)7*#()("77&,)8/77 !" Osteochondromatosis (synovial)
!" MRI !" Synovial sarcoma
!"T1-WI: intermediate intensity !" Tumoral calcinosis
!"T2-WI: may be low intensity !" Soft tissue sarcoma

References
General
1. Murphey MD, Choi JJ, Kransdorf MJ, Flemming DJ, Gannon FH. Imaging of osteochondroma: variants and
complications with radiologic-pathologic correlation. RadioGraphics 2000 Sep-Oct;20(5):1407-34. Review.
Tumoral Calcinosis
2. Steinbach LS, Johnston JO, Tepper EF, Honda GD, Martel W. Tumoral calcinosis: radiologic-pathologic
correlation. Skeletal Radiol 1995 Nov;24(8):573-8.
3. Martinez S, Vogler JB 3rd, Harrelson JM, Lyles KW. Imaging of tumoral calcinosis: new observations.
Radiology 1990 Jan;174(1):215-22.
4. Olsen KM, Chew FS. Tumoral calcinosis: pearls, polemics, and alternative possibilities. RadioGraphics
2006;26:871-85.
PVNS
5. Al-Nakshabandi NA, Ryan AG, Choudur H, Torreggiani W, Nicoloau S, Munk PL, Al-Ismail K. Pigmented
villonodular synovitis. Clin Radiol 2004 May;59(5):414-20. Review.
6. Murphey MD, Rhee JH, Lewis RB, Fanburg-Smith JC, Flemming DJ, Walker EA. From the Archives of the
AFIP: Pigmented Villonodular Synovitis: Radiologic-Pathologic Correlation. RadioGraphics 2008:28:1493-
518.
7. Nassar WA, Bassiony AA, Elghazaly HA. Treatment of diffuse pigmented villonodular synovitis of the knee
with combined surgical and radiosynovectomy. Health Soc Serv J 2009; 5:19-23.
Soft Tissue Ganglion
8. Ortega R, Fessell DP, Jacobson JA, Lin J, Van Holsbeeck MT, Hayes CW. Sonography of ankle Ganglia with
pathologic correlation in 10 pediatric and adult patients. AJR Am J Roentgenol. 2002 Jun; 178(6):1445-9.
9. Kim MG, Kim BH, Choi JA, et al. Intra-articular ganglion cysts of the knee: clinical and MR imaging
features. Eur Radiol 2001;11:834-840.
10. Teefey SA., Dahiya N., Middleton WD., Gelberman RH., Boyer MI. Ganglia of the hand and wrist: A
sonographic analysis. AJR Am J Roentgenol 2008;191:716-20.
11. Omoumi P, de Gheldere A, Leemrijse T, Galant C, Van den Bergh P, Malghem J, Simoni P, Vande Berg
BC, Lecouvet FE. Value of computed tomography arthrography with delayed acquisitions in work-up of
ganglion cysts of the tarsal tunnel: report of three cases. Skeletal Radiol 2010;39:381-6.
Myxoma
12. V&-:9,<)V!M)V%L/,)J^M)K/.1&-2?Q8"(9)RFM)P,8:',)_PM)H,E".,)^VM)^1*&'/$/)^RS))U8/2".2)*#)Q*#()P"77&,)
Myxoma with Emphasis on CT and MRI and Comparison of Radiologic and Pathologic. Radiology 2002;
225:215-24.
Synovial Cyst
14. P7%9"-%9)KPM)Q%98"+)VLM)G$--8/..)FNM)L*8,-*)RM)_*+',-)RM)n/.,((")VS))G-,E/',.%,)/.+)7"`,)*#)8,."7%/')
%<7(7M)2/.2'"*."%)%<7(7M)7<.*E"/')%<7(7)*#)(9,):*:'"(,/')7:/%,M)C&"+?$'',+)1&-7/,M)/.+)*(9,-)C&"+)%*'',%("*.7)
in asymptomatic knees on MR imaging. AJR Am J Roentgenol 2003 May;180(5):1431-6.
Synovial Lipoma
15. Vilanova JC, Barceló J, Villalón M, Aldomà J, Delgado E, Zapater I. MR imaging of lipoma arborescens and
the associated lesions. Skeletal Radiology 2003;32:504-9.
Synovial Chondromatosis
16. Robinson P, White LM, Kandel R, Bell RS, Wunder JS. Primary synovial osteochondromatosis of the hip:
extracapsular patterns of spread. Skeletal Radiol 2004 Apr;33(4):210-5. Epub 2004 Feb 18.
17. Murphey MD, Vidal JA, Fanburg-Smith JC, Gajewski DA. Imaging of synovial chondromatosis with
radiologic-pathologic correlation. RadioGraphics 2007;27:1465-88.

Heterotopic Bone
18. h-/.7+*-#)VRM)V,"7)RVM)R,'".,W)RQS)V<*7"("7)*77"$%/.7[)VL)/::,/-/.%,)a"(9)-/+"*'*2"%?:/(9*'*2"%)
correlation. AJR Am J Roentgenol 1991 Dec;157(6):1243-8.
Synovial Sarcoma
19. Valenzuela RF, Kim EE, Seo JG, Patel S, Yasko AW. A revisit of MRI analysis for synovial sarcoma. Clin
Imaging. 2000 Jul-Aug;24(4):231-5.
20. Murphey, MD, Gibson MS, Jennings, BT, Crespo-Rodriguez, AM, Fanburg-Smith JC, Gajewski, DA.
From the archives of the AFIP: Imaging of synovial sarcoma with radiologic-pathologic correlation.
Clear Cell Sarcoma
22. Memis A, Arkun R, Basdemir G, Sabah D, Ustun EE. Clear cell chondrosarcoma: unusual radiologic
appearances with histologic correlation. Eur Radiol 2002;12:427-30.
927
928
Musculoskeletal Angiomatous Lesions
Mark D. Murphey, MD
Angiomatous Lesions Osseous Hemangioma: Radiology
!" Hemangioma (vascular malformation) [Figures 1 to 5]
!" Lymphangioma (lymphatic malformation) !" Vertebrae: focal or diffuse – vertical
!" Glomus tumor striations (corduroy or polka dot)
!" Angiomatosis and associated syndromes posterior element involvement more likely
!" Hemangioendothelioma symptomatic
!" Hemangiopericytoma !" Calvarium/mandible radiating web-like
!" Angiosarcoma trabecular pattern
!" Long bone: multifocal lytic honeycomb
Osseous Hemangioma pattern, cortical lesions/erosions in
Clinical Characteristics diaphysis
!" V)o)K)p)X[@Y)#*&-(9?$#(9)+,%/+, !" Bone overgrowth
!" Majority asymptomatic !" Arthritis from intraarticular bleeding
!" May have soft tissue components
!" Common sites: vertebral body (at
least 11% of spines; 25% multifaced),
calvarium (30% of lesions)
Soft Tissue Hemangioma:

!" 7% of all benign soft tissue neoplasms
!" 1.5% of the general population; 10%
children under 1 year old; 20% multiple
!" Most frequent soft tissue neoplasm in
children
!" More common in young women - may
increase in size with pregnancy Figure 1 A & B
!" Subcutaneous, intramuscular, or synovial
Vertebral hemangiomas with thickened vertical
Hemangioma: Pathology trabeculae (corduroy appearance) (arrows) on
radiograph and coronally sectioned gross specimen
!" Subtype based on predominant vascular (different patients).
component but usually mixed tumor
!" F/:"''/-<[)8*7()%*88*.)?)$-7()<,/-7)*#)
life - skin, subcutaneous, vertebrae (low
C*a4
!" Cavernous: childhood - larger and deeper
0'*a)C*a4
!" ^-(,-"*E,.*&7[)+,,:)*-)7&:,-$%"/')?)
:,-7"7(,.()#,(/')%/:"''/-<)1,+)09"29)C*a4
!" Venous: adults - deep involvement - (low
C*a4)L,(-*:,-"(*.,&8M)8,7,.(,-<M)*-)
extremities
!" Epithelioid: dermis/subcutis
Hemangioma or Vascular Malformation

!" Vascular malformation: dysplastic vessels
without cellular proliferation or regression
and present at birth
!" Hemangioma: rapid growth and
cellular proliferation of endothelial cells Figure 2 A, B, C & D
in neonatal period followed by slow
Vertebral hemangioma (asymptomatic) of lumbar
involution spine with “polka dot” appearance and fat between
!" Hemangioma: benign nonreactive process trabeculae on CT.
with increased number of normal or
abnormal appearing vessels
Musculoskeletal Angiomatous Lesions 929 Musculoskeletal Radiology

Soft Tissue Hemangioma Radiology:
Soft Tissue Changes [Figure 6]
!" F/'%"$%/("*.[)%&-E"'".,/-)*-)/8*-:9*&7M)
phlebolith (30%-50% of lesions)
!" Angiography: irregular enlarged feeding
arteries, contrast pooling, arteriovenous
shunting
!" Venous lesions seen only with venography
Figure 3 A, B & C
Vertebral hemangioma (symptomatic patient) with

“polka dot” appearance on CT (arrowheads) and soft
tissue extension. Sagittal T1-W and T2-W MR images
show vertebral fracture and spinal canal compromise
caused by anterior epidural soft tissue component
(arrows) but diagnostic trabecular thickening is
)34&/.0!*!1*#::"(/3#!(D*
Figure 6 A & B
Soft tissue hemangioma of the hand with phleboliths

on radiograph (arrows) and intraoperative photograph.
Soft Tissue Hemangioma: Imaging

[Figures 7 to 12]
Figure 4 A, B & C
!" T1WIs – low to intermediate
Calvarial hemangioma with spoke wheel pattern of heterogeneous mass; look for fat
trabecular thickening (arrows) on radiograph, CT overgrowth
and vascular channels/spaces on gross specimen
(arrowheads).
!" g,-<)9"29)".(,.7"(<)PX?NU7)0'*a)C*a4
!" Serpentine vessels/cavernous spaces may
9,':)+"7(".2&"79)(<:,7Y)9"29)E7)'*a)C*a
!" Enhance with contrast
!" Phleboliths: CT > MRI
!" Bone scan: often only limited activity
!" Sonography: solid mass Doppler may
79*a)'*a)-,7"7(/.%,)C*a
Figure 7
A&B
Soft tissue
hemangioma
Figure 5 A & B of axilla
(intramuscular
Femoral hemangioma on coronal T1-W MR image and cavernous)
before and after contrast shows multifocal round on CT showing
areas of marrow replacement (arrowheads) enhancing
representing vascular channels with enhancement and vascular
serpentine feeding vessels (arrows). channels (large
arrows), fat
overgrowth
(small arrows),
and phlebolith
(arrowhead).

Figure 11
J14!*!3%%.(*6(>#$E31>#*@63E6*?1<*#"!("31=($1.%A*
about knee with low-signal intensity serpentine vessels
(arrows) on coronal T2-W MR image.
Figure 8 A, B & C
Soft tissue hemangioma of forearm (intramuscular

and cavernous) on sagittal T1-W MR images before
and after gadolinium showing intermediate signal
intensity serpentine vascular channels and spaces
(arrows) that enhance following contrast and fat
overgrowth (arrowheads). Axial T2-W MR reveals
multiple circular high signal areas corresponding to
%01<*?1<*/#=("$1.%*%:#/(%*@RAD
Figure 9 A & B
Soft tissue hemangioma of the thigh on sagittal T1-W
(left image) and axial STIR (right image) MR images
with associated fat atrophy (arrowheads) and slow Figure 12 A, B & C
?1<*/3"/.0#"*=#%/.0#"*%:#/(%*@#""1<A*/1""(%:1$)3$E*!1*
Capillary hemangioma on T2-W MR image (arrow) with
!6(*E"1%%*%:(/3>($*#$)*63%!101E,*@$('!*&E."(AD
$1$%:(/3&/*63E6*%3E$#0*3$!($%3!,*3$*!6(*4#/(*<3!6*!,:3/#0*
extensive strawberry nevus clinically. No characteristic
features of fat overgrowth or serpentine vascular
structures are seen to suggest hemangioma as the
vessels in this type of lesion are too small (capillary) to
discern on imaging as demonstrated on the histology.
Hemangioma: Treatment
!" Surgical resection/laser therapy
!" Q%',-*(9,-/:<)0'*a)C*a)',7"*.7)ZA64
Figure 10 A & B
!" ]81*'"`/("*.)09"29)C*a)',7"*.7)@A64
Soft tissue hemangioma (arrows) with associated fat !" Radiation in symptomatic unresectable
atrophy (arrowheads) in surrounding thigh muscle on
gross specimen (left image). Histology (right image)
lesions – spine
reveals :60(+103!6%*@RA*<3!6*/#0/3&/#!31$*:("3:6("#00,* !" Vertebroplasty
(arrows) and fat atrophy of muscle (arrowheads). !" Recurrence (15%-30%) – large lesions

Lymphangioma:
(Lymphatic Malformation)
!" Rare lesion in bone, usually soft tissue
!" Often present at birth (50%-65%)
!" 90% apparent by 2 years old
!" Head, neck, axilla – 75% of cases
!" Q*#()C&%(&/.()8/77
Lymphangioma:
Pathology
!" Sequestrated noncommunicating lymphoid
tissue (macrocystic or microcystic)
!" Large multiloculated cystic spaces
!" Lined by lymphatic endothelium
!" Filled with proteinaceous material
Lymphangioma: Figure 15 A & B

Radiology [Figures 13 & 14]
Glomus tumor with erosion of the terminal phalanx
!" Radiographs: Soft tissue mass 14*!6(*01$E*&$E("*1$*"#)31E"#:6*@#""1<%A*#$)*%#E3!!#0*
!" Imaging: large cystic spaces less common macrosection (*).
serpentine component may appear
complex – solid components (high signal
on T1 – 25%)
!" Cystic hygroma: hydrops fetalis, Turner
syndrome
Angiomatosis
!" !"%)-.&$*%+&1+9-.."#(+-,4%)1*)-&,+
of bone by hemangiomatous or
Figure 13
lymphangiomatous lesions with or
Lymphangioma without soft tissue involvement
of the neck
on CT with a Angiomatosis: Clinical Characteristics
homogeneously !" j*&.2):/(",.(7)c)$-7()5)+,%/+,7)
low attenuation
!" M > F = 2:1
mass (*).
!" Osseous involvement only – benign
course
!" Visceral involvement – poor prognosis
!" No malignant potential
Angiomatosis: Pathology
Figure 14 !" Capillary or cavernous hemangioma
!" H<8:9/.2"*8/)'<8:9/("%)1/%WC*a
Lymphangioma !" V"3,+)E/7%&'/-)',7"*.)+"#$%&'()(*)
of the neck in distinguish
an infant on
coronal T1-W
MR image with
Angiomatosis: Radiology [Figure 16]
heterogeneous !" MR imaging/CT: some as solitary
mass (arrow) angiomatous lesions more extensive
showing both !" Imaging to evaluate visceral involvement/
high and low extent
signal intensity
areas extending !" Lymphangioma: proven with
along the lymphangiography and contrast in lesion
chest wall !" Diffuse round/oval medullary lytic lesions
(arrowhead). !" May have sclerotic margins
!" Location: femur, ribs, spine, pelvis,
humerus, scapula, other long bones,
clavicle
Glomus Tumor [Figure 15]
!" G/(",.(7)#*&-(9)(*)$#(9)+,%/+,
!" Tumor of neuromyoarterial glomus
!" Almost all terminal phalanx soft tissue
!" Bone erosion/invasion (15%-65%)

Figure 17 B & C
Klippel-Trenaunay-Weber syndrome on clinical
photograph and coronal T1-W and T2-W MR images
Figure 16 A & B showing classic triad of hemihypertrophy, varicose
Angiomatosis (lymphangiomatosis) with extensive =(3$%*#$)*('!($%3=(*:"()1>3$#$!0,*%01<*?1<*
3$&0!"#!31$*14*!6(*($!3"(*01<("*('!"(>3!,*/#.%3$E* #$E31>#!1.%*0(%31$*@#""1<6(#)%AD*J>#00("*63E6*?1<*
elephantiasis on coronal T1-W MR image and clinical component is also seen on T2-W image (arrows).
photograph.
Angiomatous Syndromes Massive Osteolysis of Gorham:

!" Maffucci syndrome “Vanishing Bone” Disease [Figure 18]
!" Osler-Weber-Rendu !" Patients < age 40 years old
!" Klippel-Trenaunay-Weber !" History of trauma 50%
!" Massive osteolysis of Gorham !" Upper extremity favored, may extend
!" Associated osteomalacia and across joint
thrombocytopenia !" Progressive bone resorption and
fragmentation (simulate neuropathic)
Maffucci Syndrome !" Pathology: proliferating vascular channels
!" Multiple enchondromata
!" Cavernous soft tissue hemangiomata
!" Often hands/feet, unilateral predominance
!" Malignant potential both lesions and
viscera
Osler-Weber-Rendu
!" Hereditary hemorrhagic telangiectasia
!" Dilated capillaries and veins
!" Autosomal dominant
!" GI, GU, lung, spinal; bone – rare
Klippel-Trenaunay-Weber [Figure 17]

!" Nonhereditary, lower extremity
!" Unilateral cutaneous capillary
hemangioma
!" Varicose veins and local gigantism
!" Can have arteriovenous component
Figure 18 A & B
Gorham “vanishing bone” disease involving the
foot with radiograph and gross specimen showing
Figure 17A ('!($%3=(*%6#":0,*)(&$()*+1$(*"(%1":!31$*@#""1<6(#)%*
and arrow).
Klippel-Trenaunay-
Weber syndrome on Osteomalacia and Thrombocytopenia
clinical photograph.
!" Tumor induced osteomalacia – most
frequent vascular lesions
!" Hemangioma/hemangiopericytoma
!" Kasabach-Merritt syndrome -
hemangioendothelioma/hemangioma/
hemangiopericytoma associated with
thrombocytopenia and purpura
Intermediate to Malignant Radiology of HE, HPC, ASC:
Musculoskeletal Angiomatous Lesions Advanced Imaging [Figures 20 to 22]
!" Hemangioendothelioma !" Angiography: intensely vascular with
!" Hemangiopericytoma peripheral vessels displaced by tumor
!" Angiosarcoma early; dense blush late
!" Sonography: hypo or hyperechoic mass
Hemangioendothelioma (HE) !" Doppler: arteriovenous shunting
!" Intermediate: benign or malignant !" MRI
!" Composed of vascular endothelial cells !"T1-W: usually similar to muscle
!" Often in young patients !"Can be high intensity hemorrhage
!" Bone or soft tissue !"Feeding vascular pedicle (35% HPC)
!" Locally aggressive, unusual to metastasize !" H**W)#*-):-*8".,.()7,-:,.(".,)9"29)C*a)
vessels and solid regions (biopsy with
Hemangiopericytoma (HPC) caution)
!" Intermediate: benign or malignant (more !" Fluid levels, contrast enhancement
likely in large lesions > 10 cm) !" Dominant skin mass in chronic
!" Q/8,)/7)7*'"(/-<)$1-*&7)(&8*- lymphedema (ASC)
!" Tumor of cells around vessels - pericytes
!" Tumor of middle-aged adults; M = F
!" Sites: soft tissue of lower extremity
(35%), head/neck, pelvis, and
retroperitoneum (25%)
!" Rare in bone
Angiosarcoma (ASC)
!" Malignant; M > F = 2:1
!" Composed of hemangiosarcoma or
lymphangiosarcoma cellular elements
!" Location: skin, muscular, viscera, bone
!" Associated with lymphedema post-
mastectomy (Stewart-Treve syndrome)
Osseous HE, HPC, ASC:

Skeletal Location
!" Hemangioendothelioma: skull, vertebrae,
lower extremity
!" Hemangiopericytoma (rare): pelvis,
proximal long bones, vertebrae, mandible
!" Angiosarcoma: long tubular bone lower
extremity
Figure 20
Osseous HE, HPC, ASC: Radiographic A to E
Findings [Figure 19]
!" Multifocal lytic lesions, “honeycomb” Angiosarcoma
appearance developing in
!" Aggressive bone destruction with a patient with
chronic leg
expansion and soft tissue mass lymphedema.
Axial T1-W,
T1-W post-
contrast and
Figure 19 T2-W MR
A&B images show
the enlarged
Malignant leg with
hemangioendothelioma subcutaneous
of bone with multifocal edema (arrows) and dominant skin mass (arrowheads)
lytic lesions (arrowheads) "(:"(%($!3$E*!6(*#$E31%#"/1>#D*;6(*%.:("&/3#0*
3$*!6(*!3+3#*#$)*&+.0#* angiosarcoma is also seen on the clinical photograph
on radiograph and (next image) (black arrows).
osseous replacement by
hemorrhagic tissue (*) on
photograph of coronally
sectioned gross specimen.

Cannot distinguish HE, HPC, or ASC from
other soft tissue masses if prominent
serpentine vessels are not recognized.
HE, HPC and ASC cannot be

differentiated from each other
radiologically.
Distinction of HE, HPC, and ASC from

Hemangioma
!" Large masses
!" ^22-,77"E,)%9/-/%(,-"7("%7)a"(9)".$'(-/("*.
!" No fat overgrowth
Treatment and Prognosis: HE, HPC, and

ASC
!" Surgical resection
!" Malignant lesions: radiation and
chemotherapy
Figure 21
!" Local recurrence common
Angiosarcoma developing in a patient with chronic !" Metastates common to lung in ASC
leg lymphedema. Axial T1-W, T1-W postcontrast,
and T2-W MR images show the enlarged leg with Summary:
subcutaneous edema (arrows) and dominant skin
mass (arrowheads) representing the angiosarcoma.
Musculoskeletal Angiomatous Lesions
;6(*%.:("&/3#0*#$E31%#"/1>#*3%*#0%1*%(($*1$*!6(* !" Osseous – multifocal bone lysis
clinical photograph (black arrows). !"“Honeycomb” appearance
!" Soft tissue – MRI
!"Look for serpentine vascular pattern
!"Overgrowth of fat
!" Multiple associated syndromes and
angiomatosis
!" Higher grade lesions – HE, HPC, ASC
!"Larger aggressive lesions
!"U.$'(-/("E,)%9/-/%(,-"7("%7
Figure 22 A, B & C
W(>#$E31:("3/,!1>#*3$*!6(*!63E6*%61<3$E*63E6*?1<*
vessels (arrows) in the soft tissue mass (*) and
feeding the lesion on both axial T1-W and coronal
T2-W MR images. Photograph of the sectioned gross
specimen also shows the soft tissue mass (*) and the
63E6*?1<*=(%%(0%*@#""1<6(#)%AD

References
1. Baudrez V, Galant C, Vande Berg BC. Benign vertebral hemangioma: MR-histological correlation. Skeletal
Radiol 2001 Aug;30(8):442-6.
2. Coldwell DM, Baron RL, Charnsangavej C. Angiosarcoma. Diagnosis and clinical course. Acta Radiol 1989
Nov-Dec;30(6):627-31.
3. Fayad L, Hazirolan T, Bluemke D, Mitchell S. Vascular malformations in the extremities: emphasis on MR
imaging features that guide treatment options. Skeletal Radiol 2006;35:127-37.
4. Laredo JD, Assouline E, Gelbert F, Wybier M, Merland JJ, Tubiana JM. Vertebral hemangiomas: fat content
as a sign of aggressiveness. Radiology 1990 Nov;177(2):467-72.
5. Lorigan JG, David CL, Evans HL, Wallace S. The clinical and radiologic manifestations of
hemangiopericytoma. AJR Am J Roentgenol 1989 Aug;153(2):345-9.
6. Murphey MD, Fairbairn KJ, Parman LM, Baxter KG, Parsa MB, Smith WS. From the archives of the
AFIP. Musculoskeletal angiomatous lesions: radiologic-pathologic correlation. RadioGraphics 1995
Jul;15(4):893-917. Review.
7. Persaud T. The polka-dot sign. Radiology 2008;246:980-1.
8. Navarro OM, Laffan EE, Ngan B. Pediatric soft-tissue tumors and pseudo-tumors: MR imaging features
with pathologic correlation: Part 1. Imaging approach, pseudotumors, vascular lesions, and adipocytic
tumors. RadioGraphics 2009;29(3):887-906.
9. V*&W/++/8)_M)G*''/W)RM)_/"87)^_S)VLU)%9/-/%(,-"7("%7)/.+)%'/77"$%/("*.)*#):,-":9,-/')E/7%&'/-)
malformations and tumors. Skeletal Radiol 2009;38:535-47.
10. N"2./'')BRM)V*7W*E"%)]FM)P9a/<)hM)P9*8/7)RVS)Q*'"(/-<)$1-*&7)(&8*-7)*#)(9,)7*#()("77&,[)-,E",a)*#)(9,)
imaging and clinical feature with histopathologic correlation. AJR Am J Roentgenol 2010;195:W55-62.

Paget Disease
Mark D. Murphey, MD
Paget Disease: Clinical Characteristics
!" Described in 1877 by Sir James Paget
!" Osteitis deformans
!" Common disease (some researchers
believe it is decreasing in frequency)
!"3% over age 40
!"10% over age 80
!" Slightly more common in men
!" Common in Great Britain and descendents
(USA, Australia)
!"Also continental Europe
!" Uncommon in Asia and Africa
!" Many patients asymptomatic (20%)
!" Tendency to increase in age, decrease in
severity, more monostotic
Paget Disease: Clinical Presentation Figure 1 A & B

!" Pain (11%-54%) -#""1<*"(:0#/(>($!*+,*&+"1=#%/.0#"*!3%%.(*3$*#/!3=(*
!" Osseous bowing and enlargement Paget disease (left image) versus fat in marrow with
!" Neurologic symptoms inactive disease (right image).
!" High output congestive failure
!" Lab
!"Serum alkaline phosphatase
(blastic phase)
!"Urinary and blood hydroxyproline
(lytic phase)
Paget Disease: Etiology

!" Unknown
!" Possible etiologies
!" Infection: viral: intranuclear inclusions:
paramyxovirus (measles)
!" Autoimmune
!" Connective tissue disease
Figure 2
!" Genetic
!" Neoplastic Paget disease:
skeletal
Paget Disease: Pathology [Figure 1] distribution.
!" Initially osteoclastic resorption
!" Subsequently osteoblastic response
(active)
!"Excessive and disorganized
!"“Mosaic” or “jigsaw” pattern
!"V/--*a[)$1-*E/7%&'/-)-,/%("*.
!"Marrow: fat (inactive)
Paget Disease: Skeletal Distribution

[Figure 2]
!" Calvarium, spine (lumbosacral), and
pelvis (25%-75%)
!" Proximal long bones (25%-30%)
!" Humerus (31%), scapula (24%),
clavicle (11%)
!" Initially monostotic (10%-35%) most Paget Disease: Radiologic Evaluation
polyostotic !" Radiographs: diagnosis
!" Bone scan: assess areas involved
!" CT/MRI: to assess complications or
unusual cases
Paget Disease 937 Musculoskeletal Radiology

Paget Disease: Radiologic Stages
!" Active
!"Lytic: osteoclastic activity
!"Mixed: majority of cases
!" Inactive
!"Mixed: majority of cases
!"Blastic: osteoblastic activity
!" Usually progresses through these phases
but not always
!"Recrudescent lytic phase in patients at
rest; simulates tumor
Paget Disease: Radiologic Lytic Phase

[Figures 3 to 5]
!" QW&''[)'/-2,)a,''?+,$.,+)/-,/7Y)
involve both inner and outer tables of
frontal/occipital bones (osteoporosis Figure 5 A & B
circumscripta) Lytic phase of Paget disease with sharp margins and
!" Long Bones: subchondral location with subchondral extension.
advancing wedge/V shape – “blade of
2-/77lDl%/.+',)C/8,l
Paget Disease: Radiographs –

Mixed/Blastic Disease
!" Sclerosis and lucency Termina en V
!" Trabecular and cortical thickening
!"Along the lines of stress
!"But some disorganization
!" Bone enlargement
Paget Disease: Radiographs –

Mixed/Blastic Disease [Figures 6 to 9]
!" Skull: “cotton-wool” appearance obscures
inner and outer tables, often spares facial
bones
!" Spine: vertebral body “picture frame” –
ivory vertebral body; posterior elements
may be involved
Pictorial representations of skeletal distribution of
Paget disease in the skull (osteoporosis circumscripta)
and long bone (“blade of grass” appearance).
Figure 6
“Cotton-wool” appearance on radiograph with

multifocal areas of sclerosis and thickening of the
diploic space anteriorly.
Figure 4 A & B
Osteoporosis circumscripta with sharply marginated

large area of bone lysis.

Figure 9 A & B
Ivory vertebral body in Paget disease on radiograph
and intense uptake on radionuclide bone scan.
Figure 7
A to F
Ivory Vertebral Body:
Mixed lytic/ Differential Diagnosis
blastic !" Blastic metastasis: breast, prostate,
Paget adenocarcinoma GI tract, carcinoid,
disease in transitional cell carcinoma bladder
skull with !" Lymphoma
diploic
space !" Chronic infection
expansion !" Chordoma
and
hyperemic Paget Disease: Radiographs –
bone on Mixed/Blastic Phase [Figures 10 to 12]
CT, gross
specimen, !" Pelvis: asymmetric involvement
and !"Thickened iliopubic and ischial lines
histology. !"Enlarged pubic rami and ischium
!" Long bones: epiphyseal involvement
!"Rarely diaphyseal (tibia)
!"Enlarged bone
Figure 10
Paget
disease with
coarsened
trabecular
pattern and
thickening
of the
iliopectineal
line
involving
the entire
hemipelvis.
Figure 8 A & B
“Picture frame” appearance of Paget disease of the
spine (multiple levels) on radiograph and coronal
macrosection.

Figure 11
Paget disease
mixed lytic
and blastic
in left pubic
rami.
Figure 13 A & B
Paget disease in the tibial metaepiphysis with mixed
lytic and blastic and typical trabecular and cortical
thickening on CT scout view and coronal image.
Figure 14
Paget disease
(noncomplicated)
in right iliac crest
with trabecular
and cortical
thickening
Paget disease in the humeral metaepiphysis with (arrowheads).
mixed lysis and sclerosis and typical trabecular
(arrowheads) and cortical thickening (arrows) on
radiograph, CT, and gross specimen.
Paget Disease: MRI
Noncomplicated Disease [Figures 15 to 18]
!" T1-WIs
!"Cortical and trabecular thickening
Paget Disease: Bone Scintigraphy !"Enlarged bone
!" Active disease: marked uptake !"Low signal (sclerosis)
!"Dynamic and static images !"Yellow marrow/fat (inactive disease)
!" Abnormal before radiographs !"Heterogeneous signal (active disease)
!" Overview of disease: look at distribution !"Marrow replacement nonmasslike
!" Monitor disease and therapy !" T2-WIs
!"Low signal (sclerosis)
Paget Disease: CT/MRI Noncomplicated !"Fat signal intensity (inactive disease)
Disease [Figures 13 & 14] !"Heterogeneous intermediate/high
!" Not usually needed for diagnosis 7"2./')0$1-*E/7%&'/-)8/--*a)?)/%("E,)
!" CT: thickened trabeculae disease)
!"Bone enlargement !"No focal mass (marrow or soft tissue)
!"Lytic areas
Figure 15 A & B
Paget disease involving the calcaneus

(noncomplicated), mixed lytic/blastic on radiograph,
with maintained yellow marrow on T1-W MRI.

Paget Disease: Osseous Deformity
[Figure 19]
!" Effects of bone softening
Figure 16 !" Bowing common in long bones
!" Acetabulae protrusio
Paget !" Basilar invagination – 30% of patients
disease with skull involvement
mixed lytic/
blastic with
cortical
thickening
(arrow)
involving the
tibia.
Figure 19 A & B
Acetabulae protrusio on radiograph and coxa varus

deformity of the femur on the coronally sectioned
macrosection in patients with Paget disease. Note the
axial narrowing of the hip joints.
Paget Disease: Fractures [Figure 20]

!" G/-("/')*-)%*8:',(,)0".7&#$%",.%<4
!" True acute fractures
Figure 17 A & B !" Horizontal lucencies (“banana fracture”)
Coronal T1-W (noncontrast) and axial T1-W (after !" Convex surface of bone
contrast) MR images show speckled marrow pattern !" Single or multiple
with enhancement in more active Paget disease !" Often symptomatic
(noncomplicated) (*) and more intense enhancement !" Sites: femur, humerus, pelvis
of the intracortical component that is most active. !" Spine: central compressions
!" May heal but high nonunion rate
!" ^()-"7W)#*-)7/-%*8/)01"*:7<I4
Figure 20
Paget disease
of femur with
complete and
incomplete
fractures
(arrowheads).
Figure 18 A & B
Axial T2-W MR image shows speckled pattern of

increased intensity (*) in more active Paget disease
(noncomplicated) (same patient as previous MRI and
radiograph). Paget Disease: Neurologic Symptoms
[Figure 21]
!" Symptoms: impingement of cranial and
spinal nerves (spinal stenosis 33%)
Paget Disease: Complications !" Caused by skull and spine involvement
!" Osseous deformity !" Bone enlargement, fractures, bone
!" Fractures softening with basilar invagination
!" Neurologic symptoms !" Increased osseous vascularity with cord
!" Arthropathy hypoxia
!" Neoplasm !" CT/MRI for evaluation

Figure 21
Figure 22
Paget disease
at C7 with
marked Pictorial
osseous representation
enlargement of malignant
of both the transformation
anterior and in Paget
posterior disease.
elements
(*) resulting
in spinal
stenosis.
Paget Disease: Arthropathy

!" Rheumatic diseases with poor
association: rheumatoid arthritis, calcium
pyrophosphate deposition (CPPD),
ankylosing spondylitis
!" Gout: higher incidence hyperuricema
(40%) from increased cell turnover
!" Osteoarthritis
!"Hip and knee most common
!"Abnormal mechanics from deformity
!"Bone weakening
!"Hip narrowing can be axial
!" Q*#()("77&,)%/'%"$%/("*.
!"Tendinitis with vitamin D treatment
Paget Disease: Neoplasm Figure 23 A to E

!" Sarcomatous transformation Paget disease with malignant transformation to
!"1% patients with Paget disease osteosarcoma in the proximal tibia where there is
!"5%-10% patients with extensive mass-like marrow replacement (*) and soft tissue
extension (arrow) on radiograph and multiple sagittal
disease T1-W MR images.
!" Patients 55-80 years old
!" Common sites: femur, pelvis, humerus
!" Osteosarcoma (50%-60%)
!" VK_D$1-*7/-%*8/)0XA6?X>64
!" Chondrosarcoma (10%)
!" GCT
!" Metastasis, myeloma, lymphoma
Paget Disease: Neoplasm – Radiology

[Figures 22 to 24]
!" Bone destruction predominates
!" Cortical involvement and soft tissue mass
!" No periosteal reaction
!" Persistent nonhealing fracture
!" Compare with old radiographs
!" Bone scan: photopenic area
!" Gallium scan: increased uptake
!" MRI Figure 24 A to E
!"T1-W: mass-like marrow replacement Paget disease with malignant transformation to
!"T2-W: focal mass of high intensity osteosarcoma in the humeral midshaft where there
!"Soft tissue mass is mass-like marrow replacement (*) and soft tissue
extension (arrows) on radiograph and multiple sagittal
T1-W MR images, CT, and gross specimen.

Paget Disease: Neoplasm [Figure 25] Hereditary Hyperphosphatasia:
!" GCT: skull or facial bones Juvenile Paget Disease
!"More often benign !" Described 1956 by Bakwin/Eliger
!"Rarely multiple (familial) !" Autosomnal recessive
!"Lytic expansile lesion !" Disorder of infants/children
!" Metastasis: likely related to hyperemia !" Elevated alkaline and acid phosphatase,
uric acid
Juvenile Paget Disease:

Radiographic Findings [Figure 26]
!" Generalized cortical thickening
!" All bones including skull involved
!" Osteopenia and bowing
!" Epiphyses may be spared
!" Patients severely deformed
Figure 26
Figure 25 A, B, C & D A&B
Paget disease with benign GCT of the clavicle Juvenile Paget
associated with pathologic fracture showing cortical disease (hereditary
thickening (arrows) and destructive lesion (*) on CT hyperphosphatasia)
scans, gross specimen radiograph, and gross specimen. on radiographs with
osseous bowing
and shortening as
well as trabecular
thickening.
Paget Disease: Differential Diagnosis

!" Diffuse sclerosis: chronic renal faliure
0FLK4M)8<,'*$1-*7"7M)8,(/7(/7"7M)
Paget Disease: Summary
lymphoma, sickle cell anemia
!" Common disease: 3%-4%
!" Trabecular thickening: hemangioma,
!" Diagnosis: radiographs
%9-*."%)".#,%("*.M)*7(,*8/'/%"/M)C&*-*7"7
!"H<("%[)a,''?+,$.,+M)7&1%9*.+-/')))))))
!" Polyostotic lesions: CRF
0mEl)*-)a,+2,)79/:,)c)%/.+',)C/8,4
(hyperparathyroidism), Langerhans
!"Thickened trabeculae and cortex
cell histiocytosis, unusual infection,
!"Osseous enlargement
8,(/7(/7"7M)$1-*&7)+<7:'/7"/M)lymphoma,
!" Bone scan: overview
Gaucher disease, mastocytosis
!" Complications: fracture, osseous
Paget Disease: Treatment deformity, neurologic symptoms, arthritis,
!" Calcitonin: inhibits resorption neoplasm
!" Bisphosphonates: inhibits bone resorption !" CT/MRI: to evaluate complications
and production; may restore bone !" CT/MRI: noncomplicated case
histology/radiology !"Bone enlargement
!" Mithramycin: cytotoxic antibiotic !"Trabecular thickening
!" Often relieve pain !"T1-W: low signal (sclerosis), yellow
marrow, heterogeneous nonmass-like
Paget Disease: marrow replacement
Radiology Posttreatment !"T2-W: low signal (sclerosis), yellow
!" Often subtle or no change marrow, heterogeneous high signal,
!" Occasionally improved radiographs no focal mass
!" Watch for fractures: may increase with !" CT/MRI: complicated case
bisphosphonates !"CT: focal bone destruction/
!" Bone scans best treatment indicator soft tissue mass
!"T1-W: mass-like marrow replacement
!"T2-W: focal mass in marrow with high
signal and soft tissue mass

References
1. Boutin RD, Spitz DJ, Newman JS, Lenchik L, Steinbach LS. Complications in Paget disease at MR imaging.
Radiology 1998 Dec;209(3):641-51.
2. Cooper C, Dennison E, Schafheutle K, Kellingray S, Guyer P, Barker D. Epidemiology of Paget’s disease of
bone. Bone 1999 May;24(5 Suppl):3S-5S.
3. Moore TE, Kathol MH, el-Khoury GY, Walker CW, Gendall PW, Whitten CG. Unusual radiological features in
Paget’s disease of bone. Skeletal Radiol 1994 May;23(4):257-60.
4. Smith SE, Murphey MD, Motamedi K, Mulligan ME, Resnik CS, Gannon FH. From the archives of the
AFIP. Radiologic spectrum of Paget disease of bone and its complications with pathologic correlation.
RadioGraphics 2002 Sep-Oct;22(5):1191-216.
5. Vande Berg BC, Malghem J, Lecouvet FE, Maldague B. Magnetic resonance appearance of uncomplicated
Paget’s disease of bone. Semin Musculoskelet Radiol 2001;5(1):69-77.
6. Vellenga CJ, Bijvoet OL, Pauwels EK. Bone scintigraphy and radiology in Paget’s disease of bone: a review.
Am J Physiol Imaging 1988;3(3):154-68.
7. Dell’atti C, Cassar-Pullicino VN, Lalam RK, Tins BJ, Tyrrell PN. The spine in Paget’s disease. Skeletal Radiol
2007;36:609-26.
8. Reid IR. Bisphosphonates. Skeletal Radiol 2007;36:711-4.

Musculoskeletal Infection: Part 1
Mark D. Murphey, MD
Musculoskeletal Infection: Routes of
Innoculation
!" Hematogenous
!" Contiguous spread
!" Direct implantation/postsurgical
Hematogenous Vascular Supply Tubular

Bones [Figure 1]
!" Diaphyseal
!"Enter through cortex
!"Ascending/descending branches
Figure 2 A, B & C
!" Metaphyseal
!"Sharp turns beneath growth plate Vascular supply of tubular bone by patient age.
!" Epiphyseal
!" Artery from epiphysis/metaphysis
!" Periosteal
!"From diaphyseal/muscle/soft tissue
vessels
!" Synovial
!"From epiphysis/surrounding vessels
Figure 3 A to E
Progression of osteomyelitis through cortex into the
soft tissues and subperiosteal space: (A) deposition (B)
extension (C) lateral spread (D) subperiosteal lifting
and (E) subperiosteal stripping.
Figure 1 A & B
Vascular supply to long bone and joint.
Radiographic Abnormality:
Acute Osteomyelitis
Hematogenous Vascular Supply !" Deep soft tissue swelling
Tubular Bones [Figure 2] (within three days)
!" Age dependent !" Osteoporosis to focal bone lysis
!" Infant: vessels penetrate growth plate (7-14 days)
!" Child: vessels do not extend across plate !" Periosteal reaction (10-14 days)
!" Adult: vessels cross closed growth plate !" U.%-,/7,+)1'**+)C*a[)7%".("2-/:9<)0,/-'<4
!" !,%-,/7,+)1'**+)C*a[)7%".("2-/:9<)0'/(,-4
Pathophysiology of Acute Osteomyelitis
[Figure 3] Other Radiologic Studies: MSK Infection
!" Inoculation/colonization/immunologic !" Nuclear medicine – BS: three phase
response studies
!" Marrow and soft tissue edema !"Gallium: with BS, acute infection
!" Bone destruction: trabecular/cortical !"NOF[)".%-,/7,+)7:,%"$%"(<
!" Subperiosteal/soft tissue/medullary !" Q*.*2-/:9<[)C&"+)%*'',%("*.7D,##&7"*.7
abscess !" CT: bone destruction/sequestra/abscess
!" Vascular thrombosis: infarction !" Sonography: sinus tract extent
(sequestrum) !" MRI: marrow involvement, abscess,
!" Periosteal new bone (involucrum) very sensitive (STIR, GADO)
Musculoskeletal Infection 1 945 Musculoskeletal Radiology

Osteomyelitis: Organisms
!" S aureus
(80%-90% of pyogenic cases)
!" W*3$?.($K#(, strep (shoulder, trauma
from delivery)
!" Gram negatives, uncommon except
enterics (25% of infections)
!" Pseudomonas: penetrating trauma/IVDA
!" Salmonella: sickle cell (20% of patients)
!" Blood cultures positive 50%
Hematogenous Osteomyelitis:
Infant (Up to 1-2 Years) [Figures 4 to 8]
!" May be clinically silent (NICU/catheters)
!" Group B strep more common than other
ages
!" Metaphysis/epiphysis location Figure 6 A & B
!" Extend into joint Subsequent radiographs at 1 week (left image) and
!" Most prominent sequestrum/involucrum 2 weeks (right image) later reveal development
!" Common soft tissue/subperiosteal abscess of periosteal reaction initially (arrows) followed by
!" Fracture/sinus tracts uncommon extensive involucrum (arrowheads) and sequestrum
(*) formation.
!" May lead to late sequelae
Figure 4
Pictoral
representation
of infection
deposition sites
in an infant
long bone.
Figure 7 A, B & C
Continued follow-up radiographs at 1 month (left
image), 3 months (middle image), and 1 year (right
image) later show progressive resorption of sequestra
representing the majority of the humerus (”bone within
bone” appearance*) and subsequent remodeling to
nearly normal appearance.
Figure 8
A&B
Civil war
gross
specimen and
radiograph
showing
extensive
involucrum
(arrows) and
sequestrum
(*) resulting
from war
Figure 5 A & B injury induced
osteomyelitis.
Osteomyelitis in an infant with soft tissue swelling
@/3"/0(*#$)*#""1<A*#%*!6(*1$0,*3$3!3#0*&$)3$ED*51>:#"(*
to normal left arm (right image).

Hematogeneous Osteomyelitis:
Child (1-16 Years) [Figures 9 & 10]
!" Tubular bones (75%)
!" Metaphysis/lower extremity
!" Can involve joint (hip/shoulder)
!" Sequestrum/involucrum common
!" Soft tissue/subperiosteal abscess common Figure 11
!" Fracture uncommon
!" Sinus tracts can occur Pictorial
representation
of a
subperiosteal
abscess.
Figure 9
Pictorial
representation
of infection
deposition sites
in a child long
bone.
Figure 12 A & B
Figure 10 A & B
Aggressive bone destruction (arrow) and periosteal
reaction (arrowheads) in the distal ulnar metaphysis
on radiograph and marked uptake of radionuclide on
bone scan resulting from acute bacterial osteomyelitis
in a child.
Figure 13 A & B
Subperiosteal Abscess [Figures 11 to 13] Osteomyelitis in the distal femoral metaphysis of
!"Common in children/infants the femur with bone destruction (arrows). There
!"Loose periosteum is marrow replacement on the T1-W MR image
!" Femur/tibia: long extension with focal rim enhancing subperiosteal abscess
!" Adults: sinuses/orbit (arrowheads) posteriorly showing high signal on T2-W
(*).
!" Often do not recognize on radiographs
!" Nuclear medicine: rim with photopenia
(BS, WBC)
!" FPDVLUDQB;B[)C&"+)%*'',%("*.)1*.,)
surface
Luego de diagnisticar la OM es importante descartar la presencia de un absceso porque cambia el tto y pronóstico.
Figure 15 A, B & C
Acute bacterial osteomyelitis in an adult. Initial

radiograph reveals only soft tissue swelling posterior
to olecranon (*). Subsequent radiographs two
weeks later (right images) show motheaten to
permeative bone destruction resulting from S aureus
Figure 13C osteomyelitis.
Osteomyelitis in the distal femoral metaphysis of
the femur with bone destruction (arrows). There is
marrow replacement on the T1-W MR image with focal
rim enhancing subperiosteal abscess (arrowheads) Subacute Osteomyelitis:
posteriorly showing high signal on T2-W (*). Brodie Abscess [Figure 16]
En los adultos son raros los abscesos excepto !" Described in 1832 – chronic/subacute
en las cavidades perinasales. !" N/'',+?*##)a"(9)%,.(-/')C&"+M)*#(,.)7(,-"',)
(staph)
Hematogeneous Osteomyelitis: !" Children (M > F), metaphysis, tibia
Adult (Over 16 Years) [Figures 14 & 15] !" Intramedullary channel-like lucencies
!" Tubular bones less common !" May cross growth plate or be cortical
!" Spine/pelvis/small bones more common: !" Periosteal reaction/sequestra may be seen
subchondral focus
!" Joint involvement/sinus tracts common
Figure 16 A, B & C
!" Involucrum/sequestrum/abscess
uncommon Brodie abscess
!" Fracture uncommon except neglected with sequestra
cases (arrows) in the
cortex of the
proximal femur on
radiograph, axial
CT, and coronal
CT reconstruction.
Debrided
sequestered
fragment is also
demonstrated (*).
Figure 14
Pictorial representation of infection deposition sites

in an adult long bone.

Chronic Osteomyelitis [Figure 17]
!" Bone formation results in sclerosis
!" Sclerosing osteomyelitis of Garre
!" No pus, may have mixed radiolucency
!" Active infection: new bone destruction,
sequestra, aggressive periosteal reaction
on radiographs
!" MRI, scintigraphy (bone, gallium, WBC)
Figure 17
Chronic
osteomyelitis
of the ulna with Figure 18 A & B
diffuse sclerosis
Diabetic patient with ulcer lateral to 5th MTP joint.
on radiograph.
Radiograph shows underlying destruction of distal 5th
metatarsal head and proximal phalanx resulting from
osteomyelitis and pyarthrosis. Amputation specimen
%61<%*%3>30#"*&$)3$E%D
Osteomyelitis: Diabetes Mellitus

Osteomyelitis/Septic Arthritis !" Bone destruction/periosteal reaction
Contiguous Spread: Source !" Bone scan: normal – no osteomyelitis
!" Soft tissue infection !" WBC scan: good predictive value
!"Trauma !" MRI: marrow replacement geographic
!"Human/animal bites area T1 and increased signal STIR,
!"Puncture wounds postcontrast (90% sensitivity; 83%
!"Ulcers sensitivity)
!"Surgery !"Normal on T1 or subtle/subcortical
only; then probably marrow reaction
Osteomyelitis/Septic Arthritis not osteomyelitis (Collins, et al. AJR.
Contiguous Spread: Radiographs 185:2005)
!" Soft tissue swelling/air !"K*%/')C&"+)%*'',%("*.7
!" Cortical destruction into marrow Osteomyelitis vs Neuropathic
!" Joint space loss Diabetes Mellitus
!" Factors favoring infection: Sinus tract
Osteomyelitis/Septic Arthritis (84%/0%); ST replacement (68%/32%);
Contiguous Spread: Hand C&"+)%*'',%("*.)0Z>6D=d64Y),3(,.7"E,)
!" Tendon sheaths, fascial planes, lymphatics marrow abnormality (41%/12%) (+
!" Felon-volar tuft destruction “ghost” sign)
!" Bites !" Factors favoring neuropathic: thin rim
!"_&8/.[)VFG)T*".()a"(9)$29()))))) enhancement of effusion (68%/21%);
(Staph/strep) presence of subchondral cysts (76%/2%);
!"Animal: intraarticular bodies (53%/12%)
#" Dog (90%), 5% infected;
#" Cat (10%), 20%-50% infected Ahmadi, et al. Radiology. 2006;238:622-631.
(Pasteurella multocida)
Complications of Osteomyelitis [Figure 19]
Osteomyelitis/Septic Arthritis !" Sequestra discharged through sinus tracts

!" Avascular necrosis
Contiguous Spread: Other Sites [Figure 18]
!" Fracture/slipped epiphysis
!" Foot: pathways: medial, intermediate
!" Growth plate disturbance
lateral
!" Osteolysis
!"Puncture: pseudomonas
!" Systemic amyloidosis (rare)
!"Diabetes: multiple organisms (25%
!" Epidermoid carcinoma
ulcers)
!"0.5% long term draining sinus
!"Aerobic/anaerobic
!"M > F; 20-40 year latent period
!" Pelvis: decubitus ulcers (paraplegics)
!"Tibia/femur
!"Ischial tuberosity chronic osteomyelitis
!"Arise deep in sinus tract
!" Postoperative: ring sequestra

Figure 21 A & B
Septic arthritis and osteomyelitis of the 4th MTP
joint with joint narrowing and bone destruction
(arrowhead).
Figure 19 A & B Septic Arthritis: Hip Infant/Childhood

Chronic osteomyelitis with sinus tract and secondary [Figure 22]
epidermoid carcinoma. Aggressive bone destruction !" Staphlococcus aureus
is seen distally and medially corresponding to !" Spread from adjacent osteomyelitis
malignancy (arrow and *) as sinus tract enters bone. !" Radiologic signs
!"Widened hip joint/effusion
(sonography)
Septic Arthritis: Bacterial EMERGENCIA Qx !"Displaced pericapsular fat planes
!" Cause
!" Surgical emergency
!"Hematogenous, contiguous spread,
direct implantation, postsurgical
!" Polyarticular (20%)
!" Organisms
!"W*3$?.($K#( - leading cause up to age
2
!"Staph, alpha/beta hemolytic strep
!"Pneumococcus, E. coli, Pseudomonas
Septic Arthritis: Pathology [Figure 20]

!" Q<.*E"/')".C/88/("*.D9<:,-,8"/DC&"+) Figure 22
production
Septic arthritis in the right hip of a young child
!" Fibrin deposits inhibit cartilage nutrition with joint widening indicating a joint effusion on
!" Attract WBC’s release enzymes radiography.
(collagenase)
!" Pannus formation
!" Cartilage destruction/bone erosion
Septic Arthritis: Complications/
Sequelae [Figure 23]
!" Avascular necrosis
Figure 20 !" Slipped epiphysis
!" Growth disturbance
Pictorial !" Osteomyelitis
representation !" Secondary osteoarthritis
of septic !" Synovial cyst, tendon/capsule injury
arthritis.
Figure 23
Complication
of septic
Septic Arthritis: Radiology [Figure 21] arthritis
!" Soft tissue swelling/joint effusion with right
(sonography) hip osseous
ankylosis
!" Periarticular osteopenia on
!" Increased vascularity - scintigraphy radiography.
!" Pannus – arthrography – gadolinium –
enhanced MRI

Other Soft Tissue Infection Necrotizing Fasciitis: Imaging
!" Septic bursitis – usually injury !" Skin-thickening
!"Staph/prepatellar (child) !" Subcutaneous edema and air
!" Septic tenosynovitis !" Involves deeper tissue unlike cellulitis
!" Cellulitis !" K*%/')C&"+)%*'',%("*.7)0/17%,774
!" Necrotizing fasciitis !" Gadolinium enhancement
!" Soft tissue abscess – pyomyositis
Chronic Granulomatous Disease of
!"Staph (90%)
Childhood
Soft Tissue Infection: Radiology !" X-linked recessive (males) (1/225,000 live
[Figure 24]
births)
!" Radiographs !" WBC’s (neutrophils) cannot kill organisms
!"Soft tissue swelling (catalase positive Staph/Nocardia/
!"Air (rare): clostridia, E coli (coliform), Mycobact./Aspergillus)
bacteroides !" Skin lesions, lymphadenitis (cervical),
!" CT/MRI/sonography hepatosplenomegaly (90%), and
!"U.C/88/(*-<)%9/.2,7 abscesses (55%)
!"To detect focal abscess !"Pneumonias (80%), chronic
(penumbra sign) osteomyelitis (25%-35%)
!"Contrast enhancement of rim !" Fatal: 40% cases (prognosis is improving)
- low virulent organisms
Figure 24 !" Symptoms of osteomyelitis limited
A, B & C !" Bone destruction/limited sclerosis (later
Soft tissue stages)
abscess in !" Small bones hands/feet, chest wall, spine
the buttock
on CT and Chronic Recurrent Multifocal
MR showing Osteomyelitis (CRMO) [Figure 25]
41/#0*?.3)*
collection (*)
!" Chronic symmetric plasma cell
with internal osteomyelitis
foreign material !" Indolent/recurrent bone infection
(arrows) after !" Age 5-15 years; F > M; metaphyses
accident. (49%-86%)
!" Lower extremity (40%), spine (26%),
pelvis (21%), clavicle (30%), mandible
(5%)
!" Mixed lysis/sclerosis; symmetric (85%),
edema signal MR (100%); periosteal
reaction (48%)
!" May be sterile, plasma cells, lymphs, and
histiocytes
!" SAPHO: young adults (Synovitis, Acne,
Pustular rash palms/soles, Hyperostosis,
Osteitis
Cellulitis
!" ^%&(,)".C/88/(*-<):-*%,77)*#)+,,:)
subcutaneous tissues
!" Location
!"Extremities, thorax, abdomen, neck
!" Organisms
!"Streptococci, staphylococci,
W*3$?.($K#(
Necrotizing Fasciitis: Clinical

!" Infection and necrosis of fascia (Staph/
Strep)
!" Important to distinguish from cellulitis
!" Systemic severe toxicity – IVDA
!" Extremities, neck, face, perineum Figure 25 A & B
!" High mortality (> 70% if not treated)
CRMO with patchy areas of lucency and sclerosis in the
!"Need prompt aggressive treatment distal tibial metaphysis on radiography. Contralateral
!" Treatment: fasciotomy, debridement, ankle, ipsilateral knee, and iliac bone showed similar
antibiotics &$)3$E%*@$1!*%61<$AD

Musculoskeletal Infection in Spine Infections: CT/MR Imaging
Drug Abusers !" MR imaging optimal
!" Altered WBC function and infected needles !" Bone destruction/marrow replacement
!" “S” joints: spine, SI, and sternal joints (T1-W)
!" AC joint, symphysis, ischial tuberosity !" High signal T2-W MR images
!" Pseudomonas, Klebsiella, Serratia !"Disc and adjacent vertebra
!" Candida in heroin addicts !" Postgadolinium images helpful
!"Focal abscess detection
Spine Infections: !" Paravertebral soft tissue masses (20%
Routes of Contamination pyogenic cases)
!" Hematogenous !"Anterior and lateral (psoas)
!"Arterial !"Epidural
!"Venous: Batson plexus
!" Contiguous source
!" Direct implantation/postoperative
!"Discography (-ectomy), biopsy,
laminectomy
Spine Infections: Clinical Characteristics

!" Spondylodiskitis
!" 2%-4% of all osteomyelitis cases
!" M > F = 1.5-3:1; age 40-60 years old
!" Lumbar (50%) > thoracic (35%) >
cervical/sacrum
!" Vertebral body
!" History: recent primary infection
!" Symptoms: back pain, fever, neurologic
Figure 27 A & B
Spine Infections: Pathology Bacterial spondylodiskitis with rapid disk space
!" S aureus (55%-90%) loss and endplate destruction over 2 weeks (right
!" Localizes to anterior subchondral bone image) due to S aureus infection. Left image initial
radiograph.
!" Rapidly extends into disc (1-3 weeks)
!" Can extend into paravertebral soft tissue
Spine Infections: Radiology

[Figures 26 & 27]
!" Initially radiographs normal or subtle Spine Infections: Differential Diagnosis
subchondral destruction !" Amyloid in CRF
!" Usually seen radiologically after disc !"Low signal T2-W MR images
involved !" Tumor-crossing disc
!" Rapid disc narrowing with irregular !"Chordoma, lymphoma, myeloma, GCT
endplate destruction !" B(9,-)%/&7,7)+"7%)./--*a".2)0a,''?+,$.,+)
!" Later osteosclerosis (10-12 weeks) bone margins)
!" Treatment: diffuse sclerosis, DDD, !"DDD, CPPD, neuropathic, RA, trauma,
disc ankylosis sarcoid
Intervertebral Discitis:
!" Hematogenous: children (1-16 years)
!"Disc vascularized
!" Symptoms: mild after primary infection
!" Cultures negative (50%-90%);
S aureus
!" Antibiotics given empirically
Intervertebral Discitis: Radiology

!" Scintigraphy positive early
!" Late disc narrowing and erosion
Pictorial representation of progression of virulent !" VLU)$.+".27)7"8"'/-)(*)/+&'(7
bacterial spondylodiskitis. !" Paravertebral soft tissue changes unusual
!" Disc often reconstitutes after therapy but
may remain deformed with sequelae

953
954
Musculoskeletal Infection: Part 2
Mark D. Murphey, MD
Unusual Bacterial Musculoskeletal
Infection
!" Brucella
!" Mycobacteria (acid-fast bacilli)
!"Tuberculosis
!"Atypical
!"Leprosy
!" Actinomycosis
Brucellosis
!" Malta fever – undulant fever
!" WHO – 500,000 cases annually
!" Brucella – abortius, melitensis, suis, canis
!" Endemic Midwest USA, Saudi Arabia,
South America, Spain, and Italy
!" Ingested milk/meat: reticuloendothelial
system (marrow)
Brucellosis [Figure 1]
!" Musculoskeletal infections (30%-85%)
!" Septic arthritis: knee, SI joint, shoulder
!" Prepatellar bursitis
!" Spine – 53% – lumbar (lower L4)
!"Focal: subchondral anterior superior
endplate (parrot beak phyte)
!"Diffuse: vertebral body maintained,
less disc and paravertebral
involvement, disc gas (25%-30%)
Al-Shaheed. RadioGraphics. 94;14:333-348.
Musculoskeletal Tuberculosis:
!" Increasing – immunocompromised Figure 1 A, B, C & D
patients
Brucellosis spondylodiscitis on radiograph, CT, and
!" 1%-3% of TB patients – MSK involvement sagittal T1-W and T1-W postcontrast MR images show
!" Pain, swelling, stiffness – long delay to multilevel involvement of the discs and vertebral
diagnosis bodies (arrows, open arrows, arrowheads, and *) and
!" V*-(/'"(<)7("'')7"2."$%/.( :#"#%:3$#0*#$)*#$!("31"*(:3)."#0*3$?#>>#!1",*/6#$E(%*
!" Negative skin test – MSK TB unlikely (curved arrows and arrows on MR). Note the lack of
vertebral collapse and “parrot beak” osteophytes.
!" Negative CXR (child) – MSK TB unlikely
Musculoskeletal Tuberculosis: Pathology

!" Hematogenous, pulmonary changes 50%
!" Tubercles: central giant and epitheloid
cells
!"Central caseating necrosis
(may calcify)
!"Peripheral: lymphocyte mantle
!" Q<.*E"/')("77&,DC&"+[)))
!"80%-90% positive culture
!"Newer DNA and PCR tests more rapid
"+,.("$%/("*.

Musculoskeletal Tuberculosis:
Sites of Involvement
!" Spine: 25%-60% of MSK cases
!" Other osseous sites unusual
!" Dactylitis
!" Arthritis: knee, hip
!" Bursitis/tenosynovitis – hand/wrist
!" BCG related
Tuberculous Spondylodiscitis
!" May result in neurologic symptoms
!" Hematogenous: venous (Batson) plexus
!" L1 most common: decreases above/below
!" More than one level frequent
!"Usually contiguous
!"Separate foci (1%-4%)
Tuberculous Spondylodiscitis: Radiology

[Figures 2 to 7]
!" Subchondral vertebral body (2-5 months)
!"Anterior 82%; posterior 18%
!" Disc extension
!" Less common involvement: posterior
elements, isolated vertebral body (ivory)
!" Subligamentous extension: “gouge”
defects
!" Kyphosis (gibbus): thoracic
!" Paraspinal extension: psoas (L1-L5)
!"F/'%"$%/("*.[)/8*-:9*&7D(,/-+-*:
!"Abscess (5% psoas)
!" MR imaging usually optimal
!"Assess extent/relationship to canal
!"Abscess shows rim enhancement
Figure 3 A to E
Tuberculous spondylodiscitis.
A, B) Radiographs show myelographic block
(arrowhead) with endplate destruction, collapse, and
disc involvement (arrow).
Figure 2 A & B C) CT reveals large paraspinal mass (*).
D) Sagittal T1-W MR images show marrow
Pictorial representation of tuberculous spondylodiscitis. replacement and disc involvement at two levels
(arrowheads) as well as anterior paraspinal and
posterior epidural masses (arrows).
Absceso paraespinal calcificado: Lo más probable es que sea TBC E,F,G.) Sagittal and axial postcontrast T1-W MR
images reveal rim enhancement about anterior
paraspinal and posterior epidural abscesses (arrows).
Continued to next page.

Figure 5 A & B
Anterior gouge defects on sagittal T2-W MR image
and sagittal macrosection resulting from tuberculous
spondylodiscitis extending under the anterior
longitudinal ligament (arrows) and invading other
vertebral segments (arrowheads).
Figure 3 F, G, H & I
Tuberculous spondylodiscitis.
Continued from previous page.
H, I.) High signal intensity is seen on the axial and
sagittal T2-W MR images in the involved vertebrae, Figure 6
discs, and paraspinal abscesses (*).
Teardrop
paraspinal
/#0/3&/#!31$*
(*) in a
tuberculous
paraspinal
abscess
related to
spondylo-
discitis.
Figure 7
CT of the
spine in a
patient with
tuberculous
Figure 4 A & B spondylo-
discitis and
Sagittal dried bone specimen and gross specimen /#0/3&()*
show effects of tuberculous spondylodiscitis with paraspinal
gibbus deformities (arrows) and anterior epidural abscesses
3$?#>>#!1",*>#%%*@RA*)3%:0#/3$E*!6(*%:3$#0*/1")*@/A* (arrows).
posteriorly.

Tuberculous Spondylodiscitis:
Differential Diagnosis Pyogenic
!" F/.)1,)+"#$%&'(
!" Findings favoring tuberculosis
!"Multilevel involvement
!"Slow vertebral/disc destruction
!"F/'%"$,+):/-/7:"./')8/77
!"Lack of sclerosis
Tuberculous Osteomyelitis
!" Not common, usually with arthritis
!" Often epiphyseal, any bone, joint
!" Children metaphyseal cross plate
!" F<7("%)E/-",(<)c)8&'("#*%/')+,$.,+)'<("%)
foci
!" Dactylitis: < age 5 (0.5%-14% cases)
!"Multifocal (25%-35%)
!"Spina (spike-like) ventosa Figure 9 A & B
(puffed full of air) Radiograph of tuberculous arthritis with diffuse joint
space loss, marginal erosions (arrows) and osteopenia
Tuberculous Arthritis [Figure 8]
(Phemister triad) and sagittal macrosection showing
&+"3$1.%*('.)#!(*@RA*!6"1.E61.!*!6(*G13$!D
!" Large joints (knee/hip) monoarticular
!" Q<.*E"/')(9"%W,.".2)%*E,-,+)1<)$1-".
!" Granulation tissue erodes cartilage bone
!" Slow process/lack proteases
!" Areas of cartilage contact spared
Figure 10 A & B
Pelvis radiographs over a 2-month interval show slow
pancompartmental loss of the right hip joint resulting
from tuberculous arthritis.
Atypical Mycobacterium [Figure 11]

!" Immunocompromised patients
!" Early diagnosis/treatment important –
skin/pulmonary
!" Types: photochromogens (M. kansasii),
nonchromogens (M avium); rapid growers
Figure 8 A & B !" Bone/joint: multiple lesions, less
Pictorial representation of tuberculous arthritis (right osteopenia, hand/wrist, metaphysis/
image) and normal joint (left image). diaphysis lysis/sclerosis, abscess/sinus
tracts common
Se cubre la sinovial con fibrina y como la irrigación de la articulación
es a través de la sinovial, dismunuye esta tb.
Tuberculous Arthritis: Radiology Figure 11A

[Figures 9 & 10]
Sagittal T1-W and axial
!" Phemister triad T2-W MR images reveal
!"Juxtaarticular osteopenia marked thickening
!"Slow joint space loss (arrowheads) about the
!"Peripheral erosions F$)*?('1"*!($)1$*"(0#!()*
!" Joint effusion to atypical mycobacteria
tenosynovitis. Chronic
!" MRI: nodular synovial thickening (60%), &+"1%3%*/#.%(%*!6(*
marrow edema (80%), myositis (40%) intermediate signal on
!" Less reactive bone, periostitis, osseous T2-W (arrow).
ankylosis
Artritis monoarticular es infeccioso hasta que se demuestre lo contrario.
Leprosy Indirect: N&,#;($-4$+Signs
[Figure 13]
Figure 11B
!" Neural abnormalities: common
Sagittal T1-W !" (98% MSK changes)
and axial T2-W !" _/.+)0".+,3M)'*.2)$.2,-74M)a-"7(M)/.W',)
MR images and feet (distal)
reveal marked !" Fracture, bone erosion, and resorption
thickening
(arrowheads)
(tapered appearance – “licked candy
about the stick”)
F$)*?('1"* !" Q,%*.+/-<)".#,%("*.M).,-E,)%/'%"$,+)
tendon related (ulnar), squamous cell carcinoma skin
to atypical
mycobacteria
tenosynovitis.
56"1$3/*&+"1%3%*
causes the
intermediate signal on T2-W (arrows).
Leprosy: Mycobacterium Leprae

!" Africa, South America, Asia
!" USA: Texas, Louisiana, Hawaii, Florida
!" Long incubation (3-6 years)
!" Infection through skin/mucous
membranes
!" M > F; usually detected before age 20
Leprosy: Pathology Types

!" Lepromatous: many bacilli more severe/
Figure 13 A to E
generalized
!" Tuberculoid: more reaction/less bacilli/ L(:"1%,*<3!6*>.0!341/#0*$("=(*3$?#>>#!1",*/6#$E(%*
skin and nerve involvement (arrowheads) on multiple MR images.
!" Dimorphous: features of both Cambios inflamtorios multifocales en el nervio.
!" Indeterminate
Leprosy Direct: S;($-4$+Signs [Figure 12]

!" Related to bacilli presence Actinomycosis: Clinical Characteristics
!" f.%*88*.)@6?X6)$.+".27 !" Anaerobic higher bacteria; acid fast-like
!" Small bones hands/feet (direct spread) !" Actinomyces israelii, Nocardia asteroides
!" Punched out or lace-like osseous !" ;*-8/')C*-/)".)8*&(9
destruction phalanges, nasal bone !" Trauma often results in inoculation
!" Periosteal reaction, fragmentation, !" Immunocompromised patients
arthritis
Actinomycosis: Radiology [Figure 14]
!" Sites mandible, axial skeleton (rib, spine,
pelvis) large joints
!" Lysis and sclerosis (bone proliferation)
!" Spine (posterior elements) and rib
!" Q".&7)(-/%(7D/17%,77,7)0.*)%/'%"$%/("*.4)
common
Figure 14 A & B
Figure 12 A & B
Actinomyces osteomyelitis in the mandible on
Lattice-like lucencies in the phalanges representing a radiograph showing patchy areas of destruction and
direct sign of leprosy infection on radiography. sclerosis (arrowheads).
imita la sarcoidosis
Spirochetes Congenital Syphilis: Late Changes
!" Syphilis: 10-12 million new cases/year !" Periostitis/osteomyelitis/osteitis
!" Yaws !" Gumma: any bone caseous necrosis
!" Lyme disease related to degenerating spirochete
!" Tropical ulcer !"Bone resorption: carries sicca
!" Bejel, rat bite, fever, leptospirosis !"Bone lysis/reactive sclerosis
!" Arthritis: uncommon – ankles, MTP,
Congenital Syphilis: Early Changes elbows, knees
!" Toxic effects degenerating spirochetes/ !"Swelling, effusion, narrowing,
infection destruction
!" Osteochondritis: metaphyseal lucent !"Neuropathic (5%-10%): knee, hip,
bands/irregularity ankle, spine
!"Long bone (tibia: Wimberger sign),
rib, spine, sternum Yaws
!"Epiphyseal widening/separation !" Treponema pertenue
!"Heal quickly with treatment !" ^#-"%/M)Q*&(9)^8,-"%/M)Q*&(9)G/%"$%
!" Osteomyelitis: diaphyseal lysis/sclerosis/ !" Very similar to syphilis – less nose
periostitis changes, more phalanges (spares distally)
!" Diffuse periostitis !" Exostosis maxilla – goundou
Congenital Syphilis: Late Changes Tropical Ulcer

[Figure 15] !" Central/East Africa
!" Congenital syphilis: 75% diagnosed after !" Lower leg ulcer destroys muscle/tendon
age 10 !" To bone focal osseous production tibia/
!" Hutchinson triad (Hutchinson teeth, $1&'/
interstital keratitis, nerve deafness) !" Multiple organisms including spirochetes
!" May be similar to early changes !" Epidermoid carcinoma 25% (> 10 years
!" f7&/''<)8*-,)'"W,)/%b&"-,+)$.+".27 latency)
!" !/%(<'"("7[)$.2,-7)8*-,)%*88*.
!" Painless knee effusions (Clutton joints) Lyme Disease: Clinical Characteristics
!" Recognized 1975; 23,763 new cases
(2002)
!" Most common vector-borne illness in USA
!" US (NE/Mid-Atlantic), Europe, Far East,
Australia
!" Tick bite: ixodes dammini (transmission)
!" Spirochete: Borrelia burgdorferi (deer,
mice)
!" Skin lesions (Erythema chronicum
migrans 20%)
!" Joint symptoms (usually 2-6 months; 2
weeks – 2 years)
!"80% cases reported May-August
Lyme Disease: Radiology [Figure 16]

Figure 15 !" Knee (80%), shoulder, elbow,
temporomandibular, ankle, wrist, hip,
Congenital syphilis of the lower extremity showing hand/foot
periosteal reaction (arrows) and osteochondritis
(arrowheads) of the proximal tibiae (Wimberger sign). !" Monoarticular, oligo or polyarticular
!" Soft tissue swelling/effusion (MRI
synovitis)
!" Adenopathy, myositis, lack subcutaneous
Congenital Syphilis: Early Changes edema
!" Bone changes in up to 20% (early as 6 !" Chronic changes (10%): osteopenia,
weeks) joint loss (25%), erosions, secondary
!" Proliferative periostitis carcinoma
!"V*7()%*88*.)$.+".2 Ddx: Artritis reumatoide juvenil
!"Tibia (saber shin), skull, ribs, sternum
!"Solid/laminated (rarely perpendicular)
!" Osteomyelitis/osteitis/septic arthritis
!"Much less common
!"Skull: outer table aggressive lysis
!"Nasal bone collapse – saddle nose

Blastomycosis
!" B dermatiditis (North American)
!"Ohio, Miss. River Valleys, Mid-Atlantic
!" B brasiliensis – Mexico, Central/South
America
!" Skin/pulmonary entry from soil
Figure 16 A, B & C !" Bone involved in up to 60% patients
!" Ribs, spine, tibia, carpus, tarsus, skull
Lyme arthritis of !" Arthritis < 10% patients
the knee on lateral
radiograph with Candidiasis (Moniliasis)
joint effusion (* ) !" C albicans but many other species
and MR revealing !" Patients on hyperalimentation, antibiotics,
synovitis (arrows),
intraarticular steroids
myositis (M), and
adenitis (A). !" Bone involvement rare (1%-2%)
!" Monostotic/monarticular: long bone,
sternum, spine, knee
!" Arthritis more often precedes
osteomyelitis
Coccidioidomycosis
!" C immitis – soil – inhalation
!" Southwest US, Mexico
!" < 1% disseminated; (10%-50% MSK
changes)
!" Metaphyseal, may be symmetric
!" Joints: ankle, knee, also migratory
arthritis
Cryptococcosis
!" Torulosis, C neoformans
!" Soil - inhalation
Musculoskeletal Infection Fungal
!" Disseminated disease, 5%-10% MSK
!" Aspergillosis
changes
!" Blastomycosis
!" Arthritis unusual
!" Candidiasis
!" Cryptococcosis Histoplasmosis
!" Histoplasmosis !" H capsulatum – US (Miss. River valley)
!" Mucormycosis !" H dubosii – Africa – MSK changes 80%
!" Sporotrichosis cases
!" Madura foot !" Soil – inhalation; most common fungal in
US
Fungal Musculoskeletal Infection:
!" Pelvis, skull, ribs, small tubular bones
Common Changes
!" Arthritis – knee, ankle, wrist, hand
!" Frequently in immunocompromised
!" Osteomyelitis large punched out lytic Mucormycosis
lesions !" Phycomycetes – Rhizopus, Mucor, Absidia
!" May have surrounding sclerosis !" Diabetes, uremia, burns
!" Often multifocal/may involve bone !" Entry via sinuses
protuberances !" Skull/face (max/ethmoid sinuses)
!" Joint involvement – slow progressive !" Bone destruction
destruction
!"MRI: nodular synovial thickening Sporotrichosis [Figures 17 to 21]
!" Sporothrix schenckii
Aspergillosis !" Saprophyte on vegetation
!" A fumigatus (saprophyte, > 300 species) !" Inhalation/skin wound (rose thorn)
– normal upper respiratory tract organism !" Disseminated form 80% MSK changes
!" Sites related to pulmonary changes !" Arthritis (monoarticular) common – knee
(children) or (66%) hand/wrist (52%) ankle, elbow
!"Hematogenous (adult): rib, sternum, !" Osteopenia often not prominent
spine !" Osteomyelitis due to arthritis
!" Arthritis rare
!" Mortality rate with osteomyelitis
(25%-29%)

Figure 20
Sporotrichosis
of the
knee with
CT (post-
arthrogram)
and MR
showing
enhancing
Figure 17 $1$%:(/3&/*
nodular
Aspergillus synovial
infection with thickening
pulmonary (arrowheads)
and rib after
(arrowheads) intravenous
involvement. contrast.
Figure 21 A & B
Sporotrichosis of the knee with CT (postarthrogram)

#$)*-7*%61<3$E*($6#$/3$E*$1$%:(/3&/*$1).0#"*
synovial thickening (arrowheads) after intravenous
Figure 18 contrast.
Blastomycosis
of the humerus Madura Foot: Mycetoma [Figures 22 & 23]
with extensive !" Chronic granulomatous infection
involvement !" Foot (65%-70%), hand, legs, back/head
demonstrating !" Many organisms can be cause –
mixed lysis and
sclerosis. Eumycetes (Madurella), actinomycosis,
Monosporium apiospermum (US)
No puede ser displasia !" Tropics: India, Africa, Arabia, Latin
fibrosa pq tiene engrosamiento America
cortical. Aunq se origina en la !" Tarsals/metatarsals most involved
cavidad medular
Figure 22
A, B & C
135-137
Mycetoma
(Madura
foot) on
radiographs,
sagittal T1-W
and T2-W
MR images
and gross
specimen
show
Figure 19 A & B extensive
Histoplasmosis with multifocal
multifocal area of destruction
lysis, many of which with sclerosis/
involve tuberosities and &+"1%3%*
trochanteric regions representing
(“lumps and bumps” of chronicity.
bone).

Figure 24
Coronal STIR
MR shows
#*41/#0*?.3)*
collection (*)
representing
pyomyositis in
an HIV patient.
Helminths/Worms
!" Musculoskeletal changes usually soft tissue
%/'%"$%/("*.
!" Loa loa[)^#-"%/)c)7&1%&(/.,*&7)%/'%"$%/("*.)
0$.,)'/%,?'"W,)*-)(9"%W)1,/+?'"W,4
!" Filiarasis: lymphatic obstruction
(elephantiasis)
!" Guinea worm (dracunculosis): long
%/'%"$%/("*.)#,8/',)a*-8)'*a,-),3(-,8"(<)
Mycetoma (Madura foot) on radiographs, sagittal and hand – can cause arthritis
T1-W and T2-W MR images and gross specimen show !" Cystocercosis: linear/oval rice drain
('!($%3=(*>.0!341/#0*)(%!"./!31$*<3!6*%/0("1%3%N&+"1%3%*
%/'%"$%/("*.)/'*.2)/3"7)*#)8&7%',)&:)(*)XA?
representing chronicity.
25 mm length
Echinococcus Musculoskeletal Changes

[Figure 25]
!" Echinococcus (multilocularis/granulosus)
Viral Protozoan !" Bone disease: 0.5%-4% (E granulosus)
Musculoskeletal Infection !" Spine, long bone epiphysis, ilium, skull, rib
!" TORCH: metaphyseal lucent bands (celery !" Multiloculated (bundle of grapes) lysis/
stalking) expansion
!" Cat-scratch disease: viral like bacteria !" May be soft tissue loculated, cyst margins
!" S&:3#*4(03% (R hensalae and Bartonella may calcify
species)
!"Look for adenitis (epitrochlear)
AIDS: Musculoskeletal Changes

[Figure 24]
!" Seronegative arthopathy
!" Osteomyelitis, septic joint/bursitis any
organism
!" Pyomyositis (staph); lower extremity Figure 25
A&B
(95%), multiple (50%)
!" Bacillary angiomatosis (Rochalimaea Paraspinal
hensalae, R quintana) skin lesion/bone echinococcus
infection with
destruction (cortex prominent) multiloculated
!" Neoplasm: Kaposi sarcoma, lymphoma ?.3)C&00()*
cysts (*) on
axial T1-W
and T2-W
MR images
and gross
specimen.

Figure 25C
Paraspinal echinococcus infection with multiloculated Figure 26 A & B

?.3)C&00()*/,%!%*@RA*1$*#'3#0*;BCT*#$)*;FCT*-7*
images and gross specimen. Typical lattice-like multifocal lucencies of several
phalanges resulting from sarcoid.
Sarcoid: Musculoskeletal
!" Usually have chest changes (80%-90%)
!" Muscle: myositis (50%-80% patients)
!"MRI low signal central scar
!" Subcutaneous soft tissue nodules (5%)
!" Arthritis (10%-35%): acute/chronic
!"Hand, wrist, ankle, knee, elbow
Sarcoid: Musculoskeletal - Osseous

Changes [Figures 26 & 27]
!" 1%-13% of patients; may be
asymptomatic
!" Lattice-like lysis (hands)
!" Punched out lytic lesions
!" May appear aggressive
!" Acroosteolysis, acrosclerosis (30%-50%)
!" Areas of sclerosis
!" Marrow replacement creating mottled Figure 27 A & B
appearance (MRI)
Sarcoid marrow involvement showing heterogeneous
or mottled marrow signal intensity diffusely on sagittal
T1-W cervical spine MR images.

References for Part 1 and 2
Acute Osteomyelitis
1. Unger E, Moldofsky P, Gatenby R, Hartz W, Broder G. Diagnosis of osteomyelitis by MR imaging. AJR Am J

Roentgenol 1988 Mar;150(3):605-10.
2. Erdman WA, Tamburro F, Jayson HT, Weatherall PT, Ferry KB, Peshock RM. Osteomyelitis: characteristics
and pitfalls of diagnosis with MR imaging. Radiology 1991 Aug;180(2):533-9.
3. Palestro CJ, Kipper SL, Weiland FL, Love C, Tomas MB. Osteomyelitis: diagnosis with (99m)Tc-labeled
antigranulocyte antibodies compared with diagnosis with (111)In-labeled leukocytes - initial experience.
Radiology 2002 Jun;223(3):758-64.
4. Averill LW, Hernandez A, Gonzalez L, Pena AH, Jaramillo D. Diagnosis of osteomyelitis in children: utility
of fat-suppressed contrast-enhanced MRI. AJR Am J Roentgenol 2009;192:1232-8.
Chronic Osseous Infection
5. Khanna G, Sato TS. Ferguson P. Imaging of Chronic recurrent multifocal osteomyelitis. RadioGraphics
2009;29:1159-77.
6. Fritz J, Tzaribatchev N, Claussen CD, Carrino JA, Horger MS. Chronic recurrent multifocal osteomyelitis:
comparison of whole-body MR imaging with radiography and correlation with clinical and laboratory data.
Radiology 2009;252:842-51.
Diabetic Related Infection
7. Donovan A, Schweitzer ME. Use of MR imaging in diagnosing diabetes-related pedal osteomyelitis.

Soft Tissue Infection
8. Weishaupt D, Schweitzer ME. MR imaging of the foot and ankle: patterns of bone marrow signal
abnormalities. Eur Radiol 2002;12:416-26.
Brucellosis and Musculoskeletal Tuberculosis
9. Sharif HS, Aideyan OA, Clark DC, Madkour MM, Aabed MY, Mattsson TA, al-Deeb SM, Moutaery KR.
Brucellar and tuberculous spondylitis: comparative imaging features. Radiology 1989 May;171(2):419-25.
10. Sharma P. MR features of tuberculous osteomyelitis. Skeletal Radiol. 2003 May;32(5):279-85. Epub 2003
Mar 25.
11. Jung NY, Jee WH, Ha KY, Park CK, Byun JY. Discrimination of tuberculous spondylitis from pyogenic
spondylitis on MRI. AJR Am J Roentgenol 2004 Jun;182(6):1405-10.
12. Burrill J, Williams CJ, Bain G, et al. Tuberculosis: a radiologic review. RadioGraphics 2007;27:1255.
13. Sanghvi DA, Iyer VR, Deshmukh T, Sumedh SH. MRI features of tuberculosis of the knee. Skeletal Radiol
2009;38:267-73.
Lyme Disease
14. H/a7*.)RGM)L/9.)!NS)H<8,)+"7,/7,)/.+)-/+"*'*2"%)$.+".27)".)H<8,)/-(9-"("7S)^RL)^8)R)L*,.(2,.*')@ZZX)
May;158(5):1065-9. Review.
Spine Infection
15. Hong SH, Choi JY, Lee JW, Kim NR, Choi JA, Kang HS. MR imaging assessment of the spine: Infection or
/.)"8"(/("*.I)L/+"*J-/:9"%7)XAAZYXZ[>ZZ?e@XS
Other Unusual Organisms
16. Naraghi AM, Salonen DC, Bloom JA, Becker EJ. Magnetic resonance imaging features of osseous
manifestations of early acquired syphilis. Skeletal Radiol 2010;39;305-9.
17. Winterstein AR, Bohndorf K, Vollert K, Wagner T, Gnekow A, Roemer FW. Invasive aspergillosis
osteomyelitis in children – a case report and review of the literature. Skeletal Radiol 2010;39;827-31.
18. Gould ES, Gilet AG, Vigorita VJ. Granulomatous salmonella osteomyelitis associated with anti-tumor
necrosis factor therapy in a non-sickle cell patient: a case report. Skeletal Radiol 2010;39:821-5.

966
Imaging of Cervical Spine Trauma
Mark D. Murphey, MD
Cervical Spine Trauma: Demographics Trauma Oblique: Radiographs
!" Most common portion of spine injured !" Developed by Gehweiler and Abel
!" Responsible for 65% of all spinal injuries !" X-ray tube angled 30°-40° from horizontal
!" Mechanism: MVA/fall/sports injury !" Add 15° cranial tube tilt
!" Spinal cord injury: 40% (10,000 annually) !" Better than Swimmer view for cervico-
thoracic junction
Cervical Spine Trauma: Patterns
!" Areas most commonly involved Flexion and Extension: Radiographs
!" C1-2 (particularly in children) !" f7,)&:-"29()'/(,-/')$-7()(*),E/'&/(,)
!" C5-7 cervical spine straightening/reversal
!" Other fractures 20% !" To evaluate abnormal alignment/stability
!" Particular association of low cervical !" False negative from muscle spasm
fracture with high thoracic and !"Repeat after delay
thoracolumbar injury !" Performed under physician guidance
!"Passive motion
Cervical Spine Trauma:
Radiographic Signs – Normal Cervical Spine Trauma: CT
!" ABC’s: alignment, bone integrity, cartilage !" Indispensable, widely available, rapid
(joint/disc space), soft tissues study
!" Lateral view: anterior/posterior vertebral !"1-3–mm sections, coronal/sagittal
body arcs reconstructions
!"Spinolaminal arc (except childhood !"Spiral/multichannel/holography
pseudosubluxation C2-3) !"3D helpful to depict spatial
!" AP view: spinous and lateral mass arcs relationships
Cervical Spine: Normal Measurements Cervical Spine Trauma:

!" Lateral atlantoaxial offset MR Imaging/Myelography
!"(“Open mouth” view) – 2 mm !" MRI indications
!" Predental space: 3 mm adult; 5 mm child !"Posttraumatic cervical myelopathy/
!" Anterior vertebral height vs posterior radiculopathy
!"2 mm (except C5) !"Clinical symptoms unexplained by
!" Pretracheal space at C6: 22 mm adult, other radiologic studies
14 mm child !"Assess ligamentous injury
!" Facet width: 2 mm !" Myelography (CT) largely replaced by MRI
!" H"7(9,7"7)a"(9)C,3"*.D,3(,.7"*.[)X)88 !"CSF obstruction
!" Retropharyngeal space at C2: 7-8 mm !"Nerve root avulsion, dural tear
!"Exceptions: ET/NG tubes;
".C/88/(*-<):-*%,77D%-<".2)%9"'+ Cervical Spine Trauma: Stability
!" Interspinolaminar space: 2 mm !" Mechanical: ability to not deform under
!"Between 3 continuous levels physiologic stress
!" Neurologic: potential to produce new or
Cervical Spine Trauma: ".%-,/7,):-,E"*&7)+,$%"(
Radiographic Evaluation !" Acute/chronic
!" Standard 3 view series
!"AP, lateral, open mouth Cervical Spine Trauma:
!"h/7/1/%9)E",a)8*+"$,+)*1'"b&,)*:,.) Radiographic Signs-Instability
mouth !" Widened interspinous spaces (> 2 mm)
!" Oblique views !" Widened apophyseal joints (> 2 mm)
!"Trauma oblique views !" Anterior listhesis > 3.5 mm
!" Swimmer (Twining) views !" Narrowed/widened disc space
!" f:-"29(M)'/(,-/'M)C,3"*.M),3(,.7"*. !" K*%/')/.2&'/("*.)*#)o)@@q
!" Vertebral compression > 25%
Imaging of Cervical Spine Trauma 967 Musculoskeletal Radiology

C%*##-4$*)-&,+:5+Mechanism
!" _<:,-C,3"*.
!"V*+"$,+)1<)-*(/("*.D'/(,-/')C,3"*.
!" Hyperextension
!"V*+"$,+)1<)-*(/("*.
!" Axial loading – burst
!" Complex, poorly understood mechanism

H5;(1=(B-&,+Injuries
!" Account for 50%-80% of injuries
!" Flexion forces maximal at C4-C7 anterior;
distraction posterior
!" Sprain; compression fracture
!" Facet fracture/subluxation/dislocation
!" Flexion teardrop fracture
!" Clay (coal) shovelers fracture
!" H/(,-/')C,3"*.)#-/%(&-,7[)&."'/(,-/')
occipital condyle/lateral mass C1 Figure 2
!"Uncinate or transverse process
L#!("#0*"#)31E"#:6*14*?('31$*%:"#3$*/("=3/#0*
injury with distraction forces posteriorly causing
Cervical Spine Trauma: interspinous widening or fanning at C6-7 (arrows).
H5;(1=(B-&,+Sprain [Figures 1 & 2]
!" Disrupted one-level posterior ligaments
by distraction
!" Acute focal pain/limited ROM
!" Delayed instability (30%-50%): lack Cervical Spine Trauma:
7<8:(*87)0+,'/<,+)C,3"*.D,3(,.7"*.) Compression Fracture [Figures 3 & 4]
views) !" ^77*%"/(,+)9<:,-C,3"*.)7:-/".)%*88*.
!" L/+"*2-/:9"%)$.+".27 !" Usually stable unless > 25% compression
!"Focal kyphosis, mild anterolisthesis !" Radiographs
!"Widened facet, interspinous/ !"Loss of height superior endplate
interlaminar spaces !"Focal cortical angulation
!"Widened posterior, narrowed anterior !"Band of increased density from
disc impaction
!"Compression fracture often associated
!"^'')$.+".27)/%%,.(&/(,+)a"(9)C,3"*.Y)
VLU)(*)%*.$-8)'"2/8,.()".T&-<
Figure 3 A & B
L#!("#0*"#)31E"#:6*#$)*%#E3!!#0*5;*%61<*#*?('31$*
compression fracture (arrows) at C6.
Figure 1
93/!1"3#0*"(:"(%($!#!31$*14*?('31$*%:"#3$*/("=3/#0*3$G.",*
with distraction forces posteriorly causing interspinous
widening or fanning (*).

Figure 6 A & B
Radiographs (AP and lateral) of a unilateral facet
injury (circle) with subluxation. Note that on the AP
&0>*!6(*%:3$1.%*:"1/(%%(%*#+1=(*!6(*0(=(0*14*3$G.",*
Figure 4 A & B #"(*%634!()*!1*!6(*0(4!D*S0%1*1$*!6(*0#!("#0*&0>*!6(*
J#E3!!#0*-7*@:"1!1$*)($%3!,*#$)*;FA*14*?('31$*%:"#3$* facets below the level of injury are projected as in a
cervical injury with superior endplate fracture (arrow) lateral projection whereas above the level of injury
and distraction forces posteriorly causing interspinous they are obliqued consistent with the rotational
widening or fanning at C6-7 (*). component of force.
Unilateral Facet Injury:

Cervical Spine Trauma: Radiologic Characteristics [Figure 7]
Unilateral Facet Injury !" CT
!" _<:,-C,3"*.)/.+)-*(/("*. !"“Naked” facet (may be subtle and
!" Common: 13% of cervical injuries partial)
!" Radicular symptoms common !"Contralateral facet subluxation
!" Most frequent C4-C6 common
!" Often mechanically stable, PLL partially !"Articular mass fracture (73%),
intact isolating pillar (17%), posterior
!" Unstable with prominent articular mass/ vertebral body fracture (25%)
laminar fractures !"MRI/MRA: disc herniation and
vertebral artery injury not uncommon
Unilateral Facet Injury:
Radiologic Characteristics [Figures 5 & 6]
!" Anterolisthesis < 50% vertebral width
!" Dislocated facet anterior
(oblique view in foramen)
!" Abnormal spinolaminar space/facet
rotation
!"“Bow tie” sign
!" Spinous process rotation toward side of
dislocation
Figure 5
Pictorial
representation
of a unilateral
facet injury
(circle).
Figure 7
Sagittal CT of a unilateral facet injury with locked

facets (IF - inferior facet of the level above; SF -
superior facet of the level below).

Cervical Spine Trauma
Facet Injury: Bilateral [Figures 8 & 9] Figure 10
!" _<:,-C,3"*.)8/<)1,)7*8,)-*(/("*.
!" At least as common as unilateral injury Lateral
!" Disrupted PLL, disc and often ALL radiograph
!" Unstable injury of a
bilateral
!" High incidence of cord damage facet
!"(72% quadriplegia) dislocation
!" Bilateral facet dislocation may be partial with
or complete antero-
listhesis
(arrow)
Mechanism of Locking [Figure 8]
at C4-5.
Also on
the lateral
&0>V*!6(*
inferior
facets
(IF) of
the level
above are
anterior
to the
superior
facets
(SF) of
the level
below.
Figure 8
Pictorial representation of a bilateral facet injury with

perched facets.
Locked Facets [Figure 9]
Figure 9
Pictorial
representation
of a bilateral
facet injury
with locked
facets. Figure 11 A & B
Sagittal CT’s of bilateral facet dislocation in two
different patients with the inferior facets (IF) of the
level above anterior to the superior facets (SF) of the
level below.
Bilateral Facet Dislocation:

Radiologic Characteristics
[Figures 10 & 11]
!" Anterolisthesis > 50% vertebral body Flexion Teardrop Fracture [Figure 12]
diameter !" V*7()7,E,-,)+,E/7(/(".2)C,3"*.)".T&-<

!" Dislocated inferior facets, anterior to !" Usually lower cervical spine C5-6
superior facets (70% of cases)
!" Dislocated facets in foramen – oblique !" Diving accident shallow pool common
views cause
!" K".+".27)*#)9<:,-C,3"*.)c)#/..".2M)#*%/') !" Immediate, complete, and permanent
kyphosis, disc narrowing quadriplegia (90% of cases)
!" Spinous processes not rotated !" Acute anterior cord syndrome: loss pain,
!" CT: “naked” facets, small fracture temperature, and touch
fragments often not seen on radiographs !"Retention position, motion, vibration
(posterior column senses)

Cervical Spine Fracture:
Clay Shoveler Fracture
!" Avulsion C7, C6, T1 spinous process
!" L,7&'()*#)/1-&:()C,3"*.)/2/".7()*::*7".2)
interspinous ligament
!" Stable injury
!" Oblique fracture spinous process
!" May see “double” spinous process sign
(AP radiograph)
!" Spinous process fractures can also result
from extension/direct trauma

Hyperextension Injuries [Figure 14]
!" Usually caused by force to face/forehead
!" Compression posteriorly, distraction
Figure 12 anterior
!" H,77)%*88*.)(9/.)9<:,-C,3"*.)".T&-",7)
93/!1"3#0*"(:"(%($!#!31$*14*#*?('31$*!(#")"1:*3$G.",D
(19%-38%)
!" Atlas and laminar fractures
!" Hyperextension teardrop fracture
!" Hangman fracture
!" Pillar fracture
Flexion Teardrop Fracture:
Radiologic Characteristics [Figure 13]
!" Involved vertebrae and levels above in
7,E,-,)C,3"*.
!" Vertebral body fracture with triangular
fragment from anteroinferior corner
!" Central vertebral body not severely
involved but posteriorly displaced
!" Bilateral facet subluxation/dislocation
!" MRI/MRA: disc herniation and vertebral
artery injury not uncommon
Figure 14
Pictorial representation of an extension injury.
Atlas Fractures
!" Avulsion of anterior arch C1
!"Rare stable injury
!"Results from anterior atlantoaxial
Figure 13 A & B ligament
!"Horizontal cleft in anterior arch
7#)31E"#:6%*@S9*#$)*0#!("#0A*14*#*?('31$*!(#")"1:* 0+"#$%&'()*.)FP4
injury with facet widening (circles and solid arrows),
interspinous fanning (*) and vertebral fracture with
!" Posterior C1 arch fracture
teardrop fragment anteriorly (open arrow). !"Bilateral posterior fractures (no
anterior component)
!"No anterior soft tissue swelling; stable
!"Distinguish from normal congenital
cleft

Laminar Fractures Hyperextension Fracture/Dislocation
!" Lamina crushed on extension from above/ Pedicolaminar Fracture-Separation
below !" Combined hyperextension, compression
!" Often in older patients with spondylosis and rotation
!" Usually C5 to C7 !" Fractures of pillar, lamina, pedicles
!" !"#$%&'()(*)+,(,%()*.)-/+"*2-/:97 and spinous process opposite side of
!" CT optimal translation
!" Mechanically stable !" Vertebral body often mildly (3-6 mm)
(intact anterior column/facets) anteriorly displaced
!" Neurologically unstable due to cord !" Spinous process not rotated
impingement by fragments
Hyperextension Fracture/Dislocation:
Hyperextension Dislocation Pedicolaminar Fracture-Separation
!" Common in older patients with Radiologic Characteristics
spondylosis !" Disc narrowing and vertebral rotation
!"Also bone forming diatheses AS, DISH above injury
!" Rupture of ALL, disc and stripping of PLL !" Opposite facet may be widened/dislocated
(unstable) !" Commonly involve foramen
!" Patients usually severe neurologic transversarium
symptoms !"Vertebral artery (MRA)
!"Acute central cord syndrome !" U8:*-(/.()(*)+"7(".2&"79)#-*8)C,3"*.)
!" Spinal cord impinged by subluxation and injury
intact posterior elements
!" Often recoils back to relatively normal Pillar Fracture
position !" Not common, 3%-11% of cervical injuries
(C6-C7)
Hyperextension Dislocation: !" Hyperextension and rotation
Radiographic Characteristics [Figure 15] !" Articular mass compressed on side of
!" Relatively normal cervical alignment in rotation
quadriplegic patient !" Stable, radiculopathy common without
!" Soft tissue swelling (100%) cord damage
!"B.'<)$.+".2)556
!" Avulsed fragment anteroinferior vertebrae Pillar Fracture:
(65%) Radiologic Characteristics [Figure 16]
!"Longer horizontally (unlike extension !" Subtle on radiographs
teardrop fracture) !" Disrupted lateral cortical margin (AP view)
!"In young patients ring apophysis, no !" Visualize facets on AP radiographs
.,&-*'*2"%)+,$%"( !" Loss of posterior articular mass overlap
!" Widened disc anteriorly and vacuum !"Lateral radiograph (“double outline”
(15%) sign)
!" CT optimal: degree of fragmentation and
additional other fractures
!"Pedicle, transverse process, lamina
Figure 15
Lateral
radiograph
of an
extension
fracture
subluxation
at C5-6
(arrow) in a
patient with
ankylosing
spondylitis.
(syndes-
mophytes
(arrowhead).
Figure 16 A & B
Radiograph, AP tomogram, and axial CT of an articular

pillar fracture with offset at the facet (solid arrows)
and fracture (open arrow) separating the articular
pillar from the remainder of the vertebrae.

Figure 16C Traumatic Spondylolisthesis
“Hangman”/“Hangee” Fracture
Radiograph, AP
tomogram, and axial
!" Common: 5% of all cervical spine injuries
CT of an articular !" Hyperextension is probably transient
pillar fracture with 8*+"$,+)1<)C,3"*.D%*8:-,77"*.D
offset at the facet distraction
(solid arrows) and !" Unstable injury
fracture (open arrow)
separating the !" Neurologic symptoms unusual unless
articular pillar from distraction
the remainder of !"Large canal relative to cord at C2
the vertebrae. !"“Autodecompression” from bilateral
posterior fractures
Hyperextension: Teardrop Fracture
Traumatic Spondylolisthesis: Radiologic
[Figures 17 & 18]
!" Often occur in older osteoporotic patients
Characteristics [Figures 19 & 20]
!" ]##,.+")%'/77"$%/("*.
!" Avulsion by ALL of triangular fragment
!"I: Minimally displaced fracture
!" Anterioinferior vertebral body (usually C2)
!"II: More displacement, involves C2-3
!" Fragment vertical height same or larger
disc (widening)
than length
!"III: Bilateral facet dislocation
!"Unlike avulsion with hyperextension
!" Oblique C2 pedicle fracture: lateral view
dislocation
!" Mild anterolisthesis, posteriorly displaced
!" Soft tissue swelling more prominent in
spinolaminar line
younger patients
!" Associated injuries: anterior corner
!" Unstable in extension
fractures C2/C3
!"C1/high thoracic fractures (10%)
!"Vertebral artery injuries
Axial Compression Injury:
Figure 19
Pictorial
representation
of the different
types of traumatic
spondylolisthesis.
Figure 17
Pictorial representation of an extension teardrop
fracture.
Figure 20A
Lateral
radiograph
and axial CT
of a type 1
traumatic
spondylo-
listhesis
showing
the linear
nondisplaced
fracture
(arrows).
Figure 18 A, B & C
Lateral radiograph and sagittal CT of an extension
teardrop fracture with avulsed fragment (arrows) from
the attached anterior longitudinal ligament (ALL).

Figure 20B
Lateral Figure 22
radiograph and
axial CT of a Axial CT of
type 1 traumatic a Jefferson
spondylo- fracture
listhesis showing with four
the linear components
nondisplaced (arrows).
fracture
(arrows).
Burst Fracture
!" Not common, 4% of cervical injuries Cervical Burst Fracture
!" Only occurs where cervical spine in !" Caused by vertical force driving nucleus
neutral position pulposis through endplate with body
!" C1: Jefferson fracture exploding from within
!" Lower cervical burst fracture C3-7 !" Mechanically stable unless posterior
ligament injury
Jefferson Fracture [Figure 21]
!" ;,&-*'*2"%/''<)&.7(/1',)c)+,$%"()8/<)
!" Axial compression drives occipital
progress
condyles toward atlas
!"Fragments change position
!" Bilateral fractures anterior/posterior
!"Symptoms transient paresthesias to
!"Lateral displacement
quadraplegia
!" Unstable, neurologic symptoms unusual
!"Large neural canal Cervical Burst Fracture:
!"Outward displacement of fragments
Radiologic Characteristics [Figures 23 & 24]
!" Soft tissue swelling with straightening
(but no kyphosis)
!" Retropulsed fragments disrupted posterior
vertebral body line
!" Degree of vertebral body comminution
variable
!" Vertical fracture: midline/eccentric
!" Disrupted joints of Lushka (facets)
Figure 21
Pictorial representation of a Jefferson fracture.
Jefferson Fracture:
Radiologic Characteristics [Figure 22]
!" Open mouth view best
!"Laterally displaced lateral masses
!" Lateral radiograph may only show
soft tissue swelling; look for posterior
fractures
!" CT optimal for bilateral fractures
!"Jefferson variants
Figure 23
!" Lateral mass displacement > 7 mm/
predental space > 6 mm = ruptured Lateral radiograph, axial CT, and sagittal CT of burst-
transverse atlantal ligament type fractures in different patients showing the
!" Small nondisplaced fragment medial to comminuted fracture (circle), retropulsed fragments
(solid arrows), and fracture at the junction of the
articular mass – intact ligament lamina and spinous process (open arrow).

Odontoid Fracture:
Radiologic Characteristics [Figures 25 to 28]
!" Prevertebral soft tissue swelling (may be
*.'<)$.+".24
!" Type I
!"Rare (if occurs) avulsion at tip from
alar ligaments
!" Type II
!"At base (60%-70%)
!"May miss on CT
!"High nonunion rate (72%), higher if
displacement > 5 mm
!"Open mouth view (simulated by Mach
effect); atlantoaxial instability
!"Os odontoideum distinguished by
sclerotic margins
!" Type III (30%-40%)
!"C2 body
!"Disruption of Harris ring
!"“Fat” C2 sign, invariably heal
Figure 25
Pictorial
representation
of different
types of
odontoid
fractures.
Figure 24 A to E Figure 26
Lateral radiograph, axial CT, and sagittal CT of Lateral

burst- type fractures in different patients showing the radiograph
comminuted fracture (circle), retropulsed fragments of a type
(solid arrows), and fracture at the junction of the 2 odontoid
lamina and spinous process (open arrow). fracture
(arrows).
Indeterminate Mechanism:
Cervical Injuries
!" Odontoid fractures
!" Occipitoatlantal dissociation
!" Torticollis
!" Rotary atlantoaxial subluxation/dislocation
Odontoid Fracture
!" Most common of C2 fractures (41%)
!" 11%-13% of all cervical spine injuries
!" V,%9/."78[)C,3"*.)/.+)*-),3(,.7"*.
!" Other fractures (13%): face, mandible,
posterior arch C1, extension teardrop,
hangman, atlantoaxial dissociation
Figure 27
!" ^.+,-7*.D!k^'*.`*)%'/77"$%/("*.
Open mouth radiograph of a type 3 odontoid fracture
(arrows).

Figure 28 A & B
Coronal and sagittal CT of a type 3 odontoid fracture
(arrows).
lo mas imp ver si hay hemorragia

Role of MR Imaging
!" Thecal sac/spinal cord impingement
!" Disc herniation/extrusion: 20%-40% of
patients
!"Highest (100%) in patients with
anterior cord syndrome
!" Epidural hematoma (1%-2%); spinal cord
edema/hematoma
!" Ligamentous disruption; cervical
spondylosis
!" Subsequent complications
!"Syringomyelia, myelomalacia
MR Imaging: Spinal Cord Injury

!" Intramedullary swelling
!"T1-W: increased cord caliber Figure 29 A, B, C & D
!"T2-W: increased signal
Sagittal T1-W and T2-W MR images show high signal
!" Intramedullary edema intensity in the spinal cord (yellow arrows) that
!"T2-W: increased signal subsequently reveal low signal intensity on T2-W on a
!" Intramedullary hemorrhage follow-up MR all indicative of hemorrhage as seen on
!"Variable MR appearance (often the gross specimen (black arrows).
heterogeneous)
!"Poor prognostic sign
MR Imaging:
Intramedullary Hemorrhage [Figure 29]
!" Oxyhemoglobin
!"Hyperacute (minutes to hours,
< 24 hours)
!"Intermediate signal T1-W
!"High signal T2-W
!" Deoxyhemoglobin
!"f7&/''<)$-7()X=)9*&-7
!"Can be up to 8 days with hypoxia
!"Intermediate signal T1-W
!"Low signal T2-W
!" Methemoglobin
!"Usually after 24 hours (3-14 days)
!"High signal T1-W (begins peripherally)
!"Low signal T2-W (early subacute
intracellular)
!"High signal T2-W (late subacute
extracellular)

References
1. Blackmore CC, Mann FA, Wilson AJ. Helical CT in the primary trauma evaluation of the cervical spine: an
evidence-based approach. Skeletal Radiol 2000 Nov;29(11):632-9. Review.
2. Jarolimek AM, Coffey ECC, Sandler CM, West OC. Imaging of uppercervical spine injuries - Part III: C2
below the dens. Applied Eadiology 2004 July; 9-21
3. Murphey MD, Batnitzky S, Bramble JM. Diagnostic imaging of spinal trauma. Radiol Clin North Am 1989
Sep; 27(5):855-72.Stabler A, Eck J, Penning R, Milz SP, Bartl R, Resnick D, Reiser M. Cervical spine:
postmortem assessment of accident injuries - comparison of radiographic, MR imaging, anatomic, and
:/(9*'*2"%)$.+".27S)L/+"*'*2<)XAA@);*EYXX@0X4[5=A?eS
4. Daffner RH, Hackney DB. ACR Appropriateness Criteria on suspected spine trauma. J Am Coll Radiol
2007;4:762-75.
5. Miyanji F, Furlan JC, Aarabi B, Arnold PM, Fehlings MG. Acute cervical traumatic spinal cord injury: MR
"8/2".2)$.+".27)%*--,'/(,+)a"(9).,&-*'*2"%)*&(%*8,??:-*7:,%("E,)7(&+<)a"(9)@AA)%*.7,%&("E,):/(",.(7S)
Radiology 2007;243:820-7.

978
Musculoskeletal Seminar I
Mark D. Murphey, MD
Unknown Case History 1: History
!" A 15-year-old boy with longstanding
hindfoot pain
Unknown Case 1:
Differential Diagnosis: Lesions with
Sequestra-Like Appearance
!" Osteomyelitis
!" Metastasis
Unknown Case History 1: Findings
!" K"1-*7/-%*8/D8/'"2./.()$1-*&7)
!" Diffuse sclerosis of calcaneus
histiocytoma (MFH)
!" CT: solid periosteal reaction causing
!" Lymphoma
sclerosis on radiographs
!" Osteoblastoma
!" Subchondral low density lesion with
Unknown Case 1: %,.(-/')%/'%"$%/("*.
!" Diffuse edema/focal lesion related to
Differential Diagnosis Cortical Lucency/
posterior subtalar joint with joint effusion
Central C*%$-4$*)-&,
!" Langerhans cell histiocytosis Unknown Case 1: Osteoid Osteoma
!" Osteoid osteoma !" 10-25 years, M > F = 3:1
!" Brodie abscess !" Night pain relieved by ASA
!" Lytic nidus (< 1.5-2.0 cm); central CA++
!" Intracortical: extensive periosteal reaction
!" Intramedullary: often subtle little sclerosis
!" Lymphofollicular synovitis
!" CT/MRI important for surgical guidance
Musculoskeletal Seminar I 979 Musculoskeletal Radiology

Unknown Case 1: Osteoid Osteoma
Treatment Options
!" Surgical excision
!" Percutaneous removal
!" Percutaneous ablation
!" Medical
Unknown Case 2: History

!" A 27-year-old woman with 5-year chronic
left hip pain
Unknown Case 2: PVNS

!" Young men – third to fourth decade
!" Synovial proliferation with hemosiderin
deposition
!" Extrinsic erosions common in hip
!" Joint space normal; limited osteopenia
!" Can appear like OA in hip
!" R*".()C&"+?.*+&'/-)(9"%W,.".2)/()
arthrography
!" VLU)*#(,.)%9/-/%(,-"7("%)'*a)".(,.7"(<M)C&"+)
foci
!" Treatment: synovectomy-adjuvant
radionuclide therapy

!" A 5-year-old boy with mild midfoot pain
Unknown Case 2: Osseous Lesions Both

Sides of the Joint
!" Arthritis
!" Infection
!" PVNS
!" Synovial chondromatosis
!" Amyloidosis

Unknown Case 3: Osteochondroses
!" Fragmentation
!" Sclerosis
!" Collapse
!" AVN, trauma, normal
Unknown Case 3: Kohler Disease

!" Described in 1908
!" M > F = 4-6:1; 3-7 years old
!" Often asymptomatic
!" Unilateral (75%-80%)
!" ^g;I
!" Treatment: immobilization

!" A 13-year-old girl with 1 year of pain now Unknown Case 4: Brodie Abscess
severe and worsening !" Subacute osteomyelitis
!" Medullary or cortical lucency surrounding
sclerosis
!" Channel-like lesion may extend to or
across growth plate
!" S aureus
!" MRI or CT to evaluate soft tissue
extension

!" A 30-year-old woman with progressive
%'&11".2)*#)$.2,-7
Unknown Case 5: Band-like

Acroosteolysis - Differential Diagnosis
!" Hyperparathyroidism
!" Polyvinyl chloride
!" Hajdu-Cheney syndrome
!" Posttraumatic

Unknown Case 5: Differential Diagnosis
– Wormian Bones
!" Normal
!" Cleidocranial dysplasia
!" Cretinism
!" Osteogenesis imperfecta
!" Hypophosphatasia
!" Pyknodysostosis
Unknown Case 5:
Hajdu-Cheney Syndrome
!" Autosomal dominant; described in 1948
!" Bathrocephaly, wormian bones, open
sutures
!" Acroosteolysis
!" Poor dentition
!" Osteoporosis

!" A 4-year-old boy with left hip pain
Unknown Case 6: Differential Diagosis –

Epiphyseal Lesions
!" Chondroblastoma
!" GCT
!" Subchondral cyst/intraosseous ganglion Unknown Case 6:
!" Infection Eosinophilic Granuloma (LCH)
!" Langerhans cell histiocytosis (LCH) !" 5-15 years; M:F = 2:1
!" Osteoid osteoma/osteoblastoma !" 95% of patients Caucasian
!" Clear cell chondrosarcoma !" Solitary (67%)
!" Flat bones involved (70%)
Unknown Case 6: Findings
!" Lytic hole within hole appearance
!" Lytic lesion epiphysis and metaphysis
!" Diaphysis (58%), metadiaphysis (18%),
!" Small amount surrounding sclerosis
metaphysis (28%), epiphysis (2%)
!" VLU)/.+)FP)c).*)T*".()C&"+)*-)%/'%"$%/("*.

983
984
Musculoskeletal Seminar II
Mark D. Murphey, MD
Unknown Case 1: History Unknown Case 1: Findings
!" A 62-year-old man with polyarticular joint !" Asymmetric erosive arthritis hands and
pain feet: MCP and IP joints
!" New bone formation
!" Limited osteopenia
Unknown Case 1: Seronegative

Spondyloarthropathy Characteristics
!" Asymmetry
!" Bone production
!" Less juxtaarticular osteopenia
!" Distribution
Unknown Case 1: Psoriatic Arthritis

Possible Presentations
!" DIP and PIP joints
!" Arthritis mutilans
!" Oligoarthritis or ray distribution
!" Rheumatoid-like (rare)
!" Sacroiliitis/spondylitis

!" A 42-year-old woman with right lower
back pain
Musculoskeletal Seminar II 985 Musculoskeletal Radiology

Unknown Cases 2: Findings Unknown Case 3: Findings
!" Unilateral destruction on both sides right !" Q*#()("77&,)7a,''".2)/1*&()7,E,-/')$.2,-7
SI joint !" Periosteal reaction along several rays:
!" Thickening of iliacus muscle phalanx hand, metacarpal, and metatarsal
!" Focal sclerotic fragments in joint
Unknown Case 3:
Unknown Case 2: Differential Diagnosis - Dactylitis
Differential Diagnosis – Sacroiliitis !" Infection
!" Unilateral: infection, RA, gout, psoriatic, !"Pyogenic
Reiter !"Unusual organism: TB
!" Bilateral asymmetric: RA, gout, psoriatic, !" Sickle cell anemia (50% of children)
Reiter !" Thermal injury
!" Bilateral symmetric: AS, enteropathic,
psoriatic, Reiter, RA Unknown Case 3: Sickle Cell Anemia
!" Musculoskeletal changes
Unknown Case 3: History !"Osteomyelitis (up to 18%)
!" A 1-year-old girl with hand and foot pain (salmonella)
!"Avascular necrosis AVN (up to 50% by
age 35)
!"H-type vertebrae
!"Osteopenia
!"Diffuse sclerosis

!" An 11-year-old boy with ankle pain after
previous fracture
Unknown Case 4:
Salter-Harris Fractures
!" 25%-33% growth sequelae
!" Only 10% important
!" Follow for 2 years with X-rays
!" Look for bowing/shortening

!" A 38-year-old man with calf pain and
mass, no history of trauma

!" Initial Salter-Harris IV fracture without
good reduction
!" Q&17,b&,.()'/(,-/')1*a".2)*#)$1&'/)/.+)
tibia
!" Epiphyseal plate irregular
!" CT/conventional tomography: osseous bar
bridging plate

!" ;*.7:,%"$%),.9/.%".2)".C/88/("*.)
and edema in calf with more focal mass
medially
!" Biopsy: soft tissue osteosarcoma
!" 5)a,,W7)'/(,-M),/-'<)%/'%"$%/("*.)*.)FP)
predominantly peripheral
!" =)a,,W7)'/(,-M)(9"%W)-".+)*#)%/'%"$%/("*.)
peripherally
Unknown Case 5: Myositis O##-4$*,#+

(Heterotopic Bone Formation)
!" No history of trauma (25%)
!" Soft tissue mass
!" Q&17,b&,.()%/'%"$%/("*.
!" Zonal phenomenon X-ray and path
!" Follow-up for maturation

!" A 14-year-old girl with enlarging right foot
mass

C*%$-4(9+Soft Tissue Mass Unknown Case 6: Findings
!" Soft tissue mass plantar aspect mid- to
!" V<*7"("7)*77"$%/.7
forefoot
!" Gout, collagen vascular disease
!" K/".()%/'%"$%/("*.[)FP)/.+)8/2)E",a7Y)
!" Hyperparathyroidism, tumoral calcinosis
smooth erosion of 2nd and 3rd
!" Hemangioma
metatarsals
!" Soft tissue chondrosarcoma/osteosarcoma
!" Large soft tissue mass on MRI mildly
!" Synovial sarcoma
heterogeneous and hyperintense T2-W

Unknown Case 6: Synovial Sarcoma
!" 20-40 years old
!" 68% lower extremity – particularly knee
!" Most begin periarticular
(< 10% intraarticular)
!" Biphasic: epithelioid and spindle cell
element on histo (also monophasic)
!" Radiographs: soft tissue mass, joint
,##&7"*.)0@A6?XA64M)%/'%"$%/("*.)05A64M)
erosion or destruction adjacent bone
!" Metastases: lungs and lymph node

990
Musculoskeletal Seminar III
Mark D. Murphey, MD
!" A 63-year-old woman with vague calvarial
pain
Paget Disease
!" Common: 3% of people over 40 years old
!" Lytic, blastic, or mixed phases
!" Most frequent to involve: spine, skull,
pelvis
!" Trabecular thickening: bone enlargement
Paget Disease: Complications

!" Osseous deformity
!" Fractures
!" Neurologic symptoms
!" Arthropathy
!" Neoplasm

!" A 14-year-old boy with thigh pain

– Lytic Skull Lesions
!" Metastases
!" Myeloma
!" Paget disease
!" Brown tumor

!" Focal skull lytic lesions: frontal and
parieto-occipital
!" Bone scan: multifocal area increased
activity
!" Radiographs: multiple lesions trabecular
thickening
Musculoskeletal Seminar III 991 Musculoskeletal Radiology

!" Cortical scalloping - femur
!" “Hair-on-end” periosteal reaction
!" Broad-based soft tissue mass
!" No medullary involvement
Unknown Case 2: Periosteal

Osteosarcoma
!" Most chondroblastic
!" 85% diaphysis femur/tibia
!" Same age group as conventional
osteosarcoma
!" Better prognosis

!" A 55-year-old man with hip pain

!" Osteopenia of left hip
!" MRI: decreased intensity left proximal
femur T1-W and diffuse increased signal
T2-W
!" No focal defects on MRI; effusion
!" Enhances with gado; hot on BS
!" Returns to normal in several months
Unknown Case 3:
Transient Osteoporosis Hip/
Bone Marrow Edema Syndrome
!" Middle-aged men
!" Spontaneous pain; worsened by weight-
bearing
!" Symptoms regress in 2-6 months
!" Migratory form may recur at nearby joint
!" Cause unknown: bone marrow edema
!" L,'/("*.79":)(*)^g;I

!" An 82-year-old man with slowly enlarging
mass in the thigh

!" Large mass thigh with mineralization
%/'%"$%/("*.D*77"$%/("*.
!" MRI/CT:
!"Fat component
!"Hemorrhagic component
!"Myxoid component
Unknown Case 4: Myxoid Liposarcoma

!" Myxoid variety second most common type
of liposarcoma (30%-40%)
!" Intermediate grade
!" See lipomatous components with CT/MRI
Unknown Case 4: Differential Diagnosis (40%-50%) (We believe 90%-95% by
– C*%$-4(9+Soft Tissue Mass MR)
!" V<*7"("7)*77"$%/.7 !" Mineralization not rare in liposarcoma
!" Aneurysm
!" Lipoma/liposarcoma
!" A 40-year-old woman with arthralgias
!" Soft tissue osteosarcoma/chondrosarcoma
!" Synovial sarcoma

!" Interphalangeal joint subluxations
!" No erosions
!" Osteopenia

- Subluxations/No Erosions
!" Systemic lupus erythematosis (SLE)
!" Mixed connective tissue disease (MCTD)
!" Juvenile chronic arthritis
!" Ehlers-Danlos syndrome
!" Jaccoud arthropathy

Unknown Case 5: SLE Unknown Case #6: Differential
!" Musculoskeletal changes Diagnosis – Benign Polyostotic Lesions
!"Deforming nonerosive arthropathy !" Langerhans cell histiocytosis
!"Tendon rupture !" Enchondromatosis
!"Avascular necrosis (AVN) !" Fibrous dysplasia
!"Joint and bone infection !" Hereditary multiple exostoses
!"Acrosclerosis !" Paget disease
!" ;,&-*$1-*8/(*7"7)0(<:,)@4
Unknown Case 6: History !" Angiomatous lesions
!" 37-year-old woman with progressive
ankle deformity
!"N9/()"7)(9,)&.+,-'<".2)+"7,/7,I
!"What process involves the ankle
7&17,b&,.('<I
!"_*a)%/.)(9,):-*%,77,7)1,)%*--,'/(,+I
Unknown Case 6: Neuropathic Joint

!" Cause: pain sensation vs neurovascular
!" Destruction, debris, density increase,
disorganization
!" Diabetes, syphilis, cord damage – syrinx

!" Lytic expansile benign-appearing
polyostotic lesions
!" Fibula, femur, metatarsal
!" Subsequently ankle – fragmentation,
debris, destruction, increased density
Unknown Case 6: Fibrous Dysplasia

!" Endocrine abnormalities
!"Sexual precocity
!"Cushing disease
!"Acromegaly
!"Hyperthyroidism
!"Diabetes mellitus (hypothalamic
dysfuntion)
!"!"/2.*7"7)%/7,)e[)$1-*&7)+<7:'/7"/)
(polyostotic) with neuropathic ankle
due to diabetes mellitus

995
996
Musculoskeletal Seminar IV
Mark D. Murphey, MD
!" Several patients with various wrist
subluxation patterns: match with pattern
!"Lunate
!"Perilunate
!"Barton fracture/subluxation
Unknown Case 1: Wrist Subluxations

!" Perilunate: 75%; usually with
transscaphoid fracture rest of carpus-
dorsal
!" Lunate: 25% lunate rotated volar, capitate
remains aligned to radius
Unknown Case 1: Wrist Subluxations

!" Barton: fracture of dorsal rim of radius
with dislocation of carpus
!" Reverse Barton: fracture of volar rim of
radius – with dislocation of carpus
Musculoskeletal Seminar IV 997 Musculoskeletal Radiology

!" A 31-year-old woman with underlying
systemic disorder

!" Dysplastic changes thoracolumbar
junction
!" Short segment scoliosis
!" Posterior vertebral body scalloping

Posterior – Vertebral Scalloping
!" Normal variant L4-5
!" ;,&-*$1-*8/(*7"7)0(<:,)@4
!" Tumor/increased intraspinal pressure
!" Achondroplasia
!" Acromegaly
!" Ehlers-Danlos, Marfan,
osteogenesis imperfecta
!" Mucopolysaccharides

- Dysplastic Thoracolumbar Junction
!" ;,&-*$1-*8/(*7"7)0(<:,)@4
!" Cretinism
!" Idiopathic
!" Achondroplasia
Unknown Case 2: N("1&4:1&8*)&#-#+

Type 1 Musculoskeletal Manifestations
!" Cranium: enlarged empty orbit, left
lambdoid suture defect
!" Spine: scoliosis, posterior vertebral
scalloping, lateral meningocoeles
!" Pseudarthrosis (3.6%-5%) (tibia),
bowing, fractures
!" Ribbon ribs
!" ;,&-*$1-*8/[)>6)8/'"2./.()
degeneration
!" Localized gigantism
!" V&'(":',).*.*77"#<".2)$1-*8/7

!" A 13-year-old boy with bilateral hip pain

Unknown Case 3: Differential Diagnosis Unknown Case 3: Musculoskeletal
– Irregular Epiphyses (Multiple) Changes in Hypothyroidism
!" Normal variant !" Delayed skeletal maturation,
!" Avascular necrosis (AVN) wormian bones
!" Hypothyroidism !" Epiphyseal dysgenesis with osteoarthritis
!" Epiphyseal dysplasia !" Thoracolumbar junction gibbus
!" Trevor disease !" SCFE; ligamentous laxity
!" Mucopolysaccharidosis !" B7(,*:*-*7"7Y)7*#()("77&,)%/'%"$%/("*.
!" Soft tissue edema, carpal tunnel
syndrome
Unknown Case 3:
Epiphyseal Dysgenesis
!" B77"$%/("*.)#-*8)8&'(":',)7"(,7
!" Femoral, humeral centers and talus
!" ;*()+&,)(*)E/7%&'/-)".7&#$%",.%<
!" May disappear with treatment
!" May lead to premature osteoarthritis (OA)

!" A 45-year-old man with wrist pain

!" Multiple irregular epiphyses
!"Bilateral femora Unknown Case 4: Differential Diagnosis
!"Right humerus – Chondrocalcinosis
!" Delayed skeletal maturation !" CPPD deposition/arthropathy
!" Changes of slipped capital femoral !" Hemochromatosis
epiphysis (SCFE) !" Hyperparathyroidism
!" All other poor associations
Unknown Case 3: Causes of SCFE
!" Idiopathic Unknown Case 4: Findings
!" Rickets – renal !" Osteoarthritic changes: unusual locations
!" Trauma, obesity radiocarpal and MCP joints (2nd through
!" Hypothyroidism, hypoparathyroidism 5th)
!" Radiation !" Chondrocalcinosis: TFFC, no scapholunate
separation
!" Hook-like osteophytes metacarpal heads

Unknown Case 4: Hemochromatosis –
Musculoskeletal Changes
!" Osteoporosis
!" Chondrocalcinosis (20%-60%)
!" Arthropathy (24%-50%) looks like OA
!" Differences from CPPD arthropathy –
involvement of 4th and 5th MPC joints;
hook-like osteophytes metacarpal heads;
less scapholunate separation; pericapitate
narrowing

!" A 39-year-old woman with lower back
pain

– Narrow Disk Space
!" Degenerative disk disease (DDD);
herniated disk (trauma)
!" U.C/88/(*-<)/-(9-"("7
!" Scheuermann disease
!" Osteomyelitis
!" Neoplasm (very rare)
!" Amyloid – CRF

!" Rapid disk space narrowing L2-3 over 2
week interval
!" Subtle endplate destruction L2-3 level
!" T1-W MR: marrow replacement L2-3 with
disk involvement
!" T2-W MR: increased marrow intensity
L2-3 with disk involvement
Unknown Case 5:
Infectious Spondylodiscitis
!" Usually starts in anterior subchondral
bone then spreads rapidly to disk
!" Bacterial vs unusual cause (TB)
!" Drug abusers predisposed

!" A 68-year-old woman with history of
bilateral breast cancer and left distal thigh
pain

!" Mixed lytic and sclerotic lesion distal
femur
!" Matrix on radiograph: chondroid
!" Cortical permeation and periosteal
reaction
!" Pathologic fracture and soft tissue mass
!" Soft tissue mass best seen on MRI
!" Two different signal patterns in
intraosseous and soft tissue components

- Chondroid Lesion
!" Benign
!"Enchondroma, bone infarct,
chondroblastoma, CMF, osteoblastoma
!" Malignant
!"Chondrosarcoma: intramedullary,
juxtacortical, clear cell, mesenchymal,
myxoid, dedifferentiated extraskeletal
Radiologic Differentiation of
Chondrosarcomatous Lesions
!" Aggressive chondroid lesion with soft
tissue mass
!"High-grade conventional
chondrosarcoma
!"Mesenchymal chondrosarcoma
!" H/-2,)C&"+)%*8:*.,.()1*.,)*-)7*#()("77&,
!"Myxoid chondrosarcoma
!" Change (rapid) in appearance or two
differing foci (collision two tumors) and
aggressive morphology
!"Diagnosis: dedifferentiated
chondrosarcoma

1005
1006
Musculoskeletal Seminar V
Mark D. Murphey, MD
!" A 60-year-old man with 6 months of knee
pain
!"Biopsied and diagnosed as myeloma
!"U7)(9"7)/)(,./1',)+"/2.*7"7I
!"What is the correct diagnosis and why
a/7)(9,)"."("/'):/(9*'*2<)".%*--,%(I

!" Radiographs: geographic IA lesion with
channel/tract-like component inferiorly
(subtle)
!" MRI: marrow replacement T1-W
!"L"8),.9/.%,8,.()0C&"+?$'',+)8/774
!"Homogeneous very high signal T2-W
!"Surrounding edema
!"Tract-like component inferiorly
!" Differential diagnosis: UBC, ABC (no
expansion) intraosseous hematoma,
ablated lesion, Brodie abscess
Unknown Case 1: Subacute

Osteomyelitis Brodie Abscess
!" Described in 1832 – chronic/subacute
!" N/'',+?*##)a"(9)%,.(-/')C&"+M)*#(,.)7(,-"',)
(Staph – only cultured in 50% of cases)
!" Children (M > F), metaphysis, tibia
!" Intramedullary; channel-like lucencies
!" May cross growth plate or be cortical
!" Periosteal reaction/sequestra may be seen
Unknown Case 1: Brodie Abscess

!" Biopsied at margin in reactive tissue
!"Led to erroneous diagnosis
!" Myeloma (untreated) not a tenable
diagnosis
!"As this is a solid lesion
!"Importance of radiologic/pathologic
correlation
Musculoskeletal Seminar V 1007 Musculoskeletal Radiology

!" A 59-year-old veteran involved in mild
Vg^)0$-7()$'84)a"(9):-*2-,77"E,):/".)
07,%*.+)7,()*#)$'87)5)a,,W7)'/(,-)/.+)
MRI)

!" Relatively rapid destruction of shoulder
!" Fragments in joint
!" Sharp “surgical” margin
!" MRI: replacement of humeral head with
high intensity on T2-W
!" History of drained syrinx (40 years ago)
and cervical spine MRI shows severe
myelomalacia
Unknown Case 2: Neuropathic Shoulder

– Syrinx
!" Cause: pain sensation vs neurovascular
!" Radiologic: destruction, debris, density
increase, disorganization
!" Diabetes, syphilis, cord damage - syrinx
Second
radiograph 3
weeks prior to Unknown Case 3: History
&"%!*"#)31E"#:6,D !" A 15-year-old boy with hip pain

!" Marrow replacement right femoral neck
T1-W
!"Medial transcervical region
!" High signal on STIR
!"Surrounding edema periosteum/ST
!"Horizontal low signal linear band
medially
!" Subsequent near total resolution

Stress Fracture: Femur
!" Medial femoral neck: fatigue type
!"Heal with symptomatic treatment
(3-12 months)
!"Crescentic MR abnormality above
lesser trochanter
!" H/(,-/')#,8*-/').,%W[)".7&#$%",.%<)(<:,)
!"Possible cause most subcapital
fractures
!"Do not heal: complete/displaced
!"Garden staging (< grade 2
percutaneous pins) (> grade 2 THA
due to development of AVN)
!" Usually horizontal/oblique rarely
longitudinal
!"Thigh splints (stress reaction)

!" A 23-year-old man with knee pain,
masses, and lesions on radiographs
!"Diagnosis of bone lesions
!"Underlying condition
N("1&4:1&8*)&#-#+Type 1:
Skeletal Manifestations
!" Mesodermal dysplasia
!" Kyphoscoliosis
!" Facial, orbital, lambdoid suture (left)
defects
!" V&'(":',).*.*77"#<".2)$1-*8/7
!" Meningocele
!" Posterior vertebral scalloping
!" Rib deformity (ribbon ribs)
!" Congenital pseudarthrosis (tibia)
!" Focal hypertrophy (gigantism)
!" H*%/'"`,+).,&-*$1-*8/[)8*7()%*88*.
!"Least characteristic, often deep/
multiple
!"Q&:,-$%"/')',7"*.7)0$1-*8/)
molluscum)
!" G',3"#*-8).,&-*$1-*8/[):/(9*2.*8*."%
!"Early childhood
!"G-,%,+,7)%&(/.,*&7).,&-*$1-*8/7

!" A 53-year-old man with lateral knee mass
and pain
Unknown Case 5: Findings Ganglion/Synovial Cyst

!" P"1"*$1&'/-D'/(,-/')("1"*#,8*-/')T*".() !" Etiology unknown: neoplasm, trauma,
osteoarthritis ".C/88/(*-<
!" _"29)C&"+)%*.(,.()8&'("'*%&'/-)8/77) !" Young adults: most common mass hand/
laterally wrist
!"Multilocular/surrounding edema !" Pain: may affect adjacent nerves
!"^::,/-7)(*)/-"7,)#-*8)("1"*$1&'/-)T*".( !" Location
!"Components in bone (tibia and femur) !"ST: hand, foot, knee, hip, shoulder
and soft tissue !"Intraosseous: medial malleolus, wrist,
!" Differential diagnosis: ganglion/synovial knee
cyst, myxoid tumor !"BOTH
!" Thick-walled unilocular/multilocular
!"High protein content affects CT/T1-W
MR
!"Walls/septa may enhance
!" CT/MRI/sono: cystic mass
!"May rupture causing surrounding
edema
Case 6: History
!" A 47-year-old woman with mid to low
back pain
!"V*7()'"W,'<)+"/2.*7"7I
!"Pa*)*(9,-):*77"1',)+"/2.*7,7I

!" Multifocal bone scan areas increased
radionuclide activity
!"Spine, SC joints, SI joints
!" CT: multifocal sclerosis
!"Anterior/posterior paralleling
endplates
!"Erosions/bone production
costovertebral joints
!"Cause of hot bone scan
!" MRI: multifocal areas marrow abnormality
!"Low T1-W, high T2-W/STIR
!"Anterior/posterior paralleling
endplates
!"No soft tissue mass
!" Radiographs: subtle sclerosis, sacroiliitis
!" Differential diagnosis: metastases,
myeloma, lymphoma

Ankylosing Spondylitis:
!" Peak age of onset 15-35 years
!" M:F = 3-5:1
!" Incidence: 6.6/100,000
!" HLA-B27 > 90%
!" Predilection axial involvement
Ankylosing Spondylitis: Distribution

!" Osseous ankylosis
!" H"2/8,.(D(,.+*.)*77"$%/("*.
!" Spine/SI joints
!"Symmetric
!" Pelvis: symphysis, ischium, iliac, hips
!" Peripheral changes unusual early
(10%-50%)
!"Asymmetric
Ankylosing Spondylitis: Spine Change

!" Osteitis – ”shining corners”
!" Squared vertebral bodies
!" Syndesmophytes
!" Bamboo spine
!" F/'%"$,+)+"7%M)#&7,+)#/%,(7D'"2/8,.(7
!" Pseudarthrosis/fractures
!" Atlantoaxial disease/cauda equina
!" Other diagnoses: Reiter/psoriatic, SAPHO

1013
1014
MRI of the Knee: Part 1
Lecture Outline Summary: Pulse Sequences
!" Part 1 !" Menisci
!"Technique !"Short TE (T1, PD, GRE) – caution with
!"Menisci fast spin echo
!" Articular Cartilage !" Bone marrow
!" Part 2 !"Fat saturation (STIR, fat sat FSE T2) –
!"Bones not GRE
!"Stabilizers !"T1-W in one plane
!"Miscellaneous !" Other soft tissues (ligaments, tendons)
!"T2-W with fat saturation (STIR, fat sat
Technique FSE T2)
!" Surface coil !" Cartilage
!" High resolution !"F*.(-/7()1,(a,,.)C&"+)/.+)%/-("'/2,
!" T1, T2, fat saturation
!" Sagittal, coronal, axial planes Menisci [Figures 1 & 2]
!" Fibrocartilage
Technique: Pulse Sequences !" Medial/lateral
!" T1 !" Functions:
!"Anatomy !"Joint congruity
!"Bones (marrow) !"Shock absorption
!"Fat/hemorrhage !"Load transmission
!"Muscle (atrophy) !" Segments
!"(Menisci) !"Anterior horn
!" Proton density !"Body
!"Menisci !"Posterior horn
!"Cartilage
!"Fat saturation
!" T2
!"Pathology
!"Fluid/edema
!"Soft tissue injury
!" Fast spin echo (T2)
!"Fast acquisition
!"Caution:
#" Bright fat: T2 (marrow pathology)
#" Blurring effect: proton density
Figure 1
(meniscal tears)
!" Gradient echo (T2*) Cadaveric dissection showing medial and lateral
!"Menisci menisci from above.
!"Articular cartilage (3D)
!"$ susceptibility effects
#" Good
#" Bad
!"Caution: marrow pathology
!" STIR (fat suppressed T2)
!"Marrow pathology
!"Soft tissue injury
!"Articular cartilage
MR Arthrography
!" MR arthrography
!" 0.2 cc Gd + 20 cc saline (off label use) Figure 2 A, B & C
!" T1W with fat saturation A. Diagram of a meniscus cut in cross section (black
!"Postoperative meniscus dashed line = superior articular surface; white dashed
!"Cartilage repair assessment line = inferior articular surface).
B. Sagittal image through the posterior horn of the
medial meniscus.
C. Arthroscopic view of a normal meniscus (F =
femoral condyle; T = tibial plateau).
MRI of the Knee: Part 1 1015 Musculoskeletal Radiology
Medial Meniscus [Figure 3]
!" Larger “C”
!" Posterior horn > anterior horn
Figure 5
!" Covers 1/2 contact surface of tibial
plateau Transverse
intermeniscal
ligament
(arrows).
Figure 3 A, B,
C&D
Figure 6
Sagittal gradient
echo images
(corresponding Diagram of
to lines on the knee
diagram) (posterior view)
through demonstrating the
the medial meniscofemoral
meniscus. ligament of
Wrisberg (arrow).
Lateral Meniscus [Figure 4]

!" Tighter “C”
!" Posterior horn = anterior horn
!" Covers 3/4 contact surface of tibial
plateau Menisci: Variants [Figure 7]
!" Posterolateral corner !" Discoid
!"Popliteus tendon !"Enlarged meniscus
!"Meniscal fascicles !"Lateral > medial
!"Prone to tear
!" Buckled
!"m'/3lM)mC*&.%,l
!"Medial mensicus
!"Positional
!" Ossicle
!"g,7("2"/'M):*7((-/&8/("%I
!"May be symptomatic
Figure 4 A, B, !"PHMM most common
C&D
!"Variable MRI SI
Sagittal Park JS, et al. Meniscal Flounce on Knee MRI:
gradient
echo images
Correlation With Meniscal Locations After Posi-
(corresponding tional Changes. AJR. 2006.
to lines on
diagram)
through
the lateral
meniscus.
Menisci: Attachments [Figures 5 & 6]

!" Ligaments
!"Transverse Figure 7 A & B
!"Meniscofemoral
A. Diagram illustrating a discoid lateral meniscus (L)
#" Humphrey from above.
#" Wrisberg B. Normal-sized medial meniscus (thin arrow) and
enlarged, discoid lateral meniscus (large arrow).

Meniscus Meniscal Tears [Figure 9]
!" Microstructure !" Vertical
!"Collagen bundles !"Radial
#" Circumferential !"Longitudinal
#" P-/.7E,-7,)0m(",)$1,-7l4 !"Traumatic
!"Resist longitudinal loading !"Result in anterior/posterior or medial/
#" “Hoop stresses” lateral fragments
!" Horizontal
Menisci: Pathology !"Degenerative
!" Degeneration !"Result in superior/inferior fragments
!" Tear
!"Traumatic vs degenerative
!" Surgeon’s goal
!"Preserve as much meniscus as
possible
Meniscal Tear: MRI

!" Abnormal Figure 9 A, B & C
!"Signal intensity
A. Radial tear. B. Longitudinal tear. C. Horizontal
!"Morphology tear.
Meniscal Tear: MRI [Figure 8]
!" Signal intensity (grades)
!"1: Globular Meniscal Tear: Radial [Figures 10 & 11]
!"2: Linear !" Perpendicular to axis
!"3: Contact with articular surface !" !" Vertical
%"TEAR !" U--,:/-/1',I
!" 20% asymptomatic patients > age 50 !"Always involve white zone
show MR evidence of tear
!" Morphology
!"Irregular Figure 10
!"Truncated
!"Size (large or small) Diagram of a
radial tear of
the meniscus.
Figure 11 A & B
Radial tear involving the body of the lateral meniscus
(arrow).
Meniscal Tear: Longitudinal [Figure 12]

!" Vertical
!" Long axis of meniscus
Figure 8 A & B
!"Peripheral
A. Diagram of a meniscus cut in cross section revealing #" Potentially reparable
an oblique undersurface tear. #" Outer 1/3 (red zone)
B. Similar tear in the posterior horn of the medial
meniscus on sagittal image.
!"Bucket handle
#" Displaced fragment

Figure 14
Figure 12
Diagram of
Longitudinal a bucket
tear. handle
tear of the
meniscus.
Meniscal Tear: Horizontal [Figure 13]

!" Often degenerative
!" Older patients
!" May be asymptomatic
!" Meniscal cysts
!"Parameniscal
!"Intrameniscal
Figure 13
A&B
A. Diagram of Figure 15 A & B

a horizontal
tear. B. Coronal image corresponding to the dashed line
Horizontal tear demonstrates the displaced meniscal fragment of
of the body of this bucket handle tear (large arrow) and irregular,
the meniscus truncated body of the mensicus (thin arrow).
(large arrow)
and an
associated
parameniscal
cyst (small
arrow).
Displaced Meniscal Tears [Figures 14 to 18]

!" Bucket handle
!"Medial meniscus
!"!"7:'/%,+)C/:)c).*(%9
!"“Too few bow ties”
!"“Double PCL”
!" Flipped Figure 16 A & B
!"Lateral meniscus
Sagittal image corresponding to the dashed line shows
!"“Double ant horn” the large bucket handle fragment within the notch
!"“Too much meniscus” (arrows) creating the “double PCL” sign (P = PCL).
!" Gutter

Menisci: Postsurgical
!" Truncated, absent, “normal”
!" Healed tear can look like new tear
!"H**W)#*-)C&"+)".)(,/-
!" MR arthrography (off label use)
!"Gd extending into tear
Meniscal Tear: Pitfalls

!" Anatomy
!"Transverse ligament
Figure 17 A & B
!"Meniscofemoral ligaments
!"Oblique meniscomeniscal ligament
SD*X3#E"#>*14*#*Y?3::()Z*@01$E3!.)3$#0A*>($3%/#0*!(#"D** !"Lateral inferior geniculate artery
B. Sagittal image at the level of the dashed line !"Popliteus tendon
%61<%*!6(*?3::()*4"#E>($!*@%61"!*#""1<A*#)G#/($!*!1* !"Edge artifact
the anterior horn (long arrow) creating the “double
!" Artifacts
anterior horn” sign. Note also the small residual
posterior horn (circle). !"Patient motion
!"Phase artifact (artery)
!"Magic angle
!"Gas/hemosiderin
!"Chondrocalcinosis
Figure 18 A & B
A. Coronal image demonstrating a displaced meniscal

fragment along the medial joint line (arrow).
QD*X3#E"#>*300.%!"#!3$E*!6(*61"3K1$!#0*!(#"*#$)*?3::()*
fragment.
References
1. Anderson MW. MR imaging of the meniscus. Radiol Clin North Am 2002 Sep;40(5):1081-94.
2. DeMaeseneer M, Shahabpour M, Vanderdood K, Van Roy F, Osteaux M. Medial meniscocapsular
separation: MR imaging criteria and diagnostic pitfalls. Eur J Radiol 2002;41:242-52.
3. !,Q8,()^^M)V&W9,-T,,)LS)F'"."%/'M)VLU)/.+)/-(9-*7%*:"%)$.+".27)/77*%"/(,+)a"(9)#/"'&-,)(*)+"/2.*7,)/)
lateral meniscal tear on MRI. AJR Am J Roentgenol 2008;190:22-6.
4. DeSmet AA, Tuite MJ. Use of the “two-slice-touch” rule for the MRI diagnosis of meniscal tears. AJR Am J
Roentgenol 2006;187:911-4.
5. _/-:,-)hNM)_,'87)F^M)H/81,-()_Q)5-+M)_"22".7)H!S))L/+"/')8,."7%/')(,/-7[)7"2."$%/.%,M)".%"+,.%,M)/.+)
MR appearance. AJR Am J Roentgenol 2005 Dec;185(6):1429-34.
6. Sanders TG, Miller MD. A systematic approach to magnetic resonance imaging interpretation of sports
medicine injuries of the knee. Am J Sports Med 2005 Jan;33(1):131-48.
7. Vande Berg BC, Malghem J, Poilvache P, Maldague B, Lecouvet FE. Meniscal tears with fragments
displaced in notch and recesses of knee: MR imaging with arthroscopic comparison. Radiology 2005
Mar;234(3):842-50.
8. White LM, Schweitzer ME, Weishaupt D, Kramer J, Davis A, Marks PH. Diagnosis of recurrent meniscal
tears: prospective evaluation of conventional MR imaging, indirect MR arthrography, and direct MR
arthrography. Radology 2002;222:421-9.

1020
MRI of the Knee: Part 2
Lecture Outline Acute Trauma: Contusion
!" Part 1 !" Contusion, bone bruise
!"Technique !" Edema, hemorrhage
!"Menisci !" Trabecular bone
!"Articular cartilage !" Impaction
!" Part 2
!"Bones Acute Trauma: Contusion [Figure 2]
!"Stabilizers !" MRI
!"Miscellaneous !"U''?+,$.,+)8/-2".7
!"& T1, $ STIR
Bones: Injuries !"100% heal; 2-4 months
!" Acute !" Detection
!"Impaction (contusion, occult fracture) !"Explains symptoms
!"Avulsion !"Avoids unecessary surgery
!"Mechanism of injury
Bones !"May change Rx plan
!" Cortical
!"“Compact”
!"Subchondral plate
!" Cancellous
!"“Trabecular,” “spongy”
!"Dissipates forces
!"Supports subchondral plate
!"Protects cartilage
Acute Impaction Injuries: Spectrum

[Figure 1]
Figure 2
Focal contusion involving the posterolateral tibial

plateau.
Contusion Patterns: ACL Tear [Figure 3]

!" Lateral femoral condyle (sulcus terminalis)
!" Postlateral tibial plateau
!" Mechanism
!"Twisting/valgus impaction
!" Q:,%"$%
Figure 1 A, B, C & D !"95% (adults)
!"75% (children)
Spectrum of acute osseous injuries.
!" “Contrecoup”
!"Postmedial tibial plateau
!"Peripheral injury

Knee Stability
!" Primary motions
!"Flexion/extension
!"Rotation
Figure 3
!" Forces (tibia)
!"Ant/post
ACL contusion !"Varus/valgus
pattern (lateral
femoral !"Int/Ext rotation
condyle and !" Stabilizers
posterolateral !"Static (ligaments)
tibial plateau). !"Dynamic (muscles/tendons)
Knee Stabilizers
!" Central
!"ACL, PCL
!" Medial
!"MCL
!" Lateral
Patterns: Patellar Dislocation [Figure 4]
!"Biceps femoris tendon
!" Lateral dislocation
!"Lateral collateral ligament
!" Contusions
!"G*:'"(,*$1&'/-)'"2/8,.(
!"Lateral femoral condyle
!"Iliotibial band
#" Anterior/non-weight bearing
!" Anterior
!" Medial patella
!"Patellar retinacula
!" Medial retinacular injury
!" Cartilage injury Cruciate Ligaments [Figure 6]
!" Avulsion fracture !" Named for tibial attachments
!" Anterior (lateral)
!" Posterior (medial)
Figure 4
Patellar
dislocation
contusion
pattern
(lateral
margin
of lateral
femoral
condyle
and medial
patella).
Acute Trauma: Fracture [Figure 5]

!" Linear
!"T1
#" & SI Figure 6
!"STIR
Diagram of the knee (frontal view) demonstrating the
#" $ or & SI anterior (A) and posterior (P) cruciate ligaments.
ACL
!" Anterior plateau
!"Between tibial spines
!"Lateral meniscus
!" Restrains
!"Anterior tibial translation
!"Tibial rotation
!" Functional bundles
!"Anteromedial
#" P/&()".)C,3"*.
Figure 5 A & B !"Posterolateral
Occult fracture of the lateral tibial plateau on sagittal #" Taut in extension
T1-W and coronal fat-saturated T2-W images.

ACL: Sagittal [Figure 7] MCL [Figure 9]
!" Signal intensity !" Medial side of knee (3 layers)
!"Low/intermediate !"U[)7&:,-$%"/')#/7%"/
!"Striations !"UU[)7&:,-$%"/')VFH
#" Fiber geometry !"III: deep MCL (meniscus)
!" Morphology !" Posteromedial capsule
!"Taut !"B1'"b&,)$1,-7
!"Parallel !"“Postoblique ligament”
#" Intercondylar roof !" Semimembranosus
!"Dynamic
Figure 9
Medial
collateral
ligament:
%.:("&/3#0*
&+("%*@1:($*
arrows)
and deep
&+("%*@+0#/2*
arrows).
MCL [Figure 10]

!" Q&:,-$%"/')%*8:*.,.(
Figure 7 !" Deep component
Normal anterior cruciate ligament. !"Meniscofemoral
!"Meniscotibial (coronary)
!" Bursa
PCL [Figure 8]
!" Medial intercondylar notch
!" Posterior tibia
!"Between post horns
Figure 10
!"Below joint line
!" Meniscofemoral ligaments
Normal MCL
!"Humphrey, Wrisberg on coronal
!" Restricts posttibial translation STIR image
!"P/&()".)C,3"*. @%.:("&/3#0*
!" MRI &+("%*[*1:($*
arrows; deep
!"Homogenous, low-signal intensity
&+("%*[*%103)*
arrows).
Lateral Stabilizers [Figure 11]

Figure 8 !" Complex anatomy
!"Biceps femoris
PCL. #" Long/short heads
!"LCL
!"Popliteus tendon
!"G*:'"(,*$1&'/-)'"2/8,.(
!"K/1,''*$1&'/-)'"2/8,.(
!"Arcuate ligament
#" Medial/lateral limbs
!"Iliotibial band
!" “BLT”
Figure 11
Diagram
of lateral
stabilizers (B =
biceps femoris Figure 13
tendon; P
= popliteus
tendon; F Complete
[*&+.0#"* ACL rupture.
collateral
ligament; I =
iliotibial tract).
Posterolateral Corner
!" Biceps tendon
!" LCL (conjoined tendon)
!" Popliteus complex ACL Tear: MRI
!"Popliteus tendon !" Secondary signs
!"G*:'"(,*$1&'/-)'"2/8,.( !"Bone contusions
!"Popliteomeniscal fascicles !"Deep notch LFC
!"Segond fracture
Ligament Injuries: ACL [Figure 12] #" 10% ACL tears – fx
!" 75% of all ligament injuries #" 75%-100% fx – ACL tear
!"Twisting + valgus force !"“Anterior drawer” (uncovered PHLM)
!"Hyperextension
!" Associated injuries Postop ACL [Figure 14]
!"Meniscal tear (40%-70%) !" Graft
!"O’Donoghue triad !"Integrity
#" ^FHM)VFHM)8,+"/')8,."7%&70I4 !"Signal intensity
!" (Acute: lateral; chronic: medial) #" Variable, especially early
!" Roof impingement
!" “Cyclops” lesion
!"^.(,-"*-)/-(9-*$1-*7"7
Figure 12
ACL Tear: MRI [Figure 13]

!" MRI: 90%-95% accurate
!" Primary signs Figure 14 A & B
!"Edematous mass (48%) A. Normal ACL graft (dashed arrow).
!"Nonvisualization (18%) QD*5,/01:%*0(%31$*@#"!6"1&+"1%3%A*#01$E*=($!"#0*>#"E3$*
of ACL graft (arrow).
#" “Empty notch”
!"Disruption (11%)
!"Irregular, wavy, horizontal contour Ligament Injuries: PCL [Figure 15]
!"Focal $ SI !" Tear
!"^.(,-"*-)("1"/)c)C,3,+)W.,,
#" “dashboard” injury
!"Complete tear (45%)
!"Partial tear (47%)
!" Avulsion (8%)

Figure 15 Figure 17
Full thickness Tear of

PCL tear (mid- the lateral
substance). collateral
ligament
(arrow).
ITB Friction Syndrome

!" Lateral pain
Ligament Injuries: MCL [Figure 16] !" Abnormal contact ITB/LFC
!" Bursa develops
Grade Clinical MRI
!"Fluid collection/edema
1 Sprain Thickened
!"H/(,-/')-,%,77I
Irregular
Adj edema Extensor Tendons [Figure 18]
2 Partial tear Focal SI
!" Quadriceps
3 Complete tear Discontinuity !" Patellar
!" Tears
!"Trauma
!"Degeneration
#" Renal disease, steroids,
#" Rheumatoid arthritis, systemic
lupus erythematosus
!" Partial vs complete
Figure 16
Partial
tear of
proximal
MCL
(arrow). Figure 18
Extensor
mechanism
(quadriceps
and patellar
tendons).
Posterolateral Corner Injury [Figure 17]

!" Imaging diagnosis
!"Radiographs
#" Arcuate sign
#" Segond fracture
#" Anteromedial tibial fx (MRI)
!" MRI accuracy
!"ITB, biceps, LCL (90%-95%)
!"Popliteus tendon (85%) Patellar Tendinopathy
K/1,''*$1&'/-)'"2/8,.( !" “Jumpers knee”
!"G*:'"(,*$1&'/-)'"2/8,.()0e>64 !" Enlarged (proximal)
LaPrade. AJSM. 2000. !" $ Intrasubstance signal
Theodorou. Acta Radiol. 2005. !" Spectrum
!"Partial ! complete tears

Patellofemoral Syndrome Other Cystic Masses [Figure 20]
!" Anterior pain !" Meniscal cysts
!" Patellar tilt/subluxation !" Ganglia
!" Impingement of infrapatellar fat !"Intraarticular
#" (Cruciates)
“Cystic” Structures !"Intraosseous
!" Recesses #" (Cruciate insertions)
!" Bursae !" Vascular masses
!" Ganglia !"Aneurysm
!"Cystic adventitial disease
Normal Recesses
!" Suprapatellar “bursa”
!" Infrapatellar cleft
!" Popliteus hiatus
!" Gastrocnemius/semimembranosus
Figure 20
Bursae [Figure 19]
!" Prepatellar Popliteal
artery
!" Infrapatellar aneurysm
!"0Q&:,-$%"/'D+,,:4 (A).
!" Semimembranosus
!" Pes anserine
!" Tibial collateral
!" LCL – biceps femoris
Cystic Adventitial Disease

!" Cystic degeneration vessel wall
!" Popliteal artery common
!" Sudden onset claudication
!" VLU)$.+".27
!"Intramural cysts
!"Along long axis of vessel
!"Extrinsic compression
Figure 19 A & B !"MR angiography
A. Prepatellar bursitis.
B. Semimembranosus bursitis.
References
1. Barr MS, Anderson MW. The knee: bone marrow abnormalities. Radiol Clin North Am 2002
Sep;40(5):1109-20.
2. DeMaeseneer M, Van Roy F, Lenchik L, Barbaix E, DeRidder F, Asteaux M. Three layers of the medial
capsular and supporting structures of the knee: MR imaging-anatomic correlation. RadioGraphics
2000;20:Spec No. S83-9.
3. Fritz RC. MR imaging of meniscal and cruciate ligament injuries. Magn Reson Imaging Clin N Am. 2003
May;11(2):283-93.
4. LaPrade RF, Wentory FA, Fritts H, Gundry C, Hightower CD. A prospective magnetic resonance imaging
study of the incidence of posterolateral and multiple ligament injuries in acute knee injuries presenting
with a hemarthrosis. Arthroscopy 2007;23:1341-7.
5. Lee J, Papakonstantinou O, Brookenthal KR, Trudell D, Resnick DL. Arcuate sign of posterolateral knee
injuries: anatomic, radiographic, and MR imaging data related to patterns of injury. Skeletal Radiol
2003;32:619-27.
6. Mohana-Borges AV, Resnick D, Chung CB. Magnetic resonance imaging of knee instability. Semin
Musculoskelet Radio 2005 Mar;9(1):17-33.
7. Vinson EN, Major NM, Helms CA. The posterolateral corner of the knee. AJR Am J Roentgenol
2008;190:449-58.

MRI of the Wrist
MRI Technique
!" Supine (arm at side)
!" Prone (arm overhead)
!" Dedicated surface coil
!" High resolution parameters Figure 2
!"Thickness 1-3– mm
Scaphoid
!"Matrix 512 x 512 fracture.
!"FOV 10 cm
Technique: Pulse Sequences

!" T1: anatomy overview
!" T2*: ligaments, tendons
!" QPUL[)8/--*aM)C&"+
!" Gd: cyst/solid, infection
synovitis “screen” Scaphoid AVN [Figure 3]
!" Normal T1 = normal
Outline: Image Analysis !" & T1 & T2 = necrotic T1 & T2 $)p)II
!" Bones !" F*.(-/7(),.9/.%,8,.(I
!" Intrinsic ligaments !" P@).*.%*.(-/7(I
!"(SL, LTL)
!" TFCC
!" Tendons
!" Nerves
!" Masses
Bones: Normal
!" Signal intensity
!" Alignment
!"Sagittal alignment Figure 3 A & B
!"Ulnar variance
Scaphoid fracture with abnormal marrow signal
intensity throughout the proximal pole.
Occult Osseous Injuries [Figure 1]
!" Contusion AVN Lunate
!"Bone marrow edema !" Kienböck disease
!" Fracture !" Repetitive trauma, fracture, ulna (-)
!"Edema + fx line variance
!" End arteries
!" Central position
Figure 1
AVN Lunate: MRI [Figure 4]
!" Abnormal marrow signal
Occult !" &T1 &T2 = diagnostic; &T1 $T2 = earlier
fracture of stage
triquetrum. !" More than 50% of lunate
Figure 4
Scaphoid Fracture [Figure 2]
!" 16% not detected initially Avascular
!" Complications necrosis of
!"AVN the lunate
!"Nonunion (Kienböck
Disease
disease).
MRI of the Wrist 1027 Musculoskeletal Radiology

Ulnolunate Impaction [Figure 5]
!" Ulna plus variance
!" Degenerative changes
Figure 7
!"Especially lunate
!" TFC tears
Small
scapholunate
ligament
perforation.
Figure 5
Ulnolunate Carpal Stability

impaction !" Scaphoid '% Lunate '% Triquetrum
syndrome.
Scapholunate Dissociation [Figure 8]
!" Tear or stretching of SLL
!"!*-7/')$1,-7
!"Q%/:9*"+):/'8/-)C,3,7
#" “Signet ring” deformity
!" H&./(,)+*-7"C,3,7
#" S-L angle > 60°
!" DISI deformity
Intrinsic Ligaments [Figure 6]
!"Can result from scaphoid fx
!" Scapholunate
!"“Humpback” deformity
!"g*'/-[)*1'"b&,)%*''/2,.)$1,-7
!"V"++',[)(9".)$1-*%/-("'/2,
!"Dorsal: strong transverse bundles
!" Lunotriquetral
!"Smaller (2 mm)
!"Q(-*.2,7()$1,-7[)E*'/-
Figure 8
!"Close to TFC
Dorsal
intercalated
segmental
instability
(DISI)
deformity.
S-L Instability: SLAC Wrist [Figure 9]

!" Scapho
!" Lunate
!" Advanced
!" Collapse
!" DISI
!" Arthropathy
!" Trauma, RA, CPPD
Normal scapholunate ligament (cadaveric specimen
and coronal MR images).
Ligament Pathology [Figure 7]

!" Absent
!" Distorted/elongated
!" Widened joint
!" Discontinuous
Figure 9 A & B
!" Fluid signal on T2
SLAC wrist.

Lunotriquetral Instability [Figure 10]
!" LTL tear
!" Associated with TFC tears
!" VISI deformity
!" !"#$%&'()+"/2.*7"7
Figure 12
Small
perforation
of the TFC
(arrow).
Figure 10
Volar
intercalated
segmental
instability Radioulnar Ligaments [Figure 13]
(VISI) !" Volar/dorsal margins of TFC
deformity. !" Flat margins – attach directly to bone
!" Injury...DRUJ instability
Triangular Fibrocartilage Complex

!" P-"/.2&'/-)$1-*%/-("'/2,
!" Radioulnar ligsments
!" Meniscus homologue
!" UCL and ulnocarpal ligaments
!" ECU tendon sheath Figure 13 A, B & C
TFC: Normal Anatomy [Figure 11] Normal volar and dorsal

!" Fibrocartilage radioulnar ligaments
!" “Bow tie” (arrows) (open arrow =
!" Ulnar styloid % dist radius TFC).
!" Attaches to radial cartilage
Extensor Carpi Ulnaris Sheath [Figure 14]

!" Ulnar-sided support
!" Injury leads to
Figure 11 !"Subluxation
!"Tenosynovitis
Normal !"Tears
triangular
&+"1/#"!30#E(D
Figure 14
Subluxed
extensor
carpi ulnaris
tendon
(arrow).
TFC: Pathology [Figure 12]
!" Tear/perforation
!"95% accuracy
!"Partial vs full thickness Tendons
!"Radial/ulnar !" Axial plane
!"Central/peripheral !" Flexors
!" Associated injuries !"Carpal tunnel
!"LTL, ECU sheath !" Extensors
!"Dorsal compartments
!"Extensor retinaculum

Extensor Compartments Carpal Tunnel [Figure 17]
!" 1st – Abd. pollicis longus !" Floor: carpal bones
!"Ext. pollicis brevis !" L**#[)C,3*-)-,("./%&'&8
!" 2nd – Ext. carpi radialis longus/brevis !" Contents
!" Lister tubercle !"Flexor tendons
!" 3rd – Ext. pollicis longus !"Median nerve
!" 4th – Ext. digitorum
!"Ext. indicis
!" 5th – Ext. digiti minimi
Figure 17
!" 6th – Ext. carpi ulnaris
Tendon Pathology Normal

carpal tunnel
!" Tenosynovitis (long arrow
!"Q&--*&.+".2)C&"+ [*?('1"*
!"Stenosing (septations) retinaculum;
!" Partial tear short arrow
!"Enlarged/thinned/focal SI = median
nerve).
!" Complete tear
Magic Angle Phenomenon [Figure 15]

!" Artifactual signal within tendon Median Nerve [Figure 18]
!"r)>>s)(*)8/".)8/2.,("%)$,'+ !" Volar/radial position in carpal tunnel
!" Short TE images !" Stable to decreasing size
!" Disappears on long TE images !" V/<)/::,/-)C/((,.,+)/()9/8/(,
Figure 18
Figure 15 A & B A, B & C
SD*S"!34#/!.#0*3$!(">()3#!(*%3E$#0*3$*!6(*?('1"*:1003/3%* Normal
longus tendon on gradient echo image. median
B. Tendon appears normal on fat-saturated T2-W nerve within
image. the carpal
tunnel.
Tendon Pathology [Figure 16]

!" Flexor tendons
!"Tenosynovitis
!"Carpal tunnel syndrome
Carpal Tunnel Syndrome
!" Compressive neuropathy
!" Pain, paresthesias
!"Thumb, index, long, radial 1/2 ring
Figure 16
!" Worse at night
!" Dx: clinical exam, nerve conduction
Severe
tenosynovitis Carpal Tunnel: Postop
14*!6(*?('1"* !" Volar displacement: tendons/nerve
tendons. !" Free edges or absence of retinaculum
CT: Postop Complications

!" Incomplete retinacular release
!" Proximal swelling of median nerve
!" Scarring around nerve
!" Mass lesion in carpal tunnel
!" Median nerve neuroma

Guyon Canal [Figure 19]
!" “Ulnar tunnel”
!" Ulnar nerve, artery, vein
!" Boundaries
!"K'**-[)C,3*-)-,("./%&'&8
!"Roof: fascia
!"Lateral to pisiform and hook of hamate Figure 20
A&B
Lipoma
compressing
the structures
within the
ulnar tunnel.
Figure 19
A&B
Normal ulnar
tunnel (Guyon
canal).
Figure 21
Accessory
palmaris
Ulnar Tunnel Syndrome [Figure 20]
longus muscle
(M).
!" Ganglion cyst or other mass
!" Fracture (hook of hamate)
!" Repetitive trauma
Masses: Anomalous Muscles [Figure 21]

!" Accessory palmaris longus
!"Volar
!"Q&:,-$%"/')(*)C,3*-)(,.+*.7
!" Extensor digitorum manus brevis
!"Dorsal
!"Near extensor indicis tendon
!" Isointense to muscle on all sequences
References
1. F,-,`/')HM)+,')G"./')KM)^1/7%/')KM)J/-%"/?g/'(&"'',)LM)G,-,+/)PM)F/.2/)^S)U8/2".2)$.+".27)".)&'./-?7"+,+)
wrist impaction syndromes. RadioGraphics 2002;22(1):105-21.
2. Moser T, Dosch JC, Moussaoui A, Dietemann JL. Wrist ligament tears: evaluation of MRI and combined
MDCT and MR arthrography. AJR Am J Roentgenol 2007;188:1278-86.
3. Nikken JJ, Oei GH, Ginai AZ, Krestin GP, Verhaar JA, van Vugt AB. Acute wrist trauma: value of a short
dedicated extremity MR imaging examination in prediction of need for treatment. Radiology 2005
Jan:234(1):116-24.
4. L&,22,-)FM)Q%98"+)VLM)G$--8/..)FNM);/2<)HM)J"'&'/)H^M)n/.,((")VS)G,-":9,-/')(,/-)*#)(9,)(-"/.2&'/-)
$1-*%/-("'/2,[)+,:"%("*.)a"(9)VL)/-(9-*2-/:9<)*#)(9,)+"7(/')-/+"*&'./-)T*".(S)^RL)^8)R)L*,.(2,.*')XAA\)
Jan:188(1):187-92.
5. Sofka CM, Potter HG. Magnetic resonance imaging of the wrist. Semin Musculoskelet Radiol 2001
Sep;5(3):217-26.
6. P9,&8/..);_S)G$--8/..)FNM)^.(*."*)J]M)F9&.2)FOM)J"'&'/)H^M)P-&+,'')!RM)L,7."%W)!S)]3(-".7"%)%/-:/')
ligaments: normal MR arthrographic appearance in cadavers. Radiology 2003 Jan;226(1):171-9.
7. Yu JS, Habib PA. Normal MR imaging anatomy of the wrist and hand. Radiol Clin North Am
2006;44(4):569-81, viii. Review.
8. n'/(W".)VOM)L*7.,-)RS)VL)"8/2".2)*#)'"2/8,.(7)/.+)(-"/.2&'/-)$1-*%/-("'/2,)%*8:',3)*#)(9,)a-"7(S)L/+"*')
Clin North Am 2006;44(4):595-623.

1032
MRI of the Ankle and Foot
Technique Bones: Osteochondral Lesion [Figure 2]
!" Surface coil !" Terminology
!" T1, T2, fat saturation !"Osteochondritis dissecans (OCD)
!" VL)/-(9-*2-/:9<I !"Osteochondral fracture
!" J+I !"Osteochondral injury
!"Mass: cyst vs solid !" Ankle
!"Infection: abscess, sinus !"Acute trauma
!"Synovitis screening !"Talar dome
#" Mid 1/3 lateral
Ankle/Foot: Imaging Planes #" 0U.E,-7"*.M)+*-7"C,3"*.4
Ankle Foot #" Posteromedial
!" Axial Long axis #" 0U.E,-7"*.M):'/.(/-C,3"*.4
!" Coronal Short axis
!" Sagittal Sagittal
Ankle/Foot: Image Analysis

!" “Inside out”
!"Bones
!"Ligaments Figure 2
!"Tendons
!"Nerves Osteochondral
!"Other soft tissues lesion, medial
talar dome.
Bones
!" Marrow “edema”
!" Differential diagnosis
!"Activity related
!"Contusion/occult fracture
!"Osteonecrosis Bones: Osteochondral Lesion [Figure 3]
!"Osteomyelitis !" Staging
!"Transient bone marrow edema !"0 Normal cartilage
!"Tumor !"1 Abnormal SI but intact
!"2 Fissuring not to bone
Bones: Acute Trauma [Figure 1]
!"3 Flap or exposed bone
!" Contusion, bone bruise
!"4 Loose fragment
!"Marrow edema
!"5 Displaced fragment
!"Hemorrhage
!"Trabecular fx Mintz DN, et al. Arthroscopy. 2003;19:353-359.
!" Fracture (marrow edema + fracture line)
Figure 1 Figure 3
Fracture of
the anterior Osteo-
process of the chondral
calcaneus. lesion with
overlying
cartilage
loss
(arrow).
MRI of the Ankle and Foot Musculoskeletal Radiology

1033
Bones: Os Trigonum [Figure 4]
!" Ununited tubercle
!" Os trigonum syndrome
!"Posterior pain
#" G'/.(/-)C,3"*.)01/'',(4
!"MRI Figure 6
#" Marrow edema
Calcaneonavicular
#" FHL tenosynovitis (stenosing) coalition (arrow).
Ligaments
!" Syndesmotic
!" Lateral
!" Medial
!" Spring
!" Lisfranc
!" Sinus tarsi
!" Plantar fascia
Figure 4 Ligaments: Syndesmotic [Figure 7]

Os trigonum syndrome. !" Interosseous ligament
!" ^.(,-"*-)("1"*$1&'/-
!" G*7(,-"*-)("1"*$1&'/-
Bones: Accessory Navicular [Figure 5] !" Talus = rectangular
!" Type I: distal PT tendon
!" Type II: close proximity to bone
!" Cornuate navicular
!" Pain syndrome
!"Type II and cornuate Figure 7
!"MRI: marrow edema
Normal
anterior and
posterior
!3+31&+.0#"*
ligaments.
Ligaments: Lateral [Figure 8]

!" “Fibular collateral ligament complex”
!" ^.(,-"*-)(/'*$1&'/-
!" F/'%/.,*$1&'/-
!" G*7(,-"*-)(/'*$1&'/-
!" Talus = elongated
Figure 8
Figure 5
Accessory navicular.
Normal
Bones: Tarsal Coalition [Figure 6] anterior
!#01&+.0#"*
!" Second and third decade ligament.
!" Vague hindfoot pain
!" Calcaneonavicular
!" Talocalcaneal
!" F/-("'/2".*&7M)$1-*&7M)*77,*&7
MRI of the Ankle and Foot 1034 Musculoskeletal Radiology

Ligaments: Medial [Figure 9]
!" Deltoid
!"“Tibial collateral lig complex”
!" Deep (tibiotalar) Figure 11
!" Q&:,-$%"/'
!"Tibionavicular Scar tissue in
!"Tibiocalcaneal anterolateral
!"Posterior tibiotalar gutter (arrow)
secondary to
chronic anterior
!#01&+.0#"*
ligament injury.
Figure 9
Normal Ligaments: Sinus Tarsi [Figure 12]

)((:*&+("%* !" Cone-shaped space
of the
deltoid !" Fat, nerves, vessels, ligaments
ligament. !"Inferior extensor retinaculum
!"Cervical ligament
!"Talocalcaneal interosseous ligament
!" Lateral: wide
!" Medial: narrow (tarsal canal)
Ligaments: Injuries [Figure 10]

!" Interruption
!" Laxity
!" Thickening/irregularity
Figure 12
!" Edema (acute)
!" Nonvisualization
Normal
sinus tarsi.
Sinus Tarsi Syndrome [Figure 13]

!" Lateral pain
!" Sense of hindfoot instability
!"Prior trauma (70%)
!"U.C/88/(*-<)/-(9-"("7)05A64
!" MRI Findings
!"Replacement of normal fat
!"& SI T1
!"$ or & SI T2
2do
1er
Figure 10 Figure 13
;1"$*#$!("31"*!3+31&+.0#"*03E#>($!*@#""1<A*[*
syndesmotic injury. Abnormal
low signal
intensity
Ligaments: Chronic Injury [Figure 11] throughout
!" Anterolateral impingement syndrome the sinus
!"ATAF ligament injury tarsi that can
be seen in
!"Persistent pain
patients with
!"Scar tissue in lateral gutter sinus tarsi
!"MRI syndrome.
#" Intermediate SI tissue
#" T1-W and T2-WI

Ligaments: Plantar Fascia [Figure 14] Tendon Pathology: TEAR [Figure 16]
!" Calcaneus ! toes
!" Two bands
!"Medial
!"Lateral
Figure 14
Normal
plantar
fascia.
Figure 16
Spectrum of tendon pathology.
Achilles Tendon [Figure 17]

Plantar Fasciitis [Figure 15] !" Gastrocnemius/soleus
!" U.C/88/("*. !" No tendon sheath (paratenon)
!"Mechanical (pes cavus, etc) !" Bursae
!"Degenerative (age related) !"Retrocalcaneal
!"Systemic disease (RA, seroneg) !"Retro-achilles (acquired)
!" MRI !" Flat/concave ventral margin
!"Thickened fascia (> 4 mm)
!"SI
#" Fascia and perifascial tissues
#" Calcaneus
Figure 17
Normal
Figure 15
Achilles
tendon.
Severe
plantar
fasciitis
with partial
tearing at
its origin
(arrow).
Achilles Tendon: Pathology [Figures 18 & 19]

!" Insertional tendinitis
!"Hagland syndrome
!"Bursitis
Tendons !"Thickened tendon
!" Change orientation !"“Pump bump”
!" Pulleys !" Noninsertional
!"Osseous or soft tissue !"Overuse
!" Magic angle effect #" 30-50 years old – “weekend
warrior”
Tendons: Magic Angle Artifact !"Systemic disease
!" Highly ordered collagen
#" RA, SLE
!"Tendons, ligaments
!"Local/systemic steroids
!" Oriented near 55° to B°
!" Spectrum
!" Increased signal
!"Peritendinitis
!"Short TE sequences
!"Chronic tendinopathy
#" (T1, PD, GRE)
!"Partial tear
!"Disappears on long T2
!"Complete tear

Posterior Tibial Tendon
!" Oval – 2x size of FDL
!" Insertion sites
Figure 18 !"Medial navicular
!"Cuneiforms
Hagland !"Bases of metatarsals 1-4
syndrome
(insertional
!" Pathology
Achilles !"Degenerative (middle-aged women)
tendinopathy !"RA
and partial !"Abnormal stresses
tearing; !" Loss of arch
retrocalcaneal
bursitis).
PTT Pathology: MRI [Figure 21]
!" P,.*7<.*E"("7[)C&"+
!" Partial tear: thick, thin, split
!" Complete tear: disruption
Figure 19
Chronic, non-
insertional
Achilles
tendinopathy
and partial
tearing.
Figure 21 A,
B&C
Medial Tendons [Figure 20] Spectrum

!" Post Tibial “Tom” of posterior
tibial tendon
!" Flex Digitorum “Dick” pathology (A =
!" Artery, vein, nerve “and” tenosynovitis;
!" Flex Hallucis “Harry” B = partial
tear; C =
complete tear).
Lateral Tendons [Figure 22]

!" Peroneus longus and brevis
!" Posterior to lateral malleolus
!"L,(-*$1&'/-)2-**E,
!" Peroneus brevis
!"Anterior or medial
!" Common sheath
Figure 20
O1">#0*>()3#0*?('1"*!($)1$%*@;*[*:1%!("31"*!3+3#0\*
X*[*?('1"*)3E3!1".>\*W*[*?('1"*6#00./3%\*S*[*
neurovascular structures in tarsal tunnel).

Figure 22
Normal Figure 24
peroneus
tendons Ganglion (G)
(L = within the
peroneus tarsal tunnel
longus; displacing
B= neurovascular
peroneus structures
brevis). (arrow).
Peroneus Tendons: Pathology [Figure 23]

!" Tenosynovitis
!" Partial/complete tear Morton Neuroma [Figure 25]
!" Entrapment (calcaneal fx) !" Plantar digital nerve
!" Subluxation/dislocation !" G,-".,&-/')$1-*7"7
!"H/(,-/')8/-2".)*#)$1&'/ !" Third (second) web space
!"Retinacular injury or small avulsion fx !" MRI
!"Acute or chronic !" & SI T1 & SI T2
!"Variable enhancement
Figure 25
Enhancing
Morton
neuroma
(arrow).
Masses: Accessory Muscle [Figure 26]

!" Accessory soleus
!"Ventral to achilles tendon
!" Peroneus quartus
Figure 23
!"Adjacent to peroneus brevis
Lateral dislocation of the peroneus tendons (arrow). !" Isointense to muscle on MRI
Peroneus Brevis Split Syndrome

!" Longitudinal tear (lateral malleolus)
!" May be asymptomatic
!" MRI
!"C-shaped
Figure 26
!"Two tendons
!"^+T/%,.()C&"+D,+,8/
Accessory
soleus
Tarsal Tunnel Syndrome [Figure 24] muscle.
!" Fibro-osseous tunnel
!" PT, FDL, FHL tendons
!" Tibial nerve, artery, vein
!" Pain, paresthesias: sole of foot
!" Etiologies:
!"Tumor, ganglion cyst, dilated veins,
:*7((-/&8/("%)$1-*7"7

References
1. O,/-%-*#()GNM)J&<)QM)O-/+',<)VM)L*1".7*.)KS)VLU)*#)(9,)/.W',[),##,%()*.)+"/2.*7("%)%*.$+,.%,)/.+):/(",.()
management. AJR Am J Roentgenol 2006 Nov;1287(5):1327-31.
2. Bencardino JT, Rosenberg ZS. Normal variants and pitfalls in MR imaging of the ankle and foot. Magn
Reson Imaging Clin N Am 2001 Aug;9(3):447-63.
3. Cheung Y, Rosenberg ZS. MR imaging of ligamentous abnormalities of the ankle and foot. Magn Reson
Imaging Clin N Am 2001 Aug;9(3):507-31.
4. Dunfree WR, Dalinka MK, Kneeland JB. Imaging of athletic injuries to the ankle and foot. Radiol Cliln
North Am 2002 Mar;40(2):289-312.
5. H,#C,-)QM)!"7',-)!JS)VL)"8/2".2)*#)(,.+*.M)'"2/8,.(M)/.+)*77,*&7)/1.*-8/'"(",7)*#)(9,)/.W',)/.+)
hindfoot. Radiol Clin North Am 2002 Sep;40(5):1147-70.
6. Major NM, Helms CA, Fritz RC, Speer KP. The MR imaging appearance of longitudinal split tears of the
peroneus brevis tendon. Foot Ankle Int 2000 Jun;21(6):514-9.
7. Mintz DN, Tashjian GS, Connell DA, Deland JT, O’Malley M, Potter HG. Osteochondral lesions of the talus
new magnetic resonance grading system with arthroscopic correlation. Arthroscopy 2003 Apr;19(4):353-
9 Review.
8. Newman JS, Newberg AH. Congential tarsal coalition: multimodality evaluation with emphasis on CT and
MR imaging. RadioGraphics 2000 Mar-Apr;20(2):321-32, quiz 526-7, 532.
9. Palaniappan M, Rajesh A, Rickett A, Kershaw CJ. Accessory soleus muscle:a case report and review of the
literature. Pediatr Radiol 1999 Aug;29(8):610-2. Review.
10. Q/&:,);M)V,.2"/-+")OM)G$--8/..)FNM)g",..,)GM)Q,"#,-()OM)n/.,((")VS)^./(*8"%)E/-"/.(7)/77*%"/(,+)a"(9)
:,-*.,/')(,.+*.)+"7*-+,-7[)VL)"8/2".2)$.+".27)".)E*'&.(,,-7)a"(9)/7<8:(*8/("%)/.W',7S)L/+"*'*2<)XAA\)
Feb;242(2):509-17.
11. n&1',-)gM)V,.2"/-+")OM)G$--8/..)FNM)!&%)QLM)Q%98"+)VLM)_*+',-)RM)n/.,((")VS)O*.,)8/--*a)%9/.2,7)*.)
STIR MR images of asymptomatic feet and ankles. Eur Radiol 2007;17:3066-72.

1040
C;;1&*$0+)&+)0(+3,=*88*)&15+C1)01&;*)0-(#
Part I: Objectives "Sausage" Digit [Figures 2 & 3]
!" Discuss systematic evaluation of
radiograph
!" Discuss manifestations of RA
!" Discuss manifestations of psoriatic
arthritis
Part II: Objectives

!" Discuss manifestations of reactive arthritis
!" Discuss manifestations of AS
!" Discuss manifestations of JIA Figure 2 A & B
!" Discuss manifestations of osteoarthritis AP radiograph of patient with psoriatic arthropathy
and diffuse swelling of the second toe producing a
I,=*88*)&15+Arthropathies sausage appearance of the digit. Clinical photograph
!" Rheumatoid Arthritis (RA) in a different patient with psoriatic arthropathy and
!" Spondyloarthropathies sausage enlargement of the third and fourth toes.
!"Ankylosing spondylitis
!"Enteropathic arthritis
#" Crohn, ulcerative colitis, Whipple
!"Psoriatic arthritis
!"Reactive arthritis
!" Juvenile idiopathic arthritis
Radiographic Assessment
!" Soft tissue swelling
!" Q*#()("77&,)%/'%"$%/("*.
!" Mineralization
!" Joint space change
!" Erosion
!" Bone production
!" Subluxation
!" Distribution
Soft Tissue Swelling [Figure 1]

!" Symmetrical around joint (fusiform) Figure 3 A & B
!" Diffuse (“sausage" digit)
MR of "sausage" digit with intermediate signal of
!" Lumpy, bumpy !($1%,$1=3!3%*%.""1.$)3$E*!6(*?('1"*!($)1$*%6(#!6*
14*%(/1$)*)3E3!D*;($)1$*%6(#!6*14*&"%!*)3E3!*3%*$1">#0D*
MIP projections following intravenous contrast
administration show diffuse enhancement of second,
third, and fourth toes in patient with psoriatic arthritis
and "sausage" digits.
Mineralization
!" Normal
!" Juxtaarticular
!" Diffuse
Figure 1 A & B
S9*"#)31E"#:6*<3!6*$1$%:(/3&/*4.%341">*%14!*!3%%.(*
swelling surrounding the proximal interphalangeal joint
14*!6(*"3$E*&$E("D*503$3/#0*:61!1E"#:6*3$*#*)344("($!*
patient with RA and synovitis and fusiform soft tissue
swelling involving the proximal interphalangeal of the
3$)('*#$)*>3))0(*&$E("%D*
S::"1#/6*!1*!6(*8$?#>>#!1",*S"!6"1:#!63(% 1041 Musculoskeletal Radiology
Juxtaarticular Osteoporosis [Figure 4]
Figure 6 A & B
Joint space narrowing is important for differential

Figure 4 A & B diagnosis. Both patients have erosions involving the
wrist presenting as lucencies in the carpal bones.
A 27-year-old man with reactive arthritis and erosive Patient A has RA with diffuse narrowing of all of
)3%(#%(*3$*!6(*"3E6!*&"%!*>(!#!#"%#0*:6#0#$E(#0*G13$!D* the carpal articulations. Patient B has gout with
Loss of subchondral bone is seen in the second, maintenance of joint space despite extensive erosive
!63")V*41."!6V*#$)*&4!6*>(!#!#"%#0*:6#0#$E(#0*G13$!%* disease.
3$)3/#!3$E*6,:("(>3#*#%%1/3#!()*<3!6*3$?#>>#!31$D*
Erosions [Figures 7 & 8]

Joint Space Change [Figures 5 & 6] !" Aggressive
!" Widening !"Marginal
!" Normal !"Central
!" Uniform narrowing !" Nonaggressive
!" Asymmetrical narrowing !" Early erosions
!" Ankylosis !"Thin cartilage
!"Absent cartilage
Figure 5
The interphalangeal joints should all be similar in
dimension as should the metacarpal phalangeal joints
when compared to the neighboring articulations. A
“horizontal” scan pattern is useful to detect subtle joint
space narrowing. Note the loss of joint space in the
)3%!#0*3$!(":6#0#$E(#0*G13$!*14*!6(*"3$E*&$E("*3$*!63%*
patient with posttraumatic osteoarthritis.
Figure 7
961!1*>3/"1E"#:6*14*#'3#00,*%(/!31$()*&4!6*>(!#!#"%#0*
head showing destruction of subchondral bone that
would present as an erosion on radiography.

RA
!" Most common in women (2-4:1)
!" V*7()%*88*.)".)(9,)#*&-(9)/.+)$#(9)
decades
!" Female incidence: 0.2-0.4/1000
!" Prevalence: 0.5%-1.0%
!" Probably heterogeneous disorder
!" RA
!" J,.,("%)".C&,.%,[)_H^?!L=
!" Pregnancy: increased risk postpartum
!" U.#,%("*&7)/2,.(7I
!"Chlamydia
RA: Presentations
!" Gradual onset, polyarthritis: typical
!" Mono- or pauciarticular: unusual
!" Abrupt, acute polyarthritis: unusual
!" Systemic disease
Figure 8
!" Felty syndrome
Typical diarthrodial joint anatomy. In early disease, !"RA
the articular cartilage (light blue) prevents synovial !"Splenomegaly
3$?#>>#!31$*@"()A*4"1>*)#>#E3$E*%.+/61$)"#0*+1$(* !"Leukopenia
(white). Erosions are seen earliest where cartilage is
thinnest or where cartilage is absent. Minimal or no RA: Diagnostic Criteria
cartilage is present at the margins of a typical synovial
G13$!*#)G#/($!*!1*!6(*#!!#/6>($!*14*&+"1.%*/#:%.0(D* !" Morning stiffness: three or more joints
involved
!" Arthritis of hand joints
!" Symmetric arthritis
Bone Production [Figure 9] !" Rheumatoid nodules
!" Reparative response !" Rheumatoid factor: 90% patients
!"“Whiskering”/“brush stroke" erosions !"G*7"("E,)FFG)".%-,/7,7)7:,%"$%"(<
!"Overhanging edge of cortex !" Radiographic changes
!"Subchondral bone !" Four criteria needed to have diagnosis
!"Osteophytes
!" Enthesopathy RA: Radiographic Manifestations
!" Periostitis !" Fusiform soft tissue swelling
!" Ankylosis !" Diffuse or juxta-articular osteoporosis
!" Uniform joint space narrowing
!" Aggressive marginal erosions
!" No bone production
!" Synovial/subchondral cysts
!" Bilateral symmetrical – distribution
RA: Hand and Wrist [Figure 10]

!" “100%” of patients
!" MCP, PIP joint space loss/erosions
!" Pancarpal joint space loss/erosions
!"Ulnar styloid/pisotriquetral early
!" Ulnar drift: carpus and digits
!" Swan-neck, boutonniere deformities
!" Ankylosis rare: limited to carpus
Figure 9 A & B Figure 10
Classic
Patient A has psoriatic arthritis with erosions and manifestations
bone production in the metatarsal phalangeal of RA. Erosions
and interphalangeal joints. Bone formation is and joint space
present amongst the erosive changes producing a narrowing are
“whiskering” appearance and the digits are dense present in
secondary to osteitis. Patient B has RA with erosive the proximal
disease in the metatarsal phalangeal joints but no interphalangeal,
bone production. metacarpal
phalangeal,
and wrist joints
in a bilateral
and symmetric
distribution.
Ball Catcher View (Norgaard View) Figure 13
[Figure 11]
Classic
manifestations
of RA of the
feet. Erosions
and joint space
narrowing are
seen in the
metatarsal
phalangeal
joints. The
erosions are
Figure 11 A & B
more readily
PA view (A) of the wrist shows subtle joint space %(($*1$*!6(*>()3#0*#%:(/!*14*!6(*&"%!*!6"1.E6*&4!6*
narrowing in this RA patient's wrist. The Norgaard view >(!#!#"%#0*6(#)%*#$)*!6(*0#!("#0*#%:(/!*14*!6(*&4!6*
(B) reveals erosive disease in the pisotriquetral joint metatarsal head.
that is impossible to appreciate in the PA projection.
RA: Knee and Hip [Figure 14]
!" Knee (80%)
!"Pancompartmental joint space loss
RA: MR Findings [Figure 12] !"Minimal erosions
!" Synovial hypertrophy !" Hips (50%)
!"Fat saturated fast spin echo T2-WIs !" Axial migration
!"Gadolinium !" Acetabular protrusio
!" “Erosions” !"Medial deviation beyond ilioischical
!"Low signal T1-W line
!"Low to high signal on T2-W !"Males (3 mm); females (6 mm)
!"Surrounding edema
!" Hyaline cartilage loss
Figure 14 A & B
Figure 12 A & B RA involving the knee. Note tricompartmental loss of

joint space without erosions or osteophyte formation.
Coronal T1-W
MR of the
wrist shows
numerous RA: Shoulder and Elbow
erosions !" Shoulder (60% of patients)
depicted by !"Erosion in humeral head tend to be
intermediate
signal lateral
replacing fat !"Rotator cuff tear common
in subchondral !"Bilateral AC joint erosive disease
bone that are !" Elbow (~ 34% of patients)
)34&/.0!*!1*#::"(/3#!(*1$*!6(*9S*"#)31E"#:6*@QAD*
RA: Cervical Spine [Figure 15]
!" 60%-80% of patients
RA: Feet [Figure 13] !" Atlantoaxial subluxation
!" 80%-90% of patients !" Craniocervical settling
!" May precede hand dz (10%-20%) !" Odontoid process erosion
!" Forefoot: MTP disease predominates !"VLU)1,7()+,$.,7),3(,.()*#):/..&7
!" Midfoot: talocalcaneonavicular joint !" Apophyseal joint dz
!"May see osseous ankylosis !" Erosion of joints of Luschka
!" Hindfoot: retrocalcaneal bursa !" Spinous process erosions

Psoriatic Arthritis: Radiographic
Manifestations
!" Fusiform soft tissue swelling
!" Maintenance of mineralization
!" Dramatic joint space loss
!" Bone proliferation
!" Marginal erosions predominate
!"“Pencil-in-cup” erosions
!" Bilateral asymmetric dz
Psoriatic Arthritis:
Radiographic Manifestations [Figure 16]
!" Hand/feet
!"Distribution
Figure 15 A & B #" IP joints - asymmetric
RA of the cervical spine with instability at C1-C2. #" Ray distribution
Widening of the atlantoaxial joint is seen only in #" RA distribution
?('31$*3$*!63%*:#!3($!D* !"Acroosteolysis
!"Ankylosis (~ 15%)
!"Calcaneal erosion (plantar bone)
Spondyloarthropathies proliferation
!" K/8"'<)*#)".C/88/(*-<)/-(9-"("+,7)*#) !" Wrist (pancarpal)
synovium and entheses
!" Axial and asymmetric peripheral arthritis
!" Genetic predisposition – HLA B27
!" Infectious etiology
Spondyloarthropathy: Criteria
!" U.C/88/(*-<)7:".,):/".)*-)7<.*E"("7)/.+)
one or more of following
!"Positive family hx
!"Psoriasis/IBD
!"Urethritis/cervicitis/diarrhea – within 1
month
!"Buttock pain
!"Enthesopathy
!"Sacroiliitis
Figure 16
Psoriatic arthropathy of the hands involving the

interphalangeal joints of both hands in a bilateral but
asymmetric pattern.
HLA B27
!" Normal population (USA) ~0%-8%
!" Ankylosing spondylitis > 90%
!" Reactive Arthritis 63%-75%
Erosive Osteoarthritis [Figure 17]
!" Psoriasis not increased without arthritis
!" Asymmetrical soft tissues around joint
!"With peripheral arthritis (20%)
!" Normal mineralization
!"With axial arthritis (50%)
!" Nonuniform loss of joint space
!" IBD with axial arthritis (50%)
!" Central “seagull” erosions
Psoriatic Arthritis !" Osteophytes
!" Peak ages (20-40 years) !" Subchondral sclerosis
!" M:F = 1:1 !" Distribution: symmetrical
!"Spine and DIP – M > F
!"Symmetric polyarthritis – F > M
!" Arthritis in 5%-8% of patients with
psoriasis
!" Skin dz before arthritis in 75%
!" Arthritis before skin dz in 10%

Reiter Disease/Reactive Arthritis:
Radiographic Manifestations
[Figures 18 & 19]
!" Feet (40%-55%)
!"IP and MTP joints
!"Erosions with repair
!"Periostitis along diaphyses
!" Calcaneus (25%-50%)
!"May be “sole” sight of disease
!"Plantar and posterior erosions
!"Enthesophytes
Figure 17 A & B
Typical central erosion in patient with erosive

osteoarthritis compared to marginal erosions seen in
patient with psoriatic arthritis.
Psoriatic Arthritis: Radiographic

Figure 18
Manifestations
!" SI joints (30%-50%) ;,:3/#0*?.44,*3$?#>>#!1",*:0#$!#"*/#0/#$(#0*
enthesophyte that parallels the undersurface of the
!"Bilateral asymmetrical (symmetrical) calcaneus in patient with reactive arthritis. The bone
!"Erosion (iliac > sacral) and repair is dense and an erosion is present in the posterior
!" Spine (17%) superior aspect of the calcaneus.
!"Large, bulky, lateral bone outgrowths
!"Unilateral or bilateral, asymmetrical
!"Infrequent apophyseal involvement in
lumbar spine
Part II: Objectives

!" Discuss manifestations of reactive arthritis
!" Discuss manifestations of AS
!" Discuss manifestations of JIA
!" Discuss manifestations of osteoarthritis
Reactive Arthritis (Reiter Disease)

!" Young adults
!" M:F = 50-1:1
!" Annual incidence 30-40/100,000 Figure 19 A & B
!" Frequently associated with infection A 25-year-old man has reactive arthritis. Erosions and
!"Urethritis/cervicitis subluxation are seen in the metatarsal phalangeal
!"Diarrhea: shigella, salmonella, joints in a bilateral but asymmetric pattern. Subtle
campylobacter bone formation is present along the medial aspect of
the navicular and the medial cuneiform of the left foot
Reiter Disease/Reactive Arthritis: as a manifestation of the asymmetric nature of this
disease.
Radiographic Manifestations
!" Diffuse soft tissue swelling
!" Early: juxtaarticular osteoporosis Reiter Disease/Reactive Arthritis:
!" Late: normal mineralization Radiographic Manifestations
!" Uniform joint space loss [Figure 20]
!" Aggressive marginal erosions !" Ankle (30%-50%)
!" Bone production !"Joint space loss and periostitis
!" Bilateral asymmetrical distribution !" Knee
!" Feet, ankles, knees, and SI joints !"Effusion
!"Joint space loss and periostitis
!" SI joints
!"Bilateral asymmetric
!"Erosions and repair

Figure 20
Bone formation at
the posteromedial
aspect of the distal
tibia in a patient
with psoriatic
arthritis.
Figure 21B
Ferguson view of the pelvis with bilateral symmetric

sacroiliitis in patient with ankylosing spondylitis.
Reactive Arthritis vs Psoriatic Sacroiliitis: Differential Diagnosis

!" Juxtaarticular osteoporosis !" AS
!" G,-"*7("("7)a"(9*&()T*".()$.+".27 !" Enteropathic arthropathy
!" Less ankylosis of IP joints !" Psoriasis
!" Tendency to involve MTP vs IP joints !" Reactive arthritis
!" Lower extremity involvement !" Hyperparathyroidism
predominates !" Osteiitis condensans
!" Infection
Ankylosing Spondylitis (AS)
!" Peak age of onset (15-35 years) AS: Radiographic Manifestations
!" M:F = 3-5:1 [Figures 22 & 23]
!" Incidence ~ 6.6/100,000 !" Spine disease: ascends from lumbar to
!" Strong association with HLA B27 cervical
!" Rare in African Americans !" Discovertebral destruction
!" Predilection for axial involvement !"Romanus and Andersson lesions
!" "Shiny corner" sign
AS: Radiographic Manifestations !" Squaring of vertebral body
[Figure 21] !" Syndesmophyte
!" Sacroiliac disease !" Bamboo spine
!"Bilateral symmetric – same as !" "Trolley track" and "dagger" signs
enteropathic !" Atlantoaxial disease
!"Erosions predominate iliac vs sacrum
!"Sclerosis
!"Ankylosis
!" Other pelvic dz
!" Pubic symphysis: 16%-23% erosion and
ankylosis
!" Enthesitis: ilium and ischium
Figure 22
Density con-
Figure 21A &$()*!1*!6(*
anterior,
Typical superior, and
presentation inferior end
of ankylosing plates of the
spondylitis lumbar spine
with erosions resulting in the classic “shiny corner” presentation
and sclerosis of ankylosing spondylitis. Note the lack of anterior
involving the concavity of the vertebral bodies that contributes to
inferior aspect its “squared” appearance.
of the SI joints in a bilateral and symmetric pattern.

Figure 24 A & B
Figure 22 A & B
Q.02,*:#"#=("!(+"#0*1%%3&/#!31$*3$*:#!3($!%*<3!6*X8JW*
The normal lumbar vertebral body is concave is usually distinguished easily from the thin anterior
anteriorally. The 41-year-old patient with ankylosing syndesmophytes of ankylosing spondylitis that typically
spondylitis shows bone formation at the anterior has no horizontal component.
aspect of the vertebral bodies resulting in a squared
appearance.
AS: Extraskeletal Manifestations

!" Uveitis
!" Ascending aortitis/aortic valve disease
!" Cardiac conduction abnormalities
!" Interstitial lung dz – upper lobes
Juvenile Idiopathic Arthritis

!" JRA (seronegative): 70%
!"Still disease, pauci-/mono-/
polyarticular
!" Juvenile-onset adult type RA (10%)
!" Juvenile-onset ankylosing spondylitis
!" Psoriatic arthritis
!" Enteropathic arthritis
!" Reactive/Reiter arthritis
Still Disease: Systemic Disease (Classic)

!" M:F = 1:1
!" Age usually less than 5 years
!" Acute febrile illness
Figure 23 A & B !" Rash
Lateral radiograph of the cervical spine in patient !" Generalized adenopathy/
with ankylosing spondylitis shows thin posterior and hepatosplenomegaly
anterior syndesmophytes and fusion of the facet !" Pericarditis
joints. Lateral radiograph of the thoracic spine also !" V"'+)T*".()$.+".27)c)/-(9-/'2"/7D8"'+)
shows thin posterior and anterior syndesmophytes. arthritis
JRA: Still Disease: Pauci-/Monoarticular

!" Woman more common than mem
Diffuse Idiopathic Skeletal Hyperostosis !" Large joint disease
(DISH) [Figure 24]
!" Knees, ankles, elbows, and wrists
!" Common disease: 12% of elderly
JRA: Polyarticular
population
!" M:F = 1:1
!" K'*a".2)1&'W<):/-/E,-(,1-/')*77"$%/("*.
!" Symmetric arthritis
!"Four contiguous vertebral bodies
!" Hands: MCP, PIP
!" Thoracic > lumbar > cervical
!" Wrists
!" Enthesophytes (particularly pelvis)
!" Knees/ankles
!" Absence of erosions/joint abnormality
!" Feet: intertarsal, MTT, MTP, IPs
!" Cervical spine

Juvenile-Onset Adult Type RA
(Seropositive JRA)
!" F>M
!" > 10 years old at onset
!" Polyarticular
!" Subcutaneous nodules
!" Vasculitis
JRA: Radiographic Manifestations

[Figures 25 to 29]
!" Fusiform soft tissue swelling
!" Osteoporosis
!" Joint space loss
!"Not prominent in monoarticular
!"May be rapid in sero (+) JRA
!"Ankylosis: hands, wrists, cervical spine Figure 27
!" O*.,),-*7"*.)c).*():-*8".,.()$.+".2
Coronal SPGR image of the left hip in a patient with
!" Periostitis JRA showing marked irregularity in the articular
!"Phalanges, metacarpals, metatarsals cartilage.
!" Ballooned epiphyses
!" Accelerated skeletal growth
!" Premature fusion of physes
Figure 28 A & B
Polyarticular JRA of the hands. Generalized

osteoporosis and joint space narrowing is present with
Figure 25
striking lack of erosions.
Classic manifestation of mono- or pauciarticular JRA.
The left knee is enlarged and shows advanced bone
age in comparison to asymptomatic right knee. Note
the lack of erosions and joint space narrowing.
Figure 29 A & B
Adult patient with JRA as a child. Note "ballooned"

appearance of the metacarpal heads (right greater
Figure 26 than left). Wrist involvement was also aymmetric in
this patient. Minimal erosions are seen.
A 17-year-old man has polyarticular JRA and left hip
pain. The femoral heads are enlarged resulting in
“ballooned” appearance of the epiphyses.

Osteoarthritis Osteoarthritis: Radiographic
!" Most common arthropathy Manifestations
!" ~ 80% of patients over 75 years old !" Normal mineralization
!" Second only to CHD as cause of work !" Nonuniform joint space loss
disability for men > 50 years old !" Absence of erosions
!" Primary: no underlying abnormality !" Subchondral new bone formation
!" Secondary: preexisting metabolic, !" Osteophyte formation
/./(*8"%M)(-/&8/("%M)*-)".C/88/(*-<) !" Subchondral cysts
condition !" Subluxations
Osteoarthritis: D(4,-)-&, Osteoarthritis: Subchondral “Cysts”

!" American College of Rheumatology: [Figure 30]
"a heterogeneous group of conditions that !" Not true cysts
lead to joint symptoms and signs which !" Intrusion
are associated with defective integrity of !"Defect in cartilage leads herniation of
articular cartilage, in addition to related T*".()C&"+)".(*)1*.,
changes in the underlying bone at the joint !"Cyst size based on joint pressure
margins.” !" Contusion
!"Repeated insult to subchondral bone
Osteoarthritis: Clinical leads to resorption
!" Increasing prevalance with age over 40
!" Pain, stiffness, and loss of range of motion
!" Symptoms may regress or be cyclic
!" Risk factors
!"Heredity: AD trait with Heberden nodes
!"Obesity: risk factor for knee and
possibly hand
#" Not risk factor for hip
!" Osteoarthritis
!" Clinical
!" Risk factors (continued)
!"Hypermobility: increases risk
!"Occupation: increased risk in heavy
manual labor
#" No increased risk from recreational
sports
!"Diabetes: increases risk
!"OA in one joint increases risk for other
joints
!"Osteoporosis: protective effect in hip
OA
!"Cigarette smoking: protective effect
Osteoarthritis and Pain

!" Most common and important complaint
!" Source
!"Raised intraosseous pressure
!"Synovitis/bursitis/tenosynovitis
!"Periosteal elevation
!"Muscular imbalance Figure 30
!" Less common in very old or young Typical subchondral lucencies in specimen radiograph
!" Psychosocial factors of osteoarthritic femoral head.
!" Osteoarthritis and pain
!" Radiographic predictors
!"Osteophytes in knee good predictor Osteoarthritis: Osteophytes
!"Joint space narrowing in hip predictor
[Figures 31 to 33]
!"J**+)".)$-7()FVF)T*".(
!" Tend to occur at the margins of joints
!"Poor in hand IP joints
!" Produce “enlargement” of joint
!" MR predictor of pain
!"Attempt to stabilize joint
!"Subchondral bone marrow edema
!" Can be central – “button osteophyte”
!" May not be dramatic in osteoporotic
women

Figure 33
Large osteophytes
projecting from the
articular surfaces
of the medial and
lateral femoral
condyles.
Figure 31
Osteophytes of the interphalangeal joints of the hands
are usually best appreciated on lateral radiographs.
Osteoarthritis: Subchondral Sclerosis

!" Also known as eburnation
!" Stimulated by loss of hyaline cartilage
!" Combination of new bone on existing
trabeculae from microfracture and repair
Osteoarthritis: Radiographic
Manifestations [Figures 34 & 35]
!" Hands
!"DIP joints – Heberden nodes
!"PIP joints – Bouchard nodes
!" Wrist
!"First metacarpal-carpal joint
Figure 32
Osteoarthritis of the hip with superior lateral joint

space narrowing accompanied by subchondral
sclerosis, subchondral cyst formation, and osteophyte
production.
Figure 34 A & B
Patient A shows Heberden nodes from osteophytes

and soft tissue swelling at the distal interphalangeal
joints. Bouchard nodes are seen at the proximal
interphalangeal joints of patient B.

Figure 37 A & B
Figure 35
A 56-year-old woman with acromegaly. Manifestations
Hooked osteophytes are seen involving the
of osteoarthritis are seen but the joint spaces are
second and third metacarpal heads. These may be
widened rather than narrowed.
seen in hemochromatosis, CPPD arthropathy, or
osteoarthritis.
Osteoarthritis: Hip – Radiographic

Osteoarthritis: Knee – Radiographic Manifestations
!" Superolateral migration
Manifestations [Figures 36 & 37]
!" May require weight-bearing views !"60%
!"M > F
!" Medial compartment (75%)
!" Medial migration
!" Patellofemoral joint (48%)
!"25%
!" Lateral compartment (26%)
!"F > M
!" Pancompartmental
!" Axial migration
!"Think deposition dz or prior
!"Think deposition dz or prior
".C/88/(*-<)/-(9-*:/(9<
".C/88/(*-<)+`
Hip Joint Space Narrowing
Figure 36 A & B
Nonweight-bearing AP of the knee (A) shows

osteoarthritis in the medial compartment with
subchondral sclerosis and osteophyte formation but
the joint space appears maintained. AP weight-bearing
view of the knee (B) shows the expected loss of joint
Osteoarthritis: Foot - Radiographic
space in the medial aspect of the knee. Manifestations
!" Occurs along lines of weight-bearing
!" First MTP joint
!"Hallux rigidus
!"Hallux valgus
!" First MTT joint
!" Talonavicular joint
!"Dorsal talar beak (coalition vs DJD)

References
1. R/%*17*.)R^M)J"-"79)JM)R"/.2)jM)L,7."%W)!S)L/+"*2-/:9"%),E/'&/("*.)*#)/-(9-"("7[)".C/88/(*-<)%*.+"("*.7S)
Radiology 2008 Aug;248(2):378-89.

1054
MRI of the Rotator Cuff
MRI of Rotator Cuff Tears CT and Ultrasound [Figure 2]
Figure 2 A & B
CCS-Clinical Community; ESS-Experienced Spe-

Coronally reconstructed CT image following a direct
cialist, Arthroscopy. 1997;13:710-719.
arthrogram shows a small full thickness rotator cuff
tear in the supraspinatus tendon. Coronally acquired
MRI of the Rotator Cuff: Goals ultrasound image in the same patient demonstrates
!" Review anatomy/positioning the full thickness tear as a focal hypoechoic defect in
!" Review MR appearance of tears the hyperechoic tendon.
!" Discuss problem tears
!" Discuss clinical mimics of rotator cuff tear
!" Discuss the radiologic report MRI of the Shoulder
!" Rotator cuff
Shoulder Pain !" Glenoid labrum
!" Rotator cuff disease !" Capsule
!" Impingement !" Biceps tendon
!" Arthritis !" Bone marrow
!" Adhesive capsulitis !" Acromial shape
!" Cervical spine !" AC joint
!" Referred pain !" Subdeltoid bursa
!" Instability !" Supraspinatus notch
!" Fracture !" Coracohumeral ligament
!" Osteonecrosis !" Humeral head shape
!" Nerve entrapment syndromes
!" Bursitis MRI of the Rotator Cuff
!" Coil-dedicated shoulder
Shoulder Imaging !" Slice thickness (3-4 mm)
!" Radiographs !" Matrix: 256 x 192 or higher
!" Arthrography !" FOV: 14-16 cm
!" CT arthrography !" Patient position
!" Ultrasound !" External rotation vs neutral
!" MRI !" ABER
!" Contrast: indirect or direct
Radiography [Figure 1]
!" Humeroacromial space < 7 mm Pulse Sequences
!" Massive tear !" Spin echo
!" Fast spin echo (fat saturated)
!" Sensitive for cuff tear
!" STIR
!" Gradient echo
!" 3D volume
Imaging Planes
!" Axial
!" Assess subscapularis, biceps tendon
Figure 1 A & B !" Coronal obliques
!" Parallel to supraspinatus tendon
AP radiograph of the shoulder shows superior
narrowing of the humeral acromial space indicative of !" Assess all tendons
a large rotator cuff tear. Coronal oblique T2-W in the !" Sagittal oblique (FSE T2)
%#>(*:#!3($!*/1$&">%*#*0#"E(*!(#"*3$*!6(*%.:"#%:3$#!.%* !" 90° to coronals
tendon.
MRI of the Rotator Cuff 1055 Musculoskeletal Radiology

Plane of Scan [Figure 3]
Figure 6 A & B
Figure 3 A, B & C Coronal oblique T1-WI through the subscapularis with

corresponding gross anatomy.
Axial gradient echo image (A) with typical planscan
for coronal oblique images drawn perpendicular to
the glenoid. Axial gradient echo image through the
supraspinatus at the superior aspect of the shoulder in Sagittal Anatomy [Figure 7]
internal rotation (B) shows the plane of acquisition will
cross the tendon obliquely. Axial gradient echo image
through the supraspinatus at the superior aspect of
the shoulder in external rotation (C) shows the plane
of acquisition will parallel the tendon.
Rotator Cuff
!" Dynamic stabilizer
!" Complex coordination Figure 7 A & B
!" Five layers histologically
Sagittal oblique T2-WI at the level of the glenohumeral
!" Components joint shows the normal rotator cuff muscle anatomy.
!" SITS muscles
!" Rotator cuff interval
!" Coracohumeral ligament
!" Long head biceps tendon Axial Anatomy [Figure 8]
Coronal Anatomy [Figures 4 to 6]
Figure 8 A & B
Figure 4 A & B
Coronal oblique T1-WI through the infraspinatus with Axial gradient echo image shows the normal
corresponding gross anatomy. subscapularis tendon anteriorally. The long head
biceps tendon is normally situated in the bicipital
groove.
Normal Anatomy
http://rad.usuhs.mil/rad/anatomy/shoulder/
intro.html
Rotator Cuff Tear

!" Impingement
!" Overuse
!" Aging
Figure 5 A & B
!" F9-*."%)".C/88/(*-<)+"7,/7,
Coronal oblique T1-WI through the supraspinatus with !" Acute trauma
corresponding gross anatomy. !" Instability

Pathogenesis RCT: Neer
!" Stage I (< 25 years old)
!"Edema/hemorrhage
!" Stage II (25-40 years old)
!" Fibrosis/thickening
!" Stage III (> 40 years old)
!"Partial/complete tear Figure 10 A, B & C
Impingement Syndrome Coronal oblique T1-WI posterior to the

acromioclavicular joint (A) shows the syndesmosis of
!" Clinical: not radiologic diagnosis the accessory ossicle. Coronal oblique T1-WI at the
!"Pain with abduction and external acromioclavicular joint (B) shows the AC joint and
rotation supraspinatus tendon. The os acromiale is best seen
!"Pain with elevation and internal on the axial image (C) at the level of the AC joint.
rotation
!"(Neer impingement sign)
!" Mechanical causes
!"Acromial shape, position
Rotator Cuff Tear: Types
!"AC joint osteophyte
!" Full thickness
!"Thick coracoacromial ligament
!"Communication between joint space
!"Instability
and SA bursa
Impingement [Figure 9] !" Partial thickness
!"Partial undersurface
!"Partial Bursal surface
!"Intrasubstance
!"“Rim rent”
Rotator Cuff Tear

!" Primary
!"Increased signal in tendon
!"Interruption of tendon
!" Secondary
!"Retraction of musculotendinous
Figure 9 A & B junction
T3!6*#+)./!31$V*?('31$*#$)*3$!("$#0*"1!#!31$V*!6(* !"Obliteration of subacromial bursal fat
rotator cuff may impinge on the coracoacromial arch. plane
!"Fluid in subacromial bursa
!"Atrophy of muscles
!"Fluid in muscle belly
Acromial Variation
!" Shape Increased Signal within Tendon: Short
!"Type I TE Images
!"Type II !" Magic angle
!"Type III !" Connective tissue between fascicles
!" Lateral downsloping !" Tendon overlap (internal rotation)
!" Anterior downsloping !" Degeneration
!" Os acromiale !" Tear
!" Partial volume
Acromial Variation !" Injection
!" P<:,)U[)C/(
!" Type II: curved
!" Type III: hooked
!" Increased risk of tear with type II and III
!" Assess on sagittal images
Os Acromiale [Figure 10]

!" U.%-,/7,+)-"7W)*#)%&##)(,/-I
!" Best seen on axial images
!" Injury to syndesmosis

Tendon Overlap [Figure 11] Intrasubstance vs Partial US: Value of
ABER [Figure 13]
Figure 13 A & B
T1 fat-saturated image of the shoulder following
indirect arthrography in the ABER position (A) shows
the undersurface of the infraspinatus tendon is intact.
The conventional coronal oblique T1-WI through
infraspinatus tendon suggested an undersurface tear.
Figure 11 A, B & C
Rim Rent Tear [Figure 14]
Axial gradient echo image at the superior aspect of !" Seen in young patients
the humeral head (A) shows the anterior aspect of !" Usually anterior
infraspinatus tendon overlapping (lateral) the posterior
aspect of the supraspinatus tendon (medial). Coronal !" Intrasubstance vs partial undersurface
T1-WI at the level of infra- and supraspinatus tendon
overlap shows normal high signal within the junction Figure 14
of the two tendons.
Coronal oblique
fat-saturated
T2-WI shows
horizontally
Partial Tears oriented
!" Twice as common as full thickness increased signal
in the insertional
!" Intrasubstance most common portion of
!" Bursal surface least common the posterior
!"Poor response to conservative Rx supraspinatus
!" Increased detection tendon consistent
!"Contrast with a tear
+.!*3!*3%*)34&/.0!*!1*)(!(">3$(*<6(!6("*!6(*!(#"*3%*#$*
!"ABER undersurface or intrasubstance defect.
!" Q"2."$%/.()"#)o)>A6)*#)(,.+*.)(9"%W.,77)
Partial Undersurface [Figure 12]

Subscapularis Tears [Figure 15]
!" Abnormal lift-off or belly press test on PE
!" Uncommon (5%-13% of all tears)
!"Associated with LHBT sublux or disloc
!" Look for on axial and sagittals
!"Anterior coronals provide more clues
!" Only superior 25% of tendon visible on
routine arthroscopy
Figure 12 A & B
Coronal T2-WI through the supraspinatus tendon (A)

shows a deep partial undersurface tear. Coronal T2-WI
through the supraspinatus tendon of a different patient
@QA*%61<%*?.3)*%3E$#0*3$!("".:!3$E*!6(*#"!3/.0#"*%."4#/(*
of the supraspinatus tendon but the bursal surface is
intact indicating an undersurface tear. Both patients
have SLAP tears of the superior labrum.
Figure 15 A & B
Sagittal T2-WI at the level of the lesser tuberosity

shows a focus of high signal in the subscapularis
tendon representing a partial undersurface tear. The
tear is also seen on the axial T1-W gradient echo
image following indirect arthrography (B) but is easier
to see on the sagittal image.

Long Head of Biceps Tendon Spinoglenoid Notch Entrapment
!" Abnormality frequently associated with [Figure 17]
RCT !" Infraspinatus atrophy
!" Medial dislocation
!"Coracohumeral ligament tear
!"Subscapularis tendon must be torn
#" Can be intra- or extraarticular
!" Associated with degeneration of tendon
!" Tendinopathy
!" Tear: partial or rupture
Subscapularis Insertion
[Figure 16]
Figure 17 A, B & C
Coronal oblique fat saturated T2-WI shows a paralabral
cyst extending from a posterior superior labral tear
into the spinoglenoid notch. A clinical photograph (B)
in the same patient shows marked atrophy of the right
infraspinatus muscle belly as indicated by the loss of
soft tissue inferior to the scapular spine. Sagittal T2
image (C) medial to the spinoglenoid notch shows
atrophy and denervation edema in the infraspinatus
muscle belly.
Figure 16 A, B & C
Axial gradient echo image through the subscapularis

tendon (A) that appears to only insert on the lesser
tuberosity on this image. However, photo of a
gross specimen and a photomicrograph through the QSS [Figure 18]
insertion of the subscapularis show that the tendon !" Axillary nerve compression
inserts on both the lesser and greater tuberosity. The !" Fibrous band
transverse ligament covering the bicipital groove is !" Pain, paresthesia
not actually a ligament but represents the portion of !" Atrophy of deltoid and/or teres minor
the subscapularis tendon that inserts on the greater
tuberosity. !" Weightlifters
Rotator Cuff Atrophy

!" Rotator cuff tear
Figure 18
!" Acute brachial neuritis
!" Nerve entrapment syndromes The
!"Suprascapular nerve entrapment quadrilateral
!"Quadrilateral space syndrome (QSS) space is
bounded by
teres minor,
Suprascapular Nerve Entrapment teres major,
!" Suprascapular notch long head
!"Supraspinatus/infraspinatus triceps, and
innervation the humerus.
!" Spinoglenoid notch
!"Infraspinatus innervation
!" Atrophy of SSM and ISM
!" Look for mass in region of suprascapular
notch Clinical Mimics of Rotator Cuff Tear
!" F/'%"$%)(,.+*."("7
!" Adhesive capsulitis
!" Subacromial bursitis

C*%$-4$+Tendonitis
!" Rotator cuff most common site
!" G-"8/-<)*-)7,%*.+/-<)+"7*-+,-I
!" HADD in tendon
!" Concretion: low T1 and T2
!" Variable surrounding edema
Figure 19 A & B
!" May erode cortex/invade marrow
Axial T1-W
Adhesive Capsulitis [Figure 19] gradient echo
!" Clinical mimic of cuff tear image (A)
!" Capsule thickened shows marked
enhancement
!" Abnormal enhancement – IV gad in the anterior
inferior capsule
Radiologic Report following
!" Acromion: Os acromiale IV contrast
!" Tendon: normal, tendinosis, tear administration
!"Size and Location of tear indicating
adhesive
!" Small – 3 cm; moderate – 4 cm; massive capsulitis in
> 5 cm the atraumatic
!" Partial thickness tear setting.
!"> or < 50% thickness of tendon
!" Retraction/muscle atrophy
References
1. Steinbach, et al. Shoulder Magnetic Resonance Imaging. Lippincott-Raven Publishers Philadelphia, 1998.
2. Zlatkin MB. MRI of the shoulder. Raven Press, 1991.

Lesions of Unknown Histogenesis: Ewing Sarcoma and
Langerhans Cell Histiocytosis
Unknown Histogenesis
!" Ewing sarcoma
!"Eosinophilic granuloma
!"Hand-Schüller-Christian disease
!"Letterer-Siwe disease
Learning Objectives
!" Recognize the spectrum of imaging
/::,/-/.%,7)*#)(9,7,)7:,%"$%)*77,*&7)
lesions
!" Identify differentiating features
Ewing Sarcoma
!" Highly malignant primary bone sarcoma Figure 1
!" ]a".2):-*E"+,+)$-7()%*8:-,9,.7"E,) Sheets of monotonous malignant “round
cells“ with indistinct cytoplasmic areas of necrosis and
description in 1921, designating it “diffuse
hemorrhage are frequent.
endothelioma” of bone
!" Later (1924) termed “endothelial
myeloma” of bone, and “Ewing tumor” by Radiologic Features: Intergroup Ewing
Codman Sarcoma Study [Figure 2]
!" Distribution: diaphysis 35%,
Ewing Sarcoma: Incidence and
metadiaphysis 59%, metaphysis 5%,
Distribution epiphysis < 1%
!" About 5% of all biopsied tumors
!" Lesions medullary, symmetric, or
!" Long bones involved most commonly
eccentric
!" Usually major long bones, femur most
!" Soft tissue mass in about 90%
common (25%), then humerus (8%)
!" Reactive bone (40%), but tumor produces
!" U.)C/()1*.,7M)8*7()%*88*.):,'E"7)0XA64)
no cartilage or bone A diferencia del esteosarcoma
followed by ribs (11%)
!" Cortical thickening (20%)
!" Periosteal reaction due to irritation or
Ewing Sarcoma: Clinical Presentation
edema or tumor permeation (~ 85%)
!" Q,E,.(<?$E,):,-%,.()@A?X>)<,/-7
!" “Onion skin” appearance due to cyclic
!" Peak incidence 10-15 years
pattern of periosteal irritation (55%)
!" Ranges 5 months-83 years
!" Perpendicular striations due to rapid
!" Slight male predominance (1.5:1)
continuous lifting of periosteum (30%)
!" Pain and swelling most common
!" Pathologic fracture in 10%-15%; soft
symptoms Simula proceso infeccioso como OM
("77&,)%/'%"$%/("*.)0@A64
!" Constitutional signs to include local heat,
fever, anemia, leukocytosis, etc
!" Chromosomal trans in 90%; t(11;22)
most common, others t(21;22), t(7;22)
!" Predilection for Caucasians (95%)
!" Usually solitary and nonfamilial; 10% are
reported to be multiple at presentation
Ewing Sarcoma: Pathologic Features

[Figure 1]
!" Characterized by sheets of monotonous
malignant “round cells”
!" Indistinct cytoplasmic borders
!" Frequent areas of necrosis and
hemorrhage
!" Virtually all PAS positive (glycogen)
!" Ewing family includes Ewing sarcoma and
primitive neuroectodermal tumor (PNET) Figure 2 A & B
Ewing sarcoma. Radiograph. Note metadiaphyseal

01/#!31$*#$)*#+%($/(*14*3)($!3&#+0(*>#!"3'D
Lesions of Unknown Histogenesis 1061 Musculoskeletal Radiology

Ewing’s Description [Figures 3 to 11]
!" “…characteristic features on which a
diagnosis may be based with considerable
certainty
!" “…large portion or the whole of the shaft
is involved, but the ends are generally
spared…”
!" “…shaft is slightly widened, but the main
alteration is a gradual diffuse fading of the
bone structure…”
!" “…bone production has been entirely
absent…”
!" “…some of the bones appeared
honeycombed…”
!" “The radiograph is therefore rather
7:,%"$%l
Figure 5 A & B
MR imaging. Typical features. MR shows large
heterogeneous circumferential soft tissue mass. Soft
tissue changes seen to better advantage on MR.
Coronal T1 (left) and T2 (right).
Figure 3
Scintigraphy.
P1/#0*3$/"(#%()*!"#/("*#//.>.0#!31$*1$*?1<*%!.),D
Figure 6 A & B
Note diaphyseal location, complex periosteal reaction,

and cortical thickening.
Figure 4 A & B
Scintigraphy. Figure 7 A & B

Focal increased tracer accumulation on delayed
static images. Ewing sarcoma with pathological fracture. Radiograph
(left) and bone scan (right).

Figure 8
Ewing sarcoma. Flat bone. Radiograph. Figure 11 A & B
Ewing sarcoma. Note permeative osteolysis with

evidence of associated mass.
Treatment and Prognosis: Ewing

Sarcoma [Figures 11 & 12]
!" Ablative surgery, chemotherapy, and
radiation therapy
!" About 30% present with metastases
!" Mets typically to lungs (85%), bones
Figure 9 A & B (69%), pleura (46%), CNS (12%)
Ewing sarcoma. Flat bone. MR T2 (left) and T1 (right). !" The 5-year survival rate for patients
without mets at presentation is 55%-70%
Figure 10
Ewing sarcoma. Flat bone (rib). Figure 12 A & B

Large soft tissue mass obscures osseous origin. Ewing sarcoma. Posttreatment change.

Osseous LCH: Clinical Presentation
!" About 90% are 5-15 years old (average
10-12 year old)
!" M:F about 2:1
!" More than 95% of patients are Caucasian
!" Most patients present with pain/
tenderness
!" Fever may be present and presentation
may suggest osteomyelitis
Osseous LCH: Pathologic Features

[Figures 13 & 14]
!" Characterized by a collection of histiocytes
!" Histiocytes are oval, lobulated, or
reniform, with clefts or indentations
!" Eosinophils may be seen individually, in
Figure 13 A & B sheets, in clusters, or not at all
!" Birbeck bodies on EM
Ewing sarcoma. Local recurrence.
Figure 14
Langerhans Cell Histiocytosis (LCH) Histiocytosis.

!" Eosinophilic granuloma Note
!" Hand–Schüller–Christian disease histiocytes
with reniform
!" Letterer-Siwe disease shape and
clefts.
LCH: History Scattered
!" 1940: Jaffe and Lichtenstein eosinophilic eosinophils are
granuloma seen.
!" 1941: Farber, Green, and Farber - EG
could be solitary or multiple
!" 1953: Lichtenstein proposed the name
9"7("*%<(*7"7)i)#*-)(9,)".C/88/(*-<)
histiocytoses
LCH: C%*##-4$*)-&,
!" 1987: Writing Group of the Histiocyte
Society endorsed the term Langerhans
cell histiocytosis (LCH)
!" 1997: Histiocyte Society grouped LCH
according to the number of sites and
types of tissues/organs involved and the
presence or absence of involved organ
failure
!" Single system (one organ system): single Figure 15
site or multifocal Histiocytosis. EM. Note Birbeck bodies.
!" Multisystem (two or more organ
systems): further separated into patients Osseous LCH: Radiologic Features
with or without “risk organ involvement” [Figures 16 to 26]
!" Risk organ involvement: liver, spleen, !" Usually permeative destruction in early
hematopoietic system or lungs phase with periosteal reaction
!" More sharply delineated although lesion
Osseous LCH: Incidence and may still be enlarging as time progresses
Distribution !" Lesions may have a rind of sclerosis
!" LCH involves bone most commonly; about !" There may be an associated soft tissue
1% of all biopsied osseous tumors mass in 5%-10% of patients
!" Solitary EG 2x multifocal EG !" Skull: beveled edge, button sequestrum
!" ^1*&()\A6)".E*'E,)C/()1*.,7M)8*7() !" Flat bone: hole within a hole
commonly skull (25%), pelvis (20%) !" Long bone distribution: diaphysis (58%),
!" In long bones, femur then humerus metadiaphysis (18%), metaphysis (28%),
!" Hands and feet rare in solitary disease epiphysis (2%)
!" Spine: vertebra plana
!" V/.+"1',D8/3"''/[)C*/(".2)(,,(9

Figure 16 A & B Figure 19 A & B
Skull. Beveled edge. Flat bone (left) and long bone (right). “Hole within a
hole.”
Skull. Button sequestrum. Indolent radiographic appearance. Note epiphyseal

lesion.
Figure 21 A & B
Figure 18 A & B
Flat bone. “Hole within a hole.” Spine. Vertebral plana.

Figure 22 A & B
Figure 25 A & B
MRI. Spine. Single lesion. T1 (left) and T2 (right). LCH distal humerus. Radiographs.
Figure 26 A & B
Floating teeth.
LCH. MR. Sagittal T1 (left) and T2 (right).
Osseous LCH: Prognosis and Treatment

!" Benign course
!" Simple curettage or intralesional
prednisone
!" Large lesions and vertebral lesions may
be treated with low dose RTX (300-1000
rad)
!" May regress spontaneously
Summary
!" Review the imaging appearances of Ewing
sarcoma and the osseous LCH
!" Demonstrate how the radiologic images
Figure 24 A & B -,C,%()(9,)&.+,-'<".2):/(9*:9<"*'*2<
Clavicular lesion. Radiograph (top) and macrosection !" Recognize appropriate differentiating
(bottom). features

References
1. Davis, et al. Radiographic features of eosinophilic granuloma of bone. AJR Am J Roentgenol
1989;153:1021.
2. K/E/-/M),()/'S)F*.(,8:*-/-<)%'/77"$%/("*.)*#)9"7("*%<("%)+"7*-+,-7S)V,+)G,+"/(-)B.%*')@ZZ\YXZ[@>\S
3. Shapeero, et al. Ewing sarcoma. Radiology 1994;191:825.
4. Stull, et al. Langerhans cell histiocytosis of bone. RadioGraphics 1992;12:801.
5. The Writing Group of the Histiocyte Society. Histiocytosis syndromes in children. Lancet 1987;1:208.
6. Wilkins, et al. Ewing’s sarcoma of bone. Cancer 1986;58:2551.

1068
Common Lipomatous Soft Tissue Tumors

Learning Objectives C%*##-4$*)-&,A+Weiss and Goldblum
!" Identify the radiologic appearance of !" Lipoma: “tumor of mature adult fat”
7:,%"$%)%*88*.)#/((<)8/77,7 !"Q&:,-$%"/'
!" Recognize the spectrum of common !"Deep
lipomatous soft tissue masses !"Multiple
!" Identify imaging limitations and pitfalls !" Lipomatous tumors: “intimately
associated with nonadipose tissue”
Outline !"Intramuscular lipoma
!" Incidence !"Intermuscular lipoma
!" Common tumors !"Lipomatosis nerve
!"F'/77"$%/("*. !"Lipoma tendon sheath
!"Imaging features !"Lipoma joint
!" Mimics !" Variants of lipoma: “characteristic
!" Cases _"7(*'*2<)/.+)7:,%"$%)%'"."%/')7,((".2l
!"Lipoblastoma
Incidence: New Cancers by Site (2010) !"Spindle cell lipoma
!" Breast 222,520 !"Pleomorphic lipoma
!" Lung 209,060 !"Angiolipoma
!" Colon/rectum 142,570 !"Chondroid lipoma
!" CNS 22,020 !" U.$'(-/(".2)'":*8/7[)m:-*'"#,-/("E,)?)
!" Soft tissue 10,520 Compressing adjacent structures”
!" Bone 2,650 !"Lipomatosis
Jamel, et al. CA Cancer J Clin. 2010. !"Symmetric lipomatosis
!"Adiposis dolorosa
Incidence !"Lipomatosis syndromes
!" It is estimated that the relative frequency !" Hibernoma: “tumor of brown fat”
of benign to malignant tumors is 100:1
!" Lipomatous tumors are the single largest C%*##-4$*)-&,
group of mesenchymal tumors !" H":*8/) ) ) Q&:,-$%"/'
!" About half of all surgically excised tumors !" Lipomatous tumors Intramuscular
are lipomatous Lipoma
!" Variants of lipoma Lipoblastoma
C%*##-4$*)-&,A+Benign Lipomatous !" U.$'(-/(".2)'":*8/7) ZA)t)6
Tumors !" Hibernoma
!" World Health Organization subdivides
benign lipomatous tumors into 9 groups Lipoma: Clinical
!" For imaging purposes, it is more useful to !" P&8*-)*#)8/(&-,)#/(Y)".%"+,.%,I
&7,)(9,)%'/77"$%/("*.):-*:*7,+)1<)N,"77) !" Presents age 40-60, uncommon < age 20
and Goldblum !" M ~ F, recent reports male predominance
!" Q&:,-$%"/')/.+)+,,:
Weiss SW, Goldblum JR. Enzinger and Weiss’s
Soft Tissue Tumors. 5th ed. St. Louis; 2008. !"(Deep: chest wall, retroperitoneum,
deep tissues hands and feet)
!"Deep seated tumors rare, < 1%
lipomas
!" Typically asymptomatic
!" More common in obese, tumor fat not
available for metabolism
!" Usually small, 80% < 5 cm; 1% > 10 cm
!" Clinical diagnosis 85% accurate
!" Usually solitary, 5%-15% multiple
!" 50%-80% transloc chromosome 12 q13-
15
Soft Tissue Lipomatous Tumors 1069 Musculoskeletal Radiology

Lipoma: Radiology [Figures 1 to 9]
!" Demonstrate a fat density mass
!" Fatty nature well-demonstrated on CT/MR
!" CT tissue attenuation -65 to -120HU
!" Visual comparison more reliable than #
!" Signal intensity equals SQ fat on MR
!" No enhancement with contrast (CT/MR)
!" May contain other mesenchymal elements
!" P9,)8*7()%*88*.)"7)$1-*&7)("77&,
!" P,-8,+)m$1-*'":*8/l)a9,.)7"2."$%/.()
$1-*&7)("77&,):-,7,.(
!" May be associated with cortical thickening
!" Occasional chondroid and/or osseous
metaplasia; when long-standing – termed
“benign mesenchymoma”
Figure 4 A & B
MR. Fibrolipoma. Note corresponding linear septations

of decreased signal intensity (arrows).
Figure 1
CT.
Subcutaneous
Figure 5
@%.:("&/3#0A*
lipoma
MR. Unencap-
(arrows).
sulated
lipoma of the
right thigh.
Figure 6
CT. Deep
lipoma. Retro-
peritoneum.
Figure 2
;BCT*-7D*J.+/.!#$(1.%*@%.:("&/3#0A*03:1>#*@RAD
Figure 3
Figure 7 A & B
CT. Subcutaneous lipoma (*) in right shoulder. Lipoma with metaplastic bone formation (benign
Imaging contralateral side may be useful in identifying mesenchymoma). Radiograph (left) and macrosection
subcutaneous lesions. (right).

Figure 10 A & B
Figure 8
Lipoma with metaplastic bone formation (benign 8$!"#>.%/.0#"*03:1>#D*O1!(*3$&0!"#!3$E*>#"E3$D*

mesenchymoma).
Figure 11 A & B
MR. Intramuscular lipoma.
Figure 9 A & B
Lipoma with metaplastic bone formation (benign

mesenchymoma). CT (left) and MR (right).
Intramuscular Lipoma
!" Lipoma arising in skeletal muscle
!" Most common member of subgroup of
lipomatous tumors (fatty tumors arising
in intimate association with nonadipose
tissue)
!" Other entities in this category include: Figure 12 A & B
intermuscular lipoma, lipoma of tendon,
sheath, and lipomatosis of nerve -7D*8$!"#>.%/.0#"*03:1>#*<3!6*3$&0!"#!3$E*>#"E3$D*
T1-W (left) and fat-suppressed T1-WI (right).
Intramuscular Lipoma: Clinical
[Figures 10 to 12]
!" Most common fourth–seventh decades
!" Men more commonly affected
!" Most frequent large muscle extremities
(thigh, shoulder, upper arm)
!" Typically asymptomatic
!" B#(,.)".%"+,.(/')$.+".2

“The concept that lipomas can undergo
malignant transformation to liposarco-
mas is no longer accepted...histologic
variability…and/or poor sampling of the
original tumor are the most likely expla-
nations for apparent transformation”
Weiss and Goldblum Enzinger and Weiss’s Soft
Tissue Tumors. 5th ed. 2010.
Lipoblastoma [Figure 13]

!" Relatively rare cellular immature lipoma
!" Originally termed embryonic lipoma
!" Occurs almost exclusively in infants
!" Usually presents by 3, but occasionally at
birth
!" Males affected 2-3x more
Figure 14 A & B
!" 67%-75% are discrete
!" When diffuse, termed “lipoblastomatosis” Lipomatosis upper extremity. Clinical photograph. MR
!" May image similar to liposarcoma upper extremity in a different patient.
!" Liposarcoma very rare in children
!" Most pediatric fatty masses are
lipoblastomas
Figure 15
CT.
Lipomatosis
trunk.
Figure 13 A & B
Lipoblastoma in a 18-month-old child. This appearance

in an adult suggests liposarcoma.
Figure 16 A & B
Lipomatosis [Figures 14 to 16] MR. T1-W axial images show mild lipomatosis right
!" Diffuse overgrowth mature adipose tissue lower extremity.
!" Rare; mild cases may go undiagnosed
!" Usually present before age 2
!" Considered congenital
!" Bone hypertrophy frequently associated
C%*##-4$*)-&,A+World Health
Liposarcoma
!" Malignant mesenchymal tumor Organization (WHO) (from low to high)
!" Second most common STT, after UPS !" Well-differentiated
!" Approximately 16%-18% of all sarcomas !" Myxoid
!" Presents ages 40-60 years !" Pleomorphic
!" Exceedingly rare in children !" Dedifferentiated
!" Usually extremities or retroperitoneum;
present 5-10 years earlier in extremity

C%*##-4$*)-&,A+DEF+G+Radiologic Liposarcoma: Atypical Lipoma [Figure 19]
Organization !" Lesion histologically indistinguishable
!" Well-differentiated from well-differentiated liposarcoma
!" Myxoid !" Localized in subcutaneous tissue
!" Pleomorphic !" In sites such as the retroperitoneum and
!" Dedifferentiated mediastinum where it is impossible to
obtain a wide margin
C%*##-4$*)-&,A+DEF+G+Radiologic WHO C0#%%3&/#!31$*14*Tumors. IARC Press. 2002.
Organization
!" Well-differentiated % dedifferentiated
!" Myxoid
!" Pleomorphic
Liposarcoma: Well-Differentiated
[Figures 17 & 18]
!" Predominantly fatty mass, usually more
than 75% fat
!" Irregularly thickened or nodular septa
!" Presence of nodular/globular areas
!" A small number of lipomas will have a
similar imaging appearance
!" 50%-80% of lipomas will have
cytogenetic abnormalities. The most
common aberration involves translocation Figure 19 A & B
between 12q13-15 and various other
Well-differentiated liposarcoma (atypical lipoma).
chromosomes, most commonly 1, 2, 3, Typical features. STIR (left) and T1-W (right) MR
and 21. images.
Liposarcoma: Dedifferentiated
[Figures 20 to 22]
!" Bimorphic lesion with:
!"WD liposarcoma
!"Juxtaposed high-grade sarcoma (MFH)
!" Most common dedifferentiated sarcoma
!" May be a time-related phenomenon
!" Imaging typically shows a well-
differentiated fatty mass
!" Fatty mass associated with a focal
dominant nonadipose component
Figure 20
Figure 17 A & B
Dediffer-
Well-differentiated liposarcoma. Typical features.
entiated
liposarcoma,
well-
differentiated
component.
Figure 21
Dedifferentiated
liposarcoma,
high-grade
nonlipomatous
Figure 18 A & B component.
Well-differentiated liposarcoma. Typical features. MR
imaging T1 (left) and T2 (right).

Liposarcoma: Myxoid-Round Cell
Lesions [Figure 24]
!" Since 2002, these lesions are now
accepted by WHO as ends of a common
spectrum
!" About 20% of myxoid lesions will have a
“cyst-like” appearance
Figure 22 A & B
Dedifferentiated liposarcoma. Note well-differentiated
/1>:1$($!*3$&0!"#!3$E*!6(*:(0=3%*@RAD
Liposarcoma: Higher Grade Lesions

[Figure 23]
!" Only 50%-80% of the myxoid, round cell,
or pleomorphic types show fat on imaging
studies
!" Fat usually minor component (< 25%)
!" Round cell and pleomorphic types are
typically more heterogeneous Figure 24 A & B
Myxoid liposarcoma, cyst-like appearance. T1-W (left)

and T2-W (right) MR images.
Liposarcoma: Distribution
Type % Retro Extremity
!" Well-differentiated 54 54 54
!" Myxoid 23 9 27
!" Pleomorphic 7 5 8
!" Dedifferentiated 10 32 4
Figure 23 A & B *Includes hypercellular myxoid liposarcoma
Myxoid liposarcoma, typical imaging features. T1 Liposarcoma: Mimics

(left) and T2 (right). !" Hemorrhage
!" Encased/engulfed/reactive fat
!" Muscle atrophy with fat replacement
!" Myxoid tumors
!" Neural tumors
Lipomatous Tumors: Summary

!" Fatty tumors are common
!" There is a wide spectrum of appearances
!" Imaging is frequently characteristic
References
1. Peterson, et al. Malignant fatty tumors. Skeletal Radiol 2003;32:493.

2. Kransdorf, et al. Fat-containing masses of the extremities. RadioGraphics 1991;11:81.
3. Fletcher, CD, Unni D, Mertens F. Pathology and genetics of tumours of soft tissue and bone. WHO
%'/77"$%/("*.)*#)(&8*-7S)H<*.M)K-/.%,S)U^LF)G-,77Y)XAAXS
4. Weiss & Goldblum. Enzinger and Weiss’s soft tissue tumors, 5th ed. St. Louis. CV Mosby; 2008.

Metabolic Bone Disease

Learning Objectives
!" Identify the pathophysiological alterations
that occur in rickets and osteomalacia
!" Recognize the spectrum of radiological
features of these diseases
Metabolic Bone Disease

!" Systemic diseases which affect the
skeleton diffusely and are the result of
metabolic disorders
Rickets
!" Abnormal mineralization and development
of the growth plate
Osteomalacia
!" Inadequate or delayed mineralization of
Figure 2 A & B
mature cortical or spongy bone*
Normal enchondral bone formation.
*Pitt MJ. Rad Clin. 1991;29:97.
Osteoporosis
!" U.7&#$%",.()b&/.("(<)*#).*-8/')1*.,
Osteopenia
!" Increased radiolucency of bone
Osteoporosis
!" Paucity of bone
Osteomalacia
Figure 3 A & B
!" Malformed bone
Normal bone formation (left) and richetic bone
formation (right).
Vitamin D: Prohormone
!" D2: synthetic
!" D3: natural
Vitamin D: Biochemistry [Figure 1]
Figure 1 Figure 4
Biochemistry of vitamin D. Osteoid seams.
Rickets: Radiographic Features

Pitt MJ. Rad Clin. 1991;29:97. !" ;*.7:,%"$%)#,/(&-,7
!" Growth plate abnormalities
Vitamin D: 1, 25 Dihydroxyvitamin D !" Skeletal deformities
[Figures 2 to 4]
!" Most active form of vitamin D Rickets: N&,#;($-4$+Features
!" Calcium/phosphorus homeostasis !" Osteopenia
!" Maintenance bone mineralization !" Growth retardation
Metabolic Bone Disease 1075 Musculoskeletal Radiology

Rickets: Growth Plate Abnormalities
[Figures 5 to 8]
!" Axial widening
!" Metaphyseal lucency
!" Metaphyseal cupping
Figure 8 A & B
Healing rickets with

metaphyseal lucent
bands (right) and
macrosection (upper
left).
Rickets: Skeletal Deformities

[Figures 9 to 12]
!" Craniotabes
!" Rachitic rosary
Figure 5 A & B !" Bowing of long bones
Radiographic changes of rickets. !" Scoliosis
!" Basilar invagination
!" Triradiate pelvis
Figure 6 A & B
Dietary rickets with treatment. Presentation (left) and Figure 9
one month following treatment (right). Craniotabes.
Dietary rickets with treatment. Two months (left) and Overgrowth wrist cartilage (left) with corresponding
four months (right) following treatment. clinical photograph (right).

Figure 13 A & B
Figure 11 A & B
Skeletal deformities. Coarse trabecular pattern and Looser zone.
Radiograph (left) and specimen radiograph (right).
Figure 14 A & B
Figure 12 A & B
Looser zone with (left) and without (right) fracture.
Basilar invagination (left) and triradiate pelvis (right).
Osteomalacia: Classic Radiographic

Features [Figures 13 to 15]
!" Osteopenia
!" Coarse trabecular pattern with unclear
margins
!" Looser zones
!" Features can be seen in rickets
Figure 15 A & B
Looser zones.

Vitamin D: [Figures 16 & 17]
!" g"(/8".)!?+,$%",.(
!" GI malabsorption
!" Neonatal
Figure 18 A & B
Osteomalacia (left) from anticonvulsant therapy and
rickets (right) from neonatal hepatitis.
Figure 16 A & B
Rickets with fracture distal left femur.
Figure 19 A & B
Figure 17
Renal osteodystrophy (left) and Fanconi syndrome
Rickets from necrotizing enterocolitis. (right).
25-OH Vitamin D [Figure 18]

!" Liver disease
!" Anticonvulsant therapy
Renal Related [Figures 19 to 21]

!" 1, 25 Dihydroxyvit D
!"Renal osteodystrophy
!"Vitamin D dependent rickets
!"Tumor related
!" Renal tubular disorders
!"X-linked hypophosphatasia
!"Familial vitamin D resistant rickets
!"Fanconi syndrome
!"Tumor related
!"Ifosfamide Figure 20 A & B
Rickets due to ifosfamide therapy.

Oncogenic osteomalacia. Metaphyseal chondrodysplasia.
No Abnormality [Figure 22] Summary

!" Axial osteomalacia !" The radiographic features of metabolic
!" Hypophosphatasia bone disease or frequently characteristic
!" Metaphyseal chondrodysplasia !" P9,7,)%9/.2,7)/%%&-/(,'<)-,C,%()(9,)
underlying pathophysiology
References
1. Sundaram, et al. Oncogenic osteomalacia. Skeletal Radiol 2000;29:117.

2. _*'"%WS)g"(/8".)!)+,$%",.%<[)a9/()/):/".)"()"7S)V/<*)F'".)G-*%)XAA5Y\d[@=>\S
3. Narchi, et al. Symptomatic rickets in adolescence. Arch Dis Chil 2001;84:501.
4. Pitt. Rickets and osteomalacia. In: Resnick. Diagnosis of bone and joint disorders, 4th ed. Philadelphia,
W.B. Saunders Company, 2002:1901.

1080
Osteonecrosis, Related Conditions, and Femoroacetabular
Impingement
Learning Objectives Location
!" Identify the spectrum of radiological !" Osteonecrosis is most common in the
features of osteonecrosis epiphysis
!" Recognize various associated conditions !" Ischemic necrosis or bone infarct
!" Identify differentiating features occur almost exclusively in areas of
predominantly fatty marrow
Outline
!" !,$."("*.7 Osteonecrosis: Radiologic - Pathologic
!" Pathophysiology of osteonecrosis Correlation [Figures 2 to 4]
!" Infarct geometry !" Phase I: cellular death initial response
!" Radiologic-pathologic correlation !" Phase II: cell modulation
!" Associations !" Phase III: emergence reactive interface
!" Complications !" Phase IV: remodeling reactive interface
!" Phase V: crescent sign and collapse
D(4,-)-&,#
!" Osteonecrosis: ischemic death of cellular
components of bone and marrow
!" Aseptic necrosis: equivalent to ischemic
necrosis and avascular necrosis
!" Bone infarct: osteonecrosis involving the
metaphysis or diaphysis
Pathophysiology: Osteonecrosis
!" Cellular changes from ischemic injury
!"Interruption of intracellular enzymes
!"Cessation intracellular metabolic
activity
!"Cell death
!" Cellular sensitivity to anoxia
Figure 2
!"Hematopoietic elements (6-12 hours)
Bilateral femoral head osteonecrosis.
!"Bone cells (12-48 hours)
!"Marrow fat cells (48 hours - 5 days)
Infarct Geometry: Zones [Figure 1]

!" Central zone of cell death
!" Ischemic injury
!" Active hyperemia
!" Normal tissue
Figure 3 A & B
Radiograph (left) and specimen radiograph (right)

showing osteonecrosis with collapse and crescent sign.
Figure 1 A & B
Figure 4 A & B
Infarct geometry. Corresponding gross (left) and macro section (right)
showing osteonecrosis with collapse and crescent
sign.
Osteonecrosis and Related Conditions 1081 Musculoskeletal Radiology

Associations
!" Dysbaric disorders
!" Gaucher disease
!" Pregnancy
!" Irradiation
!" Pancreatitis
!" Trauma
!" Hemoglobinopathy
!" Steroids
!" Alcoholism
!" Collage vascular disease
Osteonecrosis: Causes
!" Thrombophilia (increased tendency to
develop thrombosis)
!" _<:*$1-".*'<7"7)0-,+&%,+)/1"'"(<)(*)'<7,)
thrombi) Figure 6
!" Found in 76% of patients with
7#)31E"#:6*%61<3$E*?#!!($3$E*<3!6*/100#:%(*#$)*
osteonecrosis* crescent sign.
*Glueck, et al. Osteonecrosis. AAOS. 1997.
Osteonecrosis: Causes [Figure 5]

!" Increased size fat cell ! compresses
sinusoid vascular bed ! impedes blood
C*a
Figure 5
Radiograph
showing
typical
serpentine
margin of Figure 7
infarct.
Osteonecrosis of proximal pole of scaphoid with
surrounding osteopenia.
Imaging Features: Scintigraphy [Figure 8]

!" Decreased or absent uptake initially
!" Increased uptake with repair and
“ASEPTIC” revascularization
!" Trauma
!" Idiopathic
!" Caisson disease (dysbaric)
!" Alcoholism
!" Sickle cell anemia
!" Exogenous steroids
!" Pancreatitis
Imaging Features: Radiographs

[Figures 6 & 7]
!" Patchy lucent/sclerotic areas
!" Serpentine sclerosis
!" Arc-like subchondral lucencies
Figure 8 A & B
!" Articular collapse
!" Preservation of joint space Bilateral osteonecrosis with increased tracer
!" Surrounding osteopenia accumulation on right, whereas left is normal.

Imaging Features: CT [Figures 9 & 10]
!" g/-"/1',)$.+".27)a"(9)/2,)*#)',7"*.
!" Alterations in osseous architecture
!" Useful to evaluate the integrity of the
articular surface
Figure 12 A & B
Osteonecrosis with edema pattern.
Figure 9
CT showing reactive interface bilaterally. Transient Osteoporosis [Figures 13 & 14]
!" Described originally in third trimester
!" Typically young and middle-aged adults
!" Progressive hip pain, symptoms regress in
2-6 months
!" Edema pattern on MR, osteoporosis on
radiographs
Figure 10
Bilateral osteonecrosis with collapse on left.
Imaging Features: MRI [Figures 11 & 12]

!" Ring or band pattern
!" Homogeneous or heterogeneous
!" ”Double line” sign
!" Joint effusion
!" Marrow edema
!" Articular collapse
Figure 13 A & B
Transient osteoporosis with edema pattern and no
osteonecrosis.
Figure 11 A & B
Figure 14
Osteonecrosis and infarcts with “double line” sign.
Note regional osteoporosis of right hip.

Radiologic Staging [Figure 15]
Stage Findings
0 Clinically suspected, imaging normal
)))@))))F'"."%/')$.+".27M)/1.*-8/')7%".("2-/8
2 Osteopenia, cysts, bone sclerosis
3 Crescent sign without collapse
4 Flattening with normal joint space
5 Joint narrowing with abnormal acetabulum
Figure 15
Bilateral
osteonecrosis.
Figure 17 A & B
Note “screw treads” extending through infarct with
associated high grade sarcoma.
Complications: Osteonecrosis
[Figures 16 & 17]
!" Cartilaginous abnormalities Summary:
!" Intraarticular loose bodies !" Morphologic changes in osteonecrosis are
!" Cyst formation relatively characteristic, although they will
!" Malignant transformation vary with location
!" There are a variety of predisposing
conditions, as well as those patients in
which no cause is found
!" Imaging features are usually
characteristic
Figure 16 A & B
Infarct with malignant transformation.

FAI: Radiographic Features
Learning Objectives:
!" Identify the types of femoroacetabular
impingement (FAI)
!" Identify diagnostic criteria
!" Recognize potential imaging pitfalls
FAI
!" Characterized by abnormal contact
between the femoral head and the
acetabulum
!" H"8"(7)9":)8*("*.M),7:,%"/''<)".)C,3"*.)/.+)
internal rotation
!" Major cause of early osteoarthritis
FAI: Presentation
!" Young patients, 20-40 years Figure 20
!" Estimated prevalence ~ 15%
Positioning is critical for accurate diagnosis.
!" Groin pain with hip rotation
!" Limited hip mobility
FAI: Types
!" Cam: abutment of abnormally shaped
femoral head against the acetabular rim
!" Pincer: acetabular overcoverage limits hip
motion
!" Both types may be present
FAI: Cam Type [Figure 18]

!" More common in young men
!" Nonspherical shape to femoral head at
head-neck junction
!" Reduced depth of femoral waist
!" Abutment of head-neck junction against
acetabulum
Figure 21 A & B
Figure 18
Radiographs showing cam type FAI.
Tannast, et al. AJR. 2007;188:1540–1552.
FAI: Pincer Type [Figure 19]

!" More common in middle-aged women
!" Acetabular overcoverage leads to contact
between acetabular rim and femoral
head-neck junction
!" Contrecoup injury to posterior inferior
joint
Figure 19
Figure 22 A & B
MR arthrogram of 16-year-old adolescent with cam

type FAI (left) with corresponding intraoperative
photograph (right).

Figure 24 A & B
Pincer type FAI with abnormal CE (center-edge) angle

(left) vs normal (right).
Figure 25
Tannast, et al. AJR. 2007;188:1540–1552.
Figure 23 A & B
Pincer type FAI with protrusio acetabuli (left) vs

normal (right).
Figure 26 A & B
Positive “cross-over” sign.

FAI Summary
!" Two forms; both may be present
!" Usually in young, active individuals
!" Radiographic features may be
characteristic
References
General
1. Sweet, et al. Osteonecrosis: pathogenesis. In: Resnick D, ed. Diagnosis of bone and joint disorders, 4th
ed. Philadelphia: WB Saunders, 2002.
2. Iida, et al. Correlation between bone marrow edema and collapse of the femoral head in steroid-induced
osteonecrosis. AJR Am J Roentgenol 2000;174:735.
3. Vande Berg, et al. MR imaging of avascular necrosis and transient marrow edema of the femoral head.
RadioGraphics 1993;13:501.
4. J'&,%WM),()/'S)P9-*8*:9"'"/M)9<:*$1-".*'<7"7M)/.+)*7(,*.,%-*7"7S)F'".)B-(9*:)@ZZ\Y55=[=5S
Femoracetabular Impingement
5. Ganz R, Parvizi J, Beck M, Leunig M, Nötzli H, Siebenrock KA. Femoroacetabular impingement: a cause for
osteoarthritis of the hip. Clin Orthop Relat Res 2003;417:1–9.
6. Tannast M, Siebenrock KA, Anderson SE. Femoroacetabular impingement: radiographic diagnosis—what
the radiologist should know. AJR Am J Roentgenol 2007;188:1540–52.
7. G$--8/..)FN^M)V,.2"/-+")OM)!*-/)FM)h/'1,-,-)KM)n/.,((")VM)_*+',-)RS)F/8)/.+):".%,-)#,8*-*/%,(/1&'/-)
"8:".2,8,.([)%9/-/%(,-"7("%)VL)/-(9-*2-/:9"%)$.+".27)".)>A):/(",.(7S)L/+"*'*2<)XAAe[X=A[\\d?d>S

1088
Skeletal Metastases, Myeloma, Lymphoma
Michael E. Mulligan, MD
Incidence of Metastases [Figure 1]
!" 30% of all patients with cancer
!" Skeleton is most common site
!" More than 80% due to PTBLK
!" #1 breast, #2 prostate, #3 lung
!" Spine lesion: breast 75%
!" Femur lesion: breast 50%
!" Skull lesion: MM, B, L
!" Hands/feet: lung
!" PTBLK: P=prostate, T=thyroid, B=breast, Figure 2
L=lung, K=kidney. “P.T. barnum loves
A 55-year-old
Kids” man with lung
cancer and cortical
“cookie bite”
metastasis.
Figure 1
A 48-year-
old man with
renal cell
carcinoma
metastases
mimicking
multiple
myeloma.
Bone Metastases: Systemic Features
[Figure 3]
!" Hypercalcemia
Mechanism of Spread to Bones !" Hypertrophic ostearthropathy
Hematogenous/Contiguous Classic Triad
Marrow vessels unusual, rich sinusoidal
!" !"Joint swelling, 30%-40% patients
system with large endothelial gaps !"5% patients with lung cancer
!" Batson’s plexus has direct connection to !"F/&7,I)V/<)1,):/-/.,*:'/7("%M)2-*a(9)
IVC/SVC with no valves hormone releasing factor
!" ^-(,-"/'[)8,%9/."78)#*-)+"7(/')8,(7I)
Batson OV. Ann Surg. 1940;112:138.
Bone Metastases
!" Symptoms and signs
!"Pain most common symptom, but only
in 2/3 patients
!"Pathologic fracture
Figure 3
#" Common sign, especially bad in
spine, femur Typical thick,
solid, smooth
Pathologic Fractures [Figure 2] periosteal
!" 5%-10% of all patients with metastases reaction along
the tibia and
!" > 50% cortex gone; 25%-66% will
&+.0#*!6#!*3%*
develop pathologic fracture characteristic
!" Less than 50% cortex gone; 10%-20% of hypertrophic
will develop pathologic fracture osteoarthropathy
!" Any lesion in femoral neck in this 54-year
old-man with
!" Avulsion of lesser trochanter lung cancer.
!" Any lesion femoral cortex > 3 cm long1
!" Mirels score: site, size, l/b, pain2
!" 3- cm lesion with persistent pain after
XRT
1
Van der Linden, et al. JBJS [Br]. 2004;86:566-573.
2
Mirels H. Clin Ortho Rel Res. 1989;249:256-264.
Metastases, Myeloma, Lymphoma 1089 Musculoskeletal Radiology

Bone Metastases Radiologic Features Breast Carcinoma [Figure 5]
“Mets can look like anything” !" The most common source of bone mets in
!" Pure lysis women
!" Lysis with blowout (renal, thyroid) !" Spine #1 site
!" Mixed lytic/blastic (breast, lung, GI) !" 65% lytic, 25% mixed, 10% blastic
!" Pure blastic (prostate, carcinoid,
medulloblastoma)
Osteoclast: Activating Factor (A

Cytokine)
!" Stimulates clasts to synthesize
collagenase
!" Produced by normal activated leukocytes
!" Dependent on prostaglandin E
!" Prostaglandin inhibitors can reduce/
obliterate osteolysis
JBJS. 68A:310, FEB 1986.
Osteoclast: Stimulating Factor

!" A cytokine (lymphotoxin alpha)
!" Similar to osteoclast - activating factor
!" Produced by myeloma cells, T cells
!" Interferon is a cytokine antagonist
!" Bisphosphonates used to counter
osteoclastic resorption
Cancer. 1997;80:1557-1563. Figure 5
Somewhat unusual blastic breast cancer metastasis
Bone Metastases: Radiologic Features centered at the base of the middle meningeal artery
!" Ivory vertebra groove of this 46-year-old woman.
!" Pathologic fx
!" Periosteal rx: prostate, lung
neuroblastoma, GI tumors Prostate [Figure 6]
!" Missing pedicle !" The most common source of metastases
!" Intracortical: lung cancer in men
!" Soft tissue mass (lung) !" More than 1/3 of patients
!" 75% blastic, 15% mixed, 10% lytic
Ivory Vertebra (AE) [Figure 4] !" Humoral factor stimulates osteoblasts
!" #1 Paget 50%
!" #2 Hodgkin 30%
!" #3 Metastasis 20%
Souques A, Lafourcade, T. “Vertebra D’Ivoire”
Dans un cas de Cancer Matastatique de la Col-
onne Vertebrale. Rev Neurol. 1925;32:3-10.
Figure 6
A 76-year-
old man
<3!6*?1"3)*
Figure 4 periosteal
reaction
A 59-year-old around
woman with )3%!#0*&+.0#*
multiple ivory metastasis.
vertebrae
secondary to
breast cancer
metastases.

Lung Cancer [Figure 7]
!" 15% of patients have mets to bone
!" 80% lytic, 15% mixed, 5% blastic
!" Small cell – 20% blastic
Figure 9
A 3-year-
Figure 7 old boy with
neuroblastoma.
Lung
Metastasis
cancer.
in proximal
radius shows
permeative
appearance
similar to
Ewing sarcoma.
Renal Cell Carcinoma [Figure 8]

!" 25%-30% of patients have mets to bone
!" 90% lytic
Workup of Patient with Metastases

From Unknown Primary
!" 1 – History/physical
!" 2 – Lab studies
!" Direct workup based on 1, 2
!" Primary not found in up to 60% patients
Cancer. 1986;58:1088-1095.
Solitary Focus Tc99m Bone Scan or

PET/CT [Figure 10]
!" Seen in 2%-15% of cancer patients
!" % due to metastatic disease varies by site
of involvement and technique
!" 10% solitary rib lesions on BS1
!" 50%-60% in other BS locations (spine)2
!" 10% malignant even if there is “DJD” in
the area
!" 98% PPV when PET and CT agree3
Figure 8 A & B
1
J Nucl Med. 1985;26:1140-1143.
A 71-year-old man with blowout type metastasis
from renal cell cancer. Note active hyperemia on
2
Radiology. 1976;121:663-667.
angiogram.
3
Radiology. 2007;243:204-211.
Thyroid Cancer
!" 8% of patients have mets, lytic
Neuroblastoma [Figure 9]
!" 1st choice any patient under 10 years old
!" Can mimic primary malignancy
!" Usually multiple, often symmetric
!" Histology can be confused with Ewing
!" Periosteal Rx – aggressive

Durie/Salmon PLUS staging* radiolo-
gist’s role is to help determine, for stag-
ing the total myeloma cell mass within
the skeleton. [Figure 11]
!" Stage IA: normal skeletal survey or single
lesion
!" Stage IB: < 5 focal lesions or mild diffuse
Figure 10 disease
!" Stage IIA/B: 5-20 focal lesions or
A 65-year-
old man with moderately diffuse
solitary rib !" Stage IIIA/B: > 20 focal lesions or severe
abnormality diffuse disease
on whole body !" Subclasses A and B (A = normal renal
bone scan,
proven to be
function, B = abnormal)
esophageal !" Stage is generally predictive of survival
cancer !"IA median survival = 60 months
metastasis. !"IIIB median survival = 15 months
*Durie, et al. Myeloma Management Guidelines:
a Consensus Report. The Hematology Journal.
2003;4:379-398.
Malignant Round Cell Tumors of Bone

!" Myeloma
!" Lymphoma
!" Ewing sarcoma
!" Neuroblastoma
!" Rhabdomyosarcoma
!" Small cell carcinoma
!" PNET
Myeloma: Pathologic Features

!" Plasma cells proliferate in erythropoietic
areas Figure 11 A, B & C
!" Grossly: dark red, tan; soft The three types of myelomatous spinal involvement
!" Histology: sheets of malignant plasma for the Durie/Salmon PLUS staging system (T1-WIs).
cells obliterate the marrow
!" Special studies: markers for light chains
!" Amyloid (10%)
!" Osteoclast stimulating factors and blast
suppression result in focal lytic lesions Myeloma: Imaging Features [Figure 12]
!" 80/100 new MM patients: will have
Classic Multiple Myeloma: Clinical abnormal skeletal survey. May want
Features to add spine MRI (3 patterns: mild,
!" Signs and symptoms: pain, bleeding moderate, severe) and/or PET/CT.
+"/(9,7"7M)".#,%("*.M)-,./')".7&#$%",.%< !" V&'(":',)8<,'*8/)c)C/()1*.,7Y):&.%9,+)
!" H/1)$.+".27[)8*.*%'*./')7:"W,7)0U2JM) out lesions – long bones; endosteal
IgA), Bence-Jones (B-J) proteinuria, scalloping
anemia, hypercalcemia, elevated alkaline !" Solitary plasmacytoma: bubbly, any
phosphatase margin +/- soft tissue mass
!" Imaging W/U: X-rays, CT, MRI, Nucs, PET, !" Generalized form: just osteopenia
PET/CT1 !" Sclerosing < 3%, associated with POEMS
!" Multiple myeloma (MM) has a highly syndrome
malignant course
International working group consensus
1.
statement on imaging. Leukemia. 2009;23:1545-

1556.

Primary Lymphocytic Lymphoma of
Bone [Figure 13]

Lateral spine radiographs of two men with the a 70-year-old man with PLB. Skull radiograph shows
generalized form of myeloma. multiple lytic lesions, some with central sequestra.
Left Image: 35-year-old man.
Right Image: 64-year-old man.
Primary Lymphoma: Path Features

Sclerotic Myeloma !" J-*77[):".W"79?2-/<M)m$79)C,79l
!" Two types: MM with sclerosis and POEMS !" Histology: similar to nodal lymphoma
syndrome round cells of various sizes (Ewing
!"Polyneuropathy* monotonous)
!"Organomegaly !" L,("%&'".)7(/".[)8,79a*-W)*#)$1,-7)/-*&.+)
!"Endocrinopathy each cell
!"Monoclonal gammopathy*
!"Skin changes Primary Lymphoma: Clinical Features
* = major criteria !" Non-Hodgkin (94%), Hodgkin (6%)
Dispenzieri A (Mayo Clinic). Hematology. 2005; !" Rare 3% malignant bone tumors
360-367. !" Any age, but rare under age 10
!" Stage like soft tissue lymphoma
POEMS Syndrome !" Solitary or multifocal (skull, femur, tibia,
!" Two major criteria spine)
!"Polyneuropathy and monoclonal !" Osteoclast stimulating factor
plasma cell disorder !" Excellent prognosis (100% 5-year survival
!" Minor criteria Clev Clin)
!"Sclerotic bone lesions (often a single Kirsch, et al. Skeletal Radiol. 2006;35:590-594.
lesion)
!"Castleman disease (giant Primary Lymphoma Bone (PLB): 237
lymphadenophathy) AFIP CASES
!"Organomegaly !" 151 M, 86 F, ratio 1.8:1
!"Endocrinopathy (diabetes) and/or !" Average age 42 years old (range: 2-88
edema years old)
!"Skin changes (hyperpigmentation) !" Long bones n = 162 (71%)
!"Papilledema !" Flat bones n = 78 (22%)
!" Treatment: radiotherapy for bone lesions, !" Other sites (including spine, small bones)
steroids and chemotherapy for other n = 17
symptoms Mulligan, et al. AJR. 1999;173:1691-1697.
!" Prognosis: 14-year median survival
Myeloma: Differential Diagnosis

!" Metastatic disease
!" B cell malignancy:
!"ALL, NHL, CLL, Waldenström
macroglobulinemia
Plasmacytoma: Differential Diagnosis

!" Metastasis: thyroid, renal
!" G-"8/-<[)$1-*7/-%*8/M)VK_

PLB: Typical Features [Figure 14]
!" Location: metadiaphyseal n = 120 (54%)
!" Pattern: permeative n = 130 (55%)
!" Cortical involvement: n = 148 (62%)
!" Periosteal reaction: interrupted or solid
single layer n = 57 (65.5%)
!" Soft tissue mass: n = 113 (48%)
Mulligan, et al. AJR. 1999;173:1691-1697.
Figure 15B
Markedly
abnormal
bone scan
Figure 14 and MR
exam in a
A 57-year-old 57-year-old
woman with man with
PLB. Tibia lesion thigh pain
shows all of the and normal
most common X-rays.
radiographic
features.
PLB: Variations [Figure 15]

!" Location
!"Epiphysis n = 11 (5%) PLB: Variations [Figure 16]
!"Diaphysis n = 45 (19%) !" Periosteal reaction
!"Intracortical n = 16 (7%) !"Multiple layers n = 26 (10.2%)
!" Patterns !"Sunburst n = 4 (1.6%)
!"Normal X-ray n = 12 (5%) !" Pathologic fracture n = 52 (22%)
!"Geographic n = 26 (11%) !" Sequestra n = 37 (15.6%)
!"“Blow out” n = 2 (< 1%) !" Crossing joint n = 12 (5%)
!"Blastic n = 4 (2%)
AJR. 1999;173:1691-1697.
Figure 15A
This type of
extensive
marrow Figure 16
replacement
pattern Large lytic
with normal lesions with
X-rays soft tissue
is highly mass and
suggestive of sequestra
“round blue should put
cell tumors” PLB high
like PLB up in the
and Ewing differential
sarcoma. diagnosis.

Radionuclide, CT, and MRI Findings PLB: Summary
!" Radionuclides n = 56, markedly increased !" Usually has an aggressive appearance
uptake n = 36 (64%) !"CT or MRI showing large soft tissue
!" CT n = 45 mass without large cortical holes is
!" MRI n = 20 typical
!" “Cortical holes” by CT or MR !" Wide range of appearances
!" Large n = 20 (31%), small n = 45 (69%) !"Normal X-rays
!" Soft tissue mass !"Geographic lesions
!"Seen by CT n = 36 (80%) !"“Blow out” lesions
!"Seen by MR n = 20 (100%) !"Blastic lesions
PLB: Differential Diagnosis

!" Metastatic lymphoma
!" Ewing sarcoma
!" Neuroblastoma/PNET
!" Rhabdomyosarcoma
!" Osteomyelitis
!" Eosinophilic granuloma
References
1. Mulligan M, et al. Skeletal Metastatic Disease. In Pope, et al. Imaging of the Musculoskeletal System.
Philadelphia: Elsevier, 2008.
2. Roodman GD. Mechanisms of bone metastasis. N Engl J Med 2004;350:1655-64.
3. Mirels H. Metastatic disease in long bones. Clin Orthop Relat Res 1989;249:256-64.
4. Van der Linden, et al. Comparative analysis of risk factors for pathological fracture with femoral
metastases. J Bone Joint Surg Br 2004;86:566-73.
5. Weber K. et al. An approach to the management of the patient with metastatic bone disease. Instr Course
Lect 2004;53:663-76.
6. Durie B, et al. Myeloma management guidelines: a consensus report. The Hematology Journal
2003;4:379-98.
7. Mulligan M. Imaging techniques used in the diagnosis, staging, and follow-up of patients with myeloma.
Acta Radiologica 2005;46:716-24.
8. Mulligan M, Badros A. PET/CT and MR imaging in myeloma. Skeletal Radiol 2007;36:5-16.
9. Dimopoulos M, et al. International myeloma working group consensus statement and guidelines regarding
the current role of imaging techniques in the diagnosis and monitoring of multiple myeloma. Leukemia
2009;23:1545-56.
10. Dispenzieri A. POEMS syndrome. Blood Rev 2007;21:285-99.
11. Mulligan M, McRae G, Murphey M. Imaging features of primary lymphoma of bone. AJR Am J Roentgenol
1999;173:1691-7.

1096
Imaging of Hematologic Disease

Objectives Economic Impact of SC Disease
!" To identify the most common hematologic !" 75,000 hospitalizations yearly
disorders !" $475 million in healthcare costs alone
!" To identify the major clinical and !" Does not include lost wages, productivity,
epidemiological aspects of these entities etc
!" P*)+,8*.7(-/(,)(9,)8*7()7"2."$%/.() !" Cost > $1 billion annually
"8/2".2)$.+".27)0,7:,%"/''<)(9,)VQh)
features) Major MSK Imaging Features SC Disease
!" To expose you to a little “nonradiology” [Figures 1 to 5]
along the way !" Hand and foot syndrome
!"Dactylitis
Hematologic Disease !" Infarction (any site)
!" Hereditary anemias !" Infection
!"Sickle cell anemia !" Marrow hyperplasia
!"Thalassemia
!"Rare anemias: Fanconi
thrombocytopenia with absent radii
syndrome (TARs)
!" Coagulation disorders
!"Hemophilia
!"V<,'*$1-*7"7
Characteristics of the Hereditary

Anemias
!" Aberrations and/or abnormalities of RBC
shape
!" Molecularly distinctive
!" Electrophoresis
!" The Five “In’s”
!"In)7&#$%",.()*77"$%/("*.
!"In farction
!"In fection
!"In failure (anemia) Figure 1 A & B
!"In volution (spleen) Radiographic manifestations of Hand and foot
syndrome. Left image: hand. Right image: foot.
Sickle Cell Disease
!" One of the most common inherited blood
disorders (> 100,000 born with the
disease worldwide per year)
!" One of the most prevalent genetic
disorders in the US (> 80,000 African
Americans)
!" Hemoglobin SC disease (carrier state)
!"Autosomal dominant inheritance Figure 2A
!"8% of African Americans at birth
(2 million US African Americans) Radiographic
changes of hand
!" Hemoglobin SS disease (Sickle cell and foot syndrome
anemia) in the forearm and
!"Autosomal recessive inheritance lower extremity.
!"0.3%-1.3% of North American Blacks
(50,000 in the US)
Imaging of Hematologic Disease 1097 Musculoskeletal Radiology

Figure 2B
Radiographic
changes
of hand
and foot
syndrome in
the forearm
and lower
extremity.
Figure 3 A & B
“Rim sign” in avascular necrosis of the femoral head
(stage III).
Figure 5 A & B
Intramedullary infarction in patient with sickle cell
anemia.
Differential Diagnosis: “Bone within

Bone” Appearance
!" S – Sickle cell disease
!" T – Thoratrast
!" O – Osteopetrosis
!" P – Paget disease
!" Heavy metal
!" Hypervitaminosis D
http://chorus.mcw.edu
“H-Shaped” Vertebral Bodies

[Figure 6]
!" > 10 years old
!" Ischemia and infarction
!" Incidence:
Figure 4 A & B
!"43% of SS
Stage C (top) Stage D (bottom) and AVN of the !"36% of sickle/thalassemia
femoral heads in an 11-year-old sickle cell patient with
bilateral hip pain (Mitchell staging system). !"25% of SC

Figure 6 A & B
“H-shaped” or “Lincoln log” vertebral bodies in patient
with sickle cell anemia.
Osteomyelitis [Figure 7]
!" 100 times > SC patients
!" S aureus most common
!" Salmonella 5x > in sickle cell patients
!" Proposed mechanisms: Figure 7B
!"g/7%&'/-)".7&#$%",.%< Chronic Salmonella osteomyelitis (B = cloaca
!"Decreased phagocytosis-low O formation).
!"Decreased splenic function
!"Multiple hospitalizations
Thalassemia
!" Cooley and Lee (1925)
!" Synonyms: Cooley anemia, mediterranean
anemia, leptocytosis
!" Impaired alpha or beta chain Hgb
production
!" Homozygous beta thalassemia (800-1000
US persons – NE corridor between Boston
and NY)
!" Heterozygous trait (2.5% of Italian
Americans, 7%-10% of Greek Americans)
Types of Thalassemia
!" Alpha
!"Africa, Middle East, India, SE
Asia, Southern China, occasionally
Mediterranean descent
!" Beta:
!"Mediterranean descent (Italians and
Greeks), less commonly in Arabian
Peninsula, Iran, Africa, SE Asia, and
China
Types of Thalassemia
!" Alpha
!"Silent carrier = loss of 1 alpha globulin
2,.,)0".%"+,.(/')$.+".24M)(*)9<+-*:7)
fetalis = loss of 4 alpha globulin genes
(die before birth)
!" Beta
!"Minor (slight anemia) to major (life-
threatening anemia); Fe++ overload
with chelation therapy to prevent
Figure 7A
organ failure
Chronic Salmonella osteomyelitis (A = sequestrum
formation).

Imaging Features of Thalassemia Imaging Features
[Figures 8 & 9] !" AVN of the hip and femoral head
!" Diffuse marrow expansion !" Osteoporosis
!"Skull: (“hair-on-end” appearance) !" Marrow expansion with cortical thinning
!"Face: (“rodent-like facies”) !" ]-',.8,<,-)C/7W)+,#*-8"(<
!"H*.2)1*.,7[)m]-',.8,<,-)C/7Wl) !" Lytic lesions and sometimes periostitis
deformity
!" Extramedullary hematopoeisis Erlenmeyer Flask Deformity
!" Rare minor features: growth disturbances, !" Osteoporosis
fractures, crystal deposition !" Chronic anemia (sickle cell disease)
!" Gaucher disease
Figure 8 !" ;",8/..?G"%W)0,.`<8,)+,$%",.%<4
!" Fibrous dysplasia
Lateral !" Metaphyseal dysplasia (Pyle disease)
skull
radiograph
of a patient
Extramedullary Hematopoeisis
with [Figure 10]
thalassemia !" Blood production in fetal regions
showing !"Liver, spleen, adrenal, thymus, heart,
the classic
(“Aunt
lung, nodes, renal pelvis, GI tract,
Minnie”) dura mater (almost anywhere)
appearance !" Major causes:
of “hair-on- !"Hematologic disease (SS and
end.” thalassemia)
!"V<,'*$1-*7"7
!"Leukemia
!"Hodgkin
!"Hyperparathyroidism
!"Rickets
!"Carcinomatosis
Figure 9 A & B
Hand and forearm
&0>%*3$*:#!3($!*<3!6*
thalassemia showing
marrow expansion.
Gaucher Disease
!" Ashkenazic Jews of Eastern European
descent
!" Defect of beta glucosidase
!" Accumulation of glycosyl ceramide in the
RE cells of BM, spleen, and liver Figure 10 A & B
!" Hepatosplenomegaly, yellow skin,
Extramedullary hematopoesis in thalassemia. Note
scleral pigmentation, acid and alkaline hepatosplenomegaly and paravertebral soft tissue
phosphatase elevation masses (arrows).

Fanconi Anemia
!" B.7,()/#(,-)$-7()+,%/+,
!" Severe anemia, pancytopenia, brown
pigmentation
!" Death 2-3 years after appearance
!" Anomalies:
!"Radius absent (50%)
!"Thumb always absent
!"Short stature, microcephaly, delayed
*77"$%/("*.
!"Hip dysplasia, renal anomalies
Thrombocytopenia with Absent Radii

(TAR)
!" Congenital hypomegakaryocytic
thrombocytopenia
Figure 12 A & B
!" Apparent at birth or shortly thereafter
!" Anomalies: Standing AP
!"Bilateral radial aplasia always present radiograph of
both knees and
!"Thumb is present (differentiation from “tunnel” view
Fanconi) of left knee of
!" U#)W"+7)7&-E"E,)#*-)(9,)$-7()(a*)<,/-7M)(9,) a patient with
anemia often spontaneously resolves hemophilia
showing
widening of the
Hemophilia [Figures 11 to 13]
intercondylar
!" Oldest known hereditary bleeding disorder notch.
!" Group of X-linked recessive disorders
!" Gene carried by women and expressed in
men
!" Common associations:
!"F*/2&'/("*.)/.*8/'<)*-)+,$%",.%<)*#)
clotting factor
!" 20,000 hemophiliacs in US
!" 400 new cases/year
!" Severity of disease related to the amount
of clotting factor in blood
Figure 13 A & B
Figure 11 A & B
Lateral knee Lateral elbow
radiographs in and frontal pelvic
two patients with radiographs in
hemophilia showing a patient with
dense effusions hemophilia showing
and irregularities of ectopic soft tissue
the distal femoral 1%%3&/#!31$D
condyles.

Major Types of Hemophilia
!" Hemophilia A
!"85% of all cases
!"Lack of antihemophiliac factor (AHF)
+,$%",.%<)0#/%(*-)gUUU4
!"70% have < 1% of normal amounts of
AHF
!" Hemophilia B (Christmas disease) Figure 14
!"15% of all cases Coned-down
!"!,$%",.%<)*#):'/78/)(9-*81*:'/7(".) left iliac view
component (PTC) (factor IX) of patient with
hemophilia
Joint Disease showing an iliac
!" Acute hemarthroses: tense, swollen, intraosseous
pseudotumor.
red, and tender joints; pain; LOM; fever;
increase in WBC
!" Stages of joint disease:
!"Stage I: STS
!"Stage II: Osteoporosis
!"Stage III: Osseous lesions
!"Stage IV: Cartilage destruction
!"Stage V: Joint disorganization
Differential Diagnosis of Hemophilia

!" Juvenile chronic arthritis
!"Single joint tough to differentiate M5(%&4:1&#-#++++++++[Figure 15]
!"Distribution may be helpful !" Other designations:
#" JCA: hands/feet/big joints !"U+"*:/(9"%)8<,'*$1-*7"7
#" Hemophilia: knee, ankle, elbow !"Myeloid metaplasia
!" PVNS, infection, especially TB !"Agnogenic myeloid metaplasia
(monoarticular) !" Uncommon disease associated with
!" NM diseases: CP, muscular dystrophy, $1-*("%)*-)7%',-*("%)1*.,)8/--*a)/.+)
polio extramedullary hematopoiesis
!" Affects progenitor (stem) cells of the bone
Other Less Common Imaging Findings marrow
!" ]%(*:"%)QP)*77"$%/("*.)0:,-"/-("%&'/-[) !" Primary (idiopathic) and secondary forms
pelvis, thigh, paraspinal, knee)
!" Hemophiliac pseudotumor
!" Osteonecrosis (epiphyseal fragmentation)
!" Fractures
!" Chondrocalcinosis
Pseudotumor [Figure 14]

!" 2% of patients
!" Femur, pelvis, tibia, hands, and feet
!" Intraosseous, subperiosteal, soft tissue
!" ST: hard SQ masses
!" IO and subperiosteal: lytic, expansile,
destructive, aggressive process
Differential Diagnosis for Hemophiliac

Pseudotumor
!" Malignancy
!"Osteosarcoma
!"Chondrosarcoma
!"Ewing tumor
!"Metastases
!" Infection
Figure 15A
S*:#!3($!*<3!6*>,(01&+"1%3%*%61<3$E*)344.%(*+1$,*
sclerosis characteristic of the disease.

Secondary M5(%&4:1&#-#
!" Malignant diseases
!"Leukemias, polycythemia vera, MM,
Hodgkin, NHL, cancer
!" Chronic infections
!"Tuberculosis, osteomyelitis
!" Toxins
!"X- or gamma radiation, benzene
exposure
Imaging Findings
!" Generalized osteosclerosis (most
common)
!" Cortical thickening
!" Osteopenia
!" Rarely periostitis
!" Extramedullary hematopoiesis
Review
!" Sickle cell
!"Hand and foot syndrome representing
infarction from vaso-occlusion,
AVN and bone infarcts…“H-shaped”
Figure 15B (“Lincoln log”) vertebral bodies, “bone
S*:#!3($!*<3!6*>,(01&+"1%3%*%61<3$E*)344.%(*+1$,* within a bone” appearance, Salmonella
sclerosis characteristic of the disease. infection
!" Thalassemia
!"“Hair-on-end,”
Primary (Idiopathic) M5(%&4:1&#-# “pseudohemangiomatous”
!" O*.,)8/--*a)-,:'/%,+)1<)$1-*7"7 /::,/-/.%,M)m]-',.8,<,-)C/7Wl)
!" Unknown cause deformity (differential-Gaucher),
!" > 50 years old, incidence: 2/100,000 “rodent” facies
!" Findings: !" Hemophilia
!"OV)$1-*7"7)a"(9)9,:/(*7:',.*8,2/'< !"Knee-wide intercondylar notch,
!"Anemia erosions, medial slope of distal tibia at
!"Increased nucleated RBC’s ankle, pseudotumor of hemophilia
!"Leukocytosis or leukopenia !" V<,'*$1-*7"7
!"Abnormal WBC’s !"Diffusely dense bones,
hepatosplenomegaly, primary and
Primary (Idiopathic) M5(%&4:1&#-# secondary forms
!" Diagnosis: BM aspiration
!" Rx: transfusions, chemotherapy,
interferon, splenectomy, radiation
!" 50%-80% of patients have elevated
serum or urinary uric acid levels
!" Secondary gout occurs in 5%-20% of
patients
References
1. Greenspan A. Orthopedic Imaging: A practical approach: Lippincott Williams & Wilkins 4th edition, 2004.
2. Lonergan GJ, Cline DB, Abbondanzo SL. Sickle cell anemia. RadioGraphics 2001;21:971-94.

1104
Generalized Musculoskeletal Disorders

Learning Objectives
!" To describe a group of entities not well
covered in the rest of the course
!" To outline the imaging features of these
diseases
!" To introduce the listener to these entities
so that they can study about them further
Outline of Diseases
!" Osteoporosis (and its sequelae)
!" Osteogenesis imperfecta
!" ;,&-*$1-*8/(*7"7
!" Collagen vascular-like diseases
!"SLE
!"Scleroderma
!"Polymyositis/dermatomyositis
Terminology
!" Osteopenia – “paucity of bone”
!" Osteoporosis
!"Decreased bone mineral density
!"Normal in quality
!"Decreased in quantity
!" 30%-50% of cancellous bone must be
gone to recognize
Types of Osteopenia/Osteoporosis
!" Localized
!" Regional or segmental
!" Generalized or diffuse
Localized Osteopenia/Osteoporosis
!" Focal areas of bone loss
!" Differential diagnosis:
!"Infection Figure 1 A, B, C & D
!"Arthritides
Chronic regional
Regional Osteopenia/Osteoporosis pain syndrome
!" Segmental decrease in BMD (RSD) in the left
!" Differential diagnosis: hand.
!"Disuse (immobilization)
!"Chronic regional pain syndrome
0FLGQ4Y)L,C,3)7<8:/(9,("%)+<7(-*:9<)
(RSD) [Figure 1]
!"Transient osteoporosis (bone marrow
edema)
!"Regional migratory osteoporosis
Generalized Musculoskeletal Disorders 1105 Musculoskeletal Radiology

Disuse/Immobilization Osteoporosis
!" Major cause
!"Immobilization for traumatic injury
!"Motor paralysis
!"U.C/88/(*-<)',7"*.7)*#)1*.,7)/.+)
joints
!" Changes take 7-10 days (maximal at 2-3
months)
!" Patterns: uniform, spotty, bands, cortical
lamination, or scalloping, may appear
very aggressive
Figure 2D
Transient Regional Osteoporosis Transient regional osteoporosis (bone marrow edema)
[Figure 2] of the right hip.
!" General term
!" Conditions sharing features of Transient Regional Osteoporosis (Bone
!"Rapidly developing, self-limited, Marrow Edema) of the Hip
reversible osteoporosis !" 1st: women in the third trimester of
!"Absence of clear cut inciting events pregnancy
!" Major types: !" Middle-aged men
!"Transient osteoporosis (bone marrow !" LE > UE
edema) of the hip !" Osteoporosis and BM edema
!"Regional migratory osteoporosis !" Differential diagnosis: AVN, infection
!" Generally spontaneously resolves in 9-12
months
Generalized Osteopenia/Osteoporosis
!" Diffuse decreased BMD
!" Differential diagnosis:
!"Senile osteoporosis
!"Medications (steroids, heparin)
!"Q<7(,8"%)+"7,/7,7)0+,$%",.%<)7(/(,74
#" Scurvy
#" Malnutrition
#" F/'%"&8)+,$%",.%<
Senile Osteoporosis [Figures 3 & 4]

!" Pommer 1885 – “increased porosity”
!" Most commonly encountered metabolic
disease
!" Reduction in bone “quantity,” normal in
“quality.” F > M, 4:1, (equal incidence >
80 years old).
!" Most pain source: compression fx’s and
kyphosis
!" PE: kyphosis, shortened stature, and
spinal rigidity
Figure 3
Cross-
sectional
photo-
micrograph
of
osteoporotic
rib (top) and
normal rib
Figure 2 A, B & C (bottom)
rib. Note
Transient regional osteoporosis (bone marrow edema) normal but
of the right hip. decreased
trabeculae
in the
osteoporotic
bone.

Figure 5B
DEXA hip
printout.
Localized osteopenia in four different disorders (A and
B = Brodie abscess, C = gout, D = osteoarthritis).
Economic Impact: Osteoporosis

!" United States
!"44 million (M/F > 50 years old) or
55% of the population are at risk
!"Estimated 10 million women have
osteoporosis today Dual Energy X-Ray Absorptiometry
#" 12M by 2010 and 14M by 2020
(DEXA)
!" 1.3 million fractures/year in women > 45
!" Relative tissue attenuation from dual
years old
energy X-ray source
!" $17 billion annually in direct medical costs
!" Easy to perform
from treating fractures
!" Most reproducible technique with the least
!" Q"2."$%/.()*(9,-)8*-1"+"(<)/.+)8*-(/'"(<
%*,#$%",.()*#)E/-"/("*.)0FBg4
Osteoporosis Measurement [Figure 5]
!" Detects changes of 1%-3%
!" Dual energy X-ray absorptiometry (DEXA) !" Expressed in gm/cm2
!" Conventional X-ray (radiogrammetry) !" G-"8/-<)".+"%/("*.[),7(-*2,.)+,$%",.%<)(*)
!" Single photon absorptiometry (SPA) determine therapy
!" Dual photon absorptiometry (DPA)
BMD Terms
!" Neutron activation analysis
!" BMD measured in gm/cm2
!" Quantitative CT (QCT)
!" T score: number of standard deviations
of patient’s BMD from that of normal
25-year-old women
!" Z score: number of standard deviations of
patient’s BMD from that of aged-matched
controls
!" World Health Organization uses T scores
to classify a patient’s bone mineral status
Figure 5A
WHO C%*##-4$*)-&,+F.+H!I
DEXA spine !" Standard: mean BMD of 25-year-old
printout. women
!" Normal: BMD from the mean to 1
standard deviation below the mean (mean
to -1SD)
!" Osteopenia: BMD from 1 to 2.5 SD below
mean (-1SD and -2.5 SD)
!" Osteoporosis: BMD below 2.5 SD below
mean (> -2.5 SD)
!" Established osteoporosis includes the
presence of a nontraumatic vertebral
fracture

Senile Osteoporosis: Imaging Features Osteogenesis Imperfecta (OI)
!" Increased radiolucency on X-ray [Figure 7]
(osteopenia) !" Inherited disorder of skeleton, skin,
!" Cortical thinning sclera, dentin
!" Altered trabecular patterns !" Defect:
!"Conversion of procollagen to type I
Senile Osteoporosis: Complications collagen with abnormal crosslinking
!" Acute fractures !"Type I collagen: bones, organ
!"Spine (L>T>C) capsules, fascia, cornea, sclera,
!"Distal radius (Colles) tendons, meninges, and dermis
!"Proximal femur !"Failure of collagen maturation,
!"Humerus (neck) ".,#$%",.()*7(,*"+
!"Ankle (malleoli) !"No effect on osteoblasts or
!" U.7&#$%",.%<)#-/%(&-,7 intramembranous bone formation
!"Covered in osseous stress injury talk !" 1/30,000 affected, 1/50,000 severely
affected, no sex predilection
Spinal Effects of Osteoporosis [Figure 6]
!" 20,000-50,000 people in US
!" Decreased bone density !" 85% of cases autosomal dominant
!"Accentuation of primary trabeculae
!" Cortical thinning
!" Changes in vertebral shape
!"mO"%*.%/E,l)c)%*+$79)79/:,
!"Endplate deformities (Schmorl’s
nodes, cortical irregularities)
!"Wedged vertebrae
!"Vertebrae plana (pancake/silver dollar
shape)
Figure 6 A & B
Elderly women with osteoporotic compression

4"#/!."(%*3$*!61"#/3/*%:3$(*@0(4!*3>#E(A*#$)*Y51)&%6Z*
type vertebra in lumbar spine (right image).
Figure 7A
OI (tarda type). Note the exuberant callous formation

at the fracture sites.

NF
!" Two distinct clinical forms:
!"NF-1 (von Recklinghausen): café au
'/"()7:*(7M).,&-*$1-*8/7M)7W,',(/')
deformities
!"NF-2: Acoustic neuromas
!" F/.)',/+)(*)+"7$2&-,8,.(M)1'".+.,77M)
deafness, dermal/brain/spinal tumors,
loss of limbs, malignancies, learning
disabilities
!" Was not “elephant man’s disease”…
John Merrick had proteus syndrome (cell
growth disturbance with hemihypertrophy
and macrodactyly)
Imaging Features [Figures 8 to 10]

!" Spinal changes:
!"Dural ectasia
#" Vertebral scalloping
#" Foraminal enlargement
#" Pedicle erosion
!"Mesodermal dysplastic changes:
#" Scoliosis
#" Typical
#" Dysplastic, sharply angulated,
< 6 segments of lower T spine
(pathognomonic of NF)
Figure 7B #" Penciling and spindling of the
transverse processes
OI (tarda type). Note the exuberant callous formation
at the fracture sites. !" H*.2)1*.,7)0+&,)(*).,&-*$1-*8/7)*-)
mesodermal dysplastic changes)
!"Penciling
!"Bone erosions
N("1&4:1&8*)&#-#+6JK7 !"Pseudarthrosis (characteristically of
!" !,7%-"1,+)$-7()1<)P"-,7"&7)0@\\54)/.+) the tibia)
Smith (1849) !"^77*%"/(,+)a"(9).*.*77"#<".2)$1-*8/7
!" Named for von Recklinghausen – noticed !" Ribs
association of neural and cutaneous !"Scalloped and irregular (“twisted
elements in 1882 ribbons”)
!" Defects of all three cell layers = !"Erosions of inferior rib surfaces
phakomatosis
!" 1/3000 births
!" Estimated ~100,000 in US
!" One of humanity’s most common genetic
disorders
!" Mutation rate is 1/10,000 gametes/
generation
!" Greater than that for all other common
genetic disorders
!" AD with variable gene expression (FH in
60%)
!" Equal incidence in men and women and
Caucasian and non-Caucasian
Figure 8 A & B
Cervical spine in NF.

Figure 10C
Penciling of bone and erosions in NF.
Meningoceles [Figures 11 & 12]

!" Seen in up to 66% of patients with NF
!" 70%-80% of all meningoceles occur in
patients with NF
!" Protrusion of dura and arachnoid through
IV foramen and posterior rib cage into the
extrapleural thoracic cavity
!" 1-6 cm in size
!" N"(9*&()%/'%"$%/("*.)c)F/tt):-,7,.%,)
rules out meningocele
!" Presents most commonly as
asymptomatic posterior mediastinal mass
Figure 9 A, B, C & D !" Often laterally and on the right
Dural ectasia of NF in lumbar spine.
Figure 11A
Intrathoracic meningocele in NF (arrow).
Figure 10 A & B
Penciling of bone and erosions in NF.

Systemic Lupus Erythematosus (SLE)
!" Lupus is Latin for wolf; malar erythema
looked like the bite of a wolf
!" Generalized connective tissue disorder
!" F > M, second to fourth decade, rare over
the age of 45
!" Higher incidence in AAs and Hispanics
Figure 11B !" Fever, anorexia, weight loss,
polyarthralgias, skin rash
Intrathoracic
meningocele !" Chronic disease with acute episodes
in NF !" Variable prognosis
(arrow).
Categories of SLE
!" Discoid-skin rash only, 20% of patients
with SLE
!" Q<7(,8"%?%9-*."%M)".C/88/(*-<M)
multisystem disorder of the immune
system
!" Drug-induced: chlorpromazine,
hydralazine, isoniazid, methyldopa,
procainamide
Musculoskeletal Imaging Findings

[Figures 13 & 14]
!" Major: deforming nonerosive arthropathy
!" Minor:
!"Osteonecrosis
!"U.7&#$%",.%<)#-/%(&-,7
!"QP)%/'%"$%/("*.
!"Acroosteolysis
!"Tendon weakening and rupture
!"Subchondral cysts
!"Myositis
!"Polyarthritis
!"Osteomyelitis and septic arthritis
Figure 13
A&B
Deforming
non-erosive
arthropathy
in SLE.
Figure 12 A, B & C
Intrathoracic meningocele in NF (arrows). Density and
%3E$#0*3$!($%3!,*3%*3)($!3/#0*!1*!6#!*14*!6(*%:3$#0*?.3)D

Calcinosis
!" Abnormal calcium deposition in ST
without calcium metabolism abnormality
!" Fingers, forearms, and extensor surfaces
of elbows and knees
Sclerodactyly
!" Replacement of the normal connective
tissue with dense collagen bundles
!" Skin is thin, appears smooth, and is
tightly bound
!" Fingers are narrow and taper distally
Telangiectasia
!" Permanent dilatation of capillaries and
venules
!" K/%,M)'":7M)(*.2&,M)/.+)$.2,-7
I,=*88*)&15+Muscle Disease
!" Dermatomyositis and polymyositis
!" F:M = 2:1
!" U88&.,?8,+"/(,+I
!" Rare
IMD and Malignancy

!" Dermatomyositis
!"Men > 40 years old
!"Skin rash and muscle weakness
!"Precedes appearance of tumor months
to years
!"Primary malignancies:
#" Lung, prostate, female pelvic
organs, breast, or GI tract
Figure 14 A & B
!" Polymyositis:
I'!($%3=(*/#0/3&/#!31$*3$*!6(*6#$)%*#$)*<"3%!%*3$* !"Primary malignancies: lung, NHL
dermatomyositis.
Imaging Findings
!" ST abnormalities
Symmetric Polyarthritis
!"ST thickening and edema
!" Articular symptoms and signs common:
!"Q*#()/.+):,-"/-("%&'/-)%/'%"$%/("*.)0UV)
75%-90% of patients
> SQ)
!" Frequently bilateral and symmetric
!" Articular abnormalities
!" 5%-40% with disease
!"Radial subluxation or dislocation of
!" Hands > knees > wrists > shoulders
UG)*#)(9&81)0mC*::<)(9&81l4)p)b&"(,)
!" ST swelling, periarticular osteopenia
characteristic
!" Reversible and little functional effect
!"Erosions of multiple sites in hands
!" Cartilage and osseous destruction rare
!"Flexion deformities (MCP)
without underlying osteonecrosis
#" “Swan neck” deformity
CREST Syndrome
Other Imaging Findings
!" First described by Winterbauer in 1964 as
!" RBS
CRST syndrome
!"Increased accumulation at sites of
!" Velayos added esophageal involvement to
%/'%"$%/("*.)0(,%9.,("&8)/.+)2/''"&84
make CREST in 1979
!" MR imaging
!" 50,000 to 100,000 in US
!"Muscle atrophy
!" 7x more common in women
!"Fatty replacement
!" Calcinosis
!"Decreased SI correlating with activity
!" Raynaud’s phenomenon
of disease
!" Esophageal abnormalities
!"Increased SI on T2-WI and STIR
!" Sclerodactyly
!" Telangiectasia

Remember
!" PM, DM, scleroderma, SLE, mixed CVD,
and overlap syndromes may all look alike
!"QP)%/'%"$%/("*.
!"Articular and osseous abnormalities
Summary
!" Osteoporosis
!"Most common metabolic disease
!"Thoracic spine compression fractures
/-,)m".7&#$%",.%<l)#-/%(&-,7
!"U.7&#$%",.%<)#-/%(&-,7)8/<)8"8"%)
mets/myeloma
!" OI
!"Diagnosis of exclusion in young
patients with osteopenia out of
proportion to age
!"Easily fractured and exuberant callous
formation
!" NF
!"Penciling, pseudarthrosis, posterior
scalloping, thoracic meningocele
!" Systemic lupus erythematosis
!"Ulnar deviation without erosions
(differential is Jacoud-post-
streptococcal arthritis)
!" Scleroderma
!"CREST, acroosteolysis
!" U.C/88/(*-<)8&7%',)+"7,/7,
!"Dermatomyositis and polymyositis
!";*.7:,%"$%)$.+".27)0'**W)'"W,)
scleroderma)
!"Must look for malignancy in these
patients
References
1. Brower AC, Flemming DJ. Arthritis in Black and White: Saunders, 1988.
2. Greenspan A. Orthopedic Imaging: a practical approach: Lippincott Williams & Wilkins, 2004.

1114
Crystal Deposition Diseases and Neuropathic Osteoarthropathy
Crystal Deposition Diseases
!" Gouty arthritis Figure 1
!"Monosodium urate
!" CPPD crystal deposition disease Gouty arthritis.
Radiograph
!"Calcium pyrophosphate dihydrate
of the distal
!" HA crystal deposition disease interphalangeal
!"Calcium hydroxyapatite joint shows
characteristic
Related Disorders <(00C)(&$()*
!" Hemochromatosis erosion of
bone with
!"Iron deposition overhanging
!" Alkaptonuria edge of new
!"Homogentisic acid bone (arrow).
Note also
Gout preservation of
!" Monosodium urate crystals joint space.
!" Intraarticular, periarticular
!" ^%&(,)".C/88/(*-<)-,7:*.7,
!" Chronic granulomatous reaction
Gout: Primary (Idiopathic)

!" M:F = 20:1
!" 40-50 years old
!" (Familial history)
Gout: Secondary
!" Hereditary diseases
!" Myeloproliferative diseases
!" Endocrine disorders
!" Drug therapy
Gout: Clinical Stages

!" Asymptomatic hyperuricemia
!" Acute gouty arthritis
!" Interval phase
!" Recurrent arthritis
!" Chronic tophaceous gout Figure 2 A & B
Gouty arthritis. Left Image: Pathological specimen
Gouty Arthritis shows tophaceous material (star) and sharp interface
!" Polyarticular with adjacent bone (arrow). Right Image: Clinical
!" Asymmetric "#)31E"#:6*%61<%*0#"E(V*<(00C)(&$()*("1%31$%*14*!6(*
!" 1st MTP joint (90%) &"%!*>(!#!#"%#0*6(#)*<3!6*1=("6#$E3$E*()E(*14*$(<*
bone (arrow). Note multiple other erosions including
!" Tarsometatarsal !6(*+#%(*14*!6(*&"%!*>(!#!#"%#0D
!" Carpometacarpal
!" Olecranon bursitis
Gouty Arthritis [Figures 1 to 3]

Figure 3
!" Soft tissue swelling
!" P*:9")0%/'%"$%/("*.)-/-,4 Gouty
!" N,''?+,$.,+),-*7"*.7 Por que es un proceso lento. arthritis. There
are multiple
!" Overhanging edge <(00C)(&$()*
!" Preserved joint space erosions,
!" Extraarticular erosions particularly
at the
bases of the
metacarpals at
the common
carpometa-
carpal joint.
Crystal Deposition Diseases and Neuropathic Osteoarthropathy Musculoskeletal Radiology

1115
CPPD Crystal Deposition Disease:
Figure 4
Terminology
!" Pseudogout CPPD crystal
deposition disease.
!" Chondrocalcinosis
Frontal radiograph
!" Pyrophosphate arthropathy of the knee shows
chondrocalcinosis
CPPD Crystal Deposition Disease including meniscal
!" Usually idiopathic &+"1/#"!30#E(*
!" Occasionally hereditary /#0/3&/#!31$*@<63!(*
arrows) and hyaline
!" Over 50 years old /#"!30#E(*/#0/3&/#!31$*
!" Incidence: 5%-34% (black arrow).
.
CPPD Crystal Deposition Disease:
Related Disorders
!" Primary hyperparathyroidism
!" Hemochromatosis
CPPD Crystal Deposition Disease: Sites

of C*%$-4$*)-&, Figure 5
!" Fibrocartilage
!" Hyaline cartilage CPPD crystal
!" Synovial membrane deposition
disease.
!" Joint capsule Lateral
!" Ligaments radiograph
!" Tendons shows
!" Bursae complete
loss of
patellofemoral
Fibrocartilage C*%$-4$*)-&, joint space.
!" Knee menisci
!" P-"/.2&'/-)$1-*%/-("'/2,
!" Symphysis pubis
Pyrophosphate Arthropathy CPPD Crystal Deposition Disease: Wrist

!" Joint space narrowing and Hand [Figures 6 & 7]
!" Bone sclerosis !" P-"/.2&'/-)$1-*%/-("'/2,)%/'%"$%/("*.
!" Osteophyte formation !" Radiocarpal arthropathy
!" Subchondral cysts !" mQ(,:'/++,-l)%*.$2&-/("*.)0QH^F4
!" Metacarpophalangeal arthropathy
Differentiation of Pyrophosphate !" Absence of erosions
Arthropathy from Degenerative Joint
Disease
!" Unusual articular distribution
!" Unusual intraarticular distribution
!" Variable osteophyte formation
!" Prominent subchondral cysts
!" Progressive destruction
!" F/'%"$%/("*.
Figure 6
CPPD Crystal Deposition Disease: Knee CPPD crystal

[Figures 4 & 5) deposition
!" V,."7%/')%/'%"$%/("*. disease.
!" _</'".,)%/-("'/2,)%/'%"$%/("*. Frontal
radiograph
!" Patellofemoral arthropathy of the wrist
!" Subchondral cysts shows
!" Osseous bodies joint space
narrowing
between the
radius and
scaphoid
and
between the lunate and capitate (scapholunate advanced
collapse [SLAC]). There is extensive chondrocalcinosis
3$/0.)3$E*!6(*!"3#$E.0#"*&+"1/#"!30#E(*@#""1<A*#%*<(00*#%*#*
large subchondral cyst in the radius (star).

1116
Figure 8
Figure 7 Hemochromatosis. Frontal radiograph shows narrowing

14*!6(*%(/1$)*!6"1.E6*&4!6*>(!#/#":1C:6#0#$E(#0*
CPPD crystal deposition disease. Frontal joints as well as multiple, large hook-like osteophytes
radiograph shows narrowing of the second and (arrows).
third metacarpophalangeal joints with sclerosis,
osteophytes, and subchondral cysts. Note hyaline
/#"!30#E(*/#0/3&/#!31$*@<63!(*#""1<A*#$)*:"1+#+0(*
%,$1=3#0*#$)*/#:%.0#"*/#0/3&/#!31$*@+0#/2*#""1<%AD
Primary Periarticular HA Crystal
Deposition Disease (C*%$-4$+Tendinitis)
!" Middle-aged
Hemochromatosis !" Monoarticular
!" Primary !" (Asymptomatic)
!"Increased iron absorption !" Localized pain
!" Secondary !" Tenderness to palpation
!"Increased iron intake !" Restriction of motion
!"Multiple blood transfusions !" (Fever and malaise)
Hemochromatosis: Clinical Findings Primary Periarticular HA Crystal
!" Onset between 40 and 60 years old
Deposition Disease (C*%$-4$+Tendinitis)
!" Men more often than women [Figure 9 & 10]
!" Bronze pigmentation !" Soft tissue swelling
!" Cirrhosis !" G**-'<)+,$.,+)%/'%"$%/("*.
!" Diabetes mellitus !" Q9/-:'<)+,$.,+)%/'%"$%/("*.
!" Cardiac failure !" L,7*-:("*.)*#)%/'%"$%/("*.
!" Arthropathy
Hemochromatosis: Pathologic/
Radiologic Findings [Figure 8]
!" Iron in synovioblasts
!" CPPD crystal deposition
!" Osteoporosis
!" Q<8:9<7"7):&1"7)%/'%"$%/("*.
!" _</'".,)%/-("'/2,)%/'%"$%/("*.
!" Uniform MCP joint involvement
!" Hook-like osteophytes
HA Crystal Deposition Disease

!" Primary
!" Secondary
!" Periarticular
!" Intraarticular
Figure 9
5#0/3&/*!($)3$3!3%D*7#)31E"#:6*14*!6(*%61.0)("*3$*
('!("$#0*"1!#!31$*%61<%*:11"0,*)(&$()*/#0/3&/#!31$*
corresponding to the supraspinatus tendon (arrow).

1117
Alkaptonuria: Radiologic Findings
[Figures 11 & 12]
Figure 10 !" Knees, hips, shoulders
Radiograph of !" Symmetric cartilage loss
the shoulder !" Osseous sclerosis
in internal !" Collapse and fragmentation
rotation
shows sharply !" Intraarticular bodies
)(&$()*
/#0/3&/#!31$*
corresponding
to the Figure 11
infraspinatus
or teres Alkaptonuria.
minor tendon Lateral
(arrow). radiograph of
the lumbar
spine shows
uniform loss
Intraarticular Hydroxyapatite Crystal of disc height
and associated
Deposition Disease: Milwaukee Shoulder bone sclerosis.
!" Elderly women There is disc
!" Shoulder pain /#0/3&/#!31$*
!" Decreased mobility bridging
!" HA crystal shedding all levels
anteriorly
!" Activated collagenase except for
!" Neutral protease L4-L5, which
!" Tissue destruction shows large
osteophytes
Milwaukee Shoulder: Radiologic and a vacuum
phenomenon.
Findings
!" ^8*-:9*&7)%/'%"$%/("*.
!" Glenohumeral joint narrowing
!" Subchondral sclerosis
!" Bone destruction
!" Rotator cuff disruption
!" Acromiohumeral abutment
Alkaptonuria: Clinical Findings

!" _*8*2,.("7"%)/%"+)*3"+/7,)+,$%",.%<
!" Onset between 20 and 30 years
!" Bluish-black pigmentation (ochronosis) Figure 12
!" Dark colored urine Alkaptonuria.
!" Cardiovascular Frontal
!" Genitourinary radiograph
!" Upper respiratory of the knee
!" Articular shows uniform
joint space
loss and bone
Alkaptonuria: Pathologic Findings sclerosis.
!" Connective tissue pigmentation
!" Fibrocartilage and hyaline cartilage
!" Fibrillation, fragmentation
!" Granulation tissue
!" Osseous proliferation
Alkaptonuria: Radiologic Findings

!" !"7%)%/'%"$%/("*.
!"^..&'&7)$1-*7&7
!"Diffuse
!" Multilevel disc narrowing Neuropathic Osteoarthropathy
!" Vacuum phenomena !" Charcot joint
!" Osseous sclerosis !" Tabetic arthropathy
!" Neurotrophic joint
!" Neuropathic arthropathy
!" Neuroarthropathy

1118
Neuroarthropathy: Etiologies
!" Diabetes mellitus
!" Alcoholism
!" Syringomyelia
!" Syphilis
!" Leprosy
!" Meningomyelocele
!" Congenital insensitivity to pain
!" Steroid administration (intraarticular)
Neuroarthropathy: Pathogenesis
!" French theory
!" German theory
!" Neurotraumatic
!" Neurovascular
Figure 13
Neuroarthropathy: French Theory Neuropathic osteoarthropathy. Frontal radiograph of
!" Mitchell (1831) the shoulder shows almost complete resorption of the
!" Charcot (1868) humeral head except for some osseous debris medially
!" Damage to CNS trophic centers (arrow). Note the extremely sharp margin of the
remaining portion of the humeral shaft.
!" Altered bone and joint nutrition
!" Osseous and articular atrophy
Neuroarthropathy: German Theory

!" Volkmann, Virchow
!" Insensitivity to pain
!" Recurrent trauma
Neuroarthropathy: Neurotraumatic
Theory
!" Eloesser (1917)
!" Posterior sensory nerve section
!" Continued weightbearing
!" Joint destruction
!" Chemical analysis: no atrophy
Neuroarthropathy: Neurovascular
Theory Figure 14
!" ;,&-/''<)"."("/(,+)E/7%&'/-)-,C,3
Neuropathic osteoarthropathy. Lateral radiograph of
!" U.%-,/7,+)1*.,)1'**+)C*a the foot shows extensive destruction of the bones of
!" Osteoclastic bone resorption the midfoot with dislocation and disorganization. Note
!" Fracture and repair ('!($%3=(*=#%/.0#"*/#0/3&/#!31$*4"1>*)3#+(!(%D
Neuroarthropathy: Clinical/Pathologic
Findings
!" Swollen, deformed joint
!" Usually painless
!" Detritic synovitis
!" Rapid progression
Neuroarthropathy: Radiologic Findings

[Figures 13 to 16]
!" Destruction (atrophy)
!" Dislocation
!" Disorganization
!" Debris
!" Detritus
!" Density (sclerosis)
!" Distension (effusion)
Figure 15
Neuropathic osteoarthropathy. Follow-up lateral
radiograph less than one month later shows further
bone destruction with almost complete disappearance
of the talus and the anterior portion of the calcaneus.

1119
Figure 16
Neuropathic osteoarthropathy.
Frontal radiograph of the foot shows characteristic
destruction, disorganization, and debris around the
tarsometatarsal joints.

1120
MR Arthrography of Glenohumeral Instability
Glenohumeral Joint Normal Superior Labrum
!" Intrinsically unstable joint !" Seen best in the coronal plane
!"Shallow glenoid fossa !" Superior labrum:
!"Large articular surface of the humeral !"Dark on all pulse sequences
head !"Triangular
!" Static stabilizers !"Extends off of superior glenoid
!"Joint capsule
!"Glenohumeral ligaments Superior Glenohumeral Ligament
!"Glenoid labrum [Figure 1]
!" Dynamic stabilizers !" Prevents inferior subluxation with arm in
!"Rotator cuff 0º abduction
!"Long head of the biceps tendon !"Courses from superior glenoid tubercle
to lesser tuberosity
C%*##-4$*)-&, !"Parallels coracoid process
!" TUBS
!"Traumatic
!"Unidirectional
!"Bankart
Figure 1
!"Surgery
!" AMBRI Superior
!"Atraumatic glenohumeral
!"Multidirectional ligament.
!"Bilateral
!"Rehabilitation
!"Inferior capsular shift
Multidirectional Instability
!" AMBRI patient
!" Causes of multidirectional instability Middle Glenohumeral Ligament
!"Hypermobility or laxity [Figure 2]
!"Stretching or overuse of support !" Prevents external rotation of humeral
structures head when arm is between 45º and 60º of
!" MR imaging not usually required abduction
!"VL)$.+".27).*.7:,%"$% !" Originates at superior glenoid tubercle
!"MR useful if direction unknown to rule !" F*&-7,7)*1'"b&,'<)7&:,-$%"/')(*)(9,)
out conventional causes anterior labrum
!" O',.+7)a"(9)(9,)+,,:)$1,-7)*#)
Anterior Stabilizers
subscapularis
!" Labrum
!" Most variable of the glenohumeral
!" Glenohumeral ligaments
ligaments
!" Capsule
!" Subscapularis muscle
!" Most important anterior stabilizer: inferior
glenohumeral labroligamentous complex
!"Anteroinferior labrum Figure 2
!"Anterior band of the inferior Middle
glenohumeral ligament glenohumeral
ligament.
Normal Labrum
!" Anterior and posterior labrum best seen in
the axial plane
!" LABRUM:
!"Dark on all pulse sequences
!"May be triangular, rounded, or blunted
MR Arthrography of Glenohumeral Instability Musculoskeletal Radiology

1121
Inferior Glenohumeral Ligament !"No signal extends into the black
[Figure 3] triangle of the superior labrum
!" Most important GHL with regard to !"Can mimic a SLAP tear
stability !" Buford complex [Figure 5B]
!" Prevents anterior subluxation with arm in !"1.5% of patients
full abduction and external rotation !"Can mimic anterior labral tear
!" Extends from anterior inferior labrum to !"Thick cord-like MGHL
humeral neck !"Absent or diminutive anteriorsuperior
!" Lax with arm in neutral position labrum
!" Redundant when the arm is in neutral
position
Figure 3
Inferior
glenohumeral
ligament.
Figure 5 A & B
Scout Position and Scan Plane for ABER
[Figure 4]
Left Image: Sublabral recess.
Right Image: Buford complex.
!" Coronal scout with arm in ABER position
!" Scan plane along the long axis of the
humeral shaft
!" Stretches anterior band of IGHL
Anterior Instability
!" 95% of all dislocations
!" Mechanism
!"Fall on outstretched arm
!"Abduction and external rotation
Bankart Lesions [Figure 6]

!"Most common injury following anterior
dislocation
!"First-time dislocators under 35 years
old
Figure 4 A & B
!"Anterior labroligamentous avulsion
with disruption of the medial scapular
Left Image: Scan plane for the ABER view. periosteum
Right Image: Normal ABER view.
Normal Anatomic Variants

!" Cartilage undermining
!"Articular cartilage hyaline intermediate
signal intensity
!"H/1-&8)$1-*%/-("'/2,)'*a)7"2./')
intensity
!"Smooth, tapering
!"Does not extend completely beneath
labrum
!" Sublabral foramen (hole)
Figure 6 A & B
!"Occurs only in the anterosuperior
quadrant
Bankart lesion.
!"Complete detachment of the labrum
from the glenoid
!" Sublabral recess [Figure 5A]
!"Smooth, tapering
!"Extends toward the glenoid
MR Arthrography of Glenohumeral Instability 1122 Musculoskeletal Radiology

Osseous Bankart Lesion [Figure 7]
!" Fracture of inferior glenoid
!" Disruption of the cortex of the
anteroinferior glenoid
Figure 9 A & B
Perthes lesion.
Figure 7 A & B
Medialized Bankart Lesion [Figure 10]
!" ALPSA: anterior labroligamentous
Osseous Bankart.
periosteal sleeve avulsion
Hill-Sachs Lesion
!" Results from impaction of humeral head
against anteriorinferior glenoid
!" Associated with Bankart lesion
!" Normally: top 3 images round
!" _"''?Q/%97[)C/((,.".2)*-)%*.%/E"(<
!" Acute: + edema
Double Axillary Pouch Sign [Figure 8]

!" Double axillary pouch: small collection
of contrast in inferior labrum seen on Figure 10 A & B
coronal images
ALPSA lesion.
Chronic Medialized Bankart Lesion

!" Labrum scars down medially
!" Scar tissue mounds up covering
medialized labrum and resynovializes
!" Treatment: surgically complete Bankart,
followed by reconstruction
Axillary Nerve Neuropraxy [Figure 11]

!" Axillary nerve can be stretched at
Figure 8 A & B
time of anterior dislocation resulting in
Double axillary pouch. denervation atrophy: deltoid and teres
minor muscles
!" Denervation atrophy:
Perthes Lesion !"Acute: edema (high signal on T2)
!" Bankart variation (nondisplaced) !"Chronic: fatty (high signal on T1)
!" Labroligamentous disruption
!" Medial scapular periosteum intact
!" May resynovialize in place
!" Best detected on ABER view
Nondisplaced Tear Anteroinferior

Labrum Perthes Lesion [Figure 9]
Figure 11
ALPSA Lesion
!" Anterior labroligamentous periosteal Denervation
atrophy of
sleeve avulsion deltoid muscle.
!" Intact medial periosteal periosteum
!" Medialized Bankart lesion
!" Surgical repair technique differs from
Bankart

First Time Dislocation Over Age 35
!" Clinical presentation can be confusing
!" Tear supraspinatus tendon
!" Fracture greater tuberosity
!" Avulse subscapularis and anterior capsule
from the humerus
!" MRI can play pivotal role in directing
patient therapy
Tear of the Supraspinatus Tendon

!" First time dislocation over age 35
!" Bankart lesion uncommon
Figure 12 A & B
!" Rotator cuff tendon becomes the weak link
HAGL lesion.
First Time Dislocation Over Age 35
!" Avulsion fracture of the greater tuberosity
Greater Tuberosity Fracture Posterior Instability [Figure 13]

!" Avulsion of the greater tuberosity is often !" Repetitive microtrauma: nondisplaced
occult radiographically posterior labral tear
!" Can mimic RCT !" Reverse Bankart
!" Treated conservatively !" Reverse Hill-Sachs
!" MRI can accurately distinguish
Avulsion of Subscapularis
!" Subscapularis muscle can avulse off of
lesser tuberosity
!" Associated with dislocation of the biceps
tendon
!" Seen best in axial plane
Disruption of Subscapularis
Figure 13 A & B
!" Disruption of subscapularis at
musculotendinous junction Reverse Bankart and Hill-Sachs lesions.
!" Requires surgical repair
HAGL Lesion GLAD Lesion [Figure 14]

!" Humeral avulsion of the glenohumeral !" Glenolabral articular disruption
Ligament !" Forced adduction injury (humeral head
!" Results from dislocation impacts the glenoid fossa)
!" No age predilection !" Clinically a stable lesion
!" MR Findings: contrast extravasation from !" Partial tear anteroinferior labrum/articular
joint capsule/avulsion of subscapularis cartilage injury
HAGL Lesion [Figure 12]
!" Inferior GHL can disrupt anywhere along
course
!" Humeral attachment/midsubstance
!" !"#$%&'()(*)+,(,%()a"(9)7%*:,
!" Cause of failed repairs
!" Can present on MRI as avulsion of Figure 14
subscapularis muscle
GLAD lesion.
Posterior Instability
!" 2%-4% of all traumatic dislocations
!" 20%-25% of shoulder instability cases in
active duty military population
!" Adduction with internal rotation
!" Seizure, electrocution, weight lifting,
swimming, lineman blocking
!" “Reverse” Hill-Sachs, Bankart

GLAD Lesion [Figure 15] Glenohumeral Internal Rotation D(4$-)+
!" Nondisplaced tear anteroinferior labrum (GIRD) [Figure 17]
!" Best seen on ABER !" Scarring and thickening of the posterior
!" Articular cartilage injury capsule and has recently been described
!" Best seen on axial or coronal as a source of potential pain in throwing
athletes
!" MR imaging demonstrates thickening of
the posterior capsule
Figure 17
GIRD.
Figure 15 A & B
GLAD lesion.
Posterior Superior Glenoid “SLAP” Tears

Impingement !" The “superior labrum, anterior-to-
!" Also known as “internal impingement” posterior” lesion, can include biceps
!" Undersurface tearing of posterior rotator tendon
cuff (posterior SST or IST) !" Mechanism
!" Impingement between posterior labrum !"Fall on outstretched arm
and greater tuberosity !"Repetitive overhead activity (throwing,
!" Throwing athletes posterior shoulder pain swimming)
!" Associated with anterior instability !" Symptoms: pain with overhead activity,
catching, popping sensation
Posterior Superior Glenoid
Impingement [Figure 16]
Important Factors to Observe
!" Undersurface of posterior rotator cuff !" Abnormal signal in superior labrum
impinged between the greater tuberosity !" Extent of lesion
and the posterosuperior labrum !"Posterior labrum
!" Seen best on ABER view !"Anteroinferior quadrant
!" Biceps involvement
!" Type of SLAP tear
SLAP Lesion
!" Type 1 [Figure 18]
Figure 16 !"Fraying and degeneration, but labrum
$-8'<)/((/%9,+
Posterior
superior !" Type 2 [Figure 19]
glenoid !"Fraying of labrum and superior labrum
impingement. avulsed from glenoid
!"Signal extends into the triangle of the
superior labrum
!"Bucket-handle tear of the superior
labrum; biceps tendon remains intact
Posterior Superior Glenoid !"On MR imaging: fragment seen
displaced into superior joint space
Impingement
!" VL)$.+".27[
!"Bucket-handle tear of superior labrum
!"Undersurface tear of posterior rotator
involves biceps anchor
cuff
!"Biceps involvement best seen on axial/
!"Degenerative changes of
coronal images
posterosuperior labrum
!"Cystic change in greater tuberosity
!"Internal impingement seen on ABER
view

!"SLAP on axial images: irregular
contrast collection
!"Sublabral recess: coronal images
!"No displacement of superior labrum
!"SLAP Type 2 tear
!"Labrum pulled away from glenoid
Paralabral Cyst
!" High association with labral tears and GH
joint instability
Figure 18 A & B !" Superior labral cyst: SLAP tears
SLAP Type I. Fraying of the undersurface of labrum. !" Posterior labral cyst: posterior labral tears
!" Labral tear may resynovialize
!" Can result in shoulder pain and adjacent
nerve entrapment
!" DDX: intramuscular cysts of rotator cuff
associated with PT tear of the cuff tendon
Figure 19 Paralabral Cysts [Figure 22]
SLAP Type II. !" SLAP tear with superior paralabral cyst
Avulsion of !" Suprascapular notch
labrum from !" Suprascapular nerve entrapment
glenoid. !" Denervation edema: supraspinatus and
infraspinatus muscles
Figure 22 A & B
Left Image: SLAP tear with paralabral cyst.

Figure 20 A & B Right Image: Denervation edema within supraspinatus
SLAP Type III. Bucket-handle tear of the superior and infraspinatus muscles.
labrum.
Paralabral Cysts
!" Posterior paralabral cysts
!" Extend into spinoglenoid notch
!" Entrapment of suprascapular nerve
!" Persistent shoulder pain for 3 years
!" Small anterior labral tear with small
adjacent paralabral cyst
Paralabral Cysts
Figure 21 A & B !" Small inferior labral cyst
SLAP Type IV. Bucket-handle tear with involvement of !" Teres minor normal
biceps anchor. !" 3 years later; persistent pain
!" Paralabral cyst larger
Pitfalls: SLAP Tears !" Axillary nerve entrapment
!" Sublabral recess
!" Atrophy teres minor
!"Smooth, tapering
!"No signal in superior labrum
!"SLAP tear: any signal extending into
black triangle
!" Sublabral recess: axial images
!"Smooth linear collection of contrast

Labral Repair: Surgical Approach Failed Bankart Repair [Figure 25]
!" Direct repair of labral and capsular lesions !" Missed HAGL lesion
!"Q%-,a)$3/("*.) !" In one series: up to 30% of failed repairs
!" Indirect repairs
!"Staple capsulorapphy (Du Toit and
Roux)
!"Subscapularis manipulation to
tighten anterior capsule (Putti-Platt/
Magnuson-Stack)
!"Movement of the coracoid process
(Bristow procedure)
Direct Repairs
!" Arthroscopic/open (deltopectoral interval)
!"Suture anchors 3, 4, 5, o’clock
position Figure 25 A & B
!" Capsulorapphy (open/arthroscopic) Left Image: Missed HAGL lesion. IGHL avulsed from
!"Staple redundant capsule humeral neck.
Right Image: HAGL lesion.
!"Done in conjunction with direct repair
!"High failure rate if done as isolated
procedure
!" Osseous Bankart Recurrent SLAP Following Repair
[Figure 26]
MR Findings of Bankart Repair !" Displaced fragment anterosuperior labrum
[Figure 23] !" Osteochondral defect anterosuperior
!" Suture anchor artifact from repair may glenoid
obscure visualization
Figure 26
Figure 23 Recurrent
SLAP tear with
Direct a displaced
arthroscopic fragment.
repair of
Bankart lesion.
Suture anchors
at the 3, 4,
and 5 o’clock
positions.
MR Findings of Failed Bankart Repair 5 Months Following SLAP Repair:

[Figure 24] Recurrent Pain
!" Recurrent displaced anterior labrum !" Fraying and irregularity of superior
labrum; no displaced fragment
!" Partial thickness articular surface tear
rotator cuff
Figure 24
Recurrent
displaced
Bankart lesion.

Multidirectional Instability [Figure 27]
!" P-,/(,+)$-7()a"(9)-,9/1"'"(/("*.
!" Surgery
!"Inferior capsular shift/plication
!"Decrease volume of GHJ anteriorly, Figure 29
inferiorly, posteriorly
Postoperative
!"MR capsular thickening infection.
Figure 27
Normal
postoperative
MR appearance
following
inferior
Acute Chondrolysis of the Glenohumeral
capsular shift. Joint [Figure 30]
Thickened !" Rapid onset chondrolysis refers to
capsule. a condition in which widespread
chondrocyte death occurs within a joint
over a relatively short period of time
!" Devastating complication reported
following arthroscopy and reconstruction
of the GHJ in young individuals
Hardware Complication [Figure 28] !" Rapid onset pain
!" Proud suture anchor !" Marked loss of motion
!" Treatment supportive; eventually total
joint arthroplasty
Figure 28
CT appearance
of a proud
suture anchor.
Figure 30 A & B
Acute chondrolysis of the glenohumeral joint following

Synovitis: Prior SA Decompression and shoulder arthroscopy.
Rotator Cuff Debridement - Recurrent
Pain
!" Synovitis: 4-mm adhesive capsulitis
!" Normal postop capsule:
!"2-4 mm after surgical procedure Chondrolysis Shoulder: Proposed
!"Thickened and nodular capsule Etiologies
!" Damage from use of thermal probe for
Postop Infection [Figure 29] capsular shrinkage
!" Infectious versus reactive synovitis !" Marcaine pump
+"#$%&'()(*)+"##,-,.("/(,)a"(9)"8/2".2 !" Unknown infectious agent
!" Thickened enhancing capsule; effusion/ !" Bioabsorbable material
joint destruction/cartilage loss/cysts, !" Mechanical trauma at time of arthroscopy
erosions !" Chemical trauma to the chondrocytes
!" Event during arthroscopy that triggers
an immune response and subsequent
8"2-/("*.)*#)".C/88/(*-<)%,''7)".(*)(9,)
GH joint

References
1. Bankart AB. Recurrent or habitual dislocation of the shoulder joint. Br J Surg 1938;26:23-9.
2. Beltran J, Rosenberg ZS, Chandnani VP, et al. Glenohumeral instability: Evaluation with MR arthrography.
3. Chandnani VP, Gagliardi JA, Murnane TG, et al. Glenohumeral ligaments and shoulder capsular
mechanism: Evaluation with MR arthrography. Rad 1995;196:27-32.
4. Cvitanic O, Tirman PFJ, Feller JF, et al. Using abduction and external rotation of the shoulder to increase
the sensitivity of MR arthrography in revealing tears of the anterior glenoid labrum. AJR Am J Roentgenol
1997;169:837-44.
5. Kaplan PA, Bryans KC, Davick JP, et al. MR imaging of the normal shoulder: Variants and pitfalls. Rad
1992;184:519-24.
6. Linker CS, Helms CA, Fritz RC. Quadrilateral space syndrome: Findings at MR imaging. Rad
1993;188:675-6.
7. Neviaser RJ, Neviaser TJ, Neviaser JS. Concurrent rupture of the rotator cuff and anterior dislocation of
the shoulder in the older patient. JBJS 1988;70-A:1308-11.
8. Neviaser TJ. The anterior labroligamentous periosteal sleeve avulsion lesion: A cause of anterior
instability of the shoulder. Arthroscopy 1993;9:17-21.
9. Neviaser TJ. The GLAD lesion: Another cause of anterior shoulder pain. Arthroscopy 1993;9:22-3.
10. Palmer WE, Brown JH, Rosenthal DI. Labral-Ligamentous complex of the shoulder: Evaluation with MR
arthrography. Rad 1994;190:645-51.
11. Petersilge CA, Witte DH, Sewell BO, et al. Normal regional anatomy of the shoulder. MRI Clin North Am
1997;5:667-81.
12. Sanders TG, Tirman PFJ, Linares R. The Glenolabral articular disruption lesion: MR arthrography with
arthroscopic correlation. AJR Am J Roentgenol 1999;172:171-5.
13. Schweitzer ME. MR arthrography of the labral-ligamentous complex of the shoulder. Rad 1994;190:641-3.
14. Synder SJ, Karzel RP, Pizzo WD, et al. SLAP lesions of the shoulder. Arthroscopy 1990;6:274-9.
15. Tirman PFJ, Bost FW, Garvin GJ, et al. Posterosuperior glenoid impingement of the shoulder: Findings at
MR arthrography and MR arthrography with arthroscopic correlation. Rad 1994;193:431-6.
16. Tirman PFJ, Feller JF, Jansen DL, et al. Association of glenoid labral cysts with labral tears and
2',.*9&8,-/')".7(/1"'"(<[)L/+"*2-/:9"%)$.+".27)/.+)%'"."%/')7"2."$%/.%,S)L/+)@ZZ=Y@ZA[e>5?dS)
17. Tirman PFJ, Feller JF, Palmer WE, et al. The Buford complex—A variation of normal shoulder anatomy: MR
arthrographic imaging features. AJR Am J Roentgenol 1996;166:869-73.
18. Tirman PFJ, Steinbach LS, Feller, FJ. Humeral avulsion of the anterior shoulder stabilizing structures after
anterior shoulder dislocation: demonstration by MRI and MR arthrography. Skeletal Radiol 1996;25:743-
8.
19. Wolf EM, Cheng JC, Dickson K. Humeral avulsion of glenohumeral ligaments as a cause of anterior
shoulder instability. Arthroscopy 1995;11:600-7.
MR Arthrography Glenohumeral Instability 1129 Musculoskeletal Radiology

1130
MRI of the Elbow
Mark E. Schweitzer, MD; William B. Morrison, MD William.morrison@jefferson.edu
Anatomic Variation/Pitfalls Effusion [Figure 3]

[Figures 1 & 2] !" Fat pads are intracapsular and
!" Trochlear sulcus extrasynovial
!" Capitellar pseudodefect !" DDx:
!"DDx: location; no underlying edema !"Fracture
!" Residual hematopoietic marrow !"Arthritis (RA, OA, septic)
!"Internal derangement (eg, ligament,
cartilage)
Figure 1 A & B
Top Image:
Normal
variation- Figure 3 A & B
trochlear sulcus. Left Image: Joint effusion on lateral radiograph. Note
displacement of fat pads.
Bottom Image: Right Image: Complex joint effusion on sagittal MRI in
Capitellar a patient with rheumatoid arthritis.
pseudodefect.
Note lack of
underlying Cartilage Loss [Figure 4]
marrow !" !"#$%&'()(*)7,,)+"-,%('<)0%/-("'/2,)(9".4
abnormality. !" Subchondral marrow edema best sign
!" Osteophytes: posterior/medial/coronoid
process
!"F*.$-8)%/-()'*77D%/&7,)"8:".2,8,.(
!" Associated with effusion and bodies
Figure 4
Focal
cartilage
defect with
underlying
Figure 2 subchondral
Hematopoietic cystic
marrow at change.
proximal radius
on STIR image.
MRI of the Elbow 1131 Musculoskeletal Radiology

Osteochondral Defect [Figure 5]
!" Capitellum: third most common site (after
ankle, knee)
!" Repetitive microtrauma during valgus
(associated with MCL)
!" Symptoms: pain, locking
!" Sequellae: bodies/OA Figure 7
!" Q(/2".2[)C&"+D%<7()&.+,-)#-/28,.()p)
Intraarticular
loose (unstable)
body on MR
arthrogram.
Note contrast
completely
surrounding
the body,
/1$&">3$E*
the diagnosis.
Synovial Fold [Figure 8]

!" Lateral plica syndrome
!"Posterolateral catching /locking
Figure 5
H5X*#!*!6(*/#:3!(00.>*<3!6*.$)("0,3$E*?.3)*@.$%!#+0(*
fragment) on MR arthrogram.
Intraarticular Bodies [Figures 6 & 7]

!" May not be visible on X-ray
!" Variable signal on MRI
!" May not have apparent donor site Figure 8
!" Often adherent to synovium
!"Intraarticular, not loose Posterolateral
#" H**W)#*-)C&"+)7&--*&.+".2) synovial fold.
Note overlying
questioned body cartilage
#" DDx synovial fold, extracapsular loss and
focus cystic change
indicating
pathology.
Figure 6
Intra- Ulnar Nerve Impingement: Cubital
articular
body in the Tunnel Syndrome [Figure 9]
annular !" Cubital tunnel
recess. !"Fibro-osseous tunnel next to medial
epicondyle
!"Osborne ligament overlies tunnel
!"Look for:
#" Increased T2 signal in nerve
#" Fascicular anatomy (“dots”)
#" Enlargement
#" Subluxation from groove
#" Distal muscle edema

Biceps Anatomy
!" Long head: superior glenoid
!" Short head: coracoid
!"Two heads merge distal to the bicipital
groove
!" Insertion onto radial tuberosity at elbow
!"Intimate with brachialis
!" Proximal: synovial sheath
!" Distal: paratenon, bicipitoradialis bursa
Figure 9 /.+)'/%,-(&7)$1-*7&7
A&B
Top Image: Biceps Injury

Normal ulnar
nerve in
the cubital
tunnel.
Bottom
Image:
Abnormal
ulnar nerve in
a patient with
cubital tunnel
syndrome.
Note edema
and ‘dots’
(fascicular
pattern) in
nerve.
Biceps: Partial Tears [Figures 11 & 12]

Epicondylitis [Figure 10] !" Attritional
!" V,+"/'[)2*'#,-k7),'1*a)0%*88*.)C,3*-) !" Pain
origin) !" No pop, usually no ecchymosis
!" Lateral: tennis elbow (common extensor !" More marrow edema and bursitis
origin) !" Surgery not usually needed unless large
!" Spectrum from degeneration to partial to !" U.(/%()'/%,-(&7)$1-*7&7)8/<):-,E,.()
complete tear retraction of tear
!" Increased T1 signal
!" Increased STIR, T2 signal
!" Linear vs diffuse
!" Histologically: angioblastic changes/
$1-"''/-)%*''/2,.)+,2,.,-/("*.
Figure 11 A & B
Left Image: Partial biceps tendon tear.
Right Image: Complete biceps tear with retraction.
Figure 10 A & B
Left Image: Partial tear of the common extensor origin
(tennis elbow).
Right Image: Following acute injury, complete tear of
!6(*/1>>1$*?('1"*1"3E3$D

Todos la tenemos, no es adquirida por fricción.
Bicipitoradialis Bursitis [Figure 12] Olecranon Bursitis [Figure 14]
!" Distal biceps lacks a sheath !" Anatomic bursa
!" ^::/-,.()C&"+)/-*&.+)"7)1&-7/' !" ;*-8/''<).*)C&"+)E"7"1',
!" Close to insertion !" O&-7"("7[)C&"+M)'*77)*#)7&1u)#/()/+T/%,.()(*)
!" DDX; vessel olecranon
!" Associated with biceps tears (esp partial), !" Causes
!" L^M)8,%9/."%/')c)8/<1,)$-7( !"Trauma, RA, gout, infection
!" Mechanical
!"Student’s elbow
!"Plumber’s elbow
!"Roofer’s elbow
Figure 12
Massive
bicipitoradialis
bursitis
associated
with a partial
tear of the
biceps tendon.
Triceps Injuries [Figure 13]

!" Fairly uncommon
!" Spectrum tendonitis (posterior tennis
elbow/posterior impingement), snapping,
to tear
!" Risk factors: steroids, SLE, CRF, RA, gout
!" Within 2-3 cm of insertion, usually at
!"Associated olecranon bursitis
!"Associated soft tissue edema
Figure 14
!" Look for avulsion fx
Olecranon bursitis: mechanical.
Medial Collateral Ligament

[Figure 15]
!" AKA ulnar collateral ligament (UCL)
!" Three segments
!"Anterior bundle Más importante
#" Most important soft tissue static
constraint to valgus stress
!"Posterior bundle
!"Transverse bundle
!" Anatomy: anterior/posterior/transverse
bands
!"Strongest is anterior
!" Pathophysiology: overhead throwing,
valgus overuse, weakens/incompletely
heals, reinjures
!" Partial tears: “T” sign vs complete tears
!" Old tears show thickening +/- bowing
Figure 13 !" Association with epicondylitis
Triceps tear with olecranon bursitis.

Figure 15
A, B & C
Figure 16 A & B
Top Left Left Image: Normal radial collateral ligament.
Image: Right Image: Proximal tear of the radial collateral
Normal MCL ligament.
(medial
collateral LUCL
ligament !" Posterior “hammock” for radial head
also known
!" Major stabilizer rotational and varus
as the ulnar
collateral stress
ligament). !" Injuries caused by a fall on an
outstretched hand
Top Right !" Iatrogenic injury during release or repair
Image: Tear
of the distal
of lateral epicondylitis
aspect of the
MCL with Posterolateral Rotatory Instability
surrounding !" Instability of the elbow manifested by
edema on painful clicking of the elbow in extension
STIR image. !" Radial head moves posteriorly in relation
Bottom Right to the capitellum
Image: !" Essential lesion – tear of the LUCL
“T-sign.” Partial thickness undersurface tear of the !" Lateral pivot shift test
MCL from the sublime tubercle. Contrast extending !"Supination with axial and valgus stress
under ligament on MR arthrography.
LUCL Injuries [Figure 17]
Lateral Ligaments
!" Three main components
!"Lateral collateral ligament proper
(LCL) (radial collateral ligament)
!"Annular ligament
!"Lateral ulnar collateral ligament
(LUCL)
Annular Ligament
!" Fibro-osseous ring that encircles and
stabilizes the radial head
!" Attaches on the anterior and posterior
edges of the lesser sigmoid notch
!" Anterior portion taught in supination and
posterior portion taught in pronation
!" “Nursemaid’s elbow” in children
!" Atretic in adults
Radial Collateral Ligament [Figure 16]

!" Extends from the lateral epicondyle and
attaches to the annular ligament
!" Immediately deep to the common Figure 17A
extensors LUCL.

Figure 17B
Tear of the proximal aspect of the LUCL.
Osseous Injury [Figure 18]

!" Effusion on X-ray: presumed fx
!" Follow-up X-ray vs MR
!" Bone marrow edema after trauma: bone
bruise vs fracture
!"T1: focal low signal (linear) = fracture
!";*)'".,M)"''?+,$.,+),+,8/)p)1-&"7, Figure 18B
STIR image showing edema in the radial neck.
Osteochondral Impaction [Figure 19]

!" Analogous bruises from ACL tears
!" Transient disloc/sublux
!" Often both sides of joint
Figure 18A
(A) T1-WI showing a low signal line representing

fracture through the radial neck.
Figure 19
Osteochondral impaction injury of the capitellum.

References
1. Kijowski R, Tuite M, Sanford M. Magnetic resonance imaging of the elbow. Part I: normal anatomy,
imaging technique, and osseous abnormalities. Skeletal Radiol 2004 Dec;33(12):685-97.
2. Kijowski R, Tuite M, Sanford M. Magnetic resonance imaging of the elbow. Part II: Abnormalities of the
ligaments, tendons, and nerves. Skeletal Radiol 2005 Jan;34(1):1-18.
3. Fowler KA, Chung CB. Normal MR imaging anatomy of the elbow. Radiol Clin North Am. 2006
Jul;44(4):553-67, viii.
4. Rosenberg ZS, Bencardino J, Beltran J.MR imaging of normal variants and interpretation pitfalls of the
elbow. Magn Reson Imaging Clin N Am 1997 Aug;5(3):481-99.
5. Ly JQ, Sanders TG, Beall DP.MR imaging of the elbow: a spectrum of common pathologic conditions. Clin
Imaging 2005 Jul-Aug;29(4):278-82.
6. Saliman JD, Beaulieu CF, McAdams TR. Ligament and tendon injury to the elbow: clinical, surgical, and
imaging features. Top Magn Reson Imaging 2006 Oct;17(5):327-36.
7. Ouellette H, Kassarjian A, Tétreault P, Palmer W.Imaging of the overhead throwing athlete. Semin
Musculoskelet Radiol 2005 Dec;9(4):316-33.
8. Bencardino JT, Rosenberg ZS.Entrapment neuropathies of the shoulder and elbow in the athlete. Clin
Sports Med 2006 Jul;25(3):465-87, vi-vii.

1138
Neuroradiology
1139
1140
Imaging of Demyelinating Diseases

Demyelinating Disorders [Figure 1] Revised McDonald Criteria
!" K/43..3)"+A(2".!"/'/)()*3)($/a,+'#( !" Space
white matter !"Three of the following:
!" Oligodendrocyte: wraps axon to form #" j(Z(-30"&$/$,.W'/*3/2$/-(&'#$"/(
myelin sheath or 9 T2 hyperintense lesions if
!" These disorders affect: there is no gadolinium enhancing
!"Oligodendroglial survival lesion
!"Oligodendroglial metabolism #" j(Z($/6+3)'/)"+$3&(&'#$"/
!"Myelin sheath #" j(Z(a,L)32"+)$23&(&'#$"/
!" Now evidence that myelin is not only #" j(^(!'+$5'/)+$2,&3+(&'#$"/#
tissue damaged !" Time
!"Detection of gadolinium enhancement
j(^(."/)*#(36)'+("/#')("6($/$)$3&(
clinical event, if not at site
corresponding to initial event
!"Detection of new T2 lesion if it
appears at any time compared with
+'6'+'/2'(#23/(0"/'(j(^>(03A#(36)'+(
onset of initial clinical event
Multiple S/&1%"(,(7+Preferred Locations

[Figure 2]
!" Periventricular region
!" Corpus callosum
!" Subcortical
!" Optic nerves and visual pathways
!" Posterior fossa
!" Cervical region of spinal cord
Figure 1 A & B
Acute disseminated encephalomyelitis (ADEM):
Diffusion weighted image and ADC map in a patient Figure 2
with ADEM reveals a lesion with reduced diffusion
Multiple
(arrow), but many of the lesions demonstrate T2 shine
sclerosis:
through.
Sagittal T2-
weighted
image in a
patient with
Demyelinating Diseases MS reveals
hyperintense
!" Primary
ovoid lesion
!" Secondary perpendicular
!"Infectious to the lateral
!"Vascular ventricle
!"Metabolic/nutritional consistent
with Dawson
!"Toxic &-8'+4/
P%,*'%!7+Multiple Sclerosis
!" Most common demyelinating disease Multiple S/&1%"(,(7+Pathology
!" Etiology: unknown !" C*+"/$2($/43..3)"+A(!+"2'##
!" Peak age: 30 years !" Active lesion:
!" Diagnosis: clinical and paraclinical criteria !"Gitter cells
!" CSF oligoclonal bands !"`'+$53#2,&3+($/43..3)"+A(2,68/-(I$)*(
!" Time and space T and B lymphocytes
!" Inactive lesion:
!"Hypocellular
!"E"(!'+$53#2,&3+($/43..3)$"/
Imaging of Demyelinating Diseases 1141 Neuroradiology

Multiple S/&1%"(,(7+Imaging TDL
!" T1: Plaques iso- or low intensity !" 7$682,&)A($/(0$3-/"#$/-(B7;#("6)'/(&'30#(
!"“Black holes” to surgical biopsy
!" T2: High intensity !" k$#)"!3)*"&"-$2(8/0$/-#(23/(%'(.$#&'30$/-(
!" FLAIR does not detect lesions in posterior !"Misdiagnosis of glial neoplasm
fossa, brain stem, and spinal cord as well #" Hypercellularity
as T2 #" Atypical reactive astrocytes
#" <$)")$2(8-,+'#(
Multiple S/&1%"(,(7+Imaging [Figure 3] !" Unnecessary and potentially harmful
!" Enhancement: seen in active lesions surgical resection or radiation therapy
!"Solid
!"Ring-like TDL [Figure 5]
!"Arc-like !" Pathologically, highest Lac found in
!" MR spectroscopy: !&3l,'#(I$)*(*$-*($/43..3)"+A(32)$5$)A
!"Decreased N-acetylaspartate (NAA)
!"Increased choline, lipids, and lactate
!" Chronic cases: atrophy
Figure 3
Multiple
sclerosis.
Sagittal T2-
weighted
image of a
32-year-
old patient
with long-
standing MS.
Note marked
atrophy of
the body of
the corpus
callosum.
Figure 5
TDL: MR spectroscopy reveals an elevation in choline,

Tumefactive Demyelinating Lesions #%6%(4@)"-()#"$3"3')G?%$?)"+')&-(%-84)3?"3)$"-)"#4,)*')
seen in high grade glial neoplasms.
(TDL) [Figure 4]
!" Appearance mimics tumor
!" Clues
!"History
!"Other white-matter abnormalities
!"Less mass effect than expected for Multiple S/&1%"(,(7+Spine
size !" Can affect cord alone: 5%-24%
!"Leading edge of enhancement, !" Cervical region most common
incomplete ring !" 90% less than 2 vertebral body segments
!"Perfusion not increased in length
!"Veins course through
Multiple Sclerosis Syndromes [Figure 6]
!" Balo Concentric Sclerosis (BCS):
Figure 4
!"Multiple concentric rings
TDL. Axial !"Thought to be recurrence at same site
T1-weighted !" Neuromyelitis optica: cord and optic nerve
image reveals symptoms NMO-IgG
an incomplete
ring of
!"No longer considered MS syndrome
enhancement Now thought to be separate disorder
surrounding !" Schilder disease:
a right !"Aggressive/diffuse sclerosis
frontal lobe !"Bilateral relatively asymmetric
lesion. This
enhancement demyelination
pattern !" Marburg:
is highly !"Severe form with widespread white-
suspicious for matter lesions and rapid progression
a tumefactive
demyelinating
lesion.

A@=E7+Imaging [Figure 8]
!" Multiple lesions, may be large
Figure 6 !" T1: hypointense
!" T2: hyperintense
BCS.
Sagittal T1-
!" May enhance: nodular or ring pattern
WI reveals !" No new lesions after 6 months
a lesion in !" May be incomplete resolution of lesions
the temporal !" Periventricular: 50%
lobe. !" Brainstem, spinal cord, and cerebellar
Concentric
rings are white matter: 30%-50%
noted within
the lesion.
Neuromyelitis Optica (aka Devic

Disease) [Figure 7]
Figure 8 A & B
ADEM. Axial T2 FLAIR reveals multiple round and ovoid
lesions within the periventricular white matter. On the
postcontrast imaging, many of the lesions demonstrate
ring enhancement.
Figure 7 A & B
Neuromyelitis optica (NMO). Coronal T2-WI through the
orbits reveals an enlarged and hyperintense right optic
Acute Hemorrhagic Leukoencephalitis
nerve. Sagittal T2-WI demonstrates abnormal signal [Figure 9]
within the cervical cord.
Infectious
!" Acute disseminated encephalomyelitis
(ADEM)
!" HIV-associated encephalitis
!" Progressive multifocal
leukoencephalopathy
!" Subacute sclerosing panencephalitis
!" Lyme disease Figure 9 A & B
Acute hemorrhagic leukoencephalitis. Axial non-
ADEM contrast CT demonstrates large areas of low
!" Can look like MS – history different attenuation involving the left hemisphere. Foci of
!"Monophasic high attenuation are present in the left frontal lobe
!" Etiology: allergic or autoimmune reaction consistent with hemorrhage, and there is mass
effect with subfalcine herniation. The gross image
with viral protein demonstrates the hemorrhagic area within the left
!" 10%-30% neurologic sequelae frontal lobe.
!"Acute hemorrhagic leukoencephalitis
(Hurst disease) rapidly progressive
variant – fatal within one week
!" Diagnosis: history and lab AIDS Encephalopathy
!"CSF: may demonstrate increased !" HIV-associated chronic,
WBC’s and increased myelin basic neurodegenerative syndrome
protein !" 15%-20% of AIDS patients
!" 7$66,#'(!'+$5'/",#($/43..3)"+A(!+"2'##( !" Diagnosis: clinical
!"V'#,&)#($/(2"/4,'/)(3+'3#("6( !" Pre-HAART median survival after onset of
demyelination dementia: 6 months
!" Cortical and deep gray matter also
involved

AIDS E./10?'&"0')?!7+Imaging [Figure 10]
!" CT:
!"Cerebral atrophy
!"Low density periventricular and deep
white matter
!" MR:
!"T2 prolongation: symmetric patchy or
2"/4,'/)(3+'3#($/(!'+$5'/)+$2,&3+(3/0(
deep white matter
!"No evidence of mass effect or
enhancement
!"MRS: reduced NAA, increased Ch and
lactate
Figure 11 A & B
PML. Coronal T2 FLAIR demonstrates multifocal
areas of T2 prolongation involving the subcortical
white matter that do not exert mass effect. On
the postcontrast T1-WI there is no associated
enhancement.
Subacute Sclerosing Panencephalitis

(SSPE)
!" Slow virus infection
!" About half of patients had measles before
age 2
!" Mean age: 7 years
!" Insidious onset of behavior changes and
Figure 10 A & B mental deterioration
AIDS encephalopathy. Axial T2-WI from a 42-year- !" Death: 1-3 years
old man demonstrates a marked prominence of the !" Diagnosis:
ventricles and sulci for age. There are symmetric !"Characteristic periodic EEG discharges
regions of hyperintensity within the periventricular
!"Raised measles antibody titre in
white matter. On the postcontrast imaging there is no
associated enhancement. plasma and CSF
SSPE [Figure 12]

Progressive Multifocal !" <3A(%'(/"+.3&(8+#)(^W](."/)*#(
Leukoencephalopathy (PML) !" T2 hyperintensity:
!" Progressive demyelinating disorder !"Cerebral cortex and white matter:
!" Results from CNS infection with JC Asymmetric but bilaterally in parietal
papovavirus and occipital lobes (acute)
!"Up to 80% of people infected prior to !"Periventricular, corpus callosum, basal
adulthood without producing illness ganglia, cerebellum, and pons
!"Latent in CNS – reactivates in setting !" May enhance
of immune compromise !" Generalized atrophy (late)
!" Found in 5% of autopsies in patients with
AIDS
!" AIDS patients with very low CD4 counts
Figure 12
!"50-100 cells/mm3
!" Oligodendrocytes infected unable to Subacute
maintain myelin: focal demyelination sclerosing
panen-
FEG7+Imaging [Figure 11] cephalitis:
!" CT: Axial T2
weighted
!"Asymmetric, focal zones of image
hypodensity: periventricular or demonstrates
subcortical white matter asymmetric
!" MR T2
hyperintensity
!"Asymmetric, multifocal T1/T2 involving
prolongation the bilateral
!"K/5"&5'.'/)("6(#,%2"+)$23&(M(8%'+# parietal lobes
!"Mass effect, hemorrhage, and
enhancement usually absent – mild if
present

Lyme Disease PRES [Figure 15]
!" Borrelia burgdorferi !" A disorder of cerebral vascular
!" CNS: 10%-15% autoregulation
!" Multiple parenchymal abnormalities + CN !" Most have history of recent elevated BP
enhancement + endemic area !" Symptoms: headache, seizures,
confusion, drowsiness, and visual
L!*17+Enhancement of CN V [Figure 13] disturbance
!" 2 pathophysiologic mechanisms proposed:
!"Cerebral vasospasm with resulting
ischemia
!"Hyperperfusion due to breakdown of
cerebral autoregulation with interstitial
'L)+353#3)$"/("6(4,$0

Lyme disease. Coronal and axial T1-WI with contrast
reveals enhancement of the bilateral trigeminal PRES. Axial
nerves. T2-WI
demonstrates
Vascular White Matter Disease symmetric
!" Senescent white-matter changes vasogenic
!" Cerebral autosomal dominant arteriopathy edema
involving
with subcortical infarction and the bilateral
leukoencephalopathy (CADASIL) occipital
!" Posterior reversible encephalopathy lobes.
syndrome (PRES)
!" Vasculitis
Cadasil [Figure 14]

!" Familial, nonamyloid microangiopathy
!"Mutation of Notch3 gene on
chromosome 19 PRES
!" Early onset ischemic stroke (40-50’s) !" CT and MR:
!"Migraine in younger !"Symmetrical areas of vasogenic
!" Multi-infarct dementia edema predominantly posterior
!" Affects frontal lobes, temporal lobes, and circulation
insula !"Localized mass effect, hemorrhage,
!" BA!$23&&A($/5"&5'#(#,%2"+)$23&(M(8%'+# and subtle enhancement described
!" Primarily white matter, but cortex also
involved
!" DWI:
!"Distinguish vasogenic edema in PRES
from cytotoxic edema
!" Reduced rCBV
!" When promptly recognized and
treated, the symptoms and radiologic
abnormalities can be reversed
!" Untreated patient can progress to
ischemia, infarction, and death
Vasculitis
!" k')'+"-'/'",#(-+",!("6($/43..3)"+A(
disorders
!" Primarily affect small leptomeningeal and
parenchymal vessels
!" Etiologies:
Figure 14 !"Autoimmune disease: SLE
CADASIL. Axial T2 FLAIR image in a 52-year-old adult !"Radiation
+':'"#4)$,-01'-3)+'8%,-4),<)5J)?>6'+%-3'-4%3>)G%3?%-) !"Infection: syphilis, TB, HIV
the white matter of the bilateral temporal lobes. The !"Cocaine
41*$,+3%$"#)E)&*'+4)"+')%-:,#:'(/

V'(/9&,),(7+Imaging [Figures 16 & 17]
!" Multiple areas of T2 hyperintensity
!"Deep and subcortical white matter
!" May enhance
!" May appear identical to MS
!" Infarction and hemorrhage may be seen
!" Angiography: segmental narrowing and Figure 18
dilatation
Osmotic
myelinolysis.
Axial T2 FLAIR
image through
the level of
the basal
ganglia reveals
hyperintensity
involving the
bilateral basal
ganglia and
thalami.
Axial T2 FLAIR
image through
the level of the
pons reveals
T2 prolongation
within the pons
Figure 16 A & B that spares the
periphery.
Vasculitis secondary to methamphetamine. Axial
There is
T2-WI reveals multiple foci of hyperintensity
also some
predominantly in the right parietal region. On the
sparing of the
diffusion-weighted image, reduced diffusion is present.
corticospinal
tracts.
Figure 19
Figure 17
]"4$1#%3%49)[F)3%.'2,<20%8?3)CAB)+':'"#4)4'8.'-3"#)
narrowing and dilatation. Figure 20
Metabolic/Nutritional
!" Osmotic demyelination
!" Alcoholism
!" 9ZO(0'82$'/2A
Osmotic Myelinolysis [Figures 18 to 20]

!" Acute demyelination involving central
pons and/or basal ganglia, thalami, or
cerebral white matter
!"Oligodendroglial cells most susceptible
to osmotic stresses
!" Rapid shifts in serum osmolality
!"Classic setting ! rapid correction of
hyponatremia
Osmotic Demyelination [Figure 21]
!" Sparing of blood vessels, most nerve
cells, and axons
!" T2 hyperintensity: central pons,
extrapontine structures Figure 23
!" DWI: may be reduced
Axial T2 FLAIR
!" Typically no enhancement demonstrates
!" Demyelination characterized vacuolization cystic
and rupture of myelin sheaths presumably degeneration
due to osmotic effects along the
corpus.
Figure 21
Osmotic
demyelination.
Myelin stain
reveals loss of
myelin within Wernicke [Figure 24]
the central
region of the
pons with
sparing of
the periphery
and the
corticospinal
tracts.
Figure 24 A & B
Alcohol [Figures 22 & 23]
!" Atrophy: cerebral hemispheres, superior Wernicke encephalopathy. Coronal T1-WI of an
alcoholic patient demonstrates enhancement of
vermis
the bilateral mammillary bodies. Photograph of the
!" Marchiafava-Bignami gross specimen from the same patient demonstrates
!"Demyelination of corpus callosum petechiae within the mammillary bodies.
!"Typically severe alcoholics
!"Usually fatal although various forms of
disease: acute, subacute, chronic B12 D1#/,1./!+++++++[Figure 25]
!" Wernicke encephalopathy !" Most common cause in US: pernicious
!"B*$3.$/'(0'82$'/2A anemia
!"Severe memory impairment !" Subacute combined degeneration
!"Atrophy of mammillary bodies !"Loss of position and vibration,
paresthesias of hands and feet, lower
extremity weakness
!"Can affect brain, optic tracts, and
peripheral nerves
!"Demyelination and axonal loss
posterior and lateral spinal cord
columns
!"MR: T2 hyperintensity posterior
columns

Marchiafava-Bignami. Sagittal T1-W image ]%3".%-)ISJ)('&$%'-$>/)BU%"#)5J)2^7)('.,-43+"3'4)
demonstrates marked thinning of the body of the hyperintensity along the dorsal columns of the
corpus callosum. Axial T2 FLAIR demonstrates cystic cervical cord. Myelin stain reveals loss of myelin in the
changes in the region of the corpus callosum. posterior columns and to a lesser degree in the lateral
columns.
Toxic Methotrexate [Figure 27]
!" Radiation !" Major cause of acute neurotoxicity
!" Drugs !"Leukoencephalopathy
!"Incidence: 9%-35%
Radiation [Figure 26] !" Pathophysiology: unclear
!" Can produce demyelination !" T2 hyperintensities in PVWM
!" May cause mineralizing microangiopathy !"Centrum semiovale
!" Telangiectasia !" Reduced diffusion: cytotoxic edema
!" Hemosiderin deposition !"Suggests direct neurotoxic effect on
!" BBB disruption cell
!" Delayed radionecrosis can come on as late
as 20 years after radiation
Figure 26 A & B
Radiation
necrosis in
a patient
who received
radiation
therapy for
carcinoma Figure 27 A & B
of the right
external ear. Methotrexate toxicity. Axial T2 FLAIR demonstrates
Axial T2 FLAIR a focus of T2 hyperintensity within the right centrum
demonstrates semiovale. The ADC map reveals low signal in the same
abnormality +'8%,-)$,-&+.%-8)+'(1$'()(%<<14%,-/
within the right
temporal lobe
with extensive Methanol Poisoning [Figure 28]
vasogenic
edema.
On the
postcontrast
imaging there
is “lacy”
enhancement
within the
right temporal
lobe. MR
spectroscopy
reveals
a global
reduction in
metabolites. Figure 28 A & B
Methanol poisoning. Axial noncontrast CT

demonstrates low attenuation within the bilateral
putamen and the subcortical white matter. Photograph
of the gross specimen from the same patient reveals
hemorrhagic necrosis of the bilateral putamen.
Toxins/Drugs Heroin
!" IV drug abuse !" Leukoencephalopathy
!" Chemotherapy !"Likely due to impurity in heroin
!" Methanol: optic nerve atrophy with !" Inhalation of heroin vapor
necrosis of putamen and subcortical white !"Drug heated on tinfoil – “chasing the
matter dragon”
!" Mercury: calcarine area, cerebellum, and !" Cerebellar or extrapyramidal syndromes
postcentral gyri !" MR imaging:
!" Toluene: atrophy of cerebrum, corpus !"Involvement of the posterior limbs of
callosum, and cerebellar vermis the internal capsule
!"“Bearded” skull

Conclusions
!" Demyelinating processes can have similar imaging appearances
!"Age of patient, clinical history important
!" May mimic neoplasm – keep in back of mind
References
1. Lisanti CJ, Asbach P, Bradley WG, Jr. The Ependymal “Dot-Dash” Sign: An MR Imaging Finding of Early
Multiple Sclerosis. Am J Neuroradiol Sep 2005;26:2033-6.
2. Benedict HB, Zivadinov R, Carone DA, Weinstock-Guttman B, Gaines J, Maggiore C, Sharma J, Tomassi
M, Bakshi R. Regional Lobar Atrophy Predicts Memory Impairment in Multiple Sclerosis. Am J Neuroradiol
Aug 2005;26:1824-31.
3. Bakshi R, Ariyaratana S, Benedict RH, Jacobs L. Fluid-attenuated inversion recovery magnetic resonance
imaging detects cortical and juxtacortical multiple sclerosis lesions. Arch Neurology 2001;58:742-8.
4. Miller DH, Grossman RI, Reingold SC, McFarland HF. The role of magnetic resonance techniques in
understanding and managing multiple sclerosis. Brain 1998;121:3-24.
5. Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG. Multiple sclerosis. N Engl J Med
2000;343:938-52.
6. Cha S, Pierce S, Knopp EA, Johnson G, Yang C, Ton A, Litt AW, Zagzag D. Dynamic contrast-enhanced
T2*-weighted MR imaging of tumefactive demyelinating lesions. Am J Neuroradiol 2001 Jun-
Jul;22(6):1109-16.
7. Prayson RA. 2005. Neuropathology. Philadelphia, PA: Elsevier. pp. 200-7.
8. Barkovich AJ. Pediatric Neuroimaging 4th ed. Philadelphia, PA: Lippincott. pp. 110-8.
9. Grossman RI, Yousem DM. The Requistes: Neuroradiology 2nd ed. Philadelphia, PA: Moby pp. 331-61.
10. C3+322$"&"(XB1(<,+)3-*(V71(V"a$3/$(@<1(<,+)3-*(:VT(`3)*"-/"."/$2(<V($.3-$/-(8/0$/-#($/(%3&"(2"/2'/)+$2(
sclerosis. Am J Neuroradiol Feb 2001;22:292-3.
11. Honkaniemi J, Dastidar P, Kahara V, Haapasalo H. Delayed MR Imaging changes in acute disseminated
encephalomyelitis. Am J Neuroradiol Jun 2001;22:1117-24.
12. Bonsack TA, Robertson RL, Lacson A, Casadonte JA, Buonomo C. Pediatric case of the day. Myelinoclastic
diffuse sclerosis (MDS) (Schilder disease). RadioGraphics 1996;16:1509.
13. Donovan Post MJ, Yiannoutsos C, Simpson D, Booss J, Clifford DB, Cohen B, McArthur JC, Hall CD.
`+"-+'##$5'(.,&)$6"23&(&',D"'/2'!*3&"!3)*A($/(@K7GN(3+'()*'+'(3/A(<V(8/0$/-#(,#'6,&()"(!3)$'/)(
management and predictive of patient survival? Am J Neuroradiol Nov 1999;20:1896-906.
14. Usiskin SI, Bainbridge A, Miller RF, Jager HR. Progressive multifocal leukoencephalopathy: serial high-b-
53&,'(0$66,#$"/WI'$-*)'0(<V($.3-$/-(3/0(3!!3+'/)(0$66,#$"/(2"'682$'/)(.'3#,+'.'/)#()"(3##'##(+'#!"/#'(
to highly active antiretroviral therapy. Am J Neuroradiol Feb 2007;28:285-6.
15. Sener RN. G,%32,)'(#2&'+"#$/-(!3/'/2'!*3&$)$#(8/0$/-#(3)(<V($.3-$/-1(0$66,#$"/(<V($.3-$/-1(3/0(!+")"/(
MR spectroscopy. Am J Neuroradiol May 2004;25:892-4.
16. Garg RK. Subacute sclerosing panencephalitis. Postgrad Med J 2002;78:63-70.
17. Singhal S, Rich P, Markus HS. The spatial distribution of MR imaging abnormalities in cerebral autosomal
dominant arteriopathy with subcortical infarcts and leukoencephalopathy and their relationship to age and
clinical features. Am J Neuroradiol 2005 Nov-Dec;26(10):2481-7.
18. Ruzek KA, Campeau NG, Miller GM. Early diagnosis of central pontine myelinolysis with diffusion-weighted
imaging. Am J Neuroradiol Feb 2004;25:210-13.
19. Fisher MJ, Khademian ZP, Simon EM, Zimmerman RA, Bilaniuk LT. Diffusion-weighted MR imaging of early
methotrexate-related neurotoxicity in children. Am J Neuroradiol Aug 2005;26:1686-9.
20. Keogh CF, Andrews GT, Spacey SD, Forkheim KE, Graeb DA. Neuroimaging features of heroin inhalation
toxicity. Am J Roentgenol 2003;180:847-50.
21. Filley CM, Kleinschmidt-DeMasters BK. Toxic leukoencephalopathy. N Engl J Med 2001;345:425-32.
22. Barkovich AJ. Concepts of myelin and myelination in neuroradiology. Am J Neuroradiol 2000 Jun-
Jul;21(6):1099-109.
23. Polman CH, Reingold SC, Edan G, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the
“McDonald Criteria.” Annals of Neurology. 2005;35(6):840-6.

1150
Cerebral Intraventricular Neoplasms
Intraventricular Lesions Ependymoma
!" Signs and symptoms: !" WHO grade II (low grade, well-
!"Increased intracranial pressure differentiated) or III (anaplastic)
!"Hydrocephalus !" 5-year survival 60%-70%
!"Fourth ventricle: cerebellar ataxia and !"Less favorable prognosis for children
paresis < years old and fourth ventricular
location
Intraventricular Neoplasms (T?,.H7+ !" Recurrence after resection – if subtotal
Location and Age) !"5-year survival after recurrence: 15%
!" Ependymoma
!" Subependymoma Ependymomas [Figure 2]
!" Central neurocytoma !" M#,3&&A(8&&(5'/)+$2,&3+(&,.'/
!" Subependymal giant cell astrocytoma !" May extend into adjacent brain
!" Choroid plexus papilloma and carcinoma parenchyma
!" Meningioma !" Fourth ventricle: frequently extend
!" Chordoid glioma through foramen of Luschka and foramen
!" Craniopharyngioma magnum
!" Metastasis !" C3&2$823)$"/N(]>?WQ>?
!" Epidermoid/dermoid/teratoma !" May have CSF dissemination (3%-17%)
!" Astrocytoma
!" Primitive neurectodermal tumor
!" Ganglioglioma
!" Fibroma
Ependymoma [Figure 1]
!" 3%-5% of intracranial neoplasms
!" Any age
!"1/3 of brain tumors in patients < 3
years old
!"Most posterior fossa ependymomas
arise in children (mean age 6 years)
!"Supratentorial mean age 18-24 years
!" Arise from ependymal cells of ventricular
wall
!" Supratentorial ependymomas more
commonly extraventricular
!"May arise from embryonic rests
of ependymal tissue trapped in
developing cerebral hemisphere Figure 2
Ependymoma. Photograph of a gross specimen
demonstrates a 4th ventricular ependymoma that
extends through the foramen of Luschka into the
cerebellopontine angle.
Figure 1
Intraparen- E01.5!*"*'7+Imaging [Figure 3]

chymal !" CT:
ependymoma. !"Iso- to hyperattenuated
Axial T2- !"Ca++ common
WI reveals
a large !"Variable enhancement
cystic lesion !"May have cysts or hemorrhage
involving the !" MR:
right parietal !"T1: iso- to hypointense
lobe. !"T2: iso- to hyperintense
!"May see cystic foci, hemorrhage, or
23&2$823)$"/(
!"Heterogeneous enhancement
Cerebral Intraventricular Neoplasms 1151 Neuroradiology

Figure 4
Subependymoma.
Axial noncontrast
Figure 3 A & B CT reveals a well-
circumscribed
Ependymoma. lesion involving
Sagittal T1-WI the frontal horn
demonstrates of the left lateral
a hypointense ventricle. There
#'4%,-)&##%-8)3?') is no associated
4th ventricle edema within the
and extending adjacent brain
through the parenchyma.
foramen
magnum. On
the sagittal T2-
WI the lesion is
hyperintense.
There is S9$101.5!*"*'7+EI+Imaging [Figure 5]
associated !" T1: hypo- to isointense to white matter
hydrocephalus. !" T2: hyperintense
!" Heterogeneity due to cystic changes,
blood, calcium
!" Enhancement varies – typically none to
mild
!" Typically, no edema in adjacent brain
Subependymoma
!" Most likely arise from subependymal glial
layer surrounding cerebral ventricles
!" WHO grade I
!" 0.7% of intracranial neoplasms
!" Majority occur in fourth (60%) and lateral
ventricles
!" 82% of patients > 15 years old
!" Male predominance Figure 5 A & B
!" Most < 2 cm
!" Many patients asymptomatic (60%) – Subependymoma.
Coronal T1-weighted with contrast image reveals
$/2$0'/)3&(8/0$/- an uncommon case of bilateral subependymomas.
!" Recurrence after surgical resection rare The lesions do not demonstrate any enhancement.
Photograph of the corresponding gross specimen.
Subependymoma [Figure 4]
!" Well circumscribed
!" CT: hypo- to isointense
!" Enhance variably Ependymoma vs Subependymoma
!" C3&2$823)$"/(3/0(2A#)$2(0'-'/'+3)$"/(
common

Central Neurocytoma [Figure 6 ]
!" 0.25%-0.5% of intracranial tumors
!" WHO grade II
!" Etiology unclear: may be derived from
bipotential progenitor cells that are
capable of both neuronal and glial
differentiation
!" Lateral and third ventricles
!" Arise from septum pellucidum or
ventricular wall
!" Mean age: 29 years
!" Histologic features similar to
oligodendroglioma
!" “Fried egg” appearance
Figure 7 A, B & C
Central
neurocytoma.
Figure 6 Axial noncontrast
CT reveals an
Central intraventricular
neurocytoma. lesion with
Photograph $"#$%&$"3%,-4/))
of a gross Axial T2-WI
specimen demonstrates a
demonstrates centrally located
a centrally neoplasm with foci
located of hyperintensity
lesion with consistent with
attachment cystic areas. On
to the septum the postcontrast
pellucidum. image the lesion
heterogeneously
enhances.
Central Neurocytoma
!" Well-circumscribed, lobulated mass with
Subependymal Giant Cell A()%"/!)"*'7+
intratumoral cyst-like areas
!" F6)'/(2"/)3$/(23&2$823)$"/(HR>?J(3/0((
Imaging [Figure 8]
!" C3&2$823)$"/(53+$3%&'
may hemorrhage (rare)
!" May have hydrocephalus
!" Extraventricular neurocytoma: brain
!" Typically > 1 cm
parenchyma, cerebellum, and spinal cord
!" CT:
!" Gross total resection usually curative
!"Hypo- to isodense
Central N19%"/!)"*'7+Imaging !"Strong enhancement
[Figure 7] !" MR:
!" CT: !"T1: hypo- to isointense to gray matter
!"Iso- to hyperdense !"T2: iso- to hyperintense
!"Moderate, heterogeneous !"Avid enhancement
enhancement !"Does not seed CSF pathways
!" MR:
!"T1: mostly isointense to gray matter
!"T2: hyperintense, heterogeneous
“bubbly”
!"Moderate to strong enhancement -
heterogeneous
!"Craniospinal dissemination very rare
Subependymal Giant Cell Astrocytoma

!" Most common cerebral neoplasm in
tuberous sclerosis (up to 15%)
!" Probably arise from subependymal nodule
!" WHO grade I
!" Uncommon Figure 8
!" <"#)(23#'#N(8+#)(3/0(#'2"/0(0'230'
!" Near foramen of Monro Subependymal giant cell astrocytoma.
!" Resection: symptoms or growth on MR Coronal T1 postcontrast reveals an enhancing lesion
!"Recurrence after resection rare adjacent to the foramen of Monro.

Choroid Plexus Papilloma (CPP) [Figure 9]
!" Choroid plexus tumors:
!"2%-4% of pediatric brain tumors
!"0.5% of adult brain tumors
!" May be present at birth
!" CPP WHO grade I
!" Lateral ventricle most common site: 50%
(no gender predilection)
!"Fourth ventricle more common in
males (M:F = 3:2)
!"Can occur in multiple sites (5%)
!" Hydrocephalus
!" Seeding of cells occurs with both CPP and
CPC
Figure 10
CPP. H and E stain of a CPP demonstrates a papillary
architecture with rows of columnar cells surrounding
")&*+,:"4$1#"+)$,+'/)5?%4)%4)")4%.%#"+)"66'"+"-$')3,)
normal choroid plexus.
4FF7+Imaging
!" CT:
!"Iso- or hyperattenuating
!"Intense enhancement
!"CTA: enlarged choroidal artery
(trigonal CPPS)
!" MR:
!"T1: iso- to hypointense
!"T2: iso- to hyperintense
Figure 9 !"_3#2,&3+(4"I(5"$0#
!"Avid enhancement - homogeneous
Choroid plexus papilloma. Sagittal T1-WI
demonstrates an avidly enhancing intraventricular
!" Imaging alone cannot distinguish CPP
neoplasm in an infant. There is marked hydrocephalus from CPC
and enlargement of the head circumference.
Choroid Plexus Carcinoma (CPC)
!" Malignant tumor arising from choroid
Results plexus epithelium
!" Of 65 patients in the AFIP archives with !"WHO grade III
choroid plexus neoplasms of the lateral !" Median age 26 months
ventricle : !" 5-year survival: 26%-50%
!"50 were CPP (77%): age range 4 days !" Necrosis and parenchymal invasion
m(]Z(A'3+#Y(=>?(n(R(A'3+# !" C3&2$823)$"/N(O>?WOR?
!"4 were atypical (6%): ages 3 months,
20 months, 2 years, 51 years 4F47+Imaging [Figures 11 and 12]
!"11 were CPC (17%): Age range 7 !"Iso- to hyperattenuating
."/)*#(W(R(A'3+#Y(QO?(n(O(A'3+# !"Heterogeneous enhancement
!" MR:
CPP [Figure 10] !"T1: iso- to hypointense
!" G"6)(I'&&W2$+2,.#2+$%'0(23,&$4"I'+W&$D'( !"T2: variable
masses !"Heterogeneous enhancement
!" Histologically similar to normal choroid !"CSF seeding: image entire neuraxis
plexus prior to surgery
!" Hemorrhage and cyst formation may be
seen
!" C3&2$823)$"/N(O]?
!" Can extend from one ventricle to another
or to CPA
!" May be attached by vascular pedicle
to choroid plexus ! can move causing
intermittent ventricular obstruction

Meningioma
!" Common intraventricular neoplasms in
adults
!" 0.7% of all meningiomas
!" Peak age 30-60 years
!" Females 2:1
!" Pediatrics: 1/5 of meningiomas
!" Risk of sarcomatous change
!" Suspect NF II when found in children
!" Believed to arise from arachnoidal cap
cells trapped in choroid
!" Trigone of lateral ventricle most common
site
Figure 11 A & B !" C3&2$823)$"/(HR>?J
!" Periventricular edema may be seen
CPC. Axial T2-W image !" Preoperative embolization may be
demonstrates a heterogeneous
mass arising from the left lateral %'/'82$3&
ventricle. Vasogenic edema is !" MRS:
present within the left hemisphere. !"Decreased NAA and Cr
Sagittal T1-W image postcontrast !"Increased Ch
demonstrates an enhancing
!"Variable amounts of lactate, lipid, and
."44)"#,-8)3?')&#1.)3'+.%-"#')$,-4%43'-3)G%3?)!;_)
dissemination. alanine (1.47 ppm)
Meningioma [Figure 14]

!" CT: hyperdense, avid enhancement
!" MR: iso- to hypointense on T1; iso- to
hyperintense on T2; avid enhancement
Figure 12
CPC. H and E
stain reveals
loss of the
papillary
architecture.
Diffuse
sheets of
cells are
seen and
there are
numerous
mitotic
&81+'4/
Figure 14 A & B
Meningioma. Noncontrast CT reveals a large, well-
circumscribed, hyperattenuating lesion in the region
of the atrium of the left lateral ventricle. There is
As Nasty as This One Looks? [Figure 13] associated vasogenic edema. Axial T1 postcontrast
('.,-43+"3'4)":%()'-?"-$'.'-3)"-()$,-&+.4)3?')
intraventricular location.
Chordoid Glioma
!" Recently described neoplasm – WHO II
!" Rare
!" Occurs in region of anterior third ventricle
and hypothalamus
!" Sxs: Headaches, hydrocephalus,
hypothalamic dysfunction, and
Figure 13 A & B homonymous hemianopsia
!" Mean age 46 years
CPP. Axial T2 and sagittal T1 with contrast images !" Chordoma-like histology
demonstrate a large cystic and solid lesion with !"Cell of origin unknown
surrounding vasogenic edema. On histologic analysis,
this was shown to be a CPP.

Chordoid Glioma [Figure 15]
!" CT: well-circumscribed, hyperdense,
Figure 17
enhance
!" MRI: isointense to gray matter on T1,
Intra-
avidly enhance, slightly hyperintense on ventricular
T2 cranio-
pharyngioma.
Sagittal
T1-WI
demonstrates
a lesion
involving
the third
ventricle and
extending
superiorly into the lateral. The suprasellar cistern is not
involved.
Metastasis
Figure 15 A & B !" 0.9%-4.6% of cerebral metastases
Chordoid glioma. Sagittal T1-WI with contrast reveals
!" Most common in adults: renal and lung
a well-circumscribed avidly enhancing lesion in the !" Most common in children: neuroblastoma,
region of the third ventricle and hypothalamus. On Wilms, retinoblastoma
T2-weighted imaging the lesion demonstrates mild !" Lateral ventricle > third > fourth
hyperintensity.
Renal Cell Metastasis
!" Can produce solitary metastatis up to 50
years after detection of primary
Craniopharyngioma [Figure 16]
!" Purely intraventricular rare Colon Adenocarcinoma [Figure 18]
!"0.7%-11% of all craniopharyngiomas
!" Floor of the third ventricle intact Figure 18 A & B
!" Arise from squamous epithelial rests –
remnants of Rathke pouch Metastatic
!"Delayed development of pial colon
membrane allows Rathke pouch adenocarcinoma.
cells to come in contact with Axial T1
neuroectoderm of developing cerebral postcontrast
image reveals
vesicle multiple
Figure 16 enhancing
lesions lining
Intraventricular the ventricles.
cranio- Photograph
pharyngioma. of the gross
Photograph specimen
of the gross demonstrates
specimen the extent of
reveals that the ventricular
lesion is entirely involvement.
within the third
ventricle and
3?"3)3?')0,,+)
of the third
ventricle is
intact.
Intraventricular Craniopharyngioma
[Figure 17]
!" Normal suprasellar cistern and pituitary
stalk
!" Absence of sellar abnormality
!" C3&2$823)$"/(+3+'($/($/)+35'/)+$2,&3+(
variety
!" Variable imaging due degree of solid/
cystic component

Epidermoid Dermoid [Figure 20]
!" Congenital inclusion cyst !" CT: cystic mass, lipid hypodense
!" Squamous epithelium - only ectoderm !" MRI: T1 hyperintense areas, T2
!" 17% occur in fourth ventricle heterogeneous, possible thin rim
!" Located off midline peripheral enhancment
!" Most asymptomatic
!" If rupture $ chemical meningitis
Epidermoid [Figure 19] Figure 20 A & B

!" CT: hypodense
!" MRI: T1 hypointense, T2 hyperintense, Dermoid: Axial
DWI hyperintense, does not completely T2-WI reveals a
suppress on FLAIR, no enhancement heterogeneous
intraventricular
."44)G%3?)&-')
curvilinear
hypointense
elements that
correspond to
the hair that is
seen in the gross
specimen.
Figure 19 A, B,
C&D
Epidermoid.
Sagittal T1
postcontrast
demonstrates a
nonenhancing
lesion in the
fourth ventricle
with a similar
signal intensity
to CSF. On
T2-W imaging
the lesion is
hyperintense Intraventricular Cysts [Figure 21]
similar to CSF. !" Colloid cyst
Axial diffusion !" Neurocysticercosis
weighted image
demonstrates !" Choroid plexus cyst
high signal !" Ependymal cyst
within the
lesion. Intra-
operative
photograph Figure 21
shows a pearly,
$"1#%0,G'+2#%M') Neuro-
mass in the cysticercosis.
fourth ventricle. Axial
noncontrast CT
demonstrates
a cystic lesion
Dermoid within the right
!" Congenital ectodermal inclusion cyst ventricle. A
!" Squamous epithelium + dermal adnexa – linear structure
only ectoderm consistent
!" Increase in size by glandular secretion with the larvae
projects from
and epithelial desquamation the anterior
!" Extremely rare aspect of the
!" Tend to occur in midline cyst.
!" Complications:
!"Rupture $ chemical meningitis
!"Malignant transformation $ SCC

Colloid Cyst Neurocysticercosis
!" Wedge into foramen of Monro !" Systemic illness caused by dissemination
!" Embryonic endoderm of pork tapeworm Taenia solium
!" Age: third-fourth decade !"Rare in US
!"Rare in children !" Dead larvae incite foreign body reaction
!" Headache most common symptom 3/0(.3A(+'#,&)($/(23&2$823)$"/
!" Hydrocephalus: variable !" May involve spine and result in cord
compression
Colloid Cyst [Figure 23]
!" Benign, mucous-containing cyst Summary
!" Foramen of Monro !" Lateral ventricle
!" Density correlates with hydration state !"Anterior half
!"2/3 hyperdense #" Subependymoma: older male
!" Size variable #" Central neurocytoma: 20’s
!" Rarely has rim enhancement #" Subependymal giant cell
!" Rarely hemorrhage astrocytoma: TS
!" C3&2$823)$"/(+3+' #" Ependymoma: young
!" Complication $ sudden acute !"Posterior half
hydrocephalus #" CPP/CPC: infant and young
#" Meningioma: middle age female
#" Metastasis: primary cancer
!" Third ventricle
!"Colloid cysts (foramen of Monro)
Figure 23
!"Craniopharyngioma
!"Others less common
Colloid cyst. !" Fourth ventricle
Axial noncontrast !"Ependymoma
CT reveals a
hyperattenuating
!"Subependymoma
lesion at the !"Choroid plexus papilloma
foramen of
Monro.

References
1. Koeller KK, Sandberg GD. From the Archives of the AFIP: Cerebral intraventricular neoplasms: radiologic-
2. Hoeffel C, et al. MR manifestations of subependymomas. Am J Neuroradiol 1995;16:2121-9.
3. Tomura N. et al. Central neurocytoma with clinically malignant behavior. Am J Neuroradiol 1996;18:1175-
8.
4. Osborn AG, Preece MT. Intracranial cysts: radiologic-pathologic correlation and imaging approach.
Radiology 2006;239:651-664.
5. Osborn AG. Choroid plexus cyst. In: Diagnostic imaging: brain. Salt Lake City, Utah, Amirsys 2004;1-7-
30.
6. Pollock BE, Schreiner SA, Huston J 3rd. A theory on the natural history of colloid cysts in the third
ventricle. Neurosurgery 2000;46:1077-81.
7. Furie DM, Provenzale JM. Supratentorial ependymomas and subependymomas: CT and MR appearance. J
Comput Assist Tomogr 1995;19:518-26.
8. Spoto GP, Press GA, Hesselink JR, et al. Intracranial ependymoma and subependymoma: MR
manifestations. Am J Roentgenol 1990;154:837-45.
9. Pollack IF, Gerszten PC, Martinez AJ, et al. Intracranial ependymomas of childhood: long-term outcome
and prognostic factors. Neurosurgery 1995;37:655-66.
10. Hoeffel C, Boukobza M, Polivka M, et al. MR manifestations of subependymomas. Am J Neuroradiol Nov
1995;16:2121-9.
11. Baron Y, Barkovich AJ. MR imaging of tuberous sclerosis in neonates and young infants. Am J Neuroradiol
May 1999;20:907-16.
12. Braffman BH, Bilaniuk LT, Naidich TP, et al. MR imaging of tuberous sclerosis: pathogenesis of this
phakomatosis, use of gadopentetate dimeglumine, and literature review. Radiology 1992;183:227-38.
13. Anderson DR, Falcone S, Bruce JH, et al. Radiologic-pathologic correlation. Congenital choroid plexus
papillomas. Am J Neuroradiol Nov 1995;16:2072-6.
14. Berger C, Thiesse P, Lellouch-Tbiana A, et al. Choroid plexus carcinomas in childhood: clinical features and
prognostic factors. Neurosurgery 1998;42:470-5.
15. Pomper MG , Passe TJ, Burger PC, et al. Chordoid Glioma: A Neoplasm Unique to the Hypothalamus and
Anterior Third Ventricle. Am J Neuroradiol Mar 2001;22:464-9.
16. Behari S, Baneji D, Mishra A, et al. Intrinsic third ventricular craniopharyngiomas: report on six cases and
a review of the literature. Surg Neurol 2003 Sep;60(3):245-52.

1160
Vascular Malformations of the Brain
Vascular Malformations
!" Arteriovenous malformation (AVM)
Figure 2
!"Classic
!"7,+3&(3+)'+$"5'/",#(8#),&3(H0@_:J Classic AVM.
!"Vein of Galen malformation (VOG) H and E
!" Developmental venous anomaly (DVA) stain of the
nidus of an
!" Cavernous malformation arteriovenous
!" Capillary telangiectasia malformation.
!" Mixed malformation = combo The vessel
walls are
Classic AVM [Figures 1 to 3] thickened
!" Arteriovenous shunting and no intervening (arrow)
and brain
capillary bed parenchyma
!"Enlarged feeding artery lies between
!"Nidus the vessels
!"Early draining vein/varix of the nidus
(star).
!" Congenital
!"Usually neural tissue in between
!" Occur anywhere in brain or spinal cord
!" 98% solitary
!"Multiple AVMs usually syndromic:
#" Hereditary hemorrhagic
telangiectasia (HHT)
#" Cerebro facial arteriovenous
metameric syndromes (CAMS)
Figure 3
A&B
Classic AVM.
Axial T2-WI
demonstrates
numerous
0,G):,%(4)
in the right
hemisphere.
Note the right
hemisphere is
not enlarged
despite the
large AVM.
The gross
specimen
demonstrates
volume loss
involving
the right
hemisphere.
Figure 1
Classic AVM. Catheter angiogram reveals an enlarged

feeding artery (internal carotid), a well-formed nidus,
and an early draining vein. HHT
!" > 3 concurrent cerebral AVMs – rare
!" An angiodysplastic disorder with AD
inheritance
Vascular Malformations of the Brain Neuroradiology

1161
AVM AVM I*'-,.-7+Conventional
!" Dysregulated angiogenesis ! continued Angiography
vascular remodeling !" Best method of imaging
!" Peak age: 20-40 years old !" Must image ICA, ECA, and vertebral
!" Risk of hemorrhage: 2%-4%/year circulations
!"~50% present with symptoms of !"27%-32% of AVMs have dual arterial
hemorrhage supply
AVM G%'5,.-7+Spetzler-Martin Scale LME7+Associated Abnormalities

!" Size !" Flow-related aneurysm on feeding artery:
!"Small (< 3 cm) = 1 10%-15%
!"Medium (3-6 cm) = 2 !" Intranidal aneurysm: > 50%
!"Large (> 6 cm) = 3 !" Vascular “steal:” Ischemia in adjacent
!" Location brain
!"Noneloquent = 0
!"Eloquent = 1 Increased Risk of Hemorrhage
!" Venous drainage !" Location
!"G,!'+82$3&(g(> !"Periventricular
!"Deep = 1 !"Basal ganglia
!"Thalamus
AVM I*'-,.-7+4J !" Arterial
!" Variable hemorrhage !"Pedicle aneurysm
!" C3&2$823)$"/N(OR?W^>? !"Intranidal aneurysm
!" Enhance postcontrast #" 7$682,&)()"(0')'2)(%A(<V
!" CTA: enlarged arteries and draining veins !" Venous
AVM I*'-,.-7+EIK+++++++++[Figure 4] !"Central venous drainage
!" Flow voids: “bag of worms” !"F%#)+,2)$"/("6(5'/",#(",)4"I
!" Variable hemorrhage !"Varix
!"“Blooming” on T2* GRE !" Small nidus
!" T2: increased signal ! gliosis
LME7+Treatment
!" Contrast: strong enhancement
!" Combination
!" MRA/MRV
!"Embolization
!"Radiation: stereotaxic radiosurgery
#" Eloquent
!"Surgery
Arteriovenous Fistulas No tiene nido a diferencia de la MAV

!" Distinguished from AVMs by presence of
0$+'2)1(*$-*(4"I(8#),&3(%')I''/(3+)'+A(
and vein
Figure 4 !"Dural AVF (dAVF)
A&B !"C35'+/",#(23+")$0(8#),&3(HCC:J
!"Vein of Galen malformation
CAMS.
Sagittal T1
and axial T2 dAVF [Figure 5]
FLAIR images !" Arteriovenous shunts within dura
demonstrate !" 10%-15% of intracranial vascular
a large malformations
arteriovenous
malformation !" 2 types:
involving !"Adult: tiny vessels in wall of
the entire thrombosed dural venous sinus
left cerebral $ typically middle-aged and older
hemisphere patients
and the scalp.
#" Usually acquired – trauma
!"K/63/)$&'N(.,&)$!&'(*$-*W4"I(@_W#*,/)#(
involving several thrombosed dural
sinuses
Vascular Malformations of the Brain 1162 Neuroradiology

Figure 6
dAVF.
Coronal T1
postcontrast
MR reveals
multiple
“corkscrew”
vessels in the
right cerebral
hemisphere.
5LMN7+Conventional Angiography
[Figure 7]
!" Multiple arterial feeders
!"Dural/transosseous branches from
ECA: most common
!"Tentorial/dural branches from ICA or
Figure 5
VA
dAVF. Axial single shot fast spin echo of a fetal brain !" Involved dural sinus frequently
reveals a large subdural hematoma in the posterior thrombosed
fossa that resulted from a dAVF. !" Flow reversal in dural sinus/cortical
veins $ progressive symptoms, risk of
hemorrhage
dAVF G%'5,.-7+Cognard C&'((,#/'),".
!" Tortuous engorged pial veins $
!" Type I: in sinus wall, normal antegrade
“pseudophlebitic pattern”
venous drainage
!" Type II: in main sinus
!"@N(+'4,L($/)"(#$/,#
!"9N(+'4,L($/)"(2"+)$23&(5'$/#N(Z>?WO>?(
hemorrhage
!" Type III: direct cortical drainage
!"40% hemorrhage
!" Type IV: direct cortical drainage and
venous ectasia
!"2/3 hemorrhage
!" Type V: spinal perimedullary venous
drainage
!"Progressive myelopathy
dAVF Figure 7
!" Most common near skull base A, B & C
!"Transverse sinus most common
dAVF:
!" Hemorrhage incidence: 2%-4% per year
Axial contrast
!" Spontaneous closure rare enhanced
!"Most are type I CT reveals
multiple
dAVF I*'-,.-7+4J++++ small veins.
!" NECT: may be normal Catheter
angiogram
!" CECT: may see tortuous dural feeders and reveals a direct
enlarged dural sinus communication
from a fetal
dAVF I*'-,.-7+EIK++++++[Figure 6] origin posterior
!" Flow voids around dural venous sinus communicating
!" Thrombosed sinus artery to the
transverse
!" Dilated cortical veins without parenchymal sinus in the
nidus arterial phase.
!" T2: focal hyperintensity in adjacent brain Late venous
!" MRA: may be negative phase reveals multiple engorged pial referred to as
the pseudophlebitic pattern.
!" <V_N("22&,0'0(#$/,#1(2"&&3)'+3&(4"I

Carotid Cavernous Fistula (CCF) 5LMN7+Treatment
!" dAVF second most common site !" Endovascular
!" Abnormal communication between carotid !" Surgical resection
artery and cavernous sinus !" Stereotaxic radiosurgery
!"Enlarges cavernous sinus !" Observation:
!"Usually see enlarged superior !"Indirect CCF
ophthalmic vein
#" CCF may be contralateral to dilated Vein of Galen Malformation (VOGM)
SOV !" @+)'+$"5'/",#(8#),&3($/5"&5$/-(3/',+A#.3&(
!" C&3##$8'0(%A(3+)'+$3&(#,!!&A(3/0(5'/",#( dilatation of median prosencephalic vein
drainage (Barrow): (MPV)
!"A: Direct ICA-cavernous sinus high- !" Neonatal > infant presentation
4"I(#*,/) !"Rare adult presentation
!"B: Dural ICA branches-cavernous !" C&3##$823)$"/N
shunt !"Choroidal: multiple feeders
!"C: Dural ECA-cavernous shunt from pericallosal, choroidal, and
!"D: ECA/ICA dural branches shunt to thalamoperforating arteries
cavernous sinus !"Mural: few feeders from collicular or
posterior choroidal arteries
44N7+Imaging [Figures 8 & 9] !" Falcine sinus drains the MPV in 50% of
!" CT: cases
!"Marked dilation and enhancement of
cavernous sinus VOGM [Figure 10]
!"May see prominent SOV !" Newborns: Most common extracardiac
!" MRI: cause of high-output congestive heart
!"@%/"+.3&(4"I(5"$0#($/(235'+/",#( failure
sinus !" < 1% of cerebral vascular malformations
!"Enlargement of cavernous sinus
Figure 8
CCF.Axial
noncontrast
CT
demonstrates
proptosis
of the right
eye. There is
asymmetry of
the cavernous
sinus with
widening on
the right.
Figure 10 A & B
VOGM.
Chest x-ray
Figure 9 demonstrates
a markedly
CCF. Axial enlarged cardiac
T1-WI silhouette due
demonstrates to congestive
multiple heart failure.
0,G):,%(4) Axial contrast
in the right CT reveals
cavernous the enlarged
sinus. and enhancing
venous pouch
parenchymal
volume loss is
also present.

Figure 11
Cavernous
malformation.
Photograph
of a resected
specimen
demonstrates
multiple
cavernous
spaces.
Figure 10C
Atrophy is also
demonstrated on the gross image. The enlarged Cavernous M'&3"%*'),".7+Imaging
venous pouch is annotated by the arrow. [Figure 12]
!" Little or no mass effect
VOPE7+4J+Findings !"Unless complicated by hemorrhage
!" Venous pouch
!" May have internal areas of thrombosis or
!" May have hydrocephalus
hemorrhage
!" Parenchymal atrophy
!"Peripheral hemosiderin causes T2
!" Intraventricular hemorrhage: rare
shortening resulting in a black “halo”
!" Postcontrast: avid enhancement of
around the lesion
feeding arteries and vein
VOPE7+EI+Imaging Figure 12
!" Flow voids
!" T1 hyperintensity Cavernous
!"In pouch $ thrombus malformation.
!"In brain $($#2*'.$31(23&2$823)$"/ Axial T2-WI
demonstrates
!" DWI: restricted diffusion if acute
a cavernous
infarction malformation
in the anterior
VOPE7+Angiography right temporal
!" Choroidal or mural lobe. There
!" Dural venous sinus anomalies is a low
signal “halo”
!"Falcine sinus in 50% surrounding
!"+/- absence or stenosis of other the lesion.
sinuses
VOPE7+Treatment
!" Choroidal Cavernous Malformation
!"Medical therapy for congestive heart !" CT Findings
failure until 5 or 6 months !"Negative: 30%-50%
!"5-6 months: transcatheter !"40%-60% Ca++
embolization !"No mass effect
!" Mural !"Surrounding brain normal
!"Transcatheter embolization performed !"Little or no enhancement
later !"CTA usually negative
POP CORN Cavernous Malformation [Figure 11] Cavernous Malformation
!" AKA: angioma, cavernoma, cavernous !" MRI
hemangioma !"Variable
!" Variable size intercapillary vascular !"”Popcorn ball”
spaces, sinusoids, and larger cavernous !"Surrounding edema in acute
spaces hemorrhage
!"No intervening brain !"Postcontrast: minimal/no enhance $
!"2 types: look for DVA
#" Inherited: multiple and bilateral !"Angiography: usually occult
#" Sporadic
Cavernous Malformation [Figure 13]
!" Risk of hemorrhage: 0.25%-0.7%/year
!"More common in posterior fossa
lesions
!"In patients with prior hemorrhage
annual rate of rehemorrhage $ 4.5%
!" Treatment:
!"Observation: asymptomatic or
inaccessible lesions
!"Surgical excision
!"Radiosurgery: progressively
symptomatic but surgically
Figure 15 A & B
inaccessible
DVA. Axial T1-WI reveals a DVA in the left frontal
region. On a more inferior slice an associated
Figure 13 cavernous malformation is present.
Cavernous DVA I*'-,.-7+4J
malformation. !" C3&2$823)$"/(3/0($#2*'.$3(.3A("22,+($/(
Axial T2-WI of
a cavernous the region drained $ most likely due to
malformation chronic venous obstructive disease
with an acute !"Rare
hemorrhage
reveals a DVA I*'-,.-7+EIK+
“popcorn-like”
!" Surrounding T2 hyperintensity
lesion involving
the right frontal !"May occur in asymptomatic
lobe. There is !"Acute edema from thrombosis
a small rim of !"\&$"#$#(6+".(2*+"/$2(",)4"I(
edema. The obstruction
lesion results in
mass effect on
the foramen of @ML7+Treatment
Monro causing !" None
hydrocephalus. !"Removal may cause venous infarction
Capillary Telangiectasia [Figure 16]

CABEZA DE Developmental Venous Anomaly (DVA) !" Dilated capillaries interspersed within
MEDUSA [Figures 14 and 15]
normal brain
!" May represent anatomic variant !" Usually small, asymptomatic incidental
!"Seen in up to 3% of autopsies 8/0$/-#
!" Enlarged medullary veins !"Rare reports of hemorrhage exist
!" Drain into dural sinus or deep ependymal !" Most located in brainstem ! pons
vein
!" Usually solitary
!" “Medusa head” or “palm tree”
!" Isolated or associated with cavernous
angioma
!" Hemorrhage unusual
Figure 14
DVA. Venous
phase from
a catheter
angiogram
reveals a large
anterior DVA
with the classic
“palm tree”
appearance.
The anterior
portion of the
Figure 16
sagittal sinus is
aplastic. Capillary telangiectasia. Photograph of a gross
specimen reveals a capillary telangiectasia located
centrally within the pons.
Capillary Telangiectasia [Figure 17]
!" T2: increased signal
!" T2*: low signal
!" K&&W0'8/'0('/*3/2'.'/)(36)'+(2"/)+3#)(
administration: stippled
!" Occult on angiography
!" Treatment: none
Figure 18C
Figure 17 A & B Sinus Pericranii

Capillary telangiectasia: Axial T1 postcontrast image !" Spontaneous regression rare
reveals an area of stippled enhancement located !" Risk of hemorrhage
centrally within the pons. On axial T2-weighted !" Treatment
imaging, a focus of high signal is present centrally
within the pons. !"Surgery
!"Endovascular
Vascular Malformations
Sinus Pericranii !" Arteriovenous malformation (AVM)
!" Communication between extracranial !"Classic
venous system and dural venous sinus !"7,+3&(3+)'+$"5'/",#(8#),&3(H0@_:J
!" Rare !"Vein of Galen malformation (VOG)
!" May be congenital or acquired !" Developmental venous anomaly (DVA)
!" Cavernous malformation
Sinus Pericranii [Figure 18] !" Capillary telangiectasia
!" CT: single/multiple bone defects
!" Vascular enhancement
!" Conventional angiogram: seen during
venous phase
Figure 18 A & B
Sinus pericranii.
Axial CT in bone algorithm reveals small defects
within the calvarium and there is a prominence of the
soft tissue posteriorly at this level. The postcontrast
image reveals the associated vascular structures.
Catheter angiogram demonstrates the communication
between the sagittal sinus and the extracranial veins.

References
1. Chappell PM, Steinberg GK, Marks MP. Clinically documented hemorrhage in cerebral arteriovenous
malformations: MR characteristics. Radiology 1992;183:719.
2. Marks MP, Lane B, Steinberg GK, Chang PJ. Hemorrhage in intracerebral arteriovenous malformations:
angiographic determinants. Radiology 1990;176:807.
3. Marks MP, Lane B, Steinberg GK, Snipes GJ. Intranidal aneurysms in cerebral arteriovenous
malformations: evaluation and endovascular treatment. Radiology 1992;183:355.
4. Meder JF, Oppenheim C, Blustajn J, et al. Cerebral arteriovenous malformations: the value of radiologic
parameters in predicting response to radiosurgery. Am J Neuroradiol Sep 1997;18:1473-83.
5. Putman CM, Chaloupka JC, Fulbright RK, et al. Exceptional multiplicity of cerebral arteriovenous
malformations associated with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome). Am
J Neuroradiol Oct 1996;17:1733-42.
6. ;,2$3/(@$1(k",03+)(U1(<",/3A'+(C1(')(3&T(G!"/)3/'",#(2&"#,+'("6(0,+3&(3+)'+$"5'/",#(8#),&3#N(+'!"+)("6(
three cases and review of the literature Am J Neuroradiol May 2001;22:992-6.
7. SI"/(9X1(k3/(<k1(S3/-(k1(C*3/-(ST(<V($.3-$/-(8/0$/-#("6($/)+32+3/$3&(0,+3&(3+)'+$"5'/",#(8#),&3#N(
relations with venous drainage patterns. Am J Neuroradiol Nov 2005;26:2500-7.
8. ;''(G1(b$&&$/#DA(V@1(<"/)3/'+3(b1()'+9+,--'(S\T(<V($.3-$/-("6(0,+3&(3+)'+$"5'/",#(8#),&3#(0+3$/$/-($/)"(
cerebellar cortical veins. Am J Neuroradiol Sep 2003;24:1602-6.
9. Willinsky R, Goya M, terBrugge K, Montanera W. Tortuous. Engorged pial veins in intracranial dural
3+)'+$"5'/",#(8#),&3#N(2"++'&3)$"/#(I$)*(!+'#'/)3)$"/1(&"23)$"/1(3/0(<V(8/0$/-#($/(ZOO(!3)$'/)#T(@.(X(
Neuroradiol Jun 1999;20:1031-6.
10. Dillon WP. Cryptic vascular malformations: controversies in terminology, diagnosis, pathophysiology, and
treatment. Am J Neuroradiol Nov 1997;18:1839-46.
11. Vilanova JC, Barcelo J, Smirniotopoulos JG, et al. Hemangioma from head to toe: MR imaging with
12. S$A"#,'(k1(k"+$(o1(FD3*3+3(<1(')(3&T(B+'3).'/)("6($/)+32+3/$3&(0,+3&(3+)'+$"5'/",#(8#),&3#N(2,++'/)(
strategies based on location and hemodynamics, and alternative techniques of transcatheter
embolization. RadioGraphics 2004;24:1637-53.
13. Carpenter JS, Rosen CL, Bailes JE, Gailloud P. G$/,#(`'+$2+3/$$T(C&$/$23&(3/0($.3-$/-(8/0$/-#($/()I"(23#'#(
of spontaneous partial thrombosis. Am J Neuroradiol Jan 2004;25:121-5.
14. <"+"/(:U1(S&,2f/$D(V`1(<3I30(<U1(G)+")*'+(C<T(U/0"53#2,&3+()+'3).'/)("6(*$-*W4"I(23+")$0(235'+/",#(
8#),&3#(%A(#)'/)W3##$#)'0(2"$&(!&32'.'/)T(@.(X(E',+"+30$"&(X,/(O>>RYO[NZ^==W]>](
15. \".'f(:1(U#2"%3+(b1(\".'f(@<1(')(3&T(B+'3).'/)("6(23+")$0(235'+/",#(8#),&3#(,#$/-(2"5'+'0(#)'/)#N(
midterm results in seven patients. Am J Neuroradiol Oct 2007;28:1762-8.
16. Chen CC, Chang PC, Shy C, et al. CT Angiography and MR angiography in the evaluation of carotid
235'+/",#(#$/,#(8#),&3(!+$"+()"('.%"&$f3)$"/N(3(2".!3+$#"/("6()'2*/$l,'#T(@.(X(E',+"+30$"&(F2)(
2005;26:2349-56
17. Wilms G, Bleus E, Demaerel P, et al. Simultaneous occurrence of developmental venous anomalies and
cavernous angiomas. Am J Neuroradiol Aug 1994;15:1247-54.
18. Lee C, Pennington MA, Kenney CM, 3rd. MR evaluation of developmental venous anomalies: medullary
venous anatomy of venous angiomas. Am J Neuroradiol Jan 1996;17:61-70.
19. Brunereau L, Labauge P, Tournier-Lasserve E, et al. Familial form of intracranial cavernous angioma: MR
$.3-$/-(8/0$/-#($/(RZ(63.$&$'#T(V30$"&"-A(O>>>YOZ]NO>=T(

Cerebral Ischemia and Infarction
Ischemia/Infarction Imaging F,.5,.-(7+4J++++++[Figure 1]

!" Role of imaging in infarction !" 1-7 days
!"C"/8+.(0$3-/"#$#(3/0(+,&'(",)(.$.$2# !"Mass effect
!"Complications !" Contrast enhancement
#" Hemorrhage !"Rule of 3’s: starts 3 days, peaks 3
#" Herniation weeks, gone 3 months
!"Location !" Weeks to years
!"Size !"Atrophy
!"Acuity
!"Etiology
I(/?1*,'7+Radiologic Workup
!" CT:
!"CTA
!"CT perfusion Figure 1
!" MR
!"MRA T1-WI
demonstrates
!"MR perfusion an infarction
!" Carotid US of the right
!" Conventional angiography basal ganglia
with ring
Perfusion Imaging enhancement.
!" C'+'%+3&(%&""0(4"I(HC9:JN(5"&,.'("6(
%&""0(4"Id,/$)("6(%+3$/()$##,'d.$/,)'
!" Cerebral blood volume (CBV): volume of
blood/unit of brain tissue
!" Mean transit time (MTT): time difference
%')I''/(3+)'+$3&($/4"I(3/0(5'/",#(
",)4"I
Imaging F,.5,.-(7+EI
!" Increased signal T2
!" Decreased signal T1
!" @%#'/)(4"I(5"$0
!" Gradient: hemorrhage, clot in vessel
!" DWI positive within 30 minutes
DWI ADC
0-6h Bright Low
6h-4d Bright Low
7-14d T2 shine through Pseudonormalize
Chronic T2 shine through High
Perfusion
Ischemia Differential D,'-."(,(7+Reduced

!" Can divide into three compartments Diffusion
!"Infarct core !" Highly cellular tumors
!"Penumbra !" Demyelinating lesions
!"Oligemic region !" Extracellular methemoglobin
!" Creutzfeldt Jakob
Imaging F,.5,.-(7+4J !" Abscess
!" 0-24 hours !" Epidermoid
!"Sulcal effacement !" Herpes encephalitis
!"Hyperdense artery
!"Loss of gray-white differentiation
#" Middle cerebral artery (MCA):
insular ribbon, basal ganglia
Cerebral Ischemia and Infarction 1169 Neuroradiology

Gross Pathologic Changes [Figure 2]
!" Day 0-2 (acute) – appears normal
!" Day 2-10 (subacute) – swelling and
softening
!" Chronic – encephalomalacia and cystic
change
Figure 2
Gross photograph
of a brain with
both subacute and
chronic infarction.
The right Figure 3 A & B Top of the basilar
middle cerebral
artery territory “Top of the basilar” syndrome. Diffusion-weighted
demonstrates imaging reveals (A) infarction of the midbrain, bilateral
swelling with occipital lobes, bilateral medial temporal lobes, and (B)
associated midline bilateral thalami.
shift. The left
middle cerebral
artery territory
reveals a chronic
infarct with Watershed Infarction [Figure 4]
encephalomalacia !" Occur at junction between larger arterial
and cystic change. territories
!" Pathogenesis
!"Carotid stenosis or occlusion
!"Systemic hypotension
Middle Cerebral Artery !"Embolic events
!" 7'82$) !" More commonly hemorrhage
!"Face and arm weakness !" Commonly enhance earlier than
!"Aphasia: motor (anterior), receptive thromboembolic
(posterior)
!" Location
!"Lateral areas of frontal, temporal,
and parietal lobes, and lateral Figure 4
lenticulostriate
Watershed
infarction:
Anterior Cerebral Artery Axial
!" 7'82$) diffusion-
!"Leg weakness weighted
!" Location image
!"Medial frontal and parietal lobes, and reveals foci
of reduced
medial lenticulostriate diffusion
(“string of
Posterior Cerebral Artery pearls”)
!" 7'82$) between
!"Distal (beyond P1) the anterior
#" Unilateral: hemianopsia and middle
cerebral
#" Bilateral: cortical blindness, artery
memory loss territories.
!" Location
!"Occipital and medial and temporal lobe
Posterior Cerebral Artery [Figure 3]

Cerebellar Infarction
!" Proximal (‘top of the basilar’) !" Less than 5%
!"B*3&3.$2(#'/#"+A(0'82$)#(3/0(!3$/( !" Male predominance
syndromes !" Mean age 65
!"Impaired arousal !" Signs: Posterior headache, dysarthria,
!"Midbrain pupils severe vertigo, nausea, vomiting,
!"Extra-ocular muscle palsies unsteady gait, nystagmus
!" Risk of herniation – potential surgical
emergency

stroke en paciente joven: Simpre pensar en disección.
Etiologies of Decreased Perfusion
!" Arterial
!"Embolic
!"Thrombus
!"Vasospasm
!" Venous
!"Thrombus
!"Stenosis
!" Hypoperfusion
!"Decreased cardiac output
!"Shock
!"Decreased circulating volume
Ischemic Cerebrovascular Disease

!" 5 major subtypes*
!"Large artery Figure 5
!"Cardioembolic
Fungal stain reveals Aspergillus hyphae invading the
!"Small vessel/lacunar wall of an artery.
!"Other known etiology
!"Etiology unknown
*Trial of the Drug Org 10172 in Acute Stroke
Treatment (TOAST). HIV [Figure 6]
!" Vascular complications: 1.3%
Large Artery
!"Arteritis with development of fusiform
!" Thrombosis at site or plaque or emboli
aneurysms
from plaque
!"Arterial sclerosis with vascular
!" Carotid bifurcation – most common site
occlusion
for plaque formation
!" Etiologies other than atherosclerosis:
!"Vasculopathy
!"Dissection
!"Hypercoagulable states
Atherosclerotic Plaque
!" Slowly develop Figure 6
!" Located at arterial bifurcation
Photograph
!" Composition of the circle
!"Transformed smooth muscle cells of Willis
!"Collagen from a
!"Macrophages and lymphocytes patient with
!"Central necrotic core (cholesterol HIV. Areas
of fusiform
crystals) aneurysm
!"Intact endothelial layer formation
as well as
I.Q'**')"%!+4RS+Vasculitides sclerosis are
[Figure 5] present.
!" Non-infectious
!"Drugs
!"Primary angiitis of the central nervous
system (PACNS)
!"Immune-related diseases
!"Giant cell arteritis
!" Infectious
!"Bacterial Arterial Dissection [Figure 7]
!"Viral !" Consider in young adult with infarction
!"Fungal !" Can result from relatively minimal trauma
– sneezing, chiropractic manipulation
!" Fibromuscular dysplasia and collagen
vascular diseases predispose

Figure 7
Figure 9
Arterial
dissection. Lacunar
Axial T1- infarcts.
WI with fat Photograph
saturation of a gross
reveals specimen
high signal reveals
intensity lacunar
intramural infarcts in
hematoma the bilateral
within the basal
wall of the ganglia.
right internal
carotid
artery.
Small Vessel or Lacunar [Figure 10]
Cardioembolic !" Etiologies

!" Relative stasis !"Atherosclerotic
!"Myocardial infarction !"Infectious or noninfectious vasculitides
!"Ventricular aneurysm !"Meningitis
!"@)+$3&(8%+$&&3)$"/ !"Vasculopathies associated with
!"Cardiomyopathy collagen vascular disease
!" Valvular heart disease !"Cerebral autosomal dominant
!" Cardiac tumors arteriopathy with subcortical infarction
!" Right to left shunt and leukoencephalopathy (CADASIL)
Septic Embolism [Figure 8]

!" May lead to:
!"Cerebrovascular occlusions
!"Intracerbral abscesses
Figure 10
!"Arterial mycotic aneurysms A&B
Top Image:
Tuberculous
Figure 8 meningitis.
Photograph
Mycotic of the gross
aneurysm. specimen
Catheter reveals thick
angiogram exudate along
reveals the region of
a small the basilar
aneurysm artery.
along a
distal middle
cerebral
artery
branch.
Bottom
Image:
Small Vessel or Lacunar [Figure 9] Axial CT
!" Generally involve perforating arteries reveals
a region
!" Common locations:
of low
!"Basal ganglia attenuation
!"Internal capsule within the
!"Brainstem left aspect
!"Deep white matter of the hemispheres of the pons
consistent
!" Less than 1.5 cm with an
!" Hypertension infarct.

Differential D,'-."(,(7+Lacunar
[Figure 11]
!" Dilated Virchow-Robin spaces Figure 12
!"Most common in basal ganglia
Fat
!"Increase in size and frequency with embolism.
age Axial
!"Cryptoccocus diffusion-
weighted
image
Figure 11 A & B reveals
mutiple foci
Cryptococcus of reduced
(A) Axial T2-WI diffusion
demonstrates involving
dilated both gray
perivascular and white
spaces in the matter.
region of the LO43"+)&'#(W)
basal ganglia. pattern).
(B) Photograph
of the gross
specimen
demonstrates
the gelatinous
pseudocysts
(arrows) in the
region of the
basal ganglia.
Figure 13
Fat embolism. Cross section from a gross specimen

reveals numerous petechial hemorrhage.
CADASIL Venous Infarction [Figure 14]

!" Familial, non-amyloid microangiopathy !" Wide range of etiologies
!"Mutation of Notch 3 gene on !"Risk factors
chromosome 19 (blood test) #" Acquired: dehydration, sepsis,
!" Early onset ischemic stroke (40-50s) traumatic occlusion
!" Multi-infarct dementia #" Genetic: factor V Leiden, protein C,
!" Affects frontal lobes, temporal lobes, and protein S
insula !" GA.!)".#("6)'/(/"/W#!'2$82
!" BA!$23&&A($/5"&5'#(#,%2"+)$23&(M(8%'+# !"G,00'/(0'82$)
!"Often heralded by seizure
Fat Embolism [Figures 12 & 13]
!" Typically hemorrhage
!" Uncommon, potentially life-threatening,
complication of long bone fractures
!"Incidence: 0.9%-2.2%
!" Fat emboli pass through pulmonary
vasculature $"systemic embolization
!" Hypoxia, deteriorating mental status and
petechiae
!" CT usually negative
!" MRI: Multiple, small, scattered inc T2;
7bK(h#)3+(8'&0i

Stoke in Pediatric Population
!" Rare
!" Subtle presentation
!":"23&(/',+"&"-$2(0'82$)#(+3+'($/(
newborns
!"Seizures are more common in
newborns
!"> 50% of children diagnosed 24 hours
after presentation
!" Initial CT misses acute ischemic stroke in
40% of children
DDx Ischemia/Infarction in Childhood

[Figure 16]
Figure 14
!" Moyamoya
!" Hypercoagulable state
Venous infarction. Photograph of a cross section of a !" Sickle cell
brain from a patient with a sagittal sinus thrombosis !" Carotid or vertebral arterial dissection
reveals bilateral parasagittal hemorrhage.
!" Vasculitis
!" Mitochondrial encephalopathy with lactic
acidosis and stroke (MELAS)
Venous Infarction [Figure 15]
!" Imaging patterns:
!"May be bilateral and/or multifocal
!"Does not conform to vascular territory
!"Superior sagittal sinus $ cortical veins
$ parasagittal
!"Vein of Labbe $ temporal lobe
!"Straight sinus $ thalamostriate veins
$ thalamus
Figure 16 A & B
Moyamoya in a 17-year-old adolescent.
(A) Axial T2 FLAIR reveals an old right occipital lobe
infarction. There is increased signal within the sulci
consistent with the “ivy sign.” (B) 3D TOF imaging
demonstrates multiple prominent lenticulostriate
vessels.
Figure 15 A & B
Moyamoya
Venous infarction. !" Progressive narrowing of distal ICA
(A) Dense sinus sign. Axial non-contrast CT reveals and proximal COW with secondary
a hyperdense right transverse sinus. (B) Empty delta
4%8-/)!5):'-,8+".)('.,-43+"3'4)")&##%-8)('<'$3)%-)3?')
collateralization
sagittal sinus. !" “Puff of smoke”
!" Multiple etiologies:
!"Primary: inherited
!"Secondary: SSD, Down syndrome, TS,
Venous Infarct
connective tissue disorder
!" Reduced diffusion not constant feature
!" Much of edema is vasogenic
Mimics of Dural Sinus Thrombosis

!" Anatomic variant
!" “Giant” arachnoid granulation
!"> 1 cm
!" Hemoconcentration

Conditions Associated With Global Global Ischemic/Hypoxic I.T9%!7+Adult
Ischemic/Hypoxic Injury !" Mild to moderate $ watershed zone
!" Transient cardiac arrest !" Severe:
!" Arterial hypotension !"Deep gray
!" Strangulation !"Cortex
!" Near drowning !"Cerebellum
!" Carbon monoxide poisoning !"Hippocampi
!" Increased intracranial pressure
!" Vasospasm Multifocal Infarction
!" Systemic vasculopathy
A 9-Month-Old Child not Responding !"Hypertension, diabetes
[Figure 17] !"Vasculitis
!"Mitochondrial disease
!"CADASIL
!" Central embolic source
!"Cardiac or aortic arch emboli
Figure 17 !"Infective endocarditis
!"Fat emboli
Pseudo- !" Venous infarction
subarachnoid !" Meningitis
sign.
Global
hypoxic Complications
injury in a !" Herniation
9-month-old !" Hemorrhage
child. Axial
noncontrast Hemorrhagic Transformation
CT reveals low
attenuation
!" Hemorrhagic transformation of ischemic
of the lesion
supratentorial !"> 24 hours after onset
brain. The !" Mechanism:
cerebellum !"Reperfusion of ischemic territory
appears
higher in !"Episodes of hypertension
attenuation !"Partial occlusion of arterial lumen
(white cerebellar sign), and the vessels of the circle of !" Pathologic features
Willis appear dense (pseudosubarachnoid sign). !"Cortical petechial hemorrhages
!"Hematoma
Laminar Necrosis [Figure 18]

!" Usually seen in setting of anoxic
Global Ischemic/Hypoxic I.T9%!7+ encephalopathy
Imaging Findings !" Hyperintense T1 cortical lesions
!" Highly variable !" Mechanism unclear
!" Variety of factors impact !" Subacute or chronic phase
!"Brain maturity !" Third layer of cortex most commonly
!"Severity and duration of insult affected
!"Type of imaging studies
!"Timing of imaging
!" U3+&A($.3-$/-(8/0$/-#(23/(%'(#,%)&'
Hypoxic-Ischemic I.T9%!7+Infants
Figure 18
!" Premature:
!"Mild: caudothalamic notch, Laminar
periventricular necrosis.
!"Profound: thalamus, basal ganglia, Axial T1-WI
brainstem in an infant
with history
!" Perinatal: of non-
!"Mild: parasagittal watershed accidental
!"Profound: dorsal brainstem, trauma
ventrolateral thalamus, basal ganglia, demonstrates
high signal
hippocampi
along the
!" Infant (> 4 months): cortex
!"Mild: parasagittal watershed consistent with laminar necrosis. Parenchymal atrophy
!"Profound: basal ganglia, diffuse and bilateral subdural hematomas are present.
cortical

Wallerian Degeneration [Figure 19]
!" Secondary degeneration of axons from
cortical or subcortical injury
!" Associated with poor neurological
outcome Figure 19B
!"Presence in corticospinal tracts is
associated with persistent hemiparesis The right
cerebral
peduncle
demonstrates
volume loss
consistent
with Wallerian
Figure 19A degeneration.
Photo of
a gross
specimen
from a
patient with
a chronic @UK7+F%1BU'&&1%,'.+Degeneration
right middle !" Altered water diffusion in white matter
cerebral
tracts thought to be sequelae of MCA
territory
artery ischemia
infarction. !" Axonal injury in descending motor
pathways determinant of magnitude of
.")"+(0'82$)($/(!3)$'/)#(I$)*(#)+"D'
!" Resolves after 2 weeks
Summary
!" Role of imaging in infarction
!"C"/8+.(0$3-/"#$#(3/0(+,&'(",)(.$.$2#
!"Complications
!"Location
!"Size
!"Acuity
!"Etiology
References
1. Hess, WD. The concept of the penumbra: can it be translated to stroke management? Int J Stroke 2010
Aug;5(4):290-5.
2. Lazzaro NA, et al. Artery of Percheron infarction: imaging patterns and clinical spectrum. Am J
Neuroradiol 2010 Aug;31:1283-9.
3. Uchino A, et al. Transient detection of early wallerian degeneration on diffusion-weighted MRI after an
acute cerebrovascular accident. Neuroradiology 2004;46(3):183-8.
4. Kidwell CS, Wintermark M. The role of CT and MRI in the emergency evaluation of persons with suspected
stroke. Curr Neurol Neurosci Rep 2010 Jan;10(1):21-8.
5. Kloska, et al. Acute stroke magnetic resonance imaging: current status and future perspective.
Neuroradiology 2010;52(3):189-201.
6. Wintermark M. FDA investigates the safety of brain perfusion CT. Am J Neuroradiol 2010;31(1):2-3.
7. Ledezma CJ, et al. Modern imaging of the infarct core and the ischemic penumbra in acute stroke
patients: CT versus MRI. Expert Rev Cardiovasc Ther 2009 Apr;7(4):395-403.
8. `3+$f'&(`<1(')(3&T(U3+&A(0$3-/"#$#("6(2'+'%+3&(63)('.%"&$#.(#A/0+".'(%A(0$66,#$"/mI'$-*)'0(<VK(H#)3+8'&0(
pattern). Stroke 2001;32:2942-4.
9. Muller C, et al. The incidence, pathogenesis, diagnosis and treatment of fat embolism. Orthop Rev
1994;23:107-17.
10. k,3/-(9o1(C3#)$&&"(<T(kA!"L$2WK#2*'.$2(%+3$/($/a,+AN($.3-$/-(8/0$/-#(6+".(%$+)*()"(30,&)*""0T((

1177
1178
Neuroradiology Seminar 1
Case 1 Alexander Disease anterior

!" A 6-month-old child vomiting for 7 weeks, !" Rare, nonfamilial leukoencephalopathy
now listless !" Frontal preponderance of WM
!" Head circumference noted to be large abnormalities and macrencephaly
!" Different clinical subtypes:
!"Infantile variant (most common):
early onset macrocephaly and rapid
neurologic deterioration early death
!"Neonatal variant: even more rapidly
fatal
T1 !"Juvenile variant: macrocephaly
less consistent feature and onset of
neurologic deterioration occurs later in
childhood and is less rapid
!"Adult variant also described
!" 7$#'3#'(*3&&.3+DN(V"#'/)*3&(8%'+#(
throughout CNS
!"Intracytoplasmic proteinaceous
inclusions
Alexander D,(1'(17+Imaging Findings

!" CT:
!"Low density FWM $ PWM, internal
capsule, caudate heads
!"CE adjacent to tips of frontal horns
early
!" MR:
!"Extensive cerebral WM changes –
frontal predominance
!"Periventricular rim high T1, low T2
!"Abnormalities of basal ganglia,
T2 thalami, brainstem
!"Enhancement of certain gray and
white matter structures
!"MRS: decreased NAA, increased myo-
inositol
T1
Postcontrast
Canavan Disease. T2 prolongation throughout the
white matter.
Neuroradiology Seminar 1 1179 Neuroradiology

Canavan Disease
!" AR
!" Most common in Ashkenazi Jews
!" 7'82$'/2A($/(3#!3+)"32A&3#'
!" Macrocephaly, seizures
!" Death usually occurs in second year of life
Canavan Disease
!" Diffuse, symmetric involvement of T1
cerebral white matter
!" SC WM preferentially affected early
!" No contrast enhancement
!" MRS: elevation of NAA
T1 + GD
Canavan. MR spectroscopy demonstrates a marked

elevation in NAA.
Big-Headed K,5(7+MACrencephaly
!" M: Mucopolysaccharidosis
!" A: Alexander
!" C: Canavan
Case 2
!" 1-day-old infant – marked abnormality Congenital Neoplasms
noted on prenatal ultrasound !" Congenital cerebral tumors are extremely
!" Macrocephaly noted rare
!"0.5%-1.5% of cerebral tumors in
children
!"Teratoma most frequent: account for
50%
!"Gliomas second most common: 25%
!" Teratomas: mixed solid and cystic
component
!"When cystic component predominates,
.3A(%'(0$682,&)()"(0$#)$/-,$#*(6+".(
arachnoid cyst
!" Associated with:
!"Hydrocephalus
!"Macrocrania
!"Hydramnios
!"Vascularized tumors may result in
heart failure
T2

Case 3 Hemimegalencephaly
!" A 29-month-old child with intractable !" Pachygyria
seizures since birth !" Polymicrogyria
!" Macrocephaly noted !" Heterotopia
!" Enlarged neurons
!" Balloon cells
!" Astrogliosis of hemispheric white matter
!" If intractable seizures – surgery only if no
cortical malformation on contralateral side
Hemimegalencephaly
!" Most typical imaging appearance: cortex
dysplastic, with broad gyri, shallow sulci,
blurring of gray white junction, and
cortical thickening
Case 4
!" A 6-year-old boy presented with broad
based gait and decreased vision
!" Normal head circumference
Hemimegalencephaly
!" Hamartomatous overgrowth
!" Defects in neuronal proliferation,
migration, and organization
!" Affected portion has little or no function
!" Can be associated with cutaneous
abnormalities or ipsilateral body
hemihypertrophy

Periventricular C'&/,#/'),".(7+
Congenital
!" CMV
!" Toxoplasmosis
!" Congenital lymphocytic choriomeningitis
!" Pseudo – TORCH
!"AR
!"Progessive cerebral and cerebellar
demyelination
!"93#3&(-3/-&$3(23&2$823)$"/
!"pdW(!'+$5'/)+$2,&3+(23&2$823)$"/
Toxoplasmosis
!" Protozoan
!" 1/10 as frequent as CMV
!" C3&2$823)$"/#(#23))'+'0
!" Migrational anomalies not as common
X-Linked Adrenoleukodystrophy
!" Inherited disorder of peroxisome
metabolism
!" Males: 3-10 years old
!" Classic imaging:
!"Peritrigonal demyelination
!"Leading edge of enhancement
!"Reduced diffusion in involved white
matter
!"MRS: % NAA, & Cho/MI/Lactate
!" Rare frontal involvement
!" Death in 2-5 years without BMT
Case 5
!" 34 and 3/7 weeks gestation premature
female. Pregnancy complicated by
polyhydramnios, breech presentation.
!" Microcephaly noted
Cytomegalovirus
!" CMV: DNA virus of herpes-virus family
!" Maternal primary infection during
pregnancy or reactivation of latent
infection
!" Cerebral Ca++: 40%-70%
!"Periventricular
!" Microcephaly
!" Migrational anomalies:
!"Agyria
!"Pachygyria
!"Polymicrogyria

Neuroradiology Seminar 2
Case 1 GBM
!" A 47-year-old man with seizure !" Necrosis within tumor
!" May have intratumoral hemorrhage and
subarachnoid seeding
!" Multicentricity occurs in 4%-6% of cases
!" Frequently have large degree of
surrounding edema
!" Ring enhancement
Case 2
!" A 53-year-old woman with proptosis
lesión en mariposa que cruza por

el esplenio del cuerpo calloso
Corpus Callosum Mass Lesions

!" Neoplasm: glioblastoma (GBM),
oligodendroglioma, lymphoma
!" White matter disorders: MS, Marchiafava-
Bignami disease
!" Acute shearing injuries
!" Stroke
!" Lipoma
!" Infection: toxoplasmosis

Intraconal Masses
!" Vascular: cavernous hemangioma, varix,
lymphangioma
!" Hematoma
!" Metastasis
!" Lymphoma
!" Schwannoma
!" Optic nerve lesions: glioma, meningioma
!" Rhabdomyosarcoma
!" Orbital pseudotumor
!" Hemangiopericytoma
Cavernous Hemangioma Differential Diagnosis

!" Vascular intraconal masses
!" Diffuse dural enhancement:
!"Cavernous hemangiomas
!"Intracranial hypotension
!"Combined venous lymphatic
!"Postoperative
malformation
!"Dural metastasis (less linear)
!"Varices
!"Sarcoid (more nodular)
!"Capillary hemangioma: infants,
!" Low-lying cerebellar tonsils
usually extraconal
!"Chiari I
!" Slow onset of proptosis
!"Intracranial hypotension
!" `+'#'/)#(#'2"/0()"(86)*(0'230'
!"Tonsillar herniation
!" Smoothly marginated intraconal mass,
.3+D'0('/*3/2'.'/)1(/"(4"I(5"$0# Intracranial Hypotension
!" Brain sagging is not present in
Cavernous H1*'.-,"*'7+Imaging approximately 30% of cases
!" CT:
!" May develop subdural hematomas
!"Smoothly marginated
!" Prominence of pituitary due to venous
!"High density
dilation
!"Enhance
!" CSF studies: normal or increased protein,
!" MR:
primary lymphocytic pleocytosis – can
!"T1: Isointense
mimic aseptic meningitis
!"T2: Hyperintense
!"Enhance Intracranial H!0")1.(,".7+Etiology
!" Ruptured perineural cyst
Case 3 !" Transdural osteophyte
!" A 35-year-old woman with headache
!" Surgery
!" Lumbar drain
!" Lumbar puncture
!" Trauma
!" Connective tissue disorder: Ehlers-Danlos
syndrome, Marfan syndrome
Case 4
!" @(QWA'3+W"&0(-$+&(I$)*(5$#,3&(8'&0(&"##

Suprasellar Tumors in Children
!" Germ cell tumor
!" Craniopharyngioma
!" Astrocytoma
!" Hypothalamic hamartoma
!" Langerhan cell histiocytosis
!" Arachnoid cyst
Germinoma
!" Approximately 35% of intracranial
germinomas occur in suprasellar region
!" Most common neoplasm of pineal body
!" Suprasellar germinomas affect men and
women with equal frequency
!"Pineal: M:F = 10:1 Intraparenchymal H1*"%%?'-17+Etiology
!" Histologically similar to testicular !" Hemorrhagic infarction
seminomas and ovarian dysgerminomas !" Aneurysm
!" CSF spread not infrequent – screen the !" Hypertensive
spine !" Neoplasm
!" Trauma
Case 5 !" Cerebral amyloid angiopathy (CAA)
!" A 29-year-old postpartum woman who !" Coagulopathy
developed a severe headache !" Drugs: cocaine, meth
!" Vasculitis
!" Vascular malformation
!" Postpartum cerebral angiopathy
Sinus Thrombosis
!" Causes:
!"Hypercoagulable states
!"Pregnancy
!"Dehydration
!"Infection
!"Neoplasm
!"Blood dyscrasias
!"Trauma
!"Drugs: OCP, HRT, chemotherapeutic
agents

Sd Lemierre: Sepsis luego de una infección por
anaerobios.
Trombosis de una vena de cabeza o cuello.
Al menos 1 sitio de infección a distancia.
Teenager and young adults.
Tto: ATB.
1186
Imaging of Intracranial Infections

Summary Extra-Axial I.31/),".7+Epidural and
!" Extra-axial infections Subdural [Figure 2]
!"Epidural abscess !" Usually starts in paranasal sinuses,
!"Subdural empyema mastoids, calvarium
!"Meningitis, ependymitis !" Low density on CT
!" Parenchymal infection !" % SI T1, & SI on T2, FLAIR
!"Evolution of cerebritis to abscess !" Restricted diffusion
!"Encephalitis: HSV, CJD, ADEM !" Enhancing periphery and dura
!"AIDS-related infections !" Check for osteomyelitis of calvarium and
!"Parasitic: cysticercosis, Lyme disease sinusitis
!"Tuberculosis
!"Mycotic
Intracranial Infection [Figure 1]

!" Location
!" Intra-axial Figure 2
!"Parenchymal
!" Extra-axial Epidural
abscess
!"Epidural
on CECT
!"Subdural with typical
!"Leptomeningeal enhancing dural
!"Ependymal surface.
!" Response to infection: acute
!"Edema and swelling
!"Mass and mass effect
!"Abnormal enhancement Epidural/Subdural [Figure 3]
!" Response to infection: chronic !" Epidural
!"Atrophy !"Crosses midline
!" Subdural
!"Does not cross midline
!"K/)'+*'.$#!*'+$2(8##,+'
Figure 1 A, B & C
Left Image: Intra-axial abscess.

Middle Image: Pachymeningeal.
Right Image: Leptomeningeal infections.
Blood-Brain Barrier (BBB)

!" Tight junctions (no gaps) exist between
normal endothelial cells
!" Little communication between capillary
and extracellular space or neurons
!" Infection results in loss of tight junctions,
with increased permeability of endothelial
membranes = loss of BBB
!" Loss of BBB + increased local blood
volume = abnormal enhancement
Left Image: Epidural abscess crosses midline (arrows).
Right Image: Subdural abscess extends along
%-3'+?'.%46?'+%$)&441+')L"++,GX/
Imaging of Intracranial Infections Neuroradiology

1187
Acute Bacterial Meningitis
!" Organisms
!"Neonates: group B Streptococcus
!"Children: `"'.,6?%#14)%-01'-a"'
!"Adults: Streptococcus pneumoniae
!" Pathogenesis
!"Hematogenous seeding, choroid,
leptomeninges
!"Contiguous spread from sinusitis,
mastoiditis
!"Neonatal meningitis – maternal GU
infxn, PROM
!" Clinical
!"Headache, neck stiffness,
photophobia, cranial nerve
dysfunction, lethargy
M1.,.-,),(7+Role of Imaging
!" Is there hydrocephalus?
!"Relative contraindication to lumbar
puncture
!" Complications?
!"Hydrocephalus (especially
communicating)
!"Subdural effusions, empyema
!"Venous sinus thrombosis/infarction Figure 4 A, B, C & D
!"Arterial infarction Meningitis on FLAIR and T1 C+.
!"Vasculitis
!"Cerebritis or abscess
!"Ventriculitis/ependymitis M1.,.-,),(7+Complications [Figure 5]
!" Hydrocephalus
M1.,.-,),(7+4J+Findings !"Communicating
!" Early, CT usually normal !" Ependymitis or ventriculitis
!" Sulcal or cisternal effacement !"Ependyma never enhances normally
!" Pia/subarachnoid enhancement (BBB loss) !"Poor prognosis
!" Hydrocephalus
!" ? Source: paranasal sinus, mastoid, skull
base defect with CSF leak
Acute M1.,.-,),(7+EI+Findings
[Figure 4]
!" T1 and T2 images may be normal
!" FLAIR: best sequence
!" & SI in SAS
!" Post Gd: leptomeningeal enhancement
!" ? Hydrocephalus, infection source,
infarction? Figure 5 A & B
M1.,.-,),(7+Complications Left Image: Diffuse ependymal enhancement.

Right Image: Loculated ependymal enhancement.
!" Hydrocephalus
!"Communicating
!"K/43..3)"+A(0'%+$#(3)(3+32*/"$0(
granulations
Diffusion Weighted Imaging (DWI)
!" Powerful tool, physiologic information
!" Ependymitis/ventriculitis
!" Differentiates unrestricted from restricted
!" Infarction
free water diffusion
!"May be arterial or venous
!" “Restricted” diffusion
!"Tuberculous meningitis especially
!"Acute and subacute infarction
prone to vasospasm
!"Intracranial abscess
!"Well-demarcated: best way to
!"Creutzfeldt-Jakob disease (CJD)
differentiate from cerebritis
!"Rare acute MS plaque
!"Typical CT/MR features with restricted
!"Epidermoid (vs arachnoid cyst)
diffusion on DWI
!"Malignant neoplasms (variable)
DWI es util para evaluar si hay abseso o si hay infartos.
Neuroradiology
Imaging of Intracranial Infections 1188
M1.,.-,),(7+Complications [Figure 6] Cerebritis $ Brain Abscess
[Figure 8]
!" Early capsule
!"2-4 weeks
!"Collagenous capsule +/- daughter
abscesses
!"Necrotic core, extensive edema
!"Mass effect
!" Late capsule
!"Weeks/months
!"Rarely seen as patients are treated
earlier
!"Thick capsule
Figure 6 A & B
!"Edema, mass effect resolve
T2- and diffusion-weighted images show acute
thalamic and basal ganglia infarctions from acute
meningitis.
Figure 8
Cerebritis to Brain Abscess
!" Temporal progression from Chronic
abscess on T1
unencapsulated infection to discrete Gd. Note lack
abscess of mass effect
!" Etiology or edema.
!"Direct spread (sinus, mastoid,
odontogenic)
!"Hematogenous
!"Surgery or trauma
!"25% – no source found
Cerebritis ! Brain Abscess [Figure 7] MRI F,.5,.-(7+Abscess [Figure 9]

!" Temporal progression shown in animal !" Mass effect, edema, enhancement
model, rarely see all stages clinically !" T2-WI – % SI rim
!" Early cerebritis !" DWI/ADC
!"3-5 days after infection !"Restricted diffusion
!"Unencapsulated – white cells, edema, !" MR spectroscopy
necrosis, petechial hemorrhage !"Lactate (1.3 ppm)
!"& SI on T2, +/- enhancement !" ? Complications
!" Late cerebritis !"Herniation
!"4-14 days after infection !"Intraventricular rupture
!"Poorly delineated rim, necrotic !"Choroid plexitis
2"+'1(I*$)'(2'&&#d$/43..3)"+A(2'&&#1( !"Leptomeningitis
granulation tissue
!"& SI on T2, ++ enhancement
Figure 9 A & B
Left Image: Right frontal abscess, note low SI rim
Figure 7 A & B (arrow).
Right Image: Restricted diffusion from intraventricular
FLAIR (left image) and post-Gd (right image) of pus.
early and late cerebritis, two different patients. Note
multifocal cerebritis (arrows).
Neuroradiology
A$(/1((7+Pyogenic [Figure 10] Herpes Encephalitis [Figures 11 & 12]
!" Supratentorial is most common !" Imaging may be normal early in disease
!" Usually solitary (may have small !" Limbic system: temporal lobes, insula,
surrounding cysts) cingulate gyrus, subfrontal
!" Streptococcus, Staphylococcus !" MR > CT, especially early
!" Infants: Streptococcus, Citrobacter, !" MR
Proteus, Pseudomonas, Serratia !"Increase SI on T2 and FLAIR
!"Mass effect usually mild
!"+/- enhancement, subtle, gyral
!"60% bilateral
!"May have small punctate hemorrhages
Figure 11 A & B
Herpes encephalitis of left frontal and temporal lobes

on CECT and T2 MR.
Abscess with vasogenic edema, rim enhancement,
+'43+%$3'()(%<<14%,-),-)F^7@)$,-&+.'(),-)BF!)."6/
E./10?'&,),(7+VI.Q'**'),".+"3+)?1+
Brain”
!" Viral or bacterial
!" Usually more diffuse than cerebritis
!" May be postinfectious/immunization
!"Acute disseminated encephalomyelitis
(ADEM)
!" Viral
!"Herpes simplex virus
!"Others: measles, mumps, etc
Herpes Encephalitis [Figures 11 & 12]

!" Adults: HSV-1 (oral)
!" Neonates: HSV-2 (genital) Figure 12 A, B, C & D
!" Confusion, rapid progressing to coma
!" 50%-70% mortality, especially when Two different patients with herpes encephalitis
with high SI in temporal lobes and patchy gyral
delay enhancement.
!" to diagnosis
!" Most common cause of fatal encephalitis
!" Necrotizing hemorrhagic encephalitis,
severe
!"CSF may have RBC’s
!" Diffuse atrophy in chronic or treated stage
!" Mechanism of spread: axonal spread from
reactivation in trigeminal ganglion
Neuroradiology
CJD [Figure 13]
!" Transmissible spongiform encephalopathy
Figure 14
(TSE)
!" Microscopic: brain full of holes (“sponge”) DWI shows
!" Invariably fatal, 200 cases/year in US symmetric
!" Prion: proteinaceous infectious particle restricted
!" 3 types diffusion,
bilateral,
!"Sporadic: most common, no known in pulvinar
risk factor (85%-90%) of thalami,
!"Genetic: genetic mutation (10%-15%) caudate heads,
!"Infectious: (rare) globus pallidus,
and putamen.
Figure 13
Pathologic
AIDS-Related Conditions
specimen !" HIV encephalitis
shows typical !" Toxoplasmosis (vs lymphoma)
spongiform !" Cryptococcal meningitis
appearance. !" Progressive multifocal
leukoencephalopathy (PML)
Human Retroviruses
!" HIV (HIV-1 and HIV-2) and HTLV-1
Prion Proteins
!" HIV-1 found in CNS in AIDS
!" No RNA or DNA
(neurotrophic)
!" Normal, nonpathologic forms present
!" Encephalopathy, myelopathy, peripheral
!" 7$682,&)()"(D$&&
neuropathy
!" Very long incubation (> 40 years)
!" HIV replicates in multinucleated giant
!" Exposure to diseased neural tissue
cells and infected macrophages in CNS
!" Iatrogenic: dural graft, transplanted
!" Oligodendrocytes, astrocytes, neurons
corneas, contaminated growth hormone
less frequently directly infected
!" No case of infection from blood
transfusion 1. Subacute HIV Encephalitis AIDS
!" Normal sterilization does not eradicate
Dementia Complex (ADC) [Figure 15]
prion
!" Most common CNS complication (30%)
!" Chlorine bleach
!" Dementia, behavior changes, headache
CJD !" Virus in multinucleated giant cells (MNGC)
!" CLASSIC CJD !" CT: normal
!"Older (mean 68 years) !" MR: atrophy, periventricular white matter
!"Sporadic lesions; gray matter (late)
!"Shorter duration !" NAA/Cho and NAA/Cr ratios reduced due
!"Dementia to neuronal loss
!"“Pulvinar” sign may be present
!"Variable amounts of protease resistant
prion protein (PrPres)
!" VARIANT CJD Figure 15
!"Younger (mean 28 years)
!"BSE contaminated food Patchy frontal
symmetric
!"Longer duration abnormal
!"Behavior changes signal intensity
!"“Pulvinar” sign on MR > 75% on T2 image
!"Lots of PrPres in patient
with HIV
encephalitis.
4W@7+Imaging [Figure 14]
!" Symmetric high signal on T2 and FLAIR
!" Caudate head, basal ganglia, thalamus
(“pulvinar” sign)
!" Diffusion restriction > 2 weeks (longer
than infarction)
!" Cortical, limbic system involvement 1/3
!" Occipital lesions: 20%
!" Rapidly progressive to atrophy
Neuroradiology
2. PML [Figure 16] Toxoplasmosis
!" Opportunistic infection !" `3)*N(/'2+")$2(0'%+$#1($/43..3)"+A(2'&&#1(
!" Papovavirus (JC virus) organisms
!" Patchy nonenhancing white matter lesions !" Imaging: vasogenic edema, robust
!" Hypointense on T1 enhancement
!" No mass effect !" 15% are solitary
!" Asymmetric !" Tx: pyrimethamine + sulfa or clindamycin
!" Life-long maintenance antibiotics
!" With therapy, lesions may calcify
!" Resolution of vasogenic edema
!" New lesions or new edema develop if
medication is stopped
4. Cryptococcus Neoformans
!" Ubiquitous fungi within contaminated soil
!" Most common fungus in AIDS (6%-7%)
!" Inhaled, then hematogenous spread in
immune-compromised hosts
Figure 16 A & B !" Subacute meningitis, HA, AMS, fever
!" Dx: India ink preparation, antigen in CSF,
PML has low SI on T1 images (arrows) with no fungal culture of CSF
enhancement.
!" Path: perivascular spaces distended with
mucoid material and fungus. Lack of
endo- or exotoxins partly explains lack of
necrosis or destruction.
HIV Encephalitis vs PML
!" Tx: antifungal agents
HIV PML
!" Diffuse Asymmetric Cryptococcus Meningitis [Figure 18]
!" Central Peripheral !" Basal ganglia, often bilateral
!" T1 images normal Decrease on T1 !" CT may be normal
!" Nonenhancing Nonenhancing !" Nonenhancing low density lesions
in Virchow-Robin spaces “gelatinous
3. Toxoplasmosis [Figure 17] pseudocysts”
!" Protozoan Toxoplasma gondii !" On MR, pseudocysts are isointense to CSF
!" Soil organism !" E"(#$-/$823/)('/*3/2'.'/)('L2'!)($6(
!" Endemic in US patient treated with antiretrovirals
!" Reactivates in CNS in immune-
compromised host
!" Most common opportunistic infection
!" CD 4 < 100 cell/mm3
!" :'5'+1(k@1(/',+"&"-$2(0'82$)#1(#'$f,+'#
!" Basal ganglia, cerebral hemispheres
Figure 18 A & B
Dilated perivascular spaces in cryptococcosis. Low SI

on T1 without enhancement (right).
Figure 17 A & B
Left Image: Single large toxoplasmosis abscess with

surrounding edema and mass effect.
Right Image: Cerebritis pattern.
Neuroradiology
Highly Active Antiretroviral Tx (HLLIJC7+ CNS T9$1%/9&"(,(7+Tuberculoma
Immune Reconstitution Syndrome [Figure 20]
!" AIDS treatment regimen that includes !" Supratentorial > infratentorial
protease and reverse transcriptase !" Small or coalesced larger nodules
inhibitors !" Edema, mass effect
!" Suppresses viral replication !" Wall may have & SI on T1, % SI on T2
!" Increase in CD4 counts, decrease in viral !" Old/treated lesions often Ca+ and can be
load source for seizures
!" Increased survival
!" Ability to mount immune response may
2*3/-'($.3-$/-(8/0$/-#1('#!'2$3&&A(
enhancement patterns
!" Cryptococcal lesions may enhance
Miscellaneous Infections Figure 20

!" Tuberculosis
Multiple
!"Meningitis
tuberculous
!"Pachymeningitis abscesses on
!"Cerebritis T1 Gd.
!"Abscess “tuberculoma”
!" Neurocysticercosis
!" Lyme disease
CNS Tuberculosis
!" Granulomatous Mycobacterium
tuberculosis
!" Increasing incidence: homeless,
prisoners, immigrants (2%-5% of patients Neurocysticercosis
with pulmonary TB) !" Taenia solium (Pork tapeworm)
!" AIDS population !" Worldwide, most common CNS infection
!" Hematogenous dissemination from lungs !" Worldwide, most common cause of
!" Drug resistance increasing and ominous, epilepsy
especially in Africa !" Central/South America, East/SE Asia,
!" Multiple forms in CNS, may have more India, Africa
than one type !" CNS disease: 60%-90%
!" C$#)'+/#(8&&(I$)*(-'&3)$/",#('L,03)' !" Seizures, intracranial hypertension, focal
!" Hydrocephalus, infarctions, CN palsies 0'82$)
!" MR/CT: leptomeningeal enhancement, !" Can occur in four locations in CNS
hydrocephalus !"Parenchymal: temporal progression
!" Disease at COW: arteritis and infarctions, from vesicular to Ca++ stage
especially in children !"Intraventricular
!"Cisternal
CNS T9$1%/9&"(,(7+Cerebritis !"Spinal
[Figure 19]
Parenchymal Cysticercosis Intra-Axial
Form
!" Vesicular stage
!"Eccentric nodule (scolex), no edema
or enhancement
!" Colloidal stage
!"Dying scolex, capsule thickens,
extensive edema and enhancement
Figure 19 A, B & C !" Granular nodular stage
TB cerebritis with typical pattern of right temporal !"Cyst % in size, small enhancing
edema and enhancement. nodules, no edema
!" E"0,&3+(23&2$8'0(#)3-'
!"CA#)($/5"&,)'#1(23&2$8'#1(/"('0'.3("+(
enhancement
Neuroradiology
Parenchymal C!(),/1%/"(,(7++++++++++++++++++++++ Parenchymal C!(),/1%/"(,(7+++++++++++++
Vesicular Stage [Figure 21] Nodular C'&/,#15+Stage
!" Larva is fully grown, viable, with thin !" Ca++, no edema, no enhancement
intact capsule surrounding distended
bladder Intraventricular and Cisternal
!" Fluid in bladder is clear, no surrounding Cysticercosis [Figure 23]
$/43..3)"+A(+'32)$"/ !" 10%-20% of neurocysticercosis
!" b'&&W0'8/'0(2A#)1(#2"&'L('/*3/2'#(H.,+3&( !" Fourth ventricle: most common site
nodule) !" Basilar and sylvian cisterns
!" Wall does not enhance, no edema !" +/- hydrocephalus
!" Cyst can parallel CSF density/SI, making
$)(0$682,&)()"(0')'2)
!" Does not calcify
Figure 21
Vesicular
stage with Figure 23
larva and
eccentric Intraventricular
scolex. and cisternal
(arrows)
cysticercosis
with
hydrocephalus
on T2 image.
Parenchymal C!(),/1%/"(,(7+++++++++++++++++++++
Colloidal Stage [Figure 22]
!" ;3+53(0'-'/'+3)'#1(2A#)(4,$0(),+%$0(
!" Cyst wall thickens CNS Lyme Disease [Figure 24]
!" Vasogenic edema !" Borrelia burgdorferi, spirochete
!" Cyst wall % SI on T2-WI !"\+3.(m(%32)'+$31(43-'&&3
!" Severe vasogenic edema and !" Tick-borne disease in NE US, deer
enhancement !" Presents as skin rash (erythema migrans),
meningitis, neuritis (incl. CN), vasculitis
!" Multifocal wm lesions, +/- enhancement,
similar in appearance to MS
!" Cranial nerves may enhance
!" Tx: doxycycline
Figure 22 A & B
Colloidal stage of CNS cysticercosis, with thick

enhancing capsule, severe edema, and mass effect.
Figure 24 A & B
Typical white matter lesions (top) and enhancement

in both CN III (arrows).
Parenchymal C!(),/1%/"(,(7+++++++++++++++++++++++++
Granular Nodule Stage
!" Cyst retracts, capsule thickens, and scolex
23&2$8'#
!" +/- perifocal edema
!" CBN(K#"0'/#'(2A#)1(23&2$8'0(#2"&'L
!" MR:
!"T1-WI – isointense to brain
!"T2-WI – hypointense to brain
Neuroradiology
Fungal Disease in CNS [Figure 25] Important Points
!" No reliable or characteristic imaging !" Appearance of infection depends on host’s
8/0$/-# ability to mount a response
!" Cryptococcosis: 5%-10% of AIDS patients !" Role in meningitis is to assess for
!" Coccidioidomycosis: initial pulmonary infx complications
!"SW USA !" Temporal progression of cerebritis $
!" Candidiasis: common in diabetes, immune abscess
compromised !" Abscess
!" Mucormycosis !"% SI rim restricted diffusion
!"Most common in diabetics, especially !" AIDS
rhinocerebral form !"HIV infection vs PML
!"Angioinvasive: arteritis, infarction !"Toxoplasmosis
(bland and hemorrhagic), mycotic !"Cryptococcal meningitis “gelatinous
aneurysms pseudocysts”
!" Aspergillosis !" Enhancing cranial nerves with white
!"Ubiquitous, inhaled, often rhinocerebral matter lesions suggests Lyme disease or
!"Angioinvasive borreliosis
!" Fungi may not have distinct appearance
but if hemorrhagic think angioinvasive
form
Figure 25 A & B
Left Image: Cocci fungal abscesses.
Right Image: Hemorrhagic Aspergillus cerebritis.
References
1. Foerster BR, et al. Intracranial infections: clinical and imaging characteristics. Acta Radiol
2007;48(8):875-93.
2. Van de Beek D, et al. Community-acquired bacterial meningitis in adults. N Engl J Med 2006;354(1):44-
53.
3. Goldberg AN, et al. Complications of frontal sinusitis and their management. Otolaryngol Clin North Am
2001;Feb(34):211-25.
4. Reid JR. Complications of pediatric paranasal sinusitis. Pediatr Radiol 2004;34(12);933-42.
5. Mao-Draayer Y, et al. Emerging patterns of diffusion-weighted MR imaging in Creutzfeldt-Jakob disease:
case report and review of the literature. Amer J Neuroradiolog 2002;23(4):550-6.
6. Weihl CC, et al. Creutzfeldt-Jakob disease, new variant creutzfeldt-jakob disease, and bovine spongiform
encephalopathy. Neurol Clin 1999;17(4):835-859 Yiannoutsos CT, et al. Regional patterns of brain
metabolites in AIDS dementia complex. Neuroimage 2004;23:928-35.
7. Flisser A, et al. Neurocysticercosis: regional status, epidemiology, impact and control measures in the
Americas. Acta Trop 2003;87(1):43-51.
8. F683*(CU1(')(3&T(B*'($.3-$/-(3!!'3+3/2'#("6($/)+32+3/$3&(CEG($/6'2)$"/#($/(30,&)(kK_(3/0(@K7G(!3)$'/)#T(
Clin Radiol 2006;61(5):393-401.
9. Chang KH, et al. MRI of CNS parasitic diseases. J Mag Res Imaging 1998;8(2):297-307.
10. GD$'#)(7X1(')(3&T(C+A!)"2"223&($..,/'(+'2"/#)$),)$"/($/43..3)"+A(#A/0+".'N(+'!"+)("6(6",+(23#'#(3/0(
review of the literature. J Infec 2005;51(5):e289-297.
Neuroradiology
1196
The Sella and Parasellar Region

Imaging Techniques [Figure 1]
!" MR Imaging
!"Multiplanar: sagittal and coronal
!"Small FOV 16-18
!"3 mm Figure 2
!"T1-WI, T2-WI
!"Post Gd + T1-WI + FS Note & SI on
posterior lobe
#" Addition of Gd+ & sensitivity by on T1 sagittal
10%-15% (no Gd).
!"Dynamic enhanced for microadenoma
Figure 3
Normal graphic
through
the sella,
including the
Figure 1 A & B
pituitary gland,
suprasellar
Normal adult pituitary gland on T1 Gd (left) and T2 cistern,
images (right). infundibulum,
and cavernous
sinuses
P,)9,)'%!7+Normal Anatomy [Figure 2] (courtesy of
!" Adenohypophysis Amirsys, Inc).
!"Lateral
#" PRL (10%-30%)
#" GH (50%)
!"Midline Parasellar R1-,".7+Normal Anatomy
#" ACTH (10%-30%) [Figure 4]
#" TSH (5%) !" Parasellar structures
#" FSH/LH (10%) !"Optic chiasm
!"Location of adenomas parallel !"Hypothalamus
pituicytes #" Tuber cinereum
!"Indirect arterial supply, venous via #" Mammillary bodies
hypothalamus !"Sphenoid sinus
!" Neurohypophysis
!"Vasopressin (ADH) and Oxytocin
!"Synthesized in hypothalamus Figure 4
!"Axonal processes via infundibulum Normal
!"Posterior “bright spot” & SI on T1 suprasellar
!"Direct arterial supply: posterior lobe structures
enhances prior to anterior lobe including
optic chiasm
Parasellar R1-,".7+Normal Anatomy (long arrow),
[Figure 3] mammillary
body (short
!" Parasellar structures arrow)
!"Cavernous sinus and tuber
!"Cranial nerves cinereum of
#" III, IV, V1, V2, VI hypothalamus
!"Cavernous ICA (thick arrow).
!"Optic chiasm
!"Hypothalamus
!"Sphenoid sinus
Sella and Parasellar Region 1197 Neuroradiology

Parasellar R1-,".7+Normal Bony Empty Sella
Anatomy [Figure 5] !" G'&&3(),+2$23(8&&'0(I$)*(CG:1(-&3/0(,#,3&&A(
!" Bony structures 43))'/'0("/(#'&&3+(4""+
!"Planum sphenoidale !" Usually incidental
#" Sphenoid roof !" & in incidence with aging
!"Tuberculum sellae !" Finding present in chronic intracranial
#" Anterior margin of sella hypertension
!"Sella turcica
!"Dorsum sellae Ectopic Posterior Lobe [Figure 7]
#" Posterior margin of sella !" Normal posterior lobe & SI on T1 in
posterior sella
!" Ectopic lobe located immediately inferior
to hypothalamus
!" Infundibulum usually small or absent
!" May be congenital or acquired, especially
following trauma with stalk transection
Figure 7
Figure 5 A & B
Bony structures include planum sphenoidale, On sagittal

tuberculum sellae (long arrow), and dorsum sellae non-Gd T1
(short arrow). note & SI
(arrow)
beneath
hypothalamus
instead of
Normal Gland S,X17+Physiologic posterior sella.
Hypertrophy
!" Maximum normal height (estimates)
!"6 mm infants and children
!"8 mm men, menopause/andropause
(concave)
Intrasellar Pathology
!" Nonneoplastic lesions
!"10 mm young women of childbearing
!"Hyperplasia (physiologic, end-organ
age (convex superiorly)
failure)
!"12 mm late pregnancy, postpartum
!"Cysts (Rathke cleft cyst, pars
women (convex superiorly)
intermedia cyst)
!" Abnormal hypertrophy
!" Primary neoplasms
!"End-organ failure (hypothyroid)
!"Pituitary adenoma (most common)
!"Neuroendocrine tumor
!"Craniopharyngioma (only 5% purely
Pituitary Gland Hypertrophy intrasellar)
[Figure 6]
!"Meningioma (purely intrasellar rare)
!"Pituitary carcinoma (extremely rare)
!" Metastasis (1%)
!" Other
!"Pituitary apoplexy
!"Lymphocytic adenohypophysitis
S1&&'7+Rathke Cleft Cyst (RCC)

!" Benign, usually incidental sellar or
parasellar cyst of ectodermal origin
!"Intrasellar 40%
!"Suprasellar 60%
!" Size: 3 mm—3 cm
Figure 6 A & B !" No malignant potential
!" Symptomatic
Large, superiorly convex, enhancing gland with no
focal mass in patient with hypothyroidism. !"Pituitary dysfunction
!"Visual change, HA
1198 Neuroradiology
Sella and Parasellar Region
Rathke Cleft C!()7+Imaging Pituitary Microadenoma [Figures 10 & 11]
[Figure 8] !" 10 mm or less
!" CT !" Present in 10%-20% of autopsies
!"75% hypodense, 25% iso to & & !" Micro >>> macro
!"Ca++ rare !" Convex margin
!"<3A(%'(0$682,&)()"(0$66'+'/)$3)'( !" Stalk deviation to contralateral side
from other benign cysts or !" G'&&3(4""+()*$/
craniopharyngiomas
!" MR
!"Signal variable, depending on cyst
protein content Figure 10
#" 50%-60% & SI on T1
T1 post Gd
#" 40% isointense to CSF image shows
!"75% nodule in cyst 7 mm right
!"+/- rim enhancement inferolateral
adenoma
(arrow) in a
patient with
an elevated
prolactin level.
Figure 8 A & B
b'<3)7."8'9)b,G)('-4%3>)-,-$"#$%&'()4'##"+)."44),-)
CT.
Right Image: Sellar cyst with peripheral enhancement
on T1 MR.
Figure 11 A & B
Pituitary Neoplasms [Figure 9]
!" Adenoma Left inferolateral microadenoma on T2 (left) and post
Gd T1 (right) MR images.
!"Prolactinoma 30%
!"Null cell 25%
!"GH 20%
!"ACTH 10% Pituitary M,/%"'51."*'7+Dynamic
!"FSH/LH 10% Imaging Technique [Figure 12]
!"PRL-GH 5% !" Increases sensitivity (10%-30% seen only
!"Mixed, TSH 1-5% on dynamic MR)
!"Incidental pituitary lesions are !" 3 coronal slices, Gd bolus, image every
common (17%) and may mimic 10-15 seconds
adenoma !" Adenoma enhances slower than normal
gland
Figure 9
Graphic Figure 12
shows < 10
mm right Coronal image
adenoma obtained every
with gland 12 seconds at
convexity same location.
on right Shows left
and stalk adenoma
displaced to (arrow) with
left delayed
(Courtesy enhancement
Amirsys, compared to
Inc). gland.
1199 Neuroradiology
Pituitary Macroadenoma > 10 mm Cavernous Sinus Invasion [Figure 15]
[Figure 13] !" More aggressive tumor
!" Clinical !" Prolactin
!"Most common suprasellar mass (50%) !" Considered unresectable
!"> 10 mm !" Best imaging features:
!"10% of all intracranial tumors !"2/3 surrounds ICA
!"Compressive symptoms !"Inferior venous sulcus compartment
!"Rare in children and adolescent men 8&&'0
Figure 13 Figure 15
Right
Sella and cavernous sinus
suprasellar invasion by
macroadenoma macroadenoma,
elevating and &##%-8)%-<'+%,+)
0"33'-%-8)3?') venous sulcus.
chiasm (arrows) Note ICA
(courtesy of remains normal
Amirsys, Inc). in caliber.
Prolactinoma Lymphocytic Adenohypophysitis

!" 30% of adenomas !" Clinical and imaging
!" Female >> Males !"Occurs during late pregnancy or
!" Galactorrhea, amenorrhea shortly after delivery
!" Treatment !"Females >> Males
!"Bromocriptine: will decrease prolactin !"`+'#'/)#(I$)*(!$),$)3+A($/#,682$'/2A1(
!"Surgery: transsphenoidal headache and visual changes
hypophysectomy !"Amenorrhea or inability to lactate
!" Serum prolactic levels: !"Diffuse enlargement of
!"> 150 ng/mL – prolactinoma present adenohypophysis, posterior lobe or
!"> 1000 ng/mL – invasion of cavernous stalk (neurohypophysis) or both
sinus !"May mimic hyperplasia or adenoma,
history important
Pituitary M'/%"'51."*'7+EI+B+
CECT with Coronal Reform (If MR Lymphocytic Adenohypophysitis
Contraindicated) [Figure 14] [Figure 16]
!" Imaging features !" Pathology
!"Isointense to GM on T1, T2 !"7$66,#'($/8&)+3)$"/("6()*'(30'/"(pdW(
!"May have hemorrhage, cystic neurohypophysis by lymphocytes and
components rare plasma cells
!"Extension through diaphragm sella ! !"? Autoimmune ?
h8-,+'W'$-*)i("+(h#/"I.3/i
!"Marked, sometimes heterogeneous
enhancement
!"Determining cavernous sinus invasion
important
Figure 16
Figure 14 Man with

hypogonadism
Pituitary $,-&+.'()
macroadenoma lymphocytic
with left neuro-
cavernous sinus hypophysitis.
invasion.
Note tumor
encircling left
cavernous ICA
(arrow).
1200 Neuroradiology
Pituitary Apoplexy [Figure 17] Suprasellar Meningioma [Figure 18]
!" Clinical syndrome !" Second most common suprasellar mass
!"Acute onset (adults)
!"Visual changes, HA, vomiting !" 15% of meningiomas occur here
!"Probably hemorrhage into pituitary !"Tuberculum sellae
adenoma !"Clinoid processes
!"Infarction, necrosis !"Cavernous sinus
!"Rare, life-threatening !" Look for pituitary gland distinct from mass
!"Sheehan syndrome: pituitary apoplexy !"Pituitary macroadenoma treated
in postpartum period surgically via transsphenoidal
approach
!"Suprasellar meningioma, when
operated, approached via craniotomy
Figure 17
Hemorrhagic
pituitary
apoplexy.
Note high SI
sella contents
consistent
with blood.
Figure 18
A, B & C
Other Intrasellar M'((1(7+Uncommon
!" Craniopharyngioma (5% intrasellar)
Note plane between
!" Metastasis (1% of sellar masses, found at meningioma and normal
autopsy) pituitary gland (arrows).
!" Aneurysm (project medial from cavernous Extension along planum
ICA) is characteristic of
meningioma (arrowhead).
!" Meningioma (rare purely intrasellar)
Suprasellar M'((1(7+Most Common

!" Pituitary macroadenoma (35%-50%)
!" Approximately 10% each P'%'(1&&'%7+Aneurysm [Figure 19]
!"Meningioma !" CT
!"Aneurysm !"E"/23&2$8'0("+(!'+$!*'+3&&A(C3pp(
!"Craniopharyngioma suprasellar mass
!"Astrocytoma (hypothalamic- !"C3/(%'(0$682,&)()"(0$#)$/-,$#*(6+".(
chiasmatic) adenoma, meningioma
!" MRI
Suprasellar Differential Diagnosis !"Flow void or complex mass separate
!" Adult lesions from pituitary gland
!"Pituitary macroadenoma !"Phase encode artifact
!"Meningioma
!"Aneurysm
!" Pediatric lesions
!"Craniopharyngioma
!"Chiasmatic/hypothalamic glioma Figure 19
!"Hypothalamic hamartoma
Left
cavernous
ICA
aneurysm,
with phase
encode
artifact
parallel to
vessel.
1201 Neuroradiology
Suprasellar M'((7+Adult [Figure 20]
!" Macroadenoma
!"Pituitary is mass Figure 22
!"Enhances
!"Does not narrow ICA Complex
!" Meningioma suprasellar
!"Pituitary is separate mass with
bulky peripheral
!"Enhances
Ca++. Note
!"Dural tail 01%(201%()#':'#)
!"When involves cavernous ICA, vessel (arrow) common
may be narrow in multicystic
cranio.
C%'.,"0?'%!.-,"*'7+EI+++++++[Figures 23 & 24]

!" Variable signal
!"& SI on T1 without Gd
!" Often heterogeneous
!" C3pp(0$682,&)()"(0')'2)
!" Nodular and rim enhancement
!" Occasionally optic tract hyperintensity on
Figure 20 A & B
T2 – mass effect
Macroadenoma vs suprasellar meningioma.
S90%'(1&&'%7+Craniopharyngioma
[Figure 21]
!" Clinical
!"Most common suprasellar mass in
children
!"Bimodal age range
#" 5-15 years
#" 50-60 years
!"Presents with mass effect
#" Headache, nausea, vomiting
papilledema
#" Pituitary dysfunction
Figure 21
Complex,
multicystic,
nodular Figure 23 A & B
suprasellar High SI complex mass on T1 sagittal noncontrast MR
mass with (left image), remains high SI on T2 (right image).
intrasellar
extension
(Courtesy
Amirsys, Inc).
C%'.,"0?'%!.-,"*'7+4J++++++[Figure 22]
!" Often bizarre imaging appearance
!" Enlarged sella
!" Ca++ common
!" Solid and cystic
Figure 24 A & B
!" Fluid/debris levels
!" 90% enhance – rim or nodular Craniopharyngioma has invaded central skull base,
&##%-8)-"4,6?"+>-U)"-()#'<3)-"4"#)$":%3>/
1202 Neuroradiology
Chiasmatic-Hypothalamic Glioma
!" Clinical
!"Second most common suprasellar
mass in children
!"Often large at presentation
!"HA, visual, endocrine
!"Males = Females
!"15%-30% NF 1
Figure 25 A, B & C
!" Pathology
!"75% pilocytic astrocytoma Comparison of suprasellar masses in children.
!"OR?(&"I(-+30'(8%+$&&3+A((
!"Long term survival: 90% 5 years
Chiasmatic-Hypothalamic Glioma I.39.5,$9&9*7+Differential Diagnosis

!" MR !" Common lesions
!"Variable signal intensity !"LCH
#" T1-WI: Iso to hypointense !"Sarcoidosis
#" T2-WI Hyperintense !"Lymphoma, metastasis
!" Variable enhancement !" Rare lesions
!" Spread along optic tracts common !"Germinoma
!"Hypophysitis
Hypothalamic H'*'%)"*'7+LYL+ !"Pituicytoma
Hamartoma of Tuber Cinereum
!" Clinical LCH [Figure 26]
!"Precocious puberty !" Clinical
#" Usually < 2 years !"First decade
!"Gelastic seizures !"Males > Females
#" Inappropriate episodic laughter !"Presents with diabetes insipidus
!" Males > Females !"Increase SI of neurohypophysis is
!" Pathology commonly absent
!"Hamartoma of tuber cinereum !"Thickening of stalk
!"Congenital nonneoplastic heterotopia !"Formerly histiocytosis X
!"Between infundibular stalk,
mammillary bodies
Hypothalamic H'*'%)"*'7+EI
!" Signal follows gray matter
!" Isointense on T1
!" May be slightly T2 hyperintense
!" Pedunculated or sessile
!" May project into third ventricle
!" No enhancement
!" Benign, no malignant potential
Suprasellar M'((7+Child [Figure 25] Figure 26 A & B

!" Craniopharyngioma Post Gd images show typical thickened and enhancing
!"Complex mass infundibulum.
!"90% cystic
!"=>?(23&2$8'0
!" Astrocytoma
!"Chiasm/hypoth
!"T2 hyperintense Sarcoidosis
!"Variable enhancement !" C*+"/$21(.,&)$#A#)'.1($/43..3)"+A(
!" Hamartoma disease
!"Hypothalamus !" Noncaseating granulomas
!"GM signal !" E',+"&"-$2(8/0$/-#(R?(
!"No enhancement !" 7$3%')'#($/#$!$0,#("+(*"+."/'(0'82$'/2A((
!" Central diabetes insipidus
!"Lack of antidiuretic hormone (ADH)
!"Excessive thirst and dilute urine
volume
!" Steroid responsive
!" Can be both intra- and suprasellar
1203 Neuroradiology
Lymphoma [Figure 27] Germinoma [Figure 28]
!" Clinical !" Clinical
!"NHL (B-cell) !"Suprasellar region is second most
!"90% supratentorial common site
!"Sixth-seventh decade !"Male = Female suprasellar
!"AIDS: fourth decade !"90% present < 20 years
!" Imaging !"Endocrine dysfunction
!"Pituitary gland, hypothalamus, stalk #" Diabetes insipidus
!"Hyperdense on CTT1 iso- to #" Panhypopituitarism
hypointense !" Radiosensitive
!"T2 hypointense !" Up to 90% 10-year survival
!"Homogeneous enhancement
Figure 27 A & B
Large robustly enhancing suprasellar lymphomatous

mass (left image) and smaller mass (arrow) at tuber
cinereum (right image).
Enhancing suprasellar and pineal region masses.
References
1. Bartynski WS, et al. Dynamic and conventional spin-echo MR of pituitary microlesions. Am J Neuroradiol
1997;18:965-72.
2. :+$'0.3/(BC1(')(3&T(7A/3.$2(!$),$)3+A(<VK(*3#(*$-*(#'/T(3/0(#!'2$82$)AT(k"+.(<')3%(V'#(O>>PY^=N]RZW[T
3. Vieira JO, et al. Evaluation of MRI criteria for cavernous sinus invasion. Surg Neurol 2006;65:130-5.
4. Cottier JP, et al. Cavernous sinus invasion by pituitary adenoma: MR imaging. Radiology 2000;215:463-9.
5. Molitch ME. Nonfunctioning pituitary tumors and pituitary incidentalomas. Endo Metab Clin North Am
2008;37:151-71.
6. Saleem SN, Said AH, Lee DH. Lesions of the hypothalamus: MR imaging diagnostic features.
RadioGraphics 2007;27:1087. Review
7. 9"//'5$&&'(:1(')(3&T(BZ(#$-/3&(*A!'+$/)'/#$)A($/()*'(#'&&3+(+'-$"/N(#!'2)+,.("6(8/0$/-#T(V30$"\+3!*$2#(
2006;26:93-113.
8. Molitch ME, Gillam MR: Lymphocytic hypophysitis. Horm Res 2007;68:145-50.
9. Ohmori K, Collins J, Fukushima T. Craniopharyngiomas in children. Pediatr NS 2007;43:265-78.
1204 Neuroradiology
K*'-,.-+"3+)?1+K.3%'?!",5+R1/H7+G!*0?+R"51(+'.5+K.31/),".

Infrahyoid N1/H7+Summary
!" Part 1
!"Spaces and fascia Figure 2
!"Lymph nodes
#" Levels The most
common
#" Malignant characteristics neck lesion
#" Squamous cell carcinoma in adults is a
#" Lymphoma, other nodal conditions lymph node
!"Infection/abscess described
!" Part 2 as a certain
location or
!"Visceral space level
#" Larynx (Courtesy
#" Hypopharynx Amirsys Inc).
#" Thyroid
!"Retropharyngeal space
!"Carotid space
Lymph N"51(7+Summary
Infrahyoid Neck [Figure 1] !" Nodal levels
!" :3#2$3(0'8/'#(#!32'#N !" Nodal characteristics
!"Visceral space (VS) !"Location
!"Larynx, hypopharynx !"Size
#" Thyroid, parathyroid !"Central lucency or necrosis
#" Recurrent laryngeal nerve !"Shape
#" Trachea !"Ca++ or enhancement
#" Esophagus !" Nodal staging for head and neck cancer
!"Carotid space (CS) !" Lymphoma
#" CCA, IJV, CN X
!"Retropharyngeal space Cervical Node L"/'),".7+VLevels”
!"Perivertebral space !" 7 discrete cervical anatomic levels used
universally by all medical specialists
!" Nodal levels/locations are important
means to communicate to surgeons,
oncologists
Figure 1 !" Routine use of nodal level in radiology
report recommended
Spaces in the !" :"+(GCC31("/&A(8+#)(R(+",)$/'&A(,#'0
infrahyoid neck !" Other nodal groups named by anatomic
separated by
layers of deep location
cervical fascia !"Ex: facial, parotid, and
(Courtesy retropharyngeal
Amirsys Inc).
P1%(01/),217+Cervical Lymph Node in
Adult [Figure 3]
!" > 90% head and neck cancers are SCCa
Infrahyoid Neck [Figure 2] !" #1 prognostic factor for SCCa is presence,
:3#2$3(0'8/'#(#!32'#
!" number of metastatic nodes
C'+5$23&(/"0'#(/")(2"/8/'0()"(#!'2$82(
!" !" # nodes correlates with survival
space !" Single unilateral node: 5-year survival %
!" Nodes are described as locations or levels, 50%
but not “spaces” !" Bilateral nodes: decrease by 75%
!"IA Submental !" Extracapsular extension (ECE): 15%
!"IB Submandibular 5-year survival
!" Jugular chain !" New chemoradiotherapy regimens have
HIOIDES !"II High *30(#$-/$823/)('66'2)("/(#,+5$53&((
CRICOIDES !"III Mid !" Survival curves may change but nodal
!"IV Low status still important for prognosis
CLAVÍCULA
!"V Posterior triangle
Infrahyoid Neck: Lymph Nodes and Infection Musculoskeletal Radiology

1205
Level I Nodes [Figure 4]
Figure 4 A & B
Imaging examples of small IA and IB nodes.
Level IA and IB N"51(7+S01/,#/(+++++++++++++

[Figure 5]
!" Most nodes here are reactive/incidental
!" In a patient with SCCa, upper limits of
normal size is 1.5 cm
!" Sentinel node for oral cavity SCCa (also II
and III)
Figure 5
Figure 3 A, B & C
Left enlarged
A new neck mass in an adult, if no signs of infection IB node
and not a goiter, is a metastatic squamous cell with central
carcinoma until proven otherwise. lucency,
metastatic
from left
buccal sulcus
carcinoma.
Sentinel Nodal Chain

!" “Sentinel node” – primary lymphatic
0+3$/3-'(6"+(#!'2$82(*'30(3/0(/'2D(
primary tumor Node Level S!()1*7+Levels II, III and
!" Nasopharynx IV
!"Retropharyngeal, all levels !" Nodes beneath the sternocleidomastoid
!" Oral cavity (SCM) muscle, usually close to the
!"Levels I and II internal jugular vein
!" Oropharynx !" Divided into:
!"Levels II and III !"Level II (high): from skull base to
!" Larynx – supraglottic hyoid bone
!"Levels II and III !"Level III (mid): from hyoid to bone
!" Hypopharynx bottom of cricoid cartilage
!"Level III !"Level IV (low): from bottom of cricoid
cartilage to clavicles
Node Level System – Level IA and IB
!" All nodes underneath the mandible and .
above the hyoid bone
!" Divided into two groups:
!"IA: midline nodes between the
anterior bellies of the digastric
muscles
!"IB: all other nodes, esp submandibular
#" Anterior to submandibular gland

1206
Internal Jugular Chain Nodes [Figure 6] Level IIA and IIB Nodes
!" In a patient with SCCa, upper limits of
normal size is 1.5 cm
!" Reactive nodes common, may be large,
> 1.5 cm if bacterial or viral infection is
present
!" Sentinel node for most H and N ca,
including
!"Oropharynx
!"Nasopharynx
!"Oral cavity
!"Larynx
!"Hypopharynx
Figure 6
Level III (Middle Chain Nodes)
The hyoid bone separates level II from level III. [Figure 9]
Level III is between the hyoid and cricoid.
Level IV extends from the cricoid cartilage to the
!" Jugular chain, from lower hyoid body to
clavicle. inferior cricoid margin
!" Anterior to posterior aspect of SCM
muscle
!" In patient with SCCa, up to 10 mm is
normal
Level II (Upper Chain Nodes) !" Commonly involved
[Figures 7 & 8] !"Advanced oropharynx
!" Above inferior hyoid, anterior to posterior !"Nasopharynx
margin of SCM !"Supraglottic larynx
!" IIA: Anterior, medial, lateral, or posterior !"Hypopharynx
and “touching” the IJV
!" IIB: Posterior and separate from the IJV
Figure 9
Large
partially
necrotic
Figure 7
level III
node, at
level of
Level IIA thyroid
nodes anterior cartilage
and posterior (arrows).
to right IJV.
Level IV
!" Jugular chain, between cricoid and clavicle
!" In patient with SCCa, up to 10 mm is
normal
!" Commonly involved
!"Advanced oropharynx
!"Larynx
!"Hypopharynx
!"Thyroid
!"Esophagus
Figure 8
Lines denote
posterior
SCM muscle.
Bilateral
IIB nodes
(arrows).

1207
Level V [Figure 10] Central Defect, SCCa [Figure 11]
!" Nodes behind posterior border of the SCM !" In a patient with SCCa of head and neck,
muscle – “posterior cervical space nodes” central defect is never normal, regardless
!" VA: nodes above the cricoid cartilage level of nodal size
!" VB: nodes below the cricoid and above
the clavicle
!" SCCa unusual; lymphoma, melanoma,
systemic metastases more likely
Figure 11 A & B
Large necrotic level IB node, but notice small left level

IIB node. Even though node is < 1 cm, central necrosis
4%8-%&'4).'3"43"3%$)(%4'"4')3,)-,('/
Figure 10 A & B
Level V node (arrow) in a patient with lymphoma.
Note smaller level III node (arrowhead) on right.
Nodal Necrosis [Figures 12 & 13]
!" SCCa, 90% of nodes > 3 cm have central
Node Level System necrosis
!" Levels VI and VII !" Patient has both SCCa and lymphoma,
!"Nodes in visceral space: pre- and notice different nodal appearance
paratracheal
!"Superior mediastinal nodes
!" NAMED NODES
!"Parotid nodes: from skin carcinoma, Figure 12
parotid primary
!":32$3&(/"0'#N(#,!'+82$3&(632$3&(#"6)( Left necrotic
SCCa
tissues, including occipital, mastoid,
conglomerate
etc metastatic
!"Retropharyngeal nodes: only in the nodal mass
suprahyoid neck (arrows) and
!"Supraclavicular nodes: on the same elsewhere
typical diffuse
slice or immediately above the clavicle nodes from
lymphoma.
Anatomic Nodal Imaging
!" CT
!"Spatial resolution, 2.5 mm
!"IV contrast to detect necrosis
!"Size criteria has low sensitivity, higher
#!'2$82$)A($/(GCC3
!" MR
!"Contrast resolution
!"May be limited by artifact
!"K_(2"/)+3#)()"(2"/8+.(/'2+"#$#
!" Ultrasound common in Europe and Asia
!" Operator dependent, must have organized
approach to examining bilateral cervical
nodes
Determination of a “Malignant” Node

!" Central defect or lucency – necrosis
!" Size Figure 13 A & B
!" Shape
!" Number of nodes (cluster) Gross specimen of node involved by SCCa shows a
focus of tumor and necrosis (arrow).
!" Positive PET
!" Extracapsular (perinodal) extension

1208
Second Branchial Cleft Cyst vs Nodal Extracapsular Disease [Figures 15 & 16]
Met [Figure 14] !" Reduced survival by 50%
!" Thick, enhancing “fuzzy” irregular nodal
margin in early stages
!" Fixation of muscles or vessels, often
clinically apparent
!" C3+")$0(3+)'+A('/23#'.'/)(3/0(8L3)$"/(
are associated with high mortality
Figure 15
Bulky,
conglomerate
right level
II and III
nodal mass
with irregular
interface
between
nodes and
SCM muscle
(arrow).
Figure 16
Microscopic
Top Right Image: Gross specimen of “cystic” SCCa specimen
nodal met. shows
Top Left Image: True 2nd BCC. intranodal
Bottom Images: level IIA left necrotic SCCa nodal necrosis and
mets. extracapsular
tumor.
Size
!" K.!'+6'2)(#A#)'.1(0$682,&)(%3&3/2'(
AJCC Nodal Staging
%')I''/(#'/#$)$5$)A(3/0(#!'2$82$)A
!" N0 – no metastatic nodes
!" Options
!" N1 – single ipsilateral, < 3 cm
!"Long axis: most common criteria used
!" N2
in US
!" N2a – single ipsilateral, > 3 cm < 6 cm
!"Short axis
!" N2b – multiple ipsilateral, none > 6 cm
!"Length/width ratio (in other words,
!" N2c – bilateral or contra, none > 6 cm
round node is worse than long one)
!" N3 – node or nodes > 6 cm
S,X17+K.+'+F'),1.)+<,)?+SCCa Head and
Unusual Nodal Characteristics
Neck !" Ca++
!" Most widely used size criteria: !"Mycobacterium, other infections
!"1.5 cm for level I and II !"Treated bacterial infection
!"1 cm for other levels !"Sarcoidosis
!"0.8 cm for retropharyngeal region !"Differentiated thyroid CA
!" These measurements not applicable to !"Nodal mets: breast, lung, colon
patient without SCCa !"Treated lymphoma
!"Active infection, especially !" Bright or enhancing
mononucleosis EBV infection, nodes !"K/43..3)"+A
often > 1.5 cm !"Differentiated thyroid CA
!"Lymphoma nodes may be any size #" Papillary
!" \'/'+3&&A(!""+(#'/#$)$5$)Ad#!'2$82$)A1(%,)( #" Follicular
best compromise !" Castleman disease
!" Kaposi sarcoma
Ca papilar de tiroides: mas común, mujeres, 30-50 años.

1209
Tuberculous Adenitis [Figure 17] S)'-,.-7++L..+Arbor Criteria
!" Aerobic bacteria [Figure 19]
!" Imaging variable !" Stage I
!"Multiple large nodes !"Single nodal or extralymphatic site
!"Single node (“cold” abscess) !" Stage II
!"Varying appearance in same patient !"2 nodal stations, or single extranodal
!"May Ca++ site + nodes
!"Single side of diaphragm
!" Stage III
!"Nodes on both sides diaphragm
Figure 17 !" Stage IV
!"Multifocal disease with extralymphatic
Variable nodal organ involved
appearance
including
Ca++,
enhancing and
nonenhancing
nodes, in
patient with TB
adenitis.
Figure 19 A & B
Differentiated Thyroid Carcinoma Left Image: Multiple small homogeneous nodes in 2
[Figure 18] different patients with lymphoma.
!" Papillary carcinoma is common Right Image: Single large low-density node.
!" Females >> Males
!" 30-50 years most common
!" Thyroid primary may be microscopic Nodal D,(1'(17+Summary
!" May have nodal metastases with !" In the adult patient, a new neck mass
microscopic disease (unless obviously thyroid in origin) is
!" Nodal mets may go “upstream” to levels SCCa nodal met until proven otherwise
II and III !" CECT or MR (US) of the neck is next step
!" No predictable nodal spread !"C"/8+.()*'(.3##($#(3(/"0'
!"Look for other metastatic nodes
Figure 18 !"(location, side, size, necrosis, ECE)
!"Carefully look for primary tumor
CECT
shows large !" <')3#)3)$2(30'/"!3)*A(*3#(#$-/$823/)(
enhancing clinical prognosis
right level II !" CT “upstages” the neck 30% c/w with
node lateral clinical examination
to internal !" E"03&(/'2+"#$#(."#)(#!'2$82($/0$23)"+
jug. Vein
(arrowhead) !" Combination of CT/PET probably best
and carotid current determinant of nodal metastases
bifurcation !"But staging CT/PET not standard of
(arrows). care unless distant metastases are
suspected
Nodal Lymphoma !"Nodal disease treated with neck
!" Lymphoma in head and neck may be dissection or radiation
!"Nodal
!"Non-nodal, lymphatic Neck Infection and Abscess
#" Tonsils, base of tongue, adenoids !" Can occur in any location
!"Extra – nodal, lymphatic !" Primarily suprahyoid neck
!" Variable appearance when nodal !"Sublingual space (odontogenic)
!"Single enlarged node !"Submandibular space (SMG stone)
!"Multiple large, medium, or small nodes !"Tonsillar/peritonsillar
!"Most commonly non-necrotic !" Infrahyoid neck
!"Rarely solid, cystic, necrotic nodes (all !"Anterior cervical space
in same patient) !"Posterior cervical space
!"No standard size criteria !"Retropharyngeal space
!"Bidimensional nodal sizes reported to !" Once identify location, methodically look
follow treatment response for source and local extension

1210
Infrahyoid Neck Infection and Abscess MRSA RTP Abscess [Figure 21]
!" Describe extent
!" Effect on airway (is there airway
compromise?)
!" Proximity to ICA and IJV (involve carotid
space, is internal jugular vein still
patent?)
!" Discrete ring-enhancing collection may
not be seen
!"Necrotizing fasciitis/myositis
!" Methicillin-resistant Staphylococcus
aureus (MRSA)
Figure 21 A & B
Infrahyoid Neck Abscess [Figure 20] RTP abscess originating in suprahyoid neck (left),
!" Anterior and posterior cervical spaces extending into infrahyoid neck in RTP space and lateral
to thyroid gland (arrows).
Infrahyoid Neck Retropharyngeal Space

!" Midline potential space
!" Behind visceral space
!" Extends from skull base to T3
!" Communicates with “danger space,”
extends to mediastinum
!" Only content in infrahyoid neck is fat
!" <"#)(2".."/(&'#$"/($#(4,$0("+(!,#
!" G)'+$&'(4,$0(6+".(X_()*+".%"#$#1(
Figure 20 A & B
trauma (may be blood), effusion from
b"+8').1#3%#,$1#"3'()*"$3'+%"#)"*4$'44)&##4)*,3?) degenerative disease at skull base
anterior and posterior spaces (left image) and !" Infection
posterior cervical space (right image).
!"Discitis/osteomyelitis in adults
!"Suppurative node in children
Summary
MRSA Community Acquired !" Most common lesion in infrahyoid neck is
!" 26 cases/100,000 (Atlanta highest in US) nodal disease
!" African Americans > others !" Nodal level system commonly used
!" Occurs in any age group, but < 2 years !" Characteristics of SCCa nodal mets
old is common !" F)*'+(/"03&(0$#'3#'N(('/*3/2$/-1(23&2$8'0
!" Necrotizing pneumonia and fasciitis !" Lymphoma
!" Often looks “watery” without discrete !" Infection and abscess in infrahyoid neck
enhancing capsule
References
1. Vogl T, et al. Lymph node staging. Top Magn Reson Imaging 2007;18(4):303-16.
2. Som P. Lymph nodes of the neck. Radiology 1987;165:593-600.
3. Moon W, et al. CT and MR imaging of head and neck tuberculosis. RadioGraphics 1997;17:391-402.
4. Yanir Y, et al. Regional metastases in well-differentiated thyroid carcinoma: pattern of spread.
Laryngoscope 2008;118(3):433-6.
5. Som P, et al. The varied presentations of papillary thyroid carcinoma cervical nodal disease: CT and MR
8/0$/-#T(@.'+(X(E',+"(V30(Z==]YZRNZZO^WQT

1211
1212
K*'-,.-+"3+)?1+K.3%'?!",5+R1/H7++F'%)+Z

Infrahyoid N1/H7+Summary Larynx – Subsites [Figure 2]
!" Part 1 !" 2 lines
!"Spaces and fascia !"1. Through ventricle
!"Lymph nodes !"2. 1 cm below that line
#" Levels !" Supraglottic
#" Malignant characteristics !"Above line 1
#" Squamous cell carcinoma !" Glottic
#" Lymphoma, other nodal conditions !"Between lines
!"Infection/abscess !" Infraglottic
!" Part 2 !"Below line 2, to bottom of cricoid
!"Central compartment cartilage
#" Larynx
#" Hypopharynx
#" Thyroid
#" Parathyroid
!" Carotid space
!" Retropharyngeal space
Infrahyoid Neck [Figure 1]

!" :3#2$3(0'8/'#(#!32'#
!"Middle and deep layers of deep
cervical fascia
!"Extent: hyoid bone to mediastinum
!"Central compartment or visceral space
(VS)
#" Larynx, hypopharynx
#" Thyroid, parathyroid
#" Recurrent laryngeal nerve
#" Trachea
#" Esophagus
!" Carotid space (CS)
!" Retropharyngeal space
Figure 2
Graphic of divisions of larynx into
supraglottic, glottic, and infraglottic portions.
Laryngeal Sites
!" Supraglottic
#" Epiglottis
#" Aryepiglottic folds
#" False vocal folds
#" Preepiglottic fat/space
#" Paraglottic fat
!" Glottic
!"True vocal cord
!"Anterior commissure
!"Posterior commissure
!" Subglottic
!"Mucosa lining airway
Figure 1
Spaces in the infrahyoid neck, separated
by layers of deep cervical fascia
(Courtesy of Amirsys Inc).
Infrahyoid Neck: Part 2 1213 Neuroradiology

Laryngeal Cartilaginous and Bony Laryngocele [Figures 4 & 5]
Structures !" Compressible neck mass, Males >
!" U!$-&"))$#N(8%+"'&3#)$2(23+)$&3-'1(0"'#(/")( Females
ossify !" Secondary to obstruction at ventricle, so
!" kA"$0N("##$8'0(3)(%$+)*1()+$!3+)$)' check for lesion at that level
!" Thyroid: shield shaped, incomplete ring !" <3A(%'(8&&'0(I$)*(3$+1(.,2,#1("+(!,#
!" Cricoid: complete ring !"Internal
!" Arytenoid: bilateral, small, perched on !"Mixed
cricoid !"External
!" K/2".!&')'(3/0(3#A..')+$2("##$823)$"/(
common
Vocal Cord Palsy (VCP) [Figure 3]

!" R($.3-$/-(8/0$/-#
!"Dilated pyriform sinus
!"Dilated laryngeal ventricle
!"Paramedian AEF
Figure 4
!"Paramedian or atrophied TVC
!"Arytenoid cartilage is anterior and Internal
medialized laryngocele
on right,
!" Etiology may be neural or laryngeal mixed on
left.
Figure 3
VCP CT shows dilated laryngeal ventricle (white
arrow), low density fatty replaced left TVC, and
medialized arytenoid cartilage (black arrow).
VCP
!" Etiology may be neural or laryngeal
!" Neural
!"Follow course of vagus nerve
from jugular foramen to tracheo -
esophageal groove
!" Laryngeal
!"Mass on TVC
!"Mass at crico-arytenoid joint
!"Crico-arytenoid dislocation
Figure 5 A & B
b'<3)7."8'9)C%U'()01%(2&##'()#"+>-8,$'#'/
A%8?3)7."8'9)7-<'$3'()"%+)"-()01%(2&##'()'U3'+-"#)
laryngocele.

Laryngeal Carcinoma [Figure 6] Supraglottic Carcinoma [Figure 8]
!" Over 95% of laryngeal malignant tumors !" Epiglottis
are squamous cell CA (SCCa) !" Aryepiglottic folds
!" Risk factors: smoking, ETOH !" False vocal folds (“cords”)
!" > 50 years, Males > Females !" Preepiglottic or paraglottic fat
!" Clinical presentation depends on location !" Involvement of preepiglottic fat = T3
!" Supraglottic: often large at diagnosis, stage
dysphagia
!" Glottic: presents early with voice change
!" Subglottic: rare, presents with
hoarseness, airway obstruction
Figure 6
Figure 9 A & B
Graphic of Supraglottic CA, involving AEF and preepiglottic fat
invasive (arrows).
supraglottic Different patient (right image) tumor on false vocal
carcinoma fold, paraglottic fat with thyroid cartilage sclerosis
with (arrowheads).
cartilage
invasion
(Courtesy
of Amirsys Supraglottic S44'7+Staging
Inc). !" T1: one subsite, normal VC mobility
!" BON(e("/'(#,%#$)'1(/"(&3+A/-'3&(8L3)$"/
!" T3:
!"Fixed vocal cord
!"Invasion of postcricoid or pre-
epiglottic regions
Laryngeal SCCa !" T4a: moderately advanced
!" Glottic – 60% !"Tumor through thyroid cartilage
!" Supraglottic – 30% !"Extension to surrounding soft tissues
!"Rich lymphatic drainage, 35% have !" T4b: very advanced
metastatic nodes at presentation !"Invades carotid sheath, prevertebral
!" Subglottic – 5% muscles, mediastinal structures
!" Role of imaging
!"Extent of disease
Glottic Carcinoma [Figure 9]
!" True vocal cord
!"Does it involve the true vocal cords?
!" Anterior commissure
!"Is the cartilage involved?
!"< 1 mm soft tissue thickness
!"Does tumor extend through cartilage?
!" Cartilage sclerosis? May be due to tumor
Tumor outside of larynx?
abutting but not invading cartilage –
!"Is the airway compromised?
),."+($/0,2'0($/43..3)$"/
!"Are there metastatic cervical nodes?
Supraglottic Carcinoma [Figure 7]
Figure 9
Figure 7 A & B Glottic carcinoma extending across anterior
Supraglottic tumor is entirely above laryngeal commissure (short arrow) with arytenoid cartilage
ventricles (arrows). sclerosis (arrowhead).

Subglottic Carcinoma [Figure 10]
Figure 11
!" Beneath TVC to lower cricoid cartilage
!" Should see no tissue on airway side of Gross
subglottis specimen
!" Always look below TVC shows
extension of
tumor through
thyroid notch
but also
destruction of
medial thyroid
ala (arrows).
Miscellaneous Laryngeal Lesions

!" Juvenile papillomatosis
!" C*"/0+"#3+2".3N(#!'2$82($.3-$/-(
Figure 10 A & B
appearance
Tumor on undersurface of right TVC (left image), with !" Supraglottitis
subglottic extension (right image). !" \3#)+"'#"!*3-'3&(+'4,L(0$#'3#'(H\UV7J
!" Rheumatoid arthritis
Cartilage Involvement by Tumor
!" ;3+A/-'3&(23+)$&3-'("##$8'#( Hypopharynx [Figure 12]
asymmetrically !" 3 subsites
!" Cartilage destroyed by tumor can look like !"Pyriform sinus
,/"##$8'0(23+)$&3-' !"Posterior pharyngeal wall
!"F##$8'0(23+)$&3-'(."+'(#,#2'!)$%&'()"( !"Postcricoid region
$/53#$"/()*3/(/"/"##$8'0 !" Primary tumors less common than larynx,
!" Cartilage involvement: spectrum of but often involved by laryngeal tumors
invasion !" Rich lymphatic drainage, nodal mets
!"Inner perichondrium invaded common
!"Tumor penetrates through medullary
space
!"Tumor involves outer portion of
Figure 12
cartilage
!"Extralaryngeal extension into Small
surrounding soft tissues carcinoma of
!" C3+)$&3-'(#2&'+"#$#(m(/"/#!'2$82(8/0$/-( left pyriform
sinus,
that may mean either tumor invasion or extending into
$/43..3)"+A(2*3/-'#(H%,)(EFB(),."+J( paralaryngeal
from tumor abutting cartilage fat (arrow).
Note necrotic
Cartilage Involvement by Tumor level III node
on left.
!" CT
!"G$/-&'(#2&'+")$2(23+)$&3-'N($/43..3)$"/(
vs tumor
!"Sclerosis of 3 cartilages (thyroid, Hypopharynx S44'7+Staging
cricoid, arytenoid) means invasion is !" T1
likely !"1 subsite
!"Frank destruction with tumor on both !"< 2 cm
sides of cartilage best predictor !" T2
!" MRI !"> 1 subsite OR
!"If signal in cartilage is normal on T1, !"> 2 but < 4 cm
T2, and fat-saturated Gd images, NO !"/"(&3+A/-'3&(8L3)$"/
tumoral invasion !" T3
!"If signal is abnormal on T1, abnormal !"> 4 cm OR
on T2 but && than tumor, and if !";3+A/-'3&(8L3)$"/
enhancement more robust than tumor, !" T4a
2*3/-'#(3+'(&$D'&A(0,'()"($/43..3)$"/( !"Invasion of cartilage, cervical soft
tissues, thyroid gland
Extralaryngeal Extension [Figure 11]
!" T4b
!" Important indication for total
!"Invasion of prevertebrae fascia,
laryngectomy, vs nonsurgical treatment
encases carotida, mediastinal
!" Can directly invade through cartilage or
extension
extend through thyroid notch

Thyroid T?!%",57+Malignant
!" Central portion of VS !" Differentiated
!" Thyroid gland entirely encapsulated !"Papillary (60%-80%)
!" CT/MR and ultrasound routinely used in !"Follicular (5%, low grade)
evaluation !"Medullary (MEN IIA and IIB)
!" Thyroid lesions may present with !" Undifferentiated
!"Neck mass !"Anaplastic (10%, aggressive)
!"Hormonal, hypo- or hyperthyroid !" K.3-$/-(8/0$/-#
!"Airway compromise !"Intrathyroidal mass
!"Vocal cord paralysis !"Cervical adenopathy
!"Extracapsular invasion
T?!%",57+Benign vs Malignant !"Local extension
Characteristics #" Trachea
!" 9'/$-/(8/0$/-# #" IH strap muscles
!"Diffuse, enlarged, heterogeneous #" Tracheoesophageal groove
gland (goiter) #" Vocal cord paresis or palsy
!"Encapsulated and smooth
!"Colloid and adenomatous nodules are Papillary C'%/,."*'7+Thyroid [Figure 13]
common !" Young adult woman
!"No vocal cord paralysis !" Females >> Males
!"No metastatic nodes !" Painless thyroid nodule
!"Surgery only if sxs severe !" 90% 20-year survival
!"Goiter: check for retrosternal !" Adenopathy common
extension !"Heterogeneous
#" Scan with arms by side !"Ca++
!" <3&$-/3/)(8/0$/-# !"High density on CT
!"Extracapsular extension !"Enhancing
!"Local invasion !"May be hyperintense on T1-WI
!"Vocal cord paralysis: invasion of
recurrent laryngeal nerve
!"Cervical metastatic adenopathy
!"High suspicion if MEN or history of
neck radiation
Incidental Thyroid Lesion

!" 50% adults have thyroid nodule
!" 7'2$#$"/(+'-3+0$/-(8/'(/''0&'(3#!$+3)$"/(
usually determined by ultrasound
!" Incidence of cancer in nonpalpable
nodules = same as in palpable nodule Figure 13 A & B
!"Hh2"++'&3)'(I$)*(2&$/$23&(8/0$/-#i(/")( b'<3)7."8'9);,#%(@)6"+3%"##>)$"#$%&'()."44)%-)+%8?3)
recommended) thyroid lobe, without extension through capsule.
!" Worrisome features Right Image: Note bulky metastatic adenopathy and
enhancing right level IIA node.
!"Solid nodule with Ca++
!"C'/)+3&(4"I(3)(7"!!&'+(MdG
Semin Ultrasound CT MR. 2005;26:37-46.
Recommendations for FNA Anaplastic (Undifferentiated) Carcinoma

!" < 1 cm: no FNA
[Figure 14]
!" Entirely cystic: no FNA
!" Elderly, Females > Males
!" 1 cm: FNA if solid with micro Ca++
!" Thought to arise from differentiated
!" > 1.5 cm: FNA if solid with macro Ca++
carcinoma or multinodular goiter
!" > 2 cm: FNA if any solid component or
!" Large invasive thyroid mass
growth
!" Necrosis, hemorrhage common
Frates, et al. Radiology. 2005;237:794-800. !" Adenopathy common
!" Poor long-term prognosis

Figure 14
CT shows
heterogeneous
density both
thyroid lobes,
with bulky
necrotic
bilateral level
III nodes. Figure 17 A & B
Early (left image) and late (right image) CECT show
robust early enhancement with minimal washout in
CBT.
Carotid Space Lesions [Figure 15]
!" Carotid artery in origin
!"Dissection, aneurysm
!"Carotid body tumor: paraganglioma Schwannoma/N19%"#$%"*'+"3+4S+++++++
!" Jugular vein [Figure 18]
!"Thrombosis !" 7$682,&)(I$)*($.3-$/-()"(0$66'+'/)$3)'(
!" Vagus nerve #2*I3//".3(6+".(/',+"8%+".3
!"Glomus vagale: suprahyoid neck !" Infrahyoid schwannoma rare
!"E',+"8%+".3d#2*I3//".3 !" NF path: benign spindle cells
!" E',+"8%+".3("6)'/(&""D#(&"I(0'/#$)A1(
almost “cystic” without enhancement
!" From sympathetic chain or vagus nerve
Figure 15
!" Sporadic or associated with NF
Graphic shows
bilateral
carotid spaces
lateral to
thyroid and Figure 18
airway. Low density
nonenhancing
right carotid
space mass
displaces
CCA (arrow)
Infrhyoid N1/H7+Carotid Space [Figure 16] medially.
Infrahyoid N1/H7+Retropharyngeal
Space
!" Midline potential space
!" Behind visceral space
!" Extends from skull base to T3
!" Communicates with “danger space,”
extends to mediastinum
Figure 16 A & B !" Only content in infrahyoid neck is fat
Graphic shows lesion contained within carotid sheath. !" Lesions
;16'+&$%"#)-'$M)"*4$'44)G%3?)+%8?3)V181#"+):'%-)4'63%$) !"9'/$-/(4,$0
thrombosis (arrow). #" Blood – trauma
#" Jugular vein thrombosis
!"K/6'2)'0(4,$0
#" Check for discitis/osteomyelitis
Carotid Body Tumor, Paraganglioma
[Figure 17] Summary
!" Sporadic: may be bilateral !" Most common lesion in infrahyoid neck is
!" Multiple paragangliomas in other locations nodal disease
suggest familial type !" Larynx and hypopharynx
!" Tumor of glomus body !" Thyroid and parathyroid glands
!" Characteristic splaying of ECA/ICA at !" Carotid space
carotid bifurcation, tumor around vessels !" Retropharyngeal space

The Paranasal Sinuses

Summary Maxillary Sinus [Figure 1]
!" Anatomy, especially for endoscopic sinus !" Drainage
surgery (ESS) !"Ostium is at superomedial portion
!"Review sinus drainage pathways !"Drains into infundibulum
!" Infection !" Uncinate process
!"Acute bacterial !"Medial wall of ostium
!"Complications of sinusitis !"Located at insertion of inferior
!"Fungal: acute invasive vs allergic turbinate on lateral nasal wall
fungal !"Contiguous with lacrimal bone
!" Neoplasms anteriorly
!"Benign, including tumor-like lesions
!"Malignant
S,.9(7+Anatomy and Development

!" Nose and nasal cavities functions
!"V'#!$+3)$"/N(*,.$0$8'#(3/0(I3+.#(
inspired air
!"Defense: mucus blanket
!"F&632)$"/N(8%'+#(!3##()*+",-*(
cribriform plate to CN I
!" Nose: protective, external nose, pyriform
aperture Figure 1 A & B
!" Nasal septum: cartilage, ethmoid bone,
septum Maxillary sinus recesses.
Coronal sinus CT: Note uncinate processes (arrows).
!" Mucosa: serous and mucinous glands
!" “Mucoperiosteum”: mucosa attached to
bone Maxillary S,.9(7+Variants
!" Nasal cavities: internal nasal airways !" Hypoplasia: congenitally small
!" Turbinates !" Atelectatic: small volume acquired,
!"Inferior: nasolacrimal duct ,#,3&&A(36)'+(2*+"/$2($/43..3)$"/
!"Middle: maxillary, frontal, anterior !" C*+"/$2($/43..3)$"/
ethmoid !"Small volume
!"Superior: posterior ethmoid, sphenoid !"Thickened sclerotic walls
sinus !"If roof of sinus sags, enophthalmous
occurs “silent sinus syndrome”
Endoscopic Sinus Surgery
!" Haller cell: ethmoid cell at maxillary
!" Theory: mucosa is secondarily involved
ostium
%A($/43..3)"+A(0$#'3#'1(,#,3&&A(0,'()"(
sinus ostial obstruction Maxillary S,.9(7+Variants [Figure 2]
!" Surgically relieve obstructing lesion !" Haller cell
(polyp, anatomic variant, etc) will allow !"Inferior ethmoid cells at max sinus
sinus to drain normally and mucosal ostium
'0'.3(3/0($/43..3)$"/(I$&&($.!+"5' !"Usually incidental
!" Recurrent or chronic sinusitis should !"<3A("%#)+,2)(.3L$.,.(#$/,#(",)4"I
improve
!" Each individual sinus drainage pathway
important Figure 2
Maxillary Sinus [Figure 1] Bilateral

!" First to form, small at birth Haller cells,
!" Final pneumatization during second inferomedial
ethmoid
decade cells (circles)
!" Recesses between
!"Zygomatic uncinate
!"Palatine process
!"Alveolar: common location for benign (arrows) and
orbital wall.
cysts or polyps
Paranasal Sinuses 1219 Neuroradiology

Ethmoid Sinus [Figure 3] Frontal Sinus [Figure 5]
!" Bilateral !" Absent at birth, fully pneumatized in
!" Groups of cells formed by septa and second decade
lamella !" Essentially an anterior ethmoid cell
!" Anterior ethmoids !" Drainage: best on sagittal
!"Multiple small cells !"Frontal recess then
!"Drainage: Middle turbinate !"Ethmoid infundibulum
!" Posterior ethmoids !" Usually asymmetric, may be septated
!"Fewer but larger cells
!"Drainage: Superior turbinate
!" Basal lamella
!"Lateral insertion of middle turbinate
!"Separates ant- from postethmoids
Figure 3
Thick line
delineates
separation Figure 5 A & B
between
)_+,-3"#)+'$'44)%4)(%<&$1#3)3,)%('-3%<>),-)$,+,-"#)%."8'/))
anterior and
Note recess immediately behind the agger nasi cell
posterior
(short lines) on sagittal image.
ethmoid air
cells.
Ostiomeatal Complex/Unit [Figure 6]

!" Final drainage for frontal, max and ant.
ethmoid sinuses
Anterior Ethmoid S,.9(7+Anatomy !" Complex and variable anatomy
[Figure 4] !" Coronal and sagittal images
!" Boundaries !" Obstruction = recurrent or chronic sinus
!"Anterior: agger nasi cell infection
!"Lateral: lamina papyracea !"Maxillary ostium
!"V""6N(4""+("6(3/)'+$"+(#D,&&(%3#' !"Uncinate process
!" Frontal cells: small cells above the agger !"Frontal recess
nasi, single or multiple !"Ethmoid bulla
!" Ethmoid bulla: usually largest cell !"Middle turbinate
!" Drainage !"Middle meatus
!"Infundibulum, middle meatus
Normal ethmoid anatomy. Note agger nasi cells

(arrow) on coronal image on left. Note one cell above c43%,.'"3"#)$,.6#'U)%4)")$,.6#'U)1-%3)3?"3)%4)&-"#)
right agger nasi multiple small cells above left agger drainage pathway for ethmoids, maxillary and frontal
nasi cell. Note agger nasi (arrow) on sagittal image. sinus.

Sphenoid Sinus [Figure 7] !" Mucosal thickening may suggest acute
!" Extremely variable pneumatization sinusitis
!" Developmentally complete by second !"Moderate or severe
decade !"E"/#!'2$82
!" Planum sphenoidale, posterior and !"Thickened enhancing mucosa with
anterior walls, inferolateral and pterygoid submucosal edema
recesses !" @$+d4,$0(&'5'&#(
!" Anterior wall is roof of nasopharynx !"Frontal = sinusitis
!" Rarely nonpneumatized, consider anemia !"Maxillary = sinusitis in correct setting
or ciliary dysmotility syndrome !"Ethmoid: rare, usually complete
!" Drainage: sphenoethmoidal recess "!32$823)$"/1($/0$5$0,3&(2'&&#(3+'(#.3&&
!"G!*'/"$0N(/"/#!'2$82
Figure 7 Acute S,.9(,),(7+Complications

!" Local extension
Coronal CT !"Orbital: subperiosteal abscess
shows bilateral !"Intracranial: epidural or subdural
extensive
pneumatization empyema
into pterygoid !" Venous occlusion: cavernous sinus,
recesses transverse sinus (mastoiditis), superior
(arrows). Right sagittal sinus
sinus chamber
!" Chronic sinusitis
,6"$%&'(/
!"C*+"/$2($/43..3)"+A(0$#'3#'(6"+([(
weeks, despite antibiotics
!"Recurrent acute bouts of sinusitis
Final C?1/H7+Integrity of Skull Base, !"Chronic: patient has no periods
Lamina Papyracea [Figure 8]
without disease
!" Anterior ethmoid roof defect
S,.9(,),(7+Subperiosteal Infection
!"Check cribriform plate, lamella, roof
[Figure 9]
!"Defects may be congenital or acquired
(trauma, surgery, tumor, increased !" Most common local complication in
intracranial pressure) children and young adults
!" Sphenoid sinus wall defect !" Sxs: Preseptal swelling, discharge
!"Check all walls in axial, coronal, !" Postseptal infection best detected with
sagittal planes imaging
!"Defect may be congenital or acquired !" CECT is test of choice, to exclude post-
(trauma, spontaneous, tumor, & ICP) septal, subperiosteal abscess
!" May have orbital involvement without
destruction of bony orbital wall
Figure 8 A, B & C
Left Image: defect in left ethmoid roof with
meningocele.
Middle Image: defect in superior sphenoid sinus wall
(arrow) with small meningocele.
Right Image: defect in lamina papyracea.
I.31/),".7+Acute Sinusitis
!" No indications for imaging common cold
or clinically obvious sinusitis
!" Secondary bacterial sinusitis
!";/)6-'1.,-%"'@)`/)%-01'-a"'@)*'3"2
hemolytic strep
!" Sxs: facial pain, fever, nasal discharge
Figure 9 A & B
!" Clinical diagnosis
!" Ethmoids often primary source Orbital subperiosteal infection. Graphic and axial CECT
4?,G)'3?.,%(),6"$%&$"3%,-@)"-()6'+%6?'+"##>)'-?"-$%-8)
!" Usually asymmetric sinus involvement
mass in medial extraconal location
(Courtesy of Amirsys, Inc).
S,.9(,),(7+Intracranial Extension
[Figure 10]
!" Noncontrast sinus CT not enough Figure 12
!" Enhanced CT and MR are indicated for
Axial CT from
complicated sinusitis sinus study
!" Intracranial infection can occur without shows small
bone defect colloid cyst,
!" Subdural or epidural empyema very the likely
dangerous, patient usually sick out of explanation
for “sinusitis
proportion to size of collection symptoms.”
!" Cortical vein thrombosis may result in
parenchymal hemorrhage
Fungal Sinus D,(1'(17+Z+Types

!" Acute invasive
!"Immunosuppressed patient acute
pain, fever, local invasion
!"May be fulminant, rapidly progress
!"Spaces and soft tissues surrounding
sinuses and nasal cavity infected >
sinuses
!"Antifungal agents
Figure 10 A & B
!"Often treated surgically with local
Axial CECT shows small interhemispheric subdural resection, orbital exenteration
abscess. Note posterior frontal wall is intact on axial !"High mortality
bone CT. !" Allergic fungal
!"Immunocompetent
!"Clinically well
S,.9(,),(7+Intracranial Abscess !"Aspirin intolerance
[Figure 11] !"Chronic
!"Presents with nasal obstruction
!"Txed with endoscopic polyp resection
!"High rate of recurrence
Allergic Fungal Sinusitis with Polyps

(AFS-SNP) [Figures 13 & 14]
!" Immuno-competent, +/- eosinophilia
!" Chronic nasal obstruction, “recurrent
Figure 11 A, B & C
sinusitis”
T2, sagittal and axial post-Gd T1 MR images show !" Cycle of sinusitis, mucosal edema, polyp
right frontal abscess with surrounding edema. Low formation, ostial stenosis, sinusitis…
signal rim on T2-WI suggests abscess. Note thin !" Polyps
(1+"#)'-?"-$'.'-3@),6"$%&'()<+,-3"#)4%-14'4)"-()4,<3) !" CT
3%441')%-0".."3%,-/
!"`3/#$/,#d/3#3&(235$)A("!32$823)$"/
!"Expanded airless sinuses
Sinusitis “Mimics” [Figure 12] !"B*$/(0'"##$8'0(#$/,#(I3&&#
!" Be careful, aggressive sinus processes or !"Sinus contents variable in density,
intracranial lesions can present clinically may rarely Ca++
like simple bacterial sinusitis with nasal !"Mixed low and high density on
#),68/'##1(.$/"+('!$#)3L$#1(!3$/ noncontrast CT
!" Carefully look at extrasinus sites, for: !" MRI
!"Subarachnoid hemorrhage !"Extremely complex SI
!"Glial neoplasm !"May be & or % on T1
!"Meningioma !"Variable on T2, regions of frank signal
!"Colloid cyst void
!"Hydrocephalus !"T1 Gd shows enhancement of mucosa
!"Subdural hematoma but rarely sinus contents
!"Esthesioneuroblastoma !"Marked expansion may encroach on
!"Lymphoma of maxillary antrum surrounding structures, including orbit
!"SCCa maxillary sinus and skull base
!"Adenoid cystic CA

Fungal S,.9(,),(7+Invasive
[Figure 16]
!" Variable SI
!" May have dramatic % SI on T1 and T2
!" Heterogeneous enhancement pattern
!" Look for extension
!"Cavernous sinus
!"Orbit
!"Intracranial
Figure 13 A & B
Noncontrast CT shows massive expansion of ethmoid

and frontal sinuses with contents both low and high
density.
Complex, Left Image: Complex sinus contents on T2 with signal

mixed signal void (arrow) from fungal sinusitis.
intensity within Right Image: Intracranial extension on T1-Gd.
expanded
airless sinuses
on T2-WI
(Courtesy of Benign Sinus Lesions
Amirsys, Inc). !" No bone destruction
!" G$/,#(I3&&#(.3A(%'()*$//'0(3/0(0'"##$8'0
!" F6)'/(2"$/2$0'/)3&(#$/,#("!32$823)$"/
!"Obstructed sinus ostium = sinusitis
Fungal S,.9(,),(7+Invasive [Figure 15] #" Antrochoanal polyp
!" K..,/'(0'82$'/)1('#!'2$3&&A(0$3%')'# #" Mucocele
!" U3+&AN(/"/#!'2$82(!+'#'/)3)$"/ #" Fibrous dysplasia
!" CT: early #" Osteoma
!"Minimal sinus mucosal disease !"Benign but more aggressive
!"Nasal cavity soft tissue due to #" Juvenile nasopharyngeal
mucosal, septal or turbinate necrosis 3/-$"8%+".3(HXE@J
!" CT: late #" Inverted papilloma
!"Local invasion
#" Retroantral fat, cheek Antrochoanal Polyp [Figure 17]
!"Intracranial/orbital spread !" Benign maxillary polyp

!"Bone destruction !" Extends from maxillary antrum through
ostium into nasal cavity
!" When large, may extend to nasopharynx
!" Entire lesion must be removed to avoid
recurrence
Figure 15 A & B
Figure 17 A, B & C
Left Image: Axial CT shows small mass in posterior
left nasal cavity, necrotic sloughed mucosa. Antrochoanal polyp extending through left maxillary
Right Image: Axial CT shows cheek and retroantral fat ostium into nasopharynx.
induration. Note necrotic debris in nasal cavity.

Mucocele [Figure 18] F,$%""((1"9(7+Osteoma
!" “Airless, expanded sinus” !" Benign proliferation of mature bone
!" Sinus walls thinned, may appear !" Frontal and ethmoid sinus: most common
dehiscent location
!" Frontal, ethmoid, maxillary, sphenoid in !" Usually small and incidental
order of frequency !" May obstruct sinus ostium with sinusitis or
!" CT/MR signal intensity variable, mucocele formation
depending on age and protein content of !" CBN(.3A(%'(5'+A(0'/#'("+(."+'(8%+",#
secretions !" MR: % SI if primarily osseous
!"Early: % SI T1 & SI T2
!"Mid: & SI T1 & SI T2 Juvenile Nasopharyngeal A.-,"#$%"*'+
!"Late: & SI T1 %% SI T2 (JNA) [Figure 20]
!" Is mucocele secondary to mass at sinus !" Benign but aggressive vascular mass
ostium? !" Exclusively in men, usually adolescents
!" Presenting sxs depend on location
!"Nasal obstruction
!"Minor or major epistaxis
!"Facial asymmetry/deformity
!"Proptosis
!"Serous otitis media
!"Headache
!" Nasal cavity and nasopharyngeal mass
!" Expansion of pterygopalatine fossa (PPF)
!" Anterior bowing of posterior maxillary
sinus wall
Figure 18 A & B
T1 (left) and T2 (right) images show expanded, airless

right frontal sinus, mucocele.
Figure 20
!#"44%$)&-(%-84)
Fibrous Dysplasia [Figure 19] include
!" <'0,&&3+A(%"/'(+'!&32'0(%A(8%+""##'",#( nasal cavity/
tissue nasopharyngeal
mass, wide
!" Presents < 30 years PPF (arrow),
!" Facial asymmetry, especially cheek posterior
!" Most common: maxilla and mandible maxillary sinus
!" Obstruction of sinus ostium results in wall displaced
mucocele, especially ethmoid anteriorly.
!" Fibroosseous……
!" Therefore, often heterogeneous
!" CT: ground glass
!" MR: complex appearance
!"Mixed & and % SI
!"Enhances robustly – often leads to
misinterpretation as tumor
Figure 19 A & B
Monostotic (left image) and severe polyostotic (right

%."8'X)&*+,14)(>46#"4%"/

JNA [Figure 21] Sinonasal Malignant Neoplasms
!" Arises in posterior nasal cavity !" Location
!" Involves nasal cavity, nasopharynx (NP), !"Maxillary 70%
masticator space (MS), sphenoid sinus, !"Ethmoid 10%-20%
cavernous sinus !"Other (sphenoid, nasal cavity) 20%
!" Blood supply
!"ECA: int. max and asc. pharyngeal
arteries
!"ICA supply usually implies intracranial
extension
!"Both ipsi- and contralateral ECA/ICA
supply
Sinonasal Neoplasms
!" G$-/#d#Lq#(/"/#!'2$82
!" Present similar to “chronic sinusitis” or
Figure 21 A & B
“allergy”
!" Often present with unilateral nasal
Robustly enhancing JNA in nasal cavity, NP, MS, obstruction
left PPF, sphenoid sinus. Note left cavernous sinus !" Therefore, most are advanced stage at dx
invasion. !" Long delay to dx typical
!" Nodal mets uncommon at initial
Inverted Papilloma [Figure 22] presentation, but increase with recurrence
!" Epithelial tumor of mucosa
!" Endophytic growth pattern Malignant Sinus Lesions
!" Benign appearing mass in nasal cavity/ !" Squamous cell carcinoma (most common)
middle meatus !" Glandular origin
!" Associated with SCCa 10%-20% of time !"Adenocarcinoma
!" Bone remodeling without destruction !"Mucoepidermoid carcinoma
!" On MR !"Adenoid cystic carcinoma
!"Enhancement !" Olfactory neuroblastoma
!"Convoluted cerebriform pattern (esthesioneuroblastoma)
!" Sinonasal undifferentiated carcinoma
(SNUC)
!" Melanoma
!" Lymphoma
!" COMMON IMAGING FINDINGS
!"Bone destruction
!"Local extension/invasion
!"Intracranial extension
Most Important Imaging G"'&7+

Extension of Disease [Figure 23]
Figure 22 A & B
CECT and Gd + enhanced MR show characteristic

“cerebriform” pattern of enhancement.
Sinonasal Malignant Neoplasms

!" 3%-4% head and neck tumors
!" M:F = 2:1
!" Most common > 50 years Figure 23 A & B
!" Risk factors – ? Chronic sinusitis?
!"HPV, EBV, HIV Graphics show patterns of spread of sinus malignancy.
!"Inverted papilloma
!"+/- smoking
!"Wood, leather, textile, etc
Sinonasal S)'-,.-7+Critical Findings
!" Primary site
!"Where did tumor arise?
!"Size
!"Bone: maxillary or orbit walls, skull
base
!"Local: cheek, nasal cavity,
nasopharynx, orbit
!"Intracranial
#" Smooth interface suggests extra-
dural
Figure 25 A & B
#" Irregular borders suggests dural
invasion Subtle erosion of planum sphenoidale on CT (arrow)
from nasal cavity and sphenoid sinus SCCa.
Most Important Imaging G"'&7+ Note on T2 the tumor is lower SI than benign
Extension of Disease [Figure 24] secretions in mastoid/middle ear.
Malignancies of Glandular Origin

!" 10% of all sinus malignancies
!" Typical local extension and bony erosion
!" May be & SI on T2
!"Adenocarcinoma
!"Adenoid cystic CA
#" Propensity for perineural spread
#" Check all foramen, especially
vidian canal, foramen rotundum,
foramen ovale
!"Mucoepidermoid CA
Figure 24 A & B
Adenoid Cystic CA
Left Image: Extension through medial orbital wall !" Sinus mass with osseous erosion
(arrows), sphenoid sinus invasion (arrowhead).
Right Image: Intracranial extension (arrow).
!" Perineural spread
!"Widened foramen or canal
!"Enlarged enhancing nerve
!"Obliteration of fat at skull base
SCCa Staging (Maxillary)
foramen
!" T1: Antral mucosa without bone
destruction or erosion E()?1(,".19%"$&'()"*'7+'H'+Olfactory
!" T2: Hard palate or sinus walls
Neuroblastoma
!" T3: Cheek, orbital walls, pterygoid plates,
!" Tumor of neural crest origin
ethmoids
!" Accounts for 2% of sinonasal
!" T4: Skull base (cribriform plate
malignancies
or sphenoid sinus), frontal sinus,
!" Arises in nasal cavity near cribriform plate
nasopharynx, orbital apex
!" Age range: 3 years to elderly
!" Nasal cavity mass, erosion of cribriform
Malignant S,.9(7+SCCa [Figure 25]
plate, often with intracranial extension
!" Most arise in max sinus or nasal cavity
!" Peripheral intracranial tumoral cysts
!" Males > Females, adults > 50 years
!" Usually advanced at detection
!" Obstructed sinus secretions may make
imaging appearance complex
!" CT: bone thinning or destruction
!" MR: T2 differentiates tumor from benign
secretions
!"Tumor: % SI
!"Secretions: & SI

Malignant Characteristics Summary
[Figure 26] !" Sinus development and variants
!" Bone destruction !" Anatomy, especially for endoscopic sinus
!" Local invasion surgery (ESS)
!" Restricted diffusion !" Infection
!" Esthesioneuroblastoma !"Acute
!"Complications
!"Fungal: invasive and noninvasive
!" Neoplasms
!"Benign, including tumor-like lesions
!"Malignant
Figure 26 A, B & C
CT and MR show enhancing sinus mass, intracranial
extension and restricted diffusion.
References
1. Meyers RM, et al. Interpretation of anatomic variations of computed tomography scans of the sinuses: a
surgeon’s perspective. Laryngoscope 1998;104:422-5.
2. Younis RT, et al. The role of computed tomography and magnetic resonance imaging in patients with
sinusitis with complications. Laryngoscope 2002;112(2):224-9.
3. Eustis HS, et al. MR imaging and CT of orbital infections and complications in acute rhinosinusitis. Radiol
Clin North Am 1998;36(6):1165-83.
4. 7'&\3,0$"(X<1(')(3&T(C".!,)'0()"."-+3!*$2(8/0$/-#($/(!3)$'/)#(I$)*($/53#$5'(6,/-3&(#$/,#$)$#T(@+2*(
Otolaryngol Head Neck Surg 2003;129(2):236-40.
5. <,D*'+a$(GS1(')(3&T(@&&'+-$2(6,/-3&(#$/,#$)$#N(CB(8/0$/-#T(V30$"&"-A(Z==QYO>PHOJN]ZPWOOT
6. C*,/-(GS1(')(3&T(G,+-$23&1(+30$"&"-$21(3/0(*$#)"&"-$2(8/0$/-#("6()*'(3/)+"2*"3/3&(!"&A!T(@.(X(V*$/"&(
2002;16(2):71-6.
7. Loevner LA, et al. Imaging of neoplasms of the paranasal sinuses. Magn Reson Imaging Clin N Am
2002;10(3):467-93.
8. Li C, et al. Olfactory neuroblastoma: MR evaluation. Am J Neuroradiol 1993;14(5):1167-71.

1228
Lymphoma and Uncommon Neuroepithelial Tumors

CNS Lymphoma Histopathology [Figure 2]
!" 6.6%-15.4% of all primary brain tumors !" “Small blue cell tumor”
!" Only GBM, meningioma, and low-grade !" Almost always B-cell type
astrocytoma are more common !" Perivascular space
!"Less than 1% of all body lymphomas Koeller, et al. RadioGraphics. 1997;17:1497-
!" Primary lymphoma much more common 1526.
than secondary
Miller, et al. Cancer. 1994;74:1383-1397.
Henry, et al. Cancer. 1974;34:1293-1302.
Figure 2
Clinical
!" Wide age range Perivascular
!"`'3DN(6",+)*()"(86)*(0'230'# distribution
of small blue
!"G.3&&'+(!'3DN(8+#)(0'230'(H@K7GJ lymphocytes
!" E"/#!'2$82(2&$/$23&(!+'#'/)3)$"/ (arrow, blood
!"Expanding mass lesion vessel).
!"Encephalitis
!"Stroke
!"Cranial nerve palsies
Koeller, et al. RadioGraphics. 1997;17:1497-526. CT/MR Findings [Figures 3 to 5]
!" NCCT: Hyperattenuated mass
Immunocompromised Patients !"Negative CT does not exclude
!" “Opportunistic neoplasm” diagnosis
!"Incidence much higher than in !" MR:
immunocompetent patients !"T1-WI: iso-to-hypointense to gray
!" @K7GW0'8/$/-(0$3-/"#$#($/(kK_p(!3)$'/)# matter
!" 2% of AIDS patients develop CNS !"T2-WI: hypointense
lymphoma !"Little mass effect for size of lesion
!" CNS mass lesion in AIDS patient !" Virtually all enhance
!"Toxoplasmosis #1, lymphoma #2 !"Ring-like: necrosis; common in
!"Lymphoma: #1 in pediatric AIDS immunocompromised hosts
patient Lee, et al. AJR. 1986;147:747-752.
Rosenblum, et al. Ann Neurol. 1988:23:S13-S16. Schwaighofer, et al. AJNR. 1989;10:725-729.
Koeller, et al. RadioGraphics. 1997;17:1497-526. Dina. Radiology. 1991;179:823-828.
Gross Pathology [Figure 1]

!" Intra-axial nodule
!"Grayish-pink, homogeneous,
circumscribed
!"Multifocal: 50%
!" Leptomeningeal
!" Uveal
!" Intradural spinal
Koeller, et al. RadioGraphics. 1997;17:1497-526.
Figure 1
Two masses,
both
lymphoma,
with one
located around Figure 3 A & B
the ventricle
while the other Lymphoma with characteristic CT hyperattenuation
arises from the and T2 hypointensity.
leptomeninges.
Lymphoma and Uncommon Neuroepithelial Tumors 1229 Neuroradiology

Figure 6
Lymphoma of right
basal ganglia.
Figure 4 A & B
CNS lymphoma with true water restricted diffusion.
Left Image: DWI hyperintensity
Right Image: ADC hypointensity.
PET/SPECT-Thallium [Figure 7]
!" Hypermetabolic
!" Non-neoplastic lesions: hypometabolic
!" k$-*(#!'2$82$)A(3/0(#'/#$)$5$)A
!" False positives: interpretation errors,
occasional hypermetabolic abscess
Hoffman, et al. J Nucl Med. 1993;34:567-575.
Villringer, et al. J Comput Assist Tomogr.
1995;19:532-536.
Figure 5 A & B
Lymphoma in AIDS patient with ring-like

enhancement secondary to necrosis.
General Neuroimaging Features

[Figure 6]
!" Supratentorial location
!"Deep gray matter: “classic”, 33%
!"Cerebral white matter: 55%
!"Cerebellar lesions: 10%
!" Multiple lesions: 11%-47% Figure 7 A, B & C
!"More common in immunocompromised
Toxoplasmosis or
!" Recurrences: 50% at original site lymphoma? PET image
Koeller, et al. RadioGraphics. 1997;17:1497- shows hypermetabolic
1526. activity consistent with
lymphoma.
General Neuroimaging Features
!" “Hugs” ependyma or leptomeninges
!" h9,))'+4Ai(!3))'+/N(2"+!,#(23&&"#,.
!" “Ghost” tumor: vanishes with steroid or
radiation therapy
!"Avoid prior to biopsy
!" V3+'N(23&2$823)$"/1(*'."++*3-'
Jiddane, et al. J Neurosurg. 1986;65:592-599.
Vaquero, et al. J Neurosurg. 1984;60:174-176.

Neuroepithelial Tumors Ganglioglioma [Figure 9]
!" Astrocytic !" Typically peripheral mass
!"Pleomorphic xanthoastrocytoma !"Cyst-like/solid: 52%
!" Oligodendroglial !"Solid: 43%
!" Mixed glial !"Purely cyst-like: 5%
!" Ependymal !" Little mass effect or surrounding edema
!" Choroid plexus !" C3&2$823)$"/(2".."/
!" Pineal parenchymal !" Skull remodeling
!" Neuroblastic !" Enhancement variable
!"Glial of uncertain origin Zentner, et al. AJNR. 1994;57:1497-502.
!"Neuronal and mixed neuronal-glial Dorne, et al. AJNR. 1986;7:281-5.
!"Ganglioglioma/gangliocytoma Castillo, et al. AJNR. 1990;11:109-14.
!"Desmoplastic Infantile ganglioglioma
!"Dysplastic cerebellar gangliocytoma
!"Dysembryoplastic neuroepithelial
tumor
!" Embryonal
!"Supratentorial PNET
!"Atypical teratoid/rhabdoid tumor
Figure 9
Ganglioglioma/Gangliocytoma
Ganglioglioma
!" About 1% of all brain tumors with typical
!" Children and young adults peripheral
!"80% < 30 years old; peak: 10-30 location and
years of age $"#$%&$"3%,-/
!"Men slightly more common
!" Most common tumor seen in chronic
temporal lobe epilepsy
!"15%-25% of medically refractory
seizures
!" Cerebral hemisphere predilection
!"Temporal lobe: most common (38%)
!"Optic nerves, pituitary and pineal
glands, spinal cord, ventricles, cranial
nerve (1 report) Ganglioglioma [Figures 10 to 12]
Johnson, et al. Pediatr Neurosurg. 1997;27:203- !" BA!$23&(<V(8/0$/-#
207. !"T1-WI: iso-to-hypointense
Athale, et al. Neuroradiology. 1999;16:790-792. !"T2-WI: hyperintense
!"Occasional T1 hyperintensity
Ganglioglioma/Gangliocytoma [Figure 8] !"May or may not enhance
!" Good prognosis overall !" Leptomeningeal spread: rare
!" Ganglioglioma: WHO I or II Castillo, et al. AJNR. 1990;11:109-114.
!"Biphasic tumor: neoplastic ganglion Tampieri, et al. AJNR 1991;12:749-755.
cells and glial cells Tien, et al. AJR. 1992;159:391-393.
!"Malignant degeneration of glial cells
(WHO III): 6%
!" Gangliocytoma
!"Only mature ganglion cells
!"WHO grade I
!"AFIP: really cortical dysplasia?
Silver, et al. Surg Neurol. 1991;35:261-266.
Kalyan, et al. Neurosurgery. 1987;20:428-433.
Figure 8
Ganglioglioma
with biphasic Figure 10 A, B & C
appearance on
histology. Arrow Ganglioglioma in temporal lobe.
points to a
ganglion cell.

Desmoplastic Infantile Ganglioglioma /
Astrocytoma [Figure 13]
!" WHO grade I
!" Desmoplastic stroma
!"Neuronal component: ganglioglioma
!"Neoplastic astrocytes: astrocytoma
!" Meningocerebral: involves cortex and
leptomeninges
Duffner, et al. Neurosurgery. 1994;34:583-589.
Figure 13
Desmoplastic
Figure 11 A & B infantile
Large ganglioglioma. ganglioglioma.
Desmoplastic Infantile Ganglioglioma/

Astrocytoma [Figures 14 & 15]
!" Large heterogeneous mass
!" Cyst-like areas
!" G,!'+82$3&(#"6)()$##,'(3+'3
!"Slightly hyperattenuated
!"Isointense compared to brain
!"Frequently attached to dura
!"Intense enhancement
!" E"(23&2$823)$"/
!" Occasional vasogenic edema
Duffner, et al. Neurosurgery 1994;34:583-9.
Martin, et al. AJNR. 1991;12:1195-1197.
Tenreiro-Picon, et al. Pediatr Radiol.
1995;25:540-543.
Figure 12 A & B
Ganglioglioma in medial portion of right temporal lobe.
Ganglioglioma
!" Positron Emission Tomography (PET):
heterogeneous metabolic activity
!" MR Spectroscopy: increased choline-
creatine ratio
Desmoplastic Infantile Ganglioglioma

(DIG)/Astrocytoma
!" First described in 1987
!"hG,!'+82$3&(2'+'%+3&(3#)+"2A)".3i
!"“Desmoplastic cerebral astrocytoma of
infancy”
!" Rare: 0.6% of brain tumors
!"16% of all infant brain tumors Figure 14 A & B
!"Vast majority: less than 1 year DIG with intensely enhancing soft tissue component
(range: up to 17 years) along meningocerebral interface.
!"Males more common (2:1)
!" Rapid onset: increasing head
circumference
!" Usually more than one lobe: typically
frontal and parietal

Dysplastic Cerebellar Gangliocytoma
(Lhermitte-Duclos Disease) [Figure 16]
!" <V(8/0$/-#
!" “Classic” appearance
!"Cerebellar mass
!"“Striated”
!"No edema
!"No enhancement
!"E"/2&3##$2(23#'#N(/"/#!'2$82(
appearance
Meltzer, et al. Radiology. 1995;194:699-703.
Figure 15 A & B
DIG with intensely enhancing soft tissue component
along meningocerebral interface.

(Lhermitte-Duclos Disease)
!" Original case, 1920 (Lhermitte and
Duclos)
!" A 36-year-old man with progressive
/',+"&"-$2(0'82$)#
!"Cerebellar mass: “diffuse
ganglioneuroma”
!" Dysplastic cerebellar gangliocytoma
!"Numerous other names proposed
!" Histogenesis: hamartoma vs neoplasm Figure 16 A & B
!"Hamartoma favored Classic “striated cerebellum” appearance in Lhermitte-
Duclos disease.
Lhermitte, Duclos. Bull Assoc Fr Etude Cancer.
1920;9:99-107; Wiestler, et al. WHO C#"44%&$"-
tion, 2000;235-237.
(Lhermitte-Duclos Disease) !" T1 hypointensity/T2 hyperintensity:
!" 50%: Cowden disease #" Inner molecular layer, granular
!"Autosomal dominant: susceptibility cell layer, and loss of central white
gene 10q23 matter within folia
!"Colonic polyps, cutaneous tumors,
thyroid tumors, breast tumors, Kulkantrakorn, et al. Neurology. 1997;48:725-
meningioma, glioma 731.
!"MR screening of family members
Dysembryoplastic Neuroepithelial
recommended
!"Diagnosis established when Lhermitte- Tumor
Duclos combined with either: !" First described in 1988 (Daumas-Duport,
#" Thyroid cancer et al)
#" Breast cancer !" Benign tumor of cortex or deep gray
#" Macrocephaly matter
!" Children and young adults with partial
Robinson and Cohen. Neurosurgery seizures
2000;46:371-83; Kulkantrakorn, et al. Neurol- !"Peak age: 10-30 years
ogy. 1997;48:725-31; Nelen, et al. Nat Genet. !"Males more common
1996;13:114-116. !" E',+"&"-$2(0'82$)#(/")(2".."/
!" Excellent prognosis even with partial
resection
!"Very rare malignant transformation
!" CB(8/0$/-#
!"Usually slightly hypoattenuated Daumas-Duport, et al. Neurosurgery.
!"Isoattenuated: “normal” 1988;23:545-56.
!"C3&2$823)$"/(,/2".."/ Daumas-Duport, et al. WHO C#"44%&$"3%,-/)JQQQD)
Hammond, et al. J Neurosurg. 2000;92:722-725.
Meltzer, et al. Radiology. 1995;194:699-703.
Tumor [Figure 17]
!" WHO Grade I Figure 17
!" Simple form vs complex form:
controversial DNT with
O0,"3%-8)
!" Multinodular: complex form neuron.”
!" Cortical dysplasia: focal
!" hG!'2$82(-&$"/',+"/3&('&'.'/)Ni(2"&,./3+(
pattern
!"h:+''&A(4"3)$/-(/',+"/#i
!" Temporal lobe: 62%
!"Frontal lobe: 31%
!"Other sites: caudate nucleus,
cerebellum, pons
Daumas-Duport, et al. Neurosurgery.
1988;23:545-556.
Daumas-Duport, et al. WHO C#"44%&$"3%,-/)JQQQ/
Tumor [Figure 18]
!" CB(8/0$/-#
!"Hypoattenuated
!"C3&2$823)$"/N(,/2".."/((Hr(R?J
!"May remodel skull
!"No surrounding edema
!"May or may not enhance
!" <V(8/0$/-#
!"T1-WI: hypointense
!"T2-WI: hyperintense
!"May or may not enhance
!"Occasional “soap bubble” appearance
!"More multinodular than ganglioglioma?
Koeller, Dillon. AJNR. 1992;13:1319-25; Kuroi-
wa, et al. JCAT, 1994;18:352-6; Ostertun, et al.
AJNR. 1996;17:419-430.
Pleomorphic Xanthoastrocytoma
!" *Originally described in 1979
!"12 cases of supratentorial tumors
involving the leptomeninges
!" Believed to arise from subpial astrocytes
of the cortex
!" Less than 1% of all brain neoplasms
!" Importance: characteristic imaging
appearance, highly amenable to surgical
resection
*Kepes, et al. Cancer. 1979:44:1839-1852.
!" Usually adolescents or young adults
(average age: 26 years)
!"Wide age range: 5-82 years
!" No gender predilection
!" Long history of seizures
!" Supratentorial: 98%
!"Temporal lobe: 47%
!"Multi-lobe: 10%
!"Rare: thalamus, cerebellum, spinal
cord, orbital globe
Figure 18 A to F
Giannini, et al. Cancer. 1999;85:2033-45.
Pahapill, et al. Neurosurgery. 1996;38:822-829. DNT in classic cortical location and showing exophytic
extension with pressure erosion of inner table of skull.

[Figure 19]
!" WHO Grade II
!"Pleomorphism
!"“Lipidized” neoplastic glial cells:
xanthoma-like
!"Overall good prognosis
#" 81% 5-year survival
#" 70% 10-year survival
!"Higher recurrence rate
!" Malignant transformation: 20%
Kepes, et al. WHO C#"44%&$"3%,-)JQQQDdJ2dT/)
Giannini, et al. Cancer. 1999;85:2033-2045.
Figure 19
Figure 20 A & B
PXA with PXA as large heterogeneous mass and enhancing soft
vacuoles tissue component.
secondary
to
“lipidized”
neoplastic Supratentorial Primitive
glial cells. Neuroectodermal Tumor
!" E"/#!'2$82(2&$/$23&(6'3),+'#(+'&3)'0()"(#$)'
!"Cerebrum: seizures, increased
$/)+32+3/$3&(!+'##,+'1(.")"+(0'82$)#
Pleomorphic Xanthoastrocytoma !"Suprasellar region: visual or endocrine
[Figure 20] problems
!" “Classic:” large cyst-like lesion with an !"Not pineal: pineoblastoma
enhancing mural nodule (< 50%) !" Poor prognosis, especially in children < 2
!" Meningocerebral location years old
!"<'/$/-'3&($/8&)+3)$"/(+3+' !"34% 5-year survival rate (85% for
!"Cortical involvement common cerebellar medulloblastoma)
!"Perivascular space extension
Rorke, et al. WHO C#"44%&$"3%,-/)JQQQDSTS2STT/
!" C3&2$823)$"/(+3+'
!" Usually no surrounding edema Supratentorial Primitive
Tien, et al. AJR. 1992:159:1397-1404. Neuroectodermal Tumor
Lipper, et al. AJNR. 1993;14:1397-1404. !" WHO grade IV
Pahapill, et al. Neurosurgery. 1996;38:822-829. !" Virtually identical to medulloblastoma
!" Undifferentiated or poorly differentiated
Pleomorphic Xanthoastrocytoma neuroepithelial cells
[Figure 20] !" Dense cellularity: “small blue cell tumor”
!" <V(8/0$/-# !"Pleomorphism
!"Heterogeneous mass !"Rosette formation
!"T1-WI: hypo-to-isointense
!"T2-WI: hyper-to-isointense Rorke, et al. WHO C#"44%&$"3%,-/)JQQQDSTS2STT/
!"Soft tissue component usually
enhances intensely
!"Leptomeningeal enhancement:
characteristic
Lipper, et al. AJNR. 1993;14:1397-1404.
Supratentorial Primitive
Neuroectodermal Tumor
!" “Cerebral medulloblastoma”
!" 1% of all pediatric CNS neuroepithelial
tumors
!"6% of all pediatric PNETs
!" Age range: 4 weeks to 10 years (mean
age: 5.5 years)
!"Boys more common (2:1)
Rorke, et al. WHO C#"44%&$"3%,-/)JQQQDSTS2STT/

Supratentorial Primitive Atypical Teratoid/Rhabdoid Tumor
Neuroectodermal Tumor [Figure 21] !" 2.1% of all primary CNS tumors in
!" Large heterogeneous mass children
!"CT: iso- to hyperattenuated !" 94%: < 5 years old
!"Cysts or necrosis common !"Rarely presents in adults (4 cases)
!"C3&2$823)$"/N(R>?WP>? !"Boys more common (1.4:1)
!"Vasogenic edema present but not !" E"/#!'2$82(#A.!)".#
usually extensive !" Lethargy, failure to thrive
!"T1-WI: hypointense to gray matter !" Head tilt
!"T2-WI: hypointense predominantly !" Cranial nerve palsy: usually VI or VII
Rorke, et al. WHO C#"44%&$"3%,-/)JQQQDSTS2STT/ Rorke, Biegel. WHO C#"44%&$"3%,-/)JQQQDSTd2Z/)
Burger, et al. Am J Surg Pathol. 1998;22:1083-
1092.
Atypical Teratoid/Rhabdoid Tumor

!" WHO grade IV
!" Soft lobulated mass
!"Necrosis and hemorrhage common
!" Rhabdoid cells
!"Mixed with primitive neuroepithelial,
epithelial, and mesenchymal elements
!"Not a germ-cell tumor
!" Poor prognosis: most die within one year
Rorke, Biegel. WHO C#"44%&$"3%,-/)JQQQDSTd2Z/

[Figure 22]
!" Posterior fossa: most common location
(52%)
!"Especially cerebellopontine angle
!" Supratentorial: 39%
!"Including intraventricular
!" Pineal: 5%
!" Spinal: 2%
!" Multifocal: 2%
Rorke, Biegel. WHO C#"44%&$"3%,-/)JQQQDSTd2Z/
Supratentorial PNET with CSF dissemination.
Figure 22
!" First reported in 1978 Posterior
fossa ATRT.
!" Various names
!"“Rhabdomyosarcomatoid variant of
Wilms tumor”
!"“Embryonal small cell tumor”
!"“Rhabdoid tumor”
!" Biologic behavior and some histologic
features similar to malignant rhabdoid
tumor of the kidney (sometimes
associated)
Beck, Palmer. Cancer. 1978;41:1937-48.
Rorke and Biegel. WHO C#"44%&$"3%,-/)JQQQDSTd2
148.
Rorke, et al. J Neurosurg 1996;85:56-65.
Hanna, et al. AJNR. 1993;14:107-115.

Atypical Teratoid/Rhabdoid Tumor S9**'%!7+Lymphoma
[Figure 23] !" Rapid increase in prevalence
!" Imaging: often mimics medulloblastoma !" Fourth most common primary cerebral
!" CT: hyperattenuated neoplasm
!"Cysts and hemorrhage common !" Second most common intracranial mass in
!"Vasogenic edema common immunocompromised patient
!"Variable enhancement !" Periventricular
!" CT: hyperattenuated
Hanna, et al. AJNR. 1993:14:109-114.
Caldemyer, et al. Pediatr Neurosurg. 1994;21: !" T2-W: hypointense
232-236.
Rorke, Biegel. WHO C#"44%&$"3%,-/)JQQQDSTd2
Peripheral Mass
148. !" Ganglioglioma
!"_3+$3%&'(#$f'(I$)*(2".."/(23&2$823)$"/
Atypical Teratoid/Rhabdoid Tumor !"Most common tumor cause of chronic
[Figure 23]
temporal lobe epilepsy
!" Large heterogeneous mass !"Gangliocytoma: lacks glial component
!" <V(8/0$/-# !" Dysembryoplastic neuroepithelial tumor
!"T1-WI: hypo-to-isointense (DNT)
!"T2-WI: variable !"Almost always involves cortical margin
#" Soft tissue: iso-to-hypointense !"M/2".."/(23&2$823)$"/
#" Cyst-like: hyperintense !"Temporal lobe: 62%
!"Heterogeneous enhancement !"“Soap bubble” appearance
!"Subarachnoid seeding: 33% at
Cerebellar Mass
presentation
!" “Striated” cerebellar mass
Hanna, et al. AJNR. 1993;14:109-115. !"Dysplastic cerebellar gangliocytoma
Rorke, Biegel. WHO C#"44%&$"3%,-/)JQQQDSTd2STZ/ (Lhermitte-Duclos)
Large Heterogeneous Mass

!" Meningocerebral interface
!"Desmoplastic infantile ganglioglioma
#" Large heterogeneous cerebral
hemisphere mass
#" E"(23&2$823)$"/
!"Pleomorphic xanthoastrocytoma
#" “Cyst-like mass with enhancing
mural nodule”
#" C3&2$823)$"/(+3+'
#" Older patients: adolescents and
young adults
Large Heterogeneous Mass

!" Young child
!"Supratentorial PNET
#" Large heterogeneous cerebral
hemispheric mass
#" “Cerebral medulloblastoma”
!" Atypical teratoid/rhabdoid tumor
#" Mimics medulloblastoma
#" Predilection for foraminal extension
in posterior fossa
#" Subarachnoid seeding common
Posterior fossa ATRT. Hyperattenuation on CT is similar

to medulloblastoma but shows foraminal extension on
MR images.

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50. B$'/(V71(C3+0'/3#(C@1(V3a3-"!3&3/(GT`&'"."+!*$2(L3/)*"3#)+"2A)".3("6()*'(%+3$/N(<V(8/0$/-#($/(#$L(
patients. AJR Am J Roentgenol 1992 Dec;159(6):1287-90.
51. Tien RD, Tuori SL, Pulkingham N, Burger PC.Ganglioglioma with leptomeningeal and subarachnoid spread:
results of CT, MR, and PET imaging. AJR Am J Roentgenol 1992 Aug;159(2):391-3.
52. VandenBerg SR, May EE, Rubinstein LJ, et al. Desmoplastic supratentorial neuroepithelial tumors of
infancy with divergent differentiation potential (“desmoplastic infantile gangliogliomas”). Report on 11
cases of a distinctive embryonal tumor with favorable prognosis. J Neurosurg 1987;66:58-71.
53. Vaquero J, Martinez R, Rossi E, Lopez R. Primary cerebral lymphoma: the “ghost tumor”. Case report. J
Neurosurg 1984;60:174-6.
54. Villringer K, Jager H, Dichgans M, et al. Differential diagnosis of CNS lesions in AIDS patients by FDG-PET.
J Comput Assist Tomogr 1995;19:532-6.
55. Wiestler OD, Padberg GW, Steck PA. Cowden disease and dysplastic gangliocytoma of the cerebellum/
;*'+.$))'W7,2&"#(0$#'3#'T(K/N(S&'$*,'#(`1(C35'/''(bS1('0#T(b"+&0(k'3&)*(F+-3/$f3)$"/(C&3##$823)$"/("6(
Tumours: Pathology and genetics of tumours of the nervous system. Lyon, France: IARC, 2000;235-7.
56. c'/)/'+(X1(b"&6(kS1(F#)'+),/(91(')(3&T(\3/-&$"-&$".3#N(2&$/$23&1(+30$"&"-$23&1(3/0(*$#)"!3)*"&"-$23&(8/0$/-#(
in 51 patients. J Neurol Neurosurg Psychiatry. 1994;57:1497-502.

1240
K*'-,.-+"3+)?1+J1*0"%'&+:".17+L.')"*!+'.5+4".-1.,)'&+G1(,".(

Middle Ear
!" Epitympanum Figure 3
!"Malleus head
Superior
!"Short process of incus portion of
!" Mesotympanum vestibule
!"Muscles: tensor tympani (V3), with malleus
stapedius (VII) (anterior)
and incus
!"Ossicles: rest of malleus and incus, (posterior)
stapes within the
!"Ligaments epitympanum.
!"Nerves: chorda tympani (VII),
Jacobson nerve (IX)
Figure 4
I..1%+='%7+Cochlea
!" Anterior to vestibule Superior
!" Promontory: bony ridge portion of
!" Modiolus: central axis, cochlear nerve internal
auditory
!" Apex (cupola)
canal with
!" Basal turn labyrinthine
!" Cochlear aqueduct: perilymphatic duct canal
containing the
I..1%+='%7+Vestibule facial nerve
!" Posterior to cochlea on its way to
the geniculate ganglion and tympanic facial segment
!" Oval window niche: partition from middle along medial wall of middle ear.
ear
!" Lamina cribrosa: partition from internal
auditory canal (IAC)
!" Vestibular aqueduct: endolymphatic duct Figure 5
I..1%+='%7+Semicircular Canals (SCC) Superior

portion of
[Figures 1 to 15] cochlea and
!" Lateral (horizontal) internal
!" Superior: arcuate eminence auditory
!" Posterior canal. Note
vestibular
!" Oriented ~90 degrees to each other aqueduct
!" Rotational acceleration arising from
posterior margin of temporal bone.
Figure 1
Axial CT at Figure 6
superior
portion of Mid-portion
temporal of internal
bone shows auditory
lumen of canal and
superior cochlea.
semicircular Sinus
canal and tympani is
upper portion of mastoid antrum and epitympanum. located just
lateral to
Figure 2 vestibule.
Small bony peak lateral to vestibule is pyramidal
Subarcuate eminence. Facial nerve canal is located
artery canal posterolateral to pyramidal eminence. Middle
traversing ear shows “parallel lines sign:” tensor tympani
through tendon anteriorly and incudostapedial junction with
“hoop” of stapedial struts posteriorly. Struts mark the site of
superior the oval window.
semicircular
canal.
Temporal Bone Anatomy and Congenital Lesions 1241 Neuroradiology

Figure 11
Figure 7
Cochlea is
separated
Inferior by cochlear
portion of promontory
cochlea. from middle
Bony plate ear. Anterior
separating portion of
it from the internal
middle ear is auditory canal
the cochlear is just coming
promontory. into view. Scutum is well seen along superior margin
Note jugular bulb in posterior temporal bone. of medial external auditory canal.
Figure 8
Figure 12
Basilar turn
of cochlea. Mid-portion
Internal of internal
carotid artery auditory canal
is seen with crista
anterior to falciformis
the cochlea along its
and is lateral margin.
delimited Vestibule now
from appears with
the middle ear by a bony plate. Eustachian tube lateral and
arises just lateral to the artery and heads along an superior semicircular canals. Facial nerve is located
anteromedial pathway towards the nasopharynx. immediately inferior to lateral semicircular canal and
above oval window.
Figure 9
Coronal
Figure 13
view shows
internal
Posterior
carotid artery
margin of
inferiorly
vestibule with
separated
facial nerve
from middle
as small
ear by bony
soft tissue
plate. Cochlea
just prior
is located
to reaching
immediately
posterior
superior. Geniculate ganglion is located just
genu.
superolateral to cochlea. Middle ear contains ossicles
(malleus anterior to incus) within epitympanum.
Tegmen tympani is bony plate separating middle ear
from brain.
Figure 14
Figure 10
Facial nerve
Moving at posterior
posteriorly, genu.
facial nerve
segments are
seen above
and lateral to
cochlea. Figure 15
Mastoid
segment of
facial nerve
extending
inferiorly
to the
stylomastoid
foramen.

Congenital Anomalies
!" Outer ear
!" Middle ear
!" Inner ear
!" Vascular
!"Internal carotid artery
!"Jugular vein
!" Cholesteatoma Figure 16
!" Encephalocele
Anomalous
Congenital Malformations shortening
!" External and middle ear (1st and 2nd and widening
of lateral
branchial arch) develop independent of
semicircular
inner ear (ectodermal) canal.
!" IAC development separate from inner ear
development
!" Anomalies of all 3 parts are rare
!"Dysplasias and trisomies 13, 18, 21
Fisher, Curtin. Otolaryngol Clin North Am.
1994;27:511-531.
Outer Ear Anomalies Incomplete Partition/Dilatational

!" Congenital aural dysplasia
Defects [Figure 17]
!" Bilateral: 33%
!" Mondini dysplasia (1791): cochlea with 1
!" Genetic disorder association
and 1/2 turns
!" External auditory canal (EAC) atresia:
!" Second most common form of congenital
failure of recanalization (26th gestational
deafness (Schiebe deafness #1)
week)
!" Seventh gestational week
!"Fibrous vs. bony plate
!" Small cochlea with incomplete or absent
!"CT: middle ear dysplasia or
intrascalar septum
cholesteatoma
!" Basilar turn present
Robson, et al. Neuroimag Clin North Am. !" Common cavity in place of middle and
1999;9:133-135. apical turns
Mayer, et al. AJNR. 1997;18:53-65.
Paparella. Ann Otol Rhinol Laryngol Suppl.
Middle Ear Anomalies 1980;89:1-10.
!" Temporomandibular joint (TMJ) anomalies
!" TMJ higher and more posterior than
normal
!" Facial nerve displaced
!"Vertical portion more anterior than
normal
!"_'+A($.!"+)3/)(!+'"!'+3)$5'(8/0$/-
Figure 17
Robson, et al. Neuroimag Clin North A.
1999;9:133-5. Mondini
Mayer, et al. AJNR. 1997;18:53-65. dysplasia.
Inner Ear Anomalies [Figure 16]

!" Lateral semicircular canal anomaly
!"Last semicircular canal to form
!"Usually short and wide, less commonly
narrow
Jackler, Luxford. Laryngoscope 1987;97:2-14.
Complete Labrynthine Aplasia

!" Michel deformity
!" Third gestational week
!" Inner ear absent
!" Small cystic cavity: single or multiple
Jackler, Luxford. Laryngoscope. 1987;97:2-14.

Other Cochlear Anomalies Inner Ear A."*'&,1(7+Associations
!" Common cavity !" Otocraniofacial
!"Fourth gestational week !"Crouzon, Apert, etc
!"Cochlea and vestibule fused !" Otocervical
!"25% of all cochlear anomalies !"Klippel-Feil, Goldenhar, etc
!" Cochlear aplasia !" Otoskeletal
!"Fifth gestational week !"Osteogenesis imperfecta,
!"Rest of inner ear normal or malformed osteopetrosis, etc
!" Cochlear Hypoplasia Romo, Casselman, and Robson in Som and Cur-
!"Sixth gestational week tin, Head and Neck Imaging, 4th ed, Mosby;
!"Small cochlear bud 2003.
Jackler, Luxford. Laryngoscope. 1987;97:2-14.
Aberrant Internal Carotid Artery
Large Endolymphatic Duct and Sac [Figure 19]
(LEDS) [Figure 18] !" 90% females
!" Large vestibular aqueduct syndrome !" More common on right side
!" Dilated vestibular aqueduct !" Pulsatile tinnitus, conductive hearing loss
!"<"#)(2".."/(+30$"&"-$2(8/0$/-($/( (HL), otalgia
early-onset progressive sensorineural !" Enhancing mass in hypotympanum
hearing loss (SNHL) (inferior tympanic canaliculus)
#" > 1.5 mm diameter (lateral SCC) Sinnreich, et al. Otolaryngol Head Neck Surg.
#" MR: look at T2-W images 1984;92:194-206.
!" Often associated with incomplete partition Thiers, et al. AJNR. 2000;21:1551-1554.
cochlear anomalies
!" Progressive sensorineural hearing loss
!" Etiology: hyperosmolar protein
transmission?
Figure 19
Valvassori, Clemis. Laryngoscope. 1978;88:723-
728. Aberrant
Mafee. AJNR. 1992;13:805-819. internal
Ackler, De la Cruz. Laryngoscope. 1989;99:1238- carotid
1243. artery with
Dahlen, et al. AJNR. 1997;18:67-75. soft tissue
attenuation
Davidson, et al. AJNR 1999;20:1435-1441. within middle
ear and absent bony margin (Case courtesy of Wendy
Smoker, M.D, FACR).
Absent Internal Carotid Artery

Figure 18 !" May be incidental discovery
!" High association with intracranial
Enlarged aneurysms
vestibular
aqueduct. !" Nearly 30% present with subarachnoid
Note size in hemorrhage
comparison Keen. Clin Proc. 1946;4:588-94.
to lateral
semicircular Martinez-Granero, et al. Rev Neurol.
canal. 1997;25:1207-1209.
Persistent Stapedial Artery

!" Rare: most seen at surgery
!" Precursor for middle meningeal artery
!" Small canal from carotid canal
!" Crosses cochlear promontory
!" Widened facial canal
!" Absence of foramen spinosum
Thiers, et al. AJNR. 2000;21:1551-1554.

High Jugular Bulb (“Megabulb”)
[Figure 20]
!" _3+$",#(0'8/$)$"/#(0'#2+$%'0
!" Most common vascular anomaly of
petrous temporal bone
!"3%-7% incidence
!" More common on right side Figure 21
!"75%: jugular vein larger on right
!" Usually poorly pneumatized mastoids Pial siderosis
with thin
!" No bony dehiscence bands of T2
!" Importance: surgical impact hypointensity
secondary to
Overton, Ritter. Laryngoscope. 1973;83:1986-
subarachnoid
1991. hemorrhage.
Caldemyer, et al. RadioGraphics. 1997;17:1123-
1139.
Figure 20
High jugular
bulb with
dehiscence
along internal
auditory
canal.
Figure 22 A, B & C
B*-,+."#)0,G):,%(4)4'$,-("+>)3,)"+3'+%,:'-,14)&431#"/
Other Jugular Vein Anomalies Congenital Cholesteatoma

!" Dehiscent jugular bulb (Epidermoid) [Figures 23 & 24]
!"Direct communication with middle ear !" Child with conductive HL
!"Lateral: pulsatile tinnitus, conductive !" Aberrant epithelial rests
hearing loss !" Epitympanum, incudostapedial joint >
!"Medial: Meniere disease petrous apex
!" Jugular diverticulum !" Globular mass +/- bone destruction
!"Above, medial, posterior to petrous !" :"&&"I#(4,$0(#$-/3&($/)'/#$)A
pyramid !" May have peripheral enhancement
!"More common on left side and in Peron, Schuknecht, Arch Otolagol. 1975:101:
women 498-505.
Couloigner, et al. Eur Arch Otorhinolaryngol Gao, et al. AJNR. 1992;13:863-872.
1999;256:224-229.
Pappas, et al. Otolaryngol Head Neck Surg,
1993;109:847-852.
Pulsatile Tinnitus Lesions [Figures 21 & 22]

!" Congenital
Figure 23
!"Aberrant internal carotid artery
!"Dehiscent jugular bulb Ossicular
!" Tumor epidermoid with
!"Paraganglioma bone erosion.
!"Hemangioma
!" Vascular
!"@+)'+$"5'/",#(.3&6"+.3)$"/d8#),&3
!"Aneurysm
!"Pial siderosis: VIII n. especially prone

Figure 24
Figure 25
Epidermoid
with peripheral Encephalocele
contrast with focal T2
enhancement hyperintensity
on coronal MR of
image. epitympanum
and soft tissue
attenuation on
CT.
Congenital Dehiscence of Tegmen

Tympani [Figures 25 & 26]
!" Fusion of petrosquamosal suture by 1
year of age
!" Tiny openings: up to 34% of population
!"U/2'!*3&"2'&'1(8#),&3N(+3+'(H+'l,$+'#(
dural weakening)
!" Coronal plane best
Gavilan, et al. Arch Otolaryngol. 1984;110:206-
207.
Gottlieb, et al. Arch Otolaryngol. 1998;124:1274-
1277.
Figure 26 A & B
Encephalocele with focal T2 hyperintensity of

epitympanum and soft tissue attenuation on CT.

References
1. Caldemeyer KS, Mathews VP, Azzarelli B, Smith RR. The jugular foramen: a review of anatomy, masses,
and imaging characteristics. RadioGraphics 1997;17:1123-39.
2. Couloigner V, Grayeli AB, Bouccara D, Julien N, Sterkers O. Surgical treatment of the high jugular bulb in
patients with Meniere’s disease and pulsatile tinnitus. Eur Arch Otorhinolaryngol 1999;256:224-9.
3. Dahlen RT, Harnsberger HR, Gray SD, et al. Overlapping thin-section fast spin-echo MR of the large
vestibular aqueduct syndrome. AJNR Am J Neuroradiol 1997;18:67-75.
4. Davidson HC, Harnsberger HR, Lemmerling MM, et al. MR evaluation of vestibulocochlear anomalies
associated with large endolymphatic duct and sac. AJNR Am J Neuroradiol 1999;20:1435-41.
5. Gao PY, Osborn AG, Smirniotopoulos JG, Harris CP. Radiologic-pathologic correlation. Epidermoid tumor of
the cerebellopontine angle. AJNR Am J Neuroradiol 1992;13:863-72.
6. Gavilan J, Trujillo M, Gavilan C. Spontaneous encephalocele of the middle ear. Arch Otolaryngol
1984;110:206-207.
7. Gottlieb MB, Blaugrund JE, Niparko JK.Imaging quiz case 1. Tegmental encephalocele. Arch Otolaryngol
Head Neck Surg 1998 Nov;124(11):1274, 1276-7.
8. Jackler RK, De La Cruz A. The large vestibular aqueduct syndrome. Laryngoscope 1989;99:1238-42;
discussion 1242-33.
9. X32D&'+(VS1(;,L6"+0(b<1(k",#'(b:T(C"/-'/$)3&(.3&6"+.3)$"/#("6()*'($//'+('3+N(3(2&3##$823)$"/(%3#'0("/(
embryogenesis. Laryngoscope 1987;97:2-14.
10. Keen JA. Absence of both internal carotid arteries. Clin Proc 1945-1946;4:588.
11. Mafee MF, Charletta D, Kumar A, Belmont H. Large vestibular aqueduct and congenital sensorineural
hearing loss. AJNR Am J Neuroradiol 1992;13:805-19.
12. Martinez-Granero MA, Martinez-Bermejo A, Arcas J, et al. [Unilateral agenesis of the internal carotid
artery in childhood: description of a case]. Rev Neurol 1997;25:1207-9.
13. Mayer TE, Brueckmann H, Siegert R, Witt A, Weerda H. High-resolution CT of the temporal bone in
dysplasia of the auricle and external auditory canal. AJNR Am J Neuroradiol 1997;18:53-65.
14. Overton SB, Ritter FN. A high placed jugular bulb in the middle ear: a clinical and temporal bone study.
Laryngoscope 1973;83:1986-91.
15. Paparella MM. Mondini’s deafness. A review of histopathology. Ann Otol Rhinol Laryngol Suppl 1980;89:1-
10.
16. Pappas DG, Jr., Hoffman RA, Cohen NL, Holliday RA, Pappas DG, Sr. Petrous jugular malposition
(diverticulum). Otolaryngol Head Neck Surg 1993;109:847-52.
17. Peron DL, Schuknecht HF. Congenital cholesteatomata with other anomalies. Arch Otolaryngol
1975;101:498-505.
18. Robson CD, Robertson RL, Barnes PD. Imaging of pediatric temporal bone abnormalities. Neuroimaging
Clin N Am 1999;9:133-55.
19. Romo LV, Casselman JW, Robson CD. Temporal Bone: Congenital Anomalies. In: Som P.M., Curtin H.D.
(eds) Head and Neck Imaging, 4th ed. Mosby-Year Book Inc., St. Louis, 2003, pp:1275-360.
20. Sinnreich AI, Parisier SC, Cohen NL, Berreby M. Arterial malformations of the middle ear. Otolaryngol
Head Neck Surg 1984; 92:194-206.
21. Smith ME, Fisher C, Weiss SW. Pleomorphic hyalinizing angiectatic tumor of soft parts. A low-grade
neoplasm resembling neurilemoma. Am J Surg Pathol 1996;20:21-9.
22. B*$'+#(:@1(G3D3$(F1(`"'(7G1(C,+)$/(k7T(`'+#$#)'/)(#)3!'0$3&(3+)'+AN(CB(8/0$/-#T(@XEV(@.(X(E',+"+30$"&(
2000;21:1551-4.
23. Valvassori GE, Clemis JD. The large vestibular aqueduct syndrome. Laryngoscope 1978;88:723-8.

1248
K*'-,.-+"3+)?1+J1*0"%'&+:".17+K.31/),"9(+'.5+R1"0&'(),/+G1(,".(

Conductive Hearing Loss
!" Ossicular motion impeded
!" Differential diagnosis
!" Cholesteatoma
!" Hemangioma
!" Glomus tympanicum
!" Trauma: disruption
!" Congenital
!" Otosclerosis
I.Q'**')"%!+Disease
!" Mechanism
!"Eustachian tube dysfunction
!"Decreased intratympanic pressure
!"Children: otitis media Figure 2
!"Adults: nasopharyngeal carcinoma Gross photograph of an acquired cholesteatoma, a sac
!" B*$/W#'2)$"/(CBN(#"6)()$##,'(3/0(4,$0(&""D( of keratin lined with squamous epithelium.
alike
!"k",/#8'&0(,/$)#(/")(*'&!6,&
Nemzek and Schwartz in Som and Curtin, Head
and Neck Imaging, 4th ed, Mosby; 2003.
Acquired Cholesteatoma [Figures 1 to 4]

!" UL6"&$3)'0(D'+3)$/(I$)*$/(#32("6(#)+3)$8'0(
squamous epithelium
!" 98% of middle ear cholesteatomas
!"Probably from retraction pocket in
!3+#(4322$03
!" Prussak’s space: ossicles displaced
medially
!" Bone destruction
!"Scutum and ossicles: coronal plane
best
Figure 3 A & B
!"Pars tensa: lateral semicircular canal,
axial plane best
Coronal CT image of acquired cholesteatoma with
Buckingham, Valvassori. Otolaryngol Clin North erosion of the scutum and ossicles.
Am. 1973;6:363.
Figure 1 A & B
Figure 4 A & B
Left Image: Artist rendition of retraction pocket
at superior tympanic annulus caused by negative Middle ear “soft tissue” without bone erosion (not
intratympanic pressure. cholesteatoma).
A%8?3)7."8'9)A'3+"$3%,-)6,$M'3)&##4)G%3?)'6%3?'#%"#) Left Image: Granulation tissue.
debris from external auditory canal, creating a A%8?3)7."8'9)C%((#')'"+)01%(/
cholesteatoma.
Temporal Bone: Infectious and Neoplastic Lesions 1249 Neuroradiology
Acquired Cholesteatoma
!" May not be able to distinguish from simple
Figure 6
debris early in course
!" MR: T1 and T2 prolongation Coalescent
!" Does not enhance (granulation tissue mastoiditis. Only
does) a single cavity
remains within
!" Treatment: excision or exteriorization the mastoid bone
!"Open cavity (canal wall down) as a result of
mastoidectomy osteomyelitis.
#" Radical: stapes left
#" <"0$8'0(+30$23&(H9"/0AJN(3&&(
ossicles left
Phelps, Lloyd. Radiology. 1986;37:359-364.
O’Donoghue, et al. Clin Otolaryngol. 1987;12:89.
Ishii, et al. JCAT. 1991;15:934-937.
Nemzek and Swartz in Som and Curtin, Head and
Neck Imaging, 4th ed, Mosby; 2003.
Acquired C?"&1()1')"*'7+Complications
[Figure 5]
!" ;3%A+$/)*$/'(8#),&3N(&3)'+3&(GCC(."#)(
common
!"Labyrinthitis
!" Facial nerve canal
!" *Tegmen tympani: intracranial
!" *Sigmoid sinus erosion/thrombosis
!" “Automastoidectomy:” into EAC
*MR Recommended
Silver, et al. Radiology. 1987;164:47.
Schwartz. Radiology. 1984;153:443-447. Figure 7 A & B
Nemzek and Schwartz in Som and Curtin, Head Mastoiditis with posterior fossa epidural abscess
and Neck Imaging, 4th ed, Mosby; 2003. (Case courtesy of Vanessa Albernaz, MD).
Necrotizing External Otitis

Figure 5
!" Osteomyelitis: bone destruction
!" Diabetics: pseudomonas
Cholesteatoma with
erosion of mastoid !" AIDS: aspergillus
bone adjacent to !" C3+)$&3-'(!"+)$"/N(8##,+'#("6(G3/)"+$/$
sigmoid dural sinus. !"Spreads rapidly into adjacent spaces
!"Parotid, facial nerve, intracranial
!" Goal: determine extent of disease by CT
and MR
!" In-111 WBC study: posttherapy
Slattery, Brackmann. Otolaryngol Clin North Am.
1996;29:795-806.
Ress, et al. Laryngoscope. 1997;107:456-460.
Grandis, et al. Radiology. 1995:196:499-504.
Mastoiditis [Figures 6 & 7]
!" F#)'".A'&$)$#N(!3)2*A("!32$823)$"/ .
!"Loss of mastoid septations
!"Demineralization
!" Coalescent: single cystic cavity
!" Complications
!"Bezold abscess: zygomatic root, EAC
!"Gradenigo syndrome: petrous apicitis
#" VI palsy, V neuralgia, chronic otitis
!"Sigmoid sinus thrombosis
!"Meningitis, epidural abscess
Castillo, et al, AJR. 1998;17:1491-5.
Mafee, et al. Radiology. 1985;155:391.

External Ear Masses [Figure 8]
!" Exostosis: chronic cold water exposure
!" Usually broad-based and bilateral
!" Bony portion of EAC
!" Not an osteoma Figure 9
!"Usually unilateral, pedunculated, and
lateral to EAC External
auditory
DiBartolomeo. Ann Otolaryngol. 1979;88:2-20. canal erosion
Turetsky, et al. AJNR. 1990;11:1217-1218. secondary to
neoplasm.
Cerebellopontine Angle M'((1(7+J?1+

“AMEN” Differential Diagnosis
!" Acoustic schwannoma (60%-91%)
!" Meningioma (3%-7%)
!" Epidermoid (2%-6%)
!" Nonacoustic schwannoma (1%-5%): V,
VII
!" Others
Figure 8
!"Ependymoma, medulloblastoma,
Bilateral exostoses. pilocytic astrocytoma
!"Paraganglioma
!"Arachnoid cyst
!"Lipoma, dermoid, teratoma
External Ear Masses Brackmann, Bartels. Otolaryngol Head Neck Surg
!" Keratosis obturans 1980;88:555-559.
!"< 40 years old Valavanis, et al. Clinical Imaging of the Cer-
!"Sinusitis, bronchiectasis ebellopontine Angle, Springer-Verlag, 1980.
!"Hearing loss Gonzalez-Revilla, Johns Hopkins Hosp Bull.
!"Smooth external auditory canal (EAC) 1948(83):187-189.
widening
!"U/)$+'(U@C("6)'/(8&&'0 Acoustic Schwannoma [Figure 10]
!" EAC cholesteatoma: 0.5% of all !" 8%-10% of intracranial tumors
cholesteatomas !" 60%-90% of CPA tumors
!"Otorrhea !" Most: 30-70 years old
!"Focal erosions !" E',+"8%+".3)"#$#(O(HE:WOJN(2*$&0+'/1(
Piepergerdes, et al. Laryngoscope. 1980;90:383- bilateral in 96%
391. !"Schwann cell tumors, multiple
meningiomas, gliomas
External Ear Neoplasms [Figure 9]
!"First-degree relative counseling +/-
!" Skin cancers
imaging screening
!"Squamous cell carcinoma
#" Most common malignant ear tumor Kasantikul, et al. J Neurosurg. 1980;52:28-35.
!" Basal cell carcinoma Martuza and Eldridge. N Engl J Med.
!" Melanoma 1988;318:684-688.
!" Ceruminoma Kishore and O’Reilly. Clin Otolaryngol.
!" Parotid tumors 2000;25:561-565.
!" Metastasis
Schuknecht. Pathology of the Ear. Harvard 1974.
Maya, et al. In Som and Curtin, Head Neck Im-
aging, 4th ed, Mosby; 2003.
Figure 10
Canalicular vestibular schwannoma with smooth
remodeling of the canal wall and loss of crista
falciformis.
Acoustic (Vestibular) Schwannoma
[Figure 11]
!" Sensorineural hearing loss, vertigo,
tinnitus
!"Speech discrimination impaired:
telephone use
!" Arise from vestibular division CN VIII
usually
!"Direct pressure on cochlear division
!" Benign neoplasm
!"Slow growth (0.2 cm per year)
!"Well-circumscribed globular mass
!" k$#)"&"-AN(@/)"/$(@(3/0(9(8%'+#
Komatsuzaki, Tsunoda. J Laryngol Otol.
Figure 12 A & B
2001;115:376-379.
NIH Consensus Development Conference, Arch Vestibular schwannoma with classic mushroom
Neurol. 1994;51:201-207. morphology on precontrast and postcontrast axial T1-
Lanser, et al. Otolaryngol Clin North Am. weighted images.
1992;25:499-520.
Figure 11 A & B
Figure 13 A & B
Antoni A (left image) and Antoni B (right image) cell Left Image: Coronal T2-weighted FSE image of right-
populations of a schwannoma. sided vestibular schwannoma.
Right Image: Focal enhancement of deep portion of
internal auditory canal secondary to arteriovenous
malformation (not vestibular schwannoma).
Vestibular S/?<'.."*'7+Imaging
[Figures 12 to 14]
!" Internal auditory canal (IAC) widening
with “mushroom” expansion
!"“Giant:” usually no IAC involvement
!" CT: usually isodense to cerebellum
!"C3&2$823)$"/(3/0(*'."++*3-'(+3+'
!" T1-WI: iso- to hypointense
!" T2-WI: hyperintense
!" Intense enhancement: into porus
acousticus and no dural tail
Maya, et al. In Som and Curtin, Head and Neck
Imaging, 4th ed, Mosby; 2003.
Moller, et al. Neuroradiology. 1978;17:25-30.
Tali, et al. AJNR. 1993;14:1241-1247.
Schmalbrock, et al. AJNR. 1999;20:1207-1213.
Figure 14 A & B
Cystic degeneration of large vestibular schwannoma.

Vestibular S/?<'.."*'7+Therapy
!" Surgical resection
!"Larger masses
#" Translabyrinthine: protect facial
nerve
!" Smaller masses
#" Retrosigmoid: suboccipital
approach
#" Middle cranial fossa
!" Stereotactic radiosurgery (gamma knife):
up to 4 cm
!" Poor surgical risk patients: serial MR
Jackle, Pitts. Otolaryngol Clin North Am.
1992;25:361-387.
House, Shelton. Otolaryngol Clin North Am. Figure 16 A & B
1992;25:347-359. Cerebellopontine angle meningioma with numerous
Fucci, et al. Am J Otol. 1999;20:497-508. 0,G):,%(4)"-()01%(201%()#':'#/)=,3')'U3'-4%,-)3?+,18?)
Nakamura, et al. AJNR. 2000;21:1540-1546. foramina.

!" Usually eccentric to porus acousticus
!"IAC involvement uncommon (16%)
!"Frequently “trans-spatial”
!" Broad dural base: hemispherical
!"Obtuse bone-tumor angle
!"Dural tail: 52%-72%
!"Hyperostosis: highly characteristic
!" ECCBN(,#,3&&A(*A!'+0'/#'(H23&2$823)$"/N(
25%)
!" T1-WI: isointense to gray matter
!" T2-WI: variable
House and O’Conner. Handbook of Neurotological
Diagnosis, Marcel-Dekker, 1987.
Valavanis, et al. Neuroradiology. 1981;22:111- Figure 17 A & B
121.
Moller, et al. Neuroradiology. 1978;17:25-30. Epidermoid of middle cranial fossa with extension into
posterior fossa.
Facial Nerve Palsy

Figure 15
!" MR: imaging study of choice
!" Bell palsy: > 50%, nerve not enlarged
Tentorial meningioma
with extension into !"K0$"!3)*$21(%A(0'8/$)$"/(H!+"%3%&A(
cerebellopontine angle. HSV)
!"Imaging usually not performed
!" Tumors: 6%, enlarged nerve
!"Geniculate ganglion
#" Schwannoma
#" Hemangioma
!" Epidermoid
!" Parotid tumor spread
Epidermoid [Figures 16 & 17]
Tien, et al. AJNR. 1990;11:735-741.
!" Soft, “pearly” tumor Daniels, et al. Radiology. 1989;17:807-809.
!" K++'-,&3+(.3+-$/#N(h23,&$4"I'+i
Temporal Bone Paragangliomas
!" Follows CSF density and signal
!" Glomus jugulare: jugular foramen
!" Usually no enhancement
!"Jacobson (IX) and Arnold (X) nerve
!" Diffusion-weighted imaging: hyperintense
!" Glomus tympanicum: cochlear
to CSF
promontory
!" Differential diagnosis: arachnoid cyst,
!"Most common middle ear tumor
cysticercosis, atypical dermoid, lipoma
!"Most common etiology of
Berger, Wilson. J Neurosurg. 1985;62:214-9. retrotympanic vascular mass
Gao, et al. AJNR. 1992;13:863-72. !" Vagal paraganglioma: jugular ganglion
Tampieri, et al. AJNR. 1989;10:351-6. !" Women 5:1; peak age: 40-60 years old

Jugulotympanic Paraganglioma
[Figure 18]
!" Neuroendocrine tumor
!"Paraganglia: chemoreceptor function
!"Functioning: 1%-3%, catecholamine
secretion
!" Early symptoms
!"Conductive HL, pulsatile tinnitus
!" Slow growth but locally invasive
!"Mortality rate: 15%
!" Metastasis very rare
!" Path: chief cells (Zellballen), sustentacular
cells
Rao, et al. RadioGraphics. 1999;19:1605-1632.
Figure 20 A & B
Glomus tympanicum (paraganglioma)

(Case courtesy of William Kelly, MD).
Figure 18
Zellballen
histologic
appearance of
paraganglioma.
Jugulotympanic P'%'-'.-&,"*'7+
Imaging [Figures 19 to 22]
!" CT: irregular margins, “moth-eaten”
erosion
!" Glomus jugulare: may extend down
carotid sheath
!" MR: “salt and pepper” appearance
!"hG3&)Ni(*A!'+$/)'/#'(6"2$(H#&"I(4"I1(
hemorrhage)
!"h`'!!'+Ni(#'+!'/)$/'(4"I(5"$0#
!" Intense enhancement
!" Angiography: ascending pharyngeal artery
!" V30$"&"-$#)q#(-"3&N(0'8/'('L)'/)
Rao, et al. RadioGraphics. 1999;19:1605-1632.
Glomus jugulotympanicum (paraganglioma).
Figure 19 A & B
Glomus tympanicum (paraganglioma) (Case courtesy

of William Kelly, MD).

Figure 23 A & B
Papillary endolymphatic sac tumor in different
patients.
Differential D,'-."(,(7+Petrous Apex

!" Cholesterol granuloma (cyst): most
common
!" Epidermoid
!":"&&"I#(2'+'%+"#!$/3&(4,$0(HCG:J(
signal
!"Solid mass: resection
!" Chondrosarcoma
!" Mucocele
!" Carotid artery aneurysm
!" Meningocele
Curtin, Som. Otolaryngol Clin North Am.
1995;28:473-496.
Figure 22 A, B, C & D Cholesterol Granuloma (Cyst)

!" Retention cyst: obstruction in petrous
“Salt and pepper” appearance of glomus jugulare on
MR images. apex
!"“Chocolate cyst,” “blue-domed cyst:”
within mastoidectomy cavity
!" Young, middle-aged adults
Jugular Foramen Masses !" Hearing loss, tinnitus, cranial nerve
!" Paraganglioma: 90% palsies
!" Schwannoma: 9% !" Hemorrhage and foreign-body reaction:
!" Meningioma: < 1% cholesterol crystals and blood (brownish
!" Malignant neoplasms: < 1% 4,$0J
!"Carcinoma
!"Sarcoma Lo, et al. Radiology. 1984;153:705-711.
!"Mets Graham, et al. Laryngoscope. 1985;95:1401-
1406.
Papillary Endolymphatic Sac Tumor Latack, et al. AJNR. 1985;6:409-413.
[Figure 23]
G+%<&-@)'3)"#/)AJNR. 1988;8:825-829.
Greenberg, et al. AJNR. 1988;9:1205-1214.
!" Ipsilateral hearing loss, facial nerve palsy,
vestibular dysfunction Cholesterol Granuloma (Cyst)
!" Women more common
[Figure 24]
!" von Hippel-Lindau association
!" CT
!" Adenomatous tumor
!"Isodense to brain
!" Bone destruction, intratumoral bone
!"Expansile, especially posterior
spicules
!"Sharp smooth margins
!" MR: hemorrhage
Heffner. Cancer. 1989;64:2292-2302. !"Hyperintense on T1-WI
Lo. AJNR. 1993;14:1322-1323. !"Hyperintense on T2-WI
Palmer, et al. Otolaryngol Head Neck Surg.
1989;100:64-68. Lo, et al. Radiology 1984;153:705-711.
Mukherji, et al. Radiology. 1997;202:801-808. Graham, et al. Laryngoscope. 1985;95:1401-
1406.
Latack, et al. AJNR. 1985;6:409-413.
G+%<&-@)'3)"#/)AJNR. 1988;8:825-829.
Greenberg, et al. AJNR. 1988;9:1205-1214.

Temporal Bone Fracture
Figure 24 A & B Schwartz, Curtin. In Som and Curtin, Head and

Neck Imaging, 4th ed, Mosby; 2003.
Cholesterol granuloma.
Ossicular Derangement [Figure 26]
!" Need 1 mm CT images or thinner
Chondrosarcoma [Figure 25] !" Incus: most vulnerable
!" Most common primary neoplasm of !"Subluxation from malleus
petrous apex !"Dislocation
!" Off the midline: sutures !" Incudostapedial disruption
!"Petrosphenoidal !"Most common cause of posttraumatic
!"Petrooccipital conductive HL
!" Locally invasive !"Normal: < 1 mm between lenticular
!" Bone destruction: no sclerosis process of incus and stapes head
!" T1 and T2 prolongation Lourenco, et al. Am J Otol. 1995;16:387-392.
!" Intense but heterogeneous enhancement Swartz, et al. Radiology. 1989;171:309-317.
Grossman, Davis. Radiology. 1981;141:403-408.
Meyers, et al. Radiology. 1992;184:103-108.
Bourgouin, et al. JCAT. 1992;16:268-273.
Figure 26
Ossicular
derangement.
Figure 25 A & B
Chondrosarcoma.
Otosclerosis
!" Primary endochondral bone within otic
capsule replaced by spongy vascular bone
(“otospongiosis”)
!" Slowly progressive
!" Presents 10-30 years old with tinnitus
!"Hearing loss later
!" Females more common (70%)
!" Bilateral 80% (usually asynchronous)
Valvassori. Otolaryngol Clin North Am.
1973;6:379-389.
Reudi. Arch Otolaryngol. 1963;78:469-747.

Otosclerosis Summary
!" Fenestral type (80%): CHL !" Challenging complex anatomy
!"Begins at anterior oval window !" Facial nerve course: critical for pre-
!" Cochlear type (20%): SNHL operative evaluation
!"Almost always with fenestral type !" Bony plate between hypotympanum and
!"“Double ring” sign ICA canal
!" Demineralized areas: active disease !" Tegmen tympani
!" Chronic disease: may appear normal !" Cholesteatoma: bone erosion
!" MR: punctate enhancement !" Cerebellopontine angle: “AMEN”
Mafee, et al. Radiology. 1985;156:703-708. !"Vestibular schwannoma: most common
Swartz, et al. Radiology. 1985;155:147-150. !"Meningioma
Sakai, et al. Am J Otolaryngol. 2000;21:116-118. !"Epidermoid
!"Nonacoustic schwannoma
!" Jugular foramen
!"Paraganglioma
!"Schwannoma
!" Petrous apex
!"Cholesterol granuloma vs epidermoid
!"Chondrosarcoma, chordoma,
metastasis
!" Otosclerosis
!" V30$"&"-$#)q#(-"3&N(0'8/'('L)'/)("6(&'#$"/
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Temporal Bone: Infectious and Neoplastic Lesions 1259 Neuroadiology

1260
K*'-,.-+"3+)?1+O%$,)7+J?1+P&"$1+'.5+4".'&+G1(,".(

The Bony Orbit [Figure 1]
!" Bones
!"Frontal Figure 3
!"Maxilla
!"Sphenoid Nasolacrimal
ducts in
!"Zygoma
inferomedial
!"Ethmoid portions of
!"Lacrimal bony orbit.
!"Palatine
Globe [Figure 4]
!" Anterior chamber: aqueous humor
!" Iris and ciliary body
!" Posterior chamber: aqueous humor
!" Lens apparatus
!" _$)+'",#(%"0AN(-'&W&$D'(H2"&&3-'/(8%+$&#J
!"Most: free water
Figure 4
Normal globe
with anterior
and posterior
chambers located
Figure 1 anterior to the
The bony orbit.
lens and the
vitreous body
constituting most
The Bony Orbit of the globe.
!" G,!'+$"+("+%$)3&(8##,+'
!"Middle cranial fossa
!"Cranial nerves III, IV, VI, V1
!"Superior and inferior ophthalmic veins Globe [Figure 5]
!" K/6'+$"+("+%$)3&(8##,+' !" Retina
!"Pterygopalatine (V2) and !"Neural sensory inner layer
infratemporal fossa (photoreceptors)
!"Retinal pigment epithelium (RPE):
Anterior Orbit [Figures 2 & 3]
outer layer
!" Orbital septal system
!"Ora serrata
!"Anterior: well-developed (preseptal
!" Uvea: choroid (vascular); Bruch’s
space)
membrane
#" Arises from periosteum of anterior
!"Iris
bony orbit
!"Ciliary body
#" Attaches to tarsal plates of eyelids
!" G2&'+3N(8%+",#(&3A'+Y(2"+/'3(3/)'+$"+&A
!"Posterior: incomplete
!" Tenon’s capsule (bulbar fascia)
!" Lacrimal gland
!" Normal: only one “layer” seen
!" Lacrimal sac and nasolacrimal duct
Figure 5
Figure 2
Close-up view of the
Lacrimal posterior globe layers.
glands in Retina is innermost,
superolateral followed by choroid and
portion of the sclera. The macula is
bony orbit. located lateral to the optic
disk.
Imaging of the Orbit: The Globe and Conal Lesions 1261 Neuroradiology
Retrobulbar (Postseptal) Space Senile Macular Degeneration
[Figures 6 to 8] !" Most common cause of legal blindness in
!" :3)(I$)*(8%+",#(#'!)3 the elderly
!" Extraocular muscles (EOM) (cone) !" Hyalinization of macula, thickening of
!"Rectus: medial, lateral, superior, Bruch’s membrane
inferior !"Pigment epithelium detachment
#" Annulus of Zinn: optic canal !"G'+",#(#,%+')$/3&(#!32'(4,$0
#" Intermuscular septa (incomplete !" k'."++*3-'N(8%+",#(#23+1(.32,&3+(&"##
posteriorly) !" Computed tomography (CT): mimics
!" Oblique: superior (trochlear), inferior uveal melanoma
!" Levator palpebrae superioris !" Magnetic resonance (MR): variable
!" Optic nerve: glial-lined Mafee, in Som and Curtin. Head and Neck Imag-
!" Vessels ing, 4th ed, Mosby; 2003.
Retinal Detachment (RD) [Figure 9]

Figure 6
!" Sensory retina separates from RPE
Extraocular muscles.
!" Rhegmatogenous RD: tear in retina
The superior oblique !" RPE: can heal (laser therapy)
muscle travels !" Ultrasonography (US) superior to MR or
through the trochlea, CT for detection
a bony strut near the !"C3,#'#N(.3##1(8%+"!+"&$6'+3)$5'(
superomedial margin of
the bony orbit. disease, toxocara, choroidal lesions
!" V-shape: apex at optic disk
Mafee, Peyman. Radiol Clin North Am.
1987;25:487-507.
Figure 9
Figure 7
Retinal detachment
Coronal view of with characteristic
the six extraocular V-shape created by
muscles and levator anchor points at optic
palpebrae superioris. disk and ora serrata.
Choroidal Detachment [Figure 10]

!" Hemorrhagic: contusion
!" Serous: ocular hypotony (choroidal
Figure 8 $/43..3)$"/1()+3,.31(-&3,2".3()*'+3!AJ
Papilledema with
!" U-shaped
%-$+'"4'()01%() !"Anchor points: short posterior ciliary
surrounding optic artery, vortex vein
nerves bilaterally !" No connection with optic disk
caused by a
supratentorial Mafee, Peyman. Radiol Clin North Am.
oligodendroglioma. 1987;25:487-507.
Cranial Nerves III, IV, VI Figure 10

!" Motor control of EOMs
!" Cranial nerve III: all EOMs except- Choroidal detachment,
!"Lateral rectus: cranial nerve VI with typical U-shape
created by anchor
!"Superior oblique: cranial nerve IV points at ciliary body
!"“LR6SO4” and vessels away from
!" Sensory control: V1 primarily, V2 the optic disk.
(infraorbital region)
Leukocoria R1),."$&'()"*'7+Pathology
!" Retinoblastoma !" Neuroectodermal origin: primitive
!" Persistent hyperplastic primary vitreous embryonal retinal cells (retinoblasts)
(PHPV) !" Rosettes: Flexner-Wintersteiner or
!" Retinopathy of prematurity (ROP) Homer-Wright
!" Congenital cataract !" k$-*&A(.3&$-/3/)N(/'2+"#$#1(.$)")$2(8-,+'#
!" Coats disease !" C3&2$823)$"/
!" Toxocariasis Kyritsis, et al. Nature 1984;307:471-473.
!" Total retinal detachment
Mafee. In Som and Curtin, Head and Neck Imag- R1),."$&'()"*'7+Imaging [Figure 12]
ing, 4th ed, Mosby; 2003. !" CT: imaging study of choice
!"C3&2$823)$"/N(e(=>?("6(23#'#
Retinoblastoma #" Child < 3 years old: highly
!" Most common intraocular tumor of suggestive for diagnosis
childhood !" Tri- or tetralateral retinoblastoma with
!"Incidence 1:15,000 pineal and/or suprasellar masses
!"Virtually all patients < 6 years old !" <VN(/")(3#(#!'2$82(3#(CB
!"80% 3 years old or younger !"Hyperintense on T1-WI and PD
!"13 months: average age at !"Hypointense on T2-WI
presentation !"May miss lesions as large as 4 mm
!" No gender or racial predilection !"Better for intracranial extension,
!" “Retinoblastoma gene:” chromosome extraocular spread
13q14 Char. Ophthalmology. 1984;91:1347-5130.
!"“Germinal” (inherited): 85% bilateral Mafee. Radiol Clin North Am. 1987;25:667-681.
!"“Somatic” (notinherited): unilateral Mafee, et al. Ophthalmology. 1989;96:965-976.
!" Unilateral: 60%-70% Jakobeic, et al. Cancer. 1977;39:2048-58.
!" Association: osteosarcoma, other El-Naggar, et al. Ann Ophthalmol. 1995;27:360-
sarcomas 336.
Abramson, et al. Ophthalmology. 1984;91:1351-
1355. Pendergrass, Davis, Arch Ophthalmol.
1980;98:1204-1210. Ellsworth. Trans Am Oph-
thalmol Soc. 1969;67:462-534. Kaufman, et al.
Radiol Clin North Am. 1998;36:1101-1117.
Retinoblastoma [Figure 11]

!" Ophthalmoscopic diagnosis primarily
!"Small gray-white intraretinal lesions,
23&2$823)$"/1(#''0$/-
!"Ultrasonography: 80% accurate
!" G)3-'(ZN(2"/8/'0()"()*'(-&"%'
!" Stage 2: extraocular extension to orbit or
optic nerve
!" Stage 3: extra-orbital extension
!" 92% 5-year survival for intraocular lesions
but near 100% mortality when extends
beyond eye
Kodilyne. Am J Ophthalmol. 1967;63:467-
481; Abramson, et al. Arch Ophthalmol.
1981;99:1761-1762.
Figure 11
Gross photograph Figure 12

of retinoblastoma. A'3%-,*#"43,.")G%3?)$?"+"$3'+%43%$)$"#$%&$"3%,-),-)!5/
Persistent Hyperplastic Primary Toxocariasis
Vitreous (PHPV) [Figure 13] !" Chorioretinitis: toxocara canis (nematode)
!" Failure of embryonic hyaloid system !" Granuloma: eosinophilic abscess
(primary vitreous) to regress normally !" CT: homogeneous intravitreal density
3/0(6"+.()*'(#'2"/03+A(5$)+'",#(%A(86)*W !"Retinal detachment, organized
sixth gestational month 5$)+'",#1($/43..3)"+A('L,03)'
!" Isolated or part of more complex !"Irregular thickening of uveoscleral
abnormality coat
!"Bilateral: Norrie, Warburg !" MR: subretinal exudate, variably
!" Usually unilateral leukokoria and hyperintense on all sequences
microphthalmos Margo, et al. Pediatr Ophthalmol Strabismus.
!"Lens opacity, RD, vitreous hemorrhage 1983;20:180-184; Wilder. Trans Am Acad Oph-
!" Persistent hyaloid (Cloquet) canal thalmol Otolaryngol. 1950;55:99-104.
!"E"(23&2$823)$"/
Mafee, Goldberg. Radiol Clin North Am. Uveal Melanoma
1987;25:683-692. !" Uvea
!"Choroid, ciliary body, iris
!" Derived from mesoderm and
neuroectoderm
!"Highest vascular part of eyeball
!" Melanoma: most common neoplasm of
choroid
!" Whites (15:1)
!"Incidence increases with age
!" Arises from choroid, elevates and may
rupture Bruch’s membrane (mushroom
shape)
Yanoff, Fine. Ocular Pathology. Harper and
Row, 1975; Mafee, Radiol Clin North Am.
1998;36:1083-1099.
Uveal Melanoma [Figures 15 & 16]

!" Metastasis: liver > lung > bone > kidney
Figure 13 A & B
> brain
PHPV with hyaloid canal. !" Diagnosis usually made by
ophthalmoscopy or US
!" CT: elevated, hyperdense, sharply
Coats Disease [Figure 14] marginated (usually) solid mass
!" Juvenile males most common !" MR
!" Usually unilateral (85%-90%) !"Hyperintense on T1-WI and PDW
!" Peripheral telangiectasias !"Hypointense on T2-WI
!"Leak lipoproteinaceous exudate !" Moderate enhancement
!"Retinal detachment
D1<&-@)'3)"#/)Arch Ophthalmol. 1981;99:1827-
!" May mimic retinoblastoma clinically
1830. Enochs, et al. Radiology. 1997;204:417-
Coats. R Lond Ophthalmol Hosp Rep. 423; Mafee in Som and Curtin, Head and Neck
1908;17:440-525. Imaging, 4th ed, Mosby; 2003.
Reese, Am J Ophthalmol. 1956;42:1-8.
Edward, et al. Radiol Clin North Am.
1988;36:1119-1131.
Figure 14
Gross
photograph of
Coats disease.
Figure 15 A, B & C
Uveal melanoma.
!"Sub-Tenon capsule
!"Subdural (optic nerve sheath)
!" Optic nerve Injury
!" Eyeball injury: phthisis bulbi
!" Foreign body
Figure 16
Uveal melanoma.
Figure 18 A & B
Uveal Metastasis [Figure 17] Blow-out

!" Usually in the plane of the choroid with fracture.
little increased thickness
!" Mottled appearance, diffuse outline
!" Breast and lung cancer most common
!" Retina or choroid
!" Bilateral 1/3 (melanoma rarely bilateral)
!" Mucinous adenocarcinoma: mimic
melanoma
Mafee. Radiol Clin North Am. 1998;36:1083-
1099.
Figure 17
A&B Figure 19 A & B
Bilateral
Orbital fracture
uveal
extending
metastasis.
towards optic
canal.
Conal Lesions
!" Graves disease
Orbital Trauma [Figures 18 & 19] !" Pseudotumor
!" CT: imaging modality of choice !" Others
!" Fractures !"Lymphoproliferative disease
!"Isolated: orbital rim (Waters view) !"Metastasis: 7%, breast carcinoma,
!"Blow-out: inferior wall; medial wall: nodular
1/2 !"@+)'+$"5'/",#(8#),&3("+(53#2,&3+(
!"Nasoethmoidal (NOE) complex congestion
#" Canthal injury common !"Acromegaly
!"Zygomatic complex (ZC) !"Amyloid
!"Lefort types: I, II, III !"Cysticercosis/trichinosis
!"Orbital apex-optic canal
!" Hemorrhage
!"Retrobulbar: most common
!"Extraconal
!"Subperiosteal
Thyroid Orbitopathy (Graves Disease) Graves D,(1'(17+Imaging
!" Autoimmune disorder: orbital soft tissues, [Figure 21]
thyroid, extremities !" Muscle enlargement IMSLOW
!"Superior cervical lymph channel: !"Inferior rectus
drains both thyroid and orbit !"Medial rectus
!" Incidence: 0.5% (US) !"Superior muscle complex
!" Most common orbital disorder !"Lateral rectus
!" Most common cause of exophthalmos in !"s(V'&3)'0()"($//'+53)$"/(3/0(8%'+(#$f'
adults !" Tendon spared
!"15%-28% of unilateral exophthalmos !" h7$+)Ai(+')+"%,&%3+(63)N($/43..3)$"/
!"80% of bilateral exophthalmos !" Apex: optic nerve compression
Rubin and Sadun in Yanoff and Duker, Ophthal- Mafee in Som and Curtin, Head and Neck Imag-
mology. Mosby, 1999. ing, 4th ed, Mosby; 2003.
Mafee in Som and Curtin, Head and Neck Imag-
ing. 4th ed, Mosby; 2003.
Graves Disease
!" Most (up to 80%) patients are or will be
hyperthyroid
!"Euthyroid (10%)
!" Family history: 30%
!" Range: 15-86 years old (peak: 30-50 Figure 21
years old) A&B
!" Women much more common (4:1) Graves
!" Males, patients > 50 years old: more disease with
severe disease sparing of
the tendinous
Kendler, et al. Arch Ophthalmol. 1993;111:197- insertions.
201.
Graves Disease [Figure 20]

!" Acute phase
!"K/43..3)"+A(+'32)$"/N(2"/-'#)$"/1(
*A!'+)+"!*A1(8%+"#$#("6("+%$)3&(63)d
muscles
!"Mucopolysaccharides accumulate in
EOMs Pseudotumor
!" Chronic phase: exophthalmos (34%-93%) !" E"/-+3/,&".3)",#($/43..3)$"/
!"Fibrosis !" No known cause
!"Restrictive myopathy !" Diagnosis of exclusion
!"Diplopia !" Second most common (~5%) orbital
Rubin and Sadun in Yanoff and Duker. Ophthal- disease (after Graves disease)
mology. Mosby; 1999. !" Children: 6%-16% of all cases, more
frequently bilateral
Blodi, Gass, Br J Ophthalmol. 1968;52:79-93.
Flanders, et al. J Comput Assist Tomogr.
1989;13:40-47.
Weber, et al. Radiol Clin North Am.
1999;37:151-168.
Figure 20
A&B Pseudotumor
Graves !" Acute form
disease. !"Abrupt onset of pain usually
!"Lid swelling, redness, ptosis, proptosis
!" Chronic form
!"Fixation signs: diplopia, proptosis
!" Sites
!"Lacrimal gland (lacrimal adenitis)
!"Extraocular muscles (myositic form)
!"Cavernous sinus (Tolosa-Hunt)
Tolosa, J Neurol Neurosurg Psychiatry. 1954;
17:300-302.
Hunt. Neurology. 1961;11:56-62.
P(195")9*"%7+=OE+++++++++[Figure 22] P(195")9*"%7+Imaging
!" Tendons involved (unlike Graves disease) [Figure 23]
!" V3--'01(h4,66Ai(.,#2&'(%"+0'+ !" CT
!" Inward bowing of muscle contour at globe !"E"/#!'2$82
insertion !"Moderate enhancement
!" “Dirty” retrobulbar fat !" MR
!" May extend intracranially (apical orbital !"Hypointense on T1-WI and T2-WI
$/43..3)$"/J("+("/)"("!)$2(/'+5'(HFEJ(
sheath (perineuritis)
!" Bone destruction rare
Trokel, Hilal, Am J Ophthalmol. 1979;87:503-
512.
Flanders, et al. J Comput Assist Tomogr.
1989;13:40-47.
Figure 23
A&B
Pseudotumor
with
Figure 22 characteristic
A&B T1 and T2
hypointensity.
Top Image:
Pseudotumor
with tendinous
involvement.
Bottom Image:
Rapid response
to steroid
therapy on
follow-up.
Secundario a la fibrosis. Tb podría ser

linfoma
References
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2. Abramson DH, Ellsworth RM, Tretter P, Javitt J, Kitchin FD. Treatment of bilateral groups I through III
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3. 9&"0$(:C1(\3#(X7T(K/43..3)"+A(!#',0"),.",+("6()*'("+%$)T(9+(X(F!*)*3&."&(Z=[QYRONP=W=^T
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6. 7,68/(V<1(G)+33)#.3(9V1(:""#(Vo1(S'+.3/(9<T(G.3&&(.3&$-/3/)(.'&3/".3("6()*'(2*"+"$0(I$)*(
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$/43..3)"+A(!+"2'##'#T(X(C".!,)(@##$#)(B"."-+(Z=Q=YZ^N]>WPT
12. k,/)(bU1(<'3-*'+(XE1(;'6'5'+(kU1(c'.3/(bT(`3$/6,&("!)*3&."!&'-$3T(K)#(+'&3)$"/()"($/0"&'/)($/43..3)$"/(
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of Gd-DTPA contrast enhancement. Radiol Clin North Am 1998;36:1101-17.
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16. Kodilinye HC. Retinoblastoma in Nigeria: problems of treatment. Am J Ophthalmol 1967;63:469-81.
17. Kyritsis AP, Tsokos M, Triche TJ, Chader GJ. Retinoblastoma - origin from a primitive neuroectodermal
cell? Nature 1984;307:471-3.
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21. Mafee MF, Peyman GA. Retinal and choroidal detachments: role of magnetic resonance imaging and
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24. Margo CE, Katz NN, Wertz FD, Dorwart RH. Sclerosing endophthalmitis in children: computed tomography
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32. Yanoff K, Fine BS, Ocular Pathology. Hagerstown: Harper & Row, 1975.
1269
1270
K*'-,.-+"3+)?1+O%$,)7+K.)%'/".'&+'.5+=>)%'/".'&+G1(,".(

Intraconal Lesions Optic Nerve Sheath Meningioma
!" Optic nerve glioma !" 5% of all orbital tumors
!" Optic nerve sheath meningioma !" Less than 1% of all meningiomas
!" Cavernous hemangioma !" “Extradural” meningiomas: associated
!" Schwannoma with “blistering” of adjacent bone
!" Lymphoma !" Slowly progressive loss of vision,
!" Fibrous histiocytoma proptosis
!" Varix, arteriovenous malformation !"Optociliary venous shunts, disk pallor,
visual loss: highly suggestive
Optic Nerve Glioma
Sibony, et al. Ophthalmology. 1984;11:1313-
!" 3% of all orbital tumors; 4% of gliomas
1326.
!" Peak age: 2-8 years (range: birth to 60
years) Optic Nerve Sheath Meningioma
!" R>?(3##"2$3)'0(I$)*(/',+"8%+".3)"#$#( [Figure 2]
type 1 (NF-1) and frequently bilateral !" b'&&W0'8/'0(),%,&3+()*$2D'/$/-("6(FE
!"10%-15% of all NF-1 cases !" CBN(C3&2$823)$"/(2".."/
!" Optic atrophy on ophthalmoscopy !" T1-WI: isointense to ON
!" Arise from glial cells of optic nerve !" T2-WI: iso- to hyperintense
!" Slow growth usually; may grow in spurts !" “Tram-track” enhancement
Azar-Kia, et al. Radiol Clin North Am. !"Fat suppression essential
1987;25:561-581. !" May be eccentric, extend intracranially
Daniels, et al. AJNR. 1982:3:181-183.
Optic Nerve Glioma [Figure 1]
Azar-Kia, et al. Radiol Clin North Am.
!" Juvenile: pilocytic astrocytoma
1987;25:561-581.
!" Adult: glioblastoma multiforme (non-NF-1
cases)
!" Fusiform enlargement: kinking, buckling
!" CT: iso- to hypodense
Figure 2
!"C3&2$823)$"/(+3+' A&B
!" T1-WI: hypointense; T2-WI: hyperintense
!" Heterogeneous enhancement Optic nerve
sheath
Azar-Kia, et al. Radiol Clin North Am. meningioma
1987;25:561-81. with tram-
Haik, et al. Ophthalmology. 1987;94:709-717. track
enhancement
(top
image) and
$"#$%&$"3%,-)
(bottom
image) in
2 different
patients.
Figure 1
Optic nerve
glioma with
characteristic
“kinking” of
the nerve.
Imaging of the Orbit: Intraconal and Extraconal Lesions 1271 Neuroradiology

Cavernous Hemangioma [Figure 3] Schwannoma [Figure 4]
!" Most common vascular orbital tumor in !" Fusiform to oval-shaped mass
adults !" CT: isodense to extraocular muscles
!" Peak age: 25-40 years old (range 25-70 !"More hyperdense areas = Antoni A
years old) cells
!" Well-circumscribed mass (pseudocapsule) !" T1WI: iso- to hypointense
!" Intraconal (83%) !" T2WI: hyperintense
!" 9'/$-/(/"/$/8&)+3)$5'(*3.3+)".3 !" Marked enhancement
!"Large dilated sinusoid-like spaces
!"Slowly progressive enlargement
!"Prominent arterial supply usually
absent
!" CT
!"Hyperdense
!"Phleboliths Figure 4
!"Bone remodeling Schwannoma.
!"Variable enhancement
!" MR
!"T1-WI: mixed
!"T2-WI: iso- to hyperintense
!" Hemorrhage occasionally
Bilaniuk. Radiol Clin North Am. 1999;37:169-
183.
Mafee, et al. Radiol Clin North Am. 1987;25:529-
559.
Orbital Lymphoma
!" Lymphoid tumors: 10%-15% of orbital
masses
!"Lymphoma, pseudolymphoma,
lymphoid hyperplasia
Figure 3 !" 10% of all lymphomas as primary site
A&B !"75% have or will have systemic
Cavernous lymphoma
hemangioma !"Lacrimal gland: most common site
with pressure !"EOMs rarely involved
erosion of !" Non-Hodgkin (B-cell): majority
orbital roof.
!" Proptosis, ptosis, diplopia
!" V,%%'+A(8+.(.3##'#
Valvassori, et al. Radiol Clin North Am.
1999;37:135-150.
Flanders, et al. Radiol Clin North Am.
1997;25:601-612.
Orbital Lymphoma [Figure 5]

!" Molds itself along margins of normal
structures
!"9"/'('+"#$"/N(&3)'(8/0$/-
!" M#,3&&A(I'&&W0'8/'01(+",/0()"("53&
!" CT: homogeneous, mildly hyperdense
Schwannoma !" T1-WI: hypointense
!" 1% of all orbital tumors: usually !" T2-WI: iso- to hypointense
intraconal !" Mild to marked enhancement
!"Arise from cranial nerves, not optic
Valvassori, et al. Radiol Clin North Am.
nerve
1999;37:135-150.
!"K#"&3)'0("+(/',+"8%+".3)"#$#(
Flanders, et al. Radiol Clin North Am.
association
1997;25:601-612.
!" Benign with slow growth
!"Well-encapsulated
!" Painless proptosis
!" Compresses or engulfs optic nerve
Carroll, et al. Radiol Clin North Am.
1999;37:195-202.

Figure 5
Figure 7
Orbital lymphoma A&B
with characteristic
molding of the tumor Orbital
against the orbital varix with
globe. enlargement
upon Valsalva
maneuver on
postcontrast
image (bottom
image).
Fibrous Histiocytoma [Figure 6]

!" Most common primary orbital
mesenchymal tumor in adults
!" 1% of all primary orbital tumors
!" Mean age: 42 years old
!" Usually benign (66%)
!"Malignant: bone erosion,
hemorrhage, postradiation therapy for
retinoblastoma
!" b'&&W0'8/'0($/)+3W("+('L)+32"/3&(.3##
!" Moderate to marked enhancement
Font, Hidayat. Hum Pathol. 1982;13:199.
Mafee in Mafee, Valvassori, and Becker, Imaging
of the Head and Neck, 2nd ed, Thieme; 2005. Figure 8
A, B & C
Carotid-
Figure 6 cavernous
&431#")G%3?)
Malignant enlarged
&*+,14) superior
histiocytoma. ophthalmic
vein. Lateral
view from
cerebral
angiogram
shows
abnormal
Orbital Varix [Figure 7] 0,G)3?+,18?)
!" Most common cause of spontaneous cavernous
sinus, petrosal
orbital hemorrhage sinuses, and
!" Focal venous dilatation superior
!" Valsalva: stress proptosis ophthalmic
!"Lobulated mass vein.
!" Phleboliths
!" Spontaneous thrombosis common
Bilaniuk. Radiol Clin North Am. 1999;37:169-83.
Arteriovenous Fistula [Figure 8]

!" Usually posttrauma Extraconal Lesions
!"Spontaneous less common (Ehlers- !" Lymphangioma*
Danlos, osteogenesis imperfecta, !" Metastasis*
pseudoxanthoma elasticum) !" Rhabdomyosarcoma*
!" Orbital bruit, proptosis, chemosis !" Dermoid/epidermoid
!" CT/MR: dilated superior ophthalmic vein !" Paranasal sinus disease
!" Angiography diagnostic !"Infection
!" Endovascular occlusion: treatment of !"Neoplasm
choice
*Commonly “intercompartmental”
Tan, et al. Radiol Clin North Am 1987;25:849-61.

Lymphangioma [Figures 9 & 10]
!" Children and young adults
!" Exophthalmos with viral infection
!" Lymphoid follicles, dilated spaces
!"K/8&)+3)$5'N(0"(/")(+'#!'2)(63#2$3&(
planes Figure 11
A&B
!"Hemorrhage common
!" Extraconal space primarily Orbital
!" CT/MR: heterogeneous appearance metastasis
!"k'."++*3-'("+(2A#)$2(4,$0 from unknown
!" Variable enhancement (venous channels) primary
neoplasm.
Bilaniuk. Radiol Clin North Am. 1999;37:169-
183.
Mafee, et al. Radiol Clin North Am. 1987;25:529-
559.
Metastatic Lesions
Figure 9 !" 9 months average survival (lung
A&B carcinoma, melanoma worst)
Lymphangioma !" Hematogenous spread
with !" Diplopia, proptosis, pain, vision loss
hemorrhage !" Enophthalmos: breast carcinoma
in 2 different !" Isolated lateral rectus enlargement:
patients.
metastasis or pseudotumor
Rhabdomyosarcoma
!" Most common primary orbital malignancy
tumor in children
!"Most: 2-5 years old; 90% younger
than 16 years old
!"Rapidly progressive but usually
painless
!" Arise from undifferentiated mesenchyme
in orbital fat (not from extraocular
muscles)
Figure 10
!"Children: embryonal (70%) and
Lymphangioma alveolar types
with !"Adults: pleomorphic type
hemorrhage !" 90% 5-year survival with complete
in 2 different resection
patients.
!"^R?($6(#$-/$823/)(+'#$0,3&(0$#'3#'
Mafee, et al. Radiol Clin North Am.
1998;36:1215-1227.
Rhabdomyosarcoma [Figure 12]

Metastatic Lesions [Figure 11]
!" Superior orbit predilection
!" 10% of orbital tumors
!" Homogeneous mass
!"1/3 bony orbit, 1/3 globe, 1/3
!" CT: isodense to muscle
scattered
!"Bone destruction common in larger
!" Increasing incidence (longer survival)
lesions
!" Primary site
!"E'2+"#$#1(23&2$823)$"/1(*'."++*3-'(
!"Breast: 42%
uncommon
!"Lung: 11%
!" T1-WI: hypointense
!"Unknown primary: 11%
!"Prostate: 8%
!" Moderate to marked enhancement
!"Melanoma: 5%
!"Children: neuroblastoma, leukemia, Mafee, et al. Radiol Clin North Am.
Ewing 1998;36:1215-1227.

Figure 12 Figure 14B
Rhabdomyo- Peri-orbital
sarcoma with cellulitis.
characteristic
bone
destruction.
Dermoid/Epidermoid [Figure 13]

!" Most common congenital orbital lesion
!"Many manifest in second-third
decades
!" Superolateral: most common location
!" Arise at sutures or diploe
!" b'&&W0'8/'0(.3##(I$)*(63)("+(4,$0(#$-/3&( Figure 15
in upper corners of orbit A&B
!" Remodel bone without destruction Orbital
cellulitis. Note
Kaufman, et al. Radiol Clin North Am. involvement
1998;36:1149-1163. along lamina
papyracea.
Figure 13
Dermoid.
Fungal Sinusitis [Figure 16]

!" Immunocompromised patients
!"Rhino-orbital mucormycosis
!"Aspergillosis
!" V'5'+#3&("6()A!$23&(8/0$/-#($/(#$/,#(
disease
Orbital Cellulitis [Figures 14 & 15] !"Increasing protein, decreasing water
!" C&3##$823)$"/ content
!"Preseptal cellulitis: eyelid !"CT: hyperattenuated
!"Postseptal cellulitis !"T1-WI: hyperintense
!"Subperiosteal phlegmon and abscess !"T2-WI: hypointense (can mimic air)
!"Cavernous sinus thrombosis Chandler, et al. Laryngoscope. 1970;80:1414;
!" Usually paranasal (ethmoid) sinusitis Eustis, et al. Radiol Clin North Am.
!" Usually does not extend into intraconal 1998;36:1165-1183.
space
Chandler, et al. Laryngoscope. 1970;80:1414.
Eustis, et al. Radiol Clin North Am.
1998;36:1165-1183.
Figure 14A
Perioribital
cellulitis. Figure 16 A, B & C
Fungal sinusitis.

Lacrimal Gland Lesions Lacrimal Sac Lesions [Figure 18]
!" R>?($/43..3)"+Ad&A.!*"!+"&$6'+3)$5' !" Benign: 43%
!"Sarcoid !"Diverticulum
!"Sjogren !"Pneumatocele
!"Lymphoma: frequent anterior/ !"Mucocele
posterior extension !"Papilloma
!"Pseudotumor: 15% of all orbital !"Polyp
pseudotumor !"Fibroma
!" 50%: epithelial tumors !"Dermoid
!"50%: benign (pleomorphic adenoma, Stefanyszyn, et al. Ophthal Plast Reconstr Surg.
benign mixed cell tumor) 1994;10:169-184.
!"50%: malignant (adenoid cystic, Pe’er, et al. Ophthalmology. 1996;103:1601-
malignant mixed, mucoepidermoid, 1605.
adeno, squamous cell, anaplastic)
!" Imaging: pre-op planning
Zimmerman, et al. Int Ophthalmol Clin.
Figure 18
1962;2:337-367.
Mafee, et al. Radiol Clin North Am. 1987;25:767- Lacrimal sac
779. malignancy
with bone
Lacrimal Gland Lesions [Figure 17] destruction.
!" K/43..3)"+A(&'#$"/#
!"Oblong mass
!"Molded enlargement of lacrimal gland
!" Pleomorphic adenoma
!"Long duration Summary
!"Rounded mass !" Retinoblastoma: most common intraocular
!"Bone remodeling malignancy of childhood
!"Bone destruction: malignant epithelial !" Uveal melanoma: most common
tumors malignancy of the globe in adults
Jakobiec, et al. Am J Ophthalmol Clin. !" Uveal metastasis: frequently bilateral
1962;2:337-267. !" Most common disease of the orbit
!"Graves: no tendon involvement
!"Lymphoma
!"Pseudotumor: tendon involvement
!" Intraconal lesions
!"Optic nerve tumors
#" Glioma
#" Nerve sheath meningioma
!"Cavernous hemangioma
!"Nerve sheath tumors
!"Lymphoma
!"Fibrous histiocytoma
!"Varix
!"C3+")$0W235'+/",#(8#),&3
!" Extraconal lesions
!"Lymphangioma
Figure 17 A & B !"Metastases: 10% of orbit masses
!"Rhabdomyosarcoma
Left Image: Lacrimal lymphoma.
Right Image: Lacrimal pleomorphic adenoma. !"Dermoid
!"Sinus disease
!" Lacrimal gland lesions
!"“The 50% gland”
Lacrimal Sac Lesions [Figure 18] !"R>?($/43..3)"+Ad&A.!*"!+"&$6'+3)$5'
!" Malignant: 57% !"50% neoplasms
!"Epithelial: 75% #" 50% benign, 50% malignant
#" Squamous cell !" Lacrimal sac lesions: most are malignant
#" Transitional cell
#" Mucoepidermoid
!"<'#'/2*A.3&N(8%+",#(*$#)$"2A)".3
!"Lymphoid: lymphoma
!"Neural
!"Metastasis

References
1. Azar-Kia B, Naheedy MH, Elias DA, Mafee MF, Fine M. Optic nerve tumors: role of magnetic resonance
imaging and computed tomography. Radiol Clin North Am 1987;25:561-81.
2. Bilaniuk LT. Orbital vascular lesions. Role of imaging. Radiol Clin North Am 1999;37:169-183, xi.
3. Carroll GS, Haik BG, Fleming JC, Weiss RA, Mafee MF. Peripheral nerve tumors of the orbit. Radiol Clin
North Am 1999; 37:195-202, xi-xii.
4. Chandler JR, Langenbrunner DJ, Stevens ER. The pathogenesis of orbital complications in acute sinusitis.
5. Daniels DL, Williams AL, Syvertsen A, Gager WE, Harris GJ. CT recognition of optic nerve sheath
meningioma: abnormal sheath visualization. AJNR Am J Neuroradiol 1982;3:181-3.
6. Eustis HS, Mafee MF, Walton C, Mondonca J. MR imaging and CT of orbital infections and complications in
acute rhinosinusitis. Radiol Clin North Am 1998;36:1165-83, xi.
7. Flanders AE, Espinosa GA, Markiewicz DA, Howell DD. Orbital lymphoma. Role of CT and MRI. Radiol Clin
North Am 1987;25:601-13.
8. Font RL, Hidayat AA. Fibrous histiocytoma of the orbit. A clinicopathologic study of 150 cases. Hum Pathol
1982;13:199-209.
9. Haik BG, Saint Louis L, Bierly J, et al. Magnetic resonance imaging in the evaluation of optic nerve
gliomas. Ophthalmology 1987;94:709-17.
10. Jakobiec FA, Yeo JH, Trokel SL, et al. Combined clinical and computed tomographic diagnosis of primary
lacrimal fossa lesions. Am J Ophthalmol 1982;94:785-807.
11. Kaufman LM, Villablanca JP, Mafee MF. Diagnostic imaging of cystic lesions in the child’s orbit. Radiol Clin
North Am 1998;36:1149-63, xi.
12. Mafee MF, Haik BG. Lacrimal gland and fossa lesions: role of computed tomography. Radiol Clin North Am
1987;25:767-79.
13. Mafee MF, Pai E, Philip B. Rhabdomyosarcoma of the orbit. Evaluation with MR imaging and CT. Radiol Clin
North Am 1998;36:1215-27, xii.
14. Mafee MF, Putterman A, Valvassori GE, Campos M, Capek V. Orbital space-occupying lesions: role of
computed tomography and magnetic resonance imaging. An analysis of 145 cases. Radiol Clin North Am
1987;25:529-59.
15. Mafee MF. Eye and Orbit. In: Mafee MF, Valvassori GE, and Becker M, eds. Imaging of the head and neck.
2nd ed., Thieme, 2005.
16. Pe’er J, Hidayat AA, Ilsar M, Landau L, Stefanyszyn MA. Glandular tumors of the lacrimal sac. Their
histopathologic patterns and possible origins. Ophthalmology 1996;103:1601-5.
17. Sibony PA, et al: Optic Nerve Sheath Meningiomas. Ophthalmology 1984, 91(11):1313-26.
18. Stefanyszyn MA, Hidayat AA, Pe’er JJ, Flanagan JC. Lacrimal sac tumors. Ophthal Plast Reconstr Surg
1994;10:169-84.
19. Tan WS, Wilbur AC, Mafee MF. The role of the neuroradiologist in vascular disorders involving the orbit.
Radiol Clin North Am 1987;25:849-61.
20. Valvassori GE, Sabnis SS, Mafee RF, Brown MS, Putterman A. Imaging of orbital lymphoproliferative
disorders. Radiol Clin North Am 1999;37:135-150, x-xi.
21. Zimmerman LE, Sanders TE, Ackerman LV. Epithelial tumors of the lacrimal gland: prognostic and
)*'+3!',)$2(#$-/$823/2'("6(*$#)"&"-$2()A!'#T(K/)(F!*)*3&."&(C&$/(Z=[OYON^^PW[PT

1278
Congenital Brain Malformations
Si encuentras una, buscar otras.
Callosal Anomalies Migrational Disorders
!" Migrational disorders
!" Holoprosencephaly Gray Matter Heterotopia [Figure 2]
!" Dandy-Walker syndrome !" Arrest of migration b nerve cells in
!" “Molar Tooth” disorders abnormal locations
!" Cerebellar dysplasias !"Subependymal
!"Focal subcortical
CC Development !"Band (double cortex)
!" 8-20 weeks gestation !" Present with sz
!" Signals from meninx primitiva guide
axons to and across midline
!" Genu b body b splenium b rostrum
!"Hippocampal commisure can mimic
splenium
!"Exceptions: injury, HPE
Corpus Callosum Anomalies

!" Associated with
!"Dandy Walker spectrum, migrational
disorders, midline facial anomalies,
encephaloceles
!" Probst bundle – WM tract lateral to
cingulate gyrus, medial to ventricle
!" Lipomas, interhemispheric cysts common
!"Syndromes with agenesis:
#" Aicardi
#" Fetal alcohol
#" X-linked hydrocephalus
#" Metabolic disorders (PDH)
Aicardi Syndrome [Figure 1]

!" X-linked dominant
!"Clinical: infantile spasms, chorioretinal
lacunae, severe DD
!"Imaging: absent/hypog CC, IH cysts,
Figure 2
PMG, PF cysts, Cb hypoplasia, CP
cysts/papillomas, microphthalmia Postmortem gross specimen showing subependymal
gray matter heterotopia lining the wall of the lateral
ventricle (Courtesy of L Rorke-Adams, MD).
Subependymal Heterotopia [Figure 3]
Two Forms:
!" Few, asymmetrical, at trigones and occ
horns
!"Assoc with Chiari II, agenesis CC
!"When isolated, mild clinical signs,
normal development, seizures in
second decade
!" Many, symmetrical, completely line lateral
ventricles
!"Familial, Xq28 mutation (Filamin A)
Figure 1 #" Girls: mega cisterna magna
#" Boys: cortical malformations,
Sagittal T1 showing absence of the corpus callosum,
multiloculated interhemispheric cysts, and inferior syndactyly, ear anomalies, severe
vermian hypogenesis. Note the enlargement of the mental retardation
massa intermedia.
Congenital Brain Malformations 1279 Neuroradiology

Polymicrogyria [Figure 5]
!" Focal or diffuse, multiple small gyri
!" Error in late migration or early cortical
organization
Figure 3 !" Infxn (CMV), vascular injury
!" Polymicrogyria
Large focus !" Congenital bilateral perisylvian syndrome
of gray
matter !"Pseudobulbar palsy, sz, variable MR,
heterotopia arthrogryposis
in the !" Heterog genetics, Xq28 most common
atrium of
the left
lateral
ventricle on
an axial T2-
weighted
image.
Focal Subcortical Dysplasia

Figure 5
!" Variable cognitive and motor delay A&B
!"70% CC anomalies and BG dysplasia
!" E'3+&A(3&&(0'5'&"!(#f(8+#)W#'2"/0(0'230' Axial and
!" Surgical resection potentially useful coronal
!" Imaging: large, heterogeneous, thin volumetric
T1-weighted
cortex, shallow sulci, small hemisphere images
!"Distortion can mimic mass effect and through a
tumor region of
polymicrogyria
Band Heterotopia [Figure 4] in a small
!" Variable delay, mixed sz right cerebral
hemisphere.
!" > 90% female, Xq22 (DCX)
!" Imaging: bands GM between ventricles
and cortex, shallow sulci, normal-
appearing WM
!"When partial, frontal predominance
(unlike classical lissencephaly – LIS1)
Figure 4
Postmortem
gross
specimen
highlights
the band of
heterotopic
gray matter Lissencephaly
(light) in !" Classical (type I) [Figure 6]
the more !"Arrest of migration aka agyria-
normal-
appearing pachygria
white matter !"LIS1 (17p3): posterior > anterior
(dark) !"DCX (Xq22): anterior > posterior
between #" Incomplete much more common
the cortex
!" Thin outer cortex, cell-sparse zone, thick
and the
ventricle. inner cortex
!" Cobblestone (type II): overmigration
!"Congenital muscular dystrophies, etc

Focal Cortical Dysplasia [Figure 8]
!" Dysmorphic neurons without balloon cells
(Palmini IIA)
!"Often abnormality of lamination
!" Blurring of gray-white junction, frequently
overlooked
!" Partial seizures
Figure 6
A&B
Sagittal and
axial T1-WIs Figure 8
in classical
lissencephaly. Coronal
The normal volumetric
gyral pattern T1-weighted
is absent. image reveals
Note the cell- the unusually
sparse zone deep gyrus
between the in the
thin peripheral parasagittal
cortex and the right frontal
thick lobe with
inner cortex. associated
blurring of
the gray-
white
junction.
Focal Cortical Dysplasia [Figure 9]

!" Dysmorphic neurons with balloon cells
(Palmini IIB)
Lissencephaly [Figure 7] !" May be transmantle
!" Microlissencephaly (radial microbrain) !"GM traversing WM from ventricle to
!"HC > 3 SD below, too few gyri, cortex
shallow sulci, thick cortex !" Cortex may be hyperintense
!"Reduced proliferation in germinal !" Frequently b partial epilepsy
zones
!"Must exclude acquired causes
(infection, ischemia, metabolic, toxins/
radiation)
Figure 9
Figure 7 Axial T1-WIs demonstrates the dysplastic gray matter

running from the right frontal cortex to the ependyma
Sagittal T1-WI in profound microcephaly with a nearly of the frontal horn of the right lateral ventricle.
absent gyral pattern.

Schizencephaly [Figure 10] Semilobar Holoprosencephaly
!" Acquired – mid-second trimester [Figure 12]
ischemia, infection !" Callosal splenium present, anterior extent
!" Dysplasia GM lines cleft from ependyma correlates with IHF
to pia, near central sulcus !" Deep gray nuclei partially separated,
!" Open or closed, 60% unilateral small third ventricle
!" Dorsal cyst common
Figure 12
Axial T2-
WI through
the level of
the deep
gray nuclei
with lack of
separation
of the
frontal
cortex,
Figure 10 A & B
caudate
nuclei, and
Axial T2-WIs show the gray-matter lined cleft through putamina.
the right posterior frontal lobe. Note the absence of
the septum pellucidum.
Holoprosencephaly
!" Classical holoprosencephaly: lack of
separation of basal forebrain
!"Alobar > semilobar > lobar Lobar Holoprosencephaly [Figure 13]
!" Middle interhemispheric variant: lack of !" IHF and falx further anteriorly
separation of dorsal brain !" Frontal lobes and frontal horns of lat
ventricles small
Alobar Holoprosencephaly [Figure 11]
!" More separation of deep gray nuclei
!" Pancake-like cerebrum, rostral-most !" Lobar holoprosencephaly
calvarium !" Posterior callosum more well formed
!" Crescentic holoventricle continuous with !" Hippocampus, third ventricle, temporal
dorsal cyst horns of lateral ventricles nearly normal
Figure 11 Figure 13
Axial T1-WI through the monoventricle and dorsal Axial T2-WI shows the lack of separation of the
cyst of alobar holoprosencephaly. Note the lack of basal forebrain. Note that the deep gray nuclei are
separation of the brain parenchyma anteriorly. separated.

Dorsal Cyst of HPE [Figure 14] Hindbrain Development
!" Distinguish from IHF cyst with agenesis
CC Dandy Walker Syndrome
!" @CC(3/0(Kk:(2A#)N(#$-/$823/)&A(%'))'+( !" Prominent retrocerebellar CSF space
clinical outcome (formerly mega cisterna magna)
!" ~40% of cases diagnosed with HPE are !" Inferior vermian hypogenesis
not !" DW “variant”
!"Partial vermian agenesis, cystic fourth
ventricle, normal-slightly enlarged PF
!" DW malformation
!"Absent vermis, hypoplastic Cb
hemispheres, cystic fourth ventricle,
large PF, high tentorium
!" Prognosis depends on associated
anomalies: hydro, ag CC, heterotopia
Joubert Syndrome
!" Most common “molar tooth” disorder
!" Lack of decussation of superior cerebellar
peduncles and pyramids
!" Clinical: episodic hyperpnea, abnormal
eye movement, ataxia, mental retardation
!" Imaging: cleft in vermis with loss of
normal folia, large SCP, “bat wing” fourth
vent, hemispheres in apposition
Figure 14 Rhombencephalosynapsis [Figure 16]

!" Fused hemispheres, absent vermis +/-
Enlargement of the massa intermedia in agenesis of
the corpus callosum is not thalamic fusion.
fused dentate nuclei, SCP, thalami
!" Associated with: absent ant commissure
and septum pellucidum, ventriculomegaly,
hippocampal hypoplasia, polymicrogyria
Middle Interhemispheric Variant !" C&$/$23&N(+'&3)'0(."+'()"(3##"2(8/0$/-#1(
[Figure 15] reports of relatively asymptomatic adults,
!" Callosal genu and splenium formed, body no genetic predisposition
absent
!" Posterior frontal and parietal affected
!" Anteroinferior frontal, deep gray nuclei
separated
Figure 16
A&B
Sagittal T1-
and axial
T2-weighted
imaging
shows the
absent
inferior
vermis
and the
enlargement
of the
posterior
fossa.
Figure 15
Sagittal T1-WI with the anterior and posterior aspects
of the corpus callosum present, but the body is absent.
Note the atretic cephalocele over the affected region.

Congenital Malformations [Figure 17]
!" Callosal anomalies
!" Migrational disorders
!" Holoprosencephaly
!" Dandy-Walker syndrome
!" “Molar tooth” disorders
!" Cerebellar dysplasias
!" Diagrams from Neuropathology, Ellison
and Love, eds. Mosby International, Ltd.
1998
!" Skull photograph from Nature Reviews
Neuroscience, Nature Publishing Group,
London, England
Figure 17 A & B
Axial and coronal T2-weighted imaging of the fusion of the cerebellar hemispheres.

Congenital Spinal Anomalies

Spinal Dysraphism Myelomeningocele [Figure 3]
!" Defect of closure of neural tube !" Most LS, also more proximal, normal
!" For defects of primary neurulation appearing distal cord
!"Involves: !"j(](#$)'#($/$)$3)$/-(/',+,&3)$"/1(#$)'(
#" Tubulation of neural plate that fails determines defect location
#" Separation from ectoderm
#" 7$#a,/2)$"/("6(#,!'+82$3&(6+".(
neural ectoderm
Reprinted from Neuropathology, Ellison and
Love, 1998 with Permission from Elsevier.
Spinal Dysraphism [Figure 1]
Figure 3
Sagittal MR
(22 weeks
gestation)
showing
posterior
osseous
defect and
neural tissue
traversing
expanded CSF
space.
Myelomeningocele [Figure 2]
!" Failure of neurulation and placode
elevation from expansion of SAS
!"Placode protrudes through osseous Myelocele (Myeloschisis) [Figure 4]
and cutaneous defect !" Placode of OSD in plane with back
!" Less common, embryologically similar
From Barkovich, Pediatric Neuroimaging, ©LWW,
!"Clinical signs and function similar
2000, with Permission.
Figure 4
Figure 2 Axial lumbar myelocele with placode at level of skin
Axial schematic of lumbar MMC with placode forming defect.
dorsal wall of expanded CSF space.
Congenital Spinal Anomalies 1285 Neuroradiology
Chiari II Malformation [Figure 5] Lipomyelomeningocele [Figure 6]
!" Absence raises suspicion that “MMC” !" Lipoma outside canal, expanded SAS
really terminal myelocystocele or lipoMMC !"Placode deformed, with rotation
!" From % distention rhombencephalic toward lipoma and protrusion of
vesicle meninges contralaterally
!" Herniation, CSF leakage !"Nerve roots short on side of lipoma
!" Not associated with CSD (also tether cord), elongated on side
of meninges
2000, with permission.
Figure 6
Axial lumbar lipomyelo-meningocele with asymmetrical

placode/lipoma interface outside canal.
Lipomyelocele (Lipomyeloschesis)
Figure 5
[Figure 7]
Sagittal MR (22 weeks gestation) with small posterior !" Lipoma traverses defect to attach to
fossa, hindbrain herniation, loss of supratentoral CSF placode within or along edge of canal
spaces.
CSD with Subcutaneous Mass

!" Lipoma with dorsal defect (lipoMMC/
lipomyelocele (schisis)
!" Terminal myelocystocele
!"Meningocele
!" Cervical myelocystoceles and
meningoceles extremely rare
Lipoma With Dorsal Defect

!" Premature disjunction of cutaneous
ectoderm from neuroectoderm allows
Figure 7
mesenchyme to contact inner portion of
neural tube Axial lumbar lipomyelocele with placode/lipoma
!" As tube tries to close, mesenchyme ! fat, interface along edge of canal.
interferes with neurulation
!" Lipomas contain ectodermal, mesodermal,
endodermal elements
!" Grows in proportion to overall adipose, &
retether vs MMC

Meningocele [Figure 8]
!" Meningeal-lined CSF sac protruding
through defect
!" Cord does not enter sac, may be
3##"2$3)'0(I$)*(*A!'+)+"!*A("6(8&,.("+( Figure 9
cord tethering
!" ? From CSF pulsations Schematic
!" Lateral meningoceles associated with NF of terminal
myelocystocele.
1, also posttraumatic, connective tissue The expanded
disorders CSF spaces are
separate from the
markedly dilated
terminal ventricle.
CSD without Subcutaneous Mass

!" Simple dysraphic states
!" `"#)'+$"+(#!$/3(%$803
!" K/)+30,+3&1($/)+3.'0,&&3+A1(8&,.()'+.$/3&'(
lipoma
!" Persistent terminal ventricle
!" Cutaneous stigmata7 dimple,
hemangioma, hair
!" 4.8% nl neonates (74% simple, No SB)
!" Atypical dimples = high risk
!"Larger than 5 mm
!"> 2.5 cm cephalad to anus
!"Hemangiomas, hairy patches, tails
Posterior Spina B,#5'

!" Most basic, commonly encountered
!" L5 or S1, in isolation or with CSD when
cord tethered
!" Posterior arch of L5 can remain unfused
until 5-6 years
Intraspinal Lipoma [Figure 10]

!" Mesodermal cells contact primitive
ependyma
!" LS, any level
!" Usually intradural, rarely entirely
intramedullary
Figure 8
Thoracic meningocele. Figure 10
Intradural
extramedullary
Terminal Myelocystocele [Figure 9]
lipoma.
!" Large, skin-covered lumbosacral mass
!" Dilatation of terminal ventricle
!" Herniates through SB
!" High assoc with caudal cell mass
anomalies (GU, lower GI, abdominal wall)
!" Incontinent, extremely poor LE function

Fibrolipomatous I.#&)%'),".+"3+Filum Persistent Terminal Ventricle [Figure 13]
[Figure 11] !" Incomplete regression of TV of 2°
!" Anomaly of 2° neurulation, from neurulation, continuity with central canal
totipotential caudal cell mass $ small cavity
!" Axial T1 most sens !" PTV vs terminal myelocystocele (? severe
!"Unclear if small amount of fat is manifestation from inability of CSF to
anatomical variant vs any fat or escape)
thickening (> 1 mm) = tethered spinal From Barkovich, Pediatric Neuroimaging, ©LWW,
cord 2000, with permission.
Figure 11
Fat Figure 13
deposition Development of distal spine from caudal cell mass via
within retrogressive differentiation.
&#1.)
terminale.
Persistent Terminal Ventricle

[Figure 14]
!" C".."/1()+3/#$'/)(8/0$/-(,/)$&(R(A'3+#
!" K0'/)$23&()"(CG:1($/(2"/,#("+(2"/,#W8&,.(
transition
!" Anatomic variant, no clinical sig, but >
4-5 mm can $ pain and neuro signs
Tight Filum Terminale [Figure 12]

!" Impaired retrogressive differentiation $
#*"+)1(*A!'+)+"!*$2(8&,.(
!" Conus low, assoc with SB, scoliosis, ±
dermal sinus
!" Axial T2 for detection
_%*+,14)3?%$M'-%-8),<)&#1.)3'+.%-"#')4''-)"4) Terminal ventricle on axial ultrasound through conus

hypointense on axial T2. medullaris.

Complex Dysraphic States Split Cord Malformation
!" Disruption during gastrulation $ !" Diastematomyelia (splitting) and
notochordal derangement diplomyelia (duplication), not always
!" 7"+#3&('/)'+$2(8#),&3 distinguishable
!" Neurenteric cysts !" Type I: less common, osseous septum
!" Split cord malformation dividing two dural tubes and hemicords,
!" Dorsal dermal sinus assoc vertebral anomalies
!" Caudal regression syndrome !" Type II: more common, hemicords in
!" Segmental spinal dysgenesis #$/-&'(0,+3&(),%'(t(8%+",#(#'!),.
!" Each hemicord contains a central canal,
Gastrulation [Figure 15] dorsal horn and ventral horn, each $ 1
!" Cells migrate towards primitive streak, nerve root
through primitive groove $ endoderm !" Can be asymmetrical, smaller easily
and mesoderm missed
!" Prospective notochordal cells in cranial !" Split cord malformation
margin of Hensen node become !" Septum $ tethering, ?SCM at CTJ under-
notochordal process recognized
!" Despite lack of s/sx, ~ 75% abnormal
voiding
!" Cutaneous stigmata (type I), females >
males
!" Present: scoliosis, ULE weak, wasting,
tether
!" 8%-45% of OSD, separate from site of
non-neurulation $ rarity of hemiMMC
!" Type I SCM
!" Type II SCM
Dorsal Dermal Sinus [Figure 16]

!" Epith-lined tube from dorsal skin to cord/
coverings
!" Focal nondisjunction neuroectoderm and
cutaneous ectoderm
!" Risk for bacterial infection
!" Epithelium secretes squamous debris, can
exude cheesy material
!" P/w mass or recurrent infection?
Figure 15 A & B !" > 10% intraspinal dermoid
Migration of prospective notochordal cells during From Barkovich, Pediatric Neuroimaging, ©LWW,
gastrulation 2000, with Permission.
(From Neurosurg Focus, 2004).
Dorsal Enteric Fistula

!" Most multifaceted, failure of notochordal
integration
!" Persistence of neurenteric canal $ cleft
from bowel to dorsal skin surface, through
vertebral column and spinal canal Figure 16
!" Usually lumbar
!" High assoc with other CNS and non-CNS Dorsal
anomalies (renal, GI, CDH, pulmonary) dermal sinus,
associated
dermoid,
Neurenteric Cyst spinal cord
!" From partial regression of neurenteric tethering.
canal
!" Lined by secretory epith, contents iso to
CSF or proteinaceous
!" Intraspinal, ventral to T cord, anywhere
!" Associated with dysplastic vert > GI, resp
anom
!" Present late teens, compressive signs and
sx

Caudal Regression Syndrome
[Figure 17]
!" Spectrum from coccygeal/LS hypogenesis
$ sirenomelia
!" Infants of diabetic mothers, 1 in 7500 live
births
!" Associated with:
!"OEIS (omphalocele, exstrophy,
imperforate anus, spinal anomalies) Figure 17
!"VACTERL (vertebral, renal, cardiac,
limb anomalies with anorectal atresia Blunted
and TEF) conus and
absent
!"Currarino triad (sacral hypogenesis,
distal
anorectal malformations, presacral sacrum/
teratoma or meningocele) coccyx
!" Level determines type and severity of caudal
!"Type I: = S1, even mid-T, cord regression
syndrome.
terminates high, blunted tip and
deformation of cauda common, ant-
and postseparation of roots
!"Type II: = S2, less severe, distal-most
2"/,#(3%#'/)1()')*'+'0(%A()$-*)(8&,.1(
lipoma, or CSD with subQ mass
!"Mild CRS: only tip of conus absent,
cord not tethered, may be missed
Segmental Spinal Dysgenesis

!" Focal segment of lumbar or thoracic
spine agenetic-markedly hypogenetic,
cord segmentally disrupted, distal canal
unaffected
!" Distal cord large, focal kyphosis $ early
presentation
!" Anomalous lower extremities,
incontinence
!" ? Within caudal regression spectrum,
morphology depends on level of
notochordal disruption
!" Distal $ CRS, proximal $ SSD
!"Frequency of CRS (11:1), indicates
higher degree of susceptibility of the
caudal cell mass to derangement
References
1. Barkovich AJ. Pediatric Neuroimaging. 4th Ed. Lippincott, Williams & Wilkins, Philadelphia 2000.
2. Dias MS, Partington M. Embryology of myelomeningocele and anencephaly. Neurosurg Focus 2004;16:E1.
3. Ellison D, Love S, Chimelli L, Harding BN, Lowe J, Vinters HV. Neuropathology: A Reference Text of CNS
Pathology. 1st ed. Mosby International Ltd, London 1998.
4. Tortori-Donati P, Rossi A, Cama A. Spinal dysraphism: a review of neuroradiological features with
'.%+A"&"-$23&(2"++'&3)$"/#(3/0(!+"!"#3&(6"+(3(/'I(2&3##$823)$"/T(E',+"+30$"&"-A(O>>>Y]ON]PZW=ZT

Patterns of Enhancement
Contrast Enhancement Time Density Curves [Figure 1]
!" Vascularity
!"Arteries and veins > capillary
!"Perfusion MTT
!"Blood volume (rCBV)
!"9&""0(4"I(H+C9:J
!" Permeability
!"Capillary (leakage)
When Endothelium Goes bad!
Mechanisms of Enhancement
Contrast Enhancement
!" Vascular (intravascular) phase
!"K/2T(%&""0(4"Id*A!'+53#2,&3+(
neoplasm Figure 1 A & B
!"AVM, meningioma, GBM
The bolus creates a high intravascular concentration
!"True “luxury” perfusion gradient that pushes contrast across a permeable
!"Hyperemic swelling (“malignant brain membrane into the tissue interstitial space.
edema”)
!" Interstitial (extravascular) phase
!"Blood-brain barrier breakdown
!"@2,)'($/43..3)$"/(H<GJ Ultrastructure of BBB [Figure 2]
!"Neoplasm, abscess, “granulation”

tissue
!"Ischemia, “luxury” perfusion,
contusion
!"Gliosis?
Figure 2
Schematic of ultrastructure of blood-brain barrier.
Patterns of Enhancement 1291 Neuroradiology

4RS7+Normal Tissues without BBB Cranial Nerve Enhancement
!" Dura (falx and tentorium) !" Optic nerve – never normal
!" Arachnoid? (it is avascular) !" * Seventh nerve:
!" Choroid plexus !"Inside facial canal – yes, asymmetric
!" Pineal gland (epiphysis) ~70%
!" Pituitary gland (hypophysis) !"Geniculate ganglion – 98%
!" CTZ (area postrema of medulla !"Tympanic > labyrinthine > mastoid
oblongata) !"May represent perineural vessels
!"One of the “circumventricular organs” !" Eighth nerve – never normal
* Neuroradiology. 1997;39(3):207-212.
Survival Strategy
!" Tastes bitter Contrast E.?'./1*1.)7+Phases
!"Alkaloids, most medicines
!" Absorbed in stomach VASCULAR BBBB
!" Carried via bloodstream to brain !" ANGIO (I-) ++++ -
!" Medulla oblongata !" VWE(HB2pJ( p(H4"IJ( ((((p(H#)3)$2J
!"@+'3(!"#)+'.3(H4""+("6(6",+)*( !" CT (I-) + +++
ventricle) !" MRI (Gd+) +/- +++
!"CTZ: chemoreceptor trigger zone
Enhancement vs Vasogenic Edema
!"Vomiting control center of autonomic
[Figure 4]
system
Normal Enhancement
!" Choroid plexus (blood CSF barrier)
!" Pineal gland
!" Pituitary stalk
!" Pituitary gland
!"Anterior: adenohypophysis
!"Posterior hypophyseal portal system
!" C35'+/",#(#$/,#(3/0(0,+3&(+'4'2)$"/#
!" Nasal turbinates
!" Sinonasal mucosa
!" Extracranial muscles and mucosa
Nasal Cycle
!" Vasocongestion ~/~ vasoconstriction
!"6-8 hour cycle alternation
!" Humidify and warm the air
!" Secrete mucus (1–2 liters/day)
!" Chronic vasocongestion would cause
submucosal edema
!" Breathe mostly through the
vasoconstricted side (~ 75%-85%)
!" Yogi can control which nostril
!"So can Tom Cruise (Minority Report)
Fat-Suppressed T1-W Gd [Figure 3]
Figure 3
Figure 4 A to F
Abnormal
optic nerve Patterns of enhancement.
enhancement Images Left to Right: Normal patchy, dura-arachnoid
– optic (pachymeningeal), pia arachnoid, dural-based
neuritis. extraaxial, intraaxial subcortical, cortical.

Contrast Morphologic Patterns Intracranial Hypotension [Figure 7]
!" Homogeneous (solid)
!" Heterogeneous (nonuniform)
!" Ring lesions
!"Unilocular or multilocular
!"Smooth thin ring
!"Thick irregular ring
!"Incomplete ring
!"“Cyst” with mural nodule
!" Serpentine (“gyriform“)
!"Serpiginous?
Contrast Location Patterns

!" G,!'+82$3&(H#'+!'/)$/'("+(-A+3&J
!"Pachymeningeal
#" Dura-arachnoid
!"Leptomeningeal
#" Pia arachnoid (subarachnoid
space)
!" Cortical-gyral
!" Gray-white junction Figure 7 A to E
!" Deep white matter Pachymeningeal enhancement.
!" Periventricular
!"Ependymal
Patterns of Enhancement [Figure 5] Spontaneous Intracranial Hypotension

< 60 mm H2O Opening Pressure
!" Orthostatic headache, worse upright
!" <V($#(+'&3)$5'&A(#'/#$)$5'(3/0(#!'2$82((
!" Thick linear dural enhancement
!" No enhancement of sulci or brain surface
!" Enhancement above and below tentorium
!" Enlargement of the pituitary gland
!" Descent of brain
!"Low cerebellar tonsils
!"Third ventricle iter below the
Figure 5 A, B & C tentorium incisural line
!" Some patients have second subdural
Patterns of enhancement.
effusions and/or hemorrhage
Dural E.?'./1*1.)7+Meningioma
D9%'&7+Pachymeningeal [Figure 6] [Figure 8]
!" Globose nodular enhancement + linear
“dural tail”
Figure 6 A & B
Intracranial hypotension – shunted hydrocephalus.
There is widespread and diffuse thickening and
continuous enhancement of the dura, including the Figure 8 A & B
falx and tentorium
Meningioma - dural tail.
(Courtesy Laszlo Mechtler, DNI).

Linear Dural Enhancement Meningioma CSF S0%1'57+Zuckerguss [Figure 10]
!" Curvilinear enhancement !" Carcinomatous Meningitis
!"7,+3&()3$&(3D3(h0,+3&(43$+i
!" First reported with meningioma
!" First reported to be neoplastic invasion
!" What is it really?
!" Thickening of the dura
!" Vasocongestion of the dura
!" Edema of the dura
Pia Arachnoid Enhancement

!" Infectious meningitis
!"Bacterial Figure 10 A, B & C
!"Viral Diffuse leptomeningeal (pia arachnoid) enhancement
!" Chemical meningitis from disseminated CSF seeding of a medulloblastoma.
!"Subarachnoid hemorrhage
!"Ruptured dermoid, epidermoid,
Teratoma, cranio S1%01.),.17+Cortical Gyral
!" Neoplastic meningitis
!"CSF dissemination Contrast Enhancement
!" Cortical/gyriform
Enhancement? [Figure 9] !"Cerebral ischemia/infarction
!" Leptomeningeal enhancement - #" Ischemia
pneumococcal meningitis #" Infarction
!" Bacterial glycopeptides cause breakdown #" Hyperemia
in the BBB #" PRES, seizure, migraine
!"Meningoencephalitis
#" Herpes virus: HSV1, HSV2
#" Creutzfeldt-Jakob
!" CSF or subpial spread
!" SAH (rarely seen)
!" Leptomeningeal malformation (SW)
!" Meningioangiomatosis (NF2)
Ischemic Enhancement
!" Acute and/or reperfusion enhancement
Figure 9 A, B & C !"True “luxury perfusion” 2° to acidosis
Multiple symmetric areas of abnormal leptomeningeal !"BBBB after 4-6 hours of ischemia
enhancement from meningitis. Notice the abnormal !" Subacute to chronic enhancement
enhancement of the entire suprasellar cistern.
Zulmarie Roig, MD and Gil Gonzalez, MD, MGH. !"Capillaries grown in from surface
!"Primarily in GM (cortex and deep)
!"Peak intensity at 2-3 weeks
!"Fades away over weeks to months
!" Atrophy replaces enhancement
CNS Bacterial Infections
!" Birth to 4 Weeks Reperfusion Injury [Figure 11]
!"2-10 cases/10000 births !" Hemorrhagic infarction
!"Group B Streptococcus
!"E coli
!"Listeria monocytogenes
!" 3 months to 3 years
!"`"'.,6?%#14)%-01'-a"' (type B)
!"Strep pneumoniae
!"Meningococcus (Neisseria
meningitidis)
!" Over 3 years to adult
!"Strep pneumoniae
!"Neisseria meningitidis
Figure 11 A & B
Hemorrhagic infarction shows early and dense
enhancement due to reperfusion.

Subacute Stroke vs SWS [Figure 12]
!" Enhancement with atrophy (left image)
!" Enhancement without atrophy (right
image)
Figure 12 A & B
Re-perfusion of ischemic brain (left image) vs Sturge-

Weber syndrome (right image).
Herpes Encephalitis [Figure 13] Figure 14 A to F
Ependymitis.
Diffuse enhancement of the lining (ependyma) of both
lateral ventricles from CMV ependymitis
(Courtesy of Vince Mathews, MD).
Figure 13 A, B & C
Herpes encephalitis. Abnormal cortical signal in
multiple vessel territories.
S1%01.),.17+Cortical Gyral
Periventricular or Ependymal Figure 15 A, B & C

!" CMV
Rimphoma.
!"Thin smooth linear enhancement A thick rind of abnormal enhancing tissue surrounds
!"Herpes virus family *,3?)#"3'+"#):'-3+%$#'4)L4%8-%&$"-3#>).,+'),-)3?')+%8?3X/
!"Ependymitis
!" Lymphoma
!"Thick irregular enhancement
!"Primary CNS lymphoma Ring Lesion Causes
!" Necrotic neoplasm
Cytomegalovirus Ependymitis !" Fluid-secreting neoplasm
!" Advancing infection: cerebritis
RIM PHOMA [Figures 14 & 15] !" Organized abscess with pus and necrosis
!" Subacute hematoma
Ring-Enhancing Lesions !" @053/2$/-($/43..3)$"/(H'-(<GJ
!" Ring lesion
!"Circumferential or peripheral/marginal
enhancement, surrounding a central
non-enhancing region
!"In turn, this is often surrounded by a
large area of “edema”
!"May be unilocular or multilocular

Abscess [Figure 16] WHO 1 vs WHO 4 [Figure 19]
Figure 16 A & B
Two different patients with cerebellar abscess. Figure 19 A & B

Right Image: CT showing the formation of a daughter One patient has a WHO grade 4 tumor (Glioblastoma
abscess. multiforme – GBM) and the other has a WHO grade 2
tumor (Pilocytic astrocytoma).
Which is which? COME TO CLASS.......
Rules for Ring-Enhancing Masses

[Figure 17]
!" Benign Abscess [Figure 20]
!"Round and convex !" Round
!"Smooth, uniform !" Smooth
!"Thin (< 10 mm) !" Regular
!" Malignant !" Convex all around
!"Undulating !" Rim of edema
!"Irregular, variable !" Restricted diffusion
!"Thick !" MRS shows
!"AA peaks
Figure 17 !"Acetate
!"Succinate
Differential
appearance
of ring-
enhancing
lesions.
Ring-Enhancing Lesions [Figure 18]

Figure 20
Cerebral
abscess in
thalamus.
Figure 18
Four different types of “ring lesion.”

Abscess [Figure 21]
Figure 21 A to E Figure 23 A & B

Cerebral abscess. Corresponding CT, T2-Gd, T2, and Glioblastoma multiforme vs abscess (toxoplasmosis).
DWI image. The ring is thin and smooth, hypointense 5?'):%4$,14)614)"-()G?%3')$'##)%-&#3+"3')%-)3?')
on T2. Centrally there is restricted diffusion. abscess causing restricted diffusion (bright on DWI).
Glioblastoma Multiforme [Figures 24 & 25]
Abscess [Figure 22]

!" Viscous pus and coagulation necrosis
Figure 22 A, B & C
Abscess. Figure 24 A & B
Viscous pus and coagulation necrosis cause restricted
diffusion. Glioblastoma multiforme (WHO Grade 3). Portions
of this ring-enhancing lesion are smooth and thin.
However, there are multiple linear enhancing strands
extending into the center. This is inconsistent with an
abscess or cerebritis. This represents residual islands
@UK7+Necrosis vs Pus [Figure 23]
of enhancing living tumor surrounding vessels.
!" “We conclude that viable cell density is
the main biological parameter responsible
for restricted diffusion in brain abscess,
3/0($)($#(/")($/4,'/2'0(%A()*'(')$"&"-$23&(
agents responsible for its causation.”
Magn Reson Med. 2005;54:878-885.
Figure 25 A & B
Ring-enhancing lesion. Glioblastoma (WHO Grade 4).

Tumefactive Demyelination H1*')"*'7+Halo of Serum
[Figure 26] [Figure 27]
!" Absent vasogenic edema … signal
abnormality ends at edge of enhancement
Figure 27 A & B
Acute hematoma. Halo of edema.
Subacute to chronic may have vasogenic edema.
Reactive Ring Enhancement

[Figure 28]
Tumefactive demyelination.
Figure 28 A & B
Acute hematoma. Halo of edema.

Open (Incomplete) Ring Sign Subacute to chronic may have vasogenic edema.
!" Demyelinating disease
!" Fluid-secreting “cystic” neoplasms
Masdeau JC, Moreira J, Trasi S, et al. The open Postoperative Enhancement
ring. A new imaging sign in demyelinating dis- !" Residual tumor
ease. J Neuroimaging. 1996;6:104-107. !"Left behind
Masdeu JC, Quinto C, Olivera C, et al. Open-ring !" Recurrent tumor
%."8%-8)4%8-9)?%8?#>)46'$%&$)<,+)"3>6%$"#)*+"%-) !"It grew back
demyelination. Neurology. 2000;54:1427-1433. !" Infection
!" Normal postoperative change
Contrast E.?'./1*1.)7+Hematoma !"Surgical “trauma,” healing, gliosis
!" Early: hyperdense, round/oval !" Radiation necrosis
homogeneous mass of RBC’s with
proportional mass effect for volume
edema “halo”, not spreading
!" Later: iso-/hypodense, smaller. Reactive
capillaries form outside. Uniform rim
of enhancement. May see “vasogenic”
edema spreading.

Surgical Change and/or Residual Ring-Enhancing Lesions [Figure 29]
Neoplasm?
!" Surgical enhancement typically begins
after 24-48 hours
!"Scan early (24 hours) or scan late (4-6
weeks)
!"May fade after a few weeks but may
last for months
!"Gd+ enhancement may begin in 4-6
hours
!" In the operative bed
!"Mixed with residual tumor?
!"Along the margins of resection
!"Thin and uniform in brain (CT/MR)
!" LINEAR meningeal/dural enhancement on
MR Figure 29 A, B, C & D
!"NOT lumpy-bumpy
Ring-enhancing lesions.
!" Small amounts of air, blood are normal
!"No instruments or sponges, etc
References
1. Andreula CF, Recchia-Luciani ANM. Rationale for the use of contrast media in MR imaging. Neuroimaging
Clinics of North America 1997;7[3]:461-98.
2. Blatt DR, Friedman WA, Agee OF. Delayed computed tomography contrast enhancement patterns in
biopsy proven cases. Neurosurgery 1993;32:560-93.
3. Brant-Zawadski M, Enzmann DR, Placone RC Jr, et al. NMR imaging of experimental brain abscess:
comparison with CT. Am J Neuroradiology 1983;4:250-253.
4. 9+$))(Vk1(U/f.3//(7V1(o'3-'+(@GT(E',+"!3)*"&"-$23&(3/0(2".!,)'+$f'0()"."-+3!*$2(8/0$/-#($/(
experimental brain abscess. J Neurosurg 1981;55:590-603.
5. Britt RH, Enzmann DR, Placone RC Jr, Obana WG, Yeager AS. Experimental anaerobic brain abscess. J
Neurosurg 1984;60:1148-59.
6. Cairncross JG, Pexman JH, Rathbone MP, DelMaestro RF. Postoperative contrast enhancement in patients
with brain tumor. Ann Neurol 1985;17:570-27.
7. Cairncross JG, Pexman JH, Rathbone MP. Post-surgical contrast enhancement mimicking residual brain
tumour. Can J Neurol Sci 1985;12:758.
8. Dolinskas CA, Simeone FA. Surgical site after resection of a meningioma. Am J Neuroradiol 1998;19:419-
69.
9. Ekinci G, Akpinar IN, Baltacioglu F, et al. Early-postoperative magnetic resonance imaging in glial tumors:
prediction of tumor regrowth and recurrence. Eur J Radiol 2003;45:99-110.
10. Forsyth PA, Petrov E, Mahallati H, et al. Prospective study of postoperative magnetic resonance imaging in
patients with malignant gliomas. J Clin Oncol 1997;15:2076-81.
11. Henegar MM, Moran CJ, Silbergeld DL. Early postoperative magnetic resonance imaging following
nonneoplastic cortical resection. J Neurosurg 1996;84:174-212.
12. Jeffries BF, Kishore PR, Singh KS, Ghatak NR, Krempa J. Postoperative computed tomographic changes in
the brain: an experimental study. Radiology 1980;135:751-13.
13. Jeffries BF, Kishore PR, Singh KS, Ghatak NR, Krempa J. Contrast enhancement in the postoperative
brain. Radiology 1981;139:409-13.
14. ;")'(S1(U-'&3/0(B1(k3-'+(91(')(3&T(G,+5$53&1(!+"-/"#)$2(632)"+#1(3/0()*'+3!',)$2('68232A($/(&"IW-+30'(
glioma: a retrospective study in 379 patients. J Clin Oncol 1997;15:3129-40.
15. Nicoletti GF, Barone F, Passanisi M, Mancuso P, Albanese V. Linear contrast enhancement at the operative
site on early post-operative CT after removal of brain tumors. J Neurosurg Sci 1994;38:131-5.
16. F#'+(@91(<"+3/(CX1(S3,6.3/(9@1(`3+D(BGT(K/)+32+3/$3&(),."+($/(2*$&0+'/N(<V($.3-$/-(8/0$/-#(I$)*$/(O](
hours of craniotomy. Radiology 1997;205:807-12.
17. Provenzale JM, Mukundan S, Dewhirst M. The role of Blood-Brain Barrier Permeability in Brain Tumor
Imaging and Therpeutics. Am J Roentgenol 2005;185:763-7.
18. Spellerberg b, Prasad S, Cabellos C, Burroughs M, Cahill P, Tuomanen E. Penetration of the blood-
brain barrier: enhancement of drug delivery and imaging by bacterial glycopeptides. J Exp Med
1995;182:1037-43.

19. Spetzger U, Thron A, Gilsbach JM. Immediate postoperative CT contrast enhancement following surgery
of cerebral tumoral lesions. J Comput Assist Tomogr 1998;22:120-5.
20. G)3/'#2,(CV1(_3+&')(`1(9',5"/(:1(')(3&T(7A#'.%+A"!&3#)$2(/',+"'!$)*'&$3&(),."+#N(CB1(<V(8/0$/-#(3/0(
imaging follow-up: a study of 53 cases. J Neuroradiol 2001;28:230-40.
21. Stark AM, Tscheslog H, Buhl R, Held-Feindt J, Mehdorn HM. Surgical treatment for brain metastases:
prognostic factors and survival in 177 patients. Neurosurg Rev 2005;28:115-9.
22. Smirniotopoulos JG, Murphy FM, Rushing EJ, Rees JH, Schroeder JW. Patterns of contrast enhancement in
the brain and meninges. RadioGraphics. 2007 Mar-Apr;27(2):525-51.
23. Symon L, Murota T, Pell M, Bordi L. Surgical management of haemangioblastoma of the posterior fossa.
Acta Neurochir (Wien) 1993;120:103-10.
24. b$0a3a3(U1(C"//"&&A(7X1(\3)#2*'+(G1(<2<,&&'/(X1(\+$68)*#(`7T(G!,+$",#(&'!)".'/$/-'3&('/*3/2'.'/)("/(
immediate post-operative MRI for paediatric brain tumours. Pediatr Radiol 2005;35:334-8.

Approach to Astocytoma
Pattern A.'&!(,(7+Location Childhood CNS Tumor Demographics
!" Basic approach !" 367 Syrian children, collected from 1993-
!"Where is the lesion? 2002
#" Intraaxial !"Supratentorial – 47%
#" Extraaxial !"Infratentorial – 53%
#" Intraventricular !"52% boys; 48% girls
!"Where is the lesion? !" Overall incidence:
#" Supratentorial !"Medulloblastoma 27%
#" Infratentorial !"Astrocytoma 26%
!"How old is the patient? !"Craniopharyngioma 14%
#" Child !" Posterior fossa only:
#" Adult !"Medulloblastoma (PNET) 54%
!"What about sex? !"Astrocytoma 23%
!"Ependymoma 17%
Primary N1"0&'(*(7+Neuroectodermal
Kadri H, Mawla AA, Murad L. Incidence of Child-
!" Neuroectoderm
hood Brain Tumors in Syria (1993-2002).
!"Embryologic neural tube Pediatric Neurosurgery. 2005;41:173-177.
!"“Neuroepithelial”
!" Broad categories Pediatric Posterior Fossa
!"Glial tumors (gliomas) !" 194 posterior fossa masses
!"Embryonal/immature (PNETs) !"Posterior fossa only:
!"Neuronal (neurocytoma) #" Medulloblastoma (PNET) 54%
!"Mixed (ganglioglioma) #" Astrocytoma 23%
#" Ependymoma 17%
Brain N1"0&'(,'7+Frequency
[Figure 1]
Kadri H, Mawla AA, Murad L. Incidence of Child-
hood Brain Tumors in Syria (1993-2002).
Pediatric Neurosurgery. 2005;41:173-7.
Pediatric Posterior Fossa

!" 454 posterior fossa patients
!" All under the age of 18
!" 402 tumors:
!"37.1% cerebellar astrocytoma (149)
!"34.6% medulloblastoma (PNET) (139)
!"11.4% brain stem astrocytoma (46)
!"7% ependymoma (28)
!"9.9% “other” (40)
Parizek J, et al. Posterior Cranial Fossa Surgery
in 454 Children. Childs’ Nerv Syst. 1998;14:426-
439.
Figure 1
The frequency of the various primary central nervous

Traditional Tumor Perspectives
system tumors range from 2% !" Pathologist: grading
for meningioma and mixed oligoastrocytoma to 40% !"Low grade
for glioblastoma multiforme (GBM) !"High grade
"-()TJe)<,+)%-&#3+"3%:')"43+,$>3,."/ !" Radiologist: imaging
Levin VA, et al. Cancer: Principles & Practice of !"Nonenhancing
Oncology. 1997;2022-2082. !"Enhancing
!" Neurosurgeon: removal
!"“Suckable”
!"“Nonsuckable”
Approach to Astocytoma 1301 Neuroradiology

WHO 1 vs WHO 4 [Figure 2] Grading Systems
Figure 2 A & B
M,(%&'()from Sem Rad Onc. 1991;1:2-9.
One patient has a WHO grade 4 tumor (Glioblastoma
multiforme – GBM) and the other has a WHO Grade 2
tumor (pilocytic astrocytoma). WHO C&'((,#/'),".
(Courtesy of Paul Sherman and RD Zimmerman) !" 7'8/'#(*$#)"&"-$2(#,%)A!'#
!" Grades biologic potential
!" Allows international cooperation
!" Ascending scale of aggression from 1-4
D1#.1+)?1+P%"$&1*7
!" Some low grade enhance WHO Correlation
!" Some low grade do not !" Low grade – grade 1
!" Some low grade ! GBM !" Possible surgical cure
!" Some low grade do not !"Long-term survival
!"Stable histology no progression
Kernohan Grading of Astrocytoma Five-
Year Survival [Figure 3] CNS Neoplasm-GGKLG7+Prognostic
Factors
Lesion Aggression and Grading
Figure 3
For diffuse astrocytomas, the Kernohan and Sayer

(Mayo Clinic/AFIP) remains a good predictor of
survival. However, pilocytic astrocytomas enjoy the
best survival.
.

Pathologic–Radiologic Correlation What Can We Diagnose?
!" Circumscribed astrocytoma
!"WHO grade 1 pilocytic astrocytoma
!"WHO grade 1 subependymal giant cell
astrocytoma
!"WHO grades 2,3 pleomorphic
xanthoastrocytoma
!" Diffuse astrocytoma
!"WHO grade 2 (“astrocytoma”)
!"WHO grade 3 (“anaplastic
astrocytoma”)
!"WHO Grade 4 (“glioblastoma
multiforme” - GBM)
Circumscribed Astrocytoma
Astrocytoma
WHO G%'51+[7+Pilocytic Astrocytoma
“Benign” Astrocytoma
!" Two types
!"Low grade “benign”
#" Diffuse in adults
#" WHO grade 2
!"Low grade “special”
#" Circumscribed in children
#" WHO grade 1
Major Concept
Circumscribed astrocytoma, like pilocytic astrocytoma,
?":')O614?%-8)."+8%-4W)"-()"+'),<3'-)01%(24'$+'3%-8/
A()%"/!)"*'7+Circumscribed
!" “Special” astrocytomas
!" Astrocytoma of young
!" Various locations
!" Well-circumscribed (yet, no capsule)
!" Do not spread along WM
!" Do not change grade (except PXA)
!" C"/#)'&&3)$"/("6(8/0$/-#(2"++'&3)'#(I$)*(
histology
Pilocytic Astrocytoma
!" Cystic cerebellar astrocytoma Juvenile
pilocytic astrocytoma (PA or JPA)

Pilocytic Astrocytoma Astrocytoma Pathology
!" Synonyms: polar spongioblastoma, cystic !" Cyst and mural nodule
cerebellar astrocytoma !" Balanced morphology
!" Cell of Origin: astrocyte (bipolar, hair-like) !" Wall may not enhance
!" Associations: in on with nf-1 !" CA#)(4,$0(*3#(!+")'$/
!" Incidence: 3%-6% of all cranial, 32% of !" Not identical to CSF
child !" Nodule low density on CT
!" Age: 5-15 (Zulch 3-7) !" May calcify up to 25%
!" Sex: slight F (11/9) !" No increase in vascularity
!" Location: cerebellum, chiasm/hypothal, !" WHO grade 1
optic !" Peak at ~10 years
!" Treatment: surgery, patience
!" Prognosis: 77% at 5 years, 75% at 10 Pathology
years, 75% at 15 years !" Biphasic pattern
!"Dense pilocytic glia
Pilocytic Astrocytoma [Figure 4] !"V"#'/)*3&(8%'+#
!" Cyst and mural nodule !"Loose microcystic areas
!"Balanced morphology !" No necrosis
!" Wall may not enhance !" Low grade
!" CA#)(4,$0(*3#(!+")'$/ !" Abnormal capillaries
!"Not identical to CSF !"Allow enhancement
!" Nodule low density on CT !"Fluid production
!"May calcify up to 25%
!" No increase in vascularity Grading Problems in Gliomas
!" WHO grade 1 51 Pilocytic (WHO Gr. 1)
!" Peak at ~10 years KERNOHAN MAYO-ST.ANNE
1 26% 1 2%
2 69% 2 55%
3 6% 3 35%
4 0% 4 8%
By conventional “feature counting,” most pi-
locytic astrocytomas were overgraded.
Figure 4
Pilocytic Astrocytoma
Pilocytic !" Variant appearance
astrocytoma.
Classic cyst-
!" Variant location
with-nodule
morphology. Pilocytic Astrocytoma [Figures 5 to 7]
Copyright 2007.
Pilocytic A()%"/!)"*'7+Radiology
!" Cerebellum, diencephalon
!"Rare in BS or Cerebrum
!" <3a"+$)A(*35'(#$-/$823/)(h2A#)i
!"“Cyst and mural nodule”
#" Part of lining does NOT enhance Figure 5 A, B & C
!"Nodule may be heterogeneous
!"Exceptional purely solid Pilocytic astrocytoma may have a variant appearance.
!" Nodule has increased water
!" C3&2$823)$"/($/(R?WOR?

Figure 6 A & B
Pilocytic astrocytoma. Figure 8 A & B
Pilocytic astrocytoma of hypothalamus.
WHO Grade 1 Tumors

!" Circumscribed astrocytoma
!"Juvenile pilocytic astrocytoma (JPA)
!"Subependymal giant cell (SGCA)
!" Ganglioglioma
!" Meningioma
SGCA [Figure 9]
!" 85%-95% associated with tuberous
sclerosis
This is an unusual pilocytic astrocytoma as the lesion Figure 9 A & B
%4)4,#%()L-,)01%(X@)3?')!5)4?,G4)('-4')$"#$%&$"3%,-@)
and there is no enhancement after contrast. SGCA. These neoplasms are covered by an intact
#">'+),<)'6'-(>.")"-()3?'>)(,)-,3)%-&#3+"3')%-3,)
the adjacent brain. They are most common near
Pilocytic A()%"/!)"*'7+Locations the forman of Monro, attached to the head of the
[Figure 8] caudate nucleus (star). Typically, they show contrast
!" Cerebellum enhancement on both MR and CT.
!" Diencephalon
!"Chiasm and optic nerve
!"Hypothalmus/thalamus
!" Cerebral hemisphere
!" Spinal cord (intramedullary)
Astrocytomas
!" “Special” astrocytomas
Pilocytic Astrocytoma !"Circumscribed growth:
(Juvenile Pilocytic) #" JPA
!" Childhood, young adults #" SGCA
!" Benign, no mitosis/necrosis #" Pleomorphic xanthoastrocytoma
!" Circumscribed – enhancing
!" Cyst formation, mural nodule
!" Cerebellum and diencephalon
!" (Optic tracts, hypothalmus)

Circumscribed Astrocytoma Pilomyxoid Astrocytoma (PMA)
[Figure 12]
[Figure 10]
!" Rare variant of astrocytoma
!" Arises from subpial astrocytes
!" @66'2)#(#,!'+82$3&(2'+'%+3&(2"+)'L(3/0(
meninges
!" Skull erosion (scalloped excavation)
!" Temporal > frontal > parietal
!" WHO grade 2, 3
!" 50% progress over time
Figure 12 A & B
These are uncommon neoplasms and may not have
any typical nor suggestive features on imaging. PMA is
a recently described type of brain tumor. PMA shares
similar features with pilocytic astrocytoma (PA), the
most common central nervous system (CNS) tumor in
the pediatric population.
Med Gen Med. 2004;6(4):42. Published online 2004
November 24. PMCID: PMC1480592 Copyright
Medscape from WebMD.
Figure 10 A & B
Pleomorphic xanthoastrocytoma. The nodule is

6'+%6?'+"#)%-)")416'+&$%"#)"-()41*6%"#)#,$"3%,-/)5?'4')
$%+$1.4$+%*'()31.,+4)"+')"#4,)3>6%$"##>)01%(24'$+'3%-8)
and enhancing. “Ordinary“ Astrocytomas
!" 7$66,#'($/8&)+3)$"/("6(b<(%AN
!"Fibrillary astrocytes
Ganglioglioma [Figure 11] !"Protoplasmic astrocytes
!"Gemistocytic astrocytes
!" WHO 2, 3, 4 (NOT 1)
!" KS and Mayo grades 1-4
Astrocytoma [Figure 13]
Figure 11 A, B & C
K"-8#%,8#%,.").">)"#4,)6+'4'-3)"4)")01%(24'$+'3%-8)
“cyst-with-nodule” lesion.
Figure 13 Astrocytoma.

Astrocytes GFAP Stain Glioblastoma Multiforme … Too Many
Cells, Atypia, Mitoses, Vessels, and
Normal Appearing White Matter … Few Necrosis [Figure 16]
Cell Bodies
Figure 16
Diffuse Grade 2 Astrocytoma … Too
Many Cells [Figure 14] Diffuse
astrocytoma.
Vascular
changes
(endothelial
hyperplasia,
angiogenesis)
and necrosis
characterized
WHO Grade 4 – glioblastoma multiforme.
Daddy, Where do Glioblastomas Come

From?
!" Progressive transformation from lower
grade diffuse astrocytoma or arise de
novo
Figure 14 Astrocyte Mutation

Diffuse astrocytoma. Individual neoplastic cells spread
out through the white matter. In WHO Grade 2, this is
only noted as “increased cellularity.”
Diffuse Grade 2 Astrocytoma … Too

Many Cells
Diffuse Anaplastic Astrocytoma …

Anaplastic Cells [Figure 15]
Diffuse Astrocytoma [Figure 17]

!" WHO grade 4
!" WHO grade 3
!" WHO grade 2
!" Normal
Figure 15
Diffuse astrocytoma Grade 3. Even more cells, mitoses

and cellular atypia – no margin or edge.
Figure 17
All three grades of astrocytoma in one patient.

A()%"/!)"*'7+Radiologic Grading Gliomatosis Cerebri [Figure 19]
!" Type 1: WHO grade 2, KS grade 1-2, !" T2
“benign” !" T1-gad
!"Homogeneous !" NOTE: looks like “vasogenic edema” yet
!"No enhancement, no vasogenic edema there is no enhancement
!" Type 2: WHO grade 3 anaplastic !" This is NOT edema secondary to a lesion,
!"Variable enhancement, edema rather it is tumor signal from the primary
!"50% enhance – 50% do not tumor
!" Type 3: WHO grade 4 glioblastoma
!"Heterogeneous (necrosis, blood)
!"Ring enhancement, edema
“Benign” A()%"/!)"*'7+U;O+Grade 2,
KS 1-2, Mayo 1
!" Younger patient
!"Childhood
!"Young adults (20-40 years old)
!" NL vessels (no neovascularity)
!"BBB intact
!"No edema
!"No enhancement
!"No tumor vessels
B1.,-.7+Diffuse
!" Homogeneous Figure 19 A & B
!"No necrosis
K#%,."3,4%4)$'+'*+%/)B)(%<<14')"43+,$>3,.")%-&#3+"3%-8)
!"No hemorrhage two or more lobes of the brain.
!"Increased water
!"Dark and poorly demarcated on CT
#" Dark and sharp on T1-W
#" Bright and sharp on T2-W A()%"/!)"*'7+Microcystic Change
#" Microcyst >>> macrocyst [Figure 20]
(Macrocysts Occur in JPA, etc.)
Grade 2 Fibrillary Astrocytoma

[Figure 18] Figure 20
!" T1-non (left image)
!" T1-gad (right image) Astrocytoma.
Microcystic
change.
Spread Along White Matter Tracts

[Figure 21]
Figure 18 A & B
K+"(')J)&*+%##"+>)"43+,$>3,."/)=,)'-?"-$'.'-3)"<3'+)
gadolinium.
Figure 21 A & B
Diffuse grade 2 astrocytoma spreading through white

matter including corpus callosum.

MRS for the Complete Idiot [Figure 22] Diffuse Astrocytoma [Figure 23]
Figure 22
Hunter’s angle. Urban legend suggests a neurosurgeon

pulled out a pocket comb to demonstrate that in a
normal MRS there is a rising diagonal line connecting
from choline (Cho) to creatine (CR) to n-acetyl-
aspartic acid (NAA). NAA is unique to the brain of
vertebrate animals.
Nature 203, 658 (08 August 1964).
Pontine astrocytoma. WHO Grade 2.
EIS7+Hypothetical Neoplasm
Spread Along WM Tracts
!" Corpus callosum
!" Corona radiata
!" Peduncles
!" Anterior commissure
!" @+2,3)'(8%+'#1(')2
Modes Of Spread
!" Expansion of brain
!" Along white matter tracts
!" Along surfaces: pia and ependyma
!" Across the meninges, across the dura
WHO 2 $ GBM [Figure 24]
Brainstem Glioma
!" Usually in the pons
!" Usually astrocytoma
!"Diffuse astrocytoma Grade 2-4
!" Often ventrally exophytic
!"Surround basilar artery – elevate from
clivus
!" Often pilocytic
!"Midbrain - mesencephalon
!"Dorsally exophytic
Figure 24 A & B
Progressive transformation of WHO Grade 2

astrocytoma to glioblastoma multiforme.

Expanded Brain [Figure 25]
Figure 25
Tracking along
WM – uncinate
fasciculus.
Anaplastic A()%"/!)"*'7+Overall
Characteristics
!" WHO grade III malignant glioma
!" Less aggressive than GBM, malignant with
somewhat better prognosis
!" Frequency: highest in young adults (30–40
years old)
!" Recurrence: often as a higher grade
glioma
!" C*3&&'/-'N(0$682,&)()"(+'."5'(2".!&')'&A(
with surgery
!" Median survival: 3–4 years
Anaplastic Astrocytoma [Figure 26]

!" Enhancement but no necrosis …
!" WHO 2007 makes this GBM Figure 27 A, B, C & D
Anaplastic astrocytoma. No enhancement in this

example – about 50% will enhance.
Review of Anaplastic Astrocytoma

!" 21 pathologically proven AA (WHO grade
3)
!" 11 Upgraded to GBM using the WHO 2007
!"18 showed contrast enhancement
#" 10 upgraded to GBM
#" 7 because of microvascular
changes
#" 3 because of necrosis
#" 8 remained as AA but had
h$/#,682$'/)()$##,'i
Figure 26 A & B !"3 cases did not show enhancement
#" 1 upgraded to GBM because of
A 47-year-old right-handed woman with 2 weeks of vascular changes
HA, followed by mild hemiparesis for 2 days.
Nf9)^,+(2&-(%-8)(%<&$1#3>@)#'<3)<"$%"#)(+,,6@).%#()bEfg
LLE weakness. “Malignant” Astrocytoma
Stereotactic Bx for Dx, followed by resection 7 days !" Older patients
later. !"40’s and up
!"Exceptions (PNET)
!"~ 1/2 arise from previous low grade
(2-3)
Anaplastic Astrocytoma [Figure 27]
!" Abnormal vessels (neovascularity)
!" No enhancement – abnormal MRS !"BBB abnormality
!"Vasogenic edema
Increased Cellularity, +/- Minimal
!"Contrast enhancement
Vascular Changes, No Necrosis, No !"Irregular vessels, shunting, etc
Hemorrhage !" Heterogeneous
!"Hemorrhage (old/new)
!"Tumor necrosis
!"Tumor itself
Glioblastoma Multiforme [Figure 28] P:E7+Thicker on Surface
Pseudopalisading Necrosis [Figure 31]

Figure 28
Glioblastoma
multiforme.
Photo-
micrograph
at high power
shows both
angiogenesis
and
pseuopalisading
necrosis.
Figure 31 A & B
Glioblastoma multiforme with pseudopalisading

(Grade 4) G&,"$&'()"*'7+FUKB4:M++++++++++ necrosis.
[Figure 29]
Glioblastoma Multiforme (Surrounding

Zone of I.#&)%'),".C
!" GBM arose from a preexisting low grade
!"Surrounding lower grade neoplasm
!"May also transform over time
!" GBM arose de novo
!"Sends cells to invade the brain
Glioblastoma Multiforme [Figure 32]
Figure 29 A & B
Increased perfusion due to angiogenesis in a
glioblastoma multiforme.
CT Perfusion
X-Ray Perfusion Imaging [Figure 30]

!" Hypervascularity means rCBV and rCBF
!" Early draining veins mean short MTT
Figure 32 A & B
Neoplasm in the edema … neoplasm in NAWM.
Astrocytes Track Along WM
Figure 30 A & B
Glioblastoma multiforme. The early draining veins

+'0'$3)%-$+'"4'()6'+<14%,-)"-()")4?,+3'-'().'"-)
transit time (MTT).

DTI and Tumor Spread
Ring Enhancing Mass [Figure 33]

!" Round
!" Smooth
!" Thin wall
!" Undulating
!" Irregular
!" Thick wall
!" Benign
!" Malignant
Figure 33
Figure 35 A & B
Original biopsy was reported as anaplastic astrocytoma

– WHO grade 3.
MRI of Tumor Necrosis

!" Prolonged T1, T2
!"Fluid change – CSF-like
!" Shortened T1, T2
!"Hemorrhage
!"Iron deposition
!"Free radicals
!"Proteinaceous debris (T1)
!" High ADC (dark on DWI in core)
DWI of Glioblastoma (Grade 4)
B9))1%Q!+Glioma [Figures 34 to 36]

Figure 36 A & B
Rapid growth and progression in a glioblastoma

multiforme.
D1#.1+)?1+Problem
!" Some low grade enhance*
!" Some low grade do not
!" Some low grade $ GBM
!" Some low grade do not *
D1#.1+)?1+P%"$&1*7+Answers
!" Some low grade enhance*
!" Some low grade do not
!" Some low grade $ GBM
Figure 34 A & B !" Some low grade do not*
* These are the circumscribed astrocytomas.
I133'+0>)8#%,.")h)glioblastoma multiforme.
The others are the diffuse astrocytomas
References
1. Kadri H, Mawla AA, Murad L. Incidence of childhood brain tumors in Syria (1993-2002) Pediatric
Neurosurgery 2005;41:173-7.
2. Levin VA, Leibel SA, Gutin PH. Neoplasms of the central nervous system. In: DeVita VT Jr, Hellman S,
Rosenberg SA, eds. Cancer: Principles & Practice of Oncology. Vol 2. 5th ed. Philadelphia, Pa: Lippincott-
Raven Publishers; 1997:2022-82.
3. Parizek J, et al. Posterior cranial fossa surgery in 454 children. Childs’ Nerv Syst 1998;14:426-39.
4. Pobereskin LH, Chadduck JB: Incidence of brain tumours in two English counties: a population based
study. J Neurol Neurosurg Psychiatry 2000;69:464-71.

Non-Astrocytic Gliomas
Primary N1"0&'(*(7+Neuroectodermal Oligodendroglioma
!" Neuroectoderm !" bkF(2&3##$823)$"/(
!"Embryologic neural tube !"Oligodendroglioma (WHO grade 2)
!"Neuroepithelial !"Anaplastic oligodendroglioma (WHO
!" Broad Categories grade 3)
!"Glial tumors (gliomas)
!"Embryonal/immature (PNETs) Oligodendroglioma
!"Neuronal (neurocytoma) !" Grade 1: rare
!"Mixed (ganglioglioma) !" Grade 2: conventional oligodendroglioma
!" Grade 3: anaplastic oligodendroglioma:
Gliomas !"Hypercellularity, atypia, mitoses,
!" Astrocytoma endothelial proliferation, necrosis
!"Circumscribed (children, cerebellum + !" Grade 4: GBM-like (rare)
diencephalon) !"Not biologically equivalent to grade 4
!"Diffuse (adults, cerebral hemisphere) 8%+$&&3+A(3#)+"2A)".3
!" Oligodendroglioma
!"Adult, cerebral hemisphere, O&,-"51.5%"-&,"*'7+Gross Pathology
23&2$823)$"/ !" Arise in white matter
!" Ependymoma !" Grow toward cortex
!"Intraventricular, children >> adults !" Unencapsulated
!" Choroid plexus papilloma/carcinoma !" E")(3#($/8&)+3)$/-(3#(3#)+"2A)".3
!"Intraventricular, children >>>> adults !" Heterogeneous
!" Medulloblastoma – PNET !"Myxoid areas (“cystic”)
!"Cerebellar vermis, children >>> !"Hemorrhage
adults !" C3&2$823)$"/
What is it? O&,-"51.5%"-&,"*'7+Radiology

!" Solitary, intraaxial, mass lesion !" Heterogeneous hemispheric mass
!"Primary neoplasm !"Ca++, cysts – “myxoid change,” blood
#" Glioma products
#" Astrocytoma !" UL)'/0()"(2"+)'L(3/0($/8&)+3)'(\<
'" 7$66,#'(8%+$&&3+A !"Gyriform or dot-dash Ca++
WHO grade 2 !"Scalloped erosion inner table
WHO grade 3 – anaplastic !" 1/3-2/3 will enhance
WHO grade 4 – glioblastoma !"+/- anaplasia
#" Oligodendroglioma !" MR +/- special pulse sequences for Ca++
!"Metastasis detection
!"Abscess !"T2*, GRE, magnetic susceptibility
!"Tumefactive demyelination !" MR spectroscopy?
!"Potential for tumor grade, but not
Oligodendroglioma subtype or genetics
!" Cell of origin
!"Oligodendrocyte
!"Makes central myelin
!"51%-90% oligos, remainder
astrocytes
!" 1%-8% of ALL CNS primary
!" Adults > children (8:1)
!" Age peak 35–45 years
!" Supratentorial – 85%, extend to cortex
!" Slow growth, long Hx (10 years)
!" Prognosis better with 1p and 19q
mutations
Non-Astrocytic Gliomas 1313 Neuroradiology

Oligodendroglioma [Figure 1] “Fried Egg” Appearance [Figure 3]
!" Signal and attenuation are water-like
Figure 3
The cells have

distinct cell
membranes
and resemble
“fried eggs.”
“Chicken Wire” Vascularity [Figure 4]
Figure 4
Fried Egg.
Round dark
nucleus
surrounded by a
clear halo which
is an artifact of
&U"3%,-/)
Figure 1 A to E Chicken-wire.
The capillary
c#%8,('-(+,8#%,."/)!5)4?,G4):'+>)('-4')$"#$%&$"3%,-4) vessels form a “chicken wire” pattern around nests of
which are highly suggestive and characteristic of cells.
oligodendroglioma.
Courtesy of JP Parisi, Mayo Clinic.
Oligodendroglioma [Figure 2] Oligodendroglioma

!" Combined 1p and 19q chromosome loss
!"Associated with prolonged survival
!"Response to PVC (Procarbazine,
Vincristine
!"CeeNU® (Lomustine) chemotherapy
!"50% volume decrease in 100% of
patients
!"Median survival 10 years vs 2 years
!"95% 5-year survival
!"Most powerful predictor of prognosis
on multivariate analysis
Cairncross, et al. J NCI. 1998;90:1473.
O&,-"51.5%"-&,"*'7+Bleed
Gliomas
!" Astrocytoma
Figure 2 A & B !"Circumscribed (children, cerebellum +
diencephalon)
c#%8,('-(+,8#%,."/)F'-4')$"#$%&$"3%,-4)L43%##):%4%*#'),-)
!"Diffuse (adults, cerebral hemisphere)
wide window) and expansile remodeling.
!" Ependymoma
!"Intraventricular, children >> adults
!" Choroid plexus papilloma/carcinoma
!"Intraventricular, children >>>> adults
!" Oligodendroglioma
!"Adult, cerebral hemisphere,
23&2$823)$"/
!" Medulloblastoma: PNET
!"Cerebellar vermis, children >>>
adults

Medulloblastoma Subtypes (Grade 4) Kadri H, Mawla AA, Murad L. Incidence of child-
!" ICD-0 9470/3 Medulloblastoma hood brain tumors in Syria (1993-2002). Pediat-
!" ICD-0 9471/3 Desmoplastic/nodular ric Neurosurgery. 2005;41:173-177.
medulloblastoma
!" ICD-0 9471/3 Medulloblastoma with Medulloblastoma [Figure 5]
extensive nodularity
!" ICD-0 9474/3 Anaplastic medulloblastoma Figure 5
!" ICD-0 9474/3 Large cell medulloblastoma
!" ICD-0 9472/3 Medulloblastoma with Medullo-
myogenic differentiation blastoma
!" ICD-0 9470/3 Medulloblastoma with (PNET).
melantoic differentiation Rounded mass
in the central
posterior
Medulloblastoma fossa.
!" Cell of origin:
!"“Medulloblast” – not
!" Bipotential embryologic cells:
!"Migrate from fourth to form CRBLL
!"Glial and neuronal differentiation M159&&"$&'()"*'7+Gross Pathology
!"External granular cells (fetus) !" Arise from:
!"Internal granular layer (mature) !"Posterior (inf.) medullary vellum
!" A type of primitive neuroectodermal !"Vermis (midline cerebellum)
tumor – PNET !" Morphology:
!"Expansile, spherical, unencapsulated
M159&&"$&'()"*'7+Demographics !"Posterior fourth ventricle
!" First or second most common cerebellar !"Residual ANT. crescent of CSF
neoplasm in children !"“Homogeneous”
!"1/5–1/3 of all pediatric CNS #" (Ca++, Cyst, Heme are UN-
!"M:F 1.1–2:1 common)
!" May be congenital
!"Present at birth up to 60 days M159&&"$&'()"*'7+Micro Pathology
!" Most (1/2) < 15 years [Figure 6]
!" However; 1/3 present from 15-35 years !" Small round “blue cell” tumor
!" 5-year survival approaching 75%-85% !"Immature, high nuclear: cytoplasm
!" Primitive neuroectodermal tumor !"Both neuronal and glial features
(occasional astrocytic differentiation)
Pediatric Posterior Fossa !"Form “Homer-Wright Rosettes”
!" 454 posterior fossa patients #" Cells arranged in a circle surround
!" All under the age of 18 2"+'(I$)*(&$/'3+(8%+$&#
!" 402 tumors: !"Densely cellular
!"37.1% Cerebellar astrocytoma (149) !"Necrosis/hemorrhage is not rare
!"34.6% Medulloblastoma (PNET) (139)
!"11.4% Brain stem astrocytoma (46)
!"7% Ependymoma (28)
!"9.9% “Other” (40) Figure 6
Parizek J, et al. Posterior cranial fossa surgery in
Medullo-
454 children. Childs’ Nerv Syst. 1998;14:426- blastoma. A
439. small, round,
blue-cell
Childhood CNS Tumor Demographics tumor.
!" 367 Syrian children, collected from 1993-
2002
!"Supratentorial 47%
!"Infratentorial 53%
!"Male 52%:female 48%
!"Overall incidence:
#" Medulloblastoma 27%
#" Astrocytoma 26%
#" Craniopharyngioma 14%
!"Posterior fossa only:
#" Medullo (PNET) 54%
#" Astrocytoma 23%
#" Ependymoma 17%

M159&&"$&'()"*'7+Radiology
[Figure 7]
!" Posterior fossa, behind/in fourth ventricle
!" hk"."-'/'",#i(H*'($#(&A$/-J(%,)1(8/'&A(
heterogeneous
#" Grossly uniform
#" Hyperdense on CT (without Ca++)
#" Hypo-/isointense to GM on MR
#" Cellularity and high N:C ratio
Figure 9 A, B & C
#" Ca++ and “cysts” < 15%
!" Enhance with contrast Medulloblastoma (PNET). Rounded mass in the central
posterior fossa.
Medulloblastoma [Figure 10]

!" ‘Homogeneous’
!"Finely irregular
!" Cyst and hemorrhage are uncommon
< 10%
!" Hyperdense on NCT
!"Up to 75%
!"Densely cellular
!"Small round blue cells
!" Center is behind fourth ventricle
!" Rounder, not angular
Figure 7 A & B
Medulloblastoma (PNET): Rounded mass in the central

posterior fossa.
Fourth V1.)%,/&17+Schematic Figure 10
Medulloblastoma.
Central Masses [Figure 11]
Medulloblastoma (PNET) [Figures 8 & 9]
Figure 8 A & B
Medulloblastoma (PNET). Rounded mass arising in the Figure 11 A & B
cerebellum and not from the fourth ventricle roof.
Schematic diagram of medulloblastoma and
ependymoma.
(Copyright 2005).

PR=J7+Reduced Diffusion Desmoplastic Variant of
Medulloblastoma
Atypical M159&&"7+Hemorrhage !" About 1/10 medulloblastomas are
desmoplastic
Posterior Fossa !" @%,/03/)(+')$2,&$/(8%'+#(3/0(2"&&3-'/
!" Incidence/location: !" Dense reticulin areas surround nodules
!"Medulloblastoma (PNET) (1/4-1/3) (‘pale islands’) without reticulin
#" Posterior to fourth !" Like medulloblastoma, the cell of origin is
!"Brainstem glioma (1/6) not clear:
#" Anterior to fourth !"‘Medulloblasts’
!"Ependymoma (1/6) !"External granular cells
#" Inside fourth !"Subependymal matrix cells
!"Pilocytic astrocytoma (1/4-1/3) !"More than one cell of origin
#" Lateral and/or posterior to fourth !" WHO grade 4
#" These are often a cyst with nodule !" More often peripheral/lateral than midline
!" Older patients than typical
Medulloblastoma (PNET)
medulloblastoma
“Zuckerguss” or “Sugar Icing” !" Better outcome than medulloblastoma
(CSF Dissemination) M159&&"$&'()"*'7+Desmoplastic
CSF Dissemination Cerebral Neuroblastoma [Figure 13]
!" Neuroectodermal:
!"PNET (medulloblastoma)
!"GBM (reaches ventricle or pia)
!"Ependymoma
!"Oligodendroglioma (micro curiosity –
no Sx)
!"CPP and CPC
!" Nonglial:
!"Germinoma
!"Lymphoma (usually secondary)
!"Leukemia Figure 13 A & B
!"Carcinomatous meningitis Cerebral neuroblastoma – PNET.
CSF S0%1'57+Zuckerguss [Figure 12]
CSF spread of medulloblastoma (PNET).

References
1. Kadri H,Mawla AA, Murad L. Incidence of childhood brain tumors in Syria (1993-2002. Pediatric
Neurosurgery 2005;41:17377.
2. Parizek J, et al. Posterior cranial fossa surgery in 454 children. Childs’ Nerv Syst 1998;14:426-39.
3. Jenkinson MD, Smith TS, Joyce K, Fildes D, du Plessis DG, Warnke PC, Walker C. MRS of oligodendroglial
tumors: correlation with histopathology and genetic subtypes. Neurology 2005 Jun 28;64(12):2085-9.
4. C3$+/2+"##(X\1(M'D$(S1(c&3)'#2,(<C1(')(3&T(G!'2$82(-'/')$2(!+'0$2)"+#("6(2*'.")*'+3!',)$2(+'#!"/#'(3/0(
survival in patients with anaplastic oligodendrogliomas. J Natl Cancer Inst 1998;90:1473-9.
5. Korshunov A, Remke M, Werft W, Benner A, Ryzhova M, Witt H, Sturm D, Wittmann A, Schöttler A,
:'&#%'+-(X1(V'$6'/%'+-'+(\1(V,)D"I#D$(G1(G2*',+&'/(b1(S,&"f$D(@U1(5"/(7'$.&$/-(@1(;$2*)'+(`1(`8#)'+(
SM. Adult and pediatric medulloblastomas are genetically distinct and require different algorithms for
."&'2,&3+(+$#D(#)+3)$823)$"/T(X(C&$/(F/2"&T(O>Z>(X,/(O>YOQHZQJN^>R]W[>T(U!,%(O>Z>(<3A(ZPT
6. Rutkowski S, Gerber NU, von Hoff K, Gnekow A, Bode U, Graf N, Berthold F, Henze G, Wolff JE, Warmuth-
Metz M, Soerensen N, Emser A, Ottensmeier H, Deinlein F, Schlegel PG, Kortmann RD, Pietsch T, Kuehl
J; German Pediatric Brain Tumor Study Group. Treatment of early childhood medulloblastoma by
postoperative chemotherapy and deferred radiotherapy Neuro Oncol. 2009 Apr;11(2):201-10. Epub 2008
Sep 25.
7. Giangaspero F, Perilongo G, Fondelli MP, Brisigotti M, Carollo C, Burnelli R, Burger PC, Garrè ML.
Medulloblastoma with extensive nodularity: a variant with favorable prognosis. J Neurosurg. 1999
Dec;91(6):971-7.
8. Koeller KK, Rushing EJ. From the archives of the AFIP: medulloblastoma: a comprehensive review with
radiologic-pathologic correlation. Radiographics. 2003 Nov-Dec;23(6):1613-37.
9. Koral K, Gargan L, Bowers DC, Gimi B, Timmons CF, Weprin B, Rollins NK. Imaging characteristics of
atypical teratoid-rhabdoid tumor in children compared with medulloblastoma. AJR Am J Roentgenol. 2008
Mar;190(3):809-14.
10. Rodallec M, Colombat M, Krainik A, Kalamaridès M, Redondo A, Feydy A. Diffusion-weighted MR imaging
3/0(!3)*"&"-$2(8/0$/-#($/(30,&)(2'+'%'&&3+(.'0,&&"%&3#)".3T(X(E',+"+30$"&T(O>>](X,/Y^ZH^JNO^]WPT

Neoplasms of the Meninges
Pattern A.'&!(,(7+Location Primary Meningeal Neoplasms
!" Basic approach !" Meningioma (arachnoid cap cell):
!"Where is the lesion? !"Meningioma (typical and metaplastic)
#" Intraaxial !"Atypical meningioma
#" Extraaxial !"Anaplastic (malignant) meningioma
#" Intraventricular #" Papillary meningioma
!"Where is the lesion? !" Mesenchymal (non-meningothelial)
#" Supratentorial !" Primary melanocytic lesions
#" Infratentorial !" Uncertain origin
!"How old is the patient? !"Hemangiopericytoma (pericyte)
#" Child !"Hemangioblastoma (mesenchyme)
#" Adult
!"What about sex? Meningeal T9*"%(7+U;O+Grades
!" 91% of meningioma – grade 1
Extra-A>,'&7+R".BGlial !"Includes most subtypes/metaplastic
!" Meningioma changes
!"Hemangiopericytoma !"B+3/#$)$"/3&1(8%+"%&3#)$21(
!" Schwannoma meningothelial
!" Pituitary !" 8.3% are ATYPICAL meningioma – grade
!" Cysts 2
!"Epidermoid, dermoid !" Hemangiopericytoma – grade 2/3
!"Colloid, craniopharyngioma !" Papillary meningioma – grade 3
!"Arachnoid !" < 1% are anaplastic meningioma -
!" Chordoma grade 3
!" Pineal Sandhyamani, Rao, Nair, Radhakrishan. Atypical
Meningioma: A Clinicopathological Analysis.
Educational Objectives Neurology India. 2000;48:338-342.
!" Meningioma is the most common nonglial
primary tumor M1.,.-,"*'7+Benign Subtypes – WHO 1
!" Meningioma is the most common !" Syncytial (meningothelial)
extraaxial neoplasm !" :$%+"%&3#)$2(H8%+",#J
!" Most meningiomas have “typical imaging” !" Transitional (features of both)
!"Hemispheric, homogeneous, broad !" Psammomatous
based on the dura, hyperostosis, !" Microcystic (humid), secretory
hormonally sensitive !" Metaplastic features
!" Some meningiomas have “atypical !"Lipoblastic, osteoblastic,
imaging” chondroblastic
!" Hemangiopericytoma is not a meningioma !"Myxoid, xanthomatous, melanotic
Meningioma M1.,.-,"*'(7+Cell of Origin [Figure 1]
!" 75% are histologically typical !" 7,+3&(8%+"%&3#)s(m(/"
!" 75% are radiologically typical !" Arachnoid cap cell
!"CT !"“Meningothelial cell”
!"MR !"Arachnoid granulations
!"Angiography !"Dural sinuses
!" Atypical imaging =/= atypical histology #" Sup. sag.
!" “The atypical appearance of a common #" Sphenoparietal
lesion may be seen more often than the
classic appearance of an uncommon
lesion.”
Figure 1
Inset. HE of
arachnoid
granulation.
Neoplasms of the Meninges 1319 Neuroradiology

M1.,.-,"*'7+Etiologic Factors M1.,.-,"*'7+=.+Plaque
!" Trauma !" U/(!&3l,'(H&$D'(3(43)(%+'30J
!" Radiation !" Pancake
!" Viruses !" Crepe
!" Familial (non-NF2) meningioma !" Wonton wrapper
!" E',+"8%+".3)"#$#(m()A!'(O !" Tortilla
!"MISME syndrome !" Arepa (Colombia)
!" Sopapilla (Chile)
M1.,.-,"*'7+Radiation !" Bolo de milho (Brazil)
!" Low Dose (< 800 cGray) !" Pita (Greece and Middle East)
!"Immigrants to Israel (1940s) !" Naan (India)
!"Tinea capitis (ringworm) !" Lavaash (Farsi/Iran)
!"G,!'+82$3&(+30$3)$"/ !" Injera (Ethiopia)
!"High incidence of meningioma
!" High dose (> 2000 cGray = 2000 RADS) M1.,.-,"*'7+4J+Imaging
!"Used for skull base tumors !" Noncontrast
!"Pituitary adenoma !"Sharply circumscribed
!"Homogeneous
M1.,.-,"*'7+Molecular Biology !"Hyperdense (+/- Ca++)
!" Postulate tumor suppressor gene #" NOT from psammoma bodies
!" Chromosome 22 – deletion in tumor cells !"Broad dural surface
!"Both sporadic and inherited !"Bone changes (hyperostosis)
!"With or without NF2 !" Enhanced CT
!" Homozygous for TWO wild-type copies is !"Homogeneous enhancement
normal
!" Heterozygous for 22 develops neoplasm M1.,.-,"*'7+Early CT [Figure 3]
!"Because there is a subsequent loss of
the other wild-type gene
!" Inherited (germline) deletion of 22
!"With schwannoma = NF2
Meningiomas
!" 1/7-1/4 of all intracranial primary
!"~ 6/100000 per year
!"Small ones in ~ 1.4% of autopsies
!" 1/4–1/3 of all intraspinal tumors
!" Middle age (40-60 years)
!" Female > male
!"Cranial 2-4:1
!"Spinal 4-8:1 Figure 3 A & B
!"Progesterone receptors in 2/3 Meningioma with classic features of hyperdensity and
!"Estrogen receptors less common hyperostosis.
M1.,.-,"*'7+Sharp Margin [Figure 2]

Psammomatous Meningioma [Figure 4]
Figure 2 A & B
Meningioma – parasagittal.
Figure 4 A & B
Spinal masses.

M1.,.-,"*'7+Vasogenic Edema Meningioma and Edema
!" Vascular
!"Parasitization of MCA, etc Edema and Prognosis
!"Compression of cortical aa./vv. !" Edema =/= histology
!" Compressive trauma !" Edema =/= size
!" Secretory effect !" Edema ~ pial vascularity
!" hB+3/#2"+)$23&(4"Ii !" Edema is related to resectability
!"Close apposition of tumor to brain !"Smaller “pseudocapsule”
!"Thinned cortex !"Surgical “cleavage plane”
!"pdW($/8&)+3)$"/("6(%+3$/ !"Tumor “sticks” to underlying brain
!"Fluid gradient from meningioma into !" Resectability is related to prognosis
brain !" Edema is indirectly related to prognosis
Meningioma and Edema [Figure 5] M1.,.-,"*'(7+EI+Imaging

!" “Meningiomas are ISO-intense”
!"Usually on T1-W
!"Vary pulse sequence to see
!" Extra-axial features
!"Gray matter buckling
!"Pseudo-capsule of vessels
!"Meningeal/dural “TAIL”
!" Gadolinium enhancement
Tentorial Meningioma [Figure 6]

Figure 5 A, B & C
Meningioma. WHO grade 1 – benign, yet with
extensive vasogenic edema.
M1.,.-,"*'7+Peritumoral Edema
!" Male > female (p = 0.026)
!" Hyperintense to GM on T2W (p = 0.016)
!" Pial blood supply (p = 0.001)
!"G)3)$#)$23&&A(#$-/$823/)
!" Pathology
!"Grade 1: 23/79 cases had edema
(32% G1)
!"Grade 2-3: 7/79 cases had edema Figure 6 A & B
(87% G2-3)
Gross (Courtesy Tom Naidich, Mt. Sinai, NY).
Lee K, Joo W, Rha H, et al. Peritumoral brain
edema in meningiomas. Surgical Neurology.
2008;69:350-355.
M1.,.-,"*'7+F%1B+'.5+Post- Gd
[Figure 7]
Figure 7 A & B
Frontal Meningioma. Notice the bone thickening

(hyperostosis) under the center of the lesion.

MR Signal and Meningioma Types Dural T',&7+Histology [Figure 9]
!" Most are isointense to GM
!"On both T1-W and T2-W
!" Hyperintense to GM on T1-W
!"Lipoblastic (fatty) meningioma
!"Hemorrhage into meningioma
!" Hypointense on T2-W
!"Fibroblastic
!"Transitional
!" Hyperintense on T2-W
!"Meningothelial
!"Angioblastic
!" Microcystic (“humid”)
M1.,.-,"*'7+Dural Tail [Figure 8]

Figure 9
Dural T',&7+Differential Diagnosis

!" Extraaxial lesions
!"Meningioma
#" Most common lesion with dural tail
#" Most common lesions overall
!"Schwannoma
!"Hemangiopericytoma
!"Sarcoidosis
!"Dural Lymphoma and metastases
!"Gumma (syphilis)
!" Intraaxial lesions
!"Pleomorphic xanthoastrocytoma
!"G,!'+82$3&(2'+'%+3&(3#)+"2A)".3
!"GBM (rare)
Cavernous Sinus Meningioma

[Figure 10]
Meningioma - dural tail.
The upper right image shows branching hypointensities
3?"3).">)+'6+'4'-3)0,G):,%(4)<+,.)31.,+):'44'#4/
Dural Tail Figure 10 A & B

!" Curvilinear enhancement Cavernous Sinus Meningioma with extensive dural
!" h7,+3&(43$+i enhancement along the tentorium.
!" First reported with meningioma
!" First reported to be neoplastic invasion
!" What is it really? Meningioma CT and MR Features
!"Thickening of the dura !" Mass effect 88% 90%
!"Vasocongestion of the dura !" Extraaxial location 42% 70%
!"Edema of the dura !" Broad dural attach 74% 98%
!" Typical dense/intensity 92% 74%
!" Hyperostosis 10% 14%
!" Homogeneous 76% 76%
!" Enhancement 96% (78%) 96% (80%)
(Homogeneous)
!" Meningeal. Enhance (tail) 2% 50%
!" “Capsule” 14% 68%
Neuroradiology. 1990;32:467-473.

Other Locations for Meningioma
!" Intraventricular
!" Orbit
!"Intraconal
!"Periorbital
!" Nasal cavity
I.)%'21.)%,/9&'%7+\+]^++++[Figure 11]
!" Usually adult
!" Females > Males
!" Usually lateral ventricle
!" Usually trigone/atrium
!" Always attached to choroid plexus
!" Vascular pedicle from choroid
Figure 12 A & B
Meningioma. Supplied by branches of the ECA showing
classic spoke-wheel vascularity.
Figure 11
Intraventricular
meningioma.
Figure 13
Meningioma.
Venous phase
showing
persistent and
dense tumor
blush.
Optic Nerve Meningioma
Meningioma Arterial Supply

!" External carotid 85% Delayed Washout [Figure 14]
!" Internal carotid 63%

!" Tumor blush 95%
M1.,.-,"*'7+Angiography – Transit
Time [Figure 12]
!" Blush or stain
!"Early arterial
!"Prominent in venous phase
!"Capillaries/small arterioles
!"(Too small to see individually)
!" _'/",#(8&&$/-
!"Characteristic if delayed
!"<3A(8&&(I$)*("+(%'6"+'(E&T(5'$/#
Meningioma – Angiography – Long

Transit Time [Figure 13]
!" _'/",#(8&&$/-(HG)3))$/1(Z==[J
Figure 14 A to E
!"170 meningiomas
!"Delayed in 136 (80%) MR perfusion study showing delayed washout from
!"With Nl. vv In 10 (6%) meningioma (Courtesy of Dra. Perla Salgado, Mexico
!"Earlier in 24 (14%) City, Mexico).
!"(8 in early arterial phase)
!" Leeds and Taveras (1969)
!"EDV in 6/36 (16%)

M1.,.-,"*'7+Effect on Skull M1.,.-,"*'7+Mostly Intraosseous
[Figure 15] [Figure 17]
!" Hyperostosis (15%-25%)
!"With or without micro invasion
!" Pressure erosion
!"Periosteal remodeling
!" Bone destruction
!"Microscopic invasion
Figure 17 A, B & C
A 57-year-old woman with a long Hx of seizures.
Figure 15
Meningioma Hyperostosis
Variable patterns of hyperostosis from meningioma. !" Does not mean invasion of bone
Inner table, inner and outer table, diploic space,
combinations.
!" Implies chronicity and benign behavior
!" Skull base
!"Invasion via Haversian canals
Hyperostosis [Figure 16] M1.,.-,"*'7+Atypical Imaging (Yet,

Typical Histology)
M1.,.-,"*'7+U;O+[++++++++[Figure 18]
Figure 16 A & B
Hyperostosis from meningioma.
Figure 18 A & B
En Plaque Meningioma Meningioma with typical histology yet aggressive

!" Meningioma: radiologic appearance.
!"Intradural soft tissue mass
!"Extradural soft tissue mass
!" Fibrous dysplasia:
!"Intraosseous lesion
!"No extraosseous mass

Meningioma Atypical Imaging Hemangiopericytoma [Figure 20]
!" Focal lucency outside (arachnoid cyst) !" Synonym: “angioblastic meningioma”
!" Focal lucency inside (necrosis, cyst) !" Cell of origin: perivascular pericyte of
!" Hypodensity (“humid”, lipoblastic) Zahn and/or Zimmerman
!" Focal hyperdensity (metaplasia, !" < 1% of primary CNS
hemorrhage) !" M:F = 1.4:1
!" Heterogeneous !" Age: 40s
!" Hyperintensity on T1-W !" Dural-based, bone destruction, lobulated
!" Hyperintensity on T2-W
Fatty Metaplasia [Figure 19]
Figure 19 A & B
WHO grade 1 meningioma with fatty metaplasia.
Meningioma with Cysts

!" Inside of neoplasm
!"(rim enhancement)
!" Between tumor and brain Figure 20 A, B, C & D
!"(Arachnoid cysts) Hemangiopericytoma. WHO grade 2, 3.
!" Inside brain Top Image: Lobulated mass - narrow attachment base.
!"Pia separates tumor from brain
!"?? results of chronic Edema
!"Vacuolization of white matter Hemangiopericytoma (HPC)
!" Narrow dural base (“mushrooming”)
M1.,.-,"*'7+Atypical Histology !" No hyperostosis
!" Atypical meningioma ~ 5%-7% !" E"(23&2$823)$"/($/(),."+
!" Anaplastic meningioma ~ 1%-3% !" Lobulated (not hemispheric)
!" ~ 0.2%/100000 per year !" Internal signal voids (on MRI)
!" Higher incidence of recurrence !"Irregular and multiple
!" Shorter time to recurrence
!" “Atypical histology” M1.,.-,"*'7+Radiologic F1')9%1(7+4J
!"Necrosis
Feature Benign/”Malignant”
!"Excessive mitoses
!" Homogeneous enhance 72%/36%
!"Invasion into brain*
!" Heterogeneous enhance 23%/64%
Malignant Meningioma !" Hyperostosis 18%/7%
!" < 3% of all meningioma !" C3&2$823)$"/((( ( ((((OP?d>?
!" Anaplastic (malignant) meningioma !" “Mushrooming” 0%/57%
!" Papillary meningioma !"Narrow attachment and larger “cap”
!" Benign metastasizing meningioma !"Invaginating into brain
!" Hemangiopericytoma (HPC)
!" <3&$-/3/)(8%+",#(*$#)$"2A)".3(H<:kJ
Parkway Delight vs Rueben
!" Parkway delight Rueben
!" Pastrami Corned beef
!" Coleslaw Sauerkraut
!" Thousand island Russian
!" Muenster Swiss cheese
!" Pumpernickel Rye bread
HPC vs Meningioma Meningioma
HPC Meningioma !" The 4H+ tumor
!" Narrow base Broad base !" Homogeneous
!" Lobulated Hemispheric !" Hyperdense
!" Heterogeneous Homogeneous !" Homogeneous enhancement
!" Bone destruction, Hyperostosis !" Hemispheric shape
!" No Ca++ Psammomatous, !" Hyperostosis
No Ca++ !" Hormonally modulated
!" Irregular vessels Spoke wheel vessels
References
1. Ahmadi J, Hinton DR, Segall HD, Couldwell WT. Surgical implications of magnetic resonance-enhanced
dura. Neurosurgery. 1994 Sep;35(3):370-7;discussion 377.
2. Aoki S, Sasaki Y, Machida T, Tanioka H. Contrast-enhanced MR images in patients with meningioma:
importance of enhancement of the dura adjacent to the tumor. AJNR Am J Neuroradiol 1990 Sep-
Oct;11(5):935-8.
3. Asari S, Yabuno N, Ohmoto T. Magnetic resonance characteristics of meningiomas arising from the
falcotentorial junction. Comput Med Imaging Graph 1994 May-Jun;18(3):181-5.
4. Berger MS. Perfusion MR and the evaluation of meningiomas: is it important surgically? AJNR Am J
Neuroradiol 2003;24:1499-500.
5. Goldsher D, Litt AW, Pinto RS, Bannon KR, Kricheff II. Dural “tail” associated with meningiomas on Gd-
DTPA-enhanced MR images: characteristics, differential diagnostic value, and possible implications for
treatment. Radiology 1990 Aug;176(2):447-50.
6. Helie O, Soulie D, Sarrazin JL, Derosier C, Cordoliani YS, Cosnard G. [Magnetic resonance imaging and
meningiomas of the posterior cerebral fossa. 31 cases] J Neuroradiol 1995 Dec;22(4):252-70. French.
7. Hutzelmann A, Palmie S, Buhl R, Freund M, Heller M. Dural invasion of meningiomas adjacent to the
tumor margin on Gd-DTPA-enhanced MR images: histopathologic correlation. Eur Radiol 1998;8(5):746-
8.
8. Hutzelmann A, Palmie S, Freund M, Buhl R, Heller M. [Dura thickening adjacent to intracranial, para-dural
space-occupying lesions in MRI. Histologic correlation] Aktuelle Radiol 1997 Nov;7(6):305-8. German.
9. Hutzelmann A, Palmie S, Zimmer C, Benz T, Leweke F, Freund M. [The meningeal sign: a new appraisal]
Rofo 1996 Apr;164(4):314-7. German.
10. Ildan F, Tuna M, Gocer AP, Boyar B, Bagdatoglu H, Sen O, Haciyakupoglu S, Burgut HR. Correlation of the
+'&3)$"/#*$!#("6(%+3$/W),."+($/)'+632'#1(.3-/')$2(+'#"/3/2'($.3-$/-1(3/0(3/-$"-+3!*$2(8/0$/-#()"(!+'0$2)(
cleavage of meningiomas. J Neurosurg 1999 Sep;91(3):384-90.
11. Kawahara Y, Niiro M, Yokoyama S, Kuratsu J. Dural congestion accompanying meningioma invasion into
vessels: the dural tail sign. Neuroradiology 2001 Jun;43(6):462-5.
12. Maiuri F, et al. Intracranial meningiomas: correlations between MR imaging and histology. Eur J Radiol
1999;31:69-75.
13. Nagele T, Petersen D, Klose U, Grodd W, Opitz H, Voigt K. The “dural tail” adjacent to meningiomas
studied by dynamic contrast-enhanced MRI: a comparison with histopathology. Neuroradiology 1994
May;36(4):303-7.
14. Nakasu S, Nakasu Y, Matsumura K, Matsuda M, Handa J. Interface between the meningioma and the brain
on magnetic resonance imaging. Surg Neurol 1990 Feb;33(2):105-16.
15. E3D3,(k1(<$A3f3I3(B1(B3.3$(G1(B#,2*$A3(S1(G*$.3(S1(G*$+")3/$(B1(C*$-3#3D$(kT(`3)*"&"-$2(#$-/$823/2'("6(
.'/$/-'3&('/*3/2'.'/)(Hh43+'(#$-/iJ("6(.'/$/-$".3#("/(<VKT(G,+-(E',+"&(Z==P(7'2Y]QH[JNRQ]W=>Y(
discussion 590-1.
16. Quekel LG, Versteege CW. The “dural tail sign” in MRI of spinal meningiomas. J Comput Assist Tomogr.
1995 Nov-Dec;19(6):890-2.
17. Sakai K, Tada T, Fukasaku K, Kyoshima K, Kobayashi S. Histological examination of the gadolinium-
enhanced dura mater around meningiomas on magnetic resonance imaging. Neurol Med Chir (Tokyo)
1993 Jul;33(7):429-33.
18. Sandhyamani, Rao, Nair, Radhakrishan: Atypical Meningioma: A Clinicopathological Analysis.Neurology
India 2000;48:338-42.
19. Sato M, Matsumoto M, Kodama N. Meningeal enhancement surrounding meningiomas on Gd-DTPA MRI.
Fukushima J Med Sci. 1998 Jun;44(1):1-11.
20. Sekiya T, Manabe H, Iwabuchi T, Narita T. [The dura mater adjacent to the attachment of meningiomas:
$)#('/*3/2'0(<V($.3-$/-(3/0(*$#)"&"-$23&(8/0$/-#u(E"(G*$/D'$(\'D3(Z==O(F2)YO>HZ>JNZ>[^WQT(X3!3/'#'T(

21. Takeguchi T, Miki H, Shimizu T, Kikuchi K, Mochizuki T, Ohue S, Ohnishi T. The dural tail of intracranial
.'/$/-$".3#("/(4,$0W3))'/,3)'0($/5'+#$"/W+'2"5'+A($.3-'#T(E',+"+30$"&"-A(O>>](:'%Y][HOJNZ^>WRT(U!,%(
2004 Jan 28.
22. Wilms G, Lammens M, Marchal G, Van Calenbergh F, Plets C, Van Fraeyenhoven L, Baert AL. Thickening of
dura surrounding meningiomas: MR features. J Comput Assist Tomogr 1989 Sep-Oct;13(5):763-8.
23. Yamaguchi N, Kawase T, Sagoh M, Ohira T, Shiga H, Toya S. Prediction of consistency of meningiomas
with preoperative magnetic resonance imaging. Surg Neurol 1997 Dec;48(6):579-83.

1328
“Pinealomas” and Other Pineal Region Masses
Pineal Gland Introduction Mammalian Biological Clock
!" “Seat of the soul” [Figure 2]
!" Daily (diurnal) biorhythms !" Pineal day-night diurnal rhythms
!"Life-cycles (puberty, migration) !"Darkness stimulates melatonin release
!" Responds to light/dark !" Pineal melatonin suppresses gonadotropin
!"Melatonin levels releasing hormone (GnRH)
!"Accessory optic pathway !" Longer daylight decreases melatonin
#" Retinohypothalamic tract, RAS, !" % MT leads to increased GnRH
Sympathetic n. to gland !" & GnRH ! & LH and increase FSH
!" Third eye !" Increased sexual drive and activity in the
!"Phylogenetically spring
!"Developmentally
!"Embryologically
Pineal Region
!" 60% Germ cell neoplasm
!"Seminoma (2/3 or 40% of all pineal
region)
!"Teratoma
!"Other: “nongerminoma GCT”
!" 15% Pineal parenchymal
!"Pineocytoma
!"Pineoblastoma (PNET)
!" OTHER lesions
!"VOG malformations
!"Astrocytoma
#" Splenium, tectum, thalamus
!"Meningioma, lipoma Figure 2 A & B
P,.1'&7+Third Eye [Figure 1] Pineal gland and surrounding region. Third ventricle,
quadrigeminal plate and cistern, and bilateral thalami.
!" In lower vertebrates, it may have a lens 5?')!5)4?,G4)-,+."#)6%-'"#)$"#$%&$"3%,-)3?"3)%4)
and a retina physiologic after puberty.
!" Iguana
!"Third eye
!"Photoreceptor Normal Pineal
!"Radiometer for sunlight !" A reddish-brown pinecone-shaped
structure behind the third ventricle
Pineal R1-,".7+Normal Anatomy

[Figure 3]
Figure 1
There is a hole
in the skull
to allow light
to reach the
pineal gland.
Figure 3
The internal cerebral veins, great vein of Galen, and

straight sinus are important landmarks.
Pineal Region 1329 Neuroradiology

Pineal Region Mass Symptoms and #" Endodermal sinus tumor
Signs !" Choriocarcinoma
!" Parinaud syndrome !"Teratoma
!"Not paranoid #" Immature, mature, malignant
!" Precocious puberty !" Mixed germ cell
!"Male < 8 year old and female < 9 year
old Intracranial Germ Cell Tumors
!" Headache, nausea, vomiting !" Usually primary in the CNS
!" E"/#!'2$82(.3##('66'2) !"Arise from “germ cell rests”
!" & ICP (intracranial pressure) !"Pineal/quadrigeminal and suprasellar
cistern
Parinaud Syndrome Aqueduct/Tectal !" Exceptional cases metastatic to CNS
Syndrome !"Testicular veins/lymphatic drainage to
!" Failure of conjugate vertical eye renal hilus
movement !"Para-artic nodes $ lung
!"Upward >> downward !"Rare cases of testicular seminoma
!" <A0+$3#$#1(8L'0(!,!$&#( CNS mets
!" Failed ocular convergence !"Lance Armstrong had a mixed chorio/
!"Lateral midbrain tegmentum embryonal testicular with CNS
!" Blepharospasm metastases
!"Eyelid spasm
Pineal Region GCT
Pineal Region Masses !" If not metastatic, then how?
!" Germ cell tumors ~ 2/3 !" Multipotential “germ cells” migrate
!"Germinoma !" Misplaced, they reach midline of
!"Teratoma developing brain
!" Pineal parenchyma ~ 1/7 !"Suprasellar cistern
!"Pineocytoma !"Quadrigeminal cistern - pineal region
!"Pineoblastoma !" Secondary factors induce neoplasms
!" Pineal cyst - common !" Germinoma most common ~ 2/3 (40% of
!" Vascular lesions all)
!"Vein of Galen malformation !" Teratoma second most common (20% of
all)
Pineal Region Mass
!" 369 patients Hoffman series, Toronto Germ Cell Migration [Figure 4]
!" Primordial germ cells migrate out into
Tumor %
yolk sac by third week of gestation
!" Germ cell 59
!" Abnormal migration: ectopic “rests” in
!" Germinoma 39
sacral, mediastinal, and pineal regions
!" Teratoma (malignant) 11
!" Primordial germ cells migrate back into
!" Teratoma (benign) 2
'.%+A"(0,+$/-(6",+)*(3/0(86)*(I''D#
!" Yolk sac 2
!" Gonads form in sixth week
!" Choriocarcinoma 2
!" Embryonal CA 1
!" Mixed germ cell 1
Pineal Region Mass

369 Patients Hoffman*
!" Epidermoid 1+
!" True pineal 14
!"Pineoblastoma 2
!"Pineocytoma 2
!" Other neoplasms 27
!"Gliomas (thalamus, callosum) 26
!"Nonglial (meningioma, etc)
*Dr. Hoffman Neurosurgeon Toronto, Ont, CA.
CNS Germ Cell T9*"%(7+Primary or

Metastatic to the CNS?
Figure 4
!" bkF(2&3##$823)$"/(((
!"Germinoma Diagram of primordial germ cells. By 3 weeks they
!"Embryonal carcinoma have left the embryo to park in the yolk sac. At 4-5
!"Yolk sac weeks they migrate back into the embryo and then
form the gonads during the 6th week.

Anterior Mediastinal Teratoma Germinoma Imaging
[Figure 5] !" Sharply circumscribed midline mass
!" Surrounds/engulfs pineal Ca++
!" Alternate locations
!"Thalamus, third ventricle, suprasellar
cistern
!" NCT: Homogeneous hyperdense
!" ECT: Homogeneous enhancement
!" MR” Isointense to gray matter
!" +/- CSF spread, tumor Ca++
Germinoma/Seminoma
!" Central
!"Pineal region
!"Suprasellar cistern
!" Homogeneous
Figure 5 A & B !" Hyperdense to GM
Anterior mediastinal teratoma. !" Isointense to GM
!" Uniform enhancement
!" CSF seeding?
!" May engulf pineal
Basic Approach to Pineal Region !" Ca++
Germinoma/Seminoma [Figures 6 & 7]
Pineal Region Masses

!" Germ cell tumors ~ 2/3
!"Germinoma
!"Teratoma
!" Pineal parenchyma ~ 1/7
Figure 6 A & B
!"Pineocytoma
!"Pineoblastoma Pineal region germinoma.
!" Pineal cyst
!" Vascular lesions
!"Vein of galen malformation
Intracranial Germinoma
!" Synonyms: pinealoma, seminoma,
dysgerminoma, atypical teratoma Figure 7
!" Cell of origin: germ cell rests, 2-cell
pattern Pineal Region
!" Incidence: 1%-2% of all cranial Germinoma.
Homogeneous
neoplasms and
!"2%-4% of childhood neoplasms hyperattenuating
!"9%–15% of childhood in Japan mass
!" Age: 5-35 (remember precocious puberty surrounding
< 8-9 years) an “engulfed”
$"#$%&$"3%,-/
!" Sex: 2-7 M/F
!" Location: 60%-80% pineal, 22%
suprasellar
!" Treatment: Bx, radiation, chemoTx
!" Prognosis: up to 90% at 5 years
!"Radiosensitive and chemosensitive
tumor
!"Median survival ~19 years

G1%*,."*'7+J<"BCell Pattern EI7+N".(01/,#/+Signal [Figure 11]
[Figure 8]
!" One cell looks like a lymphocyte
Figure 8 A & B
Pineal region germinoma. Two-cell pattern, one cell
resembles a lymphocyte. The dense cellularity and Figure 11 A & B
“small round blue cell” component contribute to the
high attenuation noted on CT. N%-'"#)+'8%,-)8'+.%-,."),-)CA/)=,-46'$%&$)4%8-"#2
intensity with prominent gadolinium enhancement.
G1%*,."*'7+J<"BCell Pattern
[Figure 9] Where is the Lesion? [Figures 12 & 13]
!" Mass is below tentorium
Figure 12
Pineal region
germinoma
extending below
the tentorium.
Figure 9 A & B
Pineal region seminomas are usually hyperdense on

plain CT.
Sometimes Eccentric Ca++

[Figure 10]
Figure 13 A & B
Figure 10
Pineal region seminoma (germinoma). Two different
patients. The mass extends below the tentorium like a
wedge.
Sometimes
the mass is
eccentric in the
quadrigeminal
cistern.
The pineal Surgical Planning
$"#$%&$"3%,-) !" Find the internal cerebral veins and the
is displaced vein of Galen (VOG)
leftward.
!" If tumor is below these veins
!"Suboccipital infratentorial approach
!" If tumor is above these veins
!"Interhemispheric approach
!"Subtemporal approach
!"Various other techniques

Suboccipital Infratentorial Approach Pineal Region
[Figure 14] !" Teratoma BUSCAR GRASA!!!
!"Sharply circumscribed
!"Lobulated and multicystic
!"Heterogeneous tissues
!"Heterogeneous attenuation and signal
Figure 14 #" <$L),+'("6(4,$01(&$!$01(#"6)W)$##,'1(
Ca++
The surgical !"Enhancement of solid areas
approach may
be suggested T1%')"*'7+LIPID [Figure 15]
by the tumor
relation to !" Gd T1-W: enhancement of solid areas
the internal
cerebral veins
(ICV), including
supratentorial
interhemispheric, transcallosal, supracerebellar,
transtentorial, and transventricular.
Chandy MJ, Damarju SC. Benign tumours of the

pineal region: a prospective study from 1983 to
1997. Br J Neurosurgery. 1998;12:228-233.
Basic Approach to Pineal Region
Figure 15 A & B
Pineal region teratoma. Note the small peripheral

focus of very low attenuation (less than water) and
corresponding T1-shortening from lipid. This could
be sebaceous (ectodermal) lipid or mesodermal lipid
(adipose tissue). The lipid focus does not enhance
after contrast.
T1%')"*'7+Rupture [Figure 16]

!" Note: chemical shift artifact – frequency
Pineal Region Masses encoding direction
!" Germ cell tumors ~ 60%
!"Germinoma
!"Teratoma is ~1/3 of all GCT
!"Pineocytoma
!"Pineoblastoma
!" Pineal cyst
!" Vascular lesions
Epidermoid/Dermoid/Teratoma
!" Histology
!" Epidermoid: an inclusion cyst lined by
squamous epithelium – only
!" Dermoid – an inclusion cyst lined by
squamous epithelium plus dermal
appendages (eg hair follicles, sebaceous Figure 16 A & B
glands, sweat glands) A1631+'()6%-'"#)+'8%,-)3'+"3,."/)=,3')3?')#%6%(g01%()
!" Teratoma: complex differentiation, tissues levels in the frontal regions of both lateral ventricles.
from two or more germ layers; most The primary tumor is seen in the midline pineal region.
often mainly ectoderm, “benign cystic” There is a “chemical shift” artifact.
teratoma.

Teratoma vs Dermoid CSF Dissemination [Figure 19]
!" Teratoma is a neoplasm
!"From multipotential cells/tissues
!"“Included twin” from embryo/fetus
!"Ectoderm (skin, occ. brain) common
!"Lipid (mesodermal fat or sebaceous)
!"Multiloculated, lobulated
!" Dermoid is an inclusion cyst
!"Only skin (ectoderm)
!"Water and/or sebaceous lipid
!"Unilocular
Two Theories for Teratoma

!" Progressive differentiation from multi-
potential (“omnipotential”) germ cells –
“primordial germ cells”
!" Inclusion of a twin during early gestation Figure 19 A & B
- embryogenesis
Pineal region seminoma. The lesion is hyperdense
without contrast and surrounds or engulfs a central
Famous Quote from Aunt Voula $?1-M),<)$"#$%&$"3%,-/)5?')6,43$,-3+"43)4"8%33"#)#1.*"+)
!" “You family now, so I tell you a story. All spine MR demonstrates multiple areas of CSF seeding.
my life ... I have this lump on the back of
my neck. When I reach the menopause,
the lump get bigger. I go to the doctor,
and he performs a...bo-bobopsy. And Pineal Neoplasms Serum and CSF
$/#$0'()*'(&,.!1(*'(8/0#()'')*1(3/0(3( Hormone Tests [Figure 20]
spinal column.”
NOT Hyperdense on CT [Figure 17]

!" Endodermal sinus tumor
Figure 20
Pineal region masses may abnormally elevate CSF and

serum hormones.
Basic Approach to Pineal Region

Figure 17 A & B
Nonseminomatous germ cell tumor. This lesion is NOT Pineal Region Masses
hyperdense on plain CT, but does surround or engulf a !" Germ cell tumors ~ 2/3
$'-3+"#)$?1-M),<)$"#$%&$"3%,-/ !"Germinoma
!"Teratoma
G1%*,."*'7+Seeding [Figure 18] !" Pineal parenchyma ~ 1/7
!"Pineocytoma
!"Pineoblastoma
!" Pineal cyst
Figure 18
!" Vascular lesions
Germinoma. CSF
seeding along the
edge of the tentorium
(arrows).

Pineal Parenchymal Tumors Pineoblastoma [Figure 22]
!" The 2007 WHO recognized these tumors !" hUL!&"0'0(23&2$823)$"/#i
of the pineal region:
!"ICD-0 9361/1 Pineocytoma (WHO
grade 1)
!"ICD-0 9362/3 Pineal parenchymal
tumor with intermediate differentiation
(WHO grade 2 or 3)
!"ICD-0 9362/3 Pineoblastoma (WHO
grade 4)
!"ICD-0 9395/3 Papillary tumor of pineal
region (WHO grade 2, 3)
Pineal Parenchyma
!" Pineoblastoma (PNET)
!"o",/-(!3)$'/)#(H8+#)()I"(0'230'#J(
!"B,."+($)#'&6(23&2$8'#( Figure 22 A & B
!"”Exploded” pineal Ca++
N%-',*#"43,."/)OfU6#,('()$"#$%&$"3%,-4W)"+,1-()3?')
!" Pineocytoma (mature pineal cells) outside rim of the tumor.
!"Young or old
!" Trilateral retinoblastoma
!"Inherited Rb (chromosome 13)
!"1/3 inherited but 2/3 heritable Pineoblastoma [Figure 23]
!"Look at orbits for signs of Tx
Pineal Parenchyma Mass [Figure 21]

!" UL!&"0'0(!$/'3&(23&2$823)$"/#(
!" Pineoblastoma
!"Some hyperdense on CT
!" Pineocytoma
!"Isodense on CT
Figure 21
Pineal
parenchyma
mass schematic.
“Exploded Figure 23 A & B
$"#$%&$"3%,-4W)
from a mass Pineoblastoma.
arising inside the
pineal gland. This
pattern is seen P,.1"$&'()"*'7+N".(01/,#/+++++++[Figure 24]
in both pineal !" CSF seeding along tentorium
cysts and pineal
neoplasms.
Figure 24 A & B
Pineoblastoma with seeding along the edge of the

tentorium. Using this T1-W MR alone, this mass is
indistinguishable from a pineal region germinoma.

Germinoma/Pineoblastoma Pineal Cysts [Figure 27]
[Figure 25] !" Autopsy Pathology
!" E"/#!'2$82(<V(3!!'3+3/2'(3/0(CG:( !"~ 5%-40% of adults
seeding along tentorium !"< 2 mm in a normal size gland
!" MR visible
!"2%-8% of adults
!"2-7 mm common
!"14-25– mm cysts are not rare
!"May expand the gland
!"Ring enhancement should be smooth
and thin (only 1-2 mm)
!" Why do they grow? – Unknown.
Figure 25 A & B
Pineoblastoma with seeding along the edge of the

tentorium. Using this T1-W MR alone, this mass is
indistinguishable from a pineal region germinoma.
Left Image: Germinoma.
Right Image: Pineoblastoma. Figure 27 A & B
Pineal Cyst. The lesion is surrounded by a uniform and
Pineoblastoma [Figure 26] thin rim of enhancement. This is the normal pineal
!" Note: This mass also extends below the parenchyma that does not have a blood-brain barrier.
tentorium
Pineal Cyst [Figure 28]

!" Typical cysts:
!"Round or oval
!"T1 ~ WM
!"T2 ~ CSF
!"T2 homogeneous
!"Rim enhancement < 2 mm
!"No nodularity
!" hB*'#'(8/0$/-#(#,--'#)()*3)()A!$23&(!$/'3&(
Figure 26 A & B
cysts may be followed up on a clinical
basis alone rather than on imaging.”
Pineoblastoma. Note how the lesion extends below Barbouriak DP, Lee L, Provenzale JM. Serial MR
the tentorial hiatus (dotted line) and into the posterior imaging of pineal cysts: implications for natural
fossa. history and follow-up. AJR. 2001;176:737-743.
Pineal Region Masses [Figure 27]

Figure 28
!"Germinoma
Pineal cyst.
!"Teratoma Note: the
!" Pineal parenchyma ~ 1/7 lesion is now
!"Pineocytoma below the
!"Pineoblastoma tentorium due
!" Pineal cyst to secondary
hydrocephalus,
!" Vascular lesions and the lesion
!"Vein of Galen malformation has a uniform
thin rim of contrast enhancement.
Barbouriak DP, Lee L, Provenzale JM. Serial MR

imaging of pineal cysts: implications for natural history
and follow-up. AJR. 2001;176:737-743.

Pineal Region Masses Vein of Galen Malformation [Figure 30]
!"Germinoma
!"Teratoma
!"Pineocytoma
!"Pineoblastoma
!" Pineal cyst
!" Vascular lesions
Vein of Galen M'&3"%*'),".7+Symptoms

and Signs
!" Childhood: large shunt
!"High output failure
!"Persistent ductus
!"Hydrocephalus
!"Cranial bruit/thrill
Figure 30 A & B
!" Adult: small shunt
!"Asymptomatic Vein of Galen malformation.
!"Pineal symptoms
Vein of Galen Malformation – Types And VOG Sagittal T1-W MRI [Figures 31 to 33]
Causes
!" Parenchymal AVM (shunt)
!" 7$+'2)(8#),&3()"(5'$/((
!" 7,+3&(8#),&3(H0+3$/#()"(5'$/J((
!" Sinus thrombosis (fetal)
!" Hypoplastic straight sinus
Sagittal T1-W MRI [Figure 29]

!" All of these increase the deep venous
!+'##,+'("+(4"I
!"Parenchymal AVM (shunt)
!"7$+'2)(8#),&3'()"(5'$/
!"7,+3&(8#),&3(H0+3$/#()"(5'$/J Figure 31 A & B
!"Sinus thrombosis (fetal)
!"Hypoplastic straight sinus Vein of Galen malformation. Persistence of the falcine
vein draining the vein of Galen.
Figure 29
Schematic for
vein of Galen
malformations. Figure 32
Any cause
of increased Sagittal T1-W
deep venous MRI showing
pressure or classic balloon-
0,G).">)$"14') like enlargement
aneurysmal of the vein of
dilatation of the Galen. In this
vein of Galen. case, the VOG
Straight sinus drains into the
,*43+1$3%,-@)4%-14)?>6,6#"4%"@)B]C@),+)(1+"#)&431#") straight sinus;
draining into the VOG are all possible causes. however, in
many cases the
drainage is through a persistent prosencephalic vein
of Markowsky.

Headaches and Parinaud Syndrome
[Figure 36]
Figure 36
Astrocytoma
of the
quadrigeminal
plate. Note how
the mass is
displaced into
Figure 33 A & B the posterior
fossa due to
Vein of Galen malformation with 3D CTA. the obstructive
hydrocephalus.
Intracranial Lipoma
!" Congenital, not a true neoplasm
!" Midline (usually) Pineal Region
!" Usually around corpus callosum !" 60% germ cell neoplasm
!" Occasional tectal, hypothalamic, CPA !"Seminoma (2/3 or 40% of all pineal
!" Abnormal differentiation region)
!"Meninx primativa into fat !"Teratoma
!"Other: “nongerminoma GCT”
Lipoma [Figure 34] !" 15% pineal parenchymal
!"Pineocytoma
!"Pineoblastoma (PNET)
!" Other lesions
!"VOG malformations
!"Astrocytoma
#" Splenium, tectum, thalamus
!" Meningioma, lipoma
Figure 34 A & B
Intracranial lipoma of the quadrigeminal plate.
Notice how the mass presents below the tentorium
because of the herniation caused by obstructive
hydrocephalus.
A()%"/!)"*'7+Splenium [Figure 35]
Figure 35 A & B
Left Image: Mass in the splenium of the corpus

callosum – Glioblastoma multiforme. Note how the
mass is above the deep veins.
Right Image: Mass in the splenium of the corpus
callosum – glioblastoma multiforme.

References
1. Barboriak DP, Lee L, Provenzale JM. Serial MR imaging of pineal cysts: implications for natural history and
follow-up. Am J Roentgenol 2001 Mar;176(3):737-43.
2. Barbouriak DP, Lee L, Provenzale JM: Serial MR Imaging of Pineal Cysts: Implications for Natural History
and Follow-Up. Am J Roentgenol 2001;1737-43.
3. Fain JS, Tomlinson FH, Scheithauer BW, Parisi JE, Fletcher GP, Kelly PJ, Miller GM. Symptomatic glial cysts
of the pineal gland. J Neurosurg. 1994 Mar;80(3):454-60.
4. Fleege MA, Miller GM, Fletcher GP, Fain JS, Scheithauer BW. Benign glial cysts of the pineal gland: unusual
imaging characteristics with histologic correlation. AJNR Am J Neuroradiol 1994 Jan;15(1):161-6.
5. Fujimaki T, Matsutani M, Funada N, Kirino T, Takakura K, Nakamura O, Tamura A, Sano K.J Neurooncol.
CT and MRI features of intracranial germ cell tumors 1994;19(3):217-26.
6. Hayashida Y, Hirai T, Korogi Y, Kochi M, Maruyama N, Yamura M, Yamashita Y. Pineal cystic germinoma
I$)*(#A/2A)$")+"!*"%&3#)$2(-$3/)(2'&&#(.$.$2D$/-(<V($.3-$/-(8/0$/-#("6(3(!$/'3&(2A#)T(@XEV(@.(X(
Neuroradiol 2004 Oct;25(9):1538-40.
7. Jinkins JR, Xiong L, Reiter RJ. The midline pineal “eye”: MR and CT characteristics of the pineal gland with
and without benign cyst formation. J Pineal Res 1995 Sep;19(2):64-71.
8. Koenigsberg RA, Faro S, Marino R, Turz A, Goldman W. Imaging of pineal apoplexy. Clin Imaging 1996
Apr-Jun;20(2):91-4.
9. Korogi Y, Takahashi M, Ushio Y. MRI of pineal region tumors. J Neurooncol 2001 Sep;54(3):251-61.
10. Lee DH, Norman D, Newton TH. MR imaging of pineal cysts. J Comput Assist Tomogr 1987 Jul-
Aug;11(4):586-90.
11. <3.",+$3/(@1(B"I8-*$(XT(<V("6(!$/'3&(2A#)#T(@XEV(@.(X(E',+"+30$"&(Z==](F2)YZRH=JNZP=[WPT(
12. <3.",+$3/(@C1(B"I8-*$(XT(`$/'3&(2A#)#N(<V($.3-$/-T(@XEV(@.(X(E',+"+30$"&T(Z=Q[(E"5W7'2YPH[JNZ>QZW[T(
13. Mamourian AC, Yarnell T. Enhancement of pineal cysts on MR images. AJNR Am J Neuroradiol. 1991 Jul-
Aug;12(4):773-4. No abstract available.
14. Osborn RE, Deen HG, Kerber CW, Glass RF. A case of hemorrhagic pineal cyst: MR/CT correlation.
Neuroradiology 1989;31(2):187-9.
15. Reis F, Faria AV, Zanardi VA, Menezes JR, Cendes F, Queiroz LS. Neuroimaging in pineal tumors. J
Neuroimaging 2006 Jan;16(1):52-8.
16. Sener RN. The pineal gland: a comparative MR imaging study in children and adults with respect to
normal anatomical variations and pineal cysts. Pediatr Radiol 1995;25(4):245-8.
17. Welton PL, Reicher MA, Kellerhouse LE, Ott KH. MR of benign pineal cyst. AJNR Am J Neuroradiol 1988
May-Jun;9(3):612.

1340
Other Non-Glial Lesions Radiology-http://PassMyBoards.org
Chordoma [Figure 1] Chordoma
!" Rich corinthian leather vs physaliphorous !" Origin: notochordal rests
cells “bubble” or vacuolated !" Age: 30-60 years old
!" Location:
Figure 1 !"Clivus 35%
!"Spine 15% (especially Cx)
Chordoma.
!"Sacrum 50%
physaliphorous
cells’ bubbly
appearance C?"%5"*'7+Imaging
(Courtesy of !" Location
Joe Parisi, MD). !"Midline clivus
#" May extend lateral, dorsal, ventral
!"Midline sacrum
!" Lobulated heterogeneous bulky mass
C?"%5"*'7+Normal Notochord !" Bone destruction
!" Nucleus pulposis of intervertebral disk !" No remodeling
!" Ecchordosis of clivus !" Variable density/signal
!"Size/shape like a grain of rice !" Bone sequestra
!"Dorsal to clivus !" 7A#)+"!*$2(23&2$823)$"/#
Sclerotomes and Notochord [Figure 2] Chordoma [Figures 4 to 6]
Figure 2
Schematic of sclerotomes surrounding the notochord. Figure 4 A & B

Two adjacent sclerotomes fuse into one vertebral Large bulky mass with destruction of the clivus. The
body. The notochord tissue is extruded into the odontoid and C1 are preserved.
intervertebral disc, forming the nucleus pulposis.
(Copyright 2003).
N")"/?"%57+Chordoma and Thornwaldt

[Figure 3]
Figure 5 A & B
Chordoma. Destruction of the clivus, the basilar and

vertebral arteries are stretched over a large bulky,
hypovascular mass. Air and contrast remain from an
earlier myelogram.
Figure 3 A & B
Chordoma (left image) and Thornwaldt cyst (right

image). The orange line is the embryologic location of
the notochord the green triangle is the clivus.
Other Non-Glial Lesions 1341 Neuroradiology

Eccentric Mass [Figure 10]
Figure 10
Chondrosarcoma
(low grade).
Notice the dense
mineralization
Figure 6 A, B & C and the
eccentric
Lobulated mass arising eccentrically from the vertebral location of the
body. mass.
T1 Pre and Post, T2 [Figure 7]
Chondrosarcoma [Figure 11]
Figure 7 A, B & C
Sacrococcygeal chordoma.
Chordoma [Figures 8 & 9]
Figure 11 A & B
Chondrosarcoma.
Dermoid/Epidermoid
!" True cysts of the CNS
!" Subepidermoid
!" Lined by an epithelium
True Cysts of the CNS

!" Epidermoid
!" Dermoid
!" Colloid
!" Craniopharyngioma
!" Rathke cleft
!" Ependymal
Figure 8 A & B
!" Endodermal
Chordoma: Destruction of the sacrum and bulky soft
tissue mass. This patient presented with symptoms of
constipation and rectal fullness.
Figure 9
Chordoma.
Destruction
of the sacrum
and bulky soft
tissue mass.

True Cysts Epidermoid Inclusion Cyst
!" @(4,$0W8&&'0(#!32'1(&$/'0(%A(3/('!$)*'&$,. [Figure 12]
!" C&3##$8'0(%A()*'()A!'("6('!$)*'&$3&(&$/$/-N
!"Epidermoid
#" Squamous epithelium: ectoderm
!"Dermoid
#" Squamous and dermal adnexa:
ectoderm
!"Colloid cyst
#" Ciliated cuboidal/columnar
epithelium, mucus secreting cells -
similar to endoderm?
!"Craniopharyngioma (two types)
#" Adamantinomatous: children,
2A#)$21(23&2$8'0(
#" Squamous and papillary: adult,
solid Figure 12 A & B
!"Rathke cleft cyst Epidermoid inclusion cyst. Note: the lesion is nearly,
#" Ciliated cuboidal/columnar but not exactly, like CSF in signal. The sagittal images
epithelium – possibly endoderm? demonstrate internal layers of keratin.
Myth of the Mesoderm

!" One germ cell layer = epidermoid E0,51%*",57+@%!+Waxy Keratin
!"Ectoderm [Figure 13]
!" Two germ cell layers = dermoid
!"Ectoderm and mesoderm
!" Three germ cell layers = teratoma
!"Ectoderm, mesoderm, endoderm
Dermoid/E0,51%*",57+Histology
!" Epidermoid: squamous epithelium – only
!" Dermoid: squamous epithelium plus
Dermal appendages
!"(Hair, sebaceous, sweat glands, etc)
!"No mesoderm Figure 13 A, B & C
!" Teratoma: complex tissues, 2 or more
germ layers Epidermoid inclusion cyst.
!"(Often mainly ectoderm, “benign Top Left Image: A “keratin pearl.” The cyst lining is
squamous epithelium and the cyst contents are dry,
cystic”) G"U>@)0"M'>)M'+"3%-)%-).1#3%6#')#">'+4)#%M')"-),-%,-/
Epidermoid Inclusion Cyst
!" Age: fourth-sixth decades
!" Location: midline or lateral (CPA)
!" Composition: squamous epithelium, Epidermoid [Figures 14 to 17]
keratin
!" Thin wall, no Ca++ or vascularity
!" NCT: lipid to brain attenuation
!"Ca++/enhance. rare
!" MRI: hetero., CSF to brain signal
!"Usually not bright on T1-W (although
reported)
!"Bright on DWI and dark on ADC
!"vv(:&,$0W4,$0(&'5'&(+3+'1(,/&'##(
ruptured
Tercera masa mas comun del angulo pontocerebeloso.

Meningioma y schwanoma que son los más frec ahi realzan.
Figure 14 A & B
Epidermoid inclusion cyst. Faint peripheral
enhancement from gliosis. Internal wisps from layers
of keratin and marked hyperintensity on the FLAIR
image.

Figure 15
Epidermoid
with
invagination
into the left
temporal
lobe.
Figure 18 A & B
Dermoid inclusion cyst. Expansile remodeling of

the occipital bone, subcutaneous, intra-diploic, and
intradural components seen on axial CT. Note the
very low attenuation regions resembling subcutaneous
fat. These are not mesodermal fat, but rather oily
sebaceous material.
Dermoid [Figure 19]
Figure 16 A & B
Epidermoid cyst. Water-like attentuation on CT.
Figure 19
Dermoid with hair and sebaceous material.
Dermoid Inclusion Cyst [Figure 20]

!" Skin, hair, sebaceous and sweat glands
Figure 17 A & B
Epidermoid inclusion cyst. Water-like on T1-W but

grossly different on FLAIR.
Dermoid Inclusion Cyst [Figure 18]

!" Age: third decade
!" Location: midline
!" Composition: Squamous epithelium and
appendages
!" Thicker wall, Ca++ and vascularity
!" ECBN(&$!$0()"(%+3$/1(&$!$0d4,$0(&'5'&#
!"Ca++/enhance. often Figure 20
!" MRI: hetero., lipid to brain Epidermal surface but with sebaceous glands, hair
!"Bright on T1-W shafts, and follicles, making this a dermoid inclusion
cyst.
!"** Watch for dysraphism, sinus tract
D1%*",57+Rupture [Figure 21] Arachnoid Cyst [Figures 24 & 25]
Figure 21 A & B
Ruptured dermoid inclusion cyst. Notice the “hairball” Figure 24 A & B
at the lipid-CSF interface.
Arachnoid cyst. No enhancement. & diffusion.
Body Soil
!" “As gross as it is, the average person
excretes up to 50 grams of body soil per
day! This is because on a normal day
we each use 1 liter of sweat, eliminate
1 billion dead skin cells, and run off 50
grams of sebum, otherwise known as
body oil.”
Figure 25 A, B & C
Clorox Commercial, May 2005. Contrast cisternogra. The contrast in the SAS does not
communicate with the CSF in the cyst.
Intradiploic Epidermoid
[Figures 22 & 23]
!" “Paraphyseal” cyst
!"Ependymal cyst, choroid cyst
!" Congenital lesion
!" Cuboidal, low columnar epithelium
!" Filled with “mucus”
!" Scant connective tissue
!" Foramen on Monro
Figure 22 A & B
Intradiploic epidermoid inclusion cyst.
Figure 26 A & B
Colloid cyst.
Masa benigna en una localización maligna

Puede ocluir el foramen de monro en forma aguda y producir
hidrocefalia aguda obstructiva.
Figure 23
Intradiploic epidermoid cyst. The lesions grow slowly
so that there is a scalloped and sclerotic rim.

Ciliated Columnar Epithelium Aqueous Protein Solution
[Figure 27]
Figure 27 A & B
Colloid cyst. Ciliated cuboidal to low columnar Cysticercosis
epithelium. The cyst contents are like mucus and vary
in consistency from a watery substance to a gel, to C%'.,"0?'%!.-,"*'7+Z+Types
hard and inspissated.
[Figures 29 to 31]
!" Child
!"Adam ant – inomatous
#" Enamel organ of tooth
!" Location: foramen of Monro
!"Commonly cystic
!" CT: sharply demarcated
!"“Machine oil”
!"Hyperdense to hypodense
!"C".."/&A(23&2$8'0
!"<< half enhance
!"Adherent to brain
!" MR: sharply demarcated
#" Pilocytic astrogliosis
!"T1-W: iso. to bright
!" Adult
!"T2-W: bright to dark
!"Papillary and squamous
!"Note: dark cysts are too thick for
!"Commonly solid
stereotactic aspiration
!"C3&2$823)$"/(&'##(6+'l,'/)
!"Easier to resect
#" Less adherent
Figure 29 A & B
Craniopharyngioma. Expansile remodeling of sella

turcica.
Figure 30 A & B
Colloid cyst. Craniopharyngioma.

Figure 31 A, B & C
Craniopharyngioma.
Suprasellar mass, heterogeneous and multi-loculated,
with enhancement of the soft-tissue components.
5?')O01%(W)%4)#%M')O."$?%-'),%#W)G%3?)OG'3)M'+"3%-W)"-()
cholesterol.
References
1. Smith AS. Myth of the mesoderm. AJNR Am J Neuroradiol 1989 Mar-Apr; 10(2):449.
2. Ochi M, Hayashi K, Hayashi T, Morikawa M, Ogino A, Hashimi R, Iwanaga M Yasunaga A, Shibata S.
Unusual CT and MR appearance of an epidermoid tumor of the cerebellopontine angle. American Journal
of Neuroradiology 1998;19:1113-5.
3. Horowitz BL, Chari MV, James R, Bryan RN. MR of intracranial epidermoid tumors: correlation of in vivo
imaging with in vitro 13C spectroscopy. American Journal of Neuroradiology 1990;11:299-302.

1348
The Phakomatoses Part 1
Educational Objectives Tumor Suppressor G1.17+VJ<"+;,)_+
!" Describe why NF-1 is truly Hypothesis [Figure 1]
h/',+"8%+".3)"#$#i
!" Describe 3 neoplasms caused by the
chromosome 22 mutation in NF-2
!" Describe the vascular abnormalities of
Sturge-Weber syndrome
!" Explain why tuberous sclerosis is a
disorder of neuronal migration
!" Distinguish von Hippel-Lindau from the
‘neurocutaneous’ phakomatoses
P?'H"*')"(1(7+U?!+Study Them?
!" They are common diseases
!" Diagnosed by imaging
!" Genetic implications
!" Screen relatives Figure 1
!" Surveillance of affected Tumor suppressor gene: “two hit” hypothesis.
Phakomatoses Mnemonic Tool

!" NF-1 (von Reck’s)
!"BVMU(/',+"8%+".3)"#$#(wZP P?'H"*')"(1(7+Genes and Proteins
!" NF-2 (bilateral vs syndrome)
!"MISME #22 múltiples scwanomas
!" Sturge-Weber (Dimitri) syndrome
!"Congenital vascular lesion
!"Perhaps not inherited
!" Tuberous sclerosis
!"Pringle’s “hamartoma” disease
!" von Hippel-Lindau syndrome
!"No cutaneous lesions
!"Hemangioblastomas and visceral
lesions
P?'H"*')"(1(7+Plan
!" Demographics N19%"#$%"*')"(,(
!" Diagnostic criteria !" NF-1, von Recklinghausen (“peripheral” –
!" Ocular/orbit lesions bad term)
!" Skin !" NF-2, bilateral acoustic (“central” – bad
!" Brain term)
!" Visceral manifestations !" NF-3, overlap of 1 and 2
!" Complications of disease !" NF-5, segmental (eg a quadrant)
!" NF-6, cafe au lait, without CNS/PNS
CNS N1"0&'(*(7+Chromosomes !" NF-7, late onset
!" Loss of Heterozygosity (LOH) !" NF-8, other
!"Schwannoma – 22q
!"Meningioma – 22q (long arm) N19%"#$%"*')"(1(7+Types
!"Ependymoma – 22 !" E',+"8%+".3)"#$#()A!'(Z(HE:WZJ
!"Medulloblastoma – 17p (short arm) !"von Recklinghausen disease
!"E',+"8%+"#3+2".3(m(ZP! !"hB+,'i(/',+"8%+".3)"#$#
!"Retinoblastoma – 13q !"Prominent cutaneous signs
!"Pilocytic astrocytoma – none !"Chromosome 17q
!" ! Tumor suppressor genes !" E',+"8%+".3)"#$#()A!'(O(HE:WOJ
!"Bilateral acoustic schwannoma
Molecular Biology !"hC'/)+3&(/',+"8%+".3)"#$#i
!" Mutations and the genetic “two hit” theory !"Minimal skin manifestations
!"Chromosome 22q
Phakomatoses Part 1 1349 Neuroradiology

N19%"#$%"*')"(,(+Type 1 or von NF-1 Optic Nerve Glioma [Figure 3]
Recklinghausen Disease
!" Chromosome 17
N19%"#$%"*')"(,(
!" 1768 Mark Akenside (New York)
!" 1793 Tilesius (Leipzig)
!" 1849 RW Smith (England)
!" 1822 Wishart (Edinburg) NF-2
!" 1882 von Recklinghausen (Germany)
NIH Diagnostic C%,)1%,'7+Z+3%"*+List

!" Café au lait spots
!"6 or more Figure 3 A & B
!"5 mm child, 15 mm adult Optic nerve glioma. Extending to the chiasm. In
!" E',+"8%+".3#(m(O("+(."+' NF-1 patients these are almost always pilocytic
!" Plexiform E',+"8%+".3(W(Z astrocytomas. Unlike their cerebellar counterparts,
they are usually solid in the optic nerve.
!" Axillary (intertriginous) freckling – 1
!" Optic glioma
!" Lisch nodules (Iris) – 2 or more
!" “Distinctive bone lesions” NF-1 Optic Nerve Glioma [Figure 4]
!" First degree relative with NF-1 !" Note: dilated perioptic subarachnoid space
RNB[7+=!1+Manifestations
!" LISCH nodules (iris hamartomas)
!"Penetrance > 90%
!"G!'2$82$)A(e(=>?
!"Translucent/pigmented
!"Small (< 3 mm), slit-lamp exam
!" Optic glioma
!"Up to 15% of patients Figure 4 A, B, C & D
!"Pilocytic astrocytomas Top Image: Bilateral
!"Benign (“hamartoma-like”), Tx? dilated perioptic
!"True neoplasms, spread along SAS subarachnoid spaces
!"Up to 1/2 of childhood ONG with NF-1 and a beaded
appearance to the
nerve.
Lisch Nodules [Figure 2] Bottom Image:
NF-1 patient
with chiasmatic/
hypothalamic
astrocytoma.
N19%"#$%"*')"(,(+`+[
!" Cutaneous manifestations
!"Café au lait spots
!"Intertriginous freckling
!"E',+"8%+".3#(H#D$/(3/0(
subcutaneous)
!"Fibroma molluscum (TNTC NFB)
!"Elephantiasis neuromatosa
#" Diffuse skin thickening/plexiform
NFB or
#" Focal gigantism
Figure 2 A & B
Café au Lait Spot [Figure 5]
Lisch nodules. Named for the 19th century German
6?>4%$%"-)G?,)&+43)('4$+%*'()3?'.@)F+/)B1814314) Figure 5
Nodule. They are small, often translucent, and a slit-
lamp exam is often required. Café au lait spot. A
."$1#"+)L0"3X)"+'"),<)
hyperpigmentation.
There are several
subcutaneous
-'1+,&*+,."4/

N19%"#$+Omatosis – 1 Progressive Pseudoarthrosis
!" Bone dysplasia and remodeling [Figure 8]
!"Macrocephaly !" Bowing deformity
!"Craniofacial dysplasia !" 8 months later
#" Especially sphenoid
!"Vertebrae (scalloping, scoliosis)
!"Pseudoarthrosis
#" Especially congenital
!"Genu Valgum/Varum
!"Twisted “ribbon ribs”
“Empty Orbit” [Figure 6]
Figure 6
“Empty orbit”
from sphenoid
dysplasia.
The right Figure 8 A & B
orbit shows
the outline Progressive bowing leading to a fracture and
of normal pseudoarthrosis.
sphenoid
densities –
lesser wing
(upper line) Focal Gigantism [Figure 9]
and greater
wing (lower
line). The
left orbit is
dysplastic.
Sphenoid Dysplasia [Figure 7]
Sphenoid dysplasia of the left orbit with secondary Focal gigantism. The overgrowth may affect all
temporal lobe herniation into the orbit, causing elements equally, bone, muscle, fat, vessels, etc.
proptosis. This patient also has a subcutaneous
6#'U%<,+.)-'1+,&*+,."/
Nerve Sheath Tumors
!" Schwannoma (sporadic >> NF-2 > NF-1)
!"Focal mass
!"Usually sensory root, cranial and
spinal nerves
!" E',+"8%+".3
!"Usually NF-1, especially if spinal or
paraspinal
!"Spindle or dumbbell lesion
!" Plexiform /',+"8%+".3(H,#,3&&A(E:WZJ
!"Diffuse or fusiform enlargement
!" Malignant peripheral nerve sheath tumor
!"NF-1 or sporadic

N19%"#$%"*'+2(+Schwannoma Intraspinal Neoplasms
!" E',+"8%+".3 !" 68 patients with 86 spinal nerve sheath
!"Schwann cells neoplasms
!"Fibroblasts !" Sporadic patients: 42 (65%)
!"Acellular material !"40 schwannoma and 2 /',+"8%+".3
!"K/8&)+3)$/- !" NF-1 patients: 12 (18%)
!"Fusiform or spindle !"All were /',+"8%+".3
!"Resect parent nerve !" NF-2 patients: 7 (11%)
!" Schwannoma !"6 schwannoma/1 “mixed” tumor
!"Schwann cell neoplasm !" Unknown (did not meet Dx criteria)
!"Vascular changes 5 patients
!"Mostly cellular
!"Encapsulated N19%"#$%"*')"(,(7+Spine
!"Eccentric to nerve !" Scoliosis (NF-1, only?)
!"Nerve sparing surgery !"Simple (“idiopathic”)
!"Acute cervical kyphosis
Schwannoma !" Dural ectasia (NF-1, only?)
!" 7.5% all primary CNS tumors (CBTRUS !"Vertebral scalloping
1995-1999) !"Arachnoid “cysts”
!" Origin from sensory nerves !"Lateral thoracic meningocele
!" Most common in adults
!"(Fifth decade) Acute Cervical Kyphoscoliosis
!" Predominance in women [Figure 11]
!" 95% solitary
!" 5% bilateral (NF-2)
S/?<'.."*'7+Encapsulated
[Figure 10]
Figure 10 A & B
Left Image: Schwannoma. A focal mass, even at the

microscopic level, within a single nerve fascicle. Figure 11 A & B
Right Image: ='1+,&*+,."/)B)(%<<14')#'4%,-@)':'-)"3)
the microscopic level within a single fascicle. Acute cervical kyphoscoliosis is one of the
“characteristic” bone lesions of NF-1.
Distribution of Nerve Sheath Tumors

!" Intracranial ! schwannoma
!" Sporadic >> NF-2
!" Spinal ! both types (S >> N)
!" Dumbbell ! both (N >> S)
!" PNS ! both
!" Cutaneous ! /',+"8%+".3
!" Usually N in NF-1
N19%"#$%"*')"(,(7+Spine
!" E',+"8%+".3(HE:WZJ
!" Osteoporosis (NF-1, only?)
!"Idiopathic
!"Parathyroid adenoma
!" NF-2
!"Schwannoma
!"Meningioma
!"Ependymoma

Enlarged Neural Foramen [Figure 12] N19%"#$%"*'+2(+Schwannoma
!" DDx: [Figure 15]
!" Nerve sheath tumor !" “Stringy” (top image)
!"E',+"8%+".3 !" “Localized” (bottom image)
!"Schwannoma
!" Arachnoid cyst
Figure 15
!" Bone dysplasia A, B & C
='1+,&*+,.")
vs
schwannoma.
The
schwannoma is
encapsulated
and focal. The
-'1+,&*+,.")
%-&#3+"3'4)"-()
tracks along the
nerve, passing
through the
intervertebral
neural foramen.
Causes of Rib Notching [Figure 16]

!" Aortic coarctation
Figure 12 A & B !"Older than 5-6 years
!"Ribs 3-9 possible
Enlarged neural foramina from multiple plexiform
-'1+,&*+,."3"/ !"Ribs 5-8 most often
!"Intercostal 1-2 arise from subclavian
artery
Multiple Dumbbell Lesions [Figure 13] !"Usually bilateral
!"Unilateral on the right
#" If coarctation involves left
Subclavian origin
!"@W_(8#),&3
!"Nerve sheath tumors
Figure 16
Rib notching
from extensive
plexiform
-'1+,&*+,."4)
involving all of
the intercostal
nerves.
Figure 13 A, B & C
C1#3%6#')(1.**'##)#'4%,-4)h)-'1+,&*+,."4/
Multiple N19%"#$%"*'(++++++++[Figure 17]
Dumbbell N19%"#$%"*'+++++++++[Figure 14]
Figure 14 A, B & C Figure 17 A & B
C1#3%6#')(1.**'##)-'1+,&*+,."4/)5?'4')#'4%,-4) C1#3%6#')-'1+,&*+,."4/)]%+31"##>)':'+>)$'+:%$"#)"-()
%-&#3+"3')3?')-'+:')"-()3+"$M)"#,-8)%34)6"3?@)6"44%-8) lumbar nerve root is massively enlarged in a fusiform
through the neural foramen into the paraspinal area. shape.

N19%"#$%"*'(++++++++++++[Figure 18] Arachnoid Cyst and N19%"#$%"*'+++++++++++
[Figure 21]
!" E")'N(#"6)W)$##,'(),."+(H/',+"8%+".3J(
and dural ectasia
Figure 21
Arachnoid
cysts on the
right – actual
Figure 18 A & B enlargement of
the axillary nerve
C1#3%6#')-'1+,&*+,."4/)5?'+')"+')*%#"3'+"#)#,G2 root sleeves
attenuation lesions within the psoas muscles and in and a large
the subcutaneous tissues of the buttocks. -'1+,&*+,."),-)
the left, with an
extensive and
Plexiform N19%"#$%"*'(++++++++++[Figure 19] bulky paraspinal
mass.
N19%"#$%"*')"(,(+`+[
!" Posterior meningocele (sporadic)
!"Dorsal dysraphism, closure of tube
!" Anterior meningocele (sporadic)
!"Neurenteric canal/cyst
!"Anterior vertebral cleft
!" Lateral thoracic meningocele (NF-1)
!"“Pulsion diverticulum” of SAS
!"Negative intrathoracic pressure
!"No overlying paravertebral MM
N19%"#$%"*')"(,(+`+[7+DBOs MR Signal
Abnormalities
Figure 19 A & B !" T1-W bright foci
N#'U%<,+.)-'1+,&*+,."4/)!'-3+"#)?>6,%-3'-4%3>)h)3?') !"Globus pallidus
“target sign.” Note: The “target” sign occurs more !" T2-W bright foci
,<3'-)%-)-'1+,&*+,.")$,.6"+'()3,)schwannoma, but
!"Without mass, do not enhance
by itself is not pathognomonic.
Jee W, Oh S, McCauley T, et al. Extraaxial !"Cerebellar peduncles, pons, midbrain
-'1+,&*+,."):'+414)-'1+%#'..,."9)(%4$+%.%-"3%,-) !"Globus pallidus, thalamus, optic
with MRI. AJR. 2004;183:629-633. radiations
!" What in the heck are they?
!"Ectopic schwann cells, melanocytes?
!"Dysmyelination?
N19%"#$%"*')"(,(+`+[7+Spine !"K/)+32'&&,&3+(!+")'$/32'",#(4,$0s
!" Scoliosis (acute Cx kyphoscoliosis)
!" Vertebral scalloping High Signal in Brain on T2 Resolves as
!" Enlarged neural foramina Adults [Figure 22]
!" Lateral thoracic meningocele
Vertebral Body Scalloping [Figure 20]
Figure 20 A & B
Vertebral body
scalloping
and one
-'1+,&*+,.")
(circled). Both
of these lesions
may cause
enlargement/
erosion of the
intervertebral Figure 22 A & B
neural foramina.
='1+,&*+,."3,4%4)deep bright objects (DBOs).

DBOs and NF-1 D:O(+"3+RNB[7+Cerebellar Peduncle
!" Incidence: a considerable body of [Figure 25]
knowledge suggests that these deep
bright objects (DBOs) are very common
in children with NF-1 (> 90% in some
series)
!" Age: They are most frequent from 4-12
years of age. They are uncommon under
the age of 4 and begin to fade away after
the age of 16.
!" Location: deep bright objects
!"Globus Pallidus 30%
!"Cerebellum 23%
!"Midbrain 16%
Figure 25 A & B
An 11-Year-Old boy with NF-1 [Figure 23]
='1+,&*+,."3,4%4)FIc4)4?,G%-8)46,-3"-',14)
improvement.
N19%"#$%"*')"(,(+Type 2
D1#.15+$!+Wishart
!" Genetics based on your parents – your
63.$&A(/3.'1(/")(A",+(8+#)(/3.'
N19%"#$%"*')"(1(+B+Types
!" E',+"8%+".3)"#$#()A!'(Z(HE:WZJ(
!"von Recklinghausen disease
!"hB+,'i(/',+"8%+".3)"#$#
!"Prominent cutaneous signs
Figure 23 A & B !"Chromosome 17q
DBOs of NF-1. !" E',+"8%+".3)"#$#()A!'(O(HE:WOJ
!"Bilateral acoustic schwannoma
!"hC'/)+3&(/',+"8%+".3)"#$#i
!"Minimal skin manifestations
DBOs of NF-1 [Figure 24] !"Chromosome 22q
N19%"#$%"*')"(,(7+Type 2
!" Incidence: 1/50,000
!" Inheritance: autosomal dominant
!" Age at presentation: birth to 40’s (peak in
20’s)
!" Sx at presentation: hearing loss from VS
!" Diagnostic criteria: VIII masses
!" Chromosome abnormal: 22 cutaneous
Findings: minimal (skin tags)
!" CEG(8/0$/-#N(schwannoma, meningioma,
ependymoma (intramedullary spinal cord)
CNS N1"0&'(*(7+Chromosome Loss of

Figure 24 A & B
Heterozygosity
!" NF-2
='1+,&*+,."3,4%4)FIc4)4?,G%-8)6+,8+'44%,-/ !"Schwannoma - 22q
!"Meningioma - 22q (long arm)
!"Ependymoma - 22
!" Not /',+"8%+".3
!" Not astrocytoma NF1
!" Not optic glioma

NF-2 (“Central”), 1 or More Multiple Meningiomas [Figure 27]
!" Bilateral VIIIth masses
!" Relative with NF-2 and either:
!"Unilateral VIIIth mass
!"Any two:
#" “E',+"8%+".31i(meningioma,
glioma, schwannoma, (congenital)
lens opacity
Figure 27 A, B & C
N19%"#$%"*')"(,(+`+Type 2
!" NEJM 319:278-83, 1988 (Gulf of Mexico) Multiple meningiomas. With an associated
schwannoma this would probably be due to NF-2.
!" 23 Patients (15M/8F), kindred of 137 However, without any schwannomas this is likely
!" 0.95 penetrance caused by a different mutation.
!" 18 acoustic schwannoma (17 billion)
!" 8 meningioma (3 mult.)
!" 4 ependymoma Bilateral Vestibular Schwannomas
!" 2 spinal “/',+"8%+".3i [Figure 28]
Intracanalicular Schwannoma
[Figure 26]
Figure 26 A & B
Figure 28 A & B
Intracanalicular schwannoma. They all begin inside the
IAC because that is where the Schwann cells are. The Bilateral intracanalicular vestibular schwannomas. On
cisternal segment of the nerve has oligodendrocytes. the right side, the lesion is beginning to grow out of
the IAC and into the cerebellopontine angle cistern.
Schwannoma Multiple Schwannomas and

!" 5%-10% of all CNS tumors Meningiomas
!" Benign, slowly growing
N19%"#$%"*')"(,(+`+Z
!" F > M (intracranial), M > F (spinal)
!" Multiple meningiomas (up to 45% of NF-
!" 30’s-60’s, with NF-2 10’s-30’s
2)
!" Sensory nerves (usually):
!"Intraventricular meningiomas
!"CNN VIII (sup. vestibular), V, X
!"Childhood meningiomas
!"Spine: dorsal roots
!" Multiple meningiomas
!" Majority (> 90%) are sporadic
!"1%-10% of all patients with
!" Multiple in NF-2, bilat.VIII pathognomonic
meningioma
N19%"#$%"*')"(,(+`+Z !"SPORADIC in 80%-90% of cases
!" Meningiomas: !" Intraventricular meningiomas
!"Multiple transitional type meningioma !"Sporadic in 90%
!"NOT meningothelial !" Childhood meningiomas
!" Meningioangiomatosis: !"Sporadic vs inherited (NF-2 or not)
!"Cortical (intracortical) vascular tissue
!"Resembles a vascular malformation
!"<'/$/-")*'&$3&(3/0(8%+"%&3#)W&$D'(2'&&#

Multiple Schwannomas, Meningiomas,
and Ependymomas [Figure 29]
Figure 30 A & B
Figure 29 A & B
Bilateral vestibular schwannoma.
Multiple schwannomas, meningiomas, and
ependymomas. The MISME syndrome.
MISME Syndrome
Bilateral Vestibular Schwannoma !" M - Multiple
[Figure 30] !" I - Inherited
!" S - Schwannoma
!" M - Meningioma
!" E - Ependymoma
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E',+"8%+".3)"#$#T(@XEV(Z==]YQNQ^ZW[T
32. V$223+0$(_T(E',+"8%+".3)"#$#T(`*'/")A!'1(E3),+3&(k$#)"+A1(3/0(`3)*"-'/'#$#T(Ond ed. Baltimore: The Johns
Hopkins University Press, 1992.
33. Russell DS, Rubinstein LJ. Dysgenetic Syndromes (Phacomatoses) Associated with Tumors and
Hamartomas of the Nervous System. Chap 11 (pgs 766-784) in Pathology of Tumors of the Nervous
System Williams and Wilkins, Baltimore, 1989.
34. Seizinger BR, Martuza RL, Gusella JF. Loss of Genes on Chromosome 22 in Tumorigenesis of Human
Acoustic Neuroma. Nature 1986;322:644-7.
35. Smirniotopoulos JG, Murphy FM. The Phakomatoses. AJNR Am J Neuroradiol 1992;13:725-46.
36. Stull MA, Moser RP, Kransdorf MJ, Bogumill GP, Nelson MC. Magnetic Resonance Appearance of Peripheral
Nerve Sheath Tumors. Skeletal Radiology 1991;20:9-14.

The Phakomatoses Part 2
Tuberous Sclerosis Complex or Pringle Disease
Bourneville Disease !" Pringle’s name
!" Chromosomes 9 and 16 !"Entire disease
!"Facial lesion only
Tuberous Sclerosis !" Mild mental retardation
!" Bimalar red papules
!" No racial/sexual
!" Seizures
!" High spontaneous mutation
!" Hard potatoes (sclerosis)
!" High penetrance
!" Tubular can – ‘tuberous’
!"“Sporadic” overreported
!" Multiple genes Subungual/Periungual Fibroma
!"TSC1 – 9q [Figure 1]
!"TSC2 – 16p
Tuberous Sclerosis
!" Original “Vogt triad”
!"Facial nevus (adenoma sebaceum)
!"Seizures
!"<'/)3&(0'82$'/2A
Tuberous Sclerosis, NIH Consensus
Conference
!" Major features:
!":32$3&(3/-$"8%+".3("+(6"+'*'30(!&3l,'
!"M/-,3&("+(!'+$,/-,3&(8%+".3
!"> 3 hypomelanotic macules Figure 1 A & B
!"Shagreen patch Subungual (right image) and periungual (left image)
!"Multiple retinal nodular hamartomas O&*+,."W)%-)tuberous sclerosis. These are actually
!"Cortical tuber "-8%,&*+,."4@)4%.%#"+)3,)3?')N+%-8#')<"$%"#)#'4%,-/)
!"Subependymal nodule They may erode the distal phalangeal tuft – DDx –
scleroderma, frostbite, glomus tumor, metastasis.
!"Subependymal giant cell astrocytoma
!"Cardiac rhabdomyoma
!"Lymphangiomyomatosis
!"Renal angiomyolipoma
!" Minor features:
!"Multiple dental enamal pits
!"Hamartomatous rectal polyps D10,-*1.)'),".7
!"Bone cysts !" Ash-leaf spots
!"White matter migration lines !"(Lance-ovate shaped)
!"\$/-$53&(8%+".3# !" Confetti-like hypopigmentation
!"Nonrenal hamartoma !"(Inverse freckle)
!"Retinal achromic patch
!"“Confetti” skin lesions Other Cutaneous Manifestations
!"Multiple renal cysts !" G,%'!$0'+.3&(8%+"#$#N
!" 7'8/$)'(BG(m(HO(.3a"+J("+(HZ(.3a"+(p(O( !"Dorsal surfaces
Minor) !"“Shagreen patch”
!" Probable TS – (1 major + 1 minor) !"“Peau d’orange”
!" Possible TS – (1 major) or (2 minor) !"“Pigskin”
Hyman MH, et al. National Institutes of Health Con- !"“Elephant hide”
sensus Conference: tuberous sclerosis complex. Arch
Neurol. 2000;57:662-665. Tuberous S/&1%"(,(7+Ocular
!" Phakoma
Adenoma Sebaceum !"Benign astrocytic hamartoma
!" AKA Pringle disease !"Leukokoria
!" NOT present at birth #" b*$)'(&$-*)(+'4'L
Ddx con retinoblastoma
!" Develop before puberty !" C3&2$823)$"/(2".."/
!" Nasolabial fold $ bimalar lesions #" Especially over optic nerve
!" `3!,&'#("6(3/-$"8%+".3 !" May be multiple and bilateral

Astrocytic Hamartoma [Figure 2] Periventricular Ca++ [Figure 4]
Figure 4 A & B
Tuberous sclerosis. Multiple deep (periventricular)

$"#$%&'()41*'6'-(>."#)-,(1#'4/
Figure 2 A & B
Tuberous sclerosis. Astrocytic hamartoma of the

retina – the original “phakoma” of van der Hoeve. The Subependymal Nodules [Figures 5 to 8]
lesions are multiple with one located over the optic
nerve head.
Figure 5
Neonatal
sonogram.
Tuberous S/&1%"(,(7+Brain Subependymal
!" Heterotopias and hamartomas nodules in
!"In white and gray matter tuberous
!" Cortical tubers sclerosis are
developmental
!"“Hamartomas” and are present
!"But with abnormal “N” cells during fetal life
!"Neither astrocyte nor neuron before birth.
!"Decreased myelination
!"No laminar architecture
Tuberous S/&1%"(,(7+Brain
!" Subependymal nodules (almost 100%)
!"“Hamartomas” vs neoplasia
!"Caudothalamic groove
!"Polypoid “candle gutterings”
!" Dilated ventricles
Figure 6 A & B
!"Variable
!"Obstructive, atrophic vs ”idiopathic” Subependymal nodules may enhance without
!" TUMORS 15% neoplastic transformation.
!" Subependymal giant cell astrocytoma
!"True neoplasm, Benign WHO grade I
Cortical Tubers [Figure 3]

!" Cortical tuber: focal enlarged gyrus,
abnormal WM Figure 7
Tuberous
sclerosis is
a disorder
of neuronal
migration and
maturation.
Figure 3 A, B & C
Cortical tuber. Focal enlarged gyrus and abnormal

WM.

Renal Cysts [Figures 11 & 12]
Figure 8
Tuberous
sclerosis.
Cortical
tubers and
white matter
hyperintensities
from the
abnormal
migration and
maturation of Figure 11 A & B
the brain.
Tuberous sclerosis. In addition to angiomyolipoma, the
patients may also develop multiple and bilateral renal
cysts.
Subependymal Giant Cell Astrocytoma Figure 12

[Figure 9]
Tuberous
sclerosis. In
addition to
angiomyolipoma,
the patients may
also develop
multiple and
bilateral renal
cysts.
Figure 9 A, B & C
Angiomyomatosis vs
Lymphangiomyomatosis
Subependymal giant cell astrocytoma in tuberous !" “Sporadic” cases (all female)
sclerosis. This is a low grade WHO 1 neoplasm. !"50% chylothorax
!"Perilymphatic smooth mm.
!"May have abdominal LN involvement
A.-,"*!"&,0"*'7++++++++++++++++++[Figure 10] !" In TS, men can be affected
!" Z>?(I$)*('/",-*(:@B(6"+(!&3$/(8&. !"Chylothorax is rare
!" 1/6 of solitary AML patients have TS !"Periarterial smooth mm. around
!" 1/3-1/2 of solitary AML patients have pulmonary aa
other stigmata of TS
!" 50%-80% of patients with TS will have Pulmonary Lymphangioleiomyomatosis
AML [Figure 13]
!" 3/4 multiple
!" 1/3-1/2 Bilateral (probably more)
!" Variable amounts of FAT, smooth mm.,
and vessels
Figure 10 Figure 13
Multiple renal angiomyolipomas in tuberous sclerosis Pulmonary interstitial smooth muscle proliferation,
complex. These masses are often easily recognizable similar to lymphangioleiomyomatosis, occurs in
as fat attenuation. This patient also has a renal cyst tuberous sclerosis. It may be associated with
(C), another feature of TSC. spontaneous pneumothorax but chylothorax is
uncommon.
AML > de 4 cm tiene mucho riesgo de hemorragia, se sugiere extirpación qx

Sturge-Weber Disease or Encephalo- Port-Wine Stain [Figure 14]
Trigeminal Angiomatosis
!" Inheritence?
!" Autosomal dominant?
!" Autosomal recessive?
!" Sex-linked?
Sturge-W1$1%7+D1#.,),".
!" A telangiectatic venous angioma of the
leptomeninges, face, and choroid of the
eye
Sturge-W1$1%7+History
!" 1879 STURGE, clinical description
!" 1897 Kalischer, vascular nature
!" 1922 Weber, published radiography
!" 1923 Dimitri, “tram-track” Ca++
!" 1934 Krabbe, Ca++ in cortex
Figure 14 A & B
!" 1937 van der Hoeve, phakomatosis
Trigeminal angiomatosis in SWS.
Sturge-W1$1%7+Classic Triad Dilated small vessels in the skin with deoxygenated
blood. Pressing on the skin blanches the lesion.
!" :32$3&(/'5',#(43..',#
!"Port-wine stain
!" Seizures Port-Wine Stain
!" <'/)3&(0'82$'/2A !" Not everyone with a port-wine stain has
Sturge-Weber syndrome
Sturge-W1$1%7+Variants !" Association of PWS with SWS:
!" Facial and intracranial without eye !"More extensive PWS
!" Intracranial and eye without face !"Includes medial canthus of eye
!" Intracranial alone #" V1 or V2
!"(Cerebral and leptomeningeal) !" Mikhail Sergeyevich Gorbachev - 1990
!" Klippel-Trenaunay (KT Weber) Nobel Peace Prize
!"Extracranial soft tissue angiomas !" Time Magazine: Man of the Decade
(1980s), Time Magazine: Man of the Year
Sturge-W1$1%7+Manifestations (1987)
!" Facial “angioma”
!"Present at birth Sturge-W1$1%7+What do we Know?
!" Leptomeningeal “angioma” !" Usually unilateral
!" Seizures, mental decline !" Usually supratentorial
!"M#,3&&A(%'-$/#($/(8+#)(O](."/)*# !"Cerebral >>> cerbellum
!" Angiomatous overgrowth of soft tissue !" Neurologically normal at birth
and bone of head !" Seizures in early life (< 24 months)
!" Ipsilateral cerebral atrophy with Ca++ !" Normal cerebral arteries
!" Contralateral somatic atrophy !" Impaired cortical venous drainage
Sturge-W1$1%7+Port-Wine Stain (PWS) Medullary Veins [Figure 15]
!" :32$3&(/'5,#(43..',#
!" Blanches with pressure
!" Trigeminal dermatome
!"V1 - Ophthalmic
!"V2 - Maxillary
!"V3 - Mandibular
No todas las personas con manchas en vino de oporto

tienen el Sd. Si no desarrollan compromiso neurológico Figure 15
los primeros 2 años, lo más probable es que no tengan The medullary veins are abnormally prominent
nada. and bridging veins are absent over the occipital
and posterior parietal lobes. These medullary veins
are draining the cortex in an abnormal centripetal
direction because the cortical veins are missing.

Abnormal Medullary Veins Atrophy and C'&/,#/'),".+++++[Figure 17 ]
[Figure 16]
!" Drain cortex inward through white matter
instead of outward to SAS and dura
Figure 16
Sturge-Weber
syndrome.
T1-W MR with
contrast shows
prominent Figure 17 A & B
medullary veins
that drain the In an older patient with SWS the cortex is atrophic
cortex into the "-()$"#$%&'(/)=,G)3?')$,##"3'+"#)(+"%-%-8):'%-4)"+')-,)
periventricular longer prominent in the subarachnoid space.
white matter.
Also note the
widened diploic
space of the Normal vs Venous O9)Q"<+Obstruction
frontal bone [Figure 18]
and gyriform
surface
enhancement
posteriorly.
Sturge-W1$1%7+Vascular
!" Absence of cortical bridging veins
!"`""+(8&&$/-("6(#3-$))3&(#$/,#
!" Persistent primitive plexus (SAS)?
!" Recruitment of Collateral veins
!"Deep medullary veins
!"Prominent choroid plexus
!" Impaired venous drainage $ reduced
cerebral perfusion
Figure 18
Parsa DF. Sturge-W'*'+)4>-(+,.'9)B)1-%&'()
pathophysiologic mechanism. Current Treatment Impaired venous drainage leads to chronic cerebral
Options in Neurology. 2008;10:47-54. ischemia. Rather than an abrupt ischemic event
causing infarction, there is low level ischemia that
Cranial Vascular Development leads to progressive atrophy.
!" Begins with primitive plexus
!" Progressive differentiation
!"Arteries
!"Capillaries
Sturge-W1$1%7+C'&/,#/'),".
!" Abnormal (sluggish) circulation
!"Veins
!" Chronic cerebral ischemia
!" Progressive lamination
!" Progressive cell loss (atrophy)
!"Cerebral (brain) circulation
!" `+"-+'##$5'(2'+'%+3&(23&2$823)$"/
!"Dura and bone circulation
!"Early – cortical WM (?)
!"Scalp circulation
!"Later – middle layers of cortex
!" Development and/or retention of collateral
venous drainage Atrophy and C'&/,#/'),".++++++++[Figure 19]
Sturge-W1$1%7+Orbit/Eye
!" Buphthalmos (‘ox eye’)
!" Congenital glaucoma
!" Enlarged globe
!" Choroidal angioma
!" Episcleral telangiectasia
!" Angiomatous overgrowth of EOM’s
Figure 19 A & B
Sturge-Weber syndrome with extensive occipital and
6"+%'3"#)$"#$%&$"3%,-)"-()"3+,6?>/

Dyke, Davidoff, M'((".7 Hemiatrophy [Figure 22]
“Cerebral Hemiatrophy with Homolateral Hyper- !" Enlarged choroid plexus
trophy of the Skull and Sinuses.” Surgery, Gyne-
cology, and Obstetrics. 1933:589-600.
Progression in SWS [Figure 20]
Figure 22 A & B
Figure 20 A & B SWS showing the classic features of cerebral

hemiatrophy, widened diploic space, gyriform
Progression in SWS. Same patient scanned two years enhancement, and enlargement of the choroid plexus.
apart.
Sturge-Weber
Dyke, Davidoff, Masson [Figure 21] !" Gyral gadolinium enhancement
!" Abnormal BBB in cortex
!"(Chronic ischemia)
!" “Epicortical” enhancement
!"HG&"I(4"I($/(#,!'+82$3&(5'$/#J
Gyral C'&/,#/'),".++++++++++[Figure 23]
Figure 21 A & B
Dyke, Davidoff, Masson skull changes, secondary to

cerebral hemiatrophy in SWS.
Figure 23 A & B
Sturge-Weber disease. T2-W MR and CT in the same

6"3%'-3)4?,G)$?"-8'4)<+,.)8>+"#)$"#$%&$"3%,-/
Sturge-W1$1%7+Treatment
!" Symptomatic (anticonvulsants)
!" Cosmetic tattooing
!" Laser treatment of skin lesions
!" Hemispherectomy
!" Aspirin (mild antiplatelet)?

Half a Brain !"Hemangioblastoma
!" Uncontrolled Sz !"Viscera
!" Under age 2 !"Pheochromocytoma
!" Up to age 5-7 !"Renal cancer
!" Plasticity
!" Uncrossed tracts von Hippel-L,.5'97+RK;+C&'((,#/'),".
!"5%–15% !" Type I - VHL without pheo
!"Renal/pancreatic cysts, RCC
Outcome of Sturge-Weber in Adults !"Most common type
!" Craniofacial PWS 98% !" Type II - VHL with pheo
!"96% had PWS with seizures and/or !"IIA islet cell tumors (no cysts)
glaucoma !"IIB renal/pancreatic disease
!" Extracephalic PWS 52% #" Least common type
!" Seizures 83% (88% presented <= 5
years) von Hippel-L,.5'97+S,>+Classic Lesions
!"[]?($/(8+#)(A'3+ !" Hemangioblastoma
!"76% by second year !" Retinal angioma (hemangioblastoma)
!" E',+"&"-$2(0'82$)#([R? !" Pancreatic cyst
!" Headaches 62% !" Renal cysts and CA
!" Intellectual functioning !" Pheochromocytoma
!"“Subnormal” 55% !" Epididymal cystadenoma
!"Normal 45% !" Endolymphatic sac tumor
!" Glaucoma 60%
!" Body asymmetry 48% Hemangioblastoma
!" All patients without seizures able to live !" True neoplasm endothelial origin
independently !" Hypervascular
!" 41% with seizures did not require !"Capillary to sinusoidal
“supervised arrangements” !"Dilated feeding artery
!"Dilated draining vein
Hemangioblastomatosis or von Hippel- !"G&"I(4"I
Lindau Disease !" Stromal cells
!" Chromosome 3 !"Foamy, lipid-laden
!" VHL has 3 letters
no tiene hallazgos cutaneos H1*'.-,"$&'()"*'7+Fluid Secreting
von Hippel-Lindau [Figure 24]
!" Incidence of 1/35000-40000 !" “Cyst with nodule”
!"6-7000 patients in US
!" Autosomal dominant Figure 24
!"No racial/sexual predilection
Hemangio-
!" variable penetrance/expressivity blastoma. The
!" Mutation on chromosome 3p25-26 classic “cyst
!"Associated with renal cell carcinoma with nodule”
morphology.
von Hippel-L,.5'97+History
!" 1864 scattered reports of angiomatous
lesions of both retina and cerebellum
!" 1894 Collins (England) Hemangioblastoma [Figures 25 to 27]
!"Two sibs with retinal angioma

!" 1904 von Hippel (Germany)
!"Familial retinal hemangioblastoma
!" 1926 Lindau (Sweden)
!"Familial retinal and cerebellar
hemangioblastomas
!" 1964 Melmon and Rosen
von Hippel-Lindau
!" CNS and retinal hemangioblastoma
Figure 25 A & B
!" Hemangioblastoma and one:
!"Renal, pancreatic, hepatic, epididymal Hemangioblastoma with capillaries and stromal cells.
cyst
!"Pheochromocytoma
!"Renal cancer El hemangioblastoma se en pctes con VHL aparece
!" Family history and one: dp de los 20 años y es hipervascular.

M;G7+Renal Manifestations
!" Cysts 25%-63%
!" Angiomas 7%
!" Adenomas 14%
!" Clear cell CA 15%-50%
von Hippel-L,.5'97+I44
!" Renal cell carcinoma
!"Multiple
!"Bilateral
!"Conservative surgery
Multicystic RCC [Figure 29]

Figure 26 A & B
Hemangioblastoma showing the classic “cyst with

-,(1#'W).,+6?,#,8>),<)3?'4')01%(24'$+'3%-8)31.,+4/
Figure 29 A & B
von Hippel-Lindau. Multicystic renal cell carcinoma.

The septations are thick and enhancing; composed of
neoplastic cells.
Figure 27 A & B
Endolymphatic Sac Tumor [Figure 30]
Hemangioblastomas span a spectrum from largely !" Petrous apex mass
cystic to mostly solid. !"Cholesterol granuloma
!"Glomus tumor
!"Vascular variant
Hemangioblastoma [Figure 28]
!"Cystadenoma (endolymphatic sac
tumor)
Figure 30 A & B
Endolymphatic sac tumor.
Summary
!" E',+"8%+".3)"#$#()A!'(Z
Figure 28 A & B !" Skin, nerves, optic astrocytoma, brain
von Hippel-Lindau. Syringohydromyelia with multiple DBOs, spine and bone
enhancing nodules of hemangioblastoma. !" Proband with stigmata

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K*'-,.-+"3+)?1+S90%'?!",5+R1/H+K7+
S901%#/,'&a+F'%'0?'%!.-1'&a+'.5+4'%"),5+S0'/1(
Cervical Fascia S901%#/,'&+S0'/17+Pathology

!" G,!'+82$3&(2'+5$23&(63#2$3 !" Hair follicles
!":3)W8&&'0(&3A'+("6(2"//'2)$5'()$##,'( !"Sebaceous cyst
that completely surrounds the neck !" Congenital/blood vessels
and permits the skin to glide easily !"EJV thrombosis, hemangiomas/
over deeper structures vascular malformations
!" Deep cervical fascia !" Lymph nodes
!"G,!'+82$3&(&3A'+(H$/5'#)$/-(63#2$3J !"Reactive/suppurative adenopathy
!"Middle layer (visceral or pretracheal !"Nodal metastases
fascia) !" Fat
!"Deep layer (perivertebral fascia) !" Lipoma/liposarcoma
!" Pseudomass
Fascial Spaces of the Suprahyoid Neck !"Fibromatosis coli
[Figure 1]
!" G,!'+82$3&(#!32' Hemangiomas (Proliferating
!" Parapharyngeal space Hemangioma of Infancy) [Figure 2]
!" Carotid space !" Most common head and neck tumor of
!" Masticator space infancy and childhood
!" Parotid space !" Rarely present at birth but manifests in
!" Pharyngeal mucosal space early infancy, grows slowly, and involutes
!" Retropharyngeal/danger space by adolescence
!" Perivertebral space !" 80% are isolated lesions
!" Posterior cervical space !" Females > males
!" Isointense on T1-WI, hyperintense on T2-
WI
!" + enhancement
Figure 1
Fascial spaces of the suprahyoid neck.
S901%#/,'&+S0'/17+Contents
!" Sternocleidomastoid muscle
!" Trapezius muscle
!" Platysma muscle
!" Lymph nodes Figure 2 A, B, C & D
!" Blood vessels/EJV
!" Hair follicles Large facial hemangioma.
Note isointense on T1-WI, hyperintense on T2-WI, and
!" Fat intense enhancement.
;16+"?>,%()='$M9);16'+&$%"#@)N"+"6?"+>-8'"#@)!"+,3%();6"$'4 1369 Neuroradiology

Lymphatic Malformations [Figure 3]
!" Arise from sequestrations of the primitive
embryonic yolk sac
!" C&3##$8'0(322"+0$/-()"(&A.!*3)$2(5'##'&(
size (capillary, cavernous, cystic) –
Largest is the cystic variety, previously
termed cystic hygroma
!" Typically multiseptated
!" :&,$0W4,$0(&'5'&#(I$)*$/()*'(&'#$"/#(3+'(
almost pathognomonic
Figure 5 A & B
Madelung disease.
Fibromatosis Coli (Stenocleidomastoid

Tumor of Infancy) [Figure 6]
!" Diffuse SCM enlargement
!" Most common type of congenital torticollis
!" :$%+"2"&&3-'/",#($/8&)+3)$"/(W(23,#'s
!" Typical course:
!"Not detected at birth
Figure 3
A, B & C !"Palpable neck mass at 2-4 weeks of
age
!"Increases in size for a few weeks
Lymphatic
malformation. (growth phase)
Thin-walled cysts, !"Most recede spontaneously at 4-8
very bright on T2- months of age
WIs and rim or !" This is a leave-alone lesion
no enhancement
(Courtesy Dr. S.
Blaser).
Veno-Lymphatic Malformation [Figure 4]
Figure 6
A, B & C
Fibromatosis
coli.
Note diffuse
enhancement.
Figure 4 A & B
Large, mixed, venolymphatic malformation in a
2-year-old child.
Madelung Disease [Figure 5]

!" Almost exclusively a disease of middle-
aged alcoholic men
!" 50 years of age
!" Appearance of lesions is preceded by 10
years of heavy drinking
!" Nonencapsulated fatty masses
!" Sight diagnosis

Parapharyngeal Space (PPS) [Figure 7] Parapharyngeal S0'/17+Pathology
!" Is an “in-between” space lying between !" Pseudomass
")*'+(63#2$3&&AW0'8/'0(#!32'#T(E")( !"Asymmetric pterygoid plexus of veins
63#2$3&&AW0'8/'0($)#'&6T !" Congenital/vascular
!" Few lesions actually arise within this !"Atypical second BCC, hemangioma,
space but typically originate from lymphatic malformation, aneurysm
surrounding spaces and produce !" K/43..3)"+A
characteristic encroachment on the PPS !" Cellulitis/abscess
63)T(C3/()*'+'%A(0'8/'()*'(#!32'("6( !" Benign tumor
origin. !"Pleomorphic adenoma from ectopic
!" The “parapharyngeal space” can salivary gland rests, neurogenic tumor,
be considered as consisting of two lipoma
compartments: !" Malignant tumor
!"Prestyloid = parapharyngeal space !"MECa and ACCa from ectopic salivary
(PPS) gland rests, direct spread from
!"Retrostyloid = carotid space (CS) malignancies in surrounding spaces,
liposarcoma, distant mets (rare)
Hemangioma [Figure 8]
Figure 7 A & B
T1-W MR images optimally demonstrate the

4>..'3+%$@)O<"32&##'(W)NN;)46"$'4)L"++,G4X/
Figure 8 A to E
Figure 7C PPS hemangioma

(arrows)
The normal “in-between” location of the PPS is shown demonstrates
in yellow. enhancement on
the CT image.
The lesion is iso-
intense on T1-
WI, hyperintense
on T2-WI, and
exhibits intense enhancement (arrows). Flow voids are
best appreciated on the T1- and T2-WIs.
Parapharyngeal S0'/17+Contents
!" Fat
!" Branches of the mandibular nerve (V3)
!" Internal maxillary artery branches
!" Ascending pharyngeal artery
!" Pharyngeal venous plexus
!" Ectopic salivary gland tissue

Lymphatic Malformation [Figure 9] Pleomorphic Adenoma [Figure 11]
Figure 9 A,
B&C
PPS lymphatic
malformation
(arrows) is iso-
intense on T1-WIs
and demonstrates
")01%(201%()#':'#)
on the T2-WI Figure 11
(arrow). A to E
PPS pleomorphic
adenoma,
well-centered
within the
PPS Abscess [Figure 10] PPS, is clearly
separated from
the deep lobe
of the parotid
gland.
Lipoma [Figure 12]
Figure 10
A, B & C
Odontogenic
PPS
abscess.
Figure 12 A & B
Lipoma-predominantly PPS. Since the PPS is not
<"4$%"##>2('&-'(@)%-3+%-4%$)6"3?,#,8>)%4)<+'')3,)'U3'-()
along fascial planes, as can be seen with this lipoma.
Carotid S0'/17+Contents
!" Internal carotid artery
!" Cranial nerves (IX-XII)
!" Sympathetic chain
!" Internal jugular vein
!" Deep cervical (internal jugular) lymph
node chain

Carotid S0'/17+Pathology
!" Pseudomass Figure 14C
!"Ectatic CCA or ICA, asymmetric IJV
(can mimic a vascular tumor) Second branchial
!" Congenital cleft cyst with
classic “beak”
!"Second branchial cleft cysts between the ECA
!" K/43..3)"+A and ICA (arrow).
!"Cellulitis/abscess, adenopathy
!" Vascular lesions
!"IJV thrombosis or thrombophlebitis,
ICA thrombosis, aneurysm, or
dissection
!" Benign tumor
!"Paragangliomas (jugular, vagal,
carotid body), nerve sheath tumors,
meningioma (from jugular foramen) Lymphatic Malformation [Figure 15]
!" Malignant tumor
!"SCCa nodal metastases, direct
invasion by SCCa, NHL, other nodal
mets
Second Branchial Cleft Cyst [Figures 13 & 14]

!" The most common of the branchial cleft
cysts
!"66%-75% in children
!" “Classic location” at, or just caudal to, the
angle of mandible (but may present in a
variety of locations):
!"Posterior to the submandibular gland
!"Anterior to the SCM
!"Lateral to the carotid space
!"Occasionally see a “beak” with the
cyst pointing medially between the
ECA and ICA (track) Figure 15 A to F
!" Often enlarge with URIs and become Lymphatic malformation. The multiloculation
painful if infected distinguishes this from a second branchial cleft cyst
although the displacements of surrounding structures
Figure 13 is the same.
Second branchial
cleft cyst. Classic
displacements. ICA Dissection [Figure 16]
Anterior displacement
of the submandibular
gland (SMG), medial
displacement of the
carotid space (CS)
structures, and posterior
displacement of the
sternocleidomastoid
muscle (SCM).
Figure 16 A & B
Internal carotid artery dissection.

Hemorrhage in the wall of the vessel is best
demonstrated on the noncontrast T1-WI (arrows).
Figure 14 A & B
Second branchial cleft cyst with classic “beak”
between the ECA and ICA (arrow).

Jugular Paragangliomas [Figure 17]
!" Arise in adventitia of IJV from Arnold
nerve (IX) and Jacobson’s nerve (X)
!" Represent the most common tumor found
in the jugular foramen
!" Permeative erosive changes with
amputation of the jugular spine
demonstrated on CT
!" Multicentric in up to 25% of familial cases
!" Sx: pulsatile tinnitus; IX-XI cranial
neuropathy +/- XII
!" Malignant with mets in approximately 3%
Figure 16 C & D
Internal carotid artery dissection.

Hemorrhage in the wall of the vessel is best
demonstrated on the non-contrast T1-WI (arrows).
Paragangliomas
!" Highly vascular tumors arising from non-
2*+".368/(2'&&#("6(/',+3&(2+'#)("+$-$/
!" Usually asymptomatic from endocrine
standpoint but rare catecholamine-
secreting lesions do occur
!" Not true resemblance to glomus tumors
6",/0($/(#D$/(3/0(#,!'+82$3&(#"6)()$##,'#1(
so some prefer term “paraganglioma”
instead of “glomus” tumor
!" Familial and nonfamilial patterns exist
with synchronous lesions seen in up to
25% of familial cases
!" Highly vascular “salt and pepper”
appearance of larger lesions on MR
suggestive in correct locations
!" Both regional and distant (lung, liver)
metastatic disease are reported in 10%- Figure 17 A to F
15% of cases
Jugular paraganglioma on the right extends inferiorly
!" Etiology is unclear probably due to %-3,)3?')?%8?)$"+,3%()46"$')L"++,G4X/)N+,.%-'-3)0,G)
hypoxic stimuli voids are seen on the T1-WIs. The lesion erodes the
!" Four common locations: V181#"+)31*'+$#')"-()&##4)3?')?>6,8#,44"#)$"-"#@)3?')
!"Middle ear cavity-tympanicum normal counterparts arrowed on the left.
Note late chronic denervation atrophy of the right
paragangliomas hemitongue.
!"Jugular foramen-jugular
paragangliomas
!"High carotid space-vagal
paragangliomas
!"Carotid bifurcation-carotid body
paragangliomas

Meningioma is isointense on T1-WI, mixed intensity on

5J2^7@)"-()."+M'(#>)'-?"-$'4)L"++,G4X/)!"#$%&$"3%,-)
demonstrated on CT (arrow) mitigates against
consideration of a paraganglioma. Figure 19 A, B, C & D
Vagal paraganglioma displaces the ICA anteriorly

G%3?)3?')f!B)L"++,G4X/)b"+8')0,G):,%(4)"+')4''-/)5?')
MRA optimally demonstrates the anterior vascular
Vagal Paraganglioma [Figure 19] displacements (arrows).
!" Arise from paraganglia located around
nodose ganglion, the more caudal of the
two vagus nerve ganglia
!" Situated just below skull base, lower than
typical jugulare tumors and higher than
typical carotid body tumors
!" Usually lie entirely within carotid space
!" As vagus nerve lies dorsal to ICA, these
tumors usually displace ICA anteriorly
!" Approximately 10% incidence of
malignancy
Vagal Meningioma [Figure 20]
Figure 20 A to E
Meningioma.
Enhancing lesion
in the high carotid
space which displaces
the ICA anteriorly
(arrows), suggesting a
vagal paraganglioma.
`,G':'+@)%('-3%&$"3%,-)
of associated
$"#$%&$"3%,-)"-()
sclerosis (arrows) of
the jugular tubercle
and lack of destruction
makes the diagnosis of
meningioma.

Vagal Schwannoma [Figures 21 & 22] Carotid Body Paragangliomas
[Figure 23]
!" Arise from paraganglia located in the
“crotch” of the carotid bifurcation (most
common location)
!" `3)*"-/"."/$2(8/0$/-($#(h#!&3A$/-i("6(
)*'(UC@(3/0(KC@(3/0(h8&&$/-W$/i("6()*'(
bifurcation
!" Multiple in up to 33% of familial cases
!" Sx: Only 8% of these lesions are large
enough to present as carotid space mass;
may have X and/or XII neuropathy
!" Malignant in 10%-15% of cases
Vagal schwannoma displaces the ICA anteriorly
(arrows). The lesion is very homogeneous and exhibits
-,)0,G):,%(4/
.
Figure 22 A, B, C & D Figure 23 A to G
Vagal schwannoma displaces the ICA anteromedially Carotid body tumor.

(arrows). Note splaying of the internal and external carotid
arteries (arrows) and the marked vascularity on
the postcontrast images. MR angiogram also shows
characteristic vessel splaying as well as the marked
hypervascularity.

Jugular and Vagal Paragangliomas [Figure 24]
Figure 24 A to E
Vagal and jugular paragangliomas.
References
1. @%&$/(7G1(')(3&T(M&)+3#",/0(3/0(<V($.3-$/-("6(8%+".3)"#$#(2"&&$(H#)'+/".3#)"$0(),."+("6($/63/2AJT(`'0$3)+(
Radiol 1998;28(4):230-3.
2. @*,a3(@1(')(3&T(<30'&,/-(0$#'3#'N(7$#)+$%,)$"/("6(2'+5$23&(63)(3/0(!+'"!'+3)$5'(8/0$/-#(3)(#"/"-+3!*A(<V(
and CT. AJNR Am J Neuroradiol 1998;19(4):707-10.
3. Alkadhi H, et al. Evaluation of topography and vascularization of cervical paragangliomas by magnetic
resonance imaging and color duplex sonography. Neuroradiology 2002;44(1):83-90.
4. 9",##"/(_1(')(3&T(7$##'2)$"/#("6()*'($/)'+/3&(23+")$0(3+)'+AN(B*+''W0$.'/#$"/3&()$.'W"6W4$-*)(<V(
angiography and MR imaging features. AJR Am J Roentgenol 1999;173(1):139-43.
5. U&0'5$D(F`1(')(3&T(K.3-$/-(8/0$/-#($/(#2*I3//".3#("6()*'(a,-,&3+(6"+3.'/T(@XEV(@.(X(E',+"+30$"&(
2000;21(6):1139-44.
6. Gilbert MR, et al. Meningioma of the jugular foramen: Glomus jugulare mimic and surgical challenge.
Laryngoscope 2004;114(1):25-32.
7. Gilmer-Hill HS, et al. Neurogenic tumors of the cervical vagus nerve: Report of four cases and review of
the literature. Neurosurgery 2000;46(6):1498-503.
8. Harnsberger, et al. Diagnostic Imaging: Head and Neck. Amirsys Publishers, 2005.
9. Heis HA, et al. Carotid body tumors. Int Surg 2003;88(4):226-30.
10. Koeller KK, et al. Congenital cystic masses of the neck: Radiologic-pathologic correlation. RadioGraphics
1999;19(1):121-46.
11. Mafee MF, et al. Glomus faciale, glomus jugulare, glomus tympanicum, glomus vagale, carotid body
tumors, and simulating lesions: Role of MR Imaging. Radiol Clin North Am. 2000;38(5):1059-76.
12. Macdonald AJ, et al. Primary jugular foramen meningiomas: Imaging appearance and differentiating
features. AJR Am J Roentgenol 2004;182(2):373-7.
13. Nadgir RN, et al. Simultaneous bilateral internal carotid and vertebral artery dissection following
chiropractic manipulation: Case report and review of the literature. Neuroradiology 2003;45(5):311-4.
14. Rao AB, et al. From the archives of the AFIP. Paragangliomas of the head and neck: Radiologic-pathologic
correlation. Armed Forces Institute of Pathology. RadioGraphics 1999;19(6):1605-32.
15. Sharma S, et al. Fibromatosis colli in infants: A cytologic study of eight cases. Acta Cytol
2003;47(3):359-62.
16. G/$)f'+(U;1(')(3&T(<3-/')$2(+'#"/3/2'($.3-$/-(3!!'3+3/2'("6(8%+".3)"#$#(2"&&$T(<3-/(V'#"/(K.3-$/-(
1997;15(7):869-71.

1378
K*'-,.-+"3+)?1+S90%'?!",5+R1/H+KK7+
Masticator and Parotid Spaces
Masticator Space – Contents [Figure 1] Masticator S0'/17+Pathology [Figure 3]

!" Muscles of mastication !" Pseudotumors
!"Lateral and medial pterygoid muscles !"Denervation atrophy patterns
!"Masseter muscle !"“Benign” masseteric hypertrophy
!"Temporalis muscle !"Accessory parotid tissue
!" Inferior alveolar nerve (branch of V3) !" Congenital lesions
!" Inferior alveolar artery and vein !"Hemangiomas, lymphatic
!" Ramus and posterior body of the mandible malformations
!" Vascular
!"Aneurysm
!" K/43..3)"+Ad$/6'2)$"/
!"Odontogenic abscess with or without
osteo is most common
!" Benign neoplasms
!"Neurogenic tumors
!"Lipomas
!"@--+'##$5'(8%+".3)"#$#(H0'#."$0J
!"Hemangiopericytomas
!" Malignant neoplasms
!"Malignant schwannomas
!"Non-Hodgkin lymphoma
!"Chondrosarcoma
!"Osteosarcoma
!"SCCa spread from contiguous spaces
!"Osseous mets to mandible
Normal anatomy of the masticator space. Axial
images best demonstrate muscles within this space.
The coronal and parasagittal images demonstrate
the mandibular division of the trigeminal nerve (V3) Figure 3
(arrows) and are best to assess for perineural tumor.
Masticator
space
Masticator S0'/17+Normal Anatomy pathology.
Coronal Plane [Figure 2]
Figure 2
5?')416'+&$%"#)
layer of the
deep cervical
fascia attaches
to the skull
base MEDIAL Chronic V3 Denervation Atrophy
to the foramen (Meningioma) [Figure 4]
ovale putting
the foramen
within the
masticator
space fascial
compartment.
The cortical
margins of the foramen ovale are arrowed. V3 is well-
visualized traversing the foramen.
(Harnsberger, et al. Diagnostic Imaging: Head and
Neck)
Suprahyoid Neck: Masticator and Parotid Spaces 1379 Neuroradiology

Masseter Hemangioma [Figure 6]
Masseter hemangioma (arrows). Isointense on T1-WI,

hyperintense on T2-WI, and exhibits enhancement.
Figure 4 A to E
Chronic right Masticator Space Infections [Figure 7]

V3 denervation
atrophy. There is !" Most common cause is seeding
volume loss and from infected tooth following dental
complete fatty manipulation
replacement of the !" In patients s/p zygomatic arch wiring for
muscles innervated treatment of facial fractures, evaluate the
by V3, including
those innervated suprazygomatic MS
by the mylohyoid !" Check bone windows for mandibular
branch (mylohyoid osteomyelitis
and anterior digastric muscles). The responsible !" Check all spaces for pus pockets
meningioma is indicated by the arrow.
(Long Parotid Tails and) Accessory

Parotid Tissue [Figure 5]
!" Encountered in approximately 20% of the
population
!" May be unilateral or bilateral
!" Has separate ductal system draining into
Stensen’s duct
!" Neoplastic involvement is uncommon, but
when it does occur, 50% of lesions are
malignant (as oppossed to main parotid
gland in which majority of tumors are
benign)
Figure 7 A, B & C
Masticator space infection. Note multiple abscesses

(arrows).
Benign Neoplasms
!" Neurogenic tumors
!" Lipomas
Figure 5 A & B
!" @--+'##$5'(8%+".3)"#$#(H'L)+33%0".$/3&(
desmoid)
Long right parotid tail. The right parotid tail is covering !" Hemangiopericytomas
the entirety of the masseter muscle (arrows). Patient
complained of a right cheek mass.

V3 Schwannoma [Figures 8]
Mandibular nerve (V3) schwannoma in the masticator
space (dots). Note enlargement of the foramen ovale
and the inferior alveolar canal.
Non-Hodgkin lymphoma.
There is loss of the fat planes within the masticator
Malignant Neoplasms 46"$'@)%-$#1(%-8)'-#"+8'.'-3)"-()%-&#3+"3%,-),<)3?')
!" Malignant schwannoma temporalis muscle in the suprazygomatic masticator
!" Non-Hodgkin lymphoma space (arrow). The right pterygopalatine fossa
!" Chondrosarcoma is enlarged indicating V2 perineural extension.
!" Osteosarcoma Involvement of the extraconal orbit and extraaxial
middle cranial fossa are evident. Involvement of the
!" SCCa spread from contiguous spaces lateral pterygoid and temporalis muscles are evident
!" Metastases (usually mandibular) (arrows) and extension along V2 and V3 is noted
(open arrows).
Non-Hodgkin Lymphoma [Figures 9 & 10]
Mandibular Osteosarcoma [Figures 11 & 12]
Figure 9 A,
B&C
Non-Hodgkin Figure 11 A, B & C

lymphoma.
There is loss
of the fat Osteosarcoma.
planes within )=,3')%-&#3+"3%,-)
the masticator of the mandibular
space, including marrow, best
enlargement appreciated on the
"-()%-&#3+"3%,-) T1-WI (arrow).
of the
temporalis muscle in the suprazygomatic masticator
space (arrow). The right pterygopalatine fossa
is enlarged indicating V2 perineural extension.
Involvement of the extraconal orbit and extraaxial
middle cranial fossa are evident. Involvement of the
lateral pterygoid and temporalis muscles are evident
(arrows) and extension along V2 and V3 is noted
(open arrows).

The Stylomandibular Tunnel [Figure 14]
Figure 14
Deep lobe
parotid space
pathology
may push
through
and enlarge
the stylo-
Figure 12 A to E mandibular
tunnel and
Osteosarcoma. compress
=,3')%-&#3+"3%,-) the PPS
of the mandibular fat from a
marrow, best posterolateral
appreciated on the direction.
T1-WI (arrow).
Parotid S0'/17+Anatomy [Figure 15]
Figure 15
Normal
anatomy.
Dots=parotid
glands.
Parotid
ducts (black
arrows)
traverse the
buccal space
fat and
pierce the
buccinator
V3 Perineural Tumor Spread [Figures 13] muscles (white arrows) to enter the vestibule of the
oral cavity opposite the second maxillary molar.
Figure 13
V3 Perineural
Tumor
Parotid S0'/17+Pathology
extension. !" Pseudomass
!"Long parotid tails, accessory parotid
glands, parotid agenesis
!" Congenital
!"First branchial cleft cyst,
hemangiomas, lymphatic
malformations
!" K/43..3)"+Ad$/6'2)$"/
Parotid Space Contents !"Abscess or cellulitis, benign
!" Parotid gland and duct (Stenson’s duct) lymphoepithelial lesions, reactive
coursing through buccal space adenopathy, sialoliths, sialectasis
!" Facial nerve (VII): creates a surgical (including autoimmune)
!&3/'()*3)(0$5$0'#(!3+")$0($/)"(#,!'+82$3&( !" Benign neoplasm
3/0(0''!(&"%'#Y(/")(,#,3&&A($0'/)$83%&'( !"Pleomorphic adenoma, Warthin’s
on either CT or MR; courses immediately tumor, oncocytoma, lipoma, VII
lateral to retromandibular vein neurogenic tumor
!" Retromandibular vein (lateral to ECA) !" Malignant neoplasm
!" External carotid artery !"Mucoepidermoid CA, adenoid cystic
!" Intraparotid lymph nodes: 20-30 nodes; CA, NHL, acinic cell CA, malignant
8+#)("+0'+(0+3$/3-'(6"+(30a(#23&!1(U@C1( myxoid tumor, metastases (SCCa,
and deep face melanoma, NHL)

Parotid Gland Agenesis with Accessory Parotid Hemangioma [Figures 18]
Parotid Gland [Figures 16]
Figure 16
Right
parotid
gland
agenesis
with
accessory
parotid
gland.
First Branchial Cleft Cysts [Figure 17]

!" Account for 8% of BCCs
!" Typical history: middle-aged woman with Figure 18 A, B, C & D
history of multiple parotid abscesses Hemangioma (arrows) replaces much of the left
unresponsive to drainage and antibiotics parotid gland, isointense on T1-WI, hyperintense on
!" If there is an external sinus, it is typically T2-WI, and exhibiting marked enhancement.
found in the skin at angle of mandible
!" b$&&($.3-'(3#(2A#)(#,!'+82$3&()"1(I$)*$/1(
or deep to parotid gland. Wall thickness
53+$'#(I$)*(0'-+''("6($/43..3)$"/T Parotid Lymphatic Malformation
!" 9")*(CB(3/0(<V(23/(0'8/'(2A#)$2(/3),+'( [Figure 19]
of lesion but easiest to appreciate on
T2-W MR
Figure 19
A, B, C & D
Multiseptated
parotid
Figure 17 lymphatic
A, B & C malformation.
First branchial
cleft cyst
(arrows).
Other cystic
lesions
cannot be
differentiated.

S,'&"(,(7+++++++++[Figure 20] Sjogren Syndrome [Figure 22]
!" (Usually) diffuse bilateral parotid swelling; !" Clinical triad:
/"/W/'"!&3#)$21(/"/$/43..3)"+A1( !"Enlarged salivary glands with
nontender parotid enlargement xerostomia
!" Usually insidious onset, associated with !"Enlarged lacrimal glands with
variety of endocrine diseases, nutritional keratoconjunctivitis sicca
states, or certain medications !"Connective tissue disease (RA most
common)
!" Increased risk of developing a lymphoma,
often aggressive biologically
!" Sialography: punctate, globular, cavitary,
and destructive lesions can all be seen
Figure 20
!" CT/MR: enlarged glands with honeycomb
appearance. Some cysts may be quite
Sialosis in large and indistinguishable from LEL of
a diabetic
women. AIDS by imaging alone.
Benign Lymphoepithelial Lesions

[Figure 21]
!" Old term of benign lymphoepithelial cysts
replaced as both solid and cystic lesions
occur
!" Typical history: bilateral parotid swelling
associated with cervical adenopathy,
usually in a patient seropositive for HIV
virus (parotid lesions may occur prior to
seroconversion and may be the initial
presentation)
!" Imaging features: bilateral parotid
enlargement associated with intragladular Figure 22 A, B, C & D
cystic and solid lesions. May see Sjogren syndrome. The noncontrast CT scan
associated cervical adenopathy. demonstrates cystic enlargement of the parotid glands
G%3?)46'$M4),<)$"#$%&$"3%,-)%('-3%&'(@)4188'43%:'),<)
an infectious process. The MR images reveal multiple,
:"+%,1424%a'()$>434)%-)3?')416'+&$%"#)"-()(''6)#,*'4),<)
both glands.
Parotid Sialocele [Figure 23]
Lymphoepithelial lesions.
There are multiple cystic and solid lesions in the
parotid glands bilaterally in this 27-year-old HIV-
positive hemophiliac patient.
Figure 23
Parotid sialocele.
Note the large sialocele and enlargement of Stensen’s
duct, all the way back to the parotid gland (arrows).

Pleomorphic Adenoma [Figures 24 & 25] Deep Lobe Pleomorphic Adenoma
!" Most common benign parotid tumor [Figure 26]
(80%). If left untreated, estimated 25%
will undergo malignant degeneration.
!" Path: mixture of epithelial and
myoepithelial cells
!" Typical patient: > 50 years of age with
slow-growing lump in the cheek
!" Sharply marginated; round, oval, or
lobulated
!" CT: variable enhancement, infrequent
0A#)+"!*$2(23&2$823)$"/1(3/0($/)'+/3&( Figure 26 A, B & C
pockets of low density when large due to
“mucoid matrix” Large deep lobe
!" MR: very hyperintense on T2-WI. pleomorphic
adenoma. Lesion
May have internal pockets of greater herniates through
hyperintensity if “mucoid matrix.” and widens the right
stylomandibular
tunnel (arrows).
The size of the left
tunnel is indicated
by the straight line.
Warthin Tumor (Papillary [Figure 27]

Cystadenoma Lymphomatosum)
!" Second most common benign tumor of
the parotid space
!" 80% men, older than 50 years
!" Usually slow-growing mass in region of
parotid tail
!" Arise from ectopic salivary gland rests
within intraparotid lymph nodes
!" Limited to parotid gland only
!" Bilateral in 10%-15% of patients
!" Imaging: well-circumscribed, usually 3-4
cm
Figure 24 A to E !"Complex mixture of solid and cystic
components
!#"44%$)416'+&$%"#) !"Appears more complex than typical PA
lobe pleomorphic
adenoma.
Figure 27 A,
B&C
Bilateral
warthin
tumors.
Seeding of the buccal space with multiple pleomorphic

adenomas after “spilling” at surgery.

Lipoma [Figure 28] Malignant Tumors
!" The smaller the salivary gland, the higher
the chance a mass is malignant
!" Sublingual mass: 70% malignancy
!" Submandibular mass: 60% malignancy
!" Parotid mass: 20% malignancy
!" Mucoepidermoid carcinoma: more than
80% occur in parotid glands; most
common malignant salivary gland tumor
in most series
!" Adenoid cystic carcinoma: 2%-6% of
parotid tumors
!" Acinic cell carcinoma: 10%-30% of
Figure 28
A, B & C parotid tumors
!" Adenocarcinoma: rare in major salivary
glands
Lipoma.
Note fat signal Mucoepidermoid Carcinoma [Figure 30]
suppression !" Most common malignant lesion in parotid
on the post-
contrast, fat- gland
suppressed !" Most common between 35 and 60 years
image. of age but may be found at any age; most
common malignant tumor in people under
20 years old
!" Slight predilection for women
!" Clinical: rock hard mass with associated
pain and itching over the course of the
Facial Nerve Schwanoma [Figure 29] facial nerve
!" Imaging features depend on grade:
!"Low grade: benign appearance;
cannot distinguish from pleomorphic
adenoma
!"k$-*'+(-+30'N($/8&)+3)$/-1($/0$#)$/2)(
margins; look for PNT along VII
!"Low to intermediate signal on T1- and
T2-WI
Figure 30
A, B & C
Figure 29 A to D Mucoepider-
moid
Facial nerve carcinoma
schwanoma (low-grade,
involving 416'+&$%"#)
parotid and parotid
mastoid lobe).
segments. Note
the mastoid The lesion is
segment somewhat
enlargement complex
is easily and exhibits
appreciated indistinct
on the coronal margins
image (arrows). laterally
(arrows)
leading away
from the
diagnosis
of a benign
neoplasm.

VII Perineural Tumor [Figure 32]
Figure 30
D&E
Mucoepider-
moid
carcinoma
(low-grade,
416'+&$%"#)
parotid
lobe).
Figure 32 A, B & C
The lesion is
somewhat VII perineural tumor.
complex This patient has
and exhibits recurrent adenoid
indistinct cystic carcinoma of the
margins parotid gland. Note
laterally perineural extension
(arrows) of the tumor along
leading the facial nerve
away from the diagnosis of a benign neoplasm. (VII), up through the
stylomastoid foramen (arrow on coronal), extending to
the geniculate ganglion (arrow on axial).
Parotid Node Metastases [Figure 31]
Parotid metastases.
Left Images: Met from forehead SCCa.
Right Images: Met from medial canthus SCCa.

References
1. Curtin HD. Detection of perineural spread: Fat suppression versus no fat suppression. AJNR Am J
Neuroradiol 2004;25(1):1-3.
2. Go JL, et al. The trigeminal nerve. Semin Ultrasound CT MR 2001;22(6):502-20.
4. Holliday RA, et al. Benign lymphoepithelial parotid cysts and hyperplastic cervical adenopathy in AIDS risk
patients: A new CT appearance. Radiology 1998;168:439-41.
5. Izumi M, et al. MR imaging of the parotid gland in Sjogren’s syndrome: A proposal for new diagnostic
criteria. Am J Roentgenol 1996;166:1483-7.
6. Palacios E, et al. Benign asymmetric hypertrophy of the masticator muscles. Ear Nose Throat J
2000;79(12):915.
7. Russo CP, et al. MR appearance of trigeminal and hypoglossal motor denervation. AJNR Am J Neuroradiol
1997;18(7):1375-83.
8. Shah GV. MR imaging of salivary glands. Magn Reson Imaging Clin N Am 2002;19(4):631-62.
9. Triglia JM, et al. First branchial cleft anomalies: A study of 39 cases and a review of the literature. Arch
Otolaryngol Head Neck Surg 1998;124(3):291-5.
10. Williams LS, et al. MR imaging of the trigeminal ganglion, nerve, and the perineural vascular plexus:
Normal appearance and variants with correlation to cadaver specimens. AJNR Am J Neuroradiol
2003;24(7):1317-23.
11. Yonetsu K, et al. Deep facial infections of odontogenic origin: CT assessment of pathways of space
involvement. Am J Neuroradiol 1998;19:123-8.

K*'-,.-+"3+)?1+S90%'?!",5+R1/H+KKK7+
Pharyngeal Mucosal Space and Oral Cavity
Pharyngeal Mucosal Space Pharyngeal Mucosal S0'/17+Contents

!" Extends from skull base to hyoid bone and !" Mucosa
includes the nasopharynx, oropharynx, !" Waldeyer’s ring of lymphatic tissue
and hypopharynx !" Minor salivary glands (especially in soft
!" The mucosa lining the upper aerodigestive palate)
tract !" Superior and middle pharyngeal
constrictor muscles
Nasopharynx [Figure 1] !" Cartilaginous (distal) end of eustachian
tube (torus tubarius) (nasopharynx)
!" Levator palatini muscle (nasopharynx)
Pharyngeal Mucosal S0'/17+Pathology

!" Pseudomass
!"Lymphoid hyperplasia
!" Congenital
!"Tornwaldt cyst
Figure 1
!" K/6'2)$"/d$/43..3)"+A
!"`"#)$/43..3)"+A(2A#)#(H+')'/)$"/(
Limits of
the naso- cysts); cellulitis/abscess
pharynx. !" Benign neoplasms
!"Pleomorphic adenoma
!"NPCa, non-Hodgkin lymphoma,
minor salivary gland neoplasms
(mucoepidermoid CA, adenoid cystic
CA, etc)
Nasopharyngeal Carcinoma (NPCa)

[Figures 3 & 4]
Naso-PMS Anatomy [Figure 2] !" Centered in lateral pharyngeal recess
!" Invasion of levator palatini results in
eustachian tube dysfunction and serous
Figure 2 A, B otitis media with CHL (check mastoids)
&C !" Perivascular spread (via foramen lacerum)
and perineural extension (mainly V3) are
Normal common so skull base must be carefully
anatomy of the assessed
nasopharynx. A. !" Nodal metastases present in 90% at
Arrows indicate
presentation (retropharyngeal, level II,
cartilaginous
ends of 3/0(&'5'&(_W8+#)J
eustachian !" Distant metastases uncommon at
tubes. B. Short presentation (< 10%) (bone, lung, and
arrows indicate liver)
medial pterygoid muscles and long arrows indicate
PPS fat. C. Long arrows indicate PPS fat and short
!" Strong relationship with Epstein-Barr
arrows indicate air in lateral pharyngeal recesses. virus (EBV)
Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity 1389 Neuroradiology
Nasopharyngeal Carcinoma [Figure 4]
Figure 4 A to E
Nasopharyngeal
carcinoma. A 48-year-
old man with bilateral
7i2i77)('&$%34/)b"+8')
tumor replaces the
Figure 3 A to E entire basiocciput
(distal clivus), occipital
Nasopharyngeal condyles, jugular
Carcinoma. tubercles, and portions
A 19-year-old of the C1 lateral
man presenting masses (best seen on
with conductive the coronal images).
hearing loss. Note Coronal images also
,6"$%&$"3%,-),<) demonstrate extensive
left mastoid air bilateral adenopathy.
cells secondary to
eustachian tube
obstruction.
I Found the Tumor... Now Where are

the Nodes?
PMS Non-Hodgkin Lymphoma (NHL)

[Figure 5]
!" Tends to remain localized and grow slowly
!" NHL in H&N from nasopharyngeal
lymphoid tissue in 35% of cases (versus
palatine tonsil lymphoma in 50% and
lingual tonsil lymphoma in 15%)
!" 50% have associated adenopathy at
presentation
!" 20% may have GI tract NHL involvement
!" AIDS and Sjogren syndrome predispose Figure 5 A, B, C & D
!" Usually > 50 years; M:F = 1.5:1 Non-Hodgkin lymphoma.
!" 9,&DA(.3##(8&&$/-(/3#"!*3+A/L 5?%4)?,.,8'-',14@)*1#M>)."44)&##4)3?')-"4,6?"+>-U)
!" T1-WI isointense, T2-WI hyperintense, *13)'U?%*%34)-,)%-&#3+"3%,-),<)"(V"$'-3)46"$'4)"-()
enhance -,)4M1##)*"4')%-:,#:'.'-3/)=,3')+%8?3)."43,%()01%()
indicating eustachian tube dysfunction.
Oropharynx [Figure 6] Oro-PMS Pathology
!" Congenital
!"Thyroglossal duct cyst; lingual thyroid
!" K/6'2)$"/d$/43..3)"+A
!"`"#)$/43..3)"+A(2A#)#(H+')'/)$"/(
cysts); cellulitis/abscess (tonsillar)
!" Benign neoplasms
!"Pleomorphic adenoma
Figure 6 !"SCCa (base of tongue and faucial
pillars); non-Hodgkin lymphoma;
Limits of the minor salivary gland malignancies
oropharynx.
(especially soft palate)
!" Pseudomass
!"Lymphoid hyperplasia (lingual tonsil)
Thyroglossal Duct Cysts [Figure 8]

!" Most common nonodontogenic
extracranial head and neck cyst
!" 20% are suprahyoid in location
!" Well-circumscribed
!" 2-4 cm
!" Occasionally septated
Oral-PMS Anatomy [Figure 7] !" Capsular enhancement
!" Smooth margins
!" DDx: submental node
Figure 8 A & B
Foramen cecum thyroglossal duct cyst (arrows).
Lingual Thyroid Gland [Figure 9]

!" Failure of thyroid descent from foramen
cecum
Figure 7 A, B, C & D !" Accounts for 90% of ectopic thyroid
Oropharyngeal mucosal space anatomy. !" High female predominance (7:1)
A. Arrows indicate tonsillar pillars. B. Long arrows !" Only functioning thyroid tissue in 70%-
indicate tonsillar pillars and short arrows indicate fat 80%
in PPS. C. Long arrows indicate tonsillar pillars and !" CT: hyperdense with avid enhancement
short arrow indicates soft palate. D. Arrows indicate !" MR: iso- to hyperintense to muscle
regions of glossotonsillar sulci.
on both T1- and T2-WI with strong
enhancement
!" ;""D($/(&"I'+(/'2D()"(2"/8+.(&32D("6(
gland in normal location
!" Subject to typical “thyroid pathology”
Tonsillar SCCa [Figure 11]
Lingual thyroid gland.
Note absence of thyroid tissue in its normal location
in the lower neck. Figure 11 A, B & C
Tonsillar SCCa (T3N2cM0).

Note extension along glossotonsillar sulcus into left
Tonsillar Abscess [Figure 10] soft palate and bilateral nodes.
Base of Tongue SCCa [Figure 12]

!" Is there extension across the midline?
!" Is there extension to the oral tongue?
!" K#()*'+'('L)'/#$"/()"(4""+("6(.",)*d
sublingual space?
!" Is there extension along glossotonsillar
sulcus to reach the anterior tonsillar
Figure 10 A & B pillar?
Bilateral tonsillar abscesses. !" Is there inferior extension to reach the
vallecula and preepiglottic space?
Tonsillar S44'7+What the Surgeon Needs !" What is the status of regional nodes?
to Know
!" Is there extension superiorly along the
anterior and/or posterior tonsillar pillars
to involve the soft palate?
!" Is there direct extension to involve the
lateral and/or posterior pharyngeal wall?
!" Is there antero-inferior extension along
the glossotonsillar sulcus to reach the
tongue base?
!" Is there postero-inferior extension to
involve the hypopharynx
!" Is there extension to involve the PPS or
MS? Any PNTS?
Figure 12
!" What is the status of regional lymph A, B & C
nodes?
Base of tongue
SCCa.
Figure 14 A & B
Normal anatomy of the oral cavity.
The Mylohyoid Muscle [Figure 15]

!" Subdivides the lower oral cavity into two
major spaces:
!"Sublingual space (intraoral approach)
!"Submandibular space (external
approach)
Figure 12 D to I
Base of tongue SCCa. Note extension along

glossotonsillar sulcus to tonsil and soft palate.
Oral Cavity [Figures 13 & 14]
Figure 15
The mylohoid muscle (arrows) separates the
sublingual (above and medial) from the submandibular
(below and lateral) spaces.
Oral Cavity Pathology

!" Congenital lesions
!"Hemangiomas/vascular
malformations; dermoids/epidermoids
!" K/43..3)"+A(&'#$"/#
!"Cellulitis/abscesses; sialoliths; ranulas
Figure 13 !" Benign neoplasms
Extent of the oral cavity. !"Pleomorphic adenomas; aggressive
The oral cavity is separated from the oropharynx by 8%+".3)"#$#
the circumvallate papillae, the soft palate complex, !" Malignant neoplasms
and the anterior tonsillar pillars. !"GCC3(H4""+("6(.",)*1("+3&()"/-,'1(
etc); minor salivary gland neoplasms
(SMG, SLG)
SMS Lymphatic Malformation [Figure 16]
Figure 18 A & B
Tongue abscess.
Wharton’s Duct Sialoliths [Figure 19]
Submandibular space lymphatic malformation.
Dermoid Cysts [Figure 17]

!" Refers to dermoid, epidermoid, and
teratoid lesions
!" Most uncommon of the congenital lesions
!" Sublingual and submandibular locations
!" Low density/intensity, unilocular,
!" Well-circumscribed Figure 19 A, B & C
!" Cyst wall enhances with contrast
!" Individual fat globules = dermoid
!" In absence of fat, cannot DDx epidermoid Large
from dermoid submandibular
duct stone.
Ranulas [Figure 20]

!" Mucoceles/mucous retention cysts of the
4""+("6()*'(.",)*
!" Secondary to trauma or obstruction of
sublingual gland/ducts
!" Thin-walled, unilocular, nonenhancing
!" Two varieties:
!"Simple ranula-in SLS (true)
!"Plunging ranula-in SMS (pseudocyst)
Dermoid cysts in two patients.

Note classic “bag of marbles” appearance.
Tongue Abscess [Figure 18]

Figure 20 A & B
Plunging ranulas in three different patients.
Figure 22
Figure 20 C & D
Plunging ranulas in three different patients.
Pleomorphic Adenomas [Figure 21]

!" Most common benign glandular tumor
majority in parotid gland
!" 8% in submandibular gland; 0.5% in
sublingual gland
!" Well-demarcated; homogeneous when
small
!" Heterogeneous (cystic changes necrosis,
hemorrhage)
!" Hypoisointense on T1-WI
!" Hyperintense on T2-WI Figure 23
A, B & C
!" Homo-/heterogeneous enhancement
Exostoses.
Arrows indicate
torus palatinus,
bilateral
mandibular tori
interna, and
bilateral maxillary
tori externa.
Floor of Mouth SCCa

!" What is the degree of submucosal
extension?
!"Is there evidence for involvement of
the ipsilateral and/or contralateral
Figure 21 A, B, C & D neurovascular bundles?
Sublingual gland pleomorphic adenoma. !"Is there evidence of extension into the
oral tongue or base of the tongue?
!"Is there evidence of submandibular
gland duct obstruction?
Exostosis [Figures 22 & 23]
!"Is there evidence of upper neck
!" Dense cortical bone with or without
involvement?
cancellous bone
!" What is the status of regional lymph
!" Incidental unless they preclude proper
nodes (I and II)?
0'/),+'(8))$/-
!" Is there evidence of mandibular invasion?
!" Occasionally very large and interfere with
swallowing
!" Torus palatinus
!" Torus mandibularis
!"Interna/externa
!" Torus maxillaris
!"Interna/externa
I Found the Tumor...Now Where are the Oral Tongue SCCa [Figure 25]
Nodes? !" Critical to follow same type of assessment
6"+()*'#'(),."+#(3#(6"+(!+$.3+A(4""+("6(
mouth lesions (FOM, mandible? nodes?
SMD? BOT? GT sulcus extension)
!" Most important for these tumors is the
relationship to midline + NVB
!" G$-/$823/)(2"/)+3&3)'+3&($/53#$"/(.3A(
indicate total glossectomy or nonsurgical
organ preservation therapy
!" Level I, II, and III nodes
Floor of Mouth SCCa [Figure 24]
Oral tongue SCCa (arrows).
Note invasion of the ipsilateral mylohyoid muscle
(dots). An ipsilateral malignant 2A node is indicated
by the single arrow.
Figure 24 A to E
Floor of mouth SCCa (T2N1M0).
Tumor has extended to sublingual space/
neurovascular pedicle as evidenced by submandibular
duct obstruction. Note 1B necrotic node.
References
2. King AD, et al. In vivo proton MR spectroscopy of primary and nodal nasopharyngeal carcinoma. AJNR AM
J Neuroradiol. 2004;25(3):484-90.
3. Mukherji SK, et al. Squamous cell carcinoma of the oropharynx and oral cavity: How imaging makes a
difference. Semin Ultrasound CT MR. 1998;19:463-75.
4. Roh JL, et al. Nasopharyngeal carcinoma with skull base invasion: A necessity of staging subdivision. Am
J Otolaryngol 2004;25(1):26-32.
5. G$-3&(V1(')(3&T(CB(3/0(<V($.3-$/-("6(#l,3.",#(2'&&(23+2$/".3("6()*'()"/-,'(3/0(4""+("6()*'(.",)*T(
6. Smoker WRK. The Oral Cavity in Head and Neck Imaging (4th ed) Som and Curtin, eds. Mosby Year Book
Publishers. 2002 pp 1377-464.
7. Weber AL, et al. Malignant tumors of the oral cavity and oropharynx: Clinical, pathologic, and radiologic
evaluation. Neuroimaging Clin N Am 2003;13(3):443-64.
S0,.1+K7+R1"0&'(*(
First Things First - Localize the Lesion [Figure 1]
Figure 1 A, B & C
Localize the lesion. Localizing a spinal lesion to the appropriate “compartment” [intramedullary (left image),
extramedullary-intradural (center image), or extradural (right image)] allows a tailored differential diagnosis.
Common Intramedullary Lesions

!" Non-neoplastic:
!"Acute trauma (contusion, edema…)
!"Syringohydromyelia
#" Syrinx-cavity in cord NOT lined by
ependyma
#" Hydromyelia-dilatation of the
central canal lined by ependyma
!"Demyelinating disease (MS, ADEM…)
!" Neoplastic
!"Ependymoma
!"Astrocytoma
T?1%1+,(+."+(01/,#/+,*'-,.-+0'))1%.+)?')+
reliably permits differentiation between
ependymomas and astrocytomas.
Ependymomas [Figure 2]
!" Most common intramedullary tumor in
adults 60% Figure 2 A, B & C
!" Mean age 43 years; women predominate Ependymoma.
(slightly) Note lesion isointensity on T1-WIs, heterogeneous
!" Arise from ependymal cells lining central hyperintensity on the T2-WIs, and relatively
canal homogeneous enhancement on the post-Gd images
(dots). Associated syringohydromyelia is indicated by
!" Slow-growing; canal expansion is typical
the arrows.
!" 56% cervical; 28% thoracic; 16% lumbar
!" 75% are isointense on T1-WI; 100%
hyperintense on T2-WI
!" Cystic degeneration and hemorrhage are
common
!" Hemosiderin deposition – common at
periphery
!" Heterogeneous enhancement in 65%
Spine I: Neoplasms 1397 Neuroradiology

Figure 2 D, E & F
Ependymoma.
Note lesion
isointensity on T1-
WIs, heterogeneous
hyperintensity
on the T2-WIs,
and relatively
homogeneous
enhancement on
the post-Gd
images (dots).
Associated syringo-
hydromyelia is
indicated by the
arrows. Pilocytic
astrocytoma. Lesion
demonstrates
isointensity on T1-
WI, hyperintensity
on T2-WI,
and manifests
enhancement on
post-Gd images.
Cyst formation
is present both
cephalad and
caudal to the
tumor.
Astrocytomas [Figure 3]
!" Second most common IM tumor overall;
most common tumor in children Rare
!" Cervical = thoracic; M=F; mean age 21 !" Non-neoplastic lesions
years !"Vascular lesions (cavernomas, AVM,
!" BA!$23&&A(!$&"2A)$2(3/0(0$66,#'(8%+$&&3+A( etc)
types !"Infections (sarcoid, TB, lyme disease,
!" May extend to involve the entire cord etc)
!" Cyst formation is common; Syrinx - above !" Neoplastic lesions
or below !"Metastases
!" T1: Iso- to hypointense; T2: hyperintense !"Lipoma
!" Enhancement !"Subependymoma
!" Hemorrhage is less common than in !"Oligodendroglioma
ependymomas !"Ganglioma
!" Virtually 100% enhance !"Paraganglioma
Uncommon Hemangioblastoma [Figure 4]

!" Non-neoplastic lesions !" Uncommon; 1%-5% of cord tumors
!"Acute cord ischemia/stroke !" Peak age between 30 and 40 years
!"Myelitis (post viral ADEM, etc) !" 1/3 associated with VHL syndrome
!" Neoplastic lesions !" 85% intramedullary or combined
!"Hemangioblastoma intramedullary/extramedullary-intradural
!"Astrocytoma (anaplastic and GBMs) !" 50% thoracic; 40% cervical; 80% are
solitary
!" Isointense on T1-WI; hyperintense on T2-
bKY(#)+"/-('/*3/2'.'/)Y(.3A(#''(4"I(
voids, etc
!" On angio, highly vascular mass; dense
prolonged tumor stain, prominent draining
veins

Intramedullary
metastasis in a 56-
year-old woman
with a history of
total mastectomy
8 years ago, now
with new radicular
symptoms. We
were asked to
Figure 4 A to E assess for HNP.
Note subtle
Hemangioblastoma. enlargement of
Classic appearance the spinal cord
of an intramedullary G%3?,13)4%8-%&$"-3)
hemangioblastoma signal change on
with T1 isointensity, the T1-WI, hyperintensity on the T2-WI, and lesion
T2 hyperintensity, and enhancement.
marked enhancement
G%3?)-1.'+,14)0,G)
voids, best seen on the
T2 and post-Gd images
(arrows).
Intramedullary Metastases [Figure 5]

!" Intramedullary metastases are rare
!" 1%-3% of all intramedullary tumors
!" E"(#!'2$82($.3-$/-(2*3+32)'+$#)$2#(
to clearly distinguish from other
intramedullary lesions; breast and lung
most common
!" Also lymphoma, leukemia, and malignant
melanoma
Subpial Lipomas [Figure 6]

!" Originate from fat cells in subpial region
!" Conus region seems most common
!" Congenital malformation with proliferating
fat cells
!" Very rare
!" Excessive weight gain and pregnancy may
aggravate
Non-Neoplastic Intramedullary
Pathology
Figure 6 A to E
Subpial Lipoma. A 21-year-old woman with right
great toe numbness. Note the high signal of fat on the
T1-WIs and fat suppression on the FS postcontrast
images.
Syringohydromyelia [Figure 7] Extramedullary-Intradural Lesions
Common Uncommon
!" Neurogenic neoplasms Lipomas
!"E',+"8%+".3#( (((@+32*/"$0(2A#)#
!"Schwannomas Epidermoids/
aaaaaaaaaaaaaaaa dermoids
!" Meningiomas Drop metastases
!" Myxopapillary AVM
!"Ependymomas Infection
!" Arachnoiditis Paragangliomas
Nerve Sheath Tumors [Figures 9 to 11]

!" Most common extramedullary-intradural
tumors (70%-75%); 15% extradural;
15% dumbbell
!" Schwannomas more common than
/',+"8%+".3#(,/&'##(!3)$'/)(*3#(E:
!" E',+"8%+".3#N(<g:Y(O>W^>(A'3+#Y(/"(
true capsule
Figure 7 A & B
!"Localized, diffuse, or plexiform
Syringohydromyelia in a 2-year-old child with a Chiari !" Schwannomas: M=F; 30-60 years;
I malformation. encapsulated
!"40% cystic changes; 10%
Multiple Sclerosis [Figure 8] hemorrhage; target sign
!" Neural foraminal enlargement; pedicle
thinning
!" Isointense on T1-WI; hyperintense on T2-
WI; enhance
!" <,&)$!&'($/(/',+"8%+".3)"#$#
N19%"#$%"*'+2( Schwannoma [Figure 9]
Figure 8 A to E
Multiple sclerosis.
=,3')"*4'-$'),<)4%8-%&$"-3)
spinal cord expansion. The
MS plaque is not appreciated
on the T1-WI. The lesion
can be seen in the center
of edema on the T2-WIs.
Marked enhancement of this
active lesion is seen on the Figure 9 A & B
postcontrast images.
='1+,&*+,."):4)4$?G"--,."/
='1+,&*+,."4)L3,6)%."8'X)"+')%-&#3+"3%-8)"-()+'j1%+')
resection of the parent nerve while schwannomas
(bottom image) are encapsulated, usually permitting
nerve-sparing surgery.

Dumbbell N19%"#$%"*'++++++++[Figure 10] Meningiomas [Figures 12 & 13]
!" Second most common spinal tumor (25%)
!" 90% intradural; 10% extradural or
dumbbell
!" :(e(<(g(]NZY(!+$.3+$&A(86)*W#$L)*(0'230'#
!" Thoracic (80%) > cervical (16%) >
lumbar (4%)
!" More often anterior in cervical region
!" Below C7, more common posterior to cord
!" Usually single unless NF-2
!" Iso- on T1-WI; iso- or hyperintense on
T2-WI; hypointense if Ca++
!" Marked homogeneous enhancement
Meningioma (C Spine-Ventral) [Figure 12]
Figure 12 A to D
Meningioma-cervical spine (anterior location).

The sagittal images clearly localize this lesion as
extramedullary-intradural by demonstrating a nice
subarachnoid cap (widening of the subarachnoid
space-arrows). The lesion severely compresses the
spinal cord, best appreciated on the axial T2-WI image
(outlined). The lesion is essentially isointense to cord
Figure 10 A to F on T1- and T2-WIs and enhances intensely.
Classic dumbbell -'1+,&*+,."/)=,3')%4,%-3'-4%3>)
,-)5S2^7@)?>6'+%-3'-4%3>),-)5J2^7@)"-()4%8-%&$"-3)
enhancement on the post-Gd images. The dumbbell Meningioma (T Spine-Dorsal) [Figure 13]
nature of this lesion is easily appreciated on the axial
images. The coronal image shows a nice subarachnoid
cap (arrow).
Schwannoma [Figure 11]
Figure 13 A to D
Figure 11 A to D
Meningioma-thoracic spine
Schwannoma at the level of the conus. Sagittal images
(posterior location). Patient
nicely demonstrate the classic subarachnoid cap at
is a 62-year-old woman with
the inferior margin of the lesion with widening of the
lower extremity weakness
subarachnoid space. Note hypointensity on the T1-WI
and bladder incontinence.
and hyperintensity on the T2-WI. The postcontrast
Note lesion isointensity
images demonstrate a nice “target sign.” The lesion
on T1- and T2-WIs and
,$$16%'4).,43),<)3?')46%-"#)$"-"#)"-()4%8-%&$"-3#>)
homogeneous enhancement.
compresses the spinal cord, best seen on the axial
The subarachnoid cap is easily
postcontrast image (arrow).
appreciated.
Myxopapillary Ependymoma [Figure 14]
!" =>?("6(8&,.(),."+#
!" F22,+('L2&,#$5'&A($/(2"/,#(3/0(8&,.(
)'+.$/3&'(6+".('!'/0A.3&(2'&&#($/(8&,.(
!" M:F = 2:1; peak between 30 and 40
years
!" G&"IW-+"I$/-(3/0(.3A(8&&('/)$+'(&,.%3+(
spinal canal
!" Vertebral scalloping; canal enlargement
!" Highly vascular; hemorrhage is common
!" Isointense on T1-WI; hyper on T2-WI;
hypointense margin if hemosiderin
!" Intense enhancement in 100%
Figure 15 A to E
Implantation
epidermoid cyst.
Patient is a 7-year-old
girl with back pain. She
had LP as an infant.
The lesion is slightly
hyperintense on the T1-
WI, very hyperintense on
the T2-WI, and does not
Figure 14 A to E
enhance.
A tract from the prior LP
Myxopapillary %4)-,3)%('-3%&'(/
ependymoma.
A 38-year-old
man with radicular
symptoms. Note T1
isointensity, slight
hyperintensity on the
T2-WI, and intense
enhancement.
Dermoid Cysts [Figure 16]
!" Congenital (100%)
!" Symptomatic before age 20; M=F
!" 80% in lumbosacral or cauda
“Other” Extramedullary-Intradural !" Hypointense areas? Water content from
Neoplastic Lesions sweat gland secretions.
!" Fat hyperintensity on T1-WI
Epidermoid Cysts [Figure 15] !" May cause chemical meningitis if rupture
!" Less than 1% of spinal tumors with cholesterol crystals discharged into
!" Congenital 60%; aquired 40% CSF
!" Strong association with lumbar puncture
in neonatal period (implantation
epidermoid)
!" Isointense or slightly hyperintense on T1- Figure 16
WI; Hyperintense on T2-WI
!" Mild rim enhancement Dermoid cyst.
The complex nature
!" DWI can DDx from arachnoid cysts and of the lesion with
other lesions %('-3%&$"3%,-),<)
hypointense areas (?
water) and fat signal
(high) on this T1-WI
should suggest the
diagnosis
(Courtesy Dr. M.
Modic).

Drop Metastases [Figure 17] Diffuse Mantle Cell Lymphoma
!" CNS primary tumors [Figure 18]
!"Astrocytomas
!"Medulloblastomas
!"Pineal cell tumors
!"Ependymomas
!"Germ cell tumors
!" Non-CNS primary tumors
!"Breast Figure 18
A, B, C & D
!"Lung
!"Lymphoma
Diffuse
!"Melanoma mantle cell
!"Pituitary lymphoma.
Note marrow
signal in the
thoracic spine
is diffusely
abnormal
(darker than
that of the
intervertebral
discs).
5?'+')%4)%-&#3+"3%,-)
of virtually all of
the nerve roots of
the cauda equina
such that they are
not visualized as
separate entities
on the sagittal
image.
Enlargement of
Figure 17 A to E
individual roots is
best appreciated
on the axial
Drop images.
metastases.
Numerous
enhancing
lesions on the
cauda equina
"+')%('-3%&'()
in this 25-year-
old woman
with breast
carcinoma.
Extradural Lesions
!" Common
!"Epidural metastases
!"Herniated discs, etc
!"Degenerative lesions (osteophytes,
ligament infoldin, etc)
!"Lymphoma
!"Infection (discitis, etc)
!" Uncommon
!"Epidural abscess
!"Meningeal cysts
!"Vertebral tumors (benign)
!"Vertebral tumors (malignant)
!"Paget disease
!"Epidural hematoma
!"Epidural lipomatosis
!"Extramedullary hematopoesis
!"Angiolipomas

Extradural Metastases [Figure 19] Primary Vertebral Neoplasms (Benign)
!" Most common extradural malignant tumor !" Hemangioma
in adults !" Aneurysmal bone cyst
!" Spine metastases occur in 15%-40% of !" Osteoblastoma
disseminated cancers !" Osteochondroma
!" Breast, lung, prostate (adults); Ewing !" Eosinophilic granuloma
sarcoma and neuroblastoma (children) !" Giant cell tumor
!" Complications
!"Epidural mass Hemangiomas [Figures 21 & 22]
!"Pathologic fracture !" Common benign hamartomatous lesions
!"Cord compression (10% of adults)
!" Mean age = 50 years (range = 9-77
Diffuse Prostate Metastases [Figure 19] years)
!" Multiple in 25%-30%
!" When discovered incidentally, M = F
!" b*'/(#A.!)".3)$2(H/',+"&"-$2(0'82$)1(
pain, etc) F > M
!" Features of “compressive/aggressive”
hemangiomas:
!"Location between T3 and T9
!"Entire vertebral body involved +/-
extension to neural arch
!"Cortex expansion with indistinct
margins; soft tissue mass
!"Irregular honeycombing (corduroy
appearance)
!" `&3$/(8&.#N(I'&&W0'8/'0(5'+)$23&(#)+$3)$"/#(
or honeycombed appearance
!" CT: stippled, polka dot appearance
(course trabeculae)
Figure 19 A, B & C
!" MR (typical):
!"T1-WI: hyperintense (due to fat)
Diffuse prostate metastases.
!"T2-WI: hyperintense (probably due
T1, T2, and postcontrast images.
to cellular elements within the tumor/
blood)
Diffuse Marrow Replacement [Figure 20] !" Treatment for agg. lesions: sclerotherapy,
!" Marrow should be higher in signal vertebroplasty, surgery, postop radiation
intensity than the intervertebral discs on therapy, etc
T1-WIs
!" Idiopathic
!" Leukemia/lymphoma
!" <A'&"8%+"#$#
!" HIV
Diffuse marrow replacement. A 7-year-old child with Figure 21 A, B, C & D

leukemia (left images). Note that the signal intensity Compressive hemangioma.
of marrow is less than that of the intervertebral discs
on the T1-WI which is the reverse of normal. This may
be idiopathic or seen in conditions such as leukemia,
#>.6?,."@).>'#,&*+,4%4@)`7]@)'3$/)5S2)"-()5J2^74),<)
a normal 7-year-old child are presented on the right
for comparison.

Primary Vertebral Neoplasm (Malignant)
!" Chordomas
!" Plasmacytomas
!" Ewing sarcoma
!" Hodgkin disease
!" Malignant lymphoma
!" Chondrosarcoma
!" Osteogenic sarcoma
Chordomas [Figure 24]

!" Slow-growing, rare, malignant tumors
arising from notochordal remnants
!" Sacrococcygeal 50%; clivus 35%-40%;
Vertebral body 10%-15% [C (20%-50%)
> L > T]
!" G!$/'N(<N:(g(ONZY(!'3D($/(86)*W#$L)*(
decades
!" `&3$/(8&.#dCBN(0'#)+,2)$5'(&'#$"/Y(!+$.3+$&A(
lytic with scattered areas of sclerosis/
(Same patient intratumoral Ca++
continued from !" MR: hypointense on T1-WI
previous page) !"Hyperintense on T2-WI
Compressive !"Enhancement is typical
hemangioma
!" Distant mets: 5%-40% (lung, liver, lymph
with epidural
extension and cord nodes, bone)
compression.
Aneurysmal Bone Cyst [Figure 23]

!" 1%-2% of primary bone tumors
!" 10%-30% in spine/sacrum
!" Arise in neural arch
!" 80% < 20 years of age
!" Nonmalignant hamartomatous lesion;
progressively destructive
!" Most common presenting sx = pain,
especially at night (72%)
!" hU--#*'&&i(2"+)'LY(4,$0W8&&'0(&'5'&#(6+".(
hemorrhage sedimentation
!" Rx: embolization +/- excision
C3 chordoma.
Note characteristic hyperintensity on the T2-WI.
Plasmacytoma [Figure 25]

!" Mean age 55 years; M>F
!" Most common presenting sx = pain
!" Osteolytic expansion/compression; easily
mimics metastases or benign compression
fracture
!" Hypointense on T1-WI
!" Hyperintense on T2-WI
!" Mild-mod diffuse enhancement
Aneurysmal bone cyst. Expansile lesion of pedicle and
adjacent vertebral body seen in 3 planes on CT. T2
MR images show the cystic nature of the tumor which
('.,-43+"3'4)01%(201%()#':'#4/

Figure 25 A to F
N#"4."$>3,."/)=,3')4%8-%&$"-3):'+3'*+"#)*,(>)$,##"64'@)'6%(1+"#)'U3'-4%,-)G%3?)4':'+')$,+()$,.6+'44%,-@)"-()
paravertebral extension (arrows).
References
1. Alorainy IA. “Dural tail sign in spinal meningiomas”. Eur J Radiol 2006;60:387-91.
2. Arslanoglu A, et al. “MR imaging characteristics of pilomyxoid astrocytomas”. AJNR Am J Neuroradiol
2003;24(4):1906-8.
3. Baudrez V, et al. “Benign vertebral hemangioma: MR-histological correlation”. Skeletal Radiol
2001;30(8):442-6.
4. Boriani S, et al. Aneurysmal bone cyst of the mobile spine: report on 41 cases. Spine 2001;26(1):27-35.
5. Boriani S, et al. “Chordoma of the spine above the sacrum. Treatment and outcome in 21 cases”. Spine
1996;21(13):1569-77.
6. Chan MS et al. “Spinal aneurismal bone cyst causing acute cord compression without vertebral collapse:
CB(3/0(<VK(8/0$/-#iT(`'0$3)+(V30$"&(O>>OYÔHQJN[>ZW]T
7. C3+!'/)$'+(@1(')(3&T(hG,%"22$!$)3&(3/0(2'+5$23&(2*"+0".3#N()*'(53&,'("6(3--+'##$5'()+'3).'/)(3)(8+#)(
presentation of the disease. J Neurosurg 2002;97(5):1070-7.
8. C*,(9C1(')(3&T(h<V(8/0$/-#($/(#!$/3&(*'.3/-$"%&3#)".3N(C"++'&3)$"/(I$)*(#A.!)".#(3/0(I$)*(
3/-$"-+3!*$2(3/0(#,+-$23&(8/0$/-#iT(@XEV(@.(X(E',+"+30$"&(O>>ZYOOHZJNO>[WZPT(
9. Cohen-Gadol AA, et al. “Spinal meningiomas in patients younger than 50 years of age: A 21-year
experience”. J Neurosurg. 2003 98(3 Suppl):258-63.
10. Conti P, et al. “Spinal neurinomas: Retrospective analysis and long-term outcome of 179 consecutively
operated cases and review of the literature”. Surg Neurol 2004;61(1):34-43; discussion 44, 2004.
11. Doppman JL, et al. “Symptomatic vertebral hemangiomas: treatment by means of direct intralesional
injection of ethanol”. Radiology 2000;214(2):341-8.
12. Durr HR, et al. “Multiple myeloma: surgery of the spine: retrospective analysis of 27 patients”. Spine
2002;27(3):320-24; discussion 2002:325-26.
13. Fujiwara F, et al. “Intradural spinal lipomas not associated with spinal dysraphysm: A report of four
cases”. Neurosurgery 1995;37(6):1212-5.
14. Gabal AM. “Percutaneous technique for sclerotherapy of vertebral hemangioma compressing spinal cord”.
Cardiovasc Intervent Radiol 2002;25(6):494-500.
15. Garg RK. “Acute disseminated encephalomyelitis”. Postgrad Med J. 2003;79(927):11-17.
16. Hickman SJ, et al. “Imaging of the spine in multiple sclerosis”. Neuroimaging Clin N Am. 2000;10(4):689-
704.
17. Kikuchi K, et al. “The utility of diffusion-weighted imaging with navigator-echo technique for the diagnosis
of spinal epidermoid cysts”. AJNR Am J Neuroradiol 2000;21(6):1164-6.
18. Khong PL, et al. “Childhood acute disseminated encephalomyelitis: The role of brain and spinal cord
MRI”. Pediatr Radiol 2002 32(1):59-66.

19. S"'&&'+(SS1(')(3&T(hE'"!&3#.#("6()*'(#!$/3&(2"+0(3/0(8&,.()'+.$/3&'N(V30$"&"-$2W!3)*"&"-$2(2"++'&3)$"/iT(
20. Kransdorf MJ, et al. “Aneurysmal bone cyst: concept, controversy, clinical presentation, and imaging”. AJR
1995;164:573-80.
21. Lee S, et al. “Extraosseous extension of vertebral hemangioma, a rare cause of spinal cord compression”.
Spine 1999;24(20):2111-4.
22. Murphey MD, et al. “Imaging of musculoskeletal neurogenic tumors: Radiologic-pathologic correlation”.
RadioGraphics 1999 19:1253-80.
23. Murphey MD, et al. “Primary tumors of the spine: radiologic-pathologic correlation”. RadioGraphics 1996
16:1131-58.
24. Potgieter S, et al. “Epidermoid tumours associated with lumbar punctures performed in early neonatal
life”. Dev Med Child Neurol 1998;40(4):266-9.
25. V3*.",/)(@1(')(3&T(h9"/'(.3++"I(I$)*(0$66,#'(),."+($/8&)+3)$"/($/(!3)$'/)#(I$)*(&A.!*"!+"&$6'+3)$5'(
diseases: dynamic gadolinium-enhanced MR imaging”. Radiology 2003;229(3):710-17.
26. Shah BK, et al. “Magnetic resonance imaging of spinal plasmacytoma”. Clin Radiol 2000;55:439-45.
27. Simon JH. “Brain and spinal cord atrophy in multiple sclerosis”. Neuroimaging Clin N Am 2000;10(4):753-
70.
28. Sun B, et al. “MRI features of intramedullary spinal cord ependymomas”. J Neuroimaging.
2003;13(4):346-51.
29. B*3DD3+(G71(')(3&T(hG!$/3&(),.",+#($/(/',+"8%+".3)"#$#()A!'(KN(@/(<VK(#),0A("6(6+'l,'/2A1(.,&)$!&$2$)A(
and variety”. Neuroradiology 1999;41(9):625-9.
30. Vazquez E, et al. “Neuroimaging in pediatric leukemia and lymphoma: differential diagnosis”.
Radiographics 2002;22(6):1411-28.
31. Wanebo JE, et al. “The natural history of hemangioblastomas of the central nervous system in patients
with von Hippel-Lindau disease”. J Neurosurg. 2003;98(1):82-94.
32. Wilder RB, et al. “Persistence of myeloma protein for more than one year after radiotherapy is an adverse
prognostic factor in solitary plasmacytoma of bone”. Cancer 2002;94(5):1532-7.
33. Wippold FJ 2nd, et al. “Clinical and imaging features of cervical chordoma. AJR Am J Roentgenol
1999;172(5):1423-6.

1408
S0,.1+KK7+@1-1.1%'),21+@,(1'(1+'.5+K.31/),".(

Low Back Pain Annual Costs Annular Tear/Fissure [Figure 3]
!" 250,000 operations/year !" Typically seen with degenerated discs but
!" 18-56 billion dollars/year even seen in 25% of patients < 20 years
!" 85% of costs are due to recurrent or old
chronic disability !" Disc protrusions/extrusions often
associated
Degenerative Disc D,(1'(17+Lumbar !" Primary failure of the annulus (all layers
Nomenclature [Figure 1] involved)
!" Normal !" Present with back/radicular pain
!" Bulge (symmetric, asymmetric) !" MR: 1-2 mm band of increased T2 signal
!" @//,&3+()'3+d8##,+' (high intensity zone-HIZ)
!" Herniation (focal or broad-based) !"Linear area of contrast enhancement
!"Protrusion (96%)
!"Extrusion !"Not as sensitive as discography
!"Extrusion with free fragment
Figure 1 A & B
Disc bulges: Symmetric (left image) and asymmetric

(right image) (www.asnr.org/spine_nomenclature).
Figure 3 A & B
B--1#"+)3'"+g&441+'/)=,3')?%8?)%-3'-4%3>)a,-'),-)3?'4')
Multilevel Disc Bulges [Figure 2]
T2-WIs (arrows).
Disc Herniation and Types

[Figures 4 & 5]
Multilevel disc bulges in a 77-year-old man.

Figure 4
Disc herniation and types.
Top Left Image: Focal.
Top Right Image: Broad based.
Bottom Left Image: Protrusion.
Bottom Right Image: Extrusion.
Spine II: Degenerative Disease and Infections 1409 Neruoradiology Radiology

L4-5 Disc Extrusion with Inferior
Migration [Figure 7]
Figure 5
Disc protrusions
and extrusions
(www.asnr.
org/spine_
nomenclature).
Figure 7 A, B & C
Disc extrusion, L4-L5. This extruded disc retains a

connection to the parent L4-5 disc as it migrates
down behind the L5 vertebral body (arrows).
L5-S1 Focal Disc Protrusion [Figure 6]

L4-5 Disc Extrusion with Sequestered
Fragment [Figure 8]
Figure 8 A to E
Disc extrusion with

sequestered fragment,
L4-L5. Note that the
fragment does NOT
retain its connection
to the parent disc
Focal disc protrusion, L5-S1. (arrows). The signal
A 31-year-old man with left S1 radiculopathy. The intensity differs from
normal right S1 nerve root is indicated by the arrows. the parent disc on the
T2-WI.

Degenerative Changes Typically Induce
Secondary Changes in the Adjacent
Vertebral Bodies (Degenerative
Discovertebral Changes) (Modic Figure 11
A&B
Changes) [Figures 9 to 11]
Type III
modic
changes.
Sclerosis.
Hypointense
on both T1-
and T2-WIs.
Figure 9
A, B, C & D
Type I modic Lumbar Spinal Canal and Foraminal

changes. Stenosis [Figure 12]
Vascularized
marrow
(edema).
Hypointense
on T1-
WI and
hyperintense
on T2-WI.
Multilevel degenerative disease. Note severe right L1-2
foraminal stenosis from a combination of disc bulge,
<"$'3)"+3?+,6"3?>@)"-()#%8".'-31.)0":1.)*1$M#%-8/)))))))))
All T1-WI images.
Facet Joint Synovial Cysts [Figure 13]

!" Intraspinal juxta-articular synovial cysts
Figure 10
A, B & C are uncommon; associated with facet
arthopathy
Type II !" Most in lumbar spine, especially L4-5
modic !" Slight female preponderance; mean age
changes. 58 years
Proliferation
of end- !" Origin: DJD? trauma?
plate fatty !" E"(#!'2$82(#A.!)".(*$#)"+AY(I3L$/-(3/0(
marrow. waning symptoms as these increase and
Hyperintense decrease in size
on both T1- !" CBN(2A#)$2(&'#$"/(I$)*("+(I$)*",)(23&2$8'0(
and T2-WIs.
rim adjacent to degenerated facet
!" MR: Iso- or slightly hyperintense on SE
sequences
!" DDx: ganglion cyst (does not
communicate with joint)

Synovial Cyst [Figure 13]
Figure 14 D, E & F
Failed back surgery
– recurrent disc
Figure 13 protrusion. A
A, B, C & D large recurrent
disc (arrows)
Synovial cyst. demonstrates mild
Cyst produces enhancement but the
compression surrounding epidural
on the thecal &*+,4%4)'-?"-$'4)3,)")
sac from a much greater degree.
posterolateral
location
(arrows).
Compression
of the nerve
roots is best appreciated on the MR
myelogram (right image). F:SS7++Type I Arachnoiditis [Figure 15]
Failed Back Surgery Syndrome (F:SSC7+++++

Avoid the Knife [Figures 14 to 16]
!" 10%-40% of patients
!" Intractable pain with variable
incapacitation
!" Differential considerations include:
!"Recurrent/residual disc herniation
!"Postop infection
!"Second level disease
!"Facet disease
!"Arachnoiditis
!"Neuritis
!"U!$0,+3&(8%+"#$#(Hh#23+iJ
!"Miscellaneous
F:SS7+VRecurrent” Disk [Figure 14]
Figure 15 A, B & C
Type I arachnoiditis.
Nerve roots are
clumped centrally
within the thecal sac
(arrows).
Figure 14 A, B & C
Failed back surgery – recurrent disc protrusion. A
large recurrent disc (arrows) demonstrates mild
'-?"-$'.'-3)*13)3?')41++,1-(%-8)'6%(1+"#)&*+,4%4)
enhances to a much greater degree.

F:SS7++Type II Arachnoiditis [Figure 16]
Figure 16
A, B, C & D
Type II
arachnoiditis.
Nerve roots are
“plastered” to
the margins
of the thecal
sac producing
an “empty”
appearance (large
arrows). The more Figure 18 A to F
proximal nerve
roots are seen as Acquired cervical
distinct entities spinal canal stenosis.
(small arrows). Disc disease, coupled
with ligamentum
0":1.)*1$M#%-8@)
produces severe canal
Cervical Spinal Canal Stenosis stenosis at multiple
levels (dark arrows)
[Figures 17 & 18] with associated
!" Congenital spinal canal stenosis pathologic signal in
!" Acquired spinal canal stenosis the spinal cord (white arrows), most severe at C5-6.
O((,#/'),".+"3+)?1+Posterior
Longitudinal Ligament (OPLL)
[Figures 19 & 20]
!" 9'-$/#(I$)*(23&2$823)$"/(6"&&"I'0(%A(6+3/D(
"##$823)$"/("6()*'(!"#)'+$"+(&"/-$),0$/3&(
ligament in upper C-spine and progresses
into upper T-spine
!" C3/(#''("/(!&3$/(8&.#($/(>TZO?("6(
asymptomatic North Americans and 20%-
30% of symptomatic patients
!" Most easily seen on CT
!" On MR, thick band of decreased signal on
T1- and T2-WI with mass effect on thecal
sac and cord
!" Associated with DISH
Figure 17 A, B & C
Congenital cervical spinal canal stenosis. Left Image:

Normal. This may be produced by pedicle (middle
image) or lamina (right image) hypoplasia. The
underlying dimensions of the canal should be assessed
on every study as even mild degenerative disease
$"-)*')4%8-%&$"-3)%-)3?')<"$'),<)1-('+#>%-8)$,-8'-%3"#)
stenosis.

OPLL and DISH [Figure 19] Infections
Pyogenic Osteomyelitis [Figure 21]

!" K&&W0'8/'0(BZW*A!"$/)'/#'(5'+)'%+3&(
marrow with loss of adjacent endplate
0'8/$)$"/("/(%")*(#$0'#("6($/6'2)'0(0$#2Y(
hyperintense on T2-WI; enhances
!" Lumbar 48%; thoracic 35%; cervical
6.5%
!" Paraspinal and/or epidural involvement in
75%
!" S aureus most common; E coli if gram
negative; salmonella in sickle cell
!" Source: GU, GI, lung, cardiac, cutaneous/
mucous-seeds vascularized subchondral
bone
!" Bimodal: pediatric patients and sixth to
seventh decade; also IV drug abusers and
those with HIV
!" Pain, tenderness, and fever
Figure 19 A to E
c44%&$"3%,-),<)3?')6,43'+%,+)#,-8%31(%-"#)#%8".'-3/)
5?%$M)?>6,%-3'-4')4%8-"#)%4)%('-3%&'()*'3G''-)3?')
spinal cord and posterior vertebral bodies on MR
L"++,G4X/)!5)$,-&+.4)3?')(%"8-,4%4),<)cNbb)4':'+'#>)
compromising the spinal canal diameter. DISH is
present at lower levels.
O((,#/'),".+"3+Ligamentum Flavum
(OLF) [Figure 20]
Figure 21 A to E
Pyogenic osteomyelitis. Note paraspinal and epidural
involvement (arrows).
Tuberculous Osteomyelitis [Figure 22]

!" AKA Pott disease
!" Typical: gibbus vertebrae with relatively
intact disc and paraspinal abscess
!" Abscesses dissect over considerable
length
Figure 20 A, B & C !" Mid-thoracic or thoracolumbar most
common
c44%&$"3%,-),<)3?')#%8".'-31.)0":1./)C"+M'()3?'$"#)
!" Inoculum in anterior vertebral body;
sac and cord compression produced by OLF.
spreads under anterior longitudinal
ligament; spares discs due to absence of
proteolytic enzymes
!" M = F; presents in 50’s; fever infrequent
!" Concomitant pulmonary TB in 10%

Tuberculous Osteomyelitis [Figure 22] S Aureus Epidural Phlegmon [Figure 23]
Figure 22 A, B,
C&D
Tuberculous
osteomyelitis.
Note gibbus
deformity and
extension
anteriorly under
the anterior Figure 23 A to E
longitudinal
ligament S aureus epidural phlegmon. A 20-month-old boy
(arrows). with 5 days of fever, now failing to ambulate or move
?%4)-'$M/)B)('&-%3')"*4$'44)$":%3>)%4)-,3)('&-'()*13)
"*-,+."#)'-?"-$%-8)4,<3)3%441')&##4)3?')6,43'+%,+)
epidural space (arrows).
Epidural Phlegmon/Abscess
[Figures 23 & 24] S Aureus Epidural Abscess [Figure 24]
!" S aureus most common (57%-73%), then
TB (25%)
!" Predisposing conditions: IV drug users,
immunocompromised states, DM, CRF,
alcoholis, etc
!" Anterior from adjacent discitis or
osteomyelitis
!" Posterior from GU, GI, lung, cardiac, etc
!" Direct inoculation from penetrating
trauma, surgery, etc
!" `'3D#($/(86)*(3/0(#'5'/)*(0'230'#
!" Lumbar EA may mimic herniated disc
Figure 24 A to E
S aureus epidural abscess. Note rim enhancement and

low ADC (arrows).

References
1. Akman S, et al. Magnetic resonance imaging of tuberculous spondylitis. Orthopedics 2003;26(1):69-73.
2. 9'/(k3.",03(S1(')(3&T(B*"+32$2(.A'&"!3)*A(23,#'0(%A("##$823)$"/("6()*'(&$-3.'/),.(435,.N(@(+'!"+)("6(
18 cases. J Neurosurg. 2003;99(2 Suppl):157-61.
3. 9""#(E1(')(3&T(C&3##$823)$"/("6(3-'W+'&3)'0(2*3/-'#($/(&,.%3+($/)'+5'+)'%+3&(0$#2#N(O>>O(_"&5"(@I3+0($/(
basic science. Spine. 2002;27(23):2631-44.
4. Carragee EJ. The clinical use of magnetic resonance imaging in pyogenic vertebral osteomyelitis. Spine
1997;22(7):780-85.
5. Cinotti G, et al. Stenosis of lumbar intervertebral foramen: Anatomic study on predisposing factors. Spine
2002;27(3):223-29.
6. Eastwood JD, et al. Diffusion-weighted imaging in a patient with vertebral and epidural abscesses. AJNR
Am J Neuroradiol 2002;23(3):496-98.
7. Modic MT, et al. Degenerative disk disease: Assessment of changes in vertebral body marrow with MR
imaging. Radiology 1988;166(1 Pt 1):193-99.
8. Munter FM, et al. Serial MR imaging of annular tears in lumbar intervertebral disks. AJNR Am J
Neuroradiol 2002;23(7):1105-9.
9. C"/#'/#,#(#)3)'.'/)("/(/".'/2&3),+'(3/0(2&3##$823)$"/("6(&,.%3+(0$#2(!3)*"&"-A(%A(E@GG1(@GGV1(3/0(
ASNR. © 2001 Lippincott Williams & Wilkins, Inc. Volume 26(5) 1 March 2001 pp E93-E113.
10. Van Goethem JW, et al. Review article: MRI of the postoperative lumbar spine. Neuroradiology
2002;44(9):723-39.
1416 Neruoradiology Radiology

Spine II: Degenerative Disease and Infections
S0,.1+KKK7+M'(/9&'%+'.5+E,(/1&&'.1"9(+G1(,".(

Vascular Lesions Cervical Type I Dural AVF [Figure 2]
!" AVM/AVF
!"Type I = DAVF
!"Type II = intramedullary “glomus”
type AVM
!"Type III = “juvenile” type AVM
!"Type IV = intradural (perimedullary)
AVF
!" Cavernous malformations
!" Spinal cord infarction
!" EDH/SDH/SAH
Type I Dural AVF [Figure 1]

!" Most common type of spinal vascular
malformation (80%)
!" Presentation: acquired lesion; 80%
Figure 2 A, B & C
= male; 40-60 years; back/leg pain,
progressive myelopathy from venous Type I dural AVF. Note edema in lower cervical
hypertension (Foix-Alajouanine syndrome and upper thoracic cord with diffuse enhancement
= subacute necrotic myelopathy) (arrows). T2 shows extensive increased signal within
3?')$,+()"-()4'+6%8%-,14)&##%-8)('<'$34)G%3?%-)3?')
!" `"$/)("6(8#),&$f3)$"/(/'3+("+("/(!+"L$.3&( thecal sac anteriorly (Courtesy ME Jensen).
nerve root; usually intradural
!" <A'&"dCBN(#'+!$-$/",#(8&&$/-(0'6'2)#($/(
subarachnoid space; normal to mildly
swollen spinal cord
!" MR: abnormal intramedullary T2 signal; Type II “Glomus” AVM [Figure 3]
#I"&&'/(2"+0Y(4"I(5"$0#(3+",/0(2"+0 !" Congenital lesion with discrete nidus
!" Angiography: single/multiple feeders located within spinal cord
from radicular branches; single intradural !" Presentation: young adults; acute
draining vein; small nidus of AV shunting neurologic symptoms from hemorrhage;
at intervertebral foramen progressive myelopathy from steal,
venous hypertension, cord compression
!" Location: throughout cord; cervical/
thoracolumbar junction most common
!" Associated with Klippel-Trenaunay-Weber
and Rendu-Osler-Weber syndromes
!" Feeding vessel aneurysms in 40%
!" <A'&"dCBN(#'+!$-$/",#(4"I(5"$0#Y(
enlarged cord
!" CT: subarachnoid/intraparenchymal
Figure 1 hemorrhage
!" <VN($/)+3.'0,&&3+Ad!'+$.'0,&&3+A(4"I(
Type I dural voids; hematomyelia; myelomalacia; cord
AVF. Note
multiple edema
0,G):,%(4) !" Angiography: enlarged anterior and/or
surrounding the !"#)'+$"+(#!$/3&(3+)'+$'#(8&&$/-(2".!32)(
thoracic cord nidus; rapid shunting into dilated veins;
(Courtesy CD intranidal/perinidal aneurysms
Phillips).
Spine III: Vascular and Miscellaneous Lesions 1417 Neruoradiology Radiology

Figure 3 A, B,
C&D
Type II
“glomus”
AVM
(Courtesy
CD Phillips).
Type III “Juvenile” AVM

!" AKA juvenile AVM; intramedullary
-extramedullary AVM
!" Most uncommon of spinal AVMs
!" Usually cervical Figure 4 A to H
!" May be associated with Cobb syndrome
Type IV perimedullary AVF. A 20-year-old woman with
(metameric vascular malformation long-standing abdominal pain (due to steal). Note
involving cord, bone, and skin) enhancing structures within the spinal canal on the CT
!" Poor prognosis; complete resection not images (arrows). The spinal angiogram demonstrates
possible; palliative treatment the supply from the artery of Adamkiewicz (arrows).
Type IV “Perimedullary” AVF [Figure 4] POP CORN

!" 10%-20% of spinal AVMs/AVFs Cavernous Malformations [Figure 5]
!" All ages; M = F !" Peak = fourth decade (12-88 years); M:F
!" 7$+'2)(8#),&3(%')I''/(@G@d`G@(3/0( = 1:2
draining vein; no nidus !" Spinal cord = only 3%-5% of all CMs
!" Fistulae usually ventral in region of conus !" Thoracic (50%) > cervical (40%) > conus
!" Congenital or acquired after trauma (10%)
!" Associated with Rendu-Osler-Weber !" Familial in 20% (autosomal dominant);
!" Generally good outcome highest hemorrhage risk
!" Embolization and/or resection (vary for !" Scan brain for additional lesions; GRE-
Types A, B, and C) best
!" <A'&"dCBN(#'+!$-$/",#(4"I(5"$0#Y( !" Clinical presentations:
enlarged cord !"Discrete episodes of neurologic
!" CT: subarachnoid and/or intraparenchymal deterioration with variable recovery
hemorrhage !"Slow neurologic decline
!" <VN(K/)+3.'0,&&3+Ad!'+$.'0,&&3+A(4"I( !"Acute onset with rapid decline
voids; hematomyelia; myelomalacia; cord !"Acute onset with mild symptoms and
edema subsequent gradual decline
!" Angiography: enlarged anterior and/or
posterior spinal arteries directly draining
into ectatic, tortuous veins; intranidal/
peripheral aneurysms

Cavernous Malformations [Figure 5]
Figure 6C
Spinal cord
infarction
from a type
I dural AV
&431#"/
Spinal E0,59%'&7+Subdural Hematomas

[Figure 7]
!" U7kN(%$."03&N(2*$&0+'/(H<(g(:JY(86)*(3/0(
sixth decades (M:F = 4:1)
Figure 5 A, B, C & D !" SDH: all ages; M = F
Cavernous malformation (Courtesy CD Phillips).
!" Sx: acute knife-like neck/back pain,
extremity weakness, sphinctor
disturbances, altered DTRs
!" Thoracic/lumbar > cervical (except EDH in
Spinal Cord Infarction [Figure 6] children are more common in C-T region)
!" Typically in thoracic cord (due to arterial !" May be spontaneous (EDH = 40%-50%;
border zone) SDH = 15%)
!" Most patients > 50 years; M = F !" Predisposing causes include: vascular
!" Slightly expanded cord with T2 malformations, anticoagulation, tumors,
hyperintensity coagulopathies, trauma, prior surgery/
!" Multiple etiologies: idiopathic, procedure (LP, spinal anesthesia, etc)
atherosclerosis, aortic aneurysm/ !" Rx: may resolve spontaneously or
surgery, hypotension, infection, need decompressive laminectomy for
embolic, AVM, decompression sickness, evacuation
coagulopathy, HNP, postanesthesia
complications (epidurals, etc) “Spontaneous” Epidural Hematoma
St son agudos !" Main DDx: MS, transverse myelitis, cord [Figure 7]
tumor, type I spinal DAVF
AVF and Spinal Cord Infarction [Figure 6]
Spontaneous epidural hematoma in a 3-year-old child

with a 2-day history of neck pain and both upper
Figure 6 A & B and lower extremity weakness. A large epidural
hematoma (from C2 to T5) produces severe spinal cord
Spinal cord %-<"+$3%,-)<+,.)")3>6')7)(1+"#)B])&431#"/ $,.6+'44%,-/))=,3')3?')01%(201%()#':'#)%-(%$"3'()*>)3?')
arrows.
Uncommon Non-Neoplastic Extradural Type III Meningeal Cysts (Intradural
Lesions Arachnoid Cysts) [Figure 10]
!" Meningeal cysts !" Intradural arachnoid cysts are rare
!" Epidural lipomatosis !" Unclear etiology: ?congenital;
!" Meningoceles s*'."++*3-'Y(s$/43..3)$"/((
!" Transdural cord herniation !" Thoracic spine is most common location
!" Subacute combined degeneration !" 80% arise near septum posticum and
located posterior to cord
Meningeal C!()(7+C&'((,#/'),".++++++++++++++++ !" Most communicate with subarachnoid
!" Type I: extradural MC without nerve root space
8%'+# !" CTM: compressed cord displaced
!"IA: extradural arachnoid cyst anteriorly
!"IB: occult sacral meningocele !" MR: signal intensity of CSF so may not be
!" Type II: extradural MC with nerve root able to identify unless cord is displaced/
8%'+# deformed
!"Tarlov perineural cyst
!" Type III: intradural MC
!" Intradural arachnoid cyst
T!01+KL+E47+AExradural Arachnoid Cyst)

[Figure 8]
Figure 8 A, B & C
Type IA meningeal
cyst (extradural
arachnoid cyst).
Note displacement of
epidural fat (arrows)
(Courtesy M Modic).
T!01+KK+E47+ATarlov Perineural Cyst)

[Figure 9]
Figure 10 A to G
Type III meningeal

cyst (intradural
arachnoid cyst).
MR demonstrates
an intradural cystic
lesion.
The myelogram
$,-&+.4)3?')
Figure 9 A, B & C intradural
location and the
Type III
communicating
meningeal cyst
nature of the cyst
(Tarlov perineural
which is slowly
cyst).
&##%-8)G%3?)$,-3+"43/)
=,3')01%(201%()#':'#)
(arrows) (Courtesy
CD Phillips).

Epidural Lipomatosis [Figure 11]
!" Most often associated with chronic steroid
use (exogenous or endogenous Cushing
syndrome)
!" Also associated with rapid weight gain and
obesity
!" Thoracic spine most common
!" Myelopathic symptoms predominate
Figure 12 B, C, D & E
Lateral thoracic meningoceles.
The MR images demonstrate meningoceles originating
from two separate levels, one anterior and one
posterior (arrows).
Brachial Plexus Avulsions [Figures 13 & 14]

!" AKA traumatic meningocele
!" Avulsion of root(s) of brachial plexus
invariably from traumatic injuries
!" Patients will often present with “dead
arm” and the question arises as to
whether the brachial plexus is disrupted in
cords or trunks (which might be amenable
to repair) or whether the roots are torn
Figure 11 A to F from the cord (not reparable)
!" Demonstration of “rootless” meningoceles
Epidural lipomatosis. Note fat density posterior to the
spinal cord on the CT study. Compression of the cord are diagnostic
results in abnormal T2 signal and cord enhancement.
Lateral Thoracic Meningoceles [Figure 12]
Figure 13 A & B
Figure 12A
Brachial plexus avulsions. An 8-year-old boy s/p ATV
Lateral thoracic meningoceles. accident with a dead right arm. Note avulsions at
A 30-year-old woman with decreased breath sounds on multiple levels (arrows).
the right.

Idiopathic Transdural Cord Herniation
Figure 13C
[Figures 15 & 16]
Brachial plexus !" Occur in the left anterolateral dura
avulsions. An !" Present with a long history of subtle
8-year-old boy s/p
hemisensory abnormality before the
ATV accident with
a dead right arm. motor symptoms
Note avulsions !" MR shows a typical pattern of an
at multiple levels interruption of the usually smooth ventral
(arrows). margin of the cord being thrust anteriorly
over a short segment
!" Primary differential is whether cord is
being displaced by a posterior mass, such
as an arachnoid cyst, or whether the cord
is tethered ventrally
Figure 15
Idiopathic
Transdural
spinal cord
herniation.
Figure 14 A to F
Brachial plexus
avulsion.
A 24-year-old woman
s/p ATV accident with
right arm weakness
and Horner syndrome.
Note single right
C8 root avulsion
(pseudomeningocele).
All images are T2-WI.
Idiopathic Transdural Cord Herniation

[Figures 15 & 16]
!" Typical presentation is Brown-Séquard
syndrome
!" C&$/$23&(0'82$)#()'/0()"(%'(!+"-+'##$5'(
unless treated
!" Surgical reduction of the herniated cord
can lead to improvement in the motor
0'82$)
!" Typical patient is an adult female, affected
location is the upper and mid-thoracic
level (T2-T7).
Figure 16 A to E
Idiopathic transdural cord herniation.

Subacute Combined Degeneration
[Figure 17]
!" _$)3.$/(9ZO(0'82$'/2A
!" Accumulation of methylmalonic acid
(myelin toxic) with selected degeneration
of dorsal +/- lateral columns
!" Mild cord enlargement and abnormal T2
signal in dorsal columns (inverted “V” on
axial images)
!" Etiologies: malabsorption (most
common), inadequate B12 intake (rare),
nitrous oxide (inactivates B12)
Subacute combined degeneration. Note high T2 signal involving the posterior columns.
References
1. Acosta FL, et al. Diagnosis and management of sacral Tarlov cysts. Case report and review of the
literature. Neurosurg Focus 2003;15(2): Article 15.
2. Acosta FL, et al. Diagnosis and management of sacral tarlov cysts. Case report and review of the
literature. Neurosurg Focus 2003;15(2): Article 15.
3. Bemporad JA, et al. Magnetic resonance imaging of spinal cord vascular malformations with an emphasis
on the cervical spine. Neuroimag Clin North Am 2001;11:111-29.
4. Boukobza M, et al. Spinal subdural haematoma: a study of three cases. Clin Radiol 2001;56(6):475-80.
5. Caspar W, et al. Microsurgical excision of symptomatic sacral perineurial cysts: a study of 15 cases. Surg
Neurol 2003;59(2):101-05; discussion 105-06.
6. Deutsch H, et al. Spinal intramedullary cavernoma: clinical presentation and surgical outcome. J
Neurosurg 2000;93(1 Suppl):65-70.
7. Dix JE, et al. Spontaneous thoracic spinal cord herniation through an anterior dural defect. AJNR Am J
Neuroradiol 1998;19(7):1345-8.
8. Doi K, et al. Cervical nerve root avulsion in brachial plexus injuries: Magnetic resonance imaging
2&3##$823)$"/(3/0(2".!3+$#"/(I$)*(.A'&"-+3!*A(3/0(2".!,)'+$f'0()"."-+3!*A(.A'&"-+3!*AT(X(E',+"#,+-(
2002;96(3 Suppl):277-84.
9. Dorsay TA, et al. MR imaging of epidural hematoma in the lumbar spine. Skeletal Radiol
2002;31(12):677-85.
10. Dubuisson AS, et al. Brachial plexus injury: a survey of 100 consecutive cases from a single service.
Neurosurgery 2002;51:673-83.
11. Fassett DR, et al. Spinal epidural lipomatosis: A review of its causes and recommendations for treatment.
Neurosurg Focus 2004;16(4):Article 11.
12. Geers C, et al. Polygonal deformation of the dural sac in lumbar epidural lipomatosis: Anatomic
explanation by the presence of meningovertebral ligaments. AJNR Am J Neuroradiol 2003;24(7):1276-82.
13. Hung KS, et al. Traumatic spinal subdural hematoma with spontaneous resolution. Spine
2002;27(24):E534-E538.
14. Hurst RW, et al. Peripheral spinal cord hypointensity on T2-weighted MR images: a reliable imaging sign
of venous hypertensive myelopathy. AJNR Am J Neuroradiol. 2000;21(4):781-86.
15. K&/$2fDA(G1(')(3&T(<V(8/0$/-#($/(#,%32,)'(2".%$/'0(0'-'/'+3)$"/("6()*'(#!$/3&(2"+0(23,#'0(%A(/$)+",#(
oxide anaesthesia—two cases. Eur J Neurol 2002;9(1):101-04.

16. Khosla A, et al. CT myelography and MR imaging of extramedullary cysts of the spinal canal in adult and
pediatric patients. AJR Am J Roentgenol 2002;178:201-07.
17. Liao CC, et al. Experience in the surgical management of spontaneous spinal epidural hematoma. J
Neurosurg 2004;100(1 Suppl):38-45.
18. Mascalchi M, et al. Spinal vascular malformations: MR angiography after treatment. Radiology
2001;219(2):346-53.
19. Massicotte EM, et al. Idiopathic spinal cord herniation. Report of eight cases and review of the literature.
2002 Spine. 27:E233-E243.
20. Paulsen RD, et al. Prevalence and percutaneous drainage of cysts of the sacral nerve root sheath (Tarlov
cysts). AJNR Am J Neuroradiol 1994;15:293-97.
21. V35$/3(91(')(3&T(<V(8/0$/-#($/(#,%32,)'(2".%$/'0(0'-'/'+3)$"/("6()*'(#!$/3&(2"+0N(3(23#'("6(+'5'+#$%&'(
cervical myelopathy. AJR Am J Roentgenol 2000;174(3):863-5.
22. V$2"&8(:1(')(3&T(\$3/)(!'+$.'0,&&3+A(3+)'+$"5'/",#(8#),&3#("6()*'(#!$/'N(2&$/$23&(3/0(+30$"&"-$2(6'3),+'#(3/0(
endovascular treatment. AJNR Am J Neuroradiol 1997;18(4):677-87.
23. Salvador de la Barrera S, et al. Spinal cord infarction: prognosis and recovery in a series of 36 patients.
Spinal Cord 2001;39(10):520-25.
24. Sandalcioglu IE, et al. Intramedullary spinal cord cavernous malformations: clinical features and risk of
hemorrhage. Neurosurg Rev 2003;26(4):253-56.
25. G3+36W;35$(U1(')(3&T(7')'2)$"/("6(#!$/3&(0,+3&(3+)'+$"5'/",#(8#),&3'(I$)*(<V($.3-$/-(3/0(2"/)+3#)W
'/*3/2'0(<V(3/-$"-+3!*AN(#'/#$)$5$)A1(#!'2$82$)A1(3/0(!+'0$2)$"/("6(5'+)'%+3&(&'5'&T(@XEV(@.(X(E',+"+30$"&(
2002;23(5):858-67.
26. Sasaoka R, et al. Idiopathic spinal cord herniation in the thoracic spine as a cause of intractable leg pain:
Case report and review of the literature. J Spinal Cord Tech 2003;16(3):288-94.
27. G!')f&'+(V:1(')(3&T(<"0$8'0(2&3##$823)$"/("6(#!$/3&(2"+0(53#2,&3+(&'#$"/#T(X(E',+"#,+-(HG!$/'(OJT(
2002;96:145-56.
28. Srikanth SG, et al. MRI in subacute combined degeneration of spinal cord: a case report and review of
literature. Neurol India 2002;50(3):310-12.
29. G,+'(M1(')(3&T(G!$/3&()A!'(K_(3+)'+$"5'/",#(.3&6"+.3)$"/#(H!'+$.'0,&&3+A(8#),&3#J($/(2*$&0+'/T(C*$&0#(E'+5(
Syst 2000;16(8):508-15.
30. Wang MY, et al. Intradural spinal arachnoid cysts in adults”. Surg Neurol 2003;60(1):49-55; discussion
55-56.
31. Watters MR, et al. Transdural spinal cord herniation: Imaging and clinical spectra. AJNR Am J Neuroradiol
1998;19(7):1337-44.
32. Weidauer S, et al. Spinal cord infarction: MR imaging and clinical features in 16 cases. Neuroradiology
42002;4(10):851-7.
Spine III: Vascular and Miscellaneous Lesions Neruoradiology Radiology

1424
Nuclear Radiology
1425
1426
Hepatobiliary Imaging (HBI)
What Imaging Modality (NM, US, CT, HBI Acute Cholecystitis Detection
MRI) Should be Employed to C".#%*+ Technique
the Clinical Impression of Acute/ !" Patient preparation
Chronic Disorder of the Hepatobiliary !"Nothing by mouth at least 4 hours
Tree? prior to examination
!" Acute cholecystitis !" Radiopharmaceutical
!" Chronic acalculous cholecystitis !"5 mCi technetium 99-m disofenin
!" The cystic duct syndrome !" Image acquisition
!" Gallbladder dyskinesia !"Anterior 500 K images of the liver and
!" Sphincter of oddi dyskinesia biliary tree q 10 minutes
!" A bile leak !"Delayed 4-hour images in patients in
whom the gallbladder did not visualize
Acute Cholecystitis Imaging Modality within 60 minutes
Options
!" Imaging options HBI, US, CT, MRI RTUS Acute Cholecystitis Detection
!" Optimal imaging HBI Technique
modality !" Patient preparation
!"Nothing by mouth at least 6 hours
The Sensitivity of HBI and Real-Time prior to examination
Ultrasonography in the Detection of !" Technique
Acute Cholecystitis !"Real-time sonograms in transverse,
horizontal, and left lateral decubitus
Fink-Bennett D, Freitas J, Ripley S, Bree R. Ar- positions
chives of Surgery. Vol. 120 (August 1985).
HBI Acute Cholecystitis Detection
Product Line/Diagnostic Algorithm
Results
Guideline Inclusion J9(),#/'),".b
Protection Calculous AC Acalculous AC
!" HBI 97% 100%
HBI vs RTUS (Strict- and Liberal- !" RTUS
Criteria Real-Time Ultrasonography) !"Liberal 86% 89%
Acute Cholecystitis Detection Subjects !"Strict 24% 44%
!" Patients
A R12,(,)7+A Means to Protect HBI’s Role
!"100
in the Acute Cholecystitis Diagnosis
!" Inclusion criteria
!"Path DX: Product Line
!"Acute cholecystitis (Hemorrhagic
Hepatobiliary Scintigraphy is Superior
necrosis of the gallbladder wall)
!"RTUS and HBI (48 hours of each
to Abdominal Ultrasound in Suspected
other) Acute Cholecystitis
Chatziioannou S, Moore W, Ford P, Dhekne R.
HBI/RTUS Acute Cholecystitis Surgery, Vol. 127,Pg. 609-613 June 2000.
Diagnostic Criteria
!" HBI Baylor’s HBI vs US Acute Cholecystitis
!"Gallbladder non visualization up to 4 Detection Revisit Objectives
hours postradiotracer administration !" To determine which imaging modality
!" RTUS k9K("+(MG($#(%'#)()"(2"/8+.()*'(2&$/$23&(
!"Liberal diagnosis of acute cholecystitis.
#" Stones, thick wall, nonshadowing !" To determine the incremental diagnostic
echos, and/or Murphy sign value of each modality in patients with
!"Strict suspected acute cholecystitis, ie do the
#" Wall edema and/or pericholecystic h'L)+3*'!3)$2d3/A(8/0$/-#i("6(#"/"-+3!*A(
4,$0($6($/()*'(3%#'/2'("6( warrant its use in AC detection
hypoalbuminemia, cirrhosis, or
ascites
Hepatobiliary Imaging Nuclear Radiology

1427
Baylor’s HBI vs US Acute Cholecystitis Morphine Augmented Cholescintigraphy
Detection Revisit Methods !" An intervention that decreases the time to
!" Final medical: surgical diagnosis/scan diagnosis from 4-1.5 hours
result correlation
!"107 Morphine Augmented Cholescintigraphy
!" Patients Rational
!"Referred for HBI and GB US in patients !" Morphine sulfate .04 mg/Kg IV
with suspected AC (1 day of each " " %
other) !" Increased common bile duct resistance
!" Calculated the incremental diagnostic (12.7 ± 2.4 - 20.0 ± 2.4 cm/saline)
value of HBI and US in patients with !" Increased resistance
suspected AC
" " %
!"Nominal logistic analysis
!" K/2+'3#'(%$&'(4"I()"(-3&&%&300'+($6(2A#)$2(
Baylor’s HBI vs US Revisit Acute duct patent
Cholecystitis Diagnosis Criteria Does it Work?
Imaging Modality: Acute Cholecystitis
HBI: Persistent nonvisualization E3#/'/!+"3+Morphine Augmented
of the gallbladder, 30 min Cholescintigraphy
postmorphine augmenta-
tion or on 3-hour delayed
images
Sonography Murphy sign, gallblad-
der wall-thickening, gall-
bladder size (> 5 cm),
gallbladder wall edema,
sludge, pericholecystic
(( ( ( 4,$01(#&",-*'0(.,2"#3((
with Murphy sign
Bottom Line
Examples [Figures 1 to 6]
Baylor’s HBI vs US Acute Cholecystitis
Detection Revisit Results in 107
Medical/Surgically Rx Patients
Baylor’s HBI and US Incremental

Diagnostic Value Results (Nominal
Logistics Analysis)
!" All Patients: Figure 1 A & B
!"Both tests demonstrated diagnostic
value, but scintigraphy had a much
higher diagnostic value than US
(global c2 = 58.1 (p < 0.001)
and global c2 = 9.7 (p = 0.002)
respectively)
!"The addition of the information
derived from U.S. to that from
scintigraphy did not improve the
diagnositic accuracy compared to that
from scintigraphy alone (global c2 =
58.2)
How Do We Do This Today?
Figure 2 A & B

1428
Figure 3 A to N
Figure 4 A & B
Figure 5 A & B
Figure 6 A to U

1429
The Liver Sign [Figure 7]
Figure 7
A to G
RIM Sign [Figures 8 & 9]
Figure 8
A to K
Figure 9
A to L

1430
RIM Sign [Figure 10]
Figure 10
A&B
Or Time? [Figures 11 to 17]
Figure 11 A to I
Figure 12
Figure 13

1431
Morphine Augmented Cholescintigraphy
Potential Pitfalls/Methods to Prevent
[Figure 18]
Potential Pitfall Action to Prevent

!" Increased biliary Booster dose
to bowel transit
!" The “cystic duct sign” Recognition of it
!" Acute acalculous Ultrasonography
Figure 14
cholecystitis Indium-111 WBC’s
Figure 18
Figure 15 A & B
Morphine Augmented Cholescintigraphy

!" Contraindications
!"Allergy
!"Known addiction
!"Pancreatitis
Bile Leaks
Post Cx Bile Leak Incidence

Surgery Incidence
!" Conventional Cx 0.1%
(1/3-500 Sx)
!" Laproscopic Cx 0%-7%
!" # Cx/Yr = 600,000; 80% performed
laproscopically
Figure 16 Laproscopic Cholecystectomy

Advantages
!" Decreased hospital stay (2.8-1.96 days)
!" Time to return to work reduced (34-6.2
days)
!" Decreased postoperative respiratory
complicaions
!" 7'2+'3#'0(0$#8-,+'.'/)
How Do We Do This?
Figure 17 A & B

1432
Bile Leak Detection Technique
!" Radiopharmaceutical
!"Tc-99 Disofenin
!" Dose
!"5 mc
!" Image acquisition
!"Dynamic
#" 1 min/image x 33 x 64 x 64 word
matrix
!"Analog*
#" 750 k anterior images at 5 mins
#" Anterior images at 10, 20, 30 mins
#" Lateral image at 35 mins Figure 21 A & B
#" 3-hours delayed anterior image**
*All analog images are acquired for the time re-
quired to obtain the 750 K 5 min postinjection
image.
**If not obtained, sensitivity % by >50%.
Scintigraphic Patterns of Bile Leaks

!" B2W==.(0$#"6'/$/($#($0'/)$8'0()*+",-*",)(
the abnormal cavity
!" Tc-99m disofenin is located within the
parcolic gutters
!" Tc-99m disofenin is located within the
splenic bed
!" Tc-99m disofenin is encapsulated between Figure 22 A & B
loops of bowel or encapsulated in the
gallbladder fossa
Examples [Figures 19 to 22] Bile Leak Therapeutic/Prognostication

Patterns
Bile Flow Treatment
!" &Aberrant pathway Surgery
!" %Aberrant pathway Conservative
management
The Chronic Acalculous Disorders of the

Hepatobiliary Tree
Chronic Acalculous Biliary Disorders

Figure 19 A & B !" Chronic acalculous cholecystitis
!" The cystic duct syndrome
!" Gallbladder dyskinesia
!" Sphincter of oddi dyskinesia
Chronic Acalculous Biliary Disease

Imaging Modality Options
!" Imaging options
!"CCK cholescintigraphy
!"CCK biliary sonography
!" Optimal imaging modality
!"CCK biliary scintigraphy (tried and
true)
Figure 20 A & B

1433
The Chronic Acalculous Biliary Disorders The E.,-*'7+A Test to C".#%*+)?1+
Presence of a Chronic Acalculous
Disorder of the Hepatobiliary Tree
CCK Cholescintigraphy Procedure

Rational
!" Normal response to CCK
!"Gallbladder contraction (greater than
35%)
!"Sphincter of oddi relaxation
!"Increased bowel motility
!"Pyloric sphincter augmentation
!"Increased secretion of pancreatic
enzymes and enterokinase
!" Abnormal response to CCK
!"Reduced gallbladder contraction (less
than 35%)
!"Dilated common bile duct sign
Clinical/Laboratory Manifestations of
Chronic Acalculous Biliary Disorders E3#/'/!+"3+44Y+Cholescintigraphy in
!" Laboratory C".#%*,.-+)?1+Diagnosis of a Chronic
!"0 Acalculous Biliary Disorder
!" Clinical
!"Recurrent post prandial right E3#/'/!+"3+44Y+Cholescintigraphy in
Upper quadrant pain Detecting ABD
!"Biliary colic
#" Fatty food intolerance
#" Heartburn
#" Flatulence
#" Epigastric fullness
#" Upper abdominal discomfort
The Surgeon’s Gastroenterologist’s

Nightmare
Chronic Acalculous Biliary Disease

Treatment
E3#/'/!+"3+44Y+Cholescintigraphy in
Detecting ABD (Revisited)
“Cholecystokinin Cholescintigraphy - Is
it a Victim of its Own Success?”
Journal of Nuclear Medicine, 12/99.

1434
CCK Cholescintigraphy Editorial E3#/'/!+"3+44Y+Cholescintigraphy in
(Potential Recall) Alert Detecting A.B.D.
!" A change is occurring in the type
of patients referred for a CCK
cholescintigram, ie, “mimickers of ABD not
excluded”
!" CCK cholescintigraphy is being employed
3#(3(#2+''/$/-1(/")(2"/8+.3)"+A()'#)(6"+(
symptomatic ABD
!" To maintain CCK cholescintigraphies high
PPV in diagnosing ABD, a procedural
."0$823)$"/($#(+'l,$+'01($'1(3(^>W1(/")(^W1(
minute CCK infusion
Examples [Figures 23 to 26]
Figure 23
A to O
Figure 24
A to O

1435
Examples [Figure 25 & 26 ]
Figure 25 A & B
Figure 26 A & B
CCK Cholecystography Potential Pitfall

!" K)q#(,#'0(3#(3(#2+''/$/-()'#)1(/")(3(2"/8+.3)"+A()'#)
!"Loop(s) of bowel residing within the region of the gallbladder fossa

1436
Thyroid Cancer
Well-Differentiated Thyroid Cancers Clinical Manifestations

!" Papillary !" Asymptomatic nodule
!" Follicular !" 50% found serendipitously
!" Papillary/Follicular !" 50% noticed by patient
!" Hurthle Cell (variant of follicular thyroid
cancer) How Do We Find Out? [Figure 1]
Points of Information/Demographics Thyroid Cancer Diagnosis Algorithms

!" Uncommon; 17,000 new cases Dx 1998 Clinical Presentation Dx Algorithm
!" 14th Ranked cancer among malignancies !" Thyroid nodule Thyroid scan
of internal organs " " " " " " %
!" Peak incidence Cold/isointense
!"40 years (females) nodule
!"60 years (males) " " " " " " %
!" Lifetime risk of being diagnosed with Fine needle Bx
thyroid cancer
!"1%
#" .75% females
#" .25% males
!" Mortality
!"Greater in males if Dx @ or after 60
years of age
!" Thyroid cancer prevalence
!"Lower in African Americans
Incidence
!" Papillary 80%
!" Follicular 11%
!" Hurthle 3%
!" Medullary 4%
!" Anaplastic 2%
(1985-1995 31,513 Patients)
Figure 1
Prognosis
Type of Cancer 10-Year Survival
!" Papillary 93% The Treatment of Well-Differentiated
!" Follicular 85% Thyroid Cancer
!" Hurthle 76%
(National Cancer Data Base Pts = 53,856) Thyroid Cancer Therapy Surgery
Recurrence Rate + +
!" Rate I-131 ablation therapy T4 suppression
!"30% if therapy
#" Od^(8+#)(Z>WA'3+# Ablation Indications Present
#" 1/3 second 10-years
!" Increased rate I-131 Ablation Therapy Indicators
!"Age<20; >60 !" Age <15; >40 years
!" Tumor size > 1-1.5 cm
Recurrence Location
(>Size;>R/R-M/R)
Site Recurrence Rate
!" Cervical lymph node 74%
!" Thyroid bed 20%
!" Trachea/neck muscles 6%
!" Distant 21%
(60% Lungs 50% Mortality)
Thyroid Cancer Nuclear Radiology

1437
I-131 Ablation Therapy Indicators I-131 Ablation Therapy Dose and
!" Tumor histology Release Requirements/Recomendations
!"Pure follicular CA !" R/R
!"Papillary CA variant !";$6'#)A&'(l,3&$823)$"/#(.')
#" Tall cell !"K/-'#)()3+)(23/0Ad4,$0(
#" Columnar !"Vanilla ice cream
#" Follicular !"Arrange 7 day post-Tx total body
#" Diffuse sclerosing scan
!"Transformed (anaplastic) papillary CA !"Rx T4
!" Tumor aggressiveness !"Resume normal diet
!"Capsular/vascular invasion !" Rationale
!"METS !"D and R permitted
!" I-131 neck and chest scan !"Decrease parotid and submandibular
!"Iodine accumulating tissue present $/43.d)")3&(%"0A(+30$3)$"/
(M/R (10years) up to: 90% Coll; 25% Tall Cell; !"Decrease nausea
20% Foll) !" +/- mets
(R/R Foll Var up to 80%) - Up to 25% post-Tx scans
demonstrates tumor
I-131 Ablation Therapy Doses !"Correct iatrogenic hypothyroidism
Site of Iodine
Accumulating Tissue Dose/mCi Method to Prevent Xerostomia
!" Thyroid bed 100 - 150 !" EVOXACTM
!" Lymph nodes 150 - 175 !"(Cevimeline HCl)
!" Lung 175 - 200 #" Cholinergic agent that increases
!" Bone > 200 salivary production and thus
decreases salivary iodine residence
I-131 Neck and Chest Scan time
!" Dose 2-3 mCi (prevents #" Well tolerated
stunning) #" 30 mg three times per day for
!" I-131 uptake @ 24 hours 3 days prior to and after I-131
!" *Scan @ 48 hours Ablation Tx
*Follicular and agressive papillary cancer vari-
ants should undergo a neck and chest scan plus I-131 Postablation Therapy Lifetime
total body scan. Follow-up
!" Ablation Rx
I-131 Neck and Chest Scan Preparation !"1-Year follow-up neck/chest/total body
!" Thyroid Approximately 6 scan (-):Tg(-)
hormone/betadine weeks !"2-Year follow-Up neck/chest/total body
Depletion scan (-):Tg(-)
!" Serum TSH value > 40 uIU/ml !"5-Year follow-up neck/chest/total body
!" Low iodine diet Begin 7 days prior to scan (-):Tg(-)
I-131 adm !"Q 10-Year thereafter
!" Beta HCG Negative (within 48 (Annual Evaluation:TSH, FT4, Serrum tg, Neck
hours of adm. dose) Ultrasound)
(Increase Tg or Abn Neck US = N/C/TBS)
Pre I-131 Ablation Safety Work-up
Orders Rationale Thyroid Cancer Surveillance/
!" CBC Bone marrow adq. Therapeutic Controversial Issues/
!" C*'.(!+"8&'( ( E"+.3&(+'/3&((((((((((((((( Enigmas
Function !" Use of recombinant human TSH (rhTSH,
!" Urinalysis No bladder infection ThyrogenTM) vs endogenously stimulated
!" Chest X-ray No mets/trach shift TSH I-131 imaging
!" Beta HCG R/O pregnancy !" Treatment of patients with an elevated Tg
(within 48 hrs of Tx) but negative I-131 scan
!" TG Assay Baseline tumor
marker

1438
Thyroid Cancer Therapy Enigma Reimbursable/Medical Necessity
!" Enigma ThyrogenTM Criteria
!"I-131 WBS (-) !" Patients with renal failure in whom
!"Tg>10 ng/ml off T4 prolonged hypothyroidism will affect
or clearance of Na I-131 (GFR < 59 ml/
!"Tg>2/5 - 5.0 ng/ml after rh TSH adm min/1.73m2 or less)
!" Work-up/Rx !" Patients with an active psychiatric
!"All imaging modalities negative disorder (depression) that will be
exacerbated by hypothyroidism
%
!" National Kidney Foundation Stage 3 or
!"k100-150 mCi Na I-131, if Tg up to 10
greater (normal GFR > 90)
(>20)
!" Patients on medications with a narrow
Recombinant TSH (Thyrogen ) TM therapeutic index (Digoxin, Lithium,
!" A series of amino acids synthesized in Warfarin) for which clearance of
3(-'/')$23&&A(."0$8'0(*3.#)'+("53+A( medications may be impaired by
cell line whose properties are identical hypothyroidism
to human pituitary thyroid stimulating !" Patients whose overall performance status
hormone may be severely compromised during
hypothyroidism (ECOG performance
Recombinant TSH (ThyrogenTM) status > 2)
Properties !" Patients over 65 years of age regardless
!" Binds to TSH receptor sites on normal of the presence or absence of other
thyroid follicular cells and on well- concurrent medical conditions
differentiated thyroid cancer cells
ECOG Performance Status
!" Stimulates iodine uptake and
"+-3/$823)$"/1(#A/)*'#$#1(3/0(#'2+')$"/("6(
Tg, T4 and T3
!" Mean peak concentration:
!"3-24 hours post
!"Im injection
!"(Mean: 10 hours)
!" Elimination half life:
!"25 ± 10 hours
When Should it be Used? or When is it a

Covered B1.1#)6
Reimbursable ThyrogenTM Indications

!" Postop I-131
!"N/C/TBS
#" If contraindication to THW ie, there
is an increased risk of side effects/
complications from iatrogenic
hypothyroidism
!" Follow-up I-131 N/C/TBS in patients with
elevated Tg
!" Follow-up I-131 N/C/TBS in high-risk
thyroid cancer patients with non-
detectable Tg
!" Contraindication to THW or history of
#$-/$823/)(0$#)+'##(+'#,&)$/-(6+".(!+'5$",#(
THW
Criteria For High-Risk Thyroid Cancer

!" Macroscopic tumor invasion
!" Incomplete tumor resection
!" Distant metastases
!" Thyroglobulinemia out of proportion
to what is seen on the patients post-
treatment scan

1439
!" Postop or follow-up N/C / TBS
!"M/3%&'()"(!+"0,2'(#,682$'/)(
endogenous TSH post THW
!" Pituitary failure
!" & tumor burden
!" Thyroid remnant ablation therapy
!"No postop I-131 N/C / TBS, minimal
dose 100 mCi, post ablation Tx scan
2-10 days
!" Stimulated Tg assessment
!"History of non-Iodine avid tumor,
assess for persistent recurrent tumor
!" Preparation for PET scan
!"History of non-Iodine avid tumor, &Tg
Recombinant TSH (ThyrogenTM)

Diagnostic/Surveillance Imaging
Protocol
Weekday Procedure
Monday IM injection, 0.9 mg ThyrogenTM
Tuesday IM injection, 0.9 mg ThyrogenTM
Wednesday 4.0 mCi sodium I-131, orally
TSH determination
Thursday 24-hour I-131 uptake
Friday 48-hour I-131 scan Tg assay
Example of Thyroid Cancer [Figures 2 to 5]
Figure 4 A & B
Figure 2 A, B & C
Figure 4C
Figure 3 A & B

1440
R1/"*$,.'.)+JS;7+K)(+Role in Thyroid
Cancer Surveillance (The Bottom Line)
!" Second Post Ablation Therapy Follow-up
G23/1($6(8+#)(/'-3)$5'
!" Post Ablation Therapy Follow-up Scan,
if patient unable to tolerate THW
Hypothyroidism
I-131 Post Ablation Therapy Lifetime

Follow-Up
!" Ablation Rx
!"1-Year follow-up neck/chest/total body
scan (-):Tg (-)
scan (-):Tg (-)
scan (-):Tg (-)
!"10-Year follow-up neck/chest/total
body scan (-):Tg (-)
!"Q 10-Years thereafter
(Annual evaluation: TSH, FTI, Tg, serum CA,
chest X-Ray)

!" Postop I-131 N/C / TBS
!"If contraindication to THW N/C / TBS,
ie, secondary malignancy, frailty,
myasthenia gravis, mental disease
(depression), elderly (CHF, % renal/
function)
!" Follow-up I-131 N/C / TBS
!"k$#)"+A("6(#$-/$823/)(0$#)+'##(+'#,&)$/-(
from previous THW N/C / TBS and -Tg
value
Figure 5 A & B
Figure 5 C & D

1441
1442
Thyroid Imaging
Common Disorders of the Thyroid Gland Common Disorders of the Thyroid
Disorder Facts
Hyperthyroidism
- Plummer disease
Multinodular Autonomous function
vs superimposed Graves
disease on multinodular
goiter
Common Disorders of the Thyroid

Disorder Facts
Hyperthyroidism
- Hashitoxicosis Superimposed Graves
The Thyroid D1*!(),#15 disease

- T3 toxicosis Recurrent Graves, early
Common Disorders of the Thyroid hyperthyroidism
Disorder Facts
- T4 toxicosis Graves in “ill” individual
Hashimoto disease O+-3/$823)$"/(0'6'2)
Most frequent disorder Common Disorders of the Thyroid
of childhood and Disorder Facts
adolescence (peak 10-
Hyperthyroidism
11 years) and middle-aged
adults - Factitious toxicosis Iatrogenic/self imposed
Associated disorders: normal thyroglobulin
Graves disease (5%-10%) assay
Spectrum
Compensated "!#Decompensated
Disorder Facts
Common Disorders of The Thyroid Thyroiditis
Disorder Facts - Subacute Viral infection
Hyperthyroidism thyroiditis
- Graves disease Autoimmune disorder (Granulomatous, Self-limiting (6-12 weeks)
(Thyroid stimulating De Quervain)
immunoglobulin) & SED rate and serum thyro-
& Incidence in adulthood; globulin
Unusual in childhood
Less than 10 years - 10%
Disorder Facts
Greater than 15 years =
Thyroiditis
adulthood
- Autoimmune
Common Disorders of the Thyroid (lymphocytic)
Disorder Facts painless & antibodies
Hyperthyroidism postpartum & antibodies
- Plummer disease 7%-11% 4-6 weeks post-
Uninodular = 5% Solitary nodules delivery if in conjunction
(ATFA) with & AB
2.5 cm - 6 year FU = toxicity (8%)
3.0 cm - 6 year FU = toxicity (20%)
Thyroid Imaging Nuclear Radiology
1443
Disorder Facts
Silent thyroiditis Self limiting
& SED rate
Etiology unknown

Disorder Facts
Simple goiter Failing thyroid
“Colloid”
“Dyshormonogenesis,
( ( '/fA.3)$2(0'82$'/2Ai Figure 1
“Nodular” Adenoma vs. malignancy
Tc-99m Pertechnetate Thyroid Imaging
“The 20-Minute Diagnosis”
Rationale
Figure 2
How Do We Do This?
Method to Distinguish the Etiology of

Thyroid Disorders [Figures 1 to 4]
1. Visually calculate TcO4- trapping estimate

from a 5-6 minute–parallel hole image of the
thyroid and salivary glands.
2. Obtain a 20-minute–TcO4- pinhole thyroid

scan.
3. Categorize the individual into “hyper, Figure 3

hypo, or normal TcO4- trappers.”
4. Assess thyroid morphology

scintigraphically, ie, homogeneous vs
inhomogeneous distribution of radiotracer.
5. Establish tentative diagnosis(es).
6. Finalize diagnosis postclinical/biochemical Figure 4

evaluation(s).

1444
Clinical Applications of a Hypertrapping Clinical Applications of a Hypotrapping
Functional Estimate Functional Estimate
Clinical Applications of a Hypotrapping

Functional Estimate
Clinical Applications of a Hypertrapping
Functional Estimate
Examples [Figure 6]
E>'*0&1(7+Hypertrapping Estimate/
Scan [Figure 5]
Figure 6 A & B
Clinical Applications of a Normal

Functional Estimate
Figure 5 A & B

1445
Clinical Applications of a Normal I-131 Therapy (Hyperthyroidism)
Functional Estimate
Thyroid Therapy
Etiology Treatment
Factitious/Iatrogenic Dc T4/% T4
Hyperthyroidism
Subacute/silent Tincture of time
Thyroiditis Tylenol if needed,
No steroids if possible,
Beta blocker (PRN)
E>'*0&1(7+Normal [Figure 7]
Postpartum thyroiditis Beta blocker
Thyroid Therapy
Disease Tx
Hypothyroidism T4
Euthyroid with goiter T]($6(j(]>(-.#(
Can You Do It?.... Doctor, Name That

Disorder
Diagnosis [Figure 9]
Figure 7 A & B
E>'*0&1(7+GLO+c+ILO+F;+Images
[Figure 8]
Figure 9
Figure 8 A & B
Autonomously Functioning Thyroid

Tissue Therapy
Tx Options Recommendations
I-131 +
Surgery Cold nodule/FNA (+)
Antithyroid T+$3&(H#.3&&(-&3/0(z(O>?J
Medication Remission
I-131 + PTU Elderly, heart disease,
or tapazole or exquisitely HT emic

1446
Therapy? [Figures 10 to 12] Diagnosis [Figure 13]
Figure 13 A & B Age: 15
Diagnosis/Treatment [Figures 14 & 15]
Figure 10
Figure 14 A & B Age: 91 Atrial Fib
Figure 11
Figure 12
Figure 15 A & B

1447
Trapping Estimate/Diagnosis? [Figure 16] Diagnosis [Figure 19]
!" TSH < 0.03 uIU/ml
Figure 19 A & B
Figure 16
Next Step? [Figure 20]

Diagnosis/Treatment [Figure 17]
Figure 20 A & B
Figure 17
Now What? [Figure 18] Diagnosis? [Figure 21]
Figure 21 A & B
Figure 18

1448
Diagnosis? [Figure 22] Surgery? [Figure 25]
Figure 22 A & B
Figure 25 A & B
Surgery vs I-131 Therapy [Figure 23] Optimal Imaging [Figure 26]
Figure 23 A & B
What is It? [Figure 24]
Figure 26 A, B & C
Figure 24

1449
1450
R9/&1'%+I'5,"&"-!7+S1*,.'%+[
Interesting Cases
What Is It? [Figure 1]
Figure 1
A to O
Should This Patient Be Cathed? [Figure 2]
Figure 2
A to VV
Seminar 1 Nuclear Radiology

1451
Cath? [Figure 3]
Figure 3
A to DD
Cath? [Figure 4]
Figure 4
A to U
What Happened? [Figure 5]
Figure 5
A to HHH

1452
ACS/Agent? [Figure 6]
Figure 6 A to R
Preoperatve Risk S)%'),#/'),".++Study
SPECT Rest/Stress MPI [Figure 7]
Figure 7 A & B

1453
Surgery?
PET Rest/Stress PET MPI [Figure 8]
Figure 8 A to TTT
SPECT Imaging - Is It Worth While?
Diagnosis? [Figures 9 & 10] Diagnosis?

!" 15 min post RT ADM !" 2 hr post RT ADM
Figure 9 Figure 10

1454
Diagnosis? [Figure 11] Diagnosis? [Figure 12]
!" 15 min post RT ADM !" 2 hr post RT ADM
Figure 11 Figure 12
A, B & C A, B & C
What’s Wrong? [Figure 13]
Figure 13
A to AA
The Cause? [Figure 14]
Figure 14
A to N

1455
To Treat or not to Treat? [Figure 15]
!" Y90 Zevalin yes or no? !" Y90 Zevalin? !" Y90 Zevalin TX?
Figure 15 A, B & C
To Treat or Not to Treat? [Figure 16]
Figure 16 A to E

1456
Y-90 Intra-Arterial Brachytherapy [Figure 17]
Figure 17 A to J
Pre Lasix Diuresis Renal Scan

[Figure 18]
Figure 18 A to AA

1457
Post Lasix Diuresis Renal Scan [Figure 19]
Figure 19 A to AA
Diagnosis [Figure 20] Surgery? [Figures 22 to 25]
Figure 20 Figure 22
Surgery or Medical Management
Surgery or Medical TX [Figure 21]
Figure 21
Figure 23

1458
Diagnosis? [Figure 26]
Figure 26
Figure 24
?WBC Image/Diagnosis [Figure 27]
Figure 27
?WBC Image/Diagnosis [Figure 28]
Figure 28
Figure 25 A & B

1459
Damage Control? [Figure 29]
Figure 29
Tc RBC Scan? [Figures 30 & 31]
Figure 30 A to F
Surgery, Radiation, Both? [Figure 32]
Figure 32
Figure 31 A & B

1460
RAO Chest? [Figure 33] Diagnosis [Figure 35]
Figure 33
Figure 35
???? [Figure 34]
Figure 34 A to F

1461
DX? [Figures 36 & 37]
Figure 36 A & B
Figure 37 A to G
MET/Fracture? [Figure 38]
Figure 38 A & B

1462
Figure 39 A to J
Foot Pain in 9 Year-Old Child [Figure 40] Next Test? [Figure 41]
Figure 40
Figure 41 A to I

1463
Fever Of Unknown Etiology
[Figures 42 to 43]
Figure 42 Figure 44
IN 111 WBC SCAN DIAGNOSIS? [Figure 45]
Figure 45 A & B
Figure 43
Figure 46
A to E

1464
? Periprosthetic Infection [Figure 47]
Figure 47 A, B & C
Exchange Arthroplasty? [Figure 48]
Figure 48 A, B & C
Infection [Figure 49]
Figure 49 A, B & C
Headache Etiology? [Figures 50 & 51]
Figure 50
A&B

1465
Figure 51 A & B
Etiology of Dementia [Figures 52 & 53]
Figure 52 A to R
Figure 53 A to L

1466
Recurrent Abdominal Pain Why?
[Figure 54]
Figure 54
A, B, C
& D
Bariatric Risk S)%'),#/'),".a+,1+++++++++++++

No Event Postop
Surgery Yes/No? [Figure 55]
Figure 55 A to V V

1467
1468

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Radiologic

Leonard M. Glassman, MD, FACR, FAIUM

Grant E. Lattin Jr., MD, Maj, MC, USAF

Rachel B. Lewis, LCDR, MC, USN

Mark D. Murphey, MD Illustrators

Alice B. Smith, Lt. Col., MC, USAF

© Copyright 2011 by the American Institute for Radiologic Pathology.

Made in the United States of America

Library of Congress Cataloging-in-Publication Data [in process]

Breast Radiology Mark J. Kransdorf, MD, FACR

Angela M. Pansera, DO, Maj, USAF, MC Michael E. Mulligan, MD

Donald J. Flemming, MD Mark E. Schweitzer MD

Patricia A. Hudgins, MD, FACR

Kelly K. Koeller, MD, FACR

Erin Simon Schwartz, MD

Wendy R. K. Smoker, MS, MD, FACR

Leonard M. Glassman, MD, FACR, FAIUM

Jennifer A. Harvey, MD, FACR

Angela M. Pansera, DO, Maj, MC, USAF

Mark J. Kransdorf, MD, FACR

Thomas Lee Pope Jr., MD, FACR

Mark E. Schweitzer, MD/William B. Morrison, MD

Alice Boyd Smith, MD, Lt. Col., MC, USAF

Patricia A. Hudgins, MD, FACR

Kelly K. Koeller, MD, FACR

Erin Simon Schwartz, MD

Leonard M. Glassman, MD, FACR

Cancer has Two Predominant Signs

What You Need to Remember

Rad Path Correlation – What You Need

Rad Path Correlation – What You Need

Pathologic Basis of Breast Imaging Breast Radiology

Pathologic Basis of Breast Imaging Breast Radiology

Fibroepithelial Lesions Horizontally

Pathologic Basis of Breast Imaging Breast Radiology

Left Image: Benign phyllodes tumor.

Invasive Ductal Cancer [Figures 13 & 14]

Pathologic Basis of Breast Imaging Breast Radiology

Types of Invasive Ductal Carcinoma

Types of Invasive Ductal Carcinoma

Pathologic Basis of Breast Imaging Breast Radiology

Pathologic Basis of Breast Imaging Breast Radiology

Spindle Cell Sarcoma [Figure 22]

Pathologic Basis of Breast Imaging Breast Radiology

Pathologic Basis of Breast Imaging Breast Radiology

Leonard M. Glassman, MD, FACR

Breast Disease in Men and Young Women 753 Breast Radiology

Nodular Glandular Pattern [Figure 2]

Breast Disease in Men and Young Women 754 Breast Radiology

Male Breast Cancer

Male Breast Cancer

Breast Disease in Men and Young Women 755 Breast Radiology

Presenting Signs and Symptoms

Diagnosis in Young Women

Breast Disease in Men and Young Women 756 Breast Radiology

Less Common Benign Lesions

Breast Disease in Men and Young Women 757 Breast Radiology

Granular Cell Tumor [Figure 12]

Juvenile Papillomatosis [Figure 14]

Top Image: Circumscribed granular cell tumor.

Breast Disease in Men and Young Women 758 Breast Radiology

Breast Disease in Men and Young Women 759 Breast Radiology

Angiosarcoma [Figure 20]