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Imaging modalities
Simple radiography
USG:
NEUROSONOGRAPHY
NICU
Assist in diagnosis:
PVL; ICH;
hydrocephalous
etc
Monitor
complications and
interventions:
ventriculoperitone
al shunts
Hypodense lesions
Hyperdense
1. Infarct
2. Non-haemorrhagic
contusion
3. Tumours
4. Edema
5. Metabolic
encephalopathy
6. Hypertensive
encephalopathy
7. Encephalitis
8. Lipoma
1.
2.
3.
Intracranial calcifications
Infection (TORCH)
Tumors
1. lymphoma
2. medulloblastoma
3. meningioma
4. metatasis
a. mucin-producing
adenocarcinoma
b.
hemorrhagic metatasis:
breast/lung; melanoma/RCC
choriocarcinoma
4.
5.
6.
7.
Cysts: Colloid
Endocrinal:
hypoparathyroidism
Neurocutaneous syndromes
Arteriovenous lesions
Metastasis
Abscess
Glioblastoma
Infarction
Contusion
Demylinating disease
Radiation necrosis
INTRACRANIAL
CALCIFICATIONS
Normal intracranial calcificationscan be
defined as all age-related physiologic and
neurodegenerative calcifications that are
unaccompanied by any evidence of disease and
have no demonstrable pathological cause.
PINEAL GLAND: 60% adult; >14mm: neoplasm
HABENULA: 30%
CHOROID PLEXUS: 10%
BASAL GANGLIA
DURA
PETROCLINOID LIGAMENTS
SSS
CRANIOCEREBRAL
TRAUMA
Secondary injury:
These are consequences of primary
injuries
Frequently more devastating than the
primary injury
Primary injuries:
Skull #, scalp hematoma/ lacerations
Extracerebral hemorrhage
Epidural hemorrhage
Subdural hemorrhage
Subarachnoid hemorrhage
Intraaxial lesions:
Secondary lesions:
Cerebral herniations
Traumatic ischemia, infarction
Diffuse cerebral edema
Hemorrhages
Imaging Strategy
Imaging of acute head trauma is performed
to detect treatable lesions before secondary
neurologic damage occurs.
Currently, this is best performed by CT for
several reasons:
it is quick & widely available
Highly accurate in the detection of acute intraaxial and extra-axial hemorrhage, as well as
skull, temporal bone, facial, and orbital fractures.
Monitoring equipment is easily accommodated.
Skull Fractures:
Types:
Linear #
Depressed #; ping-pong/pond fracture
(newborn)
Comminuted #
Compound #
Growing #: (leptomeningeal cyst)
Can involve:
Cranial vault
Base of the skull
Sutural diastases
Epidural hematoma
1-4% pt imaged for craviocerebral trauma
Etiology- # that lacerates MMA or dural venous sinus
Location:
Between skull & dura (biconvex shape)
Temporoparietal region commonest site
95% unilateral
Do not cross suture
Secondary herniation common
Imaging :
Biconvex extra-axial collection
May be heterogeneous due to hyperdense blood
and hypodense serum or due to active bleeding
Chronic- Peripheral enhancement representing
dura and membrane formation between
hematoma & adjacent brain parenchyma.
Subdural Hematoma
Most lethal of all head injuries
Mortality rates upto 50-85%
Stretching and tearing of bridging cortical veins
as they cross sd space common
disruption of penetrating branches of superficial
cerebral arteries less common
Location:
Tumor bleeding
Mycotic aneurysm
Cortical thrombosis
Dural AV fistula
Arterial Dissection
Hydrocephalus
Denotes an increase in the volume of CSF
and thus of the cerebral ventricles.
Obstructive and non-obstructive (on
the grounds of whether or not there is
obstruction of CSF pathways in the
ventricles or in the subarachnoid space)
Communicating and noncommunicating (addressing where
theobstructionis located).
Obstructive hydrocephalus
passage of CSF within the ventricular system or in the
subarachnoid space isimpaired at some point
communicating obstructive hydrocephalus
passage of CSF from the ventricular system and into the
subarachnoid space is unimpeded butabsorption of CFS via
arachnoid granulations is impaired
subarachnoid haemorrhageormeningitis
extra-axial CSF spaces (e.g. Sylvian fissures and sulci) are also
distended
Non-obstructive hydrocephalus
often referred to asex-vacuo
dilatation of the ventricles
CSF can pass out of the ventricles and
into the basal cisterns without
impediment, and is readily absorbed
ventricles are enlarged due to loss of
adjacent brain parenchyma
Characteristics of
Hydrocephalus
Ventricular enlargement disproportionate to the
degree of sulcal widening
Enlargement of temporal horns
Periventricular fluid secondary to
transependymal CSF permeation
Enlarged 3rd ventricle (outward bowing of the
lateral wall) with large suprapineal and
chiasmatic receses and inferior bowing of the
floor
In children < 2 years the head circumference is
often the best distinguishing feature between
hydrocephalus and atrophy.
MEASUREMENTS
Frontal horns (Monro):
<40 yrs= <12mm
>40 yrs=<15
Ventriculohemispheric ratio:
<33% in adults
<40% in children
Third ventricle
<5mm: children
<7mm: <60yrs
<9mm:>60yrs
Hydrocephalic
Brain
Normal CT Brain
Colloid cyst
STROKE
On CT 60% of
infarcts are seen
within 3-6 hrs and
virtually all are
seen in 24 hours.
ADV: Hge stroke
(MRI confusing)
MRI- Diffusion
restriction (DWI)
with reduced ADC
has been observed
as early as 30
minutes after the
onset of ischemia.
Imaging protocal
Nonenhanced scanning must be performed as
soon as possible after the stroke is suspected.
and the key role of nonenhanced CT is the
detection of hemorrhage or other possible
mimics of stroke (eg,neoplasm, arteriovenous
malformation).
CT Findings in Infarction
Hyperacute: <12 hrs
Normal 50-60%
Hyperdense artery (dense MCA sign)
Obscuration of the lenticular nucleus
loss of gray-white interfaces (insular ribbon sign
Axial unenhanced CT
images in a proximal
segment of the left MCA
in a 53-year-old man (a)
and a distal segment of
the left MCA in a 62year-old woman (b),
obtained 2 hours after
the onset of right
hemiparesis and aphasia,
show areas of
hyperattenuation (arrow)
suggestive of intravascular
thrombi
Axial unenhanced CT
image obtained in a 53year-old man shows
hypoattenuation and
obscuration of the left
lentiform nucleus (arrows),
which, because of acute
ischemia in the
lenticulostriate distribution,
appears abnormal in
comparison with the right
lentiform nucleus
Axial unenhanced CT
image, obtained in a 73year-old woman 212 hours
after the onset of left
hemiparesis, shows
hypoattenuation and
obscuration of the posterior
part of the right lentiform
nucleus (white arrow) and
a loss of gray matterwhite
matter definition in the
lateral margins of the right
insula (black arrows).The
latter feature is known as
the insular ribbon sign.
Drawings (top) illustrate the territories(blue) of the ACA, middle cerebral artery (MCA)
, and posterior cerebral artery. CT scans (bottom) show established infarctions of
these arteries
CVA
Intracerebral
hematoma
basal nuclei
region with
mass effect
INFECTIONS
CMV
DNA virus
Most common cong. CNS infection
(also cause cardiac anomalies, hepatosplenomegaly)
Predilection for periventricular subependymal germinal matrix
Widespread periventricular tissue necrosis and subsequent
dystrophic calcification.
Plain film microephaly with egg shell- like periventricular
calcification
US/CT/MRI encephaloclastic lesions, periventricular ca++,
subependymal paraventicular cyst, ventriculomegaly
MRI- delayed myelination, encephalomalacia, migrational
disorder (lissencephaly, polymicrogyria, pachygyria)
TOXOPLASMOSIS
MENINGITIS
Role of CT in meningitis
toidentify contraindicationsof a lumbar puncture
to identify complicationsthatrequire prompt
neurosurgical interventions such assymptomatic
hydrocephalus, subdural empyema, and cerebral abscess.
CT scans may reveal the cause of meningeal infection.
Otorhinologic structures and congenital and posttraumatic
calvarial defects can also be evaluated
CT cisternography may depict CSF leaks, which may be the source
of infection in cases of recurrent meningitis
Contrast-enhanced CT scans
Meningeal & ependymal enhancement
Help in detecting complications of meningitis, such as
subdural empyema
Venous thrombosis, infarction
Cerebritis/abscess
Ventriculitis.
Bilateral subdural
empyema in a patient
with bacterial meningitis.
This computed
tomography scan
demonstrates the
important diagnostic
features of meningitis:
prominent enhancement
of the margin and
increased attenuation of
the empyema.
CNS tuberculosis
Hematogenous dissemination usually from pulmonary
infection
Meningitis- most common manifestation
Parenchymal lesions
Caseating granuloma
Usually solitary, multiple in 1/3
Cortical, subcortical, basal ganglia lesions. Cerebellum in
children
Tubercular abscess
indistinguishable from caseating granuloma/ pyogenic
abscess
thinner & smoother wall
multiloculated
larger(>3cm)
surrounding edema is less than that in pyogenic abscess
Parasitic infections
NCC
Echinococcosis
Amebiasis
Paragonimiasis
Spargonimiasis
Malaria
Neurocysticercosis
Larval form of T. solium
Most common CNS parasite
location
Brain parenchyma- corticomedullary junction
Intraventricular in 20-50% cases
Subarachnoid space
NCC
Brain tumors
Classification by histology
A)Glial tumors-
Astrocytomas
Oligodendroglioma
Ependymal
Choroid plexus tumors-CPP/CPC
E) Embryonal tumorsneuroblastoma
retinoblastoma
PNETS
F) Hematopoetic tumorslymphoma
leukaemia
plasmacytoma
G) Pitutary tumors
H) Cyst and tumor like lesions
BRAIN TUMOURS
Most common
GLIOMA/NEUROGLIAL
Tumours
Glial cells: 5-10X (trillion) neurons
Among Primary brain tumours :
approx are glioma
Among glioma: > are astrocytoma
Glioblastoma multiforme
Most common and malignant of all
primary intracranial tumours ( 50%
astrocytomas)
Rapidly enlarging malignant
astrocytic tumor characterized by
necrosis and neovascularity
Common in older age >50yrs; Rare
below 30yrs
Location:
o Supratentorial white matter most
common
Frontal, temporal, parietal lobes
Occipital lobes relatively spared
o Cerebral hemispheres> brainstem >
cerebellum
o Brainstem, cerebellum - common in
children
Worst prognosis
CT: Marked
intratumoral
heterogenicity with
central low density
region (s/o necrosis or
cyst form) is present in
95% of all GBM
Hemorrhage & peripheral
oedema (Fingers of
edema) is common
Enhancement is strong &
inhomogenous with thick
irregular rim
enhancement
MR: T1 shows poorly
delineated mixed signal
mass with necrosis or cyst
formation with marked
inhomogenous
enhancement
T2 shows heterogenous
mass with mixed signal,
central hemorrhage &
necrosis
Spread of GBM:
signal abnormalities!
Common
Along compact white matter tracts- corona
radiata, corticospinal tracts, corpus callosum
(Butterfly glioma) and hippocampal
commissures
Around ventricular ependyma
Into leptomeninges
CSF seeding of subarachnoid space
Uncommon
Dural invasion
Rare
Extracerebral metastasis
SPINE
SPINE
D/D: Collapsed vertebra
1. Vascular: hemangioma, ABC
2. Infective
3. Neoplastic:
1. Metastatic
2. MM/Plasmocytoma
4.
5.
6.
7.
Drug/metabolic: osteoporosis
LCH
Traumatic
Pagets
Tubercular spine
common in NEPAL
RADIOLOGY
Plain radiography
signs :
Reduced disc space
Blurred paradiscal
margins
Destruction of bodies
Loss of trabecular
pattern
Increased
Prevertebral soft
tissue shadow
Subluxation/dislocatio
n
Decreased Lordosis/
kyphosis
Tuberculous
Spondylitis
Pyogenic
Spondylitis
Onset
Insidious/ chronic
Acute
Progress
Slow
Rapid
Site
Thoraco-lumbar
Lower lumbar
X ray changes
At presentation
Bone sclerosis
Lack sclerosis
Present
Periosteal reaction
Little or absent
Present
Multifocal
involvement
Multiple contiguous
vertebrae
Two or one
Disc involvement
Late
Early
Posterior element
inv
More frequent
Less
Subligamentous
spread
common
+/-
Paraspinal mass
Large
Small
Calcification
Hallmark
Rare
Spinal deformity
Common (kyphosis)
Not so
Spinal tuberculosis
A destructive bone
lesion associated with
a poorly defined
vertebral body
endplate, with or
without a loss of disk
height.
Better prognosis
Metastatic tumor
A destructive bone
lesion associated with a
well preserved disk
spaces with sharp end
plates s/o neoplastic
infiltrates.
Bad prognosis
Vertebral Metastasis
General Information
Metastatic disease is the most common
tumor affecting the spinal column.
Approximately 70% of all spinal tumors
are metastatic in nature.
Primary carcinoma of the prostate,
breast, lung, thyroid gland or intestinal
tract.
Vertebral Metastases of C5
Conventional Radiographs
Conventional radiography is relatively insensitive to bone
metastases.
50% destruction of the bone mineral content is necessary
for detection, thus it is not apparent on conventional
radiographs the early stages of disease.
As a rule, lesions need to be 2 cm to be detected.
Conventional radiography is still the preferred imaging
method to determine behavior (i.e.) sclerotic, osteolytic or
mixed.
Osteolytic metastases can mimic:
o OA, Subchondral cysts or Schmorl nodes of the spine
Sclerotic metastases of L2
Common signs of spinal
metastases found on
conventional radiographs
include:
Destruction of the
pedicle
Associated soft-tissue
mass
MRI
Imaging method of choice for evaluating
suspected metastatic spinal pathology.
Apparent diffusion coefficient (ADC)
values calculated from diffusion-weighted
MR images is a reliable factor to
distinguish vertebral metastases
from normal vertebrae.
MRI can also help detect metastatic
lesions before changes in bone
metabolism make the lesions detectable
on bone scintiscans
Criteria
Infection
Tumour
No & pattern of
vertebral involve
At least 2 around
affected disc
Portion of
vertebral involve
Mostly
endplates; post
elements relatively
spared
Disc involvement
Yes
Marrow signal
T1 low, T2 high,
normal diffusion
Epidural
component
Granulation tissue;
extends several
levels above &
below