The parasellar region: Normal Anatomic and Pathologic

Appearances
Poster No.:

C-0661

Congress:

ECR 2015

Type:

Educational Exhibit

Authors:

I. Mezhoud, S. Majdoub, A. Messoud, H. Zaghouani, M. Limeme,

D. Bakir, C. Kraeim; Sousse/TN

Keywords:

CNS, Head and neck, Neuroradiology brain, CT, MR, Diagnostic

procedure, Aneurysms, Hemangioma, Neoplasia

DOI:

10.1594/ecr2015/C-0661

Any information contained in this pdf file is automatically generated from digital material
submitted to EPOS by third parties in the form of scientific presentations. References
to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in
any way constitute or imply ECR's endorsement, sponsorship or recommendation of the
third party, information, product or service. ECR is not responsible for the content of
these pages and does not make any representations regarding the content or accuracy
of material in this file.
As per copyright regulations, any unauthorised use of the material or parts thereof as
well as commercial reproduction or multiple distribution by any traditional or electronically
based reproduction/publication method ist strictly prohibited.
You agree to defend, indemnify, and hold ECR harmless from and against any and all
claims, damages, costs, and expenses, including attorneys' fees, arising from or related
to your use of these pages.
Please note: Links to movies, ppt slideshows and any other multimedia files are not
available in the pdf version of presentations.
www.myESR.org

Page 1 of 20

Learning objectives
Normal 0 21 false false false FR X-NONE AR-SA
1/To review the complex anatomic, relationship between structures in the parasellar
regions.
2/To understand the main patterns and radiological characterization, mainly by MR, of
the lesion that alter the structures of parasellar region.

Background
Normal 0 21 false false false FR X-NONE AR-SA
The parasellar region is an anatomically complex area that represents a critical
junction for important contiguous structures. A wide range of neoplastic, inflammatory,
infectious, developmental and vascular diseases may embroil vital structures in this
region.
The most frequently involved are the brain parenchyma, meninges, the optic pathways
and cranial oculomotor nerves (III, IV, VI) and the V1 and V2 branches of the trigeminal
nerve, major blood vessels, hypothalamo-pituitary system, tuber cinereum, and bone
compartments. Presently MR is the method of choice for diagnosis and characterization
of this disease[1].

Findings and procedure details

Normal 0 21 false false false FR X-NONE AR-SA
The cavernous sinus (CS) contains vital neurovascular structures that may be affected
by vascular, neoplastic, infective, and infiltrative lesions arising in the CS proper or via
extension from adjacent intra- and extracranial regions. Patients with CS syndrome
usually present with paresis of 1 or more cranial nerves (III_VI), which may be associated
with
painful ophthalmoplegia. The clinician needs to know the type of CS lesion, its relationship
to crucial neurovascular structures,and its extension into the surrounding tissues.

Page 2 of 20

MR is enormously valuable, in the study of parasellar region, CT or nuclear studies can

also provide relevant information.

Normal Anatomy
The parasellar region is considered a cranial area around the sella turcica.The anatomical
definition of the parasellar region, includes all the structures that border the sella turcica.
The parasellar region includes, laterally, the dural walls of the cavernous sinus

The relationships of the cavernous sinus are: inferiorly with the basisphenoid and
sphenoid sinus, superiorly and above the diaphragm sellae, with the suprasellar
subarachnoid spaces containing the optic nerves and chiasm, the polygon of Willis,
hypothalamus, tuber cinereum and anterior third ventricle. The gasserian ganglion region,
though it is not anatomically related to the sellar region, can be considered as a parasellar
structure. Nasopharynx and the medial aspects of the temporal lobes are closely related
to the parasellar region, and pathological processes in this region can be disclosed by
symptoms related to intrinsic parasellar structures[3].

Fig. 1: A Coronal schematic drawing of the parasellar region with reference to the
main structures found in this area.
References: farhat hached - Sousse/TN

Page 3 of 20

Pathologic Conditions
Pathological conditions that affect the parasellar region can arise from the pituitary
gland, meninges, vessels, cranial nerves and nasopharynx. Pathological processes are
represented by primary and secondary neoplasms, inflammatory/granulomatous and
vascular lesions[3].

Fig. 2
References: farhat hached - Sousse/TN

Imaging Protocol
CT Scan : CT better delineates primary or secondary bony changes and intralesional or
perilesional calcifications and still represents a quite good approach for the detection and
characterization of lesions.CT Angiography can be used to evaluate the cavernous part
of the internal carotid arteries.

Page 4 of 20

MRI : provides detailed information about the contents of the para-sellar regions. Multiplanar views are possible and the different MR sequences help to reach accurate
diagnosis in case of diagnostic delimma. Post-gadolinium enhanced MR sequences
obtained with fat suppression are helpful to obtain contrast between pathology and
surrounding structures.
Current MRI protocols for the correct imaging of the sellar and parasellar regions are
based on sagittal and coronal T1-weighted images (T1WIs) without and with contrast
enhancement. Other pulse sequences generating T2-weighted, FLAIR and FE images
are complementary for characterisation of some specific processes. Magnetic resonance
(MR) spectroscopy is rarely used in this region.
Digital subtraction angiography is helpful for vascular lesions and tumoral vascularisation
for therapeutical Planning [3].

I.Vascular Lesions :
Carotid Cavernous Fistula Fig. 3 on page 9 Fig. 4 on page 10
Carotid
:
cavernous fistula (CCF) is an abnormal connection between the carotid arterial system
and the CS, which may be classified into 4 types. Direct CCF (type A) is a high-flow
communication between the ICA and the CS that occurs after trauma or secondary to a
ruptured aneurysm of the cavernous ICA. These lesions present acutely with pulsating
exophthalmos, chemosis, and CS syndrome. Dural CCFs (types B_D) are low-flow
fistulas occurring between meningeal branches of the carotid artery and CS, which tend
to have milder symptoms than direct fistulas. MR imaging findings of CCFs include a
dilated CS with multiple signal-intensity void structures that are associated with proptosis
and an enlarged superior ophthalmic vein. Ongradient-echo images, these flow voids
shows high signal intensity. The presence of flow related enhancement in the CS on MR
angiography suggests the diagnosis in the right clinical setting [4].
Normal 0 21 false false false FR X-NONE AR-SA
Anevrysms :Cavernous carotid anevrysms may produce CS syndrome by virtue of mass
effect, inflammation, or rupture into the CS, with subsequent development of a CCF.
Most are idiopathic, but they may occasionally be traumatic or mycotic in nature. A patent
aneurysm shows signal-intensity void on spin-echo MR imaging sequences[5].

Thrombosis Fig. 5 on page 11 CS

: thrombosis may be secondary to infection of the
sinonasal cavities, orbits, and/or the middle third of the face. MR imaging signs of CS
thrombosis include changes in signal intensity and/or in the size and contour of the CS.

Page 5 of 20

Indirect signs that help to suggest the diagnosis are dilation of the superior ophthalmic
veins, exophthalmos, and increased dural enhancement along the lateral border of CS
and ipsilateral tentorium[6].

II. Neoplastic Lesions

Adenomas Fig. 6 on page 12 :Large adenomas are the most frequent tumours
involving the cavernous sinus [7]. The extent of the adenomas invading or infiltrating the
cavernous sinus is an important feature, to be diagnosed or excluded by imaging studies
in order to define not only the way to approach surgically, but also to show whether the
tumour can be completely or partially removed [3].

Meningiomas Fig. 7 on page 13 : represent, after adenomas, the most frequent

intracranial tumours, a great majority of them localized in the surroundings of the sella
turcica, arising from the tuberculum sellae, jugum sphenoidal, floor of the frontal fossa,
greater and lesser wing of the sphenoid or in the dural wall of the cavernous sinus.
Meningiomas are generally isointense with cortical grey matter on T1- and T2-weighted
images and enhances intensely. A dural tail frequently can be seen extending away from
the edge of the tumor and often into the ipsilateral tentorium[8] .

Cavernous Hemangioma: CS hemangioma is more commonly seen during the fifth

decade of life in female patients. This tumor is formed by sinusoidal spaces with
endothelial lining that contain slow-flowing or stagnant blood. A preoperative diagnosis
is important because of its propensity to bleed at the time of resection. These tumors are
nearly hyperintense on T1- and T2-weighted images and are attached to the outer wall
of the CS, and their diagnosis may be suggested when they show progressive "filling in"
after contrast administration[9].

Schwannomas: infiltrating or invading the cavernous sinus come from the trigeminal
nerve and affect its cisternal portion, the ganglion or one of its terminal branches.
They can be found isolated or in the context of NF-1. Schwannomas are isointenseto-hypointense masses on T1 images, mostly T2 hyperintense, and show contrast
enhancement. They may havean appearance very similar to meningiomas[10].
Chordoma and chondrosarcoma: are rare neoplasms developing within the clivus [11]
and affecting the parasellar region. Although pathologically distinct, they have similar
imaging features. Chordomas are slow-growing neoplasms developed from notocord
Page 6 of 20

remnants, while chondrosarcomas are malignant bone tumours whose cells produce
hyaline cartilage. Both lesions have prolonged T1 and T2 relaxation times and enhance
intensely by contrast media. CT is very useful for demonstrating the structure and bone
destruction as well as the pattern of intratumoral calcifications.
Differential diagnosis has to be made with infiltrative adenomas as well as metastases
from lung, breast or prostatic carcinomas, which affect the sphenoid sinus and clivus[3].
Metastases :Metastases to the CS can be hematogenous or perineural in nature. Distant
tumors with hematogenous spread to the CS are generally renal, gastric, thyroid, lung,
and breast cancers. MR imaging shows CS enlargement, outward bowing of its lateral
wall, and replacement of the Meckel cave with soft tissue that homogeneously enhances.
Perineural tumor spread is commonly seen along branches of cranial nerve V. Perineural
spread is most commonly seen with adenoid cystic or squamous cell carcinoma but
may also be seen with lymphoma, melanoma, basal cell carcinoma, rhabdomyosarcoma,
neurogenic tumors, and juvenile angiofibroma. MR imaging features of perineural tumor
spread include nerve enlargement and enhancement and foraminal enlargement and
destruction [12].

Lymphoma and Leukemia Fig. 8 on page 14As

: with metastases, lymphoma and
leukemia reach the CS by direct extension from a primary lesion or from hematogenous
spread. MR imaging may show infiltrative lesions of the skull base invading the CS without
arterial narrowing[13] Normal 0 21 false false false FR X-NONE AR-SA

Nasopharyngeal Carcinoma Nasopharyngeal carcinoma is the most common primary

malignant extracranial neoplasm to invade the CS. Intracranial extension may occur
directly via the skull base erosion or by perineural spread along branches of the trigeminal
nerve . Tumor can extend through the petro-occipital synchondrosis and foramen lacerum
into the inferior CS or via the carotid canal to gain access to the CS without destroying
bone.
Once the CS is invaded, bulky masses are present in the nasopharynx. The tumor is
generally hypointense to isointense (relative to muscles) on T1-weighted images and T2
hypointense and shows moderate-to-intense contrast enhancement[14].

Other tumors:Case reports described a lot of other tumors arising

in the parasellar region:hemangioblastomas [15], hemangiopericytomas[16],
fibrosarcomas[17], rhabdomyosarcomas of the sphenoid sinus[18], solitary fibrous
tumors [19]

Page 7 of 20

III. Inflammatory, Infectious, and Granulomatous Lesions :

Tolosa-Hunt Syndrome:Tolosa-Hunt syndrome is a term applied to a retro-orbital
pseudotumor extending to the CS. Its clinical triad includes unilateral ophthalmoplegia,
cranial nerve palsies, and a dramatic response to systemic corticosteroids. The process
is usually unilateral but may be bilateral. MRI shows a mild asymmetry of the affected
sinus, together with an asymmetric hypersignal on proton density (PD) images and some
degree of narrowing of the intracavernous carotid artery[20].

Tuberculous Pachymeningitis :Tuberculosis is, in some parts of the world, a relatively

common cause of pachymeningitis that produces diffuse or focal extra-axial masses
along the surfaces of the CS[21].
Sarcoidosis Fig. 10 on page 16 :Dural involvement can occur with sarcoidosis
and extend to the CS. The presence of multiple dural-based lesions, pachymeningitis
or leptomeningeal enhancement, thickened cranial nerves, thickened hypothalamus,
multiple scattered brain lesions, and periventricular multifocal white matter lesions should
raise the possibility of the diagnosis of sarcoidosis[21].

Wegener Granulomatosis:Wegener granulomatosis is a rare disorder of unknown

etiology associated with necrotizing granulomas in the paranasal sinuses, nasal cavities,
and/or orbits. CS involvement is rare. MR imaging shows meningeal thickening and
enhancement that may extend to the CS[22].

Images for this section:

Page 8 of 20

Fig. 1: A Coronal schematic drawing of the parasellar region with reference to the main
structures found in this area.

Fig. 2

Page 9 of 20

Fig. 3: Contrast-enhanced computed tomography, arterial phase. Female 73- year-old

patient with diagnosis of Direct Carotid Cavernous Fistula. Early contrast enhancement
shows proptosis and an enlarged superior left ophthalmic vein. Orbital Doppler
ultrasonog-raphy: Exuberant shows blood flow at color Doppler study and is arterialized
at spectral Doppler study

Page 10 of 20

Fig. 4: Female 45-year-old patient with a diagnosis of Dural Carotid cavernous fistula

Page 11 of 20

Fig. 5: CS thrombosis. Coronal postcontrast T1-weighted image shows an enlarged and

inhomogeneous-appearing left CS that contains areas of low signal intensity compatible
with clot.

Page 12 of 20

Fig. 6: Large adenomas tumours involving the cavernous sinus. Coronal T1,T2
and postcontrast T1-weighted image shows a large inhomogeneous-appearing mass
involving the CS, sella, supra-sellar region.

Page 13 of 20

Fig. 7: Meningiomas. T1 and T1 post contrast weighted image shows a meningioma that
is isoattenuated to white matter with homogeneously enhancing involving the left CS.

Page 14 of 20

Fig. 8: Lymphoma:Coronal T1 ,T2 and postcontrast T1-weighted image shows diffuse

enlargement and enhancement of the CS.

Page 15 of 20

Fig. 9: nasopharyngeal fibroma involving the CS

Page 16 of 20

Fig. 10: hypothalamic pituitary SARCOIDOSIS

Page 17 of 20

Conclusion
Normal 0 21 false false false FR X-NONE AR-SA
Profound understanding and knowledge of the anatomy, clinical dysfunctions and all
possible pathological processes that may arise in the parasellar region are necessary to
diagnose correctly the pathological processes . MRI is the modality of choice to assess
the complete information needed for patient management

Personal information
References

1. Boardman JF, Rothfus WE, Dulai HS. Lesions and pseudolesions of the cavernous
sinus and petrous apex. Otolaryngol Clin North Am 2008;41:195-213.
2. Gallioud P, Ruiz D, Muster M, et al Angiographic anatomy of laterocavernous
sinus(2000). Am J Neuroradiol 21:1923-29.
3. J. Ruscalleda .Imaging of parasellar lesions. Eur Radiol (2005) 15: 549-59.
4. Hirai T, Korogi Y, Hamatake S, et al. Three-dimensional FISP imaging in the evaluation
of carotid cavernous fistula: comparison with contrast enhanced CT and spin-echo MR.
AJNR Am J Neuroradiol 1998;19:253-59
5. Rubinstein D, Sandberg EJ, Breeze RE, et al. T2-weighted three-dimensional turbo
spin-echo MR of intracranial aneurysms. AJNR Am J Neuroradiol 1997;18:1939-43
6. Schuknecht B, Simmen D, Yuksel C, et al. Tributary venosinus occlusion and septic
cavernous thrombosis: CT and MR findings. AJNR Am J Neuroradiol 1998;19:617-26
7. Cottier J, Destrieux C, Brunereau J, et al (2000) Cavernous sinus invasion by pituitary
adenoma: MR imaging.
Radiology 215:463-469

Page 18 of 20

8. Hirsch WL, Sekhar LN, Lanzino G, et al. Meningiomas involving the cavernous
sinus: value of imaging for predicting surgical complications. AJRAmJ Roentgenol
1993;60:1083-88
9.Jinhu Y, Jianping D, Xin L, et al. Dynamic enhancement features of cavernous sinus
cavernous hemangiomas on conventional contrast-enhancedMRimaging. AJNR Am J
Neuroradiol 2008;29:577-81
10. Weber A, Motandon C, Robson C. Neurogenic tumors of the neck. Radiol Clin North
Am 2000;39:1077-90
11. Oot RF, Melville GE, New PFJ, et al (1988) The role of MR and CT in valuating clival
chordomas and chondrosarcomas. Am J Nueroradiol 9:715-723
12. Caldemeyer K, Mathews V, Righi P, et al. Imaging features and clinical significance of
perineural spread or extension of head and neck tumors. Radiograhics 1998;18:97-110
13. Heisman T, Tschirch F, Schneider J, et al. Burkitt's lymphoma with bilateral cavernous
sinus and mediastinal involvement in a child. Pediatr Radiol 2003;33:719-21
14. Chong VF, Khoo JB, Fan YF. Imaging of the nasopharynx and skull base.
Neuroimaging Clin N Am 2004;14:695-719
15. Rumboldt Z, Gnjidic Z, Talan-Hranilovic J, & Vrkljan M. (2003). Intrasellar
hemangioblastoma: characteristic prominent vessels on MR imaging. AJR American
Journal of Roentgenology, Vol. 180, pp. 1480-1481.
16. Jalali R, Srinivas C, Nadkarni TD, & Rajasekharan P. (2008). Suprasellar
haemangiopericytoma - challenges in diagnosis and treatment. Acta Neurochirurgica,
Vol. 150, pp. 67-71.
17. Lopes MB, Lanzino G, Cloft HJ, Winston DC, Vance ML, & Laws Jr ER. (1998).
Primary fibrosarcoma of the sella unrelated to previous radiation therapy. Modern
Pathology,Vol. 11, pp. 579-84.

Page 19 of 20

18. Jalalah S, Kovacs K, Horvath E, Couldwell W, Weiss MH, & Ezrin C.

(1987).Rhabdomyosarcoma in the region of the sella turcica. Acta Neurochirurgica, Vol.
88, pp. 142-146.
19. Furlanetto TW, Faria Pitta Pinheiro C, Oppitz PP, de Alencastro LC, & Asa SL. (2009).
Solitary Fibrous Tumor of the Sella Mimicking Pituitary Adenoma: An Uncommon Tumor
in a Rare Location-A Case Report. Endocrine Pathology Vol. 20, pp. 56-61.
20. Cakirer S (2003) MRI findings in the patients with the presumptive clinical diagnosis
of Tolosa-Hunt syndrome.
Eur Radiol 13(1):17-28

21. Wilson JD, Castillo M. Magnetic resonance imaging of granulomatous inflammations:

sarcoidosis and tuberculosis. Top Magn Reson Imaging 1994;6:32-40
22. Provenzale JM, Allen NB. Wegener granulomatosis: CT and MR findings. AJNR Am
J Neuroradiol 1996;17:785-92

Page 20 of 20