Magnetic Resonance Imaging of Sellar and Suprasellar Pathology: A Pictorial Review

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Magnetic Resonance Imaging of Sellar andSuprasellar Pathology: A Pictorial Review

Jyoti Kumar, MD, DNB, Atin Kumar, MD, DNB, Raju Sharma, MD,
and Sushma Vashisht, MD
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he sellar and suprasellar locations contain a variety oftructures with complex anatomic relationships. A diverseroup of pathologic processes can occur here. Magneticesonance (MR) imaging is the modality of choice forvaluating this region. We discuss and illustrate theseesions and discuss the MR imaging features that are helpfuln formulating an appropriate differential diagnosis.

he sellar and suprasellar locations contain a varietyf structures with complex anatomic relationships. Aiverse group of pathologic processes can occur in thisegion including developmental, infectious/inflamma-ory, vascular pathology, and neoplasms. Neoplasmsre the most common among the group of pathologicrocesses. Due to the complex anatomy of this regionnd small size of the pituitary gland, magnetic reso-ance (MR) imaging is the modality of choice for thisegion. We present MR imaging characteristics andifferential diagnoses of common and some rare le-ions at this location.

echniquehin-section T1-weighted images (3 mm or less) arebtained in the sagittal and coronal planes, before andfter intravenous contrast administration. Because ofifferential rates of contrast enhancement betweendenomas and normal pituitary gland, dynamic imag-ng is useful in detection of microadenomas. The usualose of gadolinium is 0.1 mmol/kg. Some authorsave also recommended the use of half the usual dose

rom the Department of Radiology, All India Institute of Medicalciences, New Delhi, India.eprint requests: Atin Kumar, MD, DNB, 175 Minakshi Garden, P.O.ilak Nagar, New Delhi 110018, India. E-mail: [email protected] Probl Diagn Radiol 2007;36:227-36.2007 Mosby, Inc. All rights reserved.

363-0188/2007/$32.00 � 0
aoi:10.1067/j.cpradiol.2007.04.004
urr Probl Diagn Radiol, November/December 2007

f contrast (0.05 mmol/kg) for the investigation ofituitary adenomas with comparable results.1 Occa-ionally, T2-weighted images, fat-suppressed images,uid-attenuated inversion recovery, constructive inter-erence in steady state, diffusion-weighted images,

R angiography, and spectroscopy may be used toiscriminate between certain lesions.

umors

ituitary AdenomasPituitary adenomas are the most common cause of

ellar mass in an adult. They are classified accordingo size and functional activity. Adenomas greater than0 mm are referred to as macroadenomas, while lesshan 10 mm are designated microadenomas. Approx-mately 75% adenomas are functional2 and, hence, aremall when they present clinically. Prolactin-secretingdenomas are the most common functioning adeno-as.2 Nonfunctioning adenomas are detected inciden-

ally or as a result of symptoms related to compressionf adjacent structures. Optic chiasmal compressionay result in visual field defect. Compression of the

hird ventricle/foramen of Monroe can cause hydro-ephalus. Parasellar invasion into the cavernous si-uses may result in cranial nerve palsies.

Macroadenomas (Fig 1) almost always cause sellarnlargement. Sellar wall erosion may also occur.ecrosis and hemorrhage can result in a variable

ppearance on imaging. Generally, they are isointenseo gray matter on T1WI and hyperintense on T2WI.ecrosis/cystic change is seen in 5 to 18% of mac-

oadenomas.3 Intratumoral hemorrhage occurs in 20 to0% of patients, which alters the signal intensity.4 Auid level is highly suggestive of hemorrhage. En-ancement is mild and inhomogenous. Differentiating
pituitary adenoma with central necrosis from pitu-
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tary abscess may be difficult. Adjacent meningealnhancement, if present, may aid in the differentiation.

The issue of cavernous invasion is also difficult ashe medial wall of the cavernous sinus is not wellelineated. The presence of abnormal tissue betweenhe lateral wall of the cavernous sinus and the cavern-us internal carotid artery is the most reliable imaginganifestation of invasion.5 A high serum prolactin

evel (1,000 ng/mL) also correlates well with cavern-us sinus invasion.4 However, luminal reduction ofnternal carotid artery is not a feature of macroadeno-as.Microadenomas (Fig 2) are best seen on coronal

mages as hypointense lesions relative to normalituitary on unenhanced T1WI. After contrast admin-stration, they are again hypointense due to theirifferential enhancement. Dynamic imaging afterapid contrast administration is particularly helpful indentification. They are best seen in the early phasehen a normal gland has relatively higher signal

ntensity. Peak enhancement of the adenoma occursetween 1 and 4 minutes when a normal gland mayegin to show reduced signal intensity.2

Focal abnormalities may be seen incidentally in theituitary gland. They may be due to several factors—symptomatic coincidental cysts, microadenomas, orrtifactual hypointensities. Incidental pituitary lesions2 mm are nearly always either pituitary adenomas or

IG 1. Pituitary macroadenoma. Coronal CE T1WI shows 8-shapedomogenously enhancing lesion arising from sella extending intouprasellar cistern and invading cavernous sinuses. Internal carotidrteries are encased but not constricted.

athke cleft cysts. Focal susceptibility artifacts are d

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ommon near the junction of the sphenoid sinuseptum and the sellar floor.6

eningiomasApproximately 15 to 25% of meningiomas (Fig 3)

ccur in the parasellar region.7 They can arise from thelanum sphenoidale, tuberculum, and dorsum sellae orrom the dural covering of the cavernous sinuses onither side. They are generally isointense to grayatter on T1WI. Fifty percent remain isointense on2WI; 40% are hyperintense.8 Calcification may beeen as hypointense foci on both T1W and T2Wequences. Homogenous enhancement, suprasellar ep-center with broad dural base, and dural enhancementdural tail) help in differentiating meningiomas fromdenomas.3 Cerebrospinal fluid (CSF) cleft may beeen between the pituitary gland and the tumor. Sellaurcica is only mildly enlarged as opposed to macroad-nomas. Meningiomas constrict the carotid lumen,nlike adenomas.4

raniopharyngiomasCraniopharyngiomas arise from squamous epithe-

ial cell remnants of Rathke’s pouch. They have aimodal age distribution. Two-thirds occur in child-ood and adolescence with a peak at 5 to 10 years; aecond smaller peak occurs in the fifth through seventh

IG 2. Pituitary microadenoma. Postcontrast coronal image shows aelatively nonenhancing focal lesion within the enhancing pituitaryland on the right side with superior bulging and stalk deviation toontralateral side.

ecades. Seventy percent are in the suprasellar and

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ellar regions; 20% are suprasellar and 10% are purelyntrasellar.9

Based on histopathology, they can be classified asdamantinomatous and squamous papillary type ofraniopharyngiomas.10 The adamantinomatous typeFig 4) are the most common variety. They areobulated, typically with cystic components, and 90%ave solid or rim calcification. Cystic areas are hyper-ntense on T1WI and T2WI in 33% of cases due toigh protein content or methemoglobin. The cysts maylso show signal isointensity to CSF.9 Solid portionsre hypo- to isointense on T1 and iso- to hyperintensen T2WI and enhanced moderately. Rim enhancementf the cystic component may be seen.

Squamous papillary craniopharyngiomas are moreommon in adults. They are solid and spherical aspposed to lobulated. They are less likely to havealcification and rarely recur after excision. MR ap-earance is nonspecific—isointense to gray matter on1WI and hyperintense on T2WI.10 Unlike macroad-nomas, the suprasellar component induces edemalong optic tracts.11

ypothalamic and Chiasmatic GliomasGliomas of the visual pathway are seen predomi-

antly in the first decade of life and account for 25 to0% of pediatric suprasellar neoplasms. Twenty to

IG 3. Meningioma. Contrast-enhanced sagittal T1WI shows intenseomogenously enhancing mass with a suprasellar epicenter. A duralail is also noted extending over planum sphenoidale.

fty percent of these patients have neurofibromatosis t


ype I.12 These patients present with visual loss,ydrocephalus, or hypothalamic dysfunction.

These tumors (Fig 5) are often quite large onresentation and may have areas of cystic degenera-ion. Contrast enhancement is seen in 50% of theseesions and is usually homogenous or occasionallyim-like.13 Differentiation of chiasmatic from hypo-halamic glioma is often difficult, depending mainlyn the epicenter of the lesion. These are seen as aypo- to isointense mass on T1WI with moderateyperintensity on proton density and T2WI. The tu-ors can spread along the optic tracts, anteriorly into

he optic nerve and posteriorly through the optic tractsnd optic radiations.

etastasesMetastatic tumor to the pituitary gland most com-

only arises from a breast or bronchogenic primarynd is present in approximately 3% of terminally illatients with carcinoma. However, it becomes symp-omatic in only 5 to 15% of these patients. It is usuallyrelatively small enhancing pituitary lesion with lackf sellar enlargement. A dumbbell morphology result-ng from invasion of diaphragma sella and invasionather than displacement of third ventricle are other

IG 4. Craniopharyngioma. Sagittal contrast-enhanced T1WI showsheterogeneous mass in the suprasellar cistern extending into the

ella. Inferiorly, it shows heterogeneous enhancement and, superiorly,here is a high signal intensity cyst consistent with proteinaceousontent.

ypical features.14,15

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Metastatic disease in the suprasellar region occurso the pituitary infundibulum or hypothalamus (Fig 6).he most common primary carcinomas responsible arereast and lung carcinoma, with hematogenouspread. Primary brain tumors with high propensityor CSF seeding (ependymoma, medulloblastoma,erminoma, pineoblastoma) may also spread to theuprasellar location. Leukemia and lymphoma may

IG 5. Hypothalamic glioma. Plain (A) and contrast-enhanced (Bypothalamus. The optic chiasm is displaced anteriorly.

IG 6. Metastases. Axial T1WI (A) in a follow-up case of carcinomahich represents metastasis. Also, note another focal metastatic lesionhancement of the suprasellar mass and the thickened infundibular s

lso spread to this region through leptomeninges. m

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uch metastases may be loculated and appear as aolid mass.9

thersOther lesions that may be seen in this location are

ermoids and epidermoids, germ cell tumors;athke’s cleft cysts, chordomas, schwannomas, and

ittal T1WI demonstrate a homogenously enhancing mass in the

shows a hemorrhagic mass lesion in the region of suprasellar cistern,the right eye globe. On post-contrast T1 coronal image (B), there is

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umor-like Conditionsrachnoid CystsArachnoid cysts account for 1% of all intracranial

asses and 9% occur in the suprasellar cistern. Rarely,hey may be seen in the intrasellar location. They areostly seen in infancy and in children under the age of

0 years.9

On MR, they are seen as smoothly marginated

IG 7. Arachnoid cyst. Axial T1 (A) and T2WI (B) show a well-define

IG 8. Hypothalamic hamartoma. Coronal postgadolinium T1WI (A) seviating the stalk to the left. MR spectroscopy (B) reveals myoinosito

asses with homogenous signal isointense to CSF on d


ll sequences (Fig 7). The optic chiasm is lifted andnteriorly displaced. Although usually indistinguish-ble from a Rathke’s cleft cyst with low proteinoncentration, they typically displace the anterior pi-uitary and infundibulum posteriorly rather than ante-iorly.16

ypothalamic HamartomaHypothalamic hamartomas (Fig 8) are composed of

mogenous lesion isointense to CSF.

a rounded nonenhancing mass lesion in the region of hypothalamus,k.

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isorganized heterotopic neural tissue.4 Patients

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resent mostly with isosexual central precocious pu-erty. Seizures, including the characteristic gelasticeizures, are another mode of presentation. These areessile or pedunculated nonneoplastic masses isoin-ense to gray matter on T1WI. They may be hyperin-ense on T2WI. Contrast enhancement, a differentiat-ng feature from gliomas, is usually not seen.17

omparison of proton MR spectra between hypotha-amic hamartomas and normal tissues reveals elevatedyoinositol.18

angerhans Cell HistiocytosisLangerhans cell histiocytosis (Fig 9) is mainly a

isease of childhood and may involve the hypothala-us or the pituitary stalk. Patients may present with

iabetes insipidus, as seen in Hand Schuller Christianisease.19

On MR, there is thickening of the pituitary stalkith intense contrast enhancement. The hypothalamusay also show soft-tissue mass, which enhances on

ontrast administration. The bright spot of the normaleurophysis is absent in patients with diabetes insipi-us. The lesion may be hyperintense on T2WI.9,19

nflammatory and Infectious Lesionsymphocytic Hypophysitis

Lymphocytic hypophysitis (Fig 10) is an inflamma-ory disorder of the pituitary gland which is probablyutoimmune in origin. It occurs primarily in women,articularly during pregnancy or the postpartum

IG 9. Langerhan cell histiocytosis. Sagittal T1W1 (A) shows soft-tissunhancement on postcontrast T1WI sagittal (B) and coronal (C) imarecontrast image (A).

eriod.20 At disease onset, the pituitary gland is a

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nlarged and edematous with lymphocytic infiltration.he mass effect on adjacent structures leads to head-che, visual field impairment, or diplopia. At thistage, subclinical hypopituitarism can be present butpontaneous remission can occur if the pituitary tissues not destroyed. In a subsequent stage, the pituitaryarenchyma, destroyed by the inflammatory process,s substituted with fibrous tissue, progressing some-imes to atrophy. At this stage, symptoms of partial oranhypopituitarism usually appear.21

The anterior lobe is diffusely enlarged, whichhows marked and homogenous enhancement withdjacent dural enhancement. The posterior pituitaryright spot is preserved. It frequently extends along thenfundibulum and does not enlarge the sella.22-24 Since aossible spontaneous remission can occur, a carefulollow-up may be done in subclinical patients withoutymptomatic mass effect or hypopituitarism. This entitylso shows good response to corticosteroid therapy.urgical removal of the expanding mass may be required

o decrease the pressure on adjacent structures.21

uberculosis

Tuberculosis (Fig 11) has a predilection for theasal cisterns and can present with leptomeningealnhancement in the suprasellar cistern. Enlargementnd enhancement of the pituitary stalk and mass-ike suprasellar lesions may be seen.4 Other brainesions and pulmonary tuberculosis may be associ-

ion in the region of hypothalamus, which shows intense homogenousNote also the absence of the posterior pituitary bright spot in the

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ted and help in the diagnosis.


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ascular and Ischemic Lesions

ituitary ApoplexyPituitary apoplexy is caused by sudden expansion

f the gland due to massive necrosis of tumor or

IG 10. Lymphocytic hypophysitis. Sagittal T1WI (A) shows a large hhis resolved on corticosteroid therapy (B).

IG 11. Tuberculosis. Axial (A) and coronal (B) contrast-enhanced T1uberculous meningitis. Exudates are also seen in bilateral CP angle c

emorrhage into tumor. This may be accompanied by o


poplectiform clinical event or may be asymptomatic inany cases. MR (Fig 12) reveals an enlarged sella

ontaining a macroadenoma or rarely other tumors likeathke’s cleft cyst. Signal characteristics depend on thege of the hemorrhage.25 Follow-up appearances may be

genously enhancing pituitary mass with involvement of infundibulum.

hows diffuse enhancement of the suprasellar cistern in a patient withs.

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f pituitary volume loss or a persistent cystic mass.

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neurysmsAneurysms of the sellar region mainly arise from

he cavernous or supraclinoid portions of the internalarotid artery. They present as eccentric sellar

IG 12. Pituitary apoplexy. Sagittal T1 (A) and T2WI (B) demonyperintensity on both T1 and T2 represent subacute hemorrhage.

IG 13. Aneurysm. Axial T1 (A) and T2WI (B) show a giant partially thhe sella.

asses.25 Suprasellar cistern aneurysms (Fig 13) arise r

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rom the anterior communicating artery, posteriorommunicating artery, or ophthalmic or supraclinoidnternal carotid artery. They may be detected inciden-ally or with subarachnoid hemorrhage. Giant aneu-

a sellar-based mass extending into suprasellar cistern. Areas of

osed aneurysm of the cavernous internal carotid artery projecting into

strate

romb

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resent with mass effect.9 Nonthrombosed aneurysmsith rapid flow are seen as signal void lesions arising

rom a normal-sized artery. Slow flow is seen as aeterogenous T1 signal. Lamellated thrombus of vari-ble signal intensity may be seen. Calcification, seens hypointensity, may be seen in the outer rim of theesion. MR angiography can detect most aneurysms.26

onventional angiography is required for treatment

IG 14. Empty sella. Sagittal (A) and coronal (B) T2WI show CSF fiisplaced inferiorly and the infundibulum is elongated.

IG 15. Ectopia of the posterior pituitary gland. T1-weighted coronahere is no bright spot in the posterior sella.

lanning. q


iscellaneous

mpty SellaEmpty sella is caused by incompetence of dia-

hragma sella, which allows CSF to pulsate throughn opening from the suprasellar cistern into the sella.t can also be postsurgical or secondary to ischemicecrosis of the pituitary gland as a delayed conse-

the sella, which is enlarged. The pituitary gland is thinned out and

nd sagittal (B) images show a high signal spot in the hypothalamus.

lling

l (A) a

uence of Sheehan’s syndrome. This may present

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ncidentally or with nonspecific symptoms. Patientsay also present with endocrine dysfunction, CSF

hinorrhea, or visual loss.25

On MR, sellar contents with same intensity as CSF areeen on all sequences. Infundibulum is seen in its normalocation but is elongated. It is seen extending from tuberinereum to the pituitary gland, which is flattened againsthe floor of the enlarged sella (Fig 14). With time, theella becomes larger without significant erosion of dor-um sella.4,16

ctopia of the Posterior Pituitaryland (EPP)The posterior lobe of pituitary gland is normally

ituated within the sella and is seen as a “bright spot”n sagittal T1WI of the sella. It is the presence ofntidiuretic hormone within neurosecretory vesicleshat is thought to be responsible for the T1 shorten-ng.9 EPP may be incidentally detected. It is seen in3% of patients with idiopathic growth hormoneeficiency.27 Pituitary or hypothalamic tumors, iatro-enic or traumatic stalk transection, sarcoidosis, andangerhans’ cell histiocytosis are disease entities thatay interrupt the normal transport of antidiuretic

ormone from the hypothalamus, resulting in ectopicosterior pituitary. MR (Fig 15) is the only study todentify EPP. Differential diagnoses include lipoma,ermoid, or teratoma, all of which may be hyperin-ense on T1WI.9

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7. Burton EM, Ball WS Jr, Crone K, et al. Hamartoma of thetuber cinereum: A comparison of MR and CT findings in fourcases. AJNR Am J Neuroradiol 1989;10:497-501.

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Documents

Magnetic Resonance Imaging of Sellar and Suprasellar Pathology: A Pictorial Review