nonadenomatous tumors of the pituitary and sella...

Nonadenomatous Tumors of the Pituitaryand Sella Turcica

Benjamin Y. Huang, MD, MPH, and Mauricio Castillo, MD, FACR

Abstract: While pituitary adenomas make up over 90% of all sellar

masses, there are a number of less known tumors, both malignant

and benign, which may arise within the sella turcica. These include

relatively common tumors such as meningiomas and craniophar-

yngiomas, as well as extremely rare tumors such as pituitary

astrocytomas and granular cell tumors. Unfortunately, many of these

tumors lack characteristic imaging features, often making it

extremely difficult to distinguish them by imaging alone from the

more common pituitary adenoma. In this article, we review several

nonadenomatous tumors of the sella, with a focus on their clinical

features and typical MR imaging characteristics.

Key Words: nonadenomatous tumors, pituitary

(Top Magn Reson Imaging 2005;16:289Y299)

A lthough pituitary adenomas are the most common sellartumors, accounting for more than 90% of sellar masses1

and 10% to 15% of all intracranial neoplasms,2 there are othertumors that arise in the sella turcica. These tumors arise fromnormal pituitary elements (craniopharyngiomas, pituitarycarcinomas, astrocytomas, and granular cell tumors) may beof nonpituitary origin (meningiomas, germ cell tumors, andlymphoma) or may be metastases.

Many of these nonadenomatous tumors lack specificimaging characteristics and are often indistinguishable fromadenomas by imaging alone. In many instances, a definitivediagnosis is made only postoperatively, and the finalhistological diagnosis is often unexpected. Despite this,there are imaging findings that may be helpful in suggestingthat a sellar lesion may not be an adenoma. In this article, wereview several nonadenomatous sellar tumors and theirimaging characteristics (Table 1).

CRANIOPHARYNGIOMASCraniopharyngiomas are common, benign neoplasms,

accounting for 2% to 5% of all intracranial tumors.2,3 Theyhave a bimodal age distribution with a primary peak between5 and 14 years and a second smaller peak somewhere betweenthe fifth and seventh decades. Approximately two thirds occurin individuals younger than 20 years.4,5 Craniopharyngiomas

account for 5.6% to 13% of intracranial tumors in childrenand are 10 to 20 times more common than adenomas in thispopulation.3,6 The incidence does not vary by race or sex.4

Craniopharyngiomas are derived from squamous cellrests in the remnant of Rathke pouch between the adenohy-pophysis and neurohypophysis and can occur anywhere alongthe path of the craniopharyngeal duct, from the nasopharynxto the third ventricle.3,6,7 Most craniopharyngiomas have asuprasellar component, with only 4% to 25% being purelyintrasellar.3,5,8 Two subtypes of craniopharyngioma havebeen described: the adamantinomatous type, which ispredominantly a tumor of children and adolescents butwhich can be seen at any age, and the papillary type, which isseen almost exclusively in adults.9

Patients commonly present with nonendocrine symp-toms, including headache, nausea, vomiting, and symptomsrelated to compression of the optic chiasm.6 Endocrinedysfunction is less common and may be manifested inchildren as growth disturbances.2,3,6 Up to 80% of childrenwith craniopharyngiomas have endocrine dysfunction atdiagnosis, with 75% demonstrating growth hormone defi-ciency.10 Patients may present with hypopituitarism, hyper-prolactinemia, or diabetes insipidus (DI).3 Treatment usuallyconsists of surgical resection with or without adjuvantradiotherapy, based on whether gross total resection isachieved. Recurrence is rare after gross total resection.With subtotal resection, only 47% of patients are recurrence-free at 5 years, and only 38% are recurrence-free at 10 years.3

On magnetic resonance imaging (MRI), craniophar-yngiomas can appear cystic, solid, or both.2,3 Cysts are seenin 85% of craniopharyngiomas.11 Predominantly solid tumorsare 2 times more likely to be seen in adults than in children,whereas predominantly cystic tumors are seen in childrenroughly 50% of the time and less frequently in adults.3 Cystscontain variable amounts of cholesterol, keratin, protein,methemoglobin, and necrotic debris, which accounts for theirvariable appearance on MRI.12 Cystic components aretypically hyperintense, and less commonly isointense, tocerebrospinal fluid (CSF) on T1-weighted images.2 Fluid-debris levels can be seen within the cysts. Solid componentshave variable signal intensities, and they usually enhanceafter gadolinium administration.2,13

Calcification is typical of craniopharyngiomas and ispresent in approximately two thirds of all cases; tumorcalcification is seen in approximately 90% of childhoodcraniopharyngiomas and in 50% to 70% of adult craniophar-yngiomas.2,7,14 Calcification is rare in papillary-type cranio-pharyngiomas.9 Computed tomography is the preferredmodality for detecting calcification.13

REVIEW ARTICLE

Top Magn Reson Imaging & Volume 16, Number 4, July 2005 289

From the Department of Radiology, University of North Carolina at ChapelHill, NC.

Reprints: M. Castillo, MD, FACR, CB no. 7510, Department of Radiology,University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7510(e-mail: [email protected]).

Copyright * 2005 by Lippincott Williams & Wilkins

Copyr ight © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Solid craniopharyngiomas can be difficult to distinguishfrom adenomas. However, the apparent diffusion coefficientof craniopharyngiomas is higher than that of adenomas onaverage49 (Fig. 1).

RATHKE CLEFT CYSTSRathke cleft cysts, like solid craniopharyngiomas, occur

along the craniopharyngeal duct and are felt to arise whenthere is incomplete obliteration of the central embryonic cleftseparating the anterior lobe of the pituitary from the parsintermedia. Rathke cleft cysts are differentiated from cranio-pharyngiomas by having single-layered walls of columnar orcuboidal epithelium, often containing ciliated and gobletcells.2,15 They are common lesions and usually asymptomatic,reported incidentally in up to 33% of autopsy cases. Rathkecleft cysts are 2 to 3 times more common in females than inmales.2,16 They can be seen at any age but, when symptomatic,usually present between 40 and 60 years of age.2

Symptoms are more likely to be present when the cystsare large enough to cause mass effect on adjacent structures

and are similar to symptoms observed with other sellar andsuprasellar masses.16,36 Rathke cleft cysts range in size from afew millimeters to very large, in excess of 4.5 cm.15Y17 Whensymptomatic, cysts can be treated with partial removal or cystaspiration, with a low rate of recurrence.

The primary imaging differential diagnosis is a cysticcraniopharyngioma. As with craniopharyngiomas, signalintensities of the fluid in Rathke cleft cysts can be variable onMRI, reflecting the heterogeneous composition of the fluid,which ranges from serous to mucinous.2,15Y17 The cysts areusually of higher T1 signal intensity than CSF, with themajority being isointense to hyperintense to white matter,probably reflecting the proteinaceous nature of the cystfluid.16,17 On T2-weighted imaging, Rathke cleft cysts demon-strate variable signal intensity; with high protein concentra-tions, there may be low signal intensity on T2-weighted images.In contradistinction to the cysts of craniopharyngiomas, Rathkecleft cysts usually demonstrate thin and uniform walls, andenhancement of the walls is uncommon.2,16,17 Enhancement ofthe walls of a Rathke cleft cyst may reflect inflammation orinfection. Wall calcification is uncommon.2

One group reported the presence of T1 hyperintense, T2hypointense, nonenhancing intracystic nodules in 10 of 13patients with pathologically confirmed Rathke cleft cysts,corresponding to waxy, solid, intracystic masses intraopera-tively, probably representing concretions of desquamatedcellular debris.18 They suggest that these nodules can bedistinguished from soft tissue nodules seen in craniopharyngio-mas by their signal intensities and lack of enhancement (Fig. 2).

PITUITARY CARCINOMAPituitary carcinomas are extremely rare tumors, with

fewer than 150 cases reported.19 They are tumors of theadenohypophysis that undergo discontinuous craniospinal orsystemic spread.19,20 In patients with pituitary carcinoma,

TABLE 1. Nonadenomatous Tumors of the Sella Turcica

Tumors of pituitaryorigin

Craniopharyngioma/Rathke cleft cyst

Pituitary carcinoma

Astrocytoma (pilocytic or pituicytoma)

Granular cell tumor

Gangliocytoma and MGA

Nonpituitary origin Meningioma

Germ cell tumors

Primary CNS lymphoma

Dermoid/epidermoid

Schwannoma

Metastases (breast and lung cancers most common)

FIGURE 1. Craniopharyngioma. Coronal T2-weighted (A), unenhanced (B) and enhanced (C) coronal T1-weighted, andenhanced sagittal T1-weighted MR images through the sella turcica demonstrate a multiloculated, mixed cystic, and solidsuprasellar mass. The walls of the mass enhance, and there are solid enhancing nodules (arrows) in the right anterolateral aspect ofthe tumor (C). In this case, the mass is entirely suprasellar and can be easily distinguished from the normally enhancing pituitarygland.

Huang and Castillo Top Magn Reson Imaging & Volume 16, Number 4, July 2005

290 * 2005 Lippincott Williams & Wilkins


47% have only systemic metastases, 40% have craniospinalmetastases, and 13% have both.20 Common sites ofhematogenous spread are the liver and bone; less commonreported sites include the lungs, lymph nodes, ovaries, heart,pancreas, and myometrium.19,21 Craniospinal metastasesusually involve the cortex, cerebellum, and cerebellopontineangles.19

The pathogenesis of pituitary carcinomas is not under-stood. It is likely that most develop secondary to transforma-tion of an existing pituitary adenoma rather than develop denovo.21 Most pituitary carcinomas are initially diagnosed asinvasive macroadenomas, and there is generally a latencyperiod of 5 to 10 years before finding metastases.19,21

Histologically, there are no reliable criteria for distinguishingadenomas from pituitary carcinomas.20 A diagnosis of

pituitary carcinoma cannot be made without evidence ofdistant spread.

There is no sex predilection, and pituitary carcinomascan be seen in adults of any age (mean, 44 years).19,21

Approximately 75% of pituitary carcinomas are endocrino-logically active; most are prolactin or adrenocorticotropichormoneYproducing tumors.20Y22

Clinical features of pituitary carcinoma are similar tothose of invasive adenomas, with symptoms due to masseffect on surrounding structures or to the excessive hormoneproduction.19,21,22 A common clinical presentation is earlyrecurrence of tumor after resection, followed by a prolongedcourse of repeated surgeries for local recurrences, beforemetastatic disease.22 Once metastases are detected, the meansurvival time is 4 years; survival varies with endocrinologic

FIGURE 2. Rathke cleft cyst. Unenhanced sagittal (A) and coronal (B) T1-weighted, and enhanced coronal T1-weighted (C) MRimages demonstrate a well-circumscribed, nonenhancing, hyperintense intrasellar lesion, which displaces the normally enhancingadenohypophysis superiorly (arrows). Enhanced sagittal T1-weighted MR image in a different patient (D) shows a thin enhancingrim; note that the contents of the cyst are hyperintense to CSF and isointense to hyperintense relative to adjacent brain parenchyma.

FIGURE 3. Pituitary carcinoma. Unenhanced sagittal T1-weighted (A) and enhanced coronal T1-weighted (B) MR imagesdemonstrate a bilobed sellar and suprasellar mass with heterogeneous enhancement. Note the circumferential Bwaisting^ thatoccurs at the level of the diaphragma sella (arrows), which is commonly seen in pituitary macroadenomas. This mass isradiographically indistinguishable from an adenoma.

Top Magn Reson Imaging & Volume 16, Number 4, July 2005 Tumors of the Pituitary and Sella Turcica

* 2005 Lippincott Williams & Wilkins 291


tumor subtypes, with adrenocorticotropic hormoneYprodu-cing tumors having the worst prognosis.19 Patients with onlycentral nervous system (CNS) involvement seem to havelonger survival than those with systemic metastases.19

From a neuroimaging standpoint, distant spread is theonly feature which distinguishes pituitary carcinomas fromadenomas. With regard to the primary sellar tumor,carcinomas cannot be differentiated from invasive macro-adenomas.19,21 Like macroadenomas, pituitary carcinomasappear as enhancing sellar masses with suprasellar/parasellarextension and invasion of the cavernous sinus or bone. Themetastases of pituitary carcinoma are indistinguishable frommetastases of other carcinomas21 (Figs. 3 and 4).

PITUITARY ASTROCYTOMASAstrocytomas arising from the pituitary gland are rare

and arise from the neurohypophysis. Astrocytomas of thepilocytic type have been reported.23 In addition, there havebeen several reports of low-grade neurohypophyseal glialtumors, histologically distinct from pilocytic astrocytomas,which have been referred to as pituicytomas.24Y29 Someconfusion in terminology has arisen as some authors haveused the term pituicytoma to encompass all astrocytomasarising from the gland, whereas others consider thepituicytoma to be a distinct entity.

The neurohypophysis contains specialized glial cellsreferred to as Bpituicytes.^ Five different types of pituicyteshave been described,30 with most pituicytomas arising frommajor and dark cell types.31 Pituicytomas are differentiatedfrom pilocytic astrocytomas by having plump, spindle-shapedcells with a slightly fibrillar cytoplasm and by lack of Rosenthalfibers, microcysts, and granular bodies found commonly inpilocytic astrocytomas.24

Pituicytomas are seen from the third to ninth decades inpatients with a mean age of 40 years.24,28 There is a malepredominance.24,25,28 Pituicytomas may be entirely intrasel-lar or suprasellar or involve both compartments. Clinicalpresentation is similar to that of other sellar and suprasellarmasses, with the most common presenting complaint beinghypopituitarism, followed by visual disturbances.28 Despitethe neurohypophyseal origin of these tumors, DI is not acommon presenting symptom.25,28 Total resection is usuallycurative.25

Pituicytomas and pituitary pilocytic astrocytomas areindistinguishable from one another radiographically and, ingeneral, cannot be distinguished from other neurohypophy-seal tumors. Diagnosis of pituitary astrocytoma can only bemade pathologically. For the sake of simplicity, we refer topituitary tumors of glial origin as pituitary astrocytomas.

MRI features of pituitary astrocytomas are nonspecificand are those of a solid, circumscribed, enhancing sellar orsuprasellar mass, usually isointense to gray matter on T1-weighted and hyperintense on T2-weighted sequences.24,31,29

Anterior displacement of the normally enhancing adenohy-pophysis by the tumor may suggest that it is of neurohypo-physeal origin.24 A pituitary astrocytoma containing solid andcystic components has been reported, but the presence ofcysts is an uncommon feature.24

GRANULAR CELL TUMORSGranular cell tumors are rare and benign tumors of the

neurohypophysis and have also been referred to as choristo-mas, myoblastomas, and infundibulomas. They arise fromgranular cellYtype pituicytes,31 but structurally identical

FIGURE 4. Pituitary carcinoma metastases. Enhanced sagittal(A) and axial (B) T1-weighted MR images demonstrateenhancing extraaxial, dural-basedmasses (arrows). The patienthad undergone resection of a prolactinoma in the past. Biopsyof 1 of these lesions revealed metastatic prolactinoma.




tumors have been described elsewhere in the CNS.32 They arethe most common primary tumor of the neurohypophysis33

and are seen in up to 17% of nonselected adult autopsies.34

The tumors are twice as common in females than in males.32

Granular cell tumors are usually asymptomatic but,when symptomatic, usually present in the fifth decade.32,35 Aswith other nonfunctional pituitary tumors, symptoms areprimarily related to size and mass effect. Tumors are usuallyvery large when discovered.32,35 Approximately 90% ofsymptomatic patients have visual complaints, and 50% haveclinical or laboratory signs of hypopituitarism or hyperpro-lactinemia.32 Headache is a common complaint. Treatmentfor symptomatic granular cell tumors is surgical; post-operative radiation is controversial but appears to increasemean survival time and time to recurrence after surgery.32,37

The imaging appearance of granular cell tumors isnonspecific, with an enhancing sellar or suprasellar mass seenon MRI. Eleven percent of symptomatic granular cell tumorsare intrasellar, 42% are suprasellar, and 47% involve bothcompartments.32 The masses are isointense to gray matter onboth T1- and T2-weighted sequences.32,37,35 Intense enhance-ment may be seen and reflects the high vascularity of thesetumors. Calcifications may be present. Absence of the normalpituitary bright spot may be a clue that the tumor is ofneurohypophyseal origin, but this finding is nonspecific, asthe posterior pituitary bright spot may be absent in 10% to20% of normal subjects38 (Fig. 5).

GANGLIOCYTOMASAlthough the pituitary gland does not contain neurons,

a small number of reports of pituitary tumors composed atleast partly of ganglion cells can be found in the literature.These tumors are referred to as gangliocytomas. The exacthistogenesis of these tumors is debated, with some authorssuggesting that they arise from embryonal pituitary cell reststhat have features between neurons and adenohypophysealcells and others suggesting a common hypothalamic origin.39

The tumors are found in adults and are more common infemales.40

Although these tumors may consist exclusively ofganglion cells, the majority (65%Y76%) of gangliocytomasare found in association with adenomas.39Y41 Because of this,some suggest the name, mixed gangliocytoma-adenoma(MGA).42 Approximately 75% of patients with pituitarygangliocytomas demonstrate pituitary hormone hypersecretion,with oversecretion of growth hormone being the most commonmanifestation, followed by Cushing disease.40,41 Interestingly,the MGAs are more likely to be hormonally active than the puregangliocytomas.40 In addition to the endocrine abnormalitiesseen with MGAs, visual changes and headaches can alsooccur.39

On MRI, intrasellar gangliocytomas and MGAs maynot be distinguishable from pituitary macroadenomas andappear as an enhancing sellar and suprasellar mass. Somehave noted that the suprasellar portion of an MGA tends to bemore spherical than macroadenomas and that they do notdemonstrate the waist at the level of the diaphragma sella thatmacroadenomas do42 (Fig. 6).

MENINGIOMASMeningiomas can originate from any dural surface,

including the tuberculum sella, olfactory groove, sphenoidwing, diaphragma sella, and sella turcica.2 They account forapproximately 20% of all intracranial neoplasms; are tumorsof adults, increasing in incidence with increasing age (peakincidence, 60Y70 years); and are 2 times more common infemales.2,43 Whereas 10% to 15% of meningiomas arise inthe parasellar region, purely intrasellar meningiomas arerare.2,44 The majority of intrasellar meningiomas arise fromthe undersurface of the diaphragma sella, but meningiomasoriginating from the floor or walls of the sella have beenreported.44

FIGURE 5. Granular cell tumor. Unenhanced (A) andenhanced (B) coronal T1-weighted MR images through thepituitary demonstrate a well-circumscribed, enhancing nodulearising from the pituitary stalk.




Meningiomas are benign, slow-growing tumors. Intra-sellar meningiomas may mimic nonfunctioning adenomas intheir clinical presentation, with primary symptoms beingheadache, visual disturbances, visual field defects, andendocrinologic abnormalities (hypopituitarism or hyper-prolactinemia).44Y46 Cases of an intrasellar meningiomamimicking pituitary apoplexy have been reported.46,47

Although benign, meningiomas can be locally aggressive andrecur after incomplete resection. Encasement and, ultimately,occlusion of an internal carotid artery can occur.2

Preoperative diagnosis of an intrasellar meningioma isextremely useful in surgical planning and may sway surgeonsaway from the transsphenoidal approach used for mostadenomas in favor of a transcranial approach.47Y49 The highdegree of vascularity of most meningiomas predisposes toexcessive intraoperative bleeding during resection, which isgenerally more easily controlled from a transcranial approach.Because of the vascularity of meningiomas, preoperativeembolization of tumors is advocated by some as being helpfulin reducing intraoperative blood loss.44 Diaphragma sellameningiomas are typically supplied by arteries of theophthalmic segment of the internal carotid arteries.45

Purely intrasellar meningiomas can be extremelydifficult to distinguish from adenomas by imaging.45,48

Intrasellar meningiomas typically appear as masses whichare hypointense to isointense to gray matter on both T1- andT2-weighted sequences.2,7 Sellar enlargement is com-mon.44,45,48 Enhancement after administration of gadoliniumis marked and homogeneous, with homogeneous enhance-

ment seen in more than 90%.7,50 The rate of enhancement isusually rapid.51 The enhancement profile of meningiomasmay aid in distinguishing them from adenomas, as adenomasgenerally enhance less intensely and more heterogeneouslythan meningiomas and demonstrate a longer time-to-peakenhancement on dynamic imaging.7,50,51 The presence ofan enhancing dural tail is not a feature of intrasellarmeningiomas.45,52

Identification of the pituitary gland as separate from asellar mass is probably the single most useful finding indifferentiating adenomas from sellar meningiomas. Visuali-zation of a CSF cleft between a tumor and the gland, althoughuncommon, virtually excludes the diagnosis of adenoma.7,53

Another finding which may favor meningioma is hyperostosisof the floor of the sella or adjacent bony structures, seen in34% of sellar meningiomas.7,51 Prominent vessels may beseen in approximately 65% of sellar meningiomas.7 Macro-scopically detectable calcifications are uncommon and areseen in just over 10% of sellar meningiomas7,44 (Fig. 7).

GERM CELL TUMORSIntracranial germ cell tumors are rare malignant

tumors, representing only 0.1% to 2% of all primary brainneoplasms. They are believed to arise from totipotent germcells that fail to migrate to the genital crest during embryoniclife. Primarily midline tumors, germ cell tumors aresubdivided into teratomas, germinomas, embryonal cellcarcinoma, choriocarcinoma, endodermal sinus (yolk sac)tumors, and mixed germ cell tumors. Pure germinomas

FIGURE 6. Gangliocytoma. Coronal T2-weighted (A) and enhanced sagittal T1-weighted (B) MR images demonstrate aheterogeneous, enhancing sellar and suprasellar mass. Note the spherical configuration of the mass and the absence of a Bwaist^ atthe level of the diaphragma sella.




account for two thirds of intracranial germ cell tumors, withnongerminomatous mixed germ cell tumors accounting formost of the rest.54

Germ cell tumors are primarily tumors of childhood,with a peak presentation at 10 to 12 years. Pure germinomasoccur at an older age than nongerminomatous tumors.54 Themajority of intracranial germ cell tumors are found in thepineal or suprasellar regions. Intracranial germ cell tumorsoccur twice as often in males than females, but this malepredominance is limited to tumors arising in the pinealregion. Suprasellar germ cell tumors occur slightly morefrequently in females.55,56 Pure germinomas are radio-sensitive and carry a favorable prognosis. More than 90%of germinomas can be treated effectively with radiation.Prognosis for patients with nongerminomatous tumors is lessfavorable, with only 40% to 60% demonstrating diseasecontrol with radiation therapy alone.55

Primarily intrasellar germinomas are rare and have afemale predominance.57 Most suprasellar germinomas origi-nate either in the floor of the third ventricle or in theinfundibulum. It is felt that intrasellar germinomas representinfundibular tumors with primarily intrasellar growth.57

Patients most commonly present with endocrine abnormal-ities, with DI being the most common symptom to promptpatients to seek medical attention.57,58 Development of DI isrelated to invasion or compression of the posterior lobe orinfundibulum and may persist for years before a diagnosis ismade. Other manifestations include hypopituitarism inchildren and adolescents and hypogonadism in adults.57

Hyperprolactinemia and precocious puberty have beenobserved.57,59 Large tumors and primarily suprasellar tumorsmay present with visual changes or oculomotor palsies. 58,59

Serum tumor markers can be extremely useful inestablishing the diagnosis of a germ cell tumor. Production ofeither >-fetoprotein (AFP) or A-human chorionic gonado-tropin (BHCG) can be seen in a number of subtypes of germcell tumors. Tumors with a yolk sac component secrete AFP.Choriocarcinomas produce high levels of BHCG. Patientswith pure germinomas can secrete BHCG into the CSF at lowlevels, and this is considered an early indication of CSFdissemination. Because other intracranial tumors do notproduce AFP or BHCG, the presence of these markers in CSFor serum in the setting of an intracranial tumor is essentiallydiagnostic of a germ cell tumor.54,55

Because intracranial germ cell tumors have a predilec-tion to disseminate via CSF, MRI of the entire craniospinalaxis and lumbar puncture for cytology are mandatory.54 MRIcannot reliably differentiate the different types of germ celltumors. The earliest finding in cases of neurohypophysealgerm cell tumors is probably absence of the normal posteriorlobe bright spot on T1-weighted images. This can be followedby swelling of the stalk and subsequent mass formation,which may displace the enhancing pituitary gland anteriorly.Loss of the normal pituitary bright spot and thickening of thestalk are also seen with idiopathic DI, granulomatousprocesses, and lymphocytic hypophysitis. Because of this,some have proposed serial MRI and endocrinologic evalua-tions in patients presenting with DI and loss of the posteriorbright spot without a definite mass.60

Larger sellar/suprasellar germ cell tumors have anonspecific imaging appearance and usually cannot bedistinguished from other tumors. The MR findings are thoseof an enhancing solid sellar mass, with or without suprasellarextension. Cysts and calcifications may be seen.61 Differentialenhancement of the tumor and the enhancing displacedanterior lobe may aid in distinguishing these tumors fromadenomas.60,62 Although rare, cavernous sinus invasion hasbeen reported to occur with larger tumors58 (Fig. 8).

LYMPHOMACNS lymphoma may be primary or metastatic. Less

than 1% of metastases to the pituitary are secondary tolymphoma.63 Primary CNS lymphoma refers to diseaselimited to the craniospinal axis, without systemic disease.64

It represents up to 2% of all primary CNS malignancies and ispractically always of the non-Hodgkin type, with the majoritybeing B-cell lymphoma.65 The incidence of CNS lymphomahas more than tripled in the United States since the early1980s,66 due to the increase in number of immunocompro-mised individuals. In patients with AIDS, primary CNSlymphoma makes up 3% of intracranial neoplasms. Interest-ingly, the incidence of primary CNS lymphoma has also beenincreasing in the nonimmunocompromised population.64,66,67

Primary CNS lymphoma is considered by the US Centers forDisease Control to be an AIDS-defining illness in thoseinfected with HIV. The mean age at presentation issignificantly lower for immunocompromised patients (meanage, 30Y40 years) versus immunocompetent patients (meanage, 60Y70 years); males are more frequently affected. Theredoes not appear to be a sex predilection in the immunocom-petent population.65

Primary lymphoma arising in the sella is exceedinglyrare, with only a handful of cases reported.68Y74 Patients range

FIGURE 7. Meningioma. Enhanced coronal T1-weighted MRimage demonstrates a sellar and suprasellar mass with markedenhancement.




in age from 44 to 86 years. Presenting symptoms are notspecific and include headaches, hypopituitarism, visual fielddeficits, and oculomotor palsies.

The imaging appearances of primary CNS lymphomatend to differ based on whether patients have normal orsuppressed immunity. CNS lymphoma in patients with

normal immune systems usually appears as a solitary masswith intermediate to low signal intensity relative to graymatter on both T1- and T2-weighted sequences; enhancementwith gadolinium is seen in nearly all cases and is homogenousin approximately three quarters of cases.75,65 The relativelack of T2 prolongation in CNS lymphoma is generallyattributed to dense cellularity and to a high nuclear-cytoplasmic ratio and may be helpful in distinguishinglymphoma from other CNS tumors; unfortunately, thisfinding is relatively insensitive, as it is seen in just over50% of cases.65 Calcification and hemorrhage in CNSlymphoma are rare.75

In immunocompromised patients, lesions of CNSlymphoma are likely to be multiple and to demonstratenecrosis.65 In the setting of necrosis, the center of the lesion isT2 hyperintense, whereas the periphery remains of inter-mediate to low signal.75 Contrast enhancement is hetero-geneous in this population, and rim enhancement is morecommon.65,75

MRI characteristics of sellar lymphomas are largelynonspecific, with most cases appearing as homogeneously orheterogeneously enhancing sellar masses.70,72Y74 Isointensityto hypointensity of masses relative to gray matter on T2-weighted imaging has been reported in sellar lymphoma70,74

and may be helpful in distinguishing it from pituitaryadenoma.

METASTASESMetastases to the pituitary gland and sella are

uncommon. In surgical series examining patients undergoingtranssphenoidal surgery for sellar or parasellar tumors,metastases are found in less than 1% of cases.63 In autopsyseries, evidence of metastases to the pituitary is seen inapproximately 5% of patients with known malignancy. Inapproximately two thirds of these cases, the pituitary ismacroscopically normal.75 The most common primarymalignancies to metastasize to the pituitary gland are breastand lung cancers which together account for more than 60%of all pituitary metastases.63,76 In 1 review, metastases to thepituitary were found in 17.6% of autopsies of patients withbreast cancer.63 Although breast and lung cancers are themost common primaries to metastasize to the pituitary,metastases from tumors of nearly every tissue type have beenreported.63

Metastases can reach the sella turcica via hematogen-ous spread, spread from a hypothalamic or hypophysealmetastasis through portal vessels, direct extension from skullbase tumors, or meningeal spread.63 Hematogenous metas-tases to the pituitary have a predilection to involve theposterior lobe. In 1 review of 201 cases of pituitarymetastases, the posterior lobe alone was involved in 50.8%of cases, both lobes were involved in approximately 33.8% ofcases, and the anterior lobe was involved in 15.4% of cases.77

The relative infrequency of metastases exclusive to theanterior lobe has been attributed to its lack of a direct arterialblood supply.2,63 It is hypothesized that the first capillary bedof the portal system may trap metastases before they cantravel to the anterior lobe.2 Therefore, metastatic involvementof the adenohypophysis is more often due to contiguous

FIGURE 8. Germ cell tumor. Unenhanced (A) and enhanced(B) sagittal T1-weighted images demonstrate a bilobed sellarand suprasellar mass with heterogeneous enhancement.Cysts are present within the mass.




spread from the posterior lobe than to direct hematogenousspread.78

Probably because of the predilection for metastases toinvolve the posterior lobe, the most common symptomobserved in patients with pituitary metastases is DI, whichoccurs in 45% of cases.63 Other signs/symptoms include visual

field deficits, anterior pituitary insufficiency, oculomotorpalsies, and headache.63,76

Imaging features of pituitary metastases are variable,and in the absence of coexistent brain metastases, differentia-tion from an adenoma is difficult. On MRI, pituitarymetastases appear as sellar or suprasellar masses whichoften are isointense or hypointense to gray matter on T1-weighted images and are usually of increased T2 signal. Theyenhance after gadolinium administration. Enhancement maybe homogeneous or heterogeneous, and rim enhancement canalso be seen.2,63 Like macroadenomas, metastases can appearas dumbbell-shaped intrasellar and suprasellar tumors.Invasion of the cavernous sinus and underlying sphenoidsinus may be seen.63 Loss of the normal posterior bright spot

FIGURE 9. Metastasis. Coronal T2-weighted (A) andunenhanced (B) and enhanced (C) coronal T1-weightedimages through the sella demonstrate a predominantly rimenhancing sellar mass with suprasellar extension. Central areasof T1 hyperintensity in B and T2 hypointensity in A probablyreflect hemorrhage. The mass displaces the optic chiasmsuperiorly. This was a metastasis from breast cancer.

FIGURE 10. Melanoma metastasis. Unenhanced sagittalT1-weighted (A) and coronal T2-weighted (B) MR imagesdemonstrate a sellar mass which is markedly hyperintense onthe T1-weighted image and hypointense on the T2-weightedimage relative to adjacent brain parenchyma. The signalcharacteristics presumably are due to the presence of melanin.




has been reported.79 Rapid growth of tumor, infundibularenlargement, and apparent destruction rather than remodelingof the bone of the sella turcica have also been reported andmay favor metastasis over adenoma2,79,80 (Figs. 9 and 10).

CONCLUSIONDifferentiating pituitary adenomas from any of the

above entities can be extremely difficult and, at times, evenimpossible. In some patients, however, there are specificimaging findings which, when present and when correlatedwith appropriate clinical information, can lead the radiologistto make the diagnosis or at least to suggest the actualdiagnosis.

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