(25-72) Sagittal graphic shows lymphocytic hypophysitis. Note thickening of the infundibulum and infiltration into the anterior lobe of the pituitary gland .

Miscellaneous Lesions

Hypophysitis

Hypophysitis is an inflammation of the pituitary gland that comprises an increasingly complex group of disorders. There are two main histologic forms of hypophysitis: lymphocytic hypophysitis (LH) and nonlymphocytic hypophysitis. Recent reports of other variants broaden the hypophysitis spectrum even further. In this section, we focus on LH, the most common form. We then briefly discuss nonlymphocytic hypophysitis, including granulomatous hypophysitis and some of the newly described entities that are often characterized by plasma cell infiltrates.

Lymphocytic Hypophysitis

Terminology. LH is also called lymphocytic adenohypophysitis, primary hypophysitis, and stalkitis. A variant form of LH is called lymphocytic infundibuloneurohypophysitis (LINH).

Etiology. LH is an uncommon autoimmune inflammatory disorder of the pituitary gland that most often occurs in women of child-bearing age, usually late in pregnancy or shortly after childbirth. Immune competence is reestablished in the late pregnancy/peripartum period. Antipituitary antibodies co-react with both the pituitary gland and the placenta.

LH is also associated with other autoimmune disorders. Approximately 25% of patients have coexistent systemic inflammatory/autoimmune disease. Thyroiditis, polymyositis, type 1 diabetes, and psoriasis have all been associated with LH.

(25-73) Lymphocytic adenohypophysitis is typified by numerous infiltrating cytologically benign lymphocytes overrunning the gland. (Courtesy B. K. DeMasters, MD.)

Pathology. The pituitary gland and stalk in LH appear diffusely enlarged and firm although inflammatory changes are predominantly or exclusively in the anterior lobe (25-72). Microscopic features include a dense infiltrate mostly composed of T-cell lymphocytes (25-73). Varying degrees of gland destruction and fibrosis may be present. Granulomas and giant cells are absent.

LINH typically involves both the neurohypophysis and the adenohypophysis (25-76).

Clinical Issues. Between 80 and 90% of patients with LH are female; 30-60% of cases occur in the peripartum period. There is no adverse effect on the fetus.

The most common presenting symptoms are headache and multiple endocrine deficiencies with partial or total hypopituitarism. Diabetes insipidus is common. Adrenocorticotrophic hormone deficits often appear first. Hyperprolactinemia occurs in one-third of all patients, probably secondary to stalk compression.

Men, women past child-bearing age, and children are affected in 10-20% of cases. Middle-aged men typically present with diabetes insipidus.

Treatment is hormone replacement with or without corticosteroids.

Imaging. LH is typically both intrasellar and suprasellar. Adjacent dural or sphenoid sinus mucosal thickening is common.

Imaging shows a thickened, nontapering infundibular stalk. A rounded, symmetrically enlarged pituitary gland is common (25-74). The sellar floor is intact, not expanded or eroded. The

posterior pituitary "bright spot" is absent in 75% of cases. LH enhances intensely and uniformly.

HYPOPHYSITIS vs. NONSECRETING PITUITARY ADENOMA

Hypophysitis

•Clinical profile

○Younger patients (mean: women = 35 years, men = 45 years)

○Patient age < 40 years favors hypophysitis

○Pregnant/peripartum patient

○Diabetes insipidus common

•Smaller mass

•Symmetric pituitary expansion

•Loss of normal posterior pituitary "bright spot" (PPBS)

•Stalk enlarged, nontapering

•Homogeneous signal, strong enhancement

Pituitary Adenoma

•Clinical profile

○Older patients (peak = 60 years)

○Diabetes insipidus rare

•Larger mass

○Volume > 6 cm³ favors adenoma

•Asymmetric pituitary expansion

•PPBS generally preserved

•Stalk displaced but otherwise normal

•Heterogeneous signal, moderate enhancement

Differential Diagnosis. The major differential diagnosis for LH is nonsecreting pituitary macroadenoma. The distinction is important, as treatment differs significantly. LH is treated medically, whereas surgical resection is the primary treatment for pituitary macroadenoma. Macroadenomas can be giant, but LH only occasionally exceeds 3 cm in diameter. Clinical findings are also helpful, as LH commonly presents with diabetes insipidus (25-76).

The stalk is usually normal in pituitary hyperplasia, although patient age and sex are similar. Metastasis usually occurs in older patients with known systemic primary tumor.

Granulomatous hypophysitis may occur secondary to infection, sarcoidosis, or Langerhans cell histiocytosis. Granulomatous hypophysitis is less common than LH, has a different epidemiologic profile, and tends to enhance more heterogeneously. IgG4and drug-related hypophysitis is very rare.

Granulomatous Hypophysitis

Granulomatous hypophysitis has different epidemiologic characteristics than LH does. Granulomatous hypophysitis is equally common in both sexes, and there is no association with pregnancy.

Granulomatous hypophysitis can be primary (idiopathic) or secondary (2575). Secondary granulomatous hypophysitis is far more common than primary granulomatous hypophysitis and typically results from necrotizing granulomatous inflammation. Infectious/inflammatory secondary granulomatous hypophysitis can be caused by TB, sarcoid, fungal infection, syphilis, Langerhans cell histiocytosis, Wegener granulomatosis, ErdheimChester disease, granulomatous autoimmune hypophysitis, ruptured Rathke cleft cyst, or craniopharyngioma. Secondary granulomatous hypophysitis may also occur as a reaction to systemic inflammatory disorders, such as Crohn disease. Imaging findings are nonspecific, resembling those of LH or pituitary adenoma.

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(25-74A) Coronal T1WI in a 19y pregnant woman with vision problems shows a "figure eight" or snowman-shaped intraand suprasellar mass .

(25-74B) Coronal T2WI shows that the lesion is mildly hyperintense. Note elevation and draping of the optic chiasm over the mass.

(25-74C) T1 C+ shows that the mass appears virtually identical to pituitary macroadenoma. This is lymphocytic hypophysitis.

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(25-75) This is granulomatous hypophysitis. (Top) Fat pituitary gland , stalk , and pseudotumor . (Bottom) Steroids resolved it.

(25-76) LINH in a middle-aged man with diabetes insipidus is seen here as an enhancing mass in the hypothalamus.

(25-77) Patient on ipilimumab for metastatic melanoma developed drug-induced hypophysitis with infiltration of the stalk and pituitary gland.

Primary granulomatous hypophysitis is a rare inflammatory disease without identifiable infectious organisms. The precise etiology of primary granulomatous hypophysitis is unknown. Nonnecrotizing granulomas with multinucleated giant cells, histiocytes, and various numbers of plasma cells and lymphocytes are typical. Primary granulomatous hypophysitis usually presents with diabetes insipidus. A symmetric sellar mass that enhances strongly but heterogeneously is seen on imaging studies.

Other Hypophysitis Variants

A number of new hypophysitis variants have been recently described. IgG4related hypophysitis has a marked mononuclear infiltrate mainly characterized by increased numbers of IgG4-positive plasma cells. Imaging findings resemble those of lymphocytic infundibuloneurohypophysitis. The pituitary stalk and posterior pituitary lobe are enlarged and enhance intensely following contrast administration.

Drug-related hypophysitis has been reported in cases of cancer immunotherapy with antibodies that stimulate T-cell responses (e.g., ipilimumab) (25-77). Clinicians and radiologists should be aware of autoimmune-induced hypophysitis as a complication of new treatments. Imaging of drug-related hypophysitis usually shows enlargement of the pituitary gland with or without infundibulum.

Langerhans Cell Histiocytosis

Terminology

Langerhans cell histiocytosis (LCH) is now considered a neoplastic disease with BRAF V600E mutations and LCH clonality. LCH is discussed in more detail in Chapter 24. This section focuses more specifically on the pituitary axis.

Clinical Issues

Presentation. Patients with pituitary axis LCH typically present with diabetes insipidus. There may be associated visual disturbances or hypothalamic dysfunction.

Demographics. LCH typically presents in patients less than 2 years of age. The peak age at onset is 1 year old for isolated LCH and between 2 and 5 years of age in multifocal disease. Female patients are more commonly affected 2:1.

Natural History. The overall survival rates of patients with LCH at 5, 15, and 20 years are 88%, 88%, and 77%, respectively. Late sequela are often present and include diabetes insipidus in 25% and growth failure in 20%. Therapeutic options depend on symptoms, location, and extent of disease. Patients with diabetes insipidus are treated with oral or nasal vasopressin. They may also be treated with chemotherapy and radiation therapy.

Imaging

The classic imaging of LCH of the pituitary axis is an absent posterior bright spot with a thickened, enhancing pituitary infundibulum (25-78A). LCH may also present as a sellar and suprasellar mass (25-78B).

Differential Diagnosis

The major differential diagnosis of LCH in a child is germinoma. Both LCH and germinoma may present with an absent posterior "bright spot" and a thickened, enhancing pituitary infundibulum. Germinomas typically present in young patients (peak of 10-12 years) with diabetes insipidus. There is

significant imaging overlap of LCH and germinoma although the age of the patient can be a helpful distinguishing feature, as LCH is most common in the first 2 years of life.

In an adult, the major differential diagnosis of LCH affecting the pituitary axis is neurosarcoid or hypophysitis.

Neurosarcoid patients often present with solitary or multifocal CNS masses as well as pulmonary hilar lymphadenopathy. Patients with neurosarcoid are usually between 20-30 years of age or over 50 years of age and have diabetes insipidus if the pituitary axis is affected. Although hypophysitis may present with loss of the normal pituitary "bright spot," hypophysitis usually affects the pituitary gland and the infundibulum, whereas LCH is usually centered in the infundibulum only. Additionally, patients with hypophysitis are typically young adults who may have another autoimmune disorder.

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Neurosarcoid

Neurosarcoid is a multisystem inflammatory disease characterized by noncaseating epithelioid-cell granulomas. Neurosarcoid is discussed in more detail in Chapter 15. This section will focus on the pituitary axis.

Etiology

The etiology of neurosarcoid remains unknown. It may be related to stimulation of the immune system by one or more antigens and/or an abnormal immune response.

Pathology

Sarcoidosis may affect many body parts, especially the lymph nodes and lungs. The hilar lymph nodes are the most common site. The CNS is usually affected in combination with disease elsewhere. However, approximately 5-10% of neurosarcoid

(25-78A) Sagittal T1WI in a young adult shows a thickened pituitary infundibulum with absence of a normal posterior pituitary bright spot, typical of Langerhans cell histiocytosis. (25-78B) Axial T1 C+ MR image in the same patient 9 months later shows an enhancing suprasellar mass. Patient was lost to follow-up and returned with progressive pituitary dysfunction at the time of this MR. Langerhans cell histiocytosis was diagnosed at resection.

(25-79) Sagittal T1 C+ MR in a 50y woman with diabetes insipidus shows marked thickening of the infundibulum . Patient was diagnosed with neurosarcoid. Differential considerations include lymphocytic hypophysitis, lymphoma, and metastatic disease. (2580) Coronal T2WI shows a hypointense sella/suprasellar mass in this female patient with pituitary dysfunction. Neurosarcoid was diagnosed at resection.

(25-81) Coronal graphic shows a macroadenoma with acute hemorrhage , causing pituitary apoplexy.

(25-82) Autopsy specimen of pituitary apoplexy shows hemorrhagic macroadenoma extending into both cavernous sinuses . (Courtesy R. Hewlett, MD.)

cases are confined to the CNS and occur without systemic sarcoid.

Clinical Issues

Presentation. Sarcoid symptoms vary with lesion location. The CNS is involved in approximately 5-10% of sarcoid patients. Patients with lesions affecting the pituitary axis result in pituitary and hypothalamic dysfunction, including diabetes insipidus and panhypopituitarism.

Demographics. There is a bimodal age peak with the initial peak in the third and forth decades and a later peak age in women greater than 50 years old. In the United States, the lifetime risk of sarcoid in African Americans is nearly three times higher than in Caucasians. In Europe, Caucasians are most commonly affected. Sarcoidosis may occur in families.

Natural History. Neurosarcoid has a variable clinical course. It is often an indolent disease that is up to 50% asymptomatic. Approximately 65-70% of neurosarcoid patients have selflimited monophasic illness. The remainder of patients with neurosarcoid have a remitting-relapsing course. The majority of patients respond rapidly to steroids.

Imaging

Neurosarcoid may present as diffuse or focal dural (pachymeningeal) and/or leptomeningeal thickening and enhancement, pituitary infundibulum and/or hypothalamic thickening and enhancement, cranial nerve enhancement, brain parenchymal lesions, or less commonly choroid plexus lesions (25-79) (25-80).

Differential Diagnosis

The main differential diagnoses for pituitary axis neurosarcoid are lymphocytic hypophysitis, lymphoma, and metastatic disease. Lymphocytic hypophysitis often presents with loss of the normal pituitary "bright spot" and shows abnormal enhancement in the pituitary gland and the infundibulum. Lymphoma often has an enhancing, infiltrative appearance and may affect the hypothalamus and pituitary gland as well as the infundibulum. Metastatic disease affecting the pituitary axis often has other sites of disease and a known primary cancer.

INFUNDIBULAR STALK MASSES

Adults

•Neurosarcoid (isolated stalk lesion rare)

•Hypophysitis ("stalkitis")

•Metastasis

•Lymphoma

•Pituicytoma

Children

•Germinoma (diabetes insipidus may occur before lesion is visible on MR!)

•Langerhans cell histiocytosis (look for other lesions)

•Ectopic neurohypophysis (displaced PPBS)

•Leukemia

Pituitary Apoplexy

Pituitary apoplexy (PAP) is a well-described acute clinical syndrome with headache, visual defects, and variable

endocrine deficiencies. In some cases, profound pituitary insufficiency develops and may become life-threatening.

Etiology

PAP is caused by hemorrhage into—or ischemic necrosis of—the pituitary gland. A preexisting macroadenoma is present in 65-90% of cases, but PAP can also occur in microadenomas or histologically normal pituitary glands. What precipitates the hemorrhage or necrosis is unknown.

In rare cases, patients undergoing treatment with bromocriptine or cabergoline for pituitary adenoma have developed life-threatening PAP. More often, this medical therapy results in a subclinical hemorrhage into the adenoma.

Pathology

The most common gross appearance of PAP is that of a large intrasellar or combined intraand suprasellar mass (25-81). Between 85 and 90% of cases demonstrate gross hemorrhagic infarction (25-82). Nonhemorrhagic ("bland") pituitary infarction causes an enlarged, edematous-appearing pituitary gland. Microscopic features are nonspecific and generally unremarkable.

Clinical Issues

Epidemiology and Demographics. PAP is rare, occurring in approximately 1% of all patients with pituitary macroadenomas. Peak age is 55-60 years. PAP is rare in patients under the age of 15 years. The M:F ratio is 2:1.

Presentation. Headache is almost universal in patients with PAP and is the most common presenting symptom, followed by nausea (80%) and visual field disturbance (70%). Hemorrhagic tumors that extend into the cavernous sinus may compress cranial nerves III, IV, V, and VI.

Almost 80% of patients with PAP have panhypopituitarism. Acute adrenal crisis with hypovolemia, shock, and disseminated intravascular coagulation may occur. Occasionally, diffuse subarachnoid hemorrhage may be seen.

Rarely, pituitary apoplexy with panhypopituitarism and diabetes insipidus develops in patients with hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome.

Natural History. PAP varies from a clinically benign event to catastrophic presentation with permanent neurologic deficits. Coma or even death may ensue in severe cases.

Long-term survivors often have permanent pituitary insufficiency requiring hormone replacement (most commonly steroids or thyroid hormone). Almost half of all male patients with PAP require testosterone replacement.

Patients with pituitary adenomas and PAP may show recurrent pituitary tumor growth and therefore merit continued postoperative surveillance.

A rare variant of PAP is Sheehan syndrome (SS). Sheehan syndrome is acute postpartum ischemic necrosis of the anterior pituitary gland, typically caused by blood loss and hypovolemic shock during or after childbirth. SS may result in long-term loss of hormone function. Remote SS is a rare cause of partially empty sella on imaging studies.

Treatment Options. Surgical decompression is generally necessary in patients with compromised visual acuity. Supportive therapy with steroids and fluid/electrolyte/hormone replacement is often required.

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(25-83A) T1WI in a 68y man with "thunderclap" headache and visual changes shows mostly isointense intraand suprasellar mass .

(25-83B) Coronal T2WI shows that the mass is very heterogeneous in signal intensity with multiple hemorrhagic foci .

(25-83C) Coronal T1 C+ FS shows thin peripheral enhancement , pituitary apoplexy with necrotic, hemorrhagic adenoma found at surgery.

(25-84) Pituitary apoplexy in a 50y woman with 4 days of visual changes shows subacute hemorrhage in the pituitary gland with a blood-fluid level.

Imaging

General Features. An enlarged pituitary gland with peripheral rim enhancement is typical of pituitary apoplexy (25-83). Gross intraglandular hemorrhage is common but not invariably present.

CT Findings. NECT scans are often normal. Hemorrhage into the pituitary gland with a hyperdense sellar/suprasellar mass can be identified in 20-25% of cases. Occasionally, subarachnoid hemorrhage into the basal cisterns can be identified.

MR Findings. MR is the procedure of choice to evaluate suspected PAP. Signal intensity depends on whether the PAP is hemorrhagic or nonhemorrhagic. Hemorrhage can be identified in 85-90% of cases (25-84).

Signal intensity depends on clot age. Acute PAP is heterogeneously isoto hypointense to brain on T1WI. Initially isoto mildly hyperintense on T2WI, PAP rapidly becomes hypointense on T2WI. Acute compression of the hypothalamus and optic chiasm may cause visible edema along the optic tracts on T2/FLAIR scans.

"Blooming"/susceptibility artifact on T2* is common if blood products are present but may be obscured by artifact from the adjacent paranasal sinuses. T1 C+ shows rim enhancement (25-85). Dural thickening and enhancement is seen in 50%, and mucosal thickening in the adjacent sphenoid sinus occurs in 80% of all patients. PAP usually restricts on DWI.

(25-85) (Top left) T1WI shows an enlarged pituitary gland , thick hypothalamus . (Top right) FLAIR hyperintensity is along both optic tracts . (Bottom) Rim enhancement is shown. This is nonhemorrhagic pituitary apoplexy.

PITUITARY APOPLEXY

Etiology

•Hemorrhagic or nonhemorrhagic pituitary necrosis

•Preexisting macroadenoma (65-90%)

Clinical Issues

•Sudden onset

•Headache, visual defects

•Hypopituitarism (80%)

•Can be life-threatening

•Can result in permanent pituitary insufficiency

•Sheehan syndrome = postpartum pituitary necrosis

Imaging

•Enlarged pituitary

○± Hemorrhage (85-90%)

•Rim enhancement around nonenhancing gland

•May cause hypothalamic, optic tract edema

Differential Diagnosis

•Hemorrhagic macroadenoma without apoplexy

•Rathke cleft cyst apoplexy

•Pituitary abscess

•Acute thrombosed aneurysm

Differential Diagnosis

The major differential diagnosis of PAP is hemorrhagic macroadenoma. Focal hemorrhages in adenomas are common, but, in contrast to PAP, the clinical course is typically subacute or chronic. Most adenomas enhance strongly but heterogeneously, whereas PAP demonstrates rim enhancement around a predominantly nonenhancing, expanded pituitary gland.

(25-86A) Sagittal T1WI in a patient with longstanding acromegaly shows well-aerated sphenoid sinus extending posteriorly to clivus . Pneumatization is classified as postsellar. Note well-defined sellar bulge into sphenoid sinus.

Rathke cleft cyst (RCC) can contain thick proteinaceous fluid that appears hyperintense on T1WI and mimic intrapituitary hemorrhage. Most RCCs are asymptomatic and found incidentally. With some exceptions, RCCs that become symptomatic typically follow a subacute/chronic course. Apoplexy is a rare but distinct presentation caused by sudden hemorrhage into the cyst. RCC with apoplexy can mimic the symptoms of PAP, but the cyst can usually be identified as separate from the pituitary gland.

Pituitary abscess is a rare entity that may be difficult to distinguish from PAP with "bland" (ischemic) infarction. Clinical signs of infection may be minimal or absent. T1 shortening around the rim rather than the center of the mass is characteristic of abscess. Rim enhancement with restriction on DWI is typical for both pituitary abscess and PAP.

Acute thrombosis of a large intraor parasellar aneurysm can present with panhypopituitarism and subarachnoid hemorrhage. "Mixed age" laminated clot is common, and a small residual "flow void" from the residual patent lumen can often be identified on MR.

Lymphocytic hypophysitis can cause a relatively sudden onset of symptoms and thus mimic PAP clinically. LH usually causes only modest gland enlargement. The pituitary enhances intensely and uniformly.

Preand Postoperative Sella

Two approaches are almost universally used in sellar surgery: traditional sublabial transsphenoidal surgery and minimally invasive completely endoscopic surgery. Image-guided surgery with robotics and stereotactic intraoperative MR is increasingly used with microsurgical and endoscopic

(25-86B) Coronal T2WI shows the exceptionally thick skull of this patient. The intercarotid distance measured 24 mm. Transsphenoidal surgery was successful because of the favorable anatomy.

techniques. Subfrontal craniotomy is now uncommon and is generally used only for lesions with very large supradiaphragmatic tumors.

Each of these techniques requires careful preoperative imaging evaluation. In this section, we focus on the preoperative evaluation for—and postoperative imaging of—transsphenoidal and endoscopic surgery. Both involve safely navigating the sphenoid sinus and avoiding the many critical structures in and around the sella.

Preoperative Evaluation

Most surgical approaches (transethmoid, transnasal, or transseptal) pass through the sphenoid sinus to reach the sella. Regardless of which operative technique—microscopic or endoscopic—is used, delineating sphenoid sinus anatomy and identifying anatomic variants that might impact surgery are important to successful patient outcome.

CT and MR each has a unique contribution to the full preoperative evaluation of sellar lesions. Multiplanar MR is the procedure of choice to characterize the lesion and define its extent. In concert with MR, preoperative CT helps define relevant bony anatomy.

Four key features of sphenoid sinus anatomy should be identified: the location and extent of pneumatization, the sellar configuration, any septation, and the intercarotid distance.

Pneumatization. Location and extent of sphenoid sinus pneumatization are the major concern. Pneumatization is classified as sellar (57%), postsellar (22%), presellar (21%), or conchal (2%). The specific type of pneumatization is generally determined from sagittal MRs (25-86).

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(25-87A) Preoperative sagittal T1WI shows a large sellar/suprasellar solid and cystic mass that expands, erodes, and deepens the sella turcica.

(25-87B) Postoperative T1 C+ scan after tumor debulking shows fat packing , residual tumor, and sphenoid air-fluid level .

(25-87C) T1 C+ FS scan shows suppressed fat and a thin rim of enhancing tissue .

The rare conchal nonpneumatized sphenoid is important to recognize preoperatively, as it makes transsphenoidal surgery more difficult. At the opposite end of the spectrum, a highly pneumatized sphenoid sinus may make the surgery technically easier but also distorts the anatomic configuration, attenuating the bone and potentially uncovering the carotid arteries and optic nerves.

A pneumatized dorsum sellae can be penetrated during surgery, resulting in a CSF leak.

Sellar Configuration. The presence (well defined) or absence (ill defined) of sellar bulging in relation to the sellar floor and the degree of sphenoid pneumatization should be reported. Pneumatization of the planum sphenoidale and dorsum sellae should also be noted. These are determined from sagittal MR.

A prominent sellar bulge into a pneumatized sphenoid sinus is seen in 75% of patients (25-86A). The other 25% have an absent or ill-defined sellar bulge. A well-pneumatized sphenoid sinus with a prominent sellar bulge facilitates surgery, which is further eased if the sellar floor is thinned or disrupted by tumor. Dorsum sellae pneumatization is present in the majority.

Septation. The presence or absence of an intersphenoid septum should be determined. If present, note whether there is a single intersinus septum or more than one septa. The position of the septal insertion (in the sellar floor, at the carotid canal, or at the optic canal) should be identified. This is best evaluated on both axial and coronal bone CT.

Axial scans show no septum in 10-11% of patients and a single intersphenoid septum in 70%. An accessory septum is seen in 10% of patients, and 7-9% have multiple septa.

The intersphenoid septum must be removed to expose the sellar floor, so determining its location is crucial. The septum is rarely located in the midline. It typically deviates to one side or the other, dividing the sphenoid sinus into two unequal cavities. This results in an asymmetric appearance of the sellar floor. In 30-40% of patients, the septum deviates quite laterally and terminates adjacent to the internal carotid artery.

Intercarotid Distance. The intercarotid distance is measured between the medial aspects of the two signal "voids" of the cavernous ICA segments as seen on midsellar coronal MR. Intercarotid distance varies widely, ranging from 10-12 mm to 30 mm (mean of 23 mm). Narrow distances (< 12 mm) increase the chance of vascular injury during transsphenoidal surgery.

Postoperative Evaluation

To evaluate the postoperative sella, thin-section, small FOV imaging in both the sagittal and coronal planes is mandatory. Precontrast T1and T2WI images plus postcontrast fat-saturated sequences are standard.

The appearance on postoperative MR scans is complicated by hemorrhage, use of hemostatic agents, packing materials (muscle, fat, fascia lata), and residual tumor. Typical findings include a bony defect in the anterior sphenoid sinus wall, fluid and mucosal thickening in the sinus, fat packing within the sella turcica, hemorrhage, and varying amounts of residual mass effect (25-87).

The first postoperative scan provides the baseline against with which subsequent imaging is compared. With time, hemorrhage evolves and resorbs, fat packing fibroses and retracts, and mass effect decreases. A partially empty sella with or without traction on the infundibular stalk and optic chiasm is typical in the months and years following the initial surgery.

Complications such as diabetes insipidus, stalk transection, and electrolyte disturbances are usually temporary. Long-term complications include CSF leaks and cranial neuropathy.

Differential Diagnosis of a

Sellar Region Mass

In establishing a helpful differential diagnosis of a sellar mass, determining anatomic sublocation is the first, most important step. Is the lesion (1) intrasellar, (2) suprasellar, or (3) in the infundibular stalk? Or is it a combination of these locations?

Whether a sellar/suprasellar mass is the pituitary gland itself or is separate from the mass is the most important imaging task and the most helpful finding (25-88) (25-89) (25-90)

(25-91). Masses that can be clearly distinguished as separate from the pituitary gland are rarely—if ever—macroadenomas.

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The most helpful clinical feature is patient age. Some lesions are common in adults but rarely occur in children. Sex and endocrine status are helpful ancillary clues. For example, pituitary macroadenomas rarely cause diabetes insipidus, but it is one of the most common presenting symptoms of hypophysitis.

Lastly, consider some specific imaging findings. Is the mass cystic? Is it calcified? What is the MR signal intensity? Does the lesion enhance?

Intrasellar Lesions

Intrasellar lesions can be mass-like or non-mass-like. Keep two concepts in mind: (1) not all "enlarged pituitary glands" are abnormal. Pituitary size and height vary with sex and age. A "fat" pituitary can also occur with intracranial hypotension. (2) Pituitary "incidentalomas" are common (identified in 15-20% of normal MR scans), often cystic microadenomas or Rathke cleft cysts.

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WHEN THE MASS CANNOT BE SEPARATED FROM THE PITUITARY GLAND

Common

•Pituitary macroadenoma

•Pituitary hyperplasia (physiologic, pathologic)

Less Common

•Neurosarcoid

•Langerhans cell histiocytosis

•Hypophysitis

Rare But Important

•Metastasis

•Lymphoma

•Germinoma

INTRASELLAR LESION

Common

•Pituitary hyperplasia (physiologic, pathologic)

•Pituitary microadenoma

•Empty sella

Less Common

•Pituitary macroadenoma

•Rathke cleft (or other) cyst

•Craniopharyngioma

•Neurosarcoid

Rare But Important

•Lymphocytic hypophysitis

•Intracranial hypotension (venous congestion)

•Vascular ("kissing" carotids, aneurysm)

•Meningioma

•Metastasis

•Lymphoma

Common Suprasellar Masses

The five most common overall suprasellar masses, i.e., the "Big Five," are pituitary macroadenoma, meningioma, aneurysm, craniopharyngioma, and astrocytoma. Together they account for 75-80% of all sellar region masses. Three of the "Big Five" (the "Big Three")—adenoma, meningioma, aneurysm—are common in adults but rare in children (25-92) (25-93).

COMMON SUPRASELLAR MASSES

Adults

•Pituitary adenoma (mass = gland)

•Meningioma (mass separate from gland)

•Aneurysm ("flow void," pulsation artifact)

Children

•Craniopharyngioma (90% cystic, 90% calcify, 90% enhance)

•Hypothalamic/optic chiasm astrocytoma (solid, no calcification)

Less Common Suprasellar Masses

The presence of some less common lesions can often be inferred from imaging studies.

LESS COMMON SUPRASELLAR MASSES

•Rathke cleft cyst (well delineated, separate from pituitary)

•Arachnoid cyst (behaves just like CSF)

•Dermoid cyst (looks like fat)

•Neurocysticercosis (usually multiple)

Rare Suprasellar Masses

Keep these lesions in mind—they can mimic more common lesions, but the appropriate treatment differs sharply.

RARE BUT IMPORTANT SUPRASELLAR MASSES

•Hypophysitis (may look like adenoma)

•Hypothalamic hamartoma ("collar button" between stalk, mammillary bodies)

•Metastasis (systemic cancer; look for other lesions)

•Lymphoma (often infiltrates adjacent structures)

Cystic Intra-/Suprasellar Mass

If an intraor suprasellar mass is primarily or exclusively cystic, the differential diagnosis considerations change. The key issue is to distinguish a cystic mass that originates within the sella versus intrasellar extension from a suprasellar lesion (25-94). Other than Rathke cleft cyst, completely intrasellar nonneoplastic cysts are rare, as is a totally intrasellar craniopharyngioma without suprasellar extension.

In a child with a suprasellar cystic mass, consider an enlarged third ventricle, craniopharyngioma, neurocysticercosis, and astrocytoma. In an adult, consider arachnoid cyst, neurocysticercosis, Rathke cleft cyst, adenoma, and aneurysm

(25-95).

CYSTIC INTRASELLAR MASS

Common

•Empty sella

•Idiopathic intracranial hypertension

Less Common

•Cystic pituitary adenoma

•Rathke cleft cyst

•Neurocysticercosis cyst

Rare But Important

•Craniopharyngioma

•Epidermoid cyst, arachnoid cyst

•Pituitary apoplexy

•Thrombosed aneurysm

CYSTIC SUPRASELLAR MASS

Common

•Enlarged third ventricle

•Arachnoid cyst

•Craniopharyngioma

•Neurocysticercosis cyst

Less Common

•Rathke cleft cyst

•Dermoid cyst

•Epidermoid cyst

Rare But Important

•Pituitary macroadenoma, apoplexy

•Astrocytoma (usually solid)

•Ependymal cyst

•Aneurysm (patent or thrombosed)

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CALCIFIED SUPRASELLAR MASS

Common

•Atherosclerosis

•Craniopharyngioma

•Meningioma

•Aneurysm

○Saccular

○Fusiform, atherosclerotic

Less Common

•Neurocysticercosis

•Pilocytic astrocytoma

•Dermoid cyst

Rare But Important

•Macroadenoma

•Tuberculosis

•Chondroid tumor

(25-92) Autopsy specimen demonstrates an unruptured suprasellar aneurysm . (Courtesy R. Hewlett, MD.) (25-93) NECT in a 55y man with headaches shows hyperdense noncalcified mass in the suprasellar cistern. Considerations in an adult include macroadenoma, meningioma, and aneurysm. This is large basilar tip aneurysm.

(25-94) Coronal T2WI shows a cystic intrasellar mass in a young adult with elevated prolactin. Cystic microadenoma was found at resection. Imaging mimics a Rathke cleft cyst. (25-95) Coronal T2WI shows a cystic intraand suprasellar mass . The optic chiasm is elevated and draped over the cyst. Arachnoid cyst was found at surgery. ACs follow CSF signal intensity on all MR sequences.