Diagnosis of pituitary adenoma This is virtually certain when a chiasmal syndrome is combined with an endocrine syndrome of either hypopituitary or hyperpituitary type. Laboratory data that are confirmatory of an endocrine disorder, as described above, and sometimes a ballooned sella turcica on plain films of the skull are occasionally found. Patients who are suspected of having a pituitary adenoma should be examined by MRI with gadolinium; this procedure will visualize pituitary adenomas as small as 3 mm in diameter and show the relationship of the tumor to the optic chiasm (Fig. 30-21). This also provides the means of following the tumor’s response to therapy. It should be kept in mind that pituitary tissue normally enhances on CT and MRI, revealing small tumors as relatively hypoenhancing nodules.
Tumors and lesions other than pituitary adenomas may sometimes expand the sella. Enlargement may be the result of an intrasellar craniopharyngioma, meningioma, carotid aneurysm, or cyst of the pituitary gland. Intrasellar epithelium-lined cysts are rare lesions. They originate from the apex of the Rathke pouch, which may persist as a cleft between the anterior and posterior lobes of the hypophysis. Rarer still are intrasellar cysts that have no epithelial lining and contain thick, dark brown fluid, the product of intermittent hemorrhages. Both types of intrasellar cysts may compress the pituitary gland and mimic the endocrine-suppressive effects of pituitary adenomas. Neoplasms originating in the nasopharynx or sinuses may invade the sella and pituitary gland, and sarcoid lesions at the base of the brain may do the same. Also, the pituitary gland and the infundibulum (and the chiasm) may be the site of metastases, most of them from the lung and breast (Morita et al); they give rise to diabetes insipidus, pituitary insufficiency, or orbital pain, and rarely may be the first indication of a systemic tumor.
Empty sella syndrome More common than the aforementioned conditions is a nontumorous enlargement of the sella (“empty sella”). This results from a defect in the dural diaphragm, which may occur without obvious cause or with states of raised intracranial pressure, such as pseudotumor cerebri (see Chap. 29) or hydrocephalus, or may follow surgical excision of a pituitary adenoma or meningioma of the tuberculum sellae or pituitary apoplexy (see later). The arachnoid covering the diaphragm sellae will bulge downward through the dural defect, and the sella then enlarges gradually, presumably because of the pressure and pulsations of the CSF acting on its walls. In the process, the pituitary gland becomes flattened, sometimes to an extreme degree; however, the functions of the gland are usually unimpaired. Flattening of the pituitary gland precedes bony expansion of the sella in many cases. Erosion or dishiscence of the sellar floor does not occur and the appearance of these changes implicates another type of lesion. Downward herniation of the optic chiasm occurs occasionally and may cause visual disturbances simulating those of a pituitary adenoma (Kaufman et al). As mentioned earlier, a bitemporal hemianopia with a normal-sized sella is usually caused by a primary suprasellar lesion (saccular aneurysm of the distal carotid artery, meningioma, or craniopharyngioma).