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Craniopharyngiomas may vary greatly in size. Small intrasellar tumors only 6 or 7 mm in diameter may be detected in amenorrheic young women and may be mistaken for prolactin-secreting adenomas whereas large tumors may occupy a significant portion of the intracranial volume. Almost all of these tumors have both solid and cystic portions, and even portions that appear densely calcified on diagnostic studies usually contain small cysts. The fluid in these cysts may be yellow, light tan, greenish, dark black (like machine oil), or even milky white, and can range in viscosity from watery to sludgelike. Cystic craniopharyngioma fluid contains suspended cholesterol crystals, which can be recognized by their characteristic birefringency.

The microscopic appearance typically shows an external layer of high columnar epithelium, a variable portion of polygonal cells, and a central network of epithelial cells. These epithelial bands are supported by a mesodermal connective tissue stroma. Papillary structures are common and are recognized as islands of squamous cells showing stellate forms in their interior. Regressive changes in the epithelial cells may vary from cellular liquefaction to cellular swelling with deposition of keratin-like material. The central stroma may degenerate, leading to cyst formation. Cysts may coalesce to produce large cystic components. Cyst walls can vary from thin, diaphanous membranes to thick, tough structures, which may be hard and rigid because of calcium salt deposition. Calcification is found on microscopic examination in approximately half of adult craniopharyngiomas and in almost all those in children.

Craniopharyngiomas often cause an intense glial reaction in subjacent brain. This reaction is particularly dense around small papillary tumor projections toward the hypothalamus. Some authors have stated that traction on this glial attachment will always lead to hypothalamic infarction and thus preclude safe total removal of the tumor. However, the attachment to the nervous system has proved to be very limited in some cases. Hoffman and colleagues reported autopsy findings in two children with large tumors in which the only attachment of the tumor was at the tuber cinereum. Others have reported similar experiences, especially with cystic tumors of the papillary type. Moreover, others have found that this "glial envelope" often provides a plane in which it is possible to dissect without damaging neural tissue.

Craniopharyngiomas may be adherent to major arteries at the base of the brain. The internal carotid artery was the only site of attachment that prevented total removal in 6 of a series of 23 chil­dren. Tumor remaining after attempted total removal is more likely to be adherent to a major artery than to the hypothalamus or chiasm. It may be that the mesenchymal reaction of the vessel wall to tumor produces a tougher and more tenacious attachment than does glial proliferation.

Craniopharyngiomas in the suprasellar region derive their blood supply from small arterial feeders arising from the anterior cerebral and anterior communicating arteries or from the internal carotid and posterior communicating arteries. Pertuiset makes the important point that craniopharyngiomas do not receive blood from the posterior cerebral arteries or from the basilar artery bifurcation unless the blood supply of the floor of the third ventricle is parasitized, a fact basic to removal of retrosellar portions of tumors. Within the sella, the tumor may be supplied by small arteries that penetrate the dura of the cavernous sinuses.

Occasional cases of extremely aggressive craniopharyngiomas with rapid growth and recurrence are reported, including postirradiation cases, but it is generally held that these tumors do not undergo malignant degeneration. Matson and Crigler specifically denied that craniopharyngiomas invade the brain.

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