Although uncommon, the possibility of a cerebral aneurysm masquerading as a pituitary adenoma has always been an important, if not a nagging, diagnostic consideration in the evaluation of an endocrine-inactive sellar mass (Fig. 9).
Indeed, the inadvertent rupture of an unsuspected intrasellar aneurysm during the course of transsphenoidal exploration for a presumed pituitary adenoma represents one of the classic neurosurgic disasters. That cerebral angiography was, until recently, a regular practice in the radiological evaluation of pituitary adenomas further emphasizes the fact that aneurysms do periodically involve the sellar region, and their exclusion is essential. Fortunately, one of the many benefits of MRI is its ability to exclude an aneurysm as a potential aetiology of a sellar region mass, thus obviating the routine use of angiography. The majority of aneurysms involving the sellar region derive from the intracavernous segment of the carotid artery, and less often from the supraclinoid carotid and the anterior communicating artery complex. The clinical picture may be indistinguishable from a NFPA or other sellar mass; headache and retro-orbital pain, visual symptoms, low-grade hyperprolactinemia, and, less commonly, hypopituitarism and DI may all be presenting features. Should such aneurysms erode into and occupy the sella, the resulting sellar enlargement can be indistinguishable from that occurring with pituitary adenomas or other intrasellar mass lesions.
In addition to mimicking pituitary adenomas, aneurysms have also coexisted with pituitary adenomas. As reviewed by Weir, the incidence of coexisting pituitary adenomas and incidental cerebral aneurysms approaches 7.4% in various reports (195). GH-producing pituitary tumors in particular have been repeatedly reported to coexist with incidental aneurysms at a frequency above what would be expected by chance alone. The basis of this association is uncertain. Because generalized arterial ectasia is a recognized feature of acromegaly, some have speculated that the local effects of GH or, more likely, of IGF-1 on cerebral blood vessels (which are known to have IGF-1 receptors) may in some way predispose or contribute to aneurysm formation.
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