A pituitary stroke is a sudden hemorrhagic infarction of a pituitary adenoma. The clinical presentation of pituitary stroke is typical and usually includes acute headache, signs of meningeal irritation, visual disturbances, ocular muscle palsy, and changes in consciousness. Sometimes patients die from severe subarachnoid hemorrhage and hypopituitarism. Pituitary adenomas present with pituitary strokes in 1-2% of cases, but subclinical hemorrhage with few symptoms accounts for about 10% of all pituitary tumors. The literature is inconsistent as to which type of pituitary tumor is associated with stroke, with some suggesting that hormonally active tumors such as acromegaly and Cushing’s disease are prone to hemorrhage, while others suggest that large, nonfunctional adenomas have a higher incidence of hemorrhagic infarction. The pathophysiological basis for the occurrence of pituitary stroke is unclear, and possible mechanisms include ischemic necrosis due to rapid tumor growth, vascular abnormalities in the tumor itself, and compression of the superior pituitary artery, among others. Other relevant factors: apocryptine therapy, anticoagulation therapy, diabetic ketoacidosis, head trauma, estrogen therapy, and pituitary radiotherapy. The cause of most pituitary strokes is unknown. Stroke causes a sudden increase in pressure within the tumor, which can result in mechanical compression of the optic nerve and involvement of structures within the cavernous sinus. The hematoma cavity in pituitary stroke is usually confined to the tumor, and sometimes blood enters the subarachnoid space. Stroke in tumors with significant suprasellar growth may trigger obstructive hydrocephalus. Stroke brings about destruction of the glandular structures, resulting in varying degrees of pituitary hypoplasia. In general, the adenohypophysis has a very impressive reserve capacity and persistent hypopituitarism occurs only if more than 75-90% of the gland is destroyed.