In pituitary apoplexy, headache is universal and usually occurs abruptly and is severe in intensity. Meningeal signs including stiff neck, nausea, and vomiting may be present because of blood entering the subarachnoid space. Deterioration of visual fields is common because of compression of the proximate optic chiasm. The compression of crossed nasal retinal fibers, which represents the temporal visual fields, produces a characteristic bitemporal hemianopia. The proximity of the pituitary gland to the cavernous sinuses may result in opthalmoparesis and diplopia due to dysfunction of the third, fourth, and sixth cranial nerves and a Horner syndrome, ptosis, and miosis due to compression of the sympathetic plexus within the cavernous sinus. Some patients will complain of facial pain or altered sensation, which is related to trigeminal nerve compression. Hypotension may occur because of deficiency of adrenocorticotropic hormone (ACTH).

Pituitary apoplexy usually occurs without any specific provoking factor. Most patients are found to have an underlying pituitary adenoma. Several proposed pathophysiological mechanisms that may trigger the apoplectic event include (a) reduced blood flow in the pituitary gland related to either systemic hypoperfusion or transient elevated intracranial pressure; (b) acute increased blood flow; (c) stimulation of the pituitary gland by exogenous or endogenous sources; and (d) coagulopathic conditions. Some of the common clinical scenarios in which the previous conditions occur include surgical or procedural interventions, pregnancy, and acute systemic illnesses.