Which physical findings are characteristic of pituitary apoplexy?

Updated: Apr 19, 2019
  • Author: Michael S Vaphiades, DO; Chief Editor: Edsel Ing, MD, MPH, FRCSC  more...
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Clinical presentation is marked by headache in 95% of cases. The headache is sudden and postulated to result from stretching and irritation of the dura mater in the walls of the sella supplied by the meningeal branches of cranial nerve V. The headache also may result from irritation of the trigeminal nerve from the expanding mass. Frequently, it is retro-orbital in location and may be unilateral at onset, then becomes generalized.

Vomiting occurs in 69% of patients and often accompanies the headache. The mechanism is unclear but may be due to meningeal irritation or increased intracranial pressure.

Visual acuity defects (52%) and visual field defects (64%) result from upward expansion of the tumor, which compresses the optic chiasm, optic tracts, or optic nerve. The classic visual field defect is a bitemporal superior quadrantic defect. Optic tract involvement from a prefixed chiasm is less common and results in a contralateral homonymous hemianopia. Optic nerve compression from a postfixed chiasm is rare and may mimic optic neuritis with pain on eye movement, monocular visual acuity loss, and a central scotoma on visual field testing. See the image below.

Automated visual field showing a bitemporal field Automated visual field showing a bitemporal field defect due to compression of the optic chiasm from below.

Ocular paresis (78%) results from compression of the cavernous sinus, which makes cranial nerves III, IV, and VI vulnerable to compression. If consciousness is maintained, diplopia may be present. Of the cranial nerves, the oculomotor nerve (cranial nerve III) is involved most commonly, resulting in a unilateral dilated pupil, ptosis, and a globe that is deviated inferiorly and laterally. [8]

Less commonly, cranial nerve IV is involved. A fourth cranial nerve palsy typically manifests as vertical diplopia that worsens when the patient gazes in a direction opposite or tilts the head toward the direction of the hypertropic (affected) eye. It also is worsened by downgaze.

Cranial nerve VI is least commonly involved, perhaps because, in the cavernous sinus, it is more sheltered from the pituitary expansion than are cranial nerves III and IV. Abducens involvement produces horizontal diplopia owing to the inability to abduct the involved eye.

Trigeminal nerve (cranial nerve V) involvement may produce facial pain or sensory loss.

Horner syndrome may develop from damage to the sympathetic fibers. Hemispheric deficits may also develop.

The carotid siphon may be compressed against the anterior clinoid process, leading to stroke and vasospasm from subarachnoid blood.

Leakage of blood and necrotic tissue into the subarachnoid space may lead to meningismus, stupor, and coma.

The cerebrospinal fluid frequently is marked by increased pressure and pleocytosis (even in the absence of hemorrhage), increased numbers of red blood cells, and xanthochromia.

Involvement of the hypothalamus may alter thermal regulation. Destruction of adenohypophyseal tissue may lead to endocrinologic deficiencies.

Rarely, pituitary apoplexy can occur in ectopic sites. Hori examined normal adult brains at autopsy and found ectopic pituitary cells in the leptomeninges of the peri-infundibular region in 75%. [9] He postulated that these cells may produce an ectopic pituitary adenoma. Ectopic pituitary adenomas commonly present late because they displace rather than invade vital nervous structures. They may be discovered only after the patient has pituitary apoplexy. Only one case of an ectopic pituitary adenoma that underwent apoplexy has been reported.

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