CRANIAL NERVE III (oculomotor)PALSY

SIGNS AND SYMPTOMS
The patient will usually present with sudden onset unilateral ptosis (or rarely, a bilateral ptosis if the damage occurs to the third nerve nucleus), which is frequently accompanied by significant eye or head pain. The patient rarely complains of double vision because the ptosis obscures the vision in the affected eye; however, if the lid is manually elevated, the patient will experience diplopia. Acuity is typically unaffected unless damage occurs in the superior orbital fissure and cranial nerve II is also involved. The affected eye positions in a non-comitant exotropic, hypotropic position (down and out).

There will be limitation of elevation, depression and adduction. There is an underaction of the superior, inferior, and medial recti muscles and inferior oblique muscle, which may be total or partial. The pupil may be dilated and minimally reactive to light (pupillary involvement), totally reactive and normal (pupillary non-involvement), or may be sluggishly responsive (partial pupillary involvement). The patient is frequently elderly and often has concurrent diabetes and/or hypertension.

PATHOPHYSIOLOGY
Third nerve palsy results from damage to the oculomotor nerve anywhere in its course from the nucleus in the dorsal mesencephalon, its fascicles in the brainstem parenchyma, the nerve root in subarachnoid space, or in the cavernous sinus or posterior orbit. Damage to the third nerve nucleus results in an ipsilateral third nerve palsy with contralateral superior rectus under action and bilateral ptosis. Damage to the third nerve fascicles results in an ipsilateral third nerve palsy with contralateral hemiparesis (Weber's syndrome), contralateral intention tremor (Benedikt's syndrome), or ipsilateral cerebellar ataxia (Nothnagel's syndrome). Vascular infarct, metastatic disease and demyelinization are the common causes of brainstem involvement.

Damage to the third nerve within the subarachnoid space produces an isolated third nerve palsy. The main causes are compression of the nerve by an expanding aneurysm of the posterior communicating artery or the basilar artery, and ischemic vasculopathy. There will always be pain in aneurysmal compression and pupillary involvement is typical, though there have been infrequent cases of aneurysmal compression that did not initially affect pupillary function. In ischemic vascular nerve third palsies, pain is frequent and the pupil is typically normal and reactive.

Damage to the third nerve in the cavernous sinus, superior orbital fissure, or posterior orbit is unlikely to present as third nerve palsy due to the confluence of other structures in these areas. Cavernous sinus involvement may also include pareses of cranial nerves IV, VI and V-1, and an ipsilateral Horner's syndrome. The most common causes of damage in these areas include metastatic disease, inflammation, herpes zoster, carotid artery aneurysm, pituitary adenoma and apoplexy, and sphenoid wing meningioma.

MANAGEMENT
In complicated third nerve palsies where other neural structures are involved, have the patient undergo an MRI. In isolated third nerve palsies with no pupillary involvement where the patient is over 50, MRI scanning, an ischemic vascular evaluation, and daily pupil evaluation is indicated.

If the patient is under 50 and has a non-pupillary involved isolated third nerve palsy, intracranial angiography is indicated since ischemic vasculopathy is less likely to occur in this age group than is aneurysm. If the adult patient of any age presents with a complete or incomplete isolated third nerve palsy with pupillary involvement, consider this to be a medical emergency and have the patient undergo intracranial angiography immediately. In these cases, the cause is likely subarachnoid aneurysm and the patient may die if the aneurysm ruptures. Children under the age of 14 rarely have aneurysms; the majority of third nerve palsies in this age group are traumatic or congenital.

CLINICAL PEARLS

Isolated third nerve palsy due to ischemic vasculopathy will spontaneously resolve and recover over a period of three to six months. If the palsy fails to resolve in this time frame, repeat the MRI to search for the true etiology.

Myasthenia gravis has the ability to mimic virtually any cranial neuropathy, including isolated third nerve palsies. Myasthenia gravis must remain a possible diagnosis when encountering a third nerve palsy, especially when the course is variable or atypical.