Third cranial nerve disorders can impair ocular motility, pupillary function, or both. Symptoms and signs include diplopia, ptosis, and paresis of eye adduction and of upward and downward gaze. If the pupil is affected, it is dilated, and light reflexes are impaired. If the pupil is affected or patients are increasingly unresponsive, CT is done as soon as possible.

Etiology

Third cranial (oculomotor) nerve disorders that cause palsies and affect the pupil commonly result from aneurysms (especially of the posterior communicating artery) and transtentorial brain herniation (see Coma and Impaired Consciousness: Brain herniation.) and less commonly from meningitis affecting the brain stem (eg, TB meningitis). The most common cause of palsies that spare the pupil, particularly partial palsies, is ischemia of the 3rd cranial nerve (usually due to diabetes or hypertension) or of the midbrain. Occasionally, a posterior communicating artery aneurysm causes complete oculomotor palsy and spares the pupil.

Symptoms and Signs

Diplopia and ptosis (drooping of the upper eyelid) occur. The affected eye may deviate slightly out and down in straight-ahead gaze; adduction is slow and may not proceed past the midline. Upward gaze is impaired. When downward gaze is attempted, the superior oblique muscle causes the eye to adduct slightly and rotate. The pupil may be normal or dilated; its response to direct and to consensual light may be sluggish or absent (efferent defect). Mydriasis (pupil dilation) may be an early sign.

Diagnosis

• Clinical evaluation
• CT or MRI

Differential diagnosis includes midbrain lesions that disrupt the oculomotor fascicle (Claude syndrome, Benedict syndrome), leptomeningeal tumor or infection, cavernous sinus disease (giant carotid aneurysm, fistula, or thrombosis), intraorbital structural lesions (eg, orbital mucormycosis) that restrict ocular motility, ocular myopathies (eg, due to hyperthyroidism or mitochondrial disorders), and disorders of the neuromuscular junction (eg, due to myasthenia gravis or botulism). Differentiation may be clinical. Exophthalmos or enophthalmos, a history of severe orbital trauma, or an obviously inflamed orbit suggests an intraorbital structural disorder. Graves orbitopathy (ophthalmopathy) should be considered in patients with bilateral ocular paresis, paresis of upward gaze or abduction, exophthalmos, lid retraction, lid lag during downward gaze (Graefe sign), and a normal pupil.

CT or MRI is required. If a patient has a dilated pupil and a sudden, severe headache (suggesting ruptured aneurysm) or is increasingly unresponsive (suggesting herniation), CT is done immediately. If ruptured aneurysm is suspected and CT does not show blood or is not available rapidly, other tests, such as lumbar puncture, magnetic resonance angiography, CT angiography, or cerebral angiography, are indicated. Cavernous sinus disease and orbital mucormycosis require immediate MRI imaging for timely treatment.

Treatment

Treatment depends on the cause.

Last full review/revision July 2012 by Michael Rubin, MDCM

Content last modified November 2012