The third, fourth, and sixth cranial nerves innervate the extraocular muscles that position the globes in the orbits. Extraocular muscle paralysis resulting from lesions in one or all of these cranial nerves results in failure of one or both eyes to rotate in concert with the other eye.
The primary symptom is diplopia caused by misalignment of the visual axes, and the pattern of image separation is the key to diagnosing which particular ocular motor cranial nerve (and extraocular muscle) is involved. With unilateral third cranial nerve palsy (ie, oculomotor nerve palsy), the involved eye usually is deviated "down and out" (ie, infraducted and abducted), and there may or be partial or complete ptosis. In addition, pupillary dilatation can cause anisocoria (greater in the light), symptomatic glare in bright light, and accommodation deficit that may cause blurred vision for near objects.
Recognition of oculomotor nerve palsy is critical to ensure prompt and appropriate evaluation and treatment.
A painful pupil-involved oculomotor nerve palsy may result from a life-threatening intracranial aneurysm.
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The anatomical relationship of the various portions of the oculomotor (third) cranial nerve accounts for many of the clinical features of third cranial nerve palsy as outlined below.
Nuclear portion: The cell bodies for axons that travel in the oculomotor nerve reside in the column-shaped nuclear groups on either side of the midbrain tegmentum. The axons destined for each extraocular and intraocular muscle derive from a specific subnucleus. 
Fascicular intraparenchymal midbrain portion: The fascicular portion of the oculomotor nerve courses ventrally from the nucleus in the dorsal midbrain tegmentum, passes through the red nucleus, and emerges from the medial aspect of the cerebral peduncle.
Subarachnoid portion: The cisternal portion of the nerve is in the subarachnoid space anterior to the midbrain and in close proximity to the posterior communicating artery. Berry aneurysm at the junction between the posterior communicating artery and the internal carotid artery is an important cause of oculomotor nerve palsy.
Cavernous sinus portion: The next segment of the oculomotor nerve runs through the lateral wall of the cavernous sinus superiorly. It enters the cavernous sinus just above the petroclinoid ligament and inferior to the interclinoid ligament. Masses invading the cavernous sinus from within the sella often cause third cranial nerve dysfunction prior to involvement of the other cranial nerves in the cavernous sinus. This is probably because of the oculomotor nerve's close proximity to the unyielding interclinoid ligament above and the petroclinoid ligament below.
Orbital portion: The oculomotor nerve enters the orbit through the superior orbital fissure adjacent to the fourth cranial nerve. The nerve branches into superior and inferior divisions, usually within the posterior orbit, but, occasionally, the branching occurs as far back as the cavernous sinus segment. The superior division innervates the levator palpebrae and the superior rectus muscles; the inferior division innervates all the other muscles innervated by the third nerve, including the iris sphincter, which constricts the pupil.
The axons for most of the muscles are uncrossed from the nucleus to the eye, but there are 2 exceptions: (1) Axons for the levator palpebrae come from both sides of the central caudal subnucleus via bilateral, crossed, and uncrossed pathways. (2) Those for the superior rectus muscle come from the superior rectus subnucleus on the contralateral side.
The pupillomotor and ciliary muscle neurons derive from the Edinger-Westphal subnucleus, which is in the midline in the most rostral and anterior part of the oculomotor nerve nucleus. These autonomic pathways are all ipsilateral or uncrossed.
The oculomotor nerve innervates the following extraocular muscles of either eye: superior rectus, inferior rectus, medial rectus, inferior oblique, levator palpebrae, ciliary muscle, and iris sphincter.
Oculomotor nerve palsy is uncommon.
Morbidity and mortality are essentially those of the diseases that cause oculomotor nerve palsy and are beyond the scope of this article.
The most significant causes of mortality and morbidity along with oculomotor nerve palsy are subarachnoid hemorrhage from berry aneurysm of the posterior communicating artery, and meningitis or meningeal infiltrative disorders, both infectious and neoplastic.
The prognosis of an oculomotor palsy depends on the etiology. Posttraumatic, postinfectious, postinflammatory, and ischemic oculomotor palsies may partially or completely recover spontaneously. Compressive lesions (eg, aneurysm or tumor) that are treated endovascularly or surgically may also improve or resolve following treatment. Patients with chronic and stable ptosis or ophthalmoplegia due to oculomotor nerve palsy may benefit from reconstructive lid or strabismus surgery.
Patients should be informed of the potentially life-threatening etiologies of unexplained oculomotor nerve palsy. They should undergo appropriate evaluation and treatment of underlying etiologies and understand the prognosis for recovery.
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