Oculomotor Nerve Palsy

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Background

The third, fourth, and sixth cranial nerves innervate the extraocular muscles that position the globes in the orbits. Extraocular muscle paralysis resulting from destructive 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 from misalignment of the visual axes, and the pattern of image separation is the key to diagnosing which particular cranial nerve (and extraocular muscle) is involved. With unilateral third cranial nerve palsy, the involved eye usually is deviated down and out (infraducted, abducted), and there is ptosis, which may be severe enough to cover the pupil. In addition, pupillary dilatation can cause symptomatic glare in bright light (if the ptotic lid does not cover the pupil), and paralysis of accommodation causes blurred vision for near objects.

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Patient with left posterior communicating artery aneurysm and third cranial nerve palsy. Courtesy of James Goodwin, MD.

Pathophysiology

The anatomical relationship of the various portions of the 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.[1]

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.

Fascicular 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.

Fascicular 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 are most likely to 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.

Fascicular 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, 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 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.

Epidemiology

Frequency

United States

Rare

Mortality/Morbidity

History

Physical

Initially, physical findings attributable to involvement of the fascicles of one or the other third cranial nerve are described. Subsequently, additional physical findings that are associated with lesions of particular portions or segments of the third cranial nerve are described.

Causes

Any focally destructive lesion along the course of the third cranial nerve can cause oculomotor nerve palsy or dysfunction. Some of the most frequent causes include the following:

Imaging Studies

Procedures

Histologic Findings

Cytologic examination of cerebrospinal fluid is used to diagnose meningeal carcinomatosis and lymphomatous or leukemic infiltration.

Medical Care

Surgical Care

Consultations

Activity

Medication Summary

NSAIDs commonly are used to treat the pain in ischemic third cranial nerve palsy.

Ibuprofen (Ibuprin, Motrin)

Clinical Context:  Can be used to treat the acute pain that commonly occurs with ischemic third cranial nerve palsy.

Class Summary

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Further Inpatient Care

Further Outpatient Care

Complications

Prognosis

Author

James Goodwin, MD, Associate Professor, Departments of Neurology and Ophthalmology, University of Illinois College of Medicine; Director, Neuro-Ophthalmology Service, University of Illinois Eye and Ear Infirmary

Disclosure: Nothing to disclose.

Specialty Editors

Edsel Ing, MD, FRCSC, Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Toronto East General Hospital, Canada

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Brian R Younge, MD, Professor of Ophthalmology, Mayo Clinic School of Medicine

Disclosure: Nothing to disclose.

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

References

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Patient with left posterior communicating artery aneurysm and third cranial nerve palsy. Courtesy of James Goodwin, MD.

Angiography anteroposterior and lateral views, left posterior communicating artery aneurysm, indicated by red arrow. Courtesy of James Goodwin, MD.

Angiography anteroposterior and lateral views, left posterior communicating artery aneurysm, indicated by red arrow. Courtesy of James Goodwin, MD.

Patient with left posterior communicating artery aneurysm and third cranial nerve palsy. Courtesy of James Goodwin, MD.