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3rd Nerve Palsy

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Title: 3rd Nerve Palsy
Author: Patrick Commiskey, 4th Year Medical Student, University of Michigan Medical School
Description: The 3rd cranial nerve (CN III), or oculomotor nerve, is a motor nerve responsible for many eye-related functions. The third cranial nerve innervates four of the six extraocular muscles: medial rectus, superior rectus, inferior rectus, and inferior oblique. Parasympathetic nerve fibers originating from the Edinger-Westphal nucleus travel circumferentially with CN III to the pupil. causing pupillary constriction when activated. The levator palpebrae superioris muscle, which is the primary muscle in elevating the eyelid is innervated by the superior division of CN III.

A complete lesion of CN III would result in ipsilateral ptosis (droopy eyelid) and a “down and out” eye due to denervation of most extraocular muscles leaving the lateral rectus (innervated by CN VI, abducts) and superior oblique (innervated by CN IV, depresses) unopposed.  A dilated pupil (mydriasis) resulting from disruption of the parasympathetic fibers are the result of denervation of the sphincter pupillae.

Understanding the anatomy of CN III is important to deciphering important the etiology of a CN III palsy. Most lesions of the 3rd cranial nerve are from vascular insults causing ischemia and can be attributed to known vascular risk factors such as diabetes or hypertension.  These presentations typically have ptosis, a down-and-out eye but a normal pupil.  However, a compressive or space-occupying lesion such as an aneurysm or tumor would cause disruption of the parasympathetic fibers because of their superficial location on the outside of CN III. In fact, an acutely “blown” pupil in conjunction with the above mentioned ptosis and motility deficits may be an ominous sign of a growing aneurysm. Retrospective review studies have shown that we cannot completely rely upon the pupil to differentiate vascular from compressive causes because numerous exceptions have occurred. Therefore, a “blown” pupil is treated emergently and requires neuro-imaging, but the lack of this sign does not exclude an acute space-occupying pathology.

Additional etiologies of 3rd nerve palsy to consider include Myasthenia Gravis, Thyroid disease, internuclear ophthalmoplegia, orbital tumor or pseudotumor, and temporal arteritis (giant cell arteritis).

References:

  1. Jacobson DM , BrosteSK. Early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies.Arch Ophthalmol.1995;113(12):1535–1537.
  2. Trobe JD . Managing oculomotor nerve palsy.Arch Ophthalmol.1998;116(6):798.

Identifier: Moran_CORE_ID: 24487