Oculomotor Nerve Palsy

Description

• There are six muscles that control eye movement innervated by three cranial nerves (CN):
  • CN III, or oculomotor nerve, innervates 4 of the 6 eye muscles and also innervates the lid and pupil:
    • Medial rectus:
      • Adduction – moves eye medially toward nose
    • Superior rectus:
      • Elevation – moves eye upward
      • Intorsion – rotates top of eye toward nose
      • Slight adduction
    • Inferior rectus:
      • Depression – moves eye inferiorly
      • Extorsion – rotates top of eye away from nose
      • Slight adduction
    • Inferior oblique:
      • Extorsion – rotates top of eye away from nose
      • Slight elevation and abduction
    • Levator palpebrae superioris:
      • Raises eyelid
    • Iris sphincter pupillae and ciliary muscles
      • Constricts pupil (miosis)
      • Innervated by parasympathetic fibers of CN III
  • CN IV innervates the superior oblique:
    • Extorsion – rotates top of eye away from nose
    • Depression and slight abduction (lateral rotation)
  • CN VI innervates the lateral rectus:
    • Moves eye laterally (abduction)
• Oculomotor nerve palsy results from damage to CN III or a branch thereof resulting in abnormal eye movements, lid ptosis, and/or changes to the pupil:
  • Complete oculomotor nerve palsy:
    • Eye “down and out,” ptosis, pupil dilated
    • Most often caused by compressive lesions
      • 95–97% of compressive lesions involve the pupil
      • Parasympathetic fibers sit peripherally in CN III
      • Mydriasis is often first symptom of compression
    • Pupil-sparing complete oculomotor nerve palsy:
      • Almost always ischemic from microvascular disease due to underlying diabetes, hypertension, and/or hyperlipidemia
      • Ischemic injuries often spare the pupil because the outer parasympathetics are not affected
      • Often benign and fully resolves in 3 mo
  • Incomplete oculomotor nerve palsy (more common):
    • Partial loss of function of CN III
    • Most often caused by ischemia of vasa vasorum
• Pathophysiology of oculomotor nerve palsy:
  • Midbrain lesions of the oculomotor nucleus leads to bilateral CN III palsy (ischemia of the basilar artery)
  • Lesions leaving CN III nucleus are often associated with other neurologic findings such as hemiplegia or ataxia (Weber syndrome, Benedikt syndrome)
  • Lesions in the subarachnoid space cause complete palsy with pupil involvement (compressive aneurysms) or complete palsy with pupil sparing (ischemia due to risk factors)
  • Lesions in the cavernous sinus and superior orbital fissure can cause isolated CN III palsy, but often are associated with CN IV, CN VI, and maxillary division of CN V dysfunctions
  • Lesions in the orbit are associated with visual loss (CN II), ophthalmoplegia (CN III, IV, VI), and proptosis and caused by trauma, mass, inflammation:
    • Incomplete CN III palsy originates here as the nerve divides into superior and inferior divisions

Etiology

• Acquired etiologies:
  • Vascular disorders:
    • Diabetes mellitus (DM)
    • Hypertension and heart disease
    • Atherosclerosis
    • Aneurysm (esp posterior communicating artery)
    • Arteriovenous malformation (AVM)
    • Intracranial hemorrhage (nonaneurysmal)
    • Cerebral vascular accident
    • Cavernous sinus thrombosis
  • Infectious:
    • Meningitis
    • Syphilis
    • Herpes zoster
  • Inflammatory:
    • Sarcoidosis
    • Giant cell arteritis, vasculitis
    • Systemic lupus erythematous
  • Neoplastic:
    • Intracranial tumor
    • Pituitary tumor
    • Orbital tumor
    • Leukemia
  • Degenerative:
    • Myasthenia gravis
    • Guillain–Barré
  • Trauma – head injury, recent or remote
  • Migraine headache
  • Iatrogenic:
    • Chemotherapy
    • Radiation therapy
  • Idiopathic:
    • Idiopathic intracranial hypertension (IIH)
  • Congenital etiologies are often unknown but some with familial tendency

• Trauma is the most common cause of acquired oculomotor nerve palsies:
  • Includes birth trauma
• Can also see in neurofibromatosis, ophthalmologic migraine with recurrent CN III palsy, and spontaneous intracranial hypotension