Clinical Examination of the Oculomotor Nerve (CN III)
Test the oculomotor nerve by assessing extraocular movements (asking the patient to follow your finger in an "H" pattern), checking for ptosis, evaluating pupil size and reactivity, and looking for the characteristic "down and out" eye position at rest if CN III is damaged. 1, 2
Motor Function Testing
Extraocular Muscle Assessment
- Ask the patient to follow your finger through all fields of gaze to test the four extraocular muscles innervated by CN III: superior rectus (upward gaze), inferior rectus (downward gaze), medial rectus (inward/adduction), and inferior oblique (upward and outward gaze). 3, 2
- The superior oblique (CN IV) and lateral rectus (CN VI) are NOT innervated by CN III, so isolated weakness in depression while adducted or abduction suggests involvement of other cranial nerves. 3, 4
- In complete CN III palsy, the eye assumes a "down and out" position due to unopposed action of the lateral rectus (CN VI) and superior oblique (CN IV) muscles. 5, 6
Eyelid Position (Levator Function)
- Observe for ptosis (drooping of the upper eyelid), which occurs because CN III innervates the levator palpebrae superioris muscle. 5, 2
- Ptosis in CN III palsy is typically complete or near-complete, distinguishing it from the mild ptosis seen in Horner's syndrome. 5
- Nuclear CN III lesions may cause bilateral incomplete ptosis due to the shared central caudal nucleus that innervates both levator muscles. 7
Parasympathetic Function Testing
Pupillary Examination
- Assess pupil size in both eyes - CN III carries parasympathetic fibers that constrict the pupil via the sphincter pupillae muscle. 2, 4
- Test direct and consensual light reflexes by shining light in each eye and observing both pupils for constriction. 8, 4
- Pupil-involving CN III palsy (dilated, unreactive pupil) requires urgent evaluation for compressive lesions, especially posterior communicating artery aneurysm, as parasympathetic fibers run superficially on the nerve and are vulnerable to external compression. 1, 5
- Pupil-sparing CN III palsy suggests vasculopathic/ischemic etiology (diabetes, hypertension) as the parasympathetic fibers are relatively preserved when the nerve's vascular supply is compromised. 1
Key Clinical Distinctions
Differentiating CN III from Other Causes of Ophthalmoplegia
- CN VI palsy causes isolated limitation of abduction WITHOUT ptosis or pupillary abnormalities, with the eye positioned "in" (esotropia). 6
- Myasthenia gravis causes variable, fatigable ptosis without pupillary abnormalities, distinguishing it from CN III palsy. 5
- Horner's syndrome presents with mild ptosis, miosis (small pupil), and anhidrosis, contrasting with the dilated pupil and complete ptosis of CN III palsy. 5
Nuclear vs. Fascicular vs. Peripheral Localization
Nuclear Lesions (Brainstem)
- Characteristic triad: unilateral CN III palsy, bilateral incomplete ptosis, and contralateral superior rectus weakness due to the unique nuclear organization where the superior rectus subnucleus innervates the contralateral muscle. 7
Fascicular Lesions (Midbrain)
- Associated with other brainstem signs such as contralateral hemiparesis (Weber syndrome) or contralateral tremor/ataxia (Claude syndrome). 7, 2
Peripheral Lesions (Cisternal, Cavernous Sinus, Orbital)
- Isolated CN III palsy without other neurological signs suggests peripheral involvement. 1, 2
- Aberrant regeneration (eyelid elevation with attempted adduction or downgaze) may occur months to years after peripheral CN III injury, never with ischemic lesions. 7
Common Pitfalls
- Do not assume all ptosis is CN III-related - consider Horner's syndrome, myasthenia gravis, mechanical causes, and orbital inflammatory conditions. 5
- Pupil-involving CN III palsy is a neurological emergency requiring immediate vascular imaging (CTA or MRA) to exclude aneurysm. 1
- Complete evaluation requires assessment from brainstem nuclei to orbital end-organs, as pathology can occur anywhere along this pathway. 1