oculomotor nerve
The oculomotor nerve is the third cranial nerve. Its nuclear complex lies in the midbrain at the level of the superior colliculus, ventral to the Sylvian aqueduct.1 In the anterior cavernous sinus the nerve divides, and both divisions enter the orbit through the superior orbital fissure within the annulus of Zinn. The superior division supplies the levator and superior rectus. The inferior division supplies the medial rectus, inferior rectus and inferior oblique.1 The branch to the inferior oblique also carries preganglionic parasympathetic fibers from the Edinger-Westphal subnucleus to the sphincter pupillae and the ciliary muscle.1
A complete third nerve palsy causes profound ptosis and leaves the eye down and out, because the lateral rectus and superior oblique act unopposed. Adduction, elevation and depression are limited, and the pupil is dilated with defective accommodation.1 The pupillomotor fibers run superficially in the superomedial part of the nerve, so compressive lesions such as aneurysms, trauma and uncal herniation characteristically involve the pupil. Microvascular palsies from hypertension and diabetes usually spare the pupil, because their ischemia affects the main trunk of the nerve. The rule is not infallible.1
Microvascular disease is the most common cause, at about 40% of cases.1 In an adult with an acquired, isolated third nerve palsy, especially one that involves the pupil, an aneurysm at the junction of the internal carotid and posterior communicating arteries must be excluded emergently. Immediate computed tomography or magnetic resonance imaging, with noninvasive angiography, is required.2
More detail
The levator subnucleus is a single midline structure that supplies both levators, so a lesion there causes bilateral ptosis. Each superior rectus subnucleus supplies the contralateral superior rectus, so a nuclear palsy spares the ipsilateral superior rectus and affects the contralateral one.1 Fascicular lesions produce named syndromes. Benedikt syndrome adds contralateral extrapyramidal signs, Weber syndrome adds contralateral hemiparesis, Nothnagel syndrome adds cerebellar ataxia, and Claude syndrome combines Benedikt and Nothnagel syndromes.1
In diabetes-related palsy, about 80% of cases show relative or complete pupil sparing.1 Aberrant regeneration may follow traumatic and compressive palsies but not vascular ones. Misdirected regenerating axons then produce signs such as elevation of the upper eyelid on attempted adduction or depression, the pseudo-Graefe phenomenon.1
Sources (8)
- Kanski's Clinical Ophthalmology (2024), ch. 19
- Liu, Volpe and Galetta, Neuro-Ophthalmology: Diagnosis and Management, ch. 15
- Brazis, P.W. 2011. Localization of lesions of the oculomotor nerve: recent concepts. Mayo Clinic Proceedings, 86(10), pp.1029-1035.
- Ehlers, J.P., Shah, C.P. and Fenton, G.L. eds. 2008. The Wills eye manual: office and emergency room diagnosis and treatment of eye disease. 5th ed. Philadelphia: Lippincott Williams & Wilkins.
- Lavin, P.J.M. 2005. Pupillary dilatation in oculomotor nerve palsy. Archives of Ophthalmology, 123(4), pp.555-556.
- Prasad, S. and Volpe, N.J. 2010. Paralytic strabismus: third, fourth, and sixth nerve palsy. Neurologic Clinics, 28(3), pp.803-833.
- Rucker, J.C. and Tomsak, R.L. 2005. Binocular diplopia: a practical approach. The Neurologist, 11(2), pp.98-110.
- Rutstein, R. and Daum, K. 1997. Anomalies of Binocular Vision: Diagnosis & Management. St. Louis: Mosby.
Reviewed October 2026