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.
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
- Morbidity and mortality are essentially those of the diseases that cause oculomotor nerve palsy and are beyond the scope of this article.
- The most significant causes of mortality and morbidity along with oculomotor nerve palsy are subarachnoid hemorrhage from berry aneurysm of the posterior communicating artery, and meningitis or meningeal infiltrative disorders, both infectious and neoplastic.
Warwick R. Representation of the extraocular muscles in the oculomotor nuclei of the monkey. J Comp Neurol. Jun 1953;98(3):449-503. [Medline].
Vieira JP, Castro J, Gomes LB, et al. Ophthalmoplegic migraine and infundibular dilatation of a cerebral artery. Headache. Oct 2008;48(9):1372-4. [Medline].
Bharucha DX, Campbell TB, Valencia I, et al. MRI findings in pediatric ophthalmoplegic migraine: a case report and literature review. Pediatr Neurol. Jul 2007;37(1):59-63. [Medline].
Acierno MD, Trobe JD, Cornblath WT, et al. Painful oculomotor palsy caused by posterior-draining dural carotid cavernous fistulas. Arch Ophthalmol. Aug 1995;113(8):1045-9. [Medline].
Bahmani Kashkouli M, Khalatbari MR, Yahyavi ST, et al. Pituitary apoplexy presenting as acute painful isolated unilateral third cranial nerve palsy. Arch Iran Med. Jul 2008;11(4):466-8. [Medline].
Quisling SV, Shah VA, Lee HK, et al. Magnetic resonance imaging of third cranial nerve palsy and trigeminal sensory loss caused by herpes zoster. J Neuroophthalmol. Mar 2006;26(1):47-8. [Medline].
Yamada K, Shiga K, Kizu O. Oculomotor nerve palsy evaluated by diffusion-tensor tractography. Neuroradiology. Mar 15 2006;[Medline].
Chen W, Yang Y, Xing W, et al. Sixteen-row multislice computed tomography angiography in the diagnosis and characterization of intracranial aneurysms: comparison with conventional angiography and intraoperative findings. J Neurosurg. Jun 2008;108(6):1184-91. [Medline].
Uysal E, Oztora F, Ozel A, et al. Detection and evaluation of intracranial aneurysms with 16-row multislice CT angiography: comparison with conventional angiography. Emerg Radiol. Sep 2008;15(5):311-6. [Medline].
Asbury AK, Aldredge H, Hershberg R, et al. Oculomotor palsy in diabetes mellitus: a clinico-pathological study. Brain. 1970;93(3):555-66. [Medline].
Trobe JD. Isolated pupil-sparing third nerve palsy. Ophthalmology. Jan 1985;92(1):58-61. [Medline].
Jacobson DM, McCanna TD, Layde PM. Risk factors for ischemic ocular motor nerve palsies. Arch Ophthalmol. Jul 1994;112(7):961-6. [Medline].
Trobe JD. Third nerve palsy and the pupil. Footnotes to the rule. Arch Ophthalmol. May 1988;106(5):601-2. [Medline].
Jacobson DM. Pupil involvement in patients with diabetes-associated oculomotor nerve palsy. Arch Ophthalmol. Jun 1998;116(6):723-7. [Medline].
Daniell MD, Gregson RM, Lee JP. Management of fixed divergent squint in third nerve palsy using traction sutures. Aust N Z J Ophthalmol. Aug 1996;24(3):261-5. [Medline].
Chen PR, Amin-Hanjani S, Albuquerque FC, et al. Outcome of oculomotor nerve palsy from posterior communicating artery aneurysms: comparison of clipping and coiling. Neurosurgery. Jun 2006;58(6):1040-6; discussion 1040-6. [Medline].
Leivo S, Hernesniemi J, Luukkonen M, et al. Early surgery improves the cure of aneurysm-induced oculomotor palsy. Surg Neurol. May 1996;45(5):430-4. [Medline].
Burgess AW, Scheraga HA. A hypothesis for the pathway of the thermally-induced unfolding of bovine pancreatic ribonuclease. J Theor Biol. Sep 1975;53(2):403-20. [Medline].
Jacobson DM, Broste SK. Early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies. Arch Ophthalmol. Dec 1995;113(12):1535-7. [Medline].
Keane JR. Aneurysms and third nerve palsies. Ann Neurol. Dec 1983;14(6):696-7. [Medline].
Keane JR, Ahmadi J. Third-nerve palsies and angiography. Arch Neurol. May 1991;48(5):470. [Medline].
Miller NR. The ocular motor nerves. Curr Opin Neurol. Feb 1996;9(1):21-5. [Medline].
Trobe JD. Isolated third nerve palsies. Semin Neurol. Jun 1986;6(2):135-41. [Medline].

