For more information regarding 3rd nerve palsy, watch my video, with the transcript below.

Hi, today I am looking at assessing a patient with a new onset 3rd cranial nerve palsy, also called an oculomotor nerve palsy.

So what are the clinical features?Well the oculomotor nerve supply’s the levator palpabrae superioris muscle, responsible for elevating the upper eyelid. It also supply’s 4 of the 6 extraocular muscles: superior rectus, medial rectus, inferior oblique and inferior rectus. It has no sensory action.

Loss of function of the 3rd nerve therefore causes the remaining lateral rectus and superior oblique muscles to act unnapposed and deviate the eye down and out. It also carries parasympathetic innervation to the pupil, responsible for pupil constriction. A palsy may therefore leave the pupil dilated. This pupil involvement is typically spared in microvascular palsy. Finally the deviated eye is hidden behind the drooping or ptotic eyelid due to loss of levator function. This ptosis may relieve the unpleasant diplopia caused by the deviation of the affected eye.

Lets look at the pathway of the oculomotor nerve.

If we look at the brainstem from the side, through the temporal lobe, the oculomotor nerve nucleus lies at the level of the superior colliculus in the midbrain. The nerve exits ventrally, as the subarachnoid portion, into the cavernous sinus where it splits into superior and inferior branches before entering the orbit through the superior orbital fissure.

In section, the oculomotor nerve nuclei lie centrally, close to the midline. The superior rectus subnucleus is distinct in supplying the contralateral eye, while there is a single midline subnucleus supplying both levator muscles. Dorsal midbrain infarction may therefore cause an ipsilateral 3rd nerve palsy with in addition a contralateral upgaze palsy and partial ptosis. The infarct may be visible on MRI.

Pretectal nuclei lie dorsally and receive innervation from the optic tracts as part of the pupil light reflex. These then pass fibres bilaterally to the edinger-westphal nuclues, which is the parasympathetic nucleus responsible for pupil constriction and closely related to the oculomotor nucleus. Fibres from both pass ventrally through the red nucleus and cerebral peduncles and exit as the fascicular subarachnoid oculomotor nerve. Lesions affecting the red nucleus or cerbral peduncles cause ipsilateral flapping tremor or contralateral hemiplegia respectively. Both are easily detected by asking the patient to stretch out their arms.

The parasympathetic fibers run superficially within the nerve and as mentioned are typically spared by microvascular ischaemia which is a common cause of oculomotor nerve palsy in diabetics. Pain in and around the eye is quite common, but neck stiffness or decreased consciousness are not features. The palsy evolves over a period of around 3 days, shows improvement within 4 weeks and has completely resolved within 4 months. A painless 3rd nerve palsy with pupil sparing should make the possibility of ocular myasthenia a consideration where the patient is not diabetic. Check blood pressure, fasting glucose, ESR and a CT head in patients under 50. Re-examine the patient in 1-3 days if the symtoms are less than 48 hours duration, to check the pupils remain normal.

The circle of willis lies immediately beside the subarachnoid oculomotor nerve, with supply from the single basilar artery and two internal carotid artery’s. The major branches of these are the anterior cerebral, middle cerebral and posterior cerebral artery’s. These are connected into a circle by the single anterior communicating artery – which is the most common site of berry aneurysm, and the two posterior communicating artery’s. Posterior communicating artery aneurysms occur at the origin of the artery from the internal carotid and compress the adjacent oculomotor nerve, especially upon rupture with subarachnoid haemorrhage. The patient presents with severe headache, reduced consciousness, neck stiffness and vomiting. The associated oculomotor nerve palsy is isolated, may take 3 days to maximise but normally becomes complete and pupil dilation is the rule. Formal angiography is indicated to exclude aneurysm in all isolated oculomotor nerve palsys with a dilated pupil, with MR angiography an option where the index of suspicion is lower, for example an otherwise well diabetic patient with an oculomotor nerve palsy and slight pupil dilation.

The subarachnoid portion of the 3rd nerve is also vulnerable to basal meningeal infection, inflammation or neoplastic infiltration and these usually affect multiple cranial nerves.

Next the oculomotor nerve enters the cavernous venous sinus. This dural sinus lies beneath the frontal lobes of the brain, with the temporal lobes laterally. The sphenoid sinus lies inferiorly and the pituitary gland sits in the middle within the sella turcica. The optic chiasm crosses in front of the pituitary stalk and the internal carotid artery’s loop through the sinus. Laterally the oculomotor nerve sits against the lateral wall, as do the 4th nerve and upper 2 branches of the trigeminal nerve. The Abducens nerve is more medial and is most often the first nerve to be affected by cavernous sinus pathology. Lesions here tend to affect multiple cranial nerves although a 4th or 6th nerve deficit can be difficult to demonstrate clinically when combined with a 3rd nerve palsy. Therefore particular attention should be paid to features suggestive of trigeminal nerve involvement. This would be burning pain and numbness affecting the forehead or cheek, representing the first or second division of the trigeminal nerve. Pupil involvement here is variable, with both sympathetic and parasympathetic pupillary fibres present. The pupil may therefore be small, large or normal. Causes of cavernous sinus lesions include Tolosa-Hunt granulomatous inflammation, Pituitary, Nasopharyngeal or Metastatic Neoplasms and Intracavernous aneurysms. Herpes zoster may also affect the oculomotor nerve, associated with ophthalmic shingles.

Finally the 3rd nerve enters the orbit as superior and inferior branches through the superior orbital fissure and may be damaged by orbital fractures. The superior branch supply’s levator and superior rectus, the inferior supplying medial rectus, inferior oblique, inferior rectus, pupil and ciliary muscle. A partial 3rd nerve palsy affecting one of these branches may be a feature of oculomotor palsy elsewhere along its path, and doesn’t necessarily localise pathology to the cavernous sinus or orbit. Pathology within the orbit usually also features an abduction deficit, as well as proptosis, lid swelling, conjunctival injection, and chemosis.

Assessment and follow-up of oculomotor nerve palsy is usually by an ophthalmologist in conjunction with orthoptists, who as well as measuring the degree of deficit, may prescribe prisms to control diplopia during recovery.

A few key points once more:
The oculomotor palsy is characterized by unilateral ptosis and an eye that is down and out.

Pupil dilation suggests compression, possibly by berry aneurysm.

A contralateral ptosis or upgaze palsy suggest a dorsal midbrain lesion.

An ipsilateral ataxia or contralateral hemiparesis suggesting ventral midbrain lesion, check by asking the patient to stretch out their arms.

Check for facial parasthesia, corneal sensation, and ask about burning facial pain or numbness to consider cavernous sinus lesions.