Mohd Alhalki

West Middlesex University Hospital, London

Introduction:

The oculomotor cranial nerve has 2 major components which collectively control eye movements, pupil constriction, and upper eyelid elevation. Accordingly, third nerve palsy will cause diplopia, failure of pupil constriction, and upper eyelid ptosis

Third nerve palsy can be divided into a partial or complete palsy and has a variety of causes which can be life-threatening.

Pathophysiology:

The oculomotor nerve nucleus presents in the midbrain, at the level of the superior colliculus, and consists of a motor nucleus and a parasympathetic nucleus

The oculomotor nerve exits the midbrain through the interpeduncular fossa between the posterior cerebral artery and the superior cerebellar artery to reach the cavernous sinus. During this course, the oculomotor nerve lies lateral to the posterior communicating artery. The nerve then divides into a superior and inferior division and enters the orbit through the superior orbital fissure.

Causes:

There are many aetiologies for oculomotor nerve palsy. The aetiology and presentation will depend on the level and course of nerve damage.

The most common causes of 3rd cranial nerve palsy are

• compression of the nerve: such as aneurysm, neoplasm, or haemorrhage

• Inadequate blood supply to the nerve (ischaemia): such as stroke, HTN, diabetes, or vasculitis.

Main parts of Oculomotor nerve and most common causes of nerve dysfunction: Oculomotor Nucleus (Midbrain): Vascular diseases, and tumours are the main cause of third-nerve palsy.

Oculomotor Nerve Fascicles: similar to the nuclear lesions.

Subarachnoid space (interpeduncular): The primary causes of isolated palsy include aneurysms, diabetes mellitus, and extradural hematoma.

Cavernous Sinus and Superior Orbital Fissure: The common causes are diabetes, pituitary apoplexy, aneurysm, or carotid-cavernous fistula.

Presentation:

Third nerve palsy presentation depends on the location of the lesion.

The most common ocular manifestations are diplopia and ptosis.

Diplopia occurs due to ocular deviation which brings the eye in a “down and out” position.

In ischemic third-nerve palsy, the pupil is spared, and there is no loss of accommodation

In compressive third-nerve palsy, the pupil becomes fixed and dilated. Therefore, In a patient presenting with ophthalmoplegia, ptosis and mydriasis, a compressive aetiology, such as an intracranial aneurysm, must be ruled out

Investigations:

Brain imaging is usually done if intracranial pathology is suspected

If an intracranial aneurysm is suspected, a CT angiography (CTA) or MR angiography (MRA) should be urgently performed,

Generally speaking, MRI is a more sensitive imaging modality for detecting intracranial anomaly than CT scan

Patients with pupil-sparing third-nerve palsy should be evaluated to exclude any vascular cause. Basic workup includes vital signs and blood pressure

recording, complete blood count (CBC), blood sugar including Hb1AC and erythrocyte sedimentation rate (ESR).

Management:

Treatment of 3rd cranial nerve palsy depends on the cause.

Conservative management:

The majority of complete or incomplete third-nerve palsies without pupil involvement are secondary to an ischemic process.

Most patients with ischemic third-nerve palsy demonstrate improvement within 1 month and complete recovery in 3 month

Surgical management:

Emergency treatment is required if a compressive third-nerve palsy such as intracranial haemorrhage or aneurysm is the cause.

Differential diagnosis:

• Myasthenia Gravis (should be considered in any painless pupil-sparing ophthalmoplegia with or without ptosis)

• Thyroid eye disease

• Pituitary apoplexy

• Ophthalmoplegic migraine

• Internuclear ophthalmoplegia

• Orbital pseudotumor

• Giant cell arteritis