Lesion of the oculomotor (III) nerve (n. oculomotorius)

Topical diagnostics of oculomotor nerve damage is possible at the following five levels:

1. Nuclear complex of the oculomotor nerve and its root in the brainstem.
2. Nerve trunk in the subarachnoid space.
3. Cavernous sinus.
4. Superior orbital fissure.
5. Eye socket.

Unilateral lesion at the level of the nuclear complex or root of the third nerve in the brainstem

Lesion of the entire nucleus of the third nerve	Ipsilateral - complete paralysis of the third nerve Contralaterally - ptosis and paresis of the m. rectus superior
Damage to a single nucleus of the nuclear complex	Isolated paralysis of any muscle (for example, m. rectus inferior)
Isolated lesion of the nucleus for m. levator	Isolated bilateral ptosis
Paramedian mesencephalic lesion	Plus-minus syndrome (ipsilateral ptosis and contralateral eyelid retraction
Isolated lesion of the root of the third nerve	Isolated partial or complete palsy of the third nerve with (or without) involvement of the pupillary innervation
Lesion of the root of the third nerve, red nucleus and superior cerebellar peduncle	Ipsilateral third nerve palsy with contralateral ataxia and tremor (Claude syndrome)
Lesion of the root of the third nerve and conductors in the cerebral peduncles	Ipsilateral palsy of the third nerve and contralateral hemiparesis (Weber syndrome)
Lesion of the root of the third nerve of the red nucleus, substantia nigra and subthalamic region	Ipsilateral III nerve palsy and contralateral choreiform movements (Benedict's syndrome - strongenedikt)

Lesion of the trunk of the third nerve in the subarachnoid space

There is complete paralysis of the muscles innervated by the third nerve with (or without) involvement of other cranial nerves; upward and downward movements of the eyeball are impossible.

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Damage to the third nerve in the cavernous sinus

There is paralysis of the muscles innervated by the III nerve (with or without pain), with (or without) combined damage to the IV, VI nerves (ophthalmoplegia) and the first branch of the V nerve with Horner's syndrome on the same side.

Lesion of the third nerve in the superior orbital fissure

Paralysis of the muscles innervated by the III nerve with (or without) involvement of the IV, VI and first branch of the V nerves is observed, often exophthalmos.

Lesion of the third nerve in the orbit

Paralysis of the muscles innervated by the third nerve is observed. If the optic nerve is involved, a decrease in visual acuity develops. Exophthalmos and chemosis are possible.

Possible causes of damage to the third nerve

Polyneuropathies and mononeuropathies (diabetes mellitus, etc.), aneurysms, tumors, tuberculoma, cerebral infarctions, encephalitis, demyelinating diseases, meningitis, trauma, temporal lobe entrapment in the tentorium foramen, Tolosa-Hunt syndrome, sinus thrombosis, carotid-cavernous fistula, arteriovenous malformation, ophthalmic herpes, orbital pseudotumor, pituitary apoplexy, "nerve stroke", syphilis, congenital nerve hypoplasia, ophthalmic migraine, vasculitis, sarcoidosis, infectious mononucleosis and other viral infections, post-vaccination neuropathy and other diseases. Unknown cause of isolated palsy of the third nerve - about 30% of all cases.

Diseases that simulate damage to the third nerve: thyrotoxicosis, myasthenia, internuclear ophthalmoplegia, concomitant strabismus, progressive external ophthalmoplegia.

Symptoms of damage to the left third cranial nerve

• Weakness of the levator is manifested by complete ptosis, as a result of which diplopia is often absent.
• The unopposed lateral rectus muscle abducts the eye to the primary position.
• An intact superior oblique muscle causes eye intorsion at rest, which increases with downward gaze.
• Normal abduction because the lateral rectus muscle is intact.
• Weakness of the internal rectus muscle limits adduction.
• Weakness of the superior rectus and inferior oblique muscles limits elevation.
• Weakness of the inferior rectus muscle limits descent.
• Damage to the parasympathetic fibers causes pupil dilation with impaired accommodation.

Aberrant regeneration may be a complication of aneurysm and acute traumatic, but not vascular, lesions of the third cranial nerve. This is explained by the fact that the endoneural sheath, which can be damaged by traumatic and compressive lesions, remains intact in vascular pathology. Bizarre disturbances of ocular motility, such as raising the upper eyelid when trying to adduct or depress the eye (pseudo-Gracie phenomenon), are associated with abnormal growth of axons that reinnervate inappropriate muscles. Pupillary disturbances are possible.

Causes of isolated damage to the third pair of cranial nerves

1. Idiopathic lesion: the cause is unknown in 25% of cases.
2. Vascular diseases such as hypertension and diabetes are the most common causes of third cranial nerve lesions without pupillary abnormalities, so all patients should have blood pressure, glucose levels, and urine tests. Most cases spontaneously resolve within 6 months. Diabetic third cranial nerve lesions are often accompanied by periorbital pain and are sometimes the first manifestation of diabetes, so the presence of pain does not help differentiate aneurysmal from diabetic third cranial nerve lesions.
3. Trauma, direct and secondary to subdural hematoma with hook wedging, is a common cause. However, lesion of the third pair of cranial nerves after minor head trauma without loss of consciousness should alert the physician to the possibility of a basal intracranial tumor causing tension on the nerve trunk.
4. Aneurysm of the posterior communicating artery at its junction with the internal carotid artery is a very important cause of isolated painful damage to the third pair of cranial nerves with pupillary disturbances.
5. Other uncommon causes include tumors, syphilis, and vasculitis in collagenoses.

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Treatment of damage to the third pair of cranial nerves

Nonsurgical treatment includes the use of Fresnel prisms if the deviation angle is small, unilateral occlusion to eliminate diplopia (if ptosis is partial or decreasing), and injection of CI boiulinum toxin into the intact lateral rectus muscle to prevent its contracture until the deviation decreases or stabilizes.

Surgical treatment, as with other oculomotor nerve lesions, should be considered only after spontaneous improvement has ceased, usually not earlier than 6 months after the onset of the disease.