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The defeat of the oculomotor (III) nerve (n. Oculomotorius)

, medical expert
Last reviewed: 23.04.2024
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Topical diagnosis of oculomotor nerve damage is possible on the following five levels:

  1. The nuclear complex of the oculomotor nerve and its spine in the brain stem.
  2. The nerve trunk in the subarachnoid space.
  3. Cavernous sinus.
  4. Upper orbital crack.
  5. The Sacrament.

One-sided defeat at the level of the nuclear complex or root of the third nerve in the trunk of the brain

The defeat of the entire nucleus of the III nerve

Ipsilateral - complete paralysis of the 3rd nerve

Contralateral - ptosis and paresis m. Rectus superior

The defeat of an individual nucleus of the nuclear complex Isolated paralysis of any muscle (eg, M. Rectus inferior)
Isolated damage to the nucleus for m. Levator Isolated bilateral ptosis
Paramedian defeat of mesencephalon Plus-minus syndrome (ipsilateral ptosis and contralateral retraction of the eyelid
Isolated lesion of root of nerve III Isolated partial or complete paralysis of the 3rd nerve with or without involvement of pupillary innervation
The defeat of the root of the third nerve, the red nucleus and the upper leg of the cerebellum Ipsilateral paralysis of the third nerve with contralateral ataxia and tremor (Claude-Claude syndrome)
Defeat of root of the third nerve and conductors in the legs of the brain Ipsilateral paralysis of the third nerve and contralateral hemiparesis (Weber-Weber syndrome)
The defeat of the root of the third nerve of the red nucleus, the black substance and the subthalamic region Ipsilateral paralysis of the third nerve of the nerve and contralateral choreiform movements (Benedict syndrome - strongenedikt)

Damage to the trunk of the third nerve in the subarachnoid space

There is complete paralysis of the muscles innervated by the III nerve with or without the involvement of other cranial nerves; eyeball movements up and down are impossible.

trusted-source[1], [2], [3], [4], [5], [6]

The defeat of 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 IV, VI nerves (ophthalmoplegia) and I of the V branch of the nerve with Horner's syndrome on the same side.

The defeat of the third nerve in the upper orbital gap

There is paralysis of the muscles innervated by the III nerve with or without IV, VI and the first branch of the V nerves, often exophthalmos.

The defeat of the third nerve in orbit

There is paralysis of the muscles innervated by the III nerve. If the optic nerve is involved, visual acuity decreases. Possible exophthalmos, chemosis.

Possible causes of damage to the III nerve

Polyneuropathy and mononeuropathy (diabetes mellitus, etc.), aneurysms, tumors, tuberculosis, cerebral infarctions, encephalitis, demyelinating diseases, meningitis, trauma, infringement of the temporal lobe in the opening of the cerebellum, Tolosa-Hunt syndrome, sinus thrombosis, carotid cavernous fistula , arterio-venous malformation, ophthalmic herpes, orbital pseudotumor, pituitary apoplexy, "nerve stroke", syphilis, congenital nerve hypoplasia, ophthalmic migraine, vasculitis, sarcoidosis, infectious mononucleosis and other viral infections, postvaccinal neuropathy and other diseases. The unknown cause of isolated paralysis of the third nerve is about 30% of all cases.

Diseases simulating the defeat of the third nerve: thyrotoxicosis, myasthenia gravis, internuclear ophthalmoplegia, friendly strabismus, progressive external ophthalmoplegia.

Symptoms of lesion of the left third cranial nerve

  • The weakness of the levator is manifested by complete ptosis, due to which diplopia is often absent.
  • A non-counteracting lateral rectus leads the eye to the primary position.
  • The intact upper oblique muscle causes an intortus of the eye at rest, amplified when trying to look down.
  • Normal lead, tk. The external rectus muscle is intact.
  • The weakness of the inner rectus restricts the reduction.
  • The weakness of the upper and lower oblique muscles limits the uplift.
  • The weakness of the lower rectus restricts the subsidence.
  • The defeat of parasympathetic fibers is the cause of the dilated pupil with accommodation disruption.

Aberrant regeneration may be a complication of an aneurysm and an acute traumatic, but not vascular injury, III. This is explained by the fact that the zondoneural envelope, which can be damaged by traumatic and compression lesions, remains intact in vascular pathology. Bizarre violations of eye mobility, such as the raising of the upper eyelid when trying to bring or lower the eye (the phenomenon of pseudo-Gracie), are associated with abnormal growth of axons, rhea and unnerving inappropriate muscles. Possible pupillary disorders.

Causes of isolated defeat of the third pair of cranial nerves

  1. Idiopathic defeat: the cause is unknown in 25% of cases.
  2. Vascular diseases, such as hypertension and diabetes, are the most common cause of injury to the third pair of cranial nerves without pupillary disorders, so all patients need to measure blood pressure, blood glucose and urinalysis. In most cases, spontaneous recovery occurs within 6 months. Diabetic lesion of the third pair of cranial nerves is often accompanied by periorbital pain and sometimes is the first manifestation of diabetes, so the presence of pain does not help differentiate the aneurysmal and diabetic lesions of the third pair of cranial nerves.
  3. Trauma, direct and secondary to the subdural hematoma with the incision of the hook, is a common cause. However, the defeat of the third pair of cranial nerves after minor head trauma, not accompanied by loss of consciousness, should alert the doctor with regard to the possible presence of a basal intracranial tumor, which causes tension of the nerve trunk.
  4. An aneurysm of the posterior connective artery in its connection with the internal carotid is a very important reason for the isolated painful lesion of the third pair of cranial nerves with pupillary disorders.
  5. Other infrequent causes: tumors, syphilis and vasculitis with collagenoses.

trusted-source[7], [8], [9], [10], [11], [12]

Treatment of defeat of the third pair of cranial nerves

Non-surgical treatment involves the use of Fresnel prisms, if the angle of deflection is small, one-sided occlusion to eliminate diplopia (if ptosis is partial or decreased) and injections of CI toxin. Boiulinum in intactial lateral rectus to prevent its contracture until the deviation is reduced or stabilized.

Surgical treatment, as with lesions of other oculomotor nerves, should be considered only after the termination of spontaneous improvement, usually no earlier than 6 months after the onset of the disease.

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