oculomotor nerve palsy
Introduction
Introduction Lesions of the oculomotor nerves and their dominating tissues caused by lesions in various regions are called oculomotor nerve palsy. When the oculomotor nerves are paralyzed, the upper eyelids are drooping, the eyeballs are restricted inward, upward and downward, and exotropia and diplopia appear, and the pupils are scattered, and the adjustment and aggregation reflexes disappear. The cyclical phenomenon is caused by the rhythmic impulse of the midbrain nerve center directly acting on the oculomotor nerve. The cause is divided into: 1. Congenital oculomotor nerve palsy: This type is rare, the vast majority is monocular, the cause is dysplasia or birth injury. 2. Acquired oculomotor nerve palsy: Acquired oculomotor nerve palsy is more common than congenital oculomotor nerve palsy, but it is less common in the three pairs of cranial nerves associated with eye movement.
Cause
Cause
Congenital oculomotor nerve palsy: This type is rare, the vast majority is monocular, the cause is dysplasia or birth injury.
Acquired oculomotor nerve palsy: Acquired oculomotor nerve palsy is more common than congenital oculomotor nerve palsy, but it is less common in the three pairs of cranial nerves associated with eye movement. Branch palsy of the oculomotor nerve is more common than oculomotor palsy. The oculomotor palsy is more common than the lower palsy. Specific causes include:
First, brain stem lesions
1, Benedikt syndrome, manifested as ipsilateral oculomotor palsy and contralateral intentional tremor.
2, Weber syndrome, manifested as ipsilateral oculomotor nerve paralysis and contralateral hemiplegia.
Second, the inflammatory environment
1, meningitis.
2, encephalitis.
3. Polyneuritis caused by alcohol, lead, arsenic and carbon monoxide poisoning or diabetes.
4. Herpes zoster virus infection.
5, Echo virus infection.
Third, vascular disease
1, microaneurysms.
2, internal carotid artery (ICA) peeling, ICA stenosis.
3, carotid cavernous fistula.
Fourth, the tumor
Glioblastoma multiforme.
Fifth, demyelinating disease
1, multiple sclerosis.
2. Chronic inflammatory demyelinating polyneuropathy.
Sixth, trauma
Seven, other
1. Anterior communicating aneurysm.
2, bilateral chronic subdural hematoma.
3. Congenital toxoplasmosis.
4, "Crack" cocaine.
5. Diagnostic angiography.
6, optic eosinophilic granuloma.
7, frontal sinus mucus cyst.
8. Infectious mononucleosis.
9, leukemia.
10. Vaccination against measles.
11, myasthenia gravis.
12, eye muscle paralysis migraine.
13, nodular polyarteritis.
14, porphyria.
15, sarcomatoid disease.
16, Schwann cell tumor.
17, temporal arteritis.
18, Viagra drug treatment (citronium citrate tablets).
Examine
an examination
Related inspection
Oculomotor examination
The diagnosis of oculomotor nerve paralysis mainly relies on detailed ophthalmic neurological examination, including drooping of the eyelid, exotropia of the eye, dilation of the pupil, poor coordination of the two eyes, etc. Retinal and optic papilla examinations are also a focus, and another examination The direction is to exclude diseases that are harmful to other tissues and organs. Therefore, in addition to the basic ophthalmic neurological examination, we must also perform some imaging examinations (computed computed tomography CT, nuclear magnetic resonance MRI, angiography) to eliminate some progressive diseases, if the patient itself If there is no special systemic disease (such as hypertension, diabetes, etc.), it is necessary to suspect whether there are diseases such as blood, blood vessels, tumors, etc., that is, to exclude the third pair of lesions on the cranial nerve path, if necessary It is also very important to have a proper consultation with a neurologist.
Diagnosis
Differential diagnosis
1. Oculomotor paralysis regeneration error syndrome: When the oculomotor nerve paralysis is regenerative disorder, the extraocular muscles are dominated by the nerve fibers with the wrong direction of regeneration, which can be accompanied by various eye movements, and the strange eye movements are manifested as eye infections. There is no orbital retraction when there is a downward or internal rotation. Generally, there is no automatic rhythm change. In some cases, the periodic paralysis and the regenerative mismatch are more common in the acute or recovery phase of congenital or traumatic oculomotor nerve paralysis.
2. Marcus-Gunn syndrome: also known as the mandibular blink syndrome, named after MarcusGunn first described. Cyclic oculomotor paralysis is common in patients with congenital ptosis and superior rectus paralysis. It is characterized by congenital ptosis and special joint movement of the pterygoid muscle, that is, when the ipsilateral pterygoid muscle is stimulated, the ptosis and eyelid retraction occur. This type of eyelid retraction often occurs when the mouth is open, the mandible is chewing, and the tongue is extended. The abnormality of the pupil may be related to the position of the trigeminal nerve branch to the position of the third cranial nerve.
3. Marin-Amat syndrome: also known as anti-mandibular blink syndrome. Cyclic oculomotor nerve paralysis is characterized by the appearance of drooping eyelids when the mouth and jaw move, and the ptosis disappears when closing or stopping chewing.
4. ocular myopathy myasthenia gravis: periodic oculomotor palsy is a post-synaptic acetylcholine receptor involved in the neuro-muscle junction, resulting in neuro-muscular excitation transmission disorder, with repeated An autoimmune disease that relapses and relieves. It is characterized by early appearance of ptosis with one eye or both eyes, morning light and heavy afternoon, and pupillary sphincter involvement later. The degree of paralysis and the degree of strabismus in the paralyzed muscles are often diplopia. After the injection of neostigmine or Teng Xilong, the above symptoms are alleviated or disappeared.
