Can't keep eyes open

Introduction The fourth-grade hemifacial spasm can have severe paralysis and dysfunction, and the patient cannot read because he cannot keep blinking. The facial muscle spasm is twitching on one side of the face (some people have bilateral sputum), the more nervous the spirit, the more severe the excitement. Because the initial symptoms of hemifacial spasm are eyelid beating, the folks also have the title of left eye jumping for money and right eye jumping for disasters, so they generally do not attract peoples attention. After a period of lesion formation, they develop into hemifacial spasm. Move to the corner of the mouth, severely with the neck. The hemifacial spasm can be divided into two types, one is the original facial muscle spasm, and the other is the facial muscle spasm caused by facial sequelae. Both types can be distinguished from symptom manifestations. The facial hair spasm of the original hair can also occur in a static state, relieved after a few minutes, and is uncontrolled; the facial muscle spasm caused by facial sequelae is only caused by blinking, raising eyebrows and the like.

Cause

(1) vascular factors

In 1875, Schulitze et al reported that a case of HFS was found to have a "cherry"-sized basal aneurysm in the facial nerve. It is currently known that about 80% to 90% of HFS is caused by vascular compression in the brainstem region of the facial nerve. Clinical data indicate that the anterior cerebellar artery (AICA) and the posterior inferior cerebellar artery (PICA) are the main vascular factors leading to HFS, and the superior cerebellar artery SCA is the second. It is known that SCA originates from the junction of basilar artery and posterior cerebral artery, and the walking is most constant, while PICA and AICA are relatively mutated, so it is easy to form vasospasm or ectopic compression to the facial nerve; in addition, the artery and other variant aorta For example, vertebral artery and basilar artery may also cause compression of the facial nerve to cause HFS. In the past, it was thought that HFS was caused by pulsating compression of arteries. In recent years, studies have shown that single vein venous compression of facial nerve can also cause HFS, and the above-mentioned blood vessels can form combined compression on the facial nerve, which is to some extent. It affects the prognosis of HFS surgery.

(2) non-vascular factors

Non-vascular occupying lesions of the cerebellopontine angle (CPA), such as granuloma, tumors and cysts, can also produce HFS. The reason may be due to:

1 occupancy causes normal vascular displacement. Singh et al reported a case of CPA epidermoid cysts that caused AICA displacement to the facial nerve leading to HFS;

2 placeholders directly oppress the facial nerve;

3 Occupation of abnormal blood vessels such as arteriovenous malformations, meningiomas, aneurysms, etc. In addition, some space-occupying lesions in the posterior fossa can also cause HFS. Such as the rare interneuronal Schwann cell tumor compression of the facial nerve caused by HFS. Hirano reported that a patient with a cerebellar hematoma had a first symptom of HFS. In younger patients, local arachnoid thickening may be one of the main causes of HFS, and some congenital diseases such as Arnold-Chiari malformation and congenital arachnoid cyst can occur HFS.

(3) Other factors

The presence of oppressive factors in the brainstem region of the facial nerve is the main cause of HFS, and most scholars observed in the cerebellopontine angle surgery that there is vascular compression outside the brainstem region and does not produce HFS. In Kuroki et al., it was observed in animal models that the facial nerve demyelination lesions outside the brainstem region and the EMG can be similar to HFS changes. Mar-tinelli also reported that HFS can occur after a lesion around the facial nerve. Whether there is a compression factor in the area other than the facial nerve outside the brainstem region leads to further investigation.

In addition, HFS can also be seen in some systemic diseases such as multiple sclerosis. Familial HFS has only been reported so far, and its mechanism is still unclear. It is speculated that it may be related to heredity.

an examination

Related inspection

Ophthalmologic examination electromyogram

Most patients with primary hemifacial spasm develop after middle age, and more women. At the beginning of the course of the disease, the convulsions of one side of the orbicularis muscle are involuntarily involuntarily, and gradually spread to other facial muscles on one side of the face. The twitching of the horn muscles is most noticeable. In severe cases, the ipsilateral platysma can be involved. But the frontal muscles are less involved. The degree of convulsions varies, ranging from paroxysmal, rapid, and irregular convulsions. At the beginning, the convulsions are lighter and last only a few seconds. Afterwards, the gradual length can be ash for a few minutes or longer, and the intermittent time is gradually shortened, and the convulsions are gradually increased.

Severe cases are tonic, so that the ipsilateral eye can not be opened, the mouth angle is skewed to the same side, unable to speak, often exacerbated by fatigue, mental stress, and spontaneous movement, but can not imitate or control its seizure. A convulsion is as short as a few seconds and as long as more than ten minutes. The interval is uncertain. The patient feels upset and unable to work or study, seriously affecting the patient's physical and mental health. Most convulsions stop after falling asleep.

Bilateral tendons are rare. If there is, it is often on both sides of the disease, after the side of the convulsions stop, the other side of the attack, and the side of the convulsion is light and heavy on the other side, both sides of the simultaneous onset, while convulsions have not been reported. A small number of patients have mild facial pain during convulsions, and some cases may be accompanied by ipsilateral headache and tinnitus.

According to the strength rating of Cohen et al:

Level 0: no flaws;

Level 1: External stimuli cause increased blinking or mild facial muscles;

Level 2: The eyelids and facial muscles spontaneously flutter and have no dysfunction;

Level 3: obvious, with mild dysfunction;

Level 4: severe paralysis and dysfunction. If the patient is unable to read because he cannot continue to blink, it is difficult to walk alone. The nervous system examination showed no other positive signs except for paroxysmal convulsions of the facial muscles. A small number of patients may be accompanied by mild paralysis of the lateral muscles in the later stages of the disease.

Differential diagnosis

Clinically, it should be differentiated from the following diseases:

Facial paralysis

In the past, there was a clear history of facial paralysis. Due to the incomplete recovery of facial paralysis, the axonal regeneration was caused by confusion. The affected side left different degrees of facial muscle weakness and paralysis.

Blinking into a coma

Blinking into a coma is manifested by the patient's clear mind, but in addition to the movement of the eyeball, the other can not move, can follow the instructions to close the eye or do eye movement in all directions.

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