What Causes Facial Twitching?

Facial muscle spasm, also known as facial muscle twitch, hemifacial spasm, refers to paroxysmal, involuntary, irregular muscle twitches on one side of the face, without other positive signs of neurological damage. The cause is unclear.

Hemifacial spasm

Facial spasm usually refers to hemifacial spasm

Hemifacial spasm

The incidence is mostly middle-aged women, and the onset is usually a slight convulsion of the orbicularis muscle of the lower eyelid, which gradually expands to one side of the face later, with the corner muscle convulsions being the most obvious. The degree of convulsions varies, which worsens during stress, excitement or fatigue, and disappears during quietness or sleep. In a few severe cases, facial muscle twitches can affect the entire lateral muscle. Convulsions are mostly limited to one side, and bilaterals are rare.

The disease is a chronic, progressive development that generally does not resolve spontaneously. Some patients develop paralysis and atrophy of the lateral muscles at a later stage, and the seizures also stop. At the beginning of the course, when facial muscle convulsions are limited to orbicularis oris, it should be distinguished from functional eyelid spasm, which does not spread to the face and is often bilateral. When facial muscle convulsions are accompanied by other cranial nerve damage, or limb dysfunction, or involuntary movements of the limb, intracranial lesions should be considered and should be treated in the hospital.

Facial spasm is mainly treated with drugs, such as phenytoin, rimienine, diazepam, and lumina. And with reasonable treatment. Symptoms can be slightly reduced after treatment. In severe cases, when the drug treatment is not effective, facial nerve closed surgery can be used.

Hemifacial spasm, also known as facial myoclonus, is a paroxysmal involuntary convulsion of the hemifacial muscles. It is more common in women over the middle age. The spasm usually starts from one eye or mouth corner, and then spreads to the ipsilateral hemifacial muscles, but the frontal muscles are less affected. There was intermittent involuntary rhythmic twitching, and self-control was not possible. The duration of each twitch ranges from a few seconds to a few minutes, with varying intervals. Human fatigue, emotional excitement, blinking of laughter, etc. can induce or aggravate it. Although there is no pain in the face during convulsions, frequent attacks can affect vision, speech, or chewing function, and the patient is also intolerable.

The cause of the disease is unknown. Most scholars and clinicians believe that the facial nerve is caused by compression of the posterior inferior cerebellar artery near the inner ear portal; symptoms occur when the blood vessels are excessively tortuous, stretched, tightened or hardened. It is presumed that the myelin sheath of the facial nerve atrophied at the compression point, the afferent sensory fibers and the efferent motor fibers "short-circuited", activating the motor fibers and causing facial muscle spasm. Another way of saying this is that the motion-inhibiting fibers from the facial nerve are also distributed in the muscles. When certain factors make the inhibition fibers disappear, the facial muscles spasm.

According to clinical manifestations, the diagnosis of this disease is relatively easy, but clinical, otolaryngological and neurological examinations should be performed to try to trace possible causes. The examination should include X-ray tomography and CT examination to exclude the possibility of facial nerve compression by tumors (mainly cerebellar pontine angles or tumors of the temporal bone). For example, cholesteatoma in the temporomandrosus initially manifests as facial muscle spasm, as well as facial schwannomas and rare acoustic neuromas. Idiopathic hemifacial spasm can only be diagnosed if the above tests are negative.

Hemifacial spasm

For the treatment of hemifacial spasm, due to the unknown etiology, many lack specific treatments. The current clinical methods are:

often combined with sedatives, weak tranquilizers and antiepileptic drugs in the early stages. Drugs such as diazepam, belladonna, phenytoin, carbamazepine, and tonidine are available. At the same time with acupuncture (selection of acupoints: Dicang, cheek car, qifeng, Hegu, etc., strong stimulation, leaving the needle for 20 minutes), infrared, ultraviolet, ultra-short wave physiotherapy can be used to alleviate the symptoms of mild patients.

Patellar facial nerve block: 0.5ml of 80% alcohol is injected into the spleen foramen around the nerve trunk below to block its conduction function and relieve spasm. May relapse after 2 to 3 years, but the degree will be significantly reduced, and repeated injections are possible. Block therapy has the advantages of less damage and simple operation. The disadvantages are that it cannot avoid recurrence and cannot predict the duration and extent of facial paralysis or spasm. Although it can be used repeatedly after relapse, the effect is poor due to the effect of scar.

(3) Surgical treatment: Facial nerve coagulation, temporal nerve facial nerve decompression, neurotomy, facial nerve decompression and nerve cut and electrocoagulation are used together.

Traditional Chinese medicine believes that the disease is caused by wind, phlegm, and stasis. The cure should be to stop the liver from experiencing wind, dredge the wind and clear the collaterals, and to relieve phlegm and calm the mind. Zhengan Xifeng Decoction and Ditan Decoction can be added and subtracted: 20g of vermiculite, 20g of rehmannia glutinosa, 12g of angelica, 20g of white peony, 15g of calcined keel, 15g of calcined oyster, 10g of bile star, 15g of pinellia, 15g of silkworm, 15g of pupa , Whole worm 10g, Polygala 10g. After the acute phase, you can take Chinese medicine such as Dahuoluodan for a long time.

Causes of hemifacial spasm

Hemifacial spasm review

Hemifacial Spasm (HFS) is an involuntary twitch of paresthesia. Generally, it is limited to one side of the face, so it is also called hemifacial spasm, which is occasionally seen on both sides. It starts from the orbicularis oris muscle gradually, and gradually develops toward the cheek and even the entire semi-lateral side, and the reverse development is rare. It can be exacerbated by fatigue and tension, especially when talking and smiling, and can be convulsive when severe. Onset is most common in middle age, with the youngest reported being two years old. In the past, women were thought to be more prone, and statistics in recent years have shown that the incidence is not related to gender. In the end of HSF, mild facial paralysis may occur in a few cases.

Hemifacial spasm vascular factor

In 1875, Schulitze et al reported that a HFS patient underwent an autopsy and found a "cherry" 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 area of the facial nerve. Clinical data show that the anterior inferior cerebellar artery (AICA) and posterior inferior cerebellar artery (PICA) are the main vascular factors leading to HFS, followed by the superior cerebellar artery (SCA). It is known that SCA originates from the junction of the basilar artery and the posterior cerebral artery, and the path is the most constant, while PICA and AICA are relatively variably, so it is easy to form vascular crests or ectopic compression to the facial nerve; in addition, labyrinth arteries and other mutated aorta For example, the vertebral artery and the basilar artery may also cause compression of the facial nerve and cause HFS. In the past, HFS was thought to be caused by pulsatile compression of arteries. In recent years, research has shown that a single venous blood vessel can also cause HFS when it compresses the facial nerve, and the aforementioned blood vessels can form a combined compression of the facial nerve by two or more, which is to a certain extent This affects the prognosis of HFS surgery.

Non-vascular causes of hemifacial spasm

Non-vascular occupying lesions of the cerebellopontine angle (CPA), such as granulomas, tumors, and cysts, can also produce HFS. The reason may be due to: Occupation leads to normal blood vessel displacement. Singh et al. Reported a case in which CPA epidermoid cysts displaced AICA to the facial nerve and caused HFS; direct compression of the facial nerve by the occupancy; the effects of abnormal blood vessels such as arteriovenous malformations, meningiomas, and aneurysms. In addition, some space-occupying lesions in the posterior cranial fossa can also cause HFS. Such as rare Schwann cell tumors of the intermediate nerve, HFS caused by compression of the facial nerve. Hirano reported that a patient with cerebellar hematoma had HFS as the first symptom. In young patients, localized arachnoid thickening may be one of the main causes of HFS, and some congenital diseases such as Arnold-Chiari malformations and congenital arachnoid cysts can occasionally cause HFS.

Hemifacial spasm other factors

The presence of compression factors in the brain stem area of the facial nerve is the main cause of HFS, and most scholars have observed during the cerebellopontine angle surgery that vascular compression in areas outside the brain stem area of the facial nerve does not produce HFS. And Kuroki et al. Observed in animal models that the facial nerve demyelinating lesions outside the brainstem area, the EMG of the facial nerve can be similar to HFS. Mar-tinelli also reported a case of HFS after peripheral facial nerve branch injury. Whether the presence of compressive factors outside the brainstem outside the facial stem leads to HFS needs further investigation.

In addition, HFS is also found in some systemic diseases such as multiple sclerosis. Familial HFS has so far been reported in only a few cases, the mechanism of which is unknown, and it is speculated that it may be genetically related.

Hemifacial spasm treatment

Hemifacial spasm medication

Traditional drug treatments often use antiepileptic drugs such as phenytoin, carbamazepine, and diazepam, and other drugs, such as carbachol, non-urethane, etc., are reported to have specific effects on certain HFS, but they are not enough to promote application.

Hemifacial spasm closure treatment

When the drug treatment of HFS is not effective in the past, alcohol can be used for local closure in clinical practice, but it often causes facial paralysis and is easy to relapse.

In recent years, Botuline Toxin A (BTA) has been widely used in closed treatment of HFS. Compared with alcohol closure, complete facial paralysis occurs less frequently and lasts longer. More than 90% of patients have improved to varying degrees, and the efficacy can be maintained for 3 to 4 months. Its side effects are dry eyes, drooping upper eyelid, and mild facial paralysis. Its toxicity is dose-dependent and can produce a psychosis known as the "lighting phenomenon." In addition, it also affects the autonomic nervous system. Can cause palpitation, palpitations, and elevated blood pressure. When combined with other drugs that damage neuromuscular junctions, the toxic effect increases. It is recommended to use BTA in small doses (12.5u), multiple times (3 to 4 times / year), and intermittently when treating HFS.

Hemifacial spasm surgery

Since Campbell and Kendy began to use surgery to treat HFS caused by basal aneurysm compression in 1944, with Carden (19 58), Maroon (1960) and other further improvements in surgery, Jannetta officially proposed microvascular decompression (microv as cular decompression (MVD). MVD has become the preferred method of treating HFS. The operation method is as follows: craniotomy, exposure of the facial nerve, and compression of blood vessels in the brainstem area of the facial nerve. Gelatin sponge, muscle sheet or Teflon sheet is used to reduce the pressure. This procedure was once thought to be the only cure for HFS without sequelae.

Hemifacial spasm treatment effect

Many scholars have found in long-term follow-up that the long-term effectiveness of MVD for HFS can reach 60% to 70%, and some patients can have different degrees of relief or even cure during follow-up. A few patients completely disappeared after 5 months after surgery. . In the analysis of its influencing factors, Barker et al. Showed that the age, spasticity, duration of the disease, and the presence or absence of facial paralysis before surgery were not related to long-term efficacy. The typical degree of detection of gender and disease is the main indicator of prognostic evaluation. Follow-up shows that there is still a 4% -12% recurrence rate of HFS in MDV treatment. The reason may be related to the following factors: Materials inserted: gelatin sponge and muscle pieces may be absorbed after insertion and cause recurrence. Teflon tablets It has been reported that after being used for decompression, cholesteatoma can be formed and then the facial nerve can be compressed again; implants fall off: if the pad is not placed properly, the imperfect operation of the surgeon before closing the skull can cause the pad to drift; Postoperative arachnoid adhesions cause compression of the facial nerve; decompression is insufficient: due to various reasons, such as the technique of the operator, accidents during the operation and the concealed blood vessels, the decompression is insufficient; in addition, combined vascular compression is only available Single vessel decompression can cause recurrence after surgery. Jannetta believes that most cases of relapse are caused by insufficient decompression. Some scholars have suggested that reoperation for these patients can still achieve good clinical results, but it has little significance for reoperation due to adhesion. HFS recurrence is mostly within 2 years (January to 5 years) after surgery, and the recurrence rate after 2 years can be less than 1%.

The mortality rate of MDV surgery is very low, but most patients will experience symptoms such as nausea, vomiting, hearing loss, facial dysfunction, and dizziness. Most patients can disappear within two weeks after surgery; only a few patients can survive. There are permanent sequelae such as hearing loss and even deafness (2.6%), facial paralysis (0.9%), facial paresthesia (0.4%), and brain stem infarction (0.3%), and these sequelae are relatively elevated with reoperation.

Hemifacial spasm

Facial spasm is an involuntary twitch or spasm of paroxysmal irregular hemifacial muscles. It often occurs on one side of the face, and bilateral cases are rare. Idiopathic facial spasm mostly occurs after middle age, and there are more women than men. Facial twitching starts from the orbicularis oris muscle, which is intermittent, and then gradually spreads to other facial muscles on the same side. . Facial twitches worsen when you are nervous or tired, and stop when you sleep. There were no other positive signs of neurological examination. Show muscle fiber tremor and muscle bundle tremor wave on electromyogram. The disease generally does not heal itself, and treatment is not ideal. Currently, it is mostly symptomatic.