Facial muscle spasm, also known as facial twitch, is an episodic, recurrent, involuntary twitching of the facial muscles innervated by the facial nerve. The incidence of facial muscle twitching: trigeminal neuralgia = 1:2.8. The disease mostly starts in adulthood, with the most patients between 30-40 years of age, and there is no significant difference in the gender of patients.
I. Etiology
Facial myospasm is still classified into two categories: primary and secondary. Secondary facial myoclonus refers to those whose etiology is clear, such as peripheral facial palsy caused by some facial nerve trauma or facial neuritis, which can cause facial myoclonus during the recovery period; some tumors of the pontocerebellar angle or skull base arachnoiditis involving the facial nerve root can also cause the occurrence of this disease.
The pathogenesis of primary facial myospasm is the same as that of primary trigeminal neuralgia, which is thought to be caused by abnormal vascular compression of the facial nerve root out of the pontocerebellar segment, resulting in demyelination of the nerve and “short-circuiting” of the current between nerve fibers. In recent years, a large number of clinical practices have shown that once the compression of the nerve root by the blood vessel is released, the facial muscle spasm can be stopped immediately or gradually.
Clinical manifestations
Most of the facial muscle spasms are limited to one side, often occurring first in the lower eyelid, and then gradually expanding in scope, spreading to the corners of the mouth, other facial muscles and broad neck muscles after 1 to 2 years. There is no aura before the attack, and the attack is characterized by rapid and frequent muscle twitching for a few seconds to a few minutes each time, with everything as normal in the interval.
The seizures can have voluntary facial movements and chewing, . They can be triggered by transient or random facial movements, and can be aggravated by emotional excitement, stress, exertion or prolonged reading time, and reduced when resting or emotionally stable. If the seizures are severe, the twitching may continue throughout the day, even during sleep. In some patients, the eyelid fissures may become smaller due to compulsive contraction of the eyelids, and in some patients, even the facial muscles may contract tensely, causing the corners of the mouth to be continuously tilted to the side of the disease.
The disease has a chronic course and can be prolonged for many years, affecting the patient’s work, mind and life to a certain extent. Individual patients with facial twitches may have trigeminal neuralgia (about 0.8% of patients with facial twitches). The two symptoms have their own attacks and are not obviously related to each other. In addition, some patients may also have tinnitus and hearing loss on the affected side.
Neurological examination: Patients with primary facial twitches usually have no obvious positive features. A few patients may show incomplete facial muscle paralysis because they have been treated with acupuncture, closure or radiofrequency thermocoagulation. Electromyography examination: the affected muscles can show a high frequency of rhythmic motor unit discharge (50-100 M min).
Third, auxiliary examination
EMG examination of facial muscle spasm patients can find high amplitude F and abnormal muscle response wave pattern when EMG examination is performed; stimulation of the mandibular rim branch of facial nerve can induce the muscle potential of orbicularis oculi muscle; EMG monitoring during microvascular decompression of facial nerve reveals that once the blood vessels compressing the facial nerve are separated, the abnormal EMG of the face can disappear.
2.Imaging examination
2.1 CT, MRI and other examinations: can make a clear diagnosis of secondary facial muscle spasm caused by some occupational and organic lesions.
2.1 Magnetic resonance tomographic angiography (MRA): This examination technique can show the relationship between cerebral blood vessels and cranial nerves, which can help to diagnose primary facial muscle spasm caused by vascular compression of facial nerve.
Diagnosis and differential diagnosis
The clinical diagnosis of this disease can often be made based on the typical medical history and observation of facial muscle spasm, but attention should be paid to differentiate it from the following diseases in the diagnostic process.
Facial muscle twitching after facial nerve paralysis Facial nerve injury or facial neuritis-induced facial nerve paralysis can produce facial muscle twitching when recovery is incomplete. This facial muscle twitch is often accompanied by contracture or associated movement of the paralyzed muscle (such as involuntary closure of the eyes when opening the mouth), and the facial muscle on the side of the twitch does not contract when performing autonomous movements such as showing the teeth, while the contraction of the facial muscle on the healthy side is normal and the corner of the mouth is crooked to the healthy side.
2, pontocerebellar horn lesions such as tumors and arachnoiditis, but rare. These patients often show damage to the adjacent cranial nerves (VII, VIII, IX and other cranial nerves). CT and MR brain scans are feasible if tumor is suspected.
Hysterical blepharospasm is common in middle-aged and older women. The spasm is confined to the eyelids, and the twitching is bilaterally synchronized, but does not accumulate the facial muscles in the lower part of the face.
4. Habitual facial twitching Commonly seen in children and young adults, it is a transient forced facial muscle movement that is bilateral, and the muscle contractions that appear on electromyography are the same as those produced during voluntary movements.
5, chorea and tardive dyskinesia may have involuntary twitching of the facial muscles, but they are bilateral and accompanied by similar involuntary movements of the extremities, which can be distinguished.
The twitching may also be limited motor epilepsy, but the magnitude of the twitching is larger and often involves the neck, upper extremities or even the lateral limbs, or there is a typical cortical motor area sequential diffusion of limited seizures. It is not uncommon to see seizures confined to the facial muscles only, and epileptic waves are visible on EEG.
V. Treatment
In primary facial spasms, medications are usually difficult to control the seizures. In the past, various destructive methods have been used to treat the disease by causing partial paralysis of the facial muscles, such as alcohol closure, percutaneous puncture of the facial nerve with radiofrequency thermocoagulation, severance of most of the branches or trunk of the facial nerve, intracranial facial nerve extrusion, partial injury of the nerve in the facial nerve canal, etc.
In recent years, with the clarification of the cause of primary facial spasm, microvascular decompression of the facial nerve root has become the preferred surgical treatment method. For those who are too old for surgery or unwilling to undergo surgery, the use of botulinum toxin A (botulinum toxin A) closure also has certain efficacy.
This method was first proposed by Gardner (1962) and Jannetta (1970). The procedure is performed from the posterior cranial fossa, exposing the affected pontocerebellar angle, searching for the compressed vessels at the pontocerebellar initiation of the facial nerve root, confirming them and then freeing them, and filling them with Tefleon cotton mass to separate the vessels from the nerve. Postoperatively, spasticity was controlled in more than 90% of patients.
In half of these patients, the spasticity stops immediately, and in the other part, it gradually stops within one week to six months. Since the authors began performing microvascular decompression of the facial nerve roots in ’83, they have performed approximately 3,500 such procedures, and intraoperative compression of the facial nerve roots by blood vessels was found in 99% of the patients. The key to achieving a definitive outcome is adequate decompression of the responsible vessels and avoiding the omission of the responsible vessels.
With the introduction of neuroendoscopic techniques, the cure rate has now been increased to 95%, with a recurrence rate of approximately 5% to 7% at long-term follow-up. Patients with recurrence may be considered for reoperation. The main complication of this procedure is hearing loss on the operative side. With the improvement of surgical techniques and the adoption of intraoperative electrophysiological monitoring, the incidence of this complication is now about 2%.
2. Botulinum toxin A closure treatment This method is also commonly used nowadays, especially for those with blepharospasm. Botulinum toxin A is injected into the branches of the main facial nerve to cause partial facial muscle paralysis, but does not affect the overall facial activity. A single injection can last for 3 to 4 months, and the closure can be repeated after a relapse, but permanent facial paralysis may result after too many closures.