Facial myoclonus is a paroxysmal, involuntary twitching of one or both facial muscles (orbicularis oculi, expression muscles, orbicularis oris), which is aggravated by emotion or tension, and in severe cases, there may be difficulty in opening the eyes, distorted corners of the mouth, and a twitch-like murmur in the ear.
Typical facial spasm is a spasm that starts from the eyelids and gradually develops downward to the lower facial muscles such as the cheek expression muscles, while atypical facial spasm is a spasm that starts from the lower facial muscles and gradually develops upward to eventually involve the eyelids and frontal muscles. Atypical facial spasms are less common in clinical practice, and the vast majority are typical facial spasms.
Facial myospasm is more common in middle-aged and elderly people, with slightly more women than men, but there is a trend toward younger age of onset. Although most facial myospasms are located on one side, bilateral facial myospasms are not uncommon.
Diagnosis and differential diagnosis
The diagnosis of facial myasthenia gravis depends mainly on the characteristic clinical manifestations. Patients without characteristic clinical manifestations need to be clarified by auxiliary tests, including electrophysiological examinations, imaging examinations, and carbamazepine treatment tests.
Electrophysiological examinations include electromyography (EMG) and abnormal muscle response (AMR), or lateral spread response (LSR). In patients with facial spasm, EMG can record a high frequency of spontaneous potentials (up to 150 per second) and AMR is an abnormal electromyographic response specific to facial spasm, and a positive AMR supports the diagnosis of facial spasm.
Imaging studies include CT and MRI to identify intracranial lesions that may be causing the facial spasm, and 3D-TOF-MRA to help understand the distribution of blood vessels around the facial nerve. Patients with facial myasthenia are generally effective with carbamazepine treatment at the beginning of the disease (with a small number of patients experiencing ineffectiveness), so a carbamazepine treatment trial is useful for diagnosis.
Differential diagnosis of facial dystonia Facial dystonia needs to be differentiated from bilateral blepharospasm, Major’s syndrome, occlusal dystonia, post-facial palsy, and other facial dystonia disorders.
(1) Bilateral blepharospasm: This is characterized by recurrent episodes of involuntary eye closure of both eyelids, often at the same time, and the patient often shows difficulty in opening the eyes and reduced tearing.
(2) Meijer syndrome: Patients often start with recurrent episodes of involuntary eye closure of the eyelids bilaterally, but with the prolongation of the disease, involuntary twitching of the muscles below the eye fissure will gradually appear, manifesting as involuntary abnormal movements of the face bilaterally, and with the aggravation of the disease, the scope of muscle spasm will gradually expand downward, even involving the muscles of the neck, limbs and trunk.
③ Bite muscle spasm: It is a spasm of unilateral or bilateral masticatory muscles. Patients may have different degrees of upper and lower jaw bite disorder, teeth grinding and mouth opening difficulties, and trigeminal nerve motor branch lesion is one of the possible causes.
④ Posterior facial palsy: It is manifested by restricted movement of the ipsilateral facial expression muscles, involuntary twitching of the ipsilateral corners of the mouth and associated movement of the corners of the mouth and eyelids, which can be identified based on the exact history of facial palsy.
Treatment methods
Drug treatment
Except for phenytoin sodium or carbamazepine, which may be effective in some mild cases, general central sedatives, depressants and hormones have no significant effect.
Acupuncture in Chinese medicine
It is best not to use acupuncture for facial muscle spasm, because the disease itself is afraid of stimulation, sometimes acupuncture will aggravate the disease, and some people see results at the time, but later relapse will be powerful. In addition to taking carbamazepine or phenytoin sodium these anti-sedative anti-epileptic drugs only control, and long-term taking side effects are also very big, dependence is also relatively strong. You can take some B1 and B12, but the effect is very little.
Botulinum toxin injection
To a certain extent, facial muscle spasms can be controlled, generally one injection can control the longest one year, a long time injection will produce resistance, and because type A botulinum toxin can paralyze the nerves of the face to cause artificial facial paralysis, so at that time after playing facial muscle spasms will be controlled. However, patients who have been injected for a long time will have more or less symptoms of facial paralysis.
Surgical treatment
1) Facial nerve stem compression and branch severance
Under local anesthesia, an incision is made under the stem mammary foramen, the nerve trunk is identified, and the nerve trunk is pressed with a vascular clamp. The force of the press should be appropriately controlled; in light cases, it will recur in a short period of time, and in heavy cases, permanent facial paralysis will be left. If the distal branches are identified, the nerve branch responsible for the main spasm is identified under electrical stimulation and selectively cut, the effect is better than compression, but mild facial palsy still has to occur after the operation, and there is also recurrence after 1 to 2 years, which is rarely used now.
(2) Facial nerve decompression surgery
The decompression of the facial nerve by grinding the bony canal out of the skull was first adopted by Proud in 1953. In 1972, Pulec thought that the scope of decompression in the mastoid process alone was too small, and the top of the internal auditory canal and the vagus segment should be decompressed at the same time. In 1965, Cawthorne reported 13 cases in which no abnormalities were found. Decompression is complex, and especially total segmental decompression is not only difficult but also dangerous. It is also debatable whether the so-called efficacy is due to the trauma to the facial nerve during surgery and not the effect of decompression.
3) Combing of the vertical segment of the facial nerve
Scoville (1965) used, after grinding the vertical segment of the facial nerve canal, the vertical segment was dissected 1 cm longitudinally with a fibrous knife and spaced with silicone film. The purpose was to cut the crossed nerve fibers to reduce abnormal impulse conduction, the disadvantage was that it was difficult to achieve the exact degree of neither obvious facial paralysis nor spasm.
4) Microvascular decompression
In 1967, Professor Jennatta of the United States pioneered microvascular decompression to treat facial spasm. It is a method commonly used internationally in neurosurgery for the radical treatment of HFS. Under general anesthesia, a straight incision is made in the hairline behind the ear, and the anatomical relationship between the facial auditory nerve and the surrounding blood vessels in the pontocerebellar angle is observed under a microscope. Teflon spacers of appropriate size are inserted. If the responsible vessel is clearly identified intraoperatively, the vessel that may be compressing the nerve is treated and decompression is performed.