I. Overview
Facial muscle spasm, also known as facial muscle twitching, is manifested as involuntary twitching of one side of the face. The twitching is paroxysmal and irregular, with varying degrees, and may be aggravated by fatigue, mental stress and voluntary movements. The onset of the twitching mostly starts from the orbicularis oculi muscle and then involves the whole face. The disease occurs mostly after middle age and is commonly seen in women.
II. Introduction
The initial symptom of facial myospasm is eyelid jumping, which is also known as “left eye jumping for money, right eye jumping for disaster”, so it usually does not attract people’s attention, but after a period of time, it develops into facial myospasm, even to the corners of the mouth, and in serious cases, even to the neck. Facial muscle spasm can be divided into two types, one is primary facial muscle spasm, one is secondary facial muscle spasm, that is, facial muscle spasm produced by the sequelae of facial paralysis. The two types can be distinguished from each other in terms of symptoms. Primary facial muscle spasm can occur even in the resting state, and the spasm is relieved after several minutes and is not controlled; facial muscle spasm produced by the sequelae of facial palsy is produced only when doing actions such as blinking and raising eyebrows.
III. Clinical manifestations
Most of the primary facial muscle spasms develop after middle age, and there are more women. At the beginning of the disease, it is mostly paroxysmal involuntary twitching of the orbicularis oculi muscle on one side, gradually and slowly expanding to other facial muscles on one side of the face, the twitching of the corners of the mouth muscle is most easily noticed, and in severe cases, it can even involve the ipsilateral broad neck muscle, but the frontal muscle is less involved. The degree of twitching varies, and it is paroxysmal, rapid and irregular twitching. The initial convulsion is light and lasts for only a few seconds, and then it gradually grows for several minutes or longer, while the interval is gradually shortened and the convulsions gradually increase in frequency. In severe cases, it is tonic, causing the ipsilateral eye to be unable to open, the corner of the mouth to be skewed to the ipsilateral side and unable to speak, often aggravated by fatigue, mental tension and voluntary movement, but it cannot imitate or control its seizure by itself. A convulsion can last from a few seconds to more than 10 minutes, with intervals of variable length. The patient feels distracted and unable to work or study, which seriously affects the patient’s physical and mental health. Most of the convulsions stop after sleep. Bilateral lateral muscle spasms are rarely seen. If there is, it often starts on both sides successively, and most of the convulsions stop on one side and then the other side seizes again, and the convulsions are light on one side and light on the other side, and bilateral simultaneous onset and convulsions have not been reported. A few patients have mild facial pain during convulsions, and individual cases may be accompanied by ipsilateral headache and tinnitus.
V. Onset factors
Vascular factors
In 1875, Schulitze et al. reported a case of HFS in which a “cherry” sized basilar artery aneurysm was found in the facial nerve during autopsy. It is now known that approximately 80% to 90% of HFS is due to vascular compression of the facial nerve exiting the brainstem region. Clinical data show that the anterior inferior cerebellar artery (AICA) and posterior inferior cerebellar artery (PICA) are the main vascular factors causing HFS, while the superior cerebellar artery (SCA) is less common. In the past, HFS was thought to be caused by pulsatile compression of the artery, but in recent years, studies have shown that a single venous vessel can also cause HFS when it compresses the facial nerve, and both of these vessels can compress the facial nerve at the same time, which affects the prognosis of HFS surgery to some extent.
Non-vascular factors
Non-vascular occupying lesions in the pontocerebellar angle (CPA), such as granulomas, tumors, and cysts, can also cause HFS, which may be due to.
(i) displacement of normal vessels due to the occupancy. singh et al. reported a case of a CPA epidermoid cyst that displaced the AICA to compress the facial nerve resulting in HFS;
(ii) Direct compression of the facial nerve by the occupancy;
(iii) the influence of the abnormal vessels of the occupancy itself such as arteriovenous malformation, meningioma, and aneurysm.
In addition, some occupational lesions in the posterior cranial fossa can also cause HFS, such as a rare case of HFS due to compression of the facial nerve by a Chewang’s cell tumor of the intermediate nerve, and Hirano reported a patient with a cerebellar hematoma whose first symptom was HFS. HFS can occasionally occur in congenital disorders such as Arnold-Chiari malformation and congenital arachnoid cysts.
Other factors
The presence of compression factors in the exocortical region of the facial nerve is a major cause of HFS, and most authors have observed during pontocerebellar horn surgery that the presence of vascular compression in areas other than the exocortical region of the facial nerve does not produce HFS, whereas Kuroki et al. observed in an animal model that demyelinating lesions of the facial nerve in areas other than the exocortical region of the facial nerve can show electromyographic changes similar to those of HFS. Further investigation is needed to determine whether the presence of compression factors in areas other than the brainstem region of the facial nerve leads to HFS.
IV. Treatment Drug therapy
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 the effect at that 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 time, and in heavy cases, permanent facial paralysis will remain. 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 full-segment 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, not the effect of decompression.
3. Combing of the vertical segment of facial nerve
Scoville (1965) used, after grinding the vertical segment of the facial nerve canal, the vertical segment was dissected 1cm longitudinally with a fibrous knife and spaced with a 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 in international 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 the 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.