Facial spasm, also known as facial twitch, is a paroxysmal painless, involuntary twitching of the hemifacial muscles, usually limited to one side of the face, so the English translation is Hemi-facial Spasm (HFS), which is one of the difficult conditions of the facial motor nervous system. HFS is one of the most difficult disorders of the facial motor nervous system. Most of them develop after middle age, slightly more in women, and slightly more on the left side than on the right. The twitching of the orbicularis oculi muscle at the beginning of the disease is mostly paroxysmal involuntary twitching on one side of the face, which gradually and slowly extends to other facial muscles on one side of the face. The degree of twitching varies, and it is paroxysmal, rapid and irregular twitching. The initial twitch is light and lasts only a few seconds, and then it gradually lengthens for several minutes or longer, while the interval is gradually shortened and the twitches are gradually increased frequently. 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 the inability to speak, often aggravated by fatigue, nervousness, and voluntary movement, but it cannot imitate or control the seizure by itself. A convulsion is short for a few seconds or long for more than 10 minutes, with variable intervals. Patients feel distracted and unconfident, which seriously affects their physical and mental health. Most of the convulsions stop after falling asleep.
It is worth mentioning that bilateral facial muscle spasms are rarely seen, while bilateral eye muscle twitches are relatively common clinically, but most of them are not facial muscle spasms, and the pathogenesis is not yet understood.
According to the spasticity intensity grading developed by Cohen et al.
Grade 0: no spasm.
Grade 1: increased transients or mild fluttering of the facial muscles caused by external stimuli.
Grade 2: spontaneous mild tremors of the eyelids and facial muscles without functional impairment.
Grade 3: marked spasticity and mild dysfunction.
Grade 4: severe spasticity and dysfunction, e.g., the patient is unable to read and has difficulty walking alone because he or she cannot open the eyes continuously. Neurological examination is not positive for signs other than paroxysmal twitching of facial muscles. A small number of patients may have mild paralysis of the affected facial muscles in the late stage of the disease.
The quality of life of patients with facial muscle spasm is greatly affected, and they tend to rush to doctors and believe in false advertisements such as “one shot” and “miracle drug” advertised in magazines and newspapers, so the treatment often takes many detours. The best and most fundamental way to treat facial muscle spasm is microvascular decompression surgery (microsurgery to separate and displace the compressed blood vessels in the facial nerve root with special materials). The misconceptions that patients often take to treat facial spasm are often the following.
Misconception one, botulinum toxin injections on the face, can cure facial muscle spasm
Botox injections on the face can have a certain relief effect on local muscle spasms, mainly because Botox can block the conduction of facial nerve endings to facial muscles, is a conservative peripheral treatment method, if the injection location is accurate, there can be a certain effect, the ideal relief time in about 3 months, if the injection site is not accurate, not only the symptoms can not be relieved, and even the emergence of long-term sequelae such as facial paralysis, the patient is very Another problem with Botox treatment is that the early treatment effect may be okay, but after several injections, the effect is more and more unsatisfactory, and the maintenance time is getting shorter and shorter, and multiple treatments are prone to facial nerve paralysis, resulting in difficulty in closing the eyes and salivation from the corners of the mouth. The second misconception is that facial closure is not a good idea.
The second misconception is that facial closure “needle” can cure facial muscle spasm.
The main method of needling is to destroy the peripheral branches of the facial nerve (such as radiofrequency thermal coagulation, alcohol destruction) to prevent it from inducing spasms. In fact, the destruction of peripheral nerves can relieve spasm for a short period of time, but the long-term effect is not good, as the conduction of the nerve trunk behind the regeneration of peripheral nerves can be transmitted to the facial muscle again, and spasm can be triggered again. Moreover, peripheral nerve destruction can lead to permanent facial paralysis, which is a greater side effect than Botox.
Misconception 3: Chinese medicine and acupuncture can cure facial muscle spasm
The cause of this disease is the compression of the facial nerve root which is near the center by blood vessels, so lifting the compression is the most fundamental treatment method.
Misconception 4: Facial nerve microvascular decompression can have many complications
Facial nerve microvascular decompression surgery is an extremely delicate, minimally invasive cranial nerve surgery that requires a physician with a strong foundation in microsurgery. The surgical procedure is performed in the arachnoid space between the cerebellum and the meninges, which is a normal cranial space for surgical operation, and strictly speaking, there is no obvious damage to the brain tissue. For experienced physicians, the treatment effect of facial nerve microvascular decompression surgery can reach about 95%, which is much higher than other treatments. Complications of microvascular decompression surgery mainly include facial palsy, hearing loss, choking on water and hoarseness, but the overall incidence is 3-5%, which is still a relatively low incidence.
Myth 5: The face continues to jump after microvascular decompression surgery and the surgery is not effective
The purpose of facial nerve microvascular decompression surgery is to separate the blood vessels compressing the facial nerve root (responsible vessels) and the facial nerve out of the brainstem through microsurgery, and decompress them by cushioning them with a special soft material, so as to stop its involuntary discharge and fundamentally release the cause of spasm. In a small number of patients, the facial nerve itself is quite fragile, and partial degeneration of the nerve occurs after being compressed by ectopic vessels for a longer period of time, resulting in the continuation of its discharge process. Therefore, patients who continue to have spasticity after surgery are seen clinically, not because the surgery is ineffective, but because the majority of them can have delayed recovery. If spasticity persists 2 years after surgery, further treatment should be considered.
In conclusion, there are more treatment methods for facial spasm, as a doctor, and do not want patients to take too many detours in the process of treating the disease, the above is my simple experience in the actual clinical work, take out and share with the majority of patients, hope to help more patients.