What Is a Hemifacial Spasm?
Because the initial symptoms of facial muscle spasm are eyelid beating, and folks also call it "left eye jumping fortune, right eye jumping." , Severe joint neck. Facial spasm can be divided into two types, one is primary facial spasm, and the other is secondary facial spasm, that is, facial spasm caused by the sequelae of facial paralysis. The two types can be distinguished from the symptoms. Facial spasm of the original type can also occur in a static state. The spasm is relieved after a few minutes and is not controlled. Facial spasm caused by the sequelae of facial paralysis is only caused by blinking and eyebrow raising.
- Western Medicine Name
- Facial spasm
- English name
- Hemifacial Spasm, HFS
- Affiliated Department
- Surgery-Neurosurgery
- Disease site
- Facial
- Contagious
- Non-contagious
- Whether to enter health insurance
- Yes
| Bao Yuhai | (Chief physician) | Department of Neurosurgery, Xuanwu Hospital, Capital Medical University |
| Liang Jiantao | (Deputy Chief Physician) | Department of Neurosurgery, Xuanwu Hospital, Capital Medical University |
- Facial muscle spasm (Hemifacial Spasm, HFS), also known as facial muscle twitch, manifested as involuntary twitching of one side of the face. Convulsions are paroxysmal and irregular in varying degrees and can be exacerbated by fatigue, mental stress, and voluntary movements. The onset usually begins with the orbicularis orbicularis muscle, and then involves the entire face. The disease mostly occurs after middle age and is common in women.
Facial muscle spasm
- Because the initial symptoms of facial muscle spasm are eyelid beating, and folks also call it "left eye jumping fortune, right eye jumping", so people generally don't pay attention to it. After a period of time, it develops into facial muscle spasm, which moves to the corner of the mouth. , Severe joint neck. Facial spasm can be divided into two types, one is primary facial spasm, and the other is secondary facial spasm, that is, facial spasm caused by the sequelae of facial paralysis. The two types can be distinguished from the symptoms. Facial spasm of the original type can also occur in a static state. The spasm is relieved after a few minutes and is not controlled. Facial spasm caused by the sequelae of facial paralysis is only caused by blinking and eyebrow raising.
Causes of Facial Spasm
Facial muscle spasm vascular factors
- In 1875, Schulitze et al. Reported that a cherry basal aneurysm was found in the facial nerve at the autopsy of a HFS patient. 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, while the superior cerebellar artery (SCA) is rare. SCA originates from the junction of the basilar artery and the posterior cerebral artery, and the movement is relatively 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 such as vertebrae Arteries and basilar arteries may also cause facial nerve compression and cause HFS. In the past, HFS was thought to be caused by the pulsatile compression of the arteries. In recent years, research has shown that a single venous blood vessel can also cause HFS when the facial nerve is compressed, and the above blood vessels can simultaneously compress the facial nerve, which affects to a certain extent Prognosis of HFS surgery.
Non-vascular factors of facial 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.
Facial 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.
Genetic factors for facial spasm
- 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.
Clinical manifestations of facial spasm
- Most of the primary facial muscle spasms develop after middle age, and there are many females. In the early stage of the disease, most of the orbicularis muscles are involuntarily convulsed, and gradually spread to other facial muscles on one side of the face. The convulsions of the corner muscles are most noticeable. In severe cases, the platysma on the ipsilateral side can be involved , But the frontal muscle is less involved. The degree of convulsions varies from paroxysmal, rapid, and irregular. The convulsions are mild at the beginning, lasting only a few seconds, and then gradually can be grayed for several minutes or longer, while the intermittent time is gradually shortened, and the convulsions gradually increase. Severe cases are tonic, causing the ipsilateral eyes not to open, the corners of the mouth to the ipsilateral side, unable to speak, often exacerbated by fatigue, nervousness, and voluntary movements, but they cannot imitate or control their own attacks. A seizure lasts for a few seconds and lasts for more than ten minutes. The length of the rest period varies. The patient feels upset and unable to work or study, which seriously affects the physical and mental health of the patient. Most twitches stop after falling asleep. Bilateral muscle spasms are rare. If there is, it usually starts on both sides. After the seizures on one side stop, the other side recurs, and the seizures are lighter on the other side and on the other side. A few patients have mild facial pain during convulsions, and individual cases may be accompanied by ipsilateral headaches and tinnitus.
- Graded by Cohen et al.
- Level 0: no spasms;
- Level 1: External stimulus causes blinking or facial muscles to tremble slightly;
- Level 2: Spontaneous slight tremor of eyelids and facial muscles without dysfunction;
- Level 3: Obvious spasms and slight dysfunction;
- Level 4: Severe spasms and dysfunctions, such as patients unable to read because they cannot keep their eyes open, and walking alone is difficult. Except for facial paroxysmal twitching of the nervous system, there were no other positive signs. A small number of patients may be accompanied by mild paralysis of the lateral muscles at a later stage. [1]
Facial spasm treatment
Facial spasm medication
- Except that phenytoin sodium or carbamazepine may be effective for some light patients, central sedatives, inhibitors and hormones have no significant effect.
Facial spasm Chinese medicine acupuncture
- Facial spasm is best not to use acupuncture, because the disease itself is afraid of stimulation. Sometimes acupuncture will aggravate the condition, and some people will take effect at that time, but it will be worse in the future. In addition, taking carbamazepine or phenytoin sodium as anti-sedative antiepileptic drugs is only controlled, and long-term side effects are also very large, and the dependence is also relatively strong. Can take some B1, B12 but with little effect.
Facial spasm injection of botulinum toxin
- Facial spasm can be controlled to a certain extent. Generally, a single injection can control up to one year. Long-term injection will produce resistance, and because type A botulinum toxin can paralyze the facial nerves and cause artificial facial paralysis, so it was completed at the time. Facial spasms will be controlled. However, patients with long-term injections will have more or less facial paralysis.
Facial spasm surgery
- 1) Facial nerve squeeze and branch amputation
- Under local anesthesia, make an incision under the stem and stomata to find the nerve trunk. Squeeze the nerve trunk with vascular forceps. The squeezing force should be properly controlled. It will recur in a short period of time, and will leave permanent facial paralysis in severe cases. If the distal branch is found, the responsible nerve branch that mainly produces spasms is found under electrical stimulation, and selective cutting is performed. Although the effect is better than that of squeezing, mild facial paralysis will still occur after surgery, and it will also occur after 1 to 2 years. There has been relapse and it is rarely used now.
- 2) Facial nerve decompression
- The decompression of the osteocanal tube of the facial nerve out of the skull was first used by Proud in 1953. Under local anesthesia, the mastoid was excised, and the horizontal and vertical bone canals of the facial nerve were completely abraded with an electric drill. The nerve sheath was cut longitudinally to reduce the nerve fibers. In 1972, Pulc believed that the range of decompression within a simple mastoid was too small, and the top of the inner auditory canal and the labyrinth section should be completely decompressed at the same time. Pathological changes in the nerves such as neuroedema, diffuse hypertrophy, and nerve sheath fibrillation have also been found during surgery to contradict the cause, but some patients have been cured after surgery. In 1965, Cawthorne reported 13 cases of surgery and found no abnormalities. Decompression is more complicated, especially the whole stage of decompression is not only difficult but also dangerous. It is also questionable whether the so-called curative effect is caused by trauma during surgery and is not a decompression effect.
- 3) Facial nerve combing
- Scoville (1965) adopted that after grinding the vertical facial nerve bone canal, the vertical segment was cut open 1cm vertically with a fiber knife, and a silicone film was used at the interval. The purpose was to cut off the intersecting nerve fibers to reduce abnormal impulse. Conduction, the disadvantage is that it is difficult to reach the exact level of neither 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 neurosurgery to cure HFS. The specific method is: under general anesthesia, use a straight incision in the postauricular hairline, observe the anatomical relationship between the facial auditory nerve and the surrounding blood vessels under the microscope during the operation, carefully find the vascular crests that compress the facial nerve, and confirm the responsible blood vessels (ie, compression After the facial nerves cause clinical symptoms, the arachnoid trabeculae and the nerves and blood vessels are loosened. After confirming that the blood vessels and the roots of the facial nerves are sufficiently separated, a Teflon gasket of an appropriate size is inserted. If a clear responsible blood vessel is found during the operation, the blood vessels that may compress the nerves are treated and decompression is performed. [2]
Facial spasm care
Facial spasm preoperative care
- 1) Preoperative preparation In addition to the routine preparations before neurosurgery, electrical audiometry and magnetic resonance angiography (MRA) examinations must be done, and the frequency, intensity and duration of facial spasms should be carefully evaluated to provide postoperative care. Observation provides contrast.
- 2) Psychological care: Although HFS is not life-threatening, its involuntary face seriously hinders patients' social life and mental health, and even adversely affects marriage and employment of some young patients. Coupled with the prolonged course of the disease, repeated medical treatments, and experienced repeated medications or even botulinum toxin injections, some patients have been in a state of high mental stress and emotional irritability for a long time, have doubts about the effect of the operation, and are eager to speak, be understood and concerned. Therefore, after the patient was admitted to the hospital, we patiently listened to the patient's complaint while understanding the medical history in detail, and provided understanding, sympathy, and comfort to the patient's suffering and the unsatisfactory life caused by the disease, and guided his release. At the same time, the purpose, methods, effects and postoperative precautions of the operation will be explained in detail, so that the patient can enhance their confidence and be in the best state of treatment.
Facial spasm postoperative care
- 1) General Nursing: Go to the supine supine position 24h postoperatively, and closely observe whether there is active bleeding and changes in vital signs, pupils, and body movement language. Postoperative nurses must understand the situation during the operation in detail, so that they have the heart and have abnormalities. Report to the doctor in a timely manner and treat accordingly. Continuous low-oxygen inhalation was performed 24 hours postoperatively to prevent edema of the brain tissue around the incision. Pay attention to the symptoms of brain stem damage, observe the symptoms of increased intracranial pressure such as severe headache, frequent vomiting, slow pulse, and elevated blood pressure, and be alert to the occurrence of secondary intracranial bleeding. Water was absent for 24 hours after the operation, and then transitioned from liquid food to a digestible, high-calorie, high-vitamin, and high-protein diet. If temporary numbness occurs, food should not be too hard, too cold or too hot, so as not to damage the oral mucosa.
- 2) Observation of the efficacy after surgery After the patient is awake, the frequency, intensity and duration of facial muscle spasm shall be assessed in time, and the time of facial muscle spasm to stop convulsions shall be recorded. In patients with severe facial spasm, the affected eye can be seen to be larger than before surgery. This is caused by the relaxation of the previously tense facial muscles after the disease is lifted, rather than the facial nerve injury. It is the first sign of successful surgery. . However, immediate failure after surgery does not mean that treatment is ineffective. Although MVD surgery relieves vascular compression, it takes time to complete the regeneration and repair of facial nerve root myelin sheath and facial nerve motor nucleus excitement. The observation of postoperative curative effect should be continued for more than 6 months.
Facial spasm with microvascular decompression for facial spasm
- Microvascular decompression surgery for facial spasm
- Facial muscle spasms are paroxysmal, irregular, and involuntary convulsions in the hemifacial region, ranging in severity from severe to severe. There are countless daily convulsions and even facial atrophy and small eyelid fissures, which seriously affects patients' work, study and Self-esteem.
- Microvascular decompression is a method recognized by the medical community to cure facial muscle spasm. The surgical technique is mature, simple to operate, less risky, effective and immediate. In order to make it easier for patients without medical background and their families to understand what is facial muscle spasm and microvascular decompression, one of our cases is illustrated to illustrate the surgical process. [3]
- MRI showed that the right facial nerve was compressed by a blood vessel at the exit of the brain stem