Facial muscle twitching refers to the painless contraction of the muscles innervated by the facial nerve. The first symptom often starts with a slight tremor of the orbicularis oculi muscle of the lower lid, and gradually extends upward to all the orbicularis oculi muscle, and then to the lower half of the facial muscle, especially the corner of the mouth twitches more often. In severe cases, the whole facial muscles and the ipsilateral broad neck muscles can be spasmed, and when the orbicularis oculi muscle is severely spasmed, the eyes cannot be opened, thus affecting walking and work, and may be accompanied by mild weakness and muscle atrophy. The spasm may be aggravated by mental stress, fatigue and voluntary movement, and disappears during sleep. Facial muscle twitches are not accompanied by pain, and the random contraction of facial muscle is generally unaffected during non-facial muscle twitches. I. Treatment with medication. Sedative drug treatment: (1) Carbamazepine: Generally, symptoms start to improve when 400-600mg/d is taken orally, and the seizures disappear completely when 600-1000mg/d is taken. However, relapse can occur rapidly after discontinuation of the drug, thus requiring long-term maintenance treatment. The sustained improvement rate is 35% and the complete control rate is 22%. Therefore, carbamazepine can be used to treat facial twitches with certain efficacy, but a larger dose is needed for long-term administration. Long-term use of higher doses of carbamazepine often results in side effects such as dizziness, drowsiness, ataxia, and leukopenia. Its effective mechanism of action may be related to reducing the excitability of the facial nucleus, thereby reducing its abnormal discharge. (2) Clonazepam (clonidine): 0.5~1mg per dose, 3 times/d, can reduce symptoms, and side effects such as weakness and drowsiness are often observed after the dose is increased. (3) Baclofen (chlorambucil): 5~10mg/d for the first time, divided into 1~2 doses, increase by 5~10mg every 2~3 days until 30mg per day. 48h after the symptoms can be significantly improved, and after 3 months the symptoms completely disappear. Second, botulinum toxin A (BTXA) treatment. The injection sites for BTXA are: (1) Lower eyelid: divided into 4 equal parts from the inner canthus to the outer canthus, inject BTXA 5-5.5 U at the midpoint of each 1 equal part, 5 mm from the lower eyelid margin. if the degree of blepharospasm is mild, the injection dose of BTXA can be reduced appropriately. (2) Upper eyelid: From the midpoint between the inner canthus and outer canthus, move 5 to 8 mm outward on each side and inject 5 to 5.5 U of BTXA 5 mm from the upper lid margin. When injecting BTXA into the upper eyelid, care should be taken to avoid injecting directly into the central part of the upper eyelid. This is because this area is where the levator muscle attaches, and injecting BTXA directly into this area can paralyze the levator muscle and cause ptosis. (3) Outer corner of the eye: The lateral part of the canthus has more orbicularis muscle, so many patients with primary blepharospasm complain that their muscle spasm here is very severe, so the injection sites here are relatively concentrated. Generally, 3 to 4 dots are injected 5 to 8 mm lateral to the outer canthus, with each dot spaced about 5 mm apart and arranged in a triangular or quadrilateral shape. More injection sites are added to the temporal and zygomatic twitching muscles on the affected side. On the lateral side of the nose and the nasolabial folds, 2 to 3 sites are injected accordingly. The upper lip injection sites should be minimized because if more BTXA is injected in the upper lip and lateral corners of the mouth, it will inevitably lead to the dropping of the corresponding corners of the mouth, and in severe cases, there may be salivation in the corners of the mouth and memory of rice. The lower lip and cheek injection sites also depend on the condition, and there are more injection sites to choose from. The maximum dose of BTXA is 5 to 6 U per site, and too large a dose per site may cause more side effects. Patients are generally satisfied with the results within 4 to 7 months after treatment. As the effect of BTXA gradually diminishes and the manifestation of area spasm gradually recurs, most patients need to repeat the treatment after six months of the first treatment. However, because the degree of facial twitching has been significantly reduced, the dose of BTXA required is greatly reduced. The treatment can be applied continuously for several years, but fewer patients achieve recovery. A small number of patients can be treated with Botulinum toxin type F (BTXF) instead due to more BTXA antibodies produced after the treatment, which affects the therapeutic effect. Third, surgical treatment. Facial muscle twitching, if not given treatment, usually does not improve naturally, and facial muscle twitching gradually attacks frequently and lengthens in duration, which seriously affects the patient’s mental and physical health. Some patients may develop facial muscle paralysis after several years. 648 patients with facial muscle twitching had a 5-year follow-up rate of 92% and a 10-year follow-up rate of 88% after microvascular decompression surgery. The early outcome within 1 month after surgery was 86% complete remission, 5% partial remission, and 9% ineffective. 10 years later, the outcome was 79% complete remission, 5% partial remission, and 16% ineffective. For early ineffective cases, early reoperation was performed, and long-term complete remission was also obtained. Fourth, complications. In severe cases, the orbicularis oculi muscle is severely spastic, so that the eye cannot be opened, and the whole facial muscle and ipsilateral cervical muscle can be spastic, thus affecting walking and work, and may be accompanied by mild weakness and muscle atrophy.