I. Overview Epidemiological surveys at home and abroad tend to vary somewhat, probably related to race, environment, climate, geography and sample size. Studies have shown that BP facial palsy accounts for 60%-75% of all peripheral facial palsy, with an annual incidence of 11.5~40.2/100,000 people and an average of one in 60 people having suffered from the disease in their lifetime. There is no obvious seasonality, but some scholars have shown that the incidence is relatively low in summer; the high incidence age is 15-45 years old, with an average age of 40-44 years old, and patients younger than 15 years old and older than 60 years old are rare; there is no significant gender difference in prevalence, with women slightly higher than men (1.2:1), and the incidence is especially high in women during their reproductive years. The risk of Bell’s palsy is 3.3 times higher than that of non-pregnant women in the same age group, and is common in the third trimester (i.e., late pregnancy, last trimester) and puerperium. The incidence is generally reported to be the same on both sides, but some report a higher incidence on the right side (63%) than on the left; 0.3% of patients present with bilateral facial palsy; 4% to 13% of patients are recurrent cases, either ipsilateral or contralateral. Patients with a history of recurrence are more likely to have a third episode, and patients with a history of three episodes have a 50% chance of having a fourth episode. 1/3 of patients with this type of recurrence have abnormal glucose tolerance, although they do not necessarily have clinical diabetes. It has been investigated that about 2.5% to 12.5% of patients are diabetic, and Adour confirmed that the risk of Bell’s palsy is 4.5 times higher in diabetic patients than in normal people. Other investigations have found that patients with hypertension are at a much higher risk, with 14.1% of Bell facial palsy patients having hypertension. Familial Bell palsy is not uncommon, with Adour reporting a family history in 8% of patients and May’s case in 17% of patients. The onset of the disease is rapid, and most patients have a history of exposure to cold and wind, often with salivation and tilting of the corners of the mouth when brushing the teeth and washing the face in the morning. The disease may be accompanied by pain in the posterior mastoid area of the paralyzed side, in the ear or in the angle of the jaw, or there may be no conscious symptoms. 50% of the patients reach the most severe degree of facial paralysis within 2 days, and the majority of patients can reach the peak within 5 days, and the progress should not exceed 2~3 weeks in general. Clinical manifestations 1. The expression muscle is paralyzed on one side. The frontal lines disappear, and the forehead cannot be wrinkled and frowned; the eye fissure becomes larger, and the eyelid cannot be closed or closed incompletely; when the eye is closed, the eyeball on the paralyzed side turns upward, revealing the white sclera, which is called Bell’s sign; the transient eyes on the diseased side are reduced, dulled or disappeared; the nasolabial folds on the affected side become shallow, the corners of the mouth droop, and the saliva flows out; when the teeth are exposed, the corners of the mouth are crooked to the healthy side; when the orbicularis oris muscle is paralyzed, the cheeks are puffed or the air is leaked when whistling; when the buccal muscle is paralyzed, the food is easily retained in the affected side of the teeth and cheeks The cheek muscle is paralyzed and food is retained between the cheek and the tooth on the affected side. In addition, the lower lid is flaccid and ectropic, causing the tear point to turn outward and the tear drainage to become poor. In addition to facial muscle paresis, some patients also have hypoesthesia or loss of taste in the anterior 2/3 of the tongue on the affected side, indicating that the facial nerve injury has reached the bulbar nerve in the foramen; if, in addition to facial muscle paresis, hypoesthesia or loss of taste in the anterior 2/3 of the tongue on the affected side is accompanied by auditory hypersensitivity, the lesion is in the stapedius muscle branch nerve; if, in addition to facial muscle paresis, hypoesthesia or loss of taste in the anterior 2/3 of the tongue on the affected side, auditory hypersensitivity is also accompanied by pain in the mastoid region on the affected side, pain in the auricular region and external auditory canal, dullness of sensation in the external auditory canal or the external auditory canal, and pain in the mastoid region. If, in addition to facial muscle paralysis, hypoesthesia or loss of taste in the anterior 2/3 of the tongue, hearing hypersensitivity, pain in the affected mastoid region, pain in the auricle and external auditory canal, and herpes in the external auditory canal or tympanic membrane, it is called Hunt syndrome, with lesions in the geniculate ganglion; lesions above the geniculate ganglion may also invade the superficial large nerve and show Hunt syndrome, but without herpes in the external auditory canal or tympanic membrane. 3, a few patients with incomplete facial nerve recovery can produce complications: facial muscle fibrous spasm, facial muscle contracture, facial muscle spasm, joint band movement, crocodile tear syndrome, etc., mostly seen in the 12th to 18th month of onset. Fibrous spasm of the facial muscles is a small, rapid, non-constant muscle contraction on the affected side, often accompanied by an increase in transient eye movements. Facial muscle contracture is characterized by narrowing of the eye fissure on the affected side, deepening and lengthening of the nasolabial fissure, recoil of the corners of the mouth toward the affected side, and poor contraction of the facial muscles during voluntary movements. However, if the patient does active movement, such as showing teeth, it can be found that the facial muscle on the contracted side does not contract, while the contraction of the healthy side is normal. The reason for this may be related to partial fibrosis of the facial expression muscles, or it may be due to local muscle hypertonia after nerve regeneration. Its severity depends on the severity of facial nerve paralysis. Facial muscle spasm is a painless, regular clonic facial muscle twitching, mainly located in the zygomaticus, orbicularis oculi, superior labialis square, and orbicularis raphe, with involuntary twitching of the zygomaticus being the most common, often combined with contractures and joint band movements. The spasms may be aggravated by talking, eating, nervousness and fatigue, and each spasm lasts from a few seconds to several minutes. Facial muscle association band movement refers to the patient appearing to open the mouth, show teeth, puff the cheeks, sucking when the eye fissure becomes smaller, on the contrary when the patient transient upper lip slight trembling or even closed eyes when the affected side of the mouth corner involuntary lifting. This is due to poor recovery of the myelin sheath of the facial nerve after damage, and the nerve fibers innervating the orbicularis oculi muscle travel into the innervated descending orbicularis muscle, resulting in misdirected regeneration of the nerve. With treatment, the symptoms can disappear when the nerve is completely repaired. The incidence of joint band movement varies widely in the literature, ranging from 18.3% to 55%, and studies have shown that the incidence depends on the severity of facial nerve palsy and the recovery time. Crocodile tear syndrome refers to the tearing of the affected side when the patient chews food (especially strongly flavored food), or even when he sees or thinks of delicious food. Auriculotemporal syndrome is a condition in which the patient experiences flushing of the temporal skin, localized heat, and sweat secretion when eating. It is due to the regeneration of the parasympathetic nerve of the facial nerve when the nerve fibers innervating the submandibular and sublingual glands travel into the nerve fibers innervating the sweat glands in the temporal region. Contraction of the stapedial tendon manifests as distention and roaring in the affected ear during facial muscle movement, often accompanied by facial muscle contracture. It is a hyperactive motor function that occurs due to the regeneration of misaligned nerve fibers and has a low incidence. The pathogenesis of facial neuritis is not fully understood, but according to some patients, the onset of the disease is due to overexertion and cold, so the main thing is to prevent overexertion and avoid local cold. In addition, strengthen the exercise, strengthen the body, can make the positive energy full, external evil can not invade. Also pay attention to mental regulation, keep a happy mood, and avoid bad mental stimulation. Prognosis Peitersen observed 1011 cases of untreated facial palsy, 85% of them started to improve within 3 weeks, and most of them recovered completely in 1~3 months, and no obvious sequelae were left. If there were signs of recovery only after 3 months, the recovery time could be six months to a year and all had sequelae; all patients recovered to some extent, and permanent complete facial palsy was not reported.