What’s wrong with “crooked mouth”? Minnie 9-year-old boy, has been in the second grade, smart and lively, the day before or well, slept a sleep, get up in the morning, found that he spoke to the right side of the mouth crooked, laugh more crooked terrible, the left eye can not be closed, the family was very nervous, rushed to the hospital to send him to the doctor, anxious to ask: how our Minnie will get “crooked mouth madness”? Will there be sequelae? After examination, the doctor diagnosed Minnie with “idiopathic peripheral left facial nerve palsy”. Idiopathic peripheral facial nerve palsy, also known as Bell’s facial paralysis (Bellspalsy), is an acute-onset, self-limiting, non-progressive, spontaneously relieved, non-life-threatening disease. Its incidence is (20~30)/100,000 people, there is no significant difference in the incidence between men and women, it can occur at any age, and the chances of Bell’s palsy occurring on both sides of the facial nerve are equal. Cold and wind stimulation, excessive fatigue, unbearable psychological stimulation, upper respiratory infections, pregnancy, etc. can be the triggering factors of this disease, but the exact cause of its development is still unclear. Many Bell’s palsy develops after being stimulated by cold and cool wind, so it is presumed that the sudden stimulation of cold or other causes of stimulation causes the motor-neural reflexes of the blood vessels, leading to spasmodic contraction of the neurotrophic blood vessels, resulting in ischemia, edema, and compression of the nerves. After the facial nerve enters the internal auditory canal, it has been traveling in the curved and narrow bony canal, which is the longest nerve in the human body residing in the bony canal, and it is easy to cause ischemic damage. Facial nerve ischemia, edema after pressure, facial nerve bone tube pressure increases, affecting the blood supply of the facial nerve, these factors are interlinked to form a vicious circle, so that the nerve dysfunction and facial muscle paralysis. In addition, there is also caused by viral infection. Since some patients with Bell’s palsy have fever, nasal congestion, sore throat, herpes in the mouth and lips and other symptoms similar to upper respiratory tract viral infection at the onset of facial paralysis, the occurrence of facial paralysis may be related to viral infection. Some studies suggest that herpes simplex virus infection may be the cause of Bell’s facial paralysis. Clinical symptoms of Bell’s facial paralysis: generally acute onset, most patients in the onset of 2~3 days of facial paralysis to reach the most serious degree, facial paralysis progression is not more than 2~3 weeks, manifested as peripheral facial nerve paralysis, all the branches of the facial nerve area all involved, static frontal lines, eye fissure, nasolabial folds, the corners of the mouth asymmetric, dynamic knit the forehead, frowning, closing the eyes, teeth and other facial expression asymmetric, the corners of the mouth to the healthy side of the tilt. Some patients may have ear temporal pain. Some patients may have ear-temporal pain. There may be decreased tear secretion on the affected side, decreased sense of taste in the anterior 2/3 of the tongue, and auditory hypersensitivity; acoustic impedance examination may find that the stapedius muscle reflex has disappeared, and so on. CT of the temporal bone and MRI of the cranium are not necessary for Bell’s palsy, but imaging is necessary if there is a suspicion of temporal bone space-occupying lesions or other neurologic disease, and enhanced MRI may reveal edema of the facial nerve. Electrophysiologic examination is also important in the diagnosis and prognostic evaluation of Bell’s palsy. Bell’s palsy is an unexplained “idiopathic facial nerve palsy.” Therefore, peripheral facial nerve palsy must be excluded if there is a clear cause for the palsy before a diagnosis of Bell’s palsy can be made. Firstly, central facial nerve palsy should be excluded. Central facial nerve palsy manifests as the presence of upper facial muscle movement, knitting the forehead, closing the eyes, lifting the eyebrow function is normal, while the lower facial muscles are paralyzed, unable to complete the shrug of the nose, show the teeth, puffing out the cheeks and other movements, while taste, lacrimal secretion, salivary secretion function is normal; secondly, through the inquiry of the patient’s medical history, the ear and head and neck examination to exclude other diseases that cause peripheral facial paralysis; thirdly, the patient cannot be determined can be clinically audiologically examined to determine the causes. Third, for patients who cannot be identified, clinical audiology, vestibular function, and head and neck imaging can be performed to further exclude other central nervous system diseases or diseases of the ear or posterior cranial fossa, and for recurrent Bell’s palsy, a thin-layer temporal bone CT scan or MRI should be performed to exclude facial nerve tumors. Although about 70% of untreated Bell’s palsy patients can recover their facial nerve function, 20-30% of Bell’s palsy patients cannot recover their facial nerve function by themselves, and the psychological and daily life of patients with Bell’s palsy will be greatly affected, so timely and effective treatment is very necessary. In the treatment of Bell’s palsy, the best therapeutic effect was obtained by adding acyclovir or other antiviral drugs to the hormone treatment at the early stage of the disease (within 3 d), and the overall recovery rate of facial nerve function was 95.7%, while the recovery rate of prednisolone treatment alone was 88.6%; moreover, the recovery rate of those who received the combination of treatments within 3 days of the onset of the disease was 100%, and the recovery rate of those who received the combination of treatments after the onset of the disease was 86.6%. patients who received combination therapy within 3 days of onset had a 100% recovery rate, whereas patients who received combination therapy 4 d after onset had a recovery rate of 86.2%. Therefore, it is believed that the treatment of Bell’s palsy should be started within 3 days of the onset of the disease. Glucocorticosteroids are commonly used, including prednisone, prednisolone, and dexamethasone, and the dose of hormone therapy is prednisone 1 mg? kg? day (maximum not more than 80 mg), usually taken in the morning at once, can also be divided into doses, continued to take 5-7 days, and then gradually reduce the amount of 10-14 days to stop. Hormone therapy should be started as early as possible, within 24h of the onset of symptoms. Antiviral drugs are commonly used such as acyclovir. Other than that, patients with Bell’s palsy are prone to exposure keratitis due to incomplete eyelid closure with reduced tear secretion, so eye protection is very important for patients with Bell’s palsy. Protective measures include avoiding wind and continuous eye use, eye drops, and using non-irritating ointment during sleep. Vitamin B drugs such as vitamin B1 or methylcobalamin are also beneficial in restoring peripheral nerve function. Vasodilators and agents to improve microcirculation and neurotrophic factors may also have a role. Surgical decompression of the facial nerve may improve the prognosis if more than 90% of the nerve is degenerated within 2 weeks of facial nerve injury.