Idiopathic facial neuritis or Bell’s palsy is a peripheral facial nerve paralysis caused by nonspecific inflammation of the facial nerve within the stoma. Etiology: The exact etiology is unknown, and the disease has long been thought to be associated with neurotropic viral infections. The onset of the disease after exposure to cold or upper respiratory tract infection may be due to acute viral infection and edema of the facial nerve in the foramen ovale resulting in nerve compression or local blood circulation disorders and facial nerve palsy. Most believe that this disease is also an autoimmune reaction. Some patients may have geniculate ganglionitis caused by herpes zoster virus. Pathology: mainly facial nerve edema, swelling and loss of myelin sheath, and axonal degeneration of varying degrees in advanced stages, especially in the stem mammary foramen and parts of the facial nerve canal. Clinical manifestations: The disease can develop at any age, but it is most common in males aged 20-40. The vast majority of cases are unilateral and few are bilateral. The onset of the disease is not related to the season. The onset of the disease is usually acute, and is characterized by a skewed mouth, salivation, leakage of speech, whistling or laughing. It may reach its peak within 48 hours. Some patients have mild pain behind the ipsilateral ear, in the ear, in the mastoid region or on the face for a few days before the onset of the disease. On physical examination, paralysis of the facial expression muscles is seen. The frontal lines disappear, the eye fissures widen, the nasolabial folds flatten, the corners of the mouth droop, and the face is drawn toward the healthy side. When the facial muscles are exercised, the contraction of the healthy side of the face makes the above signs more obvious. The sick side could not make movements such as frowning, frowning, closing the eyes, showing teeth, puffing and whistling. When the eyes are closed, the eye on the paralyzed side turns inward, exposing the white sclera under the cornea, called Bell’s phenomenon. When puffing and whistling, the affected side of the mouth leaks air because the lips cannot be closed. When eating, food is often retained in the buccal gingival sulcus on the affected side, and saliva often flows down from that side. The lacrimal punctum is ectropioned with the lower lid, which prevents normal tear absorption and causes overflow. The clinical symptoms of facial nerve damage vary from site to site. 1, anterior damage of the geniculate ganglion, due to the involvement of the bulbar nerve, the appearance of the anterior 2/3 of the tongue taste disorder; stapedius muscle branch involvement, auditory hypersensitivity, excessive echo; 2, the geniculate ganglion lesions in addition to the manifestation of facial nerve palsy, auditory hypersensitivity and anterior 2/3 of the tongue taste disorder, there are auricular and external auditory canal sensory dullness, external auditory canal and tympanic membrane on the herpes, called Hunter syndrome, due to herpes zoster virus infection;. 3. In the case of lesions near the stem mammary foramen, the typical peripheral facial palsy signs and pain behind the ear described above are present. Patients with facial nerve palsy usually begin to recover within 1 to 2 weeks after the onset of the disease, and about 80% of the patients basically return to normal within a few weeks and 1 to 2 months. About 1/3 of patients have partial paralysis and 2/3 have complete paralysis. In the latter, about 16% do not recover. Facial neuritis with incomplete recovery can often be accompanied by contractures of the paralytic muscles, facial muscle spasms, or joint band movements. Contractures of the paralytic muscles are manifested by deepening of the nasolabial fold on the diseased side, recoil of the corners of the mouth toward the affected side, and narrowing of the eye fissure. However, if the patient is asked to make active movements such as showing teeth, it can be found that the facial muscles on the contracted side do not contract, while the facial muscles on the healthy side contract normally and the eye fissure on the diseased side is smaller. The common clinical sign of the band is a slight fluttering of the upper lip on the diseased side when the patient’s eyes are transient; involuntary closure of the eyes on the diseased side when the teeth are exposed; contraction of the frontalis muscle on the diseased side when trying to close the eyes; tearing on the diseased side with flushing of the temporal skin, local heat and sweat secretion when eating and chewing. These phenomena may be due to the regeneration of nerve fibers into other nerve sheath cell pathways in the vicinity of the lesion and innervate the peripheral apparatus that originally belonged to other nerve fibers. Diagnosis: Based on the form of onset and typical clinical features, the diagnosis of peripheral facial palsy is not difficult, but it needs to be differentiated from other diseases that can cause peripheral facial nerve palsy. Treatment: Efforts should be made to promote the early resolution of local inflammation and edema, and to promote the recovery of facial nerve function. 1, corticosteroids: dexamethasone 5~10mg/d intravenously; or prednisone 20~30mg/d, once in the morning, gradually stop after 1 week; caused by herpes zoster, corticosteroids combined with aciclovir (ACV) 0.2g, 5 times a day, for 7~10 days. 2, B vitamins: vitamin B 1100mg, vitamin B12 500μg, intramuscular injection, once a day. 3.Physiotherapy and acupuncture treatment: give hot compresses near the stem mastoid, or infrared irradiation or short-wave transheat therapy. Acupuncture should be performed 1 week after the onset of the disease. 4.Physical therapy: The patient massages the paralyzed facial muscle by hand against the mirror several times a day for 5~10 minutes each time. When the nerve function starts to recover, the patient can practice the random movement of the paralyzed individual facial muscles against the mirror. 5.Protect the exposed cornea and prevent conjunctivitis by using eye shields, eye drops, eye ointment, etc. 6.Surgical treatment: Facial nerve decompression surgery is effective for some patients. Facial-sublingual nerve and facial-paraneoplastic nerve anastomosis can be considered for those who do not heal for a long time, but the efficacy is not certain.