Facial neuritis, also known as Bell’s palsy, is an acute nonspecific inflammation of the facial nerve in the facial neural tube above the foramen magnum. Etiology: Facial neuritis is more common in cerebral neurological disorders, which is related to the anatomical structure of the facial neural tube as a long and narrow bony tube. When the rocky bone develops abnormally, the facial neural tube may be even narrower, which may be an intrinsic factor in the development of facial neuritis. The extrinsic cause of the development of facial neuritis is not yet understood. According to the early pathological changes of facial nerve edema, myelin sheath and axial space with different degrees of degeneration, some people speculate that it may be due to the cold wind blowing on the face, the nutrient microvascular spasm of the facial nerve, resulting in ischemia and hypoxia of the local tissues. It is also thought to be related to viral infection, but no virus has been isolated. In recent years it has also been suggested that it may be an immune response. Ramsay-Hunt Syndrome is caused by herpes zoster virus infection, which leads to inflammation of the geniculate ganglion and facial nerve. Clinical manifestations: Can be seen at any age, no gender differences. It is mostly unilateral and rarely bilateral. The onset of the disease has nothing to do with the season, usually acute onset, one side of the facial expression muscles suddenly paralyzed, can be a few small into the peak. Some patients have pain in the postauricular mastoid area of the external auditory canal 1-3 days prior to the onset of the disease, and they often find it in the morning when they are washing up, or are found by others to have a crooked mouth. Examination shows the disappearance of forehead lines on the same side, inability to frown, due to paralysis of the orbicularis oculi muscle, the eye fissure is enlarged, and when the eyes are closed, the eyelids cannot be closed or are incompletely closed while the eyeballs rotate outwardly and expose the white sclera, which is known as Bell’s phenomenon. The lower eyelid is ectropion, and the tears do not easily flow into the nasolacrimal duct and overflow out of the eye. The nasolabial folds become shallow on the sick side, the corners of the mouth droop, and the corners of the mouth are pulled toward the healthy side when showing teeth. When showing teeth, the corners of the mouth are pulled towards the healthy side. The patient cannot make pouting and whistling movements, and when puffing the cheeks, the corners of the mouth on the diseased side leak out, and when eating and mouthwashing, the soup leaks out from the corners of the mouth on the diseased side. Due to the paralysis of the buccal muscles, food often stays between the teeth and cheeks. If the lesion affects the tympanic nerve, in addition to the above symptoms, there may be loss of taste in the anterior 2/3 of the tongue on the same side. Involvement of the upper part of the peduncle muscle branch, due to the paralysis of the peduncle muscle, there may also be ipsilateral auditory hypersensitivity. In addition to facial paralysis, dysgeusia and auditory hypersensitivity, there are also ipsilateral salivary and lacrimal secretion disorders, intra- and postauricular pain, and herpes zoster in the external auditory canal and auricular area in the involvement of the geniculate ganglion, which is known as the geniculate ganglion syndrome (Hunt’s syndrome ). Diagnosis and differentiation: According to the form of onset and clinical features, the diagnosis is not difficult. However, it should be differentiated from the following diseases: (1) central facial paralysis: it is caused by the damage of the contralateral cortical brainstem bundle, and it only manifests as the paralysis of the lower facial muscles on the contralateral side of the lesion. (b) Peripheral facial paralysis caused by other reasons: (i) acute infectious polyneuritis: there may be peripheral facial nerve paralysis, but it is often bilateral, and most of them are accompanied by symmetrical paralysis of other cranial nerves and limbs, and the phenomenon of cerebrospinal fluid protein cell separation, etc. (ii) pontine facial paralysis: it is caused by damage to the contralateral cortical brainstem bundle, and only shows the lower facial muscle paralysis on the side opposite to the lesion. (ii) Pontine damage: damage to the facial nerve nucleus and its fibers in the pontine brain can have peripheral facial paralysis, but it is often accompanied by damage to adjacent structures within the pontine brain, such as the abducens nerve, trigeminal nerve, pyramidal fasciculus, and spinal cord thalamus system, etc., which may result in the paralysis of the extraocular muscles of the ipsilateral eye, facial sensory deficits, and paralysis of the contralateral limbs (cross paralysis). It is seen in tumors, inflammation, and vascular lesions in this part. (C) Cerebellar pontine angle damage: more damage to the trigeminal nerve, auditory nerve, cerebellum and medulla oblongata at the same time, so in addition to peripheral facial paralysis, there can also be ipsilateral facial pain sensory impairment, tinnitus, deafness, vertigo, nystagmus, limb ataxia and contralateral limb paralysis and other symptoms, called “cerebellar pontine angle syndrome”, mostly due to tumors of the Department, Inflammation. (d) Structural lesions adjacent to the facial neural tube: these can be seen in otitis media, mastoiditis, middle ear mastoid surgery, and skull base fracture, etc., and may have corresponding history and clinical symptoms. (e) Lesions outside the stem mastoid foramen: seen in parotitis, parotid tumors, surgery of the maxillo-neck and parotid region, etc. In addition to peripheral facial paralysis only, there are history and clinical manifestations of corresponding diseases. Treatment: Early to improve the local blood circulation, eliminate the inflammation and edema of facial nerve, and later to promote the recovery of nerve function as its main treatment principle. (I) Hormone therapy: Dexamethasone (10-15mg)1/d, intravenous drip, 3-5 days to prednisone oral 30mg/d, one week after the gradual reduction of the amount. (B) improve microcirculation, reduce edema: low molecular dextrose 250-500ml, intravenous drip 1 / d, for 7-10 days, can also add dehydration diuretic. (C) the application of neurotrophic metabolic drugs: vitamin B1 50-100mg, vitamin B 12 1000μg, cytidine 250mg, coenzyme Q105-10mg, etc., intramuscular injection 1 / d. (D) Knee Ganglion Syndrome (Hunt’s Syndrome): antiviral therapy can be used acyclovir or ganciclovir. Or use interferon 1-3 million u intramuscularly once a day for one week. (e) Acupuncture treatment: take cataract, hearing, sun, dicang, Xiaguan, cheek car, and with Quchi, Hegu and other points. (F) Vasodilator and cervical sympathetic ganglion block: Tolazoline 25mg or niacin 100mg can be used, orally, 3/d or cervical stellate ganglion block on the affected side, 1/d, for 7-10 days. (VII) Physiotherapy: ultrashort wave hyperthermia near the stem and breast orifices, infrared irradiation, direct current iodine ion introduction, in order to promote the dissipation of inflammation. Transistor pulse therapy can also be used to stimulate the facial nerve trunk to prevent facial muscle atrophy and reduce the excessive traction of the paralyzed side muscle by the healthy side muscle. In addition to the above treatments during the recovery period, vitB1 and vitB8 can be taken orally, 10-20mg each, 3/d; dibazole, 10-20mg, 3/d; and galantamine, 2.5-5mg, intramuscularly, 1/d, to promote the recovery of nerve function. In addition, to protect the exposed cornea, to prevent the occurrence of conjunctivitis, keratitis, can be used eye masks, eye drops, eye ointment and other methods. Prognosis and prevention: Enhance the physical fitness, pay attention to the face and the area behind the ear to keep warm in the cold season, avoid sitting or sleeping with the head facing the windy window to prevent the onset or recurrence of the disease. The general prognosis is good, usually 1 to 2 weeks after the onset of the disease began to recover, 2 to 3 months within the cure. About 85% of the cases can be fully recovered without sequelae. However, those who have not recovered for more than 6 months have a poorer prognosis, and some of them may be left with facial muscle spasm or facial muscle twitching. The former is characterized by the deepening of the nasolabial folds on the sick side, the corner of the mouth is pulled towards the sick side, the eye fissure is small, and it is easy to mistake the healthy side for the sick side; the latter is characterized by the involuntary twitching of the facial muscles on the sick side, and the symptoms are more pronounced when the patient is tense, which may affect the normal work in case of seriousness. In a few cases, the “crocodile tears sign”, i.e., tears flowing from the sick side of the eye when eating, may be caused by the regeneration of nerve fibers in the process of facial nerve repair, which may be mistakenly inserted into adjacent nerve sheaths with different functions. Electromyography and measurement of facial nerve conduction function are of considerable value in determining the degree of damage to the facial nerve and the extent of its possible recovery, and can be performed two weeks after the onset of the disease.