Facial Neuritis Facial neuritis, also known as facial nerve palsy, facial nerve palsy is a peripheral facial paralysis (referred to as facial palsy) caused by facial neuritis. Clinically, it is characterized by distortion of the eyes and mouth, and is mostly unilateral, with very few cases of bilateral onset. The onset of the disease is rapid, with paralysis of the facial expression muscles, disappearance of forehead wrinkles, drooping eyebrows, enlarged eyelid fissures, flattened nasolabial folds, drooping corners of the mouth, and the face being pulled toward the healthy side. This disease is a common and frequent disease in neurology clinic, which can develop at any age, but is most common in 20-40 years old. It can occur in any season. If facial paralysis is mild and treated in time, the prognosis is good; the longer the duration of facial paralysis, the worse the prognosis. In Chinese medicine, facial nerve paralysis is called “facial paralysis” and “oral remoteness”, which belongs to the category of “stroke”. Pathogenesis and pathology of 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, but 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 hours 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 or are found by others to have a skewed angle of the 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. When the geniculate ganglion is involved, 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, which is called Ramsay-Hunt syndrome. Diagnosis and differentiation, according to the form of onset and clinical features, the diagnosis is not difficult. However, it needs to be differentiated from the following diseases: i. Central facial paralysis: it is caused by damage to the contralateral cortical brainstem bundle, and only manifests as paralysis of the lower facial muscles on the contralateral side of the lesion. ii. (b) Peripheral facial paralysis caused by other reasons: (i) acute infectious polyradiculoneuritis: peripheral facial nerve paralysis can be present, but it is often bilateral, and most of the cases are accompanied by symmetrical paralysis of other cranial nerves and limbs, and the phenomenon of protein cell separation in cerebrospinal fluid. (ii) Pontine damage: damage to the facial nerve nucleus and its fibers in the pontine brain may cause peripheral facial paralysis, but it is often accompanied by damage to adjacent structures in the pontine brain, such as the abducens nerve, trigeminal nerve, pyramidal fasciculus, and spinal cord thalamus system, which results in paralysis of the extraocular muscles of the ipsilateral eye, sensory disturbances in the face, and paralysis of the contralateral limbs (cross paralysis). Tumors, inflammation, and vascular lesions in this area are seen. (C) Cerebellar pontine angle damage: the trigeminal nerve, auditory nerve, cerebellum and medulla oblongata are damaged at the same time. Therefore, in addition to peripheral facial paralysis, there may be ipsilateral facial dysesthesia, tinnitus, deafness, vertigo, nystagmus, ataxia and contralateral limb paralysis, which is known as cerebellar pontine angle syndrome, and it is often seen in tumors of this part of the brain, 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 medical history and clinical symptoms. (e) Lesions outside the mastoid foramen: seen in parotitis, parotid tumors, surgery of the maxillo-cervical and parotid regions, etc. In addition to peripheral facial paralysis only, there are history and clinical manifestations of corresponding diseases. Treatment: Improve local blood circulation and eliminate inflammation and edema of facial nerve in early stage, and promote the recovery of nerve function in later stage as its main treatment principle. (I) Hormone therapy: prednisone (20-30mg) or dexamethasone (1.5-3.0mg) 1/d, orally for 7-10 days. (B) improve microcirculation, reduce edema: available 706 plasma or low molecular dextrose 250-500ml, 1 / d, for 7-10 days, can also add dehydration diuretic. (C) the application of neurotrophic metabolic drugs: vitamin B150-100mg, vitamin B12100μg, cytidine 250mg, coenzyme Q105-10mg, etc., intramuscular injection 1 / d. (D) Physiotherapy: ultra-short-wave hyperthermia near the stems and breasts of the holes, infrared irradiation, DC iodine ion implantation, in order to promote inflammation dissipation. 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. (e) Acupuncture treatment: take cataract, hearing, sun, dicang, Xiaguan, cheek car, and with quchi, hegu, etc. (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. 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. Galantamine 2.5-5mg, intramuscular injection, 1/d can also be used to promote the recovery of neurological function. In addition, to protect the exposed cornea and prevent the occurrence of conjunctivitis and keratitis, eye masks, eye drops and eye ointment can be used. Nerve grafting can be considered for those who do not recover for a long time. Generally take the peroneal nerve or neighboring auricular nerve, with vascular muscle, transplantation to the facial nerve branch, the effective rate of about 60%. Prognosis and prevention, strengthen the body, 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 1~2 weeks after the onset of the disease began to recover, 2~3 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 nasolabial folds on the diseased side, the corner of the mouth is pulled towards the diseased side, the eye fissure is small, and it is easy to mistake the healthy side for the diseased side; the latter is characterized by the involuntary twitching of the facial muscles on the diseased side, and the symptoms are more pronounced in times of nervousness, which may affect the normal work in case of seriousness. 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 repairing the facial nerve, 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 extent of facial nerve damage and the degree of possible recovery, and can be performed two weeks after the onset of the disease.