Definition: Facial palsy is a disease in which the mouth and eyes are skewed to one side, also known as “skewed mouth and eyes”. The onset of this disease is rapid (mostly occurs after blowing wind or getting cold, or after overexertion, and many patients find it after waking up in the morning), but there is no hemiplegia or unfavorable speech. The disease can occur at any age, and used to be seen in the autumn, winter and spring, but with the development of society, air conditioning and cold air increase, now there is no obvious seasonality. Facial nerve anatomy: The facial nerve travels from the caudal end of the cerebral bridge to the nucleus of the facial nerve ventral to the cover, first bypassing the nucleus of the spreading nerve near the midline, then descending forward and penetrating at the lower edge of the cerebral bridge adjacent to the auditory nerve. It crosses the subarachnoid space, enters the inner ear foramen above the auditory nerve, then descends through the facial nerve canal, crosses the geniculate ganglion at the bend, and finally exits the stem mammary foramen, innervating the facial muscles other than the masticatory muscles and the levator palpebrae, as well as the ear muscles, the occipital muscles, the broad neck muscles, and the stapedius muscles. Sensory: Gustatory fibers originate from the neurons of the geniculate ganglion in the facial nerve canal. The peripheral branch follows the facial nerve path down the facial nerve canal, leaves the facial nerve and travels anteriorly to form the bulbar nerve, which joins the lingual nerve and terminates in the taste buds in the first 2/3 of the tongue. The central branch forms the middle branch of the facial nerve and enters the pons, where it joins the taste fibers of the glossopharyngeal nerve and terminates in the nucleus tractus solitarius. From the nucleus tractus solitarius, fibers emanate to the thalamus and finally terminate in the inferior aspect of the postcentral gyrus. The facial nerve is a mixed nerve and contains three main fiber components: 1. Special visceral motor fibers: originate in the facial nucleus and mainly innervate the movement of the facial muscles. 2. 2. General visceral motor fibers: originate from the supraglottic nucleus and innervate the secretion of the glands (lacrimal, sublingual, submandibular, and mucosal glands of the nose and palate). 3.Special visceral sensory fibers: i.e., gustatory fibers, whose cytosol is located in the geniculate ganglion, the peripheral protrusions are distributed in the anterior 2/3 of the taste buds of the tongue, and the central protrusions end in the nucleus of the solitary bundle. Branches in the facial nerve canal: 1. bulbar nerve: innervates the anterior 2/3 of the tongue for taste and the secretion of the sublingual and submandibular glands. 2. Iguanodal nerve: innervates the secretion of the lacrimal gland, palate and glands of the nasal mucosa. 3.Stapedius muscle nerve: innervates the stapedius muscle. Third, the main pathological mechanism: ischemia and edema It is generally believed that the bony facial nerve canal can just accommodate the facial nerve, once there is ischemia and edema, there will be a vicious circle of edema and ischemia, so that the facial nerve is compressed, lack of nerve nutrition, and even cause nerve demyelination and degeneration and cause disease. The stimulating factors can be viral infection, various ways of cold stimulation and autonomic instability. Clinical manifestations The disease usually has an acute onset, with the sudden appearance of facial expression muscle paralysis on one side, the frontal line disappears, the eye fissure becomes larger, the eyes are exposed to tears, the nasolabial fissure becomes shallow, the corners of the mouth droop to the healthy side; the sick side cannot make frown, frown forehead, close the eyes, drum cheeks, show teeth and other actions; some patients initially have pain behind the ear or below the ear, but also the affected side of the front 2/3 of the tongue loss of taste, auditory hypersensitivity, tear secretion disorder and cause corneal dryness In some patients, there may also be a loss of taste in the anterior 2/3 of the tongue, auditory hypersensitivity, lacrimation disorder and corneal dryness. If the disease is prolonged, the corners of the mouth may recoil to the affected side due to muscle contracture, forming the phenomenon of “inverted error”. V. Diagnosis and differential diagnosis The diagnosis can be made based on the acute onset of peripheral facial palsy without hemiplegia and confusion. The localized diagnosis of facial nerve palsy should first distinguish between peripheral facial nerve palsy and central facial nerve palsy. The former is often heavier than the latter, with paralysis of the facial expression muscles above and below the eyes, resulting in loss of expression movements; the latter is paralysis of the lower part of the opposite side of the lesion, with no damage to the frontal muscles, so forehead frowning, frowning and eye closing movements are unimpeded, while the random movements of the opposite side disappear and crying and laughing movements are still preserved, often with ipsilateral hemiparesis and central hypoglossal nerve palsy, mostly seen in stroke and brain tumor. 2, inside or outside the brainstem After identifying peripheral facial nerve palsy, additional symptoms should be combined to determine the site and cause of facial nerve damage, according to the presence or absence of other cranial nerve palsy and the presence or absence of symptoms of damage to the long tract of the brainstem, to distinguish whether the damage to the facial nerve is inside or outside the brainstem. Brain bridge damage is often accompanied by cranial nerve palsy on the diseased side V, VI and VIII and contralateral hemiparesis or bilateral damage. 3. Intracranial or extracranial cavity (including temporal bone). If the intracranial cavity lesion invades the cerebral base near the foramen ovale, it may be accompanied by auditory nerve disorder, which is common in tumor, skull base fracture, various meningitis, etc. 4.Decide the depth of the disease location according to the accompanying symptoms When the facial nerve canal and other structures in the temporal bone are damaged, the disease location is deep, the facial nerve damage is serious and the recovery is poor according to whether it is accompanied by taste deficiency (damage to the bulbar branch), auditory hypersensitivity (damage to the stirrup muscle branch), and urinary delay disorder, etc. If the above conditions occur, the disease location is deep, the facial nerve damage is serious and the recovery is poor. 5.Hunt syndrome When facial nerve paralysis on one side is accompanied by pain in the external auditory canal and herpes, it suggests herpes zoster virus infection in the geniculate ganglion, which is called Hunt syndrome. It is often seen in patients who are overly fatigued and stay up late for long periods of time (more than 3 consecutive days). Treatment: Combination of Chinese and Western medicine, early intervention with acupuncture (preferably without electroacupuncture), recovery usually starts in 7-12 days and heals in 3-4 weeks. Hunt (Hunt) syndrome recovery is slower, 2-3 months have a chance to recover, but more difficult to fully recover. Prevention 1. Do more exercises to enhance physical fitness. 2, regular life, avoid staying up late (90% of clinical patients with Hunter facial palsy are caused by staying up late for more than 3 days in a row). 3. Don’t blow the cold air conditioner against your face for a long time, especially for drivers. In addition, during the cold season, you should avoid exposing your face when you go out in the morning, especially for patients with poor physical condition or old age.