Idiopathic facial nerve palsy, also known as facial neuritis, is an acute nonsuppurative facial neuritis within the stomastoid foramen that clinically manifests as peripheral facial nerve palsy, also known as Bell’s palsy. The etiology of this disease is not fully elucidated. It is generally believed that the bony facial nerve canal can only accommodate the facial nerve, and once there is ischemia and edema, it will inevitably lead to compression of the facial nerve. Exciting factors can include wind chill, viral infection (e.g., herpes zoster) and autonomic instability leading to neurotrophic vasoconstriction ischemia, capillary dilation, and tissue edema compression. Early pathological changes of the facial nerve are edema and demyelination, and in severe cases, axonal degeneration. The disease can develop at any age, with no seasonal differences, and is slightly more common in males. The onset is usually acute, with a peak within hours or 1-3 days. The disease is often preceded by prodromal symptoms of viral infection and a history of exposure to wind and cold. The main symptom is mostly unilateral facial expression muscle paralysis. The main symptom is unilateral facial expression muscle paralysis, which is characterized by loss of frontal lines, inability to frown, inability to close the eye fissure or incomplete closure, and the phenomenon of the paralyzed side of the eye turning upward and outward when trying to close the eye. The white sclera is exposed on the affected side, which is called Bell’s phenomenon. The nasolabial fissure on the affected side becomes shallow, the corners of the mouth droop, and the corners of the mouth are skewed to the healthy side when the teeth are exposed; due to paralysis of the orbicularis oris muscle, the air leaks when puffing or whistling. Due to the paralysis of the buccal muscle, food is easily retained between the teeth and cheeks on the affected side. If the lesion is above the knee of the tympanic cord branch and the facial nerve, loss of taste and auditory hypersensitivity may occur on the ipsilateral side of the anterior tongue if it is damaged above the branch of the stapedius muscle; if the lesion reaches the geniculate ganglion, in addition to the above-mentioned manifestations, there is pain in the affected mastoid region and hyposensitivity in the auricle and external auditory canal. If herpes is also present in the external auditory canal or tympanic membrane, it is called Hunt’s syndrome, which is usually caused by herpes zoster virus infection. In cases of incomplete facial palsy, recovery begins after 1-3 weeks of onset and gradually heals after 1-2 months of marked improvement. The prognosis is better in young cases. Facial nerve conduction examination is a useful method to determine the prognosis of early (5-7 days after onset) complete facial palsy. If the amplitude of the evoked action potential M wave on the affected side is 30% or more of that on the healthy side, recovery is expected within 2 months; if 10-30%, recovery will take 2-8 months with possible complications; if only 10% or less, recovery will take 6-12 months with complications such as facial muscle spasm and joint band movements. The common associated band movement is a slight tremor of the affected upper lip during transient eyesight, involuntary eye closure during tooth exposure or contraction of the frontalis muscle when trying to close the eyes, and tearing of the affected eye when chewing food, called the crocodile tear sign, which may be caused by some fibers growing into the adjacent Schwann cell membrane canals belonging to other functional nerves during nerve fiber regeneration. The diagnosis is based on the acute onset of peripheral facial palsy. The disease should be differentiated from otogenic facial nerve palsy complicated by Guillain-Barré syndrome, otitis media, labyrinthitis, mastoiditis, etc., as well as from peripheral facial palsy caused by mumps, purulent lymphadenitis, tumors, etc., and tumors in the posterior cranial fossa or meningitis. The treatment principle of this disease is to improve local blood circulation, reduce facial nerve edema, and promote functional recovery. 1. Adrenocorticotropic hormone: Within a week after the onset of the disease, a course of adrenocorticotropic hormone is mostly recommended to reduce the edema and pressure on the nerve. Such as prednisone tablets, dexamethasone injection, etc. 2, antiviral drugs: such as virazole, acyclovir, ganciclovir, etc. 3, neurotrophic drugs: vitamin B drugs can promote the recovery of nerve myelin. Such as vitamin B1, B12, etc., gangliosides can also be applied. In the acute stage, ultrashort wave heat therapy, infrared radiation or local hot compresses near the stem mammary foramen can help improve local blood circulation and eliminate neuroedema. In the recovery period, iontophoresis, acupuncture or electroacupuncture can be done. Prevent ocular complications, as the cornea is exposed for a long time due to the inability to close the eyes and transient eyes, it is prone to infection, so eye shields, eye drops and eye ointment can be used for protection. Functional training: Massage the paralyzed facial muscles with your hands as early as possible. When the function starts to recover, frowning, raising the forehead, showing the teeth, puffing the cheeks, whistling and other movements can be performed in the mirror for several minutes each time, several times a day. Those who have not recovered for one year or more after the onset of the disease can consider cosmetic surgery. Chinese herbal medicine can often be very effective in the treatment of this disease.