Facial paralysis

Introduction to facial muscle spasm The facial muscles are divided into two parts: the expression muscle and the masticatory muscle. The former is dominated by the facial nerve and the latter is dominated by the trigeminal motion branch. The facial muscle spas described here only discuss the expression of facial muscle paralysis, that is, facial nerve paralysis. Facial nerve paralysis is more common in cranial nerve diseases. It is divided into specific diseases according to the cause, trauma, infection, tumor, and neural source. There are five main types of sex. Idiopathic facial paralysis, Bell palsy, is described in detail as a separate disease, and other types of facial nerve palsy are described here. basic knowledge The proportion of illness: 0.37% Susceptible people: no special people Mode of infection: non-infectious Complications: facial muscle twitching necrotic otitis externa

Hemifacial spasm

(1) Causes of the disease

1. idiopathic facial paralysis

The main type of facial paralysis is idiopathic facial paralysis, often called Bell paralysis, accounting for 60% to 75% of all facial paralysis cases, the most common is unilateral nerve paralysis, the degree of facial nerve paralysis can be complete or incomplete Paralysis, considering this diagnosis after excluding other causes, the complete recovery rate of Bell's palsy was 71% without treatment, 13% of patients had only mild sequelae, and 16% had moderate recovery or poor recovery.

The incidence of Bell's palsy in the United States is 13/100,000 to 34/100,000 per year. The literature in Western countries reports that the incidence of Bell's palsy is 20/100,000 per year, Japan's annual rate is 30/100,000, and Ramsay Hunt's syndrome is 3. /10 million people, 1/10 of Bell's paralysis.

In 1982, the prevalence of this disease in 6 cities in China was 425.7/100,000. The annual incidence rate was not reported, and it is estimated to be similar to Japan.

2. Infection

Infection is the second most common cause of facial paralysis. Common causes of infection are viruses, spirochetes and bacteria.

In a 5-year study by Ratanaprasatporn et al., about 5.7% of patients with facial paralysis were infected with infection. Ramsay Hunt syndrome with herpes zoster is one of the most common causes of infection, and is generally more severe.

This type of facial nerve paralysis accounts for 12% of all facial nerve paralysis, with varying degrees of cochlear nerve involvement, accounting for about 20% of the symptoms of the cochlear and vestibular nerves. Other viral infections include herpes simplex virus, measles virus and giant Cytomegalovirus (CMV) can also produce clinical symptoms similar to herpes zoster.

Lyme disease is another cause of facial paralysis. Lyme disease was discovered by Steere in Lyme, Conn., in 1977. It is a system that can invade nerves, skin, eyes, heart and joints. A vector-borne disease, the disease is a regional epidemic, more common in the summer, the population is generally susceptible, living in forests and rural areas are more likely to occur, the incidence is often related to tourism, hunting, camping, etc., age of onset and gender Differences, the disease is prevalent in more than 20 countries on five continents and has an expanding trend. The Lyme disease investigation and research team of China conducted a Lyme disease survey in 19 cities and districts across the country from 1987 to 1992, and found that the disease is also distributed in China. Widespread, 11 provinces (cities, districts) have occurred and prevailed, the prevalence rate in the northeast forest area is 1% to 4%, and the prevalence rate in some forest areas in Sichuan Province is as high as 9%.

Facial paralysis can also be secondary to middle ear infections. Otitis media is not treated in time and can cause facial paralysis. Ratanaprasat-porn et al reported that 161 cases of facial paralysis were caused by otitis media, and middle ear infections caused 1.96 per year in the United States. Ten cases of facial nerve paralysis.

3. Tumor

Tumors are the second most common cause of infection. About 5% of patients with facial paralysis are caused by tumors. These tumors include acoustic neuroma, parotid adenoma, primary cholesteatoma and jugular bulb tumor. In abnormal cases, the tumor itself and Surgical removal of tumors can cause facial nerve paralysis.

The annual incidence of acoustic neuroma in the United States is about 1/100,000, and the incidence of parotid tumors is 5.8/100,000. From this, it can be calculated that there are 17,200 cases of facial paralysis caused by tumors in the United States each year. The proportion calculation (1.3 billion × 6.8 / 100,000) was 88,400 cases.

4. Neurogenicity

The results of studies published by Ratanaprasatporn and May indicate that facial nerve palsy caused by neurogenic causes account for 5% of all facial paralysis, and there are many intracranial, non-traumatic neurogenic facial paralysis and cerebrovascular diseases, which are the causes of facial paralysis. Ratanaprasatporn et al found that about 2.5% of facial nerve palsy was caused by cerebrovascular disease.

Guillain-Barré syndrome and Melkersson-Rosenthal syndrome are rare neurogenic causes of facial paralysis. According to the above-mentioned incidence, it is estimated that about 172,000 new facial paralysis patients in the United States are caused by neurogenic causes. of.

5. Traumatic

Traumatic injury is one of the common causes of facial paralysis. The fracture of the humerus is the most common cause of facial nerve palsy in traumatic causes. The fracture can be either longitudinal or lateral. It can be caused by a car accident of 58,000 patients with skull fracture. About 3275 of them caused facial nerve palsy.

Neonatal traumatic facial paralysis is most common in childbirth, with an annual incidence of 1.8 . There are approximately 4 million newborns per year in the United States, which results in 7200 neonates with facial nerve palsy, and approximately 9.0% (700 patients) will be permanently Tormented by facial nerve paralysis.

In neonates, facial paralysis is not common, with an incidence of 0.2% to 6.9% of neonates. In the facial nerve clinic of Kochi School of Medicine, the incidence of neonatal facial paralysis accounted for 1.4% of patients with peripheral facial paralysis. %.

Neonatal facial nerve palsy is mainly divided into three types:

(1) Congenital facial paralysis: including developmental disorders that occur during embryonic development, leading to facial paralysis or other symptoms.

(2) Pre-natal acquired facial paralysis: the result of an intrauterine environment or factor that affects neurogenesis.

(3) acquired facial paralysis after birth: from infection, trauma, to skull and cranial diseases of various causes.

A review of the medical literature on the causes of facial paralysis in the 90 years from 1900 to 1990 reported many causes of facial paralysis. Wang Xinglin et al. summarized it.

Hemifacial spasm prevention

To prevent facial paralysis and hemifacial spasm, the key is to pay attention to cold protection, especially to avoid cold winds and long-term sputum according to the climate (not to be cool), to exercise more, to strengthen exercise, and to improve the body's righteousness. "Dry", the human body is full of vitality, wind evil is not easy to invade; also pay attention to keep the spirit happy and comfortable, enough sleep time, pay attention to the diet, not only enhance physical fitness, but also enhance disease resistance. If you have suffered from facial paralysis, you should seek medical treatment in time. The treatment with traditional Chinese medicine should be the first choice. It can achieve both the symptoms and the root causes, in order to prevent the sequelae.

Hemifacial spasm complications Complications facial muscle twitching necrotic otitis externa

Facial paralysis is complete or incomplete, facial paralysis and herpes at the same time. Although the facial nerve also transmits the proprioception from the facial muscles and a small range of skin sensations from the ear and outer ear canal, these sensations are rarely detected. Partial facial nerve injury causes weakness in the upper and lower half of the face. Occasionally, the lower half of the face is more severely affected than the upper half of the face. The recovery of facial paralysis depends on the severity of the lesion. If the nerve has been severed, the chances of complete or even partial recovery are small. Most patients with facial paralysis can partially or completely restore function. Complete recovery is at rest or During exercise, there is no difference in facial expressions on both sides. Partial recovery has a "collapse" change on the temporal side. Surface examination seems to indicate that the normal side muscles are weak. This incorrect impression is more obvious as the patient smiles or tries to exercise the facial muscles.

Symptoms of hemifacial spasm Common symptoms Facial pattern disappears Sensory disorders Tinnitus and ear mites Ear pain after earache valgus valgus ptosis Hearing hypersensitivity Nasal labial groove shallow

Clinically, it can be divided into two types: central facial paralysis and peripheral facial paralysis.

1. The central facial sputum is caused by the damage of the contralateral cortex-cerebral pons. Because of the involvement of the upper facial muscles, it is only manifested as the paralysis of the facial muscles of the contralateral side of the lesion, and often accompanied by hemiplegia on the side.

2. In addition to idiopathic facial paralysis, there are mainly the following facial paralysis caused by other causes. The main causes can be seen in Table 2.

(1) Guillain-Barré syndrome (brain nerve type): peripheral facial paralysis may occur, but the lesions are often bilateral, most of which are accompanied by other cranial nerve damage, and the cerebrospinal fluid may have protein (increased) cells (normal or slightly high). Separation phenomenon.

(2) cerebral bridge lesions: because the facial nerve movement nucleus is located in the pons, its fibers bypass the nucleus, so the pons lesions except the peripheral facial paralysis, often accompanied by damage to the adjacent structures inside the pons, like lateral lateral rectus paralysis, facial sensation Obstructions and paralysis of the contralateral limbs.

(3) Cerebellar pons damage: more than the same side of the V and VIII on the cranial nerve and cerebellum and medulla, so in addition to peripheral facial paralysis, there may be the same side of the sensory, tinnitus, deafness, dizziness, nystagmus, Limb ataxia and contralateral limb paralysis.

(4) lesions in the vicinity of the facial nerve tube: such as otitis media, mastoiditis, middle ear mastoid surgery and skull fracture, in addition to peripheral facial paralysis, there may be other corresponding signs and medical history.

(5) lesions other than the stem of the stem: Because the facial nerve exits the stem of the stem and passes through the parotid gland to control the facial expression muscle, the parotid inflammation, tumor, jaw neck and parotid area surgery can cause peripheral facial paralysis, but in addition to facial paralysis, Often have a history of the disease and characteristic clinical manifestations, no hearing allergies and taste disorders.

The signs of facial nerve palsy are divided into three categories of exercise, secretion and sensation, often acute onset. The upper and lower facial muscles are also the main clinical manifestations, often accompanied by diseased lateral external auditory canal and/or post-auricular mastoid pain. And/or tenderness.

The upper facial muscle spasm causes the frontal frontal line to disappear, can not lift the amount, the eyebrows, the eyelids can not be closed or closed, and the eyeballs turn upwards when the eyes are closed to expose the white sclera (called the Bell phenomenon), due to the orbicularis tendon, The lower eyelids are everted, and the tears do not easily flow into the nasolacrimal duct and ooze out of the eyes.

The lower group of hemifacial spasm showed that the nasolabial fold was shallow, the mouth was drooping, the mouth was pulled to the opposite side of the lesion, and the mouth and whistle could not be licked. When the drumsticks were leaking at the corner of the disease side, due to buccal tendon, it was easy to chew. Biting the buccal mucosa, food often stays between the cheeks.

In severely injured, the facial muscle paralysis is significant. Even when the facial rests, the lower part of the patient's facial muscles relax, the facial pattern disappears, the platysma muscle fissure is wider than normal, and the facial muscles and platysma muscles disappear completely and synergistically. When the patient tries to smile, the lower half of the facial muscles pulls to the opposite side, causing the illusion of deflection when the tongue is extended or the mouth is open. The saliva and food gather on the temporal side, the patient cannot close the eye, and the eye movement is visible with the eye movement. Turning inward, when the lesion is located in the peripheral nerve to the ganglion, the lacrimal gland nerve loses its function, and the tear can not be pressed into the nasolacrimal duct through the eyelid movement, resulting in excessive accumulation of tears in the capsular sac, and the corneal reflex disappears due to the upper eyelid paralysis. The afferent portion of the corneal sensation and corneal reflex is indicated by swaying the other side of the eyelid.

If the lesion spreads to the tympanic nerve, there may be a 2/3 taste loss or disappearance in front of the ipsilateral tongue.

If the upper part of the iliac crest is involved, in addition to the dysgeus, ipsilateral hypersensitivity may also occur.

If the geniculate ganglion is involved (mostly herpes zoster virus infection), in addition to facial paralysis, 2/3 taste disorder in front of the tongue, hypersensitivity, ipsilateral saliva, tear secretion disorder, pain in the ear and behind the ear, external auditory canal and Auricular herpes, called Ramsay Hunt's syndrome, generally predicts that the facial paralysis of Ramsay Hunt syndrome is worse than Bell's paralysis. About 66% of patients with complete paralysis can recover completely, and only 10% Complete paralytic patients recovered normal facial function, and the risk factors for poor prognosis included age, degree of ear pain, facial nerve palsy was complete or incomplete, facial paralysis and herpes were common.

Although the facial nerve also transmits the proprioception from the facial muscles and a small range of skin sensations from the ear canal and the external auditory canal, it is rarely found that these sensations are missing.

Partial facial nerve injury causes weakness in the upper and lower half of the face. Occasionally, the lower half of the face is more severe than the upper half of the face. The contralateral side is rarely affected. The recovery of facial paralysis depends on the severity of the lesion. If the nerve has been cut, The chances of complete function and even partial recovery are small. Most patients with facial paralysis can partially or completely restore their function. When restoring or exercising, there is no difference in facial expressions on both sides; partial recovery is on the temporal side. There has been a change in "collapse".

The surface examination seems to indicate that the normal side muscles are weak, and this incorrect impression is more pronounced as the patient smiles or tries to move the facial muscles.

Examination of hemifacial spasm

Select the necessary selective tests based on the likely cause.

1. Blood routine, blood electrolytes: generally no specific changes, the blood picture can be slightly higher at the onset.

2. Blood sugar, immune items, cerebrospinal fluid examination, if abnormal, there is a differential diagnosis.

Melkersson-Rosenthal syndrome: from the point of view of etiology must exclude certain inflammation, such as tuberculosis, sarcoidosis, etc., for this should be done related tests, usually to do tuberculin test, Kveim reaction, serum gamma globulin determination.

Lyme disease can increase erythrocyte sedimentation rate; serum GOT, GPT and LDH increase, acute pathogen can be found from blood, cerebrospinal fluid, joint fluid and skin lesions, cerebrospinal fluid initial examination is normal, white blood cells increase after weeks to months, Lymphocyte elevation is dominant, protein can be slightly increased, enzyme-linked immunosorbent assay (ELISA) and immunofluorescent antibody assay anti-BB antibody positive, is of great significance for diagnosis, IgM and IgG titer is more than 1:64 positive, IgG of this patient And IgM titer was measured 3 to 6 weeks, 90% of patients >1:128, early IgM increased, followed by elevated IgG, and its potency can be maintained for several years.

If the following items are abnormal, there is a differential diagnosis.

3. CT, MRI examination.

4. Skull base film.

5. EEG, fundus examination.

6. ENT examination.

Hemifacial spasm diagnosis

1. Identification of lesions

(1) Central facial paralysis: the contralateral cortex-brain bridge is damaged, because the upper group is not affected by the facial muscles, only the paralysis of the facial muscles of the contralateral side of the lesion, the nasolabial fold becomes shallow, the mouth angle is drooping, the mouth Was pulled to the opposite side of the lesion, the mouth of the disease side leaked when the drumsticks, often accompanied by the tongue and limbs on the side.

(2) Peripheral facial paralysis: on the disease side, the lower facial muscles are also the main clinical manifestations, often accompanied by pain and/or tenderness in the external auditory canal and/or posterior mastoid region, upper facial muscle spasm Lead to the disappearance of the frontal line of the disease, can not lift the amount, eyebrows, eyelids can not be closed or closed, because the orbicularis tendon, lower eyelid valgus, tears do not easily flow into the nasolacrimal duct and exudate the eye, the lower group of facial muscle spasm It is manifested as a shallow nasolabial fold on the disease side, a drooping mouth, and the mouth is pulled to the opposite side of the lesion. It is not allowed to pout and whistle. When the drumsticks, the mouth of the disease side leaks.

2. Rare cause identification

The differential diagnosis of facial paralysis may sometimes be complicated, but efforts should be made to determine the cause. The appropriate treatment can be used after the cause is determined. Detailed medical history and comprehensive examination are very important in the diagnosis and differential diagnosis. After excluding other causes of facial paralysis, Bell palsy can be diagnosed and patients should continue to be followed up until new signs of recovery or other causes.

(1) Melkersson-Rosenthal syndrome: In the diagnosis of patients with recurrent facial paralysis, it is necessary to consider the rare Melkersson-Rosenthal syndrome, the cause of which is unknown, including infection (virus or bacteria), neurotrophic, allergies, immunity And heredity, the characteristics of this syndrome include paralysis of one or both sides, chronic facial swelling (especially the lips) and tongue wrinkles (scrotal-like tongue), family reports, but mostly sporadic cases, Symptoms are clearly diverse, and only a subset of patients have typical facial paralysis, edifice edema and fissured tongue triads, which are sometimes difficult to diagnose due to different symptoms.

Many scholars believe that the intrinsic is a hereditary disease, but it has not been finally confirmed. Therefore, there are many hypotheses about the etiology of the intrinsic.

1 bacterial infection: It is considered that the intrinsic is a secondary manifestation of bacterial infection, but it has not been consistently recognized. In addition, it is found that when it is bitten by insects, it can cause symptoms due to insect venom, thus emphasizing biological infection or foreign Pathogenic factors.

2 tuberculosis theory: Although some clues were found from the pathological changes, they were not proved.

3 part of the symptoms of sarcoidosis: the pathological histology of the intrinsic is similar to sarcoidosis, so it is speculated that the intrinsic part may be part of sarcoidosis, but according to the systemic symptoms and lymph nodes of sarcoidosis See, we can see that the two are not a disease.

4 allergic reaction: It is considered that the intrinsic is an allergic reaction caused by local infection such as dental caries and tonsillitis, but it has not been confirmed.

5 Mechanical stimulation of dentures, caries, etc.: It is believed that the chronic stimulation of dentures and caries can cause the intrinsic, but it has not been finalized.

In short, the etiology of the intrinsic complex has not yet been elucidated. Once the lips are swollen, the tongue becomes rough and thick, and the condition quickly spreads to the facial nerve canal. The facial nerve in the facial nerve canal is edematous and facial paralysis occurs.

The syndrome is divided into 6 types from the pathological histological point: 1 type tuberculosis type. 2 nodular disease type. 3 granulation type. 4 diffuse infiltration type. 5 edema type. 6 mixed type, usually tuberculosis type, diffuse invasive type is common, histopathological changes include edema and / or sarcoidosis-like granuloma.

(2) One side muscle twitching and hyperkinetic disease: facial motor hyperactivity includes a lateral muscle twitch, eyelid and facial multiple fibrous myoclonus, one of which is the most common of these diseases. Severe lateral muscle twitching, patients may have eyelids and upper lip muscle contracture and associated movement, facial expression muscles to the affected side skew, should be differentiated from facial nerve paralysis sequelae and facial nerve paralysis.

(3) malignant otitis externa: in some cases, refractory external auditory canal infection may be combined with a systemic disease. Elderly patients with diabetes may have an infection that is not effective in general treatment. The disease was first reported by Chandler. It is called malignant otitis externa and is usually caused by Pseudomonas aeruginosa (Pseudomonas aeruginosa).

Contrary to other otitis externa, "malignant" is characterized by severe pain, purulent discharge, gradual aggressive processes, lesions extending to the parotid glands and tibia, and the degree of paralysis and the severity of the patient when facial paralysis occurs. Closely related, if the infection directly erodes the facial nerve, the prognosis is poor, and the prognosis is better due to facial nerve palsy or parotid swelling caused by edema or toxin swelling and facial nerve palsy caused by facial nerve.

(4) Facial numbness caused by otitis media and mastoiditis:

1 otitis media: acute suppurative otitis media is an acute suppurative inflammation of the middle ear mucosa. The main pathogens are Streptococcus pneumoniae, Haemophilus influenzae, Streptococcus hemolyticus and Staphylococcus.

Facial paralysis may be a complication of otitis media, due to inflammation of the middle ear edema, compression of the facial nerve or affecting the supply of blood vessels in the facial nerve tube to stagnant blood, or toxic substances absorbed by the facial nerve through the bone fracture, causing facial nerve paralysis, due to the high incidence of otitis media in children Therefore, acute otitis media is the most common cause of facial paralysis in children.

2 acute mastoiditis: acute mastoiditis is the mastoid airway mucosa - periosteum, especially the suppurative inflammation of the mastoid bone, occurs in children, but the infantile breasts under 2 to 3 years old began to develop, so This disease does not occur.

Acute suppurative otitis media, not only the tympanic membrane, but also the inflammatory changes of the mucosa and periosteum of the eustachian tube, the sinus sinus and the mastoid air chamber. In the case of the mastoid, there is also acute inflammation, but the ear science Experts did not call it "acute mastoiditis", nor did they treat it as a separate disease, because the acute inflammation of the mastoid is only part of the inflammation of the middle ear, with the absorption of inflammation in the middle ear, the local part of the mastoid The muco-periosteum is gradually returning to normal, and there is no need for special treatment in the clinic. The clinically known acute mastoiditis is mostly caused by the spread of some severe acute suppurative otitis media and is a complication of acute suppurative otitis media.

3. Disease and prognosis identification

In the differential diagnosis of facial nerve palsy, careful medical history, detailed clinical examination and necessary electrical and laboratory tests are critical to help diagnose and determine the extent of facial nerve damage.

(1) Time and extent of onset of paralysis: The onset time of facial paralysis and complete facial paralysis itself are not diagnostic, but the onset time and complete paralysis have prognostic significance and help guide the diagnosis process, for example, paralysis is born. When it occurs, it can be either developmental or traumatic. If it is developmental, it is often accompanied by other congenital anomalies. There is no improvement in postnatal paralysis. If it is traumatic, there are often other traumatic symptoms. improve.

In normal people with a history of trauma, complete facial facial paralysis suddenly occurs after trauma, most likely due to facial nerve transection, and gradually increased to complete facial nerve paralysis, may be caused by tumor or hematoma compression facial nerve, if paralysis is incomplete, in the onset There was no increase in the first 2 weeks, and Bell palsy or other non-neoplastic lesions were more likely.

(2) the same side of the nerve paralysis: the same side of the nerve paralysis recurrence has the characteristics of idiopathic (Bell) paralysis, usually herpes simplex virus infection, but also seen in herpes zoster virus infection, suggesting that Bell's paralysis may be caused by herpes simplex virus in the early stage of recurrence Infection, facial nerve palsy of Melkersson-Rosenthal syndrome can also recur, but it usually recurs in the contralateral side, and one side facial paralysis recurs in the same side, which may be caused by Bell paralysis, but the possibility of tumor must be considered. Of the 164 patients with a history of recurrence of the same lateral nerve palsy, 16 (10%) had facial nerve tumors, and 69 (5%) of the 1455 patients had recurrence of ipsilateral paralysis, and in some patients the second episode was mild. Unless it is carefully and comprehensively examined, it is easy to ignore, but there is also a second onset, and the symptoms gradually worsen.

(3) alternating or bilateral lateral paralysis: although alternating recurrent facial paralysis is associated with some rare diseases, contrary to the ipsilateral, facial paralysis with contralateral recurrence is also common in Bell paralysis, while Melkersson-Rosenthal syndrome is the most Commonly alternating or bilateral lateral paralysis, the syndrome has characteristics of lips, face, recurrent edema of the eyelids, cheilitis and cracked tongue, which can be distinguished from Bell's paralysis. In addition, there may be a genetic predisposition, presumably one of sarcoma-like diseases. Types.

Simultaneous facial nerve palsy on both sides is rare. If there are bilateral facial paralysis on both sides, there may be life-threatening diseases or low systemic resistance. It is reported that 2 of 2856 patients have bilateral paralysis and 49 patients have acute onset. 13 cases were developmental, of which 10 were Mobius syndrome, 10 were due to bilateral acoustic neuroma; 9 were humeral fractures; Bell palsy, Guillain-Barré syndrome was 6 cases, and 1 case was acute leukemia. 1 case of medullary palsy (ball paralysis) caused by rabies pre-emergence immunization, 1 case of otitis media, 1 case of sarcoma-like disease, and 1 case of positive Epstein-Barr virus.

(4) Recurrent facial palsy (RFP): another disease that can be seen in Bell's palsy or completely different from Bell's palsy. It is known that the cause of recurrent facial paralysis caused by other diseases is sarcomatoid disease, diabetes, leukemia. Infectious mononucleosis, the tumor involving the facial nerve must be considered in the diagnosis process. The recurrent facial paralysis caused by the tumor is twice as high as Bell's paralysis. May noticed that in 895 patients with Bell's palsy, recurrent facial paralysis. The incidence was 4%, and 91 patients with facial nerve palsy caused by tumors had a recurrent facial paralysis of 9%.

Yanagihara et al. showed that in 2414 patients with Bell's palsy, the incidence of recurrent facial paralysis was 2%, and of 51 patients with recurrent facial paralysis, only 5 patients had facial paralysis 3 or more times. The incidence of recurrent facial paralysis on both sides, including both sides, alternating and recurring was 3%.

Adour et al combined a prospective and retrospective study of 1,700 cases of Bell's palsy, the incidence of recurrent facial paralysis was 5.7% to 7.3%, and the average interval from the first onset to the first recurrence was 9.8 years; The average interval from the first recurrence to the second recurrence was 6.7 years, and only 15% of recurrent facial paralysis recurred more than twice.

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