idiopathic facial paralysis
Introduction
Introduction to idiopathic facial nerve spasm Idiopathic facial nerve spasm, namely facial neuritis, also known as Bell's palsy, refers to a peripheral facial paralysis caused by an acute non-specific inflammation of the facial nerve in the facial nerve canal. Facial neuritis is mainly Bell palsy and genic ganglion syndrome (RamsayHunt syndrome). The cause of Bell's palsy is not fully understood, but tends to be caused by a neurotropic virus. RamsayHunt syndrome is caused by herpes zoster virus. basic knowledge The proportion of illness: 0.003% Susceptible people: no specific population Mode of infection: non-infectious Complications: facial muscle twitching
Cause
Idiopathic facial nerve spasm
(1) Causes of the disease
Facial neuritis is more common in cranial nerve disorders, which is related to the anatomy of the facial nerve canal. The facial nerve canal is a narrow bony duct. The normal person is about 2 to 3 mm wide and about 30 mm long. When the rock bone is abnormal, the facial nerve is The tube may be narrower and become an intrinsic factor for the facial nerve to be easily affected.
In addition, because the facial nerve is superficial in the face and close to the pharynx, it is susceptible to cold wind or acute pharyngeal infection, which may lead to facial vascular spasm, ischemia, hypoxia and edema. And become an external factor that is easily affected by facial nerves.
At present, there are two main causes of Bell's paralysis: fatigue and facial, facial nerve paralysis after cold in the ear, such as cold wind blowing by the car or cold wind or electric fan blowing after sleep, obviously the body's resistance is reduced. One of the causes of facial paralysis, but the real cause of Bell's palsy is not very clear. After decades of research, it tends to be a neuropathy caused by a virus, or a herpes simplex.
The cause of Bell's palsy is still a goal of clinical research. In the past few decades, extensive research has been carried out, and many researchers have proposed genetic, metabolic, autoimmune, vascular, nerve incarceration and infection.
(two) pathogenesis
The pathogenesis of facial neuritis has not been fully elucidated. Because the facial facial nerve can only accommodate the facial nerve, once the facial nerve has inflammatory edema, it will inevitably lead to facial nerve compression, cold, viral infection (such as herpes zoster) and autonomic dysfunction. Can cause local neurotrophic vasospasm, leading to nerve ischemia and edema.
The early pathological changes of facial neuritis are neuroedema and demyelination. In severe cases, axonal degeneration can occur. There are two main theories:
Demyelinating theory
It is believed that Bell's palsy is mainly caused by viruses. It is not completely clear how the virus damages the facial nerve in the body. Herpes simplex virus may be an important cause of Bell's palsy. Herpes simplex virus is well understood in other aspects of human pathophysiology. The pathophysiological mechanism of Bell's palsy can be inferred.
The virus lurks in the trigeminal ganglion, and other brain nerves such as the knee ganglia and the spinal nerve sensory ganglia, the virus is activated in an unclear way, replicates in the ganglion, and avoids the attack of circulating antibodies, the nerves in the virus replication The injury of the joint causes a decrease in nerve function, and the clinical appearance of the face, the pharynx, the head and the neck are dull, and then the virus enters the axon, causing spinal radiculitis, and ascending to the brain stem causes local meningoencephalitis. Changes can be evidenced by increased cerebrospinal fluid protein and lymphocytosis, which can also be seen by Gadolinium-enhanced MRI.
In the affected nerve, the virus infects Schwann cells to cause inflammation. The virus accumulates in the fibrin sheath of nerve cells. When the virus breaks through the cell membrane, the autoimmune reaction of nerve cell membrane damage occurs, leading to myelin rupture and demyelination. The chromatin of the sheath and facial nucleus cells dissolves, and then the lymphocytes infiltrate the peripheral nerve fibers. After the inflammation and autoimmune reaction are eliminated, these nerve cells are damaged, but can be repaired and re-formed into the myelin sheath. The degree of recovery of neuromuscular function depends on the degree of recovery. The extent of the damage.
2. Indentation theory
Some scholars believe that facial nerve palsy is due to inflammation caused by facial neuritis, so that the facial nerve in the facial nerve canal congestion, because the facial nerve canal is a bone tube, the swollen facial nerve is squeezed by the facial nerve canal in a fixed space, causing facial nerve Embedding damage.
The basic theory of facial nerve decompression is to release the facial nerve and its blood vessels from the incarceration pressure, regardless of the cause of the injury, due to intra-neural edema, damaged nerve swelling, nerve edema increases the pressure inside the neural tube, resulting in facial nerve in the facial nerve canal Inlay, in Bell's paralysis, the appearance of muscle paralysis, which is one of the clinical symptoms of nerve compression, Sunderland pointed out that venous return block is the first stage of nerve damage, early relief of this pressure is important for better recovery of facial nerve The findings of surgery support this invasive theory. Fisch and Esslen observed a pathological swelling of the facial nerve during surgery, which was embedded at the bottom of the internal auditory canal. This study suggests that facial paralysis originates from inflammatory lesions in narrow veins. Internal nerve swelling makes the lesion complex, followed by demyelination, and facial neuritis can also occur in Guillain-Barré syndrome.
There are few reports on the pathological study of Bell's palsy. The main reason is that it is difficult to obtain facial nerve specimens. It is generally derived from facial nerve palsy and died of other diseases such as car accidents, myocardial infarction, and cerebral infarction. Part of the material was derived from facial nerve decompression. Early reports were difficult to accurately explain the pathological changes of facial paralysis. Alexander, Proctor, Ulrich and Odonoghue and Michaels observed inflammatory cells infiltrating the facial nerve. O'Donoghue and Michaels reported a case of Bell paralysis. In the knee of the facial nerve, the nerve sheath is congested, and the bone changes. In their study, the bone is absorbed in the lesion, accompanied by abundant osteolytic cells, and the case of Stephen et al reported that the nerve sheath is not affected, along the drum. Suo found that there is a change in bone quality.
Fisch and Esslen electrophysiological studies indicate that the nerve block of Bell's paralysis is mainly located at the proximal end of the knee ganglion. Before the facial nerve enters the facial facial nerve tube, the facial nerve can be seen with staining changes. McKeever et al. noticed that the facial nerve entered the facial nerve tube first. The facial nerve has demyelination during the segment.
Ylikoski et al reported that when performing surgical nerve anastomosis or transplantation, the nerve specimens were obtained for microscopy and electron microscopy. The motor nerve fibers at the distal end of all specimens had Wallerian degeneration and demyelination, and most of the nerve fibers were partially regenerated, but Regeneration is not complete.
Summarize the above-mentioned scattered pathological reports, the results are as follows:
Early changes: edema of nerve edema, venule congestion, occasional small focal, fresh intraneural hemorrhage, nerve fiber myelin collapse, part of axon disappeared, lymphocytes infiltrated around nerve bundle or nerve.
Middle and late changes: severe Wallerian degeneration, axonal pulp is foamy, axonal pulp disappears, lymphocytes can be seen extensively infiltrated around the blood vessels in the main nerve of the facial nerve; nerves become thinner, atrophy, and connective tissue hyperplasia.
Prevention
Idiopathic facial nerve spasm prevention
1. Enhance physical fitness, pay attention to prevent facial cold wind and upper respiratory tract infection.
2. Early comprehensive treatment to reduce complications and sequelae.
Complication
Idiopathic facial nerve spasm Complications, facial muscle twitching, ptosis
Complications are a symptom that occurs after recovery or recovery of facial paralysis. It is mainly characterized by facial contracture muscle contraction, joint movement, facial muscle twitching, ptosis and crocodile tears.
Facial muscle movement and lacrimal gland abnormalities can be secondary to facial paralysis. Whenever a patient blinks (associated with movement), the lips muscles are slightly twitched, or when the saliva is secreted, it causes excessive secretion of the lacrimal gland; The contracture of the hair, which looks like a localized seizure, is occasionally seen in patients who have never had a significant facial nerve disease. The etiology of these conditions is unclear, and some researchers attribute it to inappropriate regeneration of nerve fibers. Or impulsive conduction between fibers (false synaptic conduction) occurs within the nerve trunk.
Symptom
Idiopathic facial paralysis symptoms Common symptoms After the ear, the pain, the mouth, the sagging, the facial slamming, the nasolabial fold, the shallow valgus, the valgus, the squint, the squint, the earache
Common symptoms
The signs of facial nerve palsy are divided into three categories: exercise, secretion and sensation. Often acute onset, the upper and lower facial muscles are also the main clinical manifestations, often accompanied by diseased lateral ear canal and/or posterior mastoid pain. And/or tenderness.
1. Facial nerve paralysis earache, auricle and external ear canal herpes, oropharyngeal symptoms: taste disorder or loss of taste, pharyngitis, oral blisters and ulcers.
2. Eye symptoms Reduced tears, conjunctivitis, tears, pupil contraction, uveitis, visual impairment and ptosis.
3. Hearing/vestibular symptoms, acoustic horror and hearing allergy, sensorineural hearing loss, tinnitus, dizziness and nystagmus.
4. Central, neck and distal symptoms of fever and discomfort, accompanied by facial or body herpes, trigeminal sensation abnormalities, local lymphadenopathy, side sweating, encephalitis, sympathetic ganglia involvement, including Horner syndrome; The neck is damaged and the limbs are affected.
Symptoms of different parts of the injury
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, Lower eyelid valgus, tears do not easily flow into the nasolacrimal duct and ooze out of the eye, the lower group of facial muscle spasm appears to be shallow on the diseased nasolabial fold, the mouth angle drooping, the mouth is pulled to the opposite side of the lesion, can not pout and whistle, When the drumsticks are leaking at the corners of the side of the disease, due to buccal muscle spasm, it is easy to bite the buccal mucosa when chewing, and the 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 part of the corneal sensation and corneal reflex is indicated by swaying the other side 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.
Although the facial nerve may conduct a 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. A change in "collapse" occurs, and 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 attempts to exercise the facial muscles.
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 syndrome, was first described in 1907 by Ramsay Hunt, which consists of facial ganglion herpes syndrome, including facial nerve palsy, ear pain and typical ear herpes triad, 1977 Djupesland, Degre and Stien proposed Ramsay Hunt syndrome as multiple neuropathy based on viral histology and immunological findings.
Examine
Examination of idiopathic facial nerve spasm
Necessary selective inspection:
1. Blood routine, blood electrolytes generally have 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.
If the following items are abnormal, there is a differential diagnosis.
3. EEG, fundus examination.
4. Skull base film.
5. CT and MRI examinations.
6. Chest, ECG.
Diagnosis
Diagnosis and differentiation of idiopathic facial nerve spasm
Diagnostic criteria
Diagnosis of acute Bell palsy should be an exclusionary diagnosis. When other causes of facial paralysis are not found, the diagnosis of Bell palsy is accurate. Typical characteristics of Bell palsy are:
1. Usually acute onset, one side facial expression tendon; early symptoms and signs of facial nerve paralysis also include facial numbness, pain, dysgeus, hearing hypersensitivity (hyperpractic), tearing and tearing reduction.
2. In 50% of patients, the ear, the face, the mastoid, the neck or the tongue are numb or painful. The pain is usually behind the ear, but sometimes it is radiated to the face, the pharynx or the upper limb. These symptoms are usually one-sided, but It can also be symmetrical.
3.60% of patients have prodromal symptoms of viral infection.
4. Fewer patients have recurrent facial paralysis (13%).
5. Patients with a family history of Bell's palsy accounted for 14%.
6. There may be a decrease in the secretion of the affected eye or submandibular gland (10%).
7. In most patients (90%), the ipsilateral sacral muscle reflex is weakened or disappeared. Because of the inhibition of nerve fiber involvement in the cochlear ganglia, auditory hypersensitivity (hyperpractice, sound horror) even appears in the complete iliac muscle reflex. The patient represents a collateral nerve dysfunction.
8. In the first 10 days after onset, the tympanic membrane of 40% of patients can be seen to have congestion.
9. In patients with acute facial paralysis, there is a taste disorder or hypersensitivity, which is enough to confirm Bell palsy.
In short, facial nerve palsy is peripheral, accompanied by acute history and infectious polyneuritis. Without other diseases, Bell's palsy can be diagnosed without further diagnostic tests.
10. Typical knee cerebral herpes syndrome (Ramsay Hunt syndrome), including facial nerve palsy, ear pain and typical ear herpes triad, Djupesland, Degre and Stien proposed Ramsay Hunt syndrome as multiple neuropathy:
(1) facial nerve paralysis earache, auricular and external ear canal herpes, oropharyngeal symptoms: taste disorder or loss of taste, pharyngitis, oral blisters and ulcers.
(2) Eye symptoms: reduced tearing, conjunctivitis, tears, pupil contraction, uveitis, visual impairment and ptosis.
(3) Hearing/vestibular symptoms: acoustic horror and hearing allergy, sensorineural hearing loss, tinnitus, dizziness and nystagmus.
(4) central, neck and distal symptoms: fever and discomfort, accompanied by facial or body herpes, trigeminal sensation abnormalities, local lymphadenopathy; suffering from side sweating, encephalitis, sympathetic ganglia involvement, including Horner synthesis Signure; neck deformation is impaired, limb movement is involved.
Differential diagnosis
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. Peripheral facial paralysis caused by other causes
(1) acute infectious multiple radiculitis neuritis (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 cerebrospinal fluid may have protein (increased) cells (normal or Mildly 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.
