Facial lines disappear

Introduction In the lower part of patients with idiopathic facial nerve spasm, the facial muscles are loose, the facial pattern disappears, the platysma crevices are wider than normal, and the facial muscles and platysma muscles disappear completely and synergistically. The signs of facial nerve palsy are divided into three categories: exercise, secretion and sensation. Often acute onset, the upper and lower facial muscles of the disease side are also the main clinical manifestations, often accompanied by pain and/or tenderness in the external auditory canal and/or posterior mastoid region. In severely injured, facial paralysis is significant, even when the face is resting. The lower part of the patient's facial muscles relax, the facial pattern disappears, the platysma muscle crevices are wider than normal, and the facial muscles and platysma muscles disappear completely and synergistically.

Cause

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 abnormally developed, the facial nerve can be more narrow and become an intrinsic factor that the facial nerve is easily affected.

an examination

Related inspection

EMG

The signs of facial nerve palsy are divided into three categories: exercise, secretion and sensation. Often acute onset, the upper and lower facial muscles of the disease side are also the main clinical manifestations, often accompanied by pain and/or tenderness in the external auditory canal and/or posterior mastoid region.

The upper facial muscle spasm causes the frontal frontal line to disappear, unable to lift the amount, eyebrows, and the eyelids cannot be closed or closed. When the eye is closed, the eyeball turns upward to expose the white sclera (called the Bell phenomenon). Because of the orbicularis tendon, the lower eyelids are everted, and the tears do not easily flow into the nasolacrimal duct and ooze out of the eye. 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. Due to buccal muscle spasm, it is easy to bite the buccal mucosa when chewing, and food often stays between the cheeks.

In severely injured, facial paralysis is significant, even when the face is resting. The lower part of the patient's facial muscles relax, the facial pattern disappears, the platysma muscle crevices are 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 opened. Saliva and food gather on the temporal side, the patient can't close the eye, and the eye movement can be seen as the eyeball moves upwards and turns slightly 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 combined capsule. Because of the upper eyelid paralysis, the corneal reflex disappears, and 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 transmit a proprioception from the facial muscles and a small skin feel from the ear and outer ear canal, it is rarely found that these feelings are missing. Partial facial nerve damage causes weakness in the upper and lower faces, and occasionally the lower half is more severe than the upper half. The opposite side is rarely affected. 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, and complete recovery is at rest. Or exercise, the facial expressions on both sides are indistinguishable; partial restorers have 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.

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 Herpes has a herpes, called Ramsay Hunt syndrome. In 1907, Ramsay Hunt first described the knee ganglion herpes syndrome, including facial nerve palsy, ear pain, and a typical triad of ear herpes. In 1977, Djupesland, Degre, and Stien proposed Ramsay Hunt syndrome as multiple neuropathy based on viral histology and immunological findings.

1. Facial nerve paralysis earache, auricle and external ear canal herpes. Oropharyngeal symptoms: dysgeusia or loss of taste, pharyngitis, oral blisters and ulcers.

2. Eye symptoms are reduced in tears, conjunctivitis, and 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; suffering from side sweatiness; encephalitis; sympathetic ganglia involvement, including Horner syndrome; cervical neck sensation; limb movement involvement.

Diagnosis of acute Bell palsy should be an exclusionary diagnosis. When no other cause of facial paralysis is found, the diagnosis of Bell's palsy is accurate. Typical characteristics of Bell's paralysis are:

1. Usually acute onset, facial expression on one side of the tendon; early symptoms and signs of facial nerve paralysis also include facial numbness, pain, dysgeus, hearing hypersensitivity (hyperpractic), tears and tears reduced.

2. In 50% of patients, numbness or pain in the ear, face, mastoid, neck or tongue occurs. The pain is usually behind the ear, but sometimes it is radiated to the face, throat or upper limbs. These symptoms are usually one-sided, but they 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. No further diagnostic tests are required.

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, auricle and external ear canal herpes. Oropharyngeal symptoms: dysgeusia or loss of taste, pharyngitis, oral blisters and ulcers.

(2) Eye symptoms: reduced tearing, conjunctivitis, and 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 sweatiness; encephalitis; sympathetic ganglia involvement, including Horner syndrome; cervical neck sensation; limb movement involvement.

Differential diagnosis

1. Central facial paralysis: the contralateral cortex-brain bridge is damaged. Because of the involvement of the upper facial muscle, it is only manifested as the paralysis of the facial muscle in 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 polyneuritis (Cerebrovascular): peripheral facial paralysis can occur, but the lesions are often bilateral, most with other cranial nerve damage. Cerebrospinal fluid can have protein (increased) cells (normal or slightly high) separation.

(2) pons lesions: because the facial nerve nucleus is located in the pons, its fibers bypass the nucleus. Therefore, in addition to peripheral facial paralysis, the pons lesions are often accompanied by damage to the adjacent structures inside the pons, such as lateral lateral rectus paralysis, facial sensory disturbances, and contralateral limb paralysis.

(3) Cerebellar pons angle damage: more damage to the ipsilateral V and VIII to the cranial nerve as well as the cerebellum and medulla. Therefore, in addition to peripheral facial paralysis, there may also be sensory disturbances on the same side, 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 inflammation of the parotid gland, the tumor, the neck and the parotid gland can cause peripheral facial paralysis. However, in addition to facial paralysis, there are often medical history and characteristic clinical manifestations of the corresponding diseases, without hearing allergies and taste disturbances.

The signs of facial nerve palsy are divided into three categories: exercise, secretion and sensation. Often acute onset, the upper and lower facial muscles of the disease side are also the main clinical manifestations, often accompanied by pain and/or tenderness in the external auditory canal and/or posterior mastoid region.

The upper facial muscle spasm causes the frontal frontal line to disappear, unable to lift the amount, eyebrows, and the eyelids cannot be closed or closed. When the eye is closed, the eyeball turns upward to expose the white sclera (called the Bell phenomenon). Because of the orbicularis tendon, the lower eyelids are everted, and the tears do not easily flow into the nasolacrimal duct and ooze out of the eye. 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. Due to buccal muscle spasm, it is easy to bite the buccal mucosa when chewing, and food often stays between the cheeks.

In severely injured, facial paralysis is significant, even when the face is resting. The lower part of the patient's facial muscles relax, the facial pattern disappears, the platysma muscle crevices are 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 opened. Saliva and food gather on the temporal side, the patient can't close the eye, and the eye movement can be seen as the eyeball moves upwards and turns slightly 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 combined capsule. Because of the upper eyelid paralysis, the corneal reflex disappears, and 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 transmit a proprioception from the facial muscles and a small skin feel from the ear and outer ear canal, it is rarely found that these feelings are missing.

Partial facial nerve damage causes weakness in the upper and lower faces, and occasionally the lower half is more severe than the upper half. The opposite side is rarely affected. 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, and complete recovery is at rest. Or exercise, the facial expressions on both sides are indistinguishable; partial restorers have 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.

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