Facial muscle atrophy

Introduction Facial muscle atrophy refers to dystrophy of striated muscle, muscle volume is reduced compared to normal, muscle fibers become thinner or even disappear. Neuromuscular disease is hypertrophy. In addition to the pathological changes of muscle tissue itself, muscle nutrition is closely related to the nervous system. Spinal cord disease often leads to muscular dystrophy and muscle atrophy.

Cause

First, the peripheral circulation is poor; the second is due to nerve damage leading to nerve conduction disorder; the third is caused by nerve endings or facial nerve paralysis sequelae and other diseases.

Common causes of neurogenic facial muscle atrophy are disuse, dystrophies, ischemia, and poisoning. Anterior horn lesions, nerve roots, nerve plexus, and peripheral nerve lesions can cause conduction disturbances of nerve excitation impulses, thereby dissipating part of the muscle fibers and causing disuse of facial muscle atrophy.

Myogenic pancreatic muscle atrophy is caused by muscle disease itself, and may include other factors, such as shoulder or facial scapular type of muscular dystrophy, confirmed by morphological examination of spinal muscular atrophy. On the other hand, when any part of the motor neurons is damaged, the acetylcholine released from the distal part is reduced, and the sympathetic nutrient effect is weakened, resulting in muscle atrophy.

an examination

Related inspection

Electromyography

History: For facial muscle atrophy, attention should be paid to the age, the location of the disease, the onset of disease, the length of the disease, etc.; acute onset, or chronic onset, is gradually progressing, or rapid development, whether there is sensory disturbance, urinary dysfunction, atrophy is a limitation or Systemic, muscle strength, muscle weakness and muscle atrophy, with or without muscle agitation and pain, exacerbation or reduction after activity, past history should be noted with or without systemic diseases such as malignant tumors, connective tissue diseases, consumptive Disease, diabetes, uremia, trauma, alcohol consumption, disc herniation, myelitis, optic neuritis, history of drug application and history of poisoning, etc., with or without a special hereditary family history, pay attention to the history of infection and vaccination history.

Physical examination: Muscle shape observation: Clinical diagnosis of facial muscle atrophy should be compared on both sides, that is, the extent of muscle atrophy, the comparison of bilateral symmetrical parts, observation of fasciculation, muscle strength and muscle tension: muscle atrophy More often accompanied by low muscle strength, so should pay attention to the comparison of muscle volume and muscle strength, pay attention to the muscle strength of muscle atrophy. Muscle tone should be checked in a warm environment and in a comfortable position. The patient should be relaxed as much as possible by touching the stiffness of the muscle and the resistance felt when the patient flexibly flexes and flexes the patient's limb. When the muscle tension is reduced, the muscles are slack, the resistance is reduced or disappeared during passive exercise, and the range of motion of the joint is enlarged, which is more common in lower motor neuron lesions. Some myopathy, such as disuse muscle atrophy, facial muscle atrophy: such as deformation of bones and joints, skin symptoms, whether there is tenderness and mass along the nerve, etc., pay attention to the distribution of sensory disturbances, the scope and Properties such as deep sensory disturbance or complex sensory disturbance, sensory separation, etc., atrophic muscles with or without spontaneous pain and tenderness.

Auxiliary examination: neurogenic facial muscle atrophy: examination according to the extent and distribution of atrophy, general electromyography, CT or MRI of the corresponding site, lumbar puncture examination, neuromuscular biopsy, etc.; muscle-derived facial muscle atrophy: should be examined for myoelectricity Figure, serum muscle enzyme series, serum potassium antibody, creatinine test, muscle biopsy, etc.

Differential diagnosis

Clinically, it should be differentiated from the following diseases:

1. Facial paralysis of facial paralysis: In the past, there was a significant history of facial paralysis. Due to the incomplete recovery of facial paralysis, the axonal regeneration was caused by confusion. The affected side left different degrees of facial muscle weakness and paralysis.

2. Idiopathic spasm: bilateral orbital tendon, often accompanied by mental disorders, EMG shows that the facial muscles are not synchronized discharge, the frequency is normal, may be caused by dysfunction of the pyramidal system.

3. Facial muscle twitch: for the facial muscles, the individual muscle bundles are slightly vibrating, often invading the surrounding orbital muscles, mostly limited to one side, can be relieved by themselves, may be caused by benign lesions of the brain stem and cranial nerve.

4. Habitual sputum: for small sputum, facial muscles have no purpose stereotypes or repeated beating, more common in one side, mostly in childhood.

5. The movement of the hand and foot caused by lesions in the midbrain and cone system.

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