Facial weakness

Introduction The facial nerve consists of two parts: the motor fiber and the middle nerve that govern the facial expression muscle. The interneuron is composed of sensory and parasympathetic fibers. The site of facial nerve damage can be in the brainstem, the skull base, the facial nerve canal and its distal end. The nucleus and the pons are adjacent to the facial nucleus. Therefore, brain stem lesions involving the facial nerve are often accompanied by cross-sectional convulsions composed of ocular abduction or lateral paralysis. Facial nerve injury mainly manifests as peripheral facial spasm or hemifacial spasm.

Cause

A common cause of facial nerve injury is fractures in the cranial fossa and the mastoid, with approximately 50% of longitudinal fractures and 25% of transverse fractures associated with VII cranial nerve injury. In particular, longitudinal fractures parallel to the long axis of the rock cone, the facial nerve is most susceptible to involvement, contusion or fracture of the fracture piece leading to early or delayed facial paralysis.

It is a group of chronic progressive degenerative diseases with selective etiology of spinal cord anterior horn cells, motor brain neurons, cortical pyramidal cells and pyramidal tract. The clinical features are that the symptoms and signs of upper and lower motor neurons are coexisting and manifested as muscle weakness. The combination of different degrees of muscle atrophy and pyramidal tract, sensation and sphincter function are generally unaffected.

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Upper and lower motor neurons have symptoms and signs of impaired coexistence, manifested as muscle weakness, and the combination of different degrees of muscle atrophy and pyramidal tract, sensation and sphincter function are generally unaffected. The specific manifestations are atrophy of the tongue muscle, eating cough, drinking water from the nostrils, speech speech is unclear, hoarseness, often accompanied by lateral weakness of the head; pharyngeal reflex disappears, soft palate does not move, and lingual muscle bundle vibrates.

Early-onset, facial muscle spasm occurs immediately after injury, the affected side loses expression, the eyelids are incompletely closed, and the mouth is biased toward the healthy side, especially when crying and laughing, and the exposed eye often has exposed keratitis. If the facial nerve is injured at the proximal end of the tympanic nerve, the 2/3 taste in front of the ipsilateral tongue is also lost. Late-onset patients often have hemifacial spasm 5 to 7 days after injury, mostly due to bleeding, ischemia, edema or compression, and the prognosis is good.

Differential diagnosis

Facial muscle weakness symptoms need to be distinguished from the following symptoms.

Facial muscle atrophy: The most difficult to cure in muscular atrophy is facial muscle atrophy, and it has the greatest impact on patients' lives. Facial muscle atrophy refers to the weight loss of normal developing parenchyma, organs and cells, the volume is reduced, the function is low, the protein synthesis of atrophic cells is reduced, and the decomposition is increased to adapt to the living environment with low nutritional level. The facial nerve has a regulating effect on the metabolism of facial muscles. When the nerve trunk is damaged, the corresponding tissue may undergo facial muscle atrophy due to the loss of nerve regulation.

Disuse atrophy (when the facial muscles are inactive for a long time, the neurosensory receptor lacks centripetal stimulation, so the centrifugal impulse is reduced, causing the blood supply and material metabolism to gradually shrink and atrophy), and the cells that are atrophied after the cause can Return to normal. A large number of organelles in the cytoplasm of atrophy cells are degraded, and autophagosomes are increased, so that a large number of residues (ie, lipofuscin) which are not degraded by lysosomal enzymes and rich in phospholipids can be accumulated. This is why patients with heavier facial muscle atrophy are gray or brown in color.

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.

According to the pathogenesis of facial muscle atrophy:

(1) Facial muscle atrophy caused by systemic dystrophies, disuse, endocrine abnormalities, muscle degeneration, and abnormal muscle structure.

(2) facial muscle atrophy caused by genetics, poisoning, metabolic abnormalities, infections, allergies, etc., the clinical significance of this classification is not large, because the cause is difficult to be clear.

According to the classification of primary lesions of facial muscle atrophy:

(1) Neurogenic facial muscle atrophy. (2) Myogenic pancreatic muscle atrophy. (3) Disuse of facial muscle atrophy.

Neurogenic muscle atrophy mainly refers to the lesions of the lower motor neurons such as the anterior horn cells and peripheral nerves of the spinal cord, and belongs to the primary neurogenic muscle atrophy. The three were related to each other, and the upper motor neuron lesions also showed muscle atrophy. Some people listed it as secondary, and the late stage was disuse atrophy. Myogenic muscle atrophy is caused by the muscle itself. Disuse muscle atrophy can still be mailed to systemic wasting diseases.

Myasthenia gravis: Myasthenia gravis is an autoimmune disease of the nerve to muscle transmission disorder. It is a chronic disease that transmits disorders at the neuromuscular junction. Acetylcholine receptor (AChR) antibody is the main autoantibody that causes its pathogenesis. It mainly produces Ach receptor antibodies that bind to the Ach receptor, causing neuromuscular junction block, leading to the eye. Muscle, swallowing muscles, respiratory muscles, and skeletal muscle weakness in the limbs, that is, the nerves that govern muscle contraction cannot transmit the signal command to the muscles under the influence of various etiologies, so that the muscles lose their contractile function, clinically There are eyelid drooping, diplopia, strabismus, expression muscles and masticatory muscle weakness, manifested as apathy, can not be suffocated, etc., medullary muscle weakness, language disadvantage, lack of tongue, eating difficulties, eating cough, And limb muscle weakness.

Facial spasm: 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 spasm described here only discusses the expression of facial muscle paralysis, which is the facial nerve paralysis. The facial nerve paralysis is more common in cranial nerve diseases, and it is divided into specific diseases (Bell), trauma, infection, tumor, and neural source according to the cause. There are five main types of sex. Idiopathic facial paralysis, Bell palsy, is described in detail as a separate disease. Other types of facial nerve paralysis are described here.

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