extrapyramidal damage

Introduction

Introduction to extrapyramidal damage Extrapyramidal disease is an involuntary movement and muscle tension that is not controlled by human will. It is aggravated by emotion, tension, and relieves when it is quiet, and disappears when it is sleeping. This type of phenomenon is called extrapyramidal disease. Cone system damage manifests as spastic paralysis, while extrapyramidal damage mainly manifests as involuntary movement, muscle rigidity, and slow movement, rather than true paralysis. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people. Mode of infection: non-infectious complication:

Cause

Extrapyramidal damage

An integral part of the movement system. The genus occurs in the ancient part of the nervous system. The main function is to regulate muscle tension under the control of the cerebral cortex, maintain and adjust body posture, and control habitual and rhythmic movements (such as swinging arms, imitation, gestures, facial expressions, certain defensive reaction movements, etc.) . When completing complex motor functions, the extrapyramidal system and the cone system are inseparable continuums. Only when the extrapyramidal system maintains a certain stability and proper muscle tension and coordination of the limbs, the cone system can dominate the precise Feel free to exercise. Cone system damage manifests as spastic paralysis, while extrapyramidal damage mainly manifests as involuntary movement, muscle rigidity, and slow movement, rather than true paralysis.

Extrapyralidal diseases

A disease that occurs in the extrapyramidal system of the nervous system. Mainly manifested dystonia (hypertension or too low) and dyskinesia (including tremor, hand and foot, dance-like movements, twisting sputum, etc.). Related diseases mainly include:

(1) Parkinson's disease and various types of Parkinson's syndrome.

(2) Small dance disease.

(3) Chronic progressive chorea or Huntington.

(4) Hepatolenticular degeneration, also known as Wilson's disease.

(5) Abnormal muscle tension.

(6) Slang tic syndrome.

(7) Delayed dyskinesia.

(8) Throwing a dance.

(9) Paroxysmal hand and foot Xu levitation or paroxysmal sports-derived dance hand and foot Xu levy, twisting sputum and so on.

Prevention

Extrapyramidal damage prevention

Prevention of dyskinesia with a genetic background is even more important. Preventive measures include avoiding the marriage of close relatives, conducting genetic counseling, genetic testing of carriers, prenatal diagnosis and selective abortion to prevent the birth of children. Early diagnosis, early treatment, and intensive clinical care are important for improving the quality of life of patients with dyskinesia.

Complication

Extrapyramidal complication Complication

No complications.

Symptom

Symptoms of extrapyramidal damage Common symptoms Myasthenia gravis pharyngeal muscle dyskinesia

It mainly includes two aspects, namely dystonia and dyskinesia. Dystonia manifests as an increase or decrease in muscle tone; dyskinesia includes tremor, hand and foot movements, dance-like movements, and twisting sputum. Reduced muscle tone caused by extrapyramidal diseases often coexists with involuntary movements (excessive exercise). The patient presented with irregular and arrhythmic continuous activity and slow and complex involuntary movement. This kind of action occurs when you are awake, increases when you are excited, decreases when you are quiet, and disappears when you sleep. A typical case is chorea. The other group is characterized by increased muscle tone and bradykinesia. A typical case is Parkinson's syndrome. The causes of dyskinesia and dystonia are: a variety of neurotransmitters in the striatum of the human brain, in which dopamine and its metabolites have the highest content of vanillinic acid (HVA), and also contain high concentrations of acetylcholine. -aminobutyric acid, serotonin and norepinephrine. There are two major ascending dopaminergic pathways in the brain. The largest is the nigrostriatal bundle, and its neurons are located in the dense part of the substantia nigra. The main function is related to the initiation and control of the movement. The other is the brain pathway in the midbrain. Dopamine is the inhibitory medium of the acetylcholine system of the striatum, while acetylcholine is a striatum excitatory medium, and the two media are in a state of dynamic equilibrium. If the substantia nigra occurs, the ascending dopaminergic neuronal pathway is blocked, and the reduction or loss of dopamine causes the striatum to lose its inhibitory effect. The acetylcholine excitatory effect is relatively enhanced, and the clinical manifestations of tremor. Experiments have shown that electrical stimulation of globus pallidus or thalamus can cause characteristic resting tremor in patients with Parkinson's syndrome. Therefore, Parkinson's syndrome can be treated with levodopa plus decarboxylase inhibitor and anticholinergic drugs. Surgery destroys the lateral ventral nucleus of the thalamus, and the motor cortex or globus pallidus can also interrupt resting tremors.

New striatum lesions cause another group of muscle tension reduction, hyperactivity syndrome. For example, in Huntington's disease, the striatum nerve is significantly degenerated, and the -aminobutyric acid (GABA) in the caudate, caudate nucleus and substantia nigra is significantly reduced, and the glutamate decarboxylase which catalyzes the synthesis of GABA in the basal ganglia is also significantly reduced. GABA is an inhibitory medium, its lack of hyperactivity, basal ganglia dopamine content, acetylcholine reduction can induce hyperactivity symptoms, so Huntington's disease can block dopamine receptor drugs (such as haloperidol, trifluoperazine) , perphenazine), drugs that increase central GABA (such as isoniazid) and drugs that strengthen acetylcholine (such as choline chloride).

Examine

Examination of extrapyramidal damage

Transcranial color Doppler imaging: through the sputum window, pillow window, sputum window exploration, can explore the cerebral artery, according to the intracranial blood vessel flow rate, bandwidth, abnormal flow or audio abnormalities, etc., applied to cerebrovascular diseases Diagnosis and cause classification.

Electroencephalography is a graph obtained by amplifying and recording the spontaneous biopotentials of the brain from the scalp by means of an instrument.

CT or MRI examinations, such as patients with Wilson's disease, may show low-density lesions in the bilateral lenticular nucleus or abnormal MRI signals.

Diagnosis

Diagnosis and diagnosis of extrapyramidal damage

Electrical stimulation of the globus pallidus or thalamus can cause characteristic resting tremor in patients with Parkinson's syndrome. Therefore, Parkinson's syndrome can be treated with levodopa plus decarboxylase inhibitor and anticholinergic drugs. Surgery destroys the lateral ventral nucleus of the thalamus, and the motor cortex or globus pallidus can also interrupt resting tremors.

Age of onset: often can indicate the cause, such as infant or early onset may be cerebral hypoxia, birth injury, bilirubin encephalopathy or genetic factors. Juvenile tremor may be hepatolenticular degeneration, also help to determine prognosis, such as The primary torsion mites of childhood onset are far more severe than those of adult onset; on the contrary, the onset of late onset dyskinesia is more stubborn than younger.

Onset: often can cause the cause, such as acute onset of children or adolescents dystonia may suggest adverse drug reactions, slow onset is mostly primary torsion spasm, hepatolenticular degeneration, etc., severe onset of serious dance Symptoms or eccentric throwing tips may be vascular causes, and slow insidious onset may be neurodegenerative diseases.

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