Movement disorders

Introduction to movement disorders Movement disorder (also known as extra-existing disease) (extrapyramidaldiseases), mainly characterized by voluntary motor regulation dysfunction, muscle strength, sensory and cerebellar function are not affected. This group of diseases stems from basal ganglia dysfunction, usually divided into two categories: increased muscle tone - decreased exercise and decreased muscle tone - excessive exercise. The former is characterized by poor exercise and the latter is characterized by abnormal involuntary movement. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: mental disorders

Causes of dyskinesia

(1) Causes of the disease

The regulation of motor function can be accomplished by the close cooperation of the pyramidal system, the basal ganglia and the cerebellum. These three are not independent and independent systems, but are functionally an inseparable whole, dyskinesia disease (ie Extrapyramidal disease), mainly due to basal ganglia dysfunction.

(two) pathogenesis

The basal ganglia has complex fiber connections that primarily constitute three important neural circuits:

1 cortical-cortical loop: cerebral cortex - caudate putamen - medial globus pallidus - thalamus - cerebral cortex;

2 substantia nigra-striatum loop: the substantia nigra and caudate nucleus, the core between the crest and the nucleus;

3 striatum - globus globule loop: caudate nucleus, putamen nucleus - lateral globus pallidus - subthalamic nucleus - medial globus pallidus.

There is a direct pathway in the cortical-cortical loop (striatum-medial globus pallidus/black matter reticular) and indirect pathway (striatum-lateral globus pallidus-thalamic nucleus-medial globus pallidus/black matter reticular The loop is the anatomical basis for the basal nucleus to achieve motor regulation. The balance of activity between the two pathways is critical to achieving normal motor function.

Degeneration of the nigrostriatal striatum DA pathway leads to excessive basal ganglia export, excessive inhibition of thalamic-cortical feedback activity, impaired cortical motor function facilitation, and less motility diseases such as Parkinson's disease, striatal neurons Degeneration leads to a decrease in basal ganglia output, and thalamic-cortical feedback is too powerful for cortical motor function, resulting in hyperactive diseases such as Huntington's disease. Therefore, basal cytoplasmic biochemical abnormalities and loop activity disorders are symptoms of various dyskinesias. The main pathological basis, treatment of dyskinesia, whether the drug or surgical treatment principles are based on the correction of transmitter abnormalities and loop activity disorders.

Dyskine disease prevention

Prevention of dyskinesia with genetic background, prevention is more important, preventive measures include avoiding close relatives marriage, carrying out genetic counseling, carrier genetic testing and prenatal diagnosis and selective abortion, to prevent the birth of children, early diagnosis, early Treatment and strengthening clinical care are important for improving the quality of life of patients with dyskinesia.

Dyskinesia disease complications Complications

The ability to take care of themselves is declining. Some dyskinesias are accompanied by mental retardation and/or mental and behavioral disorders.

Symptoms of dyskinesia disease Common symptoms Body shake signs of lack of exercise Syndrome play piano finger (toe) sign rhythmic stereotypes repeated ... muscle hypertonia limb or trunk posture abnormal involuntary movement exercise conduction beam involvement exercise endurance reduce exercise ignorance

The clinical manifestations of basal nucleus diseases are mainly:

1. Involuntary action.

2. The movement is missing or slow and innocent.

3. Poor posture and muscle tension.

The function of the indirect pathway causes movement loss and stiffness, and the indirect pathway function is insufficient to cause chorea and throwing; the function of the direct pathway causes dystonia, hand and foot dyskinesia or tics, and the lack of direct pathway function causes slow movement. .

Examination of movement disorders

Blood electrolytes, trace elements and biochemical tests are helpful for the diagnosis of dyskinesia diseases, such as serum copper, urinary copper and serum ceruloplasmin in patients with Wilson's disease, which has important diagnostic significance.

1. CT or MRI examination: such as hepatolenticular degeneration, can show bilateral low density lesions in the lenticular nucleus or MRI display signal abnormalities.

2. Positron emission tomography (PET) or single photon emission tomography (SPECT): can show decreased function of striatum DA transporter (DAT), decreased DA transmitter synthesis and D2 type DA receptor activity, etc. The diagnosis of Parkinson's disease is quite meaningful.

3. Genetic analysis: It is of great significance for the diagnosis of certain hereditary dyskinesia diseases.

Diagnosis and diagnosis of dyskinesia

Diagnostic points

History

(1) Age of onset: often can cause the cause, such as infant or early onset may be cerebral hypoxia, birth injury, bilirubin encephalopathy or genetic factors, tremor in juvenile may be hepatolenticular degeneration; also help Judging the prognosis, such as the primary torsion of the onset of childhood is far more severe than the onset of adult disease; on the contrary, the onset of late onset dyskinesia is more stubborn than the young.

(2) 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.; acute onset Severe chorea or eccentric throwing may suggest a vascular cause, and a slow insidious onset may be a neurodegenerative disease.

(3) Course of disease: It is also helpful for diagnosis. For example, small chorea usually relieves within 6 months of onset, which is different from other choreas that start from childhood.

(4) Drugs such as phenothiazines and butyrylbenzenes can cause movement disorders.

(5) Certain diseases such as rheumatic fever, thyroid disease, systemic lupus erythematosus, polycythemia vera, etc. may be accompanied by dance-like movements.

(6) Family history: Diagnostic significance, such as Huntington's disease, benign hereditary chorea, idiopathic tremor, torsion spasm, tics-slang syndrome, etc. have a genetic background.

2. Physical examination

Can understand the characteristics of dyskinesia symptoms, clear the presence or absence of other symptoms of the nervous system, such as resting tremor, lead tube-like or gear-like muscle tonic prompted Parkinson's disease, corneal KF ring prompted hepatolenticular degeneration, Huntington's disease and liver In addition to dyskinesia, such as nuclear degeneration, often accompanied by mental and intellectual damage.

Differential diagnosis

Extrapyramidal diseases should be distinguished from motor dysfunction caused by diseases of the pyramidal system. The main clinical features of the latter are sputum (reduced muscle strength), which is generally not difficult to identify. In addition, between different types of extrapyramidal diseases Identification is more important.

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