extrapyramidal damage
Introduction
Introduction Extrapyramidal diseases occur in extrapyramidal diseases of the nervous system. Mainly manifested dystonia (hypertension or too low) and dyskinesia (including tremor, hand and foot, dance-like movements, twisting sputum, etc.). Cone system damage manifests as spastic paralysis, while extrapyramidal damage mainly manifests as involuntary movement, muscle rigidity, and slow movement, rather than true paralysis.
Cause
Cause
The extrapyramidal system is part of the motor 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. 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.
The regulation of motor function can be accomplished by the close cooperation of the pyramidal system, basal ganglia and cerebellum. These three are not independent and independent systems, but are functionally an inseparable whole. Dyskine disorders (ie, extrapyramidal diseases) are mainly caused by basal ganglia dysfunction.
Examine
an examination
Related inspection
Auburnham brain CT examination abdominal wall reflex knee reflex brain Doppler ultrasound (TCD)
Clinical manifestations and treatments mainly include 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. 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).
History
(1) 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 primary torsion in childhood, is far more severe than adult onset; on the contrary, late onset dyskinesia is more persistent than younger.
(2) onset of disease: often can indicate 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.
Diagnosis
Differential diagnosis
Cone beam lesion: the original reflex that occurs as a result of upper motor neuron damage. Mainly refers to a network system of vertebral cells in the cerebral cortex and its axons (like tentacles) and the spinal cord, mainly governing limbs and trunk movement. When the pyramidal tract is damaged, it loses its inhibitory function on the brainstem and spinal cord and releases the reflex effect of the sacral and toe extension. The above-mentioned reflection phenomenon may occur in infants and young children within 1 year and a half because the pyramidal tract is not yet fully developed. Adult patients, if present, are pathological reflexes. include:
1.Babinski sign
2.Oppenheim sign
3.Gorden sign
4.Chaddock sign
5.Gonda sign
6. Hoffmann sign.
Increased muscle tone in the extremities: Tillering is both tonic. Increased spasm of the sacral muscles is associated with damage to the cone, and spinal cord reflexes are facilitated. When passively moving a patient's joint, a sense of impedance occurs in the case of increased muscle tone, which is related to the speed of being exercised. When the muscles in the shortened state are quickly drawn, they immediately cause contraction and feel paralyzed state. When the force is stretched to a certain extent, the resistance suddenly disappears, that is, the so-called knives-like muscle tension is increased. Increased spastic muscle tension is not related to "sputum", which refers to an involuntary muscle contraction. Increased tonic muscle tone is seen in some extrapyramidal lesions with special tension changes, which are selective for increased muscle tone. The upper limbs are mainly adductor, flexor and pronator, and the lower extremities are superior to extensor muscle tension. The resistance encountered when passively moving a patient's limb is generally smaller than that of a sputum, but it has nothing to do with the length of the muscle at that time, ie, the contraction morphology. There is no difference between the extensor and the flexor. Regardless of the speed, amplitude, and direction of the action, the same resistance is encountered. This increase in muscle tone is called lead-like tonic, such as alternating loose and tight changes due to tremor, called gear-like rigidity.
Nerve Root Injury: A series of conditions caused by nerve damage in the body-related parts caused by factors such as squeezing, pulling, rubbing, and surgery.
Spinal nerve root injury: mostly with spinal cord injury. In the case of a spinal fracture, the spinal nerve root can be compressed by the compressed or dislocated vertebral body and the protruding intervertebral disc, and can also be contused, torn or severed by the broken bone piece and the dislocated vertebra.
Clinical manifestations and treatments mainly include 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. 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).
History
(1) 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 primary torsion in childhood, is far more severe than adult onset; on the contrary, late onset dyskinesia is more persistent than younger.
(2) onset of disease: often can indicate 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.
