Alcoholic neurological disease
Introduction
Introduction to alcoholic neurological diseases Alcohol absorption through the gastrointestinal tract is about 25% in the stomach. Others absorb milk and fat through the upper small intestine to hinder alcohol absorption. There is also a difference between men and women. The blood alcohol concentration of women is higher than that of men. Because of the low alcohol dehydrogenase activity of women's gastric mucosa, the metabolism of alcohol in the "first pathway" of the stomach reduces the alcohol mainly into the body with the plasma. Alcohol-toxic neurological organs, cerebrospinal fluid (CSF), and urine alveolar, the alcohol concentration in these areas is a constant relationship with the concentration in the blood. Alcohol is mainly excreted from the urine sweat glands and respiration by oxidative metabolism of only 10%. basic knowledge Probability ratio: up to 10% of long-term drinking patients Susceptible people: long-term heavy drinkers Mode of infection: non-infectious Complications: arrhythmia congestive heart failure thrombosis cardiomyopathy myocardial infarction hypertension
Cause
Causes of alcoholic neurological diseases
Drinking (86%)
The cause of the disease has now been confirmed to be greatly damaging to many organ systems in the body due to a large amount of uncontrolled drinking. The nervous system is one of the main target organs for alcohol abuse.
Pathogenesis
Similar to general anesthetics, alcohol acts directly on the nerve cell membrane. These substances are fat-soluble like barbiturates. They act by lysing the cell membrane to interact with the lipoproteins of the cell membrane. Alcohol is an inhibitor of CNS rather than excitement. Agents, some early symptoms of alcoholism suggest brain excitement, such as chatter, aggressiveness, excessive activity, and increased electrical excitation in the cerebral cortex, which is due to certain structures under the cortex that normally regulate cerebral cortical activity (possibly upper brain stem As a result of inhibition of the reticular structure, the same early sputum reflexes may reflect the transient loss of control of the motor neurons in the spinal cord by the advanced inhibitory center. However, as the amount of alcohol increases, the inhibitory effect extends to the brain, brainstem and spinal cord nerves. cell.
The mechanism by which alcohol causes secondary damage to the nervous system has not yet been fully elucidated and is thought to be related to the following factors:
1. Affect vitamin B1 metabolism
Influencing and inhibiting the absorption of vitamin B1 and storage in the liver, the level of vitamin B1 in patients is significantly lower than that in normal people. In general, the main energy of nerve tissue is derived from sugar metabolism. In the absence of vitamin B1, due to sulfur deficiency The reduction of amines can cause disorders of glucose metabolism, causing a decrease in the energy supply of nerve tissue, which in turn leads to abnormalities in nerve tissue function and structure. In addition, the deficiency of vitamin B1 can also cause metabolic pathways of pentose phosphate metabolism, affecting phospholipids. The synthesis causes demyelination and axonal degeneration-like changes in the surrounding and central nervous tissues.
2. Has fat solubility
It can rapidly pass through the blood-cerebrospinal fluid barrier and nerve cell membranes, and can act on certain enzymes and receptors on the membrane to affect cell function.
3. Other
Free radicals and other metabolites produced during alcohol metabolism can also cause damage to the nervous system.
The main pathological changes of alcohol-induced neurological diseases: chronic chronic alcoholism causes chronic damage to nerve cells, decreased synapses, and neuronal loss.
Prevention
Alcohol-induced neurological disease prevention
A small amount of reasonable drinking may have certain benefits for the human body. Avoiding long-term heavy drinking is the main measure to prevent alcoholic neurological diseases.
Complication
Alcoholic neurological complications Complications arrhythmia congestive heart failure thrombosis cardiomyopathy myocardial infarction hypertension
Alcohol abuse has a great detrimental effect on many organs of the human body. It has been confirmed that alcoholism can cause severe arrhythmia, congestive heart failure, cardiac wall thrombosis, cardiomyopathy, myocardial infarction, hypertension, and increased platelet count. Increased agglutination function and prolonged spontaneous dissolution of fibrin, etc., a large number of alcoholic mothers found that the placenta has ultrastructural changes, may indirectly affect the fetus, make the fetus dysplasia or deformity, a large amount of alcohol can occur acute neuropsychiatric symptoms Long-term drinking produces chronic neuropsychiatric symptoms and even irreversible damage to the nervous system.
Symptom
Symptoms of alcoholic neurological diseases Common symptoms Coma fetal alcohol syndrome ataxia dementia convulsion pathological drunken
1. Classification of Algal Alcoholic Diseases Alcoholic diseases are classified into the following categories based on the mechanism of pathological effects of known alcohols.
(1) Acute alcoholism: simple drunkenness, complicated drunkenness, pathological drunkenness.
(2) Prohibition of alcohol or withdrawal syndrome: tremor, delusions, convulsions, spastic tremors.
(3) Nervous system malnutrition diseases secondary to alcoholism:
1 Wernicke-Korsakoff syndrome.
2 more peripheral neuropathy.
3 optic atrophy (smoke-alcoholic syndrome).
4 pellagra.
(4) Diseases with unclear pathogenesis associated with alcoholism:
1 cerebellar degeneration.
2 Marchiafava-Bignami disease.
3 cerebral bridge central myelinolysis.
4 alcoholic cardiomyopathy and myopathy.
5 alcoholic dementia.
6 brain atrophy.
(5) Fetal alcohol syndrome.
(6) Nervous system diseases caused by cirrhosis and portal vein shunt:
1 hepatic stupor and coma.
2 chronic liver and brain degeneration.
2. The main clinical manifestations of alcoholic neurological damage
(1) Alcohol affects various motor functions to varying degrees, including simple standing, speaking, eye movement and highly sophisticated, complex motor skills. The movement becomes slow and inaccurate, and it is abrupt, so it is not qualified for skilled work.
(2) Alcohol also damages intelligence by interfering with perceived speed and continuous mental activity. The learning process is slow and the effect is poor. It is easy to form too many links between words and numbers. The ability to concentrate and last attention is reduced. Patients cannot fully consider the problem. And simplifying the problem, eventually alcohol will damage judgment and cognitive ability, and even lose all thinking and reasoning ability.
(3) Miles established a set of blood alcohol and functional impairment scales in non-addicted people many years ago. When the blood ethanol concentration was 30 mg/dl, mild euphoria could occur; at 50 mg/ Mild ataxia occurred at dl; ataxia was evident at 100 mg/dl; confusion was observed at 200 mg/dl, and the level of intelligent activity was reduced; at 300 mg/dl, the patient was in a coma; at 1000 mg/dl Deep anesthesia, there is a possibility of death.
(4) Tolerance to alcohol: Habitual drinking can increase the amount of alcohol, thus lowering the alcohol effect. This is the reason why chronic alcoholics drink plenty of alcohol without obvious signs of drunkenness. After short-term alcohol exposure, the nervous system can adjust and adapt. The presence of alcohol, therefore, if the concentration of ethanol in the blood rises very slowly, even if the concentration reaches a high level, symptoms rarely occur. Conversely, the faster the peak blood of ethanol rises, the heavier the degree of poisoning, as in the previous It is pointed out that the important factor affecting this rapid adaptability is not the concentration of ethanol in the blood, but the length of time that ethanol exists in the body. The understanding of the underlying mechanism of alcohol tolerance has just started, and the alcoholics have a certain degree of tolerance. The increase in metabolism with ethanol does not seem to explain, and the increased adaptation of neurons to ethanol may be a better explanation.
As mentioned above, ethanol has a strong physiological and biochemical effect on the cell membrane. Ethanol dissolves lipids in the lipid bilayer, which increases the proportion of liquid delipidation and reduces the proportion of colloid. This process makes other membrane structures special. It is a protein disorder. It has been suggested that ethanol-like inhalation anesthetics can cause toxic effects through the "liquefied membrane structure". With the development of nerve cell membrane tolerance, it is resistant to the liquefaction of ethanol. The role of the cell membrane receptor system, which is a chloride and calcium channel, is equally important.
Chronic administration of ethanol increases the number of calcium channels in the nerve cell membrane; in addition, administration of a calcium channel blocker during chronic administration of ethanol prevents an increase in neuronal calcium channels and alcohol tolerance.
Examine
Examination of alcoholic neurological diseases
1. Determination of blood and urine alcohol concentration
There is a diagnostic and the degree of toxicity assessment.
2. Other blood tests
Including blood biochemistry, liver function, kidney function, coagulation function and immunoglobulin.
3. ECG, EEG, brain CT or MRI examination, there is a differential diagnosis and the significance of the degree of poisoning assessment.
4. Electromyography and neurophysiological examination have differential diagnosis significance.
Diagnosis
Diagnosis and diagnosis of alcoholic neurological diseases
Diagnosis can be made mainly based on the history of drinking, clinical manifestations and appropriate auxiliary examinations such as blood and urine alcohol concentration.
Symptoms of central nervous system depression in acute alcoholism should be differentiated from diseases that cause coma, such as sedative hypnotic poisoning, carbon monoxide poisoning, stroke, craniocerebral trauma, psychosis and seizures of withdrawal syndrome, and psychosis Seizures, epilepsy, asphyxiating gas poisoning, hypoglycemia, etc., intelligent disorders and personality changes in chronic alcoholism should be differentiated from dementia caused by other causes.
