Alcoholism dementia

Introduction to alcoholic dementia Alcoholic dementia (alcoholic dementia) or alcoholic dementia is a primary, characteristic dementia caused by the chronic direct action of alcohol on brain tissue. It is the brain damage caused by long-term heavy drinking, which is the most serious state of chronic alcoholism. It is characterized by tremors, convulsions, seizures, acute or chronic personality changes, mental retardation, and memory impairment. Alcoholic dementia accounts for about 2% of chronic alcoholism patients. This diagnostic name has been widely used, but its name is not uniform. The similar diagnostic names are: alcoholic decline, chronic alcoholic psychosis, alcoholic chronic or organic brain syndrome. There is no satisfactory limit to the disease both clinically and pathologically. In recent years, people have tried to precisely define alcoholic dementia. However, due to the different materials reported, the clinical manifestations are extensive and it is difficult to have consistent standards. basic knowledge The proportion of sickness: 0.01% Susceptible people: long-term heavy drinkers Mode of infection: non-infectious Complications: chronic alcoholism, liver cirrhosis, peripheral neuritis, brain atrophy, arrhythmia, congestive heart failure, thrombosis, cardiomyopathy, myocardial infarction, hypertension

Causes of alcoholic dementia

The occurrence may be related to the direct toxic effects of alcohol on brain tissue, as well as the sputum caused by alcoholism, hypoglycemia, B vitamin deficiency and other comprehensive damage to the brain. Alcohol has many factors affecting brain damage, such as drinking time and time. Quality of wine, diet, history of head trauma, liver disease, malnutrition and drug abuse.

The mechanism of chronic alcoholism causing alcoholic dementia (alcoholic dementia) is still unclear. Most believe that the neurotoxic effects of alcohol cause degeneration, necrosis and loss of cerebral cortical neurons, atrophy of nerve cell bodies, dehydration of brain cells and reduction of synapses.

Genetic factors (30%):

The incidence of alcoholism is seven times higher in the first-degree relatives than in the general population. The sensitivity of alcohol to brain damage is also affected by genetic factors. CT and neuropsychological tests show that some patients with alcoholism have obvious brain atrophy and brain. Abnormal function, other alcohol poisoning patients have similar brain atrophy and brain dysfunction despite the similar drinking time and amount. The neurotoxicity and thiamine deficiency of alcohol are related to the genetic susceptibility of different parts, and the neurotoxicity of alcohol. Usually damage to the cortex and basal ganglia, thiamin deficiency is more damaging to the basal ganglia, the diencephalon, the upper stem and the papillary body, the alcoholic neurotoxicity is highly susceptible to individuals, prone to brain atrophy and cognitive dysfunction, thiamine deficiency Sensual individuals are prone to develop Wernicke-Korsakoff syndrome, and a few have a dual susceptibility to alcohol neurotoxicity and thiamine deficiency.

Neurobiochemistry and metabolism (30%):

(1) Toxic products: Metabolites of ethanol, acetaldehyde is a poison that can bind to various proteins. Alcohol can activate certain special exogenous enzymes, producing abnormal toxic substances such as phosphatidyl alcohol and fatty acid ethyl ester, which can cause brain cell poisoning. And death.

(2) Metabolic abnormalities: alcohol inhibits protein synthesis, affects cell membrane lipid and protein structure, changes neuronal membrane fluidity, triphosphate adenosine activity and impedes calcium transport, causes nerve cell dysfunction, leading to nerve cell death; alcoholism leads to Deficiency of thiamine reduces transketolase activity, reduces lipid and protein synthesis, affects intracellular calcium regulation, and leads to neuronal cell death.

(3) Metabolic synthesis disorders: alcohol neurotoxicity and thiamine deficiency can interfere with the synthesis, uptake and release of neurotransmitters, leading to nucleus nucleus damage, reducing acetylcholine and norepinephrine synthesis, and memory impairment in Korsakoff syndrome. And dementia may be associated with a significant reduction in acetylcholine.

Neuroimaging and neuropathology (10%):

Studies have shown that brain structural abnormalities in patients with chronic alcoholism are the basis of neuropsychological damage. The frontal cortex is most sensitive to alcohol damage. Chronic alcoholism patients have cognitive and memory impairments, and the operation related to frontal lobe is poor. Chronic alcoholism Patients often have visual motor coordination, visual spatial orientation, visual adjustment and memory impairment, and are related to right hemisphere dysfunction. Chronic alcoholism is mostly diffuse brain damage, alcohol inhibits hippocampal N-methyl-D-aspartate Receptors, the latter play an important role in learning and memory.

Pathological changes of chronic alcoholism can be seen in brain atrophy, ventricular enlargement, brain weight loss, cortical neuron degeneration, loss, decreased number of nerve cells, cell body atrophy, axonal and dendritic reduction, increased white matter water content, lipid and phospholipid content cut back.

However, the pathological reports on primary alcoholic dementia are still inconsistent. Most reports suggest that the pathology of patients with alcoholic dementia or degenerative state proves that there are pathological changes of Wernicke-Korsakoff syndrome, often with varying degrees of traumatic injury; In some cases, there are hypoxia or hepatic encephalopathy, traffic hydrocephalus, Alzheimer's disease, ischemic necrosis, and other pathological changes unrelated to alcoholism. According to practical experience, this pathological condition may be one of them. The result of a disease, or a combination of multiple diseases, cannot be inferred from the hypothesis that alcohol has a brain toxicity. Except for a few cases, such as alcoholism and Alzheimer's disease, they believe that the pathology of all alcoholic dementia is only confirmed. Characteristics of chronic lesions.

In short, the most serious shortcomings of the concept of primary alcoholic dementia are not clearly defined. The characteristic pathology definition, before the morphological basis is clear, the clinical pathological entity of alcoholic dementia is still unclear.

Alcoholic dementia prevention

Promote the harm of alcohol to the human body, improve the cultural quality of the whole nation, strictly enforce the law on minors, strictly prohibit the drinking of minors, strengthen legal supervision, attach importance to and strengthen the mental health propaganda of wine, promote civilized drinking, do not persuade alcohol, do not drink alcohol, Do not drink on an empty stomach, treat physical or mental illnesses, avoid alcohol substitutes, promote the use of beverages to replace alcohol, reduce alcohol dependence caused by occupational reasons, promote the production of low-alcohol, control and ban the production of spirits, and crack down on illegal acts of illegal counterfeiting .

Complications of alcoholic dementia Complications chronic alcoholism cirrhosis peripheral neuritis brain atrophy arrhythmia congestive heart failure thrombosis cardiomyopathy myocardial infarction hypertension

The special psychological state caused by long-term excessive drinking is chronic alcoholism, and ultimately manifests as chronic alcoholism syndrome. It is a long-term (several years to decades, usually more than 10 years), a variety of physical and mental disorders, even irreversible Sexual pathological damage, such as liver damage or cirrhosis, multiple peripheral neuritis, central nervous system degeneration or brain atrophy.

In addition, the abuse of alcohol 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 platelet count. Increased, increased agglutination function and prolonged spontaneous dissolution of fibrin.

Symptoms of alcoholic dementia in alcohol Symptoms Symptoms of dullness, hallucinations, dementia, weakness, ataxia, insomnia, gait, instability, dizziness, coma, urinary incontinence

1. Most patients with alcoholic dementia have insidious onset, chronic disease, initial manifestation of burnout, lack of concern for things, feelings of dullness, anxiety, irritability, clothing dirt, no hygiene and loss of etiquette, etc. Vomiting and nystagmus can occur, gradually inattention, insomnia, irritability or lethargy, extraocular muscle spasm and strabismus, and then cerebellar ataxia, such as gait instability or instability, severe cases Insanity or coma can occur.

2. The onset of illness is often caused by sudden stimulation of mental stimulation. There may be significant obstacles in space and time orientation, abnormal emotions and behaviors, and even hallucinations, near memory impairment, fictional and delusional mental symptoms, due to the etiology of AD. Complex, so the clinical manifestations are also complex, can show a variety of clinical syndromes, and even some physical lesions, such as facial telangiectasia, muscle relaxation, weakness, tremors and seizures.

3. After more than a year of gradual emergence of cognitive impairment, and orientation and memory disorders, subsequent learning, abstract thinking, attention, visual space, visual movement coordination and spatial perception, etc., can be exaggerated, lack of rationality and self-knowledge , no language and dyslexia, with the increase in alcohol poisoning, memory loss, do not know their loved ones, the surrounding environment, general things or the return of serious cognitive dysfunction.

4. The patient's personal life ability is gradually lost in the later stage, and there may be a distinct personality degeneration. The demand for drinking exceeds everything, self-centered, selfish, no sense of responsibility for family or work, and moral standards are reduced. Get the wine without any means, even stealing, fraud and strong robbing, loss of self-control, rude behavior, cruel, duration of disease for several years, can be combined with Korsakoff syndrome, Wetnicke encephalopathy, chronic alcoholic peripheral neuropathy, etc., late language function Loss, only words, and finally bedridden, urinary incontinence, and more deaths due to serious complications.

5. Patients with EEG can appear low amplitude slow wave, CT examination shows ventricular enlargement, cerebral cortex, especially the frontal lobe significantly atrophy.

Examination of alcoholic dementia

1. Determination of blood and urine alcohol concentration.

There is a diagnosis and the significance of the degree of alcoholism.

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 and diagnosis of alcoholic dementia

Diagnostic criteria:

1 memory impairment manifests as the ability to learn new information or to recall previously acquired knowledge;

2 memory impairment caused severe social and occupational impairment, and the previous functional level decreased significantly;

3 memory disorders persist in the course of dementia;

4 medical history, physical examination showed that memory impairment is related to the sustained action of alcohol.

After 3 weeks of drinking, if the above symptoms persist, the diagnosis of alcoholic dementia can be diagnosed. Young patients with chronic alcoholism have spatial cognitive impairment and coordinated movement disorder. In the early stage of suspected alcoholic dementia, measures should be taken in time to prevent progress. .

The disease must be differentiated from brain-induced dementia caused by other causes, as well as changes in consciousness that occur in chronic alcoholism withdrawal.

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