Wernicke's encephalopathy
Introduction
Introduction to Wernicke's encephalopathy Wernicke'sencephalopathy (WE) or Wernicke-Korsakoff syndrome is a common metabolic encephalopathy of chronic alcoholism and is an acute illness caused by thiamine deficiency. In the Chinese classification of mental illness, WE is classified as a mental disorder caused by alcoholism, but currently there is no clear diagnostic criteria. Patients diagnosed and treated in time can be fully recovered, and the mortality rate of WE is 10% to 20%. basic knowledge The proportion of illness: 0.001-0.003% Susceptible people: between 30 and 70 years old Mode of infection: non-infectious Complications: hypotension, liver disease, pancreatitis, heart failure, alcohol-toxic peripheral neuropathy
Cause
Wernicke encephalopathy
(1) Causes of the disease
The cause of Wernicke's encephalopathy is thiamin deficiency. The causes of thiamine deficiency include vomiting in pregnant women, malnutrition, anorexia nervosa, liver disease, total removal of the stomach, jejunal resection, gastric cancer, malignant tumor, pernicious anemia, chronic diarrhea, and long-term renal dialysis. Parenteral nutrition lacks thiamine, long-term fluid replacement and magnesium deficiency. Animal experiments have shown that chronic alcoholism can lead to malnutrition, mainly thiamine deficiency, which can aggravate chronic alcoholism.
(two) pathogenesis
Thiamine (vitamin B1) is mainly taken from the diet, alcoholics often substitute meals for wine, and even do not eat for several days; long-term alcohol abuse causes gastrointestinal dysfunction and intestinal mucosal lesions cause malabsorption, the incidence of chronic liver disease increases, so that sulfur Amine storage, the ability of thiamine to convert to active thiamine pyrophosphate decreased, resulting in insufficient intake of thiamine, thiamine pyrophosphate is an important coenzyme in cell metabolism, making pyruvate dehydrogenase, -ketoglutarate Dehydrogenase and transketolase act to convert pyruvate decarboxylation to acetyl-CoA, linking anaerobic glycolysis to the tricarboxylic acid cycle; converting alpha-ketoglutarate to succinic acid, the latter An important part of the tricarboxylic acid cycle, thiamine or thiamine pyrophosphate deficiency makes the tricarboxylic acid cycle unable to proceed normally. It can not produce ATP as an energy source by oxidation of glucose. Metabolic disorders cause lactic acid accumulation and acidosis in brain tissue, interfering with neurotransmission. Synthetic, release and uptake, leading to central nervous system dysfunction, producing Wernicke encephalopathy.
Wernicke (1881) first described the pathological changes of this disease as the third, and there were many punctate lesions in the gray matter of the fourth ventricle and midbrain. The study found that patients with WE had multiple brain lesions, such as papillary body, brain stem, and third. The ventricles, the pericardium, the thalamus, the hypothalamus, the upper cerebellum and the vestibular nuclei, etc., the midbrain, pons, medulla and brain lesions are obvious.
The brain histopathology study of WE found that typical histological features are neuronal degeneration, necrosis and loss, myelin degeneration and necrosis, astrocytes, oligodendrocytes and capillary proliferation, cell edema and spotted Bleeding, etc.
Prevention
Wernicke encephalopathy 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 .
Complication
Wernicke encephalopathy complications Complications hypotension liver disease pancreatitis heart failure alcoholic peripheral neuropathy
Most patients can be accompanied by hypothermia, hypotension and tachycardia, and some patients are associated with liver disease, pancreatitis, heart failure and peripheral neuropathy.
Symptom
Wernicke encephalopathy symptoms common symptoms ambiguity heart failure consciousness disorder dementia eyeball tremor tachycardia diplopia retinal hemorrhage ataxia hypotension
1. The onset age of WE is 30-70 years old, with an average of 42.9 years old. There are a few males, mainly characterized by sudden onset of nervous system dysfunction, typical WE appearance of extraocular muscle paralysis, mental disorders and ataxia. Sexual symptoms.
(1) Extraocular muscle paralysis is common with bilateral nerve palsy and diplopia. Other eye symptoms may have nystagmus, ptosis, optic disc edema, retinal hemorrhage and pupillary light reflex or disappear; nystagmus appears early, with horizontal and Verticality is the main, often with abnormal vestibular function test, eye muscle paralysis such as timely treatment often recover within 24h, nystagmus needs 1 to 2 weeks to recover.
(2) Mental abnormalities manifested as attention, memory and disorientation, mental distraction, irritability, apathy and dementia, sometimes difficult to distinguish from alcohol withdrawal, often referred to as generalized turbidity; often accompanied by Korsakoff syndrome It is characterized by memory impairment, learning failure, fiction, apathy and disorientation, with confusion, sleepiness or coma.
(3) Ataxia is mainly caused by the trunk and lower limbs. The upper limbs are less common, standing and walking difficult. It takes 2 weeks or more to recover.
2. Only 10% to 16.5% of patients have three groups of symptoms. Studies have shown that 66% of patients have mental disorders, 73% have ocular symptoms, 82% have ataxia, and most patients have hypothermia, hypotension and Tachycardia, some patients with liver disease, heart failure, pancreatitis and peripheral neuropathy and other complications, eye muscle paralysis recovered faster, the recovery of mental symptoms often takes weeks to months.
Examine
Wernicke encephalopathy check
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. CT can see low-density or high-density lesions of bilateral thalamus and brainstem, and 25% of patients have low-density areas around the aqueduct. MRI is an ideal tool for the diagnosis of WE. Early diagnosis is sensitive, and bilateral thalamus and brainstem symmetry can be seen. The typical change of the lesion in the acute phase is the high signal intensity of the symmetric T2WI around the ventricle and the aqueduct. The high signal of the recovery period is reduced or disappeared after 6 to 12 months. The atrophy of the papillary body is a characteristic neuropathological abnormality of WE, the papillary body. Significantly reduced volume is not only a special marker of thiamin deficiency, but also a distinguishing feature of WE and Alzheimer's disease.
4. Electrocardiogram, EEG has differential diagnosis and the significance of the degree of poisoning assessment.
Diagnosis
Diagnosis and diagnosis of Wernicke's encephalopathy
Mainly based on medical history, clinical manifestations and typical changes in head MRI, autopsy studies found that the clinical diagnosis rate of WE (0.2% to 0.5%) is about 80% lower than the pathological diagnosis rate (1% to 3%), due to WE typical The three groups of symptoms are not common, even if they appear, it is difficult to identify, easy to miss diagnosis and misdiagnosis, clinical patients with chronic alcoholism or malnutrition with disturbance of consciousness, should pay attention to the possibility of WE for early treatment.
The disease must be differentiated from other causes of brain-induced dementia, extraocular muscle paralysis, mental disorders and ataxia.
