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Korsakovsky psychosis
Last reviewed: 23.04.2024
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Korsakov psychosis (AWP) is a late complication of Wernicke's persistent encephalopathy, which is manifested by impaired memory, confusion and changes in behavior. The syndrome classically proceeds with the manifestation of a clinical triad of symptoms: confusion, ataxia and nystagmus. In 1881, Wernicke first described the disease in 3 patients, which was characterized by paralysis of eye movements, ataxia, confusion. At the autopsy, Wernicke found pinpoint hemorrhages in the gray matter around the third and fourth ventricles and sylvian aqueduct. Sergey Korsakov, a Russian psychiatrist, described memory impairment in patients with chronic alcoholism in his articles from 1887-1891.. He called this psychosis syndrome "polyneuritica", believing that a typical memory impairment combined with polyneuropathy is different facets of the same disease.
Causes of the korsakovsky psychosis
Korsakovsky psychosis (Korsakovsky amnestic syndrome) is observed in 80% of untreated patients with Wernicke's encephalopathy. Severe or repetitive alcohol withdrawal with delirium can provoke the development of Korsakov's psychosis, regardless of whether initially typical signs of Wernicke's encephalopathy were observed. Thiamine deficiency (vitamin B1) is responsible for the development of the Wernicke-Korsakov syndrome complex.
Risk factors
The provoking factors include subarachnoid hemorrhage, hemorrhage in the thalamus, thalamic ischemic stroke and, infrequently, tumors in the posterior paramedial region of the thalamus. It remains unclear why Korsakov's psychosis develops only in some patients with Wernicke encephalopathy.
Other risk factors:
- Bariatric surgery. Recovery usually occurs within 3-6 months from the start of treatment, but may be incomplete.
- Specific diets.
- Persons with anorexia nervosa, schizophrenia, or incurable forms of cancer.
- Vomiting in pregnant women.
- Inflammatory bowel disease.
- Abscesses of the abdominal cavity.
- Tuberculosis.
- Acquired Immunodeficiency Syndrome (AIDS).
- Uraemia.
- Stem cell transplantation.
- Chronic hemodialysis.
- Breast-fed infants with insufficient thiamine intake.
[14]
Pathogenesis
Thiamine is absorbed from the duodenum. Thiamine is metabolized to the active form - thiamine pyrophosphate in neuronal and glial cells. Thiamine pyrophosphate serves as a cofactor for a number of enzymes, including transketolase, pyruvate dehydrogenase, and alpha-KG. The main function of these enzymes is participation in lipid and carbohydrate metabolism, the synthesis of amino acids, glucose, and neurotransmitters.
Thiamine plays a role in conducting nerve impulses along axons, especially in GABA-ergic and serotonergic neurons. Reducing the function of these enzymes leads to diffuse lesions, impaired glucose metabolism in key areas of the brain, which leads to metabolic disorders at the cellular level.
Symptoms of the korsakovsky psychosis
Observed pronounced violations of short-term memory; retrograde and anterograde amnesia are expressed in varying degrees. Patients may have memories of long-standing events, while memory of recent events is more disturbed. As a rule, there is disorientation in time. Often there are emotional disturbances: apathy, indifference, slight euphoria with a reduced or absent reaction to events, even life-threatening. Spontaneity and initiative may decrease.
Confabulations are often an early bright sign; confused patients unconsciously produce fictional or distorted stories about events they cannot recall; these stories can be so convincing that the underlying disorder can not be recognized.
Treatment of the korsakovsky psychosis
Treatment consists of prescribing thiamine and adequate hydration.
Forecast
The prognosis is quite favorable for patients with traumatic brain injury, subarachnoid hemorrhage, or a combination thereof. Worse prognosis in cases of thiamine or heart attack deficiency; long-term inpatient treatment is required in approximately 25% of patients, and only 20% recover completely. However, improvement may occur even 12-24 months after the onset of the disease, and patients should not be prematurely placed in boarding homes.
Mortality in severe cases is 10-15%.