Korsakovsky psychosis

Korsakoff's psychosis (KPP) is a late complication of persistent Wernicke's encephalopathy, which is characterized by memory impairment, confusion, and behavioral changes. The syndrome classically occurs with the 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, and confusion. At autopsy, Wernicke found punctate hemorrhages in the gray matter around the third and fourth ventricles and the Sylvian aqueduct. Sergei Korsakov, a Russian psychiatrist, described memory impairment in patients with chronic alcoholism in his articles from 1887 to 1891. He called this syndrome of psychosis "polyneuritica", believing that typical memory impairment combined with polyneuropathy are different aspects of the same disease.

[ 1 ], [ 2 ], [ 3 ], [ 4 ]

Epidemiology

According to statistics in countries such as Australia, Austria, Belgium, Czech Republic, Slovakia, France, Germany, Norway, England, the United States, the prevalence of the disease ranges from 0-2.8%.

[ 5 ], [ 6 ], [ 7 ], [ 8 ], [ 9 ]

Causes Korsakovsky psychosis

Korsakoff's psychosis (Korsakoff's amnestic syndrome) is observed in 80% of untreated patients with Wernicke's encephalopathy. Severe or repeated alcohol withdrawal with delirium may trigger the development of Korsakoff's psychosis regardless of whether typical features of Wernicke's encephalopathy were initially observed. Thiamine (vitamin B1) deficiency is responsible for the development of the symptom complex of Wernicke-Korsakoff syndrome.

[ 10 ], [ 11 ], [ 12 ], [ 13 ]

Risk factors

Precipitating factors include subarachnoid hemorrhage, thalamic hemorrhage, thalamic ischemic stroke, and, uncommonly, tumors in the posterior paramedian thalamus. It remains unclear why Korsakoff'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 not be complete.
• Certain diets.
• People with anorexia nervosa, schizophrenia, or incurable forms of cancer.
• Vomiting in pregnant women.
• Inflammatory bowel disease.
• Abdominal abscesses.
• Tuberculosis.
• Acquired immunodeficiency syndrome (AIDS).
• Uremia.
• Stem cell transplantation.
• Chronic hemodialysis.
• Breastfed infants with inadequate thiamine intake.

[ 14 ]

Pathogenesis

Thiamine is absorbed from the duodenum. Thiamine is metabolized into 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-ketoglutarate. 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 the conduction of nerve impulses along axons, especially in GABAergic and serotonergic neurons. Decreased function of these enzymes leads to diffuse lesions, disruption of glucose metabolism in key areas of the brain, which leads to disruption of metabolism at the cellular level.

[ 15 ], [ 16 ], [ 17 ]

Symptoms Korsakovsky psychosis

There are marked short-term memory impairments; retrograde and anterograde amnesias are expressed to varying degrees. Patients may retain memory of old events, while memory of recent events is more severely impaired. Disorientation in time is usually observed. Emotional disturbances are common: apathy, indifference, mild euphoria with reduced or absent reaction to events, even life-threatening ones. Spontaneity and initiative may decrease.

Confabulations are often an early, salient sign; confused patients unconsciously produce fictitious or distorted stories about events they cannot remember; these stories may be so convincing that the underlying disorder may not be recognized.

[ 18 ], [ 19 ]

Treatment Korsakovsky psychosis

Treatment consists of thiamine and adequate hydration.

Forecast

The prognosis is quite good for patients with traumatic brain injury, subarachnoid hemorrhage, or a combination of the two. The prognosis is worse in cases of thiamine deficiency or infarction; long-term hospital treatment is required in about 25% of patients, and only 20% recover completely. However, improvement may occur 12–24 months after onset of the disease, and patients should not be prematurely placed in nursing homes.

Mortality in severe cases is 10-15%.

[ 20 ], [ 21 ], [ 22 ]