korsakoff's syndrome
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2020 ◽  
Vol 12 (6) ◽  
pp. 124-130
Author(s):  
N. A. Tyuvina ◽  
T. N. Maksimova ◽  
S. V. Prokhorova ◽  
V. O. Vysokova

Approaches to treating cognitive-amnestic disorders of various origins, including Korsakoff's syndrome (KS), are currently being actively elaborated. KS is manifested by severe memory impairment, leading to disability. It is quite common in alcohol abusers. There is still no proven effective treatment for KS. In view of the fact that studies on the treatment of KS have been very few, there are no clear recommendations for its most effective treatment. There has been evidence that in addition to thiamine deficiency, the toxic effect of glutamate that is actively released through binding to NMDA receptors during the ethanol withdrawal period is the basis for KS development. Memantine, a noncompetitive NMDA receptor antagonist, has recently been used successfully to treat KS. The paper describes a clinical case of a 55-year-old patient with KS treated with akatinol memantine, in which the latter has demonstrated its high efficacy and good tolerance. Analysis of the data available in the literature and the presented clinical case suggest that it is advisable to prescribe memantine for patients with alcohol-related memory impairment.


Author(s):  
Ken Wilson

Like the liver, the brain is commonly affected by long-term alcohol misuse. While neurocognitive dysfunctions are widely known in their most extreme presentations, such as Korsakoff’s syndrome and Wernicke’s encephalopathy (WE), there are other less explicit manifestations of neurocognitive damage which occur more frequently. This chapter explores these conditions under the umbrella term ‘alcohol-related brain damage’ (ARBD), more specifically employing the term Wernicke–Korsakoff’s syndrome (WK) when referring to the acute and chronic effects of thiamine deficiency. The correlation between excessive alcohol consumption and thiamine intake is explored, along with the body’s response of boosting gamma-aminobutyric acid (GABA)–benzodiazepine and NMDA receptors. In acute and non-acute cases of ARBD, prompt diagnosis and treatment are essential due to the risk of long-term cognitive and intellectual damage it can yield. As such, psychosocial treatment in the aftermath of the clinical phase is equally important, focusing on assessment, therapeutic intervention, adjustment, and social integration.


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