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1.
Journal of Korean Geriatric Psychiatry ; : 89-96, 2012.
Artículo en Coreano | WPRIM | ID: wpr-118958

RESUMEN

Chronic alcohol use may have direct or indirect neurotoxic effects on the brain that can lead to cognitive impairment. However, the precise relationship between alcohol and dementia remains unclear. There are several epidemiological studies suggest that the protective effect of light-moderate alcohol drinking in dementia. But obviously the heavy alcohol drinking can lead to brain damage and increase the risk of various types of dementia. The clinicopathological issues and criteria regarding so-called 'alcoholic dementia' remain under debate. Alcohol-induced persisting amnestic disorder, alcohol-induced persisting dementia, and Wernicke-Korsakoff syndrome (thiamine deficiency) may constitute distinct disease entities, but they may also share some common features. Based on this theory, Oslin and colleagues proposed the broader diagnostic scheme and criteria for Alcohol Related Dementia (ARD), which may include cases of Wernicke-Korsakoff syndrome and also other cases of dementia that appear to be alcohol-related. In pathogenesis of the alcoholic dementia, the chronic exposure to ethanol results in the adaptive up-regulation of NMDA receptor sensitivity, which can result in an increased vulnerability to glutamate induced excitotoxicity. Despite the clinical importance of ARD, few medical treatments for ARD have been proposed and studied. Most of all, the gold standard of the treatment in alcoholic dementia is the maintaining abstinence. Some therapeutic trials with cholinesterase inhibitors (donepezil and rivastigmine) and memantine (NMDA receptor antagonist) have been conducted for the patients with Wernicke-Korsakoff syndrome and alcohol-related dementia, and these studies reported favorable outcomes. Especially memantine can be a more effective agent in the treatment of alcoholic dementia because of anti-craving effect reported in several studies.


Asunto(s)
Humanos , Trastorno Amnésico Alcohólico , Consumo de Bebidas Alcohólicas , Alcohólicos , Encéfalo , Inhibidores de la Colinesterasa , Cognición , Demencia , Etanol , Ácido Glutámico , Síndrome de Korsakoff , Memantina , N-Metilaspartato , Regulación hacia Arriba
2.
Korean Journal of Psychopharmacology ; : 5-14, 2009.
Artículo en Coreano | WPRIM | ID: wpr-123145

RESUMEN

Despite epidemiological studies reporting no negative effects of mild to moderate alcohol drinking on cognitive functioning, a recent well-controlled study showed that chronic mild drinking diminished the volume of the brain and was associated with cognitive decline that worsened as a function of the amount of alcohol consumed. Animal studies have demonstrated that neural cell damage follows chronic alcohol intake and withdrawal. In addition, acute excessive alcohol intake has been shown to result in temporary impairment of memory, and chronic alcohol drinking is often related to neuronal damage and cognitive disorders. Even though a diverse spectrum of cognitive disorders can develop after sustained alcohol drinking, no definite diagnostic criteria existed before those proposed by Oslin; the availability of these criteria will provide more structured clinical and academic approaches to alcohol-related cognitive decline, including dementia. In general, diminished cognitive functioning has been related to excessive alcohol consumption, with cognitive functioning gradually recovering over time. With the exception of the administration of thiamine in Wernicke-Korsakoff syndrome, only supportive pharmacotherapies have been provided for patients with alcohol-related cognitive disorders. However, experimental trials with rivastigmine or donepezil have been conducted for special populations with persistent cognitive impairments, and these studies reported favorable outcomes. We administered memantine for alcohol-related dementia and observed improvements in verbal memory and scores on the mini-mental status exam. We anticipate that novel and appropriate therapeutic agents for various conditions in this domain will be developed based on systematic diagnostic criteria and the accumulation of neurobiological evidence about alcohol-related cognitive decline.


Asunto(s)
Animales , Humanos , Consumo de Bebidas Alcohólicas , Alcoholismo , Encéfalo , Demencia , Ingestión de Líquidos , Indanos , Síndrome de Korsakoff , Memantina , Memoria , Neuronas , Fenilcarbamatos , Piperidinas , Tiamina , Rivastigmina
3.
Journal of the Korean Medical Association ; : 84-89, 2008.
Artículo en Coreano | WPRIM | ID: wpr-127652

RESUMEN

Alcohol-induced cognitive disorder is a very severe problem in problem alcohol drinker and alcohol itself seems to be one of the main causalities in the development of senile dementia. However, the spectrum of alcohol induced cognitive disorder is quite broad, for example, it covered from alcohol-induced persistent amnestic disorder to Wernicke-Korsakoff syndrome and alcohol-induced persistent dementia. By that reason, broad spectrum of cognitive impairment by excessive alcohol drinking is regarded as alcohol related dementia. The pharmacological treatment is not well established yet in alcohol related dementia, except Wernicke-Korsakoff syndrome which is definitely related to thiamine deficiency. Therefore we introduced that some reports about the clinical efficacies by rivastigmine or donepezil trial and recent outcomes of memantine trial by authors in this review.


Asunto(s)
Consumo de Bebidas Alcohólicas , Enfermedad de Alzheimer , Demencia , Indanos , Síndrome de Korsakoff , Memantina , Fenilcarbamatos , Piperidinas , Rivastigmina , Tiamina , Deficiencia de Tiamina
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