Alcohol and Cognitive Disorder / 대한정신약물학회지

ABSTRACT

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.