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Blackout (Alcohol Related Amnesia) : ウィキペディア英語版
Blackout (drug-related amnesia)

A drug-related blackout is a phenomenon caused by the intake of any substance or medication in which short term and long term memory creation is impaired, therefore causing a complete inability to recall the past. Blackouts can be caused by any substance, but are most frequently associated with GABAergic drugs. Blackouts are frequently described as having effects similar to that of anterograde amnesia, in which the subject cannot recall any events after the event that caused amnesia. Research on alcohol blackouts was begun by E. M. Jellinek in the 1940s. Using data from a survey of Alcoholics Anonymous (AA) members, he came to believe that blackouts would be a good determinant of alcoholism. However, there are conflicting views whether this is true. The negative psychological effects of an alcohol-related blackout are often worsened by those who suffer from anxiety disorders. Impairment of the liver will also allow more alcohol to reach the brain and hasten the individual's blackout.
The term "blackout" can also refer to a complete loss of consciousness, or syncope.〔http://medical-dictionary.thefreedictionary.com/blackout〕
==Alcohol and long-term memory==
Various studies have also given rise to proof of links between general alcohol consumption and its effects on memory capacity. These studies have shown in particular, how the inebriated or intoxicated individual makes poorer associations between words and objects than does the sober individual. Later blackout-specific studies have indicated that alcohol specifically impairs the brain's ability to take short-term memories and experiences and transfer them to long-term memory.
It is a common misconception that blackouts generally occur only in alcoholics; research suggests that individuals who engage in binge drinking, such as many college students, are often at risk as well. In a 2002 survey of college students by researchers at Duke University Medical Center, 40% of those surveyed who had consumed alcohol recently reported having experienced a blackout within the preceding year.
In one study, a sample of individuals was gathered and divided into groups based on whether they had had a fragmentary blackout within the last year or not. Groups were also divided based on those who had received alcohol and those who had not. In their beverage challenge, participants were given one drink per ten minutes until the target of .08%BAC was achieved. Drinks for the alcohol condition contained a 3:1 ratio of mixer to vodka. After 30 minutes, breathalyzer samples were recorded and recorded every 30 minutes thereafter. In the test for narrative recall those who received alcohol and FB+(those who admitted to having a fragmentary blackout within the last year) recalled fewer narrative details after a 30-minute delay, but there were no significant interaction effects. The next day participants were called and tested on their narrative recall and cued recall and the results were that those who consumed alcohol showed poorer 30-minute delay recall and next-day recall than those who did not consume alcohol, but there were no significant effects on cued recall of details. Their study also revealed that those who were FB+ and consumed alcohol also performed worse on contextual recall than the other participants.〔Wetherill, R. R., & Fromme, K. (2011). Acute alcohol effects on narrative recall and contextual memory: An examination of fragmentary blackouts. Addictive Behaviors, 36(8), 886-889. doi: 10.1016/j.addbeh.2011.03.012〕
Alcohol impairs delayed and next-day narrative recall, but not next-day cued recall which suggests that information is available in memory but is temporarily inaccessible. Those with a history of fragmentary blackouts also performed worse on delayed recall than those with no prior blackouts. Neuroimaging shows that cued recall and free recall are associated with differential neural activation in distinct neural networks: sensory and conceptual. Together, these findings suggest that the differential effects of alcohol on free and cued recalls may be a result of substance altering neural activity in conceptual rather than sensory networks. Prior blackout experiences also appear to be related to impaired conceptual networks.〔Wetherill, R., Schnyer, D., & Fromme, K. (2012). Acute Alcohol Effects on Contextual memory BOLD
response: Differences Based on Fragmentary Blackout History. Alcoholism: Clinical and Experimental Research, 36(6), 607-617. Doi: 10.1111/j.1530-0277.2011.01702.x


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