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black outs (notes)

Blackout (alcohol-related amnesia)

From Wikipedia, the free encyclopedia

A blackout is a phenomenon caused by the intake of alcohol or other substance in which long term memory creation is impaired or there is a complete inability to recall the past. Blackouts are frequently described as having effects similar to that of anterograde amnesia, in which the subject cannot create memories after the event that caused amnesia. ‘Blacking out’ is not to be confused with the mutually exclusive act of ‘passing out‘, which means loss of consciousness. 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 predictor of alcoholism.[1] However, there are conflicting views as to whether or not this is true.[2]

Alcohol and long-term memory

Various studies have also proven links between general alcohol consumption and its effects on memory creation.[3] Particularly, these studies have shown that associations made between words and objects when intoxicated are less easily recalled than associations made when not intoxicated. 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.[4]

It is a common misconception that blackouts generally occur only to alcoholics; research suggests that social drinkers, such as 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.[5]

Types of blackouts

Blackouts can generally be divided into two categories, “en bloc” blackouts, and “fragmentary” blackouts. En bloc blackouts are classified by the inability to later recall any memories from the intoxicated period, even when prompted. These blackouts are characterized also by the ability to easily recall things that have occurred within the last 2 minutes, yet inability to recall anything prior to this period. As such, a person experiencing an en bloc blackout may not appear to be doing so, as they can carry on conversations or even manage to accomplish difficult feats. It is difficult to determine the end of this type of blackout as sleep typically occurs before they end.[6] Fragmentary blackouts are characterized by the ability to recall certain events from an intoxicated period, yet be unaware that other memories are missing until reminded of the existence of these ‘gaps’ in memory. This phenomenon is also termed a brownout. Research indicates that fragmentary blackouts, or brownouts are far more common than en bloc blackouts.[7]

Causes

Blackouts are commonly associated with the consumption of large amounts of alcohol; however, surveys of drinkers experiencing blackouts have indicated that they are not directly related to the amount of alcohol consumed. Respondents reported they frequently recalled having “drunk as much or more without memory loss”, compared to instances of blacking out.[6] Subsequent research has indicated that blackouts are most likely caused by a rapid increase in a person’s blood-alcohol concentration. One study, in particular, resulted in subjects being stratified easily into two groups, those who consumed alcohol very quickly, and blacked out, and those who did not black out by drinking alcohol slowly, despite being extremely intoxicated by the end of the study.[8]

Benzodiazepines

Benzodiazepines such as clonazepam (Klonopin), diazepam (Valium), and alprazolam (Xanax), which also act as GABA agonists, are known to cause blackouts as a result of high dose use.

Predisposition to blackouts

Research indicates that some users of alcohol, particularly those with a history of blackouts, are predisposed to experience blackouts more frequently than others.[9] One such study indicated a link between prenatal exposure to alcohol and vulnerability towards blackouts, in addition to the oft-cited link between this type of exposure and alcoholism.[10] Alternatively, another study has indicated that there appears to be a genetic predisposition towards blacking out, suggesting that some individuals are made to be susceptible to alcohol related amnesia.[11]

What Happened? Alcohol, Memory Blackouts, and the Brain

Aaron M. White, Ph.D.

Mechanisms underlying alcohol–induced memory impairments include disruption of activity in the hippocampus, a brain region that plays a central role in the formation of new auotbiographical memories.

In addition to impairing balance, motor coordination, decisionmaking, and a litany of other functions, alcohol produces detectable memory impairments beginning after just one or two drinks. As the dose increases, so does the magnitude of the memory impairments.

Early anecdotal evidence suggested that blackouts might actually reflect state–dependent information storage—that is, people might be able to remember events that occurred while they were intoxicated if they returned to that state. Regardless of how compelling such stories can be, clear evidence of state–dependent learning under the influence of alcohol is lacking. In one recent study, Weissenborn and Duka (2000) examined whether subjects who learned word lists while intoxicated could recall more items if they were intoxicated again during the testing session. No such state–dependency was observed. Similarly, Lisman (1974) tried unsuccessfully to help subjects resurrect lost information for events occurring during periods of intoxication by getting them intoxicated once again.

During the 2 weeks preceding the survey, an equal percentage of males and females experienced blackouts, despite the fact that males drank significantly more often and more heavily than females. This outcome suggests that at any given level of alcohol consumption, females—a group infrequently studied in the literature on blackouts—are at greater risk than males for experiencing blackouts. The greater tendency of females to black out likely arises, in part, from well–known gender differences in physiological factors that affect alcohol distribution and metabolism, such as body weight, proportion of body fat, and levels of key enzymes. There also is some evidence that females are more susceptible than males to milder forms of alcohol–induced memory impairments, even when given comparable doses of alcohol (Mumenthaler et al. 1999).

a recent study by Hartzler and Fromme (2003a) suggests that people with a history of blackouts are more vulnerable to the effects of alcohol on memory than those without a history of blackouts.

n an impressive longitudinal study, Baer and colleagues (2003) examined the drinking habits of pregnant women in 1974 and 1975, and then studied alcohol use and related problems in their offspring at seven different time points during the following 21 years. These authors observed that prenatal alcohol exposure was associated with increased rates of experiencing alcohol–related consequences, including blackouts, even after controlling for the offsprings’ general drinking habits.

Substantial evidence now indicates that alcohol selectively alters the activity of specific complexes of proteins embedded in the membranes of cells (i.e., receptors) that bind neurotransmitters such as gamma–aminobutyric acid (GABA), glutamate, serotonin, acetylcholine, and glycine (for a review, see Little 1999)

More than 30 years ago, both Ryback (1970) and Goodwin and colleagues (1969a) speculated that alcohol might impair memory formation by disrupting activity in the hippocampus. This speculation was based on the observation that acute alcohol exposure (in humans) produces a syndrome of memory impairments similar in many ways to the impairments produced by hippocampal damage. Specifically, both acute alcohol exposure and hippocampal damage impair the ability to form new long–term, explicit memories but do not affect short–term memory storage or, in general, the recall of information from long–term storage.

Research conducted in the past few decades using animal models supports the hypothesis that alcohol impairs memory formation, at least in part, by disrupting activity in the hippocampus (for a review, see White et al. 2000b). Such research has included behavioral observation; examination of slices of and brain tissue, neurons in cell culture, and brain activity in anesthetized or freely behaving animals; and a variety of pharmacological techniques.

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