Alcohol primarily interferes with the ability to form new long–term memories, leaving intact previously established long–term memories and the ability to keep new information active in memory for brief periods. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments.
Large amounts of alcohol, particularly if consumed rapidly, can produce partial or complete blackouts, which are periods of memory loss for events that transpired while a person was drinking. Blackouts are much more common among social drinkers—including college drinkers—than was previously assumed, and have been found to encompass events ranging from conversations to intercourse.
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. If recreational drugs were tools, alcohol would be a sledgehammer. Few cognitive functions or behaviors escape the impact of alcohol, a fact that has long been recognized in the literature.
As Fleming stated nearly 70 years ago, “the striking and inescapable impression one gets from a review of acute alcoholic intoxication is of the almost infinite diversity of symptoms that may ensue from the action of this single toxic agent”.
In addition to impairing balance, motor coordination, decision making, 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.
Under certain circumstances, alcohol can disrupt or completely block the ability to form memories for events that transpire while a person is intoxicated, a type of impairment known as a blackout. This article reviews what is currently known regarding the specific features of acute alcohol–induced memory dysfunction, particularly alcohol–induced blackouts, and the pharmacological mechanisms underlying them.
EFFECTS OF ALCOHOL ON MEMORY
To evaluate the effects of alcohol, or any other drug, on memory, one must first identify a model of memory formation and storage to use as a reference. One classic, often–cited model, initially proposed by Atkinson and Shiffrin, posits that memory formation and storage take place in several stages, proceeding from sensory memory (which lasts up to a few seconds) to short–term memory (which lasts from seconds to minutes depending upon whether the information is rehearsed) to long–term storage.
This model often is referred to as the modal model of memory, as it captures key elements of several other major models. Indeed, elements of this model still can be seen in virtually all models of memory formation.
In the modal model of memory, when one attends to sensory information, it is transferred from a sensory memory store to short–term memory. The likelihood that information will be transferred from short–term to long–term storage, or be encoded into long–term memory, was once thought to depend primarily on how long the person keeps the information active in short–term memory via rehearsal.
Although rehearsal clearly influences the transfer of information into long–term storage, it is important to note that other factors, such as the depth of processing (the level of true understanding and manipulation of the information), attention, motivation, and arousal also play important roles.
Variability in the use of terms, particularly in operational definitions of short–term memory, makes it difficult to formulate a simple synopsis of the literature on alcohol–induced memory impairments.
As Mello (1973) stated three decades ago with regard to the memory literature in general, “The inconsistent use of descriptive terms has been a recurrent source of confusion in the ‘short–term’ memory literature and ‘short–term’ memory has been variously defined as 5 seconds, 5 minutes, and 30 minutes”.
In spite of this inconsistency, several conclusions can be drawn from research on alcohol–induced memory impairments. One conclusion is that the impact of alcohol on the formation of new long–term “explicit” memories—that is, memories of facts (e.g., names and phone numbers) and events—is far greater than the drug’s impact on the ability to recall previously established memories or to hold new information in short–term memory.
Intoxicated subjects are typically able to repeat new information immediately after its presentation and often can keep it active in short–term storage for up to a few minutes if they are not distracted, though this is not always the case.
Similarly, subjects normally are capable of retrieving information placed in long–term storage prior to acute intoxication. In contrast, alcohol impairs the ability to store information across delays longer than a few seconds if subjects are distracted between the time they are given the new information and the time they are tested.
In a classic study, Parker and colleagues reported that when intoxicated subjects were presented with “paired associates”—for example, the letter “B” paired with the month “January”—they were impaired when asked to recall the items after delays of a minute or more.
However, subjects could recall paired associates that they had learned before becoming intoxicated. More recently, Acheson and colleagues observed that intoxicated subjects could recall items on word lists immediately after the lists were presented but were impaired when asked to recall the items 20 minutes later.
Large amounts of alcohol, particularly if consumed rapidly, can produce partial or complete blackouts, which are periods of memory loss for events that transpired while a person was drinking. Blackouts are much more common among social drinkers—including college drinkers—than was previously assumed, and have been found to encompass events ranging from conversations to intercourse.
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. If recreational drugs were tools, alcohol would be a sledgehammer. Few cognitive functions or behaviors escape the impact of alcohol, a fact that has long been recognized in the literature.
As Fleming stated nearly 70 years ago, “the striking and inescapable impression one gets from a review of acute alcoholic intoxication is of the almost infinite diversity of symptoms that may ensue from the action of this single toxic agent”.
In addition to impairing balance, motor coordination, decision making, 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.
Under certain circumstances, alcohol can disrupt or completely block the ability to form memories for events that transpire while a person is intoxicated, a type of impairment known as a blackout. This article reviews what is currently known regarding the specific features of acute alcohol–induced memory dysfunction, particularly alcohol–induced blackouts, and the pharmacological mechanisms underlying them.
EFFECTS OF ALCOHOL ON MEMORY
To evaluate the effects of alcohol, or any other drug, on memory, one must first identify a model of memory formation and storage to use as a reference. One classic, often–cited model, initially proposed by Atkinson and Shiffrin, posits that memory formation and storage take place in several stages, proceeding from sensory memory (which lasts up to a few seconds) to short–term memory (which lasts from seconds to minutes depending upon whether the information is rehearsed) to long–term storage.
This model often is referred to as the modal model of memory, as it captures key elements of several other major models. Indeed, elements of this model still can be seen in virtually all models of memory formation.
In the modal model of memory, when one attends to sensory information, it is transferred from a sensory memory store to short–term memory. The likelihood that information will be transferred from short–term to long–term storage, or be encoded into long–term memory, was once thought to depend primarily on how long the person keeps the information active in short–term memory via rehearsal.
Although rehearsal clearly influences the transfer of information into long–term storage, it is important to note that other factors, such as the depth of processing (the level of true understanding and manipulation of the information), attention, motivation, and arousal also play important roles.
Variability in the use of terms, particularly in operational definitions of short–term memory, makes it difficult to formulate a simple synopsis of the literature on alcohol–induced memory impairments.
As Mello (1973) stated three decades ago with regard to the memory literature in general, “The inconsistent use of descriptive terms has been a recurrent source of confusion in the ‘short–term’ memory literature and ‘short–term’ memory has been variously defined as 5 seconds, 5 minutes, and 30 minutes”.
In spite of this inconsistency, several conclusions can be drawn from research on alcohol–induced memory impairments. One conclusion is that the impact of alcohol on the formation of new long–term “explicit” memories—that is, memories of facts (e.g., names and phone numbers) and events—is far greater than the drug’s impact on the ability to recall previously established memories or to hold new information in short–term memory.
Intoxicated subjects are typically able to repeat new information immediately after its presentation and often can keep it active in short–term storage for up to a few minutes if they are not distracted, though this is not always the case.
Similarly, subjects normally are capable of retrieving information placed in long–term storage prior to acute intoxication. In contrast, alcohol impairs the ability to store information across delays longer than a few seconds if subjects are distracted between the time they are given the new information and the time they are tested.
In a classic study, Parker and colleagues reported that when intoxicated subjects were presented with “paired associates”—for example, the letter “B” paired with the month “January”—they were impaired when asked to recall the items after delays of a minute or more.
However, subjects could recall paired associates that they had learned before becoming intoxicated. More recently, Acheson and colleagues observed that intoxicated subjects could recall items on word lists immediately after the lists were presented but were impaired when asked to recall the items 20 minutes later.
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