Alcohol-Induced Sleepiness and Memory Function

Article excerpt

Alcohol is known to impair various aspects of cognitive functioning, including learning and memory (Birnbaum and Parker 1977). Alcohol-induced memory impairment has been studied extensively both by researchers and clinicians, partly because memory impairment has everyday practical consequences for the affected patient. In addition, precise methods exist to assess memory functions. However, despite the large number of studies on alcohol-induced memory impairment, there is little consensus about the specific components of memory affected by alcohol or about the neurobiological mechanisms underlying alcohol's effects.

A useful method of conceptualizing the way alcohol may affect memory is offered by Curran (1991). This concept entails that mood, level of sleepiness/alertness (or, as Curran describes it, arousal), and memory all are interrelated. Alcohol is known to affect directly each of these factors. And by acting on one factor, alcohol also can indirectly affect the other factors because of their interrelations.

This article reviews a wide range of research findings contributing to the hypothesis that alcohol's direct sedative effects (i.e., alcohol-induced sleepiness)--in addition to its direct memory effects--contributes to alcohol's amnestic (i.e., memory impairing) effects. Studies on both healthy, sleep-deprived people and on patients with sleep disorders and studies of the effects of sedative drugs provide the basis for this hypothesis. Studies separately assessing alcohol's sedative and amnestic effects or simultaneously measuring alcohol's sedative and performance-disruptive effects provide further support. The article also describes some of the neurotransmitter systems controlling sleep and wakefulness that are affected by alcohol and other sedative drugs and that may underlie the association of sedation and memory impairment. Finally, some important practical implications of the potential correlation between alcohol's sedative and memory-impairing effects are discussed.


Like hunger and thirst, sleepiness is considered a basic physiological drive state. It reflects the organism's need or pressure for sleep. Like other physiological drive states, the level of sleepiness is difficult to assess. Despite a general tendency toward increasing sleepiness after sleep loss, most a sleep deprivation studies find some inconsistencies in the subjects' personal assessment of how sleepy they are (Monk 1991; Roth et al. 1994).

Research has shown that people's ability to accurately judge their degree of sleepiness depends on several factors, such as internal point of reference, environmental demands, and time of day (Roth et al. 1994). For example, a person not getting enough sleep for an extended period will lose the internal reference to the experience of full alertness and therefore may underestimate his or her level of sleepiness. Similarly, people often judge their level of sleepiness to be higher in boring, nonstimulating situations in which environmental demands to stay alert or to pay attention are reduced. Finally, most people experience a circadian fluctuation with increased sleepiness over the midday and increased alertness in the early evening.

To assess sleepiness or alertness or the sedative effects of drugs, such as alcohol, scientists have asked people to self-rate their sleepiness or have used standard laboratory tests of performance. However, for the reasons stated above, self-ratings of sleepiness or sedative drug effects may be inaccurate (Roth et al. 1982). Similarly, performance tests sometimes are insensitive to the effects of small doses of sedative drugs or low breath alcohol concentrations.

A method to assess sleepiness objectively has been developed, however. This method conceptually is based on an observation originating in the 19th century that as sleep loss progresses over time, people increasingly experience uncontrollable brief naps or microsleeps (Patrick and Gilbert 1896). …


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