Alcohol and the sleeping brain

Abstract

Alcohol acts as a sedative that interacts with several neurotransmitter systems important in the regulation of sleep. Acute administration of large amounts of alcohol prior to sleep leads to decreased sleep-onset latency and changes in sleep architecture early in the night, when blood alcohol levels are high, with subsequent disrupted, poor-quality sleep later in the night. Alcohol abuse and dependence are associated with chronic sleep disturbance, lower slow-wave sleep, and more rapid-eye-movement sleep than normal, that last long into periods of abstinence and may play a role in relapse. This chapter outlines the evidence for acute and chronic alcohol effects on sleep architecture and sleep electroencephalogram, evidence for tolerance with repeated administration, and possible underlying neurochemical mechanisms for alcohol's effects on sleep. Also discussed are sex differences as well as effects of alcohol on sleep homeostasis and circadian regulation. Evidence for the role of sleep disruption as a risk factor for developing alcohol dependence is discussed in the context of research conducted in adolescents. The utility of sleep-evoked potentials in the assessment of the effects of alcoholism on sleep and the brain and in abstinence-mediated recovery is also outlined. The chapter concludes with a series of questions that need to be answered to determine the role of sleep and sleep disturbance in the development and maintenance of problem drinking and the potential beneficial effects of the treatment of sleep disorders for maintenance of abstinence in alcoholism.

Keywords: REM; acute alcohol K-complex; alcoholism; slow-wave sleep.

Figure 1

The percentage of (A) slow wave sleep (SWS) and (B) rapid eye movement (REM) sleep in the first half of the night across multiple nights of drinking. Data are drawn from (Feige et al. 2006; Prinz et al. 1980; Rundell et al. 1972).

Figure 2

The percentage of the night spent in different sleep stages (Rechtschaffen and Kales 1968) in men and women with alcohol dependence and sex-matched control. Data are dawn from (Colrain, Turlington, and Baker 2009b).

Figure 3

Figure 1: All-night NREM sleep slow wave activity (; 0.3 – <4 Hz) at Fz (upper panel) and O2 (lower panel) for 34 alcoholics (21 men) and 41 controls (18 men). Values are averaged within the 0.3–1 Hz bin, and within each 1-Hz frequency bin thereafter. Bins are identified by their lower boundary. Data are dawn from (Colrain, Turlington, and Baker 2009b).

Figure 4

Examples of averaged evoked responses from stage 2 NREM sleep. The left panel (KC+) shows the result of averaging responses that included K-complexes. The right panel (KC-) show the result of averaging responses not including K-complexes. Waveforms are presented from Fz, FCz, Cz, CPz and Pz.

Figure 5

Grand mean evoked potential waveforms for alcoholics (red lines) and control subjects (black lines) for the FP1, Fz, FCz and Cz electrode sites. Data are presented with negative voltages up the Y axis. Data are drawn from (Colrain et al. 2009).

Figure 6

A structural model of rapid eye movement (REM) sleep control highlighting the role of GABAergic interneurons (McCarley 2011). LDT, laterodorsal tegmental nucleus; PPT, pedunculopontine tegmental nucleus; RF, reticular formation; GABA, gamma-aminobutyric acid; NE, norepinephrine.

Figure 7

Grand mean evoked potential waveforms for alcoholics at initial assessment(redlines) and at 12 month follow-up (blue lines) Fz, FCz, Cz, CPz and Pz. Data are presented with negative voltages up the Y axis. Data are drawn from (Colrain, Padilla, and Baker 2012).