Sleep EEG as a potential marker of alcoholism predisposition-commentary on "Adolescence and parental history of alcoholism: insights from the sleep EEG".

THE PAPER BY Tarokh and colleagues (2012) in the current issue of ACER provides the first longitudinal investigation of sleep architecture in normal healthy children and adolescents who are family history positive for alcoholism compared with those who are family history negative. The longitudinal design permits assessment of the impact of familial predisposition on developmental trajectories. Even with only two time points, the design informs the question of whether differences predate onset of alcohol use disorders, and when alcoholism-related deviations from normal development emerge. Alcoholism has a significant familial component with data from numerous sources, indicating that it has a genetic predisposition. Starting in the 1980s (Begleiter et al., 1984), investigators have evaluated the hypothesis that observed differences between adult alcoholics and controls in awake electroencephalogram (EEG) measures (e.g., P300) possibly reflected genetic predisposition rather than, or in addition to, the consequence of alcohol abuse. This literature has revealed that alcohol-naı̈ve children of alcoholics are likely to show some of the deficits in EEG that had previously been assumed to be the consequences of alcohol abuse (Ehlers et al., 2003). Recent data from the Consortium on Genetics of Alcoholism have identified theta and delta frequency differences during wakefulness as an endophenotype of alcoholism susceptibility (Rangaswamy et al., 2007). Sleep quality and sleep EEG show reliable differences between adult alcoholics and controls, with alcoholics typically showing poorer-quality sleep and altered EEG during sleep. An unusual but reliable finding in this context is evidence for greater amount, proportion, or intensity of rapid eye movement (REM) sleep in alcoholics compared with controls (Gillin et al., 1990). Previously (Colrain et al., 2009), we suggested that determination of whether more REM sleep in abstinent alcoholics represents a predisposition to altered sleep rather than a consequence of alcohol abuse would require careful study of sleep in those with a genetic familial risk of alcoholism along the lines of the investigations conducted in wake EEG and evoked potentials (Porjesz et al., 2005). While it does not address genetics directly, the study by Tarokh and colleagues (2012) provides evidence that a familial predisposition is not associated with greater REM sleep, suggesting that increased REM sleep is more likely to be a consequence of alcohol abuse. Another commonly reported finding in the sleep of adult alcoholics is deficient slow-wave sleep (SWS; Benca et al., 1992), which has also been shown to be a predictor of relapse (Brower, 2003). Spectral analysis of the EEG during nonrapid eye movement (NREM) sleep reveals alcoholics to have significantly less delta power in the first NREM period (Armitage et al., 2012) or across the entire night (Armitage et al., 2012; Colrain et al., 2009; Irwin et al., 2002). The study of sleep EEG is important and challenging in children and adolescents. SWS shows marked reduction of approximately 40% during the second decade of life (Carskadon, 1982). Quantitative analysis of the sleep EEG has provided a more detailed description of the changes in sleep across adolescence with an emphasis on changes in the characteristics of slow waves. Cross-sectional studies have reported a dramatic decrease in slow-wave (delta) activity (Feinberg et al., 2006), slow-wave amplitude, and slope of slow waves (Kurth et al., 2010), across adolescence. Recent longitudinal studies of adolescents across the age range of 9 to 18 years have confirmed the decline in delta power during NREM sleep and provided further insight into the timing of maturational development in adolescence (Campbell and Feinberg, 2009; Tarokh et al., 2011). Delta power is maintained between the age of 9 and 11 years, followed by a steep decline of about 66% beginning between the age of 11 and 12 years (about 15% per year; Campbell and Feinberg, 2009; Feinberg et al., 2012). It has been hypothesized (Feinberg, 1982) that the decline in NREM EEG power across adolescence is driven by the decrease in synaptic density or “pruning” and represents a process of brain maturation during adolescence. Support for this hypothesis has recently From the Human Sleep Research Program (IMC, FCB), SRI International, Menlo Park, California; Department of Psychological Sciences (IMC), University of Melbourne, Parkville, Victoria, Australia; and Brain Function Research Group (FCB), School of Physiology, University of the Witwatersrand, Johannesburg, South Africa. Received for publicationMay 11, 2012; accepted May 23, 2012.  IanM. Colrain PhD, SRI International, 333 Ravenswood Avenue, Menlo Park, CA, 94025; Tel.: 650-859-3915; Fax: 650-859-2743;  ian.colrain@sri.com

Field of study: Medicine