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Volume 66, Issue 2, Pages 177-184 (15 July 2009)


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The Impact of Alcoholism on Sleep Evoked Δ Frequency Responses

Ian M. ColrainabCorresponding Author Informationemail address, Kate E. Crowleyc, Christian L. Nicholasb, Mayra Padillaa, Fiona C. Bakerad

Received 19 August 2008; received in revised form 16 September 2008; accepted 4 October 2008. published online 08 December 2008.

Background

K-complexes (KCs) are evoked δ frequency electroencephalogram (EEG) responses during sleep that occur when large numbers of healthy cortical cells burst fire in a synchronized manner. The KC amplitude and incidence are sensitive measures of normal healthy brain aging. Given the known neurodegenerative consequences of alcohol abuse it was hypothesized that alcoholism would be associated with further KC amplitude and incidence reductions.

Methods

Eighty-four subjects (42 alcoholics) screened for medical, psychiatric, and sleep problems participated. The protocol involved the presentation of auditory stimuli during stage 2 sleep throughout a night in the laboratory. The KCs were identified and averaged, to enable measurement of the P2, N550, and P900 peaks.

Results

Compared with control subjects, alcoholic men and women had lower KC incidence (p < .001) and P2 (p < .001), N550 (p < .05), and P900 (p < .05) amplitudes. There was a significant diagnosis × site interaction (p < .001), indicating the group difference was largest at frontal sites. Longer sobriety correlated with increased N550 amplitude (p < .01).

Conclusions

The KC incidence and amplitude were negatively impacted in alcoholic men and women with exacerbation of the normal aging effects, particularly over frontal scalp regions. The observed relationship between improvements in KC measures and increased time of abstinence suggests that these measures might provide a useful marker of brain recovery with continued abstinence from alcohol.

a Center for Health Sciences, SRI International, Menlo Park, California

b Department of Psychology, The University of Melbourne, Parkville, Australia

c Optalert, Richmond, Victoria, Australia

d Brain Function Research Unit, School of Physiology, University of the Witwatersrand, Johannesburg, South Africa

Corresponding Author InformationAddress reprint requests to Ian M. Colrain, Ph.D., SRI International, 333 Ravenswood Ave., Menlo Park, CA, 94025

PII: S0006-3223(08)01239-0

doi:10.1016/j.biopsych.2008.10.010


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