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The online version of this article, along with updated information and services, is located on the World Wide Web at: http://www.neurology.org/cgi/content/full/74/21/1732
Neurology® is the official journal of the American Academy of Neurology. Published continuously since 1951, it is now a weekly with 48 issues per year. Copyright © 2010 by AAN Enterprises, Inc. All rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X.
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Sleep disturbance and melatonin levels following traumatic brain injury
J.A. Shekleton, BBNSc (Hons) D.L. Parcell, DPsych J.R. Redman, PhD J. Phipps-Nelson, BBSc (Hons) J.L. Ponsford, PhD S.M.W. Rajaratnam, PhD
Objectives: Sleep disturbances commonly follow traumatic brain injury (TBI) and contribute to ongoing disability. However, there are no conclusive findings regarding specific changes to sleep quality and sleep architecture measured using polysomnography. Possible causes of the sleep disturbances include disruption of circadian regulation of sleep-wakefulness, psychological distress, and a neuronal response to injury. We investigated sleep-wake disturbances and their underlying mechanisms in a TBI patient sample.
Methods: This was an observational study comparing 23 patients with TBI (429.7 287.6 days post injury) and 23 age- and gender-matched healthy volunteers on polysomnographic sleep measures, salivary dim light melatonin onset (DLMO) time, and self-reported sleep quality, anxiety, and depression. Results: Patients with TBI reported higher anxiety and depressive symptoms and sleep disturbance than controls. Patients with TBI showed decreased sleep efficiency (SE) and increased wake after sleep onset (WASO). Although no significant group differences were found in sleep architecture, when anxiety and depression scores were controlled, patients with TBI showed higher amount of slow wave sleep. No differences in self-reported sleep timing or salivary DLMO time were found. However, patients with TBI showed significantly lower levels of evening melatonin production. Melatonin level was significantly correlated with REM sleep but not SE or WASO.
Address correspondence and reprint requests to Dr. Shantha M.W. Rajaratnam, School of Psychology and Psychiatry, Monash University, Building 17, Clayton Campus, Victoria 3800, Australia
Conclusions: Reduced evening melatonin production may indicate disruption to circadian regulation of melatonin synthesis. The results suggest that there are at least 2 factors contributing to sleep disturbances in patients with traumatic brain injury. We propose that elevated depression is associated with reduced sleep quality, and increased slow wave sleep is attributed to the effects of mechanical brain damage. Neurology® 2010;74:1732–1738 GLOSSARY
AUC area under the curve; DLMO dim light melatonin onset; EOG electrooculogram; ESS Epworth Sleepiness Scale; HADS Hospital Anxiety and Depression Scale; MEQ Morningness Eveningness Questionnaire; NREM non-REM; PSQI Pittsburgh Sleep Quality Index; PTA posttraumatic amnesia; SE sleep efficiency; SOL sleep onset latency; SWS slow wave sleep; TBI traumatic brain injury; WASO wake after sleep onset.
Supplemental data at www.neurology.org
Sleep disturbances are common following traumatic brain injury (TBI), reported by 30%–75% of individuals and contributing to ongoing disability.1-6 Reported sleep complaints include insomnia, hypersomnolence, and altered sleep-wake cycles.7 Understanding of changes to sleep following TBI is limited. Reduced sleep efficiency8 and increased sleep fragmentation post-TBI9-11 have been reported. Some studies have shown...