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Abstract

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.
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.

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Published In

Neurology®
Volume 74Number 21May 25, 2010
Pages: 1732-1738
PubMed: 20498441

Publication History

Published online: May 24, 2010
Published in print: May 25, 2010

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Affiliations & Disclosures

J.A. Shekleton, BBNSc (Hons)
From the School of Psychology and Psychiatry (J.A.S., D.L.P., J.R.R., J.P.-N., J.L.P., S.M.W.R.), Monash University, Victoria; and Monash-Epworth Rehabilitation Research Centre (J.L.P.), Epworth Hospital, Victoria, Australia.
D.L. Parcell, DPsych
From the School of Psychology and Psychiatry (J.A.S., D.L.P., J.R.R., J.P.-N., J.L.P., S.M.W.R.), Monash University, Victoria; and Monash-Epworth Rehabilitation Research Centre (J.L.P.), Epworth Hospital, Victoria, Australia.
J.R. Redman, PhD
From the School of Psychology and Psychiatry (J.A.S., D.L.P., J.R.R., J.P.-N., J.L.P., S.M.W.R.), Monash University, Victoria; and Monash-Epworth Rehabilitation Research Centre (J.L.P.), Epworth Hospital, Victoria, Australia.
J. Phipps-Nelson, BBSc (Hons)
From the School of Psychology and Psychiatry (J.A.S., D.L.P., J.R.R., J.P.-N., J.L.P., S.M.W.R.), Monash University, Victoria; and Monash-Epworth Rehabilitation Research Centre (J.L.P.), Epworth Hospital, Victoria, Australia.
J.L. Ponsford, PhD
From the School of Psychology and Psychiatry (J.A.S., D.L.P., J.R.R., J.P.-N., J.L.P., S.M.W.R.), Monash University, Victoria; and Monash-Epworth Rehabilitation Research Centre (J.L.P.), Epworth Hospital, Victoria, Australia.
S.M.W. Rajaratnam, PhD
From the School of Psychology and Psychiatry (J.A.S., D.L.P., J.R.R., J.P.-N., J.L.P., S.M.W.R.), Monash University, Victoria; and Monash-Epworth Rehabilitation Research Centre (J.L.P.), Epworth Hospital, Victoria, Australia.

Notes

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

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