Sleep architecture as correlate and predictor of symptoms and impairment in inter-episode bipolar disorder: taking on the challenge of medication effects
- PMID: 20408930
- PMCID: PMC2965266
- DOI: 10.1111/j.1365-2869.2010.00826.x
Sleep architecture as correlate and predictor of symptoms and impairment in inter-episode bipolar disorder: taking on the challenge of medication effects
Abstract
This study was designed to clarify the association between inter-episode bipolar disorder (BD) and sleep architecture. Participants completed a baseline symptom and sleep assessment and, 3 months later, an assessment of symptoms and impairment. The effects of psychiatric medications on sleep architecture were also considered. Participants included 22 adults with BD I or II (inter-episode) and 22 non-psychiatric controls. The sleep assessment was conducted at the Sleep and Psychological Disorders Laboratory at the University of California, Berkeley. Follow-up assessments 3 months later were conducted over the phone. Results indicate that, at the sleep assessment, BD participants exhibited greater rapid eye movement sleep (REM) density than control participants with no other group differences in sleep architecture. Sleep architecture was not correlated with concurrent mood symptoms in either group. In the BD group, duration of the first REM period and slow-wave sleep (SWS) amount were positively correlated with manic symptoms and impairment at 3 months, while REM density was positively correlated with depressive symptoms and impairment at 3 months. The amount of Stage 2 sleep was negatively correlated with manic symptoms and impairment at 3 months. In contrast, for the control group, REM density was negatively correlated with impairment at 3 months. SWS and Stage 2 sleep were not correlated with symptoms or impairment. Study findings suggest that inter-episode REM sleep, SWS and Stage 2 sleep are correlated with future manic and depressive symptoms and impairment in BD. This is consistent with the proposition that sleep architecture may be a mechanism of illness maintenance in BD.
© 2010 European Sleep Research Society.
Conflict of interest statement
Disclosure: Dr. Harvey is a consultant to Actelion Pharmaceuticals and a speaker for Sanofi-aventis and the Sleep Medicine Education Institute. All other authors declare that they have no conflicts of interest. Funding for this study was provided by NARSAD (AGH).
References
-
- Bastien CH, LeBlanc M, Carrier J, Morin CM. Sleep EEG power spectra, insomnia, and chronic use of benzodiazepines. Sleep. 2003;26:313–317. - PubMed
-
- Benca RM, Obermeyer WH, Thisted RA, Gillin C. Sleep and psychiatric disorders: A meta-analysis. Arch Gen Psychiatry. 1992;49:651–668. - PubMed
-
- Borbely AA. A two process model of sleep regulation. Human Neurobiology. 1982;1:195–204. - PubMed
-
- Borbely AA. The S-deficiency hypothesis of depression and the two-process model of sleep regulation. Pharmacopsychiatry. 1987;20:23–29. - PubMed
-
- Brunner DP, Dijk DJ, Borbely AA. Repeated partial sleep deprivation progressively changes the EEG during sleep and wakefulness. Sleep. 1993;16:100–113. - PubMed