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Link to original content: http://www.ncbi.nlm.nih.gov/pubmed/21397252
Antidepressant effects of selective slow wave sleep deprivation in major depression: a high-density EEG investigation - PubMed Skip to main page content
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Clinical Trial
. 2011 Aug;45(8):1019-26.
doi: 10.1016/j.jpsychires.2011.02.003. Epub 2011 Mar 11.

Antidepressant effects of selective slow wave sleep deprivation in major depression: a high-density EEG investigation

Affiliations
Clinical Trial

Antidepressant effects of selective slow wave sleep deprivation in major depression: a high-density EEG investigation

Eric C Landsness et al. J Psychiatr Res. 2011 Aug.

Abstract

Sleep deprivation can acutely reverse depressive symptoms in some patients with major depression. Because abnormalities in slow wave sleep are one of the most consistent biological markers of depression, it is plausible that the antidepressant effects of sleep deprivation are due to the effects on slow wave homeostasis. This study tested the prediction that selectively reducing slow waves during sleep (slow wave deprivation; SWD), without disrupting total sleep time, will lead to an acute reduction in depressive symptomatology. As part of a multi-night, cross-over design study, participants with major depression (non-medicated; n = 17) underwent baseline, SWD, and recovery sleep sessions, and were recorded with high-density EEG (hdEEG). During SWD, acoustic stimuli were played to suppress subsequent slow waves, without waking up the participant. The effects of SWD on depressive symptoms were assessed with both self-rated and researcher-administered scales. Participants experienced a significant decrease in depressive symptoms according to both self-rated (p = .007) and researcher-administered (p = .010) scales, while vigilance was unaffected. The reduction in depressive symptoms correlated with the overnight dissipation of fronto-central slow wave activity (SWA) on baseline sleep, the rebound in right frontal all-night SWA on recovery sleep, and the amount of REM sleep on the SWD night. In addition to highlighting the benefits of hdEEG in detecting regional changes in brain activity, these findings suggest that SWD may help to better understand the pathophysiology of depression and may be a useful tool for the neuromodulatory reversal of depressive symptomatology.

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Conflict of interest statement

Conflict of interest statement

Dr. Peterson has received unrelated research support from Sanofi-Aventis. Dr. Tononi has consulted for Sanofi-Aventis and Takeda, and he is currently the David P. White Chair in Sleep Medicine at the University of Wisconsin – Madison, endowed by Phillips Respironics. Dr. Tononi has also received unrelated research support from Phillips Respironics. Dr. Benca has consulted for Merck and Sanofi-Aventis. The other authors have indicated no financial conflicts of interest.

Figures

Figure 1
Figure 1
Global SWA time course across the night for baseline (BSL), slow wave deprivation (SWD), and recovery (RCV) nights. Artifact-free NREM epochs for each night were divided into quintiles. Inset: comparison of SWA dissipation across the entire night for BSL, SWD, and RCV, expressed as the first quintile (Q1) minus the last quintile (Q5).
Figure 2
Figure 2
Impact of slow wave deprivation (SWD) on the (A) modified Inventory of Depressive Symptomatology, self-rated (mIDS-SR) and (C) Hamilton Rating Scale for Depression (HRSD-13) scores. (B) The amount of REM sleep obtained during the treatment correlates with the antidepressant response (displayed with 95% confidence regression bands), but (D) initial severity of depression does not predict level of response.
Figure 3
Figure 3
Topographic correlation of antidepressant response (via mIDS-SR) with (A) dissipation of SWA across the baseline (BSL) night (high sleep pressure – low sleep pressure, expressed as a percentage of SWA averaged across the entire night) and (B) all-night SWA rebound on RCV (relative to BSL). (C–D) Frequency-specific correlations are shown for the central channel in the cluster (white dot) of each SWA measure.

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References

    1. Aeschbach D, Cutler AJ, Ronda JM. A role for non-rapid-eye-movement sleep homeostasis in perceptual learning. J Neurosci. 2008;28:2766–2772. - PMC - PubMed
    1. American Psychiatric Association., & American Psychiatric Association. Task Force on DSM-IV. Diagnostic and statistical manual of mental disorders : DSM-IV-TR. 4th ed. Washington, DC: American Psychiatric Association; 2000.
    1. Benca R, Obermeyer W, Thisted R, Gillin J. Sleep and psychiatric disorders. A meta-analysis. Arch Gen Psychiatry. 1992;49:651–668. discussion 669-70. - PubMed
    1. Benedetti F, Smeraldi E. Neuroimaging and genetics of antidepressant response to sleep deprivation: implications for drug development. Curr Pharm Des. 2009;15:2637–2649. - PubMed
    1. Borbély A. The S-deficiency hypothesis of depression and the two-process model of sleep regulation. Pharmacopsychiatry. 1987;20:23–29. - PubMed

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