From Clinical Neurophysiology, 10 January 2015 (published online before print),
Slow wave sleep in the chronically fatigued: power spectra distribution patterns in chronic fatigue syndrome and primary insomnia
Daniel Neu (1,2,*), Olivier Mairesse(1,2,3,4,*), Paul Verbanck(1,2), Olivier Le Bon (2,5)/
1) Brugmann University Hospital, Sleep Laboratory & Unit for Chronobiology U78, Université Libre de Bruxelles (U.L.B), Brussels, Belgium
2) UNI, ULB Neurosciences Institute, Faculty of Medicine, Laboratory for Medical Psychology ULB312, Université Libre de Bruxelles (U.L.B.), Brussels, Belgium
3) Department of Experimental and Applied Psychology (EXTO), Vrije Universiteit Brussel (V.U.B.), Brussels, Belgium
4) Royal Military Academy, Department LIFE, Brussels, Belgium
5) Tivoli University Hospital, Department of Psychiatry, U.L.B., La Louvière, Belgium
* Both authors contributed equally to this work)
Corresponding authors. Address: Université Libre de Bruxelles – Brugmann University Hospital, Sleep Laboratory & Unit for Chronobiology U78, 4, Arthur Van Gehuchten Square – Building Hh, 1020 Brussels, Belgium. Tel.: +32 24772554; fax: +32 24772162.
• Evidence for similarly lower central ultra slow (US) delta power (0.3-0.79 Hz) proportions during slow wave sleep (SWS) in both primary insomnia and chronic fatigue syndrome in comparison to controls.
• Lower US power proportions relate mainly to perceived sleep quality impairment and daytime fatigue intensity.
• Clinical distinction between both conditions relates to a different frontal EEG power distribution during SWS in primary insomnia.
To investigate slow wave sleep (SWS) spectral power proportions in distinct clinical conditions sharing non-restorative sleep and fatigue complaints without excessive daytime sleepiness (EDS), namely the Chronic Fatigue Syndrome (CFS) and Primary Insomnia (PI). Impaired sleep homeostasis has been suspected in both CFS and PI.
We compared perceived sleep quality, fatigue and sleepiness symptom-intensities, polysomnography (PSG) and SWS spectral power distributions of drug-free CFS and PI patients without comorbid sleep or mental disorders, with a good sleeper control group.
Higher fatigue without EDS and impaired perceived sleep quality were confirmed in both patient groups. PSG mainly differed in sleep fragmentation and SWS durations. Spectral analysis revealed a similar decrease in central ultra slow power (0.3-0.79Hz) proportion during SWS for both CFS and PI and an increase in frontal power proportions of faster frequencies during SWS in PI only. The latter was correlated to affective symptoms whereas lower central ultra slow power proportions were related to fatigue severity and sleep quality impairment.
In combination with normal (PI) or even increased SWS durations (CFS), we found consistent evidence for lower proportions of slow oscillations during SWS in PI and CFS.
Observing normal or increased SWS durations but lower proportions of ultra slow power, our findings suggest a possible quantitative compensation of altered homeostatic regulation.