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Sleep restriction attenuates amplitudes and attentional modulation of pain-related evoked potentials, but augments pain ratings in healthy volunteers

Tiede, Wiebkea,1,2; Magerl, Waltera,*,1; Baumgärtner, Ulfa; Durrer, Bennob; Ehlert, Ulrikec; Treede, Rolf-Detlefa

doi: 10.1016/j.pain.2009.08.029
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The experiment investigated the impact of sleep restriction on pain perception and related evoked potential correlates (laser-evoked potentials, LEPs). Ten healthy subjects with good sleep quality were investigated in the morning twice, once after habitual sleep and once after partial sleep restriction. Additionally, we studied the impact of attentional focussing on pain and LEPs by directing attention to (intensity discrimination) or away from the stimulus (mental arithmetic). Laser stimuli directed to the hand dorsum were rated as 30% more painful after sleep restriction (49 ± 7 mm) than after a night of habitual sleep (38 ± 7 mm). A significant interaction between attentional focus and sleep condition suggested that attentional focusing was less distinctive under sleep restriction. Intensity discrimination was preserved. In contrast, the amplitude of the early parasylvian N1 of LEPs was significantly smaller after a night of partial sleep restriction (−36%, p < 0.05). Likewise, the amplitude of the vertex N2–P2 was significantly reduced (−34%, p < 0.01); also attentional modulation of the N2–P2 was reduced. Thus, objective (LEPs) and subjective (pain ratings) parameters of nociceptive processing were differentially modulated by partial sleep restriction. We propose, that sleep reduction leads to an impairment of activation in the ascending pathway (leading to reduced LEPs). In contradistinction, pain perception was boosted, which we attribute to lack of pain control distinct from classical descending inhibition, and thus not affecting the projection pathway. Sleep-restricted subjects exhibit reduced attentional modulation of pain stimuli and may thus have difficulties to readily attend to or disengage from pain.

aDepartment of Neurophysiology, Center for Biomedicine and Medical Technology Mannheim (CBTM), Ruprecht Karls-University Heidelberg, Medical Faculty Mannheim, Ludolf-Krehl-Strasse 13–17, 68167 Mannheim, Germany

bDepartment of General Internal Medicine, University Hospital/Inselspital, 3010 Bern, Switzerland

cDepartment of Psychology, Clinical Psychology and Psychotherapy, University of Zürich, Binzmuehlestrasse 14, 8050 Zürich, Switzerland

*Corresponding author. Address: Center for Biomedicine and Medical Technology (CBTM), University of Heidelberg, Medical Faculty Mannheim, Ludolf-Krehl-Strasse 13–17, 68167 Mannheim, Germany. Tel.: +49 621 383 9936; fax: +49 621 383 9921.

E-mail address:walter.magerl@medma.uni-heidelberg.de

1These authors contributed equally to this work.

E-mail address:walter.magerl@medma.uni-heidelberg.de

2Present address: Alan Edwards Centre for Research on Pain, Faculty of Dentistry, McGill University, Montreal, Quebec, Canada H3A2B2.

E-mail address:walter.magerl@medma.uni-heidelberg.de

Submitted October 20, 2008; revised August 12, 2009; accepted August 25, 2009.

© 2010 Lippincott Williams & Wilkins, Inc.
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