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The effect of sleep restriction on laser evoked potentials, thermal sensory and pain thresholds and suprathreshold pain in healthy subjects.

Research paper by Siv Steinsmo SS Ødegård, Petter Moe PM Omland, Kristian Bernhard KB Nilsen, Marit M Stjern, Gøril Bruvik GB Gravdahl, Trond T Sand

Indexed on: 13 Jan '15Published on: 13 Jan '15Published in: Clinical Neurophysiology



Abstract

Sleep restriction seems to change our experience of pain and reduce laser evoked potential (LEP) amplitudes. However, although LEP-habituation abnormalities have been described in painful conditions with comorbid sleep impairment, no study has previously measured the effect of sleep restriction on LEP-habituation, pain thresholds, and suprathreshold pain.Sixteen males and seventeen females (aged 18-31years) were randomly assigned to either two nights of delayed bedtime and four hours sleep (partial sleep deprivation) or nine hours sleep. The study subjects slept at home, and the sleep was measured with actigraphy both nights and polysomnography the last night. LEP, thermal thresholds and suprathreshold pain ratings were obtained the day before and the day after intervention. The investigator was blinded. ANOVA was used to evaluate the interaction between sleep restriction and day for each pain-related variable.LEP-amplitude decreased after sleep restriction (interaction p=0.02) compared to subjects randomized to nine hours sleep. LEP-habituation was similar in both groups. Thenar cold pain threshold decreased after sleep restriction (interaction p=0.009). Supra-threshold heat pain rating increased temporarily 10s after stimulus onset after sleep restriction (interaction p=0.01), while it did not change after nine hours sleep.Sleep restriction reduced the CNS response to pain, while some of the subjective pain measures indicated hyperalgesia.Since LEP-amplitude is known to reflect both CNS-pain-specific processing and cognitive attentive processing, our results suggest that hyperalgesia after sleep restriction might partly be caused by a reduction in cortical cognitive or perceptual mechanisms, rather than sensory amplification.