Experimental Sleep Restriction Facilitates Pain and Electrically Induced Cortical Responses

Abstract

Study objectives: Sleep restriction (SR) has been hypothesized to sensitize the pain system. The current study determined whether experimental sleep restriction had an effect on experimentally induced pain and pain-elicited electroencephalographic (EEG) responses.

Design: A paired crossover study.

Intervention: Pain testing was performed after 2 nights of 50% SR and after 2 nights with habitual sleep (HS).

Setting: Laboratory experiment at research center.

Participants: Self-reported healthy volunteers (n = 21, age range: 18-31 y).

Measurements and results: Brief high-density electrical stimuli to the forearm skin produced pinprick-like pain. Subjective pain ratings increased after SR, but only in response to the highest stimulus intensity (P = 0.018). SR increased the magnitude of the pain-elicited EEG response analyzed in the time-frequency domain (P = 0.021). Habituation across blocks did not differ between HS and SR. Event-related desynchronization (ERD) was reduced after SR (P = 0.039). Pressure pain threshold of the trapezius muscle region also decreased after SR (P = 0.017).

Conclusion: Sleep restriction (SR) increased the sensitivity to pressure pain and to electrically induced pain of moderate, but not low, intensity. The increased electrical pain could not be explained by a difference in habituation. Increased response magnitude is possibly related to reduced processing within the somatosensory cortex after partial SR.

Keywords: EEG; event-related desynchronization (ERD); event-related potential (ERP); pain; pressure pain threshold (PPT); time-frequency analysis.

Figure 1

Group-level average event-related potentials elicited by high-density electrical stimulation. (A) Group-level average N2P2 potential after habitual sleep, (HS, black) and sleep restriction (SR, red) in the time domain. (B) Group-level average time-frequency representation of pain-elicited modulation of electroencephalographic oscillation magnitude (ER%). The color scale represents average increase or decrease of oscillation magnitude relative to a prestimulus reference interval (−0.9 to −0.1 sec) before the electrical stimulus. Statistically defined regions of interest (ROI) used in the time-frequency analysis are shown in yellow. Responses are from recording position Cz, referenced to linked mastoid (A1A2). ERD, event-related desynchronization; α-ERD, ERD in the α-frequency range; β-ERD, ERD in the β-frequency range; ‘ERP,’ event-related potential ROI; ERS, event-related synchronization.

Figure 2

Changes in pain. (A) Mean pain intensity increased with stimulus intensity (**P < 0.001) and showed an interaction with sleep condition (P = 0.022). Post hoc analysis showed that pain ratings were higher after sleep restriction (SR) versus after habitual sleep (HS) for stimulus intensity C (**P = 0.018, Bonferroni corrected). (B) Mean pain intensity decreased with stimulus block (**P = 0.004), but the decrease did not change between sleep conditions (P = 0.99). Values are mean ± standard error of the mean. NRS, numerical rating scale; HS, habitual sleep; SR, sleep restriction.

Figure 3

Changes in N2P2 amplitude. (A) Average N2P2 amplitude by sleep condition and electrode. There was no difference in amplitude after 2 nights of habitual sleep versus after 2 nights with 50 % sleep restriction at any of the recording electrodes (Cz, Cc; P > 0.69). (B) N2P2 amplitude did not change with stimulus intensity (P = 0.48, main effect) and there was no sleep × intensity interaction (P = 0.66). (C) N2P2 amplitude habituated across stimulus blocks (P < 0.001, main effect), but the degree of habituation was not different between sleep conditions (P = 0.63, sleep × block interaction). Values are mean ± standard error of the mean. HS, habitual sleep; SR, sleep restriction.

Figure 4

Changes in ‘ERP’ magnitude. (A) Average event-related synchronization (in % of the pre-stimulus reference interval) by sleep condition and electrode. At electrode Cc the magnitude was significantly larger after SR versus after habitual sleep, *P = 0.021. There was no sleep related differences at electrode Cz (P = 0.56). (B) ‘ERP’ magnitude increased with stimulus intensity (*P = 0.045), but there was no sleep × intensity interaction (P = 0.35). (C) The ‘ERP’ response habituated with stimulus block (**P < 0.001), but there was no sleep × block interaction (P = 0.68). Values are mean ± standard error of the mean. ‘ERP’, event-related potential in time-frequency domain; HS, habitual sleep; SR, sleep restriction.

Figure 5

Changes in α-ERD magnitude. (A) Average event-related desynchronization (in % of the pre-stimulus reference interval) by sleep condition and electrode. α-ERD at electrode Cc was significantly weaker in magnitude after sleep restriction (*P = 0.039). (B) α-ERD magnitude increased with stimulus intensity (**P < 0.001), but no sleep × intensity interaction (P = 0.50). (C) α-ERD habituated with stimulus block (**P < 0.001), but no sleep × block interaction (P = 0.84). Values are mean ± standard error of the mean. ERD, event-related desynchronization; HS, habitual sleep; SR, sleep restriction.