Shift work and pain : a quantitative EEG investigation into the effects of shift work and nocebo on pain perception
Master thesis
Permanent lenke
http://hdl.handle.net/11250/2437125Utgivelsesdato
2016Metadata
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Sammendrag
Introduction: Shift work is associated with increased prevalence of pain and shift workers commonly report reduced sleep, which is related to increased pain sensitivity. Thus, night shift work (NSW) may potentially lead to increased pain sensitivity. This study investigates electroencephalogram (EEG) recordings in response to nociceptive electrical stimuli following NSW and habitual sleep (HS) with and without negative expectation (nocebo).
Methods: 53 nurses participated in the study. They received nociceptive electrical stimuli following NSW and HS that were either correctly signalled or signalled as higher than the actual intensity delivered (in the case of nocebo). Pain scores were recorded using a visual analogue scale (1-10). EEG measurements were recorded from 32 electrodes and analysed in the time-frequency domain using Analyzer, EEGlab and Matlab. Linear Mixed Models in SPSS was used for statistical analysis.
Results: Following NSW, the participants exhibited increased event-related synchronisation (ERS) in response to nociceptive stimuli in the 1-400 ms/1-25 Hz, post stimulus interval across several electrodes, which was significant at p < 0.05 level. Nocebo was significantly associated with lower ERS magnitude than correctly signalled stimuli (p < 0.05). Finally, there was a significant effect of NSW and nocebo on pain scores (p < 0.05), in which the participants rated the electrical stimuli as more painful following NSW and nocebo, however, nocebo was not facilitated by NSW (p = 0.438).
Conclusion: NSW leads to sleep induced hyperalgesia accompanied by increased ERS across several electrodes following exposure to nociceptive electrical stimuli. There is also hyperalgesia in response to nocebo, which is accompanied by reduced ERS compared to correctly signalled stimuli. However, the present study does not find support for nocebo as a principal underlying factor in SIH, but rather, SIH and NIH appear to stem from cortical processes that do not overlap.