206 Figure 2. Complexity of neuronal oscillations at baseline predicts pain response to nocebo treatment. Spatial topographies show Spearman’s rank correlation coefficient values (rho) of magnitude of nocebo hyperalgesia and EEG measures (n = 33). Magnitude of nocebo hyperalgesia was defined as the difference between mean pain response of all nocebo trials and all control trials during the evocation phase, per individual. Top row shows the association between magnitude of nocebo hyperalgesia and EEG parameters for the difference condition ECRPOST – ECRPRE. Bottom row shows the correlation of nocebo hyperalgesia with EEG condition ECRPRE. (a-c) Magnitude of nocebo hyperalgesia was negatively associated with DFA within beta and gamma bands. (d-f) Individuals with high DFA beta and gamma at baseline (ECRPRE) show a larger nocebo effect during evocation. Red colors indicate positive correlations, whereas blue colors indicate negative correlations. Open white circles show statistical significance at P < .05. Closed white circles indicate significance after correcting for multiple comparisons using a False Discovery Rate procedure (FDR) with q = 0.05, per topography. Nocebo conditioning suppresses power of alpha and beta oscillations Next, we assessed whether parameters of resting-state EEG are altered during nocebo acquisition. To this end, non-parametric paired Wilcoxon signed-rank tests were conducted to compare differences in power and DFA between nocebo and control trials during the induction phase of the study (Fig. 3a-c; Table 1). Relative power of alpha oscillations was significantly lower during nocebo compared to control trials, in particular above parietal and occipital regions (Electrode PO3, Z = 2.73, p = 0.0064) (Fig. 3d). Relative power beta was significantly lower during nocebo than during control trials above central regions (Electrode Cz,
RkJQdWJsaXNoZXIy MTk4NDMw