Background: Patients with chronic fatigue syndrome (CFS) and chronic whiplash associated disorders (cWAD) present a reduced ability to activate central descending nociceptive inhibition after exercise, compared to measurements before exercise. It was hypothesised that a dysfunctional motor-induced inhibition of nociception partly explains this dysfunctional exercise-induced hypoalgesia. This study investigates if engagement of the motor system during movement preparation inhibits nociception-evoked brain responses in these patients as compared to healthy controls (HC).

Methods: The experiment used laser-evoked potentials (LEPs) during three conditions (no task, mental task, movement preparation) while recording brain activity with a 32-channel electroencephalogram in 21 patients with cWAD, 20 patients with CFS and 18 HC. Two-factor mixed design Analysis of variance were used to evaluate differences in LEP amplitudes and latencies.

Results: No differences in N1, N2, N2P2, and P2 LEP amplitudes were found between the HC, CFS, and cWAD groups. After nociceptive stimulation, N1, N2 (only at hand location), N2P2, and P2 LEP amplitudes significantly decreased during movement preparation compared to no task (within group differences).

Conclusion: Movement preparation induces a similar attenuation of LEPs in patients with CFS, patients with cWAD and HC. These findings do not support reduced motor-induced nociceptive inhibition in these patients.

Objective: Laser-evoked potentials (LEPs) are among the reliable neurophysiological tools to investigate patients with neuropathic pain, as they can provide an objective account of the functional status of thermo-nociceptive pathways. The goal of this study was to explore the functioning of the nociceptive afferent pathways by examining LEPs in patients with chronic whiplash-associated disorders (cWAD), patients with chronic fatigue syndrome (CFS), and healthy controls (HCs).

Design: Case-control study.

Setting: A single medical center in Belgium.

Subjects: The LEPs of 21 patients with cWAD, 19 patients with CFS, and 18 HCs were analyzed in this study.

Methods: All participants received brief nociceptive CO2 laser stimuli applied to the dorsum of the left hand and left foot while brain activity was recorded with a 32-channel electroencephalogram (EEG). LEP signals and transient power modulations were compared between patient groups and HCs.

Results: No between-group differences were found for stimulus intensity, which was supraliminal for Aδ fibers. The amplitudes and latencies of LEP wave components N1, N2, and P2 in patients with cWAD and CFS were statistically similar to those of HCs. There were no significant differences between the time-frequency maps of EEG oscillation amplitude between HCs and both patient populations.

Conclusions: EEG responses of heat-sensitive Aδ fibers in patients with cWAD and CFS revealed no significant differences from the responses of HCs. These findings thus do not support a state of generalized central nervous system hyperexcitability in those patients.

Introduction: Despite the worldwide increase in prevalence of chronic pain and the subsequent scientific interest, researchers studying the brain and brain mechanisms in pain patients have not yet clearly identified the exact underlying mechanisms. Quantifying the neuronal interactions in electrophysiological data could help us gain insight into the complexity of chronic pain. Therefore, the aim of this study is to examine how different underlying pain states affect the processing of nociceptive information.

Methods: Twenty healthy participants, 20 patients with non-neuropathic low back-related leg pain and 20 patients with neuropathic failed back surgery syndrome received nociceptive electrical stimulation at the right sural nerve with simultaneous electroencephalographic recordings. Dynamic Causal Modeling (DCM) was used to infer hidden neuronal states within a Bayesian framework.

Results: Pain intensity ratings and stimulus intensity of the nociceptive stimuli did not differ between groups. Compared to healthy participants, both patient groups had the same winning DCM model, with an additional forward and backward connection between the somatosensory cortex and right dorsolateral prefrontal cortex.

Discussion: The additional neuronal connection with the prefrontal cortex as seen in both pain patient groups could be a reflection of the higher attention towards pain in pain patients and might be explained by the higher levels of pain catastrophizing in these patients.

Conclusion: In contrast to the similar pain intensity ratings of an acute nociceptive electrical stimulus between pain patients and healthy participants, the brain is processing these stimuli in a different way.

Objectives: Spinal cord stimulation (SCS) is considered an effective pain-relieving treatment for patients with Failed Back Surgery Syndrome (FBSS). Despite the clinical effectiveness, it is unknown whether the altered functional connectivity in such patients, as compared to healthy persons, can be influenced by SCS. Therefore, the goal of this study is to evaluate whether brain connectivity assessed by EEG differs between baseline and SCS in patients with FBSS.

Materials and methods: Eight patients with FBSS underwent a resting-state EEG protocol before SCS, 1.5 months and 2.5 months after receiving SCS. At each frequency band, power spectrums were compared for no SCS, conventional (CON) SCS and High Dose (HD) SCS. Functional connectivity, with the aid of eConnectome was also calculated.

Results: Significant differences in the average power density spectrum over the whole scalp were observed between no SCS, CON SCS and HD SCS in delta, theta and beta frequency bands (p < 0.01). The average power spectrum for CON SCS was significantly lower than the average power spectrum for HD SCS. Marked increases in strength of the information flow between electrode pair FC3-TP9 in the beta frequency band (p = 0.006) were found in favor of HD SCS.

Conclusions: The differences in power spectrum and connectivity between the three conditions lead to the hypothesis that HD SCS differs from CON SCS on average power spectrum, suggesting that HD SCS may have a higher contribution on the excitatory bottom-up pathway.

Background: Descending nociceptive inhibitory pathways often malfunction in people with chronic pain. Conditioned pain modulation (CPM) is an experimental evaluation tool for assessing the functioning of these pathways. Spinal cord stimulation (SCS), a well-known treatment option for people with failed back surgery syndrome (FBSS), probably exerts its pain-relieving effect through a complex interplay of segmental and higher-order structures.

Objective: To the best of our knowledge, no clinical studies have thoroughly investigated the associations between SCS and CPM.

Design: This was a prospective cohort study in people with FBSS.

Methods: Seventeen people who had FBSS and were scheduled for SCS were enrolled in this study. The CPM model was evaluated at both sural nerves and was induced by electrical stimulation as the test stimulus and the cold pressor test as the conditioning stimulus.

Results: Before SCS, less than 30% of the participants with FBSS showed a CPM effect. Significant increases in the electrical detection threshold on the symptomatic side and the nonsymptomatic side were found. On the symptomatic side, no differences in the numbers of CPM responders before and after SCS could be found. On the nonsymptomatic side, more participants showed a CPM effect during SCS. Additionally, there were significant differences for CPM activation and SCS treatment.

Limitations: Limitations were the small sample size and the subjective outcome parameters in the CPM model.

Conclusions: This study revealed a bilateral effect of SCS that suggests the involvement of higher-order structures, such as the periaqueductal gray matter and rostroventromedial medulla (key regions in the descending pathways), as previously suggested by animal research.

The goal of this study was to capture the electroencephalographic signature of experimentally induced pain and pain-modulating mechanisms after painful peripheral electrical stimulation to determine one or a selected group of electrodes at a specific time point with a specific frequency range. In the first experiment, ten healthy participants were exposed to stimulation of the right median nerve while registering brain activity using 32-channel electroencephalography. Electrical stimulations were organized in four blocks of 20 stimuli with four intensities - 100%, 120%, 140%, and 160% - of the electrical pain threshold. In the second experiment, 15 healthy participants received electrical stimulation on the dominant median nerve before and during the application of a second painful stimulus. Raw data were converted into the time-frequency domain by applying a continuous wavelet transform. Separated domain information was extracted by calculating Parafac models. The results demonstrated that it is possible to capture a reproducible cortical neural response after painful electrical stimulation, more specifically at 250 milliseconds poststimulus, at the midline electrodes Cz and FCz with predominant δ-oscillations. The signature of the top-down nociceptive inhibitory mechanisms is δ-activity at 235 ms poststimulus at the prefrontal electrodes. This study presents a methodology to overcome the a priori determination of the regions of interest to analyze the brain response after painful electrical stimulation.