Key result
Chronic pain patients had significantly lower peak alpha frequency and higher alpha/theta and alpha/beta power ratios at rest compared to healthy controls (p < 0.0002).
Why the study?
Central sensitization in chronic pain is clinically detected using subjective measures, creating a need for reliable, direct neural measurements of response to controlled stimuli to quantify neuronal dysfunction.
Does cortical activity recorded via EEG differ between chronic pain patients and healthy controls at rest and during objective painful stimulation?
Case-Control (n=16)
Does cortical activity recorded via EEG differ between chronic pain patients and healthy controls at rest and during objective painful stimulation?
p-value: p=<0.0002
EEG activity patterns at rest and during acute painful stimulation differ between chronic pain patients and healthy controls, suggesting potential diagnostic biomarkers for central sensitization.
EEG spectral differences in central sensitization patients during rest and QST may aid objective assessment; leaves open biomarker validation in larger prospective cohorts.
Objective. Central sensitization, or increased responsiveness of the central nervous system to sensory input, is present in many chronic pain patients. Clinically, it is detected through subjective, patient-reported measures. There is a need for reliable, direct measurements of neural response to controlled stimuli to quantify neuronal dysfunction in pain. The goal of this work is to investigate cortical activity, recorded via electroencephalogram (EEG), during objective and calibrated painful stimulation in chronic pain patients. Approach. Chronic pain patients (N = 8) and healthy controls (N = 8) participated in this study. We recorded electroencephalography (EEG) at rest (baseline) and during evoked pain tasks, including thermal and mechanical stimuli. The evoked pain was applied following the quantitative sensory testing (QST) protocol, which is a research technique that applies objective, calibrated painful stimuli. Main results. Peak alpha frequency at rest was significantly lower in chronic pain patients compared to healthy controls (p < 0.0002), while EEG alpha/theta and alpha/beta power ratios at rest were higher in patients (p < 0.0002). During thermal QST, these power ratios decreased in patients and increased in controls (p < 0.0002 for both). During mechanical QST, power ratios decreased or did not change. Furthermore, the peak theta–beta frequency difference at baseline was significantly lower in patients compared to controls (p < 0.0002). During thermal QST, this difference increased in patients and decreased in controls; during mechanical QST, this difference increased in both patients and controls (p < 0.0002). Functional connectivity analysis showed that controls had greater baseline theta connectivity strength that increased during mechanical QST (p < 0.0002). Significance. This work demonstrates differential patterns of EEG activity at rest and during acute painful stimulation in chronic pain patients compared to healthy controls. These measures may quantify an individual’s tendency to experience chronic pain and central sensitization and serve as diagnostic biomarkers.
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Ding et al. (2024) conducted a case-control in Chronic pain (n=16). Chronic pain vs. Healthy controls was evaluated on Peak alpha frequency at rest (p=<0.0002). Chronic pain patients had significantly lower peak alpha frequency and higher alpha/theta and alpha/beta power ratios at rest compared to healthy controls (p < 0.0002).
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