Previous studies comparing laser (LEPs) and contact heat evoked potentials (CHEPs) consistently reported higher amplitudes following laser compared to contact heat stimulation. However, none of the studies matched the perceived pain intensity, questioning if the observed difference in amplitude is due to biophysical differences between the two methods or a mismatch in stimulation intensity. The aims of the current study were twofold: (1) to directly compare the brain potentials induced by intensity matched laser and contact heat stimulation and (2) investigate how capsaicin-induced secondary hyperalgesia modulates LEPs and CHEPs. Twenty-one healthy subjects were recruited and measured at four experimental sessions: (1) CHEPs + sham, (2) LEPs + sham, (3) CHEPs + capsaicin, and (4) LEPs + capsaicin. Baseline (sham) LEPs latency was significantly shorter and amplitude significantly larger compared to CHEPs, even when matched for perceived pain. Neither CHEPs nor LEPs was sensitive enough to detect secondary hyperalgesia. These differences provide evidence that a faster heating rate results in an earlier and more synchronized LEPs than CHEPs. To our knowledge, this was the first study to match perceived intensity of contact heat and laser stimulations, revealing distinct advantages associated with the acquisition of LEPs.
Objective Widespread pain hypersensitivity and enhanced temporal summation of pain (TSP) are commonly reported in patients with complex regional pain syndrome (CRPS) and discussed as proxies for central sensitization. This study aimed to directly relate such signs of neuronal hyperexcitability to the pain phenotype of CRPS patients. Methods Twenty-one CRPS patients and 20 healthy controls (HC) were recruited. The pain phenotype including spatial pain extent (assessed in % body surface) and intensity were assessed and related to widespread pain hypersensitivity, TSP, and psychological factors. Quantitative sensory testing (QST) was performed in the affected, the contralateral and a remote (control) area. Results CRPS patients showed decreased pressure pain thresholds in all tested areas (affected: t(34)=4.98, p < 0.001, contralateral: t(35)=3.19, p = 0.005, control: t(31)=2.65, p = 0.012). Additionally, patients showed increased TSP in the affected area (F(3,111)=4.57, p = 0.009) compared to HC. TSP was even more enhanced in patients with a high compared to a low spatial pain extent (F(3,51)=5.67, p = 0.008), suggesting pronounced spinal sensitization in patients with extended pain patterns. Furthermore, the spatial pain extent positively correlated with the Bath Body Perception Disturbance Scale (ρ = 0.491; p = 0.048). Conclusion Overall, we provide evidence that the pain phenotype in CRPS, i.e., spatial pain extent, might be related to sensitization mechanism within the central nociceptive system. This study points towards central neuronal excitability as a potential therapeutic target in patients with more widespread CRPS.
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