Brain potentials evoked by intraepidermal electrical stimuli reflect the central sensitization of nociceptive pathways

Central sensitization (CS), the increased sensitivity of the central nervous system to somatosensory inputs, accounts for secondary hyperalgesia, a typical sign of several painful clinical conditions. Brain potentials elicited by mechanical punctate stimulation using flat-tip probes can provide neural correlates of CS, but their signal-to-noise ratio is limited by poor synchronisation of the afferent nociceptive input. Additionally, mechanical punctate stimulation does not activate nociceptors exclusively. In contrast, low-intensity intra-epidermal electrical stimulation (IES) allows selective activation of type-II A mechano-heat nociceptors (II-AMHs), and elicits reproducible brain potentials. However, it is unclear whether hyperalgesia from IES occurs and co-exists with secondary mechanical punctate hyperalgesia, and whether the magnitude of the EEG responses evoked by IES within the hyperalgesic area is increased. To address these questions, we explored the modulation of the psychophysical and EEG responses to IES by intra-epidermal injection of capsaicin in healthy human subjects. We obtained three main results. First, the intensity of the sensation elicited by IES was significantly increased in participants who developed robust mechanical punctate hyperalgesia after capsaicin injection (i.e., responders), indicating that hyperalgesia from IES co-exists with punctate mechanical hyperalgesia. Second, the N2 peak magnitude of the EEG responses elicited by IES were significantly increased after the intra-epidermal injection of capsaicin in responders only. Third, a receiver-operator characteristics analysis showed that the N2 peak amplitude is clearly predictive of the presence of CS. These findings suggest that the EEG responses elicited by IES reflect secondary hyperalgesia, and therefore represent an objective correlate of CS.

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