Sympathetic skin response as an objective tool to estimate stimulus-associated arousal in a human model of hyperalgesia

Salameh, Charbel; Perchet, Caroline; Hagiwara, Koichi; García-Larrea, L.

doi:10.1016/j.neucli.2022.10.002

Cited by 5 publications

(1 citation statement)

References 44 publications

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“…In individuals with chronic pain, autonomic responses to noxious stimuli are enhanced (e.g., increased SSRs) ( 8 – 12 ), paralleling that seen in healthy individuals after the experimental induction of secondary hyperalgesia ( 7 ). Emerging from these observations is the concept that autonomic readouts could serve as reliable and objective markers of nociceptive sensitization ( 7 , 13 , 14 ), discussed as one of the main potential underlying mechanisms of chronic pain ( 15 , 16 ). Increased autonomic responses could, on the one hand, be directly attributable to sensitization of nociceptive and autonomic pathways.…”

Section: Introductionmentioning

confidence: 99%

Priming of the autonomic nervous system after an experimental human pain model

Scheuren,

Bösch,

Rosner

et al. 2023

Journal of Neurophysiology

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Modulated autonomic responses to noxious stimulation have been reported in experimental and clinical pain. These effects are likely mediated by nociceptive sensitization, but may also, more simply reflect increased stimulus-associated arousal. To disentangle between sensitization- and arousal-mediated effects on autonomic responses to noxious input, we recorded sympathetic skin responses (SSRs) in response to 10 pinprick and heat stimuli before (PRE) and after (POST) an experimental heat pain model to induce secondary hyperalgesia (EXP) and a control model (CTRL) in 20 healthy females. Pinprick and heat stimuli were individually adapted for pain perception (4/10) across all assessments. Heart rate (HR), heart rate variability (HRV) and skin conductance (SCL) were assessed before, during, and after the experimental pain model. Both pinprick- and heat-induced SSRs habituated from PRE to POST in CTRL, but not EXP (p=0.033). Background SCL (during stimuli application) was heightened in EXP compared to CTRL condition during pinprick and heat stimuli (p=0.009). Our findings indicate that enhanced SSRs after an experimental pain model are neither fully related to subjective pain, as SSRs dissociated from perceptual responses, nor to nociceptive sensitization, as SSRs were enhanced after both modalities. Our findings can, however, be explained by priming of the autonomic nervous system during the experimental pain model, which makes the autonomic nervous system more susceptible to noxious input. Taken together, autonomic readouts have the potential to objectively assess not only nociceptive sensitization, but also priming of the autonomic nervous system, which may be involved in the generation of distinct clinical pain phenotypes.

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