Physiological mechanisms
descending pain, hyperalgesia, pain
So far, physiological measurements taken during OA included functional magnetic resonance imaging [Interestingly, results of this study showed that, contrary to our prediction, EDA responses to OT were not decreased alongside pain perception. In turn, the increase of the temperature during a T2 interval significantly elevated the EDA level which persisted during the T3 interval, whereas the pain response was reduced. Indeed, a lowered pain intensity overlapped with higher EDA level in offset compared to constant trial. It can be suggested that the higher stimulus in T2 of the OT activates the descending pain inhibition pathways and therefore inhibits pain. In fact, the EDA level during CT gradually decreased over-time which was, in general, associated with higher pain compared to OTs. During OA, endogenous modulatory mechanisms have been shown to be activated [However, whether this EDA response represents a physiological correlate of the OA via pain response is not clear. Indeed, no differences were found for the EDA data within the OT (as is usual for the pain response) when the time intervals T1 and T3 were considered. One can therefore assume that the increased EDA response within T3, may related to an (still) ongoing EDA response caused by a higher stimulation during the T2 interval. Thus, it should be further investigated whether the EDA within an OA paradigm may also reflect the pain predictions that may involve perception of both temperature decreases (OA) and temperature increases (onset hyperalgesia) as shown by Alter et al. 2020 [Our psychological manipulation did not influence the EDA signal. Although EDA has been used extensively to capture reported pain intensity and has been shown to be a potent biomarker in pain prediction [