Temporal Profile and Limb-specificity of Phasic Pain-Evoked Changes in Motor Excitability

Abstract

A fundamental function of nociception is to trigger defensive motor responses to threatening events. Here, we explored the effects of phasic pain on the motor excitability of ipsilateral and contralateral arms. We reasoned that the occurrence of a short-lasting nociceptive stimulus should result in a specific modulation of motor excitability for muscles involved in the withdrawal of the stimulated limb. This was assessed using transcranial magnetic stimulation (TMS) of the left and right primary motor cortex to elicit motor-evoked potentials (MEPs) in three flexor and two extensor muscles of both arms. To assess the time-course of nociception-motor interactions, TMS pulses were triggered 50-2000 ms after delivering short-lasting nociceptive laser stimuli to the left or right hand. We made three main observations. First, nociceptive stimuli induced an early-latency (100 ms) enhancement of MEPs in flexor muscles of the stimulated hand. Considering its latency, this modulation is likely consequent to nociceptive-motor interactions at spinal level. This early and lateralized enhancement was followed by a later (150-400 ms) MEP reduction in extensor muscles of the stimulated hand and flexor muscles of both hands, predominant at the stimulated hand. Finally, we observed a long-lasting (600-2000 ms) MEP enhancement in muscles of the non-stimulated hand. These later effects of the nociceptive stimulus could reflect nociception-motor interactions occurring at cortical level.

The effect of experimental pain on the excitability of the corticospinal tract in humans: A systematic review and meta‐analysis

“…maintenance of the thermal pain during TMS). Considering that phasic pain may produce a series of time‐dependent decrease and increase of the MEP amplitude (and EMG) for a same muscle (Algoet et al., 2018; Kofler et al., 2001), it was difficult to perform a meta‐analysis. Thus, data were presented separately (a) for each interstimulus interval (ISI, i.e.…”

“…For electrical stimulation, the latency of the somatosensory evoked potential following the stimulation of median nerve is ~20 ms for Caucasians and the onset is ~18 ms (Cruccu et al, 2008;Lenoir et al, 2017) and reduction in corticospinal excitability prior to this latency likely comes from the spinal level. This reduction in corticospinal excitability is possible because noxious electrical stimulus bypasses the cutaneous receptors and depolarizes not only Aδ and C nociceptive fibres with a slow conduction velocity, but also the non-nociceptive Aβ-fibres, which are larger and have a lower threshold and a faster velocity of conduction (Algoet et al, 2018;Beall et al, 1977;Mouraux et al, 2010). A similar reduction in corticospinal excitability is also present consecutive to a non-noxious electrical stimuli (Tamburin et al, 2001(Tamburin et al, , 2005 supporting that some of the reduction in corticospinal excitability is secondary to the activation of non-nociceptive fibres.…”

Motor training strengthens corticospinal suppression during movement preparation

“…, double-coil TMS) eliciting MEPs in one or in both hands, respectively. Importantly, in double-coil trials, a 1-ms interval separated the onset of the two pulses, eliciting MEPs in both hands at a near simultaneous time (Algoet et al, 2018; Grandjean et al, 2018; Vassiliadis et al, 2018; Quoilin et al, 2019). This interval was used to avoid direct electromagnetic interference between the two coils (Cincotta et al, 2005), while preventing transcallosal interactions that would occur between motor areas with longer delays (Ferbert et al, 1992; Hanajima et al, 2001).…”

The Role of Sensorimotor Processes in Pain Empathy

“…Combined TMS-EEG or TMS-fMRI experiments could help to reconcile the contradictory results from different methods. It should be also considered that the activity of the skeletomotor system in response to observed pain may be highly dynamic and may differ at various levels of the nervous system, as indicated by the effects of experimentally induced pain on CSE (Bank et al 2013; Algoet et al 2018).…”