Pain influences plasticity within the sensorimotor system and the aim of this study was to assess the effect of pain on changes in motor performance and corticospinal excitability during training for a novel motor task. A total of 30 subjects were allocated to one of two groups (Pain, NoPain) and performed ten training blocks of a visually-guided isometric pinch task. Each block consisted of 15 force sequences, and subjects modulated the force applied to a transducer in order to reach one of five target forces. Pain was induced by applying capsaicin cream to the thumb. Motor performance was assessed by a skill index that measured shifts in the speed–accuracy trade-off function. Neurophysiological measures were taken from the first dorsal interosseous using transcranial magnetic stimulation. Overall, the Pain group performed better throughout the training (p = 0.03), but both groups showed similar improvements across training blocks (p < 0.001), and there was no significant interaction. Corticospinal excitability in the NoPain group increased halfway through the training, but this was not observed in the Pain group (Time × Group interaction; p = 0.01). These results suggest that, even when pain does not negatively impact on the acquisition of a novel motor task, it can affect training-related changes in corticospinal excitability.

When a movement repeatedly generates pain, we anticipate movement-related pain and establish self-protective strategies during motor preparation, but the underlying mechanisms remains poorly understood. The current study investigated the effect of movement-related pain anticipation on the modulation of behaviour and corticospinal excitability during the preparation of arm movements. Participants completed an instructed-delay reaction-time (RT) task consisting of elbow flexions and extensions instructed by visual cues. Nociceptive laser stimulations (unconditioned stimuli) were applied to the lateral epicondyle during movement execution in a specific direction (CS+) but not in the other (CS-), depending on experimental group. During motor preparation, transcranial magnetic stimulation was used to measure corticospinal excitability in the biceps brachii (BB). RT and peak end-point velocity were also measured. Neurophysiological results revealed an opposite modulation of corticospinal excitability in BB depending on whether it plays an agonist (i.e. flexion) or antagonist (i.e. extension) role for the CS+ movements (P < 0.001). Moreover, behavioural results showed that for the CS+ movements RT did not change relative to baseline, whereas the CS- movements were initiated more quickly (P = 0.023) and the CS+ flexion movements were faster relative to the CS- flexion movements (P < 0.001). This is consistent with the pain adaptation theory which proposes that in order to protect the body from further pain, agonist muscle activity is reduced and antagonist muscle activity is increased. If these strategies are initially relevant and lead to short-term pain alleviation, they may potentially have detrimental long-term consequences and lead to the development of chronic pain.

Background and objective Pain influences motor control. Previous reviews observed that pain reduces the excitability of corticospinal projections to muscles tested with transcranial magnetic stimulation. However, the independent effect of the type of pain models (tonic, phasic), pain location and tissues targeted (e.g. muscle, skin) remains unexplored. The objective of this review was to determine the influence of experimental pain and of different methodological factors on the corticospinal excitability. Databases and data treatment Three electronic databases were searched: Embase, Pubmed and Web of Science. Meta‐analyses were conducted in three consecutive steps to reduce methodological variability: (a) all studies; (b) same pain location; (c) same tissues, pain location and muscle state. Strength of evidence was assessed for each analysis performed. Results Forty studies were included in the review and 26 in the meta‐analysis as it focused only on studies using tonic pain. Overall, there was conflicting/moderate evidence of a diminution of corticospinal excitability during and after tonic pain. When considering only pain location, tonic hand and face pain induced a reduction in corticospinal excitability (limited evidence). Both muscle and cutaneous hand pain reduced corticospinal excitability (limited/conflicting evidence). Similar results were observed for phasic pain (limited evidence). Conclusions Our results confirm the inhibitory effect of pain on corticospinal excitability for both tonic and phasic pain. This reduction was specific to hand and face pain. Also, both cutaneous and muscle hand pain reduced excitability. The strength of evidence remains limited/conflicting. More high‐quality studies are needed to confirm our conclusions. Significance This study adds evidence on the effect of specific factors on the modulation of corticospinal excitability during/after experimental pain. The reduction in corticospinal excitability was driven by hand and face pain. We confirmed previous results that muscle pain reduces corticospinal excitability and provided evidence of a similar effect for cutaneous pain. Both models may inform on the influence of different types of pain on motor control. Future studies are needed to determine the origin of the effect of pain.

Sensorimotor reorganization is believed to play an important role in the development and maintenance of phantom limb pain, but pain itself might modulate sensorimotor plasticity induced by deafferentation. Clinical and basic research support this idea, as pain prior to amputation increases the risk of developing post-amputation pain. The aim of this study was to examine the influence of experimental tonic cutaneous hand pain on the plasticity induced by temporary ischemic hand deafferentation. Sixteen healthy subjects participated in two experimental sessions (Pain, No Pain) in which transcranial magnetic stimulation was used to assess corticospinal excitability in two forearm muscles (flexor carpi radialis and flexor digitorum superficialis) before (T0, T10, T20, and T40) and after (T60 and T75) inflation of a cuff around the wrist. The cuff was inflated at T45 in both sessions and in the Pain session capsaicin cream was applied on the dorsum of the hand at T5. Corticospinal excitability was significantly greater during the Post-inflation phase (p=0.002) and increased similarly in both muscles (p=0.861). Importantly, the excitability increase in the Post-inflation phase was greater for the Pain than the No-Pain condition (p=0.006). Post-hoc analyses revealed a significant difference between the two conditions during the Post-inflation phase (p=0.030) but no difference during the Pre-inflation phase (p=0.601). In other words, the corticospinal facilitation was greater when pain was present prior to cuff inflation. These results indicate that pain can modulate the plasticity induced by another event, and could partially explain the sensorimotor reorganization often reported in chronic pain populations.

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