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.

Objective: We conducted a systematic review/meta-analysis to evaluate noninvasive brain stimulation (NIBS) efficacy to alleviate pain and improve disability in low back pain (LBP). Materials and Methods:A systematic literature search was performed by a librarian in MEDLINE, Embase, EBM Reviews, CINAHL, and Web of Science databases (last search: January 14, 2021). Data were pooled by the number of sessions and follow-up periods. Independent reviewers performed screening, data extraction, and risk of bias. Pain reduction and disability were used as outcomes.Results: Twelve articles were included in the qualitative synthesis and 8 in the meta-analysis. A single session of NIBS reduced pain compared with sham (standardized mean difference: −0.47; P < 0.001; very low-quality evidence). Repeated sessions of NIBS did not impact pain at short-term (mean difference [MD]: −0.31; P = 0.23) or midterm (MD: −0.56; P = 0.33; moderate quality evidence). Combining NIBS with cointerventions did not influence pain (MD: −0.31; P = 0.30; moderate quality evidence). NIBS did not have a statistically significant impact on disability.Discussion: There is very low-quality evidence suggesting that a single NIBS session reduces LBP intensity. In contrast, there is moderate quality evidence that repeated NIBS sessions or combination with cointervention did not improve pain or disability. Thus, current results do not support NIBS use to treat chronic LBP. Considering that tDCS was tested in 8 of 12 studies with little success, studies focusing on different NIBS techniques or innovative parameters are required to determine their potential to improve pain and disability in chronic LBP.

Introduction: Exercise is the most recommended treatment for chronic low back pain (CLBP) and is effective in reducing pain, but the mechanisms underlying its effects remain poorly understood. Exercise-induced hypoalgesia (EIH) may play a role and is thought to be driven by central pain modulation mechanisms. However, EIH appears to be disrupted in many chronic pain conditions and its presence in people with CLBP remains unclear. As people suffering from chronic pain often exhibit psychological factors and central sensitization symptoms influencing pain perception, EIH might be associated with these factors. Objective: The aim of this study is to compare the level of EIH between participants with and without CLBP following back and wrist exercises and to assess the associations between EIH, psychological factors, and symptoms of central sensitization (using the central sensitization inventory -CSI) in CLBP. Method: Twenty-eight participants with CLBP and 23 without pain were recruited. Pressure pain thresholds (PPT) were measured at 4 sites (2 bony sites = capitate, S1|2 muscle sites = wrist flexors, lumbar erector spinae) before and after each of two exercises (wrist flexion and lumbar extension). Exercise-induced hypoalgesia was defined as percent change in PPT from pre-to post-exercise. Participants with CLBP also completed questionnaires to measure psychological factors (e.g., kinesiophobia, catastrophizing, anxiety, and self-efficacy) and symptoms of central sensitization (CSI), and correlations with EIH were calculated. Results: After wrist exercise, EIH measured at the muscle sites was lower in the CLBP group compared with the pain-free group (p = 0.047) but no differences were found at bony sites (p = 0.49). No significant differences for EIH were observed following back exercise at muscle sites (p = 0.14) or at bony sites (p = 0.65). Exerciseinduced hypoalgesia was not correlated with any psychological factors or with the CSI score. Conclusion:The lower EIH following wrist exercises may represent an alteration in pain modulation control in CLBP. However, psychological factors and central sensitization symptoms may not explain the differences observed.