Different directions of transcranial magnetic stimulation (TMS) can activate different neuronal circuits. While posteroanterior current (PA-TMS) depolarizes mainly interneurons in primary motor cortex (M1), an anteroposterior current (AP-TMS) has been suggested to activate different M1 circuits and perhaps axons from the premotor regions. Although M1 is also involved in the control of axial muscles, no study has explored if different current directions activate different M1 circuits that may have distinct functional role. The aim of the study was to compare the effect of different current directions (PA- and AP-TMS) on the corticomotor control and spatial cortical organisation of the lumbar erector spinae muscle (LES). Thirthy-four healthy participants were recruited for two independent experiments and LES motor-evoked potentials (MEP) were recorded. In experiment 1 (n=17), active motor threshold (AMT), MEP latencies, recruitment curve (90 to 160% AMT), excitatory and inhibitory intracortical mechanisms using paired-pulse TMS (80% followed by 120% AMT stimuli at 2-3-10 and 15ms inter-stimulus intervals) were tested using a double cone (n=12) and a figure-of-eight (n=5) coils. In experiment 2 (n=17), LES cortical representations were tested using PA- and AP-TMS. AMT was higher for AP- compared to PA-TMS (p=0.002). Longer latencies with AP-TMS were compared to PA-TMS (p=0.017). AP-TMS produced more inhibition compared to PA-TMS at 2ms and 3ms (p=0.010), but no difference was observed for longer intervals. No difference was found for recruitment curve and mapping. Those findings suggest that each PA- and AP-TMS may activate different cortical circuits controlling low back muscles as proposed for hand muscles.

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.

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