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.

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In the presence of experimental low back pain, spinal, subcortical, and cortical motor networks involved in the control of back muscles were not modified. However, once the pain disappeared, a reduction in motoneuronal excitability was observed without change in corticospinal and vestibulospinal excitability, suggesting a reduction in descending drive. Experimental low back pain may elicit long-term plasticity even after pain extinction.