The immediate effect of anodal tDCS over the motor cortex on postural control and cortical activation in patients with chronic low back pain: A preliminary study

Background: Impaired postural control, attributed to abnormal function of motor-related cortices, has been proven as one of the potential mechanisms of chronic low back pain (CLBP). Based on available evidence, anodal transcranial direct current stimulation over the primary motor cortex (M1-tDCS) can significantly enhance cortical activation and improve postural control. However, the neuromechanism underlying the effect of anodal M1-tDCS on patients with CLBP remains unclear. Methods: Twenty-six participants with CLBP were randomly assigned to the active tDCS group or sham group. A 20-minute session of anodal M1-tDCS or sham intervention was applied. Before and after the intervention, postural control performance and cortical activity during unipedal standing were assessed by center of pressure displacement and functional near-infrared spectroscopy (fNIRS), respectively. Regions of interest (ROIs) included bilateral primary motor cortex (M1), dorsolateral prefrontal cortex (DLPFC), frontopolar area (FpA), and supplementary motor area (SMA). Functional connectivity (FC) among these ROIs was also analyzed. Results: Significant interactions (Group × Time) were observed in anterior-posterior (AP) velocity, sway length, left M1 activation, and FC between left M1 and right DLPFC, as well as between the left M1 and bilateral FpA (ps<0.05). Post-hoc comparisons demonstrated that AP velocity and sway length significantly decreased after the anodal M1-tDCS intervention (p_FDR<0.001, effect size (d)= 2.060). Additionally, participants in the active tDCS group exhibited significantly reduced left M1 activation (p_FDR<0.001, d=1.894), FC between the left M1 and right DLPFC (p_FDR=0.008, d=1.420), and FC between the left M1 and bilateral FpA (left: p_FDR=0.006, d=1.461; right: p_FDR=0.027, d=1.227) after the intervention. Conclusion: The improvement in postural control of patients with CLBP following anodal M1-tDCS, accompanied by reduced cortical activation and functional connectivity, suggests enhanced neural efficiency (more efficient neural processing) and reduced compensatory demands within sensorimotor networks.