The influence of experimental low back pain on neural networks involved in the control of lumbar erector spinae muscles.

Low back pain (LBP) often modifies spine motor control, but the neural origin of these motor control changes remains largely unexplored. This study aimed to determine the impact of experimental low back pain on the excitability of cortical, subcortical, and spinal networks involved in the control of back muscles. Thirty healthy subjects were recruited and allocated to pain (capsaicin and heat) or control (heat) groups. Corticospinal excitability (motor-evoked potential; MEP) and intracortical networks were assessed by single- and paired-pulse transcranial magnetic stimulation, respectively. Electrical vestibular stimulation was applied to assess vestibulospinal excitability (vestibular MEP; VMEP) and the stretch reflex for excitability of the spinal or supraspinal loop (R1 and R2, respectively). Evoked back motor responses were measured before, during, and after pain induction. Nonparametric rank-based ANOVA determined if pain modulated motor neural networks. A decrease of R1 amplitude was present after the pain disappearance ( = 0.01) whereas an increase was observed in the control group ( = 0.03) compared with the R1 amplitude measured at prepain and preheat period, respectively (group × time interaction, < 0.001). No difference in MEP and VMEP amplitude was present during and after pain ( > 0.05). During experimental LBP, no change in cortical, subcortical, or spinal networks was observed. After pain disappearance, the reduction of the R1 amplitude without modification of MEP and VMEP amplitude suggests a reduction in spinal excitability potentially combined with an increase in descending drives. The absence of effect during pain needs to be further explored. 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.