• Luke C Jenkins, Wei-Ju Chang, Valentina Buscemi, Matthew Liston, Patrick Skippen, Aidan G Cashin, James H McAuley, and Siobhan M Schabrun.
• School of Health Sciences, Western Sydney University, Penrith, New South Wales, Australia; Centre for Pain IMPACT, Neuroscience Research Australia (NeuRA), Randwick, New South Wales, Australia.
• J Pain. 2022 Feb 1; 23 (2): 289-304.

AbstractDetermining the mechanistic causes of complex biopsychosocial health conditions such as low back pain (LBP) is challenging, and research is scarce. Cross-sectional studies demonstrate altered excitability and organization of the somatosensory and motor cortex in people with acute and chronic LBP, however, no study has explored these mechanisms longitudinally or attempted to draw causal inferences. Using sensory evoked potential area measurements and transcranial magnetic stimulation derived map volume we analyzed somatosensory and motor cortex excitability in 120 adults experiencing acute LBP. Following multivariable regression modelling with adjustment for confounding, we identified lower primary (OR = 2.08, 95% CI = 1.22-3.57) and secondary (OR = 2.56, 95% CI = 1.37-4.76) somatosensory cortex excitability significantly increased the odds of developing chronic pain at 6-month follow-up. Corticomotor excitability in the acute stage of LBP was associated with higher pain intensity at 6-month follow-up (B = -0.15, 95% CI: -0.28 to -0.02) but this association did not remain after confounder adjustment. These data provide evidence that low somatosensory cortex excitability in the acute stage of LBP is a cause of chronic pain. PERSPECTIVE: This prospective longitudinal cohort study design identified low sensorimotor cortex excitability during the acute stage of LBP in people who developed chronic pain. Interventions that target this proposed mechanism may be relevant to the prevention of chronic pain.Copyright © 2021 United States Association for the Study of Pain, Inc. Published by Elsevier Inc. All rights reserved.

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