Low somatosensory cortex excitability in the acute stage of low back pain causes chronic pain

Abstract

BACKGROUND: Determining 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 organisation of the primary somatosensory and primary motor cortex in people with acute and chronic LBP, however, no study has explored these mechanisms longitudinally or attempted to draw causal inferences. METHODS: Prospective, longitudinal, cohort study including 120 people with an acute episode of LBP. Sensory evoked potential area measurements were used to assess primary and secondary somatosensory cortex excitability. Transcranial magnetic stimulation derived map volume was used to assess corticomotor excitability. Directed acyclic graphs identified variables potentially confounding the exposure-outcome relationship. The effect of acute-stage sensorimotor cortex excitability on six-month LBP outcome was estimated using multivariable regression modelling, with adjusted and unadjusted estimates reported. Sensitivity analyses were performed to explore the effect of unmeasured confounding and missing data. RESULTS: Lower primary (OR = 2.08, 95% CI = 1.22 to 3.57) and secondary (OR = 2.56, 95% CI = 1.37 to 4.76) somatosensory cortex excitability in the acute stage of LBP increased the odds of developing chronic pain at six-month follow-up. This finding was robust to confounder adjustment and unmeasured confounding (E-Value = 2.24 & 2.58, respectively). 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. CONCLUSION: These data provide the first evidence that low somatosensory cortex excitability in the acute stage of LBP is a cause of chronic pain. Interventions designed to increase somatosensory cortex excitability in acute LBP may be relevant to the prevention of chronic pain.

Cortical function and sensorimotor plasticity predict future low back pain after an acute episode: the UPWaRD prospective cohort study

“…For example, in sub-acute LBP, greater functional connectivity of corticostriatal circuitry predicts chronic LBP at 1-year [8;72]. Further, using causal inference analyses, we have shown that low sensory cortex excitability (N80 SEP area) in acute LBP is a cause, and not an epiphenomenon, of chronic pain [50]. Our findings also demonstrate that BDNF genotype MET allele carriers are more susceptible to future LBP.…”

Mechanisms and manifestations in musculoskeletal pain: from experimental to clinical pain settings

“…Measures recorded in the acute pain phase of LBP may also represent an epiphenomenon, but the reduced sensory-evoked potentials were demonstrated as causative of chronic pain after 6 months in contrast to the changes in the motor mapping. 105 Such data indicate that the cortical sensory-discriminative function is impaired in candidates vulnerable to developing chronic musculoskeletal pain. How this links with the sensory-discriminative function in painful stimulations is unknown, although previous studies demonstrated augmented nociceptive-evoked potentials (short latency) in patients with chronic LBP 49 and fibromyalgia 50 compared with controls.…”

BackWards – Unveiling the Brain’s Topographic Organization of Paraspinal Sensory Input

“…With respect to supraspinal mechanisms, growing evidence suggests that chronic low back pain (CLBP) is linked to neuroplastic adaptations of the brain (Flor et al, 1997, Ung et al, 2014, Rodriguez-Raecke et al, 2014, Konno and Sekiguchi, 2018). Thus, in light of its potential clinical relevance, neural reorganization, specifically in the primary somatosensory and in the motor cortices, has been studied with growing interest in back pain contexts (Flor et al, 1997, Flor, 2003, Tsao et al, 2010, Van Dieën et al, 2017, Zhang et al, 2019, Jenkins et al, 2022, Moseley and Flor, 2012).…”