Sensorimotor cortical activity is altered in both the immediate acute and chronic stages of musculoskeletal pain. However, these changes are opposite, with decreased cortical activity reported in experimentally induced acute pain (lasting minutes to hours), and increased cortical activity in chronic, clinical pain (lasting >6 months). It is unknown whether sensorimotor cortical activity is altered in acute, clinical musculoskeletal pain (lasting <4 weeks). In 36 individuals with acute, nonspecific, clinical low back pain (LBP) and 36 age- and sex-matched, pain-free controls, we investigated the processing of non-noxious afferent inputs using sensory evoked potentials (SEPs), as well as corticomotor excitability and organization of the primary motor cortex using transcranial magnetic stimulation. Processing of non-noxious sensory inputs was lower (smaller area of the N80-N150-P260 SEP complex) in acute LBP (F1,70 = 45.28, P < .01). The examination of specific SEP components revealed a smaller area of the N150 and P260 SEP components in acute LBP, although interindividual variability was high. Motor cortical map volume was lower in acute LBP (F1,70 = 5.61, P = .02). These findings demonstrate that acute LBP is characterized by lower sensorimotor cortical activity at the group level. However, individual variation was high, suggesting individual adaptation of cortical plasticity in acute pain. PERSPECTIVE: This is the first study to examine sensorimotor cortical activity in the acute stage of clinical LBP. This information is critical for understanding the neurophysiology of acute LBP.
Keywords: Low back pain; primary motor cortex; primary sensory cortex; sensory evoked potentials; transcranial magnetic stimulation.
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