To investigate whether recurrent low back pain (LBP) is associated with changes in motor cortical representation of different paraspinal muscle fascicles.
Fascicles of the lumbar paraspinal muscles are differentially activated during function. Human studies indicate this may be associated with a spatially separate array of neuronal networks at the motor cortex. Loss of discrete control of paraspinal muscle fascicles in LBP may be because of changes in cortical organization.
Data were collected from 9 individuals with recurrent unilateral LBP and compared with 11 healthy participants from an earlier study. Fine-wire electrodes selectively recorded myoelectric activity from short/deep fascicles of deep multifidus (DM) and long/superficial fascicles of longissimus erector spinae (LES), bilaterally. Motor cortical organization was investigated using transcranial magnetic stimulation at different scalp sites to evoke responses in paraspinal muscles. Location of cortical representation (center of gravity; CoG) and motor excitability (map volume) were compared between healthy and LBP groups.
Individuals with LBP had a more posterior location of LES center of gravity, which overlapped with that for DM on both hemispheres. In healthy individuals, LES center of gravity was located separately at a more anterior location to that for DM. Map volume was reduced in LBP compared to healthy individual across muscles.
The findings highlight that LBP is associated with a loss of discrete cortical organization of inputs to back muscles. Increased overlap in motor cortical representation of DM and LES may underpin loss of differential activation in this group. The results further unravel the neurophysiological mechanisms of motor changes in recurrent LBP and suggest motor rehabilitation that includes training of differential activation of the paraspinal muscles may be required to restore optimal control in LBP.
Loss of differential motor activation of lumbar paraspinal muscles is a feature of recurring low back pain. This is associated with loss of discrete organization of neuronal networks at the motor cortex. The findings help unravel neural mechanisms that underpin changes in motor coordination with back pain.
*Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia;
†Department of Rehabilitation Sciences and Physiotherapy, Ghent University, Ghent, Belgium.
Address correspondence and reprint requests to Paul Hodges, NHMRC Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, QLD 4072 Australia; E-mail: firstname.lastname@example.org
Acknowledgment date: October 14, 2010. Acceptance date: March 24, 2011.
The manuscript submitted does not contain information about medical device(s)/drug(s).
Institutional funds were received to support this work (P.H.). No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.