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REORGANISATION OF THE MOTOR CORTEX IN CHRONIC LOW BACK PAIN



Abstract

Introduction: Deficits in motor control of the trunk muscles have been extensively reported in individuals with chronic low back pain (LBP). Recent evidence suggests that these deficits can be improved with motor training. However, whether these changes in motor control are mediated by changes in the motor cortex remains unclear. As deficits in postural activation of transversus abdominis (TrA) is consistently observed in individuals with LBP, the present study aimed to investigate the representation of TrA at the motor cortex in individuals with and without chronic LBP. The potential to change the cortical representation of TrA following motor training in individuals with chronic LBP was also examined.

Methods: Eleven healthy volunteers and twenty individuals with chronic LBP participated. Chronic LBP individuals were randomly allocated into two training groups: specific motor control training that involved practice of skilled activation of TrA, or walking exercise, and trained twice per day for two weeks. Recordings of electromyographic activity (EMG) of TrA were made bilaterally with intramuscular fine-wire electrodes. Motor control of TrA was assessed as the postural activation of the muscle associated with repetitions of rapid arm flexion and extension movements. To evaluate the representation of TrA, transcranial magnetic stimulation (TMS) was delivered over pre-marked scalp sites. EMG amplitude of the responses to TMS at each site was superimposed over the grid to produce a map of response amplitude relative to scalp site. All procedures were repeated two weeks post-training for the chronic LBP group. Onset of TrA EMG relative to prime mover deltoid and the location of the centre of gravity (CoG) of TMS map were compared between individuals with and without chronic LBP, and between pre- and post-training in individuals with chronic LBP.

Results: The CoG of the cortical representation of TrA was located 2 cm anterior and lateral to the vertex in healthy individuals. However, individuals with chronic LBP showed a posterior and lateral shift in the CoG. The shift in location of the CoG of the TrA representation was associated with timing of activation during rapid arm movement tasks. Following two weeks of skilled training of TrA, motor cortical representation shifted towards that observed in healthy individuals. Changes in representation were not observed for the walking exercise group.

Discussion: These findings provide evidence of reorganisation of trunk muscle representation at the motor cortex in individuals with chronic LBP, and that cortical changes are associated with deficits in motor control. Furthermore, this study provides the first evidence that training can induce plasticity of the motor cortex in this group.

Correspondence should be addressed to Dr Owen Williamson, Editorial Secretary, Spine Society of Australia, 25 Erin Street, Richmond, Victoria 3121, Australia.