PAIN CHANGES THE BRAIN
17th January 2013
Smudging the motor brain in young adults with recurrent low back pain.
ISSLS prize winner
Tsao H, Danneels LA, Hodges PW.
Spine 2011 Oct 1;36(21):1721-7. doi: 10.1097/BRS.0b013e31821c4267.
This research paper demonstrates that low back pain is associated with a loss of discrete cortical organisation of the back muscles. Increased overlap in the motor cortical representation of Deep Multifidus and Longissimus Erector Spinae may explain motor control changes noted in people with low back pain. Helps to explain why it is difficult to retrain the motor control impairment in people with low back pain.
To investigate whether recurrent low back pain (LBP) is associated with changes in motor cortical representation of different paraspinal muscle fascicles.
SUMMARY OF BACKGROUND DATA:
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.
RESULTS: 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.