Abstract
ObjectiveCortical reorganization is one of the most plausible mechanisms underlying impairment of anticipatory postural adjustments (APAs) in low back pain (LBP) patients. In order to clarify changes in corticomotor neurophysiology, APAs were assessed by using electromyography (EMG) and electroencephalography (EEG).MethodsAn equal number (29) of nonspecific LBP patients and healthy subjects performed unilateral rapid arm movements in response to auditory imperative stimulus preceded by warning stimulus within 2 s interstimulus interval. Burst onset activity was calculated in relation to the activity of anterior deltoid for bilateral transverse abdominis/internal oblique (TrA/IO), and also postural muscles on left side, including rectus abdominis, external oblique (E.O), erector spinae and medial head of gastrocnemius (Gc.M). Contingent negative variation (CNV) potentials were recorded by scalp EEG, and the area under receiver operating characteristic curve (AUC) was analyzed.ResultsIn LBP patients, there was a significant onset delay for E.O and bilateral TrA/IO, but a significant earlier activity for Gc.M (for both P < 0.05). The CNV parameters were considerably greater in LBP patients (P < 0.01). The AUC was significant just for left TrA/IO and E.O muscles (P < 0.05).ConclusionsThe CNV amplitudes were increased, and APA onset times re-organized to be delayed at the trunk and early at the distal limb in LBP cases. These findings support the hypothesis about reorganized activity of cerebral cortex in LBP patients.
Highlights
Low back pain (LBP) is considered as pain limited to the region between the 12th rib and the inferior gluteal fold, whether it is accompanied by leg pain or not (Krismer and Van Tulder 2007)
Based on the scientific literature, there is a high prevalence for LBP which involves 70–85 % of all people during their lifetime so that it is estimated that the mean ± SEM of point prevalence is 11.9 ± 2.0 % and one-month prevalence is Sadeghi et al SpringerPlus (2016) 5:674
The present study showed that Gc.M had significant earlier activation in the LBP patients than the healthy subjects, while E.S onset latency showed no considerable change
Summary
Low back pain (LBP) is considered as pain limited to the region between the 12th rib and the inferior gluteal fold, whether it is accompanied by leg pain or not (Krismer and Van Tulder 2007). One plausible mechanism that has been mentioned for inducing chronic recurrent LBP is the change in postural control of the trunk muscles (Tsao et al 2008). LBP patients display delay in the feedforward activation of deep abdominal muscles before onset of focal movement (Hodges and Richardson 1999; Hodges 2001), and these patients exhibit changes in spatial representation and magnitude of somatosensory-evoked potentials (SEPs) of brain in response to painful or painless stimuli (Flor et al 1997). Alteration of lumbar paraspinal muscle activity occurs in LBP cases due to changes in nervous system including reflex inhibition, muscle’s nerve supply loss and supraspinal changes (Tsao et al 2011). There is a loss of discrete control of paraspinal muscles in LBP patients; for instance, superficial and deep multifidus fascicles are recruited simultaneously during trunk perturbation. Cortical reorganization in motor cortex seems to be responsible for the changes in activity of paraspinal muscles (Tsao et al 2011)
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