Cortical excitability and multifidus activation responses to transcranial direct current stimulation in patients with chronic low back pain during remission.

Evidence indicates that patients with chronic low back pain (CLBP) have lumbar multifidus muscle (LM) activation deficit which might be caused by changes in cortical excitability. Anodal transcranial direct current stimulation (a-tDCS) can be used to restore cortical excitability. This study aimed to (1) determine the immediate effects of a-tDCS on the cortical excitability and LM activation and (2) explore the relationship between cortical excitability and LM activation. Thirteen participants with CLBP during remission and 11 healthy participants were recruited. Cortical excitability (peak-to-peak motor evoked potential amplitude; P2P and cortical silent period; CSP) and LM activation were measured at pre- and post-intervention. We found significant difference (P < 0.05) in P2P between groups. However, no significant differences (P > 0.05) in P2P, CSP and LM activation were found between pre- and post-intervention in CLBP. The CLBP group demonstrated significant correlation (P = 0.05) between P2P and LM activation. Although our finding demonstrates change in P2P in the CLBP group, one-session of a-tDCS cannot induce changes in cortical excitability and LM activation. However, moderate to strong correlation between P2P and LM activation suggests the involvement of cortical level in LM activation deficit. Therefore, non-significant changes could have been due to inadequate dose of a-tDCS.

Multifidus Muscle Contractility Deficit Was Not Specific to the Painful Side in Patients with Chronic Low Back Pain During Remission: A Cross-Sectional Study.

Purpose: Morphology studies demonstrated that patients with chronic low back pain (CLBP) have bilateral multifidus muscle (LM) atrophy. This atrophy should result in LM contractility deficit bilaterally. Additionally, a recent study showed the effect of sex on LM thickness. Researchers proposed percentage LM contractility (LMCONT) as standardization to enable the comparison across participants. This study aimed to determine side-to-side difference in LMCONT and to determine the difference in LMCONT between males and females. Patients and Methods: Twenty-five healthy individuals (NoLBP group; 10 males and 15 females) and 35 with CLBP (CLBP group; 16 males and 19 females; 23 unilateral pain and 12 bilateral pain) were recruited. Ultrasound imaging was used to measure LM thickness at rest, during maximum voluntary isometric contraction, and during combined maximum voluntary isometric contraction with electrical stimulation. These data were used to calculate LMCONT. For unilateral CLBP, right and left LMCON were renamed to painful and non-painful sides. Results: Data demonstrated no significant difference (p > 0.05) between right (87.3 ± 13.7%) and left (87.2 ± 14.0%) in NoLBP, right (71.2 ± 15.7%) and left (76.5 ± 19.7%) in bilateral CLBP, and painful (70.3 ± 17.5%) and non-painful (77.7 ± 18.4%) in unilateral CLBP. No difference (p > 0.05) was found between males and females in both NoLBP (male 84.8 ± 6.5%, female 88.9 ± 15.4%) and CLBP groups (male 76.3 ± 15.5%, female 71.9 ± 14.0%). Conclusion: The findings suggested that LM contractility deficit in CLBP is not specific to painful side. No effect was found of sex on LM contractility. Therefore, we can use averaged LM activation across painful and non-painful sides and across males and females to compare between NoLBP and CLBP groups.