Clinical observation of aberrant movement patterns during active forward bending is one criterion used to identify patients with non-specific low back pain suspected to have movement coordination impairment. The purpose of this study was to describe and quantify kinematic patterns of the pelvis and trunk using a dynamics systems approach, and determine agreement between clinical observation and kinematic classification. Ninety-eight subjects performed repeated forward bending with clinical observation and kinematic data simultaneously collected. Kinematic data were plotted using angle-angle, coupling-angle, and phase-plane diagrams. Accuracy statistics in conjunction with receiver operating characteristic curves were used to determine agreement between clinical observation and kinematic patterns. Kinematic patterns were consistent with clinical observation and definitions of typical and aberrant movement patterns with moderate agreement (kappa = 0.46–0.50; PABAK = 0.49–0.73). Early pelvic motion dominance in lumbopelvic coupling-angle diagram ≥59° within the first 38% of the movement represent observed altered lumbopelvic rhythm. Frequent disruptions in lumbar spine velocity represented by phase-plane diagrams with local minimum occurrences ≥6 and sudden decoupling in lumbopelvic coupling-angle diagrams with sum of local minimum and maximum occurrences ≥15 represent observed judder. These findings further define observations of movement coordination between the pelvis and lumbar spine for the presence of altered lumbopelvic rhythm and judder. Movement quality of the lumbar spine segment is key to identifying judder. This information will help clinicians better understand and identify aberrant movement patterns in patients with non-specific low back pain.

Motor control exercise (MCE) is commonly prescribed for patients with low back pain. Although MCE can improve clinical outcomes, lumbar multifidus muscle (LM) activation remains unchanged. Neuromuscular electrical stimulation (NMES) can be used to re-activate motor units prior to MCE which should result in increased LM activation. Therefore, this study aimed to explore the immediate effects of NMES combined with MCE on LM activation and motor performance. Twenty-five participants without low back pain (NoLBP) and 35 participants with movement control impairment (MCI) were recruited. Participants with MCI were further randomized to combined NMES with MCE (COMB) or sham-NMES with MCE (MCE) group. Ultrasound imaging was used to measure LM thickness at rest, maximum voluntary isometric contraction (MVIC), and NMES with MVIC. These data were used to calculate LM activation. Quadruped rocking backward was used to represent motor performance. LM activation and motor performance were measured at baseline and after one-session of intervention. Results showed that both COMB and MCE groups had significantly lower (P < 0.05) LM activation compared with NoLBP group at baseline. Additionally, both COMB and MCE groups demonstrated significant improvement (P < 0.05) in motor performance while COMB group demonstrated significantly greater improvement (P < 0.05) in LM activation compared with MCE group. Individuals with MCI still have persisting LM activation deficit. Our key findings suggest that combined NMES and MCE may have better ability to improve LM activation in individuals with MCI. These findings would support the utility of NMES to induce a priming effect before MCE.

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.