Elsevier

Clinical Biomechanics

Volume 20, Issue 5, June 2005, Pages 465-473
Clinical Biomechanics

Trunk muscle recruitment patterns in specific chronic low back pain populations

https://doi.org/10.1016/j.clinbiomech.2005.01.007Get rights and content

Abstract

Background. It is hypothesized that injury or degeneration of osteoligamentous spinal structures would require compensation by trunk musculature and alterations in motor control to maintain spine stability. While, biomechanical modeling has supported this hypothesis, studies of muscle recruitment patterns in chronic low back pain patients both with and without significant osteoligamentous damage have been limited. This study utilized a non-randomized case-control design to investigate trunk muscle recruitment patterns around the neutral spine position between subgroups of patients with chronic mechanical low back pain and asymptomatic controls.

Methods. Twenty subjects with chronic low back pain attributed to clinical lumbar instability were matched to 20 asymptomatic controls. In addition 12 patients with non-specific chronic low back pain were studied. Surface EMG from five trunk muscles was analyzed to determine activation levels and patterns of recruitment during a standing reach under two different loading conditions.

Findings. The chronic low back pain group with symptoms attributed to clinical instability demonstrated significantly higher activation levels of the external oblique and rectus abdominus muscles and lower abdominal synergist ratios than the control group. No significant differences were found between patient subgroups.

Interpretation. While these data demonstrate altered muscle recruitment patterns in patients with chronic low back pain, the changes are not consistent with Panjabi’s theory suggesting that these alterations are driven by passive subsystem damage. However, the higher activation of global abdominal musculature and altered synergist patterns may represent a motor control pattern that has consequences for continued dysfunction and chronic pain.

Introduction

Differences in trunk muscle recruitment or neuromuscular control in patients with mechanical low back pain have been reported by several investigators (Hodges and Richardson, 1999; O’Sullivan et al., 1997a; Radebold et al., 2000; Van Dieen et al., 2003). It has been hypothesized that these changes in muscle recruitment patterns are an adaptation to underlying spinal instability resulting from osteoligamentous laxity or damage, muscle dysfunction or reduced neuromuscular control (Panjabi, 1992; Paris, 1985). Panjabi (1992) proposed a model for a spinal stabilization system which partitioned the responsibility for joint stability and movement into three subsystems: a passive subsystem (connective tissue, bones, and intervertebral discs), an active subsystem of muscles and tendons, and a neural (motor) control subsystem. Panjabi further hypothesized that spinal instability created by dysfunction of the passive support system, resulting in loss of control or excessive motion of a spinal segments neutral zone, would trigger compensation strategies by trunk musculature under the guidance of the neural control systems. The objective of the compensation would be to maintain spinal stability (Panjabi, 1992).

Biomechanical modeling and experimental studies have demonstrated that trunk muscle co-contraction is necessary for spinal stability particularly in neutral upright postures even in the healthy spine (Cholewicki et al., 1997; Granata et al., 2001). Moreover, reduction of a model’s passive stiffness component predicts that muscle activation would increase to maintain stability of a spine (Cholewicki et al., 1997). Gardner-Morse and Stokes (2001) lend further support to this hypothesis, by demonstrating that a 10% reduction in segmental stiffness can compromise spine stability. They further suggest that this reduction in segmental stiffness, in conjunction with poor neuromuscular control and reduction in muscle stiffness could result in clinical instability. These modeling predictions are supported by data from animal models (Kaigle et al., 1995; Wilke et al., 1995) and through experiments using healthy individuals, who upon challenges to trunk stability responded by increasing muscle co-contraction (Granata and Orishimo, 2001). This co-contraction is particularly necessary around the neutral spine position and during low load conditions (Cholewicki and McGill, 1996).

While numerous investigators have reported activation pattern differences in patients with non-specific mechanical low back pain, the hypothesis that changes in trunk muscle recruitment patterns are an adaptation to underlying passive subsystem damage that results in an increased neutral zone, segmental hypermobility, and/or clinical spinal instability has not been systematically investigated (Lariviere et al., 2000; Newcomer et al., 2002; Van Dieen et al., 2003). The few investigators who studied patients with radiographic findings associated with clinical lumbar instability (i.e., spondylolisthesis) have found differences in muscle recruitment; however, these findings were demonstrated during the performance of a specific therapeutic exercise or non-functional activity (Lindgren et al., 1993; O’Sullivan et al., 1997a; Sihvonen et al., 1997). These investigators did not study muscle activation patterns of the trunk flexors and extensors simultaneously nor did they consistently address muscle co-contraction or synergist ratios (i.e., trunk flexors/extensors, internal oblique/rectus abdominus).

On the basis of the assumption that chronic mechanical low back pain (CLBP) patients with significant passive subsystem damage adapt muscle recruitment to compensate for the loss of spinal stability, we have formulated several hypotheses regarding muscle activation levels and patterns. Patients with chronic mechanical low back pain attributed to clinical lumbar instability (CLBPI) from significant passive subsystem damage would demonstrate increased muscle activation and greater co-contraction of the trunk muscular than asymptomatic controls during a functional reaching task. In addition, work by Bergmark (1989) and Panjabi et al. (1989) suggests that muscle architecture plays a role in effective spine stability. They found through biomechanical modeling that activation of segmentally inserting muscles would be more effective at increasing stability than multi-segmental muscle inserting on the thorax and pelvis. Based upon this work, we also hypothesized that synergist muscle ratios represented by activation of segmental relative to multi-segmental muscles when acting synergistically (i.e., internal oblique/rectus abdominus) would be higher in the CLBPI group as an attempted to increase stability. To further establish if passive subsystem damage associated with findings of clinical lumbar instability was the determinate of muscle pattern changes, a separate subset of patients with non-specific chronic mechanical low back pain (CLBPN) was compared to the CLBPI group. Pattern differences between CLBPI and CLBPN; would also lend support to the idea that unique impairments exist between these subgroups of the chronic low back pain population. These hypotheses were tested by recording activity of ten trunk muscles during functional reach under two loading conditions.

Section snippets

Participants

A total of 39 participants with recurrent or chronic low back pain were recruited from an orthopedic surgery practice and completed the testing protocol. Inclusion criteria were current pain episode greater than 3 months, primary complaint of back and not leg pain, and inability to work or perform essential activities of daily living secondary to pain. All of these individuals had failed to resolve their symptoms in a course of conservative care, which included medical management, as well as

Muscle activation levels

Fig. 2 provides group mean muscle activations with standard error for the no load and 5 lb load condition at 0° of trunk flexion. The rectus abdominus (F1,36 = 5.226, P = 0.0001) and external oblique (F1,35 = 18.541, P = 0.028) muscles had significantly higher activation levels in the CLBPI group compared to matched asymptomatic controls. There was a significant main effect for load in all muscle groups except the external oblique (Table 2). A significant load x group interaction (F1,38 = 6.406, P = 0.016)

Muscle activation levels and patterns

This study compared trunk muscle recruitment pattern between two subgroups of CLBP patients and asymptomatic control using both normalized muscle activation and RMS sEMG patterns of co-activation. The findings demonstrate differences in activation strategies of the CLBPI subgroup and matched control subjects, but not between the CLBP subgroups themselves. Using both normalized muscle activity and RMS ratios of activation to describe muscle recruitment allowed us to address the limitations

Conclusions

The data from our subjects does not support the theory that passive subsystem damage drives the muscle recruitment patterns of patients with CLBP. While the altered abdominal recruitment patterns demonstrated by our CLBP patients suggest reliance on multi-segmental abdominal musculature, the 1–2% mean group difference in individual muscle activation, although statically significant, may have limited clinical implications. However, we believe the synergists ratios are a better and more

Acknowledgments

The authors would like to thank Dr. Susan Smith for her manuscript review and editorial suggestions. This study was supported in part by grants from the Orthopaedic Section of the American Physical Therapy Association and the US Department of Education, National Institute on Disability and Rehabilitation Research.

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