Trunk muscle activation in low-back pain patients, an analysis of the literature

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Abstract

This paper provides an analysis of the literature on trunk muscle recruitment in low-back pain patients. Two models proposed in the literature, the pain–spasm–pain model and the pain adaptation model, yield conflicting predictions on how low- back pain would affect trunk muscle recruitment in various activities. The two models are outlined and evidence for the two from neurophsysiological studies is reviewed. Subsequently, specific predictions with respect to changes in activation of the lumbar extensor musculature are derived from both models. These predictions are compared to the results from 30 clinical studies and three induced pain studies retrieved in a comprehensive literature search. Neither of the two models is unequivocally supported by the literature. These data and further data on timing of muscle activity and load sharing between muscles suggest an alternative model to explain the alterations of trunk muscle recruitment due to low-back pain. It is proposed that motor control changes in patients are functional in that they enhance spinal stability.

Introduction

Low-back pain (LBP) is one of the most prevalent and costly health problems in western society [7]. In spite of extensive research efforts, the causes of LBP are still elusive and treatment effects are unsatisfactory. It is often suggested that the occurrence of LBP should be accepted as a fact of life and efforts of researchers and clinicians should focus on preventing LBP from becoming chronic rather than at prevention of first-time occurrence [7].

To design a rational program for secondary prevention, it needs to be established whether behavioral responses displayed by patients should be considered adaptive and supportive of recovery or as adverse and contributing to a vicious cycle leading to chronicity. An important debate in the literature on LBP in this respect focuses on the interpretation of changes in trunk muscle activity in LBP patients. On the one hand, these changes are interpreted in the context of the pain–spasm–pain model, postulating that pain results in increased muscle activity, which in turn will cause pain [110], [129]. In contrast, the pain adaptation model postulates that pain reduces activation of muscles when active as agonists and increases activation of muscles when active as antagonists. This will reduce movement velocity and range of motion, which would prevent mechanical provocation of pain in damaged tissues and further damage of these tissues [78].

It is striking that proponents of both models have found evidence supporting their interpretation in reviews of the literature on electromyographically recorded back muscle activation in LBP patients [78], [110]. The aim of the present paper therefore is to more systematically review the literature on effects of clinical and experimentally induced LBP on trunk muscle activation in terms of levels of activation, the timing of activation, and load sharing between muscles. First, the two models will be outlined and specific predictions on trunk muscle activation will be derived for each model. Second, studies on trunk muscle activation in LBP patients will be reviewed. The results from the studies reviewed will be compared to the model predictions. Finally, an alternative interpretation for the experimental results based on spinal instability as an important component of LBP will be proposed.

Section snippets

Pain–spasm–pain model

Pain occurring immediately after acute trauma is often accompanied by intense contractions of muscles surrounding the injured structures. This is thought to be functional, since it will prevent motion of the injured structures. In clinical practice, it is often assumed that similar muscular reactions occur following non-traumatic pain. In these cases, it is not the functional, adaptive nature of such a response that is emphasized but rather its possible adverse consequences. The pain–spasm–pain

Pain-adaptation model

The pain-adaptation model was proposed by Lund et al. [78] to account for clinical findings on muscle activity in pain syndromes. The model states that pain decreases the activation of muscles when active as agonists and increases it when the muscle is active as antagonist [78]. The effects of such a control strategy would be that movement velocity is reduced and movement excursions are limited. These kinematic effects are believed to prevent pain provocation.

A neural pathway suggested to

Methods

This review was based on a literature search in PubMed using the search terms ‘low-back pain and muscle activity’ or ‘low-back pain and electromyography’ and several similar combinations. The references thus retrieved were screened on the basis of titles and abstracts and those papers apparently fulfilling our inclusion criteria (see below) were selected for further study. The literature retrieved in this way was supplemented with references from the authors’ own databases, from previous

Effects of clinical pain on EMG amplitudes

Of the total number of 44 studies retrieved fulfilling the inclusion criteria, 30 reported a comparison of lumbar erector spinae (LES) EMG amplitudes between patients and controls (Table 3). This material was used for testing the predictions of the pain–spasm–pain model and the pain-adaptation model. The 30 studies together described 101 separate experimental tasks, which were classified according to Table 1, Table 2. This classification made it necessary to include two extra categories. A

Discussion

The literature reviewed here reveals that neither one of the two models adequately predicts the effects of back pain on trunk muscle activation. In some cases evidence for reduced activation is found in line with the pain-adaptation model and in conflict with the pain–spasm–pain model. These changes appear to be adaptive in that heavy exertion of painful muscles and high accelerations that may impose a risk of pain provocation are avoided. In line with this Marras et al. [84], [85] reported

Conclusion

Findings on trunk muscle recruitment in LBP patients fit neither the pain–spasm–pain model, nor the pain-adaptation model. The changes observed are task-dependent, related to the individual problem and hence highly variable between and probably within individuals. We propose that the alterations in trunk muscle recruitment in patients are functional in that they reduce the probability of noxious tissue stresses by limiting range of motion and providing stabilization of the spine. This

Acknowledgements

The authors would like to thank Onno Meijer and Claudine Lamoth, for reviewing earlier versions of the text. This project was partially supported by NIH grant 5R01 AR 46844 and a grant provided by the Institute for Fundamental and Clinical Human Movement Sciences.

Jaap van Dieën obtained a PhD in Human Movement Sciences from the Faculty of Human Movement Sciences at the ‘Vrije Universiteit Amsterdam’ in the Netherlands. Since June 1996 he has been employed at this faculty, currently as professor of biomechanics. He is chairing the ergonomics program at this faculty. In addition, he is the head of a research group focusing on mechanical and neural aspects of musucloskeletal injuries. His main research interest is on control of muscles of the trunk and

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    Jaap van Dieën obtained a PhD in Human Movement Sciences from the Faculty of Human Movement Sciences at the ‘Vrije Universiteit Amsterdam’ in the Netherlands. Since June 1996 he has been employed at this faculty, currently as professor of biomechanics. He is chairing the ergonomics program at this faculty. In addition, he is the head of a research group focusing on mechanical and neural aspects of musucloskeletal injuries. His main research interest is on control of muscles of the trunk and upper extremity, where especially the interaction of muscle coordination, fatigue, joint load and stability is an important research topic. Jaap van Dieën was the first author of over 30 and a co-author of a similar number of papers in international scientific journals. In addition he has (co-) authored numerous abstracts and book chapters in the international literature and over 50 technical reports and publications in Dutch. He serves on the editorial boards of the Journal of Electromyohraphy and Kinesiology and Human Movement Sciences and is a regular reviewer for several other journals and funding agencies.

    Luc P.J. Selen received a BS degree in Applied Physics from the Hogeschool Enschede in 1999 and completed his MS in 2002 at the Faculty of Human Movement Sciences at the Vrije Universiteit in Amsterdam. He is currently a PhD student in the Institute for Fundamental and Clinical Human Movement Sciences (IFKB) at the Vrije Universiteit. His research interests include the influence of joint stiffening through co-contraction on movement variability.

    Jacek Cholewicki is a spinal biomechanist and Associate Professor of Orthopaedics and Rehabilitation at Yale University School of Medicine in New Haven, Connecticut. He holds cross-appointments to the departments of Mechanical Engineering and Biomedical Engineering where he teaches a graduate and undergraduate course in biomechanics. He received his Bachelor, Masters, and PhD degrees in Kinesiology from the University of Waterloo in Canada in 1986, 1990, and 1994, respectively. His research addresses the issues of lumbar and cervical spine function, spine injury mechanisms, tissue loading, and biomechanical modeling using both in vivo and in vitro experimental approaches. His current research interests include motor control of spine stability and the effectiveness of abdominal belts.

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