Gluteus medius muscle activation patterns as a predictor of low back pain during standing
Introduction
It is well known that low back pain (LBP) is a major contributor to escalating health care costs and disability in North America. It is estimated that 70–85% of all adults will experience a significant episode of LBP at some point in their lives (Giesecke et al., 2004). There are over 700,000 workers’ compensation claims for work-related LBP in the United States each year (Waddell, 2004), and one third of worker’s compensation costs are related to LBP (Abenhaim et al., 2000). While occupational manual material handling tasks have been extensively identified as an important contributing factor in LBP and discomfort (Norman et al., 1998, Adams et al., 1999), static low magnitude exposures such as prolonged standing have also been associated with the development of LBP and discomfort (Macfarlane et al., 1997). Mechanisms for development of LBP are widely considered to be multi-factorial (Linton, 2000, Kumar, 2001, Waddell, 2004), therefore the effective prediction of who will develop LBP remains complex and problematic (Leboeuf-Yde et al., 1997).
Many researchers have reported differences in muscle activation patterns in people with LBP (Hungerford et al., 2003, Van Dieen et al., 2003b, Ferguson et al., 2004, Pirouzi et al., 2006, Gregory et al., 2007). A primary finding that is consistent across studies is the presence of agonist–antagonist muscle co-activation in people who report LBP. One known consequence of increased muscle co-activation is a commensurate increase in spine loading (Granata and Marras, 2000). There has been an assumption that this altered muscle activation pattern in people with LBP is in response to, or an adaptation to their condition (Van Dieen et al., 2003a, Van Dieen et al., 2003b, O’sullivan, 2005). The bulk of the existing literature deals with cohort investigations (i.e., clinical LBP populations compared with healthy, asymptomatic populations). A limitation of this methodology is that it cannot be ascertained if altered muscle activation patterns were present in the clinical groups prior to the onset of their dysfunction, and therefore it remains unknown whether these patterns are adaptive, or in fact contributory to the problem of LBP. There are relatively few studies that have examined muscle activation patterns during prolonged exposures to static postures, such as those commonly seen in real-world workplace environments (Gregory et al., 2007). Typically, studies focused on examining LBP have not included the hip musculature in their analyses. However, hip function has been shown to be an important contributor to both trunk and spine function, and therefore likely plays a role in the development and response to LBP (Kankaanpaa et al., 1998, Leinonen et al., 2000, Nadler et al., 2001, Gombatto et al., 2006). Winter and colleagues (1996) identified synergistic muscle activity at the hip as a fundamental mechanism for medio-lateral postural control during standing, therefore the hip musculature should be considered during the study of any activity involving standing.
The primary purpose of this work was to investigate differences in trunk and hip muscle activation patterns in asymptomatic individuals during prolonged standing while performing simulated occupational tasks. A secondary purpose was to determine whether identification of individuals who would develop LBP during prolonged standing could be achieved based upon their muscle activation patterns.
A small percentage of the participants were expected to develop significant levels of LBP during the prolonged standing task. It was hypothesized that there would be differences in trunk and hip muscle activation patterns between those who developed pain and those who did not. Specifically, we expected to find increased agonist–antagonist muscle co-activation in LBP developers. Furthermore, it was expected that these differences would be sufficient to enable separation of subjects into pain and non-pain groups prior to viewing their self-reported pain ratings.
Section snippets
Methods
Data for this work was collected by two independent researchers, using identical protocols, and was analyzed retrospectively for this research study.
Prediction of low back pain development
Seventeen of 23 participants were correctly predicted to have presence or absence of LBP during prolonged standing based upon the single factor of Rxy–LGM–RGM polarity. Fig. 1, Fig. 2 show example EMG recordings for the left and right GM muscles with the corresponding cross-correlation values. Fig. 1 shows a typical pattern of synergistic GM muscle activity during standing from a non-LBP subject, with a corresponding negative Rxy value. Conversely, Fig. 2 shows a typical pattern of GM muscle
Discussion
The primary aim of this work was to determine whether muscle activation patterns differed among asymptomatic individuals performing occupational tasks during standing. The secondary aim was to determine whether differences in muscle activation patterns could be used to differentiate individuals who would experience LBP during a low-demand functional activity from those who would not. A large percentage of previously asymptomatic individuals (65%) in this study experienced significant levels of
Conclusion
Participants who developed LBP during prolonged standing demonstrated co-activation of the left and right GM muscles versus synergistic, reciprocal activation of these muscles in those who did not develop LBP. These participants were a non-clinical population, yet LBP was functionally induced through a low demand, common activity of standing. We were able to predict, with moderate success, those individuals who would develop LBP based upon the single factor of co-activation of hip musculature
Acknowledgments
The authors wish to acknowledge the Natural Sciences and Engineering Research Council Canada, AUTO21-Network of Centres of Excellence, Canadian Institute for the Relief of Pain and Disability, and Canadian Institutes for Health Research for financial support, as well as Sandy Sperling for her assistance with data collection. Dr. Jack Callaghan is also supported by a Canada Research Chair in Spine Biomechanics and Injury Prevention. Erika Nelson-Wong is supported in part by a scholarship through
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