Is muscle co-activation a predisposing factor for low back pain development during standing? A multifactorial approach for early identification of at-risk individuals.

Abstract

PURPOSE AND SCOPE: Low back pain development has been associated with static standing postures in occupational settings. Previous work has demonstrated gluteus muscle co-activation as a predominant pattern in previously asymptomatic individuals who develop low back pain when exposed to 2-h of standing. The purpose of this work was to investigate muscle co-activation as a predisposing factor in low back pain development while including a multifactorial approach of clinical assessment tools and psychosocial assessments to identify individuals who are at risk for pain development during standing. RESULTS: Forty percent of participants developed low back pain during the 2-h of standing. Pain developers demonstrated bilateral gluteus medius and trunk flexor-extensor muscle co-activation prior to reports of pain development. Pain developers and non-pain developers demonstrated markedly different patterns of muscle activation during the 2-h of standing. A novel screening test of active hip abduction was the only clinical assessment tool that predicted pain development. CONCLUSIONS: Gluteus medius and trunk muscle co-activation appears to be a predisposing rather than adaptive factor in low back pain development during standing. A combination of a positive active hip abduction test and presence of muscle co-activation during standing may be useful for early identification of at-risk individuals.

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IS MUSCLE CO-ACTIVATION A PREDISPOSING FACTOR FOR LOW BACK PAIN
DEVELOPMENT DURING STANDING?
Erika Nelson-Wong and Jack P. Callaghan
Department of Kinesiology, University of Waterloo, Waterloo, ON
email: enelsonw@uwaterloo.ca
INTRODUCTION
Occupations involving static postures such as
prolonged standing have been associated with low
back pain (LBP) development [1]. While trunk
muscle co-activation has been found in people with
LBP compared with healthy controls [2], it is
unknown whether these differences preceded the
development of the LBP problem. Therefore, it
cannot be determined whether the muscle co-
activation is an adaptation to LBP or a predisposing
factor.
Previous work [3] has found muscle co-activation to
be associated with LBP development in previously
asymptomatic individuals. The purpose of this study
was to investigate whether muscle co-activation is a
predisposing versus adaptive factor in standing-
induced LBP. A multifactorial approach including
clinical assessment tools
questionnaires was used to enhance the clinical
relevance of the work.
and psycho-social
METHODS
43 volunteers, 22 male and 21 female, with no
history of LBP were enrolled. Following a clinical
examination by a physical therapist, 16 channels of
continuous electromyography (EMG) from the
trunk and hip were collected during 2-hrs of
standing. Participants were instructed to ‘stand in
their usual style’ as they completed light
occupational tasks. Participants rated LBP on a 100
mm visual analog scale (VAS) every 15 min.
Participants who exhibited increases of LBP > 10
mm were considered to be pain developers (PD).
Muscle co-activation was quantified with co-
contraction index [4] (CCI). Three-way general
linear models (group, gender and time) were used
for statistical analyses with p<0.05 for significance.
RESULTS
Participants clearly separated into two groups with
40% of participants being classified as PD (Figure
1). There were no gender differences in pain
development, gluteus
flexor/extensor co-activation as quantified by CCI.
medius or trunk

Figure 1: PD and NPD were clearly separated
based upon VAS scores during the 2-hours of
standing.

Figure 2: PD demonstrated higher gluteus medius
muscle CCI than NPD, especially during early and
late stages of standing (*p < 0.05).
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Time (min)
NPD
PD
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15 30 45 60 75 90 105 120
CCI (% MVC)
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PD
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The only clinical assessment tool that predicted PD
was a novel Active Hip Abduction (AHAbd) test (p
< 0.05) [5]. Bilateral gluteus medius and trunk
flexor/extensor CCI values were higher in PD
versus NPD during the initial and final stages of
standing (Figure 2).
PD and NPD groups demonstrated different
modulation of co-contraction throughout the
standing period. PD had a decrease in both trunk
and gluteus medius co-contraction during the
middle portion of standing, corresponding to the
period of acute pain development (Figure 3), while
the NPD group had an overall increase in their co-
contraction levels during the same time period
(Figure 4).

Figure 3: Pain Developers had a decrease in both
trunk and gluteus medius CCI during time period of
greatest pain development (30-90 minutes).
DISCUSSION
Low back pain developers had increased co-
contraction prior to any subjective reports of pain,
leading us to conclude muscle co-activation is a
predisposing rather than adaptive factor for LBP
development during this task. PD also demonstrated
decreased frontal plane control and reported more
difficulty in performance during the AHAbd clinical
test. Muscle co-activation during standing in this
group may be present as a compensatory motor
control pattern for an underlying deficiency in trunk
control that has not yet manifested with clinical
LBP symptoms. A combination of the above
findings could be useful in early identification of
individuals who are at-risk for LBP, especially
those exposed to occupational tasks involving
prolonged standing.

Figure 4: Non-Pain Developers had a general
increase in both trunk and gluteus medius CCI
during the same time period (30-90 minutes).
CONCLUSIONS
Individuals who develop LBP during standing
demonstrate different muscle activation patterns
than individuals who do not develop LBP.
Differences exist prior to pain development, and
therefore may be a predisposing factor for LBP
during standing. Some increase in muscle co-
activation during a relatively static, prolonged task,
may provide some protection against LBP
development.
REFERENCES
1. Kim J, et al. Appl Ergon 25 (1), 9-34, 1994.
2. Van Dieen J, et al. Journal of Electromyography
and Kinesiology 13, 333-351, 2003.
3. Nelson-Wong E, et al. Clinical Biomechanics
23, 545-553, 2008.
4. Lewek, M, et al. Osteoarthritis and Cartilage 12
(9), 745-751, 2004.
5. Nelson-Wong, et al. J Orthop & Sports Physical
Therapy, submitted in revision, 2009.
ACKNOWLEDGMENTS
The authors wish to acknowledge the Natural
Sciences and Engineering Research Council of
Canada. Dr. Nelson-Wong is also supported through
a PODS II scholarship, Foundation for Physical
Therapy, American Physical Therapy Association.
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