Full length articlePain catastrophizing and trunk muscle activation during walking in patients with chronic low back pain
Introduction
Individuals with low back pain (LBP) tend to walk slowly [1], which may be a means of reducing spine motion [2]. This should normally lead to lower trunk muscle activation [3], but there is evidence that some individuals with LBP increase trunk muscle activity during gait, possibly as a “guarding strategy” to further limit spine motion [4], [5]. Furthermore, it has been suggested that muscle guarding is more closely related to the psychological response to pain than to pain intensity [6].
There are conflicting findings on pain-induced trunk muscle guarding during gait. Arendt-Nielsen et al. [7], for example, reported a decrease in the phasic nature of EMG patterns during gait in individuals with chronic LBP, which could reflect an attempt to splint the spine. Lamoth et al. [8], on the other hand, found that induced pain has only minimal effects on the global pattern of lumbar erector spinae activity. The influence of psychological factors on trunk muscle activity during gait is also unclear. Two previous studies have found no relationship between fear-avoidance beliefs and lumbar EMG [4], [9]. Pain catastrophizing, however, has been linked to increase erector spinae activity during gait [10].
The objective of this cross-sectional study is twofold: first, to investigate whether the amplitude of trunk muscle activation differs between individuals with and without chronic LBP, when walking on a treadmill at a self-selected speed; second, to determine if the amplitude of trunk muscle activation is affected by pain catastrophizing in individuals with chronic LBP. We hypothesized that higher trunk muscle activation is used by persons with LBP during walking as a guarding strategy that can be influenced by pain catastrophizing.
Section snippets
Participants
Thirty individuals with chronic LBP were divided into two age- and gender-matched groups, based on their scores on the Pain Catastrophizing Scale (PCS) [11]: high (HLBP: PCS ≥ 21/52) and low (LLBP: PCS ≤ 20/52). The cut-off value of 20/52 was chosen based on the median value for the PCS, as reported in the PCS User Manual [12]. Inclusion criteria for both groups were: nonspecific LBP (excluding serious pathology, spinal stenosis and radiculopathy [13]) primarily located between the lower ribs and
Results
A significant main effect of Group was found for the percentage sub-MVIC EMG amplitude of MF, bilaterally (RMF: F = 4.546, p = 0.016; LMF: F = 3.998, p = 0.026) as well as for LRA (F = 4.604, p = 0.016). Post-hoc comparisons revealed that amplitudes for these 3 muscles were significantly higher for the HLBP group than for controls (Fig. 1).
Significant interactions between Group and Sub-phase of gait were found in EO (REO: F = 3.719, p = 0.015; LEO: F = 3.477, p = 0.014) and ESI (RESI: F = 2.749, p = 0.033; LESI: F =
Discussion
Our findings indicate that, at self-selected gait speeds, the activation amplitude for certain trunk muscles is higher among individuals with chronic LBP who exhibit high pain catastrophizing (HLBP) than for healthy controls, when normalized to a standardized, sub-maximal task. This pattern was significant across the whole gait cycle (main effect of Group) for 3 of the 10 trunk muscles assessed (LRA and MF bilaterally), with another 2 (EO bilaterally) showing similarly elevated levels of
Conclusion
The findings of this study provide evidence for an association between pain catastrophizing and altered neuromotor behavior during gait, among individuals with LBP. This underscores the biopsychosocial nature of LBP, where the psychological response to pain may influence not only the patient’s perception of their condition, but may manifest in physical behaviors that are generally controlled at a subconscious level. The findings of the current study also provide some support to the “guarding
Conflicts of interest
The authors have no relevant financial activities and no conflicts of interest to disclose in relation to this work.
Acknowledgements
This work was supported partially by funding from the Physiotherapy Foundation of Canada, the Quebec Rehabilitation Research Network (REPAR), and the Quebec health research funds (FRQS).
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