Objectives: The purpose of this study was to examine the relationship between pain-related fear, lumbar flexion, and dynamic EMG activity among persons with chronic musculoskeletal low back pain. It was hypothesized that pain-related fear would be significantly related to decreased lumbar flexion and specific patterns of EMG activity during flexion and extension.
Study Design: Data was obtained from subjects who, on a single day, completed self-report measures of pain and pain-related fear, and were interviewed to determine demographic and pain information. Subjects then underwent a dynamic EMG evaluation for which they were asked to stand, then bend forward as far as possible, stay fully flexed, and return to standing. Lumbar EMG and angle of flexion were recorded during this time. A flexion-relaxation ratio (FRR) was computed by comparing maximal EMG while flexing to the average EMG in full flexion.
Subjects: Seventy-six persons with chronic musculoskeletal low back pain.
Results: Zero-order correlations indicated that pain-related fear was significantly related to reduced lumber flexion (r = -0.55), maximum EMG during flexion (r = -0.38) and extension (r = -0.51), and the FRR (r = -0.40). When controlling for pain and demographic factors, pain-related fear continued to be related to reduced lumbar flexion. Using a path-analytic model to examine whether angle of flexion mediated the relationship between fear and EMG activity, the models examining maximal EMG during flexion and extension supported the notion that pain-related fear influences these measures indirectly through its association with decreased range of motion. Conversely, pain-related fear was independently related to higher average EMG in full flexion, while angle of flexion was not significantly related. Pain-related fear was directly related to a smaller FRR, as well as indirectly through angle of flexion.
Conclusions: Pain-related fear is significantly associated with reduced lumbar flexion, greater EMG in full flexion, and a smaller FRR. The relationship between pain-related fear and EMG during flexion and extension appears to be mediated by reduced lumbar flexion. These results suggest that pain-related fear is directly associated with musculoskeletal abnormalities observed among persons with chronic low back pain, as well as indirectly through limited lumbar flexion. These musculoskeletal abnormalities as well as limited movement may be involved in the development and maintenance of chronic low back pain. In addition, changes in musculoskeletal functioning and flexion associated with pain-related fear may warrant greater attention as part of treatment.
Chronic low back pain (CLBP), particularly of musculoskeletal origin, has become a major focus of concern for both employers and health care professionals. Although several factors have been proposed to be responsible for or to perpetuate CLBP, little is known about the disorder. Several theories have been advanced to explain the disorder, and research addressing the tenability of each one has been mixed. One major theory, the biomechanical model, proposes that CLBP may be the result of muscle asymmetries or abnormally low levels of muscle activity. 1 This theory suggests that abnormal electromyographic (EMG) activity is a result of poor posture and guarding that develops in response to an original injury. 2 Several investigators proposed that this irregular muscle activity contributes to spinal instability, which in turn enhances the potential of infringement upon nerve endings and thereby produces pain. 1,3,4 It has also been suggested that pain may also originate from muscle secondary to microcontractures as in myofascial pain, 5 as well as other structures such as the disks, joints, and ligaments. 6-8
Another major theory of chronic back pain is the reflex-spasm model. While proponents of this theory debate the relative importance of physical or psychosocial stressors in the development of CLBP, one or both of these factors are believed to contribute to an ongoing cycle of reflex-spasm. 1,9-11 The model that emphasizes the contribution of psychosocial stress to reflex-spasm has been referred to as the diathesis-stress 12 or stress-hyperactivity model of chronic pain. 13
Evidence for these various theories is mixed. Studies supporting the biomechanical model have found that persons with CLBP display lower EMG levels compared with controls while sitting and during movement, 3,13-15 as well as abnormal muscle patterns or asymmetries compared with controls. 2,16,17 In support of the reflex-spasm model, studies have found increased EMG in response to painful stimulation, and greater EMG in static postures. 9,17,18 Research has also demonstrated that persons with CBP have elevated EMG during dynamic activity, greater EMG in response to stress, and higher left-right asymmetries. 19-22 Additional studies have failed to support the reflex-spasm model. 10,23
Several methodological issues have been raised to explain these discrepancies, including heterogeneous groups of patients with different pathology and pain in different sites. 24 Many authors encourage the evaluation of dynamic EMG activity, as EMG in static positions may not be representative of what occurs during activities of daily living. 25 Two studies have examined continuous ambulatory monitoring of EMG activity in persons with CBP. One found that paraspinal muscle activity did not differ between persons with CBP and controls, nor was it related to self-reported pain intensity. 26 Geisser et al 27 found a significant relationship between physical activity and pain among persons with CLBP, as well as an association between perceived stress and pain. No relationship between EMG activity and pain was observed.
One pattern of abnormal muscle activity that has consistently been shown to be associated with CLBP is an absence of relaxation of the lumbar paraspinal muscles in full-flexion. In healthy persons who are asked to stand quietly, the surface EMG signals from the paraspinal muscles are generally low. As a person bends forward, EMG activity increases as the muscles support the trunk at a greater angle to gravity. Near full flexion, ligamentous support becomes more important and lumbar EMG activity drops, often to a level less than the activity recorded when standing upright. This paraspinal relaxation on terminal flexion, first reported in the late 1940s by Allen, 27 is known as the flexion-relaxation phenomenon (FRP). Many studies conducted among persons with CLBP indicate that the FRP is absent in this population. 3,28-30 Ahern et al 3 reported that the presence or absence of the FRP correctly identified 86% of persons with CLBP and healthy controls, and Watson et al 8 reported a similar rate of 89%. This response has been shown to be significantly related to disability ratings and pain behavior among persons with CLBP, 31-32 and has been shown to be sensitive to spinal pathology such as disk herniation. 33 Studies indicate that the FRP has good test-retest reliability, even in clinical populations. 8,34
Little is known about the factors that contribute to the absence of the FRP in persons with CLBP. Ahern et al suggested that the absence of the FRP in persons with CLBP may be a result of limited lumbar flexion. 3 Most argue that limited flexion is not responsible for this finding, as persons with CLBP can generally reach 40 degrees of flexion, where the FRP is believed to begin. 31 However, some observe that there is substantial variability in the angle where the FRP starts. 3,31 In addition, due to altered body mechanics, persons with CLBP have been observed to display only 27 degrees of true lumbar flexion. 3 Alternatively, it has been proposed that muscle EMG abnormalities may be a response to pain, as pain has been shown to have some influence on muscle firing. 35 However, two studies failed to find a relationship between pain state and EMG among persons with CLBP. 3,36 Finally, it has been suggested that changes in paraspinal activity may be a compensatory response to improve spinal stability and decrease pain during movement. 8,35
Several authors have suggested that EMG abnormalities in persons with back pain may be due to pain-related fear or volitional guarding during movement. 3,8 It has been demonstrated that persons with CLBP display abnormal muscle activity while watching a videotape of persons performing strenuous activity. 37 The authors predicted that muscular reactivity would be greater for persons high in pain-related fear, and that this effect would be moderated by negative affect. Unexpectedly, the authors found that subjects responded to the videotape with decreased muscle tension, although subjects high in pain-related fear tended to display less of a decrement compared with persons with CLBP who reported low fear. Vlaeyen and Linton 38 propose that pain-related fear and resulting muscular reactivity may be related to the development and maintenance of CLBP. 38 This assertion seems reasonable given that pain-related fear has been shown to be consistently related to disability among persons with CLBP, and has also been found to be a potent predictor of chronicity among persons with acute low back pain. 39
Watson et al 40 examined the relationship between pain-related fear and the flexion-relaxation ratio (FRR), defined as the ratio of maximal muscle activity in flexion to the average EMG activity in full flexion, among persons with CLBP. The authors found a significant, inverse relationship between pain-related fear and the FRR, whereby persons with higher pain-related fear tended to display a lower ratio. In addition, the authors found a significant increase in the FRR following a pain management program, which was significantly associated with decreased pain-related fear. Changes in range of motion or self-report of pain as a function of treatment were not related to changes in the FRR. The authors concluded that pain-related fear promotes muscle guarding during flexion, which in turn contributes to the development and maintenance of chronic pain. However, the authors did not examine how fear was related to each component of the FRR, as previous studies have suggested that persons with CLBP demonstrate reduced EMG during flexion as well as higher EMG activity in full flexion. 3,8
In the present study, we wished to directly examine the relationship between pain-related fear, as measured by the Tampa Scale of Kinesiophobia-2 (TSK-2), 41,42 and EMG activity and angle of flexion among persons with CLBP. Extending the findings of Watson et al, 40 we wished to determine how pain-related fear influences the components of the FRR (maximum EMG in flexion and average EMG in full flexion) as well as the FRR itself. We hypothesized that persons with CLBP who demonstrated higher pain-related fear would display decreased EMG levels in flexion and extension, greater EMG levels in full flexion, and a lower FRR compared with persons with CLBP who exhibited low pain-related fear. In addition, we hypothesized that pain-related fear would be significantly associated with decreased flexion. Lastly, we wished to examine whether angle of flexion might account for any observed relationship between pain-related fear and lumbar EMG by statistically examining the independent influence of pain-related fear and angle of flexion on EMG activity. As pain-related fear has been shown to be associated with restricted movement, 43 it is possible that fear may be related to abnormal EMG activity through limited movement or flexion.