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ABSTRACT
Background: One of the diagnostic characteristics of the manipulable spinal lesiona musculoskeletal disturbance
detected by manual palpation and corrected with manipulationis said to be altered segmental tissue texture. Various manual therapy authors have speculated on the possible nature of this tissue change, with some authors hypothesizing that it represents deep segmental muscle overactivity. Objectives: To review the literature relating to the detection and nature of altered paraspinal tissue texture, proposed explanations for altered tissue texture, evidence for the plausibility of paraspinal muscle spasm, and evidence of muscle dysfunction associated with low back pain (LBP). Data Source: MEDLINE and CINAHL databases were searched using various combinations of the keywords paraspinal, muscle, palpation, EMG, spine, low back pain, pain, myofascial, hardness, manipulation, reliability, and somatic dysfunction, along with searching the bibliographies of selected articles and textbooks. Data Extraction: All relevant data were used. Results: Little direct evidence exists for the nature of abnormal paraspinal tissue texture detected by palpation. Palpation for tenderness is more reliable than palpation for tissue texture change. Indirect evidence from animal studies and experimental muscle inflammation support the plausibility of protective paraspinal muscle contraction. Increased paraspinal electromyographic (EMG) activity observed in subjects with LBP appears to be a result of voluntary and nonvoluntary changes in motor control, modified by psychophysiological responses to perceived stress rather than a simple protective reflex. Conclusion: Although little direct evidence exists of the nature of clinically detected paraspinal tissue texture change, the concept of reactive muscle contraction appears plausible. Increased paraspinal EMG activity associated with LBP does not appear to be mediated by a simple protective reflex. (J Manipulative Physiol Ther 2004;27:267-74) Key Indexing Terms: Spine; Muscle; Palpation; Chiropractic; Osteopathic Medicine
INTRODUCTION
alpation of musculoskeletal tissues forms a major part of physical examination for practitioners in many disciplines of manual therapy. For practi-
a School of Health Science, Victoria University, Melbourne, Australia. b Faculty of Human Development, Victoria University, Melbourne, Australia. Submit requests for reprints to: Gary Fryer, School of Health Science, City Campus Victoria University, PO Box 14428 MCMC, Melbourne 8001, Australia (e-mail: gary.fryer@vu.edu.au). Paper submitted December 2, 2002. 0161-4754/$30.00 Copyright n 2004 by National University of Health Sciences. doi:10.1016/j.jmpt.2004.02.006
tioners of osteopathy and chiropractic, paraspinal tissue texture changes are thought to be associated with the manipulable spinal lesion and are proposed by some authors to be a diagnostic indicatorand even a causeof intervertebral dysfunction.1-3 The nature of deep paraspinal tissue abnormalities detected by palpation, however, has been underresearched and is largely speculative. This is the first of two papers that will review and examine the proposed explanations for deep paraspinal tissue texture change and the evidence supporting these explanations. MEDLINE and CINAHL databases were searched using various combinations of the keywords paraspinal, muscle, palpation, EMG, spinal, low back pain, pain, myofascial, hardness, manipulation, reliability, and somatic dysfunction, along with searching the bibliographies of selected articles and textbooks. 267
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This article will review the practice of palpation to detect altered paraspinal tissue texture, explanations for paraspinal muscle dysfunction, evidence for the rationale of paraspinal muscle spasm, and the evidence for increased paraspinal muscle electromyographic (EMG) activity associated with low back pain (LBP). Part 2 will examine the evidence for decreased paraspinal EMG activity associated with LBP, deep paraspinal muscle atrophy, nonparaspinal muscle dysfunction, the effect of manipulation on paraspinal muscle EMG activity, and how this evidence may relate to tissue texture abnormalities detected with palpation. Finally, it will outline directions for future research that is needed to determine the exact nature of altered paraspinal tissue texture detected with manual palpation.
DISCUSSION
The Manipulable Lesion
Authors in the field of manual therapy claim that intervertebral dysfunction (known as somatic dysfunction, segmental dysfunction, chiropractic subluxation, joint blockage, or fixation by the various manipulating professions)1,3-8 can be detected by skilled manual palpation.1,3-5 In osteopathy, the diagnostic indicators of segmental dysfunction are said to be segmental asymmetry of bony landmarks, range of motion abnormality (increased, decreased, or a change in quality), tissue texture changes, and tenderness.1-3 Other manipulative professions use similar diagnostic criteria to diagnose manipulable lesions. Physiotherapists place emphasis on the altered quality of joint motion or end-feel,9-11 whereas the chiropractic profession has traditionally emphasized static asymmetry, sometimes employing radiographic analysis to determine positional asymmetry.6,7
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Proposed Explanations for Altered Tissue Texture Associated with Intervertebral Dysfunction
There has been much speculation on the etiology of the manipulable lesion, with various authors implicating the paraspinal muscles, zygapophysial joints, and the intervertebral disk as the underlying cause of motion restriction and tissue texture change. The model most accepted in the field of osteopathy and still quoted in most osteopathic texts3,5,34-36 is Korrs neurological concept of the facilitated segment, which implicates the deep paraspinal musculature as the prime cause of restricted segmental mobility and tissue texture change. From the 1940s to the early 1960s, osteopathic researchers Denslow et al and Korr et al37-42 conducted studies that they claimed provided evidence of segmental spinal cord hyperactivity, which Denslow first called the central excitatory state. They reported evidence of increased segmental muscle activity and segmental sympathetic nervous system output at spinal levels associated with clinically detected segmental dysfunctions. Korr43 developed the facilitated segment concept, where he proposed that minor unanticipated trauma could produce a discordant barrage of afferent input into the spinal cord from muscle spindle proprioceptors. This discordant noise would enter the dorsal horn of the spinal cord and alter the firing thresholds and excitability of the interconnecting neurons, bringing the normally anonymous segment into view of the central nervous system. All activity passing through that segment would become exaggerated, producing increased nociception, a and g motor activity to segmental muscles, and sympathetic output. This model attempted to explain the clinical findings of segmental dysfunction: tenderness and pain due to facilitated ascending nociception, joint range of motion restriction due to the resistance of shortened and overactive muscles, and tissue texture changes due to sustained muscle contraction and sympathetic induced circulatory changes.43 The concepts of muscle spasm and pain-spasm-pain cycle are popular explanations for hard and tender muscles, but the evidence to support these concepts is lacking.44 Lederman45 has criticized the belief, common in manual therapies, that relaxed muscles normally display a low level of motor contraction (neurological muscle tone) that may be turned up when dysfunction occurs. Neurological muscle tone appears to be controversial, as some authorities in the field of EMG claim that relaxed muscles have no motor activity,46 whereas others state that low-level motor unit firing contributes to resting muscle tone.47 The assessment of very low-level EMG activity in paraspinal muscles is complicated by the electrical noise generated by the heart, respiratory muscles, and extraneous sources of noise.48 The greatest weakness in all models that attribute muscle spasm as the cause of altered tissue texture and joint motion loss is the lack of evidence of abnormal motor activity associated with these clinical findings. The studies by
Denslow et al and Korr et al37-42 are over 50 years old and were, by todays standards, poorly described with insufficient data reported and no statistical analysis. Slosberg49 suggested that the diameter of the needles used by Denslow were larger and more disruptive than the fine-wire needle electrodes used today. Reproduction of these studies with modern equipment would help verify their significance. Hubbard et al50 recently examined the EMG activity of relaxed paraspinal muscles and found no significant differences between those detected as tender and abnormal with palpation and nontender muscles. This pilot study should be regarded as inconclusive due to its small sample size and problems encountered with noise and cardiac artefact. Interestingly, the one symptomatic subject in the study displayed a large increase in EMG activity over the painful site. Even Denslow51 had misgivings about their original research. In 1975, 34 years after the publication of his original article, Denslow conceded that not all palpable paraspinal tissue texture changes could be explained by muscle contraction. He suggested that it was possible that some inflammatory process may account for the abnormal tissues.51 Despite these admissions and the lack of corroborating evidence, Denslows work is still commonly cited to support the theory of paraspinal muscle spasm.34-36,52
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Researchers have demonstrated that electrical stimulation and mechanical deformation of the supraspinous ligament can produce reflex activation of the paraspinal muscles, which are most likely to be protective reflexes to produce unloading of the injured ligament. Stubbs et al54 electrically stimulated the supraspinous ligaments of 6 anesthetized cats and recorded fast and powerful reflex paraspinal muscle contraction. Williams et al55 demonstrated that prolonged flexion of the feline lumbar spine (by placing a load on the supraspinous ligament) produced initial reflex activity of the multifidus, which diminished in 3 minutes, and was followed by random bursts of activity, which Williams et al55 termed spasms. Solomonow et al56 examined the effect of mechanical deformation of the supraspinous ligament in 12 cats and reported that strong reflex multifidus activation was produced in the isolated ligament only when the stress in the ligament approached magnitudes causing risk or rupture of the tissue. Solomonow et al56 also electrically stimulated the supraspinous ligaments in 3 patients undergoing spinal surgery and recorded EMG discharges from the paraspinal muscles of 2 patients. Thus, Solomonow et al56 were able to confirm that electrical stimulation and mechanical deformation of the supraspinous ligament can elicit reflex paraspinal muscle activity and that such a reflex exists in humans.
the stretch reflexes of the jaw muscles of volunteers. Matre et al60 used hypertonic saline infusions to create muscle pain in the tibialis anterior and soleus muscles of 14 human volunteers. Matre et al61 reported an increase in the amplitude of the stretch reflex, suggesting increased muscle spindle sensitivity, but no change in the excitability of the a-motor neurone pool (as evidenced by the H-reflex). The increased stretch reflex appeared to occur only in the relaxed muscle. Increased spindle sensitivity may be less important when the muscle is functionally active, but it may be relevant to the detection of tissue changes due to the slight stretch produced when palpating a relaxed muscle. Although these studies support the theory of chemically induced muscle spindle sensitivity, 2 recent studies have failed to support the proposal of increased spindle sensitivity in LBP.62,63 The evidence for protective reflex muscle contraction and increased muscle spindle sensitivity lends credibility to the theory of muscle contraction as a component of intervertebral dysfunction. Although this theory would seem to have a plausible foundation, what must follow is evidence establishing increased or altered EMG activity of paraspinal muscles in regions detected as tender and abnormal to palpation.
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or adaptation to it and whether it could be a spinal cord reflex or a more complex change in central nervous system (CNS) control.
Decreased Flexion-Relaxation
The most consistent demonstration of increased paraspinal muscle activity in LBP, relative to healthy control subjects, has been the lack of lumbar muscle relaxation when the trunk is fully flexed.63-69 When pain-free subjects perform active full trunk flexion, there is normally minimal activity of the lumbar paraspinal muscle at the end of flexion, presumably as the trunk can be supported in this position by the tension of the posterior spinal ligaments. Many researchers have reported the loss of this flexionrelaxation response63-69 in LBP, as well as a reduced range of flexion63-65,67 and decreased paraspinal EMG activity when reextending.63,64,66,68,69 It is unknown whether the lack of paraspinal muscle relaxation during full trunk flexion is produced by a reflex from injured spinal ligaments, an unconscious guarding action as painful ligaments are stretched, or simply due to apprehension of a patient who believes further flexion will produce more pain and injury. Nouwen et al68 suggested that patients with chronic LBP move differently, possibly flexing from the hips and keeping their backs extended, which would explain the increased paraspinal activity in the flexed position. Ahern et al64,65 noted that the majority of chronic LBP patients failed to achieve the range of flexion where the relaxation response was likely to occur (63j F 13j) and concluded that guarded movement (slow cautious movement and/or decreased velocity relative to baseline; nonmethodical or jerky movement) explained approximately 27% of the variability in the relaxation response. Mannion et al70 reported, however, that there was no significant relationship between changes in the degree of flexion-relaxation and the range of lumbar flexion. Zedka et al63 examined the effect of experimentally induced pain (computer regulated saline infusion into the right lumbar erector spinae muscles) on paraspinal muscle activity. During trunk flexion, pain spontaneously decreased the velocity and range of trunk motion, paraspinal relaxation in maintained flexion was absent, and decreased paraspinal EMG activity occurred on reextension. When subjects were asked to voluntarily overcome this guarding strategy and be guided to perform flexion and extension at a prepain velocity and range, the EMG activity was similar, with only the left nonpainful paraspinal muscles achieving some degree of relaxation. Zedka et al63 questioned the view that the increased muscle activity in full flexion was a protective reflex initiated from the loading of injured spinal ligaments, because in their study the ligaments were uninjured and painless. They argued that the persistence of EMG changes, even when subjects overcame their natural tendency to move more slowly and over a smaller range while in pain,
suggested a more complex mechanism. They proposed that pain in any lumbar structure (ligament, joint, or muscle) may have produced a change in CNS strategy, which resulted in the muscle working in pain mode to protect the spine from extreme movement whenever pain was signalled.63 It is likely that the lack of flexion-relaxation exhibited by subjects with LBP can be due to both voluntary guarding behavior and a change in CNS strategy. Protective reflex contraction initiated from injured ligaments seems unlikely, given that the phenomena occurred with experimentally induced muscle pain alone. The relevance of this increased paraspinal activity to abnormally palpable resting paraspinal muscles is unclear. If a change in CNS strategy as a reaction to spinal pain results in paraspinal muscles working in an overprotective pain mode, it may be possible that nonvoluntary muscle guarding also occurs when the muscles are being palpated. This hypothesis has not yet been examined. No study has yet examined whether the resting activity of paraspinal muscles changes during the procedure of palpation.
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studies lend support to the proposal of muscle overactivity being associated with LBP and palpable paraspinal abnormalities, there still remains a lack of evidence demonstrating this increased activity in muscles that are detected as tender and abnormal to palpation.
episodes of acute pain may produce a stronger stereotypical, psychophysiological response in susceptible individuals. It seems possible that most reports of increased paraspinal EMG activity in LBP patients may be explained as a combination of voluntary guarding behavior65,68 and a change in CNS strategy, producing exaggerated pain mode muscle activity to limit excessive or unanticipated movement.63 Emotional and psychological experience of chronic pain may further modify or reinforce this altered CNS strategy to produce stereotypical patterns of guarding activity in response to real or imagined stress. The relevance of this abnormally increased muscle activity to paraspinal regions that are tender and feel abnormal to palpation remains untested, but it is feasible that increased muscle activity may be detectible with palpation and even the act of palpation may provoke further muscle guarding.
CONCLUSION
Although there is little direct evidence to support the belief that sustained muscle contraction is a feature of intervertebral dysfunction, the concept of protective muscle spasm appears plausible. Reflex multifidus muscle contraction has been demonstrated following electrical and mechanical stimulation of deep spinal structures in animals, and such a reflex has been demonstrated to exist in humans. Additionally, experimental muscle inflammation has been demonstrated to produce increased fusimotor activity and reflex-mediated muscle stiffness. Increased paraspinal muscle activity has been observed in LBP patients during full flexion, static postures, and as a reaction to stressful imagery. It appears that while voluntary guarding behavior may be responsible for increased activity in some patients, increased muscle activity is, in part, due to a nonvoluntary change in CNS control, a proposed pain mode strategy in response to pain originating from any spinal structure. There is evidence to support the proposal of abnormally increased paraspinal muscle activity as a consequence of spinal injury. Similar changes to those found in LBP patients may occur in the muscles adjacent to intervertebral injury and produce the commonly reported clinical findings of tenderness and altered tissue texture at a single intervertebral level. What must follow, however, is direct evidence of increased EMG activity associated with the detection of tender and abnormal to palpation paraspinal regions.
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