The Biological Rationale For Possible Benefits of Spinal Manipulation
SOURCE: Chapter X; AHCPR Publication No. 98-N002: December 1997
By Howard T. Vernon, DC
Manipulation is a form of treatment that dates to antiquity and has been practiced in some form in most cultures since that time (Lomax, 1997; Anderson, 1992). One of the first theories related to manipulation might be the statement attributed to Hippocrates: “Look to the spine as the cause of disease.” The theories of the early pioneers of chiropractic were firmly grounded in notions that had been widely held in the 1800s, particularly the idea of “spinal irritability” and its correlation with disease (Lomax, 1997; Terrett, 1987). Theories on the nature of the primary spinal disorder amenable to manipulation and on the mechanisms of action of spinal manipulation abound within chiropractic, osteopathy, physiotherapy, and manual medicine. The original chiropractic theory suggested that misaligned spinal vertebrae interfered with nerve function, ultimately resulting in altered physiology that could contribute to pain and disease. In recent decades, chiropractic theories about how mechanical spinal joint dysfunction might influence neurophysiology have undergone significant modification and reflect more contemporary views of physiology (Gatterman, 1995).
Spinal manipulative procedures produce a short-lasting (100-300 milliseconds), high velocity impulse into the body (Herzog, 1996; Triano, 1992). Herzog (1996, p.271) has summarized the work done on manipulative forces in his laboratory (Conway, 1993; Gal, 1995; Kawchuk, 1992; Kawchuk, 1993; Herzog, 1991; Herzog, 1993a; Herzog, 1993b; Herzog, 1995; Hessel, 1990; Suter, 1994) as follows:
- “The peak and preload forces achieved in CSMT (chiropractic spinal manipulative therapy) were lowest for (manipulations) in the cervical spine” while being similar in the thoracic and lumbo-pelvic regions.
- “The peak forces achieved using a (mechanical assistive adjusting device) were considerably smaller than any of the peak forces resulting from CSMT.”
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Triano and colleagues (Triano, 1992; Brennan, 1992) have quantified the applied forces of a manipulation and correlated them with physiologic responses (changes in leukocyte function) such that a threshold of approximately 500 N distinguishes potentially effective from “noneffective” procedures.
When joint structures are rapidly stretched in this manner, cavitation occurs internally and an audible “pop” may be heard. Brodeur (1995) reviewed the historical literature on joint cavitation, particularly the work of Sandoz (1976) in defining the “paraphysiologic space” and Mierau, (1988) in identifying the vacuum phenomenon created by rapid joint distraction with cavitation. The work of Mierau (1988) also provided the first experimental evidence of increased range of motion after cavitation.
Herzog’s group has addressed the issue of whether vertebrae actually move. Gal, (1995) provide evidence of absolute and relative intervertebral movements resulting from CSMT (see review by Herzog, 1996).
The hypothesized effects of manipulation common to most modern schools of thought can be categorized as either mechanical or neurological. In fact, manipulation has been described “as mechanical treatment with reflex effects” (Arkuszewski, 1988).
In terms of mechanical issues, the manipulable spinal disorder (traditionally termed “subluxation” in chiropractic, “somatic dysfunction” in osteopathy, and “fixation” or “functional blockage” in manual medicine) is characterized as a spinal joint strain/sprain with associated local and referred pain and muscle spasm. The function of the spinal joint is deranged by virtue of static misalignment and/or reduction of motion (i.e., “fixation,” “blockage,” or the more generic term “hypomobility”). Mechanisms that have been proposed for this dysfunction, particularly the hypomobility, include:
- Entrapment of a zygapophyseal joint inclusion or meniscoid (which have been shown to be heavily innervated by nociceptors (Giles, 1987; Bogduk, 1985).
- Entrapment of a fragment of posterior annular material from the intervertebral disc (again, innervated by nociceptors) (Bogduk, 1981, 1985).
- Stiffness induced by adhesions and scar tissue from previous injury and/or degenerative changes and adaptive shortening of myofascial tissues (Arkuszewski, 1988; Lantz, 1995).
- Excessive activity (spasm, hypertonicity) of the deep intrinsic spinal musculature, particularly in unilateral, asymmetric patterns (Blunt, 1995; Buerger, 1983).
Mechanisms of action of manipulation, which have been proposed to affect these mechanical issues, include: (1) release of entrapped synovial or disc tissues, thus reducing pain and restoring mobility; (2) stretching and breaking of adhesions; (3) the dynamic stretching of musculature and myofascial tissues. Korr (1975), Grice (1974), and Buerger (1983) proposed that manipulation might exert its effect by dynamic stretching of the muscle spindles and Golgi Tendon Organs (copiously located in the deep spinal muscles) thereby resetting the length/tension ratio in these muscles.
Herzog, (1995), Suter, (1994), and Triano (1992) have studied reflex muscular responses to CSMT and have reported brief but substantial reflex contractions which appear to be contingent on the speed of impulse (high-velocity) rather than the presence or absence of cavitation. Whether these brief bursts of spinal EMG activity represent a prerequisite to subsequent relaxation or “resetting of muscle spindle gain” remains to be demonstrated conclusively, although preliminary clinical studies have demonstrated attenuation of spinal EMG activity post-manipulation (Thabe, 1982; Shambaugh, 1987).
The second category of hypothesized mechanisms involves “neurological” issues. The classical theory of “pinched nerve” has given way to a model that includes both direct and indirect effects on the function of the peripheral and central nervous system resulting from spinal dysfunction. Direct effects (or what Korr (1975) calls “non-impulse”-based mechanisms) involve compression/irritation of the neural structures in and around the intervertebral foramen. This area is a fertile zone for entrapment of neural structures responsible for pain, sensation, motor, and autonomic function. Effects of partial occlusion of the nerve bed, such as those that might occur with disc herniation, foraminal stenosis, or spinal instability, have been investigated (Triano, 1982). Dynamic perturbations of the nerve rubbing across a partial obstruction give rise to inflammatory responses. The putative effects of such neural compressions are currently better understood in “orthopedic” terms as neurogenic pain, and reduced sensation and motor power (i.e., as a radiculopathy). The effects of compression on autonomic structures (nerves, rami, and ganglia), however, are only just beginning to be understood, although chiropractors have theorized that these effects may extend to visceral function (Lantz, 1995).
The indirect effect of spinal dysfunction (what Korr (1975) called “impulse-based” mechanisms) involves the effects of persistent spinal pain and hypomobility on the reflex activities of the associated spinal cord levels (or “neuromere”). Korr (1975) proposed a model of “central facilitation.” Many mechanisms have been elucidated suggesting that spinal cord sensorimotor processing leads to “activity-dependent changes” or “neuroplasticity,” which results in long-lasting firing patterns that reinforce pain perception (Woolf, 1989; Mense, 1993; Gillette, 1995). The current term for such changes at the spinal cord level is “central sensitization” (Coderre, 1993). This model is now used to explain the clinical features of chronic pain, persistent motor changes, and autonomic dysfunction resulting from neuropathic and somatic pain. There is evidence that axial or spinal structures have particularly strong capacities to induce central sensitization (Gillette, 1995; Patterson, 1986; Hu, 1993) and thereby produce the clinical features described above, most predominantly back and neck pain.
Proposed mechanisms of action of manipulation on these “neurological” phenomena can be divided into two categories: reduction of compressive insult to neural tissues, and the creation of stimulus-induced reflex changes. The former mechanism is relatively straightforward in that manipulation is hypothesized to relieve the compressive insult on nerve roots and autonomic fibers within the intervertebral foraminae, or affect disc/facet athropathy (and inflammatory or noninflammatory mechanisms). In the latter mechanism it is proposed that the dynamic stretching produced by manipulation (particularly when the “crack” of cavitation occurs) induces a barrage of activity in joint and muscular mechanoreceptors that is transmitted along “large-fibre” afferents and which produces inhibitory effects within the nervous system. These effects are proposed to be both local (i.e., at the spinal level) and “central,” in that they may involve so-called descending inhibitory pathways (Gillette, 1995; Le Bars, 1992; Vernon, 1986). These same mechanisms have been proposed to explain the therapeutic effects of acupuncture and TENS, and are generically known as “stimulus-produced analgesia” (Pressman, 1984). In other words, it is hypothesized that the deleterious effects of excitation in the pain and sensorimotor pathways are “turned down” (clinically = “relieved”) by precise, therapeutic somatic stimulation. The spinal tissues appear to be particularly amenable to this process, probably because of their unique patterns of afferent input into the central nervous system, with a high level of convergence existing with other somatic and visceral inputs onto the same spinal tract projection cells (Gillette, 1995; Patterson, 1986; Hu, 1993).
Although of great interest to many neuropathologists and chiropractors, these theories described remain largely speculative. A recent review of the limited basic science research in chiropractic noted that nearly all of the theories of the effects and mechanisms of action of spinal manipulation still lack adequate research and that no definitive anatomic or biomechanical studies have yet identified the lesion manipulated (Brennan, 1997). The few animal studies performed to date have failed to provide conclusive support for or against the existence of a spinal lesion. Human studies have also been inconclusive. For example, of three studies of the effect of spinal manipulation on plasma beta-endorphin levels (which could be involved in relief of pain), one found a slight but statistically significant increase (Vernon, 1986) while the other two failed to confirm this (Christian, 1988; Sanders, 1990). Other studies of the effect of spinal manipulation on the immune system has shown strong consistency of the mechanistic action on chemiluminescence, but its clinical importance is not known (Brennan, 1997). The review by Brennan, concluded with recommendations for specific lines of investigation that are likely to produce more definitive conclusions regarding the potential physiological and anatomic mechanisms underlying the effects of spinal manipulation. The effect of spinal manipulation on patients with co-morbid metabolic and neurogenic complications, structural anomalies, injury, and aging continues to be fertile ground for further investigation. Models of biomechanical and physiological effects of these complications and natural events and discussions of manipulation effects are now emerging in the literature (Triano, in press).
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