The reduction of pain and disability from spinal manipula- tion is well recognized and clinically documented.147,194,199,334-340
“Numerous studies suggest that SM alters central processing of noxious stimuli because pain tolerance or pain threshold levels can increase after manipulation.”261 The mechanisms by which manip-
ulation inhibits pain, however, are matters of speculation and still under investigation. Proposed hypotheses have suggested that manipulation has the potential to remove the source of mechanical pain and inflammation or induce stimulus-produced analgesia.
The case for decreasing pain by removing its mechanical source is empiric and deductive. The pain associated with mechanical disorders of the musculoskeletal system is a product of physical deformation, inflammation, or both.341 It is reasoned that
manual therapy effective at reversing or mitigating underlying structural and functional derangements will remove the source of pain and the associated pain-producing agents as structures are returned to normal function.
The argument for stimulus-produced analgesia is bolstered by experimental evidence that suggests that chiropractic adjustments induce sufficient force to simultaneously activate both superficial and deep somatic mechanoreceptors, proprioceptors, and nocicep- tors. The effect of this stimulation is a strong afferent segmental barrage of spinal cord sensory neurons, capable of altering the pat- tern of afferent input to the central nervous system and inhibiting the central transmission of pain (Figure 4-20).341-345
Gillette342 suggests that spinal adjustments may initiate both
a short-lived phasic response triggered by stimulation of superfi- cial and deep mechanoreceptors, and a longer-lived tonic response triggered by noxious-level stimulation of nociceptive receptors. The phasic response is hypothesized to initiate a local gating effect, but pain inhibition terminates with cessation of therapy. The tonic response initiated by noxious levels of mechanical stim- ulation is more powerful and capable of outlasting the duration of applied therapy.344
Adjustments that induce joint cavitation and capsular distrac- tion may be a source of nociceptive stimulation capable of initiat- ing relatively long-lasting pain inhibition. This concept supports the premise that the slight discomfort that may be associated with adjustments is causally associated with a positive therapeu- tic effect.334
The potential for spinal adjustments to act directly on the pain system opens up the possibility that manipulation may have the ability to diminish persistent pain that is neuropathic in ori- gin.345 Chronic neuropathic pain may result from plastic changes
and central sensitization of the nervous system. Central sensiti- zation refers to plastic changes in the nervous system that result from persistent amplification of nociceptive synaptic transmis- sion. This can result in the persistence of pain states even after the offending peripenial pathologic injury and inflammation have resolved.344
The short-term bursts of proprioceptive and nociceptive input associated with adjustments, much like transcutaneous electrical nerve stimulation and acupuncture, have also been theorized to increase the levels of neurochemical pain inhibitors.337 Both a local
release of enkephalins, initiated by stimulation of the neurons of substantia gelatinosa, and a systemic increase in plasma and cere- brospinal fluid endorphin levels, initiated by simulation of the hypothalamic pituitary axis, have been proposed. Both substances act as endogenous opioid pain inhibitors and may play a role in the analgesic effects of adjustments.
Doctor reassurance and the laying-on of hands may also impart a direct analgesic effect, which must be factored into the equation when calculating the effects of adjustments and manual therapy. The contact established during a skilled evaluation of the soft tis- sues indicates the doctor’s sense of concern and skill. Paris331 states
that with the addition of a skilled evaluation involving palpation for soft tissue changes and altered joint mechanics, the patient becomes convinced of the clinician’s interest, concern, and manual skills. If the examination is followed by treatment and an adjustive cavitation (crack), further positive placebo effects may be regis- tered. The astute clinician accepts and reinforces this phenom- enon if it influences the patient’s recovery. This does not excuse misrepresentation or irresponsible exaggeration of the therapeutic effect.
Muscle spasm (hypertonicity)
Numerous authors have presented the potential causative role of hypertonic muscles in the development of joint dysfunction and spi- nal pain.24,238,289,292,346-349 The concept that restricted joint movement
may result in increased segmental muscle tone or spasm is supported by the knowledge that muscles not only impart movement but also impede movement. Joint movement depends on a balance between its agonist and antagonists. If this balance is lost and antagonistic muscles are unable to elongate because of involuntary hypertonicity, the joint may be restricted in its range or quality of movement.
Increased resting muscle tone or spasm may be initiated by direct provocation or injury to myofascial structures or indi- rectly by stimulation or injury to associated articular structures. Direct overstretching and tearing of muscle lead to stimulation of myofascial nociceptors and protective muscle splinting. The intersegmental muscles of the spine may be especially vulnerable to incidents of minor mechanical stress and overstretching. They are not under voluntary control. They act primarily to stabilize and integrate segmental movements in response to global move- ments of the trunk. As a result, they may be especially vulnerable to unguarded movements and the induction of reactive splinting.
Korr346 suggests that unguarded and uncoordinated move-
ments may approximate the short segmental muscles of the back and reduce annulospiral receptor activity in the muscle spindle complex and produce muscle spasm. Maigne291 envisions a similar
lesion (articular strain), but speculates that it results from abnormal
sustained postures or poorly judged movements that induce minor intersegmental muscle overstretching and cramping. Both specu- late that segmental muscle spasm, once initiated in the back, may be hard to arrest. Contracted segmental muscles of the back, unlike the voluntary appendicular muscles, are not easily stretched by the contraction of antagonistic muscle groups. As a result, this condi- tion may not be inhibited by active stretching and therefore may be less likely to be self-limiting.291 Research published in 2000
demonstrated that muscle spasm reduced the ability of paraspinal muscle stimulation to evoke cerebral potentials.350 “Spinal manipu-
lation reversed these effects, reducing muscle spasm and restoring the magnitude of the evoked cerebral potentials.”261
Myofascial Cycle
A central complicating feature of many of the internal and exter- nal derangements of the motion segment is the induction of a self- perpetuating myofascial cycle of pain and muscle spasm. The articular soft tissues are richly innervated with mechanoreceptors and nocice- ptors, and traction or injury to these structures may lead to the ini- tiation of local muscle splinting. With time, the continued muscle contraction may lead to further muscle fatigue, ischemia, pain, and maintenance of muscle spasm and joint locking (Figure 4-21).
High-velocity adjustments are suggested as treatments that may be effective in interrupting this cycle. Several theories exist as to the mechanism by which adjustments relieve muscle spasm. Both are speculated to induce a reflex response in muscle—one
Figure 4-20 Diagram suggesting the mechanism by which a high-velocity chiropractic adjustment inhibits the central transmission of pain through activation of mechanoreceptors and nociceptors. (Modified from Gillette, Cassidy JD, Lopes AA, Yong-Hing K: The immediate effect of manipulation versus mobilization on pain and range of motion in the cervical spine: A randomized controlled trial, J Manipulative Physiol Ther 15:570, 1992.)
Pain transmission cell A mechanoreceptors
A and C nociceptors Pain Posterolateral quadrant white matter Anterolateral quadrant white matter Supersegmental descending analgesic system Inhibitory interneuron
through direct action on muscle and the other reflexly through joint distraction (cavitation). The direct muscle model346 specu-
lates that quick traction and excitation of the Golgi tendon organ (GTO), located in the muscle tendon junction, act as brakes to limit excessive joint movement and possible injury by inhibiting motor activity. The concept is that adjustments induce a strong stretch on the muscle tendon complex, activate the GTO, and induce reflex muscle relaxation (autogenic inhibition). Although this model seems reasonable, evidence suggests that the GTO has a less profound effect than initially envisioned. Watts and associ- ates349 found that stimulation of the GTO produces a very mea-
ger inhibitory effect on motor neuron activity. This information implies that the GTO plays a more minor role in the inhibition of muscle spasm than initially proposed and brings into question its relationship to postadjustment muscle relaxation.
In contrast, stimulation of articular low- and high-threshold mechanoreceptors and nociceptors has demonstrated a notable inhibitory effect on segmental motor activity.342 Mechanoreceptors
and nociceptors are also widely embedded in articular soft tissues, muscle, and skin. High-velocity adjustments induce enough force to stimulate these structures and induce a burst of somatic afferent receptor activity.281,342 Based on this information, it seems reason-
able to assume that joint and soft tissue mechanoreceptors and nociceptors have the potential to play a material role in the inhibi- tion of muscle spasm and the interruption of painful myofascial cycles and joint locking.
Clinical investigations on the effects of spinal manipulation on muscle activity are very limited. Investigations have centered on the effects of manipulation during and after the application of manipulation. Using surface electromyograph (EMG), Herzog and others351–353 investigated the immediate effects of thoracic
SMT on paraspinal muscle activity. They applied prone unilateral quick (HVLA) and slow (3- to 4-second) “manipulations” to the
thoracic transverse processes. Both procedures consistently induced momentary increased muscle activity during their application. The high-velocity manipulations were associated with a fast, burst- like EMG signal, and the slow manipulation with a gradual increase in EMG activity. Cavitations induced during the application of the slowly applied manipulation were not associated with increased EMG activity, leading the researchers to speculate that cavita- tion alone is not sufficient to induce a reflex muscular response. The myoelectric response recorded during thoracic adjustments did conflict with the application of the adjustive forces. In con- trast, Triano and Schultz161 were unable to record any significant
myoelectric activity or muscular responses with the application of HVLA SP lumbar-adjusting procedures.
Investigations into more prolonged effects on resisting mus- cle activity, although very limited, have shown reductions in paraspinal muscle activity and imbalance with full-spine adjusting procedures.352,353
nerve root Compression
Chiropractic, osteopathy, and manual medicine has envisioned manual therapy affecting not only somatic disorders, but also vis- ceral disorders through neurologic means.17 The early paradigm
presented in chiropractic stressed a model of altered NR func- tion as the basis for secondary somatic or visceral dysfunction. It was theorized that subluxations induce structural alteration of the intervertebral foramina, leading to compression of the contained neurovascular structures and altered function of the NR as electri- cal transmission or axoplasmic flow is impaired. The postulated net result of this process (nerve interference) was dysfunction or dis- ease in the somatic and visceral structures supplied by the affected NR.17,354-359 The subluxation-induced narrowed intervertebral fora-
men (IVF) was hypothesized to induce NR dysfunction through direct bony compression (pinched-hose model) or indirectly by increasing pressure around the NR and its vascular structures.
In 1973, Crelin360 challenged the anatomic plausibility of sub-
luxated motion segments producing NR compression. His ana- tomic dissections and measurements, made at the lateral borders of the IVF, demonstrated a minimum of 4 mm of space around the NR. He concluded that the space was more than adequate and that the NR was not anatomically vulnerable to compression. More recently in 1994, Giles361 revisited the issue of NR vulner-
ability but at a different anatomic site. His measurements were taken at the interpedicular zone and demonstrated an average of only 0.4 to 0.8 mm of space around the NR and the NR gang- lion. He concluded that the NR was anatomically vulnerable, but at the interpedicular zone, not at the lateral borders of the IVF. Furthermore, “dorsal roots and dorsal root ganglia [DRG] are more susceptible to the effects of mechanical compression than are axons of peripheral nerves because impaired or altered func- tion is produced at substantially lower pressures.”361
A potential site of anatomic vulnerability does not, by any means, validate chiropractic models of subluxation-induced NR dysfunction. The plausibility of uncomplicated subluxations com- monly inducing NR compression still seems unlikely.355-360 It does,
however, raise an interesting issue about the potential for spinal motion segment dysfunction to contribute to NR compression when it is associated with other compromising joint patholo-
Figure 4-21 The self-perpetuating cycle of myofascial pain and muscle spasm. Uncoordinated movements Articular strain Pain Vasoconstriction ischemia Joint dysfunction Retained metabolites
Edema (inflammation) Muscle spasm Chronic postural stress
gies.300,361,362 Disc herniation and exposure of the NR to discal
material increase spontaneous nerve activity and the mechanical sensitivity of the NR and possible mechanical hyperalgesia. Spinal NRs already compromised by disc herniation, degenerative joint and disc disease, or central or lateral stenosis and the associated inflammation may become more serious when associated with dys- function that fixes the joint in a more compressive and compromis- ing position. In such circumstances, adjustive therapy that reduces a position of fixed subluxation and root irritation may have an effect on reducing NR traction, compression, or inflammation.
reflex dysfunction
Beginning with the work of Homewood,358 the profession has
gradually moved away from reliance on NR compression and toward a more dynamic model of subluxation-induced neurodys- function. As presented in Chapter 3, the reflex paradigm pres- ents a model in which somatic dysfunction or joint dysfunction induces persistent nociceptive and altered proprioceptive input. This persistent afferent input triggers a segmental cord response, which in turn induces the development of pathologic somatoso- matic or somatovisceral disease reflexes357-359,363-368 (Figure 4-22). If
these reflexes persist, they are hypothesized to induce altered func- tion in segmentally supplied somatic or visceral structures.
Chiropractic adjustive therapy has the potential for arresting both the local and the distant somatic and visceral effects by nor- malizing joint mechanics and terminating the altered neurogenic reflexes associated with joint dysfunction. For example, a patient with a strained posterior joint capsule accompanied by reflex mus- cle spasm may have nociceptive bombardment of the spinal cord. If the nociceptive bombardment is of sufficient strength and dura- tion, it may cause segmental facilitation. The spinal adjustment may reduce the strain on the joint capsule and reduce muscle spasm that stops nociception from these tissues into the spinal cord. At the same time, adjustments stimulate many different types of mechanoreceptors. The result is a reduction of a harm- ful somatosomatic and potential somatoautonomic reflex. This model has become the focus of more attention and investigation as
chiropractors search for an explanation to the physiologic effects that they have clinically observed to be associated with spinal adjus- tive therapy. This relationship is not consistent, and the frequency of response is undetermined, but the anecdotal and empiric expe- riences of the profession are significant enough to warrant serious further investigation.
An additional model of subluxation-induced neurodysfunc- tion focuses attention on the potential direct mechanical irritation of the autonomic nervous system. The paradigm for irritation of sympathetic structures is based on the anatomic proximity and vulnerability of the posterior chain ganglion, between T1 and L2, to the soma of the posterior chest wall and costovertebral joints. Altered spinal and costovertebral mechanics are hypothesized to mechanically irritate the sympathetic ganglia and to induce seg- mental sympathetic hypertonia.368 The target organs within the
segmental distribution then theoretically become susceptible to altered autonomic regulation and function as a result of altered sympathetic function.
In contrast to the sympathetic chain, the parasympathetic sys- tem, with its origins in the brain, brainstem, and sacral segments of the spinal cord, does not have anatomic proximity to the spinal joints. Models of mechanically induced dysfunction of the para- sympathetic system propose dysfunction in cranial, cervical, and pelvic mechanics as potential sources of entrapment or tethering of the parasympathetic fibers. Altered cervical, cranial, or craniosacral mechanics are theorized to induce traction of dural attachments and the cranial nerves as they exit through the dura and skull foram- ina. The treatment goal in mechanically induced autonomic dys- function is to identify the sites of joint dysfunction and implement appropriate manual therapy to balance membranous tension.369
From the discussion of spinal dysfunction and its potential neurobiologic effects on health, it must be remembered that spinal dysfunction and pain may be the product of, not the cause of, somatic or visceral dysfunction or disease.370 Spinal pain and
dysfunction may be secondary to a disorder that needs direct treat- ment. Manual therapy may be a fitting component of appropri- ate care, but would be inadequate as the singular treatment. The patient with caffeine-induced gastritis who develops secondary midback pain and dysfunction (viscerosomatic) should not receive manual therapy without also being counseled to discontinue ingestion of caffeinated beverages. The spine is a common site of referred pain, and when a patient with a suspected mechanical or traumatic disorder does not respond as anticipated, the possibility of other somatic or visceral disease should be considered.
neuroimmunology
An interaction exists between the function of the central nervous system and the body’s immunity that lends support to the chiroprac- tic hypothesis that neural dysfunction is stressful to the body locally and globally. Moreover, with the resultant lowered tissue resistance, modifications to the nonspecific and specific immune responses occur, as well as altered trophic function of the involved nerves. This relationship has been termed the neurodystrophic hypothesis.
Selye371-373 demonstrated neuroendocrine-immune connections
in animal experiments and clinical investigations. Physiologic, psychologic, psychosomatic, and sociologic components compose the stress response. From studies of overstressed animals, Selye Afferent from joint 2 2 4 3 1 Efferent blood vessels Efferent to muscle Visceral efferent Visceral afferent
Figure 4-22 Afferent and efferent pathways from and to the viscera and somatic structures that can produce (1) somatosomatic, (2) soma- tovisceral, (3) viscerosomatic, and (4) viscerovisceral reflex phenomena. (Modified from Schmidt,188.)
observed nonspecific changes that he labeled the general adaptive
syndrome. He also observed very specific responses that depended
on the stressor and on the part of the animal involved, which he termed local adaptive syndrome. Furthermore, he established a stress index comprising major pathologic results of overstress, including enlargement of the adrenal cortex, atrophy of lymphatic tissues, and bleeding ulcers. Selye also felt that long-term stress would lead to diseases of adaptation, including cardiovascular disease, high blood pressure, connective tissue disease, stomach ulcers, and headaches.
Stressors can produce profound health consequences.374
Theorists propose that stressful events trigger cognitive and affec- tive responses that, in turn, induce sympathetic nervous system and endocrine changes, and these ultimately impair immune function.375-379 Stressful events cannot influence immune func-
tion directly. Instead, stress is thought to affect immune function through central nervous system control of the hypothalamic- pituitary-adrenal (HPA) axis and sympathetic-adrenal-medul- lary axis.377,380-383 Stressors produce reliable immune changes.374
Segerstrom and Miller384 analyzed different types of stressors sepa-
rately and found that the immunologic effect of stressors depends on their duration.
However, because all individuals do not develop the same syn-