44 Spinal Adjustments and Reflex Physiology
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Dynamic Chiropractic – October 22, 2007, Vol. 25, Issue 22

Spinal Adjustments and Reflex Physiology

By Nancy Martin-Molina, DC, QME, MBA, CCSP

The original contribution of chiropractic to the healing arts was observed from a pathologenic and a therapeutic point of view. Review of the literature reveals strong evidence for both the mechanical model of disease production (structural) and the neurophysiologic model (functional).

Today, chiropractic researchers are focusing on the multiple components of the chiropractic vertebral subluxation complex (CVSC), as a definitive, provable clinical entity. Chiropractic has become revitalized in favor of an evolution of our concepts to make them conform to newly established facts. Perhaps in this manner, no longer can "informed" critics support the accusation that chiropractic is not evidenced-based.

Chiropractic was first to postulate that the spine can be the seat of mechanical derangements other than major boney pathologies. These mechanical derangements can affect a detrimental effect not only locally on the spine itself, but also in areas remote from the spine through mediation of the nervous system. The remedy of choice for these mechanical derangements and their local and remote effects should be of a mechanical nature (remedy) also, mainly in the form of adjustments performed by hand.

The main reflex physiology associated with vertebral spinal derangements and adjustments in the literature often has pertained to referred pain, the regulation of the tonic and phasic activity of the autonomic spinal musculature, and the peripheral modulation of the pain perception. Let us review these physiological processes or mechanisms.

Nociception is the process by which nociceptive receptors receive tissue-damaging stimuli that are then carried into the CNS by nociceptive axons (A-delta and C fibers). Potential outcomes of nociceptive input to the cord include pain, autonomic symptoms, and vasoconstriction and muscle spasm. Nociceptive input to the cord appears to be the driving force behind the pathogenesis of subluxation.

Nociception and pain are completely different. For example, pain may be felt in an area far from the site of the lesion due to distortion of the sensory pathways. This is called referred pain. Pain may originate in an internal organ or a spinal structure, particularly a joint such as the spinal facet joint. A devastating consequence of both pain and nociceptive stimulation of the hypothalamus is the release of cortisol by the adrenal glands. Over time, elevated levels of cortisol will promote glucose intolerance, inhibit collagen formation and increase protein degradation. Heightened levels of cortisol are not conducive to the patient's healing process.

Mechanoreceptor refers to the process by which tissue mechano-receptors are stimulated by mechanical input such as touch, muscle stretching and joint motion. A-alpha and A-beta fibers carry mechanoreceptor information into the CNS. Segmental reflex effects of mechanoreceptor input can elicit excitatory and inhibitory effects. An important inhibitory effect is the presynaptic and postsynaptic inhibition of the nociceptive pathways.

It is thought that the adjustment stimulates joint mechanoreceptors by increasing joint motion. Besides the direct mechanical effects, the adjustment is thought to produce a reflex inhibition of the hypertonic spinal muscles, brought about by an intense activation of the mechanical receptors located on the spinal joint capsules (known as facets), ligaments and muscle tendons due to stretching. The increase in mechanoreceptor input produced by the adjustment brings about a peripheral modulation of pain perception in the sense of alleviation (gate-control mechanism).

The converse also may be true, in that increased mechanoreceptor input from degenerated joints which favor a selective destruction of large mechanoreceptor fibers may lead to increased pain perception (negative feedback control). There also are suprasegmental reflex effects of mechanoreceptor stimulation which are proprioceptive in nature.

Proprioception occurs as a consequence of the integration of vestibular input, visual input and tissue mechanoreceptor input to the cerebral cortex and cerebellum. It is thought that mechanoreceptor input is of the utmost importance for proprioception. Thus, mechanoreceptors give rise to local segmental reflexes and suprasegmental proprioceptive reflex effects.

Nociception, mechanoreceptor and proprioception are all intimately associated with the normal and abnormal function of vertebral joints. Can it be that nociception induces subluxation which subsequently reduces mechanoreception and proprioception? Our bodies and their organ systems do primarily operate on a negative feedback mechanism to allow a return to normal or to the set point.

A recent study from the Department of Orthopedic Surgery, Fukushima Medical University School of Medicine in Japan investigated the association between lumbar facet joint inflammation and radiculopathy using behavioral, histological and immunohistochemical testing in rats. When inflammation was induced in a spinal facet joint, inflammatory reactions spread to nerve roots and leg symptoms were induced by chemical factors. The conclusions of their results support the possibility that facet spinal joint inflammation induces radiculopathy. Interestingly, in chiropractic, this is considered to be part of the histological component of a CVSC or subluxation complex.

Today, an experimental body of evidence exists indicating that spinal manipulation impacts primary afferent neurons from paraspinal tissues, the motor control system and pain processing. Biomechanical changes caused by spinal manipulation are thought to have physiological consequences by means of their effects on the inflow of sensory information to the central nervous system. Muscle spindle afferents and Golgi tendon organ afferents are stimulated by spinal manipulation and affect the extra cellular fluid reducing inflammatory mediators at the effectors organ. Substantial evidence demonstrates that spinal manipulation evokes paraspinal muscle reflexes and alters motoneuron excitability. The effects of spinal manipulation on these somatosomatic reflexes may be quite complex, producing excitatory and inhibitory effect; whereas substantial information also shows that sensory input, especially noxious input from paraspinal tissues, can reflexively elicit sympathetic nerve activity.

In conclusion, in their 1992 study, the RAND Corporation confirmed that chiropractors perform 94 percent of all spinal manipulation procedures in the U.S., with osteopaths delivering just 4 percent and general practitioners and orthopedic surgeons performing the remaining 2 percent. In light of the AHCPR's findings, we must be prepared for these figures to change as spinal manipulation becomes more accepted as a viable treatment of choice.

References

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  2. Sandoz R. Some reflex phenomena associated with spinal derangements and adjustments. Annuals of the Swiss Chiropractors' Association, 1976;Vol VI.
  3. Suter E, Herzog W, Conway PJW, Zhang WT. Reflex response associated with manipulative treatment of the thoracic spine. Journal of the Neuromusculoskeletal System, 1994;2(3):124-30.
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  5. Budgell BS. Reflexes effects of subluxation : the autonomic nervous system. J Manipulative Physiol Ther, February 2000;23(2):104-6.
  6. Dishman, JD. Review of the literature supporting a scientific basis for the chiropractic subluxation complex. J Manipulative Physiol Ther, September 1985;8(3):163-74.
  7. Dishman JD, Burke JR. Spinal reflex excitability changes after cervical and lumbar joint manipulation. A comparative study. Spine, 2003;3:204-12.
  8. Herzog W. On sounds and reflexes. J Manipulative Physiol Ther, 1996;19(3): 216-18.
  9. Ross JK, Berznick DE, McGill SM. Determining cavitation location during lumbar and thoracic spine manipulation. Spine, 2004;29(13):1452-7.
  10. Herzog W, Kats M, Symons B. The effective forces transmitted by high-speed low-amplitude thoracic manipulation. Spine, 2001;26(19):2105-111.
  11. Tachihara H, Kikuchi S, Konno S, Sekiguchi M. Does facet joint inflammation induce radiculopathy? Spine, Feb. 15, 2007;32(4):406-12.

Click here for previous articles by Nancy Martin-Molina, DC, QME, MBA, CCSP.


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