*Please note that the following content is solely a brief introduction to the chiropractic subluxation complex for the purpose of promoting the clarification of chiropractic care.
Repetitive postural strain or trauma to the spine, overuse or under use of the spine, such as caused by over training, immobilization, contact sports, or prolonged poor postural habits in front of a desk; can adversely affect the normal way in which a vertebral segment of the spine (a component of the spine) functions and moves. This can place additional stress on the facet joint capsule, muscles, tendons and ligaments which support the normal functioning and movement of the vertebral segment and alter its normal segmental spinal reflex arc activity with subsequent weakness and/ spasm of the associated muscle(s), and cause spinal pain (neck pain, back pain and low back pain).
Repetitive postural strain, trauma to the spine, overuse of the spine and under use of the spine can cause alterations in the normal anatomical, physiological and / or biomechanical dynamics of individual vertebral segments and produce relatively large vertebral motions that achieve a new position of stable equilibrium. The higher energy level needed to achieve the new position of stable equilibrium can place additional mechanical stress or overload on the static stabilizers (ligaments and bones) and dynamic stabilizers (muscles and tendons) of the vertebral segment including the facet joint capsular tissue and / or cause uneven or increased unilateral facet joint loading. These alterations in the vertebral segment can cause tension, pressure, stretching or irritation of the facet joint capsular tissue as well as the displacement of collagen in the facet joint capsular ligament, and thereby stimulate (depolarize and sensitize) mechanoreceptors and/ or nociceptors within the facet joint tissue and subsequently increase their afferent discharge frequency.
The raised Aβ-fiber afferent discharge from the facet joint tissue can cause alterations in its arthrokinetic reflex activity with subsequent neurogenic inhibition and weakness of the homonymous muscles in the presence and absence of pain, namely arthrogenic muscle inhibition (AMI). Particularly type I joint mechanoreceptors called the Ruffini end-organs are extremely sensitive to a change in intra-articular pressure and are found around the collagen fibers of the superficial layers of the facet joint capsular tissue. Alterations in the biomechanical dynamics of a vertebral segment (a chiropractic subluxation) can induce tension and pressure inside the facet joint capsular tissue, thereby causing AMI by mechanically stimulating the Ruffini end organs. Any induced alteration in the joint mechanoreceptor’s discharge may affect the position sense and kinesthetic sense (proprioception) of the affected joint and give rise to symptoms of disequilibrium. Alterations in the biomechanical dynamics of a vertebral segment (a chiropractic subluxation) can produce relatively large vertebral motions that achieve a new position of stable equilibrium. The higher energy level needed to achieve the new position of stable equilibrium can place additional mechanical stress or overload on the facet joint capsular tissue and hold the capsular ligament of the facet joint in a subtle stretched position. Although the alterations in the vertebral segment does not cause gross laxity of the facet joints or may be too subtle to cause symptoms of disequilibrium; the alterations in the biomechanical dynamics of the vertebral segment (a chiropractic subluxation) may affect the facet joint position sense to the extent of solely increasing its mechanoreceptor Aβ-fiber afferent discharge with subsequent AMI (see scientific support).
The additional mechanical loading placed on the facet joints and / uneven or increased unilateral facet joint loading by the presence of a chiropractic subluxation can mechanically stimulate nociceptors in the facet joint capsular tissue and synovium and act as a mechanical irritant to the capsular tissue which cause the release of inflammatory cytokines. The released inflammatory cytokines can stimulate their specific nociceptive receptors in the facet joint capsular tissue and synovium and induce a change in enzyme protein cascade, which can sensitize mechano-insensitive nociceptors and make them respond to mechanical and thermal stimuli. Once activated, these nociceptors become mechanosensitive and lead to the development of peripheral- and central sensitization (activity-dependent synaptic plasticity). In addition, the released inflammatory cytokines can also lead to the upregulation of existing receptors on the membrane of the nociceptors, which is one of the main mechanisms responsible for peripheral sensitization (increase the number of nociceptors present). When the nociceptors are activated by chemical irritants, the nociceptive nerve endings also respond by releasing neuropeptides and neuromodulators such as substance P and calcitonin gene related peptide (CGRP), to increase the excitability of adjacent nociceptors so that tissue repair is facilitated and inflammation is modulated. The released substance P is likely to be responsible for the initiation of the facet joint pain and CGRP is associated for the persistence of the pain and referred pain with subsequent spinal pain; neck pain, back pain or low-back pain. The sensitized nociceptors can cause peripheral sensitization and cause an increase in nociceptive responsiveness and a decrease in nociceptive threshold in the periphery to stimulation of their receptive fields. Thus, making non-noxious stimuli such as light touch or normal joint movement able to depolarize the nociceptors and excite the nociceptor afferents, and produce an increase of stimulation frequency. A chiropractic subluxation may thereby cause spinal pain in the acute setting as well as induce an abnormal stimulus that may lead to central sensitization with subsequent chronic spinal pain (see scientific support).
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