By Neil Davies
It is axiomatic that consistently accurate clinical decisions are irrevocably intertwined with the understanding that the subluxation is not a random, unpredictable biomechanical event. But rather, a neuropathological state which exhibits multifaceted, measurable manifestations in the neuromusculoskeletal system which occur in patterns as predictable as a mathematical formula.
The role of the chiropractor, then, is not simply the mobilization of a stuck joint' as some have wrongly imagined, but correction of patterns of functional neuropathology. In this, the chiropractor must make a carefully weighted decision in each and every patient consultation, keeping accurate and exhaustive records in order to facilitate recognition of recurring patterns of subluxation.
That functional neuropathology accompanies disease and biological imbalance, and freedom from such neuropathology is necessary for the individual to enjoy the benefits of homeostasis, has always been, and always will be, the fundamental philosophic premise upon which the science and art of chiropractic is predicated (Palmer 1910).
The relentless search for the specific in each individual which, when corrected, will result in the elimination of neuropathology, and the restoration of homeostasis (Strang 1984) remains the original franchise of the chiropractor.
The subluxation complex is based on precise, predictable patterns of neuropathology, kinesiopathology and compensation pattern (Lantz 1995). Each of these elements of the subluxation complex must be present every time and in every case before a precise chiropractic adjustment of the subluxation complex can occur.
The inherent importance of the above rule is that it provides for specific subluxation diagnosis. Working in this way and in particular in allowing the neuropathology to guide examination and diagnosis provides for the treatment of one subluxation complex and not of many compensations which display one but not all of the properties required for subluxation diagnosis.
Additionally, the precise and predictable patterns allow for the testing and proving of subluxation correction before any care is implemented. The neuropathology of the subluxation complex, involves the synthesis of four neuro-physiological mechanisms which provide an explanation of the neurological effect that the subluxation has on neurological function.
Mechanism #1: The Effect of Dural Tension
The major mechanical attachments of the dura are at the cranium, upper cervical spine and lumbar-sacral junction and involve attachments to the occiput, ligamentum flavum, rectus capitis posterior minor, directly to C2 and C3 and via Hoffman's and Trolard's ligaments to L5 and sacrum (Snell 1992, Barbaix et al. 2000, Wadhwani et al. 2004).
Cerebro-spinal fluid flow is dependent upon, among others, the appropriate function of the contractible meninges (Greitz 1993). If the biomechanical lie of the dura is changed due to aberrant kinesiology, then the contractible function of the meninges becomes impaired and thus contributes to a change in CSF flow, changing the CSF pressure and affecting the function of a number of central nervous system structures.
Kinesiopathology results in a change in the lie of the dura, and is associated with a change in CSF pressure. This results in aberrant reticular formation function causing the processing of inappropriate neurological signals which reach the cerebral cortex and must be processed into a meaningful efferent output.
The cerebral cortex is also challenged by a change in CSF pressure and in so doing fails to adequately synthesize the sensory information resulting in the process known as dysafferentation (Seaman 1998, Knutson 1999).
Mechanism #2: Noxious Mechanoreceptor Input from the Dura
The major innervation of the dura is through slow reacting type C fibres and fast reacting type A fibres, principally at the cervico-cranial junction (Snell 1992). Additionally the ventral dura is richly innervated by the sinuvertebral nerve plexus and from a number of perivascular nerve plexi (Groen et al. 1988, Fricke et al. 2001).
As with any ascending sensory information, the ascending tract for the transmission of nociceptive information is mainly via the spinothalamic tract. This tract communicates directly with the thalamus but also sends some fibres via the reticular formation. The spinoreticular tract is also thought to be involved in nociception (Mense 2004).
If dural tension is created by aberrant kinesiology the contractibility of the meninges is effected (Greitz 1993) and nociceptor stimulation will occur. This creates a noxious input from the dural system into the central nervous system creating a type of sensory overload. The sensory information must be adequately processed by the reticular formation and thalamus so that the cortex receives appropriate sensory information.
Failure to adequately process sensory information into appropriate efferent information is known as dysafferentation.
Mechanism #3: Noxious Mechanoreceptor Input from the Facet Joints
The facet joints are innervated by a variety of types of nerve endings. Principally types I,II, III and IV have been recognised (Mclain 1994, Mclain and Pickar 1998, Snell,1992). The type IV nerve ending is a free nerve ending and is particularly relevant to nociception.
The mechanoreceptor pathways which feed in to the CNS are the spinothalamic and spinocerebellar tracts and the posterior columns. This contribution of sensory information is transmitted via a number of central nervous system structures including the cerebellum, reticular formation and thalamus.
Aberrant kinesiopathology, changes the orientation of the facet joint and its capsule and may expose the synovium to mechanical stress (Inami et al. 2000). Aberrant facet position and the physiological irritation of the anatomical structures can result in the sensory overload discussed in mechanism 2.
Mechanism #4: Aberrant Sympathetic Activity
The superior cervical ganglion communicates with the upper four cervical nerves via the grey rami communicantes (Snell 1992). Furthermore the sympathetic fibres communicate with the ventral nerve plexus which surrounds the vertebral column (Groen et al. 1990).
The sympathetic nervous system has many functions but one of particular relevance to central nervous system function is the control of cerebral hemodynamics including the Circle of Willis. The Circle of Willis provides the blood supply to the cerebral cortex.
Aberrant sympathetic activity which may occur due to excessive facet irritation (Suseki et al. 1996) or in very extreme cases through prolonged stress (Kadojic et al. 1999) results in vasoconstriction and a change in cerebral hemodynamics.
If this is the case, the already challenged cerebral cortex will again be negatively influenced adding to the inability to adequately synthesis afferent information in to appropriate (motor) output.
The Common Elements
Each of the discussed neurological mechanisms contributes to the neuropathology of the subluxation. Each mechanism results in the process known as DYSAFFERENTATION and it is this which is crucial to the understanding of the neurological effect of the subluxation complex.
Additionally, all sensory pathways decussate. This means that adverse sensory events initiated on the left side of the body are interpreted by the right brain and vice versa. Finally, the effect on the autonomic nervous system is noted by the interconnections of the reticular formation and the superior cervical ganglion.
The Chiropractic Adjustment
The chiropractic adjustment is a precise and specific intrusion into the nervous system. Delivering any adjustive thrust, and in particular, repeated adjustive thrusts to a compensated region of the spine or extremities must be assiduously avoided at all times if inappropriate neurological input is to be avoided.
Repeated adjustive thrusts will put the patient at risk of developing an iatrogenic hypermobility syndrome at that level (Cox 1997). The chiropractic adjustment can be seen as providing a sort of resetting mechanism to the nervous system. It overrides the gating mechanism and activates specific neurological pathways (Carrick 1997).
The Subluxation-Compensation Relationship
One of the most poorly misunderstood clinical relationships is that of the compensatory response to the subluxation. A compensation is a biomechanical aberration which is invariably devoid of the full complement of physical examination findings that would define it as a subluxation (Herbst 1968) and will be manifest as a predictable pattern of movement loss, hypermobility or both (Davies 2000) with little capacity to cause neuropathology (Plaugher 1993).
Compensation is a kinesiopathologic response to the subluxation and may involve a single motion segment or a whole area of the spine (Gatterman 1995).
Compensation is frequently found as far from the subluxation as the occiput is from the sacrum. Compensatory kinesiopathologic response to the subluxation may be demonstrated on postural assessment and motion palpation examination with the elements related alteration of primary curve contour and disc shape most reliably seen on X-ray.
When is a Subluxation really a Subluxation?
The essence of sound decision-making in chiropractic is the result of a process of clinical logic and deductive reasoning which has taken into account all the available physical evidence. The conclusion that a chiropractic adjustment is an appropriate clinical intervention should only be arrived at when adequate evidence of all five fundamental aspects of the subluxation can be demonstrated.
It is illogical to decide to 'adjust' a given spinal motion segment when only hypomobility, for example, can be demonstrated. Such hypomobility, existing in the absence of other findings, almost certainly represents a compensation (Davies 1997.)
Dr Neil Davies D.C, is the author Chiropractic Pediatrics A Clinical Handbook (Churchill Livingstone 2000) and developer of the NeuroImpulse Protocol and Adjusting the Child seminar programmes for chiropractors. His passion for improving the clinical skills of practicing chiropractors is known in international circles and he will be commencing new courses in USA in 2008.
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