Which Of The Following Displays The Result Of A Formula Understanding the Chiropractic Subluxation

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Understanding the Chiropractic Subluxation

It is axiomatic that consistently accurate clinical judgment is irrevocably intertwined with the understanding that subluxation is not a random, unpredictable biomechanical event. But rather a neuropathological condition with multifaceted, measurable manifestations in the neuromusculoskeletal system that occur in patterns that are as predictable as a mathematical formula.

The role of the chiropractor, then, is not simply to mobilize a stuck joint, as some have wrongly imagined, but to correct patterns of functional neuropathology. In doing so, the chiropractor must make a carefully considered decision in each consultation with the patient, keeping accurate and comprehensive records to facilitate the identification of recurrent subluxation patterns.

That functional neuropathology accompanies disease and biological imbalance, and that the individual needs to rid himself of such neuropathology in order to enjoy the benefits of homeostasis, has always been, and always will be, a fundamental philosophical premise upon which the science and art of chiropractic rests (Palmer 1910).

The chiropractor’s original franchise remains the unceasing search for specificity in each individual, which when corrected leads to elimination of neuropathology and restoration of homeostasis (Strang 1984).

The subluxation complex is based on precise, predictable patterns of neuropathology, kinesiopathology and compensation (Lantz 1995). All of these elements of the subluxation complex must be present every time and in every case before accurate chiropractic adjustment of the subluxation complex can take place.

The intrinsic importance of the above rule is that it prescribes the diagnosis of a specific subluxation. Working in this way, and especially enabling the study and diagnosis of neuropathology, makes it possible to treat one subluxation complex and not many compensations that have one, but not all, of the features necessary to diagnose a subluxation.

In addition, accurate and predictable patterns allow subluxation correction to be tested and proven before any maintenance is applied. The neuropathology of the subluxation complex involves the synthesis of four neurophysiological mechanisms that explain the neurological effects of subluxation on neurological function.

Mechanism #1: Effect of dural tension

The main mechanical attachments of the dura are located in the skull, upper cervical spine, and lumbosacral junction and attach to the occiput, ligamentum flavum, rectus capitis posterior minor, directly to C2 and C3, and through the ligaments of Hoffman and Trolard to L5 and the sacrum. (Snell 1992, Barbaix et al. 2000, Wadhwani et al. 2004).

CSF flow depends, among other things, on the appropriate function of the contractile meninges (Greitz 1993). When the biomechanical position of the dura is altered due to abnormal kinesiology, the contractile function of the meninges is impaired and thus contributes to altered CSF flow, altering CSF pressure and affecting the function of several CNS structures.

Kinesiopathology causes dural repositioning and is associated with changes in CSF pressure. This results in abnormal function of the reticular formation, which results in the processing of inappropriate neurological signals that reach the cortex and must be processed into meaningful efferent output.

The cerebral cortex is also challenged by changes in CSF pressure and thereby fails to adequately synthesize sensory information, resulting in a process known as dysafferentation (Seaman 1998, Knutson 1999).

Mechanism #2: Noxious mechanoreceptor input from the Dura

The main innervation of the dura is via slow-reacting C-type fibers and fast-reacting A-type fibers, mainly at the cervical-cranial junction (Snell 1992). In addition, the ventral dura is richly innervated by the sinuvertebral nerve plexus and several perivascular nerve plexuses (Groen et al. 1988, Fricke et al. 2001).

As with any ascending sensory information, the ascending pathway of nociceptive information transmission occurs primarily via the spinothalamic tract. This tract communicates directly with the thalamus but also sends some fibers through the reticular formation. The spinoreticular tract is also thought to be involved in nociception (Mense 2004).

When aberrant kinesiology produces dural tension, contractility of the meninges is exerted (Greitz 1993) and nociceptor stimulation occurs. This creates a noxious input from the dural system to the CNS, creating a type of sensory overload. Sensory information must be adequately processed by the reticular formations and the thalamus in order for the cerebral cortex to receive relevant sensory information.

The inability to adequately process sensory information into appropriate efferent information is called dysafferentation.

Mechanism #3: Toxic mechanoreceptor input from facet interfaces

Facet joints are innervated by different types of nerve endings. Basically, types I, II, III and IV are recognized (Mclain 1994, Mclain and Pickar 1998, Snell, 1992). Type IV nerve endings are free nerve endings and are particularly important for nociception.

The mechanoreceptor pathways entering the CNS are the spinothalamic and spinocerebellar tracts and the posterior columns. This input of sensory information is relayed through several CNS structures, including the cerebellum, reticular formation, and thalamus.

Aberrant kinesiopathology alters 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 physiological irritation of anatomical structures can lead to the sensory overload discussed in mechanism 2.

Mechanism #4: Abnormal sympathetic activity

The superior cervical ganglion communicates with the four superior cervical nerves via the gray rami communicantes (Snell 1992). In addition, sympathetic fibers communicate with the ventral plexus surrounding the spinal column (Groen et al. 1990).

The sympathetic nervous system has many functions, but one particularly important to CNS function is cerebral hemodynamics, including the control of the circle of Willis. The circle of Willis ensures blood supply to the cerebral cortex.

Aberrant sympathetic activity, which can occur due to excessive solid irritation (Suseki et al. 1996) or, in very extreme cases, prolonged stress (Kadojic et al. 1999), causes vasoconstriction and changes in cerebral hemodynamics.

If this is the case, the already damaged cortex is again negatively affected, increasing the inability to adequately synthesize afferent information into an appropriate (motor) output.

Common elements

All of the neurological mechanisms discussed contribute to the neuropathology of subluxation. Each mechanism results in a process called DYSAFFERENTATION, which is crucial to understanding the neurological effects of the subluxation complex.

In addition, all sensory pathways are decussated. 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 interrelationships between the reticular formation and the superior cervical ganglion note the effects on the autonomic nervous system.

Chiropractic adjustment

A chiropractic adjustment is a precise and specific penetration of the nervous system. Any regulatory thrust, especially repetitive thrusts to the compensated region of the spine or limbs, must be consistently avoided to avoid inappropriate neurological input.

Repetitive regulatory drives place the patient at risk for iatrogenic hypermobility syndrome at this level (Cox 1997). A chiropractic adjustment can be viewed as a resetting mechanism for the nervous system. This overrides the gating mechanism and activates specific neurological pathways (Carrick 1997).

Subluxation-compensation relationship

One of the least misunderstood clinical associations is the compensatory response to subluxation. Compensation is a biomechanical aberration that always lacks any physical examination findings that would define it as a subluxation (Herbst 1968) and manifests as a pattern of predictable movement with little movement, hypermobility, or both (Davies 2000). the ability to cause neuropathology (Plaugher 1993).

Compensation is a kinesiopathological response to subluxation and may involve a single motion segment or the entire spinal region (Gatterman 1995).

Compensation is often found as far from the subluxation as the occipital sacrum. A compensatory kinesiopathological response to subluxation can be demonstrated by assessment of position and palpation of range of motion, with the contour of the primary curve and disc shape associated with the elements most reliably seen on radiographs.

When is a subluxation actually a subluxation?

The nature of sound chiropractic decision-making is the result of clinical logic and deductive reasoning that has taken into account all available physical evidence. The conclusion that chiropractic adjustment is an appropriate clinical intervention should only be reached when sufficient evidence can be demonstrated for all five key aspects of subluxation.

It is illogical to decide to “adjust” a certain segment of spinal motion when, for example, only hypomobility can be demonstrated. Such hypomobility, which exists in the absence of other findings, is almost certainly compensatory (Davies 1997).

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