Major models and hypotheses of chiropractic subluxation ii neurologic models
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Major Models and Hypotheses of Chiropractic Subluxation: II. Neurologic Models. II. Neurological Models. Nerve compression B. Dorsal Root Ganglion compression C. Spinal Cord compression/traction D., E., F.: The Reflex Models. Reference:. Sato, A. Chapter 8: “ Spinal Reflex Physiology ”

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Ii neurological models
II. Neurological Models

  • Nerve compression

    B. Dorsal Root Ganglion compression

    C. Spinal Cord compression/traction

    D., E., F.: The Reflex Models


Reference
Reference:

Sato, A.

Chapter 8:“Spinal Reflex Physiology”

Swenson, R.

Chapter 9: “Clinical Investigations of Reflex Function”

in:

Haldeman, S.

Principles and Practice of Chiropractic, 1992


Reflex models
Reflex Models:

  • Can be understood as different combinations of communications (reflexes) between somatic and visceral structures:

    1. Somato-somatic (aka somato-motor)

    2. Somato-visceral (aka somato-autonomic)

    3. Viscero-somatic (aka viscero-motor)

    4. Viscero-visceral (not currently discussed as subluxation model; no somatic component)


Reflex models1
Reflex Models:

Somato-somatic (aka somato-motor)

local spinal effects of subluxation- muscle hypertonicity/imbalance, fixation, etc…

Somato-visceral (aka somato-autonomic)

subluxation effects on visceral function

Viscero-somatic (aka viscero-motor)

visceral cause/perpetuation of subluxation


D. Somato-Somatic ReflexHypothesis (aka somato-motor; proprioceptive “insult”)somatic afferents somatic efferents


Somato somatic reflex model
Somato-somatic Reflex Model

  • Korr and early researchers felt that richly-innervated somatic tissues in and around the spine were the source of afferent “bombardment” of neurologic signals, leading to a state of hyperstimulation, or facilitation

  • This state was considered to be self-perpetuating, leading to reflexive errors in postural muscle tone and other somatic structures involved in posture and locomotion


Somato somatic reflex model cont
Somato-somatic Reflex Model, cont.:

  • Seaman and others currently propose that nociceptive neurons are the afferents which produce this facilitation. (“nociceptive facilitation”)

  • Among the various effects are “nociceptive spasm” of isolated segmental spinal muscles which than do not act in coordination with the rest of the spine. (“out of step”, “segmental consternation”)



“The disturbance in the cord is caused by distorted afferent impulse patterns from either (a) affected musculoskeletal tissues, (b) lesions of nerves, roots and ganglia due to irritation. Or both, preventing adaptive, appropriate responses.”

Korr


Inflammatory model of facilitation
Inflammatory Model of Facilitation: afferent impulse patterns from either (a) affected musculoskeletal tissues, (b) lesions of nerves, roots and ganglia due to irritation. Or both, preventing adaptive, appropriate responses.”

Damaged skeletal tissues associated with SDF (segmental dysfunction) release vasoneuractive substances such as bradykinin, prostaglandinE2, substance P, histamines, etc., which facilitate neural pathways, including nociceptors. This may give rise to the initial stages of segmental facilitation of the spinal cord.


INJURY afferent impulse patterns from either (a) affected musculoskeletal tissues, (b) lesions of nerves, roots and ganglia due to irritation. Or both, preventing adaptive, appropriate responses.”


“Once this facilitation occurs, despite the removal of the afferent source of stimulation, the abnormal reflex circuit itself participates in maintaining the symptoms, thus creating a cycle of increased output with any sensory input.”

Leach, 1994, p. 101


  • “Activation of deep (type IV) nociceptive afferents from the involved joint tissues project polysynaptically to alphamotoneurones of the muscles related to the involved joints, thereby giving rise to abnormal reflex activity in the muscles…contributing to further pain, and joint and muscle dysfunction.”

    Terrett and Terret, “Referred Posterior Thoracic Pain,” Chiropr J of Australia 2002; 32: 44


  • “…a positive feedback cycle of proprioceptive excitability may be triggered, refreshed and maintained within pain-signaling neurons by periodic nociceptive and non-nociceptive paraspinal input.”

  • Terrett and Terret, “Referred Posterior Thoracic Pain,” Chiropr J of Australia 2002; 32: 45



The deafferentation concept
The “Deafferentation” Concept: “vicious circle”:

  • Some authors suggest that an effect of spinal fixation/hypomobility associated with subluxation process may cause diminished afferent signals from somatic structures

  • Primarily implicated are mechanoreceptors (especially types I & II)

  • CNS is therefore deprived of information needed for balance and coordination; ataxia and dizziness can be clinical symptoms


“Chiropractors don’t take pressure off nerves- they put pressure on mechanoreceptors.”

“Ninety-nine percent of all neurologic syndromes are related to deafferentation.”

F. Carrick, D.C.


“”Ninety percent of the incoming sensory impulses to the brain come from the joints and muscles. That’s why contracting muscles and moving joints have a profound effect on all neurologic function, which then affects every other system in the body.”

Gregory Malakof: The Neurology Behind the Health Benefits of Yoga


The deafferentation concept1
The “Deafferentation” Concept: the brain come from the joints and muscles. That’s why contracting muscles and moving joints have a profound effect on all neurologic function, which then affects every other system in the body.”

  • It is further known that mechanoreception affects the transmission of nociceptor information:

    “Nociceptive transmission can be modulated through “gateway” synapses in the basal spinal nucleus by peripheral (joint and muscle) mechanoreceptor (type I and II) discharge.”

    Terrett and Terret, “Referred Posterior Thoracic Pain,” Chiropr J ofAustralia 2002; 32: 44


“…it is proposed that decreased mechanoreceptor input associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”

Terrett and Terret, “Referred Posterior Thoracic Pain,” Chiropr J of Australia 2002; 32: 44


Somato somatic reflex model is it increased afferentation or decreased afferentation
Somato-somatic reflex model: Is it associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”increased afferentation, or decreased afferentation?

  • It is both: increased nociceptor traffic and decreased mechanoreceptor signals could be jointly referred to as “somatic dysafferentation”

  • Reflexive effects of this cause altered postural muscle tone or imbalances, leading to errors in posture and coordination and segmental somatic dysfunction which is self-perpetuating

  • There may also be increased pain perception because of pain gate modification


associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”Somatic Dysafferentation”

Increased nociception

and/or

Decreased mechanoreception


What to tell patients regarding somato somatic reflexes
What to associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”Tell Patients (regarding somato-somatic reflexes):

  • Abnormal motion and alignment of spinal joints can cause persistent muscle tightness in and around the spine; this can be a factor in spinal stiffness and pain

  • Balance and coordination can be affected by abnormal signals coming from spinal joints

  • This becomes a “vicious cycle”; a subluxation is self-perpetuating; i.e… its effects cause it to become worse


What to tell patients regarding somato somatic reflexes1
What to associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”Tell Patients (regarding somato-somatic reflexes):

  • A subluxation can be like a “bad habit:” easily started, and hard to “break.” It can take repeated adjustments and consistent work to achieve full correction of subluxations.

  • Loss of spinal motion can cause increased perception of pain; consequently, improved spinal motion can help relieve pain.


Article of interest
Article of Interest: associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”

Bolton, P

“Somatosensory system of the neck and its effects on the CNS”

JMPT 21:8; Oct 1998


E somato visceral reflex hypothesis aka somato autonomic somatic afferents visceral efferents
E. associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”Somato-Visceral ReflexHypothesis (aka somato-autonomic)somatic afferents visceral efferents


New text of note
New Text of Note: associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”

Masarsky and Masarsky, 2008:

Somatovisceral Aspects of Chiropractic: An Evidence-Based Approach


Somato visceral reflex model
Somato-Visceral reflex model: associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”

  • Somatic dysafferentation can reflexively change output from the lateral horn regions of the spinal cord (sympathetic preganglionic efferents); facilitation can occur

  • Increased sympathetic stimulation of target tissues and organs can result; this can be termed sympatheticotonia

  • Visceral dysfunction can directly follow, or happen due to vasomotor effects


Somato visceral reflex
Somato-Visceral reflex: associated with decreased or restricted joint mobility (hypomobile subluxations) causes increased perception of pain.”


“The spinal and supraspinal pathways allow a rich access of somatic afferents to sympathetic neurons. Therefore, when the motion of intervertebral joints is even slightly amiss, there will be autonomic effects, with resulting circulatory, metabolic, and visceral repercussions.”

Korr


“…once viscus and soma have become linked in a vicious circle, it no longer matters, from a therapeutic viewpoint, in which of these the vicious circle started. What matters is the interruption of the circle.”

Korr


The “Meric” clinical approach is based on segmental arrangement and distribution of nerves of the autonomic nervous system


Visceral correlations with vsc

Colic arrangement and distribution of nerves of the autonomic nervous system

High blood pressure

Urinary output

Enuresis

Gastric acidity and motility

Pituitary circulation

Anemia

Blood sugar levels

Asthma, allergic rhinitis

Coronary arteriospasm, dysrhythmias

Pupillary diameter

Migraine

dysmenorrhea

“Visceral” correlations with VSC


Alternative hypothesis the simulated visceral disease model
Alternative hypothesis: the “simulated” visceral disease model:

  • Somatic afferents and visceral afferents converge on, and may facilitate common neuronal pools, leading to the misperception by higher levels of the CNS that visceral dysfunction may be occurring, when, in fact, the somatic afferent signaling is the problem

  • So, some apparent remission of visceral symptoms after adjustments may have not been visceral in origin


Common sets of indistinguishable perceptive, somatic, autonomic and neuroendrocrine responses

Primary somatic dysfunction or disease:

Somatic afferent signals

Leading to:

Equally indistinguishable sets of signs and symptoms

CNS Afferent Convergence

Visceral afferent signals

Facilitation of common neuronal pool by either visceral or somatic afferents

Primary visceral dysfunction or disease:


What to tell patients regarding somato visceral reflexes
What to autonomic and neuroendrocrine responsesTell Patients (regarding somato-visceral reflexes):

  • Neural effects of subluxation include alteration of the blood supply and other controls of body organs and systems

  • Neural interference from VSC can cause or contribute to dysfunction of all body systems- chiropractic is not just about back and neck pain


F viscero somatic reflex hypothesis aka viscero motor visceral afferents somatic efferents
F. autonomic and neuroendrocrine responsesViscero-Somatic ReflexHypothesis (aka viscero-motor) visceral afferents somatic efferents


Viscero somatic reflex model
Viscero-Somatic reflex model: autonomic and neuroendrocrine responses

  • Visceral dysafferentation due to viscus (organ) injury/pathology can cause or predispose the spine to develop subluxation or somatic precursors

  • Facilitation of the anterior horn of the cord allows visceral input to cause reflexive muscle hypertonicity and other somatic effects

  • suggests that VSC can be caused by chemical stressors and other insults to body organs


Viscero-Somatic Reflex autonomic and neuroendrocrine responses


“The same mechanisms are at work when the viscera produce the main disturbance of the cord and the somatic (musculoskeletal) involvement is secondary (as in referred pain).”

Korr


“Referred pain of visceral and somatic origin, and the associated phenomena, are an example of dysfunctional segmental coupling.”

Korr


Possible clinical correlations in viscero somatic reflexes
Possible Clinical Correlations in Viscero-Somatic Reflexes: associated phenomena, are an example of dysfunctional segmental coupling.”

  • Lung irritation due to inhalation of toxins (i.e., smoking, air pollution, etc..) reflexively can cause somatic manifestations in the upper thoracic and midcervical regions of the spine

  • Stomach-mid-thoracic spine

  • Colon-lower thoracic & upper lumbar spine


“From baby in the high chair to grandma in the rocker, the axial bones are as liable to be displaced by noxious substances which enter the system in our food and drink or by inhalation as they are by direct accident.”

D.D. Palmer


What to tell patients regarding viscero somatic reflexes
What to the axial bones are as liable to be displaced by noxious substances which enter the system in our food and drink or by inhalation as they are by direct accident.”Tell Patients (regarding viscero-somatic reflexes):

  • “Toxins” and chemical stresses to body organs can be a factor in causing subluxations

  • This can cause a recurrence or relapse of one’s subluxation pattern, or make “holding” corrections difficult

  • What we eat, drink, and inhale can influence our spine and nerve system


Reflex models review
Reflex Models Review: the axial bones are as liable to be displaced by noxious substances which enter the system in our food and drink or by inhalation as they are by direct accident.”

  • The implication is that altered neurologic activity tends to be a self-sustaining phenomenon because of the naturally-circuitous, reflexive fashion in which the nervous system works.

  • Altered messages may elicit maladaptive responses, which in turn reinforce or worsen the original message, in a positive feedback fashion.


Osteopathic researchers “Patterson and Steinmetz concluded that in an area of SDF with accompanying motion disorder and muscle tension, visceral spasm, or other initiating disorder, if the initial stimulus is sufficient or lasts long enough, there may be segmental facilitation even after the instigating stimulus is removed.”


Some of the current thinking is that the resultant postural muscle hypertonicity not only creates hypomobility, but that the muscle contraction chokes off its own blood supply, and ischemic conditions worsen the inflammatory state.

(a vicious circle is established)


INJURY muscle hypertonicity not only creates hypomobility, but that the muscle contraction chokes off its own blood supply, and ischemic conditions worsen the inflammatory state.


Trauma muscle hypertonicity not only creates hypomobility, but that the muscle contraction chokes off its own blood supply, and ischemic conditions worsen the inflammatory state.


Anterior horn effects: muscle hypertonicity not only creates hypomobility, but that the muscle contraction chokes off its own blood supply, and ischemic conditions worsen the inflammatory state.

Trauma


Lateral horn effects: muscle hypertonicity not only creates hypomobility, but that the muscle contraction chokes off its own blood supply, and ischemic conditions worsen the inflammatory state.

Trauma


“Referred pain of visceral and somatic origin, and the associated phenomena, are an example of dysfunctional segmental coupling.”

Korr


“Somatic and visceral structures that, in the course of normal body activity or adaptive response patterns, do not have a functional link become clinically coupled only because their innervating neurons are segmentally related.”

Korr


Reflex models review1
Reflex Models Review normal body activity or adaptive response patterns, do not have a functional link become clinically coupled only because their innervating neurons are segmentally related.”:

  • The implication is that altered neurologic activity tends to be a self-sustaining phenomenon because of the naturally-circuitous, reflexive fashion in which the nervous system works.

  • Altered messages may elicit maladaptive responses, which in turn reinforce or worsen the original message, in a positive feedback fashion.


“Manipulative therapy is effective when it establishes coherent patterns of afferent input… The proper articular, interosseous, muscular, fascial, and ligamentous adjustments allow the tissues to report in logical proprioceptive patterns, thereby improving afferent input, and also relieve mechanical irritation or deformation of neural structures.”

Korr


G neurodystrophic hypothesis is also being referred to currently as the neuroimmune hypothesis
G. coherent patterns of afferent input… The proper articular, interosseous, muscular, fascial, and ligamentous adjustments allow the tissues to report in logical proprioceptive patterns, thereby improving afferent input, and also relieve mechanical irritation or deformation of neural structures.”Neurodystrophic Hypothesis( Is also being referred to currently as the “Neuroimmune Hypothesis”)


Neurodystrophic neuroimmune hypothesis
Neurodystrophic/Neuroimmune Hypothesis: coherent patterns of afferent input… The proper articular, interosseous, muscular, fascial, and ligamentous adjustments allow the tissues to report in logical proprioceptive patterns, thereby improving afferent input, and also relieve mechanical irritation or deformation of neural structures.”

  • Neural dysfunction as a result of VSC is stressful to the body and lowers tissue resistance, modifying specific and nonspecific immune responses

  • Specific effects of VSC are not well researched, but may include alteration of the trophic function of nerves

  • Most-accepted current concept is modification of sympathetic nerve activity locally and globally (i.e..sympatheticotonia)


“…it appears that the SNS significantly influences the response, including resistance of tissues, to antigenic, infectious, irritative, toxic, and even carcinogenic agents. Processes such as allergic manifestations, anaphylaxis, and immune reactions…also seem to be under some sympathetic influence.”

Korr


“…the SNS regulates all aspects of immune function in vivo, including proliferation, cytokine production, antibody production, and lymphocyte migration.”

Madden, K., Chapter 5, “Catecholamines, Sympathetic Nerves, and Immunity,” in Psychoneuroimmunology, Ader, Felton and Cohen, 2001, p. 198


Handout
Handout: vivo, including proliferation, cytokine production, antibody production, and lymphocyte migration.”

  • Elenkov et al; “The Sympathetic Nerve: An Integrative Interface between two Supersystems: The Brain and Immune System,” Pharmacol Rev, Vol 52, #4, 595-638, Dec. 2000;

    Dr. Dan Murphy’s “best article of all time”


“Subluxation reduces brain/cortical summation.” vivo, including proliferation, cytokine production, antibody production, and lymphocyte migration.”

Murphy



“Correcting the subluxation will: nervous system.”reduce SNS activity, reduce catecholamine release, enhance the Th1 response which will improve infection fighting; and inhibit the Th2 response, which will reduce allergy/atopic disease signs and symptoms.”

Murphy


“…the most critical effect [of manipulative therapy] is the quieting of sympathetic hyperactivity.”

Korr


Adjustments anti inflammatory
Adjustments: Anti-inflammatory? the quieting of sympathetic hyperactivity.”

  • Recent research suggests an effect of one type of adjustment (HVLA with cavitation) may be to help control the systemic inflammatory response

  • Study showed this type of adjustment was associated with a short-term decreases in production of TNF-a (Tumor Necrosis Factor a)

  • Subluxation may result in sustained increased production of TNF-a, which is not the normal function of this cytokine (usually short-term)


Adjusting and tnf a
Adjusting and TNF- the quieting of sympathetic hyperactivity.”a

“Spinal manipulative therapy can exert a modulatory and/or stabilizing effect on the inflammatory response in vivo.”

Teodorczyk-Injeyan et al, “Attenuation of Tumor Necrosis Factor Secretion following Spinal Manipulative Therapy in Normal Subjects”; J of Chiro Ed; 18(1), Spring 2004


Conclusion
Conclusion: the quieting of sympathetic hyperactivity.”

  • Subluxation can disrupt the body’s ability to keep this part of the inflammatory response short-term

  • Ordinarily, balance between sympathetic and parasympathetic portions of the autonomic nervous system keeps this in check

  • Subluxation leads to “dysautonomia” (Kent)


Recall kent s 3 d model of vsc
Recall Kent’s 3-D Model of VSC? the quieting of sympathetic hyperactivity.”

1. Dyskinesia

(somatic dysafferentation)

2. Dysponesis

(dysafferentation leads to dysefferentation… i.e. aberrant adaptive responses)

3. Dysautonomia

“functional autonomic dystonia”


Further conclusions
Further Conclusions: the quieting of sympathetic hyperactivity.”

  • Correction of subluxations:

    1. improves spinal motion

    2. improves spinal alignment

    3. leads to improvement in somatic afferentation, which:

    4. enhances immune response by balancing the sympathetic and parasympathetic divisions of the autonomic nervous system


“Amazingly, Palmer’s concept of altered “tone” of the nervous system being the cause of disease then has some support in the current neurophysiologic literature regarding facilitation and sympatheticotonia.” (“dysautonomia”)

Leach, ’94, p. 114


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