1 / 71

Major Models and Hypotheses of Chiropractic Subluxation: II. Neurologic Models

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 ”

Download Presentation

Major Models and Hypotheses of Chiropractic Subluxation: II. Neurologic Models

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Major Models and Hypotheses of Chiropractic Subluxation:II. Neurologic Models

  2. II. Neurological Models • Nerve compression B. Dorsal Root Ganglion compression C. Spinal Cord compression/traction D., E., F.: The Reflex Models

  3. 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

  4. Diagram of a Reflex higher center integrative center afferent efferent receptor effector stimulation response Adapted from Sato, A. in “Spinal Reflex Physiology” in Haldeman, S. Principles and Practice of Chiropractic, 1992, p. 87

  5. Diagram of a Reflex higher center (cerebral cortex) (descending inhibition/stimulation) integrative center (“sub-cortical” CNS, spinal cord) afferent efferent receptor effector stimulation response Adapted from Sato, A. in “Spinal Reflex Physiology” in Haldeman, S. Principles and Practice of Chiropractic, 1992, p. 87

  6. 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)

  7. 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

  8. When a response causes stimulation of afferent pathways involved in a reflex, a self-perpetuating positive feedback loop can emerge- a “vicious cycle”: higher center integrative center afferent efferent receptor effector stimulation response Adapted from Sato, A. in “Spinal Reflex Physiology” in Haldeman, S. Principles and Practice of Chiropractic, 1992, p. 87

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

  10. 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

  11. 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”)

  12. Somato-somatic reflex

  13. “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

  14. Inflammatory Model of Facilitation: 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.

  15. “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

  16. “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

  17. “…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

  18. Facilitation can result in a positive feedback cycle, or a “vicious circle”: Input Output

  19. The “Deafferentation” Concept: • 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

  20. “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.

  21. “”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

  22. The “Deafferentation” Concept: • 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

  23. “…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

  24. Somato-somatic reflex model: Is it 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

  25. “Somatic Dysafferentation” Increased nociception and/or Decreased mechanoreception

  26. What toTell 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

  27. What toTell 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.

  28. Article of Interest: Bolton, P “Somatosensory system of the neck and its effects on the CNS” JMPT 21:8; Oct 1998

  29. E. Somato-Visceral ReflexHypothesis (aka somato-autonomic)somatic afferents visceral efferents

  30. Somato-Visceral reflex model: • 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

  31. Somato-Visceral reflex:

  32. “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

  33. “…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

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

  35. Colic 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

  36. 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

  37. 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:

  38. What toTell 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

  39. F. Viscero-Somatic ReflexHypothesis (aka viscero-motor) visceral afferents somatic efferents

  40. Viscero-Somatic reflex model: • 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

  41. Viscero-Somatic Reflex

  42. “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

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

  44. Possible Clinical Correlations in Viscero-Somatic Reflexes: • 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

  45. “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

  46. What toTell 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

  47. Reflex Models Review: • 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.

  48. 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.”

  49. 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)

  50. Trauma

More Related