1. 1 Module 5 Subluxation Theories Highlights from Section III, chapters 8-18, of The Chiropractic Theories: A Textbook of Scientific Research, 4 th Edition, Leach 2004 [there is a copy in the reference books on the top floor of the library] Biomechanics (TECH 71613) James W. DeVocht, DC, PhD

2. 2 The Cardinal Signs of Inflammation (classic clinical signs) from Leach pages 131, 132 Rubor - redness Tumor - swelling Calor – heat, fever Dolor - pain Functio Laesa – loss of function Chapter 8: Inflammation Hypothesis

3. 3 Inflammatory Process is not all bad from Leach page 132 Maintenance of tissues Allows for remodeling

4. 4 Two Distinct Forms of Inflammation from Leach page 131 Acute – 3 phases 1. Vasodilation 2. Slowing of blood flow 3. Migration of white blood cells (can be self sustaining) Chronic - Accumulation of lymphocytes & macrophages - Angiogenesis - Connective tissue proliferation

5. 5 Chiropractic Management of Inflammation (according to Lantz, Chapter 8 in Leach) from Leach page 136 Ice Nutrition Exercise Strategies

6. 6 Segmental dysfunction: the most common spinal lesion recognized by lessened or otherwise altered mobility, altered pressure threshold to pain, and signs of neuromuscular dysfunction. from Leach pages 137, 138 Chapter 9: Segmental Dysfunction Hypothesis: Joint and Muscle Pathology and Facilitation

7. 7 from Leach page 138 Segmental facilitation: a lowered threshold for firing a neuron in the spinal cord as a result of afferent bombardment associated with spinal lesions.

8. 8 adapted from Leach Fig 9-1 Neurobiology of Muscle Spindles Gamma efferent fibers Group Ia afferent fiber Group II afferent fiber Intrafusal muscle fibers Capsule

9. 9 Leach Fig 9-3 Muscle Spindle Response to a Thrust on a Cat Lumbar Vertebra

10. 10 Leach Fig 9-4 Discharge of an Afferent Nerve in Response to Movement of the L5-L6 Facet Joint in a Cat

11. 11 Hypothesized Effects of Entrapped Joint Meniscoid (Jones 1989) from Leach page 149 Increased joint capsule tension  Increased mechanoreceptor activity  Increased nociception  Decreased pain threshold & hypertonic paraspinal musculature (classic signs of segmental dysfunction) Joint hypomobility  Capsular adhesions  Obliteration of joint cavity (no movement at all) The decreasing joint mobility  Loss of bone minerals  Premature degeneration

12. 12 Extensive Investigations of Lumbar Zygapophyseal Joints (Giles 1987,1989) from Leach page 148 Conclusion: Chiropractic benefit could be due to releasing trapped intra-articular synovial folds and stretching the joint capsule

13. 13 Leach Fig 9-9 Henderson’s Animal Model of Facet Pathophysiology

14. 14 The Korr Model of Segmental Dysfunction Leach Fig 9-10 A. CNS orders skeletal muscle contraction B. At same time, external forces push segments closer together than expected C. CNS turns up gain for motor neuron based on input from spindles D. Body recoils but muscles now resist E. Muscle is stretched at normal length (CNS in confused by bad info from spindles) (seems consistent with EMG data)

15. 15 Patterson-Steinmetz Model of SDF (1986) Leach Fig 9-11 Cerebral lesion  rear leg flexion Cord was then severed - if done immediately, no flexion - if > 45 min, full flexion remained - if < 35 min, some flexion remained Spinal learning occurs if lesion is sustained over time

16. 16 Mense Model (1991) Leach Fig 9-14 Mechanical spinal lesion, spasm  local ischemia  edema  release of vasoneuroactive substances  reinforces the spasm (self propagating) As a result of the local ischemia  decreased ATP  failure of Ca ++ pump  increased muscle contracture (spasm)  more ischemia There must be some sort of self-reinforcing cycle

17. 17 Instability hypothesis: Severe or repeated trauma and postural stresses can cause tissue damage and resultant instability and/or misalignment. This can predispose the spine to painful episodes and ultimately lead to premature stabilization of the involved motion segments. from Leach page 207 Chapter 10: Instability Hypothesis

18. 18 Postural Deviations Leach Fig 10-2 A & B: Reversed cervical curvature C: Significant DJD at C3-C4 level D: Spondylolisthesis of L5

19. 19 4 Methods of Quantifying Cervical Lordosis Leach Fig 10-3 1. Curve depth 2. C2-C7 angle 3. Chord-C7 angle 4. Radii of curvature

20. 20 Leach Fig 12-1 Chapter 12: Neuropathology Hypothesis Mechanical susceptibility of nerve root to distortion - compression - stretch Biological susceptibility of nerve root to distortion - inflammation - edema - venous obstruction of IVF

21. 21 Leach Fig 12-2 Susceptibility of cat nerves to compression block Dorsal roots much more susceptible than peripheral nerves

22. 22 Leach Fig 12-3 Structural Effects of Nerve Compression (MacGregor 1975) Displaced fluid resulting from blockage forces radial distention and lengthening

23. 23 Hypothesis: spinal joint lesions may trigger facilitation- induced reflexes that impair or disturb visceral function from Leach pages 269-271 Chapter 13: Somatoautonomic Reflex Hypothesis A. Central modulation: disturbance of lateral fibers of the spinothalamic system and/or medial fibers of the dorsal column system B. Peripheral modulation: segmental facilitation from prolonged bombardment of the dorsal horn to cause habituation of certain spinal reflex arcs. This could result from failure of damaged skeletal tissues to heal promptly.

24. 24 Sympathicotonia – hyperactive sympathetic function associated with segmental dysfunction (SDF) Leach page 274

25. 25 from Leach pages 277-282 Purported Chiropractic Success with Somatoautonomic Dysfunction Bell Palsy Down Syndrome Dysphagia Migraine headaches Myoclonus Nystagmus Seizure disorders Spasmodic dysphonia Vertigo (cervicogenic)

26. 26 Leach Fig 13-1 Fitz-Ritson’s Test for Cervicogenic Vertigo (cervicogenic or vestibular?)

27. 27 adapted from Leach Fig 13-4 Proposed Mechanism for PNS Mediation of Plasma Extravasation (major feature of acute inflammation) - Substance P (SP) released from primary afferent fibers - Acts on mast cells to initiate release of prostaglandin (PG) which causes plasma extravasation - Adjustments are thought to affect plasma levels of SP

28. 28 Hypothesis: Intervertebral subluxation may, in some severe cases (and even in the absence of fracture- dislocation), irritate, compress, or destroy portion of the spinal cord. from Leach page 311 Chapter 14: Myelopathy Hypothesis

29. 29 Leach Fig 14-1 Anterior Subluxation of C1 – Flattening Cord

30. 30 Leach Fig 14-2 MRI Evidence of Direct Pressure on Cord

31. 31 Dentate Ligament Hypothesis

32. 32 Chapter 15: Hypothesis of Vertebrobasilar Insufficiency Hypothesis: cervical joint lesions may compromise the vertebral arteries, especially in the presence of anomalies within the vertebrobasilar system. from Leach page 327

33. 33 Leach Fig 15-1 Vertebral artery is most susceptible in the upper cervical spine to deflection and obstruction by subluxation, osteophytic spurring, increased tortuosity from lower cervical degenerative joint disease, and even cervical spine manipulation itself.

34. 34 Chapter 16: Neuroimmune Hypothesis Hypothesis: immune response is significantly affected by neural influence and therefore can be positively affected by chiropractic adjustments. This theory was developed primarily from D.D. Palmer’s early writing. from Leach page 359

35. 35 Selye’s General Adaptation Syndrome (GAS) A general model concerning the effects of stress 1. Alarm reaction (increased secretion of cortisone, ACTH etc.) (misc. signs of damage or shock) from Leach pages 344 - 345 2. Stage of resistance (body seeks to function normally in spite of the stress) (lasts as long as endocrine & other systems hold up) 3. Diseases of adaptation (develops if the body is unable to maintain normal function while the stress continues)

36. 36 Diseases of Adaptation Includes a wide variety of diseases – not only things like hypertension and gastrointestinal ulcers but possibly many others including nephrosis, nephritis, rheumatic fever, and some tumors. from Leach page 345 Exposure to stress Conditioning factors Physiologic adaptation syndrome Disease of adaptation from Leach Fig 16-3