Chapter #3 CHIROPRACTIC MANAGEMENT OF SPINE RELATED DISORDERS
1. According to Palmer, what is the cause of disease?
Interference with the nervous system, primarily at the site
where the spinal nerve exited the IVF. Her attributed
interference with normal nerve function to approximation of
vertebrae, which he termed subluxation
(NERVE INTERFERENCE – AN OPEN-ENDED STATEMENT).
2. How does the nervous system affect the body's ability to fight disease?
Through its interplay with the endocrine system in maintaining
homeostasis - primarily through the immune response.
3. How do chiropractors view health?
A continuously active homeostatic process that maintains a
disease-free state (HOMEOSTASIS – SYSTEM OF BALANCES).
4. What is the body's ability to deal with stress contingent upon?
An intact neuroendocrine system regulating the host’s immune
5. According to Selye, what are the three responses of the body to stress?
Adrenocortical enlargement, thymicolymphatic involution, and
6. What neurological influences affect lymphatic tissue?
The neuroendocrine response and the ANS, both controlled by the
hypothalamus, that directly affects the pituitary and adrenal
glands. Branches of the ANS that secrete NE and ACh directly
affect lymphatic tissue.
7. What has been identified on the surfaces of lymphocytes?
Adrenalin, NE, and ACh receptors.
8. What is the neurodystrophic hypothesis according to Leach?
Immunity is under direct influence by neuroendocrine factors
as well as by direct neural modulation.
9. What three mechanisms suggested by Homewood may result in a
Mechanical, chemical, and mental stresses.
10. According to Faye, what does a chiropractic adjustment do?
Restores normal physiological motion to fixed joints and their
adjacent compromised tissues (REMOVE FIXATIONS).
11. What are two means by which a subluxation complex may result in
The subluxation complex has basis on the model that spinal joint
fixation compromises neural elements producing irritation
and/or compression of these structures (IRRITATION AND
12. What does nerve irritation lead to?
Increased neuronal activity through facilitation
(INCREASED CONDUCTION OR DIS-EASE).
13. What does nerve compression lead to?
Tissue degeneration (DECREASED CONDUCTION OR DISEASE).
14. According to Korr, where is the site of nerve irritation?
The spinal cord segments adjacent to the fixed vertebral motion
15. Which neurons are in a state of hyperexcitability?
Sensory, motor, and autonomic.
16. Where does facilitation of the anterior horn cells have an effect?
Motor outflow, sustained muscular tensions, postural
asymmetries, and limited and painful motion intense and
exaggerated streams of afferent impulses with resultant pain
CNS stimulation that will perpetuate spasms or ascend to the
reticular formation, fusimotor neurons, thalamus, and cortex
trigger points, spasm, and restricted motion.
17. What may facilitation of lateral horn cells affect?
Autonomic outflow deleterious effects on viscera, blood
vessels, and glands segmental musculoskeletal strain,
trauma, deep and superficial tenderness, and electromyographic
activity of paraspinal muscles.
18. What is the most widely acknowledged cause of nerve compression?
Intervertebral disc pathology, including disc bulge, disc
protrusion, and frank herniation with or without sequestration
19. Other than disc, what may cause IVF compression?
IVF narrowing Z-joint subluxation (facet syndrome),
inflammation, osteophytic formation, soft tissue compromise,
venous congestion, lateral recess entrapment, metabolic (B
deficiency, diabetes), MS, polio, toxicity.
20. To what are the earliest signs of nerve compression due?
Venous congestion [because the veins are the primary structures
passing in the IVF that are affectable].
21. What are the combined effects of nerve compression?
Decreased axoplasmic flow and resultant Wallerian degeneration
areflexia, motor weakness, and muscle atrophy, with sensory
loss producing numbness and paresthesia (DEFICITS IN REFLEXES,
STRENGTH AND TONE, AND SENSATION).
22. What autonomic response may occur from nerve compression?
Somatoautonomic reflexes and sympathetic atonia from
23. According to Korr, where are neural structures especially
vulnerable to compression?
In their passage over highly mobile joints, through bony canals,
IVF, fascial layers, and tonically contracted muscles.
24. How does Gillet define spinal fixation?
The element which in a subluxation holds the vertebra in its
abnormal placement and hinders its normal movement.
25. How does the ACA define fixation?
As a component of subluxation; under kinetic intersegmental
subluxations – hypomobility.
26. What does an adjustment accomplish?
The aim of manipulative therapy is not to reposition a displaced
vertebra, but to remove the obstacle that prevents normal
movement at that vertebral motion segment (REMOVE NERVE
27. How is coordination between agonists and antagonists achieved?
28. Which muscles voluntarily move the spine?
The long spinal muscles.
29. What movements do the voluntary spinal muscles accomplish?
Spinal flexion, extension, lateral flexion, rotation, and
30. How does segmental movement occur?
Short intersegmental muscles (interspinales,
intertransversarii, rotatores, and deep fibers of multifidus)
not under voluntary control.
31. What service do these involuntary muscles provide?
Vertebral motion segment stabilizers during spinal motion and
as factors in spinal articular blockage.
32. What happens when unguarded movement approximates short spinal muscles?
Silencing of the annulospiral receptor activity the lack of
input to the CNS in a turning up of the -motoneuronal gain,
increasing the intensity of the muscle contraction producing
the muscle spasm.
33. Why can't the short spinal muscles be stretched by the patient?
They are involuntary.
34. How would a high velocity, manipulative thrust work to reduce
joint fixation due to spa
HVLA at the extreme of the restricted joint’s motion activates
the GTO’s inhibiting muscle activity, thereby reducing muscle
35. According to Wyke, where are the nociceptors and mechanoreceptors which
influence the intersegmental spinal muscles?
In the spinal joints arising in individual vertebral motion segments.
36. What inhibits nociception?
Static and dynamic mechanoreceptors (type I and II).
37. What is contraindicated for hypermobile joints?
Repeated manipulation (>12Tx’s).
38. What is Gillet's postulate of the etiology of joint immobility?
A progressive degenerative process, with ligamentous shortening occurring
in the wake of long-standing muscular hypertonicity, wherein the contiguous
parts of adjacent vertebrae pull together.
39. To what does Stoddard attribute joint fixation?
Adhesions that form following a joint sprain, with unilateral restriction
of bending toward one side and ligamentous shortening affecting z-joints.
40. What are two causes of adhesions?
Fibrous – with collagen scar tissue or fibrosis.
Articular - glycosaminoglycans, water, and intermolecular
cross-links in collagen fibers.
41. What do Schmorl and Junghans believer to be the etiology of joint
Meniscoid fragments or small discs that incarcerate in the z-joint, or villi
of synovial membrane that project into the articular space.
42. What does Hadley propose as the cause of sudden facet locking?
Tabs of synovial tissue projecting inward from the facet joint margins
pinching of soft tissue structures between the articular surfaces procuring
the ‘sudden catch’ spontaneous type of localized back pain.
43. What has Giles demonstrated to exist in synovial folds?
Small myelinated nerves (0.6-12m) coursing through the
synovial folds not in association with blood vessels,
suggesting that these nerves are nociceptive.
44. What does Maigne accept as the cause of joint locking?
The herniated disc acting as a wedge between the vertebral bodies, thereby
modifying the reciprocal relationships of the posterior articulations and
their function, so that they assume the position that they occupy in
hyperflexion movement or they assume an asymmetric position, that they
occupy in a movement of lateroflexion.
45. Where is hypermobility commonly found?
In combination with hypomobility as a compensatory mechanism.
46. What are other common causes of joint hypermobility?
Esthenic individuals with ligamentous laxity, pregnancy, disc
degeneration, and ligamentous sprains.
47. What elicits pain in a hypermobile joint?
Sustained stretching of the involved joint.
48. Describe the pain associated with a hypermobile joint.
Dull, diffuse ache accompanied by sustained muscle spasm to
protect the joint.
49. What provides relief to a hypermobile joint?
Stabilization of the involved joint.
50. What explains the temporary relief following adjustment of a
Splinted muscles undergo tractioning with muscle spasm removal, but
it returns as motion reintroduces into the hypermobile area.
51. With what are zygapophyseal joints innervated?
Proprioceptive and nociceptive fibers.
52. Where are articular mechanoreceptor nerve fibers distributed?
They give off collateral branches that distribute
intersegmentally as well as segmentally throughout the
53. According to Mennell, where may one perceive pain from a
In any distant structure that shares its nerve supply with the
54. How does immobility damage a diarthrodial joint?
It interferes with the furnishing of nutrition by the synovial
fluid as well as the removal of waste products.
55. From where does the cartilage receive nutrition?
Diffusion of low molecular weight nutrients either from the
subchondral capillaries in the underlying bone or from the
56. How does mobilization differ from manipulation?
Mobilization is a passive movement that tractions the joint to
the end point of the elastic barrier.
Manipulation consists of forcing the joint beyond the elastic
barrier that produces a cracking noise as the articular surfaces
suddenly move apart.
57. What is cavitation?
The cracking noise resulting from a sudden liberation of the
dissolved synovial gases. The liberation of gases is
58. What is the refractory period, and how long does it usually last?
A period of time wherein the synovial gases are redissolving.
It lasts approximately 20 minutes.