Philosophy Final

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Dysfunction
Trauma or uncoordinated muscle contraction leads to facet subluxation, local pain, synovitis, segmental, hypertonicity, splinting
If stays for long time = instability or stabilization
Instability
Trauma or long-standing dysfunction leads to laxity of the facet joint capsule and bulging of the annulus, causing abnormal motion at the 3-joint complex and increasing stability, often with local and referred pain
Stabilization
Chronic, poor biomechanics results in degenerative changes, including destruction of disk and endplates, osteophytic changes, enlargement of the facets, resulting in stiffness and decrease in ROM (ranges of motion) and mobility
Body tries to support itself
Radial tears
Tears that go thru fibers
Circumference tears
Tears around ring
Stress due to faculty mechanics
Increase dysfunction and weakness of capsule
Primary functions of a Meniscoid
1. Fill space at the periphery of the joint surface
2. Increase SA contact and therefore transfer load
3. To cover exposed particular surfaces and protect joint margins during flexion and extension
Fibroadipose or Loose CT base
Arising from the joint capsule
Synovial inclusion zone
Highly vascularized
Tip of dense CT or cartilaginous tissue
Projects between the articular surfaces
Entrapped Meniscoid Released
Distraction of the articular surfaces and allow resolution of the consequent muscle spasm
Facet Syndrome Symptoms
1. Low Back Pain
2. Hip and buttocks pain
3. Cramping pain above knee
4. Low back stiffness in AM or after decreased activity
Facet Syndrome Signs
1. Local paralumbar tenderness
2. Pain on spine (hyperextension)
3. Absence of neurologic deficit
4. Absence of root tension signs
5. Hip, buttocks or Back Pain with Straight Leg Raise (Signs are found with orthopedic tests)
Kemp's Test
Disc problem from facet problem
Facet Syndrome Correlates
1. Postural increase in Weight Bearing (An observation is that facet loading with prolonged standing relieves pain
2. Increase in Lumbar lordotic curve (same as 1)
3. Anterior Sacral Tipping (flexion relieves loading)
Effects Manipulation has on Facet Articulations
1. Release of entrapped meniscoid
2. Reduction in articular cartilage displacement by chronically entrapped meniscoid
3. Pain relief by coactivation of various receptors
4. Reduced weight bearing
5. Reduction of intervertebral forman stenosis caused by segmental hyperexntension
6. Reduced intracapsular and extracapsular adhesions (tear adhesions)
7. Relief of abnormal tension on jt. capsule
8. Reduction of local vascular stasis
9. Release of osseous mechanical locking
General Adaptation Syndrome (Selye's Work) (GAS)
3 stages
1. Alarm Reaction (Rx)
2. Stage of Resistance
3. State of Exhaustion
Alarm Reaction
1. First exposed
2. A person's ability to withstand or resist any type of stressor is lowered by the need to deal with the stressor (increased secretion of gluccocorticoids
3. Good stress can lead to subluxation too
4. Parts of adrenal gland can burn out deplete ability to function (associated with immune system)
Stage of Resistance
1. PAS body tries to balance itself, but the "conditioning factors" of the individual will modify the results
2. If interaction with the stressor is prolonged, the ability to resist becomes depleted
State of Exhaustion
1. Ability to resist is depleted, the person becomes ill
2. Diseases of adaptation
3. Someone going to a job that they hate and having mental stressors
4. Patient with taking many medications
Emotional Brain
HPA axis (Hypothalamic-Pituitary-Adrenal)
-Cortisol include the mobilization of energy stores for immediate energy needs, the enhancement of tissue sensitivity to other stress-related neurohomones and the INHIBITION OF THE IMMUNE RESPONSE
Hypothalamic-Pituitary-Adrenal (HPA)
1. Hypothalamus receives a stress or fear reaction from the limbic system
2. Responds by secreting corticotrophin-releasing hormone (CHR)
3. Pituitary gland to release an ACTH
4. ACTH stimulates the adrenal cortex to release cortisol
Vora and Bates Research
-1980
-8 patients with CHRONIC musculoskeletal conditions were given spinal manipulation 2 a week for 2 weeks
-5 patients exhibited an INCREASE in levels of circulating B-lymphocytes
-T-lymphocytes INCREASED in 1 patient ONLY
-Postulated that spinal manipulation resulted in the removal of a 'physiological barrier' in the lymph nodes proximal to the spinal column
Brennan Research
-1991
-Thoracic adjustment/manipulation, sham manipulation, soft tissue manipulation groups were compared
-Blood was drawn both before and after interventions
-Both polymorphonuclear neutrophils and monocytes demonstrated INCREASE activity after T manipulation compared to the sham or soft tissue manipulation
-Difference between groups as statistically significant
Hayek Research
-2002
-Done at 16 tx centers in Australia 420 patients
-Finding out the effects spinal manipulation has on symptoms IgA and Immunosuppressant (cortisol)
-Spinal manipulation displayed significant improvement in asthma symptoms and depression and anxiety scores
-INCREASES IgA and DECREASES cortisol thru post-tx pd
-2 million people Australia suffer from Asthma
SympatheticOtonia
Increase in your sympathetics
SymatheticAtonia
Decrease in your sympathetics
Stress Causes
INCREASE in the Sympathetic Nervous System
Sympathetic Nervous System
1. ThoracoLumbar portion of ANS
2. Fight or flight
3. Iris- Dilation of pupil
4. Heart- HR increases (distress)
5. Stomach- (Decreases peristalsis
6. Colon sphincters constricted
7. Hypertension
8. Patient will most likely have a subluxation with these sympathetic issues
9. Patient will show exhaustion
10. Adrenal glands won't work properly
Parasypathetic Nervous System
1. Craniosacral
2. Conserves Energy
3. CN III
4. CN VII
5. CN IX
6. CN X
7. S2-S3
8. Balances itself out
9. Iris-Constriction
10. Heart- HR decreases and BP decreases
11. Gastro Instestinal Peeristalsis- INCREASES
Myelopathy
Functional disturbances in the spinal cord
Can result in Bone spurs and degeneration
Spinal Stenosis
Gradually develops
Patient dx have weakness, difficulty with gait and have balance problems
BJ Palmer (HIO technique)
RADICULAR pain (LMN- lower motor neuron)
Cervical Radiculopathy
Pain in the distribution of a specific cervical nerve root as a result of compressive pathology from disc herniation and more
Stenosis
Reduction of cross-sectional area of the spinal canal
-11-12 mm of A-P dimension of canal signifies stenosis
-SOL- m/c disc herniation
-Hypertrophy of PLL, ligamentum flava, anterior and posterior capsular ligament
-Laxity ligamentous structure
-Post-surgical complications (Fibrosis, Hypertrophic bone formation)
AtlantoDental Interspace (N-Range)
Adult 1-3mm
Children 1-5mm
HIO (Hole in One) Technique
C1-C2 (Atlas and Axis)
-Adjusting a patient with this technique would heal the whole spine
B.J. Palmer came up with the technique
Down's Syndrome
Cervical Spine Involved (C1-C2)
Integrity of Transverse ligament
Up to 20% born w/o transverse ligament
Detection of missing transverse ligament can be done and seen in a Flexion Radiograph
-AtlantoDental Interspace (N Range)
-Adults 1-3mm
-Children 1-5mm
Rheumatoid Arthritis
Generalized C.T. disorder
Targets synovial Tissue
Upper cervical spine is most critical
AtlantoAxial Joint (C1-C2)
Atlas instability
Bilateral condition Osteoarthritis is a unilateral condition
Oblique x-rays are used to view IVFs on C/S
-Increased AtlantoDental Interspace (N Range)
Altered Cerebrospinal Fluid Flow
1. Improper circulation of the cerebospinal fluid has been suggested as a mechanism in spinal dysfunction that si amenalbe to manipulation
2. Craniopelvic manip. thought by some to normalize
3. Postural disorders and head symptoms may occur
4. A condition of CSF stasis or aberrant flow leads to DECREASED nutritional supply to those CNS components bathed by the fluid
Axoplasmic Aberration
Axoplasmic Transport may be altered in certain cases in which the spinal nerve roots or spinal nerves are compressed or irritated by intervertebral subluxation or facilitation
-Dr. Korr
Trophic
Nutrition
Axoplasmic Transport
Nonimpulse mechanism based NOT on transmission of signals along the surface of the neuron's outermost layer of the nerve fiber but on the intra-axonal transport and exchange of macromolecular materials
Anterograde Transport
From cell body out to the periphery
Fast transport = 410mm/day +/- 50 mm
Slow transport called BULK FLOW = 1-3mm/day (form storage mechanism)
Transfers product for nerve growth
Provides function and repair for synaptic processes
Retrograde Transport
From periphery to the cell body (going back up)
Recycling of enzymes and building blocks
Transfers of information about status of an axon on its terminals and target cells
Transport is 110-220mm/day
Axoplasmic Flow Disturbances
OCHS, KORR< SJOSRAD all found that any type of neuronal constriction, compression or ischemia will cause a local transport block and an accumulation of the fluid proximal to the restriction
Weiss- described these disturbances as a form of persistent endoneurial edema found just proximal to a compressed area
Decreased Axoplasmic Transport
1. Affects intra-axonal transport mechanisms for neurotrophic substances to end organs (target cells)
2. Affects development, growth, and maintenance of cells or strctures dependent on this trophic (growth) influence expressed by the nerve
3. Depriving an end organ structure of trophic materials results in lack of growth or atrophy of these structures
Peripheral Nerves
1. Compression can cause injury to the nerve fibers and blood vessels in the nerve
2. Variables in Injury (pressure level, duration, mode of pressure application)
3. Regeneration (nerve fibers grow at a max. speed about 1mm/day)
Nerve irritated or compressed
1. Will see an alteration of AXT
2. Change in protein composition
3. Nerve conduction capacity changes function
4. Increase pressure= more repair
5. Increase time = Increase pressure = increase recovery
Peripheral Nerve Compression
Low Pressure (20-150 mmHg)
-Decrease in intraneural blood flow, cell nucleus, intrafascicular edema, increase in endoneurial fluid pressure, Epineural fluid pressure (chronic), CTS (carpal tunnel syndrome)
High Pressure (200-1000mmHg)
-Displacement of nodes of Ranvier, decrease microcirculation, increase endoneurial fluid pressure, direct mechanical injury and deformation
Carpal Tunnel Syndrome
CTS
Critical pressure 40-50mmHg
Median nerve compromised
Neurapraxia
1st degree
Conducting blocked but continuity of axon preserved
NO Wallerian Degeneration
After latent period lasting from hrs. to days, conduction across the affected segment returns and funciton is fully restored
Endoneurium is fine (NOT damaged)
Axonotmesis
Endoneurial sheath intact
Axons are damaged- Wallerian Degeneration
Regeneration of axon is confined to the endoneurial tube which originally contained it
Recovery is complete (more slowly for the restoration of axonal continuity w/periphery)
Neurotmesis 3rd Degree
Intrafunicular Damage (axon continuity lost, endoneurial continuity lost)
Intact perineurial sheath
Regeneration is incomplete and imperfect
Hard to get full funciton back
Neurotmesis 4th Degree
Ruptured and disorganized by the injury
Continuity of trunk maintained by damage disorganized tissue
Considerable obstacles to useful regeneration
NO useful recovery to be expected
Neurotmesis 5th Degree
NERVE SEVERED: CLEANLY or RAGGEDLY
Double Crush Syndrome
-Nerves being irritated up in the cervical region causing peripheral nerve entrapment like CPT at the wrist or ulnar
-Compromised nerve has less reserve and resilience to cope with the second compression. Because of the initial compression farther up in the TOS, CPT
-1st compression causes lack of nutrient flow on an axon thru smaller surface area causing 2nd compression bc nerve is irritated which causes edema and inflammation
DRG
Far more sensitive to mechanical stimulation than peripheral nerves (Lantz)
Vertebrobasilar Arterial Insufficiency (V.B.A.I.)
Cervical spine joint lesions may compromise the vertebral arteries, thereby altering cerebral circulation, especially in the presence of anomalies within the vertebrobasilar system
C6
Vertebral artery enters the transverse foramen at
VBAI anatomy
Subclavian Artery
Goes through transverse foramina C6 to C2
VA makes the Basilar Artery
VABI Signs and Symptoms
Dizziness/vertigo/giddiness/light headedness
Drop attacks/loss of consciousness
Diplopia
Dysphagia (not able to swallow)
Dysarthria (difficult to speech)
Gaitaxia/extremities
Nausea
Numbness on one side of body, face
Nystagmus
Predisposing to brainstem ischemia
1. Unilateral VA obstruction by congenital or development factors
-arteriosclerosis, vascular anomaly, unilateral vertebral artery occlusion
2. DJD
-loss of disc height, shortens C/S become more tortuous
3. Osteophytic Outgrowths
-zygapophyses, can obstruct the course of the V, outgrowths can obstruct the course of the VA's on the side on the osteophytic outgrowth reducing
Signs of Stroke
1. Can the patient smile?
2. Can they raise both arms?
3. Can they stand steady on both feet with their eyes closed?
4. Can they speak a simple sentence with several vowels that run together such as : Simple SImon Says?
5. Can they stick out their tongue?
Cerebral Dysfunction Theory
Possible mode of action of spinal manipulation in some patients with visual disorders, dizziness, depression, anxiety, memory problems
Diminished blood flow thru brain "hibernate"
Ischemic Penumbra- cerebral flow was btw normal blood flow and blood flow low enough to result in irreversible tissue damage
Semental Dysfunction
Daniel David (D.D.) Palmer and Henri Gillet
-Life is the expression of tone
-Tone is the normal degree nerve tension
-Tone is expressed in functions by normal elasticity, activity strength, and excitability of various organs, as observed in a state of health
-Consequently, the cause of disease is any variant of tone
Facilitation
Irwin Korr (SympatheticOtonia)
-Chronic neural dysfunction associated with persistent segmental dysfunction, including lowered skin resistance, aberrant sudomotor responses; high vasomotor and sudomotor activity, and may result in abnormal
-SOMATOAUTONOMIC REFLEX activity
Somatoautonomic Reflex
-Spinal Joint lesions may trigger facilitation-induced that impair or disturb visceral function
-A proprioceptive insult
-A kidney stone which cause back pain is an example of viscerosomatic reflex
Vertebral Subluxation Complex (VSC)
John Faye, Charles Lantz
-Model of motion segment dysfunction (subluxation, articular spinal lesion) that incorporates the complex interaction of inflammatory, degernerative, and pathologic changes in nerve, muscle, lig. , vascular, and C.T. may influence organ system function and health
Neuropathology- Nerve Compression
D.D. Palmer
-Intervertebral Subluxations may interfere with the normal transmission of nerve energy by irritating or compressing the spinal nerve roots
-Inflammatory changes associated with spinal joint lesions may affect the blood nerve barrier and neuroplasmic transport and impair verve, muscle and organ function
Myelopathy- Compressive Myelopathy
Bartlett Joshua (B.J.) Palmer
-(Spinal cord compression): intervertebral subluxation may, in some caes (even in the absence of fracture/dislocation) irritate, compress, or destroy the spinal cord
-HIO (Hole in One) technique (C1-C2 Atlas and Axis)
Denticulate (Dentate) Ligament/Cord Distortion
John Grastic
-Misalignments of the upper cervical vertebrae, bc of their unique attachment to the spinal cord by means of the dentate ligament, can directly stress and deform the spinal cord. Subsequently, this stress on the cord, in addition to direct mechanical irritation, may produce venous occlusion with stasis of blood and resulting anoxia (decreases in oxygen) in particular areas of the upper cervical cord
2 components of Denticulate (Dentate)
Hypothesis uses the anatomy of C1 or C2 misalignment producing neurological insult directly via mechanical irritation of the spinal cord, and indirectly via the vascular compromise of the cervical cord
Upper cervical technique
Vertebrobasilar Arterial Insufficiency Hypothesis
Alan Terrett, John Triano, Dr. Scott Haldemann
-Cervical spine joint lesions may compromise the vertebral arteries, thereby altering cerebral circulation, especially in the presence of anomalies within the vertebrobasilar system
Neuroimmune Neurodystrophy
Dr. Hans Selye
-Neuroimmodulation, Neuroimmunology: Spinal Joint lesions, thru largely sympathetic mediated influences, modify nonspecific and specific immune responses and alter the trophic function of the involved nerves
-GAS
Axoplasmic Aberration
Dr. Korr
-Axoplasmic transport may be altered in certain cases in which the spinal nerve roots or spinal nerves are compressed or irritated by intervertebral subluxation or facilitation
Meniscoid Entrapment
Wolf
-Becoming entrapped btw the articular surfaces. An adjustment that separates the articular cartilages releases the trapped meniscus and relieves the capsular strain
(Joint blockage Theory)
Immobilization Degeneration
Kirkaldy Willis
-Articular overstress in the spinal joints, especially when combined with trauma, commonly promotes pro-inflammatory changes, cartilage and disc destruction, and osteophytic bony and architectural changes
Wellness
Leach and Redwood
-Chiropractic adjustive intervention, in a prevention-based practice, that enhances patient health and well-being
SOT
Dejarnett
VBAI Injury SItes
1. Between C1-C2 TP
2. Level C2-C3 compression of VA superior articular facet of C3 on ipsil. rotation
3. C1 TP compressing the internal carotid artery
4. C4-C5 or C5-C6 due to osteoarthrosis of the uncovertebral joints
5. C6 transverse process, traction over a prominent longus colli muscle
6. Constriction of the VA the ventral ramus second cervical nerve
7. Atlanto-occipital aperture on extension
98. C1 and C2 compression by the oblique capitis inferior muscle
Arterial wall trauma
Trauma to the wall producing damage to the wall
Trauma to the arterial wall producing vasospasm
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