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226 Cards in this Set
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INSTABILITY hypothesis
(slides 3 and 4 of Instability lecture) |
1. SEVERE/REPEAT TRAUMA
POSTURAL STRESS 2.SCARRING (ligaments, capsular, disc tissue) 3. OBSERVABLE INSTABILITY/ MISALIGNMENT via XRAY 4. predispositon to PAIN 5. PREMATURE STABILIZATION of those MOTION SEGMENTS |
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EXAMPLE of:
radiographic operationally-defined INSTABILITY *example of observable unstable segment on an x-ray |
SPONDYLOLISTHESIS
A-P Shearing crashes pedicle and pars interarticulars = spondylo *we actually can say when this is not to be adjusted, based on evidence |
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VSC2 is ___________
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INSTABILITY
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Some epidemiologic evidence for cause of spondylolisthesis via activities that use ____________ of motion.
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full ranges
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Name 5 causes for INSTABILITY (VSC2)
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1. PARS INTERTICULARIS defect
2. BIPED STANCE 3. REPETITIVE ROTATION/FLEXION/EXTENSION/LATERAL BENDING PROFESSIONS! 4. POSTURE 5. TRAUMA |
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Developmental instability problem
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CONGENITAL defect of
TRAUMA + NORMAL LORDOSIS |
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biped stance problem instability
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ANTERIOR THICKENING of vertebrae
POSTERIOR THINNING of vertebrae |
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Occupational problem instability
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PROLONGED ANYTHING
*flexion/extension/rotation/lateral bending |
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Postural problem instability
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Unilateral subluxation during SLEEP
BAD POSTURE IS WORSE THAN UPRIGHT POSTURE |
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Trauma problem instability
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MVA's - DIVING - BLOWS TO THE HEAD - WHIPLASH, etc.
UNILATERAL + FORWARD + ROTARY CERVICAL MOTION = atlantoaxial subluxation *esp when taken by surprise, however I disagree. Drunks and people asleep at the wheel are never as injured. Awareness allows us to clench up tight and shatter. |
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Instability and TRAUMA: posterior branches of spinal nerves affected by derangement of posterior joints due to ACUTE OR CHRONIC trauma causes nerve _________.
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TRACTION
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Regarding TRAUMA instability, what also may injure the nerve besides traction?
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EDEMA
PERI-ARTICULAR BRUISE LIGAMENT/CAPSULE TEARS |
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OCCUPATIONAL instability of repetitious nature may cause
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FORAMINAL ENCROACHMENT
*you keep using what isn't meant to be used that way at work and your body is going to deposit bone. Friction is a real kicker for osteoblasts. |
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WHIPLASH instability
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Both severe and mild
76% WHIPLASH HYPERLORDOSIS in car crashes *seizures can occur w/ whiplash even with NO fracture or dislocation |
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LOW BACK TRAUMA instability
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DISC NARROWING & EXTENSION
****70% body weight shifts to discs versus normal 16% |
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LOW BACK TRAUMA instability
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narrowing and extension is bad but also FACET SYNDROME...
microtrauma repetition |
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what else is whiplash instability called
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acceleration/deceleration syndrome
(Foreman and Croft) |
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What's the main cause of low back pain after trauma?
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NONE 27%
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Disc Degeneration GRADE I
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BULGE
ages 14-40 |
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Describe a NORMAL IVD
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AVASCULAR
SEMIGELATINOUS NUCLEUS P. COLLAGEN/PROTEIN POLYSACCHARIDE GEL |
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What is the cause of IVD displacement in teens? In adults?
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Teens Trauma drama
Adults - dehydration, loss of disc height, changes to COARSE collagen instead of gel. Cartilage plates start to APPROXIMATE (touch), allowing BULGING DISC. |
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GRADE 1 disc degen
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BULGE degeneration
15-40 yrs. old |
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GRADE 2 disc degen
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INTACT NUCLEUS
decreased disc space larger bulge 35 - 70 yrs |
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GRADE 3 disc degen
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Nucleus BULGING INTO ANNULUS
Damage to INFERIOR END PLATE moderate degeneration |
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GRADE 4 disc degen
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SEVERE degeneration
BOTH END PLATES crack ANNULUS INTERNAL COLLAPSE LOSS of disc HEIGHT |
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Why does a bulging disc produce BONY SPURS?
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pressure on LONGITUDINAL LIGAMENT
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When nucleus GONE (grade 4), the narrow disc space leads to
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SUBLUXATION of FACET
NERVE ENCROACHMENT (pinch) |
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In the PASSIVE SUBSYSTEM (load-rate dependency), what fails first?
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END PLATE at low load
vertebral bony elements @ higher loads |
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Schmorl's nodes (end plate fractures w/ nucleus extravasation into bone) is often misdiagnosed as>..
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herniated disc
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The disc must be at full end range in order to
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herniate.
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Since DISC HERNIATION is assoc w/ EXTREME deviated posture, and repeated loading, what is a primary cause of INJURY?
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FATIGUE
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Is it the grossly unstable or the minor instabilities we question? Yes, minor. Why does this threaten VSC-2?
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Because if it's MINOR INSTABILITY, then VSC-2 is irrelevant. Most agree that phase 2 is NOT typically PART OF the overall progression from SEGMENTAL DYSFUNCTION to FIXATION
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Use it or lose it
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IMMOBILIZATION DEGENERATION hypothesis
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IMMOBILIZATION DEGENERATION is basically
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Lack of use leads to hypomobility then fixation, degeneration, then immobilization.
If something is immobilized, the body tries to kill it (degenerates it) with inflammation and destruction. |
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Hallmarks of Immobilization degeneration
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Inflammation
Destruction of cartilage and disc Osteophytes Architecture changes permanent |
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Notion of FIXED or RESTRICTED JOINTS
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MOTION PALPATION
(MOPAL) |
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Degeneration as a PROCESS in the LUMBAR SPINE
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SANDOZ
*described spinal lesion in distinct phases, long before K-W in '83 |
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First person to use TERM "immobilization degeneration" {I.D.}
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LANTZ
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VSC -3 CLINICAL FINDINGS (3)
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you can SEE IT on an X-RAY!
Yay!!! other degenerative signs, too. OSTEOPHYTES, SCLEROTIC END PLATES ANKYLOSIS |
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{I.D.} HISTOPATHOLGY of cartilage
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Distraction causes FACET JOINT CARTILAGE DEGENERATION
thick cartilage, rich in proteoglycans> loss of proteoglycans> channels develop due to thinning between SUBCHONDRAL & SYNOVIAL SPACE> VASCULAR INVASION!! CONVERSION of end cartilage to TRAEBECULAR BONE (spongy) |
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Molecular effects of immobilization on cartilage (what did the rat tails lose?)
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HYALURONAN (a glycosaminoglycan that attracts water when in binds to AGGRECAN)
LUBRICIN also protein for joint viscosity |
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Cartilage immobilization:
LUBRICIN AGGRECAN HYALURONAN |
LOST during immobilization (causes dehydration)
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{I.D.} SYNOVIAL MEMBRANE changes
EARLY |
VISCOUS!! even more viscous!!
FIBRO-FATTY CONSOLIDATION HYDROXYAPATITE |
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FIBRO-FATTY CONSOLIDATION
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SYNOVIAL membrane EARLY change
in Immobilization degeneration |
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RE-mobilization can restore much lost GAG content after lengthy immobilization, but..
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it is an INCOMPLETE restoration
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What is the problem with immobilization of an ARTICULAR CAPSULE during a FRACTURE?
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if it is neutral, great!
If it is immobilized in FLEXION = inside SLACK< outside STRETCHED Slack side thickens, Stretched side becomes hypermobile |
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Remember the channels (canalization) that develops between the subchondral zone and the synovial space during cartilage immobilization? Vascular invasion!
What happens to SUBCHONDRAL BONE during {I.D.}? |
LOSS of TRABECULAR MASS (spongy)
EXPANSION of sinuses allow diffusion. INVASION OF SUBCHONDRAL BONE INTO SYNOVIAL SPACE causes ACCELERATED ANKYLOSIS |
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{I.D} COLLATERAL LIGAMENTS
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EITHER stretched OR shortened
SHORT CONTRACTS and RESTRICTS joint even after ID. |
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{I.D.} TENDON
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EITHER stretched OR shortened
Like ligaments in ID, TENDONS LOSE INTEGRITY at bony insertion |
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What happens specifically to tendons during immobilization degeneration that is DIFFERENT from ligaments?
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Both stretch or shorten but TENDONS LOSE INTEGRITY AT INSERTION at bony insertion
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{I.D.} IVD changes
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similar to ligament (stretch or shorten)
NUCLEUS PULPOSIS DEHYDRATES because cannot exchange fluid through end plates LOTS OF CARTILAGE FISSURES in annulus fibrosis DISC HERNIATION OSTEOPHYTES |
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{I.D.} MUSCLE
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SHORT CONTRACTURE
LOSS OF MASS CONNECTIVE TISSUE replaces contractile tissue |
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Immobilization degeneration muscles due to SCOLIOSIS
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SHORT SIDE = ATROPHY
STRETCHED SIDE = HYPERTROPHY loss of mitochondria and proteins |
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Which muscles are MOST SUSCEPTIBLE to {I.D.}?
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POSTURAL muscles...
slow fiber slow fiber justin beiber slow fiber stand up straight, justin bieber you are fucking up your slow fibers |
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{I.D} NERVE
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TETHERING at contact w/ CONNECTIVE TISSUE
EFFERENT FAIL creates LACK OF COORDINATION in immobilized limbs |
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What is the biggest difference between SANDOZ and KIRKALDY-WILLIS?
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K-W leave out Sandoz' PHASE 3 TEMPORARY FIXATION
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Provide TORSIONAL RIGIDITY and structural support for AXIAL LOADING
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Z-JOINT
*TROPISM predisposes z-joint to degeneration/derangement |
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What happens to Z-JOINTS as we AGE?
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Z-joints TAKE UP LOAD for degenerating, shrinking disc
PROTEOGLYCAN CRASH and is LOWEST in L5-S1 disc, the point of GREATEST LOAD BEARING! |
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point of GREATEST LOAD BEARING suffers how with age?
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L5/S1
Loss of PROTEOGLYCANS |
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Other changes affecting z-joint besides fail of IVD?
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PRESSURE
loss of pH CARBON DIOXIDE |
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athletics
smoking occupation factors (heavy lifting) |
all contribute to disc degeneration (overuse and dehydration)
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Which test does not correlate with size or position of herniation
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Straight leg raise
because Inflammation, not distortion, is the cause of pain. SLR distorts. |
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Does a disc herniation on an MRI confirm nerve compression
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NO.
*because inflammation, not distortion, causes pain. |
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A 'stabilized' or ankylosed joint is bad. Might go through a period of laxity and mobility in isolated joints. This is paradoxical because...
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it is followed by CONTRACTURE of the HOLDING ELEMENTS
and loss of tissue compliance and elasticity |
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Bed rest is harmful in acute back injury. What is done now?
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PASSIVE MOBILIZATION
to prevent contracture |
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z-joint degeneration:
FIBROSIS (dysfunction) HYPERTROPHY (unstable) LOCKING (stable) |
KIRKALDY-WILLIS
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4 phases:
articular overstress insufficiency & instability EPISODIC fixations stabilization |
Sandoz
EPISODIC FITS OF RAGE! |
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phase 1 sandoz
vs dysfunction K-W |
both localized
overstress sandoz paraspinal and spinal pain KW |
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phase 2 sandoz
vs unstable KW |
rest relieves instability
catching unstable |
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phase 3 sandoz
vs stabilization KW |
EPISODIC FIXATION sandoz anytime near end range acute or normal chronic
Stabilization - KW ends w/ less LBP but scoliosis and reduced movement |
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phase 4 sandoz
vs KW |
stabilization stiffness in morn better as day goes, reduced ROM sandoz
NO KW 4 |
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Is complete immobilization necessary to full degeneration?
How chiros help... |
NO, degeneration w/ less than complete immobilization
chiro reduces fixations, delays onset Trauma + immobilization kills joints |
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Ruffini
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type 1 spray
boys in blue always reporting in on joint position, velocity, pressure slow to react |
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Pacino
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Al is a deep, thoughtful actor
Lightning-quick reflexes to sudden change |
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Goligi
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you cant GO without your GOlgi
If the joint is immobile,no golgi slowest responders of all only in tendons ligaments and capsules |
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type IV
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nociceptors
free nerve endings that are everywhere |
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neuropathology/compression hypothesis
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ISCHEMIA & EDEMA
Nerve ROOT, not peripheral, is prone to COMPRESSION and distortion |
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why are NERVE ROOTS more susceptible to pathology of compression than peripheral
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they aren't protected - they are CRUSHABLE
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HOYLAND
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BABES IN TOYLAND
IVD FIBROSIS = VASCULAR ISCHEMIA ROOT & DORSAL ROOT GANGLION ARTERIAL OR VENOUS SUPPLY CAUSES FIBROSIS & DEGENERATION |
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venous stasis first, then nerve degeneration at root
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HOYLAND = VASCULAR STASIS
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LARGER fibers more susceptible
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HOYLAND
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PRESSURE effects nerve due to ISCHEMIA
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HOYLAND
ischemia screws axoplasmic flow |
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VENOUS STASIS EFFECTS
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HOYLAND
more CO2 more negative pH less blood and O2 |
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ADJUSTMENTS on venous stasis
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relieve torque of posture on a/v
restore flow clear inflammatory mediators |
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___________ sensory inputs from selective loss of certain fibers or cells
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DIFFERENTIAL
#12 result of nerve damage |
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Neural COMPRESSION hypothesis (neuropathology) upshot
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VELOCITY SAME
AMPLITUDE (STRENGTH) CHANGES PERMANENTLY MECHANICAL DISTORTION ISCHEMIA |
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pain when I move
stops when I rest |
CLAUDICATION
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___________alters AXONAL TRANSPORT
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FACILITATION
compression/subluxation/whatever |
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growth factors OUT to terminal of axon
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ANTEROGRADE = OUT
fast |
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can block either antero or retrograde axoplasmic flow
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chemicals
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What would INTERFERE w/ axoplasmic flow
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CRUSH
COMPRESSION ISCHEMIA |
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*ROOTS
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MORE SUSCEPTIBLE to injury
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NEUROPRAXIA
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LOCAL BLOCK
DUE TO INJURY RECOVERS |
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AXONTOMESIS
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CRUSH INJURY BUT LEAVES ENDOMETRIUM INTACT
TINEL'S SIGN COMPLETE, SLOW RECOVERY |
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NEUROTEMESIS
*Timm-eh! gets KILLED in every episode of South Park |
TOTAL TRANSECTION
DEATH OF NERVE SURGERY |
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SOMATO-AUTONOMIC (VISCERAL) REFLEX hypothesis
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Hypomobile facilitated SPINAL LESIONS
REFLEXIVELY SHOOT VISCERA W/ abnormal signals = CRAP FUNCTION RESULTS |
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CRAP FUNCTION OF VISCERA
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SOMATO-AUTONOMIC (VISCERAL) REFLEX hypothesis
HYPOMOBILE SEGMENTS SHOOT NERVE SIGNALS TO VISCERA, BAD RESULTS |
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autonomic evidence of S-A/(visceral) R hypothesis
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HTN
HYPERACTIVITY AROUSAL |
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NOCICEPTORS
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GROUP II
PAIN |
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SILENT/SLEEPING NOCICEPTORS
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C FIBERS
GROUP IV EFFERENTS EVERYWHERE ASLEEP UNTIL INFLAMMATION |
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POLYMODALS PROMOTE
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HEALTH
THEY ARE AWAKE DURING ALL NOXIOUS & NON-NOXIOUS STIMULII -FIREMEN RETURN OF HOMEOSTASIS group III C-FIBERS |
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There is a balance between SYMPATHETIC innvervation of spinal structures and __________
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GROUP IV AFFERENTS (SILENT/SLEEPING)
FIREMEN |
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drive CHRONIC NOCICEPTIVE & NEUROPATHIC PAIN in a
pro-inflammatory environment |
POLYMODAL NOCICEPTORS
& SILENT/SLEEPING NOCICEPTORS FIREMEN work in pro-inflammatory situation |
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Only YOU can prevent forest fires.
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FIREMEN:
polymodals (homeostasis) and silent/sleeping (inflammation awake!) |
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once the FIREMEN (PMNC and Silent Sleepers) are stuck in a fire, they become ______________.
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SENSITIZED (SHELL SHOCKED)
AND FIRE AT WILL |
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3 ways a nociceptor can make a subluxation worse:
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PAIN
SPLINTING OF MUSCLES KEEP INFLAMMATION HOT (remember the firemen have PSTD and are firing at will) |
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expensive word for chronic inflammation
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NEUROGENIC INFLAMMATION
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SEAMAN and the VSC
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FIREMEN (Polymodal III's and Silent/Sleeping nociceptors IV's) are slowly being irritated by subtle PRO-INFLAMMATORY CHANGES in the joint.
FIREMEN develop post traumatic stress and HYPERSENSITIZE, firing at anything that moves GLIAL cells react w/ inflammatory chemicals to VSC ALPHA & GAMMA -MOTOR NEURONS promote muscle splinting HYPERSENSITIVE POSTGANGLIONIC SEGMENTS release inflammation chems,too! It's one great big fuckarow of HYPERSENSITIZATION due to PTSD, according to SEAMAN |
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Think of DORSAL HORN REORGANIZATION as tic- doloreaux
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WRONG NUMBER!! mechanoreceptors that usually synapse on LAMINAE III & IV and end at I - II - V. If they start ending DIRECTLY on I - II- V, then PAIN is the signal. No buffering.
COLLATERAL SPROUTING due to inflammation (nerves are trying to get normal input so, they move!) makes ANY STIMULATION PAINFUL. |
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dorsal horn reorganization/collateral sprouting/tic doloreaux of the back causes CHRONIC INFLAMMATION:
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SCARRING
FIBROSIS INTRAcellular ADHESION EXTRAcellular ADHESION PAIN LOSS OF FUNCTION/ROM ATROPHY RE-INJURY |
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DYS-AFFERENT-ATION
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DYS- loss
AFFERENT- mechanoreceptor movement signals to spine ATION- makes dysafferentation a word |
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You have ___________pain in yours shoulder where your ribs punctured your pleura and ruined the nerves. IT BURNS.
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NEUROGENIC BURNS
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3 types of pain
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NEUROGENIC BURNS
NOCICEPTIVE PSYCHO-GENIC |
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ADRENAL EXHAUSTION causes
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EPINEPHRINE that was released from the ADRENAL MEDULLA to perpetuate INFLAMMATION of the SYMPATHETIC nervous system.
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Joint afferents are 75% ______ and 25% __________.
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75% PAIN (nociception and polymodals)
25% MOVEMENT (mechanoreceptors) |
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Hypomobility means no stimulation to mechanoreceptors so, you lose them because you don't use them.
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DYSAFFERENTATION
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pain caused by SALINE injection
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NOCICEPTIVE
NAUSEA, PALLOR, SWEATING, BRADYCARDIA, HYPOTENSION, FAINTING = didn't matter how much saline was injected; the autonomic SYMPATHETIC RESPONSE was overwhelming |
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sympathetiKOnia + KOrr
sympathetaconia+ korr |
sympathetaKOnia+KOrr:
means TOO MUCH SYMPATHETIC INPUT (agghhhhh!) so... DYSAFFERENTATION (loss of mechanoreceptor response = HYPOMOBILITY) would cause sympathetiKOnia+KOrr |
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sympathetiKOnia+KOrr means
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too much sympathetic input causes VASOCONSTRICTION
and this leads to VISCERAL DYSFUNCTION |
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DYSAFFERENTATION
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LOSS OF MOVEMENT-BASED MECHANORECEPTOR STIMULATION (hypomobility/facilitation causes NO stimulation to reach receptors and they wither up/die from lack of stimulation)
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a FACILITATED spinal segment
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CENTRAL NOCICEPTIVE SENSITIZATION
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somato-somato
somato-visceral visceral-somato |
somato-somato: sublux to sublux
somato-visceral: sublux to organ dysfunction visceral-somato: organ causes sublux |
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who is the SomATOvisceral response king?
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SATO = SomATOvisceral
SATO is an MD, PhD |
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SATO is SomATOvisceral...
ASTHMA |
ANS imbalance
MAST CELLS increased |
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SATO is SomATOvisceral...
ARTERIAL PATHOLOGY |
ARTERIOSCLEROSIS
from SYMPATHECTOMY OR INJURY |
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SATO is SomATOvisceral...
HEART |
HYPERTENSION
****remove LEFT SIDED cardiac sympathetic nerve = less ischemia and fibrillation*** lesions association with MYOCARDIAL INFARCT (we already said ischemia causes infarct - this is not new) |
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SATO is SomATOvisceral...
KIDNEYS |
RENAL PARENCHYMA
gets screwed by high Aldosterone levels when heart is no longer able to send proper signal to regulate RENAL PARENCHYMA SYMPATHETICS project through DORSAL ROOT GANGLION so lesion may cause FIGHT OR FLIGHT REACTION (hypertension) |
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SATO is SomATOvisceral...
ANGINA PECTORIS |
chest pain from VAGAL activity and AUTONOMIC IMBALANCES
CORRECTED W/ ADJUSTMENTS upper cervical, ribs |
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ASTO: SomATOvisceral..
DYSRHYTHMIAS |
HOLE IN ONE - BJ
dizziness, numbness, paralysis, urinary frequency, oliguria, belly pain, weakness |
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SATO
NO EVIDENCE FOR |
MI improvement w/ somatic
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SATO
HYPERTENSION |
SUSTAINED DROP IN B.P. w/ adjusting
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SATO
GI disorders |
THORACIC LESION
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SATO
GASTRITIS |
VAGAL STIM increases gastric tone w/ upper cervical adjustment
GASTRIC ACIDITY INCREASED FROM SPINAL LESIONS IN ANIMAL MODELS - definitive visceral response to stress! |
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SATO
PEPTIC ULCERS & PANCREATITIS, OH MY! |
SYMPATHETIC
MICROBIAL |
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BJ'S work with __________flutter showed half of the subjects improved. That's meaningful!
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ATRIAL
*sinus bradycardia improved, too |
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"Anatomical abnormalities of the cervical spine at the level of the ___________ vertebra are associated with relative _________ of the brainstem circulation and INCREASED BLOOD PRESSURE."
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ATLAS
ISCHEMIA ~fm Journal of Human Hypertension, 2007, abstract |
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gastric acidity increased from ______________ in animal models
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spinal lesions
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There is evidence that sympathetic stim alters non-lethal, mild bile induced pancreatitis to HEMORRHAGIC, NECROTIZING LETHAL KIND associated with ___________
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VASOCONSTRICTION
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GUILLAIN-BARRE SYNDROME
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CERVICAL MANIPULATIVE THERAPY decreased parasthesias
REDUCED CALCITONIN (puts the bone in) of the immunoreactive pituitary type |
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Can the AUTONOMIC n.s. distinguish between + and - EMOTIONS?
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YES
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ALTERS EEG & hippocampal spiking
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WHIPLASH
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SEIZURE & CMT
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30-70 a day down to 6 a day
LENNOX GASTAUT syndrome : tonic, atonic or tonic-clonic seizures brain lesion or elsewhere. Psychomotor retardation. Poor turnout. |
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Physical and mental exercise offsets seizures. When do they occur?
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EPILEPSY
when sleeping, off-guard, resting, idling |
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Kind of diet for anti epilepsy
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KETOGENIC
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RSD also called
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COMPLEX REGIONAL PAIN SYNDROME
is RSD=Reflex Sympathetic Dystrophy |
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RSD cause
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not severe - can be small cut
POST LUMBAR DISC SURGERY estab. ABNORMAL SYNAPSES of rami communicantes w/ sympathetic chain. BAM! ACUTE PAIN, SWELLING, DYSFUNCTION, ATROPHY OF LIMB DUE TO C-FIBER HYPERACTIVITY |
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This syndrome progresses in stages from weeks to years: ACUTE, DYSTROPHIC, ATROPHIC
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RSD/COMPLEX REGIONAL PAIN SYNDROME
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BELL's PALSY
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86% spontaneously recover in 10-21 days
HIGH VOLT GALVANIC ADJUSTING |
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DYSPHAGIA & CMT
HEADACHE & CMT MIGRAINE & CMT NYSTAGMUS & CMT VERTIGO & CMT |
dysphagia: MYASTHENIA GRAVIS
headache: TENSION, CERVICOGENIC migraine: CERVICAL PLAY ROLE, VERTEBROGENIC nystagmus: DECREASED vertigo: DECREASED if from abnormal spinal mm tension |
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TYPE II DIABETES
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There is altered sympathetic activity in Diabetics.
HYPER-RESPONSIVE to EPINEPHRINE EXAGGERATED INSULIN RESP. SENSITIVE ALPHA-2 PANCREAS RECEPTORS HIGH LEVELS CATECHOLAMINES + OPIODS |
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NON-ADAPTIVE "entanglement"
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ABNORMAL COUPLING OF AN ORGAN TO A SOMATIC STRUCTURE
sympathetiKOnia + KOrr |
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IMMUNOCOMPETENCE and sympathetics
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THYMUS direct innervation
STIMULATION OF LUMBAR SYMPATHETICS causes bone marrow to release inflammatory mediators (reticulocytes & PMN's) |
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BOWEL & BLADDER
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dysfunction SECONDARY to LUMBAR DYSFUNCTIONAL SYNDROME
SIDE POSTURE improved sx ****PELVIC PAIN AND ORGAN DYSFUNCTION 2ND TO LOWER SACRAL NERVE ROOT COMPRESSION is greater in women than men. Duh. |
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LOWER SACRAL N. ROOT COMPRESSION SYNDROME
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frequency, urgency
incontinence, retention nocturia, sluggishness dysuria, difficulty emptying chronic bladder infection vaginal discharge painful, irregular menstruation protastovesiculitis, ED decreased penile sensitivity miscarriage, dyspareunia CPP disorder constipation proctalgia, flatus, sphincter spasm spotting |
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DYSFUNCTIONAL UTERINE BLEEDING & CMT
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yes
this is secondary to a nervous system dysfunction |
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CULPRIT in dysmenorrhea (not PMS)
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LAMINA II
NSAIDS WORK |
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PPOD & CMT
*you know this is about ADHESIONS, right? Not rocket science. |
IMPROVED
ILIOPSOAS SPASM reduces blood flow to internal repro/genitalia - LEACH |
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UTERINE DISORDERS
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HYPOGASTRIC N.
adjusting relieves SYMPATHETIkoNIA+koOR |
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PREGNANCY & LBP
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YES, DUH.
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PEDIATRICS &
ADHD, INFANTILE COLIC, DYSLEXIA, ENURESIS scoliosis... |
ADHD: maybe, CMT instead of stimulants
Infantile Colic: yes, CMT better than meds Enuresis: maybe Scoliosis: TENS, Flex/Distract |
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REDUCTION in MECHANORECEPTOR input
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dysafferentation
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the transmission of AFFERENT nerve impulses
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afferentation
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DESTRUCTION of AFFERENT nerve impulses, not just reduction
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DE-afferentation
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Describe nociceptors (fm JMPT article)
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mechanical, mechanothermal, polymoday - depends on TYPE OF ENERGY used to activate
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activated by noxious mechanical and thermal stimulation and by chemical mediators released from injured tissues..as per JMPT article
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POLYMODALS (promote homeostasis)
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chicken wire
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NOCICEPTORS
weaving all directions/tri-dimensionally UNMYELINATED |
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ARTICULAR nociceptors w/ thresholds soooooo high, they can't be bothered unless there is
ACUTE NOXIOUS STIMULII |
silent/sleeping nociceptors
solely CHEMOSENSITIVE may promote central sensitization since only react to INFLAMMATION |
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Where do nociceptors terminate
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SPINAL
BRAINSTEM NUCLEI LIMBIC SYS FRONTAL LOBE PARIETAL LOBE INSULA CORTEX TEMPORAL LOBE pretty much everywhere from your ass to your eyeballs |
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How are nociceptors depolarized
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DAMAGED TISSUE
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peripheral sensitization happens when
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NOCICEPTORS get LOWERED THRESHOLDS for firing
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when can LIGHT TOUCH and MOVEMENT (MECHANO) stimulate a nociceptor?
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PERIPHERAL SENSITIZATION
ABNORMAL!! sensitivity due to low thresholds for firing |
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GENERAL substances and PHYSIOLOGIC PROCESSES of peripheral sensitization
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CHEMICAL MEDIATORS
RELEASED AFTER TISSUE INJURY |
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CENTRAL SENSITIZATION
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HYPERexcitability of nociceptors in the CENTRAL nervous system
*get it? CENTRAL sensitization is CENTRAL nervous system nociception lowered thresholds (vs. peripheral sensitization which would be in the...periphery!) |
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Which is more prone to central sensitization,
JOINT & MUSCLE OR SKIN/CUTANEOUS? |
JOINT AND MUSCLE
*remember: joints are 75% nociceptors, 25% mechanoreceptors |
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older terms for central sensitization?
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FACILITATION
CENTRAL FACILITATION = CENTRAL SENSITIZATION |
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SPINAL CORD PLASTICITY
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just like brain, can change in response to environment -specifically at SYNAPSES
involves increase in GENE EXPRESSION |
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allodynia
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NORMAL STIMULI CAUSES PAIN
ie, gentle palpation causes searing pain |
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SUBCORTICAL centers and nociception (pain registry)
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SUPRA-SEGMENTAL REFLEX RESPONSE from medulla breathing and circulation centers, hypothalamus (sympathetic) of neural hormones, and some limbic structures...
all are affected by PAIN ramps every response sky high!! decrease effectiveness of normal fight or flight responses because they are always ON! Battery dies. |
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PAIN effect on nervous system hormones:
CATABOLIC (BREAK DOWN) vs. ANABOLIC (BUILDERS) |
catabolic hormones UP
catecholamines UP cortisol UP ACTH, glucagon, cAMP, ADH, GH, renin...UP anabolic hormones DOWN insulin DOWN testosterone DOWN (estrogen breasts from stress) coagulation cascade DOWN |
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Negative effects of CATABOLIC hormones (increased during pain subcortical response)
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Crashes:
REM cell-mediated immunity osteoblasts collagen synthesis antagonizes insulin, screws glucose lipogenesis! spare tire, face downs ratio of type I muscle fibers to type II, wh/ deconditons spinal/postural muscles |
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Pallor/sweating/bradycardia/HYPOtension/fainting/nausea...
no, not a migraine or your period but... |
SYMPTOMS OF NOCICEPTION TO SUBCORTICAL CENTERS
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Autonomic CO-COMITANTs are likely caused by
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MEDULLA gets PAIN signals
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All those bad things catabolic hormones do because the medulla is receiving pain signals/nociceptive signals could be MISDIAGNOSED as...
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PRIMARY VISCERAL disease
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What receptors are classified as MECHANOreceptors?
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CORPUSCULAR mechanoreceptors
MUSCLE SPINDLE FIBERS GOLGI TENDON ORGANS |
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What does REDUCED MECHANORECEPTOR ACTIVITY do?
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ramps up PAIN input assoc. w/ joint complex dysfunction
enhances segmental sympathetics enhances somatomotor output **pain drives activity up and over the top of mechanoreception. PAIN TRUMPS EVERYTHING |
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mechanoreceptors CAN reduces sympathetic hyperactivity until
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they receive reduced input associated w/ JOINT COMPLEX dysfunction
this mimics VESTIBULAR lesions, CEREBELLAR lesions, CEREBRAL CORTEX & BASAL GANGLIA lesions like ataxia, cervical vertigo |
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positive message from cerebellum
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HYPOTHALAMUS & medial AMYGDALA
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negative message from cerebellum
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The cerebellum doesn't send negative messages. It INHIBITS them from going to the HIPPOCAMPUS and lateral AMYGDALA
*guess what happens if mechanoreceptor input to cerebellum gets reduced? Then cerebellum isn't going to inhibit those negative messages, is it? No. |
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MYELOPATHY hypothesis beginnings
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'mye' as in 'myelin' means spinal cord
BJ's subluxations cause cord compression |
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MYELOPATHY hypothesis meaning
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VASCULAR INSUFFICIENCY
+ nerve ROOT FIBROSIS & OSTEOPHYTES = mild cord COMPRESSION w/ clinical findings |
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affected FIRST and are SLOWEST to RECOVER in myelopathy hypothesis of cord compression
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DORSAL COLUMN FIBERS
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according to myelopathy hypothesis of cord compression due to vascular insufficiency, osteophytes and nerve root fibrosis, how does the CERVICAL CORD DAMAGE PROGRESS?
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STEP-WISE fashion
(vs linearly) added to HTN, hypotension, occlusion of spinal artery, etc |
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NEURO-IMMUNE hypothesis
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spinal joint lesions may, through SYMPATHETIC-mediated influence, change SPECIFIC & NON-SPECIFIC IMMUNE RESPONSES, and alter TROPHIC (growth) FUNCTION of involved nerves.
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What's the problem with Acute Otitis Media claims for chiropractic as cure?
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AOM clears up on its own in 1-7 days, with or without antibiotics. Chiropractors cannot, ergo, take credit for it.
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Antibiotics do not appear to reduce the ___________ complications of AOM, however children that responded well to antibiotics also...
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suppurative
responded well to chiropractic adjustments |
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CHRONIC OTITIS MEDIA
antibiotics? chiropractic? |
chiro not proven to be very effective - these kids didn't respond well to antibiotics or they wouldn't have chronic AOM to begin with, and they also didn't respond much to adjustments, HOWEVER...
POSITIVE SOMATIC DYSFUNCTION IMPROVEMENTS & REDUCED MONTHLY EPISODES, ANTIBIOTICS |
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adjusting for PNEUMONIA
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effective thoracic pump
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spinal joint lesions
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NEUROIMMUNE/NEURODYSTROPHIC HYPOTHESIS
Gillet, Selye, BJ, Homewood, Janse, Watkins |
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part of brain linked to IMMUNE COMPETENCE
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HYPOTHALAMUS
NOREPINEPHRINE RELEASED FROM HYPOTHALAMIC NUCLEUS modulates immune response |
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what part of the brain and what neuro-endocrine hormone do you want to be healthy and regulated
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hypothalamus
norepinephrine (immune responder) |
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BURNET'S B-CELLS
neuroimmune hypothesis slant |
BURNET's B-cells
CLONAL SELECTION Ab-Ag complexes ONLY B-CELLS MAKE Ab that tags antigen for destruction |
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NETWORK THEORY
neuroimmune hypothesis slant |
the immune system is a WEB
responds SIMULTANEOUSLY provides STABILITY & responsiveness |
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CELL-MEDIATED IMMUNITY
neuroimmune hypothesis slant |
LYMPHOCYTES
NON-SPECIFIC/GENERAL IMMUNITY + SPECIFIC HUMORAL/BLOOD IMMUNITY |
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THYMUS IMMUNITY
neuroimmune hypothesis slant |
PRECIPITIN Ab-Ag BLOOD
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GENETIC IMMUNITY
neuroimmune hypothesis slant |
T-LYMPHOCYTES
B-LYMPHOCYTES ...both have CODED IMMUNITY programmed into their DNA |
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Selye's GAS
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General Adaptation Syndrome
3 stages: ALARM RESISTANCE EXHAUSTION ***lead to DISEASES of ADAPTATION |
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Selye's GAS:
1. ALARM! |
ALARM! = ADRENALS
cortisone and ACTH (ulcers, eosinopenia, lymphopenia) |
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Selye's GAS:
2. RESISTANCE~~ is futile |
RESISTANCE works as long as endocrine functions normally
(heredity, age, nutrition, protein increases ACTH, stress) |
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It's not the INTENSITY of the STRESS, but how
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you PERCEIVE it.
Like, this test, for instance, has blown about 20 hours so far, and it's not the most important, nor the hardest test I have out of 11, but I have spent all damn day sitting here because I am terrified of failure, not of dying. |
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What are the options regarding developing a disease of adaptation in response to perceived stress?
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Will either be PHYSIOLOGIC actual adaptation
OR will develop a DISEASE of adaptation (HTN, inflammatory, collagen-vascular, hyperthyroid) |
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Are hormonal changes developed during a disease of adaptation permanent?
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Yes
also can STORE UP STRESS HORMONES and this deranges organ response |
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based on the notion that the body can respond to stressors by adapting to them
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Selye's G>A>S
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What are some GAS responses?
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HYPO-POPHYSEAL ADRENO-CORTICAL SYSTEM (HPAC)
VASOCONSTRICTION (the 'stiffening up in the face of danger' response) to get ready for the CORTISOL/CORTISONE onslaught |
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Anesthesia/Euphoria/Depression
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Ah, CORTISOL!
GLUCOCORTICOIDS AND CATECHOLAMINES |
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Selye's GAS proved? but did NOT PROVE?
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proved relationship between hormones and stress
but DID NOT PROVE RELATIONSHIP BETWEEN THE STRENGTH OF YOUR NERVOUS SYSTEM AND YOUR IMMUNE COMPETENCE |
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What does the NEUROENDOCRINE system do?
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COORDINATES immune response
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specific things the NEUROENDOCRINE SYSTEM does:
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GH, TSH
PITUITARY FACTOR reduces immune response w/ age HYPOTHALAMUS (social stress that gets to your psyche can make a disease more infectious than it was going to be) The above is true with CANCER |
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vis medicatrix naturae
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VITALISM
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humans are not a collection of parts.
correcting subluxations may have MULTIDIMENSIONAL effects patients must learn self-care, not just relief or doctor band-aide care |
HOLISM
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AUTONOMY & DIGNITY
PATIENT-CENTERED CARE means active participation by patient TAILORED CARE |
HUMANISM
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DO ONLY WHAT IS NECESSARY
PREVENT, not react ANTICIPATE, not need a cure MANUAL METHODS, not pills |
THERAPEUTIC CONSERVATISM
1. Primary prevention - illness never occurs in the first place 2. Secondary prevention - catch problem early 3. Tertiary prevention - slow or decrease symptoms |
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NATURAL REMEDIES
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NATURALISM
(not natural philosophizing about this and that but actual herbal remedies) |
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DISEASE model
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REACTIVE
SYMPTOMATIC REDUCTIONISTIC MECHANISTIC *DOCTOR-CENTERED |
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BIOPSYCHOSOCIAL model
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PROACTIVE
HOLISTIC MULTIFACTORIAL CAUSES ALL PATIENTS ARE DIFFERENT, EVEN IF PROBLEM IS THE SAME PATIENT-CENTERED |
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HEALTH and UN-HEALTH are true __________, versus Health and Disease.
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opposites
*disease is only a symptom of unhealth, with unhealth being the overarching theme |
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Health is a state of
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OPTIMAL WELLBEING
*and wellness is HOW WE GET TO HEALTH, the process of optimal functioning and creative adaptation across a lifetime |
