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293 Cards in this Set
- Front
- Back
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SDF = Fixation is what phase of the vertebral subluxation complex phase?
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Phase 1 of VSC is FIXATION
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When group III and IV afferents talk to skeletal muscle, and then back again, what is this called?
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Reflex arc
*pain, tenderness, altered tone |
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SDF for Leach is~
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spinal fixation
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Most common spinal lesion recognized by:
a. _______ mobility of a segment (more/less) b. altered pressure ________ for pain (doorway/threshold) c. signs of _____ dysfunction like taut muscles (CNS,NMS) |
-LESSENED mobility of a segment
-altered pressure THRESHOLD for pain (hypersensitivity) -signs of NMS dysfunction like taut muscles |
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Spinal FIXATION
of {VSC phase 1} Segmental DysFunction is whose model? |
Leach!
Leeches fixate at the segment and cause dysfunction! |
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Whose definition of SDF does Medicare accept?
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Medicare is for people on FIXED incomes because their bosses were leeches.
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Name 3 classic signs of SDF
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point tenderness, loss of normal motion in one or more planes, abnormal contraction of paraspinal muscles
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"a lowered threshold for firing in a spinal cord segment as a result of AFFERENT bombardment."
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segmental facilitation=lowered threshold
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In SDF, facilitation is bad. Why? What does it mean?
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Lowered threshold, leading to central sensitization (abnormally low threshold/response to pain)
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Segmental facilitation is bad. What does it lead to?
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CENTRAL SENSITIZATION! OWWW!
(lowered threshold/response to pain) |
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model that uses trigger points as core
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Gatterman and Coe, touch me some'mo
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FIXATION }} FACILITATION }}}}} HYPERSENSITIZATION
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LEACH
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model that uses "FACILITATED AS A NASTY WORD...YOU DON'T WANT THIS,"
meaning less pressure evokes more potential and causes spasm |
Denslow - less/low is more
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model of slack muscle SPINDLE & CNS adjusting FUSIMOTOR system (the gamma motor neuron)
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Korr spindle fibers and Korr CNS adjusting fusimotor, controlling heart, smooth muscles, organs, and glands =
SOmatic-AutOnomic FusimOtor is KOrr |
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uses somato-autonomic reflex hypothesis
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Korr
Body controls automatic reflex (slack muscle Korr spindle fibers cause adjustment of fusimotor system - gamma motor neurons) |
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What does 'somato-autonomic reflex' mean?
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affects organs in the Korr of your body
(2 neuron system versus somatic that is a 1 neuron system) |
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Explain a muscle spindle example of Korr
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weight lifter squats, compressive load allows floppiness of certain muscle spindles in fibers. CNS senses slack and turns up gain to avoid injury. SPASM!
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Korr hypothesized both motor & autonomic fcns are affected in a ________ zone - maybe associated with SDF.
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facilitated zone
Hypersensitivity WILL affect your Korr autonomics via muscle spindles and CNS to the fusiforms |
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mediating variable for VSC phase 1
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SDF
*segmental dysfunction |
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the independent variable is what is ___________
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observed the SITUATION
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What is the independent variable (the SDF, the adjustment, the improvement)?
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the adjustment
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What is the dependent variable (what is changed/the result)?
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Improvement in pain, function, etc.
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List the independent variable, the mediating variable, and the dependent variable.
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1. independent action/adjustment/what you do
2. mediating SDF ('med'-ical problem) 3. dependent children are improvements upon ourselves So this is stupid. The definition of mediation: Intervene in a dispute to bring about an agreement or reconciliation. Intervene in (a dispute) to bring about an agreement. Why isn't this the independent variable? I don't know. Why do we use the word 'subluxation' instead of fixation, when there is already a definition of subluxation in the medical world? Stupid. Stupid. Stupid. |
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In the example, "Aging leads to increased wisdom which results in better driving," name the independent, mediating and dependent variable. Switch the word "MEDiating" to MEDical problem or condition/state.
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independent (observed) is Aging, mediating/MEDical problem or condition/state is Increased wisdom, dependent (what changed) is Better driving
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the subluxation is which variable?
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the mediating variable
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the adjustment is what variable?
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independent
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the result/improvement is what variable?
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the dependent (the outcome)
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List which variables for each: Adjusting the spine, SDF of VSC1, Clinical improvement
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Adjusting = independent
SDF of VSC1 = mediating Clinical improvement = dependent |
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defined as lowered threshold for firing in a spinal cord segment as a result of afferent bombardment associated with spinal lesions
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Segmental facilitation, according to Leach
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What kind of nerves (afferents or efferents) bombard the spinal cord during segmental facilitation, according to Leach?
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AFFERENT!!!! Segmental facilitation can't happen from outside in - must come from outside stimulus - too much of it.
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__________ occurs before segemental facilitation occurs.
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Myopathology
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The hypothesis of myopathology
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MUSCLE SPASM as a precursor to SDF (of VSC1)
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Afferent and efferent nerves, Joint receptors, Muscle receptors, Posterior facet joints, Inflammatory triggers, Noninflammatory triggers
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Myopathology of muscle spasm hypothesis
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the mediating variable is the _______ (the SDF)
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"MED-ical problem"
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Describe afferent group I
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FASTEST - THICKEST - LARGEST
*not in skin, Proprioception & kinesthesia Why you can rub your shin when you bang it to override pain to cortex |
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what's the problem, what's the treatment, what's the desired result
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the SDF/low back pain (mediating), the adjustment (independent), decreased pain (dependent outcome)
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Describe group II afferents
THE ADJUNCTS TO THE COMMANDER IN CHIEF (GP 1 SMALL, LITHE HOTDOG UNDERGROUND FLIERS UPHILL) |
ADJUNCTS: run ABOVE GROUND
GROUP II MEDIUMS HOTDOG THICK MYELIN FAST UPHILL ALPHA BETA BALANCE ABOVEGROUND IN THE SKIN!!!!!!!! |
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Describe group III afferents do 3 things. Describe them physically and the 3 (III) things...
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small, thin myelin, slow, alpha - delta,
Mechanical/Heat:cold/Nociception Think Greek! Alpha Delta small thin slow, the last to know |
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Describe group IV afferents
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Tiniest, most painful - a dentist pokes your cavity to see where it is. That is the group IV afferents - they have NO myelin so they wear their heart on their sleeve. Everything hurts group IV, long and slow and thin skinned, throbbing group IV.
think of IV as an open mouth with the eyes clamped shut, screaming sideways in a text message |
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Afferents are to the cord - include groups I - IV. What are efferents and their groups?
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Away from cord, Alpha motor neurons and Gamma motor neurons
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Describe efferent Alpha motor neurons
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Well, they are ALPHAS, for crying out loud, so they are myelinated, innervate FORCE-producing extrafusal muscle, LARGER & FASTER, LOUDER!
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Describe efferent Gamma motor neurons
OKAY, EFFERENT MEANS OUT TO WHAT? YEP, THOSE. |
MUSCLES!
An efferent gamma is slow and small like your beloved gramma. Gamma efferents innervate the intrafusal fibers, SMALLER & SLOWER but will get there eventually. |
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Posterior vertebral facet joints are _________ joints enclosed in a capsule; the articular surfaces are covered with ________ cartilage.
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Posterior vertebral facet joints: synovial, surfaces covered with hyaline cartilage
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Myopathology occurs before segmental facilitation occurs. Describe joint receptors:
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respond to chemical/mechanical changes near joints. May respond to direction of movement. Nociceptors like substance P may alter threshold of mechanoreceptors, causing them to fire
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Myopathology occurs before segmental facilitation occurs. Describe afferent and efferent nerves:
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afferent (groups I - IV)
efferent (Alpha motor and Gamma motor) |
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Myopathology occurs before segmental facilitation occurs. Describe Muscle receptors:
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Both mm. spindles and Golgi tendon organs may act in concert to regulate muscle stiffness. SMT may change afferent groups I and II discharge
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How would mm. spindles and Golgi tendons act in concert to regulate mm. stiffness?
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the ratio of mm. TENSION CHANGE mm. muscle LENGTH CHANGE
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What might modify the discharge of group I and II afferents, thus relaxing muscle tension?
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SMT
*Spinal Manipulative Therapy |
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They are generally silent at rest, but are more activated by the IMPULSE of SMT, rather than the pre-load.
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GTO
*Golgi Tendon Organs |
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Just like Golgi Tendon Organs, these are more activated/having a resting discharge that increases more with IMPULSE than pre-load.
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mm. SPINDLES
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REFLEX interaction between these small, slow thin nerve types that have little to no myelin and your skeletal muscle might actually cause PAIN, TENDERNESS and ALTERED MUSCLE tone
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AFFERENTS III & IV
(small, slow, thin to no myelinated, A-delta and C-fibers, Mechanica/heat/cold/nociception |
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Hypothesized that both motor and autonomic fcns are affected in a facilitated zone
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KORR
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The FACILITATED ZONE, according to KORR, may be associated with _____
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SDF (segmental dysfunction)
facilitated zone of Korr |
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What part of the spinal cord pathways did Korr include?
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Anterior and Lateral HORN cells of ASCENDING pain pathways
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Which neurons in the cord become hyper-responsive, according to Korr?
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Anterior and Lateral HORN cells of ASCENDING pain pathways
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Korr blamed ________ rather than joint receptors as the coordinators that decrease or increase muscle contraction
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mm. SPINDLES
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KORR SPINDLES INCREASE OR DECREASE
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BASED ON JOINT MOVEMENT
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(Korr). The CNS detects slack muscle spindles during extrafusal contraction and then?
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adjusts the background activity in the fusimotor system. GAMMA
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(Korr) The CNS sets and resets mm spindle sensitivity through an automatic _____. Chrios call this innate.
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GAIN
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How would a chiro compel the CNS to reduce gamma motor discharge?
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If you STRETCH A SPINDLE, IT SHUTS GAMMA
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If a chiro stretched the intrafusal fibers (Forceful stretching AGAINST SPINDLE resistance) and lowered Gamma discharge, what else is stimulated besides spindles?
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the GTO's:
FORCEFUL STRETCH AGAINST SPINDLE STOPS ALPHA & GAMMA |
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Forced stretch of the muscle causes both ______ and ______ motor neuron INHIBITION.
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The Golgi Tendon Organ would be stimulated by forced stretch of the mm. causing both GAMMA & ALPHA motor neuron INHIBITION
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Korr predicted that 2 kinds of adjusting would be successful:
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Slow, long-lever
Rapid, high-velocity/short lever |
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How might spinal adjusting normalize spindle (Korr) biomechanics?
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When you STRETCH, it restores SPINDLE to NORMAL
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Cord learning model Patterson-Steinmetz summary from Leach: 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...
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there may be segmental facilitation even after the initiating stimulus is removed. Once this facilitation occurs, despite the removal of the AFFERENT (internal) source of stimulation, the abnormal segmental REFLEX CIRCUIT itself participates in maintaining the symptoms, thus creating a cycle of INCREASED OUTPUT with any sensory input. According to this model, ADJUSTMENT would be highly effective in stopping the signal, especially if done soon after the initiating stimulus.
HOWEVER, once the changes were fixed in the cord, a NEURAL SCAR of HYPERexcitable neurons remain, and are ABNORMALLY RESPONSIVE to stimuli. STRESORS INCREASE spinal fixation in rats (swimming, loud noises) |
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How did they find out that CORD involvement is necessary for FIXATION?
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Experimenters Patter(n)son-Steinmetz induced cerebellar lesions in dogs and rats= caused HINDLIMB FLEXION
Basically they caused an UMNL spasticity |
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Stimulation of the severed ventral roots controlling the hindlimb does NOT result in retention of hindlimb flexion. What does this mean?
Patterson-Steinmetz... |
BECAUSE THE MESSAGE IS STUCK IN THE BRAIN/CNS, NOT IN THE PERIPHERY. THE MESSAGE AFFERENTS ARE SCREWING UP THE INPUT OR THE REFLEXES, NOT THE MUSCLE ITSELF.
>>>>>>>>>>>>PATTER(N)SON-STEINMETZ>>>>>>>>>> |
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Conclusion of Patter(n)son-Steinmetz?
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FIXATION/CORD LEARNING is a Patternson.
DUE TO CENTRAL OR PHERIPHERAL INPUT NEURAL SCAR HYPERSENSITIVITY |
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In an area of SDF with Motion disorder (altered biomechanics) and Muscle tension with Visceral spasm, may be an area of _________, even after stimulus removed!
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SEGMENTAL FACILITATION,
even after stimulus removed if sufficient quantity/duration |
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What maintains symptoms of segmental facilitation in the cord, according to Patter(n)son-Steinmetz?
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Abnormal segmental reflex circuit --- causes INCREASED output w/ increased sensory input
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IF Patter(n)son-Steinmetz model is correct, spinal adjustments are effective at breaking cycle if performed when?
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SOON after initiating stimulus
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Patter(n)son-Steinmetz: if adjustment is not perfomed soon after insult, facilitation may become?
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fixed/learned into the cord = Patternsoned.
. A 'neural scar' of hyperexcitability and subliminally excited neurons would remain, creating CENTRAL SENSITIZATION |
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*model of NOCICEPTORS where joint/reflex changes depend on FIBER type (fast twitch vs. slow twitch)
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Dvorak fast or slow anorak fiber model
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Dvorak proposed that segmental dysfunction creates?
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Dvorak: both mechanical & chemical stimulation to activate NOCICEPTORS and ST tract activity
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Dvorak said that after SDF creates activated nociception & ST tract, it then creates _______ pain and ______ muscle changes.
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articular, reflex
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Muscles with more slow twitch fibers and shorten in response to SDF and overuse
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POSTURAL muscles
*tough Russian Dvorak fast and slow fiber anorak theory - he had good posture. |
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Postural/slow twitch muscles respond to fatigue with _________
DVORAK WAS A MAN OF SHORT STATURE |
Postural/Short twitch = SHORTENING when overused
SHORT STATURE. A muscle recoils and shortens when it gets fatigued (probably to protect itself). Dvorak in his short twitch anorak stood up |
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Postural/slow twitch muscles respond to OVERUSE with shortening. Larger, fast twitch muscles like quadriceps respond to overuse with ________.
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Large/Fast twitch = fatigue when overused
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Using 1a alpha-motor neuorns, SDF increases sensory discarge because of increased _________ activity.
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spindle activity up due to SDF means up sense discharge
SPINDLE UP/ SENSORY UP/ SDF |
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Postural/slow twitch muscles respond to OVERUSE with shortening. Larger, fast twitch muscles like quadriceps respond to overuse with ________.
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Large/Fast twitch = fatigue when overused
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LEARNED PATTERNSON OF SDF leaves a
NEURAL SCAR of HYPEREXCITABILITY |
Patter(n)son-Steinmetz
LEARNED PATTERNSON OF SDF leaves a NEURAL SCAR of HYPEREXCITABILITY |
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Abnormal responses ARE PATTERNED/LEARNED IN THE CORD AND HAVE FORMED A NEURAL SCAR might not be easily removed, according to ______________, and increased susceptibility could remain for months after resolution of acute injury.
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Patter(n)son-Steinmetz
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Patter(n)son-Steinmetz key words:
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HINDLIMB flexion
-cord learning -neural scar/SDF -reflex excitability -hyperexcitable EVEN AFTER STIMULUS GONE |
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Dvorak key words;
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SDF model NOCICEPTORS
Joint/reflex chgs depend on fiber type (fast vs. slow twit) Increased spindle activity Short postural muscles INFLAMMATORY |
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Dvorak said same thing as Korr, but he added?
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inflammatory & histochemical changes
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SDF >>>> NOCICEPTORS >>>PAIN>>>FIBER
(short stature or fast fatigue) Tough Russian fiber |
Dvorak
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SDF creates articular pain and reflex mm. changes, which depend on the sort of FIBER TYPE (slow vs. fast twitch)
*Russian tough cloth |
DVORAK in his slow or fast anorak stood up straight and short
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Said POSTURAL muscles have more SLOW twitch fibers and SHORTEN in response to SDF and overuse.
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Dvorak
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POSTURAL
SLOW SHORTEN SDF/OVERUSE |
Dvorak
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Said LARGER muscles have more FAST twitch fibers and respond to OVERUSE with FATIGUE.
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Dvorak
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LARGE
FAST FATIGUE OVERUSE |
Dvorak
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Increased _____ activity with SDF increases sensory discharge.
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Spindle
*via 1a alpha-motor neurons Dvorak |
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Facet neurons that are stimulated by SDF
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1A ALPHA motor neurons
Commander in chief! neuron |
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Increase spindle fiber
Increase sensory discharge via 1a alpha-motor neurons triggers? |
Affecting COMMANDER IN CHIEF 1A's:
CONTRACT MORE - THIS EITHER SHORTENS POSTURE OR FATIGUES FAST TWITCH {Dvorak} tough Russian FIBER, short stature, fast fatigue |
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et forhold
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condition / relationship
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What kind of histochemical change does shortening of postural/slow twitch was {DvoraK} talking about?
(an increase in one of the ions in his name) |
Increasing K+ concentrations
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Postural/slow get shortened, Large/fast get fatigued, histochemical changes happen and what results:
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Relative hypoxemia
Altered Joint Movement {Dvorak} |
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MFT^P generated by traumatic or postural strain of skeletal mm.
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Gatterman^Coe, touch me some 'mo
^means trigger point |
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Paraspinal muscles
Like rotators and multifidus Develop constellations of painful trigger points Segmental DysFunction Are Us! |
Gatterman^Coe touch me some'mo
Paraspinal trigger^points from SDF, uh oh! |
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MAST CELL + HISTAMINE
SPINDLE RESET CELL PRODUCT DEPLETION |
Gatterman^Coe, touch me some'mo
mast cells and histamine are inflammatory sustained contraction depletes mm. cell resources |
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What causes RELAXATION to FAIL?
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INFLAMMATION (W/ MODULATORS)
SUSTAINED CONTRACTION MFTP! Gatterman^Coe, touch me some'mo |
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Who theorized that a reduction in blood flow and sustained contraction of an area could stimulate autonomics? What is this called?
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Gatterman^Coe, touch me some'mo
Somato-Somatic response |
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Somato-somatic response due to sustained contraction of MFT^Ps and histamine build up stimulates somato-somatic response. Then...
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resulting accumulation of metabolites (PG) causes MORE sensitization
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This model predicts a SELF-PERPETUATING cycle with pain, RESISTANCE to stretching, decreased ROM
*occur as constellations, circles of pain tightening and tightening around a center until no motion or pliability |
Gatterman^Coe touch me some'mo
resisting stretching and motion trigger points block flow! |
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model that focuses on muscle pain from SENSITIZATION of NOCICEPTORS and other mechanoreceptors
*Mensa is overly Sensa |
MENSE
*Mensa is overly Sensa |
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model that predicts the neurobiologic sequelae from SDF that could lead to facilitation and muscle pain
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MENSE
*you must be in Mens/a/e to use big words like 'sequelae' vs. sequela |
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Mense model: ______ release of inflammatory mediators _______ nociceptive threshold
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MENSE Local release of inflaming bad stuff Lowers pain threshold
*the more pain you are in, the less you can take |
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What are muscular contributions to SDF? (3)
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I. DE-STABILIZATION (meaning muscles screw up stability when under strain of SDF)
II. Muscle BALANCE (unbalanced) III. MFTP (response to SDF) |
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How do muscles STABILIZE the spine?
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position sense in space
stabilizers of spine spinal movement |
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position, stability, movement
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how muscles stabilize spine
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Culprit muscle of low back pain
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multifidus wasting
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What pathologies surround the pain point of LBP sufferers?
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mutifidus wasting
fatty inflitration changes in fiber types |
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People who did not have LPB (in the study) also did not have
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multifidus wasting
*this wasting continues long after pain stops |
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How can multifidus wasting be treated?
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exercise
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What causes muscle wasting?
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SHARED INNERVATION of multifidus and joint
LATE FIRING of core muscles |
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Components of PASSIVE subsystem of spine stabilicers: (haha get it? It's cold as f*** here)
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Passive think bones & ligs:
Vertebrae LIgaments Discs Certain muscular activity |
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ACTIVE subsystem members of spine stabilizers:
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MUSCLES AND TENDONS that apply forces to the spinal column
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3 subsystems of spinal stability: PAN or NAP
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Passive
Active Neural |
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NEURAL control (mind control!! agghhh!) subsystem members:
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NERVES
CNS -determines requirements for stability of spine by monitoring TRANDUCER signals, and tells active subsystem (mm & tendons) to GET TO WORK! |
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Regarding muscle balance, what happens when mm. are immobilized?
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Pathological changes like shortening, tightening, atrophy, MFTP) and loss of function
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Muscle balance and MFTP's are considered to be part of the joint hypomobility problem and are therefore a part of ?
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SDF (segmental dysfunction hypothesis - VSC phase 1)
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What muscle types develop trigger points in cohorts?
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Imbalances between PHASIC muscles and inhibitory-POSTURAL muscles
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Well, this is predictable. You have your muscles prone to tightness (phasic) developing MFTP's and those prone to (postural) inhibition doing the same. What syndromes develop?
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Upper and Lower Crossed syndromes (due to MFTP's between tight (phasic) muscles and inhibitory (postural) muscles. Who has the valium?
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Weak muscles of upper crossed syndrome
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NECK FLEXORS ('cause you are only using your extensors when you crane your head forward), MIDDLE & LOWER TRAPS(shoulders are rounded - only ones working are uppers), RHOMBOIDS (stretched beyond belief)
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What are the overtaxed, tight muscles of upper crossed syndrome?
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Anything that holds your 15lb. bowling ball head up from the rear: UPPER traps,
LEVATOR scapulae, SCALENES, SUBoccipitals, NECK EXTENSORS, INTERNAL shoulder rotators (subscap, lats, teres major, coracobrachialis, pec minor, medial bicep) |
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Lower crossed. What core muscles weak?
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abdominals, gluteals (yes, because they are using the 5 external rotators like obdurator externus, etc. so it gives a person a flat, flabby butt. The deep external rotators are the only ones working and baby, no one sees those).
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Tight lower crossed muscles:
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Hamstrings, gastroc/soleus, psoas, QL's, extensors, piriformis
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small, hypertensive areas from which impulses bombard the CNS and give rise to referred pain
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myofascial trigger points
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MFTP's develop in response to
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muscle macro/microtrauma
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Name some characteristics of MFTP's
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1. short, tight mm.
2. JUMP sign 3. referred pain, numbness, autonomic symptoms 4. reproducible symptoms 5. resolution when MFTP addressed |
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What two patterns of pain treatment/etiology were discovered separately but work on similar neural mechanisms?
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myofascial trigger points
& acupuncture points |
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Although poo-poo'd by Melzak & Wall, what theory explains how nociceptors affect mechanoreceptors in ways other than just pain?
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Gate Theory
(overstimulation of a point releases endorphins or enkephalins, OR vibratory fibers override pain sensation) |
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Are there significant effects of synovial joint manipulation that are not seen with mobilization or simple ROM?
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yes
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What increases circulation in a joint?
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mobilization, ROM, Adjustment
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How does adjustment affect SDF
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INTERRUPTS PAIN cycle
(pain-spasm-pain wicked circle) MAY TRIGGER CIRCULATORY/NEURAL SURGE |
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What is the 3 phase of model of VSC?
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Subluxations begin a degenerative process that ends in permanent changes if not corrected. Basis of maintenance and preventative models of care.
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What is VSC phase 1?
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Segmental dysfuction hypothesis
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What is VSC phase 2?
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Instability hypothesis Injury or congenital
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What is VSC phase 3?
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Immobilization Degeneration hypothesis; typically go from 1 to 3 w/o going through 2
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What words should you associate w/ VSC phase 1, 2 and 3?
You big S.I.S.I. |
SDF
INSTABILITY STABLE but IMMOBILE 1: inflammation and segmental dysfunction 2: instability 3: stabilization and immobilization |
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What was Palmer's first hypothesis?
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INFLAMMATION
, which was, "the result of displacement of any body part: n., a., or v., bone, ligament or m. |
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How did DD refine his hypothesis?
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"Luxation on bones cause disease". He believed mm. nn. and bones were the key in displacement causing pressure which could be relieved w/ adjustments.
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What did DD believe put "pressure" on the nerves?
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Articular structures most important sources (After Renwick's hot arm).
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What does innate mean?
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Born with
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What did DD add to his theory after asserting the superiority of the nervous system?
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Vibratory theory: nerves vibrated normally at 200 per minute representing the tone of the NS.
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According to DD what causes BOP?
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S.P.A.T.
Accidents Poisons Toxins Stresses |
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What were BJ's 4 criteria for subluxation?
*hint: it makes a person mopi |
MISALIGNED
OCCLUDED PRESSURED INTERFERED |
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What did CO Watkins do for chiropractic history?
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Advocate of applying the scientific method to chiropractic practice, research and education to show evidence.
My dear WATKINS, the SCIENTIFIC METHOD divulged the DNA helix (Watson and Crick - close enough, Sherlock) |
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What did Marcel and Henri Gillet and do for chiropractic history?
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Revitalized the LPS concept of lack of proper joint motion.
GILLETT- HypOmobility, HypERmobility! |
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What did Fred Illi do for chiropractic history?
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Discovered the intraarticular sacroiliac ligament.
***It's Illi the SI and hypERmobility. Illi! It illi is! |
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What did Dr. Thomas Brown do for chiropractic history?
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Downtown Brown coined the term SPINAL IRRI-TA-TION, brothers and sisters. Spinal iri-ta-tion!!!
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RIADORE
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RIADORE Compressione Nervo
father of nerve compression theory |
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What did AR Renwick do for chiropractic history?
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"The patient, A.R. Renwick, had the left hand, arm, shoulder and on up to the spine, intensely hot. Dr. Palmer drew the attention of the class to the excessive heat condition of the portion named; the balance being normal in temperature. He then gave an adjustment in the dorsal region which relieved the pinched nerve on the left
side, also the excessive heat of the left upper limb; but he had thrown the vertebra too far, which had the effect of pinching the nerves on the right side, and immediately causing the upper limb to be excessively hot. He asked the class, "Is the body heat by blood or by nerves?" he then left them for two or three minutes. He returned and asked them, "Is the body heat by blood or by nerves?" The class unanimously answered "Nerves." Thus was this new thought originated. |
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What did Solon Langworthy, Oakley Smith and Minora Paxson do for chiropractic history?
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Made LSP text saying BOP model, by Palmer, was too old. Joint FIXATION a better model to distinguish medicine and osteopathy from chiro. (too bad they didn't ditch the word subluxation while they were at it)
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What did Tom Morris do for chiropractic history?
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MORRIS & MORIKUBO case.
Tom was a lawyer.using mixer Langworthy's book Modernized Chiropractic, attorney Tom Morris legally differentiated chiropractic from osteopathy by the differences in the philosophy of chiropractic's "supremacy of the nerve" and osteopathy's "supremacy of the artery". Morikubo was freed, and the victory reshaped the development of the chiropractic profession, which then marketed itself as a science, an art and a philosophy, and B.J. Palmer became the "Philosopher of Chiropractic". Used LSP text to defend that chiropractic used for his client is different from medicine and osteopathy. |
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What did Joy Loban do for chiropractic history? Joy M. Loban, DC, former chairman of the department of philosophy at the PSC, added a new dimension to the struggle among the schools in 1913. Loban was one of the organizers of the Universal Chiropractic College in 1910, a school formed in apparent reaction to B.J.'s curriculum. When D.D. Palmer died in 1913, Loban repeatedly sought grand jury indictments of the "Developer" for homicide, claiming that B.J. had struck the founder with his automobile during a parade in Davenport in August, 1913. No charges were ever brought, but the continuing accusations of patricide fouled the chiropractic literature for decades to come.
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Objected DD's introduction of x-ray; left Palmer school w/ 50 students to form Universal College of Chiropractic down the street.
********Made detailed Meric system. [wiki] Joy Loban, DC, executor of DD's estate, voluntarily withdrew a civil suit claiming damages against B.J. Palmer, and that several grand juries repeatedly refused to bring criminal charges against the son. |
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What did Alva Gregory do for chiropractic history?
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Accepted the Palmer hypothesis (BOP) w/o metaphysical thinking. He emphasized the effects of mechanical interference on the excitability, conductivity, reflexivity and efferent transmission of nn. at the IVF.
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What did Verner, CW Weiant and RJ Watkins do for chiropractic history? (the VW's)
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Admonished chiropractic for dogmatic adherence to Palmerism (the VW's broke away and made a new vehicle)
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What did Irvin Hoff do for chiropractic history?
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AXOPLASMIC FLOW = HOFF
Osteopathic researcher who published data related to axoplasmic flow during nerve compression. |
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What did Coulter do for chiropractic history?
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Talked down to chiropractic saying it doesn't look at data that goes against Palmerism. He suggested we research focusing on the body as a self healing organism w/o metaphysical things.
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LIGAMENT & CAPSULAR dysfunction facet
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Hadley
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What is the independent variable (Leach)?
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The adjustment
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What is the mediating variable?
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SDF (VSC phase 1)
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What is the dependent variable?
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Improvement of pain or function
*Children are our dependents. They are an improvement upon ourselves. |
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Clinical trials on the effectiveness of spinal manipulation, have they used the term "subluxation" according to Nelson?
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No, previous studies have not used subluxation at all.
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What sort of reasoning is used when assuming there is a lesion chiropractors treat w/o that lesion being verified?
|
Many chiro.s believe a lesion does exist d/t their education of anatomy, neuro, etc. Based on the article (Nelson) all science and spine related facts are being used to validate the existence of the lesion but proof is never shown.
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What does Nelson say about defining subluxation by consensus vs. reality and validity of subluxations?
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It is useless and all debators are more concerned w/ being right rather than rethinking and applying science (physiology) to their definition.
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What doesn't the VSC model accomplish as a proposed theory? (Nelson)
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Doesn't provide a coherent understanding of relationship b/w spinal dysfcn and health, a clinical phenomenon, predictions can't be made b/c it doesn't draw conclusions, is not testifiable or falsifiable.
Can't be shown as false by new evidence = no theory |
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What are problems w/ Nelson's conclusion that a theory should be falsifiable?
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A problem is that NOT all theories can be tested.
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What is tautology?
|
A circular type of argument that validates itself by renaming accepted principals or beliefs as a new theory or principle.
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In Nelson's view do clinical studies on manipulation offer any insight into subluxations?
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No, clinical studies just focus on treatment by Chiropractic in comparison to other forms of care.
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What are the necessary characteristics that would make a genuine subluxation theory? (6)
|
HISTORY
TESTABLE/FALSIFIABLE CURRENT BASIC SCIENCE STANDARDS (EDU AND PRACTICE) CLINICAL MEANING UNIQUE |
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What were Nelson's modifications to Palmer's original theories on subluxations? (4)
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1. Less emphasis on innate 2. The manipulation is not as "almighty" as it once seemed. 3. Expands BOP model 4. Shifted away from pinched nerve theory and into somato-visceral reflexes
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What are the 4 testable hypotheses?
|
1. Differences in HEALTH can be RELATED TO differences in SPINAL FUNCTION
2. Spinal DYSFUNCTION at "X, Y & Z" are related to more of CONDITION "W" 3. Ability to RELIABLY IDENTIFY and categorize spinal DYSFUNCTION that RELATES to CONDITION 4. SPECIFIC manipulation BETTER than nonspecific manipulation |
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What occurs in tissue w/ injury?
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Infiltration of histamine, protein derived factors, eicosanoids, proinflammatory cytokines, NO, degradative enzymes and substance P into tissues are caused by injury.
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What are leukotrienes?
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An eicosanoid, product of arachidonic acid
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What are proteoglycans?
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Product of arachidonic acid. TXA2 vasoconstricts and platelet aggregates and PGI2 does opposite. Inflammation destroys PGs and those pieces induce inflam.
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What does platelet activating factor do?
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Causes platelets to aggregate, mediator in anaphylaxis, inflammation and bronchoconstriction.
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What does cyclooxygenase activate?
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proteoglycan pathway
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What does lypooxygenase activate?
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Leukotriene pathway
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What does aspirin do?
|
Blocks cyclooxygenase.
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What do cytokines do?
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Regulate inflammation and immune responses. Says "cell can no longer function and needs to die."
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What does interleukin do?
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Stimulates synthesis of proteases, proteoglycans, NO (vasodilates), and CK (high in joints)
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What do tumor necrosis factor, chemokines and tissue growth factor do?
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Bind to receptors to start processes (autocrine, endocrine, paracrine)
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What does substance P do?
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Neuron protein that functions as nt, associated w/ anxiety, stress, neurogenesis, vomiting, pain or nociception. Stimulates cell growth in culture Potent vasodilator b/c releases NO from endothelium can -> hypotension
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What are arthritides?
|
Inflam destroys PGs and those pieces induce inflammation. Inflam includes tissue remodeling which may cause loss of function in long term.
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What are the characteristics of acute inflammation?
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Visible signs, often w/ vascular damage, capillary walls allow exudates. Cell level: mast cell, leukocytes, macrophages (chemotaxis). Histamine (vasoconstrictor), protein derived factors (complement system, kinin system, coagulation system)
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What are the characteristics of chronic inflammation?
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LYMPHOCYTES & MACROPHAGES
ANGIOGENESIS CT PROLIFERATION (SCAR) |
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What are the clinical characteristics of inflammation?
5 Latin words... |
Rubor (redness)
Tumor (swelling) Calor (heat) Dolor (pain) Functio Laesa (Loss of function) |
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What does diapedesis mean?
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process of WBCs when they penetrate the basement membrane out of a blood vessel and undergo chemotaxis
*same as EXTRAVASATION |
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What does OPSONization mean?
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a function of the complement system (C3b, C5a, etc) that, FLAGS BACTERIA for macrophages to destroy.
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What does autocrine mean?
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chemicals made from cell to interact w/ itself
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What does paracrine mean?
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Chemicals made from cell to communicate w/ adjacent cells
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What does endocrine mean?
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Chemicals made from cell that act on cells far away (travels a distance)
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What is involved if myopathology occurs before segmental facilitation occurs?
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Afferent and efferent nerves Joint receptors Muscle receptors Posterior facet joints Inflammatory triggers and noninflammatory triggers
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Describe Group I afferent nerve fibers.
*Group ONE is the hot dog fliers... |
Largest, thickly myelinated, fastest, not in skin, proprioception, kinesthesia
ONE LARGE PROTEIN HOT DOG! FAST UPHILL and UNDERGROUND BALANCE. |
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Describe Group II afferent nerve fibers.
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Medium sized, thickly myelinated, fast, A-beta in skin proprioception, mechanical
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Describe Group III afferent nerve fibers.
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Small, thinly myelinated, slow, A-delta mechanical, heat, cold, nociception
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Describe Group IV afferent nerve fibers.
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Smallest, unmyelinated, slowest, C mechanical, heat, cold, nociception
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What are the efferent nerve fibers? (2)
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ALPHA OUTSIDE EXTRAFUSAL FORCE
gammma inside smallers intrafusal ALPHA OUTSIDE EXTRAFUSAL FORCE |
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What are the joint receptors?
|
Group II-IV neurons respond to chemical and mechanical changes near facet joints. Some respond to movement w/in physiologic range and others might respond to greater force. Some respond to directions of movement.
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With joint receptors describe how nociceptive chemicals can act.
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Various nociceptive chemicals like substance P canALTER THE THRESHOLD of the mechanoreceptors, causing them to FIRE in an attempt to modify nociception.
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STIFFNESS?
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SPINDLE SHORTEN AND GTO'S TENSE
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1a
*Commander in Chief |
Primary muscle SPINDLE afferents:
RESPOND TO STRETCH AND TELL THE MUSCLE HOW LONG IT CAN GET |
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What does Group Ib do as a muscle receptor?
|
Golgi tendon organ afferents; respond to muscle tension and low levels of force during active muscle contraction.
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What do group II afferents do as a muscle receptor?
|
Mostly secondary m. spindles that respond to m. stretch and are inhibited by m. contraction. Respond to change in m. length (tonic response) but not so much to the rate of change in length (phasic response)
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What do non-muscle group II afferents do?
|
ADJUNCTS ARE MEDIUM SIZED ABOVE GROUND THICKLY MYELINATED UPHILL HOTDOGS
joints and skin are their domain! |
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What do group III and IV afferents do as a muscle receptor?
|
Considered together d/t their similarity. C fibers (IV) most well known pain receptors. Have highly specific responses to chemical and/or mechanical stimuli.
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What can SPINAL MANIPULATION do to muscle receptors?
|
change COMMANDER IN CHIEF AND ADJUNCT (GROUPS I & II AFFERENTS)
Might modify the discharge of group I and II afferents. |
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How does Golgi Tendon Organ react to SMT?
|
silent at rest and more activated by impulse of SMT than by preload before the thrust.
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Describe type I/slow twitch fibers.
|
POSTURE/SHORTEN/DVORAK/FIBERS
Have more mitochondria, store O2 in myoglobin, rely on aerobic metabolism, have greater capillary to volume ratio and associated w/ endurance; produce ATP more slowly. Marathon runners tend to have more type I fibers d/t training and genetics. |
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Describe type II/fast twitch fibers.
|
Fewer mitochondria, capable of more powerful (but shorter) contractions, metabolize ATP more quickly, have a lower capillary to volume ratio, and more likely to accumulate lactic acid. Weightlifters and sprinters have more type II fibers.
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What is a motion segment in reference to facets?
|
2 adjacent vertebrae, IVD, and soft tissues that cross or connect the 2 vertebrae.
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What is the anterior part of a motion segment in reference to facets?
|
Vertebral bodies, IVD, and anterior and posterior longitudinal ligaments.
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What is the posterior segment in reference to facets?
|
SP, pedicles, lamina and articular facets, posterior paraspinal muscles and ligamentum flavum.
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|
Describe a facet joint.
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True diarthrodial w/ posterolateral fibrous capsule that has reinforcing strands from the interspinous ligament; there is synovial lining and a medial capsule formed by ligamentum flavum. It has the property of shock absorption.
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What kind of joint derangements develop due to LIGAMENT & CAPSULAR INSTABILITY as a model of facet pathophysiology? (3)
Cap's off to Hadley for this one! |
FOR ROACHES
SYN-CLUSION SUPER ART PEDDLERS & MINA **Caps off to Hadley for this one!*** all HadleyFORAMINAL encROACHment; intra-articular SYNOVIAL FOLD inclusions; impingement of the SUPERIOR ARTICULAR process against the PEDICLE above and LAMINA below. ****HADLEY*** |
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What facet pathophysiology was researched by Schmorl and Junghann?
*think patho for psychos in prison |
Degenerative change w/in the joint and meniscal "INCARCERATION".
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Jackson
|
JACKSON JACKED THE CAPSULE
Joint effusion w/ capsular distention. |
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HALDEMANN
Haldemann is an effusive man with diffuse interests |
Joint EFFUSION w/ direct DIFFUSION = NERVE ROOT PAIN
Haldemann is a effusive man with diverse interests |
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What facet pathophysiology was researched by Farfan?
|
Joint adhesion
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What did Giles study in models of facet pathophysiology?
GILES AND ZEE LUMBAR JOINT STRETCH! |
GILES AND ZEE LUMBAR JOINT STRETCH!
Lumbar z-joints and favored release of trapped intra-articular fold and stretching the joint capsule as a likely mechanism for why adjusting the spine works. |
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What are the models of facet pathophysiology? (6)
|
1. Joint derangement 2. Degenerative change 3. Joint effusion w/ capsular distention 4. Joint effusion w/ direct diffusion 5. Joint adhesion 6. Z-joints
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|
What are Z-joint meniscoids?
|
Contain variable tissues such as vascular fibroadipose, synovium, calcified tissue, fibrocartilage and chondrocytes in the process of calcification. Might cause chronic SDF; mech. could explain "acute locked back"
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|
What are the hypothesized pathophysiological effects of trapped meniscoid? (4)
|
1. Joint capsule tension -> more mechanoreceptor activity 2. Capsular adhesions form 2ndary to joint hypomobility 3. Biochem change: GAG lost from cartilage and lig. related to jt 4. Deg. changes occur early as normal stresses apply to the dysfcn'l jo
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What are the hypothesized pathological effects of a
TRAPPED MENISCOID? |
1. Joint CAPSULE TENSE 2. CAPSULE ADHESION
3. BIOCHEMical alteration 4. DEGENERation *When lesbians feel trapped or menised, they tense up, adhere a cap (baseball) to their heads, go through biochemical changes and voila! Ellen Degeneres! |
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What is joint capsule tension as a pathological effect of trapped meniscoid?
|
Results in increased mechanoreceptor activity; results in increased nociception, lowering pain threshold and creates pain-spasm-pain cycle.
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What are capsular adhesions as a pathological effect of trapped meniscoid?
|
Form secondary to joint hypomobility; results in capsule contracture and connective tissue growth across the joint space which obliterates the cavity.
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What is biochemical alteration as a pathological effect of trapped meniscoid?
*the BIOCHEM change that happens to Ellen Degeners when she feels trapped and menised, tightens up, adheres a cap to her head... |
She GAG's!!!
GAG lost from cartilage and ligament related to the joint including end plates. |
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What are degenerative changes as a pathological effect of trapped meniscoid?
|
PREMATURE BONE LOSS (Ellen Degeneres)
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What current research is being done on the pathological effects of trapped meniscoid?
*are lesbians bringing back the rat tail? |
Using small animal models is ongoing using rat spine, rat tail and the inducement of facet pathophysiology by fixation
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|
Tenderness of a vertebrae corresponds to the diseased organ ~ 1832
|
Brown
"spinal irritatation" of organs |
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|
Deranged nerve compression father
|
Riadore!
|
|
|
Palmer's first hypothesis
|
INFLAMMATION ANYWHERE
DISPLACEMENT |
|
|
Why was DD's hypothesis interesting?
|
Because it's all biomechanics! In the 19th c. when he was alive and well, the mind was responsible for health acc'ding to the popular thinking
|
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|
When was DD's first adjustment, who?
|
1903 Renwick the janitor
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After DD decided the nerves were the most important, he never again discussed manipulation of non-osseous structures. He thought the _________ structures were MOST important sources of ________ on the nerves.
|
Articular, pressure
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Trial in Wisc.
|
1906 Morikubo trial in La Crosse, Wisc. forced DD to use metaphysical to distinguish chiro from osteo.
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|
|
myelopathy
|
general effects on the spinal cord
|
|
|
State DD Palmer's hypothesis:
|
BOP in the spine from
Accidents/Poisons/Toxins/Stresses of all sort resulted in: NERVE impingement, decreased OR increased BODY TONE, then>>>DISEASE |
|
|
DD's too much or too little nerve fcn is the basis of
|
neuropathology, neuroimmune hypothesis
& HOMEOSTASIS as king |
|
|
Who wrote Modernized Chiropractic just before DD published his first text?
|
Langworthy, Smith & Paxton in 1906
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|
What book was used by a lawyer to defend Morikubo and who was the lawyer?
|
Modernized Chiropractic (Langworthy, Smith & Paxton) by TOM MORRIS
|
|
|
DIFFERENCE b/w bone out of place & fixation
|
BOP the bone has moved measurably (disproved)
vs. Fixation = HYPOmobility (bone in place but not moving properly) |
|
|
Disc protrusion is the VSC phase?
|
1
|
|
|
Extrusion and cord myelopathy are VSC
|
2
|
|
|
Laminectomy for cord myelopathy from extrusion of nucleus would be VSC
|
3 (immoble but stable)
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VSC1 is the initial
|
injury
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VSC2 is the lesion, the
|
unstable spine
|
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VSC3 is the spine finally
|
immobile but stable
|
|
|
first to use the term SUBLUXATION
|
Langworthy
(of Langworthy, Smith & Paxton - Modernized Chiropractic 1906) |
|
|
Tom MORRIS, defending Morikubo with LS&P's book Modernized Chiropractic, presented the theory of ____________ and people claimed the verdict was FIXED!!!!!
|
joint FIXATION
*rejecting BOP, Langworthy used the word Subluxation for the first time and Morris perpetuated it at the trial |
|
|
"A simple subluxated vertebra differs from abnormal vertebra only in its FIELD OF MOTION and the center of its field of motion."
|
- Langworthy, Smith & Paxton players on the FIELD OF MOTION
*field of motion may be too great in some directions, and too great in others |
|
|
Precursor to Segmental Dysfunction Theory SDF
|
LS&P's subluxation theory
(vs. DD's Bone Out of Place that became the halmark) |
|
|
Meric system
|
developed by Jay LOBAN, an old student of DD's who didn't like them new-fangled x-ray machines. Formed Universal and MERIC sys of Nerve-to-Organ
|
|
|
Nerve-to-Organ
|
LOBAN, the MERIC system
|
|
|
Meric is really
|
all or nothing nerve to organ
(typically developed from a man who didn't like x-rays - Jay Loban) |
|
|
How does the nervous system respond to FIXATION?
|
with INFLAMMATION, and eventual dysfunction
|
|
|
In 1912, an MD/DC Palmer student accepted the bone out of place model but ?
|
He chucked the metaphysical crap - Dr. Alva Gregory!
MECHANICAL INTERFERENCE on excitability, conductivity, reflexivity and efferent transmission of nn. at IVF. |
|
|
Gregory
|
Dr. Alva Gregory, MD/DC, accepted BOP, chucked metaphysical crap, and emphasized
************MECHANICAL INTERFERENCE at the IVF.********* |
|
|
Nazi Germany passes the "Law for the Prevention of Hereditarily Diseased Offspring". Roosevelt signs the New Deal into law. Bonnie and Clyde are gunned down. What did BJ Palmer do that year?
|
Establishes 4 Subluxation criteria:
1. MISALIGNMENT in relation to adjacent segments 2. OCCLUSION of foramen, including canal 3. PRESSURE on nerves 4. INTERFERENCE OF TRANSMISSION of mental impulse supply (innate) |
|
|
BJ's 4 criteria (Misalignment/Occlusion/Pressure/Interference) really mean subluxation is a direct compression on the
|
cord.
*only 2 vertebrae - ATLAS & AXIS - matter |
|
|
Because BJ believed root compression could only occur at C1/C2, he developed the
|
Hole In One technique
|
|
|
Apart from Dr. Gregory, the MD/DC who accepted BOP but chucked metaphysical crap and went with mechanical, who is another science hero DC?
|
Elementary, my dear Watkins! Applied scientific method to chiropractic, research, education. Generate clinical data and publish clincial research!
|
|
|
Revitalized the LPS concept of lack of proper joint motion...
|
Gillet brothers and Fred Illi
*an injured joint is fixed due to EDEMA dev. a/r strained capsule and tissues |
|
|
discovered the interarticular sacroiliac ligament
|
Fred Illi
EDEMA around injured joint/GILLET brothers *revitalized fixation theory of LS&P |
|
|
Fred Illi discoveries (2)
|
~The sacroiliac joint moves!
~The interarticular sacroILLIac ligament (mispelled on purpose) |
|
|
What did Fred Illi, discoverer of the i.a. sacroILLIac ligament and that the SI joint is NOT diarthrotic (stuck), term chiropractors?
|
SCIENTIST-PRACTITIONER
|
|
|
Fred Illi demonstrated that the iliolumbar ligament DAMPENS?
|
dampens the effect of spinal motion on L5
|
|
|
Regarding germ theory, Palmer meant
|
restore the body so it can fight the germs that do exist
|
|
|
Problem with BJ's book Chiropractic Clinical Controlled Research?
|
there was none - he was trying to prove chiro works instead of using scientific method. Real setback. Thanks, BJ.
|
|
|
Wrote The Science & LOGIC of Chiropractic
|
VERNER THE VULCAN:
It is logical, Captain, that the body cannot meet every emergency, but NEURAL mechanisms are, indeed, always involved where there is infection and immunity. |
|
|
Eventually, VERNER, WEIANT & WATKINS (VW squared) wrote Rational Bacteriology...
|
admonishing the profession for dogmatic adherence to Palmerism. Verner is our neural mechanism involved in infection/immunity guy
|
|
|
Rational Bacteriology
HIPPIE BIOLOGISTS |
VWsq. (Verner, Wieant, Watkins)
Volkswagen squared |
|
|
Discovered at Univ. Colorado and funded by the ICA
|
HOFF - they didn't scoff!
It's true - damage to AXOPLASMIC flow results from just a small amount of insults on you! |
|
|
Hoff's
|
axoplasmic flow
|
|
|
Psychoimmunology of the 1990's guy that suggested chiropractic adopt WELLNESS CARE
|
COULTER
WELLNESS CARE |
|
|
5 Theory Characteristics
|
~predict NOVEL observat's
~explain OBSERVED phen. ~testifiable/FALSIFIABLE ~PARSIMONIOUS ~NATURAL explanation |
|
|
called 'principled chiropractors' - insist on vitalism
|
Vitalists
|
|
|
resist vitalism on the grounds that it harms the profession
|
Non-vitalists
|
|
|
What is the problem with the subluxation term itself?
|
there is NO OPERATIONAL DEFINITION of it
|
|
|
Does valid mean true?
|
no, we accepted that aspirin truly took care of pain, even when we didn't understand why (COX-inhibitor)
|
|
|
VSC views subluxation as a form of
|
pathology
|
|
|
Carver viewed subluxation as a
|
disease
|
|
|
a partial or incomplete separation; one in which the articulating surfaces remain in partial contact.
|
early DD Palmer def of subluxation=
PARTIAL CONTACT of articulating surfaces |
|
|
BJ Palmer def of subluxation
|
MISALIGNMENT
OCCLUSION PRESSURE INTERFERENCE |
|
|
A vertebral articulation can become fixed in any of the positions it normally takes in spinal movement...when we adjust _________, we do not 'replace' vertebrae.
|
Gillet (1951) subluxations as DISPLACED out of physiological boundaries
|
|
|
Does subluxation meet the criteria for disease?
|
no, neither does schizophrenia.
TB does. |
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Some cluster of signs/symptoms with Natural history of progression if left alone. Knowledge of etiology and treatment consistent with what we know about its development. This is a ________.
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disease.
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Conceptual definitions are not __________ definitions.
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operational
*operational def's are used in scientific research |
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the link between the outcome and the adjustment
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mediating variable
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the treatment itself
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independent variable
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outcome
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dependent variable
*children are dependents. They are better outcomes, improvements upon ourselves. |
