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coined the term "spinal irritation" said vertebrae tenderness corresponded to diseased organ. |
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irritation of spinal nerves alters fx and structure. encouraged manipulation. |
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1. inflammation=result of any displacement. 2. luxation on bones causes disease 3. renwick adjusted; nervous system manages circulatory system 4. innate 5. vibratory theory added. "rack" bones to normal position; BOP!! |
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adjusted by dd, caused dd to hypothesize nervous controlled circulatory. |
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wrote stuff before palmer. rejected BOP. suggested jt fixation. |
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langworthy. precursor of sdf. |
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meric system based on spinal nerves |
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bj's 4 subluxation criteria: |
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1. v misalignment 2. occlusion of foramen 3. nerve pressure 4. interference of mental impulse transmission |
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bj thought which bones were subluxated? which caused pressure? |
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scientific research about chiro |
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marcel and gellet and illi |
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revitalized no joint motion theory. strained capsule. |
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why is chiropractic a paradigm and who said it |
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coulter; some ignore the things that challenge palmerism |
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what spot is the mediating variable in? |
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sdf=fixation sdf=mediating variable adjust=independent improvement in pain=dependent. |
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what does sdf do according to leach? |
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Definition
decreased mobility, altered pressure threshold, taut muscle |
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decreased rom, point tenderness, abnormal paraspinal contracture |
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decreased threshold for firing at a segment due to afferent bomardment associated with spinal lesionsr |
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fast, myelinated thickly, big, not in skin, proprio/kinesthesia |
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medium, thick myelin, fast, a-b in skin, proprio/mechanic |
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small, thin, slow, a-delta, mechanic/temp/nociception |
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smallest, no myelin, slowest, C fibers, mechanic/temp/nociception and PAIN |
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myelinated, innervate force muscles, big, fast |
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outer fibers (collagen), inward: subsynovia (fat, blood, lymph), synovial intima |
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which fibers respond to change in facets? what kind of changes are they? |
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chemical and mechanical 2, 3, 4 |
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primary; respond to stretch, rate, and magnitude of change in length |
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afferents to Ia muscle receptors? |
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golgi tendon. muscle tension and decreased force. silent at rest. |
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change in tension/change in length |
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secondary muscle spindles. respond to stretch and INHIBITED by contraction. |
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II muscle receptor. what happens at impulse? |
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resting discharge increased |
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vertebral body, ivd, ALL and PLL |
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posterior muscle segment=? |
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sp, pedicle, lamina, facets, flavum, post. paraspinal |
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theory I of facet dysfunction |
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Definition
due to ligament and capsule instability, foraminal encroachment, and synovial fold bends |
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theory II of facet dysfunction |
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Definition
degenerative chane in joint and meniscal incarceration |
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theory III of facet dysfunction |
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Definition
joint effusion w/capsular distention |
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theory IV of facet dysfuntion |
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Definition
joint effusion with direct diffusion as cause of nerve root pain. |
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theory V of facet dysfunction |
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theory VI of facet dysfunction |
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z-joint meniscoid w/important structures, possibly causing chronic SDF. |
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effects of trapped meniscoid |
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Definition
1. joint capsule tension (increased mechanoreceptor activity leads to increased nociception leads to decreased pain threshold) 2. capsular adhesion 3. biochemical alteration 4. degenerative changes |
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describe capsular adhesion in effects of trapped meniscoid |
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Definition
secoindary to joint hypomobility; ct growth around joint |
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describe biochemical alteration in effects of trapped meniscoid |
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Definition
GAG lost from cartilage and ligament of joint in question |
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describe degenerative changes of effecs of trapped meniscoid |
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Definition
abnormal stress--> bone loss and increased hypomobility |
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which cells affected in Korr's facilitated zone? What do they do? |
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Definition
ant and lat horn AND efferent pain become hypersensitive |
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what do muscle spindles do to contraction |
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Definition
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how does cns deal with lazy muscles? |
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Definition
muscle spindle adjusted during extrafusal contraction and adusts gamma motor neuron |
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so cns is adjusting to muscle slack. then what? |
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Definition
gain is set too high-->spasm. |
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in korr's model, the gain set too high leads to what two things |
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resist-->spasm, and golgi tendon organs inhibit alpha and gamma motor neurons |
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no. stretching muscle is all you need |
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cord necessary for fixation but cerebellum isn't. it's caused by central or peripheral input to segments. hindleg flexion! |
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in patterson-steinmetz, how do you prevent neural scarring? |
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don't wait to find fixation |
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what did wells say was his conclusion of patterson-steinmetz? |
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slow-twitch fibers (postural) shorten in sdf from overuse. sdf increases sensory discharge via 1a alpha to contract same muscle; altered joint movement results. |
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mood regulation, pain, nociception, stress, nausea, stimulates cell growth, vasodilates, reverses diabetes in mice. |
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what kills proteoglycans? |
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histamine causes depletion of atp which makes muscle never reset decreased blood makes somato-somato resopnse which leads to more histamine and more sensitization self-perpetuating for joints and/or muscles |
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Evans. fixation of joint and receptor tonus. minimum E used when spine is in equilibrium. |
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punjabi. what are paraspinal m. in? |
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what does multifidus affect |
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upper trap, levator scap, scalenes, subocciputal, extensors, internal shoulder rotators |
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neck flexors, mid and low trap, rhomboid |
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ql, hammies, gastroc, psoas, extensors, piriformis |
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