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130 Cards in this Set
- Front
- Back
2 different qualities found at varying levels of CT:
1. ELASTIC stretch 2. Plastic * VISCOUS stretch |
VISCO-ELASTICITY
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elongation created by imposed load that has a reversal when load removed
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ELASTIC stretch
*visco-elasticity |
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What are the qualities of ELASTIC stretch?
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When a temporary change in length provides:
extensibility retractability spring-like behavior |
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tensile load creates NO REVERSAL when load removed.
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VISCOUS or plastic (moldable)
*PERMANENT putty |
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Tissues w/ both ELASTIC & VISCOUS PLASTIC
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VISCO-ELASTIC
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VISCOUS tissues allow either
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plastic or permanent deformation
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Elastic properties allow for ___________ deformation (returning to original length)
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RECOVERABLE
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loads/stress can be unidirectional, meaning deformation along multiple vectors
ie: |
LENGTH & SHAPE change
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3 factors determining if ELASTIC vs. VISCOUS PLASTIC dominates:
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1. AMPLITUDE of force
2. SPEED of application 3. DURATION of application |
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What determines the dominating STRETCH?
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FORCE & TIME determine whether it will result in an elastic (recoverable) stretch or a permanently deformed viscous plastic putty state.
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The condition of the muscle _________ will change the O&I length, resulting in HYPO or HYPERtonicity.
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ANTAGONIST
the opposition has a say!!! |
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SHORT
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ELASTIC
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LONG
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VISCOUS
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LOW
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ELASTIC
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HIGH
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VISCOUS
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SLOW
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ELASTIC
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RAPID
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VISCOUS
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SHORT
LOW SLOW |
ELASTIC
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LONG
HIGH RAPID |
VISCOUS
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Not only can a high amplitude, rapidly applied force cause un-recoverable change, it can lead to tissue _________
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FAILURE
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If no tearing occurs when CT structures are PERMANENTLY lengthened, there will at least be some
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MECHANICAL WEAKENING
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What procedure produces more structural WEAKENING because of its high amplitude, rapid application?
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PFS
(Please Fucking Stop) is sometimes necessary to break the cross-linked adhesions of collagen caused by IMMOBILIZATION |
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IMMOBILIZATION
1. 2. |
Loss of WATER [turgor]
CROSS-LINKING ADHESIONS *do PFS (high amp, rapid app) |
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CREEP
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VISCOUS GIRLS GONE WILD
*Progressive plastic deformation of proteinaceous tissue under a sustained load OR SUSTAINED LACK OF LOADING |
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Progressive plastic deformation of proteinaceous tissue under a sustained load OR SUSTAINED LACK OF LOADING
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CREEP
Use it or lose it, creep. |
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The gradual rearrangement of collagen, proteoglycans and the loss of turgor.
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CREEP
Use it or lose it, creep. |
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Effects of CREEP vary with
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AGE
RESPONSE TO INJURY/DISEASE |
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CREEP commonly seen in
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ADL's or REPETITIVE motion occupation
ABNORMAL POSTURAL SYNDROMES [upper & lower crossed] HABITS of living |
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HYSTERESIS
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LOSS OF ENERGY in viscoelastic tissue DUE TO CREEP having already happened
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POST creep change
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HYSTERESIS
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A change in the BEHAVIOR of the tissue
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HYSTERESIS
Post creep can be due to CONTINUOUSLY APPLIED load OR REPETITIVE cyclic LOADING & UNLOADING over time |
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Once _________ has set in, the deformation has become PERMANENT.
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HYSTERESIS
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SET
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the difference or change in LENGTH OR SHAPE that a tissue has undergone FROM its original
*AFTER creep and hysteresis have already happened |
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CHS
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Creep Hysteresis Set
*Denial Bargaining Resignation |
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Can SET be reversed?
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If the stressor is removed, SOME restoration of SHAPE & LENGTH, as well as REHYDRATION [turgor] is possible
But once permanent deformation has occurred, the tissue becomes more susceptible to injury. |
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largest single organ in body
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SKELETAL mm
40% of body weight Largest CONSUMER of energy |
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Impairment has extensive implications
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SKELETAL mm.
*waste disposal, heat production, pumping of blood and lymph all mm. jobs so all affected if mm. are impaired. |
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Functions of SKELETAL mm
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MOVEMENT of joints
PROTECTION of joints POSTURE HEAT |
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Injury of muscle results in:
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FIBROSIS w/in surround fascia
LOSS of EXTENSION & RETRACTION (elasticity and strength) JOINT DYSFUNCTION |
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OBSERVE muscle to assess
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CONTOUR & SYMMETRY
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PALPATE mm to assess
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INTERNAL ARRANGEMENT [fibrous nodes, taut bands]
TONE: Consistency~Flexibility~Response |
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Describe a normal muscle
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Think 25 year old female (yeah, this is a transitory state so enjoy it):
SUPPLE, FLEXIBLE, SMOOTH, MODERATELY FIRM, **PAIN-FREE! |
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INDICATORS of ABNORMAL mm. tissue:
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Palpable NODULES
Taut and tender BANDS FIBROSIS ROPINESS |
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MOTOR UNIT
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single ALPHA motor neuron and ALL the SKELETAL mm. fibers it innervates.
Avg = 180 per |
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Range 3-2000 fibers per.
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MOTOR UNIT = average is 180
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MYOTACTIC UNIT
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ALL of the mm involved in a SPECIFIC MOVEMENT across a GIVEN JOINT, including:
1. AGONIST {prime mover} 2. SYNERGIST = may extend line of pull or stabilize prime mover 3. ANTAGONIST - opposes movement |
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3 components of a MYOTACTIC unit
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AGONIST
SYNERGIST ANTAGONIST |
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The result of a continuous, random stream of nerve impulses from the spinal cord (LMNs)
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Muscle TONE
This sustained partial contraction is maintained by: 1. GAMMA motor cortex (impulses) out to body from brain 2. Muscle SPINDLES (reflexes) INHIBITORY that detect changes in LENGTH and send message from LMN to cortex |
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2 components maintain muscle TONE
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GAMMA motor cortex go thru anterior motor neurons to pyramidal and extrap. tracts tell body to remain upright.
Muscle SPINDLES detect changes in length |
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The principle that at any given time, some mm fibers are contracted and others are relaxed
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ASYNCHRONOUS firing
Don't shoot your wad all at once. NO motor unit can fire continuously (that would be tetany then death!) |
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occurs when mm of OPPOSING function develop ALTERED levels of RESTING TONE relative to one another
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mm IMBALANCE
*these mm are susceptible to TrP formation |
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TrP
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a fancy abbreviation for Trigger Point, like MFTP for myofascial triggerpoint or nodules or fibrosis or taut and tender bands or fasiculations - it's all related crap. Just fix it.
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occurs when mm of OPPOSING function develop ALTERED levels of RESTING TONE relative to one another
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mm IMBALANCE
*these mm are susceptible to TrP formation |
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Kind of motor neurons that send information from anterior horn to periphery
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LOWER motor neurons
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a state of readiness to CONTRACT
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RESTING tone
*the default state, influenced by joints and resting tone of all other muscles in the MYOTACTIC unit (agonist, synergists, antagonists). When RESTING TONE is normal, there is considered to be muscle BALANCE across a JOINT |
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occurs when muscles of OPPOSING FUNCTIONS develop ALTERED levels of resting tone, relative to one another
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MUSCLE IMBALANCE
*Develop TRIGGER POINTS *Antagonists will become RECIPROCALLY INHIBITED and HYPO-tonic * FAULTY movement PATTERNS as CNS overactivates the hypertonic mm and under uses the hypotonic ones (ie, you get stuck in a rut when you have mm imbalance) |
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Name 3 reasons muscle imbalance occurs:
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Sustained loading
Constrained postures Repetitive tasks Lack of activity and VARIETY of motion Gravity Familial modeling * |
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Most important factor in development of MUSCLE IMBALANCE?
*hint: it's a Bangles lyric |
TIME TIME TIME
See what's become of me As I looked around for my possibilities They were so hard to see Look around, the leaves are brown And the sky is a hazy shade of winter |
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The longer a person allows muscle imbalance, the greater the likelihood of recruiting more?
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MOTOR UNITS >>> CREEP
*leading to greater effort needed to reverse |
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When a mm develops INCREASED resting tone, it is
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HYPERTONIC
*having lost extensibility (elastic barrier has moved) *having lost strength so tires quickly *synergists may also become hypertonic, while antagonists become hypOtonic and stretched in length *joints they control develop small ROM's, increasing stress and fatigue |
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FACILITATION
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HYPERtonicity (a heightened state of readiness, usually experienced after reading forensic novels or playing Call of Duty and the #1 reason YOU should not have a gun in the house).
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a heightened state of readiness
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FACILITATION [hypertonicity]
Code Orange. We were in a constant state of FACILITATION under George Bush, Jr. |
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ADAPTIVE shortening
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CHRONIC facilitation
ADAPTIVE = CHRONIC (can't beat'em so you join'em) |
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Does a hypertonic muscle have to have a spasm?
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NO, but...Hypertonicity does not necessarily result in spasm but it may lead to spasm and adaptive shortening.
I hate this class. I love this class. I have to take this class no matter how I feel about it. Yeah, that's it. |
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ADAPTIVELY shortened mm develop
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ADHESIONS [loss of water/turgor]
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How is ADAPTIVE SHORTENING reversible?
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STRETCH
*not strength. Duh, this would shorten the mm again. You must break the pattern of FACILITATION (hypertonic state) |
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What do you have to do to a mm that is ADAPTIVELY SHORTENED?
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You have to STRETCH it.
*in response, the INHIBITED mm will REGAIN contractility and tone *the speed and magnitude of the stretch you apply depends on how chronically contracted the mm is. Meaning: if a person has been laying in the ICU and their Achilles' have shrunk them onto their tip toes, do NOT apply your 180lb frame to suddenly dorsiflex their ankles. You will be sued. |
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INHIBITION
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HYPOtonicity = inhibition is a compromised state of readiness. A dullness. Too stretched over too long at time = STRETCH WEAKENED
May also have developed ADHESIONS |
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Hypertonic mm lose
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EXTEND ability
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Hypotonic mm lose
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RETRACT ability
*can be taut or not |
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_________ must be distinguished from SPASM
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IMBALANCE
*imbalance = usually abnormal postural alignment, alteration of contour, plumb line test fail. *confirm via PALPATION, LENGTH TESTING, FUNCTIONAL TESTING of movement patterns |
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What could be the most important factor of IMBALANCE of mm patterns?
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FAMILIAL PATTERNING
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POSTURAL mm
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OVERUSED
FACILITATED (HYPER) ADAPTIVELY SHORT (more perimysium) |
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TONIC mm
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are postural mm that maintain erect standing against gravity
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Name the mm ADAPTIVE SHORTENING tendencies:
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Pec minor/major - Upper trap - Levator - SCM - Scalenes (esp FHP) - Suboccipitals - Masseter & temporalis - Gastroc/soleus - Rectus femoris - Iliacus - Psoas major/minor - Erector spinae - Quadratus lumborum
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mm that tend toward STRETCHED WEAKENING
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trunk flexors
rhomboids mid and lower traps serratus anterior longus coli and capitus (deep neck flexors) ankle dorsiflexors TIBIALIS ANTERIOR gluteus maximus hamstrings = either hyper or hypo as in lower crossed syndrome are taut hamstrings that are stretch weakened over time |
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Recognizable patterns of imbalance
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1. LOWER CROSSED
2. UPPER CROSSED 3. LAYERED {after multiple episodes of lower back pain} 4. FORWARD HEAD CARRIAGE |
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an increase in DIAMETER of muscle cells and NUMBER of myofibrils
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HYPERTROPHY
The Hulk a related increase in ATP, phosphocreatinine, glycogen |
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a decrease in size of fibers and number of myofibrils
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ATROPHY
Disuse from a hospital bed...caused by IMMOBILIZATION and/or DE-NERVATION |
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Can a muscle be re-enervated after disuse atrophy from immobilization has set in?
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YES if remobilized/moved within 3-4 mo., then full function may return.
BEYOND 4 MO. then some permanent LOSS AFTER 2 YEARS, complete and no chance of recovery |
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INVOLUNTARY CONTRACTION in response to nerve IRRITATION, INJURY or other COMPROMISE (ie, a large # of motor units firing)
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SPASM
Ca++ Mg++ HYPOTHYROIDISM STATIN DRUGS dystonia = writer's cramp, epilepsy, low Ca++ tetany, low electrolytes, myoclonus, MS, Parkinson's, Alzheimer's, alcoholism, DEHYDRATION |
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SPASM can be
1. 2. |
1. PRIMARY = direct TRAUMA to mm itself. May become widespread panic d/t pain REFLEX mechanism. Relief depends on stoppage of nerve IRRITATION. Treating the PRIMARY SPASM AGGRAVATES IT.
2. SECONDARY = irritation of nerve ROOT, PLEXUS, or PERIPHERAL nerve causes guarding/SPLINTING. *Injury to nearby structures like tendons, bones, discs can cause 2nd spasm |
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TREATMENT for spasm:
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Primary = IMMOBILIZATION
Secondary = Ice (both P&S), Compression is usual mode of tx for secondary, HOWEVER secondary spasm d/t tendon injury is painful, i.e. tendinitis or shin splints |
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How to D/DX between PRIMARY & SECONDARY SPASM?
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LOOK: posture assessment, 1 and 2 legged stance, gait analysis
TOUCH: firmness or give, identify taut bands, palpate the TPs LENGTH TEST: presence or absence of pain during test FUNCTIONAL TEST: key movement patterns (test opposing forces during 6 basic movement patterns) |
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When the trigger point is the PAIN GENERATOR
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MYOFASCIAL PAIN SYNDROME of the _________ MUSCLE
*Pain and/or autonomic phenomena referred from active MFTP and associated w/ muscular dysfunction |
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MYOFASCIAL TRIGGER POINT
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When the trigger point is the focus of HYPERIRRITABILITY in muscle or fascia and when COMPRESSED, is locally tender, giving rise to REFERRED PAIN, autonomic phenomena and DISTORTION of PROPRIORECEPTION in a place REMOTE from the source.
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What is the quick def of a MFTP?
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PREDICTABLE
REPRODUCIBLE REFERRED PAIN PATTERN that doesn't follow myo/dermatomal pattern |
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Area of pain of trigger point REFERRAL:
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REFERENCE
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The REFERENCE POINT of tp referral is either called:
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SOLID - ESSENTIAL
SPILLOVER - STIPPLED |
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TP REFERRAL PATTERNS are, according to this class, :
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PREDICTABLE & REPRODUCIBLE
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TP's are NOT _______ but may be found near them.
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not motor points
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TP's may be found in sundry tissues (cutaneous, ligamentous, periosteal) but distinguished from
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MYOFASCIAL trigger points
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ACTIVE trigger points
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Refers to whether muscle AT REST or IN MOTION:
Always TENDER PREVENT full lengthening of mm |
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ACTIVE TRIGGER POINTS always refer to a muscle at rest or in motion and are always tender.
They prevent full lengthening (may induce 2* spasm if you try to) and this might ________ the mm. |
WEAKENS the mm
FATIGUES easily REFERRAL pain ***worsens*** during COMPRESSION in active compression |
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LATENT [vs. active] trigger point
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NO spontaneous pain = MUST be COMPRESSED to refer or cause pain
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SATELLITE trigger point (vs active and latent)
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Becomes active because its mm is located within the ZONE OF REFERENCE of another ACTIVE trigger point (don't develop unless actively causing pain; SAME MYOTACTIC UNIT/agonist-synergist-antagonist is recruited so SATELLITE develops by default.
GUILT BY MYOTACTIC ASSOCIATION! |
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SECONDARY tp becomes active because it's muscle was OVERLOADED while...
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acting as a SYNERGIST or ANTAGONIST of a muscle with an active tp.
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Which is more common, LATENT or ACTIVE trigger points?
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LATENT [the kind that only refers or has pain if you compress it, titch at it]
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Are trigger points (mostly latent) more common in males or females?
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Females
*in old age, no difference |
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Pain of trigger points increases in likelihood as well as in frequency as
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we get older because we are more active
*disagree! Trigger points are most often in sedentary muscles. I worked on them for 14 years before I sat in this class. Kids get tps, but it is unusual and due to postural distortion, not dehydration, a shitty job and sitting on the couch after work because they are too tired to move. |
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With advancing age, STIFFNESS and DECREASED ROM become more prominent than...
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pain
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Studies show chief complain of pain turned out to be myofascial tp in ___% of the patients
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85-95%
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A trigger point can be SATELLITE & SECONDARY, for example:
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iliopsoas can cause LBP and anterior thigh pain similar to rectus femoris pain
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REFERRAL usually projects
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DISTALLY 85% of time
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Response of tp to SNAPPING palpation?
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TWITCH
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What is the characteristic of a tp to PALPATION?
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SPOT TENDERNESS
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Are trigger points predictable and reproducible?
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Yes (sigh)
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Where are tp's most often found
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TAUT FIBROUS BAND that is palpable in the muscle
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Histological changes to mm w/ a trigger point?
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NONE
PHYSIOLOGICAL signs are due to **OXIDATIVE stress** (inadequate ATP for the higher than usual demand) |
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Pain from a tp can occur either at AT REST OR IN MOTION, but is exacerbated by
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PASSIVE STRETCHING (lengthening)
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Severity and extent of the tp does NOT correlate w/ the _____ of the muscle.
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size
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Where is pain often referred when a muscle has a trigger point?
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to the JOINT moved by that muscle
ie, infraspinatus and subscap refer deeply to glenohumeral joint |
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What is the only mm in the body that attaches to the anterior aspect of the spine?
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Longus coli
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Some referral patterns are ______, while some are very extensive
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local
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What 5 things can directly activate a TrP?
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1. ACUTE overload: [contraction from an already shortened position]
2. CHRONIC overload: overuse. Fatigue d/t repetitive or sustained contraction, incl. postural stress] 3. OVERSTRETCHING 4. DIRECT TRAUMA 5. CHILLING |
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Trigger points can be activated by OTHER trigger points (2):
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SATELLITE: develop in mm w/in the zone of reference of other Trp's
SECONDARY: develop in synergystic or antagonistic mm that get overloaded trying to reduce the strain of a mm w/ a primary Trp |
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Trigger points can be activated by _______ DISEASE
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VISCERAL
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TrPs can be activated by ________JOINTS
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ARTHRITIC
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TrPs can be activated if the mm gets too ________
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CHILLED/COLD during post-exercise stiffness
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Holding a mm in a _________ position over time can activate a TrP.
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SHORTENED
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What kind of ILLNESS can cause Trps?
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VIRAL
*shingles, influenza |
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Intensity of a TrP can vary from day to day, even hour to hour, but stiffness & weakness is GREATEST after __________.
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INACTIVITY
*upon awakening in the morning, sitting in one position over time |
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What are some AUTONOMIC phenomena that can occur from TrP's?
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1. Local VASOCONSTRICTION
2. SWEATING 3. TEARING [mm. of head and neck] 4. SALIVATING |
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Proprioception tells us where we are relative to our environment.
INTROCEPTION tells us? |
Intero = sense of internal self
ie, pulmonary stretch receptors preventing us from holding our breath for too long. Peripheral chemoreceptors monitoring gasses. Stretch receptors in GI tract. FASCIA is the largest interoceptor in body. |
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Proprioreceptive imbalances may occur d/t to TrP:
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IMBALANCE
DIZZINESS TINNITUS = 1-3 trigger points of head and neck, esp. of mm of mastication DISTORTED perception of the WEIGHT of objects lifted by hand [SCM] |
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When a patient's TOTAL PAIN PATTERN compromises overlapping patterns from different mm, the extent of the pattern exceeds that of any one mm. [additive in nature]. This is called a ________ Pain Pattern.
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COMPOSITE pain pattern (overlapping, additive)
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If MORE than one mm refers to the same area, the area of referral may be LARGER and will also be more _______ than if produced by a single mm.
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PAINFUL
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Any one of the 3 trigger points in the _________ can reproduce any part or all of the pain referral pattern.
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ILIOPSOAS
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Trigger points have a TYPICAL response (3) to therapy that let you know they are, in fact, trigger points:
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1. Immediate DISAPPEARANCE of SPOT tenderness, REFERRED pain, and local TWITCH/ w/ a release of the mm's RESTRICTED motion
2. MOIST HEAT applied after therapy gives extra ROM, reducing post-therapy soreness 3. Relief lasts longer if tx mm are moved through MULTIPLE cycles of ACTIVE ROM directly after. |
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Rectus femoris is susceptible to TrP's when
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there is a sudden, vigorous ECCENTRIC contraction
will feel like RETRO-PATELLAR pain |