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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
elongation created by imposed load that has a reversal when load removed
ELASTIC stretch

*visco-elasticity
What are the qualities of ELASTIC stretch?
When a temporary change in length provides:
extensibility
retractability
spring-like behavior
tensile load creates NO REVERSAL when load removed.
VISCOUS or plastic (moldable)


*PERMANENT putty
Tissues w/ both ELASTIC & VISCOUS PLASTIC
VISCO-ELASTIC
VISCOUS tissues allow either
plastic or permanent deformation
Elastic properties allow for ___________ deformation (returning to original length)
RECOVERABLE
loads/stress can be unidirectional, meaning deformation along multiple vectors

ie:
LENGTH & SHAPE change
3 factors determining if ELASTIC vs. VISCOUS PLASTIC dominates:
1. AMPLITUDE of force
2. SPEED of application
3. DURATION of application
What determines the dominating STRETCH?
FORCE & TIME determine whether it will result in an elastic (recoverable) stretch or a permanently deformed viscous plastic putty state.
The condition of the muscle _________ will change the O&I length, resulting in HYPO or HYPERtonicity.
ANTAGONIST

the opposition has a say!!!
SHORT
ELASTIC
LONG
VISCOUS
LOW
ELASTIC
HIGH
VISCOUS
SLOW
ELASTIC
RAPID
VISCOUS
SHORT
LOW
SLOW
ELASTIC
LONG
HIGH
RAPID
VISCOUS
Not only can a high amplitude, rapidly applied force cause un-recoverable change, it can lead to tissue _________
FAILURE
If no tearing occurs when CT structures are PERMANENTLY lengthened, there will at least be some
MECHANICAL WEAKENING
What procedure produces more structural WEAKENING because of its high amplitude, rapid application?
PFS

(Please Fucking Stop) is sometimes necessary to break the cross-linked adhesions of collagen caused by IMMOBILIZATION
IMMOBILIZATION
1.
2.
Loss of WATER [turgor]
CROSS-LINKING ADHESIONS

*do PFS (high amp, rapid app)
CREEP
VISCOUS GIRLS GONE WILD

*Progressive plastic deformation of proteinaceous tissue under a sustained load OR SUSTAINED LACK OF LOADING
Progressive plastic deformation of proteinaceous tissue under a sustained load OR SUSTAINED LACK OF LOADING
CREEP

Use it or lose it, creep.
The gradual rearrangement of collagen, proteoglycans and the loss of turgor.
CREEP

Use it or lose it, creep.
Effects of CREEP vary with
AGE

RESPONSE TO INJURY/DISEASE
CREEP commonly seen in
ADL's or REPETITIVE motion occupation

ABNORMAL POSTURAL SYNDROMES [upper & lower crossed]

HABITS of living
HYSTERESIS
LOSS OF ENERGY in viscoelastic tissue DUE TO CREEP having already happened
POST creep change
HYSTERESIS
A change in the BEHAVIOR of the tissue
HYSTERESIS

Post creep can be due to CONTINUOUSLY APPLIED load OR REPETITIVE cyclic LOADING & UNLOADING over time
Once _________ has set in, the deformation has become PERMANENT.
HYSTERESIS
SET
the difference or change in LENGTH OR SHAPE that a tissue has undergone FROM its original

*AFTER creep and hysteresis have already happened
CHS
Creep Hysteresis Set

*Denial Bargaining Resignation
Can SET be reversed?
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.
largest single organ in body
SKELETAL mm

40% of body weight
Largest CONSUMER of energy
Impairment has extensive implications
SKELETAL mm.

*waste disposal, heat production, pumping of blood and lymph all mm. jobs so all affected if mm. are impaired.
Functions of SKELETAL mm
MOVEMENT of joints
PROTECTION of joints
POSTURE
HEAT
Injury of muscle results in:
FIBROSIS w/in surround fascia

LOSS of EXTENSION & RETRACTION (elasticity and strength)

JOINT DYSFUNCTION
OBSERVE muscle to assess
CONTOUR & SYMMETRY
PALPATE mm to assess
INTERNAL ARRANGEMENT [fibrous nodes, taut bands]

TONE: Consistency~Flexibility~Response
Describe a normal muscle
Think 25 year old female (yeah, this is a transitory state so enjoy it):

SUPPLE, FLEXIBLE, SMOOTH, MODERATELY FIRM, **PAIN-FREE!
INDICATORS of ABNORMAL mm. tissue:
Palpable NODULES
Taut and tender BANDS
FIBROSIS
ROPINESS
MOTOR UNIT
single ALPHA motor neuron and ALL the SKELETAL mm. fibers it innervates.

Avg = 180 per
Range 3-2000 fibers per.
MOTOR UNIT = average is 180
MYOTACTIC UNIT
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
3 components of a MYOTACTIC unit
AGONIST

SYNERGIST

ANTAGONIST
The result of a continuous, random stream of nerve impulses from the spinal cord (LMNs)
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
2 components maintain muscle TONE
GAMMA motor cortex go thru anterior motor neurons to pyramidal and extrap. tracts tell body to remain upright.

Muscle SPINDLES detect changes in length
The principle that at any given time, some mm fibers are contracted and others are relaxed
ASYNCHRONOUS firing

Don't shoot your wad all at once. NO motor unit can fire continuously (that would be tetany then death!)
occurs when mm of OPPOSING function develop ALTERED levels of RESTING TONE relative to one another
mm IMBALANCE

*these mm are susceptible to TrP formation
TrP
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.
occurs when mm of OPPOSING function develop ALTERED levels of RESTING TONE relative to one another
mm IMBALANCE

*these mm are susceptible to TrP formation
Kind of motor neurons that send information from anterior horn to periphery
LOWER motor neurons
a state of readiness to CONTRACT
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
occurs when muscles of OPPOSING FUNCTIONS develop ALTERED levels of resting tone, relative to one another
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)
Name 3 reasons muscle imbalance occurs:
Sustained loading
Constrained postures
Repetitive tasks
Lack of activity and VARIETY of motion
Gravity
Familial modeling *
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
The longer a person allows muscle imbalance, the greater the likelihood of recruiting more?
MOTOR UNITS >>> CREEP

*leading to greater effort needed to reverse
When a mm develops INCREASED resting tone, it is
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
FACILITATION
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).
a heightened state of readiness
FACILITATION [hypertonicity]

Code Orange. We were in a constant state of FACILITATION under George Bush, Jr.
ADAPTIVE shortening
CHRONIC facilitation

ADAPTIVE = CHRONIC (can't beat'em so you join'em)
Does a hypertonic muscle have to have a spasm?
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.
ADAPTIVELY shortened mm develop
ADHESIONS [loss of water/turgor]
How is ADAPTIVE SHORTENING reversible?
STRETCH

*not strength. Duh, this would shorten the mm again. You must break the pattern of FACILITATION (hypertonic state)
What do you have to do to a mm that is ADAPTIVELY SHORTENED?
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.
INHIBITION
HYPOtonicity = inhibition is a compromised state of readiness. A dullness. Too stretched over too long at time = STRETCH WEAKENED

May also have developed ADHESIONS
Hypertonic mm lose
EXTEND ability
Hypotonic mm lose
RETRACT ability

*can be taut or not
_________ must be distinguished from SPASM
IMBALANCE

*imbalance = usually abnormal postural alignment, alteration of contour, plumb line test fail.
*confirm via PALPATION, LENGTH TESTING, FUNCTIONAL TESTING of movement patterns
What could be the most important factor of IMBALANCE of mm patterns?
FAMILIAL PATTERNING
POSTURAL mm
OVERUSED

FACILITATED (HYPER)

ADAPTIVELY SHORT (more perimysium)
TONIC mm
are postural mm that maintain erect standing against gravity
Name the mm ADAPTIVE SHORTENING tendencies:
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
mm that tend toward STRETCHED WEAKENING
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
Recognizable patterns of imbalance
1. LOWER CROSSED
2. UPPER CROSSED
3. LAYERED {after multiple episodes of lower back pain}
4. FORWARD HEAD CARRIAGE
an increase in DIAMETER of muscle cells and NUMBER of myofibrils
HYPERTROPHY

The Hulk
a related increase in ATP, phosphocreatinine, glycogen
a decrease in size of fibers and number of myofibrils
ATROPHY

Disuse from a hospital bed...caused by IMMOBILIZATION and/or DE-NERVATION
Can a muscle be re-enervated after disuse atrophy from immobilization has set in?
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
INVOLUNTARY CONTRACTION in response to nerve IRRITATION, INJURY or other COMPROMISE (ie, a large # of motor units firing)
SPASM

Ca++
Mg++
HYPOTHYROIDISM
STATIN DRUGS
dystonia = writer's cramp, epilepsy, low Ca++ tetany, low electrolytes, myoclonus, MS, Parkinson's, Alzheimer's, alcoholism, DEHYDRATION
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
TREATMENT for spasm:
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
How to D/DX between PRIMARY & SECONDARY SPASM?
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)
When the trigger point is the PAIN GENERATOR
MYOFASCIAL PAIN SYNDROME of the _________ MUSCLE

*Pain and/or autonomic phenomena referred from active MFTP and associated w/ muscular dysfunction
MYOFASCIAL TRIGGER POINT
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.
What is the quick def of a MFTP?
PREDICTABLE
REPRODUCIBLE
REFERRED PAIN PATTERN that doesn't follow myo/dermatomal pattern
Area of pain of trigger point REFERRAL:
REFERENCE
The REFERENCE POINT of tp referral is either called:
SOLID - ESSENTIAL

SPILLOVER - STIPPLED
TP REFERRAL PATTERNS are, according to this class, :
PREDICTABLE & REPRODUCIBLE
TP's are NOT _______ but may be found near them.
not motor points
TP's may be found in sundry tissues (cutaneous, ligamentous, periosteal) but distinguished from
MYOFASCIAL trigger points
ACTIVE trigger points
Refers to whether muscle AT REST or IN MOTION:
Always TENDER
PREVENT full lengthening of mm
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
LATENT [vs. active] trigger point
NO spontaneous pain = MUST be COMPRESSED to refer or cause pain
SATELLITE trigger point (vs active and latent)
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!
SECONDARY tp becomes active because it's muscle was OVERLOADED while...
acting as a SYNERGIST or ANTAGONIST of a muscle with an active tp.
Which is more common, LATENT or ACTIVE trigger points?
LATENT [the kind that only refers or has pain if you compress it, titch at it]
Are trigger points (mostly latent) more common in males or females?
Females

*in old age, no difference
Pain of trigger points increases in likelihood as well as in frequency as
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.
With advancing age, STIFFNESS and DECREASED ROM become more prominent than...
pain
Studies show chief complain of pain turned out to be myofascial tp in ___% of the patients
85-95%
A trigger point can be SATELLITE & SECONDARY, for example:
iliopsoas can cause LBP and anterior thigh pain similar to rectus femoris pain
REFERRAL usually projects
DISTALLY 85% of time
Response of tp to SNAPPING palpation?
TWITCH
What is the characteristic of a tp to PALPATION?
SPOT TENDERNESS
Are trigger points predictable and reproducible?
Yes (sigh)
Where are tp's most often found
TAUT FIBROUS BAND that is palpable in the muscle
Histological changes to mm w/ a trigger point?
NONE

PHYSIOLOGICAL signs are due to **OXIDATIVE stress** (inadequate ATP for the higher than usual demand)
Pain from a tp can occur either at AT REST OR IN MOTION, but is exacerbated by
PASSIVE STRETCHING (lengthening)
Severity and extent of the tp does NOT correlate w/ the _____ of the muscle.
size
Where is pain often referred when a muscle has a trigger point?
to the JOINT moved by that muscle

ie, infraspinatus and subscap refer deeply to glenohumeral joint
What is the only mm in the body that attaches to the anterior aspect of the spine?
Longus coli
Some referral patterns are ______, while some are very extensive
local
What 5 things can directly activate a TrP?
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
Trigger points can be activated by OTHER trigger points (2):
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
Trigger points can be activated by _______ DISEASE
VISCERAL
TrPs can be activated by ________JOINTS
ARTHRITIC
TrPs can be activated if the mm gets too ________
CHILLED/COLD during post-exercise stiffness
Holding a mm in a _________ position over time can activate a TrP.
SHORTENED
What kind of ILLNESS can cause Trps?
VIRAL

*shingles, influenza
Intensity of a TrP can vary from day to day, even hour to hour, but stiffness & weakness is GREATEST after __________.
INACTIVITY

*upon awakening in the morning, sitting in one position over time
What are some AUTONOMIC phenomena that can occur from TrP's?
1. Local VASOCONSTRICTION
2. SWEATING
3. TEARING [mm. of head and neck]
4. SALIVATING
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.
Proprioreceptive imbalances may occur d/t to TrP:
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]
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.
COMPOSITE pain pattern (overlapping, additive)
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.
PAINFUL
Any one of the 3 trigger points in the _________ can reproduce any part or all of the pain referral pattern.
ILIOPSOAS
Trigger points have a TYPICAL response (3) to therapy that let you know they are, in fact, trigger points:
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.
Rectus femoris is susceptible to TrP's when
there is a sudden, vigorous ECCENTRIC contraction

will feel like RETRO-PATELLAR pain