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Osteopathic Theory > Posture and Movement Dysfunction > Flashcards

Posture and Movement Dysfunction Flashcards

1
Q

What are the prerequisites of Posture?

A
  1. It creates an optimal load on the joints/skeletal system
  2. There is a balance in length/strenght between antagonistic muscle groups
  3. Support and orientation of the body sytems such as respiratory/nervous/digestive/cirgulatory (Think how these might be comrimised by posture change)
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2
Q

Posture is effected by what?

A
  1. Age - ie disc height, rib movement/muscle atrophy/instability
  2. gender - pelvis shape - changes femur relationship to knee - posible lumbar spine postural differences between sexes - women lordosis. Breasts might change posture (weight or embarassment).
  3. enviroment - affecting how you use your body - sitting/vs active/vs over active
  4. Psycho aspects - depressed = upper crossed posture
  5. Physicality ie how you use your body.
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3
Q

Alignment is ?

A

the relationship of position of bones/semental organisation and how they are moved in relationship to each other.

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4
Q

Alignment assumes that controlling elements are?

A

Optimised ie balance of muscles/fascia that support the joint or segment.

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5
Q

Movement strategy is important for alignment why?

A

Body use can volunteerly move from optimised aligment to poor alignment - can result in over stressing of tissue beyond ability to adapt.

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6
Q

optimal movement precision = technique of body use, is useful because ?

A

it should result in less wear and tear.

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7
Q

What are the different functions a muscle may have?

A
  1. Agonists - prime mover
  2. Antagonists - resist the prime mover (may add stiffness/support to a joint i.e. useful
  3. Synergistic muscles - support primemover
  4. Fixators - provide a base of support for other muscles to work ie those muscls that support the shoulder blade so that GH movement can occur
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8
Q

what are the three ways that muscles act?

A
  1. Concentric - shortening to produce movement
  2. Eccentric contraction - resisting lengthening - antigravity
  3. Isometric contraction - maintaining length ie posture/fixators
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9
Q

What are the characteristics of sway back posure?

A
  1. lumbar slight extn
  2. Pelvis poster tilt
  3. hips hyper extended
  4. knees hyper extended
  5. Ankles possibly planter flexed if knees hyper extended otherwise fwd movement pelvis = increased dorsiflexion
  6. Shortened muscles - hamstrings - potential recurrent strain/tight QL and Erector Spinae
  7. Lengthened/weak -glutes/ext obliques/rect ab/hipflexors
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10
Q

what are the characteristics of Kyphosis Lordosis posture?

A
  1. forward head posture
  2. upper back = strong kyphosis
  3. Lower back = strong lordosis
  4. pelvis = anterior tilt
  5. shortened muscles = iliopsoas/hipflexors, lumbar ES,Upper traps
  6. lengthened muscles (weak) = hamstrings/abdominal ex obl,front of neck, upper back es
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11
Q

Discuss Sarhmans model (kinesiologic) of movement?

A
  • Movement is considered a physiological system that functions to produce motion of the body as a whole or of its component parts.
  • The functional interaction of structures that contribute to the act of moving
  • system is comprised of 4 components
  1. base - muscle/skeletal
  2. modulator - nervous system - motor/sensory cortices
  3. biomechanical - statics/dynamics -
  4. support - cardiac/pulmonary/nutrition - GIT
  • each component a necessary interdependant part of the whole system
  • movement system needs movement varied and periodic-frequent
  • to remain optimal
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12
Q

kinesopathologic Model?

A
  • movement dysfunciton → pathology/pathology → movment dysfunction
  • repeated and poor movement → dysfunction → pathology
  • repeated movement over a day → will alter the NMS system ie sit in a chair-become a chair
  • woolfs law
  • atrophy of muscle/decreased fascial support if stimulus is low/unused
  • hypertrophy if muscles/facial thickening → if required to work too much -
  • facial elasticity vs static fascial support
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13
Q

how might atrophy be observed?

A

decreased power, resisted muscle tests

less stability/control - i.e muscle cant do its job, increased chance of wear/tear

test by - movement - gait, lunge, squats, single leg stance

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14
Q

muscle length increase dysfunction is?

A
  • outside its mechanical advantage/ability to contract compromised why?
  1. strain
  2. prolonged lengthened positions
  3. sustained stretching
  • results in → overstretch weakness or an increased length following strain (or stretch adaption??)
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15
Q

muscle length shortness dysfunction?

A
  • loss of sacromeres in length - immobilisation/movement demanding a shorter position/protection injury
  • stiffness is the resistence felt to passive lengthaning due to
  1. fluid properites (thixotrophy - temp+viscosity)
  2. titin (important in the contraction of striated muscle tissues as it connects the Z line to the M line in the sarcomere, responsible for passive elasticity of muscle)
  3. hypertrophy? or (pseudo hypertrophy-increased connective tissue deposition)
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16
Q

increasing series length (sarcomeres) is useful?

A
  • if muscles are overly short and strong
  • sacromeres added via extensive stretching?
  • purpose of stretching what does it add? - depends on functional needs of the individual
  • stretching as injury prevention - contrevsersial
  • also question of neural adaption ie pattern of movement - people dont necessarily use the increased length
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17
Q

Nervous System mediated dysfunction is what?

A
  • the way muscles are recruited ie motor patterns/execution - can become faulty ie due to pain inhibition
  • dominance and synergists - ie muscles being over recruited - ie because they are attempting to stabilise when usually they are phasic?
  • muscles being shorter protect nerves
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18
Q

Janda’s model of movement is based on muscle roles they are?

A

muscle roles as being

  1. stabilisers - “postural”/”tonic”- role is genetic
  • one joint/assist postural holding-anitgravity, stability
  • tend towards overactivity - loss of extensibility
  1. mobility - “phasic”
  • multi jt, assist rapid movt and produce high force/power - for moving the body
  • tend towards inhibition/flexibility,laxity,weakness
19
Q

Jandas muscle imbalance syndromes?

A

upper x’d

  • upper Cx: hyperextended → fascilitated suboccipitals/uppertraps/Levat scap →headache/movt dysfunction
  • lower cx: flexn →faciliated SCM,Sca - inhibited deep cervicals
  • shoulder: protracted/depressed/ GH internal rotation → facilitated pec → impingement as decreases subacromial space+less dwnward rotation + endrange earlier in overhead movts
  • CT - flexn but Ts extn till T4
  • Thoracic: hyper kyphosis - inhibited low/midTrap and seratus ant. Ribs are held more in an exhalation position therefore breathing also restricted - pump/bucket - diaprhragm tight

lower x’d

  • Lumbar:hyper lordosis- inhibited abs/fascilitate QL, lumbar ext.
  • Hip Joint - held in flexn - inhibited glutes-all, fasciliated rec fem/psoas
20
Q

Features of local muscles?

A
  1. control posture - ie spine curve + intersegmental motion
  2. mechanical stiffness
  3. respond to changes in posture/changes in low extrinsic load.
  4. deep/1 jt
  5. less force but stiff
  6. control in all directions mutiplanar
  7. tonic regardless of loading
  8. no atagonists
21
Q

Features of Global muscles?

A
  1. large torque/leveraging, for rotation
  2. global muscles + intraab pressure transfer load between pelvis and throracic cage (by fascial networks+hyraulic support of lumbar)
  3. Responsive to changes in line of action/magnitude of load - ie direction important for activation
  4. deep single joint or superficial multijoint
  5. concentric - ROM, plus
  6. eccentric l- ROM limiter
  7. no translation control
  8. direction specific/antagonist influenced
22
Q

Local muscles produce stability how?

A
  • increase the muscle stiffness - control segmental motion/translation
  • control the neutral jt position
  • contraction - isometric or slight changes in legnth
  • anticpatory - active before prime movers e.g TVA BUT not if alreadly loaded
  • muscle is independant of direction of activity
  • continuous throughout movement
  • highly innervated - likely to be proprioceptive allows body to know positioning\
23
Q

Dysfunction of local stablisers manifests how?

A
  1. delayed timing or inadequate recruitment/activation
  2. reacts to pain/path by inhibition
  3. results in decreases jt stiffenss and loss of segment control
  4. neutrality of jt position compromised
24
Q

Global stability by global muscles how?

A
  1. generates force to control ROM
  2. eccentric contraction controls range
  3. BUT also a) shorten through inner ROM b) isometrically mainting jt position c) eccentric for anti grav+ hypermobile outer ROM
  4. deceleration esp axial rotation
  5. direction dependant = influenced my line of action + antagonists
  6. high threshold activation under load and speed.
25
Q

Dysfunction of Global stabilisers manefest how?

A
  1. activates and low threshold = more tonic
  2. fails to activate in inner range/iso contract/ or eccentric control of return
  3. poor rotation disassociation = lack control
  4. poor contol of hyper mobile ROM
  5. inhibited by dominant antags
  6. uncontrolled or poor movement control + strength deficit with high threshold activity
26
Q

Global mobility role achieved how?

A
  1. Generates torque for ROM
  2. concentric esp sagital plane = flexn/ext
  3. shock absorbtion via high load
  4. activity is direction dependant
  5. intermittant activity brief bursts highly Phasic
27
Q

Dysfunction of global muscles for mobility manifests how?

A
  1. loss of extensiblity of myofascia = decrease ROM that has to compensated elsewhere
  2. overactive at low threshold = more tonic
  3. reacts to pain/path via SPASM
  4. deficiencies in Sagital plane control with high threshold
28
Q

Muscle has low and high threshold motor units describe them?

A
  1. Low threshold = slow twitch =slow contraction/low force/fatique resistant
  2. High = fast twitch= fast contraction, high force,fatique easily
29
Q

Pain affects muscle recruitment how?

A
  1. guarding/spasm
  2. increase tone
  3. resulting in antagonist changes/postural changes/compensations
  4. may persist after healing as inhibition/defaciltiation
30
Q

motor restrictions are common and the body can compensate but what may result?

A

If compensation pattern is poorly controlled then microtrauma/damage pathology may result.

31
Q

Motion restriction is adaptive by can become pathological how?

A
  • restriction → compensation →uncontrolled movement → healing → return to normal movement
  • restriction → compensation →uncontrolled movement →damage→pain/pathology
32
Q

what are the common causes of movement restriction?

A
33
Q
  1. increase scar tissue/injury
  2. protective/guarding
  3. postural shortening due to habit and/or lack of movement
  4. degenerative change in jts/cartilage/bone
  5. over use
  6. hypertrophy and increased stiffness of intrinsic/local stabilisers
  7. recruitment dominance - habit overuse or past injury
  8. Behaviour/pshychology - physical expression of underlying states
  9. Enviroment/occupation factors - daily use of body
A
34
Q

describe the features of the Joint by Joint Model?

A

some joints are more for stability and others for stablity

  • ankle = mob
  • knee = stability
  • hip = mob - triaxial
  • lumbar = stability
  • thoraci spine = mob
  • Scap = stability
  • GH = mob
35
Q

what are the problems of this model?

A
  • too simple - good for screen -
  • not all jts described
  • very basic view of jts ie what about SI
  • T spine tends not to be mobile - or parts are and parts are not
  • Mobile is good but hypermobility is?
  • mobility and stability depends on the movement being performed
  • dysfunction in one area will affect another
  • no discussion of other players such as muscles/fascia and nervous system control.
  • jts need both elements of stab/mob
36
Q

analyse a hyper mobile foot with the jt by jt ?

A
  • pronation - allows more movement at ankle = increase stretch soleus/gastroc
  • mobille = need muscles also to provide control
  • pronation is not necessarily a local problem
  • instability = proprioceptive but too much control at ankle = Knee compensation
  • OA is more common at knee = knee more mobile - subject to wear and tear?
37
Q

hypomobile ankle results in what via jt by jt?

A
  • less shock absorbance
  • knee has to compensate = more movement in knee - rotatory impacts/jt laxity
  • hip become less mobile due to less movement at ankle = gait effects less hipROM
  • stiff hip + stiff ankle = more motion required at knee
38
Q

dysfunction of one joint results in?

A
  • compensation across whole body
  • e.g hyper mobile ankle = less knee stability
  • alter force transfer/posture
  • gait change
  • effects of primary function of a joint.
  • e.g limited dorsiflexion may result in back pain ie pain symptom is not primary reason
39
Q

in the jt by jt knee = stable but ?

A

knees do require movement in all planes even though limited such that those forces can be absorbed and transfered to other jts.

40
Q

jts work together to absorb shock and forces ie triple flexion,

triple flexion test is a screen assessment test that looks at ?

A
  • double leg squat
  • single leg squat
  • and a single leg landing from a 50cm horizontal hop
41
Q

why triple flexion an issue for adolescent athletes?

A
  • hipflexors become tight due to growthspurt
  • effect of this lower x’d issues - inhibted glutes/pelvic tilt/lumbar lordosis-disc facet pressure/SI jt
  • increased knee flexion at heal strike = more loading of patella tendon/ increased compressional load at contact between patella and femoral condyles = path
42
Q
  • decribe the effect of increased femoral internal rotation?
A
  • increased turning in of the femur shaft anteversion
  • decreases strength external rotators/hip adductors
  • neurological control might change ie fascilitation/inhibition - psoas/quads/vs glutes/hamstrings
  • ROM deficeit ie lack of extension of hip, or flexion of lumbar
  • tight adductors
43
Q

describe effects of increased knee valgus?

A
  • knocked knees
  • structural from tibial shape, kneck of the femur shape resulting in valgus
  • strength deficit - hip ext rot/abductors/hamstrings and quads
  • altered control of the lumbo/pelvic muscles ie fascilitated QL, inhibited external rotator,
  • abductors - trendelenburg - weak glutes esp med.

Osteopathic Theory (3 decks)

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