Posture and Movement Dysfunction

Question 1

What are the prerequisites of Posture?

Answer 1

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)

Question 2

Posture is effected by what?

Answer 2

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.

Question 3

Alignment is ?

Answer 3

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

Question 4

Alignment assumes that controlling elements are?

Answer 4

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

Question 5

Movement strategy is important for alignment why?

Answer 5

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

Question 6

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

Answer 6

it should result in less wear and tear.

Question 7

What are the different functions a muscle may have?

Answer 7

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

Question 8

what are the three ways that muscles act?

Answer 8

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

Question 9

What are the characteristics of sway back posure?

Answer 9

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

Question 10

what are the characteristics of Kyphosis Lordosis posture?

Answer 10

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

Question 11

Discuss Sarhmans model (kinesiologic) of movement?

Answer 11

• 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

Question 12

kinesopathologic Model?

Answer 12

• 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

Question 13

how might atrophy be observed?

Answer 13

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

Question 14

muscle length increase dysfunction is?

Answer 14

• 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??)

Question 15

muscle length shortness dysfunction?

Answer 15

• 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)

Question 16

increasing series length (sarcomeres) is useful?

Answer 16

• 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

Question 17

Nervous System mediated dysfunction is what?

Answer 17

• 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

Question 18

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

Answer 18

muscle roles as being

1. stabilisers - “postural”/”tonic”- role is genetic

• one joint/assist postural holding-anitgravity, stability
• tend towards overactivity - loss of extensibility

2. mobility - “phasic”

• multi jt, assist rapid movt and produce high force/power - for moving the body
• tend towards inhibition/flexibility,laxity,weakness

Question 19

Jandas muscle imbalance syndromes?

Answer 19

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

Question 20

Features of local muscles?

Answer 20

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

Question 21

Features of Global muscles?

Answer 21

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

Question 22

Local muscles produce stability how?

Answer 22

• 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\

Question 23

Dysfunction of local stablisers manifests how?

Answer 23

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

Question 24

Global stability by global muscles how?

Answer 24

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.

Question 25

Dysfunction of Global stabilisers manefest how?

Answer 25

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

Question 26

Global mobility role achieved how?

Answer 26

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

Question 27

Dysfunction of global muscles for mobility manifests how?

Answer 27

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

Question 28

Muscle has low and high threshold motor units describe them?

Answer 28

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

Question 29

Pain affects muscle recruitment how?

Answer 29

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

Question 30

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

Answer 30

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

Question 31

Motion restriction is adaptive by can become pathological how?

Answer 31

* restriction → compensation →uncontrolled movement → healing → return to normal movement * restriction → compensation →uncontrolled movement →damage→pain/pathology

Question 32

what are the common causes of movement restriction?

Question 33

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

Question 34

describe the features of the Joint by Joint Model?

Answer 34

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

Question 35

what are the problems of this model?

Answer 35

* 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

Question 36

analyse a hyper mobile foot with the jt by jt ?

Answer 36

* 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?

Question 37

hypomobile ankle results in what via jt by jt?

Answer 37

* 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

Question 38

dysfunction of one joint results in?

Answer 38

* 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

Question 39

in the jt by jt knee = stable but ?

Answer 39

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

Question 40

jts work together to absorb shock and forces ie triple flexion, triple flexion test is a screen assessment test that looks at ?

Answer 40

* double leg squat * single leg squat * and a single leg landing from a 50cm horizontal hop

Question 41

why triple flexion an issue for adolescent athletes?

Answer 41

* 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

Question 42

* decribe the effect of increased femoral internal rotation?

Answer 42

* 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

Question 43

describe effects of increased knee valgus?

Answer 43

* 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.