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DPT 730: MSK > Shoulder Complex I and II: Test 3 > Flashcards

Shoulder Complex I and II: Test 3 Flashcards

1
Q

what are the normal dominant side asymmetries

A

ips shoulder depression
less IR
ips thoracolumbar SB and RT
hyperextended knee
flat foot

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2
Q

functional ROM for: washing, donning shirt, reaching high shelf, and fastening bra

A

washing = 120 flex (hair) and 75 (trunk)

shirt = 90 flex

high shelf = 150 flex

bra = 50+ ext, 70 horizontal add, and full IR

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3
Q

movement of humerus is accompanied by

A

scapula

AC

SC

upper thoracic

upper costotransverse

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4
Q

importance of companion motions of shoulder complex

A

Optimal motion
prevents impingement
keeps actin/myosin overlap efficient (prevents active insufficiency)

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5
Q

humerus motions with overhead reach 0-150

A

FLX/ABD/ER

concentric control of flexors, abductors, and ERs

eccentric control of opposite muscles

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6
Q

scapula motions with 0-150 overhead reach

A

elevation, upward RT, and protract around AC

concentric control of elevators, up RTs, and protractors

eccentric of opposite

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7
Q

when is there max tension on the brachial plexus with overhead reach

A

at 150 degrees as clavicle posteriorly rotates

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8
Q

what are the motions of the humerus with 150-200 overhead reach

A

FLX/abd/ER

same muscle actions as below 150

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9
Q

motions of the scapula with 150-200 overhead reach

A

depress/retract/post tilt around SC

concentric control of these above muscle groups especially LT if there is 150 degrees of motions with GH and ST motion and upper T spine ext

eccentric = opposite

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10
Q

how does the upper t spine move with 150-200 overhead reach

A

ips SB and RT

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11
Q

why is it important motion at the upper T spine is unilateral with overhead reach

A

triggers concentric control of LT along with subclavius for scap and clavicle motions

prevents excess tension on brachial plexus by limiting more post clavicular RT

hypo mobility leads to GH and AC joints becoming hyper mobile to compensate

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12
Q

upper T spine hypomobility causes what

A

inhibits LT (up RT and depression) = impaired scap motion

compensatory motion at AC and GH

excessive posterior clavicular RT and tension on medial cord of brachial plexus (median and ulnar n paresthesias)

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13
Q

movements of humerus with reaching behind back

A

hyper ext/ADD/IR

concentric control = hyperextenders, adductors, and IRs

eccentric = opposite

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14
Q

movement of scapula with reaching behind back

A

elevation/Down RT/retract

concentric control = elevators, down RT, and retractors

eccentric = opposite

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15
Q

JMs effectiveness for shoulder injuries

A

useful for a variety of common RC disorders, shoulder disorders, adhesive capsulitis, and soft tissue disorders

applied to shoulder complex joints

effective intervention with or without exercise and or multimodal therapy

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16
Q

more recent systematic reviews of RC tendinopathy say what

A

do not rely on manual therapy alone

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17
Q

TherEx effectiveness for shoulder interventions

A

good for various shoulder conditions

effective as an intervention

no added benefits with STM was added with nonspecific shoulder pain, ROM and function

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18
Q

MET order and emphasis for shoulder complex

A
  • tight grip RC muscles
    -ER during exercises when you can (better scap muscle activation)
    -Local muscle activation (RC and scap)
    -prone scap exercises
    -Ex on both sides (motor cortex activity)
    -Global muscles
    -higher level goals (i.e. LE and multiplanar ex)
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19
Q

how can serratus anterior be better activated

A

closed chain activities

wall slides = lower activation of LT/MT/LS/RM

advance to UE weight shifts, push ups, off/on unstable surfaces

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20
Q

why are prone scap exercises good? examples?

A

limit compensation of UT and activate more needed muscles

I, T, W, Y

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21
Q

compare the effectiveness of JM and TherEx

A

combo of both was as effective as TherEx alone

one isnt conclusively better than the other

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22
Q

is exercsie or MT more beneficial for RC tendinopathy

A

exercise

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23
Q

effects of cervical manipulation

A

diminished severity if shoulder pain

improved shoulder and neck mobility

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24
Q

effectiveness of C5-C6 JM

A

immediate increase in muscle strength of the ERs

carry over for 10 minutes but not after 20 minutes

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25
Q

evidence of what conditions may be high indicators for a future shoulder problem

A

cervical trauma
cervical hyper mobility/instability
age related neck changes
prolonged FHP

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26
Q

why it is important to minimize FHP

A

thoracic extensors overwork to compensate for excessive flexion and decreased diagram fxn

thoracic stiffness develops

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27
Q

dry needling support for non traumatic shoulder pain and disability

A

moderate quality of evidence of a small and short term effect

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28
Q

4 positive factors fro those referred to PT with shoulder pain

A

lower baseline disability
lower symptoms at rest
high pt expectation with PT
higher self efficacy despite symptoms

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29
Q

what is impingement syndrome

A

aka subacromial pain syndrome

cluster of symptoms

doesn’t indicate definitive signs/cause

44-65% all shoulder complaints

30
Q

pathomechanics of impingement syndrome

A

sub and coracoacromial space compromised resulting in impingement or compression of tendons

increased tension on tendons when loaded and as they wrap around the bone it results in compression

31
Q

how is the supraspinatus tendon involved in impingement syndrome

A

most commonly involved

tendiopathy

can tear gradually

the limited vascularity in the distal supraspinatus affects healing

32
Q

how is the biceps tendon involved in impingement syndrome

A

may gradually tear

tendinopathy

33
Q

how are the labrum and subacromial bursa involved with impingement syndrome

A

labrum may gradually tear

subacromial bursa can develop bursitis

34
Q

primary cause/pathomechanics of impingement is limited motion. This can be caused by

A

trauma with fibrotic capsule

disuse/immobilization = muscle inhibition/shortening

persistent FHP

regional interdependence

spurring/hooking of acromion

35
Q

secondary cause of impingement is hyper mobility. This is caused by what

A

trauma/adj joint hypo mobility

disuse/immobilization = muscled inhibition limiting stabilization

regional interdependence

36
Q

regional interdependence associated with secondary impingement syndrome leads to what

A

insufficient shoulder stabilization

proprioceptive impairments greatest at higher elevations

kinesthetic impairment is greater than proprioceptive so emphasize coordination

37
Q

how is impingement a combo of hyper mobility and hypomobility

A

scapular hypo mobility and GH hyper mobility

38
Q

what is posterior superior glenoid impingement

A

more common in overhead athletes

ER ROM and ant GH glide are typically excessive

impingement that occurs at the posterior superior glenoid on the labrum

39
Q

typical age, pain pattern, and reversibility of stage I impingement

A

age = less than 25 is most common; any is possible

worse with > 90 elevation

it IS reversible

40
Q

typical age, pain pattern, and reversibility of stage II impingement

A

age = 25-40

pain = with all ADLs and sleep

not fully reversible bc of tissue changes

41
Q

typical age, pain pattern, and reversibility of stage III impingement

A

age = > 40

pain = persistent/repetitive

not reversible; tissues are degenerative; tendinosis

42
Q

symptoms of impingement

A

varied

pain typically at tip of shoulder and referred to lateral shoulder/arm

pain/limits with elevation, pushing, lifting, pulling, reaching behind back

can become nociplastic

43
Q

observation signs with impingement syndrome

A

scapular compensations possible (increased elevation and possible increase or decrease with upward RT)

44
Q

what symptoms alteration tests are reliable with the scapula

A

scapular assistance test - passive up RT

scap repositioning test - passive up RT and post tilt

scap retract test - voluntary retraction

taping for LT assistance

45
Q

function/ROM signs of impingement

A

limited/painful reaching overhead and behind

ROM often worse with FLX, ABD, and ER but IR can be too

post shoulder pain with ER indicates posterior impingement

46
Q

signs with resisted/MMT with impingement syndrome

A

inhibited scapular and cuff muscles

most scap muscle groups except elevators

proprioceptive impairments greatest at higher elevations

47
Q

AM test results with impingement

A

primary = hypomobile (especially with posterior glide)

secondary = hypermobile

48
Q

special tests for impingement

A

GIRD ratio > 1

infraspinatus or ER test in 0 degrees ABD = P!/giving away

IR resisted strength test if IR is weaker than ER at 90 abd

49
Q

RC pathology prevalence in MRI related to age

A

youngest = 32%

middle = 48%

Oldest = 78%

RC pathology not associated with impingement syndrome

50
Q

what is a tendon made out of

A

dense regular connective tissue

type I collagen

low elastin

fibrocytes

parallel fibers for more unidirectional loads

51
Q

what do tendons resist/release

A

resist tension and release energy with muscle action

more stiffness = better force transmission or storing potential energy

52
Q

describe the mid portion of a tendon

A

hypo vascular and hyponeural

53
Q

describe the insertion of a tendon

A

hyper vascular and hyperneural

54
Q

prevalence of tendinopathy

A

30% of general MSK injuries

30-50% of sports injuries

55
Q

what is tendinitis and what is the prevalence

A

inflammation of tendon without structural changes due to overuse

uncommon

56
Q

S&S of tendinitis

A

acute and classic presentation

tender to palpation

pain/limit with lengthening

pain with resisted test/MMT especially in lengthened portion

57
Q

what is tendinosis

A

most common tendinopathy

degenerative changes with some inflammation

58
Q

what can tendon inflammation with tendinosis be due to

A

repetitive stress and tendinitis

impingement pathomechanics

neural/vascular insufficiency

exercise induced hyperthermia

older age

hormonal fluctuation

59
Q

symptoms of tendinosis

A

acute irritation = tendinitis S&S

persistent (>4-6 wks) often with previously failed PT

dercreased tendon tolerance

mislabeled as tendinitis and treated as such

60
Q

signs of tendinosis

A

enlarged tendon

ROM possibly painful and limited with lengthening if aggravated but may be WNL

resisted/MMT possibly limited if acute but also possible WNL

no association with strength deficits and tendinopathy

61
Q

palpation signs with tendinosis

A

localized TTP with decreased pain threshold

increased in growth of vessels/nerves

elevated pain neurotransmitters

SO ROM and resisted/MMT can all be WNL but still very TTP

62
Q

pathogenesis of tendinosis

A

little to no inflammation

fiber changes seen on imaging

corticospinal (voluntary movement) influences

sounds similar to neoplastic pain

63
Q

what fiber changes are seen with tendinosis

A

degeneration and disorganization

causes weakening and greater likelihood of overload

increased non-collagen matrix

fatty infiltration

64
Q

describe corticospinal influences of tendinosis

A

increased inhibition

increased excitability (abberant/excessive firing)

bilateral influence

65
Q

what can cause a rare type of tendon tear

A

higher and oblique forces during fast eccentric loading

happens with prior degeneration or tendinosis

66
Q

how do tendon tears occur with age and disuse

A

elastin and vascularity decrease

atrophy and drying

shorter and smaller tendons are less pliable/durable

67
Q

when does tendonitis inflammation generally resolve

A

at most in 4-6 weeks

68
Q

primary focus with tendinosis and tendon tears

A

proliferating tendon

69
Q

tensile strength of tendons initially approves when? when does even greater strength occur?

A

initially at 3-5 weeks

even greater hen dense fibrous tissue fills in at 8-12 weeks

70
Q

what tears can/can’r be improved with PT

A

partial tear can improve with PT

full tear will require sx

10-12 months post op to regain normal strength after a tear

DPT 730: MSK (14 decks)

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