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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
evidence of what conditions may be high indicators for a future shoulder problem
cervical trauma cervical hyper mobility/instability age related neck changes prolonged FHP
26
why it is important to minimize FHP
thoracic extensors overwork to compensate for excessive flexion and decreased diagram fxn thoracic stiffness develops
27
dry needling support for non traumatic shoulder pain and disability
moderate quality of evidence of a small and short term effect
28
4 positive factors fro those referred to PT with shoulder pain
lower baseline disability lower symptoms at rest high pt expectation with PT higher self efficacy despite symptoms
29
what is impingement syndrome
aka subacromial pain syndrome cluster of symptoms doesn't indicate definitive signs/cause 44-65% all shoulder complaints
30
pathomechanics of impingement syndrome
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
how is the supraspinatus tendon involved in impingement syndrome
most commonly involved tendiopathy can tear gradually the limited vascularity in the distal supraspinatus affects healing
32
how is the biceps tendon involved in impingement syndrome
may gradually tear tendinopathy
33
how are the labrum and subacromial bursa involved with impingement syndrome
labrum may gradually tear subacromial bursa can develop bursitis
34
primary cause/pathomechanics of impingement is limited motion. This can be caused by
trauma with fibrotic capsule disuse/immobilization = muscle inhibition/shortening persistent FHP regional interdependence spurring/hooking of acromion
35
secondary cause of impingement is hyper mobility. This is caused by what
trauma/adj joint hypo mobility disuse/immobilization = muscled inhibition limiting stabilization regional interdependence
36
regional interdependence associated with secondary impingement syndrome leads to what
insufficient shoulder stabilization proprioceptive impairments greatest at higher elevations kinesthetic impairment is greater than proprioceptive so emphasize coordination
37
how is impingement a combo of hyper mobility and hypomobility
scapular hypo mobility and GH hyper mobility
38
what is posterior superior glenoid impingement
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
typical age, pain pattern, and reversibility of stage I impingement
age = less than 25 is most common; any is possible worse with > 90 elevation it IS reversible
40
typical age, pain pattern, and reversibility of stage II impingement
age = 25-40 pain = with all ADLs and sleep not fully reversible bc of tissue changes
41
typical age, pain pattern, and reversibility of stage III impingement
age = > 40 pain = persistent/repetitive not reversible; tissues are degenerative; tendinosis
42
symptoms of impingement
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
observation signs with impingement syndrome
scapular compensations possible (increased elevation and possible increase or decrease with upward RT)
44
what symptoms alteration tests are reliable with the scapula
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
function/ROM signs of impingement
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
signs with resisted/MMT with impingement syndrome
inhibited scapular and cuff muscles most scap muscle groups except elevators proprioceptive impairments greatest at higher elevations
47
AM test results with impingement
primary = hypomobile (especially with posterior glide) secondary = hypermobile
48
special tests for impingement
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
RC pathology prevalence in MRI related to age
youngest = 32% middle = 48% Oldest = 78% RC pathology not associated with impingement syndrome
50
what is a tendon made out of
dense regular connective tissue type I collagen low elastin fibrocytes parallel fibers for more unidirectional loads
51
what do tendons resist/release
resist tension and release energy with muscle action more stiffness = better force transmission or storing potential energy
52
describe the mid portion of a tendon
hypo vascular and hyponeural
53
describe the insertion of a tendon
hyper vascular and hyperneural
54
prevalence of tendinopathy
30% of general MSK injuries 30-50% of sports injuries
55
what is tendinitis and what is the prevalence
inflammation of tendon without structural changes due to overuse uncommon
56
S&S of tendinitis
acute and classic presentation tender to palpation pain/limit with lengthening pain with resisted test/MMT especially in lengthened portion
57
what is tendinosis
most common tendinopathy degenerative changes with some inflammation
58
what can tendon inflammation with tendinosis be due to
repetitive stress and tendinitis impingement pathomechanics neural/vascular insufficiency exercise induced hyperthermia older age hormonal fluctuation
59
symptoms of tendinosis
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
signs of tendinosis
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
palpation signs with tendinosis
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
pathogenesis of tendinosis
little to no inflammation fiber changes seen on imaging corticospinal (voluntary movement) influences sounds similar to neoplastic pain
63
what fiber changes are seen with tendinosis
degeneration and disorganization causes weakening and greater likelihood of overload increased non-collagen matrix fatty infiltration
64
describe corticospinal influences of tendinosis
increased inhibition increased excitability (abberant/excessive firing) bilateral influence
65
what can cause a rare type of tendon tear
higher and oblique forces during fast eccentric loading happens with prior degeneration or tendinosis
66
how do tendon tears occur with age and disuse
elastin and vascularity decrease atrophy and drying shorter and smaller tendons are less pliable/durable
67
when does tendonitis inflammation generally resolve
at most in 4-6 weeks
68
primary focus with tendinosis and tendon tears
proliferating tendon
69
tensile strength of tendons initially approves when? when does even greater strength occur?
initially at 3-5 weeks even greater hen dense fibrous tissue fills in at 8-12 weeks
70
what tears can/can'r be improved with PT
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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