Week 4: Multifactorial/Multicomponent MSK conditions Flashcards
What aggravates PFP
tasks that increase patellofemoral joint loading
such as
- jumping, running, squatting, stairs, prolonged sitting
Differentials for PFP
chrondomallacia patella patellar tendinopathy osgood schlatters sinding larsen-johansson's disease bursitis pleural of neuromas intra-articular pathology plica syndrome
What is the most common alternative diagnosis to PFP
patellar tendinopathy
How to differentiate between PFP and patellar tendinopathy
Onset
running, stairs, WB knee flexion vs jumping, change direction, stairs
pain
nonspecific, vague vs patella inferior pole
Aggrav
activities that load PFJ vs jumping, early to mid squat
Inspection
normal or VMO wasting vs general quads wasting
TOP
medial, lateral patella facets, inf patella or non vs inferior pole and possibly tibial tuberosity, rare mid tendon
Swelling
occasional vs tendon thickening
Differentiation #2
click, clunks and crepitus
give way = occasionally
knee ROM = normal, reduced in severe cases vs normal with OP
Quads concentric contraction = normally no pain but not quality vs possibly painful
PFJ= potential restriction any direction but commonly medial vs normal unless combined with PFPS
VMO =potential for weakness & deficits in tone and timing vs general quads weakness
function = stairs & squats may aggrav, PFJ taping decreases pain vs decline squat aggravtes, PFJ tape less effect
Extrinsic factors that lead to PFP
excess training load
altered training surface
incorrect footwear
intrinsic factors that lead to PFP
gender weak medial tight lateral torsion of the femur /tibia eversion of the foot larger Q angle sulcus sign patella tilt decreased abduction strength of the hip and decreased ER strength of the hip lead to lower knee peak extension torque
Proximal treatments of PFP
hip abductor and ER strengthening
Distal treatment for PFP
orthoses
Local treatment for PFP
taping
PF mobes
vasti retraining
what is considered gold standard approach to treatment for PFP
multimodal approach including taping vasti retraining gluteal strength patella mobes and stretches
Sum up conservative treatment success for PFP
high success rate short term but long term is questionable
what is the role of supraspinatus
superior role of HOH
compresses HOH into glenoid fossa
restricts excessive superior translation of humerus
role of infraspinatus, teres minor and subscap
depression force on HOH
Role of infraspinatus and teres minor together
externally rotate humerus
Primary external impingement is
abnormalities of superior structures encroach into subacromial space
undersurface of the acromion may be beaked, curved, hooked
thickening of the coracoacromial arch or osteophytes on inf AC joint in older populations
Secondary external impingement includes
excessive angulation (anterior tilt and IR) of acromion due to inadequate muscular stabilisation of scapula in younger athletes - altered activation patterns or strength imbalances (eg. deltoid vs RC)
RC tendons weakened by large volumes of activity
Internal impingement is
occurs mainly in overhead sportspeople during late cocking stage of throwing (ext, abd+ER)
RC undersurface impinged against posterosuperior glenoid surface
may become pathologic due to repetitive trauma/overuse and injury to superior labrum
Tendinopathy development involves
tendon becoming swollen and hypercellular
collagen matrix disorganised and tendon is weaker
increased vascularity and nerve density
volume is major determinant
3 stages of tendon pathology
tendon pathology continuum
reactive tendinopathy
- non-inflammatory proliferative response
- acute overload
tendon dysrepair
- similar, but greater matrix breakdown
- chronic overload
degenerative
-progression of both matrix and cell changes/breakdown
areas of cell death
Ageing or chronic overload
clinical presentation of supraspinatus tendinopathy
complaints of pain with overhead activities
activities <90 degrees may be pain free
ER can be a problem
possible Hx of associated symptoms of instability including recurrent subluxation
Episodes of dead arm
night pain is extremely common
difficulty sleeping
symptoms may be reproduced with impingement tests
EOR passive flexion - symptomatic
Resisted supraspinatus contraction
- resisted upward movement in 90 degrees abduction, 30 degrees horizontal flexion +IR
MRI = investigation of choice to determine presence of partial tears
treatment of supraspinatus tendinopathy #1
avoid aggrav activities
Ice
single corticosteroid injection
treatment of supraspinatus tendinopathy #2
correction of abnormalities GH instability Muscle weakness or imbalance ST tightness Impaired scapulohumeral rhythm Training errors
Exercise therapy for the shoulder
the shoulder is highly muscular dependant
muscle recruitment patterns, coactivation and force couples are vital for normal function
minimise pain to avoid pain inhibition
- pain relief is a key to success
Exercise rehab for supraspinatus tendinopathy can include
addressing decreased rotator cuff strength or imbalance
- target ERs
Restore correct SH rhythm
Stretching of the posterior capsule + Tx spine mobilisation
Closed chain exercises can be used in supraspinatus rehabilitation, what are the suggested parameters
proximal to distal sequencing allows optimum force generation
safe muscle loads and activation levels
decreases tensile stresses on ligament and tendons
enhances proprioceptive function
provides stability to the ST joint
force closure to the GH joint
abnormalities along the kinetic chain must be identified and corrected
- training errors such as technique and overuse should be corrected-
Plyometrics for supraspinatus rehabilitation
development of power
utilise stretch-shortening cycle
heightens excitability of nervous system
goal is to decrease amortization time phase
What is a SLAP lesion
due to excessive traction through labrum via LH biceps
extend from ant to biceps tendon to posterior to tendon
stable or unstable depending on amount of superior labrum and LH biceps tendon firmly attached to glenoid margin
4 types - classification
Non-Slap
- degenerative, flap and vertical labral tears, Bankart lesions, Hill-Sachs
the 4 types of SLAP lesions are
Type 1: attachment of the labrum to glenoid attached but fraying and degeneration present
Type 2: lesions with detachment of Sup labrum and LH biceps tendon from glenoid rim
Type 3: meniscoid superior labrum torn away & displaced into joint but tendon & its labral rim attachment intact
Type 4 : tear of sup labrum extends into tendon and these are displaced into joint
Clinical presentation of glenoid labrum injuries
Hx - often MOI or excessive traction on labrum via LH biceps
Pain in posterior or posterosuperior joint line esp in abduction
pain increased by overhead and HBB positions
popping, catching, grinding
TOP ant shoulder
pain on resisted biceps contraction
dynamic labral shear test +ve
MRI often unnecessary with combination of clinical tests more sensitive
Treatment of glenoid labrum injuries
conservative Mx is generally unsuccessful except in extremely minor cases (always SLAP type 1)
-if so, avoid heavy weights
surgical repair generally indicated
-arthroscopic SL repair +/- debridement
Post surgery - exercise program - no gold standard
Evidence on rate of return to participation post surgery is in consistent
- return to pre injury levels of participation in athletes that perform overhead activities consistently lower than non-throwing/non overhead athletes
