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Flashcards

Peripheral Musculoskeletal Science

gault.kirsten English 178 cards

Cards in this deck (178)

  1. 1What is the most popular graft for ACL reconstructions?Patellar Tendon Graft
  2. 2Why is the patellar tendon graft the most popular graft for ACL reconstructions?Due to easily performed interference screw fixation and the rapid bone to bone healing to the graft
    -Less likely to fail than hamstring
  3. 3Why is the patellar tendon graft not useful-Possible OA
    -Patella Baja 5-10%
    -Decreased knee flexion during stance
    -Women and for people who kneel
  4. 4What are the negatives to hamstring recon?-Graft Laxity
    -Patellar tendon joined to tunnels within 6 weeks (compared to hamstring at 8 weeks)
    -However if fixation is standardised there are no differences in laxity
  5. 5What are the stats for recons for ACL'sFor every 100 patients 2 per year (20%) will suffer a further cruciate ligament injury regardless of patellar or hamstring
  6. 6Following a patellar graft, what are you also likely to injure?Contralateral ACL
  7. 7What are the factors that determine surgery vs. conservative management?Degree of instability
    Presence of meniscal lesions
    Patients veel of activity
    Patients age
  8. 8What is the stats for OA post ACL recon?10-87%
  9. 9What did the Mueffells' study in regards to conservative vs. surgical post ACL-Insufficient evidence to show that reconstructing the ACL is better surgically than conservative
    -Higher OA surgically
    -Higher meniscectomy surgically
    -No differences in functional outcome
    -Instability in conservative group is present
  10. 10At what time period are ACL's at their most vulnerable to tears?6-8 weeks
    The ligament is revascularising, however the pain goes so the patient is ready to go
    DO NOT LET THEM DO ANYTHING THEY SHOULD NOT BE DOING
  11. 11Why are open kinetic chain exercises not appropriate at 6 weeks?Due to the patient not being able to achieve terminal end range, therefore OKC are not appropriate
  12. 12What are the goals for weeks 0-2 for ACL-Educate and manage pain
    -Protect graft, however do not stay in bed all day
    -0-90 degrees flexion
    -co-contraction work
    -Gait progression
  13. 13Weeks 2-6 ACL recon-Educate and manage pain
    -0 degrees extension- 90-120 degrees flexion
    -improve gait
    -co-contraction
    -muscle conditioning
    -STATIONARY CYCLE
    -SWIMMING NO KICK
  14. 14Weeks 7-12 ACL recon-Educate and manage swelling
    -Near full knee ROM
    -Normal gait
    -SQUATS
    -SIDE STEPS
    -DEAD LIFTS
    -LL conditioning
    -Cycle and swimming (No kick)
    -Walk treadmill
  15. 15Weeks 13-26 ACL recon-3 hours/ week exercise
    -RUNNING
    -JUMPING
    -CONTROLLED AND CAREFUL RUNNING
    HOP
    -SQUATS
    -LUNGES
    -HURDLE DRILLS
    -Proprioception
    -Bike
    -STATIONARY SPORTS (weeks 16- gold and tennis)
  16. 16Weeks 26+ ACL recon-Running and agility
    -Fartlek training
    -Interval training
    -NM control
    -Squats
    -Swimming
    -Ski Machine
    -Team scratch match
  17. 17Functional outcome measures RTS for ACL-Single hop
    -6m hop
    -Triple hop
    -Figure 8 hop
    -Must have 100% contralateral symetry
  18. 18What is the major problem post- ACL tear-Feelings of rotational instability of the lateral tibiofemoral compartment
  19. 19What are the three types of Polar Classification of InstabilityType One- atraumatic/ structural (TUBS)
    Type Two- atraumatic/ structural (micro-trauma)
    Type Three- Musculoskeletal patterning disorder/ non-structural (AMBRII)
  20. 20What are the benefits of Polar Classification of Instability-Allows patients to be between poles
    -Recognises the stages as a continuum
    -Recognises instability as a continuum
    -Takes into account the shifting nature of pathology
    -Graduation from traumatic to atraumatic causes
  21. 21Ottawa Ankle Rules:-Top midline distal 6cm of fib or top of lateral malleolus
    -Top midline distal 6cm of tin or top of medial malleolus
    -Unable to WB at time of injury and unable to walk 4 steps
    -Top base of 5th metatarsal
    -Top of navicular
  22. 22Dorsiflexion restrictionAP glide of talus
    -Patient in supine
  23. 23Plantar-flexion restrictionPA glide of talus
    -Patient in prone with feet on bed
    -
  24. 24What joint is involved with lack of dorsiflexion/ plantar flexion for AP and PA glide of talusTalocrural joint
  25. 25Why would you perform a medial/ lateral glide of the calcaneus?Lack of eversion and inversion
  26. 26What joint is involved with medial and lateral glide of calcaneus?Sub-talar joint
  27. 27What ligament is stressed in the anterior drawer test?ATFL
    Anterior band of deltoid ligament
  28. 28What ligament is stressed in the talar tilt test?-Ankle in PG= CFL
    -Ankle in 20 degrees PF= CFL and ATFL
  29. 29Rupture to Achilles Tendon- Clinical Presentation-Pain on resisted tests
    -Irritability
    -Pain on eccentric and concentric loading
  30. 30A 30 year old man has trouble squatting 6 weeks post fractured tibia- the movement is only slightly painful and irritability is low -WHICH DIRECTIONS OF ACCESSORY GLIDE MAY BE RESTRICTED?-AP glide will be restricted (DF)
  31. 31How would you determine if a loss of ankle DF is due to soft tissue or stiffness to the jointMuscle- muscle length test
    Joint- reduced PAMS; AROM and PROM
  32. 32What is the role of the talocalcaneal ligament complexStabilises the sub-taler joint (supination sprain)
  33. 33Ligaments of antero-lateral ligamentATFL
    CFL
    Talocalcaneal ligament
  34. 34Medial ankle complexTibionavicular ankle complex
    Tibiospring Ligament
    Tibiocalcaneal Ligament
  35. 35Low ankle sprain mechanisms of injury-Supination injury
    -PF, inversion and adduction
  36. 36Pronation sprainsInjuring distal TFJ/ syndesmosis
    -deltoid ligament
  37. 37Lateral ankle sprains- why are they more commonSize and extent of ligament support- deltoid ligament is larger
    -Loose pack position of TCJ
    -Speed of NM protective response
    -Side of lateral vs. medial malleolus- the MM block inversion of the calcaneus and talus to a lesser extent that the LM block eversion
  38. 38Mild supination sprainLigaments are stretched
  39. 39Moderate supination sprainLigaments are torn slightly
  40. 40Severe supination sprainLigaments torn completely
  41. 41Grade 1 supination sprainPartial ATFL and CFL
    -10-12 days RTS
  42. 42Grade 2 supination sprainComplete ATFL and/or partial CFL
    -RTS 2-3 weeks
  43. 43Grade 3A supination sprainComplete ATFL and CFL and/or partial PTFL
    -6 weeks return to sport
    NORMAL STRESS RADIOGRAPHS
  44. 44Grade 3BComplete ATFL, CFL and/or PTFL
    10 weeks RTS
    -Stress radiographs more than 3mm of difference
  45. 45Which grade is most likely to have reinjuryGrade 1 or 2
  46. 46High ankle sprain- Ankle syndemsosis-Fibrous joint in which two adjacent bones are linked by a strong membrane
    -Realtively uncommon injury
    MECHANISMS- external rotation (pronation) of the foot or hyperdorsiflexion
  47. 47Weber A fracture-Break in the fibula
    -Below talar dome
  48. 48Weber B fracture-Medial malleolus may be broken
    -Torn deltoid ligament
  49. 49Weber C fractureAbove the level of the malleolus
    Syndemosis disrupted
    Medial malleolus fracture w/ deltoid torn
    usually requires ORIF
  50. 50Mechanisms of injury for syndemosis injuries-Forces external rotation (widening the mortise)
    -Powerful abduction
    -Hyperdosriflexion with the talus forcing the malleoli apart
  51. 51Symptoms of syndemsotic injuryFocal pain above the ankle
    May radiate superiorly
    No significant swelling or bruising
    Poor tolerance of WB
    -SQUEEZE TEST WILL SHOW GAPPING
  52. 52Four landmarks for significant swelling of ankle (oedema)1. Navicular tuberosity
    2. Distal tip of lateral malleolus
    3. Distal tip of medial malleolus
    4. Base of fifth metatarsal
  53. 53Rehabilitatio for ankle sprainEarly ankle ROM
    Proprioception day 1-2
    Local muscle strengthening
    Gradual return to function i.e. normalise gait pattern, brace, taping, return to sport is guided by pain and swelling
  54. 54Chronic ankle instability-Functional ankle instability- giving way
    -Mechanical instability- excessive inversion and/or laxity
    BOTH
    Mechanical instability, perceived instability and recurrent sprain
  55. 55CAI- clinical featuresHistory of ankle trauma
    Recurrent giving way and or ankle sprains
    Feelings of instability, hollowness or weakness
    Manual stress tests= POSITIVE
    Time in SLS- less than 26 secs
    -More than 10% difference in jump landings
    -Hopping test fails
  56. 56Talar dome fracture/ lesion -Mechanism of injury-Atypical sprain event with dominance of compression and shearing forces
    Severe pain with WB post injury
    Poor tolerance of compression
    Persistent ache at rest
    Generalised TC joint swelling
    Injury fails to resolve in expected manner
    Recurrent effusion
  57. 57Post-traumatic synovitis-Observable swelling
    -Usually mild
    -Pain at EROM
    -Focal top along joint line
    -Thickened odematous synovium at joint margins
  58. 58Medial tibial stress syndromePain at attachment of posterior compartment muscles to tibia
    Especially tib post
    Comes under the broad heading of exercise-related leg pain
    "tenoperiostial stress reaction through overt bony stress fractures of the tibia"
  59. 59Causes of medial tibial stress syndrome AKA SHIN SPLINTSIntrinsic-
    -Excessive uncontrolled pronation
    -Muscle tightness
    -Running technique
    Extrinsic-
    -High and unaccustomed training loads
    -Hard training surfaces
    -Poor footwear
  60. 60What is the most important predictor of ingoing instability in ankle sprain patients-Perceived ankle instability is more than mechanical instability
  61. 61SPRICEMMSupport
    Protect
    Rest
    Ice
    Compression
    Elevation
    Movement
    Medication
  62. 62POLICEProtection
    Optimal Loading
    Ice
    Compression
    Elevation
  63. 63Grade 1 tear what management?GraSPRICEMM and POLICE
  64. 64Grade 2SPRICEMM and POLICE
  65. 65Grade 3 tear- what management?SPRICEMM and conservative or surgical
  66. 66Plantar FasciosisNon-inflammatory stress reaction to the plantar aponeurosis of the medial calcaneal tubercle
    DEGENERATIVE
  67. 67Symptoms of plantar fasciosisGradual onset of burning sensation
    Common in running athletes or sedentary people who begin high training schedule
    Post rest stiffness
    Symptoms easing with activity
    Tender on medial calcaneal palpation
    -Loss of DF, PF
    -Calf weakness
    -Sub-optimal hip control also...
  68. 68Compartment SyndromePain secondary to the muscle and nerve schema
    -Caused by increased compartment pressure during exercise and results in poor vascular flow
    -Relieved with rest
    -TOP on compartment
  69. 69Three compartments of compartment syndromeAnterior- deep fibular nerve
    Lateral- superficial nerve
    Deep posterior- tibial nerve
  70. 70Purpose of the foot posture indexQuantifies degree of supination/ pronation
    Considers all regions of the foot (RF/STJ), mid-foot, forefoot in three planes (transverse, frontal and sagittal)
  71. 71FPI Normal score0-5
  72. 72FPI Pronated score+6-+9
    highly pronated 10+
  73. 73FPI Supinated foot-1 to -4
    highly supinated -5 to -12
  74. 74FPI criteria-Talar head palpation
    -Curves above and below the malleoli
    -Calcaneal inversion/ eversion
    -Talo-navicular congruence
    -Medial arch height
    -Forefoot abduction/ adduction
  75. 75Talar head palpationLateral- -2
    Medial- +2
  76. 76Curves above and below the malleoliCurve below the malleoli= straight -2
    Curve below the malleoli= concave +2
  77. 77Inversion/ eversion of the calcaneousInversion from achilles= -2
    Eversion from achilles= +2
  78. 78Talo-navicular congruenceTalo-navicular congruence- concave= -2
    Talo-navicular congruence- bulging out= +2
  79. 79Medial longitudinal archArch high= -2 (supinated)
    Arch very low and flat= +2 (pronated)
  80. 80Forefoot abduction and adductionNo lateral toes visible= -2 (supination)
    No medial toes visible= +2 (pronation)
  81. 81Tendinopathy (COOK)Pain
    Decreased exercise tolerance
    Reduction in function
    Repetitive energy storage and release and excessive compression appear to be key factors
  82. 82Intrinsic factors that cause tendinopathiesGenes
    Age
    Circulating and local cytokine production
    Sex
    Biomechanics
    Body composition
  83. 83Three stages of tendinopathyReactive tendinopathy
    Tendon disrepair
    Degenerative tendinopathy
  84. 84Reactive tendinopathyAcute tensile or compressive overload
    Thickening portion of tendon
    Excessive load
    Unaccustomed physical activity
    Falling directly onto the tendon
    Initial changes in ground substance
    Increased stiffness
    More common in younger people
  85. 85Imaging for reactive tendinopathyTendon is swollen in fuisform manner
  86. 86Treatment for reactive tendinopathyReduce load
    Modifcation of FITT
    Cycling
    Weight training
    NSAID's
  87. 87Tendon disrepairAttempt at tendon healing similar to reactive tendinopathy but with greater matrix breakdown
    Increase in vasculatiry and assoc. neuronal growth
  88. 88Imaging for tendon disrepairMatrix and collagen disorganisation
  89. 89Tendon disrepair clinicallyChronically overloaded tendons in the young
    However can include many ages
    Or old people with stiff tendons
  90. 90Treatment for tendon disrepairEccentric exercises
  91. 91Degenerative tendinopathyMatrix and cell changes
    Areas of cell death
    Matrix disorganisation
    Little capacity for reversibility of pathological changes
    Degenerative pathology with some normal tendon
    CAPACITY FOR HEALING IS SEVERELY REDUCED
  92. 92Imaging of degenerative tendinopathyHyperechoic regions with decreased tendon size
  93. 93Degenerative tendinopathy clinicallyOlder people
    Elite athletes with chronically overloaded tendons
    Middle-ages, recreational athlete with focal nodular areas with or without thickening
  94. 94What exercises are best for the acute stages of tendon healing?Isometric exercises
  95. 95Once a patient has begun to be less irritable with their tendinopathy, what exercises will they undertake?Eccentric (for high demand RTS) and concentric (for concentric sport deficits) exercises
  96. 96Stretch shortening training-Eccentric lengthening of muscle action with elastic energy storage
    -Concentric muscle action coupled with released of elastic
    2-5 mins of session with 2-5 days of recovery
  97. 97Examples of stretch shortening exercises:Jumping
    DL/SL trampette
    DL bunny hops
    SL hop
    Triple extensions
    Walk, jog, running
    --
    DL borad jumps
    SL hopping
    Box jumping
  98. 98Criterion for SSC trainingLate stage rehab progression
    Tolerating high-intensity tendon loading
    Low irritability
    Pain free walking
    But can begin some early form of gentle SSC if non-irritable
  99. 99In Sherry et al. study on hamstring strains who is prone to getting hamstring strains?Males more than females
    Field sports more than courts
  100. 100In Sherry et al. study on hamstring strains what are the risk factors for hamstring strains?Increased age
    Decreased quads flexibility
    muscle imbalances
  101. 101In Sherry et al. study on hamstring strains what are the likely mechanisms for injury?Terminal swing of gait
    Biceps femoris experiencing the greatest strain
  102. 102In Sherry et al. study on hamstring strains what are the best methods for reconditioning the injured hamstring?-Eccentric training
    -NM control of muscles of lumbopelvic region
    -Trunk stabilisation and NM control exercises
    -Warmup is critical
  103. 103In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 1AFatigue induced muscle disorder
    -Dull diffuse, tolerable pain in involved muscles
  104. 104In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 1BDOMS
    -Swelling, stuff muscles, limited ROM, pain on iso contraction
  105. 105In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 2ASpine-related neuromuscular disorder
    -Aching muscle firmness, increasing with continued activity
    -No pain at rest
  106. 106In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 2BMuscle related NM disorder
    -Cramp like pain, swelling, pressure pain and aching
  107. 107In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 3AMinor partial tear
    -Well-defined localised pain, palpable, stretch induce pain aggravating
  108. 108In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 3BMOderate/ partial muscle tear
    -Stabbing, sharp pain well-defined and localised
    -Patient experiences a sharp snapping sound on experience
  109. 109In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 4Sub-total muscle tear/ tendinous avulsion
    -Dull pain at the time of the injury
    -noticable tearing 'snap'
  110. 110In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS CONTUSION-Dull pain at time of injury
    -Iccreasing pain due to haematoma
    -Definite external mechanism
  111. 111According to: The association of scapular kinematics and glenohumeral joint pathologies by Ludewig and Reynolds WHAT IS SHOULDER IMPINGEMENT DEFINED AS?Compression
    Entrapment
    Mechanical Irritation of the rotator cuff structures and/ or long head of biceps tendon
  112. 112According to: The association of scapular kinematics and glenohumeral joint pathologies by Ludewig and Reynolds WHAT CAUSES SHOULDER IMPINGEMENT?1. Anatomical reductions in available space beneath the coracoacromial arch or within the supraspinatus outlet area
    2. Intrinsic tendon degeneration from eccentric overload, schema, raging or inferior tissue properties
    3. Scapular or humeral movement alterations compromising the rotator cuff tissues through sub acromial impingement
  113. 113According to: The association of scapular kinematics and glenohumeral joint pathologies by Ludewig and Reynolds WHAT CLINICAL SIGNS ARE SEEN WITH SHOULDER INSTABILITY?-Less scapular upward rotation at beginning of elevation/ faster at end
    -Significantly more scapular winging
    -Significant differences in scapulohumeral rhythm
  114. 114According to Rotator Cuff Tendinopathy by JS Lewis WHAT ARE THE MAIN REASONS PEOPLE EXPERIENCE SHOULDER PAIN?-Rotator cuff pathology
    -Sub acromial bursa
  115. 115According to Rotator Cuff Tendinopathy by JS Lewis HOW WOULD YOU DESCRIBE SHOULDER DIAGNOSIS?-High sensitivity
    -Low specificity
  116. 116According to Rotator Cuff Tendinopathy by JS Lewis WHY CANT THE CLINICAL ASSESSMENT PROCEDURES FOR ROTATOR CUFF TENDIOPATHY DIAGNOSE INDIVIDUAL TENDON OR OTHER STRUCTURES?-Morphology of rotator cuff
    -The position and innervation of sub-acromial bursa
    -Lack of correlation between symptoms and contemporary methods of imaging
  117. 117According to Rotator Cuff Tendinopathy by JS Lewis WHAT IS THE SHOULDER SYMPTOMS MODIFICATION PROCEDURE-Series of four mechanical techniques that are applied while the patient performs the activity or movement that most closely reproduces the symptoms experienced
  118. 118According to Rotator Cuff Tendinopathy by JS Lewis WHAT ARE THE FOUR CATEGORIES OR SHOULDER SYMPTOM MODIFICATION PROCEDURE?1. Humeral head procedure
    2. Changing scapular position
    3. Cervical and thoracic procedures (as structures within the spine may cause symptoms)
    3. Thoracic kyphosis technique
  119. 119According to Rotator Cuff Tendinopathy by JS Lewis WHAT ARE THE ADVANTAGES OF THE SHOULDER SYMPTOMS MODIFICATION PROCEDURE?-Recognises the inadequacy of the present method of assessment and proposes that patient management may be guided by the response to symptom modification
    -The program is graduated according to the individuals needs and aims to restore normal function
    -Flexible and capable of modification and evolution
  120. 120According to Rotator Cuff Tendinopathy by JS Lewis WHAT ARE THE DISADVANTAGES OF THE SHOULDER SYMPTOM MODIFICATION PROCEDURE?-No means for determining the origin of the symptoms
    -Lacks validity
  121. 121According to the J S Lewis' study on subacromial impingement WHAT IS SAPS?-Based on the hypothesis that lacrimal irritation leads to external abrasion of the bursa and rotator cuff
  122. 122According to the J S Lewis' study on subacromial impingement WHAT ARE THE MAJOR FINDINGS OF THE STUDY?Lacks evidence in regards to:
    -The areas of tendon pathology and accordion irritation
    -The shape of the accordion and symptoms
    -The proposal that irritation leads to the development of tendinitis and bursitis
    -Imaging changes and symptoms of the condition
  123. 123According to the J S Lewis' study on subacromial impingement STATS91% of partial thickness tears are on the inferior (articular or joint) side of the supraspinatus tendon
    9% on the superior or bursal side
  124. 124According to the J S Lewis' study on subacromial impingement WHAT IS THE EVIDENCE IN REGARDS TO POSTURE AND SAPSThere is little evidence to state that posture will lead to SAPS
  125. 125According to the J S Lewis' study on subacromial impingement WHAT ARE THE THREE TYPES OF ACROMIAL SHAPE-Type 1: Flat
    Type 2: Round
    Type 3: hooked
  126. 126According to the J S Lewis' study on subacromial impingement WHAT ARE THE TYPES OF ACROMIAL SHAPE THAT WILL CAUSE SAPSType 2: round
    Type 3: hooked
    *however studies have disproved this theory*
  127. 127What are the upward rotators of the scapular?-Lower trapezius
    -Upper trapezius
    -Serratus anterior
  128. 128What attaches to the inter tubercular sulcus?Latissimus dorsi
    Trees major
    Pectoralis Major
  129. 129What are the attachments of levator scapulae?Medial spine of scapular
    to
    T7-T12
  130. 130Contribution of supraspinatus and middle deltoid to abductionSupraspinatus- first 30 degrees of abduction
    Deltoid- remainder of abduction
  131. 131Attachments of rotator cuffSupraspinatus- superior facet
    Infraspinatus- middle facet
    Teres Minor- inferior facet
    Subscapularis- lesser tubercle
  132. 132Ligaments of glenohumeral jointSuperior GHL
    Middle GHL
    Inferior GHL
    Coraco-acromial Ligament
    -Transverse humeral
  133. 133External types of impingement-Sub acromial
    -Sub coracoid- Structures possibly impinged= subscap tendon, LHB middle GHL
  134. 134Internal types of impingement-Posterior superior impingement
    (SS or IS , RC and posterior labrum/ deep IS/ SS)
    -Anterior superior impingement
    (Subscap and biceps)
  135. 135Structures which can sub acromial pain syndrome-supraspinatus tendon
    -long head of biceps
    -superior capsule
    -superior glenohumeral ligament
    -sub acromial bursa
  136. 136Functional outcome measures to allow for testing for chronic ankle instabilityNo effusion
    Full ROM
    Pain free walking
    Normal walking gait
    Straight line running
  137. 137What are the benefits of eccentric training?Allows for heavier weight
  138. 138Extrinsic causes of shoulder region pain-Cervical spine referral
    -Thoracic spine referral
    -Heart--> Left side
    -Live--> Right side
    -Gall bladder--> right side
    -Spleen--> Left side
    -Apical lung tumors
  139. 139Why is there lack of specificity in shoulder tests?-Morphology of RC (all have one insertion)
    -Position and inversion of sub acromial bursa- richly innervated and blends with bursa
    -Weakness on testing (weakness during testing shows pain rather than actual structural pathology
    -Pain/ weakness during testing can be influenced by spinal, scapular or head position
  140. 140What is primary impingement of the shoulder?True structural narrowing leading to impingement of structures in sub acromial or sub coracoid spaces
  141. 141What is secondary impingement of the shoulder?Functional narrowing leading to impingement of structures due to:
    -Sub-topimal/ impaired RC function/ GHJ MC impairment
    -Instability
    -Hypomibility
    -Poor scapula kinematics
    -Sub-optimal postures in spine
  142. 142Sub acromial impingement- encroachment of which structures?-SA spur/ osteophytes
    -Calcified caraco-acromial ligament
    -ACJ arthropathy
    -Malunion of ACROMIAL or greater tuberosity
  143. 143Structures potentially impinged in SAPS-Sub-acromial bursa
    -SUperior GH:
    -RC tendons
    -LHB
  144. 144Symptoms of SAPS-Pain w/ overhead movements
    -Loaded shoulder IR
    -EOR
    -Pain with loading RC due to failure of RC to keep the HH centred
  145. 145Possible causes for sub-optimal RC function-Structural pathology of RC
    -Pain inhibition of RC
    -Disuse of RC
    -Disuse/ reconditioning leading to weakness or loss of endurance of RC
    -Muscle fatigue
    -Abnormal GHJ mobility leading to sub-optimal RC function
    -Sub-optimal spinal/ scpaula postures and scpaula kinematics
    -If RC is impaired--> poor HH control during loading or movement//> excessive superior or antero-superior HH translation (therefore impingement)
  146. 146Consequences of gross of subtle GHJ hypo mobilityInability to centre HH
    -Loss of ER ROM (this affects the ability of greater tuberosity to clear coraco-acromial arch during shoulder elevation)
    which means there is a risk for secondary impingement
  147. 147Normal scapular positionUpward rotation 2 degrees
    IR 33 degrees
    Anterior tilt 8 degrees
  148. 148How can scapular mechanics changePain
    Soft tissue tightness over activity
    Altered function of scap force couples- reduced strength, endurance and sub-optimal timing
    Sub-optimal thoracic postures
  149. 149Excessive medial border winging-Secondary to sub-optimal serratus anterior
    -results in lack of normal upward rotation and posterior tilt (i.e. the coraco-acromial arch fails to rotate out of the way)
  150. 150Excessive downward rotation- muscles involved-Overtight levator scap or rhomboids
    -Weak serratus anterior and upper and lower traps
  151. 151Excessive anterior tilt- muscles involvedTight pectoralis minor
    -Results in scap IR, DR and anterior tilt
  152. 152Alterations in scpaular kinematics common in patients w/ impingement, RC pathology, GHJ instability, GHJ hypomobility-Upward rotation
    -Posterior tilt
    -Increase in IR (medial winging)
  153. 153Result of flexed/ kyphotic thoracic postures-Lengthened/ reconditioned scap upward rotators
    -Tight pec minor and major
    -Restriction in UR and post tilt
    -Decreased thoracic extension ROM
    -LITTLE EVIDENCE TO SUPPORT
  154. 154Is impingement a diagnosis or clinical sign?CLINICAL SIGN
  155. 155Acromial irritation model- limitations-Common location of RC pathology doesn't support this model (most RC pathology (i.e. 90%) occurs on deep articular side)
    -Acromial shape and relationship to pathology doesn't support this model
    -Acromial shape- SA spur formation may be secondary not primary
  156. 156Why does 90% of RC pathology occur on intra-articular/ deep side-Deeper side fibres relatively weaker and fail earlier than large acromial side fibres
    -Pathology due to intrinsic tendon degeneration or failure without direct mechanical irritation
  157. 157Risk factor predisposing to RC tears-Increased age
    -SMoking
    -Hypercholesterolemia
    -Family predisposition
    -High BMI
  158. 158Classification of RC tears-Partial thickness tear (start in the deep articular side)--> the progresses to involve subscap
    -Full thickness tear
  159. 159Diagnosis of RC tear-Age more than 60
    -Night pain
    -Abduction weakness (initiation)
    -ER weakness
    -Positive impingement signs
    -Imaging (however symptoms do not always correlate)
    -Antero-lateral shoulder pain
  160. 160Calcific tendinopathies-Causes of calcium deposits in RC unknown
    -Unclear if assoc. with tendon degenerative process
    -Usually supraspinatus
    -More common in those above 30
    -Deposits chemically irritate the tendon leading to inflammatory process and therefore pain!
    -The size of the deposit is not always linked to pain
    -usually managed conservatively
  161. 161Joint LaxityDegree of translation which falls within physiological range and is asymptomatic
    -Increased of developing shoulder pathology is higher
  162. 162Joint instabilityAbnormal symptomatic motion
    -Abnormal motion of HH relative to the gleaned during active shoulder motion
    -Feelings of looseness, slipping, shoulder falling out, apprehension, lack of power, sense of displacement
  163. 163Multi-directional joint instability-Instability in atleast 2 direction
    -TRUE JOINT INSTABILITY= instability in posterior and anterior w/ inferior component
  164. 164Anterior instability-Hand behind head
    -Abduction
    -ER
  165. 165Inferior instabilityCarrying objects/ lifting things when HH gets pulled down
  166. 166Posterior instabilityPushing something out front or when throwing (VERY COMMON)
  167. 167General classifciation system TUBSTraumatic
    Unidirectional
    Bankart
    Surgery
  168. 168General classification system- AMBRIIAtraumatic
    Multidirectional
    Bilateral
    Rehab- restore optimum NM control
    -Inferior capsule shift- tightening
    -Interval RC closer and reconstructing
  169. 169Mechanisms of injury for anterior dislocation-Forced abduction and internal rotation
  170. 170Posterior dislocation- MOIMore than 90 degrees flexion
    -Adduction
    -IR
    (i.e. falling on outstretched arm)
  171. 171Structures affected w/ anterior dislocation-Inferior glenohumeral ligament
    -Antero-inferior glenoid labrum (Bankart lesion)
    -Axillary nerve injury- reduced sense of lateral sensation and deltoid weakness
    -RC possibly (more if over 40)
  172. 172Structures affected w/ posterior dislocation-Bankart lesion (tearing labrum)
    -Bony bankart (pulling glenoid rim as well)
    -Hills Sach's lesion (compression)
    -Bennet lesion (calcification of posterior band of inferior GH ligament)
    -RC damage
  173. 173Common symptoms w/ non-acute instability-In direction of symptoms
    -Feelings of apprehension
    -Less firm ER
    -RC weakness
    -Laxity tests positive
    -Impairments of static and dynamic scapula and GHJ motor control
  174. 174Adhesive capsulitis -aka frozen shoulder-GLOBAL limitation of GH motion resulting from contracture and loss of compliance of GHJ capsule
  175. 175Clinical features of adhesive capsulitis-Females more than males
    -40-60 yrs
    -Diabetic population (meaning to do with immune system)
    -Thyroid disorders assoc.
    -Unknown cause
    -10-30% become bilateral
    -Night pain
    -Pain w/ quick movements
    -Pain lying on shoulder
    -Pain at end range of movement
  176. 176Stages of adhesive capsulitis1. Inflammatory- pain and synovitis
    2. Freezing- pain and synovitis w/ progressive stiffening
    LOSS OF CAPSULAR MOVEMENT- ER, abd, IR, flexion
    3. Frozen- contracture and fibrosis of capsule (min pain)
    4. Thawing- recovery @2 years however uncertain timeframe (min pain)
  177. 177Closed packed position of shoulderAbduction and external rotation
  178. 178Open packed position of the shoulder50 degrees abduction, slight horizontal adduction, external rotation

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Musc E-Test Week 11 Curtin University
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