Week 8 Lecture

Involves passive restraints and dynamic stabilisers Key source of stability=concavity-compression mechanism. A stabilising mechanism in which compression of the convex humeral head into the concaved glenoid stabilises and protects it against translating forces. Its directly related to depth of concavity and magnitude of compressive force. GHJ depth = glenoid depth + labrum Depth is greater superior inferiorly and most shallow A-P There is negative atmospheric pressure within the joint, the greater the depth of the labrum the greater the negative atmospheric pressure t/f greater resistance to translation. Static stabilisers GHJ motion passively controlled by tightening of GHJ ligs and capsule at EROM Geometry of the GHJ Glenoid labrum Dynamic stabilisers Rotator cuff; ideally positioned biomechanically to provide a compressive force throughout the entire ROM of the GHJ. Scapular stabilising muscles; provide a mobile yet stable BOS for GHJ functi

A torn labrum> decreased neg atmospheric pressure, decreased concavity t/f decreased stability Torn labrum > break in circle > channeling effect of laxity as compared to opposite side Leads to SLAP tears, Traumatic dislocations, Atraumatic laxity GHJ depth = glenoid depth + labrum Depth is greater superior inferiorly and most shallow A-P There is negative atmospheric pressure within the joint, the greater the depth of the labrum the greater the negative atmospheric pressure t/f greater resistance to translation.

Focal thickenings of the GHJ capsule, can be divided into 4 parts. -Tendon of longhead of biceps, -SGHL,Superior glenohumeral ligment -MGHL,Middle glenohumeral ligament -IGHL,Inferior glenohumeral ligament: Anterior band of IGHL,auxillary pouch of IGHLC, Posterior band of IGH *Coracohumeral ligament (CHL) posterior band IGHL -most important restraint to posterior subluxation at 90° flexion and IR -tightness leads to internal impingement and increased shear forces on superior labrum (linked to SLAP lesions) anterior band IGHL -primary restraint to anterior/inferior translation 90° abduction and maximum ER(late cocking phase of throwing) -anchors into anterior labrum forms weak link that predisposes to Bankart lesions superior band IGHL most important static stabilizer about the joint 100% increased strain on superior band of IGHL in presence of a SLAP lesion *-Inferior glenohumeral ligament is like a hammock Bands reciprocally tighen as the head is rotated in the abducted postion Stability further enhanced by tightening ligaments increasing joint compression External rotation winds it up so it acts like a sling

Mid-range stability(45/60-120 ) of GHJ is provided by Rotator cuff which provide a muscular compressive force which results in the concavity compression mechanism. ER – infraspinatus ER HOH and imparts posterior roll, additionally holds posterior capsule relatively taut. Creates additional tensioning of passsive stability system -Passive tension on otherside of joint by subscapularis and anterior capsular ligament when stretched during ER. If the RC becomes damaged or weakened, the HOH may migrate upwards and forwards with a resultant increased risk of impingement of subacromial structures. (Deltoid may act unopposed) Rotator cuff has an anti-impingement function. Deltoid pulls the humerus outward and upward towards the acromion. Balanced action of the RC opposes this and keeps the humeral head centred, preventing upward dislocation. RC also generates ER needed to prevent impingement of the GT against the glenoid.

GHJ force couples Coronal force couple: Deltoid and Supraspinatus vs Inferior cuff Trasverse force couple: Anterior(Subscap) vs Posterior cuff(Infraspinatus, Teres minor * critical for providing superior-inferior stability. SA impingement often develops secondary to compromise of the transverse force couple. Supraspinatus becomes the “victim” not the culprit.

Scapulohumeral rhythm 120 GHJ: 60 Scap 2:1 ratio Initial phase (Setting phase) 30 GHJ Abduction(20-80) Scapula mostly stable (0-30 degrees) Midphase/critical phase 2:1 60 GHJ abduction 30 scap upwards rotation GHJ externally rotates to clear GT from acromion and depress humeral head Final phase 3:5:1 60 GHJ abduction 30 scap upwards rotation Slight extension and lateral flexion of thorax to assist elevation

Cervical spine referral (c5/6) Thoracic spine referral(upper) Heart(angina)L Liver via diaphragm R Cholecystitis (gall bladder) R Spleen L Apical lung tumours Vascular compromise( thoracic outlet syndrome)

Diagnosis requires identification of the specific Patho anatomical source of symptoms& related pathology. Shoulder PE tests not good at identifying structural pathology and structural pathology as seen in imaging is common in those with no pain. Lack of specificity of common shoulder tests coz: Morphology of RC means tendons don’t function as separate entities anatomically or functionally. Fuse to form common insertional aponeurosis t/f cant test 1 tendon in isolation. Position and innervation of subacrominal bursa Richly innervated and anatomically blends with GHJ capsule and RC insertions. Any test of interity and pain response from any RC tendons would inherently involve bursal tissue. No test can distinguish between them Weakness on testing- pain inhibition vs structural failures. Injection studies suggest weakness detected during testing may be better explained by pain inhibition rather than structural pathology. *2/3 of RC tears are asymptomatic in general population FTT common & commonly asymptomatic in general population

PRIMARY subacromial impingement: ( true structural narrowing) Impingement leading to impingement of structures in SA space caused by outlet stenosis in Sub acromial space in a stable shoulder. Due to Encroachment from above: Sub acromial spur/osteophytes, thickened calcified coracoacromial ligament, Acromiocalvicuar joint arthropathy/spur formation, mal-union of acromial or greater tuberosity fracture SECONDARY subacromial impingement: (functional narrowing Pinching/mechanical compression of any structures between HOH ( greater tuberosisty) and acrominon/CAL as a concequency of functional narrowing. An impairment of musculoskeletal function.

INTERNAL • PSI(posterior superior)*more common • ASI(Anterior superior) EXTERNAL • Subacromial (Primary or Secondary) *most common • Subcoracoid(Primary or Secondary)

Suacromial bursa Superior glenohumeral capsule and superior glenohumeral ligment Rotatorcuff tendons and most superior fibres of infraspinatus Long head of biceps tendon

Pain with overhead activities / activities involiving loaded shoulder IR rotation with shoulder elevation g tennis serve, swimming, throwing. Painful arc during active shoulder elevation. Point in range where mechanical impingement of sensitised SA structures is occurring. Usually (45/60- 130 abduction) Pain commonly absent or eases in early and late ROM.May be painfull at EOR again Pain usually worse in abduction compared to flexion In middle range humerus needs to clear acromioclavicular space, scap needs to upwardly rotate at this point, if it cant they may get functional narrowing. @ end range scap does most of the work. If it cant glenohumeral joint may jam up to try and get more range. Pain with loading RC ( empty can test, full can test) due to failure of RC to keep HH centred. Othopaedic specific tests for impingement may reproduce pain: Hawkins kennedy test, Relocation test.

• Suboptimal/impaired RC function/GHJ impairment • GHJ instability or hyperlaxity • GHJ hypomobility • Sub optimal scapula kinematics/MC • Suboptimal spinal postures • Combination of the above

Can be post or posterior-superior impingement(PSI) Anterio-superior impingement(ASI) less common PSI Pinching/mechanical compression of articular(deeper most) fibres of subscapularis and infraspinatus & posterior labrum between greater tuberosity and posterior superior glenoid rim as consequence of FUNTIONAL NARROWING. (during abd/ER)eg throwing motion,late cocking phase. >Posterior shoulder pain ASI Impingement of under surface subscapularis and biceps pulley against anterosuperior glenoid rim in positions of horizontal adduction and IR in flexion. Damage to pulley can lead to LHB instability • biceps pulley is soft tissue sling that encloses LHB to stabilise it at at entrance to bicipital groove

Primary or secondary narrowing of space between coracoid process and humerus and lesser tuberosity. Structures potentially impinged: -Subscapularis tendon -LH biceps tendon -Middle Glenohumeral ligament and capsule.

Sub-acromial pain syndrome (SAPS) Associated with symptoms of subacromial impingement Limitations to the acromial irritational model 1. Most AC pathology is of the deeper structures(articular side) Deeper fibres are relatively weaker and fail earlier than larger acromial side fibres. Intrinsic tendon degeneration without direct mechanical irritation. • Acromial shape has a poor relationship to pathology and symptoms(Flat, curved, hooked) • Subacromial spur (osteophyte) may not be primary may be secondary to chronic strain or tension in coracoacromial ligament increasing bone stress @ the acromial insertion > spur formation( seconday ossification of CAL) Strain/ tension in CAL due to: -Failure of RC to stop HH superior translation during elevation -Increased tendon volumes (reactive tendonopathy) -Increased bursal volume associated with SA bursitis t/f type 3 acromion may not be morphological variation but a result of increased strain on CAL as a result of a degenerative process. THEEEN failure to control superior HH migration and eventual spur formation result in irritation of bursal tissue and bursal side of RC patholgoy Can be one or the other first -Subacromial pathology then impingement Injury to RC leads to superior migration of HH t/f impingement signs -Or subacromial impingement leading to SA injury Pathomechanics mean functional narrowing of subacromial space then subacromial strucures become sensitised and secondary SA pathology occurs *Rotator cuff pathology is more likely due to intrinsic tendon degeneration or failure than extrinsic acromial mechanical compression.

• Tendinopathy (early reactive – disrepair -degenerative) reveiw this • Partial / full thickness tears Clinical presentation: >60 yrs Night pain Abduction weakness ER weakness Positive impingement signs Presence of all above = 98% chance of RC tear MRI or US, can have large asymptomatic tears In young trauma> dislocation more likely than RC tear If older than 40> RC tears associated with traumatic GHJ dislocation + gt tuberosity # LHB pathology Frequently associated with other shoulder pathology. (SAPS & RC) Same spectrum of pathology as RC

Anterolateral shoulder pain SA structures may refer to deltoid tuberosity Can refer more distally, C5,6 distribution Hx variable gradual onset, overuse, traumatic Pain with movement/loading with OH activities(worse in positions of IR Signs of SA impingement usually present

Risk factors: increasing age Smoking ( tear size and surgical outcomes) Hypercholesterolemia Familiar predisposition Limited healing ability

Calcium deposits chemically irritates tendon> inflamm resonse > edema> increased intratendon pressure> pain Cause unknown May be associated with tendon degenerative process, usually subscap just distal to tendon insertion. Most common > 30 yrs female, diabetic Bilateral Asymptomatic Site of deposit not strongly associated with pain severity Management Conservative NSAID’s, deposits usually reabsorbed. Acutely painful at this stage Address impairments secondary to pain and altered function: GHJ mobility RC function Needle lavage if non responsive to above> aspirate Surgical removal , bursectomy, acromioplasty

• Joint laxity – Degree of translation which falls within physiological range & is asymptomatic = not pathological • Joint instability – Abnormal symptomatic motion – Shoulder instability: “symptomatic abnormal motion of the HH relative to the glenoid during active shoulder motion”

Classification Aetiology- traumatic vs atraumatic Directional-ant, inf, posterior, multi‐directional (MDI) Severity-subluxation vs dislocation Position(s) of symptom provocation eg: – Anterior instab: HBH, abd+ER – Inferior instab: carrying object – Posterior instab: pushing something out front -MDI( multidirectional instability) Instability in at least 2 directions – True MDI should have both anterior & posterior instability with inferior component Thomas & Matsen Classification over simplification of a complex issue… T.U.B.S Traumatic Unidirectional/ Unilateral Bankart Surgery to fix A.M.B.R.I.I Atraumatic/Acquired Multidirectional Bilateral Rehab (1st)– Restore optimum NM control Inferior capsular shift/tightening* Interval (RC) closure/recon* *Surgery only if conservative measures fail Stanmore Classification of GHJ Instability: “Polar” Groups Concept Type I: traumatic / structural (=TUBS) Type II: atraumatic /structural (microtrauma) Type III: m/s patterning disorders / non-structural (=AMBRII) (ie NM control STJ/GHJ) Continuum b/w 3 groups with some pts falling b/w groups (iesub-groups) *Direction of instab NOT as impt to effective Mx as whether instab is structural, non‐structural or both • Usually atraumatic or repetitive micro‐ traumatic – In sports requiring large GHJ ROM eg swimming • May be associated with generalised ligament laxity • Often bilateral & more common in young

• Diagnosis: Symptoms of instability are required: – Feelings of looseness, slipping, shoulder going out/falling out, - apprehension, ‘dead arm’, - lack of power, - ‘sense of displacement’ (subluxation, dislocation) +/‐ pain

Anterior Dislocation – >90% of dislocations – MOI: forced abd + ER Key stabilising structures damaged: – Capsulo‐ligamentous structures ‐ IGHLC especially – Tearof Antero‐inf glenoid labrum = Bankart Lesion – Bony injury: • BonyBankartLesion/# = #of Antero‐inferior glenoid margin • Hill‐Sachs Lesion= Compression # posterior(lateral) HH Impaction of humerus against anterior rim of glenoid +/‐ tearing of posterior or superior labrum – Axillary nerve injury – reduced sens lat shoulder & deltoid weakness – RC damage possible • More common if > 40 yo Posterior Dislocation – <5% of dislocations – MOI: • >90 flex + add +/ IR eg FOOSH in some IR/add • Reverse Hill‐Sachs Lesion Compression fracture antero‐medial HH • Reverse Bankart Lesion Postero‐inferior glenoid rim – fracture or labral Lesion • Bennett Lesion Calcification of posterior band of inferior GH ligament at postero‐ inferior glenoid secondary to traction / avulsion injury • RC damage