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    REVIEW

    MRI of impingement syndromes of the shoulder

    E. Mulyadia, S. Harisha,b,*, J. ONeilla,b, R. Rebelloa,b

    aDepartment of Diagnostic Imaging, St Josephs Healthcare, 50, Charlton Avenue East, Hamilton, Ontario

    L8N 4A6, Canada, and bFaculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada

    Received 30 March 2008; received in revised form 31 July 2008; accepted 7 August 2008

    The diagnosis of shoulder impingement is primarily a clinical one. Imaging has a role in assisting clinicians in devel-oping a treatment strategy by identifying and characterizing the cause of shoulder impingement. In this review,the relevant anatomy, cause/pathomechanics, clinical features, and magnetic resonance imaging (MRI) findings ofthe different types of impingement syndromes are presented. 2008 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.

    Introduction

    Shoulder impingement syndromes are commoncauses of shoulder pain. They are broadly classi-fied into external (also known as extrinsic) andinternal impingements, which refer to extra-artic-ular and intra-articular impingements of the rota-tor cuff tendons respectively. Subacromial and

    subcoracoid impingement are primary externalimpingements. Secondary extrinsic impingementresults from glenohumeral instability in theabsence of outlet stenosis of the rotator cufftendons. Internal impingement refers to intra-articular impingement involving the glenoid la-brum and is named according to the portion ofthe glenoid that is involved in the impingementprocess, namely posterosuperior and anterosupe-rior impingements. Radiographs, ultrasound (US),and MRI can all be used to evaluate the shoulder inthe context of impingement syndromes. Radio-graphs are useful to evaluate osseous abnormali-ties of the coracoacromial arch, such asacromioclavicular degenerative change, acromialmorphology, acromial spurs and cystic/erosivechanges of the greater tuberosity. US has high

    accuracy for detecting rotator cuff tears and hasadvantages in dynamic assessment for subacromialbursal impingement and also in assessing the longhead biceps in the bicipital groove. This reviewfocuses on the assessment of shoulder impinge-ment by means of conventional MRI and MRarthrography (MRA).

    Primary extrinsic impingement

    Subacromial impingement

    Causes and clinical featuresThe supraspinatus outlet is bounded superiorly bythe coracoacromial arch, which is made up of thecoracoacromial ligament, coracoid process, andthe acromion (Fig. 1). The supraspinatus tendonand the subacromial subdeltoid (SASD) bursa passthrough this narrow outlet. Primary extrinsic suba-cromial impingement refers to pain caused by con-

    tact between the rotator cuff and thecoracoacromial arch. The pain is thought to becaused by irritation of the well-innervated SASDbursa.

    Patients are usually older than 50 years of age,although it is not uncommon to see subacromialimpingement in younger patients. Patients typi-cally present with anterior or lateral shoulder painthat is essentially produced by impingement of theSASD bursa and supraspinatus tendon between the

    * Guarantor and correspondent: S. Harish. Department ofDiagnostic Imaging, St Josephs Healthcare, Hamilton, Facultyof Health Sciences, McMaster University, Hamilton, Ontario,Canada

    E-mail address: [email protected] (S. Harish).

    0009-9260/$ - see front matter 2008 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.doi:10.1016/j.crad.2008.08.013

    Clinical Radiology (2009) 64, 307e318

    mailto:[email protected]:[email protected]
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    greater tuberosity of the humerus and the cora-coacromial arch during abduction and externalrotation or forward elevation and internal rotation

    of the shoulder.1

    On physical examination, theimpingement sign is classically present (painon passive shoulder elevation between 70e120)and this can be confirmed with the impingementtest, which is pain relieved by injection of5e10 ml 1% xylocaine into the SASD bursa.2

    Treatment includes avoiding symptom-provok-ing activities, anti-inflammatory medications,physiotherapy, and SASD steroid injections.1,3,4

    Surgery, in the form of rotator cuff repair and sub-acromial decompression (open or laparoscopictechnique), is indicated in symptomatic cuff tearsand in cases of failed conservative treatment.1,3,4

    Imaging featuresAcromial morphology is implicated in the patho-genesis of subacromial impingement. It is classifiedbased on the appearance of the undersurface astype 1 flat (12%), type 2 concave (56%), type 3hooked (29%), and type 4 inferiorly convex (3%).5e7

    Type 3 (Fig. 2) and, to a lesser extent, type 2 acro-mion are associated with increased incidence andseverity of cuff tears.5 Both are associated withsubacromial spurs and can be evaluated on obliquesagittal MRI.3,6 Os acromiale due to failure of the

    acromial ossification centres to fuse by age 25years can also be a substrate for impingement.8

    It is important to identify the os acromiale preop-

    eratively, which is best done on the most superiorsections of the axial MRI, as standard subacromialdecompression may weaken the os, further in-creasing its mobility and causing detachment ofthe deltoid tendon to which it provides attach-ment.8,9 In combination or independent from acro-mial morphology, subacromial spur can contributeto subacromial impingement (Fig. 2).3 It arises atthe origin of the coracoacromial ligament as a re-sult of an enthesopathic reaction to repeatedabutment of humerus against the undersurface ofthe coracoacromial ligament.10

    Acromioclavicular joint (ACJ) degeneration withinferior osteophytes can also narrow the supra-spinatus outlet (Figs. 1 and 3).11 A laterally or an-terior down-sloping acromion and a low-lyingacromion may also narrow the supraspinatus outlet(Fig. 2).12,13

    On MRI, rotator cuff tendinosis and tears aretypically seen at the anterior aspect of the supra-spinatus tendon. Rotator cuff tears in subacromialimpingement may be partial or full thickness.Bursal-side partial-thickness tears are encoun-tered more commonly in subacromial impingement(Fig. 2c).14 The dimensions and extent of rotator

    Figure 1 Diagram illustrating the normal outlet of the supraspinatus (a) and the narrowing of the outlet by ACJdegenerative changes (b). The black arrow indicates the coracoacromial ligament.

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    cuff tears, the condition of the involved tendon,morphological features of the tear, involvementof other rotator cuff tendons, and evidence ofmuscle atrophy may all have implications for rota-tor cuff treatment and prognosis. Significant SASDbursal fluid can be seen in the setting of impinge-ment (Fig. 3). Features suggested to indicate

    significant SASD bursitis include thickness greaterthan 3 mm, presence of bursal fluid medial to theACJ, and presence of fluid in the anterior aspectof the bursa (Fig. 3).15

    Subcoracoid impingement

    Aetiology and clinical featuresThe coracohumeral interval is a space between the

    coracoid process and the anterior humeral cortex.Subcoracoid impingement syndrome refers to im-pingement of subscapularis tendon in the coraco-humeral interval.

    Loetal.16proposed a mechanism called the Roll-ereWringer effect, by which during internal rota-tion of the shoulder, the coracoid process indentsthe superficial surface of the upper subscapularis

    Figure 2 Sagittal, T1-weighted, fat-saturated MRA image (a), sagittal, T1-weighted, MR image (b), and coronal, T2-weighted, fat-saturated MR image (c) in different patients with external subacromial impingement shows type 3 acro-mion (white arrow) with full thickness rotator cuff tear (black arrow) in (a), anterior acromial enthesophyte (blue

    arrow) in (b), bursal-side partial thickness supraspinatus tear (brown arrow) and lateral tilt of acromion (yellow arrow)in (c).

    Figure 3 Coronal, proton density-weighted, fat-satu-rated, MR image in a patient with subacromial impinge-ment demonstrates ACJ degenerative changes (whitearrow), low-lying acromion with a slight lateral tilt(black arrow), SASD bursitis (white arrowhead), partialthickness supraspinatus tear (black arrowhead) and en-theseal changes in the greater tuberosity (yellow arrow).

    Figure 4 Diagram illustrating the rollerewringer ef-fect in subcoracoid impingement. The coracoid processindents the anterior surface of the subscapularis. TheTUFF lesion (black arrow) on the deep surface of thetendon is the side of the tensile forces.

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    tendon while stretching (tensile loading) the deepsurface of the tendon (Fig. 4). This leads to a TUFF(tensile undersurface fibre failure) lesion, which isan articular-sided subscapularis tear (Fig. 4).

    Patients present with anteromedial shoulder

    pain/click during flexion, adduction, and internalrotation.17 There is tenderness to palpation overthe coracoid region. There are three common

    causes of subcoracoid impingement, namely idio-pathic, iatrogenic, and traumatic.18 Congenitalcauses include any anatomic variations that mayreduce the coracohumeral distance, such as anexcessively long coracoid process and protuberantlesser tuberosity.19 Iatrogenic causes include a vari-

    ety of operative procedures that may alter the re-lationship between the coracoid process with thelesser tuberosity or change the orientation of thecoracoid or glenoid.17,20,21 Fractures of the glenoidneck, coracoid process and lesser tuberosity canalso diminish the coracohumeral distance.17,22,23

    The majority of patients with subcoracoid impinge-ment syndrome respond favourably to conservativetreatment with physiotherapy and anti-inflamma-tory medication. Surgical management includesopen or arthroscopic coracoplasty.17,20,21,24

    Imaging features

    The coracohumeral distance is measured on theaxial MRI images with the greatest amount ofsubcoracoid narrowing from the cortical marginof the coracoid to the cortical margin of thehumeral head (Figs. 5 and 6).19,25,26 In one study,the mean coracohumeral distance in patientswith subscapularis tears was 5 1.7 mm as op-posed to 10 1.3 mm in the control group.25 Sub-coracoid stenosis, defined as a coracohumeralinterval of less than 6 mm, has a high specificityfor subcoracoid impingement (Figs. 5 and 6).16,19

    As subcoracoid impingement is an uncommon

    cause of anterior shoulder pain,17

    the identifica-tion of a narrow coracohumeral interval and sub-scapularis tendinosis/tears on MRI could influence

    Figure 5 Axial, T2-weighted, gradient-echo, MR imagein a patient presenting with anterior shoulder pain dem-onstrates subcoracoid stenosis with coracohumeral in-terval of 5.4 mm (white arrows). The subscapularistendon demonstrates marked tendinosis and fraying(black arrows).

    Figure 6 Axial, T2-weighted, gradient-echo (a) and sagittal, T2-weighted, fat-saturated (b) MR images in a patientpresenting with anterior shoulder pain demonstrates subcoracoid stenosis with coracohumeral interval of 5.6 mm(white arrows). The subscapularis tendon demonstrates mild to moderate tendinosis (black arrows). There are asso-ciated subcortical cysts near the lesser tuberosity (white arrowhead) and subcoracoid bursitis (black arrowheads).

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    further management by prompting the clinician tothe possibility of subcoracoid impingement, whichmay have not been recognized before imaging. Be-cause subcoracoid impingement is a cause of per-sistent shoulder pain following supraspinatusrepair,17,21,27 alerting the surgeon to the possibility

    of subcoracoid impingement on preoperative MRImay be the necessary clue in leading to a thorougharthroscopic examination of the subscapularisecoracoid relationship, which may ultimately leadto the decision to perform a subcoracoid decom-pression. However, it should be noted that in tworecent studies in the imaging literature,

    Figure 7 Coronal, T2-weighted, fat-saturated (a) and sagittal, T1-weighted, fat-saturated (b) MR arthrographic im-ages in a patient presenting with clinical suspicion of subacromial impingement demonstrates tendinosis and under-surface fraying of the supraspinatus (black arrow), SASD bursitis (white arrow), and a lax anterior capsular recess(white arrowheads).

    Figure 8 Diagram illustrating posterosuperior internalimpingement. In ABER position of the shoulder, thegreater tuberosity abuts against the posterosuperior gle-noid, entrapping the rotator cuff causing undersurfacetears (black arrow).

    Figure 9 Sagittal, oblique, T1-weighted, fat-satu-rated, MR arthrographic image in the ABER position ina patient with PSI clinically demonstrates the delaminat-ing undersurface tear of the posterior supraspinatus(black arrows), posterosuperior labral fraying (whitearrowhead), and mild anterior capsular redundancy(white arrow).

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    a statistically significant relationship between de-creasing coracohumeral distance and subscapularistendon abnormalities was not found in patientswith full-thickness supraspinatus tendon tears.28,29

    Apart from subscapularis tendinosis/tears (Figs.5 and 6), other findings that can be seen on MRI in

    the setting of subcoracoid impingement includesubcoracoid bursal distension (Fig. 6), cortical ir-regularities of the lesser tuberosity (Fig. 6) andabnormalities of long head of biceps (LHB).

    Secondary extrinsic impingement

    Secondary extrinsic impingement refers to rotatorcuff impingement secondary to glenohumeral in-stability.30 It is typically seen in patients who per-form repetitive overhead or throwing motions, andis the most common cause of impingement pain inathletes.31 The instability may itself be asymptom-atic, and results from a stretched/lax anterior cap-sule that develops over time. The instability leadsto increased workload for the rotator cuff resultingin cuff fatigue, which in turn allows superior mi-gration of the humeral head narrowing the supra-spinatus outlet.30,32 MR arthrography could playa role in influencing further management by iden-tifying anterior capsular laxity and noting the ab-sence of anatomical factors causing primaryextrinsic impingement (Fig. 7). This could be im-portant for the clinician to know as the treatmentmay be directed to correcting the capsuloligamen-

    tous laxity rather than performing a subacromialdecompression.33

    Figure 10 Diagram illustrating pathogenesis of PSI. InABER, there is a posterosuperior shift in the glenohum-eral rotation point (O to X). As a result, the LHB (blackarrow) vector shifts and twists posteriorly causinga peel-back type SLAP tear (white arrow).

    Figure 11 Axial, proton density-weighted, fat-saturated (a) and sagittal, T1-weighted, fat-saturated (b) MR arthro-graphic images in a patient with PSI demonstrates SLAP tear (white arrow) with associated paralabral cyst (black ar-row), impingement cysts in the humeral head (black arrowhead) and undersurface tear of the infraspinatus (whitearrowhead).

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    Internal impingement

    Posterosuperior impingement (PSI)

    Aetiology and clinical featuresPSI was first described as a physiological phenom-enon whereby the greater tuberosity abuts againstthe posterosuperior glenoid with the arm in ab-duction, external rotation (ABER).34 It becomespathological in the athletes with overhead armmotion, such as baseball pitchers, racquet sportathletes, competitive swimmers, javelin throwers,etc, whereby extreme ABER causes repetitive/ex-cessive impaction of the humeral head on the post-erosuperior glenoid with entrapment of the

    posterior fibres of the supraspinatus tendon, ante-rior fibres of the infraspinatus tendon, and theposterosuperior labrum (Fig. 8).34,35

    PSI might be progressively worsened by anteriorhumeral subluxation secondary to anterior jointinstability produced by repetitive stretching of theanterior capsuloligamentous structures duringABER motion (Fig. 9).35e37 Another theory proposestightening of the posteroinferior aspect of the cap-sule produced by repetitive microtrauma duringABER motion as the main initiating pathologic

    lesion in PSI.38,39 This progressively results in post-erosuperior shift of the glenohumeral contactpoint and allows hyperexternal rotation duringthe late cockingethrowing phase (Fig. 10). The

    Figure 12 Sagittal, T1-weighted, fat-saturated (a) and axial, gradient-echo (b, c), MRA images in a patient with PSIshows thickened posterior labrum and adjacent capsular tissues (white arrows) in keeping with posterior capsular con-tracture and impingement cysts in the humeral head (black arrow).

    Figure 13 Coronal, T2-weighted, fat-saturated (a, b) and sagittal, T1-weighted, fat-saturated (c) MRA images ina patient with PSI demonstrates a SLAP lesion (short white arrow) with associated paralabral cyst (black arrow),greater tuberosity bone marrow oedema (long white arrow) and rim-rent tear of the infraspinatus (blue arrow), Thereis also an intrasubstance tear of the supraspinatus at the footprint (brown arrow).

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    combination of humeral translation and repetitivetorsional loading from hyperexternal rotationcause articular-side posterior supraspinatus and in-fraspinatus cuff injuries. The shift of the gleno-humeral contact point also allows excessivetwisting of the LHB tendon, which in turn produces

    a peel-back tear of the superior labrum (Fig. 10).39

    Patients present with posterior shoulder painduring the throwing motion.38 Many also have sig-nificant glenohumeral internal rotation deficit(GIRD) in abduction, an indication of a tight post-eroinferior capsule.38 Symptoms and signs of ante-rior instability and superior labral anterior toposterior SLAP tear may be present.38,39 Patientswith symptomatic GIRD are usually treated byphysiotherapy to stretch the posteroinferior cap-sule.38 Posteroinferior capsulotomy and SLAP le-sion repair is sometimes performed in patientsnot improving on physiotherapy.38,39

    Imaging featuresConventional MRI or MRA demonstrates labral in-juries in suspected PSI.40 MRA, by virtue of its in-creased sensitivity for demonstrating SLAP tearsand undersurface partial thickness rotator cufftears, is the preferred technique for investigatingsuspected PSI. There is a triad of direct signs of

    PSI on MRA performed with the arm in neutralposition,41,42 namely: (a) cystic changes withinthe posterolateral humeral head subjacent to in-sertions of the posterior cuff (Figs. 11 and 12);(b) articular surface tears of the infraspinatusand posterior supraspinatus (Figs. 9,11 and 13);

    Figure 14 Sagittal, T1-weighted, fat-saturated, MR ar-thrographic image of a normal rotator interval demon-strates blended CHL and SGHL (white arrow) traceinferior and medial to LHB (white arrowhead) before in-serting on lesser tuberosity.

    Figure 15 Diagram illustrating pathogenesis of ASI.With humerus in adduction and internal rotation, thereis tearing in the pulley ligaments (white arrow), medialsubluxation of the LHB (black arrow) and deep surfacetear of the subscapularis tendon (black arrowhead).

    Figure 16 Diagram showing tears of the SGHLeCHLcomplex (thin white arrow) with partial articular-sidedsupraspinatus (thick white arrow) and subscapularis(thin black arrow) tears and medial subluxation of LHB(thick black arrow) from the bicipital groove.

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    and (c) tear/fraying of the posterosuperior la-brum, including SLAP type 2 (Figs. 9,11 and 13).It should be noted that this triad can be seen onMRI in non-athletes where tension overload ofthe rotator cuff and repetitive shearing of the hu-meral head against the superior labrum is thought

    to be the causative mechanism rather than PSI.43

    MRA with ABER sequences can reproduce thearthroscopic criteria for the diagnosis of PSIincluding posterosuperior labral tear, articular-sided tear of the supraspinatus and/or infraspina-tus and demonstrating contact of the posterior

    cuff on the posterosuperior glenoid (Fig. 9).41,42,44

    MRA with ABER position has increased sensitivityfor detecting and characterizing undersurface de-laminating cuff tears in the setting of PSI. How-ever, the ABER sequence does not necessarilyneed to be done in all cases of suspected PSI, es-

    pecially if the conventional sequences reveal thecuff tears and the SLAP lesions. Athletes withPSI and GIRD tend to have an increased labrallength and a shallow posterior capsular recessnear the attachment of the posterior band IGHLon MRA (Fig. 12).45

    Figure 17 Axial, proton density-weighted, fat-saturated (a), double oblique, axial, T1-weighted, fat-saturated (b),and sagittal, T1-weighted, fat-saturated (c, d) MR arthrographic images in a patient with ASI demonstrates medialsubluxation of LHB (white arrows), tear of the subscapularis (black arrows), and lesser tuberosity cyst/erosion (whitearrowhead). There is irregularity of the rotator interval (black arrowheads) in keeping with tear of the pulley liga-ments; compare with normal biceps pulley in Fig. 14.

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    Anterosuperior impingement

    Aetiology and clinical featuresThe union of the coracohumeral ligament (CHL),superior glenohumeral ligament (SGHL), anterioraspect of supraspinatus tendon, and the superior

    aspect of subscapularistendon insertiontowards theentrance to the bicipital groove forms a pulleyaround the LHB called the biceps pulley, theprimary function of which is to keep the LHB in thegroove during active movements (Fig. 14).46e49 An-terosuperior impingement (ASI) is described as aninternal impingement of the pulley system and thearticular surface of the subscapularistendon againstthe anterosuperior glenoid causing friction injuryduring anterior/horizontal elevation, adduction,and internal rotation of the shoulder (Fig. 15).50

    Contact between the rotator cuff and thesuperior labrum is physiological, when the shoul-der is rotated in the forward flexed position.However, this phenomenon becomes pathologicalin the presence of a pulley lesion and a partialarticular-sided subscapularis tendon tear (Figs. 15and 16).50e52 A pulley lesion can be produced bytrauma or degenerative changes.50,53 Traumaticcauses include a fall on the outstretched armwith full external rotation and a forcefully stoppedoverhead throwing motion. The LHB plays a part inanterior stabilization of the glenohumeral joint,especially during rotational movement. Hence,with medial subluxation/dislocation of LHB due

    to a pulley lesion (Figs. 16 and 17), this anteriorstabilizing effect is lost leading to anterosuperiorhumeral translation during arm rotation.54e56 Thesubscapularis tendon tear further augments thisanterosuperior humeral translation, resulting inASI. An articular-sided anterior supraspinatus ten-don tear may also supplement ASI (Fig. 16).

    Clinical features include chronic anterior shoul-der pain without instability provoked by anteriorelevation and internal rotation, which is unrespon-sive to subacromial local anaesthetic infiltration. ASIaffects patients in the 35e45 years age group and

    affects the dominant arm.

    50e52

    ASI affected patientshave been noted to perform regular overhead activ-ity during daily work, such as bricklaying, carpentry,or in sports, such as swimming and tennis.50

    Imaging features

    The lesions associated with ASI such as deep surfaceinsertional subscapularis tear, tear of the SGHLeCHL complex, LHB subluxation, and superior labraltears can be seen on conventional MRI or MRarthrography. Axial sequences demonstrate LHB

    subluxation and the subscapularis tendon tears(Fig. 17). Sagittal sequences delineate the superiorsubscapularis tears, deep surface anterior supraspi-natus tears and the tear of the pulley ligaments(Fig. 17). Features suggestive of the presence ofa pulleylesionon MR arthrography include irregular-

    ity of the superior margin of the subscapularis ten-don, extra-articular contrast medium collection,and LHB tendon subluxation (Fig. 17).46e49 Theserotator interval lesions are by no means specific toASI, which is essentially a clinical diagnosis. How-ever, as ASI can be mistaken for subacromial im-pingement clinically, MRI could play a role indirecting further appropriate management. If giventhe clinical history of chronic anterior shoulderpain, the presence of the spectrum of lesions de-scribed above in conjunction with lack of the typicalimaging features of external subacromial impinge-ment could alert the radiologist to suggest ASI asa possible cause for these findings in the report.

    Summary

    Shoulder impingement syndromes are a commoncause of shoulder pain that may be isolated oroccur with related pathology such as glenohumeralinstability. Knowledge of the relevant anatomy,aetiology and clinical features, allows a betterunderstanding of the important imaging featuresas well as highlighted areas that will impactclinical decisions.

    Acknowledgements

    The authors thank Glen Oomen for preparation ofthe illustrations, and Joanna Andrews for the smallfinancial contribution from the Department ofDiagnostic Imaging, St Josephs Healthcare, to-wards preparation of this manuscript.

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