MRI of impingement syndromes of the shoulder

MRI of impingement syndromes of the shoulder

Clinical Radiology (2009) 64, 307e318 REVIEW MRI of impingement syndromes of the shoulder E. Mulyadia, S. Harisha,b,*, J. O’Neilla,b, R. Rebelloa,b ...

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Clinical Radiology (2009) 64, 307e318

REVIEW

MRI of impingement syndromes of the shoulder E. Mulyadia, S. Harisha,b,*, J. O’Neilla,b, R. Rebelloa,b a

Department of Diagnostic Imaging, St Joseph’s 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 developing 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 of the different types of impingement syndromes are presented. ª 2008 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.

Introduction Shoulder impingement syndromes are common causes of shoulder pain. They are broadly classified into external (also known as extrinsic) and internal impingements, which refer to extra-articular and intra-articular impingements of the rotator cuff tendons respectively. Subacromial and subcoracoid impingement are primary external impingements. Secondary extrinsic impingement results from glenohumeral instability in the absence of outlet stenosis of the rotator cuff tendons. Internal impingement refers to intraarticular impingement involving the glenoid labrum and is named according to the portion of the glenoid that is involved in the impingement process, namely posterosuperior and anterosuperior impingements. Radiographs, ultrasound (US), and MRI can all be used to evaluate the shoulder in the context of impingement syndromes. Radiographs are useful to evaluate osseous abnormalities of the coracoacromial arch, such as acromioclavicular degenerative change, acromial morphology, acromial spurs and cystic/erosive changes of the greater tuberosity. US has high * Guarantor and correspondent: S. Harish. Department of Diagnostic Imaging, St Joseph’s Healthcare, Hamilton, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada E-mail address: [email protected] (S. Harish).

accuracy for detecting rotator cuff tears and has advantages in dynamic assessment for subacromial bursal impingement and also in assessing the long head biceps in the bicipital groove. This review focuses on the assessment of shoulder impingement by means of conventional MRI and MR arthrography (MRA).

Primary extrinsic impingement Subacromial impingement Causes and clinical features The supraspinatus outlet is bounded superiorly by the coracoacromial arch, which is made up of the coracoacromial ligament, coracoid process, and the acromion (Fig. 1). The supraspinatus tendon and the subacromial subdeltoid (SASD) bursa pass through this narrow outlet. Primary extrinsic subacromial impingement refers to pain caused by contact between the rotator cuff and the coracoacromial arch. The pain is thought to be caused by irritation of the well-innervated SASD bursa. Patients are usually older than 50 years of age, although it is not uncommon to see subacromial impingement in younger patients. Patients typically present with anterior or lateral shoulder pain that is essentially produced by impingement of the SASD bursa and supraspinatus tendon between the

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

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

greater tuberosity of the humerus and the coracoacromial arch during abduction and external rotation or forward elevation and internal rotation of the shoulder.1 On physical examination, the ‘‘impingement sign’’ is classically present (pain on passive shoulder elevation between 70e120 ) and this can be confirmed with the ‘‘impingement test’’, which is pain relieved by injection of 5e10 ml 1% xylocaine into the SASD bursa.2 Treatment includes avoiding symptom-provoking activities, anti-inflammatory medications, physiotherapy, and SASD steroid injections.1,3,4 Surgery, in the form of rotator cuff repair and subacromial decompression (open or laparoscopic technique), is indicated in symptomatic cuff tears and in cases of failed conservative treatment.1,3,4 Imaging features Acromial morphology is implicated in the pathogenesis of subacromial impingement. It is classified based on the appearance of the undersurface as type 1 flat (12%), type 2 concave (56%), type 3 hooked (29%), and type 4 inferiorly convex (3%).5e7 Type 3 (Fig. 2) and, to a lesser extent, type 2 acromion are associated with increased incidence and severity of cuff tears.5 Both are associated with subacromial spurs and can be evaluated on oblique sagittal MRI.3,6 Os acromiale due to failure of the

acromial ossification centres to fuse by age 25 years can also be a substrate for impingement.8 It is important to identify the os acromiale preoperatively, which is best done on the most superior sections of the axial MRI, as standard subacromial decompression may weaken the os, further increasing its mobility and causing detachment of the deltoid tendon to which it provides attachment.8,9 In combination or independent from acromial morphology, subacromial spur can contribute to subacromial impingement (Fig. 2).3 It arises at the origin of the coracoacromial ligament as a result of an enthesopathic reaction to repeated abutment of humerus against the undersurface of the coracoacromial ligament.10 Acromioclavicular joint (ACJ) degeneration with inferior osteophytes can also narrow the supraspinatus outlet (Figs. 1 and 3).11 A laterally or anterior down-sloping acromion and a low-lying acromion may also narrow the supraspinatus outlet (Fig. 2).12,13 On MRI, rotator cuff tendinosis and tears are typically seen at the anterior aspect of the supraspinatus tendon. Rotator cuff tears in subacromial impingement may be partial or full thickness. Bursal-side partial-thickness tears are encountered more commonly in subacromial impingement (Fig. 2c).14 The dimensions and extent of rotator

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Figure 2 Sagittal, T1-weighted, fat-saturated MRA image (a), sagittal, T1-weighted, MR image (b), and coronal, T2weighted, fat-saturated MR image (c) in different patients with external subacromial impingement shows type 3 acromion (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).

cuff tears, the condition of the involved tendon, morphological features of the tear, involvement of other rotator cuff tendons, and evidence of muscle atrophy may all have implications for rotator cuff treatment and prognosis. Significant SASD bursal fluid can be seen in the setting of impingement (Fig. 3). Features suggested to indicate

significant SASD bursitis include thickness greater than 3 mm, presence of bursal fluid medial to the ACJ, and presence of fluid in the anterior aspect of the bursa (Fig. 3).15

Subcoracoid impingement Aetiology and clinical features The coracohumeral interval is a space between the coracoid process and the anterior humeral cortex. Subcoracoid impingement syndrome refers to impingement of subscapularis tendon in the coracohumeral interval. Lo et al.16 proposed a mechanism called the ‘‘RollereWringer effect’’, by which during internal rotation of the shoulder, the coracoid process indents the superficial surface of the upper subscapularis

Figure 3 Coronal, proton density-weighted, fat-saturated, MR image in a patient with subacromial impingement demonstrates ACJ degenerative changes (white arrow), low-lying acromion with a slight lateral tilt (black arrow), SASD bursitis (white arrowhead), partial thickness supraspinatus tear (black arrowhead) and entheseal changes in the greater tuberosity (yellow arrow).

Figure 4 Diagram illustrating the rollerewringer effect in subcoracoid impingement. The coracoid process indents the anterior surface of the subscapularis. The TUFF lesion (black arrow) on the deep surface of the tendon is the side of the tensile forces.

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causes of subcoracoid impingement, namely idiopathic, iatrogenic, and traumatic.18 Congenital causes include any anatomic variations that may reduce the coracohumeral distance, such as an excessively long coracoid process and protuberant lesser tuberosity.19 Iatrogenic causes include a variety of operative procedures that may alter the relationship between the coracoid process with the lesser tuberosity or change the orientation of the coracoid or glenoid.17,20,21 Fractures of the glenoid neck, coracoid process and lesser tuberosity can also diminish the coracohumeral distance.17,22,23 The majority of patients with subcoracoid impingement syndrome respond favourably to conservative treatment with physiotherapy and anti-inflammatory medication. Surgical management includes open or arthroscopic coracoplasty.17,20,21,24 Figure 5 Axial, T2-weighted, gradient-echo, MR image in a patient presenting with anterior shoulder pain demonstrates subcoracoid stenosis with coracohumeral interval of 5.4 mm (white arrows). The subscapularis tendon demonstrates marked tendinosis and fraying (black arrows).

tendon while stretching (tensile loading) the deep surface of the tendon (Fig. 4). This leads to a TUFF (tensile undersurface fibre failure) lesion, which is an articular-sided subscapularis tear (Fig. 4). Patients present with anteromedial shoulder pain/click during flexion, adduction, and internal rotation.17 There is tenderness to palpation over the coracoid region. There are three common

Imaging features The coracohumeral distance is measured on the axial MRI images with the greatest amount of subcoracoid narrowing from the cortical margin of the coracoid to the cortical margin of the humeral head (Figs. 5 and 6).19,25,26 In one study, the mean coracohumeral distance in patients with subscapularis tears was 5  1.7 mm as opposed to 10  1.3 mm in the control group.25 Subcoracoid stenosis, defined as a coracohumeral interval of less than 6 mm, has a high specificity for subcoracoid impingement (Figs. 5 and 6).16,19 As subcoracoid impingement is an uncommon cause of anterior shoulder pain,17 the identification of a narrow coracohumeral interval and subscapularis tendinosis/tears on MRI could influence

Figure 6 Axial, T2-weighted, gradient-echo (a) and sagittal, T2-weighted, fat-saturated (b) MR images in a patient presenting 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 associated subcortical cysts near the lesser tuberosity (white arrowhead) and subcoracoid bursitis (black arrowheads).

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

further management by prompting the clinician to the possibility of subcoracoid impingement, which may have not been recognized before imaging. Because subcoracoid impingement is a cause of persistent shoulder pain following supraspinatus repair,17,21,27 alerting the surgeon to the possibility of subcoracoid impingement on preoperative MRI may be the necessary clue in leading to a thorough arthroscopic examination of the subscapularise coracoid relationship, which may ultimately lead to the decision to perform a subcoracoid decompression. However, it should be noted that in two recent studies in the imaging literature,

Figure 8 Diagram illustrating posterosuperior internal impingement. In ABER position of the shoulder, the greater tuberosity abuts against the posterosuperior glenoid, entrapping the rotator cuff causing undersurface tears (black arrow).

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

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a statistically significant relationship between decreasing coracohumeral distance and subscapularis tendon abnormalities was not found in patients with 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 include subcoracoid bursal distension (Fig. 6), cortical irregularities of the lesser tuberosity (Fig. 6) and abnormalities of long head of biceps (LHB).

Secondary extrinsic impingement

Figure 10 Diagram illustrating pathogenesis of PSI. In ABER, there is a posterosuperior shift in the glenohumeral rotation point (O to X). As a result, the LHB (black arrow) vector shifts and twists posteriorly causing a peel-back type SLAP tear (white arrow).

Secondary extrinsic impingement refers to rotator cuff impingement secondary to glenohumeral instability.30 It is typically seen in patients who perform repetitive overhead or throwing motions, and is the most common cause of impingement pain in athletes.31 The instability may itself be asymptomatic, and results from a stretched/lax anterior capsule that develops over time. The instability leads to increased workload for the rotator cuff resulting in cuff fatigue, which in turn allows superior migration of the humeral head narrowing the supraspinatus outlet.30,32 MR arthrography could play a role in influencing further management by identifying anterior capsular laxity and noting the absence of anatomical factors causing primary extrinsic impingement (Fig. 7). This could be important for the clinician to know as the treatment may be directed to correcting the capsuloligamentous laxity rather than performing a subacromial decompression.33

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

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

Internal impingement Posterosuperior impingement (PSI) Aetiology and clinical features PSI was first described as a physiological phenomenon whereby the greater tuberosity abuts against the posterosuperior glenoid with the arm in abduction, external rotation (ABER).34 It becomes pathological in the athletes with overhead arm motion, such as baseball pitchers, racquet sport athletes, competitive swimmers, javelin throwers, etc, whereby extreme ABER causes repetitive/excessive impaction of the humeral head on the posterosuperior glenoid with entrapment of the

posterior fibres of the supraspinatus tendon, anterior fibres of the infraspinatus tendon, and the posterosuperior labrum (Fig. 8).34,35 PSI might be progressively worsened by anterior humeral subluxation secondary to anterior joint instability produced by repetitive stretching of the anterior capsuloligamentous structures during ABER motion (Fig. 9).35e37 Another theory proposes tightening of the posteroinferior aspect of the capsule produced by repetitive microtrauma during ABER motion as the main initiating pathologic lesion in PSI.38,39 This progressively results in posterosuperior shift of the glenohumeral contact point and allows hyperexternal rotation during the late cockingethrowing phase (Fig. 10). The

Figure 13 Coronal, T2-weighted, fat-saturated (a, b) and sagittal, T1-weighted, fat-saturated (c) MRA images in a 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), There is also an intrasubstance tear of the supraspinatus at the footprint (brown arrow).

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combination of humeral translation and repetitive torsional loading from hyperexternal rotation cause articular-side posterior supraspinatus and infraspinatus cuff injuries. The shift of the glenohumeral contact point also allows excessive twisting of the LHB tendon, which in turn produces a peel-back tear of the superior labrum (Fig. 10).39 Patients present with posterior shoulder pain during the throwing motion.38 Many also have significant glenohumeral internal rotation deficit (GIRD) in abduction, an indication of a tight posteroinferior capsule.38 Symptoms and signs of anterior instability and superior labral anterior to posterior SLAP tear may be present.38,39 Patients with symptomatic GIRD are usually treated by physiotherapy to stretch the posteroinferior capsule.38 Posteroinferior capsulotomy and SLAP lesion repair is sometimes performed in patients not improving on physiotherapy.38,39 Imaging features Conventional MRI or MRA demonstrates labral injuries in suspected PSI.40 MRA, by virtue of its increased sensitivity for demonstrating SLAP tears and undersurface partial thickness rotator cuff tears, is the preferred technique for investigating suspected PSI. There is a triad of direct signs of

Figure 14 Sagittal, T1-weighted, fat-saturated, MR arthrographic image of a normal rotator interval demonstrates blended CHL and SGHL (white arrow) trace inferior and medial to LHB (white arrowhead) before inserting on lesser tuberosity.

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Figure 15 Diagram illustrating pathogenesis of ASI. With humerus in adduction and internal rotation, there is tearing in the pulley ligaments (white arrow), medial subluxation of the LHB (black arrow) and deep surface tear of the subscapularis tendon (black arrowhead).

PSI on MRA performed with the arm in neutral position,41,42 namely: (a) cystic changes within the posterolateral humeral head subjacent to insertions of the posterior cuff (Figs. 11 and 12); (b) articular surface tears of the infraspinatus and posterior supraspinatus (Figs. 9,11 and 13);

Figure 16 Diagram showing tears of the SGHLeCHL complex (thin white arrow) with partial articular-sided supraspinatus (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 labrum, including SLAP type 2 (Figs. 9,11 and 13). It should be noted that this triad can be seen on MRI in non-athletes where tension overload of the rotator cuff and repetitive shearing of the humeral head against the superior labrum is thought to be the causative mechanism rather than PSI.43 MRA with ABER sequences can reproduce the arthroscopic criteria for the diagnosis of PSI including posterosuperior labral tear, articularsided tear of the supraspinatus and/or infraspinatus and demonstrating contact of the posterior

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cuff on the posterosuperior glenoid (Fig. 9).41,42,44 MRA with ABER position has increased sensitivity for detecting and characterizing undersurface delaminating cuff tears in the setting of PSI. However, the ABER sequence does not necessarily need to be done in all cases of suspected PSI, especially if the conventional sequences reveal the cuff tears and the SLAP lesions. Athletes with PSI and GIRD tend to have an increased labral length and a shallow posterior capsular recess near the attachment of the posterior band IGHL on 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 medial subluxation of LHB (white arrows), tear of the subscapularis (black arrows), and lesser tuberosity cyst/erosion (white arrowhead). There is irregularity of the rotator interval (black arrowheads) in keeping with tear of the pulley ligaments; compare with normal biceps pulley in Fig. 14.

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Anterosuperior impingement Aetiology and clinical features The union of the coracohumeral ligament (CHL), superior glenohumeral ligament (SGHL), anterior aspect of supraspinatus tendon, and the superior aspect of subscapularis tendon insertion towards the entrance to the bicipital groove forms a pulley around the LHB called the ‘‘biceps pulley’’, the primary function of which is to keep the LHB in the groove during active movements (Fig. 14).46e49 Anterosuperior impingement (ASI) is described as an internal impingement of the pulley system and the articular surface of the subscapularis tendon against the anterosuperior glenoid causing friction injury during anterior/horizontal elevation, adduction, and internal rotation of the shoulder (Fig. 15).50 Contact between the rotator cuff and the superior labrum is physiological, when the shoulder is rotated in the forward flexed position. However, this phenomenon becomes pathological in the presence of a pulley lesion and a partial articular-sided subscapularis tendon tear (Figs. 15 and 16).50e52 A pulley lesion can be produced by trauma or degenerative changes.50,53 Traumatic causes include a fall on the outstretched arm with full external rotation and a forcefully stopped overhead throwing motion. The LHB plays a part in anterior 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 anterior stabilizing effect is lost leading to anterosuperior humeral translation during arm rotation.54e56 The subscapularis tendon tear further augments this anterosuperior humeral translation, resulting in ASI. An articular-sided anterior supraspinatus tendon tear may also supplement ASI (Fig. 16). Clinical features include chronic anterior shoulder pain without instability provoked by anterior elevation and internal rotation, which is unresponsive to subacromial local anaesthetic infiltration. ASI affects patients in the 35e45 years age group and affects the dominant arm.50e52 ASI affected patients have been noted to perform regular overhead activity 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 surface insertional subscapularis tear, tear of the SGHLe CHL complex, LHB subluxation, and superior labral tears can be seen on conventional MRI or MR arthrography. Axial sequences demonstrate LHB

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subluxation and the subscapularis tendon tears (Fig. 17). Sagittal sequences delineate the superior subscapularis tears, deep surface anterior supraspinatus tears and the tear of the pulley ligaments (Fig. 17). Features suggestive of the presence of a pulley lesion on MR arthrography include irregularity of the superior margin of the subscapularis tendon, extra-articular contrast medium collection, and LHB tendon subluxation (Fig. 17).46e49 These rotator interval lesions are by no means specific to ASI, which is essentially a clinical diagnosis. However, as ASI can be mistaken for subacromial impingement clinically, MRI could play a role in directing further appropriate management. If given the clinical history of chronic anterior shoulder pain, the presence of the spectrum of lesions described above in conjunction with lack of the typical imaging features of external subacromial impingement could alert the radiologist to suggest ASI as a possible cause for these findings in the report.

Summary Shoulder impingement syndromes are a common cause of shoulder pain that may be isolated or occur with related pathology such as glenohumeral instability. Knowledge of the relevant anatomy, aetiology and clinical features, allows a better understanding of the important imaging features as well as highlighted areas that will impact clinical decisions.

Acknowledgements The authors thank Glen Oomen for preparation of the illustrations, and Joanna Andrews for the small financial contribution from the Department of Diagnostic Imaging, St Joseph’s Healthcare, towards preparation of this manuscript.

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