eMedicine Specialties > Sports Medicine > Shoulder

Supraspinatus Tendonitis

Author: Thomas M DeBerardino, MD, Associate Professor of Orthopaedic Surgery, University of Connecticut Health Center
Coauthor(s): Wing K Chang, MD, Musculoskeletal Spine Fellow, Department of Physical Medicine and Rehabilitation, University of Michigan Medical Center
Contributor Information and Disclosures

Updated: Jan 21, 2010

Introduction

Background

Supraspinatus tendonitis is often associated with shoulder impingement syndrome. The common belief is that impingement of the supraspinatus tendon leads to supraspinatus tendonitis (inflammation of the supraspinatus/rotator cuff tendon and/or the contiguous peritendinous soft tissues), which is a known stage of shoulder impingement syndrome (stage II) as described originally by Neer in 1972.¹

The causes of supraspinatus tendonitis can be broken down into extrinsic and intrinsic factors.^2,3 Extrinsic factors are further broken down into primary impingement, which is a result of increased subacromial loading, and secondary impingement, which is a result of rotator cuff overload and muscle imbalance. In athletes whose sport involves stressful repetitive overhead motions, a combination of causes may be found.

Recent studies

Lewis et al demonstrated the presence of neovascularity in individuals with a clinical diagnosis of rotator cuff tendinopathy and, to a lesser extent, in asymptomatic shoulders. Twenty patients (mean age, 50.2 y; range 32-69 y) with a clinical diagnosis of unilateral rotator cuff tendinopathy received a clinical examination then underwent bilateral grey scale and color Doppler ultrasound assessment.

Neovascularity was found in the symptomatic shoulder in 13 of 20 patients (35%) as well as in the asymptomatic shoulder in 5 of the 20 patients (25%).⁴ Of 6 other patients who withdrew from the study before entering the trial, 1 withdrew due to cessation of symptoms and did not have neovascularity in either shoulder; 5 withdrew due to bilateral symptoms, of whom 2 had signs of bilateral neovascularity, 1 had unilateral neovascularity, and the remaining 2 did not have neovascularity in either shoulder.⁴ No association was identified between the presence of neovascularity and pain, duration of symptoms, and neovascularity and shoulder function. The investigators noted more research is needed to evaluate the relevance of their findings.

In another study, Millar et al suggested proinflammatory cytokines may have a role in supraspinatus tendinopathy.⁵ The investigators used custom micro-arrays to assess rat supraspinatus tendinopathy produced by running overuse. In addition, samples of torn supraspinatus tendon and matched intact subscapularis tendon from patients undergoing shoulder surgery for rotator cuff tears, as well as control samples of subscapularis tendon from 10 individuals with normal rotator cuffs undergoing arthroscopic shoulder stabilization, were collected and examined with semiquantitative reverse transcription polymerase chain-reaction (RT-PCR) and immunohistochemistry.⁵ The presence of significant upregulation of proinflammatory cytokines and apoptotic genes was found in the rat samples (P = 0.005) as well as in the supraspinatus and subscapularis tendons obtained from the patients with rotator cuff tears (P = 0.0008).

Frequency

United States

Supraspinatus tendonitis is a common cause of shoulder pain in athletes whose sports involve throwing and overhead motions.

Functional Anatomy

The shoulder consists of 2 bones (ie, humerus, scapula), 2 joints (ie, glenohumeral, acromioclavicular), and 2 articulations (ie, scapulothoracic, acromiohumeral). Several interconnecting ligaments and layers of muscles join these bones. The relative lack of bony stability in the shoulder permits a wide range of motion. Soft tissue structures are the major glenohumeral stabilizers.

The static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. The dynamic stabilizers include the rotator cuff muscles, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles such as the pectoralis major, latissimus dorsi, and serratus anterior.

The rotator cuff consists of 4 muscles, which control 3 basic motions: abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor for controlling external rotation, and the subscapularis for controlling internal rotation. The rotator cuff muscles provide dynamic stabilization to the humeral head on the glenoid fossa, forming a force couple with the deltoid to allow elevation of the arm. It is responsible for 45% of abduction strength and 90% of external rotation strength.

The supraspinatus outlet is a space formed by the acromion, coracoacromial arch, and acromioclavicular joint on the upper rim and the humeral head and glenoid below. It accommodates passage and excursion of the supraspinatus tendon. Abnormalities of the supraspinatus outlet have been identified as a cause of impingement syndrome and rotator cuff tendonitis.

Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described that variations in acromial size and shape can contribute to impingement. From cadaveric studies, 3 different variations in the morphology of the acromion are described. Type I is flat, type II is curved, and type III is anteriorly hooked. Although the curved configuration is the most common (43% prevalence, compared with 17% for flat and 40% for hooked), the hooked configuration is associated most strongly with rotator cuff pathology.

Other sites of impingement in the supraspinatus outlet space include the coracoacromial ligament, where thickening can occur, and the undersurface of the acromioclavicular joint, where osteophytes can form. Only rarely is the medial coracoid involved. These impingement sites in the supraspinatus outlet are compressed further when the humerus is placed in the forward flexed and internally rotated position, forcing the greater tuberosity of the humerus into the undersurface of the acromion and coracoacromial arch.

Nonoutlet impingement can also occur. The causes may be loss of normal humeral head depression either from a large rotator cuff tear or weakness of the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. Another way this may occur is with thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.

Sport-Specific Biomechanics

Overuse or repetitive microtrauma sustained in the overhead position may contribute to impingement and rotator cuff tendonitis. Shoulder pain and rotator cuff tendonitis are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, tennis).

Secondary impingement

Supraspinatus tendonitis is often attributed to impingement, which is seldom mechanical in athletes. Rotator cuff tendonitis in this population may be related to subtle instability and therefore may be secondary to such factors as eccentric overload, muscle imbalance, and glenohumeral instability or labral lesions. This has led to the concept of secondary impingement, which is defined as rotator cuff impingement that occurs secondary to a functional decrease in the supraspinatus outlet space due to underlying instability of the glenohumeral joint.

Secondary impingement may be the most common cause in young athletes who use overhead motions and who frequently place repetitive large stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures and leading to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendon. These increased demands may lead to rotator cuff pathology such as partial tearing or tendonitis, and, as the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging on the coracoacromial arch, which leads to rotator cuff inflammation. In these patients, treatment should be directed at the underlying instability.

Glenoid impingement

Recently, the concept of glenoid impingement has been suggested as an explanation for partial-thickness rotator cuff tears in throwing athletes, particularly those tears involving the articular surface of the rotator cuff tendon. Such tears might occur in the presence of instability due to increased tensile stresses on the rotator cuff tendon either from abnormal motion of the glenohumeral joint or from increased forces on the rotator cuff necessary to stabilize the shoulder.

Arthroscopic studies of these patients have noted impingement between the posterior superior edge of the glenoid and the insertion of the rotator cuff tendon with the arm placed in the throwing position, abducted and externally rotated. Lesions are noted along the area of impingement at the posterior aspect of the glenoid labrum and articular surface of the rotator cuff. This concept is believed to occur most commonly in throwing athletes and must be considered when assessing for impingement and rotator cuff tendonitis.

Clinical

History

• Age
  • Younger than 40 years: It is usually glenohumeral instability. The cause is acromioclavicular joint disease or injury.
  • Older than 40 years: Consider glenohumeral impingement syndrome or rotator cuff tendonitis. Additionally, consider degenerative joint disease of the glenohumeral joint.
• Occupation
  • Laborers and persons with jobs that require repetitive overhead activity (most at risk).
  • Athletes (eg, swimmers, those participating in throwing sports, tennis players, volleyball players)
• Athletic activity
  • Onset of symptoms related to specific phases of the athletic event performed
  • Duration and frequency of play
  • Duration and frequency of practice
  • Level of play (Little League [elementary school], middle school, high school, college, professional)
  • Actual playing time (starter, backup, bench player)
  • Position played
• Symptom onset
  • Sudden onset of sharp pain in the shoulder with tearing sensation - More suggestive of a rotator cuff tear
  • Gradual increase in shoulder pain with overhead activities - More suggestive of an impingement problem
• Chronicity of symptoms
• Location of symptoms (ie, pain)
  • Usually lateral, superior, anterior shoulder; occasionally referred to deltoid region
  • Posterior shoulder capsule - Usually consistent with anterior instability causing posterior tightness
• Setting during which symptoms appear (eg, pain during sleep or various sleeping positions, at night, with activity, types of activities, at rest)
• Quality of pain (eg, sharp, dull, radiating, throbbing, burning, constant, intermittent, occasional)
• Severity of pain (ie, on a scale of 1-10, with 10 being the worst)
• Alleviating factors (eg, change of position, medication, rest)
• Aggravating factors (eg, change of position, medication, increase in practice, increase in play, change in athletic gear, change in position played)
• Associated manifestations (eg, chest pain, dizziness, abdominal pain, shortness of breath) - May indicate a more ominous problem than supraspinatus tendonitis
• Provocative positions
  • Pain with humerus in forward flexed and internally rotated position - Suggestive of rotator cuff impingement
  • Pain with humerus in abducted and externally rotated position - Suggestive of anterior glenohumeral instability and laxity
• Other history - Previous or recent trauma, stiffness, numbness, paresthesias, clicking, catching, weakness, crepitus, symptoms of instability, neck symptoms

Physical

• Inspection
  • Men should wear no shirt; women are instructed to wear a tank top to the visit.
  • Visualize the entire shoulder girdle and scapular area, noting muscle mass asymmetry/atrophy or bony asymmetry.
• Active range of motion:
  • Test this if possible; if not, then test passive range of motion.
  • Test forward flexion. The average range is 150-180°.
  • Test abduction. The average range is 150-180°.
  • Test external rotation. The average range with the arm in adduction is 30-60°, and the average range with the arm in abduction is 70-90°.
  • Test internal rotation. The average range is measured by how high the patient can reach up his or her back with the ipsilateral thumb (ie, ipsilateral hip, T12, L5). The average range is above T8.
  • Test adduction. The average range is 45°.
  • Test extension. The average range is 45°.
  • Note that stiffness with external/internal rotation is best tested with the arm in 90° of abduction. Also, for an optimal evaluation, test external and internal rotation in the supine position with the scapulothoracic articulation stabilized. Moreover, most high-level pitchers have increased external rotation and decreased internal rotation in the pitching arm compared with the nonpitching arm. However, the overall absolute arc of motion when measured in degrees is usually equal. This may not be pathologic in the high-level athletic population. Finally, a painful arc of motion may be experienced with elevation above the shoulder level in patients with impingement (typically 80-150°).
• Palpation
  • Areas that are palpated include the joints, biceps tendons, supraspinatus and subscapularis tendons, and anterolateral corner of the acromion.
  • The entire shoulder girdle is palpated (noting tenderness, deformities, or atrophy) from the acromioclavicular joint, clavicle, glenohumeral joint, scapula, scapulothoracic articulation, anterior/posterior shoulder capsule, supraspinous fossa, infraspinous fossa, and humerus, especially proximally.
• Manual muscle testing
  • Concentrate on the shoulder girdle muscles (especially external and internal rotation, abduction).
  • The supraspinatus may be isolated by having the patient rotate the upper extremity so that the thumbs are away from the floor and resistance is applied with the arms at 30° of forward flexion and 90° of abduction.
  • Note that pain is felt with tendonitis or partial injury to the supraspinatus tendon with the supraspinatus isolation test, but weakness can also be found accompanying partial- or full-thickness disruption of the supraspinatus tendon. Also, weakness may be found with tendonitis because of muscle inhibition from the pain stimulus.
• Special tests (impingement signs)
  • For the Neer test, the examiner forcefully elevates an internally rotated arm in the scapular plane, causing the supraspinatus tendon to be impinged against the anterior inferior acromion.
  • For the Hawkins-Kennedy test, the examiner forcefully internally rotates a 90° forwardly flexed arm, causing the supraspinatus tendon to be impinged against the coracoacromial ligamentous arch. Pain and a grimacing facial expression indicate impingement of the supraspinatus tendon, and this is a positive Neer/Hawkins-Kennedy impingement sign.
  • For the impingement test, the examiner injects 10 mL of a 1% lidocaine solution into the subacromial space and then repeats the tests for the impingement sign. Elimination or significant reduction of pain constitutes a positive impingement test result.
  • With the drop arm test, the patient places the arm in maximum elevation in the scapular plane and then lowers it slowly. The test can be repeated following subacromial injection of lidocaine. Sudden dropping of the arm suggests a rotator cuff tear.
  • With the supraspinatus isolation test/empty can test (ie, Jobe test), the supraspinatus may be isolated by having the patient rotate the upper extremity so that the thumbs are pointing to the floor and resistance is applied with the arms in 30° of forward flexion and 90° of abduction (simulates emptying of a can). The result is positive when weakness is present compared with the unaffected side, suggesting a disruption of the supraspinatus tendon.
• Tests for instability
  • To elicit the sulcus sign, the examiner grasps the patient's elbow and applies inferior traction. Dimpling of the skin subjacent to the acromion (the sulcus sign) indicates inferior humeral translation, which suggests multidirectional instability.
  • The apprehension test is performed most effectively with the patient supine, stabilizing the scapulae. The examiner gently brings the affected arm into an abducted and externally rotated position. The patient's apprehension and guarding by not allowing further motion by the examiner denotes a positive test result, which is consistent with anterior shoulder instability.
  • The relocation test is usually performed in conjunction with the apprehension test. After placing the patient in an apprehensive position, posteriorly directed pressure is applied to the anterior proximal humerus, simulating a relocation of the glenohumeral joint that was presumably partially dislocated from the apprehension test. The adept examiner may feel posterior translation of the humeral head on the glenoid. A positive test result is when the patient's apprehension is relieved by the application of pressure on the anterior proximal humerus, which suggests anterior shoulder instability.
• Note: Any tests completed should compare both shoulders in order to detect bilateral pathology or have a control for comparison with the affected shoulder.
• Other tests: These should be performed during the shoulder examination to rule out other pathology affecting the biceps tendon, glenoid labrum, cervical spine, sternoclavicular joint, acromioclavicular joint, and scapulothoracic joint. A survey of other joint range of motion should also be performed to assess for generalized ligamentous laxity.
• Neurovascular examination
  • To complete the shoulder examination, a full neurologic examination must be performed along with an assessment of all upper extremity vascular pulses.
  • The neurologic examination should include all neurologic segments from C5 through T1 myotome and dermatome, with the corresponding stretch reflexes.

Causes

• Extrinsic causes
  • Primary impingement
    • Increased subacromial loading
    • Trauma (direct macrotrauma or repetitive microtrauma)
    • Overhead activity (athletic and nonathletic)
  • Secondary impingement
    • Rotator cuff overload/soft tissue imbalance
    • Eccentric muscle overload
    • Glenohumeral laxity/instability
    • Long head of the biceps tendon laxity/weakness
    • Glenoid labral lesions
    • Muscle imbalance
    • Scapular dyskinesia
    • Posterior capsular tightness
    • Trapezius paralysis
• Intrinsic causes
  • Acromial morphology (ie, hooked acromion, presence of an os acromiale or osteophyte, calcific deposits in the subacromial space, all of which predispose to primary impingement)
  • Acromioclavicular arthrosis (inferior osteophytes)
  • Coracoacromial ligament hypertrophy
  • Coracoid impingement
  • Subacromial bursal thickening and fibrosis
  • Prominent humeral greater tuberosity
  • Impaired cuff vascularity
  • Aging (primary)
  • Impingement (secondary)
  • Primary tendinopathy
  • Intratendinous
  • Articular side partial-thickness tears
  • Calcific tendinopathy

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