Wing K. Chang, MDa,b,* aDepartment of Rehabilitation Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA bNYCONN Orthopaedic and Rehabilitation Specialists, 1421 Third Avenue, Penthouse, New York, NY 10028, USA
Neer first introduced the concept of rotator cuff impingement in 1972. He described the syndrome as a mechanical impingement of the rotator cuff tendons beneath the anterior-inferior portion of the acromion occurring when the shoulder is placed in the forwardly flexed and internally rotated position. Neer described three stages in the spectrum of rotator cuff impingement. Stage I, which is seen most commonly in patients younger than 25 years of age, has acute inflammation, edema, and hemorrhage in the rotator cuff. This stage usually is reversible with nonoperative treatment. Stage II usually is seen in patients age 25 to 40 and represents a progression from acute edema and hemorrhage to fibrosis and tendinitis of the rotator cuff. Stage II pathology may not respond to conservative treatment and may require operative intervention. Stage III is typified by mechanical disruption of the rotator cuff tendons and changes in the coracoacromial arch with osteophytosis along the anterior acromion. This stage commonly affects patients older than 40 years of age and commonly requires surgical anterior acromioplasty and rotator cuff repair. In all stages, Neer believed the etiology to be impingement of the rotator cuff tendons under the acromion and the rigid coracoacromial arch, eventually leading to degeneration and tearing of the rotator cuff tendon. Although rotator cuff tears are more common in older populations, impingement and rotator cuff disease are increasingly more common in athletes whose sports involve repetitive overhead motions. The increased forces and repetitive overhead motions can cause attritional changes in the distal part of the supraspinatus tendon, which is most at risk due to its poor blood supply. Impingement syndrome and rotator cuff disease affect athletes at a younger age than in the general population as described by Neer.
The shoulder consists of two bones (humerus and scapula), two joints (glenohumeral and acromioclavicular), and two articulations (scapulothoracic and acromiohumeral), which are joined by several interconnecting ligaments and layers of muscles. Minimal bone stability in the shoulder permits awide range of motion (ROM). Soft tissue structures are the major glenohumeral stabilizers. Static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. Dynamic stabilizers include the rotator cuff muscles (supraspinatus, infraspinatus, teres minor, and subscapularis), long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles (eg, pectoralis major, latissimus dorsi, and serratus anterior). The rotator cuff consists of four muscles that control three basic motions: abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor control external rotation, and the subscapularis controls internal rotation. The rotator cuff muscles provide dynamic stabilization to the humeral head in the glenoid fossa (fulcrum effect) and form a ‘‘force couple’’ with the deltoid to allow elevation of the arm. The rotator cuff 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 attributed as the cause of impingement syndrome and rotator cuff disease. Other causes since have been discovered. Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani et al discovered and described variations in acromial size and shape that can contribute to impingement. Based on cadaver studies, there seem to be three different variations in the morphology of the acromion: Type I is flat, type II is curved, and type III is hooked anteriorly. Although the curved configuration was the most common (43% prevalence compared with 17% for flat and 40% for hooked), the hooked configuration was associated most strongly with full-thickness rotator cuff tears. 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 various 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 also can occur. The causes may be loss of normal humeral head depression from a large rotator cuff tear or weakness of the rotator cuff muscles from a C5-6 neural segmental lesion or a suprascapular mononeuropathy. Another way this impingement may occur is through thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.
Athletes with shoulder pain and rotator cuff disease most often are involved in sports requiring repetitive overhead arm motions, such as swimming, baseball, and tennis. Rotator cuff disease in this population more likely is related to subtle instability and secondary to factors such as eccentric overload, muscle imbalance, glenohumeral instability, and labral lesions. These instances of rotator cuff disease have led to the concept of secondary impingement, which is defined as rotator cuff impingement that occurs secondary to a functional dynamic decrease in the supraspinatus outlet space due to underlying instability of the glenohumeral joint. Young overhead athletes frequently place repetitive large stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures and generating subclinical glenohumeral instability. This instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendons. These increased demands lead to rotator cuff pathology, such as partial tearing or tendinitis. As the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging on the coracoacromial arch, leading to rotator cuff inflammation. In these patients, treatment should be directed at the underlying instability. The concept of glenoid impingement has been advanced as an explanation for partial-thickness tears in throwing athletes, particularly tears involving the articular surface of the rotator cuff tendon. These 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 were 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.
In patients younger than 40 years of age, history may include the
- Usually glenohumeral instability
- Acromioclavicular joint disease/injury
In patients older than 40 years of age, history may include the following:
- Glenohumeral impingement syndrome/rotator cuff disease
- Glenohumeral joint degenerative joint disease
Most at risk for impingement are laborers with jobs requiring repetitive overhead activity and athletes (eg, wimming, throwing sports, tennis, volleyball). The following need to be considered in regard to athletic activity:
- Onset of symptoms in relation to specific phases of the athletic event performed
- Duration and frequency of play
- Duration and frequency of practice
- Level of play (little league, pre–high school, high school, college,
- Actual playing time (starter, backup, bench player)
- Position played
The following need to be considered in regard to symptoms:
- Sudden onset of sharp pain in the shoulder with tearing sensation suggests rotator cuff tear
- Gradual increase in shoulder pain with overhead activities suggests an impingement problem
Chronicity of symptoms
Location of symptoms
- Pain usually lateral, superior, anterior shoulder, occasionally refers to deltoid region
- Posterior shoulder capsule pain usually consistent with anterior instability causing posterior tightness
- Setting during which symptoms come on Quality of pain (eg, sharp, dull, radiation, throbbing, burning, constant, intermittent, occasional)
Quantity of pain (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/footwear, change in position played)
Associated manifestations (eg, chest pain, neck pain, dizziness, abdominal pain, shortness of breath, numbness, weakness)
- Pain with humerus in forward flexed and internally rotated position suggests rotator cuff impingement
- Pain with humerus in abducted and externally rotated position suggests anterior glenohumeral instability and laxity
Other questions to ask in regard to the history include questions about previous or recent trauma, stiffness, numbness, paresthesias, clicking, catching, weakness, crepitus, symptoms of instability, and neck symptoms.
For the inspection portion of the physical examination, the clinician needs to:
- Visualize the entire shoulder girdle and scapula
- Note muscle mass asymmetry/atrophy and bony asymmetry
Range of motion
Active ROM is tested if possible; if not, passive ROM is tested, as follows:
- Forward flexion (average range 150–180º)
- Abduction (average range 150–180º)
- External rotation (average range with arm in adduction 30–60º; with arm in abduction 70–90º)
- Internal rotation (average range measured by how high the patient can reach the back with the ipsilateral thumb
(average range above T8)
- Adduction (average range 45º)
- Extension (average range 45º)
The following considerations apply in regard to ROM testing:
Stiffness with external/internal rotation is best tested with the arm in 90º of abduction.
It is best to test external/internal rotation in the supine position with the scapulothoracic articulation stabilized.
Most high-level pitchers have increased external rotation and decreased internal rotation in the pitching arm compared with the nonpitching arm. This may not be pathologic in high-level athletes.
Palpation is performed along the joints, noting the biceps tendons, supraspinatus and subscapularis tendons, and anterolateral corner of the acromion. The entire shoulder girdle is palpated (noting tenderness, deformities, and 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
For manual muscle testing, the clinician should concentrate on the shoulder girdle muscles (especially external/internal rotation, abduction). The supraspinatus may be isolated by having the patient rotate the upper extremity so that the thumbs are pointing to the floor; resistance is applied with the arms in 30 of forward flexion and 90 of abduction (called the supraspinatus isolation test or empty can test (position imitates the position of emptying of a can). The following considerations apply in regard to manual muscle testing:
Pain is felt with tendinitis or partial injury to the supraspinatus tendon with the supraspinatus isolation test, but weakness also is found accompanying partial-thickness or full-thickness disruption of the supraspinatus tendon.
Weakness also may be found with tendinitis due to muscle inhibition from the pain stimulus.
All tests performed should compare both shoulders either to detect bilateral pathology or to establish a control for comparison with the affected shoulder.
Impingement signs. There are two tests for impingement signs. In 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. In the Hawkins-Kennedy test, the examiner forcefully internally rotates a 90º 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—a positive Neer/Hawkins impingement sign.
Impingement test. The examiner injects 10 mL of a 1% lidocaine solution into the subacromial space, then repeats the tests for impingement sign. Elimination or significant reduction of pain constitutes a positive impingement test.
Drop arm test. The examiner places the patient’s arm in maximum elevation in the scapular plane. The patient is asked to lower it slowly to the side (the test can be repeated after subacromial injection of lidocaine). Sudden dropping of the arm suggests rotator cuff tear.
Supraspinatus isolation test. The supraspinatus tendon may be isolated by having the patient rotate the upper extremity so that the thumbs are pointing to the floor; resistance is applied with the arms in 30º of forward flexion and 90º of abduction (called the supraspinatus isolation test or empty can test). The test is positive when weakness is present compared with the unaffected side, suggesting a disruption of the supraspinatus tendon.
Tests for instability
For 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, suggesting multidirectional instability.
The apprehension test is done most effectively with the patient in supine position stabilizing the scapula. 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 that is consistent with anterior shoulder instability.
Other tests should be performed to rule out other pathology affecting the biceps tendon, the glenoid labrum, the cervical spine, the sternoclavicular joint, the acromioclavicular joint, and the scapulothoracic joint. A survey of other joint ROM also should be performed to assess for generalized ligamentous laxity.
To complete the shoulder examination, a full neurologic examination must be performed along with assessment of all upper extremity vascular pulses. The neurologic examination should include all neurologic segments from C5 through T1 myotome, dermatome, and the corresponding stretch reflexes.
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