In 1972, Neer first introduced the concept of rotator cuff impingement to the literature, stating that it results from mechanical impingement of the rotator cuff tendon beneath the anteroinferior portion of the acromion, especially when the shoulder is placed in the forward-flexed and internally rotated position. 
Neer describes the following 3 stages in the spectrum of rotator cuff impingement:
Stage 1, commonly affecting patients younger than 25 years, is depicted by acute inflammation, edema, and hemorrhage in the rotator cuff. This stage usually is reversible with nonoperative treatment.
Stage 2 usually affects patients aged 25-40 years, resulting as a continuum of stage 1. The rotator cuff tendon progresses to fibrosis and tendonitis, which commonly does not respond to conservative treatment and requires operative intervention.
Stage 3 commonly affects patients older than 40 years. As this condition progresses, it may lead to mechanical disruption of the rotator cuff tendon and to changes in the coracoacromial arch with osteophytosis along the anterior acromion. Surgical l anterior acromioplasty and rotator cuff repair is commonly required.
In all Neer stages, etiology is impingement of the rotator cuff tendons under the acromion and a rigid coracoacromial arch, eventually leading to degeneration and tearing of the rotator cuff tendon.
Although rotator cuff tears are more common in the older population, impingement and rotator cuff disease are frequently seen in the repetitive overhead athlete. The increased forces and repetitive overhead motions can cause attritional changes in the distal part of the rotator cuff tendon, which is at risk due to poor blood supply. Impingement syndrome and rotator cuff disease affect athletes at a younger age compared with the general population.
Magnetic resonance imaging (MRI) is considered the imaging study of choice for evaluation of shoulder pathology. In general, conservative measures for shoulder impingement syndrome are applied for at least 3-6 months or longer if the individual is improving, which is usually the case in 60-90% of patients. If the patient remains significantly disabled and has no improvement after 3 months of conservative treatment, the clinician must seek further diagnostic work-up, as well as reconsider other etiologies or refer the person for surgical evaluation.
No documented information on the occurrence of shoulder impingement syndrome exists.
The shoulder consists of 2 bones (humerus, scapula), 2 joints (glenohumeral, acromioclavicular), and 2 articulations (scapulothoracic, acromiohumeral) that are joined by several interconnecting ligaments and layers of muscles. Minimal bony stability in the shoulder permits a wide 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, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles (eg, pectoralis major, latissimus dorsi, serratus anterior).
The rotator cuff consists of 4 muscles that control 3 basic motions, abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor muscles control external rotation, and the subscapularis muscle controls 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. This force couple is responsible for 45% of abduction strength and 90% of external rotation strength.
The supraspinatus outlet is a space formed on the upper rim, humeral head, and glenoid by the acromion, coracoacromial arch, and acromioclavicular joint. This outlet accommodates passage and excursion of the supraspinatus tendon. Abnormalities of the supraspinatus outlet have been attributed as a cause of impingement syndrome and rotator cuff disease, though other causes have been discovered. Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described how variations in acromial size and shape can contribute to impingement. 
Cadaveric studies show 3 variations in acromion morphology, as follows: type 1 is flat, type 2 is curved, and type 3 is hooked anteriorly. Although the curved configuration was the most common (43% prevalence, compared to 17% flat and 40% hooked), the hooked configuration most strongly was associated 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). The medial coracoid rarely is 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 also can occur. Causes may be loss of normal humeral head depression from either a large rotator cuff tear or weakness in the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. This condition also may occur because of thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.
Overuse or repetitive microtrauma sustained in the overhead position may contribute to impingement and rotator cuff pathology. Shoulder pain and rotator cuff disease are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, volleyball, tennis).
Secondary impingement often is attributed to impingement, which seldom is mechanical in nature in young athletes. Rotator cuff disease in this population may be related to subtle instability, and, therefore, may be secondary to such factors as eccentric overload, muscle imbalance, 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 frequently place large, repetitive overhead stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures, which leads to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendons.
These increased demands may lead to rotator cuff pathology (eg, partial tearing, tendonitis). Furthermore, as the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging upon the coracoacromial arch. This leads to rotator cuff inflammation. In these patients, treatment should address underlying instability.
The concept of glenoid impingement has been advanced as an explanation for partial-thickness tears in throwing athletes, particularly those involving the articular surface of the rotator cuff tendon. Such tears may occur in the presence of instability due to increased tensile stresses on the rotator cuff tendon from abnormal motion of the glenohumeral joint or increased forces on the rotator cuff necessary to stabilize the shoulder.
Arthroscopic studies of these patients note 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.
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