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L i s te n to T h e A B M P Po d c a s t a t a b m m /p o d c a s t s o r w h e reve r yo u a cce s s yo u r favo r i te p o d c a s t s 87 prominent roles in keeping the humeral head partially depressed during overhead shoulder motions. These muscles are critical for ensuring the humerus doesn't migrate in a superior direction and pinch tissues under the coracoacromial arch. Now that we have explored the architecture and mechanics of this region, let's examine some of the main causes of SAPS. DESCRIPTION OF PATHOLOGY There are two primary models of SAPS: the mechanistic and the biological. We now realize many shoulder complaints are a combination of both. The mechanical has been the dominant model for decades and is a bit more complex, so we'll take a detailed look at it first. The mechanical model suggests there is a biomechanical problem leading to the subacromial pain. 2 As noted earlier, this condition was previously referred to as subacromial impingement syndrome. Subacromial impingement is usually divided into two categories. The first is primary impingement, which results from problematic architecture of the subacromial region. For example, if there is very little space between the acromion process and the upper part of the humeral head, this narrow space would make impingement more likely and be considered a cause for primary impingement. Secondary impingement is a result of biomechanical dysfunction or overuse in the shoulder region but does not necessarily result from decreased subacromial space. The original description of subacromial impingement was presented by Charles Neer in a paper he wrote in the early 1970s. 3 According to his classification, the pathology begins with edema and thickening of the bursa in the first stage. It progresses to fibrosis and other inflammatory changes within the supraspinatus in the second stage. Eventually this can lead to a complete tear of the supraspinatus tendon in the third stage. However, more recent findings have called into question this tissue progression, so Neer's classification is no longer considered a standard sequence of events. Most models of mechanical impingement now focus on the subacromial region, thus they're being labeled as subacromial impingement syndrome. Pain is generally felt more in the lateral aspect of the shoulder and is most aggravated during shoulder abduction movements but may be felt during forward-flexion movements, as well. The tissues most involved in subacromial impingement include the subacromial bursa, supraspinatus tendon, upper margin of the glenohumeral joint capsule, coracohumeral ligament, and long head of the biceps brachii tendon (Image 2). There is another region of potential impingement that does not get as much attention as the subacromial space. Tissue compression under the coracoid process, or the lower margin of the coracoacromial ligament, is called anterior or subcoracoid impingement. Possible causes of subcoracoid pain include entrapment of the superior border of the subscapularis tendon, bursitis, subscapularis tendon calcification, or ossification and inflammatory enlargement of the glenohumeral ligaments. 4 Pathology of the bicep tendon may also be a cause (Image 3). Some research also points toward subcoracoid pain arising from the underside of the subscapularis where it comes in contact with the glenohumeral joint. In some cases, excess friction can irritate the Tissues involved in subacromial pain: 1. Subacromial bursa; 2. Supraspinatus tendon; 3. Upper margin of the glenohumeral joint capsule; 4. Coracohumeral ligament; and 5. Long head of the biceps brachii tendon. Image from 3D4Medical's Complete Anatomy application. Tissues involved in subcoracoid pain: 1. Upper margin of subscapularis tendon; 2. Coracobrachialis bursa; and 3. Upper margin of the glenohumeral joint capsule. Image from 3D4Medical's Complete Anatomy application. 2 3 1 1 2 2 3 3 4 5

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