Any accompanying soft tissue pathology surrounding the glenohumeral ( Shoulder ) joint including but not limited to:
1) Impingement syndrome
2) Calcific tendinitis
3) Subacromial bursitis
4) Supraspinatus tendonitis
5) Bicipital tendonitis
The rotator cuff tendons provide a major contribution to the dynamic stabilization of glenohumeral joint by stabilizing the humeral head within the concavity of glenoid, resulting in the compression force in the joint. The balance between the superior force generated by the deltoid muscle and the central inferior direction of rotator cuff force couple is lost during rotator cuff pathologies. The result is diminution of joint reaction force and the change in overall direction of the joint force that leads to an unstable glenohumeral joint with superior displacement of the humeral head.
Resulting in shoulder Impingement-A shoulder impingement is the main extrinsic cause of the RC tendinopathy. It occurs with mechanical compression of the external portion (bursal side) of the tendon, which leads to inflammation and degeneration. Upon repeated occurrence, the coracoacromial ligament may thicken, decreasing the subacromial space. Overuse activities coupled with coracoacromial arch changes have a significant effect on the tendon injury. Significant relationships have been demonstrated between acromion morphology, the patient's self reported shoulder function, and the severity of the RC pathology.
Resulting in subacromial bursitis-Muscle deficits, soft tissue tightness and abnormal posture directly influence shoulder kinematics. Weakness or dysfunction of the rotator cuff muscles can set up a situation that leads to Sub Acromial Impingement Syndrome due to a narrow Subacromial Space. There is a superior humeral head translation and decreased abduction torque when there is reduced force of RC muscles, especially infraspinatus. The RC tendinopathy is seen in individuals with significant decreases in muscle peak isometric, eccentric and concentric torque when compared to those without these deficits. Decreased muscle co‐activation ratios between subscapularis, infraspinatus, and supraspinatus during the first 30 degrees of arm elevation and an increase at above 90 degrees was seen in patients exhibiting impingement as compared to the control group with no impingement
Resulting in bad posture and movement abnormalities-Individuals who have some sort of impingement are thought to develop compensational movement patterns that relieve the compression and increase the subacromial space.
Capular dyskinesis in subjects with the RC tendinopathy has been theorized to include aberrant scapular and the RC neuromuscular activation and muscle performance, thoracic kyphosis, pectoralis minor shortening, and posterior shoulder tightness. A shortened pectoralis minor muscle at rest has been indirectly correlated with the RC tendinopathy, functional deficits, and pain. This is again thought to be attributed to abnormal scapular kinematics. In subjects with the RC tendinopathy, it was found that the serratus anterior and lower trapezius muscles demonstrate reduced muscle force and performance
Resulting in Tendinopathy-Tendons must be able to handle tensile loads and their ability to do so relies on Type 1 collagen. However, a key feature of tendinopathy can be seen through collagen structure analysis by showing the disruption of tendon microarchitecture, which helps to understand the response to variable amounts of cyclic loading. The process starts with tendonitis, then progressed to tendinosis with degeneration and partial thickness tears, and finally resulted in full thickness tears.
Resulting in AC joint degeneration -The AC joint could be another contributing factor. Over time, this joint degenerates and osteophytes can form on the inferior aspect of the distal clavicle. These arthritic signs have been correlated with the presence of the RC pathology. The spurs are termed an enthesopathy and are thought to form from a coracoacromial ligament sprain. These spurs may also be a secondary formation after sustaining a bursal‐side RC tear.
Resulting in further blood circulation, tendinosis and rupture-Decreased microvascular blood supply has been discussed as a possible cause of the intrinsic pathology but it can also come from an extrinsic cause. For example, when the arm is in full abduction, and the supraspinatus is compressed by the humeral head, the reduction in perfusion may be significant
Resulting in dislocation The scapulohumeral rhythm affects the scapula during the arm elevation. Most of the posterior tilting occurred after the 90° elevation, but as the arm is not elevating properly beyond 90°, the posterior tilting of scapula is affected along its long axis can also be affected that can cause degeneration of the acromioclavicular joint. Normally the scapular strength increases joint stability by placing the glenoid fossa under the humeral head serving as a stable base for the glenohumeral function. Rotator cuff muscles which function as dynamic stabilizers to the humeral head, when weakened would create an added stress for the static shoulder stabilizers, that is a capsule and ligaments, which in turn increases the chance of the dislocation in the future. Because the rotator cuff muscle weakness and, inharmonious scapular moment due to fatigued scapular muscles must put the cuff muscles at even further disadvantage. The combination of the abnormal scapulothoracic rhythm distress, the levator scapula and upper trapezius, creating myo fascial trigger points and painful nodes
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