Pathology
The greatest range of motion of any joint in the body occurs in the glenohumeral joint. While freedom of movement is necessary in performing various actions of the shoulder, there is increased potential for soft-tissue injury. Without stabilization from the bony structures of the joint, much of the structural support must come from soft-tissue support. Thus, muscles, tendons, ligaments and the joint capsule make up the primary support for this joint.

The joint capsule's fundamental role is in restricting excess motion. However, because there is such a great range of motion in the shoulder joint, the capsule must be able to allow a wide range of movement before it restricts that motion. The glenohumeral joint capsule is looser than many other joint capsules in the body in order to accommodate this greater range of motion.

The above image shows the glenohumeral joint capsule with the shoulder in a neutral position. Notice that when the shoulder is in this position, there is a slackening of the joint capsule on the underside. The underside of the capsule is made up of capsular tissue as well as the inferior glenohumeral ligament. In order to allow the full range of glenohumeral motion, the capsule must be slack on the underside. As other shoulder motions are performed, this portion of the capsule will become taut while others slacken.

The pathology in adhesive capsulitis develops when a portion of the capsule (usually the underside) adheres to itself and prevents full movement. The joint capsule is richly innervated, so when the adhesions pull on the capsular tissues, it is very painful.

There are two categories of adhesive capsulitis: primary and secondary. In primary capsulitis, there is no easily apparent cause for the condition. It is frustrating for many health-care providers because they aren't able to identify what created the problem and help the patient/client better understand why it happened. It is difficult to avoid the aggravating factors of the condition without understanding what triggered the problem.

What can make primary capsulitis more challenging is that, in some cases, there seems to be a correlation between significant emotional trauma and the development of adhesive capsulitis. While there is not a clear cause/effect relationship, this correlation can lead some health-care practitioners to presume the condition is primarily psychological in nature. However, the seriousness of the problem should not be minimized simply because a structural or mechanical cause cannot be found.

In this case, the capsular adhesion occurs as a result of some other pathology. For example, in the glenohumeral joint, secondary capsulitis will often develop as a result of rotator-cuff tears, arthritis, bicipital tendinosis (an abnormal condition of the tendon when no inflammatory cells are present), shoulder trauma, surgery or other problems. There appears to be a process of fibrosis that is initiated by these other conditions. Consequently, the individual is usually limiting motion in the shoulder at the same time that fibrous proliferation is occurring. As a result, the fold on the underside of the joint capsule never gets fully elongated, and the fibrous proliferation causes the two sides of the fold to adhere to each other. A vicious cycle then follows. The adhesion causes pain and limitation to movement, thus worsening the problem.

Another possible cause of secondary capsulitis is the presence of myofascial trigger points. There is an indication that trigger-point activity in the subscapularis muscle can set off a cascade of adhesion in the capsule. This may result from irritation of the attachment site of the subscapularis, which is very close to the joint capsule. Local inflammation at the attachment site will then cause fibrous adhesion in the capsule.

Adhesive capsulitis can be a stubborn condition and last for many months. In fact, it is not unusual for the problem to last 18 months or more. The severity of the problem and its recuperation time depend upon how early in its development it can be halted.

The problem is often divided into three different stages:

• Freezing: Onset is usually between 10 and 36 weeks. This stage is characterized by a gradual decrease in range of motion and an increase of pain.

• Frozen: This period occurs between four and 12 months after initial onset. Motion is likely to remain limited though a gradual decrease in pain may be occur.

• Thawing: This period is characterized by a gradual return of range of motion and decreased pain. This stage may be as short as several months, but it is not uncommon for it to last for years.

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