Capsuloligamentous Constraint.

Last updated Thursday, February 10, 2005

Figure 1 - Maximum humeroscapular angle
Figure 1 - Maximum humeroscapular angle

Figure 2 - Amount of internal and external rotation
Figure 2 - Amount of internal and external rotation

Common functional positions
Common functional positions

No capsular tension
No capsular tension

Shoulders were stressed to the clinical end point
Shoulders were stressed to the clinical end point

The amount of translation was highly reproducible
The amount of translation was highly reproducible

This group of normal shoulders demonstrated substantial translations on these clinical laxity tests
This group of normal shoulders demonstrated substantial translations on these clinical laxity tests

The magnitudes of the passive glenohumeral translations measured in the unstable shoulders were remarkably similar to those measured in the normal subjects
The magnitudes of the passive glenohumeral translations measured in the unstable shoulders were remarkably similar to those measured in the normal subjects

About capsuloligamentous constraint

The capsule and its ligaments

The capsule and ligaments of the glenohumeral joint serve as check reins to glenohumeral translation and rotation. They are not "primary stabilizers" in that they do not effectively hold the humeral head centered in the glenoid socket in most functional positions of the joint.

The capsule and its ligaments arise in continuity with the articular surface of the glenoid through the glenoid labrum, so that when they are under tension they provide a smooth continuation of the glenoid concavity. By serving as check reins at the limits of glenohumeral motion, the capsule and ligaments control the maximum humeroscapular angle that can be achieved in a given direction as well as the amount of internal and external rotation that is allowed at each humeroscapular position. For example, the posterior capsule limits how far the elevated arm can be brought across the body. Glenohumeral joints with lax posterior capsules can reach the 90 degree anterior humeroscapular plane. Shoulders with tight posterior capsules have difficulty reaching the 45 degree anterior humeroscapular plane. Similarly, the anterior capsule limits posterior motion of the elevated arm. Shoulders with anterior capsular laxity achieve significantly more posterior humeroscapular planes than shoulders with tight anterior structures. In this way, the capsule prevents the humerus from deviating far from positions of glenohumeral balance.

Certain portions of the capsular complex that serve major roles are condensed and thickened in the form of capsular ligaments. These ligaments appear to represent capsular reinforcements in directions where large torques may be encountered at the extremes of motion, as in swinging from branch to branch or in the transition between the cocking and the acceleration phases in a baseball pitch. These motions apply major torques to the joint. The strong anterior band of the inferior glenohumeral ligament is strategically positioned to check the range of rotation of the joint when the arm is elevated and forced into external rotation.

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Necessary for large range of joint positions

The capsule and its associated ligaments are lax in most of the common functional positions of the glenohumeral joint.

To see this compare the common functional positions with the envelope of motion in which there is no capsular tension (see figures). This laxity is necessary for the joint to achieve its large range of positions. Because of this midrange laxity, the capsule cannot stabilize the joint in many important functional positions. Instead, centering of the humeral head in the glenoid fossa must depend on other mechanisms, such as concavity compression.

To demonstrate the degree of laxity present in eight normal shoulders, electromagnetic sensors were pinned to the humerus and scapula to allow accurate measurement of the magnitude of translation on standard clinical tests of glenohumeral laxity: the anterior and posterior drawer tests, the sulcus test, and the push-pull test. The anterior and posterior drawer tests were performed by stabilizing the scapula and clavicle with one hand while grasping the proximal humerus with the other hand. The arm was placed in a relaxed position at the subject's side. The humeral head was pushed forward to assess maximal anterior translation and then pushed posteriorly to assess maximal posterior translation. In the sulcus test, downward traction was applied to the subject's arm while the shoulder girdle was stabilized with the other hand.

The push-pull test was performed with the subject supine and the arm elevated 90 degrees in the plus 20 degrees thoracic plane. The examiner pushed down on the proximal humerus with one hand while pulling up on the subject's wrist with the other.

The shoulders were stressed to the clinical end point. Even though the force applied was not quantified, the amount of translation was highly reproducible. The results of these tests indicate that this group of normal shoulders demonstrated substantial translations on these clinical laxity tests. These data indicate that, in the positions tested, the capsule and ligaments were lax and were not contributing to the centering of the humeral head in the glenoid fossa. We conclude that in these midrange positions, the head is centered by stabilizing mechanisms other than the capsule and ligaments.

Because laxity is a feature of stable shoulders, it is of interest to ask whether unstable shoulders have more laxity than stable shoulders. Of greater clinical relevance are the questions: Are laxity tests useful in discriminating stable from unstable shoulders? Do laxity tests reveal the primary pathology in glenohumeral instability? As a step toward answering these questions, we measured the laxity of 16 patients requiring surgery because of symptomatic recurrent instability that was refractory to non-operative management. We then compared these results with those of normal shoulders presented earlier. Eight of these patients had classic anterior traumatic instability and eight had classic atraumatic instability. Each patient was studied under anesthesia just prior to surgical repair, with our electromagnetic position sensors rigidly attached to the humerus and scapula. The laxity tests were carried out exactly as described earlier for the normal subjects. The magnitudes of the passive glenohumeral translations measured in the unstable shoulders were remarkably similar to those measured in the normal subjects.

These results suggest that glenohumeral laxity is not the preponderant factor in determining the clinical stability of the shoulder. Shoulders that are quite lax may be completely stable, while those without major laxity may be clinically unstable. These data further serve to caution against using the magnitude of translation on these laxity tests to distinguish between clinically stable and unstable shoulders. As we will see, the diagnosis of instability must rest on a careful history and physical examination which endeavor to define the problem that is symptomatic for the patient.

In conclusion, substantial translational laxity is allowed by the normal glenohumeral joint capsule, especially in midrange positions. The wide variance in translation among normal shoulders precludes the definition of a "normal" amount of translation on laxity tests. Translation on clinical laxity tests is not an indication of instability. Stability of the glenohumeral joint, especially in midrange positions, must be due to factors other than tension in the capsular structures.

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