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Multidirectional Glenohumeral Instability: Background, Anatomy, Pathophysiology
9/26 11:26:35

Background

Multidirectional instability (MDI) is a relatively common, generally bilateral, typically atraumatic condition affecting shoulder function. MDI is caused by generalized capsular laxity—that is, insufficiency of the static ligament constraints of the glenohumeral joint (GHJ). There is excessive mobility of the GHJ in all directions: anterior, posterior, and inferior. However, there may be a predominance of one direction, typically anteroinferior or posteroinferior.[1]

The history of MDI of the shoulder is neither as colorful nor as ancient as that of traumatic shoulder instability. Whereas traumatic shoulder dislocation and its treatment can be traced back to ancient Egypt, MDI was acknowledged as a real entity only as recently as 1980, when it was first described in detail by Neer and Foster. Although Perthes[2] in 1906 and Bankart[3] in 1923 described the essential lesion of recurrent traumatic glenohumeral dislocations (ie, detachment of the labrum and inferior glenohumeral ligament from the glenoid), the role of generalized capsular laxity in glenohumeral instability was not appreciated until 1980.

A patient with symptomatic MDI may complain of instability symptoms but often presents only with pain, and therefore, a high index of suspicion is required. The diagnosis is highly clinical. Suggestive history and physical examination findings are the basis of a diagnosis of MDI (see Presentation). Imaging studies, including plain radiography, magnetic resonance imaging (MRI), and magnetic resonance (MR) arthrography, may be of marginal help (see Workup). Examination under anesthesia (EUA) and arthroscopic findings are highly supportive.

Initial treatment is conservative, focusing on strengthening the dynamic components of shoulder stability—the rotator cuff and the scapular stabilizers. A conservative approach is most often successful; however, when a period of prolonged rehabilitation (3-6 months) fails, surgical management may be undertaken to enhance static stabilization by tightening the shoulder capsule. (See Treatment.) Historically, this was classically accomplished with an open procedure, but arthroscopic management is evolving rapidly. The prognosis for MDI is generally good.

For patient education resources, see the First Aid and Injuries Center, as well as Shoulder Dislocation and Shoulder Separation.

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Anatomy

The GHJ is a relatively nonconstrained joint, and the GHJ in MDI is excessively so. Typical characteristics of MDI are that of a loose capsule, with poorly developed glenohumeral ligaments, and a variable labral anatomy. The labrum may be normal and unimpressive for an unstable joint, or attenuated or hypoplastic, or even sometimes torn or abraded. Anterior and/or posterior labral tears or separation may be present (Bankart lesions[3] ).

Capsular tissue is typically thin and redundant, especially inferiorly, with small anterior and posterior bands of the inferior glenohumeral ligaments, and superiorly, at the cuff interval. The axillary recess or pouch is impressively patulous. The articular surfaces are most often normal or show minimal condromalacia, and Hill-Sachs impaction type lesions are quite atypical. For more anatomic details, see Treatment.

Pathophysiology

Physicians must thoroughly understand basic shoulder biomechanics to understand MDI, to make the diagnosis in appropriate cases, and to prescribe a proper treatment plan. The best-written, most elegant, most concise, and most readable summary of shoulder stability is that of Matsen et al.[4] Review of this text is encouraged; highlights are summarized in this section.

The shoulder is unlike other joints in the body in that for it to meet the demands for extreme motion, osseous- and ligamentous-based stability is sacrificed. Matsen et al described the following concepts, which contribute to the stability of the shoulder joint:

  • Balance
  • Concavity compression
  • Superior stability
  • Adhesion-cohesion
  • Glenohumeral suction cup
  • Limited joint volume
  • Capsuloligamentous constraints

Balance

Balance refers to the passage of the net joint-reaction forces on the humeral head through the center of the glenoid fossa. An analogy is made to a golf ball on a tee. The key components of balance include alignment of the humerus with the glenoid center line, facilitated by the surface arcs and areas of the glenoid and humeral head and by the muscles that position these two bones relative to each other—namely, the rotator cuff and scapular positioners. Factors that affect balance stability include loss of glenoid surface area, scapular malalignment, and muscle imbalance or weakness (eg, rotator-cuff dysfunction).

Concavity and compression

The concept of concavity compression refers to the stabilizing effect of the depth of the concave glenoid fossa on translation of the convex humeral head. This is augmented by (1) the increased thickness of the glenoid articular cartilage at the periphery of the glenoid relative to its center, (2) the glenoid labrum, and (3) the compressive force of an appropriately functioning rotator cuff. Factors that affect this component include deficiencies of glenoid concavity (congenital flatness); labral hypoplasia, attrition, or tearing; and rotator-cuff dysfunction.

Superior stability

Superior stability refers specifically to the superior-inferior component of glenoid concavity, which resists proximal migration of the humeral head within the glenoid. Coupled with the compressive function of the rotator cuff, even with a torn supraspinatus, this component can resist the upward pull of the deltoid. Factors that affect such superior stability include a deficient superior glenoid and the biceps-labral anchorage.

Adhesion-cohesion

Adhesion-cohesion is a mechanism by which fluid on coated surfaces provides an intrinsic adherence between the surfaces. This may be affected by changes in the fluid chemistry (secondary to inflammatory disease), loss of smoothness of the surfaces (secondary to degenerative disease), and alterations in the contact areas.

Glenohumeral suction cup

The glenohumeral suction-cup effect depends upon the tendency for matched concave and convex surfaces with a flexible periphery to center and stabilize after expressing any intervening air and fluid, thereby forming a seal. Deficiencies of the glenoid labrum or of the margin of the glenoid can adversely affect this stabilizing mechanism.

Limited joint volume

The limited joint volume mechanism reflects the fact that the normal GHJ is really a potential space, contains minimal fluid, and has an inherent negative pressure. A sealed joint ensures an increase in this negative pressure with attempted distraction, thus increasing the joint reactive force independent of other muscular forces. Joint puncture by any means, increase in joint fluid secondary to trauma or inflammation, and laxity of the capsule (increasing joint volume) all contribute to the loss of this stabilizing mechanism.

Capsuloligamentous restraints

Matsen et al stressed that the aforementioned components provide midrange stability—that is, stability in the middle of the range of motion (ROM), where the ligaments and capsule provide little tension-dependent static stability. These factors act independently of the capsuloligamentous restraints. The capsule serves as a passive leash that can restrain glenohumeral motion within a given ROM. The insertion of the capsule upon the glenoid labrum provides continuity for the concavity mechanisms described above. The glenohumeral ligaments are ideally positioned thickenings within the capsule that serve to check large forces encountered within the capsule during specific arm positions and activities.

Numerous studies have elucidated the role of the capsuloligamentous complex in the static stabilization of the shoulder, and it has been shown that the inferior glenohumeral ligament is clearly the most crucial component.[5, 6, 7]

The value of the dynamic supports of shoulder stability (ie, rotator cuff, scapular stabilizers) cannot be overstated. Proper compressive functioning of the rotator cuff is essential for glenohumeral stability and remains the primary focus of rehabilitative management for this problem. Deficits of shoulder proprioceptive function have been reported in MDI.[8]

Etiology

Shoulder instability has been classified by Hawkins et al,[9] as well as others,[4, 10] on the basis of a number of different variables, including direction (eg, anterior, posterior), degree (dislocation vs subluxation), etiology (eg, traumatic, atraumatic, overuse), and chronology (eg, acute, recurrent, fixed).

It may be helpful to keep in mind the mnemonic device TUBS, defined as follows:

  • Traumatic etiology
  • Unidirectional instability
  • Bankart lesion
  • Surgical repair

When the diagnosis of MDI is under consideration, it is helpful to remember the mnemonic device AMBRII, defined as follows:

  • Atraumatic etiology
  • Multidirectional instability
  • Bilateral involvement
  • Rehabilitative initial management
  • Rotator Interval tightening with Inferior capsular shift repairs

Epidemiology

The prevalence of MDI (atraumatic shoulder instability) in the general population is not known. Traumatic shoulder instability is a much more common surgical indication.

Prognosis

In general, patients who have had open capsular shifts do reasonably well. Published studies indicate that the recurrence rate for MDI after surgery is about 10%. Loss of ROM after open capsular shift repair was greater in the early case series than in the later series, particularly for external rotation and abduction. Reported complications are rare.

Good results tend to persist with time as well. Stability does not seem to be lost at later follow-up on individuals with conventional open shift repair.

The long-term follow-up of arthroscopic management of MDI cannot yet be assessed. Advocates of both suture techniques have reported results that are somewhat less favorable in some cases than those of open surgery at follow-ups of up to 2 years, with recurrence rates of approximately 20-30%[11, 12, 13] versus 10% for open repairs.[14, 15] -[16] However, others have reported similar results 4 years or longer after treatment.[17]

Thermal repairs have generally shown poorer outcomes, with failure rates of 60%.[18, 19]  Because of these poorer outcomes, the unacceptable risks, and the reported complications, thermal capsulorraphy is no longer recommended.

Clinical Presentation    

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