Introduction

Multidirectional shoulder instability is a complex entity and nearly 30 years after its first discussion in contemporary literature, relatively few series of patients with this condition have been reported. An accurate and encompassing definition of this clinical entity also remains elusive. The pathognomonic anatomic finding is redundancy of the inferior capsule, allowing the shoulder to sublux, not only anteriorly but also inferiorly and posteriorly. Patients with multidirectional instability (MDI) possess two clinical features. First, most symptoms are experienced in the midrange positions of the glenohumeral motion, such as occur during activities of daily living. Second, the physical examination demonstrates the ability to dislocate or subluxate the glenohumeral joint in three directions (anteriorly, posteriorly, and inferiorly) with concurrent reproduction of symptoms in one of these directions. Importantly, both features are thought to be necessary for a diagnosis of MDI and are useful in distinguishing this instability pattern from other types of instability. More recent investigations and analysis of this unique type of instability pattern suggest that pathology of the rotator interval may be implicated in the etiology of this clinical syndrome.¹ Despite the increased awareness of MDI and the increased attention in research efforts to better clarify its etiology, understanding of this disorder remains woefully incomplete. Patient presentations are quite variable, the etiology multifactorial, and treatment algorithms incomplete. In addition, MDI still lacks a uniform definition accepted by the body of orthopaedic surgeons. Because of these ambiguities, the diagnosis of MDI is somewhat subjective, with the current tendency being to overdiagnose this once overlooked complex condition.

Definition

Multidirectional instability has been defined simply as “global instability” or “instability in more than one direction,” and in more complex terms, as part of a classification system with multiple subtypes.² A useful and comprehensive description of MDI defines it as a global shoulder laxity (anterior, posterior, and inferior) that is associated with the concurrent reproduction of symptoms inferiorly and in at least one other direction. Additionally most symptoms are experienced in the midrange of glenohumeral motion, resulting in frequent limitation in activities of daily living.³

It is important to discern the difference between instability and laxity. Laxity is the clinical condition associated with ligaments that have the ability to stretch beyond what is considered normal. Bear in mind that there is no absolute “norm” in measuring or assessing ligament compliance to tensile force. The more important concept to understand is that laxity, by definition, is not symptomatic in itself nor does any “lax” joint lead to clinical awareness or complaint. By contrast, “instability” is a clinical syndrome manifested by patient complaint, pain, and apprehension or fear that application of a physiologic or nonphysiologic force may result in a mechanical dissociation of the joint.

Pathology

There is no single pathologic lesion in MDI; there is no “essential” lesion, although a patulous inferior pouch is always present. It is the combination of inferior translation that is symptomatic that most appropriately defines MDI. Current understanding, though perhaps incomplete, focuses on structural or anatomic abnormalities, biochemical abnormalities, and neuromuscular abnormalities.

In the normal shoulder, glenohumeral stability is conferred by an intricate balance of static and dynamic mechanisms that include muscle, nerves, ligaments, bone, and geometry. The capsuloligamentous restraints in the shoulder should be considered as checkreins that provide stability at the extremes of motion. The function of these individual ligaments has been defined by several authors through basic science and cadaveric studies.⁴ However, outside the endpoints of motion, stability of the glenohumeral joint is conferred by other mechanisms. The precise centering of the humeral head on the glenoid by the rotator cuff muscles is achieved by a mechanism defined as concavity-compression. The presence of synovial fluid within the finite volume of the glenohumeral joint contributes to the formation of passive stabilizing articular adhesion-cohesion forces. Also of importance is that an intact glenohumeral joint possesses negative intra-articular pressure. These factors combine to create a stabilizing vacuum effect when inferior translation is placed on the glenohumeral joint. Studies have shown that when a cadaver shoulder has been stripped of all muscle, the humeral head remains centered on the glenoid, but when the joint is vented with a needle, the head then demonstrates increased inferior translation. In MDI, a defect in the rotator interval capsule may “vent” the joint and reduce the effectiveness of the dependent passive restraints. With recurrent instability, there is deconditioning of the dynamic stabilizers and ultimately, loss of effective concavity-compression. Furthermore, with loss of labral integrity, which functionally deepens the glenoid fossa by 50%, concavity-compression is further compromised. The importance of concavity-compression and glenoid positioning may be reflected by the fact that many patients respond to a rehabilitative exercise program directed at improving strength and neuromotor coordination of the rotator cuff and scapular musculature.

Two other anatomic lesions that result in MDI include a redundant inferior capsule and deficient rotator interval tissue. The triangular space separating the anterior edge of the supraspinatus from the superior edge of the subscapularis is defined as the rotator interval. It is normally bridged by a tissue considered capsule and is further defined as “rotator interval capsule.” Anatomically, the rotator interval includes the underlying superior glenohumeral ligament and is reinforced by the overlying coracohumeral ligament. Although controversial, anatomic studies in cadaver specimens have led to the understanding that these structures together resist the inferior and posterior displacement of the humeral head. The superior glenohumeral ligament is thought to be the primary biomechanical restraint to inferior subluxation in the adducted arm. Patients with MDI consistently are found to have incompetence of this tissue. The rotator interval capsule is consistently characterized by the presence of either a discrete cleft or insubstantial and attenuated tissue. Defects in the rotator interval further disrupt the concavity-compression negative intra-articular pressure and may contribute to instability in this respect. As the arm is progressively abducted, the inferior glenohumeral ligament complex functions as the primary restraint to inferior translation. In this abducted position, the anterior and posterior bands of this ligament reciprocally tighten with internal and external rotation. With a very large and redundant inferior capsule, it is easy to see how a patient may be clinically unstable in various positions of arm rotation while the arm is abducted.

Despite much investigation, a consistent biochemical explanation for capsular laxity remains elusive. Numerous studies have failed to identify a difference in the type or quantity of collagen between patients with MDI and controls. Bell found that although there is no difference in the types of collagen between patients with MDI and controls, he did find that the patients with MDI had a significant increase in the rate of collagen formation.⁵ Skin samples from these same patients revealed significantly smaller mean collagen fibril diameter in patients with MDI than in those with unidirectional instability. This may suggest a possible underlying connective tissue abnormality.

More recent investigations of the etiology of clinically significant MDI have sought a neurologic explanation.⁶^–⁸ Several observations support the idea of an underlying neuromuscular etiology. Many patients with MDI in one shoulder have an equal or greater amount of laxity in their other, asymptomatic shoulder. In this condition, most symptoms occur in the midrange of motion where contribution of the ligaments to stability is minimal. High speed photography of patients with symptomatic MDI reveals altered glenohumeral and scapulothoracic rhythms. Most importantly, mechanoreceptors have been identified in shoulder joint capsule and proprioceptive deficits have been demonstrated both in patients with anterior instability and more recently in patients with MDI. It is possible that known proprioceptive receptors in the glenohumeral joint capsule, in addition to providing joint position sense, reflexively modulate rotator cuff forces during arm use to promote shoulder stability. Patients with recurrent traumatic anterior instability appear to have deficits in joint-position sense compared with normal controls.⁹ Although yet to be proven scientifically, a defect in proprioception may be a component of the etiology of MDI. Interestingly, these deficits were shown to be reversible by surgical stabilization.

One further plausible hypothesis is that the provocation of MDI occurs when the system of dynamic restraint is overwhelmed such as occurs when the arm is suddenly and unexpectedly moved or is fatigued as a result of repetitive use. This event, whether or not it results in identifiable trauma, results in pain and initiates a self-perpetuating cycle of increasing symptoms. When the now painful shoulder is protected, muscular weakness and subtle losses of refined neuromotor coordination are thought to ensue. Continued disuse further deconditions the dynamic constraints against glenohumeral instability, which are critical to maintaining stability in lax shoulders. With the further use of a deconditioned shoulder, the patient is more prone to experience painful episodes of instability, which promotes further disuse, and so on.

A relatively atraumatic onset of instability strongly suggests MDI. However, an episode of significant trauma can be a factor in a shoulder with excessive laxity. Reports in the literature suggest that athletes with symptomatic instability have such a history.¹⁰^,¹¹ In this scenario, the athlete has a multidirectionally unstable shoulder in the presence of a Bankart lesion. Therefore, the presence of a Bankart lesion either on a radiograph or on a magnetic resonance arthrogram (MRA), does not rule out MDI as the correct diagnosis. As Neer noted, this is a critical distinction to make.¹² He noted that when there is a history of significant traumatic event, MDI can be mistaken for a traumatic unidirectional instability. If a surgical repair designed for a unidirectional instability is preformed, it is likely to result in a fixed subluxation in the opposite direction. Not only will the surgery fail in the short term, but also the likelihood of developing arthritis of dislocation becomes a very concerning consequence.