Shoulder instability encompasses a wide scope of pathologies and presentations.^{1, 2, 3 and 4} Physicians have long recognized the inherent differences between traumatic instability, whether it be anterior or posterior, and atraumatic instability. Multidirectional instability (MDI) falls into a relatively unique category of shoulder instability. Patients can often have more global instability, with combined anterior, posterior, and inferior instability and often atraumatic in etiology. Further challenging the diagnosis and management of the patient with MDI is the spectrum of laxity inherent to some patients in their shoulder versus pathologic instability.^5,6 In 1980, Neer and Foster⁷ defined MDI as symptomatic, involuntary inferior subluxation with anterior and posterior instability. Others mention instability in at least two directions, with some requiring one of those directions to be inferior.^1,2 The lack of standardized criteria for MDI directly influences treatment algorithms, and consequently, the literature is lacking in guidance to physicians managing patients with MDI.^8,9 While many patients with MDI do well with nonoperative management, often the mainstay of treatment, some patients will have more favorable outcomes following surgical treatment.^{1,3,4,10, 11, 12 and 13} It is crucial that surgeons understand the nuances between MDI and classic traumatic anterior or posterior instability in order to provide the optimal care of their patients.

Shoulder stability is conferred by static (bony architecture, glenohumeral ligaments, capsule, labrum, negative intra-articular pressure) and dynamic stabilizers (rotator cuff, long head of biceps, deltoid, scapulothoracic muscles).^2,3,12 The static stabilizers function at the extremes of motion and, as such, are commonly involved in traumatic instability. Dynamic stabilizers provide stability in midrange positions through the concavity-compression mechanism and scapular motion. Recently, there has been an increased focus on the concept of functional stability, or the coordinated actions of both stabilizing mechanisms during active shoulder motion.^1,2 The hallmark of functional stability is articular proprioception, which is the combination of limb movement and joint position awareness. In 2004, Barden et al¹⁴ demonstrated through electromyographic analysis that patients with MDI have an asynchronous activation pattern of the rotator cuff and scapulothoracic muscles. Subsequent studies have confirmed that altered scapular kinematics is a universal finding in patients with MDI.^15,16 A study in 2006 by Illyés¹⁵ also demonstrated altered scapulohumeral rhythm by the relative displacement of the centers of rotation of the scapula and humeral head, in patients with MDI compared with controls. The combination of improper scapular alignment and muscle imbalance leads to off-centering of the humeral head on the glenoid. Inherent glenohumeral laxity may theoretically increase the risk of injury to static stabilizers due to excessive relative translation.² As some patients with MDI have normal static stabilizers, this presents the possibility of insufficiency of the dynamic stabilizers playing a primary role in the pathogenesis of this condition.

A critical concept related to shoulder instability is the distinction between laxity and instability. Laxity is a physiologic property of the capsuloligamentous structures of the shoulder that is necessary for normal range of motion (ROM). Instability, on the other hand, is a pathologic condition in
which abnormal motion of the humeral head on the glenoid during active shoulder motion causes symptoms and loss of function.^{1,2,5,12,13,17} The normal parameters of laxity, however, are highly variable.¹⁸ Inferior capsular redundancy and rotator interval deficiency are common, but nonspecific, findings in MDI, as they are also seen in asymptomatic controls. The presence of hyperlaxity, either congenital or acquired, is not sufficient to diagnose instability.

MDI is a clinical diagnosis, and therefore, a thorough history and physical examination is important for every patient with instability. Clinicians should maintain a degree of suspicion when treating patients with instability. It typically presents as the insidious onset of nonspecific, activity-related shoulder pain or loss of function.^1,2,12,13 Providers should inquire about any prior trauma, prior surgery, generalized laxity, or connective tissue disorders. Additional information regarding specific provocative positions or activities assists with determining the directions of instability. Traction paresthesias with the arm at the side is associated with inferior instability. The patient’s activity level should also be determined. Repetitive microtrauma, such as in overhead athletes, does alter the biomechanical properties of the injured capsule.^{4,12,19, 20 and 21} Plastic deformation of the capsule leads to a substantial decrease in peak force with unrecovered elongation as well as loss of the mechanoreceptors responsible for proprioception. This raises the question of whether the dysfunction of the dynamic stabilizers is a primary or secondary factor in the development of MDI.

An accurate physical examination is imperative for appropriate treatment. Without specific parameters for laxity, there is a wide range in the realm of normal; therefore, the examiner must always relate positive signs of laxity with the patient’s symptoms.¹⁸ The examiner should inspect for asymmetry, atrophy, or old incisions. All patients with instability should be evaluated for generalized hyperlaxity. Signs of hyperlaxity include hyperextension of the elbow, metacarpophalangeal joints, or knees; patellar instability; and the ability to touch the thumb to the volar forearm. The Beighton score can be used as a more objective way to quantify hyperlaxity.^1,22 Shoulder ROM is measured, and apprehension and relocation tests are performed. The examiner should look for scapular dyskinesis or winging during shoulder motion and can employ the scapular activation or scapular retraction tests. Provocative tests, including the Kim test, jerk test, and active compression test, should be performed to evaluate for any internal derangement. The contralateral shoulder should also be examined as it is not uncommon for bilateral shoulders to be affected, as well as to understand the patient’s inherent laxity versus instability. Shoulder laxity should be evaluated in all directions. Patients with MDI will commonly have increased rotation, both internal and external, especially in abduction in the pathologic shoulder compared with the contralateral shoulder.^2,3,6 The commonly cited sulcus sign is also suggestive of inferior laxity; however, it should again be noted that it is not diagnostic of inferior instability unless it reproduces symptoms.⁵

Failure to address all elements during surgical stabilization can lead to failed procedures. The anterior and posterior load and shift tests are used for assessing anterior and posterior laxity, respectively. External rotation >85° is indicative of anterior laxity.^1,2,13,22 The hyperabduction test, developed by Gagey and Gagey, indicates inferior laxity with passive abduction >105° or a difference of 20° compared with the contralateral shoulder.^1,2,13,22

Diagnostic imaging for MDI should always start with plain radiographs. Although often normal, standard radiographs can occasionally show glenoid dysplasia (hypoplasia, abnormal version, shallow concavity), bone loss, or humeral head defects. Computerized tomography can be obtained for further delineation if concerned for bone loss. Stress radiographs, although described, are rarely used.¹² Magnetic resonance imaging is the standard imaging study for MDI due to its excellent soft tissue detail. Magnetic resonance arthrography may be more helpful since the capsular distension allows better appreciation of the rotator interval, patulous capsule, and possible labral tears.^{2,13,22, 23 and 24}

Currently, the mainstay of treatment of MDI is still physiotherapy. Biomechanical studies have led to rehabilitation protocols that focus on neuromuscular control and proprioceptive training to attempt to restore normal shoulder kinematics.^{14, 15 and 16,25} Nyiri et al²⁵ reported, however, that while
physiotherapy can improve shoulder kinematics, physiotherapy alone cannot restore normal kinematics. Additionally, at long-term follow-up, patients’ shoulder kinematics were nearly the same as pretreatment, implying the need of a maintenance program.