Secondary Logo

Journal Logo

SECTION I SYMPOSIUM: Recent Basic Science and Clinical Advances in Anterior Glenohumeral Instability

Classification of Glenohumeral Joint Instability

Gerber, Christian; Nyffeler, Richard, W.

Author Information
Clinical Orthopaedics and Related Research: July 2002 - Volume 400 - Issue - p 65-76

Abstract

Many different classifications of glenohumeral joint instability have been proposed, based on etiology, the direction of the instability, or on combinations thereof. 19,22,23,25,32–36 None provide all the information necessary to classify a given case and allow easy communication between orthopaedic surgeons.

The etiology of instability has been considered a key element for classification. 32 If a patient has recurrent anterior instability develop because of major trauma, it is called posttraumatic. TUBS 32 is an acronym that describes instability caused by a traumatic event, which is unidirectional, associated with a Bankart lesion, and requires surgical treatment. These patients would, by definition, not have multidirectional instability. Unfortunately, individuals with hyperlaxity also may sustain trauma that causes instability. The term hyperlax commonly is used but is defined poorly. Indeed, laxity (joint play) is a trait of body constitution that is different from one individual to another. Individuals may be loose jointed or tight jointed without a definition of what laxity is pathologic. A shoulder is termed hyperlax if the examiner can easily subluxate the humeral head out of the socket anteriorly and posteriorly on drawer testing and inferiorly with sulcus testing. Nonetheless, being hyperlax may be a risk factor for having shoulder pain and instability develop. If a patient with such a hyperlax shoulder sustains a macrotrauma, this may result in unidirectional instability in a shoulder with a grossly positive sulcus sign. In addition, repetitive microtrauma can occur in a shoulder with prior macrotraumatic anterior instability. The need to distinguish between instability and hyperlaxity and between macrotrauma and repetitive microtrauma makes classification of instability based on etiology extremely difficult.

Classifications based on the direction of instability avoid these problems. Before the introduction of the term multidirectional instability by Neer and Foster, 27 instability usually was considered to be either anterior or posterior. Multidirectional instability was described as a problem caused, presumably, by enlargement of the capsule from genetic or microtraumatic origin. They described the sulcus sign as the clinical hallmark of such an excessively wide joint capsule. The description of multidirectional instability has widened the spectrum of recognized instabilities and stimulated research of joint instability. Unfortunately, abuse of the term multidirectional instability also has created confusion among orthopaedic surgeons. The positive sulcus sign has been used as the diagnostic hallmark for multidirectional instability and has become virtually synonymous with multidirectional instability. However, the sulcus sign 27 and the ability to passively sublux the glenohumeral joint, either in adduction 32 or in abduction, 13 only determines the degree of laxity. If a sulcus sign is found on physical examination, it always is bilateral and the expression of hyperlaxity. None or only one of the shoulders, however, may be symptomatic. Use of a positive sulcus sign to define the diagnosis of multidirectional instability, therefore would require the classification system to differentiate symptomatic from asymptomatic shoulders.

It is crucial for the classification of shoulder instability to distinguish instability and hyperlaxity and to recognize that both can be present independently. A simple form of the classification 10,11 described in the current study has been helpful to determine diagnostic and therapeutic strategies and to establish a basis of communication with other orthopaedists. Description of static instabilities and recognition of osseous lesions to this classification may be an additional aid. A basis for this classification is that hyperlaxity (either generalized or of the shoulder) is an individual trait and not pathologic. However, hyperlaxity may be a factor of risk for having shoulder problems develop.

STATIC INSTABILITIES

Static instabilities (Class A) are defined by absence of classic symptoms of instability yet, the humeral head is displaced and fixed superior, anterior, or posterior relative to its normal position on the glenoid fossa (Fig 1). The diagnosis is radiologic, not clinical. Static instability may remain asymptomatic for a long period. If treatment becomes necessary, the consequences are entirely different from those imposed by a diagnosis of dynamic instability. In addition, these static instabilities currently are difficult to treat successfully. Static instabilities can coexist with dynamic instabilities (recurrent anterior instability in a massive cuff tear with superior humeral migration) and then require a decision as to which instability has priority in treatment. Usually the more disabling instability is dynamic and is best treated initially.

Fig 1.
Fig 1.:
This radiograph shows static superior subluxation. The acromiohumeral distance is less than 7 mm, indicating that there is a supraspinatus and infraspinatus tendon tear.

Static Superior Subluxation

Static superior migration (Class A1) of the humeral head is present if the normal distance between the undersurface of the acromion and the most cranial aspect of the humeral head on an anteroposterior (AP) radiograph with the shoulder in neutral rotation is decreased. In 1970, Weiner and MacNab 40 described diminution of this distance, associated with rotator cuff tears. Cotty et al 4 correlated the acromiohumeral distance with arthrographic findings. They showed that the subacromial space in shoulders with intact cuffs measured 10.5 mm on average, whereas it measured only 8.2 mm if a tear of the rotator cuff tendons was present. In their study, a distance less than 9 mm was suggestive, whereas a distance less than 7 mm was proof of full-thickness rotator cuff tear. Therefore, 7 mm currently is the value used to define static superior subluxation. These values only are valid for conventional radiographs taken with the technique described. Specifically, there is no correlation between the acromiohumeral distance measured on such radiographs with that measured on magnetic resonance imaging (MRI) scans.

The cause of cranial migration of the humeral head seems to be insufficiency of the infraspinatus in the presence of a supraspinatus tear. Isolated supraspinatus, isolated infraspinatus, or combination tears of the supraspinatus and subscapularis tendons do not cause static superior instability. This concurs with a prior study that found single tendon tears do not lead to changes in the movement pattern of the shoulder. 20 Loss of the acromiohumeral distance to less than 7 mm also is associated with loss of strength of abduction and of external rotation. In addition, such static superior subluxation carries a poor prognosis for repair of the rotator cuff tear 6,38 and some consider it to be a predictor of an irreparable tear. 12,18,38 In the current authors’ experience, superior static subluxation essentially is irreversible by conventional repair techniques.

Static Anterior Subluxation

Static anterior subluxation (Class A2) is a fixed anterior position of the humeral head on the glenoid fossa and often is manifest clinically as moderate to severe shoulder pain, partly caused by impingement under the coracoid and coracoacromial arch and loss of anterior elevation. It usually is detected on computed tomography (CT) scans or MRI scans taken with the arm in neutral rotation but occasionally may be evident on axillary lateral radiographs (Fig 2). Static anterior subluxation usually is not associated with recurrent anterior shoulder instability.

Fig 2.
Fig 2.:
A radiograph shows static anterior subluxation. The center of the humeral head is anterior to the center of the glenoid fossa, indicating a lesion of subscapularis, supraspinatus, and probably infraspinatus.

The cause of static anterior subluxation is not well-established. The current authors caused static anterior subluxation with transfer of the pectoralis major tendon in a case of severe fatty degeneration of the subscapularis (Fig 3). Static anterior subluxation also occurred in a few cases early in the authors’ experience with latissimus dorsi transfers when this procedure was done in the presence of a large subscapularis tear. To develop without any previous operation, it seems that a combination of a subscapularis tear, a supraspinatus tear, and fatty degeneration of the infraspinatus muscle is necessary. 28 An isolated tear of the subscapularis tendon and posterosuperior tears usually do not lead to anterior static subluxation.

Fig 3A–B.
Fig 3A–B.:
(A) A computed arthrotomograph of a patient with anterosuperior rotator cuff deficiency shows that the humeral head is centered in the glenoid fossa. (B) A CT scan of the same patient shows static anterior subluxation of the humeral head after pectoralis major transfer. Tendon transfer surgery may unbalance the glenohumeral joint and lead to static subluxations.

Current treatment attempts include repair of the supraspinatus tendon plus pectoralis major tendon transfer with the transferred tendon being rerouted behind the conjoined tendon 31 or a Latarjetlike procedure to provide better anterior stability. In the current authors’ experience to date, static anterior subluxation has been irreversible with soft tissue procedures alone.

Static Posterior Subluxation

Static posterior subluxation (Class A3) is a fixed posterior position of the humeral head on the glenoid fossa on CT or MRI scans with the arm in neutral rotation (Fig 4). This condition is most frequently but not always associated with congenital dysplasia of the glenoid or with degenerative glenohumeral joint disease. Static posterior subluxation may be associated with glenoid deformations such as classified by Walch and coworkers. 39 This static subluxation may be present without any rotator cuff deficiencies. To date, most authors have found static posterior subluxations to be irreversible.

Fig 4.
Fig 4.:
A CT scan shows static posterior subluxation. The center of the humeral head remains behind the center of the glenoid fossa irrespective of the rotation of the humerus.

The fact that posterior static subluxation occurs without cuff degeneration raises the question of whether the cuff alterations really are the major cause of static subluxations. The current authors observed that the orientation of the supraspinatus vector relative to the glenoid fossa was associated with the type of rotator cuff tear. This suggests that the relation of the supraspinatus vector to the center of the glenoid fossa might play a role in the development of anterior or posterior subluxation. The authors think that specific anatomic variants are more likely to explain these static subluxations than rotator cuff disorders alone. With a new aiming device that allows precise reorientation of the glenoid fossa during total shoulder arthroplasty, the current authors observed correction of posterior subluxation with time (Fig 5). Whether such posterior subluxations can be corrected regularly with proper reorientation of the glenoid is being studied in a larger series of patients.

Fig 5A–D.
Fig 5A–D.:
(A) An AP radiograph of a shoulder with severe osteoarthritis is shown. (B) An axillary radiograph shows posterior subluxation of the humeral head. (C) An AP of the same shoulder as in Figure 5B taken after total joint replacement is shown. (D) An axillary radiograph shows correction of posterior subluxation after correction of glenoid version during total shoulder replacement.

Static Inferior Subluxation

Inferior subluxation (Class A4) of the shoulder is characterized by straight inferior translation of the humerus relative to the glenoid fossa. This may occur from trauma, 30 neurologic injury, septic arthritis, 37 or inadequate restoration of humeral length after arthroplasty. 26 Inferior subluxation after trauma and surgery, if not associated with permanent nerve injury, usually resolves within 6 weeks but always resolves within 2 years. 30 Conversely, inferior subluxation caused by infection tends to result in joint surface destruction and only successful treatment of infection results in resolution of the inferior subluxation. Inferior subluxation caused by neurologic injury or shortening of the humerus also remains symptomatic unless the primary problem can be resolved.

Subluxation must be distinguished from traumatic inferior dislocation, which occasionally is encountered as luxatio erecta. This entity is part of the dynamic instabilities that can momentaneously be reduced and may recur.

DYNAMIC INSTABILITIES

Dynamic instabilities (Class B) are characterized by subjective loss of normal glenohumeral joint stability and momentaneous but restorable loss of joint congruency. Dynamic instabilities always are initiated by trauma. This may be repetitive microtrauma or one macrotraumatic event. Being able to passively displace the humeral head out the glenoid fossa during physical examination does not describe instability but is a semiquantitative assessment of hyperlaxity. 13,27,32 Such translation testing may be a sign of instability if it is significantly different from the asymptomatic side or if it is associated with symptoms of apprehension.

Typical pathoanatomy is associated with each of the dynamic instabilities. All can be associated with major bony defects of the glenoid fossa but it often is difficult to assess the size and thereby the relevance of such lesions. Biomechanical investigations done at the authors’ institution showed that lesions involving loss of the normal anteroinferior glenoid rim of more than half of the maximal AP diameter of the glenoid lead to a loss of dislocation resistance of more than 30% (Fig 6). This may not be compensated for by soft tissue repair alone. If the superoinferior extension of a glenoid rim lesion is larger than half of the largest AP diameter of the glenoid, instability can be subclassified as with bony lesion, if this is not the case, it can be subclassified as without bony lesion. Although this neglects the humeral head impression fractures, they are not always irrelevant. If these impression fractures are large, they are relevant but are so clearly associated with specific types of instabilities (locked dislocations, dislocations in patients with epilepsy), that they invariably are recognized and reported, so that a specific classification system is not necessary.

Fig 6.
Fig 6.:
This graph shows the relation between size of an antroinferior bony glenoid rim defect (x) and dislocation resistance of the humeral head. If the glenoid rim lesion measures more than half of the maximal AP diameter of the glenoid fossa (w), the dislocation resistance decreases to no more than 70% of the value of an intact joint.

Chronic, Locked Dislocation of the Shoulder

Chronic, locked shoulder instability (Class B1) invariably is caused by major trauma 10,14,15,34,39 most frequently incurred in a motor vehicle accident, a fight, or during an epileptic seizure. Anterior or posterior dislocation may be associated with a fracture of the surgical neck region that must be recognized before treatment is initiated.

Characteristic Lesions

The most important lesions (Class 1.1) of locked shoulder dislocation are the compression fractures of the humeral head and stable contact of this lesion with the articular surface of the glenoid, whereas the majority of the cartilage of the humeral head has no contact with the glenoid fossa. The posterolateral Malgaigne 21 or Hill - Sachs compression fracture is found in anterior dislocation (Fig 7), whereas an anteromedial (McLaughlin) compression fracture is found in posterior dislocation. 24 Capsular distention is usual; rotator cuff tears are rare. If the humeral head remains outside the glenoid fossa, a disuse atrophy of the humeral head develops. Although these lesions can be identified with radiographs, they are seen best on CT scans or arthrogram CT scans. Chronic locked dislocations may be reduced and can recur. The essential lesion seems to be the humeral head defect. As opposed to humeral head compression fracture associated with recurrent dislocation, the humeral head defect associated with chronic, locked dislocation often needs to be addressed during operative repair of long-standing lesions in patients who do not respond to conservative treatment. 5,14,17,24 A large glenoid fossa lesion rarely is found.

Fig 7.
Fig 7.:
A CT scan shows a large Hill – Sachs lesion caused by locked anterior dislocation.

Unidirectional Instability Without Hyperlaxity

Unidirectional instability without hyperlaxity (Class B2) may be the most frequent form of recurrent instability, accounting for 60% of the patients treated at the current authors’ institution. Either there is a distinct injury with a frank dislocation requiring reduction by another person, or a painful subluxation followed by recurrent episodes of instability. On physical examination, the main finding is a positive apprehension test, either anterior or posterior. There is no sulcus sign and the results of the anterior and the posterior drawer tests are negative. For anterior instability, however, the hyperabduction test recently described by Gagey and Gagey 9 is positive indicating incompetence of the inferior glenohumeral ligament complex (Fig 8).

Fig 8A–B.
Fig 8A–B.:
(A) These photographs show the hyperabduction test. Abduction is normal on the right shoulder. (B) A hyperabduction test is positive on the left shoulder. A difference greater than 10° abduction in the coronal plane with the arm in internal rotation is proof of a lesion of the inferior glenohumeral ligament.

Characteristic Lesions

A traumatic lesion (Class 2.1) involving the inferior glenohumeral ligament complex can cause anterior instability without hyperlaxity. 1–3,29,38 Lesions may be at the humeral insertion site, midsubstance, at the glenoid insertion site, involving the labrum and/or the anterior glenoid rim or rarely at the humeral and the glenoid insertion sites. 7 In addition, the passage of the humeral head over the anterior glenoid rim causes a posterolateral humeral head defect that is diagnostic of anterior instability. The severity of the two lesions often are related as very large Hill - Sachs lesions often associated with small lesions of the anteroinferior capsulolabrum, whereas large capsulolabral lesions often are associated with small Hill - Sachs lesions.

Posterior instabilities without hyperlaxity have posterior capsulolabral lesions (posterior Bankart) more frequently than previously recognized. 8 These lesions, less severe than anterior capsulolabral lesions, also can be accompanied by an anteromedial humeral head compression fracture (McLaughlin lesion).

These instabilities usually can be treated with success by repair of the capsulolabral lesion. If this repair is correct technically, the results of arthroscopic procedures may be comparable with those of open repair. Finally, if a glenoid rim lesion is present and of the size defined above, either glenoid reconstruction using iliac bone or a bone block procedure may be necessary to restore stability.

Unidirectional Instability With Hyperlaxity

Unidirectional instability with hyperlaxity (Class B3) accounts for approximately 30% of the patients with instability treated at the authors’ institution. The injury is of variable severity. It includes dislocations requiring reduction, dislocations reduced by the patient, and painful subluxation followed by frequent and almost pain-free episodes of recurrence, generally self-treated. The position of discomfort occurs with the shoulder either in external rotation and abduction, or in anterior elevation. The physical examination shows either a positive anterior or a positive posterior apprehension test, 10 but not both. There is a clear sulcus sign and the anterior and the posterior drawer tests 13 are positive. The drawer test in the direction of the instability may be associated with apprehension. In anterior instability the hyperabduction test is positive, and in posterior instability internal rotation of the 90° abducted arm usually is increased over the opposite asymptomatic side. If on physical examination the contralateral shoulder is hyperlax, the instability is classified as anterior or posterior with hyperlaxity.

Characteristic Lesions

A traumatic lesion (Class 3.1) of the anteroinferior capsulolabrum also may cause anterior instability with hyperlaxity. This lesion may be similar to those without hyperlaxity. With inferior hyperlaxity, an opening in the rotator interval is expected and is addressed best during surgery. If external rotation is increased dramatically beyond normal, a dysplasia of the middle glenohumeral ligament is characteristic. It may be difficult to anatomically reinsert this structure during surgery. Typically, a small traumatic lesion of the anteroinferior labrum or a longitudinal fissure or other mild detachment is present. The capsular volume is large and the surgeon may be tempted to reef the capsule but should not. A Hill - Sachs lesion often is present, but may be small.

Posterior instabilities with hyperlaxity have only minimal labral lesions. Most frequently, the lesions are barely recognizable. The patient may have subluxated the shoulder by a movement of anterior elevation and internal rotation, but he or she is unable to subluxate the shoulder in a different direction. The patient also complains exclusively of symptoms in this position. The sulcus sign is not very marked, but persists in internal rotation. This implies that the posteroinferior capsule is functionally incompetent and needs to be addressed surgically. The variant of this instability with a relevant glenoid fossa lesion is rare.

Multidirectional Instability Without Hyperlaxity

Multidirectional instability without hyperlaxity (Class B4) is even rarer than multidirectional instability with hyperlaxity. Typically, the patient reports at least two significant injuries or instability episodes. The injuries almost invariably were of sufficient severity to warrant medical consultation. The patient is uncertain which position is the most uncomfortable. He or she is not comfortable with the shoulder in external rotation and abduction, with the shoulder in anterior elevation and internal rotation. On physical examination, there is a positive anterior and a positive posterior apprehension test, and although one apprehension test may be more positive, both clearly are not normal. There is no sulcus; external rotation of the adducted arm is not beyond 70°. The drawer tests show small displacement and therefore are negative and may be associated with apprehension. If there is no hyperlaxity, but subjective instability and history and physical examination fail to positively identify the direction of instability, multidirectional instability without hyperlaxity must be ruled out.

Characteristic Lesions

Multidirectional instability without hyperlaxity has typical lesions of anterior and posterior instability without hyperlaxity (Class 4.1). The bony and the capsulolabral lesions are present. The labrum may be avulsed anterior or posterior making open surgery difficult. Optimal treatment of this condition is complex and may require staged procedures of anterior and posterior repair. Surgery should attempt to restore the anatomy by reinserting the capsulolabral structures at their anatomic sites under as normal tension as possible.

Multidirectional Instability With Hyperlaxity

Multidirectional instability with hyperlaxity (Class B5) is the classic syndrome initially described as multidirectional instability. Today, the majority of cases described as multidirectional instability likely are unidirectional instabilities with hyperlaxity, which is much more common than true subjective multidirectional instability. Although unidirectional instability with hyperlaxity accounts for approximately 30% of the cases of instability, true multidirectional instability with hyperlaxity accounts for less than 5%. The onset of symptoms may be associated with a significant trauma, but even a minor injury may produce multidirectional instability with hyperlaxity. Patients often are females who have had repetitive microtrauma in childhood or adolescence (gymnasts, swimmers). Most patients have signs of generalized hyperlaxity, which sometimes may be limited to both shoulders. This hyperlaxity may be severe and patients already may have had surgery for ankle injuries, knee ligament lesions, or other joint instabilities. The symptoms may present as anterior, posterior, and often inferior. The patient has no control of the position of the humeral head relative to the glenoid as opposed to the voluntary type of instability, where the patient changes the relative position of humerus and glenoid at will. Subluxation may occur many times a day. The instability events are almost invariably subluxations, reduced by the patient, and frequently are not very painful. At physical examination, positive anterior, posterior, and inferior drawer tests show apprehension in at least two directions and external and internal rotation usually are increased dramatically beyond normal.

Characteristic Lesions

Multidirectional instability with hyperlaxity typically has the lesions of anterior and posterior instability and the characteristics of hyperlaxity (Class 5.1). There are only minimal skeletal lesions, but the capsular lesions are present including widening of the rotator interval, a patulous capsule, and stretched ligaments. Conservative treatment often is successful. This may be attributed to the minimal structural lesions being well compensated for by rehabilitation of the shoulder muscles.

Unidirectional or Multidirectional Instability With Voluntary Reduction (Voluntary Instability)

The form of instability, which was termed unidirectional or multidirectional with voluntary reduction (Class B6), previously has been called voluntary and habitual, 8,18,19 but these latter terms have caused confusion in recognizing this form of instability. There are children and adults whose shoulders start to dislocate anterior and/or posterior and/or inferior often without the patient noticing. However, early in the course of the disease the patient learns how to reduce the shoulder and will present to the physician with a maneuver of reduction that should not be misinterpreted as a maneuver of dislocation. With time, the patient learns how to position the shoulder so that it dislocates and willfully reduces the shoulder. To the patient, this reduction maneuver often is the instability because the prior subluxation was not noticed. The capability of subluxing the shoulder may be shown but it is not associated with any psychologic disturbance. The voluntary dislocations often are bilateral and usually are pain-free. The reduction maneuver may be associated with pain and discomfort. Children who have learned to voluntarily reduce and dislocate their shoulders have an excellent prognosis if untreated for relief of pain, as in terms of function and psychologic development. 16 Adults often have been able to dislocate their shoulders during childhood.

Although excellent success may be possible with conservative treatment, 32 the current authors have not had universally satisfactory outcomes. This especially has been the case with the posterior variant. Conversely, it was shown that patients with this form of voluntary instability can be treated successfully operatively. 8

VOLUNTARY DISLOCATIONS

There are three types of individuals who can dislocate their shoulders at will (Class C). The first group is comprised of individuals who do not suffer but are surprised to realize that that they can dislocate and relocate their shoulder at will. This condition should not be called instability because the individual has not lost control of the stability of his or her shoulder. In fact, the individual has more control over the shoulder than usual, because the position of the shoulder can be maintained whether the humeral head is in the glenoid fossa or outside. This is similar to an Indian fakir who is able to control his heartbeat. The treatment of bradycardia of the fakir’s heart is not a pacemaker. There is no need for treatment of these patients. If left untreated, these patients never develop degenerative changes of their joint; therefore, no treatment is the best option. The second group is comprised of patients who suffer involuntary dynamic instability and subsequently learn to voluntarily subluxate (and reduce) their joint. They are treated best according to their dynamic instability as under B6.

A third very small but important to identify group of patients can dislocate their joint and use this to gain attention or to mask a major psychiatric problem. Typically, these are young females. Willful instabilities should raise the suspicion of this variant, which is not an expression of shoulder instability, but of psychiatric illness. Accordingly, these patients should not be treated by an orthopaedic surgeon, but by a psychiatrist.

Classification of shoulder instabilities is controversial. For practical purposes, the classification described by the current authors has been helpful in clinical practice. It has allowed residents and students of shoulder surgery to reconcile the terms of instability and hyperlaxity and to communicate with their peers. It is hoped that future research may allow one to quantitatively describe what currently is a qualitative distinction between entities encountered in daily practice.

References

1. Bankart ASB: Recurrent or habitual dislocation of the shoulder-joint. Br Med J 2:1132–1133, 1923.
2. Bankart ASB: The pathology and treatment of recurrent dislocation of the shoulder joint. Br J Surg 26:23–29, 1938.
3. Broca A, Hartmann H: Contribution à l’étude des luxations de l’épaule (luxations dites incomplètes, décollements périostiques, luxations directes et luxations indirectes). Bull Soc Anat Paris 5:312–336, 1890.
4. Cotty P, Proust F, Bertrand P, et al: Rupture de la coiffe des rotateurs: Quantification des signes indirects en radiologie standard et manoeuvre de leclercq. J Radiol 69:633–638, 1988.
5. Dubousset J: Luxation postérieure de l’épaule. Rev Chir Orthop 53:65–85, 1967.
6. Ellman H, Hanker G, Bayer M: Repair of the rotator cuff: End-result study of factors influencing reconstruction. J Bone Joint Surg 68A:1136–1144, 1986.
7. Field LD, Boker DJ, Savoie FH: Humeral and glenoid detachment of the anterior inferior glenohumeral ligament: A cause of anterior shoulder instability. J Shoulder Elbow Surg 6:6–10, 1997.
8. Fuchs B, Jost B, Gerber C: Posterior - inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg 82A:16–25, 2000.
9. Gagey OJ, Gagey N: The hyperabduction test: An assessment of the laxity of the inferior glenohumeral ligament. J Bone Joint Surg 82B:69–74, 2001.
10. Gerber C: Les Instabilités de l’Épaule. In Duparc J (ed). Cahiers d’Enseignement de la Sofcot. Paris, Expansion Scientifique Française 51–74, 1988.
11. Gerber C: Observations on the Classification of Instability. In Warner JJP, Iannotti JP, Gerber C (eds). Complex and Revision Problems in Shoulder Surgery. Philadelphia, Lippincott-Raven 9–18, 1997.
12. Gerber C, Fuchs B, Hodler J: The results of repair of massive tears of the rotator cuff. J Bone Joint Surg 82A:505–515, 2000.
13. Gerber C, Ganz R: Clinical assessment of instability of the shoulder: With special reference to anterior and posterior drawer tests. J Bone Joint Surg 66B:551–556, 1984.
14. Gerber C, Lambert SM: Allograft reconstruction of segmental defects of the humeral head for the treatment of chronic locked posterior dislocation of the shoulder. J Bone Joint Surg 78A:376–382, 1996.
15. Hawkins RJ, Neer CS, Planta RM, Mendoza FX: Locked posterior dislocation of the shoulder. J Bone Joint Surg 69A:9–18, 1987.
16. Huber H, Gerber C: Voluntary subluxation of the shoulder in children: A long-term follow-up study of 36 shoulders. J Bone Joint Surg 76B:118–122, 1994.
17. Hughes M, Neer CS: Glenohumeral joint replacement and postoperative rehabilitation. Phys Ther 55:850–858, 1975.
18. Kaneko K, De Mouy EH, Brunet ME: Massive rotator cuff tears: Screening by routine radiographs. Clin Imaging 19:8–11, 1995.
19. Lippitt S, Matsen F: Mechanisms of glenohumeral joint stability. Clin Orthop 291:20–28, 1993.
20. Loehr JF, Helmig P, Sojbjerg JO, Jung A: Shoulder instability caused by rotator cuff lesions: An in vitro study. Clin Orthop 304:84–90, 1994.
21. Malgaigne JF: Traité des Fractures et des Luxations. Atlas de XXX Planches. Paris, JB Ballière 1855.
22. Mallon WJ, Speer KP: Multidirectional instability: Current concepts. J Shoulder Elbow Surg 4:54–64, 1995.
23. Maruyama K, Sano S, Saito K, Yamaguchi Y: Trauma-instability-voluntarism classification for glenohumeral instability. J Shoulder Elbow Surg 4:194–198, 1995.
24. McLaughlin HL: Posterior dislocation of the shoulder. J Bone Joint Surg 34A:584–590, 1952.
25. Molé D, Walch G: Traitement chirurgical des instabilités de l’épaule: Articulation glénohumérale. Ed Tech Encycl Méd Chir Orthop Trauma 244–265, 1993.
26. Neer CS: Shoulder Reconstruction. Philadelphia, WB Saunders Co 1990.
27. Neer CS, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder: A preliminary report. J Bone Joint Surg 62A:897–908, 1980.
28. Nove-Josserand L, Boulahia A, Levigne C, Noel E, Walch G: Espace coraco-huméral et rupture de la coiffe des rotateurs de l’épaule [coraco-humeral space and rotator cuff tears]. Rev Chir Orthop 85:677–683, 1999.
29. Perthes G: Ueber operationen bei habitueller schulterluxation. Deutsch Zeitschr Chir 85:199–227, 1906.
30. Pritchett JW: Inferior subluxation of the humeral head after trauma or surgery. J Shoulder Elbow Surg 7:356–359, 1997.
31. Resch H, Povacz, P, Ritter E, Matschi W: Transfer of the pectoralis major muscle for the treatment of irreparable rupture of the subscapularis tendon. J Bone Joint Surg 82A:372–382, 2000.
32. Rockwood CA, Thomas SA, Matsen FA: Subluxations and Dislocations About the Glenohumeral Joint. In Rockwood CA, Green DP, Bucholz RW (eds). Fractures in Adults. Ed 3. Philadelphia, JB Lippincott Co 1021–1079, 1991.
33. Rowe CR, Pierce DS, Clark JG: Voluntary dislocation of the shoulder. J Bone Joint Surg 55A:445–460, 1973.
34. Rowe CR, Zarins B: Chronic unreduced dislocations of the shoulder. J Bone Joint Surg 64A:494–505, 1982.
35. Salomonsson B, Sforza G, Revay S, Abbaszadegan H, Jonsson U: Atraumatic shoulder instability: Discussion of classification and results after capsular imbrication. Scand J Med Sci Sports 8:398–404, 1998.
36. Silliman JF, Hawkins RJ: Classification and physical diagnosis of instability of the shoulder. Clin Orthop 291:7–19, 1993.
37. Thomas E, Leroux JL, Azema MJ, Blotman F: Inferior glenohumeral subluxation: An indirect sign of sepsis of the shoulder. Rev Rhum Ed Fr 61:349–352, 1994.
38. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg 63A:1208–1217, 1981.
39. Walch G, Boileau P, Martin B, Dejour H: Luxations et fractures - luxations postérieures invétérées de lépaule: A propos de 30 cas. Rev Chir Orthop 76:546–558, 1990.
40. Weiner DS, MacNab I: Superior migration of the humeral head: A radiological aid in the diagnosis of tears of the rotator cuff. J Bone Joint Surg 52B:524–527, 1970.

Section Description

Patrick J. McMahon, MD; and Thay Q. Lee, PhD—Guest Editors

© 2002 Lippincott Williams & Wilkins, Inc.