Indian Journal of Orthopaedics

CURRENT CONCEPT REVIEW
Year
: 2002  |  Volume : 36  |  Issue : 4  |  Page : 214--220

Anterior inferior shoulder instability - Part I: The pathogenesis of anterior inferior shoulder instability


DV Ranjan1, NA Antao2,  
1 Sports Injury and Arthroscopy Clinic, SARC # 1, Venkatachlam Road, RS Puram, Coimbatore 641 002, India
2 Holy Spirit Hospital, Andheri (E) and Holy Family Hospital, Bandra, and Arthroscopy and Sports medicine Centre, Hillway clinic, Hill Road, Bandra ,Bombay 50., India

Correspondence Address:
D V Ranjan
Sports Injury and Arthroscopy Clinic, SARC # 1, Venkatachlam Road, RS Puram, Coimbatore 641 002
India




How to cite this article:
Ranjan D V, Antao N A. Anterior inferior shoulder instability - Part I: The pathogenesis of anterior inferior shoulder instability.Indian J Orthop 2002;36:214-220


How to cite this URL:
Ranjan D V, Antao N A. Anterior inferior shoulder instability - Part I: The pathogenesis of anterior inferior shoulder instability. Indian J Orthop [serial online] 2002 [cited 2019 Jun 18 ];36:214-220
Available from: http://www.ijoonline.com/text.asp?2002/36/4/214/35938


Full Text

 Introduction



The shoulder enjoys an enormous range of movement at the expense of stability. Common shoulder instabilities include antero-inferior, posterior and multidirectional, of which, the antero-inferior type is the most common and includes 90% of all instabilities. This review will focus on the pathophysiology of antero-inferior instability.

The unstable shoulder has been the subject of interest for over ten centuries. The detailed description of the anatomy and surgical treatment of the unstable shoulder was first documented by Hippocrates. Various mechanisms of injuries were postulated for the dislocating shoulder, and it was Bankart [1] who suggested that the capsule and the glenohumeral ligaments were responsible for the repeated dislocations. Saha contributed to the understanding of pressure dynamics and zero position in shoulder biomechanics. Although, the cause for the recurrent anterior dislocation has been identified as a Bankart's lesion and capsular disruption; non-anatomic procedures [2],[3],[4],[5],[6] such as the Putti­Platt and Bristows had been popular due to technical difficulties in performing Bankart's procedure. [6],[7],[8] These non-anatomic surgical procedures have led to an increased incidence of recurrence and complications. It was Turkel in 1981 [8] , who again stressed that the pathology was in the labrum and glenohumeral ligaments and that those structures should be addressed in order for successful treatment of recurrent anterior dislocation of the shoulder. It has also been noted, that whatever nonsurgical treatment is initiated in the first dislocation, the recurrence rate is very high in patients below 20 years. Laxity of the shoulder is necessary for normal movements and it varies from one individual to another. Excessive laxity may on the other hand render the shoulder susceptible to repeated dislocation. [9],[10] Proper correlation is necessary to differentiate from physiological laxity to pathological instability. Earlier, the teaching was that frank dislocation of the shoulder is necessary to make a diagnosis of recurrent anterior instability of the shoulder. But now, we know that there exists a spectrum of micro-instability which may not manifest with the head of the humerus coming out of the glenoid, but symptoms may vary from pain to crepitus or dead arm syndrome.

Part I: The pathogenesis of anterior inferior shoulder instability

The stability of glenohumeral joint is governed by 2 factors (1) bony stabilizers i.e. the glenohumeral articulation, and (2) soft tissue stabilizers of the glenohumeral joint [Figure 1].

Bony stabilizers

The glenohumeral articulation includes the speherical head retroverted to 15 0 and the pear shaped glenoid. According to Saha, excessive retroversion was one of the causes of dislocation. It is now believed that with repeated dislocations, fractures of the anterior rim of the glenoid (bony Bankart) render the shape of the glenoid to an inverted pear. Also, repeated dislocations result in compression/impaction fractures of the postero­medial aspect of the head of humerus, resulting in Hill- Sach's lesion. All these bony injuries result in a deficient three dimensional glenohumeral articulation.

Soft tissue stabilizers

The shoulder joint remains stable to a great extent due to a balance between the soft tissue stabilizers i.e. the static and dynamic stabilizers. Static stabilizers include the glenoid labrum, glenohumeral ligaments, capsule and rotator cuff interval. The dynamic stabilizers are comprised of the rotator cuff group of muscles (subscapularis, supraspinatus, infraspinatus, teres minor) and the scapulothoracic muscles. The biceps tendon also has a role in the depression of the head of humerus. Imbalance in the various muscles groups can result in shoulder instability. It is believed that the negative intra­articular pressure or ligament tension and concavity compression mechanism also can provide glenohumeral stability in the inferior direction.

The glenoid labrum

Normal and Variants: The glenoid labrum is a vascularised fibrocartilaginous bumper attached all along the rim of the glenoid. It is loosely attached at the superior portion and this has resulted in the mistaken identity of normal variants. The vascularity at the periphery has clinical applicability in determining whether labral tears are repairable or not. [11] The structure of the glenoid labrum is known to increase the depth of the glenoid socket by more than 50% in all directions; and also deepen the surface area of the glenoid by 9 mm in AP plane. [12] According to Gill et al [9] , the labrum functions as a "chock block" preventing "excessive translation of the humeral head" on loading. Biomechanical studies by Lippitt et al [13] showed that by resecting the labrum, the resistance to translation on compressive loading is reduced to 20%. The labrum also serves as an attachment to the superior, middle and inferior glenohumeral ligaments. Mosely and Overgaard [14] have classified three types of labrum depending upon the insertion of the capsule into the labrum. The superior part of the labrum inserts directly into the biceps tendon, distal to the insertion of the tendon into the supra glenoid tubercle. There is a synovial recess beneath the biceps tendon and it can be mistaken for a SLAP (superior labrum, anterior to posterior) lesion.[15]

Normal variations to the capsule-labral complex are quite common. This can be often be mistaken for pathological lesions. The Buford Complex[16] is a cord like middle glenohumeral ligament found in association with absent antero-superior labral complex. Another such variant is sub-labral foramen which can also be mistaken for a pathological lesion.

Labral pathology

Bankart [1] in 1938, described the classical "Bankart lesion" [Figure 2(a)],[Figure 2(b)] as detachment of the anteroinferior labrum with its attached inferior glenohumeral ligament complex as the "essential lesion" for shoulder instability and reported excellent results in patients where the labrum was reattached to the original site of disruption. Navieser in 1993 [17] described ALPSA (Anterior labral periosteal sleeve avulsion) [Figure 3] as a pathological finding similar to Bankart's lesion with one notable difference; the anterior scapular periosteum does not rupture and the inferior glenohumeral ligaments, labrum, and periosteum are stripped and displaced in a sleeve type fashion medially on the glenoid neck. Speer et al [18] created experimental Bankart lesions and came to the conclusion that pure detachment from the labrum without proper tensioning of the inferior glenohumeral ligament complex leads to failure of the surgical procedure. Therefore, arthroscopic surgical procedures that simply led to reattachment of the labrum had failure rates varying from 5% to 60%. [19],[20],[21],[22],[23]

Superior labral lesions

Synder et al [15] described the SLAP (superior labrum antero posterior) lesion characterized by complex labral detachment from 10 o'clock to 6 o'clock position of the shoulder. Such superior labral lesions can lead to subtle forms of instability. Similarly experimental studies by Pagnani et al [24] confirmed that there was significant effect on anteroposterior and superoinferior translation with a complete lesion from 10 o'clock to 3 o'clock position.

Capsule/gleno humeral ligaments

The superior glenohumeral ligament along with coracohumeral ligament limits inferior translation and external rotation of the adducted shoulder, and posterior translation of the fixed adducted and internally rotated shoulder. The middle glenohumeral ligament limits anterior translation of the humeral head when the arm is abducted between 60 0 and 90 0 . The inferior glenohumeral ligament functions like a hammock in preventing increased translation of the humeral head on the glenoid. The entire complex in abduction moves beneath the humeral head and prevents the anterior and inferior translation. Likewise, in internal rotation, the ligament complex moves posteriorly and limits posterior translation.

Lesions of the ligaments

Thomas [2] and Townley [25] introduced the "capsular mechanism" and believed that failure of the capsule and its plastic deformation was a cause of instability of the shoulder. Thomas [2] described the essential lesion as a tear in the capsule with hemarthroses which in turn resulted in stretching of the capsule, leading to an anterior inferior hernial pouch and recorded successful results after repair/shortening/obliteration of the capsule alone. Warren et al [26] introduced the "Circle concept" of capsular contribution to shoulder instability. They pointed out that the complete dislocation requires the deformation of capsule on the involved side as well as stretching in the opposite side of the joint. Therefore, it was not clear as to what the essential lesion of the inferior glenohumeral ligament really was. Bigliani et al [27] tested the inferior glenohumeral ligament to load failure in uniaxial tension, dividing the inferior glenohumeral ligament into three anatomic regions. Failure occurred 40% in the glenoid insertion (Bankart's); mid­substance 35%, and humeral insertion 25%. This led to the concept of plastic deformation of the inferior glenohumeral ligament and hypothesis that the plastic deformation of inferior glenohumeral ligament is the essential lesion in recurrent shoulder instability.

Operative repair of the capsule either by plication, double breasting, advancement or tensioning are important in successful outcome of shoulder stabilization surgery. Recently capsular shrinkage down through radiofrequency heat probes has given encouraging results.

SLAC (Superior labral anterior cuff) lesion

This lesion occurs as a result of injury to the anterior superior labrum at the site of insertion of the anterior portion of biceps and the superior glenohumeral ligaments. Because of this injury the undersurface of the supraspinatus tendon comes in contact with the anterior superior labrum and the glenoid. Repeated forceful contact result in wear down of the undersurface of the supraspinatus resulting in a partial tear at the anterior edge along with the labral injury. These patients often complain of pain, popping and fatigue with repeated overhead loading activities. It is clinically tested with Whipple test.

Rotator interval

The rotator interval is a triangular shaped space bordered by the anterior supraspinatus tendon superiorly, subscapularis tendon border and the corocoid base laterally. The capsule is structurally enhanced by the coracohumeral ligaments and the superior glenohumeral ligaments. It functions to limit the inferior translation of the gleno humeral joint in the adducted shoulder and provides stability against posterior dislocation in flexion or abduction-external rotation.

Harrymen et al [28] have stressed on the significant role of rotator cuff lesion in anterior instability, because sectioning of the rotator cuff have lead to increase in anterior, posterior and inferior instability. The rotator interval can be a small opening to a wide cleft. Clinical reports of the closure of isolated rotator interval defect on a small group of patients, have been recently reported with excellent short term results. [29]

Dynamic factors

The rotator group of muscles has a dynamic role in providing compressive load on the humeral head throughout the range of shoulder movement. Lippitt et al [13] described the "concavity compression" and proved in their experiments that with intact labrum the humeral head resists only 60% of the compressive load. When there is an anterior inferior chondral labral defect the height of the glenoid is reduced by 80% and stability by 65%. [30] Coordinated rotator cuff contraction plays significant role in maintaining the stability of the shoulder. Overhead activities in the athlete with increasing demands on the shoulder subject the shoulder to fatigue and hence increasing risk to injury. Displacement of the humeral head increased with increase in size of the rotator cuff defect. It is believed that the capsule and the ligaments are tensioned during active contraction of the rotator cuff muscles. Rodosky et al [31] , emphasised the contribution of the long head of biceps in resisting the excessive external rotation forces. They felt that the biceps tends to stabilize the joint anteriorly with the arm in internal rotation and acts as the posterior stabilizer with the arm in external rotation.

Traumatic instability

Overhead athletes like bowlers in cricket, tennis and swimmers, put their shoulder at considerable risk of injury. Placing the shoulder at extremes of motion under strenuous condition may develop instability. Improper throwing mechanisms and capsular contracture does not allow generation and energy about the shoulder. Repetitive throwing generated humeral velocity and rotational torques which overuse weaknesses the anterior static restraints and lead to trauma of the under surface of the rotator cuff against the postero superior glenoid. This cause, pain and weakness and aggravate to the instability. This has been described by Walch et al [23] . Micro Instability appear to occur as a compensation. This may be reversible by neuro-muscular conditioning exercises.

Proprioception

Ligaments can stabilize the joint by providing neurogenic feed-back and directly mediate the joint position sensibility and muscular reflex action. This feed-back mechanism is known as proprioception. Vangsness et al [32] have demonstrated existence of neuro structure and mechano receptors in the capsule and ligaments of the shoulder joint. Lephart et al [33] showed that the proprioception of the symptomatic shoulder was disrupted in patients with instability. More work is being done to understand the proprioceptive mechanism of the shoulder joint.

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