To prevent abnormal translation of the humeral head on the glenoid, the shoulder is stabilised by both static and dynamic mechanisms [1, 2]. The dynamic stabilisers include the rotator cuff and to a lesser degree the long head of the biceps and deltoid muscle. The static mechanisms include the bony configurations of the glenoid and humerus, the glenoid labrum, the joint capsule and the glenohumeral ligaments. The role of the capsular structures in preventing dislocation of the glenohumeral joint is well described [3–5]. Although the avulsion of the capsulolabral complex (Bankart lesion) accounts for more than 80% of instability cases, the humeral avulsion of the glenohumeral ligaments (HAGL) has only been reported in 1–9% of patients but may be even higher when looking at specific subgroups [6, 7]. Almost two-thirds of patients can have concurrent injury to the labrum or rotator cuff.

Nicola, in a short series of acute shoulder dislocations, was the first to describe the avulsion of the anterior inferior glenohumeral ligament (AIGHL) in 1942 [8]. Bach later described this injury in two patients with recurrent instability [9]. Wolf, in an arthroscopic study of 64 shoulders with shoulder instability, termed the acronym HAGL for humeral avulsion of glenohumeral ligaments [7].

The capsuloligamentous complex consists of the coracohumeral ligaments, superior glenohumeral ligament, middle glenohumeral ligament and inferior glenohumeral ligament (IGHL) [10]. The IGHL, which is attached medially to the glenoid labrum, is composed of the anterior band, posterior band and axillary pouch. The orientation of the pouch and bands creates a hammock-like structure on the anterior and posterior aspects of the glenoid. The anterior band of the IGHL therefore provides restraint to anterior and inferior translation with the arm in abduction and external rotation. With the arm in flexion and internal rotation, the posterior band of the IGHL spans the mid-portion of the joint providing posterior stability. The humeral insertion of the IGHL has been described as either a collar-like attachment close to the articular margin or as a V-shaped attachment with a base, anteriorly and posteriorly, close to the articular margin and the apex more distal on the humeral neck. Pouliart, in a large cadaveric and arthroscopic study, found on dissection from the outside that all had a capsular attachment in a V-form; however on visualisation this had a rounded collar-like appearance due to the presence of connecting synovial bands. Anteriorly, the most superior part of the IGHL joined the inferior fibres of the subscapularis tendon on the lesser tuberosity, while posteriorly it was attached to the distal part of the greater tuberosity adjacent to the superior fibres of the latissimus dorsi tendon [11].

The overwhelming majority of HAGL lesions are caused by traumatic injury. A small series of overhead athletes with IGHL avulsion due to repetitive microtrauma have been reported [12, 13]. Studies of arthroscopic findings in first-time dislocators have reported that traumatic shoulder dislocation or subluxation may result in (1) avulsion of the capsulolabral complex from the anterior glenoid rim (i.e. Bankart lesion), (2) avulsion of the IGHL from its humeral attachment (i.e. HAGL lesion) and (3) capsular tears or a combination of the above [14, 15]. These findings have been collaborated in cadaveric studies testing the tensile properties of the IGHL which demonstrated three possible locations of injury to occur: failure of the IGHL labral complex at the glenoid origin (40%), an intrasubstance tear (35%) and at the point of insertion on the humerus (25%) [4]. Gagey et al. however experimentally dislocated cadaver shoulders and noted capsular failure at the humeral side in as high as 63% of specimens [16].

Bui-Mansfield et al. developed the West Point classification system to organise the variety of concurrent injuries associated with the IGHL complex. The authors described six distinct forms of HAGL lesion based on anterior or posterior involvement, the presence or absence of bony avulsion and the presence of associated labral pathology: anterior HAGL, anterior bony HAGL (i.e. with associated bony avulsion), floating anterior IGHL (i.e. HAGL lesion with concurrent detachment of the anteroinferior labrum), posterior HAGL, posterior bony HAGL and floating posterior IGHL (i.e. HAGL lesion with concurrent detachment of the posterior inferior labrum). The anterior HAGL represents 93% of reported cases, whereas posterior HAGL represents only 7% of cases. This system does however not account for the finding of posterior HAGL with anterior labral pathology and vice versa as found in other studies on MR imaging of posterior HAGL lesions [17]. Furthermore, there is no evidence to suggest any correlation between the type of lesion and prognosis, and course of management using these classification systems.

In experimental sequential cutting studies evaluating the extent of humeral-based capsuloligamentous damage required for dislocation to occur, a high degree of correlation between the amount of cutting performed and the resulting degree of instability was found [18, 19]. The order in which the ligamentous cuts were made had no significant influence, but for dislocation to occur, at least three zones had to be cut.

Although large HAGL lesions can increase the passive motion of the glenohumeral joint in both neutral and external rotation, these differences are small and may be difficult to measure clinically [20]. That extensive lesions on the humeral side are required before dislocation can occur may be a factor explaining the relatively low incidence of HAGL lesions in clinical series.

From history, taking a traumatic shoulder injury event with or without subluxation or dislocation is described in 93% of the cases. It is important to ascertain the position of the arm at the time of injury, direction of instability and typically previous failed instability surgery. Although both traumatic Bankart and HAGL lesions occur with the arm in hyperabduction, HAGL lesions are more likely to occur with hyperabduction and external rotation. Bokor noted HAGL lesions in 14.6% of patients requiring revision of a previous failed procedure [21]. Occasionally, patients may present with non-specific symptoms like weakness, pain and poor function which may represent less extensive capsuloligamentous damage with subtle microinstability of the glenohumeral joint. All provocative tests to assess stability are similar to those for anterior and posterior capsulolabral pathology. Typically, the examiner should perform the apprehension, relocation, load-and-shift, posterior stress and posterior jerk tests. Examination for associated pathology of the rotator cuff should be performed including signs of subscapularis weakness.

Imaging studies should include a true AP with the shoulder in ER and IR, axillary view, Bernageau view and an outlet view. A small bony avulsion of the humeral neck is the only pathognomonic sign of inferior IGHL injury, but associated findings including humeral head impaction, glenoid rim fractures and glenohumeral malalignment must be excluded.

MRI, with or without intra-articular contrast, is the modality of choice for the assessment of a suspected HAGL lesion. The IGHL complex is best evaluated on coronal oblique or sagittal oblique T2-weighted fat-suppressed magnetic resonance images [22]. The normal IGHL anatomy appears as a U-shaped structure because of fluid distension of the axillary pouch. As a result of the loss of containment of contrast or joint fluid through the torn capsule and ligament, the presence of a HAGL lesion can cause the normally U-shaped axillary pouch to appear J-shaped.

Chronic HAGL lesions may be difficult to visualise on magnetic resonance images as the torn edge on the humeral side may scar down to the capsule with time. In a study of 42 patients with acute first-time dislocation, MRI was performed within 7 days of the injury and a follow-up MRI arthrogram after 30 days. Capsular ligament lesions were found in 22 patients (52.4%) in the acute stage and in 5 patients (11.9%) at follow-up. Nine patients (21.4%) had a humeral avulsion of the anterior glenohumeral ligament (HAGL lesion) on MRI. Three patients (7.1%) had this lesion at follow-up [23]. Understandably, only one study has determined the accuracy of standard MRI or magnetic resonance arthrography in detecting the presence of HAGL lesion. In 23 patients that underwent surgery for HAGL lesions, 16 lesions were seen on prospective MR reading [24].