The biceps brachii, innervated by the musculocutaneous nerve, has two heads that originate from different points on the scapula. The short head arises from the coracoid process as a single tendon combined with the coracobrachialis muscle (the conjoined tendon) and the long head arises from within the glenohumeral joint from both the supraglenoid tubercle and the adjacent glenoid labrum (Fig. 5.1). The tendon travels anterolaterally in the rotator interval and exits the joint through the bicipital groove which lies between the greater and lesser tuberosities of the proximal humerus. Travelling distally, the muscle bellies of each head coalesce, cross the cubital fossa and spiral towards their primary insertion on the bicipital tuberosity on the proximal radius (Fig. 5.2). This chapter will focus on the intra-articular portion of the LHB tendon since it is often implicated in the development of acute and chronic shoulder pain.

The supraglenoid tubercle of the scapula has historically been described as the origin of the LHB tendon. However, several cadaveric studies have found that the superior labrum contributes significantly to the LHB origin [1–5]. In a series of 105 cadaveric shoulders, Vangsness Jr et al. [5] found that 40–60 % of the LHB tendon originated from the supraglenoid tubercle while the remaining fibers originated from the superior labrum (Fig. 5.3). Tuoheti et al. [4] dissected 101 cadaveric shoulders and found that the LHB tendon originated from both the supraglenoid tubercle and the glenoid in every case. In addition, Gigis et al. [2] noted that the LHB not only arises from both the supraglenoid tubercle and the labrum, but it also forms a portion of the posterosuperior labrum itself. An anatomic study of 16 cadaveric shoulders by Arai et al. [1] found that the fibers of the labrum became stiffer and stronger as the LHB tendon origin was approached. These studies support other claims that the torsional strain placed upon the superior labrum by the LHB tendon in positions of hyperabduction and external rotation is at least one factor involved in the development of superior labral anterior to posterior (SLAP) tears in throwing athletes (discussed later in this chapter) [6].

One of the difficulties inherent to the diagnosis of SLAP tears, especially with regard to imaging studies, is the significant anatomic variability of the biceps anchor-superior labrum complex. According to Rao et al. [7], there are three predominant variations in superior labral anatomy that may be present in up to 10 % of the general population: the sublabral recess, the sublabral foramen, and the Buford complex (Figs. 5.4 and 5.5). The sublabral recess represents a potential space beneath the biceps anchor and the anterosuperior aspect of the glenoid labrum. The sublabral foramen is a small orifice located between the anterosuperior labrum and the articular cartilage of the anterior glenoid. The Buford complex is characterized by an absence of the anterosuperior labrum with a cord-like middle glenohumeral ligament that attaches directly to the superior labrum. It is crucial for the clinician to identify these findings as normal anatomic variants rather than pathologic lesions since inappropriate “repair” may lead to significant pain and external rotation loss as a result of stiffness [8, 9].

As the LHB tendon travels obliquely through the joint in an anterolateral direction, the tendon is encased in an outward-facing synovial membrane that is continuous with the joint capsule and renders the tendon extra-synovial [10]. As the tendon travels distally towards the bicipital groove of the proximal humerus, its position is maintained by the capsuloligamentous restraints within the rotator interval. The rotator interval is a triangular area in the anterosuperior aspect of the glenohumeral joint (Fig. 5.6). The medial base of the triangle is located at the coracoid process. The anterior margin of the supraspinatus and the superior margin of the subscapularis make up the superior and inferior borders of the rotator interval triangle, respectively. The lateral apex of the rotator interval is composed of the transverse humeral ligament which covers the bicipital groove and contributes to the bicipital sheath (discussed below). The contents of the interval include the LHB tendon, the superior glenohumeral ligament (SGHL), the coracohumeral ligament (CHL), and the glenohumeral joint capsule [11]. A more detailed description of the structure, function, and pathologies associated with the rotator interval can be found in Chap. 6.

As the LHB tendon courses towards the bicipital groove, the SGHL and the CHL form a sling around the LHB tendon, primarily preventing its medial subluxation. This sling extends to the most anterior portion of the rotator cable and the biceps reflection pulley (BRP) at the proximal end of the bicipital groove [12]. The BRP, derived from the coalition of the SGHL, CHL, and the upper 1/3 of the subscapularis tendon, redirects the anterolateral course of the LHB tendon such that the tendon travels directly inferiorly along the anterior humeral shaft (Fig. 5.7). Habermeyer et al. [14] described a 30–40° inferior turn of the LHB tendon as it exited the joint via the BRP. Tearing of the subscapularis in this region, often known as a “pulley lesion,” can allow medial subluxation of the LHB tendon producing a painful “popping” or “snapping” sensation as the arm is moved (Fig. 5.8). In addition, a biomechanical study by Braun et al. [16] found that the LHB tendon slides up to 18 mm in and out of the joint with forward flexion and internal rotation, respectively. Therefore, the LHB tendon itself is subjected to significant mechanical stresses in the area of the BRP which can lead to tendonitis, tearing or rupture of the LHB.

The bicipital sheath is another complex structure through which the LHB tendon traverses as it passes through the bicipital groove (see Fig. 5.7). The floor of this sheath is formed from the coalescence of the SGHL and the subscapularis tendons at the superior aspect of the lesser tuberosity. These fibers then travel laterally, forming the floor of the bicipital sheath. The roof of the sheath is mostly composed of fibers from both the supraspinatus and CHL ligaments. All of these fibers (the floor and the roof of the sheath) combine to form a continuous ring around the LHB tendon as it passes through the bicipital groove thus providing tendon stability (Fig. 5.9). A recent biomechanical study by Kwon et al. [17] found that the subscapularis tendon was the most important stabilizer of the LHB tendon within the bicipital groove since tears of the subscapularis in this area almost always resulted in medial subluxation of the LHB tendon.

The bony structure of the bicipital groove can also play a role in pathologies of the LHB tendon. In a radiographic study by Pfahler et al. [18], the opening angle of the groove in patients without LHB tendon pathology was between 101° and 120° with the medial wall having a greater height than the lateral wall. Patients with a shallow groove or a lower medial wall may also be susceptible to subluxation of the LHB tendon.

The vascular supply to the LHB tendon near the biceps-labral complex is variably derived from the suprascapular, circumflex scapular and posterior circumflex humeral arteries [10]. Vascularity of the tendon is richest near its origin and dissipates prior to entering the bicipital groove where the tendon is avascular and fibrocartilaginous. This infrastructure helps prevent tendon injury from the sliding action of the LHB within the sheath of the groove. Similarly, innervation of the LHB tendon is concentrated near its anchor and dissipates as the tendon travels distally [19]. This arrangement was described as a “net-like” pattern of sympathetic fibers by Alpantaki et al. [19] in a cadaveric study using neurofilament antibodies (Fig. 5.10). In addition, Tosounidis et al. [20] demonstrated the presence of sympathetic α₁-adrenergic receptors along the LHB tendon in cadaveric specimens with known acute and chronic shoulder conditions. These studies demonstrate that sympathetic innervation of the proximal LHB tendon may play a role in the pathogenesis of shoulder pain.

Although the anatomy of the proximal LHB tendon has been well described, its precise function has been debated for many years. Most studies that have aimed to describe its function are based on cadaveric models that focus on glenohumeral stability.

Pagnani et al. [21] used ten cadaveric shoulders to show that decreased anterior, superior, and inferior humeral head translation occurred when a simulated load of 55 N was applied to the LHB tendon in lower angles of elevation. Rodosky et al. [22] used a dynamic cadaveric shoulder model to simulate the forces typically applied to both the rotator cuff and the LHB tendons. They found that the LHB tendon contributed to glenohumeral stability by resisting torsional forces in the abducted and externally rotated position. The authors also noted a significantly increased strain applied to the anterior band of the inferior glenohumeral ligament (IGHL) when the biceps-labral complex was detached from its anchor at the superior aspect of the glenoid. This study provides some evidence that SLAP tears may contribute to increased anterior humeral head translation that is often found during physical examination (see Chap. 6 for more details regarding glenohumeral laxity and instability). More recently, Youm et al. [23] showed that the LHB tendon contributed significantly to anterior, posterior, superior, and inferior translation of the humeral head when a 22 N load was applied. Rotational range of motion and scapulohumeral kinematics were also affected when a load was applied to the LHB tendon. Alexander et al. [102] also noted a decrease in humeral head translation in all directions when a 20 N load was applied to the LHB tendon. Su et al. [24] studied the effects of the LHB tendon in cadaveric shoulders with variably sized rotator cuff tears. In their study, a significant decrease in anterosuperior and superior humeral head translation occurred when a 55 N load was applied to the LHB tendon.

Itoi et al. [25] contested that both the LHB and the short head of the biceps contribute significantly to glenohumeral joint stability, particularly in positions of abduction and external rotation when a simulated load of 1.5 and 3.0 kg were applied. This contribution to stability was particularly robust after attenuation of anterior stabilizing structures had occurred. In another biomechanical study, Kumar et al. [26] showed that loading of the short head of the biceps alone caused superior migration of the humeral head whereas tensioning of both the short head and the LHB simultaneously did not result in humeral head translation in any direction.

Although these studies suggest the role of the LHB tendon may be associated with glenohumeral stability, interpretation of dynamic shoulder models is difficult since replication of the in vivo environment, including complex force couples and resting tension, is quite difficult to achieve. In addition, the variability of simulated loads (11–55 N) makes their results difficult to compare, especially when the precise physiologic loads applied to the LHB tendon in different angles of abduction and rotation are currently unknown. Thus, it is possible that some studies may have obtained statistically significant results due to the application of non-physiologically high loads, making the results of these studies difficult to interpret.

To help answer these questions, electromyographic (EMG) studies have been performed to evaluate the effect of the LHB tendon on glenohumeral kinematics. However, their findings have been inconsistent to date. Levy et al. [27] found that the LHB tendon aided in glenohumeral stability both passively and in association with forearm supination or flexion. In contrast, Sakurai et al. [28] determined that the LHB tendon dynamically stabilized the humeral head, regardless of elbow activity. Other studies on pitching biomechanics found that the biceps may primarily function as a stabilizer of the elbow during flexion and supination with little effect on shoulder stability [29, 30]. Thus, the effect of the LHB tendon on glenohumeral kinematics remains controversial with respect to the most current EMG literature.

Both cadaveric and EMG studies have produced an incomplete picture of how the LHB tendon actually functions with regard to glenohumeral kinematics. Therefore, in vivo studies have also been conducted to help solve the mystery. Warner and MacMahon [31] studied a group of seven patients with rupture of the proximal LHB tendon and compared humeral head translation to their unaffected shoulders by true anteroposterior radiographs. In their study, radiographs were obtained in 0°, 45°, 90°, and 120° of abduction in the scapular plane. They found that superior migration of the humeral head was significantly increased in the shoulders with a ruptured LHB tendon compared to their contralateral, unaffected shoulders at all angles of abduction. Another radiographic study by Kido et al. [32] found similar results, noting that the humeral head was depressed as the LHB tendon was stimulated. However, the accuracy of radiographic studies has been called into question. Therefore, three-dimensional biplane fluoroscopy, a modality which has sub-millimeter accuracy, has been used to study in vivo kinematics with improved accuracy during full muscle activation. A study by Giphart et al. [33] found that, in five patients who underwent unilateral open subpectoral biceps tenodesis, humeral head translations of approximately 3 mm occurred in both the affected and unaffected shoulders during active elevation. The authors also studied various loading conditions such as forward flexion with maximal biceps activity on EMG, abduction to assess superior translation and a simulated throw (hyperabduction and external rotation) to evaluate anterior translation. Despite these loading conditions, the differences in translation between tenodesed and normal shoulders was always less than 1.0 mm, suggesting that the proximal LHB tendon may actually play a minimal role in glenohumeral kinematics in a shoulder that otherwise has an intact rotator cuff (Fig. 5.11).

The inconsistent and often contradictory findings of cadaveric, EMG, and in vivo studies have made it difficult to define the precise function of the proximal LHB tendon. While most of these studies have found that the LHB tendon may be involved with glenohumeral stability, further in vivo kinematic studies are necessary to completely elucidate the biomechanical role of the LHB tendon in shoulder motion and stability.

Inflammation of the LHB tendon most often occurs secondarily as a result of surrounding pathologies such as impingement syndrome, pulley lesions, and/or degenerative rotator cuff tears (Fig. 5.12). Primary LHB tendonitis, in which there is isolated inflammation with no apparent cause, is not uncommon in clinical practice. Although isolated inflammation of the proximal LHB tendon can occur in overhead athletes, this may be the result of repetitive microtrauma as the tendon glides back and forth in a “sawing” motion within the bicipital groove and across the BRP. It is important to remember that because the LHB tendon is encased with synovium, inflammation within the shoulder may track proximally into the biceps-labral complex or distally into the bicipital groove.

Subacromial impingement is the most common mechanism by which LHB tendonitis occurs, especially in older patients. Subcoracoid impingement can also lead to injury involving the LHB tendon and the BRP [35]. Weak rotator cuff and periscapular musculature potentially allow increased translation of the humeral head, narrowing the space available for the subacromial or subcoracoid contents to pass thus allowing impingement of these structures between the greater tuberosity and the undersurface of the acromion or between the lesser tuberosity and the coracoid (further details on subacromial impingement and subcoracoid impingement are provided in Chap. 4). In patients with subacromial impingement, LHB tendonitis almost always occurs simultaneously since the LHB is subject to the same mechanical wear from the coracoacromial arch. In addition, because the LHB tendon is encased in an outward-facing synovial membrane extending from the glenohumeral joint, any inflammatory process within the joint can thus involve the LHB tendon, producing painful inflammation and tenosynovitis (Fig. 5.12).

The acute stage of LHB tendonitis is characterized by significant anterior shoulder pain localized within the bicipital groove. The LHB tendon will swell and sometimes develop partial-thickness tearing at points of maximal wear. Later, the tendon further degenerates and may form adhesions with surrounding structures such as the bicipital sheath and rotator interval structures. In this stage, microscopic examination reveals fibrinoid necrosis and atrophy of collagen fibers [36]. As the tendon degenerates, it can either become hypertrophic or atrophic with a deterioration of its organization and infrastructure. If, or when, rupture occurs, symptoms will often resolve immediately with the formation of a “Popeye” deformity (discussed later). On the contrary, attritional tendon degeneration may occur asymptomatically and painless rupture may occur.

Evaluation of patients with bicipital tendonitis is often difficult due to vague symptoms and inconsistent physical examination findings. It is therefore critically important to obtain a detailed history to help guide the use of appropriate provocative testing. Some patients may describe a “popping” or “snapping” sensation, especially when internally and externally rotating the humerus in 90° of abduction. Although the most common finding in patients with bicipital tendonitis is bicipital groove tenderness, this type of pain is difficult to differentiate from pain related to the anterosuperior cuff which inserts in the area of the bicipital sheath. Patients who describe a history of anterior shoulder pain that suddenly resolved after a specific incident likely had spontaneous rupture of their LHB tendon.

Both upper extremities of every patient should be inspected for any evidence of asymmetry. Spontaneous rupture of the proximal LHB tendon can result in the classic “Popeye” deformity in which the muscle belly is distally retracted, appearing as distinct bulge in the distal aspect of the humerus just above the elbow (Fig. 5.13). Strength and range of motion should also be recorded for each extremity, particularly noting any discrepancies. Range of motion loss in patients with bicipital groove tenderness is most often associated with concomitant rotator cuff disease (see Chap. 4 for information regarding physical examination of the rotator cuff). Because some biomechanical data suggests that the LHB tendon functions to promote glenohumeral stability, it may also important to perform stability testing in these patients (see Chap. 6). The most important provocative tests traditionally used for the detection of bicipital tendonitis and tearing are presented below.

The pathogenesis of pulley lesions that lead to medial subluxation or dislocation of the LHB tendon has not been completely elucidated. Some have suggested that asymmetric loading of the LHB in positions of abduction and external rotation may be responsible for lesions of the BRP. However, in a biplane fluoroscopic study in cadavers performed by Braun et al. [16], the investigators demonstrated high shear-force vectors across the BRP in both the neutral and in internal rotation positions with or without forward flexion. Currently, there is insufficient data to suggest a specific pathomechanism responsible for the development of pulley lesions.

While there are some physical examination maneuvers that can be used to evaluate instability of the LHB tendon [25, 60, 61], none of these methods have been formally validated. Typically, the clinician will palpate the bicipital groove while simultaneously internally and externally rotating the humerus (see Fig. 5.14). Painful “clicking” or “popping” occurs as the LHB tendon translates over the lesser tuberosity. Complete dislocation of the LHB tendon out of the bicipital groove indicates a high probability of concomitant full- or partial-thickness tearing of the upper 1/3 of the subscapularis tendon and/or the anterior aspect of the supraspinatus tendon [59, 61]. Therefore, full examination of the anterosuperior rotator cuff is necessary in cases where instability of the LHB is suspected (see Chap. 4).

The precise pathomechanism behind the development of SLAP tears has been debated since its first description in 1985. Investigators most commonly cite forceful traction loads, forceful compression loads, and overhead sporting activities as the most common causes of SLAP tears. A forceful traction load to the biceps tendon may create a defect at the superior labrum resulting in pain and dysfunction [10, 70]. Clavert et al. [70] and Bey et al. [71] found that forward flexion and inferior traction, respectively, facilitated the development of SLAP lesions in separate cadaveric models. A forceful compression load may trap the biceps-labrum complex between the humeral head and the superior glenoid rim which may produce a mechanical shearing effect (or “grinding,” as suggested by Snyder et al. [63, 67]) resulting in a tear of the superior labrum. Repetitive traction from participation in overhead throwing sports such as baseball and softball also commonly result in tearing of the superior labrum.