The coracohumeral ligament (CHL) is a strong band of connective tissue situated within the shoulder joint. It is part of the complex capsular structure that envelops the glenohumeral joint, the articulation between the shoulder blade and the upper arm bone. The CHL functions as a static restraint, helping to keep the head of the humerus centered within the shallow socket of the shoulder blade. Understanding this structure provides insight into the biomechanics of shoulder movement and why certain conditions can lead to severe restriction of motion.
Anatomy and Attachments
The coracohumeral ligament is a broad, flat structure reinforcing the superior aspect of the shoulder joint capsule. Its name indicates its bony connections: it originates from the coracoid process of the scapula (shoulder blade), specifically near the base of this hook-like projection. It then extends laterally and downward across the top of the joint.
Moving toward the humerus (upper arm bone), the ligament splits into two bands. These bands insert onto the greater and lesser tubercles, the two bony prominences at the top of the humerus. The ligament covers the long head of the biceps tendon superiorly, forming a fibrous tunnel that holds the tendon in place.
The CHL blends with surrounding structures, including the superior joint capsule and the tendons of the supraspinatus and subscapularis muscles. This positioning means the CHL forms the roof of the rotator interval, a triangular space in the shoulder complex. This broad attachment pattern provides its stabilizing function.
Role in Shoulder Stability and Biomechanics
The primary function of the coracohumeral ligament is to provide passive, static stability to the glenohumeral joint. It acts as a superior buttress, preventing the downward displacement of the humeral head when the arm hangs at the side. This is relevant when external forces, such as carrying weight, attempt to pull the arm inferiorly. The CHL’s tautness helps maintain joint congruence in this position.
The ligament also controls the rotational movement of the arm. It becomes taut when the arm is moved into external rotation, particularly when the arm is at the side. By tightening, the CHL serves as a passive check-rein that limits the degree of external rotation possible at the shoulder joint.
Biomechanical studies show the CHL contributes significantly to maintaining inferior stability during external rotation. This differs from stability during internal or neutral rotation, where internal joint pressure is more important. The CHL and the rotator interval capsule work together to maintain the integrity of the superior joint aspect. While surrounding muscles provide dynamic stabilization, the CHL offers constant structural support.
Involvement in Adhesive Capsulitis (Frozen Shoulder)
The coracohumeral ligament is intimately involved in the pathology of adhesive capsulitis, or frozen shoulder. In this condition, the shoulder joint capsule undergoes inflammation leading to fibrosis, which is the thickening and scarring of connective tissue. The CHL and the surrounding rotator interval capsule are considered the main structures that contract in chronic cases.
This pathological contracture results in a mechanical block to shoulder movement. The thickening of the ligament is a highly suggestive finding for adhesive capsulitis and can be visualized on magnetic resonance imaging (MRI). Studies show the CHL is significantly thicker in affected shoulders compared to unaffected ones, and this increased stiffness directly causes the loss of motion.
The stiffness of the CHL contributes most significantly to the restriction of external rotation, the hallmark clinical finding of frozen shoulder. Since the ligament naturally limits external rotation, its contracture severely compounds this restriction. The restricted motion can also extend to internal rotation and arm elevation.
Treatment for persistent frozen shoulder often targets this contracted tissue. Surgical procedures, such as manipulation under anesthesia or arthroscopic capsular release, frequently involve cutting or releasing the thickened CHL and rotator interval to restore mobility. Histological analysis of the removed tissue confirms structural changes, showing clear evidence of fibrosis and abundant Type III collagen.
Acute Injuries and Clinical Assessment
While involvement in frozen shoulder is more common, the CHL can also sustain acute injuries. Sprains or tears often occur alongside traumatic events or major rotator cuff tears. Partial or full ruptures have been observed, and these injuries can destabilize the superior aspect of the joint and contribute to pain.
Clinicians assess CHL involvement primarily through a physical examination focused on passive range of motion. Since the ligament limits external rotation, a marked decrease in the arm’s ability to externally rotate suggests CHL tightness. Palpation is also used, though the ligament’s deep location makes it difficult to isolate.
Advanced imaging, such as ultrasound or MRI, provides objective evidence of CHL pathology. Ultrasound can measure the thickness of the ligament. MRI is effective at visualizing the ligament’s structure and detecting signs of thickening or inflammation, helping to differentiate CHL involvement from other causes of shoulder pain.