8 – THE MEASUREMENT OF TENSION IN THE MEDIAL COLLATERAL LIGAMENT OF THE ELBOW

Abstract

Purpose: Techniques to quantify soft-tissue forces in the upper extremity are not well described. Consequently, ligament forces of the elbow joint have not been reported. Knowledge of the magnitudes of tension of the primary valgus stabilizer, the anterior bundle of the medial collateral ligament (AMCL), would allow for an improved understanding of the load bourne by the ligament. The purpose of this in vitro study was to quantify the magnitude of tension in the native AMCL throughout flexion with the arm in the valgus orientation. We hypothesized that tension in the AMCL would increase with flexion.

Method: Five fresh-frozen cadaveric upper extremities (mean age 72 ± 10 years) were tested. To produce active muscle loading in a motion simulator, cables were affixed to the distal tendons of the brachialis, biceps brachii, triceps brachii, and brachioradialis and attached to actuators. The wrist was fixed in neutral flexion/extension and the forearm in neutral rotation. The arm was orientated in the valgus gravity-loaded position. A custom designed ligament load transducer was inserted into the AMCL. Active simulated flexion was achieved via computer-controlled actuation while passive elbow flexion was achieved by an investigator manually guiding the arm through flexion. Motion of the ulna relative to the humerus was measured using a tracking device.

Results: Both the active and passive motion pathways showed an increase in AMCL tension with increasing angles of elbow flexion (p < 0.05). There was no difference in AMCL tension levels between active and passive elbow flexion (p = 0.20). The mean maximum tension achieved was 97±33N and 94±40 N for active and passive testing respectively.

Conclusion: AMCL tension levels were observed to increase with elbow flexion, indicating that other structures (such as the joint capsule and the shape of the articulation) are likely more responsible for joint stability near full extension, and that the AMCL is recruited at increased angles of elbow flexion. With respect to load magnitudes, Regan et al. found the maximum load to failure of the AMCL was 261 N, while Armstrong et al. reported a failure load of 143 N in cyclic testing. The maximum AMCL tension level observed in this study was 160 N. Failure of the AMCL was not observed, which may be due to differences in specimen size, age, or the method of load application. In summary, this in vitro cadaveric study has provided a new understanding of the magnitudes of AMCL tension through the arc of elbow flexion, and this has important implications with respect to the desired target strength of repair and reconstruction techniques. These findings will also assist in the development and validation of computational models of the elbow.