Publications

BACKGROUND: Both the anterior cruciate ligament (ACL) and the medial collateral ligament (MCL) bear load during athletic tasks of landing, cutting, pivoting, and twisting. As dynamic knee valgus is a purported mechanism for ACL injury, the MCL should bear significant strain load with valgus force.

HYPOTHESIS: The intact MCL will demonstrate a significant increase in strain upon failure of the ACL at 25° of knee flexion.

STUDY DESIGN: Controlled laboratory study.

METHODS: In vivo kinetics/kinematics of 44 healthy athletic participants were measured to determine stratification of injury risk (ie, low, medium, and high) in 3 degrees of knee forces/moments (knee abduction moment, anterior tibial shear, and internal tibial rotation). These stratified kinetic values were input into a cadaveric impact simulator to assess ligamentous strain during a simulated landing task. Uniaxial and multiaxial load cells and differential variable reluctance transducer strain sensors were utilized to collect mechanical data for analysis. Conditions of external loads applied to the cadaveric limbs were varied and randomized.

RESULTS: ACL strain increased with increased dynamic knee abduction moment (χ2[5] = 14.123, P = .0148). The most extreme dynamic knee abduction moment condition demonstrated significantly higher ACL strain compared with lower loaded trials (P≤ .0203). Similarly, MCL strain increased with dynamic knee abduction moment (χ2[5] = 36.578, P < .0001). Matched-pairs analysis compared ACL strain with MCL strain (maximum ACL strain - maximum MCL strain) and demonstrated high strain for the ACL versus the MCL (S177 = 6223.5, P < .0001).

CONCLUSION: Although significant, MCL strain had minimal increase with increased dynamic knee abduction moment, and the event of ACL failure did not significantly increase MCL strain when compared with high dynamic knee abduction moment conditions in the cadaveric model. The ACL bears more strain than the MCL at increasing amounts of dynamic knee abduction moment at 25° of knee flexion, which may explain the limited concomitant MCL injury rate that can occur during a dynamic valgus collapse of the knee.

CLINICAL RELEVANCE: These characteristics of ACL and MCL strain are important to understand the mechanisms that drive these injuries at the knee and will improve rehabilitation and injury prevention techniques.

BACKGROUND: The existent literature has well explored knee ligament kinetics and strain at and after initial contact (IC) during landing tasks. However, little is known about knee ligament biomechanics in flight before IC.

PURPOSE: To quantify and compare change in anterior cruciate ligament (ACL) and medial collateral ligament (MCL) strain before IC relative to after IC.

STUDY DESIGN: Descriptive laboratory study.

METHODS: A total of 40 cadaveric specimens were analyzed after being subjected to simulated landings in a mechanical impact simulator. External joint loads of varying magnitudes were applied to mimic relative injury risk load levels from an in vivo cohort and were coupled with an impulse force to represent initial ground contact. Implanted strain gauges continually recorded ligament strain. Kruskal-Wallis tests evaluated the significance of risk level and pre- and post-IC factors, while Wilcoxon each-pair tests evaluated differences within both factors.

RESULTS: Strain responses during simulated landing tasks for the ACL (P ≥ .545) and MCL (P ≥ .489) were consistent after IC regardless of the level of relative injury risk simulated in each trial. Before IC, the level of injury risk kinetics applied to a specimen differentiated strain response in the ACL (P < .001) and MCL (P < .001), as higher risk profiles produced greater changes in ligament strain. Mean baseline strain was 4.0% in the ACL and 1.0% in the MCL. Mean change in strain from the ACL ranged from 0.1% to 3.9% pre-IC and from 2.9% to 5.7% post-IC, while the MCL ranged from 0.0% to 3.0% pre-IC and from 0.9% to 1.3% post-IC.

CONCLUSION: Within each ligament, post-IC strain response lacked statistical differences among simulated risk profiles, while pre-IC response was dependent on the risk profile simulated. Individually, neither pre- nor poststrain changes were enough to induce ACL failure, but when combined over the course of a full landing task, they could lead to rupture.

CLINICAL RELEVANCE: Prevention and rehabilitation techniques should aim to limit the presence of increased risk biomechanics in flight before landing, as impulse delivery at IC is inevitable.

BACKGROUND: Athletes have traditionally been subdivided into risk classifications for ACL injury relative to the biomechanical traits they display during landing. This investigation aimed to discern whether these separate risk classifications elicit strain differences on the ACL and MCL during landing. It was hypothesized that the higher risk simulation profiles would exhibit greater ACL strain and that the ACL would exhibit greater strain than the MCL under all conditions.

METHOD: The mechanical impact simulator was used to simulate landing on a cohort of 46 cadaveric specimens. The simulator applied external joint loads to the knee prior to impulse delivery. These loads were organized into a series of profiles derived from in vivo motion capture previously performed on a cohort of 44 athletes and represented various risk classifications. Strain gauges were implanted on the ACL and MCL and simulations performed until a structural failure was elicited. Differences were assessed with Kruskal-Wallis tests.

FINDINGS: The highest-risk profiles tended to exhibit greater peak ACL strain and change in ACL strain than the baseline- and moderate-risk profiles. Specimens that failed during lower-risk simulations expressed greater strain at these loads than specimens that completed higher-risk simulations. The ACL recorded greater strain than the MCL throughout all simulation profiles.

INTERPRETATION: This behavior justifies why neuromuscular interventions have greater impact on higher-risk athletes and supports the continued screening and targeted training of those athletes that express greater injury risk. The loading disparity between ACL and MCL justifies their limited concomitant injury rate.

OBJECTIVE: To measure McArdle sign (rapidly reversible weakness induced by neck flexion) both qualitatively and quantitatively and to evaluate its specificity and clinical utility for diagnosis of multiple sclerosis (MS).

PATIENTS AND METHODS: In this prospective study, McArdle sign was evaluated by a technician blinded to diagnosis by measuring changes in finger extensor strength in successive trials of neck extension and flexion, first clinically and then with a torque measurement device. We studied 25 healthy controls and 81 patients with finger extensor weakness. Patients were not selected for having McArdle sign. Fifty-two patients had MS, 24 had other myelopathies, and 5 had peripheral nerve lesions accounting for their weakness. The study was conducted between February 1, 2016, and June 30, 2017.

RESULTS: The median clinical McArdle sign and the 2 quantitative measures of neck flexion-induced strength reduction were greater in patients with MS than in the other groups (P<.001). Baseline strength did not confound the difference. The area under the receiver operating characteristic curve was 0.84 (95% CI, 0.75-0.93) comparing patients with MS vs healthy controls and 0.84 (95% CI, 0.75-0.93) comparing MS vs patients with other myelopathies. The 2 quantitative and 1 clinical measurement of McArdle sign by the technician who performed the quantitative testing were correlated (r=.57 and r=.58; P<.001), and in turn, the technician's and unblinded referring physician's clinical assessments were correlated (r=.58; P<.001). McArdle sign was evident in some patients who had minor disability and who were in early phases of MS.

CONCLUSION: McArdle sign, when defined as greater than 10% neck flexion-induced reduction in strength, is entirely specific and 65% sensitive for a diagnosis of MS when compared with other conditions that mimic MS-associated myelopathy. It may facilitate diagnosis in certain clinical situations.

TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT03122873.