Response

Abstract

Dear Editor-in-Chief: We appreciate Dr. Krishnan's thoughtful comments on, "A Neuromuscular Mechanism of Posttraumatic Osteoarthritis Associated with ACL Injury" (3). We read his remarks with interest and appreciate the opportunity to respond. It is indeed important for readers to be aware of other points of view on this topic. We remain steadfast in our hypothesis that quadriceps inhibition may serve as a potential mechanism of posttraumatic osteoarthritis (OA). Dr. Krishnan points out that limited data are available regarding the presence or absence of persistent quadriceps arthrogenic muscle inhibition (AMI) after anterior cruciate ligament reconstruction (ACLr). We do not disagree with his point and concur that more evidence is necessary before we firmly conclude that AMI causes chronic quadriceps weakness after ACLr. However, we do believe that a reasonable amount of evidence is available to lend credence to our original premise. The findings of Urbach et al. (7) and Suter et al. (6) illustrate that quadriceps AMI can be present approximately 2 yr after ACLr. Furthermore, the magnitude of this inhibition can be rather large, upward of 15%-20% (6,7). Unpublished data from our laboratory support these findings, with patients 10 months after ACLr having bilateral quadriceps inhibition (mean central activation ratios of 0.83 and 0.89 in the ACLr and uninjured limbs, respectively). It is important to note that the magnitude of quadriceps AMI seems to vary greatly after ACLr. Some patients in our ongoing study, for example, demonstrate inhibition of 40%, whereas others display minimal activation deficits of 2%, suggesting that patients can display complete activation as Dr. Krishnan points out. However, this is not a certainty, and more often than not, at least in the case of our patients and those studied previously (6,7), a substantial amount of quadriceps inhibition lingers. It is currently unknown why some evidence illustrates persistent quadriceps AMI after ACLr (6,7), whereas other research does not (1,5). This discrepancy may be attributed to the various procedures used to quantify AMI, the degree of joint damage at the time of injury, the magnitude of preoperative inhibition, and the graft selected, among other possible contributors. Dr. Krishnan also highlights the recent findings of Scopaz et al. (4), showing that baseline quadriceps activation did not hinder quadriceps strength gains after an exercise intervention in persons with knee OA. Although these findings seem to contradict our original assertion that lingering quadriceps inhibition may preclude full recovery of quadriceps strength after ACLr, it is important to consider that the results noted in patients with OA may not apply to persons after anterior cruciate ligament injury or reconstruction. In fact, Hurley et al. (2) noted that persons with traumatic knee joint injuries who have greater magnitudes of quadriceps AMI do not respond well to traditional rehabilitation. The peripheral and central mechanisms leading to OA- and ACL-induced AMI may differ, lending to varied responses to exercise. Therefore, we still assert that failure to target AMI after ACLr could promote persistent deficits in quadriceps strength. We believe that quadriceps AMI is a potential mechanism of posttraumatic OA associated with anterior cruciate ligament injury. Quadriceps inhibition can persist after ACLr and may hinder successful rehabilitation. Acknowledgments The data presented herein were supported by grant number 1K08 AR053152-01A2 from the National Institutes of Health. Riann M. Palmieri-Smith, Ph.D. Abbey C. Thomas, MEd Neuromuscular Research Laboratory Center for Clinical Biomechanics University of Michigan School of Kinesiology Ann Arbor, MI