Neuroplastic Mechanisms for Acquisition and Transfer of Injury-Resistant Movement Patterns Assessed in VR Simulated Sport

项目摘要/摘要 前交叉韧带(ACL)损伤是一种常见的与活动相关的膝关节损伤，具有很大的负面影响 在个人和社会上。年度直接成本超过130亿美元，长期间接成本远远超过 这一数字，因为前交叉韧带损伤也与几年内致残性骨关节炎的加速发展有关 受伤几年后。国家骨关节炎公共卫生议程建议扩大和加强 以证据为基础的前交叉韧带损伤预防，以减轻这一负担。我们已经确定了可改变的运动模式 这增加了年轻女运动员前交叉韧带损伤的风险。虽然神经肌肉训练针对的是那些受伤的风险 在高危运动员的运动模式和显示的统计效果，有意义的转移低风险 机械师在赛场上的发挥一直是有限的。这种目前的方法无法确保抗伤害 随着全国前交叉韧带损伤的减少，运动模式向体育运动的转变很明显 年轻女运动员中的比率，尽管标准的神经肌肉训练对修改生物力学有效果 实验室。确保有效的伤害预防转移到体育运动的关键知识差距是理解 神经系统参与获取和转移抗损伤运动模式的机制 对运动场的干预或实验室。因此，这项提案的总体目标是确定 支持将抗损伤运动模式转移到现实运动场景的神经机制。 我们发表的和最新的关于神经可塑性与损伤风险和以下方面相关的初步数据 神经肌肉训练显示了一种特定的神经机制，这种机制是耐损伤转移的基础 运动模式。这些初步数据支持这一提议的中心假设，即大脑的变化 活动是获得并将抗伤害运动模式转移到现实运动情景中的基础。 重要的是，这项工作表明，神经可塑性可以通过增强的生物反馈和其他临床应用来实现 优化大脑运动激活模式以促进抗损伤运动模式的方法 收购和转让。靶向降低伤害风险因素的神经机制的能力可能 彻底改变前交叉韧带损伤预防策略。一旦这一应用程序的目标实现，我们将 能够通过确定的神经治疗靶点提高神经肌肉训练的效果。这 对提高前交叉韧带损伤预防训练可转移性、降低损伤发生率具有重要意义 从而避免相关的长期负面健康后果。这一点对年轻人来说尤其相关 女性运动员是非接触性感觉运动错误相关前交叉韧带损伤的最高风险人群。 这是通过靶向神经肌肉的神经机制来加强前交叉韧带损伤预防的独特机会 改编和转让突出了这一附属项目为母公司U01提供的特殊机会 NIH投资公司。

Project Summary/Abstract Anterior cruciate ligament (ACL) injury is a common activity-related knee injury with a substantial negative impact on individuals and society. Annual direct costs exceed $13 billion, and the long-term indirect costs far exceed that figure, as ACL injury is also linked to the accelerated development of disabling osteoarthritis within a few years after injury. The National Public Health Agenda for Osteoarthritis recommends expanding and enhancing evidence-based ACL injury prevention to reduce this burden. We have identified modifiable movement patterns that increase ACL injury risk in young female athletes. While neuromuscular training targets those injury risk movement patterns and shows statistical efficacy in high-risk athletes, a meaningful transfer of low-risk mechanics to the field of play has been limited. This inability of current approaches to ensure injury-resistant movement pattern transfer to sport is readily apparent as there has not been a decrease in national ACL injury rates in young female athlete despite efficacy of standard neuromuscular training to modify biomechanics in the lab. The key knowledge gap to ensure effective injury prevention transfer to sport is understanding the mechanisms the nervous system engages to acquire and transfer injury-resistant movement patterns from the intervention or laboratory to the athletic field. Thus, the overall objective of this proposal is to determine the neural mechanisms underpinning the transfer of injury-resistant movement patterns to realistic sport scenarios. Our published and recent preliminary data on the neuroplasticity related to injury risk and following neuromuscular training demonstrate a specific neural mechanism underlies the transfer of injury-resistant movement patterns. These preliminary data support this proposal's central hypothesis that changes in brain activity underlie the acquisition and transfer of injury-resistant movement patterns to realistic sport scenarios. Importantly this work indicates the neuroplasticity can be targeted by augmented biofeedback and other clinical methods to optimize brain activation patterns for movement that promote injury-resistant movement pattern acquisition and transfer. The ability to target the neural mechanisms of injury risk factor reduction could revolutionize ACL injury prevention strategies. Once the objectives of this application are achieved, we will be able to enhance the efficacy of neuromuscular training with the identified neuro-therapeutic targets. This contribution will be significant to improve ACL injury prevention training transferability to reduce injury incidence and thus avoid the associated long-term negative health consequences. This is especially relevant to young female athletes as they are the population at highest risk for non-contact sensorimotor error related ACL injury. This unique opportunity to enhance ACL injury prevention by targeting neural mechanisms of neuromuscular adaptation and transfer highlights the exceptional opportunity afforded by this ancillary project to the parent U01 NIH investment.