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高、低风险重复腰椎弯曲后黏弹性组织降解的神经肌肉表现。

Neuromuscular manifestations of viscoelastic tissue degradation following high and low risk repetitive lumbar flexion.

机构信息

Musculoskeletal Disorders Research Laboratory, Bioengineering Division, Department of Orthopaedic Surgery, School of Medicine, University of Colorado, Denver, Aurora, CO 80045, USA.

出版信息

J Electromyogr Kinesiol. 2012 Apr;22(2):155-75. doi: 10.1016/j.jelekin.2011.11.008. Epub 2011 Dec 6.

Abstract

Cumulative lumbar disorder is common in individuals engaged in long term performance of repetitive and static occupational/sports activities with the spine. The triggering source and of the disorder, the tissues involved in the failure and the biomechanical, neuromuscular, and biological processes active in the initiation and development of the disorder are not known. The hypothesis is forwarded that static and repetitive (cyclic) lumbar flexion-extension and the associated repeated stretch of the various viscoelastic tissues (ligaments, fascia, facet capsule, discs, etc.) causes micro-damage in their collagen fibers followed by an acute inflammation, triggering pain and reflexive muscle spasms/hyper-excitability. Continued exposure to activities, over time, converts the acute inflammation into a chronic one, viscoelastic tissues remodeling/degeneration, modified motor control strategy and permanent disability. Changes in lumbar stability are expected during the development of the disorder. A series of experimental data from in-vivo feline is reviewed and integrated with supporting evidence from the literature to gain a valuable insight into the multi-factorial development of the disorder. Prolonged cyclic lumbar flexion-extension at high loads, high velocities, many repetitions and short in between rest periods induced transient creep/laxity in the spine, muscle spasms and reduced stability followed, several hours later, by an acute inflammation/tissue degradation, muscular hyper-excitability and increased stability. The major findings assert that viscoelastic tissues sub-failure damage is the source and inflammation is the process which governs the mechanical and neuromuscular characteristic symptoms of the disorder. A comprehensive model of the disorder is presented. The experimental data validates the hypothesis as well as provide insights into the development of potential treatment and prevention of the disorder.

摘要

累积性腰椎紊乱在长期从事重复性和静态职业/运动活动的个体中较为常见,这些活动涉及脊柱。目前尚不清楚该疾病的触发源和发病机制,也不清楚涉及的组织以及在疾病发生和发展中起作用的生物力学、神经肌肉和生物学过程。提出了一种假说,即静态和重复性(循环)腰椎屈伸以及与之相关的各种粘弹性组织(韧带、筋膜、小关节囊、椎间盘等)的反复拉伸,会导致其胶原纤维发生微损伤,随后发生急性炎症,引发疼痛和反射性肌肉痉挛/过度兴奋。随着时间的推移,持续暴露于活动中会使急性炎症转变为慢性炎症,粘弹性组织重塑/退变,运动控制策略发生改变,并导致永久性残疾。在疾病发展过程中预计会出现腰椎稳定性的变化。本文回顾了一系列来自体内猫的实验数据,并整合了文献中的支持证据,深入了解了该疾病的多因素发展过程。在高负荷、高速度、多次重复且两次休息之间时间较短的情况下,长时间的循环性腰椎屈伸会导致脊柱短暂的蠕动/松弛、肌肉痉挛和稳定性降低,数小时后会发生急性炎症/组织降解、肌肉过度兴奋和稳定性增加。主要研究结果表明,粘弹性组织的亚失效损伤是该疾病的根源,炎症是控制该疾病机械和神经肌肉特征症状的过程。提出了一种疾病综合模型。该实验数据验证了假说,并为潜在的疾病治疗和预防方法提供了新的思路。

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