The biomechanics of subsynovial connective tissue in health and its role in carpal tunnel syndrome.

The biomechanics of subsynovial connective tissue in health and its role in carpal tunnel syndrome.
复制标题

DOI:
10.1016/j.jelekin.2017.10.007
复制
发表时间:
2018-03
期刊:
Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology
影响因子:
--
通讯作者:
Amadio PC
Amadio PC
中科院分区:
其他
文献类型:
--
作者:
Festen-Schrier VJMM;Amadio PC

文献摘要

参考文献

被引文献

相似文献

腕管综合征(CTS)是手部最常见的外科治疗问题。除了神经病变本身,最常见的发现是滑膜下结缔组织纤维化(SSCT)和腕管内压力增加。正常情况下,SSCT是分布在腕腱和神经之间的多层组织。随着肌腱的移动,连续的SSCT层被招募,形成一个滑动单元,并为不同的运动提供限制。超过这一限制,会损害SSCT,正如在身体和动物模型中所显示的那样。这种损伤导致进行性纤维化和神经缺血的非炎性反应,使SSCT更容易受到损伤。虽然对患者的直接后果还不完全清楚,但超声研究表明,这种纤维化限制了肌腱负荷期间正中神经的移位。本文旨在提供对迄今为止所描述的SSCT的机械特性的见解,并将其置于CTS病理生理学的背景下。提出了一种关于SSCT的理论损伤模型,该模型显示了一系列事件和恶性循环,这些事件和恶性循环可能导致CTS中发现的神经压迫。这个模型虽然不完整,但可以解释特发性CTS的病理生理途径。
Carpal Tunnel Syndrome (CTS) is the most common surgically treated problem in the hand. Aside from the neuropathy itself, the most common findings are fibrosis of the subsynovial connective tissue (SSCT) and increased intra carpal tunnel pressure. Normally, the SSCT is a multilayer tissue interspersed among the carpal tendons and nerve. As the tendons move, successive SSCT layers are recruited, forming a gliding unit and providing a limit to differential movement. Exceeding this limit, damages the SSCT as has been shown in both cadavers and animal models. This damage leads to a non-inflammatory response with progressive fibrosis and nerve ischemia leaving the SSCT more susceptible to injury. Although the direct consequences for patients are not fully understood, ultrasound research shows that this fibrosis restricts median nerve displacement during tendon loading. This article aims to provide insights into the mechanical properties of SSCT described so far and place it in the context of CTS pathophysiology. A theoretical damage model concerning the SSCT is proposed showing a chain of events and vicious cycles that could lead to the nerve compression as it is found in CTS. Although not complete, this model could explain the pathophysiological pathway of idiopathic CTS.
DOI: 10.1002/jor.22909
发表时间: 2015-09-01
影响因子: 2.8
作者:
Filius, Anika;Scheltens, Marjan;Selles, Ruud W.
通讯作者: Selles, Ruud W.
DOI: 10.1002/jor.22489
发表时间: 2014-01
影响因子: 2.8
作者:
Filius, Anika;Thoreson, Andrew R.;Yang, Tai-Hua;Vanhees, Matthias;An, Kai-Nan;Zhao, Chunfeng;Amadio, Peter C.
通讯作者: Amadio, Peter C.
DOI: 10.3109/17453678909149305
发表时间: 1989-08-01
期刊: ACTA ORTHOPAEDICA SCANDINAVICA
影响因子: --
作者:
LUCHETTI, R;SCHOENHUBER, R;LANDI, A
通讯作者: LANDI, A
DOI: 10.1016/j.main.2010.04.002
发表时间: 2010-06-01
影响因子: --
作者:
Guimberteau, J. -C.;Delage, J. -P.;Wong, J.
通讯作者: Wong, J.
DOI: 10.1002/jor.22485
发表时间: 2014-01
影响因子: 2.8
作者:
Chikenji, Takako;Gingery, Anne;Zhao, Chunfeng;Passe, Sandra M.;Ozasa, Yasuhiro;Larson, Dirk;An, Kai-Nan;Amadio, Peter C.
通讯作者: Amadio, Peter C.