Mackinnon Susan E
Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine, 1 Barnes-Jewish Hospital Plaza, Suite 17424/East Pavilion, St. Louis, MO 63110, USA.
Hand Clin. 2002 May;18(2):231-41. doi: 10.1016/s0749-0712(01)00012-9.
Both ischemic and mechanical factors are involved in the development of compression neuropathy. Experimental studies suggest a dose response curve such that the greater the duration and amount of pressure, the more significant is neural dysfunction. With changes of axonal injury, significant neurologic dysfunction would be anticipated; however, the vast majority of patients with CTS present with symptoms in association with electrophysiologic findings of demyelination (prolonged latency). Frequently, the prolongation in latency is minimal and some patients may even present with normal electrodiagnostic studies, still complaining of significant symptomatology. This would support the concept that in the majority of patients with CTS, the symptoms relate to problems with the connective tissue "container" of the nerve rather than pathology of the nerve fiber itself. This would be in keeping with the histopathologic findings of fibrosis, with thickening of the external epineurium and perineurium. These changes would interfere with blood flow as the vessels pass through the epineurium and perineurium and produce dynamic ischemia to the nerve fibers. As well, this fibrosis would decrease the excursion of the nerve fibers, resulting in traction, and prevent the nerve fibers themselves from going through a full range of movement without traction and decreased gliding. The importance of neural gliding and movement of the nerve in the extremity has been recently emphasized in the clinical management of patients with multilevel nerve compression. Clinical maneuvers that put the nerve on stretch will provoke patients' symptoms and have been used to diagnose specific compression neuropathies (neural tension test). Similarly, physical therapy modalities to stretch the nerves and restore neural gliding are frequently successful in relieving patients' symptoms [33]. This physical therapy approach is based on the premise that the connective tissue "container" of the nerve is tight and short and needs to be mobilized. This is in keeping with the histopathologic findings of increased connective tissue at the perineurial and epineurial levels. A greater understanding of the pathophysiology of compression neuropathy will have immediate impact on our management of this problem and likely result in emphasis on conservative management and physical therapy rather than surgical intervention.
缺血因素和机械因素均参与压迫性神经病变的发生发展。实验研究表明存在剂量反应曲线，即压力的持续时间和大小越大，神经功能障碍就越显著。随着轴突损伤的变化，预计会出现明显的神经功能障碍；然而，绝大多数腕管综合征（CTS）患者的症状与脱髓鞘的电生理表现（潜伏期延长）相关。通常，潜伏期的延长很轻微，有些患者甚至电诊断检查结果正常，但仍主诉有明显症状。这支持了这样一种观点，即在大多数CTS患者中，症状与神经的结缔组织“容器”问题有关，而非神经纤维本身的病变。这与纤维化的组织病理学发现一致，表现为神经外膜和神经束膜增厚。这些变化会在血管穿过神经外膜和神经束膜时干扰血流，对神经纤维产生动态性缺血。同样，这种纤维化会减少神经纤维的移动，导致牵拉，并使神经纤维本身无法在无牵拉和减少滑动的情况下进行全方位运动。神经滑动和肢体中神经运动的重要性最近在多节段神经压迫患者的临床管理中得到了强调。使神经受牵拉的临床操作会引发患者症状，已被用于诊断特定的压迫性神经病变（神经张力测试）。同样，拉伸神经并恢复神经滑动的物理治疗方法常常能成功缓解患者症状[33]。这种物理治疗方法基于这样的前提，即神经的结缔组织“容器”紧绷且缩短，需要进行松动。这与神经束膜和神经外膜水平结缔组织增加的组织病理学发现一致。对压迫性神经病变病理生理学的更深入理解将对我们处理这个问题产生直接影响，可能会导致更强调保守治疗和物理治疗而非手术干预。
