Mizisin A P, Kalichman M W, Myers R R, Powell H C
Department of Pathology (Neuropathology), University of California, San Diego, School of Medicine 92093.
Toxicol Pathol. 1990;18(1 Pt 2):170-85. doi: 10.1177/019262339001800123.
Nerve edema is a common response to the nerve injury seen in many peripheral neuropathies and is an important component of Wallerian degeneration. However, independent pathologic effects of nerve edema that aggravate or induce nerve injury extend the role of edema beyond that of an epiphenomenon of injury. New insights into the mechanism and impact of nerve edema come largely from animal models. In the following review, we discuss the cause and consequences of nerve edema with particular reference to endoneurial fluid pressure and its relevance to the nerve microenvironment. Experimental models of nerve edema include conditions with increased vascular permeability such as lead poisoning, experimental allergic neuritis, and murine globoid leukodystrophy. Increased perineurial permeability induced by local anesthetics and neurolytic drugs can also induce nerve edema sufficient to increase endoneurial fluid pressure. Both perineurial and vascular permeability are increased after damage induced by crush, freeze, or laser injury. One of the most important forms of nerve edema is induced by external compression; the significance of this change is that edema has local compressive effects that persist after the external pressure has been relaxed. Nerve edema and increased endoneurial fluid pressure also occur in conditions in which vascular permeability appears to be unchanged such as experimental diabetic neuropathy and in hexachlorophene intoxication. In both of these conditions, reduced nerve blood flow has been demonstrated in rats and is viewed as a consequence of increased endoneurial fluid pressure. Whatever its mechanism, endoneurial edema has important structural and functional consequences for nerve fibers. A clear understanding of the underlying pathology of the nerve microenvironment may provide useful insights into treatment of clinical neuropathies.
神经水肿是许多周围神经病变中神经损伤的常见反应，也是华勒氏变性的重要组成部分。然而，神经水肿独立的病理效应会加重或诱发神经损伤，这使得水肿的作用超出了损伤附带现象的范畴。对神经水肿机制及影响的新认识很大程度上源于动物模型。在以下综述中，我们将讨论神经水肿的原因及后果，特别提及神经内膜液压及其与神经微环境的相关性。神经水肿的实验模型包括血管通透性增加的情况，如铅中毒、实验性过敏性神经炎和小鼠球状细胞脑白质营养不良。局部麻醉药和神经溶解药物引起的神经束膜通透性增加也可诱发足以增加神经内膜液压的神经水肿。挤压、冷冻或激光损伤造成损害后，神经束膜和血管的通透性都会增加。神经水肿最重要的形式之一是由外部压迫引起的；这种变化的意义在于，水肿具有局部压迫作用，在外部压力解除后仍会持续。在血管通透性似乎未改变的情况下，如实验性糖尿病性神经病变和六氯酚中毒时，也会发生神经水肿和神经内膜液压升高。在这两种情况下，大鼠都已证实存在神经血流减少的情况，这被视为神经内膜液压升高的结果。无论其机制如何，神经内膜水肿都会对神经纤维产生重要的结构和功能影响。清楚了解神经微环境的潜在病理学可能为临床神经病变的治疗提供有益的见解。
