Dyck P J, Lais A C, Giannini C, Engelstad J K
Peripheral Neuropathy Research Laboratory, Mayo Clinic, Rochester, MN 55905.
Proc Natl Acad Sci U S A. 1990 Dec;87(24):9828-32. doi: 10.1073/pnas.87.24.9828.
Whether compression nerve injury is due to ischemia, direct mechanical injury, or both remains unsettled. To assess structural changes of nerve during compression, peroneal nerves of rats were compressed at various pressures for different times, and the structural alterations were stopped by simultaneous in situ and perfusion fixation. The structural changes observed during a few minutes of compression cannot be explained by ischemic injury because the pathologic alterations characteristic of ischemia take many hours to develop and in any case are different from the ones found here. The pressure- and time-related structural changes observed in the present study under the cuff were (i) decrease in fascicular area and increase in fiber density due to expression of endoneurial fluid; (ii) compression and expression of axoplasm, sometimes to the point of fiber transection; (iii) lengthening of internodes; and (iv) obscuration of nodes of Ranvier due to cleavage and displacement of myelin and overlapping of nodes by displaced loops of myelin. At the edges of the cuff the changes were (i) increase of fascicular area probably from expressed endoneurial fluid; (ii) widening of nodal gaps, perhaps mainly from translocated axonal fluid; and (iii) disordered structure of axoplasm. We suggest that the process of paranodal demyelination and axonal transection are linked, occur during the act of compression, and are due to shear forces. The initial event is expression of endoneurial fluid, followed by compression and expression of axoplasm and cleavage and displacement of layers of myelin. Conceivably, with prolonged cuff compression ischemic injury might be found to be superimposed on mechanical injury.
压迫性神经损伤是由局部缺血、直接机械损伤还是两者共同所致，目前尚无定论。为评估神经在受压过程中的结构变化，对大鼠的腓总神经施加不同压力并持续不同时间，同时通过原位灌注固定来终止结构改变。在几分钟的压迫过程中观察到的结构变化无法用缺血性损伤来解释，因为缺血的病理改变需要数小时才会出现，而且无论如何都与这里发现的不同。本研究在袖带压迫下观察到的与压力和时间相关的结构变化包括：（i）由于神经内膜液的渗出，束状面积减小，纤维密度增加；（ii）轴浆受压和渗出，有时直至纤维横断；（iii）结间长度增加；（iv）由于髓鞘的裂开和移位以及移位的髓鞘环重叠导致郎飞结模糊不清。在袖带边缘，变化包括：（i）束状面积可能因神经内膜液渗出而增加；（ii）结间隙增宽，可能主要是由于轴突液移位；（iii）轴浆结构紊乱。我们认为，结旁脱髓鞘和轴突横断过程是相关联的，发生在压迫过程中，是由剪切力引起的。最初的事件是神经内膜液渗出，随后是轴浆受压和渗出以及髓鞘层的裂开和移位。可以想象，随着袖带压迫时间延长，可能会发现缺血性损伤叠加在机械损伤之上。
