Lundborg G, Gelberman R H, Minteer-Convery M, Lee Y F, Hargens A R
J Hand Surg Am. 1982 May;7(3):252-9. doi: 10.1016/s0363-5023(82)80175-5.
Controlled external compression was applied to the medium nerve of 16 volunteer subjects. Tissue fluid pressure in the carpal canal was monitored with a wick catheter and pressures of 30, 60 and 90 mm Hg were induced for periods varying from 30 to 90 minutes.l Sensory and motor conduction and two-point discrimination were continuously monitored. Tissue compression at 30 mm Hg caused mild neurophysiological changes and symptoms of hand paresthesias. Compression at both 60 and 90 mm Hg induced a rapid, complete sensory conduction block which consistently preceded a motor block by 10 to 30 minutes. Frequently, two-point discrimination remained normal until the last stages of preserved sensory fiber conduction. In three cases, a modification of the model utilizing an arm tourniquet, demonstrated that ischemia rather than mechanical deformation was the primary cause of the functional deterioration. It was concluded that there is a critical pressure level between 30 and 60 mm Hg where nerve fiber viability is acutely jeopardized.
对16名志愿者的正中神经施加控制性外部压迫。用灯芯导管监测腕管内的组织液压力，并诱导30、60和90毫米汞柱的压力，持续30至90分钟。连续监测感觉和运动传导以及两点辨别能力。30毫米汞柱的组织压迫引起轻度神经生理变化和手部感觉异常症状。60和90毫米汞柱的压迫均诱发快速、完全的感觉传导阻滞，且感觉传导阻滞始终比运动阻滞提前10至30分钟出现。通常，直到感觉纤维传导的最后阶段，两点辨别能力仍保持正常。在三例病例中，利用手臂止血带对模型进行的改良表明，缺血而非机械变形是功能恶化的主要原因。得出的结论是，在30至60毫米汞柱之间存在一个临界压力水平，在此压力水平下神经纤维的活力会受到严重威胁。
