Parry G J, Linn D J
Department of Neurology, Hahnemann University, Philadelphia, PA 19102.
J Neurol Sci. 1988 Apr;84(2-3):265-73. doi: 10.1016/0022-510x(88)90131-1.
Incomplete infarction of the tibial nerve was produced in 37 rats by injecting arachidonic acid into the femoral artery. Sciatic-tibial motor nerve conduction studies were performed 1, 2, 3 and 7 days later. In all animals the evoked motor responses were of low amplitude and morphological examination showed axonal degeneration. In 20 rats the response elicited by proximal stimulation was of lower amplitude than the distal response indicating focal conduction block in a proportion of those axons which had survived the ischemia and were not degenerating distally. The conduction block resolved over several days and in all but one rat had disappeared by 7 days. Morphological examination of semithin sections and single teased myelinated axons revealed no evidence of segmental demyelination. The rapid resolution of conduction block and the lack of significant segmental demyelination suggest that it has a metabolic basis. We suggest that hypoperfusion of the subperineurial region of the proximal tibial nerve, the region surrounding the infarct through which surviving axons pass, may be sufficient to temporarily block impulse transmission in these surviving axons without producing morphological changes.
通过向37只大鼠的股动脉注射花生四烯酸，造成胫神经不完全梗死。在1、2、3和7天后进行坐骨-胫神经运动神经传导研究。在所有动物中，诱发的运动反应幅度较低，形态学检查显示轴突退变。在20只大鼠中，近端刺激引发的反应幅度低于远端反应，表明在一部分存活于缺血状态且未发生远端退变的轴突中存在局灶性传导阻滞。传导阻滞在数天内消退，除1只大鼠外，所有大鼠在7天时传导阻滞均已消失。半薄切片和单个分离的有髓轴突的形态学检查未发现节段性脱髓鞘的证据。传导阻滞的快速消退以及缺乏明显的节段性脱髓鞘表明其具有代谢基础。我们认为，胫神经近端神经束膜下区域（梗死灶周围存活轴突穿过的区域）的灌注不足，可能足以暂时阻断这些存活轴突中的冲动传递，而不产生形态学变化。
