Sebille A, Hugelin A
Pathol Biol (Paris). 1982 Jan;30(1):37-41.
The study of toxic experimental models of neuropathies has been a decisive step to understand some cellular mechanisms of human neuropathies. The progressive development of toxic neuropathies allow to the possibility of isolating their initial mechanism. Dying back axonopathies are the commonest neuropathies as observed in clinical practice, and their experimental models had been extensively studied. Acrylamide and n-hexane intoxications have shown the following results : 1) The onset of the neuropathy is located at the most distal node of the longest and largest fibres. Sensory fibres are impaired before the motor ones. 2) Fast axoplasmic transport stops distally. 3) Impaired enzymes of the energetic cycle were observed distally. Proximal axonopathies as those resulting from IDPN intoxication are a possible model to clear up the cellular mechanisms of the lateral amyotrophic sclerosis. Human toxic neuronopathies and myelinopathies are uncommon. Such experimental models are described in relation to other human neuropathies.
对神经病变毒性实验模型的研究是理解人类神经病变某些细胞机制的决定性一步。毒性神经病变的逐步发展使得分离其初始机制成为可能。轴索性逆行性神经病是临床实践中最常见的神经病变，其实验模型已得到广泛研究。丙烯酰胺和正己烷中毒呈现出以下结果：1）神经病变的起始部位位于最长和最大纤维的最远端节段。感觉纤维比运动纤维更早受损。2）快速轴浆运输在远端停止。3）在远端观察到能量循环中的酶受损。由IDPN中毒导致的近端轴索性神经病可能是一种用于阐明侧索肌萎缩硬化症细胞机制的模型。人类毒性神经元病和髓鞘病并不常见。此类实验模型与其他人类神经病变相关进行了描述。
