Shiraki H
Jpn J Med Sci Biol. 1975;28 Suppl:101-64.
The detailed neuropathology of the 16 autopsy cases of the acute to chronic "SMON" of different ages together with those reported before and at the "SMON" Research Commission has been described and reviewed. This was compared with the alreadyknown neurological disorders, particularly systemic and/or pseudosystemic degeneration of the long tracts of the spinal cord with polyneuropathy together with the "SMON"-like diseases caused by certain neurotoxic and/or neurotropic agents. It has been concluded that "SMON" can be belonged to a subgroup of some endemic diseases within the main group of combined degenerations associated with complex nutritional deficiency or toxic interference of tissue metabolism. Since an excess and mal-administration of quinoform in quantity, time and space were identified in a great majority of the autopsy cases, quinoform could comprize the most important etiology for the "SMON" onset. This view also was supported by the almost complete reconstruction of the neuropathology of the human "SMON" in the experimental animals intoxicated with quinoform which disclosed a precise neurotropism from the autoradiograms of the same animals. As compared with the similar lesions in SLE,hepatocerebral diseases, etc., the pathogenesis and clinicopathological relationship of "SMON" was speculated. The accerelating and/or modifying factors for the SMON" onset aside from quinoform were discussed.
对16例不同年龄段急性至慢性“SMON”尸检病例的详细神经病理学进行了描述和回顾,并与之前在“SMON”研究委员会报告的病例以及已知的神经系统疾病进行了比较,特别是脊髓长束的系统性和/或假性系统性变性合并多发性神经病,以及由某些神经毒性和/或神经嗜性药物引起的“SMON”样疾病。得出的结论是,“SMON”可归属于与复杂营养缺乏或组织代谢毒性干扰相关的合并变性主要组中的一些地方病亚组。由于在绝大多数尸检病例中发现氯碘喹啉在数量、时间和空间上过量及使用不当,氯碘喹啉可能是“SMON”发病的最重要病因。用氯碘喹啉中毒的实验动物几乎完全重现了人类“SMON”的神经病理学,从同一动物的放射自显影片中显示出精确的神经嗜性,这也支持了这一观点。与系统性红斑狼疮、肝脑疾病等类似病变相比,推测了“SMON”的发病机制和临床病理关系。讨论了除氯碘喹啉外“SMON”发病的加速和/或调节因素。