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.