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areas of residual in ammation and demyelination are often detected at the edges of the destructive lesions For these reasons the current authors agree with Hughes in classifying this condition with the demyelinative diseases Older lesions may have left the spinal cord cavitated or collapsed over a vertical extent of 5 to 20 cm, with conical extensions of necrosis into the gray matter above and below the area of transverse damage In two cases of ours, in which death occurred many years after the onset of the myelitis, there were old cavitated and demyelinated, lesions in the cerebral white matter, typical of MS Cases of this type emphasize the overlapping relationship between the necrotizing and demyelinative processes Also, as alluded to earlier we have been unable to make a clear distinction between the necrotic myelopathy of Devic disease and the identical process occurring without optic neuropathy The optic nerve lesions also tend to be of demyelinative type In the cases of pure necrotic myelopathy described by Green eld and Turner as well as by Hughes and in our own series (Katz and Ropper), patients of all ages and both sexes were affected Under the title Subacute Necrotic Myelitis, Foix and Alajouanine and later Green eld and Turner described a disorder of adult men characterized by amyotrophic paraplegia that ran a progressive course over several months An early spastic paraplegia evolved after a few weeks or longer into a accid, are exive state Sensory loss, at rst dissociated and then complete, and loss of sphincteric control followed the initial paresis The CSF protein was considerably elevated but there were no cells In most ways, therefore, this process resembles subacute necrotizing myelopathy Postmortem examinations in two of the cases of Foix and Alajouanine and in most subsequently reported ones have shown the lumbosacral segments to be the most severely involved In the affected areas there was severe necrosis of both gray and white matter with appropriate macrophage and astrocytic reactions However, the characterizing feature was thought to be an increase in the number of small vessels; their walls were thickened, cellular, and brotic ( angiodysplastic ), yet their lumens were not occluded The veins were also thickened and surrounded by lymphocytes, mononuclear cells, and macrophages These ndings have been dif cult to interpret The possibility of spinal venous thrombosis in the pathogenesis has been emphasized, but in the case of Mair and Folkerts, only one thrombosed anterior spinal vein was seen; in the cases of Foix and Alajouanine, no thrombosed vessels were found We believe the evidence of venous or other vascular occlusion to be unconvincing and are inclined to the view of Antoni and of others, who were impressed with the prominence of large arteries and veins and have reinterpreted this pathologic process as an arteriovenous malformation (see further on) More importantly, in most cases of necrotic myelopathy that are not associated with a true vascular malformation, the vascular changes simply re ect a neovascular response to necrosis Only when enlarged and abnormal vessels involve the surface and adjacent parenchyma of the cord does the disorder deserve to be designated as Foix-Alajouanine myelopathy; the remaining cases are of the in ammatory-necrotizing type described earlier, with a secondary neovascular response to necrosis Rarely, a similar syndrome is produced by an idiopathic granulomatous or necrotizing angiitis that is con ned to the spinal cord (Caccamo et al) In these cases, there is a persistent and marked pleocytosis and some clinical stabilization with corticosteroids One of our patients with a similar subacute necrotizing myelitis, responsive to corticosteroids, had mononuclear cells in the spinal uid persistently over a year and died later as a result of in am-.

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