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romyelitis optica Its principal features are the acute to subacute onset of blindness in one or both eyes, preceded or followed within days or weeks by a severe transverse or ascending myelitis (Mandler et al) The spinal cord lesions in cases of neuromyelitis optica are often necrotizing rather than purely demyelinative in type, leading eventually to cavitation; as would be expected, the clinical effects are more likely to be permanent than those of demyelination A few of the patients have been children; in a number of instances, they suffered only a single episode of neurologic illness Although it is true that cases corresponding to this prototype are seen on occasion in every large medical center and at all age periods, the isolation of such an entity on clinical grounds alone has been unsatisfactory At least half of our patients have proved by subsequent clinical developments, and in a few instances by autopsy, to have chronic relapsing MS In one notable example, where hemiplegia and aphasia were followed within 2 weeks by a necrotizing myelitis from which there was no recovery, the patient later developed typical attacks of MS, including retrobulbar neuritis At autopsy, more than 15 cm of the spinal cord had been destroyed, reducing it to a collapsed membranous tube Elsewhere in the brain and cord the lesions were typically demyelinative One might conclude from cases such as these that neuromyelitis optica is but a variant form of MS (or some other type of demyelinative disease) Many cases of neuromyelitis optica, however, stand apart from MS by virtue of a number of distinctive clinical and pathologic features namely, a failure to develop brainstem, cerebellar, or cerebral demyelinative lesions and normality of the cerebral white matter on MRI, even after several years of illness; almost uniform absence of oligoclonal bands and other abnormalities of IgG in the spinal uid; and nally, the necrotizing and cavitary nature of the spinal cord lesion, affecting white and gray matter alike with prominent thickening of vessels but without in ammatory in ltrates On the basis of these differences, Mandler and O Riordan and their colleagues and others have favored the separation of Devic disease from MS For reasons mentioned above, we are uncertain that the distinction is quite so clear or perhaps there are two types of disease, only one of which is allied with MS Recently, evidence of antibody binding, complement activation, and eosinophilic in ltration has led to the conclusion that the Devic process is a humoral disease, in contrast to the cellular mechanism that has been proposed for MS (see Lucchinetti et al, 2002) In support of this notion is the nding of a serum IgG antibody directed against capillaries in the brainstem and cerebellum Lennon and colleagues have reported that this is a marker for neuromyelitis optica in half of the cases and is absent in MS Insofar as the cause of neither MS nor Devic disease is known, uncertainties about the relationship of these diseases cannot be resolved with nality It should also be noted that acute disseminated encephalomyelitis may occasionally present as a neuromyelitis optica syndrome There is in addition a progressive and saltatory subacute necrotic myelopathy without optic neuritis that shares all the myelopathic features of Devic disease but not the optic neuropathy and, in our view, probably represents the same entity (Katz and Ropper) In our clinics, such purely myelopathic cases outnumber those of Devic disease The differential diagnosis here is broader and includes speci cally arteriovenous malformation of the cord or dura and, of lesser resemblance, infarction or neoplasm of the cord Also, a rare isolated vasculitis of the cord may cause a necrotic myelopathy; it is associated with an active CSF pleocytosis (Ropper et al) The cord in the cases we have studied was swollen on. c# free tiff library TiffBitmapDecoder .cs source code in C# .NET
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