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EVIDENCES OF VASCULAR DISORDER IN CASES OF MULTIPLE SCLEROSIS SINCE the time of Rindfleisch,1 disturbances in circulation have been described as a part of the histologic picture of multiple sclerosis by the majority of observers. Some pathologists (Ribbert,2 Borst,3 Williamson,4 Klingman5) have ascribed an etiologic significance to the alterations observed, and one of us (T. J. P.), with various collaborators, has attempted a systematic survey of the hypothesis that the characteristic lesions are the result of vascular closure. Spotty areas of demyelination, with relative preservation of axis-cylinders and a purely ectodermal type of repair, may be produced by experimental venular obstruction,6 or may be observed in conjunction with a variety of lesions which embarrass the venous return.7 Thrombi are observed in or adjacent to the lesions in about 36 per cent of cases.8 This observation has subsequently been confirmed by Dow and

HYPERCHOLESTEREMIA in multiple sclerosis has been reported by several investigators.1 In three of these studies1a-c the number of patients was too small to permit full confidence in the findings, and in two1a,b the range of control serum-cholesterol concentrations with which the data from patients were compared was considerably below that which is usually accepted as normal. In one of these investigations1c no control values were cited. Only one recent report1d includes data on an acceptably large number of patients with multiple sclerosis. Average serum-cholesterol concentrations of 271, 267, and 230 mg. per 100 ml. were found, respectively, for 25 patients in relapse, 38 patients in remission, and 30 control subjects. The higher values for the patients were statistically significant, even though the average control concentration would be regarded by many as abnormally high.We were not satisfied that the available evidence was sufficient to establish

IT HAS been noted during the past decade that an increasing number of cases of multiple sclerosis are coming to the attention of neurologists, ophthalmologists and general practitioners. Various attempts have been made in the past by different observers to obtain statistical data on this disease (von Hoesslin,1 Brown and Putnam,2 Sachs and Friedman3). Those observations, however, were never on a large enough scale to give a clear picture of the distribution of multiple sclerosis. It has, therefore, not been possible to determine whether or not an actual increase in the number of patients is taking place or whether improved medical care and examining methods have had their share in revealing cases of the disease which previously had remained undiagnosed.The only statistical figures on a nationwide basis which so far are available come from Switzerland. There, Ackermann4 found an incidence of 4 to 5 cases

ETIOLOGY OF MULTIPLE SCLEROSIS EVIDENCE has been accumulating over recent years which indicates that vascular destruction, or, more specifically, probably a thrombosis of venules, is an essential link in the chain of causation of multiple sclerosis and the related "encephalomyelitides."1 This evidence may be summarized as follows:1. Histologic pictures indistinguishable from the lesions of "encephalomyelitis" in the acute stage, and of multiple sclerosis when sufficient time has elapsed to permit gliosis to take place, have been produced experimentally in animals by the retrograde obstruction of cerebral venules2 and by the intravenous injection of various coagulants, especially organ extracts.32. Similar lesions are also often seen in pathologic material of human origin, following spontaneous thrombosis of veins of a certain size from any cause, or compression of a pial vein by a tumor.43. Thrombi, usually in venules and veins, have been observed in a large