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AMONG the noninfective inflammatory diseases of the blood vessels is a rare form of granulomatous angiitis that is almost entirely confined to the central nervous system (CNS). The lesions, which are focal and often necrotizing, are generally associated with multinucleate giant cells. Before its delineation as a distinct clinicopathologic entity by Cravioto and Feigin,1 the condition was variously designated as "Morbus Boeck" (Zollinger2), "allergic angiitis and allergic granulomatosis" (Churg and Strauss,3 Newman and Wolf4) and "giantcell arteritis" (McCormick and Neubuerger5). To our knowledge, 14 cases of the disorder have been reported up to now,1,2,4-11 of which two appeared in the form of clinicopathologic discussions in the Cabot case series from the Massachusetts General Hospital.6,7 These two cases, and two additional ones more recently studied at this hospital, are the subject of the present communication. Serial sections of typical lesions from one of the

IN RECENT years staff members of the Neurology Service at the Massachusetts General Hospital have had the opportunity of examining three adult patients suffering from a slowly progressive neurological illness that defied all attempts at exact diagnosis and effective treatment. This strange disorder was characterized by severe impairment in the control of muscular movements, by abnormalities in posture and by involuntary motor activity. Despite serious disability, there was little muscular weakness, and mental faculties were relatively spared until the end. After years of increasing incapacity, all three patients died of the effects of the illness. Postmortem neuropathological studies showed a disease process in the central nervous system that was unlike any that we had previously seen or had been described by others. Since it appears to us that we may be dealing with a hitherto unrecognized disorder of the central nervous system, we feel justified in reporting our findings

MYOTONIA, the denominating characteristic of three genetically determined diseases of muscle (myotonia congenita, myotonia dystrophica, and paramyotonia), and dystrophy of muscle fibers, a feature of one of these diseases (myotonia dystrophica), remain obscure.Concerning the localization of myotonia, a number of investigators believe it might reside in the muscle cell. Grund1 and later Schaffer2 noted the persistence of this phenomenon after complete block of the nerve fibers supplying the muscle; and Gregor and Schilder3 and later Lindsley and Curnen4 observed it during the relaxation phase of contraction, when few nerve impulses were reaching the muscle. Brown and Harvey5 in a myotonic disease of goats also demonstrated that complete denervation of muscle failed to abolish the myotonia. Landau6 and Floyd et al7 have shown that curare has no effect on human myotonia. Denny-Brown and Nevin8 confirmed this localization but also obtained evidence