Objectives (i) To determine the prevalence of multiple sclerosis (MS) in New South Wales and South Australia; (ii) to compare these prevalences with those in other areas of Australia and to determine the relationship between prevalence and latitude; (iii) to examine the relative contribution of genetic and environmental factors in the aetiology of the disease in Australia; and (iv) to ascertain whether there had been a change in the frequency of the disease since 1961. Results The crude prevalence of MS in New South Wales on prevalence day (National Census Day, 30 June 1981) was 37.2/100000 and the age‐standardised prevalence 36.6/100000. The female:male ratio was 2.3:1. The crude prevalence in South Australia was 29.4/100 000 and the age‐standardised prevalence 28.8/100000. The female:male ratio was 2.4:1. No Aborigines or Torres Strait Islanders with MS were identified. There was a significant increase in the prevalence with increasing south latitude in Australia, MS being about seven times more frequent in Hobart than in tropical Queensland, but no genetic differences were found in the surveyed population in different parts of Australia. A significant increase in the prevalence of MS occurred in most areas of Australia between 1961 and 1981, but this may not reflect a true increase in incidence. Conclusion The increasing prevalence with increasing south latitude cannot readily be explained by genetic susceptibility, and suggests that environmental factors are important for expression of the disease.

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This combined histochemical and biochemical study has shown that acid proteinase activity (PH 3.5) is increased around histologically-defined active plaques of multiple sclerosis (MS). Biochemical estimation showed that the enzyme is more active in most samples of 'normal' white matter in MS than in controls. A gradient of enzyme activity was observed : control white matter-white matter distant from plaqueclose white matter-edgsplaque. Both electrophoretic and histochemical techniques revealed a reduction or absence of basic (encephalitogenic) protein in the plaques. Electrophoresis showed a diminution of encephalitogenic protein outside some plaques. Phospholipids that remain on the base-line of thin-layer chromatoplates were shown to be predominantly phosphoinositides combined with encephalitogenic protein

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Cimetidine inhibits the hepatic microsomal oxidation system in vitro and reduces clearance of drugs metabolised by these enzymes.' In man cimetidine increases the effect of warfarin'' and diazepam.4Phenytoin, a commonly used anticonvulsant with a narrow therapeutic index, is also metabolised by the hepatic microsomal system. We therefore investigated the effect of cimetidine on steady-state plasma phenytoin concentrations in patients with longstanding epilepsy.Patients studied and mean serum phenytoin concentrations ( SD) before, during, and after cimetidine (C)