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The EEGs of twenty-three patients and five asymptomatic siblings with Wilson's disease were correlated with their clinical states and biochemical studies related to liver function and copper metabolism. In uncomplicated cases of the disease the EEG may be normal or abnormal. When the EEG is abnormal there does not appear to be a clear correlation with a clinical or biochemical state. Severely abnormal EEGs are seen with severe complications of the disease and are appropriate to the complication. These EEGs show improvement parallel with clinical improvement. Asymptomatic siblings with the characteristic biochemical defect of copper metabolism may also show normal or abnormal EEGs, a feature which seems to have a familial tendency. The abnormal EEGs of asymptomatic siblings show improvement with treatment, supporting the argument for prophylaxis in such cases.

Seven patients are described in whom dementia developed during treatment with methotrexate for meningeal leukaemia. The patients presented with confusion, tremor, ataxia, irritability, and somnolence. There were major epileptic fits in two cases and in one case there was progression to coma and death. Necropsy findings in the latter showed infarcted areas in the temporal and parietal lobes, with no evidence of active leukaemic disease or of viral encephalitis. The condition has not responded to radiotherapy and no positive evidence of viral encephalitis has been obtained. On the other hand, when treated with folinic and folic acid the deterioration has been arrested and there has been some improvement; thus the condition appears to be due to methotrexate. The occurrence of so many cases within the past year of a condition not previously described is probably attributable to the introduction of intensive cytotoxic therapy directed against meningeal leukaemia.

One hundred and twenty-four EEGs were obtained from thirty-nine juvenile baboons during anaesthesia with phencyclidine hydrochloride (Sernyl) and pentobarbitone (Nembutal). Changing EEG patterns were found which could be related to the time interval from the onset of anaesthesia. It was found, with some variations in individual animals, that a relatively stable EEG was seen from 15 to 45 min after starting anaesthesia. It is suggested that evaluation of these variations are important in experiments where the EEG is being used to monitor changes in cerebral function.