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Five patients with either "diencephalic" or "brainstem" epilepsy or "diencephalosis" were examined EEGcally during the course of their hospitalization. The significant changes were detected, mainly by diphenhydramine activation as to the distribution of the 6-14/sec positive spike pattern on the scalp. When the patients were relatively free from their symptoms, the positive spikes were recorded partially on only one or very fre areas, and when they were experiencing clinical paroxysms, the spikes were detected diffusely in almost all areas of the scalp. Chronological EEG observations paralleling the clinical course of illness of a paroxysmal nature are unpopular. However, the necessity of efforts to record EEG's of patients during clinical paroxysms seems important and has been briefly discussed concerning the question as to whether the 6-14/sec positive spike pattern is an abnormal EEG change or perhaps a "seizure pattern".

Nialamide, a kind of monoamine oxydase inhibitor, was used for provoking centrencephalic EEG abnormalities and 6-14 Hz positive spikes. It was assumed that these EEG abnormalities have close relationship with dysfunctions of the brainstem which is rich in monoamines and monoamine oxydase. The nialamide provocation was carried out on 49 inpatients who had centrencephalic discharges in their EEG reports. These patients consisted of four cases of epilepsy, one case of anorexia nervosa, two cases of narcolepsy and 42 cases of diencephalosis. Another series of 22 patients suffering from other diseases, in whome EEG no centrencephalic EEG abnormallities were detected, were examined with nialamide. Out of the 49 patients, 35 cases (71.4+) showed increased EEG abnormalities following the administration of nialamide. It was noteworthy that this drug had provocative effect not only for EEG abnormalities, but also for the symptoms from which patients were suffering. In 26 out of 49 patients, both EEG abnormalities and clinical symptoms were provoked by nialamide. And the nialamide administration resulted in negative on all 22 patients who did not register centrencephalic EEG abnormalities. The mechanism and characteristics of this provocative procedure by the use of nialamide were evaluated.