抄録
The present author has studied the influences of haloperidol treatment in 22 schizophrenic patients electroencephalographically as well as psychopathologically. Of the 22 patients,17 were of paranoid form and five were of hebephrenic form, and all of them had been strictly free from any kind of CNS acting drug for at least one month prior to the present study. Their clinical evolutions throughout the treatment were recorded by the author in daily interview and evaluated by weekly scoring with the KMU edition of Expanded Brief Psychiatric Rating Scale (EBPRS). EEG was regularly examined during the treatment and recorded on magnetic tape for the quantitative analysis using Itil-Saito's method, which provides 22 EEG parameters representing 20 × 10 seconds' epochs as the time sample. The 22 parameters consist of ten frequency bands of primary waves, eight bands of first derivatives, mean values and standard deviations of primary wave frequency and amplitude. Based on the parameters, the author has studied their histograms of time sample EEG recorded before, three hours, one week and one month after the onset of treatment, and so-called t-profiles illustrating the changes from the base line (pre-treatment) EEG.
A controll study was don e in normal healthy male volunteers with single dose oral administration of haloperidol 0.75 and 2.25 mg, and it presented that haloperidol would induce a significant increase of 9.5-10.5 Hz alpha rhythm.
The patients' result was first examined in the form of group t-profile but the group t-profile without any significant change suggested the presence of induced EEG changes which are mutually contradictory. Actually, further examinations revealed a number of group differences as to patients' age, past history, incidence of alpha activity in base line EEG, clinical subdiagnosis, induced extrapyramidalism, and so forth. However, these group differences were finally found to be attributable to none of the above-mentioned items, but to the general improvement scores of patients' clinical features. In the groups of which the majority showed a marked clinical improvement, a significant increase of moderate alpha activity was presented, while in the groups of which the majority did not show any noticeable improvement, the increases of fast and/or slow activity due to a decrease of alpha rhythm in the contrary. The former group consited of those who were in their thirties to forties of a shorter history, less than 40% in alpha incidence, paranoid, within two weeks from the onset of extrapyramidalism, and the latter one consisted of those who were in their twenties, longer than five years in history, more than 40% in alpha incidence, hebephrenic, over two weeks from the onset of extrapyramidalism and free from any extrapyramidal disorders. These results have been confirmed by the comparison of t-profiles of the therapy responsive patients and those of the therapy resistant ones.
The increase of alpha activity which was seen in normal volunteer study seems to correspond with the normalization of EEG and also with the exertion of pharmacological influence of haloperidol. The increases of fast and slow activities seen in the patients who were not clinically improved can be interpreted as the increase of the deviation from normal EEG possibly due to the lack of their functional elasticity. The differences of the EEG changes induced during the haloperidol treatment were found to be neither influenced by the daily dose nor by the accumulated dose of halloperidol, but maily by the clinical outcomes of the patients.
The EEG changes can be seen already in the three hours postdrug recording and the author has convinced that it is quite possible to predict the patient's outcome at a high probability early after the first single administration of haloperidol solely based upon the quantitative analysis of patient's EEG.
