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TRIAL OF AZACYCLONOL MBRm 377was small (60 mg. daily). More important was an intrinsic defect in our method of assessment, which resulted in the apparent superiority of the placebo to the drug. We think that the explanation lies in the stimulant effect of the drug (equivalent to Feldman's observation of " turbulence "), which made the'patient's mental disturbance more obvious in the interview situation. That this can also be true of reserpine we can confirm from personal experience. But, even allowing for these criticisms of our method, our results do suggest that azacyclonol is unlikely to be a very useful drug in the treatment of chronic schizophrenia. The results of our clinical trial seem promising enough to warrant a more extensive trial of the drug in cases of acute schizophrenia and alcoholic hallucinosis. One difficulty in evaluating drug therapy of such acute cases is that a proportion remit spontaneously and no precise criteria are yet available for indicating which patients should have azacyclonol. Some later American papers-for example, Cohen and Parlour (1956)-suggested that azacyclonol had very little anti-hallucinatory effect. Our experience suggests that hallucinatory experience of recent onset, whether schizophrenic or toxic, is an indication for treatment with azacyclonol.The only report of any toxic side-effect of azacyclonol is contained in the paper by Forster and Henderson (1957). They found elevation of the non-protein nitrogen in 11 out of 18 patients treated with azacyclonol. We have found similar changes in two patients: One of these was later shown to have signs indicative of chronic nephritis. However, the blood urea nitrogen did fall later to near normal levels when the dose of azacyclonol was reduced. SummaryWe have described a controlled trial of azacyclonol in 40 chronic schizophrenic patients. The results suggest that azacyclonol is not going to be of great value in the treatment of this type of patient.We subsequently treated 18 patients (16 schizophrenics, 2 toxic hallucinatory states) with azacyclonol.The illness was of more recent onset in these patients than in those involved in the controlled trial: 13 patients improved and 6 have since left hospital.Our clinical impression is that azacyclonol has a central stimulant action and that part of the poor result of the drug in the controlled trial was due to the masking effects of excitement and overactivity.The only toxic effect observed was a rise of blood urea nitrogen in two patients out of a group of four who were subjected to detailed study.
TRIAL OF AZACYCLONOL MBRm 377was small (60 mg. daily). More important was an intrinsic defect in our method of assessment, which resulted in the apparent superiority of the placebo to the drug. We think that the explanation lies in the stimulant effect of the drug (equivalent to Feldman's observation of " turbulence "), which made the'patient's mental disturbance more obvious in the interview situation. That this can also be true of reserpine we can confirm from personal experience. But, even allowing for these criticisms of our method, our results do suggest that azacyclonol is unlikely to be a very useful drug in the treatment of chronic schizophrenia. The results of our clinical trial seem promising enough to warrant a more extensive trial of the drug in cases of acute schizophrenia and alcoholic hallucinosis. One difficulty in evaluating drug therapy of such acute cases is that a proportion remit spontaneously and no precise criteria are yet available for indicating which patients should have azacyclonol. Some later American papers-for example, Cohen and Parlour (1956)-suggested that azacyclonol had very little anti-hallucinatory effect. Our experience suggests that hallucinatory experience of recent onset, whether schizophrenic or toxic, is an indication for treatment with azacyclonol.The only report of any toxic side-effect of azacyclonol is contained in the paper by Forster and Henderson (1957). They found elevation of the non-protein nitrogen in 11 out of 18 patients treated with azacyclonol. We have found similar changes in two patients: One of these was later shown to have signs indicative of chronic nephritis. However, the blood urea nitrogen did fall later to near normal levels when the dose of azacyclonol was reduced. SummaryWe have described a controlled trial of azacyclonol in 40 chronic schizophrenic patients. The results suggest that azacyclonol is not going to be of great value in the treatment of this type of patient.We subsequently treated 18 patients (16 schizophrenics, 2 toxic hallucinatory states) with azacyclonol.The illness was of more recent onset in these patients than in those involved in the controlled trial: 13 patients improved and 6 have since left hospital.Our clinical impression is that azacyclonol has a central stimulant action and that part of the poor result of the drug in the controlled trial was due to the masking effects of excitement and overactivity.The only toxic effect observed was a rise of blood urea nitrogen in two patients out of a group of four who were subjected to detailed study.
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