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June 1956

Model Psychoses Induced by LSD-25 in Normals: I. Psychophysiological Investigations, with Special Reference to the Mechanism of the Paranoid Reaction

Author Affiliations

Beverly Hills, Calif.; Los Angeles; Beverly Hills, Calif.; Los Angeles

From the University of Southern California, Department of Physiology, Los Angeles.

AMA Arch NeurPsych. 1956;75(6):588-611. doi:10.1001/archneurpsyc.1956.02330240026003

INTRODUCTION  Experimental psychosis has a long history. It might have started with the administration of Cannabis indica boiling in wine to the ancient Hun warriors, resulting in mental obfuscation, as they were prepared for surgery because of wounds sustained in battle. Scientific experimental psychiatry began toward the end of the last century, in the Kraepelinian era—when the organic theory of psychoses was in its fullest vogue. Beringer's experiments with mescaline1 marked a milestone in research in that many of the symptoms induced were highly similar to those encountered in schizophrenia and the drug seemed to have had a selective affinity for the brain. The discovery of LSD-25* by Stoll and Hoffmann2 was an even more exciting event, because the drug worked similarly in infinitesimal-trace amounts. Stoll3 (1947) suggested the pharmacological designation Phantastium for this substance, and he classified the resultant model psychosis as that of the acute

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