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

Nicolas A. Bercel, Lee E. Travis, Leonard B. Olinger & E. Dreikurs

AMA Archives of Neurology and Psychiatry, 1956, 588-611

republishing :Psychopathology: A Source Book (pp. 605–639).

DOI: https://doi.org/10.4159/harvard.9780674367012

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 exogenus reaction type.

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