Despite 14 years of investigation, as intensive as accorded any biologically active chemical, a gap remains in the systematic description of human response to lysergic acid diethylamide (LSD-25). The dramatic schizophrenic-like symptoms after doses of 40 μg to 100 μg have drawn the main interest. The threshold for activity is placed at 20 μg by general consensus, while perfunctory administration of smaller doses has left their effect uncertain.

Accompanying those pharmacologic demonstrations has been the controversy whether LSD symptoms simulate the psychopathology of schizophrenia¹ or can be better explained as a toxic organic psychosis.² One of these alternatives might be favored by its resemblance to the complete dosage-response relation-ship of LSD. It is unfortunate for analogical comparison that early stages of toxic psychosis have rarely been described in a psychopathological framework³; on the other hand, there is a firm basis for comparison with various schizophrenic processes.

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