Archives of Neurology And Psychiatry
March 1, 1959
Elliot D. Luby
920 citations
Since 1921, researchers have induced temporary psychotic-like states in animals and humans using drugs such as bulbocapnine, mescaline, and LSD-25, aiming to test theories about schizophrenia. Some psychiatrists, like Ebaugh, argue these drug-induced pseudopsychoses differ so markedly from schizophrenia that their relevance to understanding the disorder is limited. Others, like Wikler, contend that for developing causal concepts of behavior, whether the model psychoses resemble schizophrenia is unimportant. The abstract presents this ongoing debate without resolving it.
Archives of Neurology And Psychiatry
May 1, 1951
Gordon R. Forrer
66 citations
Lysergic acid diethylamide (LSD-25) was studied in both psychotic and normal subjects, with findings generally confirming earlier work by Stoll. The chemistry of ergot alkaloids is reviewed: all lysergic acid alkaloids are based on lysergic acid, a polycyclic nitrogenous carboxylic acid that has not been synthesized. Natural ergot alkaloids contain d-lysergic acid and are divided into two groups—the ergotamine-ergotoxine group, where d-lysergic acid is combined with a peptide, and the ergonovine group, which comprises mono acid amides of d-lysergic acid.
Archives of Neurology And Psychiatry
January 1, 1956
Edward V. Evarts
52 citations
Bufotenine, a chemical relative of serotonin, was first synthesized in 1934 and known to cause temporary changes in blood pressure and breathing in anesthetized dogs. Its effects on unanesthetized animals had not been studied, despite bufotenine being isolated from the bean of Piptadenia peregrina, the source of cohoba, a narcotic snuff used in the West Indies to induce hallucinations and mystical states similar to those produced by mescaline, harmine, and lysergic acid diethylamide. This prompted investigation into bufotenine's behavioral effects.
Archives of Neurology And Psychiatry
May 1, 1959
Sidney Cohen
49 citations
Lysergic acid diethylamide (LSD-25) has been established in experimental psychiatry as a psychotomimetic drug, but its potential as an adjunct to psychotherapy remains underexplored. The first mention of LSD-25 in this context was in 1950 by Busch and Johnson, who reported that the drug profoundly influenced the course of eight cases of psychoneurosis, particularly by enabling patients to remember and relive early traumatic episodes. Abramson has since used LSD-25 alongside analytic treatment, giving small doses periodically when therapy stalls. He noted the drug's pharmacologic safety, maintenance of consciousness and cooperation, and lack of evidence for addiction with repeated use.
Archives of Neurology And Psychiatry
June 1, 1956
Bert E. Schwarz
49 citations
Scalp and depth electroencephalography were used to investigate the effects of mescaline, LSD-25, and adrenochrome on brain activity. Previous work had shown that chlorpromazine reverses mescaline- and LSD-induced psychoses clinically but with minimal conventional EEG changes, and these drugs failed to activate temporal-lobe epilepsy. Depth electrography was pursued to better capture drug effects, including adrenochrome's reported ability to induce psychosis without insight in volunteers and increase paroxysmal discharges in epileptics' EEGs. The study aimed to clarify these neurophysiological actions through more sensitive recording techniques.
Archives of Neurology And Psychiatry
October 1, 1958
A. B. Silverstein
30 citations
Previous studies on lysergic acid diethylamide (LSD-25) and memory suggest that memory impairment becomes evident at doses between 50 and 100 micrograms. At 40 or 50 micrograms, little or no memory impairment was found, but at 100 micrograms, scores were significantly lower on most visual and some auditory tests. One study using 1 microgram per kilogram of body weight also found impairment but only tested memory for unrelated words. The present study aims to determine whether memory for different types of material is differentially affected by LSD-25.
Archives of Neurology And Psychiatry
July 1, 1956
Santo Salvatore
29 citations
Lysergic acid diethylamide (LSD-25) consistently produces physical symptoms such as tremor, nausea, dilated pupils, perspiration, and blood pressure changes, but its mental effects vary widely across studies. Some researchers report increased activity, emotional expression, and psychopathology with brief confusion and occasional visual hallucinations, while others emphasize the reliving of repressed personal experiences due to nonselective disturbance of the unconscious. One clinical psychological study found the mood to be one of aggrandizement.
Archives of Neurology And Psychiatry
January 1, 1941
W. S. Maclay
25 citations
Theories about the cause of hallucinations have been shaped by the specific material each researcher studied, such as phantom limbs, delirious states, or electrical brain stimulation. A major limitation is that research relies on verbal descriptions from patients whose ability to describe their experiences is often impaired. To overcome this, scientists turned to studying hallucinations experimentally induced in normal subjects using drugs like mescaline. Work by Mayer-Gross, Stein, Zucker, and others demonstrated the value of this approach, termed 'experimental psychosis.' Mescaline hallucinations are predominantly visual, so having subjects describe them through drawings and pictures could provide more impressive and realistic accounts.
Archives of Neurology And Psychiatry
June 1, 1958
Julia T. Apter
9 citations
Lysergic acid diethylamide (LSD-25) protects cats against the toxic effects of large doses of pentobarbital. One hundred forty cats survived inordinate amounts of pentobarbital after receiving LSD-25 systemically. Electrophysiological evidence from other studies shows that LSD-25 antagonizes the action of anesthetic doses of barbiturates on the frontal cortex and reticular formation. Under the conditions of the present studies, LSD-25 safely and effectively reversed respiratory and central nervous system depression induced in cats by lethal doses of pentobarbital.