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Muzio JN, Roffwarg HP, Kaufman E. 
“Alterations In The Nocturnal Sleep Cycle Resulting From LSD”. 
Electroencephalography and Clinical Neurophysiology. 1966;21:313-324.
Abstract
D-Lysergic acid diethylamide (LSD-25) is a potent pharmacological agent that causes psychological and autonomic alterations in awake humans when administered in conventional doses of 1-2 mcg/kg of body weight (Bercel et al. 1956; Klee 1963; Kuramochi and Takahashi 1964). LSD's effects on the human EEG have been studied primarily in the waking state. These would seem to be minimal (Forrer and Goldner 1951; Schwarz et al. 1955) or to consist of slight increases or decreases in the frequency of the alpha rhythm (Rinkel et al 1952 Anderson and Rawnsley 1954; Bercel et ai. 1956). During a typical night's sleep there are predictable shifts in the EEG pattern (Dement and Kleitman 1957). The intervals characterized by a relatively low voltage, fast, non-spindling EEG, accompanied by rapid eye movements REMs), and loss of tones ofthe head and neck musculature – designated as REM Sleep (REM S)–alternate with spindle and high voltage slow waves, without REMs, and associated with measurable resting muscle potentials–designated as Slow Wave Sleep (SWS). REMS is a associated with complex and intense hallucinatory sequences or "dreams" in humans (Dement 1964.) Because of LSD's imagery evoking properties, it was felt that investigation of the drug's effect during sleep might be fruitful. The mechanisms which underly most hallucinatory phenomena are not well understood, but a body of neuroanatomical and neurophysiological data pertaining to brain-stem triggering zones of REMS is available (Jouvet 1965). Attention has just begun to focus on the ascending pathways which might be responsible for the hallucinations of dreaming (Roffwarg et al. 1966). Inasmuch as dreaming and other types of hallucinations may be related, we hypothesized that an enhancement of REMS by LSD might indirectly support a commonality of hallucinatory mechanisms.
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