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ALEX E. KRILL, M.D.; ANNA M. WIELAND, A.M.; ADRIAN M. OSTFELD, M.D.

Arch Ophthalmol. 1960;64(5):724-733.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

It has been shown in previous studies that visual hallucinations are part of the total response to both d-lysergic acid diethylamide (LSD-25)^1,2,3 and n-ethyl-3-piperidyl benzilate hydrochloride (JB 318).^4,5 It has never been demonstrated, however, where these drugs act to induce this phenomenon. Since visual hallucinations can arise from any level of the visual pathways (i.e., retina to the cerebral cortex),⁶ the problem of defining the hallucinogenic mechanism is quite complex. Various workers have attempted to gain insight into this problem by studying the effects of hallucinogenic drugs on different levels of the visual pathways. The objective techniques used have been primarily electrophysiological and most of the studies have been done on animals. Drug effects have been noted on (1) cortical potentials, both spontaneous and evoked, (2) synaptic transmission at different levels of the visual system, and (3) optic tract responses to photic stimuli. Retinal function evaluation . . . [Full Text PDF of this Article]

Author Affiliations
Chicago

From the Department of Ophthalmology and Preventive Medicine, University of Illinois College of Medicine.

Footnotes
Submitted for publication June 8, 1960.

Supported by United States Public Health Service Grant MY 2302.

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