Original Article
Clinical Pharmacology and Therapeutics (1988) 43, 86–90; doi:10.1038/clpt.1988.15
The P-300 event-related potential in experimental nitrous oxide exposure
William J Estrin MD*, Paul Moore DMD, PhD**, Richard Letz PhD and Heidi H Wasch BA San Francisco, Calif., Pittsburgh, Pa., and Boston, Mass.
Department of Neurology and Division of Occupational Medicine, University of California, San Francisco, the School of Dental Medicine, University of Pittsburgh, and the Division of Occupational Health, Harvard School of Public Health, Boston
Correspondence: William J Estrin MD, Department of Neurology, 4M71, San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110.
*Supported in part by National Institute of Environmental Health Sciences Clinical Investigator Award 5-KO8-ES00148-03.
**Supported in part by National Institute of Dental Research award DE-07011.
Received 28 July 1986; Accepted 22 July 1987.
Abstract
Without the availability of objective measures of central neurologic dysfunction, neuroepidemiologic investigations of individuals exposed to psychoactive drugs and potential environmental and occupational neurotoxins are extraordinarily difficult, particularly when the central nervous system manifestations are subtle, diffuse, and limited to cognitive deficits. In an attempt to assess and quantitate psychomotor dysfunction, P-300 event-related potentials, Symbol Digit Test, Continuous Performance Test, and Finger Tapping Test were obtained from six subjects sequentially exposed to nitrous oxide at 0%, 10%, 20%, and 40%. With increasing concentration of N2O, there was prolongation of P-300 latency and worsening of Continuous Performance Test and Symbol Digit Test performance; P-300 amplitude and Finger Tapping Test performance were decreased by exposure to N2O. This study demonstrates a dose-dependent reduction in P-300 amplitude and prolongation of P-300 latency in subjects in whom psychomotor impairment was induced by the acute administration of N2O.
