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Evaluation of tests of central nervous system performance after hypoxemia for a model for cognitive impairment

Centre for Human Drug Research, Leiden University Medical Center, Leiden, the Netherlandsjvdp{at}chdr.nl

L. A. W. Noordzij

M. L. de Kam

Centre for Human Drug Research, Leiden University Medical Center, Leiden, the Netherlands

G. J. Blauw

Section of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, the Netherlands

A. F. Cohen

J. M. A. van Gerven

Centre for Human Drug Research, Leiden University Medical Center, Leiden, the Netherlands

The sensitivity of several neurophysiological and cognitive tests to different levels of hypoxia was investigated. Cerebral hypoxia in healthy volunteers may be a disease model for dementia or other forms of brain dysfunction. Twelve healthy subjects were included in a randomized, single-blind, placebo-controlled, three-period cross-over trial. They received three air/N2 gas mixtures via mask breathing [aimed at peripheral oxygen saturation (SPO2) values of > 97% (placebo), 90% and 80%, with normal end-tidal CO2]. Central nervous system effects were tested regularly for 130 min by saccadic and smooth pursuit eye movements, electro-encephalogram, visual analogue scales and cognitive tests. Treatments were well tolerated. Compared to SPO2 90%, SPO2 80% reduced saccadic peak velocity by 16.4 °/s [confidence interval (CI) –26.3, –6.4], increased occipital delta power by 14.3% (CI 3.6, 25.1), and significantly increased most cognitive reaction times. SPO2 80% also decreased correct responses for the binary choice task and serial word recognition [–1.3 (–2.2, –0.3) and –3.5 (–6.2, –0.8), respectively] compared to SPO2 90%. Cognitive performance was decreased by SPO2 80% and increased by SPO2 90% compared to placebo. Sensitive effect measurements can be identified for these interventions. The applicability as a model for cognitive impairment should be investigated further.

Key Words: cognition • electro-encephalography • eye-movements • hypoxemi

Journal of Psychopharmacology, Vol. 16, No. 4, 337-343 (2002)
DOI: 10.1177/026988110201600408


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