The effects of ketamine and risperidone on eye movement control in healthy volunteers

Schmechtig, A., Lees, J., Perkins, A., Altavilla, A., Craig, K. J., Dawson, G. R., William Deakin, J. F., Dourish, C. T., Evans, Lisa Helen ORCID: https://orcid.org/0000-0002-3874-4676, Koychev, I., Weaver, K., Smallman, R., Walters, James Tynan Rhys ORCID: https://orcid.org/0000-0002-6980-4053, Wilkinson, Lawrence Stephen ORCID: https://orcid.org/0000-0002-9337-6124, Morris, R., Williams, S. C. R. and Ettinger, U. 2013. The effects of ketamine and risperidone on eye movement control in healthy volunteers. Translational Psychiatry 3 (12) , e334. 10.1038/tp.2013.109

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Abstract

The non-competitive N-methyl-D-aspartate receptor antagonist ketamine leads to transient psychosis-like symptoms and impairments in oculomotor performance in healthy volunteers. This study examined whether the adverse effects of ketamine on oculomotor performance can be reversed by the atypical antipsychotic risperidone. In this randomized double-blind, placebo-controlled study, 72 healthy participants performed smooth pursuit eye movements (SPEM), prosaccades (PS) and antisaccades (AS) while being randomly assigned to one of four drug groups (intravenous 100 ng ml−1 ketamine, 2 mg oral risperidone, 100 ng ml−1 ketamine plus 2 mg oral risperidone, placebo). Drug administration did not lead to harmful adverse events. Ketamine increased saccadic frequency and decreased velocity gain of SPEM (all P<0.01) but had no significant effects on PS or AS (all Pgreater than or equal to0.07). An effect of risperidone was observed for amplitude gain and peak velocity of PS and AS, indicating hypometric gain and slower velocities compared with placebo (both Pless than or equal to0.04). No ketamine by risperidone interactions were found (all Pgreater than or equal to0.26). The results confirm that the administration of ketamine produces oculomotor performance deficits similar in part to those seen in schizophrenia. The atypical antipsychotic risperidone did not reverse ketamine-induced deteriorations. These findings do not support the cognitive enhancing potential of risperidone on oculomotor biomarkers in this model system of schizophrenia and point towards the importance of developing alternative performance-enhancing compounds to optimise pharmacological treatment of schizophrenia.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG) Cardiff University Brain Research Imaging Centre (CUBRIC) Medicine Neuroscience and Mental Health Research Institute (NMHRI) Psychology
Subjects:	B Philosophy. Psychology. Religion > BF Psychology
Uncontrolled Keywords:	glutamate; ketamine; risperidone; saccades; schizophrenia; smooth pursuit
Publisher:	Nature Publishing Group
ISSN:	2158-3188
Last Modified:	25 Oct 2022 08:37
URI:	https://orca.cardiff.ac.uk/id/eprint/53768

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