Neuronal Substrate of the Saccadic Inhibition Deficit in Schizophrenia Investigated With 3-Dimensional Event-Related Functional Magnetic Resonance Imaging

Abstract

SMOOTH PURSUIT eye movement¹ and the inhibition of automatic saccades² is impaired in patients with schizophrenia, their healthy first-degree relatives,^3,4 and healthy subjects with high scores on a measure of schizotypy.⁵ This suggests that eye movement deficits are a vulnerability marker^6,7 or reflect an endophenotype⁸ for schizophrenia. A common feature of both smooth pursuit eye movements and antisaccade tasks is the requirement to avoid automatic intruding saccades. The failure to effectively inhibit saccades may explain the oculomotor impairments observed in patients with schizophrenia.^9,10 A potential link has been reported between the antisaccade deficit and a genetic marker on chromosome 22q.¹¹ The neural correlate of the antisaccade deficit in schizophrenia has not yet been identified. The elucidation of the neural correlate could provide a physiological measure of saccade inhibition, which could in turn prove to be a better endophenotype marker than the behavioral measure.