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Neuronal Substrate of the Saccadic Inhibition Deficit in Schizophrenia Investigated With 3-Dimensional Event-Related Functional Magnetic Resonance Imaging
Mathijs Raemaekers, MSc;
Johannus M. Jansma, PhD;
Wiepke Cahn, MD;
Josef N. Van der Geest, PhD;
Jeroen A. van der Linden, MD;
René S. Kahn, MD, PhD;
Nick F. Ramsey, PhD
Arch Gen Psychiatry. 2002;59:313-320.
Background Several studies have shown that the ability to suppress automatic saccadic
eye movements is impaired in patients with schizophrenia as well as in their
first-degree relatives, and suggest that this impairment is a potential vulnerability
marker for schizophrenia. The neurobiological mechanisms underlying normal
saccade production and inhibition, revealed in primate studies, indicate that
the impairment may result from a failure of the oculomotor system to effectively
exert inhibitory control over brainstem structures. Functional localization
of the affected brain structure(s) potentially provides a physiological measure
for the investigation of vulnerability markers in schizophrenia.
Methods The hemodynamic response to discrete visual stimuli was measured during
prosaccades (saccades toward a peripheral stimulus), antisaccades (saccades
toward a position opposite to a peripheral stimulus), and active fixation
(holding fixation and ignoring a peripheral stimulus) in 16 patients with
schizophrenia receiving atypical neuroleptics and 17 healthy control subjects
using an event-related functional magnetic resonance imaging task design.
Results Brain responses were detected in the frontal and parietal regions of
the oculomotor system in all 3 tasks. Patients made more errors during inhibition
tasks and exhibited a selective failure to activate the striatum during the
inhibition of saccades. In other regions that were active during inhibition,
specifically the supplementary and frontal eye fields, no difference was found
between patients and control subjects.
Conclusions A frontostriatal network is engaged in the suppression of automatic
eye movements. The results indicate that abnormalities in this network, rather
than the selective dysfunction of prefrontal brain regions, underlie the saccade
inhibition deficit in schizophrenia.
From the Department of Psychiatry, University Medical Center Utrecht,
Utrecht, the Netherlands.
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