Reduced attentional engagement contributes to deficits in prefrontal inhibitory control in schizophrenia.
BACKGROUND
Problems with the voluntary control of behavior, such as those leading to increased antisaccade errors, are accepted as evidence of prefrontal dysfunction in schizophrenia. We previously reported that speeded prosaccade responses, i.e., shorter response latencies for automatic shifts of attention to visual targets, were associated with higher antisaccade error rates in schizophrenia. This suggests that dysregulation of automatic attentional processes may contribute to disturbances in prefrontally mediated control of voluntary behavior.


METHODS
Twenty-four antipsychotic-naïve schizophrenia patients and 30 healthy individuals completed three tasks: a no-gap prosaccade task in which subjects shifted gaze toward a peripheral target that appeared coincident with the disappearance of a central fixation target and separate prosaccade and antisaccade tasks in which a temporal gap or overlap of the central target offset and peripheral target onset occurred. Sixteen patients were retested after 6 weeks of antipsychotic treatment.


RESULTS
Patients' prosaccade latencies in the no-gap task were speeded compared with healthy individuals. While patients were not atypical in the degree to which response latencies were speeded or slowed by the gap and overlap manipulations, those patients with diminished attentional engagement on the prosaccade task (i.e., reduced overlap effect) had significantly elevated antisaccade error rates. This effect persisted in patients evaluated after antipsychotic treatment.


CONCLUSIONS
This study provides evidence that a reduced ability to engage attention may render patients more distracted by sensory inputs, thereby further compromising impaired executive control during antisaccade tasks. Thus, alterations in attentional and executive control functions can synergistically disrupt voluntary behavioral responses in schizophrenia.
Reilly
James L
JL
Center for Cognitive Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA. jreilly@psych.uic.edu
Harris
Margret S H
MS
Khine
Tin T
TT
Keshavan
Matcheri S
MS
Sweeney
John A
JA
D000293:Adolescent; D000328:Adult; D014150:Antipsychotic Agents / Q000627:therapeutic use; D001288:Attention / Q000187:drug effects / Q000502:physiology*; D001569:Benzodiazepines / Q000627:therapeutic use; D004585:Electrooculography / Q000187:drug effects; D005260:Female; D005403:Fixation, Ocular / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D000077152:Olanzapine; D009949:Orientation / Q000187:drug effects / Q000502:physiology*; D010364:Pattern Recognition, Visual / Q000187:drug effects / Q000502:physiology*; D017397:Prefrontal Cortex / Q000187:drug effects / Q000503:physiopathology*; D011618:Psychotic Disorders / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D018967:Risperidone / Q000627:therapeutic use; D012438:Saccades / Q000187:drug effects / Q000502:physiology*; D012559:Schizophrenia / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D012815:Signal Processing, Computer-Assisted
D014150:Antipsychotic Agents; D001569:Benzodiazepines; D018967:Risperidone; D000077152:Olanzapine