***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Abstract This series of studies evaluated ( 1 ) hypotheses that poor antisaccade performance is attributable to confounding variables ( e.g. , visual attention deficits , incomplete underst and ing of task dem and s ) and ( 2 ) the specificity of poor antisaccade performance to schizophrenia . In addition to self-correcting errors before being cued to do so , schizophrenia patients also showed the expected saccadic reaction time changes to fixation condition manipulations : decreased latencies for gap and increased latencies for overlap trials . These data suggest that schizophrenia patients are adequately engaged in and underst and the antisaccade task . Schizophrenia patients made fewer correct antisaccade responses than other psychiatric patients ( obsessive-compulsive and bipolar disorder ) and normal subjects . The first-degree relatives of schizophrenia patients also generated a decreased proportion of correct antisaccade responses compared with normal subjects . For schizophrenia patients who performed below the range of normal subjects , 26 % of their relatives also performed below the normal range . Conversely , patients who performed normally did not have a single poor-performing relative . These data suggest that increased antisaccade error rates may index a liability for schizophrenia within a subset of families Background Smooth pursuit eye movement ( SPEM ) dysfunctions are considered a biological marker for schizophrenia and have been studied widely . In contrast , saccadic eye movements have received less attention , although disturbances have been described previously . Basic neurophysiologic parameters of saccades in schizophrenics , especially in unmedicated patients , have not been studied extensively . Methods Saccadic eye movements of 38 unmedicated schizophrenic patients , 32 patients with major depression and 42 non-psychiatric controls were examined using high-resolution infrared oculography . Two large-amplitude saccadic tasks were presented . The groups were compared on peak velocity , reaction time and accuracy . Results Peak velocity was significantly increased in schizophrenic patients . Depressive patients had a significantly longer reaction time . Both patient groups needed more corrective saccades to reach the target than controls . Conclusions Peak velocity distinguishes unmedicated schizophrenic patients from depressive patients and normal controls . This could be explained by deficits of the prefrontal cortex in the inhibitory control of saccades . Our findings suggest that schizophrenia affects not only SPEM but also saccadic eye movements Smooth pursuit eye movement ( SPEM ) and antisaccade deficits have been proposed as endophenotypes in the search for schizophrenia genes . We assessed these measures in 24 schizophrenia patients , 24 of their healthy siblings , and 24 healthy controls closely matched to the siblings . Between-group differences were assessed using a r and om effects regression model taking into account the relatedness between patients and siblings . Patients showed reduced SPEM gain , increased frequency of saccades during pursuit , increased antisaccade error rate , and reduced antisaccade gain compared to controls . Siblings performed intermediate , i.e. between patients and controls , on most measures , but were particularly characterised by reduced antisaccade gain . SPEM gain at one target velocity was significantly correlated between patients and siblings , highlighting the necessity of taking into account within-family correlations in the statistical analysis of between-group differences . It is concluded that subtle SPEM and antisaccade deficits are observed in clinical ly unaffected siblings of schizophrenia patients ; these deficits may be useful markers of genetic liability to schizophrenia Repeated amphetamine administration is used to examine the responsivity of cerebral dopaminergic systems . Schizophrenia spectrum personality ( SSP ) provides a unique opportunity to study the pathophysiology of schizophrenia because of shared neurobiology without the confounding factors of acute psychosis and psychotropic exposure . Previously we noted that on repeated amphetamine administration , dyskinesia and SSP symptoms were less likely to worsen in SSP than in healthy volunteers . In the current study , we report the effects of repeated amphetamine on antisaccade task performance . Eleven SSP and seven healthy subjects were given placebo once and amphetamine ( 30 mg ) twice , in r and omized double-blind fashion at least 1 week apart . Antisaccade eye measurements ( error rate and latency ) were recorded over 30 trials in each direction . Analysis of error rate showed no significant main effects of the drug . There was a significant group by field by drug interaction effect on the antisaccade latency . The SSP group showed a significant reduction in antisaccade latency for right field targets whereas no significant effects were noted in healthy control subjects . Findings from this preliminary study suggest SSP may be more receptive to the beneficial effects of repeated amphetamine on cognition than healthy controls Abstract Saccades were elicited in 30 schizophrenic patients before medication , in 17 of them during medication with neuroleptics , and in 12 healthy controls using six paradigms that tested different types of saccades : ( a ) the externally triggered and visually guided saccades ; ( b ) the externally triggered and internally guided saccades ( anti-saccades ) ; and ( c ) the internally triggered and internally guided saccades ( memory-guided saccades )  . Latency of the primary saccade , gain ( eye amplitude to target amplitude ) , and percentage of unwanted saccades ( fixation suppression errors ) were calculated . The externally triggered and externally guided saccades were only slightly affected in the patients , indicating that the function of parieto-tectal pathways was preserved . In contrast , the internally guided and externally triggered saccades showed abnormally long latencies , slightly smaller gains , and an increased rate of suppression errors regardless of the medication status . These findings were even more pronounced in the internally triggered and internally guided saccades such as memory-guided saccades . According to animal experiments and studies on patients with disorders of the basal ganglia , the performance of these saccades is based on the function of the pre- and dorsolateral frontal cortex and its connections to the basal ganglia . The minimal improvement of some of the parameters after clinical improvement and during treatment with neuroleptics suggests that the eye-movement deficits are associated with abnormalities of schizophrenia , which do not basically change under medication with neuroleptics . The observed effects of neuroleptics also argue against a primary abnormality in the dopaminergic input to the frontal cortex – basal ganglia oculomotor loop and support the view that there is a primary disturbance of the cortical input to the oculomotor loop through the basal ganglia in schizophrenics Schizotypal  personality disorder ( SPD ) is theoretically part of the schizophrenia spectrum both clinical ly and neurobiologically . A liability for developing schizophrenia may be associated with dysfunction of dorsolateral prefrontal cortex ( DLPFC ) and its cortical and /or subcortical circuitry . If so , abnormalities on tasks associated with DLPFC functioning among SPD subjects would support the thesis that SPD is neurobiologically related to schizophrenia . Antisaccade and ocular motor delayed response performance , both of which are ostensibly supported by DLPFC circuitry , were assessed among 29 SPD , 17 schizophrenia , and 25 normal subjects . Generally , the SPD subjects ' performance was more similar to normal than to schizophrenia groups . There was evidence , however , for inhibition abnormalities in a subgroup of SPD subjects . Antisaccade performance identified more SPD subjects as " abnormal " than delayed response measures Rationale The increasing dem and to develop more efficient compounds to treat cognitive impairments in schizophrenia has led to the development of experimental model systems . One such model system combines the study of surrogate population s expressing high levels of schizotypy with oculomotor biomarkers . Objectives We aim ed ( 1 ) to replicate oculomotor deficits in a psychometric schizotypy sample and ( 2 ) to investigate whether the expected deficits can be remedied by compounds shown to ameliorate impairments in schizophrenia . Methods In this r and omized double-blind , placebo-controlled study 233 healthy participants performed prosaccade ( PS ) , antisaccade ( AS ) and smooth pursuit eye movement ( SPEM ) tasks after being r and omly assigned to one of four drug groups ( nicotine , risperidone , amisulpride , placebo )  . Participants were classified into medium- and high-schizotypy groups based on their scores on the Schizotypal Personality Question naire ( SPQ , Raine ( Schizophr Bull 17:555–564 , 1991 ) ) . Results AS error rate showed a main effect of Drug ( p < 0.01 ) , with nicotine improving performance , and a Drug by Schizotypy interaction ( p = 0.04 ) , indicating higher error rates in medium schizotypes ( p = 0.01 ) but not high schizotypes under risperidone compared to placebo . High schizotypes had higher error rates than medium schizotypes under placebo ( p = 0.03 ) . There was a main effect of Drug for saccadic peak velocity and SPEM velocity gain ( both p ≤ 0.01 ) indicating impaired performance with risperidone . Conclusions We replicate the observation of AS impairments in high schizotypy under placebo and show that nicotine enhances performance irrespective of group status . Caution should be exerted in applying this model as no beneficial effects of antipsychotics were seen in high schizotypes Nicotine has been proposed to be a cognitive enhancer , particularly in schizophrenia patients . So far , the published studies of nicotine effects on antisaccade performance in schizophrenia patients only tested participants who were deprived smokers . Thus , we aim ed to test both smoking and non-smoking patients as well as healthy controls in order to extend previous findings . Moreover , we employed a paradigm using st and ard and delayed trials . We hypothesized that , if nicotine is a genuine cognitive enhancer , its administration would improve antisaccade performance both in smoking and non-smoking participants . A total of 22 patients with schizophrenia ( 12 smokers and 10 non-smokers ) and 26 controls ( 14 smokers and 12 non-smokers ) completed the study . The effects of a nicotine patch ( 14 mg for smokers , 7 mg for non-smokers ) on antisaccade performance were tested in a r and omized , double-blind , placebo-controlled , cross-over trial . Schizophrenia patients made significantly more antisaccade errors than controls ( p = 0.03 ) . Both patients and controls made fewer antisaccade errors in the delayed trials than in the st and ard trials ( p < 0.0001 ) . Nicotine significantly reduced antisaccade error rate in the st and ard trials , but not in the delayed trials ( p = 0.02 ) . Smoking status did not influence the nicotine effect on antisaccade error rate ( p = 0.10 ) indicating an equal procognitive effect of nicotine in smokers and non-smokers . Overall the present findings indicate that beneficial effects of nicotine on antisaccade performance are not confined to smoking schizophrenia patients . Instead , the findings likely represent genuine nicotine-induced enhancement of cognitive performance BACKGROUND Eye tracking deficits are one of a few widely vali date d behavioral markers of risk for schizophrenia . Recently , it has been proposed that antisaccade performance may also constitute a marker of schizophrenia risk . This study investigated whether eye tracking and antisaccade deficits could be found in another population with putative liability to schizophrenia-non clinical subjects with elevated scores on a psychometric index of perceptual aberrations . METHODS Subjects were 55 university students who received either high or normal scores on the Perceptual Aberration Scale , a measure of schizotypy indexing body image and perceptual distortions . Subjects completed a smooth pursuit eye tracking task and an antisaccade task . Eye movements were monitored using an infrared limbus tracker . RESULTS Subjects with high Perceptual Aberration Scale scores ( putative " schizotypes " ) had lower pursuit quality and a lower percentage correct on the antisaccade task than the controls . The 2 groups did not differ in antisaccade or error latencies . The increase in antisaccade errors in the schizotypes was accounted for almost entirely by an increase in perseverative errors , but virtually no difference between groups on r and om errors . Antisaccade performance was significantly related to pursuit quality . CONCLUSIONS Subjects with elevated Perceptual Aberration Scale scores have performance deficits on oculomotor tasks that have been linked to latent liability to schizophrenia , namely , smooth pursuit and antisaccade performance . The antisaccade errors in the schizotype group were primarily perseverations , a behavioral pattern often associated with frontal lobe dysfunction and observed in the performance of schizophrenic patients BACKGROUND Increased catechol-O-methyltransferase activity associated with variation in catechol-O-methyltransferase valine158 methionine genotypes may result in reduced dopamine neurotransmission in the prefrontal cortex and thus contribute to the poor performance of frontally mediated cognitive tasks and the occurrence of associated negative symptoms observed in patients with schizophrenia ; however , reported associations between catechol-O-methyltransferase valine158 methionine genotypes and measures of cognition have not been consistent . METHODS Catechol-O-methyltransferase genotyping , measures of schizotypy , cognitive measures of memory and attention , as well as the antisaccade eye movement task , a measure sensitive to prefrontal cortical function , were obtained in a sample of 5 
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Antisaccade error rate was the most consistent deficit found for schizotypy .
Relatives had intermediate antisaccade error rates between patients and controls .
Antisaccade error rate was the most consistent deficit found for high schizotypy .
Relatives had intermediate antisaccade error rates between patients and healthy controls .
Results from the limited genetic and neuroimaging studies echoed schizophrenia findings .