Measures of eye movement dysfunction have been considered as candidate endophenotypes for the study of genetic liability in schizophrenia. In this respect it is crucial to confirm a clinical state independentce of these measures. Twenty people with DSM-IV schizophrenia were assessed using a battery of oculomotor tasks in the acute phase of their disorder without being treated with antipsychotic medication and then again in the remission phase under treatment with antipsychotic medication. The saccade latency in the saccade task, the error rate and antisaccade latency in the antisaccade task, and the frequency of unwanted saccades in the active fixation task were stable in time both at the group level and within each individual, showing no relation to the significant improvement in different psychopathological dimensions of these patients. The root mean square error, gain and saccade frequency in the pursuit task were not stable over time, although again this instability was not related to the changes in psychopathological status of these patients. Finally, the saccade frequency in the active fixation task with distracters was not stable in time and was correlated with changes in specific dimensions of psychopathology. These results provide further evidence that saccade and smooth eye pursuit dysfunction measures are not affected by the substantial change in the clinical state of schizophrenia from the acute phase to remission, and strengthen the current view that they can be used as endophenotypes. On the other hand, active fixation might be state-dependent adding to the evidence against its use as a candidate endophenotype in schizophrenia.

The study tested whether the antisaccade (AS) performance and Contingent Negative Variation (CNV) measures differed between the first-episode and chronic patients to provide the evidence of PFC progressive functional deterioration. Subjects included 15 first-episode and 20 chronic schizophrenic patients (with the duration of illness more than 5 years), and 21 control subjects. The first-episode and chronic patients had significantly elevated error percent (p < .05, effect size 1.10 and p < .001, effect size 1.25), increased AS latencies (p < .01, effect size 1.18 and p < .001, effect size 1.69), and increased latencies variability (p < .01, effect size 1.52 and p < .001, effect size 1.37) compared to controls. Chronic patients had marginally significant increase of the response latency (p = .086, effect size .78) and latency variability (p < .099, effect size .63) compared to first-episode ones. Results of CNV analysis revealed that chronic patients only exhibited robustly declined frontal CNV amplitude at Fz (p < .05, effect size .70), F3 (p < .05, effect size .88), and F4 (p < .05, effect size .71) sites compared to controls. The obtained results might be related to specific changes in prefrontal cortex function over the course of schizophrenia.

Background: Despite its inhibitory control requirements, antisaccade deficits have been consistently associated with working memory impairments in schizophrenia. We investigated whether variance in antisaccade performance could be better accounted for in terms of a specific inhibitory function. Method: We assessed 48 clinically stable out-patients with schizophrenia on an antisaccade task, as well as on measures of spatial and verbal working memory, sustained selective attention, and a simple motoric go/no-go measure of response inhibition. Results: In a stepwise multiple regression analysis, go/no-go task performance accounted for a considerably greater percentage of variance in antisaccade performance (25.3%) than either working memory (8.4%) or sustained selective attention task (9.1%). Discussion: We conclude that antisaccade deficits in schizophrenia appear to be better understood in terms of a specific deficit of inhibitory control than in terms of more general difficulties with context maintenance or goal neglect. (JINS, 2006, 12, 901–906.)

Schizotypal personality disorder (SPD) is theoretically part of the schizophrenia spectrum both clinically 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.

There are few studies on the development of oculomotor functions during childhood. B. Fischer, M. Biscaldi, and S. Gezeck (1997) reported improvement of antisaccade task performance between ages 6 and 16 years. The present study is a replication and extension of those results. In three age groups (6–7, 10–11, 18–26 years), saccades during pro- and antisaccade tasks with 200-ms gap and overlap and during a fixation task were measured. Adults exhibited faster saccades and less prosaccades during the antisaccade tasks than 10–11-year-old children; these two groups had faster saccades during all tasks and less prosaccades during the anti- and the fixation task than 6–7-year-old subjects. Both children groups made more express saccades than adults. Results suggest different degrees of age-related improvement for different saccadic parameters, the effects being greatest for prosaccade inhibition during the antisaccade task and in line with the assumed protracted development of prefrontal functions.