Fifty to eighty-five percent of schizophrenic patients are impaired on ocular pursuit paradigms. However, results regarding the relatives are more discordant. The aim of this study was to investigate whether eye movement disorders could be a vulnerability marker of schizophrenia.

Contingent negative variation (CNV) topography, hemispheric asymmetry and time-course were investigated in healthy subjects and non-medicated paranoid schizophrenic patients in two antisaccade paradigms with the short (800-1000 ms) and long (1200-1400 ms) durations of the fixation period. EEG and electrooculogram (EOG) were recorded. Saccade characteristics and mean amplitudes of slow cortical potentials time-locked to peripheral target were analyzed in 23 healthy volunteers and 19 schizophrenic patients. Compared to healthy control subjects, schizophrenic patients had significantly slower antisaccades and committed significantly more erroneous saccades in the both antisaccade tasks. The prolongation of the fixation period resulted in noticeable decrease of error percent in patients group. The analysis of CNV time-course has revealed two distinct stages in both groups. The early CNV stage was represented by a negative wave with the maximal amplitude over midline fronto-central area, and the late stage was characterized by increased CNV amplitude at the midline and left parietal electrode sites. In healthy subjects the simultaneous activation of frontal and parietal areas was observed in the paradigm with the shorter fixation interval; the increase of the fixation period produced consecutive activation of these areas. Schizophrenic patients' CNV amplitude was generally smaller than that of healthy subjects. The most pronounced between-group differences of the negative shift amplitude were revealed at frontal electrode sites during the early CNV stage in both modifications of the antisaccade task. The deficit of frontal activation revealed in patients at the early stage of antisaccade preparatory set in both antisaccadic paradigms may be related to pathogenesis of paranoid schizophrenia.

Objectives: It is increasingly important to develop predictors of treatment response and outcome in schizophrenia. Neuropsychological impairments, particularly those reflecting frontal lobe function, appear to predict poor outcome. Eye movement abnormalities probably also reflect frontal lobe deficits. We wished to see if these two aspects of schizophrenia were correlated and whether they could distinguish a treatment resistant from a treatment responsive group.

Methods: Ten treatment resistant schizophrenic patients were compared with ten treatment responsive patients on three eye movement paradigms (reflexive saccades, antisaccades and smooth pursuit), clinical psychopathology (BPRS, SANS and CGI) and a neuropsychological test battery designed to detect frontal lobe dysfunction. Ten aged-matched controls also carried out the eye movement tasks.

Results: Both treatment responsive (p = 0.038) and treatment resistant (p = 0.007) patients differed significantly from controls on the antisaccade task. The treatment resistant group had a higher error rate than the treatment responsive group, but the difference was not statistically significant. Similar poor neuropsychological test performance was found in both groups.

Conclusions: To demonstrate the biological differences characteristic of treatment resistance, larger sample sizes and wider differences in outcome between the two groups are necessary.

The error negativity (Ne/ERN) and error positivity (Pe) are two components of the event-related brain potential (ERP) that are associated with action monitoring and error detection. To investigate the relation between error processing and conscious self-monitoring of behavior, the present experiment examined whether an Ne and Pe are observed after response errors of which participants are unaware. Ne and Pe measures, behavioral accuracy, and trial-to-trial subjective accuracy judgments were obtained from participants performing an antisaccade task, which elicits many unperceived, incorrect reflex-like saccades. Consistent with previous research, subjectively unperceived saccade errors were almost always immediately corrected, and were associated with faster correction times and smaller saccade sizes than perceived errors. Importantly, irrespective of whether the participant was aware of the error or not, erroneous saccades were followed by a sizable Ne. In contrast, the Pe was much more pronounced for perceived than for unperceived errors. Unperceived errors were characterized by the absence of posterror slowing. These and other results are consistent with the view that the Ne and Pe reflect the activity of two separate error monitoring processes, of which only the later process, reflected by the Pe, is associated with conscious error recognition and remedial action.

The aim of the present study was the comparative assessment of the 4-week test-retest stabilities of the saccadic CNV (sCNV) and saccadic reaction times (SRT) during the execution of pro- and antisaccades, as well as the stability of RT during execution of two neuropsychological tests of alertness and S-R incompatibility. Prosaccades were elicited under the 200-ms gap and overlap conditions, antisaccades under the overlap condition (64 trials each). The EEG was recorded from 25 channels with a DC amplifier (MES, Munich). Data of 20 healthy participants were statistically analyzed. We found high test-retest correlations for all SRT (.76 ≤ rtt ≤ .88) and neuropsychological (.62 ≤ rtt ≤ .88) measures. For the sCNV, coefficients ranging between .58 (pro/gap) and .77 (anti/overlap) were obtained. Whereas SRT were significantly faster during the second than during the first session, group means for the saccadic CNV were stable across the sessions. Our results suggest high 4-week stability of individual differences in SRT, and moderate to good stabilities of saccadic CNV amplitudes. Our results recommend these “traitlike” measures to be used in individual differences research.

The ability to identify unaffected gene carriers within families may be crucial to the success of schizophrenia genetics studies. Data collected from three family samples (N = 365) demonstrated that poor antisaccade performance is an exceptionally promising indicator of liability for schizophrenia. A particular antisaccade task version provides large separations (5–6 sigma) between proband and normal groups. Poor antisaccade performance alone correctly identified 70% of patients in California, Utah, and Micronesia schizophrenia samples. Twenty-five to 50% of these patients' nonpsychotic first-degree relatives also had poor antisaccade performance, yielding risk ratios around 20:1 for simplex and 50:1 for multiplex schizophrenia families. Poor antisaccade performance is associated with dorsolateral prefrontal cortex pathology, suggesting that dysfunction of this circuitry also may predispose individuals to developing this disease.