Increase In Perseverative Errors Research Articles

Repeated dextromethorphan administration in adolescent rats produces long-lasting behavioral alterations

Initiation of non-medical dextromethorphan (DXM) use often occurs in adolescence, yet little is known about the consequences when use begins during this developmental period. The current experiments examined the acute response and the effects of repeated exposure to DXM in adolescence on behavior in adulthood. We examined locomotor activity, locomotor sensitization, and cognitive function, in rats that received repeated administration of DXM. Groups of adolescent (PND 30) and adult (PND 60) male rats were treated with DXM (60 mg/kg) once daily for 10 days. Locomotor activity in response to DXM was assessed following the first injection, on the 10th day of injection (adolescent – PND 39; adult – PND 69), and following 20 days of abstinence (adolescent – PND 59; adult – PND 89). Acute locomotor effects and locomotor sensitization were compared in adolescents and adults; cross-sensitization to ketamine, another dissociative with abuse potential, was also examined. In a separate group of rodents cognitive deficits were assessed following a 20 day abstinence period (adolescent – PND 59; adult – PND 89) in spatial learning and novel object recognition tasks. The locomotor stimulant effect of DXM was much greater in adolescents than adults. Also, only adolescent rats that were repeatedly administered DXM demonstrated locomotor sensitization at the end of 10 days of injection. However, sensitization occurred after the abstinence period in all rats regardless of age. Nonetheless, cross-sensitization to ketamine was only evident in adolescent-treated rats. DXM also led to an increase in perseverative errors in reversal learning only in the adolescent-treated group. We conclude that repeated use of DXM produces long-lasting neuroadaptations that may contribute to addiction. Deficits in cognitive flexibility occur in adolescents, although further work is necessary to confirm these findings. The results extend the understanding of potential long-term consequences of DXM use in adolescents and adults.

Increase in cerebral microbleeds and cognitive decline.

In spite of increasing evidence of the clinical importance of cerebral microbleeds (CMBs), the relationship between CMBs and cognitive impairment is still controversial. In addition, there are very limited prior data regarding the prospective association of additional CMBs over time with a decline in cognitive function. This study thus aimed to investigate the effects of newly detected CMBs on cognitive decline in a Japanese health examination cohort. We performed a prospective cohort study involving 769 Japanese participants (mean age, 61.6 years) with a mean follow-up of 7.3 ± 3.5 years. CMBs were classified according to their locations. Cognitive functions were evaluated using Okabe's Intelligence Scale, Koh's block design test, and the Wisconsin Card Sorting Test. Multiple linear regression analyses were performed to examine the relationship between the newly detected CMBs and cognitive decline. Fifty-six (7.3%) participants (16 had new strictly lobar cerebral microbleeds and 40 had new deep or infratentorial cerebral microbleeds) developed new CMBs during the follow-up period. In multivariable analysis, newly detected strictly lobar CMBs were associated with a greater decline in the Wisconsin Card Sorting Test in the categories achieved (β: - 0.862 [95% CI: - 1.325, - 0.399]; P < 0.0001), greater increase in perseverative errors of Nelson (β: 0.603 [95% CI: 0.023, 1.183]; P = 0.04), and greater increase in the difficulty with maintaining set (β: 1.321 [95% CI: 0.801, 1.842]; P < 0.0001). Strictly lobar CMBs over time were associated with a decline in executive function.

The role of dopamine D1 receptors in MDMA-induced memory impairments

(±) 3,4-Methylenedioxymethamphetamine (MDMA) is a recreationally abused psychostimulant that impairs memory performance. This effect is often attributed to a working memory impairment resulting from compromised serotonin systems. However, recent evidence from non-human animal experimental studies suggests that acute MDMA may indirectly impair memory performance through overstimulation of dopamine (DA) D1 receptors, which increases perseverative responding during memory tasks. This hypothesis was explored using DA D1 mutant (DAD1−/−) rats which possess a selective down-regulation in functional D1 receptors. Adult male Wistar DAD1−/− rats and wild type controls were trained over 25 sessions on a spatial working memory T-maze delayed non-matching to position (DNMTP) task. Once trained, the rats were administered MDMA (1.5, 2.25 and 3 mg/kg) or saline fifteen minutes prior to testing on DNMTP with all subjects experiencing all drug doses and saline three times. We predicted that controls would demonstrate decreased task accuracy following MDMA, driven by an increase in perseverative errors. In contrast, we predicted that DAD1−/− rats would be protected from MDMA-induced perseverative errors due to their reduced D1 receptor function. As predicted, during the third block of MDMA administration, control rats demonstrated decreased task accuracy following 2.25 and 3 mg/kg doses, driven by an increase in perseverative errors. In addition, DAD1−/− rats were protected from MDMA-induced task deficits. These findings challenge the assumption that MDMA’s acute effects on memory performance are predominantly due to serotonergic mechanisms and provide support for the hypothesis that acute MDMA impairs memory performance in rats via overstimulation of D1 receptors by increasing perseverative behaviour.

Pigeons' midsession reversal: Greater magnitude of reinforcement on the first half of the session leads to improved accuracy.

In the midsession reversal task, pigeons are trained on a simultaneous two-alternative discrimination in which S1 is correct for the first half of the session and S2 is correct for the second half of the session. Optimally, pigeons should choose S1 until it stops being correct and choose S2 afterward. Instead, pigeons anticipate S2 too early and continue choosing S1 even after the reversal. Research suggests that they attempt to time the reversal rather than use the feedback from the preceding response(s). Recently, there is evidence that performance is almost optimized by generating an asymmetry between S1 and S2. For example, pigeons' accuracy improves if correct S1 responses are reinforced 100% of the time, but correct S2 responses are reinforced only 20% of the time. Similarly, accuracy improves if S1 requires one peck but S2 requires 10 pecks. Accuracy does not improve, however, if the value of S1 is less than the value of S2. In the current experiment, we manipulated the magnitude of reinforcement. For the experimental group, correct responses to S1 were reinforced with five pellets of food and correct responses to S2 were reinforced with one pellet. For the control group, all correct responses were reinforced with three pellets. Consistent with the earlier findings, results indicated that there was a significant reduction in anticipatory errors in the experimental group compared with the control, and there was no significant increase in perseverative errors.

The midsession reversal task: A theoretical analysis.

In the midsession reversal task, choice of one stimulus (S1) is correct for the first half of each session and choice of the other stimulus (S2) is correct for the last half of each session. Although humans and rats develop very close to what has been called a win-stay/lose-shift response strategy, pigeons do not. Pigeons start choosing S2 before the reversal, making anticipatory errors, and they keep choosing S1 after the reversal, making perseverative errors. Research suggests that the pigeons are timing the reversal from the start of the session. However, making the reversal unpredictable does not discourage the pigeons from timing. Curiously, pigeons' accuracy improves if one decreases the value of the S2 stimulus relative to the S1 stimulus. Another form of asymmetry between S1 and S2 can be found by varying, over trials, the number of S1 or S2 stimuli. Counterintuitively, if the number of S2 stimuli varies, it results in a large increase in anticipatory errors but little increase in perseverative errors. However, if the number of S1 stimuli varies over trials, it results in a large increase in perseverative errors but no increase in anticipatory errors. These last two effects suggest that in the original midsession reversal task, the pigeons are learning to reject S2 during the first half of each session and learning to reject S1 during the last half of each session. These results suggest that reject learning may also play an important role in the learning of simple simultaneous discriminations.

Subchronic anesthetic ketamine injections in rats impair choice reversal learning, but have no effect on reinforcer devaluation.

Previous exposure to a variety of drugs of abuse has been shown to cause long-term impairments in reversal learning and reinforcer devaluation tasks. However, there is mixed evidence in the literature for a long-term effect of ketamine exposure on reversal learning and the long-term effect of ketamine exposure on devaluation is not known. We determined whether repeated injections of an anesthetic dose of ketamine would lead to impairments in choice reversal learning after discrimination learning or impairments in reinforcer devaluation. In two experiments, rats received three injections once-daily of ketamine (100 mg/kg, intraperitoneally) or saline and then began behavioral training 19 days later so that the key reversal learning and devaluation tests would occur about 1 month after the final ketamine injection. This ketamine exposure regimen did not impair learning in our discrimination task, but led to an increase in perseverative errors in reversal learning. However, the same ketamine exposure regimen (or injections of a lower 50 mg/kg dose) had no effect on behavior in the devaluation task. The behavioral patterns observed suggest possible neural mechanisms for the effects of ketamine, but future neurobiological investigations will be needed to isolate these mechanisms.

Neural mechanisms underlying cognitive inflexibility in Parkinson's disease

Cognitive inflexibility is a hallmark of executive dysfunction in Parkinson's disease (PD). This deficit consistently manifests itself in a PD-related increase in the number of perseverative errors committed on the Wisconsin Card Sorting Test (WCST). However, the neural processes underlying perseverative WCST performance in PD are still largely unknown. The present study is the first to investigate the event-related potential (ERP) correlates of cognitive inflexibility on the WCST in PD patients. Thirty-two PD patients and 35 matched control participants completed a computerized version of the WCST while the electroencephalogram (EEG) was recorded. Behavioral results revealed the expected increase in perseverative errors in patients with PD. ERP analysis focused on two established indicators of executive processes: the fronto-central P3a as an index of attentional orienting and the sustained parietal positivity (SPP) as an index of set-shifting processes. In comparison to controls, P3a amplitudes were significantly attenuated in PD patients. Regression analysis further revealed that P3a and SPP amplitudes interactively contributed to the prediction of perseverative errors in PD patients: The number of perseverative errors was only increased when both ERP amplitudes were attenuated. Notably, the two ERP markers of executive processes accounted for more than 40% of the variance in perseverative errors in PD patients. We conclude that cognitive inflexibility in PD occurs when the neural bases of multiple executive processes are affected by the pathophysiology of PD. The combined measurement of P3a and SPP might yield an electrophysiological marker of cognitive inflexibility in PD.

Neonatal Perirhinal Lesions in Rhesus Macaques Alter Performance on Working Memory Tasks with High Proactive Interference.

The lateral prefrontal cortex is known for its contribution to working memory (WM) processes in both humans and animals. Yet, recent studies indicate that the prefrontal cortex is part of a broader network of interconnected brain areas involved in WM. Within the medial temporal lobe (MTL) structures, the perirhinal cortex, which has extensive direct interactions with the lateral and orbital prefrontal cortex, is required to form active/flexible representations of familiar objects. However, its participation in WM processes has not be fully explored. The goal of this study was to assess the effects of neonatal perirhinal lesions on maintenance and monitoring WM processes. As adults, animals with neonatal perirhinal lesions and their matched controls were tested in three object-based (non-spatial) WM tasks that tapped different WM processing domains, e.g., maintenance only (Session-unique Delayed-nonmatching-to Sample, SU-DNMS), and maintenance and monitoring (Object-Self-Order, OBJ-SO; Serial Order Memory Task, SOMT). Neonatal perirhinal lesions transiently impaired the acquisition of SU-DNMS at a short (5 s) delay, but not when re-tested with a longer delay (30 s). The same neonatal lesions severely impacted acquisition of OBJ-SO task, and the impairment was characterized by a sharp increase in perseverative errors. By contrast, neonatal perirhinal lesion spared the ability to monitor the temporal order of items in WM as measured by the SOMT. Contrary to the SU-DNMS and OBJ-SO, which re-use the same stimuli across trials and thus produce proactive interference, the SOMT uses novel objects on each trial and is devoid of interference. Therefore, the impairment of monkeys with neonatal perirhinal lesions on SU-DNMS and OBJ-SO tasks is likely to be caused by an inability to solve working memory tasks with high proactive interference. The sparing of performance on the SOMT demonstrates that neonatal perirhinal lesions do not alter working memory processes per se but rather impact processes modulating impulse control and/or behavioral flexibility.

Self-focused attention in anorexia nervosa.

The clinical presentation of anorexia nervosa (AN) is characterized by preoccupation with body experience, intrusive concerns regarding shape, and pathological fears of weight gain. These symptoms are suggestive of unrelenting self-focused attention. No research to date has characterized self-focused attention (SFA) in AN nor examined neurocognitive features that may facilitate an excessive, rigid, or sustained focus on one's appearance. This study examined SFA, body image disturbance, and executive functioning in women with current anorexia nervosa (AN-C; n = 24), a history of AN who were weight-restored at the time of the study (WR; n = 19), and healthy controls (n = 24). Private and public SFA were highest among WR and lowest among AN-C. Shape concerns were negatively correlated with SFA, especially among AN-C, after controlling for depression and social anxiety symptoms. Lower levels of SFA among AN-C were unexpected and suggest the acute state of AN may lessen pathological self-focus, negatively reinforcing symptoms. In addition, body image concerns may distract from general SFA. Deficits in executive attention may explain these findings, as each one unit increase in perseverative errors among AN-C participants was associated with an almost one-half unit decrease in public SFA.

Impairments in set-shifting but not reversal learning in the neonatal ventral hippocampal lesion model of schizophrenia: Further evidence for medial prefrontal deficits

The executive function processes of set-shifting and reversal learning in rodents are mediated by the medial prefrontal cortex and the orbitofrontal cortex, respectively. Here, we investigated both set-shifting and reversal learning in a developmental animal model of schizophrenia, the neonatal ventral hippocampal lesion (NVHL) model. The NVHL manipulation is known to disrupt development of the medial prefrontal cortex, and to impair behaviors dependent on this area, but potential orbitofrontal abnormalities and reversal learning deficits are less well studied. Animals received excitotoxic lesions of the ventral hippocampus (NVHL) or a sham treatment during the first postnatal week, and all animals were subsequently tested in adulthood on either an operant set-shifting or an operant reversal task. Results indicated that NVHL animals were able to acquire a simple discrimination rule and exhibited normal reversal learning, but were impaired on a prefrontal-dependent set-shifting task. Furthermore, this set-shifting deficit was due to an increase in perseverative errors, which indicate difficulty suppressing a previously learned strategy and result from medial prefrontal insult. Together, these results confirm and extend the idea that cognitive impairments in the NVHL animal are primarily driven by medial prefrontal abnormalities, while the orbitofrontal cortex may remain relatively unaffected.

Progressive Gray Matter Loss and Changes in Cognitive Functioning Associated With Exposure to Herpes Simplex Virus 1 in Schizophrenia: A Longitudinal Study

Longitudinal changes in gray matter volume and cognitive performance were evaluated among individuals exposed to neurotropic herpes simplex virus subtype 1 (HSV1). There is a replicable association of HSV1 exposure with smaller prefrontal volumes and cognitive impairments in schizophrenia. The authors concurrently examined the whole-brain longitudinal trajectory over 1 year of gray matter volumes and executive functioning measured with the Wisconsin Card Sorting Test among 26 first-episode antipsychotic-naive subjects with schizophrenia and 38 healthy subjects. Age, gender, socioeconomic status, and exposure to cytomegalovirus (another virus of the herpes family that was previously associated with cognitive impairments) were the covariates. Significant gray matter loss in the posterior cingulate gyrus was noted among the HSV1-seropositive schizophrenia subjects over 1 year but not among other groups. Prefrontal gray matter volumes did not show longitudinal changes. Binomial mixed-effects models indicated that improvement over 1 year in Wisconsin Card Sorting Test categories completed and perseverative errors occurred in significantly fewer HSV1-seropositive schizophrenia subjects than in the HSV1-seronegative schizophrenia subjects or the healthy subjects regardless of serological status. Three-way interactions of diagnosis, HSV1 status, and time were significant for both categories completed and perseverative errors. An increase in perseverative errors over 1 year, but not the change in the number of categories completed, correlated with longitudinal volume loss of the posterior cingulate gyrus. These observations suggest that HSV1 exposure may be associated with longitudinal gray matter loss in the posterior cingulate gyrus and decline in executive functioning among subjects with schizophrenia.

Blockade of NMDA GluN2B receptors selectively impairs behavioral flexibility but not initial discrimination learning

Behavioral flexibility is the ability to adjust behavior when environmental contingencies change and is compromised in disease states such as schizophrenia, attention deficit hyperactivity disorder, and following damage to the prefrontal cortex. The present study investigated the contribution of N-methyl-D-aspartate GluN2B receptor subunits in the initial learning and in shifting between or within discrimination strategies (i.e., strategy set-shifting and reversal learning), using tasks conducted in operant chambers. Strategy set-shifting required rats initially to learn a visual-cue discrimination (day 1) and on day 2, shift to using an egocentric spatial response strategy to obtain reward. For reversal learning, rats were trained on a response discrimination on day 1 and then required to select the opposite lever on day 2. Blockade of GluN2B receptors with systemic administration of Ro25-6981 on day 1 did not impair initial acquisition of either a response or visual-cue discrimination nor did these treatments affect performance of strategy or reversal shifts on day 2. However, administration of Ro25-6981 prior to a set-shift or reversal on day 2 significantly impaired performance on both tasks, inducing a selective increase in perseverative errors, indicative of a disruption the ability to suppress a previously acquired prepotent response. These data suggest that systemic blockade of GluN2B receptors Ro25-6981 does not appear to interfere with the initial acquisition of simple visual or response discriminations. However, these receptors do appear to play a central and selective role in the modification of previously acquired strategies or stimulus-reward associations, facilitating behavioral inhibition so that novel patterns of behavior may emerge.

Neonatal ventral hippocampal lesions disrupt set-shifting ability in adult rats

Set-shifting in a T-maze task was assessed in rats with a neonatal ventral hippocampal lesion (NVHL), a proposed animal model of schizophrenia. NVHL animals tested as adults were impaired in shifting to a new rule; an increase in perseverative errors suggested that this impairment stemmed from an inability to suppress the previously learned strategy. The NVHL animals’ performance is reminiscent of humans with prefrontal damage and patients with schizophrenia.

Thalamic-Prefrontal Cortical-Ventral Striatal Circuitry Mediates Dissociable Components of Strategy Set Shifting

The mediodorsal nuclei of thalamus (MD), prefrontal cortex (PFC), and nucleus accumbens core (NAc) form an interconnected network that may work together to subserve certain forms of behavioral flexibility. The present study investigated the functional interactions between these regions during performance of a cross-maze-based strategy set-shifting task. In Experiment 1, reversible bilateral inactivation of the MD via infusions of bupivacaine did not impair simple discrimination learning, but did disrupt shifting from response to visual cue discrimination strategy, and vice versa. This impairment was due to an increase in perseverative errors. In Experiment 2, asymmetrical disconnection inactivations of the MD on one side of the brain and PFC on the other also caused a perseverative deficit when rats were required to shift from a response to a visual cue discrimination strategy, as did disconnections between the PFC and the NAc. However, inactivation of the MD on one side of the brain and the NAc contralaterally resulted in a selective increase in never-reinforced errors, suggesting this pathway is important for eliminating inappropriate strategies during set shifting. These data indicate that set shifting is mediated by a distributed neural circuit, with separate neural pathways contributing dissociable components to this type of behavioral flexibility.

Executive system dysfunction occurs as early as middle-age in the rhesus monkey

As our understanding of age-related cognitive decline advances, studies are now focusing on identification of those areas of cognitive function that undergo the first changes with age. In the present study, in order to determine whether executive function is sensitive to the aging process, we assessed the performance of 16 monkeys of middle-age (12–19 years of age) on the conceptual set-shifting task, an analogue of the Wisconsin Card Sorting Test (WCST). We compared their performance to that of seven young adult (5–9 years of age) and 18 aged monkeys (20–30). The findings showed that middle-aged monkeys, like those of advanced age, were significantly impaired on the conceptual set-shifting task (CSST). These findings parallel those of recent studies in humans demonstrating an increase in perseverative errors on the WCST by middle-aged as well as aged individuals and, in turn, support the notion that disruption of executive function is one of the earliest changes in cognition to occur in normal aging.

Multiple Dopamine Receptor Subtypes in the Medial Prefrontal Cortex of the Rat Regulate Set-Shifting

Dopamine (DA) input to the prefrontal cortex (PFC), acting on D1 receptors, plays an essential role in mediating working memory functions. In comparison, less is known about the importance of distinct PFC DA receptor subtypes in mediating executive functions such as set-shifting. The present study assessed the effects of microinfusion of D2 and D4 receptor antagonists, and D1, D2, and D4 receptor agonists into the PFC on performance of a maze-based set-shifting task. In Experiment 1, rats were trained on a response discrimination task, and then on a visual-cue discrimination task requiring rats to suppress the use of the response strategy and approach the previously irrelevant cue to locate food. In Experiment 2, the order of training was reversed. Infusions of the D2 antagonist eticlopride, or the D4 agonist PD-168,077, impaired shifting from a response to a visual-cue discrimination strategy and vice versa, and caused a selective increase in perseverative errors. In contrast, infusions of the D4 antagonist L-745,870 improved set-shifting. Infusions of the D1 agonist SKF81297 or the D2 agonist quinpirole caused no reliable effect. These data, in combination with previous reports of impaired set-shifting following D1 receptor blockade, suggest that multiple receptors in the PFC are essential for set-shifting and that the mechanisms by which PFC DA mediates behavioral flexibility may be different from those underlying working memory. These findings may have important implications for developing novel treatments for cognitive deficits observed in disorders such as attentional deficit and hyperactivity disorder and schizophrenia.

The Contributions of Attention and Working Memory to Age Differences in Concept Identification

The contributions of attention and working memory to adult age differences in concept identification were examined in two experiments using the standard version of the California Card Sorting Test plus two modified versions. Older adults demonstrated global reductions in their ability to identify concepts whether sorting stimuli, identifying concepts used by the examiner, or generating concepts from cues. Although age differences in selective attention and interference control did not contribute to these deficits, reduced working memory accounted for the age-related increase in perseverative errors. Our conclusions focus on whether impairments in working memory might fully account for age differences in concept identification.

Perseveration for novel stimuli in Parkinson's disease: An evaluation based on event-related potentials topography

Event-related potential topography produced by novel and target stimuli was used to detect dysfunction of mental switching (perseveration) in nondemented patients with Parkinson's disease. The study participants were 15 patients with Parkinson's disease and 13 age-matched healthy control patients. Ten percent of the novelty tones with pitches of 125 and 500 Hz were added to 20% of the target tones that had a pitch of 1000 Hz. Patients were instructed to count the target tones. The modified Wisconsin Card Sorting Test was used to evaluate frontal lobe function. Patients with Parkinson's disease showed a significant decrease in the achieved categories and an increase in perseverative errors in the Wisconsin Card Sorting Test. These results indicate that the cognitive impairment of patients with Parkinson's disease can be characterized as failure of mental switching related to frontal lobe dysfunction based on basal ganglia disturbance. As compared with the control patients, patients with Parkinson's disease had shorter P3 latencies to the novel stimuli and a more frontal distribution on the P3 map, especially for the 125-Hz stimuli. This characteristic of P3 to novel stimuli in the patients with Parkinson's disease, but not in the control patients, is categorized by P3a (novelty P3). Our findings suggest that decreased mental switching causes lack of novelty P3 habituation in patients with Parkinson's disease and that it is related to learning disabilities based on dysfunction of the frontal lobe and basal ganglia.

Researching a differential impairment of frontal functions and explicit memory in early Parkinson's disease.

An impairment at tasks sensitive to frontal lobe damage has been repeatedly reported in Parkinson's disease, but the exact nature of these deficits has not yet been clarified. Similarly, deficits of visuo-spatial functions have been frequently observed, but it is still debated whether verbal and visuo-spatial memory can be differentially affected. In this study we have compared the performance of 20 mild Parkinson's disease patients (I-II Hoehn and Yahr stage) and 18 matched normal controls, at tasks assessing frontal functions and explicit memory. We detected a selective deficit in set shifting and maintaining, without impairment in categorization and set formation. The lack of a selective increase in perseverative errors might indicate that perseverations either measure something different from set shifting or that they do not represent an index sensitive enough to set shifting impairment. Parkinson's disease patients were also significantly impaired at Raven's Progressive Matrices, a task assessing both frontal and visuo-spatial aspects. However, they did not show any differential impairment of visuo-spatial memory. Indeed, despite a trend of lower performance in visuo-spatial learning, memory performance of Parkinson's disease patients was significantly different from that of controls only at a free recall test which involved both verbal and visuo-spatial memory. We suggest the exploration of set shifting and maintaining to detect 'frontal' deficits in mild Parkinson's disease. We argue that Raven's Progressive Matrices is a valuable task for detecting subclinical cognitive deficits in Parkinson's disease, even if it does not show a specific profile of impairment in these patients. According to our results, a differential evaluation of verbal vs. visuo-spatial memory is not necessary in clinical practice, whilst free recall confirms its usefulness to detect subclinical impairments of memory functions.

Antisaccades and smooth pursuit eye tracking and schizotypy.

Eye tracking deficits are one of a few widely validated 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-nonclinical subjects with elevated scores on a psychometric index of perceptual aberrations. 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. 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 random errors. Antisaccade performance was significantly related to pursuit quality. 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.