Maladaptive anticipatory saccades in schizophrenia

Hommer, Daniel W.; Clem, Thomas R.; Litman, Robert E.; Pickar, David

doi:10.1016/0006-3223(91)90234-d

Cited by 54 publications

(37 citation statements)

References 39 publications

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“…This effect was not related to minimal treatment-emergent EPS or to changes in manual motor control, suggesting that the ability to generate accurate behavioral responses based on internal representations without sensory feedback is a process adversely and selectively impacted by risperidone treatment. The demonstration of reduced accuracy of predictive saccades after treatment is consistent with findings from prior studies with medicated patients (Crawford et al, 1995a;Hommer et al, 1991;McDowell et al, 1996;Thaker et al, 1996). However, the present findings are the first to document the onset of this robust deficit after the initiation of antipsychotic therapy.…”

Section: Discussionsupporting

confidence: 91%

“…In a combined group of antipsychotic-free and antipsychotic-naive schizophrenia patients, Krebs et al (2001) reported hypometric predictive saccades, as did Hutton et al (2001) in a group of never-medicated patients. In contrast, Crawford et al (1995b) and Hommer et al (1991) reported no reductions in saccade accuracy in previously treated but medication-free patients. Thus, although medicated patients have consistently been shown to produce hypometric predictive saccades, the findings have been less consistent in medication-free patients.…”

Section: Introductionmentioning

confidence: 65%

“…Previous studies investigating predictive saccades in schizophrenia all documented hypometric (ie undershooting) predictive saccades in medicated, typically chronic schizophrenia patients (Crawford et al, 1995a;Hommer et al, 1991;McDowell et al, 1996;Thaker et al, 1996). Findings with regard to the ability to learn to accurately time predictive saccades in relation to stimulus appearance have been less consistent.…”

Section: Introductionmentioning

confidence: 98%

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Effects of Risperidone on Procedural Learning in Antipsychotic-Naive First-Episode Schizophrenia

Harris

Wiseman

Reilly

et al. 2008

Neuropsychopharmacol

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Studies of procedural learning in medicated schizophrenia patients using predictive saccade paradigms have consistently demonstrated hypometric predictive responses. Findings from antipsychotic-naive schizophrenia patients indicate fewer or no deficits. This pattern of findings suggests that antipsychotic medications might adversely affect frontostriatal systems supporting procedural learning on this task. The accuracy and latency of predictive saccades were assessed in 25 antipsychotic-naive first-episode schizophrenia patients and 22 matched healthy individuals. Patients were retested after 6 weeks of treatment with risperidone. Healthy individuals were reevaluated after a similar time period. The ability to learn to time response initiation in anticipation of target appearance (target prediction) was not impaired in patients before or after treatment. In contrast, although no deficits were evident before treatment initiation, after treatment patients showed a marked decrease in the accuracy of predictive but not sensory-guided responses. The findings from pretreatment testing indicate that procedural learning is a relatively unaffected cognitive domain in antipsychotic-naive first-episode schizophrenia. Although treatment-emergent extrapyramidal symptoms were minimal, these data suggest that D2 antagonism in striatum after risperidone treatment was sufficiently robust to disrupt the generation of planned volitional behavior guided by internalized representations.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 65%

Section: Introductionmentioning

confidence: 98%

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Effects of Risperidone on Procedural Learning in Antipsychotic-Naive First-Episode Schizophrenia

Harris

Wiseman

Reilly

et al. 2008

Neuropsychopharmacol

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“…Increased numbers of errors (premature saccades towards the target) are taken to indicate weaker inhibitory control. this task been used extensively to study inhibitory dysfunction in a number of groups such as schizophrenic patients (hommer et al 1991;Ross et al 1998), children and adults with aDhD (Ross et al 1994(Ross et al , 2000, young adults with autism (Minshew et al 1999), as well as in determining the effect of ageing (Gottlob et al 2007) and alcohol (abroms et al 2006) on inhibitory function. While these various participant groups show error rates of 20-44 %, normal healthy adults typically generate between 4 and 15 % errors.…”

Section: Introductionmentioning

confidence: 99%

Oculomotor inhibitory control in express saccade makers

Wolohan

Knox

2014

Exp Brain Res

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Express saccade makers (ESMs) produce high proportions (>30 %) of low-latency (80-130 ms) express saccades in tasks in which such responses are usually suppressed. In addition, high directional error rates on the antisaccade (AS) task suggest a failure of oculomotor inhibitory mechanisms in ESMs. However, the AS task is complex and does not provide a measure of inhibitory processes in isolation. We therefore examined inhibitory control in 25 ESM and 28 non-ESM ('Norm') participants, using a minimally delayed oculomotor response (MDOR) task. After a randomised fixation period, a pro-saccade target appeared for 200 or 1,000 ms. Participants were instructed to maintain fixation and saccade to the target position upon target offset. In a control task, they saccaded on target onset. Overall, saccade latency was considerably increased in the MDOR task compared to the control task (354 vs. 170 ms; p < 0.001), and we also observed a latency modulation with display time (200: 399, 1,000: 302 ms; p < 0.001). However, there was no evidence of a difference between groups (p = 0.29). Errors consisted primarily of responses to target onsets and error rates were comparable between the groups (p = 0.33). The overproduction of fast, reflexive responses was still observed in ESMs who generated a higher proportion of their errors within the express latency range (p < 0.001). We confirmed that in the AS task, the ESMs exhibited a higher directional error rate (p = 0.03). These results suggest that the performance 'deficit' observed on the AS task in ESMs cannot be attributed to generally weaker inhibitory control.

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“…It has been found that schizophrenics have frequent loss-of-gain relative to the target [3]. along with saccadic intrusions [4], The SPEM deficit has a segregation pattern consistent with an autosomal single-gene defect [5].…”

Section: Introductionmentioning

confidence: 99%

Fine Motor Performance in Schizophrenia

Griffith¹,

Adler²,

Freedman³

1994

Neuropsychobiology

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Peripheral and central aspects of motor dysfunction were assessed in 12 schizophrenic and 12 normal subjects, using a test of control of finger movement based on the widely used smooth pursuit eye movement task. This was performed in order to investigate the basis of neuromotor dysfunction in schizophrenia. In this task, subjects used finger movement to track a visual target. Simultaneously, an electromyogram of the extensor digitorum commu-nis, the primary muscle utilized in the task, was recorded. Smooth pursuit eye movements were also assessed. Accuracy of finger-based and smooth-pursuit eye movement tracking was analyzed by fast Fourier transform and expressed as a log signal-to-noise ratio. The electromyograms were analyzed by motor unit potential discrimination and by interspike interval histography. Schizophrenics demonstrated significantly poorer finger tracking than did controls, with a mean score of 2.01 ± 0.63 (SD) versus 2.81 ± 0.42 (t = 3.52, d.f. = 21, p < 0.005). However, there was no evidence for motor-unit dysfunction. Schizophrenics also performed more poorly on smooth-pursuit eye movement, with a mean score of 2.06 ± 0.62 versus 3.33 ± 1.21 (t= 3.21, d.f. = 22, p < 0.005). Severity of extrapyramidal symptoms was correlated with poorer performance on the finger tracking task, but not smooth-pursuit eye movement. These findings support the hypothesis that schizophrenics’ tracking abnormalities are due to central nervous system deficits rather than peripheral pathology.

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Maladaptive anticipatory saccades in schizophrenia

Cited by 54 publications

References 39 publications

Effects of Risperidone on Procedural Learning in Antipsychotic-Naive First-Episode Schizophrenia

Effects of Risperidone on Procedural Learning in Antipsychotic-Naive First-Episode Schizophrenia

Oculomotor inhibitory control in express saccade makers

Fine Motor Performance in Schizophrenia

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