Using saccade tasks as a tool to analyze executive dysfunctions in schizophrenia

Reuter, Benedikt; Kathmann, Norbert

doi:10.1016/j.actpsy.2003.12.009

Cited by 106 publications

(69 citation statements)

References 47 publications

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“…Of course, antisaccade effects and switch paradigm congruity costs, though related, are not identical. Nonetheless, it is interesting to note that, in an antisaccade/prosaccade task-switching paradigm, schizophrenic patients show intact switch capabilities combined with an increased difficulty to suppress the default prosaccade (Levy et al, 1998;Barton et al, 2002;Manoach et al, 2002;Reuter and Kathmann, 2004).…”

Section: Discussionmentioning

confidence: 99%

Effects of the NMDA Antagonist Ketamine on Task-Switching Performance: Evidence for Specific Impairments of Executive Control

Stoet

Snyder

2005

Neuropsychopharmacol

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In humans, the effects of subanesthetic doses of ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, substantially impair executive control functions. Here, we consider whether ketamine exposure can provide an animal model for the effects of ketamine on executive control. Two monkeys (Macaca mulatta) performed a cued task-switching paradigm. We studied their behavior before and after a range of ketamine doses. We found that ketamine slowed overall performance and decreased overall accuracy, strongly impaired the capacity to ignore task-irrelevant information and, to a lesser degree, decreased accuracy when a task switch was required. This pattern of results is very similar to that found in studies of schizophrenic patients performing task-switching paradigms or the Stroop task. We conclude that ketamine in monkeys provides a good animal model for exploring the relationship between the glutamate system, executive control, and the symptoms of schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Effects of the NMDA Antagonist Ketamine on Task-Switching Performance: Evidence for Specific Impairments of Executive Control

Stoet

Snyder

2005

Neuropsychopharmacol

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“…More recent accounts, however, take on board the suggestion made by currently influential models of cognitive control that inhibition of erroneous information processing occurs as a direct consequence of successful activation of processing routes required to perform the correct response (Miller & Cohen, 2001). As a result recent models of antisaccade performance emphasize cognitive constructs such as working memory, goal or intention activation, and attentional focus (Mitchell, Macrae, & Gilchrist, 2002;Nieuwenhuis, Broerse, Nielen, & de Jong, 2004;Reuter & Kathmann, 2004). Although differing somewhat in terminology and detail, these accounts suggest that correct antisaccade performance depends upon the ability to adequately maintain the relevant task instructions, or sufficiently activate the intention to make an antisaccade.…”

Section: -*9#(-:(!0$2#and''and*(610'$2-0(mentioning

confidence: 99%

“…Average antisaccade error rates in healthy humans vary considerably across studies and laboratories, with some studies reporting rates as low as 5% and others as high as 25% (Reuter & Kathmann, 2004). Recent studies using large samples suggest an error rate of around 20% is typical (Ettinger et al, 2003a(Ettinger et al, , 2005bSmyrnis et al, 2002; Tatler & Hutton, in submission; see also Everling & Fischer, 1998).…”

Section: '(4*#*and%'5(620207#((mentioning

confidence: 99%

“…Recent accounts emphasize the parallel nature of motor programming in antisaccade performance and suggest that whether an error is made or not is determined by the relative strength of activation in neural systems supporting the pro-and antisaccade (Massen, 2004;Munoz & Everling, 2004;Reuter & Kathmann, 2004). These accounts argue that at stimulus onset a "competition" ensues between processes underlying the exogenously triggered prosaccade and the endogenously initiated antisaccade -the coordinates for the antisaccade being computed as soon as the stimulus location is determined.…”

Section: -*9#(-:(!0$2#and''and*(610'$2-0(mentioning

confidence: 99%

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The antisaccade task as a research tool in psychopathology: A critical review

2006

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The antisaccade task is a measure of volitional control of behavior sensitive to fronto‐striatal dysfunction. Here we outline important issues concerning antisaccade methodology, consider recent evidence of the cognitive processes and neural mechanisms involved in task performance, and review how the task has been applied to study psychopathology. We conclude that the task yields reliable and sensitive measures of the processes involved in resolving the conflict between volitional and reflexive behavioral responses, a key cognitive deficit relevant to a number of neuropsychiatric conditions. Additionally, antisaccade deficits may reflect genetic liability for schizophrenia. Finally, the ease and accuracy with which the task can be administered, combined with its sensitivity to fronto‐striatal dysfunction and the availability of suitable control conditions, may make it a useful benchmark tool for studies of potential cognitive enhancers.

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“…Some reviewers have suggested that antisaccade deficits in schizophrenia index deficits in attentional control leading to difficulties with goal directed behaviour more generally (Nieuwenhuis et al, 2004;Reuter & Kathmann, 2004). In this view, antisaccade deficits may arise from a general difficulty with goal neglect, operationalised by Duncan (1995) as the tendency to disregard task requirements even though they are understood and remembered.…”

Section: Response Inhibition and Attentional Controlmentioning

confidence: 99%

Do antisaccade deficits in schizophrenia provide evidence of a specific inhibitory function?

Donohoe

Reilly

Clarke

et al. 2006

J. Inter. Neuropsych. Soc.

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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 go0no-go measure of response inhibition. Results: In a stepwise multiple regression analysis, go0no-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.)

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Using saccade tasks as a tool to analyze executive dysfunctions in schizophrenia

Cited by 106 publications

References 47 publications

Effects of the NMDA Antagonist Ketamine on Task-Switching Performance: Evidence for Specific Impairments of Executive Control

Effects of the NMDA Antagonist Ketamine on Task-Switching Performance: Evidence for Specific Impairments of Executive Control

The antisaccade task as a research tool in psychopathology: A critical review

Do antisaccade deficits in schizophrenia provide evidence of a specific inhibitory function?

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