Cognition and the inhibitory control of saccades in schizophrenia and Parkinson's disease

Crawford, Trevor J.; Bennett, David A.; Lekwuwa, Godwin; Shaunak, Sandip; Deakin, Bill

doi:10.1016/s0079-6123(02)40068-4

Cited by 51 publications

(36 citation statements)

References 114 publications

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“…However, there is a lack of consensus on antisaccades (Lueck et al 1990;Kitagawa et al 1994;Vidailhet et al 1994a;Crevits and DeRidder 1997;Briand et al 2001;Cameron et al 2012). Inhibition errors may depend on the extent of cognitive impairment (Crawford et al 2002) as PD is not homogenous in the extent of prefrontal impairments. Our findings in relation to the gap effect in PD are consistent with that of Chan et al (2005) and van Koningsbruggen et al (2009) who found an equivalent effect in older controls.…”

Section: Saccadic Eye Movements In Parkinson's Diseasementioning

confidence: 99%

“…For example, it has been shown that patients with AD are deficient in the strategic selection of the important items in a memory recall task (Castel et al 2009). Saccadic eye movement paradigms have been widely used as a tool to examine impairments in attention and the cognitive control of behaviour (Broerse et al 2001;Crawford et al 2002;Leigh and Kennard 2004;Hutton and Ettinger 2006). The pro-saccade task (PST) requires an eye movement to be directed towards the visual target.…”

mentioning

confidence: 99%

“…Given that the 'reverse' format provides a better estimate of working memory, we predicted that the 'reverse' format should correlate more reliably with AST errors than the 'forwards' version. Parkinson's disease (PD) is a relatively common neurodegenerative disorder that is also characterised by deficits of inhibitory control (Crawford et al 2002). We therefore examine whether these uncorrected AST errors are specific to AD or are a general feature of a neurodegenerative disorder.…”

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confidence: 99%

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The role of working memory and attentional disengagement on inhibitory control: effects of aging and Alzheimer's disease

Crawford

Higham²,

Mayes

et al. 2012

AGE

101

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Patients with Alzheimer's disease have an impairment of inhibitory control for reasons that are currently unclear. Using an eye-tracking task (the gapoverlap paradigm), we examined whether the uncorrected errors relate to the task of attentional disengagement in preparation for action. Alternatively, the difficulty in correcting for errors may be caused by the working memory representation of the task. A major aim of this study was to distinguish between the effects of healthy aging and neurodegenerative disease on the voluntary control of saccadic eye movements. Using the antisaccade task (AST) and pro-saccade task (PST) with the 'gap' and 'overlap' procedures, we obtained detailed eye-tracking measures in patients, with 18 patients with probable Alzheimer's disease, 25 patients with Parkinson's disease and 17 healthy young and 18 old participants. Uncorrected errors in the AST were selectively increased in Alzheimer's disease, but not in Parkinson's disease compared to the control groups. These uncorrected errors were strongly correlated with spatial working memory. There was an increase in the saccade reaction times to targets that were presented simultaneously with the fixation stimulus, compared to the removal of fixation. This 'gap' effect (i.e. overlap-gap) saccade reaction time was elevated in the older groups compared to young group, which yielded a strong effect of aging and no specific effect of neurodegenerative disease. Healthy aging, rather than neurodegenerative disease, accounted for the increase in the saccade reaction times to the target that are presented simultaneously with a fixation stimulus. These results suggest that the impairment of inhibitory control in the AST may provide a convenient and putative mark of working memory dysfunction in Alzheimer's disease.

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Section: Saccadic Eye Movements In Parkinson's Diseasementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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The role of working memory and attentional disengagement on inhibitory control: effects of aging and Alzheimer's disease

Crawford

Higham²,

Mayes

et al. 2012

AGE

101

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show abstract

“…These tasks have traditionally been viewed as sensitive and specific to PFCdl damage (Fuster, 1997;Malloy and Richardson, 1994). Poor performance in patients with schizophrenia is thought to reflect defective PFCdl programming of exploratory oculomotor activity (Karatekin and Asarnow, 1999), an impairment seen at a more elemental level in poor performance on delayed-saccade and anti-saccade tasks (Crawford et al, 2002;Curtis et al, 2001;Karoumi et al, 1998).…”

Section: Schizophreniamentioning

confidence: 99%

The dual origin hypothesis: An evolutionary brain-behavior framework for analyzing psychiatric disorders

Giaccio

2006

Neuroscience & Biobehavioral Reviews

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“…Everling and Fischer (1998) argued that antisaccade performance requires two intact subprocesses: 1) the ability to suppress a reflexive saccade towards the target; 2) the ability to generate a voluntary saccade in the opposite direction. In clinical research, increased antisaccade error rates are often interpreted as reflecting failures in inhibitory processing (Crawford, Bennett, Lekwuwa, Shaunak, & Deakin, 2002;Hutton et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Antisaccades in Dyslexic Children: Evidence for Immaturity of Oculomotor Cortical Structures

Bucci¹,

Nassibi²,

Gérard³

et al. 2012

Dyslexia - A Comprehensive and International Approach

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Cognition and the inhibitory control of saccades in schizophrenia and Parkinson's disease

Cited by 51 publications

References 114 publications

The role of working memory and attentional disengagement on inhibitory control: effects of aging and Alzheimer's disease

The role of working memory and attentional disengagement on inhibitory control: effects of aging and Alzheimer's disease

The dual origin hypothesis: An evolutionary brain-behavior framework for analyzing psychiatric disorders

Antisaccades in Dyslexic Children: Evidence for Immaturity of Oculomotor Cortical Structures

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