Reliability of smooth pursuit, fixation, and saccadic eye movements

Ettinger, Ulrich; Kumari, Veena; Crawford, Trevor J.; Davis, Robert E.; Sharma, Tonmoy; Corr, Philip J.

doi:10.1111/1469-8986.00063

Cited by 148 publications

(177 citation statements)

References 62 publications

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“…This interpretation also clarifies the failure to observe facilitatory effects of nicotine on antisaccade performance in a subgroup of schizophrenic patients who did not have abnormally increased antisaccade errors (Larrison-Faucher, 2004, and the fact that, in general, facilitatory effects of nicotine on antisaccade performance have been more consistently observed in patients with schizophrenia (who have high baseline levels of antisaccade errors) compared to healthy controls (Roos et al 1995;Depatie et al 2002). This interpretation is also consistent with the finding that participants with poor antisaccade performance benefit most from practice effects (Ettinger et al 2003b).…”

Section: Discussionsupporting

confidence: 75%

“…Ettinger et al, 2003b). One explanation of our findings, and those described above, is that any facilitatory effects of nicotine are more likely to be observed when performance is least optimal -as practice improves performance towards the higher end of the range of possible scores, ceiling effects reduce the potential for nicotine to induce any further improvements.…”

Section: Discussionsupporting

confidence: 50%

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The antisaccade task as an index of sustained goal activation in working memory: modulation by nicotine

2006

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Article (Unspecified) http://sro.sussex.ac.uk Rycroft, Nicola, Hutton, Samuel B. and Rusted, Jennifer M. (2006) The antisaccade task as an index of sustained goal activation in working memory: modulation by nicotine. Psychopharmacology, 188 (4). pp. [521][522][523][524][525][526][527][528][529] This version is available from Sussex Research Online: http://sro.sussex.ac.uk/738/ This document is made available in accordance with publisher policies and may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the URL above for details on accessing the published version. Copyright and reuse:Sussex Research Online is a digital repository of the research output of the University.Copyright and all moral rights to the version of the paper presented here belong to the individual author(s) and/or other copyright owners. To the extent reasonable and practicable, the material made available in SRO has been checked for eligibility before being made available.Copies of full text items generally can be reproduced, displayed or performed and given to third parties in any format or medium for personal research or study, educational, or not-for-profit purposes without prior permission or charge, provided that the authors, title and full bibliographic details are credited, a hyperlink and/or URL is given for the original metadata page and the content is not changed in any way. Recent models of antisaccade performance suggest that errors are more likely to occur when the intention to initiate an antisaccade is insufficiently activated within working memory. Nicotine has been shown to enhance specific working memory processes in healthy adults. We explored the effect of nicotine on antisaccade performance in a large sample (N=44) of young adult smokers. Minimally abstinent participants attended two test sessions and were asked to smoke one of their own cigarettes between baseline and retest during one session only.Nicotine reduced antisaccade errors and correct antisaccade latencies if delivered before optimum performance levels are achieved, suggesting that nicotine supports the activation of intentions in working memory during task performance. The implications of this research for current theoretical accounts of antisaccade performance, and for interpreting the increased rate of antisaccade errors found in some psychiatric patient groups are discussed.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionsupporting

confidence: 50%

The antisaccade task as an index of sustained goal activation in working memory: modulation by nicotine

2006

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“…However, these variables were estimated at different times and only once in each participant. Nonetheless, high test-retest reliability of our inhibition measures (Ettinger et al, 2003;Logan et al, 1984) as well as of DBP ND to d-amph (Kegeles et al, 1999) supports the interpretation that dopaminergic dysfunction is related to response inhibition deficits in ADHD. (2) Our sample size had power to detect only associations of a medium to large effect size, given the Bonferroni correction for multiple comparisons.…”

Section: Discussionsupporting

confidence: 64%

Amphetamine-Induced Dopamine Release and Neurocognitive Function in Treatment-Naive Adults with ADHD

Cherkasova

Faridi

Casey

et al. 2013

Neuropsychopharmacol

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Converging evidence from clinical, preclinical, neuroimaging, and genetic research implicates dopamine neurotransmission in the pathophysiology of attention deficit hyperactivity disorder (ADHD). The in vivo neuroreceptor imaging evidence also suggests alterations in the dopamine system in ADHD; however, the nature and behavioral significance of those have not yet been established. Here, we investigated striatal dopaminergic function in ADHD using [ 11 C]raclopride PET with a d-amphetamine challenge. We also examined the relationship of striatal dopamine responses to ADHD symptoms and neurocognitive function. A total of 15 treatment-free, noncomorbid adult males with ADHD (age: 29.87±8.65) and 18 healthy male controls (age: 25.44±6.77) underwent two PET scans: one following a lactose placebo and the other following d-amphetamine (0.3 mg/kg, p.o.), administered double blind and in random order counterbalanced across groups. In a separate session without a drug, participants performed a battery of neurocognitive tests. Relative to the healthy controls, the ADHD patients, as a group, showed greater d-amphetamine-induced decreases in striatal [ 11 C]raclopride binding and performed more poorly on measures of response inhibition. Across groups, a greater magnitude of d-amphetamine-induced change in [ 11 C]raclopride binding potential was associated with poorer performance on measures of response inhibition and ADHD symptoms. Our findings suggest an augmented striatal dopaminergic response in treatment-naive ADHD. Though in contrast to results of a previous study, this finding appears consistent with a model proposing exaggerated phasic dopamine release in ADHD. A susceptibility to increased phasic dopamine responsivity may contribute to such characteristics of ADHD as poor inhibition and impulsivity.

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“…Previous studies have shown temporally stable SPEM performance in schizophrenic patients and healthy individuals in the absence of between-session improvements (Gooding et al, 1994). We have recently demonstrated robust practice effects on antisaccade, but not SPEM measures in healthy individuals over a period of about 2 months (Ettinger et al, 2003).…”

Section: Effects Of Procyclidinementioning

confidence: 56%

“…Eye-blinks in all tasks were identified by visual inspection of position and velocity charts. The oculomotor tasks used here have very good temporal stability and internal consistency (Ettinger et al, 2003).…”

Section: Eye Movement Analysismentioning

confidence: 99%

Effects of Procyclidine on Eye Movements in Schizophrenia

Ettinger

Kumari²,

Zachariah³

et al. 2003

Neuropsychopharmacol

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Smooth pursuit eye movement (SPEM) and antisaccade deficits are observed in the schizophrenia spectrum and have been used to study the pathophysiology as well as the genetic basis of this condition. The neurotransmitter acetylcholine has been implicated in a number of cognitive processes thought to underlie SPEM and antisaccade performance. This study investigates effects on eye movements of procyclidine, an anticholinergic drug often administered to schizophrenic patients. A total of 13 patients completed a double-blind placebo-controlled crossover design, receiving 15 mg procyclidine and placebo. Seven participants received procyclidine first and placebo second, six participants were tested in the reverse order. SPEM and antisaccade (as well as fixation and prosaccade) eye movements were recorded using infrared oculography. Results showed that procyclidine overall, relative to placebo, mildly worsened SPEM performance, as indicated by nonsignificantly reduced gain (p ¼ 0.08) and increased frequency of intrusive anticipatory saccades during pursuit (p ¼ 0.06). A significant interaction of group and order of administration indicated that procyclidine increased the rate of antisaccade reflexive errors only when administered first; the opposite pattern was observed when placebo was administered first, likely due to the operation of practice effects at second assessment. These findings indicate that acute administration of a clinically relevant dose of procyclidine leads to mild impairments in eye movement performance in schizophrenic patients, suggesting the need to consider this compound in oculomotor studies in schizophrenia. The action of this anticholinergic drug on oculomotor performance is consistent with the hypothesized role of the cholinergic system in the cognitive mechanisms of attention and working memory, processes thought to underlie SPEM and antisaccade performance. Effects of order of administration and practice on the antisaccade task suggest that these factors need to be taken into consideration in future pharmacological studies.

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Reliability of smooth pursuit, fixation, and saccadic eye movements

Cited by 148 publications

References 62 publications

The antisaccade task as an index of sustained goal activation in working memory: modulation by nicotine

The antisaccade task as an index of sustained goal activation in working memory: modulation by nicotine

Amphetamine-Induced Dopamine Release and Neurocognitive Function in Treatment-Naive Adults with ADHD

Effects of Procyclidine on Eye Movements in Schizophrenia

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