{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T11:15:44Z","timestamp":1753874144938,"version":"3.41.2"},"reference-count":55,"publisher":"AIP Publishing","issue":"1","content-domain":{"domain":["pubs.aip.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,1,1]]},"abstract":"<jats:p>Huntington's disease (HD), a genetically determined neurodegenerative disease, is positively correlated with eye movement abnormalities in decision making. The antisaccade conflict paradigm has been widely used to study response inhibition in eye movements, and reliable performance deficits in HD subjects have been observed, including a greater number and timing of direction errors. We recorded the error rates and response latencies of early HD patients and healthy age-matched controls performing the mirror antisaccade task. HD participants displayed slower and more variable antisaccade latencies and increased error rates relative to healthy controls. A competitive accumulator-to-threshold neural model was then employed to quantitatively simulate the controls' and patients' reaction latencies and error rates and uncover the mechanisms giving rise to the observed HD antisaccade deficits. Our simulations showed that (1) a more gradual and noisy rate of accumulation of evidence by HD patients is responsible for the observed prolonged and more variable antisaccade latencies in early HD; (2) the confidence level of early HD patients making a decision is unaffected by the disease; and (3) the antisaccade performance of healthy controls and early HD patients is the end product of a neural lateral competition (inhibition) between a correct and an erroneous decision process, and not the end product of a third top-down stop signal suppressing the erroneous decision process as many have speculated.<\/jats:p>","DOI":"10.1063\/5.0021584","type":"journal-article","created":{"date-parts":[[2021,1,12]],"date-time":"2021-01-12T08:41:51Z","timestamp":1610440911000},"update-policy":"https:\/\/doi.org\/10.1063\/aip-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["Neural modeling of antisaccade performance of healthy controls and early Huntington's disease patients"],"prefix":"10.1063","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9005-0260","authenticated-orcid":false,"given":"Vassilis","family":"Cutsuridis","sequence":"first","affiliation":[{"name":"School of Computer Science, University of Lincoln 1 , Lincoln LN6 7TS, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shouyong","family":"Jiang","sequence":"additional","affiliation":[{"name":"School of Computer Science, University of Lincoln 1 , Lincoln LN6 7TS, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0295-2182","authenticated-orcid":false,"given":"Matt J.","family":"Dunn","sequence":"additional","affiliation":[{"name":"School of Optometry and Vision Sciences, Cardiff University 2 , Cardiff CF24 4HQ, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4716-4753","authenticated-orcid":false,"given":"Anne","family":"Rosser","sequence":"additional","affiliation":[{"name":"Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University 3 , Cardiff CF14 4XN, United Kingdom"},{"name":"Cardiff Brain Repair Group, School of Biosciences 4 , Museum Avenue, Cardiff CF10 3AX, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James","family":"Brawn","sequence":"additional","affiliation":[{"name":"School of Optometry and Vision Sciences, Cardiff University 2 , Cardiff CF24 4HQ, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jonathan T.","family":"Erichsen","sequence":"additional","affiliation":[{"name":"School of Optometry and Vision Sciences, Cardiff University 2 , Cardiff CF24 4HQ, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"317","published-online":{"date-parts":[[2021,1,11]]},"reference":[{"key":"2023080720124519700_c1","doi-asserted-by":"publisher","first-page":"165","DOI":"10.1111\/j.1750-3639.2012.00629.x","article-title":"Degeneration of the cerebellum in Huntington\u2019s disease (HD): Possible relevance for the clinical picture and potential gateway to pathological mechanisms of the disease process","volume":"23","year":"2013","journal-title":"Brain Pathol."},{"key":"2023080720124519700_c2","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1007\/978-3-319-71779-1_1","article-title":"Clinical features of Huntington\u2019s disease","volume":"1049","year":"2018","journal-title":"Adv. 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