Deficits in saccadic eye-movement control in Parkinson's disease

In contrast to their slowed limb movements, individuals with Parkinson's disease (PD) produce rapid automatic eye movements to sensory stimuli and show an impaired ability to generate voluntary eye movements in cognitive tasks. Eighteen PD patients and 18 matched control volunteers were instruc...

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Veröffentlicht in:Neuropsychologia 2005, Vol.43 (5), p.784-796
Hauptverfasser: Chan, Florence, Armstrong, Irene T., Pari, Giovanna, Riopelle, Richard J., Munoz, Douglas P.
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container_title Neuropsychologia
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creator Chan, Florence
Armstrong, Irene T.
Pari, Giovanna
Riopelle, Richard J.
Munoz, Douglas P.
description In contrast to their slowed limb movements, individuals with Parkinson's disease (PD) produce rapid automatic eye movements to sensory stimuli and show an impaired ability to generate voluntary eye movements in cognitive tasks. Eighteen PD patients and 18 matched control volunteers were instructed to look either toward (pro-saccade) or away from (anti-saccade) a peripheral stimulus as soon as it appeared (immediate, gap and overlap conditions) or after a variable delay; or, they made sequential saccades to remembered targets after a variable delay. We found that PD patients made more express saccades (correct saccades in the latency range of 90–140 ms) in the immediate pro-saccade task, more direction errors (automatic pro-saccades) in the immediate anti-saccade task, and were less able to inhibit saccades during the delay period in all delay tasks. PD patients also made more directional and end-point errors in the memory-guided sequential task. Their inability to plan eye movements to remembered target locations suggests that PD patients have a deficit in spatial working memory which, along with their deficit in automatic saccade suppression, is consistent with a disorder of the prefrontal-basal ganglia circuit. Impairment of this pathway may release the automatic saccade system from top-down inhibition and produce deficits in volitional saccade control. Parallel findings across various motor, cognitive and oculomotor tasks suggest a common mechanism underlying a general deficit in automatic response suppression.
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Their inability to plan eye movements to remembered target locations suggests that PD patients have a deficit in spatial working memory which, along with their deficit in automatic saccade suppression, is consistent with a disorder of the prefrontal-basal ganglia circuit. Impairment of this pathway may release the automatic saccade system from top-down inhibition and produce deficits in volitional saccade control. 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Their inability to plan eye movements to remembered target locations suggests that PD patients have a deficit in spatial working memory which, along with their deficit in automatic saccade suppression, is consistent with a disorder of the prefrontal-basal ganglia circuit. Impairment of this pathway may release the automatic saccade system from top-down inhibition and produce deficits in volitional saccade control. 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Leukodystrophies. Prion diseases</topic><topic>Express saccades</topic><topic>Female</topic><topic>Frontal cortex</topic><topic>Gap effect</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Ocular Motility Disorders - etiology</topic><topic>Organic mental disorders. Neuropsychology</topic><topic>Parkinson Disease - physiopathology</topic><topic>Photic Stimulation - methods</topic><topic>Pro-saccades</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychomotor Performance - physiology</topic><topic>Psychopathology. Psychiatry</topic><topic>Reaction Time - physiology</topic><topic>Saccades - physiology</topic><topic>Task Performance and Analysis</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chan, Florence</creatorcontrib><creatorcontrib>Armstrong, Irene T.</creatorcontrib><creatorcontrib>Pari, Giovanna</creatorcontrib><creatorcontrib>Riopelle, Richard J.</creatorcontrib><creatorcontrib>Munoz, Douglas P.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropsychologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chan, Florence</au><au>Armstrong, Irene T.</au><au>Pari, Giovanna</au><au>Riopelle, Richard J.</au><au>Munoz, Douglas P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deficits in saccadic eye-movement control in Parkinson's disease</atitle><jtitle>Neuropsychologia</jtitle><addtitle>Neuropsychologia</addtitle><date>2005</date><risdate>2005</risdate><volume>43</volume><issue>5</issue><spage>784</spage><epage>796</epage><pages>784-796</pages><issn>0028-3932</issn><eissn>1873-3514</eissn><coden>NUPSA6</coden><abstract>In contrast to their slowed limb movements, individuals with Parkinson's disease (PD) produce rapid automatic eye movements to sensory stimuli and show an impaired ability to generate voluntary eye movements in cognitive tasks. 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subjects Adult
Adult and adolescent clinical studies
Aged
Aged, 80 and over
Anti-saccades
Attention - physiology
Basal ganglia
Biological and medical sciences
Case-Control Studies
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Express saccades
Female
Frontal cortex
Gap effect
Humans
Male
Medical sciences
Middle Aged
Neurology
Ocular Motility Disorders - etiology
Organic mental disorders. Neuropsychology
Parkinson Disease - physiopathology
Photic Stimulation - methods
Pro-saccades
Psychology. Psychoanalysis. Psychiatry
Psychomotor Performance - physiology
Psychopathology. Psychiatry
Reaction Time - physiology
Saccades - physiology
Task Performance and Analysis
Time Factors
title Deficits in saccadic eye-movement control in Parkinson's disease
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