Deficits in saccadic eye-movement control in Parkinson's disease.
Identifieur interne : 000507 ( Ncbi/Curation ); précédent : 000506; suivant : 000508Deficits in saccadic eye-movement control in Parkinson's disease.
Auteurs : Florence Chan [Canada] ; Irene T. Armstrong ; Giovanna Pari ; Richard J. Riopelle ; Douglas P. MunozSource :
- Neuropsychologia [ 0028-3932 ] ; 2005.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Attention (physiology), Case-Control Studies, Female, Humans, Male, Middle Aged, Ocular Motility Disorders (etiology), Parkinson Disease (physiopathology), Photic Stimulation (methods), Psychomotor Performance (physiology), Reaction Time (physiology), Saccades (physiology), Task Performance and Analysis, Time Factors.
- MESH :
- etiology : Ocular Motility Disorders.
- methods : Photic Stimulation.
- physiology : Attention, Psychomotor Performance, Reaction Time, Saccades.
- physiopathology : Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Case-Control Studies, Female, Humans, Male, Middle Aged, Task Performance and Analysis, Time Factors.
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. 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.
DOI: 10.1016/j.neuropsychologia.2004.06.026
PubMed: 15721191
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pubmed:15721191Le document en format XML
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<term>Ocular Motility Disorders (etiology)</term>
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<term>Photic Stimulation (methods)</term>
<term>Psychomotor Performance (physiology)</term>
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<front><div type="abstract" xml:lang="en">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.</div>
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