Deficits in saccadic eye-movement control in Parkinson's disease
Identifieur interne : 000925 ( PascalFrancis/Corpus ); précédent : 000924; suivant : 000926Deficits in saccadic eye-movement control in Parkinson's disease
Auteurs : Florence Chan ; Irene T. Armstrong ; Giovanna Pari ; Richard J. Riopelle ; Douglas P. MunozSource :
- Neuropsychologia [ 0028-3932 ] ; 2005.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Format Inist (serveur)
NO : | PASCAL 05-0165101 INIST |
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ET : | Deficits in saccadic eye-movement control in Parkinson's disease |
AU : | CHAN (Florence); ARMSTRONG (Irene T.); PARI (Giovanna); RIOPELLE (Richard J.); MUNOZ (Douglas P.) |
AF : | Centre for Neuroscience Studies, Queen's University/Kingston, Ont., K7L 3N6/Canada (1 aut., 2 aut., 3 aut., 4 aut., 5 aut.); Department of Physiology, Centre for Neuroscience Studies, Queen's University/Kingston, Ont., K7L 3N6/Canada (1 aut., 2 aut., 5 aut.); Department of Medicine, Centre for Neuroscience Studies, Queen's University/Kingston, Ont., K7L 3N6/Canada (3 aut., 4 aut.); Department of Psychology, Centre for Neuroscience Studies, Queen's University/Kingston, Ont., K7L 3N6/Canada (5 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Neuropsychologia; ISSN 0028-3932; Coden NUPSA6; Royaume-Uni; Da. 2005; Vol. 43; No. 5; Pp. 784-796; Bibl. 2 p.1/4 |
LA : | Anglais |
EA : | 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. |
CC : | 002B18C13; 002B17G |
FD : | Parkinson maladie; Mouvement oculaire saccadé; Cortex frontal; Contrôle volontaire; Inhibition; Mémoire; Noyau gris central; Homme |
FG : | Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Encéphale; Système nerveux central |
ED : | Parkinson disease; Saccadic eye movement; Frontal cortex; Voluntary control; Inhibition; Memory; Basal ganglion; Human |
EG : | Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Encephalon; Central nervous system |
SD : | Parkinson enfermedad; Movimiento ocular brusco; Corteza frontal; Control voluntario; Inhibición; Memoria; Núcleo basal; Hombre |
LO : | INIST-11143.354000125006590130 |
ID : | 05-0165101 |
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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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<s5>13</s5>
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<s5>13</s5>
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<s5>13</s5>
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<s5>19</s5>
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<s5>19</s5>
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<s5>37</s5>
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<s5>40</s5>
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<s5>40</s5>
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<s5>41</s5>
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<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
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<s5>45</s5>
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<s5>45</s5>
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<s5>45</s5>
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<s5>46</s5>
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<s5>46</s5>
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<s5>46</s5>
</fC07>
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<server><NO>PASCAL 05-0165101 INIST</NO>
<ET>Deficits in saccadic eye-movement control in Parkinson's disease</ET>
<AU>CHAN (Florence); ARMSTRONG (Irene T.); PARI (Giovanna); RIOPELLE (Richard J.); MUNOZ (Douglas P.)</AU>
<AF>Centre for Neuroscience Studies, Queen's University/Kingston, Ont., K7L 3N6/Canada (1 aut., 2 aut., 3 aut., 4 aut., 5 aut.); Department of Physiology, Centre for Neuroscience Studies, Queen's University/Kingston, Ont., K7L 3N6/Canada (1 aut., 2 aut., 5 aut.); Department of Medicine, Centre for Neuroscience Studies, Queen's University/Kingston, Ont., K7L 3N6/Canada (3 aut., 4 aut.); Department of Psychology, Centre for Neuroscience Studies, Queen's University/Kingston, Ont., K7L 3N6/Canada (5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuropsychologia; ISSN 0028-3932; Coden NUPSA6; Royaume-Uni; Da. 2005; Vol. 43; No. 5; Pp. 784-796; Bibl. 2 p.1/4</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B18C13; 002B17G</CC>
<FD>Parkinson maladie; Mouvement oculaire saccadé; Cortex frontal; Contrôle volontaire; Inhibition; Mémoire; Noyau gris central; Homme</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Encéphale; Système nerveux central</FG>
<ED>Parkinson disease; Saccadic eye movement; Frontal cortex; Voluntary control; Inhibition; Memory; Basal ganglion; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Encephalon; Central nervous system</EG>
<SD>Parkinson enfermedad; Movimiento ocular brusco; Corteza frontal; Control voluntario; Inhibición; Memoria; Núcleo basal; Hombre</SD>
<LO>INIST-11143.354000125006590130</LO>
<ID>05-0165101</ID>
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