Motor imagery in Parkinson's disease: A PET study
Identifieur interne : 002916 ( PascalFrancis/Corpus ); précédent : 002915; suivant : 002917Motor imagery in Parkinson's disease: A PET study
Auteurs : R. Cunnington ; G. F. Egan ; J. D. O'Sullivan ; A. J. Hughes ; J. L. Bradshaw ; J. G. ColebatchSource :
- Movement disorders [ 0885-3185 ] ; 2001.
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- Pascal (Inist)
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Abstract
We used positron emission tomography (PET) with 15 O-labelled water to record patterns of cerebral activation in six patients with Parkinson's disease (PD), studied when clinically "off' and after turning "on" as a result of dopaminergic stimulation. They were asked to imagine a finger opposition movement performed with their right hand, externally paced at a rate of 1 Hz. Trials alternating between motor imagery and rest were measured. A pilot study of three age-matched controls was also performed. We chose the task as a robust method of activating the supplementary motor area (SMA), defects of which have been reported in PD. The PD patients showed normal degrees of activation of the SMA (proper) when both "off" and "on." Significant activation with imagining movement also occurred in the ipsilateral inferior parietal cortex (both "off" and when "on") and ipsilateral premotor cortex (when "off" only). The patients showed significantly greater activation of the rostral anterior cingulate and significantly less activation of the left lingual gyrus and precuneus when performing the task "on" compared with their performance when "off." PD patients when imagining movement and "off showed less activation of several sites including the right dorsolateral prefrontal cortex (DLPFC) when compared to the controls performing the same task. No significant differences from controls were present when the patients imagined when "on." Our results are consistent with other studies showing deficits of pre-SMA function in PD with preserved function of the SMA proper. In addition to the areas of reduced activation (anterior cingulate, DLPFC), there were also sites of activation (ipsilateral premotor and inferior parietal cortex) previously reported as locations of compensatory overactivity for PD patients performing similar tasks. Both failure of activation and compensatory changes are likely to contribute to the motor deficit in PD.
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Format Inist (serveur)
| NO : | PASCAL 02-0050588 INIST |
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| ET : | Motor imagery in Parkinson's disease: A PET study |
| AU : | CUNNINGTON (R.); EGAN (G. F.); O'SULLIVAN (J. D.); HUGHES (A. J.); BRADSHAW (J. L.); COLEBATCH (J. G.) |
| AF : | Neuropsychology Research Unit, Department of Psychology, Monash University/Clayton, Victoria/Australie (1 aut., 5 aut.); Howard Florey Research Institute, University of Melbourne/Parkville, Victoria/Australie (2 aut.); Centre for Positron Emission Tomography, Austin and Repatriation Medical Centre/Heidelberg, Victoria/Australie (2 aut.); Department of Neurology, Austin and Repatriation Medical Centre/Heidelberg, Victoria/Australie (3 aut., 4 aut.); Institute of Neurological Sciences and School of Medicine, Prince of Wales Hospital/Randwick, Sydney, NSW/Australie (6 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 5; Pp. 849-857; Bibl. 51 ref. |
| LA : | Anglais |
| EA : | We used positron emission tomography (PET) with 15 O-labelled water to record patterns of cerebral activation in six patients with Parkinson's disease (PD), studied when clinically "off' and after turning "on" as a result of dopaminergic stimulation. They were asked to imagine a finger opposition movement performed with their right hand, externally paced at a rate of 1 Hz. Trials alternating between motor imagery and rest were measured. A pilot study of three age-matched controls was also performed. We chose the task as a robust method of activating the supplementary motor area (SMA), defects of which have been reported in PD. The PD patients showed normal degrees of activation of the SMA (proper) when both "off" and "on." Significant activation with imagining movement also occurred in the ipsilateral inferior parietal cortex (both "off" and when "on") and ipsilateral premotor cortex (when "off" only). The patients showed significantly greater activation of the rostral anterior cingulate and significantly less activation of the left lingual gyrus and precuneus when performing the task "on" compared with their performance when "off." PD patients when imagining movement and "off showed less activation of several sites including the right dorsolateral prefrontal cortex (DLPFC) when compared to the controls performing the same task. No significant differences from controls were present when the patients imagined when "on." Our results are consistent with other studies showing deficits of pre-SMA function in PD with preserved function of the SMA proper. In addition to the areas of reduced activation (anterior cingulate, DLPFC), there were also sites of activation (ipsilateral premotor and inferior parietal cortex) previously reported as locations of compensatory overactivity for PD patients performing similar tasks. Both failure of activation and compensatory changes are likely to contribute to the motor deficit in PD. |
| CC : | 002B17G; 235 |
| FD : | Parkinson maladie; Imagerie mentale; Mouvement corporel; Tomographie émission positon; Aire motrice supplémentaire; Activation; Personne âgée |
| FG : | Homme; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique |
| ED : | Parkinson disease; Mental imagery; Body movement; Positron emission tomography; Supplementary motor area; Activation; Elderly |
| EG : | Human; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study |
| SD : | Parkinson enfermedad; Imaginería mental; Movimiento corporal; Tomografía emisión positrones; Area motriz suplementaria; Activación; Anciano |
| LO : | INIST-20953.354000099256460070 |
| ID : | 02-0050588 |
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Colebatch</name><affiliation><inist:fA14 i1="05"><s1>Institute of Neurological Sciences and School of Medicine, Prince of Wales Hospital</s1><s2>Randwick, Sydney, NSW</s2><s3>AUS</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">02-0050588</idno><date when="2001">2001</date><idno type="stanalyst">PASCAL 02-0050588 INIST</idno><idno type="RBID">Pascal:02-0050588</idno><idno type="wicri:Area/PascalFrancis/Corpus">002916</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Motor imagery in Parkinson's disease: A PET study</title><author><name sortKey="Cunnington, R" sort="Cunnington, R" uniqKey="Cunnington R" first="R." last="Cunnington">R. Cunnington</name><affiliation><inist:fA14 i1="01"><s1>Neuropsychology Research Unit, Department of Psychology, Monash University</s1><s2>Clayton, Victoria</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Egan, G F" sort="Egan, G F" uniqKey="Egan G" first="G. F." last="Egan">G. F. Egan</name><affiliation><inist:fA14 i1="02"><s1>Howard Florey Research Institute, University of Melbourne</s1><s2>Parkville, Victoria</s2><s3>AUS</s3><sZ>2 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Centre for Positron Emission Tomography, Austin and Repatriation Medical Centre</s1><s2>Heidelberg, Victoria</s2><s3>AUS</s3><sZ>2 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="O Sullivan, J D" sort="O Sullivan, J D" uniqKey="O Sullivan J" first="J. D." last="O'Sullivan">J. D. O'Sullivan</name><affiliation><inist:fA14 i1="04"><s1>Department of Neurology, Austin and Repatriation Medical Centre</s1><s2>Heidelberg, Victoria</s2><s3>AUS</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hughes, A J" sort="Hughes, A J" uniqKey="Hughes A" first="A. J." last="Hughes">A. J. Hughes</name><affiliation><inist:fA14 i1="04"><s1>Department of Neurology, Austin and Repatriation Medical Centre</s1><s2>Heidelberg, Victoria</s2><s3>AUS</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Bradshaw, J L" sort="Bradshaw, J L" uniqKey="Bradshaw J" first="J. L." last="Bradshaw">J. L. Bradshaw</name><affiliation><inist:fA14 i1="01"><s1>Neuropsychology Research Unit, Department of Psychology, Monash University</s1><s2>Clayton, Victoria</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Colebatch, J G" sort="Colebatch, J G" uniqKey="Colebatch J" first="J. G." last="Colebatch">J. G. Colebatch</name><affiliation><inist:fA14 i1="05"><s1>Institute of Neurological Sciences and School of Medicine, Prince of Wales Hospital</s1><s2>Randwick, Sydney, NSW</s2><s3>AUS</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2001">2001</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Activation</term><term>Body movement</term><term>Elderly</term><term>Mental imagery</term><term>Parkinson disease</term><term>Positron emission tomography</term><term>Supplementary motor area</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Parkinson maladie</term><term>Imagerie mentale</term><term>Mouvement corporel</term><term>Tomographie émission positon</term><term>Aire motrice supplémentaire</term><term>Activation</term><term>Personne âgée</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We used positron emission tomography (PET) with <sup>15</sup> O-labelled water to record patterns of cerebral activation in six patients with Parkinson's disease (PD), studied when clinically "off' and after turning "on" as a result of dopaminergic stimulation. They were asked to imagine a finger opposition movement performed with their right hand, externally paced at a rate of 1 Hz. Trials alternating between motor imagery and rest were measured. A pilot study of three age-matched controls was also performed. We chose the task as a robust method of activating the supplementary motor area (SMA), defects of which have been reported in PD. The PD patients showed normal degrees of activation of the SMA (proper) when both "off" and "on." Significant activation with imagining movement also occurred in the ipsilateral inferior parietal cortex (both "off" and when "on") and ipsilateral premotor cortex (when "off" only). The patients showed significantly greater activation of the rostral anterior cingulate and significantly less activation of the left lingual gyrus and precuneus when performing the task "on" compared with their performance when "off." PD patients when imagining movement and "off showed less activation of several sites including the right dorsolateral prefrontal cortex (DLPFC) when compared to the controls performing the same task. No significant differences from controls were present when the patients imagined when "on." Our results are consistent with other studies showing deficits of pre-SMA function in PD with preserved function of the SMA proper. In addition to the areas of reduced activation (anterior cingulate, DLPFC), there were also sites of activation (ipsilateral premotor and inferior parietal cortex) previously reported as locations of compensatory overactivity for PD patients performing similar tasks. Both failure of activation and compensatory changes are likely to contribute to the motor deficit in PD.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>16</s2></fA05><fA06><s2>5</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Motor imagery in Parkinson's disease: A PET study</s1></fA08><fA11 i1="01" i2="1"><s1>CUNNINGTON (R.)</s1></fA11><fA11 i1="02" i2="1"><s1>EGAN (G. F.)</s1></fA11><fA11 i1="03" i2="1"><s1>O'SULLIVAN (J. D.)</s1></fA11><fA11 i1="04" i2="1"><s1>HUGHES (A. J.)</s1></fA11><fA11 i1="05" i2="1"><s1>BRADSHAW (J. L.)</s1></fA11><fA11 i1="06" i2="1"><s1>COLEBATCH (J. G.)</s1></fA11><fA14 i1="01"><s1>Neuropsychology Research Unit, Department of Psychology, Monash University</s1><s2>Clayton, Victoria</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Howard Florey Research Institute, University of Melbourne</s1><s2>Parkville, Victoria</s2><s3>AUS</s3><sZ>2 aut.</sZ></fA14><fA14 i1="03"><s1>Centre for Positron Emission Tomography, Austin and Repatriation Medical Centre</s1><s2>Heidelberg, Victoria</s2><s3>AUS</s3><sZ>2 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Neurology, Austin and Repatriation Medical Centre</s1><s2>Heidelberg, Victoria</s2><s3>AUS</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="05"><s1>Institute of Neurological Sciences and School of Medicine, Prince of Wales Hospital</s1><s2>Randwick, Sydney, NSW</s2><s3>AUS</s3><sZ>6 aut.</sZ></fA14><fA20><s1>849-857</s1></fA20><fA21><s1>2001</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000099256460070</s5></fA43><fA44><s0>0000</s0><s1>© 2002 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>51 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>02-0050588</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>We used positron emission tomography (PET) with <sup>15</sup> O-labelled water to record patterns of cerebral activation in six patients with Parkinson's disease (PD), studied when clinically "off' and after turning "on" as a result of dopaminergic stimulation. They were asked to imagine a finger opposition movement performed with their right hand, externally paced at a rate of 1 Hz. Trials alternating between motor imagery and rest were measured. A pilot study of three age-matched controls was also performed. We chose the task as a robust method of activating the supplementary motor area (SMA), defects of which have been reported in PD. The PD patients showed normal degrees of activation of the SMA (proper) when both "off" and "on." Significant activation with imagining movement also occurred in the ipsilateral inferior parietal cortex (both "off" and when "on") and ipsilateral premotor cortex (when "off" only). The patients showed significantly greater activation of the rostral anterior cingulate and significantly less activation of the left lingual gyrus and precuneus when performing the task "on" compared with their performance when "off." PD patients when imagining movement and "off showed less activation of several sites including the right dorsolateral prefrontal cortex (DLPFC) when compared to the controls performing the same task. No significant differences from controls were present when the patients imagined when "on." Our results are consistent with other studies showing deficits of pre-SMA function in PD with preserved function of the SMA proper. In addition to the areas of reduced activation (anterior cingulate, DLPFC), there were also sites of activation (ipsilateral premotor and inferior parietal cortex) previously reported as locations of compensatory overactivity for PD patients performing similar tasks. 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F.); O'SULLIVAN (J. D.); HUGHES (A. J.); BRADSHAW (J. L.); COLEBATCH (J. G.)</AU><AF>Neuropsychology Research Unit, Department of Psychology, Monash University/Clayton, Victoria/Australie (1 aut., 5 aut.); Howard Florey Research Institute, University of Melbourne/Parkville, Victoria/Australie (2 aut.); Centre for Positron Emission Tomography, Austin and Repatriation Medical Centre/Heidelberg, Victoria/Australie (2 aut.); Department of Neurology, Austin and Repatriation Medical Centre/Heidelberg, Victoria/Australie (3 aut., 4 aut.); Institute of Neurological Sciences and School of Medicine, Prince of Wales Hospital/Randwick, Sydney, NSW/Australie (6 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 5; Pp. 849-857; Bibl. 51 ref.</SO><LA>Anglais</LA><EA>We used positron emission tomography (PET) with <sup>15</sup> O-labelled water to record patterns of cerebral activation in six patients with Parkinson's disease (PD), studied when clinically "off' and after turning "on" as a result of dopaminergic stimulation. They were asked to imagine a finger opposition movement performed with their right hand, externally paced at a rate of 1 Hz. Trials alternating between motor imagery and rest were measured. A pilot study of three age-matched controls was also performed. We chose the task as a robust method of activating the supplementary motor area (SMA), defects of which have been reported in PD. The PD patients showed normal degrees of activation of the SMA (proper) when both "off" and "on." Significant activation with imagining movement also occurred in the ipsilateral inferior parietal cortex (both "off" and when "on") and ipsilateral premotor cortex (when "off" only). The patients showed significantly greater activation of the rostral anterior cingulate and significantly less activation of the left lingual gyrus and precuneus when performing the task "on" compared with their performance when "off." PD patients when imagining movement and "off showed less activation of several sites including the right dorsolateral prefrontal cortex (DLPFC) when compared to the controls performing the same task. No significant differences from controls were present when the patients imagined when "on." Our results are consistent with other studies showing deficits of pre-SMA function in PD with preserved function of the SMA proper. In addition to the areas of reduced activation (anterior cingulate, DLPFC), there were also sites of activation (ipsilateral premotor and inferior parietal cortex) previously reported as locations of compensatory overactivity for PD patients performing similar tasks. Both failure of activation and compensatory changes are likely to contribute to the motor deficit in PD.</EA><CC>002B17G; 235</CC><FD>Parkinson maladie; Imagerie mentale; Mouvement corporel; Tomographie émission positon; Aire motrice supplémentaire; Activation; Personne âgée</FD><FG>Homme; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique</FG><ED>Parkinson disease; Mental imagery; Body movement; Positron emission tomography; Supplementary motor area; Activation; Elderly</ED><EG>Human; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study</EG><SD>Parkinson enfermedad; Imaginería mental; Movimiento corporal; Tomografía emisión positrones; Area motriz suplementaria; Activación; Anciano</SD><LO>INIST-20953.354000099256460070</LO><ID>02-0050588</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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