Stimulation of the subthalamic nucleus in Parkinson's disease does not produce striatal dopamine release. Commentary
Identifieur interne : 000A29 ( PascalFrancis/Corpus ); précédent : 000A28; suivant : 000A30Stimulation of the subthalamic nucleus in Parkinson's disease does not produce striatal dopamine release. Commentary
Auteurs : Aviva Abosch ; Shitij Kapur ; Anthony E. Lang ; Doug Hussey ; Elspeth Sime ; Janis Miyasaki ; Svlvain Houle ; Andres M. Lozano ; Philip Starr ; Giovanni Broggi ; Roy A. E. Bakay ; Nicholas Boulis ; Ali R. RezaiSource :
- Neurosurgery [ 0148-396X ] ; 2003.
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- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
OBJECTIVE: The subthalamic nucleus (STN) is a target in the surgical treatment of Parkinson's disease (PD). The mechanism by which electrical stimulation of the STN ameliorates symptoms of PD remains unknown. One consistent aspect of STN stimulation is the ability to reduce the dosage of dopaminergic medications; sometimes they can be eliminated altogether. Furthermore, nigrostriatal projection axons are apposed to the dorsal surface of the STN and are likely affected by the application of current in this region. We sought to determine whether STN stimulation could release endogenous striatal dopamine. METHODS: Five patients with PD, who had previously undergone surgical implantation of bilateral STN stimulators, underwent [11C]raclopride positron emission tomographic scanning. L-dopa was withheld for 12 hours, and both stimulators were turned off 9 hours before scanning. We assayed for striatal dopamine release by measuring radioligand displacement as a consequence of turning on the right STN stimulator after 45 minutes of a 90-minute [11C]raclopride infusion. Patients were evaluated with the motor section of the Unified Parkinson's Disease Rating Scale before and after the studies. RESULTS: Comparisons between the right and left striata, before and after right STN stimulation, demonstrated no significant differences in [11C]raclopride binding, despite significant improvements in Unified Parkinson's Disease Rating Scale motor scores with unilateral stimulation (mean improvement, 26.0 ± 16.4%; P < 0.05). This finding was also noted when the striatum was partitioned into dorsal and ventral caudate and putamen and the four regions were analyzed separately. CONCLUSION: Our results suggest that STN stimulation does not mediate its anti-PD effects via the release of dopamine, as assessed with [11C]raclopride displacement.
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| NO : | PASCAL 04-0104974 INIST |
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| ET : | Stimulation of the subthalamic nucleus in Parkinson's disease does not produce striatal dopamine release. Commentary |
| AU : | ABOSCH (Aviva); KAPUR (Shitij); LANG (Anthony E.); HUSSEY (Doug); SIME (Elspeth); MIYASAKI (Janis); HOULE (Svlvain); LOZANO (Andres M.); STARR (Philip); BROGGI (Giovanni); BAKAY (Roy A. E.); BOULIS (Nicholas); REZAI (Ali R.) |
| AF : | Department of Surgery, Division of Neurosurgery, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital/Toronto, Ontario/Canada (1 aut., 5 aut., 8 aut.); University Health Network, University of Toronto/Toronto, Ontario/Canada (1 aut., 2 aut., 3 aut., 4 aut., 6 aut., 7 aut., 8 aut.); PET Centre, Department of Psychiatry and Centre for Addiction and Mental Health/Toronto, Ontario/Canada (2 aut., 4 aut.); Department of Medicine, Division of Neurology, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital/Toronto, Ontario/Canada (3 aut., 6 aut.); PET Centre, Department of Psychiatry and Centre for Addiction and Mental Flealth/Toronto, Ontario/Canada (7 aut.) |
| DT : | Publication en série; Article; Commentaire; Niveau analytique |
| SO : | Neurosurgery; ISSN 0148-396X; Coden NRSRDY; Etats-Unis; Da. 2003; Vol. 53; No. 5; Pp. 1095-1105; Bibl. 46 ref. |
| LA : | Anglais |
| EA : | OBJECTIVE: The subthalamic nucleus (STN) is a target in the surgical treatment of Parkinson's disease (PD). The mechanism by which electrical stimulation of the STN ameliorates symptoms of PD remains unknown. One consistent aspect of STN stimulation is the ability to reduce the dosage of dopaminergic medications; sometimes they can be eliminated altogether. Furthermore, nigrostriatal projection axons are apposed to the dorsal surface of the STN and are likely affected by the application of current in this region. We sought to determine whether STN stimulation could release endogenous striatal dopamine. METHODS: Five patients with PD, who had previously undergone surgical implantation of bilateral STN stimulators, underwent [11C]raclopride positron emission tomographic scanning. L-dopa was withheld for 12 hours, and both stimulators were turned off 9 hours before scanning. We assayed for striatal dopamine release by measuring radioligand displacement as a consequence of turning on the right STN stimulator after 45 minutes of a 90-minute [11C]raclopride infusion. Patients were evaluated with the motor section of the Unified Parkinson's Disease Rating Scale before and after the studies. RESULTS: Comparisons between the right and left striata, before and after right STN stimulation, demonstrated no significant differences in [11C]raclopride binding, despite significant improvements in Unified Parkinson's Disease Rating Scale motor scores with unilateral stimulation (mean improvement, 26.0 ± 16.4%; P < 0.05). This finding was also noted when the striatum was partitioned into dorsal and ventral caudate and putamen and the four regions were analyzed separately. CONCLUSION: Our results suggest that STN stimulation does not mediate its anti-PD effects via the release of dopamine, as assessed with [11C]raclopride displacement. |
| CC : | 002B17G |
| FD : | Parkinson maladie; Stimulation instrumentale; Electrique; Noyau sousthalamique; Tomoscintigraphie; Emission; Positon; Corps strié; Dopamine; Exploration; Homme |
| FG : | Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Traitement instrumental; Encéphale; Exploration radioisotopique |
| ED : | Parkinson disease; Instrumental stimulation; Electric; Subthalamic nucleus; Emission tomography; Emission; Positron; Corpus striatum; Dopamine; Exploration; Human |
| EG : | Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Instrumentation therapy; Encephalon; Radionuclide study |
| SD : | Parkinson enfermedad; Estimulación instrumental; Eléctrico; Núcleo subtalámico; Tomocentelleografía; Emisión; Positrón; Cuerpo estriado; Dopamina; Exploración; Hombre |
| LO : | INIST-18396.354000118758050100 |
| ID : | 04-0104974 |
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Lozano</name><affiliation><inist:fA14 i1="01"><s1>Department of Surgery, Division of Neurosurgery, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Starr, Philip" sort="Starr, Philip" uniqKey="Starr P" first="Philip" last="Starr">Philip Starr</name></author><author><name sortKey="Broggi, Giovanni" sort="Broggi, Giovanni" uniqKey="Broggi G" first="Giovanni" last="Broggi">Giovanni Broggi</name></author><author><name sortKey="Bakay, Roy A E" sort="Bakay, Roy A E" uniqKey="Bakay R" first="Roy A. E." last="Bakay">Roy A. E. Bakay</name></author><author><name sortKey="Boulis, Nicholas" sort="Boulis, Nicholas" uniqKey="Boulis N" first="Nicholas" last="Boulis">Nicholas Boulis</name></author><author><name sortKey="Rezai, Ali R" sort="Rezai, Ali R" uniqKey="Rezai A" first="Ali R." last="Rezai">Ali R. Rezai</name></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">04-0104974</idno><date when="2003">2003</date><idno type="stanalyst">PASCAL 04-0104974 INIST</idno><idno type="RBID">Pascal:04-0104974</idno><idno type="wicri:Area/PascalFrancis/Corpus">000A29</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Stimulation of the subthalamic nucleus in Parkinson's disease does not produce striatal dopamine release. Commentary</title><author><name sortKey="Abosch, Aviva" sort="Abosch, Aviva" uniqKey="Abosch A" first="Aviva" last="Abosch">Aviva Abosch</name><affiliation><inist:fA14 i1="01"><s1>Department of Surgery, Division of Neurosurgery, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Kapur, Shitij" sort="Kapur, Shitij" uniqKey="Kapur S" first="Shitij" last="Kapur">Shitij Kapur</name><affiliation><inist:fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>PET Centre, Department of Psychiatry and Centre for Addiction and Mental Health</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E." last="Lang">Anthony E. Lang</name><affiliation><inist:fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Medicine, Division of Neurology, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hussey, Doug" sort="Hussey, Doug" uniqKey="Hussey D" first="Doug" last="Hussey">Doug Hussey</name><affiliation><inist:fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>PET Centre, Department of Psychiatry and Centre for Addiction and Mental Health</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Sime, Elspeth" sort="Sime, Elspeth" uniqKey="Sime E" first="Elspeth" last="Sime">Elspeth Sime</name><affiliation><inist:fA14 i1="01"><s1>Department of Surgery, Division of Neurosurgery, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Miyasaki, Janis" sort="Miyasaki, Janis" uniqKey="Miyasaki J" first="Janis" last="Miyasaki">Janis Miyasaki</name><affiliation><inist:fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Medicine, Division of Neurology, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Houle, Svlvain" sort="Houle, Svlvain" uniqKey="Houle S" first="Svlvain" last="Houle">Svlvain Houle</name><affiliation><inist:fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>PET Centre, Department of Psychiatry and Centre for Addiction and Mental Flealth</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lozano, Andres M" sort="Lozano, Andres M" uniqKey="Lozano A" first="Andres M." last="Lozano">Andres M. Lozano</name><affiliation><inist:fA14 i1="01"><s1>Department of Surgery, Division of Neurosurgery, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Starr, Philip" sort="Starr, Philip" uniqKey="Starr P" first="Philip" last="Starr">Philip Starr</name></author><author><name sortKey="Broggi, Giovanni" sort="Broggi, Giovanni" uniqKey="Broggi G" first="Giovanni" last="Broggi">Giovanni Broggi</name></author><author><name sortKey="Bakay, Roy A E" sort="Bakay, Roy A E" uniqKey="Bakay R" first="Roy A. E." last="Bakay">Roy A. E. Bakay</name></author><author><name sortKey="Boulis, Nicholas" sort="Boulis, Nicholas" uniqKey="Boulis N" first="Nicholas" last="Boulis">Nicholas Boulis</name></author><author><name sortKey="Rezai, Ali R" sort="Rezai, Ali R" uniqKey="Rezai A" first="Ali R." last="Rezai">Ali R. Rezai</name></author></analytic><series><title level="j" type="main">Neurosurgery</title><title level="j" type="abbreviated">Neurosurgery</title><idno type="ISSN">0148-396X</idno><imprint><date when="2003">2003</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neurosurgery</title><title level="j" type="abbreviated">Neurosurgery</title><idno type="ISSN">0148-396X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Corpus striatum</term><term>Dopamine</term><term>Electric</term><term>Emission</term><term>Emission tomography</term><term>Exploration</term><term>Human</term><term>Instrumental stimulation</term><term>Parkinson disease</term><term>Positron</term><term>Subthalamic nucleus</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Parkinson maladie</term><term>Stimulation instrumentale</term><term>Electrique</term><term>Noyau sousthalamique</term><term>Tomoscintigraphie</term><term>Emission</term><term>Positon</term><term>Corps strié</term><term>Dopamine</term><term>Exploration</term><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">OBJECTIVE: The subthalamic nucleus (STN) is a target in the surgical treatment of Parkinson's disease (PD). The mechanism by which electrical stimulation of the STN ameliorates symptoms of PD remains unknown. One consistent aspect of STN stimulation is the ability to reduce the dosage of dopaminergic medications; sometimes they can be eliminated altogether. Furthermore, nigrostriatal projection axons are apposed to the dorsal surface of the STN and are likely affected by the application of current in this region. We sought to determine whether STN stimulation could release endogenous striatal dopamine. METHODS: Five patients with PD, who had previously undergone surgical implantation of bilateral STN stimulators, underwent [<sup>11</sup>C]raclopride positron emission tomographic scanning. L-dopa was withheld for 12 hours, and both stimulators were turned off 9 hours before scanning. We assayed for striatal dopamine release by measuring radioligand displacement as a consequence of turning on the right STN stimulator after 45 minutes of a 90-minute [<sup>11</sup>C]raclopride infusion. Patients were evaluated with the motor section of the Unified Parkinson's Disease Rating Scale before and after the studies. RESULTS: Comparisons between the right and left striata, before and after right STN stimulation, demonstrated no significant differences in [<sup>11</sup>C]raclopride binding, despite significant improvements in Unified Parkinson's Disease Rating Scale motor scores with unilateral stimulation (mean improvement, 26.0 ± 16.4%; P < 0.05). This finding was also noted when the striatum was partitioned into dorsal and ventral caudate and putamen and the four regions were analyzed separately. CONCLUSION: Our results suggest that STN stimulation does not mediate its anti-PD effects via the release of dopamine, as assessed with [<sup>11</sup>C]raclopride displacement.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0148-396X</s0></fA01><fA02 i1="01"><s0>NRSRDY</s0></fA02><fA03 i2="1"><s0>Neurosurgery</s0></fA03><fA05><s2>53</s2></fA05><fA06><s2>5</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Stimulation of the subthalamic nucleus in Parkinson's disease does not produce striatal dopamine release. Commentary</s1></fA08><fA11 i1="01" i2="1"><s1>ABOSCH (Aviva)</s1></fA11><fA11 i1="02" i2="1"><s1>KAPUR (Shitij)</s1></fA11><fA11 i1="03" i2="1"><s1>LANG (Anthony E.)</s1></fA11><fA11 i1="04" i2="1"><s1>HUSSEY (Doug)</s1></fA11><fA11 i1="05" i2="1"><s1>SIME (Elspeth)</s1></fA11><fA11 i1="06" i2="1"><s1>MIYASAKI (Janis)</s1></fA11><fA11 i1="07" i2="1"><s1>HOULE (Svlvain)</s1></fA11><fA11 i1="08" i2="1"><s1>LOZANO (Andres M.)</s1></fA11><fA11 i1="09" i2="1"><s1>STARR (Philip)</s1><s9>comment.</s9></fA11><fA11 i1="10" i2="1"><s1>BROGGI (Giovanni)</s1><s9>comment.</s9></fA11><fA11 i1="11" i2="1"><s1>BAKAY (Roy A. E.)</s1><s9>comment.</s9></fA11><fA11 i1="12" i2="1"><s1>BOULIS (Nicholas)</s1><s9>comment.</s9></fA11><fA11 i1="13" i2="1"><s1>REZAI (Ali R.)</s1><s9>comment.</s9></fA11><fA14 i1="01"><s1>Department of Surgery, Division of Neurosurgery, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ></fA14><fA14 i1="02"><s1>University Health Network, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></fA14><fA14 i1="03"><s1>PET Centre, Department of Psychiatry and Centre for Addiction and Mental Health</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Medicine, Division of Neurology, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="05"><s1>PET Centre, Department of Psychiatry and Centre for Addiction and Mental Flealth</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>7 aut.</sZ></fA14><fA20><s1>1095-1105</s1></fA20><fA21><s1>2003</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>18396</s2><s5>354000118758050100</s5></fA43><fA44><s0>0000</s0><s1>© 2004 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>46 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>04-0104974</s0></fA47><fA60><s1>P</s1><s3>AR</s3><s3>CT</s3></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neurosurgery</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>OBJECTIVE: The subthalamic nucleus (STN) is a target in the surgical treatment of Parkinson's disease (PD). The mechanism by which electrical stimulation of the STN ameliorates symptoms of PD remains unknown. One consistent aspect of STN stimulation is the ability to reduce the dosage of dopaminergic medications; sometimes they can be eliminated altogether. Furthermore, nigrostriatal projection axons are apposed to the dorsal surface of the STN and are likely affected by the application of current in this region. We sought to determine whether STN stimulation could release endogenous striatal dopamine. METHODS: Five patients with PD, who had previously undergone surgical implantation of bilateral STN stimulators, underwent [<sup>11</sup>C]raclopride positron emission tomographic scanning. L-dopa was withheld for 12 hours, and both stimulators were turned off 9 hours before scanning. We assayed for striatal dopamine release by measuring radioligand displacement as a consequence of turning on the right STN stimulator after 45 minutes of a 90-minute [<sup>11</sup>C]raclopride infusion. Patients were evaluated with the motor section of the Unified Parkinson's Disease Rating Scale before and after the studies. RESULTS: Comparisons between the right and left striata, before and after right STN stimulation, demonstrated no significant differences in [<sup>11</sup>C]raclopride binding, despite significant improvements in Unified Parkinson's Disease Rating Scale motor scores with unilateral stimulation (mean improvement, 26.0 ± 16.4%; P < 0.05). This finding was also noted when the striatum was partitioned into dorsal and ventral caudate and putamen and the four regions were analyzed separately. CONCLUSION: Our results suggest that STN stimulation does not mediate its anti-PD effects via the release of dopamine, as assessed with [<sup>11</sup>C]raclopride displacement.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Stimulation instrumentale</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Instrumental stimulation</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Estimulación instrumental</s0><s5>04</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Electrique</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Electric</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Eléctrico</s0><s5>05</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Noyau sousthalamique</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Subthalamic nucleus</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Núcleo subtalámico</s0><s5>07</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Tomoscintigraphie</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Emission tomography</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Tomocentelleografía</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Emission</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Emission</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Emisión</s0><s5>11</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Positon</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Positron</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Positrón</s0><s5>12</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Corps strié</s0><s5>13</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Corpus striatum</s0><s5>13</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Cuerpo estriado</s0><s5>13</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>16</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>16</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Dopamina</s0><s2>NK</s2><s2>FR</s2><s5>16</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Exploration</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Exploration</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Exploración</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Homme</s0><s5>20</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Human</s0><s5>20</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Hombre</s0><s5>20</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Traitement instrumental</s0><s5>45</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Instrumentation therapy</s0><s5>45</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Tratamiento instrumental</s0><s5>45</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Encéphale</s0><s5>53</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Encephalon</s0><s5>53</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Encéfalo</s0><s5>53</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Exploration radioisotopique</s0><s5>61</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Radionuclide study</s0><s5>61</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Exploración radioisotópica</s0><s5>61</s5></fC07><fN21><s1>068</s1></fN21><fN82><s1>PSI</s1></fN82></pA></standard><server><NO>PASCAL 04-0104974 INIST</NO><ET>Stimulation of the subthalamic nucleus in Parkinson's disease does not produce striatal dopamine release. Commentary</ET><AU>ABOSCH (Aviva); KAPUR (Shitij); LANG (Anthony E.); HUSSEY (Doug); SIME (Elspeth); MIYASAKI (Janis); HOULE (Svlvain); LOZANO (Andres M.); STARR (Philip); BROGGI (Giovanni); BAKAY (Roy A. E.); BOULIS (Nicholas); REZAI (Ali R.)</AU><AF>Department of Surgery, Division of Neurosurgery, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital/Toronto, Ontario/Canada (1 aut., 5 aut., 8 aut.); University Health Network, University of Toronto/Toronto, Ontario/Canada (1 aut., 2 aut., 3 aut., 4 aut., 6 aut., 7 aut., 8 aut.); PET Centre, Department of Psychiatry and Centre for Addiction and Mental Health/Toronto, Ontario/Canada (2 aut., 4 aut.); Department of Medicine, Division of Neurology, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital/Toronto, Ontario/Canada (3 aut., 6 aut.); PET Centre, Department of Psychiatry and Centre for Addiction and Mental Flealth/Toronto, Ontario/Canada (7 aut.)</AF><DT>Publication en série; Article; Commentaire; Niveau analytique</DT><SO>Neurosurgery; ISSN 0148-396X; Coden NRSRDY; Etats-Unis; Da. 2003; Vol. 53; No. 5; Pp. 1095-1105; Bibl. 46 ref.</SO><LA>Anglais</LA><EA>OBJECTIVE: The subthalamic nucleus (STN) is a target in the surgical treatment of Parkinson's disease (PD). The mechanism by which electrical stimulation of the STN ameliorates symptoms of PD remains unknown. One consistent aspect of STN stimulation is the ability to reduce the dosage of dopaminergic medications; sometimes they can be eliminated altogether. Furthermore, nigrostriatal projection axons are apposed to the dorsal surface of the STN and are likely affected by the application of current in this region. We sought to determine whether STN stimulation could release endogenous striatal dopamine. METHODS: Five patients with PD, who had previously undergone surgical implantation of bilateral STN stimulators, underwent [<sup>11</sup>C]raclopride positron emission tomographic scanning. L-dopa was withheld for 12 hours, and both stimulators were turned off 9 hours before scanning. We assayed for striatal dopamine release by measuring radioligand displacement as a consequence of turning on the right STN stimulator after 45 minutes of a 90-minute [<sup>11</sup>C]raclopride infusion. Patients were evaluated with the motor section of the Unified Parkinson's Disease Rating Scale before and after the studies. RESULTS: Comparisons between the right and left striata, before and after right STN stimulation, demonstrated no significant differences in [<sup>11</sup>C]raclopride binding, despite significant improvements in Unified Parkinson's Disease Rating Scale motor scores with unilateral stimulation (mean improvement, 26.0 ± 16.4%; P < 0.05). This finding was also noted when the striatum was partitioned into dorsal and ventral caudate and putamen and the four regions were analyzed separately. CONCLUSION: Our results suggest that STN stimulation does not mediate its anti-PD effects via the release of dopamine, as assessed with [<sup>11</sup>C]raclopride displacement.</EA><CC>002B17G</CC><FD>Parkinson maladie; Stimulation instrumentale; Electrique; Noyau sousthalamique; Tomoscintigraphie; Emission; Positon; Corps strié; Dopamine; Exploration; Homme</FD><FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Traitement instrumental; Encéphale; Exploration radioisotopique</FG><ED>Parkinson disease; Instrumental stimulation; Electric; Subthalamic nucleus; Emission tomography; Emission; Positron; Corpus striatum; Dopamine; Exploration; Human</ED><EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Instrumentation therapy; Encephalon; Radionuclide study</EG><SD>Parkinson enfermedad; Estimulación instrumental; Eléctrico; Núcleo subtalámico; Tomocentelleografía; Emisión; Positrón; Cuerpo estriado; Dopamina; Exploración; Hombre</SD><LO>INIST-18396.354000118758050100</LO><ID>04-0104974</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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