STN‐stimulation in Parkinson's disease restores striatal inhibition of thalamocortical projection
Identifieur interne : 000964 ( Main/Exploration ); précédent : 000963; suivant : 000965STN‐stimulation in Parkinson's disease restores striatal inhibition of thalamocortical projection
Auteurs : Jacob Geday [Danemark] ; Karen Stergaard [Danemark] ; Erik Johnsen [Danemark] ; Albert Gjedde [Danemark]Source :
- Human Brain Mapping [ 1065-9471 ] ; 2009-01.
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Abstract
To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN‐stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN‐stimulation with a 4‐h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area. Hum Brain Mapp, 2009. © 2007 Wiley‐Liss, Inc.
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DOI: 10.1002/hbm.20486
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Brain Mapp.</title><idno type="ISSN">1065-9471</idno><idno type="eISSN">1097-0193</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-01">2009-01</date><biblScope unit="volume">30</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="112">112</biblScope><biblScope unit="page" to="121">121</biblScope></imprint><idno type="ISSN">1065-9471</idno></series><idno type="istex">9BFF2AF4B4382896A7269ECAFFBAA3E4C4A46750</idno><idno type="DOI">10.1002/hbm.20486</idno><idno type="ArticleID">HBM20486</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1065-9471</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PET</term><term>Parkinson</term><term>STN‐stimulation</term><term>VL</term><term>basalgangglia loop</term><term>clinical outcome</term><term>deactivation</term><term>flow</term><term>thalamus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN‐stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN‐stimulation with a 4‐h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area. Hum Brain Mapp, 2009. © 2007 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Danemark</li></country></list><tree><country name="Danemark"><noRegion><name sortKey="Geday, Jacob" sort="Geday, Jacob" uniqKey="Geday J" first="Jacob" last="Geday">Jacob Geday</name></noRegion><name sortKey=" Stergaard, Karen" sort=" Stergaard, Karen" uniqKey=" Stergaard K" first="Karen" last=" Stergaard">Karen Stergaard</name><name sortKey="Geday, Jacob" sort="Geday, Jacob" uniqKey="Geday J" first="Jacob" last="Geday">Jacob Geday</name><name sortKey="Gjedde, Albert" sort="Gjedde, Albert" uniqKey="Gjedde A" first="Albert" last="Gjedde">Albert Gjedde</name><name sortKey="Johnsen, Erik" sort="Johnsen, Erik" uniqKey="Johnsen E" first="Erik" last="Johnsen">Erik Johnsen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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