Mechanisms of deep brain stimulation
Identifieur interne : 004389 ( Main/Exploration ); précédent : 004388; suivant : 004390Mechanisms of deep brain stimulation
Auteurs : Jonathan O. Dostrovsky [Canada] ; Andres M. Lozano [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-03.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Animals, Basal Ganglia (physiopathology), Basal ganglion, Brain (vertebrata), Electric, Electric Stimulation Therapy, GABA, High frequency, Human, Humans, Instrumental stimulation, Involuntary movement, Mechanism of action, Movement Disorders (physiopathology), Movement Disorders (therapy), Neurons (physiology), Thalamus (physiopathology), Treatment, basal ganglia, deep brain stimulation, gamma-Aminobutyric Acid (metabolism), movement‐disorders, thalamus.
- MESH :
- chemical , metabolism : gamma-Aminobutyric Acid.
- physiology : Neurons.
- physiopathology : Basal Ganglia, Movement Disorders, Thalamus.
- therapy : Movement Disorders.
- Animals, Electric Stimulation Therapy, Humans.
Abstract
High frequency electrical stimulation by means of electrodes implanted into the brain (deep brain stimulation; DBS) recently has become an accepted technique for the treatment of several movement disorders and in particular for Parkinson's disease. Because the effects produced by DBS are similar to those produced by making a lesion in the same region, it has been proposed that the overall effect of DBS is to inhibit the neural activity in the region stimulated. However, whether this is actually the case is presently not known, but various mechanisms have been proposed in an attempt to explain how DBS could mimic the effects of a lesion. We describe the various mechanisms that have been proposed to account for the inhibition or disruption of the pathologic outflow by high‐frequency DBS, ranging from depolarisation block to stimulation‐evoked release of γ‐aminobutyric acid and describes preliminary findings that show that stimulation within these structures can result in inhibition. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10143
Affiliations:
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-03">2002-03</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">S3</biblScope><biblScope unit="supplement">3</biblScope><biblScope unit="page" from="S63">S63</biblScope><biblScope unit="page" to="S68">S68</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">A32B299F6F5BB098B99FF28D5F270D553EB5D8C0</idno><idno type="DOI">10.1002/mds.10143</idno><idno type="ArticleID">MDS10143</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Basal Ganglia (physiopathology)</term><term>Basal ganglion</term><term>Brain (vertebrata)</term><term>Electric</term><term>Electric Stimulation Therapy</term><term>GABA</term><term>High frequency</term><term>Human</term><term>Humans</term><term>Instrumental stimulation</term><term>Involuntary movement</term><term>Mechanism of action</term><term>Movement Disorders (physiopathology)</term><term>Movement Disorders (therapy)</term><term>Neurons (physiology)</term><term>Thalamus (physiopathology)</term><term>Treatment</term><term>basal ganglia</term><term>deep brain stimulation</term><term>gamma-Aminobutyric Acid (metabolism)</term><term>movement‐disorders</term><term>thalamus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Movement Disorders</term><term>Thalamus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Movement Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Electric Stimulation Therapy</term><term>Humans</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Electrique</term><term>Encéphale</term><term>GABA</term><term>Haute fréquence</term><term>Homme</term><term>Mouvement involontaire</term><term>Mécanisme action</term><term>Noyau gris central</term><term>Stimulation instrumentale</term><term>Traitement</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">High frequency electrical stimulation by means of electrodes implanted into the brain (deep brain stimulation; DBS) recently has become an accepted technique for the treatment of several movement disorders and in particular for Parkinson's disease. Because the effects produced by DBS are similar to those produced by making a lesion in the same region, it has been proposed that the overall effect of DBS is to inhibit the neural activity in the region stimulated. However, whether this is actually the case is presently not known, but various mechanisms have been proposed in an attempt to explain how DBS could mimic the effects of a lesion. We describe the various mechanisms that have been proposed to account for the inhibition or disruption of the pathologic outflow by high‐frequency DBS, ranging from depolarisation block to stimulation‐evoked release of γ‐aminobutyric acid and describes preliminary findings that show that stimulation within these structures can result in inhibition. © 2002 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><country name="Canada"><region name="Ontario"><name sortKey="Dostrovsky, Jonathan O" sort="Dostrovsky, Jonathan O" uniqKey="Dostrovsky J" first="Jonathan O." last="Dostrovsky">Jonathan O. Dostrovsky</name></region><name sortKey="Dostrovsky, Jonathan O" sort="Dostrovsky, Jonathan O" uniqKey="Dostrovsky J" first="Jonathan O." last="Dostrovsky">Jonathan O. Dostrovsky</name><name sortKey="Lozano, Andres M" sort="Lozano, Andres M" uniqKey="Lozano A" first="Andres M." last="Lozano">Andres M. Lozano</name><name sortKey="Lozano, Andres M" sort="Lozano, Andres M" uniqKey="Lozano A" first="Andres M." last="Lozano">Andres M. Lozano</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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