Latest view on the mechanism of action of deep brain stimulation
Identifieur interne : 000288 ( France/Analysis ); précédent : 000287; suivant : 000289Latest view on the mechanism of action of deep brain stimulation
Auteurs : Constance Hammond [France] ; Rachida Ammari [France] ; Bernard Bioulac [France] ; Liliana Garcia [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-11-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Brain (pathology), Brain (physiology), DBS, Deep Brain Stimulation (methods), Deep Brain Stimulation (trends), Deep brain stimulation, Dystonia, Electrophysiology, Humans, Mechanism of action, Nervous System Diseases (pathology), Nervous System Diseases (therapy), Nervous system diseases, Neurons (physiology), OCD, Parkinson, Spike, antidromic spikes, dystonia, electrophysiology.
- MESH :
- methods : Deep Brain Stimulation.
- pathology : Brain, Nervous System Diseases.
- physiology : Brain, Neurons.
- therapy : Nervous System Diseases.
- trends : Deep Brain Stimulation.
- Humans.
Abstract
How does deep brain stimulation (DBS) applied at high frequency (100 Hz and above, HFS) in diverse points of cortico‐basal ganglia thalamo‐cortical loops alleviate symptoms of neurological disorders such as Parkinson's disease, dystonia, and obsessive compulsive disorders? Do the effects of HFS stem solely or even largely from local effects on the stimulated brain structure or are they also mediated by actions of HFS on distal structures? Indeed, HFS as an extracellular stimulation is expected to activate subsets of both afferent and efferent axons, leading to antidromic spikes that collide with ongoing spontaneous ones and orthodromic spikes that evoke synaptic responses in target neurons. The present review suggests that HFS interfere with spontaneous pathological patterns by introducing a regular activity in several nodal points of the network. Therefore, the best site of implantation of the HFS electrode may be in a region where the HFS‐driven activity spreads to most of the identified, dysrhythmic, neuronal populations without causing additional side effects. This should help tackling the most difficult issue namely, how does the regular HFS‐driven activity that dampens the spontaneous pathological one, restore neuronal processing along cortico‐basal ganglia‐thalamo‐cortical loops? © 2008 Movement Disorder Society
Url:
- https://api.istex.fr/document/4F208B7D0277EEE629FF3B67CCB7574CCA7A3400/fulltext/pdf
- http://www.hal.inserm.fr/inserm-00483505
DOI: 10.1002/mds.22120
Affiliations:
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ISTEX:4F208B7D0277EEE629FF3B67CCB7574CCA7A3400Le document en format XML
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Hammond</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>Institut de Neurobiologie de la Méditerranée (INMED, U901), Unité mixte Inserm‐Université Aix Marseille II, Marseille Cédex 9</wicri:regionArea><wicri:noRegion>Marseille Cédex 9</wicri:noRegion><wicri:noRegion>Marseille Cédex 9</wicri:noRegion></affiliation></author><author><name sortKey="Ammari, Rachida" sort="Ammari, Rachida" uniqKey="Ammari R" first="Rachida" last="Ammari">Rachida Ammari</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>Institut de Neurobiologie de la Méditerranée (INMED, U901), Unité mixte Inserm‐Université Aix Marseille II, Marseille Cédex 9</wicri:regionArea><wicri:noRegion>Marseille Cédex 9</wicri:noRegion><wicri:noRegion>Marseille Cédex 9</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>UMR 5227 CNRS‐Université Bordeaux 2, Bordeaux Cédex</wicri:regionArea><wicri:noRegion>Bordeaux Cédex</wicri:noRegion><wicri:noRegion>Bordeaux Cédex</wicri:noRegion></affiliation></author><author><name sortKey="Bioulac, Bernard" sort="Bioulac, Bernard" uniqKey="Bioulac B" first="Bernard" last="Bioulac">Bernard Bioulac</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>UMR 5227 CNRS‐Université Bordeaux 2, Bordeaux Cédex</wicri:regionArea><wicri:noRegion>Bordeaux Cédex</wicri:noRegion><wicri:noRegion>Bordeaux Cédex</wicri:noRegion></affiliation></author><author><name sortKey="Garcia, Liliana" sort="Garcia, Liliana" uniqKey="Garcia L" first="Liliana" last="Garcia">Liliana Garcia</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>UMR 5227 CNRS‐Université Bordeaux 2, Bordeaux Cédex</wicri:regionArea><wicri:noRegion>Bordeaux Cédex</wicri:noRegion><wicri:noRegion>Bordeaux Cédex</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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>Hoboken</pubPlace><date type="published" when="2008-11-15">2008-11-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2111">2111</biblScope><biblScope unit="page" to="2121">2121</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">4F208B7D0277EEE629FF3B67CCB7574CCA7A3400</idno><idno type="DOI">10.1002/mds.22120</idno><idno type="ArticleID">MDS22120</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain (pathology)</term><term>Brain (physiology)</term><term>DBS</term><term>Deep Brain Stimulation (methods)</term><term>Deep Brain Stimulation (trends)</term><term>Deep brain stimulation</term><term>Dystonia</term><term>Electrophysiology</term><term>Humans</term><term>Mechanism of action</term><term>Nervous System Diseases (pathology)</term><term>Nervous System Diseases (therapy)</term><term>Nervous system diseases</term><term>Neurons (physiology)</term><term>OCD</term><term>Parkinson</term><term>Spike</term><term>antidromic spikes</term><term>dystonia</term><term>electrophysiology</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Nervous System Diseases</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Brain</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Nervous System Diseases</term></keywords><keywords scheme="MESH" qualifier="trends" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dystonie</term><term>Electrophysiologie</term><term>Mécanisme action</term><term>Pathologie du système nerveux</term><term>Pointe positive</term><term>Stimulation cérébrale profonde</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">How does deep brain stimulation (DBS) applied at high frequency (100 Hz and above, HFS) in diverse points of cortico‐basal ganglia thalamo‐cortical loops alleviate symptoms of neurological disorders such as Parkinson's disease, dystonia, and obsessive compulsive disorders? Do the effects of HFS stem solely or even largely from local effects on the stimulated brain structure or are they also mediated by actions of HFS on distal structures? Indeed, HFS as an extracellular stimulation is expected to activate subsets of both afferent and efferent axons, leading to antidromic spikes that collide with ongoing spontaneous ones and orthodromic spikes that evoke synaptic responses in target neurons. The present review suggests that HFS interfere with spontaneous pathological patterns by introducing a regular activity in several nodal points of the network. Therefore, the best site of implantation of the HFS electrode may be in a region where the HFS‐driven activity spreads to most of the identified, dysrhythmic, neuronal populations without causing additional side effects. This should help tackling the most difficult issue namely, how does the regular HFS‐driven activity that dampens the spontaneous pathological one, restore neuronal processing along cortico‐basal ganglia‐thalamo‐cortical loops? © 2008 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>France</li></country></list><tree><country name="France"><noRegion><name sortKey="Hammond, Constance" sort="Hammond, Constance" uniqKey="Hammond C" first="Constance" last="Hammond">Constance Hammond</name></noRegion><name sortKey="Ammari, Rachida" sort="Ammari, Rachida" uniqKey="Ammari R" first="Rachida" last="Ammari">Rachida Ammari</name><name sortKey="Ammari, Rachida" sort="Ammari, Rachida" uniqKey="Ammari R" first="Rachida" last="Ammari">Rachida Ammari</name><name sortKey="Bioulac, Bernard" sort="Bioulac, Bernard" uniqKey="Bioulac B" first="Bernard" last="Bioulac">Bernard Bioulac</name><name sortKey="Garcia, Liliana" sort="Garcia, Liliana" uniqKey="Garcia L" first="Liliana" last="Garcia">Liliana Garcia</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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