Therapeutic electrical stimulation of the central nervous system.
Identifieur interne : 000F64 ( PubMed/Corpus ); précédent : 000F63; suivant : 000F65Therapeutic electrical stimulation of the central nervous system.
Auteurs : Alim-Louis Benabid ; Bradley Wallace ; John Mitrofanis ; Celine Xia ; Brigitte Piallat ; Valérie Fraix ; Alina Batir ; Paul Krack ; Pierre Pollak ; François BergerSource :
- Comptes rendus biologies [ 1631-0691 ] ; 2005.
English descriptors
- KwdEn :
- Animals, Anorexia Nervosa (therapy), Brain (physiology), Brain (physiopathology), Central Nervous System (physiology), Central Nervous System (physiopathology), Central Nervous System Diseases (physiopathology), Central Nervous System Diseases (therapy), Electric Stimulation, Electric Stimulation Therapy (methods), Humans, Obesity (therapy), Obsessive-Compulsive Disorder (therapy), Parkinson Disease (therapy).
- MESH :
- methods : Electric Stimulation Therapy.
- physiology : Brain, Central Nervous System.
- physiopathology : Brain, Central Nervous System, Central Nervous System Diseases.
- therapy : Anorexia Nervosa, Central Nervous System Diseases, Obesity, Obsessive-Compulsive Disorder, Parkinson Disease.
- Animals, Electric Stimulation, Humans.
Abstract
The electrical effects on the nervous system have been known for long. The excitatory effect has been used for diagnostic purposes or even for therapeutic applications, like in pain using low-frequency stimulation of the spinal cord or of the thalamus. The discovery that High-Frequency Stimulation (HFS) mimics the effect of lesioning has opened a new field of therapeutic application of electrical stimulation in all places where lesion of neuronal structures, such as nuclei of the basal ganglia, had proven some therapeutic efficiency. This was first applied to the thalamus to mimic thalamotomy for the treatment of tremor, then to the subthalamic nucleus and the pallidum to treat some advanced forms of Parkinson's disease and control not only the tremor but also akinesia, rigidity and dyskinesias. The field of application is increasingly growing, currently encompassing dystonias, epilepsy, obsessive compulsive disease, cluster headaches, and experimental approaches are being made in the field of obesity and food intake control. Although the effects of stimulation are clear-cut and the therapeutic benefit is clearly recognized, the mechanism of action of HFS is not yet understood. The similarity between HFS and the effect of lesions in several places of the brain suggests that this might induce an inhibition-like process, which is difficult to explain with the classical concept of physiology where electrical stimulation means excitation of neural elements. The current data coming from either clinical or experimental observations are providing elements to shape a beginning of an understanding. Intra-cerebral recordings in human patients with artefact suppression tend to show the arrest of electrical firing in the recorded places. Animal experiments, either in vitro or in vivo, show complex patterns mixing inhibitory effects and frequency stimulation induced bursting activity, which would suggest that the mechanism is based upon the jamming of the neuronal message, which is by this way functionally suppressed. More recent data from in vitro biological studies show that HFS profoundly affects the cellular functioning and particularly the protein synthesis, suggesting that it could alter the synaptic transmission by reducing the production of neurotransmitters. It is now clear that this method has a larger field of application than currently known and that its therapeutical applications will benefit to several diseases of the nervous system. The understanding of the mechanism has opened a new field of research, which will call for reappraisal of the basic effects of electricity on the living tissues.
PubMed: 15771004
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Therapeutic electrical stimulation of the central nervous system.</title><author><name sortKey="Benabid, Alim Louis" sort="Benabid, Alim Louis" uniqKey="Benabid A" first="Alim-Louis" last="Benabid">Alim-Louis Benabid</name><affiliation><nlm:affiliation>INSERM U318, Université Joseph-Fourier, CHU Albert-Michallon, pavilion B, BP 217, 38043 Grenoble, France. alim-louis.benabid@ujf-grenoble.fr</nlm:affiliation></affiliation></author><author><name sortKey="Wallace, Bradley" sort="Wallace, Bradley" uniqKey="Wallace B" first="Bradley" last="Wallace">Bradley Wallace</name></author><author><name sortKey="Mitrofanis, John" sort="Mitrofanis, John" uniqKey="Mitrofanis J" first="John" last="Mitrofanis">John Mitrofanis</name></author><author><name sortKey="Xia, Celine" sort="Xia, Celine" uniqKey="Xia C" first="Celine" last="Xia">Celine Xia</name></author><author><name sortKey="Piallat, Brigitte" sort="Piallat, Brigitte" uniqKey="Piallat B" first="Brigitte" last="Piallat">Brigitte Piallat</name></author><author><name sortKey="Fraix, Valerie" sort="Fraix, Valerie" uniqKey="Fraix V" first="Valérie" last="Fraix">Valérie Fraix</name></author><author><name sortKey="Batir, Alina" sort="Batir, Alina" uniqKey="Batir A" first="Alina" last="Batir">Alina Batir</name></author><author><name sortKey="Krack, Paul" sort="Krack, Paul" uniqKey="Krack P" first="Paul" last="Krack">Paul Krack</name></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name></author><author><name sortKey="Berger, Francois" sort="Berger, Francois" uniqKey="Berger F" first="François" last="Berger">François Berger</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15771004</idno><idno type="pmid">15771004</idno><idno type="wicri:Area/PubMed/Corpus">000F64</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000F64</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Therapeutic electrical stimulation of the central nervous system.</title><author><name sortKey="Benabid, Alim Louis" sort="Benabid, Alim Louis" uniqKey="Benabid A" first="Alim-Louis" last="Benabid">Alim-Louis Benabid</name><affiliation><nlm:affiliation>INSERM U318, Université Joseph-Fourier, CHU Albert-Michallon, pavilion B, BP 217, 38043 Grenoble, France. alim-louis.benabid@ujf-grenoble.fr</nlm:affiliation></affiliation></author><author><name sortKey="Wallace, Bradley" sort="Wallace, Bradley" uniqKey="Wallace B" first="Bradley" last="Wallace">Bradley Wallace</name></author><author><name sortKey="Mitrofanis, John" sort="Mitrofanis, John" uniqKey="Mitrofanis J" first="John" last="Mitrofanis">John Mitrofanis</name></author><author><name sortKey="Xia, Celine" sort="Xia, Celine" uniqKey="Xia C" first="Celine" last="Xia">Celine Xia</name></author><author><name sortKey="Piallat, Brigitte" sort="Piallat, Brigitte" uniqKey="Piallat B" first="Brigitte" last="Piallat">Brigitte Piallat</name></author><author><name sortKey="Fraix, Valerie" sort="Fraix, Valerie" uniqKey="Fraix V" first="Valérie" last="Fraix">Valérie Fraix</name></author><author><name sortKey="Batir, Alina" sort="Batir, Alina" uniqKey="Batir A" first="Alina" last="Batir">Alina Batir</name></author><author><name sortKey="Krack, Paul" sort="Krack, Paul" uniqKey="Krack P" first="Paul" last="Krack">Paul Krack</name></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name></author><author><name sortKey="Berger, Francois" sort="Berger, Francois" uniqKey="Berger F" first="François" last="Berger">François Berger</name></author></analytic><series><title level="j">Comptes rendus biologies</title><idno type="ISSN">1631-0691</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anorexia Nervosa (therapy)</term><term>Brain (physiology)</term><term>Brain (physiopathology)</term><term>Central Nervous System (physiology)</term><term>Central Nervous System (physiopathology)</term><term>Central Nervous System Diseases (physiopathology)</term><term>Central Nervous System Diseases (therapy)</term><term>Electric Stimulation</term><term>Electric Stimulation Therapy (methods)</term><term>Humans</term><term>Obesity (therapy)</term><term>Obsessive-Compulsive Disorder (therapy)</term><term>Parkinson Disease (therapy)</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Electric Stimulation Therapy</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Brain</term><term>Central Nervous System</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Central Nervous System</term><term>Central Nervous System Diseases</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Anorexia Nervosa</term><term>Central Nervous System Diseases</term><term>Obesity</term><term>Obsessive-Compulsive Disorder</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Electric Stimulation</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The electrical effects on the nervous system have been known for long. The excitatory effect has been used for diagnostic purposes or even for therapeutic applications, like in pain using low-frequency stimulation of the spinal cord or of the thalamus. The discovery that High-Frequency Stimulation (HFS) mimics the effect of lesioning has opened a new field of therapeutic application of electrical stimulation in all places where lesion of neuronal structures, such as nuclei of the basal ganglia, had proven some therapeutic efficiency. This was first applied to the thalamus to mimic thalamotomy for the treatment of tremor, then to the subthalamic nucleus and the pallidum to treat some advanced forms of Parkinson's disease and control not only the tremor but also akinesia, rigidity and dyskinesias. The field of application is increasingly growing, currently encompassing dystonias, epilepsy, obsessive compulsive disease, cluster headaches, and experimental approaches are being made in the field of obesity and food intake control. Although the effects of stimulation are clear-cut and the therapeutic benefit is clearly recognized, the mechanism of action of HFS is not yet understood. The similarity between HFS and the effect of lesions in several places of the brain suggests that this might induce an inhibition-like process, which is difficult to explain with the classical concept of physiology where electrical stimulation means excitation of neural elements. The current data coming from either clinical or experimental observations are providing elements to shape a beginning of an understanding. Intra-cerebral recordings in human patients with artefact suppression tend to show the arrest of electrical firing in the recorded places. Animal experiments, either in vitro or in vivo, show complex patterns mixing inhibitory effects and frequency stimulation induced bursting activity, which would suggest that the mechanism is based upon the jamming of the neuronal message, which is by this way functionally suppressed. More recent data from in vitro biological studies show that HFS profoundly affects the cellular functioning and particularly the protein synthesis, suggesting that it could alter the synaptic transmission by reducing the production of neurotransmitters. It is now clear that this method has a larger field of application than currently known and that its therapeutical applications will benefit to several diseases of the nervous system. The understanding of the mechanism has opened a new field of research, which will call for reappraisal of the basic effects of electricity on the living tissues.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15771004</PMID><DateCreated><Year>2005</Year><Month>03</Month><Day>17</Day></DateCreated><DateCompleted><Year>2005</Year><Month>04</Month><Day>14</Day></DateCompleted><DateRevised><Year>2005</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1631-0691</ISSN><JournalIssue CitedMedium="Print"><Volume>328</Volume><Issue>2</Issue><PubDate><Year>2005</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Comptes rendus biologies</Title><ISOAbbreviation>C. R. Biol.</ISOAbbreviation></Journal><ArticleTitle>Therapeutic electrical stimulation of the central nervous system.</ArticleTitle><Pagination><MedlinePgn>177-86</MedlinePgn></Pagination><Abstract><AbstractText>The electrical effects on the nervous system have been known for long. The excitatory effect has been used for diagnostic purposes or even for therapeutic applications, like in pain using low-frequency stimulation of the spinal cord or of the thalamus. The discovery that High-Frequency Stimulation (HFS) mimics the effect of lesioning has opened a new field of therapeutic application of electrical stimulation in all places where lesion of neuronal structures, such as nuclei of the basal ganglia, had proven some therapeutic efficiency. This was first applied to the thalamus to mimic thalamotomy for the treatment of tremor, then to the subthalamic nucleus and the pallidum to treat some advanced forms of Parkinson's disease and control not only the tremor but also akinesia, rigidity and dyskinesias. The field of application is increasingly growing, currently encompassing dystonias, epilepsy, obsessive compulsive disease, cluster headaches, and experimental approaches are being made in the field of obesity and food intake control. Although the effects of stimulation are clear-cut and the therapeutic benefit is clearly recognized, the mechanism of action of HFS is not yet understood. The similarity between HFS and the effect of lesions in several places of the brain suggests that this might induce an inhibition-like process, which is difficult to explain with the classical concept of physiology where electrical stimulation means excitation of neural elements. The current data coming from either clinical or experimental observations are providing elements to shape a beginning of an understanding. Intra-cerebral recordings in human patients with artefact suppression tend to show the arrest of electrical firing in the recorded places. Animal experiments, either in vitro or in vivo, show complex patterns mixing inhibitory effects and frequency stimulation induced bursting activity, which would suggest that the mechanism is based upon the jamming of the neuronal message, which is by this way functionally suppressed. More recent data from in vitro biological studies show that HFS profoundly affects the cellular functioning and particularly the protein synthesis, suggesting that it could alter the synaptic transmission by reducing the production of neurotransmitters. It is now clear that this method has a larger field of application than currently known and that its therapeutical applications will benefit to several diseases of the nervous system. The understanding of the mechanism has opened a new field of research, which will call for reappraisal of the basic effects of electricity on the living tissues.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Benabid</LastName><ForeName>Alim-Louis</ForeName><Initials>AL</Initials><AffiliationInfo><Affiliation>INSERM U318, Université Joseph-Fourier, CHU Albert-Michallon, pavilion B, BP 217, 38043 Grenoble, France. alim-louis.benabid@ujf-grenoble.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wallace</LastName><ForeName>Bradley</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Mitrofanis</LastName><ForeName>John</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Xia</LastName><ForeName>Celine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Piallat</LastName><ForeName>Brigitte</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Fraix</LastName><ForeName>Valérie</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Batir</LastName><ForeName>Alina</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Krack</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Pollak</LastName><ForeName>Pierre</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Berger</LastName><ForeName>François</ForeName><Initials>F</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>C R Biol</MedlineTA><NlmUniqueID>101140040</NlmUniqueID><ISSNLinking>1631-0691</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000856" MajorTopicYN="N">Anorexia Nervosa</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002490" MajorTopicYN="N">Central Nervous System</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002493" MajorTopicYN="N">Central Nervous System Diseases</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004558" MajorTopicYN="N">Electric Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004599" MajorTopicYN="N">Electric Stimulation Therapy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009771" MajorTopicYN="N">Obsessive-Compulsive Disorder</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>61</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>3</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>4</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>3</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15771004</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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