Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease.
Identifieur interne : 000D69 ( PubMed/Corpus ); précédent : 000D68; suivant : 000D70Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease.
Auteurs : Harrison C. Walker ; He Huang ; Christopher L. Gonzalez ; James E. Bryant ; Jeffrey Killen ; Gary R. Cutter ; Robert C. Knowlton ; Erwin B. Montgomery ; Bart L. Guthrie ; Ray L. WattsSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2012.
English descriptors
- KwdEn :
- Aged, Analysis of Variance, Cerebral Cortex (physiopathology), Deep Brain Stimulation (methods), Electroencephalography, Evoked Potentials (physiology), Female, Humans, Male, Middle Aged, Motor Activity (physiology), Nonlinear Dynamics, Parkinson Disease (pathology), Parkinson Disease (therapy), Reaction Time (physiology), Regression Analysis, Subthalamus (physiology).
- MESH :
- methods : Deep Brain Stimulation.
- pathology : Parkinson Disease.
- physiology : Evoked Potentials, Motor Activity, Reaction Time, Subthalamus.
- physiopathology : Cerebral Cortex.
- therapy : Parkinson Disease.
- Aged, Analysis of Variance, Electroencephalography, Female, Humans, Male, Middle Aged, Nonlinear Dynamics, Regression Analysis.
Abstract
Subthalamic deep brain stimulation (DBS) is superior to medical therapy for the motor symptoms of advanced Parkinson's disease (PD), and additional evidence suggests that it improves refractory symptoms of essential tremor, primary generalized dystonia, and obsessive-compulsive disorder. Despite this, its therapeutic mechanism is unknown. We hypothesized that subthalamic stimulation activates the cerebral cortex at short latencies after stimulus onset during clinically effective stimulation for PD. In 5 subjects (six hemispheres), EEG measured the response of cortex to subthalamic stimulation across a range of stimulation voltages and frequencies. Novel analytical techniques reversed the anode and cathode electrode contacts and summed the resulting pair of event-related potentials to suppress the stimulation artifact. We found that subthalamic brain stimulation at 20 Hz activates the somatosensory cortex at discrete latencies (mean latencies: 1.0 ± 0.4, 5.7 ± 1.1, and 22.2 ± 1.8 ms, denoted as R1, R2, and R3, respectively). The amplitude of the short latency peak (R1) during clinically effective high-frequency stimulation is nonlinearly dependent on stimulation voltage (P < 0.001; repeated-measures analysis of variance), and its latency is less variable than that of R3 (1.02 versus 19.46 ms; P < 0.001, Levene's test). We conclude that clinically effective subthalamic brain stimulation in humans with PD activates the cerebral cortex at 1 ms after stimulus onset, most likely by antidromic activation. These findings suggest that alteration of the precise timing of action potentials in cortical neurons with axonal projections to the subthalamic region may be an important component of the therapeutic mechanism of subthalamic brain stimulation.
DOI: 10.1002/mds.25025
PubMed: 22648508
Links to Exploration step
pubmed:22648508Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease.</title><author><name sortKey="Walker, Harrison C" sort="Walker, Harrison C" uniqKey="Walker H" first="Harrison C" last="Walker">Harrison C. Walker</name><affiliation><nlm:affiliation>Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0017, USA. hcwalker@uab.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Huang, He" sort="Huang, He" uniqKey="Huang H" first="He" last="Huang">He Huang</name></author><author><name sortKey="Gonzalez, Christopher L" sort="Gonzalez, Christopher L" uniqKey="Gonzalez C" first="Christopher L" last="Gonzalez">Christopher L. Gonzalez</name></author><author><name sortKey="Bryant, James E" sort="Bryant, James E" uniqKey="Bryant J" first="James E" last="Bryant">James E. Bryant</name></author><author><name sortKey="Killen, Jeffrey" sort="Killen, Jeffrey" uniqKey="Killen J" first="Jeffrey" last="Killen">Jeffrey Killen</name></author><author><name sortKey="Cutter, Gary R" sort="Cutter, Gary R" uniqKey="Cutter G" first="Gary R" last="Cutter">Gary R. Cutter</name></author><author><name sortKey="Knowlton, Robert C" sort="Knowlton, Robert C" uniqKey="Knowlton R" first="Robert C" last="Knowlton">Robert C. Knowlton</name></author><author><name sortKey="Montgomery, Erwin B" sort="Montgomery, Erwin B" uniqKey="Montgomery E" first="Erwin B" last="Montgomery">Erwin B. Montgomery</name></author><author><name sortKey="Guthrie, Bart L" sort="Guthrie, Bart L" uniqKey="Guthrie B" first="Bart L" last="Guthrie">Bart L. Guthrie</name></author><author><name sortKey="Watts, Ray L" sort="Watts, Ray L" uniqKey="Watts R" first="Ray L" last="Watts">Ray L. Watts</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="doi">10.1002/mds.25025</idno><idno type="RBID">pubmed:22648508</idno><idno type="pmid">22648508</idno><idno type="wicri:Area/PubMed/Corpus">000D69</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease.</title><author><name sortKey="Walker, Harrison C" sort="Walker, Harrison C" uniqKey="Walker H" first="Harrison C" last="Walker">Harrison C. Walker</name><affiliation><nlm:affiliation>Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0017, USA. hcwalker@uab.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Huang, He" sort="Huang, He" uniqKey="Huang H" first="He" last="Huang">He Huang</name></author><author><name sortKey="Gonzalez, Christopher L" sort="Gonzalez, Christopher L" uniqKey="Gonzalez C" first="Christopher L" last="Gonzalez">Christopher L. Gonzalez</name></author><author><name sortKey="Bryant, James E" sort="Bryant, James E" uniqKey="Bryant J" first="James E" last="Bryant">James E. Bryant</name></author><author><name sortKey="Killen, Jeffrey" sort="Killen, Jeffrey" uniqKey="Killen J" first="Jeffrey" last="Killen">Jeffrey Killen</name></author><author><name sortKey="Cutter, Gary R" sort="Cutter, Gary R" uniqKey="Cutter G" first="Gary R" last="Cutter">Gary R. Cutter</name></author><author><name sortKey="Knowlton, Robert C" sort="Knowlton, Robert C" uniqKey="Knowlton R" first="Robert C" last="Knowlton">Robert C. Knowlton</name></author><author><name sortKey="Montgomery, Erwin B" sort="Montgomery, Erwin B" uniqKey="Montgomery E" first="Erwin B" last="Montgomery">Erwin B. Montgomery</name></author><author><name sortKey="Guthrie, Bart L" sort="Guthrie, Bart L" uniqKey="Guthrie B" first="Bart L" last="Guthrie">Bart L. Guthrie</name></author><author><name sortKey="Watts, Ray L" sort="Watts, Ray L" uniqKey="Watts R" first="Ray L" last="Watts">Ray L. Watts</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Cerebral Cortex (physiopathology)</term><term>Deep Brain Stimulation (methods)</term><term>Electroencephalography</term><term>Evoked Potentials (physiology)</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Motor Activity (physiology)</term><term>Nonlinear Dynamics</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (therapy)</term><term>Reaction Time (physiology)</term><term>Regression Analysis</term><term>Subthalamus (physiology)</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>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Evoked Potentials</term><term>Motor Activity</term><term>Reaction Time</term><term>Subthalamus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Electroencephalography</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Nonlinear Dynamics</term><term>Regression Analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Subthalamic deep brain stimulation (DBS) is superior to medical therapy for the motor symptoms of advanced Parkinson's disease (PD), and additional evidence suggests that it improves refractory symptoms of essential tremor, primary generalized dystonia, and obsessive-compulsive disorder. Despite this, its therapeutic mechanism is unknown. We hypothesized that subthalamic stimulation activates the cerebral cortex at short latencies after stimulus onset during clinically effective stimulation for PD. In 5 subjects (six hemispheres), EEG measured the response of cortex to subthalamic stimulation across a range of stimulation voltages and frequencies. Novel analytical techniques reversed the anode and cathode electrode contacts and summed the resulting pair of event-related potentials to suppress the stimulation artifact. We found that subthalamic brain stimulation at 20 Hz activates the somatosensory cortex at discrete latencies (mean latencies: 1.0 ± 0.4, 5.7 ± 1.1, and 22.2 ± 1.8 ms, denoted as R1, R2, and R3, respectively). The amplitude of the short latency peak (R1) during clinically effective high-frequency stimulation is nonlinearly dependent on stimulation voltage (P < 0.001; repeated-measures analysis of variance), and its latency is less variable than that of R3 (1.02 versus 19.46 ms; P < 0.001, Levene's test). We conclude that clinically effective subthalamic brain stimulation in humans with PD activates the cerebral cortex at 1 ms after stimulus onset, most likely by antidromic activation. These findings suggest that alteration of the precise timing of action potentials in cortical neurons with axonal projections to the subthalamic region may be an important component of the therapeutic mechanism of subthalamic brain stimulation.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">22648508</PMID><DateCreated><Year>2012</Year><Month>06</Month><Day>25</Day></DateCreated><DateCompleted><Year>2012</Year><Month>11</Month><Day>13</Day></DateCompleted><DateRevised><Year>2014</Year><Month>10</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>7</Issue><PubDate><Year>2012</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>864-73</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25025</ELocationID><Abstract><AbstractText>Subthalamic deep brain stimulation (DBS) is superior to medical therapy for the motor symptoms of advanced Parkinson's disease (PD), and additional evidence suggests that it improves refractory symptoms of essential tremor, primary generalized dystonia, and obsessive-compulsive disorder. Despite this, its therapeutic mechanism is unknown. We hypothesized that subthalamic stimulation activates the cerebral cortex at short latencies after stimulus onset during clinically effective stimulation for PD. In 5 subjects (six hemispheres), EEG measured the response of cortex to subthalamic stimulation across a range of stimulation voltages and frequencies. Novel analytical techniques reversed the anode and cathode electrode contacts and summed the resulting pair of event-related potentials to suppress the stimulation artifact. We found that subthalamic brain stimulation at 20 Hz activates the somatosensory cortex at discrete latencies (mean latencies: 1.0 ± 0.4, 5.7 ± 1.1, and 22.2 ± 1.8 ms, denoted as R1, R2, and R3, respectively). The amplitude of the short latency peak (R1) during clinically effective high-frequency stimulation is nonlinearly dependent on stimulation voltage (P < 0.001; repeated-measures analysis of variance), and its latency is less variable than that of R3 (1.02 versus 19.46 ms; P < 0.001, Levene's test). We conclude that clinically effective subthalamic brain stimulation in humans with PD activates the cerebral cortex at 1 ms after stimulus onset, most likely by antidromic activation. These findings suggest that alteration of the precise timing of action potentials in cortical neurons with axonal projections to the subthalamic region may be an important component of the therapeutic mechanism of subthalamic brain stimulation.</AbstractText><CopyrightInformation>Copyright © 2012 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Walker</LastName><ForeName>Harrison C</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0017, USA. hcwalker@uab.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>He</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Gonzalez</LastName><ForeName>Christopher L</ForeName><Initials>CL</Initials></Author><Author ValidYN="Y"><LastName>Bryant</LastName><ForeName>James E</ForeName><Initials>JE</Initials></Author><Author ValidYN="Y"><LastName>Killen</LastName><ForeName>Jeffrey</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Cutter</LastName><ForeName>Gary R</ForeName><Initials>GR</Initials></Author><Author ValidYN="Y"><LastName>Knowlton</LastName><ForeName>Robert C</ForeName><Initials>RC</Initials></Author><Author ValidYN="Y"><LastName>Montgomery</LastName><ForeName>Erwin B</ForeName><Initials>EB</Initials></Author><Author ValidYN="Y"><LastName>Guthrie</LastName><ForeName>Bart L</ForeName><Initials>BL</Initials></Author><Author ValidYN="Y"><LastName>Watts</LastName><ForeName>Ray L</ForeName><Initials>RL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K23 NS067053</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K23-NS067053-01</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>05</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1987 Aug;84(15):5492-5</RefSource><PMID Version="1">3474665</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 1981;6(11):2367-77</RefSource><PMID Version="1">7329552</PMID></CommentsCorrections><CommentsCorrections 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