Subthalamic nucleus stimulation reverses spinal motoneuron activity in parkinsonian patients.
Identifieur interne : 001101 ( Main/Merge ); précédent : 001100; suivant : 001102Subthalamic nucleus stimulation reverses spinal motoneuron activity in parkinsonian patients.
Auteurs : Sylvie Raoul [France] ; Vincent Roualdes ; Céline Deligny ; Dominique Leduc ; Jean-Charles Lamy ; Alexandra Lackmy-Vallée ; Jean-Paul N'Guyen ; Philippe Damier ; Rose KatzSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2012.
English descriptors
- KwdEn :
- Adult, Aged, Deep Brain Stimulation, Female, Humans, Long-Term Synaptic Depression (physiology), Male, Middle Aged, Motor Neurons (physiology), Muscle Rigidity (physiopathology), Muscle Rigidity (therapy), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Subthalamic Nucleus (physiopathology).
- MESH :
- physiology : Long-Term Synaptic Depression, Motor Neurons.
- physiopathology : Muscle Rigidity, Parkinson Disease, Subthalamic Nucleus.
- therapy : Muscle Rigidity, Parkinson Disease.
- Adult, Aged, Deep Brain Stimulation, Female, Humans, Male, Middle Aged.
Abstract
Although a cardinal symptom of Parkinsonian disease, up to now, rigidity has been investigated much less than spasticity in hemiplegic patients. Many pathophysiological mechanisms may at least theoretically contribute to Parkinsonian rigidity, from altered viscoelastic muscle properties to inability of parkinsonian patients to relax. However, as demonstrated many years ago, motoneuron responses to muscle afferent volleys are involved in rigidity since afferent volleys are suppressed after dorsal root section. To our knowledge, homosynaptic depression (i.e. the fact that motoneuron responses to Ia afferent volleys exhibit a frequency-related depression) has not been studied in parkinsonian disease, despite the fact that in spastic patients, changes in homosynaptic depression are significantly correlated at wrist and ankle levels with the severity of spasticity. Thus, in the present series of experiments, we investigated in parkinsonian patients with chronic implantation of both subthalamic motor nuclei, the amount of homosynaptic depression at wrist and ankle levels on and off deep brain stimulation. Off deep brain stimulation, the frequency-related depression disappeared, the patients became rigid and the amount of homosynaptic depression was significantly correlated with the severity of rigidity. On deep brain stimulation, the frequency-related depression was restored and the rigidity suppressed, suggesting that homosynaptic depression is one of the mechanisms underlying rigidity in Parkinson's disease. Moreover, the unexpected finding that changes in the rigidity score and the amount of homosynaptic depression are time-locked to the onset of deep brain stimulation leads us to reconsider the mechanisms underlying changes in homosynaptic depression.
DOI: 10.1093/brain/awr267
PubMed: 22075070
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Laennec,44093 Nantes</wicri:regionArea><placeName><region type="region" nuts="2">Pays de la Loire</region><settlement type="city">Nantes</settlement></placeName></affiliation></author><author><name sortKey="Roualdes, Vincent" sort="Roualdes, Vincent" uniqKey="Roualdes V" first="Vincent" last="Roualdes">Vincent Roualdes</name></author><author><name sortKey="Deligny, Celine" sort="Deligny, Celine" uniqKey="Deligny C" first="Céline" last="Deligny">Céline Deligny</name></author><author><name sortKey="Leduc, Dominique" sort="Leduc, Dominique" uniqKey="Leduc D" first="Dominique" last="Leduc">Dominique Leduc</name></author><author><name sortKey="Lamy, Jean Charles" sort="Lamy, Jean Charles" uniqKey="Lamy J" first="Jean-Charles" last="Lamy">Jean-Charles Lamy</name></author><author><name sortKey="Lackmy Vallee, Alexandra" sort="Lackmy Vallee, Alexandra" uniqKey="Lackmy Vallee A" first="Alexandra" last="Lackmy-Vallée">Alexandra Lackmy-Vallée</name></author><author><name sortKey="N Guyen, Jean Paul" sort="N Guyen, Jean Paul" uniqKey="N Guyen J" first="Jean-Paul" last="N'Guyen">Jean-Paul N'Guyen</name></author><author><name sortKey="Damier, Philippe" sort="Damier, Philippe" uniqKey="Damier P" first="Philippe" last="Damier">Philippe Damier</name></author><author><name sortKey="Katz, Rose" sort="Katz, Rose" uniqKey="Katz R" first="Rose" last="Katz">Rose Katz</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:22075070</idno><idno type="pmid">22075070</idno><idno type="doi">10.1093/brain/awr267</idno><idno type="wicri:Area/PubMed/Corpus">000897</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000897</idno><idno type="wicri:Area/PubMed/Curation">000861</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000861</idno><idno type="wicri:Area/PubMed/Checkpoint">000861</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000861</idno><idno type="wicri:Area/Ncbi/Merge">000E06</idno><idno type="wicri:Area/Ncbi/Curation">000E06</idno><idno type="wicri:Area/Ncbi/Checkpoint">000E06</idno><idno type="wicri:Area/Main/Merge">001101</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Subthalamic nucleus stimulation reverses spinal motoneuron activity in parkinsonian patients.</title><author><name sortKey="Raoul, Sylvie" sort="Raoul, Sylvie" uniqKey="Raoul S" first="Sylvie" last="Raoul">Sylvie Raoul</name><affiliation wicri:level="3"><nlm:affiliation>CHU Nantes, Neurosurgery Department, Hôpital G. et R. Laennec,44093 Nantes, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CHU Nantes, Neurosurgery Department, Hôpital G. et R. Laennec,44093 Nantes</wicri:regionArea><placeName><region type="region" nuts="2">Pays de la Loire</region><settlement type="city">Nantes</settlement></placeName></affiliation></author><author><name sortKey="Roualdes, Vincent" sort="Roualdes, Vincent" uniqKey="Roualdes V" first="Vincent" last="Roualdes">Vincent Roualdes</name></author><author><name sortKey="Deligny, Celine" sort="Deligny, Celine" uniqKey="Deligny C" first="Céline" last="Deligny">Céline Deligny</name></author><author><name sortKey="Leduc, Dominique" sort="Leduc, Dominique" uniqKey="Leduc D" first="Dominique" last="Leduc">Dominique Leduc</name></author><author><name sortKey="Lamy, Jean Charles" sort="Lamy, Jean Charles" uniqKey="Lamy J" first="Jean-Charles" last="Lamy">Jean-Charles Lamy</name></author><author><name sortKey="Lackmy Vallee, Alexandra" sort="Lackmy Vallee, Alexandra" uniqKey="Lackmy Vallee A" first="Alexandra" last="Lackmy-Vallée">Alexandra Lackmy-Vallée</name></author><author><name sortKey="N Guyen, Jean Paul" sort="N Guyen, Jean Paul" uniqKey="N Guyen J" first="Jean-Paul" last="N'Guyen">Jean-Paul N'Guyen</name></author><author><name sortKey="Damier, Philippe" sort="Damier, Philippe" uniqKey="Damier P" first="Philippe" last="Damier">Philippe Damier</name></author><author><name sortKey="Katz, Rose" sort="Katz, Rose" uniqKey="Katz R" first="Rose" last="Katz">Rose Katz</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Deep Brain Stimulation</term><term>Female</term><term>Humans</term><term>Long-Term Synaptic Depression (physiology)</term><term>Male</term><term>Middle Aged</term><term>Motor Neurons (physiology)</term><term>Muscle Rigidity (physiopathology)</term><term>Muscle Rigidity (therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Subthalamic Nucleus (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Long-Term Synaptic Depression</term><term>Motor Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Muscle Rigidity</term><term>Parkinson Disease</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Muscle Rigidity</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Deep Brain Stimulation</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although a cardinal symptom of Parkinsonian disease, up to now, rigidity has been investigated much less than spasticity in hemiplegic patients. Many pathophysiological mechanisms may at least theoretically contribute to Parkinsonian rigidity, from altered viscoelastic muscle properties to inability of parkinsonian patients to relax. However, as demonstrated many years ago, motoneuron responses to muscle afferent volleys are involved in rigidity since afferent volleys are suppressed after dorsal root section. To our knowledge, homosynaptic depression (i.e. the fact that motoneuron responses to Ia afferent volleys exhibit a frequency-related depression) has not been studied in parkinsonian disease, despite the fact that in spastic patients, changes in homosynaptic depression are significantly correlated at wrist and ankle levels with the severity of spasticity. Thus, in the present series of experiments, we investigated in parkinsonian patients with chronic implantation of both subthalamic motor nuclei, the amount of homosynaptic depression at wrist and ankle levels on and off deep brain stimulation. Off deep brain stimulation, the frequency-related depression disappeared, the patients became rigid and the amount of homosynaptic depression was significantly correlated with the severity of rigidity. On deep brain stimulation, the frequency-related depression was restored and the rigidity suppressed, suggesting that homosynaptic depression is one of the mechanisms underlying rigidity in Parkinson's disease. Moreover, the unexpected finding that changes in the rigidity score and the amount of homosynaptic depression are time-locked to the onset of deep brain stimulation leads us to reconsider the mechanisms underlying changes in homosynaptic depression.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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