Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?
Identifieur interne : 001D97 ( Main/Exploration ); précédent : 001D96; suivant : 001D98Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?
Auteurs : Moran Weinberger [Canada] ; William D. Hutchison ; Jonathan O. DostrovskySource :
- Experimental neurology [ 1090-2430 ] ; 2009.
English descriptors
- KwdEn :
- Action Potentials (drug effects), Action Potentials (physiology), Akinetic Mutism (drug therapy), Akinetic Mutism (physiopathology), Antiparkinson Agents (pharmacology), Biological Clocks (drug effects), Biological Clocks (physiology), Dopamine Agents (pharmacology), Humans, Hypokinesia (drug therapy), Hypokinesia (physiopathology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Subthalamic Nucleus (anatomy & histology), Subthalamic Nucleus (physiopathology), Synaptic Transmission (drug effects), Synaptic Transmission (physiology).
- MESH :
- chemical , pharmacology : Antiparkinson Agents, Dopamine Agents.
- anatomy & histology : Subthalamic Nucleus.
- drug effects : Action Potentials, Biological Clocks, Synaptic Transmission.
- drug therapy : Akinetic Mutism, Hypokinesia, Parkinson Disease.
- physiology : Action Potentials, Biological Clocks, Synaptic Transmission.
- physiopathology : Akinetic Mutism, Hypokinesia, Parkinson Disease, Subthalamic Nucleus.
- Humans.
Abstract
There is growing evidence that Parkinson's disease (PD) is associated with pathological synchronous oscillatory activity in the basal ganglia. These synchronized oscillations primarily occur in the 11-30 Hz range, the so-called beta band. Studies of local field potential activity in the subthalamic nucleus (STN) of PD patients suggest that exaggerated beta band oscillatory activity can disrupt function and, in particular, may contribute to slowness of movement. It has been previously shown that the degree of beta oscillatory activity in the STN of PD patients correlates with the patients' benefit from dopaminergic medications, but not with baseline motor deficits. In a paper that was recently published in Experimental Neurology, [Kuhn A.A., Tsui A., Aziz T., Ray N., Brucke C., Kupsch A., Schneider G.H., Brown P., 2009. Pathological synchronisation in the subthalamic nucleus of patients with Parkinson's disease relates to both bradykinesia and rigidity. Exp. Neurol. 215, 380-387.] the authors further establish that the degree of suppression of beta oscillations in the STN by dopaminergic medications can predict the level of improvement in bradykinesia and rigidity but not tremor. This commentary reviews some of the recent findings on beta oscillatory activity in PD and highlights the possible role of these pathological oscillations in mediating PD symptoms.
DOI: 10.1016/j.expneurol.2009.05.014
PubMed: 19460368
Affiliations:
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Hutchison</name></author><author><name sortKey="Dostrovsky, Jonathan O" sort="Dostrovsky, Jonathan O" uniqKey="Dostrovsky J" first="Jonathan O" last="Dostrovsky">Jonathan O. Dostrovsky</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19460368</idno><idno type="pmid">19460368</idno><idno type="doi">10.1016/j.expneurol.2009.05.014</idno><idno type="wicri:Area/PubMed/Corpus">000E43</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000E43</idno><idno type="wicri:Area/PubMed/Curation">000E43</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000E43</idno><idno type="wicri:Area/PubMed/Checkpoint">000E43</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000E43</idno><idno type="wicri:Area/Ncbi/Merge">000A90</idno><idno type="wicri:Area/Ncbi/Curation">000A90</idno><idno type="wicri:Area/Ncbi/Checkpoint">000A90</idno><idno type="wicri:Area/Main/Merge">001F45</idno><idno type="wicri:Area/Main/Curation">001D97</idno><idno type="wicri:Area/Main/Exploration">001D97</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?</title><author><name sortKey="Weinberger, Moran" sort="Weinberger, Moran" uniqKey="Weinberger M" first="Moran" last="Weinberger">Moran Weinberger</name><affiliation wicri:level="4"><nlm:affiliation>Department of Physiology, University of Toronto, Toronto, ON, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Physiology, University of Toronto, Toronto, ON</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author><author><name sortKey="Hutchison, William D" sort="Hutchison, William D" uniqKey="Hutchison W" first="William D" last="Hutchison">William D. Hutchison</name></author><author><name sortKey="Dostrovsky, Jonathan O" sort="Dostrovsky, Jonathan O" uniqKey="Dostrovsky J" first="Jonathan O" last="Dostrovsky">Jonathan O. Dostrovsky</name></author></analytic><series><title level="j">Experimental neurology</title><idno type="eISSN">1090-2430</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action Potentials (drug effects)</term><term>Action Potentials (physiology)</term><term>Akinetic Mutism (drug therapy)</term><term>Akinetic Mutism (physiopathology)</term><term>Antiparkinson Agents (pharmacology)</term><term>Biological Clocks (drug effects)</term><term>Biological Clocks (physiology)</term><term>Dopamine Agents (pharmacology)</term><term>Humans</term><term>Hypokinesia (drug therapy)</term><term>Hypokinesia (physiopathology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Subthalamic Nucleus (anatomy & histology)</term><term>Subthalamic Nucleus (physiopathology)</term><term>Synaptic Transmission (drug effects)</term><term>Synaptic Transmission (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" qualifier="anatomy & histology" xml:lang="en"><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Action Potentials</term><term>Biological Clocks</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Akinetic Mutism</term><term>Hypokinesia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Action Potentials</term><term>Biological Clocks</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Akinetic Mutism</term><term>Hypokinesia</term><term>Parkinson Disease</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is growing evidence that Parkinson's disease (PD) is associated with pathological synchronous oscillatory activity in the basal ganglia. These synchronized oscillations primarily occur in the 11-30 Hz range, the so-called beta band. Studies of local field potential activity in the subthalamic nucleus (STN) of PD patients suggest that exaggerated beta band oscillatory activity can disrupt function and, in particular, may contribute to slowness of movement. It has been previously shown that the degree of beta oscillatory activity in the STN of PD patients correlates with the patients' benefit from dopaminergic medications, but not with baseline motor deficits. In a paper that was recently published in Experimental Neurology, [Kuhn A.A., Tsui A., Aziz T., Ray N., Brucke C., Kupsch A., Schneider G.H., Brown P., 2009. Pathological synchronisation in the subthalamic nucleus of patients with Parkinson's disease relates to both bradykinesia and rigidity. Exp. Neurol. 215, 380-387.] the authors further establish that the degree of suppression of beta oscillations in the STN by dopaminergic medications can predict the level of improvement in bradykinesia and rigidity but not tremor. This commentary reviews some of the recent findings on beta oscillatory activity in PD and highlights the possible role of these pathological oscillations in mediating PD symptoms.</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><noCountry><name sortKey="Dostrovsky, Jonathan O" sort="Dostrovsky, Jonathan O" uniqKey="Dostrovsky J" first="Jonathan O" last="Dostrovsky">Jonathan O. Dostrovsky</name><name sortKey="Hutchison, William D" sort="Hutchison, William D" uniqKey="Hutchison W" first="William D" last="Hutchison">William D. Hutchison</name></noCountry><country name="Canada"><region name="Ontario"><name sortKey="Weinberger, Moran" sort="Weinberger, Moran" uniqKey="Weinberger M" first="Moran" last="Weinberger">Moran Weinberger</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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