Subthalamic nucleus activity dissociates proactive and reactive inhibition in patients with Parkinson's disease.
Identifieur interne : 000839 ( Main/Curation ); précédent : 000838; suivant : 000840Subthalamic nucleus activity dissociates proactive and reactive inhibition in patients with Parkinson's disease.
Auteurs : Damien Benis [France] ; Olivier David [France] ; Jean-Philippe Lachaux [France] ; Eric Seigneuret [France] ; Paul Krack [France] ; Valérie Fraix [France] ; Stéphan Chabardès [France] ; Julien Bastin [France]Source :
- NeuroImage [ 1095-9572 ] ; 2014.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (therapeutic use), Attention (physiology), Beta Rhythm (physiology), Deep Brain Stimulation, Electrodes, Implanted, Executive Function (physiology), Female, Humans, Levodopa (therapeutic use), Male, Middle Aged, Motivation (physiology), Motor Cortex (physiology), Neural Pathways (physiology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Psychomotor Performance (physiology), Reaction Time (physiology), Reactive Inhibition, Subthalamic Nucleus (physiopathology).
- MESH :
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinson Disease.
- physiology : Attention, Beta Rhythm, Executive Function, Motivation, Motor Cortex, Neural Pathways, Psychomotor Performance, Reaction Time.
- physiopathology : Parkinson Disease, Subthalamic Nucleus.
- therapy : Parkinson Disease.
- Aged, Deep Brain Stimulation, Electrodes, Implanted, Female, Humans, Male, Middle Aged, Reactive Inhibition.
Abstract
Models of action selection postulate the critical involvement of the subthalamic nucleus (STN), especially in reactive inhibition processes when inappropriate responses to a sudden stimulus must be overridden. The STN could also play a key role during proactive inhibition, when subjects prepare to potentially suppress their actions. Here, we hypothesized that STN responses to reactive and proactive inhibitory control might be driven by different underlying mechanisms with specific temporal profiles. Direct neural recordings in twelve Parkinson's disease patients during a modified stop signal task (SST) revealed a decrease of beta band activity (βA, 13-35Hz) in the STN during reactive inhibition of smaller amplitude and shorter duration than during motor execution. Crucially, the onset latency of this relative increase of βA took place before the stop signal reaction time. It could thus be thought of as a "stop" signal inhibiting thalamo-cortical activity that would have supported motor execution. Finally, results also revealed a higher level of βA in the STN during proactive inhibition, which correlated with patient's inhibitory performances. We propose that βA in the STN would here participate in the implementation of a "hold your horse" signal to delay motor responses, thus prioritizing accuracy as compared to speed. In brief, our results provide strong electrophysiological support for the hypothesized role of the STN during executive control underlying proactive and reactive response suppression.
DOI: 10.1016/j.neuroimage.2013.10.070
PubMed: 24368260
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pubmed:24368260Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term>
<term>Antiparkinson Agents (therapeutic use)</term>
<term>Attention (physiology)</term>
<term>Beta Rhythm (physiology)</term>
<term>Deep Brain Stimulation</term>
<term>Electrodes, Implanted</term>
<term>Executive Function (physiology)</term>
<term>Female</term>
<term>Humans</term>
<term>Levodopa (therapeutic use)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Motivation (physiology)</term>
<term>Motor Cortex (physiology)</term>
<term>Neural Pathways (physiology)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Parkinson Disease (therapy)</term>
<term>Psychomotor Performance (physiology)</term>
<term>Reaction Time (physiology)</term>
<term>Reactive Inhibition</term>
<term>Subthalamic Nucleus (physiopathology)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Attention</term>
<term>Beta Rhythm</term>
<term>Executive Function</term>
<term>Motivation</term>
<term>Motor Cortex</term>
<term>Neural Pathways</term>
<term>Psychomotor Performance</term>
<term>Reaction Time</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term>
<term>Subthalamic Nucleus</term>
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<term>Deep Brain Stimulation</term>
<term>Electrodes, Implanted</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
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<front><div type="abstract" xml:lang="en">Models of action selection postulate the critical involvement of the subthalamic nucleus (STN), especially in reactive inhibition processes when inappropriate responses to a sudden stimulus must be overridden. The STN could also play a key role during proactive inhibition, when subjects prepare to potentially suppress their actions. Here, we hypothesized that STN responses to reactive and proactive inhibitory control might be driven by different underlying mechanisms with specific temporal profiles. Direct neural recordings in twelve Parkinson's disease patients during a modified stop signal task (SST) revealed a decrease of beta band activity (βA, 13-35Hz) in the STN during reactive inhibition of smaller amplitude and shorter duration than during motor execution. Crucially, the onset latency of this relative increase of βA took place before the stop signal reaction time. It could thus be thought of as a "stop" signal inhibiting thalamo-cortical activity that would have supported motor execution. Finally, results also revealed a higher level of βA in the STN during proactive inhibition, which correlated with patient's inhibitory performances. We propose that βA in the STN would here participate in the implementation of a "hold your horse" signal to delay motor responses, thus prioritizing accuracy as compared to speed. In brief, our results provide strong electrophysiological support for the hypothesized role of the STN during executive control underlying proactive and reactive response suppression.</div>
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