Abnormal Dorsal Premotor-Motor Inhibition in Writer’s Cramp
Identifieur interne : 000677 ( Main/Exploration ); précédent : 000676; suivant : 000678Abnormal Dorsal Premotor-Motor Inhibition in Writer’s Cramp
Auteurs : Sarah Pirio Richardson [États-Unis] ; Sandra Beck [Allemagne, États-Unis] ; Barbara Bliem [États-Unis] ; Mark Hallett [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2014.
English descriptors
- KwdEn :
- Analysis of Variance, Case-Control Studies, Choice Behavior, Dystonic Disorders (pathology), Electromyography, Evoked Potentials, Motor (physiology), Female, Functional Laterality, H-Reflex (physiology), Humans, Inhibition (Psychology), Male, Motor Cortex (physiopathology), Neural Inhibition (physiology), Reaction Time, Spinal Cord (physiopathology), Transcranial Magnetic Stimulation.
- MESH :
- pathology : Dystonic Disorders.
- physiology : Evoked Potentials, Motor, H-Reflex, Neural Inhibition.
- physiopathology : Motor Cortex, Spinal Cord.
- Analysis of Variance, Case-Control Studies, Choice Behavior, Electromyography, Female, Functional Laterality, Humans, Inhibition (Psychology), Male, Reaction Time, Transcranial Magnetic Stimulation.
Abstract
We hypothesize that a deficient premotor-motor inhibitory network contributes to the unwanted involuntary movements in dystonia.
We studied nine controls and nine patients with writer’s cramp (WC). Dorsal premotor-motor cortical inhibition (dPMI) was tested by applying conditioning transcranial magnetic stimulation (TMS) to the dorsal premotor cortex and then a test pulse to the ipsilateral motor cortex at an interval of 6ms. We used an H-reflex in flexor carpi radialis paired with TMS over the premotor cortex to assess for spinal cord excitability change. Finally, we interrupted a choice reaction time task with TMS over dorsal premotor cortex to assess performance in a non-dystonic task.
Our results showed that WC patients exhibited dPMI at rest (88.5%, the ratio of conditioned to unconditioned test pulse) in contrast to our controls who did not show dPMI (109.6%) (p=0.0198). This difference between patients and controls persisted during contraction (100% vs. 112%) and pen-holding (95.6% vs. 111%). The H-reflex in the arm was not modulated by the premotor cortex stimulation. WC patients made more errors and the error rate improved with TMS over the premotor cortex.
These results suggest that abnormal premotor-motor interactions may play a role in the pathophysiology of focal dystonia. dPMI was not modulated by task in either group, but was constantly greater in the patients. The significance of the increased inhibition is likely to be compensatory. It appears to be a robust finding and, in combination with other features, could be further explored as a biomarker.
Url:
DOI: 10.1002/mds.25878
PubMed: 24710852
PubMed Central: 4122418
Affiliations:
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wicri:level="2"><nlm:aff id="A1">Department of Neurology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Department of Neurology, University of New Mexico Health Sciences Center, Albuquerque</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="A3">Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Beck, Sandra" sort="Beck, Sandra" uniqKey="Beck S" first="Sandra" last="Beck">Sandra Beck</name><affiliation wicri:level="1"><nlm:aff id="A2">Department of Neurology and Clinical Neurophysiology, University of Freiburg, Freiburg im Breisgau, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurology and Clinical Neurophysiology, University of Freiburg, Freiburg im Breisgau</wicri:regionArea><wicri:noRegion>Freiburg im Breisgau</wicri:noRegion><wicri:noRegion>Freiburg im Breisgau</wicri:noRegion><wicri:noRegion>Freiburg im Breisgau</wicri:noRegion></affiliation><affiliation wicri:level="2"><nlm:aff id="A3">Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Bliem, Barbara" sort="Bliem, Barbara" uniqKey="Bliem B" first="Barbara" last="Bliem">Barbara Bliem</name><affiliation wicri:level="2"><nlm:aff id="A3">Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Hallett, Mark" sort="Hallett, Mark" uniqKey="Hallett M" first="Mark" last="Hallett">Mark Hallett</name><affiliation wicri:level="2"><nlm:aff id="A3">Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region 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Inhibition (physiology)</term><term>Reaction Time</term><term>Spinal Cord (physiopathology)</term><term>Transcranial Magnetic Stimulation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dystonic Disorders</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Evoked Potentials, Motor</term><term>H-Reflex</term><term>Neural Inhibition</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Motor Cortex</term><term>Spinal Cord</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Case-Control Studies</term><term>Choice Behavior</term><term>Electromyography</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Inhibition (Psychology)</term><term>Male</term><term>Reaction Time</term><term>Transcranial Magnetic Stimulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title><p id="P1">We hypothesize that a deficient premotor-motor inhibitory network contributes to the unwanted involuntary movements in dystonia.</p></sec><sec id="S2"><title>Methods</title><p id="P2">We studied nine controls and nine patients with writer’s cramp (WC). Dorsal premotor-motor cortical inhibition (dPMI) was tested by applying conditioning transcranial magnetic stimulation (TMS) to the dorsal premotor cortex and then a test pulse to the ipsilateral motor cortex at an interval of 6ms. We used an H-reflex in flexor carpi radialis paired with TMS over the premotor cortex to assess for spinal cord excitability change. Finally, we interrupted a choice reaction time task with TMS over dorsal premotor cortex to assess performance in a non-dystonic task.</p></sec><sec id="S3"><title>Results</title><p id="P3">Our results showed that WC patients exhibited dPMI at rest (88.5%, the ratio of conditioned to unconditioned test pulse) in contrast to our controls who did not show dPMI (109.6%) (p=0.0198). This difference between patients and controls persisted during contraction (100% vs. 112%) and pen-holding (95.6% vs. 111%). The H-reflex in the arm was not modulated by the premotor cortex stimulation. WC patients made more errors and the error rate improved with TMS over the premotor cortex.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">These results suggest that abnormal premotor-motor interactions may play a role in the pathophysiology of focal dystonia. dPMI was not modulated by task in either group, but was constantly greater in the patients. The significance of the increased inhibition is likely to be compensatory. It appears to be a robust finding and, in combination with other features, could be further explored as a biomarker.</p></sec></div></front></TEI><affiliations><list><country><li>Allemagne</li><li>États-Unis</li></country><region><li>Maryland</li><li>Nouveau-Mexique</li></region></list><tree><country name="États-Unis"><region name="Nouveau-Mexique"><name sortKey="Richardson, Sarah Pirio" sort="Richardson, Sarah Pirio" uniqKey="Richardson S" first="Sarah Pirio" last="Richardson">Sarah Pirio Richardson</name></region><name sortKey="Beck, Sandra" sort="Beck, Sandra" uniqKey="Beck S" first="Sandra" last="Beck">Sandra Beck</name><name sortKey="Bliem, Barbara" sort="Bliem, Barbara" uniqKey="Bliem B" first="Barbara" last="Bliem">Barbara Bliem</name><name sortKey="Hallett, Mark" sort="Hallett, Mark" uniqKey="Hallett M" first="Mark" last="Hallett">Mark Hallett</name><name sortKey="Richardson, Sarah Pirio" sort="Richardson, Sarah Pirio" uniqKey="Richardson S" first="Sarah Pirio" last="Richardson">Sarah Pirio Richardson</name></country><country name="Allemagne"><noRegion><name sortKey="Beck, Sandra" sort="Beck, Sandra" uniqKey="Beck S" first="Sandra" last="Beck">Sandra Beck</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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