Spinal and cortical inhibition in huntington's chorea
Identifieur interne : 004960 ( Main/Exploration ); précédent : 004959; suivant : 004961Spinal and cortical inhibition in huntington's chorea
Auteurs : Alberto Priori [Italie] ; Luigi Polidori [Italie] ; Sabine Rona [Italie] ; Mario Manfredi [Italie] ; Alfredo Berardelli [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 2000-09.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Adulte.
English descriptors
- KwdEn :
- Adult, Aged, Case-Control Studies, Cerebral cortex, Cortical stimulation, Electric Stimulation, Electromyography, Exploration, Female, H-Reflex, Humans, Huntington Disease (physiopathology), Huntington disease, Hyperkinesia, Magnetic stimulus, Magnetics, Male, Middle Aged, Models, Neurological, Motor Cortex (pathology), Motor Cortex (physiopathology), Motor evoked potential, Neural Inhibition, Neural Pathways (physiopathology), Pathogenesis, Presynaptic Terminals, Reciprocal inhibition, Spinal Cord (pathology), Spinal Cord (physiopathology), Spinal cord, Transcranial route.
- MESH :
- pathology : Motor Cortex, Spinal Cord.
- physiopathology : Huntington Disease, Motor Cortex, Neural Pathways, Spinal Cord.
- Adult, Aged, Case-Control Studies, Electric Stimulation, Electromyography, Female, H-Reflex, Humans, Magnetics, Male, Middle Aged, Models, Neurological, Neural Inhibition, Presynaptic Terminals.
Abstract
In this article we studied spinal and cortical inhibitory mechanisms in patients with Huntington's disease. To evaluate spinal cord inhibitory circuitries, we assessed reciprocal inhibition between antagonist forearm muscles and the recovery cycle of the H reflex in the flexor carpi radialis. Patients showed a significant decrease in the presynaptic phase of reciprocal inhibition reaching a minimum at the conditioning‐test interval of 20 msec and an abnormal facilitation of the test H reflex at the conditioning test interval of 40 to 60 msec. Throughout its time course (10–200 msec), the H reflex recovery cycle showed a more prominent facilitation in patients than in control subjects. To assess whether the observed pathophysiological abnormalities might have arisen from an abnormal motor cortical excitability, we examined the recovery cycle of the motor potentials evoked by paired transcranial magnetic stimuli. We found that the inhibitory mechanisms controlling motor cortical excitability were normal. An interpretation of the spinal cord abnormalities is that the intrinsically normal but deafferentated motor cortex in Huntington's disease partly loses its inhibitory control, thus disinhibiting spinal cord circuitry. Our findings from paired transcranial magnetic stimulation suggest that cortical motor areas are not hyperexcitable in Huntington's disease. Hence, the postulated thalamocortical overactivity in experimental models of Huntington's disease needs to be reappraised.
Url:
DOI: 10.1002/1531-8257(200009)15:5<938::AID-MDS1026>3.0.CO;2-Q
Affiliations:
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Le document en format XML
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<term>Cortical stimulation</term>
<term>Electric Stimulation</term>
<term>Electromyography</term>
<term>Exploration</term>
<term>Female</term>
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<term>Pathogenesis</term>
<term>Presynaptic Terminals</term>
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<term>Spinal Cord (physiopathology)</term>
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<term>Neural Pathways</term>
<term>Spinal Cord</term>
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<term>Aged</term>
<term>Case-Control Studies</term>
<term>Electric Stimulation</term>
<term>Electromyography</term>
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<term>H-Reflex</term>
<term>Humans</term>
<term>Magnetics</term>
<term>Male</term>
<term>Middle Aged</term>
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<term>Neural Inhibition</term>
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<term>Chorée Huntington</term>
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<term>Inhibition réciproque</term>
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<term>Pathogénie</term>
<term>Potentiel évoqué moteur</term>
<term>Réflexe H</term>
<term>Stimulus magnétique</term>
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<front><div type="abstract" xml:lang="en">In this article we studied spinal and cortical inhibitory mechanisms in patients with Huntington's disease. To evaluate spinal cord inhibitory circuitries, we assessed reciprocal inhibition between antagonist forearm muscles and the recovery cycle of the H reflex in the flexor carpi radialis. Patients showed a significant decrease in the presynaptic phase of reciprocal inhibition reaching a minimum at the conditioning‐test interval of 20 msec and an abnormal facilitation of the test H reflex at the conditioning test interval of 40 to 60 msec. Throughout its time course (10–200 msec), the H reflex recovery cycle showed a more prominent facilitation in patients than in control subjects. To assess whether the observed pathophysiological abnormalities might have arisen from an abnormal motor cortical excitability, we examined the recovery cycle of the motor potentials evoked by paired transcranial magnetic stimuli. We found that the inhibitory mechanisms controlling motor cortical excitability were normal. An interpretation of the spinal cord abnormalities is that the intrinsically normal but deafferentated motor cortex in Huntington's disease partly loses its inhibitory control, thus disinhibiting spinal cord circuitry. Our findings from paired transcranial magnetic stimulation suggest that cortical motor areas are not hyperexcitable in Huntington's disease. Hence, the postulated thalamocortical overactivity in experimental models of Huntington's disease needs to be reappraised.</div>
</front>
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<tree><country name="Italie"><noRegion><name sortKey="Priori, Alberto" sort="Priori, Alberto" uniqKey="Priori A" first="Alberto" last="Priori">Alberto Priori</name>
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<name sortKey="Berardelli, Alfredo" sort="Berardelli, Alfredo" uniqKey="Berardelli A" first="Alfredo" last="Berardelli">Alfredo Berardelli</name>
<name sortKey="Manfredi, Mario" sort="Manfredi, Mario" uniqKey="Manfredi M" first="Mario" last="Manfredi">Mario Manfredi</name>
<name sortKey="Polidori, Luigi" sort="Polidori, Luigi" uniqKey="Polidori L" first="Luigi" last="Polidori">Luigi Polidori</name>
<name sortKey="Rona, Sabine" sort="Rona, Sabine" uniqKey="Rona S" first="Sabine" last="Rona">Sabine Rona</name>
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