From off-period dystonia to peak-dose chorea
Identifieur interne : 003E11 ( Main/Exploration ); précédent : 003E10; suivant : 003E12From off-period dystonia to peak-dose chorea
Auteurs : Paul Krack [Allemagne] ; Pierre Pollak ; Patricia Limousin [Royaume-Uni] ; Abdelhamid Benazzouz ; Gu Nther Deuschl [Allemagne] ; Alim-Louis BenabidSource :
- Brain [ 0006-8950 ] ; 1999-06.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Adulte.
English descriptors
- KwdEn :
- Adult, Antiparkinson Agents (adverse effects), Antiparkinson agent, Bilateral, Chemotherapy, Chorea, Chorea (chemically induced), Chorea (physiopathology), Chronic, Dyskinesia, Dyskinesia, Drug-Induced (physiopathology), Dyskinesia, Drug-Induced (surgery), Dystonia, Dystonia (chemically induced), Dystonia (physiopathology), Electrical stimulus, Female, Follow-Up Studies, GPi = globus pallidus internus, HFS = high-frequency stimulation, High frequency, Humans, Instrumentation therapy, LID = levodopa-induced dyskinaesias, Levodopa, Levodopa (adverse effects), Male, Middle Aged, Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Periodicity, Prognosis, STN = subthalamic nucleus, Subthalamic nucleus, Thalamic Nuclei (physiopathology), Thalamic Nuclei (surgery), Toxicity, UPDRS = Unified Parkinson's Disease Rating Scale, deep brain stimulation, dystonia, levodopa-induced dyskinaesias, subthalamic nucleus.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemically induced : Chorea, Dystonia.
- drug therapy : Parkinson Disease.
- physiopathology : Chorea, Dyskinesia, Drug-Induced, Dystonia, Parkinson Disease, Thalamic Nuclei.
- surgery : Dyskinesia, Drug-Induced, Thalamic Nuclei.
- Adult, Female, Follow-Up Studies, Humans, Male, Middle Aged, Periodicity.
Abstract
The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.
Url:
DOI: 10.1093/brain/122.6.1133
Affiliations:
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
<term>Antiparkinson Agents (adverse effects)</term>
<term>Antiparkinson agent</term>
<term>Bilateral</term>
<term>Chemotherapy</term>
<term>Chorea</term>
<term>Chorea (chemically induced)</term>
<term>Chorea (physiopathology)</term>
<term>Chronic</term>
<term>Dyskinesia</term>
<term>Dyskinesia, Drug-Induced (physiopathology)</term>
<term>Dyskinesia, Drug-Induced (surgery)</term>
<term>Dystonia</term>
<term>Dystonia (chemically induced)</term>
<term>Dystonia (physiopathology)</term>
<term>Electrical stimulus</term>
<term>Female</term>
<term>Follow-Up Studies</term>
<term>GPi = globus pallidus internus</term>
<term>HFS = high-frequency stimulation</term>
<term>High frequency</term>
<term>Humans</term>
<term>Instrumentation therapy</term>
<term>LID = levodopa-induced dyskinaesias</term>
<term>Levodopa</term>
<term>Levodopa (adverse effects)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Parkinson disease</term>
<term>Parkinson's disease</term>
<term>Periodicity</term>
<term>Prognosis</term>
<term>STN = subthalamic nucleus</term>
<term>Subthalamic nucleus</term>
<term>Thalamic Nuclei (physiopathology)</term>
<term>Thalamic Nuclei (surgery)</term>
<term>Toxicity</term>
<term>UPDRS = Unified Parkinson's Disease Rating Scale</term>
<term>deep brain stimulation</term>
<term>dystonia</term>
<term>levodopa-induced dyskinaesias</term>
<term>subthalamic nucleus</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Chorea</term>
<term>Dystonia</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Chorea</term>
<term>Dyskinesia, Drug-Induced</term>
<term>Dystonia</term>
<term>Parkinson Disease</term>
<term>Thalamic Nuclei</term>
</keywords>
<keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Dyskinesia, Drug-Induced</term>
<term>Thalamic Nuclei</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Female</term>
<term>Follow-Up Studies</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Periodicity</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Adulte</term>
<term>Antiparkinsonien</term>
<term>Bilatéral</term>
<term>Chimiothérapie</term>
<term>Chorée syndrome</term>
<term>Chronique</term>
<term>Dyskinésie</term>
<term>Dystonie</term>
<term>Haute fréquence</term>
<term>Lévodopa</term>
<term>Noyau sousthalamique</term>
<term>Parkinson maladie</term>
<term>Pronostic</term>
<term>Stimulus électrique</term>
<term>Toxicité</term>
<term>Traitement instrumental</term>
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<front><div type="abstract" xml:lang="en">The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.</div>
</front>
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<name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name>
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<country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Limousin, Patricia" sort="Limousin, Patricia" uniqKey="Limousin P" first="Patricia" last="Limousin">Patricia Limousin</name>
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