From off-period dystonia to peak-dose chorea
Identifieur interne : 002519 ( Istex/Corpus ); précédent : 002518; suivant : 002520From off-period dystonia to peak-dose chorea
Auteurs : Paul Krack ; Pierre Pollak ; Patricia Limousin ; Abdelhamid Benazzouz ; Gu Nther Deuschl ; Alim-Louis BenabidSource :
- Brain [ 0006-8950 ] ; 1999-06.
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- KwdEn :
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.
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DOI: 10.1093/brain/122.6.1133
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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>
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<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.</abstract>
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<istex:fulltextTEI uri="https://api.istex.fr/document/8F037AEB01C2F6CB70E4BD26EC8AF299425834CC/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">From off-period dystonia to peak-dose chorea</title>
<title level="a" type="sub" xml:lang="en">The clinical spectrum of varying subthalamic nucleus activity</title>
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<notesStmt><note>P. Krack, Neurology Department, University of Kiel, Niemannsweg 147, 24105 Kiel, Germany E-mail: p.krack@neurologie.uni-kiel.de</note>
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<author xml:id="author-1"><persName><forename type="first">Paul</forename>
<surname>Krack</surname>
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<affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</affiliation>
<affiliation>Neurology Department, Christian Albrecht Universität, Kiel, Germany and</affiliation>
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<author xml:id="author-2"><persName><forename type="first">Pierre</forename>
<surname>Pollak</surname>
</persName>
<affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</affiliation>
</author>
<author xml:id="author-3"><persName><forename type="first">Patricia</forename>
<surname>Limousin</surname>
</persName>
<affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</affiliation>
<affiliation>MRC Human Movement and Balance Unit, Queen Square, London, UK</affiliation>
</author>
<author xml:id="author-4"><persName><forename type="first">Abdelhamid</forename>
<surname>Benazzouz</surname>
</persName>
<affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</affiliation>
</author>
<author xml:id="author-5"><persName><forename type="first">Günther</forename>
<surname>Deuschl</surname>
</persName>
<affiliation>Neurology Department, Christian Albrecht Universität, Kiel, Germany and</affiliation>
</author>
<author xml:id="author-6"><persName><forename type="first">Alim-Louis</forename>
<surname>Benabid</surname>
</persName>
<affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</affiliation>
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<title level="j" type="abbrev">Brain</title>
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<abstract xml:lang="en"><p>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.</p>
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<item><term>Parkinson's disease</term>
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<item><term>dystonia</term>
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<subtitle>The clinical spectrum of varying subthalamic nucleus activity</subtitle>
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<contrib-group><contrib contrib-type="author"><name><surname>Krack</surname>
<given-names>Paul</given-names>
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<contrib contrib-type="author"><name><surname>Deuschl</surname>
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<contrib contrib-type="author"><name><surname>Benabid</surname>
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<aff id="AFF1"><label>1</label>
Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France, </aff>
<aff id="AFF2"><label>2</label>
Neurology Department, Christian Albrecht Universität, Kiel, Germany and </aff>
<aff id="AFF3"><label>3</label>
MRC Human Movement and Balance Unit, Queen Square, London, UK</aff>
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<author-notes><corresp>P. Krack, Neurology Department, University of Kiel, Niemannsweg 147, 24105 Kiel, Germany E-mail: <ext-link xlink:href="p.krack@neurologie.uni-kiel.de" ext-link-type="email">p.krack@neurologie.uni-kiel.de</ext-link>
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<copyright-statement>© Oxford University Press 1999</copyright-statement>
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<abstract xml:lang="en"><p>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.</p>
</abstract>
<kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>Parkinson's disease</kwd>
<kwd>levodopa-induced dyskinaesias</kwd>
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<kwd>subthalamic nucleus</kwd>
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<mods version="3.6"><titleInfo lang="en"><title>From off-period dystonia to peak-dose chorea</title>
<subTitle>The clinical spectrum of varying subthalamic nucleus activity</subTitle>
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<titleInfo type="alternative" lang="en" contentType="CDATA"><title>From off-period dystonia to peak-dose chorea</title>
<subTitle>The clinical spectrum of varying subthalamic nucleus activity</subTitle>
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<name type="personal"><namePart type="given">Paul</namePart>
<namePart type="family">Krack</namePart>
<affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</affiliation>
<affiliation>Neurology Department, Christian Albrecht Universität, Kiel, Germany and</affiliation>
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<name type="personal"><namePart type="given">Pierre</namePart>
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<affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</affiliation>
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</name>
<name type="personal"><namePart type="given">Patricia</namePart>
<namePart type="family">Limousin</namePart>
<affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France,</affiliation>
<affiliation>MRC Human Movement and Balance Unit, Queen Square, London, UK</affiliation>
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<name type="personal"><namePart type="given">Abdelhamid</namePart>
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<name type="personal"><namePart type="given">Günther</namePart>
<namePart type="family">Deuschl</namePart>
<affiliation>Neurology Department, Christian Albrecht Universität, Kiel, Germany and</affiliation>
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<name type="personal"><namePart type="given">Alim-Louis</namePart>
<namePart type="family">Benabid</namePart>
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<abstract 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.</abstract>
<note type="author-notes">P. Krack, Neurology Department, University of Kiel, Niemannsweg 147, 24105 Kiel, Germany E-mail: p.krack@neurologie.uni-kiel.de</note>
<subject lang="en"><genre>KWD</genre>
<topic>Parkinson's disease</topic>
<topic>levodopa-induced dyskinaesias</topic>
<topic>dystonia</topic>
<topic>subthalamic nucleus</topic>
<topic>deep brain stimulation</topic>
</subject>
<subject lang="en"><genre>ABR</genre>
<topic>GPi = globus pallidus internus</topic>
<topic>HFS = high-frequency stimulation</topic>
<topic>LID = levodopa-induced dyskinaesias</topic>
<topic>STN = subthalamic nucleus</topic>
<topic>UPDRS = Unified Parkinson's Disease Rating Scale</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Brain</title>
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<titleInfo type="abbreviated"><title>Brain</title>
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<genre type="journal">journal</genre>
<identifier type="ISSN">0006-8950</identifier>
<identifier type="eISSN">1460-2156</identifier>
<identifier type="PublisherID">brainj</identifier>
<identifier type="PublisherID-hwp">brain</identifier>
<identifier type="PublisherID-nlm-ta">Brain</identifier>
<part><date>1999</date>
<detail type="volume"><caption>vol.</caption>
<number>122</number>
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<detail type="issue"><caption>no.</caption>
<number>6</number>
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<extent unit="pages"><start>1133</start>
<end>1146</end>
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<identifier type="DOI">10.1093/brain/122.6.1133</identifier>
<identifier type="local">1221133</identifier>
<accessCondition type="use and reproduction" contentType="copyright">© Oxford University Press 1999</accessCondition>
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