Progression of motor and nonmotor features of Parkinson's disease and their response to treatment
Identifieur interne : 000356 ( Ncbi/Merge ); précédent : 000355; suivant : 000357Progression of motor and nonmotor features of Parkinson's disease and their response to treatment
Auteurs : Thuy Vu [États-Unis] ; John Nutt [États-Unis] ; Nicholas Holford [Nouvelle-Zélande]Source :
- British Journal of Clinical Pharmacology [ 0306-5251 ] ; 2012.
Abstract
(i) To describe the progression of the cardinal features of Parkinson's disease (PD); (ii) to investigate whether baseline PD subtypes explain disease progression; and (iii) to quantify the symptomatic and disease-modifying effects of anti-parkinsonian treatments.
Data were available for 795 PD subjects, initially untreated, followed for up to 8 years. Cardinal features [tremor, rigidity, bradykinesia, and postural instability and gait disorder (PIGD)] were derived from the total unified Parkinson's disease rating scale (total UPDRS), cognitive status from the mini-mental status exam score (MMSE) and depression status from the Hamilton depression scale (HAM-D). Analysis was performed using a nonlinear mixed effects approach with an asymptotic model for natural disease progression. Treatment effects (i.e. symptomatic and disease modifying) were evaluated by describing changes in the natural history model parameters.
Tremor progressed more slowly (half-time of 3.9 years) than all other motor features (half-time 2–3 years). The MMSE progression was negligible, while HAM-D progressed with a half-time of 5 years. Levodopa had marked symptomatic effects on all features, but low potency for effect on PIGD (
This analysis indicates that tremor progresses more slowly than other cardinal features and that PIGD is less treatment responsive in early PD patients. There was no evidence of baseline PD subtypes as a clinically useful predictor of disease progression rate. Anti-parkinsonian treatments have symptomatic and disease-modifying effects on all major features of PD.
Url:
DOI: 10.1111/j.1365-2125.2012.04192.x
PubMed: 22283961
PubMed Central: 3630747
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PMC:3630747Le document en format XML
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<author><name sortKey="Vu, Thuy C" sort="Vu, Thuy C" uniqKey="Vu T" first="Thuy" last="Vu">Thuy Vu</name>
<affiliation wicri:level="2"><nlm:aff id="au1">Department of Pharmacokinetics and Drug Metabolism, Amgen Inc., Thousand Oaks, CA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacokinetics and Drug Metabolism, Amgen Inc., Thousand Oaks, CA</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
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<author><name sortKey="Nutt, John G" sort="Nutt, John G" uniqKey="Nutt J" first="John" last="Nutt">John Nutt</name>
<affiliation wicri:level="2"><nlm:aff id="au2">Department of Neurology, Oregon Health and Science University, Portland, OR, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurology, Oregon Health and Science University, Portland, OR</wicri:regionArea>
<placeName><region type="state">Oregon</region>
</placeName>
</affiliation>
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<author><name sortKey="Holford, Nicholas H G" sort="Holford, Nicholas H G" uniqKey="Holford N" first="Nicholas" last="Holford">Nicholas Holford</name>
<affiliation wicri:level="1"><nlm:aff id="au3">Department of Pharmacology and Clinical Pharmacology, University of Auckland, New Zealand</nlm:aff>
<country xml:lang="fr">Nouvelle-Zélande</country>
<wicri:regionArea>Department of Pharmacology and Clinical Pharmacology, University of Auckland</wicri:regionArea>
<wicri:noRegion>University of Auckland</wicri:noRegion>
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<author><name sortKey="Vu, Thuy C" sort="Vu, Thuy C" uniqKey="Vu T" first="Thuy" last="Vu">Thuy Vu</name>
<affiliation wicri:level="2"><nlm:aff id="au1">Department of Pharmacokinetics and Drug Metabolism, Amgen Inc., Thousand Oaks, CA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacokinetics and Drug Metabolism, Amgen Inc., Thousand Oaks, CA</wicri:regionArea>
<placeName><region type="state">Californie</region>
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<author><name sortKey="Nutt, John G" sort="Nutt, John G" uniqKey="Nutt J" first="John" last="Nutt">John Nutt</name>
<affiliation wicri:level="2"><nlm:aff id="au2">Department of Neurology, Oregon Health and Science University, Portland, OR, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurology, Oregon Health and Science University, Portland, OR</wicri:regionArea>
<placeName><region type="state">Oregon</region>
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<author><name sortKey="Holford, Nicholas H G" sort="Holford, Nicholas H G" uniqKey="Holford N" first="Nicholas" last="Holford">Nicholas Holford</name>
<affiliation wicri:level="1"><nlm:aff id="au3">Department of Pharmacology and Clinical Pharmacology, University of Auckland, New Zealand</nlm:aff>
<country xml:lang="fr">Nouvelle-Zélande</country>
<wicri:regionArea>Department of Pharmacology and Clinical Pharmacology, University of Auckland</wicri:regionArea>
<wicri:noRegion>University of Auckland</wicri:noRegion>
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<series><title level="j">British Journal of Clinical Pharmacology</title>
<idno type="ISSN">0306-5251</idno>
<idno type="e-ISSN">1365-2125</idno>
<imprint><date when="2012">2012</date>
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<front><div type="abstract" xml:lang="en"><sec><title>AIMS</title>
<p>(i) To describe the progression of the cardinal features of Parkinson's disease (PD); (ii) to investigate whether baseline PD subtypes explain disease progression; and (iii) to quantify the symptomatic and disease-modifying effects of anti-parkinsonian treatments.</p>
</sec>
<sec><title>METHODS</title>
<p>Data were available for 795 PD subjects, initially untreated, followed for up to 8 years. Cardinal features [tremor, rigidity, bradykinesia, and postural instability and gait disorder (PIGD)] were derived from the total unified Parkinson's disease rating scale (total UPDRS), cognitive status from the mini-mental status exam score (MMSE) and depression status from the Hamilton depression scale (HAM-D). Analysis was performed using a nonlinear mixed effects approach with an asymptotic model for natural disease progression. Treatment effects (i.e. symptomatic and disease modifying) were evaluated by describing changes in the natural history model parameters.</p>
</sec>
<sec><title>RESULTS</title>
<p>Tremor progressed more slowly (half-time of 3.9 years) than all other motor features (half-time 2–3 years). The MMSE progression was negligible, while HAM-D progressed with a half-time of 5 years. Levodopa had marked symptomatic effects on all features, but low potency for effect on PIGD (<italic>ED</italic>
<sub>50</sub>
of 1237 mg day<sup>−1</sup>
compared with 7–24 mg day<sup>−1</sup>
for other motor and nonmotor features). Other anti-parkinsonian treatments had much smaller symptomatic effects. All treatments had disease-modifying effects on the cardinal features of PD. Baseline PD subtypes only explained small differences in disease progression.</p>
</sec>
<sec><title>CONCLUSIONS</title>
<p>This analysis indicates that tremor progresses more slowly than other cardinal features and that PIGD is less treatment responsive in early PD patients. There was no evidence of baseline PD subtypes as a clinically useful predictor of disease progression rate. Anti-parkinsonian treatments have symptomatic and disease-modifying effects on all major features of PD.</p>
</sec>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Br J Clin Pharmacol</journal-id>
<journal-id journal-id-type="iso-abbrev">Br J Clin Pharmacol</journal-id>
<journal-id journal-id-type="publisher-id">bcp</journal-id>
<journal-title-group><journal-title>British Journal of Clinical Pharmacology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0306-5251</issn>
<issn pub-type="epub">1365-2125</issn>
<publisher><publisher-name>Blackwell Publishing Ltd</publisher-name>
<publisher-loc>Oxford, UK</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">22283961</article-id>
<article-id pub-id-type="pmc">3630747</article-id>
<article-id pub-id-type="doi">10.1111/j.1365-2125.2012.04192.x</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Treatment of Parkinson's disease</subject>
</subj-group>
</article-categories>
<title-group><article-title>Progression of motor and nonmotor features of Parkinson's disease and their response to treatment</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Vu</surname>
<given-names>Thuy C.</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nutt</surname>
<given-names>John G.</given-names>
</name>
<xref ref-type="aff" rid="au2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Holford</surname>
<given-names>Nicholas H. G.</given-names>
</name>
<xref ref-type="aff" rid="au3">3</xref>
</contrib>
</contrib-group>
<aff id="au1"><label>1</label>
Department of Pharmacokinetics and Drug Metabolism, Amgen Inc., Thousand Oaks, CA, USA</aff>
<aff id="au2"><label>2</label>
Department of Neurology, Oregon Health and Science University, Portland, OR, USA</aff>
<aff id="au3"><label>3</label>
Department of Pharmacology and Clinical Pharmacology, University of Auckland, New Zealand</aff>
<author-notes><corresp id="cor1">Professor Nick Holford, Department of Pharmacology & Clinical Pharmacology, University of Auckland, 85 Park Road, Private Bag 92019, Auckland, New Zealand. Tel.: +64 9 923 6730. Fax: +64 9 373 7090. E-mail: <email>n.holford@auckland.ac.nz</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>8</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="epub"><day>10</day>
<month>7</month>
<year>2012</year>
</pub-date>
<volume>74</volume>
<issue>2</issue>
<fpage>267</fpage>
<lpage>283</lpage>
<history><date date-type="received"><day>21</day>
<month>1</month>
<year>2011</year>
</date>
<date date-type="accepted"><day>15</day>
<month>1</month>
<year>2012</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2012 The British Pharmacological Society</copyright-statement>
<copyright-year>2012</copyright-year>
</permissions>
<abstract><sec><title>AIMS</title>
<p>(i) To describe the progression of the cardinal features of Parkinson's disease (PD); (ii) to investigate whether baseline PD subtypes explain disease progression; and (iii) to quantify the symptomatic and disease-modifying effects of anti-parkinsonian treatments.</p>
</sec>
<sec><title>METHODS</title>
<p>Data were available for 795 PD subjects, initially untreated, followed for up to 8 years. Cardinal features [tremor, rigidity, bradykinesia, and postural instability and gait disorder (PIGD)] were derived from the total unified Parkinson's disease rating scale (total UPDRS), cognitive status from the mini-mental status exam score (MMSE) and depression status from the Hamilton depression scale (HAM-D). Analysis was performed using a nonlinear mixed effects approach with an asymptotic model for natural disease progression. Treatment effects (i.e. symptomatic and disease modifying) were evaluated by describing changes in the natural history model parameters.</p>
</sec>
<sec><title>RESULTS</title>
<p>Tremor progressed more slowly (half-time of 3.9 years) than all other motor features (half-time 2–3 years). The MMSE progression was negligible, while HAM-D progressed with a half-time of 5 years. Levodopa had marked symptomatic effects on all features, but low potency for effect on PIGD (<italic>ED</italic>
<sub>50</sub>
of 1237 mg day<sup>−1</sup>
compared with 7–24 mg day<sup>−1</sup>
for other motor and nonmotor features). Other anti-parkinsonian treatments had much smaller symptomatic effects. All treatments had disease-modifying effects on the cardinal features of PD. Baseline PD subtypes only explained small differences in disease progression.</p>
</sec>
<sec><title>CONCLUSIONS</title>
<p>This analysis indicates that tremor progresses more slowly than other cardinal features and that PIGD is less treatment responsive in early PD patients. There was no evidence of baseline PD subtypes as a clinically useful predictor of disease progression rate. Anti-parkinsonian treatments have symptomatic and disease-modifying effects on all major features of PD.</p>
</sec>
</abstract>
<kwd-group><kwd>disease progression</kwd>
<kwd>levodopa</kwd>
<kwd>motor subscales</kwd>
<kwd>Parkinson's disease</kwd>
<kwd>pharmacodynamics</kwd>
<kwd>selegiline</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Nouvelle-Zélande</li>
<li>États-Unis</li>
</country>
<region><li>Californie</li>
<li>Oregon</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Californie"><name sortKey="Vu, Thuy C" sort="Vu, Thuy C" uniqKey="Vu T" first="Thuy" last="Vu">Thuy Vu</name>
</region>
<name sortKey="Nutt, John G" sort="Nutt, John G" uniqKey="Nutt J" first="John" last="Nutt">John Nutt</name>
</country>
<country name="Nouvelle-Zélande"><noRegion><name sortKey="Holford, Nicholas H G" sort="Holford, Nicholas H G" uniqKey="Holford N" first="Nicholas" last="Holford">Nicholas Holford</name>
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