Atomoxetine for the treatment of executive dysfunction in Parkinson’s disease
Identifieur interne : 000043 ( Pmc/Curation ); précédent : 000042; suivant : 000044Atomoxetine for the treatment of executive dysfunction in Parkinson’s disease
Auteurs : Laura Marsh [États-Unis] ; Kevin Biglan [États-Unis] ; Melissa Gerstenhaber [États-Unis] ; James R. Williams [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2009.
Abstract
Executive dysfunction (ED) is a prominent and often disabling feature of cognitive impairment in Parkinson’s disease (PD). Few studies have examined treatments. Given the role of noradrenergic pathology in ED, atomoxetine, a norepinephrine reuptake inhibitor indicated for attention deficit hyperactivity disorder (ADHD), may be a potential treatment for PD-related ED.
12 patients with PD and disabling ED completed an 8-week pilot open-label, flexible dose (25 to 100 mg/day) trial of atomoxetine.
On primary outcome measures, atomoxetine was associated with improved ED based on the Clinical Global Impression-Change Scale (75% positive response rate; 95% CI: 43%-95%, p<.05) and behavioral measures of ED [Frontal Systems Behavior Scale (FrSBE) Executive Dysfunction and Connors Adult ADHD Rating Scale (CAARS) inattention/memory subscales]. Adverse effects included sleep and gastrointestinal disturbances and hypomania.
Atomoxetine is tolerable in PD and may benefit clinical manifestations of ED, warranting further study in controlled trials.
Url:
DOI: 10.1002/mds.22307
PubMed: 19025777
PubMed Central: 2683743
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Kevin Biglan<affiliation><nlm:aff id="A5">Department of Neurology, University of Rochester Medical School</nlm:aff><wicri:noCountry code="subfield">University of Rochester Medical School</wicri:noCountry></affiliation>Le document en format XML
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Udall Parkinson’s Disease Research Center of Excellence at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Morris K. Udall Parkinson’s Disease Research Center of Excellence at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD</wicri:regionArea></affiliation></author><author><name sortKey="Biglan, Kevin" sort="Biglan, Kevin" uniqKey="Biglan K" first="Kevin" last="Biglan">Kevin Biglan</name><affiliation wicri:level="1"><nlm:aff id="A2">Department of Neurology and Neurological Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology and Neurological Sciences, Johns Hopkins University School of Medicine, Baltimore, MD</wicri:regionArea></affiliation><affiliation><nlm:aff id="A5">Department of Neurology, University of Rochester Medical School</nlm:aff><wicri:noCountry code="subfield">University of Rochester Medical School</wicri:noCountry></affiliation></author><author><name sortKey="Gerstenhaber, Melissa" sort="Gerstenhaber, Melissa" uniqKey="Gerstenhaber M" first="Melissa" last="Gerstenhaber">Melissa Gerstenhaber</name><affiliation wicri:level="1"><nlm:aff id="A1">Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A3">Morris K. Udall Parkinson’s Disease Research Center of Excellence at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Morris K. Udall Parkinson’s Disease Research Center of Excellence at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD</wicri:regionArea></affiliation></author><author><name sortKey="Williams, James R" sort="Williams, James R" uniqKey="Williams J" first="James R." last="Williams">James R. Williams</name><affiliation wicri:level="1"><nlm:aff id="A3">Morris K. Udall Parkinson’s Disease Research Center of Excellence at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Morris K. Udall Parkinson’s Disease Research Center of Excellence at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A4">Department of Mental Health, Bloomberg School of Public Health, Johns Hopkins University School of Medicine, Baltimore, MD, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Mental Health, Bloomberg School of Public Health, Johns Hopkins University School of Medicine, Baltimore, MD</wicri:regionArea></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Introduction</title><p id="P2">Executive dysfunction (ED) is a prominent and often disabling feature of cognitive impairment in Parkinson’s disease (PD). Few studies have examined treatments. Given the role of noradrenergic pathology in ED, atomoxetine, a norepinephrine reuptake inhibitor indicated for attention deficit hyperactivity disorder (ADHD), may be a potential treatment for PD-related ED.</p></sec><sec sec-type="methods" id="S2"><title>Methods</title><p id="P3">12 patients with PD and disabling ED completed an 8-week pilot open-label, flexible dose (25 to 100 mg/day) trial of atomoxetine.</p></sec><sec id="S3"><title>Results</title><p id="P4">On primary outcome measures, atomoxetine was associated with improved ED based on the Clinical Global Impression-Change Scale (75% positive response rate; 95% CI: 43%-95%, p<.05) and behavioral measures of ED [Frontal Systems Behavior Scale (FrSBE) Executive Dysfunction and Connors Adult ADHD Rating Scale (CAARS) inattention/memory subscales]. Adverse effects included sleep and gastrointestinal disturbances and hypomania.</p></sec><sec id="S4"><title>Conclusion</title><p id="P5">Atomoxetine is tolerable in PD and may benefit clinical manifestations of ED, warranting further study in controlled trials.</p></sec></div></front></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8610688</journal-id><journal-id journal-id-type="pubmed-jr-id">5937</journal-id><journal-id journal-id-type="nlm-ta">Mov Disord</journal-id><journal-title>Movement disorders : official journal of the Movement Disorder Society</journal-title><issn pub-type="ppub">0885-3185</issn><issn pub-type="epub">1531-8257</issn></journal-meta><article-meta><article-id pub-id-type="pmid">19025777</article-id><article-id pub-id-type="pmc">2683743</article-id><article-id pub-id-type="doi">10.1002/mds.22307</article-id><article-id pub-id-type="manuscript">NIHMS106386</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Atomoxetine for the treatment of executive dysfunction in Parkinson’s disease</article-title><subtitle>A pilot open-label study</subtitle></title-group><contrib-group><contrib contrib-type="author"><name><surname>Marsh</surname><given-names>Laura</given-names></name><degrees>M.D.</degrees><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Biglan</surname><given-names>Kevin</given-names></name><degrees>M.D., M.P.H.</degrees><xref ref-type="aff" rid="A2">2</xref><xref ref-type="aff" rid="A5">5</xref></contrib><contrib contrib-type="author"><name><surname>Gerstenhaber</surname><given-names>Melissa</given-names></name><degrees>M.A.S, M.S.N.</degrees><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Williams</surname><given-names>James R.</given-names></name><degrees>M.H.S.</degrees><xref ref-type="aff" rid="A3">3</xref><xref ref-type="aff" rid="A4">4</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA</aff><aff id="A2"><label>2</label>Department of Neurology and Neurological Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA</aff><aff id="A3"><label>3</label>Morris K. Udall Parkinson’s Disease Research Center of Excellence at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD, USA</aff><aff id="A4"><label>4</label>Department of Mental Health, Bloomberg School of Public Health, Johns Hopkins University School of Medicine, Baltimore, MD, USA</aff><aff id="A5"><label>5</label>Department of Neurology, University of Rochester Medical School</aff><author-notes><corresp id="CR1">Correspondence to: Laura Marsh, M.D., Johns Hopkins University School of Medicine, 600 N. Wolfe Street- Phipps 300, Baltimore, MD 21287, <email>lmarsh@jhmi.edu</email>; o:410-502-6945; f: 410-614-3676</corresp><fn id="FN1"><p id="P1">The authors confirm that this work complies with the Movement Disorder Society’s policy on ghostwriting.</p></fn></author-notes><pub-date pub-type="nihms-submitted"><day>9</day><month>4</month><year>2009</year></pub-date><pub-date pub-type="ppub"><day>30</day><month>1</month><year>2009</year></pub-date><pub-date pub-type="pmc-release"><day>30</day><month>1</month><year>2010</year></pub-date><volume>24</volume><issue>2</issue><fpage>277</fpage><lpage>282</lpage><abstract><sec id="S1"><title>Introduction</title><p id="P2">Executive dysfunction (ED) is a prominent and often disabling feature of cognitive impairment in Parkinson’s disease (PD). Few studies have examined treatments. Given the role of noradrenergic pathology in ED, atomoxetine, a norepinephrine reuptake inhibitor indicated for attention deficit hyperactivity disorder (ADHD), may be a potential treatment for PD-related ED.</p></sec><sec sec-type="methods" id="S2"><title>Methods</title><p id="P3">12 patients with PD and disabling ED completed an 8-week pilot open-label, flexible dose (25 to 100 mg/day) trial of atomoxetine.</p></sec><sec id="S3"><title>Results</title><p id="P4">On primary outcome measures, atomoxetine was associated with improved ED based on the Clinical Global Impression-Change Scale (75% positive response rate; 95% CI: 43%-95%, p<.05) and behavioral measures of ED [Frontal Systems Behavior Scale (FrSBE) Executive Dysfunction and Connors Adult ADHD Rating Scale (CAARS) inattention/memory subscales]. Adverse effects included sleep and gastrointestinal disturbances and hypomania.</p></sec><sec id="S4"><title>Conclusion</title><p id="P5">Atomoxetine is tolerable in PD and may benefit clinical manifestations of ED, warranting further study in controlled trials.</p></sec></abstract><kwd-group><kwd>Executive Dysfunction</kwd><kwd>Parkinson’s disease</kwd><kwd>Cognition</kwd><kwd>Norepinephrine Reuptake inhibition</kwd><kwd>Atomoxetine</kwd></kwd-group><contract-num rid="RR1">UL1 RR025005-01</contract-num><contract-num rid="AG1">T32 AG027668-02</contract-num><contract-num rid="NS1">P50 NS038377-10</contract-num><contract-sponsor id="RR1">National Center for Research Resources : NCRR</contract-sponsor><contract-sponsor id="AG1">National Institute on Aging : NIA</contract-sponsor><contract-sponsor id="NS1">National Institute of Neurological Disorders and Stroke : NINDS</contract-sponsor></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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