Methylphenidate : a treatment for Parkinson's disease?
Identifieur interne : 000681 ( PubMed/Checkpoint ); précédent : 000680; suivant : 000682Methylphenidate : a treatment for Parkinson's disease?
Auteurs : David Devos [France] ; Caroline Moreau ; Arnaud Delval ; Kathy Dujardin ; Luc Defebvre [France] ; Regis BordetSource :
- CNS drugs [ 1179-1934 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Central Nervous System Stimulants (pharmacology), Central Nervous System Stimulants (therapeutic use), Corpus Striatum (metabolism), Dopamine (metabolism), Dopamine Plasma Membrane Transport Proteins (metabolism), Dopamine Uptake Inhibitors (pharmacology), Dopamine Uptake Inhibitors (therapeutic use), Humans, Methylphenidate (pharmacology), Methylphenidate (therapeutic use), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology).
- MESH :
- chemical , metabolism : Dopamine, Dopamine Plasma Membrane Transport Proteins.
- chemical , pharmacology : Antiparkinson Agents, Central Nervous System Stimulants, Dopamine Uptake Inhibitors, Methylphenidate.
- chemical , therapeutic use : Antiparkinson Agents, Central Nervous System Stimulants, Dopamine Uptake Inhibitors, Methylphenidate.
- drug therapy : Parkinson Disease.
- metabolism : Corpus Striatum.
- physiopathology : Parkinson Disease.
- Animals, Humans.
Abstract
Parkinson's disease (PD) affects about 1 % of the population over the age of 60 years and is characterized by a combination of rest tremor, bradykinesia, rigidity, postural instability, stooped posture and freezing of gait (FoG). However, the clinical spectrum also spans a wide range of non-motor symptoms, such as depression, apathy, cognitive disorders, sleepiness, fatigue and pain. Given that the loss of dopamine in the striatum is the primary pathochemical hallmark in PD, pharmacological treatment of the disease has focused on restoring dopaminergic neurotransmission. The currently licensed dopaminergic treatments for PD modulate all the key steps in the dopamine transmission except the most powerful determinant of extracellular dopamine concentrations: the presynaptic dopamine transporter (DaT). Methylphenidate is a CNS stimulant that blocks the DaT and the noradrenaline (norepinephrine) transporter in the striatum and the prefrontal cortex in particular. Here, we report on and discuss the main open-label studies and randomized controlled trials on the effect of methylphenidate on severe gait disorders (e.g. the FoG) and non-motor symptoms in advanced PD. The various pharmacodynamic effects of methylphenidate mean that the drug may have significant value in the treatment of PD. However, there is a lack of randomized controlled trials in this field. Furthermore, more rigorous selection of the types and doses of the associated dopaminergic treatments is required because these parameters may profoundly influence the mechanisms of action of methylphenidate and the clinical outcomes. Pharmacogenetic tools could be of use in better defining study patients as a function of their dopaminergic metabolism and drug responsiveness.
DOI: 10.1007/s40263-012-0017-y
PubMed: 23160937
Affiliations:
- France
- Hauts-de-France, Nord-Pas-de-Calais
- Lille
- Université Lille 2, Université Lille Nord de France
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xml:lang="en">Methylphenidate : a treatment for Parkinson's disease?</title><author><name sortKey="Devos, David" sort="Devos, David" uniqKey="Devos D" first="David" last="Devos">David Devos</name><affiliation wicri:level="3"><nlm:affiliation>Department of Medical Pharmacology, EA 1046, Lille Nord de France University, CHU Lille, Lille, France. david.devos@chru-lille.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Medical Pharmacology, EA 1046, Lille Nord de France University, CHU Lille, Lille</wicri:regionArea><placeName><region type="region">Hauts-de-France</region><region type="old region">Nord-Pas-de-Calais</region><settlement type="city">Lille</settlement></placeName></affiliation></author><author><name sortKey="Moreau, Caroline" sort="Moreau, Caroline" uniqKey="Moreau C" first="Caroline" last="Moreau">Caroline Moreau</name></author><author><name sortKey="Delval, Arnaud" sort="Delval, Arnaud" uniqKey="Delval A" first="Arnaud" last="Delval">Arnaud Delval</name></author><author><name sortKey="Dujardin, Kathy" sort="Dujardin, Kathy" uniqKey="Dujardin K" first="Kathy" last="Dujardin">Kathy Dujardin</name></author><author><name sortKey="Defebvre, Luc" sort="Defebvre, Luc" uniqKey="Defebvre L" first="Luc" last="Defebvre">Luc Defebvre</name><affiliation><country>France</country><placeName><settlement type="city">Lille</settlement><region type="region" nuts="2">Hauts-de-France</region><region type="old region" nuts="2">Nord-Pas-de-Calais</region></placeName><orgName type="university" n="3">Université Lille 2</orgName><orgName type="institution" wicri:auto="newGroup">Université Lille Nord de France</orgName><country>France</country><placeName><settlement type="city">Lille</settlement><region type="region" nuts="2">Hauts-de-France</region><region type="old region" nuts="2">Nord-Pas-de-Calais</region></placeName><orgName type="university" n="3">Université Lille 2</orgName><orgName type="institution" wicri:auto="newGroup">Université Lille Nord de France</orgName></affiliation></author><author><name sortKey="Bordet, Regis" sort="Bordet, Regis" uniqKey="Bordet R" first="Regis" last="Bordet">Regis Bordet</name></author></analytic><series><title level="j">CNS drugs</title><idno type="eISSN">1179-1934</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Central Nervous System Stimulants (pharmacology)</term><term>Central Nervous System Stimulants (therapeutic use)</term><term>Corpus Striatum (metabolism)</term><term>Dopamine (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins (metabolism)</term><term>Dopamine Uptake Inhibitors (pharmacology)</term><term>Dopamine Uptake Inhibitors (therapeutic use)</term><term>Humans</term><term>Methylphenidate (pharmacology)</term><term>Methylphenidate (therapeutic use)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Dopamine Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Central Nervous System Stimulants</term><term>Dopamine Uptake Inhibitors</term><term>Methylphenidate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Central Nervous System Stimulants</term><term>Dopamine Uptake Inhibitors</term><term>Methylphenidate</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) affects about 1 % of the population over the age of 60 years and is characterized by a combination of rest tremor, bradykinesia, rigidity, postural instability, stooped posture and freezing of gait (FoG). However, the clinical spectrum also spans a wide range of non-motor symptoms, such as depression, apathy, cognitive disorders, sleepiness, fatigue and pain. Given that the loss of dopamine in the striatum is the primary pathochemical hallmark in PD, pharmacological treatment of the disease has focused on restoring dopaminergic neurotransmission. The currently licensed dopaminergic treatments for PD modulate all the key steps in the dopamine transmission except the most powerful determinant of extracellular dopamine concentrations: the presynaptic dopamine transporter (DaT). Methylphenidate is a CNS stimulant that blocks the DaT and the noradrenaline (norepinephrine) transporter in the striatum and the prefrontal cortex in particular. Here, we report on and discuss the main open-label studies and randomized controlled trials on the effect of methylphenidate on severe gait disorders (e.g. the FoG) and non-motor symptoms in advanced PD. The various pharmacodynamic effects of methylphenidate mean that the drug may have significant value in the treatment of PD. However, there is a lack of randomized controlled trials in this field. Furthermore, more rigorous selection of the types and doses of the associated dopaminergic treatments is required because these parameters may profoundly influence the mechanisms of action of methylphenidate and the clinical outcomes. Pharmacogenetic tools could be of use in better defining study patients as a function of their dopaminergic metabolism and drug responsiveness.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23160937</PMID><DateCreated><Year>2013</Year><Month>01</Month><Day>18</Day></DateCreated><DateCompleted><Year>2013</Year><Month>07</Month><Day>03</Day></DateCompleted><DateRevised><Year>2016</Year><Month>09</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1179-1934</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>1</Issue><PubDate><Year>2013</Year><Month>Jan</Month></PubDate></JournalIssue><Title>CNS drugs</Title><ISOAbbreviation>CNS Drugs</ISOAbbreviation></Journal><ArticleTitle>Methylphenidate : a treatment for Parkinson's disease?</ArticleTitle><Pagination><MedlinePgn>1-14</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s40263-012-0017-y</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) affects about 1 % of the population over the age of 60 years and is characterized by a combination of rest tremor, bradykinesia, rigidity, postural instability, stooped posture and freezing of gait (FoG). However, the clinical spectrum also spans a wide range of non-motor symptoms, such as depression, apathy, cognitive disorders, sleepiness, fatigue and pain. Given that the loss of dopamine in the striatum is the primary pathochemical hallmark in PD, pharmacological treatment of the disease has focused on restoring dopaminergic neurotransmission. The currently licensed dopaminergic treatments for PD modulate all the key steps in the dopamine transmission except the most powerful determinant of extracellular dopamine concentrations: the presynaptic dopamine transporter (DaT). Methylphenidate is a CNS stimulant that blocks the DaT and the noradrenaline (norepinephrine) transporter in the striatum and the prefrontal cortex in particular. Here, we report on and discuss the main open-label studies and randomized controlled trials on the effect of methylphenidate on severe gait disorders (e.g. the FoG) and non-motor symptoms in advanced PD. The various pharmacodynamic effects of methylphenidate mean that the drug may have significant value in the treatment of PD. However, there is a lack of randomized controlled trials in this field. Furthermore, more rigorous selection of the types and doses of the associated dopaminergic treatments is required because these parameters may profoundly influence the mechanisms of action of methylphenidate and the clinical outcomes. Pharmacogenetic tools could be of use in better defining study patients as a function of their dopaminergic metabolism and drug responsiveness.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Devos</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Medical Pharmacology, EA 1046, Lille Nord de France University, CHU Lille, Lille, France. david.devos@chru-lille.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moreau</LastName><ForeName>Caroline</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Delval</LastName><ForeName>Arnaud</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Dujardin</LastName><ForeName>Kathy</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Defebvre</LastName><ForeName>Luc</ForeName><Initials>L</Initials></Author><Author 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MajorTopicYN="N">Methylphenidate</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>11</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>11</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>7</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23160937</ArticleId><ArticleId IdType="doi">10.1007/s40263-012-0017-y</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Hauts-de-France</li><li>Nord-Pas-de-Calais</li></region><settlement><li>Lille</li></settlement><orgName><li>Université Lille 2</li><li>Université Lille Nord de France</li></orgName></list><tree><noCountry><name sortKey="Bordet, Regis" sort="Bordet, Regis" uniqKey="Bordet R" first="Regis" last="Bordet">Regis Bordet</name><name sortKey="Delval, Arnaud" sort="Delval, Arnaud" uniqKey="Delval A" first="Arnaud" last="Delval">Arnaud Delval</name><name sortKey="Dujardin, Kathy" sort="Dujardin, Kathy" uniqKey="Dujardin K" first="Kathy" last="Dujardin">Kathy Dujardin</name><name sortKey="Moreau, Caroline" sort="Moreau, Caroline" uniqKey="Moreau C" first="Caroline" last="Moreau">Caroline Moreau</name></noCountry><country name="France"><region name="Hauts-de-France"><name sortKey="Devos, David" sort="Devos, David" uniqKey="Devos D" first="David" last="Devos">David Devos</name></region><name sortKey="Defebvre, Luc" sort="Defebvre, Luc" uniqKey="Defebvre L" first="Luc" last="Defebvre">Luc Defebvre</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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