Movement Disorders (revue)

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Intravenous amantadine improves levadopa-induced dyskinesias: An acute double-blind placebo-controlled study

Identifieur interne : 000311 ( PascalFrancis/Curation ); précédent : 000310; suivant : 000312

Intravenous amantadine improves levadopa-induced dyskinesias: An acute double-blind placebo-controlled study

Auteurs : Paolo Del Dotto [Italie] ; Nicola Pavese [Italie] ; Gianna Gambaccini [Italie] ; Silvia Bernardini [Italie] ; Leonard Verhagen Metman [États-Unis] ; Thomas N. Chase [États-Unis] ; Ubaldo Bonuccelli [Italie]

Source :

RBID : Pascal:01-0376775

Descripteurs français

English descriptors

Abstract

Experimental evidence suggests that glutamatergic receptor blockade may improve the motor response complications associated with long-term levodopa treatment in Parkinson's disease (PD) patients. Our objective was to evaluate the acute effect of amantadine, a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, on levodopa-induced dyskinesias, and to gain further insights into the antidyskinetic mechanism of this drug. Nine PD patients with motor fluctuations and severely disabling peak of dose dyskinesias received their first morning levodopa dose, followed by a 2-hour intravenous amantadine (200 mg) or placebo infusion, on two different days. Parkinsonian symptoms and dyskinesias were assessed every 15 minutes during the infusion and for 3 hours thereafter, while patients were taking their usual oral antiparkinsonian therapy, by means of Unified Parkinson's Disease Rating Scale (UPDRS, motor examination), tapping test, and a modified Abnormal Involuntary Movement Scale (AIMS). Intravenous amantadine acutely improved levodopa-induced dyskinesias by 50%without any loss of the anti-parkinsonian benefit from levodopa. This study confirms the antidyskinetic effect of amantadine and strengthens the rationale for using antiglutamatergic drugs in the treatment of parkinsonian motor fluctuations.
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A08 01  1  ENG  @1 Intravenous amantadine improves levadopa-induced dyskinesias: An acute double-blind placebo-controlled study
A11 01  1    @1 DEL DOTTO (Paolo)
A11 02  1    @1 PAVESE (Nicola)
A11 03  1    @1 GAMBACCINI (Gianna)
A11 04  1    @1 BERNARDINI (Silvia)
A11 05  1    @1 VERHAGEN METMAN (Leonard)
A11 06  1    @1 CHASE (Thomas N.)
A11 07  1    @1 BONUCCELLI (Ubaldo)
A14 01      @1 Department of Neuroscience, Neurology Section, University of Pisa @2 Pisa @3 ITA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 7 aut.
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C01 01    ENG  @0 Experimental evidence suggests that glutamatergic receptor blockade may improve the motor response complications associated with long-term levodopa treatment in Parkinson's disease (PD) patients. Our objective was to evaluate the acute effect of amantadine, a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, on levodopa-induced dyskinesias, and to gain further insights into the antidyskinetic mechanism of this drug. Nine PD patients with motor fluctuations and severely disabling peak of dose dyskinesias received their first morning levodopa dose, followed by a 2-hour intravenous amantadine (200 mg) or placebo infusion, on two different days. Parkinsonian symptoms and dyskinesias were assessed every 15 minutes during the infusion and for 3 hours thereafter, while patients were taking their usual oral antiparkinsonian therapy, by means of Unified Parkinson's Disease Rating Scale (UPDRS, motor examination), tapping test, and a modified Abnormal Involuntary Movement Scale (AIMS). Intravenous amantadine acutely improved levodopa-induced dyskinesias by 50%without any loss of the anti-parkinsonian benefit from levodopa. This study confirms the antidyskinetic effect of amantadine and strengthens the rationale for using antiglutamatergic drugs in the treatment of parkinsonian motor fluctuations.
C02 01  X    @0 002B17G
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C03 02  X  SPA  @0 Disquinesia @5 04
C03 03  X  FRE  @0 Amantadine @2 NK @2 FR @5 07
C03 03  X  ENG  @0 Amantadine @2 NK @2 FR @5 07
C03 03  X  SPA  @0 Amantadina @2 NK @2 FR @5 07
C03 04  X  FRE  @0 Voie intraveineuse @5 10
C03 04  X  ENG  @0 Intravenous administration @5 10
C03 04  X  SPA  @0 Vía intravenosa @5 10
C03 05  X  FRE  @0 Lévodopa @5 13
C03 05  X  ENG  @0 Levodopa @5 13
C03 05  X  SPA  @0 Levodopa @5 13
C03 06  X  FRE  @0 Antiparkinsonien @5 14
C03 06  X  ENG  @0 Antiparkinson agent @5 14
C03 06  X  SPA  @0 Antiparkinsoniano @5 14
C03 07  X  FRE  @0 Chimiothérapie @5 16
C03 07  X  ENG  @0 Chemotherapy @5 16
C03 07  X  SPA  @0 Quimioterapia @5 16
C03 08  X  FRE  @0 Traitement @5 17
C03 08  X  ENG  @0 Treatment @5 17
C03 08  X  SPA  @0 Tratamiento @5 17
C03 09  X  FRE  @0 Homme @5 20
C03 09  X  ENG  @0 Human @5 20
C03 09  X  SPA  @0 Hombre @5 20
C03 10  X  FRE  @0 Etude double insu @5 23
C03 10  X  ENG  @0 Double blind study @5 23
C03 10  X  SPA  @0 Estudio doble ciego @5 23
C07 01  X  FRE  @0 Système nerveux pathologie @5 37
C07 01  X  ENG  @0 Nervous system diseases @5 37
C07 01  X  SPA  @0 Sistema nervioso patología @5 37
C07 02  X  FRE  @0 Système nerveux central pathologie @5 38
C07 02  X  ENG  @0 Central nervous system disease @5 38
C07 02  X  SPA  @0 Sistema nervosio central patología @5 38
C07 03  X  FRE  @0 Encéphale pathologie @5 39
C07 03  X  ENG  @0 Cerebral disorder @5 39
C07 03  X  SPA  @0 Encéfalo patología @5 39
C07 04  X  FRE  @0 Extrapyramidal syndrome @5 40
C07 04  X  ENG  @0 Extrapyramidal syndrome @5 40
C07 04  X  SPA  @0 Extrapiramidal síndrome @5 40
C07 05  X  FRE  @0 Maladie dégénérative @5 41
C07 05  X  ENG  @0 Degenerative disease @5 41
C07 05  X  SPA  @0 Enfermedad degenerativa @5 41
C07 06  X  FRE  @0 Trouble neurologique @5 46
C07 06  X  ENG  @0 Neurological disorder @5 46
C07 06  X  SPA  @0 Trastorno neurológico @5 46
C07 07  X  FRE  @0 Mouvement involontaire @5 47
C07 07  X  ENG  @0 Involuntary movement @5 47
C07 07  X  SPA  @0 Movimiento involuntario @5 47
C07 08  X  FRE  @0 Voie administration @5 61
C07 08  X  ENG  @0 Route of administration @5 61
C07 08  X  SPA  @0 Vía administración @5 61
N21       @1 267

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Pascal:01-0376775

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<div type="abstract" xml:lang="en">Experimental evidence suggests that glutamatergic receptor blockade may improve the motor response complications associated with long-term levodopa treatment in Parkinson's disease (PD) patients. Our objective was to evaluate the acute effect of amantadine, a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, on levodopa-induced dyskinesias, and to gain further insights into the antidyskinetic mechanism of this drug. Nine PD patients with motor fluctuations and severely disabling peak of dose dyskinesias received their first morning levodopa dose, followed by a 2-hour intravenous amantadine (200 mg) or placebo infusion, on two different days. Parkinsonian symptoms and dyskinesias were assessed every 15 minutes during the infusion and for 3 hours thereafter, while patients were taking their usual oral antiparkinsonian therapy, by means of Unified Parkinson's Disease Rating Scale (UPDRS, motor examination), tapping test, and a modified Abnormal Involuntary Movement Scale (AIMS). Intravenous amantadine acutely improved levodopa-induced dyskinesias by 50%without any loss of the anti-parkinsonian benefit from levodopa. This study confirms the antidyskinetic effect of amantadine and strengthens the rationale for using antiglutamatergic drugs in the treatment of parkinsonian motor fluctuations.</div>
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<s0>Experimental evidence suggests that glutamatergic receptor blockade may improve the motor response complications associated with long-term levodopa treatment in Parkinson's disease (PD) patients. Our objective was to evaluate the acute effect of amantadine, a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, on levodopa-induced dyskinesias, and to gain further insights into the antidyskinetic mechanism of this drug. Nine PD patients with motor fluctuations and severely disabling peak of dose dyskinesias received their first morning levodopa dose, followed by a 2-hour intravenous amantadine (200 mg) or placebo infusion, on two different days. Parkinsonian symptoms and dyskinesias were assessed every 15 minutes during the infusion and for 3 hours thereafter, while patients were taking their usual oral antiparkinsonian therapy, by means of Unified Parkinson's Disease Rating Scale (UPDRS, motor examination), tapping test, and a modified Abnormal Involuntary Movement Scale (AIMS). Intravenous amantadine acutely improved levodopa-induced dyskinesias by 50%without any loss of the anti-parkinsonian benefit from levodopa. This study confirms the antidyskinetic effect of amantadine and strengthens the rationale for using antiglutamatergic drugs in the treatment of parkinsonian motor fluctuations.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Dyskinésie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Dyskinesia</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Disquinesia</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Amantadine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Amantadine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Amantadina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Voie intraveineuse</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Intravenous administration</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Vía intravenosa</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Lévodopa</s0>
<s5>13</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Levodopa</s0>
<s5>13</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Levodopa</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Antiparkinsonien</s0>
<s5>14</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Antiparkinson agent</s0>
<s5>14</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Antiparkinsoniano</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Chimiothérapie</s0>
<s5>16</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Chemotherapy</s0>
<s5>16</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Quimioterapia</s0>
<s5>16</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Traitement</s0>
<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Treatment</s0>
<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Tratamiento</s0>
<s5>17</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Etude double insu</s0>
<s5>23</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Double blind study</s0>
<s5>23</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Estudio doble ciego</s0>
<s5>23</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Trouble neurologique</s0>
<s5>46</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Neurological disorder</s0>
<s5>46</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Trastorno neurológico</s0>
<s5>46</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Mouvement involontaire</s0>
<s5>47</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Involuntary movement</s0>
<s5>47</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Movimiento involuntario</s0>
<s5>47</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Voie administration</s0>
<s5>61</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Route of administration</s0>
<s5>61</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Vía administración</s0>
<s5>61</s5>
</fC07>
<fN21>
<s1>267</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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