Movement Disorders (revue)

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Apathy Following Subthalamic Stimulation in Parkinson Disease : A Dopamine Responsive Symptom

Identifieur interne : 001A74 ( PascalFrancis/Curation ); précédent : 001A73; suivant : 001A75

Apathy Following Subthalamic Stimulation in Parkinson Disease : A Dopamine Responsive Symptom

Auteurs : Virginie Czernecki [France] ; Michael Schüpbach [France, Suisse] ; Sadek Yaici [France] ; Richard Levy [France] ; Eric Bardinet [France] ; Jérome Yelnik [France] ; Bruno Dubois [France] ; Yves Agid [France]

Source :

RBID : Pascal:08-0305133

Descripteurs français

English descriptors

Abstract

To evaluate the effects of the dopamine D2-D3 agonist ropinirole in patients who developed apathy after complete withdrawal from dopaminergic medication following successful subthalamic nucleus (STN) stimulation for advanced Parkinson disease (PD). We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery-Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS-III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1-18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0-78%). Mood also improved (75 ± 31%; range 0-100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2-D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo-limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively.
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A11 02  1    @1 SCHÜPBACH (Michael)
A11 03  1    @1 YAICI (Sadek)
A11 04  1    @1 LEVY (Richard)
A11 05  1    @1 BARDINET (Eric)
A11 06  1    @1 YELNIK (Jérome)
A11 07  1    @1 DUBOIS (Bruno)
A11 08  1    @1 AGID (Yves)
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C01 01    ENG  @0 To evaluate the effects of the dopamine D2-D3 agonist ropinirole in patients who developed apathy after complete withdrawal from dopaminergic medication following successful subthalamic nucleus (STN) stimulation for advanced Parkinson disease (PD). We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery-Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS-III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1-18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0-78%). Mood also improved (75 ± 31%; range 0-100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2-D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo-limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively.
C02 01  X    @0 002B17
C02 02  X    @0 002B17G
C03 01  X  FRE  @0 Maladie de Parkinson @2 NM @5 01
C03 01  X  ENG  @0 Parkinson disease @2 NM @5 01
C03 01  X  SPA  @0 Parkinson enfermedad @2 NM @5 01
C03 02  X  FRE  @0 Pathologie du système nerveux @5 02
C03 02  X  ENG  @0 Nervous system diseases @5 02
C03 02  X  SPA  @0 Sistema nervioso patología @5 02
C03 03  X  FRE  @0 Dopamine @2 NK @2 FR @5 09
C03 03  X  ENG  @0 Dopamine @2 NK @2 FR @5 09
C03 03  X  SPA  @0 Dopamina @2 NK @2 FR @5 09
C03 04  X  FRE  @0 Apathie @4 CD @5 96
C03 04  X  ENG  @0 Apathy @4 CD @5 96
C03 04  X  SPA  @0 Apatía @4 CD @5 96
C07 01  X  FRE  @0 Pathologie de l'encéphale @5 37
C07 01  X  ENG  @0 Cerebral disorder @5 37
C07 01  X  SPA  @0 Encéfalo patología @5 37
C07 02  X  FRE  @0 Syndrome extrapyramidal @5 38
C07 02  X  ENG  @0 Extrapyramidal syndrome @5 38
C07 02  X  SPA  @0 Extrapiramidal síndrome @5 38
C07 03  X  FRE  @0 Maladie dégénérative @5 39
C07 03  X  ENG  @0 Degenerative disease @5 39
C07 03  X  SPA  @0 Enfermedad degenerativa @5 39
C07 04  X  FRE  @0 Pathologie du système nerveux central @5 40
C07 04  X  ENG  @0 Central nervous system disease @5 40
C07 04  X  SPA  @0 Sistema nervosio central patología @5 40
C07 05  X  FRE  @0 Catécholamine @5 42
C07 05  X  ENG  @0 Catecholamine @5 42
C07 05  X  SPA  @0 Catecolamina @5 42
C07 06  X  FRE  @0 Neurotransmetteur @5 43
C07 06  X  ENG  @0 Neurotransmitter @5 43
C07 06  X  SPA  @0 Neurotransmisor @5 43
N21       @1 189
N44 01      @1 OTO
N82       @1 OTO

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Pascal:08-0305133

Le document en format XML

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<div type="abstract" xml:lang="en">To evaluate the effects of the dopamine D2-D3 agonist ropinirole in patients who developed apathy after complete withdrawal from dopaminergic medication following successful subthalamic nucleus (STN) stimulation for advanced Parkinson disease (PD). We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery-Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS-III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1-18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0-78%). Mood also improved (75 ± 31%; range 0-100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2-D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo-limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively.</div>
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<s1>© 2008 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>33 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>08-0305133</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Movement disorders</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>To evaluate the effects of the dopamine D2-D3 agonist ropinirole in patients who developed apathy after complete withdrawal from dopaminergic medication following successful subthalamic nucleus (STN) stimulation for advanced Parkinson disease (PD). We assessed apathy (Apathy Scale, Apathy Inventory), mood (Montgomery-Åsberg Depression Rating Scale), cognitive functions (Mattis Dementia rating scale, frontal score, executive tests) and motor state (UPDRS-III) in 8 PD patients treated with STN stimulation without dopaminergic treatment and who became apathetic. Assessments were made at baseline and after 6 weeks of ropinirole treatment (7.2 ± 5.9 mg/d; range 1-18 mg/d). Apathy improved with ropinirole in all but 1 patient (54 ± 24%; range 0-78%). Mood also improved (75 ± 31%; range 0-100%), but not in correlation with the change in apathy. Cognitive performance was not modified. Stimulation contacts were located within the STN in all patients except the one who remained apathetic in spite of ropinirole treatment (zona incerta). We suggest that apathy, which was compensated for by an enhancement of D2-D3 receptor stimulation in PD patients with STN stimulation: (1) depends on a dopaminergic deficit in associativo-limbic areas of the brain and (2) can be avoided if a dopaminergic agonist is administered postoperatively.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Pathologie du système nerveux</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Apathie</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Apathy</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Apatía</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Syndrome extrapyramidal</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Catécholamine</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Catecholamine</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Catecolamina</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Neurotransmetteur</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Neurotransmitter</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Neurotransmisor</s0>
<s5>43</s5>
</fC07>
<fN21>
<s1>189</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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