Apathy following subthalamic stimulation in Parkinson disease: a dopamine responsive symptom.
Identifieur interne : 002263 ( PubMed/Corpus ); précédent : 002262; suivant : 002264Apathy following subthalamic stimulation in Parkinson disease: a dopamine responsive symptom.
Auteurs : Virginie Czernecki ; Michael Schüpbach ; Sadek Yaici ; Richard Lévy ; Eric Bardinet ; Jérôme Yelnik ; Bruno Dubois ; Yves AgidSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Aged, Deep Brain Stimulation (adverse effects), Dopamine Agonists (therapeutic use), Female, Humans, Indoles (pharmacology), Indoles (therapeutic use), Male, Middle Aged, Mood Disorders (etiology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson Disease (psychology), Receptors, Dopamine D2 (drug effects), Receptors, Dopamine D3 (drug effects), Subthalamic Nucleus (physiopathology).
- MESH :
- chemical , drug effects : Receptors, Dopamine D2, Receptors, Dopamine D3.
- chemical , pharmacology : Indoles.
- chemical , therapeutic use : Dopamine Agonists, Indoles.
- adverse effects : Deep Brain Stimulation.
- drug therapy : Parkinson Disease.
- etiology : Mood Disorders.
- physiopathology : Parkinson Disease, Subthalamic Nucleus.
- psychology : Parkinson Disease.
- Aged, Female, Humans, Male, Middle Aged.
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-Asberg 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.
DOI: 10.1002/mds.21949
PubMed: 18398913
Links to Exploration step
pubmed:18398913Le document en format XML
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<author><name sortKey="Yaici, Sadek" sort="Yaici, Sadek" uniqKey="Yaici S" first="Sadek" last="Yaici">Sadek Yaici</name>
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<front><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-Asberg 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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