Apathy following subthalamic stimulation in Parkinson disease: A dopamine responsive symptom
Identifieur interne : 001144 ( Main/Curation ); précédent : 001143; suivant : 001145Apathy following subthalamic stimulation in Parkinson disease: A dopamine responsive symptom
Auteurs : Virginie Czernecki [France] ; Michael Schüpbach [France, Suisse] ; Sadek Yaici [France] ; Richard Lévy [France] ; Eric Bardinet [France] ; Jérôme Yelnik [France] ; Bruno Dubois [France] ; Yves Agid [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-05-15.
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. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.21949
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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. © 2008 Movement Disorder Society</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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