Olivier Rascol1,2, Laurence Negre-Pages3,4, Philippe Damier5, Arnaud Delval6, Pascal Derkinderen5, Alain Destée6, Margherita Fabbri7, Wassilios G Meissner8,9,10,11, Amine Rachdi12, François Tison8,9, Santiago Perez-Lloret13,14. 1. Centre d'Investigation Clinique CIC 1436, Services de Pharmacologie Clinique et Neurosciences, NS-Park/FCRIN Network, NeuroToul COEN Center, Université de Toulouse UPS, CHU de Toulouse, INSERM Toulouse, Toulouse, France. olivier.rascol@univ-tlse3.fr. 2. Department of Clinical Pharmacology, Faculty of Medicine, 37 Allées Jules Guesde, 31000, Toulouse, France. olivier.rascol@univ-tlse3.fr. 3. LN Pharma, Toulouse, France. 4. Unité de Recherche Clinique et Epidémiologie, Département d'Information Médicale, Hôpital la Colombière, Montpellier, France. 5. CHU de Nantes, INSERM, CIC 1413, Department of Neurology, NS-Park/FCRIN Network, Université de Nantes, Nantes, France. 6. CHU de Lille, INSERM, Department of Neurology, U 837, NS-Park/FCRIN Network, Université de Lille, Lille, France. 7. Department of Neuroscience, University of Turin, Turin, Italy. 8. Service de Neurologie, CHU de Bordeaux, NS-Park/FCRIN Network, 33000, Bordeaux, France. 9. Institut des Maladies Neurodégénératives, CNRS, UMR 5293, Univ. de Bordeaux, 33000, Bordeaux, France. 10. Department of Medicine, University of Otago, Christchurch, New Zealand. 11. New Zealand Brain Research Institute, Christchurch, New Zealand. 12. Centre d'Investigation Clinique CIC 1436, Services de Pharmacologie Clinique et Neurosciences, NS-Park/FCRIN Network, NeuroToul COEN Center, Université de Toulouse UPS, CHU de Toulouse, INSERM Toulouse, Toulouse, France. 13. Institute of Cardiology Research, University of Buenos Aires, National Research Council (CONICET-ININCA), Buenos Aires, Argentina. 14. Department of Physiology, School of Medicine, University of Buenos Aires (UBA), Buenos Aires, Argentina.
Abstract
INTRODUCTION: Immediate-release (IR) amantadine has been marketed for Parkinson's disease (PD) therapy for 50 years, while two novel extended-release formulations have only recently reached the market in the US. OBJECTIVES: The aim of this study was to describe amantadine IR utilization patterns in the French COPARK cohort, at baseline and after 2 years of follow-up. METHODS: Overall, 683 PD patients from the COPARK survey were evaluated. All patients were assessed in a standardized manner (demographics, treatments, Unified Parkinson's Disease Rating Scale [UPDRS], Hospital Anxiety and Depression Scale, Pittsburg Questionnaire and health-related quality-of-life scales (Short Form-36 [SF-36], 39-item Parkinson's Disease Questionnaire [PDQ-39]). Longitudinal data were only available for 401/683 patients (59%) with a median (P25-75) follow-up period of 23 months (18-31). Patients were assessed in the same way as in the baseline visit. RESULTS: At baseline, amantadine was prescribed to 61/683 (9%) patients (median dose 200 mg/day, range 100-300 mg/day). Amantadine was initiated after a median of 7 years from PD diagnosis, and its prescription was correlated with the presence of dyskinesia (logistic regression odds ratio [OR] 3.72, 95% confidence interval [CI] 1.95-7.08) and hallucinations (UPDRS I.2) [OR 1.57, 95% CI 1.08-2.29]. After 2 years, the amantadine prescription increased from 33 (8%) patients at baseline to 54 (14%) patients in the subset of 401 patients analysed twice (p = 0.001). Among the 33 patients receiving amantadine at baseline, 9 (27%) stopped amantadine, 5 (15%) increased the dose, 6 (18%) reduced the dose and 13 (40%) stayed at the same doses. Treatment was initiated in 30/54 new patients (55%). Patients who started amantadine or increased its dose (n = 35) had more levodopa-induced dyskinesias at baseline (OR 7.02, 95% CI 3.09-15.90) and higher Mini-Mental State Examination score at follow-up (OR 1.37, 95% CI 1.06-1.79). Undergoing deep brain stimulation was related to stopping or downtitrating amantadine (OR 22.02, 95% CI 4.24-114.44; n = 15). CONCLUSIONS: In this cohort, amantadine was used in 10% of patients. Its use increased during follow-up, despite the fact that one-third of patients who received amantadine at baseline stopped taking it. Amantadine prescription was mainly correlated with the presence of dyskinesia.
INTRODUCTION: Immediate-release (IR) amantadine has been marketed for Parkinson's disease (PD) therapy for 50 years, while two novel extended-release formulations have only recently reached the market in the US. OBJECTIVES: The aim of this study was to describe amantadine IR utilization patterns in the French COPARK cohort, at baseline and after 2 years of follow-up. METHODS: Overall, 683 PDpatients from the COPARK survey were evaluated. All patients were assessed in a standardized manner (demographics, treatments, Unified Parkinson's Disease Rating Scale [UPDRS], Hospital Anxiety and Depression Scale, Pittsburg Questionnaire and health-related quality-of-life scales (Short Form-36 [SF-36], 39-item Parkinson's Disease Questionnaire [PDQ-39]). Longitudinal data were only available for 401/683 patients (59%) with a median (P25-75) follow-up period of 23 months (18-31). Patients were assessed in the same way as in the baseline visit. RESULTS: At baseline, amantadine was prescribed to 61/683 (9%) patients (median dose 200 mg/day, range 100-300 mg/day). Amantadine was initiated after a median of 7 years from PD diagnosis, and its prescription was correlated with the presence of dyskinesia (logistic regression odds ratio [OR] 3.72, 95% confidence interval [CI] 1.95-7.08) and hallucinations (UPDRS I.2) [OR 1.57, 95% CI 1.08-2.29]. After 2 years, the amantadine prescription increased from 33 (8%) patients at baseline to 54 (14%) patients in the subset of 401 patients analysed twice (p = 0.001). Among the 33 patients receiving amantadine at baseline, 9 (27%) stopped amantadine, 5 (15%) increased the dose, 6 (18%) reduced the dose and 13 (40%) stayed at the same doses. Treatment was initiated in 30/54 new patients (55%). Patients who started amantadine or increased its dose (n = 35) had more levodopa-induced dyskinesias at baseline (OR 7.02, 95% CI 3.09-15.90) and higher Mini-Mental State Examination score at follow-up (OR 1.37, 95% CI 1.06-1.79). Undergoing deep brain stimulation was related to stopping or downtitrating amantadine (OR 22.02, 95% CI 4.24-114.44; n = 15). CONCLUSIONS: In this cohort, amantadine was used in 10% of patients. Its use increased during follow-up, despite the fact that one-third of patients who received amantadine at baseline stopped taking it. Amantadine prescription was mainly correlated with the presence of dyskinesia.
Authors: Günther Deuschl; Carmen Schade-Brittinger; Paul Krack; Jens Volkmann; Helmut Schäfer; Kai Bötzel; Christine Daniels; Angela Deutschländer; Ulrich Dillmann; Wilhelm Eisner; Doreen Gruber; Wolfgang Hamel; Jan Herzog; Rüdiger Hilker; Stephan Klebe; Manja Kloss; Jan Koy; Martin Krause; Andreas Kupsch; Delia Lorenz; Stefan Lorenzl; H Maximilian Mehdorn; Jean Richard Moringlane; Wolfgang Oertel; Marcus O Pinsker; Heinz Reichmann; Alexander Reuss; Gerd-Helge Schneider; Alfons Schnitzler; Ulrich Steude; Volker Sturm; Lars Timmermann; Volker Tronnier; Thomas Trottenberg; Lars Wojtecki; Elisabeth Wolf; Werner Poewe; Jürgen Voges Journal: N Engl J Med Date: 2006-08-31 Impact factor: 91.245
Authors: Philippe Huot; Tom H Johnston; James B Koprich; Susan H Fox; Jonathan M Brotchie Journal: Pharmacol Rev Date: 2013-01-10 Impact factor: 25.468