This symposium took place on 22nd September 2016 as a part of the 89th Deutsche Gesellschaft für Neurologie (DGN) Congress in Mannheim, Germany
Chairperson: Heinz Reichmann1
Speakers: Werner Poewe,2 Georg Ebersbach,3 Thomas Müller4
1. Universitätsklinikum Technische Universität Dresden, Dresden, Germany
2. Medizinische Universität Innsbruck, Innsbruck, Austria
3. Neurologisches Fachkrankenhaus für Bewegungsstörungen, Beelitz-Heilstätten, Germany
4. Alexianer St. Joseph Berlin-Weißensee, Berlin, Germany
Disclosure: Prof Heinz Reichmann received research grants and compensation for his involvement on advisory boards and lectures from Abbott, Abbvie, Bayer Health Care, BIAL, Boehringer/Ingelheim, Brittania, Cephalon, Desitin, GSK, Lundbeck, Medtronic, Merck-Serono, Novartis, Orion, Pfizer, TEVA, UCB Pharma, Valeant, and Zambon. Prof Werner Poewe has received honoraria for lectures and consultancy fees in relation to clinical drug development programmes for Parkinson’s disease from AbbVie, Allergan, AstraZeneca, BIAL, Boehringer Ingelheim, Boston Scientific, GlaxoSmithKline, Ipsen, Lundbeck, Medtronic, MSD, Merck-Serono, Merz Pharmaceuticals, Novartis, Orion Pharma, Teva, UCB, and Zambon. He also received royalties from Thieme, Wiley Blackwell, Oxford University Press, and Cambridge University Press. Prof Georg Ebersbach has received honoraria for consulting from AOK Nordost and in his capacity as advisor for AbbVie Pharma, Grünenthal Pharma, and UCB Pharma. Furthermore, he received honoraria for speaker engagements from AbbVie Pharma, BIAL Pharma, Britannia Pharma, Desitin Pharma, Grünenthal Pharma, Licher GmbH, Mundipharma, TEVA Pharma, UCB Pharma, and Zambon Pharma. Prof Ebersback also receives royalties from Kohlhammer Verlag. Prof Thomas Müller has received honoraria from BIAL.
Acknowledgements: Writing assistance provided by Dr Juliane Moloney, ApotheCom, London, UK.
Support: Jan Jastorff translated the transcript of the presentation and BIAL/Basilio Hernandes carried out a review for medical accuracy. The satellite symposium and the publication of this article were funded by BIAL-Portela & Ca., S.A. The views and opinions expressed are those of the authors and not necessarily of BIAL-Portela & Ca., S.A.
Citation: EMJ Neurol. 2017;5[Suppl 1]:2-10.
Parkinson’s disease (PD) is a long-term degenerative disorder of the central nervous system that mainly affects the motor system. There are currently limited treatment options, including levodopa (L-DOPA), which can be amended in dosing (e.g. schedule and strength), alternative L-DOPA formulations (e.g. quick-acting soluble formulations, extended-release formulations, and continuous infusion), as well as enzyme inhibition (catechol-O-methyl transferase [COMT] and monoamine oxidase B [MAO-B] inhibitors), dopamine agonists (DAs), and combinations thereof. Besides treating symptoms, one of the main concerns in PD is to strike a fine balance between treatment being efficacious without causing dyskinesia, and treatment ‘wearing off’ due to short therapy half-life.
Conventional COMT inhibitors, entacapone and tolcapone, have shown promising results in reducing L-DOPA fluctuations and improving motor function; however, the novel once-daily (OD) oral COMT inhibitor opicapone has an exceptionally high binding affinity with the COMT enzyme, translated into a long duration of action, and provided consistent L-DOPA fluctuation control over 24 hours. Opicapone treatment is associated with more efficient endogenous L-DOPA utilisation and less need for exogenous L-DOPA. The long-term benefits of opicapone have been demonstrated in patients initiated on opicapone and those switching from combination treatment with entacapone. The reported reductions in ‘off-time’, a state of decreased mobility, and favourable results for dyskinesia, may have a big impact on patients’ mobility and treatment adherence; however, further assessments are required.