To view this page ensure that Adobe Flash Player version 11.1.0 or greater is installed.

Movement Disorders Parkinson’s Disease Extending our Understanding of the Dopaminergic Basis of Non-motor Symptoms in Parkinson’s Disease Highlights of a Britannia symposium held at the 10th International Congress on Non-Motor Dysfunctions in Parkinson’s Disease and Related Disorders, 5th December 2014, Nice, France Expert Review by: Amos D Korczyn, 1 K Ray Chaudhuri 2 and Teus van Laar 3 1. Emeritus Professor of Neurology, Tel Aviv University, Tel Aviv, Israel; 2. Professor of Movement Disorders; Director, National Parkinson Foundation Centre of Excellence, Kings College, Denmark Hill Campus, London, UK; 3. Professor of Neurology, Movement Disorder Centre, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands. Abstract Parkinson’s disease (PD) is primarily considered as a motor disorder but there is increasing recognition of the wide range of non-motor symptoms (NMS), such as low mood, pain, apathy, fatigue and sleep problems, which may be experienced by PD patients across the spectrum of the disease. Notably, NMS often occur before motor symptoms develop and are known to place a significant burden on health-related quality of life (HRQoL) of the person with PD. Commonly, NMS go undiagnosed by the clinician and are therefore undertreated; however, to optimise patient outcomes, both motor and non-motor aspects of PD need to be recognised and managed effectively. The 10th International Congress on Non-Motor Dysfunctions in Parkinson’s Disease and Related Disorders held in Nice, France, in December 2014, offered the opportunity to look further into the dopaminergic basis of NMS and how this may affect clinical management. Britannia arranged an international faculty, chaired by Professor Amos Korczyn (Tel Aviv, Israel), to review the latest developments in our understanding of the underlying aetiology and clinical burden of non-motor features in PD that will ultimately help inform clinical practice. Surveys indicate that NMS have an extremely high prevalence among PD patients and evidence now suggests that it is the total ‘burden’ of NMS, combining frequency and severity, and not just the occurrence of individual NMS such as depression, which is the major determinant of a patient’s HRQoL. Recognising the significant contribution of NMS to the total clinical picture in PD, in order to provide a more comprehensive grading of PD severity, it is now proposed that the clinical assessment of PD patients needs a combined approach using for example the validated Non-motor Symptoms Scale (NMSS) to assess total NMS burden in addition to classic motor symptom scoring. Recent data from newly diagnosed PD patients also suggests there are different subtypes of PD that may have implications for both clinical trial design and the selection of therapy. Cognitive impairment often occurs in patients with PD, even in early disease, progressing to PD dementia in a substantial proportion of patients, which can limit therapeutic options. Posterior cortical dysfunction is a negative predictor of the progression of PD with mild cognitive impairment to PD dementia. Pronounced nigrostriatal denervation is characteristic of PD; however, cholinergic changes are also observed. Cholinergic depletion starts early in the disease process and by the time PD dementia develops patients will have a significant cholinergic deficit in various cortical regions. Current research is focused on the potential to reduce cognitive decline by decreasing beta-amyloid plaques. Keywords Parkinson’s disease (PD), non-motor symptoms, dopamine, cognitive impairment, apomorphine Disclosure: Amos D Korczyn has received honoraria for sponsored symposia in educational meetings from Britannia. K Ray Chaudhuri has received honoraria for sponsored symposia in educational meetings from AbbVie, Britannia, Mundipharma, Otsuka, UCB and US WorldMeds. He has received educational grants from AbbVie, Britannia, Medtronic and UCB. Teus van Laar has received honoraria for sponsored symposia in educational meetings from AbbVie, Britannia, UCB and Medtronic. Acknowledgements: Editorial assistance was provided by Dr Karen Wolstencroft, Helen Lawn Associates, supported by Britannia Pharmaceuticals Ltd. Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. Received: 10 March 2015 Accepted: 26 March 2015 Citation: European Neurological Review, 2015;10(1):23–7 Correspondence: Amos D Korczyn, Department of Neurology, Tel Aviv University, Ramat Aviv 69978, Israel. E: amoskor@post.tau.ac.il Support: The publication of this article was supported by Britannia Pharmaceuticals Ltd. The views and opinions expressed are those of the authors and not necessarily those of Britannia Pharmaceuticals Ltd. Tou ch ME dical ME d ia 23