Chronic dopaminergic stimulation in Parkinson's disease: from dyskinesias to impulse control disorders
Valerie Voon (a), Pierre-Olivier Fernagut (b), Jeff Wickens (c), Christelle Baunez (d), Manuel Rodríguez (e), Nancy Pavon (f), Jorge L. Juncos (g), José A. Obeso (e), Erwan Bezard (b)
(a) Wellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, London, UK
(b) Université Victor Segalen-Bordeaux 2, Centre National de la Recherche Scientifique, Bordeaux Institute of Neuroscience, UMR 5227, Bordeaux, France
(c) Neurobiology Research Unit, Okinawa Institute of Science and Technology, 12?22 Suzaki, Uruma City, Okinawa, Japan
(d) Laboratoire de Neurobiologie de la Cognition, CNRS UMR 6155, Aix-Marseille Université, Marseille, France
(e) Clínica Universidad de Navarra, Pamplona, Spain
Dopamine is an essential neurotransmitter for many brain functions, and its dysfunction has been implicated in both neurological and psychiatric disorders.
Parkinson's disease is an archetypal disorder of dopamine dysfunction characterised by motor, cognitive, behavioural, and autonomic symptoms. While effective for motor symptoms, dopamine replacement therapy is associated not only with motor side-effects, such as levodopa-induced dyskinesia, but also behavioural side-effects such as impulse control disorders (eg, pathological gambling and shopping, binge eating, and hypersexuality), punding (ie, abnormal repetitive non-goal oriented behaviours), and compulsive medication use. We review clinical features, overlapping molecular mechanisms, and a specific cognitive mechanism of habit learning that might underlie these behaviours.
We integrate these mechanisms with the emerging view of the basal ganglia as a distributive system involved in the selection and facilitation of movements, acts, and emotions.
CITATION Lancet Neurol. 2009 Dec;8(12):1140-9