The publication twenty years ago describing excessive therapeutic drug dosing in some Parkinson's disease patients foreshadowed behaviours now well recognised.
The recognition and description of a behavioural syndrome in a group of patients with Parkinson’s disease (PD) who take dopamine replacement therapy in quantities beyond what is required to treat motor symptoms 20 years ago1 sparked interest for a number of reasons. In addition to its deficiency being integral to PD, dopamine had long been regarded as a critical neurotransmitter involved in reward systems reduction in dopamine associated with depression and increased dopamine with addiction. Within the addiction field, these patients represented a real-life experiment to support the prevailing models suggesting maladaptive mesolimbic dopamine circuits underlying addiction.