Abstract
Chronic administration of levodopa, while producing an “awakening” in patients with Parkinson disease (PD), causes disabling side effects such as motor fluctuations and dyskinesia. Indeed the most common reason for deep brain stimulation (DBS) in patients with PD is for treating these complications. However, our understanding of the complexities of these complications is still in the early days. Animal models (primate and rodent) have been exceedingly helpful in elucidating some of the mechanisms. More work needs to be done. In the paper by Gilmour et al. (2011) the authors have investigated the neuronal firing properties and local field potentials of two basal ganglia structures, in response to chronic treatment, to tackle this very question. This commentary attempts to place the work in the context of PD animal models, electrophysiology and where we need to go.
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