Acute dopamine boost has a negative effect on plasticity of the primary motor cortex in advanced Parkinson's disease

• DOI: 10.1093/brain/aws124
• Publication Date: 2012-05-20T12:46:01Z
• Authors: A. Kishore; T. Popa; B. Velayudhan; T. Joseph; A. Balachandran; S. Meunier
• Keywords: Adult; Male; 0301 basic medicine; Dyskinesia, Drug-Induced; Neuronal Plasticity; Dopamine; Long-Term Synaptic Depression; Long-Term Potentiation; Motor Cortex; Parkinson Disease; Middle Aged; Evoked Potentials, Motor; Transcranial Magnetic Stimulation; Levodopa; 03 medical and health sciences; Humans; Female; Aged

Plasticity of primary motor cortex is severely impaired in Parkinson's disease and chronic dopaminergic treatment reported not to rescue it. The effect an acute dose levodopa on cortical plasticity so far variable. In this study, it was hypothesized that would be restored as a long duration response stable responders while those with complications have reduction or loss similar the decay signs. Patients were carefully stratified based their into (n = 17), fluctuating non-dyskinetics 18) dyskinetics 20). Theta burst stimulation applied induce long-term potentiation depression-like both OFF ON conditions. OFF, could express types plasticity, had potentiation, but no depression lost dyskinetics. This suggests presence early stages gradual benefit particularly for depression, when develop. An led worsening non-dyskinetic patients, did any absent dyskinetic patients. Acute dosing all groups. there paradoxical instead depression. Our results suggest non-physiological dopamine boost has negative advances. We propose doses progression may contribute pathophysiology complications. Repeated surges synaptic during potentially lead persistent dysfunction key enzymes intracellular signalling cascade are involved induction maintenance forms plasticity.