Abstract
BackgroundStriatal dopamine is functionally important for the acquisition of motor skills. However, it remains controversial as to whether intrinsic processing of motor learning is impaired in patients with Parkinson’s disease (PD), and if yes, whether the impairment is associated with altered striatal dopamine release. Additionally, most neuro-imaging studies of patients with PD have focused on motor sequence learning. In contrast, skill acquisition, specifically, the reconstruction of muscle control of isolated movements, has barely been studied.MethodIn this study, we used a repetitive skill training task to measure the peak acceleration of left thumb movement during a process to achieve fine tuning of motor skill. Using 11C-raclopride (RAC) positron emission tomography, we investigated changes in striatal dopamine levels in two conditions of a skill acquisition task: initial skill training (Day 1) and acquired condition (Day 2) with eight patients with PD and age-matched healthy subjects (HS).ResultIn HS, the mean acceleration of each session improved through repeated training sessions on Day 1. However, in patients with PD, the training-associated increase was less than that for HS, and this suggests that repetitive skill training does not result in the effective improvement of motor performance. The regions of interest (ROI) analysis revealed that the RAC-binding potential (BP) was significantly reduced in the right putamen on Day 1 compared with Day 2 in HS. In patients with PD, BP within the right putamen was unchanged. Further, we found that patients with PD had increased dopamine levels within the right ventral striatum (VST) and right caudate (CAU) on Day 2, which was greater than that in HS. These results suggest the impaired activation of the putamen during skill acquisition in patients with PD and compensated hyperactivation of the VST and CAU for the reduced dopamine release within the dorsal putamen (DPU).ConclusionOur findings suggest that patients with PD had insufficiency in the process to improve motor skills. Different patterns of striatal dopamine release are relevant to the impairment of these motor functions in patients with PD, at the early stage of the disease.
Highlights
Striatal dopamine depletion due to degeneration of the nigrostriatal dopaminergic neuron causes motor disturbances in patients with Parkinson’s disease (PD)
We investigated changes in dopamine levels in the striatum, as related to the intrinsic processing of skill acquisition between different stages, using a marker of D2/D3-receptor binding with RAC-positron emission tomography (PET) in patients with PD and aged healthy subjects (HS) [32]
There was a significant difference in the mean acceleration of baseline (PD: 0.101 ± 0.015 cm/s2 vs. HS: 0.149 ± 0.052 cm/s2; P < 0.05). (Fig 2B) In each group, the changes in the mean acceleration of sessions 1–4 on Day1 were calculated using the change ratio against baseline motor performance
Summary
Striatal dopamine depletion due to degeneration of the nigrostriatal dopaminergic neuron causes motor disturbances in patients with Parkinson’s disease (PD). The motor cortical areas project major glutamatergic fibers into the striatum, which belongs to a series of basal ganglia-thalamo-cortical loops that project back to the motor cortex via the motor thalamic nucleus [1, 2]. Disruption of these loops causes the various motor signs associated with PD [3,4,5]. It remains controversial as to whether intrinsic processing of motor learning is impaired in patients with Parkinson’s disease (PD), and if yes, whether the impairment is associated with altered striatal dopamine release. Skill acquisition, the reconstruction of muscle control of isolated movements, has barely been studied.
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