Abstract
BackgroundParkinson disease (PD) patients have difficulty with self-initiated (SI) movements, presumably related to basal ganglia thalamocortical (BGTC) circuit dysfunction, while showing less impairment with externally cued (EC) movements.ObjectivesWe investigate the role of BGTC in movement initiation and the neural underpinning of impaired SI compared to EC movements in PD using multifocal intracranial recordings and correlating signals with symptom severity.MethodsWe compared time-resolved neural activities within and between globus pallidus internus (GPi) and motor cortex during between SI and EC movements recorded invasively in 13 PD patients undergoing deep brain stimulation implantation. We compared cortical (but not subcortical) dynamics with those recorded in 10 essential tremor (ET) patients, who do not have impairments in movement initiation.ResultsSI movements in PD are associated with greater low-beta (13–20 Hz) power suppression during pre-movement period in GPi and motor cortex compared to EC movements in PD and compared to SI movements in ET (motor cortex only). SI movements in PD are uniquely associated with significant low-beta pallidocortical coherence suppression during movement execution that correlates with bradykinesia severity. In ET, motor cortex neural dynamics during EC movements do not significantly differ from that observed in PD and do not significantly differ between SI and EC movements.ConclusionThese findings implicate low beta BGTC oscillations in impaired SI movements in PD. These results provide a physiological basis for the strategy of using EC movements in PD, circumventing diseased neural circuits associated with SI movements and instead engaging circuits that function similarly to those without PD.
Highlights
Patients with Parkinson disease (PD) have difficulty in initiating movements, when those movements are self-initiated (SI) (Wu et al, 2011; Taniwaki et al, 2013; Jia et al, 2018). This motor impairment is related to a wider constellation of motor symptoms in PD, including rigidity and bradykinesia which result from dysfunction of the basal ganglia thalamocortical (BGTC) network (Kühn et al, 2009; Little et al, 2012; van Wijk et al, 2016)
This circuit might be relatively preserved in PD, allowing the motor system to bypass the disrupted BGTC network and lead to more normal motor performance with externally cued (EC) movements relative to those associated with SI movements (Ballanger et al, 2008; Wu et al, 2011; Taniwaki et al, 2013)
We focus on the activities in globus pallidus internus (GPi) because it is the critical output node of the BGTC network
Summary
Patients with Parkinson disease (PD) have difficulty in initiating movements, when those movements are self-initiated (SI) (Wu et al, 2011; Taniwaki et al, 2013; Jia et al, 2018) This motor impairment is related to a wider constellation of motor symptoms in PD, including rigidity and bradykinesia which result from dysfunction of the basal ganglia thalamocortical (BGTC) network (Kühn et al, 2009; Little et al, 2012; van Wijk et al, 2016). Parkinson disease (PD) patients have difficulty with self-initiated (SI) movements, presumably related to basal ganglia thalamocortical (BGTC) circuit dysfunction, while showing less impairment with externally cued (EC) movements
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