Dopaminergic therapy in Parkinson's disease decreases cortical beta band coherence in the resting state and increases cortical beta band power during executive control

Abstract

It is not yet well understood how dopaminergic therapy improves cognitive and motor function in Parkinson's disease (PD). One possibility is that it reduces the pathological synchronization within and between the cortex and basal ganglia, thus improving neural communication. We tested this hypothesis by recording scalp electroencephalography (EEG) in PD patients when On and Off medication, during a brief resting state epoch (no task), and during performance of a stop signal task that is thought to engage two partially overlapping (or different) frontal-basal-ganglia circuits. For resting state EEG, we measured pair-wise coherence between scalp electrodes in several frequency bands. Consistent with previous studies, in the Off medication state, those patients with the greatest clinical impairment had the strongest coherence, especially in the beta band, indicating pathological over-synchronization. Dopaminergic medication reduced this coherence. For the stop signal task, On vs. Off medication increased beta band power over right frontal cortex for successful stopping and over bilateral sensorimotor cortex for going, especially for those patients who showed greater clinical improvement. Thus, medication reduced pathological coherence in beta band at rest and increased task related beta power for two potentially dissociable cortico-basal ganglia circuits. These results support the hypothesis that dopaminergic medication in PD improves neural communication both at rest and for executive and motor function.

Elevated synchrony in Parkinson disease detected with electroencephalography

“…This is consistent with previous work, using either EEG, MEG, or ECoG, which has not shown a consistent alteration of cortical beta power in PD 6, 18, 27-29 . Similarly, there were no differences in broadband gamma power (50-150 Hz, excluding 60 and 120 Hz) (p > 0.16, Figure 3C-D ).…”

“…In that study, coherence was measured between all EEG contact pairs in PD patients and was found to be reduced with medications and DBS. That reduction with medications was replicated with the same dataset reported here, in a previous publication 18 .…”

Complexity of resting-state EEG activity in the patients with early-stage Parkinson’s disease

“…Although the exclusion criteria in our study have included atypical parkinsonism, neuropsychiatric condition and any other severe illness, it is still required longitudinal study to identify whether the observed changes in PE or OI are specific to PD rather than age-related parkinsonism or multiple system atrophy. Moreover, it has been shown that the dopaminergic replacement therapy has long effects on sensory-motor circuitry (George et al 2013;Herz et al 2014). All the patients in our study have received levodopa drugs.…”

On the Globality of Motor Suppression: Unexpected Events and Their Influence on Behavior and Cognition

“…This makes a direct connection to patients with Parkinson’s Disease (PD) who are typically ‘stuck in set’, especially with regard to switching behavior (in addition to their classic motor symptoms) (Bowen et al, 1975; Lees and Smith, 1983; Taylor et al, 1986). PD is characterized by over-synchrony between basal ganglia and cortex (Brown, 2003; George et al, 2013; Swann et al, 2015); and it is thought that this ‘locking’ prevents cortico-basal-ganglia circuits from operating properly. Indeed, multiple studies show PD patients off treatment are impaired at stopping (George et al, 2013; Obeso et al, 2014; Obeso et al, 2011; Swann et al, 2011).…”

“…PD is characterized by over-synchrony between basal ganglia and cortex (Brown, 2003; George et al, 2013; Swann et al, 2015); and it is thought that this ‘locking’ prevents cortico-basal-ganglia circuits from operating properly. Indeed, multiple studies show PD patients off treatment are impaired at stopping (George et al, 2013; Obeso et al, 2014; Obeso et al, 2011; Swann et al, 2011). We hypothesize that the mental inflexibility in PD is at least partly explained by a system that is not properly interruptible by new information (because the STN-mediated interrupt is ineffective due to oversynchrony).…”