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Influence of dopamine deficiency on interhemispheric crosstalk in Parkinson’s disease

P. Loehrer, F. Nettersheim, I. Weber, F. Jung, L. Timmermann (Marburg, Germany)

Meeting: 2018 International Congress

Abstract Number: 1669

Keywords: Dopamine, Electroencephalogram(EEG), Motor control

Session Information

Date: Monday, October 8, 2018

Session Title: Parkinson's Disease: Pathophysiology

Session Time: 1:15pm-2:45pm

Location: Hall 3FG

Objective: To identify the significance of dopaminergic depletion in Parkinson’s disease (PD) on interhemispheric crosstalk using a complex bimanual tapping task.

Background: Dopamine deficiency in PD patients causes abnormal neuronal processing within the basal ganglia subsequently impeding functional integration of distinct areas of the cerebral cortex. The precise causal interplay of bihemispheric primary motor area (M1), lateral premotor cortex (lPM), prefrontal cortex (PFC), and supplementary motor area (SMA), however, is crucial for correct bimanual coordination which is impaired in PD. Hitherto, disease related alterations of interhemispheric crosstalk remain to be elucidated.

Methods: By recording high-density electroencephalography we studied 16 PD patients in the unmedicated and medicated state as well as age-matched controls while performing a complex bimanual tapping task. Behavioral analysis was performed on parameters of motor function, i.e. error rates and performance times. We used Dynamic causal modelling (DCM) for induced responses to infer task related changes of effective connectivity. Coupling values were extracted and subsequently correlated with behavioral parameters to relate electrophysiological changes to motor performance.

Results: PD patients in the unmedicated state had significantly higher performance times as compared to medicated patients (PD OFF: 2.71 s vs. PD ON: 2.47 s, p = .04). No contrast, however, could be observed between PD ON and control subjects (PD ON: 2.47 s vs. Control: 2.58 s, p > .05). A model with reciprocal interhemispheric connections was favored by Bayesian model selection. Inhibitory β-β-coupling between left and right M1 was present in the control group. In contrast, excitatory β-γ-cross-frequency-coupling was expressed by PD patients in the OFF. Correlation analysis revealed a significant positive correlation between this connection and performance time (rho = .639, p = .047, FWE-corrected). PD patients in the ON state continued to express excitatory coupling between primary motor cortices. This coupling, however, switched to within-frequency γ-γ-coupling.

Conclusions: Our results suggest that excitatory β-γ-coupling between both primary motor cortices in the OFF increases performance time and could partially be responsible for impaired bimanual coordination in PD. Furthermore, levodopa substitution promoted a switch from antikinetic beta band to prokinetic gamma band in left M1.

To cite this abstract in AMA style:

P. Loehrer, F. Nettersheim, I. Weber, F. Jung, L. Timmermann. Influence of dopamine deficiency on interhemispheric crosstalk in Parkinson’s disease [abstract]. Mov Disord. 2018; 33 (suppl 2). https://www.mdsabstracts.org/abstract/influence-of-dopamine-deficiency-on-interhemispheric-crosstalk-in-parkinsons-disease/. Accessed May 12, 2025.
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