Alterations in cognitive action control in patients with PD are well described from a behavioral point of view. However, there is currently very little information to directly link these difficulties to functional alterations of brain areas, or of efficient communication within large scale brain networks. Thus, the objective of this project is to specify the neuronal substrates linked to the difficulties in cognitive action control observed in patients with PD. Our rational is based on the recent findings on the role of theta (4-8 Hz) neuronal oscillations in cognitive action control. Indeed, converging evidence linked this process to an increase in theta oscillatory power around midfrontal electrodes (FCz, Cz) and to an increase in theta functional connectivity with task-relevant brain areas.
Our working hypotheses are based on the hypothesis proposed by Cohen (2014). It proposes that the medial frontal cortex (MFC; around the pre-SMA) would be involved in the integration of conflicting information, observable by studying theta oscillations' power. On the other hand, the phase synchronization of theta oscillations between the MFC and the other task-relevant cortical areas would reflect the degree of recruitment of the entire network participating in the implementation of an efficient cognitive control. Thus, according to this model, a conflict situation would lead to two main measurable electrophysiological reactions in the cortex: i) an increase in the power of theta oscillations around the MFC, ii) an increase in theta phase synchronization between the MFC and the other cortical areas (such as the lateral prefrontal and parietal cortices) involved in implementing cognitive action control. These two electrophysiological effects will be the main judgment criteria of this study.
We hypothesize that the behavioral difficulties in cognitive action control observed in PD patients stem from a lack of integration of the conflicting information and / or a weaker communication of this information to the areas implementing the cognitive control of the action. The alteration of one or both of these aspects may explain the weaker cognitive action control observed in patients. Moreover, by inspecting the disrupted brain networks, we will be able to make hypotheses explaining the alteration of cognitive control in PD. For example, a weaker functional connectivity between the MFC and the posterior parietal cortex could indicate a lower redirection of attentional resources following the presentation of a conflictual stimulus. Another possibility would be a weaker functional connectivity between the MFC and the inferior prefrontal cortex, which would rather indicate a lack of recruitment of the inhibitory system.
We will test our main hypothesis by comparing the performance of a group of PD patients to that of a group of healthy participants whose brain activity will be collected during the realization of a Simon task via a high resolution electroencephalography system. The behavioral performances will be compared as well as the source-reconstructed electrophysiological data. Specifically, the power of the theta oscillations within the medial frontal cortex, as well as the phase synchronization between the other cortical areas involved will be compared between the two groups. Brain-behavior relationships will also be investigated in order to try to link PD behavioral impairments to changes in theta oscillatory power/connectivity.
From ClinicalTrials.gov, a database of the U.S. National Institutes of Health, through its National Library of Medicine. This record may not reflect the most current and accurate biomedical/scientific data available from the NLM/NIH.