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Background: The G2019S-LRRK2 gene mutation is a common cause of hereditary Parkinson's disease (PD), associated with a higher frequency of the postural instability gait difficulty (PIGD) motor phenotype yet with preserved cognition. This study investigated neurophysiological changes during motor and cognitive tasks in PD patients with and without the G2019S-LRRK2 mutation. Methods: 33 iPD patients and 22 LRRK2-PD patients performed the visual Go/NoGo task (VGNG) during sitting (single-task) and walking (dual-task) while wearing a 64-channel EEG cap. Event-related potentials (ERP) from Fz and Pz, specifically N200 and P300, were extracted and analyzed to quantify brain activity patterns. Results: The LRRK2-PD group performed better in the VGNG than the iPD group (group*task; p = 0.05). During Go, the iPD group showed reduced N2 amplitude and prolonged N2 latency during walking, whereas the LRRK2-PD group showed only shorter latency (group*task p = 0.027). During NoGo, opposite patterns emerged; the iPD group showed reduced N2 and increased P3 amplitudes during walking while the LRRK2-PD group demonstrated increased N2 and reduced P3 (N2: group*task, p = 0.010, P3: group*task, p = 0.012). Conclusions: The LRRK2-PD group showed efficient early cognitive processes, reflected by N2, resulting in greater neural synchronization and prominent ERPs. These processes are possibly the underlying mechanisms for the observed better cognitive performance as compared to the iPD group. As such, future applications of intelligent medical sensing should be capable of capturing these electrophysiological patterns in order to enhance motor–cognitive functions. [ABSTRACT FROM AUTHOR]

Background: Parkinson's disease (PD) is currently considered to be a multisystem neurodegenerative disease that involves cognitive alterations. EEG slowing has been associated with cognitive decline in various neurological diseases, such as PD, Alzheimer's disease (AD), and epilepsy, indicating cortical involvement. A novel method revealed that this EEG slowing is composed of paroxysmal slow-wave events (PSWE) in AD and epilepsy, but in PD it has not been tested yet. Therefore, this study aimed to examine the presence of PSWE in PD as a biomarker for cortical involvement. Methods: 31 PD patients, 28 healthy controls, and 18 juvenile myoclonic epilepsy (JME) patients (served as positive control), underwent four minutes of resting-state EEG. Spectral analyses were performed to identify PSWEs in nine brain regions. Mixed-model analysis was used to compare between groups and brain regions. The correlation between PSWEs and PD duration was examined using Spearman's test. Results: No significant differences in the number of PSWEs were observed between PD patients and controls (p > 0.478) in all brain regions. In contrast, JME patients showed a higher number of PSWEs than healthy controls in specific brain regions (p < 0.023). Specifically in the PD group, we found that a higher number of PSWEs correlated with longer disease duration. Conclusions: This study is the first to examine the temporal characteristics of EEG slowing in PD by measuring the occurrence of PSWEs. Our findings indicate that PD patients who are cognitively intact do not have electrographic manifestations of cortical involvement. However, the correlation between PSWEs and disease duration may support future studies of repeated EEG recordings along the disease course to detect early signs of cortical involvement in PD. [ABSTRACT FROM AUTHOR]

(1) Background: Directed functional connectivity (DFC) alterations within brain networks are described using fMRI. EEG has been scarcely used. We aimed to explore changes in DFC in the sensory-motor network (SMN), ventral-attention network (VAN), dorsal-attention network (DAN), and central-executive network (CEN) using an EEG-based mapping between PD patients and healthy controls (HCs). (2) Methods: Four-minutes resting EEG was recorded from 29 PD patients and 28 HCs. Network's hubs were defined using fMRI-based binary masks and their electrical activity was calculated using the LORETA. DFC between each network's hub-pairs was calculated for theta, alpha and beta bands using temporal partial directed coherence (tPDC). (3) Results: tPDCs percent was lower in the CEN and DAN in PD patients compared to HCs, while no differences were observed in the SMN and VAN (group*network: F = 5.943, p < 0.001) in all bands (group*band: F = 0.914, p = 0.401). However, in the VAN, PD patients showed greater tPDCs strength compared to HCs (p < 0.001). (4) Conclusions: Our results demonstrated reduced connectivity in the CEN and DAN, and increased connectivity in the VAN in PD patients. These results indicate a complex pattern of DFC alteration within major brain networks, reflecting the co-occurrence of impairment and compensatory mechanisms processes taking place in PD. [ABSTRACT FROM AUTHOR]