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Parkinson’s disease (PD) is characterised by a loss of dopamine and dopaminergic cells. The consequences hereof are widespread network disturbances in brain function. It is an ongoing topic of investigation how the disease-related changes in brain function manifest in PD relate to clinical symptoms. We present The Swedish National Facility for Magnetoencephalography Parkinson’s Disease Dataset (NatMEG-PD) as an Open Science contribution to identify the functional neural signatures of Parkinson’s disease and contribute to diagnosis and treatment. The dataset contains whole-head magnetoencephalographic (MEG) recordings from 66 well-characterised PD patients on their regular dose of dopamine replacement therapy and 68 age- and sex-matched healthy controls. NatMEG-PD contains three-minute eyes-closed resting-state MEG, MEG during an active movement task, and MEG during passive movements. The data includes anonymised MRI for source analysis and clinical scores. MEG data is rich in nature and can be used to explore numerous functional features. By sharing these data, we hope other researchers will contribute to advancing our understanding of the relationship between brain activity and disease state or symptoms. [ABSTRACT FROM AUTHOR]

The usefulness of eye-tracking tasks as potential biomarkers for motor or cognitive disease burden in Parkinson's disease (PD) has been subject of debate for many years. Several studies suggest that the performance in the antisaccade task may be altered in patients with PD and associated with motor disease severity or executive dysfunction. In this meta-analysis, random effects models were used to synthesize the existing evidence on antisaccade error rates and latency in PD. Furthermore, meta-regressions were performed to assess the role of motor and cognitive disease severity, dopaminergic medication and methodological factors. Additionally, the impact of acute levodopa administration and activation of deep brain stimulation was evaluated in two separate sub-analyses. This meta-analysis confirms that antisaccade latency and error rate are significantly increased in PD. Disease duration, Unified Parkinson's disease rating scale score and Hoehn and Yahr stage mediate the effect of PD on antisaccade latency with higher motor burden being associated with increased antisaccade latency. Acute administration of levodopa had no significant effects on antisaccade performance in a small number of eligible studies. Deep brain stimulation in the subthalamic nucleus, on the other hand, may alter the speed accuracy trade-off supporting an increase of impulsivity following deep brain stimulation in PD. According to the results of the meta-analysis, antisaccade latency may provide a potential marker for disease severity and progression in PD which needs further confirmation in longitudinal studies. [ABSTRACT FROM AUTHOR]

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Motor symptoms are defining traits in the diagnosis of Parkinson's disease (PD). A crucial component in motor function is the integration of afferent proprioceptive sensory feedback. Previous studies have indicated abnormal movement-related cortical oscillatory activity in PD, but the role of the proprioceptive afference on abnormal oscillatory activity in PD has not been elucidated. We examine the cortical oscillations in the mu/beta-band (8-30 Hz) in the processing of proprioceptive stimulation in PD patients, ON/OFF levodopa medication, as compared to that of healthy controls (HC). We used a proprioceptive stimulator that generated precisely controlled passive movements of the index finger and measured the induced cortical oscillatory responses following the proprioceptive stimulation using magnetoencephalography. Both PD patients and HC showed a typical beta-band desynchronization during the passive movement. However, the subsequent beta rebound after the passive movement that was almost absent in PD patients compared to HC. Furthermore, we found no difference in the degree of beta rebound attenuation between patients ON and OFF levodopa medication. The results demonstrate a disease-related deterioration in cortical processing of proprioceptive afference in PD. [ABSTRACT FROM AUTHOR]