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One of the hallmarks of Parkinson’s disease (PD) is the presence of abnormal synchronised oscillatory activity within the basal ganglia at certain frequencies. This activity may jam normal communication within brain circuits governing movement, leading to the symptoms of PD. It is unclear however how this activity arises, or how it may be best treated in individual patients.

Ashwini Oswal is a Clinical Lecturer in Neurology affiliated to two of NDCN's divisions: the MRC Brain Network Dynamics Unit and the Division of Clinical Neurology. He and his colleagues have integrated imaging approaches (MRI tractography, magnetoencephalography and invasive recordings) in PD patients undergoing treatment with Deep Brain Stimulation, in an attempt to provide an improved understanding of how abnormal oscillatory synchrony arises in PD. 

Using multimodal imaging and computational models they observed that a direct pathway linking the motor cortex and the basal ganglia (known as the hyperdirect pathway) may be responsible for triggering abnormal synchrony within the basal ganglia in PD.

These findings could allow the development of more intelligent brain stimulation techniques that specifically target the hyperdirect pathway and ameliorate abnormal synchrony within the basal ganglia.  

Image caption: A: visualization of Deep Brain Stimulation electrodes targeting the subthalamic nucleus in Parkinson’s disease (PD) patients. B: Top; white matter tracts passing between cortical areas and the STN in PD (‘hyperdirect pathway’). The green and blue contours represent the supplementary motor area (SMA) and primary motor cortex. Middle; coupling between cortical areas and the STN at high beta band (21-30 Hz) frequencies. Bottom; Regions where high beta band cortico-STN coupling is predicted by anatomical connectivity within the hyperdirect pathway. C: Computational models reveal that high beta band cortical inputs to the STN can trigger the generation of lower beta frequencies which are believed to be pathological.

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