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Deep brain stimulation; Parkinson’s disease; Parkinson’s disease: imaging; Subthalamic nucleus; Beta oscillations
Abstract:
Deep brain stimulation of the subthalamic nucleus is an established treatment for the motor symptoms of Parkinson’s disease.
Given the frequent occurrence of stimulation-induced affective and cognitive adverse effects, a better understanding about the role
of the subthalamic nucleus in non-motor functions is needed. The main goal of this study is to characterize anatomical circuits
modulated by subthalamic deep brain stimulation, and infer about the inner organization of the nucleus in terms of motor and
non-motor areas. Given its small size and anatomical intersubject variability, functional organization of the subthalamic nucleus is
difficult to investigate
in vivo
with current methods. Here, we used local field potential recordings obtained from 10 patients with
Parkinson’s disease to identify a subthalamic area with an analogous electrophysiological signature, namely a predominant beta
oscillatory activity. The spatial accuracy was improved by identifying a single contact per macroelectrode for its vicinity to the
electrophysiological source of the beta oscillation. We then conducted whole brain probabilistic tractography seeding from the
previously identified contacts, and further described connectivity modifications along the macroelectrode’s main axis. The desig-
nated subthalamic ‘beta’ area projected predominantly to motor and premotor cortical regions additional to connections to limbic
and associative areas. More ventral subthalamic areas showed predominant connectivity to medial temporal regions including
amygdala and hippocampus. We interpret our findings as evidence for the convergence of different functional circuits within
subthalamic nucleus’ portions deemed to be appropriate as deep brain stimulation target to treat motor symptoms in Parkinson’s
disease. Potential clinical implications of our study are illustrated by an index case where deep brain stimulation of estimated
predominant non-motor subthalamic nucleus induced hypomanic behaviour.
