Abstract
Suppression of excessively synchronous beta-band oscillatory activity in the brain is believed to suppress hypokinetic motor symptoms of Parkinson’s disease. Recently, a lot of interest has been devoted to desynchronizing delayed feedback deep brain stimulation (DBS). This type of synchrony control was shown to destabilize the synchronized state in networks of simple model oscillators as well as in networks of coupled model neurons. However, the dynamics of the neural activity in Parkinson’s disease exhibits complex intermittent synchronous patterns, far from the idealized synchronous dynamics used to study the delayed feedback stimulation. This study explores the action of delayed feedback stimulation on partially synchronized oscillatory dynamics, similar to what one observes experimentally in parkinsonian patients. We employ a computational model of the basal ganglia networks which reproduces experimentally observed fine temporal structure of the synchronous dynamics. When the parameters of our model are such that the synchrony is unphysiologically strong, the feedback exerts a desynchronizing action. However, when the network is tuned to reproduce the highly variable temporal patterns observed experimentally, the same kind of delayed feedback may actually increase the synchrony. As network parameters are changed from the range which produces complete synchrony to those favoring less synchronous dynamics, desynchronizing delayed feedback may gradually turn into synchronizing stimulation. This suggests that delayed feedback DBS in Parkinson’s disease may boost rather than suppress synchronization and is unlikely to be clinically successful. The study also indicates that delayed feedback stimulation may not necessarily exhibit a desynchronization effect when acting on a physiologically realistic partially synchronous dynamics, and provides an example of how to estimate the stimulation effect.
Highlights
Deep brain stimulation (DBS) entails the delivery of a stimulation signal to subcortical structures via implanted electrodes
When measuring the effect of proposed feedback stimulation we were interested in how delayed feedback stimulation acted on this realistically intermittent weak synchrony
It can be seen (Figure 4A) that the stimulation leads to a reduction in synchrony and more uncorrelated dynamics, i.e. the phase locking between stimulated neurons is broken by the delayed feedback and this result extends to the whole subthalamic nucleus (STN) network
Summary
Deep brain stimulation (DBS) entails the delivery of a stimulation signal to subcortical structures via implanted electrodes. DBS of different targets in the basal ganglia-thalamocortical loop is used to treat symptoms of Parkinson’s disease (PD) and other motor disorders [2]; e.g. the subthalamic nucleus (STN) is a standard anatomical target for DBS in PD. The hypokinetic symptoms of PD have been related to excessive beta-band oscillations and synchrony in the basal ganglia and other structures [3,4,5]. DBS effectiveness has been linked to the destruction of this pathological rhythmicity by reducing the bursting, oscillations and synchronization in the beta-band and increasing regularity and synchrony in the high-frequency band [6,7,8,9,10,11,12].
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