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Suppression of excessively synchronous beta-band oscillatory activity in thebrain is believed to suppress hypokinetic motor symptoms of Parkinson'sdisease. Recently, a lot of interest has been devoted to desynchronizingdelayed feedback deep brain stimulation (DBS). This type of synchrony controlwas shown to destabilize the synchronized state in networks of simple modeloscillators as well as in networks of coupled model neurons. However, thedynamics of the neural activity in Parkinson's disease exhibits complexintermittent synchronous patterns, far from the idealized synchronous dynamicsused to study the delayed feedback stimulation. This study explores the actionof delayed feedback stimulation on partially synchronized oscillatory dynamics,similar to what one observes experimentally in parkinsonian patients. We employa model of the basal ganglia networks which reproduces experimentally observedfine temporal structure of the synchronous dynamics. When the parameters of ourmodel are such that the synchrony is unphysiologically strong, the feedbackexerts a desynchronizing action. However, when the network is tuned toreproduce the highly variable temporal patterns observed experimentally, thesame kind of delayed feedback may actually increase the synchrony. As networkparameters are changed from the range which produces complete synchrony tothose favoring less synchronous dynamics, desynchronizing delayed feedback maygradually turn into synchronizing stimulation. This suggests that delayedfeedback DBS in Parkinson's disease may boost rather than suppresssynchronization and is unlikely to be clinically successful. The study alsoindicates that delayed feedback stimulation may not necessarily exhibit adesynchronization effect when acting on a physiologically realistic partiallysynchronous dynamics, and provides an example of how to estimate thestimulation effect.

Failure of Delayed Feedback Deep Brain Stimulation for Intermittent Pathological Synchronization in Parkinson's Disease