  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 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.
