Abstract
In this computational study we investigate coordinated reset (CR) neuromodulation designed for an effective control of synchronization by multi-site stimulation of neuronal target populations. This method was suggested to effectively counteract pathological neuronal synchrony characteristic for several neurological disorders. We study how many stimulation sites are required for optimal CR-induced desynchronization. We found that a moderate increase of the number of stimulation sites may significantly prolong the post-stimulation desynchronized transient after the stimulation is completely switched off. This can, in turn, reduce the amount of the administered stimulation current for the intermittent ON–OFF CR stimulation protocol, where time intervals with stimulation ON are recurrently followed by time intervals with stimulation OFF. In addition, we found that the optimal number of stimulation sites essentially depends on how strongly the administered current decays within the neuronal tissue with increasing distance from the stimulation site. In particular, for a broad spatial stimulation profile, i.e., for a weak spatial decay rate of the stimulation current, CR stimulation can optimally be delivered via a small number of stimulation sites. Our findings may contribute to an optimization of therapeutic applications of CR neuromodulation.
Highlights
Synchronization plays a fundamental role in many interacting systems (Winfree, 1980; Kuramoto, 1984; Tass, 1999; Pikovsky et al, 2001; Strogatz, 2003)
Continuous coordinated reset (CR) stimulation administered via 4 stimulation sites can reliably induce a 4-cluster state such that the phases are grouped into four clusters equidistantly spaced on the unit circle (Figure 2D)
We found that an increasing number of stimulation sites Ns can prolong the admissible rest periods, i.e., nmax increases, and improve the desynchronizing impact of the intermittent CR stimulation if the latter is spatially rather selective, i.e., the stimulation current is narrowly distributed around the stimulation site within the stimulated population (Figure 6A for σ = 0.5)
Summary
Synchronization plays a fundamental role in many interacting systems (Winfree, 1980; Kuramoto, 1984; Tass, 1999; Pikovsky et al, 2001; Strogatz, 2003). HF DBS may be ineffective or lead to side effects, and the clinical effect may decline with time (Limousin et al, 1999; Kumar et al, 2003; Volkmann, 2004; Rodriguez-Oroz et al, 2005), which motivated the development of novel stimulation methods (Tass, 1999) They are aimed at the control of undesirable neuronal synchronization, which is highlighted by the finding that the physiological dynamics of neuronal populations is characterized by uncorrelated firing (Nini et al, 1995). The main distinction of the novel methods in comparison to HF DBS is that coordinated reset (CR) stimulation (Tass, 2003a,b) as well as feedback techniques (Rosenblum and Pikovsky, 2004; Hauptmann et al, 2005; Popovych et al, 2005; Pyragas et al, 2007) selectively counteract pathological synchronization of neuronal target populations and restore uncorrelated neuronal firing
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