2011
DOI: 10.1007/s11071-011-0223-z
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Intermittent neural synchronization in Parkinson’s disease

Abstract: Motor symptoms of Parkinson’s disease are related to the excessive synchronized oscillatory activity in the beta frequency band (around 20Hz) in the basal ganglia and other parts of the brain. This review explores the dynamics and potential mechanisms of these oscillations employing ideas and methods from nonlinear dynamics. We present extensive experimental documentation of the relevance of synchronized oscillations to motor behavior in Parkinson’s disease, and we discuss the intermittent character of this sy… Show more

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Cited by 77 publications
(38 citation statements)
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“…Lowering this parameter would thus correspond to stronger striatal inhibition (GPe neuron will exhibit less of its own dynamics and will be more easily controlled by excitatory inputs from STN). This increase of striatal inhibition is expected in a Parkinsonian state, because striatopallidal synapses are presynaptically suppressed by dopamine, which degenerates in Parkinson's disease (see discussion in Terman et al, 2002; Park et al, 2011; Rubchinsky et al, 2012). As I app increases, the dynamics of the STN-GPe network becomes less synchronized (Terman et al, 2002; Park et al, 2011).…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…Lowering this parameter would thus correspond to stronger striatal inhibition (GPe neuron will exhibit less of its own dynamics and will be more easily controlled by excitatory inputs from STN). This increase of striatal inhibition is expected in a Parkinsonian state, because striatopallidal synapses are presynaptically suppressed by dopamine, which degenerates in Parkinson's disease (see discussion in Terman et al, 2002; Park et al, 2011; Rubchinsky et al, 2012). As I app increases, the dynamics of the STN-GPe network becomes less synchronized (Terman et al, 2002; Park et al, 2011).…”
Section: Resultsmentioning
confidence: 99%
“…As g syn increases (in the network without input), the dynamics of STN-GPe circuits transits from less to more synchronized network dynamics (Park et al, 2011). These synapses may be suppressed by dopamine (see discussion in Terman et al, 2002; Park et al, 2011; Rubchinsky et al, 2012), so that moving from a healthy to a Parkinsonian state would correspond to increasing g syn .…”
Section: Resultsmentioning
confidence: 99%
“…Moreover, the model reproduces experimentally observed patterns of beta activity [14]. The matching of the experimental and model synchrony patterns ensures similarity of the actual and the model phase spaces ( [18,32,33]). So, the considered model may be dynamically adequate for the study of some mechanisms of beta suppression.…”
Section: B Limitations Of Modeling and Robustness Of The Stimulationmentioning
confidence: 56%
“…In the cortex this is synchrony between different EEG electrodes; in the BG this is synchrony between STN spikes and STN LFP (which may reflect input-output synchrony for STN, which gets substantial synaptic input from the external segment of globus pallidus; see discussion in Park et al, 2010). The levels of synchrony in both brain regions fluctuate in time (e.g., EEG synchrony fluctuations (Ahn & Rubchinsky, 2013) and spike-LFP synchrony fluctuations (Park et al, 2010;Rubchinsky et al, 2012)). Using methods discussed above, the strength of the synchrony may be estimated over relatively short time intervals, allowing determination of the time course of synchrony.…”
Section: Correlation Between Dynamics Of Different Brain Regionsmentioning
confidence: 99%