Oscillations In Basal Ganglia Research Articles

Ictal and peri-ictal oscillations in the human basal ganglia in temporal lobe epilepsy

Preictal, ictal, and postictal oscillations in the basal ganglia were analyzed. Five persons with temporal lobe epilepsy who were candidates for surgery had diagonal depth electrodes implanted in the basal ganglia: four of them in the putamen, and one in the pallidum and caudate. Time–frequency and power spectral analyses were used to analyze the EEG. Significant frequency components of 2–10Hz were consistently observed in the basal ganglia. The frequency of this component slowed during seizures. There was a significant ictal increase in power spectral density in all frequency ranges. The changes in the basal ganglia were consistent while seizure activity spread over the cortex, and partially persisted after the clinical seizure ended. They were inconsistent in the period after seizure onset. Seizures originating in the mesiotemporal structures can affect physiological rhythms in the basal ganglia. The basal ganglia did not generate epileptiform EEG activity. An inhibitory role for the basal ganglia during temporal lobe seizures is suggested.

Irregular vs. Synchronized activity in Basal Ganglia Circuits

Event Abstract Back to Event Irregular vs. Synchronized activity in Basal Ganglia Circuits The basal ganglia (BG) are a group of interconnected subcortical nuclei which are, among other things, involved in neural control of movement. They become impaired in Parkinson’s disease (PD), characterized by akinetic behavior. Recent studies indicate that patterns of oscillatory synchronous activity in BG are strongly relevant to BG physiology and BG disorders. In particular, neuronal activity in the beta-band significantly contributes to akinetic symptoms. The dynamics of these oscillations, their mechanisms and potential functional significance are the subjects of this study. Experimental data: we record neuronal activity during microelectrode-guided target localization in the PD patients undergoing surgery for implantation of DBS electrodes. Extracellular spiking activity and LFPs are recorded simultaneously. Modeling: we also use conductance-based models of subthalamic and pallidal cells to model rhythmic activity in subthalamo-pallidal circuits of BG. Model LFPs are constructed from model neuron’s activity. Data analysis: after appropriate filtering, Hilbert phase is constructed for both signals. Short running window analysis (with surrogates to determine statistical significance) is used to characterize temporal patterns of synchrony in experiment and model. First return maps for the phases are also used to characterize synchronization and compare model with experiment. The results of the analysis indicate that the dynamics of beta-band oscillations in BG is marked by intermittency of synchronized episodes. Oscillations tend to be desynchronized for relatively short time, although the desynchronizing events are quite frequent. The model has large areas in the parameter space, where it generates either irregular and uncorrelated firing patterns or rhythmic correlated activities. There is also an area of intermittent synchrony and, importantly, the first return maps for the phases from model and experiment are very similar in that area. Thus the model’s phase space is organized similarly to those of experimental system during rest in PD. The domain of the existence of intermittent dynamics is in between incoherent regime and synchronized regime, in the area which is characterized by the presence of different types of dynamics. Simulation of noisy version of our model confirmed the robustness of the observed dynamics (and thus its relevance to experiment). These observations suggest that in a pathological state, BG networks operate in a regime, which is quite close (in a parameter space) to an irregular activity. Although we do not have microelectrode recordings form normal humans, vast body of other experiments with animal models and humans suggest that healthy state is characterized by the absence of beta-band oscillations at rest. BG still needs them for movement preparation. The organization of the parameter space of the model and similarity of the model and experimental phase space indicate that in a disease (Parkinsonism), BG circuits are relatively close to the presumably healthy uncorrelated state and suggest that this healthy state is very close to the birth of oscillations. This closeness of the irregular healthy state to the pathological regular synchronized state may be justified by the efficiency of producing synchronized oscillations for movement generation. Dopaminergic degeneration in PD shifts the system into a pathological synchronized activity. Conference: Computational and systems neuroscience 2009, Salt Lake City, UT, United States, 26 Feb - 3 Mar, 2009. Presentation Type: Poster Presentation Topic: Poster Presentations Citation: (2009). Irregular vs. Synchronized activity in Basal Ganglia Circuits. Front. Syst. Neurosci. Conference Abstract: Computational and systems neuroscience 2009. doi: 10.3389/conf.neuro.06.2009.03.228 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 03 Feb 2009; Published Online: 03 Feb 2009. 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A pathophysiological model of freezing of gait in Parkinson's disease

Freezing of gait (FOG) is a common phenomenon in Parkinson's disease (PD) affecting over half of those in the advanced stages of the disease and often does not respond to standard drug therapies. This article proposes a possible mechanism by which this disorder of movement comes about. Co-ordinated neural activities are dependent on a series of parallel neuronal networks passing through the basal ganglia connecting and integrating functions. In healthy subjects, these competing, yet complementary, networks permit tight regulation in the broad domains of motor, cognitive, and limbic functions. In patients with PD, the loss of striatal dopamine coupled with the limited repertoire of the output nuclei within these pathways allows for an element of ‘cross-talk’ between competing inputs, which in turn could lead to a paroxysmal excessive inhibition of the thalamus and pedunculopontine nucleus triggering freezing of gait. It is further postulated that this phenomenon may be acting via a transient period of increased synchronization within the basal ganglia oscillations.