scholarly journals Oscillatory activity in basal ganglia and motor cortex in an awake behaving rodent model of Parkinson's disease

Basal Ganglia ◽  
2014 ◽  
Vol 3 (4) ◽  
pp. 221-227 ◽  
Author(s):  
Claire Delaville ◽  
Ana V. Cruz ◽  
Alex J. McCoy ◽  
Elena Brazhnik ◽  
Irene Avila ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Motor Cortex ◽  
Rodent Model ◽  
Oscillatory Activity

scholarly journals A dynamical model for the basal ganglia-thalamo-cortical oscillatory activity and its implications in Parkinson’s disease

2020 ◽  
Author(s):  
Eva M. Navarro-López ◽  
Utku Çelikok ◽  
Neslihan S. Şengör
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Activity Patterns ◽  
Dynamical Model ◽  
Substantia Nigra Pars Compacta ◽  
Oscillatory Activity ◽  
Subcortical Structures ◽  
Neuron Models ◽  
Neuronal Patterns

AbstractWe propose to investigate brain electrophysiological alterations associated with Parkinson’s disease through a novel adaptive dynamical model of the network of the basal ganglia, the cortex and the thalamus. The model uniquely unifies the influence of dopamine in the regulation of the activity of all basal ganglia nuclei, the self-organised neuronal interdependent activity of basal ganglia-thalamo-cortical circuits and the generation of subcortical background oscillations. Variations in the amount of dopamine produced in the neurons of the substantia nigra pars compacta are key both in the onset of Parkinson’s disease and in the basal ganglia action selection. We model these dopamine-induced relationships, and Parkinsonian states are interpreted as spontaneous emergent behaviours associated with different rhythms of oscillatory activity patterns of the basal ganglia-thalamo-cortical network. These results are significant because: (1) the neural populations are built upon single-neuron models that have been robustly designed to have eletrophysiologically-realistic responses, and (2) our model distinctively links changes in the oscillatory activity in subcortical structures, dopamine levels in the basal ganglia and pathological synchronisation neuronal patterns compatible with Parkinsonian states, this still remains an open problem and is crucial to better understand the progression of the disease.

14 Pathological oscillatory activity in Parkinson’s disease; what does it mean and how should we treat it?

2020 ◽  
Vol 91 (8) ◽  
pp. e6.1-e6
Author(s):  
Peter Brown
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Side Effects ◽  
Brain Stimulation ◽  
Neural Circuit ◽  
Symptom Control ◽  
Oscillatory Activity ◽  
Deep Brain

Professor Peter Brown is Professor of Experimental Neurology and Director of the Medical Research Council Brain Network Dynamics Unit at the University of Oxford. Prior to 2010 he was a Professor of Neurology at University College London.For decades we have had cardiac pacemakers that adjust their pacing according to demand and yet therapeutic adaptive stimulation approaches for the central nervous system are still not clinically available. Instead, to treat patients with advanced Parkinson’s disease we stimulate the basal ganglia with fixed regimes, unvarying in frequency or intensity. Although effective, this comes with side-effects and in terms of sophistication this treatment approach could be compared to having central heating system on all the time, regardless of temperature. This talk will describe recent steps being taken to define the underlying circuit dysfunction in Parkinson’s and to improve deep brain stimulation by controlling its delivery according to the state of pathological activity.Evidence is growing that motor symptoms in Parkinson’s disease are due, at least in part, to excessive synchronisation between oscillating neurons. Recordings confirm bursts of oscillatory synchronisation in the basal ganglia centred around 20 Hz. The bursts of 20 Hz activity are prolonged in patients withdrawn from their usual medication and the dominance of these long duration bursts negatively correlates with motor impairment. Longer bursts attain higher amplitudes, indicative of more pervasive oscillatory synchronisation within the neural circuit. In contrast, in heathy primates and in treated Parkinson’s disease bursts tend to be short. Accordingly, it might be best to use closed-loop controlled deep brain stimulation to selectively terminate longer, bigger, pathological beta bursts to both save power and to spare the ability of underlying neural circuits to engage in more physiological processing between long bursts. It is now possible to record and characterise bursts on-line during stimulation of the same site and trial adaptive stimulation. Thus far, this has demonstrated improvements in efficiency and side-effects over conventional continuous stimulation, with at least as good symptom control in Parkinsonian patients.

scholarly journals Pallidal Thermolesion Unleashes Gamma Oscillations in the Motor Cortex in Parkinson's Disease

Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Doris D Wang ◽  
Coralie de Hemptinne ◽  
Svjetlana Miocinovic ◽  
Witney Chen ◽  
Jill L Ostrem ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Cortex ◽  
Essential Tremor ◽  
Primary Motor Cortex ◽  
Gamma Oscillations ◽  
Gamma Band ◽  
Motor Dysfunction ◽  
Oscillatory Activity ◽  
Motor Network

Abstract INTRODUCTION In Parkinson's disease, the emergence of motor dysfunction is thought to be related to an imbalance between antikinetic and prokinetic patterns of oscillatory activity in the motor network. Invasive recordings from the basal ganglia and cortex in surgical patients have suggested that levodopa and therapeutic deep brain stimulation can suppress antikinetic beta band (13-30 Hz) rhythms while promoting prokinetic gamma band (60-90 Hz) rhythms. Surgical ablation of the globus pallidus internus is one of the oldest effective therapies for Parkinson's disease and gives a remarkable immediate relief from rigidity and bradykinesia, but its effects on oscillatory activity in the motor network have not been studied. We characterize the effects of pallidotomy on cortical oscillatory activity in Parkinson's disease patients. METHODS Using a temporary 6-contact lead placed over the sensorimotor cortex in the subdural space, we recorded acute changes in cortical oscillatory activities in 3 Parkinson's disease patients undergoing pallidotomy and compared the results to that of 3 essential tremor patients undergoing thalamotomy. RESULTS In all 3 Parkinson's disease patients, we observed the emergence of an approximately 70 to 80 Hz narrow-band oscillation with effective thermolesion of the pallidum. This gamma oscillatory activity was spatially localized over the primary motor cortex, was minimally affected by voluntary movements, and was not found in the motor cortex of essential tremor patients undergoing thalamotomy. CONCLUSION Our finding suggests that acute lesioning of the pallidum promotes cortical gamma band oscillations. This may represent an important mechanism for alleviating bradykinesia in Parkinson's disease.

Slow Brain Potential and Oscillatory EEG Manifestations of Impaired Temporal Preparation in Parkinson's Disease

2007 ◽  
Vol 98 (5) ◽  
pp. 2848-2857 ◽  
Author(s):  
Peter Praamstra ◽  
Paul Pope
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Temporal Structure ◽  
Oscillatory Activity ◽  
Brain Potentials ◽  
Brain Potential ◽  
Temporal Preparation ◽  
Implicit Timing ◽  
Slow Brain Potentials

Performance in behavioral tasks is influenced by temporal expectations shaped by the temporal structure of the task. Such implicit temporal preparation is reflected in slow brain potentials and electroencephalographic oscillations and is attributed to interval timing mechanisms that probably depend on intact basal ganglia function. We investigated implicit timing in Parkinson's disease using a choice reaction task with two temporally regular stimulus presentation regimes, both including occasional deviant interstimulus intervals. Control subjects, but not patients, demonstrated temporal preparation in the form of an adjustment in time course of slow brain potentials to the duration of the interstimulus interval. However, in both groups, timing perturbations were accompanied by a slow brain potential amplitude drop at the time of expected stimulus occurrence, demonstrating intact representation of time in patients. In patients, oscillatory activity in beta and alpha bands showed attenuated preparatory desynchronization and reduced postmovement event-related synchronization, reflecting abnormal engagement and disengagement of sensorimotor and parietal areas. The results demonstrate profoundly deficient temporal preparation with preserved encoding of temporal information, a dissociation that may be explained by impaired dopamine-dependent motor learning. The results are discussed in the context of recent work on oscillatory activity in the basal ganglia.

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