The STN beta-band profile in Parkinson's disease is stationary and shows prolonged attenuation after deep brain stimulation

Brontë‐Stewart, Helen; Barberini, Crista L.; Koop, Mandy Miller; Hill, Bruce C.; Henderson, Jaimie M.; Wingeier, Brett

doi:10.1016/j.expneurol.2008.09.008

Cited by 265 publications

(241 citation statements)

References 46 publications

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“…The power in this band decreased with dopamine treatment, as shown by several authors in the analysis of STN-LFP oscillations (Giannicola et al, 2010). The same effect has been obtained with STN DBS (Kuhn et al, 2008;Bronte-Stewart et al, 2009;Giannicola et al, 2010) although the intensity of the effect has not been the same in all reports. The abnormally enhanced beta band oscillations are encountered in certain sites of the STN and some authors have found a correlation between localization of the electrode in sites of the STN where there was a predominating beta band and the efficacy of STN DBS in alleviating the patient's symptoms (Ince et al, www.intechopen.com 2010; Zaidel et al, 2010).…”

Section: Wwwintechopencomsupporting

confidence: 58%

Human Central Nervous System Circuits Examined in Patients with Parkinson's Disease Using the Electrodes Implanted for Deep Brain Stimulation

Costa¹,

Valldeoriola²,

Valls‐Solé³

2011

Diagnostics and Rehabilitation of Parkinson's Disease

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Section: Wwwintechopencomsupporting

confidence: 58%

Human Central Nervous System Circuits Examined in Patients with Parkinson's Disease Using the Electrodes Implanted for Deep Brain Stimulation

Costa¹,

Valldeoriola²,

Valls‐Solé³

2011

Diagnostics and Rehabilitation of Parkinson's Disease

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“…(ii) Currently, studies are performed to understand fundamental, attenuating effects of high-frequency deep brain stimulation on beta band LFP oscillations [59,60]. Nevertheless, the effects of DBS on oscillations of higher frequencies may be significant as well.…”

Section: Discussionmentioning

confidence: 99%

Suppression of spontaneous oscillations in high-frequency stimulated neuron models

Pyragas¹,

Tass²

2017

Lith. J. Phys.

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We analyze the influence of high-frequency current stimulation on spontaneous neuronal activity and show that it may cause a death of spontaneous low-frequency oscillations. We demonstrate the universality of this effect for typical neuron models such as FitzHugh-Nagumo, Morris-Lecar, and Hodgkin-Huxley neurons as well as for the normal form of the supercritical Hopf bifurcation. Using a multiple scale method we separate the solutions of the neuron equations into slow and fast components and derive averaged equations for the slow components. The mechanism of suppression of neuronal activity is explained by an analysis of the bifurcations in the averaged equations governing the dynamics of the slow motion. Our results may contribute to the understanding of therapeutic effects of high-frequency deep brain stimulation, the golden standard for the treatment of medically refractory patients suffering from Parkinson's disease. Furthermore, our study enables hypotheses concerning possible improvements of high-frequency deep brain stimulation.

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“…For instance, STN DBS in patients with PD suppresses beta-band oscillations in the basal ganglia and reduces the aforementioned pathological coupling between beta-band phase and gamma-band amplitudes in MC [307][308][309][310]. GPi DBS also reduces beta-band oscillations in GPi and MC [297,311].…”

Section: Dbs Mechanism Of Actionmentioning

confidence: 99%

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

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Deep brain stimulation (DBS) is highly effective for both hypo-and hyperkinetic movement disorders of basal ganglia origin. The clinical use of DBS is, in part, empiric, based on the experience with prior surgical ablative therapies for these disorders, and, in part, driven by scientific discoveries made decades ago. In this review, we consider anatomical and functional concepts of the basal ganglia relevant to our understanding of DBS mechanisms, as well as our current understanding of the pathophysiology of two of the most commonly DBS-treated conditions, Parkinson's disease and dystonia. Finally, we discuss the proposed mechanism(s) of action of DBS in restoring function in patients with movement disorders. The signs and symptoms of the various disorders appear to result from signature disordered activity in the basal ganglia output, which disrupts the activity in thalamocortical and brainstem networks. The available evidence suggests that the effects of DBS are strongly dependent on targeting sensorimotor portions of specific nodes of the basal gangliathalamocortical motor circuit, that is, the subthalamic nucleus and the internal segment of the globus pallidus. There is little evidence to suggest that DBS in patients with movement disorders restores normal basal ganglia functions (e.g., their role in movement or reinforcement learning). Instead, it appears that high-frequency DBS replaces the abnormal basal ganglia output with a more tolerable pattern, which helps to restore the functionality of downstream networks.

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The STN beta-band profile in Parkinson's disease is stationary and shows prolonged attenuation after deep brain stimulation

Cited by 265 publications

References 46 publications

Human Central Nervous System Circuits Examined in Patients with Parkinson's Disease Using the Electrodes Implanted for Deep Brain Stimulation

Human Central Nervous System Circuits Examined in Patients with Parkinson's Disease Using the Electrodes Implanted for Deep Brain Stimulation

Suppression of spontaneous oscillations in high-frequency stimulated neuron models

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

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