Publications by authors named "Robert S Raike"

Adaptive deep brain stimulation (aDBS) is an emerging advancement in DBS technology; however, local field potential (LFP) signal rate detection sufficient for aDBS algorithms and the methods to set-up aDBS have yet to be defined. Here we summarize sensing data and aDBS programming steps associated with the ongoing Adaptive DBS Algorithm for Personalized Therapy in Parkinson's Disease (ADAPT-PD) pivotal trial (NCT04547712). Sixty-eight patients were enrolled with either subthalamic nucleus or globus pallidus internus DBS leads connected to a Medtronic Percept PC neurostimulator.

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Oscillatory activity within the beta frequency range (13-30 Hz) serves as a Parkinson's disease biomarker for tailoring deep brain stimulation (DBS) treatments. Currently, identifying clinically relevant beta signals, specifically frequencies of peak amplitudes within the beta spectral band, is a subjective process. To inform potential strategies for objective clinical decision making, we assessed algorithms for identifying beta peaks and devised a standardized approach for both research and clinical applications.

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The Deep Brain Stimulation (DBS) Think Tank XI was held on August 9-11, 2023 in Gainesville, Florida with the theme of "Pushing the Forefront of Neuromodulation". The keynote speaker was Dr. Nico Dosenbach from Washington University in St.

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Objective: Despite advances in the treatment of psychiatric diseases, currently available therapies do not provide sufficient and durable relief for as many as 30-40% of patients. Neuromodulation, including deep brain stimulation (DBS), has emerged as a potential therapy for persistent disabling disease, however it has not yet gained widespread adoption. In 2016, the American Society for Stereotactic and Functional Neurosurgery (ASSFN) convened a meeting with leaders in the field to discuss a roadmap for the path forward.

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Background: Deep brain stimulation (DBS) of the globus pallidus interna (GPi) is an effective therapy for select patients with primary dystonia. DBS programming for dystonia is often challenging due to variable time to symptomatic improvement or stimulation induced side effects (SISE) such as capsular or optic tract activation which can prolong device optimization.

Objective: To characterize the safety and tolerability of active recharge biphasic DBS (bDBS) in primary dystonia and to compare it to conventional clinical DBS (clinDBS).

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In prior reports, we described the design and initial performance of a fully implantable, bi-directional neural interface system for use in deep brain and other neurostimulation applications. Here we provide an update on the chronic, long-term neural sensing performance of the system using traditional 4-contact leads and extend those results to include directional 8-contact leads. Seven ovine subjects were implanted with deep brain stimulation (DBS) leads at different nodes within the Circuit of Papez: four with unilateral leads in the anterior nucleus of the thalamus and hippocampus; two with bilateral fornix leads, and one with bilateral hippocampal leads.

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Article Synopsis
  • DBS Think Tank IX took place from August 25-27, 2021, in Orlando, FL, featuring both in-person U.S. attendees and international participants joining via video conferencing.
  • Founded in 2012, the Think Tank serves as a collaborative space for clinicians, engineers, and researchers to discuss advancements in deep brain stimulation (DBS) technologies and address related logistical and ethical challenges.
  • This year's meeting highlighted the growing application of DBS across various brain disorders, estimating over 230,000 devices implanted globally, with special focus areas including neuromodulation strategies, innovative technologies, neuroethics, and specific applications for pain, epilepsy, and traumatic brain injuries.
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: Freezing of gait (FOG) is a common symptom in Parkinson's disease (PD) and can be difficult to treat with dopaminergic medications or with deep brain stimulation (DBS). Novel stimulation paradigms have been proposed to address suboptimal responses to conventional DBS programming methods. Burst-cycling deep brain stimulation (BCDBS) delivers current in various frequencies of bursts (e.

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Background: Conventional Parkinson's disease (PD) deep brain stimulation (DBS) utilizes a pulse with an active phase and a passive charge-balancing phase. A pulse-shaping strategy that eliminates the passive phase may be a promising approach to addressing movement disorders.

Objectives: The current study assessed the safety and tolerability of square biphasic pulse shaping (sqBIP) DBS for use in PD.

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Background: Conventional deep brain stimulation (DBS) utilizes regular, high frequency pulses to treat medication-refractory symptoms in essential tremor (ET). Modifications of DBS pulse shape to achieve improved effectiveness is a promising approach.

Objectives: The current study assessed the safety, tolerability and effectiveness of square biphasic pulse shaping as an alternative to conventional ET DBS.

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Background: Dystonia often has inconsistent benefits and requires more energy-demanding DBS settings. Studies suggest that squared biphasic pulses could provide significant clinical benefit; however, dystonia patients have not been explored.

Objectives: To assess safety and tolerability of square biphasic DBS in dystonia patients.

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A role for the cerebellum in causing ataxia, a disorder characterized by uncoordinated movement, is widely accepted. Recent work has suggested that alterations in activity, connectivity, and structure of the cerebellum are also associated with dystonia, a neurological disorder characterized by abnormal and sustained muscle contractions often leading to abnormal maintained postures. In this manuscript, the authors discuss their views on how the cerebellum may play a role in dystonia.

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Objectives: Evidence suggests that nonconventional programming may improve deep brain stimulation (DBS) therapy for movement disorders. The primary objective was to assess feasibility of testing the tolerability of several nonconventional settings in Parkinson's disease (PD) and essential tremor (ET) subjects in a single office visit. Secondary objectives were to explore for potential efficacy signals and to assess the energy demand on the implantable pulse-generators (IPGs).

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Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is used to treat movement disorders, including advanced Parkinson's disease (PD). The pathogenesis of PD and the therapeutic mechanisms of DBS are not well understood. Large animal models are essential for investigating the mechanisms of PD and DBS.

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Article Synopsis
  • Abnormal dopamine transmission is linked to various dystonic disorders, caused by genetic mutations like those in GCH1 and TH, which can lead to conditions responsive to l-DOPA treatment.
  • A knock-in mouse model mimicking a human TH mutation showed symptoms similar to human dystonia, including reduced TH enzyme activity and responsiveness to treatment.
  • The study revealed structural changes in striatal synapses and significant reductions in striatal dopamine concentrations, suggesting that both pre- and postsynaptic factors contribute to dystonia; additionally, manipulating dopamine receptor activity affected movement severity.
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Cerebellar degeneration is traditionally associated with ataxia. Yet, there are examples of both ataxia and dystonia occurring in individuals with cerebellar degeneration. There is also substantial evidence suggesting that cerebellar dysfunction alone may cause dystonia.

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Article Synopsis
  • - Episodic ataxia type 2 (EA2) is a genetic disorder that leads to episodes of incoordination triggered by factors like stress, alcohol, and caffeine, caused by mutations in the CACNA1A gene.
  • - Researchers developed a mouse model with a specific EA2 mutation to investigate the disorder, finding that mice with the mutation had reduced calcium channel function but did not show major motor issues.
  • - Further tests on the mice indicated that while some motor dysfunction was present, it required the involvement of multiple types of brain cells for noticeable effects rather than being linked to dysfunction in just one type.
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Several episodic neurological disorders are caused by ion channel gene mutations. In patients, transient neurological dysfunction is often evoked by stress, caffeine and ethanol, but the mechanisms underlying these triggers are unclear because each has diverse and diffuse effects on the CNS. Attacks of motor dysfunction in the Ca(V)2.

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Dystonia is a complex neurological syndrome broadly characterized by involuntary twisting movements and abnormal postures. The anatomical distribution of the motor symptoms varies among dystonic patients and can range from focal, involving an isolated part of the body, to generalized, involving many body parts. Functional imaging studies of both focal and generalized dystonias in humans often implicate the cerebellum suggesting that similar pathological processes may underlie both.

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The Cacna1a gene encodes the α(1A) subunit of voltage-gated Ca(V)2.1 Ca(2+) channels that are involved in neurotransmission at central synapses. Ca(V)2.

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Episodic ataxia type 2 (EA2) is an autosomal dominant disorder arising from CACNA1A mutations, which commonly predict heterozygous expression of Ca(v)2.1 calcium channels with truncated alpha(1)2.1 pore subunits.

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Dystonia is a prevalent neurological disorder characterized by abnormal co-contractions of antagonistic muscle groups that produce twisting movements and abnormal postures. The disorder may be inherited, arise sporadically, or result from brain insult. Dystonia is a heterogeneous disorder because patients may exhibit focal or generalized symptoms associated with abnormalities in many brain regions including basal ganglia and cerebellum.

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Humans with the disorder episodic ataxia type 2 (EA2) and the tottering mouse mutant exhibit episodic attacks induced by emotional and chemical stress. Both the human and mouse disorders result from mutations in CACNA1A, the gene encoding the alpha(1)2.1 subunit of Ca(v)2.

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Episodic ataxia type 2 (EA2) is a dominantly inherited disorder, characterized by spells of ataxia, dysarthria, vertigo, and migraines, associated with mutations in the neuronal calcium-channel gene CACNA1A. Ataxic spells lasting minutes to hours are provoked by stress, exercise, or alcohol. Some patients exhibit nystagmus between spells and some develop progressive ataxia later in life.

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