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

2016 ◽  
Vol 13 (2) ◽  
pp. 264-283 ◽  
Author(s):  
Thomas Wichmann ◽  
Mahlon R. DeLong
Keyword(s):  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Deep Brain

Basal ganglia local field potentials: applications in the development of new deep brain stimulation devices for movement disorders

2007 ◽  
Vol 4 (5) ◽  
pp. 605-614 ◽  
Author(s):  
Sara Marceglia ◽  
Lorenzo Rossi ◽  
Guglielmo Foffani ◽  
AnnaMaria Bianchi ◽  
Sergio Cerutti ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Local Field ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Local Field Potentials ◽  
Field Potentials ◽  
Deep Brain

scholarly journals Common therapeutic mechanisms of pallidal deep brain stimulation for hypo- and hyperkinetic movement disorders

2015 ◽  
Vol 114 (4) ◽  
pp. 2090-2104 ◽  
Author(s):  
Kevin W. McCairn ◽  
Atsushi Iriki ◽  
Masaki Isoda
Keyword(s):  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Information Transfer ◽  
Motor Behavior ◽  
Global Network ◽  
Symptom Profiles ◽  
Stimulus Effect ◽  
Deep Brain

Abnormalities in cortico-basal ganglia (CBG) networks can cause a variety of movement disorders ranging from hypokinetic disorders, such as Parkinson's disease (PD), to hyperkinetic conditions, such as Tourette syndrome (TS). Each condition is characterized by distinct patterns of abnormal neural discharge (dysrhythmia) at both the local single-neuron level and the global network level. Despite divergent etiologies, behavioral phenotypes, and neurophysiological profiles, high-frequency deep brain stimulation (HF-DBS) in the basal ganglia has been shown to be effective for both hypo- and hyperkinetic disorders. The aim of this review is to compare and contrast the electrophysiological hallmarks of PD and TS phenotypes in nonhuman primates and discuss why the same treatment (HF-DBS targeted to the globus pallidus internus, GPi-DBS) is capable of ameliorating both symptom profiles. Recent studies have shown that therapeutic GPi-DBS entrains the spiking of neurons located in the vicinity of the stimulating electrode, resulting in strong stimulus-locked modulations in firing probability with minimal changes in the population-scale firing rate. This stimulus effect normalizes/suppresses the pathological firing patterns and dysrhythmia that underlie specific phenotypes in both the PD and TS models. We propose that the elimination of pathological states via stimulus-driven entrainment and suppression, while maintaining thalamocortical network excitability within a normal physiological range, provides a common therapeutic mechanism through which HF-DBS permits information transfer for purposive motor behavior through the CBG while ameliorating conditions with widely different symptom profiles.

scholarly journals Toward adaptive deep brain stimulation for dystonia

2018 ◽  
Vol 45 (2) ◽  
pp. E3 ◽  
Author(s):  
Dan Piña-Fuentes ◽  
Martijn Beudel ◽  
Simon Little ◽  
Jonathan van Zijl ◽  
Jan Willem Elting ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Neural Oscillations ◽  
Feedback Signal ◽  
New Form ◽  
Different Characteristics ◽  
Potential Biomarkers ◽  
Deep Brain

The presence of abnormal neural oscillations within the cortico-basal ganglia-thalamo-cortical (CBGTC) network has emerged as one of the current principal theories to explain the pathophysiology of movement disorders. In theory, these oscillations can be used as biomarkers and thereby serve as a feedback signal to control the delivery of deep brain stimulation (DBS). This new form of DBS, dependent on different characteristics of pathological oscillations, is called adaptive DBS (aDBS), and it has already been applied in patients with Parkinson’s disease. In this review, the authors summarize the scientific research to date on pathological oscillations in dystonia and address potential biomarkers that might be used as a feedback signal for controlling aDBS in patients with dystonia.

scholarly journals New insights into cortico-basal-cerebellar connectome: clinical and physiological considerations

Brain ◽  
2019 ◽  
Author(s):  
Angelo Quartarone ◽  
Alberto Cacciola ◽  
Demetrio Milardi ◽  
Maria Felice Ghilardi ◽  
Alessandro Calamuneri ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Human Brain ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Current Model ◽  
Tract Tracing ◽  
Deep Brain

Abstract The current model of the basal ganglia system based on the ‘direct’, ‘indirect’ and ‘hyperdirect’ pathways provides striking predictions about basal ganglia function that have been used to develop deep brain stimulation approaches for Parkinson’s disease and dystonia. The aim of this review is to challenge this scheme in light of new tract tracing information that has recently become available from the human brain using MRI-based tractography, thus providing a novel perspective on the basal ganglia system. We also explore the implications of additional direct pathways running from cortex to basal ganglia and between basal ganglia and cerebellum in the pathophysiology of movement disorders.

scholarly journals Patterned low-frequency deep brain stimulation induces motor deficits and modulates cortex-basal ganglia neural activity in healthy rats

2018 ◽  
Vol 120 (5) ◽  
pp. 2410-2422 ◽  
Author(s):  
Chintan S. Oza ◽  
David T. Brocker ◽  
Christina E. Behrend ◽  
Warren M. Grill
Keyword(s):  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Neural Activity ◽  
Low Frequency ◽  
Oscillatory Activity ◽  
Motor Deficits ◽  
Motor Symptoms ◽  
Deep Brain

Deep brain stimulation (DBS) is an effective therapy for movement disorders, including Parkinson’s disease (PD), although the mechanisms of action remain unclear. Abnormal oscillatory neural activity is correlated with motor symptoms, and pharmacological or DBS treatment that alleviates motor symptoms appears to suppress abnormal oscillations. However, whether such oscillatory activity is causal of motor deficits such as tremor remains unclear. Our goal was to generate abnormal oscillatory activity in the cortex-basal ganglia loop using patterned subthalamic nucleus DBS and to quantify motor behavior in awake healthy rats. Stimulation patterns were designed via model-based optimization to increase power in the low-frequency (7–11 Hz) band because these oscillations are associated with the emergence of motor symptoms in the 6-hydroxydopamine lesioned rat model of parkinsonism. We measured motor activity using a head-mounted accelerometer, as well as quantified neural activity in cortex and globus pallidus (GP), in response to 5 stimulation patterns that generated a range of 7- to 11-Hz spectral power. Stimulation patterns induced oscillatory activity in the low-frequency band in the cortex and GP and caused tremor, whereas control patterns and regular 50-Hz DBS did not generate any such effects. Neural and motor-evoked responses observed during stimulation were synchronous and time-locked to stimulation bursts within the patterns. These results identified elements of irregular patterns of stimulation that were correlated with tremor and tremor-related neural activity in the cortex and basal ganglia and may lead to the identification of the oscillatory activity and structures associated with the generation of tremor activity. NEW & NOTEWORTHY Subthalamic nucleus deep brain stimulation is a promising therapy for movement disorders such as Parkinson’s disease. Several groups reported correlation between suppression of abnormal oscillatory activity in the cortex-basal ganglia and motor symptoms, but it remains unclear whether such oscillations play a causal role in the emergence of motor symptoms. We demonstrate generation of tremor and pathological oscillatory activity in otherwise healthy rats by stimulation with patterns that produced increases in low-frequency oscillatory activity.

scholarly journals Deep brain stimulation in the treatment of dyskinesia and dystonia

2004 ◽  
Vol 17 (1) ◽  
pp. 9-13 ◽  
Author(s):  
Hiroki Toda ◽  
Clement Hamani ◽  
Andres Lozano
Keyword(s):  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Globus Pallidus ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Improved Outcomes ◽  
Generalized Dystonia ◽  
Clinical Conditions ◽  
Better Than ◽  
Deep Brain

Deep brain stimulation (DBS) has become a mainstay of treatment for patients with movement disorders. This modality is directed at modulating pathological activity within basal ganglia output structures by stimulating some of their nuclei, such as the subthalamic nucleus (STN) and the globus pallidus internus (GPi), without making permanent lesions. With the accumulation of experience, indications for the use of DBS have become clearer and the effectiveness and limitations of this form of therapy in different clinical conditions have been better appreciated. In this review the authors discuss the efficacy of DBS in the treatment of dystonia and levodopa-induced dyskinesias. The use of DBS of the STN and GPi is very effective for the treatment of movement disorders induced by levodopa. The relative benefits of using the GPi as opposed to the STN as a target are still being investigated. Bilateral GPi stimulation is gaining importance in the therapeutic armamentarium for the treatment of dystonia. The DYT1 forms of generalized dystonia and cervical dystonias respond to DBS better than secondary dystonia does. Discrimination between the diverse forms of dystonia and a better understanding of the pathophysiological features of this condition will serve as a platform for improved outcomes.

The Effect of Deep Brain Stimulation for Movement Disorders on Emotions

2008 ◽  
Author(s):  
Jonathan D. Richards ◽  
Paul M. Wilson ◽  
Pennie S. Seibert ◽  
Carin M. Patterson ◽  
Caitlin C. Otto ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Deep Brain

Reoperation for device infection and erosion following deep brain stimulation implantable pulse generator placement

2020 ◽  
Vol 133 (2) ◽  
pp. 403-410 ◽  
Author(s):  
Travis J. Atchley ◽  
Nicholas M. B. Laskay ◽  
Brandon A. Sherrod ◽  
A. K. M. Fazlur Rahman ◽  
Harrison C. Walker ◽  
...  
Keyword(s):  
Risk Factors ◽  
Logistic Regression ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Pulse Generator ◽  
Rank Test ◽  
Implantable Pulse Generator ◽  
Device Infection ◽  
Deep Brain

OBJECTIVEInfection and erosion following implantable pulse generator (IPG) placement are associated with morbidity and cost for patients with deep brain stimulation (DBS) systems. Here, the authors provide a detailed characterization of infection and erosion events in a large cohort that underwent DBS surgery for movement disorders.METHODSThe authors retrospectively reviewed consecutive IPG placements and replacements in patients who had undergone DBS surgery for movement disorders at the University of Alabama at Birmingham between 2013 and 2016. IPG procedures occurring before 2013 in these patients were also captured. Descriptive statistics, survival analyses, and logistic regression were performed using generalized linear mixed effects models to examine risk factors for the primary outcomes of interest: infection within 1 year or erosion within 2 years of IPG placement.RESULTSIn the study period, 384 patients underwent a total of 995 IPG procedures (46.4% were initial placements) and had a median follow-up of 2.9 years. Reoperation for infection occurred after 27 procedures (2.7%) in 21 patients (5.5%). No difference in the infection rate was observed for initial placement versus replacement (p = 0.838). Reoperation for erosion occurred after 16 procedures (1.6%) in 15 patients (3.9%). Median time to reoperation for infection and erosion was 51 days (IQR 24–129 days) and 149 days (IQR 112–285 days), respectively. Four patients with infection (19.0%) developed a second infection requiring a same-side reoperation, two of whom developed a third infection. Intraoperative vancomycin powder was used in 158 cases (15.9%) and did not decrease the infection risk (infected: 3.2% with vancomycin vs 2.6% without, p = 0.922, log-rank test). On logistic regression, a previous infection increased the risk for infection (OR 35.0, 95% CI 7.9–156.2, p < 0.0001) and a lower patient BMI was a risk factor for erosion (BMI ≤ 24 kg/m2: OR 3.1, 95% CI 1.1–8.6, p = 0.03).CONCLUSIONSIPG-related infection and erosion following DBS surgery are uncommon but clinically significant events. Their respective timelines and risk factors suggest different etiologies and thus different potential corrective procedures.

scholarly journals Deep brain stimulation of the subthalamic nucleus reestablishes neuronal information transmission in the 6-OHDA rat model of parkinsonism

2014 ◽  
Vol 111 (10) ◽  
pp. 1949-1959 ◽  
Author(s):  
Alan D. Dorval ◽  
Warren M. Grill
Keyword(s):  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Information Transmission ◽  
Brain Stimulation ◽  
Rat Model ◽  
Information Transfer ◽  
Firing Pattern ◽  
Signal Propagation ◽  
Neuronal Firing ◽  
Deep Brain

Pathophysiological activity of basal ganglia neurons accompanies the motor symptoms of Parkinson's disease. High-frequency (>90 Hz) deep brain stimulation (DBS) reduces parkinsonian symptoms, but the mechanisms remain unclear. We hypothesize that parkinsonism-associated electrophysiological changes constitute an increase in neuronal firing pattern disorder and a concomitant decrease in information transmission through the ventral basal ganglia, and that effective DBS alleviates symptoms by decreasing neuronal disorder while simultaneously increasing information transfer through the same regions. We tested these hypotheses in the freely behaving, 6-hydroxydopamine-lesioned rat model of hemiparkinsonism. Following the onset of parkinsonism, mean neuronal firing rates were unchanged, despite a significant increase in firing pattern disorder (i.e., neuronal entropy), in both the globus pallidus and substantia nigra pars reticulata. This increase in neuronal entropy was reversed by symptom-alleviating DBS. Whereas increases in signal entropy are most commonly indicative of similar increases in information transmission, directed information through both regions was substantially reduced (>70%) following the onset of parkinsonism. Again, this decrease in information transmission was partially reversed by DBS. Together, these results suggest that the parkinsonian basal ganglia are rife with entropic activity and incapable of functional information transmission. Furthermore, they indicate that symptom-alleviating DBS works by lowering the entropic noise floor, enabling more information-rich signal propagation. In this view, the symptoms of parkinsonism may be more a default mode, normally overridden by healthy basal ganglia information. When that information is abolished by parkinsonian pathophysiology, hypokinetic symptoms emerge.

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