Tic related local field potentials in the thalamus and the effect of deep brain stimulation in Tourette syndrome: Report of three cases

Bour, L.J.; Ackermans, Linda; Foncke, E.M.J.; Cath, Daniëlle C.; Linden, C. van der; Vandewalle, V.; Tijssen, Marina A. J.

doi:10.1016/j.clinph.2014.10.217

Cited by 39 publications

(28 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Low‐frequency oscillations of approximately 12 Hz were detected in the GPi and the STN in this study. These oscillations over similar frequency bands are found in the thalamus (Bour et al, ; Maling, Hashemiyoon, Foote, Okun, & Sanchez, ; Marceglia et al, ; Zauber, Ahn, Worth, & Rubchinsky, ) and GPi (Jimenez‐Shahed et al, ; Neumann et al, ). The spectral power and burst length of the oscillations are correlated with the severity of tics (Neumann et al, ).…”

Section: Discussionsupporting

confidence: 58%

“…Microelectrode recording in the thalamus of patients with TS further confirmed that the firing patterns were within the low‐frequency range (2.5–8 Hz). DBS at the thalamus tended to attenuate alpha oscillations in the contralateral thalamus and increase theta oscillations in the ipsilateral thalamus in a case study (Bour et al, ; Marceglia et al, ). Alternatively, in the globus pallidus interna (GPi), attenuated beta oscillation and elevated gamma and high‐frequency oscillations were seen along with frequent tics (Jimenez‐Shahed, Telkes, Viswanathan, & Ince, ).…”

Section: Introductionmentioning

confidence: 95%

See 1 more Smart Citation

Deep brain stimulation modulates pallidal and subthalamic neural oscillations in Tourette's syndrome

et al. 2019

View full text Add to dashboard Cite

IntroductionPrevious studies found subthalamic nucleus deep brain stimulation (STN‐DBS) has clinical effect on Parkinson's disease, dystonia, and obsessive compulsive disorder. It is noteworthy that only a few studies report the STN‐DBS for Tourette's syndrome (TS). Globus pallidus interna (GPi)‐DBS is the one of the most common targets for TS. So, this paper aims to investigate the neural oscillations in STN and GPi as well as the DBS effect between these two targets in same patients.MethodsThe local field potentials (LFPs) were simultaneously recorded from the bilateral GPi and STN in four patients with TS. The LFPs were decomposed into neural oscillations, and the frequency and time–frequency characteristics of the neural oscillations were analyzed across the conditions of resting, poststimulation, and movement.ResultsNo difference of resting LFP was found between the two targets. The poststimulation period spectral power revealed the high beta and gamma oscillations were recovered after GPi‐DBS but remained attenuated after STN‐DBS. The STN beta oscillation has fewer changes during tics than voluntary movement, and the gamma oscillation was elevated when the tics appeared.ConclusionThe high beta and gamma oscillations in GPi restored after GPi‐DBS, but not STN‐DBS. High beta and gamma oscillations may have physiological function in resisting tics in TS. The cortex compensation effect might be interfered by the STN‐DBS due to the influence on the hyper‐direct pathway but not GPi‐DBS.

show abstract

Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 95%

Deep brain stimulation modulates pallidal and subthalamic neural oscillations in Tourette's syndrome

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Unique to this study was the acquisition of chronic neural activity from awake behaving humans up to 6 months after surgery, which characterised the physiological underpinnings of human tic and facilitated a differentiation from voluntary movement. These chronic recordings of thalamic and motor cortical activity provide additional insights into TS pathology and improve on the limited existing microelectrode recordings and intraoperative LFP recordings 19 33…”

Section: Discussionmentioning

confidence: 99%

Differentiating tic electrophysiology from voluntary movement in the human thalamocortical circuit

Cagle

Okun

Opri

et al. 2020

J Neurol Neurosurg Psychiatry

View full text Add to dashboard Cite

ObjectivesTourette syndrome is a neurodevelopmental disorder commonly associated with involuntary movements, or tics. We currently lack an ideal animal model for Tourette syndrome. In humans, clinical manifestation of tics cannot be captured via functional imaging due to motion artefacts and limited temporal resolution, and electrophysiological studies have been limited to the intraoperative environment. The goal of this study was to identify electrophysiological signals in the centromedian (CM) thalamic nucleus and primary motor (M1) cortex that differentiate tics from voluntary movements.MethodsThe data were collected as part of a larger National Institutes of Health-sponsored clinical trial. Four participants (two males, two females) underwent monthly clinical visits for collection of physiology for a total of 6 months. Participants were implanted with bilateral CM thalamic macroelectrodes and M1 subdural electrodes that were connected to two neurostimulators, both with sensing capabilities. MRI scans were performed preoperatively and CT scans postoperatively for localisation of electrodes. Electrophysiological recordings were collected at each visit from both the cortical and subcortical implants.ResultsRecordings collected from the CM thalamic nucleus revealed a low-frequency power (3–10 Hz) increase that was time-locked to the onset of involuntary tics but was not present during voluntary movements. Cortical recordings revealed beta power decrease in M1 that was present during tics and voluntary movements.ConclusionWe conclude that a human physiological signal was detected from the CM thalamus that differentiated tic from voluntary movement, and this physiological feature could potentially guide the development of neuromodulation therapies for Tourette syndrome that could use a closed-loop-based approach.

show abstract

“…Electrophysiology studies of the CM-Pf target in patients undergoing DBS surgery for TS have found bursting activity in CM-Pf prior to tic production and reduction in the alpha activity and increase in the gamma activity correlated with tic reduction during DBS (49–52). This suggests that CM-Pf DBS may reduce tics by normalizing the local neuronal discharge and affecting striatal output.…”

Section: The Role Of the Cm-pf In Tourette’s Syndromementioning

confidence: 99%

Deep Brain Stimulation for Tourette’s Syndrome: The Case for Targeting the Thalamic Centromedian–Parafascicular Complex

et al. 2016

View full text Add to dashboard Cite

Tourette’s syndrome (TS) is a neurologic condition characterized by both motor and phonic tics and is typically associated with psychiatric comorbidities, including obsessive-compulsive disorder/behavior and attention-deficit hyperactivity disorder, and can be psychologically and socially debilitating. It is considered a disorder of the cortico–striato–thalamo–cortical circuitry, as suggested by pathophysiology studies and therapeutic options. Among these, deep brain stimulation (DBS) of the centromedian–parafascicular nucleus (CM-Pf) of the thalamus is emerging as a valuable treatment modality for patients affected by severe, treatment-resistant TS. Here, we review the most recent experimental evidence for the pivotal role of CM-Pf in the pathophysiology of TS, discuss potential mechanisms of action that may mediate the effects of CM-Pf DBS in TS, and summarize its clinical efficacy.

show abstract

Tic related local field potentials in the thalamus and the effect of deep brain stimulation in Tourette syndrome: Report of three cases

Cited by 39 publications

References 43 publications

Deep brain stimulation modulates pallidal and subthalamic neural oscillations in Tourette's syndrome

Deep brain stimulation modulates pallidal and subthalamic neural oscillations in Tourette's syndrome

Differentiating tic electrophysiology from voluntary movement in the human thalamocortical circuit

Deep Brain Stimulation for Tourette’s Syndrome: The Case for Targeting the Thalamic Centromedian–Parafascicular Complex

Contact Info

Product

Resources

About