Deep Brain Stimulation of Anteromedial Globus Pallidus Interna for Severe Tourette's Syndrome
University of Queensland, Brisbane, Queensland, Australia American Journal of Psychiatry
(Impact Factor: 12.3).
07/2012; 169(8):860-6. DOI: 10.1176/appi.ajp.2012.11101583
Multiple anatomical targets for deep brain stimulation (DBS) have been proposed for the treatment of severe Tourette's syndrome. In this open study, the authors evaluated the effectiveness of DBS of the anteromedial globus pallidus interna on tic severity and common comorbidities.
Eleven patients (eight of them men, mean age=39 years) with severe and medically intractable Tourette's syndrome underwent implantation of Medtronic quadripolar electrodes in the globus pallidus interna bilaterally. The primary outcome measure was the Yale Global Tic Severity Scale. Secondary outcome measures included the Yale-Brown Obsessive Compulsive Scale, the Hamilton Depression Rating Scale, the Gilles de la Tourette Syndrome-Quality of Life Scale, and the Global Assessment of Functioning Scale. Follow-up occurred at 1 month and then at a mean of 14 months after surgery (range=4-30 months).
Ten patients (91%) reported improvement in tic severity soon after DBS. Overall, there was a 48% reduction in motor tics and a 56.5% reduction in phonic tics at final follow-up. Six patients (54.5%) had a more than 50% reduction, sustained for at least 3 months, in Yale Global Tic Severity Scale score. Only two patients required ongoing pharmacotherapy for tics after surgery, and patients improved significantly on all secondary measures. One patient did not tolerate DBS and discontinued treatment after 3 months. Greater anxiety in two patients and hardware malfunction in three patients were noteworthy adverse outcomes.
The results suggest anteromedial globus pallidus interna DBS for Tourette's syndrome is an effective and well-tolerated treatment for a subgroup of patients with severe Tourette's syndrome.
Available from: Perminder S Sachdev
- "factor analysis and acceptable correlations with other rating scales and clinical variables (Cavanna et al., 2008). The scale has been used widely in the assessment of HR-QoL since its development across a number of contexts and by different research teams, including follow-up from deep brain stimulation (Cannon et al., 2012). "
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ABSTRACT: Objective: Tourette syndrome is often associated with attention deficit hyperactivity disorder, obsessive compulsive disorder and other co-morbidities, the presence of which can reduce health-related quality of life. The relationship between the number and type of co-morbidities and tic severity upon health-related quality of life has been insufficiently examined in Tourette syndrome populations and not at all in the Australian context. We hypothesised that an increased number of co-morbid diagnoses would be inversely related to health-related quality of life and that the presence of attention deficit hyperactivity disorder and obsessive compulsive disorder in particular would negatively impact health-related quality of life.
Australian and New Zealand Journal of Psychiatry 07/2015; DOI:10.1177/0004867415594429 · 3.41 Impact Factor
Available from: Christian Hauptmann
- "Today the field of application of DBS is expanding. For instance, DBS has recently been evaluated in clinical trials in patients suffering from treatment-resistant depression, and first-in-man studies have been conducted for the treatment of Tourette's syndrome (Anderson et al., 2012; Cannon et al., 2012). Despite positive clinical results, the understanding of the mechanisms of action underlying the therapeutic effects of DBS is still a matter of debate (Grill and McIntyre, 2001; Volkmann, 2004; Anderson et al., 2012). "
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ABSTRACT: Synchronization of populations of neurons is a hallmark of several brain diseases. Coordinated reset (CR) stimulation is a model-based stimulation technique which specifically counteracts abnormal synchrony by desynchronization. Electrical CR stimulation, e.g., for the treatment of Parkinson's disease (PD), is administered via depth electrodes. In order to get a deeper understanding of this technique, we extended the top-down approach of previous studies and constructed a large-scale computational model of the respective brain areas. Furthermore, we took into account the spatial anatomical properties of the simulated brain structures and incorporated a detailed numerical representation of 2 · 10(4) simulated neurons. We simulated the subthalamic nucleus (STN) and the globus pallidus externus (GPe). Connections within the STN were governed by spike-timing dependent plasticity (STDP). In this way, we modeled the physiological and pathological activity of the considered brain structures. In particular, we investigated how plasticity could be exploited and how the model could be shifted from strongly synchronized (pathological) activity to strongly desynchronized (healthy) activity of the neuronal populations via CR stimulation of the STN neurons. Furthermore, we investigated the impact of specific stimulation parameters especially the electrode position on the stimulation outcome. Our model provides a step forward toward a biophysically realistic model of the brain areas relevant to the emergence of pathological neuronal activity in PD. Furthermore, our model constitutes a test bench for the optimization of both stimulation parameters and novel electrode geometries for efficient CR stimulation.
Frontiers in Computational Neuroscience 11/2014; 8:154. DOI:10.3389/fncom.2014.00154 · 2.20 Impact Factor
Available from: Jorge Arrubla
- "TS is often accompanied by comorbidities such as obsessive-compulsive disorder (OCD), depression and attention-deficit-hyperactivity disorder (ADHD) (Khalifa and von Knorring, 2003; Robertson, 2012). However, tics respond well to treatment with typical and atypical neuroleptics (Kawohl et al., 2009a,b; Roessner et al., 2011; Neuner et al., 2012; Robertson, 2012), and in adult cases resistant to pharmacotherapy, deep brain stimulation shows promising results (Vandewalle et al., 1999; Neuner et al., 2009; Ackermans et al., 2011; Müller-Vahl et al., 2011; Cannon et al., 2012; Ackermans et al., 2013a,b). "
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ABSTRACT: Introduction: Tourette syndrome (TS) is a neuropsychiatric disorder with the core phenomenon of tics, whose origin and temporal pattern are unclear. We investigated the When and Where of tic generation and resting state networks (RSNs) via functional magnetic resonance imaging (fMRI).
Methods: Tic-related activity and the underlying RSNs in adult TS were studied within one fMRI session. Participants were instructed to lie in the scanner and to let tics occur freely. Tic onset times, as determined by video-observance were used as regressors and added to preceding time-bins of 1 s duration each to detect prior activation. RSN were identified by independent component analysis (ICA) and correlated to disease severity by the means of dual regression.
Results: Two seconds before a tic, the supplementary motor area (SMA), ventral primary motor cortex, primary sensorimotor cortex and parietal operculum exhibited activation; 1 s before a tic, the anterior cingulate, putamen, insula, amygdala, cerebellum and the extrastriatal-visual cortex exhibited activation; with tic-onset, the thalamus, central operculum, primary motor and somatosensory cortices exhibited activation. Analysis of resting state data resulted in 21 components including the so-called default-mode network. Network strength in those regions in SMA of two premotor ICA maps that were also active prior to tic occurrence, correlated significantly with disease severity according to the Yale Global Tic Severity Scale (YGTTS) scores.
Discussion: We demonstrate that the temporal pattern of tic generation follows the cortico-striato-thalamo-cortical circuit, and that cortical structures precede subcortical activation. The analysis of spontaneous fluctuations highlights the role of cortical premotor structures. Our study corroborates the notion of TS as a network disorder in which abnormal RSN activity might contribute to the generation of tics in SMA.
Frontiers in Human Neuroscience 05/2014; 8:362. DOI:10.3389/fnhum.2014.00362 · 3.63 Impact Factor
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