Cortico-basal Ganglia-thalamocortical Circuits Research Articles

Repetitive transcranial magnetic stimulation modulates cortical-subcortical connectivity in sensorimotor network.

Repetitive transcranial magnetic stimulation (rTMS) holds the ability to modulate the connectivity within the stimulated network. However, whether and how the rTMS targeted over the primary motor cortex (M1) could affect the connectivity within the sensorimotor network (SMN) is not fully elucidated. Hence, in this study, we investigated the after-effects of rTMS over left M1 at different frequencies on connectivity within SMN. Forty-five healthy participants were recruited and randomly divided into three groups according to rTMS frequencies (high-frequency [HF], 3 Hz; low-frequency [LF], 1 Hz; and SHAM). Participants received 1-Hz, 3-Hz or sham stimulation and underwent two functional magnetic resonance imaging (fMRI) scanning sessions before and after rTMS intervention. Using resting-state functional connectivity (FC) approach, we found that high- and low-frequency rTMS had opposing effects on FC within the SMN, especially for connectivity with subcortical regions (i.e., putamen, thalamus and cerebellum). Specifically, the reductions in connectivity between cortical and subcortical regions within cortico-basal ganglia thalamo-cortical circuits and the cognitive loop of cerebellum, and increased connectivity between cortical and subdivisions within the sensorimotor loop of cerebellum were observed after high-frequency rTMS intervention, whereas the thalamus and cognitive cerebellum subdivisions exhibited increased connectivity, and sensorimotor cerebellum subdivisions showed decreased connectivity with stimulated target after low-frequency stimulation. Collectively, these findings demonstrated the alterations of connectivity within SMN after rTMS intervention at different frequencies and may help to understand the mechanisms of rTMS treatment for movement disorders associated with deficits in subcortical regions such as Parkinson's disease, Huntington's disease and Tourette's syndrome.

The role of coupling connections in a model of the cortico-basal ganglia-thalamocortical neural loop for the generation of beta oscillations

Excessive neural synchronization in the cortico-basal ganglia-thalamocortical circuits in the beta (β) frequency range (12–35 Hz) is closely associated with dopamine depletion in Parkinson’s disease (PD) and correlated with movement impairments, but the neural basis remains unclear. In this work, we establish a double-oscillator neural mass model for the cortico-basal ganglia-thalamocortical closed-loop system and explore the impacts of dopamine depletion induced changes in coupling connections within or between the two oscillators on neural activities within the loop. Spectral analysis of the neural mass activities revealed that the power and frequency of their principal components are greatly dependent on the coupling strengths between nuclei. We found that the increased intra-coupling in the basal ganglia-thalamic (BG-Th) oscillator contributes to increased oscillations in the lower β frequency band (12–25 Hz), while increased intra-coupling in the cortical oscillator mainly contributes to increased oscillations in the upper β frequency band (26–35 Hz). Interestingly, pathological upper β oscillations in the cortical oscillator may be another origin of the lower β oscillations in the BG-Th oscillator, in addition to increased intra-coupling strength within the BG-Th network. Lower β oscillations in the BG-Th oscillator can also change the dominant oscillation frequency of a cortical nucleus from the upper to the lower β band. Thus, this work may pave the way towards revealing a possible neural basis underlying the Parkinsonian state.

Controversies Surrounding the Pathophysiology of Tics.

Tics are sudden, rapid, recurrent, nonrhythmic motor movements or vocalizations (phonic productions) that are commonly present in children and are required symptoms for the diagnosis of Tourette syndrome. Despite their frequency, the underlying pathophysiology of tics/Tourette syndrome remains unknown. In this review, we discuss a variety of controversies surrounding the pathophysiology of tics, including the following: Are tics voluntary or involuntary? What is the role of the premonitory urge? Are tics due to excess excitatory or deficient inhibition? Is it time to adopt the contemporary version of the cortico-basal ganglia-thalamocortical (CBGTC) circuit? and Do we know the primary abnormal neurotransmitter in Tourette syndrome? Data from convergent clinical and animal model studies support complex interactions among the various CBGTC sites and neurotransmitters. Advances are being made; however, numerous pathophysiologic questions persist.

Thalamocortical dynamics underlying spontaneous transitions in beta power in Parkinsonism

Parkinson's disease (PD) is a neurodegenerative condition in which aberrant oscillatory synchronization of neuronal activity at beta frequencies (15–35 Hz) across the cortico-basal ganglia-thalamocortical circuit is associated with debilitating motor symptoms, such as bradykinesia and rigidity. Mounting evidence suggests that the magnitude of beta synchrony in the parkinsonian state fluctuates over time, but the mechanisms by which thalamocortical circuitry regulates the dynamic properties of cortical beta in PD are poorly understood. Using the recently developed generic Dynamic Causal Modelling (DCM) framework, we recursively optimized a set of plausible models of the thalamocortical circuit (n = 144) to infer the neural mechanisms that best explain the transitions between low and high beta power states observed in recordings of field potentials made in the motor cortex of anesthetized Parkinsonian rats. Bayesian model comparison suggests that upregulation of cortical rhythmic activity in the beta-frequency band results from changes in the coupling strength both between and within the thalamus and motor cortex. Specifically, our model indicates that high levels of cortical beta synchrony are mainly achieved by a delayed (extrinsic) input from thalamic relay cells to deep pyramidal cells and a fast (intrinsic) input from middle pyramidal cells to superficial pyramidal cells. From a clinical perspective, our study provides insights into potential therapeutic strategies that could be utilized to modulate the network mechanisms responsible for the enhancement of cortical beta in PD. Specifically, we speculate that cortical stimulation aimed to reduce the enhanced excitatory inputs to either the superficial or deep pyramidal cells could be a potential non-invasive therapeutic strategy for PD.

Imaging analysis of Parkinson's disease patients using SPECT and tractography.

Parkinson’s disease (PD) is a degenerative disorder that affects the central nervous system. PD-related alterations in structural and functional neuroimaging have not been fully explored. This study explored multi-modal PD neuroimaging and its application for predicting clinical scores on the Movement Disorder Society-sponsored Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). Multi-modal imaging that combined 123I-Ioflupane single-photon emission computed tomography (SPECT) and diffusion tensor imaging (DTI) were adopted to incorporate complementary brain imaging information. SPECT and DTI images of normal controls (NC; n = 45) and PD patients (n = 45) were obtained from a database. The specific binding ratio (SBR) was calculated from SPECT. Tractography was performed using DTI. Group-wise differences between NC and PD patients were quantified using SBR of SPECT and structural connectivity of DTI for regions of interest (ROIs) related to PD. MDS-UPDRS scores were predicted using multi-modal imaging features in a partial least-squares regression framework. Three regions and four connections within the cortico-basal ganglia thalamocortical circuit were identified using SBR and DTI, respectively. Predicted MDS-UPDRS scores using identified regions and connections and actual MDS-UPDRS scores showed a meaningful correlation (r = 0.6854, p < 0.001). Our study provided insight on regions and connections that are instrumental in PD.

Deep brain stimulation of the subthalamic nucleus in obsessive-compulsive disorder: Neuroanatomical and pathophysiological considerations

Obsessive-compulsive disorder (OCD) is among the most disabling chronic psychiatric disorders and has a significant negative impact on multiple domains of quality of life. For patients suffering from severe refractory OCD, deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been applied. Reviewing the literature of the last years we believe that through its central position within the cortico-basal ganglia-thalamocortical circuits, the STN has a coordinating role in decision-making and action-selection mechanisms. Dysfunctional information-processing at the level of the STN is responsible for some of the core symptoms of OCD. Research confirms an electrophysiological dysfunction in the associative and limbic (non-motor) parts of the STN. Compared to Parkinson׳s disease patients, STN neurons in OCD exhibit a lower firing rate, less frequent but longer bursts, increased burst activity in the anterior ventromedial area, an asymmetrical left-sided burst distribution, and a predominant oscillatory activity in the δ-band. Moreover, there is direct evidence for the involvement of the STN in both checking behavior and OCD symptoms, which are both related to changes in electrophysiological activity in the non-motor STN. Through a combination of mechanisms, DBS of the STN seems to interrupt the disturbed information-processing, leading to a normalization of connectivity within the cortico-basal ganglia-thalamocortical circuits and consequently to a reduction in symptoms. In conclusion, based on the STN׳s strategic position within cortico-basal ganglia-thalamocortical circuits and its involvement in action-selection mechanisms that are responsible for some of the core symptoms of OCD, the STN is a mechanism-based target for DBS in OCD.

C.01.01 - Cognitive domains affected by major depressive disorder (MDD)

Obsessive-compulsive disorder (OCD) is among the most disabling chronic psychiatric disorders and has a significant negative impact on multiple domains of quality of life. For patients suffering from severe refractory OCD, deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been applied. Reviewing the literature of the last years we believe that through its central position within the cortico-basal ganglia-thalamocortical circuits, the STN has a coordinating role in decision-making and action-selection mechanisms. Dysfunctional information-processing at the level of the STN is responsible for some of the core symptoms of OCD. Research confirms an electrophysiological dysfunction in the associative and limbic (non-motor) parts of the STN. Compared to Parkinson׳s disease patients, STN neurons in OCD exhibit a lower firing rate, less frequent but longer bursts, increased burst activity in the anterior ventromedial area, an asymmetrical left-sided burst distribution, and a predominant oscillatory activity in the δ-band. Moreover, there is direct evidence for the involvement of the STN in both checking behavior and OCD symptoms, which are both related to changes in electrophysiological activity in the non-motor STN. Through a combination of mechanisms, DBS of the STN seems to interrupt the disturbed information-processing, leading to a normalization of connectivity within the cortico-basal ganglia-thalamocortical circuits and consequently to a reduction in symptoms. In conclusion, based on the STN׳s strategic position within cortico-basal ganglia-thalamocortical circuits and its involvement in action-selection mechanisms that are responsible for some of the core symptoms of OCD, the STN is a mechanism-based target for DBS in OCD.

Resting state functional connectivity of the subthalamic nucleus in Parkinson's disease assessed using arterial spin-labeled perfusion fMRI.

Neurophysiological changes within the cortico-basal ganglia-thalamocortical circuits appear to be a characteristic of Parkinson's disease (PD) pathophysiology. The subthalamic nucleus (STN) is one of the basal ganglia components showing pathological neural activity patterns in PD. In this study, perfusion imaging data, acquired noninvasively using arterial spin-labeled (ASL) perfusion MRI, were used to assess the resting state functional connectivity (FC) of the STN in 24 early-to-moderate PD patients and 34 age-matched healthy controls, to determine whether altered FC in the very low frequency range of the perfusion time signal occurs as a result of the disease. Our results showed that the healthy STN was functionally connected with other nuclei of the basal ganglia and the thalamus, as well as with discrete cortical areas including the insular cortex and the hippocampus. In PD patients, connectivity of the STN was increased with two cortical areas involved in motor and cognitive processes. These findings suggest that hyperconnectivity of the STN could underlie some of the motor and cognitive deficits often present even at early stages of the disease. The FC measures provided good discrimination between controls and patients, suggesting that ASL-derived FC metrics could be a putative PD biomarker.

Long-range correlation properties in timing of skilled piano performance: the influence of auditory feedback and deep brain stimulation.

Unintentional timing deviations during musical performance can be conceived of as timing errors. However, recent research on humanizing computer-generated music has demonstrated that timing fluctuations that exhibit long-range temporal correlations (LRTC) are preferred by human listeners. This preference can be accounted for by the ubiquitous presence of LRTC in human tapping and rhythmic performances. Interestingly, the manifestation of LRTC in tapping behavior seems to be driven in a subject-specific manner by the LRTC properties of resting-state background cortical oscillatory activity. In this framework, the current study aimed to investigate whether propagation of timing deviations during the skilled, memorized piano performance (without metronome) of 17 professional pianists exhibits LRTC and whether the structure of the correlations is influenced by the presence or absence of auditory feedback. As an additional goal, we set out to investigate the influence of altering the dynamics along the cortico-basal-ganglia-thalamo-cortical network via deep brain stimulation (DBS) on the LRTC properties of musical performance. Specifically, we investigated temporal deviations during the skilled piano performance of a non-professional pianist who was treated with subthalamic-deep brain stimulation (STN-DBS) due to severe Parkinson's disease, with predominant tremor affecting his right upper extremity. In the tremor-affected right hand, the timing fluctuations of the performance exhibited random correlations with DBS OFF. By contrast, DBS restored long-range dependency in the temporal fluctuations, corresponding with the general motor improvement on DBS. Overall, the present investigations demonstrate the presence of LRTC in skilled piano performances, indicating that unintentional temporal deviations are correlated over a wide range of time scales. This phenomenon is stable after removal of the auditory feedback, but is altered by STN-DBS, which suggests that cortico-basal ganglia-thalamocortical circuits play a role in the modulation of the serial correlations of timing fluctuations exhibited in skilled musical performance.

Information Processing in the Primate Basal Ganglia during Sensory-Guided and Internally Driven Rhythmic Tapping

Gamma (γ) and beta (β) oscillations seem to play complementary functions in the cortico-basal ganglia-thalamo-cortical circuit (CBGT) during motor behavior. We investigated the time-varying changes of the putaminal spiking activity and the spectral power of local field potentials (LFPs) during a task where the rhythmic tapping of monkeys was guided by isochronous stimuli separated by a fixed duration (synchronization phase), followed by a period of internally timed movements (continuation phase). We found that the power of both bands and the discharge rate of cells showed an orderly change in magnitude as a function of the duration and/or the serial order of the intervals executed rhythmically. More LFPs were tuned to duration and/or serial order in the β- than the γ-band, although different values of preferred features were represented by single cells and by both bands. Importantly, in the LFPs tuned to serial order, there was a strong bias toward the continuation phase for the β-band when aligned to movements, and a bias toward the synchronization phase for the γ-band when aligned to the stimuli. Our results suggest that γ-oscillations reflect local computations associated with stimulus processing, whereas β-activity involves the entrainment of large putaminal circuits, probably in conjunction with other elements of CBGT, during internally driven rhythmic tapping.

Parkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity

Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico-basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion-weighted magnetic resonance imaging (MRI) and resting-state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico-basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere.

RTMS with motor training modulates cortico-basal ganglia-thalamocortical circuits in stroke patients

Repetitive transcranial magnetic stimulation (rTMS) may enhance plastic changes in the human cortex and modulation of behavior. However, the underlying neural mechanisms have not been sufficiently investigated. We examined the clinical effects and neural correlates of high-frequency rTMS coupled with motor training in patients with hemiparesis after stroke. Twenty-one patients were randomly divided into two groups, and received either real or sham rTMS. Ten daily sessions of 1,000 pulses of real or sham rTMS were applied at 10 Hz over the primary motor cortex of the affected hemisphere, coupled with sequential finger motor training of the paretic hand. Functional MRIs were obtained before and after training using sequential finger motor tasks, and performances were assessed. Following rTMS intervention, movement accuracy of sequential finger motor tasks showed significantly greater improvement in the real group than in the sham group (p < 0.05). Real rTMS modulated areas of brain activation during performance of motor tasks with a significant interaction effect in the sensorimotor cortex, thalamus, and caudate nucleus. Patients in the real rTMS group also showed significantly enhanced activation in the affected hemisphere compared to the sham rTMS group. According to these results, a 10 day course of high-frequency rTMS coupled with motor training improved motor performance through modulation of activities in the cortico-basal ganglia-thalamocortical circuits.

Deep brain stimulation of the globus pallidus internus and Gilles de la Tourette syndrome: Toward multiple networks modulation

Background:Gilles de la Tourette's syndrome (GTS) is a complex neuropsychiatric disorder characterized by disabling motor and vocal tics. The pathophysiology of GTS remains poorly understood. Conventional treatment consists in pharmacological and behavioral treatment. For patients suffering severe adverse effects or not responding to pharmacological treatment, deep brain stimulation (DBS) presents an alternative treatment. However, the optimal target choice in DBS for GTS remains a divisive issue.Methods:A PubMed search from 1999 to 2012 was conducted. Thirty-three research articles reporting on DBS in patients with GTS were selected and analyzed.Results:Eighty-eight patients with Tourette's syndrome were treated since 1999 with DBS. The majority of patients received thalamic stimulation. Significantly fewer patients were treated with globus pallidus internus stimulation. Occasionally, the anterior limb of the internal capsule and the nucleus accumbens were implanted. The subthalamic nucleus was selected once. All targets were reported with positive results, but of variable extent. Only 14 patients exhibited level 1 evidence.Conclusion:In light of the wide spectrum of associated behavioral co-morbidities in GTS, multiple networks modulation may result in the most efficacious treatment strategy. The optimal locations for DBS within the cortico-basal ganglia-thalamocortical circuits remain to be established. However, at the current stage, comparison between targets should be done with great caution. Significant disparity between number of patients treated per target, methodological variability, and quality of reporting renders a meaningful comparison between targets difficult. Randomized controlled trials with larger cohorts and standardization of procedures are urgently needed.

Alterations in brain connectivity underlying beta oscillations in Parkinsonism.

Cortico-basal ganglia-thalamocortical circuits are severely disrupted by the dopamine depletion of Parkinson's disease (PD), leading to pathologically exaggerated beta oscillations. Abnormal rhythms, found in several circuit nodes are correlated with movement impairments but their neural basis remains unclear. Here, we used dynamic causal modelling (DCM) and the 6-hydroxydopamine-lesioned rat model of PD to examine the effective connectivity underlying these spectral abnormalities. We acquired auto-spectral and cross-spectral measures of beta oscillations (10–35 Hz) from local field potential recordings made simultaneously in the frontal cortex, striatum, external globus pallidus (GPe) and subthalamic nucleus (STN), and used these data to optimise neurobiologically plausible models. Chronic dopamine depletion reorganised the cortico-basal ganglia-thalamocortical circuit, with increased effective connectivity in the pathway from cortex to STN and decreased connectivity from STN to GPe. Moreover, a contribution analysis of the Parkinsonian circuit distinguished between pathogenic and compensatory processes and revealed how effective connectivity along the indirect pathway acquired a strategic importance that underpins beta oscillations. In modelling excessive beta synchrony in PD, these findings provide a novel perspective on how altered connectivity in basal ganglia-thalamocortical circuits reflects a balance between pathogenesis and compensation, and predicts potential new therapeutic targets to overcome dysfunctional oscillations.

High frequency stimulation of the subthalamic nucleus impacts adult neurogenesis in a rat model of Parkinson's disease

Chronic high frequency stimulation of the subthalamic nucleus (STN-HFS) efficiently alleviates motor symptoms of advanced Parkinson's disease (PD). Here, we looked for possible STN-HFS-induced changes on adult brain neurogenesis in the hippocampus and olfactory bulb that may be related to non-motor deficits associated to PD, such as mood disorders and olfaction deficits. Cell proliferation (Ki-67 immuno-positive-cells) and survival (bromodeoxyuridine (BrdU)-immuno-positive cells) were assessed in the subventricular zone-olfactory bulb continuum and the dentate gyrus of the hippocampus of hemiparkinsonian rats with or without continuous STN-HFS for 8days. Dopamine lesion impaired cell proliferation and survival through different mechanisms, the effect on proliferation being correlated to the level of dopamine depletion whereas the effect on survival was not. Prolonged STN-HFS did not affect cell proliferation, but increased cell survival bilaterally. In these regions of constitutive neurogenesis, the percentage of new neuroblasts (BrdU-doublecortin-positive cells) was unchanged, suggesting that STN-HFS can lead to a net increase in newly formed neurons later on. STN-HFS also increased new cell survival in the striatum and promoted dopamine system recovery detected by tyrosine hydroxylase immunostaining. These data provide the first evidence that prolonged STN-HFS has a neurorestorative action and support the view that the action of this neurosurgical treatment can bypass the cortico-basal ganglia-thalamocortical loop circuits and largely impinge neuroplasticity and brain function.

From reinforcement learning models to psychiatric and neurological disorders

Over the last decade and a half, reinforcement learning models have fostered an increasingly sophisticated understanding of the functions of dopamine and cortico-basal ganglia-thalamo-cortical (CBGTC) circuits. More recently, these models, and the insights that they afford, have started to be used to understand important aspects of several psychiatric and neurological disorders that involve disturbances of the dopaminergic system and CBGTC circuits. We review this approach and its existing and potential applications to Parkinson's disease, Tourette's syndrome, attention-deficit/hyperactivity disorder, addiction, schizophrenia and preclinical animal models used to screen new antipsychotic drugs. The approach's proven explanatory and predictive power bodes well for the continued growth of computational psychiatry and computational neurology.

Acetylcholine–dopamine balance hypothesis in the striatum: An update

The imbalance between cholinergic activity and dopaminergic activity in the striatum causes a variety of neurological disorders, such as Parkinson's disease. During sensorimotor learning, the arrival of a conditioned stimulus reporting a reward evokes a pause response in the firing of the tonically active cholinergic interneurons in targeted areas of the striatum, whereas the same stimulus triggers an increase in the firing frequency of the dopaminergic neurons in the substantia nigra pars compacta. The pause response of the cholinergic interneurons begins with an initial depolarizing phase followed by a pause in spike firing and ensuing rebound excitation. The timing of the pause phase coincides well with the surge in dopaminergic firing, indicating that a dramatic rise in dopamine (DA) release occurs while nicotinic receptors remain unbound by acetylcholine. The pause response begins with dopamine D5 receptor-dependent synaptic plasticity in the cholinergic neurons and an increased GABAergic IPSP, which is followed by a long pause in firing through D2 and D5 receptor-dependent modulation of ion channels. Inactivation of muscarinic receptors on the projection neurons eventually yields endocannabinoid-mediated, dopamine-dependent long-term depression in the medium spiny projection neurons. Breakdown of acetylcholine-dopamine balance hampers proper functioning of the cortico-basal ganglia-thalamocortical loop circuits. In Parkinson's disease, dopamine depletion blocks autoinhibition of acetylcholine release through muscarinic autoreceptors, leading to excessive acetylcholine release which eventually prunes spines of the indirect-pathway projection neurons of the striatum and thus interrupts information transfer from motor command centers in the cerebral cortex.

Effects of zonisamide on c-Fos expression under conditions of tacrine-induced tremulous jaw movements in rats: A potential mechanism underlying its anti-parkinsonian tremor effect

Objectives To examine the mechanisms underlying the anti-tremor effect of zonisamide in rats under conditions of tacrine-induced tremulous jaw movements (TJMs). Methods Male adult rats received systemic administration of either zonisamide (5 or 50 mg/kg) or vehicle at 20 min prior to the administration of tacrine hydrochloride (5 mg/kg). Animals were sacrificed 2 h later, and the brains collected and immunostained for quantitative assessment of c-Fos expression. Results There was no effect of zonisamide on tacrine-induced c-Fos expression in the ventrolateral striatum, a primary site of the pharmacological action of tacrine. Zonisamide suppressed the tacrine-induced c-Fos expression in the cortex, the dorsal striatum, and the nucleus accumbens, which are involved in the architecture of the cortico-basal ganglia-thalamocortical circuits. Conclusion The anti-TJM effect of zonisamide may not relate to suppression of neural activity specifically in primary tremor-generating sites, but may be due to a more broad inhibitory effect on tremor-related structures such as the cortex or the striatum. This effect of zonisamide may be a contributing mechanism underlying its therapeutic efficacy on parkinsonian tremor.

Deep Brain Stimulation in Tourette’s Syndrome

Tourette's Syndrome (TS) is a neuropsychiatric disorder characterized by motor and vocal tics, often associated with behavioral disorders. Symptoms often disappear before or during adulthood. The pathophysiology of TS is still a matter of considerable debate. Current knowledge of cortico-basal ganglia-thalamocortical circuits provide explanations for the beneficial effects of deep brain stimulation (DBS) on tics. When conservative treatment fails in patients with severe TS, DBS may be a therapeutic option. In 1999, thalamic DBS was introduced for intractable TS. Since then, multiple targets have been used in a small number of patients, including the globus pallidus pars interna and the nucleus accumbens. Inclusion and exclusion criteria have been formulated to identify good candidates for DBS.

The cognitive event related potentials in the basal ganglia

Event Abstract Back to Event The cognitive event related potentials in the basal ganglia Ivan Rektor1* 1 Masaryk University, St. Anne’s Hospital, Czechia In this lecture we will discuss our recordings of ERP in the basal ganglia and their relationship to the cortical ERP. We studied potentials related to a variety of cognitive activities (attentional, decisional, motor preparation, sensory processing, etc.) in brain structures that participate in cortico-basal ganglia-thalamocortical loops. We chose relatively simple and well-known protocols that had been consecutively tested. The occurrence of several cognitive potentials has partially been published in previous studies. Patients with pharmacoresistant epilepsy and with advanced Parkinson’s disease were tested. Using intracerebrally inserted electrodes (in one patient, also subdural strip electrodes) ERP recordings were obtained from 32 patients, all of whom were candidates for epilepsy surgery. Fifteen patients (12 men and 3 women; the mean age 28.5 years), had diagonal electrodes targeted in the amygdalo-hippocampal complex, with one or several contacts in the basal ganglia; in putamen, caudate and in pallidum. Ten patients with idiopathic Parkinson’s disease had ERP potentials recorded from externalised deep brain electrodes implanted in the subthalamic nucleus (STN) or in its immediate vicinity. In four other patients with Parkinson’s disease the ERP in the STN were modulated by cortical rTMS. We will present: 1. Recordings of the P3-like potentials in the basal ganglia (putamen, caudate and pallidum) and in the cortex 1.1. The distribution of P3-like potentials in the basal ganglia 1.2. The relationship between the P3-like potentials in the basal ganglia and the cortical targets of the cortico-basal ganglia-thalamocortical circuits 2. P3-like potentials in the subthalamic nucleus 3. General discussion CONCLUSION: The basal ganglia represent a very complex system with large volumes of grey matter. The role of the basal ganglia in cognitive processing is largely unknown. According to our studies, based mainly on direct intracerebral recordings of cognitive event related potentials, the cognitive activities in the basal ganglia are organized in some way other than the well-known organization of the cortico-basal ganglia-thalamocortical circuits. An integrative role of the basal ganglia, with subsequent modulation of cortical cognitive processing, is suggested. In some cases, direct connections with the cortex that bypass the circuitries might underlie the processing of specific cognitive functions. This might be the case of STN. In this nucleus, the standard oddball ERP are not generated. This result differs from all other explored basal ganglia. STN seems to be specifically involved in the processing of some cognitive activities, e.g. of the executive functions. Acknowledgement: Supported by research program MŠ ČR 112801. Conference: 10th International Conference on Cognitive Neuroscience, Bodrum, Turkey, 1 Sep - 5 Sep, 2008. Presentation Type: Oral Presentation Topic: Abstracts Citation: Rektor I (2008). The cognitive event related potentials in the basal ganglia. Conference Abstract: 10th International Conference on Cognitive Neuroscience. doi: 10.3389/conf.neuro.09.2009.01.025 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 27 Nov 2008; Published Online: 27 Nov 2008. * Correspondence: Ivan Rektor, Masaryk University, St. Anne’s Hospital, Brno, Czechia, ivan.rektor@fnusa.cz Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ivan Rektor Google Ivan Rektor Google Scholar Ivan Rektor PubMed Ivan Rektor Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.