Basal Ganglia-thalamocortical Circuits Research Articles

Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception

ObjectiveSensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used...

Catatonia, Malignant Catatonia, and Neuroleptic Malignant Syndrome

Malignant catatonia (MC) represents a life-threatening neuropsychiatric disorder that was widely reported long before the introduction of antipsychotic drugs. A review of the world literature on MC indicates that although the prevalence of the condition may have declined since the pre-antipsychotic drug era, it continues to occur and represents a syndrome rather than a specific disease. Although most often the outgrowth of a psychiatric disorder, MC may develop in association with diverse neurologic and medical conditions. From this perspective, neuroleptic malignant syndrome (NMS) may be viewed as a drug-related form of this same MC syndrome. Our review also supports the proposed conceptualization of catatonia as a continuum, with milder forms at one end (termed simple or nonmalignant catatonia) and more severe forms involving hyperthermia and autonomic dysfunction (termed malignant catatonia) at the other end. In addition, findings from our review suggest that simple catatonia, MC and NMS share a common pathophysiology involving reduced dopaminergic functioning in the basal ganglia-thalamocortical circuits, consistent with their identity as variants of the larger unitary catatonic syndrome. Electroconvulsive therapy appears to represent the preferred treatment for MC. Antipsychotic drugs should be withheld whenever MC is suspected.

Task-related “cortical” bursting depends critically on basal ganglia input and is linked to vocal plasticity

Basal ganglia-thalamocortical circuits are critical for motor control and motor learning. Classically, basal ganglia nuclei are thought to regulate motor behavior by increasing or decreasing cortical firing rates, and basal ganglia diseases are assumed to reflect abnormal overall activity levels. More recent studies suggest instead that motor disorders derive from abnormal firing patterns, and have led to the hypothesis that surgical treatments, such as pallidotomy, act primarily by eliminating pathological firing patterns. Surprisingly little is known, however, about how the basal ganglia normally influence task-related cortical activity to regulate motor behavior, and how lesions of the basal ganglia influence cortical firing properties. Here, we investigated these questions in a songbird circuit that has striking homologies to mammalian basal ganglia-thalamocortical circuits but is specialized for singing. The "cortical" outflow nucleus of this circuit is required for song plasticity and normally exhibits increased firing during singing and song-locked burst firing. We found that lesions of the striato-pallidal nucleus in this circuit prevented hearing-dependent song changes. These basal ganglia lesions also stripped the cortical outflow neurons of their patterned burst firing during singing, without changing their spontaneous or singing-related firing rates. Taken together, these results suggest that the basal ganglia are essential not for normal cortical firing rates but for driving task-specific cortical firing patterns, including bursts. Moreover, such patterned bursting appears critical for motor plasticity. Our findings thus provide support for therapies that aim to treat basal ganglia movement disorders by normalizing firing patterns.

Basal ganglia modulation of thalamocortical relay in Parkinson's disease and dystonia

Basal ganglia dysfunction has being implied in both Parkinson's disease and dystonia. While these disorders probably involve different cellular and circuit pathologies within and beyond basal ganglia, there may be some shared neurophysiological pathways. For example, pallidotomy and pallidal Deep Brain Stimulation (DBS) are used in symptomatic treatment of both disorders. Both conditions are marked by alterations of rhythmicity of neural activity throughout basal ganglia-thalamocortical circuits. Increased synchronized oscillatory activity in beta band is characteristic of Parkinson's disease, while different frequency bands, theta and alpha, are involved in dystonia. We compare the effect of the activity of GPi, the output nuclei of the basal ganglia, on information processing in the downstream neural circuits of thalamus in Parkinson's disease and dystonia. We use a data-driven computational approach, a computational model of the thalamocortical (TC) cell modulated by experimentally recorded data, to study the differences and similarities of thalamic dynamics in dystonia and Parkinson's disease. Our analysis shows no substantial differences in TC relay between the two conditions. Our results suggest that, similar to Parkinson's disease, a disruption of thalamic processing could also be involved in dystonia. Moreover, the degree to which TC relay fidelity is impaired is approximately the same in both conditions. While Parkinson's disease and dystonia may have different pathologies and differ in the oscillatory content of neural discharge, our results suggest that the effect of patterning of pallidal discharge is similar in both conditions. Furthermore, these results suggest that the mechanisms of GPi DBS in dystonia may involve improvement of TC relay fidelity.

Spinocerebellar ataxia type 1 (SCA1): new pathoanatomical and clinico‐pathological insights

Spinocerebellar ataxia type 1 (SCA1) represents the first molecular genetically characterized autosomal dominantly inherited cerebellar ataxia and is assigned to the CAG-repeat or polyglutamine diseases. Owing to limited knowledge about SCA1 neuropathology, appropriate pathoanatomical correlates of a large variety of SCA1 disease symptoms are missing and the neuropathological basis for further morphological and experimental SCA1 studies is still fragmentary. In the present study, we investigated for the first time serial tissue sections through the complete brains of clinically diagnosed and genetically confirmed SCA1 patients. Brain damage in the three SCA1 patients studied went beyond the well-known brain predilection sites of the underlying pathological process. Along with neuronal loss in the primary motor cortex, it included widespread degeneration of gray components of the basal forebrain, thalamus, brainstem and cerebellum, as well as of white matter components in the cerebellum and brainstem. It involved the motor cerebellothalamocortical and basal ganglia-thalamocortical circuits, the visual, auditory, somatosensory, oculomotor, vestibular, ingestion-related, precerebellar, basal forebrain cholinergic and midbrain dopaminergic systems. These findings show for the first time that the extent and severity of brain damage in SCA1 is very similar to that of clinically closely related spinocerebellar ataxias (that is, SCA2, SCA3 and SCA7). They offer suitable explanations for poorly understood SCA1 disease symptoms and will facilitate the interpretation of further morphological and experimental SCA1 studies.

Basal ganglia–cortical interactions in Parkinsonian patients

Parkinson's disease is a common and debilitating condition, caused by aberrant activity in a complex basal ganglia–thalamocortical circuit. Therapeutic advances rely on characterising interactions in this circuit. However, recording electrophysiological responses over the entire circuit is impractical. Dynamic causal modelling offers large-scale models of predictive value based on a limited or partial sampling of complex networks. Using dynamic causal modelling, we determined the network changes underlying the pathological excess of beta oscillations that characterise the Parkinsonian state. We modelled data from five patients undergoing surgery for deep brain stimulation of more than one target. We found that connections to and from the subthalamic nucleus were strengthened and promoted beta synchrony, in the untreated compared to the treated Parkinsonian state. Dynamic causal modelling was able to replicate the effects of lesioning this nucleus and may provide a new means of directing the search for therapeutic targets.

Altered Brain Functional Connectivity in Patients with Cirrhosis and Minimal Hepatic Encephalopathy: A Functional MR Imaging Study

To investigate patterns of whole-brain functional connectivity in patients with minimal hepatic encephalopathy (HE) by using functional magnetic resonance (MR) imaging. This study was approved by the local institutional review board and was HIPAA compliant. All participants provided written informed consent. Neuropsychiatric tests including number connection test type A and digit symbol test were used to define minimal HE. Twenty-three patients with minimal HE and 25 age- and sex-matched healthy volunteers were included in this study. Resting-state functional MR imaging was performed by using a 3-T MR imaging unit. Functional connectivities between 90 pairs of cortical and subcortical regions in patients with minimal HE were compared with those in control participants, and significantly different connectivities were chosen as connectivities of interest (COIs). Correlations between neuropsychiatric tests and correlation coefficients of COIs were calculated. Among the 51 COIs that were significantly different in patients with minimal HE from those in control participants, 44 connectivities were weaker in patients with minimal HE. All 22 COIs related to subcortical regions of interest (bilateral putamen, pallidum, and thalamus) were weaker in patients with minimal HE. Of 29 cortical COIs, 22 connectivities were weaker and seven were stronger in patients with minimal HE. Nearly all COIs with significant differences correlated with digital symbol test scores (P<.05, false discovery rate corrected). No correlation was found among blood ammonia level, Child-Pugh scores, or any COIs in patients with minimal HE (P>.05, false discovery rate corrected). Widespread cortical and subcortical network connectivity changes that correlated with neuropsychologic impairment were found in patients with minimal HE. In particular, impairment in the basal ganglia-thalamocortical circuit could play an important role in mediating neurocognitive dysfunction, especially for psychomotor speed and attention deficits in patients with minimal HE.

Cerebral White Matter Lesions and Lacunar Infarcts Contribute to the Presence of Mild Parkinsonian Signs

Mild parkinsonian signs (MPS) are common in elderly people and may be an early stage of parkinson(ism). They might be related to cerebral small-vessel disease, although this association remains incompletely understood. To identify subjects at early stages of the disease, we investigated whether the presence of MPS was dependent on the severity and location of small-vessel disease, including white matter lesions and lacunar infarcts. Four hundred thirty individuals, with small-vessel disease, aged between 50 and 85 years, without dementia or parkinsonism, were included in this analysis and underwent MRI scanning. The number and location of lacunar infarcts were rated. White matter lesion volume was assessed by manual segmentation with automated delineating of different regions. Presence of MPS was based on the motor section of the Unified Parkinson's Disease Rating Scale. Associations were determined using logistic regression analysis adjusted for age, sex, and total brain volume. Severe white matter lesions and the presence of lacunar infarcts were independently associated with the presence of MPS (OR, 2.6; 95% CI, 1.3-4.9 and OR, 1.8; 95% CI, 1.0-3.0). Frontal and parietal white matter lesions and, to a lesser extent, lacunar infarcts in the thalamus were associated with a higher risk of MPS. The presence of lacunar infarcts was independently related to the bradykinesia category of parkinsonian signs. This study shows that severe small-vessel disease, especially at certain locations, is associated with MPS signs in older adults. Our findings suggest that small-vessel disease interrupts basal ganglia-thalamocortical circuits involving both the frontal and parietal lobes and hence may result in MPS.

Metabolic and electrophysiological changes in the basal ganglia of transgenic Huntington's disease rats

Huntington's disease (HD) is characterized by neuronal loss in the striatum, ultimately leading to an ‘imbalance’ in the electrical activity of the basal ganglia-thalamocortical circuits. To restore this ‘imbalance’ in HD patients, which is held responsible for (some) of the motor symptoms, different basal ganglia nuclei have been targeted for surgical therapies, such as ablative surgery and deep brain stimulation. However, evidence to target brain nuclei for surgical therapies in HD is lacking. We reasoned that a neuronal and metabolic mapping of the basal ganglia nuclei could identify a functional substrate for therapeutic interventions. Therefore, the aim of the present study was to investigate the metabolic and neuronal activity of basal ganglia nuclei in a transgenic rat model of HD (tgHD). Subjects were 10–12month old tgHD rats and wildtype littermates. We examined the striatum, globus pallidus, entopeduncular nucleus, the subthalamic nucleus and substantia nigra at different levels. First, we determined the overall neuronal activity at a supracellular level, by cytochrome oxidase histochemistry. Secondly, we determined the subcellular metabolic activity, by immunohistochemistry for peroxisome proliferator-activated receptor-γ transcription co-activator (PGC-1α), a key player in the mitochondrial machinery. Finally, we performed extracellular single unit recordings in the nuclei to determine the cellular activity. In tgHD rats, optical density analysis showed a significantly increased cytochrome oxidase levels in the globus pallidus and subthalamic nucleus when compared to controls. PGC-1α expression was only enhanced in the subthalamic nucleus and electrophysiological recordings revealed decreased firing frequency of the majority of the neurons in the globus pallidus and increased firing frequency of the majority of the neurons in the subthalamic nucleus. Altogether, our results suggest that the globus pallidus and subthalamic nucleus play a role in the neurobiology of HD and can be potential targets for therapeutic interventions.

White matter impairment in the basal ganglia-thalamocortical circuit of drug-naïve childhood absence epilepsy

It is unknown whether white matter abnormalities exist in childhood absence epilepsy (CAE), a syndrome of idiopathic epilepsy (IGE). Diffusion tensor imaging (DTI) can noninvasively quantify white matter integrity. This study used DTI to investigate abnormal changes in white matter of untreated CAE patients. Subjects included nine patients with untreated CAE and nine age-and sex-matched healthy controls. Diffusion tensor imaging parameters were voxel based and statistically compared between patients and controls. The correlations between DTI parameters in regions of interest (ROIs) and age of seizure onset or duration of epilepsy were analyzed. Untreated CAE patients had a significantly higher fractional anisotropy (FA) value in the bilateral thalamus, anterior corpus callosum and upper brainstem, while also displaying a lower FA value in prefrontal white matter, anterior cingulate, and bilateral posterior limbs of the internal capsule compared to control subjects. An increase in mean diffusivity (MD) value was observed in parietal lobe white matter, prefrontal white matter, and posterior cerebellar hemispheres, in addition to subcortical structures including bilateral putamen and posterior limb of internal capsule. MD significant correlations between ROI diffusion parameters and the duration of the disease or the age of onset. The results showed white matter integrity impairment in the basal ganglia-thalamocortical circuit of drug-naïve CAE patients. These abnormalities in white matter may be related to increased cortical excitability and cause cognitive, linguistic, and behavioral/emotional deficits both during and between seizures.

Common Features of Neural Activity during Singing and Sleep Periods in a Basal Ganglia Nucleus Critical for Vocal Learning in a Juvenile Songbird

Reactivations of waking experiences during sleep have been considered fundamental neural processes for memory consolidation. In songbirds, evidence suggests the importance of sleep-related neuronal activity in song system motor pathway nuclei for both juvenile vocal learning and maintenance of adult song. Like those in singing motor nuclei, neurons in the basal ganglia nucleus Area X, part of the basal ganglia-thalamocortical circuit essential for vocal plasticity, exhibit singing-related activity. It is unclear, however, whether Area X neurons show any distinctive spiking activity during sleep similar to that during singing. Here we demonstrate that, during sleep, Area X pallidal neurons exhibit phasic spiking activity, which shares some firing properties with activity during singing. Shorter interspike intervals that almost exclusively occurred during singing in awake periods were also observed during sleep. The level of firing variability was consistently higher during singing and sleep than during awake non-singing states. Moreover, deceleration of firing rate, which is considered to be an important firing property for transmitting signals from Area X to the thalamic nucleus DLM, was observed mainly during sleep as well as during singing. These results suggest that songbird basal ganglia circuitry may be involved in the off-line processing potentially critical for vocal learning during sensorimotor learning phase.

Preferential networks of the mediodorsal nucleus and centromedian–parafascicular complex of the thalamus—A DTI tractography study

Distinct thalamic nuclei, like the mediodorsal (MD) nucleus and the centromedian/parafascicular complex (CM/Pf), are embedded in different basal ganglia-thalamocortical loops, which were shown to integrate cognitive and emotional aspects of human behavior. Despite well described connections on a microscopic scale, derived from tracing studies in animals, little is known about the intrinsic anatomical connections of these nuclei in humans. This lack of knowledge limits not only interpretation of functional imaging studies but also estimation of direct effects of deep brain stimulation which treats diseases as different as epilepsy or major depression. Therefore, non-invasive diffusion tensor imaging (DTI) studies are key to analyzing connectivity patterns and elaborate approaches to close this gap. For our study, we explored the structural connectivity of the MD thalamic nuclei and the CM/Pf complex towards five cortical and six subcortical regions by using a preferential fiber calculation. We found both thalamic nuclei to be preferentially associated to distinct networks: whereas the MD is preferentially connected to prefrontal and limbic cortical regions, the CM is linked to subcortical regions. The anterior insula was the only cortical region associated with the subcortical network of the CM and the cortical network of the MD comprised one subcortical hub, the caudate nucleus, suggesting an integrative role of these two regions. Adding to predescribed anatomical tract tracing connectivities in animal studies, our finding lends support to the existence of similar basal ganglia-thalamocortical circuits in humans and we could show a robust distinction of preferential connectivity for both thalamic nuclei.

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.

Potential Long-term Effects of MDMA on the Basal Ganglia–Thalamocortical Circuit: A Proton MR Spectroscopy and Diffusion-Tensor Imaging Study

To investigate the effects of 3,4-methylenedioxymethamphetamine (MDMA, commonly known as "ecstasy") on the alterations of brain metabolites and anatomic tissue integrity related to the function of the basal ganglia-thalamocortical circuit by using proton magnetic resonance (MR) spectroscopy and diffusion-tensor MR imaging. This study was approved by a local institutional review board, and written informed consent was obtained from all subjects. Thirty-one long-term (>1 year) MDMA users and 33 healthy subjects were enrolled. Proton MR spectroscopy from the middle frontal cortex and bilateral basal ganglia and whole-brain diffusion-tensor MR imaging were performed with a 3.0-T system. Absolute concentrations of metabolites were computed, and diffusion-tensor data were registered to the International Consortium for Brain Mapping template to facilitate voxel-based group comparison. The mean myo-inositol level in the basal ganglia of MDMA users (left: 4.55 mmol/L ± 2.01 [standard deviation], right: 4.48 mmol/L ± 1.33) was significantly higher than that in control subjects (left: 3.25 mmol/L ± 1.30, right: 3.31 mmol/L ± 1.19) (P < .001). Cumulative lifetime MDMA dose showed a positive correlation with the levels of choline-containing compounds (Cho) in the right basal ganglia (r = 0.47, P = .02). MDMA users also showed a significant increase in fractional anisotropy (FA) in the bilateral thalami and significant changes in water diffusion in several regions related to the basal ganglia-thalamocortical circuit as compared with control subjects (P < .05; cluster size, >50 voxels). Increased myo-inositol and Cho concentrations in the basal ganglia of MDMA users are suggestive of glial response to degenerating serotonergic functions. The abnormal metabolic changes in the basal ganglia may consequently affect the inhibitory effect of the basal ganglia to the thalamus, as suggested by the increased FA in the thalamus and abnormal changes in water diffusion in the corresponding basal ganglia-thalamocortical circuit.

Movement Initiation-Locked Activity of the Anterior Putamen Predicts Future Movement Instability in Periodic Bimanual Movement

In periodic bimanual movements, anti-phase-coordinated patterns often change into in-phase patterns suddenly and involuntarily. Because behavior in the initial period of a sequence of cycles often does not show any obvious errors, it is difficult to predict subsequent movement errors in the later period of the cyclical sequence. Here, we evaluated performance in the later period of the cyclical sequence of bimanual periodic movements using human brain activity measured with functional magnetic resonance imaging as well as using initial movement features. Eighteen subjects performed a 30 s bimanual finger-tapping task. We calculated differences in initiation-locked transient brain activity between antiphase and in-phase tapping conditions. Correlation analysis revealed that the difference in the anterior putamen activity during antiphase compared within-phase tapping conditions was strongly correlated with future instability as measured by the mean absolute deviation of the left-hand intertap interval during antiphase movements relative to in-phase movements (r = 0.81). Among the initial movement features we measured, only the number of taps to establish the antiphase movement pattern exhibited a significant correlation. However, the correlation efficient of 0.60 was not high enough to predict the characteristics of subsequent movement. There was no significant correlation between putamen activity and initial movement features. It is likely that initiating unskilled difficult movements requires increased anterior putamen activity, and this activity increase may facilitate the initiation of movement via the basal ganglia-thalamocortical circuit. Our results suggest that initiation-locked transient activity of the anterior putamen can be used to predict future motor performance.

Contribution of the parafascicular nucleus in the spontaneous object recognition task

The parafascicular (PF) nucleus, a posterior component of the intralaminar nuclei of the thalamus, is considered to be an essential structure in the feedback systems of basal ganglia–thalamo-cortical circuits critically involved in cognitive processes. The specific role played by multimodal information encoded in PF neurons in learning and memory processes is still unclear. We conducted two experiments to investigate the role of the PF in the spontaneous object recognition (SOR) task. The behavioral effects of pretraining rats with bilateral lesions of PF with N-methyl-D-aspartate (NMDA) were compared to vehicle controls. In the first experiment, rats were tested on their ability to remember the association immediately after training trials and in the second experiment after a 24h delay. Our findings provide evidence that PF lesions critically affect both SOR tests and support its role in that non-spatial form of relational memory.

Aggravated stuttering following subthalamic deep brain stimulation in Parkinson's disease - two cases

Stuttering is a speech disorder with disruption of verbal fluency which is occasionally present in patients with Parkinson's disease (PD). Long-term medical management of PD is frequently complicated by fluctuating motor functions and dyskinesias. High-frequency deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective treatment of motor fluctuations and is the most common surgical procedure in PD. Here we report the re-occurrence and aggravation of stuttering following STN-DBS in two male patients treated for advanced PD. In both patients the speech fluency improved considerably when the neurostimulator was turned off, indicating that stuttering aggravation was related to neurostimulation of the STN itself, its afferent or efferent projections and/or to structures localized in the immediate proximity. This report supports previous studies demonstrating that lesions of the basal ganglia-thalamocortical motor circuit, including the STN, is involved in the development of stuttering. In advanced PD STN-DBS is generally an effective and safe treatment. However, patients with PD and stuttering should be informed about the risk of aggravated symptoms following surgical therapy.

Role of the subthalamic nucleus (STN) in modulation of cognitive functions: recordings via deep brain stimulation electrodes (DBS)

Event Abstract Back to Event Role of the subthalamic nucleus (STN) in modulation of cognitive functions: recordings via deep brain stimulation electrodes (DBS) Ivan Rektor1* 1 Masaryk University, Germany Neuropsychiatric disturbances after DBS indicate the STN involvement in cognitive functions. We report the STN recordings via DBS electrodes in cognitive tasks (Baláž et al., 2008; Rektor et al., 2009; Baláž et al., 2010; Bočková et al., 2011). The STN is implicated in tasks with increased cognitive loads. A dual task but not the simple oddball task evoked local field of P3-like potentials (Baláž et al., 2008). Oscillations in STN were modulated by writing other letter than that which appeared on a screen, but not by simple letter copying (Bočková, in Rektor et al., 2009). In the three stimulus paradigm, the distracter stimulus evoked an early potential (latency 200 ms), not known from the scalp recordings (Bočková et al., 2011). The rTMS of the inferior frontal cortex but not of the dorsolateral prefrontal cortex increased the speed of processing the dual task (Baláž et al., 2010). The STN (1) is implicated in modulation, rather than in a direct regulation, of cognitive functions; (2) there is a spatial overlap of sites regulating various functions, the STN might modulate cognitive activities via contextual modulation of certain cortical areas; (3) implicated in the non-motor activities in some way other than the well-known organisation of the basal ganglia-thalamocortical circuits; direct cortex-STN connexions may play an important role; (4) the modulation of cognitive functions is selective, probably determined by involvement of cortical neuronal population that are interconnected with the STN. Keywords: DBS, Neuropsychiatry Conference: XI International Conference on Cognitive Neuroscience (ICON XI), Palma, Mallorca, Spain, 25 Sep - 29 Sep, 2011. Presentation Type: Poster Presentation Topic: Poster Sessions: Neuropsychiatric Applications Citation: Rektor I (2011). Role of the subthalamic nucleus (STN) in modulation of cognitive functions: recordings via deep brain stimulation electrodes (DBS). Conference Abstract: XI International Conference on Cognitive Neuroscience (ICON XI). doi: 10.3389/conf.fnhum.2011.207.00111 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: 16 Nov 2011; Published Online: 25 Nov 2011. * Correspondence: Dr. Ivan Rektor, Masaryk University, Brno, Germany, irektor@med.muni.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.

External Globus Pallidus Stimulation Modulates Brain Connectivity in Huntington's Disease

Positron emission tomography with O-15-labeled water was used to study at rest the neurophysiological effects of bilateral external globus pallidus (GPe) deep brain stimulation in patients with Huntington's disease (HD). Five patients were compared with a control group in the on and off states of the stimulator. External globus pallidus stimulation decreased neuronal activity and modulated cerebral connectivity within the basal ganglia-thalamocortical circuitry, the sensorimotor, and the default-mode networks. These data indicate that GPe stimulation modulates functional integration in HD patients in accordance with the basal ganglia-thalamocortical circuit model.

Dysfunction of executive and related processes in childhood absence epilepsy

The nature and extent of the neuropsychological difficulties associated with childhood absence epilepsy (CAE) remain unclear. Because aberrant thalamocortical rhythms have been implicated in the pathogenesis of CAE, it was hypothesized that children with CAE would show greater difficulties in neuropsychological domains that are thought to be subserved by basal ganglia–thalamocortical circuits. Multivariate analysis of variance was used to compare the neuropsychological functioning of 16 children with CAE with that of 14 children with type 1 diabetes mellitus and 15 healthy children. The CAE group did not perform differently from the other groups on measures of intellectual functioning, memory, academic achievement, fine motor speed, or processing speed. In contrast, significant differences were found in problem solving, letter fluency, complex motor control, attention/behavioral inhibition, and psychosocial functioning. These results suggest that children with CAE show difficulties in neuropsychological functions thought to be subserved by the same regions implicated in the pathogenesis of the disorder.