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Dopamine exerts modulatory signals on cortex-basal ganglia circuits to enable flexible motor control. Parkinson's disease is characterized by a loss of dopaminergic innervation in the basal ganglia leading to complex motor and non-motor symptoms. Clinical symptom alleviation through dopaminergic medication and deep brain stimulation in the subthalamic nucleus likely depends on a complex interplay between converging basal ganglia pathways. As a unique translational research platform, deep brain stimulation allows instantaneous investigation of functional effects of subthalamic neuromodulation in human patients with Parkinson's disease. The present study aims at disentangling the role of the inhibitory basal ganglia pathways in cognitive and kinematic aspects of automatic and controlled movements in healthy and parkinsonian states by combining behavioural experiments, clinical observations, whole-brain deep brain stimulation fibre connectivity mapping and computational modelling. Twenty patients with Parkinson's disease undergoing subthalamic deep brain stimulation and 20 age-matched healthy controls participated in a visuomotor tracking task requiring normal (automatic) and inverted (controlled) reach movements. Parkinsonian patients on and off deep brain stimulation presented complex patterns of reaction time and kinematic changes, when compared to healthy controls. Stimulation of cortico-subthalamic fibres was correlated with reduced reaction time adaptation to task demand, but not kinematic aspects of motor control or alleviation of Parkinson's disease motor signs. By using clinically, behaviourally and fibre tracking informed computational models, our study reveals that loss of cognitive adaptation can be attributed to modulation of the hyperdirect pathway, while kinematic depends on suppression of indirect pathway activity. Our findings suggest that hyperdirect and indirect pathways, converging in the subthalamic nucleus, are differentially involved in cognitive aspects of cautious motor preparation and kinematic gain control during motor performance. Subthalamic deep brain stimulation modulates but does not restore these functions. Intelligent stimulation algorithms could re-enable flexible motor control in Parkinson's disease when adapted to instantaneous environmental demand. Our results may inspire new innovative pathway-specific approaches to reduce side effects and increase therapeutic efficacy of neuromodulation in patients with Parkinson's disease. [ABSTRACT FROM AUTHOR]

Impairment of naming function is a critical problem for temporal lobe epilepsy patients, yet the neural correlates of the disruption of temporal lobe language networks are poorly understood. Using functional MRI, we investigated the activation and task-related functional connectivity of left temporal lobe language networks and their relation to clinical naming performance and disease characteristics. We studied 59 adult patients with temporal lobe epilepsy (35 left temporal lobe epilepsy) and 32 healthy controls with auditory and visual naming functional MRI tasks. Time series of activation maxima in the left posterior inferior temporal lobe were extracted to create a psychophysiological interaction regressor for subsequent seed-based whole-brain task-related functional connectivity analyses. Correlational analyses were performed to assess the association of functional MRI activation and functional connectivity with clinical naming scores, age of onset of epilepsy, and duration of epilepsy. Auditory naming elicited activation in the left posterior inferior temporal gyrus and visual naming in the left fusiform gyrus across all groups. Activations in the left inferior temporal gyrus, left thalamus and left supplementary motor region during auditory naming as well as left fusiform activations during picture naming correlated with better clinical naming performance. Functional connectivity analyses indicated coupling of left posterior inferior temporal regions to bilateral anterior and posterior temporal lobe regions and the bilateral inferior precentral gyrus as well as contralateral occipital cortex. Stronger functional connectivity was associated with better clinical naming performance in all groups. In patients with left temporal lobe epilepsy only, functional connectivity increased with later age of onset of epilepsy and shorter disease duration. This suggests that onset of seizures early in life and prolonged disease duration lead to disrupted recruitment of temporal lobe networks ipsilateral to the seizure focus, which might account for naming deficits in temporal lobe epilepsy. [ABSTRACT FROM AUTHOR]

Objective: In this pilot study, the purpose is to investigate if a series of sphenopalatine ganglion (SPG) blockade treatments modulate the functional connectivity within the salience and central executive network (CEN) in chronic migraine with medication overuse headaches (CMw/MOH). Background: Using intranasal local anesthesia to block the SPG for the treatment of various headache disorders has been employed in clinical practice since the early 1900s. However, the exact mechanism of how SPG modulate resting state intrinsic functional brain networks connectivity remains to be elucidated. This pilot study seeks to understand the resting state connectivity changes in salience and CENs, with emphasis on the mesocorticolimbic systems, before and after a series of SPG block treatments. Methods: Using fMRI, resting state connectivity was derived from predefined networks of nodes (regions of interests) for the salience (27 nodes, 351 connections) and CENs (17 nodes, 136 connections). After treatments, a paired samples t‐test (with 10,000 permutations to correct for multiple comparison) was used to evaluate changes in the intranetwork resting state functional connectivity within the salience and executive networks, as well as the overall network connectivity strength. Results: When comparing connectivity strength at baseline to that at the end of treatment in our cohort of 10 CMw/MOH participants, there were several connections within the salience (n = 9) and executive (n = 8) networks that were significantly improved. Within the salience network, improved connectivity was observed between the prefrontal cortex and various regions of the insula, basal ganglia, motor, and frontal cortex. Additionally, changes in connectivity were observed between regions of the temporal cortex with the basal ganglia and supramarginal gyrus. Within the CEN, improved connectivity was observed between the prefrontal cortex and regions of the anterior thalamus, caudate, and frontal cortex. After treatment, the overall CEN connectivity was significantly improved (Baseline 0.00 ± 0.08; 6 weeks 0.03 ± 0.09, P = .01); however, the overall salience network connectivity was not significantly improved (Baseline −0.01 ± 0.10; 6 weeks 0.01 ± 0.12, P = .26). Additionally, after treatment, there was a significant reduction in the number of moderate/severe headache days per month (Baseline 21.1 ± 6.6; 6 weeks 11.2 ± 6.5, P < .001), HIT‐6 (Baseline 66.1 ± 2.6; 6 weeks 60.2 ± 3.6, P < .001), and PHQ‐9 (Baseline 12.4 ± 5.7; 6 weeks 6.1 ± 3.6, P = .008) scores. Conclusion: In this longitudinal fMRI study, we observed improved functional connectivity within both networks, primarily involving connectivity between regions of the prefrontal cortex and limbic (cortical‐limbic) structures, and between different cortical (cortical‐cortical) regions after a series of repetitive SPG blockades. The overall CEN strength was also improved. Our results suggest that recurrent parasympathetic inhibition via SPG is associated with improved functional connectivity in brain regions critical to pain processing in CMw/MOH. [ABSTRACT FROM AUTHOR]

Stereotactically guided radiofrequency thermoablation (RFTA) for epilepsy has been frequently applied over the last 40 years. Radiofrequency electrodes with temperature control function generate a coagulation lesion with clearly defined borders. In combination with high-resolution MRI imaging, this technique allows minimally-invasive ablation of periventricular nodular heterotopias, small focal type II dysplasias, and hypothalamic hamartomas. This review summarises the literature addressing this topic mainly regarding technical aspects. In essence, RFTA is a safe treatment option for patients suffering from epileptogenic pathologies visible on MRI-images. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to describe a robust method with high time resolution for estimating the cortico-thalamo-cortical (CTC) loop strength and the delay when using a scalp electroencephalography (EEG) and to illustrate its applicability for analyzing the wake-sleep transition.Methods: The basic framework for the proposed method is the parallel use of a physiological model and a parametric phenomenological model: a neural field theory (NFT) of the corticothalamic system and an autoregressive (AR) model. The AR model is a "stochastic" model that shortens the time taken to extract spectral features and is also a "linear" model that is free from the local-minimum problem. From the relationship between the transfer function of the AR model and the transfer function of the NFT in the low frequency limit, we successfully derived a direct expression of CTC loop strength and the loop delay using AR coefficients.Results: Using this method to analyze sleep-EEG data, we were able to clearly track the wake-to-sleep transition, as the estimated CTC loop strength (c2) decreased to almost zero. We also found that the c2-distribution during nocturnal sleep is clearly bimodal in nature, which can be well approximated by the superposition of two Gaussian distributions that correspond to sleep and wake states, respectively. The estimated loop delay distributed ∼0.08 s, which agrees well with the previously reported value estimated by other methods, confirming the validity of our method.Conclusions: A robust method with high time resolution was developed for estimating the cortico-thalamo-cortical loop strength and the delay when using a scalp electroencephalography. This method can contribute not only to detecting the wake-sleep transition, but also to further understanding of the transition, where the cortico-thalamo-cortical loop is thought to play an important role. [ABSTRACT FROM AUTHOR]

Introduction: Previous studies have shown links of body composition and fitness measures with brain structure, as well as with different aspects of emotional adjustment and well-being. However, the possible role of trait emotion-regulation success in the relationship between fitness/body composition and emotion-related subcortical structures has never been directly addressed. Methods: Twenty-three elite helicopter pilots were assessed in fat mass percentage, an endurance test to volitional exhaustion, bench-press power output, and negative urgency (trait affect regulation failure). Their brains were scanned using magnetic resonance imaging to estimate the size of the accumbens/amygdala, considered together, and the thalamus. Resulting correlations were used to test the relationship between body composition/fitness measures and brain structures' size, and the role of negative urgency therein, using structural equation modeling. Results: Fat mass percentage was associated with the size of the thalamus and the amygdala/accumbens. In the latter case, negative urgency and bench-press power output predicted structure size (and explained the effect of fat mass percentage away). In other words, bench-press power output and emotion regulation success (but not endurance performance) were associated with a larger amygdala/accumbens size. Conclusions: Bench-press power output and emotion regulation success are independently associated with a larger amygdala/accumbens size, although present evidence does not allow for determination of causal directionality. [ABSTRACT FROM AUTHOR]

Corpus callosum agenesis (CCA) is a clinical condition accompanied by various aneuploidy and genetic syndromes. We identified the development of the corpus callosum (CC) in 278 patients before 18 weeks of gestational age by visualising the pericallosal artery (PCA) in the callosal sulcus and changes in the lengths and ratios of the midbrain (MB) and falx (F), which suggested elevation of the third ventricle and thalamus due to CCA in the first trimester. We succeeded in visualising the path of the PCA in 273 patients. As expected, we observed an increase in the lengths of the MB and F throughout the pregnancies. The MB:F ratio was 0.5-0.6, and it was independent of gestational age. In all 278 patients, the MB:F ratio was <0.6 (95th percentile = 0.79). We observed the presence of the CC during anatomical screening at gestational weeks 18-24. Visualisation of the PCA path (98% sensitivity) and calculation of the MB:F ratio <95th percentile (0.79-100% sensitivity) had very high sensitivity that indirectly confirmed the presence of the CC in the first trimester of pregnancy. Impact statement What is already known on this subject: After reading the articles for detecting the absence of corpus callosum (CC) at first trimester with midbrain (MB) and falx (F) measurement by Lachmann et al. ( 2013 ) and visualising pericallosal artery (PCA) as an indirect sign of CC agenesis by Pati et al. ( 2012 ), we aimed to have a look for our records visualising PCA in callosal sulcus and measure MB-F, as well as their ratios for an indirect sign of 'presence' of CC at first trimester. What the results of this study add: In recent literature, it is not possible to find many articles suggesting the presence of CC between 11 and 13 weeks of gestation. Díaz-Guerrero et al. ( 2013 ) and Pati et al. ( 2012 ) has researched visualising PCA path. Lachmann et al. ( 2013 ) reported an article for MB and F measurements in early suspicion of CC agenesis. Our study will be the first article in visualising PCA path and measuring MB-F lengths as well as their ratios for 'presence' of CC with high sensitivity rates (98% and 100%). What are the implications of these findings for clinical practice and/or further research: This study encourages clinicians visualising PCA path and measure MB-F lengths when they will try to visualise repetitive times and see how it is an easy procedure when you get used to it. [ABSTRACT FROM AUTHOR]

Auditory learning induces frequency-specific plasticity in the auditory cortex. Both the auditory cortex and thalamus are involved in the cortical plasticity; however, the precise role of the intracortical circuity remains unclear until the contributions of the thalamocortical inputs are controlled. Here, we induced cortical plasticity by local activation of the primary auditory cortex (AI) via intracortical electrical stimulation (ES) in C57 mice and found a similar pattern of cortical plasticity was induced by ES AI when the auditory thalamus was inactivated or remained active during the ES AI . The best frequencies (BFs) of the recorded cortical neurons shifted towards the BFs of the electrically stimulated ones. In addition, the BF shifts were linearly correlated to the BF differences between the recorded and stimulated cortical neurons. More importantly, the ratio of the linear function with thalamic inactivation was nearly the same as the ratio of the linear function in the control condition. Our data show that cortical frequency-specific plasticity was induced by ES AI with or without the thalamic inactivation; thus intracortical circuitry can be independently responsible for cortical frequency-specific plasticity. [ABSTRACT FROM AUTHOR]

Massive corticothalamic afferents originating from layer 6a of primary sensory cortical areas modulate sensory responsiveness of thalamocortical neurons and are pivotal for shifting neuronal firing between burst and tonic modes. The influence of the corticothalamic pathways on the firing mode and sensory gain of thalamic neurons has only been extensively examined in anesthetized animals, but has yet to be established in the awake state. We made lesions of the rat barrel cortex and on the following day recorded responses of single thalamocortical and thalamic reticular neurons to a single vibrissal deflection in the somatosensory system during wakefulness. Our results showed that the cortical lesions shifted the response of thalamic neurons towards bursting, elevated the response probability and the gain of thalamocortical neurons, predominantly of recurring responses. In addition, after the lesions, the spontaneous activities of the vibrissa-responsive thalamic neurons, but not those of vibrissa-unresponsive cells, were typified by waxing-and-waning spindle-like rhythmic spiking with frequent bursting. In awake rats with intact cortex, identified layer 6a corticothalamic neurons responded to a single vibrissal deflection with short latencies that matched those of layer 4 neurons, strongly suggesting the existence of an immediate corticothalamic feedback. The present results show the importance of corticothalamic neurons in shaping thalamic activities during wakefulness. [ABSTRACT FROM AUTHOR]

Background: Many cross-sectional voxel-based morphometry (VBM) investigations have shown significant inverse correlations between chronological age and gray matter (GM) volume in several brain regions in healthy humans. However, few VBM studies have documented GM decrements in the healthy elderly with repeated MRI measurements obtained in the same subjects. Also, the extent to which the APOE ɛ4 allele influences longitudinal findings of GM reduction in the healthy elderly is unclear.Objective: Verify whether regional GM changes are associated with significant decrements in cognitive performance taking in account the presence of the APOE ɛ4 allele.Methods: Using structural MRI datasets acquired in 55 cognitively intact elderly subjects at two time-points separated by approximately three years, we searched for voxels showing significant GM reductions taking into account differences in APOE genotype.Results: We found global GM reductions as well as regional GM decrements in the right thalamus and left parahippocampal gyrus (p < 0.05, family-wise error corrected for multiple comparisons over the whole brain). These findings were not affected by APOE ɛ4.Conclusions: Irrespective of APOE ɛ4, longitudinal VBM analyses show that the hippocampal region and thalamus are critical sites where GM shrinkage is greater than the degree of global volume reduction in healthy elderly subjects. [ABSTRACT FROM AUTHOR]

Neurosurgical interventions have been used to treat PD for over a century. We examined the changing landscape of surgery for PD to appraise the value of various procedures in the context of advances in our understanding and technology. We assessed the number of articles published on neurosurgical procedures for PD over time as an albeit imprecise surrogate for their usage level. We identified over 8,000 publications associated with PD surgery. Over half the publications were on DBS. The field of DBS for PD showed a rapid rise in articles, but is now in a steady state. Thalamotomy and, to a lesser extent, pallidotomy follow a biphasic publication distribution with peaks approximately 30 years apart. Articles on gene therapy and transplantation experienced initial rapid rises and significant recent declines. Procedures using novel technologies, including gamma knife and focused ultrasound, are emerging, but are yet to have significant impact as measured by publication numbers. Pallidotomy and thalamotomy are prominent examples of procedures that were popular, declined, and re-emerged and redeclined. Transplantation and gene therapy have never broken into clinical practice. DBS overtook all procedures as the dominant surgical intervention and drove widespread use of surgery for PD. Notwithstanding, the number of DBS articles appears to have plateaued. As advances continue, emerging treatments may compete with DBS in the future. © 2017 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

To safely maneuver through the environment the brain needs to compare active sensory information with ongoing motor programs. This process occurs at various levels in the brain: at the lower level, i.e., in the spinal cord, reflexes are generated for the most primitive motor responses; at the intermediate level, i.e., in the brainstem, various nuclei co-process sensory- and motor-related inputs; and, at the higher level cerebellum and thalamo-cortical networks individually compute suitable commands for fine-tuned motor output. For sensorimotor processes the integrative capacities of the cerebral cortex and the cerebellum have been the topic of detailed analysis. Here, we use higher order sensorimotor integration in the whisker system as a model to evaluate the convergence pattern of primary sensory cortex projections and the cerebellar output nuclei throughout several brain nuclei. This prospective review focuses not only on the thalamus, but also incorporates extra-thalamic structures that could function as comparators of cerebellar output and sensory cortex output. Based on the literature on anatomical and physiological studies in the rodent brain and our qualitative data on the convergence of cerebellar sensory cortical projections we identify the superior colliculus as well as the zona incerta and the anterior pretectal nucleus as suitable candidates for cerebello-cortical convergence. Including these putative comparators we discuss the potential routes for sensorimotor information flow between the cerebellum and cerebral sensory cortex with a focus on the modulation of thalamic activity by extra-thalamic structures. [ABSTRACT FROM AUTHOR]

Invasive pituitary adenomas can infiltrate the dura mater, sphenoid sinus, or cranial bone. Endoscopic transsphenoidal sinus surgery is considered the standard of care; however, several potential complications must be noted. These complications can include cerebrospinal fluid leaks, infection, bleeding, optic nerve damage, and endocrinological complications such as diabetes insipidus. We present a case of a 69-year-old female with multiple recurrent invasive pituitary adenomas who has previously undergone 5 transsphenoidal procedures. Intraoperatively, the patient suffered from a left-sided carotid artery injury that was repaired with a muscle graft. Management of carotid artery injury during transsphenoidal surgery is optimized in a step-by-step approach which includes early recognition of the injury, briefing the surgical team, immediate control using compression, use of additional tissue graft for wound repair, and postoperative care. Through the use of the approach mentioned above, we were able to control the complication successfully. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to distinguish neuronal activity patterns in the human ventral thalamus and reveal common and disease-specific features in patients with Parkinson’s disease (PD) and cervical dystonia (CD). Methods Single unit activity of neurons was recorded during microelectrode-guided thalamotomies. We classified neurons of surgical target and surrounding area into patterns and compared their characteristics and responsiveness to voluntary movement between PD and CD patients. Results We distinguished five patterns of neuronal activity: single, LTS burst, mixed, non-LTS burst and longburst patterns. The burst and mixed patterns showed significant differences in several basic and burst characteristics. We showed that there were no disease-specific patterns or significant differences in pattern distribution between studied patients. However, burst patterns had an unbalanced distribution between disease conditions. In addition, we found difference in LTS burst characteristics between surgical targets and surrounding nuclei. All identified patterns, except the long burst pattern, were reactive to the motor tasks and to contraction of the pathological muscles. Conclusions The ventral thalamus was characterised by common neuronal activity patterns which differed in characteristics between PD and CD. Significance Our findings highlight patterns of neuronal activity of the human ventral thalamus and specific pathological features. [ABSTRACT FROM AUTHOR]

Dual-process theories of recognition memory sustain that recollection and familiarity reflect different mnemonic processes and rely on separate neural substrates that are located primarily in the medial temporal lobe (MTL). Aggleton and Brown’s model (1999) assumes that this distinction extends to other brain regions, including the thalamus, and that both recognition memory processes interact with the prefrontal cortex (PFC). Nevertheless, it is still unclear whether recollection and familiarity are subtended by separate prefrontal regions. Here we provided a review of the literature that first focused on functional magnetic resonance imaging studies that adopted the Remember/Know method and reported recollection- and familiarity-based activity in the PFC. There is evidence that functional activations are differently located within the lateral (i.e., along the dorso-ventral axis), medial (i.e., along the rostro-caudal axis) and anterior (i.e., along the medio-lateral axis) prefrontal surfaces according to whether they are recollection- or familiarity-related. Overall, the findings we summarise suggest that recollection and familiarity are qualitatively different processes and rely on distinct neural pathways even outside the MTL. [ABSTRACT FROM AUTHOR]

Varicella zoster virus (VZV) infects the face and can result in chronic, debilitating pain. The mechanism for this pain is unknown and current treatment is often not effective, thus investigations into the pain pathway become vital. Pain itself is multidimensional, consisting of sensory and affective experiences. One of the primary brain substrates for transmitting sensory signals in the face is the ventral posterior medial/posterior lateral thalamus (VPM/VPL). In addition, the anterior cingulate cortex (ACC) has been shown to be vital in the affective experience of pain, so investigating both of these areas in freely behaving animals was completed to address the role of the brain in VZV-induced pain. Our lab has developed a place escape avoidance paradigm (PEAP) to measure VZV-induced affective pain in the orofacial region of the rat. Using this assay as a measure of the affective pain experience a significant response was observed after VZV injection into the whisker pad and after VZV infusion into the trigeminal ganglion. Local field potentials (LFPs) are the summed electrical current from a group of neurons. LFP in both the VPM/VPL and ACC was attenuated in VZV injected rats after inhibition of neuronal activity. This inhibition of VPM/VPL neurons was accomplished using a designer receptor exclusively activated by a designer drug (DREADD). Immunostaining showed that cells within the VPM/VPL expressed thalamic glutamatergic vesicle transporter-2, NeuN and DREADD suggesting inhibition occurred primarily in excitable neurons. From these results we conclude: (1) that VZV associated pain does not involve a mechanism exclusive to the peripheral nerve terminals, and (2) can be controlled, in part, by excitatory neurons within the VPM/VPL that potentially modulate the affective experience by altering activity in the ACC. [ABSTRACT FROM AUTHOR]

This review updates the findings about the anatomical distribution (using immunohistochemical techniques) and possible functions of D-glutamate in the central nervous system of mammals, as well as compares the distribution of D-glutamate with the distribution of the most studied D-amino acids: D-serine and D-aspartate. The protocol used to obtain highly specific antisera directed against D-amino acids is also reported. Immunoreactivity for D-glutamate was found in dendrites and cell bodies, but not in nerve fibers. Perikarya containing D-glutamate were found in the mesencephalon and thalamus. The highest density of cell bodies was found in the dorsal raphe nucleus, the mesencephalic central grey matter, the superior colliculus, and in the subparafascicular thalamic nucleus. In comparison with the distribution of immunoreactive cell bodies containing D-serine or D-aspartate, the distribution of D-glutamate-immunoreactive perikarya is less widespread. Currently, the physiological actions mediated by D-glutamate in the brain are unknown but the restricted neuroanatomical distribution of this D-amino acid suggests that D-glutamate could be involved in very specific physiological mechanisms. In this sense, the possible functional roles of D-glutamate are discussed. [ABSTRACT FROM AUTHOR]

Background: Ketamine is a frequently used intravenous anesthetic, which can reversibly induce loss of consciousness (LOC). Previous studies have demonstrated that thalamocortical system is critical for information transmission and integration in the brain. The ventral posteromedial nucleus (VPM) is a critical component of thalamocortical system. Glutamate is an important excitatory neurotransmitter in the brain and may be involved in ketamine-induced LOC. Methods: The study used whole-cell patch-clamp to observe the effect of ketamine (30 µM-1000 µM) on glutamatergic neurotransmission in VPM slices. Results: Ketamine significantly decreased the amplitude of glutamatergic spontaneous excitatory postsynaptic currents (sEPSCs), but only higher concentration of ketamine (300 µM and 1000 µM) suppressed the frequency of sEPSCs. Ketamine (100 µM-1000 µM) also decreased the amplitude of glutamatergic miniature excitatory postsynaptic currents (mEPSCs), without altering the frequency. Conclusions: In VPM neurons, ketamine attenuates the glutamatergic neurotransmission mainly through postsynaptic mechanism and action potential may be involved in the process. [ABSTRACT FROM AUTHOR]

Background: We report the accumulated experience with ventral intermediate nucleus deep brain stimulation for medically refractory orthostatic tremor.Methods: Data from 17 patients were reviewed, comparing presurgical, short-term (0-48 months), and long-term (≥48 months) follow-up. The primary end point was the composite activities of daily living/instrumental activities of daily living score. Secondary end points included latency of symptoms on standing and treatment-related complications.Results: There was a 21.6% improvement (P = 0.004) in the composite activities of daily living/instrumental activities of daily living score, which gradually attenuated (12.5%) in the subgroup of patients with an additional long-term follow-up (8 of 17). The latency of symptoms on standing significantly improved, both in the short-term (P = 0.001) and in the long-term (P = 0.018). Three patients obtained no/minimal benefit from the procedure.Conclusions: Deep brain stimulation of the ventral intermediate nucleus was, in general, safe and well tolerated, yielding sustained benefit in selected patients with medically refractory orthostatic tremor. © 2017 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Neurons in cortical layer 5B (L5B) connect the cortex to numerous subcortical areas. Possibly the best-studied L5B cortico–subcortical connection is that between L5B neurons in the rodent barrel cortex (BC) and the posterior medial nucleus of the thalamus (POm). However, the spatial organization of L5B giant boutons in the POm and other subcortical targets is not known, and therefore it is unclear if this descending pathway retains somatotopy, i.e., body map organization, a hallmark of the ascending somatosensory pathway. We investigated the organization of the descending L5B pathway from the BC by dual-color anterograde labeling. We reconstructed and quantified the bouton clouds originating from adjacent L5B columns in the BC in three dimensions. L5B cells target six nuclei in the anterior midbrain and thalamus, including the posterior thalamus, the zona incerta, and the anterior pretectum. The L5B subcortical innervation is target specific in terms of bouton numbers, density, and projection volume. Common to all target nuclei investigated here is the maintenance of projection topology from different barrel columns in the BC, albeit with target-specific precision. We estimated low cortico–subcortical convergence and divergence, demonstrating that the L5B corticothalamic pathway is sparse and highly parallelized. Finally, the spatial organization of boutons and whisker map organization revealed the subdivision of the posterior group of the thalamus into four subnuclei (anterior, lateral, medial, and posterior). In conclusion, corticofugal L5B neurons establish a widespread cortico–subcortical network via sparse and somatotopically organized parallel pathways. [ABSTRACT FROM AUTHOR]

The present study sought to elucidate the functional contributions of sub-regions of the swallowing neural network in swallowing preparation and swallowing motor execution. Seven healthy volunteers participated in a delayed-response, go, no-go functional magnetic resonance imaging study involving four semi-randomly ordered activation tasks: (i) "prepare to swallow," (ii) "voluntary saliva swallow," (iii) "do not prepare to swallow," and (iv) "do not swallow." Results indicated that brain activation was significantly greater during swallowing preparation, than during swallowing execution, within the rostral and intermediate anterior cingulate cortex bilaterally, premotor cortex (left > right hemisphere), pericentral cortex (left > right hemisphere), and within several subcortical nuclei including the bilateral thalamus, caudate, and putamen. In contrast, activation within the bilateral insula and the left dorsolateral pericentral cortex was significantly greater in relation to swallowing execution, compared with swallowing preparation. Still other regions, including a more inferior ventrolateral pericentral area, and adjoining Brodmann area 43 bilaterally, and the supplementary motor area, were activated in relation to both swallowing preparation and execution. These findings support the view that the preparation, and subsequent execution, of swallowing are mediated by a cascading pattern of activity within the sub-regions of the bilateral swallowing neural network. [ABSTRACT FROM AUTHOR]

The whisker system is an important sensory organ with extensive neural representations in the brain of the mouse. Patterned neural modules (barrelettes) in the ipsilateral principal sensory nucleus of the trigeminal nerve (PrV) correspond to the whiskers. Axons of the PrV barrelette neurons cross the midline and confer the whisker-related patterning to the contralateral ventroposteromedial nucleus of the thalamus, and subsequently to the cortex. In this way, specific neural modules called barreloids and barrels in the contralateral thalamus and cortex represent each whisker. Partial midline crossing of the PrV axons, in a conditional Robo3 mutant (Robo3R3-5cKO) mouse line, leads to the formation of bilateral whisker maps in the ventroposteromedial, as well as the barrel cortex. We used voltagesensitive dye optical imaging and somatosensory and motor behavioral tests to characterize the consequences of bifacial maps in the thalamocortical system. Voltage-sensitive dye optical imaging verified functional, bdateral whisker representation in the barrel cortex and activation of distinct cortical loci following ipsilateral and contralateral stimulation of the specific whiskers. The mutant animals were comparable with the control animals in sensorimotor tests. However, they showed noticeable deficits in all of the whisker-dependent or -related tests, including Y-maze exploration, horizontal surface approach, bridge crossing, gap crossing, texture discrimination, floating in water, and whisking laterality. Our results indicate that bifacial maps along the thalamocortical system do not offer a functional advantage. Instead, they lead to impairments, possibly due to the smaller sizs of the whisker-related modules and interference between the ipsilateral and contralateral whisker representations in the same thalamus and cortex. [ABSTRACT FROM AUTHOR]

Pain is a common complication of herpes zoster (HZ) infection which results from reactivation of a latent varicella zoster virus (VZV). A third of HZ patients’ progress to a chronic pain state known as post herpetic neuralgia (PHN), and about a quarter of these patients’ have orofacial pain. The mechanisms controlling the pain responses are not understood. Studies suggest central pathways involving the thalamus could control pain related to HZ, and studies in our lab suggest (VGAT) in the lateral thalamus influences orofacial pain. We hypothesized that thalamic VGAT functions, in part, to reduce pain, particularly orofacial pain, associated with VZV. To address this hypothesis VZV was injected into the whisker pad. Affective and motivational aspects of pain were measured using the Place Escape/Avoidance Paradigm. Thalamic neuronal activity was modulated after injecting an adeno-associated virus (AAV) expressing an engineered acetylcholine Gi-protein-coupled receptor. This receptor inhibits neuronal firing when bound by clozapine-n-oxide (CNO). VGAT expression was attenuated in the thalamus by injecting an AAV construct that expressed a VGAT silencing shRNA. VZV-induced nociception was significantly decreased after administering CNO in male rats. Nociception significantly increased concomitant with increased thalamic c-fos expression after attenuating thalamic VGAT expression. These data establish that the lateral thalamus (posterior, ventral posteromedial, ventral posterolateral and/or reticular thalamic nucleus) controls VZV-induced nociception in the orofacial region, and that GABA in this region appears to reduce the response to VZV-induced nociception possibly by gating facial pain input. [ABSTRACT FROM AUTHOR]

Approximately 7% to 10% of patients develop a chronic pain syndrome after stroke. This chronic pain condition is called central poststroke pain (CPSP). Recent studies have observed an abnormal increase in the secretion of brain-derived neurotrophic factor (BDNF) in spinal cord tissue after spinal cord injury. An animal model of CPSP was established by an intrathalamus injection of collagenase. Mechanical and thermal allodynia was induced after lesions of the thalamic ventral basal complex in rats. Four weeks after the injection, the number of neurons decreased, the number of astrocytes, microglia, and P2X4 receptors increased, and BDNF mRNA expression increased in the brain lesion area. Nociceptive activity in the medial thalamus (MT) and the coherence coefficient of spontaneous field potential oscillations in the anterior cingulate cortex were enhanced in CPSP animals, and these enhancements were blocked by an acute injection of TrkB-Fc and TrkB antagonist Tat Cyclotraxin-B. Instead of being inhibited by the γ-aminobutyric acid (GABA) system in normal rats, multiunit activity in the MT was enhanced after a microinjection of muscimol, a GABAA receptor agonist, in CPSP animals. After CPSP, BDNF expression was enhanced in the MT, whereas the expression of GABAA channels and the cotransporter KCC2 decreased in the same area. These findings suggest that neuronal plasticity in the MT that was induced by BDNF overexpression after the thalamic lesion was a key factor in CPSP. [ABSTRACT FROM AUTHOR]

The aim of the present work was to conduct an immunohistochemical study of the expression of neuronal and glial proteins, as well as gap junction contacts (connexins 36 and 43) in the ventral posteromedial (VPMN) and posterolateral (VPLN) nuclei and the reticular (RTN) nucleus of the thalamus in rats. The VPMN and VPLN of the thalamus were found to be characterized by homogeneous distributions of synaptophysin, grouping of astrocytes, a horizontal orientation of somatostatin-containing myelinated and unmyelinated nerve fibers forming bundles and passing through barreloid septa, along with expression of connexins 36 and 43, as well as parvalbumin, identifying barreloids on sections of thickness 4 μm. In the RTN, the contents of myelin basic protein, neurofilaments, parvalbumin, and somatostatin were higher and there were moderate quantities of glial fibrillary acidic protein and connexin 43, while synaptophysin and connexin 36 were absent. [ABSTRACT FROM AUTHOR]

In recent years, more and more surgeries under general anesthesia have been performed with the assistance of electroencephalogram (EEG) monitors. An increase in anesthetic concentration leads to characteristic changes in the power spectra of the EEG. Although tracking the anesthetic-induced changes in EEG rhythms can be employed to estimate the depth of anesthesia, their precise underlying mechanisms are still unknown. A prominent feature in the EEG of some patients is the emergence of a strong power peak in the β–frequency band, which moves to the α–frequency band while increasing the anesthetic concentration. This feature is called the beta-buzz. In the present study, we use a thalamo-cortical neural population feedback model to reproduce observed characteristic features in frontal EEG power obtained experimentally during propofol general anesthesia, such as this beta-buzz. First, we find that the spectral power peak in the α– and δ–frequency ranges depend on the decay rate constant of excitatory and inhibitory synapses, but the anesthetic action on synapses does not explain the beta-buzz. Moreover, considering the action of propofol on the transmission delay between cortex and thalamus, the model reveals that the beta-buzz may result from a prolongation of the transmission delay by increasing propofol concentration. A corresponding relationship between transmission delay and anesthetic blood concentration is derived. Finally, an analytical stability study demonstrates that increasing propofol concentration moves the systems resting state towards its stability threshold. [ABSTRACT FROM AUTHOR]

Identification of brain structures traversed during implantation of deep brain-stimulating ( DBS) electrodes into the subthalamic nucleus ( STN- DBS) for the treatment of Parkinson's disease ( PD) frequently relies on subjective correspondence between kinesthetic response and multiunit activity. However, recent work suggests that local field potentials ( LFP) could be used as a more robust signal to objectively differentiate subcortical structures. The goal of this study was to analyze the spectral properties of LFP collected during STN- DBS in order to objectively identify commonly traversed brain regions and improve our understanding of aberrant oscillations in the PD-related pathophysiological cortico-basal ganglia network. In 21 PD patients, LFP were collected and analyzed during STN- DBS implantation surgery. Spectral power for delta-, theta-, alpha-, low-beta-, and high-beta-frequency bands was assessed at multiple depths throughout the subcortical structures traversed on the trajectory to the ventral border of STN. Similar to previous findings, beta-band oscillations had an increased magnitude within the borders of the motor-related area of STN, however, across several subjects, we also observed increased high-beta magnitude within the borders of thalamus. Comparing across all patients using relative power, we observed a gradual increase in the magnitude of both low- and high-beta-frequency bands as the electrode descended from striatum to STN. These results were also compared with frequency bands below beta, and similar trends were observed. Our results suggest that LFP signals recorded during the implantation of a DBS electrode evince distinct oscillatory signatures that distinguish subcortical structures. [ABSTRACT FROM AUTHOR]

Aim: To assess functional rearrangement following neurodegeneration in the thalamus and dentate nucleus in patients with progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS).Methods: We recruited 19 patients with PSP, 11 with CBS and 14 healthy subjects. All the subjects underwent resting-state (rs) fMRI using a 3T system. Whole brain functional connectivity of the thalamus and dentate nucleus were calculated by means of a seed-based approach with FEAT script in FSL toolbox. Thalamic volume was calculated by means of FIRST, and the dentate area by means of Jim software.Results: Both thalamic volume and dentate area were significantly smaller in PSP and CBS patients than in healthy subjects. No significant difference emerged in thalamic volume between PSP and CBS patients, whereas dentate area was significantly smaller in PSP than in CBS. Thalamic functional connectivity was significantly reduced in both patient groups in various cortical, subcortical and cerebellar areas. By contrast, changes in dentate nucleus functional connectivity differed in PSP and CBS: it decreased in subcortical and prefrontal cortical areas in PSP, but increased asymmetrically in the frontal cortex in CBS.Conclusions: Evaluating the dentate nucleus size and its functional connectivity may help to differentiate patients with PSP from those with CBS. [ABSTRACT FROM AUTHOR]

Experimental research has shown that the centromedian-parafascicular complex (CM-Pf) of the intralaminar thalamus is activated in attentional orienting and processing of behaviorally relevant stimuli. These observations resulted in the hypothesis that the CM-Pf plays a pivotal role in goal-oriented behavior selection. We here set out to test this hypothesis with electrophysiological recordings from patients with electrodes implanted in CM-Pf for deep brain stimulation (DBS) treatment of chronic neuropathic pain. Six patients participated in (1) an auditory three-class oddball experiment, which required a button press to target tones, but not to standard and deviant tones and in (2) a multi-speaker experiment with a target word that required attention selection and a target image that required response selection. Subjects showed transient neural responses (8–15 Hz) to the target tone and the target word. Two subjects additionally showed transient neural responses (15–25 Hz) to the target image. All sensory target stimuli were related to an internal goal and required a behavior selection (attention selection, response selection). In group analyses, neural responses were greater to target tones than deviant and standard tones and to target words than other task-relevant words that did not require attention selection. The transient neural responses occurred after the target stimuli but prior to the overt behavioral response. Our results demonstrate that in human subjects the CM-Pf is involved in signaling sensory inputs related to goal-oriented selection of behavior. [ABSTRACT FROM AUTHOR]

Summary The rat limbic system contains head direction (HD) cells that fire according to heading in the horizontal plane, and these cells are thought to provide animals with an internal compass. Previous work has found that HD cell tuning correlates with behavior on navigational tasks, but a direct, causal link between HD cells and navigation has not been demonstrated. Here, we show that pathway-specific optogenetic inhibition of the nucleus prepositus caused HD cells to become directionally unstable under dark conditions without affecting the animals’ locomotion. Then, using the same technique, we found that this decoupling of the HD signal in the absence of visual cues caused the animals to make directional homing errors and that the magnitude and direction of these errors were in a range that corresponded to the degree of instability observed in the HD signal. These results provide evidence that the HD signal plays a causal role as a neural compass in navigation. [ABSTRACT FROM AUTHOR]

Dynamic thalamic regulation of sensory signals allows the cortex to adjust better to rapidly changing behavioral, physiological, and environmental demands. To fulfill this role, thalamic neurons must themselves be subjected to constantly changing modulatory inputs that originate in multiple neurochemical pathways involved in autonomic, affective, and cognitive functions. This review defines a chemical framework for thinking about the complexity of factors that modulate the response properties of relay trigeminovascular thalamic neurons. Following the presentation of scientific evidence for monosynaptic connections between thalamic trigeminovascular neurons and axons containing glutamate, GABA, dopamine, noradrenaline, serotonin, histamine, orexin, and melanin-concentrating hormone, this review synthesizes a large body of data to propose that the transmission of headache-related nociceptive signals from the thalamus to the cortex is modulated by potentially opposing forces and that the so-called 'decision' of which system (neuropeptide/neurotransmitter) will dominate the firing of a trigeminovascular thalamic neuron at any given time is determined by the constantly changing physiological (sleep, wakefulness, food intake, body temperature, heart rate, blood pressure), behavioral (addiction, isolation), cognitive (attention, learning, memory use), and affective (stress, anxiety, depression, anger) adjustment needed to keep homeostasis. [ABSTRACT FROM AUTHOR]

Oculomotor abnormalities are rarely noted in thalamic strokes. We describe isolated right pseudoabducens palsy in a young patient with acute left thalamic infarction revealed by diffusion-weighted magnetic resonance imaging. The patient's horizontal diplopia and oculomotor palsy resolved within 3 days. This case supports the hypothesis that a lesion can cause isolated esotropia by interrupting descending inhibitory convergence pathways that traverse the paramedian thalamus and decussate in the subthalamic region to innervate the contralateral third oculomotor nucleus. Esotropia contralateral to the thalamic lesion results from tonic activation of the medial rectus, producing pseudoabducens palsy. [ABSTRACT FROM AUTHOR]

Neural population equations such as neural mass or field models are widely used to study brain activity on a large scale. However, the relation of these models to the properties of single neurons is unclear. Here we derive an equation for several interacting populations at the mesoscopic scale starting from a microscopic model of randomly connected generalized integrate-and-fire neuron models. Each population consists of 50–2000 neurons of the same type but different populations account for different neuron types. The stochastic population equations that we find reveal how spike-history effects in single-neuron dynamics such as refractoriness and adaptation interact with finite-size fluctuations on the population level. Efficient integration of the stochastic mesoscopic equations reproduces the statistical behavior of the population activities obtained from microscopic simulations of a full spiking neural network model. The theory describes nonlinear emergent dynamics such as finite-size-induced stochastic transitions in multistable networks and synchronization in balanced networks of excitatory and inhibitory neurons. The mesoscopic equations are employed to rapidly integrate a model of a cortical microcircuit consisting of eight neuron types, which allows us to predict spontaneous population activities as well as evoked responses to thalamic input. Our theory establishes a general framework for modeling finite-size neural population dynamics based on single cell and synapse parameters and offers an efficient approach to analyzing cortical circuits and computations. [ABSTRACT FROM AUTHOR]

Deep brain stimulation has been used in increasing frequency to treat refractory epilepsy. Different targets have been tried, and different epileptic syndromes have been addressed in different ways. We describe the current targeting techniques for the structures presently most often implanted, namely the anterior nucleus of the thalamus, the centromedian nucleus of the thalamus, and the hippocampus. [ABSTRACT FROM AUTHOR]

Cell-type specific differences in the kinetics of inhibitory postsynaptic conductance changes (IPSCs) are believed to impact upon network dynamics throughout the brain. Much attention has focused on how GABAA receptor (GABAAR) α and β subunit diversity will influence IPSC kinetics, but less is known about the influence of the g subunit. We have examined whether GABAAR γ subunit heterogeneity influences IPSC properties in the thalamus. The γ2 subunit gene was deleted from GABAARs selectively in the dorsal lateral geniculate nucleus (dLGN). The removal of the γ2 subunit from the dLGN reduced the overall spontaneous IPSC (sIPSC) frequency across all relay cells and produced an absence of IPSCs in a subset of relay neurons. The remaining slower IPSCs were both insensitive to diazepam and zinc indicating the absence of the γ2 subunit. Because these slower IPSCs were potentiated by methyl-6,7-dimethoxy-4-ethyl-b-carboline-3-carboxylate (DMCM), we propose these IPSCs involve γ¹ subunitcontaining GABAAR activation. Therefore, γ subunit heterogeneity appears to influence the kinetics of GABAAR-mediated synaptic transmission in the visual thalamus in a cell-selective manner. We suggest that activation of γ¹ subunit-containing GABAARs give rise to slower IPSCs in general, while faster IPSCs tend to be mediated by γ2 subunit-containing GABAARs. [ABSTRACT FROM AUTHOR]

Introduction Abnormal glutamatergic transmission in cortico-striato-thalamo-cortical (CSTC) circuits is thought to be involved in the pathophysiology of Tourette’s disorder (TD) and obsessive-compulsive disorder (OCD). Using proton magnetic resonance spectroscopy, the current study aimed to investigate regional concentrations of glutamatergic compounds in TD and OCD patients in comparison to healthy control subjects (HC). Material and methods Twenty-three TD patients, 20 OCD patients and 22 HC were included. Short echo-time single-voxel 3T MRS was obtained from dorsal anterior cingulate cortex (dACC) and midline bilateral thalamus. Results The 3-group comparison showed a significant difference in choline concentration in the thalamus. Thalamic choline was highest in OCD patients, showing a significant difference with TD, and a trend compared to HC (post-hoc analyses). Glutamine in dACC correlated negatively with tic severity scores in TD patients, while glutamate in thalamus correlated positively with anxiety severity scores in OCD patients. Conclusions These findings suggest subtle differences in metabolites in CSTC areas between TD and OCD. Alterations of choline concentrations seem to be both regional (only in thalamus, not in dACC) and disease specific in OCD pathology. The findings need replication in larger groups, but encourage further research into glutamatergic metabolites in TD and OCD. [ABSTRACT FROM AUTHOR]

Evidence for the hypothesis that input to the apical tufts of neocortical pyramidal cells plays a central role in cognition by amplifying their responses to feedforward input is reviewed. Apical tufts are electrically remote from the soma, and their inputs come from diverse sources including direct feedback from higher cortical regions, indirect feedback via the thalamus, and long-range lateral connections both within and between cortical regions. This suggests that input to tuft dendrites may amplify the cell's response to basal inputs that they receive via layer 4 and which have synapses closer to the soma. ERP data supporting this inference is noted. Intracellular studies of apical amplification (AA) and of disamplification by inhibitory interneurons targeted only at tufts are reviewed. Cognitive processes that have been related to them by computational, electrophysiological, and psychopathological studies are then outlined. These processes include: figure-ground segregation and Gestalt grouping; contextual disambiguation in perception and sentence comprehension; priming; winner-take-all competition; attention and working memory; setting the level of consciousness; cognitive control; and learning. It is argued that theories in cognitive neuroscience should not assume that all neurons function as integrate-and-fire point processors, but should use the capabilities of cells with distinct sites of integration for driving and modulatory inputs. Potentially 'unifying' theories that depend upon these capabilities are reviewed. It is concluded that evolution of the primitives of AA and disamplification in neocortex may have extended cognitive capabilities beyond those built from the long-established primitives of excitation, inhibition, and disinhibition. [ABSTRACT FROM AUTHOR]

Objective : Surgical resection of thalamic and brainstem cerebral cavernous malformations (CCMs) is associated with significant operative morbidity, but it may be outweighed, in some cases, by the neurological damage from recurrent hemorrhage in these eloquent areas. The goals of this retrospective cohort study are to describe the technical nuances of surgical approaches and determine the postoperative outcomes for CCMs of the thalamus and brainstem. Materials and Methods : We reviewed an institutional database of patients harboring thalamic or brainstem CCMs, who underwent surgical resection from 2010 to 2014. The baseline and follow-up neuroimaging and clinical findings of each patient and the operative details of each case were evaluated. Results : A total of eight patients, including two with thalamic and six with brainstem CCMs, were included in the study cohort. All patients had progressive neurological deterioration from recurrent CCM hemorrhage, and the median modified Rankin Scale (mRS) at presentation was 3. The median CCM maximum diameter and volume were 1.7 cm and 1.8 cm3, respectively. The thalamic CCMs were resected using the anterior transcallosal transchoroidal and supracerebellar infratentorial approaches each in one case (13%). The brainstem CCMs were resected using the retrosigmoid and suboccipital trans-cerebellomedullary fissure approaches each in three cases (38%). After a median follow-up of 11.5 months, all patients were neurologically stable or improved, with a median mRS of 2. The rate of functional independence (mRS 0-2) was 63%. Conclusion : Microneurosurgical techniques and approaches can be safely and effectively employed for the management of thalamic and brainstem CCMs in appropriately selected patients. [ABSTRACT FROM AUTHOR]

Parkinson's resting tremor is related to altered cerebral activity in the basal ganglia and the cerebello-thalamo-cortical circuit. Although Parkinson's disease is characterized by dopamine depletion in the basal ganglia, the dopaminergic basis of resting tremor remains unclear: dopaminergic medication reduces tremor in some patients, but many patients have a dopamine-resistant tremor. Using pharmacological functional magnetic resonance imaging, we test how a dopaminergic intervention influences the cerebral circuit involved in Parkinson's tremor. From a sample of 40 patients with Parkinson's disease, we selected 15 patients with a clearly tremor-dominant phenotype. We compared tremor-related activity and effective connectivity (using combined electromyography-functional magnetic resonance imaging) on two occasions: ON and OFF dopaminergic medication. Building on a recently developed cerebral model of Parkinson's tremor, we tested the effect of dopamine on cerebral activity associated with the onset of tremor episodes (in the basal ganglia) and with tremor amplitude (in the cerebello-thalamo-cortical circuit). Dopaminergic medication reduced clinical resting tremor scores (mean 28%, range -12 to 68%). Furthermore, dopaminergic medication reduced tremor onset-related activity in the globus pallidus and tremor amplitude-related activity in the thalamic ventral intermediate nucleus. Network analyses using dynamic causal modelling showed that dopamine directly increased self-inhibition of the ventral intermediate nucleus, rather than indirectly influencing the cerebello-thalamo-cortical circuit through the basal ganglia. Crucially, the magnitude of thalamic self-inhibition predicted the clinical dopamine response of tremor. Dopamine reduces resting tremor by potentiating inhibitory mechanisms in a cerebellar nucleus of the thalamus (ventral intermediate nucleus). This suggests that altered dopaminergic projections to the cerebello-thalamo-cortical circuit have a role in Parkinson's tremor.aww331media15307619934001. [ABSTRACT FROM AUTHOR]

Background: Deep Brain Stimulation (DBS) of the thalamic ventral intermediate nucleus (VIM) is a therapeutic option for patients with essential tremor. Despite a generally low risk of side effects, declines in verbal fluency (VF) have previously been reported.Objectives: We aimed to specify effects of VIM-DBS on major cognitive operations needed for VF task performance, represented by clusters and switches. Clusters are word production spurts, thought to arise from automatic activation of associated information pertaining to a given lexical field. Switches are slow word-to-word transitions, presumed to indicate controlled operations for stepping from one lexical field to another.Patients& Methods: Thirteen essential tremor patients with VIM-DBS performed verbal fluency tasks in their VIM-DBS ON and OFF conditions. Clusters and switches were formally defined by mathematical criteria. All results were compared to those of fifteen healthy control subjects, and significant OFF-ON-change scores were correlated to stimulation parameters.Results: Patients produced fewer words than healthy controls. DBS ON compared to DBS OFF aggravated this deficit by prolonging the intervals between words within clusters, whereas switches remained unaffected. This stimulation effect correlated with more anterior electrode positions.Conclusion: VIM-DBS seems to influence word output dynamics during verbal fluency tasks on the level of word clustering. This suggests a perturbation of automatic lexical co-activation by thalamic stimulation, particularly if delivered relatively anteriorly. The findings are discussed in the context of the hypothesized role of the thalamus in lexical processing. [ABSTRACT FROM AUTHOR]

The thalamic reticular nucleus (TRN) is an inhibitory shell positioned between the thalamus and the cortex. It is uniquely situated to modulate the flow of sensory information from the surroundings to the cortex as well as influencing ongoing cortical activity by modulating cortico-thalamo-cortical transmission. Although the thinness, architecture and location of the TRN deep in the brain has previously made this a difficult structure to study, novel optical and genetic tools have allowed for more precise targeting of this area. Recent research has implicated a role for the TRN in attention and sleep. Interestingly, impairments in attention and sleep resulting from TRN perturbation are strikingly similar to the clinical deficits observed in schizophrenia. This review aims to discuss recent evidence for the role of TRN in attention and sleep born from optogenetic work and connect these findings with those clinically observed in schizophrenia. [ABSTRACT FROM AUTHOR]

A series of parallel, integrated circuits link distinct regions of prefrontal cortex with specific nuclei of the striatum and thalamus. Dysfunction of these fronto-striato-thalamic systems is thought to play a major role in the pathogenesis of psychosis. In this review, we examine evidence from human and animal investigations that dysfunction of a specific dorsal fronto-striato-thalamic circuit, linking the dorsolateral prefrontal cortex, dorsal (associative) striatum, and mediodorsal nucleus of the thalamus, is apparent across different stages of psychosis, including prior to the onset of a first episode, suggesting that it represents a candidate risk biomarker. We consider how abnormalities at distinct points in the circuit may give rise to the pattern of findings seen in patient populations, and how these changes relate to disruptions in dopamine, glutamate and GABA signaling. [ABSTRACT FROM AUTHOR]

Here, we provide a review of behavioural, cognitive, and neural studies of the thalamus, including its role in attention, consciousness, sleep, and motor processes. We further discuss neuropsychological and brain disorders associated with thalamus function, including Parkinson's disease, Alzheimer's disease, Korsakoff's syndrome, and sleep disorders. Importantly, we highlight how thalamus-related processes and disorders can be explained by the role of the thalamus as a relay station. [ABSTRACT FROM AUTHOR]

The aim of this study was to test the technical feasibility of diffusion kurtosis imaging (DKI) in the brain after acute alcohol intoxication. Diffusion tensor imaging (DTI) and DKI during 7.0 T MRI were performed in the frontal lobe and thalamus before and 30 min, 2 h, and 6 h after ethyl alcohol administration. Compared with controls, mean kurtosis values of the frontal lobe and thalamus first decreased by 44% and 38% within 30 min (p<0.01 all) and then increased by 14% and 46% at 2 h (frontal lobe, p>0.05; thalamus, p<0.01) and by 29% and 68% at 6 h (frontal lobe, p<0.05; thalamus, p<0.01) after acute intake. Mean diffusivity decreased significantly in both the frontal lobe and the thalamus at various stages. However, fractional anisotropy decreased only in the frontal lobe, with no detectable change in the thalamus. This demonstrates that DKI possesses sufficient sensitivity for tracking pathophysiological changes at various stages associated with acute alcohol intoxication and may provide additional information that may be missed by conventional DTI parameters. [ABSTRACT FROM AUTHOR]

Although motor adaptation is typically rapid, accumulating evidence shows that it is also associated with long-lasting behavioral and neuronal changes. Two processes were suggested to explain the formation of long-term motor memories: recall, reflecting a retrieval of previous motor actions, and faster relearning, reflecting an increased sensitivity to errors. Although these manifestations of motor memories were initially demonstrated in the context of adaptation experiments in reaching, indications of long-term motor memories were also demonstrated recently in other kinds of adaptation such as in locomotor adaptation. Little is known about the neural processes that underlie these distinct aspects of memory. We hypothesize that recall and faster relearning reflect different learning processes that operate at the same time and depend on different neuronal networks. Seventeen subjects performed a multisession locomotor adaptation experiment in the laboratory, together with resting-state and localizer fMRI scans, after the baseline and the locomotor adaptation sessions.Wereport a modulation of the cerebellar-thalamic- cortical and cerebellar- basal ganglia networks after locomotor adaptation. Interestingly, whereas thalamic- cortical baseline connectivity was correlated with recall, cerebellar-thalamic baseline connectivity was correlated with faster relearning. Our results suggest that separate neuronal networks underlie error sensitivity and retrieval components. Individual differences in baseline resting-state connectivity can predict idiosyncratic combination of these components. [ABSTRACT FROM AUTHOR]

The article discusses the correlation between thalamic burst and pain using the embodied predictive interoception coding (EPIC) model. Topics include the response of pain via thalamic reticular nucleus (TRN), the functional connectivity between prefrontal cortex and somatosensory cortex, and the interconnection between sensation and stimuli that evokes affective changes. A graph which shows the EPIC pain model is also presented.

Basal ganglia and the cerebellum are part of a densely interconnected network. While both subcortical structures process information in basically segregated loops that primarily interact in the neocortex, direct subcortical interaction has been recently confirmed by neuroanatomical studies using viral transneuronal tracers in non-human primate brains. The thalamus is thought to be the main relay station of both projection systems. Yet, our understanding of subcortical basal ganglia and cerebellar interconnectivity within the human thalamus is rather sparse, primarily due to limitation in the acquisition of in vivo tracing. Consequently, we strive to characterize projections of both systems and their potential overlap within the human thalamus by diffusion MRI and tractography. Our analysis revealed a decreasing anterior-to-posterior gradient for pallido-thalamic connections in: (1) the ventral-anterior thalamus, (2) the intralaminar nuclei, and (3) midline regions. Conversely, we found a decreasing posterior-to-anterior gradient for dentato-thalamic projections predominantly in: (1) the ventral-lateral and posterior nucleus; (2) dorsal parts of the intralaminar nuclei and the subparafascicular nucleus, and (3) the medioventral and lateral mediodorsal nucleus. A considerable overlap of connectivity pattern was apparent in intralaminar nuclei and midline regions. Notably, pallidal and cerebellar projections were both hemispherically lateralized to the left thalamus. While strikingly consistent with findings from transneuronal studies in non-human primates as well as with pre-existing anatomical studies on developmentally expressed markers or pathological human brains, our assessment provides distinctive connectional fingerprints that illustrate the anatomical substrate of integrated functional networks between basal ganglia and the cerebellum. Thereby, our findings furnish useful implications for cerebellar contributions to the clinical symptomatology of movement disorders. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the effects of long-term, moderate level noise exposure during crucial periods of rat infants on stereological parameters of medial geniculate body (MGB) and auditory cortex.Materials and Methods: Twenty-four male offspring of 12 pregnant rats were divided into four groups: fetal-to-critical period group, which were exposed to noise from the last 10 days of fetal life till postnatal day (PND) 29; fetal period group that exposed to noise during the last 10 days of fetal life; critical period group, exposed to noise from PND 15 till PND 29, and control group. White noise at 90 dB for 2 h per day was used.Statistical Analysis Used: Variance for variables was performed using Proc GLM followed by mean comparison by Duncan's multiple range test.Results: Numerical density of neurons in MGB of fetal-to-critical period group was lower than control group. Similar results were seen in numerical density of neurons in layers IV and VI of auditory cortex. Furthermore, no significant difference was observed in the volume of auditory cortex among groups, and only MGB volume in fetal-to-critical period group was higher than other groups. Estimated total number of neurons in MGB was not significantly different among groups.Conclusion: It seems necessary to prevent long-term moderate level noise exposure during fetal-to-critical neonatal period. [ABSTRACT FROM AUTHOR]