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Background: Stress-related gastrointestinal bleeding (SRGB) is one of the major complications after aneurysmal subarachnoid hemorrhage (aSAH), and it can present challenges in patient care and treatment. The aim of this study was to explore the clinical significance of the caudate Hounsfield unit (HU) value in the Alberta Stroke Program Early CT (ASPECT) score for predicting SRGB in patients with aSAH., Methods: We retrospectively analyzed the data of 531 aSAH patients admitted to our institution between 2019 and 2022. Potential predictors of SRGB were identified using multivariate Cox regression analysis. We used a restricted cubic spline (RCS) to evaluate whether there is a nonlinear relationship between the right caudate HU value and SRGB. MaxStat analysis (titled as maximally selected rank statistics) was performed to identify the optimal cutoff point for the right caudate HU value. Another Kaplan-Meier method with the log-rank test was used to analyze the right caudate HU value in predicting the occurrence of SRGB., Results: The incidence rate of SRGB was 17.9%. In the multivariate Cox regression analysis, the right caudate HU value was an independent predictor of SRGB [Hazard ratio (HR) = 0.913; 95% confidence interval (CI): 0.847-0.983, and p  = 0.016]. The RCS indicated that the incidence of developing SRGB reduces with increasing right caudate HU values (nonlinear p  = 0.78). The optimal cut-off value of the right caudate HU was 25.1., Conclusion: Among aSAH patients, lower right caudate HU values indicated a higher risk of developing SRGB. Our findings provide further evidence for the relationship between the gastrointestinal system and the brain., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Wang, Yuan, Li, Lin, Chen, Yang, Han, Li, Jia, Zhou, Zhang, Li, Li, Zhao, Hao, Chen and Zhao.)

Introduction: Pain catastrophizing, a measure of an individual's negative emotional and cognitive appraisals of pain, has been included as a key treatment target in many psychological interventions for pain. However, the neural correlates of pain catastrophizing have been understudied. Prior neuroimaging evidence suggests that adults with pain show altered reward processing throughout the mesocorticolimbic reward circuitry., Methods: In this study, we tested the association between Pain Catastrophizing Scale (PCS) scores and neural activation to the Monetary Incentive Delay (MID) reward neuroimaging task in 94 adults reporting a range of pain, insomnia, and mood symptoms., Results: Results indicated that PCS score but not pain intensity was significantly associated with blunted activation in the caudate and putamen in response to feedback of successful vs. unsuccessful trials on the MID task. Mediation analyses indicated that PCS score fully mediated the relationship between depression symptoms and reward activation., Discussion: These findings provide evidence that pain catastrophizing is independently associated with altered striatal function apart from depression symptoms and pain intensity. Thus, in individuals experiencing pain and/or co- morbid conditions, reward dysfunction is directly related to pain catastrophizing., Competing Interests: AE has received research grant support to her institution from Pfizer Inc, Forum Pharmaceuticals, and GK, consultation fees from Charles River Analytics, and honoraria for advisory work from Pfizer, and Kaurna Pharmaceuticals in the past 5 years for work unrelated to this project. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Cooke, Edwards, Wheeler, Schmitt, Nielsen, Streck, Schuster, Potter, Evins and Gilman.)

Huntington's disease is caused by a CAG repeat expansion in the Huntingtin gene ( HTT ), coding for polyglutamine in the Huntingtin protein, with longer CAG repeats causing earlier age of onset. The variable 'Age' × ('CAG'-L), where 'Age' is the current age of the individual, 'CAG' is the repeat length and L is a constant (reflecting an approximation of the threshold), termed the 'CAG Age Product' (CAP) enables the consideration of many individuals with different CAG repeat expansions at the same time for analysis of any variable and graphing using the CAG Age Product score as the X axis. Structural MRI studies have showed that progressive striatal atrophy begins many years prior to the onset of diagnosable motor Huntington's disease, confirmed by longitudinal multicentre studies on three continents, including PREDICT-HD, TRACK-HD and IMAGE-HD. However, previous studies have not clarified the relationship between striatal atrophy, atrophy of other basal ganglia structures, and atrophy of other brain regions. The present study has analysed all three longitudinal datasets together using a single image segmentation algorithm and combining data from a large number of subjects across a range of CAG Age Product score. In addition, we have used a strategy of normalizing regional atrophy to atrophy of the whole brain, in order to determine which regions may undergo preferential degeneration. This made possible the detailed characterization of regional brain atrophy in relation to CAG Age Product score. There is dramatic selective atrophy of regions involved in the basal ganglia circuit-caudate, putamen, nucleus accumbens, globus pallidus and substantia nigra. Most other regions of the brain appear to have slower but steady degeneration. These results support (but certainly do not prove) the hypothesis of circuit-based spread of pathology in Huntington's disease, possibly due to spread of mutant Htt protein, though other connection-based mechanisms are possible. Therapeutic targets related to prion-like spread of pathology or other mechanisms may be suggested. In addition, they have implications for current neurosurgical therapeutic approaches, since delivery of therapeutic agents solely to the caudate and putamen may miss other structures affected early, such as nucleus accumbens and output nuclei of the striatum, the substantia nigra and the globus pallidus., Competing Interests: Funding for the study was provided by the NIH under a license agreement between AnatomyWorks LLC and the Johns Hopkins University. Dr. Michael I. Miller and the University are entitled to royalty distributions related to technology described in the study. Dr. Miller is a founder of and holds equity in AnatomyWorks LLC. This arrangement has been reviewed and approved by the Johns Hopkins University in accordance with its conflict of interest policies. The other authors declare no relevant conflicts of interest., (© The Author(s) 2023. Published by Oxford University Press on behalf of the Guarantors of Brain.)

Introduction: Glutamatergic neurometabolites play important roles in the basal ganglia, a hub of the brain networks involved in musical rhythm processing. We aimed to investigate the relationship between rhythm processing abilities and glutamatergic neurometabolites in the caudate., Methods: We aquired Glutamatergic function in healthy individuals employing proton magnetic resonance spectroscopy. We targeted the right caudate and the dorsal anterior cingulate cortex (dACC) as a control region. Rhythm processing ability was assessed by the Harvard Beat Assessment Test (H-BAT)., Results: We found negative correlations between the production part of the Beat Saliency Test in the H-BAT and glutamate and glutamine levels in the caudate ( r  = -0.693, p  = 0.002) whereas there was no such association in the dACC., Conclusion: These results suggest that higher glutamatergic neurometabolite levels in the caudate may contribute to rhythm processing, especially the ability to produce meter in music precisely., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Honda, Noda, Matsushita, Tarumi, Nomiyama, Tsugawa, Tobari, Hondo, Saito, Mimura, Fujii and Nakajima.)

The striatum is an important subcortical structure with extensive connections to other regions of the brain. These connections are believed to play important roles in behaviors such as reward-related processes and impulse control, which show significant sex differences. However, little is known about sex differences in the striatum-projected fiber connectivity. The current study examined sex differences between 50 Chinese males and 79 Chinese females in their fiber connections between the striatum and nine selected cortical and subcortical regions. Despite overall similarities, males showed stronger fiber connections between the left caudate and rostral cingulate cortex, between the right putamen and the lateral orbitofrontal cortex, between the bilateral putamen and the ventro-lateral prefrontal cortex, and between the right caudate and the ventro-lateral prefrontal cortex, whereas females showed stronger fiber connections between the right putamen and the dorsolateral prefrontal cortex, between bilateral caudate and hippocampus, and between the left putamen and hippocampus. These findings help us to understand sex differences in the striatum-projected fiber connections and their implications for sex differences in behaviors.

Introducción: En la fisiopatología de algunas entidades neurológicas y psiquiátricas se involucran determinadas estructuras encefálicas. Las pruebas diagnósticas por imagen y la segmentación informática brindan la oportunidad de estudiar posibles relaciones entre ellas. Objetivo: Realizar un atlas anatómico mediante imágenes de resonancia magnética (RM) encefálica, definiendo los valores de normalidad en sujetos sanos de diversas estructuras para aplicarlos en el estudio de pacientes con patologías neurológicas y/o psiquiátricas, determinando posibles relaciones. Materiales y métodos: Diez estudios de RM de individuos sanos, analizados por dos radiólogos independientes. Se estudiaron los núcleos caudado, putamen y pálido de ambos hemisferios cerebrales, mediante la herramienta de segmentación ITK-SNAP. Se determinaron los volúmenes máximo, mínimo y medio de los núcleos, comparando ambos lados y la concordancia interobservador. Resultados: Los resultados volumétricos del caudado reflejaron una media de 4032 mm3 (+/-719'72), 4626'42 mm3 (+/-653'87) para el putamen y 1251'25 mm3 (+/- 277'3) para el pálido. Los índices de correlación entre los núcleos de ambos lados fueron de 0'974 para el caudado, 0'946 para el putamen y 0´76 para el pálido. Los índices de correlación interobservador fueron de 0'737, 0'919 y 0'082, respectivamente. Conclusiones: La segmentación en imágenes médicas -en este caso, RM- tiene un futuro prometedor para analizar patologías cerebrales con alteraciones morfológicas y/o morfométricas. Los resultados obtenidos para los núcleos putamen y caudado representan una directriz inicial para establecer la morfología y morfometría normales.Introduction: Some encephalic structures are involved into the physiopathology of some neurologic and psychiatric entities. The different imaging modalities and the computer segmentation allow the opportunity of studying the possible relationship among them. Objective: To elaborate an anatomic atlas of the encephalic structures by means of MR images, evaluating in healthy patients the normal values of these structures, in order to apply them in the study of patients with neurologic or psychiatric pathologies to determine a possible relationship. Material and methods: Ten MR studies of healthy patients, analysed by two independents radiologists. Caudate, putamen and pallidum nuclei of both hemispheres were evaluated by means of the segmentation tool ITKSNAP. The maximum, minimum and medium volumes of the nuclei were determined, comparing both sides and the interobserver correlation. Results: The volumetric results for caudate nucleus (media) were: 4032 mm3 (+/-719'72), 4626'42 mm3 (+/-653'87) for the putamen and 1251'25 mm3 (+/-277'3) for the pallidum. The correlation index between the nucleus of both sides were of 0,974 for caudate, 0,946 for the putamen and 0,76 for the pallidum. The interobserver correlation indexes were 0,737, 0,919 and 0,082 respectively. Conclusions: Medical imaging segmentation, in this case MR, has a very promising future in order to analyse brain entities with morphometric or morphologic alterations. The obtained results in case of caudate, putamen and pallidum nuclei represent an initial key in order to establish the normal morphology and morphometry of these structures.

• Reading and attention difficulties occur together more often than chance. • The neural bases of this comorbidity are not well understood. • We investigated shared neural correlates of reading and attention in healthy youth. • Grey matter correlates overlapped in the precuneus and caudate nucleus. • These are potential regions of interest for comorbid reading and attention problems. Disorders of reading (developmental dyslexia) and attention (ADHD) have a high rate of comorbidity (25–40%), yet little is known about the neural underpinnings of this phenomenon. The current study investigated the shared and unique neural correlates of reading and attention in 330 typically developing children ages 8–18 from the Philadelphia Neurodevelopmental Cohort. Multiple regression analyses were used to identify regions of the brain where grey matter (GM) volume was associated with reading or attention scores (p < 0.001, cluster FDR p < 0.05). Better attention scores correlated with increased GM in the precuneus and higher reading scores were associated with greater thalamic GM. An exploratory conjunction analysis (p < 0.05, k > 239) found that GM in the caudate and precuneus correlated with both reading and attention scores. These results are consistent with a recent meta-analysis which identified GM reductions in the caudate in both dyslexia and ADHD and reveal potential shared neural correlates of reading and attention. [ABSTRACT FROM AUTHOR]

Degeneration of neurons and circuits across the striatum shows stereotyped time-course and spatial topography patterns that are distinct for Huntington's disease, Parkinson's disease, or the Tauopathies. These patterns of neurodegeneration in humans have not yet been systematically related to developmental, connectional, cellular, and chemical factors studied in human and non-human primates, that may underlie potential differences in selective vulnerability across striatal sectors. Relating primate anatomy to human pathology could provide new venues for identifying molecular, cellular, and connectional factors linked to the degeneration of striatal neurons and circuits. This review describes and summarizes several developmental, cellular, structural, and connectional features of the primate striatum in relation to patterns of neurodegeneration in the striatum of humans and of non-human primate models. We review (1) the types of neurons in the primate striatum, (2) the cyto-, myelo-, and chemoarchitecture of the primate striatum, (3) the developmental origin of the striatum in light of modern patterning studies, (4) the organization of corticostriatal projections in relation to cortical types, and (5) the topography and time-course of neuron loss, glial reaction, and protein aggregation induced by neurodegenerative diseases in humans and in non-human primate models across striatal sectors and their corresponding cortical areas. We summarize current knowledge about key aspects of primate striatal anatomy and human pathology and indicate knowledge gaps that should be addressed in future studies. We aim to identify factors for selective vulnerability to neurodegeneration of striatal neurons and circuits and obtain hints that could help elucidate striatal pathology in humans. • Degeneration in the human striatum shows typical time-course and spatial patterns. • Striatal degeneration patterns are distinct for each degenerative disease. • Development, connections, and cytology may underlie striatal degeneration patterns. • Corticostriatal connections may underlie selective vulnerability to Huntington's disease. • Corticostriatal connections provide pathways for Tauopathies and Parkinson's disease. [ABSTRACT FROM AUTHOR]

It is well documented that some brain regions, such as association cortices, caudate, and hippocampus, are particularly prone to age-related atrophy, but it has been hypothesized that there are individual differences in atrophy profiles. Here, we document heterogeneity in regional-atrophy patterns using latent-profile analysis of 1,482 longitudinal magnetic resonance imaging observations. The results supported a 2-group solution reflecting differences in atrophy rates in cortical regions and hippocampus along with comparable caudate atrophy. The higher-atrophy group had the most marked atrophy in hippocampus and also lower episodic memory, and their normal caudate atrophy rate was accompanied by larger baseline volumes. Our findings support and refine models of heterogeneity in brain aging and suggest distinct mechanisms of atrophy in striatal versus hippocampal-cortical systems., (© The Author(s) 2022. Published by Oxford University Press.)

We have explored genome-wide expression of genes related to glycobiology in exon 1 transgenic Huntington's disease (HD) mice using a custom-designed GLYCOv2 chip and Affymetrix microarray analyses. We validated, using quantitative real-time PCR, abnormal expression levels of genes encoding glycosyltransferases in the striatum of R6/1 transgenic mice, as well as in postmortem caudate from human HD subjects. Many of these genes show differential regional expression within the CNS, as indicated by in situ hybridization analysis, suggesting region-specific regulation of this system in the brain. We further show disrupted patterns of glycolipids (acidic and neutral lipids) and/or ganglioside levels in both the forebrain of the R6/1 transgenic mice and caudate samples from human HD subjects. These findings reveal novel disruptions in glycolipid/ganglioside metabolic pathways in the pathology of HD and suggest that the development of new targets to restore glycosphingolipid balance may act to ameliorate some symptoms of HD.

Prenatal marijuana exposure (PME) is linked to neurobehavioral and cognitive impairments, however findings in childhood and adolescence are inconsistent. Type-1 cannabinoid receptors (CB1R) modulate fetal neurodevelopment, mediating PME effects on growth of functional circuitry sub-serving behaviors critical for academic and social success. The purpose of this study was to investigate the effects of prenatal marijuana on development of early brain functional circuitry prior to prolonged postnatal environmental influences. We measured resting state functional connectivity during unsedated sleep in infants at 2-6 weeks (+MJ: 20 with PME in combination with nicotine, alcohol, opiates, and/or SSRI; -MJ: 23 exposed to the same other drugs without marijuana, CTR: 20 drug free controls). Connectivity of subcortical seed regions with high fetal CB1R expression was examined. Marijuana-specific differences were observed in insula and three striatal connections: anterior insula – cerebellum, right caudate – cerebellum, right caudate – right fusiform gyrus/inferior occipital, left caudate – cerebellum. +MJ neonates had hypoconnectivity in all clusters compared with -MJ and CTR groups. Altered striatal connectivity to areas involved in visual spatial and motor learning, attention, and in fine-tuning of motor outputs involved in movement and language production may contribute to neurobehavioral deficits reported in this at-risk group. Disrupted anterior insula connectivity may contribute to altered integration of interoceptive signals with salience estimates, motivation, decision-making, and later drug use. Compared with CTRs, both +MJ and -MJ groups demonstrated hyperconnectivity of left amygdala seed with orbital frontal cortex and hypoconnectivity of posterior thalamus seed with hippocampus, suggesting vulnerability to multiple drugs in these circuits.

While prior research has shown a strong relationship between socioeconomic status (SES) and working memory performance, the relation between SES and procedural (implicit) memory remains unknown. Convergent research in both animals and humans has revealed a fundamental dissociation, both behaviorally and neurally, between a working memory system that depends on medial temporal-lobe structures and the dorsal lateral prefrontal cortex (DLPFC) versus a procedural memory system that depends on the basal ganglia. Here, we measured performance in adolescents from lower- and higher-SES backgrounds on tests of working memory capacity (complex working memory span) and procedural memory (probabilistic classification) and their hippocampal, DLPFC, and caudate volumes. Lower-SES adolescents had worse working memory performance and smaller hippocampal and DLPFC volumes than their higher-SES peers, but there was no significant difference between the lower- and higher-SES groups on the procedural memory task or in caudate volumes. These findings suggest that SES may have a selective influence on hippocampal-prefrontal-dependent working memory and little influence on striatal-dependent procedural memory.

While time is well acknowledged for having a fundamental part in our perception, questions on how it is represented are still matters of great debate. One of the main issues in question is whether time is represented intrinsically at the neural level, or is it represented within dedicated brain regions. We used an fMRI block design to test if we can impose covert encoding of temporal features of faces and natural scenes stimuli within category selective neural populations by exposing subjects to four types of temporal variance, ranging from 0% up to 50% variance. We found a gradual increase in neural activation associated with the gradual increase in temporal variance within category selective areas. A second level analysis showed the same pattern of activations within known brain regions associated with time representation, such as the Cerebellum, the Caudate and the Thalamus. We concluded that temporal features are integral to perception and are simultaneously represented within category selective regions and globally within dedicated regions. Our second conclusion, drown from our covert procedure, is that time encoding, at its basic level, is an automated process that does not require attention allocated towards the temporal features nor does it require dedicated resources.

There has been a growing interest in understanding how contemplative practices affect brain functional organization. However, most studies have restricted their exploration to predefined networks. Furthermore, scientific comparisons of different contemplative traditions are largely lacking.Here we explored differences in whole brain resting state functional connectivity between experienced yoga practitioners, experienced meditators and matched controls. Analyses were repeated in an independent sample of experienced meditators and matched controls.Analyses utilizing Network Based Statistics (NBS; Zalesky et al., 2010) revealed difference components for yoga practitioners > controls and meditators > controls in which the right caudate was a central node. Follow up analyses revealed that yoga practitioners and meditators had significantly greater degree centrality in the caudate than controls. This greater degree centrality was not driven by single connections but by greater connectivity between the caudate and numerous brain regions. Findings of greater caudate connectivity in meditators than in controls was replicated in an independent dataset.These findings suggest that yoga and meditation practitioners have stronger functional connectivity within basal ganglia cortico-thalamic feedback loops than non-practitioners. Although we could not provide evidence for its mechanistic role, this greater connectivity might be related to the often reported effects of meditation and yoga on behavioral flexibility, mental health and well-being.

There is evidence of greater cognitive deficits in attention deficit hyperactivity disorder with a comorbid reading disability (ADHD/+RD) compared to ADHD alone (ADHD/−RD). Additionally, the striatum has been consistently implicated in ADHD. However, the extent of morphological alterations in the striatum of ADHD/+RD is poorly understood, which is the main purpose of this study. Based on structural MRI images, the surface deformation of the caudate and putamen was assessed in 59 boys matching in age and IQ [19 ADHD/−RD, 15 ADHD/+RD and 25 typically developing controls (TDC)]. A vertex based analysis with multiple comparison correction was conducted to compare ADHD/−RD and ADHD/+RD to TDC. Compared to TDC, ADHD/+RD showed multiple bilateral significant clusters of surface compression. In contrast, ADHD/−RD showed fewer significant clusters of surface compression and restricted to the left side. Regarding the putamen, only ADHD/−RD showed significant clusters of surface compression. Results demonstrate for the first time a greater extent of morphological alterations in the caudate of ADHD/+RD than ADHD/−RD compared to TDC, which may suggest greater implicated cortical areas projecting to the caudate that are associated with the greater neuropsychological impairments observed in ADHD/+RD. [ABSTRACT FROM AUTHOR]

The symptoms of Parkinsonism and oral dyskinesia have been showing to be induced by neuroleptics that significantly affect its clinical use. In this study, we investigate whether Nigella sativa-oil (NS) (black cumin seeds)-a traditional medicine used for the seizure treatment in eastern country-may reduce the haloperidol (HAL)-induced extrapyramidal symptoms (EPS)-like behavior in rats. After combine treatment with HAL (1 mg/kg) on NS (0.2 ml/rat), rats displayed a significant decreased EPS-like behavior including movement disorders and oral dyskinesia as compared to controls. Immunohistochemical analysis indicates that NS reduced astrogliosis in caudate and accumbens nuclei. These results suggest that NS may consider as an adjunct to antipsychotics to reduce the EPS-like side effect. [ABSTRACT FROM AUTHOR]

Although specific brain regions have been implicated in long-term memory processes, the brain function responsible for correctly recollecting information remains incompletely understood. This study used a remember-recollection-recognition task to explore brain activities specifically associated with correct recollection. Seventy-eight subjects were first asked to remember 40 items and recollect them in the scanner. Comparison of correctly recollected trials to incorrectly recollected trials (when participants mistakenly believed they had recollected information correctly) identified greater activation of the caudate bilaterally. The involvement of caudate activation appears important in recollecting information correctly. Potential explanations and implications are discussed. Hum Brain Mapp 37:3999-4005, 2016. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

The caudate nucleus is a part of the visual corticostriatal loop (VCSL), receiving input from different visual areas and projecting back to the same cortical areas via globus pallidus, substantia nigra, and thalamus. Despite perceptual and navigation impairments in patients with VCSL disruption due to caudate atrophy (e.g., Huntington's disease, HD), the relevance of the caudate nucleus and VCSL on cortical visual processing is not fully understood. In a series of fMRI experiments, we found that the caudate showed a stronger functional connection to parahippocampal place area (PPA) compared with adjacent regions (e.g., fusiform face area, FFA) within the temporal visual cortex. Consistent with this functional link, the caudate showed a higher response to scenes compared with faces, similar to the PPA. Testing the impact of VCSL disruption on neural processes within PPA, HD patients showed reduced scene-selective activity within PPA compared with healthy matched controls. In contrast, the level of selective activity in adjacent cortical and subcortical face-selective areas (i.e., FFA and amygdala) remained intact. These results show some of the first evidence for the direct impact and potential clinical significance of VCSL on the generation of "selective" activity within PPA. [ABSTRACT FROM AUTHOR]

Background Previous proton magnetic resonance spectroscopy ( 1 H MRS) studies have reported elevated glycerophosphocholine plus phosphocholine (GPC+PC) in the basal ganglia of patients with bipolar disorders (BD), which implicates an imbalance between synthesis and degradation activity of neuronal and glia membrane phospholipids (MPLs). However, the full extent of altered metabolites of MPLs in subareas within the basal ganglia, such as caudate and putamen, as well as anterior cingulate cortex (ACC) of BD patients is poorly understood. Methods Multi-voxel 1 H MRS measurements were acquired in 50 type-one BD (BD-I) and 44 healthy controls (HC) on a 3-T MRI scanner. Four different anatomically defined voxels covering ACC, caudate and putamen were systematically extracted and quantified using LCModel. Group differences in absolute GPC+PC and other metabolites were tested with age and gender as covariates. Results BD-I patients had higher GPC+PC levels in the anterior-dorsal ACC (p = 0.037), caudate (p = 0.005) and putamen (p = 0.004) compared to HC. GPC+PC levels in the caudate were elevated most significantly in currently unmediated BD-I patients (p = 0.022) and were positively correlated with HAM-D scores (r = 0.51, p = 0.005). PCr+Cr and myo-inositol levels were also significantly higher in the caudate head (F(1,45) = 6.010, p = 0.018) of patients compared to HC. NAA and glutamate levels were not significantly different between BD-I and HC in these regions (p > 0.05). Conclusion The increased GPC+PC in BD-I patients may reflect an imbalance in the MPL metabolism. Caudate GPC+PC levels may be a potential biomarker for depressive symptoms in BD. [ABSTRACT FROM AUTHOR]

The striatum is an important subcortical structure with extensive connections to other regions of the brain. These connections are believed to play important roles in behaviors such as reward-related processes and impulse control, which show significant sex differences. However, little is known about sex differences in the striatum-projected fiber connectivity. The current study examined sex differences between 50 Chinese males and 79 Chinese females in their fiber connections between the striatum and nine selected cortical and subcortical regions. Despite overall similarities, males showed stronger fiber connections between the left caudate and rostral cingulate cortex, between the right putamen and the lateral orbitofrontal cortex, between the bilateral putamen and the ventro-lateral prefrontal cortex, and between the right caudate and the ventro-lateral prefrontal cortex, whereas females showed stronger fiber connections between the right putamen and the dorsolateral prefrontal cortex, between bilateral caudate and hippocampus, and between the left putamen and hippocampus. These findings help us to understand sex differences in the striatum-projected fiber connections and their implications for sex differences in behaviors. [ABSTRACT FROM AUTHOR]

α2 adrenoreceptors (α2-ARs) play a key role in the control of noradrenaline and dopamine release in the medial prefrontal cortex (mPFC). Here, using UV-laser microdissection-based quantitative mRNA expression in individual neurons we show that in hTH-GFP rats, a transgenic line exhibiting intense and specific fluorescence in dopaminergic (DA) neurons, α2A adrenoreceptor (α2A-AR) mRNA is expressed at high and low levels in DA cells in the ventral tegmental area (VTA) and substantia nigra compacta (SNc), respectively. Confocal microscopy fluorescence immunohistochemistry revealed that α2A-AR immunoreactivity colocalized with tyrosine hydroxylase (TH) in nearly all DA cells in the VTA and SNc, both in hTH-GFP rats and their wild-type Sprague–Dawley (SD) counterparts. α2A-AR immunoreactivity was also found in DA axonal projections to the mPFC and dorsal caudate in the hTH-GFP and in the anterogradely labeled DA axonal projections from VTA to mPFC in SD rats. Importantly, the α2A-AR immunoreactivity localized in the DA cells of VTA and in their fibers in the mPFC was much higher than that in DA cells of SNc and their fibers in dorsal caudate, respectively. The finding that α2A-ARs are highly expressed in the cell bodies and axons of mesoprefrontal dopaminergic neurons provides a morphological basis to the vast functional evidence that somatodendritic and nerve-terminal α2A-AR receptors control dopaminergic activity and dopamine release in the prefrontal cortex. This finding raises the question whether α2A-ARs might function as autoreceptors in the mesoprefrontal dopaminergic neurons, replacing the lack of D2 autoreceptors. [ABSTRACT FROM AUTHOR]

Atrial natriuretic peptide (ANP) receptors are highly expressed in the amygdala, caudate and hypothalamus. GATA4 gene encodes a transcription factor of ANP associated with the pathophysiology of alcohol dependence. We have previously demonstrated that the GATA4 single nucleotide polymorphism (SNP) rs13273672 revealed stronger alcohol-specific amygdala activation associated with lowered relapse risk to heavy drinking at 90 days in the AA-homozygotes. Our understanding however with respect to GATA4 variation on gray matter (GM) regional amygdala, caudate and hypothalamus volume is limited. We investigated GM differences specific to GATA4 and hypothesized that GM alterations will be predictive of heavy relapse. Eighty-three recently detoxified alcohol dependent patients were included. Neuroimaging data was analyzed using Voxel Based Morphometry (VBM). The main effects of GM volume and genotype as well as their interaction effect on time to heavy relapse (60 and 90 days) were analyzed using cox regression. Significant higher GM volume was found for the AA-genotype group compared with AG/GG-genotype in the hypothalamus and caudate. A significant interaction was revealed between caudate and amygdala GM volume and GATA4 genotype on time to heavy relapse. The interaction was expressed by means of higher GM in the AA genotype group to be associated with reduced risk to relapse whereas in the AG/GG group higher GM was associated with increased risk to relapse. This is the first report on GM regional volume alterations specific to GATA4 genotype [(SNP) rs13273672] and its association with relapse in alcohol dependence. Current findings further support the role of GATA4 in alcoholism. [ABSTRACT FROM AUTHOR]

Background Stress triggers impulsive and addictive behaviors, and alcoholism has been frequently associated with increased stress sensitivity and impulse control problems. However, neural correlates underlying the link between alcoholism and impulsivity in the context of stress in patients with alcohol use disorders ( AUD) have not been well studied. Methods This study investigated neural correlates and connectivity patterns associated with impulse control difficulties in abstinent AUD patients. Using functional magnetic resonance imaging, brain responses of 37 AUD inpatients, and 37 demographically matched healthy controls were examined during brief individualized imagery trials of stress, alcohol cue, and neutral-relaxing conditions. Stress-related impulsivity was measured using a subscale score of impulse control problems from Difficulties in Emotion Regulation Scale. Results Impulse control difficulties in AUD patients were significantly associated with hypo-active response to stress in the ventromedial prefrontal cortex (Vm PFC), right caudate, and left lateral PFC ( LPFC) compared to the neutral condition ( p < 0.01, whole-brain corrected). These regions were used as seed regions to further examine the connectivity patterns with other brain regions. With the VmPFC seed, AUD patients showed reduced connectivity with the anterior cingulate cortex compared to controls, which are core regions of emotion regulation, suggesting AUD patients' decreased ability to modulate emotional response under distressed state. With the right caudate seed, patients showed increased connectivity with the right motor cortex, suggesting increased tendency toward habitually driven behaviors. With the left LPFC seed, decreased connectivity with the dorsomedial PFC (Dm PFC), but increased connectivity with sensory and motor cortices were found in AUD patients compared to controls ( p < 0.05, whole-brain corrected). Reduced connectivity between the left LPFC and Dm PFC was further associated with increased stress-induced anxiety in AUD patients ( p < 0.05, with adjusted Bonferroni correction). Conclusions Hypo-active response to stress and altered connectivity in key emotion regulatory regions may account for greater stress-related impulse control problems in alcoholism. [ABSTRACT FROM AUTHOR]

Objectives: To identify activation changes assessed in functional magnetic resonance imaging (fMRI) studies of obsessive–compulsive disorder (OCD) through Activation Likelihood Estimate meta-analysis. Methods: We included 28 peer-reviewed standard stereotactic space studies assessing adult OCD patients (OCDpts) vs. healthy controls (HCs) with fMRI during executive task performance. Results: In within-group analyses, HCs showed task-related activations in bilateral inferior frontal gyri, right middle frontal gyrus, right inferior parietal lobule, right claustrum, bilateral cingulate gyri, and left caudate body. OCDpts showed task-related left-sided activations in the superior, medial, and inferior frontal gyri, and thalamus, and bilateral activations in the middle frontal gyri, inferior parietal lobule, and insular cortices. Subtraction analysis showed increased left middle frontal gyrus activation in OCDpts. In between-groups analyses, OCDpts hypoactivated the right caudate body, left putamen, left ACC, and right medial and middle frontal gyri. Right caudate hypoactivation persisted also after applying Family‐wise error algorithms. Conclusions: This meta-analysis confirms that during executive functioning OCDpts show a functional deficit of the right caudate body, which could represent a major neural functional correlate of their illness. [ABSTRACT FROM AUTHOR]

Music is often used to regulate emotions and mood. Typically, music conveys and induces emotions even when one does not attend to them. Studies on the neural substrates of musical emotions have, however, only examined brain activity when subjects have focused on the emotional content of the music. Here we address with functional magnetic resonance imaging (fMRI) the neural processing of happy, sad, and fearful music with a paradigm in which 56 subjects were instructed to either classify the emotions (explicit condition) or pay attention to the number of instruments playing (implicit condition) in 4-s music clips. In the implicit vs. explicit condition, stimuli activated bilaterally the inferior parietal lobule, premotor cortex, caudate, and ventromedial frontal areas. The cortical dorsomedial prefrontal and occipital areas activated during explicit processing were those previously shown to be associated with the cognitive processing of music and emotion recognition and regulation. Moreover, happiness in music was associated with activity in the bilateral auditory cortex, left parahippocampal gyrus, and supplementary motor area, whereas the negative emotions of sadness and fear corresponded with activation of the left anterior cingulate and middle frontal gyrus and down-regulation of the orbitofrontal cortex. Our study demonstrates for the first time in healthy subjects the neural underpinnings of the implicit processing of brief musical emotions, particularly in frontoparietal, dorsolateral prefrontal, and striatal areas of the brain. [ABSTRACT FROM AUTHOR]

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective treatment for medically refractory Parkinson's disease. Although DBS has recognized clinical utility, its biologic mechanisms are not fully understood, and whether dopamine release is a potential factor in those mechanisms is in dispute. We tested the hypothesis that STN DBS-evoked dopamine release depends on the precise location of the stimulation site in the STN and the site of recording in the caudate and putamen. We conducted DBS with miniature, scaled-to-animal size, multicontact electrodes and used functional magnetic resonance imaging to identify the best dopamine recording site in the brains of nonhuman primates (rhesus macaques), which are highly representative of human brain anatomy and circuitry. Real-time stimulation-evoked dopamine release was monitored using in vivo fast-scan cyclic voltammetry. This study demonstrates that STN DBS-evoked dopamine release can be reduced or increased by redirecting STN stimulation to a slightly different site. [ABSTRACT FROM AUTHOR]

Neostriatal abnormalities can be observed in a very large number of neurological conditions clinically dominated by the presence of movement disorders. The neuroradiological picture in some cases has been described as 'bilateral striatal necrosis' (BSN). BSN represents a condition histo-pathologically defined by the involvement of the neostriata and characterized by initial swelling of putamina and caudates followed by degeneration and cellular necrosis. After the first description in 1975, numerous acquired and hereditary conditions have been associated with the presence of BSN. At the same time, a large number of disorders involving neostriata have been described as BSN, in some cases irrespective of the presence of signs of cavitation on MRI. As a consequence, the etiological spectrum and the nosographic boundaries of the syndrome have progressively become less clear. In this study, we review the clinical and radiological features of the conditions associated with MRI evidence of bilateral striatal lesions. Based on MRI findings, we have distinguished two groups of disorders: BSN and other neostriatal lesions (SL). This distinction is extremely helpful in narrowing the differential diagnosis to a small group of known conditions. The clinical picture and complementary exams will finally lead to the diagnosis. We provide an update on the etiological spectrum of BSN and propose a diagnostic flowchart for clinicians. [ABSTRACT FROM AUTHOR]

Tobacco use during later adolescence and young adulthood may cause serious neurophysiological changes; rationally, it is extremely important to study the relationship between brain dysfunction and behavioral performances in young adult smokers. Previous resting state studies investigated the neural mechanisms in smokers. Unfortunately, few studies focused on spontaneous activity differences between young adult smokers and nonsmokers from both intra-regional and inter-regional levels, less is known about the association between resting state abnormalities and behavioral deficits. Therefore, we used fractional amplitude of low frequency fluctuation (fALFF) and resting state functional connectivity (RSFC) to investigate the resting state spontaneous activity differences between young adult smokers and nonsmokers. A correlation analysis was carried out to assess the relationship between neuroimaging findings and clinical information (pack-years, cigarette dependence, age of onset and craving score) as well as cognitive control deficits measured by the Stroop task. Consistent with previous addiction findings, our results revealed the resting state abnormalities within frontostriatal circuits, i.e., enhanced spontaneous activity of the caudate and reduced functional strength between the caudate and anterior cingulate cortex (ACC) in young adult smokers. Moreover, the fALFF values of the caudate were correlated with craving and RSFC strength between the caudate and ACC was associated with the cognitive control impairments in young adult smokers. Our findings could lead to a better understanding of intrinsic functional architecture of baseline brain activity in young smokers by providing regional and brain circuit spontaneous neuronal activity properties as well as their association with cognitive control impairments. [ABSTRACT FROM AUTHOR]

Iron is an essential micronutrient for healthy brain function and development. Because of the importance of iron in the brain, iron deficiency results in widespread and lasting effects on behavior and cognition. We measured iron in the basal ganglia of young children using a novel MRI method, quantitative susceptibility mapping, and examined the association of brain iron with age and cognitive performance. Participants were a community sample of 39 young children recruited from pediatric primary care who were participating in a 5-year longitudinal study of child brain development and anxiety disorders. The children were ages 7 to 11 years old (mean age: 9.5 years old) at the time of the quantitative susceptibility mapping scan. The differential abilities scale was administered when the children were 6 years old to provide a measure of general intelligence and verbal (receptive and expressive), non-verbal, and spatial performance. Magnetic susceptibility values, which are linearly related to iron concentration in iron-rich areas, were extracted from regions of interest within iron-rich deep gray matter nuclei from the basal ganglia, including the caudate, putamen, substantia nigra, globus pallidus, and thalamus. Controlling for scan age, there was a significant positive association between iron in the basal ganglia and spatial IQ, with this effect being driven by iron in the right caudate We also replicated previous findings of a significant positive association between iron in the bilateral basal ganglia and age. Our finding of a positive association between spatial IQ and mean iron in the basal ganglia, and in the caudate specifically, suggests that iron content in specific regions of the iron-rich deep nuclei of the basal ganglia influences spatial intelligence. This provides a potential neurobiological mechanism linking deficits in spatial abilities reported in children who were severely iron deficient as infants to decreased iron within the caudate. [ABSTRACT FROM AUTHOR]

BackgroundObsessive compulsive disorder (OCD) and social anxiety disorder (SAD) are characterized by biased perception and processing of potentially threatening stimuli. A hyper-reactivity of the fear-circuit [e.g. amygdala, anterior cingulate (ACC)] has been consistently reported using functional magnetic resonance imaging (fMRI) in SAD in comparison with healthy controls (HCs). Studies investigating the processing of specific emotional stimuli in OCD reported mainly orbitofrontal-striatal abnormalities. The goal of this study was to examine similar/common and differential neurobiological responses in OCD and SAD using unspecific emotional stimuli.MethodFifty-four subjects participated: two groups (each n = 18) of outpatients with a current diagnosis of OCD or SAD, and 18 HCs. All subjects underwent fMRI while anticipating and perceiving unspecific visual stimuli with prior announced emotional valence (e.g. positive).ResultsCompared to HCs, the combined patient group showed increased activation in amygdala, caudate and prefrontal/orbitofrontal cortex while anticipating unspecific emotional stimuli. Caudate was more active in the combined patient group during perception. A comparison between the OCD and the SAD samples revealed increased amygdala and decreased rostral ACC activation in OCD patients during perception, but no differences in the anticipation phase.ConclusionsOverall, we could identify common fronto-subcortical hyper-reactivity in OCD and SAD while anticipating and perceiving unspecific emotional stimuli. While differential neurobiological responses between OCD and SAD when processing specific stimuli are evident from the literature, differences were less pronounced using unspecific stimuli. This could indicate a disturbance of emotion regulation common to both OCD and SAD. [ABSTRACT FROM PUBLISHER]

Our attitude toward risk plays a crucial role in influencing our everyday decision-making. Despite its importance, little is known about how human risk-preference can be modulated by observing risky behavior in other agents at either the behavioral or the neural level. Using fMRI combined with computational modeling of behavioral data, we show that human risk-preference can be systematically altered by the act of observing and learning from others' risk-related decisions. The contagion is driven specifically by brain regions involved in the assessment of risk: the behavioral shift is implemented via a neural representation of risk in the caudate nucleus, whereas the representations of other decision-related variables such as expected value are not affected. Furthermore, we uncover neural computations underlying learning about others' risk-preferences and describe how these signals interact with the neural representation of risk in the caudate. Updating of the belief about others' preferences is associated with neural activity in the dorsolateral prefrontal cortex (dlPFC). Functional coupling between the dlPFC and the caudate correlates with the degree of susceptibility to the contagion effect, suggesting that a frontal-subcortical loop, the so-called dorsolateral prefrontal-striatal circuit, underlies the modulation of risk-preference. Taken together, these findings provide a mechanistic account for how observation of others' risky behavior can modulate an individual's own risk-preference. [ABSTRACT FROM AUTHOR]

Background and purpose: Neuroimaging studies of relapsing--remitting multiple sclerosis (RRMS) have found structural disconnection and large-scale neural network dysfunction. However, few studies have explored the local brain activity of RRMS patients in the resting state. Patients and methods: In this study, regional homogeneity (ReHo) and resting-state functional connectivity (FC) were used to investigate intra- and interregional synchronized activity in 22 patients with RRMS and 22 matched healthy controls (HCs). Results: Compared with HCs, patients with RRMS showed significantly decreased ReHo in the left insula and right caudate. Through further seed-based FC analysis, we found decreased FC between the left insula and left precentral gyrus in patients with RRMS compared with HCs, as well as increased FC between the right caudate and right dorsolateral prefrontal cortex. Pearson's correlation analysis showed that a decreased ReHo value in the left insula was associated with an increased total white matter lesion loads (TWMLL) score (r=-0.594, P=0.004) or a worsened paced auditory serial addition test score (r=0.536, P=0.010). No other significant correlations were observed between the FC value (left insula -- left precentral gyrus) and clinical scores (P=0.246-0.982). The ReHo value of the right caudate was negatively correlated with disease duration (r=-0.526, P=0.012) and with the TWMLL score (r=-0.596, P=0.003). Moreover, a positive correlation was observed between the FC value (right caudate -- right dorsolateral prefrontal cortex) and the TWMLL score (r=0.523, P=0.012) or the modified fatigue impact scale-5 score (r=0.608, P=0.003). Conclusion: Together, these findings suggest that the insula with regional dysfunction involves disconnection with sensorimotor regions, and demyelinating lesion-related intra- and interregional dysfunction in the caudate is associated with the impact of fatigue on cognitive control functions. Abnormal synchronization of intra- and interregional activity in the insula and caudate may play important roles in the pathology of RRMS. [ABSTRACT FROM AUTHOR]

The ability to learn new tasks rapidly is a prominent characteristic of human behaviour. This ability relies on flexible cognitive systems that adapt in order to encode temporary programs for processing non-automated tasks. Previous functional imaging studies have revealed distinct roles for the lateral frontal cortices (LFCs) and the ventral striatum in intentional learning processes. However, the human LFCs are complex; they house multiple distinct sub-regions, each of which co-activates with a different functional network. It remains unclear how these LFC networks differ in their functions and how they coordinate with each other, and the ventral striatum, to support intentional learning. Here, we apply a suite of fMRI connectivity methods to determine how LFC networks activate and interact at different stages of two novel tasks, in which arbitrary stimulus-response rules are learnt either from explicit instruction or by trial-and-error. We report that the networks activate en masse and in synchrony when novel rules are being learnt from instruction. However, these networks are not homogeneous in their functions; instead, the directed connectivities between them vary asymmetrically across the learning timecourse and they disengage from the task sequentially along a rostro-caudal axis. Furthermore, when negative feedback indicates the need to switch to alternative stimulus–response rules, there is additional input to the LFC networks from the ventral striatum. These results support the hypotheses that LFC networks interact as a hierarchical system during intentional learning and that signals from the ventral striatum have a driving influence on this system when the internal program for processing the task is updated. [ABSTRACT FROM AUTHOR]

Successful social interactions depend on the ability to anticipate other people's actions. Current conceptualizations of brain function propose that causes of sensory input are inferred through their integration with internal predictions generated in the observer's motor system during action observation. Less is known concerning how action prediction changes with age. Previously we showed that internal action representations are less specific in older compared with younger adults at behavioral and neural levels. Here, we characterize how neural activity varies while healthy older adults aged 56-71 years predict the time-course of an unfolding action as well as the relation to task performance. By using fMRI, brain activity was measured while participants observed partly occluded actions and judged the temporal coherence of the action continuation that was manipulated. We found that neural activity in frontoparietal and occipitotemporal regions increased the more an action continuation was shifted backwards in time. Action continuations that were shifted towards the future preferentially engaged early visual cortices. Increasing age was associated with neural activity that extended from posterior to anterior regions in frontal and superior temporal cortices. Lower sensitivity in action prediction resulted in activity increases in the caudate. These results imply that the neural implementation of predicting actions undergoes similar changes as the neural process of executing actions in older adults. The comparison between internal predictions and sensory input seems to become less precise with age leading to difficulties in anticipating observed actions accurately, possibly due to less specific internal action models. [ABSTRACT FROM AUTHOR]

Background: Given the high level of homology between nonhuman primates and humans in regard to anatomy, physiology and ethanol drinking patterns, nonhuman primates represent an unparalleled preclinical model for examining the neurobiological basis of ethanol abuse.Methods: Here we examined the neurochemical consequences of chronic daily ethanol use using fast-scan cyclic voltammetry in brain slices containing the nucleus accumbens core or dorsolateral caudate taken from male cynomolgus macaques following ethanol drinking.Results: We found that in both regions the ability of ethanol to decrease dopamine release was unchanged, indicating that ethanol self-administration does not produce tolerance or sensitization to ethanol effects on dopamine release at the dopamine terminal at this time point. We also found that in the nucleus accumbens core, autoregulation of dopamine release was shifted from equal D2 and D3 receptor involvement in control animals to primarily D2 receptor-mediated in drinkers. Specifically, the effect quinpirole, a D2/D3 receptor agonist, on dopamine release was equal across groups; however, dopamine signals were reversed to a greater extent by the selective D3 receptor antagonist SB-277,011A in control animals, indicating a greater contribution of D2 receptors in quinpirole-induced inhibition following ethanol self-administration. In the dorsolateral caudate, the effects of quinpirole and reversal with SB-277,011A was not different between ethanol and control slices.Conclusions: This work provides novel insight into the dopaminergic adaptations resulting from chronic ethanol use in nonhuman primates and indicates that alterations in D2/D3 dopamine autoreceptor signaling may be an important neurochemical adaptation to ethanol consumption during early use. [ABSTRACT FROM AUTHOR]

Basal ganglia (BG) abnormalities are implicated in the pathophysiology of autism spectrum disorder (ASD). However, studies measuring the volume of the entire BG in individuals with ASD have reported discrepant findings, and no study conducted volume measurement of the entire substructures of the BG (the caudate, putamen, nucleus accumbens, and globus pallidus) in individuals with ASD. We delineated the BG substructures and measured their volumes in 29 adults with ASD without intellectual disabilities and 29 age- and gender-matched typically developed adult controls. We acquired T1-weighted anatomical images and performed semi-automated delineation and volume measurements of the above-mentioned subregions. Total cerebral volumes, sex, and ages were partialed out. Compared with controls, the putamen was significantly larger in the ASD group. The increased volume of the putamen found in high-functioning adults with ASD suggests that structural or histological abnormalities of the putamen may underlie the pathologies of ASD such as repetitive and stereotyped behaviors and impaired social interactions.

Having previously used functional MRI to map the response to a reward signal in the ventral caudate in awake unrestrained dogs, here we examined the importance of signal source to canine caudate activation. Hand signals representing either incipient reward or no reward were presented by a familiar human (each dog’s respective handler), an unfamiliar human, and via illustrated images of hands on a computer screen to 13 dogs undergoing voluntary fMRI. All dogs had received extensive training with the reward and no-reward signals from their handlers and with the computer images and had minimal exposure to the signals from strangers. All dogs showed differentially higher BOLD response in the ventral caudate to the reward versus no reward signals, and there was a robust effect at the group level. Further, differential response to the signal source had a highly significant interaction with a dog’s general aggressivity as measured by the C-BARQ canine personality assessment. Dogs with greater aggressivity showed a higher differential response to the reward signal versus no-reward signal presented by the unfamiliar human and computer, while dogs with lower aggressivity showed a higher differential response to the reward signal versus no-reward signal from their handler. This suggests that specific facets of canine temperament bear more strongly on the perceived reward value of relevant communication signals than does reinforcement history, as each of the dogs were reinforced similarly for each signal, regardless of the source (familiar human, unfamiliar human, or computer). A group-level psychophysiological interaction (PPI) connectivity analysis showed increased functional coupling between the caudate and a region of cortex associated with visual discrimination and learning on reward versus no-reward trials. Our findings emphasize the sensitivity of the domestic dog to human social interaction, and may have other implications and applications pertinent to the training and assessment of working and pet dogs.