Bilateral Posterior Cingulate Cortex Research Articles

Potential correlations between asymmetric disruption of functional connectivity and metabolism in major depressive disorder

ObjectivePrevious research has suggested a connection between major depressive disorder (MDD) and certain comorbidities, including gastrointestinal issues, thyroid dysfunctions, and glycolipid metabolism abnormalities. However, the relationships between these factors and asymmetrical alterations in functional connectivity (FC) in adults with MDD remain unclear. MethodWe conducted a study on a cohort of 42 MDD patients and 42 healthy controls (HCs). Participants underwent comprehensive clinical assessments, including evaluations of blood lipids and thyroid hormone levels, as well as resting-state functional magnetic resonance imaging (Rs-fMRI) scans. Data analysis involved correlation analysis to compute the parameter of asymmetry (PAS) for the entire brain's functional connectome. We then examined the interrelationships between abnormal PAS regions in the brain, thyroid hormone levels, and blood lipid levels. ResultsThe third-generation ultra-sensitive thyroid stimulating hormone (TSH3UL) level was found to be significantly lower in MDD patients compared to HCs. The PAS score of the left inferior frontal gyrus (IFG) decreased, while the bilateral posterior cingulate cortex (Bi-PCC) PAS increased in MDD patients relative to HCs. Notably, the PAS score of the left IFG negatively correlated with both TSH and total cholesterol (CHOL) levels. However, these correlations lose significance after the Bonferroni correction. ConclusionMDD patients demonstrated abnormal asymmetry in resting-state FC (Rs-FC) within the fronto-limbic system, which may be associated with CHOL and thyroid hormone levels.

Functionality of arousal-regulating brain circuitry at rest predicts human cognitive abilities.

Arousal state is regulated by subcortical neuromodulatory nuclei, such as locus coeruleus, which send wide-reaching projections to cortex. Whether higher-order cortical regions have the capacity to recruit neuromodulatory systems to aid cognition is unclear. Here, we hypothesized that select cortical regions activate the arousal system, which, in turn, modulates large-scale brain activity, creating a functional circuit predicting cognitive ability. We utilized the Human Connectome Project 7T functional magnetic resonance imaging dataset (n = 149), acquired at rest with simultaneous eye tracking, along with extensive cognitive assessment for each subject. First, we discovered select frontoparietal cortical regions that drive large-scale spontaneous brain activity specifically via engaging the arousal system. Second, we show that the functionality of the arousal circuit driven by bilateral posterior cingulate cortex (associated with the default mode network) predicts subjects' cognitive abilities. This suggests that a cortical region that is typically associated with self-referential processing supports cognition by regulating the arousal system.

Brain functional connectivity patterns associated with symptoms of vestibular migraine.

Several functional magnetic resonance imaging (fMRI) investigations of patients with vestibular migraine (VM) have revealed abnormal functionality in different networks, indicating that VM is related to alterations in brain function. We sought to investigate the resting-state functional connectivity (FC) patterns during the interictal period in VM by combining data-driven voxel-wise degree centrality (DC) calculations and seed-based FC analyses, and thereby determine the associations between cerebral function and clinical symptoms. Thirty-eight patients with VM and 33 matched normal controls were recruited. DC was calculated and compared between the groups, and the FC of locations showing DC alterations was further tested using a seed-based technique. The participants' clinical indicators were correlated with the DC and FC values of the brain areas. In contrast to the control group, the VM group showed considerably lower DC values in the bilateral medial prefrontal cortex (mPFC) and significantly higher DC values in the right occipital lobe. In the seed-based FC analyses, patients with VM demonstrated fewer connections of the bilateral mPFC with the bilateral posterior cingulate cortex, right parahippocampus, right cerebellar posterior lobe, bilateral cuneus, and left precuneus. In addition, clinical data from patients, such as pain intensity, episode frequency, and the Dizziness Handicap Inventory score, were negatively related to these FC and DC impairments. Our findings showed changes in the default mode network and visual cortex in patients with VM, providing further insights into the complexity of the mechanisms underlying VM.

Within‐network changes in strength of the default mode network relate to Alzheimer’s Disease biomarkers in APOE e4 carriers

AbstractBackgroundResting state functional connectivity measured with MRI (rsfMRI) is disrupted in Alzheimer’s Disease (AD), although reports of rsfMRI changes in adults with the apolipoprotein E (APOE) ε4 genotype (e4+) have been inconsistent. Here, we compare default mode network (DMN) connectivity between e4+ and non‐carriers (e4‐) groups and assess the relationship to AD‐related biomarkers.MethodSixty‐five e4+ (mean age 70.2 ± 4.1; 33 males) and 60 e4‐ (mean age 71.9 ± 4.1; 28 males) subjects underwent a whole‐brain anatomical MPRAGE and a rsfMRI scan. To focus on the DMN, ROIs were placed in the bilateral posterior cingulate cortex (PCC). The most highly correlated voxels between the left and right PCC ROIs were used to calculate left and right PCC rsfMRI z‐maps. Group differences were assessed and mean connectivity in each significant region was correlated with Aβ PET centiloid values and cerebrospinal fluid (CSF) Aβ42/ Aβ40 ratio, phosphorylated‐tau (p‐tau 181), and total‐tau (t‐tau).ResultEight regions showed group differences (p < 0.05; Figure 1). In the e4+ group, right PCC connectivity to the bilateral anterior middle temporal gyri (Figure 1: ROIs 1 and 2) was negatively related to both centiloid score (p < 0.03) and to CSF p‐tau (p < 0.008; Figure 2). Left PCC connectivity to the right anterior middle temporal gyrus was negatively related to centiloid score (r = ‐0.26, p < 0.042) and CSF p‐tau (r = ‐0.31, p < 0.024). Biomarker values in the e4‐ group were not significantly related to connectivity.ConclusionOur findings are consistent with reports of weakened DMN connectivity in e4+ adults and suggest that differences in connectivity strength may be mediated by amyloid or tau deposition.This work was supported by the National Institutes of Health (R01AG022304).

Structural connectome-based predictive modeling of cognitive deficits in treated glioma patients.

In glioma patients, tumor growth and subsequent treatments are associated with various types of brain lesions. We hypothesized that cognitive functioning in these patients critically depends on the maintained structural connectivity of multiple brain networks. The study included 121 glioma patients (median age, 52 years; median Eastern Cooperative Oncology Group performance score 1; CNS-WHO Grade 3 or 4) after multimodal therapy. Cognitive performance was assessed by 10 tests in 5 cognitive domains at a median of 14 months after treatment initiation. Hybrid amino acid PET/MRI using the tracer O-(2-[18F]fluoroethyl)-L-tyrosine, a network-based cortical parcellation, and advanced tractography were used to generate whole-brain fiber count-weighted connectivity matrices. The matrices were applied to a cross-validated machine-learning model to identify predictive fiber connections (edges), critical cortical regions (nodes), and the networks underlying cognitive performance. Compared to healthy controls (n = 121), patients' cognitive scores were significantly lower in 9 cognitive tests. The models predicted the scores of 7/10 tests (median correlation coefficient, 0.47; range, 0.39-0.57) from 0.6% to 5.4% of the matrix entries; 84% of the predictive edges were between nodes of different networks. Critically involved cortical regions (≥10 adjacent edges) included predominantly left-sided nodes of the visual, somatomotor, dorsal/ventral attention, and default mode networks. Highly critical nodes (≥15 edges) included the default mode network's left temporal and bilateral posterior cingulate cortex. These results suggest that the cognitive performance of pretreated glioma patients is strongly related to structural connectivity between multiple brain networks and depends on the integrity of known network hubs also involved in other neurological disorders.

NCOG-04. WHOLE-BRAIN STRUCTURAL CONNECTIVITY PREDICTS COGNITIVE DEFICITS IN PRETREATED PATIENTS WITH CNS WHO GRADE 3 OR 4 GLIOMAS

Abstract BACKGROUND Glioma patients frequently suffer from cognitive dysfunction potentially caused by tumor invasion or treatment effects. We hypothesized that cognitive functioning in pretreated glioma patients critically depends on the maintained structural connectivity of multiple brain networks. PATIENTS AND METHODS The study included 121 pretreated glioma patients (median age, 52 years; median ECOG score, 1; CNS WHO grade, 3 or 4) who had biopsy or resection plus chemoradiation as first-line therapy. Cognitive performance was assessed by ten tests in five main cognitive domains after a median time of 14 months (range, 1-214 months) after treatment initiation. Hybrid amino acid PET/MRI using the tracer O-(2-[18F]fluoroethyl)-L-tyrosine, a network-based cortical parcellation, and advanced tractography tools were used to generate whole-brain fiber count-weighted connectivity matrices. These matrices were applied to a machine learning-based model to identify predictive fiber connections, essential cortical nodes, and the networks underlying cognitive performance in the evaluated domains. RESULTS Compared to healthy controls (n=121), the cognitive scores were significantly lower in nine cognitive tests. For each test, a subset of connections between nodes (median number, 254; range, 32-542) was identified whose fiber count sum was related to the actual scores in a linear model (median R2, 0.37; range, 0.16-0.44). Leave-one-out cross-validation confirmed the model's generalizability in 7 of 10 tests (median correlation coefficient for predicted vs. observed scores, 0.47; range, 0.39-0.57). Critically involved cortical regions (≥ 10 adjacent predictive edges) included predominantly left-sided cortical nodes of the visual, somatomotor, dorsal/ventral attention, and default mode networks. Highly critical nodes (≥ 15-20 edges) included the default-mode network’s left temporal and bilateral posterior cingulate cortex. CONCLUSION These results suggest that the cognitive performance of pretreated glioma patients is strongly related to structural connectivity between multiple brain networks and depends on the integrity of known network hubs also involved in other neurological disorders.

Altered connectivity in the cognitive control-related prefrontal cortex in Parkinson's disease with rapid eye movement sleep behavior disorder.

Rapid eye movement sleep behavior disorder (RBD) frequently occurs in Parkinson's disease (PD), however, the exact pathophysiological mechanism is not clear. The prefrontal cortex (PFC), especially ventrolateral prefrontal cortex (VLPFC), dorsolateral prefrontal cortex (DLPFC), and inferior frontal gyrus (IFG) which may play roles by regulating cognitive control processes. The purpose of this study was to investigate whether there is abnormal functional connectivity (FC) maps and volume changes in PD with RBD(PD-RBD). We recruited 20 PD-RBD, 20 PD without RBD (PD-nRBD), and 20 normal controls (NC). We utilized resting-state functional Magnetic Resonance Imaging (rs-MRI) to explore FC changes based on regions of interest (VLPFC, DLPFC, and IFG), and used voxel-based morphology technology to analyze whole-brain volumes by 3D-T1 structural MRI. Except the REM sleep behavioral disorders questionnaire (RBDSQ), the PD-RBD showed lower visuospatial/executive and attention scores than the NC group. The RBDSQ scores were significantly positively correlated with zFC of right DLPFC to bilateral posterior cingulate cortex (PCC) (P = 0.0362, R = 0.4708, AlphaSim corrected) and also significantly positively correlated with zFC of left VLPFC to right inferior temporal (P = 0.0157, R = 0.5323, AlphaSim corrected) in PD-RBD group. Furthermore, abnormal correlations with zFC values were also found in some cognitive subdomains in PD-RBD group. The study may suggest that in PD-RBD patients, the presence of RBD may be related to the abnormal FC of VLPFC and DLPFC, meanwhile, the abnormal FC of DLPFC and IFG may be related to the mechanisms of cognitive impairment.

P01.02.A WHOLE-BRAIN STRUCTURAL CONNECTIVITY PREDICTS COGNITIVE OUTCOMES IN PRETREATED PATIENTS WITH WHO GRADE 3 OR 4 GLIOMAS

Abstract BACKGROUND Glioma patients frequently suffer from cognitive dysfunction potentially related to brain damage caused by tumor invasion or therapeutic intervention. We hypothesized that, as in other neurological disorders, the long-term outcome of cognitive functions in glioma patients critically depends on maintaining the structural connectivity of multiple interconnected networks. PATIENTS AND METHODS One hundred and twenty-one glioma patients (median age, 52 years; median ECOG score, 1) with histomolecularly characterized CNS WHO grade 3 or 4 gliomas were investigated after a median time of 14 months (range, 1-214 months) following first-line therapy, including resection and chemoradiation with alkylating agents. Hybrid amino acid PET/MR imaging using the tracer O-(2-[18F]fluoroethyl)-L-tyrosine, a brain-networks-based cortical parcellation into nodes, and advanced fiber tractography tools were used for constructing fiber-count-weighted connectivity matrices. Cognitive performance was measured by ten different tests concerning various cognitive domains. The connectivity matrices and the patients' test scores were applied to a machine learning-based model that identified critical fiber connections, cortical nodes, and involved networks for predicting cognitive performance in the assessed domains. RESULTS Compared to a matched cohort of healthy subjects, the cognitive scores of the patients were significantly lower in 9 of 10 cognitive tests. The most affected domains were executive function/concept-shifting (-72%), attention/processing speed (relative performance, -53%), followed by semantic word fluency (-25%), verbal working and semantic memory (-8 and -22%, respectively), and visual working memory (-11 to -20%). For each cognitive test, a subset of connections (median number, 254; range, 32-542) was identified whose fiber count sum showed a correlation with the actual scores in a linear model (median R2, 0.37; range, 0.16-0.44). Leave-one-out cross-validation confirmed the model's generalizability in 7 of 10 tests (median correlation coefficient for predicted compared to observed scores, 0.47; range 0.39-0.57). The distribution of critical cortical regions (node degree of ≥ 5 predictive edges), found in 90% of the cross-validation iterations, varied considerably between domains. These included predominantly left-sided cortical nodes of the visual, somatomotor, dorsal/ventral attention, and default mode networks. Highly critical nodes (degree of 15-20 predictive edges) included the default-mode network’s left temporal and bilateral posterior cingulate cortex. CONCLUSION These results suggest that the cognitive performance of pretreated glioma patients is strongly related to the structural connectivity within multiple brain networks and depends on the integrity of known network hubs.

Neurobiological and genetic correlates of the dissociative subtype of posttraumatic stress disorder.

Approximately 10%-30% of individuals with posttraumatic stress disorder (PTSD) exhibit a dissociative subtype of the condition defined by symptoms of depersonalization and derealization. This study examined the psychometric evidence for the dissociative subtype of PTSD in a sample of young, primarily male post-9/11-era Veterans (n = 374 at baseline and n = 163 at follow-up) and evaluated its biological correlates with respect to resting state functional connectivity (default mode network [DMN]; n = 275), brain morphology (hippocampal subfield volume and cortical thickness; n = 280), neurocognitive functioning (n = 337), and genetic variation (n = 193). Multivariate analyses of PTSD and dissociation items suggested a class structure was superior to dimensional and hybrid ones, with 7.5% of the sample comprising the dissociative class; this group showed stability over 1.5 years. Covarying for age, sex, and PTSD severity, linear regression models revealed that derealization/depersonalization severity was associated with: decreased DMN connectivity between bilateral posterior cingulate cortex and right isthmus (p = .015; adjusted-p [padj] = .097); increased bilateral whole hippocampal, hippocampal head, and molecular layer head volume (p = .010-.034; padj = .032-.053); worse self-monitoring (p = .018; padj = .079); and a candidate genetic variant (rs263232) in the adenylyl cyclase 8 gene (p = .026), previously associated with dissociation. Results converged on biological structures and systems implicated in sensory integration, the neural representation of spatial awareness, and stress-related spatial learning and memory, suggesting possible mechanisms underlying the dissociative subtype of PTSD. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Associations of bullying perpetration and peer victimization subtypes with preadolescent’s suicidality, non-suicidal self-injury, neurocognition, and brain development

BackgroundAlthough both peer victimization and bullying perpetration negatively impact preadolescents’ development, the underlying neurobiological mechanism of this adverse relationship remains unclear. Besides, the specific psycho-cognitive patterns of different bullying subtypes also need further exploration, warranting large-scale studies on both general bullying and specific bullying subtypes.MethodsWe adopted a retrospective methodology by utilizing the data from the Adolescent Brain and Cognitive DevelopmentSM Study (ABCD Study®) cohort collected between July 2018 and January 2021. Participants were preadolescents aged from 10 to 13 years. The main purpose of our study is to examine the associations of general and specific peer victimization/bullying perpetration with preadolescents’ (1) suicidality and non-suicidal self-injury; (2) executive function and memory, including attention inhibition, processing speed, emotion working memory, and episodic memory; (3) brain structure abnormalities; and (4) brain network disturbances. Age, sex, race/ethnicity, body mass index (BMI), socioeconomic status (SES), and data acquisition site were included as covariates.ResultsA total of 5819 participants aged from 10 to 13 years were included in this study. Higher risks of suicide ideation, suicide attempt, and non-suicidal self-injury were found to be associated with both bullying perpetration/peer victimization and their subtypes (i.e., overt, relational, and reputational). Meanwhile, poor episodic memory was shown to be associated with general victimization. As for perpetration, across all four tasks, significant positive associations of relational perpetration with executive function and episodic memory consistently manifested, yet opposite patterns were shown in overt perpetration. Notably, distinct psycho-cognitive patterns were shown among different subtypes. Additionally, victimization was associated with structural brain abnormalities in the bilateral paracentral and posterior cingulate cortex. Furthermore, victimization was associated with brain network disturbances between default mode network and dorsal attention network, between default mode network and fronto-parietal network, and ventral attention network related connectivities, including default mode network, dorsal attention network, cingulo-opercular network, cingulo-parietal network, and sensorimotor hand network. Perpetration was also associated with brain network disturbances between the attention network and the sensorimotor hand network.ConclusionsOur findings offered new evidence for the literature landscape by emphasizing the associations of bullying experiences with preadolescents’ clinical characteristics and cognitive functions, while distinctive psycho-cognitive patterns were shown among different subtypes. Additionally, there is evidence that these associations are related to neurocognitive brain networks involved in attention control and episodic retrieval. Given our findings, future interventions targeting ameliorating the deleterious effect of bullying experiences on preadolescents should consider their subtypes and utilize an ecosystemic approach involving all responsible parties.

Aberrant functional connectivity of the bed nucleus of the stria terminalis and its age dependence in children and adolescents with social anxiety disorder.

Social anxiety disorder (SAD) is a prevalent and impairing mental disorder among children and adolescents. The bed nucleus of the stria terminalis (BNST) plays a critical role in anxiety disorders, including valence surveillance and hypervigilance for potential threats. However, the role of BNST and its related functional network in children and adolescents with SAD has not been fully investigated. This study examined the aberration of BNST's functional connectivity and its age dependence in adolescents with SAD. Using a sample of 75 SAD patients and 75 healthy controls (HCs) children aged 9-18 years old, we delineated the group-by-age interaction of BNST-seeded functional connectivity (FC) during resting state and movie-watching. The relationships between BNST-seeded FC and clinical scores were also examined. During movie viewing, the FC between the right BNST and the left amygdala, bilateral posterior cingulate cortex (PCC), bilateral superior temporal cortex, and right pericalcarine cortex showed a diagnostic group-by-age interaction. Compared to HCs, SAD patients showed a significant enhancement of the above FC at younger ages. Meanwhile, they showed an age-dependent decrease in FC between the right BNST and left amygdala. Furthermore, for SAD patients, FC between the right BNST and left amygdala during movie viewing was positively correlated with separation anxiety scores. The right BNST plays an essential role in the aberrant brain functioning in children and adolescents with SAD. The atypicality of BNST's FC has remarkable age dependence in SAD, suggesting an association of SAD with neurodevelopmental traits.

Electroacupuncture for psychogenic erectile dysfunction: A resting-state functional magnetic resonance imaging study exploring the alteration of fractional amplitude of low frequency fluctuation.

Psychogenic erectile dysfunction (PED) can seriously affect emotional and marital wellbeing. Electroacupuncture (EA) seems an effective method for treating PED. However, the central mechanisms underlying PED and the beneficial effects of EA treatment are unclear. The purpose of this study was to explore the central mechanisms of PED and to examine the impact of EA on erectile function. We recruited 14 PED patients and 14 matched normal controls (NCs). PED patients underwent twice rs-fMRI scans, respectively, pre- and post-treatment. The NCs only completed one rs-fMRI scan. We used the fractional amplitude of low frequency fluctuation (fALFF) to compare spontaneous neural activity between the PED patients and NCs, and to examine the differences between the pre- and post-EA treatment scans in the PED patients. Scores on the IIEF5, QEQ, and SEAR improved after EA treatment. Compared with the NCs, PED patients showed increased fALFF in the right posterior cingulate cortex (PCC), right dorsolateral prefrontal cortex (DLPFC), right supplementary motor area (SMA), and left middle occipital gyrus. Most of these regions are closely implicated in sexual inhibition. The results of the correlation analysis results indicated that the fALFF of the right PCC was negatively correlated with IIEF5 scores. After treatment, fALFF values were substantially lower in the left triangular part of the inferior frontal gyrus, right DLPFC, right SMA, bilateral PCC and the orbital part of the middle frontal gyrus, and higher in the left middle temporal gyrus and left caudate nucleus. These regions mainly belong to the default mode network (DMN), executive control network and primary sensory motor network. The results of the correlation analysis indicated a positive association between the changes in IIEF5 score and changes in the fALFF value in the right PCC after EA treatment. In conclusion, our study highlights that PED patients have abnormal patterns of activity in the right PCC, right DLPFC, and right SMA mainly involved in the DMN, executive central network, and sensory motor network which could lead to a higher levels of sexual inhibition. EA might regulate the process of sexual inhibition to improve erection function in PED patients probably by modulating spontaneous brain activity in the DMN, executive central network, and sensory motor network.

Treatment response with ketamine in chronic suicidality: An open label functional connectivity study

BackgroundKetamine has recently been proposed as a treatment option for suicidality. Whilst its mechanism of action has been explored at molecular levels, the effect on the brain at the organ level remains unclear. Here we investigate immediate post-treatment and prolonged large-scale resting-state neural network changes to elucidate the neuronal underpinnings associated with ketamine's therapeutic effects. MethodsTwenty-eight adults (aged 22–72 years) participated in the Oral Ketamine Trial On Suicidality, which is an open-label trial of weekly sub-anaesthetic doses of oral ketamine over 6 weeks. MRI was acquired at baseline, post-treatment, and follow-up. Functional connectivity changes at post-treatment and follow-up were examined using seed based and independent component analysis. ResultsThe seed-based connectivity analysis revealed significantly reduced connectivity at post-treatment from the right hippocampus to both right and left superior frontal gyrus, from the left anterior parahippocampus to right superior frontal gyrus, left superior frontal gyrus, right middle frontal gyrus, and left frontal operculum cortex. Compared with baseline, the ICA showed reduced anterior default mode network connectivities to bilateral posterior cingulate cortex, middle and anterior cingulate cortex, lingual gyrus, and cuneus and increased connectivity of the frontoparietal network to the right superior parietal lobule at post-treatment. LimitationsOpen label pilot study. ConclusionsWe have shown sub-anaesthetic doses of ketamine alters connectivity in networks which have been shown to be aberrantly hyper-connected in numerous psychiatric conditions. These neurocircuitry changes are supported by significant reductions in suicide ideation. Our results provide support for the use of ketamine as a treatment for suicidality.

Right posterior hypometabolism in Pisa syndrome of Parkinson’s disease: A key to explain body schema perception deficit?

BackgroundPisa syndrome (PS) is a trunk postural abnormality in Parkinson's disease (PD). Its pathophysiology is still debated: peripheral and central mechanisms have been hypothesized. ObjectiveTo investigate the role of nigrostriatal dopaminergic deafferentation and of brain metabolism impairment in the onset PS in PD patients. MethodsWe retrospectively selected 34 PD patients who developed PS (PS+) and who had previously undergone dopamine transporter (DaT)-SPECT and/or brain F-18 fluorodeoxyglucose PET (FDG-PET). PS + patients were divided considering leaning body side in left ((l)PS+) or right ((r)PS+). DaT-SPECT specific-to-non-displaceable binding ratio (SBR) of striatal regions (BasGan V2 software) were compared between 30 PS+ and 60 PD patients without PS (PS-) as well as between 16 (l)PS+ and 14 (r)PS + patients. Voxel-based analysis (SPM12) was used to compare FDG-PET among 22 PS+, 22 PS- and 42 healthy controls (HC) and between 9 (r)PS+ and 13 (l)PS+. ResultsNo significant DaT-SPECT SBR differences were found between PS+ and PS- groups or between (r)PD+ and (l)PS + subgroups. Compared to HC, significant hypometabolism in PS+ was found in bilateral temporal-parietal regions, mainly in the right hemisphere, whereas the right Brodmann area 39 (BA39) was relatively hypometabolic both in the (r)PS+ and in the (l)PS+. BA39 and bilateral posterior cingulate cortex were significantly hypometabolic in PS + than in PS- group. ConclusionsAs a hub of the network supervising the body schema perception, the involvement of the right posterior hypometabolism supports the hypothesis PS is a result of a somatosensory perceptive deficit rather than a nigrostriatal dopaminergic unbalance.

Alternations of neuromagnetic activity across neurocognitive core networks among benign childhood epilepsy with centrotemporal spikes: A multi-frequency MEG study.

We aimed to investigate the alternations of neuromagnetic activity across neurocognitive core networks among early untreated children having benign childhood epilepsy with centrotemporal spikes (BECTS). We recorded the Magnetoencephalography (MEG) resting-state data from 48 untreated children having BECTS and 24 healthy children. The fourth edition of the Wechsler Intelligence Scale for Children (WISC-IV) was utilized to divide the children with BECTS into two groups: the cognitive impairment (CI) group with a full-scale intelligence quotient (FSIQ) of < 90 and the cognitive non-impairment (CNI) group with an FSIQ of > 90. We selected 26 bilateral cognitive-related regions of interest based on the triple network model. The neurocognitive core network spectral power was estimated using a minimum norm estimate (MNE). In the CNI group, the spectral power inside the bilateral anterior cingulate cortex (ACC) and the bilateral caudal middle frontal cortex (CMF) enhanced within the delta band and reduced within the alpha band. Both the CI and the CNI group demonstrated enhanced spectral power inside the bilateral posterior cingulate cortex (PCC), bilateral precuneus (PCu) region, bilateral superior and middle temporal cortex, bilateral inferior parietal lobe (IPL), and bilateral supramarginal cortex (SM) region in the delta band. Moreover, there was decreased spectral power in the alpha band. In addition, there were consistent changes in the high-frequency spectrum (> 90 Hz). The spectral power density within the insula cortex (IC), superior temporal cortex (ST), middle temporal cortex (MT), and parahippocampal cortex (PaH) also decreased. Therefore, studying high-frequency activity could lead to a new understanding of the pathogenesis of BECTS. The alternations of spectral power among neurocognitive core networks could account for CI among early untreated children having BECTS. The dynamic properties of spectral power in different frequency bands could behave as biomarkers for diagnosing new BECTS.

Functional Connectivity Changes in the Insular Subregions of Patients with Obstructive Sleep Apnea after 6 Months of Continuous Positive Airway Pressure Treatment.

This study was aimed at investigating the functional connectivity (FC) changes between the insular subregions and whole brain in patients with obstructive sleep apnea (OSA) after 6 months of continuous positive airway pressure (CPAP) treatment and at exploring the relationship between resting-state FC changes and cognitive impairment in OSA patients. Data from 15 patients with OSA before and after 6 months of CPAP treatment were included in this study. The FC between the insular subregions and whole brain was compared between baseline and after 6 months of CPAP treatment in OSA. After 6 months of treatment, OSA patients had increased FC from the right ventral anterior insula to the bilateral superior frontal gyrus and bilateral middle frontal gyrus and increased FC from the left posterior insula to the left middle temporal gyrus and left inferior temporal gyrus. Hyperconnectivity was found from the right posterior insula to the right middle temporal gyrus, bilateral precuneus, and bilateral posterior cingulate cortex, which mainly involved the default mode network. There are changes in functional connectivity patterns between the insular subregions and whole brain in OSA patients after 6 months of CPAP treatment. These changes provide a better understanding of the neuroimaging mechanisms underlying the improvement in cognitive function and emotional impairment in OSA patients and can be used as potential biomarkers for clinical CPAP treatment.

Transcranial direct current stimulation (tDCS) in depression induces structural plasticity

Transcranial direct current stimulation (tDCS) is a non-invasive neuromodulation technique involving administration of well-tolerated electrical current to the brain through scalp electrodes. TDCS may improve symptoms in neuropsychiatric disorders, but mixed results from recent clinical trials underscore the need to demonstrate that tDCS can modulate clinically relevant brain systems over time in patients. Here, we analyzed longitudinal structural MRI data from a randomized, double-blind, parallel-design clinical trial in depression (NCT03556124, N = 59) to investigate whether serial tDCS individually targeted to the left dorso-lateral prefrontal cortex (DLPFC) can induce neurostructural changes. Significant (FWEc p < 0.05) treatment-related gray matter changes were observed with active high-definition (HD) tDCS relative to sham tDCS within the left DLPFC stimulation target. No changes were observed with active conventional tDCS. A follow-up analysis within individual treatment groups revealed significant gray matter increases with active HD-tDCS in brain regions functionally connected with the stimulation target, including the bilateral DLPFC, bilateral posterior cingulate cortex, subgenual anterior cingulate cortex, and the right hippocampus, thalamus and left caudate brain regions. Integrity of blinding was verified, no significant differences in stimulation-related discomfort were observed between treatment groups, and tDCS treatments were not augmented by any other adjunct treatments. Overall, these results demonstrate that serial HD-tDCS leads to neurostructural changes at a predetermined brain target in depression and suggest that such plasticity effects may propagate over brain networks.

Neural correlates of mental time travel in individuals with high level of schizotypy

BackgroundMental time travel (MTT) is the ability to re-experience past events (autobiographic memory, AM) and pre-experience possible future events (episodic future thinking, EFT) through mental simulation. Empirical findings suggest that individuals with high level of schizotypy exhibit MTT impairment. However, the neural correlates of this impairment remain unclear. MethodThirty-eight individuals with high level of schizotypy and 35 low level of schizotypy were recruited to complete an MTT imaging paradigm. Participants were required to recall past events (AM condition), imagine possible future events (EFT condition) related to cue words, or generate exemplars related to category words (control condition) while undergoing functional Magnetic Resonance Imaging (fMRI). ResultsAM showed greater activation in precuneus, bilateral posterior cingulate cortex, thalamus, and middle frontal gyrus than EFT. Individuals with high level of schizotypy exhibited reduced activation in the left anterior cingulate cortex during AM (vs. Control) and in the medial frontal gyrus during EFT (vs. Control) compared to individuals with low level of schizotypy. Although psychophysiological interaction analyses did not show any significant group difference, individuals with high level of schizotypy exhibited functional connectivity between left anterior cingulate cortex (seed) and right thalamus, between medial frontal gyrus (seed) and left cerebellum during MTT, whereas individuals with low level of schizotypy did not exhibit these functional connectivities. ConclusionThese findings suggest that decreased brain activations may underlie MTT deficits in individuals with high level of schizotypy.

Remodeling of the brain correlates with gait instability in cervical spondylotic myelopathy.

Cervical spondylotic myelopathy (CSM) is a common form of non-traumatic spinal cord injury (SCI) and usually leads to remodeling of the brain and spinal cord. In CSM with gait instability, the remodeling of the brain and cervical spinal cord is unclear. We attempted to explore the remodeling of these patients' brains and spinal cords, as well as the relationship between the remodeling of the brain and spinal cord and gait instability. According to the CSM patients' gait, we divided patients into two groups: normal gait patients (nPT) and abnormal gait patients (aPT). Voxel-wise z-score transformation amplitude of low-frequency fluctuations (zALFF) and resting-state functional connectivity (rs-FC) were performed for estimating brain changes. Cross-sectional area (CSA) and fractional anisotropy (FA) of the spinal cord were computed by Spinal cord toolbox. Correlations of these measures and the modified Japanese Orthopedic Association (mJOA) score were analyzed. We found that the zALFF of caudate nucleus in aPT was higher than that in healthy controls (HC) and lower than that in nPT. The zALFF of the right postcentral gyrus and paracentral lobule in HC was higher than those of aPT and nPT. Compared with the nPT, the aPT showed increased functional connectivity between the caudate nucleus and left angular gyrus, bilateral precuneus and bilateral posterior cingulate cortex (PCC), which constitute a vital section of the default mode network (DMN). No significantly different FA values or CSA of spinal tracts at the C2 level were observed between the HC, nPT and aPT groups. In CSM, the right paracentral lobule's zALFF was negatively correlated with the FA value of fasciculus gracilis (FCG), and the right caudate zALFF was positively correlated with the FA value of the fasciculus cuneatus (FCC). The results showed that the functional connectivity between the right caudate nucleus and DMN was negatively correlated with the CSA of the lateral corticospinal tract (CST). The activation of the caudate nucleus and the strengthening functional connectivity between the caudate nucleus and DMN were associated with gait instability in CSM patients. Correlations between spinal cord and brain function might be related to the clinical symptoms in CSM.

Alterations of Spontaneous Cortical and Subcortical Activity in Type 2 Diabetes Mellitus with and without Depression

Introduction: Type 2 diabetes mellitus (T2DM) patients with depression have a higher risk of complications and mortality than T2DM without depression. However, the exact neuropathophysiological mechanism remains unclear. Consequently, the current study aimed to investigate the alteration of cortical and subcortical spontaneous neural activity in T2DM patients with and without depression. Methods: The demographic data, clinical variables, neuropsychological tests, and functional and anatomical magnetic resonance imaging of depressed T2DM (n = 47) of non-depressed T2DM (n = 59) and healthy controls (n = 41) were collected and evaluated. The correlation analysis, stepwise multiple linear regression, and receiver operating characteristic curve were performed for further analysis. Results: Abnormal neural activities in the bilateral posterior cingulate cortex (PCC) and hippocampus were observed in depressed and non-depressed T2DM and the right putamen of the depressed T2DM. Interestingly, the subcortical degree centrality (DC) of the right hippocampus and putamen were higher in depressed than non-depressed T2DM. Furthermore, the cortical amplitude of low-frequency fluctuation (ALFF) in PCC, subcortical DC in the putamen of depressed T2DM, and hippocampus of non-depressed T2DM was correlated with cognitive scores. In contrast, the cortical fractional ALFF in PCC of non-depressed T2DM was correlated with depression scores. Conclusions: The abnormalities of spontaneous cortical activity in PCC and subcortical activity in the hippocampus might represent the neurobiological feature of cerebral dysfunction in T2DM. Notably, the altered subcortical activity in the right putamen might mainly associate with negative emotion in T2DM, which could be a promising biomarker for recognizing early cerebral dysfunction in depressed T2DM. This study provided a novel insight into the neuropathophysiological mechanism of brain dysfunction in T2DM with and without depression.