Abnormal effective connectivity of reward network in first-episode schizophrenia with auditory verbal hallucinations.

OBJECTIVE: Auditory verbal hallucinations (AVHs) in schizophrenia is proved to be associated with dysfunction of mesolimbic-cortical circuits, especially during abnormal salient and internal verbal resource monitoring processing procedures. However, the information flow among areas involved in coordinated interaction implicated the pathophysiology of AVHs remains unclear. METHODS: We used spectral dynamic causal modeling (DCM) to quantify connections among eight critical hubs of reward network in 86 first-episode drug-naïve schizophrenia patients with AVHs (AVH), 93 patients without AVHs (NAVH), and 88 matched normal controls (NC) using resting-state functional magnetic resonance imaging. Group-level connection coefficients, between-group differences and correlation analysis between image measures and symptoms were performed. RESULT: DCM revealed weaker effective connectivity (EC) from right ventral striatum (RVS) to ventral tegmental area (VTA) in AVH compared to NAVH. AVH showed stronger EC from left anterior insula (AI) to RVS, stronger EC from RVS to anterior cingulate cortex (ACC), and stronger EC from VTA to posterior cingulate cortex (PCC) compared to NC. The correlation analysis results were mostly visible in the negative correlation between EC from right AI to ACC and positive sub-score, P1 sub-score, and P3 sub-score of PNASS in group-level. CONCLUSION: These findings suggest that neural causal interactions between the reward network associated with AVHs are disrupted, expanding the evidence for potential neurobiological mechanisms of AVHs. Particularly, dopamine-dependent salience attribution and top-down monitoring impairments and compensatory effects of enhanced excitatory afferents to ACC, which may provide evidence for a therapeutic target based on direct in vivo of AVHs in schizophrenia.

Identifying two distinct neuroanatomical subtypes of first-episode depression using heterogeneity through discriminative analysis.

BACKGROUND: Neurobiological heterogeneity in depression remains largely unknown, leading to inconsistent neuroimaging findings. METHODS: Here, we adopted a novel proposed machine learning method ground on gray matter volumes (GMVs) to investigate neuroanatomical subtypes of first-episode treatment-naïve depression. GMVs were obtained from high-resolution T1-weighted images of 195 patients with first-episode, treatment-naïve depression and 78 matched healthy controls (HCs). Then we explored distinct subtypes of depression by employing heterogeneity through discriminative analysis (HYDRA) with regional GMVs as features. RESULTS: Two prominently divergent subtypes of first-episode depression were identified, exhibiting opposite structural alterations compared with HCs but no different demographic features. Subtype 1 presented widespread increased GMVs mainly located in frontal, parietal, temporal cortex and partially located in limbic system. Subtype 2 presented widespread decreased GMVs mainly located in thalamus, cerebellum, limbic system and partially located in frontal, parietal, temporal cortex. Subtype 2 had smaller TIV and longer illness duration than Subtype 1. And TIV in Subtype 1 was positively correlated with age of onset while not in Subtype 2, probably implying the different potential neuropathological mechanisms. LIMITATIONS: Despite results obtained in this study were validated by employing another brain atlas, the conclusions were acquired from a single dataset. CONCLUSIONS: This study revealed two distinguishing neuroanatomical subtypes of first-episode depression, which provides new insights into underlying biological mechanisms of the heterogeneity in depression and might be helpful for accurate clinical diagnosis and future treatment.

Predictive spread of obsessive-compulsive disorder pathology using the network diffusion model.

An increasing body of studies propose that structural abnormalities begin with focal brain regions then propagate to other regions following the architecture of healthy brain network in neuropsychiatric disorders. However, these findings are untested in obsessive-compulsive disorder (OCD), also showing widespread structural brain abnormalities. In this study, we aimed to investigate whether healthy functional brain network contributed to structural brain abnormalities in OCD. The gray matter morphological abnormalities were obtained in 98 patients with OCD in relative to matched healthy controls (n = 130, HCs). The network diffusion model (NDM) was conducted to identify putative seed regions and patterns of disease propagation from seed regions to other brain regions along the functional network in OCD. The NDM has been proved to succeeded in capturing the trans-neuronal propagation of pathology and even in predicting future longitudinal progression of pathology in neurodegenerative diseases. In this study, when seeding at the right anterior cingulate cortex, the NDM best recapitulated the patterns of gray matter morphological abnormalities, suggesting this region was the most likely seed region. Further analyses revealed that pathology preferentially propagated to higher order brain systems from seed region. For non-seed regions, the arrival time of pathology was negatively correlated with their shortest functional paths to the seed (r = -0.46, p < 0.001). These results suggest that gray matter morphological abnormalities are constrained by healthy brain network and reveal temporal sequencing of pathology progression in OCD.

Gray matter atrophy is constrained by normal structural brain network architecture in depression.

BACKGROUND: There is growing evidence that gray matter atrophy is constrained by normal brain network (or connectome) architecture in neuropsychiatric disorders. However, whether this finding holds true in individuals with depression remains unknown. In this study, we aimed to investigate the association between gray matter atrophy and normal connectome architecture at individual level in depression. METHODS: In this study, 297 patients with depression and 256 healthy controls (HCs) from two independent Chinese dataset were included: a discovery dataset (105 never-treated first-episode patients and matched 130 HCs) and a replication dataset (106 patients and matched 126 HCs). For each patient, individualized regional atrophy was assessed using normative model and brain regions whose structural connectome profiles in HCs most resembled the atrophy patterns were identified as putative epicenters using a backfoward stepwise regression analysis. RESULTS: In general, the structural connectome architecture of the identified disease epicenters significantly explained 44% (±16%) variance of gray matter atrophy. While patients with depression demonstrated tremendous interindividual variations in the number and distribution of disease epicenters, several disease epicenters with higher participation coefficient than randomly selected regions, including the hippocampus, thalamus, and medial frontal gyrus were significantly shared by depression. Other brain regions with strong structural connections to the disease epicenters exhibited greater vulnerability. In addition, the association between connectome and gray matter atrophy uncovered two distinct subgroups with different ages of onset. CONCLUSIONS: These results suggest that gray matter atrophy is constrained by structural brain connectome and elucidate the possible pathological progression in depression.

MRI Assessment of Intrinsic Neural Timescale and Gray Matter Volume in Parkinson's Disease.

BACKGROUND: Numerous studies have indicated altered temporal features of the brain function in Parkinson's disease (PD), and the autocorrelation magnitude of intrinsic neural signals, called intrinsic neural timescales, were often applied to estimate how long neural information stored in local brain areas. However, it is unclear whether PD patients at different disease stages exhibit abnormal timescales accompanied with abnormal gray matter volume (GMV). PURPOSE: To assess the intrinsic timescale and GMV in PD. STUDY TYPE: Prospective. POPULATION: 74 idiopathic PD patients (44 early stage (PD-ES) and 30 late stage (PD-LS), as determined by the Hoehn and Yahr (HY) severity classification scale), and 73 healthy controls (HC). FIELD STRENGTH/SEQUENCE: 3.0 T MRI scanner; magnetization prepared rapid acquisition gradient echo and echo planar imaging sequences. ASSESSMENT: The timescales were estimated by using the autocorrelation magnitude of neural signals. Voxel-based morphometry was performed to calculate GMV in the whole brain. Severity of motor symptoms and cognitive impairments were assessed using the unified PD rating scale, the HY scale, the Montreal cognitive assessment, and the mini-mental state examination. STATISTICAL TEST: Analysis of variance; two-sample t-test; Spearman rank correlation analysis; Mann-Whitney U test; Kruskal-Wallis' H test. A P value <0.05 was considered statistically significant. RESULTS: The PD group had significantly abnormal intrinsic timescales in the sensorimotor, visual, and cognitive-related areas, which correlated with the symptom severity (ρ = -0.265, P = 0.022) and GMV (ρ = 0.254, P = 0.029). Compared to the HC group, the PD-ES group had significantly longer timescales in anterior cortical regions, whereas the PD-LS group had significantly shorter timescales in posterior cortical regions. CONCLUSION: This study suggested that PD patients have abnormal timescales in multisystem and distinct patterns of timescales and GMV in cerebral cortex at different disease stages. This may provide new insights for the neural substrate of PD. LEVEL OF EVIDENCE: 2 TECHNICAL EFFICACY STAGE: 1.

Abnormal resting-state effective connectivity in large-scale networks among obsessive-compulsive disorder.

BACKGROUND: Obsessive-compulsive disorder (OCD) is a chronic mental illness characterized by abnormal functional connectivity among distributed brain regions. Previous studies have primarily focused on undirected functional connectivity and rarely reported from network perspective. METHODS: To better understand between or within-network connectivities of OCD, effective connectivity (EC) of a large-scale network is assessed by spectral dynamic causal modeling with eight key regions of interests from default mode (DMN), salience (SN), frontoparietal (FPN) and cerebellum networks, based on large sample size including 100 OCD patients and 120 healthy controls (HCs). Parametric empirical Bayes (PEB) framework was used to identify the difference between the two groups. We further analyzed the relationship between connections and Yale-Brown Obsessive Compulsive Scale (Y-BOCS). RESULTS: OCD and HCs shared some similarities of inter- and intra-network patterns in the resting state. Relative to HCs, patients showed increased ECs from left anterior insula (LAI) to medial prefrontal cortex, right anterior insula (RAI) to left dorsolateral prefrontal cortex (L-DLPFC), right dorsolateral prefrontal cortex (R-DLPFC) to cerebellum anterior lobe (CA), CA to posterior cingulate cortex (PCC) and to anterior cingulate cortex (ACC). Moreover, weaker from LAI to L-DLPFC, RAI to ACC, and the self-connection of R-DLPFC. Connections from ACC to CA and from L-DLPFC to PCC were positively correlated with compulsion and obsession scores (r = 0.209, p = 0.037; r = 0.199, p = 0.047, uncorrected). CONCLUSIONS: Our study revealed dysregulation among DMN, SN, FPN, and cerebellum in OCD, emphasizing the role of these four networks in achieving top-down control for goal-directed behavior. There existed a top-down disruption among these networks, constituting the pathophysiological and clinical basis.

Gray matter morphological abnormities are constrained by normal structural covariance network in OCD.

A growing body of evidences reveal that abnormal gray matter morphology is constrained by normal brain network architecture in neurodegenerative and psychiatric disorders. However, whether this finding holds true in obsessive-compulsive disorder (OCD) remains unknown. In the current study, we aimed to investigate the association between gray matter morphological abnormities and normal structural covariance network architecture in OCD. First, gray matter morphological abnormities were obtained between 98 medicine-naive and first-episode patients with OCD and 130 healthy controls (HCs). Then, putative disease epicenters whose structural connectome profiles in HCs most resembled the morphological differences pattern were identified using a backfoward stepwise regression analysis. A set of brain regions were identified as putative disease epicenters whose structural connectome architecture significantly explained 59.94% variance of morphological abnormalities. These disease epicenters comprised brain regions implicated in high-order cognitive functions and sensory/motor processing. Other brain regions with stronger structural connections to disease epicenters exhibited greater vulnerability to disease. Together, these results suggest that gray matter abnormities are constrained by structural connectome and provide new insights into the possible pathological progression in OCD.

Decreased intrinsic neural timescale in treatment-naïve adolescent depression.

BACKGROUND: Major depressive disorder (MDD) is mainly characterized by its core dysfunction in higher-order brain cortices involved in emotional and cognitive processes, whose neurobiological basis remains unclear. In this study, we applied a relatively new developed resting-state functional magnetic resonance imaging (rs-fMRI) method of intrinsic neural timescale (INT), which reflects how long neural information is stored in a local brain area and reflects an ability of information integration, to investigate the local intrinsic neural dynamics using univariate and multivariate analyses in adolescent depression. METHOD: Based on the rs-fMRI data of sixty-six treatment-naïve adolescents with MDD and fifty-two well-matched healthy controls (HCs), we calculated an INT by assessing the magnitude of autocorrelation of the resting-state brain activity, and then compared the difference of INT between the two groups. Correlation between abnormal INT and clinical features was performed. We also utilized multivariate pattern analysis to determine whether INT could differentiate MDD patients from HCs at the individual level. RESULT: Compared with HCs, patients with MDD showed shorter INT widely distributed in cortical and partial subcortical regions. Interestingly, the decreased INT in the left hippocampus was related to disease severity of MDD. Furthermore, INT can distinguish MDD patients from HCs with the most discriminative regions located in the dorsolateral prefrontal cortex, angular, middle occipital gyrus, and cerebellar posterior lobe. CONCLUSION: Our research aids in advancing understanding the brain abnormalities of treatment-naïve adolescents with MDD from the perspective of the local neural dynamics, highlighting the significant role of INT in understanding neurophysiological mechanisms. This study shows that the altered intrinsic timescales of local neural signals widely distributed in higher-order brain cortices regions may be the neurodynamic basis of cognitive and emotional disturbances in MDD patients, and provides preliminary support for the suggestion that these could be used to aid the identification of MDD patients in clinical practice.

Resolving heterogeneity in schizophrenia, bipolar I disorder, and attention-deficit/hyperactivity disorder through individualized structural covariance network analysis.

Disruptions in large-scale brain connectivity are hypothesized to contribute to psychiatric disorders, including schizophrenia, bipolar I disorder, and attention-deficit/hyperactivity disorder. However, high inter-individual variation among patients with psychiatric disorders hinders achievement of unified findings. To this end, we adopted a newly proposed method to resolve heterogeneity of differential structural covariance network in schizophrenia, bipolar I disorder, and attention-deficit/hyperactivity disorder. This method could infer individualized structural covariance aberrance by assessing the deviation from healthy controls. T1-weighted anatomical images of 114 patients with psychiatric disorders (schizophrenia: n = 37; bipolar I disorder: n = 37; attention-deficit/hyperactivity disorder: n = 37) and 110 healthy controls were analyzed to obtain individualized differential structural covariance network. Patients exhibited tremendous heterogeneity in profiles of individualized differential structural covariance network. Despite notable heterogeneity, patients with the same disorder shared altered edges at network level. Moreover, individualized differential structural covariance network uncovered two distinct psychiatric subtypes with opposite differences in structural covariance edges, that were otherwise obscured when patients were merged, compared with healthy controls. These results provide new insights into heterogeneity and have implications for the nosology in psychiatric disorders.

Dynamic brain activity states of memory impairment in stroke patients with varying motor outcomes.

Introduction: The objective of this study was to characterize the alteration patterns of dynamic spatiotemporal activity in chronic subcortical stroke patients with varying motor outcomes, while investigating the imaging indicators relevant to the assessment of potential cognitive deficits in these patients. Methods: A total of 136 patients and 88 normal controls were included in the analysis of static and dynamic intrinsic brain activity, determined by amplitude of low-frequency fluctuations. Results: The findings unveiled that subcortical stroke patients exhibited significantly aberrant temporal dynamics of intrinsic brain activity, involving regions within multiple brain networks. These spatiotemporal patterns were found to be contingent upon the side of the lesion. In addition, these aberrant metrics demonstrated potential in discerning cognitive deficits in stroke patients with memory impairment, with the dynamic indices exerting more influence than the static ones. The observe findings may indicate that subcortical stroke can trigger imbalances in the segregation and integration of spatiotemporal patterns across the entire brain with multi-domain networks, especially in patients with poor motor outcomes. Conclusion: It suggests that the temporal dynamics indices of intrinsic brain activity could serve as potential imaging indicators for assessing cognitive impairment in patients with chronic subcortical stroke, which may be associated with the motor outcomes.

Similarities and differences of dynamic and static spontaneous brain activity between left and right temporal lobe epilepsy.

To comprehensively investigate the potential temporal dynamic and static abnormalities of spontaneous brain activity (SBA) in left temporal lobe epilepsy (LTLE) and right temporal lobe epilepsy (RTLE) and to detect whether these alterations correlate with cognition. Twelve SBA metrics, including ALFF, dALFF, fALFF, dfALFF, ReHo, dReHo, DC, dDC, GSCorr, dGSCorr, VMHC, and dVMHC, in 46 LTLE patients, 43 RTLE patients, and 53 healthy volunteers were compared in the voxel-wise analysis. Correlation analyses between metrics in regions showing statistic differences and epilepsy duration, epilepsy severity, and cognition scores were also performed. Compared with the healthy volunteers, the alteration of SBA was identified both in LTLE and RTLE patients. The ALFF, fALFF, and dALFF values in LTLE, as well as the fALFF values in RTLE, increased in the bilateral thalamus, basal ganglia, mesial temporal lobe, cerebellum, and vermis. Increased dfALFF in the bilateral basal ganglia, increased ReHo and dReHo in the bilateral thalamus in the LTLE group, increased ALFF and dALFF in the pons, and increased ReHo and dReHo in the right hippocampus in the RTLE group were also detected. However, the majority of deactivation clusters were in the ipsilateral lateral temporal lobe. For LTLE, the fALFF, DC, dDC, and GSCorr values in the left lateral temporal lobe and the ReHo and VMHC values in the bilateral lateral temporal lobe all decreased. For RTLE, the ALFF, fALFF, dfALFF, ReHo, dReHo, and DC values in the right lateral temporal lobe and the VMHC values in the bilateral lateral temporal lobe all decreased. Moreover, for both the LTLE and RTLE groups, the dVMHC values decreased in the calcarine cortex. The most significant difference between LTLE and RTLE was the higher activation in the cerebellum of the LTLE group. The alterations of many SBA metrics were correlated with cognition and epilepsy duration. The patterns of change in SBA abnormalities in the LTLE and RTLE patients were generally similar. The integrated application of temporal dynamic and static SBA metrics might aid in the investigation of the propagation and suppression pathways of seizure activity as well as the cognitive impairment mechanisms in TLE.

Changes in aspartate metabolism in the medial-prefrontal cortex of nicotine addicts based on J-edited magnetic resonance spectroscopy.

This study aims to explore the changes of the aspartate (Asp) level in the medial-prefrontal cortex (mPFC) of subjects with nicotine addiction (nicotine addicts [NAs]) using the J-edited 1 H MR spectroscopy (MRS), which may provide a positive imaging evidence for intervention of NA. From March to August 2022, 45 males aged 40-60 years old were recruited from Henan Province, including 21 in NA and 24 in nonsmoker groups. All subjects underwent routine magnetic resonance imaging (MRI) and J-edited MRS scans on a 3.0 T MRI scanner. The Asp level in mPFC was quantified with reference to the total creatine (Asp/Cr) and water (Aspwater-corr , with correction of the brain tissue composition) signals, respectively. Two-tailed independent samples t-test was used to analyze the differences in levels of Asp and other coquantified metabolites (including total N-acetylaspartate [tNAA], total cholinine [tCho], total creatine [tCr], and myo-Inositol [mI]) between the two groups. Finally, the correlations of the Asp level with clinical characteristic assessment scales were performed using the Spearman criteria. Compared with the control group (n = 22), NAs (n = 18) had higher levels of Asp (Asp/Cr: p = .005; Aspwater-corr : p = .004) in the mPFC, and the level of Asp was positively correlated with the daily smoking amount (Asp/Cr: p < .001; Aspwater-corr : p = .004). No significant correlation was found between the level of Asp and the years of nicotine use, Fagerstrom Nicotine Dependence (FTND), Russell Reason for Smoking Questionnaire (RRSQ), or Barratt Impulsivity Scale (BIS-11) score. The elevated Asp level was observed in mPFC of NAs in contrast to nonsmokers, and the Asp level was positively correlated with the amount of daily smoking, which suggests that nicotine addiction may result in elevated Asp metabolism in the human brain.

Two distinct neuroanatomical subtypes of migraine without aura revealed by heterogeneity through discriminative analysis.

The neurobiological heterogeneity in migraine is poorly studied, resulting in conflicting neuroimaging findings. This study used a newly proposed method based on gray matter volumes (GMVs) to investigate objective neuroanatomical subtypes of migraine. Structural MRI and clinical measures of 31 migraine patients without aura and 33 matched healthy controls (HCs) were explored. Firstly, we investigated whether migraine patients exhibited higher interindividual variability than HCs in terms of GMVs. Then, heterogeneity through discriminative analysis (HYDRA) was applied to categorize migraine patients into distinct subtypes by regional volumetric measures of GMVs. Voxel-wise volume and clinical characteristics among different subtypes were also explored. Migraine patients without aura exhibited higher interindividual GMVs variability. Two distinct and reproducible neuroanatomical subtypes of migraine were revealed. These two subtypes exhibited opposite neuroanatomical aberrances compared to HCs. Subtype 1 showed widespread decreased GMVs, while Subtype 2 showed increased GMVs in limited regions. The total intracranial volume was significantly positively correlated with cognitive function in Subtype 2. Subtype 1 showed significantly longer illness duration and less cognitive scores compared to Subtype 2. The present study shows that migraine patients without aura have high structural heterogeneity and uncovers two distinct and robust neuroanatomical subtypes, which provide a possible explanation for conflicting neuroimaging findings.

Neurovascular coupling dysfunction in high myopia patients: Evidence from a multi-modal magnetic resonance imaging analysis.

BACKGROUND AND PURPOSE: To investigate neurovascular coupling dysfunction in high myopia (HM) patients. MATERIALS AND METHODS: A total of 37 HM patients and 36 healthy controls were included in this study. Degree centrality (DC), regional homogeneity (ReHo), amplitude of low-frequency fluctuations (ALFF), and fractional ALFF (fALFF) maps were employed to represent neuronal activity. Cerebral blood perfusion was characterized by cerebral blood flow (CBF). The correlation coefficient was calculated to reflect the relationship between neuronal activity and cerebral blood perfusion. Pearson partial correlation analysis was utilized to evaluate the association between HM dysfunction and clinical indicators. RESULTS: HM patients exhibited significant alterations in neurovascular coupling across 37 brain regions compared to healthy controls. The brain regions with marked changes varied among the four neurovascular coupling patterns, including the middle frontal gyrus, superior occipital gyrus, middle occipital gyrus, and fusiform gyrus. Additionally, the superior frontal gyrus orbital part, medial superior frontal gyrus, inferior occipital gyrus, and dorsolateral superior frontal gyrus displayed significant changes in three coupling patterns. In HM patients, the ReHo-CBF changes in the inferior frontal gyrus orbital part were positively correlated with best-corrected visual acuity (BCVA) and refractive diopter changes. Similarly, the ALFF-CBF changes in the inferior frontal gyrus orbital part showed a positive correlation with refractive diopter changes. ReHo-CBF and ALFF-CBF alterations in the paracentral lobule were positively correlated with BCVA and refractive diopter changes. CONCLUSION: Our findings underscore the abnormal alterations in neurovascular coupling across multiple brain regions in HM patients. These results suggest that neurovascular dysfunction in HM patients may be associated with an aberrant visual regulation mechanism.

Decreased intrinsic neural timescales in obsessive compulsive disorder and two distinct subtypes revealed by heterogeneity through discriminative analysis.

BACKGROUND: OCD is featured as the destruction of information storage and processing. The cognition of neurobiological and clinical heterogeneity is in suspense and poorly studied. METHODS: Ninety-nine patients and matched HCs(n = 104) were recruited and underwent resting-state functional MRI scans. We applied INT to evaluate altered local neural dynamics representing the ability of information integration. Moreover, considering OCD was a highly heterogeneous disorder, we investigated putative OCD subtypes from INT using a novel semi-supervised machine learning, named HYDRA. RESULTS: Compared with HCs, patients with OCD showed decreased INTs in extensive brain regions, including bilateral cerebellum and precuneus, STG/MTG and PCC, hippocampus in DMN; right IFG/MFG/SFG, SPL and bilateral angular gyrus in CEN and insula, SMA in SN. Moreover, many other regions involved in visual processing also had disrupted dynamics of local neural organization, consisting of bilateral CUN, LING and fusiform gyrus and occipital lobe. HYDRA divided patients into two distinct neuroanatomical subtypes from INT. Subtype 1 showed decreased INTs in distributed networks, while subtype 2 presented increased in several common regions which were also found to be decreased in subtype 1, such as STG, IPL, postcentral gyrus and left insula, supramarginal gyrus. CONCLUSION: This study showed distinct abnormalities from the perspective of dynamics of local neural organization in OCD. Such alteration and dimensional approach may provide a new insight into the prior traditional cognition of this disorder and to some extent do favor of more precise diagnosis and treatment response in the future.

Alterations in static and dynamic regional homogeneity in mesial temporal lobe epilepsy with and without initial precipitating injury.

Objectives: Initial precipitating injury (IPI) such as febrile convulsion and intracranial infection will increase the susceptibility to epilepsy. It is still unknown if the functional deficits differ between mesial temporal lobe epilepsy with IPI (mTLE-IPI) and without IPI (mTLE-NO). Methods: We recruited 25 mTLE-IPI patients, 35 mTLE-NO patients and 33 healthy controls (HC). Static regional homogeneity (sReHo) and dynamic regional homogeneity (dReHo) were then adopted to estimate the alterations of local neuronal activity. One-way analysis of variance was used to analyze the differences between the three groups in sReHo and dReHo. Then the results were utilized as masks for further between-group comparisons. Besides, correlation analyses were carried out to detect the potential relationships between abnormal regional homogeneity indicators and clinical characteristics. Results: When compared with HC, the bilateral thalamus and the visual cortex in mTLE-IPI patients showed an increase in both sReHo and variability of dReHo. Besides, mTLE-IPI patients exhibited decreased sReHo in the right cerebellum crus1/crus2, inferior parietal lobule and temporal neocortex. mTLE-NO patients showed decreased sReHo and variability of dReHo in the bilateral temporal neocortex compared with HC. Increased sReHo and variability of dReHo were found in the bilateral visual cortex when mTLE-IPI patients was compared with mTLE-NO patients, as well as increased variability of dReHo in the left thalamus and decreased sReHo in the right dorsolateral prefrontal cortex. Additionally, we discovered a negative correlation between the national hospital seizure severity scale testing score and sReHo in the right cerebellum crus1 in mTLE-IPI patients. Conclusion: According to the aforementioned findings, both mTLE-IPI and mTLE-NO patients had significant anomalies in local neuronal activity, although the functional deficits were much severer in mTLE-IPI patients. The use of sReHo and dReHo may provide a novel insight into the impact of the presence of IPI on the development of mTLE.

Static and dynamic changes of intrinsic brain local connectivity in internet gaming disorder.

BACKGROUND: Studies have revealed that intrinsic neural activity varies over time. However, the temporal variability of brain local connectivity in internet gaming disorder (IGD) remains unknown. The purpose of this study was to explore the alterations of static and dynamic intrinsic brain local connectivity in IGD and whether the changes were associated with clinical characteristics of IGD. METHODS: Resting-state functional magnetic resonance imaging (rs-fMRI) scans were performed on 36 individuals with IGD (IGDs) and 44 healthy controls (HCs) matched for age, gender and years of education. The static regional homogeneity (sReHo) and dynamic ReHo (dReHo) were calculated and compared between two groups to detect the alterations of intrinsic brain local connectivity in IGD. The Internet Addiction Test (IAT) and the Pittsburgh Sleep Quality Index (PSQI) were used to evaluate the severity of online gaming addiction and sleep quality, respectively. Pearson correlation analysis was used to evaluate the relationship between brain regions with altered sReHo and dReHo and IAT and PSQI scores. Receiver operating characteristic (ROC) curve analysis was used to reveal the potential capacity of the sReHo and dReHo metrics to distinguish IGDs from HCs. RESULTS: Compared with HCs, IGDs showed both increased static and dynamic intrinsic local connectivity in bilateral medial superior frontal gyrus (mSFG), superior frontal gyrus (SFG), and supplementary motor area (SMA). Increased dReHo in the left putamen, pallidum, caudate nucleus and bilateral thalamus were also observed. ROC curve analysis showed that the brain regions with altered sReHo and dReHo could distinguish individuals with IGD from HCs. Moreover, the sReHo values in the left mSFG and SMA as well as dReHo values in the left SMA were positively correlated with IAT scores. The dReHo values in the left caudate nucleus were negatively correlated with PSQI scores. CONCLUSIONS: These results showed impaired intrinsic local connectivity in frontostriatothalamic circuitry in individuals with IGD, which may provide new insights into the underlying neuropathological mechanisms of IGD. Besides, dynamic changes of intrinsic local connectivity in caudate nucleus may be a potential neurobiological marker linking IGD and sleep quality.

Parsing altered gray matter morphology of depression using a framework integrating the normative model and non-negative matrix factorization.

The high inter-individual heterogeneity in individuals with depression limits neuroimaging studies with case-control approaches to identify promising biomarkers for individualized clinical decision-making. We put forward a framework integrating the normative model and non-negative matrix factorization (NMF) to quantitatively assess altered gray matter morphology in depression from a dimensional perspective. The proposed framework parses altered gray matter morphology into overlapping latent disease factors, and assigns patients distinct factor compositions, thus preserving inter-individual variability. We identified four robust disease factors with distinct clinical symptoms and cognitive processes in depression. In addition, we showed the quantitative relationship between the group-level gray matter morphological differences and disease factors. Furthermore, this framework significantly predicted factor compositions of patients in an independent dataset. The framework provides an approach to resolve neuroanatomical heterogeneity in depression.

Altered topological properties and their relationship to cognitive functions in unilateral temporal lobe epilepsy.

OBJECTIVE: To investigate abnormalities in topological properties in unilateral temporal lobe epilepsy (TLE) with hippocampal sclerosis and their correlations with cognitive functions. METHODS: Thirty-eight patients with TLE and 19 age- and sex-matched healthy controls (HCs) were enrolled in this research and underwent resting-state functional magnetic resonance imaging (fMRI) examinations. Whole-brain functional networks of participants were constructed based on the fMRI data. Topological characteristics of the functional network were compared between patients with left and right TLE and HCs. Correlations between altered topological properties and cognitive measurements were explored. RESULTS: Compared with the HCs, patients with left TLE showed decreased clustering coefficient, global efficiency, and local efficiency (Eloc), and patients with right TLE showed decreased Eloc. We found altered nodal centralities in six regions related to the basal ganglia (BG) network or default mode network (DMN) in patients with left TLE and those in three regions related to reward/emotion network or ventral attention network in patients with right TLE. Patients with right TLE showed higher integration (reduced nodal shortest path length) in four regions related to the DMN and lower segregation (reduced nodal local efficiency and nodal clustering coefficient) in the right middle temporal gyrus. When comparing left TLE with right TLE, no significant differences were detected in global parameters, but the nodal centralities in the left parahippocampal gyrus and the left pallidum were decreased in left TLE. The Eloc and several nodal parameters were significantly correlated with memory functions, duration, national hospital seizure severity scale (NHS3), or antiseizure medications (ASMs) in patients with TLE. CONCLUSIONS: The topological properties of whole-brain functional networks were disrupted in TLE. Networks of left TLE were characterized by lower efficiency; right TLE was preserved in global efficiency but disrupted in fault tolerance. Several nodes with abnormal topological centrality in the basal ganglia network beyond the epileptogenic focus in the left TLE were not found in the right TLE. Right TLE had some nodes with reduced shortest path length in regions of the DMN as compensation. These findings provide new insights into the effect of lateralization on TLE and help us to understand the cognitive impairment of patients with TLE.

Altered resting-state neurovascular coupling in patients with pontine infarction.

The risk for motor and cognitive impairment is increased in patients with chronic pontine infarction (PI). In this study, we attempted to explore the alterations of neurovascular coupling (NVC) in order to understand the neural basis of behavioral impairment after PI. Three-dimensional pseudo-continuous arterial spin labeling (3D-pcASL) and resting-state functional magnetic resonance imaging (rs-fMRI) were applied in 49 patients with unilateral PI (left-sided, n = 26; right-sided, n = 23) and 30 matched normal subjects to assess whole-brain cerebral blood flow (CBF) and functional connectivity strength (FCS). We evaluated NVC in each subject by calculating the correlation coefficient between the whole-brain CBF and FCS (CBF-FCS coupling) and the ratio between voxel-wise CBF and FCS (CBF/FCS ratio). The FCS maps were then divided into long-range and short-range FCS to identify the influence of connection distance. The results indicated that the CBF-FCS coupling in the whole-brain level was significantly interrupted in PI patients, and the CBF/FCS ratio in cognition-related brain regions was abnormal. Distance-dependent results demonstrated that PI had a more serious effect on long-range neurovascular coupling. Correlation analysis revealed that the changes in neurovascular coupling were correlated with working memory scores. These findings imply that disruption of neurovascular coupling in the remote-infarction brain regions may underlie the impaired cognitive functions in chronic PI.