Multicenter mapping of structural network alterations in autism.
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ABSTRACT:
SUBMITTER: Valk SL
PROVIDER: S-EPMC6129398 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Tics are sudden stereotyped movements or vocalizations. Cases of lesion-induced tics are invaluable, allowing for causal links between symptoms and brain structures. While a lesion network for tics has recently been identified, the degree to which this network translates to Tourette syndrome has not been fully elucidated. This is important given that patients with Tourette syndrome make up a large portion of tic cases; therefore, existing and future treatments should apply to these patients. The aim of this study was to first localize a causal network for tics from lesion-induced cases and then refine and validate this network in patients with Tourette syndrome. We independently performed 'lesion network mapping' using a large normative functional connectome (n = 1000) to isolate a brain network commonly connected to lesions causing tics (n = 19) identified through a systematic search. The specificity of this network to tics was assessed through comparison to lesions causing other movement disorders. Using structural brain coordinates from prior neuroimaging studies (n = 7), we then derived a neural network for Tourette syndrome. This was done using standard anatomical likelihood estimation meta-analysis and a novel method termed 'coordinate network mapping', which uses the same coordinates, yet maps their connectivity using the aforementioned functional connectome. Conjunction analysis was used to refine the network for lesion-induced tics to Tourette syndrome by identifying regions common to both lesion and structural networks. We then tested whether connectivity from this common network is abnormal in a separate resting-state functional connectivity MRI data set from idiopathic Tourette syndrome patients (n = 21) and healthy controls (n = 25). Results showed that lesions causing tics were distributed throughout the brain; however, consistent with a recent study, these were part of a common network with predominant basal ganglia connectivity. Using conjunction analysis, coordinate network mapping findings refined the lesion network to the posterior putamen, caudate nucleus, globus pallidus externus (positive connectivity) and precuneus (negative connectivity). Functional connectivity from this positive network to frontal and cingulate regions was abnormal in patients with idiopathic Tourette syndrome. These findings identify a network derived from lesion-induced and idiopathic data, providing insight into the pathophysiology of tics in Tourette syndrome. Connectivity to our cortical cluster in the precuneus offers an exciting opportunity for non-invasive brain stimulation protocols.
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Project description:The structural organization of the brain can be characterized as a hierarchical ensemble of segregated modules linked by densely interconnected hub regions that facilitate distributed functional interactions. Disturbances to this network may be an important marker of abnormal development. Recently, several neurodevelopmental disorders, including autism spectrum disorder (ASD), have been framed as disorders of connectivity but the full nature and timing of these disturbances remain unclear. In this study, we use non-negative matrix factorization, a data-driven, multivariate approach, to model the structural network architecture of the brain as a set of superposed subnetworks, or network components. In an openly available dataset of 196 subjects scanned between 5 and 85 years we identify a set of robust and reliable subnetworks that develop in tandem with age and reflect both anatomically local and long-range, network hub connections. In a second experiment, we compare network components in a cohort of 51 high-functioning ASD adolescents to a group of age-matched controls. We identify a specific subnetwork representing an increase in local connection strength in the cingulate cortex in ASD (t = 3.44, P < 0.001). This work highlights possible long-term implications of alterations to the developmental trajectories of specific cortical subnetworks. Hum Brain Mapp 38:4169-4184, 2017. © 2017 Wiley Periodicals, Inc.
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Project description:The goal of this study was to elucidate the anatomical brain basis of social cognition through two disorders with distinctively different phenotypes of social interaction. We compared structural MR images of 20 individuals with autism spectrum disorder (ASD), 19 violent offenders with high psychopathic traits, and 19 control participants using voxel-based morphometry (VBM). Our earlier study showed lower grey matter volume (GMV) values in the insula, frontal cortex, and sensorimotor cortex of the offender group compared to controls. In the present study, the images of the ASD group revealed lower GMV in the left precuneus, right cerebellum, and right precentral gyrus in comparison with controls. The comparison between the offender and ASD groups showed lower GMV values for the right temporal pole and left inferior frontal gyrus in the offender group. There was also an overlap of both disorders in the right pre-central cortex, showing lower GMV compared to controls. Our findings suggest structural differences between violent offenders with high psychopathy traits and ASD individuals in the frontotemporal social brain network areas, previously associated with empathy. We also provide evidence of similar abnormal structures in the motor cortex for both of these disorders, possibly related to uniting issues of social cognition.
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Project description:BackgroundTo evaluate brain white matter diffusion characteristics and anatomical network alterations in betel quid dependence (BQD) chewers using high angular resolution diffusion imaging (HARDI).MethodsThe current study recruited 53 BQD chewers and 37 healthy controls (HC) in two groups. We explored regional diffusion metrics alternations in the BQD group compared with the HC group using automated fiber quantification (AFQ). We further employed the white matter (WM) anatomical network of HARDI to explore connectivity alterations in BQD chewers using graph theory.ResultsBQD chewers presented significantly lower FA values in the left and right cingulum cingulate, the left and right thalamic radiation, and the right uncinate. The BQD has a significantly higher RD value in the right uncinate fasciculus than the HC group. At the global WM anatomical network level, global network efficiency (p = 0.008) was poorer and Lp (p = 0.016) was greater in the BQD group. At the nodal WM anatomical network level, nodal efficiency (p < 0.05) was lower in the BQD group.ConclusionOur findings provide novel morphometric evidence that brain structural changes in BQD are characterized by white matter diffusivity and anatomical network connectivity among regions of the brain, potentially leading to the enhanced reward system and impaired inhibitory control.
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Project description:Persistent developmental stuttering is a speech disorder that primarily affects normal speech fluency but encompasses a complex set of symptoms ranging from reduced sensorimotor integration to socioemotional challenges. Here, we investigated the whole-brain structural connectome and its topological alterations in adults who stutter. Diffusion-weighted imaging data of 33 subjects (13 adults who stutter and 20 fluent speakers) were obtained along with a stuttering severity evaluation. The structural brain network properties were analysed using network-based statistics and graph theoretical measures particularly focussing on community structure, network hubs and controllability. Bayesian power estimation was used to assess the reliability of the structural connectivity differences by examining the effect size. The analysis revealed reliable and wide-spread decreases in connectivity for adults who stutter in regions associated with sensorimotor, cognitive, emotional and memory-related functions. The community detection algorithms revealed different subnetworks for fluent speakers and adults who stutter, indicating considerable network adaptation in adults who stutter. Average and modal controllability differed between groups in a subnetwork encompassing frontal brain regions and parts of the basal ganglia. The results revealed extensive structural network alterations and substantial adaptation in neural architecture in adults who stutter well beyond the sensorimotor network. These findings highlight the impact of the neurodevelopmental effects of persistent stuttering on neural organization and the importance of examining the full structural connectome and the network alterations that underscore the behavioural phenotype.
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Project description:Given the strong involvement of affect in obsessive-compulsive disorder (OCD) and recent findings, the current cortico-striato-thalamo-cortical (CSTC) model of pathophysiology has repeatedly been questioned regarding the specific role of regions involved in emotion processing such as limbic areas. Employing a connectomics approach enables us to characterize structural connectivity on a whole-brain level, extending beyond the CSTC circuitry. Whole-brain structural networks of 41 patients and 42 matched healthy controls were analyzed based on 83 × 83 connectivity matrices derived from cortical and subcortical parcellation of structural T1-weighted magnetic resonance scans and deterministic fiber tracking based on diffusion tensor imaging data. To assess group differences in structural connectivity, the framework of network-based statistic (NBS) was applied. Graph theoretical measures were calculated to further assess local and global network characteristics. The NBS analysis revealed a single network consistently displaying decreased structural connectivity in patients comprising orbitofrontal, striatal, insula and temporo-limbic areas. In addition, graph theoretical measures indicated local alterations for amygdala and temporal pole while the overall topology of the network was preserved. To the best of our knowledge, this is the first study combining the NBS with graph theoretical measures in OCD. Along with regions commonly described in the CSTC model of pathophysiology, our results indicate an involvement of mainly temporo-limbic regions typically associated with emotion processing supporting their importance for neurobiological alterations in OCD.
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Project description:Background and purposeAccording to reports, type 2 diabetes (T2D) is a progressive disease. However, no known research has examined the progressive brain structural changes associated with T2D. The purpose of this study was to determine whether T2D patients exhibit progressive brain structural alterations and, if so, how the alterations progress.Materials and methodsStructural magnetic resonance imaging scans were collected for 81 T2D patients and 48 sex-and age-matched healthy controls (HCs). Voxel-based morphometry (VBM) and causal structural covariance network (CaSCN) analyses were applied to investigate gray matter volume (GMV) alterations and the likely chronological processes underlying them in T2D. Two sample t-tests were performed to compare group differences, and the differences were corrected using Gaussian random field (GRF) correction (voxel-level p < 0.001, cluster-level p < 0.01).ResultsOur findings demonstrated that GMV alterations progressed in T2D patients as disease duration increased. In the early stages of the disease, the right temporal pole of T2D patients had GMV atrophy. As the diseases duration prolonged, the limbic system, cerebellum, subcortical structures, parietal cortex, frontal cortex, and occipital cortex progressively exhibited GMV alterations. The patients also exhibited a GMV alterations sequence exerting from the right temporal pole to the limbic-cerebellum-striatal-cortical network areas.ConclusionOur results indicate that the progressive GMV alterations of T2D patients manifested a limbic-cerebellum-striatal-cortical sequence. These findings may contribute to a better understanding of the progression and an improvement of current diagnosis and intervention strategies for T2D.
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Project description:Disorder of consciousness (DoC) refers to a group of clinical conditions that may emerge after brain injury, characterized by a varying decrease in the level of consciousness that can last from days to years. An understanding of its neural correlates is crucial for the conceptualization and application of effective therapeutic interventions. Here we propose a quantitative meta-analysis of the neural substrate of DoC emerging from functional magnetic resonance (fMRI) and positron emission tomography (PET) studies. We also map the relevant networks of resulting areas to highlight similarities with Resting State Networks (RSNs) and hypothesize potential therapeutic solutions leveraging network-targeted noninvasive brain stimulation. Available literature was reviewed and analyzed through the activation likelihood estimate (ALE) statistical framework to describe resting-state or task-dependent brain activation patterns in DoC patients. Results show that task-related activity is limited to temporal regions resembling the auditory cortex, whereas resting-state fMRI data reveal a diffuse decreased activation affecting two subgroups of cortical (angular gyrus, middle frontal gyrus) and subcortical (thalamus, cingulate cortex, caudate nucleus) regions. Clustering of their cortical functional connectivity projections identify two main altered functional networks, related to decreased activity of (i) the default mode and frontoparietal networks, as well as (ii) the anterior salience and visual/auditory networks. Based on the strength and topography of their connectivity profile, biophysical modeling of potential brain stimulation solutions suggests the first network as the most feasible target for tES, tDCS neuromodulation in DoC patients.
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