The second iteration of the Autism Brain Imaging Data Exchange (ABIDE II) aims to enhance the scope of brain connectomics research in Autism Spectrum Disorder (ASD). Consistent with the initial ABIDE effort (ABIDE I), that released 1112 datasets in 2012, this new multisite open-data resource is an aggregate of resting state functional magnetic resonance imaging (MRI) and corresponding structural MRI and phenotypic datasets. ABIDE II includes datasets from an additional 487 individuals with ASD and 557 controls previously collected across 16 international institutions. The combination of ABIDE I and ABIDE II provides investigators with 2156 unique cross-sectional datasets allowing selection of samples for discovery and/or replication. This sample size can also facilitate the identification of neurobiological subgroups, as well as preliminary examinations of sex differences in ASD. Additionally, ABIDE II includes a range of psychiatric variables to inform our understanding of the neural correlates of co-occurring psychopathology; 284 diffusion imaging datasets are also included. It is anticipated that these enhancements will contribute to unraveling key sources of ASD heterogeneity.

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These data support the concurrent and discriminative validity of the BDI-FS in MS. As the test is brief and not confounded with neurological symptoms, it is recommended for depression screening in this population.

Autism spectrum disorder (ASD) is characterized by atypical brain network organization, but findings have been inconsistent. While methodological and maturational factors have been considered, the network specificity of connectivity abnormalities remains incompletely understood. We investigated intrinsic functional connectivity (iFC) for four "core" functional networks-default-mode (DMN), salience (SN), and left (lECN) and right executive control (rECN). Resting-state functional MRI data from 75 children and adolescents (37 ASD, 38 typically developing [TD]) were included. Functional connectivity within and between networks was analyzed for regions of interest (ROIs) and whole brain, compared between groups, and correlated with behavioral scores. ROI analyses showed overconnectivity (ASD > TD), especially between DMN and ECN. Whole-brain results were mixed. While predominant overconnectivity was found for DMN (posterior cingulate seed) and rECN (right inferior parietal seed), predominant underconnectivity was found for SN (right anterior insula seed) and lECN (left inferior parietal seed). In the ASD group, reduced SN integrity was associated with sensory and sociocommunicative symptoms. In conclusion, atypical connectivity in ASD is network-specific, ranging from extensive overconnectivity (DMN, rECN) to extensive underconnectivity (SN, lECN). Links between iFC and behavior differed between groups. Core symptomatology in the ASD group was predominantly related to connectivity within the salience network.

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utism spectrum disorder (ASD) is characterized by sociocommunicative impairments, repetitive behaviors, and restricted interests. 1 While viewed as a neurological disorder, its precise neural bases are not well understood. Growing evidence suggests that sociocommunicative, cognitive, and sensorimotor impairments are related to abnormalities of distributed networks, rather than of single brain loci. [2][3][4] Reports of atypical hemispheric asymmetries in ASD come from anatomical [5][6][7] and functional imaging studies. [8][9][10][11][12] Eyler and colleagues 13 observed atypical rightward asymmetry of receptive language activations during natural sleep in infants down to age 12.5 months, indicating that abnormal lateralization may predate language acquisition. However, all of the studies cited above focused on brain regions or stimuli specifically related to language. A recent study on gene expression in post mortem frontal cortex showed abnormalities in patterning pathways affecting lateralization in ASD, 14 possibly suggesting a broader impact on asymmetries even outside the language domain. While far from conclusive, these intriguing findings prompt the question whether atypical asymmetry could be a fundamental feature of brain organization in ASD. Indeed, theoretical considerations about possible left-hemisphere dysfunction 15,16 or, alternatively, predominant righthemisphere impairment 17,18 have a long history in autism research. However, these conjectures were largely based on limited behavioral findings, and conclusive imaging evidence beyond the language domain is lacking. Functional asymmetries related to nonverbal processing in ASD have received little attention, with only 2 studies reporting atypical left-hemisphere processing for motor tasks. 19,20 Moreover, functional studies have typically applied a priori models of task-driven activation effects. Since ASD is a pervasive developmental disorder whose neurofunctional bases are not well understood, hypothesis-driven approaches targeting single domains may, however, fail to provide comprehensive evidence because unexpected abnormalities may be missed.IMPORTANCE Autism spectrum disorder (ASD) is a brain-based pervasive developmental disorder, which-by growing consensus-is associated with abnormal organization of functional networks. Several previous studies of ASD have indicated atypical hemispheric asymmetries for language.OBJECTIVE To examine the asymmetry of functional networks using a data-driven approach for a comprehensive investigation of hemispheric asymmetry in ASD. DESIGN, SETTING, AND PARTICIPANTSThis cross-sectional study involved 24 children with ASD and 26 matched typically developing children at

Although numerous studies have shown that brain-damaged patients tend to underestimate neuropsychological (NP) impairment when self-ratings are compared to informant ratings, the meaning of such discrepancies is not well studied in multiple sclerosis (MS). We compared patient self- and informant-report questionnaire ratings of NP functioning in 122 MS patients and 37 age- and education-matched normal controls. In addition to completing the Multiple Sclerosis Neuropsychological Questionnaire (MSNQ), participants underwent NP testing and assessment of depression, personality, and neuropsychiatric symptoms. Based on the normal distribution of discrepancy scores, patients were classified according to whether they overestimated or underestimated their cognitive ability, relative to informant ratings. ANOVAs comparing test scores derived from overestimators, underestimators, and accurate estimators were significant for multiple measures of cognitive function, depression, personality, and neuropsychiatric symptoms. Overestimators were characterized by less depression and conscientiousness, and greater degrees of cognitive impairment, euphoric behavioral disinhibition, and unemployment as compared to underestimators. We conclude that patient/informant discrepancy scores on the MSNQ are associated with the aforementioned neuropsychiatric features, and that the MSNQ has potential utility for predicting euphoria and disinhibition syndromes in MS.

Preliminary evidence suggests aberrant (mostly reduced) thalamocortical (TC) connectivity in autism spectrum disorder (ASD), but despite the crucial role of thalamus in sensorimotor functions and its extensive connectivity with cerebral cortex, relevant evidence remains limited. We performed a comprehensive investigation of region-specific TC connectivity in ASD. Resting-state functional MRI and diffusion tensor imaging (DTI) data were acquired for 60 children and adolescents with ASD (ages 7–17 years) and 45 age, sex, and IQ-matched typically developing (TD) participants. We examined intrinsic functional connectivity (iFC) and anatomical connectivity (probabilistic tractography) with thalamus, using 68 unilateral cerebral cortical regions of interest (ROIs). For frontal and parietal lobes, iFC was atypically reduced in the ASD group for supramodal association cortices, but was increased for cingulate gyri and motor cortex. Temporal iFC was characterized by overconnectivity for auditory cortices, but underconnectivity for amygdalae. Occipital iFC was broadly reduced in the ASD group. DTI indices (such as increased radial diffusion) for regions with group differences in iFC further indicated compromised anatomical connectivity, especially for frontal ROIs, in the ASD group. Our findings highlight the regional specificity of aberrant TC connectivity in ASD. Their overall pattern can be largely accounted for by functional overconnectivity with limbic and sensorimotor regions, but underconnectivity with supramodal association cortices. This could be related to comparatively early maturation of limbic and sensorimotor regions in the context of early overgrowth in ASD, at the expense of TC connectivity with later maturing cortical regions.