Anxiety is a mental state characterized by an intense sense of tension, worry or apprehension, relative to something adverse that might happen in the future. Researchers differentiate aspects of anxiety into state and trait, respectively defined as a more transient reaction to an adverse situation, and as a more stable personality attribute in experiencing events. It is yet unclear whether brain structural and functional features may distinguish these aspects of anxiety. To study this, we assessed 42 healthy participants with the State-Trait Anxiety Inventory and then investigated with MRI to characterize structural grey matter covariance and resting-state functional connectivity (rs-FC). We found several differences in the structural–functional patterns across anxiety types: (1) trait anxiety was associated to both structural covariance of Default Mode Network (DMN), with an increase in dorsal nodes and a decrease in its ventral part, and to rs-FC of DMN within frontal regions; (2) state anxiety, instead, was widely related to rs-FC of Salience Network and of DMN, specifically in its ventral nodes, but not associated with any structural pattern. In conclusion, our study provides evidence of a neuroanatomical and functional distinction between state and trait anxiety. These neural features may be additional markers in future studies evaluating early diagnosis or treatment effects.

The purpose of this paper is to review some of the psychological and neural mechanisms behind mindfulness practice in order to explore the unique factors that account for its positive impact on emotional regulation and health. After reviewing the mechanisms of mindfulness and its effects on clinical populations we will consider how the practice of mindfulness contributes to the regulation of emotions. We argue that mindfulness has achieved effective outcomes in the treatment of anxiety, depression, and other psychopathologies through the contribution of mindfulness to emotional regulation. We consider the unique factors that mindfulness meditation brings to the process of emotion regulation that may account for its effectiveness. We review experimental evidence that points towards the unique effects of mindfulness specifically operating over and above the regulatory effects of cognitive reappraisal mechanisms. A neuroanatomical circuit that leads to mindful emotion regulation is also suggested. This paper thereby aims to contribute to proposed models of mindfulness for research and theory building by proposing a specific model for the unique psychological and neural processes involved in mindful detachment that account for the effects of mindfulness over and above the effects accounted for by other well-established emotional regulation processes such as cognitive reappraisal.

Autistic spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social interactions, communication and stereotyped behaviour. Recent evidence from neuroimaging supports the hypothesis that ASD deficits in adults may be related to abnormalities in a specific frontal-temporal network [Autism-specific Structural Network (ASN)]. To see whether these results extend to younger children and to better characterize these abnormalities, we applied three morphometric methods on brain grey matter (GM) of children with and without ASD. We selected 39 sMRI images of male children with ASD and 42 typically developing (TD) from the Autism Brain Imaging Data Exchange database. We used source-based morphometry (SoBM), a whole-brain multivariate approach to identify GM networks, voxel-based morphometry (VBM), a voxel-wise comparison of the local GM concentration and surface-based morphometry (SuBM) for the estimation of the cortical parameters. SoBM showed a bilateral frontal-parietal-temporal network different between groups, including the inferior-middle temporal gyrus, the inferior parietal lobule and the postcentral gyrus; VBM returned differences only in the right temporal lobe; SuBM returned a thinning in the right inferior temporal lobe thinner in ASD, a higher gyrification in the right superior parietal lobule in TD and in the middle frontal gyrus in ASD. For the first time, we investigated the brain abnormalities in children with ASD using three morphometric techniques. The results were relatively consistent between methods, stressing the role of an Autism-specific Structural Network in ASD individuals. We also make methodological speculations on the relevance of using multivariate and whole-brain neuroimaging analysis to capture ASD complexity.

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Emotion regulation plays a crucial role in an individual's well-being, as it is known that deficits in regulating emotions can lead to psychological and psychiatric disorders. Cognitive reappraisal is widely considered to be an adaptive and effective emotionregulation strategy. People are more or less able to apply it, but it is still not clear how reappraisal affects brain structures and the psychological profile of individuals. In our study we thus aimed to explore the impact of applying reappraisal at both the neural and the psychological level. Source-based morphometry (SBM), a whole-brain multivariate method based on the Independent Component Analysis that extracts patterns of covariation of gray matter ("independent networks"), was applied to the MRI images of 37 participants. In order to enrich their psychological profiles, we measured their experienced affectivity (PANAS) and their empathic abilities (IRI). Based on the frequency of applying reappraisal (ERQ), participants were divided into low and high reappraisers (18 vs. 19). An independent source of gray matter emerged as being different between the groups: specifically, low reappraisers showed more gray matter volume concentration in a network including the frontal, temporal, and parietal regions as compared to high reappraisers. At the psychological level, low reappraisers reported a more strongly experienced negative affect, while no difference among reappraisers emerged with regard to empathic abilities. Capitalizing on a multivariate method for structural analysis that is innovative in this field, this study extends previous observations on individual differences in the ability to regulate emotions, and it describes a plausible impact of reappraisal on brain structures and affectivity.

Shame plays a fundamental role in the regulation of our social behavior. One intriguing question is whether amygdala might play a role in processing this emotion. In the present single-case study, we tested a patient with acquired damage of bilateral amygdalae and surrounding areas as well as healthy controls on shame processing and other social cognitive tasks. Results revealed that the patient’s subjective experience of shame, but not of guilt, was more reduced than in controls, only when social standards were violated, while it was not different than controls in case of moral violations. The impairment in discriminating between normal social situations and violations also emerged. Taken together, these findings suggest that the role of the amygdala in processing shame might reflect its relevance in resolving ambiguity and uncertainty, in order to correctly detect social violations and to generate shame feelings.

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Anorexia Nervosa has been associated with white matter abnormalities implicating subcortical abnormal myelination. Extending these findings to intracortical myelin has been challenging but ultra-high field neuroimaging offers new methodological opportunities. To test the integrity of intracortical myelin in AN we used 7 T neuroimaging to acquire T1-weighted images optimized for intracortical myelin from seven females with AN (age range: 18–33) and 11 healthy females (age range: 23–32). Intracortical T1 values (inverse index of myelin concentration) were extracted from 148 cortical regions at ten depth-levels across the cortical ribbon. Across all cortical regions, these levels were averaged to generate estimates of total intracortical myelin concentration and were clustered using principal component analyses into two clusters; the outer cluster comprised T1 values across depth-levels ranging from the CSF boundary to the middle of the cortical regions and the inner cluster comprised T1 values across depth-levels ranging from the middle of the cortical regions to the gray/white matter boundary. Individuals with AN exhibited higher T1 values (i.e., decreased intracortical myelin concentration) in all three metrics. It remains to be established if these abnormalities result from undernutrition or specific lipid nutritional imbalances, or are trait markers; and whether they may contribute to neurobiological deficits seen in AN.