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Restriction of food intake is a central feature of anorexia nervosa (AN) and other eating disorders, yet also occurs in the absence of psychopathology. The neural mechanisms of restrictive eating in health and disease are unclear.
This study examined behavioral and neural mechanisms associated with restrictive eating among individuals with and without eating disorders. Dietary restriction was examined in four groups of women (n = 110): healthy controls, dieting healthy controls, patients with subthreshold (non-low weight) AN, and patients with AN. A Food Choice Task was administered during fMRI scanning to examine neural activation associated with food choices, and a laboratory meal was conducted.
Behavioral findings distinguished between healthy and ill participants. Healthy individuals, both dieting and non-dieting, chose significantly more high-fat foods than patients with AN or subthreshold AN. Among healthy individuals, choice was primarily influenced by tastiness, whereas, among both patient groups, healthiness played a larger role. Dorsal striatal activation associated with choice was most pronounced among individuals with AN and was significantly associated with selecting fewer high-fat choices in the task and lower caloric intake in the meal the following day.
A continuous spectrum of behavior was suggested by the increasing amount of weight loss across groups. Yet, data from this Food Choice Task with fMRI suggest there is a behavioral distinction between illness and health, and that the neural mechanisms underlying food choice in AN are distinct. These behavioral and neural mechanisms of restrictive eating may be useful targets for treatment development.
Subgenual cingulate cortex (SCC) responses to self-blaming emotion-evoking stimuli were previously found in individuals prone to self-blame with and without a history of major depressive disorder (MDD). This suggested SCC activation reflects self-blaming emotions such as guilt, which are central to models of MDD vulnerability.
Here, we re-examined these hypotheses in an independent larger sample. A total of 109 medication-free participants (70 with remitted MDD and 39 healthy controls) underwent fMRI whilst judging self- and other-blaming emotion-evoking statements. They also completed validated questionnaires of proneness to self-blaming emotions including those related to internal (autonomy) and external (sociotropy) evaluation, which were subjected to factor analysis.
An interaction between group (remitted MDD v. Control) and condition (self- v. other-blame) was observed in the right SCC (BA24). This was due to higher SCC signal for self-blame in remitted MDD and higher other-blame-selective activation in Control participants. Across the whole sample, extracted SCC activation cluster averages for self- v. other-blame were predicted by a regression model which included the reliable components derived from our factor analysis of measures of proneness to self-blaming emotions. Interestingly, this prediction was solely driven by autonomy/self-criticism, and adaptive guilt factors, with no effect of sociotropy/dependency.
Despite confirming the prediction of SCC activation in self-blame-prone individuals and those vulnerable to MDD, our results suggest that SCC activation reflects blame irrespective of where it is directed rather than selective for self. We speculate that self-critical individuals have more extended SCC representations for blame in the context of self-agency.
Culture as shared values/beliefs and behavioral scripts not only influences human behavior and cognition but modulates the underlying brain activity as well. Cultural impacts on the human brain have been investigated by cultural neuroscience research that examines cultural group differences in brain activities involved in specific cognitive/affective processes. The findings, however, do not allow inference of causal relationships between specific cultural values/beliefs and brain activity. Cultural priming approach tests how brain activities underlying various cognitive/affective processes are modulated by recent exposure to specific cultural symbols or activation of specific cultural values/beliefs. Increasing evidence indicates that cultural priming leads to subsequent changes of brain activities in response to perception, attention, reward, self-reflection, etc. The findings suggest that culture provides a key frame in which the human brain develops and functions to mediate multiple cognitive and affective processes.
Impairments in visual perception are among the most common developmental difficulties related to being born prematurely, and they are often accompanied by problems in other developmental domains. Neural activation in participants born prematurely and full-term during tasks that assess several areas of visual perception has not been studied. To better understand the neural substrates of the visual perceptual impairments, we compared behavioral performance and brain activations during visual perception tasks in adolescents born very preterm (birth weight ≤1500 g or gestational age <32 weeks) and full-term.
Tasks assessing visual closure, discrimination of a deviating figure, and discrimination of figure and ground from the Motor-Free Visual Perception Test, Third Edition were performed by participants born very preterm (n = 37) and full-term (n = 34) at 12 years of age during functional magnetic resonance imaging.
Behavioral performance in the visual perception tasks did not differ between the groups. However, during the visual closure task, brain activation was significantly stronger in the group born very preterm in a number of areas including the frontal, anterior cingulate, temporal, and posterior medial parietal/cingulate cortices, as well as in parts of the cerebellum, thalamus, and caudate nucleus.
Differing activations during the visual closure task potentially reflect a compensatory neural process related to premature birth or lesser neural efficiency or may be a result of the use of compensatory behavioral strategies in the study group born very preterm.
This study aimed to identify and meta-analyse the neuroimaging data and hence synthesise a brain map showing the neural correlates of watching food commercials.
Published studies were retrieved and included into the analysis if they evaluated brain responses to food commercials with functional MRI and reported results based on whole-brain analysis in standard brain coordinates.
No additional restriction was placed on the search, such as the publication year and age of participants.
Seven papers that composed of a total of 442 participants fulfilled the inclusion criteria. All of them recruited children or adolescents.
Food commercials caused larger brain responses than nonfood counterparts in the cuneus on both hemispheres, which played a role in dietary self-control and modulation of food craving. Other brain regions involved in food commercials processing included the left culmen, left middle occipital gyrus and the right superior parietal lobule, which could be related to reward, emotional responses and habit formation.
These neural correlates may help explain the food choice and eating behaviours of children and adolescents that might be relevant to the development of obesity.
Neuroimaging characteristics have demonstrated disrupted functional organization in schizophrenia (SZ), involving large-scale networks within grey matter (GM). However, previous studies have ignored the role of white matter (WM) in supporting brain function.
Using resting-state functional MRI and graph theoretical approaches, we investigated global topological disruptions of large-scale WM and GM networks in 93 SZ patients and 122 controls. Six global properties [clustering coefficient (Cp), shortest path length (Lp), local efficiency (Eloc), small-worldness (σ), hierarchy (β) and synchronization (S) and three nodal metrics [nodal degree (Knodal), nodal efficiency (Enodal) and nodal betweenness (Bnodal)] were utilized to quantify the topological organization in both WM and GM networks.
At the network level, both WM and GM networks exhibited reductions in Eloc, Cp and S in SZ. The SZ group showed reduced σ and β only for the WM network. Furthermore, the Cp, Eloc and S of the WM network were negatively correlated with negative symptoms in SZ. At the nodal level, the SZ showed nodal disturbances in the corpus callosum, optic radiation, posterior corona radiata and tempo-occipital WM tracts. For GM, the SZ manifested increased nodal centralities in frontoparietal regions and decreased nodal centralities in temporal regions.
These findings provide the first evidence for abnormal global topological properties in SZ from the perspective of a substantial whole brain, including GM and WM. Nodal centralities enhance GM areas, along with a reduction in adjacent WM, suggest that WM functional alterations may be compensated for adjacent GM impairments in SZ.
Neuroimaging techniques have rapidly expanded our understanding of how the brain responds to addiction in humans. This chapter will discuss methods used to assess brain response, how the data is analyzed, and how it can be used to better understand addiction. Foundational to inferences drawn from these methods is study design. Common designs employed in human neuroimaging research are discussed, including cross-sectional designs, longitudinal/cohort designs, and experimental designs. A description of various neuroimaging methods and their strengths and weaknesses is included: functional magnetic resonance imaging (fMRI), positron-emission tomography, electroencephalogram, magnetoencephalography, structural MRI, and resting state fMRI. Given its popularity in research, discussion of MRI includes details on paradigm design and data analysis of functional and structural MRI, as well as some common oversights in data processing and interpretation of results.
Although deficits in affective processing are a core component of anorexia nervosa (AN), we lack a detailed characterization of the neurobiological underpinnings of emotion regulation impairment in AN. Moreover, it remains unclear whether these neural correlates scale with clinical outcomes.
We investigated the neural correlates of negative emotion regulation in a sample of young women receiving day-hospital treatment for AN (n = 21) and healthy controls (n = 21). We aimed to determine whether aberrant brain activation patterns during emotion regulation predicted weight gain following treatment in AN patients and were linked to AN severity. To achieve this, participants completed a cognitive reappraisal paradigm during functional magnetic resonance imaging. Skin conductance response, as well as subjective distress ratings, were recorded to corroborate task engagement.
Compared to controls, patients with AN showed reduced activation in the dorsolateral prefrontal cortex (dlPFC) during cognitive reappraisal [pFWE<0.05, threshold-free cluster enhancement (TFCE) corrected]. Importantly, psycho–physiological interaction analysis revealed reduced functional connectivity between the dlPFC and the amygdala in AN patients during emotion regulation (pFWE<0.05, TFCE corrected), and dlPFC-amygdala uncoupling was associated with emotion regulation deficits (r = −0.511, p = 0.018) and eating disorder severity (r = −0.565, p = .008) in the AN group. Finally, dlPFC activity positively correlated with increases in body mass index (r = 0.471, p = 0.042) and in body fat mass percentage (r = 0.605, p = 0.008) following 12 weeks of treatment.
Taken together, our findings indicate that individuals with AN present altered fronto-amygdalar response during cognitive reappraisal and that this response may serve as a predictor of response to treatment and be linked to clinical severity.
Given the prevalence of adolescent depression and the modest effects of current treatments, research ought to inform development of effective intervention strategies. Self-compassion is inversely associated with depression, and self-compassion interventions have demonstrated promising effects on reducing depression. However, little is known about the neural mechanisms underlying that relationship. Maladaptive self-processing is a characteristic of depression that contributes to the onset and chronicity of depression. Because our own face is an automatic and direct cue for self-processing, this study investigated whether self-compassion was associated with neural responses during sad v. neutral self-face recognition and explore their relationship with depression severity in depressed adolescents and healthy controls (HCs).
During functional magnetic resonance imaging, 81 depressed youth and 37 HCs were instructed to identify whether morphed self or other faces with sad, happy, or neutral expressions resembled their own.
Self-compassion correlated negatively with activity during sad v. neutral self-face recognition in the dorsal anterior cingulate cortex in the total sample, and in the right posterior cingulate cortex/precuneus in HCs, respectively. In depressed adolescents, higher self-compassion correlated with lower activity during sad v. neutral self-face recognition in the right dorsolateral prefrontal cortex (DLPFC), implying that less cognitive effort might be needed to avoid dwelling on sad self-faces and/or regulate negative affect induced by them. Moreover, higher self-compassion mediated the relationship between lower DLPFC activity and reduced depression severity.
Our findings imply that DLPFC activity might be a biological marker of a successful self-compassion intervention as potential treatment for adolescent depression.
We review basic science research on neural mechanisms underlying emotional processing in individuals of differing socioeconomic status (SES). We summarise SES differences in response to positive and negative stimuli in limbic and cortical regions associated with emotion and emotion regulation. We discuss the possible relevance of neuroscience to understanding the link between mental health and SES. We hope to provide insights into future neuroscience research on the etiology and pathophysiology of mental disorders relating to SES.
The default mode network (DMN) dysfunction has emerged as a consistent biological correlate of multiple psychiatric disorders. Specifically, there is evidence of alterations in DMN cohesiveness in schizophrenia, mood and anxiety disorders. The aim of this study was to synthesize at a fine spatial resolution the intra-network functional connectivity of the DMN in adults diagnosed with schizophrenia, mood and anxiety disorders, capitalizing on powerful meta-analytic tools provided by activation likelihood estimation.
Results from 70 whole-brain resting-state functional magnetic resonance imaging articles published during the last 15 years were included comprising observations from 2,789 patients and 3,002 healthy controls.
Specific regional changes in DMN cohesiveness located in the anteromedial and posteromedial cortex emerged as shared and trans-diagnostic brain phenotypes. Disease-specific dysconnectivity was also identified. Unmedicated patients showed more DMN functional alterations, highlighting the importance of interventions targeting the functional integration of the DMN.
This study highlights functional alteration in the major hubs of the DMN, suggesting common abnormalities in self-referential mental activity across psychiatric disorders.
Emotional experiences are often more likely than neutral experiences to be remembered, or to be retrieved richly. In this chapter, we provide an overview of how the effects of emotion arise, emphasizing the effects that operate during the initial experience of the event (encoding), the storage and stabilization of the memory trace for that experience (consolidation), and the accessing of that trace (retrieval). We discuss how these effects of emotion can explain both why emotion enhances many aspects of memory throughout the adult life span and also why there are often age-by-valence interactions in memory, with older adults remembering information more positively than younger adults.
In this chapter, we provide an overview of how a strategy perspective fruitfully contributes to our understanding of aging effects on cognitive functioning and brain activations. We review previous research showing that people use a wide variety of strategies to accomplish cognitive tasks and how strategy use evolves during aging. Although strategic variations are modulated by individual differences and experimental conditions, older adults have been found to use fewer strategies, to use the more demanding strategies less often, to select the most appropriate strategy on each problem less often, and to be less efficient when executing a given strategy than young adults. Adopting a strategy approach enables better characterization of age-related changes observed in brain activations during task completion and contributes to specify the mechanistic and functional significance of age-related changes in neural recruitments. Finally, we review recent evidence suggesting that cognitive control processes underlie age-related changes in strategy use.
This commentary gives an overview of two types of interaction between neuroscience and psychotherapy in BPD and beyond. First, neuroscientific research, particularly neuroimaging, can be used to better understand the mechanisms how successful psychotherapy exerts its effects. Since emotion dysregulation is one of the core features of BPD and the main target of Dialectical Behavior Therapy (DBT), neuroimaging studies have investigated emotional hyperreactivity and dysfunctional regulation before and after DBT. These studies found normalization of limbic hyper-reactivity as well as a decrease of dysfunctional pain-induced emotion regulation, which is assumed to underly self-injurious behavior. A second line of research tries to use neuroimaging in the development of new therapeutic approaches such as real-time fMRI neurofeedback. Preliminary studies revealed rapid normalization of amygdala hyperreactivity and restoration of the connectivity between amygdala and medial prefrontal cortex. This was accompanied by reductions of BPD symptomatology, affective instability, and startle response. With these new approaches, there is hope to better understand mechanisms of change in BPD treatment as well as to develop innovative therapy approaches for severe emotion dysregulation.
One hypothesis proposed to underlie formal thought disorder (FTD), the incoherent speech is seen in some patients with schizophrenia, is that it reflects impairment in frontal/executive function. While this proposal has received support in neuropsychological studies, it has been relatively little tested using functional imaging. This study aimed to examine brain activations associated with FTD, and its two main factor-analytically derived subsyndromes, during the performance of a working memory task.
Seventy patients with schizophrenia showing a full range of FTD scores and 70 matched healthy controls underwent fMRI during the performance of the 2-back version of the n-back task. Whole-brain corrected, voxel-based correlations with FTD scores were examined in the patient group.
During 2-back performance the patients showed clusters of significant inverse correlation with FTD scores in the inferior frontal cortex and dorsolateral prefrontal cortex bilaterally, the left temporal cortex and subcortically in the basal ganglia and thalamus. Further analysis revealed that these correlations reflected an association only with ‘alogia’ (poverty of speech, poverty of content of speech and perseveration) and not with the ‘fluent disorganization’ component of FTD.
This study provides functional imaging support for the view that FTD in schizophrenia may involve impaired executive/frontal function. However, the relationship appears to be exclusively with alogia and not with the variables contributing to fluent disorganization.
The Arsenic (+3 oxidation state) methyltransferase (AS3MT) gene has been identified as a top risk gene for schizophrenia in several large-scale genome-wide association studies. A variable number tandem repeat (VNTR) of this gene is the most significant expression quantitative trait locus, but its role in brain activity in vivo is still unknown.
We first performed a functional magnetic resonance imaging (fMRI) scan of 101 healthy subjects during a memory span task, trained all subjects on an adaptive memory span task for 1 month, and finally performed another fMRI scan after the training. After excluding subjects with excessive head movements for one or more scanning sessions, data from 93 subjects were included in the final analyses.
The VNTR was significantly associated with both baseline brain activation and training-induced changes in multiple regions including the prefrontal cortex and the anterior and posterior cingulate cortex. Additionally, it was associated with baseline brain activation in the striatum and the parietal cortex. All these results were corrected based on the family-wise error rate method across the whole brain at the peak level.
This study sheds light on the role of AS3MT gene variants in neural plasticity related to memory span training.
It is well-known that attention deficit hyperactivity disorder (ADHD) is associated with changes in the dopaminergic system. However, the relationship between central dopaminergic tone and the blood oxygen level-dependent (BOLD) signal during receipt of rewards and penalties in the corticostriatal pathway in adults with ADHD is unclear.
Single-photon emission computed tomography with [99mTC]TRODAT-1 was used to assess striatal dopamine transporter (DAT) availability. Event-related functional magnetic resonance imaging was conducted on subjects performing the Iowa Gambling Test.
DAT availability was found to be associated with the BOLD response, which was a covariate of monetary loss, in the medial prefrontal cortex (r = 0.55, P = .03), right ventral striatum (r = 0.69, P = .003), and right orbital frontal cortex (r = 0.53, P = .03) in adults with ADHD. However, a similar correlation was not found in the controls.
The results confirmed that dopaminergic tone may play a different role in the penalty-elicited response of adults with ADHD. It is plausible that a lower neuro-threshold accompanied by insensitivity to punishment could be exacerbated by the hypodopaminergic tone in ADHD.
A better understanding of the pathophysiology of suicidal behaviour (SB) may enable the discovery of more specific treatments and a better identification of vulnerable patients. The vulnerability to SB appears to be underlied by genetic factors coding for traits rendering the individual less able to cope with stressing situations, and more likely to be engaged in a suicidal process.
During the recent years, neuroscientific studies begun to identify potential endophenotypes.
We have shown that disadvantageous decision making (DM) was involved in the vulnerability to SB. DM impairment appears to be independent of comorbid psychiatric disorders, associated with emotional dysregulation (i.e. affective lability trait and skin conductance responses), and modulated by serotonergic genotypes associated with SB. In recent fMRI studies, the region that is likely involved in DM, is overactivited in response to angry faces, suggesting a higher sensitivity to specific negative social stimuli. Deficit in risk evaluation and excessive response to specific emotional stimuli may represent key processes in the vulnerability to SB.
These potential endophenotypes may represent future relevant markers of vulnerability for the identification of vulnerable patients, and relevant targets for the development of new treatments.
The objective of this study was to develop new standardized alcohol-associated cues and assess their effects on brain activation with functional magnetic resonance imaging (fMRI). Pictures of alcoholic and neutral beverages and affectively neutral pictures were presented to 44 abstinent alcoholics and 37 age-matched healthy control subjects. We assessed the skin conductance response, and the elicited arousal and valence. Alcoholics and control subjects did not differ in arousal, valence or skin conductance response evoked by alcohol-associated and affectively neutral stimuli, while nonalcoholic beverages were rated as more unpleasant and arousing by alcoholics compared with control subjects. In the fMRI pilot study, alcohol and abstract pictures were presented to six abstinent alcoholics and induced a significant activation of brain areas associated with visual emotional processes such as the fusiform gyrus, parts of the brain reward system (basal ganglia and orbitofrontal gyrus) and further brain regions in the frontal and parietal cortices associated with the attention network. These observations suggest that standardized pictures of alcoholic beverages can be used to assess brain circuits involved in the processing and evaluation of alcohol cues.
The functional neuroimaging studies of emotion processing in schizophrenia have revealed variable results attributed partly to differential symptomatology and sex of tested patients. The aim of the present study was to investigate the relationship between cerebral activations during exposure to emotional material and schizophrenia symptoms in men versus women.
Fifteen men and 10 women with schizophrenia, equivalent in terms of age, medication and experienced symptomatology, underwent functional MRI during viewing sad and neutral film excerpts. Data were analyzed using Statistical Parametric Mapping Software (SPM2).
Across all the patients there was a significant inverse relationship between negative symptoms and activations in the right prefrontal cortex during processing of sad versus neutral stimuli. In men, activations during sad versus neutral stimuli in the prefrontal, temporal and anterior cingulate cortex, as well as the caudate and cerebellum, were positively correlated with negative symptoms. In women, there were inverse correlations between positive symptoms and activations in the hippocampus, parietal and occipital cortex during the same condition.
Present results confirmed association of prefrontal hypofunction with negative symptoms in schizophrenia. More interestingly, the results revealed a diametrically different pattern of symptom-correlated brain activity in men and women with schizophrenia, suggesting that the processing of sadness is mediated via neurophysiological mechanism related to negative symptoms in men and the mechanism related to positive symptoms in women.