Psychoradiology最新文献

Alcohol use disorder (AUD) is a worldwide problem and the most common substance use disorder. Chronic alcohol consumption may have negative effects on the body, the mind, the family, and even society. With the progress of current neuroimaging methods, an increasing number of imaging techniques are being used to objectively detect brain impairment induced by alcoholism and serve a vital role in the diagnosis, prognosis, and treatment assessment of AUD. This article organizes and analyzes the research on alcohol dependence concerning the main noninvasive neuroimaging methods, structural magnetic resonance imaging, functional magnetic resonance imaging, and electroencephalography, as well as the most common noninvasive brain stimulation - transcranial magnetic stimulation, and intersperses the article with joint intra- and intergroup studies, providing an outlook on future research directions.

There is considerable interest in the significance of structural and functional connections between the two brain hemispheres in terms of both normal function and in relation to psychiatric disorders. In recent years, many studies have used voxel mirrored homotopic connectivity analysis of resting state data to investigate the importance of connectivity between homotopic regions in the brain hemispheres in a range of neuropsychiatric disorders. The current review summarizes findings from these voxel mirrored homotopic connectivity studies in individuals with autism spectrum disorder, addiction, attention deficit hyperactivity disorder, anxiety and depression disorders, and schizophrenia, as well as disorders such as Alzheimer's disease, mild cognitive impairment, epilepsy, and insomnia. Overall, other than attention deficit hyperactivity disorder, studies across psychiatric disorders report decreased homotopic resting state functional connectivity in the default mode, attention, salience, sensorimotor, social cognition, visual recognition, primary visual processing, and reward networks, which are often associated with symptom severity and/or illness onset/duration. Decreased homotopic resting state functional connectivity may therefore represent a transdiagnostic marker for general psychopathology. In terms of disorder specificity, the extensive decreases in homotopic resting state functional connectivity in autism differ markedly from attention deficit hyperactivity disorder, despite both occurring during early childhood and showing extensive co-morbidity. A pattern of more posterior than anterior regions showing reductions in schizophrenia is also distinctive. Going forward, more studies are needed to elucidate the functions of these homotopic functional connections in both health and disorder and focusing on associations with general psychopathology, and not only on disorder specific symptoms.

Background: Disruptive behaviors, including agitation, disinhibition, irritability, and aberrant motor behaviors, are commonly observed in patients with Alzheimer's disease (AD). However, the neuroanatomical basis of these disruptive behaviors is not fully understood.

Objective: To confirm the differences in cortical thickness and surface area between AD patients and healthy controls and to further investigate the features of cortical thickness and surface area associated with disruptive behaviors in patients with AD.

Methods: One hundred seventy-four participants (125 AD patients and 49 healthy controls) were recruited from memory clinics at the Peking University Institute of Sixth Hospital. Disruptive behaviors, including agitation/aggression, disinhibition, irritability/lability, and aberrant motor activity subdomain scores, were evaluated using the Neuropsychiatry Inventory. Both whole-brain vertex-based and region-of-interest-based cortical thickness and surface area analyses were automatically conducted with the CIVET pipeline based on structural magnetic resonance images. Both group-based statistical comparisons and brain-behavior association analyses were performed using general linear models, with age, sex, and education level as covariables.

Results: Compared with healthy controls, the AD patients exhibited widespread reduced cortical thickness, with the most significant thinning located in the medial and lateral temporal and parietal cortex, and smaller surface areas in the left fusiform and left inferior temporal gyrus. High total scores of disruptive behaviors were significantly associated with cortical thinning in several regions that are involved in sensorimotor processing, language, and expression functions. The total score of disruptive behaviors did not show significant associations with surface areas.

Conclusion: We highlight that disruptive behaviors in patients with AD are selectively associated with cortical thickness abnormalities in sensory, motor, and language regions, which provides insights into neuroanatomical substrates underlying disruptive behaviors. These findings could lead to sensory, motor, and communication interventions for alleviating disruptive behaviors in patients with AD.

Background: Resting-state functional magnetic resonance imaging (RS-fMRI) has been proved to be a useful tool to study the brain mechanism in the quest to probe the distinct pattern of inter-region interactions in the brain. As an important application of RS-fMRI, the graph-based approach characterizes the brain as a complex network. However, the network is susceptible to its scale that determines the trade-off between sensitivity and anatomical variability.

Objective: To balance sensitivity and anatomical variability, a pyramid representation of the functional network is proposed, which is composed of five individual networks reconstructed at multiple scales.

Methods: The pyramid representation of the functional network was applied to two groups of participants, including patients with Alzheimer's disease (AD) and normal elderly (NC) individuals, as a demonstration. Features were extracted from the multi-scale networks and were evaluated with their inter-group differences between AD and NC, as well as the discriminative power in recognizing AD. Moreover, the proposed method was also validated by another dataset from people with autism.

Results: The different features reflect the highest sensitivity to distinguish AD at different scales. In addition, the combined features have higher accuracy than any single scale-based feature. These findings highlight the potential use of multi-scale features as markers of the disrupted topological organization in AD networks.

Conclusion: We believe that multi-scale metrics could provide a more comprehensive characterization of the functional network and thus provide a promising solution for representing the underlying functional mechanism in the human brain on a multi-scale basis.

The link between cognitive function and emotion regulation may be helpful in better understanding the onset, maintenance, and treatment for depression. However, it remains unclear whether there are neural correlates between emotion dysregulation and cognitive deficits in depression. To address this question, we first review the neural representations of emotion dysregulation and cognitive deficits in depression (including deficits in cognitive control and cognitive biases). Based on the comparisons of neural representations of emotion dysregulation versus cognitive deficits, we propose an accessible and reasonable link between emotion dysregulation, cognitive control, and cognitive biases in depression. Specifically, cognitive control serves the whole process of emotion regulation, whereas cognitive biases are engaged in emotion regulation processes at different stages. Moreover, the abnormal implementation of different emotion regulation strategies in depression is consistently affected by cognitive control, which is involved in the dorsolateral, the dorsomedial prefrontal cortex, and the anterior cingulate cortex. Besides, the relationship between different emotion regulation strategies and cognitive biases in depression may be distinct: the orbitofrontal cortex contributes to the association between ineffective reappraisal and negative interpretation bias, while the subgenual prefrontal cortex and the posterior cingulate cortex underline the tendency of depressed individuals to ruminate and overly engage in self-referential bias. This review sheds light on the relationship between cognitive deficits and emotion dysregulation in depression and identifies directions in need of future attention.

Background: Cortical functional network alterations have been widely accepted as the neural basis of attention-deficit/hyperactivity disorder (ADHD). Recently, white matter has also been recognized as a novel neuroimaging marker of psychopathology and has been used as a complement to cortical functional networks to investigate brain-behavior relationships. However, disorder-specific features of white matter functional networks (WMFNs) are less well understood than those of gray matter functional networks. In the current study, we constructed WMFNs using a new strategy to characterize behavior-related network features in ADHD.

Methods: We recruited 46 drug-naïve boys with ADHD and 46 typically developing (TD) boys, and used clustering analysis on resting-state functional magnetic resonance imaging data to generate WMFNs in each group. Intrinsic activity within each network was extracted, and the associations between network activity and behavior measures were assessed using correlation analysis.

Results: Nine WMFNs were identified for both ADHD and TD participants. However, boys with ADHD showed a splitting of the inferior corticospinal-cerebellar network and lacked a cognitive control network. In addition, boys with ADHD showed increased activity in the dorsal attention network and somatomotor network, which correlated positively with attention problems and hyperactivity symptom scores, respectively, while they presented decreased activity in the frontoparietal network and frontostriatal network in association with poorer performance in response inhibition, working memory, and verbal fluency.

Conclusions: We discovered a dual pattern of white matter network activity in drug-naïve ADHD boys, with hyperactive symptom-related networks and hypoactive cognitive networks. These findings characterize two distinct types of WMFN in ADHD psychopathology.

Autism spectrum disorder (ASD) is a formidable challenge for psychiatry and neuroscience because of its high prevalence, lifelong nature, complexity, and substantial heterogeneity. A major goal of neuroimaging studies of ASD is to understand the neurobiological underpinnings of this disorder from multi-dimensional and multi-level perspectives, by investigating how brain anatomy, function, and connectivity are altered in ASD, and how they vary across the population. However, ongoing debate exists within those studies, and neuroimaging findings in ASD are often contradictory. Over the past decade, we have dedicated to delineate a comprehensive and consistent mapping of the abnormal structure and function of the autistic brain, and this review synthesizes the findings across our studies reaching a consensus that the "social brain" are the most affected regions in the autistic brain at different levels and modalities. We suggest that the social brain network can serve as a plausible biomarker and potential target for effective intervention in individuals with ASD.

Background: Pediatric bipolar disorder (PBD) has been proven to be related to abnormal brain structural connectivity, but how the abnormalities in PBD correlate with gene expression is debated.

Objective: This study aims at identification of cell-type-specific gene modules based on cortical structural differences in PBD.

Methods: Morphometric similarity networks (MSN) were computed as a marker of interareal cortical connectivity based on MRI data from 102 participants (59 patients and 43 controls). Partial least squares (PLS) regression was used to calculate MSN differences related to transcriptomic data in AHBA. The biological processes and cortical cell types associated with this gene expression profile were determined by gene enrichment tools.

Results: MSN analysis results demonstrated differences of cortical structure between individuals diagnosed with PBD and healthy control participants. MSN differences were spatially correlated with the PBD-related weighted genes. The weighted genes were enriched for "trans-synaptic signaling" and "regulation of ion transport", and showed significant specific expression in excitatory and inhibitory neurons.

Conclusions: This study identified the genes that contributed to structural network aberrations in PBD. It was found that transcriptional changes of excitatory and inhibitory neurons might be associated with abnormal brain structural connectivity in PBD.

[This corrects the article DOI: 10.1093/psyrad/kkab009.][This corrects the article DOI: 10.1093/psyrad/kkab017.].

Mental disorders are common health concerns and contribute to a heavy global burden on our modern society. It is challenging to identify and treat them timely. Neuroimaging evidence suggests the incidence of various psychiatric and behavioral disorders is closely related to the atypical development of brain structure and function. The identification and understanding of atypical brain development provide chances for clinicians to detect mental disorders earlier, perhaps even prior to onset, and treat them more precisely. An invaluable and necessary method in identifying and monitoring atypical brain development are growth charts of typically developing individuals in the population. The brain growth charts can offer a series of standard references on typical neurodevelopment, representing an important resource for the scientific and medical communities. In the present paper, we review the relationship between mental disorders and atypical brain development from a perspective of normative brain development by surveying the recent progress in the development of brain growth charts, including four aspects on growth chart utility: 1) cohorts, 2) measures, 3) mechanisms, and 4) clinical translations. In doing so, we seek to clarify the challenges and opportunities in charting brain growth, and to promote the application of brain growth charts in clinical practice.