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Emotional disorders inflict an enormous burden on society. Research on brain abnormalities implicated in emotional disorders has witnessed great progress over the past decades. Using cross‐sectional and longitudinal designs, resting state functional magnetic resonance imaging (rs‐fMRI) and its analytic approaches have been applied to characterize the local properties of patients with emotional disorders. Additionally, brain activity alterations of emotional disorders have shown frequency‐specific. Despite the gains in understanding the roles of brain abnormalities in emotional disorders, the limitation of the small sample size needs to be highlighted. Lastly, we proposed that evidence from the positive psychology research stream presents it as a viable discipline, whose suggestions could be developed in future emotional disorders research. Such interdisciplinary research may produce novel treatments and intervention options. This article is categorized under:Psychology > Brain Function and Dysfunction [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is characterized by progressive cognitive decline along with neuropsychiatric symptoms including depression and psychosis. Depression is a common psychiatric disorder occurring in people across the lifespan. Accumulating evidence indicates that depression may be a prodrome and/or a "risk factor" for AD. However, whether AD and depression share a common pathophysiological pathway is still unclear. The aim of this study was to identify regional alterations in brain function associated with depressive symptoms in mild AD patients. Thirty-two mild AD patients were evaluated using the Neuropsychiatric Inventory and Hamilton Depression Rating Scale, and were divided into two groups: 15 AD patients with depressive symptoms (D-AD) and 17 non-depressed AD (nD-AD) patients. Using the approach of regional homogeneity (ReHo), we characterized resting-state regional brain activity in D-AD and nD-AD patients. Compared with nD-AD patients, D-AD patients showed decreased ReHo in the right precentral gyrus, right superior frontal gyrus, right middle frontal gyrus, and right inferior frontal cortex. Our findings show regional brain activity alterations in D-AD patients. Thus, D-AD pathogenesis may be attributed to abnormal neural activity in multiple brain regions. [ABSTRACT FROM AUTHOR]

Recent studies using resting-state functional magnetic resonance imaging (rs-fMRI) demonstrate that there is aberrant regional spontaneous brain activity in obsessive-compulsive disorders (OCD). Nevertheless, the results of previous studies are contradictory, especially in the abnormal brain regions and the directions of their activities. It is necessary to perform a meta-analysis to identify the common pattern of altered regional spontaneous brain activity in patients with OCD. The present study conducted a systematic search for studies in English published up to May 2023 in PubMed, Web of Science, and Embase. These studies measured differences in regional spontaneous brain activity at the whole brain level using regional homogeneity (ReHo), the amplitude of low-frequency fluctuations (ALFF) and the fractional amplitude of low-frequency fluctuations (fALFF). Then the Anisotropic effect-size version of seed-based d mapping (AES-SDM) was used to investigate the consistent abnormality of regional spontaneous brain activity in patients with OCD. 27 studies (33 datasets) were included with 1256 OCD patients (650 males, 606 females) and 1176 healthy controls (HCs) (588 males, 588 females). Compared to HCs, patients with OCD showed increased spontaneous brain activity in the right inferior parietal gyrus (Brodmann Area 39), left median cingulate and paracingulate gyri (Brodmann Area 24), bilateral inferior cerebellum, right middle frontal gyrus (Brodmann Area 46), left inferior frontal gyrus in triangular part (Brodmann Area 45) and left middle frontal gyrus in orbital part (Brodmann Area 11). Meanwhile, decreased spontaneous brain activity was identified in the right precentral gyrus (Brodmann Area 4), right insula (Brodmann Area 48), left postcentral gyrus (Brodmann Area 43), bilateral superior cerebellum and left caudate (Brodmann Area 25). This meta-analysis provided a quantitative review of spontaneous brain activity in OCD. The results demonstrated that the brain regions in the frontal lobe, sensorimotor cortex, cerebellum, caudate and insula are crucially involved in the pathophysiology of OCD. This research contributes to the understanding of the pathophysiologic mechanism underlying OCD and could provide a new perspective on future diagnosis and treatment of OCD. [ABSTRACT FROM AUTHOR]

Background: Recent resting-state functional magnetic resonance imaging studies have provided strong evidence of abnormal regional spontaneous brain activities among anxiety-disordered patients. However, the evidence has been divergent and inconclusive. Therefore, it is necessary to perform a meta-analysis identifying a common pattern of altered regional spontaneous brain activity for anxiety disorders.Method: Corresponding research of anxiety disorders, namely, whole-brain rs-fMRI studies that measured differences in regional homogeneity, amplitude of low-frequency fluctuations, or fractional amplitude of low-frequency fluctuations, were analyzed in this study. Overall, seven studies with 235 anxiety-disordered patients and 241 healthy controls were ultimately included in the meta-analysis. The meta-analysis was processed by seed-based d mapping.Results: Compared with healthy controls, patients with anxiety disorders showed significantly decreased regional spontaneous brain activities in the right putamen, the right orbital inferior frontal gyrus, and the right temporal pole. No increases in regional spontaneous brain activities were detected in patients relative to the controls.Limitation: Limited number of available studies, only Asian samples, and insufficient information of sample characteristics.Conclusion: The present study suggests that anxiety disorders are associated with aberrant regional brain activity in areas connected with emotion processing, which extends our understanding of anxiety disorders' pathophysiology. [ABSTRACT FROM AUTHOR]