Psychiatry Research: Neuroimaging最新文献

Adverse childhood experiences (ACEs) negatively affect the function and structure of emotion brain circuits, increasing the risk of various psychiatric disorders. It is unclear if ACEs show disorder specificity with respect to their effects on brain structure. We aimed to investigate whether the structural brain effects of ACEs differ between patients with major depression (MDD) and borderline personality disorder (BPD). These disorders share many symptoms but likely have different etiologies. To achieve our goal, we obtained structural 3T-MRI images from 20 healthy controls (HC), 19 MDD patients, and 18 BPD patients, and measured cortical thickness and subcortical gray matter volumes. We utilized the Adverse Childhood Experiences (ACE) questionnaire to quantify self-reported exposure to childhood trauma. Our findings suggest that individuals with MDD exhibit a smaller cortical thickness when compared to those with BPD. However, ACEs showed a significantly affected relationship with cortical thickness in BPD but not in MDD. ACEs were found to be associated with thinning in cortical regions involved in emotional behavior in BPD, whereas HC showed an opposite association. Our results suggest a potential mechanism of ACE effects on psychopathology involving changes in brain structure. These findings highlight the importance of early detection and intervention strategies.

Altered brain network profiles in schizophrenia (SCZ) during memory consolidation are typically observed during task-active periods such as encoding or retrieval. However active processes are also sub served by covert periods of memory consolidation. These periods are active in that they allow memories to be recapitulated even in the absence of overt sensorimotor processing. It is plausible that regions central to memory formation like the dlPFC and the hippocampus, exert network signatures during covert periods. Are these signatures altered in patients? The question is clinically relevant because real world learning and memory is facilitated by covert processing, and may be impaired in schizophrenia. Here, we compared network signatures of the dlPFC and the hippocampus during covert periods of a learning and memory task. Because behavioral proficiency increased non-linearly, functional connectivity of the dlPFC and hippocampus [psychophysiological interaction (PPI)] was estimated for each of the Early (linear increases in performance) and Late (asymptotic performance) covert periods. During Early periods, we observed hypo-modulation by the hippocampus but hyper-modulation by dlPFC. Conversely, during Late periods, we observed hypo-modulation by both the dlPFC and the hippocampus. We stitch these results into a conceptual model of network deficits during covert periods of memory consolidation.

Although functional changes of the frontal and (para)limbic area for emotional hyper-reactivity and emotional dysregulation are well documented in social anxiety disorder (SAD), prior studies on structural changes have shown mixed results. This study aimed to identify differences in cortical thickness between SAD and healthy controls (CON). Thirty-five patients with SAD and forty-two matched CON underwent structural magnetic resonance imaging. A vertex-based whole brain and regional analyses were conducted for between-group comparison. The whole-brain analysis revealed increased cortical thickness in the left insula, left superior parietal lobule, left superior temporal gyrus, and left frontopolar cortex in patients with SAD compared to CON, as well as decreased thickness in the left superior/middle frontal gyrus and left fusiform gyrus in patients (after multiple-correction). The results from the ROI analysis did not align with these findings at the statistically significant level after multiple corrections. Changes in cortical thickness were not correlated with social anxiety symptoms. While consistent results were not obtained from different analysis methods, the results from the whole-brain analysis suggest that patients with SAD exhibit distinct neural deficits in areas involved in salience, attention, and socioemotional processing.

Background

The symptoms of pediatric bipolar disorder (PBD)-I and PBD-II differ, but accurate identification at an early stage is difficult and may prevent effective treatment of this disorder. Therefore, it is urgent to elucidate a biological marker based on objective imaging indicators to help distinguish the two. Therefore, this research aims to compare the functional connectivity between PBD-I patient and PBD-II patient in different brain networks.

Methods

Our study enrolled 31 PBD-I and 23 PBD-II patients from 12 to 17 years of age. They were analyzed by resting state-functional connectivity through Independent component analysis (ICA).

Results

We found differences between PBD-I and PBD-II in functional connectivity of the default network, frontoparietal network, salience network and limbic system. In addition, the clinical features, cognitive functions are associated with the functional connectivity of the intrinsic networks in PBD-I and PBD-II separately.

Conclusion

This research is the first to find differences in functional connectivity between PBD-I and PBD-II, suggesting that abnormality of the functional connectivity within large networks may be biomarkers that help differentiate PBD-I from PBD-II in the future.

This review summarizes the current state of neuroimaging research on obsessive-compulsive disorder (OCD) using diffusion tensor imaging (DTI), which allows for the examination of white matter abnormalities in the brain. DTI studies on individuals with obsessive-compulsive disorder (OCD) consistently demonstrate widespread reductions in white matter integrity in various regions of the brain, including the corpus callosum, anterior and posterior cingulate cortex, and prefrontal cortex, which are involved in emotion regulation, decision-making, and cognitive control. However, the reviewed studies often have small sample sizes, and findings vary between studies, highlighting the need for larger and more standardized studies. Furthermore, discerning between causal and consequential effects of OCD on white matter integrity poses a challenge. Addressing this issue may be facilitated through longitudinal studies, including those evaluating the impact of treatment interventions, to enhance the accuracy of DTI data acquisition and processing, thereby improving the validity and comparability of study outcomes. In summary, DTI studies provide valuable insights into the neural circuits and connectivity disruptions in OCD, and future studies may benefit from standardized data analysis and larger sample sizes to determine whether structural abnormalities could be potential biomarkers for early identification and treatment of OCD.

Backgrounds

Fatigability is prevalent in older adults. However, it is often associated with depressed mood. We aim to investigate these two psychobehavioral constructs by examining their underpinning of white matter structures in the brain and their associations with different medical conditions.

Methods

Twenty-seven older adults with late-life depression (LLD) and 34 cognitively normal controls (CN) underwent multi-shell diffusion MRI. Fatigability was measured with the Pittsburgh Fatigability Scale. We examined white matter integrity by measuring the quantitative anisotropy (QA), a fiber tracking parameter with better accuracy than the traditional imaging technique.

Results

We found those with LLD had lower QA in the 2nd branch of the left superior longitudinal fasciculus (SLF-II), and those with more physical fatigability had lower QA in more widespread brain regions. In tracts associated with more physical fatigability, the lower QA in left acoustic radiation and left superior thalamic radiation correlated with higher blood glucose (r = - 0.46 and - 0.49). In tracts associated with depression, lower QA in left SLF-II correlated with higher bilirubin level (r = - 0.58).

Discussion

Depression and fatigability were associated with various white matter integrity changes, which correlated with biochemistry biomarkers all related to inflammation.

Dimensional models of psychopathology may provide insight into mechanisms underlying comorbid depression and anxiety and improve specificity and sensitivity of neuroanatomical findings. The present study is the first to examine neural structure alterations using the empirically derived Tri-level Model. Depression and anxiety symptoms of 269 young adults were assessed using the Tri-level Model dimensions: General Distress (transdiagnostic depression and anxiety symptoms), Anhedonia-Apprehension (relatively specific depression symptoms), and Fears (specific anxiety symptoms). Using structural MRI, gray matter volumes were extracted for emotion generation (amygdala, nucleus accumbens) and regulation (orbitofrontal, ventrolateral, and dorsolateral prefrontal cortex) regions, often implicated in depression and anxiety. Each Tri-level symptom was regressed onto each region of interest, separately, adjusting for relevant covariates. General Distress was significantly associated with smaller gray matter volumes in bilateral orbitofrontal cortex and ventrolateral prefrontal cortex, independent of Anhedonia-Apprehension and Fears symptom dimensions. These results suggests that prefrontal alterations are associated with transdiagnostic dysphoric mood common across depression and anxiety, rather than unique symptoms of these disorders. Additionally, no regions of interest were associated with Anhedonia-Apprehension or Fears, highlighting the importance of studying transdiagnostic features of depression and anxiety. This has implications for understanding mechanisms of and interventions for depression and anxiety.

Recent developments in neuroimaging have improved our understanding of the biological mechanisms underlying schizophrenia. However, neuroimaging findings in treatment-resistant schizophrenia (TRS) remain unclear. In the present study, we aimed to explore potential neuroanatomical regions that may be associated with treatment resistance in schizophrenia patients by comparing neuroanatomical regions of TRS and non-TRS patients using the MRICloud method. A total of 33 schizophrenia patients (meeting DSM 5 diagnostic criteria for schizophrenia) were included in the study. Patients were dichotomized into TRS (n = 18) and non-TRS (n = 15) groups, and all patients underwent MRI. Neuroanatomical regions of TRS and non-TRS patients were compared using the MRICloud method. Disease severity was measured using the Positive and Negative Syndrome Scale (PANSS). Interestingly, a statistically significant greater left Corpus Collosum (CC) thickness was found in TRS patients compared to non-TRS patients. It is clear that further studies comparing TRS patients with non-TRS patients are needed, and these studies should focus on the circuits in the corpus callosum that are thought to play a role in treatment resistance. Further longitudinal studies are also needed to complement the cross-sectional studies, using a multimodal imaging approach in the patients with clearly defined TRS criteria.