Posttraumatic stress disorder(PTSD)and major depressive disorder(MDD)are common stress-related psychiatric disorders.Genetic and neurobiology research has supported the viewpoint that PTSD and MDD may possess common a...Posttraumatic stress disorder(PTSD)and major depressive disorder(MDD)are common stress-related psychiatric disorders.Genetic and neurobiology research has supported the viewpoint that PTSD and MDD may possess common and disorder-specific underlying mechanisms.In this systematic review,we summarize evidence for the similarities and differences in brain functional and structural features of MDD,PTSD,and their comorbidity,as well as the effects of extensively used therapies in patients with comorbid PTSD and MDD(PTSD+MDD).These functional magnetic resonance imaging(MRI)studies highlight the(i)shared hypoactivation in the prefrontal cortex during cognitive and emotional processing in MDD and PTSD;(ii)higher activation in fear processing regions including amygdala,hippocampus,and insula in PTSD compared to MDD;and(iii)distinct functional deficits in brain regions involved in fear and reward processing in patients with PTSD+MDD relative to those with PTSD alone.These structural MRI studies suggested that PTSD and MDD share features of reduced volume in focal frontal areas.The treatment effects in patients with PTSD+MDD may correlate with the normalization trend of structural alterations.Neuroimaging predictors of repetitive transcranial magnetic stimulation response in patients with PTSD+MDD may differ from the mono-diagnostic groups.In summary,neuroimaging studies to date have provided limited information about the shared and disorder-specific features in MDD and PTSD.Further research is essential to pave the way for developing improved diagnostic markers and eventually targeted treatment approaches for the shared and distinct brain alterations presented in patients with MDD and PTSD.展开更多
Background The lack of clearly defined neuromodulation targets has contributed to the inconsistent results of real-time fMRI-based neurofeedback(rt-fMRI-NF)for the treatment of chronic pain.Functional neurosurgery(fun...Background The lack of clearly defined neuromodulation targets has contributed to the inconsistent results of real-time fMRI-based neurofeedback(rt-fMRI-NF)for the treatment of chronic pain.Functional neurosurgery(funcSurg)approaches have shown more consistent effects in reducing pain in patients with severe chronic pain.Objective This study aims to redefine rt-fMRI-NF targets for chronic pain management informed by funcSurg studies.Methods Based on independent systematic reviews,we identified the neuromodulation targets of the rt-fMRI-NF(in acute and chronic pain)and funcSurg(in chronic pain)studies.We then characterized the underlying functional networks using a subsample of the 7 T resting-state fMRI dataset from the Human Connectome Project.Principal component analyses(PCA)were used to identify dominant patterns(accounting for a cumulative explained variance>80%)within the obtained functional maps,and the overlap between these PCA maps and canonical intrinsic brain networks(default,salience,and sensorimotor)was calculated using a null map approach.Results The anatomical targets used in rt-fMRI-NF and funcSurg approaches are largely distinct,with the middle cingulate cortex as a common target.Within the investigated canonical rs-fMRI networks,these approaches exhibit both divergent and overlapping functional connectivity patterns.Specifically,rt-fMRI-NF approaches primarily target the default mode network(P value range 0.001–0.002)and the salience network(P=0.002),whereas funcSurg approaches predominantly target the salience network(P=0.001)and the sensorimotor network(P value range 0.001–0.023).Conclusion Key hubs of the salience and sensorimotor networks may represent promising targets for the therapeutic application of rt-fMRI-NF in chronic pain.展开更多
Background:The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models.However,the pivotal nodes and directed causal regulation within this in...Background:The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models.However,the pivotal nodes and directed causal regulation within this inhibitory circuit in humans remains con-troversial.Objective:The main aim of the present study was to determine the causal information flow and critical nodes in the basal ganglia-thalamocortical inhibitory circuits and also to examine whether these are modulated by biological factors(i.e.sex)and behavioral performance.Methods:Here,we capitalize on the recent progress in robust and biologically plausible directed causal modeling(DCM-PEB)and a large response inhibition dataset(n=250)acquired with concomitant functional magnetic resonance imaging to determine key nodes,their causal regulation and modulation via biological variables(sex)and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus(rIFG),caudate nucleus(rCau),globus pallidum(rGP),and thalamus(rThal).Results:The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal.Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal.In addition,sex and performance influenced the functional architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation,while better inhibitory performance was associated with stronger rThal to rIFG communication.Furthermore,control analyses did not reveal a similar key communication in a left lateralized model.Conclusions:Together,these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.展开更多
基金supported by the National Natural Science Foundation of China(Grant Nos.82302159 and 82001795)Post-Doctor Research Project of West China Hospital of Sichuan University(2021HXBH025)Sichuan Province Science and Technology Program(2022YFS0069,2021YFS0242,and 2023YFS0076).
文摘Posttraumatic stress disorder(PTSD)and major depressive disorder(MDD)are common stress-related psychiatric disorders.Genetic and neurobiology research has supported the viewpoint that PTSD and MDD may possess common and disorder-specific underlying mechanisms.In this systematic review,we summarize evidence for the similarities and differences in brain functional and structural features of MDD,PTSD,and their comorbidity,as well as the effects of extensively used therapies in patients with comorbid PTSD and MDD(PTSD+MDD).These functional magnetic resonance imaging(MRI)studies highlight the(i)shared hypoactivation in the prefrontal cortex during cognitive and emotional processing in MDD and PTSD;(ii)higher activation in fear processing regions including amygdala,hippocampus,and insula in PTSD compared to MDD;and(iii)distinct functional deficits in brain regions involved in fear and reward processing in patients with PTSD+MDD relative to those with PTSD alone.These structural MRI studies suggested that PTSD and MDD share features of reduced volume in focal frontal areas.The treatment effects in patients with PTSD+MDD may correlate with the normalization trend of structural alterations.Neuroimaging predictors of repetitive transcranial magnetic stimulation response in patients with PTSD+MDD may differ from the mono-diagnostic groups.In summary,neuroimaging studies to date have provided limited information about the shared and disorder-specific features in MDD and PTSD.Further research is essential to pave the way for developing improved diagnostic markers and eventually targeted treatment approaches for the shared and distinct brain alterations presented in patients with MDD and PTSD.
基金supported by Key R&D project of Science and Technology Department of the Sichuan Province(China),Grant number M112022YFWZ0003。
文摘Background The lack of clearly defined neuromodulation targets has contributed to the inconsistent results of real-time fMRI-based neurofeedback(rt-fMRI-NF)for the treatment of chronic pain.Functional neurosurgery(funcSurg)approaches have shown more consistent effects in reducing pain in patients with severe chronic pain.Objective This study aims to redefine rt-fMRI-NF targets for chronic pain management informed by funcSurg studies.Methods Based on independent systematic reviews,we identified the neuromodulation targets of the rt-fMRI-NF(in acute and chronic pain)and funcSurg(in chronic pain)studies.We then characterized the underlying functional networks using a subsample of the 7 T resting-state fMRI dataset from the Human Connectome Project.Principal component analyses(PCA)were used to identify dominant patterns(accounting for a cumulative explained variance>80%)within the obtained functional maps,and the overlap between these PCA maps and canonical intrinsic brain networks(default,salience,and sensorimotor)was calculated using a null map approach.Results The anatomical targets used in rt-fMRI-NF and funcSurg approaches are largely distinct,with the middle cingulate cortex as a common target.Within the investigated canonical rs-fMRI networks,these approaches exhibit both divergent and overlapping functional connectivity patterns.Specifically,rt-fMRI-NF approaches primarily target the default mode network(P value range 0.001–0.002)and the salience network(P=0.002),whereas funcSurg approaches predominantly target the salience network(P=0.001)and the sensorimotor network(P value range 0.001–0.023).Conclusion Key hubs of the salience and sensorimotor networks may represent promising targets for the therapeutic application of rt-fMRI-NF in chronic pain.
基金supported by the by the National Key Research and Development Program of China (grant number:2018YFA0701400-BB)National Natural Science Foundation of China (grant numbers 31530032-KMK,91632117-BB,32200904 Qian Zhuang)Key Technological Projects of Guangdong Province (grant number 2018B030335001-KMK).
文摘Background:The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models.However,the pivotal nodes and directed causal regulation within this inhibitory circuit in humans remains con-troversial.Objective:The main aim of the present study was to determine the causal information flow and critical nodes in the basal ganglia-thalamocortical inhibitory circuits and also to examine whether these are modulated by biological factors(i.e.sex)and behavioral performance.Methods:Here,we capitalize on the recent progress in robust and biologically plausible directed causal modeling(DCM-PEB)and a large response inhibition dataset(n=250)acquired with concomitant functional magnetic resonance imaging to determine key nodes,their causal regulation and modulation via biological variables(sex)and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus(rIFG),caudate nucleus(rCau),globus pallidum(rGP),and thalamus(rThal).Results:The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal.Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal.In addition,sex and performance influenced the functional architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation,while better inhibitory performance was associated with stronger rThal to rIFG communication.Furthermore,control analyses did not reveal a similar key communication in a left lateralized model.Conclusions:Together,these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.
