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Neuroscience and Biobehavioral Reviews Apr 2022Obsessive-compulsive disorder (OCD) displays widespread disruption across brain regions revealed by resting-state functional connectivity (rsFC) with inconsistent... (Meta-Analysis)
Meta-Analysis Review
Obsessive-compulsive disorder (OCD) displays widespread disruption across brain regions revealed by resting-state functional connectivity (rsFC) with inconsistent results between studies. We performed a systematic review of 47 seed-based rsFC studies (1863 patients; 1795 healthy controls) to explore brain intrinsic connectivity alterations. Quantitative coordinate-based meta-analysis was conducted for seed regions in the striatum (putamen, caudate, nucleus accumbens [Nac]), thalamus, and anterior cingulate cortex (ACC) because there were an adequate number of studies. We found that OCD patients demonstrated (1) characteristic dysconnectivity between striatum and cortical networks (i.e., caudate hyperconnectivity with the fronto-limbic network and hypoconnectivity with frontoparietal network regions; Nac hypoconnectivity with fronto-limbic network regions), (2) hypoconnectivity between thalamus and striatum (putamen and caudate), and (3) dysconnectivity between the ACC and fronto-limbic network regions. Furthermore, there were negative correlations between particular connectivities and symptom severity and onset age. Our results characterize the traditional cortico-striato-thalamo-cortical circuit model of OCD pathophysiology through the cerebral intrinsic connectivity, and unified neurocircuitry and brain network models into one integrity to elaborate the neural mechanism of OCD.
Topics: Brain; Brain Mapping; Humans; Magnetic Resonance Imaging; Neural Pathways; Obsessive-Compulsive Disorder
PubMed: 35151769
DOI: 10.1016/j.neubiorev.2022.104574 -
Brain : a Journal of Neurology Dec 2022Brain lesions are a rare cause of tic disorders. However, they can provide uniquely causal insights into tic pathophysiology and can also inform on possible...
Brain lesions are a rare cause of tic disorders. However, they can provide uniquely causal insights into tic pathophysiology and can also inform on possible neuromodulatory therapeutic targets. Based on a systematic literature review, we identified 22 cases of tics causally attributed to brain lesions and employed 'lesion network mapping' to interrogate whether tic-inducing lesions would be associated with a common network in the average human brain. We probed this using a normative functional connectome acquired in 1000 healthy participants. We then examined the specificity of the identified network by contrasting tic-lesion connectivity maps to those seeding from 717 lesions associated with a wide array of neurological and/or psychiatric symptoms within the Harvard Lesion Repository. Finally, we determined the predictive utility of the tic-inducing lesion network as a therapeutic target for neuromodulation. Specifically, we collected retrospective data of 30 individuals with Tourette disorder, who underwent either thalamic (n = 15; centromedian/ventrooralis internus) or pallidal (n = 15; anterior segment of globus pallidus internus) deep brain stimulation and calculated whether connectivity between deep brain stimulation sites and the lesion network map could predict clinical improvements. Despite spatial heterogeneity, tic-inducing lesions mapped to a common network map, which comprised the insular cortices, cingulate gyrus, striatum, globus pallidus internus, thalami and cerebellum. Connectivity to a region within the anterior striatum (putamen) was specific to tic-inducing lesions when compared with control lesions. Connectivity between deep brain stimulation electrodes and the lesion network map was predictive of tic improvement, regardless of the deep brain stimulation target. Taken together, our results reveal a common brain network involved in tic generation, which shows potential as a therapeutic target for neuromodulation.
Topics: Humans; Tics; Deep Brain Stimulation; Retrospective Studies; Treatment Outcome; Tourette Syndrome; Brain; Neural Networks, Computer
PubMed: 35026844
DOI: 10.1093/brain/awac009 -
Journal of Neurology Jun 2022Neuroimaging studies have reported gray matter changes in patients with idiopathic dystonia but with considerable variations. Here, we aimed to investigate the... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Neuroimaging studies have reported gray matter changes in patients with idiopathic dystonia but with considerable variations. Here, we aimed to investigate the convergence of dystonia-related gray matter changes across studies.
METHODS
The whole brain voxel-based morphometry studies comparing idiopathic dystonia and healthy controls were systematically searched in the PubMed, Web of Science and Embase. Meta-analysis of gray matter changes was performed using the anisotropic effect size-based signed differential mapping.
RESULTS
Twenty-eight studies comparing 701 idiopathic dystonia patients and 712 healthy controls were included in the meta-analysis. Compared to healthy controls, idiopathic dystonia patients showed increased gray matter in bilateral precentral and postcentral gyri, bilateral putamen and pallidum, right insula, and left supramarginal gyrus, while decreased gray matter in bilateral temporal poles, bilateral supplementary motor areas, right angular gyrus, inferior parietal gyrus and precuneus, left insula and inferior frontal gyrus. These findings remained robust in the jackknife sensitivity analysis, and no significant heterogeneity was detected. Subgroup analyses of different phenotypes of dystonia were performed to further confirm the above findings.
CONCLUSION
The meta-analysis showed that consistent widespread gray matter abnormalities were shared in different subtypes of idiopathic dystonia and were not restricted to the corticostriatal circuits.
Topics: Brain; Cerebral Cortex; Dystonia; Gray Matter; Humans; Magnetic Resonance Imaging; Neuroimaging
PubMed: 35013788
DOI: 10.1007/s00415-022-10961-y -
Journal of Alzheimer's Disease : JAD 2022Affecting nearly half of the patients with Alzheimer's disease (AD), apathy is associated with higher morbidity and reduced quality of life. Basal ganglia and cortical... (Meta-Analysis)
Meta-Analysis
Cerebral Volumetric Correlates of Apathy in Alzheimer's Disease and Cognitively Normal Older Adults: Meta-Analysis, Label-Based Review, and Study of an Independent Cohort.
BACKGROUND
Affecting nearly half of the patients with Alzheimer's disease (AD), apathy is associated with higher morbidity and reduced quality of life. Basal ganglia and cortical atrophy have been implicated in apathy. However, the findings have varied across studies and left unclear whether subdomains of apathy may involve distinct neuroanatomical correlates.
OBJECTIVE
To identify neuroanatomical correlates of AD-associated apathy.
METHODS
We performed a meta-analysis and label-based review of the literature. Further, following published routines of voxel-based morphometry, we aimed to confirm the findings in an independent cohort of 19 patients with AD/mild cognitive impairment and 25 healthy controls assessed with the Apathy Evaluation Scale.
RESULTS
Meta-analysis of 167 AD and 56 healthy controls showed convergence toward smaller basal ganglia gray matter volume (GMV) in apathy. Label-based review showed anterior cingulate, putamen, insula, inferior frontal gyrus (IFG) and middle temporal gyrus (MTG) atrophy in AD apathy. In the independent cohort, with small-volume-correction, right putamen and MTG showed GMVs in negative correlation with Apathy Evaluation Scale total, behavioral, and emotional scores, and right IFG with emotional score (p < 0.05 family-wise error (FWE)-corrected), controlling for age, education, intracranial volume, and depression. With the Mini-Mental State Examination scores included as an additional covariate, the correlation of right putamen GMV with behavioral and emotional score, right MTG GMV with total and emotional score, and right IFG GMV with emotional score were significant.
CONCLUSION
The findings implicate putamen, MTG and IFG atrophy in AD associated apathy, potentially independent of cognitive impairment and depression, and suggest potentially distinct volumetric correlates of apathy.
Topics: Aged; Alzheimer Disease; Apathy; Atrophy; Basal Ganglia; Brain; Cognitive Dysfunction; Cohort Studies; Gray Matter; Gyrus Cinguli; Humans; Image Processing, Computer-Assisted; Magnetic Resonance Imaging; Prefrontal Cortex
PubMed: 34924392
DOI: 10.3233/JAD-215316 -
Progress in Neuro-psychopharmacology &... Mar 2022Abnormalities in spontaneous brain activity, measured with resting-state functional magnetic resonance imaging (rs-fMRI), may be key biomarkers for bipolar disorders....
OBJECTIVE
Abnormalities in spontaneous brain activity, measured with resting-state functional magnetic resonance imaging (rs-fMRI), may be key biomarkers for bipolar disorders. This systematic review compares rs-fMRI findings in people experiencing a bipolar depressive or (hypo)manic episode to bipolar euthymia and/or healthy participants.
METHODS
Medline, Web of Science and Embase were searched up until April 2021. Studies without control group, or including minors, neurological co-morbidities or mixed episodes, were excluded. Qualitative synthesis was used to report results and risk of bias was assessed using the National Heart, Lung and Blood Institute tool for case-control studies.
RESULTS
Seventy-one studies were included (3167 bipolar depressed/706 (hypo)manic). In bipolar depression, studies demonstrated default-mode (DMN) and frontoparietal network (FPN) dysfunction, altered baseline activity in the precuneus, insula, striatum, cingulate, frontal and temporal cortex, and disturbed regional homogeneity in parietal, temporal and pericentral areas. Functional connectivity was altered in thalamocortical circuits and between the cingulate cortex and precuneus. In (hypo)mania, studies reported altered functional connectivity in the amygdala, frontal and cingulate cortex. Finally, rs-fMRI disturbances in the insula and putamen correlate with depressive symptoms, cerebellar resting-state alterations could evolve with disease progression and altered amygdala connectivity might mediate lithium effects.
CONCLUSIONS
Our results suggest DMN and FPN dysfunction in bipolar depression, whereas local rs-fMRI alterations might differentiate mood states. Future studies should consider controlling rs-fMRI findings for potential clinical confounding factors such as medication. Considerable heterogeneity of methodology between studies limits conclusions. Standardised clinical reporting and consistent analysis approaches would increase coherence in this promising field.
Topics: Amygdala; Biomarkers; Bipolar Disorder; Brain; Default Mode Network; Gyrus Cinguli; Humans; Magnetic Resonance Imaging; Mania; Neostriatum; Parietal Lobe; Temporal Lobe
PubMed: 34736998
DOI: 10.1016/j.pnpbp.2021.110465 -
The Journal of Neuropsychiatry and... 2021The mechanisms and neuronal networks associated with anxiety in Parkinson's disease (PD) are incompletely understood. One of the best tools for investigating both...
OBJECTIVE
The mechanisms and neuronal networks associated with anxiety in Parkinson's disease (PD) are incompletely understood. One of the best tools for investigating both component function and neuronal networks associated with psychiatric symptoms is functional MRI (fMRI). Unlike structural scans, functional scans, whether task-based or resting-state, are more likely to be clinically relevant and sensitive to changes related to treatment. The investigators provide a comprehensive review of and present results for imaging studies of anxiety in PD.
METHODS
A systematic review of the literature on fMRI and anxiety in PD was conducted, and the quality of all included studies was simultaneously assessed. Eighteen studies were included: 15 studies assessed anxiety directly, and three evaluated emotional processing. Imaging methodology and behavioral assessments varied across studies, preventing direct comparison of results in most cases.
RESULTS
There was a convergence in findings across methods, implicating involvement of the amygdala, caudate, and putamen in association with anxiety in PD. For both task-based activation and resting-state connectivity, dopamine medication status was associated with differences in activation and behavioral function.
CONCLUSIONS
Although there is little consensus in the current fMRI literature studying anxiety in PD, these results suggest an overlap between structures classically involved in the brain's fear circuit (particularly the amygdala) and the alterations in the nigro-striatal system (e.g., the caudate and putamen and on-off dopamine findings) related to PD and its dopaminergic treatments.
Topics: Amygdala; Anxiety; Brain Mapping; Brief Psychiatric Rating Scale; Dopamine Agents; Humans; Magnetic Resonance Imaging; Neural Pathways; Neuroimaging; Parkinson Disease
PubMed: 34280319
DOI: 10.1176/appi.neuropsych.20110272 -
Frontiers in Psychiatry 2021Patients with Internet gaming disorder (IGD) and attention-deficit/hyperactivity disorder (ADHD) have high comorbidity but it is still unknown whether these disorders...
Patients with Internet gaming disorder (IGD) and attention-deficit/hyperactivity disorder (ADHD) have high comorbidity but it is still unknown whether these disorders have shared and distinctive neuroimage alterations. The aim of this meta-analysis was to identify shared and disorder-specific structural, functional, and multimodal abnormalities between IGD and ADHD. A systematic literature search was conducted for whole-brain voxel-based morphometry (VBM) and functional magnetic resonance imaging (fMRI) studies comparing people with IGD or ADHD with healthy controls. Regional gray matter volume (GMV) and fMRI differences were compared over the patient groups and then a quantitative comparison was performed to find abnormalities (relative to controls) between IGD and ADHD using seed-based d mapping meta-analytic methods. The meta-analysis contained 14 IGD VBM studies (contrasts covering 333 IGDs and 335 HCs), 26 ADHD VBM studies (1,051 patients with ADHD and 887 controls), 30 IGD fMRI studies (603 patients with IGD and 564 controls), and 29 ADHD fMRI studies (878 patients with ADHD and 803 controls). Structurally, VBM analysis showed disorder-specific GMV abnormality in the putamen among IGD subjects and orbitofrontal cortex in ADHD and shared GMV in the prefrontal cortex. Functionally, fMRI analysis discovered that IGD-differentiating increased activation in the precuneus and shared abnormal activation in anterior cingulate cortex, insular, and striatum. IGD and ADHD have shared and special structural and functional alterations. IGD has disorder-differentiating structural alterations in the putamen and ADHD has alterations in the orbitofrontal cortex. Disorder-differentiating fMRI activations were predominantly observed in the precuneus among IGD subjects and shared impairing function connection was in the rewards circuit (including ACC, OFC, and striatum).
PubMed: 34276447
DOI: 10.3389/fpsyt.2021.679437 -
Reviews in Endocrine & Metabolic... Aug 2022Obesity is the second most common cause of preventable morbidity worldwide. Resting-state functional magnetic resonance imaging (fMRI) has been used extensively to... (Review)
Review
Obesity is the second most common cause of preventable morbidity worldwide. Resting-state functional magnetic resonance imaging (fMRI) has been used extensively to characterise altered communication between brain regions in individuals with obesity, though findings from this research have not yet been systematically evaluated within the context of prominent neurobiological frameworks. This systematic review aggregated resting-state fMRI findings in individuals with obesity and evaluated the contribution of these findings to current neurobiological models. Findings were considered in relation to a triadic model of problematic eating, outlining disrupted communication between reward, inhibitory, and homeostatic systems. We identified a pattern of consistently increased orbitofrontal and decreased insula cortex resting-state functional connectivity in individuals with obesity in comparison to healthy weight controls. BOLD signal amplitude was also increased in people with obesity across studies, predominantly confined to subcortical regions, including the hippocampus, amygdala, and putamen. We posit that altered orbitofrontal cortex connectivity may be indicative of a shift in the valuation of food-based rewards and that dysfunctional insula connectivity likely contributes to altered homeostatic signal processing. Homeostatic violation signals in obesity may be maintained despite satiety, thereby 'hijacking' the executive system and promoting further food intake. Moving forward, we provide a roadmap for more reliable resting-state and task-based functional connectivity experiments, which must be reconciled within a common framework if we are to uncover the interplay between psychological and biological factors within current theoretical frameworks.
Topics: Brain; Brain Mapping; Humans; Magnetic Resonance Imaging; Obesity; Reward
PubMed: 34159504
DOI: 10.1007/s11154-021-09665-x -
Epilepsia Open Jun 2021Recent neuroimaging studies have revealed differences in cortical and white matter brain structure in children with self-limiting rolandic epilepsy (RE). Despite this,...
OBJECTIVE
Recent neuroimaging studies have revealed differences in cortical and white matter brain structure in children with self-limiting rolandic epilepsy (RE). Despite this, reproducibility of the findings has been difficult, and there is no consensus about where and when structural differences are most apparent. We performed a systematic review of quantitative neuroimaging studies in children with RE to explore these questions.
METHODS
Using PRISMA guidelines, we used a multilayered search strategy to identify neuroimaging studies in RE. Publications were included if they were quantitative and derived from controlled group studies and passed a quality assessment. Findings of the studies were presented and stratified by duration of epilepsy and age of participants.
RESULTS
We identified six gray matter studies and five white matter studies. Consistent findings were found inside and outside the central sulcus, predominantly within the bilateral frontal and parietal lobes, striatal structures, such as the putamen and white matter, mainly involving the left superior longitudinal fasciculus and connections between the left pre- and postcentral gyrus. Stratification of the T1 studies by age found that cortical thickness differences varied between the under and over 10 year olds. Furthermore, the longer the duration of epilepsy, the less likely differences were detected. In white matter studies, there was a reduction in differences with increased age and duration of epilepsy.
SIGNIFICANCE
These findings would suggest that the development of regions of the cortex in children with RE is abnormal. These regions are more widespread than the suspected seizure onset zone. Moreover, the findings would suggest that these differences are evidence of neurodevelopmental delay rather than apparent "damage" from the epilepsy.
Topics: Child; Epilepsy, Rolandic; Gray Matter; Humans; Magnetic Resonance Imaging; Reproducibility of Results; White Matter
PubMed: 34033258
DOI: 10.1002/epi4.12468 -
Journal of Parkinson's Disease 2021The hallmark of Parkinson's disease is depletion of dopamine in the basal ganglia. Models of Parkinson's disease include dopamine as a contributor to disease... (Meta-Analysis)
Meta-Analysis
BACKGROUND
The hallmark of Parkinson's disease is depletion of dopamine in the basal ganglia. Models of Parkinson's disease include dopamine as a contributor to disease progression. However, intraneuronal levels of dopamine have not been reported.
OBJECTIVE
Meta-analytic methods were utilized to determine intracellular dopamine levels in Parkinson's disease.
METHODS
A systematic review of the literature and frequentist meta-analyses were performed. Dopamine levels were scaled for cell and axon numbers as well as VMAT2 protein levels.
RESULTS
Reduced tissue dopamine, dopaminergic cell bodies and VMAT2 protein were confirmed. The ratio of Parkinson's to normal brain intracellular dopamine scaled for either cell or axon number, each with VMAT2 level in the caudate ranged from 1.49 to 1.87 (p = 0.51 and p = 0.12, respectively) and in the putamen from 0.75 to 4.61 (p = 0.40 and 0.001, respectively).
CONCLUSION
Free, intracellular dopamine levels are not reduced in Parkinson's disease compared to normals to a similar degree as are total tissue concentrations, supporting the relevance of modulating VMAT2, neuromelanin and/or dopamine synthesis as rational neuroprotective strategies.
Topics: Basal Ganglia; Dopamine; Dopaminergic Neurons; Humans; Parkinson Disease; Putamen
PubMed: 34024786
DOI: 10.3233/JPD-212715