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Brain Imaging and Behavior Apr 2024Post-traumatic stress disorder (PTSD) is a debilitating condition which has been related to problems in emotional regulation, memory and cognitive control. Psychotherapy... (Meta-Analysis)
Meta-Analysis Review
Post-traumatic stress disorder (PTSD) is a debilitating condition which has been related to problems in emotional regulation, memory and cognitive control. Psychotherapy has a non-response rate of around 50% and understanding the neurobiological working mechanisms might help improve treatment. To integrate findings from multiple smaller studies, we performed the first meta-analysis of changes in brain activation with a specific focus on emotional processing after psychotherapy in PTSD patients. We performed a meta-analysis of brain activation changes after treatment during emotional processing for PTSD with seed-based d mapping using a pre-registered protocol (PROSPERO CRD42020211039). We analyzed twelve studies with 191 PTSD patients after screening 3700 studies. We performed systematic quality assessment both for the therapeutic interventions and neuroimaging methods. Analyses were done in the full sample and in a subset of studies that reported whole-brain results. We found decreased activation after psychotherapy in the left amygdala, (para)hippocampus, medial temporal lobe, inferior frontal gyrus, ventrolateral prefrontal cortex, right pallidum, anterior cingulate cortex, bilateral putamen, and insula. Decreased activation in the left amygdala and left ventrolateral PFC was also found in eight studies that reported whole-brain findings. Results did not survive correction for multiple comparisons. There is tentative support for decreased activation in the fear and cognitive control networks during emotional processing after psychotherapy for PTSD. Future studies would benefit from adopting a larger sample size, using designs that control for confounding variables, and investigating heterogeneity in symptom profiles and treatment response.
Topics: Humans; Stress Disorders, Post-Traumatic; Brain; Emotions; Psychotherapy; Brain Mapping; Magnetic Resonance Imaging
PubMed: 38049598
DOI: 10.1007/s11682-023-00831-0 -
Neuroscience and Biobehavioral Reviews Sep 2019Humans have a sophisticated set of neural structures for cutaneous thermoception. Sufficiently cold temperatures are thought to evoke pain and motivation to resolve... (Meta-Analysis)
Meta-Analysis
Humans have a sophisticated set of neural structures for cutaneous thermoception. Sufficiently cold temperatures are thought to evoke pain and motivation to resolve disturbed homeostasis, while cool but not painful temperatures are evaluated as cold but do not cause thermoregulatory behaviour. Brain networks for innocuous and noxious cold temperature have been proposed but a quantitative meta-analysis comparing the two has never been conducted. As a result, we sought to perform activation likelihood estimation analysis of the brain activity associated with innocuous and noxious cold exposure. Combining data from 33 data sets revealed that innocuous cold exposure activates the posterior insular, middle/orbital and posterior parietal cortices while noxious cold activates the thalamus, putamen, and right anterior insula cortex. Both conditions respectively show greater activation in these areas and no areas are common between conditions. Our results confirm the long-standing hypothesis that noxious cold is encoded in the right anterior insula, but contradicts the selective importance of the posterior insula for cool somatosensory processing.
Topics: Brain Mapping; Cerebral Cortex; Cold Temperature; Humans; Nociception; Putamen; Thalamus; Thermosensing
PubMed: 31283953
DOI: 10.1016/j.neubiorev.2019.06.021 -
Physiology & Behavior May 2023The gastrointestinal hormones ghrelin and glucagon-like peptide-1 (GLP-1) have opposite secretion patterns, as well as opposite effects on metabolism and food intake.... (Meta-Analysis)
Meta-Analysis
The gastrointestinal hormones ghrelin and glucagon-like peptide-1 (GLP-1) have opposite secretion patterns, as well as opposite effects on metabolism and food intake. Beyond their role in energy homeostasis, gastrointestinal hormones have also been suggested to modulate the reward system. However, the potential of ghrelin and GLP-1 to modulate reward responses in humans has not been systematically reviewed before. To evaluate the convergence of published results, we first conduct a multi-level kernel density meta-analysis of studies reporting a positive association of ghrelin (N = 353, 18 contrasts) and a negative association of GLP-1 (N = 258, 12 contrasts) and reward responses measured using task functional magnetic resonance imaging (fMRI). Second, we complement the meta-analysis using a systematic literature review, focusing on distinct reward phases and applications in clinical populations that may account for variability across studies. In line with preclinical research, we find that ghrelin increases reward responses across studies in key nodes of the motivational circuit, such as the nucleus accumbens, pallidum, putamen, substantia nigra, ventral tegmental area, and the dorsal mid insula. In contrast, for GLP-1, we did not find sufficient convergence in support of reduced reward responses. Instead, our systematic review identifies potential differences of GLP-1 on anticipatory versus consummatory reward responses. Based on a systematic synthesis of available findings, we conclude that there is considerable support for the neuromodulatory potential of gut-based circulating peptides on reward responses. To unlock their potential for clinical applications, it may be useful for future studies to move beyond anticipated rewards to cover other reward facets.
Topics: Humans; Glucagon-Like Peptide 1; Ghrelin; Magnetic Resonance Imaging; Gastrointestinal Hormones; Reward
PubMed: 36740132
DOI: 10.1016/j.physbeh.2023.114111 -
Progress in Neuro-psychopharmacology &... Mar 2020In recent decades, a growing number of structural neuroimaging studies of grey matter (GM) in trigeminal neuralgia (TN) have reported inconsistent alterations. We... (Meta-Analysis)
Meta-Analysis
In recent decades, a growing number of structural neuroimaging studies of grey matter (GM) in trigeminal neuralgia (TN) have reported inconsistent alterations. We carried out a systematic review and meta-analysis to identify consistent and replicable GM volume abnormalities using effect-size signed differential mapping (ES-SDM). Furthermore, we conducted a meta-regression to explore the potential effects of clinical characteristics on GM volume alterations in patients with TN. A total of 13 studies with 15 datasets, representing 407 TN patients and 376 healthy individuals, were included in the present study. The results revealed that TN patients had GM volume abnormalities mainly in the basal ganglia, including the putamen, nucleus accumbens (NAc), caudate nucleus and amygdala, as well as the cingulate cortex (CC), thalamus, insula and superior temporal gyrus (STG). The meta-regression analysis showed that verbal rating scale (VRS) scores were negatively correlated with decreased GM volume in the left striatum and that illness duration was negatively correlated with decreased GM volume in the left STG and left insula. These results provide a thorough profile of GM volume alterations in TN patients and constitute robust evidence that aberrant GM volumes in the brain regions regulating and moderating sensory-motor and affective processing may play an important role in the pathophysiology of TN.
Topics: Adult; Aged; Female; Gray Matter; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Trigeminal Neuralgia
PubMed: 31756417
DOI: 10.1016/j.pnpbp.2019.109821 -
Frontiers in Neuroscience 2024Alzheimer's disease (AD), characterized by distinctive pathologies such as amyloid-β plaques and tau tangles, also involves deregulation of iron homeostasis, which may...
INTRODUCTION
Alzheimer's disease (AD), characterized by distinctive pathologies such as amyloid-β plaques and tau tangles, also involves deregulation of iron homeostasis, which may accelerate neurodegeneration. This meta-analysis evaluated the use of quantitative susceptibility mapping (QSM) to detect iron accumulation in the deep gray matter (DGM) of the basal ganglia in AD, contributing to a better understanding of AD progression, and potentially leading to new diagnostic and therapeutic approaches.
METHODS
Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we systematically searched the PubMed, Scopus, Web of Sciences, and Google Scholar databases up to October 2023 for studies employing QSM in AD research. Eligibility criteria were based on the PECO framework, and we included studies assessing alterations in magnetic susceptibility indicative of iron accumulation in the DGM of patients with AD. After initial screening and quality assessment using the Newcastle-Ottawa Scale, a meta-analysis was conducted to compare iron levels between patients with AD and healthy controls (HCs) using a random-effects model.
RESULTS
The meta-analysis included nine studies comprising 267 patients with AD and 272 HCs. There were significantly higher QSM values, indicating greater iron deposition, in the putamen (standardized mean difference (SMD) = 1.23; 95% CI: 0.62 to 1.84; = 0.00), globus pallidus (SMD = 0.79; 95% CI: 0.07 to 1.52; = 0.03), and caudate nucleus (SMD = 0.72; 95% CI: 0.39 to 1.06; = 0.00) of AD patients compared to HCs. However, no significant differences were found in the thalamus (SMD = 1.00; 95% CI: -0.42 to 2.43; = 0.17). The sensitivity analysis indicated that no single study impacted the overall results. Age was identified as a major contributor to heterogeneity across all basal ganglia nuclei in subgroup analysis. Older age (>69 years) and lower male percentage (≤30%) were associated with greater putamen iron increase in patients with AD.
CONCLUSION
The study suggests that excessive iron deposition is linked to the basal ganglia in AD, especially the putamen. The study underscores the complex nature of AD pathology and the accumulation of iron, influenced by age, sex, and regional differences, necessitating further research for a comprehensive understanding.
PubMed: 38469572
DOI: 10.3389/fnins.2024.1338891 -
NeuroImage Jun 2024This systematic review investigates how prefrontal transcranial magnetic stimulation (TMS) immediately influences neuronal excitability based on oxygenation changes... (Review)
Review
This systematic review investigates how prefrontal transcranial magnetic stimulation (TMS) immediately influences neuronal excitability based on oxygenation changes measured by functional magnetic resonance imaging (fMRI) or functional near-infrared spectroscopy (fNIRS). A thorough understanding of TMS-induced excitability changes may enable clinicians to adjust TMS parameters and optimize treatment plans proactively. Five databases were searched for human studies evaluating brain excitability using concurrent TMS/fMRI or TMS/fNIRS. Thirty-seven studies (13 concurrent TMS/fNIRS studies, 24 concurrent TMS/fMRI studies) were included in a qualitative synthesis. Despite methodological inconsistencies, a distinct pattern of activated nodes in the frontoparietal central executive network, the cingulo-opercular salience network, and the default-mode network emerged. The activated nodes included the prefrontal cortex (particularly dorsolateral prefrontal cortex), insula cortex, striatal regions (especially caudate, putamen), anterior cingulate cortex, and thalamus. High-frequency repetitive TMS most consistently induced expected facilitatory effects in these brain regions. However, varied stimulation parameters (e.g., intensity, coil orientation, target sites) and the inter- and intra-individual variability of brain state contribute to the observed heterogeneity of target excitability and co-activated regions. Given the considerable methodological and individual variability across the limited evidence, conclusions should be drawn with caution.
Topics: Humans; Transcranial Magnetic Stimulation; Prefrontal Cortex; Magnetic Resonance Imaging; Spectroscopy, Near-Infrared; Oxygen; Brain Mapping; Brain
PubMed: 38636640
DOI: 10.1016/j.neuroimage.2024.120618 -
The International Journal of... Apr 2023Aberrant striatal responses to reward anticipation have been observed in schizophrenia. However, it is unclear whether these dysfunctions predate the onset of psychosis... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Aberrant striatal responses to reward anticipation have been observed in schizophrenia. However, it is unclear whether these dysfunctions predate the onset of psychosis and whether reward anticipation is impaired in individuals at clinical high risk for schizophrenia (CHR).
METHODS
To examine the neural correlates of monetary anticipation in the prodromal phase of schizophrenia, we performed a whole-brain meta-analysis of 13 functional neuroimaging studies that compared reward anticipation signals between CHR individuals and healthy controls (HC). Three databases (PubMed, Web of Science, and ScienceDirect) were systematically searched from January 1, 2000, to May 1, 2022.
RESULTS
Thirteen whole-brain functional magnetic resonance imaging studies including 318 CHR individuals and 426 HC were identified through comprehensive literature searches. Relative to HC, CHR individuals showed increased brain responses in the medial prefrontal cortex and anterior cingulate cortex and decreased activation in the mesolimbic circuit, including the putamen, parahippocampal gyrus, insula, cerebellum, and supramarginal gyrus, during reward anticipation.
CONCLUSIONS
Our findings in the CHR group confirmed the existence of abnormal motivational-related activation during reward anticipation, thus demonstrating the pathophysiological characteristics of the risk populations. These results have the potential to lead to the early identification and more accurate prediction of subsequent psychosis as well as a deeper understanding of the neurobiology of high-risk state of psychotic disorder.
Topics: Humans; Schizophrenia; Magnetic Resonance Imaging; Anticipation, Psychological; Brain; Reward
PubMed: 36893068
DOI: 10.1093/ijnp/pyad009 -
Frontiers in Endocrinology 2024Iron accumulation in the brain has been linked to diabetes, but its role in subcortical structures involved in motor and cognitive functions remains unclear.... (Meta-Analysis)
Meta-Analysis
INTRODUCTION
Iron accumulation in the brain has been linked to diabetes, but its role in subcortical structures involved in motor and cognitive functions remains unclear. Quantitative susceptibility mapping (QSM) allows the non-invasive quantification of iron deposition in the brain. This systematic review and meta-analysis examined magnetic susceptibility measured by QSM in the subcortical nuclei of patients with type 2 diabetes mellitus (T2DM) compared with controls.
METHODS
PubMed, Scopus, and Web of Science databases were systematically searched [following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines] for studies reporting QSM values in the deep gray matter (DGM) regions of patients with T2DM and controls. Pooled standardized mean differences (SMDs) for susceptibility were calculated using fixed-effects meta-analysis models, and heterogeneity was assessed using I. Sensitivity analyses were conducted, and publication bias was evaluated using Begg's and Egger's tests.
RESULTS
Six studies including 192 patients with T2DM and 245 controls were included. This study found a significant increase in iron deposition in the subcortical nuclei of patients with T2DM compared to the control group. The study found moderate increases in the putamen (SMD = 0.53, 95% CI 0.33 to 0.72, p = 0.00) and dentate nucleus (SMD = 0.56, 95% CI 0.27 to 0.85, p = 0.00) but weak associations between increased iron levels in the caudate nucleus (SMD = 0.32, 95% CI 0.13 to 0.52, p = 0.00) and red nucleus (SMD = 0.22, 95% CI 0.00 0.44, p = 0.05). No statistical significance was found for iron deposition alterations in the globus pallidus (SMD = 0.19; 95% CI -0.01 to 0.38; p = 0.06) and substantia nigra (SMD = 0.12, 95% CI -0.10, 0.34, p = 0.29). Sensitivity analysis showed that the findings remained unaffected by individual studies, and consistent increases were observed in multiple subcortical areas.
DISCUSSION
QSM revealed an increase in iron in the DGM/subcortical nuclei in T2DM patients versus controls, particularly in the motor and cognitive nuclei, including the putamen, dentate nucleus, caudate nucleus, and red nucleus. Thus, QSM may serve as a potential biomarker for iron accumulation in T2DM patients. However, further research is needed to validate these findings.
Topics: Humans; Diabetes Mellitus, Type 2; Iron; Magnetic Resonance Imaging; Brain; Brain Mapping
PubMed: 38510699
DOI: 10.3389/fendo.2024.1331831 -
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 -
NeuroImage Apr 2020Adolescence is increasingly viewed as a sensitive period in the development of substance use disorders (SUDs). Neurodevelopmental 'dual-risk' theories suggest adolescent... (Meta-Analysis)
Meta-Analysis
Adolescence is increasingly viewed as a sensitive period in the development of substance use disorders (SUDs). Neurodevelopmental 'dual-risk' theories suggest adolescent vulnerability to problematic substance use is driven by an overactive reward drive mediated by the striatum, and poor cognitive control mediated by the prefrontal cortex. To this end, there has been a growing number of neuroimaging studies examining cognitive and affective neural systems during adolescence for markers of vulnerability to problematic substance use. Here, we perform a coordinate-based meta-analysis on this emerging literature. Twenty-two task-based voxelwise fMRI studies with activation differences associated with substance use vulnerability, representative of approximately 1092 subjects, were identified through a systematic literature search (PubMed, Scopus) and coordinates of activation differences (N = 190) were extracted. Adolescents were defined as 'at-risk' for problematic substance use based on a family history of SUD or through prospective prediction of substance use initiation or escalation. Multilevel kernel density analysis was used to identify the most consistent brain regions associated with adolescent substance use vulnerability. Across the included studies, substance use vulnerability was most reliably associated with activation differences in the striatum, where at-risk adolescents had hyper-activation in the dorsal subdivision (putamen). Follow-up analyses suggested striatal differences were driven by tasks sharing a motivational and/or reward component (e.g., monetary incentive) and common across subgroups of substance use risk (family history and prospective prediction studies). Analyses examining the role of psychiatric comorbidity revealed striatal activation differences were significantly more common in samples whose definition of substance use risk included cooccurring externalizing psychopathology. Furthermore, substance use risk meta-analytic results were no longer significant when excluding these studies, although this may reflect limitations in statistical power. No significant activation differences were observed in prefrontal cortex in any analysis. These results suggest striatal dysfunction, rather than prefrontal, may be a more primary neural feature of adolescent vulnerability to problematic substance use, possibly through a dimension of individual variability shared with externalizing psychopathology. However, our systematic literature search confirms this is still an emerging field. More studies, increased data sharing, and further quantitative integration are necessary for a comprehensive understanding of the neuroimaging markers of adolescent substance use risk.
Topics: Adolescent; Adolescent Behavior; Corpus Striatum; Executive Function; Functional Neuroimaging; Humans; Substance-Related Disorders
PubMed: 31875520
DOI: 10.1016/j.neuroimage.2019.116476