Structural MRI Studies Research Articles

The shared neurobiological basis of developmental dyslexia and developmental stuttering: A meta-analysis of functional and structural MRI studies

BackgroundDevelopmental dyslexia (DD) and persistent developmental stuttering (PDS) are the most representative written and spoken language disorders, respectively, and both significantly hinder life success. Although widespread brain alterations are evident in both DD and PDS, it remains unclear to what extent these two language disorders share common neural substrates. MethodsA systematic review and meta-analysis of task-based functional magnetic resonance imaging (fMRI) and voxel-based morphometry (VBM) studies of PDS and DD were conducted to explore the shared functional and anatomical alterations across these disorders. ResultsThe results of fMRI studies indicated shared hypoactivation in the left inferior temporal gyrus and inferior parietal gyrus across PDS and DD compared to healthy controls. When examined separately for children and adults, we found that child participants exhibited reduced activation in the left inferior temporal gyrus, inferior parietal gyrus, precentral gyrus, middle temporal gyrus, and inferior frontal gyrus, possibly reflecting the universal causes of written and spoken language disorders. In contrast, adult participants exhibited hyperactivation in the right precentral gyrus and left cingulate motor cortex, possibly reflecting common compensatory mechanisms. Anatomically, the analysis of VBM studies revealed decreased gray matter volume in the left inferior frontal gyrus across DD and PDS, which was exclusively observed in children. Finally, meta-analytic connectivity modeling and brain-behavior correlation analyses were conducted to explore functional connectivity patterns and related cognitive functions of the brain regions commonly involved in DD and PDS. ConclusionsThis study identified concordances in brain abnormalities across DD and PDS, suggesting common neural substrates for written and spoken language disorders and providing new insights into the transdiagnostic neural signatures of language disorders.

Anterior and posterior thalamic volumes differentially correlate with memory, attention, and motor processes in HIV infection and alcohol use disorder comorbidity

The thalamus, with its reciprocal connections to and from cortical, subcortical, and cerebellar regions, is a central active participant in multiple functional brain networks. Structural MRI studies measuring the entire thalamus without respect to its regional or nuclear divisions report volume shrinkage in diseases including HIV infection, alcohol use disorder (AUD), and their comorbidity (HIV+AUD). Here, we examined relations between thalamic subregions (anterior, ventral, medial, and posterior) and neuropsychological functions (attention/working memory, executive functioning, episodic memory, and motor skills). Volumes of thalamic subregions were derived from automatic segmentations of standard T1 weighted MRIs of 65 individuals with HIV, 189 with AUD, 80 with HIV+AUD comorbidity, and 141 healthy controls (CTRL). Total thalamic volume was smaller and cognitive and motor composite scores were lower in the three diagnostic groups relative to the CTRL group. The AUD and HIV+AUD groups had significantly smaller thalamic subregional volumes than the CTRL group. The HIV+AUD group had smaller anterior thalamic volume than the HIV-only group and smaller ventral thalamic volume than the AUD-only group. In the HIV+AUD group, memory scores correlated with anterior thalamic volumes, attention/working memory scores correlated with posterior and medial thalamic volumes, and motor skill scores correlated with posterior thalamic volumes. Exploratory analyses focused on the HIV+AUD group indicated that within the posterior thalamic region, the pulvinar and medial geniculate nuclei were related to attention/working memory scores, and the pulvinar was related to motor skills scores. This study is novel in locating volume deficits in specific thalamic subregions, in addition to the thalamus as a whole, in HIV, AUD, and their comorbidity and in identifying functional ramifications of these deficits. Taken together, this study highlights the relevance of thalamic subregional volume deficits to dissociable cognitive and motor processes.

Brain Age Gap in Early Illness Schizophrenia and the Clinical High-Risk Syndrome: Associations With Experiential Negative Symptoms and Conversion to Psychosis.

Brain development/aging is not uniform across individuals, spawning efforts to characterize brain age from a biological perspective to model the effects of disease and maladaptive life processes on the brain. The brain age gap represents the discrepancy between estimated brain biological age and chronological age (in this case, based on structural magnetic resonance imaging, MRI). Structural MRI studies report an increased brain age gap (biological age > chronological age) in schizophrenia, with a greater brain age gap related to greater negative symptom severity. Less is known regarding the nature of this gap early in schizophrenia (ESZ), if this gap represents a psychosis conversion biomarker in clinical high-risk (CHR-P) individuals, and how altered brain development and/or aging map onto specific symptom facets. Using structural MRI, we compared the brain age gap among CHR-P (n = 51), ESZ (n = 78), and unaffected comparison participants (UCP; n = 90), and examined associations with CHR-P psychosis conversion (CHR-P converters n = 10; CHR-P non-converters; n = 23) and positive and negative symptoms. ESZ showed a greater brain age gap relative to UCP and CHR-P (Ps < .010). CHR-P individuals who converted to psychosis showed a greater brain age gap (P = .043) relative to CHR-P non-converters. A larger brain age gap in ESZ was associated with increased experiential (P = .008), but not expressive negative symptom severity. Consistent with schizophrenia pathophysiological models positing abnormal brain maturation, results suggest abnormal brain development is present early in psychosis. An increased brain age gap may be especially relevant to motivational and functional deficits in schizophrenia.

Alterations in Gray Matter Structural Networks in Amnestic Mild Cognitive Impairment: A Source-Based Morphometry Study.

Amnestic mild cognitive impairment (aMCI), considered as the prodromal stage of Alzheimer's disease, is characterized by isolated memory impairment and cerebral gray matter volume (GMV) alterations. Previous structural MRI studies in aMCI have been mainly based on univariate statistics using voxel-based morphometry. We investigated structural network differences between aMCI patients and cognitively normal older adults by using source-based morphometry, a multivariate approach that considers the relationship between voxels of various parts of the brain. Ninety-one aMCI patients and 80 cognitively normal controls underwent structural MRI and neuropsychological assessment. Spatially independent components (ICs) that covaried between participants were estimated and a multivariate analysis of covariance was performed with ICs as dependent variables, diagnosis as independent variable, and age, sex, education level, and site as covariates. aMCI patients exhibited reduced GMV in the precentral, temporo-cerebellar, frontal, and temporal network, and increased GMV in the left superior parietal network compared to controls (pFWER < 0.05, Holm-Bonferroni correction). Moreover, we found that diagnosis, more specifically aMCI, moderated the positive relationship between occipital network and Mini-Mental State Examination scores (pFWER < 0.05, Holm-Bonferroni correction). Our results showed GMV alterations in temporo-fronto-parieto-cerebellar networks in aMCI, extending previous results obtained with univariate approaches.

Age-Related Changes in Sleep and Its Implications for Cognitive Decline in Aging Persons With Schizophrenia: A Critical Review.

Cognitive impairment is a core feature of schizophrenia that worsens with aging and interferes with quality of life. Recent work identifies sleep as an actionable target to alleviate cognitive deficits. Cardinal non-rapid eye movement (NREM) sleep oscillations such as sleep spindles and slow oscillations are critical for cognition. People living with schizophrenia (PLWS) and their first-degree relatives have a specific reduction in sleep spindles and an abnormality in their temporal coordination with slow oscillations that predict impaired memory consolidation. While NREM oscillatory activity is reduced in typical aging, it is not known how further disruption in these oscillations contributes to cognitive decline in older PLWS. Another understudied risk factor for cognitive deficits among older PLWS is obstructive sleep apnea (OSA) which may contribute to cognitive decline. We conducted a narrative review to examine the published literature on aging, OSA, and NREM sleep oscillations in PLWS. Spindles are propagated via thalamocortical feedback loops, and this circuitry shows abnormal hyperconnectivity in schizophrenia as revealed by structural and functional MRI studies. While the risk and severity of OSA increase with age, older PLWS are particularly vulnerable to OSA-related cognitive deficits because OSA is often underdiagnosed and undertreated, and OSA adds further damage to the circuitry that generates NREM sleep oscillations. We highlight the critical need to study NREM sleep in older PWLS and propose that identifying and treating OSA in older PLWS will provide an avenue to potentially mitigate and prevent cognitive decline.

Abnormalities of brain structure and function in cervical spondylosis: a multi-modal voxel-based meta-analysis.

Previous neuroimaging studies have revealed structural and functional brain abnormalities in patients with cervical spondylosis (CS). However, the results are divergent and inconsistent. Therefore, the present study conducted a multi-modal meta-analysis to investigate the consistent structural and functional brain alterations in CS patients. A comprehensive literature search was conducted in five databases to retrieve relevant resting-state functional magnetic resonance imaging (rs-fMRI), structural MRI and diffusion tensor imaging (DTI) studies that measured brain functional and structural differences between CS patients and healthy controls (HCs). Separate and multimodal meta-analyses were implemented, respectively, by employing Anisotropic Effect-size Signed Differential Mapping software. 13 rs-fMRI studies that used regional homogeneity, amplitude of low-frequency fluctuations (ALFF) and fractional ALFF, seven voxel-based morphometry (VBM) studies and one DTI study were finally included in the present research. However, no studies on surface-based morphometry (SBM) analysis were included in this research. Due to the insufficient number of SBM and DTI studies, only rs-fMRI and VBM meta-analyses were conducted. The results of rs-fMRI meta-analysis showed that compared to HCs, CS patients demonstrated decreased regional spontaneous brain activities in the right lingual gyrus, right middle temporal gyrus (MTG), left inferior parietal gyrus and right postcentral gyrus (PoCG), while increased activities in the right medial superior frontal gyrus, bilateral middle frontal gyrus and right precuneus. VBM meta-analysis detected increased GMV in the right superior temporal gyrus (STG) and right paracentral lobule (PCL), while decreased GMV in the left supplementary motor area and left MTG in CS patients. The multi-modal meta-analysis revealed increased GMV together with decreased regional spontaneous brain activity in the left PoCG, right STG and PCL among CS patients. This meta-analysis revealed that compared to HCs, CS patients had significant alterations in GMV and regional spontaneous brain activity. The altered brain regions mainly included the primary visual cortex, the default mode network and the sensorimotor area, which may be associated with CS patients' symptoms of sensory deficits, blurred vision, cognitive impairment and motor dysfunction. The findings may contribute to understanding the underlying pathophysiology of brain dysfunction and provide references for early diagnosis and treatment of CS. https://www.crd.york.ac.uk/PROSPERO/, CRD42022370967.

Longitudinal imaging highlights preferential basal ganglia circuit atrophy in Huntington's disease.

Huntington's disease is caused by a CAG repeat expansion in the Huntingtin gene (HTT), coding for polyglutamine in the Huntingtin protein, with longer CAG repeats causing earlier age of onset. The variable 'Age' × ('CAG'-L), where 'Age' is the current age of the individual, 'CAG' is the repeat length and L is a constant (reflecting an approximation of the threshold), termed the 'CAG Age Product' (CAP) enables the consideration of many individuals with different CAG repeat expansions at the same time for analysis of any variable and graphing using the CAG Age Product score as the X axis. Structural MRI studies have showed that progressive striatal atrophy begins many years prior to the onset of diagnosable motor Huntington's disease, confirmed by longitudinal multicentre studies on three continents, including PREDICT-HD, TRACK-HD and IMAGE-HD. However, previous studies have not clarified the relationship between striatal atrophy, atrophy of other basal ganglia structures, and atrophy of other brain regions. The present study has analysed all three longitudinal datasets together using a single image segmentation algorithm and combining data from a large number of subjects across a range of CAG Age Product score. In addition, we have used a strategy of normalizing regional atrophy to atrophy of the whole brain, in order to determine which regions may undergo preferential degeneration. This made possible the detailed characterization of regional brain atrophy in relation to CAG Age Product score. There is dramatic selective atrophy of regions involved in the basal ganglia circuit-caudate, putamen, nucleus accumbens, globus pallidus and substantia nigra. Most other regions of the brain appear to have slower but steady degeneration. These results support (but certainly do not prove) the hypothesis of circuit-based spread of pathology in Huntington's disease, possibly due to spread of mutant Htt protein, though other connection-based mechanisms are possible. Therapeutic targets related to prion-like spread of pathology or other mechanisms may be suggested. In addition, they have implications for current neurosurgical therapeutic approaches, since delivery of therapeutic agents solely to the caudate and putamen may miss other structures affected early, such as nucleus accumbens and output nuclei of the striatum, the substantia nigra and the globus pallidus.

A Systematic Review of Structural and Functional MRI Studies Investigating Social Networking Site Use.

An understanding of the neurocognitive profile underlying the use of social networking sites (SNSs) can help inform decisions about the classification of problematic SNS use as an addictive disorder and elucidate how/when 'SNS addiction' might develop. The present review aimed to synthesize structural and functional MRI research investigating problematic/compulsive forms of SNS use or regular (non-addicted) SNS use behaviours. We conducted a systematic search for research articles published in English using the Web of Science, PubMed, and Scopus databases up to October 2022. Studies meeting our inclusion criteria were assessed for quality and a narrative synthesis of the results was conducted. Twenty-eight relevant articles were identified comprising structural MRI (n = 9), resting-state fMRI (n = 6) and task-based fMRI studies (n = 13). Current evidence suggests that problematic SNS use might be characterised by (1) reduced volume of the ventral striatum, amygdala, subgenual anterior cingulate cortex, orbitofrontal cortex and posterior insula; (2) increased ventral striatum and precuneus activity in response to SNS cues; (3) abnormal functional connectivity involving the dorsal attention network; (4) inter-hemispheric communication deficits. Regular SNS use behaviours appear to recruit regions involved in the mentalising network, the self-referential cognition network, the salience network, the reward network and the default mode network. Such findings are at least partially consistent with observations from the substance addiction literature and provide some provisional support for the addictive potential of SNSs. Nonetheless, the present review is limited by the small number of eligible studies and large heterogeneity in the methods employed, and so our conclusions should remain tentative. Moreover, there is a lack of longitudinal evidence suggesting SNSs cause neuroadaptations and thus conclusions that problematic SNS use represents a disease process akin to substance use addictions are premature. More well-powered longitudinal research is needed to establish the neural consequences of excessive and problematic SNS use.

Chaos analysis of the cortical boundary for the recognition of psychosis.

Structural MRI studies in people with first-episode psychosis (FEP) and those in the clinical high-risk (CHR) state have consistently shown volumetric abnormalities that depict changes in the structural complexity of the cortical boundary. The aim of the present study was to employ chaos analysis in the identification of people with psychosis based on the structural complexity of the cortical boundary and subcortical areas. We performed chaos analysis of the grey matter distribution on structural MRIs. First, the outer boundary points for each slice in the axial, coronal and sagittal view were calculated for grey matter maps. Next, the distance of each boundary point from the centre of mass in the grey matter was calculated and stored as spatial series, which was further analyzed by extracting the Largest Lyapunov Exponent (lambda [λ]), a feature depicting the structural complexity of the cortical boundary. Structural MRIs were acquired from 77 FEP, 73 CHR and 44 healthy controls. We compared λ brain maps between groups, which resulted in statistically significant differences in all comparisons. By matching the λ values extracted in axial view with the Morlet wavelet, differences on the surface relief are observed between groups. Parameters were selected after experimentation on the examined sample. Investigation of the effectiveness of the method in a larger data set is needed. The proposed framework using spatial series verifies diagnosis-relevant features and may contribute to the identification of structural biomarkers for psychosis.

Association between late‐life air pollution exposure and medial temporal lobe atrophy in older women

AbstractBackgroundAmbient air pollution exposures increase the risk of Alzheimer’s disease (AD) and related dementias, which may be driven by structural brain alterations in the medial temporal lobe (MTL). The MTL consists of subregions critical for memory and vulnerable to AD neuropathology, including the hippocampus, parahippocampal gyrus (PHG), entorhinal cortex (ERC), and amygdala. However, previous structural MRI studies examining the hypothesized adverse effects of exposure on MTL were cross‐sectional and largely focused on hippocampus which yielded mixed results, failing to provide insights on the underlying neuropathological processes affected by air pollution exposures.MethodWe conducted a longitudinal study including 653 cognitively‐normal community‐dwelling women from the Women’s Health Initiative Memory Study with two MRI brain scans (MRI‐1: 2005‐6; MRI‐2: 2010‐11; Meanage at MRI‐1 = 77.3±3.5). Using regionalized universal kriging models, exposures at residential locations were estimated as 3‐year annual averages of fine particulate matter (PM2.5) and nitrogen dioxide (NO2; traffic‐related pollution) prior to MRI‐1. Volumes of the total MTL and MTL subregions were derived using multi‐atlas region segmentation with ensembled registration. We used linear regressions to estimate exposure effects on 5‐year standardized volume changes, adjusting for intracranial volume, sociodemographic, lifestyle, and clinical characteristics. We also examined if associations differed between APOE4 carriers (n = 123) and non‐carriers (n = 463).ResultMTL volume decreased by 0.53±1.00cm3 over 5 years. For each interquartile increase of PM2.5 (3.26µg/m3) and NO2 (6.77ppb), adjusted MTL volume had greater shrinkage by 0.32cm3 (95%CI = [‐0.43,‐0.21]) and 0.12cm3 (95%CI = [‐0.23,‐0.01]) over 5 years, equivalent to respectively 17% (95%CI = [11%, 24%]) and 6% (95%CI = [0.6%, 12%]) increased dementia risk. For PHG, we found loss of 0.24cm3 (95%CI = [‐0.30,‐0.19]) and 0.09cm3 (95%CI = [‐0.14,‐0.04]) associated with PM2.5 and NO2 respectively. There was loss of 0.06cm3 (95%CI = [‐0.10,‐0.01]) in ERC associated with PM2.5, but not with NO2. No associations were found with amygdala or hippocampal atrophy. The observed adverse exposure effects on MTL atrophy did not differ by APOE4 genotype.ConclusionMTL atrophy in older women was associated with late‐life exposures to PM2.5 and NO2, and the putative adverse effects varied across brain subregions. The PHG and ERC—the MTL subregions where AD neuropathologies likely begin, may be preferentially vulnerable to air pollution neurotoxicity.

Identification of texture MRI brain abnormalities on first-episode psychosis and clinical high-risk subjects using explainable artificial intelligence

Structural MRI studies in first-episode psychosis and the clinical high-risk state have consistently shown volumetric abnormalities. Aim of the present study was to introduce radiomics texture features in identification of psychosis. Radiomics texture features describe the interrelationship between voxel intensities across multiple spatial scales capturing the hidden information of underlying disease dynamics in addition to volumetric changes. Structural MR images were acquired from 77 first-episode psychosis (FEP) patients, 58 clinical high-risk subjects with no later transition to psychosis (CHR_NT), 15 clinical high-risk subjects with later transition (CHR_T), and 44 healthy controls (HC). Radiomics texture features were extracted from non-segmented images, and two-classification schemas were performed for the identification of FEP vs. HC and FEP vs. CHR_NT. The group of CHR_T was used as external validation in both schemas. The classification of a subject’s clinical status was predicted by importing separately (a) the difference of entropy feature map and (b) the contrast feature map, resulting in classification balanced accuracy above 72% in both analyses. The proposed framework enhances the classification decision for FEP, CHR_NT, and HC subjects, verifies diagnosis-relevant features and may potentially contribute to identification of structural biomarkers for psychosis, beyond and above volumetric brain changes.

Structural alterations of the motor cortex and higher order cortical areas suggest early neurodevelopmental origin of catatonia in schizophrenia

The neurobiology of catatonia is still poorly understood. Particularly structural MRI studies yielded conflicting results. Heterogeneity of findings was suggested to stem from specifics of different rating scales. This study sought to test grey matter differences between patients with catatonia, patients without catatonia, and healthy controls using the two main instruments of catatonia rating. We included 98 patients with schizophrenia spectrum disorders and 42 healthy controls. Catatonia was measured using the Bush Francis Catatonia Rating Scale and the Northoff Catatonia Rating Scale. According to these scales, patients were classified into those with and those without catatonia. We tested whole brain grey matter volume, cortical thickness, and local gyrification across groups. Both catatonia rating scales correlated at tau = 0.65 but failed to classify identical subjects as catatonia patients. However, group differences in grey matter parameters were broadly similar with either rating scale to identify catatonia cases. Catatonia patients had reduced grey matter volume compared to controls in a large network including orbitofrontal cortex, cingulate, thalamus, and amygdala. While there was no group difference in cortical thickness, catatonia patients had increased local gyrification in premotor, motor, and parietal cortices compared to controls. Hypergyrification of the motor cortex and higher order cortical areas was found in catatonia patients compared to patients without catatonia. Both catatonia rating scales find similar symptom severity and group differences in grey matter indices. Catatonia is linked to reduced grey matter volume and increased local gyrification, suggesting some impact of early neurodevelopmental insults.

Chaos analysis of the brain topology in first-episode psychosis and clinical high risk patients.

Structural MRI studies in first-episode psychosis (FEP) and in clinical high risk (CHR) patients have consistently shown volumetric abnormalities in frontal, temporal, and cingulate cortex areas. The aim of the present study was to employ chaos analysis for the identification of brain topology differences in people with psychosis. Structural MRI were acquired from 77 FEP, 73 CHR and 44 healthy controls (HC). Chaos analysis of the gray matter distribution was performed: First, the distances of each voxel from the center of mass in the gray matter image was calculated. Next, the distances multiplied by the voxel intensity were represented as a spatial-series, which then was analyzed by extracting the Largest-Lyapunov-Exponent (lambda). The lambda brain map depicts thus how the gray matter topology changes. Between-group differences were identified by (a) comparing the lambda brain maps, which resulted in statistically significant differences in FEP and CHR compared to HC; and (b) matching the lambda series with the Morlet wavelet, which resulted in statistically significant differences in the scalograms of FEP against CHR and HC. The proposed framework using spatial-series extraction enhances the between-group differences of FEP, CHR and HC subjects, verifies diagnosis-relevant features and may potentially contribute to the identification of structural biomarkers for psychosis.

Convergent gray matter alterations across drugs of abuse and network-level implications: A meta-analysis of structural MRI studies

BackgroundNeuroimaging studies often consider brain alterations linked with substance abuse within the context of individual drugs (e.g., nicotine), while neurobiological theories of addiction emphasize common brain network-level alterations across drug classes. Using emergent meta-analytic techniques, we identified common structural brain alterations across drugs and characterized the functionally-connected networks with which such structurally altered regions interact. MethodsWe identified 82 articles characterizing gray matter (GM) volume differences for substance users vs. controls. Using the anatomical likelihood estimation algorithm, we identified convergent GM reductions across drug classes. Next, we performed resting-state and meta-analytic functional connectivity analyses using each structurally altered region as a seed and computed whole-brain functional connectivity profiles as the union of both maps. We characterized an “extended network” by identifying brain areas demonstrating the highest degree of functional coupling with structurally impacted regions. Finally, hierarchical clustering was performed leveraging extended network nodes’ functional connectivity profiles to delineate subnetworks. ResultsAcross drug classes, we identified medial frontal/ventromedial prefrontal, and multiple regions in anterior cingulate (ACC) and insula as regions displaying convergent GM reductions among users. Overlap of these regions’ functional connectivity profiles identified ACC, inferior frontal, PCC, insula, superior temporal, and putamen as regions of an impacted extended network. Hierarchical clustering revealed 3 subnetworks closely corresponding to default mode (PCC, angular), salience (dACC, caudate), and executive control networks (dlPFC and parietal). ConclusionsThese outcomes suggest that substance-related structural brain alterations likely have implications for the functioning of canonical large-scale networks and the perpetuation of substance use and neurocognitive alterations.

Individuals with cannabis use are associated with widespread morphological alterations in the subregions of the amygdala, hippocampus, and pallidum

BackgroundCannabis is the most frequently used illicit drug worldwide. Although multiple structural MRI studies of individuals with cannabis use (CB) have been undertaken, the reports of the volume alterations in the amygdala, hippocampus, and pallidum are not consistent. This study aims to detect subregion-level morphological alterations, analyze the correlation areas with cannabis usage characteristics, and gain new insights into the neuro mechanisms of CB. MethodsBy leveraging the novel surface-based subcortical morphometry method, 20 CB and 22 age- and sex-matched healthy controls (HC) were included to explore their volumetric and morphological differences in the three subcortical structures. Afterward, the correlation analysis between surface morphological eigenvalues and cannabis usage characteristics was performed. ResultsCompared with volumetric measures, the surface-based subcortical morphometry method detected more significant global morphological deformations in the left amygdala, right hippocampus, and right pallidum (overall-p < 0.05, corrected). More obvious morphological alterations (atrophy or expansion) were observed in specific subregions (vertex-based p-value<0.05, uncorrected) of the three subcortical structures. Both positive and negative subregional correlation areas were reported by the correlation analysis. ConclusionsThe current study illuminated new pathophysiologic mechanisms in the amygdala, hippocampus, and pallidum at the subregion level, which may inform the subsequent smaller-scale CB research.

Volumetric measurements of the subcortical structures of healthy adult brains in the Turkish population.

The interest in the morphological development of brain structures during childhood and adolescence arises from discussions on subcortical anomalies and sexual dimorphism, from adolescent changes in cognitive functions supported by cortical and subcortical structures to a wide range of childhood neuropsychiatric diseases. This study aims to investigate the subcortical structures regarding age/gender changes in the healthy adult human brain using web-based volBrain. In this study, 303 normal healthy adults (males and females) were examined using a 1.5 T unit with a 20-channel head coil. The volumes of white matter, grey matter, total brain, cerebrospinal fluid, and total intracranial volume were significantly higher in males than those in females. Our analysis revealed a significantly larger accumbens volume in females. With the age of less than or equal to 50 years, older males were found to have higher total lateral ventricle, putamen, thalamus, amygdala, cerebrum, white matter and grey matter volumes than females. In the age group of 50 years and older mean total volumes of thalamus, globus pallidus and accumbens were higher in females than those in males. Right hemisphere volumes in younger and older age groups were higher except for caudate volume in the older age group; the mean of caudate was significantly higher in females than those in males. These conclusions might be important for the explanation of the effects of gender and age in cross-sectional structural magnetic resonance imaging studies. Also, knowing the volume changes of the subcortical structures can provide convenience about the prevention, diagnosis, and treatment of various neuromental disorders.

Common and specific large-scale brain changes in major depressive disorder, anxiety disorders, and chronic pain: a transdiagnostic multimodal meta-analysis of structural and functional MRI studies

Major depressive disorder (MDD), anxiety disorders (ANX), and chronic pain (CP) are closely-related disorders with both high degrees of comorbidity among them and shared risk factors. Considering this multi-level overlap, but also the distinct phenotypes of the disorders, we hypothesized both common and disorder-specific changes of large-scale brain systems, which mediate neural mechanisms and impaired behavioral traits, in MDD, ANX, and CP. To identify such common and disorder-specific brain changes, we conducted a transdiagnostic, multimodal meta-analysis of structural and functional MRI-studies investigating changes of gray matter volume (GMV) and intrinsic functional connectivity (iFC) of large-scale intrinsic brain networks across MDD, ANX, and CP. The study was preregistered at PROSPERO (CRD42019119709). 320 studies comprising 10,931 patients and 11,135 healthy controls were included. Across disorders, common changes focused on GMV-decrease in insular and medial-prefrontal cortices, located mainly within the so-called default-mode and salience networks. Disorder-specific changes comprised hyperconnectivity between default-mode and frontoparietal networks and hypoconnectivity between limbic and salience networks in MDD; limbic network hyperconnectivity and GMV-decrease in insular and medial-temporal cortices in ANX; and hypoconnectivity between salience and default-mode networks and GMV-increase in medial temporal lobes in CP. Common changes suggested a neural correlate for comorbidity and possibly shared neuro-behavioral chronification mechanisms. Disorder-specific changes might underlie distinct phenotypes and possibly additional disorder-specific mechanisms.

Meta-analysis of structural MRI studies in anorexia nervosa and the role of recovery: a systematic review protocol

BackgroundAnorexia nervosa (AN) is associated with structural brain abnormalities. Studies have reported less cerebral tissue and more cerebrospinal fluid (CSF) in individuals with AN relative to healthy controls, although findings are variable and inconsistent due to variations in sample size, age, and disease state (e.g., active AN, weight-recovered AN). Further, it remains unclear if structural brain abnormalities observed in AN are a consequence of specific brain pathologies or malnutrition, as very few longitudinal neuroimaging studies in AN have been completed.MethodsTo overcome this issue, this comprehensive meta-analysis will combine region-of-interest (ROI) and voxel-based morphometry (VBM) approaches to understand how regional and global structural brain abnormalities differ among individuals with AN and healthy controls (HCs). Additionally, we aim to understand how clinical characteristics and physiological changes during the course of illness, including acute illness vs. weight recovery, may moderate these structural abnormalities. We will create an online database of studies that have investigated structural brain abnormalities in AN. Data will be reviewed independently by two members of our team using MEDLINE databases, Web of Science, PsycINFO, EMBASE, and CINAHL. We will conduct ROI and VBM meta-analysis using seed-based d mapping in AN and HCs. We will include all studies that include structural neuroimaging of individuals with AN (both acute and weight-recovered) and HCs between January 1997 and 2020.DiscussionThis systematic review will assess the effects of AN compared to HC on brain structure. Futhermore, it will explore the role of acute AN and weight-recovered AN on brain structure. Findings will help researchers and clinicians to better understand the course of illness in AN and the nature of recovery, in terms of weight, malnutrition, and the state of the brain.Systematic review registrationPROSPERO CRD42020180921

Structural atrophy of the right superior frontal gyrus in adolescents with severe irritability.

Severe irritability is common in youths with psychiatric disorders and results in significant dysfunction across domains (academic, social, and familial). Prior structural MRI studies in the pediatric population demonstrated that aberrations of cortical thickness (CT) and gray matter volume (GMV) in the fronto‐striatal‐temporal regions which have been associated with irritability. However, the directions of the correlations between structural alteration and irritability in the individual indices were not consistent. Thus, we aim to address this by implementing comprehensive assessments of CT, GMV, and local gyrification index (LGI) simultaneously in youths with severe levels of irritability by voxel‐based morphometry and surface‐based morphometry. One hundred and eight adolescents (46 youths with severe irritability and 62 healthy youths, average age = 14.08 years, standard deviation = 2.36) were scanned with a T1‐weighted MRI sequence. The severity of irritability was measured using the affective reactivity index. In youths with severe irritability, there was decreased CT, GMV, and LGI in the right superior frontal gyrus (SFG) compared to healthy youths, and negative correlations between these indices of the SFG and irritability. Our findings suggest that structural deficits in the SFG, potentially related to its role in inhibitory control, may be critical for the neurobiology of irritability.

Age-related hearing loss and cognitive decline: MRI and cellular evidence.

Extensive evidence supports the association between age-related hearing loss (ARHL) and cognitive decline. It is, however, unknown whether a causal relationship exists between these two, or whether they both result from shared mechanisms. This paper intends to study this relationship through a comprehensive review of MRI findings as well as evidence of cellular alterations. Our review of structural MRI studies demonstrates that ARHL is independently linked to accelerated atrophy of total and regional brain volumes and reduced white matter integrity. Resting-state and task-based fMRI studies on ARHL also show changes in spontaneous neural activity and brain functional connectivity; and alterations in brain areas supporting auditory, language, cognitive, and affective processing independent of age, respectively. Although MRI findings support a causal relationship between ARHL and cognitive decline, the contribution of potential shared mechanisms should also be considered. In this regard, the review of cellular evidence indicates their role as possible common mechanisms underlying both age-related changes in hearing and cognition. Considering existing evidence, no single hypothesis can explain the link between ARHL and cognitive decline, and the contribution of both causal (i.e., the sensory hypothesis) and shared (i.e., the common cause hypothesis) mechanisms is expected.