Gray Matter Changes Research Articles

A Preliminary Study of Alterations in Iron Disposal and Neural Activity in Ischemic Stroke.

Purpose The study aimed to evaluate the postrehabilitation changes in deep gray matter (DGM) nuclei, corticospinal tract (CST), and motor cortex area, involved in motor tasks in patients with ischemic stroke. Methods Three patients participated in this study, who had experienced an ischemic stroke on the left side of the brain. They underwent a standard rehabilitation program for four consecutive weeks, including transcranial direct current stimulation (tDCS), neuromuscular electrical stimulation (NMES), and occupational therapy. The patients' motor ability was evaluated by Fugl-Meyer assessment-upper extremity (FMA-UE) and Wolf motor function test (WMFT). Multimodal magnetic resonance imaging (MRI) was acquired from the patients by a 3 Tesla machine before and after the rehabilitation. The magnetic susceptibility changes were examined in DGM nuclei including the bilateral caudate (CA), putamen (PT), globus pallidus (GP), and thalamus (TH) using quantitative susceptibility mapping (QSM). Functional MRI (fMRI) in the motor cortex areas was acquired to evaluate the postrehab functional motor activity. The three-dimensional corticospinal tract (CST) was reconstructed using diffusion-weighted imaging (DWI) and diffusion tensor tractography (DTT), and the fractional anisotropy (FA) was measured along the tract. Ultimately, the relationship between the structural and functional changes was evaluated in CST and motor cortex. Results Postrehabilitation FMA-UE and WMFT scores increased for all patients compared to the prerehabilitation. QSM analysis revealed increasing in susceptibility values in GP and CA in all patients at the ipsilesional hemisphere. By fMRI analysis, the ipsilesional hemisphere demonstrated an increase in functional activity in motor areas for all 3 patients. In the ipsilesional hemisphere, the fractional anisotropy (FA) was increased in CST in two patients, while the mean diffusivity (MD) was decreased in CA in a patient, in PT and TH in another patient, and in PT in two patients. Conclusion This preliminary study demonstrates that the magnetic susceptibility may decrease at some ipsilesional DGM nuclei after tDCS, NMES, and occupational therapy for patients with ischemic stroke, suggesting a drop in the level of iron deposition, which may be associated with an increase in the level of activity in motor cortex after rehabilitation.

Neurometabolic changes in multiple sclerosis: Fingolimod versus beta interferon or glatiramer acetate therapy.

Fingolimod has been shown to be more effective in reducing relapse rate and disability than injectable therapies in clinical trials. An increase in N-acetylaspartate (NAA) as measured by MR spectroscopy is correlated with maintaining axonal metabolic functions. This study compared the neurometabolic and volumetric changes in relapsing-remitting multiple sclerosis (RRMS) patients on fingolimod or injectable therapies with healthy controls (HCs). Ninety-eight RRMS (52 on fingolimod, 46 on injectable therapies (27 on glatiramer acetate and 19 on interferon) were age and sex-matched to 51 HCs. RRMS patients underwent cognitive, fatigue, and mental health assessments, as well as an Expanded disability status scale (EDSS). MRI/S was acquired from the hippocampus, posterior cingulate gyrus (PCG), and prefrontal cortex (PFC). Volumetric and neurometabolic measures were compared across cohorts using a univariate general linear model and correlated with clinical severity and neuropsychological scores. Clinical parameters, MR-volumetric, and neurometabolic profiles showed no differences between treatment groups (p>.05). Compared to HCs, both RRMS cohorts showed volume changes in white matter (-13%), gray matter (-16%), and cerebral spinal fluid (CSF) (+17-23%), as well as reduced NAA (-17%, p = .001, hippocampus), (-7%, p = .001, PCG), and (-9%, p = .001, PFC). MRI/S metrics in three regions were moderately correlated with cognition and fatigue functions. While both treatment arms showed overall similar volumetric and neurometabolic profiles, longitudinal studies are warranted to clarify neurometabolic changes and associations with treatment efficacy.

Altered gray matter volume in children with newly diagnosed type 1 diabetes mellitus.

Type 1 diabetes mellitus (T1DM) affects the development of cognitive function in children, which may be due to deficits in brain structures or functions. It is unclear whether children with T1DM experience alterations in the gray matter (GM) structure at the initial stages of the disease. This study investigated GM structure alterations in children with newly diagnosed T1DM. Based on 3D T1-weighted MR images, we investigated the gray matter volume (GMV) of 35 newly diagnosed T1DM children and 35 age- and sex-matched healthy controls using voxel-based morphometry. The brain regions with significant differences in GMV between the newly diagnosed T1DM children and the controls were extracted and the correlation with clinical data was assessed. Compared with the control group, children with newly diagnosed T1DM had a lower GMV in the right inferior and middle temporal gyri, right lingual gyrus, and left superior frontal gyrus. In T1DM subjects, the GMV of the right middle temporal gyrus was positively correlated with IQ but was negatively correlated with HbA1c. Our findings provide compelling evidence that GM abnormalities occur during early disease stages in T1DM children, which may be a potential neurobiological mechanism underlying cognitive deficits. Using an efficient method to analyze gray matter changes in T1DM is very important. The anterior, posterior, and temporal brain regions are susceptible to T1DM in children. Recent glucose variability may affect regional gray matter volume in children with newly diagnosed T1DM. Structural changes were documented in the gray matter of the brain even at the early stages of the disease in children with T1DM.

Gray matter abnormalities and associated familial risk endophenotype in individuals with first-episode bipolar disorder: Evidence from whole-brain voxel-wise meta-analysis.

Gray matter abnormalities have been widely reported in individuals with and at familial risk for bipolar disorder (BD). However, inconsistent findings were reported, and whether shared abnormalities exist between at-risk individuals and patients which can represent an endophenotype remained unclear. This meta-analysis aimed at identifying robust patterns of gray matter changes in patients with first-episode BD (FEBD) and associated risk endophenotype of BD. A systematic literature search was performed to identify eligible voxel-based morphometry studies comparing FEBD patients and healthy controls. Findings of included studies were integrated using the Seed-based d Mapping toolbox. Common and distinct patterns of gray matter abnormalities between FEBD patients and unaffected at-risk individuals were explored. A total of 16 VBM studies comparing 411 FEBD patients and 521 controls were included. FEBD patients showed increased gray matter volume in the cerebellum, posterior cingulate cortex and striatum, and decreased gray matter volume in the medial superior frontal gyrus and gyrus rectus. No common abnormalities were identified between FEBD patients and unaffected at-risk individuals. More gray matter loss in the medial superior frontal gyrus and insula were found in FEBD patients relative to unaffected at-risk individuals. These findings revealed robust gray matter abnormalities in the cortico-striato-cerebellar and default mode network regions in FEBD, and implicated that gray matter deficits may not represent a familial risk endophenotype of BD.

Cortical and Subcortical Alterations and Clinical Correlates after Traumatic Brain Injury.

Background: Traumatic brain injury (TBI) often results in persistent cognitive impairment and psychiatric symptoms, while lesion location and severity are not consistent with its clinical complaints. Previous studies found cognitive deficits and psychiatric disorders following TBI are considered to be associated with prefrontal and medial temporal lobe lesions, however, the location and extent of contusions often cannot fully explain the patient′s impairments. Thus, we try to find the structural changes of gray matter (GM) and white matter (WM), clarify their correlation with psychiatric symptoms and memory following TBI, and determine the brain regions that primary correlate with clinical measurements. Methods: Overall, 32 TBI individuals and 23 healthy controls were recruited in the study. Cognitive impairment and psychiatric symptoms were examined by Mini-Mental State Examination (MMSE), Hospital Anxiety and Depression Scale (HADS), and Wechsler Memory Scale-Chinese Revision (WMS-CR). All MRI data were scanned using a Siemens Prisma 3.0 Tesla MRI system. T1 MRI data and diffusion tensor imaging (DTI) data were processed to analyze GM volume and WM microstructure separately. Results: In the present study, TBI patients underwent widespread decrease of GM volume in both cortical and subcortical regions. Among these regions, four brain areas including the left inferior temporal gyrus and medial temporal lobe, supplementary motor area, thalamus, and anterior cingulate cortex (ACC) were highly implicated in the post-traumatic cognitive impairment and psychiatric complaints. TBI patients also underwent changes of WM microstructure, involving decreased fractional anisotropy (FA) value in widespread WM tracts and increased mean diffusivity (MD) value in the forceps minor. The changes of WM microstructure were significantly correlated with the decrease of GM volume. Conclusions: TBI causes widespread cortical and subcortical alterations including a reduction in GM volume and change in WM microstructure related to clinical manifestation. Lesions in temporal lobe may lead to more serious cognitive and emotional dysfunction, which should attract our high clinical attention.

Grey matter changes on brain MRI in subjective cognitive decline: a systematic review

IntroductionPeople with subjective cognitive decline (SCD) report cognitive deterioration. However, their performance in neuropsychological evaluation falls within the normal range. The present study aims to analyse whether structural magnetic resonance imaging (MRI) reveals grey matter changes in the SCD population compared with healthy normal controls (HC).MethodsParallel systematic searches in PubMed and Web of Science databases were conducted, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Quality assessment was completed using the Newcastle-Ottawa Scale (NOS).ResultsFifty-one MRI studies were included. Thirty-five studies used a region of interest (ROI) analysis, 15 used a voxel-based morphometry (VBM) analysis and 10 studies used a cortical thickness (CTh) analysis. Ten studies combined both, VBM or CTh analysis with ROI analysis.ConclusionsMedial temporal structures, like the hippocampus or the entorhinal cortex (EC), seemed to present grey matter reduction in SCD compared with HC, but the samples and results are heterogeneous. Larger sample sizes could help to better determine if these grey matter changes are consistent in SCD subjects.

The structural changes of gray matter in Parkinson disease patients with mild cognitive impairments.

ObjectivesParkinson disease (PD) is associated with cognitive impairments. However, the underlying neural mechanism of cognitive impairments in PD is still not clear. This study aimed to investigate the anatomic alternations of gray matter in PD patients with mild cognitive impairment (MCI) and their associations with neurocognitive measurements.MethodsT1-weighted magnetic resonance imaging (MRI) data were acquired from 23 PD patients with MCI, 23 PD patients without MCI, and 23 matched healthy controls. The MRI data were analyzed using voxel-based morphometry (VBM) and surfaced-based morphometry (SBM) methods to assess the structural changes in gray matter volume and cortical thickness respectively. Receiver operating characteristic (ROC) analysis was used to examine the diagnostic accuracies of the indexes of interest. The correlations between the structural metrics and neurocognitive assessments (e.g., Montreal cognitive assessment, MOCA; Mini-mental state examination, MMSE) were further examined.ResultsPD patients with MCI showed reduced gray matter volume (GMV) in the frontal cortex (e.g., right inferior frontal gyrus and middle frontal gyrus) and extended to insula as well as cerebellum compared with the healthy controls and PD patients without MIC. Thinner of cortical thickens in the temporal lobe (e.g., left middle temporal gyrus and right superior temporal gyrus) extending to parietal cortex (e.g., precuneus) were found in the PD patients with MCI relative to the healthy controls and PD patients without MCI.ROC analysis indicated that the area under the ROC curve (AUC) values in the frontal, temporal, and subcortical structures (e.g., insula and cerebellum) could differentiate the PD patients with MCI and without MCI and healthy controls. Furthermore, GMV of the right middle frontal gyrus and cortical thickness of the right superior temporal gyrus were correlated with neurocognitive dysfunctions (e.g., MOCA and MMSE) in PD patients with MCI.ConclusionThis study provided further evidence that PD with MCI was associated with structural alternations of brain. Morphometric analysis focusing on the cortical and subcortical regions could be biomarkers of cognitive impairments in PD patients.

Probing the link between the APOE-ε4 allele and whole-brain gray matter using deep learning.

The APOE-ε4 allele is a known genetic risk for Alzheimer's disease (AD). Thus, it can be reasoned that the APOE-ε4 allele would also impact neurodegeneration-associated structural brain changes. Here we probe if the APOE-ε4 genotype directly modulates the human brain's gray matter using a neural network trained on the whole-brain gray matter images from the cognitively normally aging (CN) and AD individuals. To investigate the linkage between the APOE-ε4 allele and whole-brain (voxel-wise) gray matter, we systematically profile our investigation in multiple classification tasks, including diagnostic classification and APOE-ε4 classification conjointly as well as independently. Results suggest that although the MRI data can reliably track and reflect neurodegenerative changes in the brain cross-sectionally, the APOE-ε4 status may not be distinguishable correspondingly. The nonexistence of a direct and convincing modulative effect of APOE-ε4 on the whole-brain gray matter indicates that the gray matter changes may be independent of the APOE-ε4 status, and instead characterize a non-APOE, comorbid mechanism in AD.

Gray Matter Abnormalities in Myotonic Dystrophy Type 1: A Voxel-Wise Meta-Analysis.

BackgroundA growing number of voxel-based morphometry (VBM) studies have demonstrated widespread gray matter (GM) abnormalities in myotonic dystrophy type 1 (DM1), but the findings are heterogeneous. This study integrated previous VBM studies to identify consistent GM changes in the brains of patients with DM1.MethodsSystematic retrieval was conducted in Web of Science, Pubmed, and Embase databases to identify VBM studies that met the inclusion requirements. Data were extracted. The Seed-based d Mapping with Permutation of Subject Images (SDM-PSI) software was used for meta-analysis of voxel aspects.ResultsA total of eight VBM studies were included, including 176 patients with DM1 and 198 healthy controls (HCs). GM volume in patients with DM1 was extensively reduced compared with HCs, including bilateral rolandic operculum, bilateral posterior central gyrus, bilateral precentral gyrus, right insula, right heschl gyrus, right superior temporal gyrus, bilateral supplementary motor area, bilateral middle cingulate gyrus/paracingulate gyrus, left paracentral lobule, and bilateral caudate nucleus. Meta-regression analysis found that regional GM abnormalities were associated with disease duration and Rey-Osterrieth Complex Figure (ROCF)-recall scores.ConclusionDM1 is not only a disease of muscle injury but also a multisystem disease involving brain motor and neuropsychiatric regions, providing a basis for the pathophysiological mechanism of DM1.

Basic lifestyle habits and volume change in total gray matter among community dwelling middle-aged and older Japanese adults

The brain controls human behavior, and the gray matter is the main resource of neuronal cells. We examined the longitudinal relationship between six basic lifestyle habits (diet, exercise, sleep, alcohol consumption, smoking, and social activity including employment) and total gray matter volume in community-dwelling adults in Japan.This two-year follow-up study with data derived from the National Institute for Longevity Sciences, Longitudinal Study of Aging, Aichi, Japan, included adults aged 40–87 years (n = 1665, men: 51%). Lifestyle habits were assessed at baseline (2008–2010) using self-reported questionnaires and three-day dietary records. Total gray matter volume at baseline and after two years was estimated using T1-weighted brain magnetic resonance imaging and FreeSurfer software. The association between each lifestyle factor, the total number of healthy lifestyle habits, and gray matter volume change was determined via a multiple linear regression analysis adjusting for baseline age, total gray matter volume, and other confounders. The mean ± standard deviation decrease in total gray matter volume during the two-year follow-up period was 0.94 ± 1.86% in men and 0.61 ± 2.27% in women. In the multiple regression analysis, volume loss in total gray matter positively correlated with male smoking, while it was negatively correlated with male social activity and employment, female dietary diversity, and the total number of healthy lifestyle habits (standardized beta coefficient; −0.061 in men [p = 0.07], −0.113 in women [p < 0.05]). Therefore, engaging in social activities, non-smoking, a diverse diet, or adopting one healthy lifestyle habit may help prevent gray matter volume loss.

Transcranial Direct Current Stimulation (tDCS) in chronic low back pain: Systematic review with meta-analysis

Background and objective. Changes in grey matter of cortex and other parts of brain leads to increased pain perception in chronic low back pain (CLBP) patients which could be reduced by electrical application on these areas. The objective of the present review was to evaluate the efficacy of transcranial direct current stimulation (tDCS) alone as well as tDCS in combination with other interventions on pain in chronic low back pain patients. Method. PubMed and Cochrane search engines was used to locate the literature. The eligibility criterion for the study includes articles published in English language, published till March 2020 and the application of tDCS alone as well as in combination with other interventions on CLBP patients. Pain intensity was measured by visual analogue scale (VAS), numeric rating scale (NRS) or defense and veteran pain rating scale (DVPRS). Mean difference with 95% CI for the active tDCS, sham tDCS and tDCS in combination with other interventions was calculated. Result. 7 articles, with 427 patients, were included in the quantitative meta-analysis. The result showed statistically significant reduction in pain in tDCS alone as compared to sham tDCS Z= 1.93. P= 0.05 and insignificant reduction in pain in tDCS when used in combination with other intervention as compared to sham tDCS, Z= 0.72, P= 0.47 with heterogeneity of 84 % in the included studies. Conclusion. It can be concluded that there is significant reduction of pain in patients of chronic low back pain when tDCS is applied in isolation.

Cerebellar Differences after Rehabilitation in Children with Developmental Coordination Disorder.

Developmental coordination disorder (DCD) affects a child’s ability to learn motor skills. Cognitive Orientation to daily Occupational Performance (CO-OP) is one of the recommended treatments to help achieve functional motor goals. The purpose of this study was to determine if CO-OP intervention induces functional improvements and structural changes in the cerebellum of children with DCD. Using a randomized waitlist-controlled trial, we investigated the effects of CO-OP intervention on cerebellar volume in 47 children with DCD (8–12 years old). Outcome measures included the Canadian Occupational Performance Measure, Performance Quality Rating Scale (PQRS), and Bruininks–Oseretsky Test of Motor Proficiency-2. The SUIT toolbox was used to carry out voxel-based morphometry using T1-weighted MRI scans. Children with DCD showed improved motor outcomes and increased gray matter volume in the brainstem, right crus II, bilateral lobules VIIIb, and left lobule IX following CO-OP. Significant associations were found between PQRS scores and regional gray matter changes in the brainstem, right crus II, right lobule VIIb, right and left lobule VIIIb, and vermis IX. Given the improved motor and brain outcomes with CO-OP, it is recommended that children with DCD be referred for this rehabilitation intervention.

Functional dysconnectivity of cerebellum and attention networks in emotional dysregulation shared between attention deficit hyperactivity disorder and major depressive disorder: a multimodal imaging study.

Emotional dysregulation (ED) is a common characteristic of both attention deficit hyperactivity disorder (ADHD) and major depressive disorder (MDD), especially in adolescents. However, whether ADHD and MDD may share the specific ED-related neural networks remains unknown. In total, 43 adolescents with clinical ED (22 adolescents with ADHD and 21 with MDD) were recruited; in addition, 29 sex- and age-matched healthy controls (HCs) were included. Resting-state functional connectivity (RSFC) analysis, voxel-based morphometry, and diffusion tensor imaging analysis were performed for each patient. In addition, we determined the significant regions of interest in patients with ED due to ADHD and MDD as compared with HCs and tested their correlations with clinical rating scale scores. Compared with HCs, patients with ED had greater RSFC in the cerebellum and supramarginal gyrus (SMG), especially between vermis VI and the SMG in the attention networks, and lower RSFC between the right supplementary motor area and right lateral parietal area. Lower gray matter (GM) volume in the SMG was also found. RSFC was significantly correlated with clinical rating scale scores for all patients with ED due to ADHD or MDD. GM change was correlated with ED and MDD rating scale scores. The cerebellum and attention networks might play major roles in ED pathophysiology in adolescents with ADHD and MDD. Increased connectivity of the vermis to the SMG serves as a possible underlying neural network.

Prematurity Is a Chronic Disease

Few studies have investigated neuroradiographic findings of preterm birth from a clinical perspective into adulthood, or used a sibling comparison to demonstrate these differences. In this volume of The Journal, Kuula et al report deployment of MRI to assess brain abnormalities and volumetric differences in a cohort of adults born preterm at very low birth weight (VLBW), using siblings as controls. At mean age 29 years, the investigators found significantly more structural abnormalities in VLBW subjects than control siblings, 37% vs. 13%, with periventricular leukomalacia the most common finding. The VLBW group had smaller absolute brain volumes and, after adjusting for estimated intracranial volume, also larger ventricles, less gray matter, and smaller thalami, caudate nuclei, right hippocampus, and left pallidum. No differences in total white matter were detected. While other researchers have documented chronic white matter abnormalities in adults following prematurity, the chronic gray matter changes here are intriguing and require further study. Perhaps more notable is the persistence of sequelae far into adult life. Children with cerebral palsy and visual impairments were excluded from this study, but other neurodevelopmental differences in this population may be associated with these abnormalities. Children born premature are already known to be at increased risk of hypertension and chronic cardiovascular disease, chronic pulmonary disease, diabetes mellitus, and even premature death. The findings of Kuula et al underscore that prematurity is a chronic disease also affecting the central nervous system. There are no guidelines for the long-term medical follow-up of people born preterm. Meanwhile there are survivorship guidelines for prevalent yet less common conditions of childhood, such as cancer or liver transplantation. With about 10% of US births categorized as premature and over 1% VLBW, perhaps it is time give more attention to the investigation and management of chronic diseases in adulthood that arise from prematurity. Article page 48

Morphological basis of Parkinson disease-associated cognitive impairment: an update

Cognitive impairment is one of the most salient non-motor symptoms of Parkinson disease (PD) that poses a significant burden on the patients and carers as well as being a risk factor for early mortality. People with PD show a wide spectrum of cognitive dysfunctions ranging from subjective cognitive decline and mild cognitive impairment (MCI) to frank dementia. The mean frequency of PD with MCI (PD-MCI) is 25.8% and the pooled dementia frequency is 26.3% increasing up to 83% 20years after diagnosis. A better understanding of the underlying pathological processes will aid in directing disease-specific treatment. Modern neuroimaging studies revealed considerable changes in gray and white matter in PD patients with cognitive impairment, cortical atrophy, hypometabolism, dopamine/cholinergic or other neurotransmitter dysfunction and increased amyloid burden, but multiple mechanism are likely involved. Combined analysis of imaging and fluid markers is the most promising method for identifying PD-MCI and Parkinson disease dementia (PDD). Morphological substrates are a combination of Lewy- and Alzheimer-associated and other concomitant pathologies with aggregation of α-synuclein, amyloid, tau and other pathological proteins in cortical and subcortical regions causing destruction of essential neuronal networks. Significant pathological heterogeneity within PD-MCI reflects deficits in various cognitive domains. This review highlights the essential neuroimaging data and neuropathological changes in PD with cognitive impairment, the amount and topographical distribution of pathological protein aggregates and their pathophysiological relevance. Large-scale clinicopathological correlative studies are warranted to further elucidate the exact neuropathological correlates of cognitive impairment in PD and related synucleinopathies as a basis for early diagnosis and future disease-modifying therapies.

A fuzzy membership based comparison of the grey matter (GM) in cognitively normal (CN), mild cognitive impairment (MCI), and Alzheimer’s disease (AD) using brain images

Grey matter (GM) in human brain contains most of the important cells covering the regions involved in neurophysiological operations such as memory, emotions, decision making, etc. Alzheimer’s disease (AD) is a neurological disease that kills the brain cells in regions which are mostly involved in the neurophysiological operations. Mild Cognitive Impairment (MCI) is a stage between Cognitively Normal (CN) and AD, where a significant cognitive declination can be observed. The destruction of brain cells causes a reduction in the size of GM. Evaluation of changes in GM, may help in studying the overall brain transformations and accurate classification of different stages of AD. In this work, firstly skull of brain images is stripped for 5 different slices, then segmentation of GM is performed. Finally, the average number of pixels in grey region and the average atrophy in grey pixels per year is calculated and compared amongst CN, MCI, and AD patients of various ages and genders. It is observed that, for some subjects (in some particular ages) from different dementia stages, pattern of GM changes is almost identical. To solve this issue, we have used the concept of fuzzy membership functions to classify the dementia stages more accurately. It is observed from the comparison that average difference in the number of pixels between CN and MCI= 10.01%, CN and AD= 19.63%, MCI and AD= 10.72%. It can be also observed from the comparison that, the average atrophy in grey matter per year in CN= 1.92%, MCI= 3.13%, and AD= 4.33%.

Volumetric Assessment of Hippocampus and Subcortical Gray Matter Regions in Alzheimer Disease and Amnestic Mild Cognitive Impairment.

Quantitative MRI assessment methods have limited utility due to a lack of standardized methods and measures for Alzheimer disease (AD) and amnestic mild cognitive impairment (aMCI). To employ a relatively new and easy-to-use quantitative assessment method to reveal volumetric changes in subcortical gray matter (GM) regions, hippocampus, and global intracranial structures as well as the diagnostic performance and best thresholds of total hippocampal volumetry in individuals with AD and those with aMCI. A total of 74 individuals-37 with mild to moderate AD, 19 with aMCI, and 18 with normal cognition (NC)-underwent a 3T MRI. Fully automated segmentation and volumetric measurements were performed. The AD and aMCI groups had smaller volumes of amygdala, nucleus accumbens, and hippocampus compared with the NC group. These same two groups had significantly smaller total white matter volume than the NC group. The AD group had smaller total GM volume compared with the aMCI and NC groups. The thalamus in the AD group showed a subtle atrophy. There were no significant volumetric differences in the caudate nucleus, putamen, or globus pallidus between the groups. The amygdala and nucleus accumbens showed atrophy comparable to the hippocampal atrophy in both the AD and aMCI groups, which may contribute to cognitive impairment. Hippocampal volumetry is a reliable tool for differentiating between AD and NC groups but has substantially less power in differentiating between AD and aMCI groups. The loss of total GM volume differentiates AD from aMCI and NC.

Brain Structure in Acutely Underweight and Partially Weight-Restored Individuals With Anorexia Nervosa: A Coordinated Analysis by the ENIGMA Eating Disorders Working Group

BackgroundThe pattern of structural brain abnormalities in anorexia nervosa (AN) is still not well understood. While several studies report substantial deficits in gray matter volume and cortical thickness in acutely underweight patients, others find no differences, or even increases in patients compared with healthy control subjects. Recent weight regain before scanning may explain some of this heterogeneity. To clarify the extent, magnitude, and dependencies of gray matter changes in AN, we conducted a prospective, coordinated meta-analysis of multicenter neuroimaging data. MethodsWe analyzed T1-weighted structural magnetic resonance imaging scans assessed with standardized methods from 685 female patients with AN and 963 female healthy control subjects across 22 sites worldwide. In addition to a case-control comparison, we conducted a 3-group analysis comparing healthy control subjects with acutely underweight AN patients (n = 466) and partially weight-restored patients in treatment (n = 251). ResultsIn AN, reductions in cortical thickness, subcortical volumes, and, to a lesser extent, cortical surface area were sizable (Cohen’s d up to 0.95), widespread, and colocalized with hub regions. Highlighting the effects of undernutrition, these deficits were associated with lower body mass index in the AN sample and were less pronounced in partially weight-restored patients. ConclusionsThe effect sizes observed for cortical thickness deficits in acute AN are the largest of any psychiatric disorder investigated in the ENIGMA (Enhancing Neuro Imaging Genetics through Meta Analysis) Consortium to date. These results confirm the importance of considering weight loss and renutrition in biomedical research on AN and underscore the importance of treatment engagement to prevent potentially long-lasting structural brain changes in this population.

Multimodal Brain MRI of Deep Gray Matter Changes Associated With Inflammatory Bowel Disease.

Behavioral symptoms, including mood disorders, substantially impact the quality of life of patients with inflammatory bowel disease (IBD), even when clinical remission is achieved. Here, we used multimodal magnetic resonance imaging (MRI) to determine if IBD is associated with changes in the structure and function of deep gray matter brain regions that regulate and integrate emotional, cognitive, and stress responses. Thirty-five patients with ulcerative colitis (UC) or Crohn's disease (CD) and 32 healthy controls underwent 3 Tesla MRIs to assess volume, neural activity, functional connection strength (connectivity), inflammation, and neurodegeneration of key deep gray matter brain regions (thalamus, caudate, pallidum, putamen, amygdala, hippocampus, and hypothalamus) involved in emotional, cognitive and stress processing. Associations with sex, presence of pain, disease activity, and C-reactive protein (CRP) concentration were examined. Significantly increased activity and functional connectivity were observed in cognitive and emotional processing brain regions, including parts of the limbic system, basal ganglia, and hypothalamus of IBD patients compared with healthy controls. Inflammatory bowel disease patients exhibited significantly increased volumes of the amygdala and hypothalamus, as well as evidence of neurodegeneration in the putamen and pallidum. Hippocampal neural activity was increased in IBD patients with active disease. The volume of the thalamus was positively correlated with CRP concentration and was increased in females experiencing pain. Patients with IBD exhibit functional and structural changes in the limbic and striatal systems. These changes may be targets for assessing or predicting the response to therapeutic interventions aimed at improving comorbid emotional and cognitive symptoms.

Effects of Chronic Hypoxic Environment on Cognitive Function and Neuroimaging Measures in a High-Altitude Population.

ObjectiveThis study aimed to investigate the effects of long-term hypoxic environment exposure on cognitive ability and neuroimaging characteristics in a highland population in China.MethodsHealth system workers in Maduo County (4,300 m above sea level) and Minhe County (1,700 m above sea level) were selected as research participants and divided into a high-altitude (HA) group and low-altitude (LA) group, respectively. Cognitive ability was assessed using the Montreal Cognitive Assessment (MoCA), Verbal Fluency Test (VFT), Symbol Digit Modalities Test (SDMT), Trail Making Test A and B (TMT), Digit Span Test (DST), and Rey Auditory Verbal Learning Test (RAVLT). All participants underwent a magnetic resonance imaging (MRI) scan, resting state functional MRI scan, and diffusion tensor imaging to clarify changes in regional gray matter (GM) volume, anisotropy index (FA), local consistency (ReHo), and low-frequency oscillation amplitude (ALFF).ResultsThe HA group had significantly lower MoCA, DST, VFT, RAVLT, and TMT scores compared to the control group. No significant differences were found in SDMT score. Furthermore, compared to the LA group, the HA group had significantly lower GM density of the left olfactory cortex, right medial orbital superior frontal gyrus, bilateral insula, left globus pallidus, and temporal lobe (left superior temporal gyrus temporal pole, bilateral middle temporal gyrus temporal pole, and right middle temporal gyrus). In terms of FA, compared with the LA group, the HA group had lower values for the corpus callosum, corpus callosum knee, bilateral radiative corona, and left internal capsule. The HA group had lower ALFF values of the left cerebellum, left putamen, left orbital inferior frontal gyrus, and left precuneus, but higher ALFF values of the left fusiform gyrus, bilateral inferior temporal gyrus, left orbital superior frontal gyrus and medial superior frontal gyrus, compared to the LA group. There was no significant group difference in ReHo values.ConclusionOur findings suggest that a chronic hypoxic environment can induce extensive cognitive impairment. Decreased GM density in multiple brain regions, damaged nerve fibers, and unbalanced neuronal activity intensity in different brain regions may be the structural and functional basis of cognitive impairment due to hypoxia.