Gray Matter Structural Changes Research Articles

Gray matter volume of limbic brain structures during the development of chronic back pain: a longitudinal cohort study.

This study set out to investigate in a population-based longitudinal cohort, whether chronification of back pain (BP) is related to structural gray matter changes in corticolimbic brain structures. Gray matter volume (GMV) was measured in participants with chronic BP (CBP, n = 168) and controls without chronic pain (n = 323) at 2 time points with an interval of 7 years (baseline t1, follow-up t2). Over this time period, participants with CBP showed an increase of GMV in the left ventral striatum, whereas controls showed a decrease. By contrast, participants with CBP had a GMV decrease in the left parahippocampal gyrus. Within the CBP group, pain duration was negatively associated with GMV in the left caudate. Those with emerging CBP had less GMV in the right entorhinal area, right amygdala, and left medial frontal cortex. Additional variables differing between those who had BP at t1 and later developed CBP or not were pain intensity, body mass index, and depression score. In sum, these findings are in accordance with the notion that limbic brain properties are both predisposing risk factors and drivers of brain reorganization during the development of CBP.

Cortical and subcortical gray matter abnormalities in mild cognitive impairment

Gray matter changes are thought to be closely related to cognitive decline in mild cognitive impairment (MCI) patients. The study aimed to explore cortical and subcortical structural alterations in MCI and their association with cognitive assessment. 24 MCI patients and 22 normal controls (NCs) were included. Voxel-based morphometry (VBM), vertex-based shape analysis and surface-based morphometry (SBM) analysis were applied to explore subcortical nuclei volume, shape and cortical morphology. Correlations between structural changes and cognition were explored using spearman correlation analysis. Support vector machine (SVM) classification evaluated MCI identification accuracy. MCI patients showed significant atrophy in the left thalamus, left hippocampus, left amygdala, right pallidum, right hippocampus, along with inward deformation in the left amygdala. SBM analysis revealed that MCI group exhibited shallower sulci depth in the left hemisphere and increased cortical gyrification index (GI) in the right frontal gyrus. Correlation analysis showed the positive correlation between right hippocampus volume and episodic memory, while negative correlation between the altered GI and memory performance in MCI group. SVM analysis demonstrated superior performance of sulci depth and GI derived from SBM in MCI identification. When combined with cortical and subcortical metrics, SVM achieved a peak accuracy of 89 % in distinguishing MCI from NC. The study reveals significant gray matter structural changes in MCI, suggesting their potential role in underlying functional differences and neural mechanisms behind memory impairment in MCI.

Neuroprotective Effects of Inhaled Xenon Gas on Brain Structural Gray Matter Changes After Out-of-Hospital Cardiac Arrest Evaluated by Morphometric Analysis: A Substudy of the Randomized Xe-Hypotheca Trial.

We have earlier reported that inhaled xenon combined with hypothermia attenuates brain white matter injury in comatose survivors of out-of-hospital cardiac arrest (OHCA). A predefined secondary objective was to assess the effect of inhaled xenon on the structural changes in gray matter in comatose survivors after OHCA. Patients were randomly assigned to receive either inhaled xenon combined with target temperature management (33°C) for 24h (n = 55, xenon group) or target temperature management alone (n = 55, control group). A change of brain gray matter volume was assessed with a voxel-based morphometry evaluation of high-resolution structural brain magnetic resonance imaging (MRI) data with Statistical Parametric Mapping. Patients were scheduled to undergo the first MRI between 36 and 52h and a second MRI 10days after OHCA. Of the 110 randomly assigned patients in the Xe-Hypotheca trial, 66 patients completed both MRI scans. After all imaging-based exclusions, 21 patients in the control group and 24 patients in the xenon group had both scan 1 and scan 2 available for analyses with scans that fulfilled the quality criteria. Compared with the xenon group, the control group had a significant decrease in brain gray matter volume in several clusters in the second scan compared with the first. In a between-group analysis, significant reductions were found in the right amygdala/entorhinal cortex (p = 0.025), left amygdala (p = 0.043), left middle temporal gyrus (p = 0.042), left inferior temporal gyrus (p = 0.008), left parahippocampal gyrus (p = 0.042), left temporal pole (p = 0.042), and left cerebellar cortex (p = 0.005). In the remaining gray matter areas, there were no significant changes between the groups. In comatose survivors of OHCA, inhaled xenon combined with targeted temperature management preserved gray matter better than hypothermia alone. ClinicalTrials.gov: NCT00879892.

The interplay between white adipose tissue, adipokines, and structural gray matter changes

AbstractThe growing global obesity issue emphasizes the importance of understanding its health implications. Previous research has identified consistent alterations in gray matter (GM) volume in connection with obesity. Given the various implications of distinct fat compartments and the potential role of adipose tissue‐derived adipokines in brain health, a more detailed investigation of adiposity is required. This study investigates a sample of 65 males with varying body mass indices to explore the relationship between various fat compartments, adipokine levels, and volumetric GM variations, aiming to provide a deeper understanding of the interplay between adiposity, brain structure, and metabolic signals. Whole‐body magnetic resonance imaging (MRI) was used to assess total, visceral, and subcutaneous adipose tissue, while MR spectroscopy was performed to capture liver fat content. For the assessment of adipokine levels leptin and adiponectin concentrations were measured, and structural brain images underwent cortical and subcortical segmentation for GM volume and thickness. A predictive modeling approach with leave‐one‐out cross‐validation was used to predict body composition metrics and adipokine levels based on structural GM data. Our investigation revealed diminished GM volume and thickness correlated with elevated leptin levels in areas crucial for appetite regulation, decision‐making, and cognitive control, including the anterior insula, orbitofrontal cortex, and anterior cingulate cortex. These findings suggest a potential adverse impact of heightened leptin concentrations on brain health and eating habits. Contrary to expectations, our investigation found no significant relationship between GM volume and any of the measured fat compartments. This result prompts the need for further research to elucidate the relationship between obesity, adipokines, and brain structure.

Structural Neuroimaging and Molecular Signatures of Drug‐Naive Depression With Melancholic Features

Objectives: Melancholic depression (MD) is a common subtype of major depressive disorder (MDD). It is difficult to treat because its neurobiological basis is poorly understood. Therefore, to investigate whether MD patients have any structural changes in gray matter (GM) and the molecular foundation of these changes, we combined voxel‐based morphometry (VBM) analysis with neurotransmitter system‐derived mapping from public data.Methods: 137 drug‐naive MDD patients and 75 healthy controls (HCs) were recruited for structural magnetic resonance imaging. The imaging results were analyzed using VBM analysis. MDD patients were then divided into MD and nonmelancholic depression (NMD) subgroups according to their scores on the Montgomery–Asberg Depression Rating Scale (MADRS) and the Hamilton Depression Rating Scale. Next, we analyzed the spatial correlation between the changes in the gray matter volume (GMV) maps and the neurotransmitter receptor/transporter protein density maps provided by the JuSpace toolbox.Results: Compared to HCs, patients with MD had significant GMV reduction in the bilateral hippocampus, bilateral thalamus, right amygdala, and right posterior cingulate cortex (PCC)/precuneus. Compared to patients with NMD, MD patients had significant GMV reduction in the bilateral PCC/precuneus and lateral occipital cortex. Moreover, compared to HCs, changes in GMV introduced by MD were spatially associated with the serotonin transporter, cannabinoid receptor, and μ‐opioid receptor. Compared to NMD patients, changes in GMV introduced by MD were spatially associated with the vesicular acetylcholine transporter.Conclusion: The present study discovered abnormal GMV alterations in patients with subtypes of depression. We also found a series of neurotransmitter receptors that may be associated with the alterations. The findings of the current study may provide a more comprehensive understanding of the molecular mechanisms underlying the structural abnormalities in subtypes of depression and potentially offer new insights into developing new therapeutic strategies.

GRAY MATTER CORRELATES OF ANXIETY, DEPRESSION, AND GAIT SPEED IN OLDER ADULTS WITH CHRONIC PAIN

Abstract Chronic pain and its comorbidities, (e.g., anxiety, depression, slow gait speeds) are a widespread, disabling condition prevalent among older adults. Worse anxiety and depression have been associated with slower gait speeds in individuals with chronic pain, and each comorbidity has been associated with structural gray matter changes; however, results are inconclusive or limited. Further investigation into these relationships may provide insight into neural mechanisms through which anxiety and depression contribute to slow gait speeds in this population. Therefore, the aim of this study was to identify gray matter measures associated with anxiety, depression, and gait speed in older adults with chronic pain. Participants (n = 31) walked across a GAITRite mat to obtain gait speed, and completed the State-Trait Anxiety Inventory (STAI), Center for Epidemiologic Studies Depression Scale (CES-D), and a T1-weighted anatomical scan. STAI score (mean = 7, β = - 0.015, p = 0.010) and CES-D score (mean = 30, β = - 0.014, p = 0.016) were significantly associated with gait speed. CES-D score was associated with left cuneus gyrus (β = 0.017, p = 0.0002) and frontal inferior sulcus surface area (β = 0.019, p = 0.002). Gait speed was associated with right inferior temporal gyrus surface area (β = 0.436, p = 0.019). STAI score was not associated with any measure. In conclusion, anxiety and depression symptoms contribute to gait slowing in older adults with chronic pain but without clinical depression or anxiety. This relationship, however, is not reflected in each comorbidity’s structural neural correlates.

Structural gray matter changes in primary progressive aphasia variants

BACKGROUND: Primary progressive aphasia is a rare neurodegenerative disease with high clinical, genetic, and pathomorphological heterogeneity that greatly complicates its diagnosis. Voxel-based morphometry can be used to objectively assess structural gray matter changes and determine atrophy patterns in variants of primary progressive aphasia, which can improve the diagnosis and our understanding of its pathogenesis. AIMS: This study aimed to evaluate the patterns of atrophy in each of the primary progressive aphasia variants in comparison with the control group. MATERIALS AND METHODS: Patients diagnosed with one of the primary progressive aphasia variants, established in accordance with the current diagnostic criteria, were included in the main group. The control group consisted of healthy volunteers without any neurological symptoms or structural brain changes. All participants underwent brain magnetic resonance imaging. The obtained images were processed and used for voxel-based morphometry, which was performed by comparing the gray matter volume between each of the primary progressive aphasia variants and the control group. The study was adjusted for the sex, age, and intracranial volume of the participants. RESULTS: The study enrolled 25 patients with nonfluent, 11 with semantic, and 9 with logopenic variants of primary progressive aphasia, as well as 20 healthy volunteers. Voxel-based morphometry showed a specific atrophy pattern in each of the variants of primary progressive aphasia, with predominant involvement of the frontal and insular lobes in nonfluent, temporal lobe and hippocampus in semantic, and a more diffuse frontotemporal pattern in logopenic variants. CONCLUSIONS: The study revealed gray matter atrophy patterns specific to each variant of primary progressive aphasia. The obtained results mainly correspond to the clinical presentations of the disease. Moreover, some findings (e.g., absence of the posterior perisylvian atrophy and reduced motor cortex volume in the logopenic variant, atrophy of the orbitofrontal cortex and cerebellum in the nonfluent variant, and premotor cortex, precentral, and inferior frontal gyrus degeneration in the semantic variant) do not correlate with the usual understanding of primary progressive aphasia pathogenesis and require further study.

Abnormal grey matter structural changes in patients with end-stage kidney disease and mild cognitive impairment: correlations with clinical features

End-stage kidney disease and mild cognitive impairment (ESKD-MCI) affect the quality of life and long-term treatment outcomes of patients affected by these diseases. Clarifying the morphological changes from brain injuries in ESKD-MCI and their relationship with clinical features is helpful for the early identification and intervention of MCI before it progresses to irreversible dementia. This study gathered data from 23 patients with ESKD-MCI, 24 patients with ESKD and non-cognitive impairment (NCI), and 27 health controls (HCs). Structural magnetic resonance studies, cognitive assessments, and general clinical data were collected from all participants. Voxel-based morphometry analysis was performed to compare grey matter (GM) volume differences between the groups. The patients’ GM maps and clinical features were subjected to univariate regression to check for possible correlations. Patients with ESKD-MCI displayed significantly more impairments in multiple cognitive domains, including global cognition, visuospatial and executive function, and memory, compared to patients with ESKD-NCI. Using a more liberal threshold (P < 0.001, uncorrected), we found that compared to patients with ESKD-NCI, patients with ESKD-MCI exhibited clusters of regions with lower GM volumes, including the right hippocampus (HIP), parahippocampal gyrus (PHG), Rolandic operculum, and supramarginal gyrus. The volumes of the right HIP and PHG were negatively correlated with serum calcium levels. ESKD-MCI was associated with a subtle volume reduction of GM in several brain areas known to be involved in memory, language, and auditory information processing. We speculate that these slight morphometric impairments may be associated with disturbed calcium metabolism.

Pathway-specific polygenic scores for Alzheimer's disease are associated with changes in brain structure in younger and older adults.

Genome-wide association studies have identified multiple Alzheimer's disease risk loci with small effect sizes. Polygenic risk scores, which aggregate these variants, are associated with grey matter structural changes. However, genome-wide scores do not allow mechanistic interpretations. The present study explored associations between disease pathway-specific scores and grey matter structure in younger and older adults. Data from two separate population cohorts were used as follows: the Avon Longitudinal Study of Parents and Children, mean age 19.8, and UK Biobank, mean age 64.4 (combined n = 18 689). Alzheimer's polygenic risk scores were computed using the largest genome-wide association study of clinically assessed Alzheimer's to date. Relationships between subcortical volumes and cortical thickness, pathway-specific scores and genome-wide scores were examined. Increased pathway-specific scores were associated with reduced cortical thickness in both the younger and older cohorts. For example, the reverse cholesterol transport pathway score showed evidence of association with lower left middle temporal cortex thickness in the younger Avon participants (P = 0.034; beta = -0.013, CI -0.025, -0.001) and in the older UK Biobank participants (P = 0.019; beta = -0.003, CI -0.005, -4.56 × 10-4). Pathway scores were associated with smaller subcortical volumes, such as smaller hippocampal volume, in UK Biobank older adults. There was also evidence of positive association between subcortical volumes in Avon younger adults. For example, the tau protein-binding pathway score was negatively associated with left hippocampal volume in UK Biobank (P = 8.35 × 10-05; beta = -11.392, CI -17.066, -5.718) and positively associated with hippocampal volume in the Avon study (P = 0.040; beta = 51.952, CI 2.445, 101.460). The immune response score had a distinct pattern of association, being only associated with reduced thickness in the right posterior cingulate in older and younger adults (P = 0.011; beta = -0.003, CI -0.005, -0.001 in UK Biobank; P = 0.034; beta = -0.016, CI -0.031, -0.001 in the Avon study). The immune response score was associated with smaller subcortical volumes in the older adults, but not younger adults. The disease pathway scores showed greater evidence of association with imaging phenotypes than the genome-wide score. This suggests that pathway-specific polygenic methods may allow progress towards a mechanistic understanding of structural changes linked to polygenic risk in pre-clinical Alzheimer's disease. Pathway-specific profiling could further define pathophysiology in individuals, moving towards precision medicine in Alzheimer's disease.

Assessment of Gray Matter Microstructure and Synaptic Density in Alzheimer's Disease: A Multimodal Imaging Study With DTI and SV2A PET

Multimodal imaging techniques have furthered our understanding of how different aspects of Alzheimer's disease (AD) pathology relate to one another. Diffusion tensor imaging (DTI) measures such as mean diffusivity (MD) may be a surrogate measure of the changes in gray matter structure associated with AD. Positron emission tomography (PET) imaging of synaptic vesicle glycoprotein 2A (SV2A) has been used to quantify synaptic loss, which is the major pathological correlate of cognitive impairment in AD. In this study, we investigated the relationship between gray matter microstructure and synaptic density. DTI was used to measure MD and [11C]UCB-J PET to measure synaptic density in 33 amyloid-positive participants with AD and 17 amyloid-negative cognitively normal (CN) participants aged 50-83. Univariate regression analyses were used to assess the association between synaptic density and MD in both the AD and CN groups. Hippocampal MD was inversely associated with hippocampal synaptic density in participants with AD (r=-0.55, p <0.001, df=31) but not CN (r=0.13, p=0.62, df=15). Exploratory analyses across other regions known to be affected in AD suggested widespread inverse associations between synaptic density and MD in the AD group. In the setting of AD, an increase in gray matter MD is inversely associated with synaptic density. These co-occurring changes may suggest a link between synaptic loss and gray matter microstructural changes in AD. Imaging studies of gray matter microstructure and synaptic density may allow important insights into AD-related neuropathology.

Clinical Features, Brain-Structure Changes, and Cognitive Impairment in Basal Ganglia Infarcts: A Pilot Study.

Stroke has been considered to raise the risk of dementia in several studies, but the relationship between brain structural changes and poststroke cognitive impairment (PSCI) is unclear. In this study, 23 PSCI patients with basal ganglia infarcts after 2 weeks and 29 age-matched controls underwent magnetic resonance imaging measuring cortical thickness and volume changes, as well as neuropsychological tests. CI was derived from a performance score <1.5 standard deviations for normally distributed scores. We compared Z scores in different cognitive domains and cortical thickness and volumes in two groups. Multiple linear regressions were used to investigate the relationship between cortical thickness and volumes and neuropsychological tests. A majority of PSCI patients were in their 50s (55.19±8.52 years). PSCI patients exhibited significantly decreased Z scores in multiple domains, such as memory, language, visuomotor speed, and attention/executive function. The volumes of the middle posterior corpus callosum, middle anterior corpus callosum, and hippocampus in PSCI patients were markedly lower than controls. The thickness of the right inferior temporal cortex and insula were significantly smaller than controls. It found that the reduced right hippocampus was related to executive dysfunction. Hippocampus dysfunction may be involved in language impairment (p<0.05) in PSCI patients with basal ganglia infarcts. These findings demonstrated that brain structure changed after ischemic stroke, and different gray-matter structural changes could lead to specific cognitive decline in PSCI patients with basal ganglia infarcts. Atrophy of the right hippocampus potentially serves as an imaging marker of early executive function of PSCI.

The complex interplay of hypoxia and sleep disturbance in gray matter structure alterations in obstructive sleep apnea patients.

Obstructive Sleep Apnea (OSA) characteristically leads to nocturnal hypoxia and sleep disturbance. Despite clear evidence of OSA-induced cognitive impairments, the literature offers no consensus on the relationship between these pathophysiological processes and brain structure alterations in patients. This study leverages the robust technique of structural equation modeling to investigate how hypoxia and sleep disturbance exert differential effects on gray matter structures. Seventy-four Male participants were recruited to undergo overnight polysomnography and T1-weighted Magnetic Resonance Imaging. Four structural outcome parameters were extracted, namely, gray matter volume, cortical thickness, sulcal depth, and fractal dimension. Structural equation models were constructed with two latent variables (hypoxia, and sleep disturbance) and three covariates (age, body mass index, and education) to examine the association between gray matter structural changes in OSA and the two latent variables, hypoxia and sleep disturbance. The structural equation models revealed hypoxia-associated changes in diverse regions, most significantly in increased gray matter volume, cortical thickness and sulcal depth. In contrast, sleep disturbance. Was shown to be largely associated with reduce gray matter volume and sulcal depth. This study provides new evidence showing significant effects of OSA-induced hypoxia and sleep disturbance on gray matter volume and morphology in male patients with obstructive sleep apnea. It also demonstrates the utility of robust structural equation models in examining obstructive sleep apnea pathophysiology.

White and gray matter alterations in de novo PD patients: which matter most?

This paper aimed to identify white matter (WM) and gray matter (GM) abnormalities in a sample of early PD patients, and their correlations with motor and non-motor symptom severity. We enrolled 62 de novo PD patients and 31 healthy subjects. Disease severity and non-motor symptom burden were assessed by the Unified Parkinson's Disease Rating Scale part III and the Non-Motor Symptoms Scale, respectively. Cognitive performance was assessed using Montreal Cognitive Assessment and Frontal Assessment Battery. All subjects underwent a 3-Tesla MRI protocol. MRI analyses included tract-based spatial statistics, cortical thickness, and subcortical and cerebellar volumetry. In comparison to control subjects, PD patients exhibited lower fractional anisotropy and higher mean, axial, and radial diffusivity in most WM bundles, including corticospinal tracts, the internal and external capsule, the anterior and posterior thalamic radiations, the genu and body of the corpus callosum, cerebellar peduncles, and superior and inferior longitudinal and fronto-occipital fasciculi. Correlations between Montreal Cognitive Assessment scores and fractional anisotropy values in the right posterior thalamic radiation, left superior corona radiata, right inferior-fronto-occipital fasciculus, left inferior longitudinal fasciculus, bilateral anterior thalamic radiations, and bilateral superior longitudinal fasciculi were found. Smaller cerebellar volumes in early PD patients in the left and right crus I were also found. No GM changes were present in subcortical or cortical regions. The combined evaluation of WM and GM in the same patient sample demonstrates that WM microstructural abnormalities precede GM structural changes in early PD patients.

P 1 Grey matter atrophy in Amyotrophic Lateral Sclerosis correlates with quantitative disease progression

Background: There is a growing demand for the development and evaluation of biomarkers that allow the improvement of clinical disease management and trials in Amyotrophic Lateral Sclerosis (ALS). Ideal biomarkers should be able to represent individual disease covered, independent from disease aggressiveness. The D50 model provides distinct parameters of individual clinical disease progression and a framework within with to interpret any biomarker signal. Objectives: In this study we examined Magnetic Resonance Imaging (MRI)-derived measures of grey matter in correlation with D50 model parameters. Based on our previous work, we hypothesized that loss of cortical and subcortical structural integrity would correlate with disease covered, independent from disease aggressiveness (1,2). Methods: T1-MRI images of 72 healthy controls and 100 ALS patients from a 1.5 T scanner were analyzed using surface-based morphometry to obtain cortical thickness (CT) and region-of-interest based volumetric analyses of subcortical deep grey matter (DGM). Applying the D50 model, we conducted subgroup-analyses of patients, divided by a) Phase of disease covered at the time of MRI-scan and b) individual overall disease aggressiveness. Additionally, correlations between the grey matter measures and D50 model-derived parameters were examined in multiple regression analyses. Statistical significance was set at p < 0.001 for CT and p < 0.05 Holm-Bonferroni corrected for DGM. Results: Inter-group analyses revealed ALS-related cortical and subcortical grey matter atrophy compared to healthy controls. Comparison of patients in different Phases showed further decrease of grey matter along with disease progression. However, there were no differences of CT or DGM between patients with low and high disease aggressiveness. Regression analyses identified negative correlations between CT/DGM and individual disease covered. Discussion and Conclusions: We were able to reveal structural grey matter changes in ALS compared to healthy controls that worsen along with disease progression. Application of the D50 model identified robust correlations between the decrease of GM integrity and ALS-related functional disability, but not with disease aggressiveness. This indicates that CT and DGM analyses could be biomarkers representing individual disease covered independent from the overall speed of disease progression. Our findings demonstrate the applicability of structural MRI as a biomarker in ALS.

Structural gray matter differences in Problematic Usage of the Internet: a systematic review and meta-analysis

Problematic Usage of the Internet (PUI) has been linked to diverse structural gray matter changes in individual data studies. However, no quantitative synthesis across studies has been conducted. We aimed to identify gray matter regions showing significant spatial convergence across neuroimaging studies in PUI. We searched PubMed and PsycINFO up to 10/03/2021 and included original, cross-sectional comparative studies that examined structural gray matter imaging in PUI versus control groups; reported a whole-brain analysis; and provided peak coordinates for gray matter differences. From a total of 624 potentially relevant studies, 15 (including 355 individuals with PUI and 363 controls) were included in a meta-analysis of voxel-based morphometry studies. Anatomical likelihood estimation (ALE) meta-analysis was performed using extracted coordinates and identified significant spatial convergence in the medial/superior frontal gyri, the left anterior cingulate cortex/cingulate gyrus, and the left middle frontal/precentral gyri. Datasets contributing to these findings all indicated reduced gray matter in cases compared to controls. In conclusion, voxel-based morphometric studies indicate replicable gray matter reductions in the dorsolateral prefrontal cortex and anterior cingulate cortex in PUI, regions implicated in reward processing and top-down inhibitory control. Further studies are required to understand the nature of gray matter differences across PUI behaviors, as well as the contribution of particular mental health disorders, and the influence of variation in study and sample characteristics.

Changes in brain morphometry after motor rehabilitation in chronic stroke

Purpose Recent studies have revealed structural changes after motor rehabilitation, but its morphological changes related to upper limb motor behaviours have not been studied exhaustively. Therefore, we aimed to map the grey matter (GM) changes associated with motor rehabilitation after stroke using voxel-based morphometry (VBM), deformation-based morphometry (DBM), and surface-based morphometry (SBM). Methods Forty-one patients with chronic stroke received twelve sessions of low-frequency repetitive transcranial magnetic stimulation plus intensive occupational therapy. MRI data were obtained before and after the intervention. Fugl-Meyer Assessment and Wolf Motor Function Test-Functional Ability Scale were assessed at the two-time points. We performed VBM, DBM, and SBM analyses using T1-weighted images. A correlation analysis was performed between cortical thickness in motor areas and clinical outcomes. Results Clinical outcomes significantly improved after the intervention. VBM showed significant GM volume changes in ipsilesional and contralesional primary motor regions. DBM results demonstrated GM changes contralesionally and ipsilesionally after the intervention. SBM results showed significant cortical thickness changes in posterior visuomotor coordination, precentral, postcentral gyri of the ipsilesional hemisphere and contralesional visuomotor area after the intervention. A combination of threshold p < .05, False Discovery Rate and p < .001 (uncorrected) were considered significant. In addition, cortical thickness changes of the ipsilesional motor areas were significantly correlated with the clinical outcome changes. Conclusions We found GM structural changes in areas involved in motor, visuomotor and somatosensory functions after the intervention. Furthermore, our findings suggest that structural plasticity changes in chronic stroke could occur in the ipsilesional and contralesional hemispheres after motor rehabilitation.

Progressive Neurodegeneration Across Chronic Stages of Severe Traumatic Brain Injury.

To examine the trajectory of structural gray matter changes across 2 chronic periods of recovery in individuals who have sustained severe traumatic brain injury (TBI), adding to the growing literature indicating that neurodegenerative processes occur in the months to years postinjury. Patients who experienced posttraumatic amnesia of 1 hour or more, and/or scored 12 or less on the Glasgow Coma Scale at the emergency department or the scene of the accident, and/or had positive brain imaging findings were recruited while receiving inpatient care, resulting in 51 patients with severe TBI. Secondary analyses of gray matter changes across approximately 5 months, 1 year, and 2.5 years postinjury were undertaken, using an automated segmentation protocol with improved accuracy in populations with morphological anomalies. We compared patients and matched controls on regions implicated in poorer long-term clinical outcome (accumbens, amygdala, brainstem, hippocampus, thalamus). To model brain-wide patterns of change, we then conducted an exploratory principal component analysis (PCA) on the linear slopes of all regional volumes across the 3 time points. Finally, we assessed nonlinear trends across earlier (5 months-1 year) versus later (1-2.5 years) time-windows with PCA to compare degeneration rates across time. Chronic degeneration was predicted cortically and subcortically brain-wide, and within specific regions of interest. (1) From 5 months to 1 year, patients showed significant degeneration in the accumbens, and marginal degeneration in the amygdala, brainstem, thalamus, and the left hippocampus when examined unilaterally, compared with controls. (2) PCA components representing subcortical and temporal regions, and regions from the basal ganglia, significantly differed from controls in the first time-window. (3) Progression occurred at the same rate across both time-windows, suggesting neither escalation nor attenuation of degeneration across time. Localized yet progressive decline emphasizes the necessity of developing interventions to offset degeneration and improve long-term functioning.

Exploring Cortical Thickness Alteration in Parkinson Disease Patients with Freezing of Gaits

Background: Freezing of gait (FoG) is a disabling gait disorder that commonly occurs in advanced stages of Parkinson's disease (PD). The neuroanatomical mechanisms underlying FoG in PD are still unclear. The present study aims to explore alterations of structural gray matter (GM) in PD patients with FoG. Method: Twenty-four PD patients with FoG (FoG+), 37 PD patients without FoG (FoG-) and 24 healthy controls (HC) were included. All subjects underwent a standardized MRI protocol. The cortical thickness (CTh), segmentation volume without ventricles (BrainSegVolNotVent) and estimated total intracranial volume (eTIV) were analysed using the FreeSurfer pipeline. Results: CTh differences were found in the right middle temporal gyrus (rMTG) generally. Compared to that in HCs, the CTh of the rMTG in both the FoG+ and FoG- groups was smaller, while no significant difference between the FoG+ and FoG- groups. Correlation analyses demonstrated a negative correlation between the CTh of the rMTG and the UPDRS part II score in PD subjects, and a borderline significant correlation between the score of Freezing of Gait Questionnaire (FoGQ) and rMTG CTh. Additionally, receiver operating characteristic curve (ROC) analysis revealed a cut-off point of CTh =3.08 mm in the rMTG that could be used to differentiate PD patients and HCs (AUC =0.79, P <0.01). There were no differences in the BrainSegVolNotVent or eTIV among the 3 groups. Conclusions: Our findings currently suggest no significant difference between FoG+ and FoG- patients in terms of structural gray matter changes. However, decreased CTh in the rMTG related to semantic control may be used as a biomarker to differentiate PD patients and HCs.

Multimodal structural neuroimaging markers of risk and recovery from posttrauma anhedonia: A prospective investigation.

Anhedonic symptoms of posttraumatic stress disorder (PTSD) reflect deficits in reward processing that have significant functional consequences. Although recent evidence suggests that disrupted integrity of fronto-limbic circuitry is related to PTSD development, including anhedonic PTSD symptoms (posttrauma anhedonia [PTA]), little is known about potential structural biomarkers of long-term PTA as well as structural changes in fronto-limbic pathways associated with recovery from PTA over time. We investigated associations between white matter microstructure, gray matter volume, and PTA in 75 recently traumatized individuals, with a subset of participants (n = 35) completing follow-up assessment 12 months after trauma exposure. Deterministic tractography and voxel-based morphometry were used to assess changes in white and gray matter structure associated with changes in PTA. Reduced fractional anisotropy (FA) of the uncinate fasciculus at around the time of trauma predicted greater PTA at 12-months posttrauma. Further, increased FA of the fornix over time was associated with lower PTA between 1 and 12-months posttrauma. Increased gray matter volume of the ventromedial prefrontal cortex and precuneus over time was also associated with reduced PTA. The microstructure of the uncinate fasciculus, an amygdala-prefrontal white matter connection, may represent a biomarker of vulnerability for later PTA. Conversely, development and recovery from PTA appear to be facilitated by white and gray matter structural changes in a major hippocampal pathway, the fornix. The present findings shed new light on neuroanatomical substrates of recovery from PTA and characterize white matter biomarkers of risk for posttraumatic dysfunction.

Grey matter volume and structural covariance associated with schizotypy

In this study, we applied brain grey matter volume and structural covariance methods on T1 weighted images to delineate potential structural brain changes in individuals with high schizotypy, who were defined as healthy individuals scoring in the top tenth percentile of the Schizotypal Personality Questionnaire (SPQ). Eighty-seven college students with high schizotypy and 122 controls were recruited in China. Differences in grey matter volume and volume covariance between the two groups, and correlations of grey matter volume with SPQ scores in the high schizotypy group were examined. We found that individuals with high schizotypy had decreased grey matter volume at the left medial superior frontal gyrus (medsFG) extending towards the superior frontal gyrus, decreased structural covariance within the right medsFG, between the right superior frontal gyrus (sFG), the right superior temporal gyrus and the right anterior insula; and increased structural covariance between the caudate and the right inferior temporal gyrus. Correlation analysis revealed that grey matter volume of the left middle temporal pole and the right sFG correlated positively with the SPQ total scores, volume of the bilateral cerebellum 9 sub-region correlated negatively with the SPQ cognitive-perceptual sub-scale scores, volume of the bilateral striatum correlated positively with the SPQ interpersonal sub-scale scores, and volume of the bilateral superior temporal pole correlated positively with the SPQ disorganization sub-scale scores in the high schizotypy group. These results highlight important grey matter structural changes in the medsFG in individuals with high schizotypy.