Differences In Cortical Thickness Research Articles

Orbitofrontal and Cingulate Thickness Asymmetry Associated with Depressive Symptom Dimensions.

Both clinical depression and subthreshold depressive symptoms have been associated with alterations in cortical thickness. Studies have yielded conflicting results regarding whether cortical thinning or cortical thickening best characterize the depressive state. Also unclear is whether cortical thickness differences are lateralized. This study examined the relationship between depressive symptom dimensions and cortical thickness asymmetry in cingulate and orbitofrontal regions. Fifty-four community-dwelling adults between the ages of 18 and 81 years received a 3-Tesla magnetic resonance imaging scan and completed the Center for Epidemiologic Studies Depression Scale (CES-D). Cortical thickness values were extracted for the rostral anterior cingulate, caudal anterior cingulate, posterior cingulate, isthmus cingulate, and orbitofrontal cortex. An asymmetry index was calculated for each region. Data were analyzed using separate general linear models for each region, in which the CES-D somatic symptoms, negative affect, and anhedonia subscale scores predicted the asymmetry indices, controlling for age and sex. Higher scores on the anhedonia subscale were associated with right-sided asymmetry in orbitofrontal thickness, whereas higher somatic symptom subscale scores predicted greater left-sided asymmetry in posterior cingulate thickness. Follow-up analyses showed the orbitofrontal effect was specific to the medial, not the lateral, orbitofrontal cortex. These results suggest asymmetries in cortical thickness are apparent at even subthreshold levels of depressive symptoms, as all but five participants were below the CES-D cutoff for clinical depression, and that the relationship varies for different symptom dimensions of depression. Understanding brain asymmetries across the range of depressive symptom severity is important for informing targeted depression treatment.

Structural volume and cortical thickness differences between males and females in cognitively normal, cognitively impaired and Alzheimer’s dementia population

We investigated differences due to sex in brain structural volume and cortical thickness in older cognitively normal (N=742), cognitively impaired (MCI; N=540) and Alzheimer’s Dementia (AD; N=402) individuals from the ADNI and AIBL datasets (861 Males and 823 Females). General linear models were used to control the effect of relevant covariates including age, intracranial volume, magnetic resonance imaging (MRI) scanner field strength and scanner types. Significant volumetric differences due to sex were observed within different cortical and subcortical regions of the cognitively normal group. The number of significantly different regions was reduced in the MCI group, and no region remained different in the AD group. Cortical thickness was overall thinner in males than females in the cognitively normal group, and likewise, the differences due to sex were reduced in the MCI and AD groups. These findings were sustained after including cerebrospinal fluid (CSF) Tau and phosphorylated tau (pTau) as additional covariates.

Subcortical brain volume and cortical thickness in adolescent girls and women with binge eating.

Alterations in brain structure have been implicated in the onset and acute phases of several forms of psychopathology. However, there is a dearth of research investigating brain structure in persons with binge eating, contributing to poor understanding of mechanisms associated with binge eating. Adolescent girls and women (aged 14-35 years) with binge eating (n=56) and group age-matched girls and women without binge eating (n=26) completed structural magnetic resonance imaging (MRI) scans and interview-based and self-report assessments of eating disorder and general psychopathology. MRI data were processed using FreeSurfer. Analysis of covariance tested mean differences in subcortical volume and cortical thickness of a priori selected regions of interest between binge-eating and non-binge-eating groups, controlling for age, body mass index, purging frequency, depression, and medication use. Exploratory partial correlations tested associations between brain structure and eating disorder symptoms within participants with binge eating. We did not observe differences in regional subcortical volume and cortical thickness between girls and women with and without binge eating. Within participants with binge eating, severity of attitudinal eating disorder symptoms was inversely associated with caudal middle frontal gyrus, right precentral gyrus, right postcentral gyrus, superior parietal, left inferior parietal thickness, and left accumbens volume; however, these associations would not survive multiple-comparison corrections. Correlations between attitudinal eating disorder symptoms and frontoparietal thinning may represent a state marker of binge eating. Future research could investigate whether frontoparietal thinning worsens with illness duration or persists beyond binge eating cessation.

Association between cortical thickness and distinct vascular cognitive impairment and dementia in patients with white matter lesions.

What is the central question of this study? White matter lesions (WMLs) are a brain disease characterized by altered brain structural and functional connectivity, but findings have shown an inconsistent pattern: are there distinct cortical thickness changes in patients with WMLs subtypes? What is the main finding and its importance? Patients with WMLs with non-dementia vascular cognitive impairment and WMLs with vascular dementia showed distinct pathophysiology in cortical thickness. These neural correlates of WMLs should be considered in future treatment. The effect of cortical thickness on white matter lesions (WMLs) in patients with distinct vascular cognitive impairments is relatively unknown. This study investigated the correlation between cortical thickness and vascular cognitive manifestations. WML patients and healthy controls from Beijing Tiantan Hospital between 2014 and 2018 were included. The patients were further divided into two subgroups, namely WMLs with non-dementia vascular cognitive impairment (WML-VCIND) and WMLs with vascular dementia (WML-VaD) according to the Clinical Dementia Rating (CDR) scale and the Beijing version of the Montreal Cognitive Assessment (MoCA). Changes in cortical thickness were calculated using FreeSurfer. Pearson's correlation analysis was performed to explore the relationship between cognitive manifestations and cortical thickness in WML patients. Forty-five WML patients and 23 healthy controls were recruited. The WML group exhibited significant difference in cortical thickness compared to the control group. Significantly decreased cortical thickness in the middle and superior frontal gyri, middle temporal gyrus, angular gyrus and insula was found in the WML-VaD versus WML-VCIND subgroup. Cortical thickness deficits of the left caudal middle frontal gyrus (r=0.451, P=0.002), left rostral middle frontal gyrus (r=0.514, P<0.001), left superior frontal gyrus (r=0.410, P=0.006), right middle temporal gyrus (r=0.440, P=0.003), right pars triangularis (r=0.462, P=0.002), right superior frontal gyrus (r=0.434, P=0.004) and right insula (r=0.499, P=0.001) were positively correlated with the MoCA score in WML patients. The specific pattern of cortical thickness deficits in the WML-VaD subgroup revealed the pathophysiology of WMLs, which should be considered in future treatment of WMLs.

Cortical Thickness Estimation: A Comparison of FreeSurfer and Three Voxel-Based Methods in a Test-Retest Analysis and a Clinical Application.

The cortical thickness has been used as a biomarker to assess different cerebral conditions and to detect alterations in the cortical mantle. In this work, we compare methods from the FreeSurfer software, the Computational Anatomy Toolbox (CAT12), a Laplacian approach and a new method here proposed, based on the Euclidean Distance Transform (EDT), and its corresponding computational phantom designed to validate the calculation algorithm. At region of interest (ROI) level, within- and inter-method comparisons were carried out with a test-retest analysis, in a subset comprising 21 healthy subjects taken from the Multi-Modal MRI Reproducibility Resource (MMRR) dataset. From the Minimal Interval Resonance Imaging in Alzheimer's Disease (MIRIAD) data, classification methods were compared in their performance to detect cortical thickness differences between 23 healthy controls (HC) and 45 subjects with Alzheimer's disease (AD). The validation of the proposed EDT-based method showed a more accurate and precise distance measurement as voxel resolution increased. For the within-method comparisons, mean test-retest measures (percentages differences/intraclass correlation/Pearson correlation) were similar for FreeSurfer (1.80%/0.90/0.95), CAT12 (1.91%/0.83/0.91), Laplacian (1.27%/0.89/0.95) and EDT (2.20%/0.88/0.94). Inter-method correlations showed moderate to strong values (R > 0.77) and, in the AD comparison study, all methods were able to detect cortical alterations between groups. Surface- and voxel-based methods have advantages and drawbacks regarding computational demands and measurement precision, while thickness definition was mainly associated to the cortical thickness absolute differences among methods. However, for each method, measurements were reliable, followed similar trends along the cortex and allowed detection of cortical atrophies between HC and patients with AD.

Posterior Cortical Cognitive Deficits Are Associated With Structural Brain Alterations in Mild Cognitive Impairment in Parkinson's Disease.

Context: Cognitive impairments are common in patients with Parkinson’s disease (PD) and are heterogeneous in their presentation. The “dual syndrome hypothesis” suggests the existence of two distinct subtypes of mild cognitive impairment (MCI) in PD: a frontostriatal subtype with predominant attentional and/or executive deficits and a posterior cortical subtype with predominant visuospatial, memory, and/or language deficits. The latter subtype has been associated with a higher risk of developing dementia.Objective: The objective of this study was to identify structural modifications in cortical and subcortical regions associated with each PD-MCI subtype.Methods: One-hundred and fourteen non-demented PD patients underwent a comprehensive neuropsychological assessment as well as a 3T magnetic resonance imaging scan. Patients were categorized as having no cognitive impairment (n = 41) or as having a frontostriatal (n = 16), posterior cortical (n = 25), or a mixed (n = 32) MCI subtype. Cortical regions were analyzed using a surface-based Cortical thickness (CTh) method. In addition, the volumes, shapes, and textures of the caudate nuclei, hippocampi, and thalami were studied. Tractometric analyses were performed on associative and commissural white matter (WM) tracts.Results: There were no between-group differences in volumetric measurements and cortical thickness. Shape analyses revealed more abundant and more extensive deformations fields in the caudate nuclei, hippocampi, and thalami in patients with posterior cortical deficits compared to patients with no cognitive impairment. Decreased fractional anisotropy (FA) and increased mean diffusivity (MD) were also observed in the superior longitudinal fascicle, the inferior fronto-occipital fascicle, the striato-parietal tract, and the anterior and posterior commissural tracts. Texture analyses showed a significant difference in the right hippocampus of patients with a mixed MCI subtype.Conclusion: PD-MCI patients with posterior cortical deficits have more abundant and more extensive structural alterations independently of age, disease duration, and severity, which may explain why they have an increased risk of dementia.

Sex differences in Brain Structure in individuals with knee osteoarthritis pain.

There is evidence of sex differences in the prevalence of chronic musculoskeletal pain as well as in experimental pain sensitivity. However, the neurobiological mechanisms contributing to these sex differences are poorly understood, especially with respect to brain structure. The aim of the present study is to examine sex differences in brain structure in persons with knee osteoarthritis (KOA) pain. Participants (mean age=58 years) with KOA pain (n=146, 65% female) completed demographic, self-reported and experimental pain assessments including temporal summation and conditioned pain modulation along with a 3T high-resolution, T1-weighted anatomical scan at 2 study sites in the US. FreeSurfer software (v.7.1.0, http://surfer.nmr.mgh.harvard.edu ) was used to examine sex differences in gray matter volume and cortical thickness as well as associations with experimental variables. Maps were set at a vertex-wise threshold of P 0.05). The results suggest that brain morphological differences between females and men with KOA pain are associated with distinct pain modulatory measures in men, but not in women. Future studies are needed to characterize potential neurobiological mechanisms underlying endogenous pain modulatory capacity across the sexes to further understand the individualized pain experience. R01AG059809, R01AG067757.

Differences in Cortical Thickness Associated With Apathy in Cognitively Impaired Persons

Apathy increases the risk of developing dementia, is prevalent among cognitively impaired (CI) older adults, and is associated with worse outcomes. It is also associated with deficits in frontostriatal circuits and frontotemporal association areas. However, the specific brain regions that mediate apathy remain unclear given concomitant neurodegenerative processes involved in dementias.

The association between latent trauma and brain structure in children

The developing brain is marked by high plasticity, which can lead to vulnerability to early life stressors. Previous studies indicate that childhood maltreatment is associated with structural aberrations across a number of brain regions. However, prior work is limited by small sample sizes, heterogeneous age groups, the examination of one structure in isolation, the confounding of different types of early life stressors, and not accounting for socioeconomic status. These limitations may contribute to high variability across studies. The present study aimed to investigate how trauma is specifically associated with cortical thickness and gray matter volume (GMV) differences by leveraging a large sample of children (N = 9270) from the Adolescent Brain Cognitive DevelopmentSM Study (ABCD Study®). A latent measure of trauma exposure was derived from DSM-5 traumatic events, and we related this measure of trauma to the brain using structural equation modeling. Trauma exposure was associated with thinner cortices in the bilateral superior frontal gyri and right caudal middle frontal gyrus (pfdr-values < .001) as well as thicker cortices in the left isthmus cingulate and posterior cingulate (pfdr-values ≤ .027), after controlling age, sex, and race/ethnicity. Furthermore, trauma exposure was associated with smaller GMV in the right amygdala and right putamen (pfdr-values ≤ .048). Sensitivity analyses that controlled for income and parental education were largely consistent with the main findings for cortical thickness. These results suggest that trauma may be an important risk factor for structural aberrations, specifically for cortical thickness differences in frontal and cingulate regions in children.

Strain-specific alterations in the skeletal response to adenine-induced chronic kidney disease are associated with differences in parathyroid hormone levels.

Female C57BL/6J (B6) and C3H/Hej (C3H) at 16-weeks of age were given a diet with 0.2% adenine to induce CKD for 6weeks followed by a control diet for 4weeks. Age- and strain-matched controls were fed the control diet without adenine for the 10-week period (n=8 per group per strain). Both strains of adenine-fed mice had elevated blood urea nitrogen, demonstrating compromised kidney function, compared to strain-matched controls, but only B6 adenine mice had statistically higher parathyroid hormone (PTH), greater cortical porosity, high bone turnover rate, a greater percentage of osteocytes positive for RANKL and IL-17, and lower osteocyte apoptosis compared to B6 controls. C3H mice had intracortical remodeling present in both control and adenine mice, while B6 mice had intracortical remodeling present only in adenine mice. Adenine mice of both strains had lower cortical thickness and a higher percentage of osteocytes positive for TNF-α compared to controls. While both strains of mice had biochemical markers of kidney disease, only B6 mice developed a phenotype with significantly elevated PTH, high bone turnover, and cortical porosity development. This work, in a model of progressive CKD, further confirms the role of chronically elevated PTH in the development of cortical porosity and demonstrates adenine-induced increases in PTH contribute to intracortical remodeling in B6 mice. Adenine-induced changes that occurred in both strains of mice, notably lower cortical thickness and a higher percentage of osteocytes expressing TNF-α, indicate potential PTH-independent responses to CKD.

A pilot study comparing daily teriparatide with monthly cycles of teriparatide and raloxifene.

There is no cure for osteoporosis; better medications or different approaches with current agents are needed. We hypothesized that monthly cycles of teriparatide (TPD) followed by raloxifene (RLX) might promote ongoing bone formation. Additionally, as TPD might initially adversely affect hip BMD, such effects may be mitigated by a cyclic approach. Therefore, this 6-month pilot study evaluated the effect of cyclic TPD/RLX compared to daily subcutaneous TPD on bone markers, BMD, trabecular bone score (TBS), and hip parameters assessed by 3D modeling. Postmenopausal osteoporotic women (n=26) were randomized to open-label TPD 20 daily or alternating monthly cycles of TPD followed by monthly RLX 60 mg daily. BMD was measured at the lumbar spine (LS), femur, and radius by DXA. To further assess LS BMD, QCT and opportunistic CT (L1 Hounsfield units [HU]) were performed. LS TBS and hip cortical and trabecular parameters were assessed using DXA. Baseline group comparisons were performed by unpaired T-test with change over time evaluated by repeated measures ANOVA. Participant mean age, BMI, and lowest T-score were 67.0 years, 26.0 kg/m2, and -2.7; no between-group differences in serum chemistries, 25(OH)D, or BMD were observed. LS-BMD increased (p<0.001) with TPD or TPD/RLX as measured by DXA (4.8%/5.2%), QCT (13%/9.4%), or HU (15.6%/10.2%) with no between-group difference. TPD/RLX produced beneficial between-group differences in total proximal femur BMD (1.5%, p<0.05) and cortical thickness (1.6%, p<0.05). Compared with daily TPD, cyclic TPD/RLX comparably increased spine BMD and might have favorable effects on proximal femur BMD and cortical thickness.

Cortical Thickness Changes in Chronic Ketamine Users.

Background: Previous studies have examined the effects of long-term ketamine use on gray matter volume. But it is unclear whether chronic ketamine use alters cortical thickness and whether cortical thickness changes in chronic ketamine users are associated with cognitive deficits observed in chronic ketamine users.Methods: Here, 28 chronic ketamine users and 30 healthy controls (HCs) were recruited. Cortical morphometry based on Computational Anatomy Toolbox (CAT12) was used to measure cortical thickness. Cognitive performance was measured by MATRICS Consensus Cognitive Battery (MCCB). Two-sample t-test was used to assess differences in cortical thickness and cognitive performance between the two groups. Partial correlation analysis was used for assessing correlations between cortical thickness changes and clinical characteristics, cognitive performance in chronic ketamine users.Results: Chronic ketamine users exhibited significantly reduced cortical thickness in frontal, parietal, temporal, and occipital lobes compared to HC [false discovery rate (FDR) corrected at p < 0.05]. In chronic ketamine users, the average quantity (g) of ketamine use/day was negatively correlated with cortical thickness in the left superior frontal gyrus (SFG), right caudal middle frontal gyrus (MFG), and right paracentral lobule. The frequency of ketamine use (days per week) was negatively correlated with cortical thickness in the left isthmus cingulate cortex. Duration of ketamine use (month) was negatively correlated with cortical thickness in the left precentral gyrus. The chronic ketamine users showed significantly poorer cognitive performance on the working memory (P = 0.009), visual learning (P = 0.009), speed of processing (P < 0.000), and Matrics composite (P = 0.01). There was no correlation between scores of domains of MCCB and reduced cortical thickness.Conclusion: The present study observed reduced cortical thickness in multiple brain areas, especially in the prefrontal cortex (PFC) in chronic ketamine users. Dose, frequency, and duration of ketamine use was negatively correlated with cortical thickness of some brain areas. Our results suggest that chronic ketamine use may lead to a decrease of cortical thickness. But the present study did not observe any correlation between reduced cortical thickness and decreased cognitive performance in chronic ketamine users.

Cortical Thickness Alterations in Patients With Tinnitus Before and After Sound Therapy: A Surface-Based Morphometry Study.

This study aimed to explore brain surface-based morphometry cortical thickness changes in patients with idiopathic tinnitus before and after 24 weeks of sound therapy. In this prospective observational study, we recruited 33 tinnitus patients who had undergone 24 weeks of sound therapy and 26 matched healthy controls. For the two groups of subjects, a 3D-BRAVO pulse sequence was acquired both at baseline and at the 24th week. Structural image data preprocessing was performed using the DPABISurf toolbox. The Tinnitus Handicap Inventory (THI) score was assessed to determine the severity of tinnitus before and after treatment. Two-way mixed-model analysis of variance (ANOVA) and Pearson’s correlation analysis were used in the statistical analysis. Student–Newman–Keuls (SNK) tests were used in the post hoc analysis. Significantly lower cortical thickness was found in the left somatosensory and motor cortex (SMC), left posterior cingulate cortex (PCC), and right orbital and polar frontal cortex (OPFC) of the participants in the tinnitus group at baseline than in the participants in the HC group at baseline and after 24 weeks; in the tinnitus group, significantly higher cortical thickness was found after the 24 weeks sound therapy in comparison to the baseline in the left SMC, bilateral superior parietal cortex (SPC), left inferior parietal cortex (IPC), left PCC, and right OPFC. In the HC group, no statistically significant difference in cortical thickness was found after the 24 weeks treatment in comparison to the baseline in the bilateral SMC, bilateral SPC, left IPC, left PCC, or right OPFC. The changes in cortical thickness before and after sound therapy can provide certain reference values for clinical tinnitus treatment. These brain regions could serve as potential targets for neuroimaging.

Neurodevelopmental origins of self-limiting rolandic epilepsy: Systematic review of MR imaging studies.

ObjectiveRecent neuroimaging studies have revealed differences in cortical and white matter brain structure in children with self‐limiting rolandic epilepsy (RE). Despite this, reproducibility of the findings has been difficult, and there is no consensus about where and when structural differences are most apparent. We performed a systematic review of quantitative neuroimaging studies in children with RE to explore these questions.MethodsUsing PRISMA guidelines, we used a multilayered search strategy to identify neuroimaging studies in RE. Publications were included if they were quantitative and derived from controlled group studies and passed a quality assessment. Findings of the studies were presented and stratified by duration of epilepsy and age of participants.ResultsWe identified six gray matter studies and five white matter studies. Consistent findings were found inside and outside the central sulcus, predominantly within the bilateral frontal and parietal lobes, striatal structures, such as the putamen and white matter, mainly involving the left superior longitudinal fasciculus and connections between the left pre‐ and postcentral gyrus. Stratification of the T1 studies by age found that cortical thickness differences varied between the under and over 10 year olds. Furthermore, the longer the duration of epilepsy, the less likely differences were detected. In white matter studies, there was a reduction in differences with increased age and duration of epilepsy.SignificanceThese findings would suggest that the development of regions of the cortex in children with RE is abnormal. These regions are more widespread than the suspected seizure onset zone. Moreover, the findings would suggest that these differences are evidence of neurodevelopmental delay rather than apparent “damage” from the epilepsy.

Abstract 54: Bilateral Developmental Alterations in Cortical Morphology in Children With Perinatal Stroke

Perinatal stroke (PS) causes hemiparetic cerebral palsy (CP) and lifelong disability. Compensatory changes in the nonlesioned hemisphere may mediate residual function and represent targets for neuromodulation. Region-based approaches may reveal relationships between cortical thickness of nonlesioned primary motor/sensory cortices and motor function. This study uses surface-based morphometry to explore cortical alterations in the nonlesioned hemisphere in children after perinatal stroke. Children aged 6-19 with MRI-confirmed unilateral perinatal stroke and CP underwent T1-weighted anatomical imaging. Participants were classified as arterial ischemic stroke (AIS; n=36), periventricular venous infarction (PVI; n=38), or typically developing controls (TDC; n=53). Group differences in cortical thickness (distance between grey/white matter boundary and pial surface), grey matter volume, gyrification and sulcal depth and relationships between these morphology metrics and validated measures of motor/executive function were explored. Group comparisons revealed less cortical thickness, greater gyrification, and greater surface area in the nonlesioned hemisphere in both AIS and PVI as compared to TDC. Greater volume and sulcal depth were observed in the nonlesioned hemisphere for AIS. The PVI group showed greater volume in the cingulate cortex and less volume in the precuneus relative to TDC. The AIS group showed more widespread differences than the PVI group in volume and other cortical surface parameters when compared with TDC. Only modest correlations were observed between morphometric changes and clinical function. We suggest that broad differences in structural developmental plasticity occur in the nonlesioned hemisphere after perinatal stroke, particularly the larger lesions seen with AIS, and may represent novel targets for therapeutic neuromodulation.

Apolipoprotein E homozygous ε4 allele status: Effects on cortical structure and white matter integrity in a young to mid-age sample

Apolipoprotein E (APOE) genotype is the strongest single gene predictor of Alzheimer's disease (AD) and has been frequently associated with AD-related brain structural alterations before the onset of dementia. While previous research has primarily focused on hippocampal morphometry in relation to APOE, sporadic recent findings have questioned the specificity of the hippocampus and instead suggested more global effects on the brain. With the present study we aimed to investigate associations between homozygous APOE ε4 status and cortical gray matter structure as well as white matter microstructure. In our study, we contrasted n = 31 homozygous APOE ε4 carriers (age=34.47 years, including a subsample of n = 12 subjects with depression) with a demographically matched sample without an ε4 allele (resulting total sample: N = 62). Morphometry analyses included a) Freesurfer based cortical segmentations of thickness and surface area measures and b) tract based spatial statistics of DTI measures. We found pronounced and widespread reductions in cortical surface area of ε4 homozygotes in 57 out of 68 cortical brain regions. In contrast, no differences in cortical thickness were observed. Furthermore, APOE ε4 homozygous carriers showed significantly lower fractional anisotropy in the corpus callosum, the right internal and external capsule, the left corona radiata and the right fornix. The present findings support a global rather than regionally specific effect of homozygous APOE ε4 allele status on cortical surface area and white matter microstructure. Future studies should aim to delineate the clinical implications of these findings.

Asymmetry in Cortical and Subcortical Structures of the Brain in Children and Adolescents with Attention-Deficit/Hyperactivity Disorder.

BackgroundHuman cognitive and emotional functions are asymmetrical between the left and right hemispheres. In neuroimaging studies of attention-deficit/hyperactivity disorder (ADHD) patients, the absence of aberrant asymmetry might serve as a neuroanatomical marker of ADHD. However, few studies have estimated abnormalities in cortical and subcortical asymmetry in children and adolescents of different ADHD subtypes.MethodsData were from the results collected by the Peking University site in the “ADHD-200 sample” dataset, which comprised 31 eligible ADHD (20 inattentive ADHD (ADHD-I), 11 combined ADHD (ADHD-C)) and 31 matched typically developing (TD) individuals. The Asymmetry Indexes (AIs) in cortical thickness, cortical gray-matter volume and subcortical nucleus (SN) volume were calculated based on an automated surface-based approach. The differences in cortical thickness, cortical gray-matter volume, and SN volume AIs were evaluated among groups. We also analyzed the correlation between AIs and the severity of ADHD symptoms.ResultsCompared with the TD group, SN asymmetry in ADHD group did not reveal significant differences. Altered cortical asymmetry of different subtypes in ADHD groups was located in the orbitofrontal and anterior cingulate circuits, including the medial orbitofrontal, paracentral, pars triangularis, caudal anterior cingulate, isthmus cingulate, and superior frontal regions. In the comparisons, cortical gray-matter volume AIs were significantly different in the caudal anterior cingulate, isthmus cingulate, and superior frontal regions between ADHD-I and ADHD-C groups. There were significant correlations between the severity of ADHD symptoms and asymmetric measurements in medial orbitofrontal, paracentral and isthmus cingulate regions.ConclusionThese findings provide further evidence for the altered cortical morphological asymmetry in children and adolescents with ADHD, and these differences are associated (at least in part) with the severity of ADHD symptoms. Brain asymmetry could be an appropriate precursor of morphological alterations in neurodevelopmental disorders.

The relevance of multiple sclerosis cortical lesions on cortical thinning and their clinical impact as assessed by 7.0-T MRI.

This study aimed to investigate at 7.0-T MRI a) the role of multiple sclerosis (MS) cortical lesions in cortical tissue loss b) their relation to neurological disability. In 76 relapsing remitting and 26 secondary progressive MS patients (N = 102) and 56 healthy subjects 7.0-T T2*-weighted images were acquired for lesion segmentation; 3.0-T T1-weighted structural scans for cortical surface reconstruction/cortical thickness estimation. Patients were dichotomized based on the median cortical lesion volume in low and high cortical lesion load groups that differed by age, MS phenotype and degree of neurological disability. Group differences in cortical thickness were tested on reconstructed cortical surface. Patients were evaluated clinically by means of the Expanded Disability Status Scale (EDSS). Cortical lesions were detected in 96% of patients. White matter lesion load was greater in the high than in the low cortical lesion load MS group (p = 0.01). Both MS groups disclosed clusters (prevalently parietal) of cortical thinning relative to healthy subjects, though these regions did not show the highest cortical lesion density, which predominantly involved frontal regions. Cortical thickness decreased on average by 0.37mm, (p = 0.002) in MS patients for each unit standard deviation change in white matter lesion volume. The odds of having a higher EDSS were associated with cortical lesion volume (1.78, p = 0.01) and disease duration (1.15, p < 0.001). Cortical thinning in MS is not directly related to cortical lesion load but rather with white matter lesion volume. Neurological disability in MS is better explained by cortical lesion volume assessment.

Structural brain imaging studies offer clues about the effects of the shared genetic etiology among neuropsychiatric disorders

Genomewide association studies have found significant genetic correlations among many neuropsychiatric disorders. In contrast, we know much less about the degree to which structural brain alterations are similar among disorders and, if so, the degree to which such similarities have a genetic etiology. From the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) consortium, we acquired standardized mean differences (SMDs) in regional brain volume and cortical thickness between cases and controls. We had data on 41 brain regions for: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), epilepsy, major depressive disorder (MDD), obsessive compulsive disorder (OCD), and schizophrenia (SCZ). These data had been derived from 24,360 patients and 37,425 controls. The SMDs were significantly correlated between SCZ and BD, OCD, MDD, and ASD. MDD was positively correlated with BD and OCD. BD was positively correlated with OCD and negatively correlated with ADHD. These pairwise correlations among disorders were correlated with the corresponding pairwise correlations among disorders derived from genomewide association studies (r = 0.494). Our results show substantial similarities in sMRI phenotypes among neuropsychiatric disorders and suggest that these similarities are accounted for, in part, by corresponding similarities in common genetic variant architectures.

Clinical Features and Brain MRI Findings in Korean Patients with AGel Amyloidosis.

PurposeAGel amyloidosis is systemic amyloidosis caused by pathogenic variants in the GSN gene. In this study, we sought to characterize the clinical and brain magnetic resonance image (MRI) features of Korean patients with AGel amyloidosis.Materials and MethodsWe examined 13 patients with AGel amyloidosis from three unrelated families. Brain MRIs were performed in eight patients and eight age- and sex-matched healthy controls. Therein, we analyzed gray and white matter content using voxel-based morphometry (VBM), tract-based spatial statistics (TBSS), and FreeSurfer.ResultsThe median age at examination was 73 (interquartile range: 64–76) years. The median age at onset of cutis laxa was 20 (interquartile range: 15–30) years. All patients over that age of 60 years had dysarthria, cutis laxa, dysphagia, and facial palsy. Two patients in their 30s had only mild cutis laxa. The median age at dysarthria onset was 66 (interquartile range: 63.5–70) years. Ophthalmoparesis was observed in three patients. No patient presented with muscle weakness of the limbs. Axial fluid-attenuated inversion recovery images of the brain showed no significant differences between the patient and control groups. Also, analysis of VBM, TBSS, and FreeSurfer revealed no significant differences in cortical thickness between patients and healthy controls at the corrected significance level.ConclusionOur study outlines the clinical manifestations of prominent bulbar palsy and early-onset cutis laxa in 13 Korean patients with AGel amyloidosis and confirms that AGel amyloidosis mainly affects the peripheral nervous system rather than the central nervous system.