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High-resolution 7-T imaging and quantitative susceptibility mapping produce greater anatomic detail compared with conventional strengths because of improvements in signal/noise ratio and contrast. The exquisite anatomic details of deep structures, including delineation of microscopic architecture using advanced techniques such as quantitative susceptibility mapping, allows improved detection of abnormal findings thought to be imperceptible on clinical strengths. This article reviews caveats and techniques for translating sequences commonly used on 1.5 or 3 T to high-resolution 7-T imaging. It discusses for several broad disease categories how high-resolution 7-T imaging can advance the understanding of various diseases, improve diagnosis, and guide management.

There is no definitive neural marker of suicidal thoughts and behaviors (STBs) or nonsuicidal self-injury (NSSI), and relative to adults, research in youth is more limited. This comprehensive review focuses on magnetic resonance imaging studies reporting structural and functional neural correlates of STBs and NSSI in youth to 1) elucidate shared and independent neural alternations, 2) clarify how developmental processes may interact with neural alterations to confer risk, and 3) provide recommendations based on convergence across studies. Forty-seven articles were reviewed (STBs = 27; NSSI = 20), and notably, 63% of STB articles and 45% of NSSI articles were published in the previous 3 years. Structural magnetic resonance imaging research suggests reduced volume in the ventral prefrontal and orbitofrontal cortices among youth reporting STBs, and there is reduced anterior cingulate cortex volume related to STBs and NSSI. With regard to functional alterations, blunted striatal activation may characterize STB and NSSI youth, and there is reduced frontolimbic task-based connectivity in suicide ideators and attempters. Resting-state functional connectivity findings highlight reduced positive connectivity between the default mode network and salience network in attempters and show that self-injurers exhibit frontolimbic alterations. Together, suicidal and nonsuicidal behaviors are related to top-down and bottom-up neural alterations, which may compromise approach, avoidance, and regulatory systems. Future longitudinal research with larger and well-characterized samples, especially those integrating ambulatory stress assessments, will be well positioned to identify novel targets that may improve early identification and treatment for youth with STBs and NSSI.

Objective This retrospective and exploratory study tested the accuracy of artificial neural networks (ANNs) at detecting Alzheimer’s disease patients with dementia (ADD) based on input variables extracted from resting-state electroencephalogram (rsEEG), structural magnetic resonance imaging (sMRI) or both. Methods For the classification exercise, the ANNs had two architectures that included stacked (autoencoding) hidden layers recreating input data in the output. The classification was based on LORETA source estimates from rsEEG activity recorded with 10–20 montage system (19 electrodes) and standard sMRI variables in 89 ADD and 45 healthy control participants taken from a national database. Results The ANN with stacked autoencoders and a deep leaning model representing both ADD and control participants showed classification accuracies in discriminating them of 80%, 85%, and 89% using rsEEG, sMRI, and rsEEG + sMRI features, respectively. The two ANNs with stacked autoencoders and a deep leaning model specialized for either ADD or control participants showed classification accuracies of 77%, 83%, and 86% using the same input features. Conclusions The two architectures of ANNs using stacked (autoencoding) hidden layers consistently reached moderate to high accuracy in the discrimination between ADD and healthy control participants as a function of the rsEEG and sMRI features employed. Significance The present results encourage future multi-centric, prospective and longitudinal cross-validation studies using high resolution EEG techniques and harmonized clinical procedures towards clinical applications of the present ANNs.

Background Numerous studies have suggested that structural changes in the cerebellum are implicated in the pathophysiology of bipolar disorder (BD). We aimed to investigate differences in the volume and cortical thickness of the cerebellar subregions between patients with BD and healthy controls (HCs). Methods Ninety patients with BD and one hundred sixty-six HCs participated in this study and underwent T1-weighted structural magnetic resonance imaging. We analyzed the volume and cortical thickness of each cerebellar hemisphere divided into 12 subregions using T1-weighted images of participants. One-way analysis of covariance was used to evaluate differences between the groups, with age, sex, medication, and total intracranial cavity volume used as covariates. Results The BD group had significantly increased cortical thickness of the cerebellum in all cerebellar subregions compared to the HC group. The cortical thicknesses of the whole cerebellum and each hemisphere were also significantly thicker in the BD group than in the HC group. The volume of the left lobule IX was significantly lower in patients with BD than in HCs, whereas no significant differences in the volumes were observed in the other subregions. Limitations Our cross-sectional design cannot provide a causal relationship between the increased cortical thickness of the cerebellum and the risk of BD. Conclusions We observed widespread and significant cortical thickening in all the cerebellar subregions. Our results provide evidence for the involvement of the cerebellum in BD. Further studies are required to integrate neurobiological evidence and structural brain imaging to elucidate the pathophysiology of BD.

Neurodevelopment represents a period of increased opportunity and vulnerability, during which a complex confluence of genetic and environmental factors influences brain growth trajectories, cognitive and mental health outcomes. Recently, magnetic resonance imaging (MRI) studies on twins have increased our knowledge of the extent to which genes, the environment and their interactions shape inter-individual brain variability. The present review draws from highly salient MRI studies in young twin samples to provide a robust assessment of the heritability of structural and functional brain changes during development. The available studies suggest that (as with many other traits), global brain morphology and network organization are highly heritable from early childhood to young adulthood. Conversely, genetic correlations among brain regions exhibit heterogeneous trajectories, and this heterogeneity reflects the progressive, experience-related increase in brain network complexity. Studies also support the key role of environment in mediating brain network differentiation via changes of genetic expression and hormonal levels. Thus, rest- and task-related functional brain circuits seem to result from a contextual and dynamic expression of heritability.

Background Findings on structural brain volume associated with pediatric posttraumatic stress disorder (PTSD) have been variable, and it is unclear whether any structural differences are specific to pediatric PTSD in comparison with adult PTSD or other co-occurring pediatric psychiatric conditions. Methods We tested volumetric brain differences between pediatric groups with and without PTSD in a region-of-interest meta-analysis. We conducted meta-regressions to test the effects of age and sex on heterogeneous study findings. To assess specificity, we compared pediatric PTSD with the following: adult PTSD, pediatric trauma exposure without PTSD, pediatric depression, and pediatric anxiety. Results In 15 studies examined, pediatric PTSD was associated with smaller total gray matter and cerebral, temporal lobe (total, right, and left), total cerebellar vermis, and hippocampal (total, right, and left) volumes, compared to peers without PTSD. In the pediatric PTSD group, but not the comparison group, we found a trend toward smaller total, right, and left amygdalar volumes. In an external comparison, smaller hippocampal volume was not significantly different between adult and pediatric PTSD groups. Qualitative comparisons with a pediatric trauma exposure without PTSD group, a pediatric depression group, and a pediatric anxiety group revealed differences that may be unique to pediatric PTSD, and others that may be convergent with these related clinical conditions in youth. Conclusions Pediatric PTSD is associated with structural differences that parallel those associated with adult PTSD. Furthermore, pediatric PTSD appears to be distinct from other related pediatric conditions at the structural level. Future studies employing longitudinal, dimensional, and multimodal neuroimaging approaches will further elucidate the nature of neurobiological differences in pediatric PTSD.

It has been a privilege to serve the Neuroimage community as a Handling Editor, with primary focus on machine learning, over the past six years. As I step down, I was asked to provide my thoughts on the evolution of the field over the past 10–15 years, as well as its potential future challenges and directions. It is exciting to reflect back on the spectacular growth of this field over the past decade (Fig. 1), and to ponder on some of the challenges faced currently by the field, and which are likely to become central points of investigation in the upcoming decade. Open in a separate window Fig. 1. Publications obtained from Pubmed with the following search query: ("MRI” OR “Magnetic Resonance Imaging” OR "Structural Magnetic Resonance Imaging" OR "Functional Magnetic Resonance Imaging" OR "Diffusion Tensor Imaging" OR "FDG-PET” OR "Amyloid-PET” OR “multimodal" OR "neuroimaging") AND (“brain”) AND (“Machine learning” OR “pattern classification”), on September 5, 2018. This plot reflects the exponential growth of adoption of these methods in neuroimaging.

Background Prior studies of pediatric posttraumatic stress disorder (PTSD) have reported cross-sectional and age-related structural and functional brain abnormalities in networks associated with cognitive, affective, and self-referential processing. However, no reported studies have comprehensively examined longitudinal gray matter development and its intrinsic functional correlates in pediatric PTSD. Methods Twenty-seven youths with PTSD and 21 nontraumatized typically developing (TD) youths were assessed at baseline and 1-year follow-up. At each visit, youths underwent structural magnetic resonance imaging and resting-state functional magnetic resonance imaging. Regions with volumetric abnormalities in whole-brain structural analyses were identified and used as seeds in exploratory intrinsic connectivity analyses. Results Youths with PTSD exhibited sustained reductions in gray matter volume (GMV) in right ventromedial prefrontal cortex (PFC) and bilateral ventrolateral PFC. Group-by-time analyses revealed aberrant longitudinal development in dorsolateral PFC, where typically developing youths exhibited normative decreases in GMV between baseline and follow-up, and youths with PTSD showed increases in GMV. Using these regions as seeds, patients with PTSD exhibited atypical longitudinal decreases in intrinsic PFC–amygdala and PFC–hippocampus connectivity, in contrast to increases in typically developing youths. Specifically, youths with PTSD showed decreasing ventromedial PFC–amygdala connectivity as well as decreasing ventrolateral PFC–hippocampus connectivity over time. Notably, volumetric abnormalities in ventromedial PFC and ventrolateral PFC were predictive of symptom severity. Conclusions These findings represent novel longitudinal volumetric and connectivity changes in pediatric PTSD. Atypical prefrontal GMV and prefrontal-amygdala/hippocampus development may underlie persistence of PTSD in youths and could serve as future therapeutic targets.

Exposures to fine particulate matter (PM(2.5)) and nitrogen dioxide (NO(2)) have been associated with the emergence of depressive symptoms in older adulthood, although most studies used cross-sectional outcome measures. Elucidating the brain structures mediating the adverse effects can strengthen the causal role between air pollution and increasing depressive symptoms. We evaluated whether smaller volumes of brain structures implicated in late-life depression mediate associations between ambient air pollution exposure and changes in depressive symptoms. This prospective study included 764 community-dwelling older women (aged 81.6 ± 3.6 in 2008–2010) from the Women’s Health Initiative Memory Study (WHIMS) Magnetic Resonance Imaging study (WHIMS-MRI; 2005–06) and WHIMS-Epidemiology of Cognitive Health Outcomes (WHIMS-ECHO; 2008–16). Three-year average annual mean concentrations (scaled by interquartile range [IQR]) of ambient PM(2.5) (in μg/m(3); IQR = 3.14 μg/m(3)) and NO(2) (in ppb; IQR = 7.80 ppb) before WHIMS-MRI were estimated at participants’ addresses via spatiotemporal models. Mediators included structural brain MRI-derived gray matter volumes of the prefrontal cortex and structures of the limbic-cortical-striatal-pallidal-thalamic circuit. Depressive symptoms were assessed annually by the 15-item Geriatric Depression Scale. Structural equation models were constructed to estimate associations between exposure, structural brain variables, and depressive symptoms. Increased exposures (by each IQR) were associated with greater annual increases in depressive symptoms (β(PM2.5) = .022; 95% Confidence Interval (CI) = .003, .042; β(NO2) = = .019; 95% CI = .001, .037). The smaller volume of prefrontal cortex associated with exposures partially mediated the associations of increased depressive symptoms with NO(2) (8%) and PM(2.5) (13%), and smaller insula volume associated with NO(2) contributed modestly (13%) to the subsequent increase in depressive symptoms. We demonstrate the first evidence that the smaller volumes of the prefrontal cortex and insula may mediate the subsequent increases in depressive symptoms associated with late-life exposures to NO(2) and PM(2.5).

Anorexia nervosa (AN) is a mental disorder characterized by a preoccupation with thinness and may be associated with brain structural alteration. The aim of the study was to examine the brain structural alteration in AN patients, including subcortical structure volume and cortical thickness. Thirty-five un-medicated AN patients and 20 matched healthy controls underwent structural magnetic resonance imaging brain scans. High resolution structural images were acquired on a SIEMENS 3T scanner and preprocessed using FreeSurfer software. Subcortical structure volume and cortical thickness were compared between the two groups. We found larger percentage of caudate volume relative to total grey matter (GM) volume in the AN group. Reduced cortical thickness at the left precuneus was also observed in AN patients. Moreover, an interaction between group and hemisphere was found, suggesting that cortical thinning was more prominent in the left hemisphere in AN patients. These findings provide further evidence for structural brain abnormalities in patients with AN.

Adverse childhood experiences (ACEs) potentially contribute to posttraumatic stress disorder (PTSD) after adult trauma exposure, but underlying brain changes remain unclear. The present study tested relationships between ACEs, whole thalamus and thalamic nuclei volumes, and post-trauma stress symptoms (PTSS) after adult trauma. Trauma survivors (n = 101) completed the Childhood Trauma Questionnaire (CTQ), the PTSD checklist-special stressor version 5 (PCL), and a structural magnetic resonance imaging (sMRI) scan within post-trauma 2 weeks. At post-trauma 3 months, survivors completed a second PCL survey and a PTSD diagnosis interview using the Clinician-Administered PTSD Scale (CAPS). CTQ scores significantly positively correlated with PCL scores at post-trauma 2 weeks and 3 months (respective p's0.01 and0.001). CTQ scores significantly negatively correlated with whole thalamus and 7 thalamic nuclei volumes at post-trauma 2 weeks in the PTSD (N = 50), but not the non-PTSD (N = 51) group. Whole thalamus and 22 nuclei volumes significantly negatively correlated with PCL scores at post-trauma 3 months in the PTSD, but not the non-PTSD group. These results suggest ACEs negatively influence early post-trauma thalamic volumes which, in turn, are negatively associated with PTSS in survivors who develop PTSD.

The developing brain grows exponentially in the first few years of life. There is a need to have age-appropriate brain atlases that coherently characterize the geometry of the cerebral cortex, white matter tracts, and functional organization. This study employed multi-modal brain images of an Asian cohort and constructed brain structural and functional atlases for 6-month-old infants, 4.5-, 6-, and 7.5-year-old children. We exploited large deformation diffeomorphic metric mapping and probabilistic atlas generation approaches to integrate structural MRI and diffusion weighted images (DWIs) and to create the atlas where white matter tracts well fit into the cortical folding pattern. Based on this structural atlas, we then employed spectral clustering to parcellate the brain into functional networks from resting-state fMRI (rs-fMRI). Our results provided the atlas that characterizes the cortical folding geometry, subcortical regions, deep white matter tracts, as well as functional networks in a stereotaxic coordinate space for the four different age groups. The functional networks consisting of the primary cortex were well established in infancy and remained stable to childhood, while specific higher-order functional networks showed specific patterns of hemispherical, subcortical-cerebellar, and cortical-cortical integration and segregation from infancy to childhood. Our multi-modal fusion analysis demonstrated the use of the integrated structural and functional atlas for understanding coherent patterns of brain anatomical and functional development during childhood. Hence, our atlases can be potentially used to study coherent patterns of brain anatomical and functional development.

Purpose To characterize the changes in cortical thickness of adult patients with moyamoya disease (MMD). Methods 60 patients with MMD and 60 age and sex-matched healthy volunteers were recruited. Structural images were acquired by MRI. Freesurfer was used to measure cortical thickness in patients and controls, and this was compared with MRA scores and cerebrovascular accident (CVA) scores. Results Compared with controls, the average cortical thickness of both cerebral hemispheres was lower in patients than in controls and symmetrical differences were seen in the regional cortex: bilateral precentral gyri were thinner, bilateral postcentral gyri and posterior cingulate gyri were thicker, and thinning and thickening were both found in the insula. CVA scores were negatively correlated with the average cortical thicknesses. Conclusions Cortical thickness can be used as a biological indicator to assess the severity of MMD.

Recent studies using surface-based morphometry of structural magnetic resonance imaging data have suggested that some changes in bipolar disorder (BP) might be neurodevelopmental in origin. We applied a novel analysis of cortical complexity based on fractal dimensions in high-resolution structural MRI scans of 18 bipolar disorder patients and 26 healthy controls. Our region-of-interest based analysis revealed increases in fractal dimensions (in patients relative to controls) in left lateral orbitofrontal cortex and right precuneus, and decreases in right caudal middle frontal, entorhinal cortex, and right pars orbitalis, and left fusiform and posterior cingulate cortices. While our analysis is preliminary, it suggests that early neurodevelopmental pathologies might contribute to bipolar disorder, possibly through genetic mechanisms.

Aging is associated with reductions in gray matter volume and cortical thickness. One factor that may play a role in mitigating age-associated brain decline is cardiorespiratory fitness (CRF). Although previous work has identified a positive association between CRF and gray matter volume, the relationship between CRF and cortical thickness, which serves as a more sensitive indicator of gray matter integrity, has yet to be assessed in healthy young and older adults. To address this gap in the literature, 32 young and 29 older adults completed treadmill-based progressive maximal exercise testing to assess CRF (peak VO2), and structural magnetic resonance imaging (MRI) to determine vertex-wise surface-based cortical thickness metrics. Results indicated a significant CRF by age group interaction such that Peak VO2 was associated with thicker cortex in older adults but with thinner cortex in young adults. Notably, the majority of regions demonstrating a positive association between peak VO2 and cortical thickness in older adults overlapped with brain regions showing significant age-related cortical thinning. Further, when older adults were categorized as high or low fit based on normative data, we observed a stepwise pattern whereby cortex was thickest in young adults, intermediate in high fit older adults and thinnest in low fit older adults. Overall, these results support the notion that CRF-related neuroplasticity may reduce although not eliminate age-related cortical atrophy.

Introduction Atrophy measures derived from structural MRI are promising outcome measures for early phase clinical trials, especially for rare diseases such as primary progressive aphasia (PPA), where the small available subject pool limits our ability to perform meaningfully powered trials with traditional cognitive and functional outcome measures. Methods We investigated a composite atrophy index in 26 PPA participants with longitudinal MRIs separated by 2 years. Rogalski et al. [5] previously demonstrated that atrophy of the left perisylvian temporal cortex (PSTC) is a highly sensitive measure of disease progression in this population and a promising endpoint for clinical trials. Using methods described by Ard et al. [1] , we constructed a composite atrophy index composed of a weighted sum of volumetric measures of 10 regions of interest within the left perisylvian cortex using weights that maximize signal-to-noise and minimize sample size required of trials using the resulting score. Sample size required to detect a fixed percentage slowing in atrophy in a 2-year clinical trial with equal allocation of subjects across arms and 90% power was calculated for the PSTC and optimal composite surrogate biomarker endpoints. Results The optimal composite endpoint required 38% fewer subjects to detect the same percent slowing in atrophy than required by the left PSTC endpoint. Conclusions Optimal composites can increase the power of clinical trials and increase the probability that smaller trials are informative, an observation especially relevant for PPA but also for related neurodegenerative disorders including Alzheimer's disease.

The neuroprotective effects of leptin and its role in addictive disorders has been highlighted by several recent studies. However, its potential effects on morphological alterations in alcohol dependence are yet to be investigated. Associations between leptin and the longitudinal courses of gray matter volume (GMV) and cortical thickness (CT) were investigated in N = 62 alcohol-dependent patients that underwent structural magnetic resonance imaging after a mean abstinence of 12 (baseline) and 27 days (follow-up) respectively. Blood samples were collected at baseline to determine leptin levels. A cohort of N = 74 healthy individuals served as a reference sample. At baseline, alcohol-dependent patients compared to healthy controls displayed smaller GMV in the insula, parts of the superior, middle and inferior frontal gyri and hippocampal regions and thinner CT in the insula, parts of the superior and middle frontal cortices, the lateral orbitofrontal cortex and parts of the occipital and lingual cortices that partially recovered during abstinence (pFWE

In Parkinson's disease (PD), the thalamus plays an important role in pathogenesis and disease symptoms; however, the morphological changes in thalamic subnuclei have not been clearly investigated. And there are still many challenges in individual PD diagnosis, especially clinical condition evaluations. Structural magnetic resonance imaging (MRI) was performed on 131 PD patients and 69 healthy controls (HC), and the volumes of 25 thalamic subnuclei were evaluated by FreeSurfer and a newly developed thalamus segment algorithm. Then, the individual PD diagnosis and clinical condition prediction were conducted on support vector machines (SVM) classification or regression. The bilateral thalami were enlarged; the volumes of 21 of 25 left thalamic subnuclei and 20 of 25 right thalamic subnuclei were increased, accompanied by 2 left nuclei atrophy. An accuracy of 95% with sensitivity of 97.44%, and specificity of 90.48% was achieved in PD diagnosis. United Parkinson's disease Rating Scale (UPDRS) III, limb bradykinesia, and axial akinetic symptoms score prediction were obtained with Pearson correlation coefficient of 0.5497, 0.5382, and 0.5911, respectively; however, the results of tremor, rigidity, and speech prediction were limited. Finally, accuracies of 76.92% were achieved in the UPDRS III improvement prediction. These findings confirmed that numerous left and right thalamic subnuclei were enlarged, accompanied by a few atrophies. The individual PD diagnosis, symptom, and clinical improvement prediction could be achieved based on morphology of thalamic subnuclei via machine learning.

The formation of multiple sclerosis (MS) lesions is a complex process involving inflammation, tissue damage, and tissue repair — all of which are visible on structural magnetic resonance imaging (MRI) and potentially modifiable by pharmacological therapy. In this paper, we introduce two statistical models for relating voxel-level, longitudinal, multi-sequence structural MRI intensities within MS lesions to clinical information and therapeutic interventions: (1) a principal component analysis (PCA) and regression model and (2) function-on-scalar regression models. To do so, we first characterize the post-lesion incidence repair process on longitudinal, multi-sequence structural MRI from 34 MS patients as voxel-level intensity profiles. For the PCA regression model, we perform PCA on the intensity profiles to develop a voxel-level biomarker for identifying slow and persistent, long-term intensity changes within lesion tissue voxels. The proposed biomarker's ability to identify such effects is validated by two experienced clinicians (a neuroradiologist and a neurologist). On a scale of 1 to 4, with 4 being the highest quality, the neuroradiologist gave the score on the first PC a median quality rating of 4 (95% CI: [4,4]), and the neurologist gave the score a median rating of 3 (95% CI: [3,3]). We then relate the biomarker to the clinical information in a mixed model framework. Treatment with disease-modifying therapies (p, Highlights • Pipeline to extract voxel level longitudinal profiles from four MRI sequences within lesion tissue • Propose two statistical models to relate clinical covariates to the longitudinal profiles • Develop a biomarker that identifies areas of slow, long-term intensity changes at a voxel level • We validate the biomarker with ratings by two expert MS clinicians

The purpose of this prospectively designed cross-sectional observational study was to evaluate the effect of polycystic ovary syndrome (PCOS) on pituitary gland volume (PGV) under the hypothesis that endocrinologic changes may lead to morphologic changes of the pituitary gland. Twenty-six PCOS patients and 31 control subjects underwent magnetic resonance imaging (MRI) of the pituitary. Informed consent was obtained from all subjects. PGV was significantly larger in PCOS patients than in control subjects. Luteinizing hormone/follicle-stimulating hormone ratio was the only predictor of PGV. The association between pituitary gland enlargement and PCOS should be kept in mind when pituitary hypertrophy is detected on MRI.

Highlights • White matter microstructural differences occurred between early and late puberty. • White matter regions showed reduced mean diffusivity from early to late puberty. • Regression models showed that pubertal effects could not simply be ascribed to age. • Mean diffusivity decreases were associated with increasing salivary testosterone levels., Neuroimaging studies demonstrate considerable changes in white matter volume and microstructure during adolescence. Most studies have focused on age-related effects, whilst puberty-related changes are not well understood. Using diffusion tensor imaging and tract-based spatial statistics, we investigated the effects of pubertal status on white matter mean diffusivity (MD) and fractional anisotropy (FA) in 61 males aged 12.7–16.0 years. Participants were grouped into early-mid puberty (≤Tanner Stage 3 in pubic hair and gonadal development; n = 22) and late-post puberty (≥Tanner Stage 4 in pubic hair or gonadal development; n = 39). Salivary levels of pubertal hormones (testosterone, DHEA and oestradiol) were also measured. Pubertal stage was significantly related to MD in diverse white matter regions. No relationship was observed between pubertal status and FA. Regression modelling of MD in the significant regions demonstrated that an interaction model incorporating puberty, age and puberty × age best explained our findings. In addition, testosterone was correlated with MD in these pubertally significant regions. No relationship was observed between oestradiol or DHEA and MD. In conclusion, pubertal status was significantly related to MD, but not FA, and this relationship cannot be explained by changes in chronological age alone.

Violent offenders with psychopathy present a lifelong pattern of callousness and aggression and fail to benefit from rehabilitation programs. This study presents the first, albeit preliminary, evidence suggesting that some of the structural brain anomalies distinguishing violent offenders with psychopathy may result from physical abuse in childhood.

A balanced integration of emotional and cognitive information is essential for flexible behaviour, which involves the anterior cingulate cortex (ACC) and the midcingulate cortex (MCC) [1]. Both clinical and preclinical researchers have been interested in studying the role of ACC and MCC in health and disease but preclinical rodent studies so far have suffered from a severe misconception: The definition of ACC/MCC used for rodents is not homologous to the human definition of ACC/MCC. Due to this, numerous findings of rodent studies are not directly translatable to the human situation, an issue that has been addressed in the past [2]. However, the majority of researchers still use the non-homologous definition of rodent ACC/MCC and awareness of the homologous nomenclature needs to be raised. Here, we demonstrate in a series of experiments the value of the homologous rodent ACC/MCC definition for translational research. We conducted a literature review, showing that the non-homologous definition of rodent ACC/MCC does not match human ACC/MCC anatomy and connectivity, while the homologous definition does. We then determined volumes of ACC and MCC in the BALB/cJ mouse, a model demonstrating characteristic symptoms of CD and ADHD (increased aggression and inattention). BALB/cJ mice were tested in the resident-intruder paradigm, demonstrating increased aggression (reduced attack latency: p 0.55 and all p 0.05), highlighting the importance of using the homologous ACC/MCC definition. Last, we aimed to validate our histological findings by using voxel-based morphometry (VBM) of structural magnetic resonance imaging (MRI) data to measure ACC/MCC volumes. BALB/cJ and BALB/cByJ mice were tested in the 5-choice serial reaction time task, a task probing attention. BALB/cJ mice showed a global attention deficit, indicated by an increased percentage of omissions compared to BALB/cByJ mice (p 0.25 and p

Background Substantial efforts have been made to investigate the neurobiological underpinnings of human obesity with a number of studies indicating a profound influence of increased body weight on brain structure. Although body weight is known to be highly heritable, uncertainty remains regarding the respective contribution of genetic and environmental influences. Methods In this study we used structural magnetic resonance imaging (MRI) data from the Human Connectome Project (HCP). Voxel-based morphometry (VBM) was applied to study BMI-associated differences in gray matter volume (GMV) within monozygotic (MZ) twin pairs discordant for BMI (ΔBMI ​> ​2.5 ​kg*m−2, n = 68 pairs). In addition, we investigated the relationship of ΔBMI (entire range) with GMV differences within the entire sample of MZ twin pairs (n = 153 pairs). Results Analyses of BMI discordant twin pairs yielded less GMV in heavier twin siblings (p Conclusion While MZ twins share the same genetic background, our findings indicate that non-genetic influences and the mere presence of a higher BMI constitute relevant factors in the context of body weight related structural brain alterations.

Prenatal alcohol exposure can cause a wide range of deficits in executive function that persist throughout life, but little is known about how changes in brain structure relate to cognition in affected individuals. In the current study, we predicted that the rate of white matter volumetric development would be atypical in children with fetal alcohol spectrum disorders (FASD) when compared to typically developing children, and that the rate of change in cognitive function would relate to differential white matter development between groups. Data were available for 103 subjects [49 with FASD, 54 controls, age range 6–17, mean age = 11.83] with 153 total observations. Groups were age-matched. Participants underwent structural magnetic resonance imaging (MRI) and an executive function (EF) battery. Using white matter volumes measured bilaterally for frontal and parietal regions and the corpus callosum, change was predicted by modeling the effects of age, intracranial volume, sex, and interactions with exposure status and EF measures. While both groups showed regional increases in white matter volumes and improvement in cognitive performance over time, there were significant effects of exposure status on age-related relationships between white matter increases and EF measures. Specifically, individuals with FASD consistently showed a positive relationship between improved cognitive function and increased white matter volume over time, while no such relationships were seen in controls. These novel results relating improved cognitive function with increased white matter volume in FASD suggest that better cognitive outcomes could be possible for FASD subjects through interventions that enhance white matter plasticity., Highlights • Children with prenatal alcohol exposure compared with controls longitudinally • Similar increases of white matter and cognition seen in both groups • But, brain–behavior relationships differed between groups. • Different relationships seen with neurobehavior and structure in exposed children • Results suggest interventions for white matter plasticity would be useful for FASD.

This systematic review aims to determine whether or not structural magnetic resonance imaging (sMRI) data support the DSM-5 proposal of an autism spectrum disorder (ASD) diagnostic category, and whether or not classical DSM-IV autistic disorder (AD) and Asperger syndrome (AS) categories should be subsumed into it. The most replicated sMRI findings in patients with ASD compared with healthy controls are increased total brain volume in early childhood and decreased corpus callosum volume. Regarding the notion of a spectrum , some studies support that AS and AD are similar but “quantitatively different” diagnostic categories, whereas others support that they are “qualitatively different” entities with specific brain structural abnormalities. It seems that there are still not enough arguments from sMRI data for or against subsuming DSM-IV categories under a single ASD category.

Magnetic resonance imaging is the main structural imaging in epilepsy. In patients with focal seizures, detection (and characterization) of a structural lesion consistent with electroclinical data allows therapeutic decisions without having to resort to other more expensive or invasive diagnostic procedures. The identification of some lesions may provide prognostic value, as in the case of Mesial Temporal Sclerosis (MTS) or may contribute to genetic counseling, as in the case of some Malformations of Cortical Development (MCD). The aim of this paper is to review the current state of structural MRI techniques, propose a basic protocol of epilepsy and mention the indications for structural MRI. Also, review the semiology of the main causes of epilepsy, with emphasis on MTS and MCD, by its highest frequency and by the special impact that MRI has shown in dealing with these entities.

It is well established that schizophrenia is associated with structural brain abnormalities, but whether these are static or progress over time remains controversial.A systematic review of longitudinal volumetric studies using region-of-interest structural magnetic resonance imaging in patients with schizophrenia and healthy control subjects. The percentage change in volume between scans for each brain region of interest was obtained, and data were combined using random effects meta-analysis.Twenty-seven studies were included in the meta-analysis, with 928 patients and 867 control subjects, and 32 different brain regions of interest. Subjects with schizophrenia showed significantly greater decreases over time in whole brain volume, whole brain gray matter, frontal gray and white matter, parietal white matter, and temporal white matter volume, as well as larger increases in lateral ventricular volume, than healthy control subjects. The time between baseline and follow-up magnetic resonance imaging scans ranged from 1 to 10 years. The differences between patients and control subjects in annualized percentage volume change were -.07% for whole brain volume, -.59% for whole brain gray matter, -.32% for frontal white matter, -.32% for parietal white matter, -.39% for temporal white matter, and +.36% for bilateral lateral ventricles.These findings suggest that schizophrenia is associated with progressive structural brain abnormalities, affecting both gray and white matter. We found no evidence to suggest progressive medial temporal lobe involvement but did find evidence that this may be partly explained by heterogeneity between studies in patient age and illness duration. The causes and clinical correlates of these progressive brain changes should now be the focus of investigation.

Many previous studies have shown that there exists the gender effect on the structural and functional organization in the human brain Although the reported functional differences are generally consistent, the structural differences are controversial among the various studies. In this study, we particularly focused on the gender-related effect in the gray matter (GM) We performed a structural magnetic resonance imaging (MRI) study in 184 healthy adults (90 males and 94 females) with ages ranging from 18 to 70 years Cortical thickness was measured using an automated surface-based method Based on this surface morphological feature of GM, we first compared their regional differences between males and females We then constructed the morphometry-based anatomical networks derived from cortical thickness measurement, while the anatomical connection between two cortical areas depended upon the statistical dependence of their cortical thickness across subjects Subsequently, we applied graph theoretical approaches to investigate the properties of the resultant anatomical networks The results showed that the significant gender-related differences of cortical thickness appeared extensively in the frontal, parietal and occipital lobes. And there were also some between-group differences in the interregional correlation. Additional graph theoretical analysis on the morphological networks revealed both networks exhibited the small-world efficiency and their patterns of topological vulnerability had no statistical differences The findings on the large sample may provide the evidences to study the gender consistency and difference in the human brain structures. (C) 2010 Published by Elsevier Inc.

The corpus callosum (CC) is one of focused target areas which may play an important role in the pathophysiology of attention deficit hyperactivity disorder (ADHD). Conventional structural magnetic resonance imaging (MRI) studies have revealed the macrostructural abnormalities of CC and its subdivisions in ADHD compared with controls. However, no study has examined the macrostructural and microstructural characteristics of the CC in the same ADHD group. In this study, MRI morphometric and diffusion tensor imaging (DTI) techniques were combined to explore the area and measure fractional anisotropy (FA) abnormality of CC and its seven subdivisions in children with ADHD. Twenty-eight boys with ADHD (13.3 ± 1.5 years) and 27 age- and gender- matched controls (13.2 ± 0.9 years) were included. We co-registered individual structural MRI and DTI images manually and subdivided the midsagittal CC into seven subdivisions. The area and FA of the CC and its subdivisions were then compared between the patients and the matched controls. Results showed that ADHD had decreased area of entire CC, anterior middle-body, and isthmus. Meanwhile, reduced FA value of the isthmus was found in the ADHD group compared with the controls. Our study indicated that not only macrostructural abnormalities but also microstructural alterations in CC, especially in isthmus occurred in ADHD. The abnormality of the isthmus, the subdivision that contains the fibers connecting posterior regions of brain, may play an important role in the pathophysiology of ADHD and may be implicated in the disorders of attention.

Objective To provide an overview of diffusion tensor imaging (DTI) and its application to the study of white matter in the developing brain in both healthy and clinical samples. Method The development of DTI and its application to brain imaging of white matter tracts is discussed. Forty-eight studies using DTI to examine diffusion properties of the developing brain are reviewed in the context of the structural magnetic resonance imaging literature. Reports of how brain diffusion properties are affected in pediatric clinical samples and how they relate to cognitive and behavioral phenotypes are reviewed. Results DTI has been used successfully to describe white matter development in pediatric samples. Changes in white matter diffusion properties are consistent across studies, with anisotropy increasing and overall diffusion decreasing with age. Diffusion measures in relevant white matter regions correlate with behavioral measures in healthy children and in clinical pediatric samples. Conclusions DTI is an important tool for providing a more detailed picture of developing white matter than can be obtained with conventional magnetic resonance imaging alone. J. Am. Acad. Child Adolesc. Psychiatry , 2007;46(2):213-223.

Previous research has often examined whether the asymmetrical structure of the planum temporale (PT) represents an anatomical correlate of lateralized language-processing functions, gathering diverging empirical evidence by comparing PT asymmetry in subjects with differing handedness, gender, or speech lateralization. Apart from other methodological problems, direct comparisons between studies are hampered by insufficient assessment and consideration of all three potential determinants of structural cerebral asymmetry. Based on volumetric assessment of structural Magnetic Resonance Imaging (MRI) scans of 104 healthy subjects, the present study replicated earlier observations of an overall leftward PT asymmetry, which was found to prevail irrespective of handedness, gender, or dichotic-listening ear advantage. However, the mean magnitude of this leftward asymmetry was not determined by either one of these factors in itself, but varied depending on their specific combination. A clear correspondence between structural and functional asymmetry was only observed among right-handed males. In this particular subgroup, more pronounced structural asymmetry was associated with an enlarged PT on the left side, while the enhanced leftward asymmetry of female sinistrals resulted from smaller adjusted volumes of their right PT. The existence of such complex interactions suggests that future research in this area can only be expected to overcome past inconsistencies by adequately considering handedness, gender, and speech lateralization.

Background Greater physical activity (PA) is associated with better memory performance and greater hippocampal volume in older adults. However, most studies to date assessed PA via questionnaires and thereby lacked objective characterization of PA (eg, intensity, duration, etc.). Thus, we currently do not have a comprehensive understanding of PA characteristics that are important for neuroprotection, especially among older adults with mild cognitive impairment (MCI). Thus, using triaxial accelerometers, we examined the association between light- and moderate-intensity PA, total duration of PA, hippocampal volume, and memory in older adults with MCI. Methods This cross-sectional study involved 310 older adults with MCI who completed neuropsychological tests of memory, and structural magnetic resonance imaging. Participants were instructed to wear the accelerometer on an elastic band on their hip at all times for 2 weeks. Average daily duration of light, moderate, and total PA (min/day) was calculated. Results Moderate PA was associated with hippocampal volume (β = .167, p = .003) after controlling for age, but light PA (β = -.021, p = .713) and total PA (β = .011, p = .844) were not. Both light and moderate PAs were not associated with memory performance. Structural equation modeling demonstrated that moderate PA was not directly associated with memory but significantly contributed to hippocampal volume; hippocampal volume loss was significantly and directly associated with poor memory performance. Conclusions Our results suggest that the benefits of moderate PA on memory among older adults with MCI are mediated by hippocampal volume. Furthermore, light PA may not reduce dementia risk among older adults with MCI.