Project description:Verbal learning (VL) and fluency (VF) are prominent cognitive deficits in psychosis, of which the precise neuroanatomical contributions are not fully understood. We investigated the arcuate fasciculus (AF) and its associated cortical regions to identify structural abnormalities contributing to these verbal impairments in early stages of psychotic illness.Twenty-six individuals with recent-onset psychosis and 27 healthy controls underwent cognitive testing (MATRICS Consensus Cognitive Battery) and structural/diffusion-weighted MRI. Bilaterally, AF anisotropy and cortical thickness, surface area and volume of seven cortical regions were investigated in relation to VL and VF performance in both groups.Reduced right superior temporal gyrus surface area and volume related to better VF in controls. In psychosis, greater right pars opercularis volume and reduced left lateralization of this region related to better VL, while greater right long AF fractional anisotropy and right pars orbitalis volume related to better VF, these findings not present in controls. Psychosis had reduced right pars orbitalis thickness compared to controls.Anatomical substrates for normal processing of VL and VF appear altered in recent-onset psychosis. A possible aberrant role of the right hemisphere arcuate fasciculus and fronto-temporal cortical regions in psychosis may contribute to deficits in VL and VF.
Project description:In the military, explosive blasts are a significant cause of mild traumatic brain injuries (mTBIs). The symptoms associated with blast mTBIs causes significant economic burdens and a diminished quality of life for many service members. At present, the distinction of the injury mechanism (blast versus non-blast) may not influence TBI diagnosis. However, using noninvasive imaging, this study reveals significant distinctions between the blast and non-blast TBI mechanisms. A cortical whole-brain thickness analysis was performed using structural high-resolution T1-weighted MRI to identify the effects of blasts in persistent mTBI (pmTBI) subjects. A total of 41 blast pmTBI subjects were individually age- and gender-matched to 41 non-blast pmTBI subjects. Using FreeSurfer, cortical thickness was quantified for the blast group, relative to the non-blast group. Cortical thinning was identified within the blast mTBI group, in two clusters bilaterally. In the left hemisphere, the cluster overlapped with the lateral orbitofrontal, rostral middle frontal, medial orbitofrontal, superior frontal, rostral anterior cingulate and frontal pole cortices (p?<?0.02, two-tailed, size?=?1680?mm2). In the right hemisphere, the cluster overlapped with the lateral orbitofrontal, rostral middle frontal, medial orbitofrontal, pars orbitalis, pars triangularis and insula cortices (p?<?0.002, two-tailed, cluster size?=?2453?mm2). Self-report assessments suggest significant differences in the Post-Traumatic Stress Disorder Checklist-Civilian Version (p?<?0.05, Bonferroni-corrected) and the Neurobehavioral Symptom Inventory (p?<?0.01, uncorrected) between the blast and non-blast mTBI groups. These results suggest that blast may cause a unique injury pattern related to a reduction in cortical thickness within specific brain regions which could affect symptoms. No other study has found cortical thickness difference between blast and non-blast mTBI groups and further replication is needed to confirm these initial observations.
Project description:The unique neuroanatomical underpinnings of internalizing symptoms and impulsivity during childhood are not well understood. In this study, we examined associations of brain structure with anxiety, depression, and impulsivity in children and adolescents. Participants were 7- to 21-year-olds (N?=?328) from the Pediatric Imaging, Neurocognition, and Genetics (PING) study who completed high-resolution, 3-Tesla, T1-weighted MRI and self-report measures of anxiety, depression, and/or impulsivity. Cortical thickness and surface area were examined across cortical regions-of-interest (ROIs), and exploratory whole-brain analyses were also conducted. Gray matter volume (GMV) was examined in subcortical ROIs. When considered separately, higher depressive symptoms and impulsivity were each significantly associated with reduced cortical thickness in ventromedial PFC/medial OFC, but when considered simultaneously, only depressive symptoms remained significant. Higher impulsivity, but not depressive symptoms, was associated with reduced cortical thickness in the frontal pole, rostral middle frontal gyrus, and pars orbitalis. No differences were found for regional surface area. Higher depressive symptoms, but not impulsivity, were significantly associated with smaller hippocampal GMV and larger pallidal GMV. There were no significant associations between anxiety symptoms and brain structure. Depressive symptoms and impulsivity may be linked with cortical thinning in overlapping and distinct regions during childhood and adolescence.
Project description:BACKGROUND:Evidence suggests that single nucleotide polymorphisms (SNPs) in genes involved in serotonergic signaling and stress response pathways moderate associations between PTSD and cortical thickness. This study examined a genetic regulator of these pathways, the PPM1F gene, which has also been implicated in mechanisms of stress responding and is differentially expressed in individuals with comorbid PTSD and depression compared to controls. METHODS:Drawing from a sample of 240 white non-Hispanic trauma-exposed veterans, we tested 18 SNPs spanning the PPM1F gene for association with PTSD and cortical thickness. RESULTS:Analyses revealed six PPM1F SNPs that moderated associations between PTSD symptom severity and cortical thickness of bilateral superior frontal and orbitofrontal regions as well as the right pars triangularis (all corrected p's < 0.05) such that greater PTSD severity was related to reduced cortical thickness as a function of genotype. A whole-cortex vertex-wise analysis using the most associated SNP (rs9610608) revealed this effect to be localized to a cluster in the right superior frontal gyrus (cluster-corrected p < 0.02). LIMITATIONS:Limitations of this study include the small sample size and that the sample was all-white, non-Hispanic predominately male veterans. CONCLUSIONS:These results extend prior work linking PPM1F to PTSD and suggest that variants in this gene may have bearing on the neural integrity of the prefrontal cortex (PFC).
Project description:BACKGROUND:Prefrontal subregions, including the ventromedial prefrontal cortex (PFC), dorsomedial PFC, and dorsolateral PFC (DLPFC), are differentially implicated in the pathophysiology of posttraumatic stress disorder (PTSD), though few existing studies have examined subregional differences in resting-state functional connectivity (rsFC). We hypothesized that PTSD would involve weaker positive rsFC between ventromedial PFC, dorsomedial PFC, and other default mode network regions and increased negative rsFC between DLPFC and posterior default mode network regions. Additionally, we hypothesized that prefrontal regions exhibiting group differences in rsFC would be characterized by alterations in cortical thickness. METHODS:Participants included 36 healthy control subjects, 30 trauma-exposed control subjects, and 21 individuals with current DSM-IV PTSD resulting from community-acquired trauma. Participants completed the Clinician Administered PTSD Scale, questionnaires (Childhood Trauma Questionnaire, Adverse Childhood Events, Life Events Checklist, Beck Depression Inventory), structural neuroimaging, and resting-state functional magnetic resonance imaging. rsFC of DLPFC, ventromedial PFC, and dorsomedial PFC seeds was evaluated in SPM12 and CONN. Cortical thickness for regions with significant rsFC findings was assessed using FreeSurfer. RESULTS:Relative to both healthy control and trauma-exposed control subjects, individuals with PTSD showed increased negative rsFC between the DLPFC and a region of precuneus. This finding was associated with increased overall symptom severity but not with trauma load or childhood trauma exposure. Greater negative DLPFC-precuneus connectivity was associated with greater bilateral precuneus thickness. CONCLUSIONS:Given participation of precuneus subregions in the central executive network, increased anticorrelation between right DLPFC and precuneus in this sample may reflect increased opposition between anterior and posterior central executive network hubs in PTSD.
Project description:<h4>Study objectives</h4>To test the hypothesis that greater sleep fragmentation is associated with regionally decreased cortical gray matter volume in older community-dwelling adults without cognitive impairment.<h4>Methods</h4>We studied 141 community-dwelling older adults (median age 82.9; 73% female) without cognitive impairment or stroke, and not using sedative/ hypnotic medications, participating in the Rush Memory and Aging Project. We quantified sleep fragmentation from 7 d of actigraphy using the metric kRA and related this to total cortical gray matter volume, and regional gray matter volume in 34 cortical regions quantified by automated segmentation of magnetic resonance imaging data. We determined statistical significance and accounted for multiple comparisons by empirically estimating the false discovery rate by permutation.<h4>Results</h4>Lower total cortical gray matter volume was associated with higher sleep fragmentation (coefficient +0.23, standard error [SE] 0.11, P = 0.037). Lower gray matter volumes in four cortical regions were accompanied by higher sleep fragmentation with a false discovery rate < 0.05: the left (coefficient +0.36, SE 0.10, P = 2.7 × 10(-4)) and right (coefficient +0.31, SE 0.10, P = 4.0 × 10(-3)) lateral orbitofrontal cortices, and the adjacent left (coefficient +0.31, SE 0.10, 5.4 × 10(-4)) and right (coefficient +0.39, SE 0.10, P = 1.2 × 10(-4)) inferior frontal gyri pars orbitalis. These associations were unchanged after accounting for age, sex, education, depression, cognitive function, and a number of medical comorbidities.<h4>Conclusions</h4>Lower cortical gray matter volume in the lateral orbitofrontal cortex and inferior frontal gyrus pars orbitalis is associated with greater sleep fragmentation in older community-dwelling adults. Further work is needed to clarify whether this is a consequence of or contributor to sleep fragmentation.<h4>Commentary</h4>A commentary on this article appears in this issue on page 15.
Project description:Introduction:Self-referential processing is a key component of the emotional self-concept. Previous studies have shown that emotional self-referential processing is related to structure and function of cortical midline areas such as medial prefrontal cortex (mPFC), and that it can be altered on a behavioral level by specific mental training practices. However, it remains unknown how behavioral training-related change in emotional self-concept content relates to structural plasticity. Methods:To address this issue, we examined the relationship between training-induced change in participant's emotional self-concept measured through emotional word use in the Twenty Statement Test and change in cortical thickness in the context of a large-scale longitudinal mental training study called the ReSource Project. Results:Based on prior behavioral findings showing increased emotional word use particularly after socio-cognitive training targeting perspective-taking capacities, this study extended these results by revealing that individual differences in the degree to which participants changed their emotional self-concept after training was positively related to cortical thickness change in right mPFC extending to dorsolateral PFC (dlPFC). Furthermore, increased self-related negative emotional word use after training was positively associated with cortical thickness change in left pars orbitalis and bilateral dlPFC. Conclusions:Our findings reveal training-related structural brain change in regions known to be involved in self-referential processing and cognitive control, and could indicate a relationship between restructuring of the emotional self-concept content as well as reappraisal of negative aspects and cortical thickness change. As such, our findings can guide the development of psychological interventions targeted to alter specific facets of the self-concept.
Project description:Genetic predisposition and brain structural abnormalities have been shown to be involved in the biological underpinnings of anorexia nervosa (AN). Prefrontal brain regions are suggested to contribute through behavioral inhibition mechanisms to body weight. However, it is unknown if and to which extent biological correlates for AN might be present in individuals without clinical AN symptomatology. We therefore investigated the contribution of polygenic load for AN on body weight and prefrontal brain structure in a sample of n?=?380 nonclinical individuals. A polygenic score (PGS) reflecting the individual genetic load for the trait of anorexia nervosa was calculated. Structural MRI data were acquired and preprocessed using the cortical parcellation stream of FreeSurfer. We observed a significant PGS?×?sex interaction effect on body mass index (BMI), which was driven by a negative correlation between PGS and BMI in female participants. Imaging analyses revealed significant interaction effects of sex??×?PGS on surface area of the lateral orbitofrontal cortex (OFC), the pars orbitalis (PO), the rostral middle frontal gyrus (RMF) and the pars triangularis (PT) of the left frontal cortex. The interaction effects were driven by positive correlations between PGS and prefrontal surface areas in female participants and negative correlations in male participants. We furthermore found sex-specific associations between BMI and left RMF surface area as well as between BMI and left PO and left RMF thickness. Our findings demonstrate a sex-specific association between polygenic load for AN, BMI, and prefrontal brain structure in nonclinical individuals. Hence, this study identifies structural abnormalities associated with polygenic load for AN and BMI in brain regions deeply involved in behavioral inhibition and impulse regulation as candidate brain regions for future research.
Project description:Childhood maltreatment is associated with posttraumatic stress disorder (PTSD) and elevated rates of adolescent and adult psychopathology including major depression, bipolar disorder, substance use disorders, and other medical comorbidities. Gray matter volume changes have been found in maltreated youth with (versus without) PTSD. However, little is known about the alterations of brain structural covariance network topology derived from cortical thickness in maltreated youth with PTSD. High-resolution T1-weighted magnetic resonance imaging scans were from demographically matched maltreated youth with PTSD (N?=?24), without PTSD (N?=?64), and non-maltreated healthy controls (n?=?67). Cortical thickness data from 148 cortical regions was entered into interregional partial correlation analyses across participants. The supra-threshold correlations constituted connections in a structural brain network derived from four types of centrality measures (degree, betweenness, closeness, and eigenvector) estimated network topology and the importance of nodes. Between-group differences were determined by permutation testing. Maltreated youth with PTSD exhibited larger centrality in left anterior cingulate cortex than the other two groups, suggesting cortical network topology specific to maltreated youth with PTSD. Moreover, maltreated youth with versus without PTSD showed smaller centrality in right orbitofrontal cortex, suggesting that this may represent a vulnerability factor to PTSD following maltreatment. Longitudinal follow-up of the present results will help characterize the role that altered centrality plays in vulnerability and resilience to PTSD following childhood maltreatment.
Project description:Meta-analysis of voxel-based morphometry dyslexia studies and direct analysis of 293 reading disability and control cases from six different research sites were performed to characterize defining gray matter features of reading disability. These analyses demonstrated consistently lower gray matter volume in left posterior superior temporal sulcus/middle temporal gyrus regions and left orbitofrontal gyrus/pars orbitalis regions. Gray matter volume within both of these regions significantly predicted individual variation in reading comprehension after correcting for multiple comparisons. These regional gray matter differences were observed across published studies and in the multisite dataset after controlling for potential age and gender effects, and despite increased anatomical variance in the reading disability group, but were not significant after controlling for total gray matter volume. Thus, the orbitofrontal and posterior superior temporal sulcus gray matter findings are relatively reliable effects that appear to be dependent on cases with low total gray matter volume. The results are considered in the context of genetics studies linking orbitofrontal and superior temporal sulcus regions to alleles that confer risk for reading disability.