Thickness In Brain Regions Research Articles

Susceptibility or resilience to childhood peer abuse can be explained by cortical thickness in brain regions involved in emotional regulation

Experiencing peer abuse in childhood can damage mental health, but some people exhibit resilience against these negative outcomes. However, it remains uncertain which specific changes in brain structures are associated with this type of resilience. We categorized 217 participants into three groups: resilience group, susceptibility group, and healthy control group, based on their experiences of peer abuse and mental health problems. They underwent MRI scans to measure cortical thickness in various brain regions of the prefrontal cortex. We employed covariance analysis to compare cortical thickness among these groups. Individuals who resilient to anxiety exhibited smaller cortical thickness in the bilateral inferior frontal gyrus (IFG), and with larger thickness in the right medial orbitofrontal cortex (mOFC), while those resilient to stress was associated with smaller thickness in both the bilateral IFG and bilateral middle frontal gyrus (MFG). These findings deepen our understanding of the neural mechanisms underlying resilience and offer insight into improving individual resilience.

Remote cortical atrophy and language outcomes after chronic left subcortical stroke with aphasia.

ObjectiveSubcortical stroke can cause a variety of language deficits. However, the neural mechanisms underlying subcortical aphasia after stroke remain incompletely elucidated. We aimed to determine the effects of distant cortical structures on aphasia outcomes and examine the correlation of cortical thickness measures with connecting tracts integrity after chronic left subcortical stroke.MethodsThirty-two patients and 30 healthy control subjects underwent MRI scanning and language assessment with the Western Aphasia Battery-Revised (WAB-R) subtests. Among patients, the cortical thickness in brain regions that related to language performance were assessed by the FreeSurfer software. Fiber tracts connecting the identified cortical regions to stroke lesions were reconstructed to determine its correlations with the cortical thickness measures across individual patient.ResultsCortical thickness in different parts of the left fronto-temporo-parietal (FTP) regions were positively related to auditory-verbal comprehension, spontaneous speech and naming/word finding abilities when controlling for key demographic variables and lesion size. Cortical thickness decline in the identified cortical regions was positively correlated with integrity loss of fiber tracts connected to stroke lesions. Additionally, no significant difference in cortical thickness was found across the left hemisphere between the subgroup of patients with hypoperfusion (HP) and those without HP at stroke onset.ConclusionsThese findings suggest that remote cortical atrophy independently predicts language outcomes in patients with chronic left subcortical stroke and aphasia and that cortical thinning in these regions might relate to integrity loss of fiber tracts connected to stroke lesions.

Association Between Cerebral Cortical Microinfarcts and Perilesional Cortical Atrophy on 3T MRI.

Cerebral cortical microinfarcts (CMIs) are a novel MRI marker of cerebrovascular disease (CeVD) that predicts accelerated cognitive decline. Presence of CMIs is known to be associated with global cortical atrophy, although the mechanism linking the two is unclear. Our primary objective was to examine the relation between CMIs and cortical atrophy and to establish possible perilesional atrophy surrounding CMIs. Our secondary objective was to examine the role of cortical atrophy in CMI-associated cognitive impairment. Patients were recruited from 2 Singapore memory clinics between December 2010 and September 2013 and included if they received the diagnosis no objective cognitive impairment, cognitive impairment (with or without a history of stroke), or Alzheimer or vascular dementia. Cortical thickness, chronic CMIs, and MRI markers of CeVD were assessed on 3T MRI. Patients underwent cognitive testing. Cortical thickness was compared globally between patients with and without CMIs, regionally within individual patients with CMIs comparing brain regions with CMIs to the corresponding contralateral region without CMIs, and locally within individuals patients in a 50-mm radius of CMIs. Global cortical thickness was analyzed as mediator in the relation between CMI and cognitive performance. Of the 238 patients (mean age 72.5 years, SD 9.1 years) enrolled, 75 had ≥1 CMIs. Patient with CMIs had a 2.1% lower global cortical thickness (B = -0.049 mm, 95% confidence interval [CI] 0.091 to -0.007, p = 0.022) compared to patients without CMIs, after correction for age, sex, education, and intracranial volume. In patients with CMIs, cortical thickness in brain regions with CMIs was 2.2% lower than in contralateral regions without CMIs (B = -0.048 mm [95% CI -0.071 to -0.026], p < 0.001). In a 20-mm radius area surrounding the CMI core, cortical thickness was lower than in the area 20 to 50 mm from the CMI core (mean difference -0.06 mm [-0.10 to -0.02], p = 0.002). Global cortical thickness was a significant mediator in the relationship between CMI presence and cognitive performance as measure with the Mini-Mental State Examination (B = -0.12 [-0.22 to -0.01], p = 0.025). We found cortical atrophy surrounding CMIs, suggesting a perilesional effect in a cortical area many times larger than the CMI core. Our findings support the notion that CMIs affect brain structure beyond the actual lesion site.

Impact of urban environmental exposures on cognitive performance and brain structure of healthy individuals at risk for Alzheimer’s dementia

BackgroundAir quality might contribute to incidence of dementia-related disorders, including Alzheimer’s dementia (AD). The aim of our study is to evaluate the effect of urban environmental exposures (including exposure to air pollution, noise and green space) on cognitive performance and brain structure of cognitively unimpaired individuals at risk for AD. Participants and methodsThe ALFA (ALzheimer and FAmilies) study is a prospective cohort of middle-age, cognitively unimpaired subjects, many of them offspring of AD patients. Cognitive performance was measured by the administration of episodic memory and executive function tests (N = 958). Structural brain imaging was performed in a subsample of participants to obtain morphological information of brain areas, specially focused on cortical thickness, known to be affected by AD (N = 228). Land Use Regression models were used to estimate residential exposure to air pollutants. The daily average noise level at the street nearest to each participant's residential address was obtained from noise maps. For each participant residential green exposure indicators, such as surrounding greenness or amount of green, were generated. General linear models were conducted to assess the association between environmental exposures, cognitive performance and brain structure in a cross-sectional analysis. ResultsNo significant associations were observed between urban environmental exposures and the cognitive composite (p > 0.1). Higher exposure to air pollutants, but not noise, was associated with lower cortical thickness in brain regions known to be affected by AD, especially NO2 (β = −16.4; p = 0.05) and PM10 (β = −5.34; p = 0.05). On the other hand, increasing greenness indicators was associated with greater thickness in these same areas (β = 0.08; p = 0.03). ConclusionIn cognitively unimpaired adults with increased risk for AD, increased exposure to air pollution was suggested to be associated with greater global atrophy and reduced volume and thickness in specific brain areas known to be affected in AD, thus suggesting a potential link between environmental exposures and cerebral vulnerability to AD. Although more research in the field is needed, air pollution reduction is crucial for decreasing the burden of age-related disorders.

Neuroanatomical predictors of L-DOPA response in older adults with psychomotor slowing and depression: A pilot study

Declining function in dopamine circuits is implicated in normal aging and late-life depression (LLD). Dopamine augmentation recently has shown therapeutic promise, but predictors of response are unknown. Depressed elders with slowed gait underwent baseline magnetic resonance imaging (MRI) and [11C]raclopride positron emission tomography (PET). Subjects then received open treatment with carbidopa/levodopa (L-DOPA) for three weeks. Linear regressions examined relationships between baseline MRI measures, [11C]raclopride binding, and behavioral outcomes. Among N=16 participants aged 72.5±6.8 years, higher left superior temporal gyrus volume was associated with higher processing speed at baseline, while cortical thinning in a processing speed network was associated with greater improvement following L-DOPA. Greater volume and cortical thickness in brain regions associated with mobility were associated with higher baseline gait speed. Higher baseline white matter hyperintensity volume predicted less post-L-DOPA improvement on dual task gait speed and IDS-SR scores. Higher [11C]raclopride binding in the associative striatum was associated with cortical thickness in some, but not all, processing speed brain regions, while higher binding in sensorimotor striatum was significantly associated with left caudate volume. Limiting the conclusions drawn from this pilot study are the small sample size and open administration of L-DOPA. Greater baseline brain volumes and cortical thickness in regions supporting cognition and gait were associated with higher behavioral performance, while lower structural integrity was associated with increased responsivity to L-DOPA. If substantiated in larger studies, these findings could facilitate the targeting of dopaminergic treatments to those LLD patients most likely to respond.

ASSOCIATIONS BETWEEN CYTOKINES AND CORTICAL THICKNESS IN PATIENTS WITH LATE-LIFE DEPRESSION

Introduction Late-life depression (LLD), defined as depression that occurs after the age of 60 years, is associated with a poor quality of life, cognitive impairment, and increased morbidity and mortality. Immune factors are now recognized as involved in the pathophysiology of depression. We aimed to evaluate the relationship between plasma cytokine levels and cortical thickness in patients with LLD. Methods Blood samples and structural magnetic resonance imaging scans (Siemens 3T Prisma) were acquired in 29 older adults (≥60 years old) with major depression (62% female; mean age, 70.7 (7.3) years; mean MADRS 15.9 (3.2)). Associations between plasma cytokine levels (log-transformed) and cortical thickness were evaluated in a multivariate analysis using partial least squares. Cytokines with detectable levels in at least 27 of the 29 subjects (exotaxin, IFN-a2, GRO, MDC, IL-12(p70), sCD40L, IL-8, IP-10, MCP-1, MIP-1b, TNF-a, and VEGF) were included in the analysis. Results The first latent variable was significant (accounting for 32% of the cross-block covariance, p=.036) and reflected negative correlations between exotaxin, IL-8, IP-10, MIP-1b, and TNF-a levels and cortical thickness in numerous brain regions, including cingulate, insular, temporal, orbitofrontal, and prefrontal cortices (Figure 1). Conclusions Patients with LLD who have high plasma levels of exotoxin, IL-8, IP-10, MIP-1b, and TNF-a have less cortical thickness in brain regions previously implicated in depression than patients with LLD who have lower levels of these chemokines and pro-inflammatory cytokines. The affected brain regions have functions in self-referential processes, emotional regulation, social cognition, and attentional switching. Thus, the observed reductions in cortical thickness may contribute to the emotional, cognitive, and behavioral disturbances in LLD. Recently, chemokines have been implicated in many neurobiological processes and are considered to play a role in linking peripheral and central inflammation. The present results further support the importance of chemokines and proinflammatory cytokines in depressive pathophysiology. This research was funded by Sponsored by NIMH R01 MH097892, NCCIH AT009198, MH086481; Alzheimer's Research & Prevention Foundation, Allergan, PCORI; Advisory Board: Alzheimer's Research & Prevention Foundation; Royalties for books from Oxford University Press and Hopkins University Press.

Regional estimates of cortical thickness in brain areas involved in control of surgically restored limb movement in patients with tetraplegia

Context/Objective: Spinal cord injury (SCI) causes atrophy of brain regions linked to motor function. We aimed to estimate cortical thickness in brain regions that control surgically restored limb movement in individuals with tetraplegia. Design: Cross-sectional study. Setting: Sahlgrenska University hospital, Gothenburg, Sweden. Participants: Six individuals with tetraplegia who had undergone surgical restoration of grip function by surgical transfer of one elbow flexor (brachioradialis), to the paralyzed thumb flexor (flexor pollicis longus). All subjects were males, with a SCI at the C6 or C7 level, and a mean age of 40 years (range = 31–48). The average number of years elapsed since the SCI was 13 (range = 6–26). Outcome measures: We used structural magnetic resonance imaging (MRI) to estimate the thickness of selected motor cortices and compared these measurements to those of six matched control subjects. The pinch grip control area was defined in a previous functional MRI study. Results: Compared to controls, the cortical thickness in the functionally defined pinch grip control area was not significantly reduced (P = 0.591), and thickness showed a non-significant but positive correlation with years since surgery in the individuals with tetraplegia. In contrast, the anatomically defined primary motor cortex as a whole exhibited substantial atrophy (P = 0.013), with a weak negative correlation with years since surgery. Conclusion: Individuals with tetraplegia do not seem to have reduced cortical thickness in brain regions involved in control of surgically restored limb movement. However, the studied sample is very small and further studies with larger samples are required to establish these findings.

Olfactory dysfunction in Alzheimer's disease– and Lewy body–related cognitive impairment

IntroductionOlfactory dysfunction is common in Alzheimer's disease– and Lewy body–related disorders, but its neural correlates have not been clearly elucidated. MethodsWe retrospectively recruited 237 patients with Alzheimer's disease–related cognitive impairment (ADCI) and 217 with Lewy body–related cognitive impairment (LBCI). They were identically evaluated using the Cross-Cultural Smell Identification Test, neuropsychological tests, and brain magnetic resonance imaging. ResultsLBCI had more severe olfactory dysfunction than ADCI. Patients with more severe cognitive dysfunction had worse olfactory function in both groups. In ADCI, lower Cross-Cultural Smell Identification Test scores correlated with a lower cortical thickness in brain regions typically affected in Alzheimer's disease, most prominently in the right parahippocampal cortex, whereas in LBCI, the scores correlated with white matter abnormalities in regions vulnerable to Lewy body, including subcortical regions of the orbitofrontal and frontoparietal cortices. DiscussionOur results suggest that cortical atrophy in ADCI and white matter abnormalities in LBCI play important roles in olfactory dysfunction.

Concussion History Predicts Reduced Cortical Thickness in Special Operations Forces Personnel

Special Operations Forces (SOF) personnel are at high risk for repetitive blast and head impact exposure. Non-invasive neuroimaging techniques, such as magnetic resonance imaging (MRI), have identified concussion-related structural differences even when observable behavioral and cognitive deficits are absent. The relationship between injury history, neuroimaging, and standard clinical tests has not previously been defined in the SOF population. PURPOSE: To compare cortical morphology, symptom scores, and neurocognition in SOF personnel with and without concussion history. METHODS: SOF personnel completed an assessment battery including 3T high-resolution MRI and the Immediate Postconcussion Assessment and Cognitive Test (ImPACT). We examined symptom reporting and the ImPACT composite scores for verbal and visual memory, visual-motor processing speed, reaction time, and impulse control. The SOF personnel were categorized by self-reported concussion history (no history vs. 1+ concussions). We used FreeSurfer (v6) to reconstruct and segment the cerebral cortex. Cortical thickness was regressed on concussion history controlling for estimated total intracranial volume. The symptom reporting and ImPACT composite scores were regressed on concussion history. RESULTS: We imaged 166 SOF personnel (160 males; 65 self-reported concussion history) using MRI. Of these, 155 completed the ImPACT during a healthy baseline testing session. Two brain regions had reduced cortical thickness associated with concussion history, controlling for the total intracranial volume: left pericalcarine (t164=2.00, p=0.04); and left parahippocampal (t164=2.81, p=0.006). One region had larger cortical thickness in those with a concussion history: right transverse temporal (t164=2.35, p=0.02). Concussion history did not predict symptom or ImPACT composite score differences (p>0.05). CONCLUSIONS: Concussion history predicted cortical thickness in brain regions associated with vision and memory, which are cognitive functions affected following concussive injury. The ImPACT composites were not sensitive to concussion history. Supported by the United States Army Special Operations Command (USASOC)

REGIONAL AV1451 UPTAKE AND CORTICAL THICKNESS IN RELATION TO MEMORY, LANGUAGE AND EXECUTIVE FUNCTIONING IN AMYLOID-POSITIVE SUBJECTS

Tau pathology is thought to spread in a characteristic manner, leading to cell loss and inducing cognitive decline. However, it is unclear to what degree Tau-PET, a marker of neurofibrillary tau pathology (NFT) tracks cognitive symptoms relative to structural MRI, which more directly reflects neuronal injury. In a group of amyloid positive (Ab+) controls, patients with Mild Cognitive Impairment (MCI) and dementia, we investigate the association of memory, language and executive functioning with Tau-PET and MRI-based cortical thickness in brain regions putatively associated with these domains. We included Ab+ individuals, as determined by Florbetapir PET, (10 controls, 14 MCI and 5 dementia patients) from ADNI who had AV1451 Tau-PET, structural MRI and cognitive data within 6 months of each other. Cortical thickness and normalized SUVR from the Tau-PET scans were measured in regions of interest obtained using multi-atlas segmentation. Composite z-scores of delayed recall, recognition, language and executive functioning were calculated, adjusting for age, gender and education using the linear regression equation from 122 Ab- controls from ADNIGO/2. Significant associations of AV1451 uptake in medial temporal lobe (MTL) structures with memory were found (Table 1), but AV1451 uptake did not correlate significantly with language and executive functioning in regions generally considered to support these functions. Cortical thickness measures were significantly associated with all cognitive domains. Stepwise regression analyses showed that mainly structural measures were significant predictors of memory and executive functioning, but AV1451 uptake was also included in the models for memory (Table 2). None of the predictors significantly predicted language in regression models. These preliminary findings show a stronger association of cognitive functioning with structural brain measures than with AV1451 uptake. Perhaps atrophy provides a tighter link with cognitive decline than tau pathology, possibly because NFTs precede the neurodegeneration which produces cognitive impairment and/or because tau pathology does not capture other contributors to loss of neuronal integrity. The more complementary relationship of AV1451 uptake and structural MRI 5 may reflect that in early AD tangle pathology is the primary driver of neuronal integrity in this region, as opposed to language and executive networks.

Mild traumatic brain injury is associated with reduced cortical thickness in those at risk for Alzheimer's disease.

Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for the development of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk. This study examined mild traumatic brain injury and genetic risk as predictors of reduced cortical thickness in brain regions previously associated with early Alzheimer's disease, and their relationship with episodic memory. Participants were 160 Iraq and Afghanistan War veterans between the ages of 19 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorder diagnoses. Whole-genome polygenic risk scores for the development of Alzheimer's disease were calculated using summary statistics from the largest Alzheimer's disease genome-wide association study to date. Results showed that mild traumatic brain injury moderated the relationship between genetic risk for Alzheimer's disease and cortical thickness, such that individuals with mild traumatic brain injury and high genetic risk showed reduced cortical thickness in Alzheimer's disease-vulnerable regions. Among males with mild traumatic brain injury, high genetic risk for Alzheimer's disease was associated with cortical thinning as a function of time since injury. A moderated mediation analysis showed that mild traumatic brain injury and high genetic risk indirectly influenced episodic memory performance through cortical thickness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brain regions is a mechanism for reduced memory performance. Finally, analyses that examined the apolipoprotein E4 allele, post-traumatic stress disorder, and genetic risk for schizophrenia and depression confirmed the specificity of the Alzheimer's disease polygenic risk finding. These results provide evidence that mild traumatic brain injury is associated with greater neurodegeneration and reduced memory performance in individuals at genetic risk for Alzheimer's disease, with the caveat that the order of causal effects cannot be inferred from cross-sectional studies. These results underscore the importance of documenting head injuries even within the mild range as they may interact with genetic risk to produce negative long-term health consequences such as neurodegenerative disease.

Childhood abuse and reduced cortical thickness in brain regions involved in emotional processing.

Alterations in gray matter development represent a potential pathway through which childhood abuse is associated with psychopathology. Several prior studies find reduced volume and thickness of prefrontal (PFC) and temporal cortex regions in abused compared with nonabused adolescents, although most prior research is based on adults and volume-based measures. This study tests the hypothesis that child abuse, independent of parental education, predicts reduced cortical thickness in prefrontal and temporal cortices as well as reduced gray mater volume (GMV) in subcortical regions during adolescence. Structural MRI scans were obtained from 21 adolescents exposed to physical and/or sexual abuse and 37 nonabused adolescents (ages 13-20). Abuse was operationalized using dichotomous and continuous measures. We examined associations between abuse and brain structure in several a priori-defined regions, controlling for parental education, age, sex, race, and total brain volume for subcortical GMV. Significance was evaluated at p<.05 with a false discovery rate correction. Child abuse exposure and severity were associated with reduced thickness in ventromedial prefrontal cortex (PFC), right lateral orbitofrontal cortex, right inferior frontal gyrus, bilateral parahippocampal gyrus (PHG), left temporal pole, and bilateral inferior, right middle, and right superior temporal gyri. Neither abuse measure predicted cortical surface area or subcortical GMV. Bilateral PHG thickness was inversely related to externalizing symptoms. Child abuse, an experience characterized by a high degree of threat, is associated with reduced cortical thickness in ventromedial and ventrolateral PFC and medial and lateral temporal cortex in adolescence. Reduced PHG thickness may be a mediator linking abuse with externalizing psychopathology, although prospective research is needed to evaluate this possibility.

Cortical thickness in relation to clinical symptom onset in preclinical AD.

Mild cognitive impairment (MCI) and Alzheimer's disease (AD) dementia are preceded by a phase of disease, referred to as ‘preclinical AD’, during which cognitively normal individuals have evidence of AD pathology in the absence of clinical impairment. This study examined whether a magnetic resonance imaging (MRI) measure of cortical thickness in brain regions, collectively known as ‘AD vulnerable’ regions, predicted the time to onset of clinical symptoms associated with MCI and whether cortical thickness was similarly predictive of clinical symptom onset within 7 years post baseline versus progression at a later point in time. These analyses included 240 participants from the BIOCARD study, a cohort of longitudinally followed individuals who were cognitively normal at the time of their MRI (mean age = 56 years). Participants have been followed for up to 18 years (M follow-up = 11.8 years) and 50 participants with MRIs at baseline have developed MCI or dementia over time (mean time to clinical symptom onset = 7 years). Cortical thickness in AD vulnerable regions was based on the mean thickness of eight cortical regions. Using Cox regression models, we found that lower mean cortical thickness was associated with an increased risk of progression from normal cognition to clinical symptom onset within 7 years of baseline (p = 0.03), but not with progression > 7 years from baseline (p = 0.30). Lower cortical thickness was also associated with higher levels of phosphorylated tau, measured in cerebrospinal fluid at baseline. These results suggest that cortical thinning in AD vulnerable regions is detectable in cognitively normal individuals several years prior to the onset of clinical symptoms that are a harbinger of a diagnosis of MCI, and that the changes are more likely to be evident in the years proximal to clinical symptom onset, consistent with hypothetical AD biomarker models.

Childhood abuse and reduced cortical thickness in brain regions involved in emotional processing

Childhood abuse and reduced cortical thickness in brain regions involved in emotional processing

Decreased Sensitivity to Thermal Stimuli in Adolescents With Autism Spectrum Disorder: Relation to Symptomatology and Cognitive Ability

Social communication deficits and repetitive behaviors are established characteristics of autism spectrum disorder (ASD) and the focus of considerable study. Alterations in pain sensitivity have been widely noted clinically but remain understudied and poorly understood. The ASD population may be at greater risk for having their pain undermanaged, especially in children with impaired cognitive ability and limited language skills, which may affect their ability to express pain. Given that sensitivity to noxious stimuli in adolescents with ASD has not been systematically assessed, here we measured warm and cool detection thresholds and heat and cold pain thresholds in 20 high-functioning adolescents with ASD and 55 typically developing adolescents using a method-of-limits quantitative sensory testing protocol. Adolescents with ASD had a loss of sensory function for thermal detection (P < .001, both warm and cool detection thresholds) but not pain threshold (P > .05, both heat and cold pain thresholds) in comparison to controls, with no evidence for significant age or sex effects (P > .05). Intelligence quotients and symptomatology were significantly correlated with a loss of some types of thermal perception in the ASD population (ie, warm detection threshold, cool detection threshold, and heat pain threshold; P < .05). Decreased thermal sensitivity in adolescents with ASD may be associated with cognitive impairments relating to attentional deficits. Our findings are consistent with previous literature indicating an association between thermal perception and cortical thickness in brain regions involved in somatosensation, cognition, and salience detection. Further brain-imaging research is needed to determine the neural mechanisms underlying thermal perceptual deficits in adolescents with ASD. PerspectiveWe report quantitative evidence for altered thermal thresholds in adolescents with ASD. Reduced sensitivity to warmth, coolness, and heat pain was related to impaired cognitive ability. Caregivers and clinicians should consider cognitive ability when assessing and managing pain in adolescents with ASD.

Effects of Moderate to Severe Traumatic Brain Injury on Anticipating Consequences of Actions in Adolescents: A Preliminary Study

For this pilot study, we compared performance of 15 adolescents with moderate-severe traumatic brain injury (TBI) to that of 13 typically developing (TD) adolescents in predicting social actions and consequences for avatars in a virtual microworld environment faced with dilemmas involving legal or moral infractions. Performance was analyzed in relation to cortical thickness in brain regions implicated in social cognition. Groups did not differ in number of actions predicted nor in reasons cited for predictions when presented only the conflict situation. After viewing the entire scenario, including the choice made by the avatar, TD and TBI adolescents provided similar numbers of short-term consequences. However, TD adolescents provided significantly more long-term consequences (p = .010). Additionally, for the Overall qualitative score, TD adolescents' responses were more likely to reflect the long-term impact of the decision made (p = .053). Groups differed in relation of the Overall measure to thickness of right medial prefrontal cortex/frontal pole and precuneus, with stronger relations for the TD group (p < .01). For long-term consequences, the relations to the posterior cingulate, superior medial frontal, and precentral regions, and to a lesser extent, the middle temporal region, were stronger for the TBI group (p < .01).