Patterns of change in cortical morphometry following traumatic brain injury in adults.

Progressive cortical volumetric loss following moderate-severe traumatic brain injury (TBI) has been observed; however, regionally specific changes in the structural determinants of cortical volume, namely, cortical thickness (CT) and cortical surface area (CSA), are unknown and may inform the patterns and neural substrates of neurodegeneration and plasticity following injury. We aimed to (a) assess differences in CT and CSA between TBI participants and controls in the early chronic stage post-injury, (b) describe longitudinal changes in cortical morphometry following TBI, and (c) examine how regional changes in CT and CSA are associated. We acquired magnetic resonance images for 67 participants with TBI at up to 4 time-points spanning 5 months to 7 years post-injury, and 18 controls at 2 time-points. In the early chronic stage, TBI participants displayed thinner cortices than controls, predominantly in frontal regions, but no CSA differences. Throughout the chronic period, TBI participants showed widespread CT reductions in posterior cingulate/precuneus regions and moderate CT increase in frontal regions. Additionally, CSA showed a significant decrease in the orbitofrontal cortex and circumscribed increase in posterior regions. No changes were identified in controls. Relationships between regional cortical changes in the same morphological measure revealed coordinated patterns within participants, whereas correlations between regions with CT and CSA change yielded bi-directional relationships. This suggests that these measures may be differentially affected by neurodegenerative mechanisms such as transneuronal degeneration following TBI and that degeneration may be localized to the depths of cortical sulci. These findings emphasize the importance of dissecting morphometric contributions to cortical volume change.

The Effect of Congenital and Acquired Bilateral Anophthalmia on Brain Structure.

The aim of this study was to compare the pattern of changes in brain structure resulting from congenital and acquired bilateral anophthalmia. Brain structure was investigated using 3T magnetic resonance imaging (MRI) in Oxford (congenital) or Manchester (acquired). T1-weighted structural and diffusion-weighted scans were acquired from people with anophthalmia and sighted control participants. Differences in grey matter between the groups were quantified using voxel-based morphometry and differences in white matter microstructure using tract-based spatial statistics. Quantification of optic nerve volume and cortical thickness in visual regions was also performed in all groups. The optic nerve was reduced in volume in both anophthalmic populations, but to a greater extent in the congenital group and anophthalmia acquired at an early age. A similar pattern was found for the white matter microstructure throughout the occipitotemporal regions of the brain, suggesting a greater reduction of integrity with increasing duration of anophthalmia. In contrast, grey matter volume changes differed between the two groups, with the acquired anophthalmia group showing a decrease in the calcarine sulcus, corresponding to the area that would have been peripheral primary visual cortex. In contrast, the acquired anophthalmia group showed a decrease in grey matter volume in the calcarine sulcus corresponding to the area that would have been peripheral primary visual cortex. There are both qualitative and quantitative differences in structural brain changes in congenital and acquired anophthalmia, indicating differential effects of development and degeneration.

Face processing in ADHD: A review of the N170 event-related potential.

Attention-deficit hyperactivity disorder (ADHD) is associated with deficits in social functioning, including peer difficulties and poor relationship quality. Little is known, however, about the integrity of foundational sociocognitive abilities that support interpersonal interactions in ADHD. Face processing-a fundamental component of social cognition-has been a popular topic of recent investigations in this area. Researchers have attempted to delineate face processing mechanisms in ADHD to elucidate social deficits often seen in the disorder. Investigating the N170 event-related potential, a neural marker of face processing, has been a popular approach in this endeavour. Here, we present two accounts that offer competing views of how social deficits might arise in those with ADHD. Next, we systematically review and synthesise the literature on the N170 in ADHD to identify whether atypicalities in sociocognitive domains like face processing occur in this patient population. Gaps in the literature are identified and concrete solutions are offered to improve future research in this area. We end by discussing immediate implications for treatment approaches designed to address widely observed social deficits in individuals with ADHD. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Global executive dysfunction, not core executive skills, mediate the relationship between adversity exposure and later health in undergraduate students.

Executive function (EF) represents a set of higher-order cognitive skills that permit engagement in goal-oriented behavior. EF deficits are associated with wide-ranging negative health-related consequences, including psychopathology and engagement in risky health-related behaviors. Because neural substrates supporting EF develop over a protracted period of time, an extended window of vulnerability exists whereby environmental stressors can interrupt development, culminating in lifelong EF deficits. We capitalized on this understanding of the vulnerability of EF-relevant neural structures to elucidate the link between adverse childhood experiences (ACEs) and early mortality. ACEs are highly prevalent in the general population and exert negative downstream implications for many health-related behaviors, ultimately hastening mortality. However, underlying mechanisms linking ACEs with poor health remain less understood. To address this gap in the literature, we assessed ACE history and health factors, including psychopathology and risky alcohol use behaviors in undergraduates. We further assessed EF using performance-based and rating scale measures. Results revealed that some measures of EF mediated the relationship between ACEs and current mental health, but EF did not mediate the association between ACEs and engagement in risky health-related behaviors. These results partially support a neurodevelopmental model of ACE exposure vis-à-vis future health, focusing on the role of EF.

How do adverse childhood experiences impact health? Exploring the mediating role of executive functions.

Objective: Adverse childhood experiences (ACEs) are stressful life events that occur during development. It is well-established that ACE exposure has negative downstream implications for a broad range of health-related behaviors, ultimately hastening mortality. Underlying mechanisms linking the experience of early life adversity with poor health remain less understood, however, and thus potential targets for intervention remain elusive. This work seeks to fill an important theoretical gap in the ACE literature by evaluating whether executive functions (EFs) constitute a biologically plausible mediating mechanism in this causal pathway. Methods: Two separate studies were conducted. In Study 1, undergraduate students completed measures of ACE exposure, EF, health-risk behaviors (e.g., drug and alcohol use, unsafe sexual practices), and psychopathology (e.g., anxiety, depression). Study 2 sought to replicate this work in a community sample. Results: Multivariate modeling determined that executive dysfunction in daily life mediated the relationship between childhood adversity exposure and mental health concerns but not the effect between ACEs and health-risk behaviors in an undergraduate sample. In a community sample, EF difficulties in daily life mediated the relationship between ACEs and both psychopathology symptoms and health-risk behavior, but not physical health status. Conclusions: These results partially support a neurodevelopmental model of ACE exposure vis-à-vis future health, focusing on the role of EF. (PsycInfo Database Record (c) 2021 APA, all rights reserved).