Tractography based on diffusion tensor imaging (DTI) allows visualization of white matter tracts. In this study, protocols to reconstruct eleven major white matter tracts are described. The protocols were refined by several iterations of intra-and inter-rater measurements and identification of sources of variability. Reproducibility of the established protocols was then tested by raters who did not have previous experience in tractography. The protocols were applied to a DTI database of adult normal subjects to study size, fractional anisotropy (FA), and T 2 of individual white matter tracts. Distinctive features in FA and T 2 were found for the corticospinal tract and callosal fibers. Hemispheric asymmetry was observed for the size of white matter tracts projecting to the temporal lobe. This protocol provides guidelines for reproducible DTI-based tract-specific quantification.

Impaired imitation of skilled gestures is commonly reported in autism. Questions, however, remain as to whether impaired imitation is associated with a more generalized deficit in performance of gestures consistent with a dyspraxia and whether the pattern of errors differs from that observed in typically developing children. To address these questions, praxis in 21 high-functioning children with autism spectrum disorders (ASD) was compared with 24 typically developing controls using a traditional approach in which performance was evaluated through detailed examination of error types. Children with ASD produced significantly fewer correct responses not only during Gesture to Imitation, but also during Gesture to Command and with Tool Use. The pattern of errors in ASD was similar to that of controls with spatial errors being most common in both groups; however, body-part-for-tool errors were more common in children with ASD, suggesting dyspraxia is not entirely attributable to motor deficits. The findings suggest that autism is associated with a generalized praxis deficit, rather than a deficit specific to imitation. In a developmental disorder such as autism, the findings may reflect abnormalities in frontal0parietal-subcortical circuits important for acquisition (i.e., learning) of sensory representations of movement and0or the motor sequence programs necessary to execute them.

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Health care in the United States has seen many great innovations and successes in the past decades. However, to this day, the color of a person’s skin determines—to a considerable degree—his/her prospects of wellness; risk of disease, and death; and the quality of care received. Disparities in cardiovascular disease (CVD)—the leading cause of morbidity and mortality globally—are one of the starkest reminders of social injustices, and racial inequities, which continue to plague our society. People of color—including Black, Hispanic, American Indian, Asian, and others—experience varying degrees of social disadvantage that puts these groups at increased risk of CVD and poor disease outcomes, including mortality. Racial/ethnic disparities in CVD, while documented extensively, have not been examined from a broad, upstream, social determinants of health lens. In this review, we apply a comprehensive social determinants of health framework to better understand how structural racism increases individual and cumulative social determinants of health burden for historically underserved racial and ethnic groups, and increases their risk of CVD. We analyze the link between race, racism, and CVD, including major pathways and structural barriers to cardiovascular health, using 5 distinct social determinants of health domains: economic stability ; neighborhood and physical environment ; education ; community and social context ; and healthcare system . We conclude with a set of research and policy recommendations to inform future work in the field, and move a step closer to health equity.