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Objective Most migraineurs develop cutaneous allodynia during migraines, and many have cutaneous sensitization between attacks. Atypical pain modulation via the descending pain system may contribute to this sensitization and allodynia. The objective of this study was to test the hypothesis that compared with non-allodynic migraineurs, allodynic migraineurs have atypical periaqueductal gray ( PAG) and nucleus cuneiformis ( NCF) resting-state functional connectivity (rs-fc) with other pain processing regions. Design Ten minutes resting-state blood-oxygen-level-dependent data were collected from 38 adult migraineurs and 20 controls. Seed-based analyses compared whole-brain rs-fc with PAG and with NCF in migraineurs with severe ictal allodynia ( N = 8) to migraineurs with no ictal allodynia ( N = 8). Correlations between the strength of functional connections that differed between severely allodynic and non-allodynic migraineurs with allodynia severity were determined for all migraineurs ( N = 38). PAG and NCF rs-fc in all migraineurs was compared with rs-fc in controls. Results Migraineurs with severe allodynia had stronger PAG and NCF rs-fc to other brainstem, thalamic, insula and cerebellar regions that participate in discriminative pain processing, as well as to frontal and temporal regions implicated in higher order pain modulation. Evidence that these rs-fc differences were specific for allodynia included: 1) strong correlations between some rs-fc strengths and allodynia severity among all migraineurs; and 2) absence of overlap when comparing rs-fc differences in severely allodynic vs non-allodynic migraineurs with those in all migraineurs vs controls. Conclusion Atypical rs-fc of brainstem descending modulatory pain regions with other brainstem and higher order pain-modulating regions is associated with migraine-related allodynia. [ABSTRACT FROM AUTHOR]

• Drivers with preclinical Alzheimer disease drive more slowly compared to drivers without. • Road diets decrease speed variance between older drivers. • Attentional control partially mediates observed differences in driving speed. The driving populace of the United States is aging. The prevalence of Alzheimer disease (AD) will increase in the coming decades. Road diets (that is, the reallocation of one or more lanes of car traffic to other uses) have been proposed as a modification to increase pedestrian safety, particularly for older adults. In contrast, we considered the impacts of road diets on aging drivers, and on those with early pathological accumulation of AD. We observed naturalistic driving data for 60 cognitively normal older drivers (Age Range = 62–87 years, Median = 75 years) driving across three road segments located in the St. Louis metropolitan area, Missouri, United States. We used neuroimaging and lumbar puncture derived biomarker data to determine which of the drivers had preclinical AD. Since previous AD studies identified a variety of changes in driving behavior among older drivers with preclinical AD, we examined driving speed before and after lane repurposing. We found that drivers with preclinical AD drove at lower speeds compared to those without preclinical AD prior to road diet implementation. After lanes were repurposed, there was no statistical difference in the speed between older drivers with and without preclinical AD. We evaluated cognitive performance and found that attentional control had a mediating effect on driver speed, suggesting that an individual's ability to focus on a specific task and filter out distractions was associated with faster driving. Driving speed after lane repurposing is not mediated by attentional control, suggesting that road diets are impervious to individual driver capacity. We conclude that lane repurposing has potential as an important mobility infrastructure solution that could enhance older driver safety and facilitate aging in place. [ABSTRACT FROM AUTHOR]

Objectives: The present study explored relationships among personality, Alzheimer's disease (AD) biomarkers, and dementia by addressing the following questions: (1) Does personality discriminate healthy aging and earliest detectable stage of AD? (2) Does personality predict conversion from healthy aging to early-stage AD? (3) Do AD biomarkers mediate any observed relationships between personality and dementia status/conversion?, Methods: Both self- and informant ratings of personality were obtained in a large well-characterized longitudinal sample of cognitively normal older adults (N = 436) and individuals with early-stage dementia (N = 74). Biomarkers included amyloid imaging, hippocampal volume, cerebral spinal fluid (CSF) Aβ42, and CSF tau., Results: Higher neuroticism, lower conscientiousness, along with all four biomarkers strongly discriminated cognitively normal controls from early-stage AD individuals. The direct effects of neuroticism and conscientiousness were only mediated by hippocampal volume. Conscientiousness along with all biomarkers predicted conversion from healthy aging to early-stage AD; however, none of the biomarkers mediated the relationship between conscientiousness and conversion. Conscientiousness predicted conversion as strongly as the biomarkers, with the exception of hippocampal volume., Conclusions: Conscientiousness and to a lesser extent neuroticism serve as important independent behavioral markers for AD risk.

A clinical consequence of symptomatic Alzheimer's disease (AD) is impaired driving performance. However, decline in driving performance may begin in the preclinical stage of AD. We used a naturalistic driving methodology to examine differences in driving behavior over one year in a small sample of cognitively normal older adults with ( n = 10) and without ( n = 10) preclinical AD. As expected with a small sample size, there were no statistically significant differences between the two groups, but older adults with preclinical AD drove less often, were less likely to drive at night, and had fewer aggressive behaviors such as hard braking, speeding, and sudden acceleration. The sample size required to power a larger study to determine differences was calculated.

Introduction: Traumatic brain injury (TBI) is a leading cause of death and disability in children. Metabolic failure is an integral component of the pathological aftermath of TBI. The oxygen extraction fraction (OEF) is a valuable parameter for characterization and description of metabolic abnormalities; however, OEF measurement has required either invasive procedures or the use of ionizing radiation, which significantly limits its use in pediatric research., Results: Patients with TBI had depressed OEF levels that correlated with the severity of injury. In addition, the OEF measured within 2 weeks of injury was predictive of patient outcome at 3 mo after injury. In pediatric TBI patients, low OEF-a marker of metabolic dysfunction-correlates with the severity of injury and outcome., Discussion: Our findings support previous literature on the role of metabolic dysfunction after TBI., Methods: Using a recently developed magnetic resonance (MR) technique for the measurement of oxygen saturation, we determined the whole-brain OEF in both pediatric TBI patients and in healthy controls. Injury and outcome were classified using pediatric versions of the Glasgow Coma Scale (GCS) and Glasgow Outcome Scale-Extended (GOS-E), respectively.