Demographically-adjusted norms are used to enhance accuracy of inferences based on neuropsychological assessment. However, we hypothesized that predictive accuracy regarding complex real-world activities is diminished by demographic corrections. Driving performance was assessed with a standardized on-road test in participants aged 65+ (24 healthy elderly, 26 Alzheimer’s disease, 33 Parkinson’s disease). Neuropsychological measures included Trailmaking A and B, Complex Figure, Benton Visual Retention, and Block Design tests. A multiple regression model with raw neuropsychological scores was significantly predictive of driving errors (R2 = .199, p <.005); a model with demographically-adjusted scores was not (R2 = .113, p >.10). Raw scores were more highly correlated than adjusted scores with each neuropsychological measure, and among both healthy elderly and Parkinson’s patients. Demographic corrections diminished predictive accuracy for driving performance, extending findings of Silverberg and Millis (2009) that competency in complex real-world activities depends on ability levels, regardless of demographic considerations.

Posttraumatic stress disorder (PTSD) has been linked to deficits in response inhibition, and neuroimaging research suggests this may be due to differences in prefrontal cortex recruitment. The current study examined relationships between PTSD from intimate partner violence (IPV) and neural responses during inhibition. There were 10 women with PTSD from IPV and 12 female control subjects without trauma history who completed the stop signal task during functional magnetic resonance imaging. Linear mixed models were used to investigate group differences in activation (stop-nonstop and hard-easy trials). Those with PTSD exhibited greater differential activation to stop-nonstop trials in the right dorsolateral prefrontal cortex and the anterior insula and less differential activation in several default mode regions (d = 1.12-1.22). Subjects with PTSD exhibited less differential activation to hard-easy trials in the lateral frontal and the anterior insula regions (driven by less activation to hard trials) and several default mode regions (i.e., medial prefrontal cortex, posterior cingulate; driven by greater activation to easy trials; d = 1.23-1.76). PTSD was associated with difficulties disengaging default mode regions during cognitive tasks with relatively low cognitive demand, as well as difficulties modulating executive control and salience processing regions with increasing cognitive demand. Together, these results suggest that PTSD may relate to decreased neural flexibility during inhibition.

Objective The goals of this study were to determine the relationship between anxious symptoms and cognitive functioning in a non-demented, community-dwelling elderly sample (N = 48), and to determine the effect of depressive symptoms upon this relationship. Methods Anxious and depressive symptoms were assessed using Symptom Checklist 90-Revised. Cognitive functioning was assessed with the Repeatable Battery for the Assessment of Neuropsychological Status. Results Results indicated that while both cognitive functioning and anxious symptoms were within normal limits in this sample, anxious symptoms showed a significant, inverse relationship with global cognitive function [r(47) = −.400, p = .005]. In addition, specific relationships were noted between severity of anxious symptoms and visuospatial/constructional ability as well as immediate and delayed memory. With regard to the secondary objective, both anxiety and depressive symptoms together accounted for the highest level of variance [R2 = .175, F(2, 45) = 4.786, p = .013] compared to anxiety [R2(47) = .160, p = .005] and depression [R2(47) = .106, p = .024] alone. Nevertheless, neither anxious nor depressive symptoms emerged as a unique correlate with cognitive ability [r(47)= −.278, p = .058; r(48)= −.136, p = .363, respectively]. Conclusion This study demonstrates that subthreshold anxiety symptoms and cognitive functioning are significantly related even among generally healthy older adults whose cognitive ability and severity of anxious symptoms are within broad normal limits. These findings have implications both for clinical care of elderly patients, as well as for cognitive research studies utilizing this population.

Objective Anxiety predicts cardiovascular events, though the mechanism remains unclear. We hypothesized that anxious symptoms will correlate with impaired resistance and conduit vessel function in participants aged 55–90 years. Method Anxious symptoms were measured with the Symptom Checklist-90-Revised in 89 participants with clinically diagnosed atherosclerotic cardiovascular disease and 54 healthy control participants. Vascular function was measured in conduit arteries using brachial flow-mediated dilatation (FMD) and in forearm resistance vessels (FRV) using intra-arterial drug administration and plethysmography. Results Anxious symptoms were not associated with FMD in either group. Participants with atherosclerosis exhibited significant inverse associations of anxious symptoms with FRV dilatation (β for acetylcholine =−0.302, p=0.004). Adjustment for medication, risk factors and depressive symptoms did not alter the association between anxiety and FRV dysfunction, except for BMI (anxiety β=−0.175, p=0.060; BMI β=−0.494, p<0.001). While BMI was more strongly associated with FRV function than anxiety, combined BMI and anxiety accounted for more variance in FRV function than either separately. Control participants showed no association of anxiety with FRV function. Conclusion Anxiety is uniquely and substantially related to poorer resistance vessel function (both endothelial and vascular smooth muscle function) in individuals with atherosclerosis. These relationships were independent of medication, depression and cardiovascular risk factors, with the exception of BMI. These findings support the concept that anxiety potentially increases vascular events through worsening of vascular function in atherosclerotic disease.