Examining the predictive potential of depressed mood and alcohol misuse on risky driving.

AIMS: Male driving while impaired (DWI) offenders are at heightened risk for engaging in risky driving. Males in a depressed mood are also more prone to alcohol misuse, which may further contribute to risky driving. This manuscript investigates the predictive potential of combined depressed mood and alcohol misuse on risky driving outcomes 3 and 9 years after baseline in male DWI offenders. METHODS: At baseline, participants completed questionnaires assessing depressed mood (Major Depression scale of the Millon Clinical Multiaxial Inventory-III), alcohol misuse (Alcohol Use Disorders Identification Test), and sensation-seeking (Sensation Seeking Scale-V). Risky driving data (Analyse des comportements routiers; ACR3) were collected at follow-up 3 years after baseline. Driving offence data were obtained for 9 years after baseline. RESULTS: There were 129 participants. As 50.4% of the sample were missing ACR3 scores, multiple imputation was conducted. In the final regression model, R2 = 0.34, F(7,121) = 8.76, P < 0.001, alcohol misuse significantly predicted ACR3, B = 0.56, t = 1.96, P = 0.05. Depressed mood, however, did not significantly predict ACR3 and sensation-seeking was not a significant moderator. Although the regression model predicting risky driving offences at Year 9 was significant R2 = 0.37, F(10,108) = 6.41, P < 0.001, neither depressed mood nor alcohol misuse was a significant predictor. CONCLUSIONS: These findings identify alcohol misuse as a predictor of risky driving 3 years after baseline among male DWI offenders. This enhances our prediction of risky driving, extending beyond the widely researched acute impacts of alcohol by exploring chronic patterns.

Cerebral Amyloid Angiopathy Is Associated With Executive Dysfunction and Mild Cognitive Impairment.

BACKGROUND AND PURPOSE: Autopsy studies suggest that cerebral amyloid angiopathy (CAA) is associated with cognitive impairment and risk for dementia. We analyzed neuropsychological test data from a prospective cohort study of patients with CAA to identify the prevalence of cognitive impairment and its associations with brain magnetic resonance imaging features and the apolipoprotein E genotype. METHODS: Data were analyzed from 34 CAA, 16 Alzheimer's disease, 69 mild cognitive impairment, and 27 ischemic stroke participants. Neuropsychological test results were expressed as z scores in relation to normative data provided by the test manuals and then grouped into domains of memory, executive function, and processing speed. RESULTS: Mean test scores in CAA participants were significantly lower than norms for memory (-0.44±1.03; P=0.02), executive function (-1.14±1.07; P<0.001), and processing speed (-1.06±1.12; P<0.001). Twenty-seven CAA participants (79%) had mild cognitive impairment based on low cognitive performance accompanied by cognitive concerns. CAA participants had similarly low executive function scores as Alzheimer's disease, but relatively preserved memory. CAA participants' scores were lower than those of ischemic stroke controls for executive function and processing speed. Lower processing speed scores in CAA were associated with higher magnetic resonance imaging white matter hyperintensity volume. There were no associations with the apolipoprotein E ε4 allele. CONCLUSIONS: Mild cognitive impairment is very prevalent in CAA. The overall cognitive profile of CAA is more similar to that seen in vascular cognitive impairment rather than Alzheimer's disease. White matter ischemic lesions may underlie some of the impaired processing speed in CAA.