A diagnosis of dementia implies the eventual need to relinquish driving. This is associated with significant morbidity and anticipating when it will need to occur can be important for planning. Patients, however, vary in the course of their disease. We sought to identify predictors of driving cessation in patients with dementia, including both baseline characteristics and changes in cognition and function over time as indicators of disease trajectory. A total of 779 patients with dementia were recruited from 9 memory clinics around Australia. Patients and their carers reported their driving status and completed measures of dementia severity, cognition, function, neuropsychiatric symptoms, and medication use at regular intervals over a 3-year period. Of the 247 patients still driving at baseline, 147 (59.5%) stopped driving during the study. Variables that predicted driving cessation included older age; female sex; greater dementia severity and cognitive and functional impairments at baseline; and greater increases in dementia severity and cognitive and functional impairments over 3 and 6 month periods. The findings confirm that easily assessable characteristics, including changes over time, predict future driving status. The findings underscore the value of regularly assessing patients with standardized measures to determine disease trajectory and likely prognosis
*Dementia Centre for Research Collaboration, UNSW Sydney
†Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, NSW
‡University of Melbourne Academic Unit for Psychiatry of Old Age
§National Ageing Research Institute, Melbourne
∥Austin Hospital, Heidelberg, Vic., Australia
M.H.C. analyzed the data and drafted the manuscript. H.B., D.A., and M.W. conceptualized and designed the overall PRIME study, while H.B. and M.H.C. conceptualized this study.
The Dementia Centre for Research Collaboration is funded by the National Health and Medical Research Council. Data collection was funded in part by Janssen-Cilag Pty Limited. Janssen-Cilag had no input into the design, execution, analysis, interpretation, or writing of this study.
In the last 3 years, D.A. has received grants/funds for clinical trials from Eli Lilly and PranaBio, honoraria from Lundbeck, Pfizer, and Servier. He has been a consultant for PranaBio’s data safety monitoring board. He has received royalties for edited books from Cambridge University Press and Hodder. He has attended advisory board meetings of Eli Lilly. M.W. has worked on drug trials funded by pharmaceutical companies including AbbiVie, Astra Zeneca, AZ therapies, Biogen, Buck, Eisai, Janssen, Lilly, Lundbeck, Merck/MSD, Novartis, Pfizer, Roche, Servier, Takeda, Tau Rx, vTv Therapeutics and Zinfandel. He has received honoraria for consultancy or presentations at meetings organized by CogRx, Lundbeck, Merk Sharp & Dohme, Novartis, and Nutricia. H.B. has worked on drug trials for patients with mild cognitive impairment and Alzheimer disease sponsored by Sanofi-Aventis, Servier and Tau Therapeutics. He has also been a consultant and/or advisory board member for Eli Lilly and Nutricia. M.H.C. declares no conflicts of interest.
Reprints: Henry Brodaty, MBBS, MD, DSc, Dementia Collaborative Research Centre, Level 3, AGSM Building (G27), University of New South Wales, Sydney, NSW 2052, Australia (e-mail: firstname.lastname@example.org).
Received April 19, 2017
Accepted August 23, 2017