• Perminder S Sachdev, Darren M Lipnicki, John D Crawford, Wei Wen, and Henry Brodaty.
• Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, Australia Primary Dementia Collaborative Research Centre, University of New South Wales, Sydney, Australia Neuropsychiatric Institute, Prince of Wales Hospital, Sydney, Australia.
• J. Neurol. Neurosurg. Psychiatr.. 2014 Dec 1;85(12):1324-30.

ObjectivesTo examine how cognitive deficits progress in the years following a stroke or transient ischaemic attack (TIA).MethodsA follow-up study, with neuropsychological and MRI assessments undertaken 3 years after baseline assessments made 3-6 months poststroke in 183 stroke/TIA patients and 97 healthy controls participating in the Sydney Stroke Study. Additional measures included cardiovascular risk factors and apolipoprotein E (APOE) genotype.ResultsStroke/TIA patients had poorer cognitive function and more vascular risk factors than controls at baseline, but did not show greater decline in cognitive function over 3 years except for verbal memory. Patients with a subsequent stroke/TIA showed greater decline in global cognitive function and a number of domains. Rates of incident dementia were 5.9% per year in patients and 0.4% in controls. Both groups showed increased atrophy of the hippocampus, amygdala and whole brain, and an increase in white matter hyperintensities over 3 years; whole brain atrophy was greater in patients. Cognitive decline was greater in women and in those with smaller hippocampi at baseline. For patients without a subsequent stroke/TIA, those with smaller hippocampi or the APOE ε4 allele had greater global cognitive and verbal memory decline.ConclusionsIn poststroke patients, cognitive decline was not greater than in comparison subjects, except for verbal memory, unless they had another stroke/TIA. However, dementia incidence was higher in patients, as might be expected from their poorer baseline cognitive functioning. Smaller hippocampi were associated with an increased risk of decline in memory, and APOE ε4 was a risk factor in those without a subsequent stroke/TIA.Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

33 keywords...

hide…