We could not demonstrate cognitive effects of an intensive risk factor intervention at one-year poststroke. Longer follow-up and a more heterogeneous study sample might have lead to larger effects. More effective methods for managing the risk of further cognitive decline after stroke are needed.
Background: Post-stroke dementia is defined as any dementia occurring after stroke, and includes vascular, degenerative and mixed dementia. The aim of this study was to assess the incidence of dementia and mild cognitive impairment (MCI) one year after stroke in a population free from pre-stroke cognitive decline, and to investigate the different aetiological subtypes of post-stroke dementia and MCI, using a novel method of subclassification in order to separate vascular causes of MCI or dementia from a neurodegenerative disease. Methods: All patients with a first-ever stroke and TIA admitted to the stroke unit of Asker and Bærum Hospital were invited. After 12 months, dementia and MCI were diagnosed. Sub-classification was made using MRI findings, the results of biomarkers in cerebrospinal fluid and the patients’ clinical cognitive profile. Results: 36 (19.6%) patients developed dementia during the first year after stroke and 69 (37.5%) developed MCI. Fourteen (13.3%) were diagnosed as suffering from degenerative cognitive disease, 34 (32.4%) from vascular cognitive disease, and 57 (54.3%) from mixed disease. Conclusion: Fifty-seven percent suffered from cognitive impairment one year after stroke and only one third from isolated vascular cognitive disease. Post-stroke cognitive impairment is complex with a high coexistence of vascular and degenerative changes.
A structured, multidisciplinary, multifactorial risk factor program including vascular risk factor management may be associated with reduced HADS scores and a lower prevalence of depressive symptoms one year after stroke.
Background/Aim: Post-stroke cognitive impairment and dementia may be caused by pure vascular, pure degenerative or mixed disease. The relation between post-stroke cognitive impairment and the combination of vascular pathology and degenerative changes is less evaluated. We aimed to evaluate the associations between white matter lesions (WMLs) and patient performance 1 year after stroke on tests of executive functioning, memory and visuospatial function, adjusted for the effects of lifestyle and disease-related factors, including medial temporal lobe atrophy (MTLA). Methods: Patients with a first-ever stroke or transient ischemic attack were invited to participate in the study. The associations between the cognitive test performances and WMLs were studied using linear regression [Trail Making Test B (TMT B) and 10-word test] and logistic regression (Clock Drawing Test). Results: In total, 199 patients completed the follow-up. The TMT B (p = 0.029) and the 10-word test (p = 0.014) were significantly associated with WMLs; however, the Clock Drawing Test (p = 0.19) was not. The TMT B (p = 0.018) and the 10-word test (p ≤ 0.001) were both significantly associated with MTLA. Conclusion: Impaired executive functioning and memory are significantly associated with WMLs and MTLA. The mechanisms explaining post-stroke cognitive impairment are multifactorial, including different types of vascular pathology and coexisting vascular and degenerative changes.
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