Change in cognition following ischaemic stroke and transient ischaemic attack (original) (raw)

Yan, Wenci, Quinn, Terence ORCID: https://orcid.org/0000-0003-1401-0181, McConnachie, Alex ORCID: https://orcid.org/0000-0002-7262-7000, Broomfield, Niall, Wong, Yun, Dickie, David ORCID: https://orcid.org/0000-0002-9443-8403, Forbes, Kirsten, Walters, Matthew ORCID: https://orcid.org/0000-0001-5743-5871 and Dawson, Jesse ORCID: https://orcid.org/0000-0001-7532-2475(2025) Change in cognition following ischaemic stroke and transient ischaemic attack.Annals of Clinical and Translational Neurology, (doi: 10.1002/acn3.70192) (PMID:41090322) (PMCID:PMC12588654) (Early Online Publication)

Abstract

Objective: Cognitive decline can occur following ischaemic stroke. How cognition changes over time and associations with cognitive change are poorly understood. This study aimed to explore these issues over 2 years following ischaemic stroke. Methods: This analysis used data from the XILO-FIST study, a clinical trial of allopurinol versus placebo in people with ischaemic stroke according to Tissue-Based Definition. Participants underwent clinical assessment, brain MRI at baseline, and Montreal Cognitive Assessment (MoCA) at baseline, year 1 and year 2. We defined cognitive impairment as a MoCA score <26 and cognitive change as a difference in MoCA score of 2 points or more at year 1 or year 2 after randomisation. Associations with cognitive impairment and cognitive change were assessed by univariable analysis and multiple logistic regression. Results: Three hundred and sixty participants with complete MoCA data were included. Mean age was 65.4 (SD 8.36) years, and mean baseline MoCA score was 26.4 (SD 2.7). Seventy-seven participants had second-year cognitive improvement. Eightyfour had second-year cognitive decline. After adjustment for age and education year, second-year cognitive improvement was associated with smaller brain volume, lower albumin level, smoking and greater white-matter hyperintensity, and second-year cognitive decline was associated with peripheral arterial disease, higher cholesterol level, small-vessel stroke and greater whitematter hyperintensity. Interpretation: Cognition is dynamic following stroke, with different patterns of change. Brain reserve and vascular risk factors relate to later post-stroke cognitive change. This complex nature of cognitive trajectory has implications for cognitive rehabilitation provision and cognitive impairment detection after stroke.

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Funder and Project Information

Xanthine oxidase inhibition for improvement of Long-term Outcomes following ischaemic stroke and transient ischaemic attack (XILO-FIST)

Jesse Dawson

TSA BHF 2013/01

School of Cardiovascular & Metabolic Health

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