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. Eighty-four 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 white-matter 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.
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. Eighty-four 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 white-matter 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.
| Original language | English |
|---|---|
| Pages (from-to) | 14-20 |
| Number of pages | 7 |
| Journal | Annals of Clinical and Translational Neurology |
| Volume | 13 |
| Issue number | 1 |
| Early online date | 22 Sept 2025 |
| DOIs | |
| Publication status | Published - Jan 2026 |
Keywords
- cognitive impairment
- cognitive trajectory
- post-stroke cognition
- risk factor
- stroke