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Updated: Feb 16, 2026

Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions
Published on: April 23, 2021
Cognitive Impairment Before Intracerebral Hemorrhage Is Associated With Cerebral Amyloid Angiopathy
Gargi Banerjee1, Duncan Wilson1, Gareth Ambler1
1From the UCL Stroke Research Centre (G.B., D.W., K.O.-B.A., C.S., S.L., M.M.B., D.J.W.) and Lysholm Department of Neuroradiology and the Neuroradiological Academic Unit (T.Y., H.R.J.), Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, and the National Hospital for Neurology and Neurosurgery, London, United Kingdom; Department of Statistical Science (G.A.) and Haemostasis Research Unit, Department of Haematology (H.C.), University College London, United Kingdom; University of Birmingham Institute of Cardiovascular Sciences, City Hospital, United Kingdom (G.Y.H.L.); Institute of Neuroscience & Psychology, University of Glasgow, Queen Elizabeth University Hospital, United Kingdom (K.W.M.); and Centre for Clinical Brain Sciences, School of Clinical Sciences, University of Edinburgh, United Kingdom (R.A.-S.S.).
Background And Purpose:
Although the association between cerebral amyloid angiopathy (CAA) and cognitive impairment is increasingly recognized, it is not clear whether this is because of the impact of recurrent intracerebral hemorrhage (ICH) events, disruptions caused by cerebral small vessel damage, or both. We investigated this by considering whether cognitive impairment before ICH was associated with neuroimaging features of CAA on magnetic resonance imaging.
Methods:
We studied 166 patients with neuroimaging-confirmed ICH recruited to a prospective multicentre observational study. Preexisting cognitive impairment was determined using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Magnetic resonance imaging markers of cerebral small vessel disease, including CAA, were rated by trained observers according to consensus guidelines.
Results:
The prevalence of cognitive impairment before ICH was 24.7% (n=41) and, in adjusted analyses, was associated with fulfilling the modified Boston criteria for probable CAA at presentation (odds ratio, 4.01; 95% confidence interval, 1.53-10.51; P=0.005) and a higher composite CAA score (for each point increase, odds ratio, 1.42; 95% confidence interval, 1.03-1.97; P=0.033). We also found independent associations between pre-ICH cognitive decline and the presence of cortical superficial siderosis, strictly lobar microbleeds, and lobar ICH location, but not with other neuroimaging markers, or a composite small vessel disease score.
Conclusions:
CAA (defined using magnetic resonance imaging markers) is associated with cognitive decline before symptomatic ICH. This provides evidence that small vessel disruption in CAA makes an independent contribution to cognitive impairment, in addition to effects due to brain injury caused directly by ICH.
Clinical Trial Registration:
URL: https://www.clinicaltrials.gov. Unique identifier: NCT02513316.
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