E Kövari1, F R Herrmann2, G Gold2, P R Hof3, A Charidimou4. 1. Department of Mental Health and Psychiatry, University Hospitals and University of Geneva, Geneva, Switzerland. 2. Department of Internal Medicine, Rehabilitation and Geriatrics, University Hospitals and University of Geneva, Thônex, Switzerland. 3. Fishberg Department of Neuroscience, Friedman Brain Institute, and Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 4. Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston, MA, USA.
Abstract
AIMS: Cortical microinfarcts (CMI) are frequently observed in the ageing brain independent of cognitive decline, but their aetiology is not fully elucidated. To examine the potential role of different vessel pathologies, including cerebral amyloid angiopathy (CAA), arteriolosclerosis-hyalinosis and thromboembolism in the development of CMI, we examined 80 autopsy cases with more than one CMI on routine neuropathological examination. METHODS: Pial and intracortical vessels around CMI were assessed for their integrity with haematoxylin-eosin staining and antibodies against amyloid-β protein and fibrinogen using a semiquantitative four-level rating scale (absent to severe) in the hippocampus, and the frontal, temporal and occipital cortex. Four histological categories of changes were defined: CAA, vessel pathology other than CAA, thromboembolism and absence of vessel pathology near CMI. RESULTS: A differential distribution of microvascular pathology was observed depending on brain regions. In the occipital cortex, CAA was commonly associated with CMI. In contrast, in the hippocampus and the frontal cortex, cases without any vascular pathology in pial and intracortical vessels were significantly more frequent. CONCLUSIONS: The aetiology of CMI differs depending on brain location. CAA may play a role principally in the occipital cortex. The large number of intact vessels around the CMI (mainly in the frontal cortex and hippocampus) raises the possibility that pathologies other than structural microangiopathy, including hypoperfusion/arterial hypotension or large vessel atherosclerosis, play a role in the development of microvascular lesions. These results are relevant in the context of aetiopathogenesis of vascular changes associated with conditions like vascular dementia.
AIMS: Cortical microinfarcts (CMI) are frequently observed in the ageing brain independent of cognitive decline, but their aetiology is not fully elucidated. To examine the potential role of different vessel pathologies, including cerebral amyloid angiopathy (CAA), arteriolosclerosis-hyalinosis and thromboembolism in the development of CMI, we examined 80 autopsy cases with more than one CMI on routine neuropathological examination. METHODS: Pial and intracortical vessels around CMI were assessed for their integrity with haematoxylin-eosin staining and antibodies against amyloid-β protein and fibrinogen using a semiquantitative four-level rating scale (absent to severe) in the hippocampus, and the frontal, temporal and occipital cortex. Four histological categories of changes were defined: CAA, vessel pathology other than CAA, thromboembolism and absence of vessel pathology near CMI. RESULTS: A differential distribution of microvascular pathology was observed depending on brain regions. In the occipital cortex, CAA was commonly associated with CMI. In contrast, in the hippocampus and the frontal cortex, cases without any vascular pathology in pial and intracortical vessels were significantly more frequent. CONCLUSIONS: The aetiology of CMI differs depending on brain location. CAA may play a role principally in the occipital cortex. The large number of intact vessels around the CMI (mainly in the frontal cortex and hippocampus) raises the possibility that pathologies other than structural microangiopathy, including hypoperfusion/arterial hypotension or large vessel atherosclerosis, play a role in the development of microvascular lesions. These results are relevant in the context of aetiopathogenesis of vascular changes associated with conditions like vascular dementia.
Authors: Lilah M Besser; Walter A Kukull; Merilee A Teylan; Eileen H Bigio; Nigel J Cairns; Julia K Kofler; Thomas J Montine; Julie A Schneider; Peter T Nelson Journal: J Neuropathol Exp Neurol Date: 2018-08-01 Impact factor: 3.685
Authors: Lauren E Salminen; Rand R Wilcox; Alyssa H Zhu; Brandalyn C Riedel; Christopher R K Ching; Faisal Rashid; Sophia I Thomopoulos; Arvin Saremi; Marc B Harrison; Anjanibhargavi Ragothaman; Victoria Knight; Christina P Boyle; Sarah E Medland; Paul M Thompson; Neda Jahanshad Journal: Cereb Cortex Date: 2019-12-17 Impact factor: 5.357
Authors: Valentina Perosa; Jan Oltmer; Leon P Munting; Whitney M Freeze; Corinne A Auger; Ashley A Scherlek; Andre J van der Kouwe; Juan Eugenio Iglesias; Alessia Atzeni; Brian J Bacskai; Anand Viswanathan; Matthew P Frosch; Steven M Greenberg; Susanne J van Veluw Journal: Acta Neuropathol Date: 2021-12-20 Impact factor: 15.887
Authors: Susanne J van Veluw; Andy Y Shih; Eric E Smith; Christopher Chen; Julie A Schneider; Joanna M Wardlaw; Steven M Greenberg; Geert Jan Biessels Journal: Lancet Neurol Date: 2017-07-14 Impact factor: 44.182