TY - JOUR
T1 - Neuroinflammation in long-term cognitive impairment after aneurysmal subarachnoid hemorrhage
AU - Tack, Reinier W.P.
AU - Tolboom, Nelleke
AU - Meyer Viol, Bas
AU - Golla, Sandeep S.V.
AU - van Berckel, Bart N.M.
AU - van der Schaaf, Irene C.
AU - Boellaard, Ronald
AU - de Luca, Alberto
AU - van Zandvoort, Martine J.E.
AU - Visser-Meily, Johanna M.A.
AU - Hol, Elly M.
AU - Rinkel, Gabriel J.E.
AU - Vergouwen, Mervyn D.I.
N1 - Publisher Copyright:
© 2025 World Stroke Organization. This article is distributed under the terms of the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).
PY - 2025/12
Y1 - 2025/12
N2 - BACKGROUND: Survivors of aneurysmal subarachnoid hemorrhage (aSAH) often have cognitive impairment, which may be caused by long-term inflammation. We aimed to determine whether long-term neuroinflammation or microstructural brain damage is associated with cognitive impairment after aSAH.METHODS: In this prospective cohort study, we included patients >3 years after aSAH between 2020 and 2022. Patients underwent neuropsychological evaluation, translocator protein 18 kDA (TSPO) positron emission tomography (PET) imaging using [
18F]DPA-714 to determine neuroinflammation, and brain diffusion kurtosis imaging (DKI) to determine microstructural damage. We compared TSPO PET binding potential, mean kurtosis (MK), kurtosis anisotropy (KA), axial kurtosis (AK), and radial kurtosis (RA) between groups and determined which metric was correlated with individual cognitive tests.
RESULTS: We included 27 patients with aSAH; 14 with and 13 without cognitive impairment. Whole-brain TSPO binding potential was similar between groups (mean BP
ND: -0.046 [95% confidence interval (CI): -0.105; 0.013] vs -0.047 [95% CI -0.108; 0.014], p = 0.98) and there were no regional differences. Those with cognitive impairment had a lower whole-brain MK (mean MK 0.70 [95% CI: 0.69-0.72] vs 0.73 [95% CI: 0.72-0.74], p = 0.03) and whole-brain AK (mean AK 0.81 [95% CI: 0.78-0.83] vs 0.86 [0.84-0.87], p = 0.04). Left thalamic MK and AK were correlated with tests of verbal memory (r = 0.60-0.67, p < 0.01), while other correlation tests were non-significant.
CONCLUSION: Our results do not support the hypothesis that long-term cognitive impairment after aSAH is caused by long-term neuroinflammation. Instead, microstructural damage may play a role.
AB - BACKGROUND: Survivors of aneurysmal subarachnoid hemorrhage (aSAH) often have cognitive impairment, which may be caused by long-term inflammation. We aimed to determine whether long-term neuroinflammation or microstructural brain damage is associated with cognitive impairment after aSAH.METHODS: In this prospective cohort study, we included patients >3 years after aSAH between 2020 and 2022. Patients underwent neuropsychological evaluation, translocator protein 18 kDA (TSPO) positron emission tomography (PET) imaging using [
18F]DPA-714 to determine neuroinflammation, and brain diffusion kurtosis imaging (DKI) to determine microstructural damage. We compared TSPO PET binding potential, mean kurtosis (MK), kurtosis anisotropy (KA), axial kurtosis (AK), and radial kurtosis (RA) between groups and determined which metric was correlated with individual cognitive tests.
RESULTS: We included 27 patients with aSAH; 14 with and 13 without cognitive impairment. Whole-brain TSPO binding potential was similar between groups (mean BP
ND: -0.046 [95% confidence interval (CI): -0.105; 0.013] vs -0.047 [95% CI -0.108; 0.014], p = 0.98) and there were no regional differences. Those with cognitive impairment had a lower whole-brain MK (mean MK 0.70 [95% CI: 0.69-0.72] vs 0.73 [95% CI: 0.72-0.74], p = 0.03) and whole-brain AK (mean AK 0.81 [95% CI: 0.78-0.83] vs 0.86 [0.84-0.87], p = 0.04). Left thalamic MK and AK were correlated with tests of verbal memory (r = 0.60-0.67, p < 0.01), while other correlation tests were non-significant.
CONCLUSION: Our results do not support the hypothesis that long-term cognitive impairment after aSAH is caused by long-term neuroinflammation. Instead, microstructural damage may play a role.
KW - Subarachnoid hemorrhage
KW - cognitive Impairment
KW - neuroinflammation
KW - Cognitive Dysfunction/etiology
KW - Prospective Studies
KW - Humans
KW - Middle Aged
KW - Male
KW - Positron-Emission Tomography
KW - Diffusion Tensor Imaging
KW - Neuropsychological Tests
KW - Subarachnoid Hemorrhage/complications
KW - Brain/diagnostic imaging
KW - Neuroinflammatory Diseases/diagnostic imaging
KW - Female
KW - Aged
UR - https://www.scopus.com/pages/publications/105023166945
UR - https://www.mendeley.com/catalogue/2a35167a-42d2-311a-b017-ca9af802d819/
U2 - 10.1177/17474930251362004
DO - 10.1177/17474930251362004
M3 - Article
C2 - 40662329
AN - SCOPUS:105023166945
SN - 1747-4930
VL - 20
SP - 1301
EP - 1309
JO - International Journal of Stroke
JF - International Journal of Stroke
IS - 10
ER -