Cognitive Decline After Stroke Relation to Inflammatory Biomarkers and Hippocampal Volume

Inflammation may contribute to cognitive impairment after stroke. Inflammatory markers are associated with hippocampal atrophy. We tested whether markers of inflammation, erythrocyte sedimentation rate (ESR), and serum levels of C-reactive protein are associated with reduced hippocampal volume and p...

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Veröffentlicht in:Stroke (1970) 2013-05, Vol.44 (5), p.1433-1435
Hauptverfasser: KLIPER, Efrat, BASHAT, Dafna Ben, GOLDBOURT, Uri, SHAPIRA, Itzhak, KORCZYN, Amos D, ASSAYAG, Einor Ben, BORNSTEIN, Natan M, SHENHAR-TSARFATY, Shani, HALLEVI, Hen, AURIEL, Eitan, SHOPIN, Ludmila, BLOCH, Sivan, BERLINER, Shlomo, GILADI, Nir
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Sprache:eng
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Zusammenfassung:Inflammation may contribute to cognitive impairment after stroke. Inflammatory markers are associated with hippocampal atrophy. We tested whether markers of inflammation, erythrocyte sedimentation rate (ESR), and serum levels of C-reactive protein are associated with reduced hippocampal volume and poor cognitive performance among stroke survivors. We analyzed 368 consecutive cases from our prospective study of first-ever mild-moderate stroke patients. MRI, cognitive tests, and inflammatory markers were determined. Patients were reevaluated 6 and 12 months after the event. ESR remained unchanged in follow-up examinations, suggesting a chronic inflammation background in some patients. Higher levels of C-reactive protein and ESR were associated with worse performance in cognitive tests, particularly memory scores. This association was maintained for ESR (but not C-reactive protein) after adjustment for confounders (P=0.002). Patients with smaller hippocampi had inferior cognitive results. Moreover, in a multivariate regression model, higher ESR values (but not C-reactive protein) were related to reduced hippocampal volume (P=0.049). This report shows a strong relationship between ESR and hippocampal volume, as well as with cognitive performance among poststroke patients. This could plausibly relate to incipient cognitive decline via hippocampal pathways.
ISSN:0039-2499
1524-4628
DOI:10.1161/STROKEAHA.111.000536