Abstract
BackgroundExperimental studies suggest that systemic inflammation contributes to the pathophysiology of delirium. The aim of our study was to determine blood-derived inflammatory signatures of post-stroke delirium.MethodsWe included 144 ischemic stroke patients. We assessed delirium on a daily basis during the first 7 days of hospitalization. Venous blood was collected at day 3 after the onset of stroke and stimulated ex vivo with lipopolysaccharide (LPS). We measured LPS-induced cytokine concentration (TNFα, IP-10, IL-1β, IL-6, IL-8, IL-10, and IL-12p70) as well as plasma levels of IL-6 and TNFα.ResultsDelirium was diagnosed in 21.5% of patients. After correction for monocyte count, patients with delirium had reduced LPS-induced TNFα, IP-10, IL-1β, IL-6, and IL-12 release. The plasma IL-6 level was higher in delirious patients compared to patients without delirium. After adjusting for stroke severity and infections, higher ex vivo TNFα (OR 0.29, 95%CI 0.11–0.72, P = 0.01), IP-10 (OR 0.25, 95%CI 0.08–0.73, P = 0.01), IL-1β (OR 0.42, 95%CI 0.20–0.89, P = 0.02), and IL-12 (OR 0.07, 95%CI 0.01–0.70, P = 0.02) release was associated with the reduced risk of delirium. In multivariate analysis, the higher plasma IL-6 was associated with the increased risk of delirium (OR 1.61, 95%CI 1.00–2.58, P = 0.04).ConclusionsReduced ex vivo release of pro-inflammatory cytokines after LPS stimulation and the elevated plasma IL-6 are signatures of post-stroke delirium.
Highlights
Experimental studies suggest that systemic inflammation contributes to the pathophysiology of delirium
The inclusion criteria were as follows: (1) ischemic stroke, (2) time from the onset of stroke symptoms onset to admission < 24 h, (3) pre-stroke modified Rankin Scale score 0–2, (4) National Institute of Health Stroke Scale (NIHSS) score on admission > 3, and (5) informed patient consent
Higher release of TNFα, inducible protein 10 (IP-10), IL-1β, IL-6, and IL12 was associated with the reduced risk of delirium
Summary
Experimental studies suggest that systemic inflammation contributes to the pathophysiology of delirium. The aim of our study was to determine blood-derived inflammatory signatures of post-stroke delirium. Delirium is a neuropsychiatric syndrome characterized by acute, fluctuating changes in attention, awareness, and cognition. The pathophysiology of delirium is still poorly understood. One of the current hypotheses of delirium suggests that acute peripheral inflammation induces activation of systemic inflammation is recognized as a trigger of delirium, there is still limited evidence that links circulating inflammatory mediators with delirium in humans. The most replicated finding, albeit not confirmed by some researchers, is the elevated blood interleukin (IL)-6 level during delirium [6,7,8,9]. Other blood-based inflammatory mediators which predicted delirium or were elevated
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