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Objective: Inflammatory response and neuronal damage seem to be a part of the pathogenesis of delirium, but the exact mechanism, especially in motor subtypes of delirium, remains unclear.
Methods: This study included 53 patients with delirium and 50 intensive care unit patients without delirium. Interleukin (IL)-6, Neuron-specific enolase (NSE), and S100 beta (S100B) blood levels were examined in both groups. Patients with delirium were also investigated according to the delirium motor subtypes.
Results: There was no difference between the delirium and control groups with regard to S100B and NSE. However, the IL-6 levels of patients with delirium were significantly higher than those of the controls [24.73 pg/mL (2.91-99.36) vs. 5.44 pg/mL (2.75-89.32), p<0.001]. In a comparison of the subgroups of delirium, no statistical significance was found except that the IL-6 levels of hypoactive patients were delirium [10.46 pg/mL (2.91-99.36)] were lower than those of patients with hyperactive [30.97 pg/mL (10.66-88.21), p=0.03] and mixed delirium [50.18 pg/mL (17.22-66.55), p=0.02].
Conclusion: Our data suggest that delirium was associated with elevated blood levels of proinflammatory cytokine IL-6, but not with neuronal damage biomarkers S100B and NSE. We also found that delirium motor subtypes differed from each other with elevated IL-6 levels in hyperactive and mixed-type delirium.
You may cite this article as: Özkul A, Yılmaz A, Akyol A, et al. Biomarkers of neuronal damage and inflammation in delirium. Neurol Sci Neurophysiol 2019; 36(4): 193-7