The NLR might be useful as a novel predictor for 1-year outcome and mortality in severe TBI.

BackgroundTraumatic brain injury (TBI) triggers both immediate (primary) and long-term (secondary) tissue damages. Secondary damages can last from hours to days or even a lifetime. Secondary damages implicate several mechanisms, including influence of inflammatory mediators, mainly cytokines, on excitability of ion channels. However, studies should further explore the effects of inflammatory cytokines on voltage-gated sodium channels (VGSCs) and excitability in distal intact neurons.MethodsMixed cultures of mouse cortical astrocytes and neurons were subjected to mechanical injury (trauma) to mimic TBI in vitro. Expression of various cytokines in these cultures were measured by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. A trauma-conditioned medium with or without brain-derived neurotrophic factor (BDNF) was added to mouse primary cortical neurons for 6 and 24 h to mimic combined effects of multiple inflammatory cytokines on VGSCs. Spike behaviors of distal intact neurons were examined by whole-cell patch-clamp recordings.ResultsMechanical injury in mixed cortical neuron–astrocyte cultures significantly increased expression levels of multiple cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α, monocyte chemoattractant protein-1, chemokine (C-C motif) ligand-5, IL-10, and transforming growth factor-β1, at 6 and 24 h after injury. Incubation in trauma-conditioned medium increased functional VGSCs in neuronal membranes and Na+ currents. Enhanced VGSCs were almost completely abolished by BDNF, and reinforcement of Na+ currents was also reduced in a dose-dependent manner. BDNF (30 ng/mL) also significantly reversed reduced neuronal cell viability, which was induced by medium conditioned at 6 h. At 6 and 24 h, trauma-conditioned medium significantly increased spike frequency but not spike threshold.ConclusionsIn TBI, the combined effect of inflammatory cytokines is directly involved in VGSC, Na+ current, and excitability dysfunction in distal intact neurons. BDNF may partly exert neuroprotective effects by maintaining balance of VGSC function in distal intact neurons.

Objective: To investigate the diagnostic efficiency of truncal-type occlusion and branching-site occlusion in determining the etiology of intracranial large artery occlusion related acute ischemic stroke (AIS). Methods: Patients with intracranial large artery occlusion related AIS who received stent retriever (SR) thrombectomy from November 2014 to June 2019 were included in the study. All patients underwent angiography before SR thrombectomy, which was used to evaluate the occlusion type. Differences in the distribution of occlusion types in intracranial atherosclerosis (ICAS) and embolism were assessed, and the diagnostic indicators, including the area under the ROC curve (AUC), sensitivity, and specificity were calculated. Results: Of the 115 AIS patients with intracranial large artery occlusion, 42 were classified as having ICAS, and 73 having an embolism. In the ICAS group, branching-site occlusion was responsible for 3 (7%) cases and truncal-type occlusion for 39 (93%) cases, while in the embolism group, branching-site occlusion was responsible for 66 (90%) cases and truncal-type occlusion for 7 (10%) cases; the difference was statistically significant (all P < 0.01). The AUC for ICAS predicted by truncal-type occlusion was 0.916, with a sensitivity of 92.86%, and specificity of 90.41%. Conclusion: Truncal-type occlusion showed a high predictability of ICAS. Determine the etiology of intracranial large artery occlusion related AIS before SR thrombectomy may be most helpful in setting up optimal endovascular treatment strategies.