Background In recent years, argon has been shown to exert neuroprotective effects in an array of models. However, the mechanisms by which argon exerts its neuroprotective characteristics remain unclear. Accumulating evidence imply that argon may exert neuroprotective effects via modulating the activation and polarization of microglia/macrophages after ischemic stroke. In the present study, we analyzed the underlying neuroprotective effects of delayed argon application until 7 days after reperfusion and explored the potential mechanisms. Methods Twenty-one male Wistar rats underwent transient middle cerebral artery occlusion or sham surgery randomly for 2 h using the endoluminal thread model. Three hours after transient middle cerebral artery occlusion induction and 1 h after reperfusion, animals received either 50% vol Argon/50% vol O 2 or 50% vol N 2 /50% vol O 2 for 1 h. The primary outcome was the 6-point neuroscore from 24 h to d7 after reperfusion. Histological analyses including infarct volume, survival of neurons (NeuN) at the ischemic boundary zone, white matter integrity (Luxol Fast Blue), microglia/macrophage activation (Iba1), and polarization (Iba1/Arginase1 double staining) on d7 were conducted as well. Sample size calculation was performed using nQuery Advisor + nTerim 4.0. Independent t test, one-way ANOVA and repeated measures ANOVA were performed, respectively, for statistical analysis (SPSS 23.0). Results The 6-point neuroscore from 24 h to d7 after reperfusion showed that tMCAO Ar group displayed significantly improved neurological performance compared to tMCAO N 2 group ( p = 0.026). The relative numbers of NeuN-positive cells in the ROIs of tMCAO Ar group significantly increased compared to tMCAO N 2 group ( p = 0.010 for cortex and p = 0.011 for subcortex). Argon significantly suppressed the microglia/macrophage activation as revealed by Iba1 staining ( p = 0.0076) and promoted the M2 microglia/macrophage polarization as revealed by Iba1/Arginase 1 double staining ( p = 0.000095). Conclusions Argon administration with a 3 h delay after stroke onset and 1 h after reperfusion significantly alleviated neurological deficit within the first week and preserved the neurons at the ischemic boundary zone 7 days after stroke. Moreover, argon reduced the excessive microglia/macrophage activation and promoted the switch of microglia/macrophage polarization towards the anti-inflammatory M2 phenotype. Studies making efforts to further elucidate the protective mechanisms and to benefit the translational application are of great value.

Open surgery with intended total resection remains the treatment of choice in most patients. Initial stereotactic cyst aspiration or medical pretreatment to improve the patients' condition and adequate choice of surgical approach(es) are essential to achieve that goal. Nevertheless, a moderate increase in endocrinological deficits has to be accepted. The authors recommend using radiotherapy only in cases in which there are tumor remnants or disease progression after surgery.

Argon belongs to the group of noble gases, which are regarded as chemically inert. Astonishingly some of these gases exert biological properties and during the last decades more and more reports demonstrated neuroprotective and organoprotective effects. Recent studies predominately use in vivo or in vitro models for ischemic pathologies to investigate the effect of argon treatment. Promising data has been published concerning pathologies like cerebral ischemia, traumatic brain injury and hypoxic ischemic encephalopathy. However, models applied and administration of the therapeutic gas vary. Here we provide a systematic review to summarize the available data on argon’s neuro- and organoprotective effects and discuss its possible mechanism of action. We aim to provide a summary to allow further studies with a more homogeneous setting to investigate possible clinical applications of argon.

OBJECTIVEPerforming a cranioplasty (CP) after decompressive craniotomy is a straightforward neurosurgical procedure, but it remains associated with a high complication rate. Surgical site infection (SSI), aseptic bone resorption (aBR), and need for a secondary CP are the most common complications. This observational study aimed to identify modifiable risk factors to prevent CP failure.METHODSA retrospective analysis was performed of all patients who underwent CP following decompressive hemicraniectomy (DHC) between 2010 and 2018 at a single institution. Predictors of SSI, aBR, and need for allograft CP were evaluated in a univariate analysis and multivariate logistic regression model.RESULTSOne hundred eighty-six patients treated with CP after DHC were included. The diagnoses leading to a DHC were as follows: stroke (83 patients, 44.6%), traumatic brain injury (55 patients, 29.6%), subarachnoid hemorrhage (33 patients, 17.7%), and intracerebral hemorrhage (15 patients, 8.1%). Post-CP SSI occurred in 25 patients (13.4%), whereas aBR occurred in 32 cases (17.2%). An altered posterior question-mark incision, ending behind the ear, was associated with a significantly lower infection rate and CP failure, compared to the classic question-mark incision (6.3% vs 18.4%; p = 0.021). The only significant predictor of aBR was patient age, in which those developing resorption were on average 16 years younger than those without aBR (p < 0.001).CONCLUSIONSThe primary goal of this retrospective cohort analysis was to identify adjustable risk factors to prevent post-CP complications. In this analysis, a posterior question-mark incision proved beneficial regarding infection and CP failure. The authors believe that these findings are caused by the better vascularized skin flap due to preservation of the superficial temporal artery and partial preservation of the occipital artery. In this trial, the posterior question-mark incision was identified as an easily and costless adaptable technique to reduce CP failure rates.

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