Intestinal flora influences the progression of subarachnoid hemorrhage by affecting peripheral and central inflammatory pathways.

Subarachnoid hemorrhage (SAH) is a debilitating condition that leaves survivors with neurological disability for the rest of their lives. No effective treatment for early brain injury (EBI) has been developed. Gut microbiome (GM) impact the host immune system and can influence disease processes in several organs, including the brain. However, it remains unclear whether the GM has an impact on the outcome of SAH brain injury. Here, we wondered whether microbiota could relieve the injury. We changed the microbiota of 8-week-old male rats by administering antibiotic-containing water for 2 weeks. Composition of the GM was profiled by using 16S rRNA. We induced SAH by puncture the internal carotid artery of control rats and rats with altered GM. Additionally, we studied inflammatory cells using HE stains, Intestinal lymphocyte flow cytometry, and Neuroinflammatory factor WB. SAH was significantly averted by alterations in GM using antibiotics. The altered GM significantly increased the intestinal and intracranial inflammation after SAH. This was manifested by Mosin (MSN) inflammatory cytokines. Our findings demonstrated that the brain injury following SAH is associated with GM.

Erianin promotes endogenous neurogenesis in traumatic brain injury rats.

The objective of this study was to explore the positive influence and potential mechanism of Erianin on the recovery of brain cells following a traumatic brain injury (TBI). TBI rat models were prepared and treated with Erianin injection via tail vein. The assessment included evaluating the rats' levels of oxidative stress, inflammation, neuronal damage, mitochondrial damage, neuronal regeneration, transformation of pro-inflammatory microglial cells, activation status of the ERK signal pathway, and the functionality of their learning and memory. After administering Erianin, there was a suppression of oxidative stress, inflammation, nerve cell damage, and mitochondrial damage in the TBI rats. Additionally, there was an increase in neuronal regeneration in the cortex and hippocampus, inhibition of pro-inflammatory microglial cell transformation in the cortex, improvement in learning and memory function in TBI rats, and simultaneous inhibition of the activation of the ERK1/c-Jun signal pathway. The findings suggest that Erianin has the potential to reduce oxidative stress and inflammatory reaction in rats with TBI, safeguard nerve cells against apoptosis, stimulate the growth of new neural cells, ultimately enhancing the cognitive abilities and memory function of the rats. The inhibition of the ERK signaling pathway could be closely associated with these effects.

Utilization of clinical and radiological parameters to predict cognitive prognosis in patients with mild-to-moderate traumatic brain injury.

Background: Cognitive impairment is a common sequela following traumatic brain injury (TBI). This study aimed to identify risk factors for cognitive impairment after 3 and 12 months of TBI and to create nomograms to predict them. Methods: A total of 305 mild-to-moderate TBI patients admitted to the First Affiliated Hospital with Nanjing Medical University from January 2018 to January 2022 were retrospectively recruited. Risk factors for cognitive impairment after 3 and 12 months of TBI were identified by univariable and multivariable logistic regression analyses. Based on these factors, we created two nomograms to predict cognitive impairment after 3 and 12 months of TBI, the discrimination and calibration of which were validated by plotting the receiver operating characteristic (ROC) curve and calibration curve, respectively. Results: Cognitive impairment was detected in 125/305 and 52/305 mild-to-moderate TBI patients after 3 and 12 months of injury, respectively. Age, the Glasgow Coma Scale (GCS) score, >12 years of education, hyperlipidemia, temporal lobe contusion, traumatic subarachnoid hemorrhage (tSAH), very early rehabilitation (VER), and intensive care unit (ICU) admission were independent risk factors for cognitive impairment after 3 months of mild-to-moderate TBI. Meanwhile, age, GCS score, diabetes mellitus, tSAH, and surgical treatment were independent risk factors for cognitive impairment after 12 months of mild-to-moderate TBI. Two nomograms were created based on the risk factors identified using logistic regression analyses. The areas under the curve (AUCs) of the two nomograms to predict cognitive impairment after 3 and 12 months of mild-to-moderate TBI were 0.852 (95% CI [0.810, 0.895]) and 0.817 (95% CI [0.762, 0.873]), respectively. Conclusion: Two nomograms are created to predict cognitive impairment after 3 and 12 months of TBI. Age, GCS score, >12 years of education, hyperlipidemia, temporal lobe contusion, tSAH, VER, and ICU admission are independent risk factors for cognitive impairment after 3 months of TBI; meanwhile, age, the GCS scores, diabetes mellitus, tSAH, and surgical treatment are independent risk factors of cognitive impairment after 12 months of TBI. Two nomograms, based on both groups of factors, respectively, show strong discriminative abilities.

Prevalence of pituitary dysfunction after aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis.

BACKGROUND: Pituitary dysfunction (PD) is a common complication after aneurysmal subarachnoid hemorrhage (aSAH). The prevalence of PD varies widely at a global level and no recent meta-analysis is available. Therefore, the aim of our systematic review and meta-analysis was to summarize the updated estimates of worldwide prevalence of PD after aSAH. METHODS: Scopus, Embase, Web of Science, and PubMed databases were used to comprehensively search the appropriate literature and a random-effects meta-analysis on the results of the available studies was performed. The heterogeneity in the prevalence estimates was evaluated by subgroup analysis in terms of types of PD, and acute and chronic phases of aSAH. The onset of PD within 6 months after aSAH was considered as acute, while that after 6 months was considered as chronic. RESULTS: Twenty-seven studies with 1848 patients were included in this analysis. The pooled prevalence of PD in the acute phase was 49.6% (95% CI, 32.4-66.8%), and 30.4% (95% CI, 21.4-39.4%) in the chronic phase. Among the hormonal deficiencies, growth hormone dysfunction was the most prevalent in the acute phase, being 36.0% (95% CI, 21.0-51.0%), while hypoadrenalism was the most prevalent in the chronic phase, being 21.0% (95% CI, 12.0-29.0%). Among the six World Health Organization regions, the South-East Asia Region has the highest prevalence of PD in the acute phase (81.0%, 95%CI, 77.0-86.0%, P < 0.001), while the European Region had the highest prevalence of PD in the chronic phase (33.0%, 95%CI, 24.0-43.0%, P < 0.001). Moreover, single pituitary hormonal dysfunction occurred more frequently than the multiple one, regardless of acute or chronic phase. CONCLUSIONS: Almost half (49.6%) of the included patients with aSAH developed PD complication in the acute phase, while 30.4% of the patients developed them in the chronic phase. Although prevalence varies globally, the high healthcare burden, morbidity and mortality require greater awareness among clinicians.