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To compare and analyze the efficacy and safety of traditional craniotomy and small bone window craniotomy in the treatment of hypertensive cerebral hemorrhage (HICH).Fifty-four patients with HICH treated with traditional craniotomy and small bone window craniotomy were retrospectively analyzed. The operation time, hospitalization time, preoperative, and postoperative CT analysis, Glasgow coma scale (GCS) score and Glasgow outcome scale (GOS) scores were analyzed.There were no significant differences in gender, age, hematoma volume, GCS score and pre-operative time between the 2 groups (P 0.05). The operation time and hospitalization time of the micro-bone window group were shorter than those of the traditional operation group (P 0.05). The GCS and GOS scores of the small bone window group after 3 days and 6 months were higher than those of the traditional operation group (P 0.05). However, there was no significant difference in hematoma clearance rate, re-bleeding rate and infection rate between the two groups (P 0.05).For patients with GCS 8-12 HICH, micro-bone window not only has the same effect as traditional bone window, but also has the advantages of shorter operation time and less trauma.

It was previously confirmed that the apoptotic and necrotic neurons are found during the acute post‐traumatic period, suggesting the induction of apoptosis after traumatic brain injury (TBI). To further explore the involvement of apoptotic factors in TBI, an apoptosis antibody array was conducted to measure the alterations of apoptotic factors in rat brain cortex after TBI. As a result, the Neurological Severity Scale (NSS) scores after TBI were increased, and the cell morphology of the brain cortex was destructed with increased neuronal apoptosis. Furthermore, the caspase‐3 activity was increased, and the apoptotic‐related factors TNF‐α and p53 were up‐regulated in the brain cortex. More importantly, in vitro experiments demonstrated that down‐regulation of TNF‐α in oxygen‐glucose deprivation/reoxygenation (OGD/R) cells increased cell viability and decreased apoptosis and the p53 expression. These results suggested the involvement of TNF‐α–induced apoptotic signalling pathway by activating p53 in the molecular mechanism of neurological injury.

Purpose To explore the risk factors of the evolution of traumatic subdural effusion (TSE) into chronic subdural hematoma (CSDH). Materials and Methods The 70 patients' gender, age, location of effusion, unilateral and bilateral, Glasgow coma score (GCS) at admission, presence or absence of brain contusion, the time of effusion appeared, daily amount of mannitol, mannitol number of days used, with or without atorvastatin calcium tablets, with or without antiplatelet aggregation drugs, with or without anticoagulant drugs, with or without abnormalities in blood coagulation routines, computed tomography (CT) layer height, the thickness, and CT value of the first effusion were analyzed by single factor. Logistic multivariate regression analysis was performed on the statistically significant indicators. Power of the regression model was evaluated using receiver operating characteristic (ROC) curve. Results Univariate analysis showed that the presence or absence of brain contusion, the time of effusion appeared, atorvastatin calcium tablets use or not, the CT value of the effusion, and TSE into CSDH evolution varied significantly compared to the non-evolved group (P

// Guangfu Di 1, 2, * , Hua Liu 1, 3, * , Xinhua Hu 1, * , Sansong Chen 2 , Zhichun Wang 2 and Hongyi Liu 1 1 Department of Neurosurgery, The Affiliated Brain Hospital, Nanjing Medical University, Nanjing, China 2 Department of Neurosurgery, Yijishan Hospital, Wannan Medical College, Wuhu City, China 3 Department of Neurosurgery, The First People’s Hospital of Kunshan, Jiangsu University, Suzhou, China * These authors have contributed equally to this work Correspondence to: Hongyi Liu, email: DGFYJSYY@163.com Keywords: intracranial injury, mild traumatic brain injury, infants Received: June 14, 2017 Accepted: August 28, 2017 Published: October 04, 2017 ABSTRACT Purpose : Mild traumatic brain injury (TBI) is common in children. The aim of this study was to identify clinical predictors of intracranial injuries on computed tomography (CT) in infants younger than 2 years old with mild TBI, which allow reducing number of imaging. Results : Of 214 enrolled infants with complete data, 30 (5.8%) sustained intracranial injuries. Younger age in months, severe injury mechanism and scalp hematomas were associated with traumatic intracranial injuries on CT. 71 had scalp hematomas and 143 had no scalp hematoma. Within infants with scalp hematomas, 26 sustained intracranial injuries and 45 presented normal. Intracranial injuries were significantly correlated with larger scalp hematomas and different scalp hematoma locations. Logistic regression analysis showed that scalp hematoma and mechanism of injury in infants younger than 2 years old with mild TBI was related to intracranial injuries (hazard ratio=38.291, P=0.0001; hazard ratio=0.174, P=0.001). In subgroup of mild TBI infants with scalp hematomas, logistic regression analysis showed age, scalp hematoma size and mechanism of injury were independently associated with intracranial injuries (hazard ratio=0.299, P=0.032; hazard ratio=5.272, P=0.006; hazard ratio=0.312, P=0.030). Methods : Between 2014 and 2016, we retrospectively enrolled infants

Background A skull fracture widely occurs in patients with traumatic brain injury, leading to intracranial hematoma, brain contusion, and intracranial infection. It also influences the prognosis and death of patients. This study aimed to discuss cases of patients with comminuted skull fractures. Methods From October 2015 to December 2018, 38 patients with comminuted skull fractures were admitted to the hospital. All patients underwent three-dimensional reconstruction of computed tomography scan images. Digital subtraction angiography or magnetic resonance venography was performed to find out the venous sinus. The clinical findings of the patients were significant regarding gender, age, injury mechanism, location, admission Glasgow Coma Scale (GCS), combined epidural, subdural, cerebral contusion, intracranial pneumatosis, maximum depth of depression, admission to surgery, dural tear, post-operative cerebrospinal fluid leakage, post-operative infection, and Glasgow Outcome Scale (GOS) 3 months after surgery. Results The incidence of traffic accidents, fall from a height, railway accidents, fall of an object, and chop injury was 60.5%, 18.4%, 13.2%, 5.3%, and 2.6%, respectively. Intra-operative dural trar negatively correlated with epidural hematoma, cerebral contusion, and subdural hematoma. Also, post-operative infection negatively correlated with intracranial pneumatosis, depth of fracture depression, and pre-operative cerebrospinal fluid leakage. No correlation was found between contusion, subdural hematoma, intracranial pneumatosis, depth of fracture depression, and post-operative infection. The GOS score positively correlated with age, pre-operative cerebrospinal fluid leakage, and admission GCS score. Conclusions A perfect pre-operative examination is a key to successful surgery. Further studies should be conducted to find out more effective treatments for traumatic comminuted skull fractures.

Acute lung injury (ALI) is one of the severe complications in patients with traumatic brain injury (TBI), contributing to the high mortality. Ghrelin has protective effects against various inflammatory diseases, but the effects of Ghrelin on TBI-induced ALI and its mechanisms remain unknown. In this study, Ghrelin administration was performed on the mice with TBI, then histological change in cortex and lung tissues, lung vascular permeability and macrophage number in bronchoalveolar lavage fluid (BALF) were examined, respectively. Simultaneously, the alterations of proinflammatory factors and pyroptosis-related proteins in lung tissues were detected. As a result, TBI-induced ALI was ameliorated after Ghrelin treatment, which was demonstrated by improved histology, reduced lung vascular permeability, and peripheral macrophage number. Furthermore, Ghrelin decreased the mRNA levels of proinflammatory factors (IL-1β, IL-6, TNF-α and IL-18), the protein levels of pyroptosis-related proteins (NLRP3, Caspase1-P20, HMGB1 and Gasdermin D), and the phosphorylation levels of NF-κB in lung tissues. These results showed that Ghrelin attenuating TBI-induced ALI might be via ameliorating inflammasome-induced pyroptosis by blocking NF-κB signal, which are important for the prevention and treatment of TBI-induced ALI.

Traumatic brain injury (TBI) is a primary cause of disability and mortality. Ghrelin, a gastrointestinal hormone, has been found to have protective effects for the brain, but the molecular mechanism of these neuroprotective effects of ghrelin remains unclear. In this study, an electronic cortical contusion impactor was used to establish a rat TBI model and we investigated the effect of ghrelin on brain repair by neurological severity score and histological examination. An antibody array was employed to uncover the molecular mechanism of ghrelin’s neuroprotective effects by determining the alterations of multiple proteins in the brain cortex. As a result, ghrelin attenuated brain injury and promoted brain functional recovery. After TBI, 13 proteins were up-regulated in the brain cortex, while basic fibroblast growth factor (bFGF) and fibroblast growth factor-binding protein (FGF-BP) were down-regulated after ghrelin treatment. It is known that bFGF can induce angiogenesis in the brain and accelerate wound healing, which can be further enhanced by FGF-BP. Based on the previous studies, it is hypothesized that the exogenous ghrelin curing TBI might cause the closure of bFGF and FGF-BP functions on wound healing, or ghrelin might exert the neuroprotective effects by competitively inhibiting bFGF/FGF-BP-induced neovascularization. Whether the combinational administration of ghrelin and bFGF/FGF-BP can enhance or weaken the therapeutic effect on TBI requires further research.

Objective Traumatic brain injury (TBI) occurs commonly in children. Repeat computed tomography (CT) follow up of TBI patients is often scheduled to identify progressive hemorrhagic injury (PHI). However, the utility of repeated CT scans, especially in children with mild TBI [Glasgow Coma Scale (GCS) scores of 13–15], has been debated. The purposes of the present study were to identify clinical predictors of PHI in children with mild TBI and to clarify relevant clinical factors via radiological examination. Methods From 2014 to 2016, we retrospectively enrolled children