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Objective:To evaluate the effect of remimazolam pretreatment on brain injury following thalamic hemorrhage in mice.Methods:Sixty clean-grade healthy adult CD1 male mice, weighing 25-30 g, aged 7-8 weeks, were divided into 3 groups ( n=20 each) by using a random number table method: sham operation group (Sham group), brain injury group (BI group) and remimazolam pretreatment group (Rem group). Remimazolam 25 mg/kg was intravenously injected via the tail vein in group Rem.and the equal volume of normal saline was given instead in Sham group and BI group.Ten min later, type Ⅳ collagenase 0.01 U/10 nl was microinjected into unilateral ventroposterolateral nucleus and ventromedial nucleus to develop a mouse model of brain jury induced by thalamic hemorrhage.The rats were sacrificed at 6 h after developing the model, brain tissues were taken for measurement of the wet/dry weight (W/D) ratio, and hippocampal tissues were taken and stained with haematoxylin and eosin for determination of the count of the viable neurons in the hippocampal dentategyrus area, count of apoptotic neurons in the hippocampal CA1 region (by TUNEL), expression of CCAAT/enhancer-binding protein homologous protein (CHOP), activating transcription factor 4 (ATF4) and X-box binding protein-1 (XBP1) mRNA (by real-time polymerase chain reaction) and expression of CHOP, Bcl-2, Bax and caspase-3 (by Western blot) and for microscopic examination of ultrastructure of hippocampal tissues (with a transmission electron microscope). Results:Compared with group Sham, the W/D ratio of brain tissues and count of apoptotic neurons in the hippocampal CA1 area were significantly increased, the count of viable neurons in the hippocampal dentate gyrus was decreased, the expression of CHOP, ATF4 and XBP1 mRNA in hippocampal tissues was up-regulated, the expression of CHOP, caspase-3 and Bcl-2 was up-regulated, and the expression of Bax was down-regulated in BI and Rem groups ( P<0.05). Compared with group BI, the W/D ratio of brain tissues and count of apoptotic neurons in the hippocampal CA1 area were significantly decreased, the number of viable neurons in the hippocampal dentate gyrus was increased, the expression of CHOP, ATF4 and XBP1 mRNA in hippocampal tissues was down-regulated, the expression of CHOP, caspase-3 and Bcl-2 was down-regulated, and the expression of Bax was up-regulated in group Rem ( P<0.05). Conclusion:Remimazolam pretreatment can reduce the brain injury following thalamic hemorrhage in mice, and the mechanism may be related to inhibition of cell apoptosis induced by endoplasmic reticulum stress in hippocampus.
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Objective To investigate the surgical treatment value to the deep coma patients with spontaneous cerebellar hemorrhage. Methods The clinical manifestations were recorded and analyzed in 43 patients suffering from cerebellar hemorrhage. Thirty-two patients(surgical treatment group) were treated with suboccipital decompression, clot evacuation and external ventricular drainage, and 11 patients (conservative treatment group) were managed conservatively. The level of consciousness was evaluated with Glasgow coma scale (GCS), and GCS scores of all enrolled patients was less than 5. Outcome was assessed with Glasgow outcome scale (GOS) at 6 months after onset. Results At 6 months after onset, the fatality rate in surgical treatment group was 31.25%(10/32), in conservative treatment group was 6/11, and there was no significant difference (χ2=1.04, P=0.310). The rate of bad outcome (GOS 1-3 scores) in surgical treatment group was 75.00%(24/32), in conservative treatment group was 11/11, and there was no significant difference (χ2=2.40, P=0.120). In the patients of more than 60 years old, the rate of good outcome between surgical treatment group and conservative treatment group had no significant difference:5/16 vs. 0,χ2=6.00, P=0.060. Conclusions Although fatality rate is lower, the long-term prognosis couldn′ t be improved by surgical treatment in the cerebellar hemorrhage patients with GCS≤5 scores when the brainstem function isn′t evaluated.
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Objective:To explore the risk factors its predictive value of delayed traumatic intracranial hematoma (DTICH) . Methods:Clinical data of 95 patients with acute craniocerebral trauma were collected .All patients were divided into DTICH group (n=62) and no recurrent hematoma control group (n=33) .Clinical data were compared between two groups ,Lo‐gistic regression model was used to analyze risk factors .Receiver operator characteristic curve (ROC) was used to assess pre‐dictive value of relative risk factors .Results:Compared with no recurrent hematoma group ,there were significant rise in age [(46.72 ± 6.45) years vs .(52.18 ± 7.13) years] ,hematoma volume [(51.21 ± 11.25)ml vs .(56.89 ± 12.37)ml] , level of fasting blood glucose [(8.13 ± 1.55) mmol/L vs .(10.62 ± 1.73) mmol/L] ,activated partial thromboplastin time [APTT ,(25.27 ± 6.19)s vs .(27.35 ± 7.45)s] and thrombin time [TT ,(17.53 ± 5.14)s vs .(21.26 ± 7.31)s] ,significant increase in percentages of basal cistern compression (24.2% vs .46.8% ) ,brain contusion (42.4% vs .69.4% ) ,bone flap removal (45.5% vs .67.7% ) and positive Babinski sign (39.4% vs .61.3% ) , and significant reductions in GCS score [(9.46 ± 3.29) scores vs .(7.63 ± 3.07) scores] ,systolic blood pressure [(146.57 ± 18.23)mmHg vs .(132.18 ± 17.18) mmHg] and timing of surgery [(12.74 ± 4.39)h vs .(5.47 ± 2.16)h] in DTICH group ,P<0.05 or <0.01;Logistic regres‐sion analysis indicated that coagulation function (APTT ,TT) ,skull fracture and timing of surgery were risk factors for post‐operative delayed hematoma(OR=4.076~5.430 ,P<0.05 or <0.01) ,their area under curve of ROC were 0.826 ,0.748 and 0.661 respectively .Conclusion:Coagulation function ,skull fracture and timing of surgery are risk factors and possess considerable predictive value for postoperative delayed craniocerebral hematoma in patients with craniocerebral trauma .
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Objective To identify the factors enhancing the contusive brain hemorrhage following unilateral decompression craniectomy in patients with severe traumatic brain injury (TBI),and to explore the relationship between the initial Rotterdam CT score and clinical outcomes.Methods A prospective study of 291 consecutive patients with TBI admitted from Jan 2008 through Dec 2012 was carried out.Patients treated with unilateral decompression craniectomy were enrolled for study.Patients without preoperative or postoperative cranial CT imaging were excluded.Of them,235 patients were followed up.Gender,age,the causes of injury,preoperative general condition including Glasgow Coma Scale (GCS) score,pupillary response,laboratory data and the initial CT scans before operation,contusion hematoma size in CT scans following operation and Glasgow Outcome Scale (GOS) score were recorded.With t test,x2 test and nonparametric rank sum test,differences in the above listed variables were compared between patients with enlarged hematoma size group and those without change in hematoma size.A Classification And Regression Tree (CART) was used to predict the size of hematoma.Correlation analysis was used to find the relationship between the Rotterdam CT scores and GOS scores.Results The differences in age (t =2.034,P =0.043),first Rotterdam CT score (Z =4.838,P ＜ 0.01),GCS score (Z =4.440,P ＜ 0.01),pupillary response (Z =3.235,P =0.001),the length of time elapsed between the trauma occurred and the decompressive craniectomy (Z =3.874,P ＜ 0.01),glucose level (Z =3.880,P ＜ 0.01) and cerebrum hernia magnitude (Z =2.529,P =0.012) were significant between the patients with hematoma expanded (n =120) and those without change in hematoma size (n =115).The results of the CART indicated that Rotterdam score got from the initial head CT,glucose level and the length of time elapsed between trauma occurred and decompressive craniectomy were strong predictors of the risk for expanded hemorrhagic contusions following decompressive craniectomy.Both age and size of the removed bone-flap also could predict the risk of postoperative expansion of hemorrhagic contusions.The overall predictive accuracy of the CART model was 83.3％.Correlation analysis results indicated that Rotterdam CT score was negatively correlated with GOS (r =-0.333,P ＜ 0.01).Conclusions Initial Rotterdam CT scores,glucose level and the length of time between trauma and decompressive craniectomy may predict the risk of contusions expansion following decompressive craniectomy.Rotterdam CT score was negatively correlated with GOS.