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find Keyword "脑损伤" 76 results
  • MRI Findings in Brain Radiation Necrosis Following Radiotherapy for Brain Neoplasm by γknife

    摘要:目的:探讨伽玛刀治疗颅内肿瘤并发放射性脑损伤的MRI影像表现及其组织病理学基础。方法:回顾性分析8例经手术及病理证实的放射性脑损伤的MRI表现;其中,星形胶质细胞瘤4例,转移性腺癌2例,血管母细胞瘤1例,鼻咽癌1例。结果:病变位于小脑半球、额叶、颞叶及顶叶,8例9个病灶共有2种MRI表现:5例6个病灶平扫T1WI呈低、等信号,T2WI呈稍高、高信号,增强扫描呈“结节状”、“花环状”强化;3个病灶平扫为类圆形,T1WI呈均匀低信号,T2WI呈高信号,边界清楚,增强扫描囊腔无强化,囊壁轻度均匀强化。所有病例均有占位效应。结论:伽玛刀所致放射性脑损伤具有一定的特征性,特别是囊状坏死。

    Release date:2016-09-08 09:56 Export PDF Favorites Scan
  • 急性颅脑损伤患者的临床治疗

    【摘要】目的 总结急性颅脑损伤患者的外科手术治疗效果。方法 2005年1月-2009年5月,急诊外科行手术治疗158例急性颅脑损伤患者。其中男89例,女69例;年龄5~84岁,平均40岁。受伤至入院时间为1~14 h,平均6 h。CT诊断后行开颅血肿清除手术61例,开颅血肿消除及去骨瓣减压73例,钻孔引流术8例,气管切开14例,胸腔闭式引流术2例。结果 158例共存活137例(86.7%),死亡21例(13.3%)。存活患者中植物生存2例,重度残疾18例,轻度残疾57例,恢复良好60例。死亡患者gt;65岁有15例;死亡时间1周内12例,1~3周内5例,3周以上4例。结论 应深入了解急性颅脑损伤的特点,采取正确的手术治疗方式,积极防治并发症,降低患者死亡率,改善预后。

    Release date:2016-09-08 09:31 Export PDF Favorites Scan
  • Experience in Diagnosis and Treatment of Traumatic Brain Injury with Acute Brain Tissue Expulsion during Operation

    目的:探讨颅脑损伤患者术中急性脑膨出的病因、诊断及治疗。方法:对127例术中发生急性脑膨出的颅脑损伤患者的临床资料进行回顾性分析。结果:急性脑膨出的原因为同侧脑肿胀者74例,为对侧迟发性血肿者51例,而为同侧迟发性血肿者2例。共死亡48例(37.8%),其中31例因脑疝死亡。结论:通过钻孔探查或积极的CT扫描,及时发现颅脑损伤患者术中急性脑膨出的原因,并尽早正确处理极其重要,是抢救此类患者成功的关键。

    Release date:2016-09-08 09:56 Export PDF Favorites Scan
  • 癫痫的一级预防:一项来自国际抗癫痫联盟预防工作组的报告

    目前导致癫痫的病因中,有些是可以预防的。该综述总结了由此类可预防病因所造成的癫痫的公共卫生负担,并提出了癫痫一级预防的重要性。系统性回顾针对癫痫的 4 种可预防病因的流行病学研究,这些可预防病因分别是围产期损伤、脑外伤、中枢神经系统感染和卒中。通过使用统一的标准,对每项研究进行质量评估,并从满足质量评级标准的研究中提取了相关风险度量的数据,并将这些结果以中位数和四分位数的方式汇总。高质量的基于人群的研究结果显示,在中低收入国家中,所有年龄段的癫痫患病率约为 1.11%,而在高收入国家中约为 0.7%。围产期脑损伤是儿童癫痫中最常见的可预防病因,在中低收入国家中占 17%,在高收入国家中占 15%。在中低收入和高收入国家中,卒中均是老年癫痫患者中最常见的可预防病因,占所有新发癫痫病例的半数及以上,在高收入和中低收入国家中约 5%癫痫是由卒中造成的。在中低收入国家,中枢神经系统感染是较常见的癫痫病因,约占所有癫痫病例的 5%。在一些低收入农村地区和中等收入国家社区中,地方性神经囊虫病所致癫痫占所有癫痫病例的 34%。可预防的病因所致癫痫占癫痫的总体公共卫生负担的很大一部分。在中低收入和高收入国家中,围产期损伤、感染、脑外伤和卒中所致癫痫占所有癫痫的 25%。母婴保健、免疫接种、公共卫生、预防脑损伤和卒中这些公共卫生干预措施有可能会显著减少癫痫负担。

    Release date:2020-01-09 08:49 Export PDF Favorites Scan
  • Analysis of Treatment Results of 1387 Patients with Severe Cranio-cerebral Injury

    目的:总结分析1387例重型颅脑损伤的救治情况,以利在今后的工作中进一步改善和提高对重型颅脑损伤的救治水平。方法:回顾性分析1983年1月~2008年1月间1387例重型颅脑损伤患者的救治情况。结果:1387例重型颅脑损伤患者,其中手术治疗857例,非手术治疗530例。按GOS评分,出院时恢复良好475例(34.2%),中残206例(14.8%),重残202例(14.5%),植物生存89例(6.4%),死亡415例(29.9%)。结论:重型颅脑损伤仍然具有较高的病死率和致残率,早期及时手术清除颅内血肿,解除脑疝以及采取积极恰当的综合治疗措施是抢救治疗成功的关键。

    Release date:2016-08-26 03:57 Export PDF Favorites Scan
  • ESTABLISHMENT AND EVALUATION OF ACUTE CLOSED BRAIN INJURY MODEL IN RATS ACCORDING TO FEENEY’S METHOD

    Objective To set up and to evaluate an acute closed brain injury model in rats. Methods The acute closed brain injury was produced in rats by using an impactor consisting of a stand, a guide tube, a weight and a footplate. Ninetysix SD rats were divided into a control group(n=32, no impact), a mild injury group(n=32, impact once at force level of 400 g·cm) and a severe injury group(n=32, impact once at force level of 800 g·cm) to elucidate the physiological responses, the pathophysiological changes and brain edema after brain injury at different injury levels. Results In the mild injury group and the severe injury group, a sudden rise or reduction of blood pressure, deep and fast breath apnea, and pain reflects inhibition were observed. The responses were more obvious in the severe injury group than in the mild injury group. The water content of the brain increased after 6 hours of injury. The pathological contusion and edema of brain were noted or above the impact force level of 800 g·cm. When the impact force rose to or over 1200g·cm, the animals died of persistent apnea mostly. Conclusion Although the established closed brain injury model with different biomechanical mechanisms as the clinical brain injury, it is in conformity with pathological changes and pathophysiological characteristics of acute clinical brain injury, it can be utilized extensively because of its convenient and practice.

    Release date:2016-09-01 09:28 Export PDF Favorites Scan
  • 应用液压冲击颅脑损伤仪建立大鼠外伤性视神经损伤动物模型

    Objective To observe whether the animal model of optic nerve injury in rats can be set up by fluid percussion brain injury device (FPI) or not.Methods Seventyone healthy female Wister rats were randomly divided into 2 groups, inlcuding model group with 66 rats and control group with 5 rats.The rats in model group were randomly divided into 3 groups. Eight rats in group 1 were examined by flashvisual evoked potential (F-VEP) and magnetic resonance imaging (MRI) examines before and 1, 3 days,1,2,4,6,and 8 weeks after injury; 56 rats in group 2 were randomly divided into 7 subgroups with 8 rats in each subgroup,and were detected by histopathological and terminal deoxynucleotidyl transferasemediated dUTP nick end labeling (TUNEL) apoptosis examines 1, 3 days, 1,2,4,6,8 weeks after injury;2 rats in group 3 were examined by electron microscopy 4 and 8 weeks after injury.According to the degree of injury, the injured eyes were divided into 2 groups including severe injury group with the beat pressure of (699.14plusmn;60.79) kPa and mild injury group with the beat pressure of (243.18plusmn;20.26) kPa.The right and left eyes in rats in each group were in severe and mild injury group, respectively.Results One day after injury, the latency duration of FVEP prolonged in severe injury group,wich differed much form which in the normal control group (P<0.05);the amplitude was gradually reduced during the first 2 weeks after injury and kept steady after that (P>0.05). The latency duration prolonged in mild injury group,and its difference with the normal control group was statistically significant (P<0.05);the amplitude was gradually reduced during the first 4 weeks after injury and kept steady after that (P>0.05). The abnormal high signal could be seen on optic nerve 1 day after injury, and was still obvious 8 weeks later. The results of histopathological examination showed ruptured capillary in ganglion cell layer 1 day after injury;retinal ganglion cells without nucleus could be seen 4 weeks after injury. The apoptosis of positive cells was found in each layer of the retina 3 days after injury.TUNEL results indicated that the number of apoptotic positive cells increased significantly 1-2 weeks after injury.Conclusion An animal model of optic nerve injury can be successfully set up using FPI in rats.

    Release date:2016-09-02 05:42 Export PDF Favorites Scan
  • Clinical Study of Psychotic Disorder after Gravis Type of Craniocerebral Injury

    摘要:目的:探讨重型颅脑损伤后早期精神障碍临床特征及治疗方法,以提高患者的生活质量。方法:对我院48例重型颅脑损伤后早期精神障碍患者进行回顾性分析,观察精神障碍出现的时间、精神障碍的类型及预后及颅脑损伤的部位与精神障碍的关系。结果:重型颅脑损伤后精神障碍主要出现在伤后3周内,多继发于颞叶损伤,其次为额叶。临床上主要有躁狂型、抑郁型、痴呆型、精神分裂性等四型,其中以躁狂型为多见。通过治疗后,lt;1个月精神症状痊愈25例、lt;2个月痊愈13例、治疗gt;2个月仍有精神症状10例。结论:颅脑损伤后精神障碍在原发脑损伤的有效治疗前提下,辅以抗精神障碍药物治疗、心理治疗及高压氧治疗等可取得较好疗效。

    Release date:2016-09-08 10:12 Export PDF Favorites Scan
  • 白细胞介素-1β与外伤后癫痫发生的联系——一个遗传学和生物标记物的队列研究

    外伤后癫痫(Post-traumatic epilepsy, PTE)是创伤性脑损伤(Traumatic brain injury, TBI)后的一个主要的并发症, 但遗传变异在调节PTE发生中的作用尚不清楚。假设TBI诱导的炎症可能是导致癫痫发生的原因, 对白细胞介素-1β(Interleukin-1β, IL-1β)基因的遗传变异情况, 脑脊液和血清中IL-1β水平和IL-1β的脑脊液/血清比值能否预测TBI后PTE的发生进行了评估。共调查了256例中度至重度TBI后患PTE的成年白种人。对IL-1β标记和功能性单核苷酸多态性(SNPs)进行基因分型。对遗传变异性和PTE的发生进行评估。在调查患者中抽取一部分患者(n=59)在其外伤后1周内收集血清和脑脊液的IL-1β, 并评估它们与IL-1β基因变异及PTE的关系。临时配对IL-1β的脑脊液/血清比值以反映血清IL-1β水平对脑脊液IL-1β的影响。多变量分析显示随着时间推移, 高脑脊液/血清IL-1β比值与PTE风险增加有关(P=0.008)。rs1143634的多变量分析揭示了CT基因型与PTE风险增加有关(P=0.005)。CT基因型组其血清IL-1β水平较低(P=0.014), 脑脊液/血清IL-1β比值较高(P=0.093)。这是第一个揭示PTE风险中的IL-1β基因变异, 及TBI后IL-1β基因变异与血清IL-1β水平的关系和IL-1β比值与PTE风险的关系。根据这些发现, 提出基因和IL-1β比值与PTE的相关性可能归因于TBI恢复期的血脑屏障完整性的生物变异性包括。为进一步的研究提供了理论依据, 验证遗传变异性对TBI后IL-1β产生的影响, 评估造成脑脊液/血清IL-1β比值与PTE相关性的基因介导的信号传导机制, 及评估减少PTE的靶向IL-1β治疗。

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  • RELATIONSHIP BETWEEN HYPOXIA INDUCIBLE FACTOR 1α EXPRESSION AND NEURON APOPTOSIS DURING HYPOXIA ISCHEMIA BRAIN DAMAGE IN NEONATAL RATS

    Objective To investigate the relationship between the expression of hypoxia inducible factor 1α (HIF-1α) and the neuron apoptosis during a hypoxia ischemia brain damage and explore the role of HIF1α in regulating the neuron apoptosis and repairing the brain damaged by hypoxia and ischemia. Methods Forty SD rats aged 10 days were randomly divided into the experiment group and the control group, with 20 rats in each group. In the experimental group, the rats were anesthetized with ethylether. The right common carotid artery was exposed and ligated. Then, they were exposed to hypoxia ina normobaric chamber filled with 8% oxygen and 92% nitrogen for 2.5 hours. In the control group, the right common carotid artery was exposed but was not ligated or exposed to hypoxia. The brain tissues were harvested from the rats in the both groups at 4, 8, 24, 48 and 72 hours after the hypoxia and ischemia, and fromthe rats in the control group at the same time points. The HIF-1α protein expression and the cleaved caspase 3 (CC3) protein expression were detected with the immunohistochemistry method. The apoptosis cells were detected with the TUNEL staining method. Results In the experimental group, the HIF-1α expression was significantly increased at 4 hours after operation, at the peak level at 8 hours, and began to decrease at 24 hours. The CC3 protein was expressed at 4 hours after operation, and was slightly expressed at 8 hours, but was significantly increased at 24 hours; the higher levels were maintained at 48 and 72 hours. However, in the control group, both the expression levels of HIF-1α and the CC3 protein were extremely low. So, the expression levels of HIF-1α andthe CC3 protein were significantly higher in the experimental group than in the control group (P<0.01). The TUNEL staining showed that in the experimentalgroup the positive cells were significantly increased after the hypoxia and ischemia, with a peak level at 72 hours after the hypoxia and ischemia; however, in the control group there were few positive cells.TUNEL positive cells in the experimental group were significantly more than that in the control group(P<0.01).ConclusionThe expression tendency of HIF-1α is completely different from that of CC3.HIF-1α may have a protective role in regulating the neuron apoptosis in the neonatal hypoxia-ischemia brain damage and may promote the repairing and rebuilding process in the brain that was damaged by hypoxia and ischemia.

    Release date:2016-09-01 09:22 Export PDF Favorites Scan
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