创伤性脑损伤的临床康复研究

创伤性脑损伤 (traumaticbraininjury ,TBI)在欧美发病率较高 ,初步统计是创伤性脊髓损伤的 30～ 4 0倍 ,在某些方面 ,接近于脑卒中的发病率。其病因多为交通事故、体育活动、工伤和暴力袭击 ,主要为青年男性患者 ,美国统计 ,15～ 2 4岁青年男性的发病率≥ 5 5 0人 /10 0 0 0 0人口。严重TBI的良好结局依赖于长期的综合性康复治疗 ,大多数患者的社会生活能力较差 ,家庭和社会为此负担较大。1　预后评价和影响因素对TBI急性期患者进行预后评价 ,可以获得一个有意义的功能基线 ,便于今后比较。康复治疗前的临床评价有助于判断治疗效果。有…     

Extracellular signal regulated kinases 1/2 signal pathway and responses of astrocytes after diffuse brain injury

BACKGROUND: The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE: To observe the effect of over activity of extracellular signal regulated kinases 1/2 (ERK1/2) signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN: Completely randomized grouping and controlled animal study. SETTINGS: Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: A total of 158 healthy male SD rats, of 11 weeks old, weighing 320–370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 (pERK1/2) polyclonal antibody was provided by R&D Company; rabbit-anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase (HRP)-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS: The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression: A total of 110 rats were randomly divided into sham operation group (n =5), model group (n =35), high-dosage U0126 group (n =35) and low-dosage U0126 group (n =35). Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Another 48 rats were randomly divided into sham operation group (n =3), model group (n =15), high-dosage U0126 group (n =15) and low-dosage U0126 group (n =15). The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma –4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES: pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS: ① pERK1/2 expression: After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points (P < 0.01); meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Positive expression of pERK1/2 lasted in brain tissue from 30 minutes to 72 hours after diffuse brain injury (P < 0.05). In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION: Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.     

急性重型脑损伤患者脑组织氧代谢监测及意义

目的　探讨对急性重型脑损伤患者行脑组织氧代谢监测的临床意义。　方法对2 8例急性重型脑损伤患者 (均在全麻下急诊行血肿清除术和 (或 )去骨瓣减压术 )术中及术后持续进行脑组织氧代谢监测 ,观察脑组织氧分压 (PbtO2 )、二氧化碳分压 (PbtCO2 )和pH值 (pHbt)的变化。　结果　 (1) 2 8例脑外伤患者在剪开硬脑膜后PbtO2 、pHbt分别从 (13± 4 )mmHg、(6 .96± 0 .15 )增加至 (2 1± 5 )mmHg、7.0 5± 0 .12 (P <0 .0 5 ) ,PbtCO2 从 (6 1± 6 )mmHg下降至 (5 3± 5 )mmHg(P <0 .0 5 )。(2 )其中 2 4例脑外伤患者在血肿清除后 ,PbtO2 、pHbt值分别从 (2 1± 4 )mmHg、7.0 5± 0 .11增加至 (2 8± 6 )mmHg、7.15± 0 .10 (P <0 .0 5 ) ,PbtCO2 从 (5 2± 6 )mmHg下降至 (4 5± 4 )mmHg(P <0 .0 5 )。 (3)PbtO2 <10mmHg持续 30min以上的患者预后差。　结论　 (1)脑组织氧代谢监测是一种安全、可靠的监测手段 ,能直接动态反映脑组织的病理生理变化 ,及时发现脑组织缺血缺氧 ,以指导治疗。 (2 )持续进行脑组织氧代谢监测可判断重型脑外伤患者的预后。     

黄体酮对创伤性脑损伤后炎症因子的抑制作用的研究

创伤性脑损伤（Traumatic brain injury，TBI）后的炎症反应是导致继发性脑损害的主要原因之一。在TBI发生后早期，即有大量致炎细胞因子的释放和免疫细胞的激活。免疫细胞的激活，反过来又会导致自由基和更多的炎症介质释放。无论这种炎症级联反应由何种因素启动，对炎症反应的抑制都可以减轻脑水肿，减少神经元的死亡或胶质增生。     

重型颅脑损伤后继发脑损伤的研究进展

近几年,继发性脑损伤在重型颅脑损伤病人伤后病程中的作用越来越受到重视,开展了广泛的研究。目前认为:脑灌注压不足、颅内高压、脑氧代谢率降低、脑血流量下降以及失控性炎症反应等是严重创伤后发生继发性脑损伤的重要机制。相互之间平衡关系的调节是预防和治疗继发性脑损伤的关键。颅脑损伤后继发性脑损伤病理生理的研究,对预防颅脑损伤病人的继发性脑损伤和提高疗效具有重要意义。     

低能量血管内激光照射治疗脑损伤的免疫功能变化与研究

本文对49例接受低能全血管内激光照射治（ILIB）的脑损伤病人的免疫功能改变进行研究．研究显示，低能量血管内激光照射疗法可明显改善免疫状态和免疫反应水平，增强免疫功能和机体抗感染能力．     

双瞳散大患者手术治疗经验

双瞳散大患者手术治疗经验胡开树，蔡学见，陈铮立，王玉海，顾中贤，房文峰，许永军，刘斌本文总结十年来双瞳散大病人１２２例，未手术２３例，死亡１９例，手术９９例，死亡６３例。与国内外文献报告的双瞳散大病人死亡率５７％～１００％相似（１）。现将本组病人救治...     

甲基门冬氨酸受体与兴奋毒性

本文对甲基门冬氨酸受体在继发性脑损伤兴奋毒性机制中的病理生理作用进行了综述。该领域的研究成果提示甲基门冬氨酸受体拮抗剂有希望成为防治脑损伤新的治疗药物。     

重症服外伤后脑积水34例临床分析

月经过多是妇科常见症状 ,传统的治疗方法是以缓解症状为主的药物治疗和刮宫术 ,虽有近期疗效 ,但远期治疗效果不理想。一旦药物治疗无效或不能耐受者 ,只能行子宫切除术 ,且子宫切除术后病率仍高达4 0 % [1] 。微波子宫内膜去除术 (ＥＭＡ)是目前治疗月经过多的新技术之一 ,本院采用ＥＭＡ治疗 33例难治性月经过多患者 ,结果报道如下。1　临床资料1.1　研究对象　 2 0 0 1年 3～ 11月本院应用微波宫内膜去除仪治疗月经过多患者 33例 ,均符合以下标准 :①已婚妇女无生育要求 ;②月经过多 (每次月经用卫生巾均 >2 6片 ) ;③继发性贫血中度以…     

亚低温对缺氧缺血脑损伤保护作用的研究进展

近年研究证明缺氧缺血脑损伤期间和损伤后，亚低温能够提供脑保护作用。适当延长亚低温维持时间可以抑制神经元迟发性死亡。保护机制是通过降低脑氧代谢率，改善细胞能量代谢，抑制细胞毒性过程等多个环节。在新生儿临床广泛应用前尚需解决许多问题。