神经干细胞静脉移植治疗脊髓损伤的实验研究

[目的]观察神经干细胞静脉移植对损伤大鼠脊髓功能的治疗作用。[方法]取孕14—16dSD胎鼠的脑室下区组织，体外培养后鉴定细胞。制作脊髓全切模型，伤后1周将Brdu标记好的神经干细胞通过尾静脉注射移植到大鼠体内，移植后及8周行皮层体感诱发电位（CSEP）检测和BBB功能评分，并留损伤脊髓处作病理切片及免疫组化染色。[结果]（1）移植后8周BBB评分损伤组、移植组都有所恢复，但都未达到正常水平，移植组恢复较好；（2）模型制作后，CSEP波均消失，细胞移植后8周移植组的波形有不同程度的恢复，但潜伏期延长；（3）移植组大鼠脊髓损伤处存在大量Brdu染色阳性细胞，表明移植的细胞在体内可到达损伤脊髓处并能存活；脊髓损伤部位NF-200及GFAP染色阳性的细胞表明移植的细胞可以分化为具有神经元和胶质细胞特性的细胞。[结论]静脉移植的神经干细胞能到达损伤区代替受损的神经元及神经胶质细胞，使损伤的脊髓功能得到一定程度的恢复。     

经前后路联合手术治疗L5S1椎体结核

目的 探讨一期经前路病灶清除后路植骨内固定治疗L5S1椎体结核的临床疗效.方法 对40例L5S1椎体结核患者,采用一期经前路病灶清除椎体间植骨加后路椎弓根螺钉内固定植骨融合治疗.结果 所有患者随访6～24个月,35例植骨融合良好,5例融合欠佳;有1例出现尿路感染.结论 一期经前路病灶清除椎体间植骨加后路椎弓根螺钉内固定椎板植骨治疗L5S1椎体结核能在彻底清除病灶的前提下保证脊柱的稳定性,提高植骨块的融合率和缩短患者卧床时间.     

腰椎间盘突出症合并椎管狭窄23 例治疗分析

目的探讨经后路椎间盘镜手术治疗合并腰椎管狭窄症的椎间盘突出症的临床应用。方法采用后路椎间盘镜进行单侧开窗减压术。通过术前标记腰椎正侧位片定位，于定位棘突间隙后正中偏患侧作长约1.5 cm小切口，逐级扩张后置入工作通道管，钻除部分椎板，置入内窥镜，于电视监视器下显露椎板、增生内聚的关节突、肥厚的黄韧带及突出的椎间盘髓核组织，彻底解除其对硬脊膜、神经根的压迫。结果本组共治疗合并腰椎管狭窄症的腰椎间盘突出症23例，平均随访7个月，按Prolo标准评定，治愈20例，有效2例，无效1例。结论本术式在严格掌握适应证前提下对合并腰椎管狭窄症的腰椎间盘突出症患者效果明显。     

椎管内神经鞘膜肿瘤的MRI

本文总结了椎管内神经鞘膜肿瘤的MRI表现并与病理结果进行了对照。MRI诊断准确率为82.6％。哑铃征及弄清脊髓与肿瘤的关系是MRI诊断椎管内神经鞘膜肿瘤的要点,本组病例哑铃征出现率为42.1％。但椎管内神经鞘膜肿瘤的MR信号变化与脊膜瘤和室管腆窟无法区分。     

Time for sport and health to be formally linked in a positive way

Preventing sports injury has rarely been cited as an appropriate action to respond to the obesity epidemic, and in fact a recent letter has suggested that those playing sport are as responsible for their predicament as those who are obese. This opinion piece argues that it is time for better prevention and management of sports injury to be seen as part of the complex solution to preventing obesity, rather than being a self-inflicted problem that governments should continue to ignore.     

无水酒精阻滞大鼠腹腔神经丛后脊髓、孤束核C-FOS和NOS-1的表达

目的:通过免疫组化的方法研究无水酒精阻滞大鼠腹腔神经丛后脊髓和延髓孤束核内CFOS和NOS1的表达。材料和方法:对70只Wistar大鼠实施手术,建立实验动物模型。分5组于术后不同时间取得脊髓和延髓样本,并用标准方法对其进行CFOS和NOS1免疫组化染色,观察脊髓和延髓孤束核CFOS和NOS1的表达。结果:无水酒精阻滞后脊髓后角、延髓孤束核神经元细胞内均有CFOS和NOS1表达。结论:无水酒精阻滞腹腔神经丛后,短时间内脊髓后角和延髓孤束核内CFOS和NOS1表达阳性,表明FOS和NOS1与内脏信息在脊髓水平的传导有关。CFOS和NOS1参与了内脏信息在孤束核内的传导。     

Idiopathic Spinal Cord Herniation as a Treatable Cause of Progressive Brown-Sequard Syndrome

Idiopathic spinal cord herniation is a rare spinal cord disorder caused by spinal cord prolapse through a adural defect. It is a curable disease, so early detection is of particular importance. We report a 38-year-old woman with Brown-Sequard syndrome which was caused by the thoracic spinal cord herniation. Her weakness was almost completely resolved after surgical management, which emphasizes the importance of early diagnosis and surgical management in this rare disease entity.     

PLDD治疗拒绝开放手术的脊髓型颈椎病患者的疗效观察与思考

目的：探讨经皮激光椎间盘减压术（PLDD）治疗拒绝开放手术的脊髓型颈椎病患者的疗效。方法：2002年～2006年应用PLDD治疗16例拒绝开放手术的脊髓型颈椎病患者，手术前后采用日本骨科学会（JOA）17分法进行评价．计算改善率及优良率，随访观察治疗效果。结果：手术时间平均为15min，术中无明显出血，无血管、神经损伤及感染等并发症发生。术后1、3、6、12个月时JOA评分改善率分别为28．54％、34．82％、41．09％和47．57％．优良率分别为31．3％、37．5％、37．5％和56．0％。随访24个月者11例，改善率为46．56％，优良率为54．4％。结论：PLDD治疗脊髓型颈椎病患者有一定疗效，对拒绝开放手术的脊髓型颈椎病患者是一种可供选择的微创治疗手段。     

Effect of the free radical scavenger MCI-186 on spinal cord reperfusion after transient ischemia in the rabbit

Objective: Paraplegia remains a serious complication of aortic operations. The production of free radicals during reperfusion after transient ischemia is believed to induce secondary spinal neuronal injury, resulting in paraplegia. The aim of the present study was to clarify the protective effect and method of administration of antioxidants on the neurological and histological outcome in the animal model for reperfusion injury after transient spinal cord ischemia. Methods: New Zealand white rabbits underwent surgical exposure of the abdominal aorta that was clamped for 15 minutes to achieve spinal cord ischemia. Group A animals received two 10 mg/kg doses of 3-methyl-l-phenyl-2-pyrazolin-5-one (MCI-186) at the time of release of the aortic clamp and 30 minutes later. In group B, MCI-186, 5 mg/kg, was given three times, at the time of aorta clamp release, 30 minutes and 12 hours later. In group C (control group), one dose of vehicle was administered. Neurological status was assessed using modified Tarlov’s score until 168 hours after operation. Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage. Results: Groups A and B animals had better neurological function than group C (p(0.001). In contrast, group C animals exhibited paraplegia or paraparesis with marked neuronal necrosis. The number of surviving neurons within examined sections of the spinal cord was significantly greater in group B than in group C (p(0.001). Conclusion: In a 15-minute ischemia-reperfusion model using rabbits, systemic repetitious administration of MCI-186, a free radical scavenger, was found to have a protective effect on the spinal cord neurons both neurologically and histologically. We postulate that the drug minimizes the delayed neuronal cell death for reperfusion injury after transient ischemia by reducing the free radical molecules. Moreover, it was thought that we could protect delayed neuronal cell death more effectively by administering MCI-18612 hours later.