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1.
目的 建立并验证一种新型慢性压迫性颈脊髓损伤大鼠模型. 方法 2011年6-2011年11月,将54只SD大鼠随机分为对照组(n=6)、急性压迫组(4h、24h,n=6)、慢性压迫组(4h、12 h、24 h、48 h、72 h、1周,n=6).在C5~6硬膜外间隙置入不同规格吸水聚氨酯胶片制作急、慢性压迫性脊髓损伤模型.造模后不同时间行MRI、组织学和组织化学观察,运动功能评分(BBB)评价神经功能. 结果 ①急性压迫组4 ~24 h,T2WI见脊髓明显受压、髓内高信号,组织学见脊髓出血坏死,前角神经元计数显著低于对照、慢性压迫组(P<0.05),BBB评6.0分.②慢性压迫4~12h,见脊髓水肿、中央管变形,神经元计数、髓鞘染色强度与对照组比较,差异无统计学意义(P>0.05),BBB评20.6分;24 ~ 72 h,脊髓受压明显,中央管扩大、静脉淤血,神经元计数减少(P<0.05),后索神经纤维排列紊乱、断裂,髓鞘染色强度低于对照组(P<0.05),BBB评19.3分;1周,髓内空泡化,神经元数目减少(P<0.05),后索髓鞘蓝染强度低于对照组(P<0.05),BBB评17.5分.T2WI示脊髓受压变形,髓内未见出血信号. 结论 慢性压迫组造模方法可以实现慢性压迫性脊髓损伤,符合慢性压迫性脊髓损伤的病理、影像学和神经功能变化特征.  相似文献   

2.
Chen ZJ  Qiu Y  Ma WW  Zhu F 《中华外科杂志》2010,48(15):1145-1148
目的 探讨体感诱发电位(SEP)检查在伴脊髓发育畸形的先天性脊柱侧凸(CS)中的诊断价值.方法 回顾性分析2001年9月到2007年9月诊治的187例CS患者临床资料,其中男性85例,女性102例;年龄3~22岁,平均13.8岁.所有患者均行全脊髓磁共振检查判断是否存在脊髓发育畸形.分析术前SEP的峰潜伏期及左、右侧峰潜伏期差值.SEP波形消失、峰潜伏期延长及峰潜伏期不对称定义为SEP异常.比较有无脊髓发育畸形患者的临床特征及SEP异常发生率的差异.结果 共有32例患者伴脊髓发育畸形.CSⅢ型(混合型)伴脊髓发育畸形比例(30.8%)高于Ⅰ型和Ⅱ型(P<0.05).伴脊髓发育畸形组平均侧凸Cobb角大于无脊髓发育畸形组(P<0.05),而两组平均后凸Cobb角差异无统计学意义(P>0.05).伴脊髓发育畸形组SEP异常率与无脊髓发育畸形相比,差异有统计学意义(x2=4.70,P<0.05).结论 SEP检查可以评估CS患者的神经功能状态,对CS伴脊髓发育畸形具有辅助诊断价值.  相似文献   

3.
目的 利用有限元法研究不同载荷条件下颈脊髓过伸损伤时脊髓内不同区域的应力分布特征. 方法 利用颈脊髓的三维有限元模型(此模型由8484个节点和14 297个单元组成),进入Ansys前处理器,设置边界条件和不同大小的载荷配置:第Ⅰ种载荷配置:后伸载荷0.0015 N,压缩载荷1N;第Ⅱ种载荷配置:后伸载荷0.0030 N,压缩载荷2 N;第Ⅲ种载荷配置:后伸载荷0.0045 N,压缩载荷3N;第Ⅳ种载荷配置:后伸载荷0.0060 N,压缩载荷4 N;第Ⅴ种载荷配置:后伸载荷0.0075 N,压缩载荷5N.模拟不同损伤情况,进入求解模块,进行过伸损伤负载模拟计算,最后进入Ansys后处理器,读取并分析颈脊髓横断面9个不同功能区域(颈脊髓白质前索、侧索外侧部、侧索内侧部、后索外侧部、后索内侧部、灰质前角、前角底部、后角尖和头部及后角颈部)的应力分析结果. 结果 颈脊髓损伤断面应力云图提示应力主要集中于灰质前角、后角和白质前索、侧索内侧和后索外侧内,并且其平均应力依次减小.随着施加载荷的增大,灰白质内各个部位的应力均明显增加,灰质前角内的应力增幅最大.灰质前角和白质侧索的应力增幅值比较差异有统计学意义(P<0.05),后角和白质前索分别与后索应力增幅值比较差异均有统计学意义(P<0.05),后角和白质前索应力增幅值比较差异无统计学意义(P>0.05). 结论 轻度颈脊髓过伸损伤主要造成白质前索和灰质前后角损伤,表现为以上肢为主的运动和感觉异常.随着损伤载荷加大,应力分布向相邻白质扩展,载荷加大后前角支配手内肌的神经元细胞较其他部位损伤更严重.  相似文献   

4.
绵羊慢性压迫性颈脊髓病动物模型的建立及评估   总被引:1,自引:0,他引:1  
目的:探讨颈脊髓慢性压迫动物模型的建立方法及可行性评估。方法:将9只绵羊分为对照组(A组)、1个月组(B组)和3个月组(C组)。经颈前路手术将新型注射压迫系统的致压球囊置入C4/5椎间隙并固定,将注射阀埋于颈后皮下。A组术后不注射碘海醇,B、C组术后每周经皮向注射阀注射0.1ml碘海醇,使球囊缓慢膨胀,对颈脊髓产生慢性压迫。每4周于全麻下行颈椎X线、CT和MRI检查。每次注射造影剂后和检查前后用Tarlov评分法对动物进行行为学评价。终止观察时取压迫节段脊髓进行病理观察及电镜观察超微结构变化。应用单因素方差分析评估不同组实验动物行为学的差异,用Pearson相关系数分析各观测参数的相关性。结果:A组各时间点Tarlov评分均为5分。B组及C组每次注射造影剂前后Tarlov评分不变。终止观察时B组实验动物平均椎管侵占率为54.6%,Tarlov评分1只4分,2只5分;C组实验动物平均椎管侵占率67.6%,Tarlov评分1只2分,2只3分。肉眼可见B组受压节段脊髓变扁,C组明显凹陷;病理学检查见B组受压节段脊髓前角内神经元数量减少,胞体周围间隙增大,尼氏体减少,白质轻度脱髓鞘,部分轴突空泡变性;C组白质出现片状脱髓鞘区和空泡变性,灰质内多量神经元变性,可见核固缩、尼氏体减少或消失。电镜下B组神经元胞质内粗面内质网轻度扩张,部分线粒体肿胀,轴突空泡变性,形态不规则,髓鞘松解,部分轴突髓鞘脱失;C组神经元可见胞膜崩解,核固缩,粗面内质网明显扩张,核糖体脱失,线粒体广泛空泡变性,髓鞘崩解,轴突肿胀,基质致密,部分轴突消失。A组未见异常组织学改变。结论:术后实验动物行为学、影像学和组织学检查符合慢性压迫性颈脊髓病特点,新型注射压迫系统可以辅助建立稳定、可靠的慢性颈脊髓压迫动物模型。  相似文献   

5.
[目的]探讨脊髓受压及减压后,大剂量维生素C(vitaminC)联合小剂量甲基强的松龙(MP)对脊髓灰质血流量,体感诱发电位(SEP),组织学变化,运动功能的影响.[方法]36只犬随机分为3组,每组12只.A组于SEP消失后5min静脉注射MP 30 mg/kg,以5.4 mg (kg·h)输液泵静脉注射;B组于SEP消失后5min以同样方式注射vitaminC 200 mg/kg+ MP 10 mg/kg,减压后12 h,24h各注射vitaminC 200 mg/kg;C组于SEP消失后5min静脉注射0.9%氯化钠,同样以5.4 mg(kg·h)输液泵静脉注射.均持续90 min后减压,期间检测SEP及脊髓灰质血流量,减压后3h重复检测,并进行改良Tarlov评分.减压后28 d通过病理组织学分析确定损伤的范围.[结果]在持续压迫期间A组4只犬出现了SEP,B组5只犬出现了SEP,C组无一出现.减压后A组有2只犬出现SEP,B组有2只犬出现SEP,C组有1只犬出现SEP.三组犬中出现SEP的脊髓灰质血流量明显高于没有出现SEP的犬(P<0.05).A、B组脊髓灰质血流量明显高于C组(P<0.05).A、B组动物后肢的运动功能可以较快恢复,C组不能恢复.A、B组脊髓损伤范围与C组具有显著性差异,病理改变与SEP及脊髓血流量具有相关性,与运动功能的恢复具有相关性.[结论]大剂量维生素C与小剂量甲基强的松龙联合应用在神经功能保护及恢复方面提供了显著持续的作用,可能增加了脊髓局部的血流量.维生素C可以部分替代甲基强的松龙对于脊髓损伤的作用.  相似文献   

6.
目的 探讨姜黄素对神经病理性痛大鼠脊髓背角及背根神经节(DRG)神经元大麻素受体1 (CBR1)及含NR2B亚基N-甲基-D-天冬氨酸(NMDA)受体表达的影响.方法 雄性SD大鼠72只,体重200~230 g,采用随机数字表法,将其随机分为4组(n=18):假手术组(S组)、慢性压迫性损伤组(CCI组)、姜黄素组(Cur组)和溶媒对照组(SC组).S组仅分离、暴露坐骨神经,其余3组采用慢性压迫性损伤法制备神经病理性痛模型.Cur组术后腹腔注射姜黄素100 mg·kg-1·d-1,连续14 d,SC组给予等容量二甲基亚砜.分别于术前2d、术后1、3、7、10、14 d时测定机械缩足反应阈值(MWT)和热缩足潜伏期(TWL).分别于术后3、7、14 d时处死6只大鼠,取脊髓背角和DRG,采用免疫组化法检测神经元CBR1和NR2B的表达.结果 与S组比较,其他3组术后MWT降低,TWL缩短,脊髓背角和DRG神经元CBR1和NR2B表达上调(P<0.05);与CCI组比较,Cur组术后MWT升高,TWL延长,脊髓背角和DRG神经元CBR1表达上调,NR2B表达下调(P<0.05),SC组上述指标差异无统计学意义(P>0.05).结论 姜黄素可减轻大鼠神经病理性痛,其机制与脊髓背角及DRG神经元CBR1表达上调、NR2B表达下调有关.  相似文献   

7.
目的 :探讨缺氧诱导因子-1α(hypoxia inducible factor-1α,HIF-1α)和基质金属蛋白酶-2(matrix metalloproteinases-2,MMP-2)在慢性压迫性颈脊髓损伤大鼠模型中的表达及意义。方法 :将80只成年SD大鼠随机分为假手术组和慢性压迫性颈脊髓损伤组(脊髓压迫组),每组40只。大鼠麻醉后充分显露C5和C6椎板,切除C5左侧半椎板,显露硬脊膜,脊髓压迫组在C6椎板和硬脊膜之间置入吸水后可膨胀聚氨酯薄板(1×3×1mm);假手术组只显露硬脊膜不置入压迫物。两组分别通过BBB(Basso Beattie Bresnahan)评分和体感诱发电位(somatosensory evoked potential,SEP)检测评估脊髓功能;于造模后7d、28d、42d和70d时处死大鼠取颈脊髓组织进行HIF-1α及MMP-2免疫组化染色,检测其在各时间点的表达量(IOD值),采用独立样本t检验比较两组各时间点的差异,分析HIF-1α、MMP-2与脊髓功能变化的相关性。结果:造模后7d时,两组BBB评分无显著性差异;SEP潜伏期显著性延长,波幅显著性降低;HIF-1α显著性降低,MMP-2显著性升高。28d时脊髓压迫组BBB评分显著性低于假手术组,SEP潜伏期与7d比较显著性延长(P0.05)、波幅显著性降低(P0.05),HIF-1α表达显著性增高(P0.05),而MMP-2表达显著性降低(P0.05)。42d时,脊髓压迫组BBB评分、SEP潜伏期和波幅与28d时比较无显著性差异,HIF-1α表达显著性增高(P0.05),而MMP-2表达显著性降低(P0.05);70d时脊髓压迫组神经功能较28d时显著性改善,BBB评分显著性增高(P0.05),SEP潜伏期显著性缩短(P0.05)、波幅显著性升高(P0.05);HIF-1α表达较前显著性降低,而MMP-2表达升高,但与假手术组比较仍有显著性差异(P0.05)。HIF-1α表达量与BBB评分呈显著性负相关(r=-0.458,P0.05),MMP-2表达量与BBB评分呈显著性正相关(r=0.903,P0.05)。结论:大鼠慢性压迫性脊髓损伤后具有一定程度的自我修复能力,HIF-1α、MMP-2表达变化与慢性脊髓压迫性损伤后神经功能改善相关。  相似文献   

8.
目的:观察大鼠慢性颈脊髓压迫减压术后神经功能的恢复情况,探讨其相关机制。方法:30只成年SD大鼠随机分为假手术组(A组,10只)、压迫组(B组,10只)和减压组(C组,10只)。压迫组和减压组在C6~C7椎板下置入聚乙烯醇丙烯酰胺互穿网络水凝胶制作慢性颈脊髓压迫模型,减压组于造模后4周行手术咬除椎板充分减压。三组均于造模后4周行运动诱发电位(MEP);12周先行MRI和MEP检测,再处死大鼠取出颈段脊髓,行大体形态观察和组织学切片,快蓝(LFB)染色观察三组大鼠脊髓组织髓鞘变化,免疫荧光染色观察神经元数目形态及脑源性神经营养因子(BDNF)和血管内皮生长因子(VEGF)表达的变化。结果:造模后4周时,B、C组MEP潜伏期与A组比较明显延长(P<0.05),波幅与A组比较明显降低(P<0.05),B组和C组比较潜伏期和波幅均无显著性差异(P>0.05)。造模后12周时MRI轴位和矢状位均显示B组大鼠椎管狭窄,颈脊髓明显受压,A组和C组大鼠椎管无明显狭窄,脊髓无明显受压;三组间MEP潜伏期和波幅两两比较差异有显著性(P<0.05),潜伏期A组C组>B组。大体形态观察示A组脊髓形态正常,B组脊髓受压节段压痕明显,C组压痕较B组轻。LFB染色示A组脊髓组织中髓鞘染色密集,B组轴突脱髓鞘明显,C组脱髓鞘现象较B组轻。免疫荧光染色示A组脊髓组织中可见大量形态正常的神经元;B组脊髓受压节段压迫侧神经元明显减少,胞体固缩;C组脊髓受压节段神经元数量比B组多,有轻微细胞固缩,三组神经元计数有显著性差异(P<0.05),A组>C组>B组。免疫荧光染色示A组大鼠脊髓组织有少量BDNF和VEGF的表达;B组大鼠BDNF表达水平较A组有所升高,且主要集中在脊髓受压部位附近的白质区域,VEGF表达无明显增加;C组BDNF和VEGF表达水平明显增加,主要集中在原受压部位白质周围,灰质部位有少量表达。C组BDNF和VEGF表达阳性细胞计数与A、B组比较有显著性差异(P<0.05);B组BDNF表达阳性细胞与A组比较有显著性差异(P<0.05),VEGF表达阳性细胞数与A组无显著性差异(P>0.05)。结论:大鼠慢性颈脊髓压迫减压术后神经功能有所恢复,其可能是通过减轻神经元损伤和轴突脱髓鞘改变、增加BDNF和VEGF的表达水平,从而促进受损脊髓组织的修复。  相似文献   

9.
低氧诱导因子-1α在大鼠脊髓缺血再灌注损伤中的表达   总被引:4,自引:0,他引:4  
目的 观察低氧诱导因子 1α(HIF 1α)在大鼠脊髓缺血再灌注损伤 (SCII)中的表达变化及其意义。方法 制备大鼠脊髓缺血再灌注损伤模型 ,分别于再灌注后 8、12、2 4h ,3和 5d取腰骶段的脊髓 ,以假手术组大鼠相同阶段的脊髓为对照 ,采用Westernblotting法和免疫组织化学检测伤后脊髓组织中HIF 1α的表达变化。结果 再灌注 8h左右 ,HIF 1α在整个脊髓灰质开始表达上调 ,在 2 4h达峰值 ,在伤后 3d表达回落 ,5d显著减少 ,灰度值在 8、12、2 4h ,3和 5d不同时相 ,分别为 (2 11.3 9± 5 .5 8)、(184.5 3± 6.5 6)、(167.3 9± 5 .76)、(198.44± 3 .98)和 (2 2 8.3 9± 2 .87) ,分别与假手术组比较 ,差异有显著性 (P <0 .0 5 )。HIF 1α在灰质中的表达以中央管周围和前角、后角最为显著。再灌注 2 4h和 3dHIF 1α在脊髓白质出现弱的表达 ,灰度值分别为 (2 3 8.15± 6.87)和(2 3 6.87± 7.41) ,分别与假手术组比较 ,差异有显著性 (P <0 .0 5 )。但在白质后索 ,HIF 1α的表达相对较强。HIF 1α在灰质中主要定位于神经元和星形胶质细胞 ,在白质中主要定位于神经胶质细胞。结论 HIF 1α呈现时序性的表达变化在脊髓缺血再灌注损伤中 ,可能是一种重要的脊髓缺血再灌注损伤的适应性调节。  相似文献   

10.
目的回顾性分析正中神经体感诱发电位(somatosensory evoked potential,SEP,)的检测结果和分型在脊髓型颈椎病(cervical spondylotic myelopathy,CSM)手术预后评估中的作用。方法随访76例接受手术治疗的CSM患者,男49例,女27例;年龄55—74岁,平均62.4岁。将术前检测SEP的波形分为5型:Ⅰ型为正常SEP,Ⅱa型为单独幅值异常,Ⅱb型为单独潜伏期异常,Ⅲ型为幅值和潜伏期同时异常,Ⅳ型为SEP消失。根据术前和术后随访的JOA评分评估临床症状和计算康复率,统计分析SEP与临床数据之间的相关性。结果SEPⅠ型18例,Ⅱa型16例,Ⅱb型17例,Ⅲ型14例,Ⅳ型11例。SEP与术前JOA评分有显著相关性(X^2=53.9,P〈0.05)。比较术后2年随访时的康复率发现Ⅰ型和Ⅱa型、Ⅱb型和Ⅲ型之间无显著性差异,而Ⅰ型和Ⅱa型、Ⅱb型和Ⅲ型、Ⅱb型和Ⅳ型之间有显著性差异(独立样本检验,P〈0.05)。结论SEP分型为临床提供客观、有价值的信息,有助于准确了解脊髓的受损程度和评估手术预后。  相似文献   

11.
Wang XY  Xu HZ  Chi YL  Lin Y  Huang QS  Mao FM  Ni WF  Wang S  Xu H 《中华外科杂志》2011,49(6):526-529
目的 探讨颈椎后路开门手术后脊髓减压程度的预测及方法.方法 收集2008年3月至2009年8月25例行颈椎单开门椎管成形术患者术前、术后的MRI图像.根据脊髓前方的压迫程度可分为0~4分;其中>3分(3和4分)表明有脊髓压迫,<3分表明脊髓无压迫.在开门节段上位椎体下终板做一水平线与脊髓前方成一交点,在开门节段下位椎体...  相似文献   

12.
目的 观察慢性压迫性脊髓损伤后大鼠运动功能变化及周围神经和骨骼肌中胰岛素样生长因子-1(IGF-1)表达变化.方法 将50只Wistar雌性大鼠随机分为正常组、假手术组和慢性压迫组.慢性压迫组置入平头塑料螺钉对大鼠脊髓进行后路渐进性压迫,于2个月后分别压迫至20%、40%、60%左右程度.行神经功能观察;处死大鼠后取腓肠肌作为标本,分别进行IGF-1的免疫组织化学和原位杂交染色.结果 大鼠后肢瘫痪程度随压迫程度加重而加重,各组坐骨神经和骨骼肌中IGF-1蛋白和mRNA表达分别为:20%组(236.9±3.2)、(231.5±2.9)、(245.6±3.4)、(246.6±2.7);40%组(205.3±2.7)、(202.2±3.4)、(209.4±2.6)、(214.6±2.5);60%组(215.4±3.5)、(219.3±4.1)、(231.9±2.3)、(238.5±2.7).各压迫组坐骨神经及骨骼肌中IGF-1 mRNA和蛋白表达增加,与正常组比较差异有统计学意义(P<0.05).结论脊髓压迫性损伤可引起周围神经及骨骼肌中IGF-1表达增加,提示机体调动保护因素以减轻脊髓损伤并促进其再生.
Abstract:
Objective To observe the changes in motor function and expression of insulin-like growth factor-1 (IGF-1) of peripheral nerve and skeletal muscle in rats after chronic spinal cord compression. Methods A total of 50 Wistar rats were randomly divided into normal group (n=10), sham operation group (group A,n=10) and chronic compressive group (goup B,n=30). The rats in group B were given gradual compression on the posterior spinal cord using blunt plastics screw. Compression degree reached 20% (n=10), 40% (n=10) and 60% (n=10) respectively after two months. The rats were killed, and gastrocnemius muscle cells were removed. The expression levels of IGF-1 protein and mRNA in peripheral nerve and skeletal muscle were detected by immunohistochemistry and hybridization respectively after chronic compressive spinal cord injury. Results The rat hind limb paralysis was exacerbated with the increase of the compression. In the sciatic nerve and skeletal muscle, the expression levels of IGF-1 protein and mRNA were: (236.9±3.2), (231.5±2.9), (245.6±3.4), (246.6±2.7) in 20% group; (205.3±2.7), (202.2±3.4), (209.4±2.6), (214.6±2.5) in 40% group; (215.4±3.5), (219.3±4.1), (231.9±2.3), (238.5±2.7) in 60% group. The expression levels of IGF-1 protein and mRNA in peripheral nerve and skeletal muscle were significantly up-regulated after compression (P<0.05). Conclusion The results indicate that body transfers the protective factor to relieve injury of CNS.  相似文献   

13.
Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord impairment worldwide and is a risk factor for traumatic central cord syndrome. Despite advances in surgery, there are no effective neuroprotective treatments for CSM, which reflects a limited understanding of its pathophysiology. In order to develop therapeutic strategies, we have developed a novel rat model of chronic progressive cervical spinal cord compression that mimics CSM. A titanium-screw-based chronic compression device (CCD) was designed to achieve progressive cord compression at the C6 level. The CCD was fixed to the C2 and T2 spinous processes and a threaded screw was turned to induce compression. Sprague-Dawley rats (n=75) were divided into three groups: (1) sham (no compression, n=6), (2) mild compression (1.4?mm stenosis, n=27), and (3) severe compression (2.6?mm stenosis, n=42). Compression was evaluated using micro-computed tomography (micro-CT). The area of spared white matter, extent of cord flattening ratio, and loss of neurons were assessed. Functional deficits were characterized using sensory-evoked potential (SEP) recordings, and with neurobehavioral tests: the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale, inclined plane, paw grip strength, and assessment of mechanical and thermal allodynia. Micro-CT confirmed progressive canal stenosis. The loss of intact white matter and cord flattening were significantly greater in rats with severe cord compression, and the number of neurons was reduced at the epicenter of cord compression. With chronic cord compression there was a significant decline in locomotor function, forelimb function, trunk stability/coordination, an increase in mechanical allodynia, and impaired axonal conduction. The CCD model results in chronic and precise cervical cord compression. The compression is associated with mechanical allodynia and measurable neurobehavioral, neurophysiological, and neuropathological deficits. We anticipate that the CCD model will enable the investigation of translationally-relevant therapeutic strategies for CSM.  相似文献   

14.
刘培太  廖文波 《实用骨科杂志》2009,15(9):641-645,686
目的通过磁共振分型研究,探讨过伸性颈椎颈髓损伤后合理的手术方式。方法对44例接受手术治疗的过伸性颈髓损伤患者进行回顾性分析。按MRI上显示的脊髓压迫情况将颈髓损伤分为五型,Ⅰa型(限于1~2个间盘层面前方压迫型)11例、Ⅰb型(3个间盘层面及以上前方压迫型)6例、Ⅱ型(单纯发育性椎管狭窄型)2例、Ⅲa型(限于1~2个间盘层面前后压迫型)8例、Ⅲb型(3个间盘层面及以上前后压迫型)17例。手术方式分前路、后路、前后联合入路三种减压植骨固定术式。Ⅰa型患者均采用前路术式;Ⅰb型和Ⅱ型患者7例采用后路术式,1例采用联合入路术式;Ⅲ型(Ⅲa型和Ⅲb型)患者8例采用前路术式,9例采用后路术式,8例采用联合人路术式。研究各型所采取的手术方式的疗效。结果经6~24个月随访,比较手术前后的Frankel分级及ASIA运动功能评分变化。41例脊髓功能有改善,较术前提高1~3级。Ⅰa型前路组、Ⅰb型和Ⅱ型后路组及Ⅲ型前路组、后路组、联合人路组术后较术前ASIA评分均有提高,差异有统计学意义(P〈0.05)。Ⅲ型前路组ASIA评分增加值最小,其中联合入路组大于后路组大于前路组,差异有统计学意义(均P〈0.05),但联合入路组和后路组相比差异无统计学意义(P〉0.05)。结论过伸性颈髓损伤的磁共振分型有助于术式选择,前路减压植骨内固定是治疗Ⅰa型损伤的有效术式,后路减压植骨内固定是治疗Ⅰb型和Ⅱ型损伤的有效术式;前后路联合术式和后路术式治疗Ⅲ型损伤的疗效均优于前路术式,单纯前路术式疗效较差。  相似文献   

15.
目的 探讨鞘内注射PSD-93反义寡核苷酸对神经病理性痛大鼠脊髓神经型一氧化氮合酶(nNOS)的影响.方法 雄性SD大鼠32只,体重250~350 g,随机分为4组(n=8):假手术+生理盐水组(C组);C7脊神经压迫+生理盐水组(N组);C7脊神经压迫+PSD-93误义寡核苷酸10μg组(M组);C7脊神经压迫+PSD-93反义寡核苷酸10μg组(A组).N组、M组和A组采用60 g微血管夹压迫大鼠右侧C7脊神经15 min制备神经病理性痛模型,经枕骨大孔鞘内置管至颈膨大处.术毕当日开始给药,每日1次,连续4 d.于术前2 d(T0)、术后1、3、5和7 d(T1-4)时测定机械痛阈和热痛阈,术后7 d处死大鼠取C7段脊髓,免疫组化法检测神经压迫侧脊髓PSD-93蛋白和nNOS的表达.结果 与T0时比较,N组和M组各时点机械痛阈及热痛阈降低(P<0.05);与C组比较,N组和M组各时点机械痛阈及热痛阈降低,N组、M组和A组脊髓背角PSD-93蛋白和nNOS表达上调(P<0.05);与N组和M组比较,A组各时点机械痛阈及热痛阈升高,脊髓背角PSD-93蛋白和nNOS表达下调(P<0.05).结论 鞘内注射PSD-93反义寡核苷酸可抑制神经病理性痛大鼠脊髓nNOS表达,nNOS在神经病理性痛中的作用可能受PSD-93蛋白调节.  相似文献   

16.
OBJECT: The goal of this study was to perform a biomechanical study of cervical flexion myelopathy (CFM) using a finite element method. METHODS: A 3D finite element model of the spinal cord was established consisting of gray matter, white matter, and pia mater. After the application of semi-static compression, the model underwent anterior flexion to simulate CFM. The flexion angles used were 5 degrees and 10 degrees , and stress distributions inside the spinal cord were then evaluated. RESULTS: Stresses on the spinal cord were very low under semi-static compression but increased after 5 degrees of flexion was applied. Stresses were concentrated in the gray matter, especially the anterior and posterior horns. The stresses became much higher after application of 10 degrees of flexion and were observed in the gray matter, posterior funiculus, and a portion of the lateral funiculus. CONCLUSIONS: The 5 degrees model was considered to represent the mild type of CFM. This type corresponds to the cases described in the original report by Hirayama and colleagues. The main symptom of this type of CFM is muscle atrophy and weakness caused by the lesion of the anterior horn. The 10 degrees model was considered to represent a severe type of CFM and was associated with lesions in the posterior fand lateral funiculi. This type of CFM corresponds to the more recently reported clinical cases with combined long tract signs and sensory disturbance.  相似文献   

17.
Objective: Although there are several classifications for cervical myelopathy, these do not take differences between spinal cord segments into account. Moreover, there has been no report of stress analyses for individual segments to date.

Methods: By using the finite element method, we constructed 3-dimensional spinal cord models comprised of gray matter, white matter, and pia mater of the second to eighth cervical vertebrae (C2–C8). We placed compression components (disc and yellow ligament) at the front and back of these models, and applied compression to the posterior section covering 10%, 20%, 30%, or 40% of the anteroposterior diameter of each cervical spinal cord segment.

Results: Our results revealed that, under compression applied to an area covering 10%, 20%, or 30% of the anteroposterior diameter of the cervical spinal cord segment, sites of increased stress varied depending on the morphology of each cervical spinal cord segment. Under 40% compression, stress was increased in the gray matter, lateral funiculus, and posterior funiculus of all spinal cord segments, and stress differences between the segments were smaller.

Conclusion: These results indicate that, under moderate compression, sites of increased stress vary depending on the morphology of each spinal cord segment or the shape of compression components, and also that the variability of symptoms may depend on the direction of compression. However, under severe compression, the differences among the cervical spinal segments are smaller, which may facilitate diagnosis.  相似文献   

18.
BACKGROUND AND OBJECTIVES: Pathophysiologic mechanisms underlying persistent neurologic deficits after continuous spinal anesthesia using hyperbaric 5% lidocaine are still not well understood. It has been suggested that high-dose intrathecal lidocaine induces irreversible conduction block and even ischemia in white matter tracts by breakdown of the blood-nerve barrier. In this study, we use diffusion-weighted magnetic resonance microscopy to characterize the effect of intrathecal hyperbaric 5% lidocaine in rat spinal cord. The parameter measured with DWM, is an "apparent diffusion coefficient," (ADC), which can be used to exclude the presence of ischemia. METHODS: Female Fischer CDF rats were used. Group 1 (n = 5) was exposed to ischemia, group 2 (n = 7) was exposed to intrathecal 5% hyperbaric lidocaine, and group 3 (n = 5) was exposed to intrathecal 7.5% glucose. Diffusion-weighted MR images in group 1 were acquired before and after ischemia induced by cardiac arrest and in groups 2 and 3 rats prior to and during perfusion of the spinal catheter with either 5% hyperbaric lidocaine or 7.5% glucose. RESULTS: Ischemia decreased the ADC by 40% in gray matter and by 30% in white matter of spinal cord. Continuous intrathecal anesthesia with hyperbaric 5% lidocaine did not affect the spinal cord ADC. Further, 7.5% intrathecal glucose had no effect on ADCs in gray or white matter of spinal cord. CONCLUSIONS: Ischemia reduced the ADC in both spinal cord white and gray matter. Hyperbaric 5% lidocaine did not affect the spinal cord ADC during the first 1.5 hours. We suggest that 5% hyperbaric lidocaine does not induce irreversible neurologic deficits by causing spinal cord ischemia.  相似文献   

19.
Primary damage to the blood-spinal cord barrier (BSCB) is a nearly universal consequence of spinal cord injury that contributes significantly to the overall pathology, including the introduction of reactive species that induce cytotoxicity as well as secondary insults on the BSCB itself. We have characterized quantitatively the extent and severity of primary, physical disruption of the BSCB in adult rats 5 min after graded trauma induced with the Impactor weight-drop model of spinal cord contusion. Animals were injured by dropping a 10-g mass 12.5, 25, or 50 mm (n(level) = 8) on to the exposed mid-thoracic spinal cord. The volume of extravasation of three markers of distinct size--fluorescently labeled hydrazide ( approximately 730 Da), fluorescently labeled bovine serum albumin ( approximately 70 kDa), and immunohistochemically labeled red blood cells ( approximately 5 microm in diameter)--were quantified in both the gray and white matter. The results indicate that spinal cord trauma causes immediate, non-specific vascular changes that are well-predicted by mechanical parameters. Extravasation volume increased significantly with increasing drop height and decreasing marker size. Extravasation volumes for all three markers were greater in gray matter than in white matter, and were better correlated to the rate of spinal cord compression than to the depth of spinal cord compression, which suggests that tissue-level strain rate effects contribute to primary spinal cord microvasculature pathology. The relationship between the response of the spinal cord and the injury pattern points towards opportunities to control the distribution and extent of injury patterns in animal models of spinal cord injury through a precise understanding of model and tissue biomechanics, as well as potential improvements in means of preventing spinal cord injury.  相似文献   

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