马尾受压后腰骶部脊髓中P75神经营养因子受体的表达及其与神经元凋亡的关系

目的:观察大鼠马尾受压后腰骶部脊髓中P75神经营养因子受体(P75 neurotrophic receptor.P75NTR)的表达,探讨P75NTR与前角神经元凋亡的关系.方法:48只雌性成年SD大鼠,随机分为正常组(n=6)、对照组(n=6)和实验组(n=36),正常组不作任何处理,对照组行假手术,实验组在L4平面置人半圆柱体硅胶棒,占椎管截面积约75%～80%,造成马尾急性受压.实验组分别于造模后1d、3d、5d、7d、14d、28d时取L4压迫节段近端脊髓组织(L2水平脊髓),正常组和对照组在第7天时处死取相应部位脊髓组织,切片后进行P75NTR免疫组织化学染色,观察P75NTR的表达;末端转移酶标记技术(TUNEL法)检测脊髓前角运动神经元凋亡情况.用SPSS 13.0统计软件进行组间t检验和相关性分析.结果:正常组和对照组脊髓前角有少量P75NTR表达:实验组造模后1d脊髓前角即有P75NTR表达,7d达到峰值,14d、28d表达呈减少趋势,实验组除1d时外其余各时间点与正常组和对照组比较均有显著性差异(P＜0.05).正常组和对照组脊髓组织中可见少量神经元凋亡,实验组造模后1d脊髓前角神经元凋亡数量明显增多,7d达到峰值,14d、28d凋亡呈减少趋势,实验组各个时间点与正常组和对照组比较均有显著性差异(P＜0.05).神经元凋亡率与P75NTR表达存在平行变化关系.结论:马尾受压后脊髓前角运动神经元表达P75NTR,其表达量与神经元凋亡率呈正相关.     

犬马尾神经受压后腰骶髓中一氧化氮合酶活性与神经细胞凋亡的相关性

目的：研究马尾神经受压后一氧化氮合酶（NOS）活性变化与腰骶髓神经细胞凋亡的关系。方法：将27只健康家犬随机分为3组：A组21只，水囊置于椎管内并注水加压制成马尾神经压迫模型（马尾神经压迫组）；B组3只，置入水囊但未注水加压（假手术组）；C组3只（正常组）。A组再分为7组，即马尾神经持续受压4h、8h、12h、24h、48h、72h和168h组（n=3）。检测各组腰骶髓组织中的NOS活性变化，用TUNEL法标记凋亡神经元和神经胶质细胞，光镜（HE染色）和透射电镜观察细胞形态学改变。结果：B组和C组腰骶髓神经细胞形态未见异常，A组光镜及电镜观察结果均提示神经细胞发生凋亡。B组和C组未见凋亡神经元，A组于压迫后12h可见凋亡神经元，24～48h神经元凋亡最多。B组与C组腰骶髓组织中NOS活性比较无显著性差异（P〉0．05），A组于压迫12h后，NOS活性即明显增高，与B组和C组比较有显著性差异（P〈0．05），24～48h达到高峰，72h后开始下降。结论：犬马尾神经受压后腰骶髓组织中NOS活性增高，与相应神经元凋亡存在正相关。     

大鼠脊髓慢性压迫及减压后神经细胞凋亡及其相关基因的表达

目的：观察慢性压迫性脊髓损伤后及减压后神经细胞凋亡和Bcl-2mRNA，P53mRNA,CASPASE-3神经功能恢复的影响。方法：将55只同龄Wistar大鼠，置入后路渐进式压迫装置，制作成慢性压迫性脊髓损伤模型。随机分为假手术对照组（A组5只），慢性脊髓压迫组（B组25只），减压组（C组25只）。应用原原位末端脱氧核糖核苷酸转移酶介导dUTP标记（TUNEL）技术及原位杂交检测方法，观察各组细胞凋亡率及细胞凋亡相关基因Bcl-2mRNA、P53mRNA、CASPASE－3在慢性压迫性脊髓损伤后及减压后的表达，分别于损伤后及减压后1、3、7、14、28d对慢性脊髓损伤区进行细胞凋亡及原位杂交检测。结果：A、B、C三组均发现神经细胞凋亡及细胞凋亡相关基因Bcl-2mRNA、P53mRNA，CASPASE－3的表达，A、B、C三组细胞凋亡率及阳性细胞灰度值比较，差异有显著性意义（P＜0．05）。阳性细胞表达程度与细胞凋亡的减少及神经功能的恢复相一致。结论：慢性压迫性脊髓损伤可导致大量的神经细胞凋亡，同时激活内源性保护机制，使脊髓发生适应性改变，减压可能通过激活此机制而减轻神经细胞凋亡，起到保护作用。     

脊髓损伤大鼠触液神经元中p75NTR的表达

目的 :探讨大鼠触液神经元(cerebrospinal fluid-contacting neurons,CSF-CNs)p75神经营养因子受体(p75 neurotrophin receptor,p75NTR)在脊髓损伤后的表达变化。方法 :成年雌性Sprague-Dawley(SD)大鼠36只,按随机数字表法分为正常对照组(6只)、假手术组(6只)和脊髓损伤组(24只),脊髓损伤组采用Allen′s打击模型(10g×3cm)在大鼠脊髓T10段造成急性脊髓损伤,分别于损伤3d、1周、2周、4周后进行取材;对照组不做任何处理,假手术组只暴露脊髓,不击伤脊髓。对各组大鼠运动功能行BBB评分,各时间点取材行病理切片HE染色观察。取材前48h侧脑室注射霍乱毒素B亚单位与辣根过氧化物酶复合物(CB-HRP)特异性标记触液神经元。处死大鼠后,取损伤的脊髓节段10mm,用免疫荧光双标法检测触液神经元p75NTR的表达,ImagePro Plus计数目标神经元CB-HRP/p75双阳性细胞的数目。结果 :假手术组各时间点BBB评分均为21.0±0;脊髓损伤组在术后3d、1周、2周、4周各时间点BBB评分分别为3.20±0.81、10.73±1.02、12.48±1.86、13.29±1.93,两组各时间点差异均具有统计学意义(P0.05)。HE染色可见正常对照组和假手术组脊髓组织结构完整,细胞形态正常;脊髓损伤组脊髓组织结构紊乱,神经元变性坏死,胶质细胞增生,胶质瘢痕和脊髓空洞形成。免疫荧光双标示正常对照组和假手术组可见少量CB-HRP/p75双阳性细胞,计数分别为5.16±0.55、4.31±0.61,两组比较差异无统计学意义(P0.05);脊髓损伤组伤后3d、1周、2周CB-HRP/p75双阳性细胞数分别为13.35±1.53、21.68±2.15、16.26±2.09,与正常对照组和假手术组比较差异均有统计学意义(P0.05),伤后4周时,CB-HRP/p75双阳性细胞数为4.83±0.73,与正常对照组和假手术组比较差异无统计学意义(P0.05)。结论 :p75NTR可在大鼠脊髓触液神经元中表达,且在脊髓损伤后表达增加,触液神经元可能通过p75NTR参与脊髓损伤的修复过程。     

氯胺酮对慢性坐骨神经压迫性损伤大鼠脊髓背角神经元凋亡及Bax和Bcl-2的表达影响

目的观察氯胺酮（Ket）对慢性坐骨神经压迫性损伤（CCI）大鼠脊髓背角神经元凋亡及凋亡相关蛋白Bax和Bcl-2表达的影响。方法选择雄性SD大鼠40只，随机分为4组，分别为空白对照组，假手术组，CCI组和腹腔注射Ket 50mg／kg治疗组。假手术组，CCI组和Ket治疗组又按术后取材时间的不同分别分为3个亚组，即术后3d组、术后9d组和术后14d组。用TUNEL标记法标记脊髓背角浅层凋亡细胞。应用免疫组织化学方法和免疫印迹（Western-blot）法检测大鼠脊髓背角浅层神经元凋亡相关蛋白Bax和Bcl-2表达情况。结果与空白对照组和假手术组各亚组比较，CCI3d，9d，14d亚组和Ket9d，14d亚组大鼠脊髓背角的凋亡细胞明显增多（P〈0．01）；与CCI3d亚组比较，Ket3d亚组大鼠脊髓背角的凋亡细胞明显减少（P〈0．01）。与空白对照组和假手术各亚组比较，CCI3d，9d，14d亚组大鼠脊髓背角浅层Bax阳性神经元和Bax的表达显著增加（P〈0．01），CCI9d，14d亚组大鼠脊髓背角浅层Bcl-2阳性神经元和Bcl-2的表达明显增加（P〈0．01）。与CCI3d亚组比较，Ket3d亚组脊髓背角浅层Bax阳性神经元和Bax的表达显著减少（P〈0．01），而Bcl-2阳性神经元和Bax的表达显著增加（P〈0．01）。结论Ket能抑制脊髓背角浅层神经元Bax的表达，促进Bcl-2的表达，提示Ket对神经病理性疼痛状态下脊髓背角神经元的凋亡具有保护作用。     

脊髓干细胞移植对脊髓损伤后CD-95和p75表达及神经细胞凋亡的影响

目的探讨胚胎脊髓神经干细胞移植对大鼠脊髓损伤后CD-95和p75表达及神经细胞凋亡的影响。方法160只sD大鼠随机分为空白组，假手术组，脊髓损伤组，细胞移植组，分别在细胞移植后1、3d、1、2、4周应用苏木素-伊红（HE）染色）、免疫组织化学、Tunel（凋亡测定）标记、电镜方法观察CD-95、p75和神经细胞凋亡的变化。结果移植后1、3d、1、2、4周，脊髓损伤组和细胞移植组比较，CD95（P〈0．05）；p75，P〈0．01。Tunel方法测定细胞凋亡结果，差异有统计学意义（P〈0．05）。电镜观察可见，空白对照组和假手术组未见凋亡现象，细胞移植后1周，损伤对照组电镜下可见大量神经细胞凋亡小体。细胞移植组未见凋亡小体。结论脊髓源性神经干细胞移植后减少了CD-95和p75的表达，也减少了凋亡，说明移植促进了脊髓神经功能的恢复，也抑制了继发性脊髓损伤。     

急性重度犬马尾压迫模型诱导脑源性神经营养因子的合成

目的研究实验性犬急性重度马尾神经压迫48h的相关脊髓和背根神经节(dorsal root ganglion,DRG)内脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)蛋白表达水平。方法成年雄性杂种犬(n=8),随机分为实验组和对照组。实验组(n=4)行多重马尾压缢,其中第1根束缢线使整个马尾束缢了50%~75%,另3根束缢线使马尾束缢了25%~50%。对照组(n=4)仅行马尾暴露而未行马尾束缢。于术后48h取相应脊髓及DRG行HE染色、BDNF的免疫组织化学分析。结果多重马尾束缢后48h可在相应下腰骶髓和DRG神经元群体内诱导出显著的BDNF增量调节;而脊髓、DRG和神经纤维内相关结构亦见BDNF阳性表达。结论多重马尾束缢犬模型形成急性重度马尾综合征(cauda equine syndrome,CES)时,BDNF可能有神经保护作用和炎性痛、神经痛的作用。     

大鼠慢性脊髓受压及减压后骨骼肌细胞的凋亡

目的：研究大鼠慢性脊髓损伤受压及减压后骨骼肌细胞的凋亡。方法：45只SD大鼠分成3组：①受压组15只，作成慢性脊髓受压损伤模型；②减压组25只，在压迫模型作成10d后取出压迫装置；③正常对照组5只，不做任何处理。应用HE染色、TUNEL和原位杂交技术研究慢性脊髓受压及减压后肌细胞的萎缩和凋亡。结果：正常组鲜见凋亡细胞，受压组出现骨骼肌细胞凋亡，bcl-2 mRNA表达减弱，BaxmRNA表达增强；减压后肌细胞凋亡数量明显减少，bcl-2 mRNA表达增强而Bax mRNA表达减少。结论：慢性脊髓受压肌细胞凋亡是失神经骨骼肌萎缩的机制之一，bcl-2和Bax基因参与肌细胞的凋亡。     

大鼠脊髓损伤中的细胞凋亡及甲基强的松龙的干预作用

目的：探讨脊髓损伤（SCI）继发损伤机制,研究损伤脊髓细胞的凋亡及其意义,观察甲基强的松龙（MP）对细胞凋亡的影响。方法：使用改良Allen法制作大鼠急性SCI模型,实验分3组,假损伤（脊髓未受打击）,损伤组及MP治疗组,采用HE,荧光Hoechst 33342,TUNEL(末端脱氧核苷转移酶介导的脱氧尿苷三磷酸生物素缺口末端标记技术）等技术观察SCI后4h,8h,3d,7d,14d,21d及28d时损伤中心及邻近节段脊髓细胞的凋亡,治疗组损伤后30min给予大剂量MP,比较MP治疗组与损伤组脊髓细胞凋亡的变化,同时平行观察大鼠神经学和组织学恢复情况及两组神经丝蛋白（NF）含量的变化。结果：假损伤组各检测方法未见脊髓细胞凋亡,损伤组大鼠急性SCI后1d开始出现脊髓细胞凋亡,3d达高峰,自损伤中心向头尾端递减分布,持续21d,MP治疗组在伤后3d及7d凋亡脊髓细胞较损伤组显著减少,神经学恢复及组织学评分较损伤组有显著性提高,结论：凋亡是SCI后脊髓神经元死亡的一种重要方式,在继发性损伤中起极为重要的作用。MP的治疗作用可能与其干预SCI后细胞凋亡有关。     

功能训练促进颈脊髓损伤大鼠功能恢复的机制研究

目的：探讨大鼠颈脊髓不完全性损伤后前肢功能训练促进大鼠前肢功能恢复的机制.方法：在立体定位仪的引导下,致伤大鼠双侧红核和皮质脊髓背侧束后,对大鼠行前肢功能训练6周.免疫组化检测损伤脊髓节段脑源性神经生长因子（brain-derived neurotrophic factor,BDNF）的表达,皮质脊髓束投射神经元（corticospinal neurons,CSNs）中生长相关蛋白43（growth-associated protein 43,CAP43）和神经营养素共同受体P75（P75NTR）的表达,荧光金逆行示踪CSNs存活情况.结果：大鼠不完全性颈脊髓损伤后,前肢功能训练可上调脊髓前角神经元BDNF与CSNs中GAP43和P75NTR的表达,减少CSNs死亡.结论：大鼠颈脊髓不完全性损伤后,前肢功能训练通过上调脊髓前角神经元BDNF与CSNs中GAP43和P75NTR的表达以及减少CSNs的死亡等机制增加未损伤皮质脊髓腹侧束（vCST）的出芽,进而促进大鼠前肢功能恢复.     

Presentation of cauda equina syndrome due to an intradural extramedullary abscess: a case report

Background contextCauda equina syndrome is caused by compression or injury to the nerve roots distal to the level of the spinal cord. This syndrome presents as low back pain, motor and sensory deficits in the lower extremities, and bladder as well as bowel dysfunction. Although various etiologies of cauda equina syndrome have been reported, a less common cause is infection.PurposeTo report a case of cauda equina syndrome caused by infection of an intradural extramedullary abscess with Staphylococcus aureus.Study design/settingCase report and review of the literature.MethodsThe literature regarding the infectious causes of cauda equina syndrome was reviewed and a case of cauda equina syndrome caused by infection of an intradural extramedullary abscess with Staphylococcus aureus was reported.ResultsA 37-year-old woman, with history of intravenous drug abuse, hepatitis C, and hepatitis B, presented with low back pain lasting 2 months, lower extremity pain, left greater than right with increasing weakness and difficulty ambulating, and urinary and fecal incontinence. Her presentation was consistent with cauda equina syndrome. The patient underwent a T12–L2 laminectomy, and intradural exploration revealed an abscess. Methicillin-resistant Staphylococcus aureus was found on wound culture.ConclusionsCauda equina syndrome, presenting as a result of spinal infection, such as the case reported here, is extremely rare but clinically important. Surgical intervention is generally the recommended therapeutic modality.     

Vasodilative effects of prostaglandin E<Subscript>1</Subscript> derivate on arteries of nerve roots in a canine model of a chronically compressed cauda equina

Background  

Reduction of blood flow is important in the induction of neurogenic intermittent claudication (NIC) in lumbar spinal canal stenosis. PGE₁ improves the mean walking distance in patients with NIC type cauda equina compression. PGE₁ derivate might be effective in dilating blood vessels and improving blood flow in nerve roots with chronically compressed cauda equina. The aim of this study was to assess whether PGE₁ derivate has vasodilatory effects on both arteries and veins in a canine model of chronic cauda equina compression.     

借助胸腔镜技术的胸段、上腰段脊柱前路手术

目的探讨胸腔镜辅助胸椎、上腰椎前路手术的适应证 ,单肺或双肺通气的选择以及术中注意事项。方法　应用胸腔镜、骨科常规手术器械或自制的骨科器械 ,在胸腔镜辅助下行病灶清除、脊髓减压、植骨、钢板螺丝钉内固定术。结果　全部病例手术都顺利完成 ,切口均一期愈合 ,随访 3～ 10个月 ,影像学检查显示病灶清除彻底 ,脊髓减压充分 ,除 1例骨折复位、固定后仍有轻度侧方成角畸形外 ,其他病例复位满意、内固定可靠 ,位置良好。结论胸椎、上腰椎疾患 ,不论是否并发脊髓、马尾神经压迫 ,都能在胸腔镜辅助下完成病灶清除术 ,必要时还可进行脊髓减压、脊柱前路植骨、内固定手术。原则上可选择常规气管插管、双肺通气下完成手术。     

症状性腰椎管硬膜外脂肪增多症的诊断与手术治疗

目的:探讨症状性腰椎管硬膜外脂肪增多症的诊断与手术治疗的临床疗效。方法:回顾性分析2012年2月至2018年11月进行压迫节段的半椎板切除椎间融合内固定术治疗的19例症状性腰椎管内硬膜外脂肪增多症患者的临床资料,其中男7例,女12例;年龄48～72(57.6±1.2)岁;病程6～60(18.6±5.1)个月;减压平面:L_(2,3)-L_5S_1平面4例,L_(2,3)-L_(4,5)平面5例,L_(3,4)-L_(4,5)平面2例,L_(3,4)-L_5S_1平面6例,L_(4,5)-L_5S_1平面2例。分别于术前、术后6个月采用视觉模拟疼痛评分(visual analogue scale,VAS)评价腿疼和腰疼的缓解程度,采用Oswestry功能障碍指数评分(Oswestry Disability Index,ODI)评价功能恢复情况,并采用Fischgrund标准判定总体疗效。结果:所有患者获随访,随访时间12～37(16.3±3.8)个月。19例患者均顺利完成手术,椎管内压迫节段脂肪组织全部摘除。手术时间125～260(186±15) min,出血量150～500(280±46) ml。2例患者出现部分切口脂肪液化渗液不愈,经切口撑开去除积液后积极换药抗炎处理后愈合。所有患者无马尾神经损伤、脑脊液漏、钉棒断裂等并发症。术前腰痛、腿疼VAS评分分别为(5.3±0.7)、(6.8±0.8)分,术后6个月分别为(2.1±0.4)、(2.3±0.5)分,术后6个月与术前比较差异有统计学意义(P0.05)。术后6个月ODI评分(12.1±2.3)分较术前(45.5±2.8)分明显改善(P0.05)。根据Fischgrund标准,本组优13例,良4例,可2例。结论:症状性腰椎管硬膜外脂肪增多症患者进行压迫节段的半椎板切除椎间融合内固定手术,可解除硬脊膜及马尾神经的压迫,术后能取得较好的临床疗效。     

Out of hours magnetic resonance imaging for suspected cauda equina syndrome: lessons from a comparative study across two centres

BackgroundCauda equina syndrome, a rare but disabling spinal surgical emergency, requires prompt investigation, ideally using magnetic resonance imaging as patients may require decompressive surgery. Out of hours access to magnetic resonance imaging is only routinely available in major trauma centres and neurosurgical units. Patients in regional hospitals with suspected cauda equina syndrome may require transfer for diagnostic imaging. We retrospectively studied the proportion of patients referred with suspected cauda equina syndrome who required out of hours transfer for magnetic resonance imaging and decompressive surgery.Materials ands methodsRetrospective cohort study of patients referred using online referral platforms with suspected acute cauda equina syndrome and transferred out of hours between 6pm to 8am on weekdays and all day on weekends to two of the largest neurosurgical units in the UK in Birmingham and Cambridge.ResultsA total of 441 patients were referred across both sites with a suspicion of acute cauda equina syndrome; 339 patients were transferred for diagnostic scans and only 16 of them (4.7%) were positive for cauda equina compression, necessitating prompt decompressive surgery. Of the patients with negative magnetic resonance scans, 50% had their discharge or transfer back to referring hospitals delayed by more than 24 hours.ConclusionsOver 95% of patients who were transferred for imaging did not undergo emergency decompression. The authors propose a greater role for the provision of out of hours magnetic resonance imaging in all hospitals admitting emergency patients to streamline management.     

Spinal stenosis: assessment of motor function,VEGF expression and angiogenesis in an experimental model in the rat

Reduction of blood flow in compressed nerve roots is considered as one important mechanism of induction of neurogenic intermittent claudication in lumbar spinal canal stenosis. Vascular endothelial growth factor (VEGF) is a potent stimulator of angiogenesis, and is increased in expression in hypoxic conditions. The objective of this study was to examine if cauda equina compression affects motor function and induces expression of VEGF and angiogenesis. The cauda equina was compressed by placing a piece of silicone rubber into the L5 epidural space. Walking duration was examined by rota-rod testing. The compressed parts of the cauda equina and L5 dorsal root ganglion (DRG) were removed at 3, 7, 14, or 28 days after surgery, and processed for immunohistochemistry for VEGF and Factor VIII (marker for vascular endothelial cells). Numbers of VEGF-immunoreactive (IR) cells and vascular density were examined. Walking duration was decreased after induction of cauda equina compression. The number of VEGF-IR cells in the cauda equina and DRG was significantly increased at 3, 14, and 28 days after cauda equina compression, compared with sham-operated rats (P < 0.05). Vascular density in the cauda equina was not increased at any of the time points examined. Cauda equina compression decreased walking duration, and induced VEGF expression in nerve roots and DRG.     

A study of motor and sensory evoked potentials in chronic cauda equina compression of the dog

Previous experimental studies have shown the effects of acute compression of the spinal cord and peripheral nerve roots. Recently, however, a few studies of chronic compression of the cauda equina in animal models have been reported. The purpose of this study was to determine the long-term electrophysiologic changes resulting from chronic compression of the cauda equina in dogs. An animal model of lumbar spinal stenosis was prepared according to Delamarter's method. Four experimental groups, each containing six dogs, were studied. One group underwent only laminectomy of the sixth and seventh lumbar vertbrae; these animals served as controls. In the three other groups, a laminectomy was performed and the cauda equina was constricted by 25%, 50%, and 75%, respectively, to produce chronic compression. Weekly neurologic examinations were carried out, and the neurologic deficits were graded using a modified Tarlov system. Sensory, and motor evoked potentials were recorded preoperatively, immediately after constriction, and at 2 weeks and 1, 2, and 3 months postoperatively. The animals in the control group showed no changes in sensory or motor evoked potentials. The dogs in which the cauda equina had been constricted by 25% showed no neurologic deficits and only mild changes in sensory and motor evoked potentials. The dogs in which the cauda equina had been constricted by 50% showed mild initial motor weakness, and major changes in the evoked potentials. The dogs in which the cauda equina had been constricted by 75% showed significant weakness, paralysis of the tail, and urinary incontinence; all dogs were partially recovered by the 3rd month, but all still showed neurogenic changes in the evoked potentials. Sensory and motor evoked potentials revealed neurologic abnormalities before the appearance of neurologic signs and symptoms. Constriction of more than 50% was the critical point that resulted in complete loss or reduction of the evoked potentials and in neurologic deficits. Dogs in which motor and sensory evoked potentials recovered also showed gradual disappearance of neurologic symptoms and signs. Recovery of motor evoked potentials in particular was associated with complete disappearance of neurologic symptoms and signs. For accurate prognosis in cases of chronic cauda equina compression, a combined diagnostic study of sensory and motor evoked potentials is recommended.     

硬膜外腔注射致椎管内感染6例报告

目的：研究椎管内感染的特征和预后。方法：对６例椎管内感染病例临床症状,感染细菌类型,诊断,予后进行观察和分析。结果：椎管内感染可分为急性、亚急性、慢性三种类型。急性、亚急性很快致截瘫、慢性则产徨马尾神经压迫症状。结论：急性、亚急性应立即手段,予后均残留有不同程度马尾神经损伤。慢性者手术可解除压缩、予后良好。     

腰椎后路内固定融合术并发神经损伤的原因分析和处理

目的探讨椎弓根螺钉固定植骨融合治疗腰椎病变并发神经损伤的原因及处理方法,并提出预防性措施。方法回顾性分析1995年1月—2011年12月本院采用椎弓根螺钉固定治疗腰椎病变并发神经损伤的病例48例,其中马尾神经损伤3例,神经根损伤45例。神经损伤的原因:1操作损伤;2螺钉位置不正确损伤;3植骨块卡压;4椎管血肿压迫;5其他原因。1例血肿压迫所致的马尾神经损伤病例进行了椎管探查和血肿清除术,另2例马尾神经损伤患者予非手术治疗;由于操作所致神经根损伤的15例病例予非手术治疗,螺钉位置不正确所致神经根损伤的30例患者均进行了螺钉调整术。结果失访5例,余43例获得12~60个月的随访,平均随访21.2个月。获得随访的3例马尾神经损伤的患者神经功能均有不同程度的恢复。15例因术中操作所致神经根损伤的病例,其中2例失访,其余神经功能完全恢复3例,部分恢复6例,未恢复4例;30例因螺钉位置不正确所致神经根损伤的病例,其中3例失访,其余神经功能完全恢复20例,大部分恢复5例,部分恢复1例,未恢复1例。再次手术病例除1例出现切口深部急性感染外,其余病例切口均Ⅰ期愈合。结论椎弓根螺钉固定融合术后并发神经损伤的原因除了病情的严重性和复杂性,还有手术操作、螺钉位置不正确和植骨块卡压等因素。神经损伤只要尽早发现,及时治疗,大部分病例神经功能可有不同程度的恢复。而对于神经损伤的预防,要求术者对病情全面掌握,选择合适的手术方式,术中操作严谨、细致,并借助影像系统的帮助。