经椎板间入路椎间孔镜技术治疗腰椎间盘突出症疗效分析

目的探讨经椎板间入路椎间孔镜技术治疗腰椎间盘突出症的临床疗效。方法采用经椎板间入路椎间孔镜TESSYS技术治疗54例腰椎间盘突出症患者(L4-5椎间盘突出13例、L5-S1椎间盘突出41例),分别于术前和术后1 d、3个月、1年时采用视觉模拟评分(VAS)和Oswestry功能障碍指数(ODI)评价手术前后疼痛改善情况,复查腰椎MRI评价髓核摘除情况和有无复发。结果 54例患者手术成功率为96.30%(52/54),其中2例术中出现硬脊膜破裂,改为手术显微镜下椎板开窗、髓核摘除术。平均手术时间58.35 min,中位住院时间3 d。出院时52例疼痛消失、2例疼痛减轻,其中5例患侧小腿外侧麻木感加重。与术前相比,术后1 d、3个月和1年时VAS和ODI评分均减少(均P=0.000)。术后复查腰椎MRI显示髓核摘除满意,神经根压迫解除,亦未见复发。无一例发生感染等手术相关并发症,1例L5-S1椎间盘突出患者因髓核脱出椎管内游离较远,术中对神经根牵拉较重,术后出现S1神经根分布区麻木,术后1个月缓解。结论经椎板间入路椎间孔镜技术治疗腰椎间盘突出症临床疗效满意、安全性良好。     

经皮内镜椎板间入路椎间盘切除术治疗腰椎间盘突出症的疗效分析

目的探讨经皮内镜椎板间入路椎间盘切除术（PEID）治疗腰椎间盘突出症的手术疗效。 方法回顾性分析2015年8月至2016年12月首都医科大学宣武医院功能神经外科采用PEID治疗的20例腰椎间盘突出症患者的临床资料。采用视觉模拟评分法（VAS）、Oswestry功能障碍指数（ODI）和改良MacNab疗效评估标准评价手术疗效。 结果所有患者突出髓核摘除均满意。20例均获随访,末次随访时间为术后12个月。与术前相比,术后7 d、1个月、3个月、6个月、12个月的VAS评分、ODI均较术前明显下降（均P〈0.001）。末次随访时,改良MacNab疗效评定结果显示,手术优良率为80%（16/20）。1例患者术后出现一过性下肢麻木,无感染以及神经根损伤患者。无一例复发。 结论采用PEID能够安全、有效地治疗腰椎间盘突出症。     

椎板间入路治疗腰椎间盘突出症

目的 研究椎板间入路显微椎间盘切除术治疗腰椎间盘突出症的手术效果. 方法对36例病人行显微椎间盘切除术,术中对椎间盘碎片及纤维环缺损情况进行评估,分析术前资料和术后随访情况.结果 椎板间入路在28例(78%)病人中可充分暴露椎间隙,部分椎间孔扩大术在17例(47%)病人中使用.碎片-裂隙型及碎片-包含型病人手术效果最好,复发率低.结论 椎板间入路是治疗腰椎间盘突出症的一种安全、有效的手术技术,椎间盘突出类型及椎间盘切除术后纤维环的完整性对预测腰腿痛复发有价值.     

经肌肉间隙套管椎板间入路微创治疗下腰椎椎间盘突出症

目的探讨经肌肉间隙套管椎板间入路微创治疗下腰椎椎间盘突出症的手术技巧及临床疗效。方法回顾性分析32例下腰椎椎间盘突出症病人的临床资料,均行经肌肉间隙套管椎板间入路微创治疗。并采用疼痛视觉模拟评分(VAS)、oswestry功能障碍指数(ODI)评价临床疗效。结果手术切除突出髓核32例,平均手术时间(62.4±13.6)min,术中出血量(31.0±5.6)ml,32例病人术后腰腿痛及感觉、肌力减退均有不同程度好转。32例随访6~12个月,平均8.5个月。术前与术后不同时段腰痛、腿痛VAS评分及ODI评分比较均有统计学差异(P0.01)。随访期间无腰椎间盘突出症复发病例。结论神经外科显微镜下经肌肉间隙套管椎板间入路微创治疗下腰椎椎间盘突出症具有创伤小,出血少,显露清楚,神经根减压彻底,对脊柱稳定性破坏小,术后恢复快等优点;其近期疗效明确,远期效果需进一步随访。     

经皮椎间孔镜技术治疗腰椎间盘突出症和腰椎间孔狭窄的并发症原因分析与处理

目的分析经皮椎间孔镜技术治疗腰椎间盘突出症和腰椎间孔狭窄的并发症及其原因和相应处理措施。方法采用经皮椎间孔镜技术治疗286例经X线、CT或MRI证实的腰椎间盘突出症(201例)和腰椎间孔狭窄(85例)患者,视觉模拟评分(VAS)评价手术前后疼痛情况、Macnab标准评价手术疗效,记录手术相关并发症并分析原因及相应处理措施。结果与术前相比,术后3个月随访时VAS评分减少[1.00(0.00,1.50)分对8.50(7.75,9.25)分;Z=2.825,P=0.050];Macnab标准优良率达95.45%(273/286)。286患者中神经损伤8例(2.80%)、术区出血和神经根周围血肿形成6例(2.10%)、硬脊膜囊破裂1例(0.35%)、肌肉痉挛3例(1.05%)、感染1例(0.35%)、术后复发4例(1.40%),均予对症治疗后痊愈。结论经皮椎间孔镜技术治疗腰椎间盘突出症和腰椎间孔狭窄总体疗效满意,手术相关并发症发生率较低,通过术前评估,术中精细操作、仔细止血、缩短手术时间,以及术后对症处理,可以有效减少并发症的发生。     

椎板间入路经皮完全内镜手术治疗腰椎间盘突出症

目的评价经椎板间入路的完全内镜手术治疗腰椎间盘突出症的临床效果。方法回顾性分析60例应用经椎板间入路完全内镜手术治疗腰椎间盘突出症的病例资料。病人术前均符合单节段腰椎间盘突出症诊断。记录术前、术后3d、3个月和6个月腿痛VAS和腰椎JOA评分,手术时间、术中及术后并发症。结果60例病人均顺利完成手术,术中出血量少,无任何并发症。平均手术时间65min;平均住院时间4d,切口均一期愈合。术后随访：1例k;病人手术后2个月复发,其他59例病人腿痛VAS和腰椎JOA评分术后3d、3个月、6个月各个随访时间点与术前比较,均有显著性差异（P〈0.01）,术后3个月与6个月间比较无显著性差异（P〉0.05）。结论椎板间入路完全内镜手术治疗下腰椎椎间盘突出症具有微创、术后恢复快等特点,可获得良好临床疗效。     

经皮椎板间入路完全内镜下手术治疗L_(4～5)椎间盘突出症

目的评价椎板间入路的完全脊柱内镜手术治疗L_(4~5)腰椎间盘突出症的临床效果。方法回顾性分析86例L_(4~5)腰椎间盘突出症病人的临床资料,采用经皮椎板间入路完全内镜手术治疗。比较手术前后下肢VAS和腰椎JOA评分。结果所有病人顺利完成手术,无严重并发症。术后6个月复发2例,再次手术摘除突出的椎间盘。所有病人术后3 d、6个月、12个月下肢VAS和腰椎JOA评分较术前差异有统计学意义(P0.05)。结论经皮椎板间入路完全内镜手术治疗L_(4~5)椎间盘突出症具有微创、术后恢复快等特点,可获得良好的临床疗效。     

METRx系统辅助下显微外科手术治疗腰椎间盘突出症

目的探讨METRx系统辅助下腰椎间盘突出症显微外科手术的技术特点和临床疗效。方法于METRx系统辅助下显微外科手术治疗51例腰椎间盘突出症患者(L4-5椎间盘突出24例、L5-S1椎间盘突出27例),记录手术时间、术中出血量和住院时间,并于术前和术后1周、3个月、末次随访时采用视觉模拟评分(VAS)和Oswestry功能障碍指数(ODI)评价手术前后疼痛改善情况,复查腰椎MRI评价椎管减压程度。结果 51例患者手术成功率为98.04%(50/51),平均手术时间为125 min、术中出血量为50 ml、住院时间5 d、术后随访24个月。与术前相比,术后1周(P=0.036,0.029)、3个月(P=0.018,0.023)和末次随访时(P=0.007,0.013)VAS和ODI评分均减少;至末次随访时,ODI改善率为35.37%。无手术相关感染、术后脑脊液漏和神经功能缺损加重、手术切口感染病例。术后1例出现附件炎,1例神经根刺激症状明显,均经对症治疗后痊愈。结论 METRx系统辅助下显微外科手术治疗腰椎间盘突出症,可以有效解除神经根压迫、保护硬脊膜囊和神经根、减少手术并发症的发生。     

椎间盘镜与椎间孔镜治疗腰椎间盘突出症的临床分析

目的探讨椎间盘镜与椎间孔镜治疗腰椎间盘突出症(LDH)的临床疗效。方法回顾性分析120例LDH病人的临床资料,根据手术方式不同分为椎间盘镜组及椎间孔镜组各60例。比较两组术后优良率、并发症发生率以及术后视觉模拟评分(VAS)。结果椎间盘镜组术后优良率为95.0%,并发症3例(术后终板炎2例、残留椎间盘再突出1例),术后VAS评分(4.32±1.28)分。椎间孔镜组术后优良率为93.33%,并发症2例(术后神经根激惹1例、残留椎间盘再突出1例),术后VAS评分(4.67±1.29)分。两组术后优良率、并发症发生率、术后VAS评分差异均无统计学差异(P0.05)。结论采用椎间盘镜与椎间孔镜手术治疗LDH均可获得理想效果,临床上可根据病人的具体病情选择适宜的手术方案。     

经皮椎间孔镜治疗椎间盘突出及神经根粘连松解术的围手术期护理

正腰椎间盘退变及外伤等因素均可导致腰椎间盘突出,压迫神经引起神经根粘连,导致腰痛、下肢放射性疼痛、麻木、间歇性跛行等症状,给工作、生活带来一定的困难。而椎间孔镜手术创伤小,对椎管内无干扰,不影响脊柱稳定性,被医学界称为治疗椎间盘突出最微创的治疗手段。我院脊柱外科应用椎间孔镜成功治疗椎间盘突出及神经根粘连患者42例,疗效显著。现报告如下。     

Tau-induced neurodegeneration: mechanisms and targets

The accumulation of hyperphosphorylated tau is a common feature of several dementias. Tau is one of the brain microtubule-associated proteins. Here we discuss tau’s functions in microtubule assembly and stabilization and with regard to its interactions with other proteins. We describe and analyze important post-translational modifications: hyperphosphorylation, ubiquitination, glycation, glycosylation, nitration, polyamination, proteolysis, acetylation, and methylation. We discuss how these post-translational modifications can alter tau’s biological function. We analyze the role of mitochondrial health in neurodegeneration. We propose that microtubules could be a therapeutic target and review different approaches. Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and propose a mechanism of neurodegeneration.     

The effect of risperidone on reward‐related brain activity is robust to drug‐induced vascular changes

Dopamine (DA) mediated brain activity is intimately linked to reward‐driven cerebral responses, while aberrant reward processing has been implicated in several psychiatric disorders. fMRI has been a valuable tool in understanding the mechanism by which DA modulators alter reward‐driven responses and how they may exert their therapeutic effect. However, the potential effects of a pharmacological compound on aspects of neurovascular coupling may cloud the interpretability of the BOLD contrast. Here, we assess the effects of risperidone on reward driven BOLD signals produced by reward anticipation and outcome, while attempting to control for potential drug effects on regional cerebral blood flow (CBF) and cerebrovascular reactivity (CVR). Healthy male volunteers (n = 21) each received a single oral dose of either 0.5 mg, 2 mg of risperidone or placebo in a double‐blind, placebo‐controlled, randomised, three‐period cross‐over study design. Participants underwent fMRI scanning while performing the widely used Monetary Incentive Delay (MID) task to assess drug impact on reward function. Measures of CBF (Arterial Spin Labelling) and breath‐hold challenge induced BOLD signal changes (as a proxy for CVR) were also acquired and included as covariates. Risperidone produced divergent, dose‐dependent effects on separate phases of reward processing, even after controlling for potential nonneuronal influences on the BOLD signal. These data suggest the D2 antagonist risperidone has a wide‐ranging influence on DA‐mediated reward function independent of nonneuronal factors. We also illustrate that assessment of potential vascular confounds on the BOLD signal may be advantageous when investigating CNS drug action and advocate for the inclusion of these additional measures into future study designs.     

星形胶质细胞对天冬氨酸特异性半胱氨酸蛋白酶介导β淀粉样蛋白早期突触毒性作用的影响

目的探讨星形胶质细胞(astrocyte,AS)对天冬氨酸特异性半胱氨酸蛋白酶(cysteinyl aspartate specific proteinase,caspase)介导β淀粉样蛋白(β-amyloid,Aβ)早期突触毒性作用的影响,以期为进一步研究与血管性痴呆(vascular dementia,Va D)的发病机制奠定基础。方法以原代培养大鼠海马纯神经元体系(NE-S)及混合培养体系(MIX-S,主要包含神经元及AS)为研究对象,各体系分为6组:对照组、caspase-8抑制剂组、caspase-9抑制剂组、Aβ处理组、caspase-8抑制剂预处理加Aβ组和caspase-9抑制剂预处理加Aβ组。免疫荧光检测各组近胞体10μm段树突中突触后密度蛋白(postsynaptic density-95,PSD95)表达量的变化。结果 1在NE-S与MIX-S中,与对照组相比,caspase-8抑制剂组、caspase-9抑制剂组PSD95的表达量均无明显差异,Aβ处理组PSD95的表达量均显著降低(P均0.001)。2在NE-S中,与Aβ处理组相比,caspase-9抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,caspase-8抑制剂预处理加Aβ组则无显著改变;在MIX-S中的结果则相反,即caspase-8抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,而caspase-9抑制剂预处理加Aβ组则无显著改变。3MIX-S与NE-S两种培养系统间相比较,对照组间及Aβ处理组间PSD95的表达量均无显著差异,而caspase-8抑制剂预处理加Aβ组间及caspase-9抑制剂预处理加Aβ组间PSD95的表达量差异有显著性。结论在Aβ早期突触毒性作用中,AS参与caspase-8介导的死亡受体通路激活过程,且参与抑制神经元的线粒体通路。     

Ultrastructure of non-myelinated neurons during energy deprivation

Summary This paper examines the neuropathology of oxygen-glucose deprivation uncomplicated by stagnant conditions. Rabbit vagus nerves were pulled into asmulti-compartment perfusion chamber, stimulated five times per second and deprived of energy by substituting nitrogen and deoxyglucose for oxygen and glucose in the Locke's perfusate. After incubation the compartments were perfused with gluteraldehyde solution, and the nerves were prepared for electron microscopy. Fixation in the compartments ensured precise cross and longitudinal sections which permitted quantitative comparisons. Although the action potentials ceased in 45 min, 1 h of energy deprivation did not significantly affect the ultrastructure. After 2 h of deprivation the axons were smaller and flattened and microtubules appeared packed together. In the smallest axons the microtubules were gone, the neurofilaments were compacted and the few mitochondria had a dense, homogenous appearance. By 4 h the shrinking was extreme, yet 8% were swollen much larger than any of the controls. Longitudinal views showed these balloned areas were greatly expanded regions of the smallest axons. Both tiny and huge regions were devoid of microtubules and the swollen axons contained expanded mitochondria.Calcium is indirectly implicated in the pathogenesis by the concurrence of mitochondrial alteration as the microtubules disappear coupled with the known role of mitochondria in calcium regulation and the reported effect of high calcium on microtubual dissociation. In is suggested that axons first shrink as osmotially active molecules are used or washed out. After a time without energy the mitochondria can no longer regulate the intracellular calcium, microtubules dissociate, and calcium-activated phospholipases create osmotically active molecules. Finally, high-amplitude, disruptive swelling occurs.Supported, in part, by a Grant-in-aid from the American Heart Association with funds contributed by the American Heart Association, Kansas Affiliate and by the University of Kansas Biomedical Sciences Support Grant RR0737     

Development of 18F-labeled radiotracers for neuroreceptor imaging with positron emission tomography

Positron emission tomography (PET) is an in vivo molecular imaging tool which is widely used in nuclear medicine for early diagnosis and treatment follow-up of many brain diseases. PET uses biomolecules as probes which are labeled with radionuclides of short half-lives, synthesized prior to the imaging studies. These probes are called radiotracers. Fluorine-18 is a radionuclide routinely used in the radiolabeling of neuroreceptor ligands for PET because of its favorable half-life of 109.8 min. The delivery of such radiotracers into the brain provides images of transport, metabolic, and neurotransmission processes on the molecular level. After a short introduction into the principles of PET, this review mainly focuses on the strategy of radiotracer development bridging from basic science to biomedical application. Successful radiotracer design as described here provides molecular probes which not only are useful for imaging of human brain diseases, but also allow molecular neuroreceptor imaging studies in various small-animal models of disease, including genetically-engineered animals. Furthermore, they provide a powerful tool for in vivo pharmacology during the process of pre-clinical drug development to identify new drug targets, to investigate pathophysiology, to discover potential drug candidates, and to evaluate the pharmacokinetics and pharmacodynamics of drugs in vivo.     

Norharman-induced motoric impairment in mice: neurodegeneration and glial activation in substantia nigra

Summary. The β-carboline norharman is present in cooked food and tobacco smoke and show structural resemblance to the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. C57BL/6 mice were injected subcutaneously with norharman (3 and 10 mg/kg) twice per day for five consecutive days. Eighteen hours after the last dose an increased expression of glial fibrillary acidic protein and fluoro-jade staining were demonstrated whereas the number of tyrosine hydroxylase positive cells were unchanged in the substantia nigra. Two weeks after the last treatment a decreased motor activity was observed whereas cognitive functions remained intact. In cultured PC12 cells norharman treatment induced mitochondrial dysfunction and increased the number of caspase-3 and TUNEL-positive cells. The results demonstrate that norharman induced apoptosis in cultured cells as well as early neurodegeneration, glial activation and sustained motor deficits in mice and suggest that exposure to norharman may contribute to idiopathic Parkinson’s disease.     

The ENIGMA‐Epilepsy working group: Mapping disease from large data sets

Epilepsy is a common and serious neurological disorder, with many different constituent conditions characterized by their electro clinical, imaging, and genetic features. MRI has been fundamental in advancing our understanding of brain processes in the epilepsies. Smaller‐scale studies have identified many interesting imaging phenomena, with implications both for understanding pathophysiology and improving clinical care. Through the infrastructure and concepts now well‐established by the ENIGMA Consortium, ENIGMA‐Epilepsy was established to strengthen epilepsy neuroscience by greatly increasing sample sizes, leveraging ideas and methods established in other ENIGMA projects, and generating a body of collaborating scientists and clinicians to drive forward robust research. Here we review published, current, and future projects, that include structural MRI, diffusion tensor imaging (DTI), and resting state functional MRI (rsfMRI), and that employ advanced methods including structural covariance, and event‐based modeling analysis. We explore age of onset‐ and duration‐related features, as well as phenomena‐specific work focusing on particular epilepsy syndromes or phenotypes, multimodal analyses focused on understanding the biology of disease progression, and deep learning approaches. We encourage groups who may be interested in participating to make contact to further grow and develop ENIGMA‐Epilepsy.     

缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布特点的超声造影研究

目的 应用超声造影观察缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布情况,明确其 斑块内新生血管分布特征。 方法 病例组选取因急性缺血性卒中住院的糖尿病患者40例（入组前未服用降糖药）,卒中同侧颈 动脉斑块形成;对照组为同期门诊就诊的颈动脉斑块形成患者,无卒中病史,性别及年龄匹配的非 糖尿病患者32例。两组患者行弓上计算机断层扫描血管造影（computed tomography angiography,CTA） 检查排除主动脉弓斑块及颅内动脉病变,排除卵圆孔未闭及心房颤动等。对所有患者均行常规超声 及超声造影检查。常规超声观察斑块厚度及内部回声,超声造影观察斑块增强情况,横切面多角度 观察,将超声造影结果分为近内膜处有增强（代表新生血管）及近内膜处无增强两种。 结果 两组患者颈动脉斑块厚度及回声情况差异无统计学意义。超声造影结果显示病例组颈动脉 斑块近内膜处增强者34例（85%）,对照组近内膜处增强12例（37.5%）,差异有统计学意义（χ 2=17.38, P＜0.01）。 结论 未服用降糖药的2型糖尿病并发急性缺血性卒中的患者颈动脉粥样硬化斑块内近内膜处新生 血管增生多于无糖尿病患者,提示血糖升高与颈动脉斑块内血管新生有关。     

轻型缺血性卒中静脉溶栓后双重抗血小板疗效观察

目的 观察rt-PA静脉溶栓联合双重抗血小板治疗轻型缺血性卒中的有效性及安全性。 方法 以2013年12月-2016年12月在石家庄市第一医院连续住院治疗的轻型缺血性卒中患者为研究 对象,将其随机分为对照组、溶栓+单抗组和溶栓+双抗组。对照组不进行静脉溶栓,长期口服阿 司匹林（100 mg/d）抗血小板治疗;溶栓+单抗组在rt-PA静脉溶栓（0.9 mg/kg,最大剂量90 mg）基 础上长期单用阿司匹林（100 mg/d）抗血小板治疗;溶栓+双抗组在溶栓后单抗基础上加用氯吡格雷 （75 mg/d）双重抗血小板治疗,双抗治疗21 d后改为阿司匹林长期单抗治疗。随访3个月,有效性指标 为3个月时NIHSS 0～1分、Barthel指数（Barthel index,BI）95～100分和mRS 0～1分的比例,3个月时缺 血性卒中的复发率;安全性指标为治疗24 h出血转化和症状性出血转化的发生率。另外比较三组间 基线和3个月时血清hs-CRP和IL-6的水平差异。 结果 研究共纳入85例患者,对照组28例,溶栓+单抗组28例,溶栓+双抗组29例,全部患者均完 成3个月随访,无死亡患者。对照组、溶栓+单抗组和溶栓+双抗组3个月随访时NIHSS 0～1分比例分 别为46.43%、78.57%和93.10%,BI 95～100分比例分别为53.57%、82.14%和89.66%,mRS 0～1分 的比例分别为50.00%、82.14%和93.10%,三组上述有效性指标差异均有统计学意义,两两比较显 示,溶栓+双抗组高于溶栓+单抗组和对照组,溶栓+单抗组高于对照组,差异均有统计学意义;对 照组、溶栓+单抗组和溶栓+双抗组3个月时缺血性卒中复发率分别为32.14%、7.14%和3.45%,差异 有统计学意义。安全性指标方面,三组均无出血转化事件。对照组、溶栓+单抗组和溶栓+双抗组3 个月时的hs-CRP水平分别为11.92±3.58 mg/L、9.04±2.85 mg/L和6.04±2.65 mg/L,IL-6水平分别为 26.18±4.65 ng/L、16.11±6.93 ng/L和12.84±2.57 ng/L,三组上述炎症因子水平差异均有统计学意 义,其中溶栓+双抗组低于溶栓+单抗组和对照组,溶栓+单抗组低于对照组。 结论 对于急性轻型缺血性卒中患者,rt-PA静脉溶栓治疗后短期双重抗血小板治疗可显著改善患 者神经功能,降低炎症因子水平,降低复发率,且不增加出血风险。     

Yohimbine increases the binding potential for [11C]flumazenil in the monkey brain

Summary. We evaluated the impact of yohimbine administration on benzodiazepine (BDZ) receptor binding in the central nervous system of non-human primates (rhesus monkeys). Estimates of the binding potential (B_max/K_d) of BDZ receptors were made following intravenous administration of yohimbine, an α₂-adrenoceptor antagonist. Positron emission tomography was used in conjunction with [¹¹C]flumazenil (Ro 15-1788), a tracer for central BDZ receptor binding activity. The effects of yohimbine were compared with a control condition in which saline was administered. Yohimbine significantly increased the binding potential in the hippocampus, as assessed using a Student's t-test with Bonferroni correction. The result that the administration of yohimbine readily induces an increase in the binding potential for BDZ receptors in the primate brain suggests that the presence of an anxiety state potentiates the effect of anxiolytics. Accepted August 10, 2001