神经电生理监测技术在圆锥马尾病变手术中的应用

目的探讨神经电生理监测技术在圆锥马尾病变手术中应用价值。方法回顾性分析110例圆锥马尾病变患者临床资料,其显微外科手术均在神经电生理监测下进行,感觉诱发电位(somatosensory evoked potential,SEP)和运动诱发电位(motor evoked potential,MEP)监测脊髓功能,肌电图(electromyography,EMG)确定肿瘤切除范围。结果显微镜下病变全切除92例(83.6%),次全或大部分切除18例(16.4%)。术后随访1~58个月,神经系统查体及JOA评分发现脊髓神经功能改善102例(92.8%),无变化4例(3.6%),下降4例(3.6%)。对病变切除前与切除后SEP潜伏期和波幅以及MEP潜伏期进行自身比较,脊髓神经功能改善和下降患者电生理监测指标改变差异有统计学意义(P0.05),脊髓神经功能无变化患者相关监测指标改变差异无统计学意义(P0.05),神经电生理监测指标的变化与术后脊髓神经功能改善情况基本相吻合。结论术中神经电生理监测可以实时了解脊髓神经功能的完整性,结合显微神经外科技术可以明显提高圆锥马尾病变的全切率,减少术后并发症,提高手术疗效及安全性。     

脊髓运动诱发电位监测在手术中的应用

目的 评价脊髓运动诱发电位监测在脊柱脊髓手术中的作用.方法 通过连续短脉冲头皮电刺激,应用硬膜外电极于脊髓记录18例脊柱脊髓疾病患者手术过程中的运动诱发电位.根据日本整形外科协会(JOA)评分标准对患者手术前后神经功能进行评价.结果 以手术中首次记录到的脊髓运动诱发电位D1波波幅和潜伏期作为参照值,8例脊柱侧弯患者施行脊柱矫形手术过程中记录到的脊髓运动诱发电位D1波波幅和潜伏期均无异常变化;10例行椎管内及脊髓手术患者,手术中脊髓运动诱发电位D1波波形改变、波幅降低,改变手术方向或经短暂休息后恢复正常.根据JOA评分,手术后所有患者感觉和运动功能均较手术前明显改善,差异有统计学意义(Z=-2.646,P=0.008;Z=-2.828,P=0.005).结论 手术中脊髓运动诱发电位监测可及时、客观地反映神经功能,有效避免手术中神经损伤及手术后神经功能障碍.在监测过程中,头皮电刺激记录到的脊髓运动诱发电位D1波波形清晰、稳定,且不受外界因素的影响.     

神经电生理监测在脊髓髓内肿瘤显微切除术中的应用

目的探讨神经电生理监测在脊髓髓内肿瘤显微切除术的应用价值。方法回顾性分析12例脊髓髓内肿瘤的临床资料。均行显微切除术,术中以体感诱发电位和肌电图监测辅助肿瘤切除。结果肿瘤全切除8例,大部分切除1例,部分切除3例。术后病理诊断：室管膜瘤5例,星形细胞瘤5例,脂肪瘤1例,蛛网膜囊肿1例。随访6~17个月,神经功能障碍不同程度恢复11例,术后神经功能障碍1例。结论显微手术是脊髓髓内肿瘤的有效治疗措施,术中辅以神经电生理监测可提高肿瘤切除率及手术安全性,最大程度保护神经功能,改善病人预后。     

神经电生理监测和超声技术在脊髓髓内肿瘤显微手术中的应用

目的探讨神经电生理监测及超声技术在脊髓髓内肿瘤显微切除术中的应用价值。方法回顾性分析10例脊髓髓内肿瘤病人的临床资料。均行肿瘤显微切除术,术中以体感诱发电位、自发肌电图监测和超声定位辅助肿瘤切除。结果肿瘤全切除8例,大部分切除2例。术后病理诊断:室管膜瘤6例,星形细胞瘤1例,少枝胶质细胞瘤1例,神经鞘瘤1例,蛛网膜囊肿1例。出院时神经功能改善或稳定9例,加重1例;无死亡病例。结论显微手术是治疗脊髓髓内肿瘤的有效措施,术中辅助神经电生理监测及超声技术可提高肿瘤切除率,最大程度保护神经功能,改善病人预后。     

多模式神经电生理监测在颈椎前路手术中的应用

目的 探讨多模式神经电生理监测(MIOM)在颈前路手术中的应用价值.方法 53例颈椎前路手术患者采用术中MIOM监测,记录术中各个阶段的报警情况,并采取相应措施,使术中脊髓神经损伤的可能性最小化.分析术中警报按类型、原因、术前诊断以及手术方式之间的关系,通过神经电生理监测结果以及手术前后JOA评分对手术疗效进行分析.结果 与术前基准电位相比较,术毕SEP及MEP波幅均有所提高,而潜伏期均未有明显改变.术后JOA评分较术前有明显改善(P＜0.05).脊髓型颈椎病患者以及行椎体次全切手术者术中监测“严重警报”发生率较高.结论 颈前路手术中多模式神经电生理监测能有效降低术中神经功能损伤,降低手术风险并能作为手术疗效评价以及神经功能恢复情况的客观依据.     

运动诱发电位联合体感诱发电位监测在脊髓髓内肿瘤手术中的应用

目的 探讨全静脉麻醉下运动诱发电位(MEP)联合体感诱发电位(SEP)术中监测应用于脊髓髓内肿瘤手术的优越性、可靠性及临床应用价值.方法 对72例脊髓髓内肿瘤患者术中行SEP和MEP联合监测,参照McCormick评分标准对术前、术后脊髓功能的改变和诱发电位变化之间的关系进行统计分析.结果 14例脊髓神经功能改善,18例术后脊髓神经功能下降者与诱发电位监测结果具有一致性(P＜0.05).结论 对脊髓髓内肿瘤手术进行SEP与MEP监测有利于避免"假阴性/假阳性"结果及术后神经功能障碍的发生.     

脊髓运动诱发电位在脊髓肿瘤手术中的监测应用

目的探讨脊髓运动诱发电位(SCMEP)在脊髓肿瘤手术中监测的应用价值.方法采用硬膜外电极在椎管内直接刺激脊髓记录脊髓运动诱发电位(SCMEP)监测脊髓肿瘤手术,并对17例肿瘤患者的手术监测的记录结果进行回顾性分析.结果SCMEP由于病变部位及性质、刺激电极与记录电极间的距离不同,波幅及潜伏期的差异较大,电极安放后与手术结束时的结果个体对照,相差不显著(P=0.083;P=0.387).7例术中波幅降低超过预警值20%,5例经短暂休息或改变手术方向后,波幅恢复正常.结论SCMEP的波幅变化是提示脊髓损伤的可靠性灵敏指标,对辅助医生进行手术安全操作,缩短手术时间,提高手术质量,减少术后神经功能障碍起到重要作用.     

脑干听觉诱发电位监护在脑干肿瘤手术中的应用研究

目的研究脑干及相应颅神经功能损伤时较敏感的电生理指标,为脑干肿瘤手术提供精确、准确和安全的术中监测手段。方法对18例脑干肿瘤病人,用同一进口监护仪于手术前、术中及术后分别进行脑干听觉诱发电位(BAEP)连续实时监护,测定手术操作对这些指标的影响。结果脑干肿瘤手术操作均可以引起BAEP改变,BAEP的Ⅰ、Ⅲ、Ⅴ波潜伏期(PL)及Ⅰ～Ⅴ、Ⅲ～Ⅴ峰间潜伏期(IPL)明显延长(P<0.01),Ⅴ波波幅明显降低(P<0.01),其中BAEP的Ⅴ波潜伏期及波幅改变最为显著。结论BAEP的Ⅴ波潜伏期延长和波幅下降是术中敏感的电生理指标,对其进行监护可为手术中及手术后避免神经功能损伤提供客观指标,降低手术伤残率,减少或避免病人手术后神经功能损伤。     

神经电生理监测桥小脑角手术的研究(附106例报告)

目的探讨桥小脑角(CPA)手术中行神经电生理监测的意义。方法对106例CPA肿瘤病人进行了术中神经电生理监测,主要包括面神经、三叉神经、后组颅神经以及健侧脑干听觉诱发电位(BAEP)监测,观察术后面神经功能及并发症。结果面神经解剖保留96例(91%),面神经功能Ⅰ、Ⅱ级57例(54%),Ⅲ、Ⅳ级42例(40%),Ⅴ、Ⅵ级7例(6%)。术中健侧BAEP变化最明显的是Ⅲ～Ⅴ、Ⅰ～Ⅴ峰间潜伏期。结论在CPA手术中,采用诱发电位、肌电图实时监测,可及时为术者提供脑干功能的情况;术中健侧BAEP的Ⅰ～Ⅴ、Ⅲ～Ⅴ峰间潜伏期是重要监测指标;术中肌电图监测可以提示颅神经的位置和走行,为手术时避免损伤神经提供依据。     

多模式神经电生理监测辅助显微手术治疗椎管内肿瘤的疗效分析

目的探讨多模式神经电生理检测下显微手术切除椎管内肿瘤的临床疗效。方法回顾性分析2011年5月至2016年6月显微手术切除的椎管内肿瘤57例,术中采用体感诱发电位(SEP)、运动诱发电位(MEP)及肌电图(EMG)多模式神经电生理监测(MIOM)。结果肿瘤全切49例(86.0%),次全切除6例(10.5%),部分切除2例(3.5%),失访4例,53例术后随访3个月~2年,神经功能改善45例(78.9%),无明显改善4例(12.3%),症状加重3例(7.0%),复发1例(1.8%)。结论多模式神经电生理检测辅助显微手术切除椎管内肿瘤,能有效提高肿瘤全切率,并预测和保护脊髓神经功能,提高手术疗效及安全性。     

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.     

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。     

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。     

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