接触性热痛诱发电位的临床研究

目的 进一步完善接触性热痛诱发电位(CHEP)的检测方法 和检测痛觉传导通路上段脊髓丘脑束和周围段神经传导时间及周围段神经传导速度. 方法 受检者取卧位,应用CHEP刺激器,于54.5℃应用可调节脉冲,刺激部位为手背、前臂的掌侧面和C7水平皮肤.以Keypoint.net仪器记录,记录点为Cz和Pz,测定CHEP主要波形及外周神经传导速度. 结果 于记录点记录到2个主要成分;Cz/N550、Cz/P750;刺激手背、前臂掌侧面和C7水平皮肤所得CHEP起始波潜伏期男性女性间比较差异无统计学意义(P0.05);介导此诱发电位的外周神经传导速度为(12.9±7.5)m/s,与A8纤维传导速度相对应. 结论 主观疼痛能够进行客观测定,C7点刺激进行CHEP测定有助于判断脊髓丘脑束中枢段和周围段的损害.     

接触性热痛诱发电位对糖尿病小纤维神经病变的评价作用

目的 借助接触性热痛诱发电位(CHEP)为糖尿病神经病变的小纤维神经损害寻求一种新的无创客观定量方法.方法 选取糖尿病患者46例和健康人40名,应用CHEP刺激器,控制温度52℃,分别刺激所有受试者右侧前臂、手背、小腿皮肤,采用Keypoint.net肌电图仪于cz点分别记录N波潜伏期及N-P波波幅;同时行右侧上下肢感觉传导测定.结果 健康对照组各个刺激部位CHEP的引出率为100%,而糖尿病组46例中前臂7例、手背9例、小腿16例未引出肯定CHEP波形.糖尿病组较对照组N波潜伏期延长,N-P波波幅减低.糖尿病组中25例上肢感觉传导正常,其前臂刺激Cz记录的N-P波波幅较对照组减低[分别为(34.0±12.6)、(48.4 ±17.5)μV,Z=-3.151,P<0.01],N波潜伏期差异无统计学意义;手背刺激CHEP潜伏期较对照组延长[分别为(420.4±27.8)、(407.2±24.6)ms,t=2.015,P=0.048],波幅减低[分别为(28.2±10.1)、(43.0±16.6)μV,Z=-3.712,P<0.01].18例下肢感觉传导正常,其小腿刺激CHEP潜伏期延长[分别为(473.5±46.6)、(448.6±35.0)ms,t=2.219,P=0.031],波幅减低[(23.8±7.4)、(41.5±18.5)μV,Z=-3.855,P<0.01].结论 糖尿病患者在早期即有小纤维神经选择性受累,CHEP能够为其提供新的客观定量方法,具有潜在的临床应用价值.     

痛觉诱发电位示肌萎缩侧索硬化患者痛觉通路正常

目的 研究肌萎缩侧索硬化患者痛觉诱发电位的特点,评估其痛觉通路的传导.方法 肌萎缩侧索硬化患者60例,取卧位,应用接触性热痛诱发电位刺激器,直径27 mm(面积573 mm2),加热速度70℃/s.于54.5℃应用可调节脉冲,刺激部位为手背、前臂的掌侧面、第7颈椎棘突处(C7).记录仪器:Keypoint.net仪器.记录点为Cz和Pz.同时进行躯体感觉诱发电位检测,记录其波形及潜伏期.并对60名健康对照者进行相应研究.结果 肌萎缩侧索硬化患者接触性热痛诱发电位波形无异常,潜伏期分别为:手背刺激(561.2±28.6)ms,前臂掌侧刺激(540.1±39.2)ms,C7刺激(512.7±31.4)ms,与健康对照组[(558.7±30.2)、(536.6±23.5)、(501.8±26.0)ms]比较差异均无统计学意义(t=4.23、4.51、3.74,P＞0.05).其躯体感觉诱发电位各波潜伏期、波间期均正常.结论 肌萎缩侧索硬化患者接触性热痛诱发电位正常,提示其痛觉通路正常.     

接触性热痛诱发电位在多发性硬化患者中的应用

目的 建立接触性热痛诱发电位(CHEP)标准,并对多发性硬化(MS)患者进行痛温觉传导通路功能评价,评价CHEP在MS中的应用价值.方法 选取确诊的MS患者36例和健康人40名,应用接触性热痛诱发电位刺激器(Medoc,Israel),在2个强度水平(47、51℃)应用可调节脉冲,刺激部位选择右上肢前臂掌侧前1/3处、右下肢内踝上皮肤和腰部.受试者在每次刺激后,对刺激强度分级.以Keypoint.net仪器记录,记录点为Cz.测定刺激强度和疼痛分级的关系、诱发电位的主要成分的潜伏期和波幅.结果 健康对照组予以47℃和51℃分别刺激上下肢,CHEP的引出率为100%;MS组上肢4例,下肢5例未引出肯定CHEP波形.我们通过对下肢和腰部刺激计算得出A8纤维传导速度为(18.1±7.3)m/s.MS患者存在痛温觉减退症状的上肢21例,下肢29例,其反应性疼痛分级[视觉模拟评分(VAS),上肢6.1±0.9,下肢5.6±1.3]较对照组(上肢8.0±0.7,下肢7.9±0.7)低,差异有统计学意义(Z=-3.249、-5.272,P＜0.01).存在痛温觉障碍且能够诱发出CHEP波形(上肢17例,下肢24例)的上下肢N波潜伏期[上肢(387.3±34.2)ms,下肢(489.9±70.2)ms]较对照组[上肢(346.0±25.5)ms,下肢(400.8±24.4)ms]明显延长(t=4.790、4.798,P＜0.01)、N-P波幅[上肢(30.5±12.8)μV,下肢(28.2±16.2)μV]较对照组[上肢(49.3±16.0)μV,下肢(42.2±16.7)μV]明显减低(t=-4.612、-3.144,P＜0.01).MS患者下肢CHEP检测的异常率(26/36,72.2%)高于上肢(16/36,44.4%,P=0.031)和体感诱发电位(19/36,52.8%,χ~2=4.261,P=0.039).上肢未存在痛温觉障碍的15例MS患者中,有3例CHEP异常,下肢7例中有2例CHEP异常.结论 CHEP提供了一种临床实用的、非侵入性的客观检查方法,它与侧重于结构异常的MRI不同,重点检测伤害性通路的功能改变,所以结合MRI和其他诱发电位能够更有效的辅助诊断MS,评价伤害性通路的情况,揭示亚临床病灶的存在.     

接触性热痛诱发电位在亚急性联合变性诊断中的应用

目的 应用接触性热痛诱发电位(CHEPs)技术研究亚急性脊髓联合变性(SCD)患者痛觉传导通路变化特点,探讨CHEPs在SCD中的应用价值,为其电生理诊断提供依据.方法 选取确诊型SCD患者20例和健康人34名,应用CHEPs刺激器,刺激水平为51℃,对C_7部位、上肢前臂掌侧前1/3处、下肢内踝及腰部进行刺激,记录点为Cz,记录诱发电位主要成分的潜伏期和波幅.分析周围神经Aδ纤维传导速度和中枢N波峰潜伏期、N-P波波幅,同时进行躯体感觉诱发电位(SEP)及感觉传导速度(SCV)测定并与CHEPs进行比较.结果 (1)健康对照组予以51℃刺激,CHEPs的引出率为100%.(2)患者组中存在痛温觉减退者,视觉模拟评分[VAS,上肢6.4(5.3～8.9)分,下肢5.7(2.8～8.8)分]低于健康对照组[上肢7.6(6.4～9.2)分,下肢6.9(5.7～9.1)分,Z=3.478、3.909,P＜0.01].(3)患者组上肢A8纤维传导速度(CV)为(9.77±4.28)m/s,下肢Aδ纤维CV为(8.19±0.91)m/s,与健康对照组[(12.87±1.40)m/s]比较,差异具有统计学意义(t=3.142、14.864,P＜0.01).患者组中上肢Aδ纤维CV减慢13例(65%),正中神经SCV减慢4例(20%);下肢Aδ纤维CV减慢19例(85%),胫神经SCV减慢12例(60%),A5纤维CV异常率高于SCV.(4)患者组下肢CHEPs异常者16例,而SEP异常者18例,两组间比较差异无统计学意义.结论 CHEPs能发现SCD痛觉传导通路异常部位和程度,较SCV敏感,可以作为辅助SCD电生理诊断的方便、客观的方法.     

康复期男性海洛因依赖者诱发电位P300研究

目的:探讨康复期男性海洛因依赖者(MPHD)听觉诱发电位P300(AEP-P300)与视觉诱发电位P300(VEP-P300)的特点. 方法:以Neuroscan脑诱发电位仪检测38例康复期MPHD(MPHD组)和14名健康对照者(对照组)前额区(Fz)、中央区(Cz)及顶区(Pz)AEP-P300与VEP-P300. 结果:MPHD Cz点AEP-P300波幅平均秩次为23.1μV,显著低于对照组的35.8μV(P<0.05).与对照组比较,在以动物图片为靶刺激(AT)时,MPHD组Fz点波幅显著升高,Cz、Pz点潜伏期显著缩短(u=2.37、2.56、3.10,P<0.05或P<0.01);在以药物图片为靶刺激(DT)时,两组VEP-P300各指标均差异无显著性(P>0.05).与以AT为靶刺激比较,在以DT为靶刺激时,MPHD组上述各点的Fz、cz、Pz点的VEP-P300潜伏期均显著缩短,Pz点波幅显著升高(t=3.39,P<0.01). 结论:康复期MPHD者仍然存在明显的神经电生理功能的紊乱,对药物相关刺激呈现一定的偏好.     

肯尼迪病患者60例神经电生理研究

目的对肯尼迪病患者进行神经电生理检测, 了解其神经功能状况。方法对2010年11月至2022年11月北京大学第三医院门诊和病房收治的60例肯尼迪病患者(根据是否合并糖尿病分为单纯肯尼迪病组29例、肯尼迪病合并糖尿病组31例)及60例糖尿病周围神经病(DPN)患者, 分别进行肌电图、神经传导、体感诱发电位(SEP)、接触性热痛诱发电位(CHEP)及三重刺激技术(TST)检测。采用t检验分别对组内及组间神经传导速度及动作电位波幅、SEP各波潜伏期和波间期、CHEP起始峰潜伏期等参数进行比较。结果与正常值比较, 肯尼迪病组患者感觉神经动作电位(SNAP)波幅明显降低[正中神经(0.7±0.4)μV, 尺神经(0.8±0.3)μV, 腓肠神经(1.8±0.1)μV, 波幅下降30%～80%], 正中神经和尺神经波幅低于腓肠神经(t=2.43, P=0.010;t=2.40, P=0.010);SEP和CHEP的周围段异常(潜伏期延长115%～130%), SEP中枢段异常(潜伏期延长104%～115%), 17例TST结果异常(TST测试/TST对照波幅比下降40%～60%)。DPN组患者SN...     

脊髓丘脑束中枢传导时间的研究

接触性热痛诱发电位(contact heat evoked potential,CHEP)能检测A8纤维和C纤维及脊髓丘腩束功能、反映痛觉通路中枢段和周围段的功能状况.目前多数研究注重于CHEP检测方法的建立和其周围段的功能测定并作为神经系统疾病的辅助诊断[1-3].我们对其周罔段和中枢段同时进行研究,判断其通路的中枢传导时间和传导速度.     

糖尿病周围神经病的小纤维损害

目的对糖尿病周围神经病患者进行痛觉传导通路研究,评估其小神经纤维功能。方法对56例有疼痛症状的2型糖尿病患者进行感觉传导速度测定和接触性热痛诱发电位检测;同时进行健康对照组测试。结果糖尿病组感觉传导速度和接触性热痛诱发电位检测与对照组比较,各参数差异均有统计学意义。其中Aδ纤维和C纤维传导速度:糖尿病组分别为(8.6±1.7)m/s和(0.9±0.1)m/s,对照组分别(13.1±2.4)m/s和(1.7±0.3)m/s,差异有统计学意义(t=17.23,21.62,P均<0.05)。糖尿病组中,感觉传导速度异常率与接触性热痛诱发电位异常率比较,差异有统计学意义。结论糖尿病周围神经病中存在小神经纤维的传导异常,提示小神经纤维功能受累。     

三叉神经痛微血管减压术后神经传导功能的恢复

目的 评价三叉神经痛(TN)微血管减压术(MVD)前后三叉神经的功能恢复.方法 本文研究了38例经磁共振三维层析血管成像术(MRTA)证实有神经血管接触的TN患者,在MVD过程中,通过术前、中、后记录早期头皮诱发电位监测三叉神经传导功能;同时从三叉神经出脑干区(REZ)直接记录诱发电位作为对照研究.结果 所有病例的术前头皮诱发电位均显示三叉神经根部的传导功能损害.头皮诱发电位和根部直接记录电位证实MVD后32例患者三叉神经传导功能迅速恢复,所有患者术后疼痛均缓解.结论 MVD后TN的改善常与神经生理学数值恢复正常有关,提示神经传导功能的恢复.MVD后电生理数值的迅速恢复和疼痛缓解均证明这两种现象与髓鞘再生无关.     

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