目的 探讨脑微出血病人血清β淀粉样蛋白1-42(Aβ 1-42 )、磷酸化τ-181蛋白检测的意义。方法 收集2019年11月至2020年5月在徐州医科大学附属医院经头颅磁共振成像（MRI）+磁敏感加权成像（SWI）检查证实存在脑微出血的腔隙性脑梗死病人50例为研究组，与之性别、年龄相匹配的不存在脑微出血的腔隙性脑梗死病人50例为对照组。将研究组按照脑微出血的MARS评估量表分为皮层和皮质下组（16例）、深部组（14例）、幕下组（15例）和混合组（5例）。对比各组间血清Aβ 1-42 、磷酸化τ-181蛋白浓度。结果 与对照组（36.63±12.72）ng/L相比，研究组血清Aβ 1-42 浓度（50.14±25.75）ng/L明显升高（P＜0.05）；与对照组（17.82±6.93）ng/L相比，研究组血清τ-181浓度（26.40±12.24）ng/L明显升高（P＜0.05）。且脑微出血总数目与血清Aβ 1-42 及血清磷酸化τ-181浓度均呈正相关（r=0.46、0.30,P＜0.05）。然而皮层和皮质下组、深部组、幕下组间血清Aβ 1-42 和磷酸化τ-181浓度差异无统计学意义（P＞0.05）。结论 脑微出血对认知功能的影响机制与血清Aβ 1-42 、磷酸化τ-181蛋白的水平呈正相关，临床上对潜在认知功能损害的脑微出血病人检测血清Aβ 1-42 、磷酸化τ-181蛋白有重要意义。

目的 构建自发性基底节脑出血(sBGICH)患者早期血肿扩大的预测模型并验证其预测效果.方法 回顾性分析2015年1月至2020年10月徐州医科大学附属医院收治的259例sBGICH患者临床资料,根据24 h内复查CT结果分为血肿扩大组(92例)和无血肿扩大组(167例).通过单因素分析两组患者早期血肿扩大的可能因素,包括患者入院时血压、格拉斯哥昏迷量表评分、发病至行首次头颅CT的时间、发病6 h内的血液学指标、入院时首次头颅CT和发病24 h内复查的头颅CT结果等,再通过多因素logistic回归模型筛选患者早期血肿扩大的危险因素,运用R语言rms包构建预测患者早期血肿扩大的列线图模型,运用受试者工作特征(ROC)曲线和一致性指数评价模型的区分度,用校准曲线评价模型的校准度,用决策曲线评价模型的临床有效性.结果 多因素logistic回归结果显示,入院时收缩压高[OR(95％CI):1.042(1.022～1.063)]、基础血肿量大[OR(95％CI):1.159(1.097～1.224)]、血肿生成速度快[OR(95％CI):1.208(1.083～1.347)]、存在血肿密度异质性[OR(95％CI):6.671(2.569～17.324)]、中性粒细胞/淋巴细胞比值(NLR)水平高[OR(95％CI):1.168(1.056～1.292)]、血糖高[OR(95％CI):1.141(1.026～1.270)]为sBGICH患者早期血肿扩大的危险因素.以此建立列线图模型,该模型的曲线下面积为0.836(95％CI:0.784～0.889),C指数为0.815(95％CI:0.786～0.851);校正曲线:接近斜率为1的直线;决策曲线可选阈概率范围为10％～85％.结论 入院时收缩压高、基础血肿量大、血肿生成速度快、存在血肿密度异质性、NLR水平高、血糖高为自发性基底节脑出血患者早期血肿扩大的危险因素.列线图预测模型能精准识别自发性基底节脑出血后血肿扩大的高危个体,为患者预后提供参考,此预测模型临床应用价值较高.

目的 分析复发型吉兰—巴雷综合征(rGBS)患者的临床特征及炎性因子与GBS复发的相关性.方法 选取2015年1月—2020年6月徐州医科大学附属医院神经内科收治GBS患者183例,根据其是否复发分为复发组(n=11)和未复发组(n=172),比较2组患者临床特征、血清和脑脊液炎性因子.Logistic回归分析GBS复发的独立危险因素,ROC曲线分析炎性标志物对GBC复发的预测价值.结果 GBS复发率为6.0％(11/183).与未复发组比较,复发组首发年龄较低,症状达峰时间较短,肢体无力和自主神经功能障碍比例、疾病高峰期Hughes评分较低,脱髓鞘型比例较高,差异均有统计学意义(t/χ2/P=2.488/0.028、2.853/0.021、4.329/0.037、3.908/0.047、2.320/0.029、8.440/0.015);而性别、感觉障碍、颅神经麻痹、机械通气比例,差异无统计学意义(P>0.05).与未复发组比较,复发组血清NLR、IL-8升高,LY和IL-13降低(t/Z/P=2.633/0.008、2.019/0.045、1.812/0.035、2.573/0.011).多因素Logistic回归分析表明,高NLR为GBS复发的独立危险因素[OR(95％CI)=1.363(1.027～1.808)],高IL-13为其保护因素[OR(95％CI)=0.867(0.780～0.963)].NLR联合IL-13预测GBS复发ROC曲线下面积为0.818(95％CI 0.684～0.942),敏感度为73.3％,特异度为82.5％,约登指数为0.56.结论 对于首次发作的GBS患者,高NLR、低IL-13者复发风险高;NLR和IL-13可作为预测复发的指标,二者联合预测价值更高.

背景 脑微出血(CMBs)在认知功能障碍(CI)患者中的发病率高达45％,虽然CMBs的危险因素及其与认知功能的关系获得了广泛的关注和研究,但是目前CMBs的危险因素尚无统一定论,且CMBs是否独立导致认知功能下降以及不同CMBs部位和数量与总体认知功能和具体认知域之间的关系仍需进一步探索.目的 探讨CMBs、CI的危险因素,并分析CMBs与认知功能的关系.方法 选取2019-01-01至2020-05-31在徐州医科大学附属医院神经内科住院的脑小血管病患者196例为研究对象.收集患者一般资料、实验室检查指标〔包括总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、血尿酸(BUA)、同型半胱氨酸(Hcy)、β淀粉样蛋白1-42(Aβ1-42)、磷酸化Tau-181蛋白〕、影像学资料、蒙特利尔认知评估(MoCA)量表及其各认知域得分.根据颅脑MRI检查结果,将患者分为CMBs组(84例)和非CMBs组(112例).根据微出血解剖评分量表(MARS),将CMBs分为皮质-皮质下CMBs(包括皮质下U纤维)、深部CMBs、幕下CMBs、混合CMBs.根据MoCA量表得分,将患者分为CI组(MoCA量表得分≤26分,90例)和非CI组(MoCA量表得分>26分,106例).CMBs、CI的影响因素分析采用多因素Logistic回归分析;CI组CMBs数目与MoCA量表得分的相关性分析采用Spearman秩相关分析;不同部位CMBs与MoCA量表各认知域得分之间的相关性分析采用线性混合模型分析.结果 多因素Logistic回归分析结果显示,吸烟〔OR=2.857,95％CI(1.197,6.822)〕、高血压病史〔OR=4.098,95％CI(1.949,8.618)〕、TC〔OR=0.553,95％CI(0.370,0.828)〕、Aβ1-42〔OR=1.013,95％CI(1.002,1.024)〕是CMBs的影响因素(P<0.05);年龄〔OR=1.065,95％CI(1.011,1.122)〕、受教育年限〔OR=1.086,95％CI(1.023,1.153)〕、脑白质病变(WML)〔OR=5.414,95％CI(2.411,11.213)〕和CMBs〔OR=7.857,95％CI(3.371,18.313)〕是CI的影响因素(P<0.05).CI组CMBs数目与MoCA量表得分无直线相关关系(rs=-0.147,P=0.166).线性混合模型分析结果显示,CI组皮质-皮质下CMBs与MoCA量表延迟记忆、语言能力得分呈负相关(P<0.05);深部CMBs与MoCA量表视空间及执行、定向力得分呈负相关(P<0.05);混合CMBs与MoCA量表注意力得分呈负相关(P<0.05).结论 CMBs的危险因素包括吸烟、有高血压病史、TC降低、Aβ1-42升高,CI的危险因素包括高龄、受教育年限短、发生WML与CMBs;CMBs与CI患者认知功能存在一定相关性,具体为皮质-皮质下CMBs与延迟记忆、语言能力呈负相关,深部CMBs与视空间及执行、定向力呈负相关,混合CMBs与注意力呈负相关.

目的 探讨自身免疫性脑炎的临床特点及治疗预后.方法 收集2016年6月至2019年10月于徐州医科大学附属医院确诊的19例自身免疫性脑炎患者的临床资料,回顾性分析其临床表现、脑脊液检查结果、影像学表现、脑电图表现及治疗预后.结果 19例患者中男14例,女5例,年龄18～68岁,平均年龄(42.1±16.0)岁.起病形式多呈急性或亚急性,临床表现为癫痫发作14例,精神行为异常10例,认知障碍9例,意识水平下降或昏迷4例,言语障碍3例,自主神经功能障碍3例,睡眠障碍3例,腹泻1例,低钠血症1例.脑脊液检查:白细胞数增高者18例,蛋白增高者11例,免疫球蛋白IgG增高者11例,液基细胞学见淋巴细胞增多者7例.影像学:头颅MRI检查主要表现为额叶、颞叶、海马、岛叶等部位T2加权像(T2WI)、液体衰减反转恢复(FLAIR)序列呈高信号,部分患者弥散加权成像(DWI)呈高信号,增强扫描伴强化者少见.脑电图:正常者6例,轻度异常者5例,中度异常者4例,重度异常者1例.治疗预后:多数患者使用糖皮质激素、免疫球蛋白等免疫治疗后改良Rankin量表(MRS)评分较入院时降低1～3分,症状完全恢复者6例,放弃治疗者1例.结论 自身免疫性脑炎临床表现复杂多样,以癫痫发作、精神行为异常、认知障碍急性或亚急性起病的患者,应考虑自身免疫性脑炎可能,需完善脑脊液、头颅MRI等相关检查,尽早启动免疫治疗.

神经系统副肿瘤综合征(paraneoplastic neurological syndrome,PNS)是指机体各系统的恶性肿瘤或潜在的恶性肿瘤,在非浸润、压迫或转移的情况下,产生"远隔"效应而导致神经系统临床症状[1].现报告1例确诊PNS患者的临床资料,结合相关文献探讨该病的病因、临床表现、病理及影像学特征.

目的:探究脑梗死后吞咽功能障碍患者应用早期康复治疗的疗效以及临床应用价值.方法:抽取于本院进行相关诊治的脑梗死后吞咽功能障碍患者60例作为研究对象,采取随机分组分为对照、观察组,各30例.两组患者均实施神经内科治疗,在此基础上对照组采用常规早期西医康复治疗,观察组采取早期中西医结合的康复疗法,观察两组患者治疗前后的治疗满意度、疗效以及吞咽功能障碍评估.结果:治疗后,观察组患者的治疗满意度为93.33％(28/30),对照组患者的治疗满意度为60.00％(18/30),差异具有统计学意义,P<0.05(X2=6.1442);治疗后,观察组患者的治疗有效率为86.67％(26/30),对照组患者的为43.33％(13/30),差异具有统计学意义,P<0.05(X2=12.3810);治疗后,观察组洼田饮水试验评分(1.24±0.09)分低于对照组(1.78±0.12)分,差异存有统计学意义,P<0.05.结论:脑梗死后吞咽功能障碍患者应用早期康复治疗的疗效显著,值得临床推广应用.

目的 探讨槲皮素对双转基因小鼠(APP/PS1小鼠)认知功能的影响及其可能的作用机制,寻找治疗阿尔茨海默病(AD)的新方法及靶点.方法 16只雄性APP/PS1转基因小鼠随机分为模型组(n=8)和槲皮素干预组(n=8),对照组(n=8)选雄性同窝阴性小鼠.槲皮素干预组小鼠3月龄起喂饲含槲皮素(2.5 mg/g)的饲料,模型组和对照组小鼠喂饲普通饲料,9月龄时进行Morris水迷宫实验检测各组小鼠空间学习能力;通过West-ern blot检测各组小鼠海马组织中Toll样受体4(TLR4)和核转录因子κB p65(NF-κB p65)蛋白表达;实时定量PCR(qRT-PCR)检测相关炎症因子即肿瘤坏死因子α(TNF-α)、白介素1β(IL-1β)、白介素6(IL-6)、环氧合酶-2(COX-2)、一氧化氮合成酶(iNOS)的mRNA表达.结果 与对照组相比,模型组小鼠在目标象限停留时间及游动的距离明显减少(P<0.05),第2至5天逃避潜伏期延长(P<0.05),海马组织中TLR4和NF-κB p65蛋白表达及TNF-α、IL-1β、IL-6、COX-2、iNOS mRNA表达均增多(P<0.05).与模型组相比,槲皮素干预组小鼠在目标象限停留时间及游动的距离增加(P<0.05),第2至5天逃避潜伏期缩短(P<0.05),海马组织中TLR4和NF-κB p65蛋白表达及TNF-α、IL-1β、IL-6、COX-2、iNOS mRNA表达均减少(P<0.05).结论槲皮素可显著改善APP/PS1小鼠学习记忆能力和炎症反应,其机制可能与抑制海马TLR4/NF-κB信号通路有关.

Objective: To investigate the clinical features and imaging characteristics of mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Methods: Seventeen patients with MELAS diagnosed in the Affiliated Hospital of Xuzhou Medical University from July 2014 to August 2018 were enrolled in this study and their clinical manifestations, imaging and histopathological features were retrospectively analysed. We also discussed and summarised the related literature. Results: All of the 12 patients had seizures; stroke-like episodes in 12 cases; audio-visual impairment in 12 cases; headache in six cases; dysplasia in four cases; mental retardation in three cases; ataxia in two cases. On cranial magnetic resonance (MR) scans, the most common manifestations were in temporal-occipital-parietal lobe, cortical or subcortical areas as well as frontal lobe, thalamus, and basal ganglia showing long or equal T1 signals, long T2 signals, and hyperintense or iso-intense diffusion-weighted imaging (DWI) signals accompanied by ventricular enlargement and brain atrophy. MR spectroscopy showed that lactic acid peaks could be found in lesion sites, normal brain tissues, and cerebrospinal fluid. Muscle biopsy and genetic testing are the gold standard for diagnosing MELAS, muscle biopsy revealed COX-negative muscle fibres and SDH-stained red ragged fibres (RRF) under the sarcolemma. Mutations of mtDNA A3243G locus were common on gene testing. Improvement of mitochondrial function was observed after symptomatic and supportive treatment. Conclusion: MELAS should be considered for patients with epileptic seizures, headache, stroke-like episodes, extraocular palsy, cognitive decline and other clinical manifestations with the lesion located in the temporal-occipital-parietal lobe regardless of the distribution of blood vessels, and further examinations including muscle biopsy and gene testing should be performed to confirm the diagnosis.

目的 对比分析慢性炎性脱髓鞘性多发神经根神经病(CIDP)和多灶性运动神经病(MMN)的临床特征和肌电图特点,以期指导临床诊疗.方法 收集2015-01—2020-01徐州医科大学附属医院收治的MMN患者8例,并与17例同期住院治疗的与之性别、年龄相匹配的CIDP患者临床表现、肌电图特点和脑脊液结果进行比较.结果 CIDP组患者症状多表现为对称性双下肢远端麻木或无力,多从远端向近端进展,而MMN组患者以不对称上肢肌无力为主,两者相比差异有统计学意义(P<0.05).CIDP组感觉障碍和腱反射减弱比例高于MMN组,而肌肉萎缩比例低于MMN组,差异有统计学意义(P<0.05).CIDP组脑神经麻痹比例较MMN组稍高,但两者相比差异无统计学意义(P>0.05).与正常对照组相比,CIDP组和MMN组均有复合肌肉动作电位(CMAP)波幅减低、运动神经传导速度(MNCV)减慢和F波潜伏期延长;CIDP组还表现为明显的远端潜伏期(DL)延长;MMN组虽无DL延长,但有明显的运动神经传导阻滞;CIDP组在MNCV减慢、DL延长、F波潜伏期延长、CMAP波幅减低方面的程度比MMN组重.与正常对照组相比,CIDP组感觉神经动作电位波幅(SNAP)明显减低、感觉神经传导速度(SNCV)明显减慢(P<0.001),而MMN组与正常对照组相比差异则无统计学意义(P>0.05).结论 CIDP组为弥漫性对称性的运动神经感觉神经脱髓鞘,MMN组为仅累及运动神经的局灶性脱髓鞘改变,2组患者均有继发性轴索损害,而CIDP组较重.

目的 探讨平山病的临床表现、神经电生理及影像学特征.方法 回顾性分析2011年1月至2017年12月徐州医科大学附属医院13例确诊为平山病的住院患者的临床、神经电生理及影像学资料.结果 13例患者中男性12例,女性1例;年龄15～26岁,平均(19.6±3.2)岁.所有患者均有肌肉无力和萎缩(其中6例单侧受累,7例双侧均受累),手指震颤10例,肌束颤动2例,“寒冷麻痹”1例.神经电生理:13例患者感觉传导、运动传导均未见阻滞,复合肌肉动作电位的波幅下降,均表现为慢性失神经性改变.影像学:颈椎MRI平扫(直立位)表现为生理曲度变直、颈髓变扁平,部分出现颈髓萎缩或异常信号.屈曲位均出现颈髓变扁平、硬膜外新月形信号影,增强后部分患者出现硬膜外异常信号强化.均予以营养神经治疗,其中11例患者使用颈托治疗,1例患者予颈前路关节融合术和颈托联合疗法,所有患者肌无力症状均得到一定程度的改善.结论 青少年男性如出现单侧上肢肌肉无力萎缩伴手指震颤或肌束颤动,需考虑平山病可能,应进一步完善神经电生理及颈椎MRI检查(尤其是屈曲位)以确诊.

目的 探讨结节性硬化症(TSC)的临床及影像学特点.方法 回顾性分析徐州医科大学附属医院收治的TSC患者的临床资料,总结临床和影像学特点.结果 所有患者中,颜面部血管纤维瘤8例、色素脱失斑9例、癫痫发作11例、智能减退7例.头颅CT可见室管膜下多发钙化结节;头颅MRI可见皮质及皮质下结节,T2WI、FLAIR序列均呈高信号.偶可见侧脑室占位,在头颅MRI上信号混杂,增强扫描强化明显,病理结果提示为室管膜下巨细胞星形细胞瘤.肾脏检查可发现多发结节、多发肾囊肿、血管平滑肌脂肪瘤.所有癫痫患者均使用抗癫痫药物,半数疗效不佳,其中3例行癫痫病灶切除术,病理提示为局灶皮质发育不良.结论 表现为皮肤损害和癫痫发作的患儿,无论有无家族史,均需高度怀疑TSC,需进一步完善头颅CT/MRI、肾脏超声/CT以便确诊.药物治疗无效的部分癫痫患者可行手术治疗.

目的 探讨线粒体脑肌病的临床特征及影像学特点.方法 回顾性分析2014年7月至2018年8月在徐州医科大学附属医院临床确诊为线粒体脑肌病的31例住院患者的临床资料,并结合文献予以探讨与总结.结果 所有患者中癫痫发作19例,视听障碍17例,卒中样发作16例,头痛10例,发育异常8例,智力低下7例,共济失调3例,眼外肌麻痹1例,心慌胸闷1例.头颅MRI多表现为颞、枕、顶叶皮质或皮质下多发病灶,也可见于额叶及丘脑、基底节等处,呈长或等T1、长T2信号影,弥散加权成像(DWI)呈等或高信号,伴脑室扩大和脑萎缩,氢质子磁共振波谱(1H-MRS)显示病变部位、正常脑组织及脑脊液中均可出现乳酸峰.肌电图表现为神经源性或肌源性损害.肌肉活检可见细胞色素C氧化酶(COX)阴性肌纤维及琥珀酸脱氢酶(SDH)染色肌膜下出现的破碎红纤维.基因检测示线粒体DNA(mtDNA)点突变.予以改善线粒体功能及对症支持治疗.结论 具有癫痫发作、头痛、卒中样发作、眼外肌麻痹、智能下降等临床表现且病灶位于颞、枕、顶叶,不按血管分布者,应考虑为线粒体脑肌病可能,需进一步完善血乳酸测定、肌肉活检、基因检测等以确诊.

Objective: To investigate the anatomical characteristics, clinical manifestations, and imaging features of bilateral cerebral peduncular infarction. Methods: A retrospective analysis was performed on 11 patients diagnosed with bilateral cerebral peduncular infarction in the Affiliated Hospital of Xuzhou Medical University from December 2014 to December 2018. Their clinical and imaging features were analyzed and summarized in combination with the relevant national and international literature. Results: Among all the patients, there were eight cases with a history of hypertension, four cases with a history of diabetes mellitus, and four cases with a history of smoking. Conscious disturbance was observed in nine cases, quadriplegia in seven cases, pseudobulbar paralysis in three cases, and ataxia in one case. Brain magnetic resonance (MR) scans of bilateral cerebral peduncles showed patchy abnormal shadows with a hypointense signal on T1-weighted imaging (T1WI) and apparent diffusion coefficient (ADC) and hyperintense signal on T2-weighted imaging (T2WI), fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI). Computed tomography angiography (CTA) scans of head and neck showed severe stenosis or occlusion of vertebral artery, basilar artery, or posterior cerebral artery. All the patients received standardized treatment for cerebral infarction. Six patients died while five were left disabled. Conclusion: Bilateral cerebral peduncle infarction may be related to cerebral perfusion insufficiency caused by the stenosis or occlusion of vertebrobasilar artery and its branches. The main clinical manifestations are locked-in syndrome and persistent vegetative state. The specific imaging feature of "Mickey Mouse ear"-like infarction is associated with a poor prognosis.

ObjectiveTo explore the clinical and imaging features of patients with hypertrophic cranial pachymeningitis (HCP).MethodsA retrospective study was performed on 22 patients with HCP diagnosed at the Affiliated Hospital of Xuzhou Medical University from February 2014 to September 2017.ResultsA headache was present as an initial symptom in 18 patients. The headache was associated with the loss of vision (2 cases), facial pain (1 case), and unsteady walking (1 case). Other symptoms included cranial nerve dysfunction (15 cases), cerebellar ataxia (4 cases), and sinus thrombosis (3 cases). In the laboratory tests, 7 patients showed an increased number of white blood cells, higher levels of C-reaction protein (CRP), and erythrocyte sedimentation rate (ESR). An elevated level of immunoglobulin G4 (IgG4) and the presence of the anti-neutrophil cytoplasmic antibody (ANCA) were found in 3 and 2 patients respectively. There were 17 patients who had abnormalities in their cerebrospinal fluid (CSF) on lumbar puncture. On magnetic resonance imaging (MRI), a local or generalized thickening was observed in the cerebral falx, the tentorium of the cerebellum, the fronto-parietal lobe, the occipito-parietal lobe, and the dura of skull base. A dural biopsy obtained in one case showed a variety of inflammatory changes. An immunohistochemical analysis revealed the positivity of CD138, IgG, and IgG4 in some cells. All 22 patients had a good response to corticosteroids.ConclusionHCP mainly leads to a headache and the paralysis of multiple cranial nerves. A biopsy and MRI are often required and serve as the basis for the diagnosis and effective therapy.

Objective: To analyze the clinical and imaging features of hypertrophic cranial pachymeningitis (HCP).Methods:One case of HCP was reported,and the relevant literature was reviewed and retrospectively analyzed.Results:The patient experienced headache at the onset of illness along with decreased visual acuity. Hematology test:ANA(+).Lumbar puncture:cerebrospinal fluid pressure≥330 mmH2O.Cerebral MRI,plain and enhanced: cerebral falx and tentorium of cerebellum, bilateral frontal parietal dura thickening and enhancement.Dural biopsy:fibrous hyaline tissue scattered around lymphocytes and plasma cells,most apparent surrounding blood vessels. Immunohistochemistry: CD138 (+), IgG (individual cells +), IgG4 (individual cells+).Hormone therapy significantly improved symptoms.We collected data of 189 cases of HCP reported in the last 5 years. Headache is the most presented initial symptom. Dural hypertrophy and enhancement in different parts of the head was observed in all patients by plain and enhanced cranial MRI. After hormone treatment, combined hormone and immunosuppressive treatment, or surgical treatment, more than 90% of the patients'symptoms were improved. Conclusion: The clinical symptoms of HCP can be characterized by chronic headache, cranial nerve involvement, and ataxia. It is imperative to perform hematological examination, plain and enhanced cranial magnetic resonance imaging,and,when necessary,dura mater biopsy to make a diagnosis.

目的:探讨颅内静脉窦血栓(CVST)形成合并脑出血患者的临床特点及影像学特征.方法:选取确诊为CVST合并脑出血的患者9例,收集其临床资料,并进行回顾性分析.结果:9例患者中病因为产褥期4例,服用避孕药物1例,外伤后1例,面部痤疮挤压后1例,其他既往体健.实验室检查:凝血7项示D-二聚体水平升高者3例;血常规示白细胞增多者5例,后复查降至正常.予低分子肝素治疗8例,仅予对症支持治疗者1例;1例住院期间继发脑疝死亡,另8例好转出院.结论:临床上对存在可疑病因,伴有头痛、视乳头水肿等高颅压症状,应考虑CVST可能,需及时完善实验室及影像相关检查,一旦确诊,及时予抗凝等治疗.

帕金森病(PD)的临床表现包括运动症状与非运动症状.随着抗帕金森药物的应用,PD患者的非运动症状越来越成为影响其生活质量的重要因素.PD的非运动症状主要包括抑郁、认知功能障碍、睡眠障碍及消化系统症状等.研究发现,PD患者在疾病早期即可出现消化系统症状,包括流涎、吞咽困难、便秘、小肠细菌过度生长综合征等.了解这些症状对于全面认识PD、早期诊断及进一步优化治疗都具有重要意义.本文对文献报道的常见消化系统症状进行综述.

Neuroinflammation plays a pivotal role in Alzheimer's disease (AD).A growing number of studies proved that nod-like receptor protein 3 (NLRP3) inflammasome was involved in the neuroinflammation of AD through multiple mechanisms,which are crucial to the initiation and development of AD.In this paper,we will summarize the role ofNLRP3 inflammasome and its potential mechanism in AD pathogenesis,as well as NLRP3 inflammasome inhibitors.

Activated Metabotropic glutamate receptors 5(mGluR5) exhibits protective effects against ischemic brain damage, but the underlying mechanisms are not clearly known. Brain-derived neurotrophic factor (BDNF), as a valuable member of neurotrophic factor family, exerts its protection by combining with its high-affinity receptor tyrosine protein kinase B (TrkB). To investigate the role of activated mGluR5 against oxygen-glucose deprivation (OGD)/reoxygenation (R)-mediated cytotoxicity, the cell viability, apoptosis, the release of inflammatory cytokines and accumulation of reactive oxygen species (ROS) were evaluated in BV2 cells (Microglia cell line) with or without OGD/R exposure. Our data show that CHPG (the selective mGluR5 agonist) pretreatment, as an mGluR5 agonist, protected BV2 cells against OGD/R-induced cytotoxicity, apoptosis, the release of inflammatory cytokines, and the accumulation of ROS. However, these effects were significantly reversed by the mGluR5 antagonist MPEP pretreatment. Our data also show that the expressions of BDNF and TrkB were significantly decreased in BV2 cells with OGD/R exposure. CHPG pretreatment significantly enhanced the expressions of BDNF and TrkB in BV2 cells with OGD/R exposure. However, the increased expressions were significantly abrogated by MPEP pretreatment. In addition, inhibition of BDNF/TrKB pathway by K252a also attenuated the protective effects of activated mGluR5 against OGD/R-induced cytotoxicity, apoptosis and the release of inflammatory cytokines. Morever, pretreatment with exogenous BDNF protected BV2 cells against OGD/R induced apoptosis and release of inflammatory cytokines. These data suggested that BDNF/TrKB pathway may be involved in regulating activated mGluR5' protective effects against OGD/R induced cytotoxicity in BV2 cells. (C) 2017 Elsevier B.V. All rights reserved.