硬膜下脓肿误诊为慢性硬膜下血肿1例

正1病例资料男性,67岁。因发现言语不清、右侧肢体无力3 d入院。入院体格检查:神志清楚,精神差,言语不清,思维力、理解力、定向力、记忆力明显减退;颈抵抗,左侧肢体肌力5级,右侧肢体肌力3级,四肢肌张力正常,右侧巴氏征阳性。头颅CT示左侧额颞顶部硬膜下慢性血肿。初步诊断为左侧额颞顶部慢性硬膜下血肿,给予脱水、营养神经等治疗。入院2 h突发四肢抽搐,持续3～4 min,考虑癫痫发作,给予地西泮注     

颈动脉夹层支架植入术后断裂一例

临床资料 患者男性,36岁,因"突发言语不清伴左肢无力4h"于2012年1月31日入院.患者于2010年5月因"左侧肢体麻木1d"在当地医院治疗,住院检查发现"左顶叶脑梗死、右侧颈内动脉狭窄,夹层形成",2010年6月转至上海某医院行"右侧颈内动脉夹层支架植入术",术中植入自膨式支架(美国EV3公司Protégé支架)2枚,手术顺利,恢复良好,术后每天口服阿司匹林100 mg、氯吡格雷75 mg、阿托伐他汀20 mg治疗.于2012年1月25日患者再次出现左上肢麻木、欠灵活,在当地医院治疗,症状好转.2012年1月31日凌晨2时被家属发现言语不清,左侧肢体活动不能,烦躁,急送至某医院.体检:血压120/80 mm Hg(1 mm Hg=0.133 kPa),嗜睡,言语不能,双侧瞳孔直径2.5 mm,对光反射灵敏,右向凝视,未及眼震,左侧鼻唇沟对称浅,伸舌无法配合,左侧上下肢肌力0级,右侧肢体肌力检查不合作,左侧巴宾斯基征阳性.     

社区时间管理康复治疗对1例脑出血患者肢体功能恢复的思考

1病例介绍患者女性,78岁,主因“突发左侧肢体无力3天”于2016年10月31日收入上海市第五人民医院。入院查体:嗜睡,双侧瞳孔等大等圆,双侧对光反射迟钝,伸舌左偏,露齿左侧口角下垂,颈部无抵抗,气管居中,颈静脉无怒张,心率83次/分,律齐,右侧肢体肌力正常,左上肢肌力1级,左下肢肌力2级,生理反射存在,Babinski征左侧(+),右侧(-)。急诊头颅CT检查显示:右侧放射冠区脑出血,脑室积血,多发脑梗死,脑白质疏松,脑萎缩(图1A)。     

抗中性粒细胞胞质抗体阳性的类风湿性脑膜炎一例报告

临床资料患者男性,71岁。类风湿性关节炎病史2年半。1年半前出现发作性左侧肢体无力和言语不清,此后又出现双手颤动。半年前出现持续性左侧肢体无力和言语不清。查体:双手指屈曲畸形,小关节肿胀。双下肢浮肿。患者反应迟钝,言语欠清。脑神经检查未见异常。四肢痛、触觉正常,双膝关节以下音叉振动觉减弱。左上下肢力Ⅳ级,双手意向性震颤。左上肢腱反射较右侧活跃,左侧膝腱反射未引出,右侧膝腱反射减弱,双侧跟腱反射减弱。左侧下肢病理反射阳性。无脑膜刺激征。实验室检查:血沉89mm/h(正常<15mm/h)、血清类风湿因子54·3U/ml(正常0~30·0U/ml…     

皮肤真菌感染继发白色念珠菌性脑脓肿1例报道

1临床资料 患者男性,78岁,因头痛、头晕伴左侧肢体无力8 d于2002年8月28日入院 有长期体表真菌感染病史4年,无恶心、呕吐,无肢体抽搐及其它不适.无外伤史及高血压痛史,查体生命体征正常,头皮及四肢真菌感染,双侧瞳孔等大等圆,对光反射灵敏,直径2 5 mm,颈软,四肢肌张力正常,左上肢肌力3级,左下肢肌力4级.右侧肢体肌力5级.左侧腹壁反射、提睾反射减退,左侧肱二、三头肌腱反射、膝腱、跟腱反射均活跃,右侧正常 左侧巴彬斯基征阳性。头颅CT及MRI检查提示:右顶叶震性占位性病变,丧壁厚度不均,并见壁结节。CT增强     

未经治疗的后交通动脉瘤演变为巨大动脉瘤一例

临床资料患者女性,73岁,因"言语欠清、左侧肢体无力4.5h"于2007年12月29日首次入院.患者有高血压病史2年.否认糖尿病、高脂血症史.体检:血压130/80mm Hg(l mm Hg =0.133 kPa),左鼻唇沟浅,伸舌左偏,左侧上肢肌力0级,左侧下肢肌力I级,左侧巴宾斯基征(±);临床诊断:急性脑梗死(右侧大脑中动脉供血区).     

高原地区产后并发上矢状窦静脉血栓形成1例

正1病例资料17岁女性,足月顺产分娩一健康婴儿后9 d突发左侧肢体无力,伴麻木,进行性加重,随后出现肢体抽搐,约2 min后自行缓解,期间间断发作。入院头颅CT示左侧顶叶低密度影并脑沟混杂高密度影,矢状窦高密度影。体格检查:神志浅昏迷,GCS评分11分;双侧瞳孔直径约3.0 mm,对光反射灵敏;左上肢肌力0级,其余肢体肌力正常;病理征阴性。     

椎-基底动脉扩张延长症1例报告

椎-基底动脉扩张延长症(vertebrobasilar dolichoectasia,VBD)是目前正处于研究和探索阶段的一种脑血管变异性疾病,现将我院收治的1例VBD报告如下. 1 临床资料 患者,男,76岁,因"一过性意识不清、右侧肢体无力2d"于 2012年4月15 日入院.患者于2d前由座位站起时突发头晕,继之意识不清,摔倒在地,无抽搐,无尿便失禁,约1 min意识转清,醒后自觉右侧肢体无力,伴言语略不清,病来无视物成双,无饮水呛咳.既往高血压病史10年、左侧面肌痉挛3年.查体:BP 140/90mmHg,神清,言语略不清,眼球运动充分,无眼震,双侧额纹对称,右侧鼻唇沟浅,左侧面肌痉挛,伸舌右偏,右侧肢体肌力4级,腱反射对称,右Babinski(+).     

自发性颈髓硬膜外血肿致脊髓半切征一例

患者,男,74岁。颈部、上胸部及双上肢突感剧烈疼痛,呈持续性。3小时后右侧肢体酸胀无力,左侧肢体麻木,伴小便困难。无外伤史,无出血性疾患史,未服用抗凝制剂。查体:神志清,语言流利,颅神经正常。右侧肢体肌力Ⅳ级、左侧Ⅴ级,腱反射右>左,右侧巴氏征阳性。左侧T_4以下痛、触觉减退,深感觉正常。腰     

听诊阴性的左房黏液瘤致脑栓塞一例

临床资料 患者男性,46岁,因"突发意识不清、右侧肢体无力8 h"入院.2007年10月2日晚10时患者在看电视时突发呼之不应、右侧肢体不能活动,于3日晨2时送至我院就诊.发病前3 d有发热,体温最高达37.5℃,既往3年前有右胫骨下段骨折史,否认高血压、糖尿病、冠心病史.体检:血压110/70 mm Hg(1 mm Hg=0.133 kPa),呼之不应,双侧瞳孔等大等圆,直径3 mm,对光反射存在,眼震(一),右侧中枢性面舌瘫;左侧肢体见自主活动,右侧肢体肌力0级,右侧Babinski征(+).     

1例马凡综合征所致脑栓塞分析并文献回顾

1 临床资料 男性,39岁,主因突发言语不清,右侧肢体无力3d于2010年7月22日收入首都医科大学宣武医院.患者3d前晨起穿衣时突感右侧肢体无力,抬起不能,言语含糊不清;同时伴剧烈头痛,其部位不能详述,无头晕无恶心呕吐.急至当地医院,给予对症治疗（诊断及用药不详）,病情无明显改善.既往确诊马凡综合征12年,10年前行主动脉瘤及主动脉瓣换瓣手术,一直服用华法林治疗;5年前发现腹主动脉瘤,未予处理.无高血压糖尿病及烟酒史.无明确家族史.     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

头颈部动脉夹层研究进展

头颈部动脉夹层,是指各种原因造成的头颈部动脉壁各层之间分离,血肿在动脉壁间积聚或血液在动脉壁间流通.按其发生的部位分为颅外段动脉夹层和颅内段动脉夹层,包括颈内动脉、椎动脉、基底动脉及其分支动脉的夹层形成,其中以颅外段颈内动脉夹层最为常见.     

Xenon-enhanced CT assessment of cerebral blood flow in stroke-in-progress patients with unilateral internal carotid artery or middle cerebral artery stenosis

Carotid or cerebral artery stenosis resulting in low perfusion is a major cause of ischemic stroke.Understanding the unique hemodynamic features in each patient undergoing a stroke-in-progress（SIP） and the correlation between progression and cerebral blood flow（CBF） status would help in the diagnosis and treatment of individual patients.We used xenonenhanced CT（Xe-CT） to examine cerebral perfusion in patients with or without SIP（30 patients/group）,recruited from October 2009 to October 2010.Only SIP patients with unilateral stenosis in the internal or middle cerebral artery were recruited.The occurrence of watershed infarction was higher in the SIP group than in the non-SIP group（P ＆lt;0.05）.In the SIP group,larger hypoperfused areas were found around the lesions than in the non-SIP group.In the SIP group,the CBF values in the ipsilateral areas were significantly lower than those in corresponding regions on the contralateral side.CBF values in the contralateral hemisphere were significantly lower in the SIP group than in the non-SIP group.In SIP patients,infarctions were surrounded by larger hypoperfused areas than in non-SIP patients.These larger hypoperfused areas may result in pathological damage to the brain that is responsible for the progression of stroke.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

Total saponins of Panax ginseng effects on proliferation and differentiation of human embryonic neural stem cells and in a Parkinson’s disease mouse model

BACKGROUND： Total saponins of Panax ginseng （TSPG） exhibits neuroprotection against Parkinson＇s disease in the substantia nigra. OBJECTIVE： To investigate the effects of TSPG on human embryonic neural stem cells （NSCs） proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson＇s disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING： In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS： TSPG （purity 〉 95%） was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor （bFGF） and recombinant human epidermal growth factor （EGF） were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson＇s disease model with i.p. injection of MPTP （1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine） and TSPG alone or combined with interleukin-1 （IL-1）-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS： Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment： （1） to induce proliferation, NSCs were treated with TSPG, EGF＋bFGF, or TSPG＋EGF＋bFGF, respectively; （2） to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG＋IL-1, respectively. MAIN OUTCOME MEASURES： In vitro experiment： the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment： differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS： （1） NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. （2） TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. （3） At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG＋IL-1 groups （P 〈 0.05）. CONCLUSION： TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson＇s disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson＇s disease mouse model.     

Targeting 13-secretase with RNAi in neural stem cells for Alzheimer＇s disease therapy

There are several major pathological changes in Alzheimer＇s disease, including apoptosis of cho- linergic neurons, overactivity or overexpression of 13-site amyloid precursor protein cleaving enzyme 1 （BACE1） and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein （AI3） production, and introduced it into the pSilenCircle vector to construct a short hairpin （shRNA） expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing AI3 protein production. We anticipate that this technique combining cell transplantation and gene ther- apy will open up novel therapeutic avenues for Alzheimer＇s disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.