颅内深静脉血栓形成的临床特点

目的探讨颅内深静脉血栓形成的临床表现、影像特征,提高对该病的认识。方法回顾分析2例颅内深静脉血栓形成的临床资料并结合文献分析该病病因、临床表现、影像学特点与治疗方法。结果颅内深静脉血栓形成临床表现多样,缺乏特异性,本组2例影像学均表现为双侧丘脑、基底节病变,经头MRV证实为颅内深静脉血栓形成,给予抗凝治疗,症状缓解。结论本病发病因素多,临床表现复杂,头MRV检查是重要确诊手段,及时合理抗凝治疗,可获得良好疗效。     

DSA在烟雾病诊断中的临床应用研究

目的探讨烟雾病DSA检查的影像学表现及临床意义。方法回顾性分析26例确诊烟雾病患者临床及DSA影像学资料。结果26例患者DSA影像学特征如下:脑底异常烟雾状血管网形成;受累动脉狭窄或闭塞;丰富侧支循环形成。其中单/双侧大脑前、中及后动脉均存在不同程度的狭窄或闭塞性病变者24例(92.3%);双侧颈内动脉床突上段狭窄或闭塞者18例(69.2%),单侧者7例(26.9%)。结论烟雾病患者有显著的DSA影像学特征,DSA是诊断烟雾病的主要手段,临床上对疑似病例应早行DSA检查明确诊断。     

丘脑静脉性梗死的临床和影像学分析

目的探讨丘脑静脉性梗死的临床和影像学表现,以提高对该病的认识。方法 8例经临床证实为静脉窦血栓引起的丘脑静脉性梗死,收集其临床及影像学资料并进行回顾性分析。结果 8例患者均进行MRI平扫、DWI和SWI检查,均经DSA确诊。5例双侧丘脑、基底节区长T_1长T_2信号;1例双侧丘脑长T_1长T_2信号,伴胼胝体膝部短T_1信号;1例双侧丘脑、基底节区长T_1长T_2信号,伴右侧丘脑短T_1信号;1例双侧丘脑稍长T_1稍长T_2信号,并累及右侧基底节区和中脑,DWI呈高信号,ADC呈稍低信号。1例胼胝体膝部、1例右侧丘脑SWI图像上为低信号出血,2例梗死区内灶状出血。MRV与DSA检查结果相一致,5例为双侧横窦、上矢状窦、直窦、窦汇血栓形成;1例为双侧横窦、上矢状窦、直窦、大脑大静脉血栓形成;1例为右侧横窦、乙状窦血栓形成;1例为右侧横窦、直窦血栓形成。结论临床上遇到双侧丘脑病变,要考虑静脉性梗死的可能。MRI平扫联合MRV是静脉窦血栓引起的丘脑静脉性梗死诊断及随访的首选检查方法。SWI可清晰显示微出血,是MRI平扫和MRV极好的补充。     

硬脑膜动静脉瘘导致双侧丘脑病变(附2例报告及文献复习)

目的报道2例硬脑膜动静脉瘘(DAVF)导致的双侧丘脑病变病例。方法收集2例经数字减影血管造影(DSA)明确的DAVF导致的双侧丘脑病变患者的临床和影像学资料,结合文献复习进行分析。结果病例1,男性,63岁,因反应迟钝、懒言少动近2个月就诊,头颅MRI见双侧丘脑异常信号。DSA见直窦区域DAVF,行动静脉栓塞术,每年随访反应迟钝依然存在,但生活基本能自理。病例2,男性,63岁,因记忆力下降、反应迟钝1个月收治入院。头颅MRI见直窦内少许条状等信号,考虑直窦血栓,伴大脑深静脉梗死可能,继发左侧丘脑出血。DSA见直窦-窦汇区DAVF,予瘘口栓塞术,术后2个月随访,生活自理能力已完全恢复。结论 DAVF导致丘脑病变临床少见,起病隐匿,临床表现或影像学表现相似的疾病较多,诊断困难。遇有进行性认知功能下降,且影像学检查有双侧丘脑病变伴有肿胀出血者,应考虑DAVF可能。     

以丘脑病变为影像学特征的脑静脉窦血栓形成临床分析

对3例以丘脑病变为影像学特征的脑静脉窦血栓形成患者的临床资料和发病特点进行回顾分析,均存在脑静脉窦血栓形成危险因素(急性脱水、产褥期);临床主要表现为头痛、恶心呕吐、记忆力减退、偏瘫、昏迷等。MRI检查可见单侧(1例)或双侧(2例)丘脑病变,脑血管造影(MRV和DSA)显示病变部位累及直窦(3例)、下矢状窦(2例)、上矢状窦(1例)和横窦(1例)。对于呈急性发病的单侧或双侧丘脑病变,尤其是存在脑静脉窦血栓形成危险因素的患者,应首先考虑脑静脉窦血栓形成之可能。     

表现为双侧丘脑病变的硬脑膜动静脉瘘的临床特点(附1例报告)

目的探讨以双侧丘脑病变导致认知功能减退起病的硬脑膜动静脉瘘(dAVFs)的临床、影像学特点和鉴别诊断、诊治方法。方法分析1例dAVFs患者的临床资料,结合国内外文献进行分析讨论。结果本例患者临床表现为进展性的认知功能减退,MRI T_2相见双侧丘脑高信号,经DSA确诊为dAVFs,行血管内栓塞治疗后症状基本恢复。本研究系统检索了具有相似影像学表现的dAVFs相关文献报道30例,其临床表现以记忆力减退最为显著,部分伴有精神行为异常,经介入治疗或手术治疗大多预后良好。结论以双侧丘脑受累表现为认知功能减退的dAVFs报道较少,临床中出现类似病例应考虑到该诊断。     

大脑深静脉血栓形成7例临床与MR

目的探讨大脑深静脉血栓形成(DCVST)的病因、临床表现及诊断。方法回顾性分析7例经MR证实为大脑深静脉血栓形成的临床资料并复习有关文献。结果首发症状多为头痛,易伴精神症状,均有不同程度的意识障碍。结论脑静脉血栓形成的病因与脑静脉窦血栓形成(VST)的病因相似,无特征性临床表现,常进展迅猛,病死率高。MR是理想的诊断手段。     

双侧丘脑病变:1例病例报告与综述

目的：提高对以双侧丘脑病变为主要表现的神经系统疾病的临床认知水平。方法：报道1例以“行走不稳伴言语异常”为主要临床表现,具有双侧丘脑病变患者的诊疗经过,同时结合文献,重点针对其病因及临床表现等方面的相关研究进展进行综述。结果：该例丘脑病变患者以意识障碍、言语行走功能障碍为主要表现,经过相关影像学检查在双侧丘脑发现对称病灶,最终诊断为后循环脑梗死,基底动脉尖综合征。结论：双侧丘脑病变临床上并不罕见,临床表现受病变部位、其他大脑组织部位有否合并受累等影响。其病因众多,包括肿瘤、感染或脱髓鞘疾病、代谢或中毒性疾病以及需要及时干预的血管性疾病。因缺乏具特征性的临床症状表现,为临床诊断及鉴别带来一定困难。因此,早期明确丘脑病变病因尤为重要,以期能够早诊断早治疗,本文在报导病例的同时就其病因和临床表现等方面的研究进展进行综述。     

连续40例出血型烟雾病的DSA影像学分析

目的探讨烟雾病患者的DSA影像学诊断特征。方法回顾性分析40例烟雾病病例的DSA影像学表现,40例患者均经CT诊断为颅内出血,均经DSA确诊。结果双颈内动脉末段狭窄闭塞22例,一侧颈内动脉末段狭窄闭塞8例,一侧大脑中动脉狭窄闭塞3例,双侧大脑前动脉和一侧大脑中动脉狭窄闭塞1例,双侧大脑前动脉狭窄闭塞3例,双侧大脑中动脉狭窄闭塞1例,一侧大脑中动脉及对侧大脑前动脉狭窄闭塞2例,均伴颅底异常血管网形成。结论DSA为诊断烟雾病的金标准,DSA检查可清楚显示烟雾病血管狭窄闭塞的部位、侧支循环情况及是否合并动脉瘤,据其表现可指导进一步治疗。     

影像学表现为双侧丘脑病变的临床病例分析

目的 探讨影像学表现为双侧丘脑病变患者的临床特点、影像学表现、诊断及治疗,以提高对影像学表现为双侧丘脑病变相关疾病的认识.方法 收集2015年6月至2019年12月就诊于我院的影像学表现为双侧丘脑病变的6例患者的临床资料,分析相关疾病的特点.结果 6例患者影像学均出现双侧丘脑病变,但临床诊断各异.例1为基底动脉尖综合征...     

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.     

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.     

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.     

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.     

Disrupted structural and functional brain connectomes in mild cognitive impairment and Alzheimer＇s disease

Alzheimer＇s disease （AD） is the most common type of dementia, comprising an estimated 60-80% of all dementia cases. It is clinically characterized by impairments of memory and other cognitive functions. Previous studies have demonstrated that these impairments are associated with abnormal structural and functional connections among brain regions, leading to a disconnection concept of AD. With the advent of a combination of non-invasive neuroimaging （structural magnetic resonance imaging （MRI）, diffusion MRI, and functional MRI） and neurophysiological techniques （electroencephalography and magnetoencephaJography） with graph theoretical analysis, recent studies have shown that patients with AD and mild cognitive impairment （MCI）, the prodromal stage of AD, exhibit disrupted topological organization in large-scale brain networks （i.e., connectomics） and that this disruption is significantly correlated with the decline of cognitive functions. In this review, we summarize the recent progress of brain connectomics in AD and MCI, focusing on the changes in the topological organization of large-scale structural and functional brain networks using graph theoretical approaches. Based on the two different perspectives of information segregation and integration, the literature reviewed here suggests that AD and MCI are associated with disrupted segregation and integration in brain networks. Thus, these connectomics studies open up a new window for understanding the pathophysiological mechanisms of AD and demonstrate the potential to uncover imaging biomarkers for clinical diagnosis and treatment evaluation for this disease.     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

墨蝶呤还原酶基因与精神分裂症相关性的研究进展

墨蝶呤还原酶（SPR）催化四氢生物蝶呤（BH4）从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质（如多巴胺、5-羟色胺及谷氨酸等）的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。