急性卒中的磁共振成像流程探讨

目的：探讨急性卒中发生后影像学诊断的最佳流程。方法：67例发病1～72h的急性卒中患者在CT检查后行T1加权成像（T1 WI）、T2加权成像（T2 WI）、梯度回波T2^＊加权成像（GRE-T2^＊WI）和弥散加权成像（DWI）检查，39例缺血性卒中患者均行灌注加权成像（PWI）检查。结果：28例急性脑出血的出血病灶在GRE-T2^＊WI上全部清楚显影。16例TIA患者T1 WI、T2 WI和GRE-T2^＊WI以及DWI均正常，9例PWI检查灌注降低，7例正常。23例脑梗死患者中，7例发病6h内者GRE-T2^＊WI均正常，6例PWI〉DWI，1例PWI=DWI；16例发病6～72h内的患者GRE-T2^＊WI呈高信号，DWI均可见与体征相对应的高信号病灶，14例PWI=DWI，2例PWI正常。本组14例患者GRE-T2^＊WI像上在基底节区、丘脑、脑干和皮质下发现有1～18个微出血。结论：急性卒中后通过T1 WI、T2 WI、GRE-T2^＊WI、DWI和PWI检查流程可在较短时间内一站式鉴别脑出血、梗死和TIA患者，确定缺血半暗带，帮助溶栓治疗的选择。     

DWI和MRA在超急性期脑梗死中的临床应用

目的探讨磁共振弥散加权成像(DWI)和血管成像(MRA)在超急性期脑梗死中的临床应用价值。方法回顾性分析48例超急性期脑梗死患者的临床和磁共振资料,全部患者均行CT、常规MRI、DWI和MRA检查。结果 48例超急性期脑梗死的CT、常规T2WI、FLAIR及DWI阳性率分别为0、16.7%、37.5%和100%,MRA显示靶血管正常4例,动脉硬化36例,狭窄16例,闭塞8例。结论 DWI联合MRA能够准确显示责任病灶及靶血管受累情况,为超急性期脑梗死早期溶栓治疗提供切实可行的影像学依据。     

脑肿瘤灌注成像

磁共振灌注图像 ,是反映组织血管分布、血流灌注情况的检查技术。就对比剂通过毛细血管床进行分析 ,脑肿瘤灌注成像可以评估肿瘤血管容积 ,借以判断肿瘤良恶性程度及预后、治疗效果 ,并对肿瘤鉴别诊断提供帮助。本文就PWI基本原理、定量分析方法及其在脑肿瘤中的应用作一综述。     

PWI-ASPECTS/DWI-ASPECTS不匹配与PWI/DWI不匹配相关性研究

目的探讨大脑中动脉闭塞的急性脑卒中患者PWI-ASPECTS/DWI-ASPECTS不匹配与PWI/DWI不匹配间的相关性。方法回顾性分析2017年1月～2019年6月在本院就诊且行血管再通治疗的急性脑卒中患者65例,所有患者均于血管再通前行MRI(DWI、PWI)检查。计算所有患者PWI体积、DWI体积、PWI/DWI不匹配体积及PWI-ASPECTS、DWI-ASPECTS、PWI-ASPECTS/DWI-ASPECTS不匹配评分。Spearman等级相关分析体积与ASPECTS间的相关性,ROC分析PWI-ASPECTS/DWI-ASPECTS不匹配预测PWI/DWI不匹配的价值。结果 PWI体积、DWI体积及PWI/DWI不匹配体积分别为(25. 01±23. 11) ml、(75. 90±48. 99) ml、(50. 73±27. 14) ml。DWIASPECTS、PWI-ASPECTS及PWI-ASPECTS/DWI-ASPECTS不匹配评分分别为5. 95±2. 32、3. 52±2. 57、2. 43±0. 75。Spearman等级相关分析显示PWI体积与PWI-ASPECTS、DWI体积与DWI-ASPECTS、PWI/DWI不匹配体积与PWI-ASPECTS/DWI-ASPECTS不匹配间具有较强的相关性(r=-0. 767; P=0. 000、r=-0. 817; P=0. 000、r=-0. 643; P=0. 000)。ROC分析显示当PWI-ASPECTS/DWI-ASPECTS不匹配≥2时,PWI-ASPECTS/DWI-ASPECTS不匹配预测PWI/DWI不匹配的其敏感性和特异性分别为87. 90%、100%。当PWI-ASPECTS/DWI-ASPECTS不匹配≥3时,PWI-ASPECTS/DWI-ASPECTS不匹配预测PWI/DWI不匹配的敏感性和特异性分别为93. 80%、63. 64%。结论临床工作中PWI-ASPECTS/DWI-ASPECTS不匹配可替代PWI/DWI不匹配评估缺血半暗带。     

便利实用

<正>这些天,女儿口中开始不断提到一款上线1周便掀起了整个世界出门找精灵的游戏——Pokémon GO(图1)。据她说,很多常年习惯于宅在家中玩手游的人,从此告别了每天一动不动的生活状态,开始为了捕捉精灵而走出家门,甚至长途跋涉,不知不觉中就锻炼了身体,还能同时体会到游戏的乐趣。     

磁共振张量成像对脑梗死预后的评价

目的利用磁共振弥散张量成像(DTI)探讨脑梗死病人脑白质纤维束各向异性特征和白质纤维束受损与临床预后关系。方法对23例脑梗死患者行DTI检查,以三维立体弥散张量成像为基础的色彩图进行图像后处理,评价脑梗死区周边纤维束的情况,将纤维束分为受压移位、变细萎缩和破坏中断三类,并与临床预后、神经功能缺损程度比较。结果三维成像所见与病人预后关系密切。所有脑白质纤维束萎缩和中断的患者,在随访过程中存在不同程度脑功能损伤,而脑白质受压移位的病人神经功能完全或近乎完全恢复。结论在脑梗死中,DTI能直接观察到白质纤维束的变化,对于评估临床预后具有重要作用。     

脑血管畸形的磁共振成像和磁共振血管成像

目的：分析脑血管畸形在人振成像和磁共振共振血管成像的表面,并评估ＭＲＩ和ＭＲＡ在ＥＶＭ诊断方面的应用价值。方法：１８例经ＭＲＩ诊断为ＥＶＭ的患者,其中脑动静脉畸形１５例,隐匿性血管畸形３例。用Ｓｉｅｍｅｎｓ Ｖｉｓｉｏｎ ０．５Ｔ超导磁共和ＭＲＡ检查,采用ＴＯＦ－ｔｉ３ｄ－ｍｕｌｔｉ－ｔｒａ－ｔｕｎ序列。     

二维氢质子磁共振波谱分析在胶质瘤诊治中的应用价值

目的 探讨颅内胶质瘤2D1H-MRS代谢物值和病理学分级的相关性.方法 46例幕上脑胶质瘤患者行MR平扫.2D1H-MRS及MR增强扫描.量化分析NAA、Cho、Cr及Lip-Lac,与术后病理结果 对比分析研究,得出1H-MRS几种代谢物值与肿瘤恶性程度的相关性.结果 随着胶质瘤恶性程度的增加,Cho呈上升趋势,NAA及NAA/cho呈下降趋势;Cr含量有所降低,Cho/Cr随胶质瘤恶性度的增加而增高,Cho/Cr比Cho更敏感;Lip-Lac呈升高趋势.Cho/Cr与NAA/Cho各组之间两两比较,差异均有统计学意义(P＜0.05).结论 NAA/Cho、Cho/Cr和Lip-Lac可做为脑胶质瘤恶性程度评判的综合指标.     

颅内椎-基底动脉夹层形态学与后循环缺血程度的相关性研究

目的 研究颅内椎-基底动脉夹层不同形态类型及不同狭窄程度对后循环缺血的影响.方法 回顾性分析解放军总医院第一医学中心2015年12月-2019年12月经DSA确诊的椎动脉颅内段及基底动脉夹层患者的多模式磁共振影像数据,利用MRA对后循环夹层的形态进行分组(瘤样扩张型、线珠型、狭窄-闭塞型),并根据MRA和高分辨率磁共振...     

磁共振检查对基底动脉血栓形成患者的诊断价值

目的了解磁共振检查对基底动脉血栓形成患者的诊断价值。方法17例经证实为基底动脉血栓形成的患者于发病后48h时内接受磁共振T2加权成像、磁共振血管成像、弥散加权成像检查。结果所有患者都在磁共振血管成像上可见基底动脉血流信号消失和一侧或双侧椎动脉血流信号消失；弥散加权成像可见后循环区域不同形态散在分布的多发梗死灶；T2 成像可发现基底动脉内血栓形成。结论磁共振血管成像检查对颅内血管闭塞有较高的敏感性，弥散加权成像对后循环供血区域梗死灶的诊断能力优于传统影像学检查。     

视频脑电图在小儿癫痫诊断中的应用

目的评价视频脑电图(video-EEG)在小儿癫诊断中的应用价值。方法对126例具有发作性症状的患儿进行连续8h的包括清醒、睡眠、诱发试验及必要的认知测验的视频脑电图监测。结果经发作期视频脑电图证实,39例初诊为癫性发作的患儿中14例(35%)为非癫性发作;15例其他症状发作中13例(86%)为非癫性发作。64例样放电患儿中51例(80%)确定发作类型,22例(34%)确定癫类型。视频脑电图可发现短暂轻微的癫发作及样放电引起的一过性认知损伤。结论视频脑电图在排除非癫性发作、确定癫性发作的类型、评价脑电-临床关系方面可提供准确可靠的证据,进一步提高癫的临床诊断水平。     

Role of glutathione in repair of free radical damage in hippocampus in vitro.

Depletion of glutathione (GSH), an intrinsic antioxidant, increases vulnerability to free radical damage in a number of cell systems. This study investigates the role of GSH in limiting electrophysiological damage and/or recovery from free radical exposure in slices of guinea pig hippocampus. Synaptic potentials (PSPs) and population spikes (PSs) were recorded from field CA1. Free radicals were generated from 0.006% peroxide through the Fenton reaction. Analysis of the input-output curves showed that peroxide treatment decreased PSPs and impaired ability of the PSPs to generate PSs as previously reported. Recovery was nearly total within a half hour. Treatment with 5 mM buthionine sulfoximine (BSO) for 2 h depleted hippocampal GSH to 79.2% of control values. The extent of free radical damage was not increased. Recovery, however, was only partial. GSH was further depleted by oxidation with diamide or covalent bonding with dimethyl fumarate (DMF) immediately before and during the peroxide treatment. Neither diamide nor DMF treatment in BSO-incubated tissue enhanced peroxide-induced electrophysiological deficits. Following these treatments, however, tissue showed little recovery from free radical damage. We conclude that glutathione is essential for repair processes in hippocampal neurons exposed to oxidative damage.     

Neuroprotective properties of memantine in different in vitro and in vivo models of excitotoxicity

The pathogenesis of stroke, trauma and chronic degenerative diseases, such as Alzheimer's disease (AD), has been linked to excitotoxic processes due to inappropriate stimulation of the N-methyl-D-aspartate receptor (NMDA-R). Attempts to use potent competitive NMDA-R antagonists as neuroprotectants have shown serious side-effects in patients. As an alternative approach, we were interested in the anti-excitotoxic properties of memantine, a well-tolerated low affinity uncompetitive NMDA-R antagonist presently used as an anti-dementia agent. We explored in a series of models of increasing complexity, whether this voltage-dependent channel blocker had neuroprotective properties at clinically relevant concentrations. As expected, memantine protected neurons in organotypic hippocampal slices or dissociated cultures from direct NMDA-induced excitotoxicity. However, low concentrations of memantine were also effective in neuronal (cortical neurons and cerebellar granule cells) stress models dependent on endogenous glutamate stimulation and mitochondrial stress, i.e. exposure to hypoxia, the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+) or a nitric oxide (NO) donor. Furthermore, memantine reduced lethality and brain damage in vivo in a model of neonatal hypoxia-ischemia (HI). Finally, we investigated functional rescue (neuronal capacity to migrate along radial glia) by memantine in cerebellar microexplant cultures exposed to the indirect excitotoxin 3-nitropropionic acid (3-NP). Potent NMDA-R antagonists, such as (+)MK-801, are known to block neuronal migration in microexplant cultures. Interestingly, memantine significantly restored the number of neurons able to migrate out of the stressed microexplants. These findings suggest that inhibition of the NMDA-R by memantine is sufficient to block excitotoxicity, while still allowing some degree of signalling.     

Storage of lipofuscin in neurons in mucopolysaccharidosis

Summary A histochemical and ultrastructural study was made on the brain of a 23-year-old man with Sanfilippo's syndrome. In accordance with previous reports the cortical nerve cells contained a PAS-positive lipid storage substance. This showed intense autofluorescence in UV-light and was positive with various stains for lipofuscin. The storage material appeared ultrastructurally as inclusion bodies composed of short lamellated membranes, granular material, and vacuoles. In addition, concentrically and transversely lamellated membranous cytoplasmic bodies were observed in the nerve cells. It is concluded that the PAS-positive lipid storage material in the neurons was composed partly of lipofuscin in addition to other lipids presumably glycosphingolipids.Supported by a grant from the Expressen Prenatal Research Foundation