大鼠急性期缺血再灌注血管原性脑水肿MRI表现及与血管内皮细胞明胶酶B表达的关系

目的　探讨脑缺血再灌注后血管原性脑水肿 (VBE)MRI表现及其与血管内皮细胞明胶酶B表达的相关性。方法　线栓法建立大鼠脑缺血再灌注模型 ,MR连续动态观察缺血区体积与信号变化 ,免疫组织化学方法观察血管内皮细胞明胶酶B表达。结果　缺血后 3h至 7d扫描术侧大脑半球见T2 高信号改变 ,12h至 3d见不同程度同侧侧脑室受压变窄、中线结构向对侧移位。 3h开始上述征象逐渐明显 ,1～ 2d达到峰值 ,3～ 7d则逐渐减轻。显微镜下见随时间推移而明显的血管内皮细胞肿胀、血管周围间隙增宽与无定形嗜酸物质。不同时间点明胶酶B免疫组织化学染色均可见血管内皮细胞胞质着色 ,12h、1d、2d、3d、5d与 7d染色评分分别为 (1 2 0± 0 4 2 )分、(1 70±0 4 8)分、(2 2 0± 0 71)分、(2 87± 0 5 8)分、(3 0 0± 0 0 1)分与 (2 5 0± 0 71)分 ,与MRI上缺血侧大脑半球体积增加、对侧大脑半球压迫、缺血侧T2 WI上异常高信号体积增加、缺血侧额顶叶和基底节区T2 WI信号强度 (SI)增加的相关系数为 0 89～ 0 976。结论　缺血再灌注后VBEMRI表现为脑组织体积增大与T2 WI信号增高。VBE的MRI征象与脑组织明胶酶B的表达有相关性。     

羟基红花黄色素A对局灶性脑缺血再灌注大鼠血管内皮生长因子表达的影响

目的 探讨羟基红花黄色素A对局灶性脑缺血大鼠血管内皮生长因子(VEGF)表达的影响及意义.方法 采用大鼠大脑中动脉闭塞(MCAO)模型,用免疫组化的方法观察HSYA对MCAO2 h及再灌注1、3、 6、 9、12、24、72 h及7 d、14 d时脑组织VEGF表达变化,并与对照组比较.结果 缺血2 h后VEGF在缺血灶周围小血管内皮细胞、神经细胞、胶质细胞上表达开始增高,内皮细胞在再灌注24～72 h时表达量最高,7 d后开始下降,14 d时仍偏高.神经细胞及胶质细胞在再灌注9～12 h时表达量最高,24～72 h时开始下降,7 d时已无表达.HSYA使各时间点VEGF的表达增加,并使缺血后期血管内皮生长因子表达的下降减缓.结论 HSYA具有上调脑缺血后血管内皮生长因子表达的作用,这可能是其脑保护作用的机制之一.     

高压氧对成年大鼠脑缺血再灌注损伤后脑血管内皮生长因子表达的影响

目的 探讨脑缺血模型大鼠经30 d高压氧(HBO)治疗后大脑血管内皮生长因子(VEGF)表达的变化.方法 24只成年SD大鼠随机分为3组:对照组(C组)8只、缺血再灌注组(IR组)8只、HBO治疗组(HBO组)8只.C组为正常大鼠,IR组和HBO组大鼠经大脑中动脉栓塞(MCAO)1.5 h后再灌注,HBO组行HBO治疗.HBO治疗(0.28 MPa,60 min)30 d,1次/d,于31 d麻醉处死,取脑组织切片,VEGF和CD34免疫组化染色,光镜观察并于损伤区取图,进行相关分析.结果 VECF广泛分布,缺血区表达强烈,3组间有明显差异(P＜0.05),HBO组(13497.14±397.44)低于IR组(22.097.7±616.89);C组未见CD34表达,其他2组集中表达于缺血区;HBO组(5571.16±603.63)表达少于IR组(5349.72±390.88),但差异无统计学意义(P＞0.05).结论 长期HBO治疗抑制大鼠缺血脑组织VEGF的表达,可能对神经细胞具有保护作用,有利于促进脑组织自我修复.     

丁苯酞对大鼠局灶性脑缺血再灌注损伤的保护作用

目的 观察丁苯酞对大鼠局灶性脑缺血再灌注损伤后血管内皮生长因子(VEGF)表达的影响及其对缺血再灌注损伤治疗时间窗的影响.方法 SD大鼠72只,随机分为假手术组24只,缺血再灌注组24只,丁苯酞治疗组24只.每组再分为缺血2、3和4 h 后再灌注3个亚组,每亚组8只.采用改良线栓法制作大鼠局灶性脑缺血再灌注模型,观察各组神经功能和脑梗死范围,免疫组化法检测脑组织中VEGF表达.结果 随着缺血时间延长,再灌注后,神经功能评分和脑梗死范围也随之增高,缺血再灌注组在缺血2、3和4 h的神经功能评分分别为(2.6 ± 0.6)分、(3.7 ± 1.0)分和(4.2 ± 1.0)分,脑梗死容积比率分别为(27.6 ± 5.4)%、(33.1 ± 6.1)%和(42.3 ± 7.3)%;而在丁苯酞治疗组则分别为(1.2 ± 0.5)分、(1.6 ± 0.7)分、(2.3 ± 0.9)分和(9.8 ± 1.6)%、(16.7 ± 2.3)%和(20.7 ± 3.9)%,与缺血再灌注组比较丁苯酞治疗组明显较低,差异有统计学意义(P值均＜ 0.05).并发现丁苯酞治疗组的缺血4 h的症状评分和脑梗死容积比率与缺血再灌注组缺血2 h比较,差异无统计学意义(P ＞ 0.05).随着缺血时间的延长,丁苯酞治疗组和缺血再灌注组的VEGF表达均逐渐减弱.与假手术组比较,缺血再灌注组脑组织中VEGF表达明显减弱(P ＜ 0.01).与其他两组比较,丁苯酞治疗组的VEGF表达明显较强,差异有统计学意义(P ＜ 0.01).结论 丁苯酞对大鼠局灶性脑缺血再灌注损伤具有保护作用,其作用机制可能与VEGF表达相关,并能延长缺血再灌注治疗时间窗.     

MR影像学评价VEGF对兔局灶性脑缺血再灌注损伤的有效治疗时间窗

目的:探讨MR影像学评价血管内皮细胞生长因子对家兔局灶性脑缺血再灌注损伤的有效治疗时间窗。材料和方法:采用兔大脑中动脉阻断局灶性脑缺血再灌注模型,分别在缺血2h再灌注损伤后0h、1h、3h、6h和12h应用微量进样器将VEGF立体定向导入梗死灶周,于再灌注72h,应用MR影像学、TTC染色和流式细胞术评价梗死体积、灶周缺血半暗带凋亡率、ADC值比率(ADCR),评价神经功能缺损。结果:缺血再灌注0h和1h灶周给予VEGF,MRI测得的梗死体积分别为(367.0±15.7)mm3和(393.0±19.6)mm3与对照组(468.6±29.7)mm3相比差异有显著性(P均<0.01);3h、6h和12h组梗死体积为(437.0±24.6)mm3、(444.0±29.5)mm3、(449.0±30.5)mm3与对照组相比差异没有显著性(P>0.05)。TTC染色测得的梗死体积与MRI上相一致。同时1h内用药神经功能缺损评分明显减少,凋亡率明显下降,再灌注3h后给药,则无明显作用。结论:VEGF对兔局灶性脑缺血再灌注损伤的有效时间窗在再灌注损伤1h内,MR影像学检查可作为定量评价基因疗效的可靠指标。     

促红细胞生成素对大鼠脑缺血再灌注后脑组织水肿细胞凋亡及脂质过氧化水平的影响

目的 观察促红细胞生成素(EPO)对大鼠脑缺血再灌注后脑组织水肿细胞凋亡及脂质过氧化水平的影响.方法 大脑中动脉阻断法制作大鼠单侧(左)脑缺血再灌注模型.将54只SD大鼠随机分为正常组(6只)、缺血再灌注组(24只)和EPO治疗组(24只),观察缺血后6、12、24、48小时脑组织含水量、SOD活性、MDA水平、细胞计数、TUNEL阳性细胞计数.免疫组织化学染色及WB法观察糖原合成酶激酶3β(GSK3β)和Caspase-3的表达变化.结果 EPO组病理变化较缺血再灌注组轻,脑组织含水量显著减少,缺血后24小时及48小时,脑组织细胞数显著多于缺血再灌注组、TUNEL阳性细胞数量显著少于缺血再灌注组.EPO组GSK3β和Caspase-3免疫组化染色阳性细胞数量明显下降,蛋白水平显著下降,脑组织SOD活性显著上升,MDA水平显著下降.结论 EPO能有效抑制大鼠脑缺血再灌注后脑组织水肿、细胞凋亡及脂质过氧化反应发生.     

咪唑安定对脑缺血再灌注沙土鼠血管内皮生长因子表达的调节作用

目的 观察咪唑安定对沙土鼠全脑缺血再灌注损伤过程中血管内皮生长因子(CEGF)表达的影响,为咪唑安定临床合理应用提供实验依据.方法 健康雄性沙土鼠共72只,随机分为对照组、损伤组和治疗组(n=24).采用双血管法建立沙土鼠全脑缺血再灌注模型,对照组仅游离双侧颈总动脉但不夹闭;损伤组夹闭双侧颈总动脉10min,放开动脉夹后即刻腹腔注射生理盐水50ml/kg 1次,随后每天同一时间点在动物清醒状态下腹腔注射生理盐水50ml/kg,共6d;治疗组夹闭双侧颈总动脉10min,放开动脉夹后即刻腹腔注射0.01%咪唑安定注射液5mag/kg随后每天同一时间点在动物清醒状态下腹腔注射0.01%咪唑安定5mg/kg,共6d.以双侧动脉夹放开时间为基准点,分别在放开后6h、1d、3d、7d运用正电子发射断层显像(PET)观察脑梗死体积变化,用免疫组织化学方法观察脑组织VEGF的表达,每次的观察时间点均设在腹腔注射前.结果 对照组脑内再灌注面积无明显异常;与对照组比较,损伤组与治疗组沙土鼠在再灌注后各时间点的脑内灌注面积明显缩小(P<0.01);与损伤组比较,治疗组在再灌注后6h脑内灌注面积无差异,但在1d、3d、7d时明显增加(P<0.01).对照组脑内可见少量的VEGF阳性细胞表达.损伤组沙土鼠在再灌注6h即有VEGF阳性表达,随再灌注时间延长,表达逐渐增强,于再灌注3d时表达最强,以后缓慢下降,至7d时仍有部分表达,与再灌注6h时比较,有显著差异(P<0.01).表达细胞主要为神经胶质细胞和巨噬细胞,其次为神经细胞及血管内皮细胞.治疗组VEGF的表达趋势与损伤组相似,但在再灌注后各时间点的VEGF表达均较损伤组强(P<0.01).结论 咪唑安定5mg/(kg·d)可减少沙土鼠脑缺血再灌注损伤后脑梗死的体积,促进脑缺血再灌注损伤中内源性VEGF的表达,并由此可能对损伤后神经功能中远期的恢复产生影响.     

大鼠肝肿瘤放疗及酒精治疗MRI动态灌注表现

目的 研究大鼠肝肿瘤放疗及无水酒精注射治疗后MRI动态灌注表现及其半定量指标最大相对信号强度增减率(MRSI)与免疫组织化学指标增殖细胞核抗原(PCNA)、血管内皮细胞生成因子(VEGF)及CD34的相关性. 材料与方法 (1)选取45只肝肿瘤大鼠,随机分成放疗组、酒精注射组及未治疗组,每组15只,分1天、3天、7天共3个时间点观察;(2)每组大鼠每个时间点均采集MRI动态灌注图像, 后处理得到灌注曲线及MRSI;(3)MRI检查后取标本送病理及免疫组织化学(PCNA,VEGF,CD34)检查;(4)将免疫组织化学结果与MRI图像对照分析. 结果 (1)放疗组PCNA染色增殖指数较未治疗组下降, VEGF染色阳性率稍减低, CD34染色阳性表达的微血管数减少及MRSI下降; 且MRSI与PCNA染色增殖指数、CD34染色阳性表达微血管数及VEGF表达阳性率呈正相关.(2)酒精注射组PCNA染色增殖指数较未治疗组下降明显,并见CD34染色阳性表达的微血管数显著减少,VEGF染色阳性率及MRSI明显减低;MRSI与PCNA、VEGF及CD34呈正相关. 结论 放疗及酒精注射治疗对大鼠肝肿瘤新生血管有抑制作用,MRI动态增强能反映肿瘤的血供情况.     

星形细胞瘤MR征象与VEGF表达的相关性研究

目的 :探讨星形细胞瘤MRI征象与血管内皮生长因子 (VEGF)表达程度的相关性。方法 :对 3 3例经手术和病理证实的星形细胞瘤分别行术前常规横断面T1WI、T2 WI平扫和Gd DTPA增强后三维T1WI ,术后取肿瘤组织行VEGF表达和微血管密度 (MVD)免疫组化染色 ,计算每一例肿瘤标本的VEGF表达程度和MVD ,将VEGF表达程度分别与MRI征象、MVD及病理分级进行相关分析。结果 :星形细胞瘤病理分级越高 ,VEGF表达越强 (P <0 .0 1) ;肿瘤周围水肿程度、囊变与坏死、强化形态与程度以及肿瘤MVD等与VEGF表达强度密切相关。结论 :星形细胞瘤MRI表现与VEGF表达强度具有密切的相关性 ,MRI对星形细胞瘤的分级诊断和判断其生物学行为及预后有较高的价值。     

脑梗死黏附分子表达与溶栓治疗时间窗

目的　研究选择性动脉内溶栓联合抗黏附分子抗体治疗对大鼠缺血性脑梗死黏附分子表达的影响 ,探讨溶栓治疗时间窗。方法　将 85只血栓栓塞性大鼠大脑中动脉缺血模型随机分成A、B两组。再将每组随机分成 3个亚组。A组研究缺血再灌注后细胞间黏附分子 (intercellularadhensionmolecule 1,ICAM 1)表达的动态变化。B组通过观察缺血再灌注后大鼠神经功能缺陷、体重下降、MRI上长T2 病变体积变化及缺血脑组织内ICAM 1和ICAM 1配体 (Mac 1)表达情况 ,比较尿激酶联合抗ICAM 1抗体治疗 (简称联合溶栓治疗 )与单纯尿激酶治疗 (简称单纯溶栓治疗 )的疗效。结果　缺血 30min ,再灌注 2 4h ,ICAM 1表达开始增加。ICAM 1表达到达高峰的缺血时间为 3h。每个缺血时间点内 ,ICAM 1表达到达高峰的再灌注时间是 48h。缺血 1h ,单纯溶栓治疗可减轻缺血脑组织内ICAM 1表达 (阳性血管数为 84± 16比 178± 35 ,P <0 0 5 )。而缺血 6h ,单纯溶栓治疗则增加ICAM 1表达 (阳性血管数为 490± 74比 32 8± 46 ,P <0 0 1)。与单纯溶栓治疗组相比 ,联合溶栓治疗组大鼠缺血 6h后 ,MRI上长T2 体积缩小 [(2 6 0± 2 5 ) %比 (38 6± 3 5 ) % ,P <0 0 5 ],体重下降 [(12 2±1 3) %比 (18 2± 1 5 ) % ,P <0 0 5 ]、ICAM 1(阳性血管     

弥漫性脑损伤后脑缺血的实验研究

目的　运用大鼠弥漫性脑损伤 (DBI)模型研究脑外伤后脑缺血缺氧的形态学改变。　方法　采用Marmarou的DBI模型 ,光镜下观察微血管改变并测量顶叶皮质内微血管的截面积及微血管周的水肿面积 ;电镜下观察血脑屏障结构的形态学改变并半定量测定毛细血管周围的水肿范围。　结果　光镜下可见外伤后 2 ,6 ,2 4h微血管管径变窄 ,平均微血管截面积分别为 (41.77± 2 7.37) μm2 、(45 .0 9± 2 4 .75 ) μm2 、(49.38± 2 5 .13) μm2 ,均小于对照组 [(6 2 .0 7± 2 8.4 5 ) μm2 ](P <0 .0 5 )。伤后 6 ,2 4h微血管周围存在明显水肿。电镜下 2 ,6 ,2 4h血脑屏障结构有明显损害 ;微血管有痉挛、受压变窄及淤血三种改变。　结论　弥漫性脑损伤后存在明显的脑缺血缺氧的病理形态学改变。     

白藜芦醇对大鼠创伤性脑水肿的影响及超微结构观察

目的：探讨白藜芦醇对自由落体伤大鼠脑水肿的影响及超微结构变化。方法：采用自由落体伤获得大鼠脑创伤模型，白藜芦醇腹腔注射治疗，取创伤区脑组织，烤箱内干燥，根据烘烤前后质量差，得出脑含水量，用统计方法分析数据；另取部分伤区脑组织行电子显微镜观察。结果：白藜芦醇治疗后大鼠脑含水量差异性明显，超微结构亦有不同改变。结论：白藜芦醇能减轻创伤后大鼠脑水肿，同时对伤区脑组织超微结构有保护作用。     

脾脏切除对颅脑创伤大鼠死亡率及脑含水量的影响

目的 观察脾脏切除对脑创伤大鼠死亡率及脑组织含水量的影响,为提高重型颅脑创伤患者的救治水平探讨新思路.方法 成年雄性SD大鼠采用随机数字表法分为三组:颅脑创伤假手术+脾切除假手术组(A组),颅脑创伤+脾切除假手术组(B组)和颅脑创伤+脾切除组(C组).采用改进的Feeney法对大鼠右侧大脑半球进行致伤,伤后采用Longa法进行行为学评分;观察A(23只)、B(48只)、c(47只)三组大鼠致伤后7 d内的死亡率;测定各组致伤后1 d(8只)、2 d(8只)、3 d(8只)及7 d(7只)时各组大鼠脑组织含水量.结果 致伤后B、C两组之间Longs评分差异无统计学意义(P>0.05);致伤后7 d内大鼠死亡率A、B、C组分别为0%、35.4%及14.9%,各组间比较差异均有统计学意义(P<0.05);B、C组致伤侧脑含水量于伤后1,2,3及7 d时分别为(81.98±0.35)%和(81.78%±0.41)%、(82.58±0.63)%和(81.81±0.48%)(P<0.05)、(82.54±0.54)%和(81.52%±0.84)%(P<0.05),以及(81.50±0.41)%和(81.21±0.36)%.结论 颅脑创伤大鼠于伤后行脾脏切除能够降低致伤侧脑组织水肿程度,显著降低大鼠的死亡率.     

Radiological study of the brain at various stages of human immunodeficiency virus infection: early development of brain atrophy

Summary One hundred and one persons infected with human immunodeficiency virus (HIV-1), in whom other central nervous system infections or diseases were excluded, underwent brain CT and/or MRI at various stages of HIV-1 infection: 29 were asymptomatic (ASX), 35 had lymphadenopathy syndrome (LAS), 17 had AIDS-related complex (ARC), and 20 had AIDS. A control group of 32 HIV-1-seronegative healthy persons underwent brain MRI. The most common finding was brain atrophy, found in 9% of controls, and 31% of ASX cases, 29% of LAS, 59% of ARC and 70% of AIDS. Even the difference between the ASX or LAS groups and controls was significant. The changes were bilateral and symmetrical, and they were more severe at later stages of infection. Infratentorial atrophy was seen in the early stages; supratentorial atrophy became more pronounced at ARC, and generalized atrophy was typical of AIDS. Non-specific small hyperintense foci were found on MRI in 13% of controls and 6–15% of the infected groups. Larger, diffuse, bilateral white matter infiltrates were detected in 4 demented patients with AIDS. Four patients with AIDS and 1 with LAS had focal hyperintense lesions in the internal capsules, lentiform nuclei or thalamus, often bilateral on MRI. One patient with AIDS, examined with CT only, had low density in the lentiform nucleus. Loss of brain parenchyma can occur at an early stage of HIV-1 infection, and the atrophic process becomes more intense at later stages (ARC and AIDS). Parenchymal infiltration, seen as hyperintense areas on MRI, is most often associated with severe clinical symptoms, in the later stages of the disease.     

NMR imaging of the brain

Summary The basic features of an NMR imaging system are outlined and three pulse sequences which produce images with varying dependence on proton density T₁ and T₂ are described. The first of these sequences, Repeated Free Induction Decay produces images which demonstrate changes in proton density as well as flow effects. The second sequence, Inversion-recovery, produces images which are dependent on T₁ and show a high level of grey, white matter contrast giving considerable anatomical detail. In addition pathological processes such as infarction, haemorrhage, demyelination and malignancy produce changes in T₁ enabling lesions to be localised. The third sequence, Spin-echo, produces images which are dependent on T₂. These show very little grey, white matter contrast but demonstrate acute and space occupying lesions as well as cerebral oedema. The high level of grey, white matter contrast, lack of bone artefact, variety of sequences, capacity for multiplanar imaging, sensitivity to pathological change and lack of known hazard make NMR an important addition to existing techniques of neurological diagnosis.     

大鼠二次脑损伤模型的建立

目的　建立弥漫性脑损伤 (diffusebrianinjury ,DBI)合并缺血性二次脑损伤 (secondarybrianinsult ,SBI)大鼠模型。　方法　在Marmarou模型基础上结扎双侧颈总动脉 30min ,制成缺血性SBI模型 ,观察大鼠神经损伤严重程度评分 (NSS)、脑组织含水量及室上区皮层损伤神经元数改变。　结果　合并SBI组大鼠死亡率 ( 4 8.1 % )约为单纯DBI组 ( 2 6 .2 % )的 2倍 (P <0 .0 5) ;合并SBI组在损伤 2 4h后NSS明显高于单纯DBI组 (P <0 .0 5) ;单纯DBI 1h后脑含水量明显升高 ,于 2 4h达高峰 ,随后逐渐下降 ,1 6 8h降至正常 ,而合并SBI后除 1h组外 ,其余时间组脑含水量均明显高于同时间单纯DBI组 (P <0 .0 5) ,且峰值提前至 1 2h ,1 6 8h仍未恢复正常 ;单纯DBI 6h后皮层神经元明显损伤 (P <0 .0 5) ,1 2h达高峰 ,1 6 8h恢复正常 ,而合并SBI组神经元损伤数 1 2h后还增加 ,2 4h达高峰 ,1 6 8h仍未恢复正常 (P <0 .0 5)。　结论　此模型可以复制SBI的重要临床特征 ,对SBI的基础研究有重要价值。     

放射性脑损伤和脑肿瘤复发的鉴别诊断

放射性脑损伤是放射治疗的严重的并发症,其与脑肿瘤复发的鉴别诊断非常困难,目前主要依靠影像学诊断,核磁共振弥散加权像、磁共振波谱、正电子发射型计算机体层显像、单光子发射计算机体层显像等被认为对于鉴别诊断有一定的帮助,但其敏感性和特异性还有待于进一步研究。最终确诊依赖标本的组织学检查。     

CT and MR findings of brain aspergillosis

CT and MR findings of a case of brain aspergillosis with histopathologic correlation are reported. On both CT and MR images, there were multiple lesions in the corticomedullary junction (CMJ) that appeared to disrupt the cortical sulci and that were not enhanced by intravenous contrast material. In most of these lesions, there were centrally located structures that were enhanced by intravenous contrast material and that appeared to be continuous from markedly enhanced adjacent dilated cortical vessels. Histopathologic examination of the autopsy specimen showed multiple hemorrhagic infarcts in the CMJ with remaining dilated cortical vessels that had been thrombosed by aspergillus hyphae.     

载脂蛋白E基因对轻、中型创伤性脑损伤急性期脑电活动的影响

Objective To investigate the influence of apolipoprotein E gene (APOE) polymorphism on the acute-phase brain electrical activity after mild/moderate traumatic brain injury. Methods The clinical data of 112 patients with mild/moderate traumatic brain injury were collected and the APOE genotypes were identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The brain electrical activity in every patient was recorded twice by using electroencephalogram within one week after injury. Qualitative and quantitative methods were used to determine the variations of brain electrical activity. Chi-square test, variance analysis and logistic regression analyses via SPSS version 11.5 were performed among APOE genotypes, electroencephalogram data and clinical data. Results The distributions of APOE genetypes and alleles matched Haldy-Weinberg Law in 112 patients. Of 22 patients with APOEε4, 12 patients (55%) presented with deteriorated electroencephalogram, which was significantly higher than those (16 of 90 patients, 18%) without APOEε4 (P ＜ 0. 01). Comparison of the first and second electroencephalograms demonstrated that the slow waves were increased significantly in patients with APOEε4 ( P ＜ 0. 01 ) but decreased in patients with APOEε2 and APOEε3 (P ＜0.05). The reduction of slow waves in APOEε2 carriers was more obvious than APOEε3 carriers (P ＜0.05). Univariate and multivariate logistic regression analyses showed that APOEε4 was a risk factor to electroencephalogram aggravation after traumatic brain injury. Conclusion APOEε4 is a risk factor to electroencephalogram aggravation during acute stage after mild/moderate traumatic brain injury. However,APOEε2 seems to be beneficial for recovery of brain electrical activity.     

Imaging of brain metastases

Summary For the demonstration of brain metastases both CT and MRI are available as diagnostic modalities. To compare both imaging methods as to their sensitivity in detecting brain metastases CT scans and MR images of 60 patients with suspected brain metastases were evaluated. Comparing contrast-enhanced CT and plain MRI neither modality was found to be clearly superior in this respect.