盐酸法舒地尔对脑血管造影术患者脑血管痉挛及血浆内皮素-1的影响

目的观察受检者进行全脑血管造影术前和术后血浆内皮素-1(ET-1)的变化,法舒地尔干预对患者发生脑血管痉挛及术后血浆ET-1的影响。方法 324例受检者随机分为干预组和对照组各162例,术前均留取静脉血进行ET-1检测,干预组术前静脉滴注法舒地尔,对照组给予等量的生理盐水,术中观察脑血管痉挛出现的例数,术后立即留取静脉血再次进行ET-1检测。比较所有受检者术前和术后ET-1变化,干预组和对照组出现脑血管痉挛的例数及术后ET-1的差别。结果所有受检者术后血浆ET-1较术前升高,法舒地尔干预组发生脑血管痉挛的例数明显低于对照组,术前血浆ET-1无差别,术后低于对照组。结论法舒地尔可以降低脑血管造影术受检者术后血浆ET-1的分泌,减少术中脑血管痉挛的发生。     

脑池内局部应用尼卡地平多聚体缓释微球治疗脑血管痉挛的实验研究

目的 研究脑池内注入NC -PLGA缓释微球对脑血管痉挛的治疗作用.方法 采用枕大池二次注血法制作兔蛛网膜下腔出血模型.分别采用脑池内注入NC -PLGA微球和尼卡地平的方法治疗脑血管痉挛.应用经颅多普勒技术测基底动脉的血流速度,脑血管造影测量基底动脉直径,光镜和电镜行病理检查,观察基底动脉的形态学变化,评价脑血管痉挛的严重程度.结果 脑池内注入NC - PLGA微球和尼卡地平都能降低基底动脉的血流速度(P＜0.01),基底动脉的直径明显升高(P＜0.01),并能明显改善血管壁的病理改变,但前者只需一次性注入后者总量的1/4既可达到同样的疗效.结论 经脑池内注入NC -PLGA缓释微球能明显减轻脑血管痉挛的严重程度,并可减轻痉挛血管壁的病理学变化.     

增加血流动力学导致基底动脉重构的形态学及病理学早期观察

目的 探讨基底动脉血流动力学改变后基底动脉形态及病理变化.方法 新西兰大白兔双侧颈总动脉结扎以代偿性增加椎基底动脉血流,分别于术前及术后1d、1周、2周经颅多普勒检测基底动脉血流速度;术后1周、2周分别行脑血管造影,并且测量基底动脉直径及迂曲程度;对基底动脉病理切片EVG、Masson染色分析.结果 颈总动脉结扎后基底动脉血流明显增快(10.99 ml/min对比36.53 ml/min,P＜0.001),术后1周、2周基底动脉直径增大(0.60 mm对比0.82 mm;0.73 mm对比1.03 mm,P＜0.001),内弹力层完整,平滑肌层增生;并且迂曲成角,57.1％基底动脉向左侧弯曲,较术前差异有统计学意义(P＜0.05).结论 基底动脉血流动力学增加是导致基底动脉迂曲成角的主要原因.     

维拉帕米动脉血管内灌注预防神经介入术中脑血管痉挛的价值

目的探讨维拉帕米动脉血管内灌注预防神经介入术中脑血管痉挛的价值。方法对神经介入治疗过程中出现的13例血管痉挛患者,采用动脉血管内灌注维拉帕米灌注防治。结果导致脑血管痉挛的因素:蛛网膜下腔出血9例,导丝等物理刺激3例,脑动静脉畸形1例,其中经颅内动脉灌注4例,经颈内动脉灌注9例;动脉血管灌注维拉帕米后,脑血管痉挛均得到解除,血流恢复;术中未出现病情加重情况,未造成患者神经功能损伤;患者治疗前后心率、平均动脉压差异无统计学意义(P0.05)。结论采用动脉血管内灌注维拉帕米可有效解除神经介入治疗过程中脑血管痉挛,安全可靠。     

TCD评价支架治疗颈动脉狭窄的疗效及与过度灌注的相关性

目的探讨经颅多普勒(TCD)评价颈动脉狭窄行支架植入治疗的临床疗效及与过度灌注的相关性。方法选取我科收治颈动脉狭窄行支架植入术患者68例为研究对象,所有患者术前均行TCD及脑血管造影(DSA)检查,根据TCD检查结果,分为观察组(无交通动脉开放)和对照组(交通动脉开放),观察术前和术后1 m、2 m狭窄处及狭窄远端收缩期峰值流速(PV)、平均血流速度(MV),评价临床疗效;观察组和对照组术后12 h、24 h、48 h行病变侧大脑中动脉(MCA)血流速度检测。结果术前血管狭窄处PV、MV明显升高,远端血管PV、MV降低,术后1个月、2个月支架内血流速度降低,狭窄远端血流速度升高,术前、术后比较差异有统计学意义(P0.05);术后12 h、24 h及48 h患者病变侧MCA PV、MV监测,观察组和对照组比较差异有统计学意义(P0.05)。结论 TCD观察患者血流动力学变化,可有效评价支架治疗颈动脉狭窄短期疗效,并有利于长期随访;观察组术后脑血流速度增快明显,对血压变化敏感,更容易发生过度灌注,TCD监测对支架术后严格控制血压,预防过度灌注的发生有重要意义。     

经颅多普勒检测破裂脑动脉瘤栓塞术后脑血管痉挛的临床应用

目的探讨经颅多普勒(TCD)在破裂脑动脉瘤栓塞术后脑血管痉挛(CVS)诊断中的应用价值。方法 2013年5月~2016年8月在我院接受动脉瘤栓塞术治疗的46例脑动脉瘤破裂患者,在手术前、后行TCD检查,探测大脑中动脉(MCA)血流速度和颈内动脉入颅段(e ICA)的血流速度;以此为依据判断脑血管痉挛发生与否。以DSA为金标准比较TCD诊断脑血管痉挛的敏感度和特异性。结果术后3 d起,患者MCA血流速度显著上升,术后10 d时逐渐下降,但与术前相比差异均有统计学意义(均P0.05);术后3~7 d,患者e ICA血流速度明显下降,与术前比较差均有统计学意义(均P0.05)。经DSA检查确诊CVS患者24例,非CVS患者22例。术后3 d起,CVS患者MCA血流速度均显著高于非CVS患者(均P0.05)。以DSA检查结果作为金标准,同时以MCA血流速度120 cm/s作为TCD法血管痉挛判断标准,TCD诊断CVS的敏感度为79.2%,特异度为90.9%,阳性预测值为90.5%,阴性预测值为80.0%。24例CVS患者经尼莫同治疗后病情均好转,无死亡病例。结论 TCD能够在早期发现破裂动脉瘤栓塞术后CVS的发生,具有较高的敏感度和特异度;值得进一步在临床应用。     

葛根素对椎基底动脉供血不足患者血流动力学的影响

目的 研究葛根素对椎基底动脉供血不足患者血流动力学的影响.方法 选择椎基底动脉供血不足患者105例,平均年龄(56±10)岁,每天予以葛根素400mg,加入5%葡萄糖注射液250ml或生理盐水中静滴,1次/d,连用14d.分别在用药前、用药后经颅多普勒(TCD)作脑血管左、右侧椎动脉(VA)、基底动脉(BA)血流动力学分析检查,记录椎动脉、基底动脉的血流速度平均值(Vmean)、搏动指数(PI)、血管阻力(RI),所得数据进行比较.结果 用药后较用药前椎动脉、基底动脉的血流速度平均值(Vmean)增加,搏动指数(PI)增加,血管阻力(RI)减少,在统计学上有显著性差异(P＜0.05).结论 葛根素能改善椎基底动脉供血不足患者脑动脉的血液供应,使得脑动脉血流动力学中的血流速度平均值增加,搏动指数增加,血管阻力减少,增加脑血流量,促进脑血循环,对缺血性脑血管病的防治有积极的意义.     

血管迂曲致锁骨下动脉盗血(附7例报道)

目的 探讨血管迂曲与锁骨下动脉盗血综合征(Subclavian steal syndrome,SSS)之间的关系.方法 对椎基底动脉供血不足患者行TCD检测,在检测中发现有椎动脉血流方向逆转者,行DSA检查明确盗血原因.结果 7例凶动脉迂曲造成盗血的患者中,5例存在锁骨下动脉迂曲,2例为椎动脉迂曲;1例表现为晕厥,其余6例全部表现为头晕或眩晕椎基底动脉供血不足症状,1例动脉迂曲与先天发育有关,其余6例均有高血压病史,考虑与动脉粥样硬化有关.结论 血管迂曲是引起SSS病因之一.     

Trapidil对蛛网膜下腔出血后脑血管痉挛作用的实验研究

目的 探讨蛛网膜下腔出血（SAH）后脑血管痉挛的发生机制及其可能的治疗方法。方法 利用家兔枕大池内注血构建SAH模型，观察血小板衍生生长因子（PDGF）拮抗剂trapidil对脑基底动脉的影响。结果 脑基底动脉于SAH后48h明显变细；静脉或动脉内持续灌注trapidil 15min（1．5mg／min）后，数字减影脑血管造影（DSA）显示痉挛血管已明显扩张变粗，30min时达高峰。结论 PDGF可能参与脑血管痉挛发生的病理过程，PDGF拮抗剂trapidil可有效缓解实验性SAH后脑血管痉挛，有望成为脑血管痉挛的治疗药物。     

三维CT血管成像技术在兔迟发性脑血管痉挛模型中的应用

目的 对比分析CT血管成像(CTA)和数字减影血管造影(DSA)在迟发性脑血管痉挛(DCVS)检测中的准确性、敏感性和安全性,探讨采用CTA观察DCVS的应用价值.方法 17只大耳白兔枕大池注射自体动脉血诱发DCVS,分别在术前、术后第7天行CTA和DSA检杏;另10只组成动态CTA组:分别在注血前、后第1天、第4天、第7天、第11天和第14天行CTA检查.将数据进行对比分析.结果 CTA检测兔基底动脉直径术前(1.55±0.14)mm,术后(0.95±0.20)mm,DSA检测兔基底动脉直径术前(1.61±0.19)mm,术后(1.00±0.17)mm,两种检测方法的测量值经统计学检验是完全等效的.动态CTA显示兔基底动脉住注血后第1天即出现痉挛,第4-11天血管痉挛明显加重,无明显高峰期,持续至第14天仍不能完伞缓解.结论 CTA是一种可靠、快速和无创的方法,为观察兔DCVS的动态变化提供了一种新的技术.     

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