浅谈脑脊液置换术防治SAH后脑血管痉挛的护理观察

蛛网膜下腔出血(SAH)后并发脑血管痉挛(CVS)是常见且重要并发症,同时也是致残和致死的主要原因[1].蛛网膜下腔的积血是导致CVS发生的根本原因,尽快清除蛛网膜下腔积血是防治CVS的重要措施.自1993～2002年以来,我科开展脑脊液(CSF)置换术防治脑血管痉挛,取得良好效果.本文就CSF置换术防治脑血管痉挛的护理观察介绍如下:     

动脉瘤性蛛网膜下腔出血后神经元损伤机制的研究进展

动脉瘤性蛛网膜下腔出血（aSAH）是脑卒中最严重的表现形式之一。颅内动脉瘤破裂后血液瘀滞在脑蛛网膜下腔,引起多种病理生理改变,包括脑积水、细胞凋亡、血脑屏障功能障碍、血管痉挛、微血栓形成和皮层扩散性抑制,这些机制相互作用并贯穿于整个脑损伤过程。近年来,临床试验逐渐关注aSAH发生后的两个阶段:早期脑损伤（EBI）和延迟性脑缺血(DCI)。这两个时期是导致神经元损伤的主要阶段,并与患者的预后密切相关。我们就近年来蛛网膜下腔出血后脑损伤的机制作一简要总结,主要讨论EBI和DCI在神经损伤中的作用。     

动脉瘤性蛛网膜下腔出血后神经元损伤机制的研究进展（英文）

动脉瘤性蛛网膜下腔出血(a SAH)是脑卒中最严重的表现形式之一。颅内动脉瘤破裂后血液瘀滞在脑蛛网膜下腔,引起多种病理生理改变,包括脑积水、细胞凋亡、血脑屏障功能障碍、血管痉挛、微血栓形成和皮层扩散性抑制,这些机制相互作用并贯穿于整个脑损伤过程。近年来,临床试验逐渐关注a SAH发生后的两个阶段:早期脑损伤(EBI)和延迟性脑缺血(DCI)。这两个时期是导致神经元损伤的主要阶段,并与患者的预后密切相关。我们就近年来蛛网膜下腔出血后脑损伤的机制作一简要总结,主要讨论EBI和DCI在神经损伤中的作用。     

人体组织器官间的保护作用

人体组织器官在功能和形态结构上相互联系共同作用、进行代谢、运动。研究人体解剖我们发现这些组织器官间有一定的保护作用。 一、神经系统、心脏和动脉是重点保护对象。 脑、脊髓分别固定在颅腔和椎管内,从它们表面向外有软脑膜、蛛网膜、硬脑膜包裹。硬膜下腔和蛛网膜下腔内充填着脑脊液,缓冲外力,防止震动损伤,在视神经硬膜下腔一直包到视乳头。脊柱受力明显活动量大,椎管内硬膜外尚有脂肪囊、韧带牵拉固定缓冲外力。     

蛛网膜下腔出血脑脊液置换术的护理对策

蛛网膜下腔出血多数为突然发病,最突出的症状是剧烈的局限性劈裂样头痛。药物治疗作用缓慢。我科1997年6月～2000年9月采用脑脊液(CSF)置换术治疗蛛网膜下腔出血(SAH),可在短时间内降低颅内压,改善临床症状,减轻病人痛苦。本组病例通过严密观察和精心护理,取得了满意效果,现     

脑脊液置换治疗蛛网膜下腔出血

蛛网膜下腔出血（subarachnoid hemorrhage，SAH）是指各种原因出血血液流人蛛网膜下腔的统称。临床上可分为自发性与外伤性两大类，自发性又分为原发性与继发性两种。由各种原因引起软脑膜血管破裂血液流入蛛网膜下腔者称原发性蛛网膜下腔出血；因脑实质内出血血液穿破脑组织流入蛛网膜下腔者称继发性蛛网膜下腔出血。SAH是加重继发性脑损害的重要因素。如何加速蛛网膜下腔血液的廓清，减轻继发性脑损害，多年来一直是神经外科学者关注的热点，近年来，脑脊液置换技术越来越多地应用于临床，方法多种多样，均取得了良好的治疗效果，现收集我科2003—2007年期间采用脑脊液置换治疗SAH79例的资料，进行研究和分析，并报告如下。     

U74389G预防狗蛛网膜下腔出血后脑血管痉挛

颅内动脉瘤破裂后的主要并发症包括蛛网膜下腔出血（ＳＡＨ）本身所引起的脑损害以及蛛网膜下腔出血后第７天所发生的脑血管痉挛。其发生机理为：颅内动脉瘤破裂后，去氧自由基通过直接作用于动脉壁而导致血管痉挛；此外，还可引起蛛网膜下腔红细胞脂氧化而诱发血管收缩。Ｕ７４３８９Ｇ是一种有力的脂氧化抑制剂和去氧自由基清除剂。本研究验证了去氧自由基和脂氧化在实验性狗蛛网膜下腔出血中引起血管痉挛的相关作用。１６只狗实验前均进行了脑血管造影，于第２天将新鲜血液注入到延髓池诱发蛛网膜下腔出血。随机将１６只狗分为两组：第一…     

视神经磁共振成像方法研究

目的探讨视神经磁共振(MRI)成像最佳方法及正常视神经MRI征象. 方法随机选择40例进行头部检查,无眼部疾患或视力障碍患者作为正常视神经研究对象.使用Philips ACS-NT15 1.5T超导型磁共振成像仪及正交头线圈.成像序列包括自旋回波T1加权成像(SE T1WI)及超快速自旋回波加或不加脂肪频谱饱和技术成像(TSE±SPIR T2WI).扫描方位包括与视神经平行轴位、斜矢状位及与视神经长轴垂直冠状位和标准冠状位. 结果视神经眶内段、管内段及视束粗细均匀.SE T1WI显示视神经较周围的蛛网膜下腔信号强度稍高,T2WI显示视神经呈相对低信号,与脑髓质信号相等,周围包绕高信号脑脊液.与视神经长轴平行的轴位及斜矢状位T1WI及T2WI均可显示视神经全貌,与视神经长轴垂直冠状位TSE+SPIR T2WI技术显示视神经信号均匀. 结论 MRI可以较好地显示视神经解剖,与视神经长轴垂直冠状位TSE+SPIR T2WI可以较好地显示信号特征.     

眼皮肤白化病常见亚型的基因与基因突变

白化病(albinism)是一组由黑素合成相关的基因突变导致眼或眼、皮肤、毛发黑色素缺乏引起的遗传性疾病.受累个体相应部位颜色浅淡或缺如,发育过程中眼部黑色素的缺乏又可导致视网膜中央小凹发育不良、视神经通路异常,出现眼球震颤、斜视、视力低下等.皮肤缺乏色素的保护,对紫外线敏感,易于患皮肤癌.     

氧自由基对蛛网膜下腔出血后脑血管痉挛的影响

蛛网膜下腔出血(SAH)后脑血管痉挛是SAH病人致死致残的重要原因,但血管痉挛的发生机理仍未阐明。本文主要探讨氧自由基在脑血管痉挛发病中的作用。家兔分为3组(1)对照组:蛛网膜下腔注入Ns,(2)     

Role of cerebrospinal fluid in glaucoma: Pressure and beyond

Glaucoma is the second leading cause of blindness worldwide. Primary open-angle glaucoma (POAG) is characterized by optic disc cupping and visual field impairment. Though the elevated intraocular pressure (IOP) is thought to be the major risk factor for POAG, about 50% of the POAG patients have normal IOP, called ‘normal-tension’ glaucoma. Besides, many POAG patients still experience visual field loss and/or optic disc cupping even though the IOP has been well controlled. The mechanisms underlying the pathogenesis of POAG remain unclear. Extensive studies have shed lights on the mechanisms that may be involved in the etiopathology and/or the optic neuropathic manifestations of POAG. In this article, we noticed that the changes in the cerebrospinal fluid, particularly that existing in the subarachnoid space of the optic nerve, appear to be actively involved in the pathogenesis of POAG.     

The translaminar pressure gradient in sustained zero gravity,idiopathic intracranial hypertension,and glaucoma

Papilledema has long been associated with elevated intracranial pressure. Classically, tumors, idiopathic intracranial hypertension, and obstructive hydrocephalus have led to an increase in intracranial pressure causing optic nerve head edema and observable optic nerve swelling. Recent reports describe astronauts returning from prolonged space flight on the International Space Station with papilledema (Mader et al., 2011) [1]. Papilledema has not been observed in shorter duration space flight. Other recent work has shown that the difference in intraocular pressure (IOP) and cerebrospinal fluid pressure (CSFp) may be very important in the pathogenesis of diseases of the optic nerve, especially glaucoma (Berdahl and Allingham, 2009; Berdahl, Allingham, et al., 2008; Berdahl et al., 2008; Ren et al., 2009; Ren et al., 2011) [2], [3], [4], [5], [6]. The difference in IOP and CSFp across the lamina cribrosa is known as the translaminar pressure difference (TLPD).We hypothesize that in zero gravity, CSF no longer pools in the caudal spinal column as it does in the upright position on earth. Instead, CSF diffuses throughout the subarachnoid space resulting in a moderate but persistently elevated cranial CSF pressure, including the region just posterior to the lamina cribrosa known as the optic nerve subarachnoid space (ONSAS). This small but chronically elevated CSFp could lead to papilledema when CSFp is greater than the IOP. If the TLPD is the cause of optic nerve head edema in astronauts subjected to prolonged zero gravity, raising IOP and/or orbital pressure may treat this condition and protect astronauts in future space travels from the effect of zero gravity on the optic nerve head. Additionally, the same TLPD concept may offer a deeper understanding of the pathogenesis and treatment options of idiopathic intracranial hypertension (IIH), glaucoma and other diseases of the optic nerve head.     

The translaminar pressure gradient in sustained zero gravity,idiopathic intracranial hypertension,and glaucoma

Papilledema has long been associated with elevated intracranial pressure. Classically, tumors, idiopathic intracranial hypertension, and obstructive hydrocephalus have led to an increase in intracranial pressure causing optic nerve head edema and observable optic nerve swelling. Recent reports describe astronauts returning from prolonged space flight on the International Space Station with papilledema (Mader et al., 2011) [1]. Papilledema has not been observed in shorter duration space flight. Other recent work has shown that the difference in intraocular pressure (IOP) and cerebrospinal fluid pressure (CSFp) may be very important in the pathogenesis of diseases of the optic nerve, especially glaucoma (Berdahl and Allingham, 2009; Berdahl, Allingham, et al., 2008; Berdahl et al., 2008; Ren et al., 2009; Ren et al., 2011) , , ,  and . The difference in IOP and CSFp across the lamina cribrosa is known as the translaminar pressure difference (TLPD).     

颈内动脉压迫视神经颅内段的组织学改变及其机制

目的:观察视神经受压后的组织学改变,探讨因压迫所致视野缺损发生的机制。方法:60-80岁的老年人脑,组织切片观察颈内动脉内膜钙化压迫视神经颅内段引起的神经组织学改变。结果:粥样硬化的颈内动脉可压迫视神经并在其表面形成明显压迹。神经受压后,中隔变窄,神经束呈条索状,束内营养小动脉硬化,管腔阻塞,节细胞轴突萎缩,重者可全部消失,少突胶质细胞增多,肿胀。结论:视神经纤维萎缩是由于阻塞了神经束内营养小动脉缺血所致,以乳头黄斑束受累为甚,是视野缺损发生的原因之一。     

视网膜挫伤模型兔视神经细胞的凋亡

背景：视网膜挫伤是眼外伤后导致视力损害的主要原因之一,临床治疗比较棘手。虽然对视网膜挫伤后眼底改变在临床上已有较充分的认识,但在其发病机制、药物治疗上意见仍不一致。 目的：在兔视网膜挫伤模型上,观察视神经细胞的凋亡并探讨其发生机制。 方法：健康成年无眼疾青紫蓝兔48只,随机分为8组,挫伤后1,3 h组、挫伤后1,3,7,14,28 d组及正常对照组,每组6只。右眼为致伤眼,以改良Allen’s重击法制备兔单眼挫伤性视网膜病变模型。分别于建立模型后在相应时间点获取兔眼标本,对筛板后5 mm视神经行病理切片,苏木精-伊红染色,观察组织形态并行神经胶质细胞计数,以电镜及TUNEL法观察视神经细胞凋亡情况。 结果与结论：正常对照组兔视神经纤维排列整齐,胶质细胞与神经纤维走向一致,呈极性排列。挫伤后1,3 h、挫伤后1,3,7 d兔视神经纤维排列紊乱,胶质细胞杂乱无序。挫伤后1,3 h、挫伤后1,3,7,14,28 d胶质细胞计数减少,与正常对照组相比,差异有非常显著性意义(P < 0.01)。视网膜挫伤后存在神经胶质细胞凋亡现象,正常对照组、挫伤后1 h、挫伤后28 d组几乎不见凋亡细胞;挫伤后3 h组、挫伤后1,3,7,14 d组均可见TUNEL染色阳性的凋亡细胞,其中在3 d组数量较多,与正常对照组之间比较,差异有非常显著性意义(P < 0.01)。提示视网膜挫伤后,视神经胶质细胞凋亡可能是视功能恢复不良的原因之一。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

大鼠受损视神经去分化相关基因表达谱的变化及移植预变性腓总神经的作用

为检测受损视神经基因表达谱的变化以及移植预变性周围神经的调节作用,SD大鼠随机分为正常组、损伤组和神经移植组,术后7 d取眶内段视神经,用Aglient Oligo芯片检测其基因表达谱的变化,并用实时荧光定量PCR、免疫组织化学、Western Blot验证芯片检测结果。损伤组与正常组相比,1340条基因上调,940条基因下调;去分化相关基因如神经发育早期基因表达上调,转录、凋亡、增殖、生长、分化和细胞内信号转导类差异表达基因较多,基因差异表达的变化以有利于神经再生为主,但也存在显著抑制神经再生的差异表达变化。神经移植组与损伤组相比,106条基因上调,14条基因下调,部分差异表达基因与细胞去分化有关。总之,视神经损伤早期约1/10的基因差异表达,其中包含与神经胶质细胞去分化密切相关的基因;移植预变性周围神经可调控受损视神经中部分基因的表达,促使胶质细胞去分化趋势增强,有利于视神经再生。     

Macrophages during avian optic nerve development: relationship to cell death and differentiation into microglia

Cell death is frequent during the development of the nervous system. In the developing optic nerve of chicks and quails, neuroepithelial cell death was first observable on the third day of incubation, slightly after the first cell ganglion axons appeared in the stalk. Specialized phagocytes were observed within the stalk in chronological and topographical coincidence with cell death. These cells were identified as macrophages because of their morphological features, intense acid phosphatase activity and, in quail embryos, labeling with QH1, a monoclonal antibody recognizing quail hemangioblastic cells. Macrophages in areas of cell death were round and actively phagocytosed cell debris. We used electron microscopy and histochemical and immunocytochemical labeling to study macrophagic cells of the optic nerve in avian embryos of 3–6.5 days of incubation. As development proceeded, phagocytosing, round macrophages became ameboid macrophages that migrated from areas of cell death toward regions occupied by optic axonal fascicles. Macrophages in these locations were thin and elongated, with a few processes. To elucidate the final fate of macrophagic cells in the optic nerve, sections taken from older embryonic and hatched quails were stained with the QH1 antibody. On the 8th day of incubation some slightly ramified QH1+ cells were present among axonal fascicles. In subsequent stages these cells increased in number and acquired more complex ramifications. In adult optic nerves, QH1+ cells had a small body and sent out slender processes, sometimes with secondary and tertiary branches, which were frequently orientated parallel to the course of the optic axons. These cells were considered to be microglial cells. The appearance of macrophages within the developing optic nerve at the same time as neuroepithelial cell death suggests that cell death influences the recruitment of macrophages into the nerve. When macrophages reach the areas invaded by optic axonal fascicles, they undergo structural and probably also physiological changes that appear to signal differentiation into microglia.     

肌锥间隙的断层解剖

目的：为眶区影像诊断和手术治疗提供断层解剖学资料。方法：应用36例成人头颅湿标本，制成0．5mm冠状位火棉胶连续切片，用双目解剖镜对眶区结构进行形态观察，并采用计算机图像分析系统对标本上的肌锥间隙、视神经进行了测量。结果：肌锥间隙自眼球后极层面，自前向后，面积随眶腔减小，但不同层面肌锥间隙占眶腔的比例基本一致。眶内段视神经从前向后，横径和面积先逐渐减小，而后逐渐增大，垂直径逐渐减小，其与4条直肌的距离逐渐减小。结论：熟悉肌锥间隙的显微解剖，对影像诊断，麻醉及手术均有重要意义。     

大鼠受损视神经中神经前体细胞的变化及预变性腓总神经的调节

为了研究大鼠受损视神经内神经前体细胞的变化及调节,本研究建立了成年雄性大鼠视神经损伤及自体腓总神经移植模型,分正常组、损伤组和移植组,体外培养视神经的神经前体细胞,在相差显微镜下观测各组神经前体细胞神经球的形态和数目,以免疫荧光细胞化学方法对神经球细胞进行鉴定。结果显示:正常组神经球较小、较少,多数细胞表达nestin、GFAP或半乳糖脑苷脂(GC);视神经损伤后神经球的总数有所增加,但大神经球数明显减少,nestin、GFAP或GC阳性细胞也明显减少;神经移植后增加了各类神经球数,nestin、GFAP或GC阳性细胞也明显增加。本研究提示成年大鼠视神经内神经前体细胞较少,增殖能力较弱;视神经损伤也伤及其神经前体细胞并抑制其增殖;自体神经移植能保护神经前体细胞并促进其增殖。     

视神经的断层解剖学研究及其临床意义

目的：为视神经的影像检查提供断层解剖学资料。方法：应用50侧成人头颅湿标本制成0.5mm的火棉胶连续切片，用计算机图像分析系统对36侧冠状位标本上的视神经进行测量。结果：视神经分颅内段、管内段、眶内段和球内段四部分。管内段从视神经管颅口到眶口逐渐变细，眶内段中点最细。结论：视神经的测量可在冠状面上进行，眶内段中点可作为测量标准。