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创伤性蛛网膜下腔出血后脑血管痉挛危象
刨伤性蛛网膜下腔出血(traumotic subarachnoid hemorrhage,tSAH)为神经外科常见病,可因重症脑血管痉挛(cerebral vasospasm,CVS)危及生命.
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CT血管造影诊断非动脉瘤性中脑周围蛛网膜下腔出血
自发性蛛网膜下腔出血是神经外科常见的急症,约80%~90%的出血为颅内动脉瘤破裂所致,非动脉瘤性自发性蛛网膜下腔出血中约75%患者表现为中脑周围蛛网膜下腔出血( perimesencephalic subarachnoid hemorrhage,PMSAH)[1-2].中脑周围蛛网膜下腔出血是一种影像学诊断,指自发性蛛网膜下腔出血在CT上表现为:出血局限在中脑周围的脑池,积血的中心位于中脑前方;有时出血主要局限于桥脑的前方或环次、四叠体次,但主要的是积血不扩散到侧裂池岛盖部或纵裂池,当脑室里有明显积血或脑实质内血肿时可排除本病[3-4].
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蛛网膜下腔出血后脑血管痉挛机制的研究进展
SAH后脑血管痉挛(cerebrovascular spasm,CVS)分为早期痉挛和迟发痉挛.前者多发生在SAH后0.5~1 h,发生迅速,可以起到生理止血的作用.后者是指始发于SAH后24~72 h,5~14 d达高峰,2~4周后消退.后者对患者的预后影响较大,是目前研究的重点.CVS的发病机制非常复杂,目前认识到的致痉因素包括氧合血红蛋白(oxyhemoglobin,OxyHb)、炎症反应、缩血管物质增多、血液高凝状态、血管细胞增殖和细胞凋亡等.现就此综述如下.
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动脉瘤性蛛网膜下腔出血后脑血管痉挛的现代诊断和治疗
半个世纪以来,动脉瘤性蛛网膜下腔出血(SAH)引起的脑血管痉挛(cerebral vasospasm,CVS)一直是神经科学领域的研究热点之一,现已部分解决了CVS的诊断、治疗、预防及预后等问题,但依然还存在着不少难以理解及亟待解决的问题.
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Objective To undertake animal experimentation and clinical study on the safety and efficacy of percutaneous transluminal angioplasty (PTA) and intraarterial papaverine (IAP) infusion for treatment of refractory symptomatic cerebral vasospasm (CVS). Methods In the experimental study, vasospasm was induced in rabbits by double injections of blood into the cisterna magna, IAP infusion was given on either the 4th day or the 7th day after occurrence of subarachnoid hemorrhage (SAH), and then neurological observation, angiography, light and electron microscopy were done. In the clinical study, since September 1996, 22 patients with refractory symptomatic CVS involving 50 vascular territories received dilation therapy by PTA and IAP within 24 hours of clinical neurological deterioration. Results In the experimental study, all the rabbits except two in the 'the 4th day' group showed angiographic dilation in all of the spastic basilar arteries, and neurological improvement; in the ' the 7th day' group angiographic dilation appeared in 4 (57. 1% ) out of 7 rabbits. After 24 hours, 1 rabbit in each group had recurrence of neurological deficits and angiographic constriction. In the clinical study after aneurysm clipping or endovascular coil embolization was done, within 72 hours of SAH all patients underwent endovascular treatment: PTA alone in 3 cases, IAP alone in 14 cases, PTA and IAP in the remaining 5 cases. All vessel segments were dilated satisfactorily after endovascular treatment. Clinical improvement was significant in 13 cases,moderate in 7, minimal or none in 2; 2 cases died on the 7th day after endovascular dilation treatment. Conclusion Endovascular dilating techniques, namely, PTA, IAP and a combination of PTA and IAP, are safe and effective for treatment of symptomatic CVS refractory to medical therapy.
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Synaptosomal-associated protein-25 is an important factor for synaptic functions and cognition. In this study, subarachnoid hemorrhage models with spatial learning disorder were established through a blood injection into the chiasmatic cistern. Immunohistochemical staining and western blot analysis results showed that synaptosomal-associated protein-25 expression in the temporal lobe, hippocampus, and cerebel um significantly lower at days 1 and 3 fol owing subarachnoid morrhage. Our findings indicate that synaptosomal-associated protein-25 expression was down-regulated in the rat brain after subarachnoid hemorrhage.
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CT和CT血管造影术在中脑周围非动脉瘤性蛛网膜下腔出血诊断中的价值
随着影像学的发展,CT、CT血管造影术(CTA)、磁共振血管造影术(MRA)以及数字减影血管造影(DSA)在临床上的相继应用,蛛网膜下腔出血(subarachnoid hemorrhage,SAH)的病因诊断越来越明确.而对于SAH的一种特殊类型--中脑周围非动脉瘤性蛛网膜下腔出血(perimesencephalic nonaneurysmal subarachnoid hemorrhage,PNSH),也在逐渐深入的研究之中.在我国由于病理学等基础研究滞后,对PNSH尚未真正了解,特别是在基层医院,由于缺少DSA,诊断更困难.因此,将CT平扫以及CTA在PNSH诊断中的价值综述如下,以便临床医生参考.
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中国蛛网膜下腔出血诊治指南2015
颅内血管破裂后,血液流入蛛网膜下腔称为蛛网膜下腔出血( subarachnoid hemorrhage, SAH ),临床上将SAH分为外伤性与非外伤性两大类。非外伤性SAH又称为自发性SAH,是一种常见且致死率极高的疾病,病因主要是动脉瘤,约占全部病例的85%左右,其他病因包括中脑周围非动脉瘤性出血( perimesencephalic nonaneurysmal subarachnoid hemorrhage, PNSH )、血管畸形、硬脑膜动-静脉瘘(dural arteriovenous fistula, DAVF)、凝血功能障碍、吸食可卡因和垂体卒中等。近年来,血管介入技术、诊断方法与围手术期处理均有较大进展。但是, SAH患者的预后仍然较差,病死率高达45%,且存活者的残障率也较高。中华医学会神经病学分会脑血管病学组2007年出版的《中国脑血管病防治指南》中包含有SAH的章节[1]。中华医学会神经外科学分会曾于2006年出版《临床疾病诊疗指南--神经外科》一书,其中也包含了SAH诊疗指南。近几年来不断有新的临床研究和相应的国际指南发表,几个多中心、前瞻性、随机对照试验和前瞻性队列研究对SAH的治疗提出了新的方法,因此,中华医学会神经病学分会及其脑血管病学组组织了对2007年版指南的重新修订,形成新版指南以指导临床医生的操作实践。由于其他原因的SAH的资料相对缺乏,故本指南主要是针对非外伤性、动脉瘤性SAH制定的。
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中脑周围非动脉瘤性蛛网膜下腔出血
我院2002年1月~2005年12月共收治中脑周围非动脉瘤性蛛网膜下腔出血(perimesencephalic nonaneurysmal subarachnoid hemorrhage,PNSH)14例患者,经脑血管造影检查均未发现动脉瘤.现报道如下.
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动脉瘤性蛛网膜下腔出血脑积水研究进展
脑积水是动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,aSAH )常见的并发症之一,它是由于SAH后脑脊液分泌过多或吸收障碍,而导致脑脊液循环梗阻,出现的以脑室和(或)蛛网膜下腔的病理性扩张、脑实质相应减少为特征的一类疾病.对患者的预后有很大的影响,因此,了解动脉瘤性SAH后脑积水的临床特点以及早期诊断、早期治疗脑积水是提高动脉瘤性SAH治愈率和降低并发症及致残率的关键.现对其发病机制、危险因素、诊断和防治等方面并结合文献综述如下.
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他汀类药物治疗脑血管痉挛机制的研究
脑血管痉挛(cerebral vasospasm,CVS)是神经外科的常见临床问题,其基础和临床研究是目前国内外神经外科领域内的热点问题之一,特别是动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,aSAH)是致死、致残的重要原因.CVS即"颅内动脉的持续性收缩状态",其诊断主要根据患者的临床症状体征及脑血管造影的影像,如果仅在血管造影时发现血管处于痉挛状态,而患者没有相应的神经功能缺损症状,称为无症状性血管痉挛.反之,则称为症状性血管痉挛,或迟发性缺血性神经功能障碍(delayed ischemic neurological deficit,DIND).根据现有研究成果,CVS发生的病理生理机制与下列因素有关:①血液及手术器械对血管壁的机械性刺激;②血块压迫、血管壁营养障碍等导致血管壁结构破坏;③氧合血红蛋白氧化成高铁血红蛋白并释放氧自由基造成的损伤;④各种血管活性物质,如5-HT、儿茶酚胺、血红蛋白及花生四烯酸代谢产物的缩血管作用;⑤颅内压增高,过量脱水治疗而不及时补充血容量;⑥血管壁的炎症和免疫反应[1].
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脑血管痉挛防治神经外科专家共识
一、前言脑血管痉挛(cerebral vasospasm)是神经外科的常见临床问题,其基础和临床研究是目前国内外神经外科领域内的热点问题之一,特别是动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage.aSAH)是致死、致残的重要原因.
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自发性蛛网膜下腔出血患者CT血管造影的护理
自发性蛛网膜下腔出血(spontaneous subarachnoid hemorrhage,SAH)是一种危重的疾病,有很高的病死率和致残率, 三维CT血管造影(three-dimensional computer tomography angiography 3D-CTA)是一种新的无创性诊断方法,能及早明确出血原因,提高治愈率、降低患者的死亡率.本文总结急性期SAH患者3D-CTA检查中的护理方法,现报告如下.
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CTA在自发性蛛网膜下腔出血诊断中的研究进展
自发性蛛网膜下腔出血(Spontaneous subarachnoid hemorrhage,s-SAH)是神经外科较常见的疾病,是颅内动脉瘤(AN)及动静脉畸形(AVM)的主要并发症,具有较高的致死率和致残率[1] .早期发现及治疗,特别是针对病因的诊治尤为重要[2] .
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蛛网膜下隙出血病人血管内介入治疗的护理
蛛网膜下隙出血是神经内科的危重病,其主要病因是颅内动脉瘤再次出血的风险很大,有40%~65%病人会因再次出血死亡[1].目前,血管介入栓塞动脉瘤是治疗蛛网膜下隙出血的主要手段,具有创伤小、恢复快的特点.现将我院2005年1月-2010年10月血管内介入治疗动脉瘤21例护理体会总结如下.
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蛛网膜下腔出血再发的预防及护理
蛛网膜下腔出血是以剧烈头痛、脑膜刺激征阳性,以及血性脑脊液为主要表现,有再次出血的危险性.再次出血的危险性在发病后2周内发病率高,其次为3周~6周,6个月发病率减少.
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老年自发性蛛网膜下腔出血的临床观察及护理
自发性蛛网膜下腔出血(SAH)可发生于任何年龄,经临床观察,发现不同年龄临床表现亦不同,因此对病情的观察及护理也不尽相同.现将我科1991年7月-2001年10月收治的80例老年自发性SAH病人的护理体会简述如下.
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P53蛋白在蛛网膜下腔出血后早期脑损伤和血管痉挛中的作用
p53是重要的肿瘤抑制因子,在细胞内起着抑制细胞周期、促进基因组修复和诱导凋亡等多重作用.在蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后,p53在缺氧等多种因素作用下被激活,并通过其靶蛋白、Bcl-2和Caspase家族蛋白等发挥促血管内皮细胞及脑内神经元凋亡的作用,并导致SAH后早期脑损伤和后期血管痉挛的发生.应用p53特异性的抑制剂可以阻断p53的活化,显著恢复SAH后的血脑屏障功能并缓解脑血管痉挛.本文讨论了p53在SAH后的血管内皮细胞和神经元凋亡中的作用机制,并进一步探讨应用p53抑制剂拮抗p53功能以治疗SAH后早期脑损伤和血管痉挛的可能性.
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老年性蛛网膜下腔出血非典型症状30例分析
CLINICAL DATASubjects came from 30 patients with senile subarachnoid hemrrhagetreated in our hospital from January 1999 to December 2001 in-cluding 12 males and 18 females aged 60-78(mean: 65) yearsold. 24 patients presented with onset in action, 6 patients at rest; 26cases presented with acute onset and 4 cases subacute onset. Acuteheadache as first symptom was in 13 cases; pain at neck, waist,sacral as first symptom in 7 cases. 3 patients searched medical ser-vice for headache within 1 week; 2 patients for severe pain of bothlimbs and unable to walk; 2 patients for headache and vomiting at 2week. 7 patients were once treated out of our hospital and sciaticawas diagnosed in 4 cases, cold in 3 cases. Pain at shoulder, back,upper limb in action occurred in 2 cases as first symptom, consciousdisturbance was the first symptom in 4 cases, grand mal of epilepsyas first symptom in 3 cases. 1 patient searched medical service forright head pain, auricle pain for 20 days. Stiff neck ( + ) appeared in25 patients at hospitalization and (-) in 5 patients. 24 patientspresented with positive Kernig' s sign. 21 patients were complicatedwith hypertension, 1 patient was complicated with peripheral facialparalysis and left hemihypoesthesia, 3 patients with transient hemi-paresis of both lower limhs, 2 cases with bilateral ptosis, 1 case withexotropia of bilateral eyeball, pupil dilation, 6 cases with consciousdisturbance. Auxilliary examination: (1) Skull CT scanning: Sub-arachnoid hemorrhage was found in 20 cases, no abnormality in 7cases and 3 cases didn't undergo CT scanning. (2) Examination ofspinal fluid: patients with positive CT findings didn' t undergo lumbarpuncture, even hemic spinal fluid was found in 6 patients and yellowspinal fluid and shrinking red blood cell in 4 cases. Prognosis: Allcases were treated according to subarachnoid hemorrhage, 6 patientsdied and other 24 patients were cured after 6 - 8 weeks of treatment.
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通窍活血汤预防迟发性脑血管痉挛的实验研究
Objective To investigate the prevention effects and the physicochemical mechanisms of action of Tong Qiao Huo Xue Tang on delayed cerebral vasospasm(DCD) after subarachnoid hemorrhage(SAH).Methods Macaca cynomolgus were divided into two groups and underwent craniectomy,a semipermeable microdialysis catheter was placed adjacent to right middle cerebral artery (MCA).Therapeutic group were exposed to Tong Qiao Huo Xue Tang and control group to placebo via oral .Results The diameter of proximal MCA in therapeutic group changed slightly on 7th day after operation(P >0.05),whereas it decreased prominently(P< 0.05) in control group with severe vasospasm.OxyHb concentration:There's no significant difference between the two groups on 2nd ~ 5th day(P >0.05),the concentration of therapeutic group(was zero after 8 days) was lower than that of control group (became zero after 12 days) on 6th ~ 8th day(P< 0.05).The peak value of therapeutic group (on 5th day) was lower than that of control group (on 7th day)(P< 0.05).Conclusion Tong Qiao Huo Xue Tang can prevent DCV after SAH effectively and decreasing OxyHb concentration around vessels after SAH maybe the mechanism.