脑静脉闭塞实验研究现状

脑静脉血栓形成(CVT)从19世纪早期就已被认识，但由于临床表现缺乏特异性、诊断困难等原因，一直未受到重视。近30年，随着神经影像学的进展，静脉闭塞在脑血管病中的地位日益受到重视。脑静脉和静脉窦循环在保障脑血液流通、血供稳定上的重要作用正引起人们的关注。文章就近年来的有关实验研究作了综述。     

非Galen静脉脑动静脉瘘

Galen静脉脑动静脉瘘是一种少见的先天性脑血管畸形。表现为脑内动脉与静脉间的直细血管或血管,近瘘口处静脉呈动脉瘤样扩张,引流静脉亦扩张,引流静脉亦扩张回静脉引文复习了近年来的文献资料,就本病的临床表现、病理生理、影像学诊断、鉴别诊断及治疗进行综述。     

内皮素受体拮抗剂对脑血管痉挛的治疗作用

内皮素受体介导了内皮素在蛛网膜下腔出血后脑血管痉挛时的血管舒缩功能 ,内皮素受体拮抗剂在脑血管痉挛中的作用日益受到重视。文章就内皮素受体拮抗剂对脑血管痉挛的预防和治疗作用作了介绍。     

纤维蛋白原与脑动脉系统血栓形成

近年来,纤维蛋白原与脑动脉系统血栓形成之间的关系越来越受到重视,而且随着研究的不断深入,许多机制逐渐阐明。文章就血浆高纤维蛋白原水平导致脑动脉系统血栓形成的机制以及这一研究领域存在的分歧和主要的研究方向作了综述。     

非血栓性脑静脉回流障碍的研究进展

与脑动脉系统相比,脑静脉缺乏平滑肌和弹性纤维,解剖结构更为复杂多变且不对称。随着对静脉系统认识的深入,脑静脉疾病成为脑血管病不可忽视的一部分,而静脉系统疾病因其症状和体征隐匿,易被误诊或漏诊。许多造成脑静脉窦及颈内静脉狭窄或相对狭窄的原因均可引起脑静脉回流障碍,长期慢性脑静脉回流障碍可导致脑组织静脉性缺血,进而出现不同程度的临床症状。作者综述了与非血栓性脑静脉回流障碍相关的神经系统疾病及脑静脉回流障碍的诊治方法,以提高临床医师对脑静脉疾病的认识。     

内皮素受体拮抗剂对脑血管痉挛的治疗作用

内皮素受体介导了内皮素在蛛网膜下腔出血后脑血管痉挛时的血管舒缩功能，内皮素受体拮抗剂在脑血管痉挛中的作用日益受到重视。文章就内皮素受体拮抗剂对脑血管痉挛的预防和治疗作用作了介绍。     

脑静脉血栓形成的研究进展

脑静脉血栓形成(CVT)是多种病因导致的发生于颅内静脉或静脉窦的一种少见血栓形成疾病。该文就CVT的病因、机制、诊断、治疗、预后等作一综述。     

非Galen静脉脑动静脉瘘

非Ｇａｌｅｎ静脉脑动静脉瘘是一种少的先天性脑血管畸形，表现为脑内动脉与静脉间的直接沟通，其间无畸形毛细血管床或血管巢，近瘘口处静脉呈动脉瘤样扩张，引流静脉亦扩张向静脉窄引流。文中复习了近年来的文献资料，就本病的临床表现，病理生理，影像学诊断，鉴别诊断及治疗进行综述。     

纤维蛋白原与脑动脉系统血栓形成

近年来，纤维蛋白原与脑动脉系统血栓形成之间的关系越来越受到重视，而且随着研究的不断深入，许多机制逐渐阐明。文章就血浆高纤维蛋白原水平导致脑动脉系统血栓形成的机制以及这一研究领域存在的分歧和主要的研究方向作了综述。     

脑深髓静脉与脑小血管病

脑小血管病(cerebral small vessel disease, CSVD)是指各种病因作用于脑小动脉、微动脉、小静脉及毛细血管所致的一系列病理、影像及临床综合征。CSVD的主要影像学特征包括脑白质高信号、脑微出血、腔隙性脑梗死、血管周围间隙扩大和脑萎缩。脑深髓静脉(deep medullary veins, DMVs)是侧脑室周围的实质小静脉, 参与从脑深部白质静脉到室管膜下静脉的静脉回流。近年来, 越来越多的研究显示DMVs与CSVD的发生和发展密切相关。文章对DMVs在CSVD中的作用进行了综述, 为进一步探索CSVD的发病机制和影像学标志物提供思路。     

脑静脉窦血栓形成的影像学特征与早期诊断

目的 探讨脑静脉窦血栓形成(CVT)的早期临床和影像学特点，以利于CVT的早期诊断。方法 回顾性分析42例确诊的、有完整影像学资料的CVT患者的临床表现和颅脑CT、MR、数字减影血管造影(DSA)结果。结果 42例CVT患者早期的常见症状有头痛(100％)、局灶性神经功能缺损(67％)和癫痫发作(57％)，多被误诊为动脉性脑梗死、脑内占位或脑炎。影像学上39例可见静脉性脑梗死特征(引流区域脑实质肿胀和出血性梗死)，23例颅脑MR上可见T2WI病灶远大于弥散加权项(DWI)上的病灶，且坏死灶多仅位于皮层(87％)。T2WI上脑静脉窦流空信号消失有确诊价值，对上矢状窦血栓(96％)较侧窦血栓更敏感(50％)。DSA显示相应的静脉窦闭塞及静脉侧支循环，脑动静脉循环时间延长。结论 头痛、癫痫发作和局灶性神经功能缺损是CVT早期的常见症状，但缺乏特征性。熟识影像学上静脉性脑梗死的特征性表现(脑实质肿胀明显，但坏死轻微且常常伴有出血)，对CVT的早期诊断至关重要，颅脑MR上T2WI上脑静脉窦流空信号消失有确诊价值。对于MR无法确诊的病例，颅脑磁共振静脉血管造影(MRV)或13SA可明确诊断。CVT病灶功能障碍区域大而坏死轻微时，提示预后较好。     

Intracerebral Hemorrhage from Cerebral Venous Thrombosis

Cerebral venous thrombosis (CVT) is an uncommon cause of stroke with the incidence of 0.5 % from all strokes. The clinical presentation with cerebral hemorrhage constitutes a diagnostic challenge. Approximately one- third of CVT patients developed intracerebral hemorrhage (ICH). Associated factors include older age, female sex, acute onset (48 h), headache, decreased level of consciousness, seizure, elevated blood pressure and papilledema. MRI and MR venogram is the most recommend diagnostic modality in CVT. Anticoagulation therapy is the most commonly accepted treatment even in patients with ICH related CVT. Mechanical thrombectomy/thrombolysis may be considered in patients with neurological deterioration despite intensive medical treatment. Intracerebral hemorrhage in the context of CVT is usually associated with poorer outcomes compared to CVT without ICH.     

Combined heterozygosity of factor V leiden and the G20210A prothrombin gene mutation in a patient with cerebral cortical vein thrombosis

Cerebral venous thrombosis (CVT) is a rare type of stroke with a variety of causes. Several reports have suggested that either factor V Leiden or G20210A prothrombin gene mutation is associated with an increased risk of CVT. The genetic thrombophilias are typically associated with other predisposing factors. We report a unique case of CVT in a patient with both the factor V Leiden and the G20210A prothrombin gene mutations without other identifiable precipitating factors in a 28-year-old white male in good health. MRI and cerebral arterial angiography showed cerebral cortical venous thrombosis. This case suggests that combined heterozygous individuals may be particularly prone to spontaneous thrombosis, like CVT.     

Cerebral venous thrombosis as a complication of leptospirosis

Leptospirosis is an acute infectious disease caused by a spirochete of the leptospira gender and it is characterized by severe vasculitis. It is not common for leptospirosis to present as a primary neurological disease. On the other hand, no study has been reported on the progression of cerebral venous thrombosis (CVT) in patients with leptospirosis so far. This is the first case reported which shows CVT as a complication after the leptospirosis infection. An acutely developed leptospirosis and post-infectious CVT in a 21-year-old soldier is described here.     

高分辨率核磁黑血成像技术评估颅内静脉及静脉窦血栓形成病程分期的价值

目的应用高分辨率MR黑血血栓成像(BTI)技术评价颅内静脉及静脉窦血栓形成(CVT)在病程分期中的价值。方法前瞻性纳入2015年6月至2016年10月首都医科大学宣武医院37例常规影像学检查确诊为CVT的患者,均另行BTI检查。根据临床症状出现至BTI检查时间,将患者分为急性组(≤14 d,23例)和慢性组(15 d,14例)。测量BTI图像上检测到的血栓信号噪声比(SNR)和对比噪声比(CNR),比较两组血栓信号的差异。以MR静脉成像(MRV)检查结果作为参照,计算血管节段水平BTI诊断的准确性。结果 (1)血栓SNR在急性组和慢性组分别为206±97和94±41,CNR为201±96和86±40,两组比较差异有统计学意义(t值分别为4.9和5.0,均P0.01)。(2)37例CVT患者中,MRV共检出159处脑静脉及静脉窦节段存在血栓,BTI在其中152处准确识别血栓,在352处排除血栓,诊断敏感度和特异度分别为95.6%(152/159)和98.0%(352/359)。结论 BTI技术实现脑静脉血栓直接成像,能够准确区分急性与慢性血栓,具有较高准确性。     

Reversed circulation as a possible method of preventing intra-cerebral hemorrhages (experimental study)

Possibilities of reversed cerebral circulation, with arterial blood coming to cerebral tissue through the venous network and venous blood going through the arteries, were examined in acute and chronic experiments in dogs. Arterial blood pressure in cephalic veins reached 70-120 mm Hg, venous blood pressure in the circle of Willis was 5-35 mm Hg. Liquor pressure was never beyond 20-35 mm Hg. The EEG and reflex responses of the cerebral trunk were maintained for scores of minutes under acute experiment. Animals, surviving after prolonged arterialization of the cerebral venous network in chronic experiments (3-4 days), showed no central nervous or behavior disorders.     

Association of the protein C promoter CG haplotype and the factor II G20210A mutation is a risk factor for cerebral venous thrombosis.

The factor II G20210A mutation and estrogen treatment are described as risk factors for cerebral venous thrombosis (CVT). We evaluated these known risk factors in a population of CVT patients and investigated the role of a combination of two polymorphisms in the promoter of the protein C gene (PC promoter CG haplotype), newly described as risk factors for deep venous thrombosis. A retrospective population of 26 CVT patients was compared with a control group of 84 healthy volunteers. After a multivariate analysis, we confirmed that the factor II G20210A mutation is an independent risk factor for CVT with odds ratio 4.7 (95% confidence interval, 2.83--75.3). We demonstrated that the CVT risk is increased when this mutation is associated either with the PC promoter CG haplotype (odds ratio=19.8; 95% confidence interval, 2.1--186.5) or, in females, with an estrogen treatment (odds ratio=24; 95% confidence interval, 2.26--127.3). In this work, the association of the factor II G20210A mutation and the PC promoter CG haplotype or estrogen treatment seems to be a particular risk for CVT.     

脑静脉窦血栓形成的临床特征和诊断

目的 评价脑静脉窦血栓形成（ＣＶＴ）的临床特征及影像诊断。方法 详细分析６５例ＣＶＴ患者的临床表现及影像学特征。结果 大多数病人表现有头痛、视乳头水肿等颅内压增高征象（９１％）。近半数病人（４９％）伴有局灶神经功能异常如肢体无力、癫痫发作、视力下降等,５１％的病人仅表现为单纯颅内压增高,磁共振成像（ＭＲＩ）和磁共振血和成（ＭＲＡ）能直接显示肺静脉窦闭塞及其血栓栓子。结论ＭＲＩ和ＭＲＡ对脑静脉０窦血     

Sympathetic modulation of hypercapnic cerebral vasodilation in dogs.

We measured cerebral blood flow using both the radioactive microsphere technique and the cerebral venous outflow technique in dogs anesthetized with chloralase. The effect of sympathetic stimulation on cerebral blood flow was observed during both normocapnia and prolonged hypercapnia using both blood flow techniques. The increase in blood flow with hypercapnia was the same with both methods. During hypercapnia the venous outflow method showed a 38% decrease and microspheres an 18% decrease in cerebral blood flow with sympathetic stimulation. At normal CO2, stimulation caused a decrease in cerebral venous flow: no change was observed with the microsphere method. Analysis of the blood flow patterns to extracerebral tissues and evaluation of extracerebral arterial reference samples failed to prove the existence of axial streaming and subsequent skimming of microspheres within the cephalic circulation. It is concluded that direct electrical stimulation of the sympathetic innervation of the cerebral vessels is capable of reducing cerebral blood flow even during a profound hypercapnic vasodilation.     

Cerebral venous thrombosis in COVID-19

Background and aimsInitially, novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) was considered primarily a respiratory pathogen. However, with time it has behaved as a virus with the potential to cause multi-system involvement, including neurological manifestations. Cerebral venous sinus thrombosis (CVT) has increasingly been reported in association with coronavirus infectious disease of 2019 (COVID-19). Here, we have shed light upon CVT and its possible mechanisms in the backdrop of the ongoing COVID-19 pandemic.MethodsIn this review, data were collected from PubMed, EMBASE and Web of Science, until March 30, 2021, using pre-specified searching strategies. The search strategy consisted of a variation of keywords of relevant medical subject headings and keywords, including “COVID-19”, “SARS-CoV-2”, “coronavirus”, and “cerebral venous sinus thrombosis”.ResultsCOVID-19 has a causal association with a plethora of neurological, neuropsychiatric and psychological effects. CVT has gained particular importance in this regard. The known hypercoagulable state in SARS-CoV-2 infection is thought to be the main mechanism in COVID-19 related CVT. Other plausible mechanisms may include vascular endothelial dysfunction and altered flow dynamics.ConclusionsAlthough there are no specific clinical characteristics, insidious or acute onset headache, seizures, stroke-like, or encephalopathy symptoms in a patient with, or who has suffered COVID-19, should prompt the attending physician to investigate for CVT. The treatment of COVID-19 associated CVT does not differ radically from the therapy of CVT without the infection, i.e. urgent initiation of parenteral unfractionated heparin or low molecular weight heparin followed by conventional or mostly newer oral anticoagulants.