低颅压综合征合并颅内静脉血栓形成1例及文献回顾

目的 总结分析低颅压综合征合并颅内静脉系统血栓形成的临床特征、诊断方法及治疗原则.方法 报道1例低颅压综合征合并颅内静脉系统血栓形成病例,并复习相关文献.结果 患者以体位性头痛起病,经腰椎穿刺及影像学检查诊断为低颅压综合征,继发硬膜下积液及颅内静脉系统血栓形成.头颅CT、MRI均可提供低颅压综合征的表现,MRV及全脑血管造影术(DSA)是静脉系统血栓形成的重要诊断手段.结论 低颅压综合征是静脉系统血栓形成的危险因素之一,了解两者的临床特征有利于早期诊断及治疗.     

低颅压综合征伴发颅内静脉窦血栓形成1例报告及文献复习

颅内静脉窦血栓形成(cerebral venous thrombosis,CVT)的病例报道在国内外相关文献中已屡见不鲜,而低颅压综合征(spontaneous intracranial hypotension,SIH)伴发CVT的病例报道尚不足10例。现将我科收治的1例SIH伴发CVT临床资料分析报道如下。     

自发性低颅压并发静脉血栓形成和出血性梗死一例临床分析

目的自发性低颅压(SIH)多以与体位相关的剧烈头痛为主要症状,误诊率高。SIH并发静脉和(或)静脉窦血栓形成非常罕见。方法我们报道1例SIH并发静脉血栓形成和出血性梗死的患者,并复习相关文献。结果本例患者自发性低颅压在前,静脉血栓形成和出血性梗死在后,同时经过检查排除了其他可导致静脉血栓形成的危险因素。所以我们考虑SIH是静脉血栓形成的危险因素。假如SIH患者与体位相关的间断的头痛变成持续性头痛时,应考虑到有静脉血栓形成的可能。结论因为SIH的患者有形成硬膜下血肿的风险,所以对于静脉血栓形成的抗凝治疗应谨慎。     

低颅压综合征合并孤立皮质静脉血栓形成1例

低颅压综合征和脑静脉系统血栓形成均是发病率较低的神经系统疾病,而孤立皮质静脉血栓形成发病率仅占全部脑静脉系统血栓形成的5％左右,低颅压综合征合并孤立皮质静脉血栓形成的病例在临床十分罕见.现报道1例确诊为低颅压综合征的患者,并发孤立皮质静脉血栓形成及癫痫发作,予补液、抗凝、抗癫痫治疗后症状好转.同时结合相关文献进行复习、...     

肾病综合征并发颅内皮质静脉血栓1例报告

颅内静脉系统血栓(cerebral vein and sinus thrombosis,CVT)是指颅内静脉窦和(或)静脉的血栓形成,从而引起静脉回流障碍、脑组织瘀血、水肿及颅内压增高的一种脑血管疾病。其症状与体征缺乏特异性,极易漏诊和误诊,影响预后。因此,早期诊断和治疗极为重要。现将1例影像学表现不典型的肾病综合征并发的颅内皮质静脉血栓报道如下。     

自发性低颅压并发颅内静脉窦血栓形成临床分析

目的 自发性低颅压（spontaneous intracranial hypotension,SIH）及颅内静脉窦血栓形成（cerebralvenous thrombosis,CVT）均为神经科少见疾病,而SIH合并CVT更为少见,本研究旨在探寻二者之间有无内在联系。方法 报道2例SIH并发CVT的临床资料,并复习相关文献。结果 2例患者SIH在前,CVT发生在后,同时排除了其他导致静脉窦血栓的危险因素,因此推测SIH也是CVT的危险因素之一。经补液纠正低颅压后,静脉窦血栓也随之好转。结论 SIH可能导致CVT,这一观点也被相关文献所证实。     

单发和多发脑静脉血栓形成的临床特征分析

目的 探讨单发和多发脑静脉血栓形成(CVT)患者的临床特征和短期预后. 方法 总结分析136例CVT患者的血栓部位及受累静脉窦/静脉数目,依受累颅内静脉窦/静脉数目将患者分为单发CVT组和多发CVT组,采用单变量分析比较2组患者的临床特点及预后. 结果 单发CVT组44例,多发CVT组92例(其中累及2个部位45例,3个部位35例,4个部位9例,5个部位3例).最常受累的静脉窦/静脉为横窦/乙状窦(86.8%),其后依次为上矢状窦(58.1%)、直窦(18.4%)、大脑深静脉系统(7.4%)和皮层静脉系统(2.9%).单变量分析显示单发CVT组患者平均发病年龄大于多发CVT组,但短期预后好于多发CVT组,比较差异有统计学意义(P＜0.05);多发CVT组患者出现颅内实质病变及合并颅外静脉血栓的几率高于单发CVT组,同时治疗前颅内压≥300mm H2O的患者比例高于单发CVT组,比较差异有统计学意义(P＜0.05). 结论 CVT中以多发CVT所占比例较高,最容易受累的部位为横窦/乙状窦和上矢状窦.与单发CVT相比,多发CVT患者颅内压较高,多合并颅外静脉血栓,出现静脉性脑梗死和脑出血的几率较高,临床病情重,预后相对较差.     

自发性低颅压综合征与肥厚性硬脑膜炎的临床及影像学对比分析

目的探讨自发性低颅压综合征(SIH)与肥厚性硬脑膜炎(HCP)的临床及影像学特点,以提高诊断及鉴别能力。方法回顾性分析20例SIH患者及6例HCP患者的临床及影像学资料并进行对比。结果两组患者均以头痛为主要临床表现,SIH患者的头痛多与体位改变有关,脑脊液压力明显低于正常,HCP患者除头痛之外,多组颅神经损害较SIH更为常见。影像学上两组均可表现为硬脑膜弥漫性增厚并异常强化,但HCP硬脑膜强化可为局限性,部分病例可见邻近部位感染灶,而SIH可出现硬膜下积液。结论自发性低颅压综合征与肥厚性硬脑膜炎有一定的相似之处,但在临床及影像学上均有各自的特点,应注意鉴别。     

甲状腺功能亢进合并颅内静脉窦血栓的研究进展

颅内静脉血栓形成（cerebral venous thrombosis,CVT）是指由各种病因引起的颅内静脉或静脉窦血栓形成,使血液回流受阻或脑脊液循环障碍,致使颅内高压和局灶脑损害为特征的脑血管病中的一类。如今国内外关于甲状腺功能亢进合并CVT的病例报道及研究日益增多。甲状腺功能亢进与CVT的联系越来越紧密。因此,现就对甲状腺功能亢进合并CVT的发病机制、诊断、治疗及相关研究进展等归纳总结,加深临床医生对甲状腺功能亢进合并CVT的认识。     

11例颅内静脉血栓形成的临床诊断及治疗转归分析

目的 总结分析颅内静脉血栓形成的临床表现、影像学特征及治疗方法,为该疾病的诊断和治疗提供参考. 方法 对自2002年至2007年湘雅医院神经内科收治的11例颅内静脉血栓形成患者的临床表现、实验室资料、影像学特征、治疗经过及预后进行回顾性分析. 结果 10例患者临床表现为非特异性的头痛,其次为呕吐、肢体偏瘫、脑膜刺激征、抽搐等.确诊前有2例曾分别诊断为脑出血、蛛网膜下腔出血.11例患者均行头颅CT和(或)MRI,8例行MRV检查,1例行DSA,明确诊断为静脉血栓形成者10例.所有患者均行降颅压治疗,10例患者进行抗凝/抗血小板治疗,9例好转,1例加重,1例死亡. 结论 颅内静脉血栓形成l临床表现缺乏特异性,误诊率高,确诊有赖于影像学检查,早期抗凝治疗是一种安全有效的方法.     

Superior sagittal sinus thrombosis as a rare complication of spontaneous intracranial hypotension syndrome: a case report and review of the literature

In addition to an orthostatic headache, spontaneous intracranial hypotension syndrome can lead to subdural hematoma and diffusion, subarachnoid hemorrhage, and brain sag. However, cerebral venous sinus thrombosis is rarely reported in patients with spontaneous intracranial hypotension. We present the case of a 35-year-old male who developed an orthostatic headache, nausea, vomiting, and photophobia for 5 days. An enhanced brain magnetic resonance image showed extensive linear pachymeningeal enhancement in the bilateral cerebral hemispheres. Lumbar puncture showed that cerebrospinal fluid pressure was 80 mmH₂O. Subsequent magnetic resonance scans demonstrated subdural effusion of the bilateral frontoparietal lobes, hyperintense T1-weighted images, and T2WI lesions within the superior sagittal sinus in 17?days. The patient was given low molecular weight heparin and adverse events occurred. Head computed tomography showed cerebral external fluid accumulation in the bilateral frontoparietal lobes. Then, digital subtraction angiography was performed at 22?days, which confirmed superior sagittal sinus thrombosis, and the patient recovered fully after therapy. The evolution of the disease and radiological findings support the diagnosis of spontaneous intracranial hypotension with superior sagittal sinus thrombosis. To the best of our knowledge, there are very few case reports describing superior sagittal sinus thrombosis as a complication of spontaneous intracranial hypotension. When spontaneous intracranial hypotension and cerebral venous thrombosis occur together, difficult practical questions arise regarding the treatment of these two conditions.     

Cerebral sinus venous thrombosis in two patients with spontaneous intracranial hypotension

We report 2 patients who had clinical and neuroimaging signs of spontaneous intracranial hypotension and who developed cerebral sinus venous thrombosis. This sequence of events -- known after dural puncture but not in spontaneous intracranial hypotension -- was suggested by the change in the pattern of headache, from a postural to a permanent and increasing one. The diagnostic and therapeutic difficulties that this complication raises are discussed.     

Subdural hematoma in a patient with spontaneous intracranial hypotension and cerebral venous thrombosis

We report a patient with clinical and neuroimaging findings of spontaneous intracranial hypotension (SIH) who developed cerebral venous thrombosis (CVT). An association between SIH and CVT has rarely been observed. Anticoagulation therapy was administered. The clinical course was subsequently complicated by a large subdural hematoma that required neurosurgical evacuation. The present report indicates that SIH should not be always considered a benign condition, especially when associated with CVT and subdural fluid collections. Furthermore, clinicians should be aware of the potential risks of anticoagulant therapy in patients with SIH and CVT.     

Alterations in the cerebral venous circulation as a cause of headache

The alterations of the cerebral venous circulation are a rare but clinically important cause of headache. Although any process involving the cerebral veins or sinuses may cause headache, the most frequent and important are cerebral venous thrombosis and idiopathic intracranial hypertension. The headache of cerebral venous thrombosis does not have specific features and may be isolated; therefore, all patients with headache and risk factors for venous thrombosis should undergo the appropriate neuroradiologic examinations to rule out the diagnosis. In fact, early anticoagulant treatment may dramatically change the clinical outcome. Also idiopathic intracranial hypertension, if untreated, may have serious clinical consequences such as permanent visual loss. The pathogenesis of this disorder has not been clearly established and several possibilities involving the cerebral circulation are discussed.     

Alterations in the cerebral venous circulation as a cause of headache

The alterations of the cerebral venous circulation are a rare but clinically important cause of headache. Although any process involving the cerebral veins or sinuses may cause headache, the most frequent and important are cerebral venous thrombosis and idiopathic intracranial hypertension. The headache of cerebral venous thrombosis does not have specific features and may be isolated; therefore, all patients with headache and risk factors for venous thrombosis should undergo the appropriate neuroradiologic examinations to rule out the diagnosis. In fact, early anticoagulant treatment may dramatically change the clinical outcome. Also idiopathic intracranial hypertension, if untreated, may have serious clinical consequences such as permanent visual loss. The pathogenesis of this disorder has not been clearly established and several possibilities involving the cerebral circulation are discussed.     

Cough headache secondary to spontaneous intracranial hypotension complicated by cerebral venous thrombosis

Cough headache may be the clinical manifestation, sometimes isolated, of an intracranial disease. There are several possible causes of secondary cough headache. The hypothesis that cough headache may be the expression of spontaneous intracranial hypotension has been advanced only recently. In fact, this would represent an exception to the rule that cough headache is generally secondary to conditions leading to an increase in intracranial pressure and/or volume. We report and discuss a case of cough headache secondary to spontaneous intracranial hypotension in an otherwise healthy 59-year-old man. The condition was complicated by cerebral venous thrombosis.     

Thunderclap headache

Thunderclap headache (TCH) is head pain that begins suddenly and is severe at onset. TCH might be the first sign of subarachnoid haemorrhage, unruptured intracranial aneurysm, cerebral venous sinus thrombosis, cervical artery dissection, acute hypertensive crisis, spontaneous intracranial hypotension, ischaemic stroke, retroclival haematoma, pituitary apoplexy, third ventricle colloid cyst, and intracranial infection. Primary thunderclap headache is diagnosed when no underlying cause is discovered. Patients with TCH who have evidence of reversible, segmental, cerebral vasoconstriction of circle of Willis arteries and normal or near-normal results on cerebrospinal fluid assessment are thought to have reversible cerebral vasoconstriction syndrome. Herein, we discuss the differential diagnosis of TCH, diagnostic criteria for the primary disorder, and proper assessment of patients. We also offer pathophysiological considerations for primary TCH.