Sequential magnetic resonance images of a case of cerebral sinus thrombosis--imaging of the thrombosed sinus and its recanalization

Magnetic resonance images of a case of superior sagittal sinus thrombosis before and after complete recanalization are presented. The patient was a 61-year-old man with two days history of intermittent right hemiconvulsion followed by post-ictal hemiplegia. Mild erythrocytosis was noted on admission. CT scans revealed left frontal hemorrhagic infarction with empty delta sign in the middle portion of the superior sagittal sinus. Left carotid angiogram showed occlusion of two frontal cortical veins and retrograde filling of these veins into the cavernous sinus. Lack of filling of the middle and anterior part of the superior sagittal sinus was noted. These studies led to the diagnosis of superior sagittal sinus thrombosis associated with hemorrhagic infarction. He was treated with intravenous infusion of low molecular dextran and venesection. Neither heparin, urokinase, hyperosmolar solutions nor steroids were used because of the presence of hemorrhagic infarction and of the lack of signs of increased intracranial pressure. He completely recovered neurologically and recanalization of the superior sagittal sinus was confirmed angiographically eight weeks after the onset. Magnetic resonance images were taken with a Siemens 1.5 T Magnetom scanner using spin-echo pulse sequences. A T 1-weighted mid-sagittal magnetic resonance image ten days after the onset showed hyperintensity in the middle part of the superior sagittal sinus which corresponded to the thrombus. Both T 1 and T 2 weighted coronal images revealed a small area of hypointensity indicating the existence of residual blood flow in the superior sagittal sinus in addition to the thrombus both in the sinus and in the cortical vein.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic superior sagittal sinus thrombosis with phlebosclerotic changes of the subarachnoid and intracerebral veins

An autopsy case of chronic thrombotic occlusion of the superior sagittal sinus (SSS) with an unusually protracted clinical course is reported. The patient was an 84‐year‐old man without any predisposing conditions for thrombosis. The clinical features were atypical and were characterized by recurrent cerebral subcortical hemorrhages. The autopsy revealed a large, organized thrombus in the SSS and extensive hemorrhagic infarction of the bilateral parasagittal region of the cerebral hemispheres. The hemorrhagic infarction was comprised of the aggregation of numerous minute foci of coagulation necrosis associated with petechial hemorrhages. Marked phlebosclerotic changes were observed in the subarachnoid and intracerebral veins, which were considered to be reactive changes of the venous walls against a persistent elevation in peripheral venous pressure caused by thrombosis of the SSS.     

A case of cerebral deep venous and venous sinus thromboses with anti-cardiolipin antibody]

We describe a case of cerebral deep venous and venous sinus thromboses with anti-cardiolipin antibody. A 62-year-old male with no previous illness of thrombosis but with alcohol abuse was admitted with acute onset unconsciousness. He recovered two days after with no severe sequela. Laboratory findings suggested the preceding conditions of dehydration and inflammation. X-ray CT of the head revealed symmetrical low density areas in the thalami and basal ganglia, high density signs in the cerebral deep veins, and dilation of the lateral ventricles. MRI on the second hospital day showed abnormal intensities in the thalami and basal ganglia (high signal on T 2-weighed and FLAIR image, low signals on T 1-weighed image, but almost isointensity on diffusion weighed image) and acute to subacute phase thrombus in the superior sagittal sinus. Abnormal intensities observed on MRI disappeared gradually in the following studies. Venous phase images of cerebral angiography performed in chronic phase disclosed occlusion of the superior sagittal sinus and stenosis of the vein of Galen. These radiological findings support the diagnosis of cerebral deep vein and venous sinus thromboses. Hematological examination revealed positive anti-cardiolipin IgG antibody. Several cases of cerebral deep venous thrombosis with anti-cardiolipin antibody have been reported. In our case, dehydration induced by alcohol abuse would have been the trigger of thrombosis, while the existence of anti-cardiolipin antibody might contribute to the risk of thrombosis as an underlying condition.     

MRI和MRV在脑静脉和静脉窦血栓诊断中的价值

目的探讨MRI和MRV对脑静脉和静脉窦血栓(CVST)形成的诊断价值。方法回顾性分析16例CVST患者的临床和影像学资料。结果受累的脑静脉和静脉窦有上矢状窦9例,横窦5例,直窦3例,乙状窦2例,大脑大静脉合并大脑内静脉2例。常规MRI可见受累静脉窦流空信号消失,静脉窦内信号高低不一,11例脑实质内出现静脉性脑梗死表现,其中4例合并出血。增强扫描15例静脉窦内出现充盈缺损及静脉窦壁强化表现,9例脑实质内出现脑回样强化。MRV表现为受累静脉窦部分或广泛高血流信号缺失、狭窄。结论MRI和MRV是诊断和随访CVST形成的最佳检查方法。     

Superior sagittal sinus thrombosis as first manifestation of essential thrombocythemia]

A 52-year-old previously healthy woman was admitted to our hospital for status epilepticus in November 1999. She had not taken oral contraceptives. After treatment with intravenous diazepam and phenytoin, she did not develop seizures anymore. When she became alert, there was a mild left hemiparesis. Lumbar puncture showed an opening pressure of 145 mm H2O, and the cerebrospinal fluid was acellular. Cranial MR imaging demonstrated thrombosis of the superior sagittal sinus and fresh infarction in the right frontal lobe. Plasma fibrinogen, fibrin degradation product, and prothrombin fragment 1 + 2 levels were elevated. Proteins S and C activities and anti-thrombin III levels were within the normal range. Lupus anticoagulant and anti-cardiolipin antibody were negative. She was treated with continuous heparin infusion for ten days and with oral warfarin thereafter. Six months after the first admission, platelet count became more than 400 x 10(3)/microliter. In July 2002, she developed slowly progressive monoplegia of the left arm. Cranial MR imaging demonstrated patent superior sagittal sinus, fresh infarction in the right parietal lobe, and old small infarction in the right corona radiata. The patient was maintained on warfarin and 100 mg of aspirin thereafter. In September 2002, platelet count was 737 x 10(3)/microliter. Bone marrow examination showed increased megakaryopoiesis with normal erythroid and myeloid series and no chromosomal aberrations. Serum C-reactive protein and iron levels were in the normal range. An abdominal ultrasound demonstrated mild splenomegaly. Thus, we made a diagnosis of essential thrombocythemia (ET). ET causes thrombotic events in the course of the disease at a rate of 7% per year. Cerebral infarction is not uncommon, but occurrence of cerebral sinus thrombosis has been rarely reported. Recently, several cases have been reported in which cerebral infarction was the first manifestation of ET even with platelet counts lower than 600 x 10(3)/microliter. To our knowledge, there have been no reported cases of ET presenting with cerebral venous sinus thrombosis. Platelet count should be monitored in the patients with venous sinus thrombosis of undetermined etiology.     

Cerebral cortical and deep venous thrombosis without sinus thrombosis: clinical MRI correlates

BACKGROUND: Cortical and/or deep vein thrombosis (CDVT) without dural sinus involvement is uncommon and presents diagnostic difficulty for many reasons. Our aim is to determine the relationship between magnetic resonance imaging (MRI) findings and clinical findings in patients with CDVT. METHODS: Forty-six patients with venous stroke proved on MRI included in our Registry, corresponding to 0.1% of 4650 patients with stroke, were studied. Magnetic resonance angiography (MRA) was performed in all patients, and 18 of them had follow-up MRA. Outcome was evaluated by using the Glasgow Outcome Scale at the time of discharge and during follow-up. RESULTS: Thirty-two patients presented cortical venous stroke; 21 of them had involvement of the dorsomedial venous system, six had a defect in the posteroinferior venous group, and five had a defect in the anteroinferior venous group. Thirteen patients presented simultaneous involvement of the superficial and deep venous system; seven with a defect in the parietal and internal cerebral veins (three with involvement of vein of Gallen), four with a defect in the temporooccipital (vein of Labbé) and basal vein of Rosenthal, two with a deficit in the anterior frontotemporal and uncal-pterygoid venous system. One patient had deep venous thrombosis primarily localized to the thalami bilaterally and the basal ganglia on the right because of occlusion of the thalamostriate veins. The main presenting symptoms of CDVT were headache, focal neurologic signs, partial complex or secondary generalized seizures, and consciousness disturbances in those with deep venous thrombosis, presented alone or in combination at onset. CDVT was more than twofold more frequent in women than in men. Pregnancy, puerperium, oral contraceptive use, and infections were the most common predisposing factors. CONCLUSION: Computerized tomography, conventional MRI and diffusion-weighted imaging showing ischemic and/or hemorrhagic lesion that does not follow the boundary of classical arterial boundaries without signs of sinus thrombosis, and partial or generalized seizures followed by focal neurologic signs may predict CDVT. The outcome of patients with cortical venous stroke was good, but not in those with cortical plus deep venous infarction.     

颅高压对兔静脉窦血栓后脑梗死的影响

目的利用兔静脉窦血栓的动物模型,观察兔静脉窦血栓后颅内压对脑组织的影响。方法成年健康日本大耳白兔95只,随机分为5组,其中建模成功90只:A、B、C、D组为处理组,均为结扎上矢状窦后1/3及其回流静脉,其中B、C、D组为在结扎基础上分别放置0.2 ml、0.4 ml、0.6 ml的硬膜外球囊,E组为假手术组(6只)。各组均在术后8 h、24 h、48 h观察脑含水量、脑梗死范围及病理变化。结果与E组相比,A、B、C、D组在相应时间点的脑含水量、脑梗死范围均明显增加,且随着颅内压增高呈增高趋势。结论在兔静脉窦血栓模型中,颅内压增高可加重脑水肿的程度和增加脑梗死的范围,解除颅内高压则可减轻脑水肿和脑梗死范围。     

Cerebral venous infarction following thrombosis of the draining vein of a venous angioma (developmental abnormality)

We report two cases of cerebral venous angioma presenting as venous infarction, one in the left parietal lobe, the other in the left frontal lobe. Cerebral imaging demonstrated thrombotic occlusion of the draining vein of the venous angioma associated in the latter case with thrombosis of the anterior part of the superior longitudinal sinus. Both patients were free of coagulopathy. They were treated with anticoagulant therapy. One completely recovered, while the other was left with slight residual disability. Thrombosis of the draining vein has been reported in only 6 previous cases, of whom only 2 received anticoagulant therapy. Discovery of a venous angioma in the diagnostic workup of a patient with recent neurological disorders should raise the question of a possible occlusion of the draining vein and lead to an appropriate therapy.     

Evolution of venous cerebral infarction and brain edema--an experimental study of sagittal sinus obstruction

Superior sagittal sinus with/without neighboring venous system of 36 mongrel cats were occluded by cyanoacrylate polymer after i.v. administration of Evans-blue (EB). Thereafter, the cats were sacrificed 1, 3, 6, 12, 24, 72 or 120 hours after sinus-vein occlusion. According to the degree of occluded region, the cats were divided into two groups; group A (GA) and B (GB). GA showed only superior sagittal sinus occlusion, while many cortical veins were also occluded in GB. No EB nor histological changes were found in 13 cats of GA and 4 sham operated cats, while EB distribution was observed in all 20 cats of GB. The other 3 cats of GA showed a little EB in gyrus lateralis. EB distribution of GB were divided into two types. Type 1 showed EB mainly in the cortical gray matter, while type 2 showed massive EB extravasation in the white matter as well. Edematous changes with gliosis in its resolution phase, were observed in type 1. In addition, EB free zone was formed along with U-fiber zone (cortico-medullary junction) in the cats of later phase (72 hours after occlusion). The findings of EB extension in the type 1 means the existence of blockage against edema evolution from cortex toward subcortical white matter. The cats of type 2 showed fulminant hemorrhagic changes which appeared depend on time interval. Although occurrence of pathological changes were rather earlier than that of cases of clinical cerebral sinus thrombosis, this pathological findings demonstrated the typical character of venous hemorrhagic infarction. In this paper, the similarity and difference between this model and clinical case of sinus-vein thrombosis were discussed. And the possible function of the U-fiber zone in the corticomedullary junction against edema evolution was suggested.     

Bilateral basal ganglia infarction following resection of a right parietal parasagittal dural tumour requiring sinus repair -- an atypical complication of an atypical venous drainage

The case of a 68-year old woman who underwent surgery for a right parietal parasagittal dural tumour is reported. In the preoperative angiography the straight sinus failed to show. During tumour resection the lateral wall of the parietal superior sagittal sinus was opened and reconstructed. Postoperatively, the patient remained unresponsive. A computerized tomography scan revealed bilateral infarction of the basal ganglia. Angiography showed an occlusion of the superior sagittal sinus with hypervolaemia of the deep venous system. The patient did not recover. We conclude that patency of the superficial venous drainage system can be mandatory for drainage of the basal ganglia in cases with deep venous obstruction. To our knowledge, this is an extremely rare complication of neurosurgery in cortical supratentorial areas.     

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.     

Evolution of angiographic signs of venous hypertension and clinical signs of intracranial hypertension in intracranial dural arteriovenous fistulas]

Dural arteriovenous fistulas (dAVFs) can cause cerebral venous hypertension (VHT). The most common mechanism is due to the fact that some dAVFs can drain retrogradelly in cortical (better defined as leptomeningeal) veins (directly or after drainage in a dural sinus) causing venous engorgement and consequently an impairment of the cerebral venous drainage. However, more rarely, dAVFs without a cortical venous drainage can also be responsible for VHT probably due to dAVF shunts causing insufficient antegrade cerebral venous drainage. In addition, dAVFs are often associated with stenosis and/or thrombosis of dural sinus(es) which can worsen the VHT. Raised pressure within the superior sagittal sinus causes impeded cerebrospinal reabsorption in the arachnoid villi allowing increased intracranial pressure. The venous engorgement in the cortical veins can cause a venous congestive encephalopathy analogous to the venous congestive myelopathy of the spinal dural AVFs. Clinically VHT can cause not only symptoms related to increased intracranial pressure but also seizures, neurological deficits, impairment of the cognitive functions and dementia. An important aspect is the risk of hemorrhage in dAVFs with a leptomeningeal venous drainage leading to VHT. Although the term VHT sensu strictu should be used if venous pressure measurements are performed, angiographic criteria for VHT such as delayed circulation time, venous engorgement and abnormal visualization of the cerebral veins are well established. The purpose of our study was to evaluate the angiographic signs of VHT in patients with dAVF and to study the course of the VHT and of the clinical signs of increased intracranial pressure before and after dAVF endovascular treatment. A retrospective chart analysis of 22 patients (13 males, 9 females) ranging in age from 20 to 87 years (mean: 53 ys.) with a dAVF associated with angiographic signs of VHT was performed. Ten dAVFs were located on the transverse/sigmoid sinus(es), 6 on the superior sagittal sinus, 3 on the petro-tentorial incisura, 1 on the inferior petrosal sinus, 1 on the anterior ethmoidal region and 1 on the Galen vein region. All dAVFs had a retrograde leptomeningeal venous drainage. Stenosis or thrombosis of the dural AVF sinus was observed in 17 cases and stenosis or thrombosis of another sinus(es) and/or of the jugular vein in 8 cases. In 11 patients, the angiographic signs of VHT were global affecting the entire cerebral venous drainage and, in the other 11 patients, the VHT was focal. The VHT caused clinical symptoms of increased intracranial pressure in 18 patients. Other clinical findings included: bruit (11 cases), seizures (3 cases), vertigo (3 cases), visual deficits (2 cases) and impairment of cognitive functions (4 cases). Three patients presented hemorrhage (one parenchymal hematoma, one hemorrhagic infarction and one subarachnoid hemorrhage). The 4 patients without clinical symptoms of increased intracranial pressure presented only bruit in 2 cases, bruit and vertigo in 1 case, bruit and hemorrhagic infarction in another one. The dAVFs were treated by endovascular therapy (arterial approach: 3 cases, venous approach: 6 cases and both arterial and venous approach: 13 cases). Endovascular sessions ranged from 1 to 7 (mean: 2.8) for each patient. After the endovascular treatment, in 12 patients with complete occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cure were observed. In 8 patients with partial occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cure were observed in 4 cases (almost complete dAVF occlusion in 2 cases); in the other 4 cases, only reduction the angiographic signs of VHT and clinical improvement were obtained. In all 16 patients who were clinically cured angiographic signs of VHT disappeared despite the persistence of dAVF shunts as observed in 4 cases. (ABSTRACT TRUNCATED)     

Thrombus propagation and venous drainage disturbance in cerebral sinus-vein thrombosis--38 autopsied cerebral sinus-vein thrombosis

38 autopsied cases of cerebral sinus-vein thrombosis (CSVT) in our institute were studied. In this study, special attention was paid for the evolution and fate of venous thrombus. 18 cases showed hemorrhagic infarction or intracerebral hematoma (group 1; G 1). In contrast, no cerebral parenchymal changes were observed in the other 20 cases (group 2; G 2). In 13 of 18 cases of G 1, superior sagittal sinus (SSS) were thrombosed. 10 of these 13 cases showed thrombosed cerebral cortical veins (CV) or deep cerebral veins (DV). In contrast, none of 16 cases of G 1 with thrombosed SSS showed thrombosed CV or DV. All cases of the solitary thrombosis of CV or DV (each 2 cases) belong to G 1. Venous thrombi were divided into three stages according to its process of organization; recent thrombus (R), hyalinized thrombus (H), organized thrombus (O). In the venous thrombi of G 1, 6 cases were R, 6 were partly H, 6 were partly 0. In addition to O, R and H were also observed in group O. Distribution of various stage of thrombus in same case suggested that gradual thrombus evolution had occurred before or after the clinical onset in CSVT. This study suggested: (1) CV or DV occlusion may play an important role for the advent of cerebral parenchymal changes in CSVT. (2) Gradual thrombus evolution after the onset is one of possible causes of slow clinical deteoration after the onset. Therefore, prevention of these thrombus propagation with anti-platelet drugs or fibrinolotic therapy should be recommended for the treatment of CSVT. On the contrary, hyperosmolar agents and diuretics may produce potential risk of dehydration, and as a result, accelerate secondary thrombus extension.     

脑静脉系统血栓形成的临床特点

目的探讨脑静脉血栓形成(CVT)的临床特点。方法回顾性分析27例CVT患者的临床资料。结果本组患者中25例有发病诱因(包括妊娠或产褥期18例,高热、腹泻5例等),平均年龄(29.7±9.3)岁;多以急性(7例,25.9%)、亚急性(19例,70.4%)起病。以头痛为首发症状23例(91.7%),伴呕吐21例,12例出现意识障碍,均出现不同部位的神经功能缺损表现。腰穿CSF压力增高21例。血常规检查异常22例(81.5%),凝血功能异常13例(48.2%)。影像学检查[CT、MRI、MR静脉血管成像(MRV)]显示,均有不同程度的颅内静脉或静脉窦受累,其中上矢状窦受累最多(77.8%)。24例采用肝素抗凝治疗,2例用溶栓治疗。17例痊愈,4例好转,6例死亡(其中4例并发出血性梗死,2例伴大脑大静脉血栓形成)。结论 CVT继发于循环血液不足及血液高凝状态,以急性或亚急性起病,主要表现为颅内压增高综合征,死亡率较高;MRI和MRA是早期诊断的有效手段,早期肝素抗凝治疗可取得良好疗效。     

脑静脉窦血栓形成的影像学表现及脑实质病变预测

目的总结脑静脉窦血栓形成(CVST)患者的临床和MRI表现特征并探讨继发脑实质病变的预测因素。方法回顾57例CVST患者的临床及头颅MRI资料,分析患者MRI表现特征,并对临床及影像学指标进行对比分析。结果57例患者中男22例,女35例,年龄15~72岁(平均35岁)。临床症状头痛29例,癫痫发作11例,感觉变化8例,局灶性神经功能缺损9例;头颅MRI示静脉窦血栓形成部位上矢状窦9例,横窦2例,乙状窦1例,直窦1例,其中同时累及2个或2个以上静脉窦44例。静脉窦血栓伴发脑实质病变36例,其中出血性静脉梗死20例,非出血性静脉梗死12例,脑实质内出血4例。对伴和不伴脑实质病变2组患者的对比分析显示,伴脑实质病变组女性比例明显高于不伴脑实质病变组;伴脑实质病变组癫痫、感觉异常及局部神经功能缺损症状发生率均明显高于不伴脑实质病变组;伴脑实质病变组直窦血栓的发生率明显高于不伴脑实质病变组(P<0.05)。结论MRI可清楚显示CVST的直接及间接征象,通过分析CVST患者的临床和静脉窦血栓表现特征还可帮助预测严重的脑实质病变发生风险。     

An unusual case of superior sagittal sinus thrombosis accompanied with dural AV fistula]

Benign intracranial hypertension or pseudotumor cerebri is an collective term for a number of diverse syndromes characterized by increased intracranial pressure. Neither intracranial mass nor ventricular dilatation is observed in this disorder. Moreover, the pathogenesis of this syndrome has yet to be determined. We report a case of 36-year-old female diagnosed as benign intracranial hypertension, who has developed superior sagittal sinus thrombosis and dural AV fistula during the follow up period. The patient was pointed out to have papilledema and elevated intracranial pressure six years ago. Although she was examined by both DSA and CT scan, no abnormal intracranial lesions were observed. Consequently, she was diagnosed as the benign intracranial hypertension and had been followed as an out patient. Three years later, lumboperitoneal shunting was performed because of severe headache and visual impairment. Postoperatively, the patient had been well for two years. Recently, occipital headache recurred and she was readmitted to our hospital. MRI studies demonstrated dilated vessels in the right occipital area. Additionally, angiograms revealed not only the superior sagittal sinus thrombosis but also the rich network of dural AV fistula adjacent to the occlusion. According to those results, the superior sagittal sinus was supposed to have the incomplete occlusion or delayed blood flow that were not observed by DSA, MRI and CT scan performed previously. Those occlusive change in the superior sagittal sinus impeded the CSF absorption and elevated the pressure of venous inflow, then the arterio-venous communication has been developed.(ABSTRACT TRUNCATED AT 250 WORDS)     

临时夹闭加促凝法制作颅内静脉窦血栓形成的动物模型研究

目的探讨临时夹闭加促凝法制作颅内静脉窦血栓形成（CVST）的动物模型。方法30只新西兰家兔分为3组：临时夹闭上矢状窦组、结扎静脉窦对照组和假手术对照组,每组10只。临时夹闭上矢状窦组用血管夹夹住家兔上矢状窦的前、后部,注入脑磷酯白陶土悬液促凝．建立CVST的动物模型。结扎静脉窦对照组通过结扎上矢状窦建立CVST模型,假手术对照组不作任何处理。术中监测血压、心率、呼吸,术后检测脑组织含水量、静脉窦的血流速度。结果临时夹闭上矢状窦组家兔上矢状窦夹闭5h后完全栓塞,血流速度为零：在夹闭1h后．该组家兔血压、心率、呼吸均在正常范围内。临时夹闭上矢状窦组和结扎静脉窦对照组的脑组织含水量和基底静脉血流速度,分别与假手术对照组比较,差异均有明显的统计学意义（P〈0．01）,临时夹闭上矢状窦组与结扎静脉窦对照组比较无明显差异（P〉0．05）。结论临时夹闭加促凝法制作CVST模型模拟上矢状窦血栓形成,重复性和稳定性好,可满足CVST实验研究的需要。     

Venous infarction associated with carotid-cavernous fistula]

We report an 88-year-old woman who developed a hemorrhagic venous infarction in the left cerebral hemisphere and brainstem, in association with left carotid-cavernous fistula (CCF). Without aura the patient noticed diplopia due to left abducens palsy, and exophthal mos and congestion of the left eye. Brain CT revealed extrusion of the left eye, and dilatation of left superior orbital vein and cerebral cortical veins. She received diagnosis of CCF. Brain CT also revealed a small mass in the left ethmoidal sinus, which was not attached to the CCF. Biopsy of the mass was done under local anesthesia. On the following she had high fever. Her consciousness level deteriorated and she developed right hemiparesis FLAIR images of MRI showed, extensive high signal lesions in the left frontal and temporal cortices, basal ganglia, thalamus, midbrain and pons. These findings were consisted with venous infarction, possibly associated with peri-operative infection and hypovolemia. Intracranial hemorrhage occur in 3% of cases with CCF, but venous infarction was much rarer. The patients with CCF, who show dilatation of cortical veins in CT or MRI, have a higher risk of cerebral hemorrhage or infarction, and should be carefully observed.     

A case with cerebral thrombosis receiving tamoxifen treatment.

Cerebral sinus thrombosis (CST) is known to be related to a number of underlying aetiologies including otitis media, trauma, pregnancy, birth control pills, tumours, malnutrition, dehydration, haematologic disorders and malignancy (Fishman, 2000; Raizer and Abbott, 2000). We present the case of a patient with breast cancer receiving the antioestrogen drug tamoxifen who developed CST. A 40-year-old female presented as an emergency with a 10-day history of headache and left sided weakness. On questioning her past medical history included a diagnosis of breast cancer 3 years ago treated by radical mastectomy and tamoxifen 20 mg daily. At the time of admission, neurologic examination revealed a mild left sided hemiparesis and a present Babinksi sign. Non-contrast enhanced tomography was normal. Magnetic resonance imaging (MRI) showed thrombosis in the superior sagittal sinus, right lateral sinus and jugular vein in addition venous infarction in the right temporal lobe was present (Figs 1a and b). Routine haematology and biochemistry was normal. Anticoagulation tests, antithrombin III, protein S and C levels were also found to be normal. She was treated with anticoagulation therapy and her hemiparesis improved within 3 days. Control MRI showed the resorption of the venous infarction and resolution of the thrombosis (Fig. 1c).