Thrombosis of the superior cerebral vein with hemorrhagic cerebral infarction--serial MRI and pathological study of a case

We reported an autopsy case of thrombotic occlusion of the superior cerebral vein with hemorrhagic laminar necrosis of the right parietal cortex. A 68-year-old woman was admitted to our hospital because of a severe headache and left hemiplegia of acute onset. There was a past history of hypertension, fever of unknown origin, leukocytopenia and nasal dermatitis. Magnetic resonance images (MRI) disclosed thrombosis of the superior sagittal sinus and of the right parietal cortical vein as well as right parieto-occipital cerebral infarction. Although she improved with mild sequelae, the subsequent MRI showed a recurrent thrombosis of the superior sagittal sinus. Ten months after the onset she died suddenly, presumably due to acute myocardial infarction. Pathologically, thrombotic occlusion of the right parietal cortical vein, recurrent thrombosis of the superior sagittal sinus and old hemorrhagic cortical laminar necrosis of the right parietal region were revealed. Moreover, intracranial arteritis and phlebitis were observed, as well as arteriolitis in the peripheral nerves. In our case, MRI was useful for the diagnosis and following the course of cerebral venous thrombosis. Cerebral noninfective vasculitis may well have caused the venous thrombosis.     

Superior Sagittal Sinus Thrombosis in the Presence of Idiopathic Bilateral Internal Jugular Vein Stenosis

Cerebral venous outflow obstruction and anomalies in cerebral venous circulation predispose to dural sinus thrombosis. This case report illustrates the magnetic resonance and angiographic findings in a patient who had superior sagittal sinus thrombosis secondary to idiopathic bilateral internal jugular vein stenosis, a previously unrecognized entity. The findings suggest that bilateral stenosis of the internal jugular veins at their junction with the innominate veins causes obstruction to cerebral venous outflow leading to dural sinus thrombosis.     

The clinical spectrum of intracerebral hematoma, hemorrhagic infarct, non-hemorrhagic infarct, and non-lesional venous stroke in patients with cerebral sinus-venous thrombosis

Background and purpose: The clinical spectrum of different neuroradiological features of cerebral sinus–venous thrombosis (CSVT) varies considerably. We sought the relationship between different neuroradiological aspects and clinical presentations in these patients. Methods: The diagnosis of cerebral sinus–venous thrombosis has been confirmed by conventional angiography, MRI combined with MR venography following established diagnostic criteria. We analyzed clinical data, symptoms and signs, imaging findings, location and extent of the thrombus, and parenchymal lesions, retrospectively. Results: There were 220 consecutive patients with cerebral sinus–venous thrombosis; 98 (45%) had non‐lesional sinus–venous thrombosis (NL CSVT), 51 (23%) had non‐hemorrhagic infarct (NHI), 45 (20%) had hemorrhagic infarct (HI), and 26 (12%) had intracerebral hemorrhage (ICH). In patients with hemorrhagic lesion (HI+ICH), advanced age, headache (99%), behavioral disturbances (55%), consciousness disturbances (35%), seizures (41%), and language deficits (42%) were significantly higher than the other patients (NL+NHI) (P < 0.001). High blood pressure at admission, puerperium, sigmoid and straight sinus thrombosis, multiple sinus and vein involvement were more frequent in patients with hemorrhagic lesion than those with non‐hemorrhagic lesion. Patients with hemorrhagic lesion were more dependent or died (32%) than the other patients (12%) (P < 0.001), and most of the patients with NL and NHI had no disability compared with the other patients at the 3 month of follow‐up (96% and 65%; P < 0.001). Conclusion: Headache, convulsion, behavioral disorder, seizures, and speech disorders were the most frequent clinical symptoms of patients with hemorrhagic CSVT. Specific risk factors, including pregnancy/puerberium, early and extended thrombosis of large sinus, and presence of high blood pressure at admission, are associated with hemorrhagic lesion and unfavorable outcome.     

Cerebral venous thrombosis with familial antithrombin III deficiency

A case of cerebral venous thrombosis with familial antithrombin III (AT III) deficiency was reported and we discussed the anticoagulant therapy of cerebral venous thrombosis from the viewpoint of AT III. The patient, a 17-year-old boy, was admitted to our clinic with severe bifrontal headache, generalized convulsions and progressive disturbance of consciousness. He developed deep vein thrombosis in his right leg and pulmonary emboli two years earlier when he was placed on heparin and so forth, followed by warfarin sodium. Warfarin was terminated 9 months prior to his recent illness. On neurological examination on admission, he was semicomatous with blurred disc margins, roving eye movements with right abducens nerve palsy, nuchal stiffness and right flaccid hemiplegia. Left carotid angiogram and CT scan revealed extensive superior sagittal sinus thrombosis, complicated with hemorrhagic infarcts in bilateral frontal lobes. When examined for coagulation studies, the patient and his father had decrease in AT III activity and antigen levels. He was treated successfully with antiedematous agents and anticonvulsants during acute phase of illness. He was thereafter placed on warfarin 5-6 mg/day with no further clinical thromboembolic event for 2 years 9 months. There was no neurological abnormality when he was last examined, although he was treated with valproic acid 1,200 mg/day and phenytoin 250 mg/day to control occasional adversive seizures. A coagulation study following infusion of 5,000 units of AT III was carried out. Warfarin was discontinued the day before the study. 0.64 U/kg of AT III administration resulted in a 1% increase in AT III level after the infusion. The biological half life of AT III was 14.4 hours.(ABSTRACT TRUNCATED AT 250 WORDS)     

TCD动态监测静脉窦血栓形成五例

目的评价静脉窦血栓形成患者经颅多普勒超声(TCD)检测静脉侧枝的开放和再通情况以及颅内压变化。方法用TCD 2MHz探头检测5例静脉窦血栓形成患者的颅内静脉的血流速度以及动脉频谱形态的变化。结果 5例静脉窦血栓形成患者的颅内静脉(大脑中深静脉、基底静脉)的血流速度均明显增高(139cm/s,118 cm/s,99 cm/s,103 cm/s,58cm/s),动脉频谱呈高阻力,经过治疗,随着病情的好转,颅内静脉血流速度下降,颅内动脉频谱由高阻力型恢复正常。结论 TCD能可靠无创、准确地检测颅内静脉,在病程中通过多次的TCD检查,可以评价静脉窦血栓形成静脉侧枝的开放和再通情况以及颅内压变化。     

Low-molecular-weight heparin: the optimal duration of prophylaxis against postoperative venous thromboembolism after total hip or knee replacement

Venous thromboembolism is a major health problem. In about 20% of cases, the initial clinical manifestation of venous thromboembolism is sudden death due to pulmonary embolism. Consequently, appropriate prophylaxis is critical in order to improve survival. Because patients with recent surgery have a 22-fold increased risk of postoperative venous thromboembolism, a large research effort has been directed toward identifying the safest and most effective prophylaxis after surgery, especially after total hip or knee replacement. While low-molecular-weight heparin is the most effective prophylaxis currently available, from 15% to 30% of hip or knee replacement patients still develop deep vein thrombosis by the time of hospital discharge, and another 25% develop new deep vein thrombosis by 3 weeks after discharge. Extended out-of-hospital low-molecular-weight heparin prophylaxis can safely reduce the prevalence of deep vein thrombosis by about 50%. However, essentially all of these thrombi are small, asymptomatic, and resolve without serious clinical sequelae. Based on one clinical trial, out-of-hospital low-molecular-weight heparin prophylaxis could reduce the incidence of symptomatic venous thromboembolism or all-cause death after discharge by a maximum of 2.2%. At current drug costs, universal out-of-hospital low-molecular-weight heparin prophylaxis is unlikely to be cost-effective. For most patients, 7 to 10 days of low-molecular-weight heparin prophylaxis is adequate. Future research should be directed at identifying patients at risk for out-of-hospital venous thromboembolism, and targeting extended prophylaxis to those at highest risk.     

Lokale intravenöse Fibrinolyse bei tiefer Hirnvenenthrombose

Acute cerebral vein and dural sinus thrombosis are usually treated with unfractionated intravenous heparin. Progression of symptoms after appropriate heparin dosage appears to be a rare event. In the literature only single case reports or small case series dealing with local intravenous fibrinolysis are available. Here we describe a 44-year-old woman with progressive thrombosis of the sinus rectus and right sinus transversus upon an appropriate dosage of heparin who was successfully treated with urokinase 12 h after symptom onset. This case demonstrates that local thrombolysis should be discussed in patients with progression of the clinical or radiological picture under sufficient heparin therapy.     

Anticoagulant treatment in hemorrhagic brains infarts due to large sinus venous thrombosis

Cerebral venous and sinus thrombosis is an infrequent condition which presents with a wide spectrum of signs and a variable mode of onset. Sinus thrombosis may cause isolated intracranial hypertension but also may cause cerebral venous infarcts, which are frequently hemorrhagic. Treatment with antithrombotic agents is controversial because there is only one randomised controlled trial with unfractionated heparin. We report a 46- years-old man complaining of progressive headache, paraparesis and dysphasia. After admission, his neurological status worsened and he developed tetraparesis, depressed level of consciousness and seizures. A cranial computarized tomography (CT) scan showed multiple hyperdensities suggestive of hemorrhagic infarcts. Magnetic resonance imaging (MRI) study confirmed extensive cerebral venous thrombosis. Unfractionated heparin was administered for two weeks followed by acenocumarol. Within a few days his neurological status improved, and five weeks after admission the patient only hadd slight neurological deficit. After 11 years of follow-up, he has had a complete recovery. The G20210A mutation in the prothrombin gene was detected as a likely risk factor for venous thrombosis. Therapeutical and diagnosis aspects are discussed. We review the previous literature on the topic.     

Cerebral and systemic venous thrombosis associated to prothrombin G20210 mutation: case report

Cerebral venous thrombosis is a clinical condition of difficult diagnosis, and poor prognosis when treatment is not started early. There is a long list of causes, and hereby we describe a case associated to prothrombin G20210 mutation. A 53-year-old man, white, was admitted with status epilepticus. After seizures control, he developed intracranial hypertension, with headache and vomiting, and bilateral papilledema. His past medical and familial history were unremarkable. He was a nonsmoker, no drug and alcohol user. CT scan and MRI showed right temporal and parietal infarct with hemorrhagic transformation. Spinal tap with opening pressure of 500 mmH2O showed normal CSF examination. MRI angiography disclosed superior sinus, right transverse and sigmoid sinus complete thrombosis. He was started with heparin and oral warfarin. In spite of anticoagulation, two months later he developed deep right inferior limb thrombosis. All the initial tests were normal, and test for prothrombin G20210 mutation was positive. He needed a much higher than conventional daily dose of warfarin to keep him asymptomatic.     

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。     

Unruptured dural arteriovenous malformation of the transverse-sigmoid sinus presenting with focal symptoms and coma

We are presenting the case of a 63 year-old man with a dural arteriovenous malformation of the transverse sigmoid sinus who developed focal deficits followed by less localized symptoms such a disorientation, lethargy and eventually comatose status. Initial cerebral angiography showed retrograde filling of the cortical and deep cerebral venous system with marked delay in venous empting. Following embolization clinical symptoms completely cleared at the time that control angiography showed retrograde venous flow turning anterograde. Patient's symptoms recurred four months later when there was a relapse of retrograde cerebral venous drainage at the time he developed thrombosis of the superior longitudinal and right transverse sinuses. Sinus thrombosis and thrombosis of the central retinal artery were coincidental with hypercoagulability related to hyperhomocysteinemia. Since control angiography still showed persistence of the AV shunting radical excision of the involved dural sinuses was performed. The final outcome was excellent. The physiopathological mechanism responsible for neurological deficits in our patient most likely was ischemia of venous origin secondary to venous hypertension resulting from retrograde cerebral venous drainage. The clinical and angiographic presentation in few similar cases reported in the literature is reviewed.     

Case of transient cortical blindness due to thrombosis of the transverse sinus]

An 62-year-old man presented visual impairment and generalized seizure. Brain CT performed on the day of admission showed thrombus in the right transverse sinus, and DWI showed high intensity areas in the bilateral occipital and parietal lobes. According to bilateral occipital lobe lesions, we considered his visual impairment as cortical blindness. He was diagnosed as venous sinus thrombosis and intravenous heparin, edaravone and osmotic diuretics were administered. MR venography performed after starting of intravenous treatment showed flow gap in the left transverse sinus but no abnormalities in the right transverse sinus. On the second day of hospitalization, his cortical blindness showed improvement and thrombus in the right transverse sinus were disappeared. This indicated that his left transverse sinus originally hypoplastic, thrombus and hemostatis in the right transverse sinus (his dominant side) caused his cortical blindness and generalized seizure. There was a recanalization in the right transverse sinus after heparin therapy.     

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.     

Familial hyperhomocysteinemia-related cerebral venous sinus thrombosis and pulmonary embolism: a case report

Elevated plasma homocysteine levels are associated with an increased risk of deep vein thrombosis. Herein we report a case of familial hyperhomocysteinemia-related cerebral venous sinus thrombosis and pulmonary embolism in a 21-year-old man who presented with severe headache over bilateral frontal areas. Neurological examination revealed no evidence of focal neurological deficit. Chest CT showed pulmonary thromboembolism in bilateral basal lung fields and brain MRI disclosed right transverse and sigmoid venous sinus thrombosis. Routine immunological tests, coagulation factors and occult tumor screening were normal, as were vitamin B12 and folate levels. The DIC profile was negative, The only risk factor we were able to identify was an elevated serum homocysteine level, namely 46.23 microM/L. Hyperhomocysteinemia was also noted in the patient's asymptomatic elder brother (68.0 microM/L) and, to a lesser extent, in his parents (father 12.5 microM/L; mother 11.7 microM/L). In conclusion, the cause of cerebral venous thrombosis and pulmonary embolism in this young patient was most likely related to familial hyperhomocysteinemia, with the thromboembolic events precipitated by a preceding systemic infection. After anticoagulation therapy; the patient recovered completely without any residual neurological deficit.     

Imaging characteristics of two patients with isolated cortical venous thrombosis☆

Over the past twenty years, improvements in neuroimaging have greatly improved the ability to diagnose cerebral venous sinus thrombosis, as well as isolated cortical venous thrombosis. Neuroimaging allows for variations to be detected in the cortical vein and venous sinus. Diagnosis of thromboses in the venous system should not depend entirely on angiography of undeveloped veins or venous sinus. Currently, the combination of magnetic resonance imaging and magnetic resonance venography is the gold standard for diagnosing cerebral venous sinus thrombosis, rather than digital subtraction angiography. This article summarizes clinical manifestations, results from computed tomography and magnetic resonance imaging in two cases of isolated cortical venous thrombosis, analyzed relevant literature, and discussed the clinical and imaging characteristics of isolated cortical venous thromboses.     

血管内局部溶栓治疗颅内静脉窦血栓

目的评价局部溶栓与机械碎栓治疗静脉窦血栓的影像学资料与治疗效果。方法对7例静脉窦血栓病人经股静脉穿刺,将微导管选择性插入已闭塞的静脉窦内。6例行静脉窦局部灌注尿激酶或基因重组组织型纤溶酶原激活剂,1例采用球囊机械碎栓术;3例伴脑皮质或深部静脉血栓者同时经颈动脉给予溶栓药。结果造影示6例已闭塞的静脉窦部分再通,1例无明显再通;3例侧支静脉回流增多。1例溶栓后原有脑内血肿增大,导致偏瘫加重;1例术后发生无症状出血性静脉梗死。随访10个月~3年,6例mRankin评分0~1分,1例mRankin评分2分。结论血管内局部溶栓治疗静脉窦血栓,静脉窦完全再通率低,但血管部分再通及侧支静脉回流增多,可改善病人的临床预后。     

改良溶栓方案治疗脑静脉窦合并颈内静脉血栓形成

目的探讨改良溶栓方案【静脉窦内微量持续泵点尿激酶(100,000u/24h)】治疗脑静脉窦合并颈内静脉血栓形成的疗效。方法对11例患者进行机械性破栓、静脉窦内留置微导管行最低量尿激酶100,000u/24h静脉窦直接泵点滴48～96h治疗。术后积极治疗原发病,抗凝治疗6个月。术后随访6～12个月,平均10个月。结果 11例脑静脉窦合并颈内静脉血栓形成患者,脑静脉窦均获得再通(其中8例患者应用尿激酶100,000u/24h效果良好,3例患者在应用尿激酶100,000u/24h,48h复查后增量至250,000u/24h),1例颈内静脉未通,预后良好。结论改良溶栓方案可有效治疗脑静脉窦合并颈内静脉血栓形成,有待大宗病例进一步证实。     

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.     

Overlooked early CT signs of cerebral venous thrombosis with lethal outcome

The aim of this report is to emphasize the consequences of overlooked initial CT signs of cerebral venous thrombosis. Brain CT was ordered in an afebrile patient with neck pain and occipital headache. Since no abnormalities were noted on non-contrast CT study, the patient was discharged with recommendation for routine laboratory tests and plain X-ray of the cervical spine. Right hemiparesis developed the next day with persistent headache and the patient was sent back to the Neurology Clinic where he developed myoclonic seizures compatible with focal motor status epilepticus. Neuroimaging, performed two days later, revealed a huge hemorrhagic venous infarcts in the left posterior cerebral hemisphere associated with typical signs of dural sinus thrombosis. Subtle curvilinear hyperdensities were detected within the left parietal cortico-subcortical border zone on reevaluation of the initial brain CT. A posteriori these were thought to be compatible with a developing venous infarct, associated with subtle signs most consistent with combined cortical vein and sinus thrombosis. No improvement was noted after administration of anticoagulant treatment and the patient died 11 days after the initial CT scan. Detection of early CT signs of cerebral venous thrombosis is extremely important, since delaying adequate treatment may have catastrophic consequences.