Treatment Of Cerebral Venous Thrombosis Research Articles

Epidemiology, Endovascular Treatment, and Prognosis of Cerebral Venous Thrombosis: US Center Study of 152 Patients.

BackgroundCerebral venous thrombosis is a rare cause of stroke that poses diagnostic, therapeutic, and prognostic challenges. Mainstay treatment is systemic anticoagulation, but endovascular treatment is increasingly advocated. Our objectives were to describe the epidemiology, treatment, and prognosis of 152 patients with cerebral venous thrombosis.Methods and ResultsThis was a retrospective study of consecutive cerebral venous thrombosis cases from 2006 to 2013 at a comprehensive stroke center through hospital discharge. Predictors of full recovery (modified Rankin Scale scores 0–1) were analyzed with multiple logistic regression and presented as adjusted odds ratios (AORs) with 95% confidence intervals (CIs). The population was young (average age: 42 years), majority female (69%), and commonly presenting with cerebral edema (63%), and 72% were transferred in. All patients received systemic anticoagulation; 49% (n=73) required endovascular treatment. Reasons for requiring endovascular treatment included cerebral edema, herniation, or hemorrhagic infarct (n=38); neurologic decline (n=17); rethrombosis, persistent occlusion, or clot propagation (n=10); extensive clot burden (n=7); and persistent headache despite anticoagulation (n=1). There were 7 (10%) procedural complications. Recanalization was successful (61%), partial (30%), and unsuccessful (9%). Overall, 60% fully recovered. Positive predictors of full recovery included hormonal etiology, particularly for patients who were transferred in (AOR: 7.06 [95% CI, 2.27–21.96], interaction P=0.03) and who had migraine history (AOR: 4.87 [95% CI, 1.01–23.50], P=0.05), whereas negative predictors of full recovery were cerebral edema (AOR: 0.11 [95% CI, 0.04–0.34], P<0.001) and motor weakness (AOR: 0.28 [95% CI, 0.09–0.96], P=0.04).ConclusionsAs one of the largest cohort studies, our findings suggest that cerebral edema, history of migraine, and hormonal etiology were prognostic and that endovascular treatment might be a safe and effective treatment for cerebral venous thrombosis when conventional management is inadequate.

Comparison of the efficacy of fixed-dose enoxaparin and adjusted-dose unfractionated heparin in patients with cerebral venous thrombosis

ObjectiveAnticoagulants are the standard treatment for cerebral venous thrombosis (CVT). Although low-molecular-weight heparin (LMWH) is recommended in CVT, the specific type and dosage regimen of LMWH have never been specifically suggested. This study compared the clinical outcomes and adverse events in patients who received adjusted-dose unfractionated heparin (AD-UFH) versus fixed-dose enoxaparin (FD-E). MethodsA retrospective cohort study was conducted at a university hospital in Thailand. Patients included in the study were those treated for CVT initially with either AD-UFH or FD-E followed by oral warfarin for 1year between January 2002 and December 2015. Electronic medical records were reviewed by the investigators. The baseline clinical characteristics, anticoagulant regimens, complications and outcomes at hospital discharge and 1-year follow-up were analyzed. Clinical outcomes (independency defined by modified Rankin score (mRS) 0–2 at hospital discharge and 1-year follow-up) and adverse events (gastrointestinal bleeding and intracranial hemorrhage) were compared between patients who received AD-UFH or FD-E. ResultsSeventy-five patients met the inclusion criteria. Thirty-nine patients received AD-UFH and 36 patients received FD-E. The baseline demographic and clinical characteristics between the two groups were comparable. Independency at hospital discharge accounted for 51.28% in the AD-UFH group and 61.11% in the FD-E group (p=0.392). There were no significant differences in the incidence of expansion of preexisting intracerebral hematoma (14.29% vs 18.18%; p=0.773) or new symptomatic intracranial hemorrhage (7.69% vs 8.33%; p=0.855). Independency at 1-year follow-up was also comparable between the two groups (71.78% vs 77.78%; p=0.552). ConclusionThis current study suggested a comparable efficacy and safety of FD-E and AD-UFH in patients with CVT.

Apixaban for the treatment of Cerebral Venous Thrombosis: A Report of Two Cases (P1.281)

Apixaban for the treatment of Cerebral Venous Thrombosis: A Report of Two Cases (P1.281)

Prolonged microcatheter-based local thrombolytic infusion as a salvage treatment for failed endovascular treatment for cerebral venous thrombosis: A multicenter registry (P3.078)

Prolonged microcatheter-based local thrombolytic infusion as a salvage treatment for failed endovascular treatment for cerebral venous thrombosis: A multicenter registry (P3.078)

Abstract WP10: Prolonged Microcatheter-based Local Thrombolytic Infusion as a Salvage Treatment for Failed Endovascular Treatment for Cerebral Venous Thrombosis: A Multicenter Registry

Background: Transvenous endovascular treatment including combination pharmacological and mechanical modalities is reserved for patients with cerebral venous thrombosis (CVT) not responsive to standard anticoagulation. However, transvenous endovascular treatment may not always be successful in achieving recanalization. Objective: To determine the effectiveness of prolonged microcatheter based local thrombolytic infusion in treatment of patients with CVT who achieved no or suboptimal recanalization with endovascular treatment. Methods: Patients who underwent transvenous endovascular treatment for cerebral venous thrombosis at three hospitals were identified through local registries. The final response to treatment was assessed and prolonged microcatheter based local thrombolytic infusion was instituted in selected patients as second line treatment. Serial angiograms were performed to assess treatment response and determine the duration of infusion. Results: Of the 85 patients admitted with CVT, 13 patients underwent 14 transvenous endovascular treatments. Initial treatment was considered suboptimal in 10/14 procedures due to no recanalization in 6, partial recanalization in 3, and re-occlusion in 1 patient. A prolonged microcatheter-based local recombinant tissue plasminogen activator (rt-PA) infusion was used in 9 of the 10 procedures for a median duration of 16 hours (range 15-22 hours). Follow up angiography demonstrated complete recanalization in 4 procedures and improvement of the partial recanalization in 5 additional procedures. One patient died before the follow up imaging could be acquired. None of the patients developed intracranial hemorrhage associated with local thrombolytic infusion. The microcatheter position had shifted during the infusion in one procedure. Conclusion: Prolonged microcatheter based local thrombolytic infusion appears to effective treatment in patients who have suboptimal response to acute transvenous endovascular treatment without any additional adverse events.

Xa 阻害薬を治療に用いた甲状腺機能亢進症を伴う脳静脈血栓症の1 例

Xa 阻害薬を治療に用いた甲状腺機能亢進症を伴う脳静脈血栓症の1 例

Cerebral Venous Thrombosis Associated with Intracranial Hemorrhage and Timing of Anticoagulation after Hemicraniectomy

Cerebral venous thrombosis (CVT) is a rare cerebrovascular event that can present with headache, seizure, and focal neurological deficits. Approximately 30%-40% of patients with CVT also present with intracranial hemorrhage. Current guidelines recommend anticoagulation after CVT even in the setting of intracranial hemorrhage, but the timing of initiation is unclear. We present a case of CVT where timing of anticoagulation was unclear by current guidelines. We conducted a literature search with search terms of "cerebral venous thrombosis," "intracranial hemorrhage," and "anticoagulation." Abstracted information included anticoagulation status and time of initiation of anticoagulation. We present a 30-year-old woman with sudden onset of right hemiplegia, global aphasia, and new-onset seizures diagnosed with left transverse and sigmoid sinus thrombosis with intraparenchymal hemorrhage. The patient was treated with endovascular thrombectomy and decompressive hemicraniectomy due to hemorrhage expansion, and anticoagulation was restarted 8 days after hemicraniectomy. The literature review demonstrated a wide variation of timing for anticoagulation initiation in patients with CVT and intracranial hemorrhage. Most started anticoagulation within 24 hours of admission with similar functional neurological recovery. Current guidelines on the treatment of CVT, even with intracranial hemorrhage, recommend anticoagulation. Most reports in the literature state initiation of anticoagulation within 24 hours. However, the literature does not definitively state when to initiate anticoagulation in a patient with CVT, intracranial hemorrhage, thrombectomy, and decompressive hemicraniectomy. This case illustrates the challenge of determining when to resume anticoagulation for CVT.

Treatment of Cerebral Venous Thrombosis with Rivaroxaban

Treatment of Cerebral Venous Thrombosis with Rivaroxaban

Cerebral venous thrombosis

There is ample evidence that arterial and venous links of the vascular bed are interrelated, with the venous part, as the highly organized reflexogenic zone, responsible for the development of complex reactions providing the stability of the cerebral blood flow. There is few publications devoted to the venous pathology of the brain however the prevalence of cerebral venous thrombosis (CVT) is relatively high. The annual prevalence of CVT is 4-7 per 1 million of population. Timely recognition and early diagnosis of CVT are most important for successful treatment of patients. It can lead to effective therapy, decrease the consequences of this disease and the fatal outcomes. The review and systematization of the literature on the epidemiology, etiology, risk factors, clinical presentations, diagnosis and treatment of CVT are presented.

Cerebral Venous Thrombosis

Cerebral venous thrombosis (CVT) is rare and involves thrombosis of the veins and sinuses of the brain, most commonly the superior sagittal sinus. Approximately 5 CVT cases occur per 1 million persons in western countries. CVT causes 0.5% of strokes. Early diagnosis is crucial to prevent such outcomes as hydrocephalus, intracranial hypertension, and further seizures. Standard medical treatment of CVT consists of low-molecular-weight heparin and endovascular thrombolysis. Small case reports have found that the newer oral anticoagulants can be used for CVT treatment; however, they are associated with increased risk of bleeding and other adverse effects. CVT can be triggered by an imbalance of the body's homeostasis or reduced action of the intrinsic antithrombotic mechanism. Factors influencing this change include infection, brain tumor, inflammatory conditions, genetic thrombophilias, head trauma that causes intracranial bleeding, and certain medications. CVT may cause brain infarction and increased intracranial pressure. Sometimes, idiopathic intracranial hypertension presents as the only clinical manifestation. Confirmation of the diagnosis typically is through neuroimaging. Current CVT treatment depends on disease extent and severity. CVT is a rare neurological disease with potentially serious implications and high neurological morbidity and mortality rates. Understanding the role of risk factors-such as genetic or acquired thrombophilia, pregnancy, use of oral contraceptives, and hyperhomocysteinemia-in CVT development is important. Although heparin and warfarin have been used for more than 50 years, newer oral anticoagulants (eg, dabigatran, rivaroxaban, apixaban) might offer an alternative to traditional therapy.

Malignant Cerebral Venous Sinus Thrombosis in Polycythemia.

Malignant Cerebral Venous Sinus Thrombosis in Polycythemia.

Endovascular treatment of cerebral venous thrombosis: Contemporary multicenter experience.

Endovascular therapy of cerebral venous thrombosis using modern approaches to intracranial recanalization, such as stent retrievers and aspiration thrombectomy, is not well described. We performed a retrospective review of data for consecutive patients with venous sinus thrombosis who underwent endovascular treatment between 1 January 2010 and 31 December 2013 at participating institutions. We identified a total of 13 patients with a diagnosis of cerebral venous thrombosis. The most frequently utilized type of endovascular intervention was the Penumbra aspiration system (Penumbra Inc., Alameda, California, USA) (nine cases), followed by local infusion of tissue plasminogen activator (bolus and/or drip in six cases) and stent retrievers (Solitaire FR (Covidien, Irvine, California, USA) in three cases and Trevo (Stryker, Kalamazoo, Michigan, USA) in one case). Overall, multimodality treatment (two or more different types of devices or approaches) was performed in 62% of cases. Follow-up data were available for 11 patients; of those, five had a favorable clinical outcome (defined as modified Rankin Scale score of 0-2) and three patients died. Various endovascular approaches are utilized in current clinical practice. A multimodal approach to endovascular therapy for the treatment of cerebral venous thrombosis resulted in partial or complete restoration of flow in all cases, yet the mortality rate of 27% indicates the need for improvement in recanalization strategies for this disorder.

Cerebral venous thrombosis: An Indian perspective.

Cerebral venous thrombosis (CVT) is an uncommon cause of stroke with extremely varied clinical presentations, predisposing factors, imaging findings, and outcomes, and thus can be extremely challenging to diagnose. Accurate and prompt diagnosis of CVT is crucial because timely and appropriate therapy can reverse the disease process and significantly reduce the risk of acute complications and long-term squel. In this article, we have reviewed the epidemiology, causative factors, clinical features, diagnosis and treatment of CVT from an Indian perspective. Over the last decade, a change in trends in the causative factors has been noted from India.

Cerebral Venous Thrombosis As a Complication of Treatment for Acute Lymphoblastic Leukaemia in Children and Young Adults

▪Cerebral venous thrombosis (CVT) is a significant complication of therapy in children and young adults with acute lymphoblastic leukaemia (ALL). Previous reports indicate a considerable risk of mortality and morbidity in relation to CVT. In addition, there is potential for suboptimal treatment of ALL due to avoidance of Asparaginase and the need for reversal of anticoagulant therapy for invasive procedures such as intrathecal chemotherapy. Anticoagulation may be complicated by haemorrhage.This retrospective study aimed to identify the clinical features, therapy and outcome of CVT occurring during treatment of ALL in individuals, aged 1 to 24 years, who participated in the Medical Research Council UK ALL 2003 (MRC UKALL 2003) randomised controlled trial.Cases of CVT were identified from adverse event reporting. All reports were screened for central nervous system thrombosis and grade 4 serious adverse events in the category of coagulation/thrombosis. Reporting centres were asked for additional clinical information.3126 children and young adults were enrolled in the study between 2003 and 2011, with median age 5 years, including 1776 males (56.8%). The 3 initial treatment regimens: A, B and C: corresponded to standard-risk, intermediate-risk and high-risk, respectively. 55% were treated with regimen A, 32% regimen B and 13% regimen C. 48 individuals (1.5%) developed CVT and data were returned for 42. Median age was 10 (range: 1 to 18) years and 25 cases were male (59.5%). 71.4% of cases (30/42) occurred during induction therapy. 18 cases were in individuals treated with regimen A, 22 regimen B and 2 regimen C. Median time between the most recent Asparaginase dose and CVT was 12.5 days (range: 1-111 days). 29 cases (68.4%) had received 2 doses of Asparaginase prior to thrombosis, 5 cases >2 doses and 8 cases 1 dose.Presenting symptoms were: seizures, 22 cases (52.3%); neurological impairment, 20 (47.6%); headache, 19 (45.2%); reduced conscious level, 8 (19.0%); nausea/vomiting, 8 (19.0%). Identified thrombotic risk factors included: hospitalisation, 22 (52.3%); active infection, 5; recent immobility, 5; dehydration, 6; combined oral contraceptive pill, 2. None were obese, had a high white cell count at time of CVT diagnosis or a history of recent major surgery. 13 (31.0%) had >1 thrombotic risk factor and 16 (38.1%) had no additional clinical risk factor identified. 10 had a thrombophilia screen performed, one with a repeatedly low protein S level (male, 1 year of age). 7 cases (16.7%) had cerebral infarction on imaging and 11 (26.2%) were complicated by intracranial haemorrhage (ICH).38 cases (90.5%) received anticoagulant therapy, 37 of which received low molecular weight heparin (LMWH) and one unfractionated heparin. One case had catheter-directed thrombolysis. 4 were not anticoagulated, 3 due to ICH. 2 received Antithrombin replacement therapy. Anticoagulation therapy was continued for a median of 3 months. 65.0% of cases due more Asparaginase were re-exposed (26/40), 19 of which received thromboprophylaxis during re-exposure. 2 remain on long-term therapeutic anticoagulation. In 23 cases (54.8%) CVT resulted in a delay or change to planned treatment.Neurological morbidity was reported in 4 cases (9.5%): seizure disorder, 2; hemiplegia, 1; residual hemiplegia and hemianopia with severe developmental delay, 1. 36 cases (85.7%) remain in first remission. Survival in those with CVT was 90.1%, comparable to actuarial 5-year survival of the entire cohort (91.5%). There were 4 deaths, three due to leukaemia (two in first relapse) and one due to pneumonia as a complication of stem cell transplant. There were no deaths due to CVT or bleeding on anticoagulant therapy.This study highlights the clinical features of CVT in children and young adults treated for ALL in the MRC UKALL 2003 trial, in particular the timing in relation to Asparaginase treatment, presenting features and neurological outcome. These data support LMWH as safe treatment for CVT in this clinical setting. We have demonstrated the tendency of clinicians to adjust treatment regimen and/or avoid further Asparaginase exposure in response to CVT. However, overall survival at 5 years did not differ for the cohort with CVT. Future studies should aim to further evaluate clinical predictors, alongside potential coagulation and genetic markers, in order to identify a high-risk group that may benefit from measures to reduce CVT during ALL therapy. DisclosuresNo relevant conflicts of interest to declare.

Evaluation and management of a patient with possible cerebral venous thrombosis.

Cerebral venous thrombosis (CVT) is a relatively rare form of stroke usually affecting young individuals. CVT is characterized by the diversity of its neurologic manifestations, which require a high level of clinical suspicion for diagnosis and prompt, appropriate treatment. Multiple circumstances have been associated with CVT, such as prior medical conditions, transient situations, certain medications, and some predisposing conditions. Headache, focal neurologic deficit, and seizures are the most frequent clinical manifestations at onset. MRI in combination with venography has become the imaging modality of choice, as this technique has a high sensitivity and specificity for establishing a diagnosis. CT venography is an alternative to MRI because this technique produces similar diagnostic results. Pharmacologic treatment of CVT with anticoagulants is widely accepted. Per 100 cases, the recurrence of CVT is 2.8% and the mortality of CVT is 10%.

Novel factor xa inhibitor for the treatment of cerebral venous and sinus thrombosis: first experience in 7 patients.

Thrombosis of cerebral veins and sinus (cerebral venous thrombosis) is a rare stroke pathogenesis. Pharmaceutical treatment is restricted to heparin and oral anticoagulation with vitamin K antagonists (VKAs). Between January 2012 and December 2013, we recorded data from our patients with cerebral venous thrombosis. The modified Rankin scale was used to assess clinical severity; excellent outcome was defined as modified Rankin scale 0 to 1. Recanalization was assessed on follow-up MR angiography. Patients were then divided into 2 treatment groups: phenprocoumon (VKA) and a novel factor Xa inhibitor. Clinical and radiological baseline data, outcome, recanalization status, and complications were retrospectively compared. Sixteen patients were included, and 7 were treated with rivaroxaban. Overall outcome was excellent in 93.8%, and all patients showed at least partial recanalization. No statistical significant differences were found between the groups, except the use of heparin before start of oral anticoagulation (P=0.03). One patient in the VKA and 2 patients in the factor Xa inhibitor group had minor bleeding (P=0.55) within the median (range) follow-up of 8 months (5-26). Factor Xa inhibitor showed a similar clinical benefit as VKA in the treatment of cerebral venous thrombosis. Further systematic prospective evaluation is warranted.

Advances in the treatment of cerebral venous thrombosis.

Patients with recent cerebral venous sinus thrombosis (CVT) should be fully anticoagulated with heparin as soon as the diagnosis is confirmed, even in the presence of cerebral hemorrhagic venous infarcts. Fixed-dose subcutaneous low-molecular-weight heparins (LMWH) in therapeutic dosage have a better safety profile and are probably more effective than dose-adjusted intravenous unfractionated heparin. After the patient is stabilized , oral anticoagulant treatment is started, aimed at an INR value between 2.0 and 3.0 for at least three months after the acute phase. Since about 40% of patients with CVT have epileptic seizures at onset or during the first days, many require treatment with anti-epileptics. Prophylactic anti-epileptic treatment is an option, but its efficacy has not been investigated. If no new seizures occur after the acute phase, anti-epileptics can be tapered after three to six months. The efficacy of endovascular treatment, with mechanical and/or pharmacologic thrombolysis, has only been published in small case series, and cannot be regarded as proven effective treatment for CVT. Its theoretical advantage of more rapid clearance of thrombi may be offset by severe bleeding complications, and the limited availability and higher cost of the procedure. Patients who deteriorate because of large space-occupying venous infarcts have a high risk of dying from cerebral herniation. In such cases an emergent decompressive hemicraniectomy is often life-saving. Experience from different centers with this procedure shows a good clinical outcome in the majority of these patients. Patients with CVT may develop - and sometimes present with - chronic intracranial hypertension with headache and papilledema. In such patients the priority is prevention of visual function loss; intracranial hypertension should be controlled with acetazolamide, and occasionally with repeated lumbar punctures if vision is threatened. Refractory cases will need a CSF shunting procedure.

Histopathological effects of different therapy strategies in experimental sinus thrombosis

The optimal treatment for cerebral venous thrombosis is still under debate. The histological consequences of different treatments have not been systematically studied and may be of value in this debate. Thrombosis of the superior sagittal sinus was induced in rats by topical application of ferric chloride. Animals were treated 6 h after operation with subcutaneous injection of 450 IU/kg enoxaparin twice daily (n = 10), with 10 mg recombinant tissue plasminogen activator (rt-PA)/kg (n = 12), and with 6 mg abciximab/kg (n = 10). Eleven animals were treated with saline (controls), and four animals were sham-operated without thrombosis induction. Animals were killed on day 7. Coronal brain slices were stained with hematoxylin-eosin (HE) and against glial fibrillary acidic protein (GFAP), and factor VIII. Histology was quantified in parasagittal and temporal regions of interest. Compared with controls, counts of pyknotic neurons on HE stain were significantly lower in the enoxaparin group. Counts for GFAP-expressing astrocytes were highest in the enoxaparin (p < 0.001) and rt-PA (p < 0.05)-treated groups. Angiogenesis defined as factor VIII-expressing vessels was significantly (p < 0.01) higher in the enoxaparin and significantly lower (p < 0.01) in the rt-PA group compared with controls. In this animal model, we found histological differences related to the different treatments, which cannot be explained by recanalization and its speed alone.

Letter by Cundiff Regarding Editorial, “Cerebral Venous Thrombosis: Another Heparin Controversy”

My opinion piece in Stroke challenged the evidence basis for anticoagulant drug treatment for cerebral venous thrombosis (CVT).1 Thanks to Dr Selim2 for his rebuttal. Based on my systematic review of the limited available evidence divulged by CVT study authors in published articles and personal e-mails, my article detailed the case against anticoagulants: Dr Selim2 concedes that “the efficacy of anticoagulation in CVT has not been unequivocally proven.” However, he provides justification for anticoagulants based on the theory that they can prevent CVT propagation and thereby prevent ICHs. Although full-dose heparin has …

Cerebral Venous Thrombosis and Hyperthyroidism

Cerebral venous thrombosis (CVT) is mostly caused by pro-thrombotic factors. Hyperthyroidism is not a wellknown risk factor. We present a case report on a 17 year old girl who developed life-threatening CVT after Graves’ disease. A review of the literature reveals further 34 cases of CVT and hyperthyroidism. Abnormalities in the coagulation system leading to hypercoagulability such as increased coagulation factors are detected in patients with hyperthyroidism, and these abnormalities seem to be thyroxin-dependent. The cause of CVT may be multi-factorial. Our patient used oral hormonal contraception without complications until the development of severe Graves’ disease. Hyperthyroidism is suspected as the main precipitating cause of CVT in this case. We recommend performing MRI with venous angiography when a hyperthyroid patient presents with unusual headache alone or in combination with other neurological symptoms. If CVT is proven, blood screening for coagulation abnormalities should be performed. On the other hand, diagnostics for finding the cause of CVT should include blood tests of thyroid function. Early treatment of CVT and hyperthyroidism is mandatory.