Cerebral Sinovenous Thrombosis Research Articles

Comparison of CT Venography with MR Venography in Cerebral Sinovenous Thrombosis

The purpose of this study was to compare cerebral CT venography with MR venography and determine the reliability of CT venography in the diagnosis of cerebral sinovenous thrombosis. Fifty patients who were clinically suspected of having cerebral sinovenous thrombosis, irrespective of age and sex, underwent cerebral CT venography and MR venography. Projection venograms were displayed using maximum-intensity-projection images for both CT venography and MR venography. The CT venograms were also displayed using the integral algorithm, which depicts the average intensity value of the first five voxels deep in relation to the model surface that is nearest the viewer, allowing direct visualization of the thrombus in the sinuses. All CT venograms and MR venograms were independently evaluated by experienced neuroradiologists. Of these 50 patients, 30 patients were diagnosed as having cerebral sinovenous thrombosis on both CT venography and MR venography. The total numbers of sinuses involved were 81 and 77 (CT venography and MR venography). When MR venography was used as the gold standard, CT venography was found to have both a sensitivity and a specificity of 75-100%, depending on the sinus and vein involved. CT venography is as accurate as MR venography for diagnosing cerebral sinovenous thrombosis.

Arterial contamination: a useful indirect sign of cerebral sino-venous thrombosis

Various imaging findings of cerebral sino-venous thrombosis (CSVT) have been described on magnetic resonance venography (MRV). The purpose of this study was to evaluate the significance of visualization of the arterial system on cerebral MRV, also described as arterial contamination, as an indirect sign of CSVT. Forty patients with a clinical suspicion of venous sinus thrombosis underwent MR imaging of the brain, followed by MRV sequence, based on 2D time of flight technique in the coronal oblique plane. Patient's clinical symptoms and signs were noted with particular interest for papilloedema. Twenty-seven patients were diagnosed to have cerebral venous thrombosis on MRV, and of these, arterial contamination was visualized in 16 patients. In the remaining 13 cases, in which there was no evidence of venous sinus thrombosis, arterial contamination was absent. The sensitivity of this finding was 59.25% (n = 16/27), specificity was 100%, positive predictive value was 100% and negative predictive value was 54.2%. Of these 16 patients with arterial contamination, 12 patients had evidence of increased intracranial pressure in the form of papilloedema. Visualization of the arterial system is a useful indirect sign of CSVT, and may be an indicator of increased intracranial pressure in these patients.

Cerebral sinovenous thrombosis and idiopathic nephrotic syndrome in childhood: report of four new cases and review of the literature

Nephrotic children are prone to develop thromboembolic complications secondary to an acquired hypercoagulable state. Cerebral sinovenous thrombosis (CSVT) is increasingly recognised in this population, but clinical characteristics and outcome are not well documented. The database of the Canadian Pediatric Ischemic Stroke Registry (Toronto Site) containing prospectively enrolled children from 1992-2004 with CSVT identified four children with NS. A pooled literature analysis retrieved 17 additional cases reports. CSVT presented in the majority of cases during the first flare or within 6 months after the onset of NS and was found to occur more often in SSNS/SDNS (n=13) than in SRNS (n=4). Clinical manifestations were non-specific and consisted primarily of seizures (n=8) and signs of raised intracranial pressure (n=16). Imaging studies revealed a predilection for superior sagittal sinus involvement (n=21) and rare parenchymal lesions (n=4). The most consistent biological risk factors were a severe hypoalbuminaemia (n=14) and, to a lesser extent, decreased antithrombin (AT) levels (n=9/16). Deficiency of other coagulation inhibitors (protein S, protein C) was not identified. Inherited thrombophilia was documented in a single case, suggesting that acquired, more than genetic, coagulation factors are involved. Anticoagulation was safe, and the outcome was good in most patients, and no recurrence of thrombotic event was reported. In conclusion, CSVT is now a well-described complication of NS with potential morbidity. A high index of suspicion is required, especially in young children with NS presenting neurological symptoms. Reliable biological predictors of CSVT are lacking.

Neonatal Cerebral Sinovenous Thrombosis

The presentation, treatment, and outcome of neonatal cerebral sinovenous thrombosis (SVT) were studied in 42 children, using neurology clinic records (1986-2005) at Indiana University School of Medicine.

Cerebral Sinovenous Thrombosis in the Neonate

There are few studies on neonatal cerebral sinovenous thrombosis (SVT). To describe the presentations, treatments, and outcomes of neonatal SVT and to assess infarction as a predictor of outcome. Retrospective chart study. A tertiary pediatric hospital in Indianapolis, Ind. Patients Forty-two children with neonatal SVT identified using International Classification of Diseases, Ninth Revision code searches from 1986 through June 2005 and review of neurology clinic records. None. Cognitive impairment, motor impairment, and epilepsy at last clinic visit. Gestational or delivery complications or risk factors and comorbid conditions such as dehydration, sepsis, and cardiac defects were common (gestational/delivery factors in 82% [31 of 38 with available maternal data]; comorbid conditions in 62% [26 of the 42]). Twenty-four (57%) presented with seizures. Twenty-five (60%) had infarcts, which were hemorrhagic in 22. Only 27 (64%) of 42 received prothrombotic evaluations; none had persistent deficiencies of protein C, protein S, or antithrombin III. Three (7%) received heparin sodium. All other children received only supportive care. One child died. Outcome data were available for 29 (71%) of the 41 survivors; of these, 23 (79%) had impairment(s). Two were known to be in early intervention, and no further information was available. Of the remaining 27, 16 (59%) had cognitive impairment, 18 (67%) had cerebral palsy, and 11 (41%) had epilepsy. Infarction was associated with the presence of later impairment (P = .03). The presentation of neonatal SVT is often nonspecific, the diagnosis can be difficult to make, treatment beyond supportive care is rarely used, and outcomes can be severe. Further work is needed to develop standardized guidelines for the evaluation and treatment of neonatal SVT.

Infantile Spasms as an Adverse Outcome of Neonatal Cortical Sinovenous Thrombosis

Cerebral sinovenous thrombosis is a rare but potentially serious condition often occurring in children with nonspecific presenting features. Much remains to be learned about the long-term outcome of infants with cerebral sinovenous thrombosis. We report a series of four patients taken from a prospective database of neonates with sinovenous thrombosis who subsequently developed infantile spasms, three with hypsarrythmia on electroencephalography and one with multiple independent spike foci. The first patient presented at 2 weeks of age with hypernatremia, dehydration, and seizures. He was found to have extensive thrombosis and hemorrhagic infarction of the right basal ganglia. The second patient presented at 5 weeks of life and was found to have sagittal sinus thrombosis with bilateral intracranial hemorrhage. The third patient presented with seizures on day 1 of life and was found to have venous thrombosis involving the torcular, extending into the sagittal sinus. The fourth patient presented at 3 weeks with lethargy and seizures. He was diagnosed with bacterial meningitis and also had extensive sinus thrombosis. All patients developed infantile spasms at ages 9, 7, 11, and 10 months, respectively. This is the first report in the English literature describing infantile spasms as a possible outcome of sinovenous thrombosis in early infancy.

Urgent Clinical Challenges in Children With Ischemic Stroke

Clinical trials are lacking in pediatric stroke. As a result, physicians caring for children with stroke face significant challenges. The patient characteristics and specific nature of clinical challenges facing practicing clinicians can inform the design of and priorities for developing relevant clinical trials. Physicians consulted the 1-800-NOCLOTS toll-free pediatric stroke telephone consultation service on children (birth to 18 years) with ischemic stroke. Pediatric neurologist or hematologists provided telephone consultation and documented caller and patient characteristics, antithrombotic treatments and callers' questions for entry into a computerized database. Children referred from January 1, 1995 to January 1, 2004, comprised the study cohort. Stroke consults were completed on 1065 children located predominantly in the United States (76%). Children had arterial ischemic stroke (AIS; 679; 64%) or cerebral sinovenous thrombosis (CSVT; 386; 36%) and were 54% male and 16% neonates. Risk factors and antithrombotic agents (none, aspirin, warfarin, and heparins) differed by stroke type. In 60% of patients, callers had not initiated antithrombotic therapy. Callers' questions for both stroke types usually concerned treatment selection (83%), but for AIS, questions more frequently (P<0.0001) concerned the selection and interpretation of etiological investigations. Research is urgently needed in pediatric stroke to provide direction for management in "real-life" settings. Research efforts should address the unique challenges within different stroke types and include observational studies addressing investigation of the child with AIS. For AIS and CSVT, randomized controlled trials investigating the efficacy of antithrombotic treatment are urgently needed.

Cerebral Sinovenous Thrombosis Post Head Injury - 10 Year Experience in Children.

Cerebral sinovenous thrombosis (CSVT) post head injury is infrequently diagnosed in children. We retrospectively reviewed 323 patients with histories of head injury and a computerized tomography scan of the head from June 1996 to June 2005. Twelve patients (3.7%) were diagnosed with CSVT. The mean age was 6 years (range from 2 to 15 years). Male to female ratio was 10:2. The mechanism of injury included motor vehicle accidents in 5 patients, and falls in 7 patients. Nine patients had minor head injuries (GCS> 8) whereas 3 patients had severe head injuries (GCS<8). The most common presenting symptom was vomiting in 5 patients and other less common symptoms including: headache, seizure and irritability. The commonest locations of thrombosis were sigmoid and transverse sinus. Four patients had extensive thrombus involving more than 3 sinuses. Of the 12 patients, 9 (75%) patients had skull fractures and 6 (50%) had epidural hematomas in association with CSVT. Seven patients (58%) received anticoagulant treatment. The duration of anticoagulant therapy was from 2 days to 6 months. Anticoagulation was discontinued in 3 patients (25%) due to extension of CNS bleeding. All patients receiving anticoagulation were therapeutic with an anti-factor Xa level of 0.5–1 units/mL on enoxaparin, 0.35–0.7 units/mL on standard heparin and INR level of 2–3 on Coumadin. There was complete resolution in 6 patients with the imaging done in a mean followup of 78.5 days, partial resolution in 3 patients with the mean followup imaging in 95.6 days, unchanged status in 1 patient 6 days after the diagnosis and no followup imaging in 2 patients. Six patients had thrombophilic work-up and all were normal. Of the 7 patients with full recovery, 3 patients did not receive anticoagulation. Four patients had seizure and headache, left hemiparesis, panhypopituitarism and optic atrophy, and attention deficit disorder, respectively. In conclusion, the prevalence of CSVT post head injury in children was approximately 3.7%. The etiology of CSVT in this situation might be associated with skull fracture and hematoma, which could compress the cerebral sinus. Large prospective studies involving multiple centers are required to ascertain whether prothrombotic investigations are necessary and if anticoagulation improves neurologic outcome in patients with CVST post head injury.

Accelerated myelination associated with venous congestion

Magnetic resonance imaging is currently the gold standard in the assessment of brain myelination. The normal pattern of brain myelination conforms to a fixed chronological sequence. Focal accelerated myelination is a usual pathological state and previously has only been associated with Sturge-Weber syndrome. The purpose of our study is to describe alternate causes for accelerated myelination. We retrospectively reviewed serial MR scans, MR angiography, conventional angiography and the clinical progress of three children with accelerated myelination. Two patients with accelerated myelination had an underlying cerebral sinovenous thrombosis. The third patient had Sturge-Weber syndrome. Our study strongly suggests that cerebral venous thrombosis with the consequent restriction of venous outflow could be a key factor in the induction of accelerated myelination. We recommend that in patients with accelerated myelination, the search for an underlying etiology should include careful evaluation of the intracranial vascular pathology, especially cerebral venous thrombosis.

In pursuit of evidence-based treatments for paediatric stroke: the UK and Chest guidelines

Arterial ischaemic stroke and cerebral sinovenous thrombosis are increasingly seen in infants and children. Incidence ranges from two to six per 100,000 children a year. Adverse outcome including death, neurological deficits, and reduced quality of life affect most children with stroke. Residual neurological deficits last many decades, for the rest of a patient's life. Of major concern is the risk of recurrent stroke, which affects up to 25% of children who have arterial ischaemic stroke after the newborn period. Children with ischaemic stroke are empirically treated with antithrombotics including antiplatelet (aspirin and clopidogrel) and anticoagulant (heparins and warfarin) drugs. No randomised controlled trials have been done besides those in patients with sickle-cell disease and adult trial data are not directly applicable to paediatric stroke due to maturational differences in coagulation and vascular systems as well as different stroke mechanisms. National and international networks of clinical and basic researchers focused on paediatric stroke are now developing. Recently published cohort and case-controlled studies are elucidating stroke mechanisms, outcomes, and treatment safety in children. Two sets of guidelines have been published in the past 6 months. These guidelines differ both in the scope of treatments and subgroups of patients with stroke they cover; however, both focus on ischaemic stroke beyond the newborn period. There are areas of agreement-for children with sickle-cell disease and stroke, both guidelines recommend initial and maintenance transfusion therapy to reduce the proportion of sickle-cell haemoglobin to less than 30%. For children with sinovenous thrombosis or arterial stroke due to dissection or cardiac embolism, both guidelines recommend anticoagulant therapy with warfarin or low molecular weight heparin for 3-6 months. However, the guidelines diverge in their recommendations for the initial treatment of non-haemorrhagic arterial ischaemic stroke, one recommending aspirin and the other 5-7 days of anticoagulants. The guidelines also differ in their recommendations for long-term treatment of children after arterial ischaemic stroke, one set recommending maintenance aspirin in all patients and the other only in children with vasculopathy. These differences arise from both a lack of sufficient evidence and the differing views of neurologists and haematologists in the treatment of paediatric cerebral thrombosis. WHERE NEXT?: Multicentre studies and networks provide increasingly precise data regarding mechanisms, outcomes, and treatment safety in paediatric stroke. These data and networks will enable clinical trials to address areas of divergent opinion and improve the outcome from childhood stroke in the near future.

Cerebral thrombosis in childhood nephrosis

Sinovenous thrombosis is an uncommon but serious complication associated with nephrotic syndrome in children. We describe a 9-year-old Caucasian boy who presented with dehydration, vague neurological symptoms and seizures. A diagnosis of nephrotic syndrome was made during the course of hospitalization. The serum antithrombin III level was decreased and brain imaging showed cerebral sinovenous thrombosis. Anticoagulant therapy with heparin was commenced and the patient made a slow but gradual clinical, as well as radiological recovery. We describe this case and review available literature to highlight the importance of suspecting and recognizing this potentially life threatening complication and initiating early treatment.

Early cerebral sinovenous thrombosis in a child with acute lymphoblastic leukemia carrying the prothrombin G20210A variant

This paper describes the case of a male child with acute lymphoblastic leukemia who developed cerebral sinovenous thrombosis on day 6 of induction therapy with intrathecal methotrexate and methylprednisolone. A central venous catheter had been implanted the day before. The heterozygous prothrombin G20210A variant was found together with acquired activated protein C resistance and a reduced activated partial thromboplastin time. Clinical course and magnetic resonance imaging with magnetic resonance venography gradually improved over the following days after starting anticoagulant therapy (heparin and nadroparin). Cerebral sinovenous thrombosis is a serious disease in leukemic children, occurring in up to 6% of these patients. Data from the literature are in favor of anti-coagulant treatment, even though the efficacy and safety of thromboprophylaxis during chemotherapy in leukemic children with inherited thrombophilic conditions remain to be demonstrated.

Neonatal Arterial Ischemic Stroke and Cerebral Sinovenous Thrombosis Are More Commonly Diagnosed in Boys

The risk factors for arterial ischemic stroke and cerebral sinovenous thrombosis in neonates are not well understood. We looked at gender, birthweight, and gestational age in neonates with arterial ischemic stroke and cerebral sinovenous thrombosis to see if there were trends suggesting that these were risk factors. We identified neonates with a gestational age at birth > or = 36 weeks and a diagnosis of arterial ischemic stroke or cerebral sinovenous thrombosis made by computed tomography or magnetic resonance imaging during the neonatal period from a consecutive cohort study of children with arterial ischemic stroke and cerebral sinovenous thrombosis in Ontario. Data on gender, birthweight, and gestational age were obtained by health record review. Sixty-six children with neonatal arterial ischemic stroke were identified. Forty-one (62.1%; 95% CI 49.3-73.8%) were male. Thirty-two children with neonatal cerebral sinovenous thrombosis were identified. Twenty-five (78.1%; 95% CI 60.0-90.7%) were male. One male child was identified with both arterial ischemic stroke and cerebral sinovenous thrombosis. There was a trend toward higher than average birthweights among neonates with arterial ischemic stroke and a trend toward older gestational age in female neonates with arterial ischemic stroke. Our data suggest that neonatal arterial ischemic stroke and cerebral sinovenous thrombosis are more commonly diagnosed in boys. The slightly larger size of male neonates may be contributory in arterial ischemic stroke. It is not known whether boys are at higher risk of developing arterial ischemic stroke and cerebral sinovenous thrombosis or are simply more likely to present with symptoms resulting in diagnosis. These issues need further study.

Cerebral Sinovenous Thrombosis in Children: Another Reason to Treat Iron Deficiency Anemia

Iron deficiency anemia is a rare cause of cerebral sinovenous thrombosis in children. We report three cases of cerebral sinovenous thrombosis and iron deficiency anemia treated at Primary Children's Medical Center in Salt Lake City, Utah, between 1998 and 2001. The children were 9, 19, and 27 months old at the time of admission. Hemoglobin levels ranged from 6.6 to 7.0 g/dL, mean corpuscular volume levels from 45 to 56 fL, and platelet counts from 248,000 to 586,000/microL. Magnetic resonance imaging and magnetic resonance venography revealed thrombosis of the straight sinus and internal cerebral veins in all three children, with the addition of the vein of Galen, left transverse and sigmoid sinuses, and upper left internal jugular vein in one child. Recovery ranged from excellent to poor in 3 months to 3 years of follow-up. Four additional cases, ages 6 to 22 months, were found in the English-language literature. Evaluation for prothrombotic disorders was negative in all children, including the current cases. Treatments have included thrombectomy, corticosteroids, mannitol, heparin, low-molecular-weight heparin, warfarin, aspirin, blood transfusion, and iron supplementation, but there is no consensus regarding therapy, other than to correct the anemia and treat iron deficiency. Iron deficiency anemia, a preventable cause of cerebral sinovenous thrombosis, deserves consideration when cerebral sinovenous thrombosis is detected in young children.

Cardiology patient pages. Prothrombin 20210 mutation (factor II mutation).

Testing for the prothrombin 20210 mutation, also called factor II mutation, may have been offered by your doctor because you or someone in your family, has had (1) a blood clot in one of the deep veins of the body (also called deep vein thrombosis or DVT); (2) a blood clot that has traveled to the lung (called a pulmonary embolism or PE); (3) a blood clot in an unusual site (such as the mesenteric or cerebral sinus vein); (4) a heart attack or stroke at a young age; or (5) a history of recurrent pregnancy loss or stillbirth. A history like this in yourself or a family member may be indicative of an underlying thrombophilia. Thrombophilia is a term that describes a state in which the blood has an increased tendency to clot. People can have this increased tendency because they (1) have one or more inherited (genetic) risk factors, (2) have developed a chronic condition that puts them at increased risk, such as obesity, cancer, inflammatory bowel disease, or the persistence of certain antibodies (antiphospholipid antibodies), or (3) have a temporary condition that leads to an increased clotting tendency, such as recent surgery, trauma, a cast, prolonged immobility, pregnancy, or the use of oral contraceptives or hormone replacement therapy. The purpose of this Cardiology Patient Page is to provide more information about the prothrombin mutation, which is the second most common cause of hereditary thrombophilia. Normally, there is a fine balance in the body which ensures that there is not too much bleeding or blood clotting. If this balance is disrupted, a blood clot may occur. Throughout the course of a normal day, the blood vessels sustain many minor injuries of which you are not aware. In response, the body naturally triggers the “clotting cascade”—a sequence of events …

Health-related quality of life and its relationship to neurological outcome in child survivors of stroke.

Ischemic stroke during infancy and childhood has the potential to result in neurological impairments and affect a child's ability to function at home, school, and play. There are limited data on the effect of ischemic stroke on quality of life (QOL) of child survivors of ischemic stroke. To examine parent and child perspectives on QOL and examine factors that correlate with reduced QOL for child survivors of stroke. A prospective single-center cohort design was used. Participants included children 2-18 years of age surviving ischemic stroke. The Pediatric Quality of Life 4.0 Generic Inventory Scale (PedsQL) parent proxy-report (2-18 years of age) and child self-report (5-18 years of age) were completed by participants. Scores were compared with standardized normative data of healthy children and those with chronic medical conditions. Neurological deficits were measured with the Pediatric Stroke Outcome Measure, a standardized evaluation for children. The relationships between stroke type, neurological deficit, and health-related quality of life (HRQOL) were examined. We assessed the QOL in 84 children with arterial ischemic stroke and 16 with cerebral sinovenous thrombosis at a mean age of 8.4 (4.12) years; 4.4 (2.93) years after their stroke. Results showed that both the parent-proxy and child self-report HRQOL scores were significantly reduced (P>.01) compared with normative data of healthy children. Of greatest concern for both parents and children was the effect of stroke on school, followed by its impact on emotional and social functions. In contrast to other studies, scores in physical domain were better than those in the psychosocial domain. Multivariate analysis showed that of neurological deficits after stroke was a significant predictor of poor HRQOL (P>.05). The children with poor neurological recovery had the lowest mean PedsQL scores and their QOL was significantly poorer compared with normative data of children with chronic health conditions (ie, diabetes, cancer). The PedsQL appears to be a promising assessment tool of HRQOL for children following stroke. Both parent and child perspectives should be included because of the potential for there to be significant differences in perspectives. Although severity of neurological outcome is a significant predictor of reduced HRQOL, it accounted for a small proportion of variance in QOL scores. Further research is required to delineate other factors that are significant predictors of outcome.

Venous thrombosis in children

Venous thromboembolic (VTE) events are being increasingly diagnosed in systemic and cerebral vessels in children. Systemic VTE are increasing in children as a result of therapeutic advances and improved clinical acumen in primary illnesses that previously caused mortality. The epidemiology of systemic VTE has been studied in international registries. In children older than 3 months, teenagers are the largest group developing VTE. The most common etiologic factor is the presence of central venous lines. Clinical studies have determined the most sensitive diagnostic method for diagnosing upper system VTE are ultrasound for jugular venous thrombosis and venography for intrathoracic vessels. However, the most sensitive diagnostic methods for lower system VTE and pulmonary embolism (PE) have not been established. Treatment studies for VTE consist of inadequately powered randomized controlled trials or prospective cohort studies. The long-term outcome of systemic VTE, post-thrombotic syndrome, has been reported in children. Cerebral sinovenous thrombosis (CSVT) is becoming increasingly diagnosed in children due to the recognition of the associated subtle clinical symptoms and improved cerebrovascular imaging. The etiology of CSVT includes thrombophilia, head and neck infections, and systemic illness. Estimates of the incidence and outcome of childhood CSVT have recently become available through the Canadian Pediatric Ischaemic Stroke Registry. Clinical studies have not yet been carried out in children to determine the best method of diagnosis or treatment. There have only been case-series studies carried out in the treatment of CSVT. Properly designed clinical trials are urgently required in children with systemic VTE/PE and CSVT to define the best methods of diagnosis, treatment and long-term management.

Intraventricular hemorrhage in term neonates caused by sinovenous thrombosis.

The cause of intraventricular hemorrhage in term neonates is poorly understood. Among 29 neonates of at least 36 weeks' gestation with intraventricular hemorrhage, 9 (31%) had cerebral sinovenous thrombosis. Of the 26 neonates who underwent computed tomography or magnetic resonance studies, those with thalamic hemorrhage were more likely to have sinovenous thrombosis than those without thalamic involvement (4/5 vs 5/21, p = 0.03). Term neonates with intraventricular hemorrhage should undergo neuroimaging to evaluate the presence of sinovenous thrombosis. Ann Neurol 2003

Factor V Leiden and prothrombin gene G20210A mutation in children with cerebral thromboembolism.

We investigated whether there is an association between factor V Leiden (FVL) and/or prothrombin gene G20210A mutation (PT20210A) and cerebral thromboembolism in a pediatric Argentinean population. From May 1992 to January 2002, 44 consecutive children with arterial ischemic stroke (AIS) and 23 children with cerebral sinovenous thrombosis (SVT) were prospectively studied at a single center. The prevalence of both mutations was compared with a 102 age-matched controls. In children with AIS, the frequencies (patients vs. controls), odds ratio (OR), and 95% confidence interval (95% CI) for the presence of FVL were as follows: 2.3% vs. 2%, OR/95% CI, 1.16/0.2 to 13.2; P value = 0.99. No cases of PT20210A were found in this group. In children with SVT, the frequencies (patients vs. controls), OR, and 95% CI were as follows: FVL (4.3% vs. 2%, OR/95% CI, 2.27/0.22 to 6.2; P value = 0.99) and PT20210A (4.3% vs. 1%; OR/95% CI, 4.6/0.3 to 76.3; P value = 0.3354). One child with PT20210A also had an inherited protein C deficiency. In 12 (18%) out of the 67 children with cerebral thromboembolism, without the aforementioned mutations, other prothrombotic disorders were detected. Although a multi-center prospective study with a large number of Argentinean pediatric patients is needed to obtain considerable evidence, no association between factor V Leiden and/or prothrombin gene G20210A mutation and cerebral thromboembolism was found in this pediatric series.

Cerebral sinovenous thrombosis during asparaginase treatment

A boy (age: 7 1/2 years) with acute lymphoblastic leukaemia developed thrombosis of the sinus sagitalis superior with secondary haemorrhagic infarction while on induction treatment with vincristine, prednisone, and asparaginase. Based on this report, the potential pathogenic mechanisms are discussed with respect to congenital prothrombotic defects as well as to the role of antileukaemic treatment. Current hypotheses on mechanisms for thromboembolism in children and proposed prophylactic strategies are briefly summarized.