Cerebral Sinovenous Thrombosis (cerebral + sinovenou_thrombosis)

Distribution by Scientific Domains


Selected Abstracts


Anticoagulants in pediatric cerebral sinovenous thrombosis: A safety and outcome study

ANNALS OF NEUROLOGY, Issue 5 2010
Mahendranath D. Moharir MBBS
Objective Clinical trials are lacking in pediatric cerebral sinovenous thrombosis (CSVT). Neonates and children increasingly receive anticoagulant therapy (ACT) based on adult studies. Safety data for ACT in pediatric CSVT are scant and urgently needed. The objective was to assess the safety and outcome of ACT in pediatric CSVT. Methods In a single-center prospective study, neonates and children with CSVT received ACT (standard/low molecular weight heparin, warfarin) by standardized protocol. A study neuroradiologist (M.S.) assessed all initial and follow-up neuroimaging for intracranial hemorrhage (ICH), thrombus propagation, and recanalization. Clinical outcome was assessed with the Pediatric Stroke Outcome Measure. Results Among 162 pediatric patients, 85 received ACT at diagnosis, including 29/83 (35%) neonates and 56/79 (71%) children. Major hemorrhage occurred in 6% (6/99) of treated patients, including 14% (3/21 neonates, 2/15 children) with and 2% (0/17 neonates, 1/46 children) without pretreatment ICH. ACT-associated bleeds were all nonfatal, and clinical outcome was favorable in 50%, similar to the remaining patients (53%). Early follow-up imaging demonstrated thrombus propagation in 11/57 neonates (10/35 [28%] without and 1/22 [4%] with ACT [p = 0.037]) and 10/63 children (7/19 [37%] without and 3/44 [7%] with ACT [p = 0.006]). Propagation was associated with new venous infarcts in 10% neonates and 40% children and worse clinical outcome in children (p = 0.053). Recanalization occurred earlier and more completely in neonates (p = 0.002). Clinical outcome was unfavorable in 47%. Interpretation In pediatric CSVT, ACT appears safe. Nontreatment with ACT is associated with thrombus propagation, observed in ¼ of untreated neonates and over , of children. Anticoagulants merit strong consideration in pediatric CSVT. ANN NEUROL 2010;67:590,599 [source]


Role of endogenous testosterone concentration in pediatric stroke,

ANNALS OF NEUROLOGY, Issue 6 2009
Sandra Normann MD
Previous studies have indicated a male predominance in pediatric stroke. To elucidate this gender disparity, total testosterone concentration was measured in children with arterial ischemic stroke (AIS; n = 72), children with cerebral sinovenous thrombosis (CSVT; n = 52), and 109 healthy controls. Testosterone levels above the 90th percentile for age and gender were documented in 10 children with AIS (13.9%) and 10 with CSVT (19.2%), totaling 16.7% of patients with cerebral thromboembolism overall, as compared with only 2 of 109 controls (1.8%; p = 0.002). In multivariate analysis with adjustment for total cholesterol level, hematocrit, and pubertal status, elevated testosterone was independently associated with increased disease risk (odds ratio [95% confidence interval]: overall = 3.98 [1.38,11.45]; AIS = 3.88 [1.13,13.35]; CSVT = 5.50 [1.65,18.32]). Further adjusted analyses revealed that, for each 1nmol/l increase in testosterone in boys, the odds of cerebral thromboembolism were increased 1.3-fold. Ann Neurol 2009;66:754,758 [source]


Diagnosis of perinatal stroke II: mechanisms and clinical phenotypes

ACTA PAEDIATRICA, Issue 11 2009
P Govaert
Abstract Introduction:, Here (and in an accompanying article dealing with definitions, differential diagnosis and registration), a structured sequential diagnostic flow is proposed to discern clinical phenotypes for perinatal stroke, including arterial ischaemic stroke (AIS), cerebral sinovenous thrombosis (CSVT) and haemorrhagic stroke. Material and results:, For neonatal AIS, the diagnostic sequence is infection, trauma, embolism, arteriopathy, other, primary thrombosis and unclassifiable; for neonatal CSVT, the sequence is infection, trauma, venopathy, other, primary thrombosis and unclassifiable. The proposed hierarchical diagnostic flows are an initial step towards a standard for registration of the causes of neonatal stroke. Such standardization should guide attempts at prevention and intervention. An extensive literature search and study of a retrospective cohort of 134 newborn infants with stroke suggest that embolism is the most common identifiable cause for stroke in general (25%), preceding trauma (10%) and infection (8%). Other causes, such as asphyxia, acute blood loss, extracorporeal membrane oxygenation, genetic disorders or prothrombotic conditions, are seen in <5% of cases. For neonatal AIS, the presence of an embolic phenotype is 33% in this cohort. The designation unclassifiable scored 34% for the entire stroke group and 25% for neonatal AIS. Complex arterial stroke with multiple arteries involved is often seen when the underlying cause is infection, cranial trauma or embolism. One important conclusion is that a means of prevention is avoidance of embolism from thrombosis outside the brain. Conclusion:, To prevent the occurrence and recurrence of neonatal ischaemic stroke, clinicians must develop a standardized diagnostic approach that results in characterization of the clinical phenotype. [source]