Paeds · neurology-neurodisability-and-neuromuscular
Paediatric stroke and cerebral sinovenous thrombosis
Also known as Childhood arterial ischaemic stroke · Cerebral sinovenous thrombosis · Paediatric cerebrovascular disease · Childhood stroke · Venous sinus thrombosis in children
Fellowship guide to paediatric stroke and cerebral sinovenous thrombosis. Covers the classification of childhood cerebrovascular disease into arterial ischaemic stroke, cerebral sinovenous thrombosis, and haemorrhagic stroke, the epidemiology with arteriopathy as the dominant cause and recurrence driver, the pathophysiology of arterial occlusion versus venous outflow obstruction, the clinical presentation of sudden focal deficit in the older child and seizures in the infant, the urgent MRI and MRA and MRV imaging pathway, the acute management of supportive care with antithrombotic therapy for ischaemic stroke and anticoagulation for sinovenous thrombosis, the Thrombolysis in Pediatric Stroke trial and why thrombolysis is not routine in children, the focal cerebral arteriopathy and Moyamoya subtypes, secondary prevention with aspirin, and the rehabilitation and recurrence follow-up.
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Target exams
Red flags
- Sudden focal neurological deficit in a child is a stroke until proven otherwise, and the clock starts at the time of last known well
- Headache with papilloedema, vomiting, or new seizures raises cerebral sinovenous thrombosis and demands urgent venous imaging
- Arteriopathy is the strongest predictor of recurrent childhood stroke, so vascular imaging is mandatory in every case
- Thrombolysis is not routinely recommended for paediatric arterial ischaemic stroke outside a trial, because the TIPS trial could not establish efficacy
- Anticoagulation for cerebral sinovenous thrombosis should be initiated even when haemorrhagic venous infarction is present
- A child with sickle cell disease and acute neurological deficit is having a stroke until the haemoglobin S is below thirty percent on urgent exchange transfusion
- Delayed diagnosis remains the single biggest problem in paediatric stroke, because the presentation is often attributed to migraine, postictal paresis, or a minor fall
Life stages
Care settings
Clinical exam formats
Board mappings
- Defines childhood stroke as arterial ischaemic stroke, cerebral sinovenous thrombosis, or haemorrhagic stroke and states that sudden focal deficit is a stroke until proven otherwise
- Names arteriopathy as the commonest cause and strongest predictor of recurrence in childhood arterial ischaemic stroke
- States that anticoagulation is first-line for cerebral sinovenous thrombosis even when haemorrhagic venous infarction is present
- Applies the CASCADE criteria and recognises focal cerebral arteriopathy as a dynamic and treatable arteriopathy
- Explains why thrombolysis is not routine in children using the Thrombolysis in Pediatric Stroke trial findings
- Manages acute stroke with supportive care, antithrombotic therapy, and a structured secondary prevention and rehabilitation plan
- Classification of childhood cerebrovascular disease into arterial ischaemic stroke, cerebral sinovenous thrombosis, and haemorrhagic stroke
- Urgent MRI with MRA and MRV as the imaging standard, and the role of the stroke alert pathway
- Aspirin 1 to 5 mg per kg per day for secondary prevention of arterial ischaemic stroke, and anticoagulation for cerebral sinovenous thrombosis
- Runs the acute assessment of a child with sudden focal neurological deficit within the stroke alert window
- Selects antithrombotic therapy for arterial ischaemic stroke and initiates anticoagulation for cerebral sinovenous thrombosis
- Counsels the family on the cause search, the recurrence risk, and the rehabilitation and neurodevelopmental follow-up
- Level 1: Recognition that sudden focal deficit in a child is a stroke until proven otherwise and triggers urgent imaging
- Level 2: Application of the acute stroke pathway with supportive care, antithrombotic therapy, and vascular imaging
- Level 3: Coordination of secondary prevention, arteriopathy workup, and multidisciplinary rehabilitation
- Classification and epidemiology of childhood stroke with arteriopathy as the dominant cause
- Role of the Thrombolysis in Pediatric Stroke trial and why thrombolysis is not routine in children
- Anticoagulation for cerebral sinovenous thrombosis including when haemorrhagic infarction is present
- Structured bedside assessment and drug dosing of a child with an acute focal neurological deficit
- Recognition of cerebral sinovenous thrombosis and the decision to anticoagulate
- Communication of the diagnosis, the recurrence risk, and the rehabilitation plan to the family
- Childhood arterial ischaemic stroke as a sudden focal deficit requiring urgent MRI and antithrombotic therapy
- Cerebral sinovenous thrombosis management with anticoagulation and treatment of the underlying cause
- Secondary prevention with aspirin and the role of the stroke alert pathway
- Recognition of acute paediatric stroke and activation of the stroke alert pathway
- Supportive care, antithrombotic therapy, and the reasons thrombolysis is not routine in children
- Screening for arteriopathy and arranging neurology follow-up and rehabilitation
- Canadian approach to paediatric stroke with the Canadian Paediatric Ischemic Stroke guidelines
- Arteriopathy classification and the CASCADE criteria for childhood arterial ischaemic stroke
- Anticoagulation for cerebral sinovenous thrombosis and secondary prevention with aspirin
Overview & Definition
A child who develops a sudden focal neurological deficit is having a stroke until proven otherwise, and the job is to start the clock and get vascular imaging, not to attribute the deficit to a migraine or a minor fall. Paediatric stroke is broadly defined as a cerebrovascular event occurring between twenty-eight days of age and eighteen years, and it divides into three forms. Arterial ischaemic stroke is an infarction of brain tissue from occlusion of a cerebral artery. Cerebral sinovenous thrombosis is thrombosis of the dural sinuses or cerebral veins, which raises venous pressure and can produce a haemorrhagic venous infarct. Haemorrhagic stroke is non-traumatic intracranial bleeding. Neonatal stroke, which occurs between twenty-eight weeks of gestation and twenty-eight days of life, is a separate entity with its own presentation and management. [2]
The incidence of childhood arterial ischaemic stroke is about two per one hundred thousand children per year, and the incidence of cerebral sinovenous thrombosis is about 0.67 per one hundred thousand children per year. Together these are not rare in a busy paediatric service, and the dominant problem at the bedside is delay. Children present later than adults because the deficit is attributed to a postictal state, a migraine, or a limp, and the window for acute intervention narrows or closes. Lehman and colleagues identified delayed recognition as the single biggest barrier to improving paediatric acute stroke care, which is why every fellow should treat sudden focal deficit as a stroke alert. [10]
Three principles run through this topic and structure the exam answer. The diagnosis is clinical and time-critical, and sudden focal deficit in a child triggers the stroke pathway. The management is supportive care plus antithrombotic therapy for arterial ischaemic stroke and anticoagulation for cerebral sinovenous thrombosis, with thrombolysis reserved for trial contexts. And the long game is secondary prevention, because arteriopathy drives recurrence and rehabilitation shapes outcome. The American Heart Association Scientific Statement by Ferriero and colleagues sets the standard that governs paediatric stroke management across the age range. [2]
References12ShowHide
- [1]deVeber G, Andrew M, Adams C, et al Cerebral sinovenous thrombosis in children. N Engl J Med, 2001.PMID 11496852
- [2]Ferriero DM, Fullerton HJ, Bernard TJ, et al Management of Stroke in Neonates and Children: A Scientific Statement From the American Heart Association/American Stroke Association. Stroke, 2019.PMID 30686119
- [3]Medley TL, Miteff F, Andrews I, et al Australian Clinical Consensus Guideline: The diagnosis and acute management of childhood stroke. Int J Stroke, 2019.PMID 30284961
- [4]Amlie-Lefond C, Shaw DWW, Cooper A, et al. Risk of Intracranial Hemorrhage Following Intravenous tPA (Tissue-Type Plasminogen Activator) for Acute Stroke Is Low in Children. Stroke, 2020.PMID 31842706
- [5]Amlie-Lefond C, deVeber G, Chan AK, et al Thrombolysis in acute childhood stroke: design and challenges of the thrombolysis in pediatric stroke clinical trial. Neuroepidemiology, 2009.PMID 19223687
- [6]Bernard TJ, Rivkin MJ, Scholz K, et al Emergence of the primary pediatric stroke center: impact of the thrombolysis in pediatric stroke trial. Stroke, 2014.PMID 24916908
- [7]Fullerton HJ, Stence N, Hills NK, et al. Focal Cerebral Arteriopathy of Childhood: Novel Severity Score and Natural History. Stroke, 2018.PMID 30355212
- [8]Mineyko A, Kirton A, Billinghurst L, et al. Seizures and Outcome One Year After Neonatal and Childhood Cerebral Sinovenous Thrombosis. Pediatr Neurol, 2020.PMID 31882182
- [9]Mandel-Shorer N, Sabapathy CA, Krishnan P, et al. Cerebral Sinovenous Thrombosis in Infants and Children: A Practical Approach to Management. Semin Pediatr Neurol, 2022.PMID 36456034
- [10]Lehman LL, Beslow LA, Steinlin M, et al. What Will Improve Pediatric Acute Stroke Care? Stroke, 2019.PMID 30661501
- [11]Bernard TJ, Manco-Johnson ML, Lo W, et al Inter-Rater Reliability of the CASCADE Criteria: Challenges in Classifying Arteriopathies. Stroke, 2016.PMID 27633024
- [12]Darteyre S, Renaud C, Fluss J, et al. Secondary Prevention of Childhood Arterial Ischemic Stroke. J Child Neurol, 2017.PMID 28128037