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Rawanduzy, C.A.;  Earl, E.;  Mayer, G.;  Lucke-Wold, B. Common Etiologies of Pediatric Stroke. Encyclopedia. Available online: https://encyclopedia.pub/entry/39850 (accessed on 22 December 2025).
Rawanduzy CA,  Earl E,  Mayer G,  Lucke-Wold B. Common Etiologies of Pediatric Stroke. Encyclopedia. Available at: https://encyclopedia.pub/entry/39850. Accessed December 22, 2025.
Rawanduzy, Cameron A., Emma Earl, Greg Mayer, Brandon Lucke-Wold. "Common Etiologies of Pediatric Stroke" Encyclopedia, https://encyclopedia.pub/entry/39850 (accessed December 22, 2025).
Rawanduzy, C.A.,  Earl, E.,  Mayer, G., & Lucke-Wold, B. (2023, January 06). Common Etiologies of Pediatric Stroke. In Encyclopedia. https://encyclopedia.pub/entry/39850
Rawanduzy, Cameron A., et al. "Common Etiologies of Pediatric Stroke." Encyclopedia. Web. 06 January, 2023.
Common Etiologies of Pediatric Stroke
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This entry is adapted from the peer-reviewed paper 10.3390/biomedicines11010002

Pediatric stroke is an important cause of mortality and morbidity in children.  Stroke is a neurologic injury often associated with significant mortality and morbidity. The underlying mechanism is most frequently due to occluded cerebral blood vessels, i.e., ischemic stroke; however, hemorrhagic stroke is an important etiology. 

pediatric stroke arterial ischemic stroke hemorrhagic stroke

1. Etiology and Epidemiology of Ischemic Stroke

Pediatric arterial ischemic stroke (AIS), a significant source of pediatric neurologic morbidity, can lead to numerous debilitating consequences: sensorimotor deficits, behavioral problems, intellectual disability, language impairment, and epilepsy [1]. Pediatric AIS is classified by age, as perinatal AIS broadly encompasses 20 weeks of fetal life through day-of-life 28. Perinatal AIS is further classified by the timing of presentation. Childhood AIS encompasses the first month of life and beyond [1]. Additionally, diagnosing AIS in children is frequently delayed [2][3]. Therefore, understanding and identifying risk factors and at-risk populations is vital in improving the diagnosis and management of AIS.
The risk of pediatric AIS maintains an interesting trend, as children under one year of age maintain the highest risk, with a dramatic decline after one year. This risk remains low through mid-adolescence, at which time risk begins to increase [4]. Additionally, black children have been reported to maintain an increased risk of AIS when compared to white children, and this discrepancy persists after controlling for sickle cell disease [4][5]. Male sex is also reported to be associated with a higher incidence of both childhood and perinatal AIS, and this discrepancy persists after controlling for trauma [4][5].
In 2014, Lehman and Rivkin compiled a list of risk factors among perinatal AIS.
Perinatal AIS often manifests due to pregnancy-related risk factors, including hypercoagulability and complex circulation interactions. Table 1 illustrates an adapted version of these risks [6]. Congenital heart disease and arteriopathies present in the infant remain risk factors during both the perinatal stage and beyond the first year of life [1][6]. Thrombophilia in both mother and child remains a risk factor during pregnancy and after pregnancy in childhood AIS [1][6]. These risk factors will be discussed subsequently in the setting of childhood AIS.
Table 1. Various risk factors for perinatal AIS.
Maternal Fetal Placental
Infertility Hypoglycemia Chorioamnionitis
PROM Perinatal asphyxia Placental infarcts
Pre-eclampsia Infection Weight < 10th percentile
Smoking Resuscitation efforts  
IUGR 5-min APGAR <7  
Infection    
Maternal Fever
There are numerous risk factors for AIS in children, and an overview of these causes is outlined in Table 2 [1]. By definition, pediatric AIS is an acute neurological deficit in a child aged 29 days to 18 years with radiographic evidence of cerebral parenchymal infarction in a known arterial territory that corresponds to their clinical symptoms [7]. The Childhood AIS Standardized Classification and Diagnostic Evaluation (CASCADE) criteria are used to categorize strokes according to the underlying causes [7][8], and arteriopathies are recognized as the most significant risk for childhood AIS [8]. These blood vessel abnormalities can be chronic or acute/transient changes, and they regularly appear on vascular imaging [9][10]. Underlying, inborn or acquired etiologic causes of AIS, such as cardiac disease, metabolic disturbances, thrombophilia and rheumatologic diseases such as systemic lupus erythematosus, may or may not present with vascular imaging changes [9][10]. Focal cerebral arteriopathy (FCA) is a descriptive, catch-all term used to broadly describe transient cerebral arteriopathy (TCA) and other arteriopathies that meet the CASCADE designation of AIS [7]. TCA manifests as a focal stenosis or segmental vessel wall narrowing most often in the distal internal carotid artery, proximal middle cerebral artery and circle of Willis [11]. These angiographic findings are more common in children with abnormal lipid profiles and familial cardiovascular disease [12]. The literature suggests associations between TCA and varicella infections [13], acute herpes virus infections [14] and other upper respiratory infections [15], though the impact of the inflammatory pathways in TCAs remains to be fully understood.
Table 2. Various risk factors for childhood AIS.
Arteriopathies FCA, TCA Craniocervical arterial dissection Fibromuscular dysplasia Moyamoya disease Primary CNS angiitis
Cardiac Disease Congenital heart disease Cardiomyopathy Arrhythmia Catheterization, Surgery ECMO
Inherited Thrombophilia Protein C, S, Antithrombin deficiency Factor V Leiden Prothrombin G20210A MTHFR C677T Lipoprotein A elevation
Acquired Thrombophilia Antiphospholipid syndrome Drug-induced      
Inborn Errors of Metabolism Mitochondrial disease Fabry Disease      
Rheumatologic Disease Systemic lupus erythematosus Systemic vasculitis      
Other Sickle Cell Disease Malignancy Congenital vascular syndromes
There are other, rare causes of pediatric AIS that warrant discussion, including stroke secondary to genetic disorders such as pseudoxanthoma elasticum [16]. Pseudoxanthoma elasticum is a rare genetic disorder that affects elastic fibers in the skin, eyes, gastrointestinal tract and the walls of blood vessels. The most common symptoms for children with pseudoxanthoma elasticum are retinal and vascular lesions or skin papules; however, though infrequent, cerebrovascular infarcts have been reported and can result in severe neurologic impairment and death [16].
Cardiac disease represents another significant risk factor among pediatric AIS, present in up to 30% of AIS cases [9][17]. Acquired and congenital heart diseases resulted in a 16.1-fold increased risk of AIS when compared to the general pediatric population in a study utilizing the Intermountain Pediatric Stroke Database, with single ventricle pathologies being among the highest risk [18]. Additionally, children with cardiac etiologies of AIS present at an earlier age [19][20]. Recurrent AIS among this patient population is also a concern, as one study reports that 27% of patients with cardiac causes of AIS have another event within 10 years. Recurrent AIS is associated with mechanical valves, thrombophilia, anticoagulation treatment and acute infection [21]. In terms of patent foramen ovale (PFO), pediatric AIS may be a result of embolization due to the right-to-left atrial shunt, though a definitive causation linking PFO with AIS is not established [22]. Claiming PFO as the cause of AIS is based on exclusion after thoroughly ruling out all other etiologies, and PFO closure should be considered on an individual basis [22].
Malignancy, sickle cell disease (SCD) and thrombophilia remain other prominent risk factors among pediatric AIS. The risk of AIS among patients with SCD was dramatically reduced following the 1998 STOP trial, illustrating an effective prevention with chronic transfusion therapy and dramatically reducing AIS in this population where resources are available [23]. Transcranial Doppler, where available, is also an effective screening modality [24]. In some studies, thrombophilia has been observed in up to 50% of pediatric AIS cases [25][26]. An association between thrombophilia and AIS has been established in the following biomarkers: protein C deficiency, factor V G1691A, factor II G20210A, MTHFR C677T, elevated lipoprotein A and antiphospholipid antibodies [27].

Presentation, Symptomatology and Management

Challenges arise when it comes to pediatric stroke diagnosis, in part due to a lack of clinical suspicion because of the diverse and non-pathognomonic presentation. Classically, stroke in adults presents with many universally recognized signs and symptoms. The B.E F.A.S.T. (Balance, Eyes, Face, Arms, Speech, Time) protocol not only delineates common stroke symptoms, such as face droop, unilateral arm weakness and speech difficulties, but also stresses the importance of prompt treatment. Pediatric stroke requires the same urgency but lacks similar protocols for universal recognition. Focal weakness and limb and face weakness can be presentations of pediatric AIS [28]. However, the hallmark sign of stroke, acute hemiparesis, is common only in older pediatric patients [29]. Seizures are the primary presenting symptom for younger children, while nonspecific symptoms such as fever, nausea/vomiting, headache and cardio-pulmonary dysfunction permeate all pediatric patients [29]. The lack of specific symptoms makes recognition more difficult. In addition, a broad differential diagnosis for hemiparesis adds to the complexity of diagnosis in pediatric stroke, as there are many stroke-mimicking disorders. Nearly 21–76% of children with acute-onset focal neurological deficits are found to have migraines, focal seizures, demyelinating diseases, conversion disorders and central nervous system tumors, among other possible diagnoses [30]. The rarity of pediatric AIS and subsequent lack of clinical suspicion can delay diagnosis [31]; however, due to its urgent treatment requirements, AIS should be considered in a differential diagnosis for acute-onset neurologic deficit [31].
In a pediatric patient presenting with stroke-like symptoms, magnetic resonance imaging (MRI) is the preferential imaging modality; however, there are challenges to obtaining them in the pediatric population [28]. High-quality scans can be difficult to achieve in children without sedation because of movement artifacts from restlessness in MRI scanners [32].
Perinatal AIS in the neonatal period is managed with supportive measures, including oxygenation and managing dehydration and anemia [33]. Aspirin and anticoagulation are often not pursued due to the low risk of recurrence of neonatal AIS, though these treatments are considered when AIS is due to cardiac disease [34][35]. Additionally, thrombolytics and mechanical thrombectomy are often not considered in neonates following AIS due to the lack of evidence and small size of neonatal arteries [33][36].
Management of childhood AIS includes strategies targeted towards hypertension, hypotension, hyperglycemia, fever, cerebral swelling and seizures. Acute treatment of childhood AIS focuses on neuroprotective management by maintaining cerebral perfusion and reducing metabolic demand from fevers and seizures [1]. Acute treatment with IV tissue plasminogen activator (tPA) and revascularization are revolutionary in the management of adult AIS, though evidence is lacking in terms of translating this care to children. The Thrombolysis in Pediatric Stroke (TIPS) trial offered potential criteria to safely utilize tPA in children, but these criteria have not been widely accepted [1][37]. The hallmarks of both acute and chronic therapies include anticoagulation and antiplatelet medications. Controversy exists in the literature, however, regarding the optimal treatment. This is in part due to the low risk of bleeding in pediatric AIS, while monitoring the risk of acute hemorrhagic conversion and acknowledging the prominent risk of pediatric AIS recurrence [38][39]. In cases of pediatric AIS with a specific disease etiology, management specific to each disease should be considered, i.e., chronic transfusions in SCD.

2. Etiology and Epidemiology of Hemorrhagic Stroke

Hemorrhagic stroke accounts for 35–54% of all childhood stroke [4][40][41][42]. This contrasts with its incidence in adults, where hemorrhagic stroke only accounts for 7.5–19% of all strokes [43][44][45]. As previously described, while there are widespread protocols for adult stroke recognition and management, there is a lack of any similar stroke protocols for the pediatric population. This, among other reasons, may contribute to the increased mortality rate of pediatric hemorrhagic stroke, which can be as high as 54% compared to 18–35% in adults [46][47]. Among the causes of hemorrhagic stroke, one study found that 13% of patients were found to have an underlying cerebral aneurysm, 31% had brain arteriovenous malformations, 2.5% had brain tumors, 25% had an undetermined etiology, and 28.5% had other medial and anatomical etiologies (Figure 1) [48].
Figure 1. Graph showing the commonality of the different causes of hemorrhagic stroke in pediatric populations. A total of 31% of patients had brain arteriovenous malformations, 13% had a cerebral aneurysm, 2.5% had brain tumors, 25% had an undetermined etiology, and 28.5% had other medial and anatomical etiologies.

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