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Research Article | Volume 16 Issue 2 (Feb, 2026) | Pages 727 - 733
Cardiac Findings in Pediatric Stroke: A Single-Center Descriptive Case Series
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1
Junior Resident, Department of Pediatrics, JJM Medical College, Davangere, Karnataka, India
2
Assistant Professor and Pediatric Cardiologist, Department of Pediatrics, JJM Medical College, Davangere, Karnataka, India Orcid ID: 0009-0008-1866-8988
3
Professor & Neonatologist, Department of Pediatrics, JJM Medical College, Davangere, Karnataka, India Orcid ID: 0000-0002-2342-0759
4
Head of the department and professor, Pulmonologist, Department of Pediatrics, JJM Medical College, Davangere, Karnataka, India.
Under a Creative Commons license
Open Access
Received
Jan. 1, 2026
Revised
Jan. 15, 2026
Accepted
Feb. 10, 2026
Published
Feb. 26, 2026
Abstract

Background: Pediatric stroke remains a significant cause of neurological morbidity and mortality with a diverse range of underlying etiologies. Cardiac conditions represent a critical, though sometimes under-recognized, subset of these associated conditions. Identification of specific cardiac findings is paramount for guiding further diagnostic evaluation and multidisciplinary management and improving long-term patient outcomes. Methods: This retrospective observational study analyzed clinical data from a tertiary care center, specifically focusing on pediatric stroke patients admitted between January 2023 and December 2025. Medical records of children aged 1 month to 18 years diagnosed with stroke and who underwent cardiac evaluation (electrocardiography, echocardiography) and neuroimaging were reviewed and included. Children with transient ischemic attacks, primary central nervous system infections, or trauma were excluded. Results: Echocardiographic evaluation demonstrated a heterogeneous spectrum of cardiac findings, with multiple abnormalities coexisting in individual patients. Patent foramen ovale (PFO) and atrial septal defect (ASD) were identified in n = 3 (37.5%) each. Isolated PFO and small ASD were analyzed separately and were not categorized as significant   heart disease. Hemodynamically significant heart disease was present in n = 3 (37.5%). Mitral and/or tricuspid regurgitation was documented in n = 2 (25.0%), and moderate pulmonary arterial hypertension was identified in n = 1 (12.5%1) associated with the hemodynamically significant heart disease. Neuroimaging consistently revealed acute infarcts (n = 6), most commonly involving Middle Cerebral Artery (MCA) territory (n = 4), with various sites including the frontal, parietal/temporal, and deep grey and white matter. Associated findings like mass effects (n = 2) and hydrocephalus (n = 2) were also noted. Conclusion: Children with stroke demonstrate a wide range of associated cardiac abnormalities, often with overlapping findings. While isolated intracardiac shunts such as PFO and small ASD were frequently identified, complex heart disease were less common but clinically significant. These findings highlight the importance of cardiac evaluation as part of the diagnostic workup of pediatric stroke and underscore the need for a multidisciplinary approach to optimize management and outcomes.

Keywords
INTRODUCTION

Despite its relatively low incidence, stroke in the pediatric age group contributes substantially to long-term neurological disability and adverse functional outcomes in affected children. Recent estimates suggest that the incidence of arterial ischemic stroke in children ranges from 2 to 13 per 100,000 annually, with significant geographical variation [1,2]. Although infectious, metabolic, and hematological causes are frequently reported in developing countries, cardiac disorders constitute one of the most important and potentially identifiable associated conditions for stroke in the pediatric age group [3,4].

 

In children, cardiac conditions contribute to stroke through diverse mechanisms, including congenital structural abnormalities, acquired cardiac disorders, and rhythm disturbances that facilitate thromboembolism. Children with complex cyanotic congenital heart disease appear especially susceptible to stroke, likely related to chronic hypoxemia, secondary erythrocytosis, and perioperative factors associated with cardiac surgery[5,6]. Additionally, cardiomyopathies and valvular disorders contribute to stroke risk by altering hemodynamics and promoting thrombus formation [7]. Advances in pediatric cardiology and cardiac surgery have improved survival but this has paradoxically led to an increased recognition of long-term neurological complications including stroke [8].

 

Globally, cardiac abnormalities are reported in 20–30% of pediatric stroke cases [9]. Indian studies have also highlighted the burden of cardiac disorders as an etiology, particularly in resource-limited settings where access to early corrective surgery may be delayed [10]. Despite improvements in imaging modalities such as echocardiography, cardiac MRI and advanced neuroimaging, diagnostic challenges persist due to heterogeneous presentations ranging from seizures and focal deficits to developmental delay [11,12].

 

Given this background, a systematic evaluation of cardiac findings in children presenting with stroke is essential. Early identification not only assists in accurate etiological classification but also guides appropriate management, secondary prevention, and long-term follow-up [7,13]. The present study was conducted to evaluate the cardiac findings in children with stroke at a tertiary care center and to correlate these findings with clinical and neuroimaging features.

MATERIALS AND METHODS

This was a retrospective, descriptive, observational study conducted in the Department of Pediatrics at a tertiary care referral hospital attached to a medical college in South India, serving a large catchment area. The study was conducted by collecting retrospective data over two-year period from January 2023 to December 2025, during which the clinical records of children presenting with stroke were systematically reviewed. All pediatric patients aged 1 month to 18 years with a diagnosis of stroke and who underwent cardiac evaluation, including electrocardiography, echocardiography and neuroimaging, were reviewed and included. For the purpose of this study, stroke was considered when children presented with an acute focal neurological deficit persisting beyond 24 hours and supported by neuroimaging evidence of cerebral infarction or hemorrhage. Children with transient ischemic attacks, primary central nervous system infections, or trauma were excluded. The study included all eligible cases during the defined period, admitted between January 2023 and December 2025. Clinical information was obtained through a pre-structured proforma using retrospective chart review. Data collection included demographic details (age, sex, residence), antenatal and perinatal history such as complications or neonatal admissions, family history including consanguinity and genetic predispositions, developmental milestones, presenting complaints such as seizures, weakness, altered sensorium, speech disturbances, or feeding difficulties, and past medical history including infections, trauma, or cardiac illness and neurological examination findings such as neurological status, including tone, reflexes, motor deficits, cranial nerve involvement, and developmental delay and growth parameters, neurocutaneous markers, and dysmorphic features documented were retrieved. All patients enrolled had undergone a cardiac evaluation, which included a clinical examination, an electrocardiogram to assess for rhythm disturbances, a chest radiograph to detect cardiomegaly or pulmonary hypertension, and echocardiography with doppler performed by in house Pediatric Cardiologist using standard echocardiography machine (GE Healthcare Vivid S6, manufactured in France, 2021 ) to evaluate for structural heart disease, valvular lesions, chamber dilatation, intracardiac thrombus, shunts, or cardiomyopathy. Neuroimaging data obtained retrospectively demonstrated that all children had undergone imaging tailored to their clinical condition. Emergency non-contrast CT brain scans and MRI of the brain reports were retrived and served as the preferred modality for ischemic stroke characterization, and magnetic resonance angiography/venography were utilized selectively to assess vascular occlusions, arteriopathies, or cerebral venous thrombosis. Baseline laboratory investigations included complete blood counts, renal and liver function tests, serum electrolytes, and calcium levels. Statistical analysis was performed using SPSS version 25 (IBM Corp., Armonk, NY, USA), with continuous variables summarized as mean ± standard deviation, as appropriate ,while categorical variables were presented as frequencies and percentages. The study protocol was approved by the Institutional Ethics Committee of J.J.M. Medical College (JJMMC/IEC-51-2025 on 13/08/2025). As this was a retrospective chart review, the requirement for informed consent was waived. Patient confidentiality was strictly maintained by anonymizing all identifying details during data collection and analysis.

RESULTS

A total of eight children with acute ischemic stroke were included in this study. The cohort demonstrated a heterogeneous age distribution. The median age at presentation was 2.75 (1.0–9.1) years. Three children (37.5%) were below two years of age, highlighting that stroke can occur even in infancy and is not confined to older pediatric cohorts. The sex distribution was balanced with four males (50%) and four females (50%). The demographic profile is summarized in Table 1.

 

Echocardiographic evaluation revealed a wide spectrum of structural and functional cardiac abnormalities. Multiple echocardiographic findings were observed in individual patients; therefore, the categories were not mutually exclusive. Patent foramen ovale (PFO) was identified in n = 3 (37.5%), and atrial septal defect (ASD) in n = 3 (37.5%), all demonstrating left-to-right shunting. Isolated PFOs and small ASDs were analyzed separately and were not classified as complex heart disease.

 

Hemodynamically significant heart disease was identified in n = 3 (37.5%) children. These included Tetralogy of Fallot with associated defects (large malaligned ventricular septal defect, pulmonary stenosis, atrial septal defect, and patent ductus arteriosus) in one child; dilated cardiomyopathy with severe left ventricular systolic dysfunction (left ventricular ejection fraction of 25%) in one child; and severe mitral regurgitation with moderate pulmonary arterial hypertension and vegetation on the aortic valve in one child. Overall, n = 5 (62.5%) children demonstrated at least one structural or functional echocardiographic abnormality. Additional findings included mitral and/or tricuspid regurgitation in n = 2 (25.0%) and moderate pulmonary arterial hypertension in n = 1 (12.5%) associated with the hemodynamically significant heart disease . These observations, summarized in Table 2, underscore the importance of systematic cardiac evaluation in children with stroke.

 

Among the eight children evaluated (n = 8), hemiparesis was the most common neurological deficit, documented in n=6 (75.0%), followed by seizures in n=3 (37.5%). Cranial nerve involvement was observed in n=1 (12.5%), while recurrent ischemic events were noted in n=2 (25.0%).

 

Magnetic resonance imaging (MRI) of the brain demonstrated heterogeneous patterns of ischemic injury across the cohort. Multiple neuroimaging abnormalities were present in individual patients; therefore, the imaging categories were not mutually exclusive. Middle cerebral artery (MCA) territory infarcts were identified in n = 4 (50.0%). Deep gray and white matter involvement, including periventricular leukomalacia, was also observed in n = 4 (50.0%). Frontal lobe infarcts were noted in n = 3 (37.5%).

 

Based on infarct characteristics, non-hemorrhagic infarcts were documented in n = 3 (37.5%). Additional imaging findings included mass effect in n = 2 (25.0%) and hydrocephalus in n = 2 (25.0%). Chronic structural sequelae were common, with frontotemporal atrophy and associated subdural hygroma observed in n = 7 (87.5%). Partial agenesis of the corpus callosum was identified in n = 3 (37.5%), while parenchymal calcification was noted in n = 1 (12.5%).

 

Table 1. Demographic Profile of Pediatric Stroke Patients (n = 8)

Parameter

 

Total patients

8

 

Age (years)#

 

2.75 (1.0 – 9.1)

 

Male*

4 (50.0)

 

 

 

 

 

Seizures at onset*

2 (25%)

 

Cranial nerve involvement*

1 (12.5%)

 

Stroke recurrence *

2 (25%)

 

Average hospital stay†

11.4 ± 3.7 days

 

 

 

 

*n (%); #Median (Range); †Mean ± Standard Deviation

 

Table 2. Echocardiographic findings in children with stroke (n = 8)

 

Echocardiographic finding

 

n (%)

 

Patent foramen ovale (isolated)

 

3 (37.5)

 

Atrial septal defect (isolated / small)

 

3 (37.5)

 

Hemodynamically significant  heart disease

 

3 (37.5)

 

Dilated cardiomyopathy with severe LV systolic dysfunction (LVEF 25%)

1 (12.5)

 

 

Tetralogy of Fallot with associated defects ( ventricular septal defect, pulmonary stenosis, atrial septal defect, and patent ductus arteriosus)

severe mitral regurgitation with moderate pulmonary arterial hypertension and vegetation on the aortic valve in one child

1 (12.5)

1 (12.5)

 

 

 

Valvular abnormalities (mitral/tricuspid/aortic regurgitation)

 

2 (25.0)

 

Moderate Pulmonary arterial hypertension (PAH)  associated with the hemodynamically significant heart disease

 

1 (12.5)

 

Preserved biventricular systolic function

 

3 (37.5)

             

Hemodynamically significant  heart disease included Tetralogy of Fallot with associated ventricular septal defect, pulmonary stenosis, atrial septal defect, and patent ductus arteriosus, and ostium secundum atrial septal defect with severe mitral regurgitation and moderate  pulmonary arterial hypertension and Dilated cardiomyopathy with severe LV systolic dysfunction (LVEF 25%)

 

Isolated PFO and small ASD were not classified as complex heart disease.

Multiple echocardiographic abnormalities were present in individual patients; therefore, categories are not mutually exclusive.

 

Table 3.  Neuroimaging Characteristics of Pediatric Stroke Patients (n = 8)

 

MRI Feature

n (%)

 

 

Based on vascular territory affected

 

 

 

MCA territory infarcts

4 (50.0%)

 

Deep gray/white matter infarcts / Periventricular leukomalacia

4(50.0%)

 

Frontal lobe infarcts

3 (37.5%)

Based on nature of infarct

 

 

 

Non-haemorrhagic infarcts

3 (37.5%)

Additional findings

 

 

 

Mass effect / Hydrocephalus

2 (25.0%)

 

 

Frontotemporal atrophy with subdural hygroma

7 (87.5%)

 

 

Partial corpus callosal agenesis

3 (37.5%)

 

 

Parenchymal calcification (frontal)

1 (12.5%)

 

                   

n(%)

 

 

2D Echo - Two-Dimensional Echocardiography,PFO: Patent Foramen Ovale; L→R shunt: Left-to-Right shunt; OS-ASD: Ostium Secundum Atrial Septal Defect; VSD: Ventricular Septal Defect; PDA: Patent Ductus Arteriosus; MR: Mitral Regurgitation; AR: Aortic Regurgitation; TR: Tricuspid Regurgitation; PAH: Pulmonary Arterial Hypertension; LVEF: Left Ventricular Ejection Fraction; BV: Biventricular; LA/LV: Left Atrium/Left Ventricle; PS: Pulmonary Stenosis; TAP: Transannular Patch; ICR: Intracardiac Repair; MCA: Middle Cerebral Artery; M2/A1: Segments of MCA/ACA; IC/PL: Internal Capsule/Posterior Limb; TMA: Thrombotic Microangiopathy; TOF: Tetralogy of Fallot.

 

Fig.1:  M-mode echocardiogram demonstrates a grossly dilated LV cavity thinning of wall thickness (indicated by the white arrow), and the markings on the echocardiography show severe systolic dysfunction with marked reduction in EF (25%) .



 

 

 

 

 

Table 4. Clinical Profile, Cardiac Findings, and Neuroimaging Characteristics of Pediatric Stroke Patients.

Patient

Age/Sex

Clinical Presentation

Cardiac Findings (two-dimensional Echo)

Neuroimaging Findings

Other Associated conditions/Notes

1

6 months, F

Left hemiparesis, arterial ischemic stroke

PFO (L→R shunt), trace pericardial effusion.

Acute non-hemorrhagic infarct (Rt parietotemporal, MCA territory), lacunar infarcts (Rt frontal/temporal), subtle leptomeningeal enhancement

Suggestive of meningitis with vasculitis

2

15 years, M

Recurrent stroke with hemolytic anemia

Papillary muscle hypertrophy, mild MR

Acute infarcts (Lt caudate, thalamus, Rt peduncle, Lt vermis, cerebellar hemispheres), chronic infarcts (Rt frontal/parietal/occipital, lentiform), hypoplastic A1

Thrombotic microangiopathy

3

2 years, M

Right hemiparesis, stroke

Dilated cardiomyopathy, LV dysfunction (LVEF 25%, possible cardiac source of embolism).

Acute non-hemorrhagic infarct (Lt MCA territory – fronto-parieto-temporal, putamen, insula), thrombosis of M2 MCA

Probable cardiac source of embolism

4

2 years, M

(Down’s syndrome)

Stroke with obstructive hydrocephalus

Small OS-ASD, LA/LV dilation, severe MR, vegetation over Aortic valve tip with moderate AR, moderate PAH, mild pericardial effusion.

Large Lt MCA infarct with mass effect, hydrocephalus, Rt frontal infarct

Syndromic,multiple cardiac defects

5

8 years, F

Left hemiparesis

PFO (L→R shunt), Small LV hyperechogenic focus, normal AV valve, trivial TR

Acute infarct (Rt MCA territory – caudate, lentiform, internal capsule, corona radiata), tiny diffusion restriction (centrum semiovale)

Evaluation for Protein C/D deficiency

6

3.5 years, F

Ischemic stroke with mass effect

Sinus rhythm.

Acute infarct (Lt MCA territory – fronto-parietal-temporal, caudate, lentiform, splenium), abrupt cutoff of Lt MCA (M2)

Non-cardiac embolic stroke

7

11 months, M

Stroke with left hemiparesis

TOF: OS-ASD, large malaligned subaortic VSD, severe sub-valvar and valvar PS, Small PDA

Ischemic stroke

 

8

10 years 8 months, F

Recurrent hemiparesis, arteriopathy

Small OS-ASD (L→R shunt), sinus rhythm.

Acute infarct (PL-left IC with diffusion restriction)

Transient cerebral arteriopathy

 

Fig 2: Axial FLAIR MRI of the brain demonstrates a large area of hyperintensity (shown in the white arrow mark in the image) involving the cortical and subcortical regions of the left frontoparietal lobe, corresponding to the MCA vascular territory. There is loss of gray–white matter differentiation with associated sulcal effacement and compression of the ipsilateral lateral ventricle, resulting in mild midline shift to the right. Findings are consistent with a large acute ischemic infarct with significant cerebral edema.

DISCUSSION

Pediatric arterial ischemic stroke in our cohort demonstrated a wide clinical spectrum across age groups, with the median age being 2.75 years and 37.5% presenting below two years, reiterating the susceptibility of early childhood to cerebrovascular events. In the present cohort, hemiparesis emerged as the predominant clinical manifestation, with seizures representing the next most frequent mode of presentation and cranial nerve involvement in 12.5%. Recurrent ischemic events were noted in two children, highlighting a need for long-term surveillance. Neuroimaging revealed MCA territory involvement in half of the cases, with associated deep gray/white matter ischemia and frontal involvement in 37.5%. Nearly half also demonstrated periventricular leukomalacia, whereas chronic structural sequelae such as frontotemporal atrophy with subdural hygroma were seen predominantly (87.5%). Features such as hydrocephalus (25%) and mass effect (25%) suggested large territorial infarcts in severe presentations.

 

Cardiac evaluation yielded important etiological insights. A majority (62.5%) displayed structural or functional cardiac abnormalities. Patent foramen ovale and atrial septal defect were the most frequently observed cardiac findings; however, these lesions were predominantly small and hemodynamically insignificant and were therefore analyzed separately. Only n = 3 (37.5%) children had hemodynamically significant heart disease. This distinction is clinically important, as isolated PFO or small ASD may represent incidental findings rather than definitive etiological factors for stroke. The clustering of MCA infarcts among children with intracardiac shunts may suggest a possible cardioembolic contribution in selected cases. Additionally, the presence of recurrent events in those with cardiac disease further supports the role of echocardiography as part of a evaluation and cardiology referral in childhood stroke. The coexistence of vasculitis and thrombotic microangiopathy in specific cases also suggests multifactorial etiologies rather than a single-system pathology.

 

When compared with existing literature, our age distribution mirrors international observations that strokes in children are not confined to older age groups but commonly affect infants and young children. Ferriero et al. reported increased vulnerability during early life due to immature cerebral autoregulation and metabolic demand imbalance [1], while similar demographic patterns have been documented in Indian cohorts by Srinivasan et al. [10]. Neurologically, hemiparesis as the dominant presenting symptom in our study aligns closely with Lynch’s description of focal weakness as the hallmark feature of pediatric AIS [14], with seizures frequently co-occurring during cortical involvement.

 

Cardiac pathology in our cohort was higher than the 20–30% prevalence reported in broader pediatric stroke data [9,13], reflecting referral bias or higher detection due to mandatory echocardiography. The high incidence of PFO/ASD-associated infarcts parallels observations by Monagle and Mackay et al. described septal defects as important substrates for paradoxical embolism in childhood stroke [4,7]. Our case of dilated cardiomyopathy with MCA infarct supports previous evidence by Ichord et al., identifying ventricular dysfunction and stagnant intracardiac flow as high-grade embolic associated conditions [15]. Similarly, our observation of ischemic stroke in a patient with Tetralogy of Fallot aligns with reports suggesting continued thromboembolic susceptibility, supporting recommendations for long-term follow-up in this population.[8]. In our study, the presence of vegetation over the aortic valve in a child with Down syndrome represents a potential cardioembolic source for cerebral infarction. Children with Down syndrome are additionally predisposed to stroke due to an increased prevalence of congenital heart disease, prothrombotic tendencies, and susceptibility to infective endocarditis, thereby compounding the risk of cerebrovascular events. Recurrent stroke in our cardiac patients is comparable to recurrence patterns observed by Fullerton et al., who reported increased risk in children with underlying heart disease or arteriopathies [16].

 

Neuroimaging patterns in our study cohort, with MCA predominance and deep white matter infarction, align with deVeber’s findings, where anterior circulation strokes were most frequent due to direct carotid-MCA flow continuation [11]. Structural sequelae such as frontotemporal atrophy reflect chronic post-ischemic remodeling, a phenomenon also described in long-term outcome studies of pediatric AIS [3,7].

 

Overall, our study reinforces that pediatric stroke is rarely single-cause and most often emerges from an interplay of cardiac, vascular, systemic, and neuro-inflammatory factors. Our findings highlight the diagnostic value of echocardiography in uncovering clinically relevant cardiac abnormalities in children presenting with stroke.. In the absence of transesophageal echocardiography or contrast studies, septal defects and PFO should be interpreted cautiously as potentially incidental findings.

 

The retrospective design, small sample size, and single-center nature of this study limit generalizability. Advanced cardiac investigations such as transesophageal echocardiography, contrast studies, and cardiac MRI were not performed, restricting definitive etiological attribution. Therefore, findings should be interpreted as descriptive and hypothesis-generating.

 

Despite its limitations, this study provides real-world echocardiographic data from a tertiary-care setting, highlighting the spectrum of cardiac abnormalities encountered in pediatric stroke.

CONCLUSION

This study describes a spectrum of cardiac abnormalities observed in children with stroke, most of which were incidental or of uncertain etiological significance. While cardiac lesions were frequently identified, causal relationships cannot be established due to the small sample size and retrospective design. Larger prospective studies incorporating advanced cardiac imaging are required to clarify their role. Clinically, our findings support systematic cardiovascular evaluation as part of a multidisciplinary approach in pediatric stroke.

REFERENCES

1.      Ferriero DM. Management of stroke in neonates and children. Lancet Neurol. 2004;3(9):533-42. doi:10.1016/S1474-4422(04)00880-1.

2.      deVeber GA, Kirton A, Booth FA, et al. Epidemiology and outcomes of arterial ischemic stroke in children. Lancet Neurol. 2017;16(6):473-84.

3.      Srinivasan J, Miller SP, Phan TG, et al. Pediatric stroke in developing countries. Indian J Pediatr. 2009;76(9):933-38.

4.      Monagle P, Mackay MT. Stroke in children: cardiac sources and paradoxical embolism. Stroke. 2010;41(10):e391-96.

5.      Ganesan V, Prengler M, McShane MA, Wade AM. Investigation of associated conditions in childhood arterial ischemic stroke. Ann Neurol. 2003;53(2):167-73.

6.      Roach ES, Golomb MR, Adams R, et al. Management of stroke in infants and children: a scientific statement from the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the Young. Stroke. 2008;39(9):2644-691.

7.      Mackay MT, Wiznitzer M, Benedict SL, et al. Associated conditions for arterial ischemic stroke in children: the International Pediatric Stroke Study. Int J Stroke. 2011;6(5):343-53.

8.      Fullerton HJ, Wu YW, Zhao S, Johnston SC. Risk of recurrent stroke in childhood. Ann Neurol. 2003;54(2):206-12.

9.      Lo W, Zamel K, Ponnappa K, et al. The cost of pediatric stroke care and rehabilitation. Stroke. 2008;39(1):161-65.

10.   Ichord RN, Benedict SL, Chan AK, et al. Cardiac disease and stroke in children. Circulation. 2004;109(22):2638-44.

11.   deVeber G, Andrew M, Adams C, et al. Cerebral sinovenous thrombosis in children. N Engl J Med. 2001;345(6):417-23.

12.   Kirton A, deVeber G. Advances in pediatric stroke imaging. Semin Pediatr Neurol. 2010;17(4):214-23.

13.   Goldenberg NA, Bernard TJ. Anticoagulation in pediatric stroke. Hematology Am Soc Hematol Educ Program. 2011;2011:364-70.

14.   Lynch JK. Cerebrovascular disorders in children. Curr Neurol Neurosci Rep. 2007;7(2):139-46.

15.   Ichord RN, Nowak-Göttl U. Cardioembolic stroke mechanisms in children. Stroke. 2014;45(6):e200-02.

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