Childhood infections and trauma as risk factors for stroke

Abstract

Stroke is as common as brain tumor in children. The etiology of childhood arterial ischemic stroke (AIS) appears to be multifactorial, resulting from the interaction between genetic predisposition and environmental triggers. The risk factors for AIS in children are markedly different from the atherosclerotic risk factors in adults. Trauma and infections have been identified as associations in previous studies and are exposures of particular interest because of their increased prevalence in the children. The aim of this review article is to provide an overview of the research studies that have addressed the role of infections and trauma in pediatric AIS.

Fig. 1

Case 1 illustrates the phenotype of varicella-associated AIS. Brain imaging from a 17 month old boy who presented with an acute L hemiparesis, having had chickenpox 8 months earlier. (a) coronal FLAIR images showing high signal in the basal ganglia (caudate and lentiform nuclei) on the right. (b) 2D time of flight magnetic resonance imaging showing reduced flow in the distal left M1 segment of the middle cerebral artery, extending distally. No other AIS risk factors were identified despite extensive investigation, including echocardiography. A lumbar puncture was not done and the final diagnosis was post-varicella cerebral infarction. He was treated with aspirin and followed-up until the age of 12 years. He did not have any further clinical or radiological events and made an excellent motor recovery with minimal residual L sided motor signs

Fig. 2

Case 2 illustrates the clinical presentation and imaging findings of varicella vasculitis. Scans from a 7 year old girl who presented with transient weakness of the right arm 3 months after clinical chickenpox. This was her first neurologic presentation. Axial T2 weighted MRI scans (a-c) show infarcts involving the right periventricular white matter and posterior borderzone region, which had restricted diffusion (a and b) and an additional lesion with free diffusion in the head of the left caudate (c), suggesting an older clinically silent event. 2D time of flight MRA (d) showed a focal area of signal drop-out in the M1 segment of the L MCA.CSF was acellular and negative for VZV DNA. A diagnosis of FCA was made and she was treated with aspirin. Three weeks later she presented with a further episode of transient right-sided weakness. Brain imaging did not show any further infarcts but catheter cerebral angiography (e) L ICA injection, demonstrated more severe and extensive stenosis of the L MCA. In addition there were bilateral A1 stenoses and unilateral P1 stenosis. CSF examination was repeated; the CSF remained acellular, on this occasion positive for VZV DNA low titer, and VZV IgG was demonstrated to be significantly higher in CSF than in serum. She was treated with a short course of oral steroids and 3 months of acyclovir