Abstract 174: Headache Presentation in Childhood Arterial Ischemic Stroke Differs by Arteriopathy Subtype
Introduction: Headache is common at onset of arterial ischemic stroke (AIS), with rates between 10-50%. Adult studies suggest that headache prevalence relates to stroke etiology, with highest rates observed in dissection. We hypothesized that children with arteriopathy-related stroke may have higher rates of headache than those without.
Methods: Children (29 days -18 years) with AIS enrolled in the prospective, international Vascular Effects of Infection in Pediatric Stroke (VIPS) study were analyzed for presence of headache at stroke ictus. Cases were subjected to a rigorous, centralized process for diagnostic confirmation of AIS and radiographic classification of arteriopathy as definite, possible or absent. Site investigators abstracted data from medical records regarding stroke presentation details. Headache at stroke ictus was classified as present, absent or unclear.
Results: We included all 355 VIPS cases in this secondary analysis. Headache was uncommon in subjects < 3 yo (5/90, 6%) but was present in nearly half of those ≥ 3 yo (108/265, 46%). Excluding those with an unclear headache presentation (n=31), there was no significant difference in headache at stroke ictus in children ≥ 3 yo with definite (46/92, 50%), possible (15/24, 63%) or absent (60/118, 51%) arteriopathy (p=0.53). However, in those with definite arteriopathy, a difference was found in sub-classification, with headache prevalence highest in dissection and transient cerebral arteriopathy of childhood (TCA) (70% each) (p>0.001). Acute headache was uncommon in children with moyamoya (12%).
Conclusion: No difference was found in headache prevalence in children with and without definite or possible arteriopathy. However, in children with definite arteriopathy, headache was more common in TCA and dissection. This may reflect a higher degree of nociceptive afferent activation in these childhood AIS subtypes and may provide clues to underlying pathophysiologic mechanisms.
Author Disclosures: L.L. Billinghurst: None. N.K. Hills: None. L. Jastrzab: None. M. Wintermark: None. G.A. deVeber: None. H.J. Fullerton: None. M. Dowling: None.
- © 2017 by American Heart Association, Inc.