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Transient subcortical high-signal lesions in Kawasaki syndrome
1Department of Child Neurology, Seirei-Hamamatsu General Hospital, Hamamatsu, Japan. oknsoknsokns@yahoo.co.jp
Abstract:
Kawasaki syndrome is an acute systemic vasculitis in children. The pathophysiology of Kawasaki syndrome presumably involves vascular inflammation, causing plasma leakage from systemic microvessels. From 1-30% of patients with Kawasaki syndrome exhibit central nervous system involvement, e.g., aseptic meningitis, epileptic seizures, transient hemiplegia, facial palsy, ataxia, chorea, ischemia, hearing loss, abnormal vision, disturbed consciousness, and behavioral changes. Neuroradiologically, Kawasaki syndrome demonstrates subdural effusion, infarction, atrophy, and reversible splenial lesions on magnetic resonance imaging. A 25-month-old boy developed transient hypertension with generalized seizure in the subacute phase of Kawasaki syndrome. Fluid-attenuated inversion recovery imaging, performed 5 hours and 2 days postseizure, indicated subtle, subcortical, high-signal-intensity lesions. Acute transient hypertension in this patient may have triggered the onset of lesions because of the increased permeability of brain microvessels, attributable to systemic vasculitis in Kawasaki syndrome. To our knowledge, subcortical lesions in Kawasaki syndrome were not previously reported.
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