Of 4 children with idiopathic stroke syndrome examined at the Department of Neurosciences and Pediatrics, UMD-New Jersey Medical School and the University of Rochester Medical Center, all 4 were heterozygous for human leukocyte antigen (HLA-B51). Control samples from 3 patients with non-idiopathic stroke syndrome failed to reveal the HAL-B51 marker. [1]

COMMENT. The finding of a common immunogenetic marker in children with idiopathic stroke syndrome suggests a genetic predisposition and susceptibility. The authors suggest that host factors, possibly triggered by transient viral precipitants, may contribute causally to these vascular occlusions.

Delayed onset hemiparesis and vascular thrombosis may occur approximately 6 weeks after primary varicella zoster virus infection and may explain some cases of misdiagnosed idiopathic stroke in children [2]. The importance of this clinical entity is emphasized in an editorial (Lancet June 13, 1992; 339:1449-1450). The prognosis was good regardless of therapy and all patients recovered completely or nearly completely. The MRI was more sensitive than CT or angiography in demonstrating infarction of the basal ganglia and/or internal capsule. The delay in onset of the hemiparesis may result from the time taken for the vascular media to be infected with the virus.