US Map of Deaths from Stroke in Children Similar to that Seen for Adults

Abstract & Commentary

Synopsis: In the case of this paper, the impact reaches beyond pediatrics, and makes implications about potential contributing factors to adult stroke mortality as well.

Source: Fullerton HJ, et al. Pediatric Stroke Belt: Geographic Variation in Stroke Mortality in US Children. Stroke. 2004;35(7):1570-1573.

For approximately the past half century, it has been noted that adults, both black and white, living in the Southeastern United States, had an excess stroke mortality, relative to those living in other areas of the country. The region has thus been dubbed the "Stroke Belt." This excess mortality has been variably attributed to 1, or a combination of, risk factors, particularly dietary fat intake and hypertension, but these seem to explain only part of the story. The current study was undertaken to help elucidate whether other variables, particularly those that are not considered traditional atherosclerotic stroke risk factors, might contribute. Fullerton and colleagues evaluated the geographic variation in stroke mortality in children, a population for whom hypertension, smoking, hypercholesterolemia, etc, have been shown to play little part in stroke risk. Given this, pediatric stroke mortality should not cluster geographically, as does that of adults, unless factors aside from these are at play.

Using the National Center for Health Statistics’ death certificate data, for both ischemic infarct and hemorrhage similar to those used in earlier adult studies, Fullerton et al evaluated the rates of death from childhood stroke throughout the United States from 1979 to 1998. They found that children in the Stroke Belt did have an increased relative risk (RR) of death from stroke when compared to their peers in other portions of the country (RR, 1.21, 95% CI, 1.12-1.29; P < 0.0001; similar to the RR of 1.20 in adults).

Some of the increased mortality risk could be accounted for by race. However, even after adjustment for ethnicity, the relative risk in the Stroke Belt remained significantly elevated in white children (RR, 1.10, CI, 1.01-1.19, P = 0.03) and trended toward significance in blacks (RR, 1.12, CI, 0.99-1.27, P = 0.07). The increased risk occurred at all ages from infancy through late adolescence, and as in adults, applied to both genders.

Fullerton et al conclude that their findings support the hypothesis that the disproportionately high risk of death from stroke seen in the Southeastern area of the United States must be caused by mechanisms common to both ischemic and hemorrhagic stroke, and that are in effect throughout life from infancy to adulthood. The underlying risk factors causing this Stroke Belt may do so by contributing to either an increased incidence and/or an increased case fatality rate. As atherosclerotic stroke risk factors (smoking, hypertension, etc) have been shown not to play a significant etiologic role in pediatric stroke on the population level, they are unlikely to be a significant cause of the Stroke Belt. Fullerton et al also point out that there is evidence in the literature suggesting that those born in the Stroke Belt region are at higher risk than those who move into the region from elsewhere. Thus it is the location of ones birth, rather than that of the community in which one is reared, that is more strongly associated with one’s geographic stroke mortality risk.

Whether these cryptic risk factors reflect any environmental factors, and if so which, remains to be elucidated. Fullerton et al point out that the Stroke Belt is shifting westward, prompting others to suggest that environmental factors are an unlikely explanation for the existence of a Stroke Belt. Indeed, several studies have shown that in recent years this concentration of stroke deaths has dissipated somewhat in the deep South, but has spread westward across the Mississippi to encompass much of the KS/OK/TX region, and has even skipped to include non-adjacent regions such as the Pacific Northwest. Certainly, changes in contaminants caused by changes in regional industry, environmental policies, or geographic movement of infectious agents, could cause slow shifts such as these, as could socioeconomic factors and changes in access to and quality of health care, among other factors.


This is the latest of several important publications by Dr. Fullerton and her colleagues, at The University of California at San Francisco, describing details of the epidemiology of pediatric stroke during the last 2 decades of the 20th century. This body of work is a welcome contribution to the underserved and important field of pediatric neurovascular medicine. In the case of this paper, the impact reaches beyond pediatrics and makes implications about potential contributing factors to adult stroke mortality as well. — Susan E. Snyder

Susan E. Snyder, MD, PhD, is a resident of Pediatric Neurology at New York Presbyterian Hospital, Cornell Campus.