We evaluated the risk of unprovoked seizures after febrile convulsions and the factors prognostic of them in a cohort of 687 children who had an initial febrile seizure while residing in Rochester, Minnesota. Overall, children with febrile convulsions had a fivefold excess of unprovoked seizures, and the risk until the age of 25 was 7 percent. The risk ranged from 2.4 percent among children with simple febrile convulsions to 6 to 8 percent among children with a single complex feature--i.e., focal or prolonged seizures or repeated episodes of febrile convulsions with the same illness. For children with any two of the complex features, the risk was 17 to 22 percent, and for those with all three features, 49 percent. The occurrence of subsequent partial unprovoked seizures was strongly associated with all three of the complex features, whereas the occurrence of subsequent unprovoked seizures of generalized onset was associated with the number of febrile convulsions and a family history of unprovoked seizures. These results are consistent with the view that the increased risk of generalized-onset unprovoked seizures reflects a predisposition to both simple febrile convulsions and generalized-onset unprovoked seizures. The association between complex febrile convulsions and partial seizures, on the other hand, may reflect either a causal association or the presence of preexisting brain disease that is responsible for both the complex febrile seizures and later partial seizures.
A cohort of 424 patients was followed to determine the patterns of risk for recurrence after an initial unprovoked seizure. Overall, the risk of recurrence was 36% by 1 year, 48% by 3 years, and 56% by 5 years. The risk of subsequent seizures was lower for patients with idiopathic seizures than for those whose seizures had a presumed etiology. Among cases for which initial seizure was classified as idiopathic, EEG abnormalities, abnormal neurologic examination findings, and initial partial seizures were identified as significant independent predictors of higher recurrence risks.
All-cause and heart disease mortality and ischemic heart disease incidence among patients with an initial diagnosis of epilepsy while residents of Rochester, MN, from 1935 through 1979 were determined. Death rates from heart disease were slightly elevated for persons with epilepsy. The increased death rate from heart disease was confined to persons less than 65 years of age. The incidence of ischemic heart disease and of sudden cardiac death as the initial manifestation of ischemic heart disease was significantly increased in persons with epilepsy, but the increase was primarily limited to those with symptomatic epilepsy attributed to cerebrovascular disease. The occurrence of ischemic heart disease and sudden cardiac death was not related to anticonvulsant medication status.
Elevated lung cancer mortality rates in Harris County, Texas compared with other US counties and previously published reports that suggested a causal relation between air pollution and lung cancer in Houston prompted this ecologic analysis. A weighted regression analysis was used to examine the air pollution-lung cancer mortality relation for white males in Harris County, Texas, 1979-1981. The regression model included the following census tract-specific characteristics: median age for white males, two social and demographic factors not strongly correlated with pollution (family life cycle and migration), an age-dependent smoking index, and a pollution measure based on total suspended particulates. This model indicated a statistically significant contribution of the pollution measure in explaining the intracounty variation in lung cancer mortality rates. The relation between air pollution and lung cancer mortality, however, appeared to be highly dependent on which social and demographic factors were selected for inclusion in the analysis. Air pollution was not demonstrated to be a strong determinant of lung cancer mortality in this study in that the presence of air pollution accounted for less than 5% of the total variation in intraurban lung cancer mortality. In addition, the interpretation of geographic analysis must be guarded due to the introduction of potential bias due to aggregation. The hypothesis that air pollution is contributory to lung cancer cannot be tested until other, stronger individual risk factors for lung cancer can be better measured and controlled in studies of this association.
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