This population-based, retrospective cohort study of neonatal seizures included all neonates born to residents of Fayette County, Kentucky, from 1985 to 1989. We ascertained potential cases by computer search of hospital-based medical record systems, Kentucky Center for Health Statistics birth certificate data files, and National Center for Health Statistics multiple-cause-of-death mortality data files. Medical records for potential cases were abstracted, and relevant portions were reviewed independently by three neurologists using prospectively determined case-selection criteria. Seizures occurred in 58 of 16,428 neonates (3.5/1,000 live births). An additional 15 neonates had possible seizures, for a combined risk of 4.4/1,000 live births. Neonatal seizure risk varied inversely with birth weight: 57.5/1,000 live births among very low birth weight infants (< 1,500 grams) compared with 4.4/1,000 for infants with moderately low birth weight (1,500 to 2,499 grams), 2.8/1,000 for those with normal birth weight (2,500 to 3,999 grams), and 2.0/1,000 for those with high birth weight (4,000 or more grams). Risk varied among the four hospitals in the county with obstetric units, the university hospital having the highest risk. Risk did not differ by race or gender. A Cox proportional hazards model confirmed the results of the simpler univariate analyses. Differences in birth weight of the subpopulations served by each hospital accounted for much but not all the differences in hospital-specific risk.

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Children with neurosarcoid present differently than do adults. Children are more likely to have seizures, less likely to have cranial nerve palsies, and perhaps more likely to have a space-occupying lesion. Our analysis of the cases available for review in the published literature suggests that children evolve to an adult pattern as they progress through adolescence.

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The observed inverse relationship between smoking and Parkinson disease has prompted suggestions that nicotine, a centrally active agent, might protect against the disease. In this case-control study, cases were found to have ever regularly smoked cigarettes significantly less frequently than sex-, race-, and age-matched neighbors. This report analyzes the detailed smoking histories of cases and neighbors to see if these histories support the nicotine protection hypothesis. Estimated nicotine exposure before age at onset of symptoms for smoking cases was 186.1 g; for smoking controls it was 208.3 g (p = 0.34). Among the cases, severity of disease was not related to the extent of nicotine exposure before disease onset. Age at onset of symptoms for smoking cases (52.7 years) was not delayed (57.8 years for nonsmoking cases). Since the study was unable th find further support for the nicotine protection hypothesis, it is concluded that the observed inverse relationship between smoking and Parkinson disease is likely explainable by other factors, such as selective mortality or pre-morbid behavioral and/or constitutional changes.

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In previous studies, there were fewer cigarette smokers among persons with Parkinson disease than among other patients. We reinvestigated this phenomenon, using nonpatient controls. In home interviews with 237 Parkinson patients and 474 age-, sex-, and race-matched neighbors, we inquired about consumption of tobacco, coffee, tea, and alcohol. All Parkinson patients were diagnosed by a neurologist, had two or more cardinal features of parkinsonism, and had not received chronic phenothiazine therapy. One hundred fifty (63%) of 237 cases and 224 (47%) of 474 controls never smoked cigarettes (p < 0.0001). Significantly different smoking rates were also preset at 10 and 20 years before the onset of parkinsonism.