PubMed · 964756
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D Peleg, E Sklerowski, J Goldman. 1976-06-15. [Anencephaly].. https://pubmed.ncbi.nlm.nih.gov/964756/
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Neural tube defects are thought to arise from two different embryologic mechanisms depending on the level of the defect: neurulation defects associated with anencephaly and upper spina bifida and canalization defects associated with lower spina bifida. To investigate whether the risk profiles of neural tube defect cases differ according to the level of the defect, the authors examined data from the Atlanta Birth Defects Case-Control Study. Cases were infants live- or stillborn from 1968 to 1980 with these defects, and controls were infants without defects randomly selected and frequency matched to cases by race, birth year, and hospital of birth. By multivariate polychotomous logistic regression, 1,186 controls were compared with cases: 145 with anencephaly, 59 with upper spina bifida (cervical/thoracic lesions), and 100 with lower spina bifida (lumbar/sacral lesions). Infant's sex and sibling recurrence of neural tube defects were the only factors for which the case subgroups significantly differed in risk. The risks associated with selected maternal exposures during the first trimester of pregnancy did not differ among the case subgroups. Although these results do not support the concept that upper and lower neural tube defects differ in risks from exogenous factors, differences in sibling recurrence and in risks by sex between the two groups suggest an underlying heterogeneity in genetic susceptibility factors.
OBJECTIVE: To describe the recent trends and epidemiologic characteristics of neural tube defects in the United States. RESEARCH DESIGN: Ongoing surveillance data. SETTING: Two birth defect surveillance systems: the nationwide Birth Defects Monitoring Program and the Metropolitan Atlanta (Ga) Congenital Defects Program for 1970 through 1989 and 1968 through 1989, respectively. PARTICIPANTS: Between 1970 and 1989, using discharge diagnoses of approximately 1 million live-born and stillborn infants per year, the Birth Defects Monitoring Program identified 15,503 cases of spina bifida and anencephaly. Between 1968 and 1989, using discharge diagnoses and clinical records until age 1 year of 38,000 infants per year, the Metropolitan Atlanta Congenital Defects Program identified 800 cases of spina bifida and anencephaly. INTERVENTIONS: None. MEASUREMENTS/MAIN RESULTS: Nationwide, neural tube defect rates have declined from 1.3 per 1000 births in 1970 to 0.6 per 1000 births in 1989. In Atlanta, neural tube defect rates have declined from 2.0 per 1000 births in 1968 to 0.6 per 1000 births in 1989. Several changes in the epidemiologic characteristics of neural tube defects were observed: (1) the proportion of spina bifida cases has increased; (2) the proportion of neural tube defect cases compared with the proportion of other unrelated defects has increased; (3) the race ratio of whites to other races for isolated neural tube defect cases has declined in Atlanta; and (4) the rate of isolated neural tube defects in females has also decreased. CONCLUSIONS: The declining rates of neural tube defects can be partially explained by increased widespread prenatal diagnostic techniques, strongly suggesting the role of environmental factors in neural tube defects. In particular, the use of multivitamins and folic acid to prevent the occurrence of neural tube defects needs further evaluation. Nevertheless, the changing clinical and epidemiologic characteristics of cases over time points to the etiologic heterogeneity of these conditions.
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