Summary: Neural tube defects (NTDs)—malformations secondary to abnormal neural tube closure between the third and fourth weeks of gestational age—have a complex and imperfectly understood etiology in which both genetic and environmental factors appear to be involved. A number of specific chromosomal or single‐gene disorders, presumably not affected by environmental influences, are associated with the development of NTDs, but such syndromal cases account for a small proportion of NTDs in live‐born infants. Analysis of recurrence patterns within families and of twin‐concordance data provides evidence of a genetic influence in nonsyndromal cases, but factors such as socioeconomic status and geographic area (independent of race or ethnicity) are also associated with variations in the incidence of NTDs. The prevalence at birth of both anencephaly and spina bifida has decreased, but the advent of antenatal diagnosis and elective termination of affected pregnancies has undermined the reliability of birth prevalence rate as an estimate of incidence. Some occupational and other exposures, including maternal use of antiepileptic drugs (AEDs), are associated with increased risk for NTDs. Among women who have had an NTD‐affected pregnancy, recurrence risk is markedly higher than the risk for a first NTD‐affected pregnancy in the general population. There is strong evidence, overall, for a protective effect of adequate folate consumption. In some high‐risk groups, however, such as women taking AEDs, folate supplementation has not been proven to reduce NTD risk.

Objective: To determine the risk of seizure recurrence after a first seizure due to neurocysticercosis (NC) and to evaluate risk factors for seizure recurrence, including the influence of antihelminthic treatment. Methods: The authors prospectively followed 77 patients with a first seizure and active or transitional NC for >7 years (median 24 months). Results: Thirty-one patients (40.3%) experienced seizure recurrence. Kaplan–Meier estimated recurrence was 22% at 6 months, 32% at 12 months, 39% at 24 months, and 49% at 48 and 84 months. Treatment with an antihelminthic (albendazole) did not influence recurrence. On multivariable analysis, none of the following predicted recurrence: sex, presenting seizure type, classification of NC, localization of cysts, Todd paralysis, neurologic deficits at presentation, EEG abnormalities. Only change in CT predicted recurrence: 22% in patients in whom cysts disappeared and 56% in patients with persistent cysts (p < 0.05). In this latter group, recurrence was associated with persistence of an active lesion. Of those with two seizures, estimated risk of a third seizure was 68% by 6 years after the second seizure. Conclusions: Seizure recurrence is high after a first acute symptomatic seizure due to NC, but this seems related to persistence of active brain lesions. Recurrence risk is low and in keeping with seizure risk following other brain insults leading to a static encephalopathy in those in whom the NC lesion clears. Patients with NC should receive antiseizure medications until the acute lesion clears on CT. There is no correlation between treatment with antihelminthic agents and seizure recurrence.