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PubMed1997

Neural tube defect among Palestinians: a hospital-based study.

A preliminary study was undertaken to estimate the incidence of neural tube defect (NTD) among Palestinians living in East Jerusalem and the southern part of the West Bank (600,000 inhabitants). Between 1 January 1986 and 31 December 1993, all NTD in fetuses weighing more than 500 g or of more than 22 weeks gestation, whether the product of abortion, therapeutic termination, stillborn or liveborn, were included. Mothers' data recorded included age, parity, residential area, gestational age, obstetrical history and consanguinity. The study included 26,934 consecutive newborns registered at Makassed Hospital in the study period. There were 148 cases of NTD, an incidence of 5.49 per 1000 births. The female to male ratio was 1.5:1. The incidences of spina bifida, encephalocele and anencephaly were 2.23, 0.44 and 2.41 per 1000, respectively. The incidence of NTD increased with maternal age. This preliminary report reveals a high incidence of NTD in the Palestinian community and further monitoring is necessary to confirm these findings and implement suitable policies for the detection and prevention of NTD.

Adolescent↗
PubMed2006

Schizophrenia and neural tube defects: comparisons from an epidemiological perspective.

In this review, we examine and compare epidemiological studies of schizophrenia and neural tube defects (NTDs). Although there is no apparent link between these 2 disparate disorders in terms of clinical manifestation or phenotypes, overlapping patterns in the variation of incidence of schizophrenia with that of NTDs indicate the existence of one or more shared etiological risk factors. Evidence in support of such a phenomenon may enhance our understanding of underlying pathological mechanisms and may guide future studies of etiology and prevention. The similarities that occur in a number of epidemiological observations for these disorders are in keeping with a hypothesis of nutritional deficiencies in utero acting as a risk factor for both schizophrenia and NTDs. Programes of periconceptual folate and multivitamin supplementation aimed to reduce the risk of NTDs are already in place in many countries. Nevertheless, evidence of additional effects of specific maternal micronutrient deficiency on risk of schizophrenia may not only increase enthusiasm for expansion of such programes but also enhance understanding of etiology of this disorder and offer the potential for targeted interventions in high-risk groups.

Birth Intervals↗
PubMed1996

Parental recreational drug use and risk for neural tube defects.

The authors investigated whether maternal or paternal periconceptional use of recreational drugs increased the risk of having neural tube defect (NTD)-affected pregnancies using a population-based case-control study of fetuses and liveborn infants with NTDs among 1989-1991 California births. Face-to-face interviews were conducted with mothers of 538 (88% of eligible) NTD cases and 539 (88%) nonmalformed controls, usually within 5 months of delivery. Periconceptional maternal use of cocaine (odds ratio (OR) = 0.74, 95% confidence interval (CI) 0.40-1.4), amphetamines/speed (OR = 0.68, 95% CI 0.39-1.2), or marijuana (OR = 0.64, 95% CI 0.43-0.95) or preconceptional use of alcohol as < 1 drink/day (OR = 0.80, 95% CI 0.62-1.0) or > or = 1 drink/day (OR = 0.69, 95% CI 0.42-1.2) or of cigarettes as < 1 pack/day (OR = 0.90, 95% CI 0.65-1.2) or > or = 1 pack/day (OR = 0.59, 95% CI 0.36-0.96) did not increase the risk for delivering NTD-affected offspring. Risks were not substantially altered after adjustment for maternal age, race/ethnicity, vitamin use, education, and household income. Increased NTD risk was also not generally associated with paternal drug use. The authors could not discern whether the decreased risks observed for these maternal exposures reflected a true association or were due to reporting bias, a disproportionate number of drug-exposed NTD cases among spontaneous abortuses that could not be ascertained, or some other bias.

Case-Control Studies↗
PubMedDate not supplied

[Neural tube defects and vitamin B12: a report of three cases].

Periconceptional folic acid supplementation reduces the frequency of embryological neural tube defects (NTD). This fact led the USA to fortify grain products with folic acid (140 microg/100 g) starting in January 1998, with a resultant decrease in the incidence of NTD. Folate deficiency is thus confirmed to be a risk factor for NTD. However, in a prospective study, we investigated three women who conceived a fetus with NTD; no folate deficiency was found in these women but all three had decreased vitamin B12 levels (cobalamin), which can be an other risk factor. Samples were obtained from two women in Algeria, 2 days after interruption of pregnancy, and from a vegetarian woman, in France, one month after interruption of pregnancy. Red cell folate and plasma folate, vitamin B12, B6 and homocysteine were assayed and the mutations C677T (in metylenetetrahydrofolate reductase gene), A2756G (in methionine synthase gene) and A66G (in methionine synthase reductase gene) were sought. Elevated plasma folate levels were found in both Algerian women. Vitamin B 12 levels in all three women were decreased or in the lowest quartile of normal values. One woman presented simultaneously a vitamin B 12 deficiency, and heterozygous mutations in the three genes. The second woman presented a A66G homozygous mutation and the third heterozygous C677T and A66G mutations. Acquired and inborn factors are intricated in some cases of pregnancies with NTD and B 12 deficiency can be responsible for intracellular folate cycle failure. It would therefore be advisable to consider fortifying grain products with both folic acid and vitamin B12.

Adult↗
PubMed1988

Prevention of spinal neural tube defects in the mouse embryo by growth retardation during neurulation.

Homozygous mutant curly tail mouse embryos developing spinal neural tube defects (NTD) exhibit a cell-type-specific abnormality of cell proliferation that affects the gut endoderm and notochord but not the neuroepithelium. We suggested that spinal NTD in these embryos may result from the imbalance of cell proliferation rates between affected and unaffected cell types. In order to test this hypothesis, curly tail embryos were subjected to influences that retard growth in vivo and in vitro. The expectation was that growth of unaffected rapidly growing cell types would be reduced to a greater extent than affected slowly growing cell types, thus counteracting the genetically determined imbalance of cell proliferation rates and leading to normalization of spinal neurulation. Food deprivation of pregnant females for 48 h prior to the stage of posterior neuropore closure reduced the overall incidence of spinal NTD and almost completely prevented open spina bifida, the most severe form of spinal NTD in curly tail mice. Analysis of embryos earlier in gestation showed that growth retardation acts by reducing the incidence of delayed neuropore closure. Culture of embryos at 40.5 degrees C for 15-23 h from day 10 of gestation, like food deprivation in vivo, also produced growth retardation and led to normalization of posterior neuropore closure. Labelling of embryos in vitro with [3H]thymidine for 1 h at the end of the culture period showed that the labelling index is reduced to a greater extent in the neuroepithelium than in other cell types in growth-retarded embryos compared with controls cultured at 38 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Maternal illness, including fever and medication use as risk factors for neural tube defects.

We investigated if selected maternal illnesses or medications used during the periconceptional period increased risk of having neural tube defect (NTD)-affected pregnancies. We used a population-based case-control study of fetuses and liveborn infants with NTDs among 1989-1991 California births. In-person interviews were conducted with mothers of 538 (88% of eligible) NTD cases and 539 (88%) nonmalformed controls, usually within 5 months of delivery. A maternal fever or febrile illness episode in the first trimester was associated with an increased risk for having a NTD-affected pregnancy, odds ratio (OR) = 1.91 (95% confidence interval, 1.35-2.72) for fever and OR = 2.02 (1.20-3.43) for febrile illness. Risk estimates were not substantially altered after adjustment for maternal age, race/ethnicity, education, vitamin use, and body mass index. Other reported illnesses were generally not associated with risks of 1.5 or greater, or were too infrequent to adequately estimate risk. An OR of 1.5 or greater was observed for maternal use of guaifenesin, OR = 2.04 (0.79-5.28), and an OR of 0.5 or less was observed for maternal use of calcium-containing medicines, OR = 0.38 (0.14-1.03). Our findings are consistent with previous reports that suggested elevated NTD risks from maternal fever. We could not discriminate, however, whether the increased risks observed for maternal fever were indicative of a causal relation or due to reporting bias. Our findings suggest that many of the illnesses common to reproductive-aged women and the medications commonly used to treat them during pregnancy, except, perhaps, for those illnesses that are febrile-related, do not appear to substantially contribute to the occurrence of NTDs in the population.

Adult↗
PubMedDate not supplied

Primary prevention of neural-tube defects and some other major congenital abnormalities: recommendations for the appropriate use of folic acid during pregnancy.

Neural-tube defects (NTDs) are common and serious congenital abnormalities of the central nervous system. Although some cases of NTDs are induced by hyperhomocysteinaemia, resulting from genetic polymorphism of a thermolabile enzyme, in the majority of cases the cause is unknown. Diet supplementation with a folic acid-containing multivitamin or high dose of folic acid alone in the periconception period reduced the recurrence of NTDs by 83 to 91% and 71%, respectively. Two Hungarian intervention studies demonstrated a high efficacy for periconception multivitamin supplementation (containing a physiological dose: 0.8mg of folic acid) in the primary prevention of the first occurrence of an NTD (approximately 92% reduction in the incidence of NTDs). However, a high dose of folic acid (approximately 6mg) alone during the periconception period was less efficient. Periconception folic acid-containing multivitamin supplementation reduces the occurrence of urinary tract and cardiovascular congenital abnormalities, and congenital limb deficiencies. The occurrence of orofacial cleftings may also be reduced by a high dose of folic acid. This preventive effect may be the result of other mechanisms of action (e.g. compensation of impaired mitosis caused by a folate deficiency). There are 3 options for ensuring appropriate multivitamin/folic acid consumption for women of childbearing age. First, providing a folate- and other vitamin-rich diet, which unfortunately may not be appropriate for this purpose. Second, and perhaps the best choice, the unique opportunity for multivitamin/folic acid supplementation during the periconception period. However, a major proportion of pregnancies are unplanned and, even in planned pregnancies, this type of primary prevention has not been widely used. Furthermore, it would require changes to the previous recommendations since a multivitamin containing a physiological dose of folic acid (0.5 to 0.8mg) seems to be more effective in reducing the occurrence of the first NTD and other congenital abnormalities than folic acid alone. Periconception multivitamin supplementation may also reduce the occurrence of recurrent NTDs. Thirdly, food (e.g. flour, bread) may be fortified with folic acid or 3 B vitamins (folic acid, B 12 and B6). This provides a practical means to ensure all women, especially those from lower socioeconomic backgrounds and/or with a low level of education who are more likely to have unplanned pregnancies, have an adequate folic acid intake.

Adult↗
PubMed2004

Dietary nitrites and nitrates, nitrosatable drugs, and neural tube defects.

BACKGROUND: Amine-containing (nitrosatable) drugs can react with nitrite to form N-nitroso compounds, some of which are teratogenic. Data are lacking on whether dietary intake of nitrates and nitrites modifies the association between maternal nitrosatable drug exposure and neural tube defects (NTDs) in offspring. METHODS: We examined nitrosatable drug exposure and NTD-affected pregnancies in relation to dietary nitrite and total nitrite intake in a case-control study of Mexican American women. We interviewed 184 women with NTD-affected pregnancies and 225 women with normal live births, including questions on periconceptional drug exposures and dietary intake. For 110 study participants, nitrate was also measured in the usual source of drinking water. RESULTS: Women who reported taking drugs classified as nitrosatable were 2.7 times more likely to have an NTD-affected pregnancy than women without this exposure (95% confidence interval [CI] = 1.4-5.3). The effect of nitrosatable drugs was observed only in women with higher intakes of dietary nitrite and total nitrite (dietary nitrite + 5% dietary nitrate). Women within the highest tertile (greater than 10.5 mg/day) of total nitrite were 7.5 times more likely to have an NTD-affected pregnancy if they took nitrosatable drugs (95% CI = 1.8-45.4). The association between nitrosatable drug exposure and NTDs was also stronger in women whose water nitrate levels were higher. CONCLUSIONS: Findings suggest that effects of nitrosatable drug exposure on risk for neural tube defects in offspring could depend on the amounts of dietary nitrite and total nitrite intake.

Adolescent↗
PubMed1990

Screening spinal ultrasound in newborns with neural tube defects.

Twenty-six newborns with spina bifida had complete spinal ultrasound (US) prior to initial surgical repair of the neural tube defects. Associated anomalies were found on screening US in seven infants and included diastematomyelia (two cases), hydromyelia (two cases), and dural fat deposits (three cases). Initial surgical therapy was altered in one infant with diastematomyelia. Four closed simple meningoceles showed no internal neural elements on US and none were found at surgery.

Humans↗
PubMed1981

The synaptic membrane D2-protein in amniotic fluid from pregnancies with fetal neural tube defects.

The D2-protein is a neuronal membrane protein which has an immunochemically detectable soluble derivative in cerebrospinal fluid. We used rocket-on-line immunoelectrophoresis with an antiserum against rat synaptosomal membranes for demonstration of the human D2-protein in fetal cerebrospinal fluid and in amniotic fluids from pregnancies with fetal neural tube defects. D2 was neither found in normal amniotic fluids nor in cases of amniotic fluids from pregnancies with other malformations. Analysis of D2 in amniotic fluids may thus have a future role in the antenatal diagnosis of fetal neural tube defects.

Amniotic Fluid↗
PubMedDate not supplied

Neural-tube defects in a prehistoric south-western Indian population.

Concern with the frequency and patterning of the occurrence of midline neural-tube defects among contemporary human populations is widespread. These defects are, however, quite old and occur in unusually high numbers of prehistoric skeletons. A common explanation offered for such high incidence has been inbreeding among small, reproductively isolated populations. In a sample of 54 skeletons from the prehistoric south-western Indian site of Tijeras Pueblo in New Mexico, failure of neural-tube closure occurs in 10% of sacra recovered. While a more homogeneous genetic background and inbreeding may account for a portion of this elevated prevalence, the cause appears to lie with cultural-environmental factors. It is suggested that the aetiology of these conditions has become more complex in recent human history.

Adolescent↗
PubMed1989

Neural tube defect recurrence after 'partial' vitamin supplementation.

A total of 227 mothers enrolled for periconceptional multivitamin supplementation because of previous neural tube defect (NTD) births took vitamins for less than the recommended minimum period (at least 28 days before conception until two menstrual periods have been missed). Of 213 examined infants/fetuses born to these partially supplemented mothers, two had NTD, one of whom followed four previous NTDs. The observed NTD recurrence rate is similar to that observed in fully supplemented mothers. A further 14 mothers started supplements before the second missed period but after the normal time of neural tube closure. Three of their offspring had NTD. The significance of this apparently high recurrence rate is discussed.

Ascorbic Acid↗
PubMedDate not supplied

Is maternal alpha-fetoprotein screening still of value in a low-risk area for neural tube defects?

Estimation of maternal serum alpha-fetoprotein (AFP) was used as a screening method for the detection of neural tube defects (NTDs) in 6344 women over three years. Of 88 (1.4 per cent) who had one or more serum AFP levels equal to, or greater than, 2.5 multiples of the median (MoM) for the relevant gestational age, 43 (0.68 per cent) underwent amniocentesis. There were eight NTDs. Four of these were screened by serum AFP, and all cases of spina bifida had serum AFP levels greater than 3.0 MoM, including one small open defect which was not seen on ultrasound. The other four cases of NTD, which were not screened, were identified by ultrasound. Of 64 singleton pregnancies 32 (50 per cent) had serum AFP levels between 2.5 and 3.0 MoM, and low birthweight (less than or equal to 2500 g) occurred in 29 per cent. Because of improvements in ultrasound techniques and the apparent falling incidence of NTD, the role of serum AFP as the primary screening procedure should be regularly reviewed. Effective screening is dependent on mothers booking early.

Amniocentesis↗
PubMed1983

The cause of neural tube defects: some experiments and a hypothesis.

The mouse mutant curly-tail is an animal model for human neural tube defects (NTD). Around 60% spontaneously have NTD. It has been found that maternal administration of hydroxyurea, mitomycin C, or 5-fluorouracil on day 9 of pregnancy, that is, when the fetal neural tube is in the final stages of closure, leads to a significant reduction in the proportion of NTD (to 15 to 20%) in the offspring, while total litter size is unaffected. All these substances are inhibitors of DNA synthesis, yet are apparently beneficial to subjects predisposed to NTD. As a consequence, it is suggested that the underlying mechanism causing NTD in the mice, and also in man, is a basic metabolic defect in DNA synthesis which affects cell replication and results in abnormal morphogenesis of the neuraxis.

Animals↗
PubMed1976

Amniotic fluid levels of fibrin(ogen) degradation fragment E and alpha-fetoprotein in normal pregnancy and with fetal neural tube defect.

Amniotic fluid levels of alpha-fetoprotein (AFP) and fibrin(ogen) degradation fragment E (FgE) were measured in 214 normal subjects and 27 pregnancies associated with an abnormal fetus (open neural tube defect or exomphalos). AFP levels showed no overlap between the normal and abnormal groups, thus confirming the reliability of the AFP assay in the detection of these abnormalities. FgE levels however showed considerable overlap and could not be used as a diagnostic parameter. Agarose gel chromatography of the amniotic fluid revealed the presence of large molecular weight FgE related antigen in open neural tube defect suggesting that leakage of proteins from exposed capillaries is responsible for the elevation of amniotic fluid protein levels.

Amniotic Fluid↗