Facial nerve palsy in the newborn: incidence and outcome

This study retrospectively identifies and characterizes patients with facial palsy related to birth trauma and describes the natural history of this disorder. The records of infants born with facial weakness or paralysis over a 5-year period at Brigham and Women's Hospital were reviewed, and criteria were defined to assign a diagnosis of acquired facial palsy based on birth history and documented physical examinations. The majority of patients were followed up by interview with a family member. Among 44,292 infants born between October 1, 1982 and July 31, 1987, there were 92 recorded cases of congenital seventh nerve palsy. Of these, 81 were acquired, for an incidence of 1.8 per 1000. Seventy-four of the 81 (91 percent) were associated with forceps delivery. By contrast, obstetric forceps were used in 19 percent of all deliveries during the period of the study. The average weight of subjects was 3.55 kg, versus a mean overall birth weight of 3.23 kg. Fifty-nine percent of mothers of affected children and 37 percent of controls were prima gravidas. Forceps delivery, birth weight of 3500 gm or more, and primiparity were all significant risk factors for acquired facial palsy. The incidence of additional birth injuries also was substantially higher among affected subjects than among the general population of newborns. Sixty-six of 81 patients had adequate follow-up. Recovery has been complete for 59 patients (89 percent) and incomplete for the remaining 7 (mean follow-up 34 months). In summary, congenital traumatic facial palsy has definable risk factors and a predictably favorable outcome.     

Steroid contraceptive use and pregnancy outcome

Contraceptive use in relation to pregnancy outcome was studied in 8,816 births in Chiang Mai, northern Thailand, by examination of newborn infants and interviews with their mothers. Four thousand twenty-three women used no contraception before the index pregnancy, 1,229 used the injectable contraceptive Depo Provera (DMPA), and 3,038 used oral contraceptives prior to or during pregnancy. No differences were observed between these groups with respect to still births, multiple pregnancies, and birthweight. Women who used oral contraceptives had unexpectedly low rates of major defects and may have been affected by self-selection bias, whereas the noncontraceptors had rates similar to other populations. There was a significantly increased association of polysyndactyly among infants of DMPA users relative to the other groups, which was most pronounced in offspring of women under age 30 years, and persisted after exclusion of subjects with a family history or infants with multiple abnormalities. However, in five out of the ten polysyndactyly cases, the last injection of DMPA occurred more than 9 months before conception, and only three cases had definite gestational exposure. The association of chromosomal anomalies was also significantly increased in infants of mothers who used DMPA. The unrelated nature of these defects, the lack of confirmation from other studies, the distant preconceptional exposure to DMPA in many cases, and chance effects due to multiple statistical comparisons make a causal association unlikely. Other birth defects that had been previously reported in some publications to be associated with progestational steroid exposure, such as neural tube defects, heart malformations, and limb reduction defects, were not found in this study.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of common non-synonymous Toll-like receptor 4 polymorphisms on bronchopulmonary dysplasia and prematurity in human infants

Bronchopulmonary dysplasia (BPD) is a common chronic lung disease and major risk factor for severe respiratory syncytial virus (RSV) infection among preterm infants. The Toll-like receptor 4 (TLR4) is involved in oxidative injury responses in the lungs. Two non-synonymous single nucleotide polymorphisms in the TLR4 gene have been associated with RSV infection in children. However, it is unclear to what extent this association is confounded by BPD or prematurity. In this study, we analyzed two population-based cohorts of preterm infants at risk for BPD as well as ethnicity-matched infants born at term, to test whether the TLR4 polymorphisms Asp299Gly (rs4986790) and Thr399Ile (rs4986791) are independently associated with BPD or premature birth. In a Canadian cohort (n = 269) composed of a majority of Caucasian preterm infants (BPD incidence of 38%), the TLR4-299 heterozygous genotype was significantly under-represented in infants without BPD (1.6% of infants versus 12% in infants with severe BPD) after adjusting for twins, ethnicity, gestational age, birth weight and gender (p = 0.014). This association was not replicated in a Finnish cohort (n = 434) of premature singletons or first-born siblings of Caucasian descent, although the incidence of BPD was substantially lower in this latter population (15%). We did not detect a significant association (>2-fold) between TLR4 genotypes and prematurity (p>0.05). We conclude that these TLR4 genotypes may have, at best, a modest influence on BPD severity in some populations of high-risk preterm infants. Further studies are warranted to clarify how clinical heterogeneity may impact genetic susceptibility to BPD.     

Relationship between DHA status at birth and child problem behaviour at 7 years of age

Animal studies have demonstrated behavioural effects of long-chain polyunsaturated fatty acid (LC-PUFA) deficiencies and in humans, several psychiatric disorders have been linked to abnormal essential fatty acid metabolism. The aim of this study was to examine the relationship between LC-PUFA status at birth and the later development of problem behaviour. In a sample of 393 children, higher levels of docosahexaenoic acid (DHA) at birth were associated with lower levels of internalising problem behaviour at age 7 years. The association was markedly present in the infants fed with artificial formula (n=215, Beta=-0.32, P=0.000), but absent in the infants fed with human milk (n=170, Beta=0.11, P=0.325). The associations between arachidonic acid and internalising or externalising behaviour were neither large nor significant. The results suggest that perinatal DHA status may have long-term behavioural consequences. Therefore, we suggest to include measures of problem behaviour in future trials of LC-PUFA supplementation of mothers and/or infants.     

Parental age and the risk of childhood acute myeloid leukemia: results from the Childhood Leukemia International Consortium

BackgroundParental age has been associated with several childhood cancers, albeit the evidence is still inconsistent.AimTo examine the associations of parental age at birth with acute myeloid leukemia (AML) among children aged 0–14 years using individual-level data from the Childhood Leukemia International Consortium (CLIC) and non-CLIC studies.Material/methodsWe analyzed data of 3182 incident AML cases and 8377 controls from 17 studies [seven registry-based case-control (RCC) studies and ten questionnaire-based case-control (QCC) studies]. AML risk in association with parental age was calculated using multiple logistic regression, meta-analyses, and pooled-effect estimates. Models were stratified by age at diagnosis (infants <1 year-old vs. children 1–14 years-old) and by study design, using five-year parental age increments and controlling for sex, ethnicity, birthweight, prematurity, multiple gestation, birth order, maternal smoking and education, age at diagnosis (cases aged 1–14 years), and recruitment time period.ResultsAdjusted odds ratios (ORs) and 95% confidence intervals (CIs) derived from RCC, but not from the QCC, studies showed a higher AML risk for infants of mothers ≥40-year-old (OR = 6.87; 95% CI: 2.12–22.25). There were no associations observed between any other maternal or paternal age group and AML risk for children older than one year.ConclusionsAn increased risk of infant AML with advanced maternal age was found using data from RCC, but not from QCC studies; no parental age-AML associations were observed for older children.     

Congenital heart block: evidence for a pathogenic role of maternal autoantibodies

During pregnancy in autoimmune conditions, maternal autoantibodies are transported across the placenta and may affect the developing fetus. Congenital heart block (CHB) is known to associate with the presence of anti-Ro/SSA and anti-La/SSB antibodies in the mother and is characterized by a block in signal conduction at the atrioventricular (AV) node. The mortality rate of affected infants is 15% to 30%, and most live-born children require lifelong pacemaker implantation. Despite a well-recognized association with maternal anti-Ro/La antibodies, CHB develops in only 1% to 2% of anti-Ro-positive pregnancies, indicating that other factors are important for establishment of the block. The molecular mechanisms leading to complete AV block are still unclear, and the existing hypotheses fail to explain all aspects of CHB in one comprehensive model. In this review, we discuss the different specificities of maternal autoantibodies that have been implicated in CHB as well as the molecular mechanisms that have been suggested to operate, focusing on the evidence supporting a direct pathogenic role of maternal antibodies. Autoantibodies targeting the 52-kDa component of the Ro antigen remain the antibodies most closely associated with CHB. In vitro experiments and animal models of CHB also point to a major role for anti-Ro52 antibodies in CHB pathogenesis and suggest that these antibodies may directly affect calcium regulation in the fetal heart, leading to disturbances in signal conduction or electrogenesis or both. In addition, maternal antibody deposits are found in the heart of fetuses dying of CHB and are thought to contribute to an inflammatory reaction that eventually induces fibrosis and calcification of the AV node, leading to a complete block. Considering that CHB has a recurrence rate of 12% to 20% despite persisting maternal autoantibodies, it has long been clear that maternal autoantibodies are not sufficient for the establishment of a complete CHB, and efforts have been made to identify additional risk factors for this disorder. Therefore, recent studies looking at the influence of genetic and environmental factors will also be discussed.Autoantibody-associated congenital heart block (CHB) is a passively acquired autoimmune condition in which maternal autoantibodies are thought to initiate conduction disturbances in the developing fetal heart. Hallmarks of autoantibody-associated CHB are the presence of immune complex deposits, inflammation, calcification, and fibrosis in the fetal heart and a block in signal conduction at the atrioventricular (AV) node in an otherwise structurally normal heart. Clinical signs most commonly develop during weeks 18 to 24 of pregnancy. Although autoantibody-associated CHB may initially be detected as a first- or second-degree AV block, most of the affected pregnancies will present with fetal bradycardia in third-degree (complete) AV block, and ventricular rates typically are between 50 and 70 beats per minute. A complete AV block is a potentially lethal condition associated with significant morbidity, and the majority of affected children require permanent pacemaker implantation [1-3].Whereas complete AV block is the major manifestation of autoantibody-associated CHB, other cardiac abnormalities are increasingly being recognized. Transient first-degree AV block has been shown to occur in up to 30% of fetuses of mothers with anti-SSA/Ro 52-kDa antibodies [4]. The presence of sinus bradycardia [5-7] and prolongation of the QTc interval [8,9] have also been reported; however, these findings were not replicated in another recent study [10]. Endocardial fibroelastosis and cardiomyopathy have been reported in both the presence and absence of conduction abnormalities and are associated with a poor prognosis [11-14].Since the initial observation that sera of mothers of children with CHB contain anti-SSA/Ro antibodies, the association between maternal autoantibodies and CHB has been extensively studied. Most of the current knowledge comes from the comparative analysis of sera of women with affected or healthy infants, and additional information has been generated through the use of animal models. Nevertheless, the pathogenic molecular mechanisms of autoantibody-associated CHB remain unclear. Because the risk for CHB in an anti-SSA/Ro-positive pregnancy is only 1% to 2% [5,15], the need for a better marker not only for pregnancies at risk but also for the identification of other risk factors influencing the development of CHB is still important. This review will give a broad perspective of the maternal antibodies that have been associated with CHB and then will focus on the antibody specificities that have been more specifically implicated in the pathogenesis of the disease through in vitro and in vivo studies. The current hypotheses for autoantibody-associated CHB development will be discussed with an emphasis on the potential molecular targets for maternal antibodies in the fetal heart before mentioning other risk factors that have recently come to light.     

Infant C677T MTHFR polymorphism and severe mental retardation

BACKGROUND: We investigated whether infants with homozygous genotype TT of the MTHFR gene were at increased risk of severe mental retardation. METHODS: One hundred children with severe mental retardation (cases) were investigated from a large geographic-based study of infants born in California in 1992-1993. Cases were compared to 743 randomly selected nonmalformed control infants born in California during 1987-1991. DNA was extracted from newborn screening filter papers. Cases and controls were genotyped TT if homozygous for the MTHFR C677T allele, CT if heterozygous for the C677T allele, and CC if homozygous for the C677 (wild type) allele. RESULTS: Overall, case and control infants had similar percentages of TT and CT genotypes. Percentages between cases and controls differed somewhat across race/ethnic groups. Elevated ORs of 1.9 (95% CI: 0.7-5.0) and 2.6 (95% CI: 1.1-5.8) were observed for the TT and CT genotypes, respectively, among Hispanic children. Observed results were not substantially altered for analyses that removed 41 case children who also had structural birth defects. CONCLUSIONS: Folate-related mechanisms are important to investigate for etiologies of birth defects, and such lines of inquiry may be revealing for mental retardation given the relationships between mental retardation and birth defects and potential relationships between folate, DNA methylation, and mental retardation.     

The relationship between parental age and birth order with the percentage of low birth-weight infants

Birthweight, birth order, and parental age were abstracted from 1,515,443 New York State birth certificates to study the association between the birth of an infant weighing less than 2501 g and parental age. The percentage of premature infants was greatest for birth order 1 and 6+ and showed a minimum at birth order 3. When maternal age and birth order were analyzed jointly, a strong interaction was found. Young mothers showed a tendency to have an increasing proportion of low birthweight infants with increasing birth order, whereas, the exact opposite was true for mothers older than 45. The intermediate maternal age categories reflected this change from an association of increasing proportion of low birthweight infants with increasing birth order to a pattern of decreasing proportion of premature imfants with increasing birth order. In data stratified to eliminate the influence of maternal age and to some extent birth order, paternal age was shown to affect the percentage of infants weighing less than 2501 g. This association was described by a flat n-shaped curve that was significantly different from a horizontal line (P.01) in 6 of 7 maternal age categories.     

Using birth defects registry data to evaluate infant and childhood mortality associated with birth defects: an alternative to traditional mortality assessment using underlying cause of death statistics

BACKGROUND: Although birth defects are a leading cause of death in infancy and early childhood, the proportion of all deaths to children with clinically diagnosed birth defects is not well documented. The study is intended to measure the proportion of all deaths to infants and children under age 10 occurring to children with birth defects and how and why this proportion differs from the proportion of deaths due to an underlying cause of congenital anomalies using standard mortality statistics. METHODS: A linked file of Michigan livebirths and deaths was combined with data from a comprehensive multisource birth defects registry of Michigan livebirths born during the years 1992 through 2000. The data were analyzed to determine the mortality rate for infants and children with birth defects and for children with no reported birth defect. Mortality risk ratios were calculated. The underlying causes of death for children with birth defects were also categorized and compared to cause- specific mortality rates for the general population. RESULTS: Congenital anomalies were the underlying cause of death for 17.8% of all infant deaths while infants with birth defects were 33.7% of all infant deaths in the study. Almost half of all Michigan deaths to children aged 1 to 2 were within the birth defects registry, though only 15.0% had an underlying cause of death of a congenital anomaly based upon standard mortality statistics. The mortality experience among children with birth defects was significantly higher than other children throughout the first 9 years of life, ranging from 4.6 for 5 year olds to 12.8 for children 1 to 2. Mortality risk ratios examined by cause of death for infants with birth defects were highest for other endocrine (28.1), other CNS (28.1), and heart (21.9) conditions. For children 1 through 9, the highest differential risk was seen for other perinatal conditions (39.0), other endocrine (29.7), other CNS (24.5), and heart (21.4). CONCLUSIONS: Childhood mortality analyses that incorporate birth defects registry data provide a more comprehensive picture of the full burden of birth defects on mortality in infant and children and can provide an effective mechanism for monitoring the survival and mortality risks of children with selected birth defects on a population basis.     

Do infants with major congenital anomalies have an excess of macrosomia?

BACKGROUND: Infants that develop congenital anomalies may also have an excess prevalence of macrosomia (birth weight > or =4,000 g). This may indicate that abnormalities of glycemic control play a role in the etiology of birth defects. This study was undertaken to determine whether all infants with congenital anomalies have an excess of macrosomia and whether it is confined to specific types of anomalies. METHODS: A case-control study was conducted, comparing the birth weights of 8,226 infants with congenital anomalies ascertained by the Texas Birth Defects Monitoring Division with those of 965,965 infants without birth defects. Odds ratios were calculated to determine the association between birth weight and congenital anomalies, for 45 specific defects, and for all these defects combined. RESULTS: For all 45 defects combined, a significant association occurred only in the highest birth weight category. Infants with congenital anomalies were more likely than infants without birth defects to have a birth weight > or =4,500 g (OR = 1.65; 95% CI = 1.39-1.96). Infants born with ventricular septal defects, atrial septal defects, ventricular hypertrophy, or anomalies of the great vessels were 1.5-2.5 times more likely to weigh > or =4,000 g than were infants without birth defects. Based on small numbers, a stronger excess of macrosomia was observed for infants with encephalocele, holoprosencephaly, anomalies of the corpus callosum, preaxial polydactyly, and omphalocele. CONCLUSIONS: Our data suggest that infants with specific congenital anomalies are more likely to be macrosomic than are infants without an anomaly. If these findings are confirmed, associations between macrosomia and specific types of birth defects may help to identify birth defects that are caused by alterations in glycemic control.     

Detection of specific antibodies in cord blood, infant and maternal saliva and breast milk to staphylococcal toxins implicated in sudden infant death syndrome (SIDS)

The common bacterial toxins hypothesis of sudden infant death syndrome (SIDS) is that nasopharyngeal bacterial toxins can trigger events leading to death in infants with absent/low levels of antibody that can neutralise the toxins. The aim of this study was to investigate nasopharyngeal carriage of Staphylococcus aureus and determine levels of immunity in the first year of life to toxic shock syndrome toxin (TSST-1) and staphylococcal enterotoxin C (SEC). Both toxins have been implicated in SIDS cases. Seventy-three mothers and their infants (39 males and 34 females) were enrolled onto the study. The infants had birth dates spread evenly throughout the year. In infants, S. aureus carriage decreased significantly with age (P<0.001). Between 40% and 50% of infants were colonised with S. aureus in the first three months of life and 49% of the isolates produced one or both of the staphylococcal toxins. There was a significant correlation between nasopharyngeal carriage of S. aureus in mothers and infants in the three months following the birth (P<0.001). Carriage of S. aureus in infants and their mothers was not significantly associated with levels of antibody to TSST-1 or SEC in cord blood, adult saliva or breast milk. Infants colonised by S. aureus had higher levels of salivary IgA to TSST-1 than infants who were culture negative. Analysis of cord blood samples by a quantitative ELISA detected IgG bound to TSST-1 and SEC in 95.5% and 91.8% of cases respectively. There was a marked variation in levels of maternal IgG to both TSST-1 and SEC among cord blood samples. Maternal age, birth weight, and seasonality significantly affected the levels of IgG binding to TSST-1 or SEC. Analysis of infant saliva samples detected IgA to TSST-1 and SEC in the first month after birth; 11% of samples tested positive for salivary IgA to TSST-1 and 5% for salivary IgA to SEC. By the age of two months these proportions had increased to 36% and 33% respectively. More infants who used a dummy tested positive for salivary IgA to TSST-1 compared to infants who did not use a dummy. Levels of IgA to TSST-1 and SEC detected in the breast-milk samples varied greatly among mothers. There was a trend for infants receiving breast milk with low levels of antibody to TSST-1 or SEC to have higher levels of salivary antibody to the toxins. In conclusion, passive immunity to toxins implicated in SIDS cases varies greatly among infants. Infants are able to mount an active mucosal immune response to TSST-1 and SEC in the first month of life.     

Risk factors for congenital hypothyroidism: an investigation of infant's birth weight, ethnicity, and gender in California, 1990-1998

BACKGROUND: Approximately 85% of primary congenital hypothyroidism (CH) is sporadic and due to malformations of the thyroid gland. Past studies have reported an increased birth weight among infants with CH. We have attempted to replicate and expand these observations, examining the association between different birth weight categories and CH stratified by infant's sex. We have also examined the prevalence of CH by mother's age and infant's ethnicity, gender, and year of birth. METHODS: A cross-sectional study was conducted on 5, 049,185 infants screened by the statewide California Newborn Screening Program between 1990 and 1998, an estimated 98.6% of all newborns in the state. Dried blood spots from a heel stick were assayed for thyroxine (T4), and presumptive positives had follow-up assays of thyroid-stimulating hormone (TSH) to determine definite positives. RESULTS: A total of 1,806 cases of CH were identified. The following findings are unlikely to be due to chance. Compared with infants with birth weights of 3,000-3,499 g, infants weighing <2,000 g and those weighing >/=4,500 g had a twofold or greater increase in the prevalence of CH. This was not explained as a result of confounding by the infant's ethnicity or gender. Compared with whites, elevated prevalence rates were found in most ethnic groups, which include the following: Hispanics, Chinese, Vietnamese, Asian Indians, Filipinos, Middle Easterners, and Hawaiians. As reported previously, black infants had about one-third the prevalence rate of whites. We also observed the frequently described female preponderance of CH. The female excess was maintained at all birth weights, however it varied by infant's ethnicity. Trends in the prevalence of CH were not associated with mother's age or with the time interval between 1990 and 1998. CONCLUSIONS: We observed an increased risk of CH in both low-birth-weight (<2,000-g) and macrosomic (>/=4,500-g) infants. This U-shaped association has not been described in past studies. We have also expanded the previously described ethnic differences in CH risk to include ethnic groups not previously studied. The unique pattern of CH occurrence suggests that further studies to define modifiable risk factors may be useful.     

Problems in the Early Recognition of Congenital Hip Dislocation

Seven cases of infants whose hips were clinically normal at birth, and in whom hip dislocation was later recognized, are reported. In spite of the widespread practice of routine examination of the hips of newborn babies, infants and young children are still presenting with congenital dislocation of the hip. This is probably owing to there being two aetiological types. Every opportunity to re-examine the hips of children under 2 or even 3 years of age must be taken and a high level of suspicion maintained.     

Birth order and oral clefts: a meta analysis

BACKGROUND: There is evidence that late birth order is associated with some complex disorders. For orofacial clefts there is no consensus as to whether increased birth order is associated or not. A meta-analysis of published data on cleft lip or cleft palate (CL/P and CP) was carried out to ascertain whether there is an increased risk for children of high birth order to have an oral cleft. METHODS: All data available with information regarding the frequency of live births and CL/P and CP cases by birth order (1, 2, 3, and 4 or more) were included in the analysis, and the birth order category "1" was considered to be with no risk (OR = 1.0). RESULTS: Children with higher birth order are more likely to have CL/P and CP with odds ratios increasing with birth order to a peak of 3.0 in children birth order "4 or more." Results are not different when isolated and syndromic cases are combined. CONCLUSIONS: CL/P and CP occurrence is correlated with increasing birth order. Further studies, taking into consideration sample size and factors such as income status, race, paternal age, vitamin intake, and social habits, should be done to determine conclusively the association between birth order and oral clefts.     

Use of prenatal diagnostic procedures in pregnancies affected with birth defects, Hawaii, 1986-2002

BACKGROUND: Information on the utilization of prenatal ultrasound (US), amniocentesis (AC), and chorionic villus sampling (CVS) in pregnancies affected by birth defects in the United States is limited. The intent of this study was to report on the utilization of these procedures in Hawaii. METHODS: Cases were all infants and fetuses of any pregnancy outcome with birth defects, included in a Hawaii birth defects registry, and delivered during 1986-2002. The rates of prenatal US, AC/CVS, and prenatal diagnosis were calculated. RESULTS: Prenatal US was performed in 76% of the cases and AC/CVS in 14% of the cases. Prenatal diagnosis of a birth defect was made in 16% of the cases. The prenatal US, AC/CVS, and prenatal diagnosis rates in 1998-2002 were 1.5, 1.5, and 1.7 times the rates in 1986-1991, respectively. Among all birth defects, the AC/CVS rate for women aged <35 years was 7% and for women aged > or =35 years was 48%. Among chromosomal abnormalities, the AC/CVS rate for women aged <35 years was 36% and for women aged > or =35 years was 66%. CONCLUSIONS: Only a fraction of the Hawaii birth defects cases was prenatally diagnosed. The rates for prenatal US, AC/CVS, and prenatal diagnosis among pregnancies affected by birth defects were higher in 1998-2002 than in 1986-1991. AC/CVS rates were lower for maternal age <35 years.     

Assessment of Structural Connectivity in the Preterm Brain at Term Equivalent Age Using Diffusion MRI and T2 Relaxometry: A Network-Based Analysis

Preterm birth is associated with a high prevalence of adverse neurodevelopmental outcome. Non-invasive techniques which can probe the neural correlates underpinning these deficits are required. This can be achieved by measuring the structural network of connections within the preterm infant''s brain using diffusion MRI and tractography. We used diffusion MRI and T₂ relaxometry to identify connections with altered white matter properties in preterm infants compared to term infants. Diffusion and T₂ data were obtained from 9 term neonates and 18 preterm-born infants (born <32 weeks gestational age) at term equivalent age. Probabilistic tractography incorporating multiple fibre orientations was used in combination with the Johns Hopkins neonatal brain atlas to calculate the structural network of connections. Connections of altered diffusivity or T₂, as well as their relationship with gestational age at birth and postmenstrual age at the time of MRI, were identified using the network based statistic framework. A total of 433 connections were assessed. FA was significantly reduced in 17, and T₂ significantly increased in 18 connections in preterm infants, following correction for multiple comparisons. Cortical networks associated with affected connections mainly involved left frontal and temporal cortical areas: regions which are associated with working memory, verbal comprehension and higher cognitive function – deficits which are often observed later in children and adults born preterm. Gestational age at birth correlated with T₂, but not diffusion in several connections. We found no association between diffusion or T₂ and postmenstrual age at the time of MRI in preterm infants. This study demonstrates that alterations in the structural network of connections can be identified in preterm infants at term equivalent age, and that incorporation of non-diffusion measures such as T₂ in the connectome framework provides complementary information for the assessment of brain development.     

Low birth weight, maternal birth-spacing decisions, and future reproduction

The aim of this study is an analysis of the possible adaptive consequences of delivery of low birth weight infants. We attempt to reveal the cost and benefit components of bearing small children, estimate the chance of the infants’ survival, and calculate the mothers’ reproductive success. According to life-history theory, under certain circumstances mothers can enhance their lifetime fitness by lowering the rate of investment in an infant and/or enhancing the rate of subsequent births. We assume that living in a risky environment and giving birth to a small infant may involve a shift from qualitative to quantitative production of offspring. Given high infant mortality rates, parents will have a reproductive interest in producing a relatively large number of children with a smaller amount of prenatal investment. This hypothesis was tested among 650 Gypsy and 717 non-Gypsy Hungarian mothers. Our study has revealed that 23.8% of the Gypsy mothers had low birth weight (<2,500 g) children, whose mortality rate is very high. These mothers also had more spontaneous abortions and stillbirths than those with normal weight children. As a possible response to these reproductive failures, they shortened birth spacing, gaining 2–4 years across their reproductive lifespan for having additional children. Because of the relatively short interbirth intervals, by the end of their fertility period, Gypsy mothers with one or two low birth weight infants have significantly more children than their ethnic Hungarian counterparts. They appear to compensate for handicaps associated with low birth weights by having a larger number of closely spaced children following the birth of one or more infants with a reduced probability of survival. The possible alternative explanations are discussed, and the long-term reproductive benefits are estimated for both ethnic groups.     

Reproductive parameters of female Japanese macaques: Thirty years data from the arashiyama troops,Japan

Over a 30-year period from 1954 to 1983, 975 live births were recorded for Japanese macaque females at the Iwatayama Monkey Park, Arashiyama, Japan. Excluding unknown birth dates, primiparous mothers gave birth to 185 infants (182 cases with age of mother known) and multiparous mothers gave birth to 723 infants (603 cases with age of mother known). The peak month of birth was May with 52.3% of the total births occurring during the period. Multiparous females who had not given birth the previous year did so earlier than multiparous females who had given birth the previous year and also earlier than primiparous females. Among the females who had given birth the previous year, females whose infant had died gave birth earlier than females who had reared an infant the previous year. The offspring sex ratio (1:0.97) was not significantly different from 1:1, and revealed no consistent association with mother's age. Age-fecundity exhibited a humped curve. The annual birth rate was low at the age of 4 years but increased thereafter, ranging between 46.7% and 69.0%, at between 5 and 19 years of age, but again decreased for females between 20 and 25 years of age. Some old females displayed clear reproductive senescence. The infant mortality within the first year of age was quite low (10.3%) and the neonatal (less than 1 month old) mortality rate accounted for 49.0% of all infant deaths. There was no significant difference between the mortality rates of male and female infants. A female's rank-class had no apparent effect on the annual birth rate, infant mortality, and offspring sex ratio. These long-term data are compared with those from other primate populations.     

Exogenous sex hormone exposure and the risk for VACTERL association

In several studies investigators have suggested that maternal use of exogenous sex hormones during early pregnancy may be associated with various congenital malformations. A group of malformations, the VACTERL (vertebral, anal, cardiac, trachea, esophageal, renal, limb-acronym) association, has been statistically associated with maternal exposure to exogenous sex hormones during the first trimester of pregnancy. The VACTERL association is a nonrandom group of major malformations that occur together more often than would be expected on the basis of chance. To assess this association, we conducted a case-control study of first-trimester exposure to sex hormones among mothers of 34 infants with the VACTERL association and of 1,024 comparison infants with one or more of ten major malformations or Down syndrome. The study subjects were malformed infants born between July 1970 and June 1979 and registered in a population-based birth defects registry. Information concerning the use of exogenous sex hormones during pregnancy was obtained by systematically interviewing the mothers of the malformed infants. Most of the mothers were interviewed within 6 months of their children's births. Each mother was interviewed within a year of her child's birth. We found an odds ratio of 0.98 (90% confidence limits 0.40, 2.38) for the relationship between VACTERL association and use of any sex hormone in the first trimester of pregnancy. Our study had adequate statistical power to detect a true relative risk of 2.8 or greater.     

The effect of birth interval on malnutrition in Bangladeshi infants and young children

This study was undertaken to investigate the independent effect of the length of birth interval on malnutrition in infants, and children aged 6-39 months. Data for this study were drawn from a post-flood survey conducted during October-December 1988 at Sirajganj of the Sirajgani district and at Gopalpur of the Tangail district in Bangladesh. The survey recorded the individual weights of 1887 children. Cross-tabulations and logistic regression procedures were applied to analyse the data. The proportion of children whose weight-for-age was below 70% (moderate-to-severely malnourished) and 60% (severely malnourished) of the NCHS median was tabulated against various durations of previous and subsequent birth intervals. The odds of being moderately or severely malnourished were computed for various birth intervals, controlling for: the number of older surviving siblings; maternal education and age; housing area (a proxy for wealth); age and sex of the index child; and the prevalence of diarrhoea in the previous 2 weeks for the index child. About one-third of infants and young children were moderately malnourished and 15% were severely malnourished. The proportion of children who were under 60% weight-for-age decreased with the increase in the length of the subsequent birth interval, maternal education and housing area. The proportion of malnourished children increased with the number of older surviving children. Children were at higher risk of malnutrition if they were female, their mothers were less educated, they had several siblings, and either previous or subsequent siblings were born within 24 months. This study indicates the potential importance of longer birth intervals in reducing malnutrition in children.