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PubMed1995

Neurological correlates of fetal cocaine exposure: transient hypertonia of infancy and early childhood.

OBJECTIVE: To assess whether prenatal cocaine exposure has any long-term effects on neurodevelopment. DESIGN: A prospective cohort study with examiners blind to drug exposure and human immunodeficiency virus (HIV) status. SUBJECTS: Of 144 high-risk infants enrolled in a perinatal HIV neurodevelopmental study, 119 (83%) infants with both neurological and urine toxicology measures were followed up to age 24 months. METHODS: Neurological and developmental assessments were analyzed at 6-month intervals grouped according to the presence of cocaine in urine toxicology: 51 infants were cocaine-positive. Adjusted odds ratios (ORs) and 95% confidence interval (CI) were obtained by logistic regression equations that adjusted for perinatal variables, including measures of fetal growth, gestation, HIV status, and infant toxicology results. SETTING: Harlem Hospital Center from 1988 to 1992. RESULTS: At age 6 months, 21 of 51 (41%) cocaine-positive children exhibited hypertonia of any type (hypertonic tetraparesis, hypertonic diparesis, and hypertonic hemiparesis) compared with 17 of 68 (25%) cocaine-negative infants (OR = 2.1, CI = 1.0-4.6). Cocaine-positive infants were four times more likely to show hypertonic tetraparesis (HTP) than cocaine-negative infants (OR = 4.0; CI = 1.5-10.8). The association remained significant in multivariate analyses. Hypertonia, consistent with cerebral palsy, diminished over time in both groups. In 97% of affected infants hypertonia resolved by 24 months. Arm hypertonia abated first; leg hypertonia remained in some children up to age 18 months. No differences in development scores between cocaine-positive and cocaine-negative were noted at any age interval. However, among cocaine-positive infants those with early HTP showed significantly lower mean developmental scores at 6 and 12 month compared to infants without HTP. CONCLUSION: Cocaine positivity urine toxicology at birth is associated with hypertonia during infancy. Such cocaine-induced effects are usually symmetrical, transient, and the majority of exposed children outgrow hypertonia by 24 months of life. Among cocaine-positive infants, HTP may be a marker for later developmental impairments.

Adult↗
PubMedDate not supplied

[Bronchopulmonary dysplasia. Course over 3 years in 88 children born between 1984 and 1988].

BACKGROUND: The survival and outcome of infants with bronchopulmonary dysplasia (BD) depend on the patient's maturity, the severity of the BD and nutritional problems. This study evaluates the specific role of chronic pulmonary failure in the growth and development of infants recovering from BD. POPULATION AND METHODS: 88 infants admitted for BD from January 1984 to December 1988, having gestational age from 25 to 41 weeks 5 days (mean: 29) and birth weight from 680 to 3,400 g (mean: 1,195) were studied. All infants were given respiratory support for 6 to 914 days (mean 84) and oxygen therapy for 28 to 1,232 days (mean: 119). 29 infants were given corticosteroids for more than 1 month. The outcome of the 80 infants with gestational ages of less than 33 weeks was compared to that of 272 infants with the same gestational age but not suffering from BD on their 28th day. The infants in both groups were examined at 2 years of age and classified as: a) handicapped (neurologic deficit, IQ < 80, hearing loss, blindness, convulsions); b) doubtful (transitory neurology dysfunction); c) normal. RESULTS: Of the 88 infants still living at the age of 28 days, 19 died before the age of 2 years: 16 of the 64 surviving infants who could be followed until the age of 2 years were classified as handicapped, 13 were considered doubtful and 35 were normal. The more significant risk factors for neurodevelopmental impairment were: a) the presence of porencephaly and/or ventricular dilatation on brain ultrasonography; b) head circumference < -2 SD at the end of hospital stay; c) oxygen therapy and hospitalization > 5-6 months. The group of infants with BD had a higher death rate (24% vs. 3.7 in the group without BD) and more frequent neurodevelopmental impairment at gestational ages of > 31-32 weeks. CONCLUSIONS: BD is an extra risk for the survival and neurodevelopment of infants with gestational age > 31 weeks.

Bronchopulmonary Dysplasia↗
PubMedDate not supplied

Follow-up of children born to hypertensive mothers.

Maternal hypertension has significant adverse effects on perinatal outcome. We aimed to assess whether there are long-term effects on growth and neurodevelopment in childhood. Thirty-seven children were reviewed at a median age of 56 months. Although maternal hypertension had had a significant impact on perinatal outcome of these children, most had normal growth and development in childhood. The severity of maternal hypertension was influential on perinatal outcome, but not on long-term outcome.

Child, Preschool↗
PubMed1993

[Limit of antenatal management of intrauterine growth retarded fetus].

Recent advances in perinatal medicine contributed to the survival of extremely premature infants. Nonetheless, prognosis of the fetus with intrauterine growth retardation (IUGR) especially of preterm IUGR is not satisfactory with respect to both neonatal and long term neurodevelopmental outcome. As in utero pathophysiology of the IUGR has been revealed by noninvasive fetal monitoring technique along with invasive cordocentesis to determine fetal blood gas parameters, most of the neonatal morbidity of IUGR is thought to be originated prior to birth. Excluding the IUGR due to chromosomal abnormalities, fetal anomalies and multiple gestation, severe preeclampsia contributes nearly 60 to 80% of the etiology of IUGR in our series. In IUGR with severe preeclampsia, it is noteworthy that the incidence of symmetrical IUGR is approximately 50%, suggesting disturbance in head growth is responsible for symmetrical growth. We have shown that the disturbance in head growth is particularly important not only for neurodevelopmental but also for short term neonatal mortality and morbidity. It is suggested that the reasonable timing of delivery of preterm IUGR should be before onset of fetal acidosis and/or cessation of fetal head growth for the following reasons. 1. There is a relationship between fetal acidemia at cordocentesis and subsequent neurodevelopment. 2. The incidence of neonatal morbidity including hypoglycemia, hemoconcentration and thrombocytopenia increased with the degree of disturbance in head circumference at birth. We propose that the IUGR fetus should be monitored weekly for its growth by ultrasound fetometry and noninvasive fetal monitoring methods including nonstress test, Biophysical profile scoring and Doppler velocimetry.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Brachydactyly and mental retardation: an Albright hereditary osteodystrophy-like syndrome localized to 2q37.

We report five patients with a combination of brachymetaphalangia and mental retardation, similar to that observed in Albright hereditary osteodystrophy (AHO). Four patients had cytogenetically visible de novo deletions of chromosome 2q37. The fifth patient was cytogenetically normal and had normal bioactivity of the alpha subunit of Gs (Gs alpha), the protein that is defective in AHO. In this patient, we have used a combination of highly polymorphic molecular markers and FISH to demonstrate a microdeletion at 2q37. The common region of deletion overlap involves the most telomeric 2q marker, D2S125, and extends proximally for a maximum distance of 17.6 cM. We suggest this represents a consistent phenotype associated with some deletions at 2q37 and that genes important for skeletal and neurodevelopment lie within this region. Screening for deletions at this locus should be considered in individuals with brachymetaphalangia and mental retardation. Furthermore, 2q37 represents a candidate region for type E brachydactyly.

Abnormalities, Multiple↗
PubMed1994

Rey-Martinez Kangaroo Mother Program: an alternative way of caring for low birth weight infants? One year mortality in a two cohort study.

OBJECTIVES: To assess the effectiveness and safety of the Kangaroo mother intervention (KMI). DESIGN: Observational, analytic, prospective (two cohorts) study. SETTING: Two large tertiary care obstetric hospitals, one offering "traditional" care and the other KMI. PATIENTS: Newborn infants with birth weights < or = 2000 g, who survive the neonatal period and are eligible for an in-patient minimal care unit (MCU) (having overcome major adaptation problems to extra uterine life). INTERVENTIONS: "Kangaroo infants" (KI) were discharged as soon as they were eligible for MCU, regardless of weight or gestational age. Infants were kept 24 hours a day in an upright position, in skin-to-skin contact and firmly attached to the mother's chest until the KMI was not tolerated anymore. Control babies (from the other facility) were kept in incubators at the MCU until they satisfied usual discharge criteria for the control hospital. Both groups were followed periodically up to the age of 1 year. RESULTS: Three hundred thirty-two eligible infants were recruited, 162 at the Kangaroo hospital and 170 at the control hospital. KI came from a much lower socio-economic class and were more ill before eligibility. Relative risk of death was higher for KI (RR 1.9), although this figure was reversed after adjusting for weight at birth and gestational age (RR 0.5). KI grew less in the first 3 months and had a higher proportion of developmental delay at 1 year, and a multivariate analysis failed to control for the large baseline differences in socioeconomic levels and babies' health status between the two cohorts. CONCLUSIONS: In spite of major baseline differences between studied cohorts, the survival of LBW infants in Bogotá is similar between the KMI and the "traditional care". Questions remain about quality of life, especially regarding weight gain and neurodevelopment, that may be answered by a Randomized Controlled Trial.

Cohort Studies↗
PubMed1994

Migration of ganglion cell precursors in the ileoceca of normal and lethal spotted embryos, a murine model for Hirschsprung disease.

BACKGROUND: Dopamine-beta-hydroxylase-nlacZ transgenic mice are useful for studies of enteric neurodevelopment. Expression of the transgene provides a histochemical marker for neuroblasts in wild-type embryos and embryos homozygous for the lethal spotted (ls) allele that are born with aganglionosis coli and serve as a model for the human birth defect, Hirschsprung disease. Neuroblasts, derived from the vagal neural crest, colonize the gut in a cranial-to-caudal manner. However, migration of neuroblasts in ls/ls gut is impaired when neuroblasts reach the ileocecal junction and attempt to colonize the large intestine. To learn more about neuroblast migration through this specific region of the intestinal tract, a detailed light and electron microscopic study of neuroblast colonization of the developing ileoceca from wild-type, ls/+, and ls/ls embryos was conducted. EXPERIMENTAL DESIGN: The ileoceca from wild-type, ls/+, and ls/ls, dopamine-beta-hydroxylase-nlacZ embryos (E10.5-E13.5) were treated with a histochemical substrate for the transgene product and examined by light and electron microscopy. RESULTS: Five stages of ileocecal development were defined based on distinctive gross, light, and electron microscopic features. At each stage, neuroblasts had different ultrastructural features than other mesenchymal cells. Initial colonization of the colon was different from other parts of the gut, in that a string of "pioneer" neuroblasts populated the mesenteric border of the proximal colon before circumferential invasion. Subsequently, neuroblasts were arranged in intersecting linear groups of contiguous cells that radiated around the cecum and proximal colon. In ls/ls embryos, transition from neuroblast extension along the mesenteric border to cecal invasion was delayed profoundly. However, the ultrastructural features of neuroblasts and adjacent mesenchyme were indistinguishable in ls/ls and wild-type embryos. CONCLUSIONS: This study supports the hypothesis that impaired migration of neuroblasts in ls/ls embryos is not limited to the presumptive aganglionic segment, but begins at the ileocecal junction. Migration of neuroblasts from the ileum into the proximal colon follows a different pattern than movement of neuroblasts through the small intestine. The biological bases for these differences may account for the defects observed in ls/ls mice and/or may affect the pathogenesis of human Hirschsprung disease.

Animals↗
PubMedDate not supplied

Multicystic encephalomalacia in a surviving monochorionic twin.

From a recent monochorionic diamniotic twin pregnancy seen at this hospital, one of the twins died in utero at 37 weeks' gestation. The other twin, a male infant, was delivered by Cesarean section because of fetal distress, with resuscitation performed in the delivery room. The infant developed generalized tonic seizure shortly after stabilization, and was put on anticonvulsants. The initial brain echography was normal; follow-up echograms and CT scans performed at 8 and 12 days old, respectively, revealed diffuse low density over both side of cerebral hemisphere. At one month old, the infants's brain echogram showed diffuse cystic encephalomalacia. At four months, he was noted to be spastic and significantly delayed in neurodevelopment. Disseminated intravascular coagulation caused by fetal-to-fetal transfer of thromboplastic material from the dead fetus was considered as the most possible cause of the neurological complication in this patient. In addition, perinatal hypoxic-ischemic insult may also have been a superimposed, influencing factor.

Diseases in Twins↗
PubMed1995

Effects of morphine and cocaine on breathing control in neonatal animals: a minireview.

From observational studies in humans and experimental studies in animal models, there is a strong indication that prenatal exposure to morphine or cocaine causes at least transient abnormalities of breathing control in the neonate. If these abnormalities persist, sudden death may occur in the infant. Mechanisms responsible for alterations in breathing control by drugs of abuse and the relationship of these alterations to SIDS are not proven at this time. The complex nature of breathing control and neurodevelopment, as well as the confounding variables in human drug abuse, have so far prevented a definitive understanding of the link between drug abuse during pregnancy and SIDS. Further investigations are required to explore the biology of this important public health problem.

Animals↗
PubMed1995

Main neurodevelopmental study of Seychellois children following in utero exposure to methylmercury from a maternal fish diet: outcome at six months.

Methylmercury (MeHg) is a human neurotoxin to which the developing fetal brain is especially sensitive. The lowest dose of MeHg that impairs neurodevelopment in the human fetus is not known. The Seychelles Child Development Study (SCDS) is testing the hypothesis that fetal MeHg exposure from a maternal diet high in oceanic fish is related to child neurodevelopmental outcomes. Fish is the major protein source in the Republic of Seychelles, where a cohort of 779 mother-infant pairs was enrolled in a prospective longitudinal study. Maternal total hair mercury values during pregnancy were determined by cold vapor atomic absorption and ranged from 0.5 ppm to 26.7 ppm with a median of 5.9 ppm. When the children were 6 1/2 months of age, an examiner blinded to the maternal mercury value performed a neurological examination, the Fagan test of visual recognition memory, and the Denver Developmental Screening Test-Revised (DDST-R). On the DDST-R 2% scored other than normal while 3.4% had an overall neurological score other than normal. The Fagan test of visual recognition memory showed a median score of 60.5%, and the Rose attention measure from that test showed a median score of 37.9. The association between fetal mercury exposure and neurodevelopmental endpoints was examined by multiple regression analyses. After adjusting for covariates, no association between the maternal hair mercury level during pregnancy and an adverse neurodevelopmental outcome of the child was identified at 6 1/2 months of age.

Adult↗
PubMed1995

Neurodevelopmental test selection, administration, and performance in the main Seychelles child development study.

The Seychelles Child Development Study was designed to provide data on normal neurodevelopment of Seychellois children and to examine the relationship of their neurodevelopmental outcomes to in utero fetal exposure to low concentrations of methylmercury from a maternal diet high in fish. This paper outlines the strategies used to select, modify, and field test evaluation tools used in the main longitudinal prospective study of 740 children (95% of the cohort of 779 initially enrolled in 1989). It also gives population statistics and quality assurance data for the tests administered and the evaluation of the home environments.

Child↗
PubMed1997

Reelin is a secreted glycoprotein recognized by the CR-50 monoclonal antibody.

The neurological mouse mutant strain reeler displays abnormal laminar organization of several brain structures as a consequence of a defect in cell migration during neurodevelopment. This phenotype is a result of the disruption of reelin, a gene encoding a protein that has several structural characteristics of extracellular matrix proteins. To understand the molecular basis of the action of Reelin on neuronal migration, we constructed a full-length reelin clone and used it to direct Reelin expression. Here, we demonstrate that Reelin is a secreted glycoprotein and that a highly charged C-terminal region is essential for secretion. In addition, we demonstrate that an amino acid sequence present in the N-terminal region of Reelin contains an epitope that is recognized by the CR-50 monoclonal antibody. CR-50 was raised against an antigen expressed in normal mouse brain that is absent in reeler mice. The interaction of CR-50 with its epitope leads to the disruption of neural cell aggregation in vitro. Here, we used CR-50 to precipitate Reelin from reticulocyte extracts programmed with reelin mRNA, from cells transfected with reelin clones, and from cerebellar explants. The reelin gene product seems to function as an instructive signal in the regulation of neuronal migration.

Animals↗
PubMed1997

Use of the laboratory in prediction of outcome in the high-risk newborn.

This paper reviews our ability to predict survival and neurodevelopmental outcome in the newborn period. Traditionally, prognosis is based on individual risk factors or disease states. The laboratory plays an important role in diagnosing some of these. For example, prenatal and newborn screening are important in the diagnosis of chromosomal abnormalities and inborn errors of metabolism. Abnormal bilirubin, glucose, and pH values in the newborn period are risk factors for death and abnormal neurodevelopment, and the degree of abnormality imparts additional information. Many newborns have multisystem disorders, and it is only when multiple variables are considered that outcome can be predicted. Three neonatal scores that incorporate multiple variables are discussed. Methodologic difficulties in determining outcome are reviewed and illustrated with survival and morbidity rates of very premature babies. The laboratory is one of many prognostic variables. The evaluation of how laboratory services are provided is difficult but important.

Clinical Laboratory Techniques↗
PubMed1996

Epilepsy, anticonvulsant drugs and cognition.

The use of AEDs in the management of epilepsy requires an ongoing risk-benefit analysis that attempts to maximize seizure control while minimizing adverse cognitive side-effects. Although the effects of other factors on cognition are generally greater than AED effects in patients with epilepsy, the cognitive effects of AEDs are of special concern because they are iatrogenically induced. Baseline evaluation of mental functioning is essential and should be repeated whenever a change in cognitive performance is suspected. The cognitive effects of the major AEDs, including phenytoin, carbamazepine and valproate, appear modest when dosages are kept within standard therapeutic ranges and polypharmacy is avoided. Violation of these guidelines increases the risk of alterations in arousal, attention, memory and psychomotor functioning. In turn, dysfunction in these areas can contribute to deficits in higher cognitive processes. Evidence suggests that these primary and secondary deficits are relatively greater for benzodiazepines, bromide and phenobarbital. Initial studies involving the newer AEDs suggest that the cognitive profile of these drugs is favourable, but further research is required to determine their relative effects to each other and to the older AEDs. For some patients, optimal seizure management may require the use of polypharmacy or AED dosages that exceed the standard therapeutic range. In such cases, the physician should remain sensitive to the increased risk of cognitive side-effects. The impact of such effects will be greatest for those whose daily functioning requires sustained attention or psychomotor speed. Although the cognitive risks of AEDs appear rather modest for most adults, questions remain regarding the impact of AEDs on patients at extremes of age. Initial studies with children and older adults suggest that the effects of the major AEDs are comparable across the developmental lifespan. However, during the formative years of a child's intellectual development, close scrutiny should be paid to the possibility that subtle attentional or arousal deficits could contribute to cumulative deficits in learning or memory. Preliminary studies involving both animals and humans suggest that the impact of AEDs might be greatest during in utero exposure; however, additional research is required to fully delineate the long-term effects of AED exposure in this earliest period of neurodevelopment.

Adolescent↗
PubMedDate not supplied

The association of periventricular echodensity with cerebral palsy in preterm infants.

The purpose of this study was to investigate the risk factors of development of cerebral palsy (CP) in preterm infants who had periventricular echogenic abnormalities with or without cyst formation. During a period of 66 months, 332 newborns of 34 weeks gestation or less born at our hospital received serial brain ultrasound scans. Sixty-six of the 332 infants, 36 males and 30 females, were detected increased periventricular echodensity (PVE) during admission period. Subsequently, serial brain ultrasound scans were done for the 66 preterm infants at our follow-up clinic. Their neurodevelopment outcomes were then followed up for 10-48 months. The degree of periventricular echodensity (PVE) was graded as mild; or moderate to severe, according to the extent of the echodensity. Periventricular echodensity with cyst formation was classified by the size of the cyst at its widest diameter as either large (3 mm or multiple) or small (< 3 mm) in the parasagittal image. Eighteen of 66 (27.3%) infants developed cerebral palsy (CP). Infants with PVE with large cystic formation were at significantly higher risk for development of cerebral palsy (P < 0.005). Nine of 16 (56.3%) patients in the CP group had a longer duration of PVE than the non-CP group (8 of 46 patients: 17.4%) (p < 0.005). It is concluded that large cystic periventricular echodensity and long duration of PVE are associated with later development of cerebral palsy.

Cerebral Palsy↗
PubMed1997

The characterization of the Olf-1/EBF-like HLH transcription factor family: implications in olfactory gene regulation and neuronal development.

The Olf-1/EBF helix-loop-helix (HLH) transcription factor has been implicated in olfactory gene regulation and in B-cell development. Using homology screening methods, we identified two additional Olf-1/EBF-like cDNAs from a mouse embryonic cDNA library. The Olf-1/EBF-like (O/E) proteins O/E-1, O/E-2, and O/E-3 define a family of transcription factors that share structural similarities and biochemical activities. Although these O/E genes are expressed within olfactory epithelium in an identical pattern, they exhibit different patterns of expression in the developing nervous system. Although O/E-1 mRNA is present in several tissues in addition to olfactory neurons and developing B-cells, O/E-2 and O/E-3 are expressed at high levels only in olfactory tissue. In O/E-1 knock-out animals, the presence of two additional O/E family members in olfactory neurons may provide redundancy and allow normal olfactory neurodevelopment. Further, the identification of the O/E family of HLH transcription factors and their embryonic expression patterns suggest that the O/E proteins may have a more general function in neuronal development.

Age Factors↗
PubMed1997

Neonatal nonhandling and in utero prenatal stress reduce the density of NADPH-diaphorase-reactive neurons in the fascia dentata and Ammon's horn of rats.

The density of nitric oxide (NO)-producing neurons in the fascia dentata and Ammon's horn was assessed in 6-month-old male rats using NADPH-diaphorase (NADPH-d) histochemistry. Two separate experiments investigated whether (1) the complete absence of neonatal handling or (2) the administration of periodic prenatal stress could affect the expression and distribution of NADPH-d reactivity in the hippocampus, when compared with rats raised in normal standard laboratory conditions. Experiment 1 demonstrated that adult rats that received no handling during neonatal development (from birth to postnatal day 22) showed a very substantial reduction in NADPH-d-positive neurons per unit area throughout the entire hippocampus when compared with rats that received regular daily handling in this period. Quantitative analysis further revealed that this effect was significantly more pronounced in Ammon's horn than in the fascia dentata, and within Ammon's horn the dorsal region was selectively more affected. Experiment 2 showed that prenatal stress, which involved the administration of daily restraint stress to pregnant dams throughout the gestation period, also led to a reduction in NADPH-d reactivity in the hippocampus of the offspring of these dam when they reached adulthood. The present results suggest that behavioral manipulations in the early neonatal or prenatal period can significantly alter the neurodevelopment of the hippocampal NO system and these changes might be related to some of the behavioral abnormalities that emerge later in adulthood.

Animals↗
PubMed1997

Allelic association of juvenile absence epilepsy with a GluR5 kainate receptor gene (GRIK1) polymorphism.

Juvenile absence epilepsy (JAE) is a common subtype of idiopathic generalized epilepsy (IGE). Hereditary factors play a major role in its etiology. The important function of glutamate receptors (GluRs) in excitatory neurotransmission, synaptic plasticity, and neurodevelopment suggests their involvement in epileptogenesis. A tetranucleotide repeat polymorphism in the non-coding region of the kainate-selective GluR5 receptor gene (GRIK1) on chromosome 21q22.1 provides the tool to investigate this candidate gene. The present association and linkage study tested the hypothesis that allelic variants of GRIK1 confer genetic susceptibility to the pathogenesis of JAE. Our family-based association analysis using the haplotype-based haplotype relative risk statistic revealed an association of JAE with the nine-repeat containing allele of the GRIK1 tetranucleotide polymorphism (chi2 = 8.31, df = 1, P = 0.004). Supportive evidence for linkage to a JAE related IGE spectrum (Zmax = 1.67 at GRIK1) under an autosomal dominant mode of inheritance and significant allele sharing (P < 0.05) among the affected family members suggest that allelic variants of GRIK1 contribute a major genetic determinant to the pathogenesis of JAE-related phenotypes.

Alleles↗