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PubMed2003

Plasma long-chain polyunsaturated fatty acids and neurodevelopment through the first 12 months of life in phenylketonuria.

The aims of the study were to examine the relationship between long-chain polyunsaturated fatty acid (LCPUFA) status at diagnosis of phenylketonuria (PKU) and neurodevelopment through the first 12 months of life, and to assess whether any difference exists between infants breastfed and bottlefed in the first days of life on the basis of LCPUFA status. Twenty infants with PKU were prospectively examined through the first year of life. Plasma fatty acids were measured in infants at diagnosis. Plasma phenylalanine levels were determined monthly. Main outcome measures were the Bayley Mental Developmental Index (MDI) and Psychomotor Developmental Index (PDI) at 5 and 12 months of age, and the visual function at 12 months, evaluated by P100 wave latencies with visual evoked potentials. A higher PDI score was associated with higher plasma arachidonic acid at diagnosis (adjusted correlation coefficient of PDI at 5 months, r=0.38, p=0.05). P100 wave latency at 15 minutes of arc (15') was associated with the early plasma arachidonic acid (adjusted r=-0.56, p=0.02) and phenylalanine levels at 12 months (adjusted r=0.22, p=0.05). No association was found between MDI score and any essential fatty acids. Breastfed infants exhibited higher plasma arachidonic acid (mean difference, delta, =3.4%; 95% confidence interval [CI]=1.2-5.6%) and shorter P100 wave latency at 15' (delta=-21 ms, 95%CI=-30 to -12) than bottlefed infants. Within the population of this study, a weak positive association has been found between plasma LCPUFAs at diagnosis (higher in breastfed infants) and neurodevelopmental indices through the first year of life.

Adult↗
PubMed1999

Placental pathology and neurodevelopment of the infant with intrauterine growth restriction.

The placentas of 68 infants with intrauterine growth restriction (IUGR) were examined for evidence of impaired uteroplacental circulation and compared with those of 65 appropriately grown infants. Infarcts and/or accelerated villous maturation were present in the placentas in 27 (40%) of the infants with IUGR compared with seven (11%) of the infants without IUGR (P<0.001). The infants were followed-up at 4 and 12 months of age and growth parameters recorded. Medical and developmental assessments and neuromotor developmental examinations were also performed. The 23 infants in the IUGR group with placentas with evidence of impaired uteroplacental circulation were compared with the 31 infants with IUGR with normal placentas. There was no difference between the groups in growth, cognitive development, or neuromotor abnormality. It was concluded that IUGR is strongly associated with placental markers of impaired uteroplacental blood flow while it would appear that there is no association between placental pathology and growth or neurodevelopment in the first year.

Child Development↗
PubMed2003

Neurodevelopment, impulsivity, and adolescent gambling.

The prevalence of problem and pathological gambling in adolescence and young adulthood has been found to be two- to fourfold higher than in adulthood. Given that these high rates might predict future increases across all age groups, it is important to explore the causes of the elevated rates of problem and pathological gambling among youths. This article reviews evidence for a neurobiological basis for adolescent vulnerability to problem and pathological gambling behaviors. We propose that a common trait motif of impulsivity might underlie phenomenology of pathological gambling, commonly comorbid psychiatric disorders, and related aspects of adolescent behavior. Recent advances in understanding the brain mechanisms involved in motivation, reward, and decision-making allow a discussion of neural circuitry underlying impulsivity. Emerging data indicate that important neurodevelopmental events during adolescence occur in brain regions associated with motivation and impulsive behavior. We hypothesize that immaturity of frontal cortical and subcortical monoaminergic systems during normal neurodevelopment underlies adolescent impulsivity as a transitional trait-behavior. While these neurodevelopmental processes may confer advantage by promoting a learning drive for optimal adaptation to adult roles, they may also confer an increased vulnerability to addictive behaviors such as problem and pathological gambling. An exploration of the developmental changes in neural circuitry involved in impulse control has significant implications for understanding adolescent behaviors and treating problem and pathological gambling among youths.

Adolescent↗
PubMed2003

LDL receptor-related proteins in neurodevelopment.

Low-density lipoprotein receptor-related proteins (LRPs) are evolutionarily ancient cell-surface receptors with diverse biological functions. All are expressed in the central nervous system and, for most receptors, animal models have shown that they are indispensable for successful neurodevelopment. The mechanisms by which they regulate the formation of the nervous system are varied and include the transduction of extracellular signals and the modulation of intracellular signal propagation, as well as cargo transport, the function most commonly attributed to this gene family. Here, we will summarize recent advances in our understanding of the molecular basis on which these receptors function during development.

Animals↗
PubMed2005

Intestinal perforation in very low birth weight infants: growth and neurodevelopment at 1 year of age.

OBJECTIVE: To compare growth and neurodevelopment in surviving very low birth weight (VLBW) infants with an intestinal perforation (IP) caused by necrotizing enterocolitis (NEC) versus spontaneous intestinal perforation (SIP). STUDY DESIGN: Retrospective, observational cohort study. Infants born between January 1996 and December 1999 with birth weight <1500 g and a diagnosis of intestinal perforation were identified and data extracted from NICU, surgical and hospital databases. RESULTS: IP was identified in 62 of 1357 VLBW infants (5%); 39 infants (63%) had surgical NEC and 23 (37%) had SIP. Among survivors, 21/28 with surgical NEC (75%) and 13/18 with SIP (72%) returned for follow-up. At 1-year adjusted age, there were no differences in growth parameters but the Mental Developmental Index (MDI) and Psychomotor Developmental Index (PDI) were lower in survivors with NEC versus SIP (mean difference in MDI=15; 95% confidence limits=3, 28; p=0.02; mean difference in PDI=14; 95% confidence limits=0.4, 28; p=0.04). CONCLUSIONS: Intestinal perforation caused by NEC, as compared to SIP, is associated with worse neurodevelopmental outcome at 1 year.

Child Development↗
PubMed2001

Neurodevelopment of children exposed in utero to treatment of maternal malignancy.

Cancer is the second most common cause of death during the reproductive years, complicating approximately 1/1000 pregnancies. The occurrence of cancer during gestation is likely to increase as a result of a woman's tendency to delay childbearing. Improved diagnostic techniques for malignancies increases detection of cancer during pregnancy. Malignant conditions during gestation are believed to be associated with an increase in poor perinatal and fetal outcomes that are often due to maternal treatment. Physicians should weigh the benefits of treatment against the risks of fetal exposure. To date, most reports have focused on morphologic observations made very close to the time of delivery with little data collected on children's long-term neurodevelopment following in utero exposure to malignancy and treatment. Because the brain differentiates throughout pregnancy and in early postnatal life, damage may occur even after first trimester exposure. The possible delayed effects of treatment on a child's neurological, intellectual and behavioural functioning have never been systematically evaluated. The goal of this report was to summarize all related issues into one review to facilitate both practitioners' and patients' access to known data on fetal risks and safety.

Child↗
PubMed2004

Periventricular echogenicity is related to delayed neurodevelopment of preterm infants.

Periventricular leukomalacia (PVL) is one of the most commonly seen neuropathologic lesions and is related to many neurodevelopmental handicaps in premature infants. Periventricular echogenicities (PVE) are considered to be at the milder end of the spectrum of PVL, and thus might affect the neurodevelopment of the preterm infants as well. In this retrospective cohort study medical records of 257 preterm infants who were discharged from our neonatal intensive care unit (NICU) during October 1996 to August 2000 were reviewed. A total of 114 records of preterm infants fulfilling our criteria were included in the survey. On the basis of the craniosonographic findings and birth history, the candidates were divided into three subgroups: group 1 (control) included infants with normal craniosonographic image during the neonatal period; group 2 included infants with PVEs for < 2 weeks during the neonatal period; group 3 included infants with PVEs> or = 2 weeks during the neonatal period. Neurodevelopmental assessment using the Bayley Scale of Infant Development II at 6, 12, and 18 months of corrected age of each group was compared. There were no significant differences among the three groups in gestational age, birth weight, and gender prevalence. Infants in group 3 had lower Mental Developmental Index and Psychomotor Developmental Index scores as compared with those in groups 1 and 2 at 6 ( p< 0.01), 12 ( p < 0.001), and 18 ( p < 0.01) months of corrected age, respectively. In conclusion, infants with PVEs that persisted for at least a 2-week period have significantly higher risk of delayed developmental outcomes as compared with infants with normal craniosonography or infants with PVEs that persisted for less than 2 weeks. It might be prudent to arrange therapeutic intervention for rehabilitation to these high-risk infants as early as possible to reduce the intensity of possible handicap in the future.

Cohort Studies↗
PubMed1992

Neurodevelopment in late infancy after prenatal exposure to benzodiazepines--a prospective study.

Growth and neurodevelopment at 6, 10 and 18 months of age have been studied prospectively and longitudinally in a series of 17 children born to mothers who used benzodiazepines (BZD) in therapeutic doses as their only psychotropic drug throughout pregnancy. The results were compared with a group of 29 children born to mothers without any known use of psychotropic drugs. The BZD-exposed children caught up their low mean birth-weight, at an early stage, whereas the slightly decreased head circumference at birth remained at the same low level. In five infants, a pattern of craniofacial anomalies was found. Deviating neurodevelopmental and clinical symptoms and signs were common. The gross motor development was retarded at 6 and 10 months, but was nearly normal at 18 months. Impaired fine motor functions were found on all follow-up occasions. At 18 months, the most prominent finding was a delayed development of pincer grasp. The BZD-exposed children showed deviations in muscle tone and pattern of movements more frequently than children in the reference group. The study suggests that the use of BZD in therapeutic doses throughout pregnancy can have negative effects on the development of children up to 18 months of age. The long-term hazards cannot be evaluated from these results. A further follow-up at early school age is needed and is in progress.

Abnormalities, Drug-Induced↗
PubMed1997

Neurodevelopment of children exposed in utero to antidepressant drugs.

BACKGROUND: Many women of reproductive age have depression, necessitating therapy with either a tricyclic antidepressant drug or a drug, such as fluoxetine, that inhibits the reuptake of serotonin. Whether these drugs affect fetal neurodevelopment is not known. METHODS: We studied the children of 80 mothers who had received a tricyclic antidepressant drug during pregnancy, 55 children whose mothers had received fluoxetine during pregnancy, and 84 children whose mothers had not been exposed during pregnancy to any agent known to affect the fetus adversely. The children's global IQ and language development were assessed between 16 and 86 months of postnatal age by age-appropriate Bayley Scales of Infant Development or the McCarthy Scales of Children's Abilities (for IQ) and the Reynell Developmental Language Scales. RESULTS: The mean (+/-SD) global IQ scores were 118+/-17 in the children of mothers who received a tricyclic antidepressant drug, 117+/-17 in those whose mothers received fluoxetine, and 115+/-14 in those in the control group. The language scores were similar in all three groups. The results were similar in children exposed to a tricyclic antidepressant drug or fluoxetine during the first trimester and those exposed throughout pregnancy. There were also no significant differences in temperament, mood, arousability, activity level, distractibility, or behavior problems in the three groups of children. CONCLUSIONS: In utero exposure to either tricyclic antidepressant drugs or fluoxetine does not affect global IQ, language development, or behavioral development in preschool children.

Adult↗
PubMed2006

Postnatal growth, neurodevelopment and altered adiposity after preterm birth--from a clinical nutrition perspective.

UNLABELLED: Evidence reveals a dilemma that under-nutrition and growth retardation during brain growth are associated with neurodevelopmental deficits, and nutritional supplement resulting in catch-up growth and relative visceral adiposity leads to metabolic/cardiovascular morbidities. Hyperinsulinaemia secondary to insulin resistance appears to play a central role in the development of visceral adiposity through its action on adipocyte beta3-adrenoceptor. CONCLUSION: Optimal nutritional management to minimize hyperinsulinaemia and insulin resistance may potentially improve neurodevelopment and facilitate catch-up growth with normal body composition.

Adiposity↗
PubMed2006

Omega-3 fatty acid deficiencies in neurodevelopment, aggression and autonomic dysregulation: opportunities for intervention.

Mechanisms by which aggressive and depressive disorders may be exacerbated by nutritional deficiencies in omega-3 fatty acids are considered. Early developmental deficiencies in docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may lower serotonin levels at critical periods of neurodevelopment and may result in a cascade of suboptimal development of neurotransmitter systems limiting regulation of the limbic system by the frontal cortex. Residual developmental deficits may be manifest as dysregulation of sympathetic responses to stress including decreased heart rate variability and hypertension, which in turn have been linked to behavioral dysregulation. Little direct data are available to disentangle residual neurodevelopmental effects from reversible adult pathologies. Ensuring optimal intakes of omega-3 fatty acids during early development and adulthood shows considerable promise in preventing aggression and hostility.

Adult↗
PubMedDate not supplied

Refining the effects observed in a developmental neurobehavioral study of ammonium perchlorate administered orally in drinking water to rats. II. Behavioral and neurodevelopment effects.

A developmental neurotoxicity study was conducted to generate additional data on the potential functional and morphological hazard to the central nervous system caused by ammonium perchlorate in offspring from in utero and lactation exposure. Female Sprague-Dawley rats (23 to 25/group) were given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 10.0 mg/kg-day perchlorate in the drinking water beginning 2 weeks prior to mating and continuing through day 10 of lactation for the behavioral function assessment or given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 30.0 mg/kg-day beginning on gestation day 0 and continuing through day 10 of lactation for neurodevelopment assessments. Motor activity was conducted on postpartum days 14, 18, and 22 and juvenile brain weights, neurohistopathological examinations, and regional brain morphometry were conducted on postpartum days 10 and 22. This research revealed a sexually dimorphic response, with some brain regions being larger in perchlorate-treated male rats than in comparable controls. Even so, there was no evidence of any obvious exposure-related effects on male rat brain weights or neuropathology. The most consistent exposure-related effect in the male pups was on the thickness of the corpus callosum, with both the right- and left-sided measures of the thickness of this white matter tract being significantly greater for the male pups in the 0.1 and 1.0 mg/kg-day exposure groups. The behavioral testing suggests prenatal exposure to ammonium perchlorate does not affect the development of gross motor movements in the pups.

Administration, Oral↗
PubMed2005

Abnormal infant neurodevelopment predicts schizophrenia spectrum disorders.

OBJECTIVE: The aim of this study was to detect infants who carry a schizophrenic genotype and study the development of schizophrenia spectrum disorders (SZSD) from birth. INTRODUCTION: In the 1940s, Bender described uneven maturation in childhood schizophrenics and in 1952 found this in the infant histories of 6 schizophrenic children. METHODS: We tested a possible index for defective neural integration in infants termed "pandysmaturation" (PDM). This required retarded cranial growth plus retarded and erratic gross motor development on a single exam. Twelve offspring of hospitalized schizophrenic mothers and 12 infants in a "Well Baby Clinic," were examined 10 times between birth and 2 years of age. Psychiatric interviews and psychological testing were done at 10, 15, and 22 years of age, plus follow-up at 27-35 years of age. RESULTS: Six infants had PDM at 2, 6, or 13 months of age. Five individuals have been blindly diagnosed (by KSK) as having lifetime SZSD; all 5 had PDM before 8 months. Chi-square one-tailed tests confirmed the predictions: (1) PDM was related to subsequent SZSD (chi(2) = 11.43; p < 0.0005); (2) schizophrenic mothers had more infants with PDM than nonschizophrenic mothers (chi(2) = 3.28; p < 0.05); and (3) schizophrenic mothers had more SZSD offspring than nonschizophrenic mothers (chi(2) = 6.39; p < 0.0125). DISCUSSION: These first behavioral observations of aberrant neurodevelopment in pre- SZSD infants support the evidence of early neurodevelopmental disorder seen in studies of brain pathology in SZSD adults.

Adolescent↗
PubMed1995

Passive and active maternal smoking during pregnancy, as measured by serum cotinine, and postnatal smoke exposure. II. Effects on neurodevelopment at age 5 years.

The authors sought to determine the neurobehavioral effects of prenatal exposure to maternal active smoking and environmental tobacco smoke (ETS), assessed by maternal serum cotinine level, and of postnatal exposure to smoke based on maternal report. Five-year-old children (n = 2,124) who were participants in the Child Health and Development Studies in Oakland, California, between 1964 and 1967 were evaluated with the use of the Peabody Picture Vocabulary Test (PPVT) and the Raven Coloured Progressive Matrices Test, and also assessed on a behavioral rating scale completed by the mother that included questions on activity level. Children of ETS-exposed women did not differ from children of other nonsmokers on neurobehavioral assessment. Children whose mothers smoked during pregnancy had somewhat higher adjusted Raven (p = 0.10) and PPVT scores (p = 0.06) than children of nonsmokers, although they did not differ in their activity level (p = 0.32). However, children smoke-exposed during childhood did have lower adjusted Raven (p = 0.01) and PPVT scores (p = 0.16), and were rated more active by their mothers (p = 0.04). These differences may be attributed to uncontrolled confounding of sociobehavioral variables. However, the authors cannot rule out the possibility that ETS exposure during childhood may be more hazardous to neurodevelopment than prenatal exposure.

Biomarkers↗
PubMed1998

Maternal diet fatty acid composition affects neurodevelopment in rat pups.

The effect of pre- and postnatal maternal dietary fatty acid composition on neurodevelopment in rat pups was studied. Timed pregnant dams were fed, beginning on d 2 of gestation and throughout lactation, either nonpurified diet (reference) or a purified diet whose fat source (22% of energy) was either corn oil or menhaden fish oil. On postnatal d 3, pups were randomly cross-fostered among dams of the same diet group and culled to 10 pups per dam. Milk was removed from stomachs of culled pups for fatty acid analyses. From postnatal d 4 to 30, pups were assessed daily for the appearance of neurodevelopmental reflexes. Auditory brainstem conduction times were measured on postnatal d 23 and 29. Pups were killed on postnatal d 30, and cerebrums were removed for fatty acid analyses. The fatty acid composition of maternal milk and pup cerebrums reflected maternal diet with higher levels of (n-3) and (n-6) fatty acids in the fish oil and corn oil groups, respectively. The time of appearance of auditory startle was significantly delayed (P = 0.004), and auditory brainstem conduction times on postnatal d 23 and 29 were significantly longer in pups of the fish oil- than corn oil-fed dams (P </= 0.05). A delay in the appearance of the auditory startle reflex and longer auditory brainstem conduction times in pups of dams fed fish oil-supplemented diet may be due to negative effects on myelination of the auditory brainstem pathway.

Animals↗
PubMed1996

Imaging as a tool in exploring the neurodevelopment and genetics of schizophrenia.

Neuroimaging has enabled us to address questions about the timing and origin of brain abnormalities in schizophrenia. First episode and longitudinal computed tomography (CT) and magnetic resonance imaging (MRI) studies of schizophrenic patients have shown that the brain abnormalities are present at onset of psychosis and are non-progressive. Such findings support the idea that schizophrenia is a developmental rather than a degenerative condition. Furthermore, the presence of ventriculomegaly and diminished hemispheric asymmetry in familial schizophrenics and in those of their relatives who appear to be transmitting the disorder, implies involvement of the genes controlling neurodevelopment. However, genetic factors do not fully account for the development of schizophrenia; early environmental insults such as obstetric complications are also important and may interact with genetic predisposition. Brain development continues postnatally and profound maturational events also occur in adolescence and early adulthood. Magnetic resonance spectroscopy (MRS) studies allow the investigation of the developmental biochemistry of the living brain and are being used to explore the role of maturational brain events in determining the onset of psychosis.

Brain↗
PubMed2003

The causes of schizophrenia: neurodevelopment and other risk factors.

Understanding the etiology of schizophrenia has been a considerable challenge. The neurodevelopmental hypothesis has held sway in recent years, focusing our attention on biological causes acting in early life. Much evidence supports this hypothesis and risk factors operating in early life (e.g., obstetric complications) have been shown to be associated with the later development of schizophrenia. Indicators of abnormal neurodevelopment that characterize individuals vulnerable to later developing schizophrenia have also been identified. For example, as a group, children who will later develop schizophrenia subtly differ from their peers in terms of their motor, cognitive, and social functioning. However, there is much that cannot be explained in purely neurodevelopmental terms. There is growing evidence of associations between the risk of schizophrenia and factors such as drug misuse, ethnicity/migration, life events, and urbanicity. A multifactorial model of causation that encompasses biological, social, and psychological elements is arguably both a better representation of current research findings and a more appropriate model for clinical practice.

Journal Article↗
PubMed1994

Anorexia nervosa: physical health and neurodevelopment at 16 and 21 years.

Fifty-one cases of anorexia nervosa (AN) and 51 age-, sex- and school-matched controls, all drawn from a community sample of 15- to 16-year-olds, were compared at 16 and 21 years with regard to physical health and neurodevelopment. The AN group had significantly lower mean height than the comparison group at age 21 years. There were significantly more individuals that were overweight and underweight in the AN group at age 21 years. Fractures were slightly, but significantly, more common. Dysdiadochokinesis was very much more common in the AN group at both ages, and its occurrence was not correlated with low weight. It is suggested that diadochokinesis in AN might mirror some inherent underlying immaturity or other abnormality of the central nervous system in a subgroup of cases. The presence of dysdiadochokinesis was associated with a tendency towards poorer psychosocial outcome, even in cases that were no longer underweight.

Adolescent↗