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PubMed2004

Neuregulin genotype and medication response in Finnish patients with schizophrenia.

Neuregulin 1 is involved both in neurodevelopment and neurotransmitter mechanisms in the brain. There is evidence of an association between neuregulin 1 genotype and schizophrenia. We compared neuregulin 1 genotypes in patients with schizophrenia (n=94) and control subjects (n=395) of Finnish origin by using one SNP (SNP8NRG221533) as a genetic marker. We also analyzed NRG1 genotype with regard to age at onset and between responders and non-responders to conventional antipsychotics. The NRG1 genotype or allele frequencies showed similar distributions between patient and control groups. Age at onset was not associated with NRG1 genotype. The TT genotype was overrepresented in the non-responders group compared with the responders (p=0.013). Further studies are needed to ascertain the significance of neuregulin genotype in medication response to schizophrenia.

Adult↗

PubMed1990

Detection of HIV in fetal central nervous system tissue.

Neurological disease is a common finding in children with AIDS and in others without signs of disease but with evidence of congenital HIV-1 infection. To investigate the possibility that HIV-1 can infect fetal central nervous system (CNS) tissue and therefore possibly serve as the substrate for the abnormal neurodevelopment characteristic of pediatric AIDS, eight abortus CNS samples (one set of twins) from seven HIV-1-seropositive intravenous drug users (IVDUs) and eight control abortus CNS samples from eight HIV-1-seronegative IVDUs were analyzed for HIV-1 infection. HIV-1 nucleic acid was detected only after the use of polymerase chain reaction (PCR) in three of eight CNS samples from HIV-seropositive IVDUs but not in samples from seronegative subjects. In situ hybridization confirmed that HIV-1 DNA sequences were in cells in the CNS parenchyma of two of the three positive samples. This study demonstrates that HIV-1 can infect human fetal CNS tissue in vivo, but that the use of PCR may be necessary for its detection.

AIDS Dementia Complex↗

PubMed2001

Behavioral and neural consequences of prenatal exposure to nicotine.

OBJECTIVE: To review evidence for the neurodevelopmental effects of in utero exposure to nicotine. Concerns about long-term cognitive and behavioral effects of prenatal exposure to nicotine arise from reports of increased rates of disruptive behavioral disorders in children whose mothers smoked during pregnancy. The relatively high rate of tobacco smoking among pregnant women (25% of all pregnancies in the U.S.) underlines the seriousness of these concerns. METHOD: This review examines the largest and most recent epidemiological and clinical studies that investigated the association of prenatal nicotine exposure with health, behavioral, and cognitive problems. Because of the numerous potential confounding variables in human research, findings from animal studies, in which environmental factors are strictly controlled, are also discussed. Finally, neural and molecular mechanisms that are likely to underlie neurodevelopmental disruptions produced by prenatal nicotine exposure are outlined. RESULTS: A dose-response relationship between maternal smoking rates and low birth weight (potentially associated with lower cognitive ability) and spontaneous abortion is consistently found, whereas long-term developmental and behavioral effects in the offspring are still controversial, perhaps because of the difficulty of separating them from other genetic and environmental factors. Despite the wide variability of experimental paradigms used in animal studies, common physical and behavioral effects of prenatal exposure to nicotine have been observed, including low birth weight, enhanced locomotor activity, and cognitive impairment. Finally, disturbances in neuronal pathfinding, abnormalities in cell proliferation and differentiation, and disruptions in the development of the cholinergic and catecholaminergic systems all have been reported in molecular animal studies of in utero exposure to nicotine. CONCLUSIONS: Prenatal exposure to nicotine may lead to dysregulation in neurodevelopment and can indicate higher risk for psychiatric problems, including substance abuse. Knowledge of prenatal exposure to nicotine should prompt child psychiatrists to closely monitor at-risk patients.

Animals↗

PubMed2000

Neurodevelopmental and neuroimaging correlates in nonsyndromal microcephalic children.

This descriptive study examined the relationship between head size, developmental functioning, and neuroimaging findings in children with absolute microcephaly. Subjects, aged 1 to 48 months, were assigned to one of two groups based on occipitofrontal head circumference (OFC). Group A included subjects with an OFC of 2 to 2.99 standard deviations below the mean, and Group B included subjects with an OFC of 3 or more standard deviations below the mean. Brain scan findings for 62% of the subjects were abnormal. Findings included cerebral atrophy, cortical dysplasia, myelination delay, and white matter hypoplasia. Mean scores for developmental measures in Groups A and B were less than 70. Mean developmental scores in the normal imaging group were 70 or greater, whereas developmental scores in the abnormal imaging group were 52 or less. Forty-three percent of the subjects in Group A and 80% of those in Group B had abnormal findings from imaging studies (p = .0394). Subjects with one or more brain abnormalities determined on the basis of magnetic resonance images or computed tomographic scans had significantly lower scores in all developmental areas (p < .05). The authors concluded that abnormal brain images seem to be a better reflection of developmental performance than the degree of microcephaly. J Dev Behav Pediatr 21:12-18, 2000. Index terms: microcephaly, neuroimaging, neurodevelopment.

Anthropometry↗

PubMed2002

In harm's way: toxic threats to child development.

Developmental disabilities result from complex interactions of genetic, toxicologic (chemical), and social factors. Among these various causes, toxicologic exposures deserve special scrutiny because they are readily preventable. This article provides an introduction to some of the literature addressing the effects of these toxicologic exposures on the developing brain. This body of research demonstrates cause for serious concern that commonly encountered household and environmental chemicals contribute to developmental disabilities. The developing brain is uniquely susceptible to permanent impairment by exposure to environmental substances during time windows of vulnerability. Lead, mercury, and polychlorinated biphenyls (PCBs) have been extensively studied and found to impair development at levels of exposure currently experienced by significant portions of the general population. High-dose exposures to each of these chemicals cause catastrophic developmental effects. More recent research has revealed toxicity at progressively lower exposures, illustrating a "declining threshold of harm" commonly observed with improved understanding of developmental toxicants. For lead, mercury, and PCBs, recent studies reveal that background-population exposures contribute to a wide variety of problems, including impairments in attention, memory, learning, social behavior, and IQ. Unfortunately, for most chemicals there is little data with which to evaluate potential risks to neurodevelopment. Among the 3000 chemicals produced in highest volume (over 1 million lbs/yr), only 12 have been adequately tested for their effects on the developing brain. This is a matter of concern because the fetus and child are exposed to untold numbers, quantities, and combinations of substances whose safety has not been established. Child development can be better protected by more precautionary regulation of household and environmental chemicals. Meanwhile, health care providers and parents can play an important role in reducing exposures to a wide variety of known and suspected neurodevelopmental toxicants that are widely present in consumer products, food, the home, and wider community.

Aggression↗

PubMed2005

Neurodevelopmental implications of "deformational" plagiocephaly.

Over the past decade there has been a dramatic increase in referrals to specialty clinics, craniofacial centers, plastic surgeons, and neurosurgeons for assessment and treatment of deformational plagiocephaly (DP). Though considered a medically benign condition, preliminary reports suggest that DP may be associated with developmental problems. However, mechanisms to account for this association have not been hypothesized or empirically tested. Although treatment justifications often center on prevention of atypical appearance, little is known about the cosmetic outcomes of treated and untreated children. In this review we hypothesize different etiological pathways linking DP with neurodevelopment (e.g., environmental positioning limitations with and without underlying CNS pathology). We outline directions for research on incidence and prevalence, developmental outcomes, sex differences, determinants of treatment participation, and craniofacial appearance. Despite the paucity of existing research, preliminary findings suggest that children with this condition should be screened and monitored for developmental delays or deficits, as we await more conclusive information from future studies.

Cognition Disorders↗

PubMed2001

Constipation in very-low-birth-weight children at 10 to 14 years of age.

BACKGROUND: The authors documented that very-low-birth-weight children (less than 750-g) when compared with 750-to 1,499-g birth-weight and normal-birth-weight-matched controls have higher than normal rates of neurosensory and cognitive impairments at school age. In this population, the authors found a higher rate of constipation than expected among 19 of 59 (32%) less-than-750-g-birth-weight children. The authors therefore wanted to evaluate in greater detail the problem of constipation and associated toileting problems in this population. METHODS: Nineteen less-than-750-g-birth-weight children with constipation were matched to the next less than 750-g-birth-weight child of comparable age, sex, and race who did not have constipation. A telephone questionnaire was administered to 15 of 19 parents of the less-than-750-g-birth-weight children who had constipation. RESULTS: The 15 children with constipation had significantly higher rates of neurosensory impairment (7 [47%] vs. 1 [7%]) and lower mean WISC III IQ scores (72 +/- 22 vs. 89 +/- 13) when compared with birth-weight-matched controls without constipation (P < 0.05). The constipated children also had significantly higher rates of associated toileting problems, including encopresis (8[53%] vs. 1 [7%])and stool withholding (9 [60%] vs. 2 [13%]; P < 0.05). CONCLUSION: The higher incidence of constipation among less-than-750-g-birth-weight children is associated with neurodevelopment impairment. Awareness of this problem and preventive intervention to ensure regular stools could possibly decrease the high rate of constipation and associated toileting problems.

Adolescent↗

PubMed1998

Craniocerebral trauma: protection and retrieval of the neuronal population after injury.

OBJECTIVE: To review the consequences of mechanical injury to the brain with an emphasis on factors that may explain the variability of outcomes and how this might be influenced. METHODS: Information regarding the pathophysiology of traumatic brain damage contained in original scientific reports and in review articles published in recent years was reviewed from the perspective of a clinical neurosurgeon and a neuropathologist, each with major research interests in traumatic brain damage. The information was compiled on the basis of the knowledge of and personal selection of articles that were identified through selective literature searches and current awareness profiles. A systematic literature review was not conducted. RESULTS: Mechanical input affects neuronal and vascular elements and is translated into biological effects on the brain through a complex series of interacting cellular and molecular events. Whether these lead to permanent structural damage or to resolution and recovery is determined by the balance between processes that, on the one hand, mediate the effects of initial injury and subsequent secondary insults and, on the other, are manifestations of the brain's protective, reparative response. Experimental and clinical research has identified opportunities for altering the balance in a way that might promote recovery, but data demonstrating that this can lead to substantial clinical benefit are lacking. Recent evidence of genetically determined, individual susceptibility to the effects of injury may explain some of the puzzling variability in outcome after apparently similar insults and may also provide new opportunities for treatment. CONCLUSION: The understanding of traumatic brain damage that is being gained from recent research is widening and broadening perspectives from the traditional focus on mechanical, vascular, and metabolic effects to encompass wider, neurobiological issues, drawn from the fields of neurodevelopment, neuroplasticity, neurodegeneration, and neurogenetics. Neurotrauma is a fascinating area of neuroscience research, with promise for the translation of knowledge to improved clinical management and outcome.

Animals↗

PubMed2000

Cytomegalovirus urinary excretion and long term outcome in children with congenital cytomegalovirus infection. Congenital CMV Longitudinal Study Group.

BACKGROUND: Cytomegalovirus (CMV) is the most frequent cause of congenital infection, and both symptomatic and asymptomatic infants may have long term sequelae. Children with congenital CMV infection are chronically infected and excrete CMV in the urine for prolonged periods. However, the effect of prolonged viral replication on the long term outcome of these children is unknown. OBJECTIVE: To determine whether duration of CMV excretion is associated with outcome at 6 years of life in symptomatic and asymptomatic congenitally infected children. METHODS: Longitudinal cohort study. Children congenitally infected with CMV were identified at birth and followed prospectively in a study of long term effects of congenital CMV infection. The relationship between duration of CMV urinary excretion and growth, neurodevelopment and presence and progression of sensorineural hearing loss (SNHL) at 6 years of age was determined. RESULTS: There was no significant difference in the duration of viral urinary excretion between children born with asymptomatic (median, 4.55 years) and symptomatic (median, 2.97 years) congenital CMV infection (P = 0.11). Furthermore there was no association between long term growth or cognitive outcome and duration of viral excretion. However, a significantly greater proportion of children who excreted CMV for <4 years had SNHL and progressive SNHL compared with children with CMV excretion >4 years (P = 0.019, P = 0.009, respectively). CONCLUSIONS: Children congenitally infected with CMV are chronically infected for years, but the duration of CMV urinary excretion is not associated with abnormalities of growth, or neurodevelopmental deficits. However, SNHL and progressive SNHL were associated with a shorter duration of CMV excretion.

Adolescent↗

PubMed2004

Postnatally acquired cytomegalovirus infection via breast milk: effects on hearing and development in preterm infants.

BACKGROUND: In preterm infants there is a high risk of transmission of cytomegalovirus (CMV) via breast milk from seropositive mothers with reactivation of the virus during lactation. There is little information about the long term sequel of early postnatally acquired CMV infection in pre-term infants. This study aimed to investigate whether there was an increased frequency of impaired neurodevelopmental outcome and sensorineural hearing loss in preterm infants with postnatally acquired CMV infection through transmission by CMV-positive breast milk. METHODS: Twenty-two preterm infants [median birth weight, 1020 g (range, 600 to 1870 g); median gestational age, 27.6 weeks (range, 23.6 to 32 weeks] with early postnatally acquired CMV infection by breast-feeding (onset of viruria between Days 23 and 190 postnatally) were compared with 22 CMV-negative preterm infants individually matched for gestational age, birth weight, gender, intracranial hemorrhage and duration of ventilation. At 2 to 4.5 years of age, follow-up assessments were conducted consisting of neurologic examination, neurodevelopmental assessment and detailed audiologic tests. RESULTS: None of the children had sensorineural hearing loss. There was no difference between the groups with regard to neurologic, speech and language or motor development. CONCLUSION: The results of this study suggest that early postnatally acquired CMV infection via CMV-positive breast milk does not have a negative effect on neurodevelopment and hearing in this group of patients. Because we studied a small number of infants, further follow-up studies are warranted in preterm infants with early postnatally acquired CMV infection.

Adult↗

PubMed2000

Genetics of Rett syndrome: properties of the newly discovered gene and pathobiology of the disorder.

The recent identification of mutations in the gene methyl-Cpg-binding protein-2 (MECP2) in girls with Rett syndrome (RS) has firmly established the molecular genetic basis of this unique, X-linked, dominant disorder and provides a dramatic conclusion to an intensive, decade-long search. This finding has ramifications far beyond establishing the gene for RS. Recent data indicate that the clinical phenotypes for MECP2 mutations range from mild disability in the mother of a girl with RS to rapidly progressive encephalopathy in her brother. Further, the pathobiology of MECP2 could be a prototype for other disorders of neurodevelopment. MECP2 encodes a methyl-CpG-binding protein (MeCP2), which is critical for transcriptional silencing of an as yet unknown number and type of genes responsible for the pathobiology of RS. As such, this discovery opens up completely new vistas as to fundamental neurobiologic processes, to disease mechanisms in the neurodevelopmental disabilities, and to potential new therapeutic strategies for RS and related disorders.

Child↗

PubMed1992

The influence of sociopolitical, scientific, and technologic forces on the study and treatment of neonatal pain.

This article describes how sociopolitical, scientific, and technologic forces have influenced neonatal pain research and clinical practice. Changing beliefs about pain from the perspective of patients, physicians, nurses, and scientists investigating the neurobiology of pain are discussed. The impact of the development of the specialty of neonatology and its associated technologic advances on neonatal pain is explored. In addition, the influence of increased scientific knowledge about the neurodevelopment of the neonate and neurobiology of the sensory system on neonatal pain is presented. Finally, changes in society's views of children and the role of parents are addressed. The article concludes with a discussion of the relative importance of each of the factors in stimulating recent interest in neonatal pain. The opportunities for nurses to contribute to scientific research to improve the care of neonates in pain are highlighted.

Attitude to Health↗

PubMed2005

Paternal age and intelligence: implications for age-related genomic changes in male germ cells.

BACKGROUND: A robust association between advancing paternal age and schizophrenia risk is reported, and genetic changes in the germ cells of older men are presumed to underlie the effect. If that is so, then the pathway may include effects on cognition, as those with premorbid schizophrenia are reported to have lower intelligence. There are also substantial genetic influences on intelligence, so de novo genetic events in male germ cells, which accompany advancing paternal age, may plausibly influence offspring intelligence. OBJECTIVE: An association of paternal age with IQ in healthy adolescents may illuminate the mechanisms that link it to schizophrenia. METHOD: We examined the association of paternal age and IQ scores using the Israeli Army Board data on 44 175 individuals from a richly described birth cohort, along with maternal age and other potential modifiers. RESULTS: A significant inverted U-shaped relationship was observed between paternal age and IQ scores, which was independent from a similar association of IQ scores with maternal age. These relationships were not significantly attenuated by controlling for multiple possible confounding factors, including the other parent's age, parental education, social class, sex and birth order, birth weight and birth complications. Overall, parental age accounted for approximately 2% of the total variance in IQ scores, with later paternal age lowering non-verbal IQ scores more than verbal IQ scores. CONCLUSION: We found independent effects of maternal and paternal age on offspring IQ scores. The paternal age effect may be explained by de novo mutations or abnormal methylation of paternally imprinted genes, whereas maternal age may affect fetal neurodevelopment through age-related alterations in the in-utero environment. The influence of late paternal age to modify non-verbal IQ may be related to the pathways that increase the risk for schizophrenia in the offspring of older fathers.

Cohort Studies↗

PubMed2003

Apolipoprotein and apolipoprotein receptor genes, blood lipids and disease.

PURPOSE OF REVIEW: Apolipoproteins and their receptors are the main controllers of lipid metabolism and, as such, have a major impact not only on the risk of cardiovascular disease but also on the development and degeneration of the central nervous system. Variations in the genes coding for these apolipoproteins and their receptors and the interaction with the environment determine individual susceptibility to metabolic disturbances, the response to dietary or pharmacological intervention and, finally, to disease. RECENT FINDINGS: This review will focus on recent findings, such as the latest concepts regarding apolipoprotein E in neurodevelopment, the newly identified apolipoprotein A-V and its influence in triglyceride metabolism, and the improved understanding of apolipoprotein A-I and HDL metabolism in the light of the discovery of the ABC family of transporters. Other key aspects of lipoprotein metabolism and cardiovascular disease risk such as apolipoprotein B-100, the LDL receptor, apolipoprotein C-III or apolipoprotein (a) will be updated. SUMMARY: Variations in these genes will be analysed in relation to plasma lipid levels, their interactions with diet, treatment or other environmental stimuli, and their influence on the risk of cardiovascular disease and neurological disorders.

Apolipoproteins↗

PubMed2003

Impact of trauma on children.

Millions of children are affected by physical and sexual abuse, natural and technological disasters, transportation accidents, invasive medical procedures, exposure to community violence, violence in the home, assault, and terrorism. Unfortunately, the emotional impact of exposure to trauma on children is often unappreciated and therefore untreated, and yet the impact of exposures to disaster and violence is profound and long-lasting. This article first briefly discusses the epidemiology of trauma in children, and then reviews the psychiatric and neurodevelopmental impact of trauma on children as well as the effects of trauma on children's emotional development. Trauma in children can lead to the development of posttraumatic stress disorder as well as to a variety of other psychiatric disorders, including depression, generalized anxiety disorder, panic attacks, borderline personality disorder, and substance abuse in adult survivors of trauma. Research has found that early exposure to stress and trauma causes physical effects on neurodevelopment which may lead to changes in the individual's long-term response to stress and vulnerability to psychiatric disorders. Exposure to trauma also affects children's ability to regulate, identify, and express emotions, and may have a negative effect on the individual's core identity and ability to relate to others. The authors also discuss what has been learned, based on recent experiences such as the World Trade Center catastrophe, about the role of television viewing in increasing the effects of traumatic events. The last section of the article provides guidance concerning the identification and clinical treatment of children and adolescents who are having emotional problems as a result of exposure to trauma.

Journal Article↗

PubMed2004

NMDA receptor subunit expression after combined prenatal and postnatal exposure to ethanol.

BACKGROUND: The N-methyl-D-aspartate receptor (NMDAR), a subtype of glutamate receptor, is essential for normal neurodevelopment. The brain growth spurt, which is both prenatal and postnatal in the rat, is a time when the brain is especially sensitive to the effects of a teratogen, such as alcohol. Changes in NMDAR function after early perinatal exposure to ethanol (EtOH) may be related to alterations in the expression of secondary subunits. Thus, we investigated the expression of the NR1, NR2A, and NR2B subunits after combined prenatal and postnatal exposure to EtOH. METHODS: A binge model was used to administer EtOH (5 g/kg) or isocaloric vehicle to pregnant female rats followed by EtOH (6.2 g/kg) or isocaloric control diet from postnatal days 4 through 9 via an artificial rearing method. Proteins from crude membrane homogenates isolated from cortex and hippocampus at postnatal day 10, 14, or 21 were separated in a standard Western blot procedure. RESULTS: The expression of the NR2A subunit of EtOH-exposed pups showed a significant increase at postnatal day 10 in hippocampus compared with diet controls. No significant changes were seen for any other subunit in either region. CONCLUSIONS: The up-regulation of NR2A during EtOH withdrawal is consistent with compensatory changes to prolonged inhibition of the NMDAR. These results indicate that postnatal exposure to ethanol produces distinct effects on the NMDAR, which may underlie deficits associated with alcohol-related neurodevelopmental disorder.

Animals↗

PubMed2005

Recognition and prevention of fetal alcohol syndrome.

Alcohol use among women of childbearing age is prevalent in the United States, with approximately 1 in 5 nonpregnant women reporting binge drinking (5 or more drinks on any one occasion) and 1 in 25 pregnant women reporting binge drinking. Alcohol use during pregnancy results in a spectrum of adverse outcomes known as fetal alcohol spectrum disorders. Fetal alcohol syndrome (FAS) is one of these disorders. Fetal alcohol syndrome is characterized by specific facial abnormalities and significant impairments in neurodevelopment and physical growth. Early identification of children with FAS has been shown to enhance their long-term outcomes. In an effort to improve clinical recognition of children with this condition, Centers for Disease Control and Prevention (CDC) was directed by Congress in 2002 to lead the development of uniform diagnostic criteria for FAS and other prenatal alcohol-related conditions. The purpose of this commentary is to provide clinicians a summary of the report released by CDC describing the current diagnostic criteria for FAS. In addition, advancements have been made in screening and brief interventions for alcohol use disorders in women who have the potential to make significant strides in the prevention of FAS spectrum disorders. Knowledge of the diagnostic criteria for FAS can lead to increased identification of the syndrome in infants and children and the provision of appropriate medical and support services. Screening for and intervening with women at risk for an alcohol-exposed pregnancy can prevent FAS and other fetal alcohol spectrum disorders.

Alcohol Drinking↗

PubMed2006

Deregulation of cdk5 in Hippocampal sclerosis.

Hippocampal sclerosis (HS) is the most common cause of chronic medically refractory epilepsy in adults. Histologically, HS is characterized by segmental neuronal loss and gliosis. Although neuronal loss is important to the pathophysiology of HS, the molecular mechanisms underlying the neuronal loss remain uncertain. Recently, it has been appreciated that proteins important in neurodevelopment may also have a role in neurodegeneration. Cyclin-dependent kinase 5 (cdk5), known to be crucial in development of the normal cerebral cortex, has now been shown as pivotal in several cell death paradigms, including apoptosis and necrosis. Deregulation of cdk5 by p25 causes hyperphosphorylation of tau and may contribute to pathology in several neurodegenerative conditions. Furthermore, it has been shown that after transient forebrain ischemia, cdk5 causes specific death of CA1 neurons in the rat hippocampus by direct phosphorylation of the NR2A subunit of the NMDA receptor and subsequent excitotoxicity. Because apoptosis, necrosis, and excitotoxicity are all thought to contribute to neuronal loss in HS, we hypothesized that abnormalities of the cdk5 pathway would accompany this disorder. Surgically resected cases of HS with adjacent histologically normal lateral temporal cortex were examined for cdk5 and its activator p35/p25. We consistently found increased immunoreactivity for p35/p25 in surviving neurons within areas of neuronal loss compared with areas where neurons were preserved. Western blots showed the ratio of p25 to p35 to be greater in diseased hippocampi than in the adjacent histologically normal temporal lobe. Histone-based kinase assays demonstrated increased activity of the p25-cdk5 complex in HS compared with the temporal lobe despite neuronal loss in the hippocampal samples. Our results suggest that p25 is pathologically increased in HS and that deregulation of cdk5 by p25 might contribute to neuronal death in this condition.

Adult↗