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PubMed1992

Neuroradiological findings in children with congenital myotonic dystrophy.

We studied seven children with congenital myotonic dystrophy, aged 2.1-8.3 years, and the results of computed tomography and magnetic resonance imaging of the brain were analyzed and neurological development was assessed from the neonatal period. We found that ventricular dilatation that had been seen on the first day of life in two of three infants had not progressed in sequential follow-up computed tomography scans taken at intervals of one to six years. Also, in T2-weighted magnetic resonance imagings, areas of periventricular hyperintensity were identified in all children, as well as areas of subcortical hyperintensity in one child. Further, an asphyxial episode had occurred at birth in five patients and the extent of the periventricular hyperintensity was found to correlate significantly with Apgar scores, indicating that the degree of perinatal asphyxia that had occurred was responsible for the abnormalities uncovered by the magnetic resonance imagings. However, there was no correlation between the neurodevelopment outcome and the extent of the periventricular hyperintensity or ventriculomegaly. Therefore, in patients with congenital myotonic dystrophy, a neonatal episode of asphyxia can be responsible for a finding of periventricular hyperintensity, but it is unlikely that an integral part of the mental retardation is attributable to brain damage due to perinatal asphyxia.

Apgar Score↗

PubMed1994

Influences of environmental demand on maternal behavior and infant development.

Research has shown that in conjunction with genetic factors, significant aspects of non-human primate development are influenced by the infant's physical and social environment. In addition to the direct impact of the environment on the infant, the infant's attachment relationship with the mother is seen as the primary mediating factor in shaping these influences. When the mother is able to cope with environmental demands, as a reflection of her responsivity to her infant's needs, she may prepare infants for periodic interruptions in her attention, ameliorate distress during disruptive periods and, most importantly, compensate for these disruptions with enhanced attention to her infant once they are ended. Our recent work shows that when the mother's survival requirements increase, and her coping capacities are exceeded, both short- and long-term deleterious effects on her developing offspring may emerge. Particularly when confronted with an unpredictable environment, mothers are less able to maintain effective, stress-buffering, maternal-coping mechanisms which can preserve a stable attachment relationship and permit normal infant development. When these coping mechanisms are insufficient, infants may show manifest disturbances, such as depression, during development or reveal more latent disturbances, such as reduced sociability and timidity, when psychologically challenged, even as young adults. Evidence now suggests that these long-term effects may, at least in part, be the product of altered neurodevelopment of the serotonergic and noradrenergic systems.

Adaptation, Psychological↗

PubMed1995

Infantile spasms associated with theophylline toxicity.

We report on a 6-month-old infant with asthma who developed spasms and hypsarrhythmia on the electroencephalogram (EEG) shortly after starting oral theophylline medication. Theophylline levels at that time were just above the upper normal range. The spasms stopped and the EEG normalized when theophylline was discontinued and nitrazepam therapy started. On follow-up over the next 3 years there was no recurrence of seizures and the child's neurodevelopment has been normal. Nitrazepam was stopped at 10 months and the waking and sleeping EEG were normal at 14 months. We believe that the infantile spasms were caused by theophylline.

Electroencephalography↗

PubMed1996

Effectiveness of individualized neurodevelopmental care in the newborn intensive care unit (NICU).

The individual infant's neurodevelopmental process provides an integrative framework for the delivery of medical care needed to assure the infant's survival and quality of outcome. The infant's neurobehavioral functioning and expression provides an opportunity for caregivers to estimate the individual infant's current strengths, vulnerabilities and threshold to disorganization, as well as to identify the infant's strategies in collaborating in his or her best progression. This perspective supports caregivers in seeing themselves in a relationship with the infant, and in considering opportunities to enhance the infant's strengths and reduce apparent stressors in collaboration with the infant and the family. The results of several randomized studies supporting the effectiveness of such a neurodevelopment approach to NICU care will be presented, and suggest implications for staff education and nursery-wide implementation.

Brain↗

PubMed1997

Schizophrenia: developmental disturbance of brain and mind?

Schizophrenia is the most severe of the mental illnesses and affects approximately 0.8% of the population in Western societies. Postmortem and neuroimaging studies show that patients with schizophrenia have slightly larger cerebral ventricles than normal and a decrease in cortical volume, most markedly in the left temporal lobe. These changes are present at diagnosis and appear to show little change over extended periods of follow-up. Associated findings such as lack of normal cerebral asymmetry and cytoarchitectonic changes suggestive of impaired migration of cortical neurons implicate aberrant neurodevelopment. Schizophrenics also show an excess of pregnancy and birth complications, and an association with prenatal exposure to maternal influenza. These and reports of abnormal psychological development in pre-schizophrenic children add further support to the theory that the disorder has neurodevelopmental origins.

Brain↗

PubMed2003

Influence of different types of post-discharge feeding on somatic growth, cognitive development and their correlation in very low birthweight preterm infants.

UNLABELLED: The influence of appropriate post-discharge nutrition on somatic growth and cognitive development of very low-birthweight infants in the first year of life is currently a major topic in infant nutrition. Appropriate intakes of proteins, iodine and the addition of LC-PUFAs (arachidonic acid (AA), docosahexaenoic acid (DHA)) in the "right" quantities improve cognitive development and are conducive to a good correlation between somatic growth and neurodevelopment. CONCLUSION: When mother' milk is not available post-discharge, in addition to more proteins and minerals, formula for low-birthweight infants should contain AA and DHA, since the endogenous production of these important compounds from the precursors can be reduced in the first months of life, chiefly in the very low-birthweight infants.

Breast Feeding↗

PubMed2004

Neural maturation of breastfed and formula-fed infants.

BACKGROUND: Human milk provides infants with a full complement of all polyunsaturated fatty acids, including docosahexaenoic acid (DHA) and arachidonic acid (AA). Formula milks only contain the precursors of DHA, AA and linoleic acid, and hence formula-fed infants must synthesize their own DHA and AA. AIM: To evaluate the effect of feeding--whether breastfeeding or formula-feeding--in early infancy upon subsequent neurodevelopment and achievement of optimum brain function. SUBJECTS AND METHODS: The study included 53 normal, healthy infants (30 exclusively breastfed infants and 23 exclusively formula-fed infants) at the age of 1 y (+/-1 mo). Each infant was subjected to a full physical and neurological examination together with neurophysiological studies including flash visual evoked potential (FVEP), brainstem auditory evoked potential (BAEP) and somatosensory evoked potential (SSEP). RESULTS: There was significant prolongation of P100 wave latency of FVEP in formula-fed infants, together with significant prolongation of absolute latency of waves I, III and V of BAEP in formula-fed infants compared with breastfed infants. There was significant prolongation in inter-peak latencies between cortical and Erb's components in formula-fed infants compared with breastfed infants. CONCLUSION: We can conclude that VEP, BAEP and SSEP are more mature in breastfed infants relative to formula-fed infants at 1 y of age, and thus breast milk helps earlier development and maturation of some aspects of the nervous system than milk formulas.

Arachidonic Acids↗

PubMed2005

Outcome of low birthweight in China: a 16-year longitudinal study.

AIM: To compare the growth and neurodevelopment of low-birthweight (LBW) and normal-birthweight (control) infants born and raised in China. DESIGN: Prospective cohort study. SUBJECTS AND SETTING: 203 LBW (1200-2499 g) and 71 control (> or =2500 g) infants born at two Shanghai hospitals in 1983 did not differ for date of birth, gender, parental occupation, parental weight and age. LBW <10th centile at > or =37 wk gestation was defined as small for gestational age (SGA, n=102). LBW at < 37 wk gestation was defined as preterm (n=101). MAIN OUTCOME MEASURES: Weight, height, head circumference, Gesell developmental quotient (DQ), Wechsler intelligence quotient (IQ), and scholastic achievement score. RESULTS: Of the 274 enrolled subjects, 234 (85%) returned at 6 mo, 135 (49%) at 6 y, and 104 (38%) at 16 y. SGA, preterm, and control subjects did not differ in rates of follow-up or baseline characteristics. However, SGA and preterm were lower than control subjects in weight and head circumference through 16 y, height through 4 y, DQ through 3 y, IQ at 5 and 16 y, and scholastic achievement at 16 y. Catch-up to growth in the control group, defined as >3rd centile, and normal IQ, defined as > or =85, were both more common among preterm than SGA subjects. CONCLUSIONS: Adolescents in China with birthweights of 1200-2499 g, and particularly those who were SGA, lag behind peers with birthweights >2500 g in physical growth, cognitive capacity, and school achievement. The findings suggest that LBW adolescents in China today represent a population in need of evaluation and support.

Adolescent↗

PubMed2005

Hydrolysed milk in preterm infants: an open problem.

AIM: To review knowledge about the role, indications and nutritional adequacy of protein hydrolysate formulas (HF) in the preterm newborn. METHODS: A review of the available literature was carried out. RESULTS: No data support the use of HF for atopy prevention. HF could have a positive role in the early feeding of very-low-birthweight infants, but several concerns exist about their nutritional adequacy. CONCLUSION: Further investigations addressing protein and mineral metabolism as well as long-term effects, including neurodevelopment, are needed.

Child Development↗

PubMed2004

The influence of Hox genes and three intercellular signalling pathways on enteric neuromuscular development.

Normal intestinal motility requires orderly development of the complex nerve plexuses and smooth muscular layers in the gut wall. Organization of these structures results, in part, from cell autonomous programmes directed by transcription factors, which orchestrate appropriate temporal and spatial expression of specific target genes. Hox proteins appear to function in combination to dictate regional codes that establish major structural landmarks in the gut such as sphincters and muscle layers. These codes are translated in part by intercellular signals, which allow populations of cells in the embryonic gut wall to alter the developmental fate of their neighbours. Some of the best characterized intercellular signalling pathways involved in enteric neurodevelopment are mediated by GDNF/GFRa1/RET, EDN3/ENDRB, and NETRINS/DCC. These signals affect enteric neural precursors as they colonize the gut, and perturbations of these molecules are associated with various types of intestinal neuropathology.

Animals↗

PubMed1998

VIP neurotrophism in the central nervous system: multiple effectors and identification of a femtomolar-acting neuroprotective peptide.

Vasoactive intestinal peptide has neurotrophic and growth-regulating properties. As in the case of many neurotrophic molecules, VIP also has neuroprotective properties, including the prevention of cell death associated with excitotoxicity (NMDA), beta-amyloid peptide, and gp120, the neurotoxic envelope protein from the human immunodeficiency virus. The neurotrophic and neuroprotective properties are mediated in part through the action of glial-derived substances released by VIP. These substance include cytokines, protease nexin I, and ADNF, a novel neuroprotective protein with structural similarities to heat-shock protein 60. Antiserum against ADNF produced neuronal cell death and an increase in apoptotic neurons in cell culture. A 14 amino acid peptide (ADNF-14) derived from ADNF has been discovered that mimics the survival-promoting action of the parent protein. These studies support the conclusion that VIP, PACAP, and associated molecules are both important regulators of neurodevelopment and strong candidates for therapeutic development for the treatment of neurodegenerative disease.

Amino Acid Sequence↗

PubMed2026

The Long Haul: Microtubule Motors as the Essential Supply Line for Neuronal Longevity.

The extreme morphology and polarised architecture of neurons require the highly sophisticated microtubule transport system for both construction and lifelong survival. Genomic evidence from an expanding landscape of human mutations supports the essential role of the microtubule transport machinery. During neurodevelopment, mutations disrupt the proliferation and migration of neuronal precursors, as well as the initial establishment of polarity. In the mature nervous system, the reliance on microtubule transport shifts to the long-term maintenance of axon integrity and synaptic proteostasis. Across the motor proteins responsible for long distance transport in neurons, mutations highlight a specific vulnerability of long axons to transport failure in Hereditary Spastic Paraplegia (HSP), Charcot Marie Tooth disease Type 2 (CMT2), Spinal Muscular Atrophy (SMA), Perry Syndrome, and Amyotrophic Lateral Sclerosis (ALS) amongst others. Due to the role of microtubule motors in development and maintenance, there is frequently a phenotypic spectrum within a single gene of the microtubule transport system. For example, mutations in dynein motors are linked both to malformations of cortical development and specific motor neuron loss in SMA-LED (Spinal Muscular Atrophy with Lower Extremity Predominance). By synthesising genetic evidence, this review illustrates how specific molecular failures, ranging from motor-domain kinetics to cargo binding, can inform our understanding of neuronal homeostasis. Ultimately, we argue that microtubule transport is not merely a cellular utility, but a key determinant of neuronal longevity.

Humans↗

PubMed2003

Synaptogenesis in the CNS: an odyssey from wiring together to firing together.

To acquire a better comprehension of nervous system function, it is imperative to understand how synapses are assembled during development and subsequently altered throughout life. Despite recent advances in the fields of neurodevelopment and synaptic plasticity, relatively little is known about the mechanisms that guide synapse formation in the central nervous system (CNS). Although many structural components of the synaptic machinery are pre-assembled prior to the arrival of growth cones at the site of their potential targets, innumerable changes, central to the proper wiring of the brain, must subsequently take place through contact-mediated cell-cell communications. Identification of such signalling molecules and a characterization of various events underlying synaptogenesis are pivotal to our understanding of how a brain cell completes its odyssey from "wiring together to firing together". Here we attempt to provide a comprehensive overview that pertains directly to the cellular and molecular mechanisms of selection, formation and refinement of synapses during the development of the CNS in both vertebrates and invertebrates.

Animals↗

PubMed2006

Developmental mouse brain gene expression maps.

Brain gene expression databases are providing an increasing amount of information to the neuroscience community. Most databases are focused on the adult mouse rather than embryonic development. Here we survey the major mouse gene expression databases for the developing brain. The high throughput in situ hybridization approach generates large volumes of gene expression data that can be compiled and examined in a relatively short period of time. It is of increasing importance to compare gene expression patterns of neurodevelopment in the brain in relation to the adult. Often clues to adult gene expression and gene function can be determined by examining embryonic development. It is our hope that once all genes are mapped in the brain from the embryo to the adult, studies can be conducting based on information derived from such databases in conjunction with other bioinformatics sources.

Animals↗

PubMed2003

Terbutaline is a developmental neurotoxicant: effects on neuroproteins and morphology in cerebellum, hippocampus, and somatosensory cortex.

Beta(2)-adrenoceptor agonists, especially terbutaline, are widely used to arrest preterm labor, but they also cross the placenta to stimulate fetal beta-adrenoceptors that control neural cell differentiation. We evaluated the effects of terbutaline administration in neonatal rats, a stage of neurodevelopment corresponding to human fetal development. Terbutaline administered on postnatal days PN2 to 5 elicited neurochemical changes indicative of neuronal injury and reactive gliosis: immediate increases in glial fibrillary acidic protein and subsequent induction of the 68-kDa neurofilament protein. Quantitative morphological evaluations carried out on PN30 indicated structural abnormalities in the cerebellum, hippocampus, and somatosensory cortex. In the cerebellum, PN2 to 5 terbutaline treatment reduced the number of Purkinje cells and elicited thinning of the granular and molecular layers. The hippocampal CA3 region also displayed thinning, along with marked gliosis, effects that were restricted to females. In the somatosensory cortex, terbutaline evoked a reduction in the proportion of pyramidal cells and an increase in smaller, nonpyramidal cells; again, females were affected more than males. Although abnormalities were obtained with later terbutaline treatment (PN11 to 14), in general the effects were smaller than those seen with PN2 to 5 exposure. Our results indicate that terbutaline is a neurotoxicant that elicits biochemical alterations and structural damage in the immature brain during a critical period. These effects point to a causal relationship between fetal terbutaline exposure and the higher incidence of cognitive and neuropsychiatric disorders reported for the offspring of women receiving terbutaline therapy for preterm labor.

Adrenergic beta-Agonists↗

PubMed2006

Receptor regulation of gene expression of axon guidance molecules: implications for adaptation.

Axon guidance molecules, critical for neurodevelopment, are also implicated in morphological and other neurodaptative changes mediated by physiological or pharmacological events in adult brain. As an example, the psychostimulant cocaine markedly alters axon guidance molecules in adult brain of cocaine-treated rats. To decipher a potential link between drug-induced activation of G-protein-coupled receptors (GPCRs) and modulation of axon guidance molecules, we investigated whether GPCR activity in a SK-N-MC human neuroepithelioma cell line (which expresses low levels of D1 dopamine receptors) affects gene expression of axon guidance molecules (semaphorins, ephrins, netrins, and their receptors). Using real-time polymerase chain reaction, we identified 17 of 26 axon guidance molecules in these cells, with varying levels of expression. Forskolin, which raised intracellular cAMP levels 340%, increased EphA5, EphB2, and Neuropilin1 expression, paralleling reported changes in the rat hippocampus after cocaine treatment. The dopamine receptor agonist dihydrexidine, which raised cAMP levels 22%, promoted regulatory changes in EphrinA1, EphrinA5, EphB1, DCC, and Semaphorin3C, whereas (+/-)-6-chloro-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide (SKF81297) altered EphA5, EphrinA1, EphrinA5, and neuropilin1. cAMP and other signal transduction pathways may regulate gene expression of axon guidance molecules, potentially linking monoamine receptor activation to signal transduction cascades, transcriptional regulation of axon guidance molecules, and alterations in neural networks.

Adaptation, Physiological↗

PubMed1981

Rapid eye movement storms in infants: rate of occurrence at 6 months predicts mental development at 1 year.

Intense rapid eye movements (REM) during sleep were investigated as a possible indication of delay in the neurodevelopment of infants. The rate of occurrence of REM storms was determined by monitoring the sleep of 15 normal, first-born infants during weeks 2 through 5 and at 3, 6, 12 months. The amount of REM within each 10-second interval of active sleep was rated on a four-point scale based on frequency and intensity of eye movements. When the babies were 12 months old, the Bayley Scales of Mental Development were administered. A significant negative correlation was found between the frequency of REM storms of 14 subjects was also studied. The negative correlation was confirmed. The findings support the suggestion that by 6 months of age REM storms express dysfunction or delay in the development of central inhibitory feedback controls for sleep organization and phasic sleep-related activities.

Age Factors↗

PubMed2004

Prevalence of maternal dietary iodine insufficiency in the north east of England: implications for the fetus.

BACKGROUND: Maternal subclinical hypothyroidism is a cause of poor neurodevelopment outcome in the offspring. Although iodine deficiency is the most common cause of hypothyroidism world wide, there are no screening programmes for it in the United Kingdom where the population is assumed to be iodine replete. OBJECTIVE: To determine the prevalence of reduced iodine intake by measuring urinary iodide concentrations in pregnant and non-pregnant women from the north east of England. METHODS: Urinary iodide excretion (UIE) rate was estimated using inductively coupled mass spectrometry in 227 women at 15 weeks gestation and in 227 non-pregnant age matched controls. A reduced intake of iodine is indicated by a concentration in urine of less than 50 microg/l or less than 0.05 microg iodine/mmol creatinine. RESULTS: Eight (3.5%) pregnant women and 13 (5.7%) controls had a reduced iodine/creatinine ratio. These values were higher when UIE was expressed as iodine concentration: 16 (7%) and 20 (8.8%) respectively. Ninety (40%) of the pregnant women had a UIE of 0.05-0.10, which is consistent with borderline deficiency. CONCLUSION: In this study, 3.5% of pregnant women had evidence of iodine deficiency, and 40% may be borderline deficient. Larger scale studies are required to estimate the true prevalence of iodine deficiency in the United Kingdom.

Adolescent↗