Journal articles on the topic 'Neurodevelopmental'
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Given, Joanne, Rebecca L. Bromley, Florence Coste, Sandra Lopez-Leon, and Maria Loane. "An inventory of European data sources to support pharmacoepidemiologic research on neurodevelopmental outcomes in children following medication exposure in pregnancy: A contribution from the ConcePTION project." PLOS ONE 17, no. 10 (October 14, 2022): e0275979. http://dx.doi.org/10.1371/journal.pone.0275979.
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Background Studies on medication safety in pregnancy are increasingly focusing on child neurodevelopmental outcomes. Establishing neurodevelopmental safety is complex due to the range of neurodevelopmental outcomes and the length of follow-up needed for accurate assessment. The aim of this study was to provide an inventory of European data sources for use in pharmacoepidemiologic studies investigating neurodevelopment following maternal medication exposure. Method The EUROmediSAFE inventory of data sources in Europe for evaluating perinatal and long-term childhood risks associated with in-utero exposure to medication was updated by contacting colleagues across 31 European countries, literature review and internet searches. Included data sources must record at least one neurodevelopmental outcome and maternal medication use in pregnancy must be available, either in the data source itself or through linkage with another data source. Information on the domain of neurodevelopment, measure/scale used and the approach to measurement were recorded for each data source. Results Ninety data sources were identified across 14 countries. The majority (63.3%) were created for health surveillance and research with the remaining serving administrative purposes (21.1% healthcare databases,15.6% other administrative databases). Five domains of neurodevelopment were identified—infant development (36 data sources,13 countries), child behaviour (27 data sources, 10 countries), cognition (29 data sources, 12 countries), educational achievement (20 data sources, 7 countries), and diagnostic codes for neurodevelopmental disorders (42 data sources, 11 countries). Thirty-nine data sources, in 12 countries, had information on more than one domain of neurodevelopment. Conclusion This inventory is invaluable to future studies planning to investigate the neurodevelopmental impact of medication exposures during pregnancy. Caution must be used when combining varied approaches to neurodevelopment outcome measurement, the age of children in the data source, and the sensitivity and specificity of the outcome measure selected should be borne in mind.
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Sood, Erica, Jeffrey P. Jacobs, and Bradley S. Marino. "Optimising neurodevelopmental and psychosocial outcomes for survivors with CHD: a research agenda for the next decade." Cardiology in the Young 31, no. 6 (June 2021): 873–75. http://dx.doi.org/10.1017/s1047951121002171.
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AbstractNeurodevelopmental and psychosocial impairments negatively impact health-related quality of life for survivors with CHD and complicate the transition to independent adulthood. Risk for neurodevelopmental and psychosocial impairments is influenced by a complex interplay among genetic, foetal, surgical, perioperative, family, and social factors, requiring a multi-pronged approach to neuroprotection and intervention. To ensure future research can ultimately reduce the burden of CHD for individuals, families, and society, the most pressing issues in cardiac neurodevelopment requiring scientific investigation must be identified.Through funding from an R13 Grant from the National Heart, Lung, and Blood Institute of the National Institutes of Health of the United States of America, the Cardiac Neurodevelopmental Outcome Collaborative convened a two-day meeting of international experts in cardiac neurodevelopmental and psychosocial research, clinical care, and health disparities, including patient and family stakeholders, to define the cardiac neurodevelopmental and psychosocial outcomes research agenda for the next decade. Seven multidisciplinary working groups were formed to address key domains crucial to the advancement of cardiac neurodevelopmental and psychosocial outcomes research: 1) Foetal Brain Development and Neuroprotection, 2) Surgical/Perioperative Neuroprotection and Neurodevelopment, 3) Characterization of Neurodevelopmental and Psychological Outcomes, 4) Neurodevelopmental and Psychosocial Intervention, 5) Parent Mental Health and Family Functioning, 6) Neurodevelopmental Education, Outreach and Advocacy, and 7) Health Disparities and Neurodevelopmental Outcomes. Working groups identified significant gaps in knowledge and critical questions that must be answered to further knowledge, policy, care, and outcomes. The development of a research agenda in cardiac neurodevelopmental and psychosocial outcomes is critical for informing collaborative initiatives and allocation of funding for research to scientific inquiries of highest value to key stakeholders.
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Chebet, Martin, Milton W. Musaba, David Mukunya, Brian Makoko, Agnes Napyo, Ritah Nantale, Proscovia Auma, et al. "High Burden of Neurodevelopmental Delay among Children Born to Women with Obstructed Labour in Eastern Uganda: A Cohort Study." International Journal of Environmental Research and Public Health 20, no. 4 (February 16, 2023): 3470. http://dx.doi.org/10.3390/ijerph20043470.
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Over 250 million infants in low and middle-income countries do not fulfill their neurodevelopment potential. In this study, we assessed the incidence and risk factors for neurodevelopmental delay (NDD) among children born following obstructed labor in Eastern Uganda. Between October 2021 and April 2022, we conducted a cohort study of 155 children (aged 25 to 44 months), born at term and assessed their neurodevelopment using the Malawi Developmental Assessment Tool. We assessed the gross motor, fine motor, language and social domains of neurodevelopment. The incidence of neurodevelopmental delay by 25 to 44 months was 67.7% (105/155) (95% CI: 59.8–75.0). Children belonging to the poorest wealth quintile had 83% higher risk of NDD compared to children belonging to the richest quintile (ARR (Adjusted Risk Ratio): 1.83; 95% CI (Confidence Interval): [1.13, 2.94]). Children fed the recommended meal diversity had 25% lower risk of neurodevelopmental delay compared to children who did not (ARR: 0.75; 95% CI: [0.60, 0.94]). Children who were exclusively breastfed for the first 6 months had 27% lower risk of neurodevelopmental delay compared to children who were not (ARR: 0.73; 95% CI: [0.56, 0.96]). We recommend that infants born following obstructed labor undergo neurodevelopmental delay screening.
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Miller, Thomas A., Anjali Sadhwani, Jacqueline Sanz, Erica Sood, Dawn Ilardi, Jane W. Newburger, Caren S. Goldberg, David Wypij, J. William Gaynor, and Bradley S. Marino. "Variations in practice in cardiac neurodevelopmental follow-up programs." Cardiology in the Young 30, no. 11 (October 23, 2020): 1603–8. http://dx.doi.org/10.1017/s1047951120003522.
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AbstractOver the last two decades, heart centres have developed strategies to meet the neurodevelopmental needs of children with congenital heart disease. Since the publication of guidelines in 2012, cardiac neurodevelopmental follow-up programmes have become more widespread. Local neurodevelopmental programmes, however, have been developed independently in widely varying environments. We sought to characterise variation in structure and personnel in cardiac neurodevelopmental programmes. A 31-item survey was sent to all member institutions of the Cardiac Neurodevelopmental Outcome Collaborative. Multidisciplinary teams at each centre completed the survey. Responses were compiled in a descriptive fashion. Of the 29 invited centres, 23 responded to the survey (79%). Centres reported more anticipated neurodevelopment visits between birth and 5 years of age (median 5, range 2–8) than 5–18 years (median 2, range 0–10) with 53% of centres lacking any standard for routine neurodevelopment evaluations after 5 years of age. Estimated annual neurodevelopment clinic volume ranged from 85 to 428 visits with a median of 16% of visits involving children >5 years of age. Among responding centres, the Bayley Scales of Infant and Toddler Development and Wechsler Preschool and Primary Scale of Intelligence were the most routinely used tests. Neonatal clinical assessment was more common (64%) than routine neonatal brain imaging (23%) during hospitalisation. In response to clinical need and published guidelines, centres have established formal cardiac neurodevelopment follow-up programmes. Centres vary considerably in their approaches to routine screening and objective testing, with many centres currently focussing their resources on evaluating younger patients.
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Hopkins, Stephen, Jeremy Turk, Adeniyi Daramola, and Marinos Kyriakopoulos. "Autism spectrum mixed neurodevelopmental disorder associated with 6q27 deletion and multiple copies within 20q11.23: a case study." Advances in Mental Health and Intellectual Disabilities 8, no. 3 (April 29, 2014): 210–15. http://dx.doi.org/10.1108/amhid-07-2013-0050.
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Purpose – Copy Number Variations (CNVs) are not infrequently observed in aberrant neurodevelopment. CNVs can alter gene expression and have been linked to a wide range of neuropsychiatric disorders. The purpose of this case study is to report the association of CNVs with a mixed neurodevelopmental disorder. Design/methodology/approach – Array-Comparative Genomic Hybridisation analysis was carried out in a case of an eight-year-old boy presenting with a mixed neurodevelopmental disorder including autism spectrum disorder, intellectual disability, tic disorder, anxiety and severe aggression. The child's parents also underwent the same investigation. Findings – A 6q27 deletion and multiple copies within 20q11.23 were identified. The boy's father shared the 6q27 deletion and his mother also had multiple copies within 20q11.23. Originality/value – This is the first report linking the combination of 6p27 and 20q11 CNVs with a mixed neurodevelopmental presentation. Identifying CNVs that may underlie aberrant neurodevelopment is likely to assist in unravelling the aetiology of neurodevelopmental and psychiatric disorders and lead to more effective strategies for their characterisation and management.
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Malin, Ashley J., Stefanie A. Busgang, Alejandra J. Cantoral, Katherine Svensson, Manuela A. Orjuela, Ivan Pantic, Lourdes Schnaas, et al. "Quality of Prenatal and Childhood Diet Predicts Neurodevelopmental Outcomes among Children in Mexico City." Nutrients 10, no. 8 (August 15, 2018): 1093. http://dx.doi.org/10.3390/nu10081093.
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Adequate nutrition is important for neurodevelopment. Although nutrients are ingested in combination, the impact of specific nutrients within the context of a nutrient mixture has not been studied with respect to health, such as neurodevelopment. Therefore, we examined the impact of prenatal and childhood nutrient mixtures on neurodevelopmental outcomes. Participants included mother–child pairs in the Programming Research in Obesity, Growth, Environment, and Social Stress (PROGRESS) prospective birth cohort in Mexico City. We assessed prenatal and child micro- and macronutrient profiles among 65 and 329 children, respectively, via food frequency questionnaires. Neurodevelopmental outcomes of 4–6-year-old children were measured using the McCarthy Scales of Children’s Abilities (MSCA). We conducted weighted quantile sum (WQS) regression analyses to calculate indices reflecting “good” and “poor” prenatal and childhood nutrition. After adjusting for maternal education, socioeconomic status, the Home Observation for Measurement of the Environment (HOME) score, and total caloric intake, the good prenatal and childhood nutrition indices predicted more favorable neurodevelopment, while both poor nutrition indices predicted poorer neurodevelopment. These associations were stronger in prenatal than childhood models. Monounsaturated fats predicted various neurodevelopmental abilities relatively strongly in both models. Prenatal and childhood consumption of combinations of beneficial nutrients may contribute to more favorable neurodevelopment.
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Guardiola-Ripoll, Maria, and Mar Fatjó-Vilas. "A Systematic Review of the Human Accelerated Regions in Schizophrenia and Related Disorders: Where the Evolutionary and Neurodevelopmental Hypotheses Converge." International Journal of Molecular Sciences 24, no. 4 (February 10, 2023): 3597. http://dx.doi.org/10.3390/ijms24043597.
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Schizophrenia is a psychiatric disorder that results from genetic and environmental factors interacting and disrupting neurodevelopmental trajectories. Human Accelerated Regions (HARs) are evolutionarily conserved genomic regions that have accumulated human-specific sequence changes. Thus, studies on the impact of HARs in the context of neurodevelopment, as well as with respect to adult brain phenotypes, have increased considerably in the last few years. Through a systematic approach, we aim to offer a comprehensive review of HARs’ role in terms of human brain development, configuration, and cognitive abilities, as well as whether HARs modulate the susceptibility to neurodevelopmental psychiatric disorders such as schizophrenia. First, the evidence in this review highlights HARs’ molecular functions in the context of the neurodevelopmental regulatory genetic machinery. Second, brain phenotypic analyses indicate that HAR genes’ expression spatially correlates with the regions that suffered human-specific cortical expansion, as well as with the regional interactions for synergistic information processing. Lastly, studies based on candidate HAR genes and the global “HARome” variability describe the involvement of these regions in the genetic background of schizophrenia, but also in other neurodevelopmental psychiatric disorders. Overall, the data considered in this review emphasise the crucial role of HARs in human-specific neurodevelopment processes and encourage future research on this evolutionary marker for a better understanding of the genetic basis of schizophrenia and other neurodevelopmental-related psychiatric disorders. Accordingly, HARs emerge as interesting genomic regions that require further study in order to bridge the neurodevelopmental and evolutionary hypotheses in schizophrenia and other related disorders and phenotypes.
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Cormack, Barbara E., Jane E. Harding, Steven P. Miller, and Frank H. Bloomfield. "The Influence of Early Nutrition on Brain Growth and Neurodevelopment in Extremely Preterm Babies: A Narrative Review." Nutrients 11, no. 9 (August 30, 2019): 2029. http://dx.doi.org/10.3390/nu11092029.
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Extremely preterm babies are at increased risk of less than optimal neurodevelopment compared with their term-born counterparts. Optimising nutrition is a promising avenue to mitigate the adverse neurodevelopmental consequences of preterm birth. In this narrative review, we summarize current knowledge on how nutrition, and in particular, protein intake, affects neurodevelopment in extremely preterm babies. Observational studies consistently report that higher intravenous and enteral protein intakes are associated with improved growth and possibly neurodevelopment, but differences in methodologies and combinations of intravenous and enteral nutrition strategies make it difficult to determine the effects of each intervention. Unfortunately, there are few randomized controlled trials of nutrition in this population conducted to determine neurodevelopmental outcomes. Substantial variation in reporting of trials, both of nutritional intakes and of outcomes, limits conclusions from meta-analyses. Future studies to determine the effects of nutritional intakes in extremely preterm babies need to be adequately powered to assess neurodevelopmental outcomes separately in boys and girls, and designed to address the many potential confounders which may have clouded research findings to date. The development of minimal reporting sets and core outcome sets for nutrition research will aid future meta-analyses.
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Dack, Kyle, Matthew Fell, Caroline M. Taylor, Alexandra Havdahl, and Sarah J. Lewis. "Prenatal Mercury Exposure and Neurodevelopment up to the Age of 5 Years: A Systematic Review." International Journal of Environmental Research and Public Health 19, no. 4 (February 10, 2022): 1976. http://dx.doi.org/10.3390/ijerph19041976.
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Neurodevelopmental delays can interfere with children’s engagement with the world and further development, and may have negative consequences into adulthood. Mercury is highly toxic and may negatively influence neurodevelopment because it can freely cross the placenta and accumulate in the fetal brain. We searched four publication databases (Embase, PsycINFO, PubMed/MEDLINE, Scopus) for studies examining the relationship between early life mercury exposure and scores on neurodevelopmental performance measures in children aged 0 to 5 years old. Study quality was assessed using the National Institutes of Health (NIH) Quality Assessment Tool. Thirty-two prospective studies were included in the review. Neurodevelopmental performance was measured using 23 different scales, most commonly the Bayley Scales of Infant and Toddler Development (BSID). In most cases, the evidence for an association between mercury and neurodevelopment was weak. There did not appear to be exceptions for particular childhood ages, outcome scales, or mercury levels. The small number of results to the contrary were more likely to be studies which did not meet our high-quality criteria, and could be a consequence of multiple testing, selection bias, or incomplete confounder adjustment. Based on current evidence, dietary mercury exposure during pregnancy is unlikely to be a risk factor for low neurodevelopmental functioning in early childhood.
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Tran, Nguyen Quoc Vuong, and Kunio Miyake. "Neurodevelopmental Disorders and Environmental Toxicants: Epigenetics as an Underlying Mechanism." International Journal of Genomics 2017 (2017): 1–23. http://dx.doi.org/10.1155/2017/7526592.
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The increasing prevalence of neurodevelopmental disorders, especially autism spectrum disorders (ASD) and attention deficit hyperactivity disorder (ADHD), calls for more research into the identification of etiologic and risk factors. The Developmental Origin of Health and Disease (DOHaD) hypothesizes that the environment during fetal and childhood development affects the risk for many chronic diseases in later stages of life, including neurodevelopmental disorders. Epigenetics, a term describing mechanisms that cause changes in the chromosome state without affecting DNA sequences, is suggested to be the underlying mechanism, according to the DOHaD hypothesis. Moreover, many neurodevelopmental disorders are also related to epigenetic abnormalities. Experimental and epidemiological studies suggest that exposure to prenatal environmental toxicants is associated with neurodevelopmental disorders. In addition, there is also evidence that environmental toxicants can result in epigenetic alterations, notably DNA methylation. In this review, we first focus on the relationship between neurodevelopmental disorders and environmental toxicants, in particular maternal smoking, plastic-derived chemicals (bisphenol A and phthalates), persistent organic pollutants, and heavy metals. We then review studies showing the epigenetic effects of those environmental factors in humans that may affect normal neurodevelopment.
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Keilhoff, Gerburg, Paolo Fusar-Poli, and Axel Becker. "Effects of Antipsychotics on Dentate Gyrus Stem Cell Proliferation and Survival in Animal Models: A Critical Update." Neural Plasticity 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/832757.
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Schizophrenia is a complex psychiatric disorder. Although a number of different hypotheses have been developed to explain its aetiopathogenesis, we are far from understanding it. There is clinical and experimental evidence indicating that neurodevelopmental factors play a major role. Disturbances in neurodevelopment might result in alterations of neuroanatomy and neurochemistry, leading to the typical symptoms observed in schizophrenia. The present paper will critically address the neurodevelopmental models underlying schizophrenia by discussing the effects of typical and atypical antipsychotics in animal models. We will specifically discuss the vitamin D deficiency model, the poly I:C model, the ketamine model, and the postnatal ventral hippocampal lesion model, all of which reflect core neurodevelopmental issues underlying schizophrenia onset.
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Nicksic, V. B., D. B. Allen, M. A. Stanley, M. W. Baker, J. C. Eickhoff, and D. C. Kaluarachchi. "Lack of association between gestational age adjusted TSH percentiles and neurodevelopmental outcomes among preterm infants." Journal of Neonatal-Perinatal Medicine 15, no. 2 (April 12, 2022): 243–47. http://dx.doi.org/10.3233/npm-210910.
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BACKGROUND: Limited evidence exists on whether subclinical hypothyroidism suggested by mildly elevated TSH levels affect neurodevelopment and growth in preterm infants. The objective of this study was to determine the association between gestational age adjusted TSH percentiles and neurodevelopmental outcomes among preterm infants. METHODS: Univariate linear regression analysis was conducted to determine, in infants born less than thirty-two weeks gestational age, the correlation between the TSH percentile on the last newborn screen and neurodevelopmental assessment scores and growth outcomes at eighteen to twenty-two months of corrected age. RESULTS: Seventy-four patients were enrolled in the study with a mean gestational age of 28.8 weeks. There was no correlation between the last TSH percentile value and Bayley-III cognitive composite score or other neurodevelopmental or growth outcomes. CONCLUSION: In a cohort of preterm infants, higher TSH percentiles suggesting potential subclinical hypothyroidism did not predict any adverse effect on neurodevelopmental or growth outcomes.
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Foubert, R., S. Devroe, L. Foubert, M. Van de Velde, and S. Rex. "Anesthetic neurotoxicity in the pediatric population: a systematic review of the clinical evidence." Acta Anaesthesiologica Belgica 71, no. 2 (June 2020): 51–65. http://dx.doi.org/10.56126/71.2.2.
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Background: Exposure to general anesthesia (GA) in early life is known to be neurotoxic to animals. Objectives: To evaluate the risk of GA inducing long-term neurodevelopmental deficits in human children. Design: Systematic review. Methods: We included observational and randomized studies that compared the long-term neurodevelopment of postnatal children exposed to GA to the long-term neurodevelopment of children not exposed to GA. We searched MEDLINE, Embase and Web of Science for relevant studies published in the year 2000 or later. We screened all the identified studies on predetermined inclusion and exclusion criteria. A risk of bias assessment was made for each included study. We identified 9 neurodevelopmental domains for which a sub-analysis was made: intelligence; memory; learning; language/speech; motor function; visuospatial skills; development/emotions/behavior; ADHD/attention; autistic disorder. Results: We included 26 studies involving 605.391 participants. Based on AHRQ-standards 11 studies were of poor quality, 7 studies were of fair quality and 8 studies were of good quality. The major causes of potential bias were selection and comparability bias. On 2 neurodevelopmental domains (visuospatial skills and autistic disorder), the available evidence showed no association with exposure to GA. On 7 other neurodevelopmental domains, the available evidence showed mixed results. The 4 studies that used a randomized or sibling-controlled design showed no association between GA and neurodevelopmental deficits in their primary endpoints. Limitations: The absence of a meta-analysis and funnel plot. Conclusions: Based on observational studies, we found an association between GA in childhood and neuro-developmental deficits in later life. Randomized and sibling-matched observational studies failed to show the same association and therefore no evidence of a causal relationship exists at present. Since GA seems to be a marker, but not a cause of worse neurodevelopment, we argue against delaying or avoiding interventional or diagnostic procedures requiring GA in childhood based on the argument of GA-induced neurotoxicity.
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Pu, Yiwei, Songmei Li, Siyu Ma, Yuanli Hu, Qinghui Hu, Yuting Liu, Mengting Wu, Jia An, Ming Yang, and Xuming Mo. "Brain MRI Radiomics Analysis of School-Aged Children with Tetralogy of Fallot." Computational and Mathematical Methods in Medicine 2021 (October 29, 2021): 1–8. http://dx.doi.org/10.1155/2021/2380346.
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Introduction. Radiomics could be potential imaging biomarkers by capturing and analyzing the features. Children and adolescents with CHD have worse neurodevelopmental and functional outcomes compared with their peers. Early diagnosis and intervention are the necessity to improve neurological outcomes in CHD patients. Methods. School-aged TOF patients and their healthy peers were recruited for MRI and neurodevelopmental assessment. LASSO regression was used for dimension reduction. ROC curve graph showed the performance of the model. Results. Six related features were finally selected for modeling. The final model AUC was 0.750. The radiomics features can be potential significant predictors for neurodevelopmental diagnoses. Conclusion. The radiomics on the conventional MRI can help predict the neurodevelopment of school-aged children and provide parents with rehabilitation advice as early as possible.
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Heath, Rory J., Susanna Klevebro, and Thomas R. Wood. "Maternal and Neonatal Polyunsaturated Fatty Acid Intake and Risk of Neurodevelopmental Impairment in Premature Infants." International Journal of Molecular Sciences 23, no. 2 (January 9, 2022): 700. http://dx.doi.org/10.3390/ijms23020700.
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The N3 and N6 long chain polyunsaturated fatty acids (LCPUFA) docosahexaenoic acid (DHA) and arachidonic acid (AA) are essential for proper neurodevelopment in early life. These fatty acids are passed from mother to infant via the placenta, accreting into fetal tissues such as brain and adipose tissue. Placental transfer of LCPUFA is highest in the final trimester, but this transfer is abruptly severed with premature birth. As such, efforts have been made to supplement the post-natal feed of premature infants with LCPUFA to improve neurodevelopmental outcomes. This narrative review analyzes the current body of evidence pertinent to neurodevelopmental outcomes after LCPUFA supplementation in prematurely born infants, which was identified via the reference lists of systematic and narrative reviews and PubMed search engine results. This review finds that, while the evidence is weakened by heterogeneity, it may be seen that feed comprising 0.3% DHA and 0.6% AA is associated with more positive neurodevelopmental outcomes than LCPUFA-deplete feed. While no new RCTs have been performed since the most recent Cochrane meta-analysis in 2016, this narrative review provides a wider commentary; the wider effects of LCPUFA supplementation in prematurely born infants, the physiology of LCPUFA accretion into preterm tissues, and the physiological effects of LCPUFA that affect neurodevelopment. We also discuss the roles of maternal LCPUFA status as a modifiable factor affecting the risk of preterm birth and infant neurodevelopmental outcomes. To better understand the role of LCPUFAs in infant neurodevelopment, future study designs must consider absolute and relative availabilities of all LCPUFA species and incorporate the LCPUFA status of both mother and infant in pre- and postnatal periods.
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Das, Dhananjoy, Kawsar Sultana, Golam Mohammed Tayeb Ali, Tanuka Barua, and Mahmood A. Chowdhury Arzu. "Rapid Neurodevelopmental Assessment (RNDA) : An Important Tool for Assessment of Psychomotor Development in Children with Perinatal Events." Chattagram Maa-O-Shishu Hospital Medical College Journal 20, no. 1 (May 25, 2021): 16–21. http://dx.doi.org/10.3329/cmoshmcj.v20i1.53581.
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Background: Infants with various perinatal events are at risks for long term neurodevelopmental impairments. Neurodevelopmental assessment at early life has been considered as a valuable tool for prediction of neurodevelopmental outcomes in this population. This present study aimed to identify the neurodevelopmental impairments in high risk children by Rapid Neurodevelopment Assessment (RNDA)
Materials and methods : This was a cross sectional study conducted in the Autism and Child Development Centre of Chattogram Maa Shishu-O-General Hospital during the period of 0ctober to December 2018. Babies aged 0 -2 years with different perinatal events like prematurity, birth asphyxia, neonatal jaundice, and without any adverse event; that attended RNDA clinic underwent Rapid Neurodevelopmental Assessment (RNDA) to find at risk children for long term neurodevelopmental impairments.
Results: Among the 50 study subjects,Perinatal asphyxia was found in 41(82%). 26(52%) had history of IUGR, 22(44%) had Preterm delivery and 25(50%) had history of Neonatal convulsion. History of neonatal jaundice was found in 14(28%) cases. 5(10%) children did not have any perinatal event. The Mean ± SD age of study subjects was 7.38±7.31month. Severe impairment in gross motor and fine motor function were found in 25(50%) and 24(48%) respondents respectively. Vision was severely impaired in 10(20%) cases. Severe cognition and behavior impairment were found in 8(16%) and 3(6%) cases accordingly. Severe hearing and speech impairment were found in 2(4%) & 10(20%) cases respectively. Severe seizure was found in 19(39%) cases. Study subjects with the history of delayed cry or Perinatal asphyxia had significantly decreased fine motor skills. Children born with IUGR had significant gross motor and fine motor skill impairment. Significant speech & cognitive impairment were observed in children with neonatal jaundice. Seizure was found significant in study subjects with a history of neonatal convulsion.
Conclusion: Rapid Neurodevelopment Assessment (RNDA) plays an important role for early identification of neurodevelopmental impairments of high-risk infants and thus screening for these can promote early therapeutic intervention and subsequent follow up, leading to better outcome.
Chatt Maa Shi Hosp Med Coll J; Vol.20 (1); January 2021; Page 16-21
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Lovey, Oriane, Myriam Bickle-Graz, Mathilde Morisod Harari, Antje Horsch, and Juliane Schneider. "The Joint Observation in Neonatology and Neurodevelopmental Outcome of Preterm Infants at Six Months Corrected Age: Secondary Outcome Data from a Randomised Controlled Trial." Children 9, no. 9 (September 13, 2022): 1380. http://dx.doi.org/10.3390/children9091380.
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This study aimed to evaluate the impact of a standardised joint observation (JOIN) performed in the neonatal intensive care unit (NICU) on the neurodevelopment of preterm infants at six months corrected age (CA) compared with a preterm control group. In this monocentric interventional randomised controlled trial, we allocated 76 mothers and their preterm neonates to either JOIN, an early one-session intervention, or standard care during the NICU hospitalisation. The neurodevelopment of the preterm infants was assessed by standardised developmental tests at six months CA and compared between the intervention and the control groups. This randomised controlled trial was registered on clinicaltrials.gov (NCT02736136) in April 2016. Sixty-five infants underwent neurodevelopmental assessment at six months CA. There were no significant differences between the two groups in neurodevelopmental outcome measures. The JOIN intervention was not associated with significant improvement in neurodevelopment at six months CA in preterm infants.
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Zapata-Muñoz, Juan, Beatriz Villarejo-Zori, Pablo Largo-Barrientos, and Patricia Boya. "Towards a better understanding of the neuro-developmental role of autophagy in sickness and in health." Cell Stress 5, no. 7 (July 12, 2021): 99–118. http://dx.doi.org/10.15698/cst2021.07.253.
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Autophagy is a critical cellular process by which biomolecules and cellular organelles are degraded in an orderly manner inside lysosomes. This process is particularly important in neurons: these post-mitotic cells cannot divide or be easily replaced and are therefore especially sensitive to the accumulation of toxic proteins and damaged organelles. Dysregulation of neuronal autophagy is well documented in a range of neurodegenerative diseases. However, growing evidence indicates that autophagy also critically contributes to neurodevelopmental cellular processes, including neurogenesis, maintenance of neural stem cell homeostasis, differentiation, metabolic reprogramming, and synaptic remodelling. These findings implicate autophagy in neurodevelopmental disorders. In this review we discuss the current understanding of the role of autophagy in neurodevelopment and neurodevelopmental disorders, as well as currently available tools and techniques that can be used to further investigate this association.
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Blomkvist, Eli Anne Myrvoll, Elisabet Rudjord Hillesund, Sissel Heidi Helland, Indra Simhan, and Nina Cecilie Øverby. "Diet and Neurodevelopmental Score in a Sample of One-Year-Old Children—A Cross-Sectional Study." Nutrients 11, no. 7 (July 21, 2019): 1676. http://dx.doi.org/10.3390/nu11071676.
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Environmental factors in the first years of life are crucial for a child’s neurodevelopment. Research on the association between breastfeeding and neurodevelopment is inconclusive, while research on the possible association between other dietary factors and neurodevelopment is inadequate in children as young as one year of age. The aim of the present study was to investigate associations between both breastfeeding and other dietary factors and the neurodevelopment of one-year-old children in Norway. Methods: Participants were recruited from kindergartens in four Norwegian counties in 2017. A questionnaire including questions about dietary factors and breastfeeding, and a standardised age-related questionnaire on neurodevelopment (the Ages and Stages Questionnaire), were completed by parents of one-year-olds. Linear regressions adjusting for relevant covariates were conducted to explore the associations. Results: In our sample of 212 one-year-old children, a longer duration of breastfeeding was associated with higher neurodevelopmental scores. Dietary intake of fish, fruits and vegetables was also strongly associated with higher neurodevelopmental scores, even after adjustment for breastfeeding and maternal education. Conclusion: Our results indicate that healthy dietary factors are important for neurodevelopment in young children, with measurable effects already at the age of one year.
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Masi, Anne, Syeda Ishra Azim, Christa Lam-Cassettari, Mark Dadds, Antonio Mendoza Diaz, Georgina Henry, Lisa Karlov, et al. "Co-Design of a Neurodevelopment Assessment Scale: A Study Protocol." International Journal of Environmental Research and Public Health 18, no. 23 (December 6, 2021): 12837. http://dx.doi.org/10.3390/ijerph182312837.
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Neurodevelopmental disorders are a heterogeneous group of conditions with overlapping symptomatology and fluctuating developmental trajectories that transcend current diagnostic categorisation. There is a need for validated screening instruments which dimensionally assess symptomatology from a holistic, transdiagnostic perspective. The primary aim is to co-design a Neurodevelopment Assessment Scale (NAS), a user-friendly transdiagnostic assessment inventory that systematically screens for all signs and symptoms commonly encountered in neurodevelopmental disorders. Our first objective is to undertake development of this tool, utilising co-design principles in partnership with stakeholders, including both those with lived experience of neurodevelopmental disorders and service providers. Our second objective is to evaluate the face validity, as well as the perceived utility, user-friendliness, suitability, and acceptability (i.e., ‘social validity’), of the NAS from the perspective of parents/caregivers and adults with neurodevelopmental disorders, clinicians, and service providers. Our third objective is to ascertain the psychometric properties of the NAS, including content validity and convergent validity. The NAS will provide an efficient transdiagnostic tool for evaluating all relevant signs, symptoms, and the dimensional constructs that underpin neurodevelopmental presentations. It is anticipated that this will maximise outcomes by enabling the delivery of personalised care tailored to an individual’s unique profile in a holistic and efficient manner.
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Newbury, Dianne F., Nuala H. Simpson, Paul A. Thompson, and Dorothy V. M. Bishop. "Stage 1 Registered Report: Variation in neurodevelopmental outcomes in children with sex chromosome trisomies: protocol for a test of the double hit hypothesis." Wellcome Open Research 3 (February 12, 2018): 10. http://dx.doi.org/10.12688/wellcomeopenres.13828.1.
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Background: The presence of an extra sex chromosome is associated with an increased rate of neurodevelopmental difficulties involving language. Group averages, however, obscure a wide range of outcomes. Hypothesis: The 'double hit' hypothesis proposes that the adverse impact of the extra sex chromosome is amplified when genes that are expressed from the sex chromosomes interact with autosomal variants that usually have only mild effects. Neuroligin-4 genes are expressed from X and Y chromosomes; they play an important role in synaptic development and have been implicated in neurodevelopment. We predict that the impact of an additional sex chromosome on neurodevelopment will be correlated with common autosomal variants involved in related synaptic functions. We describe here an analysis plan for testing this hypothesis using existing data. The analysis of genotype-phenotype associations will be conducted after this plan is published and peer-reviewed Methods: Neurodevelopmental data and DNA are available for 130 children with sex chromosome trisomies (SCTs: 42 girls with trisomy X, 43 boys with Klinefelter syndrome, and 45 boys with XYY). Children from a twin study using the same phenotype measures will form two comparison groups (Ns = 184 and 186). Three indicators of a neurodevelopment disorder phenotype will be used: (i) Standard score on a test of nonword repetition; (ii). A language factor score derived from a test battery; (iii) A general scale of neurodevelopmental challenges based on all available information. Autosomal genes were identified by literature search on the basis of prior association with (a) speech/language/reading phenotypes and (b) synaptic function. Preselected regions of two genes scoring high on both criteria, CNTNAP2 and NRXN1, will be tested for association with neurodevelopmental outcomes using Generalised Structural Component Analysis. We predict the association with one or both genes will be detectable in children with SCTs and stronger than in the comparison samples.
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Newbury, Dianne F., Nuala H. Simpson, Paul A. Thompson, and Dorothy V. M. Bishop. "Stage 1 Registered Report: Variation in neurodevelopmental outcomes in children with sex chromosome trisomies: protocol for a test of the double hit hypothesis." Wellcome Open Research 3 (April 24, 2018): 10. http://dx.doi.org/10.12688/wellcomeopenres.13828.2.
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Background: The presence of an extra sex chromosome is associated with an increased rate of neurodevelopmental difficulties involving language. Group averages, however, obscure a wide range of outcomes. Hypothesis: The 'double hit' hypothesis proposes that the adverse impact of the extra sex chromosome is amplified when genes that are expressed from the sex chromosomes interact with autosomal variants that usually have only mild effects. Neuroligin-4 genes are expressed from X and Y chromosomes; they play an important role in synaptic development and have been implicated in neurodevelopment. We predict that the impact of an additional sex chromosome on neurodevelopment will be correlated with common autosomal variants involved in related synaptic functions. We describe here an analysis plan for testing this hypothesis using existing data. The analysis of genotype-phenotype associations will be conducted after this plan is published and peer-reviewed Methods: Neurodevelopmental data and DNA are available for 130 children with sex chromosome trisomies (SCTs: 42 girls with trisomy X, 43 boys with Klinefelter syndrome, and 45 boys with XYY). Children from a twin study using the same phenotype measures will form two comparison groups (Ns = 184 and 186). Three indicators of a neurodevelopment disorder phenotype will be used: (i) Standard score on a test of nonword repetition; (ii). A language factor score derived from a test battery; (iii) A general scale of neurodevelopmental challenges based on all available information. Autosomal genes were identified by literature search on the basis of prior association with (a) speech/language/reading phenotypes and (b) synaptic function. Preselected regions of two genes scoring high on both criteria, CNTNAP2 and NRXN1, will be tested for association with neurodevelopmental outcomes using Generalised Structural Component Analysis. We predict the association with one or both genes will be detectable in children with SCTs and stronger than in the comparison samples.
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Sanz, Jacqueline H., Julia Anixt, Laurel Bear, Amy Basken, John Beca, Bradley S. Marino, Kathleen A. Mussatto, et al. "Characterisation of neurodevelopmental and psychological outcomes in CHD: a research agenda and recommendations from the cardiac neurodevelopmental outcome collaborative." Cardiology in the Young 31, no. 6 (June 2021): 876–87. http://dx.doi.org/10.1017/s1047951121002146.
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AbstractThe Neurodevelopmental and Psychological Outcomes Working Group of the Cardiac Neurodevelopmental Outcome Collaborative was formed in 2018 through support from an R13 grant from the National Heart, Lung, and Blood Institute with the goals of identifying knowledge gaps regarding the neurodevelopmental and psychological outcomes of individuals with CHD and investigations needed to advance science, policy, clinical care, and patient/family outcomes. Accurate characterisation of neurodevelopmental and psychological outcomes in children with CHD will drive improvements in patient and family outcomes through targeted intervention. Decades of research have produced a generalised perspective about neurodevelopmental and psychological outcomes in this heterogeneous population. Future investigations need to shift towards improving methods, measurement, and analyses of outcomes to better inform early identification, prevention, and intervention. Improved definition of underlying developmental, neuropsychological, and social-emotional constructs is needed, with an emphasis on symptom networks and dimensions. Identification of clinically meaningful outcomes that are most important to key stakeholders, including patients, families, schools and providers, is essential, specifically how and which neurodevelopmental differences across the developmental trajectory impact stakeholders. A better understanding of the discontinuity and patterns of neurodevelopment across the lifespan is critical as well, with some areas being more impactful at some ages than others. Finally, the field needs to account for the impact of race/ethnicity, socio-economic status, cultural and linguistic diversity on our measurement, interpretation of data, and approach to intervention and how to improve generalisability to the larger worldwide population of patients and families living with CHD.
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Hassen, Tahir Ahmed, Catherine Chojenta, Nicholas Egan, and Deborah Loxton. "The Association between the Five-Minute Apgar Score and Neurodevelopmental Outcomes among Children Aged 8−66 Months in Australia." International Journal of Environmental Research and Public Health 18, no. 12 (June 15, 2021): 6450. http://dx.doi.org/10.3390/ijerph18126450.
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This study aimed to evaluate the association of the five-minute Apgar score and neurodevelopmental outcomes in children by taking the entire range of Apgar scores into account. Data from the Australian Longitudinal Study of Women’s Health (ALSWH) and Mothers and their Children’s Health (MatCH) study were linked with Australian state-based Perinatal Data Collections (PDCs) for 809 children aged 8−66 months old. Generalized estimating equations were used to model the association between the five-minute Apgar scores and neurodevelopmental outcomes, using STATA software V.15. Of the 809 children, 614 (75.3%) had a five-minute Apgar score of 9, and 130 (16.1%) had an Apgar score of 10. Approximately 1.9% and 6.2% had Apgar scores of 0−6 and 7−8, respectively. Sixty-nine (8.5%) of children had a neurodevelopmental delay. Children with an Apgar score of 0−6 (AOR = 5.7; 95% CI: 1.2, 27.8) and 7−8 (AOR = 4.1; 95% CI: 1.2, 14.1) had greater odds of gross-motor neurodevelopment delay compared to children with an Apgar score of 10. Further, when continuously modelled, the five-minute Apgar score was inversely associated with neurodevelopmental delay (AOR = 0.75; 95% CI: 0.60, 0.93). Five-minute Apgar score was independently and inversely associated with a neurodevelopmental delay, and the risks were higher even within an Apgar score of 7−8. Hence, the Apgar score may need to be taken into account when evaluating neurodevelopmental outcomes in children.
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Turan, Soeren, Tom Boerstler, Atria Kavyanifar, Sandra Loskarn, André Reis, Beate Winner, and Dieter Chichung Lie. "A novel human stem cell model for Coffin–Siris syndrome-like syndrome reveals the importance of SOX11 dosage for neuronal differentiation and survival." Human Molecular Genetics 28, no. 15 (April 29, 2019): 2589–99. http://dx.doi.org/10.1093/hmg/ddz089.
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AbstractThe SOXC transcription factors Sox4, Sox11 and Sox12, are critical neurodevelopmental regulators that are thought to function in a highly redundant fashion. Surprisingly, heterozygous missense mutations or deletions of SOX11 were recently detected in patients with Coffin–Siris syndrome-like syndrome (CSSLS), a neurodevelopmental disorder associated with intellectual disability, demonstrating that in humans SOX11 haploinsufficiency cannot be compensated and raising the question of the function of SOX11 in human neurodevelopment. Here, we describe the generation of SOX11+/− heterozygous human embryonic stem cell (hESC) lines by CRISPR/Cas9 genome engineering. SOX11 haploinsufficiency impaired the generation of neurons and resulted in a proliferation/differentiation imbalance of neural precursor cells and enhanced neuronal cell death. Using the SOX11+/− hESC model we provide for the first time experimental evidence that SOX11 haploinsufficiency is sufficient to impair key processes of human neurodevelopment, giving a first insight into the pathophysiology of CSSLS and SOX11 function in human neurodevelopment.
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Kordopati-Zilou, Kalliopi, Theodoros Sergentanis, Panagiota Pervanidou, Danai Sofianou-Petraki, Konstantinos Panoulis, Nikolaos Vlahos, and Makarios Eleftheriades. "Neurodevelopmental Outcomes in Tetralogy of Fallot: A Systematic Review." Children 9, no. 2 (February 15, 2022): 264. http://dx.doi.org/10.3390/children9020264.
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BACKGROUND: Tetralogy of Fallot (TOF) represents between 7 and 10% of the total cases of congenital heart defects (CHD) and is estimated to be the most common cyanotic CHD, requiring medical or surgical intervention within the first year of life. Current advances in prenatal screening and fetal echocardiography led to increased rates of prenatal diagnosis of TOF. Furthermore, improvements in initial medical care, surgical repair, and long-term care are associated with excellent long-term survival until adulthood. Consequently, issues of morbidity have come under the spotlight, specifically neurodevelopmental and psychiatric adverse outcomes, which affect the quality of life of TOF survivors. METHOD: This study is a systematic review of English articles, using PUBMED and applying the following search terms, Tetralogy of Fallot, neurodevelopment, autism, cerebral palsy, attention-deficit hyperactivity disorder. Data were extracted by two authors. RESULTS: Most researchers suggest that TOF survivors score lower in neurodevelopmental tests than healthy populations of the same age and are in danger of neurodevelopmental impairments. Furthermore, it is suggested that TOF adolescents show higher rates of psychiatric disorders. CONCLUSIONS: The neurodevelopment of TOF survivors is not intensively studied. Existing studies in TOF survivors focus on different developmental aspects, using different evaluation methods and thus making conclusions for either one of the four aspects of neurodevelopment (executive function, cognition, and adaptive function, speech-language and motor function, or neuropsychiatric domain). The poor outcomes of these isolated studies indicate the need for future research as well as for continuous neuropsychological assessment and close monitoring of children and adolescents with TOF.
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Balagura, Ganna, Julie Xian, Antonella Riva, Francesca Marchese, Bruria Ben Zeev, Loreto Rios, Deepa Sirsi, et al. "Epilepsy Course and Developmental Trajectories in STXBP1-DEE." Neurology Genetics 8, no. 3 (May 31, 2022): e676. http://dx.doi.org/10.1212/nxg.0000000000000676.
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Background and ObjectivesClinical manifestations in STXBP1 developmental and epileptic encephalopathy (DEE) vary in severity and outcome, and the genotypic spectrum is diverse. We aim to trace the neurodevelopmental trajectories in individuals with STXBP1-DEE and dissect the relationship between neurodevelopment and epilepsy.MethodsRetrospective standardized clinical data were collected through international collaboration. A composite neurodevelopmental score system compared the developmental trajectories in STXBP1-DEE.ResultsForty-eight patients with de novo STXBP1 variants and a history of epilepsy were included (age range at the time of the study: 10 months to 35 years, mean 8.5 years). At the time of inclusion, 65% of individuals (31/48) had active epilepsy, whereas 35% (17/48) were seizure free, and 76% of those (13/17) achieved remission within the first year of life. Twenty-two individuals (46%) showed signs of developmental impairment and/or neurologic abnormalities before epilepsy onset. Age at seizure onset correlated with severity of developmental outcome and the developmental milestones achieved, with a later seizure onset associated with better developmental outcome. In contrast, age at seizure remission and epilepsy duration did not affect neurodevelopmental outcomes. Overall, we did not observe a clear genotype-phenotype correlation, but monozygotic twins with de novo STXBP1 variant showed similar phenotype and parallel disease course.DiscussionThe disease course in STXBP1-DEE presents with 2 main trajectories, with either early seizure remission or drug-resistant epilepsy, and a range of neurodevelopmental outcomes from mild to profound intellectual disability. Age at seizure onset is the only epilepsy-related feature associated with neurodevelopment outcome. These findings can inform future dedicated natural history studies and trial design.
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Wei, Chih-Fu, Mei-Huei Chen, Ching-Chun Lin, Yueliang Leon Guo, Shio-Jean Lin, Hua-Fang Liao, Wu-Shiun Hsieh, and Pau-Chung Chen. "Association between maternal shift work and infant neurodevelopmental outcomes: results from the Taiwan Birth Cohort Study with propensity-score-matching analysis." International Journal of Epidemiology 48, no. 5 (March 29, 2019): 1545–55. http://dx.doi.org/10.1093/ije/dyz045.
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Abstract Background Maternal shift work is associated with preterm delivery, small-for-gestational-age new-borns, childhood obesity and future behavioural problems. However, the adverse effects on and interactions of maternal shift work with infant neurodevelopment remain uncertain. Therefore, we examined the associations between maternal-shift-work status and infant neurodevelopmental parameters. Methods The Taiwan Birth Cohort Study is a nationwide birth cohort study following representatively sampled mother–infant pairs in 2005. The participants’ development and exposure conditions were assessed by home interviews with structured questionnaires at 6 and 18 months of age. Propensity scores were calculated with predefined covariates for 1:1 matching. Multivariate conditional logistic regression and the Cox proportional-hazards model were used to examine the association between maternal-shift-work status and infant neurodevelopmental-milestone-achievement status. Results In this study, 5637 term singletons were included, with 2098 cases selected in the propensity-score-matched subpopulation. Persistent maternal shift work was associated with increased risks of delays in gross-motor neurodevelopmental milestones [aOR = 1.36, 95% confidence interval (CI) = 1.06–1.76 for walking steadily], fine-motor neurodevelopmental milestones (aOR = 1.39, 95% CI = 1.07–1.80 for scribbling) and social neurodevelopmental milestones (aOR = 1.35, 95% CI = 1.03–1.76 for coming when called upon). Moreover, delayed gross-motor and social development were identified in the propensity-score-matched sub-cohort. Conclusions This study shows negative associations between maternal shift work and delayed neurodevelopmental-milestone achievement in the gross-motor, fine-motor and social domains at 18 months. Future research is necessary to elucidate the possible underlying mechanisms and long-term health effects.
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Bae, Seong Phil, Seung Han Shin, Young Mi Yoon, Ee-Kyung Kim, and Han-Suk Kim. "Association of Severe Retinopathy of Prematurity and Bronchopulmonary Dysplasia with Adverse Neurodevelopmental Outcomes in Preterm Infants without Severe Brain Injury." Brain Sciences 11, no. 6 (May 26, 2021): 699. http://dx.doi.org/10.3390/brainsci11060699.
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Although impaired neurodevelopment is strongly associated with severe brain injury, most preterm infants survive without severe brain injury. In this study, the association of impaired neurodevelopment and neonatal morbidities of preterm infants was assessed after excluding those with severe brain injury. This was a retrospective study of very low birthweight infants in a single tertiary center. After excluding infants with severe brain injury, the study population was categorized as infants without intraventricular hemorrhage (IVH) and with low-grade IVH. Neurodevelopmental outcomes at a corrected age (CA) of 18–24 months were evaluated using the Bayley Scales of Infant and Toddler Development 3rd Edition (Bayley-III). Cerebral palsy (CP), hearing impairment and blindness were also assessed and compared. Of 240 infants, 25 (11.6%) infants had combined neurodevelopmental impairment (NDI). In the multivariate analysis for combined NDI, small for gestational age (SGA) (adjusted OR 6.820, 95% confidence intervals (CI) 1.770–26.307), moderate to severe bronchopulmonary dysplasia (BPD) (aOR 3.21, 95% CI 1.032–9.999) and severe retinopathy of prematurity (ROP) (aOR 5.669, 95% CI 1.132–28.396) were associated with combined NDI. Among neonatal morbidities, moderate to severe BPD and severe ROP were associated with adverse neurodevelopmental outcomes in preterm infants without severe brain injury.
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Nusinovici, Simon, Bertrand Olliac, Cyril Flamant, Jean-Baptiste Müller, Marion Olivier, Valérie Rouger, Géraldine Gascoin, et al. "Impact of preterm birth on parental separation: a French population-based longitudinal study." BMJ Open 7, no. 11 (November 2017): e017845. http://dx.doi.org/10.1136/bmjopen-2017-017845.
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ObjectiveThe objective of this study was to investigate both the effects of low gestational age and infant’s neurodevelopmental outcome at 2 years of age on the risk of parental separation within 7 years of giving birth.DesignProspective.Setting24 maternity clinics in the Pays-de-la-Loire region.ParticipantsThis study included 5732 infants delivered at <35 weeks of gestation born between 2005 and 2013 who were enrolled in the population-based Loire Infant Follow-up Team cohort and who had a neurodevelopmental evaluation at 2 years. This neurodevelopmental evaluation was based on a physical examination, a psychomotor evaluation and a parent-completed questionnaire.Outcome measureRisk of parental separation (parents living together or parents living separately).ResultsTen percent (572/5732) of the parents reported having undergone separation during the follow-up period. A mediation analysis showed that low gestational age had no direct effect on the risk of parental separation. Moreover, a non-optimal neurodevelopment at 2 years was associated with an increased risk of parental separation corresponding to a HR=1.49(1.23 to 1.80). Finally, the increased risk of parental separation was aggravated by low socioeconomic conditions.ConclusionsThe effect of low gestational age on the risk of parental separation was mediated by the infant’s neurodevelopment.
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Neufeld, Jacob A. "Neurodevelopmental Disorders." NeuroRehabilitation 22, no. 5 (December 7, 2007): 339–40. http://dx.doi.org/10.3233/nre-2007-22501.
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Schleichkorn, Jay. "Neurodevelopmental Therapy." Pediatric Physical Therapy 3, no. 3 (1991): 121???122. http://dx.doi.org/10.1097/00001577-199100330-00002.
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Valvano, Joanne, and Toby Long. "Neurodevelopmental Treatment." Pediatric Physical Therapy 3, no. 3 (1991): 125???130. http://dx.doi.org/10.1097/00001577-199100330-00004.
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Dixon, Suzanne D. "Neurodevelopmental Disorders." Journal of Developmental & Behavioral Pediatrics 21, no. 6 (December 2000): 448. http://dx.doi.org/10.1097/00004703-200012000-00008.
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Donders, Jacobus. "Neurodevelopmental Disorders." Child Neuropsychology 8, no. 3 (September 2002): 149. http://dx.doi.org/10.1076/chin.8.3.149.13502.
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Thapar, Anita, Miriam Cooper, and Michael Rutter. "Neurodevelopmental disorders." Lancet Psychiatry 4, no. 4 (April 2017): 339–46. http://dx.doi.org/10.1016/s2215-0366(16)30376-5.
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Cobb, Stuart R., and Ceri H. Davies. "Neurodevelopmental disorders." Neuropharmacology 68 (May 2013): 1. http://dx.doi.org/10.1016/j.neuropharm.2013.02.001.
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Schmid, Carrie, and Joshua S. Rotenberg. "Neurodevelopmental Toxicology." Neurologic Clinics 23, no. 2 (May 2005): 321–36. http://dx.doi.org/10.1016/j.ncl.2004.12.010.
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Kolehmainen, Niina. "Neurodevelopmental Treatment." British Journal of Occupational Therapy 77, no. 1 (January 2014): 23. http://dx.doi.org/10.1177/030802261407700102.
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D'Souza, Hana, and Annette Karmiloff‐Smith. "Neurodevelopmental disorders." Wiley Interdisciplinary Reviews: Cognitive Science 8, no. 1-2 (December 2016): e1398. http://dx.doi.org/10.1002/wcs.1398.
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ARNOLD, STEVEN E. "Neurodevelopmental abnormalities in schizophrenia: Insights from neuropathology." Development and Psychopathology 11, no. 3 (September 1999): 439–56. http://dx.doi.org/10.1017/s095457949900214x.
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Growing epidemiological, genetic, and clinical neurobiological evidence indicates that abnormalities in brain development play determining roles in the pathobiology of schizophrenia. Neuropathological research has made significant progress in delineating cellular and molecular abnormalities in schizophrenia that have relevance to neurodevelopment. This paper reviews the neurodevelopmental processes of neurogenesis, neuronal migration, differentiation, synaptogenesis, neuron and synaptic pruning, and myelination and the reported neuropathological findings in schizophrenia that may be a consequence of disturbances in these processes. While many neuropathological findings in schizophrenia are controversial or await confirmation, reported abnormalities in neuron density, number and morphology, cytoarchitecture, dendritic arbors and spines, synapse-related proteins, and the well-established absence of gliosis or any other evidence of neurodegeneration or neural injury all provide support for the neurodevelopmental model of schizophrenia.
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Korček, Peter, Zuzana Korčeková, Ivan Berka, Jáchym Kučera, and Zbyněk Straňák. "Corpus Callosum Growth and Neurodevelopmental Outcome Are Negatively Influenced by Systemic Infection in Very Low-Birth-Weight Infants." Journal of Child Neurology 36, no. 10 (May 28, 2021): 883–87. http://dx.doi.org/10.1177/08830738211016239.
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Systemic infection may negatively modulate the development of cerebral white matter and long-term outcome of neonates. We analyzed the growth of corpus callosum (using cranial ultrasonography) and neurodevelopment (Bayley Scales of Infant Development, Third Edition) in 101 very low-birth-weight newborns. We observed significantly reduced corpus callosum length at 3 months of corrected age (44.5 mm vs 47.7 mm, P = .004) and diminished corpus callosum growth (0.07 mm/d vs 0.08 mm/d, P = .028) in infants who experienced systemic infection. The subgroup exhibited inferior neurodevelopmental outcomes with predominant motor impairment. The results suggest that length and growth of corpus callosum might be affected by systemic inflammatory response in preterm newborns. The changes in corpus callosum can contribute to adverse neurodevelopment at 2 years of corrected age. Serial ultrasonographic measurements of the corpus callosum may be suitable to identify preterm infants with increased risk of neurodevelopmental impairment.
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Kim, Mi Ju, Hyun Mi Kim, Hyun-Hwa Cha, Haemin Kim, Hyo-Shin Kim, Bong Seon Lim, and Won Joon Seong. "Perinatal Outcomes and Neurodevelopment 1 Year after Birth in Discordant Twins According to Chorionicity." Medicina 59, no. 3 (March 2, 2023): 493. http://dx.doi.org/10.3390/medicina59030493.
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Background and Objectives: This study aimed to compare maternal complications, perinatal outcomes, and neurodevelopment 1 year after the birth between concordant and discordant twins in monochorionic and dichorionic twins. Materials and Methods: This retrospective study included twin pregnancies delivered between 24 + 1 and 38 + 2 weeks of gestation between January 2011 and September 2019. Chorionicity was confirmed by ultrasonography and was categorized into monochorionic and dichorionic. Each was then divided into two groups (concordant and discordant) according to birth weight discordancy. Maternal complications and neonatal outcomes, including neurodevelopmental delays, were compared between the two groups. Results: A total of 298 pairs of twin pregnancies were enrolled, of which 58 (19.26%) women were pregnant with monochorionic diamniotic twins and 240 (80.54%) with dichorionic diamniotic twins. In both monochorionic and dichorionic twins, the discordant twins had a greater incidence of emergency deliveries because of iatrogenic causes than the concordant twins. Among dichorionic twins, discordant twins had lower birth weight rates and higher hospitalization rates and morbidities than concordant twins. Among monochorionic twins, discordant twins had a lower birth weight and higher neonatal mortality than concordant twins. The neonatal size was not a predictor of neurodevelopment in this group. Based on the logistic regression analysis, male sex, respiratory distress syndrome, and bronchopulmonary dysplasia were risk factors for the neurodevelopmental delay; birth weight discordancy was significant only in dichorionic twins. Conclusions: Perinatal outcomes in discordant twins may be poor, and neurodevelopment 1 year after birth was worse in discordant twins than in concordant twins. Discordancy in twins can be a risk factor for neurodevelopmental delay.
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Dufour, A., M. Gagnon, B. Marandyuk, Z. Mahdi, G. Côté-Corriveau, A. Nuyt, M. Dehaes, T. Luu, M. Simard, and EF Pinchefsky. "P.075 EEG features reflecting the neurodevelopmental assessment at term equivalent age in preterm born infants." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 49, s1 (June 2022): S27—S28. http://dx.doi.org/10.1017/cjn.2022.173.
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Background: In Canada, 7% of children are born preterm between 29 and 36 weeks gestational age (GA). Electroencephalography (EEG) provides a bedside evaluation of brain activity, yet the clinical significance of several EEG patterns requires further study. The goal of this study is to determine the EEG features at term equivalent age (TEA) that correlate with neurodevelopmental evaluation at TEA in infants born between 29-36 weeks GA. Methods: Prospective cohort study of preterm infants born 29-36 weeks GA with 1 hour EEG recording at TEA. EEG discontinuity index (proportion <25mcV amplitude) and spectral power densities were calculated as well as the mean and maximum values of interburst intervals. At TEA, neurodevelopment was evaluated using the General Movement Optimality Score (GMOS). Linear regression analyses were used to evaluate the association between EEG features and neurodevelopmental assessment. Results: Eighty-two children (median GA 33.6 weeks) were included (47 males). Median GMOS was 29.0 (IQR 24.3-35.0). A greater EEG discontinuity index was associated with reduced GMOS (B -6.85; 95% CI -12.13,-1.57; p=0.012). Conclusions: At TEA, a greater EEG discontinuity index was associated with a more abnormal neurodevelopmental assessment. Ongoing longitudinal neurodevelopmental assessments are needed to better evaluate the prognostic potential of TEA EEG.
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Rivollier, Fabrice, Marie-Odile Krebs, and Oussama Kebir. "Perinatal Exposure to Environmental Endocrine Disruptors in the Emergence of Neurodevelopmental Psychiatric Diseases: A Systematic Review." International Journal of Environmental Research and Public Health 16, no. 8 (April 12, 2019): 1318. http://dx.doi.org/10.3390/ijerph16081318.
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Background: Exposure to endocrine disruptors is on the rise, with new compounds regularly incriminated. In animals and humans, this exposure during critical developmental windows has been associated with various developmental abnormalities, including the emergence of psychiatric disorders. We aimed to review the association between perinatal endocrine disruptor exposure and neurodevelopmental disorders in humans, focusing on cognitive and psychiatric disorders. Methods: We performed a systematic review with key words referring to the fields of neurodevelopment and endocrine disruptors. We reviewed 896 titles, choosing studies on the basis of titles and abstracts. We searched through the methodology sections to find perinatal exposure and neurodevelopmental disorders, following the categories indicated in the Diagnostic and Statistic Manual of Mental Disorders (5th edition). References in some studies brought us to a total of 47 studies included here. Results: Convergent studies report an association between exposure to endocrine disruptors and autism spectrum disorder, attention-deficit hyperactivity disorder, global developmental delay, intellectual disability, communication disorders and unspecified neurodevelopmental disorders. Conclusion: Sufficient data exist to report that exposure to some endocrine disruptors is a risk factor for the emergence of neurodevelopmental disorders. Studying endocrine disruptor exposure in humans is still associated with some limits that are difficult to overcome.
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Berger, Paige K., Margaret L. Ong, Lars Bode, and Mandy B. Belfort. "Human Milk Oligosaccharides and Infant Neurodevelopment: A Narrative Review." Nutrients 15, no. 3 (January 31, 2023): 719. http://dx.doi.org/10.3390/nu15030719.
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The objective of this narrative review was to synthesize the literature on human milk oligosaccharides (HMOs) and neurodevelopmental outcomes in human milk-fed infants. We conducted a scoping review of the literature indexed in PubMed reporting observational or interventional studies on HMO exposure in relation to psychometric measures in infants. Studies were characterized based on study design and definitions of HMO exposure and neurodevelopmental outcomes. Six studies were identified; all were observational in design, and five were conducted in full-term infants. Sample sizes ranged from 35–659 infants. HMOs were defined as individual concentrations or relative abundances assessed at 1 and/or 6 months of age. Studies accounted for differences in HMO exposure based on maternal secretor status. Neurodevelopmental outcomes were assessed between 6 and 24 months of age and included four domains. Studies in full-term infants reported that total and individual fucosylated and sialylated HMOs were positively associated with cognitive, language, and motor skill domains between 18 and 24 months of age, while the single study in preterm infants reported no statistically significant findings in the full cohort. The presence of a maternal secretor did not consistently alter the associations between HMO exposure and neurodevelopmental outcomes. Emerging evidence from observational studies suggests that HMO exposure may be beneficial for neurodevelopment in infants.
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Ying, Yilin, Xuefei Hu, Peng Han, Aaron Mendez-Bermudez, Serge Bauwens, Rita Eid, Li Tan, et al. "The non-telomeric evolutionary trajectory of TRF2 in zebrafish reveals its specific roles in neurodevelopment and aging." Nucleic Acids Research 50, no. 4 (February 12, 2022): 2081–95. http://dx.doi.org/10.1093/nar/gkac065.
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Abstract The shelterin protein complex is required for telomere protection in various eukaryotic organisms. In mammals, the shelterin subunit TRF2 is specialized in preventing ATM activation at telomeres and chromosome end fusion in somatic cells. Here, we demonstrate that the zebrafish ortholog of TRF2 (encoded by the terfa gene) is protecting against unwanted ATM activation genome-wide. The terfa-compromised fish develop a prominent and specific embryonic neurodevelopmental failure. The heterozygous fish survive to adulthood but exhibit a premature aging phenotype. The recovery from embryonic neurodevelopmental failure requires both ATM inhibition and transcriptional complementation of neural genes. Furthermore, restoring the expression of TRF2 in glial cells rescues the embryonic neurodevelopment phenotype. These results indicate that the shelterin subunit TRF2 evolved in zebrafish as a general factor of genome maintenance and transcriptional regulation that is required for proper neurodevelopment and normal aging. These findings uncover how TRF2 links development to aging by separate functions in gene expression regulation and genome stability control.
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Hui, Kelvin K., Noriko Takashima, Akiko Watanabe, Thomas E. Chater, Hiroshi Matsukawa, Yoko Nekooki-Machida, Per Nilsson, et al. "GABARAPs dysfunction by autophagy deficiency in adolescent brain impairs GABAA receptor trafficking and social behavior." Science Advances 5, no. 4 (April 2019): eaau8237. http://dx.doi.org/10.1126/sciadv.aau8237.
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Dysfunctional mTOR signaling is associated with the pathogenesis of neurodevelopmental and neuropsychiatric disorders. However, it is unclear what molecular mechanisms and pathogenic mediators are involved and whether mTOR-regulated autophagy continues to be crucial beyond neurodevelopment. Here, we selectively deleted Atg7 in forebrain GABAergic interneurons in adolescent mice and unexpectedly found that these mice showed a set of behavioral deficits similar to Atg7 deletion in forebrain excitatory neurons. By unbiased quantitative proteomic analysis, we identified γ-aminobutyric acid receptor–associated protein-like 2 (GABARAPL2) to differentially form high–molecular weight species in autophagy-deficient brains. Further functional analyses revealed a novel pathogenic mechanism involving the p62-dependent sequestration of GABARAP family proteins, leading to the reduction of surface GABAA receptor levels. Our work demonstrates a novel physiological role for autophagy in regulating GABA signaling beyond postnatal neurodevelopment, providing a potential mechanism for the reduced inhibitory inputs observed in neurodevelopmental and neuropsychiatric disorders with mTOR hyperactivation.
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Armstrong, F. Daniel, T. David Elkin, R. Clark Brown, Penny Glass, Renee C. Rees, Winfred C. Wang, and The Baby HUG Investigators. "Neurodevelopment in Infants with Sickle Cell Anemia: Baseline Data from the Baby HUG Trial." Blood 112, no. 11 (November 16, 2008): 713. http://dx.doi.org/10.1182/blood.v112.11.713.713.
Full textAbstract:
Abstract Delays and deficits in neurodevelopment are known complications of sickle cell anemia (SCA) in young children1. Hydroxyurea is a chemotherapeutic agent that increases production of fetal hemoglobin, and has proven effective in reducing pain and other SCA-related complications in adults, adolescents, and school-age children. To determine whether treatment with hydroxyurea for 24 months would benefit infants with SCA, the NHLBI initiated a multi-center, randomized, double-blind, placebo-controlled clinical trial (NCT00006400) in 2003 (BABY HUG). After screening 233 infants for eligibility, 193 infants 9 to 17 months of age from 14 participating institutions were randomized. While the primary outcomes for BABY HUG are spleen and kidney function, neurodevelopment is an important safety assessment and a secondary outcome. Two hundred and seven (male=89, female = 117) infants were administered the Bayley Scales of Infant Development-2nd Edition (BSID-II) by qualified psychological examiners during the screening phase of the trial. The infants also completed a transcranial Doppler ultrasound (TCD) to determine flow velocity in seven ascending arteries of the brain. The analyses for this report focused on the relationships between neurodevelopmental function on the BSID-II, age at study entry and TCD flow velocities. Overall the mean neurodevelopmental function of the sample was in the average range (mean Motor Developmental Index= 96.8; mean Mental Developmental Index = 96.3). Age at study entry (continuous and categorical) was significantly correlated with the Mental Scale of the BSID-II (p=0.0042, p=0.0001, respectively). On average, a child’s Mental Developmental Index (MDI) decreased by 0.75 for every one month increase in age. Age (categorical) was also significantly associated with the Motor Scale of the BSID (p=0.0255). TCD velocity has been shown to be a sensitive indicator of existing and future risk for central nervous system (CNS) events in children with SCA. In children age 2–16 years, flow velocities over 200mm/ sec are associated with significant stroke risk; flow velocities between 170–200 mm/sec are associated with potential risk for neurodevelopmental deficits. Early associations between TCD and neurodevelopment could be considered important clinical indicators of risk for future CNS events. BSID Mental Scale scores were significantly associated with the maximum (of left or right) flow velocity in the M-1 artery (p=0.04) and the Behavior Rating Scale scores were significantly associated with the dICA velocity (p=0.008). In both of these cases, higher flow velocity was associated with poorer neurodevelopmental function. These results reflect the function of a large group of infants and toddlers with SCA prior to the initiation of any treatment targeting the CNS. Although the overall function of the group was in the average range, it is concerning to find strong relationships between increasing age at enrollment and decreasing MDI and between higher TCD flow velocity and decreased neurodevelopmental function in these very young children. The importance of early screening and perhaps sequential assessment of infants with both TCD and neurodevelopmental assessments is raised by these findings, as is the importance of continuing efforts to determine whether interventions, such as early HU therapy, might favorably impact the CNS complications of this disease that affect neurodevelopment.
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Blair, Lisa M., Rita H. Pickler, and Cindy Anderson. "Integrative Review of Genetic Factors Influencing Neurodevelopmental Outcomes in Preterm Infants." Biological Research For Nursing 18, no. 2 (September 15, 2015): 127–37. http://dx.doi.org/10.1177/1099800415605379.
Full textAbstract:
Preterm infants are at elevated risk for a host of neurodevelopmental problems, including disorders that appear later in life. Gene–environment interactions and prematurity may combine to increase the risk for poor neurodevelopmental outcomes. Increasing evidence supports a genetic link to risk for atypical development; however, no genomic risk profiles are currently used for infants without apparent genetic disorders. The purpose of this review was to synthesize recent evidence of genetic associations with atypical neurodevelopmental outcomes that may affect preterm infants who do not have a rare genetic disease. Electronic and hand-search strategies were used to find relevant articles that were English-language, peer-reviewed primary research or meta-analysis reports published between July 2009 and July 2014, involving human participants. Articles included in the analysis ( N = 29) used a wide range of study designs and methodologies, complicating the analysis. An integrative-review design was used to synthesize the data. Numerous genes ( n = 43) and additional large deletion copy number variants were associated with neurodevelopmental outcomes, including cognition, attention, perception, psychiatric disease, autism spectrum disorder, cerebral palsy, infant behavior, and alterations in brain architecture. The creation of genetic risk profiles for complex disorders of neurodevelopment is presently hindered by inconsistent genetic-association evidence, methodological considerations, reporting problems, and lack of replication. However, several avenues of investigation offer promise, including large (>100 kb) copy number variants and the candidate genes MET, NRG3, and SLC6A4, each of which were reported to have associations with neurodevelopmental outcomes in multiple, high-quality studies.