Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “neurodevelopment”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1995

Summary of the Seychelles child development study on the relationship of fetal methylmercury exposure to neurodevelopment.

The Seychelles Child Development Study is examining the association between fetal methylmercury exposure from a maternal diet high in fish and subsequent child development. The study is double blind and uses maternal hair mercury as the index of fetal exposure. An initial cross-sectional pilot study of 804 infants aged 1 to 25 months suggested that mercury may affect development. A follow up of 217 pilot children at 66 months of age also suggested that neurodevelopmental effects might be present, but the result was dependent on outcomes in a small number of children. On the basis of initial results in the pilot study a prospective, longitudinal main study with more covariates and expanded endpoints was begun on a new cohort of 779 children. No association with neurodevelopment was seen at 6 1/2, 19, or 29 months of age, but there was an inverse relationship at 29 months in boys only between mercury level and activity as judged by the examiner. Adverse neurodevelopmental effects from fetal mercury exposure in the pilot study are highly dependent on how the data are analyzed and no definite effects have been detected through 29 months of age in the main study. In a related study, 32 brains were obtained at autopsy from Seychellois infants. These were examined histologically and analyzed for mercury. No clear histological abnormalities were found. Mercury levels ranged from a background of about 50 ppb up to 300 ppb, and correlated well between brain regions. For 27 brains maternal hair from delivery was available and hair mercury correlated well with brain mercury.

Child Development↗
PubMed1997

Pregnancy outcome and neurodevelopment of children exposed in utero to psychoactive drugs: the Motherisk experience.

This paper presents an overview of the Motherisk Program data on pregnancy outcome and neurodevelopment of children exposed in utero to selected psychoactive drugs. First, the use of cocaine during pregnancy has been associated with increased risk of spontaneous abortions, abruptio placenta, premature labor, and stillbirth. Twenty-three adopted children exposed in utero to cocaine demonstrated an 8-fold increase in risk for microcephaly compared with controls. Global intelligence quotients (IQ) did not differ between the 2 groups, but the cocaine-exposed children achieved significantly lower scores on the Reynell language test. Second, the long-term neurobehavioral effects of fetal alcohol syndrome (FAS) were studied in 384 children to show that alcohol-induced brain insults, which consist of attention and memory deficits together, and poor adaptability and organization are not attenuated with age. Third, the rates of major malformations in children exposed in utero to fluoxetine, tricyclic antidepressants, and nonteratogenic drugs did not differ or exceed the expected rates in the general population. A 2nd phase of this study established the safety of antidepressants during pregnancy by demonstrating that the mean IQ and language scores are comparable in the 3 groups. A level 2 ultrasonography is recommended in cases of in utero exposure to lithium and carbamazepine because of an increased risk of cardiac malformations and spina bifida, respectively.

Developmental Disabilities↗
PubMed2026

Personalized functional topography-based multisite brain age prediction modeling reveals divergent neurodevelopment in major depression.

Major depressive disorder (MDD) is associated with widespread alterations in functional brain networks across the lifespan. However, heterogeneity in atypical brain development among patients with MDD remains largely uncharacterized. Using a multisite resting-state functional MRI dataset consisting of 1,105 MDD patients and 1,065 healthy controls, we constructed a harmonized multicenter brain age prediction model based on individualized functional topography and identified two patient subgroups with positive or negative brain age gaps (BAGs). In patients with a positive BAG (BAG+), expansion of the salience network (SAL) into the dorsolateral prefrontal and ventrolateral prefrontal cortices, in addition to contraction of the sensorimotor and dorsal attention networks (DAN), contributes to accelerated brain aging. Conversely, in the negative BAG (BAG-) group, SAL expansion into the orbitofrontal cortex (OFC) and contraction of the visual and sensorimotor networks (SMN) were linked to delayed brain development. These subgroups also exhibited distinct neurodevelopmental trajectories. Clinically, BAG+ patients showed stronger associations between higher-order network topography and mood symptoms, whereas BAG- patients exhibited links between visual/default mode network topography and insomnia. At the molecular level, both groups showed enrichment of genes related to synaptic signaling but displayed distinct expression patterns and divergent expression trajectories in key neurodevelopmental gene sets. Notably, antidepressant treatment modulated the brain in ways that were specific to each subgroup. These findings reveal heterogeneous neurodevelopmental profiles in MDD with distinct biological and clinical signatures, offering insights into personalized precision medicine for this disorder.

Humans↗
PubMed2000

Neurodevelopment and predictors of outcomes of children with birth weights of less than 1000 g: 1992-1995.

OBJECTIVE: To examine the neurosensory and cognitive status of extremely low-birth-weight (ELBW; < 1,000 g) children born from January 1, 1992, through December 31, 1995, and to identify the significant predictors of outcome. DESIGN: An inception cohort of ELBW infants admitted to the neonatal intensive care unit (NICU) and observed to 20 months' corrected age. SETTING: A tertiary level urban NICU and follow-up clinic at a university hospital. POPULATION: Of 333 ELBW infants without major congenital malformations admitted to the NICU, 241 (72%) survived to 20 months' corrected age. We studied 221 children (92%) at a mean of 20 months' corrected age. The mean birth weight was 813 g; mean gestational age, 26.4 weeks. MAIN OUTCOME MEASURES: Assessments of cognitive and neurosensory development. RESULTS: Major neurosensory abnormality was present in 54 children (24%), including 33 (15%) with cerebral palsy, 20 (9%) with deafness, and 2 (1%) with blindness. The mean (+/- SD) Bayley-Mental Developmental Index (MDI) score was 74.7 +/- 17. Ninety-two children (42%) had a subnormal MDI score (<70). Neurodevelopmental impairment (neurosensory abnormality and/or MDI score <70) was present in 105 children (48%). Multiple stepwise logistic regression analysis that considered sex, social risk, birth weight, and neonatal risk factors revealed significant predictors of a subnormal MDI score to be male sex (odds ratio [OR], 2.73; 95% confidence interval [CI], 1.52-4.92), social risk (OR, 1.48; 95% CI, 1.09-2.00), and chronic lung disease (OR, 2.18; 95% CI, 1.20-3.94). Predictors of neurologic abnormality were a severely abnormal finding on cerebral ultrasound (OR, 8.09; 95% CI, 3.69-17.71) and chronic lung disease (OR, 2.46; 95% CI, 1.12-5.40); predictors of deafness were male sex (OR, 2.79; 95% CI, 1.02-7.62), sepsis (OR, 3.15; 95% CI, 1.05-9.48), and jaundice (maximal bilirubin level, >171 micromol/L [>10 mg/dL]) (OR, 4.80; 95% CI, 1.46-15.73). CONCLUSION: There is an urgent need for research into the etiology and prevention of neonatal morbidity.

Brain Damage, Chronic↗
PubMed1998

Effects of prenatal and postnatal methylmercury exposure from fish consumption on neurodevelopment: outcomes at 66 months of age in the Seychelles Child Development Study.

CONTEXT: Human neurodevelopmental consequences of exposure to methyl-mercury (MeHg) from eating fish remain a question of public health concern. OBJECTIVE: To study the association between MeHg exposure and the developmental outcomes of children in the Republic of Seychelles at 66 months of age. DESIGN: A prospective longitudinal cohort study. PARTICIPANTS: A total of 711 of 779 cohort mother-child pairs initially enrolled in the Seychelles Child Development Study in 1989. SETTING: The Republic of Seychelles, an archipelago in the Indian Ocean where 85% of the population consumes ocean fish daily. MAIN OUTCOME MEASURES: Prenatal and postnatal MeHg exposure and 6 age-appropriate neurodevelopmental tests: the McCarthy Scales of Children's Abilities, the Preschool Language Scale, the Woodcock-Johnson Applied Problems and Letter and Word Recognition Tests of Achievement, the Bender Gestalt test, and the Child Behavior Checklist. RESULTS: The mean maternal hair total mercury level was 6.8 ppm and the mean child hair total mercury level at age 66 months was 6.5 ppm. No adverse outcomes at 66 months were associated with either prenatal or postnatal MeHg exposure. CONCLUSION: In the population studied, consumption of a diet high in ocean fish appears to pose no threat to developmental outcomes through 66 months of age.

Central Nervous System Diseases↗
PubMed2005

Towards creation of a unified view of the neurodevelopment of the infant.

During the twentieth century, study of the neurologic development of the fetus and infant has resulted in multiple neurodevelopmental assessments. They have been used both for determination of the integrity of the neonate as well as for assessment of the child's outcome from prenatal and neonatal medical interventions. These models of assessment have broadened our view and understanding of the development of functions such as movement, posture, attention, oromotor skills, and behavior. The link between these areas and the traditional areas of neurologic and psychiatric examination of older children and adults is explored through discussion of the maturation of movement, cranial nerve function, sensory, cognitive, and behavioral responses. Gaps in knowledge remain about the relationship between early neurodevelopmental assessments and later findings. A single unified means of examining the infant is also lacking.

Brain↗
PubMed2006

Neurodevelopment and chronic illness: Mechanisms of disease and treatment.

Successful treatment of many childhood diseases once considered terminal has resulted in the emergence of long-term effects of the disease or consequences of treatment that were previously unrecognized. Many of these long-term effects involve the central nervous system (CNS) and are developmental in the way that they emerge over time. Because we are now able to observe the natural history of childhood diseases such as sickle cell anemia or HIV, or the consequences of treatment of disease such as leukemia, brain tumors, or kidney disease, we are also able to study a number of biological mechanisms that result in long-term neurocognitive impairment. While some of the neurodevelopmental outcomes can be directly linked to structural damage of the CNS, other systems (e.g., hematologic, immunologic, pulmonary) appear to play crucial indirect roles in the development of the CNS and neurocognitive abilities because of the way that they affect the course of brain development and activity of the brain across time. Important interactions between acute disease factors, biological mechanisms, age at the time of disease or treatment effect, and disruptions in patterns of development after successful treatment or management all provide support for a neurodevelopmental model of childhood chronic illness. Testing this model may make it possible to more accurately predict the timing and degree of severity of long-term neurodevelopmental consequences, provide guidance for improved treatment and prevention, and offer better understanding of neurodevelopmental disruptions that occur in other non-chronic illness related disabilities.

Brain↗
PubMedDate not supplied

VIP as a cell-growth and differentiation neuromodulator role in neurodevelopment.

In addition to its commonly recognized status as a neuromodulator of virtually all vital functions, including neurobiological, the neuropeptide VIP plays a role in the control of cell growth and differentiation and of neuronal survival. Through these actions, VIP, whose impact appears early in ontogeny, may possess developmental functions. VIP can be stimulatory or inhibitory on cell growth in function of the model considered. The growth regulatory actions of VIP, which are often independent of cAMP, are most likely significant when mitogenic or trophic factors, eventually released by nontarget cells, are simultaneously present in the extracellular medium. The intracellular mechanisms that mediate these actions of VIP may involve different transduction cascades triggered by subsets of VIP binding sites that may coexist in the same tissue.

Animals↗
PubMed2006

Movement disorders: neurodevelopment and neurobehavioural expression.

Braak and co-workers have recently shown that movement disorders such as Parkinson's disease develop progressively over years with early neuronal losses in brainstem regions caudal to the substantia nigra. The relevance of this finding to notions of comorbidity between movement disorders and psychiatric symptoms was recognised at the recent meeting concerning, "Implications of Comorbidity for the Etiology and Treatment of Neuropsychiatric Disorders" held in Oct. 2005 in Mazagon, Spain. The identification of stages in the early development of neurodegenerative disorders appeared to unify multiple, diverse findings. These included: novel therapeutic innovations for Parkinson's disease, Alzheimer's disease and depression in the aged; the neurochemical ontogeny of drug-induced oral dyskinesias; the types of chemical agents abused in neuropsychiatric states; postnatal iron overload effects upon the functional and interactive role of dopaminergic and noradrenergic pathways that contribute to the expression of movement disorders; and the spectrum of motor symptoms expressed in schizophrenia and attention deficit hyperactivity disorder and the eventual treatment of these disorders. A continued focus on a number of neuropsychiatric diseases as progressive disorders may lead to further advances in understanding their etiology and in developing better therapeutics.

Animals↗
PubMed2006

Antiepileptic drugs and neurodevelopment.

Clinical studies have documented the teratogenic potential of antiepileptic drugs (AEDs). More recent cohort studies have been trying to sort out which AEDs impose the highest risk of teratogenicity. Currently, there is evidence demonstrating an increased risk of major congenital malformations (MCMs) for valproate, phenobarbital, and polytherapy during pregnancy. Based on the current data from multiple studies, the risk for valproate is the highest. Additional studies are needed to fully delineate if differences exist for other AEDs, especially the newer AEDs. However, although MCMs are easy to recognize and have been shown to be more common after in utero exposure to AEDs, there are insufficient data regarding their long-term effects on cognition and behavior in exposed children. Although most children born to women with epilepsy are healthy, in recent years there has been increasing awareness of the long-term effects of in utero exposure to AEDs. Recent discovery of neuronal apoptosis following in utero AED exposure in animals during a period that corresponds to the third trimester and early infancy in humans raises further concerns. Prospective clinical studies seem necessary in order to better understand the long-term neurodevelopmental effects of in utero exposure to AEDs.

Abnormalities, Drug-Induced↗
PubMed1994

Folic acid in neurodevelopment and child psychiatry.

1. Folic acid deficiency has been associated with diverse neuropsychiatric symptoms. 2. This paper discusses the impact of folate on brain development, maturation and function and reviews the role of folate in psychiatric disorders, particularly childhood disorders. 3. A brief case report examines the use of folate in the treatment of attentional problems in a child with fragile X syndrome.

Brain↗
PubMed1993

Voltage sensitive calcium channels mark a critical period in mouse neurodevelopment.

Voltage sensitive calcium channel (VSCC) probes 125I-omega-GVIA Conotoxin (omega-GVIA), (+)-[5-methyl-3H]-PN200-110 (3H-PN200), and 3H-Nimodipine were bound to developing Swiss Webster mouse whole brain from postnatal days 3 to 24. 125I-omega-GVIA binding, thought to be presynaptic, showed a 50% increase between days 11 and 14. 3H-dihydropyridine binding, thought to be postsynaptic, showed spike patterns when measured developmentally. 3H-PN200 binding showed a > 150% increase between days 11 and 15. 3H-Nimodipine binding showed a > 100% increase between days 11 and 14. Depolarization-induced 45Ca fluxes also increased between days 8 and 16 by > 500%. The dramatic increases indicated by these binding data correspond to a critical period described by Himwich (Int. Rev. Neurobiol. 4, 117, 1962) between postnatal days 11 and 14 in Swiss Webster mice; during this critical period, dendrites exhibit rapid outgrowth, sensory modalities come on line, EEG patterns mature, and the cortex reaches adult proportions. We conclude from these data that the increase in VSCC activity parallels a critical period in the development of the central nervous system in Swiss Webster mice.

Animals↗
PubMedDate not supplied

Lead-impaired neurodevelopment. Mechanisms and threshold values in the rodent.

Mechanisms underlying the cognitive deficits arising from chronic low level lead exposure are viewed as a consequence of impaired neurodevelopmental events. These events are exemplified within the cerebellum which is formed completely after birth and, therefore, encompasses all major epochs of development. Further, the unique pharmacokinetic distribution of juvenile blood lead levels is developmentally regulated and can be correlated to the periods of impaired structuring and threshold values indicating no-effect levels established. Here, the endpoint value is related to lead-induced dysfunctioning of a morphoregulator--the neural cell adhesion molecule (NCAM). During final synaptic structuring its normal developmental sequence is perturbed when blood lead levels exceed 20 micrograms/dl. These events are similar, and compared to, those seen in the cerebellum of the staggerer mouse mutant (sg/sg) where the selection of circuits to be preserved from those transiently overproduced during development is impaired.

Animals↗