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Background Magnetic resonance imaging in fetal alcohol spectrum disorder (FASD) children showed altered connectivity, suggesting underlying deficits in networks, which may be related to cognitive outcome. Functional connectivity has been of interest in neurophysiological research with quantitative electroencephalography (QEEG) as useful tool for measuring pathology, not detectable by normal EEG. The aim of this study was to investigate differences in the EEG interhemispheric coherence (ICoh) in children diagnosed with FASD compared with healthy controls and to relate the results to cognitive scores. Method Analysis of ICoh in 81 FASD children (4-Digit Code) compared with 31 controls. The children underwent cognitive assessment, and EEG was performed and used for analysis. Group comparisons and analysis of covariance interaction models were used to test for differences between FASD and controls but also to look for differences between FASD subgroups. Significant findings were correlated to cognitive scores. Results Lower ICoh was found in the frontal and temporal derivations in the FASD group. When comparing FASD subgroups, children with fetal alcohol syndrome had lower ICoh occipital. Reduced ICoh in the temporal alpha band was correlated with lower performance IQ in the FASD group. Conclusion Our findings could imply hypoconnectivity between the hemispheres with impact on cognition. We suggest that EEG coherence analysis could be a sensitive parameter in the detection of electrophysiological abnormalities in FASD with possible clinical relevance. These results may indicate that QEEG could be used as biomarker for FASD. However, further research is needed to determine the role of QEEG analysis in the diagnosis of FASD. [ABSTRACT FROM AUTHOR]

Purpose: To assess various aspects of visual function in school children prenatally exposed to opioid maintenance therapy (OMT) and to explore possible outcome differences between prenatal methadone and buprenorphine exposure. Methods: In a cross‐sectional case–control study, 63 children aged 5–13 years with prenatal OMT exposure were compared with 63 age‐ and gender‐matched, non‐exposed controls regarding important visual parameters, such as visual acuity, orthoptic status, refractive state, colour vision, and visual field. Results: The OMT‐exposed children had significantly poorer visual acuity, both for the best eye, the worst eye and binocularly. Two children had mild visual impairment. Manifest strabismus was more frequent in the OMT group, 30%, vs. 4.8% in the control group. The most frequent types of strabismus were accommodative esotropia and intermittent exotropia. Manifest nystagmus was present in 10 (16%) of the exposed children compared to one among the non‐exposed children. The accommodative amplitude was decreased in the OMT group compared to the controls. After adjusting for polydrug exposure and SGA (small‐for‐gestational‐age), the between‐group differences in visual acuity, strabismus, and nystagmus remained. The methadone‐exposed children had poorer visual acuity, increased frequency of strabismus and a higher percentage of nystagmus, hypermetropia and astigmatism compared to the buprenorphine‐exposed children. Conclusions: School‐age children exposed to methadone or buprenorphine in utero had a higher prevalence of strabismus and nystagmus, and a lower visual acuity and accommodation amplitude. Buprenorphine exposure was associated with more favourable results than methadone exposure on most visual outcome measures and should be the preferred substance in OMT. [ABSTRACT FROM AUTHOR]

Neurodevelopmental origins of functional variation in older age are increasingly being acknowledged, but identification of how early factors impact human brain and cognition throughout life has remained challenging. Much focus has been on age-specific mechanisms affecting neural foundations of cognition and their change. In contrast to this approach, we tested whether cerebral correlates of general cognitive ability (GCA) in development could be extended to the rest of the lifespan, and whether early factors traceable to prenatal stages, such as birth weight and parental education, may exert continuous influences. We measured the area of the cerebral cortex in a longitudinal sample of 974 individuals aged 4-88 y (1,633 observations). An extensive cortical region was identified wherein area related positively to GCA in development. By tracking area of the cortical region identified in the child sample throughout the lifespan, we showed that the cortical change trajectories of higher and lower GCA groups were parallel through life, suggesting continued influences of early life factors. Birth weight and parental education obtained from the Norwegian Mother-Child Cohort study were identified as such early factors of possible life-long influence. Support for a genetic component was obtained in a separate twin sample (Vietnam Era Twin Study of Aging), but birth weight in the child sample had an effect on cortical area also when controlling for possible genetic differences in terms of parental height. Our results provide novel evidence for stability in brain-cognition relationships throughout life, and indicate that early life factors impact brain and cognition for the entire life course.

There is a growing realization that early life influences have lasting impact on brain function and structure. Recent research has demonstrated that genetic relationships in adults can be used to parcellate the cortex into regions of maximal shared genetic influence, and a major hypothesis is that genetically programmed neurodevelopmental events cause a lasting impact on the organization of the cerebral cortex observable decades later. Here we tested how developmental and lifespan changes in cortical thickness fit the underlying genetic organizational principles of cortical thickness in a longitudinal sample of 974 participants between 4.1 and 88.5 y of age with a total of 1,633 scans, including 773 scans from children below 12 y. Genetic clustering of cortical thickness was based on an independent dataset of 406 adult twins. Developmental and adult age-related changes in cortical thickness followed closely the genetic organization of the cerebral cortex, with change rates varying as a function of genetic similarity between regions. Cortical regions with overlapping genetic architecture showed correlated developmental and adult age change trajectories and vice versa for regions with low genetic overlap. Thus, effects of genes on regional variations in cortical thickness in middle age can be traced to regional differences in neurodevelopmental change rates and extrapolated to further adult aging-related cortical thinning. This finding suggests that genetic factors contribute to cortical changes through life and calls for a lifespan perspective in research aimed at identifying the genetic and environmental determinants of cortical development and aging.

ImportanceThe very early postnatal period witnesses extraordinary rates of growth, but structural brain development in this period has largely not been explored longitudinally. Such assessment may be key in detecting and treating the earliest signs of neurodevelopmental disorders.ObjectiveTo assess structural growth trajectories and rates of change in the whole brain and regions of interest in infants during the first 3 months after birth.Design, setting, and participantsSerial structural T1-weighted and/or T2-weighted magnetic resonance images were obtained for 211 time points from 87 healthy term-born or term-equivalent preterm-born infants, aged 2 to 90 days, between October 5, 2007, and June 12, 2013.Main outcomes and measuresWe segmented whole-brain and multiple subcortical regions of interest using a novel application of Bayesian-based methods. We modeled growth and rate of growth trajectories nonparametrically and assessed left-right asymmetries and sexual dimorphisms.ResultsWhole-brain volume at birth was approximately one-third of healthy elderly brain volume, and did not differ significantly between male and female infants (347 388 mm3 and 335 509 mm3, respectively, P = .12). The growth rate was approximately 1%/d, slowing to 0.4%/d by the end of the first 3 months, when the brain reached just more than half of elderly adult brain volume. Overall growth in the first 90 days was 64%. There was a significant age-by-sex effect leading to widening separation in brain sizes with age between male and female infants (with male infants growing faster than females by 200.4 mm3/d, SE = 67.2, P = .003). Longer gestation was associated with larger brain size (2215 mm3/d, SE = 284, P = 4×10-13). The expected brain size of an infant born one week earlier than average was 5% smaller than average; at 90 days it will not have caught up, being 2% smaller than average. The cerebellum grew at the highest rate, more than doubling in 90 days, and the hippocampus grew at the slowest rate, increasing by 47% in 90 days. There was left-right asymmetry in multiple regions of interest, particularly the lateral ventricles where the left was larger than the right by 462 mm3 on average (approximately 5% of lateral ventricular volume at 2 months). We calculated volume-by-age percentile plots for assessing individual development.Conclusions and relevanceNormative trajectories for early postnatal brain structural development can be determined from magnetic resonance imaging and could be used to improve the detection of deviant maturational patterns indicative of neurodevelopmental disorders.

Background: Fetal alcohol spectrum disorder (FASD) comprises a combination of developmental, cognitive, and behavioral disabilities that occur in children exposed to alcohol prenatally. A higher prevalence of epilepsy and pathological electroencephalographic (EEG) features have also been reported in individuals with FASD. We examined the frequency of epilepsy, pathological EEG findings, and their implications for cognitive and adaptive functioning in children with FASD. Methods: We conducted a cross‐sectional study of 148 children with FASD who underwent a multidisciplinary assessment and a 120‐min EEG recording. Group comparisons and regression analyses were performed to test the associations between epilepsy and pathological EEG findings, FASD subgroups and neurocognitive test results and adaptive functioning. Results: The frequency of epilepsy was 6%, which compares with 0.7% in Norway overall. Seventeen percent of children without epilepsy had pathological EEG findings. Attention‐deficit hyperactivity disorder (ADHD) was diagnosed in 64% of the children. Children with epilepsy and/or pathological EEG findings had comparable cognitive and adaptive scores to those with normal EEG. However, children with frontal EEG pathology (without epilepsy) had significantly lower scores on the IQ indices Processing speed and Working memory than FASD children without such findings, irrespective of ADHD comorbidity. Conclusions: There was a greater prevalence of epilepsy among children with FASD than in the general Norwegian population. A greater frequency of EEG pathology was also evident in children without epilepsy, across all FASD subgroups. Irrespective of epilepsy, ADHD comorbidity, and FASD subgroup, children with frontal EEG pathology, despite having a normal total IQ, showed significantly slower processing speed and poorer working memory, which may indicate specific executive function deficits that could affect learning and adaptive functioning. [ABSTRACT FROM AUTHOR]

In children with cerebral palsy (CP), learning disabilities are well documented, and impairments in executive functions, such as attention, inhibition, shifting and working memory, represent significant burdens on patients, their families and the society. The aim of this study was to evaluate whether Cogmed RM working memory training could improve working memory in children with CP and investigate whether increased working memory capacity would generalize to other cognitive functions. Twenty-eight children completed the training and the results were compared to a waitlist control group (n = 32). The results yielded three main findings. First, children with CP improved with practice on trained working memory tasks. Second, the intervention group showed minimal near transfer effects to non-trained working memory tasks. Third, no effects on cognitive and behavioral far transfer measures were found. [ABSTRACT FROM AUTHOR]

Aim: The aim of this study was to assess cognitive function at the age of 19 years in individuals of very low birthweight (VLBW; less than or equal to 1500g) and in term-born comparison individuals. Method: In this hospital-based follow-up study, 55 VLBW participants (30 males, 25 females; mean birthweight 1217g, SD 233g; mean gestational age 29.1wks, SD 2.5wks) and 81 comparison individuals (42 males, 39 females; mean birthweight 3707g, SD 433g; mean gestational age 39.7wks, SD 1.2wks) were examined with a standardized IQ test (Wechsler Adult Intelligence Scale III) to assess general cognitive ability. Results: Over half (53%) of the VLBW participants achieved a low IQ score (defined as greater than 1SD below the mean in the comparison group; odds ratio 6.4 vs comparison individuals; 95% confidence interval 2.8-14.4; p less than 0.001). None of the VLBW group, compared with 22% of the comparison individuals, achieved a high IQ score (greater than 1SD above the comparison mean). VLBW participants scored lower than comparison individuals on full, verbal, and performance IQ, as well as on all four indices (p less than or equal to 0.001). The subtest profile indicated problems on all subtests, but especially on those related to arithmetic and visual-perceptual tasks. Interpretations: Few studies have undertaken a comprehensive assessment of general cognitive outcome (IQ) among young adults of VLBW. Our results indicate that VLBW seems to have a global and lasting impact on cognitive ability. Full-scale IQ assessment may reveal important learning problems in young adults of VLBW, and should be performed to inform appropriate assistance to enhance academic achievement and the chances of permanent employment as adults.