This study investigates the morphometry of Heschl’s gyrus and its included primary auditory cortex (PAC) in hearing impaired (HI) and normal hearing (NH) infants. Fourty-two infants, age 8–19 months, with NH (n = 26) or hearing impairment (n = 16) were studied using high-resolution 3D magnetic resonance imaging. Gray matter (GM) and white matter (WM) volumes were obtained using software for automatic brain imaging segmentation to estimate the volume of each tissue within manually defined regions for the anterior portion of Heschl’s gyrus (aHG) in each individual subject, transformed to an infant brain template space. Interactions among group (HI, NH), tissue type (GM, WM), and hemisphere (left, right) were examined using analysis of variance. Whole-brain voxel-based morphometry was utilized to explore volume differences between groups across the entire brain. The HI group showed increased GM and decreased WM in aHG compared with the NH group; likely effects of auditory deprivation. The HI group did not exhibit their typical L > R asymmetry pattern that the NH group showed. Increased GM in aHG in HI infants may represent abnormal cortical development in PAC as seen in animal models of sensory deprivation. Lower WM volume is consistent with studies with deaf adults.
from Cerebral Cortex
Conclusion: Although our effect sizes were small, breastfeeding for four months or longer was associated with improved developmental outcomes for children aged one to three years after adjustment for multiple confounding factors.
from Acta Paediatrica
Pleiotropic Effects of the 11p13 locus on Developmental Verbal Dyspraxia and EEG Centrotemporal Sharp Waves
We recently demonstrated genomewide linkage of centrotemporal sharp waves (CTS) in classic Rolandic epilepsy (RE) families to chromosome 11p13, and fine-mapped this locus to variants in the ELP4 gene. Speech sound disorder (SSD) is a common comorbidity in RE subjects, of unknown etiology, which co-aggregates in family members in a manner that could hypothetically be explained by shared underlying genetic risk with CTS. Furthermore, the neural mechanism of SSD is unknown, although individuals with rare, Mendelian forms of RE are described with severe verbal and oromotor apraxia. We therefore first performed genome-wide linkage analysis for SSD, operationally defined as clinical history consistent with ICD-10 speech articulation disorder, in 38 families singly ascertained through a proband with RE. We tested the hypothesis of shared genetic risk with CTS at the 11p13 locus. In the second part of the study we used computerized acoustic analysis of recorded speech to test the hypothesis of dyspraxia as a mechanism for SSD in a smaller subset of RE probands and relatives. In two-point and multipoint lodscore analysis, we found that evidence for linkage to the 11p13 locus increased substantially when the phenotype was broadened from CTS to CTS/SSD. In multipoint analysis, the LOD score rose by 3.2 to HLOD 7.54 at D11S914 for CTS/SSD, the same marker at which multipoint linkage maximized for CTS alone. Non-parametric, affected-only methods in a sub-set of the data provide further confirmatory evidence for pleiotropy. In acoustic analysis there were voice-onset time abnormalities in 10/18 RE probands, 8/16 siblings and 5/15 parents, providing evidence of breakdown in the spatial/temporal properties of speech articulation consistent with a dyspraxic mechanism. The results from genetic and physiological studies suggest a pleiotropic role for the 11p13 locus in the development of both speech sound disorder and CTS, and also indicate a dyspraxic mechanism for the speech sound disorder linked to 11p13. Taken together, these data strongly support a neurodevelopmental origin for classic RE.
Validation of Rapid Neurodevelopmental Assessment Instrument for Under-Two-Year-Old Children in Bangladesh
The RNDA can be used by professionals from a range of backgrounds with high reliability and validity for determining functional status of children who are younger than 2 years. The study findings have important practical implications for early identification and intervention to mitigate neurodevelopmental impairments in large populations that live in developing countries where professional expertise is sparse.
BACKGROUND. Infancy is a critical period for brain development. Few studies have examined the extent to which infant weight gain is associated with later neurodevelopmental outcomes in healthy populations.
OBJECTIVE. The purpose of this work was to examine associations of infant weight gain from birth to 6 months with child cognitive and visual-motor skills at 3 years of age.
PATIENTS AND METHODS. We studied 872 participants in Project Viva, an ongoing prospective, longitudinal, prebirth cohort. We abstracted birth weight from the medical chart and weighed infants at 6 months of age. We used the 2000 Centers for Disease Control and Prevention growth charts to derive weight-for-age z scores. Our primary predictor was infant weight gain, defined as the weight-for-age z score at 6 months adjusted for the weight-for-age z score at birth. At 3 years of age, we measured child cognition with the Peabody Picture Vocabulary Test III and visual-motor skills with the Wide Range Assessment of Visual Motor Abilities.
RESULTS. Mean Peabody Picture Vocabulary Test III score was 104.2, and mean Wide Range Assessment of Visual Motor Abilities test score was 102.8. Mean birth weight z score was 0.21, and mean 6-month weight z score was 0.39. In multiple linear regression adjusted for child age, gender, gestational age, breastfeeding duration, primary language, and race/ethnicity; maternal age, parity, smoking status, and cognition; and parental education and income level, we found no association of infant weight gain with child Peabody Picture Vocabulary Test III score (–0.4 points per z score weight gain increment, 95% confidence interval –1.3, 0.6) or total Wide Range Assessment of Visual Motor Abilities standard score (–0.4 points, 95% confidence interval –1.2, 0.5).
CONCLUSIONS. Slower infant weight gain was not associated with poorer neurodevelopmental outcomes in healthy, term-born 3-year-old children. These results should aid in determining optimal growth patterns in infants to balance risks and benefits of health outcomes through the life course.
from Pediatric Neurology
We used brainstem auditory-evoked responses and neurodevelopmental assessment to detect abnormalities and correlations between such responses and neurodevelopmental outcomes in 78 children (aged 4-12 years) who survived perinatal asphyxia. Twenty children had brainstem auditory-evoked response abnormalities, including increased threshold, reduced wave V amplitude, decreased V/I amplitude ratio, and prolonged I-V interval. Thirty-seven exhibited neurodevelopmental deficits, including cerebral palsy and developmental delay. The remaining 41 exhibited no deficits. Brainstem auditory-evoked response abnormalities were evident in 15 of 37 (40.5%) children with neurodevelopmental deficits, but in only 5 of 41 (12.2%) with no deficits, which differed significantly (χ2 = 8.2, P < 0.05). The sensitivity, specificity, positive predictive value, and false-negative rate of brainstem auditory-evoked responses to reflect neurodevelopmental outcomes were 40.5%, 87.8%, 75.0%, and 59.5%, respectively. These findings suggest that in children who survive perinatal asphyxia, brainstem auditory impairment occurs more frequently in those with versus those without neurodevelopmental deficits. Brainstem auditory-evoked responses display a moderate correlation with clinically determined neurodevelopmental outcomes. Despite limitations, brainstem auditory-evoked response is valuable for assessing auditory and neurodevelopmental outcomes after perinatal asphyxia.