Very low birth weight (VLBW) children are at high risk of perinatal white matter injury, which, when subtle, may not be seen using conventional magnetic resonance imaging. The relationship between clinical findings and fractional anisotropy (FA) measurements in white matter of adolescents born prematurely with VLBW was studied in 34 subjects (age = 15 years, birth weight =1500 g) and 47 age-matched controls born at term, who were examined both clinically and with diffusion tensor imaging (DTI). Perceptual and cognitive functions were evaluated by visual motor integration (VMI) with supplementary tests and sub-tests from WISC-III, motor function by movement ABC and Grooved Pegboard test and psychiatric symptoms by the schedule for affective disorders and schizophrenia for school-age children semistructured interview, the Autism Spectrum Screening Questionnaire and attention deficit hyperactivity disorder (ADHD) rating scale IV. Overall functioning was scored on the children's global assessment scale. DTI scans were performed for calculation of FA maps and areas of significant differences in mean FA values between subjects and controls were compared with their clinical data. The VLBW children had reduced FA values in the internal and external capsule, corpus callosum and superior, middle superior and inferior fasciculus. Within this group of children, visual motor and visual perceptual deficits were associated with low FA values in the external capsule, posterior part of the internal capsule and in the inferior fasciculus. Children with low IQ had low FA values in the external capsule and inferior and middle superior fasciculus. Fine motor impairment was related to low FA values in the internal and external capsule and superior fasciculus. Eight VLBW children with inattention symptoms or a diagnosis of ADHD had significantly lower FA values in several areas. Mild social deficits correlated with reduced FA values in the external capsule and superior fasciculus. We conclude that DTI was able to detect differences in FA between VLBW adolescents and controls in several white matter areas at risk of periventricular leucomalacia in VLBW newborns. Our results show that low FA values in these areas were associated with perceptual, cognitive, motor and mental health impairments. These conclusions indicate that perinatal injury of white matter tracts persist with clinical significance in adolescence.
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.here is a growing realization that events during development impact brain and cognition throughout the entire lifespan (1). For instance, the major portion of the relationship between cortical thickness and IQ in old age can be explained by childhood IQ (2), and genotype may explain a substantial part of the lifetime stability in intelligence (3). Effects of genes on the organization of the cortex have been shown in adults (4-6), but it is unknown whether and how regional differences in cortical development correspond to these regional genetic subdivisions.Although consensus has not been reached for the exact trajectories, cortical thickness as measured by MRI appears to decrease in childhood (7-12). The exact foundation for this thinning is not known, as MRI provides merely representations of the underlying neurobiology, and available histological data cannot with certainty be used to guide interpretations of MRI results. Although speculative, apparent thickness decrease may be grounded in factors such as synaptic pruning and intracortical myelination, although the link between established synaptic processes (13-15) and cortical thickness has not been empirically confirmed. After childhood, cortical thinning continues throughout the remainder of the lifespan, speculated to reflect neuronal shrinkage and reductions in number of spines and synapses (16), although sim...
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