Neocortical reorganization in spina bifida

Abstract

Normal brain development throughout childhood and adolescence is usually characterized by decreased cortical thickness in the frontal regions as well as region-specific patterns of increased white matter myelination and volume. We investigated total cerebral volumes, neocortical surface area, and neocortical thickness in 16 children with a neural tube defect, spina bifida myelomeningocele (SB), and 16 age-matched typically developing controls using a semi-automated, quantitative approach to MRI-based brain morphometry. The results revealed no significant group differences in total cerebral volume. However, group differences were observed in the global distribution of distinct tissue classes within the cerebrum: the SB group demonstrated a significant 15% reduction in total white matter and a 69% increase in cerebrospinal fluid, with no differences in total gray matter. Group comparisons of neocortical surface area assessments were significantly smaller in the occipital regions for SB, with no significant group differences in the frontal regions. Group comparisons of cortical thickness measurements demonstrated reduced cortical thickness in all regions except the frontal regions, where the SB group exhibited an increase relative to the PC group. Although regional patterns of thinning may be associated with the mechanical effects of hydrocephalus, the overall reduction in white matter and increased neocortical thickness in the frontal regions suggest that SB reflects a long term disruption of brain development that extends far beyond the neural tube defect in the first weeks of gestation.

Examination of Frontal and Parietal Tectocortical Attention Pathways in Spina Bifida Meningomyelocele Using Probabilistic Diffusion Tractography

“…Although earlier studies have demonstrated opposing findings of decreased FA in isolated frontal regions of interest within the genu of the corpus callosum, fornix, and cingulum in those with SBM (Herweh et al, 2009;Vachha et al, 2006), congenital malformations such as callosal hypogenesis along with the vulnerability of periventricular WM to structural insult after hydrocephalus may explain such decrements. Comparable FA along frontal WM pathways among the groups with SBM and TD individuals is supported by the preservation of anterior structural features in regions spared from the periventricular insults of hydrocephalus, such as preserved cortical thickness within the frontal lobes in SBM ( Juranek et al, 2008). Thus, results were congruent with earlier studies indicating preferential insult to posterior pathways in SBM while adding the new information that anterior WM is relatively intact.…”

Brain malformations in the sheep model of myelomeningocele are similar to those found in human disease: preliminary report

“…Recently, a radiological study, using quantitative MRI, has described an overall reduction in white matter and an increased neocortical thickness in the frontal regions of children with MMC [35]. Parietal, temporal and occipital cortical thinning have been observed in the non-corrected brains of our study; frontal regions seemed to be even more prominent than healthy brains, and parietal areas were particularly reduced, varying from mild thinning to virtual absence.…”

“…In terms of neurobehavioral outcomes relatively few children with MMC sustain severe mental retardation; weakness involves reading, spatial construction skills, attention, orientation and engagement, and behavioral regulation. Since cognitive skills involving language and word recognition are mediated by neuronal networks that involve the frontal regions, preservation of these skills may reflect the greater reliance on frontal components of these networks, as has already been described in humans by some radiological publications [14][15][16]35].…”

White and grey matter relations to simple, choice, and cognitive reaction time in spina bifida

“…Third, brain development in SBM is aberrant in a manner of particular interest to the study of WM and GM. In the course of development, cortical regions remain thick (Juranek et al 2008) rather than showing typical age-related thinning (O'Donnell et al 2005) resulting in a disproportionate reduction in WM as opposed to GM. Fourth, cortical regions are variously thick and thin depending on whether the measurement is cortical volume or cortical complexity/local gyrification (Juranek and Salman 2010).…”