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Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans
Published on: December 18, 2016
Structural and functional brain rewiring clarifies preserved interhemispheric transfer in humans born without the
Fernanda Tovar-Moll1, Myriam Monteiro2, Juliana Andrade2
1D'Or Institute for Research and Education (IDOR), 22281-032, Rio de Janeiro, Brazil;Institute of Biomedical Sciences (ICB) andNational Institute for Translational Neuroscience (INNT), Ministry of Science and Technology, Brazil;National Center of Structural Biology and Bioimaging (CENABIO), Federal University of Rio de Janeiro, 21941-902, Rio de Janeiro, Brazil; fernanda.tovarmoll@idor.org rlent@icb.ufrj.br.
Abstract:
Why do humans born without the corpus callosum, the major interhemispheric commissure, lack the disconnection syndrome classically described in callosotomized patients? This paradox was discovered by Nobel laureate Roger Sperry in 1968, and has remained unsolved since then. To tackle the hypothesis that alternative neural pathways could explain this puzzle, we investigated patients with callosal dysgenesis using structural and functional neuroimaging, as well as neuropsychological assessments. We identified two anomalous white-matter tracts by deterministic and probabilistic tractography, and provide supporting resting-state functional neuroimaging and neuropsychological evidence for their functional role in preserved interhemispheric transfer of complex tactile information, such as object recognition. These compensatory pathways connect the homotopic posterior parietal cortical areas (Brodmann areas 39 and surroundings) via the posterior and anterior commissures. We propose that anomalous brain circuitry of callosal dysgenesis is determined by long-distance plasticity, a set of hardware changes occurring in the developing brain after pathological interference. So far unknown, these pathological changes somehow divert growing axons away from the dorsal midline, creating alternative tracts through the ventral forebrain and the dorsal midbrain midline, with partial compensatory effects to the interhemispheric transfer of cortical function.
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