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Neuropediatrics. 2017 Apr;48(2):66-71. doi: 10.1055/s-0037-1599234. Epub 2017 Mar 10.

Plasticity during Early Brain Development Is Determined by Ontogenetic Potential.

Author information

1
Department of Paediatric Neurology and Developmental Medicine, University Children's Hospital Tübingen, Tübingen, Germany.
2
Cognitive and Social Neuroscience Unit, Department of Biomedical Magnetic Resonance, Eberhard Karls University of Tuebingen, Tübingen, Germany.

Abstract

Two competing hypotheses address neuroplasticity during early brain development: the "Kennard principle" describes the compensatory capacities of the immature developing CNS as superior to those of the adult brain, whereas the "Hebb principle" argues that the young brain is especially sensitive to insults. We provide evidence that these principles are not mutually exclusive. Following early brain lesions that are unilateral, the brain can refer to homotopic areas of the healthy hemisphere. This potential for reorganization is unique to the young brain but available only when, during ontogenesis of brain development, these areas have been used for the functions addressed. With respect to motor function, ipsilateral motor tracts can be recruited, which are only available during early brain development. Language can be reorganized to the right after early left hemispheric lesions, as the representation of the language network is initially bilateral. However, even in these situations, compensatory capacities of the developing brain are found to have limitations, probably defined by early determinants. Thus, plasticity and adaptivity are seen only within ontogenetic potential; that is, axonal or cortical structures cannot be recruited beyond early developmental possibilities. The young brain is probably more sensitive and vulnerable to lesions when these are bilateral. This is shown here for bilateral periventricular white matter lesions that clearly have an impact on cortical architecture and function, thus probably interfering with early network building.

PMID:
28282668
DOI:
10.1055/s-0037-1599234
[Indexed for MEDLINE]

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