Abstract
The human brain holds highly sophisticated compensatory mechanisms relying on neuroplasticity. Neuronal degeneracy, redundancy, and brain network organization make the human nervous system more robust and evolvable to continuously guarantee an optimal environmental-related homeostasis. Nevertheless, after injury, restitution processes appear dissimilar, depending on the pathology. Following a cerebrovascular accident, asymmetry, within- and across-network compensation and interhemispheric inhibition are key features to functional recovery. In moderate-to-severe stroke, neurological outcome is often poor, and little is known about the paths that enable either an efficient collaboration among hemispheres or, on the contrary, an antagonism of adaptative responses. In this review, we aim to decipher key issues of ipsilesional and contralesional hemispheric functioning allowing the foundations of effective neurorehabilitation strategies.
Highlights
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Data on stroke behavioral outcome are consistent with several features of asymmetrical plasticity. Those include the transient role of contralateral hemisphere in recovery of lateralized functions, the disparate recovery levels of highly lateralized functions such as language or motor function, and the reduced recovery of functions that are not typically highly lateralized [15]. It is not clear whether in this case the hindered compensation from the non-lesioned hemisphere is the consequence of the intrinsic characteristics of the involved circuits or concerns the asymmetry of receptors, dendritic spines, and molecular machinery involved in a specific functional output
Little is known on how the intact healthy human brain reshapes itself in response to a focal disturbance in the short- and long-term
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. One of the brain’s fundamental properties is the ability to adapt its processes to a wide range of complex external/internal modifications, including those generated by injury This inherent neural plasticity promotes efficient functional outputs in healthy individuals or, at least, some degree of functional outcome in disease. Drug discovery and development are seriously hindered by the incomplete understanding of the pathophysiology of neurological diseases and most of the pharmacological treatments target the symptoms instead of the cause of the disease [10,11] In this context, given the highly redundant configuration of the brain, compensatory mechanisms of neural networks potentially allow a variable degree of functional recovery. CVA neurorehabilitation might include a rational functional and structural approach relying mainly on the connectome and its dynamics In this context, affected, at-risk, and preserved networks should be identified and targeted with specific single and timedependent strategies after injury.
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