In this section, we describe the processes involved in the restitution of function (requiring tissue survival) or of functional reorganization (in permanent brain damage) following brain lesions. These become obvious as the functional recovery mechanisms of relearning, within-system recovery, substitution by related systems, or assumption of new strategies take over.
In several experiments, increased and prolonged field potentials due to an increased NMDA/GABA ratio were found in the surrounding areas and these spread widely throughout areas connected to a focal brain lesion. It has been suggested that this hyperexcit-ability supports synaptic plasticity and reorganization by facilitating heterosynaptic long-term potentation (LTP), a mechanism also involved in learning.
An increasing number of neurotrophic factors have been found to be able to promote neuronal survival (protection against the late retrograde death of distant neurons) and sprouting, synapse formation (stabilization of LTP), glial proliferation and growth of new blood vessels. Reorganization of synaptic networks due to sprouting of new pre- and postsynaptic endings has been demonstrated in cases of regenerative axonal long-distance extension after injury. Even the possibility of induction of new neurons from precursor cells from the temporal lobe subventricular zone has been shown in in vitro experiments.
In studies of motor cortex lesions, a lesion-induced reduced reciprocal inhibition of pyramidal neurons that form interconnected patterns has been considered as a potential mechanism to increase the coupling strength between pyramidal cells in order to modify motor cortical output. Various studies concerning cortical neuronal plasticity demonstrated an enlargement of areas representing specific cortical functions directly adjacent to the lesion site.
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