[Cortical plasticity and restoration of neurologic functions: an update on this topic].
BACKGROUND
Neuroplasticity is a natural property of the nervous system to change its function and to reorganize due to a lesion or environmental changes. We review some of the main experimental and clinical experiences on cortical sensorimotor plasticity related to central nervous system (CNS) lesions.


METHODS
In the last 10 years increasing interest in neuronal plasticity has been prompted by several important discoveries. Long term potentiation and depression have been described as basic synaptic mechanism mediating functional recovery after CNS lesions, modulated by the up-down regulation of inhibitory-excitatory activity related to GABA, acetylcholine and glutamate between other neurotransmitters. In humans there are evidences from functional reorganization in the affected hemisphere in patients with hemispheric lesions, and the activation of homologues areas in the contralateral healthy hemisphere. Significative changes in the topography of cortical somatosensory and motor maps have been demonstrated using non invasive mapping techniques as multichannel EEG, evoked potential, transcranial magnetic stimulation, functional magnetic resonance imaging and positron emission tomography. Axonal and dendritic sprouting take place in animal models of brain lesions; but effective neural regeneration in the CNS does not seem to be a plausible mechanism for functional restoring.


CONCLUSIONS
Plastic changes after CNS lesions make it possible the restoration of neurological functions in a high number of patients. It is important now to understand which changes are related to the clinical improvement of patients, and what might be done to promote or facilitate this changes and to inhibit maladaptive phenomena, for the design of rationale therapeutics strategies with modulatory influence on this process.
Gómez-Fernández
L
L
Laboratorio de EMG y EMT Centro Internacional de Restauración Neurológica, La Habana, Cuba. lazaro@neubas.sld.cu
D000671:Amputation, Surgical; D000818:Animals; D001930:Brain Injuries / Q000503:physiopathology / Q000534:rehabilitation; D002540:Cerebral Cortex / Q000187:drug effects / Q000293:injuries / Q000502:physiology*; D000882:Haplorhini; D006801:Humans; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology; D009044:Motor Cortex / Q000293:injuries / Q000502:physiology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D017933:Peripheral Nervous System / Q000502:physiology; D051381:Rats; D020521:Stroke / Q000503:physiopathology; D000071939:Stroke Rehabilitation