Neural Reorganization versus Functional Compensation following Brain Lesions

Lesions of brain tissue cause important damage that is usually reflected in the loss of function. In some cases there is at least some recovery of the lost function, raising the question about the responsible underlying neural mechanisms. Combined neuroimaging (electroencephalography, magnetencephalography and functional magnetic resonance imaging) was used to study the neural mechanisms of preserved visual functions after posterior cerebral artery (PCA) stroke and of degraded motor function in amyotrophic lateral sclerosis (ALS). In the first case functional magnetic resonance imaging showed that motion stimuli presented to the hemianopic field of a patient produced activation in several extrastriate areas of the lesioned hemisphere. Magnetencephalographic recordings indicated that evoked activity occurred earlier in the higher-tier area V5 than in lower-tier areas suggesting that preserved vision for motion is mediated by subcortical pathways that bypass the primary visual cortex and that require neural reorganization in area V5. In ALS fMRI was employed to test the hypothesis that the limited resources in the motor cortex of the patients require the recruitment of additional motor-related areas resulting in a different pattern of hemodynamic activity compared to controls. Patients and controls executed a motor task that indeed elicited different patterns of hemodynamic activations in patients compared to controls. Importantly, the task was more difficult for patients than for controls. At equal difficulty the elicited hemodynamic patterns of the controls matched well those of the ALS patients, suggesting that the previously observed differences in hemodynamic activity between patients and controls were mainly caused by differences in difficulty. These results point out that ALS patients use the same resources as controls, arguing for the idea that functional compensation in ALS relies on existent resources and less on the development of new pathways or synapses as a consequence of the lesion.