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.
