Abstract
Disturbance of neurologic function in disorders of the central nervous system is expressed as an altered activation pattern in functional networks used by specific tasks and can be studied by functional imaging modalities, e.g., positron emission tomography and functional magnetic resonance imaging. Language, a complex brain function, is based on the interplay of a distributed network in which partial functions are executed in various centers, the primary language areas. These areas are hierarchically organized and activated according to the complexity of the specific language task. The specialization of different centers and the lateralization of integrative functions into the dominant (usually left) hemisphere are achieved by collateral and transcallosal inhibition of secondary language areas that are not used normally for performance of a specific language task. Changes in the interaction within the functional network of language are important for the recovery from aphasia after stroke. In particular, studies of changes in the activation patterns during speech tasks have demonstrated that patients with favorable recovery predominantly activate structures in the ipsilateral hemisphere, but some activation was also seen in the right hemisphere. Increased activation within the right hemisphere may be a marker of failed or faulty recovery attempts in the sense of maladaptive plasticity or the breakdown of normal interhemispheric control within the distributed neural network. The role of activation in the right hemisphere for residual language performance can be investigated by combining repetitive transcranial magnetic stimulation (rTMS) with functional imaging [e.g., positron emission tomography (PET)]. These studies suggested a less effective compensatory potential of right-sided network areas. Overactivation of right language homologues may represent a maladaptive strategy by paradoxical functional facilitation as a result of decreased transcallosal inhibition attributable to damage of specialized and lateralized speech areas. Suppression of this paradoxical activation might therefore improve aphasic deficits.
Published Version
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