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Abstract

Copyright 2002 J.A. Barth Verlag in Georg Thieme Verlag KG

Disturbance of neurologic function in disorders of the central nervous system is expressed as altered activation pattern in functional networks after specific tasks, and can be studied by functional imaging modalities, e.g. positron emission tomography (PET). Language, a complex brain function is based on the interplay of a distributed network in which partial functions are executed in various centers and tasks are hierarchically organized according to their complexity. The specialization of different centers and the lateralization of integrative functions into the dominant (usually left) hemisphere is achieved by collateral and transcallosal inhibition of structures of lower order in the network. Patients with ischemic stroke often suffer from aphasia; the features and the prognosis of this disturbance is determined by the localization and the extent of the infarct in the dominant hemisphere. The preservation of the left superior temporal gyrus or its functional reintegration, respectively, is of utmost importance for the recovery of the deficits and for a satisfactory outcome. Reactivation of this region in repeated PET-activation studies were related to a favorable outcome, activation of other eloquent regions or of contralateral areas were accompanied by some improvements, but never indicated recovery of sufficient speech production. Symptoms develop slowly in patients with tumors in the left hemisphere, and the functional network can adapt to the lesion. In these patients a dislocation of areas activated during language tasks was observed, either to ipsilateral regions usually not involved or to contralateral homotopic areas. Aphasia was frequent in cases with activation shift to the subdominant hemisphere, and the right over left asymmetry in activation of the cerebellum was correlated to the severity of language impairment. The shift of dominance in activation could be reversed after surgical resection of the tumor leading to improved speech performance. The patterns of intrahemispheric as well as interhemispheric compensation may be explained by reduction of collateral inhibition of specific centers on other structures within the network (disinhibition): circumscript and/or slowly developing lesions disinhibit surrounding areas leading to increases and to displacements of activated centers; large morphological defects reduce the transcallosal inhibition leading to the activation of contralateral regions.