Cortical dysfunction subsequent to subcortical vascular lesions: An explanation for subcortical aphasia?

Abstract

In recent years a number of authors have documented the occurrence of aphasia following apparently subcortical lesions. The existence of so-called “subcortical aphasia,” however, remains controversial in that the mechanisms of subcortical involvement in language have not been elucidated. Although most contemporary authors appear to accept that subcortical lesions do result in language disorders, whether or not the aphasia following subcortical lesions is the direct result of subcortical damage is not certain. A number of alternative mechanisms have been proposed to explain the occurrence of language deficits following subcortical lesions. These include suggestions that the language problems are the result of factors such as the influence of mass and pressure effects, oedema etc. upon the cortex. Although these factors may exacerbate the language pathology in the acute stage, it is suggested that these mechanisms cannot explain the occurrence of long-term language disturbances often reported following subcortical lesions. Recent studies utilizing brain imaging techniques that assess the physiological functioning of brain tissue (e.g. positron emission tomography), have suggested that subcortical lesions may cause a number of distance effects upon the cortex. These distance effects include reduced cerebral blood flow and cortical hypometabolism. The present paper evaluates the importance of cortical distance effects in the production of subcortical aphasia syndromes and their implications for the development of models of cortical-subcortical interactions in language.