Expressive aphasia has most generally been considered to be a loss in expressive language function as the consequence of destruction or damage of the cerebral cortex. While there has been considerable agreement concerning the facts of brain damage, substantial disagreement has attended attempts to define the mechanisms by means of which cortical destruction results in a disruption of speech and language. Explanations of mechanism have ranged from extreme localization theories, in which specific cytoarchitectonic areas have been identified as the loci of various expressive language functions, to general functional theories, such as that of Goldstein,1 who argues in terms of the general reorganization of cortical properties and the modification of general psychological attributes.
In the course of working with a population of patients with expressive aphasia over a period of years, it appeared increasingly to us that too much attention had been devoted to the negative symptoms (i. e.,
BIRCH HG, LEE J. Cortical Inhibition in Expressive Aphasia. AMA Arch NeurPsych. 1955;74(5):514-517. doi:10.1001/archneurpsyc.1955.02330170048008