Simulating single word processing in the classic aphasia syndromes based on the Wernicke–Lichtheim–Geschwind theory

Abstract

The Wernicke–Lichtheim–Geschwind (WLG) theory of the neurobiological basis of language is of great historical importance, and it continues to exert a substantial influence on most contemporary theories of language in spite of its widely recognized limitations. Here, we suggest that neurobiologically grounded computational models based on the WLG theory can provide a deeper understanding of which of its features are plausible and where the theory fails. As a first step in this direction, we created a model of the interconnected left and right neocortical areas that are most relevant to the WLG theory, and used it to study visual-confrontation naming, auditory repetition, and auditory comprehension performance. No specific functionality is assigned a priori to model cortical regions, other than that implicitly present due to their locations in the cortical network and a higher learning rate in left hemisphere regions. Following learning, the model successfully simulates confrontation naming and word repetition, and acquires a unique internal representation in parietal regions for each named object. Simulated lesions to the language-dominant cortical regions produce patterns of single word processing impairment reminiscent of those postulated historically in the classic aphasia syndromes. These results indicate that WLG theory, instantiated as a simple interconnected network of model neocortical regions familiar to any neuropsychologist/neurologist, captures several fundamental “low-level” aspects of neurobiological word processing and their impairment in aphasia.