A unified neurocomputational bilateral model of spoken language production in healthy participants and recovery in post-stroke aphasia

Abstract

Understanding the processes underlying normal, impaired and recovered language performance has been a long-standing goal for cognitive and clinical neuroscience. Many verbally-described hypotheses about language lateralisation and recovery have been generated. However, they have not been considered within a single, unified and implemented computational framework, and the literatures on healthy participants and patients are largely separated. These investigations also span different types of data, including behavioural results and fMRI brain activations, which augment the challenge for any unified theory. Consequently, many key issues, apparent contradictions and puzzles remain to be solved. We developed a neurocomputational, bilateral pathway model of spoken language production, designed to provide a unified framework to simulate different types of data from healthy participants and aphasic patients. The model encapsulates key computational principles (differential computational capacity, emergent division of labour across pathways, experience-dependent plasticity-related recovery) and provides an explanation for the bilateral yet asymmetric lateralisation of language in healthy participants, chronic aphasia after left rather than right hemisphere lesions, and the basis of partial recovery in patients. The model provides a formal basis for understanding the relationship between behavioural performance and brain activation. The unified model is consistent with the degeneracy and variable neuro-displacement theories of language recovery, and adds computational insights to these hypotheses regarding the neural machinery underlying language processing and plasticity-related recovery following damage. Significance StatementStudies of healthy and impaired language have generated many verbally-described hypotheses. Whilst these verbal descriptions have advanced our understanding of language processing, some explanations are mutually incompatible and it is unclear how they work mechanistically. We constructed a neurocomputational bilateral model of spoken language production to simulate a range of phenomena in healthy participants and patients with aphasia simultaneously, including language lateralisation, impaired performance after left but not right damage, and hemispheric involvement in plasticity-dependent recovery. The model demonstrates how seemly contradictory findings can be simulated within a single framework. To our knowledge, this provides the first coherent mechanistic account of language lateralisation and recovery from post-stroke aphasia.