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 lateralization 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 behavioral results and functional MRI 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 labor across pathways, experience-dependent plasticity-related recovery) and provides an explanation for the bilateral yet asymmetric lateralization 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 behavioral performance and brain activation. The unified model is consistent with the degeneracy and variable neurodisplacement theories of language recovery, and adds computational insights to these hypotheses regarding the neural machinery underlying language processing and plasticity-related recovery following damage.

Highlights

  • Understanding the processes underlying normal, impaired, and recovered language performance has been a long-standing goal for cognitive and clinical neuroscience

  • We investigated whether damage to the left hidden layer in the model would be more likely to result in permanently impaired language performance compared to damage to the right

  • To tackle various key issues that appear to be contradictory in healthy and impaired language processing (Table 1), we developed a single, unified neurocomputational model of spoken language production with bilateral pathways

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Summary

Introduction

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 lateralization and recovery have been generated They have not been considered within a single, unified, and implemented computational framework, and the literatures on healthy participants and patients are largely separated. To formalize and test verbally described hypotheses, and 3) a framework that can bridge between different types of cognitive neuroscience data including language behavior, lesion locations, and task-related fMRI. This was the overarching aim of the current study. The long-standing literature on aphasia dates back to seminal 19th century studies [2,3,4] While these verbally described hypotheses advanced our understanding of language processing both theoretically and clinically, it is not clear how they work mechanistically, and they can be mutually incompatible. There is a pressing need to have an implemented neurocomputational model which can provide 1) a unified framework in which findings from healthy participants and aphasic patients can be accounted for, 2) a computationally instantiated framework

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