An Imaging-Guided Neural Model Explains Lexical Stress Alteration in Acquired Apraxia of Speech.

Acquired apraxia of speech (AOS) is a disorder of speech motor planning/programming that is induced by a lesion to the left anterior ventral precentral sulcus. This study analyses neuroimaging data from AOS in order to propose and computationally test a mechanistic explanation of how the lesion leads to the characteristic of altered lexical stress in the disorder. Neuroimaging data from 31 participants with left hemisphere stroke (15 AOS) were reanalysed to guide a 'lesioned' version of the bilateral GODIVA neuro-computational model of speech production. Structural MRI and resting-state functional MRI measurements were used to decide the model's lesion extent and atypical neural processing, respectively. The 'lesioned' model was compared with a neurotypical model on the production of an exemplar utterance with different linguistic contexts. Analyses revealed the average lesion in the AOS participants extended over 22.25% of the left anterior ventral precentral sulcus. Functional connectivity in AOS was reduced between the lateral part of that region and the right motor cortex, as well as between the left and right motor cortices themselves. The version of the model that we altered in line with these findings produced lengthening of the second of two consecutive short syllables. The lengthened syllable was a word-initial unstressed syllable, and consequently, its contrastiveness with the adjacent stressed syllable of the word was reduced. The agreement between simulation results and previously reported acoustic measurements from actual AOS patients lends support to our mechanistic explanation. In conclusion, simulations of the GODIVA model provided empirical support for a mechanistic explanation indicating permanent sub-threshold cortical activity in AOS. As a result, the speech system becomes biased away from a motor control strategy based on motor programs and toward a strategy based on sensory feedback. This both lengthens brief syllables and interferes with the mechanism to shift between syllables, ultimately altering lexical stress. Analysis of the model's neural dynamics suggests the explanation can be generalised to various contexts where lexical stress is altered in AOS.