Language networks in aphasia and health: A 1000 participant activation likelihood estimation meta-analysis

Aphasia recovery post-stroke is classically and most commonly hypothesised to rely on regions that were not involved in language premorbidly, through 'neurocomputational invasion' or engagement of 'quiescent homologues'. Contemporary accounts have suggested, instead, that recovery might be supported by under-utilised areas of the premorbid language network, which are downregulated in health to save neural resources ('variable neurodisplacement'). Despite the importance of understanding the neural bases of language recovery clinically and theoretically, there is no consensus as to which specific regions are more likely to be activated in post-stroke aphasia (PSA) than healthy individuals. Accordingly, we performed an Activation Likelihood Estimation (ALE) meta-analysis of language functional neuroimaging studies in PSA. We obtained coordinate-based functional neuroimaging data for 481 individuals with aphasia following left-hemisphere stroke and 530 linked controls from 33 studies that met predefined inclusion criteria. ALE identified regions of consistent, above-chance spatial convergence of activation, as well as regions of significantly different activation likelihood, between participant groups and language tasks. Overall, these findings dispute the prevailing theory that aphasia recovery involves recruitment of novel right hemisphere territory into the language network post-stroke. Instead, multiple regions throughout both hemispheres were consistently activated during language tasks in both PSA and controls. Regions of the right anterior insula, frontal operculum and inferior frontal gyrus (IFG) pars opercularis were more likely to be activated across all language tasks in PSA than controls. Similar regions were more likely to be activated during higher than lower demand comprehension or production tasks, consistent with them representing enhanced utilisation of spare capacity within right hemisphere executive-control related regions. This provides novel evidence that 'variable neurodisplacement' underlies language network changes that occur post-stroke. Conversely, multiple undamaged regions were less likely to be activated across all language tasks in PSA than controls, including domain-general regions of medial superior frontal and paracingulate cortex, right IFG pars triangularis and temporal pole. These changes might represent functional diaschisis, and demonstrate that there is not global, undifferentiated upregulation of all domain-general neural resources during language in PSA. Such knowledge is essential if we are to design neurobiologically-informed therapeutic interventions to facilitate language recovery.