Auditory and visual speech information are often strongly integrated resulting in perceptual enhancements for audiovisual (AV) speech over audio alone and sometimes yielding compelling illusory fusion percepts when AV cues are mismatched, the McGurk-MacDonald effect. Previous research has identified three candidate regions thought to be critical for AV speech integration: the posterior superior temporal sulcus (STS), early auditory cortex, and the posterior inferior frontal gyrus. We assess the causal involvement of these regions (and others) in the first large-scale (N = 100) lesion-based study of AV speech integration. Two primary findings emerged. First, behavioral performance and lesion maps for AV enhancement and illusory fusion measures indicate that classic metrics of AV speech integration are not necessarily measuring the same process. Second, lesions involving superior temporal auditory, lateral occipital visual, and multisensory zones in the STS are the most disruptive to AV speech integration. Further, when AV speech integration fails, the nature of the failure-auditory vs visual capture-can be predicted from the location of the lesions. These findings show that AV speech processing is supported by unimodal auditory and visual cortices as well as multimodal regions such as the STS at their boundary. Motor related frontal regions do not appear to play a role in AV speech integration.

Purpose To investigate the time-course of processing of lexical items in auditorily presented canonical (subject–verb–object) constructions in young, neurologically unimpaired control participants and participants with left-hemisphere damage and agrammatic aphasia. Method A cross modal picture priming (CMPP) paradigm was used to test 114 control participants and 8 participants with agrammatic aphasia for priming of a lexical item (direct object noun) immediately after it is initially encountered in the ongoing auditory stream and at 3 additional time points at 400-ms intervals. Results The control participants demonstrated immediate activation of the lexical item, followed by a rapid loss (decay). The participants with aphasia demonstrated delayed activation of the lexical item. Conclusion This evidence supports the hypothesis of a delay in lexical activation in people with agrammatic aphasia. The delay in lexical activation feeds syntactic processing too slowly, contributing to comprehension deficits in people with agrammatic aphasia.

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