Rethinking the Mechanisms Underlying the McGurk Illusion

The McGurk illusion occurs when listeners hear an illusory percept (i.e., “da”), resulting from mismatched pairings of audiovisual (AV) speech stimuli (i.e., auditory/ba/paired with visual/ga/). Hearing a third percept—distinct from both the auditory and visual input—has been used as evidence of AV fusion. We examined whether the McGurk illusion is instead driven by visual dominance, whereby the third percept, e.g., “da,” represents a default percept for visemes with an ambiguous place of articulation (POA), like/ga/. Participants watched videos of a talker uttering various consonant vowels (CVs) with (AV) and without (V-only) audios of/ba/. Individuals transcribed the CV they saw (V-only) or heard (AV). In the V-only condition, individuals predominantly saw “da”/“ta” when viewing CVs with indiscernible POAs. Likewise, in the AV condition, upon perceiving an illusion, they predominantly heard “da”/“ta” for CVs with indiscernible POAs. The illusion was stronger in individuals who exhibited weak/ba/auditory encoding (examined using a control auditory-only task). In Experiment2, we attempted to replicate these findings using stimuli recorded from a different talker. The V-only results were not replicated, but again individuals predominately heard “da”/“ta”/“tha” as an illusory percept for various AV combinations, and the illusion was stronger in individuals who exhibited weak/ba/auditory encoding. These results demonstrate that when visual CVs with indiscernible POAs are paired with a weakly encoded auditory/ba/, listeners default to hearing “da”/“ta”/“tha”—thus, tempering the AV fusion account, and favoring a default mechanism triggered when both AV stimuli are ambiguous.

Identifying Neural Abnormalities in Schizophrenia

This chapter considers the use of magnetoencephalography (MEG) in understanding brain dysfunction in schizophrenia. Rather than provide a comprehensive review of the MEG schizophrenia literature, this chapter focuses on MEG brain measures that have received the most attention: resting-state studies and studies examining auditory encoding processes. Studies indicate that continued research in this area is of interest, with findings suggesting a focus on resting-state and task-related low-frequency activity.

Associations and Heritability of Auditory Encoding, Gray Matter, and Attention in Schizophrenia

Background Auditory encoding abnormalities, gray-matter loss, and cognitive deficits are all candidate schizophrenia (SZ) endophenotypes. This study evaluated associations between and heritability of auditory network attributes (function and structure) and attention in healthy controls (HC), SZ patients, and unaffected relatives (UR). Methods Whole-brain maps of M100 auditory activity from magnetoencephalography recordings, cortical thickness (CT), and a measure of attention were obtained from 70 HC, 69 SZ patients, and 35 UR. Heritability estimates (h2r) were obtained for M100, CT at each group-difference region, and the attention measure. Results SZ patients had weaker bilateral superior temporal gyrus (STG) M100 responses than HC and a weaker right frontal M100 response than UR. Abnormally large M100 responses in left superior frontal gyrus were observed in UR and SZ patients. SZ patients showed smaller CT in bilateral STG and right frontal regions. Interrelatedness between 3 putative SZ endophenotypes was demonstrated, although in the left STG the M100 and CT function−structure associations observed in HC and UR were absent in SZ patients. Heritability analyses also showed that right frontal M100 and bilateral STG CT measures are significantly heritable. Conclusions Present findings indicated that the 3 SZ endophenotypes examined are not isolated markers of pathology but instead are connected. The pattern of auditory encoding group differences and the pattern of brain function−structure associations differ as a function of brain region, indicating the need for regional specificity when studying these endophenotypes, and with the presence of left STG function−structure associations in HC and UR but not in SZ perhaps reflecting disease-associated damage to gray matter that disrupts function−structure relationships in SZ.