RESUMO
Within the aphasia literature, it is common to link location of lesioned brain tissue to specific patterns of language impairment. This has provided valuable insight into the relationship between brain structure and function, but it does not capture important underlying alterations in function of regions that remain structurally intact. Research has demonstrated that in the chronic stage of aphasia, variable patterns of reduced cerebral blood flow (CBF; hypoperfusion) in structurally intact regions of the brain contribute to persisting language impairments. However, one consistent issue in this literature is a lack of clear consensus on how to define hypoperfusion, which may lead to over- or underestimation of tissue functionality. In the current study, we conducted an exploratory analysis in six individuals with chronic aphasia (>1 year post-onset) using perfusion imaging to (1) suggest a new, individualized metric for defining hypoperfusion; (2) identify the extent of hypoperfused tissue in perilesional bands; and (3) explore the relationship between hypoperfusion and language impairment. Results indicated that our individualized metric for defining hypoperfusion provided greater precision when identifying functionally impaired tissue and its effects on language function in chronic aphasia. These results have important implications for intervention approaches that target intact (or impaired) brain tissue.
RESUMO
In spoken language, audiovisual (AV) perception occurs when the visual modality influences encoding of acoustic features (e.g., phonetic representations) at the auditory cortex. We examined how visual speech (mouth movements) transforms phonetic representations, indexed by changes to the N1 auditory evoked potential (AEP). EEG was acquired while human subjects watched and listened to videos of a speaker uttering consonant vowel (CV) syllables, /ba/ and /wa/, presented in auditory-only or AV congruent or incongruent contexts or in a context in which the consonants were replaced by white noise (noise replaced). Subjects reported whether they heard "ba" or "wa." We hypothesized that the auditory N1 amplitude during illusory perception (caused by incongruent AV input, as in the McGurk illusion, or white noise-replaced consonants in CV utterances) should shift to reflect the auditory N1 characteristics of the phonemes conveyed visually (by mouth movements) as opposed to acoustically. Indeed, the N1 AEP became larger and occurred earlier when listeners experienced illusory "ba" (video /ba/, audio /wa/, heard as "ba") and vice versa when they experienced illusory "wa" (video /wa/, audio /ba/, heard as "wa"), mirroring the N1 AEP characteristics for /ba/ and /wa/ observed in natural acoustic situations (e.g., auditory-only setting). This visually mediated N1 behavior was also observed for noise-replaced CVs. Taken together, the findings suggest that information relayed by the visual modality modifies phonetic representations at the auditory cortex and that similar neural mechanisms support the McGurk illusion and visually mediated phonemic restoration. NEW & NOTEWORTHY Using a variant of the McGurk illusion experimental design (using the syllables /ba/ and /wa/), we demonstrate that lipreading influences phonetic encoding at the auditory cortex. We show that the N1 auditory evoked potential morphology shifts to resemble the N1 morphology of the syllable conveyed visually. We also show similar N1 shifts when the consonants are replaced by white noise, suggesting that the McGurk illusion and the visually mediated phonemic restoration rely on common mechanisms.
