Browsing by Author "Lyytinen, Heikki"
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- Abnormal Auditory Cortical Activation in Dyslexia 100 msec after Speech Onset
School of Science | A1 Alkuperäisartikkeli tieteellisessä aikakauslehdessä(2002) Helenius, Päivi; Salmelin, Riitta; Richardson, Ulla; Leinonen, Seija; Lyytinen, HeikkiReading difficulties are associated with problems in processing and manipulating speech sounds. Dyslexic individuals seem to have, for instance, difficulties in perceiving the length and identity of consonants. Using magnetoencephalography (MEG), we characterized the spatio-temporal pattern of auditory cortical activation in dyslexia evoked by three types of natural bisyllabic pseudowords (/ata/, /atta/, and /a a/), complex nonspeech sound pairs (corresponding to /atta/ and /a a/) and simple 1-kHz tones. The most robust difference between dyslexic and non-reading-impaired adults was seen in the left supratemporal auditory cortex 100 msec after the onset of the vowel /a/. This N100m response was abnormally strong in dyslexic individuals. For the complex nonspeech sounds and tone, the N100m response amplitudes were similar in dyslexic and nonimpaired individuals. The responses evoked by syllable /ta/ of the pseudoword /atta/ also showed modest latency differences between the two subject groups. The responses evoked by the corresponding nonspeech sounds did not differ between the two subject groups. Further, when the initial formant transition, that is, the consonant, was removed from the syllable /ta/, the N100m latency was normal in dyslexic individuals. Thus, it appears that dyslexia is reflected as abnormal activation of the auditory cortex already 100 msec after speech onset, manifested as abnormal response strengths for natural speech and as delays for speech sounds containing rapid frequency transition. These differences between the dyslexic and nonimpaired individuals also imply that the N100m response codes stimulus-specific features likely to be critical for speech perception. Which features of speech (or nonspeech stimuli) are critical in eliciting the abnormally strong N100m response in dyslexic individuals should be resolved in future studies. - Cortical activation during spoken-word segmentation in nonreading-impaired and dyslexic adults
School of Science | A1 Alkuperäisartikkeli tieteellisessä aikakauslehdessä(2002) Helenius, Päivi; Salmelin, Riitta; Connolly, J. F.; Leinonen, Seija; Lyytinen, Heikki; Service, ElisabetWe used magnetoencephalography to elucidate the cortical activation associated with the segmentation of spoken words in nonreading-impaired and dyslexic adults. The subjects listened to binaurally presented sentences where the sentence-ending words were either semantically appropriate or inappropriate to the preceding sentence context. Half of the inappropriate final words shared two or three initial phonemes with the highly expected semantically appropriate words. Two temporally and functionally distinct response patterns were detected in the superior temporal lobe. The first response peaked at ∼100 msec in the supratemporal plane and showed no sensitivity to the semantic appropriateness of the final word. This presemantic N100m response was abnormally strong in the left hemisphere of dyslexic individuals. After the N100m response, the semantically inappropriate sentence-ending words evoked stronger activation than the expected endings in the superior temporal cortex in the vicinity of the auditory cortex. This N400m response was delayed for words starting with the same two or three first few phonemes as the expected words but only until the first evidence of acoustic–phonetic dissimilarity emerged. This subtle delay supports the notion of initial lexical access being based on phonemes or acoustic features. In dyslexic participants, this qualitative aspect of word processing appeared to be normal. However, for all words alike, the ascending slope of the semantic activation in the left hemisphere was delayed by ∼50 msec as compared with control subjects. The delay in the auditory N400m response in dyslexic subjects is likely to result from presemantic–phonological deficits possibly reflected in the abnormal N100m response.