Neural entrainment to speech and nonspeech in dyslexia: Conceptual replication and extension of previous investigations.

Whether phonological deficits in developmental dyslexia are associated with impaired neural sampling of auditory information is still under debate. Previous findings suggested that dyslexic participants showed atypical neural entrainment to slow and/or fast temporal modulations in speech, which might affect prosodic/syllabic and phonemic processing respectively. However, the large methodological variations across these studies do not allow us to draw clear conclusions on the nature of the entrainment deficit in dyslexia. Using magnetoencephalography, we measured neural entrainment to nonspeech and speech in both groups. We first aimed to conceptually replicate previous studies on auditory entrainment in dyslexia, using the same measurement methods as in previous studies, and also using new measurement methods (cross-correlation analyses) to better characterize the synchronization between stimulus and brain response. We failed to observe any of the significant group differences that had previously been reported in delta, theta and gamma frequency bands, whether using speech or nonspeech stimuli. However, when analyzing amplitude cross-correlations between noise stimuli and brain responses, we found that control participants showed larger responses than dyslexic participants in the delta range in the right hemisphere and in the gamma range in the left hemisphere. Overall, our results are weakly consistent with the hypothesis that dyslexic individuals show an atypical entrainment to temporal modulations. Our attempt at replicating previously published results highlights the multiple weaknesses of this research area, particularly low statistical power due to small sample size, and the lack of methodological standards inducing considerable heterogeneity of measurement and analysis methods across studies.

Perceptual learning of acoustic noise by individuals with dyslexia.

PURPOSE: A phonological deficit is thought to affect most individuals with developmental dyslexia. The present study addresses whether the phonological deficit is caused by difficulties with perceptual learning of fine acoustic details. METHOD: A demanding test of nonverbal auditory memory, "noise learning," was administered to both adults with dyslexia and control adult participants. On each trial, listeners had to decide whether a stimulus was a 1-s noise token or 2 abutting presentations of the same 0.5-s noise token (repeated noise). Without the listener's knowledge, the exact same noise tokens were presented over many trials. An improved ability to perform the task for such "reference" noises reflects learning of their acoustic details. RESULTS: Listeners with dyslexia did not differ from controls in any aspect of the task, qualitatively or quantitatively. They required the same amount of training to achieve discrimination of repeated from nonrepeated noises, and they learned the reference noises as often and as rapidly as the control group. However, they did show all the hallmarks of dyslexia, including a well-characterized phonological deficit. CONCLUSION: The data did not support the hypothesis that deficits in basic auditory processing or nonverbal learning and memory are the cause of the phonological deficit in dyslexia.

Interhemispheric differences in auditory processing revealed by fMRI in awake rhesus monkeys.

Lesion studies in monkeys have suggested a modest left hemisphere dominance for processing species-specific vocalizations, the neural basis of which has thus far remained unclear. We used contrast agent-enhanced functional magnetic resonance imaging to map the regions of the rhesus monkey brain involved in processing conspecific vocalizations as well as human speech and emotional sounds. Control conditions included scrambled versions of all 3 stimuli and silence. Compared with silence, all stimuli activated widespread parts of the auditory cortex and subcortical auditory structures with a right hemispheric bias at the level of the auditory core. However, comparing intact with scrambled sounds revealed a leftward bias in the auditory belt and the parabelt. The left-sided dominance was stronger and more robust for human speech than for rhesus vocalizations and hence does not reflect conspecific call selectivity but rather the processing of complex spectrotemporal patterns, such as those present in human speech and in some of the rhesus monkey vocalizations. This was confirmed by regressing brain activity with a model-derived parameter indexing the prevalence of such patterns. Our results indicate that processing of vocal sounds in the lateral belt and parabelt is asymmetric in monkeys, as predicted from lesion studies.

Altered low-γ sampling in auditory cortex accounts for the three main facets of dyslexia.

It has recently been conjectured that dyslexia arises from abnormal auditory sampling. What sampling rate is altered and how it affects reading remains unclear. We hypothesized that by impairing phonemic parsing abnormal low-gamma sampling could yield phonemic representations of unusual format and disrupt phonological processing and verbal memory. Using magnetoencephalography and behavioral tests, we show in dyslexic subjects a reduced left-hemisphere bias for phonemic processing, reflected in less entrainment to ≈30 Hz acoustic modulations in left auditory cortex. This deficit correlates with measures of phonological processing and rapid naming. We further observed enhanced cortical entrainment at rates beyond 40 Hz in dyslexics and show that this particularity is associated with a verbal memory deficit. These data suggest that a single auditory anomaly, i.e., phonemic oversampling in left auditory cortex, accounts for three main facets of the linguistic deficit in dyslexia.

Optical brain imaging reveals general auditory and language-specific processing in early infant development.

This study uses near-infrared spectroscopy in young infants in order to elucidate the nature of functional cerebral processing for speech. Previous imaging studies of infants' speech perception revealed left-lateralized responses to native language. However, it is unclear if these activations were due to language per se rather than to some low-level acoustic correlate of spoken language. Here we compare native (L1) and non-native (L2) languages with 3 different nonspeech conditions including emotional voices, monkey calls, and phase scrambled sounds that provide more stringent controls. Hemodynamic responses to these stimuli were measured in the temporal areas of Japanese 4 month-olds. The results show clear left-lateralized responses to speech, prominently to L1, as opposed to various activation patterns in the nonspeech conditions. Furthermore, implementing a new analysis method designed for infants, we discovered a slower hemodynamic time course in awake infants. Our results are largely explained by signal-driven auditory processing. However, stronger activations to L1 than to L2 indicate a language-specific neural factor that modulates these responses. This study is the first to discover a significantly higher sensitivity to L1 in 4 month-olds and reveals a neural precursor of the functional specialization for the higher cognitive network.