Trent Nicol

Auditory Neurophysiologic Responses and Discrimination Deficits in Children with Learning Problems

Children with learning problems often cannot discriminate rapid acoustic changes that occur in speech. In this study of normal children and children with learning problems, impaired behavioral discrimination of a rapid speech change (/dα/versus/gα/) was correlated with diminished magnitude of an electrophysiologic measure that is not dependent on attention or a voluntary response. The ability of children with learning problems to discriminate another rapid speech change (/bα/versus/wα/) also was reflected in the neurophysiology. These results indicate that some childrens discrimination deficits originate in the auditory pathway before conscious perception and have implications for differential diagnosis and targeted therapeutic strategies for children with learning disabilities and attention disorders.

Central auditory system plasticity associated with speech discrimination training

A passively elicited cortical potential that reflects the brains discrimination of small acoustic contrasts was measured in response to two slightly different speech stimuli in adult human subjects. Behavioral training in the discrimination of those speech stimuli resulted in a significant change in the duration and magnitude of the cortical potential. The results demonstrate that listening training can change the neurophysiologic responses of the central auditory system to just-perceptible differences in speech.

Developmental changes in P1 and N1 central auditory responses elicited by consonant-vowel syllables.

Normal maturation and functioning of the central auditory system affects the development of speech perception and oral language capabilities. This study examined maturation of central auditory pathways as reflected by age-related changes in the P1/N1 components of the auditory evoked potential (AEP). A synthesized consonant-vowel syllable (ba) was used to elicit cortical AEPs in 86 normal children ranging in age from 6 to 15 years and ten normal adults. Distinct age-related changes were observed in the morphology of the AEP waveform. The adult response consists of a prominent negativity (N1) at about 100 ms, preceded by a smaller P1 component at about 50 ms. In contrast, the child response is characterized by a large P1 response at about 100 ms. This wave decreases significantly in latency and amplitude up to about 20 years of age. In children, P1 is followed by a broad negativity at about 200 ms which we term N1b. Many subjects (especially older children) also show an earlier negativity (N1a). Both N1a and N1b latencies decrease significantly with age. Amplitudes of N1a and N1b do not show significant age-related changes. All children have the N1b; however, the frequency of occurrence of N1a increases with age. Data indicate that the child P1 develops systematically into the adult response; however, the relationship of N1a and N1b to the adult N1 is unclear. These results indicate that maturational changes in the central auditory system are complex and extend well into the second decade of life.

Auditory training improves neural timing in the human brainstem

The auditory brainstem response reflects neural encoding of the acoustic characteristic of a speech syllable with remarkable precision. Some children with learning impairments demonstrate abnormalities in this preconscious measure of neural encoding especially in background noise. This study investigated whether auditory training targeted to remediate perceptually-based learning problems would alter the neural brainstem encoding of the acoustic sound structure of speech in such children. Nine subjects, clinically diagnosed with a language-based learning problem (e.g., dyslexia), worked with auditory perceptual training software. Prior to beginning and within three months after completing the training program, brainstem responses to the syllable /da/ were recorded in quiet and background noise. Subjects underwent additional auditory neurophysiological, perceptual, and cognitive testing. Ten control subjects, who did not participate in any remediation program, underwent the same battery of tests at time intervals equivalent to the trained subjects. Transient and sustained (frequency-following response) components of the brainstem response were evaluated. The primary pathway afferent volley -- neural events occurring earlier than 11 ms after stimulus onset -- did not demonstrate plasticity. However, quiet-to-noise inter-response correlations of the sustained response ( approximately 11-50 ms) increased significantly in the trained children, reflecting improved stimulus encoding precision, whereas control subjects did not exhibit this change. Thus, auditory training can alter the preconscious neural encoding of complex sounds by improving neural synchrony in the auditory brainstem. Additionally, several measures of brainstem response timing were related to changes in cortical physiology, as well as perceptual, academic, and cognitive measures from pre- to post-training.

Neural plasticity following auditory training in children with learning problems

OBJECTIVE This study examined the plasticity of the central auditory pathway and accompanying cognitive changes in children with learning problems. METHODS Children diagnosed with a learning disability and/or attention deficit disorder worked with commercial auditory processing training software for 8 weeks; control groups consisted of normal-learning and learning-impaired children who did not participate in any remedial programs. Auditory brainstem function was evaluated in response to click and speech stimuli in quiet; cortical responses to speech stimuli were obtained in quiet and noise. Academic achievement and cognitive abilities were assessed with standardized measures. RESULTS Compared to controls, the trained group improved on measures of auditory processing and exhibited changes in cortical responses in quiet and in noise. In quiet, cortical responses reflected an accelerated maturational pattern; in background noise, cortical responses became more resistant to degradation. Brainstem responses did not change with training. CONCLUSIONS Children with learning problems who practiced with auditory training software exhibited plasticity of neural encoding of speech sounds at the cortical, but not subcortical, level of the auditory pathway. This plasticity was accompanied by improvement in behavioral performance. SIGNIFICANCE This study demonstrates that in learning-impaired children working with commercial auditory processing training programs affects both the perception and the cortical representation of sound.

Right-Hemisphere Auditory Cortex Is Dominant for Coding Syllable Patterns in Speech

Cortical analysis of speech has long been considered the domain of left-hemisphere auditory areas. A recent hypothesis poses that cortical processing of acoustic signals, including speech, is mediated bilaterally based on the component rates inherent to the speech signal. In support of this hypothesis, previous studies have shown that slow temporal features (3–5 Hz) in nonspeech acoustic signals lateralize to right-hemisphere auditory areas, whereas rapid temporal features (20–50 Hz) lateralize to the left hemisphere. These results were obtained using nonspeech stimuli, and it is not known whether right-hemisphere auditory cortex is dominant for coding the slow temporal features in speech known as the speech envelope. Here we show strong right-hemisphere dominance for coding the speech envelope, which represents syllable patterns and is critical for normal speech perception. Right-hemisphere auditory cortex was 100% more accurate in following contours of the speech envelope and had a 33% larger response magnitude while following the envelope compared with the left hemisphere. Asymmetries were evident regardless of the ear of stimulation despite dominance of contralateral connections in ascending auditory pathways. Results provide evidence that the right hemisphere plays a specific and important role in speech processing and support the hypothesis that acoustic processing of speech involves the decomposition of the signal into constituent temporal features by rate-specialized neurons in right- and left-hemisphere auditory cortex.

Reading and Subcortical Auditory Function

Although it is largely agreed that phonological processing deficits are a major cause of poor reading, the neural origins of phonological processing are not well understood. We now show, for the first time, that phonological decoding, measured with a test of single-nonword reading, is significantly correlated with the timing of subcortical auditory processing and also, to a lesser extent, with the robustness of subcortical representation of the harmonic content of speech, but not with pitch encoding. The relationships we observe between reading and subcortical processing fall along a continuum, with poor readers at one end and good readers at the other. These data suggest that reading skill may depend on the integrity of subcortical auditory mechanisms and are consistent with the idea that subcortical representation of the acoustic features of speech may play a role in normal reading as well as in the development of reading disorders. These data establish a significant link between subcortical auditory function and reading, thereby contributing to the understanding of the biological bases of reading. At a more general level, these findings are among the first to establish a direct relationship between subcortical sensory function and a specific cognitive skill (reading). We argue that this relationship between cortical and subcortical function could be shaped during development by the corticofugal pathway and that this cortical-subcortical link could contribute to the phonological processing deficits experienced by poor readers.

Consequences of neural asynchrony: a case of auditory neuropathy.

AbstractAbstract The neural representation of sensory events depends upon neural synchrony. Auditory neuropathy, a disorder of stimulus-timing-related neural synchrony, provides a model for studying the role of synchrony in auditory perception. This article presents electrophysiological and behavioral data from a rare case of auditory neuropathy in a woman with normal hearing thresholds, making it possible to separate audibility from neuropathy. The experimental results, which encompass a wide range of auditory perceptual abilities and neurophysiologic responses to sound, provide new information linking neural synchrony with auditory perception. Findings illustrate that optimal eighth nerve and auditory brainstem synchrony do not appear to be essential for understanding speech in quiet listening situations. However, synchrony is critical for understanding speech in the presence of noise.

Brain stem response to speech: a biological marker of auditory processing.

The auditory brain stem response to speech mimics the acoustic characteristics of the speech signal with remarkable fidelity. This makes it possible to derive from it considerable theoretical and clinically applicable information relevant to auditory processing of complex stimuli. Years of research have led to the current characterization of these neural events with respect to the underlying acoustic information they reflect. The majority of data reviewed here originates from studies using a /da/ syllable to elicit the brain stem response, which consists of transient and periodic (frequency following) neural activity. We describe how the human auditory brain stem response separately encodes source and filter characteristics of the acoustic signal, which reflect paralinguistic and linguistic information simultaneously conveyed in speech. In normal-hearing individuals, these two classes of response components (source and filter) are highly correlated within a class but not between classes. This response dissociation becomes pronounced when stimuli are presented in background noise or with faster stimulus rates. In addition, some learning-impaired children show a selective deficiency in the neural encoding of acoustic features associated with the filter characteristics of speech. These children show no deficits in the encoding of source components, further supporting the notion of separate neural mechanisms. Overall, the auditory brain stem response to speech provides a way to access subcortical auditory processing mechanisms and may be used as a biological marker of deficient sound encoding associated with learning and auditory processing disorders.

Brainstem Timing: Implications for Cortical Processing and Literacy

The search for a unique biological marker of language-based learning disabilities has so far yielded inconclusive findings. Previous studies have shown a plethora of auditory processing deficits in learning disabilities at both the perceptual and physiological levels. In this study, we investigated the association among brainstem timing, cortical processing of stimulus differences, and literacy skills. To that end, brainstem timing and cortical sensitivity to acoustic change [mismatch negativity (MMN)] were measured in a group of children with learning disabilities and normal-learning children. The learning-disabled (LD) group was further divided into two subgroups with normal and abnormal brainstem timing. MMNs, literacy, and cognitive abilities were compared among the three groups. LD individuals with abnormal brainstem timing were more likely to show reduced processing of acoustic change at the cortical level compared with both normal-learning individuals and LD individuals with normal brainstem timing. This group was also characterized by a more severe form of learning disability manifested by poorer reading, listening comprehension, and general cognitive ability. We conclude that abnormal brainstem timing in learning disabilities is related to higher incidence of reduced cortical sensitivity to acoustic change and to deficient literacy skills. These findings suggest that abnormal brainstem timing may serve as a reliable marker of a subgroup of individuals with learning disabilities. They also suggest that faulty mechanisms of neural timing at the brainstem may be the biological basis of malfunction in this group.