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Cortical activity of children with dyslexia during natural speech processing: evidence of auditory processing deficiency.

Children with dyslexia have difficulties with phonological processing. It is assumed that deficits in auditory temporal processing underlie the phonological difficulties of dyslectic subjects (i.e. the processing of rapid acoustic changes that occur in speech). In this study we assessed behavioral and electrophysiological evoked brain responses of dyslectic and skilled reading children while performing a set of hierarchically structured auditory tasks. Stimuli consisted of auditory natural unmodified speech that was controlled for the parameter of changing rate of main acoustic cues: vowels (slowly changing speech cues: /i/ versus /u/) and consonant-vowel (CV) syllables (rapidly changing speech cues: /da/ versus /ga/). Brain auditory processing differed significantly between groups: reaction time of dyslectic readers was prolonged in identifying speech stimuli and increased with increased phonological demand. Latencies of auditory evoked responses (auditory event related potentials [AERPs]) recorded during syllable identification of the dyslectic group were prolonged relative to those of skilled readers. Moreover, N1 amplitudes during vowel processing were larger for the dyslectic children and P3 amplitudes during CV processing were smaller for the dyslectic children. From the results of this study it is evident that the latency and amplitude of AERPs are sensitive measures of the complexity of phonological processing in skilled and dyslectic readers. These results may be signs of deficient auditory processing of natural speech under normal listening conditions as a contributing factor to reading difficulties in dyslexia. Detecting a dysfunction in the central auditory processing pathway might lead to early detection of children who may benefit from phonetic-acoustic training methods.

Acoustic Stimulation↗

Auditory processing disorders in adults and children: evaluation of a test battery.

A Dutch test battery comprising six different tests for auditory processing disorders was evaluated in a group of 49 adults and children (age 8-57 years) with auditory complaints despite normal audiometric thresholds. Percentile scores were derived from normal control groups (n = 132) to determine whether a subject passed or failed a test. A composite score was computed to reflect a general score on all the auditory processing tests. In order to gain insight into underlying auditory processes, factor analysis was performed. Normal scores on all the tests were seen in five subjects. The remaining 44 subjects had at least one test score that was below the cut-off point (10th percentile). Factor analysis provided evidence for a model comprising four auditory components: auditory sequencing, word recognition in noise, auditory closure, and auditory patterning. This model could be useful in the interpretation of scoring patterns. Although there were some differences in scoring patterns between the children and adults, the test battery proved to be useful in both groups.

Acoustic Stimulation↗

[Transforming and transmitting auditory information].

A mechanism of transforming and transmitting auditory information has been introduced taking into consideration the course of occurrences on molecular level in auditory cell itself. Physical energy of the sound wave is changed into bioelectric energy of the inside of the auditory cell owing to the generated electrochemical gradient. The change of the cell membrane potential which has been caused by the energy of the sound wave influences the change of the calcium level in the cell and at a further stage energetistic processes, enzymatic proteins activity and also it regulates the exocytosis of the mediator. The relationship between the generation of the transmitter and its secretion, and the stimulation of the auditory cell has been discussed. The role of afferent and efferent innervation in the generation of the fast and slow contraction of auditory cells has been noticed. Other phenomena accompanying the process of hearing have also been noticed. They are: Coding information, pre- and post-synaptic inhibition, facilitation of impulse transmission along nervous pathways, collateral inhibition, convergence and divergence. The mechanism of stimulating the receptors in the other senses has been described. A hypothesis has been put forward about the possibility of existence of a mechanism activating ionic canals of the cell membrane of auditory cells other than purely mechanical one connected with tip-links. The mechanism mentioned above may be based on inducing conformational changes of canal proteins, especially potassium canals, by the energy of the sound wave. There is a probability that there exist sound sensitive molecules in the ear as just as there exist light sensitive molecules in the organ of sight. The ability of basement membrane to transmit auditory information, especially on the verge of auditory threshold has been questioned.

Animals↗

Parvalbumin is expressed in a reciprocal circuit linking the medial geniculate body and auditory neocortex in the rabbit.

Recent studies of the rabbit auditory forebrain have shown that antibodies directed against the calcium-binding protein parvalbumin (PV) specifically demarcate auditory neocortex and the ventral division of the medial geniculate body (MGV). The auditory cortex is characterized by two PV- immunoreactive bands: dense terminal-like labeling within layer III/IV and a prominent band of PV+ somata in the upper half of layer VI. In some cases, there are distinct patches of PV immunoreactivity within layers III/IV of auditory cortex that appear similar to the patchy termination of thalamocortical axons labeled by the injection of anterograde tracers into MGV. The presence of PV+ patches in III/IV, PV+ somata in layer VI, and the high density of PV+ neurons and terminals in the MGV suggest the existence of a reciprocal PV+ circuit linking primary auditory cortex (AI) and the MGV. In the present study, double-labeling experiments in adult rabbits were carried out to provide evidence for this circuit. Focal injections of the tracers biocytin or biotinylated dextran amine (BDA) into the MGV labeled thalamocortical afferent patches within layer III/IV and retrogradely labeled corticothalamic neurons in layer VIa of the ipsilateral auditory cortex. Adjacent sections stained with antibodies against PV revealed terminal-like PV-immunoreactive patches in III/IV and PV+ somata in VIa that were in register with those labeled by BDA injections into the MGV. Serial section reconstruction of BDA-labeled corticothalamic neurons in VIa revealed pyramidal cells with tangentially oriented basal dendrites and sparsely branched apical dendrites that ascended to layer I. Fluorescent double-labeling studies demonstrated that a subpopulation of corticothalamic neurons also express PV. PV-negative corticothalamic neurons were also found. Discrete injections of BDA into auditory cortex labeled bands of neurons in the ipsilateral MGV, whose orientation paralleled the fibrodendritic laminae characteristic of this subdivision. Retrograde double-labeling experiments showed that most MGV relay neurons also express PV. Small numbers of PV-negative relay neurons were also found. These studies provide evidence for the existence of multiple, chemically coded pathways linking primary auditory cortex and the MGV.

Animals↗

Localization of two high-threshold potassium channel subunits in the rat central auditory system.

The firing pattern of auditory neurons is determined in part by the type of voltage-sensitive potassium channels expressed. The expression patterns for two high-threshold potassium channels, Kv3.1 and Kv3.3, that differ in inactivation properties were examined in the rat auditory system. The positive activation voltage and rapid deactivation kinetics of these channels provide rapid repolarization of action potentials with little effect on action potential threshold. In situ hybridization experiments showed that Kv3.3 mRNA was highly expressed in most auditory neurons in the rat brainstem, whereas Kv3.1 was expressed in a more limited population of auditory neurons. Notably, Kv3.1 mRNA was not expressed in neurons of the medial and lateral superior olive and a subpopulation of neurons in the ventral nucleus of the lateral lemniscus. These results suggest that Kv3.3 channels may be the dominant Kv3 subfamily member expressed in brainstem auditory neurons and that, in some auditory neurons, Kv3.1 and Kv3.3 may coassemble to form functional channels. The localization of Kv3.1 protein was examined immunohistochemically. The distribution of stained somata and neuropil varied across auditory nuclei and correlated with the distribution of Kv3.1 mRNA-expressing neurons and their terminal arborizations, respectively. The intensity of Kv3.1 immunoreactivity varied across the tonotopic map in the medial nucleus of the trapezoid body with neurons responding best to high-frequency tones most intensely labeled. Thus, auditory neurons may vary the types and amount of K(+) channel expression in response to synaptic input to subtly tune their firing properties.

Animals↗

Connections of the auditory midbrain in a teleost fish, Cyprinus carpio.

Central auditory pathways were traced in Japanese carp, Cyprinus carpio, using electrophysiological mapping and HRP tract-tracing methods. Multiunit recordings made from the carp torus semicircularis, the major midbrain area for processing octavolateralis information, revealed a mediolateral segregation of auditory and lateral line sensory modalities. Iontophoretic injections of HRP were made into the medial torus to trace afferent and efferent projections of the carp auditory midbrain. Following unilateral HRP injections into the medial torus, retrogradely labeled neurons were observed within six nuclei of the carp medulla. Two octaval nuclei, the anterior octavus nucleus and descending octavus nucleus, contained HRP-filled neurons. Labeled neurons were also observed within the ipsilateral superior olive, scattered among fibers of both lateral lemnisci, and bilaterally within the medullary reticular formation. In addition, bilateral retrograde cell labeling was found within a group of Purkinje-like cells located adjacent to the IVth ventricle, just rostral to the level of the VIIIth nerve. Few labeled neurons were found within the nucleus medialis, a principal target for lateral line afferents within the medulla. At midbrain levels, retrogradely labeled neurons were observed within the contralateral torus semicircularis and the ipsilateral optic tectum. Three forebrain nuclei project to the carp auditory midbrain. Within the diencephalon, descending projections originate from the anterior tuberal nucleus, bilaterally, and from the ipsilateral central posterior thalamic nucleus. The ipsilateral caudal telencephalon also projects to the carp auditory midbrain via large multipolar neurons within area dorsalis pars centralis. Anterograde labeling of fibers and terminals revealed efferent projections of the carp auditory midbrain to the following targets: the ipsilateral superior olive, the ipsilateral medullary reticular formation, the deep layers of the optic tectum, the contralateral torus semicircularis, the anterior tuberal nucleus, and the central posterior thalamic nucleus. These results, together with recent studies of lateral line pathways in teleosts (Finger, '80, '82a), demonstrate that central auditory and lateral line pathways are anatomically distinct in the carp, at least from medullary to diencephalic levels. Furthermore, there are striking similarities in the organization of the central auditory pathways of the carp and those of amphibians and land vertebrates.

Afferent Pathways↗

BDNF-induced survival of auditory neurons in vivo: Cessation of treatment leads to accelerated loss of survival effects.

Neurotrophic factors are important for the development and maintenance of the auditory system. They have also been shown to act as survival factors for auditory neurons in animal deafness models. Studies have demonstrated recently that these neurotrophic factors not only maintain survival of auditory neurons, but that these surviving neurons retain functionality. It remains to be determined, however, if a single administration of a neurotrophic factor is sufficient to maintain auditory neuron survival after loss of hair cells, or if sustained delivery is required. This study investigated the longevity of the survival effects of BDNF on auditory neurons in deafened guinea pigs. Briefly, the left cochleae of deafened guinea pigs were infused with BDNF for 28 days via a mini-osmotic pump, and neuronal survival was analyzed at various stages after the completion of treatment. BDNF treatment prevented the degeneration of auditory neurons that normally is seen after a loss of hair cells, supporting previous studies. Our results indicate, however, that cessation of BDNF treatment leads to an accelerated decline in auditory neuron survival as compared to that observed in deafened, untreated cochleae. These findings indicate that much work remains to be done to establish a technique for the long-term survival of auditory neurons in the deaf ear.

Animals↗

Dopaminergic modulation of the P50 auditory-evoked potential in a computer model of the CA3 region of the hippocampus: its relationship to sensory gating in schizophrenia.

We modeled the neuronal circuits that may underlie a sensory-processing deficit associated with schizophrenia. Schizophrenic patients have small P50 auditory-evoked responses to click stimuli compared to normal subjects. The P50 auditory-evoked response is a positive waveform recorded in the EEG approximately 50 ms after the auditory click stimulus. In addition to relatively small amplitudes, schizophrenic patients do not gate or suppress the P50 auditory-evoked response to the second of two paired-click stimuli spaced 0.5 s apart. Neuropleptic medication, which decreases dopaminergic neuronal transmission, increases the amplitude of the P50 auditory-evoked response but does not improve gating. Normal subjects have large P50 auditory-evoked responses to click stimuli when compared to unmedicated schizophrenic patients, and they gate their response to paired click stimuli or have smaller P50 auditory-evoked response amplitudes to the second of two click stimuli spaced 0.5 s apart. Schizophrenic patients do not gate and have similar response amplitudes to both clicks. We hypothesized that the small amplitudes of unmedicated schizophrenic subjects were due to a state of occlusion whereby excessive background noise in local circuits reduced the ability of cells to respond synchronously to sensory input, thereby reducing the amplitude of the P50 waveform in the EEG. Because the P50 auditory-evoked potential amplitudes increased with neuroleptic medication, which reduces dopaminergic neuronal transmission, we hypothesized a role for dopamine in modulating the signal-to-noise (S/N) in the local circuits responsible for sensory gating. To test the hypothesis that modulation of the S/N ratio reduces sensory gating, we developed a model of the effects of dopaminergic neuronal transmission that modulates the S/N in neuronal circuits. The model uses the biologically relevant computer model of the CA3 region of the hippocampus developed in the companion paper [Moxon et al. (2003) Biol Cybern, this volume]. Modified Hebb cell assemblies represented the response of the network to the click stimulus. The results of our model showed that excessive dopaminergic input impaired the ability of cells to respond synchronously to sensory input, which reduced the amplitudes of the P50 evoked responses.

Acoustic Stimulation↗

The auditory cortical projections onto the medial geniculate body in the cat. An experimental anatomical study with silver and autoradiographic methods.

The auditory cortical projections to the medial geniculate body (MGB) were studied in the cat. Lesions carefully restricted to each one of the subdivisions of the auditory and peri-auditory cortex were made and degenerating fibres were mapped in the MGB. In other experiments L-[4-5-3-H]leucine was injected into the cortex of AI, AII and SF and its transport to the MGB was studied by autoradiography. The results show that fibres arise in the deep layers of the cortex of AI, pass through the deep subdivision of the dorsal nucleus of the MGB as well as through the magnocellular MGB. and end in the pars lateralis of the ventral nucleus of the MGB, Arising from AII, axons pass through the magnocellular MGB and end in the superficial and deep subdivisions of the dorsal nucleus extending to the most caudal part of the MGB. The ectosylvian posterior auditory cortex projects diffusely to all subdivisions of the MGB as well as to its magnocellular part. Of the peri-auditory areas, only the suprasylvian fringe projects to the parvicellular MGB, and it sends axons to the dorsal nucleus of the MGB. The SF and the ectosylvian anterior periauditory area send fibres to the magnocellular MGB. The insular cortex does not project to the MGB but sends heavy projections to lower nuclei of the auditory pathway. The complementary use of degeneration and autoradiographic methods shows that each method may be used to eliminate the drawbacks of the other. This strategy appears as being most adequate for the study of reciprocal projections such as those found between the MGB and the three auditory areas AI, AII, and the ectosylvian posterior auditory area.

Animals↗

Alterations in activity at auditory nuclei of the rat induced by exposure to microwave radiation: autoradiographic evidence using [14C]2-deoxy-D-glucose.

Autoradiographic maps of brain activity in rats exposed to pulsed or continuous-wave (CW) microwave radiation were made using [14C]2-deoxy-D-glucose ([14C]2-DG). Special emphasis was given to measurements of activity in the auditory system because previous work had shown that pulsed microwave radiation can elicit auditory responses in man and other animals. In particular, one middle ear was ablated in nine rats to attenuate the transmission of air-borne sound to one cochlea. The resulting imbalance in auditory input for four animals not exposed to microwave radiation was reflected as a bilateral asymmetry of [14C]2-DG uptake at the inferior colliculus and medial geniculate body. In contrast, a symmetrical pattern of uptake at these structures in an animal exposed to pulsed microwave radiation showed that this stimulus bypasses the middle ear in eliciting auditory responses. This result established the utility of the [14C]2-DG method for demonstrating a known effect of microwave radiation on brain activity. The results also revealed responses at auditory nuclei in 4 animals exposed to CW microwave radiation. These responses, which have not been observed with other methods, were evident at the power densities of 2.5 and 10 mW/sq. cm. To exclude the possibility that CW microwave radiation produced this result by direct action on brain tissue, additional data were obtained from two rats with one cochlea destroyed. In both animals, the uptake of [14C]2-DG at the inferior colliculus and medial geniculate body was virtually identical to the uptake in animals not exposed to microwave radiation, i.e. greatest on the side of the brain contralateral to the intact cochlea. This finding, coupled with the finding of a bilateral symmetry of [14C]2-DG uptake in the auditory pathways of animals with one middle ear ablated, confirmed the hypothesis that auditory responses to CW microwave radiation originate within the cochlea. Effects on brain activity outside of the auditory system were not found in qualitative analyses of autoradiographs for the conditions of exposure to CW microwave radiation noted above or for exposure to pulsed microwave radiation at the average power density of 2.5 mW/sq. cm.

Animals↗

Sensitization induced receptive field plasticity in the auditory cortex is independent of CS-modality.

Sensitization training with an auditory stimulus produces a general increase in response magnitude across the entire receptive field (RF) of neurons in the primary auditory cortex of the guinea pig (Bakin, J.S. and Weinberger, N.M., Brain Res., 536 (1990) 271-286). To determine if this effect reflects an auditory system-specific process or is caused by a process independent of the training stimulus modality, RFs in primary auditory cortex were characterized before and immediately after adult guinea pigs were given sensitization training with either an auditory or a visual training stimulus. General increases in auditory response magnitude across the RF were observed in 7 out of 7 auditory sensitization cases and 4 out of 5 visual sensitization cases. There were no statistical differences between the effects of auditory and visual sensitization training. These findings indicate that the general increases observed following sensitization training are the result of processes independent of CS modality, in contrast to the highly specific RF modifications that are caused by classical conditioning. The findings suggest that the 2 forms of RF plasticity, CS-specific re-tuning due to associative conditioning and polymodal general increases in gain due to non-associative sensitization, may reflect neural mechanisms involved in selective attention and vigilance, respectively.

Acoustic Stimulation↗

Sharpening of frequency tuning by inhibition in the central auditory system: tribute to Yasuji Katsuki.

Frequency analysis is a fundamental function of the auditory system. Békésy and Katsuki believed that sharpening of frequency tuning by lateral inhibition takes place in the central auditory system. However, most 'cat' auditory physiologists have believed that frequency tuning of neurons is not sharpened in the central auditory system, so that there is no lateral inhibition. Unlike quasi-triangular frequency-tuning curves of peripheral neurons, pencil- or spindle-shaped frequency-tuning curves have been found in the central auditory systems of many species of animals belonging in different classes. Inhibitory tuning curves are commonly associated with such 'level-tolerant' sharp excitatory tuning curves. It is that frequency-tuning curves of some central auditory neurons are sharpened by inhibition. Yasuji Katsuki (Professor, M.D., Ph.D.) passed away on 6 March 1994 at the age of 88. I have written this article as a tribute to him, focusing on his major contribution to auditory neurophysiology: the finding of the sharpening of frequency tuning in the cat's central auditory system. Neural sharpening of frequency tuning is an old yet still current topic, as you will read in this article dedicated to Professor Katsuki.

Animals↗

The role of the external nucleus of the inferior colliculus in the construction of the superior collicular auditory space map in the guinea-pig.

In the guinea-pig two subcortical structures have been shown to contain representations of auditory space, the deep layers of the superior colliculus (SC) and the external nucleus of the inferior colliculus (ICX). The following investigation was undertaken to determine if the ICX influences the development of the SC auditory space map. A portion of the ICX was lesioned unilaterally when guinea-pigs were between 8 and 13 days old. Following a period of recovery, the SC mapping experiments commenced in the adult guinea-pig. Electrophysiological auditory responses were recorded from the deep layers of the SC to free-field azimuthal auditory stimulation. The data from the ICX lesioned animals revealed that the spatial tuning parameter values of the auditory receptive fields from the SC were significantly greater than those recorded in the normal control group of animals. The pooled data from the ICX lesioned group indicated that the peak angle of the response of the auditory receptive fields did not display normal topographic order. Furthermore, in several cases where the ICX lesion site was small, the position of the lesion could be correlated with the site of SC auditory space map disruption. These data indicate that, during early development, the presence of the ICX is essential for the normal emergence of an azimuthal map of auditory space in the deep layers of the guinea-pig SC.

Acoustic Stimulation↗

Auditory brainstem latencies in type I (insulin-dependent) diabetic patients.

INTRODUCTION: This study was undertaken to compare auditory brainstem response latencies in insulin-dependent diabetics, and to compare these findings with metabolic control, microangiopathy, neuropathy, and the duration of diabetes. METHODS: Auditory brainstem latencies were studied in 53 type I diabetic patients and 42 randomly selected nondiabetic control subjects, aged between 20 and 40 years. Three different stimulus repetition rates (10, 30, and 50 Hz) were used. All subjects had normal hearing ability. RESULTS: Wave V latencies were longer in diabetic patients when compared with those of control subjects at all repetition rates. At repetition rates of 10 and 50 Hz, diabetic patients had a prolonged I-V interwave latency, and at a repetition rate of 50 Hz, diabetics had a longer III-V interwave latency than control subjects. These findings indicate a central disturbance in the auditory pathway. Microvascular complications (retinopathy, nephropathy) and the duration of diabetes were associated with the prolongation of auditory brainstem latencies. In contrast, poor metabolic control (high fasting blood glucose and glycated hemoglobin A1c) at the time of the present study was only marginally associated with prolonged auditory brainstem latencies. The changes in auditory brainstem latencies associated with diabetic neuropathy (measured with five cardiac autonomic nervous function tests) appeared simultaneously with microvascular complications and in patients with diabetes of long duration, and thus a causative role of diabetic neuropathy in the pathogenesis of prolonged auditory brainstem latencies remains unsolved. CONCLUSION: Delayed auditory brainstem latencies in type I diabetic patients are probably caused by the long duration of diabetes and the microvascular complications associated with it.

Adult↗

Ocular tracking as a measure of auditory motion perception.

Motion is a potent sub-modality of vision. Motion cues alone can be used to segment images into figure and ground and break camouflage. Specific patterns of motion support vivid percepts of form, guide locomotion by specifying directional heading and the passage of objects, and in case of an impending collision, the time to impact. Visual motion also drives smooth pursuit eye movements (SPEMs) that serve to stabilize the retinal image of objects in motion. In contrast, the auditory system does not appear to be particularly sensitive to motion. We review the ambiguous status of auditory motion processing from the psychophysical and electrophysiological perspectives. We then report the results of two experiments that use ocular tracking performance as an objective measure of the perception of auditory motion in humans. We examine ocular tracking of auditory motion, visual motion, combined auditory + visual motion and imagined motion in both the frontal plane and in depth. The results demonstrate that ocular tracking of auditory motion is no better than ocular tracking of imagined motion. These results are consistent with the suggestion that, unlike the visual system, the human auditory system is not endowed with low-level motion sensitive elements. We hypothesize however, that auditory information may gain access to a recently described high-level motion processing system that is heavily dependent on 'top-down' influences, including attention.

Acoustic Stimulation↗

Decrease of functional coupling between left and right auditory cortices during dichotic listening: an electroencephalography study.

The present study focused on functional coupling between human bilateral auditory cortices and on possible influence of right over left auditory cortex during dichotic listening of complex non-verbal tones having near (competing) compared with distant non-competing fundamental frequencies. It was hypothesized that dichotic stimulation with competing tones would induce a decline of functional coupling between the two auditory cortices, as revealed by a decrease of electroencephalography coherence and an increase of directed transfer function from right (specialized for the present stimulus material) to left auditory cortex. Electroencephalograph was recorded from T3 and T4 scalp sites, overlying respectively left and right auditory cortices, and from Cz scalp site (vertex) for control purposes. Event-related coherence between T3 and T4 scalp sites was significantly lower for all electroencephalography bands of interest during dichotic listening of competing than non-competing tone pairs. This was a specific effect, since event-related coherence did not differ in a monotic control condition. Furthermore, event-related coherence between T3 and Cz and between T4 and Cz scalp sites showed no significant effects. Conversely, the directed transfer function results showed negligible influence at group level of right over left auditory cortex during dichotic listening. These results suggest a decrease of functional coupling between bilateral auditory cortices during competing dichotic stimuli as a possible neural substrate for the lateralization of auditory stimuli during dichotic listening.

Acoustic Stimulation↗

EEG coherence measures during auditory hallucinations in schizophrenia.

We studied the change in EEG alpha-band average coherence between auditory hallucination (AH) and non-auditory hallucination (non-AH) states in seven auditory hallucinating schizophrenia patients. Four cortical regions were considered based on the existing dominant models for auditory hallucinations, the inner speech model and the central auditory processing deficit (CAPD) model. Coherences between electrodes located over Broca's area (BA 44/45) and Wernicke's area (BA 22/42) and between electrodes located over left-right temporal cortices were examined. There was no significant change observed in the coherence between Broca's and Wernicke's areas, but a significant increase was observed in coherence between the left and right superior temporal cortices during AHs compared with non-AHs, suggesting increased bilateral coherence between auditory cortical areas. Since coherence is a pairwise measure of functional correlation between regions, our findings suggest abnormally increased synchrony between the left and right auditory cortices during AHs in schizophrenia. Further, a significant increase in relative power was observed in the left, but not in the right auditory cortex during AHs. Thus our findings support the CAPD model and are consistent with that which postulate reduced prosodic processing during AHs.

Adult↗

Disorders of auditory processing: evidence for modularity in audition.

This article examines four disorders of auditory processing that can result from selective brain damage (cortical deafness, pure word deafness, auditory agnosia and phonagnosia) in an effort to derive a plausible functional and neuroanatomical model of audition. The article begins by identifying three possible reasons why models of auditory processing have been slower to emerge than models of visual processing: neuroanatomical differences between the visual and auditory systems, terminological confusions relating to auditory processing disorders, and technical factors that have made auditory stimuli more difficult to study than visual stimuli. The four auditory disorders are then reviewed and current theories of auditory processing considered. Taken together, these disorders suggest a modular architecture analogous to models of visual processing that have been derived from studying neurological patients. Ideas for future research to test modular theory more fully are presented.

Acoustic Stimulation↗