Central auditory processing disorders in children and adults.

Central auditory processing disorders (CAPD) can affect children and adults of all ages due to a wide variety of causes. CAPD is a neurobiologic deficit in the central auditory nervous system (CANS) that affects those mechanisms that underlie fundamental auditory perception, including localization and lateralization; discrimination of speech and non-speech sounds; auditory pattern recognition; temporal aspects of audition, including integration, resolution, ordering, and masking; and auditory performance with competing and/or degraded acoustic signals (American Speech-Language-Hearing Association, 2005a, b). Although it is recognized that central auditory dysfunction may coexist with other disorders, CAPD is conceptualized as a sensory-based auditory disorder. Administration of behavioral and/or electrophysiologic audiologic tests that have been shown to be sensitive and specific to dysfunction of the CANS is critical for a proper diagnosis of CAPD, in addition to assessments and collaboration with a multidisciplinary team. Intervention recommendations for CAPD diagnosis are based on the demonstrated auditory processing deficits and related listening and related complaints. This chapter provides an overview of current definitions and conceptualizations, methods of diagnosis of, and intervention for, CAPD. The chapter culminates with a case study illustrating pre- and posttreatment behavioral and electrophysiologic diagnostic findings.

Cochlear implants: clinical and societal outcomes.

Over the past 30 years, hearing care clinicians have increasingly relied on cochlear implants to restore auditory sensitivity in selected patients with advanced sensorineural hearing loss. This article examines the impact of intervention with cochlear implantation in children and adults. The authors report a range of clinic-based results and patient-based outcomes reflected in the reported literature on cochlear implants. The authors describe the basic assessment of the physiologic response to auditory nerve stimulation; measures of receptive and productive benefit; and surveys of life effects as reflected measures of quality of life, educational attainment, and economic impact.

Auditory hallucinations: expectation-perception model.

In this paper, we aimed to present a hypothesis that would explain the mechanism of auditory hallucinations, one of the main symptoms of schizophrenia. We propose that auditory hallucinations arise from abnormalities in the predictive coding which underlies normal perception, specifically, from the absence or attenuation of prediction error. The suggested deficiencies in processing prediction error could arise from (1) abnormal modulation of thalamus by prefrontal cortex, (2) absence or impaired transmission of external input, (3) dysfunction of the auditory and association cortex, (4) neurotransmitter dysfunction and abnormal connectivity, and (5) hyperactivity activity in auditory cortex and broad prior probability. If there is no prediction error, the initially vague prior probability develops into an explicit percept in the absence of external input, as a result of a recursive pathological exchange between auditory and prefrontal cortex. Unlike existing explanations of auditory hallucinations, we propose concrete mechanisms which underlie the imbalance between perceptual expectation and external input. Impaired processing of prediction error is reflected in reduced mismatch negativity and increased tendency to report non-existing meaningful language stimuli in white noise, shown by those suffering from auditory hallucinations. We believe that the expectation-perception model of auditory hallucinations offers a comprehensive explanation of the underpinnings of auditory hallucinations in both patients and those not diagnosed with mental illness. Therefore, our hypothesis has the potential to fill the gaps in the existing knowledge about this distressing phenomenon and contribute to improved effectiveness of treatments, targeting specific mechanisms.

Central deafness in a young child with Moyamoya disease: paternal linkage in a Caucasian family: two case reports and a review of the literature.

A case of 'central deafness' is presented in a 3-year-old male Caucasian child with Moyamoya disease (MMD); a rare, progressive and occlusive cerebrovascular disorder predominantly affecting the carotid artery system. Documentation of normal peripheral auditory function and brainstem pathway integrity is provided by acoustic admittance, otoacoustic emission and brainstem auditory evoked potential measurements. The lack of behavioral response to sound, and absent middle and long latency auditory evoked potentials suggest thalamo-cortical dysfunction. Magnetic resonance imaging showed diffuse ischemic damage in subcortical white matter including areas of the temporal lobes. In addition, there were multiple and focal cortical infarctions in both cerebral hemispheres, focused primarily in the frontal, parietal and temporal areas. Taken together, these structural and functional abnormalities in addition to severely delayed speech and language development are consistent with the diagnosis of central deafness and suggest a disconnection between higher brainstem and cortical auditory areas. The child's father also has MMD, but was diagnosed only recently. The presence of paternal linkage is informative since it rules out x-linked recessive and maternal inheritance. To our knowledge, this represents the first documented case of paternal linkage in MMD with central deafness in a Caucasian child with no apparent Japanese ancestry. Herein, we focus on central auditory dysfunction and consider how lesion-induced changes have contributed to a deficit in basic auditory responsiveness, including a severe disturbance in receptive and expressive auditory-based speech and language skills.

Lesion site in sudden deafness: study with electrocochleography and transiently evoked otoacoustic emission.

We examined electrocochleogram (ECochG) and transiently evoked otoacoustic emission (TEOAE) on five cases of sudden sensorineural hearing loss which had no abnormalities detected on diagnostic imagings and showed complete recovery of hearing. At the initial examination, three cases showed a broadened wave 1 with prolonged latency in the auditory brainstem response (ABR) at 90 dB HL. The ECochG AP showed a broad waveform, low amplitude, and high threshold. CM threshold, although increased, was relatively well preserved compared with hearing threshold measured with conventional pure-tone audiometry. The thresholds in TEOAE examination were similar to those for CM and preserved better when compared with pure-tone audiometric thresholds. These findings suggest that the location of the disorder in these three cases involved not only the cochlea but also the retrocochlear auditory pathway. The other two cases showed normal ABR waveforms at 90 dB HL at the initial examinations. ECochG examination showed that a normal AP in one case and a smaller amplitude AP, an elevated threshold, and normal waveform of AP in the other ear. CM thresholds coincided with the conventional audiometry thresholds. These findings suggest that hearing loss in these two cases involved primarily the sensory hair cells.