Unilateral auditory hallucinations.
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The authors have investigated the thesis that intermittent hearing impairment due to middle ear disease in the early years of life results in a central auditory disturbance which may persist in adulthood. The concept that, during the speech development years, auditory disturbances interfere with the normal maturation of central auditory processing appear to be clearly established. Thirty-five children, free of active ear disease and normally hearing by standard peripheral audiometry, are the basis for the study. The monotic tests employing temporal and frequency distortion and the dichotic challenges of competing stimuli and central integration provide the test data. Approximately 75% of the study group fail at least 1 segment of the battery, beyond 2 standard deviations from the normal data. A decreasing percentage of the study group exceed the normative values in 2 or more of the test components. In view of these data on aggressive program of auditory conservation is suggested during the early years of life.
16 stutterers and 16 nonstutterers between the ages of 8 and 11 yr. were administered a battery of central auditory processing tests. The six audiological tests evaluated a range of auditory functions. Analysis indicated no significant differences between the two groups; however, inspection of the data showed 6 of the stuttering subjects performed consistently more poorly on four of the tests than the nonstuttering subjects. Results are discussed in relationship to subgroups of stutterers with auditory problems.
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A 56-yr old woman developed a cortical auditory disorder after two successive strokes involving the temporal lobes. Dichotic listening tests did not show a left car advantage with right ear suppression, as shown in other cases with similar disorders. Tasks exploring phonological analysis showed an impairment limited to the stop consonants. Within this framework, processing of feature place was selectively disturbed, while voicing was normally analysed. The possible role of psychoacoustic deficits in the pathogenesis of cortical auditory disorders is discussed. Some general considerations on cortical auditory disorders are also made.
This paper is intended to lend support to the 2003 findings of Poloni, Riquier, Zimmermann, and Borgeat. Further, some extensions of these and other findings with respect to perceptual defense are suggested.
The purpose of this study was to evaluate auditory event-related potentials, and related long latency components, in children with auditory processing disorders, and to compare these results with a normal group matched for age, intelligence, and gender. Results showed a significant latency increase for the N1, P2, and P3 components in the processing disordered group. Furthermore, the interpeak latency interval P2-P3 was significantly longer in the clinical group. In terms of amplitude measures, only P3 amplitude differed significantly between groups. These results suggest that the long latency potentials may be useful in the assessment of children with processing disorders.
The ability to discriminate speech and nonspeech auditory stimuli was tested in a learning disabled child. The perception of speech stimuli was normal when the stimuli were presented in quiet but below normal when the stimuli were presented in noise. Although the perception of pure tone stimuli and environmental sounds was normal both in quiet and noise, the perception of nonspeech stimuli with rapid changes in acoustic information was impaired in noise. These findings illustrate the importance of relating performance for speech and complex nonspeech stimuli in investigating the basis of speech perceptual deficits. Whereas abnormal performance for speech stimuli coupled with normal performance for complex nonspeech stimuli argues for the existence of specialized speech processing mechanisms, abnormal performance for both types of stimuli, as was found in the present subject, argues for the existence of more generalized auditory processing mechanisms.
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This study was undertaken to determine whether some aphasic defects in aural language comprehension might be a reflection of cognitive impairment which also affects the recognition of meaningful, non-verbal sounds. Defects in sound recognition were consistently associated with aural comprehension defects of at least comparable severity and the majority of aphasics with impaired aural comprehension failed sound recognition. Although some aphasics with impaired aural comprehension performed normally in sound recognition, their language comprehension impairments were not of lesser severity than those shown by aphasics failing sound recognition. The relationship between sound recognition and reading comprehension was different in nature from that between sound recognition and aural comprehension.
Data are presented indicating a correlation between chronic recurrent otitis media of early childhood and in increased likelihood of subsequent auditory processing deficits in a group of children referred for evaluation of impaired learning. Helpful appendices are added for a better understanding a central auditory processing skills.
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Forty-four psychiatric patients were separated into four groups on the basis of presence/absence of hallucinations and reactive/process status. Reactive hallucinators were found to be singularly impaired in two aspects of cognitive processing: (1) tolerance of ambiguity; and (2) availability of alternative meanings. The perceptual errors produced by premature judgment and limited consideration of alternative meanings for misperceptions are discussed as factors predisposing to auditory hallucination.
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It has been hypothesized that receptive developmental language disorder (RDLD) may be explained by an auditory processing deficit. The neuroanatomical locus of this deficit is unknown. Brainstem auditory evoked potentials (BAEPs) reflect the functioning of the auditory nerve and auditory brainstem pathways to high-frequency acoustical stimulation in humans and reflect the first stages of auditory processing. These were studied in 12 subjects with RDLD (four females and eight males, ages 12 to 19) and twelve control subjects (three females and nine males, ages 14 to 24). Click intensity and rate of stimulation were varied. The BAEPs for the RDLD group were comparable to the control group as well as to hospital norms across intensity levels and stimulation rates. The evidence obtained suggests that a disorder in the neurophysiological systems underlying the BAEPs and reflecting initial stages of auditory processing is not essential for RDLD.