Perceptual Consequences of Disrupted Auditory Nerve Activity

Zeng, Fan‐Gang; Kong, Ying‐Yee; Michalewski, Henry J.; Starr, Arnold

doi:10.1152/jn.00985.2004

Cited by 278 publications

(323 citation statements)

References 92 publications

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“…Similar impairments are also seen in patients suffering from AN (Starr et al 1996;Rance et al 1999). Other investigations also emphasize reduced speed of neuronal transmission causing deficits in temporal processing, for example, temporal resolution, detection of amplitude modulation, and temporal aspects of frequency discrimination (Rance et al 2004;Zeng et al 2005). Similar to the results observed here, AN patients in the Zeng et al study failed in signal lateralization based on interaural time but not interaural intensity differences.…”

Section: Auditory Impairmentssupporting

confidence: 85%

Auditory Processing Disorders with and without Central Auditory Discrimination Deficits

Ludwig

Fuchs

Kruse

et al. 2014

JARO

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Auditory processing disorder (APD) is defined as a processing deficit in the auditory modality and spans multiple processes. To date, APD diagnosis is mostly based on the utilization of speech material. Adequate nonspeech tests that allow differentiation between an actual central hearing disorder and related disorders such as specific language impairments are still not adequately available. In the present study, 84 children between 6 and 17 years of age (clinical group), referred to three audiological centers for APD diagnosis, were evaluated with standard audiological tests and additional auditory discrimination tests. Latter tests assessed the processing of basic acoustic features at two different stages of the ascending central auditory system: (1) auditory brainstem processing was evaluated by quantifying interaural frequency, level, and signal duration discrimination (interaural tests). (2) Diencephalic/telencephalic processing was assessed by varying the same acoustic parameters (plus signals with sinusoidal amplitude modulation), but presenting the test signals in conjunction with noise pulses to the contralateral ear (dichotic signal/ noise tests). Data of children in the clinical group were referenced to normative data obtained from more than 300 normally developing healthy school children. The results in the audiological and the discrimination tests diverged widely. Of the 39 children that were diagnosed with APD in the audiological clinic, 30 had deficits in auditory performance. Even more alarming was the fact that of the 45 children with a negative APD diagnosis, 32 showed clear signs of a central hearing deficit. Based on these results, we suggest revising current diagnostic procedure to evaluate APD in order to more clearly differentiate between central auditory processing deficits and higher-order (cognitive and/or language) processing deficits.

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Section: Auditory Impairmentssupporting

confidence: 85%

Auditory Processing Disorders with and without Central Auditory Discrimination Deficits

Ludwig

Fuchs

Kruse

et al. 2014

JARO

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“…Thresholds for gap detection tested in free-field at ''comfortable" loudness levels were abnormally elevated in the four tested subjects (48-164 ms, the upper limit of naïve normal listeners is 7 ms, Zeng et al, 2005).…”

Section: Audiological and Neurological Measuresmentioning

confidence: 80%

“…Auditory neuropathy (AN) is a disorder of auditory nerve function (Starr et al, 1996) characterized by hearing deficits affecting auditory perceptions dependent on temporal, but not intensity or high frequency spectral cues (Zeng et al, 2005). Adult patients typically complain of difficulty in understanding speech especially in the presence of noise and the extent of their speech comprehension is impaired out-of-proportion to the pure tone hearing loss , for review).…”

Section: Introductionmentioning

confidence: 99%

Neural and receptor cochlear potentials obtained by transtympanic electrocochleography in auditory neuropathy

Santarelli

Starr

Michalewski

et al. 2008

Clinical Neurophysiology

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Objective: Transtympanic electrocochleography (ECochG) was recorded bilaterally in children and adults with auditory neuropathy (AN) to evaluate receptor and neural generators. Methods: Test stimuli were clicks from 60 to 120 dB p.e. SPL. Measures obtained from eight AN subjects were compared to 16 normally hearing children. Results: Receptor cochlear microphonics (CMs) in AN were of normal or enhanced amplitude. Neural compound action potentials (CAPs) and receptor summating potentials (SPs) were identified in five AN ears. ECochG potentials in those ears without CAPs were of negative polarity and of normal or prolonged duration. We used adaptation to rapid stimulus rates to distinguish whether the generators of the negative potentials were of neural or receptor origin. Adaptation in controls resulted in amplitude reduction of CAP twice that of SP without affecting the duration of ECochG potentials. In seven AN ears without CAP and with prolonged negative potential, adaptation was accompanied by reduction of both amplitude and duration of the negative potential to control values consistent with neural generation. In four ears without CAP and with normal duration potentials, adaptation was without effect consistent with receptor generation. In five AN ears with CAP, there was reduction in amplitude of CAP and SP as controls but with a significant decrease in response duration. Conclusions: Three patterns of cochlear potentials were identified in AN: (1) presence of receptor SP without CAP consistent with presynaptic disorder of inner hair cells; (2) presence of both SP and CAP consistent with post-synaptic disorder of proximal auditory nerve; (3) presence of prolonged neural potentials without a CAP consistent with post-synaptic disorder of nerve terminals. Significance: Cochlear potential measures may identify pre-and post-synaptic disorders of inner hair cells and auditory nerves in AN.

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“…Recently, psychoacoustic and evoked potential measures of auditory temporal processes have been compared in normal-hearing individuals and in patients with an auditory temporal processing disorder (auditory neuropathy) using gaps in continuous noise Zeng et al, 2005). Evoked potentials in normal subjects (N 1 components) were recorded in response to gaps as short as 5 ms in both active and passive listening conditions, close to the behavioral thresholds of 2-3 ms. Gap-evoked potentials in the patients with a temporal processing disorder appeared only with prolonged gap durations (10-50 ms) and in close agreement with gap detection thresholds measured psychoacoustically.…”

Section: N 1 To Speech and Acoustic Temporal Cuesmentioning

confidence: 95%

The N1 complex to gaps in noise: Effects of preceding noise duration and intensity

Pratt

Starr

Michalewski

et al. 2007

Clinical Neurophysiology

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The N1 complex to gaps in noise: Effects of preceding noise duration and intensity AbstractObjective: To study the effects of duration and intensity of noise that precedes gaps in noise on the N-Complex (N 1a and N 1b ) of EventRelated Potentials (ERPs) to the gaps. Methods: ERPs were recorded from 13 normal subjects in response to 20 ms gaps in 2-4.5 s segments of binaural white noise. Within each segment, the gaps appeared after 500, 1500, 2500 or 4000 ms of noise. Noise intensity was either 75, 60 or 45 dBnHL. Analysis included waveform peak measurements and intracranial source current density estimations, as well as statistical assessment of the effects of pre-gap noise duration and intensity on N 1a and N 1b and their estimated intracranial source activity. Results: The N-Complex was detected at about 100 ms under all stimulus conditions. Latencies of N 1a (at 90 ms) and N 1b (at 150 ms) were significantly affected by duration of the preceding noise. Both their amplitudes and the latency of N 1b were affected by the preceding noise intensity. Source current density was most prominent, under all stimulus conditions, in the vicinity of the temporo-parietal junction, with the first peak (N 1a ) lateralized to the left hemisphere and the second peak (N 1b ) -to the right. Additional sources with lower current density were more anterior, with a single peak spanning the duration of the N-Complex. Conclusions: The N 1a and N 1b of the N-Complex of the ERPs to gaps in noise are affected by both duration and intensity of the pre-gap noise. The minimum noise duration required for the appearance of a double-peaked N-Complex is just under 500 ms, depending on noise intensity. N 1a and N 1b of the N-Complex are generated predominantly in opposite temporo-parietal brain areas: N 1a on the left and N 1b on the right. Significance: Duration and intensity interact to define the dual peaked N-Complex, signaling the cessation of an ongoing sound.

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Perceptual Consequences of Disrupted Auditory Nerve Activity

Cited by 278 publications

References 92 publications

Auditory Processing Disorders with and without Central Auditory Discrimination Deficits

Auditory Processing Disorders with and without Central Auditory Discrimination Deficits

Neural and receptor cochlear potentials obtained by transtympanic electrocochleography in auditory neuropathy

The N1 complex to gaps in noise: Effects of preceding noise duration and intensity

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