Clinical sectionLate auditory evoked potentials can occur without brain stem potentialsLes potentiels évoqués auditifs tardifs peuvent apparaître sans potentiels de tronc cérébral☆
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Cited by (25)
Auditory neuropathy
2015, Handbook of Clinical NeurologyCitation Excerpt :While the tests were of great benefit for objectively defining “deafness,” there were exceptions that tested this assumption. Some subjects with “hearing problems” had relatively normal audiometric thresholds but absent or severely abnormal ABRs (Kaga and Tanaka, 1980; Worthington and Peters, 1980; Hildesheimer et al., 1985; Satya-Murti et al., 1983; Kraus et al., 1984). We identified that their deafness was due to abnormal auditory nerve function in the presence of normal-functioning cochlear sensory hair cells.
Positive auditory cortical responses in patients with absent brainstem response
2014, Clinical NeurophysiologyCitation Excerpt :This observation may be superficially somewhat curious, considering that the auditory signals basically run from ear to auditory cortex via the brainstem. However, such phenomena have also been reported in patients with various retrocochlear pathologies such as auditory neuropathy, Friedreich ataxia, spinocerebellar degeneration, and multiple sclerosis (Satya-Murti et al., 1983; Kraus et al., 1993; Starr et al., 1996, 2003, 2004; Rance et al., 2002; Michalewski et al., 2005; Takata et al., 2012). Such cortical responses have not been fully examined in patients with vestibular schwannoma, which is known to be one of the typical retrocochlear lesions associated with deteriorated ABR.
Auditory evoked magnetic fields in patients with absent brainstem responses due to auditory neuropathy with optic atrophy
2012, Clinical NeurophysiologyCitation Excerpt :Therefore, auditory neuropathy has been described as auditory dys-synchrony. Neural synchrony is important in recording auditory evoked responses, but the effects of dys-synchrony may vary with the different evoked responses; i.e., auditory N100 and P200 cortical sensory potentials to tones could be often obtained with delayed latency, despite the absence of ABR (Satya-Murti et al., 1983; Kraus et al., 1993; Starr et al., 1996, 2003, 2004; Rance et al., 2002; Michalewski et al., 2005). Differences in the degradation of such cortical responses may indicate variations in the dys-synchrony of the auditory nerve activity, so detailed assessment of the cortical response in auditory neuropathy may be important.
N100 cortical potentials accompanying disrupted auditory nerve activity in auditory neuropathy (AN): Effects of signal intensity and continuous noise
2009, Clinical NeurophysiologyCitation Excerpt :Temporal bones in this condition have not yet been examined to determine whether there are long-term effects of pre-synaptic disorders on the viability of either inner-hair cells or auditory nerve fibers. AN subjects, in spite of abnormal or absent ABRs, show auditory N100 and P200 cortical sensory potentials to tones (Kraus et al., 1993; Rance et al., 2002; Satya-Murti et al., 1983; Starr et al., 1996, 2003, 2004), speech signals (Kraus et al., 2000; Narne and Vanaja, 2008), and to silent gaps in continuous noise (Michalewski et al., 2005). These cortical potentials typically were delayed in latency sometimes by as much as 60 ms or more compared to normal hearing subjects.
Central deafness in a young child with Moyamoya disease: Paternal linkage in a Caucasian family: Two case reports and a review of the literature
1999, International Journal of Pediatric OtorhinolaryngologyStrümpell's familial spastic paraplegia: an electrophysiological demonstration of selective central distal axonopathy
1987, Electroencephalography and Clinical Neurophysiology
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This study was made possible by The Robert W. Graves Memorial Fund.