Auditory processing in individuals with auditory neuropathy

Abstract

Background: Auditory neuropathy is a disorder characterized by no or severely impaired auditory brainstem responses in presence of normal otoacoustic emissions and/or cochlear microphonics. Speech perception abilities in these individuals are disproportionate to their hearing sensitivity and reported to be dependent on cortical evoked potentials and temporal processing abilities. The disproportionate loss of auditory percept in presence of normal cochlear function is suggestive of impairment of auditory neural synchrony.

Audiological Profile of Adult Persons with Auditory Neuropathy Spectrum Disorders

“…Results of the present study showed that the detection thresholds improved with decrease in modulation frequency (better thresholds for 8 Hz modulations than for 20 and 60 Hz). Similar results have been reported earlier [7] and the findings have been well explained [17]. …”

“…Kumar and Jayaram [17], in a register-based retrospective study, reported a prevalence of 0.28% of ANSD in all the hearing impaired and 0.54% in individuals with permanent hearing loss. ANSD was diagnosed on the basis of criteria of Starr, et al [18] in this study.…”

“…ANSD was diagnosed on the basis of criteria of Starr, et al [18] in this study. Kumar and Jayaram [17] reported a ‘peaked’ audiogram as the most common pure tone configuration, widely varying speech identification scores, an association between ‘peaked’ audiogram with better speech identification scores, and no association between speech identification scores and OAEs/ABRs in their participants. Fifty-nine percent of the subjects in the study reported to have had the onset of the problem between 14 and 24 years signifying late onset of the problem in India.…”

“…This is in contrast to Berlin, et al [12] who reported less than 10% of instances of onset in individuals between 16 to 18 years. While Kumar and Jayaram [17] reported a greater prevalence of the problem in males compared to females, Narne, et al [19] reported the opposite of this (female to male ratio of 1.25:1). Narne, et al [19] also reported a ‘rising’ pattern of pure tone audiogram and good speech identification in individuals in whom cortical potentials could be recorded.…”

Hesperidin promotes lysosomal biogenesis in chronically ethanol‐induced cardiotoxicity in rats: A proposed mechanisms of protection

“…Group I (normal control group) received glucose solution equivalent to the calorific value of ethanol (15 g of glucose/kg, ie, 5 mL of 30% glucose solution/100 g). Group II (hesperidin‐treated control group) received glucose solution equivalent to the calorific value of ethanol (15 g of glucose/kg, ie, 5 mL of 30% glucose solution/100 g) alone for the initial 30 days, then combined with hesperidin treatment at a dose of (50 mg/kg) dissolved in 1% dimethyl sulfoxide (DMSO) orally for another 30 days . Group III (ethanol‐fed group) received ethanol at a dose of (7.9 g/kg, ie, 5 mL of 20% ethanol/100 g) as an aqueous solution for 60 days by intragastric intubation (per os [po]) .…”