Evidence map›Paper›PMID 42158889›Full record

ArticleNorthern clinics of Istanbul2026

Subclinical auditory dysfunction in a genetic rat model of childhood absence epilepsy.

Fatma Nur Komur, Yavuz Gundogdu, Mahmut Furkan Beyaz, Ayca Ciprut

Abstract read
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Article in Northern clinics of Istanbul, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Fatma Nur KomurDepartment of Audiology and Speech Disorders, Institute of Health Sciences, Marmara University, Istanbul, Turkiye.
Yavuz GundogduDepartment of Otolaryngology, Marmara University Faculty of Medicine, Istanbul, Turkiye.
Mahmut Furkan BeyazDepartment of Otolaryngology, Marmara University Faculty of Medicine, Istanbul, Turkiye.
Ayca CiprutDepartment of Audiology, Marmara University Faculty of Medicine, Istanbul, Turkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveChildhood absence epilepsy (CAE) is defined by cognitive, behavioral, and neurophysiological abnormalities, but its impact on auditory function remains underexplored. Using Genetic Absence Epilepsy Rats from Strasbourg (GAERS), this study aimed to examine both peripheral and central auditory pathways function to better understand the auditory consequences of CAE.

methodsThe experimental and control groups consisted of six-month-old male GAERS (n=6) and Wistar (n=6) rats. Auditory functions were assessed using distortion product otoacoustic emissions (DPOAE) and auditory brainstem responses (ABR). DPOAE amplitudes and ABR wave thresholds, latencies, and amplitudes were analyzed for group comparison.

resultsDPOAE amplitudes were significantly reduced across all tested frequencies in epileptic rats compared to controls. In addition, ABR thresholds were slightly elevated compared to controls, but remained within clinically normal limits. Prolonged latencies were obtained in all waves except Wave I, indicating subcortical auditory pathway involvement in the epileptic group. A distinct ABR amplitude pattern emerged in epilepsy, characterized by increased Wave I-II amplitudes, a marked reduction at Wave III, and subsequent increases at Waves IV-V.

conclusionThe results showed both peripheral and central auditory nervous system dysfunction in GAERS rats, providing translational insight into CAE. Subclinical abnormalities in auditory neuronal processing may contribute to speech-in-noise difficulties, language impairments, and learning problems in affected children. Early detection and follow-up are valuable for the clinical management of auditory involvement in pediatric epilepsy.

Indexed as

Childhood absence epilepsyhearing lossotorhinolaryngologypediatric epilepsysubclinical dysfunction

Identifiers

PMID42158889
PMCPMC13181549

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