Concepedia

TLDR

Auditory processing disorder is thought to stem largely from neurodevelopmental delay, and the CAEP P1‑N1 complex—whose latency decreases and amplitude increases with age—has been used to track central auditory nervous system maturation in hearing‑impaired children. The study uses CAEP to determine whether central auditory nervous system maturation differs between children with and without APD. Twenty‑seven 7‑to‑12‑year‑old children who failed an APD battery were age‑matched to peers who passed, and their CAEP responses to 500‑Hz tone bursts were recorded and analyzed for latency and amplitude. APD children exhibited significantly longer latency (~10 ms) and lower amplitude (~10 μV) of the early P1‑N1 CAEP components, with no differences in the later P2 wave, supporting an immature CANS as the basis of APD.

Abstract

Neurodevelopmental delay has been proposed as the underlying cause of the majority of cases of auditory processing disorder (APD). The current study employs the cortical auditory evoked potential (CAEP) to assess if maturational differences of the central auditory nervous system (CANS) can be identified between children who do and do not meet the diagnostic criterion for APD. The P1-N1 complex of the CAEP has previously been used for tracking development of the CANS in children with hearing impairment. Twenty-seven children (7 to 12 years old) who failed an APD behavioral test battery were age-matched (within 3 months) to children who had passed the same battery. CAEP responses to 500-Hz tone burst stimuli were recorded and analyzed for latency and amplitude measures. The P1-N1 complex of the CAEP, which has previously been used for tracking development of the CANS in children with hearing impairment, showed significant group differences. The children diagnosed with APD showed significantly increased latency (∼10 milliseconds) and significantly reduced amplitude (∼10 μV) of the early components of the CAEP compared with children with normal auditory processing. No significant differences were seen in the later P2 wave. The normal developmental course is for a decrease in latency and increase in amplitude as a function of age. The results of this study are, therefore, consistent with an immaturity of the CANS as an underlying cause of APD in children.

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