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Quantitative Assessment of Cortical Auditory-tactile Processing in Children with Disabilities
Published on: January 29, 2014
Characteristic cortical alterations in auditory neuropathy: An EEG study
Xin Zhou1, Xiaonan Wu1, Suwei Ma2
1Department of Audio-Vestibular Medicine, Senior Department of Otolaryngology-Head and Neck Surgery, the Sixth Medical Center of Chinese PLA General Hospital 100048, Beijing, China; State Key Laboratory of Hearing and Balance Science 100853, Beijing, China; National Clinical Research Center for Otolaryngologic Diseases, Medical School of Chinese PLA, Chinese PLA General Hospital 100853, Beijing, China.
Abstract:
Auditory neuropathy (AN) is a complex auditory disorder characterized by disproportionately poor speech discrimination despite preserved auditory sensitivity, substantially impacting daily communication and overall quality of life. This study conducted comprehensive audiological measurements and high-density electroencephalography (EEG) measurements in resting and auditory task states on 21 AN, 21 age-, gender-, and hearing threshold-matched sensorineural hearing loss (SNHL), and 21 age- and gender-matched normal hearing (NH) subjects. The topological network attributes, microstates, event-related potentials (ERP), cortical lateralization, phase-locking value (PLV) functional connectivity strength of EEG, and correlations with audiological indicators were compared among three groups. The results showed that in the resting state, the global field power (GFP) of microstate A differed significantly after FDR correction, with SNHL showing higher GFP 3.23 (2.46-3.93) μV than AN 2.37 (2.08-3.08) μV and NH 2.38 (2.08-2.63) μV. The transition probability (TP) from microstate A to B and from B to C were higher in SNHL than NH (both P after correction = 0.011). During task processing, N1 amplitude was lower in SNHL than NH (P after correction = 0.023), while N1 latency was shorter in AN than SNHL (P after correction = 0.006) and was correlated with low-frequency PTA (correlation coefficient = 0.362, P after correction = 0.020). AN additionally exhibited left-hemispheric lateralization (P after correction < 0.05). Source localization revealed greater cortical activation in SNHL than in AN and NH, predominantly in the superior frontal gyrus (SNHL > NH: P = 0.00020, t0.05 = 3.692, and SNHL > AN: P = 0.01140, t0.05 = -3.794). Collectively, these findings demonstrate that AN exhibits unique neural compensation patterns distinct from SNHL, supporting cortical reorganization mechanisms specific to neural dyssynchrony rather than simple auditory input reduction.

