Neurophysiology Research

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Review Article - Neurophysiology Research (2025) Volume 7, Issue 2

Neurophysiological Correlates of Auditory Processing Deficits in Autism Spectrum Disorders

Rajiv Sharma*

Department of Neurophysiology, AIIMS Delhi, India.

*Corresponding Author:
Rajiv Sharma
Department of Neurophysiology
AIIMS Delhi, India.
E-mail: r.sharma@aiims.edu

Received: 03-Apr-2025, Manuscript No. AANR-25-169345; Editor assigned: 04-Apr-2025, PreQC No. AANR-25-1693455(PQ); Reviewed: 18-Apr-2025, QC No AANR-25-1693455; Revised: 21-Apr-2025, Manuscript No. AANR-25-1693455(R); Published: 28-Apr-2025, DOI:10.35841/aanr -7.2.188

Citation: Sharma R. Neurophysiological correlates of auditory processing deficits in autism spectrum disorders. Neurophysiol Res. 2025;7(2):188.

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Introduction

Autism Spectrum Disorders (ASD) encompass a group of neurodevelopmental conditions characterized by social communication deficits, restricted interests, and repetitive behaviors. One of the less overt but critically significant features of ASD is atypical auditory processing. Individuals with ASD often exhibit hypersensitivity or hyposensitivity to sounds, difficulties in speech perception in noisy environments, and delays in language development. These behavioral manifestations point toward underlying neurophysiological abnormalities that affect the way auditory stimuli are processed in the brain. Advancements in neuroimaging and electrophysiological techniques have facilitated deeper insights into these deficits, revealing altered neural responses in both early and higher-order auditory pathways [1].

Electroencephalography (EEG) and magnetoencephalography (MEG) studies have consistently shown atypical auditory evoked potentials in individuals with ASD, particularly in components such as the M100 and N1 responses. These components, typically originating from the primary auditory cortex, are known to reflect the brain's early detection of auditory stimuli. Delays in the latency and reductions in the amplitude of these responses suggest inefficiencies in the transmission and processing of basic acoustic features. Furthermore, these abnormalities have been observed to correlate with the severity of language impairment and sensory sensitivities. For instance, prolonged M100 latencies in children with ASD have been linked to poor receptive language skills, indicating that even subtle disruptions in temporal processing can cascade into more pronounced communicative challenges [2].

Beyond primary auditory processing, deficits in auditory discrimination and integration also emerge in ASD. Mismatch negativity (MMN), an event-related potential (ERP) component elicited by deviations in auditory patterns, has been frequently studied to assess automatic sound discrimination. Research indicates that individuals with ASD often exhibit reduced MMN amplitudes, suggesting impairments in pre-attentive auditory change detection. This finding is particularly relevant in understanding the difficulties that individuals with ASD face in dynamically changing auditory environments, such as following a conversation in a noisy setting. MEG studies have further localized these MMN anomalies to bilateral superior temporal gyri, reinforcing the idea that auditory perceptual abnormalities in ASD are rooted in cortical-level dysfunctions that hinder efficient sensory encoding and prediction error signaling [3].

In addition to ERP-based measures, functional magnetic resonance imaging (fMRI) has revealed aberrant activation patterns in the auditory cortex and related networks during auditory processing tasks in individuals with ASD. While typically developing individuals show robust activation in response to speech and non-speech stimuli, those with ASD often display hypoactivation or atypical lateralization, particularly in the left hemisphere language areas. This altered functional organization may contribute to both the linguistic and social-communicative difficulties seen in ASD. Moreover, disrupted connectivity between auditory regions and higher-order cortical areas such as the prefrontal cortex and the posterior superior temporal sulcus may further impede the integration of auditory information with social cues, reducing the salience of spoken language and hindering pragmatic communication [4].

The neural oscillatory dynamics underlying auditory processing have also emerged as a critical area of investigation in ASD. Studies examining gamma-band activity—a frequency band associated with local neural synchronization—have found abnormalities in individuals with ASD during auditory tasks. Specifically, reduced gamma-band power and coherence in response to auditory stimuli have been associated with impaired perceptual binding and feature integration. Additionally, alterations in theta and alpha oscillations, which are implicated in attention and inhibitory control, suggest that deficits in auditory processing in ASD may also reflect broader impairments in cortical excitatory-inhibitory balance. These oscillatory disruptions may not only affect perception but also hinder the development of auditory learning and language acquisition over time [5].

Conclusion

The neurophysiological correlates of auditory processing deficits in Autism Spectrum Disorders underscore the complex and multifaceted nature of sensory dysfunction in this population. Electrophysiological and neuroimaging findings consistently point to disruptions in early auditory detection, sound discrimination, cortical activation patterns, and neural oscillatory rhythms. These abnormalities contribute to the sensory sensitivities, language difficulties, and social communication deficits that are hallmark features of ASD. A clearer understanding of these neurophysiological mechanisms offers promising avenues for early identification, targeted intervention, and the development of biomarkers that can guide personalized therapeutic approaches. As research continues to elucidate the neural basis of auditory impairments in ASD, it holds the potential to significantly enhance the quality of life and communication outcomes for individuals affected by this complex condition.

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