Next Article in Journal
Association Between Tinnitus and Angina Pectoris in U.S. Adults: Evidence from NHANES 2009–2018
Previous Article in Journal
The Influence of Hearing Aid Type on Reading: Results of an Eye-Tracking Study at University
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Audiology Research
Volume 16
Issue 2
10.3390/audiolres16020034
audiolres-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

Binaural Processing Deficits in Autism Spectrum Disorder

by
John A. Kara
,
Tashonda B. Vaughn
,
Tanya Gandhi
and
Charles C. Lee
*
Department of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA
*
Author to whom correspondence should be addressed.
Audiol. Res. 2026, 16(2), 34; https://doi.org/10.3390/audiolres16020034
Submission received: 17 December 2025 / Revised: 20 February 2026 / Accepted: 26 February 2026 / Published: 27 February 2026
Browse Figures
Versions Notes

Abstract

The central auditory system integrates signals received from both ears to derive information about the spatial and spectral features of the emitting sound source. This binaural processing of acoustic information is critical for both communication and environmental awareness. However, these binaural computations may become disrupted in individuals diagnosed with autism spectrum disorder (ASD), potentially leading to difficulties with speech perception, sound attention, and sensory hypersensitivity. Here, we present a narrative review of the emerging evidence regarding binaural processing deficits in ASD. These deficits include elevated thresholds for interaural time and level differences and reduced sound localization accuracy. In addition, physiological data suggests that these behavioral traits correspond with abnormal activity in central auditory structures. Molecular and cellular alterations to central auditory circuits may underlie these behavioral and physiological features, which could arise from both genetic and environmental factors. Overall, binaural processing alterations in ASD remain under-studied, with a need for future studies to identify neural circuit-level mechanisms and potential interventions.

1. Introduction

Autism spectrum disorder (ASD) represents a group of neurodevelopmental conditions that are characterized by two main criteria: restricted and repetitive interests and social communication deficits [1,2,3]. The current DSM-5 diagnostic criteria for ASD have evolved from the behaviors first described by Leo Kanner in his seminal 1943 paper, where he wrote, “these children have come into the world with innate inability to form the usual, biologically provided affective contact with people, just as other children come into the world with innate physical or intellectual handicaps,” though his description of the eleven children in his report still remains largely applicable today [4,5].
Several studies and reviews have reported the following information about ASD: (1) it represents a group of neurodevelopmental conditions that are characterized by restricted and repetitive interests and social communication deficits [1,2,3,4,5]; (2) autism was originally considered a rare disorder [6], but (3) ASD’s prevalence in the United States has grown in the past two decades from 1 in 110 to 1 in 31 children, with the world-wide prevalence currently estimated to be 1 in 127 individuals [7,8,9,10]; and (4) advances and revisions of the diagnostic questionnaire have likely impacted the increasing prevalence of ASD [11,12].
Reviews of prior investigations into the underlying characteristics noted autism-specific, sensory dysfunction in social and cognitive functioning [13,14]; individuals with ASD are atypically reactive and unable to habituate to sensory stimuli [15,16,17]. Among 43 sensory domains potentially affected in ASD, auditory processing is noted to play a particularly critical role in communication and social interactions [18,19]. Many individuals with ASD exhibit hypersensitivity to sounds, as well as difficulty understanding speech in noisy environments and in localizing sound sources, which suggest fundamental disruptions in how the brain encodes and integrates auditory spatial information [18,20,21,22,23]. To date, the neural mechanisms underlying sensory perceptual deficits in persons with ASD remain incompletely understood [24,25].
In comparison with other sensory systems, central auditory processing in the brain particularly relies on integrating different signals obtained from both ears to extract spatial and spectral cues about the location and identity of the emitting source, as reviewed in [26,27]. These computations occur through an intricate constellation of crossed connections coursing throughout the auditory brainstem, midbrain, thalamus, and cortex [28,29,30,31,32]. The neurotypical integration of this binaural information enables efficient sound localization, speech segregation in complex acoustic scenes, and the perception of auditory space [33,34]. All these processes depend on millisecond-level temporal precision and balanced excitatory/inhibitory signaling, which are highly sensitive to neurodevelopmental perturbations affecting circuit maturation and synaptic function [33,35]. Varied disruptions at each stage of the central auditory pathways can lead to critical deficits in normal auditory perception in those with ASD [36,37,38,39,40]. Indeed, recent evidence from both human and animal studies suggests that binaural auditory processing is atypical in ASD [41,42]. Psychophysical studies reveal elevated thresholds for interaural time (ITD) and level (ILD) detection, reduced accuracy in sound localization, and impaired spatial unmasking [43,44,45]. Electrophysiological and neuroimaging findings corroborate these behavioral results, demonstrating altered auditory brainstem responses, atypical cortical synchronization, and disrupted connectivity among auditory nuclei [36,46,47]. At the cellular and circuit levels, animal models of ASD exhibit abnormal inhibitory signaling, reduced temporal precision, and impaired synaptic refinement in binaural pathways [48,49,50,51,52]. Understanding how these multilevel alterations converge to produce the auditory and communicative challenges observed in ASD is of both fundamental and translational importance.
In this narrative review, we discuss the evidence for binaural processing deficits in ASD across behavioral, electrophysiological, structural, and cellular domains. To identify relevant studies, we searched all available dates in standard databases (PubMed, Web of Science, and Scopus) for publications that referenced autism terms (ASD, autism spectrum disorders, etc.) with binaural hearing terms (ITD, ILD, auditory, commissural, contralateral). In addition, we assessed the identified primary literature to determine any additional resources. From these sources, we present a narrative survey of binaural auditory processing and its potential disruption in ASD. We discuss the potential consequences of altered binaural processing in individuals with ASD, as a guide towards identifying future biomarkers and therapeutic approaches. Overall, we find that binaural processing deficits in ASD are under-studied; this requires greater attention from the auditory and ASD research communities.

2. Bilateral Connections in the Central Auditory System

Integrating binaural sound information requires that auditory information from both ears be conveyed and combined through bilateral neural connections that cross the midline throughout the central auditory system (Figure 1) [53,54]. Much of the data regarding binaural neural circuitry is derived from a wide range of animal species, e.g., cats, rats, mice, bats, gerbils, etc. Specialized neuroethological adaptations of the basic auditory neural circuits exist across species, e.g., due to head size or communication abilities, but are summarized more generally here as they pertain to humans. Broadly, after the initial neural encoding of sound in the cochlea, auditory information is sent to the cochlear nucleus (CN) via the auditory nerve [55,56]. Thereafter, the first site of binaural convergence is the superior olivary complex (SOC) of the brainstem, which receives projections from both CNs [57,58,59]. The binaural information computed in the SOC is relayed to the nuclei of the lateral lemniscus (NLL) and integrated within the inferior colliculus (IC) in the midbrain [60,61,62]. From the IC, projections ascend to the medial geniculate body (MGB) of the thalamus and then to the auditory cortex [63,64,65,66]. Overall, the brainstem SOC is the most intensively investigated structure for the bilateral integration of auditory information, although bilateral connections are also prevalent in higher auditory structures, although their functional contributions are less clear [57,58,59,67,68].
In the brainstem, the SOC consists of several nuclei: the lateral superior olive (LSO) the medial superior olive (MSO), and the lateral (LNTB) and medial (MNTB) nuclei of the trapezoid body. These structures have well-described roles in computing differences in ILDs and ITDs, respectively [57,58,59]. In general, the LSO computes high-frequency ILDs through the integration of excitatory (glutamatergic) inputs received from ipsilateral ventral CN and inhibitory (glycinergic) inputs received from the ipsilateral MNTB, which itself receives excitatory inputs from the contralateral ventral CN [32,69,70,71]. The LSO also sends axonal projections through the contralateral lateral lemniscus (LLC) to the contralateral inferior colliculus (IC) [67,68]. In comparison, the MSO computes low-frequency ITDs through the integration of ipsilateral and contralateral excitatory inputs from both CNs and inhibitory inputs from the MNTB and LNTB, which themselves receive excitatory inputs from the ipsilateral and contralateral CNs, respectively [57,72,73,74]. The convergence of these bilateral inputs in the MSO likely enables the coincident detection of time-delayed sounds [72]. However, it should be noted that both the LSO and MSO have complete representations of frequencies (both high and low). As such, both structures have overlapping and complementary roles in processing ITDs and ILDs in the envelopes and fine structure of sounds [75,76,77].
The IC is the major auditory center in the midbrain that receives convergent input from ascending brainstem and descending cortical sources [78,79,80,81]. Both ICs are bilaterally connected with one another through the commissure of the inferior colliculus [28]. These projections are primarily topographically organized, with similar nuclear and subnuclear domains connected to homotopic targets in the contralateral IC [82]. Contralateral projections are composed of both excitatory (glutamatergic) and inhibitory (GABAergic) components [28,62,83,84,85]. However, heterotopic contralateral IC projections may arise from distinct cell types based on cellular morphology and neurochemical identity [28,62,68,86]. Functionally, the role of the contralateral IC projections is less clear, but they may be broadly involved in increasing the sensitivity and gain control of binaurally related sounds; however, the contribution of the separate excitatory and inhibitory contralateral projections to these functions remain unresolved [87,88,89].
In the thalamus, the MGB receives ascending input from both inferior colliculi, which are composed of excitatory (~80% glutamatergic) and inhibitory (~20% GABAergic) components [31,65,90,91]. The majority (~70%) of the contralateral tectothalamic projections are branches of the ipsilateral projection and largely target homotopic domains in both MGB, although it remains unclear whether these also form branches to the contralateral IC [28,62,92]. The function of the contralateral tectothalamic pathways is unresolved, but they may also enable gain control or the binding of acoustic objects for higher auditory processing [31].
At the level of the cerebral cortex, all auditory areas are interconnected by bilateral projections that cross through the corpus callosum and link homotopic areas (~90%), with a minority also connecting non-homotopic areas (~10%) [29,93,94,95,96]. The primary auditory cortex (A1) may also exhibit connectional modularity along the tonotopic axis, potentially related to binaural interaction bands [97,98,99,100]. The commissural connections primarily originate from and terminate within cortical layer 3, but in dorsal auditory areas, they also originate from layer 5 [29,54,97,101,102,103]. Although commissural projections were largely believed to be solely excitatory (glutamatergic) in nature, inhibitory (GABAergic) neurons, primarily parvalbumin-positive but possibly others, have been found to contribute substantially to the interhemispheric pathways [103]. Commissural auditory connections may enable the perceptual fusion of auditory information across the midline, which may be related to separate cortical streams for processing either the location or identity of the sound source [104,105,106]. However, these functions may also be in part related to descending corticofugal pathways that target contralateral sites in the midbrain and brainstem [107,108,109]. As such, descending contralateral cortical pathways can potentially influence binaural processing throughout the ascending auditory stream, as reviewed in [79].
Developmentally, the establishment of normal bilateral connectivity requires fine-tuned mediation by both intrinsic genetic and extrinsic environmental cues [110,111,112,113,114]. As such, binaural processing circuits undergo critical periods during which auditory experience calibrates sensitivity to interaural cues, which also depend on intrinsic cues for normal circuit maturation and synaptic refinement [110,115,116]. Disruption of these processes through genetic mutations, altered sensory experience, or neurodevelopmental disorders can lead to persistent deficits in spatial hearing and sound localization [110,111,112,113,114,115,116]. Disruption in any combination of these bilateral networks may contribute to the auditory perceptual anomalies observed in ASD [117,118,119]. The following section reviews the evidence for such disruptions across behavioral, physiological, and neuroanatomical domains in individuals with autism and in a relevant animal model.

3. Binaural Processing Alterations in Autism Spectrum Disorder

Hearing deficits, including binaural processing deficits, are observed in individuals with ASD, likely arising in more than half of ASD cases [120,121]. These perceptual deficits can impact normal spatial hearing by disrupting sound localization, source identification, and stream segregation [20,43,44,122,123,124,125,126,127,128,129]. These behavioral effects correlate with concomitant alterations to neuroanatomical and physiological measures that may arise from atypical development of auditory circuits (Table 1).
Binaural hearing assessments can be performed in either an open- or closed-field environment (Figure 2), e.g., [41,129]. Open-field (or free-field) tasks typically involve an array of sound speakers that are situated at different horizontal and vertical displacements relative to the listener. In contrast, closed-field tasks involve sound stimuli presented directly to the listener via headphones. As with most experimental setups, each has unique advantages and disadvantages [34,130]. Open-field tests enable assessment of complex acoustic, environmental, and head-related cues, while closed-field tests enable fine control of direct aural stimulation, e.g., independent control of ITDs and ILDs. In each setup, the type and pattern of acoustic stimuli can be carefully designed to probe the spectral and temporal responsiveness of the listener. And, in the case of ASD, each type of test has implicated impairments to binaural hearing.
However, several important caveats exist regarding these studies on binaural hearing in ASD. First, it is unclear whether these studies reflect specific deficits in binaural integration, or whether they instead reflect general deficits in temporal processing (e.g., phase-locking for ITDs), or some combination of these factors. Second, non-sensory factors, e.g., attentional state or working memory conditions, are potential confounders to observed performance deficits, particularly in ASD. Finally, the broad range of experimental paradigms in these studies may yield convergent results through divergent mechanisms. As such, more direct interpretations will require further refined studies to disentangle these factors.
Overall, the severity of potential binaural hearing deficits correlates with the severity of ASD symptoms [20,123]. In many studies, ITD and ILD thresholds are elevated in individuals with ASD, although some studies indicate that only responses to ITD cues are affected in this manner (Table 1; Figure 2) [43,126,127,128]. The threshold elevations may be due to the nature of the stimuli that are presented across studies. In addition, spatial unmasking, the ability to exploit spatial separation between target and masking sounds, is reduced or impaired, which is most evident in noisy environments that require fine binaural computations to segregate auditory objects (Table 1; Figure 2) [122,126]. Based on two studies, these deficits are likely evident from early childhood, but direct comparisons across age groups have not been specifically investigated (Table 1) [126,128]. As such, it remains unclear whether potential developmental deficits in binaural hearing are malleable through early or late environmental interventions.
The neurophysiological basis for the observed deficits in binaural hearing has primarily been assessed at the cortical level, using either electroencephalography (EEG) or magnetoencephalography (MEG) [122,126,127,128,129]. These studies reveal reduced or absent auditory evoked potentials in response to binaural stimuli, which suggest that there is impaired cortical integration of binaural cues [122,126,127,128,129]. Interestingly, a recent study suggests that these deficits may encompass altered functional connectivity between frontoparietal and auditory cortices [126]. Moreover, at subcortical levels, one study suggests that the auditory brainstem response to binaural stimulation is diminished in those with ASD; which may be related to alterations in the pathways ascending past the SOC [41].
Neuroanatomical deficits have also been observed in the central auditory pathways of individuals with ASD; however, these have not been specifically assessed vis-à-vis binaural processing deficits [37,38,131,132]. For instance, a series of post-mortem studies have identified gross morphological differences (smaller overall structure and fewer, smaller neurons) in the superior olivary complex [37,38,132]. These likely correspond to similar morphological reductions in auditory-related structures observed through imaging studies, as reviewed in [131]. Further studies should assess the direct relations between these morphological, physiological, and behavioral observations.
Animal models of ASD could illuminate the underlying neural mechanisms of the binaural processing deficits observed in humans. Indeed, general auditory dysfunctions are common to many rodent models of ASD (genetic and environmental) [49,51]. These mouse models exhibit the typical panoply of neural deficits that may underlie binaural processing abnormalities, e.g., impaired synaptic development, disrupted myelination, altered long-range and local connectivity, unbalanced excitatory/inhibitory signaling, and impaired temporal synchrony [49,51]. However, as with human studies, these varied neuroanatomical and physiological changes have not been directly linked to binaural processing deficits in these animal models of ASD. A notable exception is a series of studies in a mouse model of Fragile X Syndrome (FXS), which is the most common single-gene condition that is comorbid with autism [133]. In this FXS mouse model, the binaural interaction component of the ABR exhibits increased latency at 0 ITD [134,135], which is similar, though not identical, to that observed in humans [41]. However, an important caveat with any rodent model of binaural hearing is their smaller head size, which results in preferential use of ILD cues, rather than ITD cues [41,134,135].
Overall, human and animal studies suggest that binaural processing deficits in ASD likely arise across multiple stages of the auditory pathway. These alterations can disrupt the precise temporal coding required for binaural computations in the central auditory system, which contribute to the communication challenges that define autism. A direction for future studies is to specify the precise contributions of alterations to the central auditory pathways that result in binaural hearing deficits.

4. Developmental Impact of Binaural Processing Deficits

How might binaural processing deficits contribute to ASD-related behaviors? Binaural cues are important for isolating sound sources in noisy environments, where competing sounds must be spatially segregated [27,105,136]. In such complex acoustic environments, individuals with ASD may become overwhelmed and have difficulty focusing on specific sound sources; the inability to spatially segregate sound sources can affect speech intelligibility, potentially leading to some communication deficits [20,23]. Moreover, deficits in binaural hearing (and hearing generally) can result in atypical language development [137,138,139]. During early development, exposure to clear speech signals is essential for the acquisition of normal rhythmic and intonation patterns, which often convey sub-textual emotional and social meaning that may be impaired in ASD [140,141,142]. Similarly, binaural hearing deficits may disrupt social orienting, which is the ability to direct attention toward salient social acoustic signals; this can also impair the navigation of complex social interactions [143,144,145].
Auditory hypersensitivity is another common feature in ASD, which may also be impacted by binaural processing deficits [105,146,147]. The reduced ability to localize or segregate sound sources could potentially increase the perceived intensity and ambiguity of auditory stimuli [136,148,149]. More generally, inaccurate filtering of spatial cues may result in sound being experienced as intrusive and unpredictable. At the neural level, the central auditory system has direct connections with the amygdala, originating as early as the MGB [150]. As such, a heightened auditory neural response could aberrantly engage these emotional circuits to reinforce avoidance behaviors and anxiety in noisy environments.
Finally, multisensory integration and attentional control could be impacted by altered binaural processing in ASD [151,152,153]. Individuals with ASD often exhibit impaired audiovisual integration, especially in noisy environments; the alignment of auditory and visual maps could be affected by binaural processing deficits, leading to difficulties in audiovisual speech perception [154]. This may impose greater demands on working memory and attention during communication. The need to rely more heavily on other cues to compensate for degraded auditory input could increase cognitive load, contributing to fatigue and social withdrawal. These effects may be especially pronounced in children, whose developing neural systems are more vulnerable to the developmental consequences of early binaural processing deficiencies [20,120,125].

5. Conclusions

Binaural processing deficits are an under-studied facet of ASD, which likely contribute to its primary and secondary behavioral symptoms. These abnormalities in binaural auditory processing can impact communication, attention, and sensory regulation in ASD. The inability to accurately localize and segregate sounds undermines speech comprehension and social interaction. Moreover, the distorted auditory spatial representations could contribute to sensory overload and anxiety.
Given the emerging evidence, binaural-specific assessments of behavior and physiology may be warranted for persons with ASD. A standard battery of assessments could include the testing of: contralateral acoustic reflexes, contralateral suppression OAEs, dichotic listening, masking level differences, and others. The implementation of such assessments could result in improved treatments and expand our understanding of the magnitude and directionality of binaural processing deficits across the spectrum of these conditions. Finally, future studies should expand on the fundamental mechanisms governing how these binaural perceptual deficits arise, in order to develop effective interventions and treatments.

Author Contributions

Conceptualization, J.A.K., T.B.V., T.G. and C.C.L.; resources, C.C.L.; writing—original draft preparation, J.A.K., T.B.V., T.G. and C.C.L.; writing—review and editing, J.A.K., T.B.V., T.G. and C.C.L.; visualization, J.A.K., T.B.V., T.G. and C.C.L.; supervision, C.C.L.; project administration, C.C.L.; funding acquisition, C.C.L. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by National Institutes of Health Grants R01 DC 019348 and R03 MH 104851 and National Science Foundation Grant IOS 1652432.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
A1Primary auditory cortex
ASDAutism spectrum disorder
CNCochlear nucleus
ICInferior colliculus
ILDInteraural level difference
ITDInteraural time difference
LNTBLateral nucleus of the trapezoid body
LSOLateral superior olivary complex
MGBMedial geniculate body
MNTBMedial nucleus of the trapezoid body
MSOMedial superior olivary complex
SOCSuperior olivary complex

References

  1. Amaral, D.G.; Schumann, C.M.; Nordahl, C.W. Neuroanatomy of autism. Trends Neurosci. 2008, 31, 137–145. [Google Scholar] [CrossRef]
  2. Taurines, R.; Schwenck, C.; Westerwald, E.; Sachse, M.; Siniatchkin, M.; Freitag, C. ADHD and autism: Differential diagnosis or overlapping traits? A selective review. Atten. Defic. Hyperact. Disord. 2012, 4, 115–139. [Google Scholar] [CrossRef] [PubMed]
  3. Belmonte, M.K.; Cook, E.H., Jr.; Anderson, G.M.; Rubenstein, J.L.; Greenough, W.T.; Beckel-Mitchener, A.; Courchesne, E.; Boulanger, L.M.; Powell, S.B.; Levitt, P.R.; et al. Autism as a disorder of neural information processing: Directions for research and targets for therapy. Mol. Psychiatry 2004, 9, 646–663. [Google Scholar] [CrossRef] [PubMed]
  4. Taheri, A.; Perry, A. Exploring the proposed DSM-5 criteria in a clinical sample. J. Autism Dev. Disord. 2012, 42, 1810–1817. [Google Scholar] [CrossRef] [PubMed]
  5. Kanner, L. Autistic disturbances of affective contact. Nerv. Child 1943, 2, 217–250. [Google Scholar]
  6. Lotter, V. Epidemiology of autistic conditions in young children. Soc. Psychiatr. 1967, 1, 163–173. [Google Scholar] [CrossRef]
  7. Baio, J. Prevalence of autism spectrum disorders—Autism and developmental disabilities monitoring network, 14 Sites, United States, 2008. Morb. Mortal. Wkly. Rep. 2012, 61, 1–19. [Google Scholar]
  8. Shaw, K.A.; Williams, S.; Patrick, M.E.; Valencia-Prado, M.; Durkin, M.S.; Howerton, E.M.; Ladd-Acosta, C.M.; Pas, E.T.; Bakian, A.V.; Bartholomew, P.; et al. Prevalence and early identification of autism spectrum disorder among children aged 4 and 8 years—Autism and Developmental Disabilities Monitoring Network, 16 Sites, United States, 2022. MMWR Surveill. Summ. 2025, 74, 1–22. [Google Scholar] [CrossRef]
  9. Kroncke, A.P.; Willard, M.; Huckabee, H. What is Autism? History and foundations. In Assessment of Autism Spectrum Disorder: Critical Issues in Clinical, Forensic and School Settings; Kroncke, A.P., Willard, M., Huckabee, H., Eds.; Springer: Berlin, Germany, 2016; pp. 3–9. [Google Scholar]
  10. Zeidan, J.; Fombonne, E.; Scorah, J.; Ibrahim, A.; Durkin, M.S.; Saxena, S.; Yusuf, A.; Shih, A.; Elsabbagh, M. Global prevalence of autism: A systematic review update. Autism Res. 2022, 15, 778–790. [Google Scholar] [CrossRef]
  11. Zablotsky, B.; Black, L.I.; Maenner, M.J.; Schieve, L.A.; Blumberg, S.J. Estimated prevalence of autism and other developmental disabilities following questionnaire changes in the 2014 National Health Interview Survey. Natl. Health Stat. Rep. 2015, 13, 1–20. [Google Scholar]
  12. Zablotsky, B.; Black, L.I.; Maenner, M.J.; Schieve, L.A.; Danielson, M.L.; Bitsko, R.H.; Blumberg, S.J.; Kogan, M.D.; Boyle, C.A. Prevalence and trends of developmental disabilities among children in the United States: 2009–2017. Pediatrics 2019, 144, e20190811. [Google Scholar] [CrossRef] [PubMed]
  13. Rogers, S.J.; Ozonoff, S. Annotation: What do we know about sensory dysfunction in autism? A critical review of the empirical evidence. J. Child. Psychol. Psychiatr. 2005, 46, 1255–1268. [Google Scholar] [CrossRef] [PubMed]
  14. Marco, E.J.; Hinkley, L.B.; Hill, S.S.; Nagarajan, S.S. Sensory processing in autism: A review of neurophysiologic findings. Pediatr. Res. 2011, 69, 48R–54R. [Google Scholar] [CrossRef] [PubMed]
  15. Hutt, S.; Hutt, C.; Lee, D.; Ounsted, C. A behavioural and electroencephalographic study of autistic children. J. Psychiatr. Res. 1965, 3, 181–197. [Google Scholar] [CrossRef]
  16. DesLauriers, A.M.; Carlson, C.F. Your Child Is Asleep: Early Infantile Autism: Etiology, Treatment, and Parental Influences; Dorsey Press: Homewood, IL, USA, 1969. [Google Scholar]
  17. Rimland, B. Infantile Autism: The Syndrome and Its Implications for a Neural Theory of Behavior; Appleton-Century-Crofts: New York, NY, USA, 1964. [Google Scholar]
  18. Lau, B.K.; Emmons, K.A.; Lee, A.K.C.; Munson, J.; Dager, S.R.; Estes, A.M. The prevalence and developmental course of auditory processing differences in autistic children. Autism Res. 2023, 16, 1413–1424. [Google Scholar] [CrossRef]
  19. Demopoulos, C.; Skiba, S.A.; Kopald, B.E.; Bangera, N.; Paulson, K.; Lewine, J.D. Associations between rapid auditory processing of speech sounds and specific verbal communication skills in autism. Front. Psychol. 2023, 14, 1223250. [Google Scholar] [CrossRef]
  20. Soskey, L.N.; Allen, P.D.; Bennetto, L. Auditory spatial attention to speech and complex non-speech sounds in children with autism spectrum disorder. Autism Res. 2017, 10, 1405–1416. [Google Scholar] [CrossRef]
  21. Poulsen, R.; Williams, Z.; Dwyer, P.; Pellicano, E.; Sowman, P.F.; McAlpine, D. How auditory processing influences the autistic profile: A review. Autism Res. 2024, 17, 2452–2470. [Google Scholar] [CrossRef]
  22. Key, A.P.; Slaboch, K.D. Speech processing in autism spectrum disorder: An integrative review of auditory neurophysiology findings. J. Speech Lang. Hear. Res. 2021, 64, 4192–4212. [Google Scholar] [CrossRef]
  23. Ruiz Callejo, D.; Boets, B. A systematic review on speech-in-noise perception in autism. Neurosci. Biobehav. Rev. 2023, 154, 105406. [Google Scholar] [CrossRef]
  24. Patil, O.; Kaple, M. Sensory processing differences in individuals with autism spectrum disorder: A narrative review of underlying mechanisms and sensory-based interventions. Cureus 2023, 15, e48020. [Google Scholar] [CrossRef] [PubMed]
  25. Narzisi, A.; Vivanti, G.; Berloffa, S.; Milone, A.; Fantozzi, P.; Tancredi, R.; Sesso, G.; Viglione, V.; Fabbri Destro, M.; Pelagatti, S.; et al. Sensory processing in autism: A call for research and action. Front. Psychol. 2025, 16, 1584893. [Google Scholar] [CrossRef] [PubMed]
  26. Yin, T.C.T.; Smith, P.H.; Joris, P.X. Neural mechanisms of binaural processing in the auditory brainstem. Compr. Physiol. 2019, 9, 1503–1575. [Google Scholar] [CrossRef] [PubMed]
  27. Avan, P.; Giraudet, F.; Büki, B. Importance of binaural hearing. Audiol. Neurotol. 2015, 20, 3–6. [Google Scholar] [CrossRef]
  28. Lee, C.C.; Yanagawa, Y.; Imaizumi, K. Commissural functional topography of the inferior colliculus assessed in vitro. Hear. Res. 2015, 328, 94–101. [Google Scholar] [CrossRef]
  29. Lee, C.C.; Winer, J.A. Connections of cat auditory cortex: II. Commissural system. J. Comp. Neurol. 2008, 507, 1901–1919. [Google Scholar] [CrossRef]
  30. Lee, C.C.; Kishan, A.U.; Winer, J.A. Wiring of divergent networks in the central auditory system. Front. Neuroanat. 2011, 5, 46. [Google Scholar] [CrossRef]
  31. Clarke, B.A.; Lee, C.C. Inhibitory projections in the mouse auditory tectothalamic system. Brain Sci. 2018, 9, 103. [Google Scholar] [CrossRef]
  32. Glendenning, K.K.; Hutson, K.A.; Nudo, R.J.; Masterton, R.B. Acoustic chiasm II: Anatomical basis of binaurality in lateral superior olive of cat. J. Comp. Neurol. 1985, 232, 261–288. [Google Scholar] [CrossRef]
  33. Swaminathan, J.; Mason, C.R.; Streeter, T.M.; Best, V.; Roverud, E.; Kidd, G., Jr. Role of binaural temporal fine structure and envelope cues in cocktail-party listening. J. Neurosci. 2016, 36, 8250–8257. [Google Scholar] [CrossRef]
  34. Carlini, A.; Bordeau, C.; Ambard, M. Auditory localization: A comprehensive practical review. Front. Psychol. 2024, 15, 1408073. [Google Scholar] [CrossRef]
  35. Młynarski, W. Efficient coding of spectrotemporal binaural sounds leads to emergence of the auditory space representation. Front. Comp. Neurosci. 2014, 8, 26. [Google Scholar]
  36. Wilson, K.C.; Kornisch, M.; Ikuta, T. Disrupted functional connectivity of the primary auditory cortex in autism. Psychiaty Res. Neuroimag. 2022, 324, 111490. [Google Scholar] [CrossRef] [PubMed]
  37. Kulesza, R.J., Jr.; Lukose, R.; Stevens, L.V. Malformation of the human superior olive in autistic spectrum disorders. Brain Res. 2011, 1367, 360–371. [Google Scholar] [CrossRef] [PubMed]
  38. Kulesza, R.J., Jr.; Mangunay, K. Morphological features of the medial superior olive in autism. Brain Res. 2008, 1200, 132–137. [Google Scholar] [CrossRef]
  39. Schelinski, S.; Tabas, A.; von Kriegstein, K. Altered processing of communication signals in the subcortical auditory sensory pathway in autism. Hum. Brain Mapp. 2022, 43, 1955–1972. [Google Scholar] [CrossRef]
  40. Karavallil Achuthan, S.; Stavrinos, D.; Argueta, P.; Vanderburgh, C.; Holm, H.B.; Kana, R.K. Thalamic functional connectivity and sensorimotor processing in neurodevelopmental disorders. Front. Neurosci. 2023, 17, 1279909. [Google Scholar] [CrossRef]
  41. ElMoazen, D.; Sobhy, O.; Abdou, R.; AbdelMotaleb, H. Binaural interaction component of the auditory brainstem response in children with autism spectrum disorder. Int. J. Pediatr. Otorhinolaryngol. 2020, 131, 109850. [Google Scholar] [CrossRef]
  42. Rosenhall, U.; Nordin, V.; Sandstrom, M. Autism and hearing loss. J. Autism Dev. Disord. 1999, 29, 349–357. [Google Scholar] [CrossRef]
  43. Fujihira, H.; Itoi, C.; Furukawa, S. Sensitivity to interaural level and time differences in individuals with autism spectrum disorder. Sci. Rep. 2022, 12, 19142. [Google Scholar] [CrossRef]
  44. Visser, E.; Zwiers, M.P.; Kan, C.C.; Hoekstra, L.; van Opstal, A.J.; Buitelaar, J.K. Atypical vertical sound localization and sound-onset sensitivity in people with autism spectrum disorders. J. Psychiatry Neurosci. 2013, 38, 398–406. [Google Scholar] [CrossRef] [PubMed]
  45. Sanglakh Ghoochan Atigh, A.; Joghataei, M.T.; Moradkhani, S.; Alizadeh Zarei, M.; Nazari, M.A. Early auditory temporal processing deficit in children with autism spectrum disorder: The research domain criteria framework. Brain Sci. 2024, 14, 896. [Google Scholar] [CrossRef] [PubMed]
  46. Miron, O.; Beam, A.L.; Kohane, I.S. Auditory brainstem response in infants and children with autism spectrum disorder: A meta-analysis of wave V. Autism Res. 2018, 11, 355–363. [Google Scholar] [CrossRef] [PubMed]
  47. Samoylov, I.; Arcara, G.; Buyanova, I.; Davydova, E.; Pereverzeva, D.; Sorokin, A.; Tyushkevich, S.; Mamokhina, U.; Danilina, K.; Dragoy, O.; et al. Altered neural synchronization in response to 2 Hz amplitude-modulated tones in the auditory cortex of children with Autism Spectrum Disorder: An MEG study. Int. J. Psychophysiol. 2024, 203, 112405. [Google Scholar] [CrossRef]
  48. Mann, R.S.; Allman, B.L.; Schmid, S. Developmental changes in electrophysiological properties of auditory cortical neurons in the Cntnap2 knockout rat. J. Neurophysiol. 2023, 129, 937–947. [Google Scholar] [CrossRef]
  49. Castro, A.C.; Monteiro, P.A. Auditory dysfunction in animal models of autism spectrum disorder. Front. Mol. Neurosci. 2022, 15, 845155. [Google Scholar] [CrossRef]
  50. Lee, E.; Lee, J.; Kim, E. Excitation/Inhibition imbalance in animal models of autism spectrum disorders. Biol. Psychiatry 2017, 81, 838–847. [Google Scholar] [CrossRef]
  51. Wilde, C.; Constantin, L.; Thorne, P.R.; Montgomery, J.M.; Scott, E.K.; Cheyne, J.E. Auditory processing in rodent models of autism: A systematic review. J. Neurodev. Dis. 2022, 14, 48. [Google Scholar] [CrossRef]
  52. Gandhi, T.; Canepa, C.R.; Adeyelu, T.T.; Adeniyi, P.A.; Lee, C.C. Neuroanatomical alterations in the CNTNAP2 mouse model of autism spectrum disorder. Brain Sci. 2023, 13, 891. [Google Scholar] [CrossRef]
  53. Middlebrooks, J.C. Auditory system: Central pathways. In Encyclopedia of Neuroscience; Squire, L., Ed.; Academic Press: San Diego, CA, USA, 2009; pp. 745–752. [Google Scholar]
  54. Winer, J.A. The functional architecture of the medial geniculate body and the primary auditory cortex. In Springer Handbook of Auditory Research, Volume 1, The Mammalian Auditory Pathways: Neuroanatomy; Webster, D.B., Popper, A.N., Fay, R.R., Eds.; Springer: New York, NY, USA, 1992; pp. 222–409. [Google Scholar]
  55. Ryugo, D.K.; Willard, F.H.; Fekete, D.M. Differential afferent projections to the inferior colliculus from the cochlear nucleus in the albino mouse. Brain Res. 1981, 210, 342–349. [Google Scholar] [CrossRef]
  56. Cant, N.B.; Benson, C.G. Parallel auditory pathways: Projection patterns of the different neuronal populations in the dorsal and ventral cochlear nuclei. Brain Res. Bull. 2003, 60, 457–474. [Google Scholar] [CrossRef] [PubMed]
  57. Yin, T.C.T.; Chan, J.C.K. Interaural time sensitivity in medial superior olive of cat. J. Neurophysiol. 1990, 64, 465–488. [Google Scholar] [CrossRef] [PubMed]
  58. Park, T.J.; Klug, A.; Holinstat, M.; Grothe, B. Interaural level difference processing in the lateral superior olive and the inferior colliculus. J. Neurophysiol. 2004, 92, 289–301. [Google Scholar] [CrossRef] [PubMed]
  59. Franken, T.P.; Roberts, M.T.; Wei, L.; Golding, N.L.; Joris, P.X. In vivo coincidence detection in mammalian sound localization generates phase delays. Nat. Neurosci. 2015, 18, 444–452. [Google Scholar] [CrossRef]
  60. Nordeen, K.W.; Killackey, H.P.; Kitzes, L.M. Ascending auditory projections to the inferior colliculus in the adult gerbil, Meriones unguiculatus. J. Comp. Neurol. 1983, 214, 131–143. [Google Scholar] [CrossRef]
  61. Moore, D.R.; Kitzes, L.M. Projections from the cochlear nucleus to the inferior colliculus in normal and neonatally cochlea-ablated gerbils. J. Comp. Neurol. 1985, 240, 180–195. [Google Scholar] [CrossRef]
  62. Chen, C.; Cheng, M.; Ito, T.; Song, S. Neuronal organization in the inferior colliculus revisited with cell-type-dependent monosynaptic tracing. J. Neurosci. 2018, 38, 3318–3332. [Google Scholar] [CrossRef]
  63. Imaizumi, K.; Lee, C.C. Auditory thalamocortical transformations. In Encyclopedia of Computational Neuroscience; Jaeger, D., Jung, R., Eds.; Springer: New York, NY, USA, 2022; pp. 315–328. [Google Scholar]
  64. Winer, J.A.; Miller, L.M.; Lee, C.C.; Schreiner, C.E. Auditory thalamocortical transformation: Structure and function. Trends Neurosci. 2005, 28, 255–263. [Google Scholar] [CrossRef]
  65. Wenstrup, J.J. The tectothalamic system. In The Inferior Colliculus; Winer, J.A., Schreiner, C.E., Eds.; Springer: New York, NY, USA, 2005; pp. 200–230. [Google Scholar]
  66. Lee, C.C. Thalamic and cortical pathways supporting auditory processing. Brain Lang. 2013, 126, 22–28. [Google Scholar] [CrossRef]
  67. Kelly, J.B.; Liscum, A.; van Adel, B.; Ito, M. Projections from the superior olive and lateral lemniscus to tonotopic regions of the rat’s inferior colliculus. Hear. Res. 1998, 116, 43–54. [Google Scholar] [CrossRef]
  68. Ito, T.; Oliver, D.L. The basic circuit of the IC: Tectothalamic neurons with different patterns of synaptic organization send different messages to the thalamus. Front. Neural Circuits 2012, 6, 48. [Google Scholar] [CrossRef]
  69. Doucet, J.R.; Ryugo, D.K. Axonal pathways to the lateral superior olive labeled with biotinylated dextran amine injections in the dorsal cochlear nucleus of rats. J. Comp. Neurol. 2003, 461, 452–465. [Google Scholar] [CrossRef] [PubMed]
  70. Henkel, C.K.; Gabriele, M.L. Organization of the disynaptic pathway from the anteroventral cochlear nucleus to the lateral superior olivary nucleus in the ferret. Anat. Embryol. 1999, 199, 149–160. [Google Scholar] [CrossRef] [PubMed]
  71. Cant, N.B.; Casseday, J.H. Projections from the anteroventral cochlear nucleus to the lateral and medial superior olivary nuclei. J. Comp. Neurol. 1986, 247, 457–476. [Google Scholar] [CrossRef] [PubMed]
  72. Couchman, K.; Grothe, B.; Felmy, F. Medial superior olivary neurons receive surprisingly few excitatory and inhibitory inputs with balanced strength and short-term dynamics. J. Neurosci. 2010, 30, 17111–17121. [Google Scholar] [CrossRef]
  73. Goldberg, J.M.; Brown, P.B. Response of binaural neurons of dog superior olivary complex to dichotic tonal stimuli: Some physiological mechanisms of sound localization. J. Neurophysiol. 1969, 32, 613–636. [Google Scholar] [CrossRef]
  74. Grothe, B.; Sanes, D.H. Bilateral inhibition by glycinergic afferents in the medial superior olive. J. Neurophysiol. 1993, 69, 1192–1196. [Google Scholar] [CrossRef]
  75. Tsuchitani, C.; Boudreau, J.C. Single unit analysis of cat superior olive S segment with tonal stimuli. J. Neurophysiol. 1966, 29, 684–697. [Google Scholar] [CrossRef]
  76. Batra, R.; Kuwada, S.; Fitzpatrick, D.C. Sensitivity to interaural temporal disparities of low- and high-frequency neurons in the superior olivary complex. I. Heterogeneity of responses. J. Neurophysiol. 1997, 78, 1222–1236. [Google Scholar] [CrossRef]
  77. Tsuchitani, C. Functional organization of lateral cell groups of cat superior olivary complex. J. Neurophysiol. 1977, 40, 296–318. [Google Scholar] [CrossRef]
  78. Casseday, J.H.; Fremouw, T.; Covey, E. The inferior colliculus: A hub for the central auditory system. In Springer Handbook of Auditory Research, Volume 15: Integrative Functions in the Mammalian Auditory Pathway; Oertel, D., Popper, A.N., Fay, R.R., Eds.; Springer: New York, NY, USA, 2002; Volume 15, pp. 238–295. [Google Scholar]
  79. Winer, J.A. Decoding the auditory corticofugal systems. Hear. Res. 2006, 212, 1–8. [Google Scholar] [CrossRef] [PubMed]
  80. Reetz, G.; Ehret, G. Inputs from three brainstem sources to identified neurons of the mouse inferior colliculus slice. Brain Res. 1999, 816, 527–543. [Google Scholar] [CrossRef] [PubMed]
  81. Winer, J.A.; Schreiner, C.E. (Eds.) The Inferior Colliculus; Springer: New York, NY, USA, 2005; p. 705. [Google Scholar]
  82. Saldaña, E.; Merchán, M.A. Intrinsic and commissural connections of the rat inferior colliculus. J. Comp. Neurol. 1992, 319, 417–437. [Google Scholar] [CrossRef] [PubMed]
  83. Smith, P.H. Anatomy and physiology of multipolar cells in the rat inferior collicular cortex using the in vitro brain slice technique. J. Neurosci. 1992, 12, 3700–3715. [Google Scholar] [CrossRef]
  84. Moore, D.R.; Kotak, V.C.; Sanes, D.H. Commissural and lemniscal synaptic input to the gerbil inferior colliculus. J. Neurophysiol. 1998, 80, 2229–2236. [Google Scholar] [CrossRef]
  85. Ma, J.; Han, Y.; Yao, Y.; Wang, H.; Chen, M.; Fu, Z.; Chen, Q.; Tang, J. Investigation of neuron latency modulated by bilateral inferior collicular interactions using whole-cell patch clamp recording in brain slices. Neural Plast. 2021, 2021, 8030870. [Google Scholar] [CrossRef]
  86. Anair, J.D.; Silveira, M.A.; Mirjalili, P.; Beebe, N.L.; Schofield, B.R.; Roberts, M.T. Inhibitory NPY neurons provide a large and heterotopic commissural projection in the inferior colliculus. Front. Neural Circuits 2022, 16, 871924. [Google Scholar] [CrossRef]
  87. Orton, L.D.; Rees, A. Intercollicular commissural connections refine the representation of sound frequency and level in the auditory midbrain. eLife 2014, 3, e03764. [Google Scholar] [CrossRef]
  88. Malmierca, M.S.; Hernández, O.; Falconi, A.; Lopez-Poveda, E.A.; Merchán, M.; Rees, A. The commissure of the inferior colliculus shapes frequency response areas in rat: An in vivo study using reversible blockade with microinjection of kynurenic acid. Exp. Brain Res. 2003, 153, 522–529. [Google Scholar] [CrossRef]
  89. Orton, L.D.; Papasavvas, C.A.; Rees, A. Commissural gain control enhances the midbrain representation of sound location. J. Neurosci. 2016, 36, 4470–4481. [Google Scholar] [CrossRef]
  90. Mellott, J.G.; Foster, N.L.; Nakamoto, K.T.; Motts, S.D.; Schofield, B.R. Distribution of GABAergic cells in the inferior colliculus that project to the thalamus. Front. Neuroanat. 2014, 8, 17. [Google Scholar] [CrossRef]
  91. Winer, J.A.; Saint Marie, R.L.; Larue, D.T.; Oliver, D.L. GABAergic feedforward projections from the inferior colliculus to the medial geniculate body. Proc. Natl. Acad. Sci. USA 1996, 93, 8005–8010. [Google Scholar] [CrossRef] [PubMed]
  92. Mellott, J.G.; Beebe, N.L.; Schofield, B.R. Bilateral projections to the thalamus from individual neurons in the inferior colliculus. J. Comp. Neurol. 2019, 527, 1118–1126. [Google Scholar] [CrossRef] [PubMed]
  93. Pan, J.; Yang, C.; Li, R.; Li, J.; Sun, P.; Liu, Y.; Liu, K.; Liao, X.; Jia, H.; Yu, Z.; et al. Brain-wide atlas of outputs and inputs of mouse auditory cortex revealed by modified viral labeling strategies. Fundam. Res. 2025. [Google Scholar] [CrossRef]
  94. Rouiller, E.M.; Simm, G.M.; Villa, A.E.; de Ribaupierre, Y.; de Ribaupierre, F. Auditory corticocortical interconnections in the cat: Evidence for parallel and hierarchical arrangement of the auditory cortical areas. Exp. Brain Res. 1991, 86, 483–505. [Google Scholar] [CrossRef]
  95. Kaas, J.H.; Hackett, T.A. Subdivisions of auditory cortex and processing streams in primates. Proc. Natl. Acad. Sci. USA 2000, 97, 11793–11799. [Google Scholar] [CrossRef]
  96. Lee, C.C.; Winer, J.A. Convergence of thalamic and cortical pathways in cat auditory cortex. Hear. Res. 2011, 274, 85–94. [Google Scholar] [CrossRef]
  97. Code, R.A.; Winer, J.A. Columnar organization and reciprocity of commissural connections in cat primary auditory cortex (AI). Hear. Res. 1986, 23, 205–222. [Google Scholar] [CrossRef]
  98. Imig, T.J.; Brugge, J.F. Sources and terminations of callosal axons related to binaural and frequency maps in primary auditory cortex of the cat. J. Comp. Neurol. 1978, 182, 637–660. [Google Scholar] [CrossRef]
  99. Kelly, J.P.; Wong, D. Laminar connections of the cat’s auditory cortex. Brain Res. 1981, 212, 1–15. [Google Scholar] [CrossRef]
  100. Middlebrooks, J.C.; Dykes, R.W.; Merzenich, M.M. Binaural response-specific bands in primary auditory cortex (AI) of the cat: Topographical organization orthogonal to isofrequency contours. Brain Res. 1980, 18, 31–48. [Google Scholar] [CrossRef]
  101. de la Mothe, L.A.; Blumell, S.; Kajikawa, Y.; Hackett, T.A. Cortical connections of the auditory cortex in marmoset monkeys: Core and medial belt regions. J. Comp. Neurol. 2006, 496, 27–71. [Google Scholar] [CrossRef] [PubMed]
  102. de la Mothe, L.A.; Blumell, S.; Kajikawa, Y.; Hackett, T.A. Cortical connections of auditory cortex in marmoset monkeys: Lateral belt and parabelt regions. Anat. Rec. 2012, 295, 800–821. [Google Scholar] [CrossRef] [PubMed]
  103. Rock, C.; Zurita, H.; Lebby, S.; Wilson, C.J.; Apicella, A.J. Cortical circuits of callosal GABAergic neurons. Cereb. Cortex 2018, 28, 1154–1167. [Google Scholar] [CrossRef]
  104. Poirier, P.; Lepore, F.; Provençal, C.; Ptito, M.; Guillemot, J.P. Binaural noise stimulation of auditory callosal fibers of the cat: Responses to interaural time delays. Exp. Brain Res. 1995, 104, 30–40. [Google Scholar] [CrossRef] [PubMed]
  105. Molis, M.R.; Reiss, L.A.J. How abnormal binaural fusion explains hearing in noise difficulties. Hear. J. 2021, 74, 34–36. [Google Scholar] [CrossRef]
  106. Lepore, F.; Lassonde, M.; Poirier, P.; Schiavetto, A.; Veillette, N. Midline sensory integration in callosal agenesis. In Advances in Behavioral Biology; Lassonde, M., Jeeves, M.A., Eds.; Springer: Boston, MA, USA, 1994; Volume 42. [Google Scholar]
  107. Bertero, A.; Garcia, C.; Apicella, A.J. Corticofugal VIP Gabaergic projection neurons in the mouse auditory and motor cortex. Front. Neural Circuits 2021, 15, 714780. [Google Scholar] [CrossRef]
  108. Saldaña, E.; Feliciano, M.; Mugnaini, E. Distribution of descending projections from primary auditory neocortex to inferior colliculus mimics the topography of intracollicular projections. J. Comp. Neurol. 1996, 371, 15–40. [Google Scholar] [CrossRef]
  109. Terreros, G.; Delano, P.H. Corticofugal modulation of peripheral auditory responses. Front. Syst. Neurosci. 2015, 9, 134. [Google Scholar] [CrossRef]
  110. Keating, P.; Dahmen, J.C.; King, A.J. Context-specific reweighting of auditory spatial cues following altered experience during development. Curr. Biol. 2013, 23, 1291–1299. [Google Scholar] [CrossRef]
  111. Yamoah, E.N.; Pavlinkova, G.; Fritzsch, B. Molecular cascades that build and connect auditory neurons from hair cells to the auditory cortex. J. Exp. Neurol. 2025, 6, 111–120. [Google Scholar] [CrossRef]
  112. Lee, M.Y.; Kim, D.H.; Park, S.K.; Jun, S.B.; Lee, Y.; Choi, J.J.; Yoo, H.J.; Raphael, Y.; Oh, S.H. Disappearance of contralateral dominant neural activity of auditory cortex after single-sided deafness in adult rats. Neurosci. Lett. 2017, 657, 171–178. [Google Scholar] [CrossRef] [PubMed]
  113. Krasewicz, J.; Yu, W.M. Eph and ephrin signaling in the development of the central auditory system. Dev. Dyn. 2023, 252, 10–26. [Google Scholar] [CrossRef] [PubMed]
  114. Mrsic-Flogel, T.D.; Versnel, H.; King, A.J. Development of contralateral and ipsilateral frequency representations in ferret primary auditory cortex. Eur. J. Neurosci. 2006, 23, 780–792. [Google Scholar] [CrossRef] [PubMed]
  115. Kral, A. Auditory critical periods: A review from system’s perspective. Neuroscience 2013, 247, 117–133. [Google Scholar] [CrossRef]
  116. Persic, D.; Thomas, M.E.; Pelekanos, V.; Ryugo, D.K.; Takesian, A.E.; Krumbholz, K.; Pyott, S.J. Regulation of auditory plasticity during critical periods and following hearing loss. Hear. Res. 2020, 397, 107976. [Google Scholar] [CrossRef]
  117. Gonçalves, A.M.; Monteiro, P. Autism Spectrum Disorder and auditory sensory alterations: A systematic review on the integrity of cognitive and neuronal functions related to auditory processing. J. Neural Transm. 2023, 130, 325–408. [Google Scholar] [CrossRef]
  118. Watanabe, T.; Rees, G. Anatomical imbalance between cortical networks in autism. Sci. Rep. 2016, 6, 31114. [Google Scholar] [CrossRef]
  119. Wang, J.; Wang, X.; Wang, R.; Duan, X.; Chen, H.; He, C.; Zhai, J.; Wu, L.; Chen, H. Atypical resting-state functional connectivity of intra/inter-sensory networks is related to symptom severity in young boys with autism spectrum disorder. Front. Physiol. 2021, 12, 626338. [Google Scholar] [CrossRef]
  120. Azouz, H.G.; Kozou, H.; Khalil, M.; Abdou, R.M.; Sakr, M. The correlation between central auditory processing in autistic children and their language processing abilities. Int. J. Pediatr. Otorhinolaryngol. 2014, 78, 2297–2300. [Google Scholar] [CrossRef]
  121. Demopoulos, C.; Lewine, J.D. Audiometric profiles in autism spectrum disorders: Does subclinical hearing loss impact communication? Autism Res. 2016, 9, 107–120. [Google Scholar] [CrossRef] [PubMed]
  122. Teder-Sälejärvi, W.A.; Pierce, K.L.; Courchesne, E.; Hillyard, S.A. Auditory spatial localization and attention deficits in autistic adults. Brain Res. Cogn. Brain Res. 2005, 23, 221–234. [Google Scholar] [CrossRef] [PubMed]
  123. Skewes, J.C.; Gebauer, L. Brief report: Suboptimal auditory localization in autism spectrum disorder: Support for the bayesian account of sensory symptoms. J. Autism Dev. Disord. 2016, 46, 2539–2547. [Google Scholar] [CrossRef] [PubMed]
  124. Groen, W.B.; van Orsouw, L.; Huurne, N.; Swinkels, S.; van der Gaag, R.J.; Buitelaar, J.K.; Zwiers, M.P. Intact spectral but abnormal temporal processing of auditory stimuli in autism. J. Autism Dev. Disord. 2009, 39, 742–750. [Google Scholar] [CrossRef]
  125. Lepistö, T.; Kuitunen, A.; Sussman, E.; Saalasti, S.; Jansson-Verkasalo, E.; Nieminen-von Wendt, T.; Kujala, T. Auditory stream segregation in children with Asperger syndrome. Biol. Psychol. 2009, 82, 301–307. [Google Scholar] [CrossRef]
  126. Osorio, S.; Tan, J.; Levine, G.; Ahlfors, S.P.; Graham, S.; Mamashli, F.; Khan, S.; Joseph, R.M.; Nayal, Z.; Losh, A.; et al. Lower cortical activation and altered functional connectivity characterize passive auditory spatial attention in ASD. Autism Res. 2025, 18, 2240–2253. [Google Scholar] [CrossRef]
  127. Lodhia, V.; Hautus, M.J.; Johnson, B.W.; Brock, J. Atypical brain responses to auditory spatial cues in adults with autism spectrum disorder. Eur. J. Neurosci. 2018, 47, 682–689. [Google Scholar] [CrossRef]
  128. Brock, J.; Bzishvili, S.; Reid, M.; Hautus, M.; Johnson, B.W. Brief report: Atypical neuromagnetic responses to illusory auditory pitch in children with autism spectrum disorders. J. Autism Dev. Disord. 2013, 43, 2726–2731. [Google Scholar] [CrossRef]
  129. Lodhia, V.; Brock, J.; Johnson, B.W.; Hautus, M.J. Reduced object related negativity response indicates impaired auditory scene analysis in adults with autistic spectrum disorder. PeerJ 2014, 25, e261. [Google Scholar] [CrossRef]
  130. Sampath, S.; Aisha, S.; Neelamegarajan, D.; Jain, C.; Nisha, K.V. Comparison of a free-field and a closed-field sound source identification paradigms in assessing spatial acuity in adults with normal hearing sensitivity. J. Audiol. Otol. 2023, 27, 219–226. [Google Scholar] [CrossRef]
  131. Seif, A.; Shea, C.; Schmid, S.; Stevenson, R.A. A systematic review of brainstem contributions to autism spectrum disorder. Front. Integr. Neurosci. 2021, 15, 760116. [Google Scholar] [CrossRef]
  132. Mansour, Y.; Kulesza, R. Three dimensional reconstructions of the superior olivary complex from children with autism spectrum disorder. Hear. Res. 2020, 393, 107974. [Google Scholar] [CrossRef] [PubMed]
  133. Abbeduto, L.; McDuffie, A.; Thurman, A.J. The fragile X syndrome–autism comorbidity: What do we really know? Front. Genet. 2014, 5, 355. [Google Scholar]
  134. McCullagh, E.A.; Poleg, S.; Greene, N.T.; Huntsman, M.M.; Tollin, D.J.; Klug, A. Characterization of auditory and binaural spatial hearing in a Fragile X Syndrome mouse model. eNeuro 2020, 7, ENEURO.0300-0319.2019. [Google Scholar] [CrossRef] [PubMed]
  135. Chawla, A.; McCullagh, E.A. Auditory brain stem responses in the C57BL/6J Fragile X Syndrome-knockout mouse model. Front. Integr. Neurosci. 2022, 15, 803483. [Google Scholar] [CrossRef]
  136. Gallun, F.J. Impaired binaural hearing in adults: A selected review of the literature. Front. Neurosci. 2021, 15, 610957. [Google Scholar] [CrossRef]
  137. Davidson, M.M.; Weismer, S.E. A discrepancy in comprehension and production in early language development in ASD: Is it clinically relevant? J. Autism Dev. Disord. 2017, 47, 2163–2175. [Google Scholar] [CrossRef]
  138. Haebig, E.; Kaushanskaya, M.; Ellis Weismer, S. Lexical processing in school-age children with autism spectrum disorder and children with specific language impairment: The role of semantics. J. Autism Dev. Disord. 2015, 45, 4109–4123. [Google Scholar] [CrossRef]
  139. Félix, J.; Santos, M.E.; Benitez-Burraco, A. Specific language impairment, autism spectrum disorders and social (pragmatic) communication disorders: Is there overlap in language deficits? A review. J. Autism Dev. Disord. 2024, 11, 86–106. [Google Scholar] [CrossRef]
  140. Kellerman, G.R.; Fan, J.; Gorman, J.M. Auditory abnormalities in autism: Toward functional distinctions among findings. CNS Spectr. 2005, 10, 748–756. [Google Scholar] [CrossRef]
  141. Foss-Feig, J.H.; Schauder, K.B.; Key, A.P.; Wallace, M.T.; Stone, W.L. Audition-specific temporal processing deficits associated with language function in children with autism spectrum disorder. Autism Res. 2017, 10, 845–1856. [Google Scholar] [CrossRef] [PubMed]
  142. Reindal, L.; Nærland, T.; Weidle, B.; Lydersen, S.; Andreassen, O.A.; Sund, A.M. Structural and Pragmatic Language Impairments in Children Evaluated for Autism Spectrum Disorder (ASD). J. Autism Dev. Disord. 2023, 53, 701–719. [Google Scholar] [CrossRef] [PubMed]
  143. Unruh, K.E.; Sasson, N.J.; Shafer, R.L.; Whitten, A.; Miller, S.J.; Turner-Brown, L.; Bodfish, J.W. Social orienting and attention is influenced by the presence of competing nonsocial information in adolescents with autism. Front. Neurosci. 2016, 10, 586. [Google Scholar] [CrossRef] [PubMed]
  144. Hedger, N.; Dubey, I.; Chakrabarti, B. Social orienting and social seeking behaviors in ASD. A meta analytic investigation. Neurosci. Biobehav. Rev. 2020, 119, 376–395. [Google Scholar] [CrossRef]
  145. Tsuji, Y.; Imaizumi, S. Autistic traits and speech perception in social and non-social noises. Sci. Rep. 2024, 14, 1414. [Google Scholar] [CrossRef]
  146. Poulsen, R.; Tan, D.W.; Sowman, P.F.; McAlpine, D.; Pellicano, E. Auditory environments influence the link between Autistic traits and quality of life. Sci. Rep. 2025, 15, 10612. [Google Scholar] [CrossRef]
  147. Danesh, A.A.; Howery, S.; Aazh, H.; Kaf, W.; Eshraghi, A.A. Hyperacusis in autism spectrum disorders. Audiol. Res. 2021, 11, 547–556. [Google Scholar] [CrossRef]
  148. Rodier, P.M.; Hyman, S.L. Early environmental factors in autism. Ment. Retard. Dev. Disabil. Res. Rev. 1998, 4, 121–128. [Google Scholar] [CrossRef]
  149. Williams, Z.J.; He, J.L.; Cascio, C.J.; Woynaroski, T.G. A review of decreased sound tolerance in autism: Definitions, phenomenology, and potential mechanisms. Neurosci. Biobehav. Rev. 2021, 121, 1–17. [Google Scholar] [CrossRef]
  150. Doron, N.N.; Ledoux, J.E. Organization of projections to the lateral amygdala from auditory and visual areas of the thalamus in the rat. J. Comp. Neurol. 1999, 412, 383–409. [Google Scholar] [CrossRef]
  151. Kawakami, S.; Otsuka, S. Multisensory processing in autism spectrum disorders. In Autism Spectrum Disorders [Internet]; Grabrucker, A.M., Ed.; Exon Publications: Brisbane, Australia, 2021. [Google Scholar]
  152. Stevenson, R.A.; Siemann, J.K.; Schneider, B.C.; Eberly, H.E.; Woynaroski, T.G.; Camarata, S.M.; Wallace, M.T. Multisensory temporal integration in autism spectrum disorders. J. Neurosci. 2014, 34, 691–697. [Google Scholar] [CrossRef]
  153. Dwyer, P.; Takarae, Y.; Zadeh, I.; Rivera, S.M.; Saron, C.D. Multisensory integration and interactions across vision, hearing, and somatosensation in autism spectrum development and typical development. Neuropsychologia 2022, 175, 108340. [Google Scholar] [CrossRef]
  154. Feldman, J.I.; Dunham, K.; Cassidy, M.; Wallace, M.T.; Liu, Y.; Woynaroski, T.G. Audiovisual multisensory integration in individuals with autism spectrum disorder: A systematic review and meta-analysis. Neurosci. Biobehav. Rev. 2018, 95, 220–234. [Google Scholar] [CrossRef]
Audiolres 16 00034 g001
Figure 1. Schematic summary of major bilateral projections in the ascending auditory system. Bilateral connections occur throughout the auditory brainstem (CN: cochlear nucleus; SOC: superior olivary complex), pons (NLL: nucleus of the lateral lemniscus), midbrain and thalamus (IC: inferior colliculus; MGB: medial geniculate body), and forebrain (AC: auditory cortex). In addition, bilateral projections are also prevalent in the descending auditory system (not depicted for clarity). The schematic is of a mouse brain. Auditory structures are depicted in their general rostrocaudal and lateromedial positions, but not necessarily in their respective dorsoventral positions.
Figure 1. Schematic summary of major bilateral projections in the ascending auditory system. Bilateral connections occur throughout the auditory brainstem (CN: cochlear nucleus; SOC: superior olivary complex), pons (NLL: nucleus of the lateral lemniscus), midbrain and thalamus (IC: inferior colliculus; MGB: medial geniculate body), and forebrain (AC: auditory cortex). In addition, bilateral projections are also prevalent in the descending auditory system (not depicted for clarity). The schematic is of a mouse brain. Auditory structures are depicted in their general rostrocaudal and lateromedial positions, but not necessarily in their respective dorsoventral positions.
Audiolres 16 00034 g001
Audiolres 16 00034 g002
Figure 2. Schematic summary of binaural stimulation setups. Open-field acoustic stimuli are delivered through arrays of speakers positioned at varying horizontal and/or vertical angular displacements from the listener, while closed-field assessments are delivered directly to the listener via headphones. Individuals with ASD display varying behavioral and electrophysiological alterations in both setups.
Figure 2. Schematic summary of binaural stimulation setups. Open-field acoustic stimuli are delivered through arrays of speakers positioned at varying horizontal and/or vertical angular displacements from the listener, while closed-field assessments are delivered directly to the listener via headphones. Individuals with ASD display varying behavioral and electrophysiological alterations in both setups.
Audiolres 16 00034 g002
Table 1. Evidence for binaural processing deficits in individuals with ASD.
Table 1. Evidence for binaural processing deficits in individuals with ASD.
StudyResults
Teder-Sälejärvi (2005)
Ref. [122]		Behavior: Males with ASD (29–39 years old) exhibited a reduction in performance in identifying a sound source in a noisy open-field environment, although performance was unaffected in a simple localization task. EEG: Individuals with ASD exhibited a more shallow fall-off of the N1 auditory event-related potentials in the noisy sound localization task.
Visser et al. (2013)
Ref. [44]		Behavior: Adults with ASD (~27 years old) exhibited worse performance in localizing sound in the vertical but not the horizontal domain in an open field. In addition, individuals with ASD exhibited shorter temporal binding windows for the precedence effect.
Brock et al. (2013)
Ref. [128]		MEG: Boys with ASD (8–11 years old) lacked an object-related negativity response in both hemispheres and exhibited increased differential responses in the right hemisphere to pitch stimuli, when presented with a dichotic stimulus with ITD-related cues.
Lodhia et al. (2014)
Ref. [129]		EEG: Adults with ASD (~22 years old) exhibited a reduction in the object-related negativity response, but no change in the P400 response, when presented with a dichotic stimulus with ITD-related cues.
Skewes and Gebauer (2016)
Ref. [123]		Behavior: Adults with ASD (~27 years old) exhibited poorer performance in a horizontal sound localization task, i.e., pure-tone, sound intensity panned between left and right headphones. Performance of individuals with ASD was ‘more sub-optimal’ than that of controls, based on a Bayesian signal-detection model.
Soskey et al. (2017)
Ref. [20]		Behavior: Youths with ASD (10–17 years old) exhibited worse performance on focusing on sound cues originating from in front of them in an open field. Performance deficits were correlated with severity of ASD diagnoses.
Lodhia et al. (2018)
Ref. [127]		Behavior: Adults with ASD (~25 years old) exhibited no difference in auditory object formation based on dichotic pitch stimuli delivered through headphones. EEG: Object-related negativity response was absent for ITD-related cues, but not ILD-related cues.
ElMoazen et al. (2020)
Ref. [41]		ABR: Children with ASD (years old) exhibited decreases in the predicted amplitude of the binaural interaction component of the auditory brainstem response, between peaks IV and VI.
Fujihira et al. (2022)
Ref. [43]		Behavior: Adults with ASD (20–45 years old) exhibited higher threshold sensitivity to ITD and ILD cues presented through headphones. Sensitivity to ITD cues varied across a greater range, while ILD sensitivity was not as diversely distributed.
Osorio et al. (2025)
Ref. [126]		MEG: Children with ASD (6–17 years old) exhibited reduced auditory cortical activation and altered functional connectivity between frontoparietal and auditory cortices, in an ITD swapping ‘jump’ stimulus presented through headphones.
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Kara, J.A.; Vaughn, T.B.; Gandhi, T.; Lee, C.C. Binaural Processing Deficits in Autism Spectrum Disorder. Audiol. Res. 2026, 16, 34. https://doi.org/10.3390/audiolres16020034

AMA Style

Kara JA, Vaughn TB, Gandhi T, Lee CC. Binaural Processing Deficits in Autism Spectrum Disorder. Audiology Research. 2026; 16(2):34. https://doi.org/10.3390/audiolres16020034

Chicago/Turabian Style

Kara, John A., Tashonda B. Vaughn, Tanya Gandhi, and Charles C. Lee. 2026. "Binaural Processing Deficits in Autism Spectrum Disorder" Audiology Research 16, no. 2: 34. https://doi.org/10.3390/audiolres16020034

APA Style

Kara, J. A., Vaughn, T. B., Gandhi, T., & Lee, C. C. (2026). Binaural Processing Deficits in Autism Spectrum Disorder. Audiology Research, 16(2), 34. https://doi.org/10.3390/audiolres16020034

Article Metrics

Back to TopTop