By Hillary Siddons, AuD Candidate at UConn
Autism spectrum disorder (ASD) is a group of multifaceted neurodevelopment disorders, characterized by significant social impairments, communication difficulties, and restricted, repetitive patterns of behavior or activities (American Psychiatric Association, 2013). ASD is a lifelong disorder that affects approximately 5.7 to 21.9 per 1,000 children, and is disproportionality more prevalent (5:1) in males than females (Centers for Disease Control and Prevention, 2014). Humans of all races, ethnicities and socioeconomic status are affected with ASD; however individuals vary tremendously in terms of cognition, social challenges, communicative abilities, and behavioral impairments. ASD has an early onset, with symptoms typically appearing by 30 months of age (Tharpe et al., 2006). Currently, the cause of ASD is unknown, but is thought to be attributed to a genetic predisposition and environmental risk factors. Further, ASD is commonly comorbid with other genetic disorders such as Cornelia de Lange’s syndrome; fragile X, Angelman syndrome, Down syndrome, tuberous sclerosis, phenylketonuria, and Cohen syndrome (Rapin, 1997; Cohen, 2005). Other pathologies have also been associated with ASD such as rubella, hydrocephalus, epilepsy, Tourette syndrome, learning disabilities, and attention deficit disorder.
ASD is primarily characterized by impaired social interaction and communicative abilities. Socially, persons with ASD tend to have few friendships and lack social reciprocity and empathy for others. Further, ASD impacts an individual’s ability to initiate social engagement, regulate social interactions, and share enjoyment and interests with others (Levy et al., 2009). Individuals with ASD tend to have difficulty interpreting social cues and emotions. Additionally, their ability to participate in joint activities, such as interactive and pretend play, is severely limited.
Communicatively, children with ASD develop speech and language later than typically developing peers. In fact, speech, language comprehension, and the use of gestures are always deficient in young children with autism (Rapin, 1997). Expressive language is often literal, repetitive, and non-informative. Further, the pragmatic aspect of language is often impaired (Levy et al., 2009). Many verbalize with a sing-song voice and topics of discussion often surround interests of the individual with ASD. Receptive language deficiency is attributed to the inability to decode the rapid acoustic fluctuations of speech (Rapin, 1997).
Behaviorally, many individuals with ASD engage in repetitive routines or activities, some of which can be self-destructive. Interests are often severely restricted. Many children with ASD have temper tantrums, especially when self-initiated activities or repetitive behaviors are interrupted. Decreased ability to concentrate and sleep is a common characteristic amongst this population. Creativity is also typically limited. Cognitively, there is a tremendously wide range of mental capacity. While, some perform above average on musical, mathematic, and visual-spatial tasks, 75% of persons with ASD have an intellectual disorder (Rapin, 1997).
Auditory Characteristics of Individuals with ASD
Abnormal auditory perception is a common finding amongst individuals with ASD, particularly sensorineural hearing loss and hyperacusis. In fact, hearing loss may affect 13.3%-46% of persons with ASD and 32 to 81% of individuals on the Autism spectrum suffer from hyperacusis (Magdalini et al., 2010; Tharpe et al., 2006). Further, children with ASD are often preoccupied or distressed by noises, relative to typically developing children. In a comprehensive review, O’Connor (2012) demonstrated the following in individuals with ASD: 1) enhanced pitch perception; 2) enhanced loudness sensitivity; 3) typical intensity discrimination; 4) reduced orientation to auditory information, especially speech stimuli; 5) atypical processing of prosodic cues; and 6) impaired processing of auditory stimuli and speech in background noise. Further, persons with ASD have been found to have deficits in temporal resolution and in the identification of the temporal order of rapidly occurring auditory events (Erviti, 2014).
Overall, individuals with ASD have shown, behaviorally, to have atypical processing of auditory information across a variety of domains such as pitch perception, loudness perception, auditory orientation, prosody processing, and speech in noise performance. These atypical processing features amongst this population can also be measured electrophysiologically via auditory evoked potentials such as the Auditory Brainstem Response (ABR), Middle Latency Response (MLR), and the cortically evoked potentials. Auditory evoked potentials (AEPs) are electrical signals generated by the auditory nervous system in response to an acoustic stimulus. These evoked potentials are typically utilized to evaluate the integrity of the auditory nervous system and to make inferences about an individual’s hearing status. Notably, the behavioral and limited communication characteristics of the ASD population present challenges for clinicians in obtaining valid and reliable behavioral audiometric and speech testing results. These characteristics include receptive and expressive language deficits, unreliable use of gestures, diminished ability to attend, hypersensitivity to auditory stimuli, aversion to novel environments and tasks, and potential for temper tantrums. Consequently, testing procedures and testing settings are modified or less specific testing measures are used in order to obtain behavioral results (Davis & Stiegler, 2005). AEPs can serve as useful, objective tools to overcome the barriers of obtaining valid and reliable behavioral audiological information in the ASD population. Further, AEPs are very valuable in diagnosing a variety of neurological disorders, perhaps even ASD in the future.
Auditory Brainstem Response in Autism
The auditory brainstem response (ABR) is a neurophysiological measure that reflects the activity and integrity of the afferent auditory system from the level of the auditory nerve up through higher midbrain structures. It consists of a sequence of seven positive-to-negative waveforms (waves I-VII), of which only waves I-V are routinely used, that occur within 10 ms of stimulus onset. The ABR has been demonstrated to be generated by the distal and proximal auditory nerve (waves I and II), the cochlear nucleus (wave III), the superior olivary complex (wave IV), and neurons of the lateral lemniscus (Møller & Jannetta, 1983).
Many researchers have demonstrated that, compared to typically developing peers, individuals on the Autism spectrum have significantly prolonged absolute latencies of wave III (Dabbous, 2012; Magliaro et al., 2010; Maziade et al., 2000; Rosenblum et al., 1980) and wave V (Kwon et al., 2007; Magliaro et al., 2010; Maziade et al., 2000; Rosenhall et al., 2003). Additionally, prolonged I-III interpeak latencies (Dabbous, 2012; Magliaro et al., 2010; Maziade et al., 2000), III-V (Rosenhall et al., 2003; Tas et al., 2007), and I-V interpeak latencies (Kwon et al., 2007; Magliaro et al., 2010; Maziade et al., 2000; Rosenhall et al., 2003) have been repeatedly observed. These prolonged latencies are exacerbated in response to complex stimuli, such as speech (Magliaro et al., 2010; Rosenhall et al., 2003) and at high presentation rates (Fujikawa-Brooks et al., 2010). Additionally, individuals with ASD elicit significantly smaller wave III amplitudes in forward masking paradigms compared to normal controls (Källstrand et al., 2010).
Together, these findings suggest individuals with ASD may have neural auditory abnormalities in the lower brainstem, particularly in the areas of the cochlear nucleus and the lateral lemniscus, considering delayed absolute latencies of waves III and V.
Given the absolute latency of wave I appears to occur within normal limits amongst this population, the auditory nerve is likely unaffected. Interestingly, there seems to be a delay in the neural conduction of auditory information as indicated by prolonged I-III, III-V, and I-V interpeak latencies. Specifically, prolonged I-III interpeak latencies represent delayed neural activity from the auditory nerve to the cochlear nucleus, while prolonged III-V interpeak latencies represent delayed neural conduction time from the cochlear nucleus to the lateral lemniscus. Further, the prolonged I-V interpeak latency indicates that the neural conduction time from the distal part of the auditory nerve to the lateral lemniscus is also delayed. Thus, children with ASD experience apparent delayed/impaired auditory processing, especially in complex and tasking auditory information. This delayed begins with the auditory structures in the low brainstem. The delayed absolute latencies of waves III and V as well as the prolonged I-III and III-V inter-peak latencies could possibly be attributable to abnormalities in myelination of auditory neurons or in the anatomy of the cerebellum. Myelin has a tremendous impact on the propagation of neural signals. Speculating, abnormalities on the ABR could be indicative of immature or abnormal myelination of the auditory brainstem in the ASD population, thereby increasing the time required to propagate the neural signal along the auditory brainstem pathway. Another explanation could be the possibility of abnormalities of cerebellar anatomy in individuals with ASD. Courchesne and colleagues (1998) demonstrated that lobules VI and VII of the vermis of the cerebellum in individuals with ASD are significantly smaller the normal controls. Abnormality in the anatomy of the cerebellum may have indirect implications on both the development and function of the auditory system, through its neural connections to the brain stem (Courchesne et al., 1998).
Middle Latency Potentials in Autism
The middle latency response (MLR) is an auditory evoked potential resulting in a waveform potentially consisting of four positive waves (Po, Pa, Pb and Pc) and three negative waves (Na, Nb, and Nc) (Musiek et al., 1984). It typically occurs between 8ms and 90ms. The earliest waves of the MLR (P0 and Na) are generated by the midbrain region (Hashimoto, 1982); while the later waves (Pa and Pb) have been shown to be generated by neural activity within the primary auditory cortex (Picton et al., 2010). Typically, only Pa, Pb, Na, and Nb are analyzed, with Pa being the most robust of the responses.
Magliario and colleagues (2010) investigated the Na-Pa amplitudes across modalities (C3/A1, C3/A2, C4/A1, C4/A2) and demonstrated significant electrode effects compared to normal controls. The authors also noted right ear effects, but these findings were not significant. These MLR alterations provide evidence for abnormal subcortical and cortical auditory processing. Specifically, these findings suggest there are structural or functional abnormalities interfering with the transmission of acoustic stimuli along the thalamic-cortical pathway in the afferent auditory system. Notably, neurological research regarding the volume of Heschl’s gyrus, the primary auditory cortex, suggests there is abnormal white matter volumetric development bilaterally in individuals with ASD (Prigge et al., 2013). Additionally, the decreased volume of Heschl’s gyrus is more notable in the right hemisphere. Interestingly, these anatomic findings correlate well with the current electrophysiological data regarding the primary auditory cortex.
However, there are studies that have shown conflicting evidence. Specifically, Grillion and colleagues (1989) investigated latencies and amplitudes of the Na, Pa, and Nb waves and concluded there were no consistent differences in MLR characteristics with normal controls. Furthermore, Buchwald and colleagues (1992) have also demonstrated that the MLR appears normal in adults with ASD. These findings suggest that individuals on the Autism spectrum do not have abnormal auditory processing with respect to the thalamic-cortical pathway.
Currently, there is equivocal evidence regarding auditory dysfunction in individuals with autism from the level of the high auditory brainstem to the primary auditory cortex. With the literature supporting anatomical abnormalities of Heschl’s Gyrus in individuals with ASD, it is surprising that there are not more substantial findings regarding MLR abnormalities. The studies concluding no differences regarding the amplitude of the MLR in individuals with ASD had small
sample sizes, thus more research regarding MLR in this population is warranted.
Cortical Evoked Potentials
Cortical evoked auditory potentials conventionally consist of the following components: P1, N1, P2 and N2 (Picton, 2010). In general, N1 and P2 are the most robust of these cortically evoked potentials. N1 is a negative-going response elicited around 100ms and P2 is a positive-going response occurring between 175 and 200ms. The N1 and P2 components are primarily exogenous potentials, in that, these potentials are easily affected by the acoustic properties of a stimulus. The neuronal generators of N1 most likely include auditory association regions, located in the superior temporal gyri, the primary auditory cortices, and various frontal regions (O’Connor, 2012). Additionally, the P2 component is thought to originate from the lateral-frontal supratemporal region (Picton, 2010).
Currently, there is considerable research to suggest there are notable differences in the N1 component in terms of both amplitude and latency. Regarding amplitude, several researchers have concluded that the N1 amplitude in individuals on the Autism spectrum is significantly reduced (Bruneau et al., 2003; Orekhova et al., 2009; Teder-Salejarvi et al., 2005). In terms of latency, the literature supports the notion that individuals with ASD have delayed latencies of the N1 component (Bruneau et al. 2003; Dunn et al., 1999; Korpilahti et al., 2007). Together, the reduced amplitude and prolonged latencies of N1 indicate that individuals with ASD have impaired auditory processing, especially regarding neural auditory encoding.
Mismatch Negativity (MMN)
The Mismatch Negativity (MMN) response is an event-related, cortically evoked potential that occurs between 150-250 ms post-stimulus. It is elicited by deviances in a sequence of ongoing stimuli. This MMN response has been attributed to neural activity from the bilateral supratemporal planes of the primary auditory cortices (Hitiguloi et al., 2010) as well as the frontal cortex (Bomba et al., 2004). The MMN serves as a valuable index of auditory discrimination in terms of pitch, intensity and duration, CV transitions, and changes in periodicity.
Research has demonstrated that MMN amplitude is increased in response to changes in pitch (Gomot et al., 2002; Ferri et al., 2003; Kujala et al., 2010; Lepisto et al., 2005); whereas MMN amplitude is decreased in response to changes in duration in individuals with ASD relative to normal control subjects (Lepisto et al., 2005). Further, the latency of the MMN is shorter in individuals with ASD during pitch discrimination tasks (Gomot et al., 2011; Ferri et al., 2003; Kujala et al., 2007; Lepisto et al., 2005). Interestingly, Kuhl and colleagues (2005) found that deviances in speech syllables do not appear to elicit an MMN in autistic individuals.
These findings suggest that individuals with ASD have superior auditory processing skills regarding pitch perception, given shortened latencies and increased MMN amplitudes. This suggests that individuals on the Autism spectrum are more sensitive to pitch changes and are quickly able to detect variations in pitch within an acoustic non-speech stimulus. However, this population is deficient regarding auditory processing of speech stimuli and duration discrimination, considering the absence or the reduced amplitude of the MMN response to changes occurring in speech syllables and duration. Overall, the MMN provides evidence that individuals with ASD can subconsciously detect deviances in acoustic stimuli with respect to pitch. Considering the exact region of the supratemporal plane of auditory cortex that is responsible for processing is dependent on the acoustic parameter that is being processed, individuals with ASD may have anatomical or functional abnormalities in regions corresponding to speech and duration processing.
The P300 is a large positive waveform that occurs at approximately 250-600ms post stimulus onset in adults and is thought to originate from the association cortex of the parietal lobes (Bomba et al., 2004; Hitoglou et al., 2010). It is elicited by the absence of an anticipated auditory stimulus. Unlike the MMN, the P300 is dependent on attention, thus reflecting higher cognitive processing of stimuli. The literature has consistently demonstrated that the amplitude of the P300 is significantly attenuated when evoked aurally in the ASD population. Specifically, P300 amplitude decreases in response to simple non-speech stimuli, such as clicks (Novick et al., 1980), pure tones (Lincoln et al., 1993; Oades et al., 1988), and novel sounds (Courchesne et al., 1986). Amplitude attenuation of the P300 has also been shown in response to phonemic speech stimuli (Dawson et al., 1988; Lepisitio et al., 2005). However, individuals with autism do not appear to have attenuated P300 waves in response to musical chords (Dawson et al., 1988), or word level speech stimuli (Courchesne et al., 1986). Regarding latency of the P300, Magilario and colleagues (2010) and Kuhl and colleagues (2005) exhibited that this potential is typically absent or delayed in individuals with Autism in response to variations in speech syllables.
Abnormalities of the P300 response in this population reflect potential deficits in attention or perhaps individuals with autism invest fewer attentional resources to process auditory stimuli. Further, these findings suggest pathological involvement of the auditory association areas and impaired auditory discrimination capacity. Lastly, a decrease in P300 amplitude in individuals on
the Autism spectrum indicates that this population presents abnormalities on central aspects of auditory processing involving the detection, registration, and memory of auditory information. Overall, it appears that the neural networks responsible for language processing are disproportionately affected relative to the neural circuits required for simple sound processing.
Table 1. Summary of findings of auditory evoked potentials in individuals with Autism.
|Auditory Brainstem Response (ABR)||Middle Latency Response (MLR)||N1P2||Mismatch Negativity||P300|
|Delayed absolute latencies of waves III and V
Prolonged I-III and III-V interpeak latencies
|Findings are equivocal||Reduced N1 amplitude
Delayed latencies of N1
|Increased amplitude and decreased latency during pitch discrimination tasks
Absent MMN to speech stimuli
|Decrease in P300 amplitude|
Therefore, deficits in speech processing reflect impairment in the neural circuitry necessary for attending to, discriminating, and prioritizing speech over non-speech sounds. These findings also reflect abnormalities in recognizing novel stimuli.
Considering the auditory evoked potential findings from the level of the brainstem up through the auditory cortex and association areas, it is apparent that individuals with ASD experience abnormal auditory processing both cortically and subcortically. Table 1. Provides a summary of the findings on auditory evoked potentials in individuals with ASD. The Auditory Brainstem Response has demonstrated that the auditory processing of this population seems to be impaired beginning with the delayed processing of cochlear nucleus. Further, the processing of the acoustic signal is further delayed by the neurons of lateral lemniscus. Abnormal ABR findings could be suggestive of a maturational defect in the myelination of the auditory brainstem (Hitaglou et al., 2010). Though the ABR provides plentiful information regarding its corresponding anatomical correlates of the auditory system in individuals with ASD, the Middle Latency Response fails to provide much knowledge about the status of the thalamic-cortical pathway at this time as the findings are in conclusive in individuals with ASD. Thus, more evidence is required in order to make conclusions regarding thalamic-cortical involvement of abnormal auditory processing in this population.
Interestingly, the Cortical Auditory Evoked Potentials (CAEPs) have provided tremendous knowledge in terms of the processing of auditory stimuli in individuals on the Autism spectrum. In general, the research has consistently demonstrated amplitude and latency differences to auditory stimuli regarding many CAEP components in individuals with ASD. The body of literature of CAEPs in the population indicates individuals with ASD experience impaired auditory processing of speech stimuli, but demonstrate superior pitch perception abilities. Further, individuals on the Autism spectrum are generally able to detect changes in the auditory stimulus subconsciously. However, this skill is diminished or absent when attention is required as demonstrated by P300 findings.
Overall, auditory evoked potentials have tremendously contributed to the knowledge of the auditory deficits in individuals with ASD. It can be concluded the AEPs have confirmed that individuals with ASD experience: 1) atypical processing of acoustic information, especially speech stimuli; 2) enhanced pitch perception; and 3) impaired processing of auditory stimuli with respect to attention. Perhaps these findings are the foundation of the abnormalities experienced regarding communication deficits. Specifically, individuals on the Autism spectrum have both expressive and receptive language deficits. This population has difficulty processing affective/emotional aspects of speech and their expressive speech is often literal. This could potentially be due to the impaired/delayed processing of various parameters of the speech signal. Lastly, Rapin (1997) has suggested that the receptive language deficiency is attributed to the inability to decode the rapid acoustic fluctuations of speech. Perhaps, the encoding of the speech signal also serves as a potential barrier.
Hillary Siddons is a fourth year student in the University of Connecticut Doctor of Audiology Program and is currently an extern at Ear, Nose and Throat Medical and Surgical Group in New Haven, CT. She has served as Secretary for the UConn Student Academy of Audiology for two years and enjoys volunteering for the Walk4Hearing, the Healthy Hearing Initiative at the Special Olympics, and Hear Here Hartford (a local support group for adolescents with hearing loss). Currently, Hillary is evaluating the current hearing screening methods in Connecticut Head Start programs and is a training team member of the Early Childhood Hearing Outreach (ECHO) Initiative. Hillary enjoys all aspects of diagnostic and rehabilitative audiology, with specific interests in early hearing detection and neuroaudiology.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Arlington, VA: American Psychiatric Association; 2013.
Bomba, M. D., & Pang, E. W. (2004). Cortical auditory evoked potentials in autism: A review. International Journal of Psychophysiology, 53(3), 161-169.
Bruneau, N., Bonnet-Brilhault, F., Gomot, M., Adrien, J., & Barthélémy, C. (2003). Cortical auditory processing and communication in children with autism: Electrophysiological/ behavioral relations. International Journal of Psychophysiology, 51(1), 17-25.
Buchwald, J., Erwin, R., Van Lancker, D., Guthrie, D., Schwafel, J., & Tanguay, P. (1992). Midlatency auditory evoked responses: P1 abnormalities in adult autistic subjects. Electroencephalogr. Clin. Neurophysiol., 84, 164–171.
Centers for Disease Control and Prevention (2014). Prevalence of autism spectrum disorders—Autism and Developmental Disabilities Monitoring Network, 11 sites, United States, 2010. Morbidity and Mortality Weekly Report, 63 (No. SS-02), 1-21.
Cohen, D., Pichard, N., Tordjman, S., Baumann, C., Burglen, L., Excoffier, E., Lazar, G., Mazet, P., Pinquier, C., Verloes, A., Heron, D. (2005) Specific genetic disorders and autism: clinical contribution towards their identification. J. Autism Dev. Disord. 35,103-116.
Courchesne, E., Yeung-Courchesne, R., Press, G. A., Hesselink, J. R., & Jernigan, T. L. (1988). Hypoplasia of cerebellar vermal lobules VI and VII in autism. New England Journal of Medicine, 318(21), 1349-1354.
Courchesne, E., Lincoln, A. J., Kilman, B. A., & Galambos, R. (1986). Visual and auditory ERPs in autism. In W.C McCallum, R Zappoli, F Denoth (Eds.), Cerebral Psychophysiology: Studies in Event-Related Potentials, Electroenceph. Clin. Neurophys., Suppl., vol. 38, Elsevier, Amsterdam, pp. 446–448.
Dabbous, A. O. (2012). Characteristics of auditory brainstem response latencies in children with autism spectrum disorders. Audiological Medicine, 10(3), 122-131.
Davis, R., & Stiegler, L. N. (2005). Toward more effective audiological assessment of children with autism spectrum disorders. Seminars in Hearing, 26(4), 241-252. doi:10.1055/s-2005-922446
Dawson, G., Finley, C., Phillips, S., Galpert, L., & Lewy, A. (1988). Reduced P3 amplitude of the event-related brain potential: its relationship to language ability in autism. J. Autism Dev. Disord., 18, 493–504.
Don, M. & Kwong, B. (2002). Auditory brainstem response: differential diagnosis. In Handbook of Clinical Audiology (5th ed.), J. Katz (Ed.), Lippincott, Williams and Wilkins, Baltimore.
Dunn M, Vaughan HG, Jr., Kreuzer J, Kurtzberg D. Electrophysiologic correlates of semantic classification in autistic and normal children. Developmental Neuropsychology 1999; 16:79-99.
Erviti, M., Semal, C., Wright, B. A., Amestoy, A., Bouvard, M. P., & Demany, L. (2014). A Late-Emerging Auditory Deficit in Autism. Neuropsychology, doi:10.1037/neu0000162
Ferri, R., Elia, M., Agarwal, N., Lanuzza, B., Musumeci, S. A., & Pennisi, G. (2003). The mismatch negativity and the P3a components of the auditory event-related potentials in autistic low-functioning subjects. Clinical Neurophysiology, 114(9), 1671-1680.
Franc, C. L., Donkers, S. E., Schipul, G. T., Baranek, K. M., … & Aysenil, B. (2013). Attenuated Auditory Event-Related Potentials and Associations with Atypical Sensory Response Patterns in Children with Autism. Journal of Autism and Developmental Disorders, 1, 1.
Fujikawa-Brooks, S., Isenberg, A., Osann, S., Spence, M., & Gage, N. (2010).The effect of rate stress on the auditory brainstem response in autism: a preliminary report. International Journal of Audiology, 49 (2), 129–140.
Gomot, M., Giard, M., Adrien, J., Barthelemy, C., & Bruneau, N. (2002). Hypersensitivity acoustic change in children with autism: Electrophysiological evidence of left frontal cortex dysfunctioning. Psychophysiology, 39(5), 577-584.
Gomot, M.,Blanc, R.,Clery, H., Roux, S., Barthelemy, C., & Bruneau, N. (2011). Candidate electrophysiological endophenotypes of hyper-reactivity to change in autism. Journal of Autism and Developmental Disorders, 41 (6), 705–714.
Grillon, C., Courchesne, E., & Akshoomoff, N. (1989). Brainstem and middle latency auditory evoked potentials in autism and developmental language disorder. Journal of Autism and Developmental Disorders, 19(2), 255-269.
Hashimoto, I. (1982). Auditory evoked potentials from the human midbrain: Slow brain stem responses. Electroencephalography and Clinical Neurophysiology, 53(6), 652-657.
Hitoglou, M., Ververi, A., Antoniadis, A., & Zafeiriou, D. I. (2010). Childhood autism and auditory system abnormalities. Pediatric Neurology, 42(5), 309-314.
Jeste, S., & Nelson, C. I. (2009). Event related potentials in the understanding of autism spectrum disorders: an analytical review. Journal of Autism & Developmental Disorders, 39(3), 495-510. doi:10.1007/s10803-008-0652-9
Kaga, K., Hink, R. F., Shinoda, Y., & Suzuki, J. (1980). Evidence for a primary cortical origin of a middle latency auditory evoked potential in cats. Electroencephalography and Clinical Neurophysiology, 50(3), 254-266. doi:10.1016/0013-4694(80)90153-4
Källstrand, J., Olsson, O., Nehlstedt, S., Skold, M., & Nielzen, S. (2010). Abnormal auditory forward masking pattern in the brainstem response of individuals with Asperger syndrome. Neuropsychiatry Disorders and Treatment, 6, 289–296.
Korpilahti, P., Jansson-Verkasalo, E., Mattila, M.-L., Kuusikko, S., Suominen, K., Rytky, S. (2007). Processing of affective speech prosody is impaired in Asperger syndrome. Journal of Autism and Developmental Disorders, 37, 1539–1549.
Kuhl, P. K., & Coffey-Corina, S., Padden, D., & Dawson, G. (2005). Links between social and linguistic processing of speech in preschool children with autism: behavioral and electrophysiological measures. Dev Sci,8: F1-12.
Kwon, S., Kim, J., Choe, B., Ko, C., & Park, C. (2007). Electrophysiologic assessment of central auditory processing by auditory brainstem responses in children with autism spectrum disorders. Journal of Korean Medical Science, 22 (4), 656–659.
Lepisto, T., Kujala, T., Vanhala, R., Alku, P., Huotilainen, M., & Naatanen, R. (2005). The discrimination of and orienting to speech and non-speech sounds in children with autism. Brain Research, 1066, 147-157.
Levy, S. E., Mandell, D. S., & Schultz, R. T. (2009). Autism. The Lancet, 374(9701), 1627-1638.
Lincoln, A. J., Courchesne, E., Harms, L., & Allen, M. (1993). Contextual probability evaluation in autistic, receptive developmental language disorder and control children: event-related brain potential evidence. J. Autism Dev. Disord., 23, 37–58.
Magliaro, F. C. L., Scheuer, C. I., Assumpcao Jr., F. B., & Matas, C. G. (2010). Study of auditory evoked potentials in autism. PRO-FONO: Revista De Actualizacao Cientifica, 22(1), 31-36.
Maziade, M., Mérette, C., & Cayer, M. (2000). Prolongation of Brainstem Auditory-Evoked Responses in Autistic Probands and Their Unaffected Relatives. Arch Gen Psychiat., 57(11), 1077-83.
McFadden, K. L., &Rojas, D. C. (2013). Electrophysiology of Autism, Recent Advances in Autism Spectrum Disorders – Volume II, Prof. Michael Fitzgerald (Ed.), ISBN: 978-953-51-1022-4, InTech, doi: 10.5772/54770.
Møller, A. R. & Jannetta, P. J. (1983). Interpretation of brainstem auditory evoked potentials: results from intracranial recordings in humans. Scand Audiology, 12, 125-133.
Musiek, F. E., Geurkink, N. A., Weider, D. J., & Donnelly, K. (1984). Past, present and future applications of the auditory middle latency response. Laryngoscope, 94(12 I), 1545-1553.
O’Connor, K. (2012). Auditory processing in autism spectrum disorder: A review. Neuroscience & Biobehavioral Reviews, 36(2), 836-854.
Oades, R. D., Walker, M. K., Geffen, L. B., & Stern, L. M. (1988). Event-related potentials in autistic and healthy children on an auditory choice reaction task. Int. J. Psychophysiol., 6, 25–37.
Orekhova, E. V., Stroganova T. A., Prokofiev, A., Nygren, G., Gillberg, C., & Elam, M. (2009). The right hemisphere fails to respond to temporal novelty in autism: evidence from an ERP study. Clinical Neurophysiology, 120 (3), 520–529.
Picton, T. (2010). Introduction: Past, Present and Potential Human Auditory Evoked Potentials. Plural Publishing: San Diego. pp. 1–23.
Prigge, M. D., Bigler, E. D., Fletcher, P. T., Zielinski, B. A., Ravichandran, C., Anderson, J., … Lainhart, J. (2013). Longitudinal heschl’s gyrus growth during childhood and adolescence in typical development and autism. Autism Research, 6(2), 78-90. doi:10.1002/aur.1265
Rapin, I. (1997). Autism. N Engl J Med, 337(2), 97-104. doi:10.1056/NEJM199707103370206
Rosenblum, S. M., Arick, J. R., Krug, D.A., Stubbs, E. G., Young, N. B., & Pelson, R. O (1980). Auditory brainstem evoked responses in autistic children. J Autism Dev Disord, 10(2):215-25.
Rosenhall, U., Nordin, V., Brantberg, K., & Gillberg, C. (2003). Autism and auditory brainstem responses. Ear and Hearing, 24(3), 206-214.
Tas, A., Yagiz, R., Tas, M., Esme, M., Uzun, C., & Karasalihoglu, A. R. (2007). Evaluation of hearing in children with autism by using TEOAE and ABR. Autism, 11(1), 73-79.
Teder-Salejarvi, W. A., Pierce, K. L., Courchesne, E., Hillyard, S. A. (2005). Auditory spatial localization and attention deficits in autistic adults. Cognitive Brain Research, 23, 221– 234.
Tharpe, A. M., Bess, F. H., Sladen, D. P., Schissel, H., Couch, S., & Schery, T. (2006). Auditory characteristics of children with autism. Ear and Hearing, 27(4), 430-441.