Both of these studies found significantly longer III-V interpeak latency (thought to represent neural conduction time between cranial nerve VIII and the lateral leminiscus). In contrast, other studies have shown prolonged latencies in child and adolescent ASD cohorts ( 14, 15). Some studies show no differences in central transmission latency nor amplitude ( 12, 13). The ABR literature reports varied and contradictory findings. Incoming auditory stimuli from the vestibulocochlear nerve (Cranial Nerve VIII) travel to processing structures in the brainstem (cochlear nuclei and the superior olivary complex) and midbrain (inferior colliculus). One way of measuring the flow of auditory information processing is through the traditional auditory brainstem response (ABR) in which the electrical activity evoked from a series of clicks or tones is recorded in milliseconds using surface electrodes. We begin by considering the processing of unimodal stimuli, then we will address multisensory integration, and finally, we will examine the role of attention on the sensory processing stream.Īs language deficits are a core feature of ASD, the study of auditory processing is essential to considering the roots of ASD as well as to conceptualize rational interventions. We will review the current literature on the neurophysiology in individuals on the autism spectrum with a focus on the processing of simple sensory input in the auditory, visual, and tactile modalities. ![]() Interestingly, these tend to be the least well studied of the sensory modalities, whereas there is mounting evidence for disruption of the auditory and visual processing pathways and a surging interest in multisensory integration (MSI). However, historically, proximal senses such as touch, smell and taste were thought to be particularly at risk and to indicate developmental immaturity ( 10, 11). There is limited consensus regarding the pattern of these sensory deficits in ASD. While sensory hyper- and hypo-responsiveness are not unique to ASD, they appear to be more prevalent in this population than in other developmental disabilities ( 4, 8, 9). The distress caused by particular sensory stimuli can cause self-injurious and aggressive behavior in those unable to communicate their duress. Sensory processing concerns have been a key feature of ASD clinical descriptions from the original independent seminal reports by Asperger and Kanner to first person accounts ( 7). Similar to the wide-range of spectrum severity found for communication and social deficits, sensory behavioral differences also range from mild to severe, and these behavioral differences can endure through adulthood ( 2- 6). Over 96% of children with ASD report hyper and hypo-sensitivities in multiple domains. What does appear to be common to individuals across the spectrum are atypical behavioral responses to sensory information. ![]() There also exists considerable phenotypic variation involving the pace of language development, the presence of epilepsy, and the range of cognitive ability. ![]() in utero valproic acid exposure), and prematurity. ![]() fragile X and tuberous sclerosis), environmental exposures (e.g. There are many known etiologies that contribute to an ASD phenotype, including genetic variations (e.g. ASD is clearly not a one size fits all diagnosis. Even within a diagnosis of autism, there can be a wide range of intellectual ability. In this review, ASD is used to include individuals with the full range of symptoms from the most severe form of the condition, autistic disorder or autism, to the milder forms, Asperger syndrome (AS) and pervasive developmental disorder not otherwise specified (PDD, NOS). Autism Spectrum Disorders (ASD) are defined clinically by impairment in communication, social interaction, and behavioral flexibility ( 1).
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