Auditory Abnormalities in Autistic Children

Hayes, R.W.; Gordon, A. G.

doi:10.1016/s0140-6736(77)90278-1

Cited by 31 publications

(17 citation statements)

References 6 publications

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“…The co-occurrence between HL and ASD was first suggested in the 1970s, 42 and it was believed that HL was a possible cause for autism, 43 pointing to social isolation, emotional distress, psychological disorders, and language deficits in children with HL as potential pathways to a subsequent diagnosis of autism. 18,44 Conditions such as cytomegalovirus, toxoplasmosis, bacterial meningitis, rubella and measles have also been proposed as possible risk factors for co-occurrence of HL and ASD.…”

Section: Discussionmentioning

confidence: 99%

Childhood vision impairment, hearing loss and co-occurring autism spectrum disorder

Kancherla

Braun

Yeargin‐Allsopp

2013

Disability and Health Journal

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Background Limited population-based data on prevalence of childhood vision impairment (VI) and hearing loss (HL), and their co-occurrence with autism spectrum disorder (ASD) exists. Objective To examine prevalence and characteristics of VI, HL and co-occurring ASD among 8-year-olds in metropolitan Atlanta 2000–2008. Methods We used data from the population-based Metropolitan Atlanta Developmental Disabilities Surveillance Program. Prevalence, birth and parental characteristics, presence and severity of other co-occurring developmental disabilities, and age of earliest identification of ASD, were examined for children with VI and HL, by co-occurring ASD. Results VI and HL prevalences were 1.2 and 1.3 per 1000 8-year-olds, respectively. Approximately 6–7% of children with VI or HL had co-occurring ASD. Children with VI or HL with co-occurring ASD differed from those without co-occurring ASD by select birth characteristics and the presence of other co-occurring DDs. The median age of earliest known ASD diagnosis was significantly later among children with VI and ASD compared to children with ASD without VI (79 vs. 56 months). Children with HL and ASD were first evaluated by a community provider significantly earlier than those with ASD without HL (40 vs. 50 months). Conclusions The frequency of co-occurring ASD with VI and HL is higher than the population prevalence of ASD. The significant delays in diagnosis of ASD in children with VI and lack of earlier diagnosis of ASD among children with HL despite earlier evaluation highlight the importance of developing screening tools for early identification of ASD among children with VI and HL.

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Section: Discussionmentioning

confidence: 99%

Childhood vision impairment, hearing loss and co-occurring autism spectrum disorder

Kancherla

Braun

Yeargin‐Allsopp

2013

Disability and Health Journal

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“…Creating animal versions of the present diagnostic behaviors would carry a very high risk of false positive effects. Several more specific measures have been reported to be abnormal in autism (e.g., vestibular reflexes: Ornitz, 1983, auditory reflexes: Hayes andGordon, 1977) and these might be useful in rodents. However, since these measures are not "diagnostic," occurring in only a subset of autistic cases, positive results would only support the idea that the subjects were brain-damaged.…”

Section: Discussion Of the Animal Studiesmentioning

confidence: 99%

Embryological origin for autism: Developmental anomalies of the cranial nerve motor nuclei

et al. 1996

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The underlying brain injury that leads to autism has been difficult to identify. The diagnostic criteria of the disease are not readily associated with any brain region or system, nor are they mimicked by vascular accidents, tumors, or degenerative neurological diseases occurring in adults. Fortuitously, a recent report of autism induced by thalidomide exposure provides evidence that the disease originates by an injury at the time of closure of the neural tube. The human data suggest that the initiating lesion includes the motor cranial nerve nuclei. To test this hypothesis, we first examined motor nuclei in the brainstem of a human autistic case. The autopsy brain exhibited near-complete absence of the facial nucleus and superior olive along with shortening of the brainstem between the trapezoid body and the inferior olive. A similar deficit has been reported in Hoxa-1 gene knockout mice in which pattern formation of the hindbrain is disrupted during neurulation. Alternatively, exposure to antimitotic agents just after neural tube closure could produce the observed pattern of deficits. Thus, the lesions observed in the autopsy case appear to match those predicted by the thalidomide cases in both time of origin and central nervous system (CNS) location. To produce similar brain lesions experimentally, we exposed rat embryos to valproic acid, a second teratogen newly linked to autism. Dams received 350 mg/kg of valproic acid (VPA) on day 11.5 (the day of neural tube closure), day 12, or day 12.5 gestation. Each treatment significantly reduced the number of motor neurons counted in matched sections of the earliest-forming motor nuclei (V, XII), and progressively later exposures affected the VIth and IIIrd cranial nerve nuclei. All treatments spared the facial nucleus, which forms still later. Counts from the mesencephalic nucleus of trigeminal, the dorsal motor nucleus of the vagus, and the locus ceruleus were not affected by exposure to VPA, even though these nuclei form during the period when exposure occurred. Despite its effects on the motor nuclei, valproic acid exposure did not alter the further development of the brain in any obvious way. Treated animals were robust and had no external malformations. The autopsy data and experimental data from rats confirm that CNS injuries occurring during or just after neural tube closure can lead to a selective loss of neurons derived from the basal plate of the rhombencephalon. The results add two new lines of evidence that place the initiating injury for autism around the time of neural tube closure.

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“…Problems in state regulation may be expressed as atypical social and emotional behaviors (e.g., Bachevalier & Loveland, 2005), low thresholds to be reactive, tantrums, difficulties in sustaining attention, and sleep disorders. The auditory processing deficits may be experienced as language and speech delays, difficulties in extracting human voice from background sounds, hyperacusis, or as a general compromise in social communication skills (Dissanayake & Sigman, 2001; Frith & Baron-Cohen, 1987; Hayes & Gordon, 1977; Klin, 1992; Lockyer & Rutter, 1969). …”

Section: 0 Introductionmentioning

confidence: 99%

Respiratory sinus arrhythmia and auditory processing in autism: Modifiable deficits of an integrated social engagement system?

Porges

Macellaio

Stanfill

et al. 2013

International Journal of Psychophysiology

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The current study evaluated processes underlying two common symptoms (i.e., state regulation problems and deficits in auditory processing) associated with a diagnosis of autism spectrum disorders. Although these symptoms have been treated in the literature as unrelated, when informed by the Polyvagal Theory, these symptoms may be viewed as the predictable consequences of depressed neural regulation of an integrated social engagement system, in which there is down regulation of neural influences to the heart (i.e., via the vagus) and to the middle ear muscles (i.e., via the facial and trigeminal cranial nerves). Respiratory sinus arrhythmia (RSA) and heart period were monitored to evaluate state regulation during a baseline and two auditory processing tasks (i.e., the SCAN tests for Filtered Words and Competing Words), which were used to evaluate auditory processing performance. Children with a diagnosis of autism spectrum disorders (ASD) were contrasted with aged matched typically developing children. The current study identified three features that distinguished the ASD group from a group of typical developing children: 1) baseline RSA, 2) direction of RSA reactivity, and 3) auditory processing performance. In the ASD group, the pattern of change in RSA during the attention demanding SCAN tests moderated the relation between performance on the Competing Words test and IQ. In addition, in a subset of ASD participants, auditory processing performance improved and RSA increased following an intervention designed to improve auditory processing.

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Auditory Abnormalities in Autistic Children

Cited by 31 publications

References 6 publications

Childhood vision impairment, hearing loss and co-occurring autism spectrum disorder

Childhood vision impairment, hearing loss and co-occurring autism spectrum disorder

Embryological origin for autism: Developmental anomalies of the cranial nerve motor nuclei

Respiratory sinus arrhythmia and auditory processing in autism: Modifiable deficits of an integrated social engagement system?

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