Article

Annotation: What Do We Know about Sensory Dysfunction in Autism? A Critical Review of the Empirical Evidence

M.I.N.D. Institute & Department of Psychiatry and Behavioral Sciences, University of California-Davis, CA 95817, USA.
Journal of Child Psychology and Psychiatry (Impact Factor: 6.46). 01/2006; 46(12):1255-68. DOI: 10.1111/j.1469-7610.2005.01431.x
Source: PubMed

ABSTRACT

Unusual responses to sensory stimuli are seen in many children with autism. Their presence was highlighted both in early accounts of autism and in more recent first-person descriptions. There is a widespread belief that sensory symptoms characterize autism and differentiate it from other disorders. This paper examines the empirical evidence for this assumption.
All controlled experimental laboratory investigations published since 1960 were identified through systematic searches using Medline/PubMed and PsycInfo search engines. A total of 48 empirical papers and 27 theoretical or conceptual papers were reviewed.
Sensory symptoms are more frequent and prominent in children with autism than in typically developing children, but there is not good evidence that these symptoms differentiate autism from other developmental disorders. Certain groups, including children with fragile X syndrome and those who are deaf-blind, appear to demonstrate higher rates of sensory symptoms than children with autism. In reviewing the evidence relevant to two theories of sensory dysfunction in autism, over- and under-arousal theory, we find that there is very little support for hyper-arousal and failure of habituation in autism. There is more evidence that children with autism, as a group, are hypo-responsive to sensory stimuli, but there are also multiple failures to replicate findings and studies that demonstrate lack of group differences.
The use of different methods, the study of different sensory modalities, and the changing scientific standards across decades complicate interpretation of this body of work. We close with suggestions for future research in this area.

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    • "According to Dunn model[9], sensory modulation disorders (SMDs) are classified into three types: over-responsivity, under-responsivity, and sensory seeking. Among sensory symptoms, differences between individuals with ASD and TD subjects were greatest for under-responsivity, which describes a high threshold for sensory input[10,11]. This trait is associated with lower adaptive functioning and poorer communication and social performance[8,12]. "
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    ABSTRACT: Atypical responsiveness to olfactory stimuli has been reported as the strongest predictor of social impairment in children with autism spectrum disorders (ASD). However, previous laboratory-based sensory psychophysical studies that have aimed to investigate olfactory sensitivity in children with ASD have produced inconsistent results. The methodology of these studies is limited by several factors, and more sophisticated approaches are required to produce consistent results. We measured olfactory detection thresholds in children with ASD and typical development (TD) using a pulse ejection system—a newly developed methodology designed to resolve problems encountered in previous studies. The two odorants used as stimuli were isoamyl acetate and allyl caproate. Forty-three participants took part in this study: 23 (6 females, 17 males) children with ASD and 20 with TD (6 females, 14 males). Olfactory detection thresholds of children with ASD were significantly higher than those of TD children with both isoamyl acetate (2.85 ± 0.28 vs 1.57 ± 0.15; p < 0.001) and allyl caproate ( 3.30 ± 0.23 vs 1.17 ± 0.08; p < 0.001). We found impaired olfactory detection thresholds in children with ASD. Our results contribute to a better understanding of the olfactory abnormalities that children with ASD experience. Considering the role and effect that odors play in our daily lives, insensitivity to some odorants might have a tremendous impact on children with ASD. Future studies of olfactory processing in ASD may reveal important links between brain function, clinically relevant behavior, and treatment.
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    • "Autism spectrum disorder (ASD) is a neurodevelopmental disorder, and according to the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), it is characterized by " an impairment in social communication and interaction, and restricted and repetitive patterns of behaviors, interests or activities. " A subset of patients with ASD tend to also display hyperactivity , anxiety, hypotonia, epilepsy, sensory abnormalities, sleep disorders, intellectual disabilities, gastrointestinal disorders, microencephaly or megalencephaly1234. The symptom severity is also heterogeneous, which is why the term ASD is used to encompass all the different severities and variations of symptoms in these disorders. "
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    ABSTRACT: Autism spectrum disorder (ASD) refers to a broad spectrum of neurodevelopmental disorders characterized by three central behavioral symptoms: impaired social interaction, impaired social communication, and restricted and repetitive behaviors. However, the symptoms are heterogeneous among patients and a number of ASD mouse models have been generated containing mutations that mimic the mutations found in human patients with ASD. Each mouse model was found to display a unique set of repetitive behaviors. In this review, we summarize the repetitive behaviors of the ASD mouse models and variations found in their neural mechanisms including molecular and electrophysiological features. We also propose potential neuronal mechanisms underlying these repetitive behaviors, focusing on the role of the cortico-basal ganglia-thalamic circuits and brain regions associated with both social and repetitive behaviors. Further understanding of molecular and circuitry mechanisms of the repetitive behaviors associated with ASD is necessary to aid the development of effective treatments for these disorders.
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    • "Given these observations , there has been discussion regarding whether alterations in the neurophysiology of basic perceptions might be more critical in the pathophysiology of ASD than previ - ously thought . Following this line of reasoning , a number of papers have focused on possible alterations in the basic visual capacities of ASD patients ( Gillberg , 2003 ; Dakin and Frith , 2005 ; Rogers and Ozonoff , 2005 ; Simmons et al . , 2009 ) . "
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