International Meeting for Autism Research: Sensory Filtering Abnormalities in Autism Spectrum Disorder (ASD)

Sensory Filtering Abnormalities in Autism Spectrum Disorder (ASD)

Friday, May 21, 2010
Franklin Hall B Level 4 (Philadelphia Marriott Downtown)
1:00 PM
J. M. Baruth , Anatomical Sciences and Neurobiology, University of Louisville, Louisville, KY
E. M. Sokhadze , Psychiatry and Behavioral Sciences, University of Louisville, Louisville, KY
L. L. Sears , Pediatrics, University of Louisville, Louisville, KY
M. F. Casanova , Psychiatry and Behavioral Sciences, University of Louisville, Louisville, KY
Background: Individuals with Autism Spectrum Disorder (ASD) often have atypical reactions to the sensory environment. Sensory abnormalities generally associated with ASD are indicated by hypersensitivity and an extraordinary interest in certain sensations. In fact, it has been suggested that altered inhibitory control of sensory intake in ASD may cause sensory overload leading to avoidance of external stimulation. Sensory overload in individuals with ASD can impair functioning, raise physiological stress, and adversely affect social interaction.  Since all senses appear involved in the sensory abnormalities of ASD, an underlying cortical pathology is inferred.  It has been suggested that sensory abnormalities in ASD may be due to a lack of cortical inhibitory tone in cortical minicolumns--specifically a reduction in peripheral neuropil space. A disturbance in inhibitory function of the brain to irrelevant sensory input, i.e. an impaired ability to suppress evoked potentials elicited by task-irrelevant distracters, has been called ‘sensory filtering’. 

Objectives:  We wanted to test the hypothesis of a sensory filtering deficit in ASD by investigating event-related potentials elicited by task-irrelevant, illusory Kanizsa figures and non-Kanizsa distracter stimuli in a visual oddball task.

Methods: A 128 channel electroencephalographic (EEG) system was used on 15 high-functioning children and young adults with autism spectrum disorder (ASD) and 15 age-matched, typically developing control subjects. Subjects were required to respond with a button-press to rare (25% probability) Kanizsa squares (targets) among Kanizsa triangles (rare non-target distracters, 25% probability) and non-Kanizsa figures (standards, 50% probability) presented on a 15" display. EEG data were segmented off-line into 1000 ms epochs spanning 200 ms pre- to 800 ms post-stimulus onset. Data were digitally screened for artifacts and sorted by condition and averaged to create ERPs.

Results: Participants with ASD had significantly increased P50 amplitudes to non-target Kanizsa stimuli compared to controls at both parieto-occipital and frontal regions-of-interest (ROI).  N100 amplitudes were significantly more negative to target stimuli over frontal ROI, and N100 latencies to target stimuli were significantly prolonged over both frontal and parieto-occipital ROI. Also, individuals with ASD had equally augmented P200 amplitudes to all stimuli over frontal ROI with a lack of stimulus discrimination, and had significantly more commission and omission errors in motor responses to target stimuli.

Conclusions: As our results indicate, individuals with ASD failed to suppress task-irrelevant sensory stimuli at pre-attentive stages of visual processing compared to controls. We found difficulty in sensory filtering at pre-attentive (P50) stages disrupted stimulus discrimination in early attentive (N100), later attentive (P200), and behavioral stages (motor responses to targets), i.e. longer latencies to target stimuli at the stage of the parieto-occipital N100, lack of stimulus discrimination at the frontal P200 stage, and a significantly higher rate of error at the stage of motor responses. A sensory filtering deficit in individuals with ASD may impair functioning, raise physiological stress, and adversely affect social interaction. Further research on sensory filtering abnormalities in ASD may lead to earlier diagnosis and intervention by defining electrophysiological endophenotypes in infants and young children at a higher risk of developing ASD.

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See more of: Brain Structure & Function