18112
Neural Correlates of Cognitive Control and Attentional Orienting in Adults with Autism Spectrum Disorders

Friday, May 16, 2014
Atrium Ballroom (Marriott Marquis Atlanta)
D. S. Karhson1 and E. J. Golob2, (1)Neuroscience Program, Tulane University, New Orleans, LA, (2)Department of Psychology, Tulane University, New Orleans, LA
Background:  

Abnormal sensory reactivity is widely reported in people diagnosed with autism spectrum disorder (ASD). Appearing first in childhood and persisting throughout adulthood, abnormal reactivity is often observed as increased responsiveness in visual and/or auditory modalities. Data from cognitive neuroscience research suggests that changes in attention can alter sensory processing at several levels of analysis. Thus, abnormal stimulus-driven bottom-up processing could be contributing to atypical sensory reactivity. Restricted, fixated interest and intense focus might describe atypical functioning of voluntary top-down attentional control. Additionally, attentional pathways are modulated by the general cognitive factor and individual difference variable of working memory capacity (WMC). Defined as the amount of related information that can be actively maintained and manipulated in an accessible state, WMC contributes to the control cognition and modulating orienting responses. Electroencephalography will be used to investigate underlying cognitive processes with excellent temporal resolution, time-locked to stimulus presentation. 

Objectives:  

Current study measured event-related potentials (ERPs) associated with endogenous and exogenous orienting responses in participants with ASD after completing a modified 3-stimulus auditory oddball paradigm. Effects of sensory reactivity, perceptual load, and WMC on auditory cortical potentials to targets, non-targets, and distractors are examined. 

Methods:  

16 adults with ASD and 16 age- and IQ-matched control participants completed (recruitment is ongoing at abstract submission) the Adolescent/Adult Sensory profile and Kaufman Brief Intelligence Test (KBIT-2) prior to completing the auditory attention task. Electroencephalography was recorded as participants performed a modified 3-stimulus (target, non-target, and distractor) oddball task under varying perceptual load (high or low). Presented stimuli were random and binaural with an inter-stimulus interval of 2000 ms (~60dB, 200ms duration, 200 stimuli/block, 4 blocks/perceptual load, 8 blocks total). Infrequent pure tone targets (1000 Hz, probability = .12) and frequent non-targets (probability = .76) were presented at 0° midline. Sounds are not masked or presented concurrently with other auditory stimuli during the task, making discrimination based on sound source location or stimulus location possible. Presentation of white noise distractors at various spatial locations (-90°, 0°, or +90˚; probability=0.12) and manipulation of non-target frequency (low load: 500Hz, high load: 950Hz) were used to vary perceptual load. ERPs examined reflect early sensory and attentional processes. 

Results:  

Preliminary analyses on the Adult Sensory Profile established atypical sensory reactivity in 9 ASD participants (4 female, mean age = 29.8) specifically for low registration, sensation seeking, and sensation avoiding items. ERP analyses suggest perceptual load was sufficiently modulated as evidenced by changes in N100 amplitude to variations in frequency. Components associated with exogenous attentional orienting (P50 and P200) were modulated by perceptual load for non-targets. Whereas potentials associated with feature classification (N200) were robustly modulated by distractor location. 

Conclusions:  

Perceptual load may differentially modulate white noise and non-target auditory stimuli processing in ASD. Atypical sensory reactivity may contribute to perceptual load changes, but further analyses are required the relationship. Further evaluation is also needed to determine if effects are specific to ASD. Measures of cognitive control will be included to establish the influence of individual difference on ASD neural activity.