Date on Master's Thesis/Doctoral Dissertation

8-2013

Document Type

Master's Thesis

Degree Name

M.S.

Department

Anatomical Sciences and Neurobiology

Committee Chair

Casanova, Manuel F.

Author's Keywords

Autism; Audiovisual; Electroencephalogram; Sensory; Event-related potential; Processing

Subject

Autism; Autism spectrum disorders; Sensory integration dysfunction; Electroencephalography

Abstract

Autism spectrum condition (ASC) consists of a set of pervasive developmental problems marked by measurable deficits in social interaction and communication, often coupled with specific and repetitive patterns of behavior. Featured restrictions in the capability to communicate and remain attentive can directly relate to the individual’s ability to interact with others within societal norms. Evidence has suggested that the deficits commonly demonstrated by individuals with autism may arise from a disconnect between neural processes governing sensory inputs. Comparing ASC subjects to controls, previous investigations had shown that electroencephalogram (EEG) recordings and event-related potentials (ERPs) evoked via separate auditory and visual stimuli do not display aberrations in latency or amplitude in the ASC individuals. However, the findings reported here suggest decreased latencies in early-evoked potentials. Additionally, during the combined audiovisual task, electrophysiological recordings revealed significant cortical activity differences between ASC subjects and controls. To investigate the aforementioned phenomena this study employed EEG recording technology while subjects participated in an oddball-paradigm reaction time test. This project reports on the differences behavioral reactions as well as variances in amplitude and latency in twelve autistic individuals and twelve matched controls. Subjects were evaluated using the event related potentials, N100, N200, and P300, as well as dipole source coherence and power of EEG gamma oscillations recorded at fronto-central and parietal sites in both hemispheres. Findings of this study suggest that the irregularities arise from deficits in the integration and combinatorial processing of multiple sensory inputs. Previous research investigating the neuropathology of autism has identified abnormalities in the structure, number and activity of the cortical minicolumns, which are believed to influence excitatory and inhibitory impulses of sensory processing. The minicolumns of ASC individuals appear in greater number coupled with increased neuronal density due to a reduction in the volume of peripheral neuropil space and neuronal cell bodies. Such a cortical and cellular arrangement favors the formation of short intralobular connections between neurons at the expense of longer interlobular fibers. This study proposes that aberrations in sensory processing and functional cortical binding, as evidenced by EEG recordings related to the tasks, further reflect underlying abnormalities of minicolumns in ASC individuals. Thus, the results of this project intuitively suggest that dysfunction of sensory processing by way of minicolumn irregularity may in turn lead to symptoms commonly associated with autism spectrum condition.

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