Objectives: The purpose of the present study was to use functional magnetic resonance imaging (fMRI) to investigate the neurobiological substrates of phonological processing in individuals with autism.
Methods: Seven adults with DSM-IV ASD and eighteen controls performed a phonological priming task while undergoing fMRI. The task consisted of four prime-target conditions including homophones (e.g., PAUSE-paws), pseudohomophones (e.g., JURM-germ), unrelated (e.g., ARCH-gash), and word-nonword (e.g., FRAIL-clute) stimuli. Primes were presented below perceptual threshold at 30ms in order to investigate the initial, automatic stages of visual word recognition. Subjects performed a lexical decision task (i.e., is it a word or nonword?) on all lowercase targets. Functional images were acquired using a GE 3T whole-body magnet with a gradient-echo T2* Blood Oxygenation Level Dependent (BOLD) contrast technique. Data were realigned to the first volume, normalized to standard space, smoothed with an 8mm FWHM kernel, and evaluated using the GLM in random effects whole-brain and region-of interest analyses in SPM8.
Results: Individuals with autism exhibited similar hemodynamic response suppression to controls for phonological priming across homophone and pseudohomophone conditions in regions associated with phonological processing including the left supramarginal gyrus and superior temporal gyrus. However, individuals with autism exhibited increased hemodynamic response relative to controls for pseudohomophone compared to homophone priming in a number of cortical regions including the left supramarginal gyrus, precentral gyrus, postcentral gyrus, and supplementary motor cortex.
Conclusions: Individuals with autism exhibited enhanced hemodynamic responses for pseudohomophone relative to homophone priming in cortical regions associated with subvocal articulatory demands as well as regions associated with phonological processing. While preliminary due to the small sample size, these findings provide evidence for the neuroanatomical basis of the phonological deficits seen in autism.
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