Objectives: In the present study, we used functional magnetic resonance imaging (fMRI) to investigate the neurobiological substrates of phonological processing in parents of individuals with autism.
Methods: Fourteen parents of a child with autism 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., BRANE-brain), unrelated (e.g., ARCH-gash), and word-nonword (e.g., FRAIL-clute) stimuli. Stimuli presentation was as follows: 500ms mask, 30ms prime, 30ms blank screen, 400ms target, and 1040ms blank screen. Primes were presented below perceptual threshold at 30ms in order to investigate the initial, automatic stages of visual word recognition and to avoid possible differences in the use of strategic or controlled processes between groups. Subjects were not informed that stimuli consisted of word pairs and 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 a random effects whole-brain analysis in SPM8.
Results: Controls, as a group, exhibited enhanced hemodynamic responses for phonologically primed stimuli (i.e., homophones and pseudohomophones) relative to unrelated stimuli in regions known to be involved in phonological processing, including left lateralized inferior frontal and inferior parietal cortex, with no response differences observed between homophone and pseudohomophone stimuli (FDR, p<0.05). The parent group did not exhibit greater responses for phonologically primed relative to unrelated stimuli. Parents, however, exhibited greater responses for pseudohomophone relative to homophone stimuli in several regions including left lateralized superior temporal, middle temporal, and insular cortex (FDR, p<0.05). Direct group comparisons revealed that controls exhibited greater responses than the parent group for primed relative to unrelated stimuli in the left inferior frontal cortex (SVC, p<0.05). Furthermore, parents exhibited greater responses than controls for pseudohomophone relative to homophone stimuli in left lateralized inferior parietal, supramarginal, middle temporal, and inferior temporal gyri (SVC, p<0.05).
Conclusions: These results provide evidence for possible neurobiological correlates of the phonological processing deficits that have been observed in parents of individuals with autism. By clarifying the familiality of these deficits, our long-term aim is to identify endophenotypes that could be used to guide future genetic linkage studies and clinical interventions in autism.