Neural Processing of Speech Sounds in Individuals with ASD and First Degree Relatives

Background: Impairments in social communication are a core feature of autism spectrum disorder (ASD), and include atypical use of prosody, or the intonation, rhythm, and rate of speech (Mesibov, 1992; VanBourgonien & Woods, 1992). The midbrain’s response to speech-evoked stimuli (i.e., the frequency following response; FFR) provides valuable information regarding an individual’s ability to make sense of sound, including information about neural processing of speech prosody. Prior research using the FFR has documented delayed latencies of neural responses and poorer tracking of speech pitch in individuals with ASD (Russo et al., 2008; Russo et al., 2009). Importantly, atypicalities in social communication and prosody have also been reported in parents of individuals with ASD (Losh et al., 2012). Evidence of similar atypicalities in the FFR among parents of individuals with ASD could implicate the FFR as a genetically meaningful neurobiological marker of ASD related to prosody and broader social communication differences.

Objectives: To examine differences in the FFR to speech-evoked stimuli in individuals with ASD, their parents, and respective control groups.

Methods: Participants include 30 individuals with ASD, 36 controls (a subset of whom (n=29)) only completed FFR to the speech syllable /da/), 40 ASD parents, and 19 parent controls. FFRs to the speech syllable /da/ and the naturally spoken syllable /ya/ with an ascending pitch contour (i.e., resembling a question) were collected. FFRs to /da/ were analyzed for response latencies reflecting processing of the onset, offset, and acoustic properties of the syllable. FFRs to /ya/ were analyzed for fidelity of pitch tracking of the stimulus. Furthermore, parent-child correlations were conducted within the ASD and ASD parent groups to assess the familiality of FFRs to speech-evoked stimuli.

Results: Both the ASD and ASD parent groups differed from their respective control groups in response latencies. Specifically, in response to the /da/ syllable, individuals with ASD and ASD parents demonstrated delayed onset timing of processing the syllable /da/ compared to controls (ps < .01). Individuals with ASD also exhibited delayed processing of other acoustic features of the syllable /da/ compared to controls (ps<.05). Furthermore, individuals with ASD (p = .06; see Figure 1) and their parents (p = .02; see Figure 2) exhibited increased error in neural tracking of the ascending pitch contour of the syllable /ya/ compared to their respective control groups. Correlational analyses revealed that increased delays in processing the acoustic features of the syllable /da/ in ASD parents were associated with increased delays in individuals with ASD (rs > .42, ps < .10).

Conclusions: Findings revealed both delayed and diminished neural processing of speech-evoked stimuli in individuals with ASD and their parents. Such evidence of inefficient neural processing of the acoustic features of speech highlights the FFR as a potential neural marker of prosodic atypicalities characteristic of ASD. Parallel findings observed in individuals with ASD and their parents suggest that the FFR to speech-evoked stimuli may be a key neural marker of genetic liability to ASD.