Group Differences in FFR
/dɑ/ Stimulus. The overall model comparing latencies between the ASD and ASD Control groups was statistically significant (F = 2.71, p = .02; see Fig. 1). The ASD group exhibited significantly greater response latencies for waves A (F = 9.11, p = .005), E (F = 7.55, p = .01), and F (F = 4.31, p = .04), and a marginally greater response latency for wave V (F = 3.64, p = .06). ASD and ASD Control groups did not differ in response latency for wave D (F = .70, p = .41) or wave O (F = .72, p = .40). The model comparing spectral amplitude between the ASD and ASD Control groups was not statistically significant (F = 1.94, p = .15). The ASD group exhibited significantly greater prestimulus noise (F = 7.53, p = .006) and reduced response consistency (F = 25.74, p < .001) compared to controls.
The overall model comparing latencies between the ASD Parent and Parent Control groups approached statistical significance (F = 2.11, p = .06). The ASD Parent group exhibited significantly greater response latencies for waves V (F = 4.77, p = .03) and A (F = 10.06, p = .002; see Fig. 1). ASD Parent and Parent Control groups did not differ in response latencies for waves D (F = 0.05, p = .83), E (F = 2.14, p = .15), or F (F = 1.52, p = .22), and O (F = 0.27, p = .61). Comparison of spectral amplitude between the ASD Parent and Parent Control groups was not statistically significant (F = 1.58, p = .21), and there were no differences in prestimulus noise (F = 0.01, p = .94). Results revealed marginally poorer response consistency (F = 3.45, p = .07) in the ASD Parent group.
/jɑ/ Stimulus. The model assessing pitch tracking in the ASD and ASD Control groups approached significance (F = 2.14, p = .11). The ASD group exhibited reduced pitch strength compared to controls (F = 6.16, p = .02). Groups did not differ in pitch error (F = 2.51, p = .12) or correlation coefficient (F = 1.47, p = .23).
The overall model assessing pitch tracking in the ASD Parent and Parent Control groups did not reach statistical significance (F = 0.55, p = .65).
Speech And Language Correlates Of Ffr
Pragmatic Language in ASD and ASD Control groups. In ASD and ASD Control groups combined, increased pragmatic language violations were associated with a longer latency for wave E (r = .33, p = .02), increased prestimulus noise (r = .36, p = .008), decreased response consistency (r=-.52, p < .001), increased pitch error (r = .34, p = .02), and reduced pitch strength (r=-.42, p < .01). Each of these FFR variables, except latency for wave E, were associated with increased difficulty with discourse management (e.g., topic initiation, interrupting; rs>|.29|, ps ≤ .05). Latency for wave E, prestimulus noise, and response consistency, were also related to impairments in nonverbal communication (e.g., atypical eye contact, gestures; rs>|.28|, ps < .05). Response consistency and pitch strength were additionally related to increased violations in the speech/language behaviors domain (e.g., overly formal speech; stereotyped utterances; rs>|.32|, ps < .05). Longer latencies for waves A and E, as well as reduced response consistency, greater pitch error, and decreased pitch strength were associated with increased suprasegmental difficulties (e.g., intonation modulation, speech rate; rs >|.28|, ps < .05).
Pragmatic Language in ASD Parent and Parent Control groups. In the parent groups collapsed, increased pragmatic language violations were associated with decreased spectral amplitude for the fundamental frequency (r=-.26, p = .04) and less response consistency (r=-.26, p = .04). Associations with spectral amplitude for the fundamental frequency were detected with dominant conversational style (e.g., tangential comments, topic preoccupation; r=-.30, p = .02) and pragmatic language violations related to listener expectations (e.g., fails to reciprocate, vague; r=-.27, p = .04). The relationship between response consistency and pragmatic language violations appeared to be driven by differences in suprasegmentals (r=-.35, p < .01).
Prosodic Ability. In the ASD and ASD control groups, associations with receptive prosody skills emerged, with increased neural response latency and reduced response consistency associated with poorer Contrastive Stress. Sporadic associations were observed between measures of response latency, spectral amplitude, and pitch tracking with Turn-End and Boundary understanding. Poorer expressive prosody, particularly in the domains of Imitation, Turn-End, and Boundary expression, was associated with increased neural response latency and reduced response consistency, as well as poorer pitch tracking. Affect, Lexical Stress, and Phrase Stress domains were not associated with FFR (see Table 2).
Similar to patterns identified in ASD and ASD Control groups, in parent groups, poorer receptive prosody skills in the domain of Contrastive Stress were associated with increased neural response latencies and reduced response consistency, as well as reduced spectral amplitude of the fundamental frequency. Poorer expressive prosody skills in the domain of Contrastive Stress were associated with reduced spectral amplitude of the fundamental frequency. Sporadic associations between Phrase Stress and Boundary expression and neural response latencies emerged. Similar to findings in the ASD and ASD Control groups, several domains of prosody were not related to FFR (see Table 3).
Familiality Of Ffr
For mother-child ASD dyads, response latencies for wave D (r = .52, p = .04) and prestimulus noise (r = .52, p = .04) were positively correlated. Further, pitch error (r=-.74, p < .01) and pitch strength (r=-.72, p < .001) were negatively correlated.
In mother-child Control dyads, responses latencies for waves V (r = .64, p < .01) and A (r = .63 p < .01) were positively associated. Additionally, spectral amplitude for the first formant frequency was positively associated (r = .60, p < .01). No significant correlations were evident in the mismatched mother-child dyads in ASD nor ASD Control families (p > .25).