Not so Automatic Imitation: Expectation of Incongruence Reduces Interference in Both Autism Spectrum Disorder and Typical Development

Background:

Individuals with autism spectrum disorder (ASD) exhibit deficits in social functioning. One prominent view is that such impairments are the result of a diminished capacity for imitation; however the underlying mechanisms remain unclear. One recent theory suggests that ASD may be characterized by an aberrant mirror neuron system (MNS), the neural system underlying imitation. Imitative response tendencies can be probed in the laboratory through automatic imitation (AI)–the degree to which observed actions modulate action execution. However, the largest study to date found evidence that AI is intact in ASD, challenging this hypothesis (Sowden et al., 2016). An alternative account suggests that social deficits may instead stem from differences in the ability to exert top-down control of imitation in those with ASD versus those with typical development (TD). Although previous research has suggested that AI is not affected by top-down control in TD (Hogeveen & Obhi, 2013), no research has examined this process in ASD.

Objectives:

To provide further evidence for or against the MNS hypothesis by examining potential differences between ASD and TD in the degree of AI (H¹), and for the control of imitation theory by examining participants’ ability to exert top-down control of imitation (H²).

Methods:

Participants completed two blocks of a paradigm that included both AI and non-imitative control trials (effector priming, EP). Across blocks the congruent/incongruent trial ratio was manipulated such that one block consisted of mostly congruent trials (MC) while the other was mostly incongruent trials (MI). The dependent variables (DVs) were accuracy, reaction times (RT), and drift rate (v) – a combination of accuracy and RT quantifying participants’ rate of information processing. Data collection is ongoing for the current study, and at present we examined the control of imitation in ASD (N=27) and an FSIQ case-controlled TD sample (N=27).

Results:

Scores for our three DV’s were collapsed across block and submitted to a 2 (stimulus type: imitation vs. effector) x 2 (congruence: congruent vs. incongruent) x 2 (diagnosis group: TD vs. ASD) ANOVA (fig.1). In contrast to the theory of a broken MNS, the degree of AI was equivalent between groups for all three variables (all Fs < 1, BF₀₁ > 2), consistent with the notion that the MNS is intact in ASD. Turning to our second hypothesis, interference scores were calculated for each DV and submitted to a 2 (stimulus type: imitation vs. effector) x 2 (block: MC vs. MI) x 2 (diagnosis group: TD vs. ASD) ANOVA (fig.2). For both groups, AI and EP interference effects decreased when the ratio of incongruent-to-congruent trials increased (MI < MC; Fs > 13, BF₁₀ > 13). The top-down control of imitation was also matched between groups across all variables (Fs < 1, BF₀₁ > 8).

Conclusions:

In agreement with previous work our results demonstrate that AI is unimpaired in ASD and cast further doubt upon the broken MNS theory. Furthermore, we demonstrated that control over AI is similarly unimpaired in ASD, suggesting that for both groups AI is not as automatic as previously theorized.