Adults imitate to send a social signal

Humans are prolific imitators, even when copying may not be efficient. A variety of explanations have been advanced for this phenomenon, including that it is a side-effect of learning, that it arises from a lack of understanding of causality, to imitation being a mechanism to boost affiliation. This thesis systematically outlines the hypothesis that imitation is a social signal sent between interacting partners, which rests on testing whether our propensity to imitate is modulated by the social availability of the interaction partner (i.e., whether our interaction partner is watching us or not). I developed a dyadic block-moving paradigm that allowed us to test this hypothesis in a naturalistic manner in four behavioural and neuroimaging studies using functional near-infrared spectroscopy (fNIRS). I found that imitative fidelity was modulated by whether the interaction partner was watching the participant make their move or not, and this effect replicated across all four studies, in both neurotypicals and autistic participants. I also examined the neural correlates of responding to irrational actions, and of being watched. I found that being watched led to a robust deactivation in the right parietal cortex across both neurotypicals (in two studies) and autistic participants (one study). Among autistic participants we also found strong engagement in the left superior temporal sulcus (STS) when being watched. For responding to irrational actions, in one study of neurotypicals we found greater deactivation in the right superior parietal lobule (SPL) when making more irrational responses. In another study of autistic and neurotypical participants we found deactivation in the bilateral inferior parietal cortex (IPL) in neurotypicals when responding to irrational actions, while this deactivation appeared confined to the left IPL for autistic participants. Autistic participants also showed differentially higher engagement in the left occipitotemporal regions when responding to irrational actions. This thesis supports the social-signalling hypothesis of imitation and is accompanied by suggestions for future directions to explore this theory in more detail

Social signalling as a framework for second-person neuroscience

Despite the recent increase in second-person neuroscience research, it is still hard to understand which neurocognitive mechanisms underlie real-time social behaviours. Here, we propose that social signalling can help us understand social interactions both at the single- and two-brain level in terms of social signal exchanges between senders and receivers. First, we show how subtle manipulations of being watched provide an important tool to dissect meaningful social signals. We then focus on how social signalling can help us build testable hypotheses for second-person neuroscience with the example of imitation and gaze behaviour. Finally, we suggest that linking neural activity to specific social signals will be key to fully understand the neurocognitive systems engaged during face-to-face interactions

Brain mechanisms of social signalling in live social interactions with autistic and neurotypical adults

The simple act of watching another person can change a person's behaviour in subtle but important ways; the individual being watched is now capable of signalling to the watcher, and may use this opportunity to communicate to the watcher. Recent data shows that people will spontaneously imitate more when being watched. Here, we examine the neural and cognitive mechanisms of being watched during spontaneous social imitation in autistic and neurotypical adults using fNIRS brain imaging. Participants (n = 44) took part in a block-moving task where they were instructed only to copy the block sequence which people normally do using a straight low action trajectory. Here, the demonstrator sometimes used an atypical 'high' action trajectory, giving participants the opportunity to spontaneously copy the high trajectory even if this slowed their performance. The confederate who demonstrated each block sequence could watch the participant's actions or close her eyes, giving a factorial design with factors of trajectory (high/low) and watched (watched/unwatched). Throughout the task, brain signals were captured from bilateral temporal/parietal/occipital cortex using fNIRS. We found that all participants performed higher actions when being watched by the confederate than when not being watched, with no differences between autistic and neurotypical participants. The unwatched conditions were associated with higher activity of the right inferior parietal lobule in all participants and also engagement of left STS only in autistic participants. These findings are consistent with the claim that people engage different neural mechanisms when watched and unwatched and that participants with autism may engage additional brain mechanisms to match neurotypical behaviour and compensate for social difficulties. However, further studies will be needed to replicate these results in a larger sample of participants

Brain mechanisms of social signalling in live social interactions with autistic and neurotypical adults

Abstract The simple act of watching another person can change a person’s behaviour in subtle but important ways; the individual being watched is now capable of signalling to the watcher, and may use this opportunity to communicate to the watcher. Recent data shows that people will spontaneously imitate more when being watched. Here, we examine the neural and cognitive mechanisms of being watched during spontaneous social imitation in autistic and neurotypical adults using fNIRS brain imaging. Participants (n = 44) took part in a block-moving task where they were instructed only to copy the block sequence which people normally do using a straight low action trajectory. Here, the demonstrator sometimes used an atypical ‘high’ action trajectory, giving participants the opportunity to spontaneously copy the high trajectory even if this slowed their performance. The confederate who demonstrated each block sequence could watch the participant’s actions or close her eyes, giving a factorial design with factors of trajectory (high/low) and watched (watched/unwatched). Throughout the task, brain signals were captured from bilateral temporal/parietal/occipital cortex using fNIRS. We found that all participants performed higher actions when being watched by the confederate than when not being watched, with no differences between autistic and neurotypical participants. The unwatched conditions were associated with higher activity of the right inferior parietal lobule in all participants and also engagement of left STS only in autistic participants. These findings are consistent with the claim that people engage different neural mechanisms when watched and unwatched and that participants with autism may engage additional brain mechanisms to match neurotypical behaviour and compensate for social difficulties. However, further studies will be needed to replicate these results in a larger sample of participants