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There is some evidence that disordered self-processing in autism spectrum disorders is linked to the social impairments characteristic of the condition. To investigate whether bodily self-consciousness is altered in autism spectrum disorders as a result of multisensory processing differences, we tested responses to the full body illusion and measured peripersonal space in 22 adults with autism spectrum disorders and 29 neurotypical adults. In the full body illusion set-up, participants wore a head-mounted display showing a view of their 'virtual body' being stroked synchronously or asynchronously with respect to felt stroking on their back. After stroking, we measured the drift in perceived self-location and self-identification with the virtual body. To assess the peripersonal space boundary we employed an audiotactile reaction time task. The results showed that participants with autism spectrum disorders are markedly less susceptible to the full body illusion, not demonstrating the illusory self-identification and self-location drift. Strength of self-identification was negatively correlated with severity of autistic traits and contributed positively to empathy scores. The results also demonstrated a significantly smaller peripersonal space, with a sharper (steeper) boundary, in autism spectrum disorders participants. These results suggest that bodily self-consciousness is altered in participants with autism spectrum disorders due to differences in multisensory integration, and this may be linked to deficits in social functioning.

Communicative gaze (e.g., mutual or averted) has been shown to affect attentional orienting. However, no study to date has clearly separated the neural basis of the pure social component that modulates attentional orienting in response to communicative gaze from other processes that might be a combination of attentional and social effects. We used TMS to isolate the purely social effects of communicative gaze on attentional orienting. Participants completed a gaze-cueing task with a humanoid robot who engaged either in mutual or in averted gaze before shifting its gaze. Before the task, participants received either sham stimulation (baseline), stimulation of right TPJ (rTPJ), or dorsomedial prefrontal cortex (dmPFC). Results showed, as expected, that communicative gaze affected attentional orienting in baseline condition. This effect was not evident for rTPJ stimulation. Interestingly, stimulation to rTPJ also canceled out attentional orienting altogether. On the other hand, dmPFC stimulation eliminated the socially driven difference in attention orienting between the two gaze conditions while maintaining the basic general attentional orienting effect. Thus, our results allowed for separation of the pure social effect of communicative gaze on attentional orienting from other processes that are a combination of social and generic attentional components. [ABSTRACT FROM AUTHOR]

The functional connection between ventral premotor cortex (PMv) and primary motor cortex (M1) is critical for the organization of goal‐directed actions. Repeated activation of this connection by means of cortico‐cortical paired associative stimulation (cc‐PAS), a transcranial magnetic stimulation (TMS) protocol, may induce Hebbian‐like plasticity. However, the physiological modifications produced by Hebbian‐like plasticity in the PMv‐M1 network are poorly understood. To fill this gap, we investigated the effects of cc‐PAS on PMv‐M1 circuits. We hypothesized that specific interactions would occur with I2‐wave interneurons as measured by the short intracortical facilitation protocol (SICF). We used different paired‐pulse TMS protocols to examine the effects of PMv‐M1 cc‐PAS on SICF, on GABAergic circuits as measured by short (SICI) and long (LICI) intracortical inhibition protocols, and varied the current direction in M1 to target different M1 neuronal populations. Finally, we examined the effects of cc‐PAS on PMv‐M1 connectivity using a dual coil approach. We found that PMv‐M1 cc‐PAS induces both a long‐term potentiation (LTP)‐ or long‐term depression (LTD)‐like after‐effect in M1 neuronal activity that is strongly associated with a bidirectional‐specific change in I2‐wave activity (SICF = 2.5 ms ISI). Moreover, cc‐PAS induces a specific modulation of the LICI circuit and separately modulates PMv‐M1 connectivity. We suggest that plasticity within the PMv‐M1 circuit is mediated by a selective mechanism exerted by PMv on M1 by targeting I2‐wave interneurons. These results provide new mechanistic insights into how PMv modulates M1 activity that are relevant for the design of brain stimulation protocols in health and disease. Key points: The I2‐wave is specifically modulated by the induction of ventral premotor cortex – primary motor cortex (PMv‐M1) plasticity.After PMv‐M1 cortico‐cortical paired associative stimulation (cc‐PAS), corticospinal excitability correlates negatively with I2‐wave amplitude.Different cc‐PAS coil orientations can lead to a long‐term potentiation‐ or long‐term depression‐like after‐effect in M1. [ABSTRACT FROM AUTHOR]