Artificial scaffolding: Augmenting social cognition by means of robot technology.

The concept of scaffolding refers to the support that the environment provides in the acquisition and consolidation of new abilities. Technological advancements allow for support in the acquisition of cognitive capabilities, such as second language acquisition using simple smartphone applications There is, however, one domain of cognition that has been scarcely addressed in the context of technologically assisted scaffolding: social cognition. We explored the possibility of supporting the acquisition of social competencies of a group of children with autism spectrum disorder engaged in a rehabilitation program (age = 5.8 ± 1.14, 10 females, 33 males) by designing two robot-assisted training protocols tailored to Theory of Mind competencies. One protocol was performed with a humanoid robot and the other (control) with a non-anthropomorphic robot. We analyzed changes in NEPSY-II scores before and after the training using mixed effects models. Our results showed that activities with the humanoid significantly improved NEPSY-II scores on the ToM scale. We claim that the motor repertoire of humanoids makes them ideal platforms for artificial scaffolding of social skills in individuals with autism, as they can evoke similar social mechanisms to those elicited in human-human interaction, without providing the same social pressure that another human might exert.

Childhood thalidomide neuropathy: a clinical and neurophysiologic study.

Thalidomide was recently reintroduced to treat several immune-mediated pathologies. Peripheral neuropathy is a significant side effect limiting its clinical use. Our aims include: (1) describing and identifying the incidence of clinical or electrophysiologic peripheral neuropathy in children, (2) determining whether peripheral neuropathy correlates with cumulative dose of thalidomide and with age, and (3) defining its reversibility rate. We studied 13 children manifesting immune-mediated pathologies treated with thalidomide at doses ranging from 25-100 mg/day. Clinical and neurophysiologic evaluation was performed before and after starting treatment. Seven children (53.8%) showed neurophysiologic signs of sensory peripheral axonal polyneuropathy. Five presented associated clinical symptoms, while the other two only presented subclinical, neurophysiologic signs of peripheral neuropathy. We found a significant correlation between the incidence of peripheral neuropathy and thalidomide cumulative dose (P = 0.02). We observed a lower incidence of peripheral neuropathy at a cumulative dose <20 gm, and a correlation with age (P < 0.01). The clinical and electrophysiologic recovery rate was 40%, and clinical improvement alone was observed in another 40%. Thalidomide induces dose-dependent and age-dependent peripheral neuropathy at a significant frequency in childhood (53.8%). In our experience a cumulative dosage at >20 gm and long-term administration for >10 months seem to increase the risk of peripheral neuropathy. We propose clinical and neurophysiologic follow-up every 3 months to identify and monitor possible side effects.