The emergence of the social brain network: Evidence from typical and atypical development
Several research groups have identified a network of regions of the adult cortex that are activated during social perception and cognition tasks. In this paper we focus on the development of components of this social brain network during early childhood and test aspects of a particular viewpoint on human functional brain development: "interactive specialization." Specifically, we apply new data analysis techniques to a previously published data set of event-related potential (ERP) studies involving 3-, 4-, and 12-month-old infants viewing faces of different orientation and direction of eye gaze. Using source separation and localization methods, several likely generators of scalp recorded ERP are identified, and we describe how they are modulated by stimulus characteristics. We then review the results of a series of experiments concerned with perceiving and acting on eye gaze, before reporting on a new experiment involving young children with autism. Finally, we discuss predictions based on the atypical emergence of the social brain network.
Face-sensitive cortical processing in early infancy
Background: Debates about the developmental origins of adult face processing could be directly addressed if a clear infant neural marker could be identified. Previous research with infants remains open to criticism regarding the control stimuli employed. Methods: We recorded ERPs from adults and 3-month-old infants while they watched faces and matched visual noise stimuli. Results: We observed similar amplitude enhancement for faces in the infant N290 and adult N170. In contrast, the infant P400 showed only a latency effect, making it unlikely to be the main precursor of the adult N170. Conclusions: We conclude that there is some degree of specificity of cortical processing of faces as early as 3 months of age.
Disordered visual processing and oscillatory brain activity in autism and Williams Syndrome
Two developmental disorders, autism and Williams syndrome, are both commonly described as having difficulties in integrating perceptual features, i.e. binding spatially separate elements into a whole. It is already known that healthy adults and infants display electroencephalographic (EEG) gamma -band bursts (around 40 Hz) when the brain is required to achieve such binding. Here we explore gamma -band EEG in autism and Williams Syndrome and demonstrate differential abnormalities in the two phenotypes. We show that despite putative processing similarities at the cognitive level, binding in Williams syndrome and autism can be dissociated at the neurophysiological level by different abnormalities in underlying brain oscillatory activity. Our study is the first to identify that binding-related gamma EEG can be disordered in humans. NeuroReport 12:2697-2700 (C) 2001 Lippincott Williams & Wilkins.