The N170 is a brain electrical potential proposed to index the earliest time of categorical perception of faces in occipitotemporal visual areas implicated in face cognition, being more negative for faces than nonface objects between 120 and 200 ms. The interstimulus variance (ISV) account instead explained N170 face-specificity as an artifact due to objects varying more visually than faces. Ganis, Smith, and Schendan (2012) tested this account directly, finding that N170 face-specificity remains even when ISV is eliminated. Here, N170 peak amplitude and face-specificity is quantified for individual stimuli and participants, revealing that the right hemisphere N170 is especially sensitive to stimulus variability. Further, ISV contributes 0 to 37% to N170 face-specificity. These findings provide evidence for optimizing face processing science. The paradigm can apply to any research in which ISV may be uncontrolled (e.g., category comparisons).
[Show abstract][Hide abstract] ABSTRACT: The study of neurophysiological approaches together with rare and common risk factors for Autism Spectrum Disorder (ASD) allows elucidating the specific underlying neurobiology of ASD. Whereas most neurophysiologically based research in ASD to date has focussed on case-control differences based on the DSM- or ICD-based categorical ASD diagnosis, more recent studies have aimed at studying genetically and/or neurophysiologically defined homogeneous ASD subgroups for specific neuronal biomarkers. This review addresses the neurophysiological investigation of ASD by evoked and event-related potentials, by EEG/MEG connectivity measures such as coherence, and transcranial magnetic stimulation. As an example of classical neurophysiological studies in ASD, we report event-related potential studies which have illustrated which brain areas and processing stages are affected in the visual perception of socially relevant stimuli. However, a paradigm shift has taken place in recent years focussing on how these findings can be tracked down to basic neuronal functions such as deficits in cortico-cortical connectivity and the interaction between brain areas. Disconnectivity, for example, can again be related to genetically induced shifts in the excitation/inhibition balance. Genetic causes of ASD may be grouped by their effects on the brain's system level to identify ASD subgroups which respond differentially to therapeutic interventions.
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