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Measurement of Fronto-limbic Activity Using an Emotional Oddball Task in Children with Familial High Risk for Schizophrenia
Published on: December 2, 2015
Source-reconstruction of event-related fields reveals hyperfunction and hypofunction of cortical circuits in
Davide Rivolta1, Nazareth P Castellanos, Cerisa Stawowsky
1Department of Neurophysiology, Max Planck Institute for Brain Research and Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, Frankfurt am Main 60528, Germany, School of Psychology, University of East London, London E15 4LZ, United Kingdom, Laboratory of Cognitive and Computational Neuroscience, Center for Biomedical Technology, Universidad Politécnica de Madrid, Madrid 28223, Spain, MEG Unit, Brain Imaging Centre, Johann Wolfgang Goethe University, Frankfurt am Main 60529, Germany, Institute for Medical Psychology, Johann Wolfgang Goethe University, Frankfurt am Main 60054, Germany, Department of Psychiatry and Psychotherapy, University of Cologne, Cologne 50924, Germany, Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim 68159, Germany, Department of General Psychiatry, Medical Faculty Heidelberg, Heidelberg University, Heidelberg 69115, Germany, Frankfurt Institute for Advanced Studies, Johann Wolfgang Goethe University, Frankfurt am Main 60438, Germany, and Institute of Neuroscience and Psychology, University of Glasgow, Glasgow G12 8QB, United Kingdom.
Abstract:
Schizophrenia is characterized by dysfunctions in neural circuits that can be investigated with electrophysiological methods, such as EEG and MEG. In the present human study, we examined event-related fields (ERFs), in a sample of medication-naive, first-episode schizophrenia (FE-ScZ) patients (n = 14) and healthy control participants (n = 17) during perception of Mooney faces to investigate the integrity of neuromagnetic responses and their experience-dependent modification. ERF responses were analyzed for M100, M170, and M250 components at the sensor and source levels. In addition, we analyzed peak latency and adaptation effects due to stimulus repetition. FE-ScZ patients were characterized by significantly impaired sensory processing, as indicated by a reduced discrimination index (A'). At the sensor level, M100 and M170 responses in FE-ScZ were within the normal range, whereas the M250 response was impaired. However, source localization revealed widespread elevated activity for M100 and M170 in FE-ScZ and delayed peak latencies for the M100 and M250 responses. In addition, M170 source activity in FE-ScZ was not modulated by stimulus repetitions. The present findings suggest that neural circuits in FE-ScZ may be characterized by a disturbed balance between excitation and inhibition that could lead to a failure to gate information flow and abnormal spreading of activity, which is compatible with dysfunctional glutamatergic neurotransmission.
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