A Neural Mass Model for Abnormal Beta-Rebound in Schizophrenia

Patients with schizophrenia demonstrate robust abnormalities of the synchronisation of beta oscillations that occur in diverse brain regions following sensory, motor or mental events. A prominent abnormality seen in primary motor cortex is a reduction in amplitude of so-called beta-rebound. Here a sharp decrease in neural oscillatory power in the beta band is observed during movement (MRBD) followed by an increase above baseline on movement cessation (PMBR). An understanding of how neural circuits give rise to MRBD and PMBR is clinically relevant to the pathophysiology of schizophrenia. Here we survey a very recent neural mass model for movement-induced changes in the beta rhythm and show that it is an ideal candidate for use in a clinical setting. The model arises as an exact mean-field reduction of a spiking network, has a realistic model of synaptic processing and is able to describe the dynamic changes in population synchrony that can underlie event-related desynchronisation/synchronisation for MRBD/PMBR. A lengthening of the synaptic response time to sensory drive, modelling NMDA receptor hypofunction, shows a reduction in beta-rebound consistent with that seen in schizophrenia.