Schizophrenia: from neurophysiological abnormalities to clinical symptoms.

Abstract

Schizophrenia (SCZ) has long been associated with multifaceted dysfunctions and multiple genetic as well as environmental etiological factors (Rethelyi et al., 2013). Therefore, after a century of inconsistent results, the search for a unifying pathogenetic mechanism has become one of the most challenging issues in SCZ research. During the last decade, a growing literature has pointed to the so-called disconnection hypothesis (Friston, 1998; Tononi and Edelman, 2000; Stephan et al., 2009), i.e., to a defective integration among distributed brain areas, which may lead to a systematic impairment of information processing. EEG is a suitable tool to probe this hypothesis in the time domain, since the EEG oscillatory activity can capture subtle functional changes of underlying neuronal systems with exquisite temporal resolution. Consistent with this prediction, several recent EEG findings have shown abnormalities in SCZ neural oscillations during both wakefulness (Uhlhaas and Singer, 2014) and sleep (Gardner et al., 2014). Cognitive and theoretical approaches of brain functioning have been used to explain phenomenological features and neural disruptions in SCZ. Since its earliest conceptualizations, abnormalities of self-experience have been identified as a critical feature of the illness (Schneider, 1950). Positive and passivity symptoms in SCZ have been hypothesized to involve a misattribution of self-generated actions, thoughts and percepts to an external agency (Frith, 2005). One possible neurophysiological explanation for this peculiar subjective experience is an aberrant generation of corollary discharge (CD) by efference copy mechanisms (Feinberg, 2011). More recently, predictive coding theories began to add an integrated and structured framework to previous observations (Van de Cruys et al., 2014; Moran et al., 2015). We herein attempt to reconcile recent major neurophysiological findings with currently established approaches to SCZ psychopathology.