The Dynamics of Group Cognition

The aim of this paper is to demonstrate that the postulation of irreducible, distributed cognitive systems (or group minds as they are also known in the literature) is necessary for the successful explanatory practice of cognitive science and sociology. Towards this end, and with an eye specifically on the phenomenon of distributed cognition, the debate over reductionism versus emergence is examined from the perspective of Dynamical Systems Theory (DST). The motivation for this novel approach is threefold. Firstly, DST is particularly popular amongst cognitive scientists who work on modelling collective behaviors. Secondly, DST can deliver two distinct arguments in support of the claim that the presence of mutual interactions between group members necessitates the postulation of the corresponding group entity. Thirdly, DST can also provide a succinct understanding of the way group entities exert downward causation on their individual members. The outcome is a naturalist account of the emergent, and thereby irreducible, nature of distributed cognitive systems that avoids the reductionists’ threat of epiphenomenalism, while being well in line with materialism

Role of N-Methyl-D-Aspartate Receptors in Action-Based Predictive Coding Deficits in Schizophrenia

BACKGROUND: Recent theoretical models of schizophrenia posit that dysfunction of the neural mechanisms subserving predictive coding contributes to symptoms and cognitive deficits, and this dysfunction is further posited to result from N-Methyl D-aspartate glutamate receptor (NMDAR) hypofunction. Previously, by examining auditory cortical responses to self-generated speech sounds, we demonstrated that predictive coding during vocalization is disrupted in schizophrenia. In order to test the hypothesized contribution of NMDAR hypofunction to this disruption, we examined the effects of the NMDAR antagonist, ketamine, on predictive coding during vocalization in healthy volunteers and compared them to the effects of schizophrenia. METHODS: In two separate studies, the N1 component of the event-related potential (ERP) elicited by speech sounds during vocalization (Talk) and passive playback (Listen) were compared to assess the degree of N1 suppression during vocalization, a putative measure of auditory predictive coding. In the cross-over study, 31 healthy volunteers completed two randomly ordered test days, a saline day and a ketamine day. ERPs during the Talk/Listen task were obtained pre-infusion and during infusion on both days, and N1 amplitudes were compared across days. In the case-control study, N1 amplitudes from 34 schizophrenia patients and 33 healthy controls were compared. RESULTS: N1 suppression to self-produced vocalizations was significantly and similarly diminished by ketamine (Cohen's d=1.14) and schizophrenia (Cohen's d=.85). CONCLUSIONS: Disruption of NMDARs causes dysfunction in predictive coding during vocalization in a manner similar to the dysfunction observed in schizophrenia patients, consistent with the theorized contribution of NMDAR hypofunction to predictive coding deficits in schizophrenia

Equivalent mismatch negativity deficits across deviant types in early illness schizophrenia-spectrum patients

Neurophysiological abnormalities in auditory deviance processing, as reflected by the mismatch negativity (MMN), have been observed across the course of schizophrenia. Studies in early schizophrenia patients have typically shown varying degrees of MMN amplitude reduction for different deviant types, suggesting that different auditory deviants are uniquely processed and may be differentially affected by duration of illness. To explore this further, we examined the MMN response to 4 auditory deviants (duration, frequency, duration + frequency “double deviant”, and intensity) in 24 schizophrenia-spectrum patients early in the illness (ESZ) and 21 healthy controls. ESZ showed significantly reduced MMN relative to healthy controls for all deviant types (p < 0.05), with no significant interaction with deviant type. No correlations with clinical symptoms were present (all ps > 0.05). These findings support the conclusion that neurophysiological mechanisms underlying processing of auditory deviants are compromised early in illness, and these deficiencies are not specific to the type of deviant presented