Online research in philosophy

This paper discusses spatial cognition in the domain of minimally invasive surgery. It draws on studies from this domain to shed light on a range of spatial cognitive processes and to consider individual differences in performance. In relation to modeling, the aim is to identify potential opportunities for characterizing the complex interplay between perception, action, and cognition, and to consider how theoretical models of the relevant processes might prove valuable for addressing applied questions about surgical performance and training.

The Phillips & Silverstein model of NMDA-mediated coordination deficits provides a useful heuristic for the study of schizophrenic cognition. However, the model does not specifically account for the development of schizophrenia-spectrum disorders. The P&S model is compared to Meehl's seminal model of schizotaxia, schizotypy, and schizophrenia, as well as the model of schizophrenic cognitive dysfunction posited by McCarley and colleagues.

Phillips & Silverstein (P&S, 2003) propose that NMDA-receptor dysfunction may be the fundamental neurobiological mechanism underlying and associating impaired holistic perception and cognitive coordination with schizophrenic psychopathology. We discuss how the P&S hypothesis shares different aspects of the weak central coherence account of autism from both theoretical and experimental perspectives. Specifically, we believe that neither those persons with autism nor those with schizophrenia integrate visuo-perceptual information efficiently, resulting in incongruous internal representations of their external world. However, although NMDA-hypofunction may be responsible for perceptual impairments in schizophrenia and possibly autism, we suggest that it is highly unlikely that NMDA-hypofunction is specifically responsible for the autistic behavioral symptomology, as described by P&S in their target article.

N-methyl-d-aspartate receptor (NMDAR) dysfunction plays a crucial role in schizophrenia, leading to impairments in cognitive coordination. NMDAR agonists (e.g., glycine) ameliorate negative and cognitive symptoms, consistent with NMDAR models. However, not all types of cognitive coordination use NMDAR. Further, not all aspects of cognitive coordination are impaired in schizophrenia, suggesting the need for specificity in applying the cognitive coordination construct.

Phillips & Silverstein offer an exciting synthesis of ongoing efforts to link the clinical and cognitive manifestations of schizophrenia with cellular accounts of its pathophysiology. We applaud their efforts but wonder whether the highly inclusive notion of “context” adequately captures some important details regarding schizophrenia and NMDA/glutamate function that are suggested by work on language processing and cognitive electrophysiology.

Empirical approaches on topics such as consciousness, self-awareness, or introspective perspective, need a conceptual framework so that the emerging, still unconnected findings can be integrated and put into perspective. We introduce a model of self-consciousness derived from phenomenology, philosophy, the cognitive, and neurosciences. We will then give an overview of research data on one particular aspect of our model, self-agency, trying to link findings from cognitive psychology and neuroscience. Finally, we will expand on pathological aspects of self-agency, and in particular on psychosis in schizophrenia. We show, that a deficient self-monitoring system underlies, in part, hallucinations and formal thought (language) disorder in schizophrenia. We argue, that self-consciousness is a valid construct and can be studied with the instruments of cognitive and neuroscience.

The human self model comprises essential features such as the experiences of ownership, of body-centered spatial perspectivity, and of a long-term unity of beliefs and attitudes. In the pathophysiology of schizophrenia, it is suggested that clinical subsyndromes like cognitive disorganization and derealization syndromes reflect disorders of this self model. These features are neurobiologically instantiated as an episodically active complex neural activation pattern and can be mapped to the brain, given adequate operationalizations of self model features. In its unique capability of integrating external and internal data, the prefrontal cortex (PFC) appears to be an essential component of the neuronal implementation of the self model. With close connections to other unimodal association cortices and to the limbic system, the PFC provides an internally represented world model and internal milieu data of the organism, both serving world orientation. In the pathophysiology of schizophrenia, it is the dysfunction of the PFC that is suggested to be the neural correlate for the different clinical schizophrenic subsyndromes. The pathophysiological study of psychiatric disorders may contribute to the theoretical debate on the neuronal basis of the self model.