Online research in philosophy

Schizophrenia patients exhibit impairments across multiple clinical, cognitive, and functional domains. A fundamental abnormality of the timing and/or efficiency of neural processes across disparate brain regions (i.e., cortico-cortical communications) may underlie many of the deficits in schizophrenia. Because gamma synchrony is temporally correlated with many cognitive processes, probing patterns of gamma activation may shed light on the functional integrity of neural circuits in schizophrenia and related disorders.

To understand schizophrenia, a linking hypothesis is needed that shows how brain mechanisms lead to behavioral functions in normals, and also how breakdowns in these mechanisms lead to behavioral symptoms of schizophrenia. Such a linking hypothesis is now available that complements the discussion offered by Phillips & Silverstein (P&S).

The target article presents a model for schizophrenia extending four levels of abstraction: molecules, cells, cognition, and syndrome. An important notion in the model is that of coordination, applicable to both the level of cells and of cognition. The molecular level provides an “implementation” of the coordination at the cellular level, which in turn underlies the coordination at the cognitive level, giving rise to the clinical symptoms.

What we call today negative symptoms are thought to descend from the very deficits that the earliest scholars of schizophrenia (such as Kraepelin and Bleuler) considered to be the key, fundamental symptoms of the disorder. In the latter half of the 20th century, delusions and hallucinations received greater prominence, which eventually changed both the concept of schizophrenia and its diagnostic criteria by placing positive symptoms at the forefront. The first decade of the 21st century witnessed a resurgence of interest in negative symptoms of schizophrenia. Persistent and clinically significant negative symptoms were declared an unmet therapeutic need in a large proportion of cases by several schizophrenia experts, who, with the support of the NIMH, held a consensus development conference in 2005 to discuss negative symptoms and how to proceed in this area. The Consensus Statement read that improved recognition and awareness of negative symptoms are the fi rst step to improving function in patients with negative symptoms of schizophrenia. According to the principles of Values-Based Practice that also means improving recognition and awareness of the diverse values involved in the conceptualization and practical assessment of negative symptoms. By analyzing selected conceptual papers on negative symptoms, instruments developed for the assessment of this area of psychopathology, and clinical vignettes, we intend to point out some values-related issues in the diagnosis of negative symptoms as well as to make the case that these symptoms may be a particularly complex aspect of schizophrenia, vis-à- vis understanding the role played by values.

The advent of functional brain imaging has revolutionized the ability to understand the biological mechanisms underlying decision-making. Although it has been amply demonstrated that assumptions of rationality often break down in experimental games, there has not been an overarching theory of why this happens. I describe recent advances in functional brain imaging and suggest a framework for considering the function of the human reward system as a discrete agent.

Schizophrenia may not have reduced reproductive success in ancestral times as much as it does today, so explaining how genes for it evolved is more understandable given this prehistoric perspective. Ethological analysis of schizophrenia – understanding how basic emotional behaviors, such as dominance striving, are affected by the condition – might prove useful for comprehending and treating its social emotional symptoms.

This commentary addresses: (a) the problems of definition which have been prominent in the use of the term context in schizophrenia research; (b) potentially useful distinctions and links with other theories of schizophrenic cognition; and (c) possible pathways to schizophrenic symptoms. It is suggested that at least two major aspects of the operation of context may be distinguished and that both may be impaired in schizophrenia.

An evolutionary theory of schizophrenia needs to address all symptoms associated with the condition. Burns' framework could be extended in a way embracing behavioural signs such as catatonia. Burns' theory is, however, not specific to schizophrenia. Since no one single symptom exists that is pathognomonic for “schizophrenia,” an evolutionary proposal of psychiatric disorders raises the question whether our anachronistic psychiatric nosology warrants revision.

Cognitive impairment in schizophrenia is a core feature of the illness (i.e., not a result of clinical symptoms or drug treatments) that is related to the daily functioning of patients. Because schizophrenia is associated with poor community functioning, there is considerable interest in finding treatments to improve cognition in schizophrenia in the hopes that such improvement will yield functional benefits. Before the U.S. Food and Drug Administration could consider granting approval to any new drug for improving cognition in schizophrenia, it was first necessary to achieve consensus on the measurements and methods that would be used in clinical trials, as well as neuropharmacological targets. The U.S. National Institute of Mental Health launched an initiative to help address these obstacles to drug approval (MATRICS). This initiative has generated several additional follow-up initiatives including a clinical trial network and consensus projects for other clinical targets, such as negative symptoms. This review describes how an area that was primarily of academic interest (cognition in schizophrenia) became a focus of public health concerns and drug-development policy.