Online research in philosophy

Evolutionary psychiatrists invariably consider schizophrenia to be a paradox: how come natural selection has not yet eliminated the infamous ‘genes for schizophrenia’ if the disorder simply crushes the reproductive success of its carriers, if it has been around for thousands of years already, and if it has a uniform prevalence throughout the world? Usually, the answer is that the schizophrenic genotype is subject to some kind of balancing selection: the benefits it confers would then outbalance the obvious damage it does. In this paper, however, I will show that the assumptions underlying such evolutionary accounts of schizophrenia are at least implausible, and sometimes even erroneous. First of all, I will examine some factual assumptions, in particular about schizophrenia’s impact on reproductive success, its genetics, its history, and its epidemiology. Secondly, I will take a critical look at a major philosophical assumption in evolutionary psychiatric explanations of schizophrenia. Indeed, evolutionary psychiatrists take it for granted that schizophrenia is a natural kind, i.e. a bounded and objectively real entity with discrete biological causes. My refutation of this natural kind view suggests that schizophrenia is in fact a reified umbrella concept, covering a heterogeneous group of disorders. Therefore, schizophrenia, as we now know it, simply doesn’t have an evolutionary history.

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.

Machine generated contents note: -- Clinical Theory -- 1. Psychiatry on schizophrenia: clinical pictures of a sublime object -- 2. Schizophrenia: the sublime text of psychoanalysis -- Cultural Theory -- 3. Antipsychiatry: schizophrenic experience and the sublime -- 4. Anti-Oedipus and the politics of the schizophrenic sublime -- 5. Schizophrenia, modernity, postmodernity -- 6. Postmodern schizophrenia -- 7. Glamorama, postmodernity and the schizophrenic sublime -- Conclusion.

The claim that the disorganized subtype of schizophrenia results from glutamate hypofunction is enhanced by consideration of current subtypology of schizophrenia, symptom definition, interdependence of neurotransmitters, and the nature of the data needed to support the hypothesis. Careful specification clarifies the clinical reality of disorganization as a feature of schizophrenia and increases the utility of the subtype.

Many with schizophrenia find social interactions a profound and terrifying threat to their sense of self. To better understand this we draw upon dialogical models of the self that suggest that those with schizophrenia have difficulty sustaining dialogues among diverse aspects of self. Because interpersonal exchanges solicit and evoke movement among diverse aspects of self, many with schizophrenia may consequently find those exchanges overwhelming, resulting in despair, the sensation of fusion with another, and/or self-dissolution. In short, compromised dialogical capacities may be a contributing factor to social dysfunction in schizophrenia.

This commentary compares clinical aspects of ketamine with the amphetamine model of schizophrenia. Hallucinations and loss of insight, associated with amphetamine, seem more schizophrenia-like. Flat affect encountered with ketamine is closer to the clinical presentation in schizophrenia. We argue that flat affect is not a sign of schizophrenia, but rather, a risk factor for chronic schizophrenia.

Impairments in cognitive coordination in schizophrenia are supported by phenomenological data that suggest deficits in the processing of visual context. Although the target article is sympathetic to such a phenomenological perspective, we argue that the relevance of phenomenological data for a wider understanding of consciousness in schizophrenia is not sufficiently addressed by the authors.