Abstract
Schizophrenia is a disorder with a large number of clinical, neurobiological, and cognitive manifestations, none of which is invariably present. However it appears to be a single nosological entity. This article considers the likely characteristics of a pathology capable of such diverse consequences. It is argued that both deficit and psychotic symptoms can be manifestations of a single pathology. A general model of psychosis is proposed in which the informational sensitivity or responsivity of a network (“hodological resonance”) becomes so high that it activates spontaneously, to produce a hallucination, if it is in sensory cortex, or another psychotic symptom if it is elsewhere. It is argued that this can come about because of high levels of modulation such as those assumed present in affective psychosis, or because of high levels of baseline resonance, such as those expected in deafferentation syndromes associated with hallucinations, for example, Charles Bonnet. It is further proposed that schizophrenia results from a process (probably neurodevelopmental) causing widespread increases of variance in baseline resonance; consequently some networks possess high baseline resonance and become susceptible to spontaneous activation. Deficit symptoms might result from the presence of networks with increased activation thresholds. This hodological variance model is explored in terms of schizo-affective disorder, transient psychotic symptoms, diathesis-stress models, mechanisms of antipsychotic pharmacotherapy and persistence of genes predisposing to schizophrenia. Predictions and implications of the model are discussed. In particular it suggests a need for more research into psychotic states and for more single case-based studies in schizophrenia.
Highlights
Despite the effort that has gone into the study of schizophrenia over the last century or so, and the discovery of a large number of abnormalities, progress in understanding the nature of this disease has been limited
A particular objective was to address some of the apparent paradoxes of schizophrenia: to present a single class of pathology which is compatible with considerable heterogeneity including asymptomatic and alternative phenotypes; to explain how this could give rise to negative and positive symptoms as different dimensions, how some individuals with schizophrenia can appear cognitively within normal limits (Chan et al, 2006), how patterns of onset and treatment effects could be explained, how the genes could persist by conferring a balancing selection advantage, and how the pathology could fit within a spectrum of psychosis alongside schizo-affective and affective psychosis, and within a continuum of psychosis shading into the psychotic-like experiences of otherwise apparently healthy individuals
An accurate model of schizophrenia faces a number of challenges
Summary
Despite the effort that has gone into the study of schizophrenia over the last century or so, and the discovery of a large number of abnormalities, progress in understanding the nature of this disease has been limited. Typically associated with upregulation (Zis and Fibiger, 1975; Burke, 2002), is known to be associated with tactile (Kooijman et al, 2000), auditory (Griffiths, 2000), and visual (Ffytche, 2005) hallucinations These examples illustrate that this hypothetical hodological hyper-resonance mechanism is consistent with psychotic symptoms caused by a variety of disorders. The unevenness (or its effect) is exacerbated following maturational synaptic elimination, perhaps because pruning produces networks with fewer connections, which have a larger variance in connectivity/resonance; and results in some networks with low activation thresholds, which can become hyper-resonant under certain conditions of neuroplasticity and neuromodulation This model (subsequently referred to as the hodological variance model) can provide some explanation for bizarre and complex phenomena such as auditory hallucinations consisting of a commentary on a patient’s actions.
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