Delusional thinking and cognitive disorder.
ABSTRACT A hypothesis is presented regarding the genesis of paranoid delusion that attempts to take into account certain data. The data of interest are (a) the failure to find evidence of cognitive impairment in diagnosed paranoid patients, (b) the evidence of perceptual disorder as a primary and prior condition in the natural history of the clinical development of delusions and the empirical relationship of the perceptual disorder to presence of "thought disorder," (c) the failure to find evidence supporting universal psychodynamic patterns of etiology, (d) appearance of "delusional" phenomena in normal subjects in situations of deviant sensory experience, and (e) the reports of articulate patients writing of their experiences. This hypothesis suggests that there exists a group of patients who suffer from primary perceptual anomalies, fundamentally biological in nature although probably fluctuating with current stresses, and that these anomalies involve vivid and intense sensory input. These experiences demand explanation which the patient develops through the same cognitive mechanisms that are found in normal and scientific theory-building. As the data that are available to the patient are crucially different from those available to an observer, the latter judges the explanation to be bizarre and pathological. Being unable to check the validity of the patient's descriptions of his sensory experience the assumption is made that the patient is having the same experience as the observer but is defective in reality-testing and/or inferential thinking. As the evidence for the presence of perceptual disorder is stronger than the direct evidence for cognitive impairment, the hypothesis outlined here places central importance on the former. In brief, it is suggested that for many paranoid patients the delusion should be seen as the reaction of a normal, "sane" individual to abnormal but genuine perceptual experiences.
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ABSTRACT: Psychosis is one of the most common conditions in later life with a lifetime risk of 23 %. Despite its high prevalence, late-onset psychosis remains a diagnostic and treatment dilemma. There are no reliable pathognomonic signs to distinguish primary or secondary psychosis. Primary psychosis is a diagnosis of exclusion and the clinician must rule out secondary causes. Approximately 60 % of older patients with newly incident psychosis have a secondary psychosis. In this article, we review current, evidence-based diagnostic and treatment approaches for this heterogeneous condition, emphasizing a thorough evaluation for the "six d's" of late-life psychosis (delirium, disease, drugs dementia, depression, delusions). Treatment is geared towards the specific cause of psychosis and tailored based on comorbid conditions. Frequently, environmental and psychosocial interventions are first-line treatments with the judicious use of pharmacotherapy as needed. There is an enormous gap between the prevalence of psychotic disorders in older adults and the availability of evidence-based treatment. The dramatic growth in the elderly population over the first half of this century creates a compelling need to address this gap.Current Psychiatry Reports 02/2015; 17(2):542. DOI:10.1007/s11920-014-0542-0 · 3.05 Impact Factor
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ABSTRACT: We review the hypothesis that the brain uses a generative model to explain the causes of sensory inputs, using prediction schemes that operate based upon assimilation of time-series sensory data. We put this hypothesis in the context of psychopathology, in particular, schizophrenia's positive symptoms. Building upon work of Helmholtz and upon theories in computational cognitive processing, we hypothesize that delusions in schizophrenia can be explained in terms of false inference. An impairment in inferring appropriate information from the sensory input reflects upon the ability to assess the environment and predict outcomes. Although the inference mechanism likely involves both conscious and unconscious processes, we hypothesize that the trigger of delusions may lie within the unconscious neural pathways. A collection of computational predictive codes have been proposed for modeling perception. We discuss two examples, which may be eligible as substrates for intuitive coding. We argue that failure of the psychotic patient to choose the correct computational scheme, or the optimal range of parameters, may readily lead to an altered reconstruction of the object and false inference, feeding into the delusion mechanism. We finally propose using these models in conjunction with cognitive and imaging data, in order to obtain more testable predictions.Philosophical Psychology 04/2011; 24(2-2):145-157. DOI:10.1080/09515089.2010.533264 · 0.59 Impact Factor
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ABSTRACT: Previous research has suggested that there are multiple psychological processes underlying delusional thought. While it appears that cognitive biases in certain reasoning and attention processes are related to delusion-proneness, the influence of emotion on these processes is not well understood. The overall objective of this study was to investigate the effect of emotional content on performance on tasks thought to measure attentional bias, preferential recall, and probabilistic reasoning in individuals with schizophrenia and demographically matched controls. In order to account for level of delusion-proneness, participants also completed a multidimensional measure of delusional thought. It was hypothesized that individuals with schizophrenia would perform more poorly on both the emotional and neutral versions of these tasks compared to controls. It was also hypothesized that within each group, there would be a statistically significant emotion effect, indicated by a difference in performance on the emotional (compared to neutral) condition of each task. This emotion effect was expected to be larger in the schizophrenia group. Finally, it was hypothesized that the emotion effect would increase as the severity of delusional proneness increased for all participants, regardless of group. As hypothesized, the schizophrenia group performed more poorly on the tasks overall, though expected emotion effects were generally absent. There were no differences in the size of emotion effects between the groups on any of the cognitive tasks administered, and the emotion effect did not appear to increase as severity of delusion-proneness increased. Factors that may have contributed to this pattern of results are discussed. Implications of these findings on theoretical models of delusions and future directions for research in this area are also discussed.