Delusion Formation Research Articles

Reduced parahippocampal volume and psychosis symptoms in Alzheimer's disease.

Establishing structural imaging correlates of psychosis symptoms in Alzheimer's disease (AD) could localise pathology and target symptomatic treatment. This study investigated whether psychosis symptoms are associated with visuoperceptual or frontal networks, and whether regional brain volume differences could be linked with the paranoid (persecutory delusions) or misidentification (misidentification phenomena and/or hallucinations) subtypes. A total of 104 patients with probable AD (AddNeuroMed; 47 psychotic, 57 non-psychotic), followed up for at least one year with structural MRI at baseline. Presence and subtype of psychosis symptoms were established using the Neuropsychiatric Inventory. Volume and cortical thickness measures in visuoperceptual and frontal networks were explored using multivariate analyses to compare with both a global (psychotic versus not) and subtype-specific approach, adjusting for potential confounding factors. There was a significant main effect of psychosis subtypes on the ventral visual stream region of interest (F30,264 =1.65, p=0.021, np2 =0.16). This was explained by reduced left parahippocampal gyrus volume (F1,97 =11.1, p=0.001, np2 =0.10). When comparisons were made across psychosis subtypes, left parahippocampal volume reduction remained significant (F7,95 =3.94, p=0.011, np2 =0.11) and was greatest for the misidentification and mixed subtypes compared to paranoid and non-psychotic groups. These findings implicate the ventral visual stream in psychosis in AD, consistent with integrative theories regarding origins of psychosis, and provide further evidence for a role in the misidentification subtype. Specifically, reduced volume in the parahippocampal gyrus is implicated in misidentification delusion formation, which we hypothesise is due to its role in context attribution. Copyright © 2017 John Wiley & Sons, Ltd.

Moment-to-moment associations between emotional disturbances, aberrant salience and persecutory delusions

IntroductionExperiences of depression and anxiety are common among patients with persecutory delusions. It has been theorized that emotional disturbances affect the formation and appraisal of persecutory delusions directly and possibly via increasing the sense of aberrant salience.ObjectivesUsing a time-lagged analysis of experience sampling data, this study modelled the role of momentary levels of negative emotions and aberrant salience in maintaining persecutory delusions in patients with active delusions.MethodsClinically acute participants with at least a mild level of persecutory delusions were assessed using experience sampling method (ESM; 7 entries per day for 14 days) and clinical rating scales. ESM data of participants who completed at least 30 ESM entries were analysed by using multilevel regression modelling.ResultsThe final sample consisted of 14 participants, with a total of 1161 momentary observations. Time-lagged analysis revealed that both negative emotions (B = 0.125, P = .009) and aberrant salience (B = 0.267, P< .001) predicted an increase in persecutory delusions in the next moment. Conversely, persecutory delusions did not predict change in negative emotions or change in aberrant salience in the next moment (ps> .05). Negative emotions also predicted an increase in aberrant salience in the next moment (B = 0.087, P = .009).ConclusionsOur results supported the hypothesis that both negative emotions and aberrant salience exacerbate persecutory delusions, rather than being merely the sequelae of the symptoms. Our results suggested both direct and indirect (via aberrant salience) pathways from negative emotions to persecutory delusions.Disclosure of interestThe authors have not supplied their declaration of competing interest.

The Psychopathology of Delusion of Control According to Subjective Experience

BackgroundDelusion of control, including thought insertion, occurs in 20% of patients with schizophrenia. However little is known of its psychopathology, and studies involving patients are scarce. AimsTo explore the subjective experience of patients with delusion of control and to propose a psychopathological explanation based on empirical evidence. MethodsQualitative exploratory study of 7 patients (6 with schizophrenia and 1 with schizophreniform disorder). A phenomenologically-oriented semi-structured interview was used. ResultsDelusion of control is not an isolated and pure symptom; it is always immersed in the context of a persecutory delusion and other psychiatric symptoms. The patient experiences partial control, i.e. the control is never complete. In all cases, it is possible to trace the history of the narrative formation of delusion of control from its origins in persecutory delusions and other concomitant symptoms. ConclusionsThe delusion of control is a narrative resulting from the joint presence of a persecutory delusion and other psychiatric symptoms. For the patient, the delusion of control is the narrative of the elaborate expression of the meaning of the anomalous experience. Delusion of control is a narrative variety of persecutory delusion.

SU32. Impact of Catechol-O-Methyl Transferase Polymorrphism on Cognition and Information Processing in Schizophrenia Using Novel MBIAL Computerized Battery—A Case-Control Study

Abstract Background: Frontal executive dysfunction have been robustly demonstrated in schizophrenia. Several fundamental information processing deficits were reported in schizophrenia underlying the various symptom dimensions. Results of previous studies of neuropsychological functioning in schizophrenia were inconsistent. Association between COMT allele type and cognition was not confirmed in all studies. This study attempted to assess the neuropsychological performance on a hypothesis-driven MBIAL-computerized neuropsychological battery in a sample of schizophrenia subjects and matched healthy comparison subjects and its relationship with the gene polymorphism. Methods: Total 34 patients and 30 matched healthy controls were recruited after obtaining informed consent. An HMSE was applied to exclude those with scores <23. The matrix reasoning module of WAIS-III was applied to obtain an estimate of their perceptual organization index as a reflection of their intellectual abilities, independent of verbal abilities. A novel MBIAL Computerized neuropsychological battery consisting of 6 tests was applied on all the subjects. Later, both the groups were assessed for symptom severity using PANSS. All Neuropsychological tests and PANSS Interviews using SCI-PANSS were Video and Audio recorded. Genotyping for COMTval158met polymorphism was accomplished by PCR-RFLP method. Genotype frequencies across groups were noted using chi-square test and later were compared using ANCOVA as we had WAIS III and HMSE as covariates. Results: Schizophrenia patients performed significantly poorly on most of the neuropsychological tests as compared with healthy matched controls. Negative symptom severity was associated with significant impairment in neuropsychological deficits as compared to positive symptoms. Separate analysis of association of gene polymorphism on these cognitive tests done on patients and controls did not reveal much results. But on pooled data, we found Val-Carriers performed poorly on most of the Neuropsychological and Information processing tasks and have high threat perception compared to Non-Val Carriers. Conclusion: Hypothesis-driven neuropsychological battery was used in schizophrenia that incorporated tests for frontal executive functioning; rostral prefrontal functioning; threat perception (aberration of which is postulated to underlie delusion formation); and cross-modal sensory integration (aberration of which is postulated to underlie development of hallucinations). The MBIAL battery is sensitive in detecting differences between patients and controls in the adult population. We suggest here that Val158Met polymorphism rather exerts a modifying influence on brain activation in general than impacts directly on performance of the particular neuropsychological task.

Rethinking Social Cognition in Light of Psychosis: Reciprocal Implications for Cognition and Psychopathology.

The positive symptoms of psychosis largely involve the experience of illusory social actors, and yet our current measures of social cognition, at best, only weakly predict their presence. We review evidence to suggest that the range of current approaches in social cognition is not sufficient to explain the fundamentally social nature of these experiences. We argue that social agent representation is an important organizing principle for understanding social cognition and that alterations in social agent representation may be a factor in the formation of delusions and hallucination in psychosis. We evaluate the feasibility of this approach in light of clinical and nonclinical studies, developmental research, cognitive anthropology, and comparative psychology. We conclude with recommendations for empirical testing of specific hypotheses and how studies of social cognition could more fully capture the extent of social reasoning and experience in both psychosis and more prosaic mental states.

Transdiagnostic Extension of Delusions: Schizophrenia and Beyond.

Delusion is central to the conceptualization, definition, and identification of schizophrenia. However, in current classifications, the presence of delusions is neither necessary nor sufficient for the diagnosis of schizophrenia, nor is it sufficient to exclude the diagnosis of some other psychiatric conditions. Partly as a consequence of these classification rules, it is possible for delusions to exist transdiagnostically. In this article, we evaluate the extent to which this happens, and in what ways the characteristics of delusions vary according to diagnostic context. We were able to examine their presence and form in delusional disorder, affective disorder, obsessive-compulsive disorder, borderline personality disorder, and dementia, in all of which they have an appreciable presence. There is some evidence that the mechanisms of delusion formation are, at least to an extent, shared across these disorders. This transdiagnostic extension of delusions is an argument for targeting them therapeutically in their own right. However there is a dearth of research to enable the rational transdiagnostic deployment of either pharmacological or psychological treatments.

Endogenous episodes of juvenile psychosis with religious delusions

To identify clinical and psychopathological features, conditions of formation and prognostic significance of delusions with religious content in endogenous psychotic states in adolescence. Fifty-three male patients, aged from 16 to 25 years, with juvenile endogenous psychosis, with a psychotic episode with religious content of delusion were examined. Clinical, psychopathological, psychometrical (The Dawkins scale) and statistical methods were used. General psychopathological features of psychotic states with religious delusions, according to the specificity of adolescent age, were identified. Common types of religious delusional episodes, forming by primal interpretive (delusion of sin, delusion of demonic possession) and sensual (messianic and antagonistic delusion, religious oneiroid) mechanisms were distinguished. A role of the previous religiosity, including overvalued religious ideas, was clarified. It was found out that the duration of the pre-manifest stage, hospitalization and the period of 'untreated psychosis', was longer in patients with religious delusions compared to patients with other types of delusions. Patients with interpretive mechanism of delusion formation demonstrated the subsequent intensification of religiosity that was not common for psychotic episodes with the sensual mechanism of delusion formation.

The Role of Emotions in Delusion Formation

Abstract The text concerns the role of emotions in delusion formation. Provided are definitions from DSM-V and DSM-IV-R and the problems found in those definitions. One of them, the problem of delusion formation, is described when providing cognitive theories of delusions. The core of the paper is a presentation of the emotional and affective disorders in delusions, especially Capgras delusion and Cotard delusion. The author provides a comparison of the kinds of delusions and the conclusions taken from neuroimaging studies. As a result of the fact that an explanation of delusion formation focusing on emotional problems turns out to be insufficient, the author provides examples of the reasoning impairments which coexist with them. At the end of the article, some hypotheses are proposed concerning the role of emotions and reasoning in delusion formation and the relation between belief disorders and emotional disorders.

Delusional Beliefs, Two-Factor Theories, and Bizarreness

In order to explain delusional beliefs, one must first consider what factors should be included in a theory of delusion. Unlike a one-factor theory, a two-factor theory of delusion argues that not only anomalous experience (the first factor) but also an impairment of the belief-evaluation system (the second factor) is required. Recently, two-factor theorists have adopted various Bayesian approaches in order to give a more accurate description of delusion formation. By reviewing the progression from a one-factor theory to a two-factor theory, I argue that in light of the second factor’s requirements, different proposed impairments can be unified within a consistent belief-evaluation system. Under this interpretation of the second factor, I further argue that the role of a mechanism responsible for detecting bizarreness is wrongly neglected. I conclude that the second factor is a compound system which consists of differing functional parts, one of which functions to detect bizarreness in different stages of delusion; moreover, I hold that the impairment can be one or several of these functional parts.

Prediction error, ketamine and psychosis: An updated model.

In 2007, we proposed an explanation of delusion formation as aberrant prediction error-driven associative learning. Further, we argued that the NMDA receptor antagonist ketamine provided a good model for this process. Subsequently, we validated the model in patients with psychosis, relating aberrant prediction error signals to delusion severity. During the ensuing period, we have developed these ideas, drawing on the simple principle that brains build a model of the world and refine it by minimising prediction errors, as well as using it to guide perceptual inferences. While previously we focused on the prediction error signal per se, an updated view takes into account its precision, as well as the precision of prior expectations. With this expanded perspective, we see several possible routes to psychotic symptoms – which may explain the heterogeneity of psychotic illness, as well as the fact that other drugs, with different pharmacological actions, can produce psychotomimetic effects. In this article, we review the basic principles of this model and highlight specific ways in which prediction errors can be perturbed, in particular considering the reliability and uncertainty of predictions. The expanded model explains hallucinations as perturbations of the uncertainty mediated balance between expectation and prediction error. Here, expectations dominate and create perceptions by suppressing or ignoring actual inputs. Negative symptoms may arise due to poor reliability of predictions in service of action. By mapping from biology to belief and perception, the account proffers new explanations of psychosis. However, challenges remain. We attempt to address some of these concerns and suggest future directions, incorporating other symptoms into the model, building towards better understanding of psychosis.

The impact of loneliness on paranoia: An experimental approach

Background and objectivesLoneliness is a common problem in patients with schizophrenia, and may be particularly linked with persecutory ideation. Nevertheless, its role as a potential risk factor in the formation and maintenance of persecutory delusions is largely unexplored. MethodsLoneliness was experimentally manipulated using a false-feedback paradigm in a non-clinical sample (n = 60). Change in state paranoia was compared between the induction of increased loneliness, the induction of reduced loneliness and a control condition. Distinct associations between pre-post scores of loneliness and state paranoia were examined at three (medium/high/low) levels of proneness to psychosis across the experimental conditions. ResultsReduction of loneliness was associated with a significant reduction of present paranoid beliefs, while induction of loneliness lead to more pronounced paranoia on trend significance level. Moreover, proneness to psychosis significantly moderated the impact of loneliness on paranoia. Persons with a pronounced level of proneness to psychosis showed a stronger reduction of paranoid beliefs as a consequence of a decrease in loneliness, than less prone individuals. LimitationsA limitation is the small size of our sample, which may have limited the power to detect significant within-group changes in state paranoia in the high-loneliness condition and changes in loneliness in the low-loneliness condition. ConclusionsThe findings support the feasibility of the experimental design to manipulate loneliness and suggest that loneliness could be a cause of paranoia. However, the findings need to be confirmed in high risk samples to draw conclusions about the role of loneliness in the genesis of clinically relevant levels of paranoia and derive implications for cognitive behaviour therapy.

Searching for meaning in meaningless gestures, pathologic activity in amygdala, hippocampus and temporal pole during planning of gestures in schizophrenia

IntroductionSchizophrenia is characterized by poor social interaction contributing to poor functional outcome. Particularly nonverbal communication is disturbed. Neural correlates of impaired gesturing are currently unclear. We thus tested functional correlates of gesturing in schizophrenia patients and healthy controls.MethodsWe tested 22 patients and 25 controls with an event-related fMRI (instructed delay) paradigm to dissociate brain activation during planning and execution of meaningful (e.g. use scissors) and meaningless novel gestures. Preprocessing included realignment, coregistration, normalization and spatial smoothing. We used a two stage mixed effects model for statistical analysis. Conditions were contrasted against a linguistic control within and between groups. We correlated psychopathological characteristics with beta estimates of brain areas with between group effects.ResultsDuring planning and execution of both gesture subtypes both groups activated brain areas of the ventral and dorsal stream. However patients’ activity was less prominent and more left lateralized. During planning patients showed additional activity in bilateral temporal poles, amygdala and hippocampus associated with the level of delusions. Furthermore patients had increased dorsomedial prefrontal cortex and precuneus activity when planning meaningless gestures.ConclusionDuring the planning of meaningless gestures we detected aberrant activation of limbic structures in patients typically implicated in delusion formation, which also correlated with current severity of delusions. Moreover, planning of meaningless gestures relied on areas relevant for strategic control and attention. These results argue for a pathologic search for meaning in neutral gestures and increased control effort during planning of meaningless gestures in schizophrenia.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Life hassles and delusional ideation: Scoping the potential role of cognitive and affective mediators

An intertemporal association between major psychological stress and subsequent delusion formation has been established by others. The current study explores (1) whether the stress from life hassles predicts delusional ideation and (2) if so, do self-criticism, self-reassurance, and positive and negative affectivity (PA and NA, respectively) mediate this link. This paper thus aimed to scope-out viable psychological processes involved in the formation of stress-induced delusions. A cross-sectional survey using a non-clinical community sample. Responses (N=251) to an online community survey were tested via a nonparametric bootstrap sampling approach to examine the effects of multiple mediators. Self-criticism and NA appear to mediate a connection found between life hassles and delusions. A second mediation analysis found that life hassles positively predicts NA directly and indirectly (via self-criticism). NA in turn predicted delusional tendencies. Life events had direct statistical effects on delusions in all models. Neither PA nor self-reassurance mediated the stress-delusion link. Self-criticism and NA seem to be viable mediators worth contemplating when elaborating upon the connection between life hassles and delusions. Compared to self-criticism, NA appears to be the intervening variable most proximal to delusions and explains more variance. Even if these cross-sectional results were interpreted as causative, life hassles and delusions remained directly interconnected in all mediation models (suggesting much of the association remains unexplained). Although the results are theory-consistent, investigations using longitudinal, known-group, and experimental methods are now warranted to establish causation and possible feedback loops - especially from delusion to life hassles. Self-criticism and negative affectivity (NA) mediate the link between stressful life events and delusions suggesting they might actively elicit delusional ideation, whereas self-reassurance and PA (although negatively associated with life hassles) have no unique predictive link to delusions. This study offers initial evidence that NA and self-criticism may be viable clinical intervention targets for early psychosis-sufferers under stress - especially for medically non-compliant and marginal (where drug treatment is not clinically indicated) cases. The clinical efficacy of alleviating self-criticism and/or negative emotional processes in those displaying early psychosis or at high risk appear worthy of exploration using both practice-based case studies and formal experimental research methods.

Neurocognitive Model of Delusion: Two-Factor Theory

The underlying nature of delusions remains unclear despite their importance in psychopathology. Here we present a review of the neurocognitive model of delusions from a cognitive neuroscience viewpoint. There have been numerous reports on cognitive impairments in delusional patients, such as in their reasoning, attention, metacognition, and attribution biases. These findings have been incorporated into several cognitive models that aim to explain the formation, maintenance, and content of delusion. Although delusions are commonly conceptualized as beliefs, not all models make reference to models of normal belief formation. This review focused on two-factor theory models that make a distinction between factors that explain the content of delusions and those that explain their presence. This cognitive theory that includes the ‘pragmatic pathology’ of delusions can address both the phenomenology and treatment of delusion-related distress. Key Words: Delusions, Neurocognitive, Belief, Two-Factor Theory

Coexistence of Reverse Capgras Syndrome, Subjective Double and Cotard Syndrome

: Misidentification syndrome is a condition in which the person thinks that familiar persons have been replaced with other one. Coexistence of some types of this syndrome has been reported with other psychiatric syndromes. In this report, we present a 47-year-old married man with coexistence of reverse Capgras and subjective double syndromes with Cotard syndrome. There is no previous report of coexistence of these three forms of delusions in a single case.

The doxastic shear pin: delusions as errors of learning and memory

ABSTRACTWe reconsider delusions in terms of a “doxastic shear pin”, a mechanism that errs so as to prevent the destruction of the machine (brain) and permit continued function (in an attenuated capacity). Delusions may disable flexible (but energetically expensive) inference. With each recall, delusions may be reinforced further and rendered resistant to contradiction. We aim to respond to deficit accounts of delusions – that delusions are only a problem without any benefit – by considering delusion formation and maintenance in terms of predictive coding. We posit that brains conform to a simple computational principle: to minimize prediction error (the mismatch between prior top-down expectation and current bottom-up input) across hierarchies of brain regions and psychological representation. Recent data suggest that delusions may form in the absence of constraining top-down expectations. Then, once formed, they become new priors that motivate other beliefs, perceptions, and actions by providing strong (sometimes overriding) top-down expectation. We argue that delusions form when the shear-pin breaks, permitting continued engagement with an overwhelming world, and ongoing function in the face of paralyzing difficulty. This crucial role should not be ignored when we treat delusions: we need to consider how a person will function in the world without them..

Anti-NMDA-receptor encephalitis

BACKGROUND In 2007 a clinical disease caused by autoantibodies directed against the N-methyl-D-aspartate (NMDA) receptor was described for the first time. Anti-NMDA-receptor encephalitis is a subacute, autoimmune neurological disorder with psychiatric manifestations. The disease is a form of limbic encephalitis and is often paraneoplastic. The condition is also treatable. In this review article we examine the development of the disease, clinical practice, diagnostics and treatment.MATERIAL AND METHOD The article is based on references retrieved from searches in PubMed, and a discretionary selection of articles from the authors' own literature archive.RESULTS The disease most frequently affects young women. It may initially be perceived as a psychiatric condition, as it usually presents in the form of delusions, hallucinations or mania. The diagnosis should be suspected in patients who later develop neurological symptoms such as various movement disorders, epileptic seizures and autonomic instability. Examination of serum or cerebrospinal fluid for NMDA receptor antibodies should be included in the assessment of patients with suspected encephalitis. MRI, EEG and assessment for tumours are important tools in diagnosing the condition and any underlying malignancy.INTERPRETATION If treatment is initiated early, the prognosis is good. Altogether 75% of patients will fully recover or experience significant improvement. Apart from surgical resection of a possible tumour, the treatment consists of immunotherapy. Because of good possibilities for treatment, it is important that clinicians, particularly those in acute psychiatry, are aware of and alert to this condition.

Perception, cognition, and delusion.

Firestone & Scholl's (F&S) critique of putative empirical evidence for the cognitive penetrability of perception focuses on studies of neurologically normal populations. We suggest that a comprehensive exploration of the cognition-perception relationship also incorporate work on abnormal perception and cognition. We highlight the prominence of these issues in contemporary debates about the formation and maintenance of delusions.

How delusion is formed?

Traditionally, delusions have been considered to be the products of misinterpretation and irrationality. However, some theorists have argued that delusions are normal or rational cognitive responses to abnormal experiences. That is, when a recently experienced peculiar event is more plausibly explained by an extraordinary hypothesis, confidence in the veracity of this extraordinary explanation is reinforced. As the number of such experiences, driven by the primary disease process in the perceptual domain, increases, this confidence builds and solidifies, forming a delusion. We tried to understand the formation of delusions using a simulation based on Bayesian inference. We found that (1) even if a delusional explanation is only marginally more plausible than a non-delusional one, the repetition of the same experience results in a firm belief in the delusion. (2) The same process explains the systematization of delusions. (3) If the perceived plausibility of the explanation is not consistent but varies over time, the development of a delusion is delayed.Additionally, this model may explain why delusions are not corrected by persuasion or rational explanation. This Bayesian inference perspective can be considered a way to understand delusions in terms of rational human heuristics. However, such experiences of “rationality” can lead to irrational conclusions, depending on the characteristics of the subject.

The relationship between cognitive insight and quality of life in schizophrenia spectrum disorders: Symptom severity as potential moderator

Cognitive insight is implicated in the formation and maintenance of hallucinations and delusions. However, it is not yet known whether cognitive insight relates to broader outcome measures like quality of life. In the current study, we investigated whether the component elements of cognitive insight—self-certainty and self-reflectiveness—were related to quality of life for 43 outpatients with schizophrenia or schizoaffective disorder. Cognitive insight was assessed using the Beck Cognitive Insight Scale (BCIS) while quality of life was assessed with Quality of Life Scale (QLS). We tested whether this relationship was moderated by clinical insight and symptom severity using the Scale to Assess Unawareness of Mental Disorder (SUMD) and the Positive and Negative Syndrome Scale (PANSS). We found that self- reflectiveness had an unmoderated positive relationship with quality of life. Self-certainty was associated with better quality of life for people with more severe symptoms. Theoretical and clinical implications of these findings are discussed and areas of future research are proposed.