-
BMC Psychiatry Dec 2023Patients with Alzheimer's disease (AD) often exhibit neuropsychiatric symptoms (NPS), particularly delusions. Previous studies have shown an association between white...
BACKGROUND
Patients with Alzheimer's disease (AD) often exhibit neuropsychiatric symptoms (NPS), particularly delusions. Previous studies have shown an association between white matter hyperintensities (WMH) and specific NPS. This study aims to explore the relationship between WMH volume and delusions in AD patients by comparing the WMH volumes of delusional and non-delusional subgroups.
METHODS
80 AD patients were divided into a delusion group (n = 36) and a non-delusion group (n = 44) based on the Neuropsychiatric Inventory (NPI). The brain cortical volume and WMH volume were quantitatively calculated for all 80 patients, including total WMH volume, periventricular WMH (PVWMH) volume, deep WMH volume, as well as bilateral frontal lobe, temporal lobe, parietal lobe, and occipital lobe WMH volumes. Firstly, we compared the differences in WMH volumes between the delusion group and non-delusion group. Then, within the delusion group, we further categorized patients based on severity scores of their delusional symptoms into mild (1 point), moderate (2 points), or severe groups (3 points). We compared the WMH volumes among these three groups to investigate the role of WMH volume in delusional symptoms.
RESULTS
There was a significant difference in left occipital lobe WMH volume between the delusion group and non-delusion group(P < 0.05). Within the delusion group itself, there were significant differences in overall WMH volume as well as PVWMH volume among patients with mild or severe levels of delusions(P < 0.05).
CONCLUSION
Left occipital lobe WMH volume may be associated with the occurrence of delusional AD patients, and the total volume of whole-brain WMH and PVWMH volume may affect the degree of severity of delusional symptoms.
Topics: Humans; Alzheimer Disease; White Matter; Temporal Lobe; Brain; Parietal Lobe; Magnetic Resonance Imaging
PubMed: 38057778
DOI: 10.1186/s12888-023-05420-5 -
Journal of Psychopathology and Clinical... Aug 2023There is widespread agreement that delusions in clinical populations and delusion-like beliefs in the general population are, in part, caused by cognitive biases. Much...
There is widespread agreement that delusions in clinical populations and delusion-like beliefs in the general population are, in part, caused by cognitive biases. Much of the evidence comes from two influential tasks: the Beads Task and the Bias Against Disconfirmatory Evidence Task. However, research using these tasks has been hampered by conceptual and empirical inconsistencies. In an online study, we examined relationships between delusion-like beliefs in the general population and cognitive biases associated with these tasks. Our study had four key strengths: A new animated Beads Task designed to reduce task miscomprehension, several data-quality checks to identify careless responders, a large sample ( = 1,002), and a preregistered analysis plan. When analyzing the full sample, our results replicated classic relationships between cognitive biases and delusion-like beliefs. However, when we removed 82 careless participants from the analyses (8.2% of the sample) we found that many of these relationships were severely diminished and, in some cases, eliminated outright. These results suggest that some (but not all) seemingly well-established relationships between cognitive biases and delusion-like beliefs might be artifacts of careless responding. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
Topics: Humans; Delusions; Artifacts; Bias; Data Accuracy; Cognition
PubMed: 37326560
DOI: 10.1037/abn0000844 -
Schizophrenia Research May 2024Schizophrenia is a highly heritable, severe mental illness characterized by hallucinations, delusions, social withdrawal, and cognitive dysfunction present in ∼1% of... (Review)
Review
Schizophrenia is a highly heritable, severe mental illness characterized by hallucinations, delusions, social withdrawal, and cognitive dysfunction present in ∼1% of populations across cultures. There have been recent major advancements in our understanding of the genetic architecture of schizophrenia. Both rare, highly penetrant genetic variants as well as common, low-penetrant genetic variants can predispose individuals to schizophrenia and can impact the way people metabolize psychoactive medications used to treat schizophrenia. However, the impact of these findings on the clinical management of schizophrenia remains limited. This review highlights the few places where genetics currently informs schizophrenia management strategies, discusses major limitations, and reviews promising areas of genetics research that are most likely to impact future schizophrenia care. Specifically, I focuss on psychiatric genetic counseling, genetic testing strategies, pharmacogenetics, polygenic risk, and genetics-guided treatment. Lastly, I emphasize important ethical considerations in the clinical use of genetics for schizophrenia management, including the exacerbation of healthcare inequalities and unintended consequences of new genetic technologies.
Topics: Humans; Schizophrenia; Pharmacogenetics; Genetic Testing; Genetic Counseling; Multifactorial Inheritance; Genetic Predisposition to Disease
PubMed: 37813777
DOI: 10.1016/j.schres.2023.09.042 -
Studies in History and Philosophy of... Aug 2023Science promises benefits, some true and some illusory. Consider a scientific agnostic who thinks that to reap the true benefits of a scientific theory he does not have...
Science promises benefits, some true and some illusory. Consider a scientific agnostic who thinks that to reap the true benefits of a scientific theory he does not have to believe in its theoretical posits. Instead, it is enough if he believes that the theory successfully predicts the behavior of the observables, as ultimately only such predictions matter. Say, however, that given the results of her thorough research, a psychologist proposes a theory describing a psychological mechanism underlying a certain class of normative judgments. Moreover, the mechanism seems unfit for the task-once you see the details of the mechanism, you will realize that this is not the way they should be produced. Therefore, if the psychologist is right, it seems that these normative judgments should not inform one's normative theorizing or one's actions (Greene, 2008; Greene, 2014; Kelly, 2014). And say that the agnostic accepts the psychologist's theory, trusting that it makes correct predictions about, for example, fMRI images and subjects' reaction times, as they are observable. He also thinks that if the psychologist's description of the mechanism is correct, the judgments should not be trusted. Yet, since the mechanism posited by the theory is not observable, the agnostic is agnostic about it. He thus cannot be convinced that these judgments are produced in a flawed way and, consequently, has no reason to distrust them. Scientific agnosticism comes, therefore, at the cost of dismissing normative arguments that invoke unobservable posits of psychological models. The ability to make such arguments is a true (rather than illusory) benefit of science, despite the agnostic's promise that his philosophical theory leaves intact benefits that genuinely matter.
Topics: Humans; Emotions; Science; Judgment
PubMed: 37348149
DOI: 10.1016/j.shpsa.2023.05.001 -
Psychopathology Mar 2024Hysteria in its most severe expression may reach psychotic manifestations. Such symptomatology has been occasionally described by various authors starting from the 19th... (Review)
Review
BACKGROUND
Hysteria in its most severe expression may reach psychotic manifestations. Such symptomatology has been occasionally described by various authors starting from the 19th century and defined as "hysterical psychosis" (HP) by Hollender and Hirsch in 1964. Currently, diagnostic psychiatric manuals such as DSM and ICD do not include the diagnosis of HP, although this term is commonly used in clinical practice. This raises a well-known problem with case definition due to an inconsistent use of terminology.
SUMMARY
Here, we propose a review of the literature that aims to highlight the clinical features of HP endorsed by the majority of authors, such as histrionic premorbid personality, acute reactive onset, short duration, altered state of consciousness, unstable delusions, typical hallucinations, labile mood, lack of flat affect. In the discussion, we focus on the differential diagnosis between HP and other diagnoses such as brief psychosis and schizophrenia, trying to point out aspects of distinction and continuity.
KEY MESSAGES
The debate about this nosographic entity still remains a huge dilemma and needs further contributions.
PubMed: 38442702
DOI: 10.1159/000536377 -
Cognitive Neuropsychiatry Jan 2024Koro is a delusion whereby a man believes his penis is shrinking into his abdomen and this may result in his death. This socially-transmitted non-neuropsychological...
INTRODUCTION
Koro is a delusion whereby a man believes his penis is shrinking into his abdomen and this may result in his death. This socially-transmitted non-neuropsychological delusional belief occurs (in epidemic form) in South-East and South Asia. We investigated whether the two-factor theory of delusion could be applied to epidemic Koro.
METHODS
We scrutinised the literature on epidemic Koro to isolate features relevant to the two questions that must be answered to provide a two-factor account: What could initially prompt the Koro delusional hypothesis? Why is this hypothesis adopted as a belief?
RESULTS
We concluded that the Koro hypothesis is usually prompted by the surprising observation of actual penis shrinkage-but only if the man has access to background beliefs about Koro. Whether the hypothesis is then adopted as a belief will depend on individual factors such as prior belief in the Koro concept or limited formal education and sociocultural factors such as deference to culture, to media, or to rumours spread by word of mouth. Social transmission can influence how the first factor works and how the second factor works.
CONCLUSION
The two-factor theory of delusion can be applied to a socially-transmitted delusion that occurs in epidemic form.
Topics: Male; Humans; Koro; Delusions
PubMed: 38348821
DOI: 10.1080/13546805.2024.2313474 -
Nature Reviews. Neurology Mar 2024Parkinson disease (PD) psychosis (PDP) is a spectrum of illusions, hallucinations and delusions that are associated with PD throughout its disease course. Psychotic... (Review)
Review
Parkinson disease (PD) psychosis (PDP) is a spectrum of illusions, hallucinations and delusions that are associated with PD throughout its disease course. Psychotic phenomena can manifest from the earliest stages of PD and might follow a continuum from minor hallucinations to structured hallucinations and delusions. Initially, PDP was considered to be a complication associated with dopaminergic drug use. However, subsequent research has provided evidence that PDP arises from the progression of brain alterations caused by PD itself, coupled with the use of dopaminergic drugs. The combined dysfunction of attentional control systems, sensory processing, limbic structures, the default mode network and thalamocortical connections provides a conceptual framework to explain how new incoming stimuli are incorrectly categorized, and how aberrant hierarchical predictive processing can produce false percepts that intrude into the stream of consciousness. The past decade has seen the publication of new data on the phenomenology and neurobiological basis of PDP from the initial stages of the disease, as well as the neurotransmitter systems involved in PDP initiation and progression. In this Review, we discuss the latest clinical, neuroimaging and neurochemical evidence that could aid early identification of psychotic phenomena in PD and inform the discovery of new therapeutic targets and strategies.
Topics: Humans; Parkinson Disease; Psychotic Disorders; Hallucinations; Brain
PubMed: 38225264
DOI: 10.1038/s41582-023-00918-8 -
Neuropharmacology Dec 2023Decreased ATPergic signaling is an increasingly recognized pathophysiology in bipolar mania disease models. In parallel, adenosine deficit is increasingly recognized in... (Review)
Review
Decreased ATPergic signaling is an increasingly recognized pathophysiology in bipolar mania disease models. In parallel, adenosine deficit is increasingly recognized in epilepsy pathophysiology. Under-recognized ATP and/or adenosine-increasing mechanisms of several antimanic and antiseizure therapies including lithium, valproate, carbamazepine, and ECT suggest a fundamental pathogenic role of adenosine deficit in bipolar mania to match the established role of adenosine deficit in epilepsy. The depletion of adenosine-derivatives within the purine cycle is expected to result in a compensatory increase in oxopurines (uric acid precursors) and secondarily increased uric acid, observed in both bipolar mania and epilepsy. Cortisol-based inhibition of purine conversion to adenosine-derivatives may be reflected in observed uric acid increases and the well-established contribution of cortisol to both bipolar mania and epilepsy pathology. Cortisol-inhibited conversion from IMP to AMP as precursor of both ATP and adenosine may represent a mechanism for treatment resistance common in both bipolar mania and epilepsy. Anti-cortisol therapies may therefore augment other treatments both in bipolar mania and epilepsy. Evidence linking (i) adenosine deficit with a decreased need for sleep, (ii) IMP/cGMP excess with compulsive hypersexuality, and (iii) guanosine excess with grandiose delusions may converge to suggest a novel theory of bipolar mania as a condition characterized by disrupted purine metabolism. The potential for disease-modification and prevention related to adenosine-mediated epigenetic changes in epilepsy may be mirrored in mania. Evaluating the purinergic effects of existing agents and validating purine dysregulation may improve diagnosis and treatment in bipolar mania and epilepsy and provide specific targets for drug development.
Topics: Humans; Bipolar Disorder; Mania; Hydrocortisone; Uric Acid; Valproic Acid; Antimanic Agents; Purines; Epilepsy; Adenosine Triphosphate; Adenosine
PubMed: 37820933
DOI: 10.1016/j.neuropharm.2023.109756 -
The Journal of Clinical Psychiatry Jul 2023Delusions and hallucinations are common in Alzheimer disease (AD) and Parkinson disease (PD), especially in the later stages of illness. Antipsychotic drugs are... (Meta-Analysis)
Meta-Analysis
Delusions and hallucinations are common in Alzheimer disease (AD) and Parkinson disease (PD), especially in the later stages of illness. Antipsychotic drugs are effective in treating these psychotic symptoms but are associated with an increased risk of serious adverse events, including mortality. There is therefore a need to explore other treatment approaches. In this context, a recent individual patient data meta-analysis of 17 randomized controlled trials (RCTs) conducted in AD (12 RCTs) and PD (5 RCTs) found that the cholinesterase inhibitor (ChEI) drugs donepezil, rivastigmine, and galantamine attenuated the severity of both delusions and hallucinations in both AD and PD. Most of these trials were 24 weeks in duration. The effect sizes, expressed as standardized mean differences (SMDs), were, however, small, lying in the -0.08 to -0.14 range. These values are so small as to be perhaps clinically insignificant. When analyses were restricted to data from patients who actually had delusions and hallucinations at baseline, all effect sizes became larger, lying in the -0.13 to -0.39 range; however, after correcting for multiple hypothesis testing, only the finding for delusions in PD remained statistically significant. The meta-analysis did not provide information on what the best doses were, how long it took for improvement to become evident, and what proportion of patients showed remission from psychotic symptoms. Whereas the signal identified in this meta-analysis merits examination in appropriately designed RCTs, the findings of the meta-analysis may not much change current treatment strategies because patients with dementia would probably anyway receive a ChEI. Therefore, if psychotic symptoms persist for 24 weeks despite optimally dosed ChEI treatment, and if behavioral and psychosocial interventions do not help, clinicians may need to consider the potential benefits vs risks of other drugs, such as atypical antipsychotics and pimavanserin, in a shared decision-making process.
Topics: Humans; Cholinesterase Inhibitors; Alzheimer Disease; Delusions; Parkinson Disease; Antipsychotic Agents; Hallucinations
PubMed: 37530610
DOI: 10.4088/JCP.23f15009 -
Cortex; a Journal Devoted To the Study... Oct 2023Reduplicative paramnesia refers to the delusional belief that there are identical places in different locations. In this case-control study we investigated the clinical,...
Reduplicative paramnesia refers to the delusional belief that there are identical places in different locations. In this case-control study we investigated the clinical, phenomenological, neuropsychological and neuroanatomical data of eleven patients with reduplicative paramnesia and compared them against a control group of eleven patients with severe spatial disorientation without signs of reduplicative paramnesia. We show that most patients with reduplicative paramnesia report that a current place is reduplicated and/or relocated to an other familiar place. Patients with reduplicative paramnesia show a higher prevalence of deficits in the executive functions compared to the control patients, while mnestic and visuo-spatial deficits were both frequent in patients with reduplicative paramnesia and the control group. Patients with reduplicative paramnesia mostly suffer from right hemispheric lesions with a maximal overlap in the dorsolateral prefrontal cortex. Using lesion network mapping we show that lesions causing reduplicative paramnesia are connected to bilateral anterior insula and the right cingulate cortex. We argue that patients with reduplicative paramnesia fail to integrate the actual context with visuo-spatial memories and personal relevant emotional information due to a disruption of the neural network within the anterior temporal lobe, the cingulate cortex and the anterior insula. Also patients with reduplicative paramnesia are not able to resolve this conflict due to the lesion of the dorsolateral prefrontal cortex and executive dysfunction.
Topics: Humans; Neuroanatomy; Delusions; Neuropsychology; Case-Control Studies; Memory Disorders
PubMed: 37515831
DOI: 10.1016/j.cortex.2023.06.006