U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Delusions

; .

Author Information and Affiliations

Last Update: September 26, 2022.

Continuing Education Activity

Delusions can precipitate in isolation or as psychiatric sequelae of ongoing disease. Delusions must be appropriately identified and managed as they can result in dire complications. This activity describes the identification, evaluation, and management of delusions, by an interprofessional team, in facilitating and improving care for patients with this condition.

Objectives:

  • Identify the psychological theories of delusion.
  • Identify at least 3 syndromes in which delusions are a characteristic feature.
  • Determine the management options available for patients with delusions.
  • Communicate the different types of delusions and the role of the interprofessional team in working together to manage patients suffering from them.
Access free multiple choice questions on this topic.

Introduction

In his Critique of Pure Reason, Kant presents the existence of the noumenon (the thing-in-itself) and subsequent phenomenon: the "thing" as it appears to the observer. The veil preventing the unblemished mirroring of the noumenon by the phenomenon is the perceiver's subjective synthesis of the incoming stimuli. Kant further elaborates that the perceiver will never truly acknowledge the objective noumenal reality, as perceiving implies the synthesis of incoming empiric sensation with a priori knowledge and intuition. As a more digestible encapsulation, all experience incorporates an incoming sensation (the noumenon) followed by an organizing concept (the phenomenon), thus engendering a distinctly individualized subjective reality.[1]

Applying this epistemological heuristic, individuals of a common ilk will experience similar phenomenological realities as they share synchronous schemata. However, in deviant sensory processing, the afflicted individual would undoubtedly experience a drastically aberrant perception of reality. This distortion is the foundation for the nosologic distinction of "delusion."

Jaspers (1883-1969) was amongst the first to describe and classify delusions.[2] In his book General Psychopathology (1913), he suggests that a delusion is a "perverted view of reality, incorrigibly held." These perversions are enigmatically derived, held with extraordinary certainty, and unamenable. He further emphasized that these false beliefs exist along a continuum of thought disturbance, increasing in severity of distortion from normal thinking patterns to "true" delusions. One hundred years later, Jaspers' postulation remains a leading candidate in the investigation of delusion morphology.[1] As per the Diagnostic and Statistical Manual (DSM) of Psychiatric Disorders, delusions are defined as firm and fixed beliefs based on inadequate grounds not amenable to the rational argument or evidence to the contrary and not in sync with regional, cultural, or educational background.[3]

Etiology

Despite over a century of interest in this phenomenon, no single unifying theory has been comforted; however, postulations suggesting psychological, neurobiological, cognitive, and emotional etiologies have been offered.

Psychodynamic Theory

No discussion of abstract psychological phenomena would be satisfactory without at least an allusion to Freud. Always in character, Freud suggests that delusions are manifestations of unresolved conflicts between an individual's psychological agencies: the superego, ego, and id. This imbroglio is none other than the repression of homosexual impulses emanating from the id. In an attempt to expiate unending denigration from the superego, the ego implements immature defenses, following the sequence of denial, reaction formation, and finally, projection. The phenomenology of this sequence precipitates as the patient initially denies his homosexual impulses and instead emphasizes his disgust for homosexuals. His repressed impulses are then projected externally, as he accuses others of harboring lascivious intentions. Thus, the inchoate psychic conflict ultimately manifests in the delusion that other men are trying to engage in lewd acts with him, inciting paranoia and distress.[1]

Anthropological Theory

Roberts (1992) proposes a model with 3 stages:

  1. Pre-Psychotic: In this phase, much like the stress-diathesis model, a person with an innate vulnerability or predisposition to a psychotic-type illness is exposed to a stressor, which serves as the antecedent.
  2. Acute phase: In this phase, the person begins to experience unusual or idiosyncratic feelings, which become the seeds of delusions. If personal meaning is attributed to these ideas and sensations, "simple delusions" are formed.
  3. Elaboration: In this phase, further form is given to these simple delusions, which are expanded upon and elaborated. This personalized meaning and associated ideas become incorporated into current thinking, increasing the complexity and rigidity and reinforcing any perceptual distortions and attribution of meaning.[1]

Neurobiological Theory

Experts suggest that elevated dopaminergic transmission can increase "signal-to-noise" differences in the neural network. Consequently, this hyperactive dopamine activity manifests as the tendency to ascribe unrelated external events with personal significance.[4][5] The aberrant dopaminergic activity can impact attention, mood, motivation, and interpersonal interactions. Areas in the brain, including the substantia nigra, dorsolateral prefrontal cortex, ventral striatum, ventromedial prefrontal cortex, hippocampus, and mesolimbic pathways, have been implicated in the experience of delusions.[6] Furthermore, the ability of dopamine antagonists to treat and reduce the intensity of delusions has been considered as evidence of the role dopamine excess plays in the neurobiology of delusions.[7]

Perceptual-Cognitive Theories

This includes the "salience" theory, in which delusions result from imbalanced attention, where more attention is paid to certain idiosyncratic aspects of a situation, excluding more relevant information. This leads to a skewed decision-making process.[8] The 2-factor theory expounds on this concept, stating that both salience and faulty cognition are required to sustain delusions.[9][10]

These faulty perceptual-cognitive processes may also be associated with a "jumping to conclusions" tendency. People with this tendency spend less time reviewing the information before making decisions, are more likely to miss or misinterpret details and feel more certain of their choices. These ideas become fixed, and perception becomes influenced by faulty logic, which supports the idiosyncratic meaning attached to people, places, and situations. This impacts the accuracy of the patient's overall perceptions and conclusions, subsequently impacting information integration and understanding, increasing the likelihood of mistaken interpretations of stimuli.[11] These distorted perceptions become integrated into an overall schema and further distort perceptions as the delusions are now accepted unquestioningly. Brain network theory proposes that disconnections between essential parts of the default mode and semantic networks lead to perceptual-cognitive-affective integration difficulties and ineffective application of cognitive resources.[12][13]

Biographical Theory

Trauma has been implicated as a risk factor for the development of psychosis and delusions, most particularly trauma involving violence of an interpersonal nature. Early childhood trauma has been linked with changes in the developing brain, including a shrinking of the hippocampus, hyperarousal of the amygdala, alterations in neurotransmitters (eg, dopamine, GABA, glutamate), and the subsequently increased diathesis towards delusional manifestations.[14][15]

Integrative Theory

Van Der Gaag (2006) proposed an integrative neuropsychiatric 4-factor model by synthesizing several theoretical perspectives, suggesting that the onset of a delusion is multifactorial.[5]

  1. Biological Component: This leads to aberrant perceptions and salience of stimuli.
  2. Cognitive Component: The aberrant perceptions are interpreted based on the person's history and integrated into their overall schemas.
  3. Psychological Integrative Component: As perceptions become integrated into a person's overall worldview, they are reinforced by faulty logic, and further delusions precipitate.
  4. Psychological Maintenance Component: As delusions become integrated into overall percepts, they are maintained, further impacting perceptions.

Epidemiology

Delusions can precipitate in isolation or as psychiatric sequelae of underlying conditions. In isolation, as in delusional disorder, epidemiologists can feasibly produce estimates of prevalence. However, when manifesting as psychiatric sequelae, accurate estimates prove untenable. With this prefaced, the prevalence of the delusional disorder in the United States, as reported by the DSM-V, is estimated at 0.02%. The female-to-male ratio ranges between 1.18 and 3 to 1. Men are more prone to develop paranoid delusions. Women are more likely than men to develop delusions of erotomania. Socioeconomic factors associated with delusions include being married, employed, recently immigrated, financial stressors, celibacy, and widowhood.[16]

Pathophysiology

Klaus Conrad appropriated 5 sequential stages involved in the progression of delusions: trema, apophany, anastrophe, consolidation, and residuum

  1. Trema: Represents the manifestation of a "delusional mood," resulting in distorted perceptions
  2. Apophany: Symbolizes the designation of new meanings for psychological events
  3. Anastrophe: The heightening of the psychosis
  4. Consolidation: Concludes in a new psychological reality or "delusional state" 
  5. Residuum: The new baseline "autistic state" [17]  

History and Physical

Delusions can manifest as primary psychiatric phenomena or secondary sequelae in the context of other mental or other medical conditions.[18][19][20] However, unlike the protean history preceding the presentation, the underlying archetypal content of the delusions proves to be relatively prosaic. Some of the most clinically encountered types of delusions are:

  1. Erotomanic: A delusion that another person, more frequently someone of higher status, is in love with the individual (Clerembault syndrome) [18] 
  2. Delusional jealousy: Believing that one's sexual partner is unfaithful (Othello syndrome) [21]
  3. Grandiose: A conviction of great talent, discovery, inflated self-worth, power, knowledge, or relationship with someone famous or deity [22]
  4. Persecutory: The central theme is being conspired against, attacked, harassed, poisoned, and obstructed in the pursuit of long-term goals [23]
  5. Religious delusions: The belief that the affected person is a god or chosen to act as a god [24]
  6. Bizarre: A delusion involving a phenomenon that is impossible, not understandable, and unrelated to normal life [25]
  7. Somatic: Involves bodily functions and sensations (eg, pseudocyesis, alien hand syndrome, Alice in Wonderland syndrome)[26]
  8. Control: The delusion that some external force is controlling one's feelings, impulses, and thoughts [27]
  9. Thought broadcasting: A delusion that one's thoughts are projected outwards and perceived by others [18][28][18]
  10. Thought insertion or withdrawal: A delusion that one's thought is not one's own but inserted into their mind by an external source or entity, or one's thoughts are being removed [28][18]
  11. Delusional Misidentification Disorder: The belief that one is dead or does not exist, or one's organs are putrifying or have been removed (Cotard Disorder) [29]; the delusional belief that different people are a single person who is in disguise (Fregoli syndrome) [30] 
  12. Delusions of infestation: Also known as the delusions of parasitosis or Ekbom syndrome; an infrequent psychotic disorder characterized by a firm and false belief that there is a parasitic infestation of the skin, with no medical evidence that could support this claim [31]
  13. Delusions of misidentification: The belief that a familiar person or place has been switched with a look-alike (Capgras disorder)[30]

Picardi (2018) noted that delusions of grandeur were commonly seen in bipolar disorder, whereas delusions of guilt were consistently associated with psychotic depression, both unipolar and bipolar. Although persecutory delusions are common across diagnostic groups, these were found more frequently in schizophrenia and delusional disorders rather than in mood disorders. Delusions of thought broadcasting, insertion, or withdrawal appear to be most frequently associated with chronic psychotic disorders.[32]

Young, Kim, and Park (2012) reviewed shifts in persecutory delusions between the differing generations. They noted a shift in delusional themes temporally related to current political issues. In the earliest group reviewed, delusions were somatic in origin, primarily of having syphilis. With the onset of the Second World War, delusions in American patients contained an increased number of references to Germans and, during the Cold War, of communists.[33]

Evaluation

Evaluating delusional states can prove difficult, even for the seasoned clinician. Before a psychiatric evaluation, the physician should rule out delusional manifestations in the setting of a medical disease. No specific diagnostic test exists to identify delusions; however, the following factors should be considered essential in any clinical evaluation.

  • Genetics and family history as a risk factor: A positive family history of mental disorders should be considered a risk factor in symptom expression.[34]
  • Environment as moderator: Smeets et al (2014) noted evidence suggesting environmental implications on the manifestation and theme of delusions.[35]
  • Early exposure to trauma as a specific risk factor: There is a significant body of research on the link between early/childhood exposure to trauma and the subsequent development and severity of delusions.[36] Some researchers have proposed that the type of trauma may impact the level of risk and the expression of the delusional material.[36][37]
  • Tenacity of beliefs: Despite their encapsulation, these beliefs are impervious to reasoning, evidence, and argument; attempts to confront the delusions may precipitate resistance, early treatment termination, and alienation from the patient.[38]
  • Content and culture: Delusions appear in many cultures. Persecutory delusions appear most frequently, followed by religious and grandiose delusions. However, recent research indicates that the delusional content and expression partly reflect the person's culture and the socio-economic and political events experienced by that person.[39][40][41]

Treatment / Management

Individuals experiencing delusions do not often seek medical attention voluntarily, as their delusions are ego-syntonic, leading to the externalization of psychic distress onto others. Often, patients are prompted to seek help by concerned family members after noticing social and occupational dysfunction.[42]

If an individual seeks treatment, creating therapeutic rapport is the quintessential aim for the clinician.[43] Direct attempts to confront delusions are unlikely to be successful and may lead to significant patient distress. A more fruitful focus for clinicians may be to suspend judgment and examine these beliefs' impact and potential function in the patient's daily life. Focusing on context, exploration, and further understanding of the patient's culture and history will likely prove more productive.

Bebbington and Freeman (2017) propose an integrated neuropsychiatric framework for understanding and treating delusions. The authors indicate that treatment requires amelioration of biological and psychological aspects and that both processes must occur to lead to remission. The remission of the biological aspect consists of the dampening of mesolimbic dopamine release with antipsychotic medication. This reduced dopaminergic activity decreases the uneven salience and attribution of personalized meaning to surrounding stimuli. With the decrease in salience intensity, the person can reassess the stimuli and more accurately distribute attention, reducing the level of over-personalized meaning and leading to a more realistic appraisal of the situation. The therapist can attempt to "shake" the once "unshakable" delusion as insight improves.[44] Psychological remission consists of the reappraisal of primary psychotic experiences. Both remission forms are partially independent, and shifts in both areas are required to remission symptoms.[45]

Differential Diagnosis

As previously mentioned, delusions can precipitate in the setting of psychotic spectrum disorders, manic depressive illness, and isolation. Some research indicates that as many as 20% of those who experience a severe mood disorder may experience delusions, most of which are persecutory or derisive. Delusions in affective disorders tend to have more of a mood component and may be slightly more organized than those seen in schizophrenia.[45]

Delusions also occur with some frequency in various dementia syndromes[46], including Alzheimer disease[47], vascular dementia, frontotemporal dementia[48], and Lewy body dementia[49]; delusional themes in dementia spectrum disease are primarily of theft.[45] It is estimated that 25 to 40% of patients diagnosed with Alzheimer disease experience delusions at some stage of their illness.

In a 2006 study, Scarmeas found that approximately 50% of patients with Lewy body dementia experienced delusions. They noted these patients were prone to delusional misidentification syndromes such as Capgras or Fregoli syndrome.[30] Delusions can also be observed in Charles Bonnet syndrome, which is linked to vision loss.[50][51]

Treatment Planning

If treatment teams decide to pursue pharmacologic management, the neuroleptic medication should be chosen based on the side effect profile, tolerability, coexisting comorbidities, age, and financial burden of the medications.[52][53][54]

Prognosis

Prognosis varies, depending on comorbid conditions. Patients with primary delusions appear to function better overall than those with primary psychotic disorders and worse than those with primary affective disorders.[55][56] Theoretically, delusions precipitating in the setting of an ongoing medical disease should terminate following the resolution of the underlying disease.

Complications

Complications are often related to associated or comorbid conditions. There have been reports of violence, stalking, and homicide associated with delusions, particularly related to jealousy in Othello syndrome, refusal to provide care or displaying aggression towards family members as seen in Capgras syndrome and putting oneself in danger, such as in Fregoli syndrome.[30][57][58][59][30] In rare but dramatic responses to somatic delusions, patients may attempt to amputate limbs or even attempt enucleation.[60] Grandiose delusions may result in injury due to feelings of invincibility. Lastly, the delusions of paranoia may lead patients to commit suicide.[61]

Deterrence and Patient Education

Increased psychoeducation for patients, families, and the public can increase awareness of delusion symptomatology, prompting more rapid recognition and ultimately resulting in more appropriate management.[62]

Enhancing Healthcare Team Outcomes

Interprofessional consultations play an integral role in the setting of delusions. Patients often present to nonpsychiatric specialties due to a lack of insight. Instead, these patients may present to emergency departments and police stations with bizarre complaints of persecution and poisoning. These eccentric presentations should incite concern, and a subsequent consultation should be requested. Once in the appropriate setting, efficient healthcare teamwork is essential. Nursing staff are paramount in orienting and addressing patient needs, while case management assists in the litigious aspects of the case. Psychiatric technicians provide security for patients and staff. Persons suffering from delusions can prove challenging to treat, but with cohesive teamwork, this daunting task becomes manageable.

Review Questions

References

1.
Kiran C, Chaudhury S. Understanding delusions. Ind Psychiatry J. 2009 Jan;18(1):3-18. [PMC free article: PMC3016695] [PubMed: 21234155]
2.
Mishara AL, Fusar-Poli P. The phenomenology and neurobiology of delusion formation during psychosis onset: Jaspers, Truman symptoms, and aberrant salience. Schizophr Bull. 2013 Mar;39(2):278-86. [PMC free article: PMC3576172] [PubMed: 23354468]
3.
Biedermann F, Fleischhacker WW. Psychotic disorders in DSM-5 and ICD-11. CNS Spectr. 2016 Aug;21(4):349-54. [PubMed: 27418328]
4.
Gawęda Ł, Staszkiewicz M, Balzan RP. The relationship between cognitive biases and psychological dimensions of delusions: The importance of jumping to conclusions. J Behav Ther Exp Psychiatry. 2017 Sep;56:51-56. [PubMed: 27527489]
5.
van der Gaag M. A neuropsychiatric model of biological and psychological processes in the remission of delusions and auditory hallucinations. Schizophr Bull. 2006 Oct;32 Suppl 1(Suppl 1):S113-22. [PMC free article: PMC2632542] [PubMed: 16905635]
6.
Howes O, McCutcheon R, Stone J. Glutamate and dopamine in schizophrenia: an update for the 21st century. J Psychopharmacol. 2015 Feb;29(2):97-115. [PMC free article: PMC4902122] [PubMed: 25586400]
7.
Carota A, Bogousslavsky J. Neurology versus Psychiatry? Hallucinations, Delusions, and Confabulations. Front Neurol Neurosci. 2019;44:127-140. [PubMed: 31220856]
8.
Broyd A, Balzan RP, Woodward TS, Allen P. Dopamine, cognitive biases and assessment of certainty: A neurocognitive model of delusions. Clin Psychol Rev. 2017 Jun;54:96-106. [PubMed: 28448827]
9.
Paolini E, Moretti P, Compton MT. Delusions in first-episode psychosis: Principal component analysis of twelve types of delusions and demographic and clinical correlates of resulting domains. Psychiatry Res. 2016 Sep 30;243:5-13. [PMC free article: PMC5014642] [PubMed: 27344587]
10.
McKay R. Measles, magic and misidentifications: a defence of the two-factor theory of delusions. Cogn Neuropsychiatry. 2019 May;24(3):183-190. [PubMed: 30987538]
11.
McLean BF, Mattiske JK, Balzan RP. Association of the Jumping to Conclusions and Evidence Integration Biases With Delusions in Psychosis: A Detailed Meta-analysis. Schizophr Bull. 2017 Mar 01;43(2):344-354. [PMC free article: PMC5605251] [PubMed: 27169465]
12.
Qian W, Fischer CE, Churchill NW, Kumar S, Rajji T, Schweizer TA. Delusions in Alzheimer Disease are Associated With Decreased Default Mode Network Functional Connectivity. Am J Geriatr Psychiatry. 2019 Oct;27(10):1060-1068. [PubMed: 31130416]
13.
Looijestijn J, Blom JD, Aleman A, Hoek HW, Goekoop R. An integrated network model of psychotic symptoms. Neurosci Biobehav Rev. 2015 Dec;59:238-50. [PubMed: 26432501]
14.
Peach N, Alvarez-Jimenez M, Cropper SJ, Sun P, Bendall S. Testing models of post-traumatic intrusions, trauma-related beliefs, hallucinations, and delusions in a first episode psychosis sample. Br J Clin Psychol. 2019 Jun;58(2):154-172. [PubMed: 30421797]
15.
Trotta A, Iyegbe C, Yiend J, Dazzan P, David AS, Pariante C, Mondelli V, Colizzi M, Murray RM, Di Forti M, Fisher HL. Interaction between childhood adversity and functional polymorphisms in the dopamine pathway on first-episode psychosis. Schizophr Res. 2019 Mar;205:51-57. [PubMed: 29653893]
16.
Manschreck TC. Delusional disorder: the recognition and management of paranoia. J Clin Psychiatry. 1996;57 Suppl 3:32-8; discussion 49. [PubMed: 8626368]
17.
Mishara AL. Klaus Conrad (1905-1961): delusional mood, psychosis, and beginning schizophrenia. Schizophr Bull. 2010 Jan;36(1):9-13. [PMC free article: PMC2800156] [PubMed: 19965934]
18.
Joseph SM, Siddiqui W. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Mar 27, 2023. Delusional Disorder. [PubMed: 30969677]
19.
Kuroda N, Kashiwase H. [Induced delusional disorder]. Ryoikibetsu Shokogun Shirizu. 2003;(38):107-10. [PubMed: 12876941]
20.
Opjordsmoen S. Delusional disorder as a partial psychosis. Schizophr Bull. 2014 Mar;40(2):244-7. [PMC free article: PMC3932094] [PubMed: 24421383]
21.
Delgado MG, Bogousslavsky J. De Clérambault Syndrome, Othello Syndrome, Folie à Deux and Variants. Front Neurol Neurosci. 2018;42:44-50. [PubMed: 29151090]
22.
Isham L, Griffith L, Boylan AM, Hicks A, Wilson N, Byrne R, Sheaves B, Bentall RP, Freeman D. Understanding, treating, and renaming grandiose delusions: A qualitative study. Psychol Psychother. 2021 Mar;94(1):119-140. [PMC free article: PMC7984144] [PubMed: 31785077]
23.
Rössler V, Walter MH, Richter R. [The phenomenology of delusions of poisoning in persons with paranoid schizophrenia]. Fortschr Neurol Psychiatr. 2019 Dec;87(12):695-701. [PubMed: 31390658]
24.
Mishra A, Das B, Goyal N. Religiosity and religious delusions in schizophrenia - An observational study in a Hindu population. Asian J Psychiatr. 2018 Feb;32:35-39. [PubMed: 29202427]
25.
Ramasamy J, Arumugam S, Thamizh JS. Atypical delusional content in a case of persistent delusional disorder: freud revisited. Indian J Psychol Med. 2014 Oct;36(4):431-3. [PMC free article: PMC4201800] [PubMed: 25336780]
26.
Krämer J, Huber M, Mundinger C, Schmitgen MM, Pycha R, Kirchler E, Macina C, Karner M, Hirjak D, Kubera KM, Depping MS, Romanov D, Freudenmann RW, Wolf RC. Abnormal cerebellar volume in somatic vs. non-somatic delusional disorders. Cerebellum Ataxias. 2020;7:2. [PMC free article: PMC6971987] [PubMed: 31993210]
27.
Riemer M. Delusions of control in schizophrenia: Resistant to the mind's best trick? Schizophr Res. 2018 Jul;197:98-103. [PubMed: 29208423]
28.
Funayama M. [Symptoms Specific to Schizophrenia]. Brain Nerve. 2018 Sep;70(9):981-991. [PubMed: 30177576]
29.
González Eizaguirre MM, Martínez Fabre D, Linge Martín M, Oquendo Marmaneu C, Fernández Minaya DC. [Cotard syndrome in an elderly patient]. Rev Esp Geriatr Gerontol. 2020 May-Jun;55(3):178-179. [PubMed: 31722789]
30.
Ventriglio A, Bhugra D, De Berardis D, Torales J, Castaldelli-Maia JM, Fiorillo A. Capgras and Fregoli syndromes: delusion and misidentification. Int Rev Psychiatry. 2020 Aug-Sep;32(5-6):391-395. [PubMed: 32378427]
31.
Reich A, Kwiatkowska D, Pacan P. Delusions of Parasitosis: An Update. Dermatol Ther (Heidelb). 2019 Dec;9(4):631-638. [PMC free article: PMC6828902] [PubMed: 31520344]
32.
Picardi A, Fonzi L, Pallagrosi M, Gigantesco A, Biondi M. Delusional Themes Across Affective and Non-Affective Psychoses. Front Psychiatry. 2018;9:132. [PMC free article: PMC5895977] [PubMed: 29674982]
33.
Varga ÉJ, Tényi T. [A short overview on the changes of the content of delusions - the impact of technological innovations, historical events and culture]. Psychiatr Hung. 2018;33(2):138-144. [PubMed: 30117428]
34.
Linscott RJ, van Os J. An updated and conservative systematic review and meta-analysis of epidemiological evidence on psychotic experiences in children and adults: on the pathway from proneness to persistence to dimensional expression across mental disorders. Psychol Med. 2013 Jun;43(6):1133-49. [PubMed: 22850401]
35.
Smeets F, Lataster T, Viechtbauer W, Delespaul P., G.R.O.U.P. Evidence that environmental and genetic risks for psychotic disorder may operate by impacting on connections between core symptoms of perceptual alteration and delusional ideation. Schizophr Bull. 2015 May;41(3):687-97. [PMC free article: PMC4393682] [PubMed: 25217481]
36.
Bailey T, Alvarez-Jimenez M, Garcia-Sanchez AM, Hulbert C, Barlow E, Bendall S. Childhood Trauma Is Associated With Severity of Hallucinations and Delusions in Psychotic Disorders: A Systematic Review and Meta-Analysis. Schizophr Bull. 2018 Aug 20;44(5):1111-1122. [PMC free article: PMC6101549] [PubMed: 29301025]
37.
Saha S, Varghese D, Slade T, Degenhardt L, Mills K, McGrath J, Scott J. The association between trauma and delusional-like experiences. Psychiatry Res. 2011 Sep 30;189(2):259-64. [PubMed: 21524800]
38.
Knorr R, Hoffmann K. [Delusions: current psychodynamic and neurocognitive approaches]. Nervenarzt. 2018 Jan;89(1):8-17. [PubMed: 28251242]
39.
Campbell MM, Sibeko G, Mall S, Baldinger A, Nagdee M, Susser E, Stein DJ. The content of delusions in a sample of South African Xhosa people with schizophrenia. BMC Psychiatry. 2017 Jan 24;17(1):41. [PMC free article: PMC5259874] [PubMed: 28118821]
40.
Varga ÉJ, Herold R, Tényi T. [Effect of culture to delusions: Introduction of the Truman Show delusion]. Psychiatr Hung. 2016;31(4):359-363. [PubMed: 28032584]
41.
Oh HY, Kim D, Park YC. Nature of Persecutors and Their Behaviors in the Delusions of Schizophrenia: Changes between the 1990s and the 2000s. Psychiatry Investig. 2012 Dec;9(4):319-24. [PMC free article: PMC3521106] [PubMed: 23251194]
42.
Kurtz MM. Symptoms versus neurocognitive skills as correlates of everyday functioning in severe mental illness. Expert Rev Neurother. 2006 Jan;6(1):47-56. [PubMed: 16466311]
43.
Mehl S, Hesse K, Schmidt AC, Landsberg MW, Soll D, Bechdolf A, Herrlich J, Kircher T, Klingberg S, Müller BW, Wiedemann G, Wittorf A, Wölwer W, Wagner M. Theory of mind, emotion recognition, delusions and the quality of the therapeutic relationship in patients with psychosis - a secondary analysis of a randomized-controlled therapy trial. BMC Psychiatry. 2020 Feb 10;20(1):59. [PMC free article: PMC7011563] [PubMed: 32041577]
44.
Kumar D. Promoting insight into delusions: Issues and challenges in therapy. Int J Psychiatry Clin Pract. 2020 Jun;24(2):208-213. [PubMed: 31928095]
45.
Bebbington P, Freeman D. Transdiagnostic Extension of Delusions: Schizophrenia and Beyond. Schizophr Bull. 2017 Mar 01;43(2):273-282. [PMC free article: PMC5605249] [PubMed: 28399309]
46.
Cloak N, Al Khalili Y. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 21, 2022. Behavioral and Psychological Symptoms in Dementia. [PubMed: 31855379]
47.
Tetreault AM, Phan T, Orlando D, Lyu I, Kang H, Landman B, Darby RR., Alzheimer’s Disease Neuroimaging Initiative. Network localization of clinical, cognitive, and neuropsychiatric symptoms in Alzheimer's disease. Brain. 2020 Apr 01;143(4):1249-1260. [PMC free article: PMC7174048] [PubMed: 32176777]
48.
Scarioni M, Gami-Patel P, Timar Y, Seelaar H, van Swieten JC, Rozemuller AJM, Dols A, Scarpini E, Galimberti D, Netherlands Brain Bank. Hoozemans JJM, Pijnenburg YAL, Dijkstra AA. Frontotemporal Dementia: Correlations Between Psychiatric Symptoms and Pathology. Ann Neurol. 2020 Jun;87(6):950-961. [PMC free article: PMC7318614] [PubMed: 32281118]
49.
Tampi RR, Young JJ, Tampi D. Behavioral symptomatology and psychopharmacology of Lewy body dementia. Handb Clin Neurol. 2019;165:59-70. [PubMed: 31727230]
50.
Makarewich C, West DA. Charles Bonnet syndrome-induced psychosis? Visual hallucinations with paranoid delusions in a visually-impaired man. J Neuropsychiatry Clin Neurosci. 2011 Fall;23(4):E6. [PubMed: 22231350]
51.
Hamedani AG, Pelak VS. The Charles Bonnet Syndrome: a Systematic Review of Diagnostic Criteria. Curr Treat Options Neurol. 2019 Jul 25;21(9):41. [PubMed: 31342218]
52.
Bouvard MP, Mouren-Siméoni MC. [Prescription of neuroleptics for children]. Encephale. 1990 Sep-Oct;16(5):389-98. [PubMed: 1979943]
53.
Abou Kassm S, Naja W, Hoertel N, Limosin F. [Pharmacological management of delusions associated with dementia]. Geriatr Psychol Neuropsychiatr Vieil. 2019 Sep 01;17(3):317-326. [PubMed: 31449050]
54.
Lally J, MacCabe JH. Antipsychotic medication in schizophrenia: a review. Br Med Bull. 2015 Jun;114(1):169-79. [PubMed: 25957394]
55.
Maj M, Pirozzi R, Magliano L, Fiorillo A, Bartoli L. Phenomenology and prognostic significance of delusions in major depressive disorder: a 10-year prospective follow-up study. J Clin Psychiatry. 2007 Sep;68(9):1411-7. [PubMed: 17915981]
56.
Opjordsmoen S. Long-term course and outcome in unipolar affective and schizoaffective psychoses. Acta Psychiatr Scand. 1989 Apr;79(4):317-26. [PubMed: 2735203]
57.
Cipriani G, Vedovello M, Nuti A, di Fiorino A. Dangerous passion: Othello syndrome and dementia. Psychiatry Clin Neurosci. 2012 Oct;66(6):467-73. [PubMed: 23066764]
58.
Ivanov P, Moral Cuesta D, Perelló Alonso M. [Capgras syndrome: The delusion of impersonation]. Rev Esp Geriatr Gerontol. 2018 May-Jun;53(3):173. [PubMed: 28964547]
59.
Coltheart M, Langdon R. Somatic delusions as motivated beliefs? Aust N Z J Psychiatry. 2019 Jan;53(1):83-84. [PubMed: 30466300]
60.
Kraft DP, Babigian HM. Somatic delusion or self-mutilation in a schizophrenic woman: a psychiatric emergency room case report. Am J Psychiatry. 1972 Jan;128(7):893-5. [PubMed: 5009271]
61.
Brown RS, Fischman A, Showalter CR. Primary hyperparathyroidism, hypercalcemia, paranoid delusions, homicide, and attempted murder. J Forensic Sci. 1987 Sep;32(5):1460-3. [PubMed: 3668484]
62.
Mottaghipour Y, Tabatabaee M. Family and Patient Psychoeducation for Severe Mental Disorder in Iran: A Review. Iran J Psychiatry. 2019 Jan;14(1):84-108. [PMC free article: PMC6505048] [PubMed: 31114622]

Disclosure: Kamron Fariba declares no relevant financial relationships with ineligible companies.

Disclosure: Fatma Fawzy declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK563175PMID: 33085322

Views

  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...