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Delusions

Editor: Fatma Fawzy Updated: 9/26/2022 5:42:38 PM

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

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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.(B2)

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.

References


[1]

Kiran C, Chaudhury S. Understanding delusions. Industrial psychiatry journal. 2009 Jan:18(1):3-18. doi: 10.4103/0972-6748.57851. Epub     [PubMed PMID: 21234155]

Level 3 (low-level) evidence

[2]

Mishara AL, Fusar-Poli P. The phenomenology and neurobiology of delusion formation during psychosis onset: Jaspers, Truman symptoms, and aberrant salience. Schizophrenia bulletin. 2013 Mar:39(2):278-86. doi: 10.1093/schbul/sbs155. Epub 2013 Jan 25     [PubMed PMID: 23354468]


[3]

Biedermann F, Fleischhacker WW. Psychotic disorders in DSM-5 and ICD-11. CNS spectrums. 2016 Aug:21(4):349-54. doi: 10.1017/S1092852916000316. Epub 2016 Jul 15     [PubMed PMID: 27418328]


[4]

Gawęda Ł, Staszkiewicz M, Balzan RP. The relationship between cognitive biases and psychological dimensions of delusions: The importance of jumping to conclusions. Journal of behavior therapy and experimental psychiatry. 2017 Sep:56():51-56. doi: 10.1016/j.jbtep.2016.08.003. Epub 2016 Aug 5     [PubMed PMID: 27527489]


[5]

van der Gaag M. A neuropsychiatric model of biological and psychological processes in the remission of delusions and auditory hallucinations. Schizophrenia bulletin. 2006 Oct:32 Suppl 1(Suppl 1):S113-22     [PubMed PMID: 16905635]


[6]

Howes O, McCutcheon R, Stone J. Glutamate and dopamine in schizophrenia: an update for the 21st century. Journal of psychopharmacology (Oxford, England). 2015 Feb:29(2):97-115. doi: 10.1177/0269881114563634. Epub 2015 Jan 13     [PubMed PMID: 25586400]

Level 3 (low-level) evidence

[7]

Carota A, Bogousslavsky J. Neurology versus Psychiatry? Hallucinations, Delusions, and Confabulations. Frontiers of neurology and neuroscience. 2019:44():127-140. doi: 10.1159/000494960. Epub 2019 Apr 30     [PubMed PMID: 31220856]


[8]

Broyd A, Balzan RP, Woodward TS, Allen P. Dopamine, cognitive biases and assessment of certainty: A neurocognitive model of delusions. Clinical psychology review. 2017 Jun:54():96-106. doi: 10.1016/j.cpr.2017.04.006. Epub 2017 Apr 18     [PubMed PMID: 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 research. 2016 Sep 30:243():5-13. doi: 10.1016/j.psychres.2016.06.002. Epub 2016 Jun 11     [PubMed PMID: 27344587]


[10]

McKay R. Measles, magic and misidentifications: a defence of the two-factor theory of delusions. Cognitive neuropsychiatry. 2019 May:24(3):183-190. doi: 10.1080/13546805.2019.1607273. Epub 2019 Apr 16     [PubMed PMID: 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. Schizophrenia bulletin. 2017 Mar 1:43(2):344-354. doi: 10.1093/schbul/sbw056. Epub     [PubMed PMID: 27169465]

Level 1 (high-level) evidence

[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. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. 2019 Oct:27(10):1060-1068. doi: 10.1016/j.jagp.2019.03.020. Epub 2019 Apr 3     [PubMed PMID: 31130416]

Level 2 (mid-level) evidence

[13]

Looijestijn J, Blom JD, Aleman A, Hoek HW, Goekoop R. An integrated network model of psychotic symptoms. Neuroscience and biobehavioral reviews. 2015 Dec:59():238-50. doi: 10.1016/j.neubiorev.2015.09.016. Epub 2015 Sep 30     [PubMed PMID: 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. The British journal of clinical psychology. 2019 Jun:58(2):154-172. doi: 10.1111/bjc.12206. Epub 2018 Nov 13     [PubMed PMID: 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. Schizophrenia research. 2019 Mar:205():51-57. doi: 10.1016/j.schres.2018.04.010. Epub 2018 Apr 10     [PubMed PMID: 29653893]


[16]

Manschreck TC. Delusional disorder: the recognition and management of paranoia. The Journal of clinical psychiatry. 1996:57 Suppl 3():32-8; discussion 49     [PubMed PMID: 8626368]

Level 3 (low-level) evidence

[17]

Mishara AL. Klaus Conrad (1905-1961): delusional mood, psychosis, and beginning schizophrenia. Schizophrenia bulletin. 2010 Jan:36(1):9-13. doi: 10.1093/schbul/sbp144. Epub 2009 Dec 4     [PubMed PMID: 19965934]


[18]

Joseph SM, Siddiqui W. Delusional Disorder. StatPearls. 2024 Jan:():     [PubMed PMID: 30969677]


[19]

Kuroda N, Kashiwase H. [Induced delusional disorder]. Ryoikibetsu shokogun shirizu. 2003:(38):107-10     [PubMed PMID: 12876941]


[20]

Opjordsmoen S. Delusional disorder as a partial psychosis. Schizophrenia bulletin. 2014 Mar:40(2):244-7. doi: 10.1093/schbul/sbt203. Epub 2014 Jan 13     [PubMed PMID: 24421383]


[21]

Delgado MG, Bogousslavsky J. De Clérambault Syndrome, Othello Syndrome, Folie à Deux and Variants. Frontiers of neurology and neuroscience. 2018:42():44-50. doi: 10.1159/000475685. Epub 2017 Nov 17     [PubMed PMID: 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. Psychology and psychotherapy. 2021 Mar:94(1):119-140. doi: 10.1111/papt.12260. Epub 2019 Nov 29     [PubMed PMID: 31785077]

Level 2 (mid-level) evidence

[23]

Rössler V, Walter MH, Richter R. [The phenomenology of delusions of poisoning in persons with paranoid schizophrenia]. Fortschritte der Neurologie-Psychiatrie. 2019 Dec:87(12):695-701. doi: 10.1055/a-0846-3950. Epub 2019 Aug 7     [PubMed PMID: 31390658]


[24]

Mishra A, Das B, Goyal N. Religiosity and religious delusions in schizophrenia - An observational study in a Hindu population. Asian journal of psychiatry. 2018 Feb:32():35-39. doi: 10.1016/j.ajp.2017.11.011. Epub 2017 Nov 27     [PubMed PMID: 29202427]

Level 2 (mid-level) evidence

[25]

Ramasamy J, Arumugam S, Thamizh JS. Atypical delusional content in a case of persistent delusional disorder: freud revisited. Indian journal of psychological medicine. 2014 Oct:36(4):431-3. doi: 10.4103/0253-7176.140742. Epub     [PubMed PMID: 25336780]

Level 3 (low-level) evidence

[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. doi: 10.1186/s40673-020-0111-8. Epub 2020 Jan 20     [PubMed PMID: 31993210]


[27]

Riemer M. Delusions of control in schizophrenia: Resistant to the mind's best trick? Schizophrenia research. 2018 Jul:197():98-103. doi: 10.1016/j.schres.2017.11.032. Epub 2017 Dec 6     [PubMed PMID: 29208423]


[28]

Funayama M. [Symptoms Specific to Schizophrenia]. Brain and nerve = Shinkei kenkyu no shinpo. 2018 Sep:70(9):981-991. doi: 10.11477/mf.1416201118. Epub     [PubMed PMID: 30177576]


[29]

González Eizaguirre MM, Martínez Fabre D, Linge Martín M, Oquendo Marmaneu C, Fernández Minaya DC. [Cotard syndrome in an elderly patient]. Revista espanola de geriatria y gerontologia. 2020 May-Jun:55(3):178-179. doi: 10.1016/j.regg.2019.08.003. Epub 2019 Nov 10     [PubMed PMID: 31722789]


[30]

Ventriglio A, Bhugra D, De Berardis D, Torales J, Castaldelli-Maia JM, Fiorillo A. Capgras and Fregoli syndromes: delusion and misidentification. International review of psychiatry (Abingdon, England). 2020 Aug-Sep:32(5-6):391-395. doi: 10.1080/09540261.2020.1756625. Epub 2020 May 7     [PubMed PMID: 32378427]


[31]

Reich A, Kwiatkowska D, Pacan P. Delusions of Parasitosis: An Update. Dermatology and therapy. 2019 Dec:9(4):631-638. doi: 10.1007/s13555-019-00324-3. Epub 2019 Sep 13     [PubMed PMID: 31520344]


[32]

Picardi A, Fonzi L, Pallagrosi M, Gigantesco A, Biondi M. Delusional Themes Across Affective and Non-Affective Psychoses. Frontiers in psychiatry. 2018:9():132. doi: 10.3389/fpsyt.2018.00132. Epub 2018 Apr 5     [PubMed PMID: 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]. Psychiatria Hungarica : A Magyar Pszichiatriai Tarsasag tudomanyos folyoirata. 2018:33(2):138-144     [PubMed PMID: 30117428]

Level 3 (low-level) evidence

[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. Psychological medicine. 2013 Jun:43(6):1133-49. doi: 10.1017/S0033291712001626. Epub 2012 Jul 31     [PubMed PMID: 22850401]

Level 2 (mid-level) evidence

[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. Schizophrenia bulletin. 2015 May:41(3):687-97. doi: 10.1093/schbul/sbu122. Epub 2014 Sep 12     [PubMed PMID: 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. Schizophrenia bulletin. 2018 Aug 20:44(5):1111-1122. doi: 10.1093/schbul/sbx161. Epub     [PubMed PMID: 29301025]

Level 1 (high-level) evidence

[37]

Saha S, Varghese D, Slade T, Degenhardt L, Mills K, McGrath J, Scott J. The association between trauma and delusional-like experiences. Psychiatry research. 2011 Sep 30:189(2):259-64. doi: 10.1016/j.psychres.2011.03.019. Epub 2011 Apr 27     [PubMed PMID: 21524800]

Level 2 (mid-level) evidence

[38]

Knorr R, Hoffmann K. [Delusions: current psychodynamic and neurocognitive approaches]. Der Nervenarzt. 2018 Jan:89(1):8-17. doi: 10.1007/s00115-017-0296-0. Epub     [PubMed PMID: 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. doi: 10.1186/s12888-017-1196-3. Epub 2017 Jan 24     [PubMed PMID: 28118821]


[40]

Varga ÉJ, Herold R, Tényi T. [Effect of culture to delusions: Introduction of the Truman Show delusion]. Psychiatria Hungarica : A Magyar Pszichiatriai Tarsasag tudomanyos folyoirata. 2016:31(4):359-363     [PubMed PMID: 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 investigation. 2012 Dec:9(4):319-24. doi: 10.4306/pi.2012.9.4.319. Epub 2012 Nov 12     [PubMed PMID: 23251194]


[42]

Kurtz MM. Symptoms versus neurocognitive skills as correlates of everyday functioning in severe mental illness. Expert review of neurotherapeutics. 2006 Jan:6(1):47-56     [PubMed PMID: 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. doi: 10.1186/s12888-020-2482-z. Epub 2020 Feb 10     [PubMed PMID: 32041577]

Level 2 (mid-level) evidence

[44]

Kumar D. Promoting insight into delusions: Issues and challenges in therapy. International journal of psychiatry in clinical practice. 2020 Jun:24(2):208-213. doi: 10.1080/13651501.2019.1711420. Epub 2020 Jan 11     [PubMed PMID: 31928095]


[45]

Bebbington P, Freeman D. Transdiagnostic Extension of Delusions: Schizophrenia and Beyond. Schizophrenia bulletin. 2017 Mar 1:43(2):273-282. doi: 10.1093/schbul/sbw191. Epub     [PubMed PMID: 28399309]


[46]

Cloak N, Schoo C, Al Khalili Y. Behavioral and Psychological Symptoms in Dementia. StatPearls. 2024 Jan:():     [PubMed PMID: 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 : a journal of neurology. 2020 Apr 1:143(4):1249-1260. doi: 10.1093/brain/awaa058. Epub     [PubMed PMID: 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. Annals of neurology. 2020 Jun:87(6):950-961. doi: 10.1002/ana.25739. Epub 2020 Apr 25     [PubMed PMID: 32281118]


[49]

Tampi RR, Young JJ, Tampi D. Behavioral symptomatology and psychopharmacology of Lewy body dementia. Handbook of clinical neurology. 2019:165():59-70. doi: 10.1016/B978-0-444-64012-3.00005-8. Epub     [PubMed PMID: 31727230]


[50]

Makarewich C, West DA. Charles Bonnet syndrome-induced psychosis? Visual hallucinations with paranoid delusions in a visually-impaired man. The Journal of neuropsychiatry and clinical neurosciences. 2011 Fall:23(4):E6. doi: 10.1176/jnp.23.4.jnpe6. Epub     [PubMed PMID: 22231350]

Level 3 (low-level) evidence

[51]

Hamedani AG, Pelak VS. The Charles Bonnet Syndrome: a Systematic Review of Diagnostic Criteria. Current treatment options in neurology. 2019 Jul 25:21(9):41. doi: 10.1007/s11940-019-0582-1. Epub 2019 Jul 25     [PubMed PMID: 31342218]

Level 1 (high-level) evidence

[52]

Bouvard MP, Mouren-Siméoni MC. [Prescription of neuroleptics for children]. L'Encephale. 1990 Sep-Oct:16(5):389-98     [PubMed PMID: 1979943]


[53]

Abou Kassm S, Naja W, Hoertel N, Limosin F. [Pharmacological management of delusions associated with dementia]. Geriatrie et psychologie neuropsychiatrie du vieillissement. 2019 Sep 1:17(3):317-326. doi: 10.1684/pnv.2019.0813. Epub     [PubMed PMID: 31449050]


[54]

Lally J, MacCabe JH. Antipsychotic medication in schizophrenia: a review. British medical bulletin. 2015 Jun:114(1):169-79. doi: 10.1093/bmb/ldv017. Epub 2015 May 8     [PubMed PMID: 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. The Journal of clinical psychiatry. 2007 Sep:68(9):1411-7     [PubMed PMID: 17915981]


[56]

Opjordsmoen S. Long-term course and outcome in unipolar affective and schizoaffective psychoses. Acta psychiatrica Scandinavica. 1989 Apr:79(4):317-26     [PubMed PMID: 2735203]

Level 2 (mid-level) evidence

[57]

Cipriani G, Vedovello M, Nuti A, di Fiorino A. Dangerous passion: Othello syndrome and dementia. Psychiatry and clinical neurosciences. 2012 Oct:66(6):467-73. doi: 10.1111/j.1440-1819.2012.02386.x. Epub     [PubMed PMID: 23066764]


[58]

Ivanov P, Moral Cuesta D, Perelló Alonso M. [Capgras syndrome: The delusion of impersonation]. Revista espanola de geriatria y gerontologia. 2018 May-Jun:53(3):173. doi: 10.1016/j.regg.2017.08.004. Epub 2017 Sep 28     [PubMed PMID: 28964547]


[59]

Coltheart M, Langdon R. Somatic delusions as motivated beliefs? The Australian and New Zealand journal of psychiatry. 2019 Jan:53(1):83-84. doi: 10.1177/0004867418815981. Epub 2018 Nov 22     [PubMed PMID: 30466300]


[60]

Kraft DP, Babigian HM. Somatic delusion or self-mutilation in a schizophrenic woman: a psychiatric emergency room case report. The American journal of psychiatry. 1972 Jan:128(7):893-5     [PubMed PMID: 5009271]

Level 3 (low-level) evidence

[61]

Brown RS Jr, Fischman A, Showalter CR. Primary hyperparathyroidism, hypercalcemia, paranoid delusions, homicide, and attempted murder. Journal of forensic sciences. 1987 Sep:32(5):1460-3     [PubMed PMID: 3668484]

Level 3 (low-level) evidence

[62]

Mottaghipour Y, Tabatabaee M. Family and Patient Psychoeducation for Severe Mental Disorder in Iran: A Review. Iranian journal of psychiatry. 2019 Jan:14(1):84-108     [PubMed PMID: 31114622]

Level 3 (low-level) evidence