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Delusional disorder

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Synonyms and keywords: Delusional disorders; DD

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

Delusional disorder is a psychiatric condition in which the patients present with delusions, but with no accompanying prominent hallucinations, thought disorder, mood disorder, or significant flattening of affect. Delusions are a specific symptom of psychosis. Delusions can be bizarre or non-bizarre in content. Non-bizarre delusions are fixed false beliefs that involve situations that could potentially occur in real life, such as being followed, having an infection, being loved, and being deceived by one’s spouse. Bizarre delusions are clearly improbable. Delusions that express a loss of control over mind or body are generally considered to be bizarre and include belief that alien thoughts have been put into one’s mind, that one’s thoughts have been removed by an outside force, or that one’s body or actions are being acted on or manipulated by an outside force. Apart from their delusions, people with delusional disorder may continue to socialize and function in a normal manner and their behavior does not generally seem odd or bizarre. However, the preoccupation with delusional ideas can be disruptive to their overall lives. For the diagnosis to be made, auditory and visual hallucinations cannot be prominent, though olfactory or tactile hallucinations related to the content of the delusion may be present.[1] Delusions are false beliefs based on incorrect assumption about external reality that persist despite the evidence to the contrary and these beliefs are not ordinarily accepted by other members of the person’s culture. Delusional disorder may be classified according to Diagnostic and Statistical Manual based on content of the delusions into seven subtypes: erotomanic, grandiose, jealous, persecutory, somatic, mixed, and unspecified.[1][2] The exact pathogenesis of delusional disorder is not fully understood. It is thought that delusional disorder may be produced by polymorphisms in genes coding for dopamine receptors (DRD3 and DRD4). The cause of delusional disorder has not been identified. Genetic, biochemical, psychological, and environmental factors may play a significant role in the development of delusional disorder. Delusional disorder must be differentiated from other diseases that cause delusions, such as substrate deficiency, neurodegenerative disorders, vascular disease, other CNS disorders, infectious diseases, vitamin deficiencies, metabolic disorders, endocrinopathies, medications, toxins, substances, and other mental disorders such as schizophrenia and mood disorders. The incidence of delusional disorders is approximately 0.7 to 3.0 cases per 100, 000 individuals annually. The prevalence of delusional disorders is approximately 24 to 30 cases per 100, 000 individuals annually. Females are more commonly affected with delusional disorder than males.[1] The diagnosis of delusional disorder is based on the DSM-5 diagnostic criteria, which include criterion A i.e the presence of one (or more) delusions with a duration of one month or longer, criterion B i.e criterion A for schizophrenia has never been met, criterion C i.e apart from the impact of the delusion(s) or its ramifications, functioning is not markedly impaired, and behavior is not obviously bizarre or odd, criterion D i.e if manic or major depressive episodes have occurred, these have been brief relative to the duration of the delusional periods, and criterion E i.e the disturbance is not attributable to the physiological effects of a substance or another medical condition and is not better explained by another mental disorder, such as body dysmorphic disorder or obsessive-compulsive disorder.[2] The optimal therapy for delusional disorder includes pharmacotherapy, cognitive-behavioral therapy, supportive psychotherapy, involuntary treatment, and insight oriented therapy.

Historical Perspective

Delusional disorder was first introduced by Emil Kraepelin, a German Psychiatrist, in the year 1883. In the year 1977 Winokur redescribed paranoia under the name of delusional disorder. In the year 1987 delusional disorder was introduced in DSM-III-R and continued to be present in subsequent editions.[3][4][5]

Classification

Delusional disorder may be classified according to Diagnostic and Statistical Manual based on content of the delusions into seven subtypes: erotomanic, grandiose, jealous, persecutory, somatic, mixed, and unspecified.[1][6]

Pathophysiology

The exact pathogenesis of delusional disorder is not fully understood. It is thought that delusional disorder may be produced by polymorphisms in genes coding for dopamine receptors (DRD3 and DRD4).[7][8][9]

Causes

The cause of delusional disorder has not been identified. Genetic, biochemical, psychological, and environmental factors may play a significant role in the development of delusional disorder.[1][10][11][12][13][14][8]

Differential Diagnosis

Delusional disorder must be differentiated from other diseases that cause delusions, such as substrate deficiency, neurodegenerative disorders, vascular disease, other CNS disorders, infectious diseases, vitamin deficiencies, metabolic disorders, endocrinopathies, medications, toxins, substances, and other mental disorders such as schizophrenia and mood disorders.[15][16][17]

Epidemiology and Demographics

The incidence of delusional disorders is approximately 0.7 to 3.0 cases per 100, 000 individuals annually. The prevalence of delusional disorders is approximately 24 to 30 cases per 100, 000 individuals annually. Females are more commonly affected with delusional disorder than males.[1]

Comorbid Conditions

Common comorbid conditions associated with delusional disorder include depression and anxiety.[18][19][20][21]

Risk Factors

Common risk factors in the development of delusional disorder are family history of paranoid personality disorder, sensory impairment, middle age (18-40 years), social isolation, personality (sensitivity; narcissistic traits), immigration, and low socioeconomic status.[22][23][24][25][26][27][28]

Screening

According to the United States Preventive Services Task Force, screening for delusional disorder is not recommended.[29]

Natural History, Complications and Prognosis

If left untreated, delusional disorder may progress to develop life-long illness. Common complications of delusional disorder include depression, violence and legal problems, and isolation. The prognosis for people with delusional disorder varies depending on the type of delusional disorder, on the person, and the person’s life circumstances, including the availability of support and a willingness to adhere with treatment.[30][31][32]

Diagnostic Criteria

The diagnosis of delusional disorder is based on the DSM-5 diagnostic criteria, which include 5 citeria:[2]

  • Criterion A: Presence of one (or more) delusions with a duration of one month or longer
  • Criterion B: Diagnostic criteria for schizophrenia have not been met
  • Criterion C: Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly impaired, and behavior is not obviously bizarre or odd,
  • Criterion D: If manic or major depressive episodes have occurred, these have been brief relative to the duration of the delusional periods
  • Criterion E: The disturbance is not attributable to the physiological effects of a substance or another medical condition and is not better explained by another mental disorder, such as body dysmorphic disorder or obsessive-compulsive disorder

History and Symptoms

The hallmark of delusional disorder is non-bizarre delusions. A positive history of self-reference, aggressiveness, irritable, angry, or low mood and hallucinations that are related to the delusion is suggestive of delusional disorder.[1][33][26][34][35]

Physical Examination

Patients with delusional disorder usually appear well groomed and well-dressed without evidence of gross impairment. Mental status examination of patients with delusional disorder is usually remarkable for dysphoria, delusional beliefs, and suicidal or violent thinking.[1]

Laboratory Findings

There are no diagnostic lab findings associated with delusional disorder.

Chest-X Ray

There are no chest-x ray findings associated with delusional disorder.

CT

There are no CT findings associated with delusional disorder.

MRI

On MRI, delusional disorder is characterized by greater lateral ventricle volume and hyper intense MRI signals in deep white matter in temporal and frontal lobes.

Other Imaging Findings

There are no other imaging findings associated with delusional disorder.

Other Diagnostic Studies

There are no other diagnostic studies associated with delusional disorder.

Medical Therapy

The optimal therapy for delusional disorder includes pharmacotherapy, cognitive-behavioral therapy, supportive psychotherapy, involuntary treatment, and insight oriented therapy.[36][37][38][39][40][41][42][43][1]

Primary Prevention

There are no primary preventive measures available for delusional disorder.

Secondary Prevention

There are no secondary preventive measures available for delusional disorder.

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015
  2. 2.0 2.1 2.2 American Psychiatric Association.Diagnostic and Statistical Manual of Mental Disorders (DSM-5®). American Psychiatric Pub, 2013.
  3. Munro, Alistair. Delusional disorder paranoia and related illnesses. Cambridge New York: Cambridge University Press, 1999. Print.
  4. Grover, Sandeep, Nitin Gupta, and Surendra Kumar Mattoo. “Delusional disorders: An overview.” German J Psychiatry 9 (2006): 62-73.
  5. Winokur, George, and Ming T. Tsuang. The natural history of mania, depression, and schizophrenia. Washington, DC: American Psychiatric Press, 1996. Print.
  6. American Psychiatric Association.Diagnostic and Statistical Manual of Mental Disorders (DSM-5®). American Psychiatric Pub, 2013.
  7. Hales, Robert E., Stuart C. Yudofsky, and Laura W. Roberts. The American Psychiatric Publishing textbook of psychiatry. Washington, DC: American Psychiatric Publishing, 2014. Print.
  8. 8.0 8.1 Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H (2002). “Delusional disorder: molecular genetic evidence for dopamine psychosis”. Neuropsychopharmacology. 26 (6): 794–801. doi:10.1016/S0893-133X(01)00421-3. PMID 12007750.
  9. Huber M, Kirchler E, Karner M, Pycha R (2007). “Delusional parasitosis and the dopamine transporter. A new insight of etiology?”. Med Hypotheses. 68 (6): 1351–8. doi:10.1016/j.mehy.2006.07.061. PMID 17134847.
  10. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
  11. Conway CR, Bollini AM, Graham BG, Keefe RS, Schiffman SS, McEvoy JP (2002). “Sensory acuity and reasoning in delusional disorder”. Compr Psychiatry. 43 (3): 175–8. PMID 11994833.
  12. Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
  13. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  14. Gorman DG, Cummings JL (1990). “Organic delusional syndrome”. Semin Neurol. 10 (3): 229–38. doi:10.1055/s-2008-1041273. PMID [ 2259800 [ Check |pmid= value (help).
  15. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  16. Manschreck TC, Petri M (1978). “The paranoid syndrome”. Lancet. 2 (8083): 251–3. PMID 79043.
  17. Manschreck, THEO C. “Delusional disorder and shared psychotic disorder.” Comprehensive textbook of psychiatry 1 (2000): 1243-64.
  18. de Portugal E, Martínez C, González N, del Amo V, Haro JM, Cervilla JA (2011). “Clinical and cognitive correlates of psychiatric comorbidity in delusional disorder outpatients”. Aust N Z J Psychiatry. 45 (5): 416–25. doi:10.3109/00048674.2010.551279. PMID 21417554.
  19. Maina G, Albert U, Badà A, Bogetto F (2001). “Occurrence and clinical correlates of psychiatric co-morbidity in delusional disorder”. Eur Psychiatry. 16 (4): 222–8. PMID 11418272.
  20. Marino C, Nobile M, Bellodi L, Smeraldi E (1993). “Delusional disorder and mood disorder: can they coexist?”. Psychopathology. 26 (2): 53–61. PMID 8321893.
  21. Hsiao MC, Liu CY, Yang YY, Yeh EK (1999). “Delusional disorder: retrospective analysis of 86 Chinese outpatients”. Psychiatry Clin Neurosci. 53 (6): 673–6. doi:10.1046/j.1440-1819.1999.00624.x. PMID 10687749.
  22. Thewissen V, Myin-Germeys I, Bentall R, de Graaf R, Vollebergh W, van Os J (2005). “Hearing impairment and psychosis revisited”. Schizophr Res. 76 (1): 99–103. doi:10.1016/j.schres.2004.10.013. PMID 15927803.
  23. Munro A, Mok H (1995). “An overview of treatment in paranoia/delusional disorder”. Can J Psychiatry. 40 (10): 616–22. PMID 8681259.
  24. Munro, Alistair. Delusional disorder paranoia and related illnesses. Cambridge New York: Cambridge University Press, 1999. Print.
  25. Kendler KS, Walsh D (1995). “Schizophreniform disorder, delusional disorder and psychotic disorder not otherwise specified: clinical features, outcome and familial psychopathology”. Acta Psychiatr Scand. 91 (6): 370–8. PMID 7676834.
  26. 26.0 26.1 de Portugal E, González N, Haro JM, Autonell J, Cervilla JA (2008). “A descriptive case-register study of delusional disorder”. Eur Psychiatry. 23 (2): 125–33. doi:10.1016/j.eurpsy.2007.10.001. PMID 18082379.
  27. Kendler KS, Masterson CC, Davis KL (1985). “Psychiatric illness in first-degree relatives of patients with paranoid psychosis, schizophrenia and medical illness”. Br J Psychiatry. 147: 524–31. PMID 4075047.
  28. Fujii, Daryl, and Iqbal Ahmed. The Spectrum of Psychotic Disorders Neurobiology, Etiology & Pathogenesis. City: Cambridge Univ Pr, 2012. Print.
  29. http://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=delusional+disorder Accessed on December 10, 2015.
  30. Grover, Sandeep, Nitin Gupta, and Surendra Kumar Mattoo. “Delusional disorders: An overview.” German J Psychiatry 9 (2006): 62-73.
  31. Fujii, Daryl, and Iqbal Ahmed, eds. The spectrum of psychotic disorders: Neurobiology, Etiology & Pathogenesis. Cambridge University Press, 2007.
  32. Sadock, Benjamin J., and Virginia A. Sadock. Kaplan and Sadock’s synopsis of psychiatry: Behavioral sciences/clinical psychiatry. Lippincott Williams & Wilkins, 2011.
  33. Manschreck TC (1996). “Delusional disorder: the recognition and management of paranoia”. J Clin Psychiatry. 57 Suppl 3: 32–8, discussion 49. PMID 8626368.
  34. Ramos N, Wystrach C, Bolton M, Shaywitz J, IsHak WW (2013). “Delusional disorder, somatic type: olfactory reference syndrome in a patient with delusional trimethylaminuria”. J Nerv Ment Dis. 201 (6): 537–8. doi:10.1097/NMD.0b013e31829482fd. PMID 23719328.
  35. Reid WH (2005). “Delusional disorder and the law”. J Psychiatr Pract. 11 (2): 126–30. PMID 15803048.
  36. Freudenmann RW, Lepping P (2008). “Second-generation antipsychotics in primary and secondary delusional parasitosis: outcome and efficacy”. J Clin Psychopharmacol. 28 (5): 500–8. doi:10.1097/JCP.0b013e318185e774. PMID 18794644.
  37. Freudenmann RW, Schönfeldt-Lecuona C, Lepping P (2007). “Primary delusional parasitosis treated with olanzapine”. Int Psychogeriatr. 19 (6): 1161–8. doi:10.1017/S1041610207004814. PMID 17397562.
  38. Manschreck TC, Khan NL (2006). “Recent advances in the treatment of delusional disorder”. Can J Psychiatry. 51 (2): 114–9. PMID 16989110.
  39. Hayashi H, Oshino S, Ishikawa J, Kawakatsu S, Otani K (2004). “Paroxetine treatment of delusional disorder, somatic type”. Hum Psychopharmacol. 19 (5): 351–2, 1p following 352. doi:10.1002/hup.590. PMID 15252828.
  40. Sondheimer A (1988). “Clomipramine treatment of delusional disorder-somatic type”. J Am Acad Child Adolesc Psychiatry. 27 (2): 188–92. PMID 3360722.
  41. Wada T, Kawakatsu S, Nadaoka T, Okuyama N, Otani K (1999). “Clomipramine treatment of delusional disorder, somatic type”. Int Clin Psychopharmacol. 14 (3): 181–3. PMID 10435772.
  42. Nagata T, van Vliet I, Yamada H, Kataoka K, Iketani T, Kiriike N (2006). “An open trial of paroxetine for the “offensive subtype” of taijin kyofusho and social anxiety disorder”. Depress Anxiety. 23 (3): 168–74. doi:10.1002/da.20153. PMID 16456863.
  43. Ota M, Mizukami K, Katano T, Sato S, Takeda T, Asada T (2003). “A case of delusional disorder, somatic type with remarkable improvement of clinical symptoms and single photon emission computed tomograpy findings following modified electroconvulsive therapy”. Prog Neuropsychopharmacol Biol Psychiatry. 27 (5): 881–4. doi:10.1016/S0278-5846(03)00118-0. PMID 12921924.

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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

Delusional disorder was first introduced by Emil Kraepelin, a German psychiatrist, in the year 1883. In the year 1977 Winokur redescribed paranoia under the name of delusional disorder. In the year 1987 delusional disorder was introduced in DSM-III-R and continued to be present in subsequent editions.[1][2][3]

Historical Perspective

  • The concept of paranoia has been used for centuries while the term of delusional disorder was only coined in 1977.
  • The word paranoia comes from Greek para, meaning along side, and noos or nous, meaning intelligence, mind. The Greeks used the term “paranoia” to describe any mental abnormality similar to how we use the word insanity. The term reappeared in the 17th century, in the modern world, and it was largely used as a generic name for mental illness.
  • In the year 1863, Karl Kahlbaum introduced the concept of paranoia as a separate mental illness: “a form of partial insanity, which throughout the course of the disease principally affected the sphere of the intellect”. He even used this term to describe an illness with persistent delusions and stable course. He noted that delusions may occur in other medical and psychiatric conditions.
  • Later Emil Kraepelin, continued to work on defining the concept of paranoia, which is reflected in several editions of his famous textbook and most closely resembles the modern definition of delusional disorder. Kraepelin viewed paranoia as uncommon, chronic condition different from dementia praecox by the presence of fixed, nonbizarre delusions, preserved thought process, lack of deterioration over time, and relatively slight involvement of affect and volition. Kraepelin described that delusions of paranoia, contrary to the delusions of dementia praecox, are relatively consistent, well systemized, and often related to real-life events. He identified grandiose, persecutory, jealous, erotomanic, and possibly hypochondriacal types of that disorder. He believed that the illness derived from the deficit in the patients’ judgments caused by environmental stress and constitutional factors.
  • Eugen Bleuler continued to recognize paranoia as a separate disorder and included hallucinations in its description (Fennig, 2005; Munro, 1999). After Kraepelin’s death, Kurt Kolle (1931) reported a detailed follow-up of 66 cases seen in Kraepelin’s former clinic in Munch (Munro, 1999). He noted a pattern of deterioration and concluded that paranoia represents a form of schizophrenia. This view continued to be popular in the psychiatric community for several decades and was reflected in DSM-I and DSM-II. Winokur (1977) had redescribed paranoia under the name of delusional disorder basing his findings on Kraepelin’s definition and the observation of case types. Additionally, Kendler (1980) and Munro (1982) substantially contributed to the current understanding of medicine of this illness.
  • In 1987, delusional disorder was introduced in DSM-III-R and continued to be present in subsequent editions.[4][5][6]

References

  1. Munro, Alistair. Delusional disorder paranoia and related illnesses. Cambridge New York: Cambridge University Press, 1999. Print.
  2. Grover, Sandeep, Nitin Gupta, and Surendra Kumar Mattoo. “Delusional disorders: An overview.” German J Psychiatry 9 (2006): 62-73.
  3. Winokur, George, and Ming T. Tsuang. The natural history of mania, depression, and schizophrenia. Washington, DC: American Psychiatric Press, 1996. Print.
  4. Munro, Alistair. Delusional disorder paranoia and related illnesses. Cambridge New York: Cambridge University Press, 1999. Print.
  5. Grover, Sandeep, Nitin Gupta, and Surendra Kumar Mattoo. “Delusional disorders: An overview.” German J Psychiatry 9 (2006): 62-73.
  6. Winokur, George, and Ming T. Tsuang. The natural history of mania, depression, and schizophrenia. Washington, DC: American Psychiatric Press, 1996. Print.


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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

Delusional disorder may be classified according to Diagnostic and Statistical Manual based on content of the delusions into seven subtypes: erotomanic, grandiose, jealous, persecutory, somatic, mixed, and unspecified.[1][2]

Classification

Diagnosis of a specific type of delusional disorder can sometimes be made based on the content of the delusions. The Diagnostic and Statistical Manual of Mental Disorders (DSM) enumerates seven types:[1][3]

Subtypes of delusional disorder Description
Erotomanic
  • The patient believes that another person is secretly in love with her or him.
  • The person which patient believes is in love may be famous or have some kind of higher status, usually not part of the patient’s social circle, and not likely to be attainable.
  • Affected individuals may attempt to communicate with the object of their affection and may attempt to meet him/her in person. Such effort can lead to stalking in some cases, with some risk for assaultive behavior.
  • Expressions of love may be intense, and rejections by the loved person is interpreted oddly as affirmations of love to deflect suspicions or jealousy from the loved person’s spouse. Other names of erotomanic delusional disorder: DeClerambault syndrome, erotomania, psychose passionelle.
Grandiose
  • The patient believes he/she has special prominence or talent, major achievements, or unusual fame.
  • Features of the patient’s thinking may suggest the grandiosity associated with mania, however in the delusional disorder, the mood disturbance and behaviors characteristic of mania are not present.
Jealous
  • The delusional theme is the patient believes that a spouse or lover is unfaithful and finds “evidence” to support the delusion, accuses him or her, and relentlessly tries to substantiate the offense.
  • The delusion of jealousy can lead to aggressive, possibly violent, and threatening behavior, including homicide and suicide. In some cases delusional jealousy and its disruptive impact may only improve through separation from the suspected unfaithful partner. Other names of jealous delusional disorder: pathological or morbid jealousy, Othello syndrome, conjugal paranoia.
Persecutory
  • The patient is typically preoccupied by a delusion that he or she is being persecuted, potentially harmed, or conspired against.
  • His/her resulting actions are generally consistent with these concerns; they are well planned and executed, and carried out with emotional vigor and determined effort.
  • The individuals with persecutory delusions may resort to the courts and even to violence to right the wrongs directed at them.
Somatic
  • The patient believes that something awful is wrong with his/her body. There are several forms: that one is ill with undiagnosed disease; that one is infested with parasites or insects (delusional parasitosis); or that parts of the body are ugly, misshapen, or emanate a foul odor.
  • Individuals generally go from one doctor to another, specialist to specialist, usually disappointed by the failure to detect and diagnose the medical problem that haunts them. Suicide may be a risk, thought due to frustration and lack of effective clinical intervention. Other names of somatic delusional disorder: hypochondriacal delusion, monosymptomatic hypochondriasis.
Mixed
  • More than one delusional theme predominates.
Unspecified
  • The dominant delusional belief cannot be clearly determined or is not described by the subtypes above.
  • Other notable differences between the DSM-IV and DSM-5 diagnostic criteria are a clearer demarcation of delusional disorder in DSM-5 from psychotic variants of obsessive compulsive disorder and body dysmorphic disorder that is made explicit with a new exclusion criterion. Such a presentation must not be better explained by obsessive compulsive or body dysmorphic disorder with lack of insight/delusional beliefs.
  • Shared delusional disorder is no longer separated from delusional disorder as in DSM-IV. If the criteria for delusional disorder are met, delusional disorder is the appropriate diagnosis. If that diagnosis cannot be made yet shared delusional beliefs are present, the appropriate diagnosis is “other specified schizophrenia spectrum and other psychotic disorder.”
  • Among them persecutory and jealous subtypes are the most common, and erotomanic and grandiose are the least common.[4][5][6][7][8]

References

  1. 1.0 1.1 Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015
  2. American Psychiatric Association.Diagnostic and Statistical Manual of Mental Disorders (DSM-5®). American Psychiatric Pub, 2013.
  3. American Psychiatric Association.Diagnostic and Statistical Manual of Mental Disorders (DSM-5®). American Psychiatric Pub, 2013.
  4. de Portugal E, Martínez C, González N, del Amo V, Haro JM, Cervilla JA (2011). “Clinical and cognitive correlates of psychiatric comorbidity in delusional disorder outpatients”. Aust N Z J Psychiatry. 45 (5): 416–25. doi:10.3109/00048674.2010.551279. PMID 21417554.
  5. Kelly BD (2005). “Erotomania : epidemiology and management”. CNS Drugs. 19 (8): 657–69. PMID 16097848.
  6. de Portugal E, González N, Miriam V, Haro JM, Usall J, Cervilla JA (2010). “Gender differences in delusional disorder: Evidence from an outpatient sample”. Psychiatry Res. 177 (1–2): 235–9. doi:10.1016/j.psychres.2010.02.017. PMID 20334930.
  7. Munro, Alistair. Delusional disorder paranoia and related illnesses. Cambridge New York: Cambridge University Press, 1999. Print.
  8. Manschreck, THEO C. “Delusional disorder and shared psychotic disorder.” Comprehensive textbook of psychiatry 1 (2000): 1243-64.


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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

The exact pathogenesis of delusional disorder is not fully understood. It is thought that delusional disorder may be produced by polymorphisms in genes coding for dopamine receptors (DRD3 and DRD4).[1][2][3]

Pathophysiology

  • The pathophysiology of delusional disorder remains unknown, although some preliminary evidence indicates that polymorphisms in genes coding for dopamine receptors (DRD3 and DRD4) are associated with the disorder. Most delusional disorder patients experience the delusional belief as “ego-syntonic” which means that the delusional thought is experienced as consistent with patient’s expectations, sense of reality and self of self in general.[4]
  • Hypothesis proposes decreased striatal dopamine transporter functioning as a cause of primary and secondary causes of delusional parasitosis. Evidence has pointed that genetic predisposition to a selective D2 receptor-related hyperdopaminergia, and to dopamine neurotransmitter dysfunction investigations suggesting that delusional disorder may be a more purely D2-related psychotic condition than more common psychoses. Another hypothesis proposes decreased striatal dopamine transporter functioning as a cause of primary and secondary cases of delusional parasitosis.[2][3].
  • Evidence has also suggested that delusional symptoms are preferentially associated with disorders involving the basal ganglia and limbic system. Approximately fifty percent of patients with idiopathic basal ganglia calcifications and with Huntington’s disease developed delusions at some point of their illness. Head trauma has also been associated with development of delusions.[5][6]
  • The neurological conditions most commonly associated with delusions affect the limbic system and the basal ganglia. Patients whose delusions are caused by neurological diseases and who show no intellectual impairment tend to have complex delusions similar to those in patients with delusional disorder. Contrarily, patients with neurological disorder with intellectual impairments often have simple delusions unlike those in patients with delusional disorder. This suggests that delusional disorder may involve the limbic system or basal ganglia in patients who have intact cerebral cortical functioning.[7]

References

  1. Hales, Robert E., Stuart C. Yudofsky, and Laura W. Roberts. The American Psychiatric Publishing textbook of psychiatry. Washington, DC: American Psychiatric Publishing, 2014. Print.
  2. 2.0 2.1 Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H (2002). “Delusional disorder: molecular genetic evidence for dopamine psychosis”. Neuropsychopharmacology. 26 (6): 794–801. doi:10.1016/S0893-133X(01)00421-3. PMID 12007750.
  3. 3.0 3.1 Huber M, Kirchler E, Karner M, Pycha R (2007). “Delusional parasitosis and the dopamine transporter. A new insight of etiology?”. Med Hypotheses. 68 (6): 1351–8. doi:10.1016/j.mehy.2006.07.061. PMID 17134847.
  4. Hales, Robert E., Stuart C. Yudofsky, and Laura W. Roberts. The American Psychiatric Publishing textbook of psychiatry. Washington, DC: American Psychiatric Publishing, 2014. Print.
  5. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  6. Koponen S, Taiminen T, Portin R, Himanen L, Isoniemi H, Heinonen H; et al. (2002). “Axis I and II psychiatric disorders after traumatic brain injury: a 30-year follow-up study”. Am J Psychiatry. 159 (8): 1315–21. doi:10.1176/appi.ajp.159.8.1315. PMID 12153823. Review in: Evid Based Ment Health. 2003 May;6(2):59
  7. Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.


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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

The cause of delusional disorder has not been identified. Genetic, biochemical, psychological, and environmental factors may play a significant role in the development of delusional disorder.[1][2][3][4][5][6][7]

Causes

The cause of delusional disorder is unknown, but genetic, biochemical, psychological, and environmental factors may play a significant role in its development. Delusional disorder is currently thought to be on the same spectrum or dimension as schizophrenia, but people with delusional disorder, in general, may have less symptomatology and functional disability. The etiology of delusional disorder is unknown, and several difficulties exist in conducting research in this area:[1][8]

Genetics

  • According to the DSM-5, on an average, global function is generally better in delusional disorder than that observed in schizophrenia. Although the diagnosis is generally stable, a proportion of individuals go on to develop schizophrenia. Delusional disorder has a significant familial relationship with both schizophrenia and schizotypal personality disorder.[9]
  • There might be a genetic factor involved in the development of delusional disorder, which is suggested by the fact that delusional disorder is more common in people who have family members with delusional disorder or paranoid personality traits. It is also believed that, as with other mental disorders, a tendency to develop delusional disorder might be passed on from parents to their children. Close relatives of persons with delusional disorder do not have higher rates of schizophrenia, schizoaffective disorder or mood disorder compared to relatives of non-delusional persons.
  • Studies comparing activity of different regions of the brain in delusional and non-delusional research participants have yielded data about differences in the functioning of the brains between members of the two groups. These differences in brain activity propose that persons neurologically with delusions tend to react as if threatening conditions are consistently present whereas non-delusional persons only show such patterns under certain kinds of conditions where the interpretation of being threatened is more accurate. With the evidence of brain activity and family heritability, a strong chance exists that there is a biological aspect to delusional disorder.[10][11][6][7]
  • Some studies have found that compared with normal participants, patients with delusional disorder showed abnormalities of voluntary saccadic eye movements and smooth pursuit eye movements, a dysfunction similar to that seen in patients with schizophrenia.[12]

Biochemical factors

  • Biological factors may play a role in the development of delusional disorder, as delusions are associated with a wide range of nonpsychiatric medical conditions. Among patients with neurologic disorders such as head injury, dementia, and seizures, problems with the basal ganglia and temporal lobe are most commonly associated with delusions.[13][6]
  • Some people with delusional disorders may have an imbalance in neurotransmitters, the chemicals that send and receive messages to the brain. Hyperdopaminergic states have been implicated in the development of delusions. In some studies an increased prevalence of a polymorphism at the D2 receptor gene at amino acid 311 (cysteine-for-serine substitution) among individuals with delusional disorder have been reported, particularly in those with persecutory delusions.
  • Individuals that had more TCAT repeats within the first intron of the tyrosine hydroxylase gene had higher levels of homovanillic acid, although it is unclear if they corrected for multiple statistical comparisons.[7] Some studies have found that compared with normal participants, patients with delusional disorder showed abnormalities of voluntary saccadic eye movements and smooth pursuit eye movements, a dysfunction similar to that seen in patients with schizophrenia.[12]

Environmental factors

Evidence suggests that delusional disorder can be triggered by stress. Alcohol and drug abuse also might contribute to the condition. People who tend to be isolated, such as immigrants or those with poor sight and hearing, appear to be more vulnerable to developing delusional disorder.

Psychological factors

It is suggested that persons with delusions selectively attend to available information, which appears to overlap with hypochondriacal patient populations.[14] They attribute negative events to external personal causes, make conclusions based on insufficient information, and have difficulty in envisaging others’ intentions and motivations. Patients with delusional disorder make probability decisions based on fewer data compared with normal controls. Despite using fewer data, they are as certain as controls regarding the accuracy of their decisions.[3]

  • The two neuropsychological models proposed for schizophrenia may also have some validity in delusional disorder.
    • A cognitive bias model (CBM) proposes that paranoia is a defense to protect a fragile self-esteem, against thoughts that threaten the idealized self. Positive events are attributed to the self whereas negative events are ascribed to the external environment.
    • The cognitive deficit model (CDM) focuses on cognitive impairments and distortions of threat evaluating mechanisms as the cause for delusion formation.

References

  1. 1.0 1.1 Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015
  2. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
  3. 3.0 3.1 Conway CR, Bollini AM, Graham BG, Keefe RS, Schiffman SS, McEvoy JP (2002). “Sensory acuity and reasoning in delusional disorder”. Compr Psychiatry. 43 (3): 175–8. PMID 11994833.
  4. Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
  5. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  6. 6.0 6.1 6.2 Gorman DG, Cummings JL (1990). “Organic delusional syndrome”. Semin Neurol. 10 (3): 229–38. doi:10.1055/s-2008-1041273. PMID [ 2259800 [ Check |pmid= value (help).
  7. 7.0 7.1 7.2 Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H (2002). “Delusional disorder: molecular genetic evidence for dopamine psychosis”. Neuropsychopharmacology. 26 (6): 794–801. doi:10.1016/S0893-133X(01)00421-3. PMID 12007750.
  8. Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
  9. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
  10. Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
  11. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  12. 12.0 12.1 Campana A, Gambini O, Scarone S (1998). “Delusional disorder and eye tracking dysfunction: preliminary evidence of biological and clinical heterogeneity”. Schizophr Res. 30 (1): 51–8. PMID 9542788.
  13. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  14. Xiong, Glen L; Bourgeois, James A; Chang, Celia H; Liu, Dandan; Hilty, Donald M (2007). “Hypochondriasis: common presentations and treatment strategies in primary care and specialty settings”. Therapy. 4 (3): 323–338. doi:10.2217/14750708.4.3.323. ISSN 1475-0708.


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Differentiating Delusional Disorder from Other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

Delusional disorder must be differentiated from other diseases that cause delusions, such as substrate deficiency, neurodegenerative disorders, vascular disease, other CNS disorders, infectious diseases, vitamin deficiencies, metabolic disorders, endocrinopathies, medications, toxins, substances, and other mental disorders such as schizophrenia and mood disorders.[1][2][3]

Differential Diagnosis

The cases of primary delusional disorder are uncommon. The occurrence of delusional thinking has many sources, mostly secondary to other conditions. Hence a practical principle is to detect or rule out other possible, usually more common causes of delusions, before arriving at the diagnosis.[4][2] These include the following:

Medical conditions associated with development of delusions is shown below in a tabular form:[5]

Medical Conditions Examples
Substrate deficiency
  • Hypoglycemia*
  • Cerebral hypoxia* causes of cerebral hypoxia include cardiac insufficiency, pulmonary insufficiency, and severe anemia.
Neurodegenerative disorders
  • Alzheimer disease
  • Pick disease
  • Huntington disease
  • Parkinson Disease
  • Basal ganglia calcification (Fahr disease)
  • Multiple sclerosis
  • Metachromatic leukodystrophy
Vascular disease
  • Atherosclerotic vascular disease, especially when associated with diffuse, temporoparietal, or subcortical lesions
  • Hypertensive encephalopathy
  • Subarachnoid hemorrhage
  • Temporal arteritis
Infectious disease
  • Human immunodeficiency virus/acquired immune deficiency syndrome (AIDS)
  • Opportunistic infections in AIDS
  • Encephalitis lethargica
  • Creutzfeldt-Jakob disease
  • Syphilis
  • Malaria
  • Acute viral encephalitis
Other CNS disorders
  • Brain tumors, especially temporal lobe and deep hemispheric tumors
  • Epilepsy, especially complex partial seizure disorder, temporal lobe epilepsy
  • Stroke*
  • Brain abscess*
  • CNS infection (meningitis, encephalitis)*
  • Interictal psychosis
  • Head trauma (subdural hematoma)*
  • Anoxic brain injury
  • Fat embolism
  • Landau Kleffner syndrome
  • SSPE*
Vitamin deficiences
  • Vitamin B-12 deficiency
  • Folate deficiency
  • Thiamine deficiency
  • Niacin deficiency
Metabolic disorder
  • Hypercalcemia
  • Hyponatremia
  • Hypoglycemia
  • Uremia
  • Hepatic encephalopathy
  • Porphyria
  • Electrolyte disturbance*Δ
  • Hepatic failure*
  • Postpartum psychosis*
Endocrinopathies
  • Addison disease
  • Cushing syndrome
  • Hyperthyroidism or hypothyroidism
  • Panhypopituitarism
  • Hashimoto thyroiditis (Hashimoto encephalopathy)
  • Thyroid storm*
  • Antiphospholipid syndrome
  • Hashimoto thyroiditis (Hashimoto encephalopathy)
Medications
  • Analgesics such as meperidine, pentazocine, indomethacin
  • Adrenocorticotropic hormones
  • Anabolic steroids such as testosterone, methyltestosterone
  • Anticholinergics such as atropine, scopolamine
  • Antidepressants such as bupropion, others if triggering a manic switch
  • Antiepileptics such as zonisamide, other anticonvulsants at high doses
  • antimalarial such as mefloquine, chloroquine
  • Anti-parkinsonian drugs such as levodopa, selegiline, amantadine, pramipexole, bromocriptine
  • Antivirals such as abacavir, efavirenz, nevirapine, acyclovir
  • Cardiovascular drugs such as digoxin, disopyramide, propafenone, quinidine
  • Corticosteroids such as prednisone, dexamethasone, etc
  • Inhalants such as toluene, butane, gasoline
  • Interferons such as interferon alfa-2a/2b
  • Over-the-counter (OTC) such as dextromethorphan (DXM), diphenhydramine, some decongestants
  • Cimetidine
  • Antibiotics (eg, cephalosporins, penicillin), disulfiram
Toxins
  • Carbon monoxide
  • Organophosphates
  • Heavy metals (eg, arsenic, manganese, mercury, thallium)
Other

Systemic lupus erythematosus

Substances
  • Amphetamines
  • Cannabinoids such as marijuana, synthetic cannabinoids (ie, “spice”), dronabinol
  • Alcohol and sedatives/hypnotics such as alcohol (intoxication or withdrawal), barbiturates and benzodiazepines (particularly withdrawal)
  • Cannabis
  • Stimulants such as cocaine, amphetamine/methamphetamine, methylphenidate, certain diet pills, “bath salts” (MDPV, mephedrone), MDMA/ecstasy
  • Hallucinogens such as LSD, PCP (phencyclidine), ketamine, psilocybin-containing mushrooms, mescaline, synthetic “designer drugs” (eg, 2-CB, “N-Bomb” [25I-NBOMe]) , salvia divinorum
  • Differential Diagnoses for delusional disorder (Adapted from Manschreck, 1996) [6]
Disorder Delusions Hallucinations Awareness Other features
Delusional disorder Present Occasional Alert Relatively free of psychopathology
Psychotic disorder due to a general medical condition, with delusion Present Present May be impaired Cognitive changes; perceptual changes;substance abuse history; impairment of functioning frequent
Substance-induced psychotic disorder Present (can be bizarre) Present Acute:impaired,Chronic:may be alert History of substance abuse; impaired functioning likely
Schizophrenia Present (bizarre) Present Alert Emotional changes, pervasive thought disorder; role impairment
Major depressive episode Present (usually mood congruent) May or may not present Alert Concerted changes in mood and neurovegetative features
Manic Episode Present (usually mood congruent) May or may not present Alert Concerted changes in mood, decreased need for sleep, energy, lack of inhibition
Obsessive–Compulsive disorder Not present Not present Alert Not psychotic; impaired functioning likely
Personality disorder Not present Not present Alert Not psychotic
Somatoform disorder Not present Not present Alert Not psychotic
Shared psychotic disorder Present Not present Alert Close associate has same delusions

References

  1. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  2. 2.0 2.1 Manschreck TC, Petri M (1978). “The paranoid syndrome”. Lancet. 2 (8083): 251–3. PMID 79043.
  3. Manschreck, THEO C. “Delusional disorder and shared psychotic disorder.” Comprehensive textbook of psychiatry 1 (2000): 1243-64.
  4. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  5. Sadock, Benjamin J., Harold I. Kaplan, and Virginia A. Sadock. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolter Kluwer/Lippincott Williams & Wilkins, 2007. Print.
  6. Manschreck, THEO C. “Delusional disorder and shared psychotic disorder.” Comprehensive textbook of psychiatry 1 (2000): 1243-64.


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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

The incidence of delusional disorders is approximately 0.7 to 3.0 cases per 100, 000 individuals annually. According to DSM-5 the prevalence of delusional disorder in the United States is estimated to be approximately 24-30 cases per 100, 000 individuals (0.02%), which is considerably lower than the prevalence of mood disorders (5%) and schizophrenia (1%). Females are more commonly affected with delusional disorder than males. Age at onset ranges from 18–90 years, with a mean age of 40 years.[1]

Epidemiology and Demographics

  • Delusional disorder accounts for approximately 1-2% of admissions to inpatient mental health facilities. The incidence of first admissions for delusional disorder is approximately 0.001-0.003%. The lifetime morbid risk of delusional disorder has been estimated to range from 0.05 to 0.1 percent.[2]
  • According to DSM-5, the estimated lifetime prevalence of delusional disorder is 0.2 percent, which is far lower than the estimated lifetime prevalence for other major psychotic disorders such as schizophrenia and bipolar I disorder with lifetime prevalence of 0.3 to 0.87 percent and 0.24 to 0.6 percent respectively.[3][4][2][5]
  • Approximate rates of delusional disorder reported in samples of patients receiving mental health treatment have ranged from 0.5 to 1.2 percent. As the majority of people with delusional disorder do not regard it as an illness or receive treatment, studies likely underestimate the prevalence of the disorder. Delusional disorders are uncommon in psychiatric practice, though this may be an underestimation due to the fact that those afflicted lack insight and thus avoid psychiatric assessment.

Incidence

The incidence of delusional disorders is approximately 0.7 to 3.0 cases per 100, 000 individuals annually.[1]

Prevalence

According to DSM-5 the prevalence of delusional disorder in the United States is estimated to be approximately 0.02%, which is considerably lower than the prevalence of mood disorders (5%) and schizophrenia (1%).[6][7]

Gender

Females are more commonly affected with delusional disorder than males. The female-to-male ratio is approximately 2 to 1 (range: 1.18-3 to 1).

  • Women are more likely than men to develop delusions of eromantia whereas men are more likely than women to develop paranoid delusions.[8][9][2]

Age

Delusional disorder commonly affects individuals in middle to late adult life. First admissions to hospital for delusional disorder occur between age 33 and 55 years of age. Age at onset ranges from 18–90 years, with a mean age of 40 years.[10]

References

  1. 1.0 1.1 Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015
  2. 2.0 2.1 2.2 Kendler KS (1982). “Demography of paranoid psychosis (delusional disorder): a review and comparison with schizophrenia and affective illness”. Arch Gen Psychiatry. 39 (8): 890–902. PMID 7103678.
  3. Perälä J, Suvisaari J, Saarni SI, Kuoppasalmi K, Isometsä E, Pirkola S; et al. (2007). “Lifetime prevalence of psychotic and bipolar I disorders in a general population”. Arch Gen Psychiatry. 64 (1): 19–28. doi:10.1001/archpsyc.64.1.19. PMID 17199051. Review in: Evid Based Ment Health. 2007 Aug;10(3):96
  4. Desk reference to the diagnostic criteria from DSM-5. Washington, DC: American Psychiatric Publishing, 2013. Print.
  5. Yamada N, Nakajima S, Noguchi T (1998). “Age at onset of delusional disorder is dependent on the delusional theme”. Acta Psychiatr Scand. 97 (2): 122–4. PMID 9517905.
  6. Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
  7. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
  8. Kelly BD (2005). “Erotomania : epidemiology and management”. CNS Drugs. 19 (8): 657–69. PMID 16097848.
  9. Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
  10. Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.


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Comorbid Conditions

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

Common comorbid conditions associated with delusional disorder include depression and anxiety.[1][2][3][4]

Comorbid Conditions

The psychiatric comorbidity rates of 35 to 72 percent have been found in small studies of patients with delusional disorder. The most commonly observed co-occurring condition is depression, but anxiety can also be a significant factor. Patients with the persecutory subtype of delusional disorder were most likely to have a mood disorder.[1][2][3][4]

References

  1. 1.0 1.1 de Portugal E, Martínez C, González N, del Amo V, Haro JM, Cervilla JA (2011). “Clinical and cognitive correlates of psychiatric comorbidity in delusional disorder outpatients”. Aust N Z J Psychiatry. 45 (5): 416–25. doi:10.3109/00048674.2010.551279. PMID 21417554.
  2. 2.0 2.1 Maina G, Albert U, Badà A, Bogetto F (2001). “Occurrence and clinical correlates of psychiatric co-morbidity in delusional disorder”. Eur Psychiatry. 16 (4): 222–8. PMID 11418272.
  3. 3.0 3.1 Marino C, Nobile M, Bellodi L, Smeraldi E (1993). “Delusional disorder and mood disorder: can they coexist?”. Psychopathology. 26 (2): 53–61. PMID 8321893.
  4. 4.0 4.1 Hsiao MC, Liu CY, Yang YY, Yeh EK (1999). “Delusional disorder: retrospective analysis of 86 Chinese outpatients”. Psychiatry Clin Neurosci. 53 (6): 673–6. doi:10.1046/j.1440-1819.1999.00624.x. PMID 10687749.


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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

Common risk factors in the development of delusional disorder are family history of paranoid personality disorder, sensory impairment, age, subtle brain abnormality, social isolation, personality (sensitivity; narcissistic traits), immigration, lower socioeconomic status.[1][2][3][4][5][6][7]

Risk Factors

Risk factors for delusional disorder include the following:[1][2][8][4][5][6][9]

  • Family history of paranoid personality disorder
  • Age (34-45 years)
  • Subtle brain abnormality (e.g, head trauma)
  • Social isolation
  • Personality (sensitivity; narcissistic traits)
  • Sensory impairment
  • Immigration
  • Lower socioeconomic status
  • Drug abuse
  • Excessive stress
  • Celibacy among men
  • Widowhood among women

References

  1. 1.0 1.1 Thewissen V, Myin-Germeys I, Bentall R, de Graaf R, Vollebergh W, van Os J (2005). “Hearing impairment and psychosis revisited”. Schizophr Res. 76 (1): 99–103. doi:10.1016/j.schres.2004.10.013. PMID 15927803.
  2. 2.0 2.1 Munro A, Mok H (1995). “An overview of treatment in paranoia/delusional disorder”. Can J Psychiatry. 40 (10): 616–22. PMID 8681259.
  3. Munro, Alistair. Delusional disorder paranoia and related illnesses. Cambridge New York: Cambridge University Press, 1999. Print.
  4. 4.0 4.1 Kendler KS, Walsh D (1995). “Schizophreniform disorder, delusional disorder and psychotic disorder not otherwise specified: clinical features, outcome and familial psychopathology”. Acta Psychiatr Scand. 91 (6): 370–8. PMID 7676834.
  5. 5.0 5.1 de Portugal E, González N, Haro JM, Autonell J, Cervilla JA (2008). “A descriptive case-register study of delusional disorder”. Eur Psychiatry. 23 (2): 125–33. doi:10.1016/j.eurpsy.2007.10.001. PMID 18082379.
  6. 6.0 6.1 Kendler KS, Masterson CC, Davis KL (1985). “Psychiatric illness in first-degree relatives of patients with paranoid psychosis, schizophrenia and medical illness”. Br J Psychiatry. 147: 524–31. PMID 4075047.
  7. Fujii, Daryl, and Iqbal Ahmed. The Spectrum of Psychotic Disorders Neurobiology, Etiology & Pathogenesis. City: Cambridge Univ Pr, 2012. Print.
  8. Munro, Alistair. Delusional disorder paranoia and related illnesses. Cambridge New York: Cambridge University Press, 1999. Print.
  9. Fujii, Daryl, and Iqbal Ahmed. The Spectrum of Psychotic Disorders Neurobiology, Etiology & Pathogenesis. City: Cambridge Univ Pr, 2012. Print.

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Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

According to the United States Preventive Services Task Force, screening for delusional disorder is not recommended.[1]

Screening

According to the United States Preventive Services Task Force, screening for delusional disorder is not recommended.[1]

References


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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

If left untreated, delusional disorder may progress to develop life-long illness. Common complications of delusional disorder include depression, violence and legal problems, and isolation. The prognosis for people with delusional disorder varies depending on the type of delusional disorder, on the person, and the person’s life circumstances, including the availability of support and a willingness to adhere with treatment.[1][2][3]

Natural History

  • The onset of delusional disorder can be acute, sudden, or less commonly the disorder develops gradually. If the onset is acute, it is usually associated with the presence of a precipitating event. Some clinicians and some research data indicate that an identifiable psychosocial stressor often accompanies the onset of delusional disorder. However, the nature of the stressor, warrant some suspicion or concern. Examples of such stressors are recent immigration, social conflict with family members or friends, and social isolation.
  • A sudden onset is more common than insidious onset. Clinicians believe that a person with delusional disorder is likely to have a below-average intelligence and the premorbid personality of such a person is likely to be extroverted, dominant and hypersensitive. Delusions are often the initial manifestation of the delusional disorder, but some premorbid traits which include odd behavior and personality changes, have been reported in some cases.
  • Chronic forms of the illness, that is, patients who present with features of the illness that have been present for more than six months, tend to have onset, early in the fifth decade.
  • Onset is generally acute in two-thirds of cases, and more gradual in the remainder. Chronicity develops in nearly 10%, and a relapsing course is seen in 37%. An acute and earlier onset of illness predicts a more favorable outcome For acute forms of the illness the age of onset is in the fourth decade and recovery occurs in over half of the cases.
  • Delusional disorder is commonly a chronic condition, but if properly treated, the majority of people with this disorder can find relief from their symptoms. Some people recover completely from delusional disorders and others experience episodes of delusional beliefs with periods of remission. Delusional disorder is generally a disabling illness.
  • The available studies on outcome in delusional disorder have shown the re-diagnoses of 3-8% as affective illness and 3-28% as schizophrenia: in others-the diagnosis was stable. The condition often disrupts progress to occupational and personal goals; patients with the delusional disorder typically achieve less in their lives than their innate abilities would propound. However, the clinical course can be influenced by the availability of personal support, personal circumstances such as education, socioeconomic status, and physical health, and willingness to maintain treatment. The other psychosocial abilities usually remain intact in patients with delusional disorders.
  • The majority of the individuals with delusional disorders may rarely seek psychiatric help, remain isolated, and often present to surgeons, internists, policemen, and lawyers rather than psychiatrists. The majority of people with the delusional disorders do not seek help. Without treatment, delusional disorder can be a life-long illness.[4][5][6]

Complications

Complications of delusional disorder include the following:

  • Depression
  • Acting on the delusions may lead to violence or legal problems
  • People with the delusional disorder can eventually become isolated from others, especially if their delusions interfere with their relationships
  • Based on several small studies, rates of suicidal ideation and behavior in patients with delusional disorder, may be greater than in patients without psychiatric disorders and comparable to rates seen in patients with schizophrenia. Individuals afflicted with somatic and persecutory delusions are more likely than other subtypes to report suicidality.[7]

Prognosis

  • The prognosis for people with delusional disorder varies depending on the type of delusional disorder, on the person, and the person’s life circumstances, including the availability of support and a willingness to adhere with treatment. The majority of people with the delusional disorder do not seek help. Without treatment, delusional disorder can be a life-long illness.
  • In approximately two-thirds of cases, the course of the delusional disorder is life-long, with delusions present continuously in some cases and periodically in others cases. In approximately one-third of cases spontaneous remission of delusional disorder is reported. The diagnostic stability of delusional disorder is usually less than that of some psychotic disorders. The most frequent change is re diagnosis of delusional disorder to schizophrenia. Data has suggested that patients with delusional disorders have a better global outcome than patients with schizophrenia.
  • Patients with persecutory, somatic, and erotic delusions have a better prognosis than patients with grandiose and jealous delusions.[8][9][10]
  • Approximately 10% of delusional disorder cases will show some improvement of delusional symptoms though irrational beliefs may remain. Approximately 33–50% of delusional disorder cases may show complete remission. In 30–40% of cases there will be persistent non-improving symptoms. The prognosis for patients with delusional disorder is largely related to the openness the person has for allowing information that contradicts the delusion and to the level of conviction regarding the delusions.[11][12][13]

Poor prognostic features of delusional disorder include the following:

  • Reclusive personality
  • Poor premorbid history
  • Onset 6 months or more before admission
  • Gradual onset
  • Lack of insight
  • Single marital status
  • Lack of precipitating factors for delusional disorder.

Good prognostic features of delusional disorder include the following:

  • High level of occupational, emotional and functional adjustments
  • Female sex
  • Onset before the age of 30
  • Sudden onset
  • Short duration of the illness
  • The presence of precipitating factors

References

  1. Grover, Sandeep, Nitin Gupta, and Surendra Kumar Mattoo. “Delusional disorders: An overview.” German J Psychiatry 9 (2006): 62-73.
  2. Fujii, Daryl, and Iqbal Ahmed, eds. The spectrum of psychotic disorders: Neurobiology, Etiology & Pathogenesis. Cambridge University Press, 2007.
  3. Sadock, Benjamin J., and Virginia A. Sadock. Kaplan and Sadock’s synopsis of psychiatry: Behavioral sciences/clinical psychiatry. Lippincott Williams & Wilkins, 2011.
  4. Opjordsmoen S (1988). “Long-term course and outcome in delusional disorder”. Acta Psychiatr Scand. 78 (5): 576–86. PMID 3232535.
  5. Craddock, N. (2008). “The Spectrum of Psychotic Disorders: Neurobiology, Etiology and Pathogenesis”. The British Journal of Psychiatry. 192 (6): 478–478. doi:10.1192/bjp.bp.107.039578. ISSN 0007-1250.
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  12. Fujii, Daryl, and Iqbal Ahmed, eds. The spectrum of psychotic disorders: Neurobiology, Etiology & Pathogenesis. Cambridge University Press, 2007.
  13. Sadock, Benjamin J., and Virginia A. Sadock. Kaplan and Sadock’s synopsis of psychiatry: Behavioral sciences/clinical psychiatry. Lippincott Williams & Wilkins, 2011.

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Diagnosis

Diagnosis

Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | Chest X Ray | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case#1

References

References

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