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==Overview== | ==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.<ref name="wiki"> Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015</ref><ref> Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.</ref><ref name="pmid11994833">{{cite journal| author=Conway CR, Bollini AM, Graham BG, Keefe RS, Schiffman SS, McEvoy JP| title=Sensory acuity and reasoning in delusional disorder. | journal=Compr Psychiatry | year= 2002 | volume= 43 | issue= 3 | pages= 175-8 | pmid=11994833 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11994833 }} </ref><ref>Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.</ref><ref>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.</ref><ref name="pmid2259800 [">{{cite journal| author=Gorman DG, Cummings JL| title=Organic delusional syndrome. | journal=Semin Neurol | year= 1990 | volume= 10 | issue= 3 | pages= 229-38 | pmid=2259800 [ | doi=10.1055/s-2008-1041273 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2259800 }} </ref><ref name="pmid12007750">{{cite journal| author=Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H| title=Delusional disorder: molecular genetic evidence for dopamine psychosis. | journal=Neuropsychopharmacology | year= 2002 | volume= 26 | issue= 6 | pages= 794-801 | pmid=12007750 | doi=10.1016/S0893-133X(01)00421-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12007750 }} </ref> | 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.<ref name="wiki"> Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015</ref><ref> Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.</ref><ref name="pmid11994833">{{cite journal| author=Conway CR, Bollini AM, Graham BG, Keefe RS, Schiffman SS, McEvoy JP| title=Sensory acuity and reasoning in delusional disorder. | journal=Compr Psychiatry | year= 2002 | volume= 43 | issue= 3 | pages= 175-8 | pmid=11994833 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11994833 }} </ref><ref>Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.</ref><ref>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.</ref><ref name="pmid2259800 [">{{cite journal| author=Gorman DG, Cummings JL| title=Organic delusional syndrome. | journal=Semin Neurol | year= 1990 | volume= 10 | issue= 3 | pages= 229-38 | pmid=2259800 [ | doi=10.1055/s-2008-1041273 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2259800 }} </ref><ref name="pmid12007750">{{cite journal| author=Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H| title=Delusional disorder: molecular genetic evidence for dopamine psychosis. | journal=Neuropsychopharmacology | year= 2002 | volume= 26 | issue= 6 | pages= 794-801 | pmid=12007750 | doi=10.1016/S0893-133X(01)00421-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12007750 }} </ref> | ||
==Causes== | ==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:<ref name="wiki"> Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015</ref ><ref>Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.</ref> | 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:<ref name="wiki"> Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015</ref ><ref>Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.</ref> | ||
===Genetics=== | ===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.<ref> Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.</ref> 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.<ref>Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.</ref><ref>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.</ref><ref name="pmid2259800 [">{{cite journal| author=Gorman DG, Cummings JL| title=Organic delusional syndrome. | journal=Semin Neurol | year= 1990 | volume= 10 | issue= 3 | pages= 229-38 | pmid=2259800 [ | doi=10.1055/s-2008-1041273 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2259800 }} </ref><ref name="pmid12007750">{{cite journal| author=Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H| title=Delusional disorder: molecular genetic evidence for dopamine psychosis. | journal=Neuropsychopharmacology | year= 2002 | volume= 26 | issue= 6 | pages= 794-801 | pmid=12007750 | doi=10.1016/S0893-133X(01)00421-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12007750 }} </ref> 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.<ref name="pmid9542788">{{cite journal| author=Campana A, Gambini O, Scarone S| title=Delusional disorder and eye tracking dysfunction: preliminary evidence of biological and clinical heterogeneity. | journal=Schizophr Res | year= 1998 | volume= 30 | issue= 1 | pages= 51-8 | pmid=9542788 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9542788 }} </ref> | *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]].<ref> Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.</ref> | ||
*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.<ref>Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.</ref><ref>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.</ref><ref name="pmid2259800 [">{{cite journal| author=Gorman DG, Cummings JL| title=Organic delusional syndrome. | journal=Semin Neurol | year= 1990 | volume= 10 | issue= 3 | pages= 229-38 | pmid=2259800 [ | doi=10.1055/s-2008-1041273 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2259800 }} </ref><ref name="pmid12007750">{{cite journal| author=Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H| title=Delusional disorder: molecular genetic evidence for dopamine psychosis. | journal=Neuropsychopharmacology | year= 2002 | volume= 26 | issue= 6 | pages= 794-801 | pmid=12007750 | doi=10.1016/S0893-133X(01)00421-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12007750 }} </ref> | |||
*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.<ref name="pmid9542788">{{cite journal| author=Campana A, Gambini O, Scarone S| title=Delusional disorder and eye tracking dysfunction: preliminary evidence of biological and clinical heterogeneity. | journal=Schizophr Res | year= 1998 | volume= 30 | issue= 1 | pages= 51-8 | pmid=9542788 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9542788 }} </ref> | |||
===Biochemical factors=== | ===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.<ref>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.</ref><ref name="pmid2259800 [">{{cite journal| author=Gorman DG, Cummings JL| title=Organic delusional syndrome. | journal=Semin Neurol | year= 1990 | volume= 10 | issue= 3 | pages= 229-38 | pmid=2259800 [ | doi=10.1055/s-2008-1041273 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2259800 }} </ref> | *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.<ref>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.</ref><ref name="pmid2259800 [">{{cite journal| author=Gorman DG, Cummings JL| title=Organic delusional syndrome. | journal=Semin Neurol | year= 1990 | volume= 10 | issue= 3 | pages= 229-38 | pmid=2259800 [ | doi=10.1055/s-2008-1041273 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2259800 }} </ref> | ||
*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.<ref name="pmid12007750">{{cite journal| author=Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H| title=Delusional disorder: molecular genetic evidence for dopamine psychosis. | journal=Neuropsychopharmacology | year= 2002 | volume= 26 | issue= 6 | pages= 794-801 | pmid=12007750 | doi=10.1016/S0893-133X(01)00421-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12007750 }} </ref> 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.<ref name="pmid9542788">{{cite journal| author=Campana A, Gambini O, Scarone S| title=Delusional disorder and eye tracking dysfunction: preliminary evidence of biological and clinical heterogeneity. | journal=Schizophr Res | year= 1998 | volume= 30 | issue= 1 | pages= 51-8 | pmid=9542788 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9542788 }} </ref> | *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.<ref name="pmid12007750">{{cite journal| author=Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H| title=Delusional disorder: molecular genetic evidence for dopamine psychosis. | journal=Neuropsychopharmacology | year= 2002 | volume= 26 | issue= 6 | pages= 794-801 | pmid=12007750 | doi=10.1016/S0893-133X(01)00421-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12007750 }} </ref> 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]].<ref name="pmid9542788">{{cite journal| author=Campana A, Gambini O, Scarone S| title=Delusional disorder and eye tracking dysfunction: preliminary evidence of biological and clinical heterogeneity. | journal=Schizophr Res | year= 1998 | volume= 30 | issue= 1 | pages= 51-8 | pmid=9542788 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9542788 }} </ref> | |||
===Environmental factors=== | ===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. | 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=== | ===Psychological factors=== | ||
It is suggested that persons with delusions selectively attend to available information, which appears to overlap with hypochondriacal patient populations.<ref name="XiongBourgeois2007">{{cite journal|last1=Xiong|first1=Glen L|last2=Bourgeois|first2=James A|last3=Chang|first3=Celia H|last4=Liu|first4=Dandan|last5=Hilty|first5=Donald M|title=Hypochondriasis: common presentations and treatment strategies in primary care and specialty settings|journal=Therapy|volume=4|issue=3|year=2007|pages=323–338|issn=1475-0708|doi=10.2217/14750708.4.3.323}}</ref>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.<ref name="pmid11994833">{{cite journal| author=Conway CR, Bollini AM, Graham BG, Keefe RS, Schiffman SS, McEvoy JP| title=Sensory acuity and reasoning in delusional disorder. | journal=Compr Psychiatry | year= 2002 | volume= 43 | issue= 3 | pages= 175-8 | pmid=11994833 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11994833 }} </ref> | It is suggested that persons with delusions selectively attend to available information, which appears to overlap with hypochondriacal patient populations.<ref name="XiongBourgeois2007">{{cite journal|last1=Xiong|first1=Glen L|last2=Bourgeois|first2=James A|last3=Chang|first3=Celia H|last4=Liu|first4=Dandan|last5=Hilty|first5=Donald M|title=Hypochondriasis: common presentations and treatment strategies in primary care and specialty settings|journal=Therapy|volume=4|issue=3|year=2007|pages=323–338|issn=1475-0708|doi=10.2217/14750708.4.3.323}}</ref> 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.<ref name="pmid11994833">{{cite journal| author=Conway CR, Bollini AM, Graham BG, Keefe RS, Schiffman SS, McEvoy JP| title=Sensory acuity and reasoning in delusional disorder. | journal=Compr Psychiatry | year= 2002 | volume= 43 | issue= 3 | pages= 175-8 | pmid=11994833 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11994833 }} </ref> | ||
*The two neuropsychological models proposed for schizophrenia may also have some validity in delusional disorder. | *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. | **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. | **The cognitive deficit model (CDM) focuses on cognitive impairments and distortions of threat evaluating mechanisms as the cause for delusion formation. | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Latest revision as of 18:31, 11 December 2015
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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]
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
- ↑ 1.0 1.1 Delusional disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Delusional_disorder Accessed on November 30, 2015
- ↑ Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
- ↑ 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.
- ↑ Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
- ↑ 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.
- ↑ 6.0 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). - ↑ 7.0 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.
- ↑ Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
- ↑ Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
- ↑ Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.
- ↑ 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.
- ↑ 12.0 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.
- ↑ 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.
- ↑ 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.