Delusional disorder causes
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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.
Causes
The cause of delusional disorder is unknown, but genetic, biochemical and environmental factors may play a significant role in its development. There does seem to be some familial component, and social isolation, immigration (generally for persecutory reasons),[3] drug abuse, excessive stress,[12] being married, being employed, low socioeconomic status, celibacy among men, and widowhood among women may also be risk factors.[13] 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:
- Genetics
The relationship to the more severe psychosis is yet unclear. According to the DSM-5, on average, global function is generally better 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. Although it can occur in younger age groups, the condition is more prevalent in older individuals.[1]
- 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.[1][2]
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.[3] 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.[4]
- Psychological factors
It is suggested that persons with delusions selectively attend to available information, which appears to overlap with hypochondriacal patient populations.[5]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.[6]
- 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
- ↑ 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.
- ↑ 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). - ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.