Delusional disorder pathophysiology
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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 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).
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.[1] 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 disease developed delusions at some point of their illness. Head trauma has also been associated with development of delusions. [4][5] 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.[6]
References
- ↑ Hales, Robert E., Stuart C. Yudofsky, and Laura W. Roberts. The American Psychiatric Publishing textbook of psychiatry. Washington, DC: American Psychiatric Publishing, 2014. Print.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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
- ↑ Sadock, Benjamin J., Virginia A. Sadock, and Pedro Ruiz. Kaplan & Sadock's synopsis of psychiatry : behavioral sciences/clinical psychiatry. Philadelphia: Wolters Kluwer, 2015. Print.