Editing Delusion (section)

==Pathophysiology==
The two-factor model of delusions posits that dysfunction in both belief formation systems and belief evaluation systems are necessary for delusions. Dysfunction in evaluations systems localized to the right lateral prefrontal cortex, regardless of delusion content, is supported by neuroimaging studies and is congruent with its role in conflict monitoring in healthy persons. Abnormal activation and reduced volume is seen in people with delusions, as well as in disorders associated with delusions such as [[frontotemporal dementia]], [[psychosis]] and [[Lewy body dementia]]. Furthermore, lesions to this region are associated with "jumping to conclusions", damage to this region is associated with post-stroke delusions, and hypometabolism this region associated with caudate strokes presenting with delusions.{{citation needed|date=April 2018}}

The [[aberrant salience]] model suggests that delusions are a result of people assigning excessive importance to irrelevant stimuli. In support of this hypothesis, regions normally associated with the [[salience network]] demonstrate reduced grey matter in people with delusions, and the neurotransmitter [[dopamine]], which is widely implicated in salience processing, is also widely implicated in psychotic disorders.{{citation needed|date=April 2018}}

Specific regions have been associated with specific types of delusions. The volume of the hippocampus and parahippocampus is related to paranoid delusions in [[Alzheimer's disease]], and has been reported to be abnormal post mortem in one person with delusions. [[Capgras delusion]]s have been associated with occipito-temporal damage and may be related to failure to elicit normal emotions or memories in response to faces.<ref>{{cite book| vauthors = Naasan G | veditors = Lehner T, Miller B, State M |title=Genomics, Circuits, and Pathways in Clinical Neuropsychiatry|publisher=Elsevier Science|pages=366–369|chapter=The Anatomy of Delusions}}</ref>