Editing Hallucination (section)

==Pathophysiology==

===Dopaminergic and serotonergic hallucinations===
It has been reported that in serotonergic hallucinations, the person maintains an awareness that they are hallucinating, unlike dopaminergic hallucinations.<ref name="newrev2018"/>

===Neuroanatomy===

Hallucinations are associated with structural and functional abnormalities in primary and secondary sensory cortices. Reduced grey matter in regions of the [[superior temporal gyrus]]/[[middle temporal gyrus]], including [[Broca's area]], is associated with auditory hallucinations as a trait, while acute hallucinations are associated with increased activity in the same regions along with the [[hippocampus]], [[parahippocampus]], and the right hemispheric homologue of Broca's area in the inferior frontal gyrus.<ref name="Brown">{{cite book |doi=10.1007/7854_2010_54 |chapter=Functional Brain Imaging in Schizophrenia: Selected Results and Methods |title=Behavioral Neurobiology of Schizophrenia and Its Treatment |series=Current Topics in Behavioral Neurosciences |date=2010 |volume=4 |pages=181–214 |pmid=21312401 |isbn=978-3-642-13716-7 | vauthors = Brown GG, Thompson WK }}</ref> Grey and white matter abnormalities in visual regions are associated with hallucinations in diseases such as [[Alzheimer's disease]], further supporting the notion of dysfunction in sensory regions underlying hallucinations.<ref>{{cite journal | vauthors = El Haj M, Roche J, Jardri R, Kapogiannis D, Gallouj K, Antoine P | title = Clinical and neurocognitive aspects of hallucinations in Alzheimer's disease | journal = Neuroscience and Biobehavioral Reviews | volume = 83 | pages = 713–720 | date = December 2017 | pmid = 28235545 | pmc = 5565710 | doi = 10.1016/j.neubiorev.2017.02.021 }}</ref>

One proposed model of hallucinations posits that over-activity in sensory regions, which is normally attributed to internal sources via feedforward networks to the inferior frontal gyrus, is interpreted as originating externally due to abnormal connectivity or functionality of the feedforward network.<ref name="Brown"/> This is supported by cognitive studies of those with hallucinations, who have demonstrated abnormal attribution of self generated stimuli.<ref>{{cite journal | vauthors = Boksa P | title = On the neurobiology of hallucinations | journal = Journal of Psychiatry & Neuroscience | volume = 34 | issue = 4 | pages = 260–262 | date = July 2009 | pmid = 19568476 | pmc = 2702442 }}</ref>

Disruptions in thalamocortical circuitry may underlie the observed top down and bottom up dysfunction.<ref>{{cite journal | vauthors = Kumar S, Soren S, Chaudhury S | title = Hallucinations: Etiology and clinical implications | journal = Industrial Psychiatry Journal | volume = 18 | issue = 2 | pages = 119–126 | date = July 2009 | pmid = 21180490 | pmc = 2996210 | doi = 10.4103/0972-6748.62273 | doi-access = free }}</ref> Thalamocortical circuits, composed of projections between thalamic and cortical neurons and adjacent interneurons, underlie certain electrophysical characteristics ([[gamma oscillations]]) that are associated with sensory processing. Cortical inputs to thalamic neurons enable attentional modulation of sensory neurons. Dysfunction in sensory afferents, and abnormal cortical input may result in pre-existing expectations modulating sensory experience, potentially resulting in the generation of hallucinations. Hallucinations are associated with less accurate sensory processing, and more intense stimuli with less interference are necessary for accurate processing and the appearance of gamma oscillations (called "gamma synchrony"). Hallucinations are also associated with the absence of reduction in P50 amplitude in response to the presentation of a second stimuli after an initial stimulus; this is thought to represent failure to gate sensory stimuli, and can be exacerbated by [[dopamine]] release agents.<ref>{{cite journal | vauthors = Behrendt RP | title = Dysregulation of thalamic sensory "transmission" in schizophrenia: neurochemical vulnerability to hallucinations | journal = Journal of Psychopharmacology | volume = 20 | issue = 3 | pages = 356–372 | date = May 2006 | pmid = 16174672 | doi = 10.1177/0269881105057696 | s2cid = 17104995 }}</ref>

Abnormal assignment of salience to stimuli may be one mechanism of hallucinations. Dysfunctional dopamine signaling may lead to abnormal top down regulation of sensory processing, allowing expectations to distort sensory input.<ref>{{cite book| vauthors = Aleman A, Vercammon A | veditors = Jardri R, Cachia A, Pins D, Thomas P |title=The Neuroscience of Hallucinations|publisher=Springer|chapter=The Bottom Up and Top Down Components of Hallucinatory Phenomenon}}</ref>