Editing Visual release hallucinations (section)

== Pathophysiology ==
[[File:Lawrence 1960 9.7.png|thumb|Anatomical illustration of neuroanatomy of human vision]]
There is no general consensus on the definition of CBS.<ref name=":0" /> Predominant factors correlated with CBS are a decrease of visual acuity, visual field loss, and elderly age.<ref name=":1" /> While characteristic features of visual hallucinations are not specifically linked to the anatomical site of the ocular injury, they usually match to the location of visual loss.<ref name=":1" /> The most commonly accepted theory for Charles Bonnet syndrome proposes that extreme visual impairment promotes sensory deafferentation, leading to disinhibition, thus resulting in sudden neural firings of the visual cortical regions.<ref name=":1" /> A few studies record that visual hallucinations are likely to be concentrated in the blind regions.<ref name=":2">{{Cite web |last1=Reichert |first1=David P. |last2=Series |first2=Peggy |last3=Storkey |first3=Amos J. |title=Hallucinations in Charles Bonnet Syndrome Induced by Homeostasis: a Deep Boltzmann Machine Model |url=https://papers.nips.cc/paper/4097-hallucinations-in-charles-bonnet-syndrome-induced-by-homeostasis-a-deep-boltzmann-machine-model.pdf |website=NIPS Proceedings |location=University of Edinburgh}}</ref> [[Functional magnetic resonance imaging]] (fMRI) of Charles Bonnet syndrome patients displays a relationship between visual hallucinations and activity in the ventral occipital lobe.<ref name=":1" /> A connection between [[Macular degeneration|age-related macular degeneration]] (AMD) and colored visual hallucinations has been presented.<ref name=":0" /> Color vision signals travel through the parvocellular layers of the [[lateral geniculate nucleus]] (LGN), later transmitting down the color regions of the ventral visual pathway.<ref name=":0" /> Due to cone photoreceptor damage located in the macula, there is a significant reduction of visual input to the visual association cortex, stirring endogenous activation in the color areas and thus leading to colored hallucinations.<ref name=":0" /> Patients with CBS alongside macular degeneration exhibit hyperactivity in the color areas of the visual association cortex (as shown in fMRIs).<ref name=":0" /> Those who have significant ocular disease yet maintain visual acuity may still be susceptible to CBS.<ref name=":0" />

The Deep [[Boltzmann machine|Boltzmann Machine]] (DBM) is a way of utilizing an undirected probabilistic process in a neural framework.<ref name=":2" /> Researchers argue that the DBM has the ability to model features of cortical learning, perception, and the visual cortex (the locus of visual hallucinations).<ref name=":2" /> Compelling evidence details the role homeostatic operations in the cortex play in regards to stabilizing neuronal activity.<ref name=":2" /> By using the DBM, researchers show that when sensory input is absent, neuron excitability is influenced, thus potentially triggering complex hallucinations.<ref name=":2" />

[[File:Acetylcholine Pathway.png|thumb|Acetylcholine pathway]]
A short-term change in the levels of feedforward and feedback flows of information may intensely affect the presence of hallucinations.<ref name=":2" /> In periods of drowsiness, CBS related hallucinations are more prone to arise.<ref name=":2" /> Disrupting cortical homeostatic processes after vision has been lost may prevent or setback the emergence of hallucinations.<ref name=":2" /> At varying stages of the cortical grading, [[acetylcholine]] (ACh) may impact the balance of thalamic and intracortical inputs as well as the balance in between bottom-up and top-down.<ref name=":2" /> Particularly in CBS, a shortage of acetylcholine at cortical locations should correspond to the onset of hallucinations.<ref name=":2" />

The syndrome can also develop after bilateral optic nerve damage due to methyl alcohol poisoning.<ref>{{Cite journal |last1=Olbrich |first1=H. M. |last2=Lodemann |first2=E |last3=Engelmeier |first3=M. P. |year=1987 |title=Optical hallucinations in the aged with diseases of the eye |journal=Zeitschrift für Gerontologie |volume=20 |issue=4 |pages=227–229 |pmid=3660920}}</ref>