User:Imr254/sandbox

-"Because there is no prescribed treatment, the first starting place is to reassure the CBS sufferer of their sanity, and some charities provide specialist hallucination counseling "buddies" (people who have had CBS, or have CBS and are no longer fazed by it) to talk to on the telephone" (copied from original wiki article. There is no citation for this...either take out or find citation for it? Also, do not like the wording "no longer fazed by it", sounds too informal. I'd change that to "...or have CBS and have found effective ways to manage the symptoms"

- the rest is all original content, no copied text

(adding to heading "History")

After Bonnet’s grandfather received bilateral cataract surgery, his vision evolved from slightly better to complete deterioration over time. It was around this period that his visual hallucinations started. Even though his health was in good shape and he had an absence of any psychiatric disorders, the source of the hallucinations remained unknown. At forty years old, Charles Bonnet himself suffered from an unrevealed cause of severe vision loss.

In 1967, French-Swiss neurologist, Georges de Morsier, coined the term Charles Bonnet Syndrome in Bonnet's honor.

(adding to "Causes")

Depending on the content, visual hallucinations can be classified as either simple or complex. By focusing on the specific type of visual hallucination, one may find an accurate diagnosis. 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. Functional magnetic resonance imaging (fMRI) of Charles Bonnet Syndrome patients display a relationship between visual hallucinations and activity in the ventral occipital lobe.

(adding to "Signs and Symptoms" or "Causes"..?)

Even though people of all ages may be impacted by Charles Bonnet Syndrome, those within the age range of seventy to eighty are primarily affected. Since CBS is not commonly recognized by clinicians, it oftentimes goes misdiagnosed and identified as psychosis, delirium, or dementia. As a result of this, it is estimated that almost 60% of CBS patients hesitate to notify their physicians.

Predominant factors correlated with CBS are a decrease of visual acuity, visual field loss, and elderly age. 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. Visual hallucinations generally appear when the eyes are open, fading once the visual gaze shifts. It is widely claimed that sensory deprivation is instrumental in the progression of CBS. During episodes of inactivity, hallucinations are more likely to occur. Majority of those suffering from CBS describe the duration of hallucinations to continue for up to a few minutes, multiple times a day or week. If a patient presents symptoms indicative of Charles Bonnet Syndrome, basic laboratory examinations like metabolic panel and blood count tests, as well as neuroimaging, may aid in an accurate diagnosis.

(making a new heading: "DBM Studies" or "Studies in Homeostasis" or "CBS and Homeostasis")

The Deep Boltzmann Machine (DBM) is a way of utilizing an undirected probabilistic process in a neural framework. Researchers argue that the DBM has the ability to model features of cortical learning and perception. This network captures differing angles of the visual cortex, the site at which visual hallucinations are conclusively recognized. Compelling evidence details the role homeostatic operations in the cortex play in stabilizing neuronal activity. Due to homeostasis, the deafferentiated cortex grows a heightened excitability. Therefore, an absence of visual input could potentially influence excitability changes in neurons. By using the DBM, some experimenters show that even when sensory input is scarce, these developments may trigger complex hallucinations.

A large proportion of those suffering from CBS develop the visual hallucinations as vision begins to deteriorate and stop hallucinating once vision is entirely gone. A long-term reorganization of the cortex’s structure to signify new input (like learning) may result in a cessation of hallucinations.

A few studies record that visual hallucinations are likely to be concentrated in the blind regions. Complex hallucinations may progress over time if the primary loss of vision is due to damage of the early cortical areas. If activation of the early cortical areas is suppressed when CBS symptoms have already been exhibited, hallucinations may temporarily terminate. A short-term change in the levels of feedforward and feedback flows of information may intensely affect the presence of hallucinations. In periods of drowsiness, CBS related hallucinations are more prone to arise. Disrupting cortical homeostatic processes after vision has been lost may prevent or setback the emergence of hallucinations. 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. Particularly in CBS, a shortage of acetylcholine at cortical locations should correspond to the onset of hallucinations. A few researchers proclaim that the main aspect of a visual hallucination model is not the generation of images, but the unprompted generation of highly detailed portrayals of images.