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.The syndrome can also develop after bilateral optic nerve damage due to methyl alcohol poisoning. Diagnosis
A variety of disciplines including optometry, ophthalmology, geriatric medicine, psychiatry, and neurology play a part in securing the diagnosis of CBS. Since CBS is not commonly recognized by all 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. By focusing on the specific type of visual hallucination, one may find an accurate diagnosis. 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. Prognosis
There is no treatment of proven effectiveness for CBS. For those experiencing CBS, knowing that they are suffering from this syndrome and not a mental illness seems to be the most comforting treatment so far, as it improves their ability to cope with the hallucinations.
Functional magnetic resonance imaging (fMRI) of Charles Bonnet Syndrome patients displays a relationship between visual hallucinations and activity in the ventral occipital lobe. A connection between age-related macular degeneration (AMD) and colored visual hallucinations has been presented. 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. 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. Patients with CBS alongside macular degeneration exhibit hyperactivity in the color areas of the visual association cortex (as shown in fMRIs). Those who have significant ocular disease yet maintain visual acuity may still be susceptible to CBS.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, perception, and the visual cortex (the locus of visual hallucinations). Compelling evidence details the role homeostatic operations in the cortex play in regards to stabilizing neuronal activity. By using the DBM, researchers show that when sensory input is absent, neuron excitability is influenced, thus potentially triggering complex hallucinations. 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.