Visual release hallucinations, also known as Charles Bonnet syndrome (CBS), are a type of psychophysical visual disturbance in which a person with partial or severe blindness experiences visual hallucinations. First described by Charles Bonnet in 1760, the term Charles Bonnet syndrome was first introduced into English-speaking psychiatry in 1982. A related type of hallucination that also occurs with lack of visual input is the closed-eye hallucination.
Signs and symptoms People with significant vision loss may have vivid recurrent visual hallucinations (fictive visual percepts). These can vary greatly in apparent size, sometimes "lilliputian" (smaller than normal) and, in other cases, enlarged or expansive, as when familiar environments appear to warp in scale. Depending on the content, hallucinations are classified as either simple or complex. Simple hallucinations often involve shapes, photopsias, and grid-like patterns. Complex hallucinations may depict silent, non-interactive figures, whether multitudes of people, animals, or surreal objects, that appear life-like, as well as highly detailed landscapes or objects. The most common hallucination is of faces or cartoons. Those affected understand that the hallucinations are not real, although in some cases, particularly when cognitive decline progresses, they may begin to perceive them as genuine. Hallucinations are purely visual, usually appearing when the eyes are open and fading once the visual gaze shifts. They are more likely to occur during periods of inactivity, and sensory deprivation is widely considered a contributing factor. Episodes typically last a few minutes and may recur several times a day or week. Even though people of all ages may be affected by Charles Bonnet syndrome, those within the age range of 70 to 80 are primarily affected. Among older adults (> 65 years) with significant vision loss, the prevalence of Charles Bonnet syndrome has been reported to be between 10% and 40%; a 2008 Australian study found the prevalence to be 17.5%. Two Asian studies, however, report a much lower prevalence. The high incidence of underreporting this disorder is the greatest hindrance to determining the exact prevalence. Underreporting is thought to be a result of those with the condition being afraid to discuss the symptoms out of fear that they will be labeled of unsound mind.
Pathophysiology
There is no general consensus on the definition of CBS. 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. 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. A few studies record that visual hallucinations are likely to be concentrated in the blind regions. 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. 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.
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