Visual release hallucinations

Last updated
Visual release hallucinations
Other namesCharles Bonnet syndrome (CBS)
Specialty Psychiatry, ophthalmology, optometry, neurology
Diagnostic method Psychosis, delirium, or dementia [1]

Visual release hallucinations, also known as Charles Bonnet syndrome or CBS, are a type of psychophysical visual disturbance in which a person with partial or severe blindness experiences visual hallucinations.

Contents

First described by Charles Bonnet in 1760, [2] [3] the term Charles Bonnet syndrome was first introduced into English-speaking psychiatry in 1982. [4] 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). [1] One characteristic of these hallucinations is that they usually are "lilliputian" (hallucinations in which the characters or objects are smaller than normal). [5] Depending on the content, visual hallucinations can be classified as either simple or complex. [1] Simple visual hallucinations are commonly characterized by shapes, photopsias, and grid-like patterns. [6] Complex visual hallucinations consist of highly detailed representations of people and objects. [6] The most common hallucination is of faces or cartoons. [7] Those affected understand that the hallucinations are not real, and the hallucinations are only visual, that is, they do not occur in any other senses (such as hearing, smell or taste). [8] [9] Visual hallucinations generally appear when the eyes are open, fading once the visual gaze shifts. [1] It is widely claimed that sensory deprivation is instrumental in the progression of CBS. [10] During episodes of inactivity, hallucinations are more likely to occur. [1] The majority of those with CBS describe the duration of hallucinations to continue for up to a few minutes, multiple times a day or week. [1]

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. [1] 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%. [3] Two Asian studies, however, report a much lower prevalence. [11] [12] The high incidence of underreporting this disorder is the greatest hindrance to determining the exact prevalence. [9] 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. [9]

Pathophysiology

Anatomical illustration of neuroanatomy of human vision Lawrence 1960 9.7.png
Anatomical illustration of neuroanatomy of human vision

There is no general consensus on the definition of CBS. [6] Predominant factors correlated with CBS are a decrease of visual acuity, visual field loss, and elderly age. [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. [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. [1] A few studies record that visual hallucinations are likely to be concentrated in the blind regions. [10] Functional magnetic resonance imaging (fMRI) of Charles Bonnet syndrome patients displays a relationship between visual hallucinations and activity in the ventral occipital lobe. [1] A connection between age-related macular degeneration (AMD) and colored visual hallucinations has been presented. [6] 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. [6] 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. [6] Patients with CBS alongside macular degeneration exhibit hyperactivity in the color areas of the visual association cortex (as shown in fMRIs). [6] Those who have significant ocular disease yet maintain visual acuity may still be susceptible to CBS. [6]

The Deep Boltzmann Machine (DBM) is a way of utilizing an undirected probabilistic process in a neural framework. [10] Researchers argue that the DBM has the ability to model features of cortical learning, perception, and the visual cortex (the locus of visual hallucinations). [10] Compelling evidence details the role homeostatic operations in the cortex play in regards to stabilizing neuronal activity. [10] By using the DBM, researchers show that when sensory input is absent, neuron excitability is influenced, thus potentially triggering complex hallucinations. [10]

Acetylcholine pathway Acetylcholine Pathway.png
Acetylcholine pathway

A short-term change in the levels of feedforward and feedback flows of information may intensely affect the presence of hallucinations. [10] In periods of drowsiness, CBS related hallucinations are more prone to arise. [10] Disrupting cortical homeostatic processes after vision has been lost may prevent or setback the emergence of hallucinations. [10] 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. [10] Particularly in CBS, a shortage of acetylcholine at cortical locations should correspond to the onset of hallucinations. [10]

The syndrome can also develop after bilateral optic nerve damage due to methyl alcohol poisoning. [13]

Diagnosis

A variety of disciplines including optometry, ophthalmology, geriatric medicine, psychiatry, and neurology play a part in securing the diagnosis of CBS. [6] Since CBS is not commonly recognized by all clinicians, it oftentimes goes misdiagnosed and identified as psychosis, delirium, or dementia. [1] As a result of this, it is estimated that almost 60% of CBS patients hesitate to notify their physicians. [1] By focusing on the specific type of visual hallucination, one may find an accurate diagnosis. [1] 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. [1]

Treatment

Prognosis

There is no treatment of proven effectiveness for CBS. [6] For those experiencing CBS, knowing that they have 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. [6] As time passes from the initial onset of visual hallucinations, studies show that around 60% of those living with CBS feel that visual hallucinations have no effect on their lives, 33% of people feel that the hallucinations are disruptive to their lives, and 7% of people even find pleasure in the hallucinations. [6]

A large proportion of those with CBS develop the visual hallucinations as vision begins to deteriorate and stop hallucinating once vision is entirely gone. [10] Complex hallucinations may progress over time if the primary loss of vision is due to damage of the early cortical areas. [10] If activation of the early cortical areas is suppressed when CBS symptoms have already been exhibited, hallucinations may temporarily terminate. [10] Also, interrupting vision for a short time by closing the eyes or blinking may be helpful. [3]

It is possible for a stressful life event to alter the disposition of hallucinatory experiences as well as the emotional experiences (from unconcerning to concerning) in CBS. [14] As expressed in some patients, an interplay between CBS and an acute or post-traumatic stress disorder may exist. [14] The role that trauma plays in CBS may affect how and when a hallucinatory episode is triggered. [14]

History

Charles Bonnet, the first person to describe the syndrome. CharlesBonnet.jpg
Charles Bonnet, the first person to describe the syndrome.

The disease was first noted by the Swiss naturalist Charles Bonnet, who described the condition in 1760. [1] He documented it in his 90-year-old grandfather [15] who was nearly blind from cataracts in both eyes. [7] After Bonnet's grandfather received bilateral cataract surgery, his vision evolved from slightly better to complete deterioration over time. [6] It was around this period that his visual hallucinations started. [6] His hallucinations consisted of perceptions of men, women, birds, carriages, buildings, tapestries, physically impossible circumstances and scaffolding patterns. [7] [16] Even though his health was in good shape and he had an absence of any psychiatric disorders, the source of the hallucinations remained unknown. [6] At forty years old, Charles Bonnet himself developed an unrevealed cause of severe vision loss and experienced the hallucinations. [6]

In 1936, Jean Lhermitte and Julian de Ajuriaguerra, concluded that visual hallucinations consist of thalamic lesions as well as ocular pathology. [6]

In 1967, French-Swiss neurologist, Georges de Morsier, coined the term Charles Bonnet syndrome in Bonnet's honor. [2] [1] De Morsier's description of CBS implies a concentrated neurodegeneration, usually occurring in the elderly with typical cognition. [6] In psychiatric literature, the most commonly accepted interpretation of CBS is that of Gold and Rabins'. [6] In 1989, they detailed that the hallucinations associated with CBS are not affecting other sensory modalities. [6] They believed that the visual hallucinations are oftentimes stereotyped, persistent, and/or repetitive in nature. [6]

Society and culture

The syndrome is discussed in:

See also

Related Research Articles

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<span class="mw-page-title-main">Micropsia</span> Medical condition

Micropsia is a condition affecting human visual perception in which objects are perceived to be smaller than they actually are. Micropsia can be caused by optical factors, by distortion of images in the eye, by changes in the brain, and from psychological factors. Dissociative phenomena are linked with micropsia, which may be the result of brain-lateralization disturbance.

<span class="mw-page-title-main">Macula</span> Oval-shaped pigmented area near the center of the retina

The macula (/ˈmakjʊlə/) or macula lutea is an oval-shaped pigmented area in the center of the retina of the human eye and in other animals. The macula in humans has a diameter of around 5.5 mm (0.22 in) and is subdivided into the umbo, foveola, foveal avascular zone, fovea, parafovea, and perifovea areas.

<span class="mw-page-title-main">Temporal lobe</span> One of the four lobes of the mammalian brain

The temporal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The temporal lobe is located beneath the lateral fissure on both cerebral hemispheres of the mammalian brain.

<span class="mw-page-title-main">Macular edema</span> Medical condition

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<span class="mw-page-title-main">Scotoma</span> Altered region in an otherwise normal field of vision

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<span class="mw-page-title-main">Usher syndrome</span> Recessive genetic disorder causing deafblindness

Usher syndrome, also known as Hallgren syndrome, Usher–Hallgren syndrome, retinitis pigmentosa–dysacusis syndrome or dystrophia retinae dysacusis syndrome, is a rare genetic disorder caused by a mutation in any one of at least 11 genes resulting in a combination of hearing loss and visual impairment. It is the most common cause of deafblindness and is at present incurable.

<span class="mw-page-title-main">Visual impairment</span> Decreased ability to see

Visual or vision impairment is the partial or total inability of visual perception. In the absence of treatment such as corrective eyewear, assistive devices, and medical treatment, visual impairment may cause the individual difficulties with normal daily tasks, including reading and walking. The terms low vision and blindness are often used for levels of impairment which are difficult or impossible to correct and significantly impact daily life. In addition to the various permanent conditions, fleeting temporary vision impairment, amaurosis fugax, may occur, and may indicate serious medical problems.

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Musical ear syndrome (MES) describes a condition seen in people who have hearing loss and subsequently develop auditory hallucinations. "MES" has also been associated with musical hallucinations, which is a complex form of auditory hallucinations where an individual may experience music or sounds that are heard without an external source. It is comparable to Charles Bonnet syndrome and some have suggested this phenomenon could be included under this diagnosis.

Anton syndrome, also known as Anton-Babinski syndrome and visual anosognosia, is a rare symptom of brain damage occurring in the occipital lobe. Those who have it are cortically blind, but affirm, often quite adamantly and in the face of clear evidence of their blindness, that they are capable of seeing. Failing to accept being blind, people with Anton syndrome dismiss evidence of their condition and employ confabulation to fill in the missing sensory input. It is named after the neurologist Gabriel Anton. Only 28 cases have been published.

Lesions in the visual pathway affect vision most often by creating deficits or negative phenomena, such as blindness, visual field deficits or scotomas, decreased visual acuity and color blindness. On occasion, they may also create false visual images, called positive visual phenomena. These images can be a result of distortion of incoming sensory information leading to an incorrect perception of a real image called an illusion. When the visual system produces images which are not based on sensory input, they can be referred to as hallucinations. The visual phenomena may last from brief moments to several hours, but they also can be permanent. They are generally associated with other symptoms but occasionally are isolated. Conditions causing these phenomena include disruptions in the visual input along the pathways lesions in the extracortical visual system, migraines, seizures, toxic-metabolic encephalopathy, psychiatric conditions and sleep apnea, among others. The mechanisms underlying positive visual phenomena are not yet well understood. Possible mechanisms may be: 1) defect in the sensory input causing compensatory upregulation of the visual cortex, 2) faulty visual processing in which inputs are normal but lesions result in an inappropriate pattern of cortical excitation, 3)variants of normal visual processing. Of all forms of hallucination, visual hallucinations are the least likely to be associated with psychiatric disorders. For example most patients with visual hallucinations do not have schizophrenia and most patients with schizophrenia do not have visual hallucinations.

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Visual hallucinations in psychosis are hallucinations accompanied by delusions.

<span class="mw-page-title-main">Visual pathway lesions</span> Visual maladies

The visual pathway consists of structures that carry visual information from the retina to the brain. Lesions in that pathway cause a variety of visual field defects. In the visual system of human eye, the visual information processed by retinal photoreceptor cells travel in the following way:
Retina→Optic nerve→Optic chiasma →Optic tract→Lateral geniculate body→Optic radiation→Primary visual cortex

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Jan, Tiffany; del Castillo, Jorge (2012). "Visual Hallucinations: Charles Bonnet Syndrome". Western Journal of Emergency Medicine. 13 (6): 544–547. doi:10.5811/westjem.2012.7.12891. ISSN   1936-900X. PMC   3555593 . PMID   23357937.
  2. 1 2 de Morsier, G (1967). "Le syndrome de Charles Bonnet: hallucinations visuelles des vieillards sans deficience mentale" [Charles Bonnet syndrome: visual hallucinations of the elderly without mental impairment]. Ann. Méd.-Psychol. (in French). 125: 677–701.
  3. 1 2 3 Vukicevic, Meri; Fitzmaurice, Kerry (2008). "Butterflies and black lacy patterns: The prevalence and characteristics of Charles Bonnet hallucinations in an Australian population". Clinical & Experimental Ophthalmology. 36 (7): 659–665. doi:10.1111/j.1442-9071.2008.01814.x. PMID   18983551. S2CID   205492511.
  4. ↑ Berrios, German E.; Brook, Peter (1982). "The Charles Bonnet Syndrome and the Problem of Visual Perceptual Disorders in the Elderly". Age and Ageing. 11 (1): 17–23. doi:10.1093/ageing/11.1.17. PMID   7041567.
  5. ↑ Vojniković, Bozo; Radeljak, Sanja; Dessardo, Sandro; Zarković-Palijan, Tija; Bajek, Goran; Linsak, Zeljko (2010). "What associates Charles Bonnet syndrome with age-related macular degeneration?". Collegium Antropologicum. 34 (Suppl 2): 45–48. ISSN   0350-6134. PMID   21305724.
  6. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 Pang, Linda (2016). "Hallucinations Experienced by Visually Impaired: Charles Bonnet Syndrome". Optometry and Vision Science. 93 (12): 1466–1478. doi:10.1097/OPX.0000000000000959. ISSN   1538-9235. PMC   5131689 . PMID   27529611.
  7. 1 2 3 Sacks, Oliver. "What hallucination reveals about our minds". Ted.com. Archived from the original on 2013-07-08. Retrieved 2013-07-03.
  8. ↑ Schultz, G; Melzack, R (1991). "The Charles Bonnet syndrome: 'phantom visual images'". Perception. 20 (6): 809–25. doi:10.1068/p200809. PMID   1816537. S2CID   22318715.
  9. 1 2 3 Mogk, Lylas G.; Riddering, Anne; Dahl, David; Bruce, Cathy; Brafford, Shannon (2000). "Charles Bonnet Syndrome In Adults with Visual Impairments from Age-Related Macular Degeneration". In Arditi, Aries; Horowitz, Amy; Lang, Mary Ann; Rosenthal, Bruce; Seidman, Karen; Stuen, Cynthia (eds.). Vision Rehabilitation. CRC Press. pp. 117–9. ISBN   978-90-265-1631-3.
  10. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Reichert, David P.; Series, Peggy; Storkey, Amos J. "Hallucinations in Charles Bonnet Syndrome Induced by Homeostasis: a Deep Boltzmann Machine Model" (PDF). NIPS Proceedings. University of Edinburgh.
  11. ↑ Tan, C S H; Lim, V. S.; Ho, D. Y.; Yeo, E; Ng, B. Y.; Au Eong, K. G. (2004). "Charles Bonnet syndrome in Asian patients in a tertiary ophthalmic centre". British Journal of Ophthalmology. 88 (10): 1325–9. doi:10.1136/bjo.2004.041947. PMC   1772345 . PMID   15377560.
  12. ↑ Abbott, Emily J.; Connor, Gillian B.; Artes, Paul H.; Abadi, Richard V. (2007). "Visual Loss and Visual Hallucinations in Patients with Age-Related Macular Degeneration (Charles Bonnet Syndrome)". Investigative Ophthalmology & Visual Science. 48 (3): 1416–23. doi: 10.1167/iovs.06-0942 . PMID   17325191.
  13. ↑ Olbrich, H. M.; Lodemann, E; Engelmeier, M. P. (1987). "Optical hallucinations in the aged with diseases of the eye". Zeitschrift für Gerontologie. 20 (4): 227–229. PMID   3660920.
  14. 1 2 3 Vukicevic, Meri (2010-08-02). "Frightening visual hallucinations: atypical presentation of Charles Bonnet syndrome triggered by the Black Saturday bushfires". The Medical Journal of Australia. 193 (3): 181–182. doi:10.5694/j.1326-5377.2010.tb03843.x. PMID   20678049. S2CID   35769299.
  15. ↑ Bonnet Charles (1760) Essai Analytique sur les facultés de l'âme. Copenhagen: Philibert, pp. 426–428
  16. ↑ "Bonnet's syndrome (Charles Bonnet)". Whonamedit. Archived from the original on 2014-02-23. Retrieved 2013-07-03.
  17. ↑ V.S. Ramachandran; Sandra Blakeslee (1988). Phantoms in the Brain. HarperCollins. pp. 85–7.
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