Abstract
purpose. The condition in which visual hallucinations (VHs) are solely associated with a visual impairment is termed Charles Bonnet Syndrome (CBS). The study was undertaken to investigate whether the extent of visual acuity (VA) loss and central visual field loss predisposes a patient with age-related macular degeneration (AMD) to develop a CBS VH and, in addition, whether the progression in loss is mirrored in the complexity of the VHs reported. VH phenomenology and CBS prevalence were also examined.
methods. Sixty-six patients (age range, 63–96 years, mean ± SD 81.2 ± 7.1 years) with bilateral AMD were questioned as to whether they had experienced any hallucinatory episodes exclusive to vision. The four-point primary inclusion criterion ensured that all patients had bilateral AMD, a bilateral central scotoma, best monocular VA poorer than or equal to 0.6 logMAR (logarithm of the minimum angle of resolution) and intact cognition (using the Mini Mental State Examination for the Blind and the Telephone Interview for Cognitive Status). The patients who did not report VH were classified into the non-VH group, with the remainder in the VH group. An extended Institute of Psychiatry Structural Interview characterized the phenomenology of the VH. A secondary inclusion criterion subdivided the VH group into the apparent CBS group, in which personal medical history may have contributed to VH generation, and the manifest CBS group, where VHs were solely as a result of the visual loss.
results. Fifty-three patients met the primary inclusion criterion: 32 were classified into the non-VH group and 21 into the VH group. The VH group were slightly younger (median difference, 4 years, P = 0.03) and appeared to have a lower VA (median difference, 0.20 logMAR, P = 0.08) and a more extensive visual field loss (P = 0.06) than did the non-VH group. However, when these variables were evaluated simultaneously by logistic regression, only age emerged as a statistically significant predictor of VH (odds ratio 0.88, 95% confidence interval [CI] 0.8–0.99, P = 0.03). The prevalence of apparent CBS and manifest CBS in the AMD population was found to be 25% and 15%, respectively. With no clinical and phenomenological differences between the two CBS groups, the secondary inclusion criterion was withdrawn, the VH group was renamed the CBS group, and a prevalence of 40% was recalculated. Of the 82 visual phenomena experienced by the CBS group, 21 were classified as simple VHs and 39 as complex VHs, with the remainder classified as either entopic phenomena or visual inference. Patients who experienced both simple and complex VHs appeared to have a greater visual field loss (P = 0.06) compared with those patients who reported either solely simple or solely complex VHs.
conclusions. The extent of visual loss did not appear to be a predictor for the likelihood of a patient with AMD experiencing a CBS VH, nor was the progression of loss reflected in the complexity of the VHs reported.
Hallucinations are perceptions in the absence of an external stimulus,
1 2 can occur in any sensory modality, and are most often generated through neurologic disease, psychopathology, and the use of drugs.
2 3 4 5 6 When visual hallucinations (VHs) follow marked visual acuity (VA) loss, in the absence of cognitive impairment, the condition is termed Charles Bonnet Syndrome (CBS),
7 8 9 with an estimated prevalence of 0.5% to 17%.
10 11 12 13 14 15 16 The content of the VH range from colored shapes and/or patterns (simple VH),
7 8 10 11 12 17 18 19 20 21 22 23 24 25 26 27 to well-defined recognizable forms such as faces, animals, objects, and scenes (complex VH).
7 8 9 10 11 12 17 19 20 21 22 23 24 25 26 28 29 30 31 The phenomenology of the VH does not appear to correlate with the underlying ocular disease, although significant bilateral loss in VA appears to be a primary trigger.
8 9 10 11 12 17 20 21 32 33
Our study was designed to investigate both VA loss and central visual field loss in a group of patients with CBS and low vision attributable to age-related macular degeneration (AMD) and to compare these measures with a control AMD group. In addition, we wanted to investigate the complexity and the phenomenology of the VH reported and to determine CBS prevalence.
To ensure that there was little likelihood that factors such as cognitive impairment would contribute to the perception of the VH we applied a four-point primary inclusion criterion to the group of patients with AMD. A secondary two-point criterion subdivided the VH group into two groups: an apparent CBS group, in which concurrent medication and/or a diagnosed medical condition could have contributed to the generation of the VHs, and a manifest CBS group, in which there were no obvious causes for the VHs other than the marked visual impairment. Our findings suggest that the VH experienced by the apparent CBS group could not be differentiated from those described by the manifest CBS group. Furthermore, the extent of visual loss did not predict which patients would visually hallucinate, nor did it determine the complexity of the VHs reported.
Apparent CBS Group.
Manifest CBS Group.
This group included patients with no obvious cause for the VHs other than marked visual impairment. The secondary two-point criterion ensured the patient had (1) no concurrent medication with known visual hallucinatory or psychotic side effects and (2) no diagnosed condition associated with hallucinatory symptoms (e.g., migraine, Parkinson’s disease, Alzheimer’s disease, Lewy body dementia, schizophrenia, narcolepsy, psychotic depression and mania, epilepsy, stroke, or delirium tremens).
To ensure that other visual phenomena (e.g., entoptic phenomena and visual inference) were not incorrectly categorized as VHs, distinctions were made based on patient’s descriptions and were further clarified by direct questioning.
Sensations that arise from within the eyes are called entoptic phenomena and include photopsias, such as phosphenes, and the appearance of moving blobs or lines.
41 These phenomena are frequently reported in patients with AMD and are often secondary to tractional forces acting on the retina or the physical movement of the vitreous. Visual inferences are based on mistakenly ascribing meaning to ill-defined perceptions of external stimuli using prior knowledge. Such descriptions are invariably prefaced with the phrase, “it looked like,” and lack the vivid and precise features that are so characteristic of a VH description.
For a visual phenomenon to be categorized as a VH, it must not be entoptic in origin or visually inferred. We categorized VH as either simple or complex. Herein, we defined a simple VH as the perception of a colored shape or pattern that did not have a recognizable form. We defined a complex VH as the perception of a shape that had a recognizable form (e.g., an object, face, or scene).
A breakdown of the content of the 60 VHs reported by the apparent and manifest CBS groups is given in
Figure 3 . The prevalence of VHs in the AMD population (
n = 53) was 15% when only patients classified into the manifest CBS group were included. Because no significant differences were found between the data relating to the apparent CBS and manifest CBS groups, except in the case of their living conditions, the secondary criterion was withdrawn, and the prevalence was recalculated by combining the two groups. This adjustment gave a prevalence of 40%, and henceforth this merged group was termed the CBS group.
The category and phenomenology of the VHs reported by the apparent CBS, manifest CBS, and CBS groups are described in
Table 4 . In summary, the VHs appeared suddenly, and patients were unable to control what subsequently happened to the image. Common triggers included relaxation, solitary conditions, and evening periods. No common stoppers were evident. The VHs generally lasted no more than a few seconds and were rarely restricted to the area corresponding to the visual field loss.
Eighty-two visual phenomena were reported: 21 (26%) were categorized as simple VHs, 39 (48%) as complex VHs, 21 (26%) as entoptic phenomena, and 1 (1%) as a visual inference. Historically, previous CBS studies had considered entoptic phenomena as simple VHs and visual inferences as complex VHs. Accordingly, our study uncovered different ratios of simple to complex VHs (1:1.9) to those previously reported. If we were to recategorize the entoptic phenomena as simple VHs and visual inferences as complex VHs the ratio would become 1:1.
The majority of patients (57%, n = 12) reported both simple and complex VHs. Five (24%) patients reported solely simple VHs and four (19%) reported solely complex VHs. Those patients who experienced both simple and complex VHs appeared to have the greater visual field loss (P = 0.06, Kruskal-Wallis ANOVA by ranks), but similar VA (P = 0.23) and age (P = 0.19) compared with those patients who reported only simple or only complex VHs. Accordingly, there was no strong evidence for the hypothesis that increasing visual loss is linked to a progression in the complexity of VH experienced.
The content of the VHs showed a broad variation, with the majority being faces (n = 19, 32%) and patterns (n = 16, 27%). Figures were often reported (n = 10, 17%) whereas colored shapes, objects, scenes, and words were less common.
Fifteen (71%) patients had no prior knowledge of CBS and did not know that VHs could be a feature of their low vision.
The purpose of this study was to explore CBS by investigating whether the extent of visual loss, in terms of VA and central visual field, predisposes a patient to develop a VH, and furthermore if the progression of visual loss is mirrored in the complexity of the VH experienced. In addition, we wanted to investigate phenomenology, prevalence, and whether, when stringent inclusion criteria were used, a homogeneous group of patients with CBS AMD could be identified and, moreover, differentiated from other visually hallucinating patients.
Despite the differences in VA and central field losses between the non-VH and the VH groups we were still unable to predict which of our 53 patients were likely to report a CBS VH. This would suggest that cognitive factors, such as state of arousal, play a central role in the appearance of the VH once the visual loss has reached a critical threshold level.
The question arises as to the nature of the visual loss and the cognitive, environmental, or medical factors required to initiate the hallucinatory process. Although we have exclusively studied patients with AMD who had both VA loss and central visual field loss, many other CBS studies have included patients with low vision attributable to a broad set of etiologies.
11 15 16 Recently, Tan et al.
15 and Madill and ffytche
42 emphasized that reduced VA (and presumably central visual field loss) may not be a prerequisite for patients to report CBS VHs. If indeed extensive peripheral field loss can trigger VHs, then quantification of this reduced sensory stimulation could indicate whether the likelihood of patients experiencing a VH is due to the percentage of visual field loss per se or the percentage loss in cortical processing.
That age was found to be a predictor of VH does not exclude the possibility that the older patients were less capable of recollecting their VHs. Although the MMblind and the TICS cognitive tests included memory assessments, these evaluations were superficial and limited in number.
In common with previous studies, we found a strong preponderance of CBS among women
11 19 33 43 44 ; reflecting the female bias of an elderly population.
We found that most patients reporting VHs had no prior knowledge of CBS despite 90% of them being registered blind or partially sighted. This finding suggests that a greater awareness of CBS is critical, not only for the provision of emotional relief
30 but ultimately to avoid inappropriate psychosis labeling and therapy.
Living alone did not appear to predispose a patient to VHs. However, we appreciate that living alone per se does not demonstrate the extent of social interaction a patient encounters since visits and excursions to and from the home are not considered.
There appeared to be no relationship between the occurrence of solely simple and solely complex VHs with the extent of visual loss, thus suggesting that there is not a progression in the complexity of the VH reported as the extent of the visual loss increases. However, those patients who experienced both simple and complex VHs exhibited greater visual field loss, which could suggest a failure in serial processing rather than a breakdown in hierarchical processing for a VH appearance.
Of the 21 patients in the CBS group just 4 experienced 44% of the complex VHs. This finding may be explained by either a predilection for certain personality types to have a complex VH (possibly reflecting a greater creative disposition), our small sample size, or recall bias in our patients.
Phenomenology alone provides no information to differentiate apparent CBS from manifest CBS, or furthermore AMD CBS from CBS caused by other visual disorders.
9 23 24 25 26 In agreement with other studies, the content of the VHs showed a broad variation, with the majority being faces and patterns.
Similar triggers and stoppers were found to be consistent with previous findings, including states of relaxation, solitary conditions, and evening periods.
9 21 45 46 The aforementioned situations universally describe conditions of reduced sensory stimulation; the patient could be considered to be on “stand-by mode” and would probably employ cognitive constructs to interpret the visual scene. Although typically associated with organic diseases and psychoactive substances, VHs among the normal population are not unusual, with frequent reports of VHs during the transitional states between waking and sleeping (hypnagogic) and sleeping and waking (hypnopompic).
31 This further emphasizes the importance of the patient’s state of arousal.
Quantifying the triggers and stoppers for the VH would be fruitful yet challenging, since thorough experimentation requires repeated measures and sustained attention. Of interest, the process of measuring the spatial and temporal characteristics of a VH may in itself act as a stopper; thus, alternative investigative methodologies must be sought. One such technique, used by ffytche et al.,
24 is functional magnetic resonance imaging. Activity in the ventral extrastriate visual cortex was found to correlate with VHs of colors, faces, texture, and objects, with the increased activity persisting between the interhallucinatory periods. Simple VHs were found to originate early in the visual pathway (V1 and/or V2),
24 27 47 48 whereas more complex VHs were generated in the higher visual areas.
24
Surprisingly, only 8% of the reported VHs were restricted to the area of binocular field loss, indicating that both bottom-up and top-down processing are operating concurrently, further emphasizing the complexity of the underlying mechanisms.
This is the first AMD study that has adopted rigid inclusion criteria to investigate the relationship between VA loss and central visual field loss with reports of VHs. We also examined the complexity and phenomenology of the VHs. In summary, CBS is a common finding in low-vision patients with intact cognition. The extent of visual loss did not appear to be a predictor for the likelihood of a patient with AMD experiencing a CBS VH, nor was it reflected in the complexity of the VH. The only statistically significant predictor was age, with the younger patients more likely to report a VH. In the present study we found a CBS prevalence of 40%. The phenomenology and prevalence of the VHs are not ocular disease specific and reflect the consequences of the profound loss of bottom-up visual processing. Factors such as states of arousal have been shown to trigger the onset of the VHs. Early reassurance is important in patient care, with sympathetic understanding and explanations providing emotional relief. Greater awareness of CBS is necessary, to avoid inappropriate labeling and treatment for nonexistent psychosis.
GBC was funded by a College of Optometrists research scholarship.
Submitted for publication August 9, 2006; revised October 6 and 31, 2006; accepted January 19, 2007.
Disclosure:
E.J. Abbott, None;
G.B. Connor, None;
P.H. Artes, None;
R.V. Abadi, None
The publication costs of this article were defrayed in part by page charge payment. This article must therefore be marked “
advertisement” in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Corresponding author: Richard V. Abadi, The University of Manchester, Faculty of Life Sciences, Moffat Building, Sackville Street, Manchester, M60 1QD, UK;
[email protected].
Table 1. Summary Details of the AMD Patients
Table 1. Summary Details of the AMD Patients
| Non-VH (n = 32) (14 Men, 18 Women) | VH (n = 21) (3 Men, 18 Women) | P |
Age (y) | 84 (72–96) | 80 (63–89) | 0.027* |
Best monocular VA (logMAR) | 0.82 (0.60–1.56) | 1.02 (0.60–1.60) | 0.081* |
Binocular field loss (deg2) | 36 (3–586) | 128 (6–711) | 0.061* |
Registered blind or partially sighted | n = 18 (56%) | n = 19 (90%) | 0.39, † |
Living alone | n = 15 (47%) | n = 11 (52%) | 0.18, † |
Table 2. Summary Details of the Apparent CBS and the Manifest CBS Groups
Table 2. Summary Details of the Apparent CBS and the Manifest CBS Groups
| Apparent CBS Group (n = 13) | Manifest CBS Group (n = 8) | P |
Age (y) | 83 (63–89) | 80 (63–83) | 0.3* |
Best monocular VA (logMAR) | 1.02 (0.6–1.6) | 1.07 (0.6–1.38) | 0.97* |
Binocular field loss (deg2) | 128 (6–711) | 88 (25–317) | 0.75* |
Registered blind or partially sighted | n = 12 (92%) | n = 7 (88%) | 1.0, † |
Living alone | n = 10 (77%) | n = 1 (13%) | 0.007, † |
Table 3. Details of the Apparent and Manifest CBS Groups
Table 3. Details of the Apparent and Manifest CBS Groups
Table 4. Phenomenology of the VH for the Apparent CBS, the Manifest CBS, and the CBS Groups
Table 4. Phenomenology of the VH for the Apparent CBS, the Manifest CBS, and the CBS Groups
| Apparent CBS (n = 13) | Manifest CBS (n = 8) | CBS (n = 21) |
Entoptic phenomena (n) | 15 | 6 | 21 |
Inferences (n) | 1 | 0 | 1 |
VHs (n) | 36 | 24 | 60 |
Simple VH:complex VH | 13:23 (36:64) | 8:16 (33:66) | 21:39 (35:65) |
VH triggers | | | |
Relaxation | 11 (85) | 8 (100) | 19 (90) |
Solitary conditions | 10 (77) | 5 (63) | 15 (71) |
With people | 1 (8) | 0 (0) | 1 (5) |
Evening periods | 10 (77) | 4 (50) | 14 (67) |
Daytime periods | 0 (0) | 1 (13) | 1 (5) |
Watching TV | 1 (8) | 1 (13) | 2 (10) |
Negative emotional state | 1 (8) | 1 (13) | 2 (10) |
Looking through window | 1 (8) | 1 (13) | 2 (10) |
VH stoppers | | | |
Walking through image | 2 (15) | 0 (0) | 2 (10) |
Change of gaze | 1 (8) | 1 (13) | 2 (10) |
Blinking | 3 (23) | 2 (25) | 5 (24) |
Intervals between VHs | | | |
Days | 7 (54) | 3 (38) | 10 (48) |
Weeks | 4 (31) | 2 (25) | 6 (29) |
Months | 2 (15) | 3 (38) | 5 (24) |
Duration of VHs | | | |
Seconds | 11 (85) | 6 (75) | 17 (81) |
Minutes | 2 (15) | 2 (25) | 4 (19) |
VH restricted to scotoma | 2 (15) | 0 (0) | 2 (10) |
Hyper-realistic VH | 6 (46) | 5 (63) | 11 (52) |
Able to hallucinate with eyes closed | 3 (23) | 1 (13) | 4 (19) |
The authors thank Dominic ffytche for discussions and for the loan of the Institute of Psychiatry Visual Hallucinations Interview; Ellen E. Lee, Chris M. Dickinson, and Maggie Harrison for assistance; Isabel Cacho and Heather Smith for collecting some of the data.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 1994; 4th ed.APA Washington DC.
BentallRP. The illusion of reality: a review and integration of psychological research on hallucinations. Psychol Bull. 1990;107:82–95.
[CrossRef] [PubMed]AbrahamHD, AldridgeAM, GogiaP. The psychopharmacology of hallucinations. Neuropsychopharmacology. 1996;14:285–296.
[CrossRef] [PubMed]FeldmanRS, MeyerJS, QuenzerLF. Principles of Neuropsychopharmacology. 1997;Sinauer Sunderland, MA.
ManfordM, AndermannF. Complex visual hallucinations: clinical and neurobiological insights. Brain. 1998;121:1819–1840.
[CrossRef] [PubMed]OhayonMM. Prevalence of hallucinations and their pathological associations in the general population. Psychiatry Res. 2000;97:153–164.
[CrossRef] [PubMed]de MonsieurG. Les automatisms visuels hallucinations rétrochiasmatiques. Schweiz Med Wochenschr. 1936;66:700–708.
FernandezA, LichtsheinG, ViewegWV. The Charles Bonnet Syndrome: a review. J Nerv Ment Dis. 1997;185:195–200.
[CrossRef] [PubMed]MenonGJ, RahmanI, MenonSJ, et al. Complex visual hallucinations in the visually impaired: the Charles Bonnet Syndrome. Surv Ophthalmol. 2003;48:58–72.
[CrossRef] [PubMed]BrownGC, MurphyRP. Visual symptoms associated with choroidal neovascularization: photopsias and the Charles Bonnet syndrome. Arch Ophthalmol. 1992;110:1251–1256.
[CrossRef] [PubMed]TeunisseRJ, CruysbergJR, VerbeekA, et al. The Charles Bonnet Syndrome: a large prospective study in the Netherlands. A study of the prevalence of the Charles Bonnet Syndrome and associated factors in 500 patients attending the University Department of Ophthalmology at Nijmegen. Br J Psychiatry. 1995;166:254–257.
[CrossRef] [PubMed]TeunisseRJ, CruysbergJR, HoefnagelsWH, et al. Visual hallucinations in psychologically normal people. Charles Bonnet Syndrome. Lancet. 1996;347:794–797.
[CrossRef] [PubMed]CohenSY, SafranAB, TadayoniR., et al. Visual hallucinations immediately after macular photocoagulation. Am J Ophthalmol. 2000;129:815–816.
[CrossRef] [PubMed]ShiraishiY, TakeshiT, IbiK, et al. The rarity of Charles Bonnet syndrome. J Psych Res. 2004;38:207–213.
[CrossRef] TanCSH, LimVSY, HoDYM, et al. Charles Bonnet syndrome in Asian patients in a tertiary ophthalmic centre. Br J Ophthalmol. 2004;88:1325–1329.
[CrossRef] [PubMed]NesherR, NesherG, EpsteinE, AssiaE. Charles Bonnet Syndrome in glaucoma patients with low vision. J Glaucoma. 2001;10:396–400.
[CrossRef] [PubMed]FitzgeraldRG. Visual phenomenology in recently blind adults. Am J Psychiatry. 1971;127:1533–1539.
[CrossRef] [PubMed]LanceJW. Simple formed hallucinations confined to the area of a specific visual field defect. Brain. 1976;99:719–734.
[CrossRef] [PubMed]SchultzG, MelzackR. The Charles Bonnet Syndrome: phantom visual images. Perception. 1991;20:809–825.
[CrossRef] [PubMed]HolroydS, RabinsPV, FinkelsteinD, et al. Visual hallucinations in patients with macular degeneration. Am J Psychiatry. 1992;149:1701–1706.
[CrossRef] [PubMed]SchultzG, MelzackR. Visual hallucinations and mental state: a study of 14 Charles Bonnet hallucinations. J Nerv Ment Dis. 1993;181:639–643.
[CrossRef] [PubMed]HolroydS. Visual hallucinations in a geriatric psychiatry clinic: prevalence and associated diagnosis. J Geriatr Psychiatry Neurol. 1996;9:171–175.
[CrossRef] [PubMed]ffytcheDH, HowardRJ. The perceptual consequences of visual loss: ‘positive’ pathologies of vision. Brain. 1999;122:1247–1260.
[CrossRef] [PubMed]ffytcheDH, HowardRJ, BrammerMJ, et al. The anatomy of conscious vision: an fMRI study of visual hallucinations. Nat Neurosci. 1998;1:738–742.
[CrossRef] [PubMed]SanthouseAM, HowardRJ, ffytcheDH. Visual hallucinatory syndromes and the anatomy of the visual brain. Brain. 2000;123:2055–2064.
[CrossRef] [PubMed]ScottIU, ScheinOD, FeuerWJ, et al. Visual hallucinations in patients with retinal disease. Am J Ophthalmol. 2001;131:590–598.
[CrossRef] [PubMed]BurkeW. The neural basis of Charles Bonnet hallucinations: a hypothesis. J Neurol Neursurg Psychiatry. 2002;73:535–541.
[CrossRef] KomelHW. Complex visual hallucinations in the hemianopic field. J Neurol Neurosurg Psychiatry. 1985;48:29–38.
[CrossRef] [PubMed]SchultzG, NeedhamW, TaylorR, et al. Properties of complex hallucinations associated with deficits in vision. Perception. 1996;25:715–726.
[CrossRef] [PubMed]MenonGJ. Complex visual hallucinations in the visually impaired. Arch Ophthalmol. 2005;123:349–355.
[CrossRef] [PubMed]CollertonD, PerryE, McKeithI. Why people see things that are not there: a novel perception and attention deficit model for recurrent complex visual hallucinations. Behav Brain Sci. 2005;28:737–974.
[PubMed]GirkinCA, MillerNR. Central disorders of vision in humans. Surv Ophthalmol. 2001;45:379–405.
[CrossRef] [PubMed]Norton-WilsonL, MunirM. Visual perceptual disorders resembling the Charles Bonnet syndrome: a study of 434 consecutive patients referred to a psychogeriatric unit. Fam Pract. 1987;4:27–35.
[CrossRef] [PubMed]FolsteinMF, FolsteinJE, McHughPR. Mini-Mental State: A practical method for grading the cognitive state of patients for the clinician. J Psychiatry Res. 1975;12:189–198.
[CrossRef] TomfbaughTN, McIntyreNJ. The Mini-Mental State Examination: a comprehensive review. J Am Geriatr Soc. 1992;40:922–935.
[CrossRef] [PubMed]ReischeisFM, GeiselmannB. Age-related cognitive decline and vision impairment affecting the detection of dementia syndrome in old age. Br J Psychiatry. 1997;171:449–451.
[CrossRef] [PubMed]BrandtJ, SpencerM, FolsteinM. The telephone interview for cognitive status. Neuropsychiatry Neuropsychol Behav Neurol. 1988;1:111–117.
CopelandJRM, KellnerMJ, KelletJM. A semi-structured clinical interview for the assessment of diagnosis and mental state in the elderly: the geriatric mental state schedule. Psychol Med. 1976;6:439–449.
[CrossRef] [PubMed]MattisS. Dementia Rating Scale. 1988;Psychological Assessment Resources Odessa, FL.
SweetmanS. Martindale: The Complete Drug Reference. 2004; 34th ed.Pharmaceutical Press London.
CraneWG, FletcherDC, SchuchardRA. Prevalence of photopsias and Charles Bonnet syndrome in a low vision population. Ophthalmol Clin North Am. 1994;7:143–149.
MadillSA, ffytcheDH. Charles Bonnet syndrome in patients with glaucoma and good acuity. Br J Ophthalmol. 2005;88:785–786.
TeunisseRJ, ZitmanFG, RaesDCM. Clinical evaluation of 14 patients with Charles Bonnet syndrome (isolated visual hallucinations). Compr Psychiatry. 1994;35:70–75.
[CrossRef] [PubMed]GoldK, RabinsPV. Isolated visual hallucinations and Charles Bonnet syndrome: a review of the literature and presentation of six cases. Compr Psychiatry. 1989;30:90–98.
[CrossRef] [PubMed]MewasinghLD, KornreichC, ChristiaensF, et al. Pediatric phantom vision (Charles Bonnet) syndrome. Pediatr Neurol. 2002;26:143–145.
[CrossRef] [PubMed]CoganDG. Visual hallucinations as release phenomena. Graefes Arch Clin Exp Ophthalmol. 1973;188:139–150.
[CrossRef] SafranAB, LandisT. Plasticity in the adult visual cortex: implications for the diagnosis of visual field defects and visual rehabilitation. Curr Opin Ophthalmol. 1996;7:53–64.
BressloffPC, CowanJD, GolubitskyM, et al. What geometric visual hallucinations tell us about the visual cortex?. Neural Comp. 2002;14:473–491.
[CrossRef] NadarajahJ. Visual hallucinations and macular degeneration: an example of the Charles Bonnet syndrome. Aust NZ J Ophthalmol. 1998;26:63–65.
[CrossRef] NixonPA, MasonJO. Visual hallucinations from age-related macular degeneration. Am J Med. 2006;119:e1–e2.
[CrossRef] RosenbaumF, HaratiY, Rolakl, FreedmanM. Visual hallucinations in sane people: Charles Bonnet Syndrome. J Am Geriatr Soc. 1987;35:66–68.
[CrossRef] [PubMed]OhayonMM. Prevalence of hallucinations and their pathological associations in the general population. Psychiatry Res. 2000;97:153–164.
[CrossRef] [PubMed]PessoaL, ThompsonE, NoeA. Finding out about filling-in: a guide to perceptual completion for visual science and philosophy of perception. Behav Brain Sci. 1998;21:723–802.
[PubMed]ErmentroutGB, CowenJD. A mathematical theory of visual hallucination patterns. Biol Cybern. 1979;34:137–150.
[CrossRef] [PubMed]ErmentroutGB. Neural networks as spatial forming systems. Rep Prog Phys. 1998;61:353–430.
[CrossRef] BressloffPC, CowanJD, GolubitskyM, et al. Geometrics visual hallucinations, Eucliden symmetry, and the functional architecture of striate cortex. Phil Trans Roy Soc Lond B. 2001;356:299–330.
[CrossRef] GrossbergS. How hallucinations may rise from brain mechanisms of learning, attention and volition. J Int Neuropsychol Soc. 2006;6:583–592.