Complex Visual Hallucinations in the Visually Impaired: The Charles Bonnet Syndrome

A. Prevalence 

Historically, hallucinatory experiences have been deemed to signify mental instability;8 patients are therefore often reluctant to admit to their hallucinatory experiences. The prevalence of CBS is thus likely to be underestimated.12, 83, 116, 132

The prevalence of complex visual hallucinations in patients with visual impairment has been estimated at between 11% and 15%.21, 44, 70, 82, 86, 109, 145, 147 A similar incidence of complex visual hallucinations has been reported in patients subjected to sensory deprivation by means of ocular masking prior to cataract surgery.92 In psychogeriatric patients over the age of 65 the prevalence of CBS has been estimated at between 1.84% and 3.5%.107, 108

Elementary visual phenomena however, occur more frequently; their incidence has been estimated at between 41% and 59% in visually impaired patients.21, 52, 89, 124, 151

B. Age distribution 

CBS is more common in the elderly.24, 32, 71, 116, 121, 128 Major case series reveal mean ages of incidence of 83.8,107 78.4,145 75.7,116 and 74.970 years. Other investigators report similar figures.53, 77, 146, 148, 150 However, the condition has also been reported in children sustaining rapid visual loss.130, 155 It has been suggested that the predilection for the elderly merely reflects the increased incidence of sudden profound visual loss in that age group.130

C. Sex distribution 

Different case series yield varying figures on the relative prevalence of CBS in men and women. De Morsier32 originally reported a male preponderance. Other studies suggest a clear preponderance of women;53, 71, 107, 108, 128, 145, 148 yet others recognize no sex bias.42, 49, 116, 146

D. Under-recognition 

CBS frequently goes unrecognized in clinical practice.21, 89, 147 Patients who admit to experiencing hallucinations are often labeled demented or psychotic,60 while potentially treatable causative factors are ignored.122

Many authors draw attention to the unfamiliarity of medical personnel with CBS and the tendency to misdiagnose mental illness.21, 59, 89, 107 In one series of 60 CBS patients, only 16 had consulted a doctor about their hallucinations; of these 16, one was diagnosed correctly.147 There is also the account of an elderly woman with CBS who would have been confined to a mental institution, had it not been for the intervention of a knowledgeable social worker.60

Arguably one of the most illustrative examples is a study of 50 patients with probable Alzheimer's disease, in which hallucinatory activity was exclusively confined to those who were visually impaired.22 It has been subsequently pointed out that, despite recognizing the association between hallucinations and impaired visual acuity, and that optimizing visual acuity by optical means often reduced the occurrence of hallucinatory experiences, the possibility of CBS as part of the differential diagnosis tends not to be considered.140

Awareness of CBS among medical personnel is therefore essential to avoid the risk of inappropriate therapy for non-existent psychiatric disease.104, 107

A. Content 

Hallucinatory content has been variously described. The most common image is that of a person.116 Disembodied distorted faces; small costumed figures and branching structures;125 vivid images of animals and figures;94 subtle geometric forms; well-defined complex figures; faces; Lilliputian (miniaturized),21, 31, 32, 83 normal-sized,32, 104 and “larger than life” images;32, 71 in black and white—or more commonly—in color,31, 49, 83, 104, 116, 128, 147, 156 of varying degrees of complexity128 have also been described.

These hallucinations are always localized in external space,31, 42, 49, 132 and the contents are well organised, defined and brilliantly clear.104, 109, 125, 128, 156 In the context of coexistent visual impairment, the clarity of the visions contrasts sharply with the blurred perception of real objects.11, 31, 49, 132, 156

Patients may perceive visions of themselves, sometimes at earlier stages in their lives, a phenomenon referred to as heautoscopia46, 82 or autoscopia.80, 83 Déjà vu experiences are rare; subjects rarely recognize the figures as living or deceased acquaintances.116 It is unclear whether the images represent playback of previous visual memories.128

The typical CBS hallucination has been variously described as a sudden sharply focused, immobile image, most often the face or figure of a person, which occurs when the patient is alert, with eyes open and vanishes spontaneously after a period of seconds.129 Alternatively it has been described as a solitary constant solid object in the central visual field, most commonly a flash, but often a complex grid, a disembodied distorted face, a small costumed figure with a hat or a branching structure.125

Atypical CBS hallucinations, classified into atypical sensory-perceptual (ASP) and atypical psychodynamic (APD) varieties, have also been described. ASP hallucinations differ from typical complex visual hallucinations in one or more characteristics such as duration, movement, volition, or participation of another sense (the latter widely considered an exclusion criterion for Charles Bonnet Syndrome), whereas APD hallucinations, similar to dreams, are more complex, mirroring the subject's psychological state, changing in content and frequency with alterations in the person's inner life or daily activities and may be repetitive.105

B. Movement 

There is no uniformity of opinion regarding the presence or absence of movement of hallucinatory images. Images have been described as static,129 moving en bloc (without internal change)42, 49, 116 or dynamic (with internal movement).31, 65, 128

C. Stereotypy 

The criteria of Gold and Rabins53 specify that the visual hallucinations in CBS be stereotyped. Recurrent themes21, 82, 100 and minimal variability in individual subjects109 have been noted in many subjects; however, many investigators have reported hallucinatory content varying between patients and even in the same patient at different times.21, 83, 104, 147, 148 It has therefore been recommended that the criterion mandating stereotypy of hallucinatory content should be abandoned.148 However, when images are dynamic (animated), the pattern of internal movement tends to be stereotyped.128

D. Triggering and relieving factors 

These hallucinations typically occur independently of any triggering factors or exercise of volition in the genesis of the image.104, 129 In some individuals however, they may be triggered by a wide variety of stimuli,42 such as conditions of general sensory reduction,91 fatigue,109 stress,82 low levels of illumination122, 128 or even by bright light.156

Once manifest, images last for periods varying from seconds through minutes to hours12, 21, 49, 83, 94, 96, 104, 109, 116, 122, 128, 152 and subsequently disappear, either spontaneously, or in response to actions such as closing the eyes27, 32, 42, 94, 128, 147, 148 and executing ocular saccades.27, 54, 82, 83, 128 Measures such as looking directly at the images,82 attempting to approach them,122 and conversing with them87 have also been reported to terminate hallucinations. A clinical approach, which investigates the utility of any such strategies, may be warranted.

Eye closure may both trigger and terminate hallucinations.31, 53, 148 Hallucinations have been reported to occur when the eyes are closed.141, 147

E. Course 

After impairment or loss of vision, hallucinations usually appear after a latent period lasting from hours to days.82 They may commence gradually, or more commonly exhibit a sudden onset, often occurring several times a day.21, 49, 83, 94, 104, 116, 128 Hallucinations may then continue to occur over varying periods from days through months to years.31, 82, 116, 122, 128 They tend to fade as sight is finally lost,42, 156 usually disappearing several months after the onset of the disorder, but are prone to reappear under conditions of physical or emotional stress.83

Three patterns of disease—episodic, periodic, and continuous—have been described.32, 116 The episodic variety, in which hallucinations occur over a period of days to months and then permanently resolve, is the least common.13 The periodic pattern of disease is characterized by phases of hallucinatory activity alternating with phases of remission, whereas patients manifesting the continuous pattern experience no hallucination-free intervals.

Elementary visual hallucinations may progressively evolve into complex visual hallucinations;31, 87, 116, 152 less frequently complex visual hallucinations regress to simple visual phenomena as they gradually cease to occur.87

F. Hallucinations of other modalities 

Most authorities maintain that the hallucinatory experiences of CBS are exclusively visual, unaccompanied by noise18, 31, 32, 87 or hallucinations of other senses.11, 109, 132 It has been recommended that such silent visual hallucinations should alert clinicians to the possibility of dysfunction of the visual pathway.151 Auditory hallucinations in association with complex visual hallucinations have, however, been described;74, 108 it has therefore been suggested that the coexistence of hallucinations of other modalities does not preclude a diagnosis of CBS, provided subjects retain insight into the unreality of their experiences.74

G. Patients' reaction to their hallucinations 

Reports on patients' reaction to the images are variable. Some investigators emphasize that patients find their hallucinations pleasant,3, 12, 31, 53, 116, 128 purportedly due to preserved central nervous function and adaptability.94 Others however, counter that CBS hallucinations are not invariably pleasant experiences.16, 21, 48, 62, 71, 96, 108, 129, 147, 148 Emotional response may be related to the nature of hallucinatory content.31 A quarter of CBS patients manifest anger, anxiety, or mild paranoia in response to the imagery.49, 125 Reactions to these visual experiences vary from indifference, through curiosity and irritation to terror.31, 38, 48, 62, 104, 128

Based on numerous reports describing patient reluctance to share their experiences16, 108, 109, 148, 156 and personal observation, it has been suggested that the positive response to hallucinations documented in the literature may be over-rated.148 Other investigators however, counter that patients with CBS discuss their hallucinations freely and objectively.152

Unlike the images seen in psychiatric states such as schizophrenia and depression, CBS hallucinations infrequently consist of images capable of generating emotional distress.94, 148, 152 Some authors draw a distinction between a predominantly positive reaction to hallucinatory content on the one hand, and anxiety and distress at the existence of hallucinatory activity on the other.104, 116 Though most patients experience no practical problems, continuous visual hallucinations occurring while the subject is in motion can interfere with navigation.104

H. Insight 

Most investigators agree that patients with CBS retain full insight into the unreality of their hallucinations,31, 82, 89, 94, 109, 132, 143, 147 which may therefore may be considered pseudohallucinations.11

However, insight may not be immediate. On initial appearance of hallucinations, patients may not recognize the unreality of their visions.31, 83, 116 Accurate insight is often achieved after initial deception,31, 49, 143 especially if the perceived images are appropriate to and fit realistically into the surroundings.143 Accordingly, patients may react to their hallucinations, trying to hit them away or grab them.71 The utility of the terms hallucinations and pseudohallucinations in CBS has been challenged on this basis.32

Furthermore, insight is not an all-or-none phenomenon; it may come and go, and even when present, may vary in degree.137 Accordingly, studies suggest that a considerable proportion of CBS patients possess partial or fluctuating insight into their symptomatology.53, 108

I. The mental state 

Lack of agreement exists regarding the mental state in CBS patients. Many authors emphasize the absence of depression or other demonstrable psychopathology in CBS.31, 70, 71, 109, 127, 128, 146, 148 It has been suggested that subtle confusional states in the elderly may be relevant in the development of CBS.16 Depression has also been observed in CBS patients with considerable frequency.127

Cognitive impairment has been documented in CBS patients;30 cases of CBS have developed dementia on follow-up.53 The prevalence of CBS may be higher in individuals with lower cognitive scores and impaired cognitive status may be a predisposing factor for CBS.70, 71 Subjects lacking insight into the unreality of their hallucinations typically demonstrate significant cognitive impairment compared with those with normal insight. On this basis, it has been suggested that patients with CBS manifest neuropsychological changes characteristic of early dementia, which are however, often overlooked due to lack of sensitivity of screening test measures such as the Mini-Mental State Examination (MMSE), to subtle cognitive decline in the early stages of dementia.114 It is therefore proposed that visual hallucinations may represent an early marker for dementia in the elderly and that visual impairment occurring in the early stages of cognitive decline unmasks these hallucinations.113, 114 This has, however, been contested on the grounds that patients who lack insight do not meet criteria53 for the diagnosis of CBS,143 and on the basis of documented stable cognitive scores on follow up of CBS patients with macular degeneration.69

It has also been argued that the failure of patients to experience distress on account of their hallucinations reflects compromised awareness of the significance of the symptom and provides further evidence that CBS and dementia lie on the same continuum of cognitive decline.115

The term Charles Bonnet Plus has been proposed in the presence of cognitive impairment.10 This has however, been deemed unnecessary, on the admittedly controversial basis that some degree of cognitive impairment is universally present in CBS patients.113

It is interesting that hypoperfusion of the mid-parietal and occipital areas of the brain, a well-recognized pattern in Alzheimer's disease and other dementias, has been documented on single photon emission computed tomography (SPECT) in a patient with CBS.58

It has been argued that cognitive or visual deficits alone are unlikely to cause hallucinations, but together they may contribute to a state of sensory deprivation.30 CBS patients with significant cognitive impairment may well represent a different sub-group to those who present to ophthalmologists primarily on account of poor vision, which may account for the diversity of views in this area.

J. fear of insanity 

Hallucinations have historically been deemed to signify psychiatric disease. Numerous reports describe patients' reluctance to admit to their hallucinatory experiences for fear of being considered psychiatrically unstable.1, 11, 15, 21, 42, 52, 54, 60, 70, 83, 89, 93, 109, 132, 139, 146, 147, 148, 149, 156

Many investigators draw attention to the fear of imminent insanity in the mind of a patient who knows their visions are not real.49, 60, 68, 83, 101, 116, 129, 149 Moreover, care providers, relatives, and friends may think the patient with CBS is mad.54 It is well recognized that many patients experience relief when told that their hallucinatory experiences are normal and do not signify psychiatric disease.70, 146, 147

K. visual function 

There is no consensus on whether visual pathology is necessary for the development of CBS. Many investigators report a strong association between CBS and impaired vision;2, 15, 31, 42, 52, 53, 65, 70, 82, 83, 89, 94, 107, 109, 116, 128, 146, 148, 156 the most commonly associated ocular pathology is age-related macular degeneration,94 although CBS has been documented in the context of visual impairment secondary to pathology anywhere along the visual pathway, from eye to occipital cortex.37, 41, 82, 85, 96, 117 Such visual hallucinations do not occur in those born blind, but only in the context of acquired visual impairment.110

It has been suggested that CBS is almost invariably associated with impaired vision;122, 128 indeed some authors mandate diminution of visual acuity,64 obligatorily secondary to ocular pathology83 to diagnose CBS. Others116, 148 concur with de Morsier's original opinion32 that visual dysfunction, though common, is not mandatory for diagnosis.

Hallucinations may occur more commonly in the context of sudden and unexpected reduction in visual function.70, 83 The degree of diminution of vision may be more relevant to the occurrence of visual hallucinations than the specific underlying ocular pathology.146 CBS occurs more frequently in higher degrees of visual impairment52, 70, 89, 146 and with bilateral as opposed to unilateral ocular pathology.21, 70, 146 In two separate studies, visual acuity of worse than 20/60 and 0.3 (20/66 approximate) in the better eye has been found to be associated with significant risk of developing visual hallucinations.70, 146

Numerous reports82, 91, 96, 116 suggest that improvement of visual function, spontaneously or by interventional means (such as cataract surgery or neurosurgical procedures) results in cessation or improvement of hallucinatory phenomena.

Some reports suggest that complex visual hallucinations have a predilection for blind areas of the visual field,82, 87 whereas other investigators recognize no relationship between the location of the hallucinatory images and objectively blind/scotomatous areas of the visual field.152

It has however, been countered that hallucinations are unrelated to the degree of visual impairment.71, 104, 114 This is supported by the observation that hallucinations may paradoxically cease in response to further deterioration of vision.150

L. quality of life in visually impaired patients 

Loss of vision, with its profound effects on employment, independence, mobility, and self-esteem, can be an overwhelming personal tragedy. The reactions of adults who have recently suffered loss of vision, include psychic stress, depression, suicidal ideation, anxiety, tearfulness, withdrawal, hallucinations, and insomnia,44 persisting as late as 5 years after the onset of visual loss.45 Patients with macular degeneration manifest poor quality of life and emotional distress ratings, comparable with those of individuals with chronic illnesses such as obstructive airways disease and AIDS.157

M. neurological features 

On the basis of normal visually evoked potentials (VEP) in a patient with CBS due to bilateral cataracts, it has been suggested that the diagnosis can be confirmed by a normal VEP, the geniculo-striate pathways and occipital lobe being normal in this condition.120 It is however, evident in the light of current knowledge that this is not so, and that CBS can occur due to pathology anywhere along the visual pathway.37, 59, 63, 82, 85, 96, 117, 135, 152

N. other risk factors 

Multiple factors have been implicated as causative for the complex visual hallucinations seen in CBS. Postulated predisposing factors include social isolation,70, 71, 144 shyness,144 and cerebrovascular disease.70 Fatigue and disturbances of vigilance have been implicated as relevant,94, 109, 116, 145, 147 since hallucinations are more likely to occur during states of drowsiness. Other factors, including stress4, 139 and suggestibility,14 have also been proposed as relevant to the genesis of visual hallucinations.

The pre-morbid personality structure and the ability to mobilize visual memories in the absence of normal stimuli has also been highlighted as relevant to the occurrence of complex visual hallucinations.82

A. Sensory deprivation—phantom vision 

Visual hallucinations occurring in the context of visual loss have been conceptualized as phantom visions28 due to de-afferentation16 and compared with the “phantom-limb” syndrome.12, 16, 104, 128 Visual sensory cortex, when deprived of normal afferent input, may exhibit spontaneous independent activity with resultant conscious imagery,12, 21, 109, 127 a hypothesis supported by the observation that such hallucinations can be abolished by normal or excessive visual stimulation.12

Reduction in sensory input to specific areas of the brain may allow memories of previous perceptions to enter consciousness as hallucinations.8 Visual hallucinations in destructive lesions of the central visual system may relate to pathological activation of other neural regions.6, 69, 123 On the basis that some hallucinatory states are associated with impaired cortical inhibition it has been suggested that images that are “screened out” or censored under normal circumstances, could, in the absence of normal inhibitory activity, reach higher centers and impinge onto consciousness.76 It has also been suggested that visual impairment alone may be insufficient to cause complex visual hallucinations, but together with impaired cognition, may contribute to a state of sensory deprivation with resultant visual phenomena.30

Musical pseudohallucinations with insight have been documented in the context of acquired deafness and have been compared with the visual pseudohallucinations of CBS.40, 57

B. Sensory deprivation experiments 

Hallucinations similar to those in CBS have been described by individuals subjected to sensory deprivation. The development of hallucinatory phenomena has been demonstrated under conditions such as ocular masking92, 158 and exposure to monotonous sensory environments.66

Heron et al66 subjected themselves to sensory (including visual) deprivation, and they noted that after a single day all investigators invariably experienced visual hallucinatory experiences, initially elementary, which later evolved in complexity and exhibited movement, both en bloc and internal. The typical progression of visual hallucinations from simple to complex, observed during experiments on perceptual isolation, has been interpreted to signify progression from lower to higher centers in the nervous system.159

Hallucinatory activity in patients undergoing bilateral ocular patching exhibits a strong relationship with duration of visual deprivation and manifests mainly during periods of reduced alertness, indicating that concurrence of sensory deprivation and reduced alertness is of causal significance in the development of hallucinatory experiences.158

C. Dreams and hallucinations 

The neurophysiological mechanisms underlying dreams and hallucinations may be similar, the former occurring during sleep and the latter during wakefulness.39 Dreams and hallucinations have been conceptualized as lying on a continuum, manifestation in the waking state being prevented by activity in ascending corticopetal nervous pathways. Disruption of such inhibitory mechanisms may “unmask” dreams—and the emergence of hallucinations.61

Reduced sensory input usually occurs during sleep; however, if specific sensory and non-specific ascending reticular input to sensory cortex drops below a threshold level even during the waking state, super-sensitivity to background activity in cerebral cortex may develop, with resultant hallucinatory experiences.94, 126 In this context it is interesting that fatigue and disturbances of vigilance have been implicated as relevant to the emergence of hallucinations,94, 109, 116, 145, 147 as they are more likely to occur during states of drowsiness.

D. Theory of perceptual release 

The brain may actively exclude irrelevant sensory impulses from conscious perception, by means of an active censorship mechanism, in turn dependent upon normal sensory input. When afferent input is reduced below a threshold level (such as in disease of the eyes or visual pathway), the brain may then allow previously registered subconscious perceptions or engrams to emerge into consciousness, resulting in a hallucinatory experience.153, 154

E. The neuromatrix theory 

Contending that the occurrence of visual hallucinations is independent of the degree of visual impairment, some authors104 challenge the theory of perceptual release and refer to the neuromatrix theory,97, 98 which proposes the existence of a network of neurons, the neuromatrix, extending throughout the brain, capable of generating sensory phantoms. This neuromatrix is said to impart a pattern, the neurosignature, on all afferent inputs from the body, so that sensory experiences may have a quality of self and possess affective tone and cognitive meaning. These authors argue that changes to sensory input may trigger or modulate the output of this neuromatrix, but do not dictate the qualities of experience.

F. Irritative and release hallucinations 

Cogan27 classified hallucinations into irritative and release variants and suggested that while the former are repetitive, stereotyped, and momentary, occurring secondary to electrical discharge at any point along the visual pathway, the latter are more likely to cause formed, continuous, variable complex visual hallucinations. He believed that complex visual hallucinations in patients with multi-factorial visual impairment represented release phenomena secondary to attenuation of visual sensory input due to pathology anywhere along the visual system, as a result of which they have much less localizing value than those of the irritative type.

Many authors believe that CBS hallucinations represent release phenomena.27, 42, 82, 89, 94, 109, 111, 128, 132, 150 It has also been suggested that coexisting pathology of the central nervous system may have a further permissive effect on the release of hallucinatory activity.132

Ictal activity from a focal irritative center, possibly in the occipital or temporal cortices has also been implicated as causative in the genesis of visual hallucinations.16, 87, 122

G. Social isolation 

Social isolation has been implicated as etiological in the genesis of CBS hallucinations,70, 71, 77, 144, 148 supported by the observation of temporary cessation of hallucinatory experiences during hospitalization. Social isolation may predispose to a state of sensory deprivation, a well recognized predisposing factor for visual hallucinations.30

H. Senescence 

The possible role of senescence has been highlighted,27 in that it may bring about the disintegration of higher centers and facilitate the release of sub-cortical phenomena, resulting in hallucinations. Complex visual hallucinations may be more likely to manifest in the context of macular disease if superimposed on age related central nervous system changes.94 The requirement for disinhibition of higher cortical centers may therefore explain the almost exclusive incidence of CBS in the elderly.49

I. Psychological factors 

It has been suggested that the psychological desire to see under conditions of partial visual loss may produce visual hallucinations. However, the disappearance of hallucinatory experiences when vision is totally lost negates this possibility.150 Hallucinations have been postulated to involve the integrative activity of the mind152 and may be due to facilitation of a general capacity of the brain for imagery;20 indeed, CBS is reported to occur predominantly in individuals with high levels of education and in the creative professions.65, 121

J. anomalies of cerebral perfusion 

Abnormalities of perfusion of the cerebral cortex have been implicated in the etiology of complex visual hallucinations. Vertebro-basilar insufficiency with ischemia of the visual pathway;107, 117 asymmetrical hyperperfusion in the lateral temporal cortex, corpus striatum, and thalamus during hallucinatory experiences;2 reduced occipital perfusion;133 and mid-parietal and occipital hypoperfusion resembling a commonly described pattern in Alzheimer's disease58 have been demonstrated in studies with SPECT and magnetic resonance imaging.

A. History taking 

Because most patients do not mention their symptoms unless specifically asked, sensitive, sympathetic, specific, and comprehensive history taking is essential to ascertain the existence of complex visual hallucinations in elderly visually impaired patients.15, 19, 21, 42, 107, 139, 147 When questioned by sympathetic, understanding, and accepting interviewers, more visually impaired subjects may admit to hallucinatory experiences.104

B. Examination 

Once hallucinations have been documented, thorough ophthalmic and neurological examination,113, 149 including formal evaluation of the neuropsychological status,114 is recommended to determine any potentially treatable causal pathology. It is also important to exclude other causes of visual hallucinations, as discussed previously. Effective communication with psychiatrists and rehabilitation therapists involved in the care of the patient is valuable in this context. However, in the alert, well-oriented patient, a simple test of cognitive function such as the Mini Mental State Examination may be adequate, with further psychiatric evaluation perhaps indicated only in the context of cognitive impairment.

C. Reassurance and counseling 

Patients with CBS may experience considerable anxiety, compounded by lack of awareness of the condition.104 Many patients express disappointment and amazement at unsympathetic reactions received from healthcare professionals when seeking advice regarding their hallucinations.60

Most patients experience relief when reassured that their condition is not a psychiatric disorder, but a recognized phenomenon with a name.147 Explanation and reassurance that the visions are benign and harmless, and do not signify mental illness therefore have a powerful therapeutic effect,15, 36, 104 so much so that it has been recommended that all blind individuals, even those who do not acknowledge the existence of hallucinations, should be informed of the possibility of their occurrence and advised that if they do occur, the hallucinations need not be a cause for distress.104 Cognitively intact patients may need no further measures, though patients in the early stages of dementia may prove more difficult to reassure, especially if lacking insight and experiencing visions of a distressing nature.149

It has been claimed that patients derive comfort from being told that their visual hallucinations will cease as their vision deteriorates further,122, 150 though it is difficult to understand how the knowledge of impending blindness can be of comfort. Reassurance and counseling are therefore the cornerstones of treatment.

D. Maximizing visual function 

Optimizing visual function often has a beneficial effect on hallucinatory activity42, 82, 91, 116, 132 and may be the most effective treatment, though correction of the visual defect may not always be possible, especially in elderly patients.150 Optical means such prescription of spectacles or visual aids and surgical procedures such as cataract surgery may be employed for this purpose.

E. Psychological therapy 

Techniques such as hypnosis, distraction, cognitive restructuring, and relaxation training, utilized in psychological therapy for phantom limb pain, have been advocated to minimize the unpleasant effects of persistent, intrusive, and troublesome visual hallucinations.104

F. Pharmacotherapy 

There is currently no universally effective pharmacotherapy for CBS. The evaluation of any potential remedy is further complicated by the fact that even without treatment, hallucinations sometimes fade away over a period of weeks to months. Moreover, because patients are often not distressed by their visions, and may even enjoy them, a therapeutic approach may not always be necessary. However, if hallucinations are frequent, non-resolving, distressing, or impairing quality of life, effective therapy is required.112

Drug therapy is rarely useful in CBS.83, 116 Anticonvulsants such as carbamazepine,17, 24, 25, 55, 77, 141 clonazepam,141 and valproate75 have been suggested as effective. A combination of carbamazepine and clonazepam has proved useful in some patients.141 It is suggested that the efficacy of carbamazepine may be due to inhibition of inter-hallucinatory persistent increased ventral extra-striate neuronal activity.24

Low-dose gabapentin (anti-convulsant) is reported to have produced permanent remission.112 On the basis that serotonergic pathways may be relevant to the pathogenesis of visual hallucinations, cisapride, a potent 5HT-3 antagonist, has also been used with reported success.106, 118

Anti-psychotic drugs (neuroleptics) have been used in treatment of CBS, but are generally only partially effective at eradicating hallucinatory activity.149 Varying degrees of success have been reported with thioridazine,62 haloperidol,26 and the atypical neuroleptics risperidone78 and melperone.13 Different neuroleptics may have varying effects on CBS (risperidone has been documented to worsen hallucinations and render them menacing); treatment should therefore be tailored to the individual patient.84

G. Social and environmental factors 

CBS is known to occur in the context of social isolation and sensory deprivation, improvement of which may have a beneficial effect.149 Symptoms may abate when alternative interests are pursued, such as television, music, and the company of friends.

Environmental changes such as improved illumination may reduce hallucinatory activity,99, 149 perhaps by increasing the overall level of sensory stimulation. Treatment of depression, modification of the environment, and establishment of support groups, in which patients can share their experiences, may also be useful.