An Overview of Visual Hallucinations

Patients who experience hallucinations secondary to a host of underlying conditions often will look to you for guidance, reassurance and treatment.

By Michael N. Block, O.D.

Release Date: march 2012
Expiration Date: march 1, 2015

Goal Statement:

This article examines the occurrence of hallucinations in healthy patients as well as in those with a host of underlying conditions, such as stroke, migraine and Parkinson's disease. Additionally, we'll examine the particulars of Charles Bonnet Syndrome, including its pathogenesis, risk factors and management strategies.

Faculty/Editorial Board:

Michael N. Block, O.D.

Credit Statement:

This course is COPE-approved for 2 hour of CE credit. COPE ID is 33853-LV. Please check your state licensing board to see if this approval counts toward your CE requirement for relicensure.

Joint-Sponsorship Statement:

This continuing education course is joint-sponsored by the Pennsylvania College of Optometry.

Disclosure Statement:

Dr. Block has no relationships to disclose.

Although healthy individuals may experience hallucinations, these visual phenomena are often associated with a variety of disease processes. Some patients who seek care for visual hallucinations first approach an internist or neurologist. However, a significant number of patients present to an optometrist when associated symptoms include headache, reduced visual acuity and restricted fields.

Bilateral vision loss predisposes some patients to intermittent visual hallucinations. The source of decreased vision may lie anywhere in the visual pathway, but macular degeneration is most often implicated. These frequently begin as simple visual hallucinations, and then progress to more complex ones. Patients usually recognize them as being distinct from reality and, after the initial few occurrences, consider the images to be both pleasant and non-threatening. This phenomenon likely is underreported because many patients fear that the hallucinations herald the onset of dementia.

Eighteenth-century Swiss scientist turned philosopher Charles Bonnet first documented visual hallucinations and impaired vision in the context of uncompromised cognition––thus, the constellation of associated symptoms later became known as Charles Bonnet Syndrome (CBS).1

Here, we'll discuss the occurrence of hallucinations in healthy patients as well as in those with a host of underlying conditions, such as stroke, migraine and Parkinson's disease. Additionally, we'll examine the particulars of CBS, including its pathogenesis, risk factors and management strategies.


Perception is the awareness that results from the brain's processing and synthesis of data that is garnered by our sensory organs. Imagery, unlike perception, occurs in the absence of adequate sensory input and lacks a sense of reality. Hallucinations differ from both perception and imagery because there are no sensory inputs that correspond to cortically generated visual experiences. Despite this, the images seem compellingly real. Although hallucinations stem from a variety of conditions, the actual visual symptoms are often quite similar, leading some researchers to suggest the existence of just a few common mechanisms that produce these phantom images.1,2

Visual hallucinations may be characterized as either simple or complex, depending upon their content. Simple (elementary) hallucinations include spots of light, lines and patterns, and are associated with the striate cortex. On the other hand, complex hallucinations yield vivid, formed, well-organized images, and are linked to the visual association areas. More specifically, complex hallucinations may feature images of people, faces, birds, animals or scenery. Additionally, miniature images (lilliputian) are often reported, and may be either dynamic or static.

No matter the form, when hallucinations occur in the visually impaired, the outstanding clarity of the phantom image sharply contrasts with the individual's habitually degraded vision.1

In one study of the cerebral cortex, the author discovered that electrical stimulation of the striate cortex (areas 17 and 18) caused simple visual hallucinations, including light flashes.3 When the visual association cortex (area 19) was stimulated, the subject experienced complex visual hallucinations. The presence of hallucinations associated with area 19 in the context of calcarine cortical infarction supports the claim that hallucinations originate in the surviving visual association areas.3

Hallucinations in Healthy Patients

Complex visual hallucinations occur in 30% of individuals who have no predisposing physical or mental conditions. Such complex hallucinations are associated with varied states of drowsiness, and usually occur at the end of the day before the onset of sleep. They may persist for as little as two seconds to more than 15 minutes; the duration possibly is related to the degree and length of fatigue.1

Occasionally, hallucinations begin as simple before transitioning to complex. However, more often than not, hallucinations both begin and remain complex. Their content may range from terrifying to pleasant.

Hallucinations not only are related to periods of drowsiness prior to sleep in otherwise healthy patients, but also are found in–– and epitomized by––narcolepsy. The hallmark of narcolepsy is excessive daytime sleep that is unrelated to the total sleep time of the prior evening. The episodes are uncontrollable and often interfere with normal activities.

During sleep, brain activity is divided into two categories based on physiologic changes and the presence of dreaming: non-rapid eye movement (NREM) and rapid eye movement (REM). NREM is the first stage of sleep and has four subcategories that usually need to be completed before entering into REM. Normally, NREM begins with shallow sleep; then progresses to deep sleep; and eventually leads into a period of REM, which is when most dreaming occurs. This process repeats itself several times each night. The initial REM phase occurs 90 minutes after the onset of sleep, and persists for approximately 10 minutes. Each successive period of REM lasts longer––the final phase persisting up to one hour.

Hallucinations occur during the first REM period. In normal individuals, the first REM phase takes place only following the deepest NREM sleep. Unlike a dream, where the individual often is a participant, the hallucinator generally is an observer. The term "hypnagogic hallucination" was first used in 1848 to describe this phenomenon.

It is postulated that hypnologic hallucinations are generated when REM sleep is entered prematurely and/or when there is still a high level of cognitive arousal. These hallucinations––found in both normals and narcoleptics––are referred to REM-related abnormalities.1 It is interesting to note that as many as 50% of narcoleptics experience hypnagogic-type hallucinations when transitioning from being awake to falling asleep.1

Posterior Cerebral Artery Infarction

The majority of cerebrovascular accidents (CVA) result secondary to embolic travel to the cerebral vasculature. This process causes an interruption in blood supply, which results in ischemia.

Hemorrhagic strokes are far less common, but may produce the same end result. Stroke patients with infarction of the middle cerebral artery often suffer from contralateral hemiparesis or weakness. Infrequently (10% of cases), infarction of this vessel will produce a contralateral hemianopsia.4 The vast majority of CVA-related hamianopsias, however, are caused by infarctions of the posterior cerebral arteries.4

Complex visual hallucinations have been reported in 13% to 41% of patients who suffer hemianopsias secondary to occipital infarction.5 Usually, the visual phenomena occur within the defective visual field. Hallucinations usually are transient, lasting days to weeks––although they may persist occasionally. Additionally, they are limited to the visual modality, except when areas other than the visual cortex are involved. Most often, there is a time delay from the ischemic event to the onset of hallucinations that may last up to several weeks.

Radiological studies have demonstrated that lesions associated with hemianopsias and visual hallucinations are significantly smaller than the more severe lesions that cause only hemianopsias without hallucinations.5

Apparently, a small portion of surviving cortex is necessary for the generation of hemianopic visual hallucinations. Larger lesions that extend anteriorly and destroy the visual association areas never are associated with hallucinations.5

Brainstem Lesions

Peduncular hallucinosis, first documented in 1922, results from vascular lesions to the rostral brainstem that affect the thalamus.2 They resemble the aforementioned vivid hypnagogic hallucinations that occur in normal patients.

Phenomena duration varies from minutes to hours, occasionally lasting all day. There is a time delay of several days prior to the onset of these phantom images. Although the hallucinations usually subside after a few weeks, they may persist for years.2 Typically, episodes occur toward the evening, but are unrelated to levels of drowsiness. Interestingly, no part of the visual pathway––beginning at the retina and terminating at the visual cortex––is directly involved.2


Complex visual hallucinations occurring in epilepsy patients bear little resemblance to hypnagogic and peduncular hallucinations. These hallucinations are brief, fragmentary and occur in the context of seizures or their aftermath. Based on intracranial electroencephalogram, they originate from pathological irritation and excitation of the visual association cortex.6


The prevalence of migraine headaches in the general population is 10%.7 Approximately one third of migraines are preceded by simple visual hallucinations known as auras. Although there are many variations, the classic aura is the fortification spectra, which begins near fixation and features shimmering lights that are restricted to half of the visual field. They enlarge in an arc of zigzag-lines oriented at 60° and are further magnified as they move from fixation to the periphery.7

Immediately following this phase is the development of a scotoma or hemianopsia. According to a 2004 report from the International Headache Society, the aura of migraine slowly and gradually develops over a span of five minutes, and may persist up to 60 minutes.8 This contrasts with the visual symptoms of occipital epilepsy, which are fragmentary and flickering.7,8 In addition to being associated with migraine and epilepsy, aura-like vision changes are found in some patients with occipital lesions. It is important to understand that this symptom overlap often poses a diagnostic challenge. Although these auras are infrequently associated with cortical lesions, the clinician still needs to differentiate the benign migrainous auras from those secondary to an intracranial pathology.7

A clinically important characteristic of the migraine aura is variability within the visual fields. The location often shifts laterally from one hemifield to the next in different episodes. Approximately 86% to 100% of patients with cortical pathology have auras that are contralateral to the lesion.7,9,10

An aura that consistently recurs on the same side should alert the practitioner to a more insidious etiology and warrants imaging and referral. Similarly, any change in the appearance of a previously diagnosed migrainous aura or the emergence of a new aura also should be of concern. Several studies documented a significant increase (58% to 67%) in the frequency of visual auras among patients who were ultimately diagnosed with an intracranial pathology. Daily auras were reported in 32% of these patients.7,9,10

Migraine sufferers rarely see complex visual hallucinations. Such hallucinations are, however, frequently found in migraine coma (an entity associated with recovery from coma) and familial hemiplegic migraine. Further differentiating these hallucinations from migraine aura is the timing; unlike the aura of a conventional migraine headache, hallucinations caused by migraine coma and familial hemiplegic migraine occur at the end of the attack.

The electrophysiological correlate to the aura is a spreading wave of glial depolarization that is followed by reduction in cortical activity, which is known as cortical spreading depression (CSD). The rate of depolarization traversing the cortex directly corresponds to the rate of the scintillating scotoma's movement from the center to the periphery.10

Expanding upon this electrophysiological data, one study indicated that the initial migraine phase of aura is due to a chemically mediated state of neuronal hyperexcitability and spontaneous discharge associated with depolarization.9 This is followed by CSD, which is responsible for the ensuing visual field defect and headache. The similarity of visual symptoms associated with cortical ischemia, intracranial lesions, epilepsy and migraines arises from the single common mechanism of CSD.9

Parkinson's Disease

Parkinson's disease is one of the most common neurological disorders associated with complex visual hallucinations. Between 8% and 40% of Parkinson's patients report these ophthalmic manifestations.11,12 The hallucinations usually occur at the end of the day; are vivid and often associated with sleep disturbances; and may be similar to the peduncular hallucinations caused by brainstem lesions.11,12

Until recently, there was widespread acceptance that these hallucinations were due to adverse reactions to long-term use of Parkinson's medication levodopa. This theory was challenged by a prospective study in which the author concluded that underlying characteristics of Parkinson's––not the duration of medical treatment––were directly associated with hallucinations.13 In fact, reduced visual acuity, depression, worsening of dementia and increased severity of Parkinson's disease were all more significant determinants of hallucinations than treatment duration.1,13,14


Hallucinations in schizophrenics usually are experienced in color and most often are multi-modal, consisting of visual and auditory components. They frequently accompany paranoia or other thought disorders. Unlike most of the hallucinations described above, these occur during the daytime and are associated with episodes of excess excitability.

Charles Bonnet Syndrome

Charles Bonnet documented hallucinations that were experienced by his 89-year-old grandfather, Charles Lullin. The images that Lullin described were varied and included people, animals, birds, scenery and carriages.

The onset of Lullin's spontaneously occurring images was linked to visual impairment that developed after bilateral cataract surgery. His cognition was intact, as was his ability to discern the hallucinations as unreal. This cognitive awareness has led some authors to characterize these visual phenomena as pseudo-hallucinations.1 Interestingly, Bonnet––who was hearing impaired since childhood––suffered vision loss at age 34 and subsequently experienced visual hallucinations similar to those described by his grandfather.


The defining characteristics of CBS have evolved since the condition was first described. In his essay, Bonnet indicated that advanced age, intact cognition, presence of eye disease and hallucinations with insight were all necessary components.1

In the 1930s, Georges de Morsier introduced the term CBS and used it to differentiate hallucinations that occurred with no cognitive deficits from those associated with cerebral degenerative disease.1 Unlike Bonnet, de Morsier maintained that eye pathology was unrelated to the hallucinations and was not a prerequisite for the syndrome.

In 1950, Julian de Ajuriaguerra expanded the definition of CBS to include visual hallucinations in the presence of eye disease. Building from this work, Klaus Podoll, M.D., established criteria to grade visual hallucinations seen by elderly patients who had normal cognition in the late 1980s. Interestingly, Podoll noted that visual acuity loss from eye disease was often––but not always––found.

Then, in 1989, Kenneth Gold, M.D., and associates took a different approach by defining CBS based on symptoms––not etiology. They suggested that CBS was a constellation of symptoms consisting of hallucinations that were exclusively visual, complex, formed and stereotyped with full or partial insight.


Complex visual hallucinations occur in 11% to 15% of patients who suffer severe bilateral vision loss. In CBS, simple visual hallucinations are documented more frequently than complex hallucinations, and affect up to 59% of patients.

One study indicated that the type of hallucination––whether simple or complex––was unrelated to the level of vision loss.16 Furthermore, the extent of visual impairment was more predictive of CBS-related hallucinations than either the type or sub-type of underlying ophthalmic disease that caused the vision deficit.16,17

There is no definitive consensus regarding the condition's gender predilection; however, most studies suggest that women are more likely to be diagnosed with CBS than men.1,16,18 And, although CBS has been reported in children who suffer sudden vision loss, the vast majority of CBS cases occur in the elderly––with an average age of onset ranging from 74 to 83 years. This age-related skew may be due to the increased prevalence of vision threatening eye disease in the geriatric population.1,16,18


Deafferentation is one of the current theories that explains the occurrence of complex visual hallucinations accompanied by severe bilateral vision loss.1,19 It is associated with sensory deprivation and is based on the premise that a steady stream of high-quality input to the primary visual cortex is a prerequisite for proper, non-hallucinogenic, visual function.

The continual flow of nondegraded input to the striate cortex is crucial to suppressing the expression of random and memory-based images that are stored in the visual association areas. Retinal or other pathologies may interrupt this data stream, resulting in the reduced ability of the primary visual cortex to effectively censor or inhibit these images, which leads to their sudden intrusion into conscious perception. When this occurs, the images are then "released" and manifested as complex visual hallucinations.

The nervous system responds to denervation (loss of neuronal connections) and deafferentaion by biochemically inducing a state of neuronal excitability. This occurs in the visual, auditory, vestibular and motor systems.20 It is thought that the cells in the visual association areas are, therefore, more likely to discharge spontaneously in this state of excitability due to the absence of quality afferent inflow.

One study evaluated the association of visual hallucinations and the activity of the occipital cortex using functional magnetic imaging (fMRI).13 During the period when hallucinations were experienced, the authors documented reduced cortical response to visual stimulation. The occurrence of hallucinations underscored their assertion that these extraneous visual images arose from reduced sensory input and a resulting lack of visual association area inhibition.13

The CBS images are analogous to the auditory and musical hallucinations of the deaf, which are also attributed to sensory deprivation. Lack of quality input to the primary auditory areas reduces its inhibition of the auditory association areas. Likewise, the effect of degraded input on the primary visual cortex leads to a lack of censorship of extraneous images that originate in the visual association areas, which results in the expression of complex visual hallucinations.

Sensory deprivation can also cause tactile hallucinations that are similar to those experienced in "phantom limb syndrome, " which is often seen in amputees (e.g., patients who have lost limbs frequently "feel" sensations or pain in the limbs that now do not exist). Similar to those affected by CBS, phantom limb patients are aware of the inauthenticity of these hallucinations, as well as display a latency period of weeks following the loss of sensory input before the tactile hallucinations begin.

In 1994, Peter V. Rabins, M.D., M.P.H., traced the similarities of hallucinations caused by either CBS or phantom limb syndrome to a common mechanism.21 Expanding upon on the aforementioned deafferentation theory, Dr. Rabins proposed that sensory interruption in afferent cells and the loss of sensory end organs are quickly followed by hypersensitivity, and then expansion or relocation of the corresponding cortical receptive fields.1 Hallucinations most likely result from spontaneous discharge of cells in the altered, newly innervated receptive fields.14,21

A type of selective deafferentation may be responsible for the colored CBS hallucinations associated with macular degeneration. Following data interruption from the highly concentrated macular cones, there is hyperexcitablity of the color area in the ventral pathway that reduces inhibition and expression of colorful hallucinations.

Interestingly, many studies indicate a high incidence of hallucinations in people who live alone.1 Because this lifestyle is a type of social sensory deprivation, deafferentation may play a role in the generation of these images. Additional support for deafferentaion is the reported elimination of CBS hallucinations following instances when visual acuity was, optically or medically, improved. Hallucinations attributed to macular degeneration were markedly reduced after photocoagulation therapy.22

Risk Factors

As might be expected, the greatest risk factor for these hallucinations is any severe, bilateral reduction in visual acuity that is consistent with the deafferentation theory. However, one study indicated that reduced contrast sensitivity is a better predictor of hallucination risk than acuity loss.7

Regardless, the high concentration of cortical input that corresponds to the macula accounts for visual hallucinations when a macular pathology degrades these afferent signals, consequently eliminating the normal inhibition and censorship of the visual association areas.23

While visual impairment can arise from disorders anywhere along the visual pathway, bilateral macular degeneration is most closely associated with the development of CBS. This is no surprise, because macular degeneration is the most prevalent cause of severe vision loss in the western world.

Other ophthalmic conditions associated with hallucinations are cataract, glaucoma, retinal detachment, enucleation, optic neuritis secondary to multiple sclerosis, cortical blindness and macular holes.

Non-ophthalmic causes are metabolic, infectious or vascular. They include diabetes mellitus with uncompromised vision, HIV with manifestations of cytomegalovirus retinitis and vertebral basilar insufficiency.1

Finally, there have been isolated reports of CBS in patients who have undergone peripheral iridotomies and intravitreal bevacizumab therapy for macular degeneration.1

These hallucinations occur more frequently in the context of sudden visual loss and are never found in the congenitally blind. The severity of acuity loss is more significant than its underlying etiology when assessing risk for CBS. Patients are at risk for CBS when the acuity in the better eye falls below 20/60.

According to several reports, improvement of acuity secondary to cataract extraction or photocoagulation decreases or eliminates these visual phenomena.16

Furthermore, a study published in 2008 showed that low vision rehabilitation was associated with a 27% reduction in hallucinations in CBS patients.24

Visual Streams and Cerebral

There are three cerebral pathways that transmit cortically processed signals to specific areas of the brain. Each stream conveys information with unique visual attributes, and projects them to specialized regions.

Relationship of CBS Hallucinations to the Visual Pathways
Hallucination Cluster Visual Stream Projection
Landscapes; small, costumed figures; vehicles;
trees; and birds
Ventral Inferior temporal cortex
Grotesque, disembodied, distorted, faces with
prominent eyes
Unnamed Superior temporal
sulcus (STS)
Visual preservation; palinopsia Dorsal Parietal cortex

One study investigated various hallucinations found in 34 CBS patients. The researchers grouped 12 common types of hallucinations into three symptom clusters and proposed that hallucinations in each cluster were commonly linked to increased activity in specific regions of the brain (see "Relationship of CBS Hallucinations to the Visual Pathways, " above).25

The ventral pathway, often referred to as the "what stream, " transports visual information that originated in the ganglionic P cells. This stream presents the resulting cortically processed data to the inferior temporal cortex. This pathway features signals that are associated with color perception, luminance, stereopsis and pattern recognition. Functional MRI studies have shown that the ventral temporal lobe is specialized for complex features of objects and landscapes.25 CBS hallucinations consisting of scenery, vehicles, trees, and figures with hats and costumes correspond to the functional specialization of this region. It is likely that the increased activity in the ventral stream's projections is responsible for these types of hallucinations.25

The dorsal stream, commonly referred to as the "where pathway, " transports signals that originate in the ganglionic M cells, which are eventually processed in the striate and extrastriate cortices. Data is then projected to the posterior parietal cortex by this stream and is associated with object location, movement and the stabilization of images during saccades. Palinopsia, a disorder involving preservation of visual images after the objects are no onger in the field of view, is linked to disorders of the parietal cortex.1

The third and final category of CBS hallucinations consists of grotesque faces with distorted and rearranged features, including oversized eyes and teeth. Of the four regions in the brain that selectively respond to different facial stimuli, these images correspond to overactivity in the superior temporal sulcus (STS).26 This area is responsible for processing variable aspects of the human face, include expressive features around the eyes. The STS is located between the dorsal and ventral pathways, suggesting a causative link.26

Further evidence linking hallucinatory syndromes and visual streams comes from a study that documented an association of dorsal projections with the peripheral visual field as well as a relationship between ventral projections and the central visual field.26 This finding corresponds well with the cluster of hallucinations that is generated by each stream. Palinopsia, for example, is an illusion that is exclusive to the peripheral field, whereas hallucinations of figures and landscapes are found in the central field.26

Content and Characteristics

CBS-induced hallucinations frequently occur upon awakening, with the eyes open and the patient alert. Images appear suddenly and usually last several seconds. Occasionally, however, some visions will persist for minutes to hours. They are exclusively visual, brilliant, sharply focused, often lack movement, and may merge or blend in with pre-hallucinogenic views. Saccadic eye movements, eyelid closure, and attempts to interact with the hallucination have been reported as effective methods of terminating CBS hallucinations.1,17,27,28

A latent period ranging from hours to days follows the onset of vision loss. Hallucinations tend to begin suddenly and last several months. There is general agreement that the CBS syndrome disappears when vision either improves or––more commonly–– declines significantly.

Hallucinations associated with CBS can follow one of three courses:

  • The appearance of images may alternate from periods of hallucinatory activity and inactivity.
  • They may last for days to months before completely vanishing.
  • They may occur continuously with no remission.

Insight and Response

CBS patients have full or partial insight and usually understand the inauthenticity of the images. However, this may not occur initially, because the images may genuinely complement the existing scene. Any conscious insight that develops may be intermittent.

Similarly to the development of insight, this neutral-to-positive response does not happen immediately. Geriatric patients who experience the sudden appearance and disappearance of images may fear for their mental wellness, and might be concerned that they are on the threshold of insanity.


Currently, there is no consensus regarding the level of cognition in CBS. As noted earlier, Bonnet's documentation indicated that intact cognition is a requirement for the syndrome. Other researchers have proposed that visual hallucinations are an early sign of dementia.29 They maintain that CBS occurs in the presence of reduced cognitive levels and visual loss.

The lack of distress shown by many hallucinators may indicate poor awareness of the potential gravity of these symptoms. Further, the combination of visual loss and early cognitive deficit may combine to facilitate the hallucinations of CBS.29


• Parkinson's disease. There are many similarities in the visual hallucinations associated with CBS and Parkinson's disease. They include insight and awareness, the involuntary nature of the images, and the occurrence of hallucinations when patients are alert with open eyes.

Characteristic differences are the clarity of CBS hallucinations compared to the reportedly blurred images of Parkinson's patients. Additionally, CBS is associated with highly colorful images that usually lack movement, unlike the hallucinations associated with Parkinson's.

• Psychosis. Visual hallucinations associated with psychosis and paranoia are multi-modal, involving visual images combined with sounds. Insight is overwhelmingly poor, further differentiating visions from those associated with CBS and Parkinson's.

• Substance abuse. Hallucinations are also prominently associated with drug intoxication and withdrawal. Further, they are a potential adverse side effect of several medications, such as donezepil, tramadol, anti-depressants and quinolones, as well as the desired effect of hallucinogenic recreational drugs.


Management of CBS includes a three-pronged, interventional approach that encompasses optics, medications and psychology. According to several reports, full or partial reversal of the vision loss that precipitated the hallucinations usually reduces or eliminates hallucinations.30 This may be accomplished medically, surgically or through low vision rehabilitation.

While the hallucinations are benign by nature, many patients still feel disturbed and/or threatened. Pharmacologic treatment is controversial and reserved for this group of hallucinators. Antipsychotics, anticonvulsants and serotonin reuptake inhibitors have been used to help these patients. Specific medications include risperidone, valproate, clonazepam and olanzapine.30 Gabapentin has been successfully used when other medications have failed to produce relief.30

Finally, the underlying fear of psychosis needs to be allayed. All CBS patients need reassurance that their symptoms are not an unexpected result of severe bilateral vision loss.

Many medical conditions are associated with visual hallucinations, and each entity possesses unique characteristics and distinctive features. Similarities do exist, however, and often result from a common, unified mechanism.

Hallucinations that occur secondary to strokes, migraines, intracranial lesions and cortical epilepsy ultimately are traceable to neuronal excitability and spontaneous discharge followed by cortically spreading depression. The aura of migraine is a function of spontaneous discharge and the ensuing headache results from cortical depression.

Sensory deprivation, deafferentation, denervation and release are all interconnected theories that explain the generation of hallucinations associated with sensory loss––specifically CBS. Visual phenomena associated with CBS arise from neuronal hyperexcitability and eventual spontaneous discharge. These hallucinations are unique, because they result from an expansion or relocation of cortical receptive fields.

The discrepancy between the number of patients who suffer from bilateral vision loss and the relatively few individuals who present with hallucinations has been a longstanding issue with the deafferentaion theory. Dr. Rabins tried to resolve this by postulating that CBS hallucinations occur following visual loss only when there was a prior injury or insult that altered the receptive fields.

Within the last 30 years, CBS has transitioned from an esoteric syndrome found mainly in the psychiatric literature to a slightly better known ophthalmological entity. Patients who experience hallucinations caused by CBS, stroke, migraine, Parkinson's disease and drugs can and often do present to an optometrist. So, it is beneficial for us to understand the potential cause and characteristic presentation of such phantom imagery. Because CBS is a diagnosis of exclusion, hallucinating patients who are suspected of suffering from CBS should be evaluated to rule out other neurological causes, including intracranial pathology.

Dr. Block is in general practice in New York, and serves as a consultant in geriatric nursing facilities. Please send questions or comments to


  1. Menon GJ, Rahman I, Menon SJ, Dutton GN. Complex visual hallucinations in the visually impaired: the Charles Bonnet Syndrome. Surv Ophthalmol. 2003 Jan-Feb;48(1):58-72.
  2. Manford M, Andermann F. Complex visual hallucinations; clinical and neurobiological insights. Brain. 1998 Oct;121(Pt 10):1819-40.
  3. Foerster O. The cerebral cortex in man. Lancet. 1931;221:309-12.
  4. Hankey G, Warlow C. Transient Ischemic Attacks of the Eye and Brain. Oxford: Oxford University Press; 1963:21.
  5. Vaphiades MS, Celesia GG, Brigell MG. Positive spontaneous visual phenomena limited to the hemianopic field in lesions of central visual pathways. Neurology. 1996 Aug;47(2):408-17.
  6. Salanova V, Andermann F, Olivier A, et al. Occipital lobe epilepsy: electroclinical manifestations, electrocorticography, cortical stimulation and outcome in 42 patients treated between 1930 and 1991. Surgery of occipital lobe epilepsy. Brain. 1992 Dec;115( Pt 6):1655-80.
  7. Shams PN, Plant GT. Migraine-like visual aura due to focal cerebral lesions: case series and review. Surv Ophthalmol. 2011 MarApr;56(2):135-61.
  8. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders: 2nd edition. Cephalalgia. 2004;24 Suppl 1:9-160.
  9. Welch KM, D'Andrea G, Tepley N, et al. The concept of migraine as a state of central neuronal hyperexcitability. Neurol Clin. 1990 Nov;8(4):817-28.
  10. Lauritzen M. Pathophysiology of the migraine aura. The spreading depression theory. Brain. 1994 Feb;117( Pt 1):199-210.
  11. Boecker H, Ceballos-Baumann AO, Volk D, et al. Metabolic alterations in patients with Parkinson disease and visual hallucinations. Arch Neurol. 2007 Jul;64(7):984-8.
  12. Ballanger B, Strafella AP, van Eimeren T, et al. Serotonin 2A receptors and visual hallucinations in Parkinson disease. Arch Neurol. 2010 Apr;67(4):416-21.
  13. Holyrod S, Currie L, Wooten GF. Prospective study of hallucinations and delusions in Parkinson's disease. J Neurol Neurosurg Psychiatry. 2001 Jun;70(6):734-8.
  14. O'Farrell L, Lewis S, McKenzie A, Jones L. Charles Bonnet syndrome: a review of the literature. J Vis Impair Blind. 2010 May;104(5):261-74.
  15. Gold K, Rabins PV. Isolated visual hallucinations and the Charles Bonnet syndrome: a review of the literature and presentation of six cases. Compr Psychiatry. 1989 Jan-Feb;30(1):90-8.
  16. Abbott EJ, Connor GB, Artes PH, Abadi RV. Visual loss and visual hallucinations in patients with age-related macular degeneration (Charles Bonnet syndrome). Invest Ophthalmol Vis Sci. 2007 Mar;48(3):1416-23.
  17. Schultz G, Melzack R. The Charles Bonnet syndrome: phantom visual images. Perception. 1991;20(6):809-25.
  18. Tueth MJ, Cheong JA, Samander J. The Charles Bonnet syndrome: a type of organic visual hallucinosis. J Geriatr Psychiatry Neurol. 1995 Jan;8(1):1-3.
  19. Lance JW. Simple formed hallucinations confined to the area of a specific visual field defect. Brain. 1976 Dec;99(4):719-34.
  20. Burke W. The neural basis of Charles Bonnet hallucinations: a hypothesis. J Neurol Neurosurg Psychiatry. 2002 Nov;73(5):535-41.
  21. De Jonghe JF, Kat MG, Rabins PV, Wattis JP. The genesis of phantom (deenervation) hallucinations: an hypothesis. Int J Geriatr Psych. 1995 Apr;4(10):333-5.
  22. Schadlu AP, Schadlu R, Shepherd JB 3rd. Charles Bonnet syndrome: a review.Curr Opin Ophthalmol. 2009 May;20(3):219-22.
  23. Ffytche DH. Visual hallucinations in eye disease. Curr Opin Neurol. 2009 Feb;22(1):28-35.
  24. Crumbliss KE, Taussig MJ, Jay WM. Vision rehabilitation and Charles Bonnet syndrome. Semin Ophthalmol. 2008 MarApr;23(2):121-6.
  25. Santhouse AM, Howard RJ, Ffytche DH. Visual hallucinatory syn dromes and the anatomy of the visual brain. Brain. 2000 Oct;123 (Pt 10):2055-64.
  26. Hoffman EA, Haxby JV. Distinct representations of eye gaze and identity in the distributed human neural system for face perception. Nat Neurosci. 2000 Jan;3(1):80-4.
  27. Schultz G, Needham W, Taylor R, et al. Properties of complex hallucinations associated with deficits in vision. Perception. 1996;25(6):715-26.
  28. Vikusevic M, Fitzmaurice K. Butterflies and black lacy patterns: the prevalence and characteristics of Charles Bonnet hallucinations in an Australian population. Clin Experiment Ophthalmol. 2008 Oct;36(7):659-65.
  29. Cole MG Charles Bonnet hallucinations: a case series. Can J Psychiatry. 1992 May;37(4):267-70.
  30. Jackson ML, Ferencz J. Charles Bonnet syndrome: visual loss and hallucinations. CMAJ. 2009 Aug 4;181(3-4):175-6.