The Royal Australian and New Zealand College of Psychiatrists? 2006409742751Review Article COMPLEX VISUAL HALLUCINATIONSR. MOCELLIN, M. WALTERFANG, D.
VELAKOULIS

Neuropsychiatry of complex
visual hallucinations
Ramon Mocellin, Mark Walterfang, Dennis Velakoulis

Objective: To describe the phenomenology and pathophysiology of complex visual
hallucinations (CVH) in various organic states, in particular Charles Bonnet syndrome and
peduncular hallucinosis.
Method: Three cases of CVH in the setting of pontine infarction, thalamic infarction
and temporoparietal epileptiform activity are presented and the available psychiatric,
neurological and biological literature on the structures of the central nervous system
involved in producing hallucinatory states is reviewed.
Results: Complex visual hallucinations can arise from a variety of processes involving
the retinogeniculocalcarine tract, or ascending brainstem modulatory structures. The
cortical activity responsible for hallucinations results from altered or reduced input into
these regions, or a loss of ascending inhibition of their afferent pathways.
Conclusions: A significant degree of overlaps exists between the concepts of Charles
Bonnet syndrome and peduncular hallucinosis. The fluidity of these eponymous
syndromes reduces their validity and meaning, and may result in an inappropriate
attribution of the underlying pathology. An understanding of how differing pathologies may
produce CVH allows for the appropriate tailoring of treatment, depending on the site and
nature of the lesion and content of perceptual disturbance.
Key words: Charles Bonnet, hallucinosis, peduncular, vascular, visual hallucination.
Australian and New Zealand Journal of Psychiatry 2006; 40:742–751

Disorders of perception comprise some of the most
important and complex phenomena encountered in psychiatric assessment. This complexity is due to the varied
clinical contexts in which these disorders occur and the
heterogeneity of their content. Perceptual disturbances,

Mark Walterfang, Consultant Psychiatrist of Neuropsychiatry Unit, Royal
Melbourne Hospital, and Research Fellow of Melbourne Neuropsychiatry
Centre, University of Melbourne (Correspondence); Ramon Mocellin,
Consultant Psychiatrist of Neuropsychiatry Unit, Royal Melbourne
Hospital, and Northwest Aged Persons’ Mental Health Program, Bundoora;
Dennis Velakoulis, Director of Neuropsychiatry Unit, Royal Melbourne
Hospital, and Clinical Director of Melbourne Neuropsychiatry Centre,
University of Melbourne
Neuropsychiatry Unit, Level 2, John Cade Building, Royal Melbourne
Hospital,
Melbourne,
Victoria
3050,
Australia.
Email:
mark.walterfang@mh.org.au
Received 19 February 2006; accepted 23 February 2006.

particularly hallucinations, are usually but not always
characteristic of psychiatric disorders such as schizophrenia and delirium. Complex visual hallucinations
(CVH) have been associated with organic brain disease,
and are a common referral reason to psychiatrists in
consultation-liaison, old age and neuropsychiatric settings. Accurate diagnostic assessment requires a detailed
elucidation of the clinical features and associated investigation findings, an understanding of alternative phenomena such as visual illusions and distortions and an
appreciation that terms such as Charles Bonnet syndrome
(CBS), peduncular hallucinosis (PH) and organic hallucinosis have been poorly defined. By presenting three
illustrative case reports, we aim to clarify the current
understanding and nosology of visual hallucinations and
discuss some of the putative biological mechanisms
involved.

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R. MOCELLIN, M. WALTERFANG, D. VELAKOULIS

Case report A
Mrs VH was an 85-year-old widow with a long history
of visual impairment who lived at home alone presented
with a 2 day history of visual changes. These began with
the experience of a ‘grey blind’ coming down over her
left visual field over a number of minutes, without other
neurological symptoms. Within hours her entire visual
field was covered by a translucent sheet ‘. . . with yellow
and pink flowers, like a nightdress’, and moving ‘like a
sheet on a washing line’. Mrs VH was not distressed,
until she subsequently saw frequent disembodied and
grimacing male faces, mainly that of a James Bond actor.
These faces then appeared on the bodies of ambulance
officers and family members. Over the next 24 hours
following hospital admission she continued to see these
faces, which melted and distorted, as well as troops of
children, one to two feet tall and in green-blue uniform,
marching around her hospital bed. These hallucinations
were prominent at night, and Mrs VH was observed stepping around perceived objects in an empty ward corridor.
When interviewed, she described the phenomena as very
real and was frightened they would recur. Thorough neuropsychiatric evaluation revealed no other neurological
symptoms, perceptual disturbance, or other psychotic
phenomena. Mrs VH also denied alterations in mood or
recent changes in memory or other function.
Mrs VH’s past medical history included 15 years of
visual impairment (thought to be secondary to glaucoma), medicated hypertension, type-2 diabetes mellitus
and hypercholesterolemia. There was no past or family

743

psychiatric history. Medications included metformin,
glipizide, amlodipine, irbesartan, simvastatin and
timolol.
On physical examination, Mrs VH was normotensive
and afebrile, with no carotid bruits or other cardiovascular findings. There were no focal neurological signs.
Opthalmoscopy revealed bilateral severe macular degeneration and cataracts. On mental state examination she
was awake and alert, and appeared anxious. Apart from
her visual hallucinations, there were no other disorders
of perception and she had partial insight. Cognitively, her
attention, verbal and spatial memory and language were
intact. There were no disorders of executive function or
praxis, although constructional abilities were limited by
poor vision. Her Mini-Mental State Examination [1]
score was 25/25, with five points unable to be tested
resulting from her visual impairment.
Routine blood investigations were within normal limits
and electroencephalogram showed no evidence of encephalopathy or epileptiform activity. A single-photon
emission computed tomography scan showed no areas
of hypoperfusion, and occipital perfusion was normal.
Magnetic resonance imaging (MRI) demonstrated
multiple subcortical white matter intensities throughout
deep white matter, and lesions bilaterally in the pons
(Fig. 1A). On the basis of her abrupt-onset formed hallucinations (with patterned, Lilliputian and grotesque
facial content), her lack of evidence of a delirious process
or cognitive impairment, lack of other neurological signs
and pontine lesions of likely vascular origin on MRI, a
diagnosis of PH was made and she was commenced on

Figure 1. Magnetic resonance imaging scans of cases A, B and C. (A) Axial fluid-attenuation inversion recovery
(FLAIR) image of the brain demonstrating pontine white matter lesions (arrow). (B) T2-weighted scans show new right
thalamic infarct (arrow), in addition to a moderate amount of periventricular white matter disease. (C) Preoperative
T2-weighted scan showing left temporal/inferior parietal arteriovenous malformation (arrow), abutting the optic
radiation.
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COMPLEX VISUAL HALLUCINATIONS

olanzapine 2.5 mg at night. The hallucinations resolved
after further 48 hours of olanzapine therapy.

Case report B
Mrs CH was a 68-year-old woman who presented with
a 3 week history of visual hallucinations. At the age of
38 years she had had a large left frontal haemorrhage, of
presumed hypertensive aetiology, which she survived
without significant cognitive or neurological sequelae.
The hallucinations were of sudden onset, initially in the
periphery of vision and without any other neurological
symptoms. The patient described seeing small children
in groups of three or four which appeared smaller than
usual. They were dressed in colourful uniforms. Occasionally she felt they were calling her name. There were
no other hallucinatory experiences. She was described as
inattentive and disoriented with worsening confusion at
night. There was no significant family or past psychiatric
history. No medications were prescribed and there was
no history of substance use.
On neuropsychiatric examination Mrs CH was afebrile
and normotensive and there were no focal neurological
findings. Fundoscopy was normal. There were no frontal
release signs or features of parkinsonism. She was euthymic, had normal language function and there was no
evidence of other disorders of perception or psychosis.
By the time of examination the inattention had resolved,
cognition was intact and Mrs CH had full insight into the
hallucinatory experiences.
Routine investigations, including electrolytes, were
within normal limits. An urgent computed tomography
scan excluded any new haemorrhage, but demonstrated
a developing lucency in the right thalamus consistent
with a new infarct. An MRI scan 5 days after this confirmed a right thalamic lacunar infarct (Fig. 1B) as well
as a frontal defect consistent with the old haemorrhage
and periventricular white matter changes in keeping with
the patients age.
A diagnosis of CVH due to a new thalamic vascular lesion was made and Mrs CH was commenced on
risperdone 1 mg at night. The symptoms resolved completely after 1 week, and medication was successfully
withdrawn.

angiographically embolized and surgically removed
without significant complications. Ms VC successfully
returned to her previous employment. One year later the
lesion was found to have recurred medial to the surgical
site, adjacent to the lateral ventricle, and although surgery was not recommended at that time, she was lost to
follow up. She periodically had ‘flashes of light’ in the
intervening 6 years, which were diagnosed as migraine.
There were no significant features in the family or developmental history and no past history of psychiatric
disorder.
At age 33 years Ms VC developed transient right visual
field loss over a period of hours without any associated
neurological features or headache. This was followed by
a witnessed grand mal seizure resulting in admission to
hospital. At that time all routine investigations were unremarkable and neuroimaging revealed no new findings.
Three days later, Ms VC reported a number of visual
hallucinations with complete maintenance of insight. She
saw red letters (W, R and K) on people’s faces and on
her own face in the mirror. She saw ‘hundreds of little
spikes’ coming in and out of the floor and small ants
moving on regularly patterned surfaces. These were
experienced predominantly in the right visual field. During the following days she saw groups of disembodied
faces and torsos floating 10 feet above the ground. These
images were monochromatic, unfamiliar, of normal size
and mobile. Although they moved their lips giving the
appearance that they were talking to her, Ms VC experienced no auditory perceptual disturbances. There was no
palinopsia and these experiences disappeared with eye
closed and were worse in fading light.
Ms VC presented as anxious, but was otherwise euthymic and there were no features of delirium. No other
psychotic features were noted, there were no focal
neurological signs and fundoscopy was normal.
Routine blood investigations including electrolytes
were normal. Electroencephalogram showed a midtemporal epileptiform focus, approximately at the site of
the recurrent AVM. Ms VC was treated with phenytoin,
which resulted in full resolution of her symptoms over
the next 24 hours. The diagnosis was made of CVH
resulting from an irritative, epileptogenic focus of the left
temporal lesion.

Discussion
Case report C
Ms VC was a 33-year-old single woman who had been
diagnosed with a left temporoparietal arteriovenous malformation (AVM – Fig. 1C) on MRI after presenting with
headache at the age of 25 years. The AVM had been

Each of the above cases describe examples of visual
hallucinations occurring in the context of structural brain
lesions and illustrate the difficulty categorizing such phenomena. In 1838 Esquirol provided the earliest and simplest definition of a hallucination as a percept without an

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R. MOCELLIN, M. WALTERFANG, D. VELAKOULIS

object, perceived as real and in the external environment
[2]. Slade refined this definition to refer to a percept-like
experience in the absence of an external stimulus that is
experienced as a true percept, is spontaneous, unwilled
and cannot be readily controlled [3,4]. Edition IV of the
Diagnostic and Statistical Manual (DSM-IV) drew on
this to define hallucinations as a ‘sensory perception that
has the compelling sense of reality of a true perception
but that occurs without stimulation of the relevant sensory organ’ [5]. Hallucinations may have a common origin in internal experiences in healthy individuals and in
neuropsychiatric illness, where in illness states a failure
in reality testing results in this internal experience being
misattributed externally [4,6].
A hallucination is phenomenologically distinct from
either a sensory distortion or a false perception. A distortion refers to perceived changes in the nature of a real
object, such as changes in intensity (louder or brighter),
or geometric properties (larger/smaller or distorted).
Other false perceptions include illusions in which an
object is transformed into another form and pseudohallucinations. Pseudohallucinations are experienced as percepts that arise from the patient’s inner world rather than
the external environment and are usually recognized as
‘not real’ and/or as vivid internal visual imagery [7,8].
These perceptual disturbances are generally considered
to occur along a continuum from reality-based percepts
through to frank hallucinations [9], in common with a
range of other psychotic symptoms such as delusions,
passivity experiences and thought alienation [10]. Visual
hallucinations are more strongly associated with
‘organic’ illness such as visual pathology, neurodegenerative disorders or central nervous system (CNS) lesions
[11–13] rather than ‘functional’ psychiatric disorders
such as schizophrenia where auditory hallucinations are
more common.
Visual hallucinations of an organic aetiology are frequently characterized by variability in insight. Although
the patient in case A described being frightened by the
hideous faces she saw, she clearly identified them as not
real once they abated. The patients in cases B and C
always identified their experiences as not real. Hence,
these experiences do not always strictly meet phenomenological criteria for hallucinations. Classificatory systems such as the International Classification of Disease
(ICD-10) acknowledge this by the use of terms such as
‘organic hallucinosis’ [14]. The use of the term ‘organic’
is problematic when used to describe psychiatric symptoms or syndromes [15] as it implies that there are ‘nonorganic’ hallucinations that lack a biological substrate.
Although the form of visual hallucinations described
in these cases is protean, there are common features: their
vivid and colourful nature(cases A, B, C), the inclusion

745

of small people or children (Lilliputian hallucinations
[LHs], cases A and C) and the involvement of regular
patterns (cases A and C) or disembodied faces or limbs
(cases A and C). These complex visual phenomena are
differentiated from more simple, unformed hallucinations such as crudely formed flashes of light and colour,
or indistinct forms. Complex visual hallucinations may
also include branching or tessellated patterns, vivid and
colourful formed animals (real or bizarre), soldiers or
others in uniform, landscapes and complex scenes. Complex visual hallucinations are frequently associated with
a variety of visual distortions, such as palinopsia, in
which repeated images of a perceived image is seen, or
distortion of a face or head (prosometamorphopsia) [16].

Complex visual hallucinations –
the role of lesion location
The anatomy of the retinogeniculocalcarine tract is
well understood, including how lesions of the tract at
different levels produce classically described visual field
defects (Fig. 2). Although these not completely characterized in mammals, basal projections onto this tract arise
from excitatory cholinergic centres (parabrachial and
parabigeminal nuclei) with inhibitory serotonergic input
coming from the dorsal raphe nuclei [16] (shown in
Fig. 3). At the centre of this tract lie the dorsal lateral
geniculate nucleus (LGN) of the thalamus and the lateral
pulvinar. The primate pulvinar has an important role in
simple visual processing, but also visual salience (generating signals related to the salience of visual objects) and
linking eye movement to this function [17].
Retinal or other proximal lesions remove or disturb
direct inputs of the external environment to the visual
system. Complex visual hallucinations may then arise
from spontaneous discharges in distal portions of this
system [18] (Fig. 4a). Brainstem lesions may disrupt
these serotonergic inhibitory raphe nucleus inputs resulting in excitation of the dorsal LGN and dysregulation of
retinal inputs resulting in CVH (Fig. 4b). The dorsal
raphe nuclei have also been implicated in both the sleepwake cycle [19] and regulation of rapid eye movement
(REM) and non-REM sleep [20] in mammals. Sleepassociated CVH may be seen in normal sleep (hypnopompic and hypnogogic hallucinations), sleep disorders
(narcolepsy–cataplexy syndromes), delirium and Lewy
Body Dementia. Complex visual hallucinations in CBS
are often accentuated in states of reduced consciousness
or fading light. These clinical findings further suggest an
important role of the dorsal raphe system in the generation of CVH. Thalamic lesions may directly affect critical structures such as the pulvinar or the associated

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COMPLEX VISUAL HALLUCINATIONS

Figure 3. Intersection of ascending pathways. Optical
information in the retinogeniculocalcarine tract (1–8, 11
as in Fig. 2) is modulated by ascending input from
pedunculo-pontine and parabrachial nuclei (9) and
raphe nuclei (10) via the superior colliculus (7). Hashed
areas show regions where interruptions are known to
produce visual hallucinations.

Figure 2. Retinogeniculocalcarine tract. Optical
information from retina (1) passes along optic nerve (2)
through the optic chiasm (3) and optic tract (4) into the
lateral geniculate nucleus of the thalamus (5) where it
receives input from the superior colliculus (7) via the
pulvinar (6) and then traverses the optic radiation (8 and
9) through temporal lobe (13) into visual cortex (10–12).
brainstem inputs described above, and disrupt visual processing and salience (Fig. 4c). Damage to retinal inputs
in this area may also operate in the same fashion as a
more proximal de-afferentating lesion.
It is also possible that CVH arise from lesions in other
cortical areas, such as the frontal and temporal lobes
which project to the visual system via the dorsal LGN and
medial pulvinar [17]. These regions are essential for
object recognition and linking ideas and concepts with the
perceptual experience of the external environment [21].
Complex visual hallucinations can also occur in lesions
of the occipital cortex usually within the dysfunctional
hemianopic field [22,23]. This may relate to disruption of
corticothalamic projections and generation of percepts
within adjoining intact visual or visual association cortex
[24]. However, this is also suggestive of ‘back-projection’

of images stored in other intact cortical systems, but in
this case into a disturbed visual field. This may represent
a normal process by which the percept generated by the
visual system is linked to visual, verbal and affective
memory (generating an ‘internal’ percept) in order for it
to be identified [21,25]. Epileptiform discharges may
generate hallucinations in a similar fashion. However,
there is some evidence visual cortex can be activated by
discharges originating in visual association areas in temporal and parietal regions, indicating a mechanism for
CVH in some cases of temporal lobe epilepsy [16].
While differing pathologies may lead to complex visual
hallucinations, the form these hallucinations take may
relate to particular cortical locations. Using factor analysis
of clinical information collected from patients with CBS
linked with predominately primate functional MRI and
neurophysiological information, Santhouse and Howard
have postulated that CVH in CBS can be linked to hierarchical visual pathway streams [26]. These workers suggest hallucinations of extended scenes and people and
objects (including LHs) are associated with the ventral
occipitotemporal cortex, hallucinations of faces and facial
distortions (prosopometamorhopsia) with the superior
temporal sulcus, and visual perseveration and delayed
palinopsia (reappearance of a percept with shift in gaze
after time delay) with visual parietal regions [26]. These
compelling findings await further study and clarification.

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R. MOCELLIN, M. WALTERFANG, D. VELAKOULIS

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lobe epilepsy. The best described conditions characterized by CVH are PH and the CBS, both clinical syndromes encompassing CVH and historically associated
with particular clinical contexts.

Peduncular hallucinosis

Figure 4. Lesions and their effect on the visual circuit.
(a) Lesions in the proximal visual system may result in deafferentation producing in ‘release’ activity in the cortex,
with CVH arising from spontaneous discharges in visual
and associated cortical areas. (b) Brainstem lesions
involving the dorsal raphe system result in loss of
ascending inhibition to the dorsal LGN may result in a
hyper-excited geniculate and generation of CVH at the
cortical level. (c) Lesions involving thalamic nuclei may
disrupt the important processing function of these
structures possibly resulting in impaired retinal signals
and CVH. 1, retina; 2, lateral geniculate nucleus;
3, pulvinar; 4, superior colliculos; 5, occipital cortex;
6, doral raphe nuclei; 7, parabrachial and
pedunculopontine nuclei; 8, reticular nucleus of thalamus.
Complex visual hallucinations have been reported in a
wide variety of clinical and non-clinical circumstances.
They may occur as hypnopompic or hypnagogic phenomena in healthy individuals or in sensory deprivation
states [27]. Complex visual hallucinations have been
described in narcolepsy–cataplexy syndrome, delirium
tremens, Parkinson’s disease, Lewy Body Dementia,
intoxication with psychoactive substances and temporal

‘Peduncular hallucinosis’ is used to describe vivid and
complex hallucinations in the presence of lesions of the
midbrain and/or thalamus [28]. PH was first described
by the French neurologist and neuropsychiatrist Jean
Lhermitte in a 72-year-old woman with hallucinations of
strangely, colourfully attired people and groups of children which occurred at dusk [29]. These were associated
with no alteration of conscious state and neurological
signs consistent with an infarct of the pons and midbrain.
Lhermitte’s colleague Von Bogaert coined the term
‘peduncular hallucinosis’ in his description of a patient
with a similar presentation, together with post-mortem
neuropathological evidence of midbrain infarction [30].
The term ‘peduncular’ was not intended as a reference
solely to the cerebral peduncles but to the whole midbrain and its surrounds. De Morsier extended the syndrome to include thalamic lesions, and re-established the
lesion model for PH [31] whereas his predecessors had
suggested sleep-wake cycle disturbances and ego dissolution as the likely origins [29,30].
PH has subsequently been associated with a range of
differing CNS pathologies, including vascular and infectious midbrain [32], pontine [33] and thalamic lesions
[34], local subarachnoid haemorrhage [35], compression
by local [36,37] and distal [38] tumours, basilar migraine
[39], basilar vascular hypoplasia [40] and following
regional surgical [41] or angiographic [42] interventions.
Most of these pathologies have been basilar in location,
and resolution of hallucinations has been noted to result
from treatment of reversible pathologies such as compression [43]. Common hallucinations include animals,
people or children, grotesque and deforming faces or
heads, landscapes and tessellated patterns, and groups of
people walking in file are commonly reported [31,34,44].
PH frequently presents with LHs, defined by Leroy as
a visual phenomenon in which a patient views detailed
miniature people in lines or groups, often undertaking
unusual postures or actions, usually accompanied by
wonder rather than terror [45,46]. LHs can occur in a
range of neuropsychiatric syndromes including schizophrenia [47], dementia [48], encephalomyelitis [49],
traumatic brain injury [50], AIDS-related dementia [50],
multiple sclerosis [51], side-effects of dopaminergic and
anticholinergic anti-Parkinsonian medication [52] and
abuse of over-the-counter substances such as cough

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Table 1.

Comparative features of peduncular hallucinosis and Charles Bonnet syndrome

Peduncular hallucinosis
Percepts predominantly visual
Percepts vivid, formed and colourful
May include Lilliputian phenomena
Stimuli animate, mobile and non-stereotypical
Predominate at night
Generally clear sensorium
May have ocular disease; CNS pathology frequently reported
Occur across age groups

Charles Bonnet syndrome
Percepts predominantly visual
Percepts vivid, formed and colourful
May include Lilliputian phenomena
Varied
Predominate at night
Generally clear sensorium
Frequently have ocular disease; CNS pathology
rarely reported
Most common in elderly

CNS, central nervous system.

syrup [53]. Generally, LHs have been felt to have no
localizing significance [54], although they have been
reported in basilar conditions such as basilar migraine
[39] and are a common presentation in PH [22].
Risser and Powell have reviewed the commonly
reported features of PH [44], seen in Table 1 alongside
those reported to characterize CBS. These are predominantly formed and colourful visual hallucinations, occurring during clear sensorium and often during night-time.
Interestingly, they also noted that peripheral (ocular)
rather than central visual (CNS) dysfunction may be
present.
The lesions responsible for PH appear to impinge on
the brainstem reticular formation or its thalamic targets
[16] (Fig. 4b,c). Whereas lesions in visual pathways
appear to produce hallucinations via release phenomena
in the visual cortex through loss of corticocortical or
thalamocortical inputs (Fig. 4a), mesencephalic lesions
may produce hallucinations via interruption to serotonergic inhibitory afferents into the dorsal LGN of the thalamus, resulting in a dysregulated LGN which then projects
to visual cortical regions [16]. Of note is that an allied
auditory form of PH has been reported and associated with
pontine lesions of varying pathologies [55,56], and the
underlying neurobiology again is reported to be loss of
serotonergic raphe nuclei ascending inhibition.

Charles bonnet syndrome
Charles Bonnet syndrome describes a group of patients
with visual hallucinations in the setting of visual loss,
and shows significant clinical overlap with PH. In 1769
Charles Bonnet described his 89-year-old grandfather
who was healthy but blind as a result of severe cataract
disease. He experienced colourful visions of men,

women, fantastical birds and buildings, which changed
in size, shape and location but were never accepted as
real [57]. Later, Bonnet described similar experiences
when he himself developed visual impairment [58].
There has been an extensive case-report based literature
over the past 200 years describing groupings of similar
phenomenology, generally including the appearance of
complex visual hallucinations without other psychopathology and in the presence of a clear sensorium. However, little agreement exists as to whether eye or brain
pathology is central to constitute this syndrome, unlike
PH where aetiology is implicit. De Morsier, who eponymized the syndrome, de-emphasized eye pathology, and
some recent authors have employed the very broad definition: ‘any state of visual hallucinations in the elderly
irrespective of accompanying symptomatology’ [59].
More recently, visual impairment has been regarded
as central to the syndrome [60]. In a large systematic
review, 12% of visually impaired people met criteria for
CBS defined as complex visual hallucinations associated
with insight and in the absence of other disorders of
perception or delusions [12]. Sufferers had a mean age
of 74.5 years, showed a female preponderance and suffered from common causes of visual loss in this age
group (macular degeneration 56%, diabetic retinopathy
17.5% and glaucoma 6.5%). Hallucinations generally
included clear, colourful and often Lilliputian images of
people, animals and inanimate objects which often varied
over time. They tended to occur in the evening, poor
light, or personal isolation. These patients were not
screened clinically or radiologically for CNS disease,
meaning that CNS lesions such as those found in PH
cannot be excluded.
Many attempts have been made to understand the neurobiological basis of CBS. In general, most authors have
agreed on the important role of reduced or absent visual

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R. MOCELLIN, M. WALTERFANG, D. VELAKOULIS

system stimulation or input. This altered input may originate not only from the retina (such as in macular degeneration or cataract disease) but from lesions at any point
in the visual system (including lesions of intracerebral
visual pathways or visual cortical areas – Fig. 4a).
Berrios and Brook understood hallucinations in CBS
as de-afferentation phenomena which resulted from
‘intracerebral perceptions’ not unlike the ‘phantom limb’
syndrome [59]. De-afferentation in the CNS has been
shown to result in cortical hyperexcitability, secondary
to presynaptic neurotransmitter vesicle changes, postsynaptic receptor up-regulation and changes in GABA
(γ-aminobutyric acid) and NMDA (n-methyl-d-aspartate)
sensitivity in surrounding CNS regions [18]. Hence,
minor stimuli may be elaborated into complex hallucinations when received by a system disordered in this
fashion. An effective de-afferentation may also occur
following ocular lesions. Downstream cortical changes
may result in ‘minor’ stimuli being amplified, distorted
and elaborated into complex hallucinations when
received by a hyper-excitable cortical network. Spontaneous activity in the absence of sensory input can also
result from de-afferentation, resulting in bursts of paroxysmal synchronous electro-physiological discharges
resembling seizure activity and potentially resulting in de
novo image formation [18,61]. This has been supported
by attenuation of hallucinations in CBS when anticonvulsants are used [62]. We would favour a more restricted
definition of CBS as a syndrome where lesions to primary visual pathway structures result in reduced visual
throughput of the retinogeniculocalcarine tract and produce a functional de-affererntation syndrome.

749

likely to have resulted from an ischaemic vascular event
affecting ascending structures superimposed on a visual
system made vulnerable by both de-afferentation (blindness) and previous vascular disease (represented by
extensive white matter disease in cortex and brainstem
seen on MRI).
In case B, although the thalamic infarct, probably
resulting from hypertensive small vessel disease would
account for the onset of delirium and CVH, pre-existing
pathology could also contribute to a vulnerable substrate.
The scarred area resulting from the frontal haemorrhage
some 30 years previous may have involved the temporal
portion (Meyer’s loop) of the optic radiation. Lesions of
the tract in this region may result in an upper and peripheral visual field defect, and the hallucinations originated
in the periphery of vision. White matter changes noted
on neuroimaging may have also contributed to this
vulnerability.
Epileptic activity most likely arising from a mid-temporal region surgical scar resulted in CVH in case C,
representing one of the other CNS conditions (temporal
lobe epilepsy) which are known to produce these symptoms. However, the symptoms of ‘flashing lights’ may
also herald the recurrence of the AVM or development of
scar tissue. The AVM is in a region closely related to the
temporal portion of the optic radiation – again suggestive
of a vulnerable substrate if this structure was impinged
upon by the AVM or damaged by embolization or surgery
when it was removed.
These three cases illustrate that anatomically disparate
lesions can result in similar forms of CVH (Fig. 4) and
that knowledge of the pathophysiology of CBS and PH
aid in understanding how such different lesions may generate similar types visual symptoms.

Complex visual hallucinations –
a common pathophysiology
Treatment of complex visual hallucinations
Without an understanding of the preceding sections the
three presented cases could be simply diagnosed as a
case of CBS in a blind, elderly patient (case A), a diagnosis of PH in a patient with a new thalamic infarct (case
B) and CVH secondary to epilepsy originating from mid
temporal scarring (case C). Further scrutiny of each of
these cases, however, allows for a more sophisticated
understanding.
The early symptoms described in case A are suggestive
of a vascular event such as infarction. Although the
descending ‘grey blind’ approximates the classic features
of amaurosis fugax (transient monocular blindness
resulting from embolization of retinal arteries), involvement of the left visual field is more suggestive of a lesion
distal to the optic chiasm. Rather than solely arising in a
de-afferented visual system the CVH in case A are more

In general, management of CVH must be broad in its
approach. An understanding of the possible pathologies
that produce CVH allow for the correct attribution of
neurobiological aetiology – for example, in a patient with
impaired vision, not overlooking the possibility of a thalamic or brainstem infarct as an underlying pathology
and thus ensuring that brain imaging is undertaken. The
reassurance provided by the explanation of the organic
basis of the symptoms is often helpful, and that symptoms often resolve spontaneously. Withdrawal of potential pro-hallucinogenic medications, if feasible, often
forms the first step. In cases A and B patients’ improvement may not be attributable to the use of atypical antipsychotics alone as the symptoms may have resolved
spontaneously. As a result it may be appropriate in some

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750

COMPLEX VISUAL HALLUCINATIONS

cases showing spontaneous improvement of symptoms
to not initiate pharmacotherapy. Evidence for pharmacological management is limited, although treatment
response has been reported with atypical antipsychotics
[63,64] and anticonvulsant medication [65,66], although
the potential seizure threshold-lowering effect of antipsychotics may worsen symptoms in some cases of
CVH. Only a brief period of antipsychotic treatment may
be required, particularly when the causative process is
thought to have resolved (such as in cases of transient
ischemia or delirium). Correction of predisposing factors
via interventions such as cataract surgery [61], laser photocoagulation of the retina [67] and the use of optical
correcting devices [68] can be important additional considerations. Additionally, there is increasing evidence
that controlling risk factors for cerebrovascular disease
in elderly populations is important in preventing stroke
and maintaining functional level [69,70]. Visual hallucinations may therefore herald underlying cerebrovascular
disease, and investigation and addressing risk factors
such as hyperlipidaemia, hypertension and diabetes control may be equally important therapeutic aims. This
does, however, need to be balanced against the potential
risk of cerebrovascular events with atypical agents such
as olanzapine and risperidone in the elders with significant cardiovascular risk factors [71].

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Conclusions

14.

Use of historical eponymous syndromes characterizes
medicine, and ensures the work of medical pioneers lives
on in current medical practice. However, in certain circumstances, the use of eponymous terms such as PH and
CBS – particularly when definitions are fluid – may
impair an accurate pathophysiological understanding of
illness and result in barriers to appropriate disease taxonomy, investigation and treatment. An understanding of
the underlying neuroanatomy and functional neurobiology of the structures where lesions are associated with
CVH can aid both clinician and patient in understanding
the underlying pathological processes responsible for
this often highly distressing neuropsychiatric syndrome.
The investigation of the processes involved in the generation of CVH can provide a structure on which the study
of other neuropsychiatric symptoms such as auditory hallucinations may be modelled.

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Acknowledgement
We thank Dr Levent Efe for his illustrations, funded
by a grant from Organon Pharmaceuticals.

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