Approach To The Patient With Visual Hallucinations

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Approach to the patient with visual hallucinations
Author: Victoria S Pelak, MD

Section Editor: Paul W Brazis, MD
Deputy Editor: Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2017. | This topic last updated: Aug 22, 2016.
INTRODUCTION — Visual hallucinations are a clinical manifestation of neuroophthalmologic dysfunction resulting from a wide variety
of underlying etiologies. They can be very disconcerting to some patients, regardless of their insight, and can significantly decrease
quality of life [1].
Familiarity with the disorders associated with visual hallucinations is essential to provide the appropriate care. The history,
accompanying symptoms, and clinical signs are important elements for determining the most likely cause. In certain patients, further
investigation may be necessary before a definitive cause can be determined.
This topic discusses the most common causes of visual hallucinations and their distinguishing features. Visual hallucinations associated
with the Charles Bonnet syndrome are discussed separately. (See "Visual release hallucinations (Charles Bonnet syndrome)".)
CLASSIFICATION AND TERMINOLOGY — A visual hallucination is a perception of an external visual stimulus where none exists. In
contrast, a visual illusion is a distortion or modification of real external visual stimuli [2]. Examples of visual illusions include distortions
of size (micropsia or macropsia), shape (metamorphopsia), and color (dyschromatopsia). Visual hallucinations and illusions are
clinically distinct phenomena, but have overlapping etiologies.
A useful classification scheme categorizes hallucinations as simple or complex [3]. Classifying the hallucination as simple or complex
can narrow the differential diagnosis for the underlying cause.
● Simple hallucinations are also referred to as "elementary" or "non-formed." They do not include complex imagery. Examples
include lights, colors, lines, shapes, or geometric designs. Simple hallucinations of light can be further classified as phosphenes,
which are visual hallucinations of lights without structure, and photopsias, which are visual hallucinations of lights with geometric-
like structure (triangles, diamonds, squares).
● Complex hallucinations can include images of people, animals, objects, or a lifelike scene. Complex hallucinations are also referred
to as "formed."
Another classification scheme divides visual hallucinations into irritative phenomena that result in brief stereotyped hallucinations, and
release hallucinations that are continuous and variable [4]. This classification scheme is somewhat limited because the generalizations
are not absolute, and some disorders have characteristics of both types. As an example, in migraine, visual hallucinations can be
stereotyped and brief, or variable and continuous. Hallucinations associated with peduncular hallucinosis are often brief, but the content
tends to be variable and not stereotyped.
ETIOLOGIES — The clinical features of various causes of visual hallucinations are summarized in the table and are discussed below
(table 1).
Retinal pathology — Traction, irritation, injury, or disease of the retina can stimulate retinal photoreceptors, causing simple
hallucinations in the form of flashes, sparks, or streaks of light.
A posterior vitreous detachment (PVD) producing traction on the retina is a common cause of retinal hallucinations, particularly in older
patients [5]. Other potential retinal causes are listed in the table (table 2).
Hallucinations associated with retinal pathology are never complex. Insight is intact. Intrinsic motion is a common feature of the
hallucinations of light; patients often describe flashes or flashing, whirls, shooting, lightning-like, or spinning pinwheels. In many cases,
the condition and the hallucinations are monocular, but some conditions (eg, cancer-associated retinopathy) can affect both retinas
concomitantly, producing binocular hallucinations. The hallucination can occur in any area of the visual field. In cases of retinal traction,
valsalva-like maneuvers may be a trigger.
The duration of the hallucination is usually measured in seconds. The frequency is variable. While some patients experience multiple,
brief hallucinations with waxing and waning frequency throughout the day, others may experience only one to three events prior to
presentation. More frequent or persistent retinal hallucinations are associated with certain types of acute zonal occult outer retinopathy
(AZOOR) and with cancer-associated retinopathies [6,7]. In contrast, patients with PVD are likely to present with only a few episodes.
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If a scotoma (a circumscribed area of decreased vision) develops after the onset of simple hallucinations, this can indicate a retinal
injury that may become permanent if not evaluated and treated promptly (eg, retinal detachment). In addition to vision loss, the
symptoms of retinal injury include seeing shadows or having distorted, warped, or blurred vision.
All hallucinations suspected to be of retinal origin should prompt an urgent evaluation by an ophthalmologist to ensure that the retina is
intact (ie, no tears, holes, detachments). If the retinal examination is normal, but other signs and symptoms suggest retinal disease,
then occult retinal disorders such as cancer-associated retinopathy or certain types of AZOOR could be responsible. A formal visual
field test, electroretinogram, and serum studies for antibodies against retinal proteins (eg, recoverin or enolase) may be useful in
revealing a cause of retinal dysfunction [8]. (See "Paraneoplastic visual syndromes".)
Vision loss (Release hallucinations or Charles Bonnet syndrome) — Visual acuity loss or visual field loss from any cause, affecting
the eye, optic nerve, chiasm, or tract, optic radiations, or the visual cortex, can cause visual hallucinations, often referred to as release
hallucinations or Charles Bonnet syndrome (CBS) [9].
CBS is most often reported in elderly patients, reflecting the mean age of the most common underlying conditions: age-related macular
degeneration, glaucoma, diabetic retinopathy, and cerebral infarction [9-14]. Cognitive impairment and social deprivation may be risk
factors [12,15-19].
These visual hallucinations can be simple or complex. Features that help distinguish CBS from psychosis are the absence of auditory
or somatosensory hallucinations and other abnormal thought content [13]. Because the hallucinations tend to occur in the area of vision
loss, they can be monocular or binocular and/or restricted to one segment of the visual field. Most patients report a duration of several
minutes, but they can last less than one minute or be continuous [1,9,14,16,20]. While the majority of patients experience hallucinations
multiple times a day or week, some patients experience only a few isolated episodes [1,11,14]. Insight is usually retained.
Patients without known ocular disease require an ophthalmologic and/or neurologic evaluation to determine the underlying cause of
vision loss. CBS is discussed in detail separately. (See "Visual release hallucinations (Charles Bonnet syndrome)".)
Migraine aura — Approximately 15 percent of individuals with migraine experience aura. Visual aura is the most common type of aura,
occurring in 90 percent of people with migraine aura [21-23]. Most studies estimate the lifetime prevalence of visual aura of migraine to
be between 0.7 to 1.2 percent [24-26].
The pathophysiology of migraine aura is not well understood, but is believed to be related to a phenomenon known as cortical
spreading depression, a self-propagating wave of neuronal and glial depolarization that spreads across the cerebral cortex [27]. (See
"Pathophysiology, clinical manifestations, and diagnosis of migraine in adults", section on 'Pathophysiology'.)
Clinical features — Migrainous visual hallucinations are usually simple and typically linear or geometric (eg, zig zag lines) in
appearance [28]. The classic visual aura is the fortification spectra, which is considered pathognomonic for migraine (figure 1). A
scintillating scotoma is another common migraine aura; this is an area of decreased vision that is outlined by a hallucination with
geometric design. Patients also describe seeing spots, dots, or shooting stars. Migraine auras tend to be black and white or
monochromatic, and are more geometric and linear in shape compared with epileptic visual hallucinations, which are more often
colorful and circular or spherical in appearance [28,29].
Migraine aura can also include vision loss and visual distortions, such as the appearance of heat waves and tunnel vision. Objects may
appear smaller or larger (micropsia and macropsia) or with distorted contours [30,31]. Complex visual hallucinations are uncommon,
but have been described in migraine [30,32]. Patients with migrainous visual hallucinations retain insight, almost without exception.
All migraine hallucinations are believed to be binocular. It is unclear if monocular visual hallucinations of migraine truly exist [33].
However, many patients report monocular symptoms, likely misinterpreting binocular, homonymous visual field hallucinations as
occurring only in the ipsilateral eye.
Migrainous visual hallucinations can occur in any area of the visual field, but commonly begin in the central portion [28]. Growth or
spread of the aura, often from the center to the periphery of the visual field, occurring over a few minutes is a common feature of
migraine that helps distinguish it from seizure (in which spread occurs more rapidly, over a few seconds) and retinal hallucinations
(which do not tend to grow or spread) [28,30,31,34]. A minority of migrainous visual auras are abrupt in onset.
The usual duration for migraine aura is between 4 and 60 minutes, contrasting with the usually much briefer duration of retinal or
epileptic hallucinations [28,30,34,35]. More prolonged migrainous visual auras are less common; however, some case series have
described patients with persistent visual aura of migraine that lasts months or longer [36-39].
The frequency of migraine aura is highly variable. It is rare for these to occur multiple times a day. Some patients experience only one
episode in a lifetime.
Associated symptoms — Common associated symptoms include headache and other features of migraine: nausea, vomiting,
photophobia, and phonophobia. These follow the aura in most patients [28]. Headache is neither sensitive nor specific for migraine as it
is also a common postictal feature of occipital epilepsy [40]. Also, isolated visual hallucinations without headache that are presumed to
be of migraine origin are common; these are often called acephalgic migraine, migraine accompaniments, or migraine aura without
headache [28]. Up to one-third of patients with visual migraine aura experience other aura symptoms such as motor and sensory
deficits or aphasia [28,34]. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults".)
Diagnosis — There is no diagnostic test that confirms a migraine diagnosis, which is based on clinical features, and sometimes the
exclusion of other causes (see 'Evaluation' below). In one study, a rating scale of five clinical features (duration of 5 to 60 minutes,
gradual onset over 5 minutes or more, scotoma, zig-zag lines, and visual field lateralization) distinguished 362 patients with migraine
aura from 108 patients with other forms of visual disturbance with a sensitivity and specificity of 91 and 96 percent respectively [41].
The International Classification of Headache Disorders, 3rd edition (ICHD-3) criteria for migraine aura require at least two attacks of
aura with fully reversible symptoms, of either visual, sensory, motor, brainstem or speech disturbance, with at least two of the following
features [42]:
● At least one aura symptom spreads gradually over ≥5 minutes, and/or two or more symptoms occur in succession
● Each individual aura symptom lasts 5 to 60 minutes
● At least one aura symptom is unilateral
● The aura is accompanied, or followed within 60 minutes, by headache
(See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults", section on 'Diagnostic criteria'.)
Treatment — Treatment of migraine headache with aura is discussed separately (see "Preventive treatment of migraine in adults"
and "Acute treatment of migraine in adults"). Treatments for visual aura without headache and persistent visual aura of migraine have
not been well-studied. In the author's experience, verapamil may be useful as a prophylactic treatment for migraine visual aura without
headache. In case reports, agents with efficacy for persistent visual aura include acetazolamide, nimodipine, isoproterenol, lamotrigine,
and valproate [37,39,43-45].
Seizures — Visual hallucinations of epileptic origin can be simple or complex [32,46,47]. The classification may have localizing value.
In a study of 20 patients, simple visual hallucinations localized to the occipital, occipitotemporal, and occipitoparietal regions of the
cortex, while complex hallucinations localized to the occipitotemporal region and the temporal lobe [46]. Complex visual hallucinations
did not occur in seizures restricted to the occipital lobe. (See "Localization-related (focal) epilepsy: Causes and clinical features".)
Seizures arising from the occipital lobe are often associated with brightly colored circles or spherical patterns that may be multiplied or
grow in size (figure 2) [17,40,46-50]. Motion is a frequent characteristic of epileptic hallucinations. The motion can be intrinsic to the
hallucination, or the entire hallucination can move rapidly (usually in seconds) across the visual field in the direction contralateral to the
seizure focus. Visual field deficits or blindness may also occur, and some patients also note visual illusions [46,47,49,50]. As with other
epileptic phenomena, ictal visual hallucinations are usually stereotyped.
Epileptic hallucinations are binocular, usually occurring in one hemifield or the other, however, some patients misinterpret bilateral,
homonymous visual field hallucinations as existing in only the ipsilateral eye. Insight in patients with epilepsy is typically, but not always,
intact.
Epileptic hallucinations are usually brief, only a few seconds, unless the seizures are continuous [40,47,48,50]. The brief duration is
especially true of idiopathic occipital epilepsy and is a differentiating feature from migraine hallucinations, which are longer in duration.
The frequency is variable, but episodes tend to occur more frequently than do migraines; daily or weekly events are more common than
less frequent occurrence [47,50]. Episodes are generally not provoked.
Although many visual seizures do not progress to other ictal manifestations, nearly all patients experience nonvisual epileptic symptoms
at some time [17,47,49-51]. Some patients, initially misdiagnosed with migraine, eventually present with secondary generalized
seizures [29,47]. Associated symptoms depend on the origin and spread of the seizure and can include deja vu, somatosensory
phenomena, head and eye deviation, motor activity, and/or impaired consciousness. Postictal headache is common in patients with
occipital epilepsy and does not help to differentiate seizures from migrainous visual hallucinations [47,50,51].
For patients suspected of having seizures, a complete neurologic evaluation and an electroencephalogram (EEG) should be performed.
An interictal EEG is abnormal in most, but not all patients [49]. Neuroimaging is also indicated to look for etiologic structural brain
disease. (See "Evaluation and management of the first seizure in adults".)
Neurodegenerative disease
Dementia with Lewy bodies and Parkinson disease — Visual hallucinations are a core clinical feature of dementia with Lewy
bodies (DLB) and are also common in Parkinson disease (PD) [52-54]. In DLB and PD, the hallucinations are characteristically
complex, binocular, and occur throughout the entire visual field. Descriptions range from well-formed images of people or animals, to
more abstract visions such as shapes or colors [55]. Insight may or may not be retained, depending in part on the degree of cognitive
impairment. The content of the images may arouse fear or only indifference. Duration and frequency of the hallucinations are variable;
but most last seconds to minutes and recur at least weekly [55].
In DLB, visual hallucinations occur in approximately two-thirds of patients and occur early in the disease course, often preceding the
development of parkinsonism [56]. In addition to dementia, parkinsonism, visual hallucinations, and prominent fluctuations of cognition
or alertness are characteristic of DLB. (See "Clinical features and diagnosis of dementia with Lewy bodies".)
In PD, visual hallucinations are more prevalent later in the disease course. Dopaminergic medications can contribute substantively to
their occurrence, as well as to other manifestations of psychosis in patients with PD. Discontinuation or dose-lowering of antiparkinson
medications may alleviate these symptoms. Risk factors for visual hallucinations in PD include the use of high doses of antiparkinson
drugs, dementia, advanced age, impaired vision, depression, and sleep disturbances [53,57-59]. (See "Clinical manifestations of
Parkinson disease", section on 'Psychosis and hallucinations'.)
The treatment of visual hallucinations in these disorders is discussed separately. (See "Prognosis and treatment of dementia with Lewy
bodies" and "Management of nonmotor symptoms in Parkinson disease".)
Other dementia syndromes — Visual hallucinations are relatively uncommon in Alzheimer disease (AD), particularly early in the
disease course [60,61]. When present, these often reflect a superimposed delirium, medication effect, or vision loss [54,62-66] (see
'Metabolic encephalopathy' below). In patients with the relatively uncommon posterior cortical atrophy variant of AD, visual
hallucinations are reported in up to 25 percent of patients [67]. (See "Clinical features and diagnosis of Alzheimer disease", section on
'Atypical presentations'.)
Visual hallucinations are also a rare, but reported, occurrence in frontotemporal dementia [68-70].
Some patients with Creutzfeldt-Jakob disease (CJD) present with prominent visual symptoms that include visual perceptual difficulties
and visual hallucinations [71-74]. These patients typically have a rapidly progressive dementia and myoclonus.
Alcohol and drug use or withdrawal — Visual hallucinations can be a feature of drug and alcohol withdrawal syndromes, as well as
intoxication with certain medications and drugs of abuse. The table lists the most common drugs associated with visual hallucinations
(table 3) [75]. The hallucinations can be simple or complex and can be monocular (in cases of drugs that affect the retina) or binocular.
Alcohol and benzodiazepine withdrawal usually produce complex hallucinations with vivid imagery [32]. These are often continuous and
are associated with agitation, tremulousness, and autonomic hyperactivity. Hallucinations in other modalities can occur and patients
often appear to lack insight, interacting with the hallucinations. (See "Management of moderate and severe alcohol withdrawal
syndromes".)
Most visual hallucinations caused by medications or recreational drug use are associated with acute intoxication. Hallucinations are
usually complex, bilateral, and full field. There is usually associated confusion or frank delirium, often with auditory and tactile
hallucinations. Many of these drugs are believed to produce these symptoms by their direct action on central neurotransmitter systems
[76].
In contrast, digoxin and sildenafil can affect retinal function and produce simple hallucinations. Therapeutic, as well as toxic, levels of
digoxin can produce simple hallucinations of black spots, dots of light, "television static," or a tint of yellow or green to the entire visual
field [77,78]. When these visual hallucinations occur with digoxin use, level should be checked, and the dose of medication should be
lowered or discontinued to prevent permanent retinal injury [79]. Visual hallucinations appear to be a dose-dependent side effect of
sildenafil without known implications for long-term retinal injury [80,81].
Associated symptoms depend on the drug's side effect profile. As an example, anticholinergic drugs typically produce an agitated
delirium, mydriasis, and urinary retention. (See "Anticholinergic poisoning".)
For most medication-induced hallucinations, dose-lowering or discontinuation of the drug may be necessary if the patient is intolerant of
the hallucinations. For patients on dopaminergic therapy for whom dose reductions or discontinuation is not possible, treatment with an
atypical antipsychotic or cholinesterase inhibitor can be considered [82-84].
Peduncular hallucinosis — Peduncular hallucinosis is a rare manifestation of lesions (usually stroke or neoplasm) affecting the
midbrain, in particular, the paramedian reticular formation [83-90]. Similar syndromes have been described with pontine and thalamic
lesions. The hallucinations are complex and binocular, involving both visual fields. The content of the complex imagery varies and is
usually described as vivid and colorful. The hallucinations may have associated tactile and auditory content [32,87,90]. Insight is
variably retained [32,87,89-91].
While some reports note a predilection for these to occur in the evening, this is not universal [89,90]. The duration is variable, ranging
from a few minutes to a few hours. The frequency is also varied from just one to two episodes in all to 15 or more per day [87,89]. This
is often a self-limited symptom that resolves spontaneously after a few weeks or months; however, symptoms can persist [89-91].
Associated symptoms include disturbances in the sleep-wake cycle, resulting in episodes of daytime somnolence and nighttime
insomnia [87,90]. Other signs of brainstem and diencephalon dysfunction are often present, such as eye movement disturbances
(vertical gaze palsies and saccadic pursuits), poor pupillary light reaction, ataxia, hemiparesis, and confusion. (See "Posterior
circulation cerebrovascular syndromes", section on 'Rostral brainstem ischemia and "top of the basilar" syndrome'.)
The underlying mechanism for the hallucinations is uncertain. Some believe that the reticular activating system may be involved, while
others invoke the role of the pontine-geniculate-occipital pathways [87,90].
Neuroimaging is essential for patients suspected of having peduncular hallucinations. Antipsychotic agents have been effective in a few
case reports [87,92].
Narcolepsy — The visual hallucinations of narcolepsy are complex, vivid, colored images, invariably occurring immediately before
falling asleep (hypnagogic), or just after wakening (hypnopompic) [93]. Associated auditory or tactile sensations can occur. The duration
and frequency are variable. Associated symptoms of narcolepsy include excessive daytime sleepiness, sleep paralysis, and cataplexy.
Poor insight may occur because of the very realistic imagery, but most patients know the hallucinations are not real [19,94]. Even when
insight is retained, fearful content can make patients dread sleep [93].
Hypnagogic and hypnopompic hallucinations are believed to result from intrusion of rapid eye movement (REM) sleep into wakefulness
[95]. While a core feature of narcolepsy, community surveys report a high lifetime prevalence (up to 38 percent) of this phenomenon
among individuals without narcolepsy [32,96,97]. Medications that disrupt sleep architecture (eg, serotonergic and anticholinergic
antidepressants) can also produce hypnagogic and hypnopompic hallucinations [98]. Hypnagogic hallucinations associated with REM
sleep abnormalities have also been described in Guillain-Barré syndrome (GBS) [99].
Diagnostic testing for narcolepsy includes an overnight polysomnogram followed by a multiple sleep latency test. (See "Clinical features
and diagnosis of narcolepsy in adults".)
While treatment in narcolepsy is usually focused on the more disabling symptoms of daytime sleepiness and cataplexy; hypnagogic
hallucinations also often improve with these interventions. (See "Treatment of narcolepsy in adults".)
Psychiatric illness — Most visual hallucinations in psychiatric illness are complex. Auditory hallucinations are approximately twice as
common and typically accompany the visual hallucinations [100,101]. The content of the hallucinations is usually disturbing and
antagonistic. Many, but not all, patients with psychiatric illness lack insight [102]. The duration and frequency of hallucinations are highly
variable.
Symptoms of depression, mania, anxiety, disordered thoughts, or delusions are usually present. Delirium can accompany psychiatric
illness as well, but if present, drug or alcohol use, metabolic encephalopathy and other diagnoses should be considered. (See
'Metabolic encephalopathy' below and 'Alcohol and drug use or withdrawal' above.)
A complete psychiatric evaluation is essential for patients suspected of having hallucinations due to psychiatric illness. Antipsychotic
medications are useful in treatment. (See "Clinical manifestations, differential diagnosis, and initial management of psychosis in
adults".)
Metabolic encephalopathy — Visual hallucinations are a common feature of delirium, occurring in 27 percent of patients in one
hospital series [103]. These patients are typically confused, often agitated, with other psychotic features including auditory or tactile
hallucinations and delusions. In this form of "activated" delirium, etiologies are often multiple and can include central nervous system or
systemic infection, hypoxia, medications, and metabolic disturbances, including hepatic or renal failure, electrolyte imbalance, and
hypothyroidism [104]. (See "Diagnosis of delirium and confusional states".)
A syndrome of agitated delirium, visual hallucinations, and hemianopia can also be produced by lesions (usually stroke) affecting the
medial aspect of the occipital lobe, the parahippocampal gyrus, and hippocampus [11]. This can be difficult to distinguish from acute
toxic metabolic encephalopathy.
Others
● Papilledema – Patients with papilledema may experience photopsias, simple visual hallucinations of lights, or brief visual
obscurations [105]. These clear completely, are often unilateral, are typically very brief (just seconds), and are likely due to irritation
of the retinal photoreceptor in the presence of significant edema of the retinal ganglion cell axons. (See "Idiopathic intracranial
hypertension (pseudotumor cerebri): Clinical features and diagnosis" and "Overview and differential diagnosis of papilledema".)
● Optic neuritis – Simple visual hallucinations, often precipitated by eye movement, have also been reported in 30 percent of
patients with optic neuritis and can occur in the absence of significant anterior optic nerve edema [106]. (See "Optic neuritis:
Pathophysiology, clinical features, and diagnosis".)
● Reversible posterior leukoencephalopathy syndrome – Visual hallucinations along with visual field deficits and visual
distortions can occur in the reversible posterior leukoencephalopathy syndrome, a phenomenon of reversible localized cerebral
edema, often restricted to the occipital lobes, that occurs in patients with hypertension, renal failure, and/or immunosuppressive
therapies [107]. Clinical features also include headache, altered consciousness, and seizures. Eclampsia and hypertensive
encephalopathy are related conditions with similar symptoms. (See "Reversible posterior leukoencephalopathy syndrome".)
● Reversible cerebral vasoconstriction syndrome – While vision loss is a more frequent accompaniment to the sudden headache
that is the clinical hallmark of this syndrome, visual hallucinations have been described in some cases [108]. (See "Reversible
cerebral vasoconstriction syndromes", section on 'Clinical features'.)
EVALUATION — In many patients, the clinical setting (eg, patient with Parkinson disease [PD] or with longstanding vision loss) will
identify the most likely cause of the visual hallucinations. In other cases, the clinical features suggest the more likely diagnoses and
direct the diagnostic evaluation (table 1 and algorithm 1).
Clinical features — Visual hallucinations are under-reported by patients who fear that the hallucinations represent psychiatric disease
or who lack insight into the unreal nature of the hallucinations [1,9]. Insight is an important feature that can distinguish among some
etiologies.
The patient should be asked to describe their hallucinations. The characteristics of the hallucination, especially whether it is classified
as simple or complex, help to determine the underlying cause (table 1). (See 'Classification and terminology' above.)
In addition, clinicians should specifically inquire about the presence of other features, including:
● Monocular versus binocular involvement

● Involved area of the visual field
● Motion, either intrinsic motion within the hallucination, or movement of the hallucination across the field of vision
● Triggers (eg, bright light, a dark room, or anxiety)
● Duration
● Frequency
● Insight that the visual perception is unreal
● Associated symptoms and medical history
Associated symptoms that can be relevant include vision loss, headache, impaired consciousness, confusion or memory loss, sensory
or motor symptoms, gait difficulty, excessive daytime sleepiness, delusions, and hallucinations involving other senses. An alcohol, drug,
and medication history should be taken in every case.
Diagnostic testing — All patients with new onset visual hallucinations should have a complete neurologic evaluation with screening for
cognitive impairment, parkinsonism, and other neurologic deficits. Medication lists should be reviewed for their potential contribution.
Serum screening tests for alcohol and drugs of abuse may be useful for patients with unknown causes for hallucinations, particularly in
the emergency room setting. An approach to diagnostic evaluation is presented in the algorithm and summarized briefly below
(algorithm 1).
● New onset of simple hallucinations that are monocular should have an urgent ophthalmologic examination.
● In the absence of neurologic abnormalities, and in the setting of known ocular disease (eg, macular degeneration) the likely
diagnosis is release hallucinations and further diagnostic evaluation may not be required. (See "Visual release hallucinations
(Charles Bonnet syndrome)", section on 'Diagnosis'.)
● Simple hallucinations that meet criteria for migraine may not require further diagnostic evaluation (see 'Migraine aura' above).
Atypical features include monocular symptoms and episodes that are atypically brief or prolonged.
● Electroencephalography is indicated when episodes are brief, frequent, and stereotyped; these features suggest seizure.
● If mental status examination is abnormal, evaluation for delirium, drug intoxication or withdrawal, or psychiatric disease is
appropriate. (See "Diagnosis of delirium and confusional states".)
● A brain magnetic resonance image is appropriate when hallucinations do not meet criteria for visual aura of migraine and when the
neurologic examination is abnormal. Formal visual field testing can be useful to rule out subtle visual deficits not appreciated on
gross examination. Some patients with acute occipital or temporal lobe infarct have visual hallucinations in the absence of a visual
field defect by bedside examination [109].
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SUMMARY — A visual hallucination is the perception of an external visual stimulus where none exists.
● Simple visual hallucinations include images of unformed light, geometric shapes or designs. Complex visual hallucinations are
formed images of people, animals, or scenes.
● Etiologies of visual hallucinations include retinal disease, migraine, vision loss, neurodegenerative disease, alcohol and drug use,
psychiatric illness, and toxic-metabolic encephalopathy.
● Clinical features that help distinguish among etiologies are simple versus complex content, monocular versus binocular
involvement, insight, and associated symptoms (table 1). (See 'Etiologies' above.)
● Clinical features direct the diagnostic evaluation (algorithm 1). New onset of simple hallucinations that are monocular should have
an urgent ophthalmologic examination. In many other cases when the clinical setting suggests the most likely cause, diagnostic
testing beyond ophthalmologic and neurologic examination may not be required. Neuroimaging, electroencephalography, and other
tests are helpful in other cases. (See 'Evaluation' above.)
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Topic 5255 Version 12.0
GRAPHICS
Disorders causing visual hallucinations
Classification
and Associated
Etiology Location Triggers Duration Frequency Insight
characteristic symptoms
features
Retinal Simple Monocular or Valsalva if due Seconds Variable Intact Possible vision
pathology Intrinsic motion is binocular, to posterior loss per
common; eg, depending on vitreous abnormal
flashing lights underlying detachment funduscopic
pathology examination
Vision loss, Simple or complex Monocular or Sensory Variable Frequent, at Often intact Related to
release Can be stationary, binocular, full deprivation, least weekly, underlying
hallucinations have intrinsic field or decreased up to multiple condition
motion, or move hemifield arousal times in one
en bloc depending on day
underlying
pathology
Migraine Usually simple and Binocular, Migraine Several Variable, Intact Migraine
geometric in form; usually triggers (eg, minutes to an usually less headache,
eg, fortification hemifield lack of sleep, hour often than often with
spectra, Often start red wine, weekly nausea,
scintillating centrally and menses) vomiting,
scotoma move to photophobia
Spread or periphery
movement across
the visual field
over minutes is
characteristic
Seizures Simple more Binocular, Usually occur Seconds to 1-2 Variable Usually intact Other ictal
common than hemifield without trigger minutes phenomena
complex (eg,
Typically circular automatisms,
and colored deja vu,
convulsions),
Movement across
postictal
the field is rapid
headache
(seconds)
common
Dementia Simple or complex Binocular, full Usually no Variable, Variable, can Variable, Dementia,
with Lewy field trigger usually minutes be daily perhaps related Parkinsonism
bodies, to cognitive
Parkinson status
disease
Alcohol Complex, often Binocular, full Abstinence Persistent Persist during Often impaired Autonomic
withdrawal associated with field withdrawal disturbances,
auditory and confusion,
tactile agitation
hallucinations
Peduncular Complex, often Binocular, full More common Variable may Variable Maybe impaired Sleep
hallucinosis associated with field in evening persist disturbances,
auditory and hours other brainstem
tactile or diencephalic
hallucinations signs
Narcolepsy Complex, often Binocular, full Usually on Variable, Often nightly Usually intact Cataplexy,
associated with field falling to or on seconds to excessive
auditory and awakening minutes daytime
tactile from sleep sleepiness,
hallucinations sleep paralysis
Psychiatric Complex, often Binocular, full No trigger Variable Frequent Usually absent Disordered
illness associated with field thoughts,
auditory and delusions
tactile
hallucinations
Graphic 73106 Version 3.0
Retinal pathologies associated with elementary visual hallucinations
Posterior vitreous detachment with retinal traction or retinal tear
Retinal detachment
Cone dystrophies
Cancer-associated retinopathy
Melanoma-associated retinopathy
Autoimmune-associated retinopathy
Acute zonal occult outer retinopathies
Other pathology causing mechanical changes in retina
Fortification spectra
https://www.uptodate.com/contents/approach-to-the-patient-with-visual-hallucinations/print?source=search_result&search=psychiatric%20evalu… 10/13
Drawing by a patient with epileptic visual hallucinations
The patient had occipital seizures with this stereotyped hallucination for
approximately 12 years without a diagnosis. He described a bright red circle that
flickered with what looked like moving flames coming out of it. The hallucination
typically lasted for seconds and was usually followed by subtle mental status
changes, headache, and nausea.
Drugs and medications associated with visual hallucinations
Non-psychotropic Psychotropic Drugs of abuse Over-the-counter
Digoxin Benzodiazepines Alcohol Phenylpropanolamine

Glucocorticoids L-dopa d-lysergic acid diethylamide (LSD) Ephedrine
Amantadine Dopaminergic (eg, bromocriptine, Mescaline Synthetic cannabinoids
Cimetidine pergolide) PCP
Ranitidine Tricyclic antidepressants Cocaine
Sildenafil Benztropine Narcotics
Beta-blockers Narcotics 3,4
Clarithromycin methylenedioxymethamphetamine
(Ecstasy)
Cyclosporine
Amphetamine
Clomiphene
Psilocybin, psilocin (mushrooms)
Angiotensin converting enzyme
inhibitors Cannabis
Linezolid
Moxifloxacin
Adapted with permission from: Liu GL, Volpe NJ, Galetta SL. Neuro-opthalmology: Diagnosis and Management. WB Saunders Company, Philadelphia
2001. Copyright © 2001 Elsevier.
Higdon E, Twilla JD, Sands C. Moxifloxacin-Induced Visual Hallucinations: A Case Report and Review of the Literature. J Pharm Pract 2016.
Palanippan P, Rajaraman V. Visual hallucinations: a treatment-emergent adverse effect of linezolid. J Neuropsychiatry Clin Neurosci 2015; 27:65.
Padilla Peinado R, Esteban Fernández J, Rodríguez Álvarez S, et al. Visual hallucinations related to use of ertapenem. Neurologia 2015; 30:520.
Doane J, Stults B. Visual hallucinations relate to angiotensin-converting enzyme inhibitor use: case reports and review. J Clin Hypertens (Greenwich)
2013: 15:230.
Goldner JA. Metoprolol-induced visual hallucinations: a case series. J Med Case Rep 2012; 15:6.
Parkes LO, Cheng MP, Sheppard DC. Visual Hallucinations Associated with High Posaconazole Concentrations in Serum. Antimicrob Agents Chemother
2015: 7;60.
Purvin VA. Visual disturbance secondary to clomiphene citrate. Arch Ophthalmol 1995; 113:482
https://www.drugabuse.gov/publications/drugfacts/synthetic-cannabinoids
An approach to the evaluation of a patient with visual hallucinations
EEG: electroencephalogram.

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10/18/2017 Approach to the patient with visual hallucinations - UpToDate

Official reprint from UpToDate®

Author: Victoria S Pelak, MD

● Each individual aura symptom lasts 5 to 60 minutes

● At least one aura symptom is unilateral

● The aura is accompanied, or followed within 60 minutes, by headache

● Monocular versus binocular involvement

● Basics topics (see "Patient education: Detached retina (The Basics)")

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Topic 5255 Version 12.0

Disorders causing visual hallucinations

Graphic 73106 Version 3.0

Retinal pathologies associated with elementary visual hallucinations

Posterior vitreous detachment with retinal traction or retinal tear

Acute zonal occult outer retinopathies

Other pathology causing mechanical changes in retina

Graphic 82416 Version 2.0

Graphic 59061 Version 1.0

Drawing by a patient with epileptic visual hallucinations

Graphic 59850 Version 2.0

Drugs and medications associated with visual hallucinations

Non-psychotropic Psychotropic Drugs of abuse Over-the-counter

Digoxin Benzodiazepines Alcohol Phenylpropanolamine

Graphic 51079 Version 5.0

An approach to the evaluation of a patient with visual hallucinations

Graphic 109600 Version 2.0

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