Version July 2025
INTRODUCTION —
Visual hallucinations can result 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 providing 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 (CBS) 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. By contrast, a visual illusion is a distortion or modification of an external visual stimulus [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]:
●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 generate brief stereotyped hallucinations and release phenomena that generate continuous and variable hallucinations [4]. This classification scheme is somewhat limited because the generalizations are not absolute, and some disorders have characteristics of both irritative and release phenomena. For example, the visual hallucinations of migraine 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.
●Causes – 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).
●Clinical features – 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.
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.
●Temporal features – 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]. By contrast, patients with PVD are likely to present with only a few episodes.
In cases of retinal traction, Valsalva-like maneuvers may be a trigger.
●Evaluation and management – 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 visual cortex can cause visual hallucinations, often referred to as release hallucinations or Charles Bonnet syndrome (CBS) [9].
CBS is most often reported in older adult 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 migrainous aura, occurring in 90 percent of those who report an aura [21-23]. Most studies estimate a lifetime prevalence of the visual aura of migraine to be between 0.7 and 1.2 percent [24-26].
The pathophysiology of migraine aura 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 so-called scintillating scotoma, which consists of an area of decreased vision (scotoma) marked by a flickering (scintillating) fortification border (figure 1). This hallucination is considered pathognomonic of migraine. Patients with migraine may also describe seeing spots, dots, or shooting stars. Migraine auras tend to be black and white or monochromatic, and they 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].
The migraine aura may also manifest as scotomas or visual distortions, including heat waves and tunnel vision. Objects may appear smaller (micropsia) or larger (macropsia) or with distorted contours [30,31]. Complex visual hallucinations are uncommon but have been described [30,32]. Patients with migrainous visual hallucinations retain insight.
Migraine auras are binocular [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) [28,30,31,34,35]. 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 [28,30,34,36]. 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 [37-40].
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 [41]. 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 — The diagnosis of migraine is based on clinical features and the exclusion of other causes (see 'Diagnostic 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 [42].
The 3rd edition of the International Classification of Headache Disorders (ICHD-3) lists criteria for migraine aura as at least two reversible attacks of visual, somatosensory, motor, brainstem, or speech disturbance, with at least three of the following features [43]:
●At least one aura symptom spreads gradually over ≥5 minutes
●Two or more symptoms occur in succession
●Each aura symptom lasts 5 to 60 minutes
●At least one aura symptom is unilateral
●At least one aura symptom reflects activation in a sensory system ("positive symptom")
●The aura is accompanied, or followed within 60 minutes, by headache
Treatment — Treatment of migraine headache with aura is discussed separately. (See "Preventive treatment of episodic 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 [38,40,44-46].
Visual snow syndrome — Visual snow is a positive visual phenomenon in which the patient perceives continuous, tiny, flickering dots throughout the visual field of both eyes. The perception is reminiscent of the "static" on old mistuned television sets [37]. Although initially described as part of the spectrum of migraine and migraine aura [37], visual snow is now recognized as a separate entity. The syndrome has been defined by the International Headache Society (IHS) [47] as follows:
●Dynamic, continuous, tiny dots across the entire visual field, persisting for more than three months
●Additional visual symptoms of at least two of the following four types:
•Palinopsia (persistent recurrence of a visual image and/or trailing images after the stimulus has been removed)
•Enhanced entoptic phenomena
•Photophobia (sensitivity or intolerance of light, which can cause some people to avoid sunlight, computers, fluorescent lights, and car headlights)
•Nyctalopia (impaired night vision)
●Symptoms are not consistent with typical migraine visual aura
●Symptoms are not better accounted for by another disorder
Other associated symptoms and signs include tinnitus, anxiety, depression, tremor, and gait imbalance. The syndrome typically begins in the third decade of life, although some patients report being symptomatic during childhood [48]. A detailed history will help to differentiate visual snow from hallucinations persisting after ingestion of a hallucinogen.
The cause of visual snow syndrome is unknown. Limited evidence supports the theory of hyperexcitability that "drives thalamocortical dysrhythmia" [49]. In support of this theory, 18-F fluorodeoxyglucose positron emission tomography (FDG-PET) revealed more hypermetabolism in lingual gyri in patients with visual snow syndrome than in control subjects [50].
Many patients report that their symptoms are disabling. They are often diagnosed as having a psychiatric disorder. There are limited reports of positive treatment effects with antiepileptic medications, such as lamotrigine and divalproex sodium, and with spectacle lenses with colored filters, although the evidence of efficacy is weak [38,40,48,49,51].
Seizures — Visual hallucinations of epileptic origin can be simple or complex [32,52,53]. The classification may be localizing. In a study of 20 patients, simple visual hallucinations localized to the occipital, occipitotemporal, or occipitoparietal regions of the cortex, while complex hallucinations localized to the occipitotemporal region or the temporal lobe [52]. Complex visual hallucinations did not occur in seizures restricted to the occipital lobe. (See "Focal epilepsy: Causes and clinical features".)
Seizures arising from the occipital lobe are often associated with seeing multiple brightly colored circles or spherical patterns that may multiply or enlarge (figure 2) [17,35,41,52-56]. The hallucinations may flicker in place or move within seconds across the visual field in the direction contralateral to the seizure focus. During or after the visual hallucinations, visual field deficits or blindness may persist ("postictal blindness"). Some patients note visual illusions during the ictus [52,53,55,56]. As with other epileptic phenomena, visual hallucinations associated with seizures ("ictal visual auras") are usually stereotyped.
Epileptic hallucinations are binocular, usually occurring in one hemifield. Patients often incorrectly localize them to the temporal field of one eye. They last only a few seconds, unless the seizures are continuous [41,53,54,56]. The brief duration is especially true of idiopathic occipital epilepsy and is a differentiating feature from migraine hallucinations, which last much longer. Episodes tend to occur more frequently than in migraine [53,56]. Insight is usually intact.
Although most visual seizures do not progress to include other ictal manifestations, nearly all patients experience nonvisual epileptic symptoms at other times [17,53,55-57]. Patients initially misdiagnosed with migraine may later present with secondary generalized seizures [29,53]. Associated symptoms depend on the origin and spread of the seizure and can include déjà vu and somatosensory phenomena, head and eye deviation, motor activity, and impaired consciousness. Postictal headache is common and does not help to differentiate epileptic visual hallucinations from migrainous visual hallucinations [53,56,57].
For patients suspected of having seizures, a complete neurologic evaluation and electroencephalography (EEG) should be performed. The interictal EEG is abnormal in most patients [55]. Neuroimaging is indicated to look for an underlying lesion. (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) [58-60]. In DLB and PD, the hallucinations are characteristically complex, binocular, and present throughout the visual field. Descriptions range from abstract shapes or colors to well-formed images of people or animals [61]. 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 hallucinations endure for seconds to minutes and recur at least weekly [61].
In DLB, visual hallucinations occur in approximately two-thirds of patients and occur early in the disease course, often preceding the development of motor parkinsonism [60]. In addition to visual hallucinations, dementia, parkinsonism, 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 to their occurrence. Discontinuation or dose lowering of antiparkinsonian medications may alleviate these symptoms. Risk factors for visual hallucinations in PD include the use of high doses of antiparkinsonian drugs, dementia, advanced age, impaired vision, depression, and sleep disturbances [58,62-64]. (See "Clinical manifestations of Parkinson disease", section on 'Psychotic symptoms'.)
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 uncommon in Alzheimer disease (AD) [65,66] except when there is a superimposed delirium, medication effect, or vision loss [59,67-71] (see 'Metabolic encephalopathy' below). However, in patients with the posterior cortical atrophy variant of AD, visual hallucinations are reported in up to 25 percent of patients [72] (see "Clinical features and diagnosis of Alzheimer disease", section on 'Atypical presentations'). Visual hallucinations occur rarely in frontotemporal dementia [73-75]. Some patients with Creutzfeldt-Jakob disease (CJD) present with prominent visual perceptual difficulties and visual hallucinations [76-79]. They typically have a rapidly progressive dementia and myoclonus.
Alcohol and drug use or withdrawal — Visual hallucinations can be a feature of drug and alcohol intoxication and withdrawal syndromes. The table lists the most common drugs associated with visual hallucinations (table 3) [80]. 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 continuous complex hallucinations with vivid imagery [32] associated with agitation, tremulousness, and autonomic hyperactivity. Auditory and somatosensory hallucinations can also occur. Patients often appear to lack insight. (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 usually are complex and bilateral, and cover the entire visual field. There is associated confusion or frank delirium, often with auditory and tactile hallucinations. Many of these drugs are believed to produce these effects by direct action on central neurotransmitter systems [81].
By contrast, digoxin and sildenafil can disrupt 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 (xanthopsia) [82,83]. When these visual hallucinations occur with digoxin use, the serum level should be checked and the dose of medication should be lowered or discontinued to prevent permanent retinal injury [84]. Visual hallucinations following sildenafil use appear to be dose dependent and without known implications for long-term retinal injury [85,86].
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 is sufficient. For patients on dopaminergic therapy, for whom dose reductions or discontinuation are not possible, treatment with an atypical antipsychotic or cholinesterase inhibitor can be considered [87-89].
Peduncular hallucinosis — Peduncular hallucinosis is a rare manifestation of lesions (usually stroke or neoplasm) affecting the midbrain, particularly the paramedian reticular formation [88-95]. 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 but is usually described as vivid and colorful. The hallucinations may have associated tactile and auditory content [32,92,95]. Insight is variably retained [32,92,94-96].
The duration of episodes ranges from minutes to hours, and their frequency varies from 1 to more than 15 episodes per day [92,94]. Some reports note a predilection for them to occur in the evening [94,95]. They usually resolve spontaneously after a few weeks or months, but some persist [94-96].
Associated symptoms include disturbances in the sleep-wake cycle, resulting in episodes of daytime somnolence and nighttime insomnia [92,95]. 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.
The underlying mechanism for peduncular hallucinations is uncertain. Some observers believe that the reticular activating system is involved; others invoke the role of the pontine-geniculate-occipital pathways [92,95]. Data suggest that the subcortical regions implicated in peduncular hallucinosis share a specific functional connectivity, such that lesions in these areas might result in hyperactivity of extrastriate brain regions [97].
Neuroimaging is essential for patients suspected of having peduncular hallucinations.
Antipsychotic agents have been effective in a few case reports [92,98].
Narcolepsy — The visual hallucinations of narcolepsy are complex, vivid, colored images, invariably occurring immediately before falling asleep (hypnagogic) or just after wakening (hypnopompic) [99]. 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 [19,100]. Even when insight is retained, fearful content can make patients dread sleep [99].
Hypnagogic and hypnopompic hallucinations are believed to result from intrusion of rapid eye movement (REM) sleep into wakefulness [101]. Although such hallucinations are a core feature of narcolepsy, community surveys report a high lifetime prevalence (up to 38 percent) of this phenomenon among individuals without narcolepsy [32,102,103]. Serotonergic and anticholinergic antidepressants that disrupt sleep architecture can also produce these hallucinations [104]. Hypnagogic hallucinations associated with REM sleep abnormalities have also been described in Guillain-Barré syndrome (GBS) [105].
Diagnostic testing for narcolepsy includes an overnight polysomnogram followed by a multiple sleep latency test. (See "Clinical features and diagnosis of narcolepsy in adults".)
Although treatment of narcolepsy is usually focused on the disabling daytime sleepiness and cataplexy, hypnagogic hallucinations also often improve with treatment. (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 [106,107]. The content of the hallucinations is usually disturbing and antagonistic. The duration and frequency of hallucinations are highly variable. Many patients lack insight [108].
Symptoms of depression, mania, anxiety, disordered thoughts, or delusions are usually present. Manifestations of delirium should prompt consideration of drug or alcohol use and metabolic encephalopathy. (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 "Psychosis in adults: Epidemiology, clinical manifestations, and diagnostic evaluation".)
Metabolic encephalopathy — Visual hallucinations are a common feature of delirium, occurring in 27 percent in one hospital series [109]. Patients are typically confused and agitated and display auditory or tactile hallucinations and delusions. In this form of "activated" delirium, consideration should be given to central nervous system or systemic infection, hypoxia, medications, and metabolic disturbances, including hepatic or kidney failure, electrolyte imbalance, and hypothyroidism [110]. (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, but homonymous hemianopia (if present) is a distinctive feature.
Others
●Papilledema – Patients with papilledema may experience simple visual hallucinations of lights (photopsias), brief visual obscurations, or both [111]. These phenomena last for seconds and occur in one eye or both. Potential mechanisms include ischemia due to a retinal arterial circulation compressed by a crowded optic disc or mechanical stimulation of the retina without ischemia. (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 optic disc edema [112]. (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 reversible posterior leukoencephalopathy syndrome (RPLS). These manifestations are attributed to localized cerebral edema, often restricted to the occipital lobes. RPLS occurs in patients with hypertension, in patients with kidney failure, and in those undergoing immunosuppressive and antineoplastic therapy [113].
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 – Reversible cerebral vasoconstriction syndrome (RCVS) is marked by sudden onset of severe holocranial headache, variably accompanied by impaired cognition and vision, as well as seizures. Visual hallucinations have been described [114]. (See "Reversible cerebral vasoconstriction syndrome", section on 'Clinical presentation and course'.)
●Postcardiac surgery without delirium – Visual hallucinations after major cardiac surgery can occur in patients without delirium or other cause such as migraine, stroke, vision loss, or psychosis. Various series have reported incidences ranging from 11 to 22 percent [115,116]. The visual hallucinations in this setting are transient, resolve without apparent sequelae, and may consist of inanimate or moving objects. They appear to be more common after cardiac artery bypass grafting procedures performed with extracorporeal circulation (ie, on-pump) compared with those performed off-pump [115].
DIAGNOSTIC EVALUATION —
In many patients, the clinical setting 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 may be underreported 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 the hallucinations, which helps to determine the underlying cause (table 1). (See 'Classification and terminology' above.)
Clinicians should also elicit other features, including:
●Monocular versus binocular involvement
●Involved area of the visual field
●Flickering 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
Relevant associated symptoms 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, including a funduscopic examination. 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 setting. An approach to diagnostic evaluation is presented in the algorithm and summarized briefly below (algorithm 1).
●New onset of simple, monocular hallucinations suggests retinal disease and should evoke urgent ophthalmologic examination.
●Brief, simple, monocular or binocular hallucinations accompanied by loss of vision should suggest papilledema and elicit funduscopic examination. (See "Overview and differential diagnosis of papilledema".)
●In the absence of neurologic abnormalities and in the setting of impaired vision with a known cause, the likely diagnosis is release hallucinations (Charles Bonnet syndrome [CBS]); further diagnostic evaluation is not required. (See "Visual release hallucinations (Charles Bonnet syndrome)", section on 'Diagnosis'.)
●Simple hallucinations that meet criteria for typical migraine aura in a patient with known migraine do not require further diagnostic evaluation. (See 'Migraine aura' above.)
Atypical features include monocular symptoms and episodes that are atypically brief or prolonged.
●Brief, frequent, multicolored, and stereotyped hemifield hallucinations suggest the possibility of occipital seizure and indicate EEG.
●If mental status is abnormal, evaluation for drug intoxication or withdrawal, medication-induced hallucinations, metabolic encephalopathy, and psychiatric disease is appropriate. (See "Diagnosis of delirium and confusional states".)
●Brain magnetic resonance imaging (MRI) 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. However, some patients with acute occipital or temporal lobe infarction have visual hallucinations without visual field defects [117].
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Adult with altered mental status in the emergency department".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Detached retina (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition and classification – A visual hallucination is the perception of an external visual stimulus where none exists. (See 'Classification and terminology' above.)
Simple visual hallucinations include images of unformed light, geometric shapes, or designs.
Complex visual hallucinations are formed images of people, animals, or scenes.
●Etiologies and clinical features – Causes of visual hallucinations include retinal disorders, migraine, severely impaired vision, neurodegenerative disease, alcohol and drug use, psychiatric illness, and disturbed body fluid chemistries.
Clinical features that help distinguish among causes include whether the hallucinations are simple or complex, whether they are monocular or binocular, whether there are relevant associated manifestations, and whether insight is intact (table 1). (See 'Etiologies' above.)
●Diagnostic evaluation – Clinical features direct the diagnostic evaluation (algorithm 1).
New onset of simple hallucinations that are monocular requires an urgent ophthalmologic examination.
Other patients should have a complete neurologic evaluation with screening for cognitive impairment, parkinsonism, and other neurologic deficits, including a funduscopic examination. Medication lists should be reviewed for their potential contribution.
In other cases when the clinical setting suggests the most likely cause, further diagnostic testing may not be required. Neuroimaging, EEG, and other tests are helpful in other cases. (See 'Diagnostic evaluation' above.)
