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 (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 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]. By contrast, patients with PVD are likely to present with only a few episodes.
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 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 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 three of the following features [42]:
●At least one aura symptom spreads gradually over ≥5 minutes
●Two or more symptoms occur in succession
●Each individual aura symptom lasts 5 to 60 minutes
●At least one aura symptom is unilateral
●At least one aura symptom is positive
●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 [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 "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 déjà 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 [54]. 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 [52,56-58]. (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 [59,60]. When present, these often reflect a superimposed delirium, medication effect, or vision loss [53,61-65] (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 [66]. (See "Clinical features and diagnosis of Alzheimer disease", section on 'Atypical presentations'.)
Visual hallucinations are also a rare, but reported, occurrence in frontotemporal dementia [67-69].
Some patients with Creutzfeldt-Jakob disease (CJD) present with prominent visual symptoms that include visual perceptual difficulties and visual hallucinations [70-73]. 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) [74]. 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 [75].
By 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 [76,77]. 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 [78]. Visual hallucinations appear to be a dose-dependent side effect of sildenafil without known implications for long-term retinal injury [79,80].
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 are not possible, treatment with an atypical antipsychotic or cholinesterase inhibitor can be considered [81-83].
Peduncular hallucinosis — Peduncular hallucinosis is a rare manifestation of lesions (usually stroke or neoplasm) affecting the midbrain, in particular, the paramedian reticular formation [82-89]. 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 [32,86,89]. Insight is variably retained [32,86,88-90].
While some reports note a predilection for these to occur in the evening, this is not universal [88,89]. The duration is variable, ranging from a few minutes to a few hours. The frequency is also varied from just 1 to 2 episodes in all to 15 or more per day [86,88]. This is often a self-limited symptom that resolves spontaneously after a few weeks or months; however, symptoms can persist [88-90].
Associated symptoms include disturbances in the sleep-wake cycle, resulting in episodes of daytime somnolence and nighttime insomnia [86,89]. 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 [86,89]. Other 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 in extrastriate brain regions, which in turn might produce the expressed symptoms [91].
Neuroimaging is essential for patients suspected of having peduncular hallucinations. Antipsychotic agents have been effective in a few case reports [86,92].
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 "Psychosis in adults: Epidemiology, clinical manifestations, and diagnostic evaluation".)
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 syndrome", section on 'Clinical presentation and course'.)
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 department 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 (EEG) 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].
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 — 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 (EEG), and other tests are helpful in other cases. (See 'Evaluation' above.)
