Visual hallucinations are the perception of visual images in the absence of external physical stimuli. Their differential diagnosis is broad, including ophthalmic, neurological, metabolic, and psychiatric causes.
Visual hallucinations can be classified by their visual content as follows:
Simple hallucinations: elementary visual phenomena such as flashes of light, geometric patterns, sparkles, or rainbow-colored spirals.
Complex hallucinations: fully formed images such as people, animals, or landscapes. These are more common with temporal lobe lesions.
Another important classification is based on the circumstances of occurrence. Hallucinations with eyes open are often seen in psychosis or delirium4). In contrast, hallucinations with eyes closed are a rare phenomenon in which vivid, colorful images appear when the eyes are closed and disappear upon opening them; this has been reported in hyponatremia1), alcohol withdrawal4), and during clarithromycin treatment7).
The epidemiology of visual hallucinations varies greatly depending on the underlying cause.
Schizophrenia: Most often diagnosed in late teens to early 30s, more common in males
Migraine: Occurs in about 8.4% of the population aged 15 and older, more common in females (12.9%), with peak in the 30s. Migraine with visual aura accounts for 31% of all migraine patients
Dementia with Lewy bodies: Complex hallucinations occur in approximately 80% of clinically diagnosed cases6)
Hyponatremia: Hallucinations have been reported in 0.5% of patients with serum Na <120 mEq/L1)
QWhat types of visual hallucinations are there?
A
Visual hallucinations are broadly classified into simple hallucinations (flashing lights or geometric patterns) and complex hallucinations (people, animals, landscapes). They may appear with eyes open or only with eyes closed, and the context of appearance is useful for differential diagnosis. For details, see the section “Main Symptoms and Clinical Findings”.
The content of visual hallucinations varies greatly depending on the underlying disease.
Migraine aura (scintillating scotoma): Zigzag patterns of light appear in the central visual field, expand toward the periphery, and leave a central scotoma. Usually resolves within 20–30 minutes.
Visual snow: A persistent phenomenon in which the entire visual field is covered with numerous tiny dots, like a snowstorm on a television screen.
Psychotic visual hallucinations: Range from flickering lights to complex scenes such as family members, animals, or religious symbols. The presence or absence of insight is important for differential diagnosis.
Delirium-related visual hallucinations: Vary from simple shapes to the sensation of crawling insects. The latter is particularly characteristic of delirium tremens.
Closed-eye hallucinations: Vivid, colorful images appear when the eyes are closed and disappear upon opening. Patients often recognize that the hallucinations are not real 4)
Hallucinations associated with dementia: Typically involve images of animals or family members, and are easily triggered in dark or dim environments 6)
Flashing lights / photopsia: Associated with papilledema or optic neuritis. Seen in up to 30% of optic neuritis patients and triggered by eye movement.
Geometric patterns / colors: Caused by abnormal discharges in the occipital cortex during epileptic seizures.
Complex Hallucinations
Images of people or animals: Typical of dementia with Lewy bodies and Charles Bonnet syndrome. CBS patients retain cognitive function.
Scenes or landscapes: Temporal lobe lesions produce complex formed visual hallucinations (people or objects), distinct from the geometric simple hallucinations of the occipital lobe.
Reproduction of past memories: Release hallucinations after resection of brain metastases may reproduce past scenes2).
Various clinical findings accompany depending on the underlying disease.
Dementia with Lewy bodies: Parkinsonian motor symptoms, fluctuating cognition. Visual hallucinations have high specificity for differentiating from Alzheimer disease6)
VGKC limbic encephalitis: MRI shows characteristic T2 hyperintensity in bilateral hippocampi, accompanied by aggression and mood swings5)
Anton-Babinski syndrome: Cortical blindness due to bilateral occipital lobe damage, plus denial of visual loss (anosognosia) and confabulation. Most commonly secondary to cerebrovascular disease
QWhat are the characteristics of visual hallucinations in Charles Bonnet syndrome?
A
Visual hallucinations in CBS patients are highly diverse, ranging from simple flashes of light to complex images of people and animals. A key feature is that cognitive function is preserved, and many patients recognize that the hallucinations are not real. The cause is thought to be deafferentation of visual input due to severe eye diseases such as age-related macular degeneration, retinal detachment, and glaucoma.
Primary psychosis: Visual hallucinations occur in psychotic states such as schizophrenia and schizoaffective disorder. Auditory hallucinations are more common, but some patients experience vivid visual scenes.
Delirium: Characterized by acute cognitive fluctuations and decreased level of consciousness, common in hospitalized elderly patients. Metabolic encephalopathy, drug side effects, and alcohol withdrawal (delirium tremens) are typical triggers.
Migraine: Occurs in 15–29% of the general population. Visual aura (scintillating scotoma) begins as a colorless flicker in the central visual field and expands peripherally.
Epileptic seizures: Simple visual hallucinations of glowing shapes or bright dots are common, but involvement of the visual association cortex can lead to complex hallucinations.
Dementia: In dementia with Lewy bodies (DLB), up to 20% present with visual hallucinations as a core symptom. Visual hallucinations are also reported in up to 25% of Parkinson’s disease and 12–53% of Alzheimer’s disease.
Drugs: Hallucinogens such as LSD, mescaline, and psilocybin stimulate 5-HT(2A) receptors to induce visual hallucinations. Hallucinogen persisting perception disorder (HPPD) can cause perceptual distortions lasting months to years.
Anticholinergic drugs: Overdose of cyproheptadine can cause anticholinergic syndrome including visual hallucinations3).
Clarithromycin: May increase neuronal excitability via inhibition of GABAergic signaling, sometimes inducing vivid, dynamic closed-eye visual hallucinations7).
Hyponatremia: Visual hallucinations are reported in 0.5% of patients with serum Na <120 mEq/L. They appear with eyes closed and resolve with electrolyte correction1).
Tumors: Visual hallucinations were observed in 13 of 59 patients with temporal lobe tumors. Tumors along the visual pathway can induce visual hallucinations. In occipital lobe tumors, hallucinations may appear due to extension from the visual cortex to other areas.
Autoimmune encephalitis: In VGKC antibody-positive limbic encephalitis, visual hallucinations are accompanied by aggression and memory impairment. Recurrence after 1.5 years has also been reported5).
After brain metastasis resection: Release hallucinations (phantom vision) due to deafferentation may occur after resection of occipital or parietal lobe metastases2).
QCan medications cause visual hallucinations?
A
In addition to hallucinogens (LSD, mescaline, psilocybin), clarithromycin and anticholinergic drugs (such as cyproheptadine) have also been reported to cause visual hallucinations. Clarithromycin-induced visual hallucinations resolve within 72 hours after discontinuation of the drug 7). If visual hallucinations are suspected to be caused by a prescribed medication, prompt consultation with the prescribing physician is necessary.
When brain lesions are identified by MRI or CT, correlating visual fields and associated neurological symptoms with neuroimaging is useful for precise estimation of the lesion location.
In VGKC limbic encephalitis, MRI shows bilateral hippocampal T2/FLAIR hyperintensity, and CSF/serum VGKC antibodies are positive 5). To rule out paraneoplastic limbic encephalitis, screening for malignancy (e.g., testicular ultrasound, chest CT) is also performed 5).
Psychosis/delirium: Manage with environmental adjustments, discontinuation of causative drugs, and antipsychotics (typical antipsychotics such as haloperidol)
Migraine:
Preventive medication: Dihydroergotamine mesylate (Dihydergot) or lomerizine hydrochloride (Migsis) are used
During aura: Use dihydroergotamine mesylate early
During attack (mild): NSAIDs, dihydroergotamine mesylate, oral triptans
During attack (severe): Oral triptans. Subcutaneous sumatriptan injection or nasal spray may also be used
Epilepsy: Manage with an appropriate antiepileptic drug regimen based on the cause of seizures
Hyponatremia: Electrolyte correction is fundamental. Aim for an increase of 8 mEq/L per day; in some cases, visual hallucinations completely resolved within 4 days1)
Anticholinergic poisoning: Symptomatically managed with benzodiazepines and antipsychotics (haloperidol)3)
Clarithromycin-induced visual hallucinations: Drug discontinuation is the only treatment, with complete resolution within 72 hours after cessation7)
Alcohol withdrawal: Severe cases require intravenous sedation (e.g., midazolam) under ICU management4)
Autoimmune limbic encephalitis: High-dose intravenous immunoglobulin (IVIG) therapy for 5 days leads to symptom resolution. The same treatment is effective for recurrence5)
Charles Bonnet syndrome: No established evidence for drug treatment. Since many cases resolve spontaneously, explaining the condition and providing reassurance to the patient is most important2)
Optic nerve damage: Treat the underlying disease (infection, inflammation)
QIs there a specific drug for visual hallucinations themselves?
A
Standard drug therapy for visual hallucinations themselves has not been established. The principle of treatment is to address the underlying disease. In Charles Bonnet syndrome, symptoms often resolve spontaneously, and there is no definitive evidence for drug treatment2). Antipsychotics are used for psychotic hallucinations and antiepileptic drugs for epileptic hallucinations, but these are treatments for the underlying disease, not for the hallucinations alone.
The pathophysiology of visual hallucinations varies depending on the underlying disease, but a common mechanism is thought to be an imbalance between excitation and inhibition in the visual cortex.
Psychosis/delirium: Involves increased dopaminergic transmission in subcortical regions and an imbalance of neurotransmitters.
Migraine: Transient ischemia occurs in the occipital visual cortex due to cerebral vasospasm, leading to scintillating scotoma. Cortical spreading depression is thought to be involved.
Visual snow: A significant increase in gamma-band (40–70 Hz) power and a decrease in phase-amplitude coupling in the primary visual cortex have been reported, suggesting hyperactivation and disorganization of cortical activity in early visual processing.
Clarithromycin: Suppresses GABAergic signaling, increasing neuronal excitability. It has been proposed that dysfunction of the reticular activating system leads to release phenomena and visual hallucinations7).
Hyponatremia: Mechanisms are speculated to include cerebral edema due to decreased plasma osmolality and increased excitability of visual cortex neurons due to membrane potential changes. Disruption of the excitation-inhibition balance contributes to hallucination generation1).
Charles Bonnet syndrome (release hallucinations): Loss of visual input (deafferentation) leads to disinhibition of the visual cortex, “releasing” visual hallucinations. This is thought to be similar to phantom limb pain after amputation (phantom vision)2).
Tumor: Compresses the visual pathway or interferes with visual information transmission, affecting the posterior visual cortex. Temporal lobe lesions produce formed complex hallucinations (people or objects), while occipital lesions produce geometric simple hallucinations (glittering lights, rainbow spirals).
Anton-Babinski syndrome: Extensive bilateral occipital lobe damage causes cortical blindness, and abnormal connections between language centers and visual association areas lead to denial of visual impairment.
Mechanism of Visual Hallucinations in Dementia with Lewy Bodies
Mehraram et al. (2022) compared 25 patients with visual hallucinations (VH) and 17 without VH in dementia with Lewy bodies (LBD) using EEG source network analysis. The VH group showed consistently reduced connectivity within the alpha-band visual ventral network, as well as between this network and the default mode network and ventral attention network. The occipital lobe was the most functionally disconnected region 6).
In the same study’s DTI analysis, the VH group had significantly reduced white matter fiber counts between the nucleus basalis of Meynert and thalamus and the cortex. This suggests that structural degeneration of the cholinergic system contributes to functional network disruption 6).
7. Latest Research and Future Perspectives (Research-Stage Reports)
Mehraram et al. (2022) demonstrated in a study combining EEG and DTI that visual hallucinations in LBD are associated with structural degeneration of the cholinergic system and functional disruption of visual and attention networks. In the non-hallucination group, the number of white matter fibers between the nucleus basalis of Meynert and the cortex correlated with cortical functional connectivity, but this correlation disappeared in the hallucination group, where instead a correlation was found with the number of white matter fibers between functionally impaired cortical regions6).
Srichawla et al. (2022) reported a case of limbic encephalitis positive for VGKC complex antibodies despite both LGI-1 and CASPR-2 antibodies being negative. This suggests the possible existence of unidentified antigenic targets within the VGKC complex, and identification of new autoantibodies remains a future challenge5).
Release Hallucinations After Resection of Brain Metastases
Ovchinnikov et al. (2024) reported two cases of complex visual hallucinations after resection of brain metastases in the occipital and parietal lobes. In case 1, the hallucinations spontaneously resolved 18 months after surgery, and no epileptic activity was detected on EEG. Antiepileptic drugs (levetiracetam) were ineffective for the hallucinations, which were considered a non-epileptic release phenomenon (phantom vision)2).
Sharma V, Shah K, Reddy Mallimala P, et al. A Rare Case of Visual Hallucinations Associated With Hyponatremia. Cureus. 2023;15(8):e44485.
Ovchinnikov A, Andereggen L, Rogers S, Gschwind M. Visual hallucinations after resection of cerebral metastases: two patients with complex phantom images. Strahlenther Onkol. 2024;200(10):832-837.
Talabaki H, Soltani M, Abbasi A, et al. Neuropsychiatric manifestations due to anticholinergic agents and anabolic steroids ingestion: A case series and literature review. Neuropsychopharmacol Rep. 2024;44:540-544.
Desai S, Toma AE, Sunik A. Closed-Eye Visual Hallucinations Preceding Severe Alcohol Withdrawal. Cureus. 2021;13(8):e17040.
Srichawla BS. Autoimmune Voltage-Gated Potassium Channel Limbic Encephalitis With Auditory and Visual Hallucinations. Cureus. 2022;14(5):e25186.
Mehraram R, Peraza LR, Murphy NRE, et al. Functional and structural brain network correlates of visual hallucinations in Lewy body dementia. Brain. 2022;145(6):2190-2205.
McGee D, Hanley C, Reynolds A, Smyth S. Clarithromycin-Induced Visual Hallucinations. Neuro-Ophthalmology. 2022;46(5):319-321.
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