Peduncular hallucinosis (PH) is a complex, realistic visual hallucination secondary to lesions of the midbrain and/or thalamus. It involves a perceptual experience that, despite the absence of external stimuli, has the same clarity and impact as a true perception (definition of hallucination by the American Psychiatric Association). It is conceptually distinct from “illusion,” which is a misinterpretation of actual external stimuli.
Lhermitte first reported this condition in 1922. The case involved a 72-year-old woman with a stroke localized to the cerebellar peduncle and pons, who presented with neurological deficits, sleep disturbances, and new-onset hallucinations. The hallucinations were vivid and featured bizarre animals (zoopsia), increasing in frequency at dusk. Over time, the content of the hallucinations shifted from animals to humans wearing strange clothing. Insight was preserved, and there was no emotional distress or auditory hallucinations. The term “l’hallucinose pedonculaire” was coined by Van Bogaert in 1927. Currently, the concept is used to include not only lesions of the cerebral peduncle but also those of the midbrain and thalamus.
Peduncular hallucinosis is caused by organic lesions of the midbrain and thalamus, and its etiology differs from that of mental illnesses (e.g., schizophrenia). It is a diagnosis of exclusion and does not overlap with DSM-5 diagnoses. The preservation of insight during hallucinations is also a distinguishing feature from hallucinations in mental illness.
They tend to improve over several months. They may also disappear rapidly with the resolution of the primary lesion. Currently, there is insufficient evidence to support or refute an association with increased dementia risk or mortality.
Initial onset typically occurs acutely immediately after an ischemic or hemorrhagic event in the midbrain, thalamus, or pons. Posterior circulation infarction is the most common cause.
Frequently observed accompanying clinical findings are as follows.
Note that there are case reports without eye movement abnormalities or classic symptoms of brainstem lesion localization. There are also cases where hallucinations were the only presenting symptom, confirmed by neuroimaging. It may also co-occur with Parkinson’s disease or sleep-wake rhythm disorders.
Ischemia of the posterior circulation is the most common cause. Possible etiologies involved are listed below.
The involved lesion sites are mainly the midbrain, thalamus, and pons, but lesions in the basal ganglia (striatum and globus pallidus) have also been reported.
Peduncular hallucinosis is a diagnosis of exclusion. Diagnosis begins by confirming the following criteria based on clinical history.
It should not overlap with any DSM-V diagnosis. MRI is useful for identifying brainstem lesions and determining the underlying disease.
Charles Bonnet Syndrome
Onset background: Visual hallucinations occur during the course of progressive vision loss.
Visual acuity and visual field: Accompanied by decreased visual acuity and visual field (preserved in PH).
Effect of eye closure: Hallucinations tend to disappear when eyes are closed (in PH, they tend to worsen with eye closure).
Insight: Often preserved.
Dementia with Lewy bodies
Nature of hallucinations: Complex, visual, non-threatening hallucinations.
Extrapyramidal symptoms: accompanied by akathisia, dystonia, parkinsonism, and tremor.
Cognitive function: chronic, progressive decline in neurocognitive function and impairment of visuospatial abilities.
Insight: often preserved.
Hypnagogic/hypnopompic hallucinations
Underlying disease: Seen in patients with narcolepsy.
Associated symptoms: Characterized by daytime sleepiness, sleep attacks, and cataplexy.
Mechanism: Inappropriately enters REM sleep and experiences hallucinations while maintaining consciousness.
Other differential diagnoses include psychiatric disorders such as schizophrenia, drug use such as LSD, delirium, epileptic seizures, migraine, and brain tumors.
Charles Bonnet syndrome develops with progressive vision loss, and hallucinations tend to disappear when the eyes are closed. In contrast, in peduncular hallucinosis, visual acuity and visual fields are preserved, and hallucinations tend to worsen when the eyes are closed. The location of the lesion also differs (CBS involves damage to the visual pathway, while PH involves organic lesions in the midbrain and thalamus).
Since it is a diagnosis of exclusion, other causes such as psychiatric disorders, drug use, and delirium should first be systematically ruled out. Identifying brainstem lesions on MRI and determining the underlying disease is the first step in treatment.
If a treatable underlying disease is identified, correcting the cause may resolve the hallucinations. There have been reports of hallucinations disappearing after resection of juvenile pilocytic astrocytoma. Visual hallucinations may also resolve spontaneously within weeks to months.
Hallucinations may resolve spontaneously, so medication is not always necessary. However, if emotional distress is significant or daily functioning is severely impaired, atypical antipsychotics or antiepileptic drugs can be effective options. Because of the black box warning for atypical antipsychotics in elderly patients, careful judgment is required.
Several hypotheses have been proposed regarding the mechanism of onset of peduncular hallucinosis.
Lhermitte’s hypothesis attributed the cause to a lesion in the pontine tegmentum (protuberantial calotte bulb). Damage to cranial nerves III, IV, and VI and dysregulation of the brainstem were considered necessary conditions, leading to activation of subcortical areas responsible for dreaming during wakefulness.
The most currently supported theory is the neurotransmitter imbalance hypothesis.
The dorsal raphe nucleus also regulates the sleep–wake cycle and REM/non-REM sleep. Damage to this area causes nocturnal awakening and daytime hypersomnia, which may explain why PH tends to worsen at night or in dim environments.
Other theories include hyperactivation of the reticular activating system and entering REM sleep while remaining conscious (a state similar to hypnagogic hallucinations). Based on five consecutive cases, Benke proposed reinterpreting peduncular hallucinosis as a “disorder of reality monitoring,” and findings supporting the mechanism of dream-like experiences intruding into wakefulness have been presented.
Benke T. Peduncular hallucinosis: a syndrome of impaired reality monitoring. J Neurol. 2006;253(12):1561-1571. doi:10.1007/s00415-006-0254-4. PMID: 17006630
Shahab M, Ahmed R, Kaur N, Masoud H. Peduncular hallucinosis after a thalamic stroke. BMJ Case Rep. 2021;14(5):e241652. doi:10.1136/bcr-2021-241652. PMID: 33986011 / PMCID: PMC8126318
Penney L, Galarneau D. Peduncular hallucinosis: a case report. Ochsner J. 2014;14(3):450-452. PMID: 25249815 / PMCID: PMC4171807
Talih FR. A probable case of peduncular hallucinosis secondary to a cerebral peduncular lesion successfully treated with an atypical antipsychotic. Innov Clin Neurosci. 2013;10(5-6):28-31. PMID: 23882438 / PMCID: PMC3719456
Garde Gonzalez J, Oliva Lozano A, Herrero Ortega P, Morillas Romerosa MA. Peduncular hallucinosis: clinical characteristics, etiology, and a case report. Eur Psychiatry. 2024;67(Suppl 1):S260. doi:10.1192/j.eurpsy.2024.549. PMCID: PMC11862547
