Hallucinations Happen When the Brain Fills in the Blanks
What Parkinson’s and psychedelics reveal about the shared roots of hallucination.
Posted November 4, 2025 | Reviewed by Monica Vilhauer Ph.D.
“ His first misperceptions occurred when he was in a nightclub; the skin of the other dancers, even their faces, seemed to be covered with tattoos. At first, he thought the tattoos were real, but they started to glow and then to pulse and writhe…”
— Oliver Sacks, Hallucinations
What if the same neural glitch that produced this Parkinson’s patient’s writhing tattoos also drives psychedelic visions? It may seem unlikely that a degenerative brain disorder and a psilocybin trip could share common pathways, but mounting evidence suggests they do. In a recent review paper my colleagues and I published in Schizophrenia Bulletin , we explored the surprising overlap between visual hallucinations in Lewy body diseases, such as Parkinson’s and dementia with Lewy bodies, and those induced by psychedelics like psilocybin and LSD. Though these conditions differ radically in their cause, the associated hallucinations seem to arise from similar disruptions in how the brain processes visual input.
Serotonergic Visions in Drugs and Disease
While Lewy body diseases are better known for producing motor and cognitive impairments, they also have profound impacts on sensory systems . Up to 75% of patients report visual distortions of size, motion, or form. More complex hallucinations are reported at rates close to 40%. Patients often report minor hallucinations months or years before complex hallucinations emerge. Early on, a patient might experience movement in still objects, fleeting figures in their periphery, or illusory faces half-glimpsed in ambiguous patterns. Later, they can experience vivid hallucinations of strange animals, people, or entire scenes.
Psychedelics compress a similar progression into hours, rather than months or years. Psychedelic visions may start with breathing walls and color shifts, then blossom into intricate imagery and animate presences. Despite the vastly different timescale, the progression in complexity over time and some of the content are remarkably similar. These perceptual similarities suggest that both Lewy body diseases and psychedelic drugs might disturb similar perceptual mechanisms.
A growing body of research points to one key player in both psychedelic and Lewy body–related hallucinations: a serotonin receptor known as the 2A receptor. Psychedelics like psilocybin and LSD act mainly through this receptor, and blocking it with drugs can prevent their hallucinogenic effects. In Lewy body diseases, the same receptor seems to become overactive or more abundant. Drugs that dampen the 2A receptor’s activity, like pimavanserin, often reduce hallucinations in these patients. In hallucinating patients, brain imaging shows that areas where these receptors are most concentrated tend to be those with the most neurodegeneration.
Together, these converging findings make a compelling case that the serotonin 2A receptor forms a shared molecular bridge between drug-induced and disease-related hallucinations: one transient and pharmacological, the other gradual and pathological. In other words, the impact of Lewy body diseases on the visual system may act like a slow-motion psychedelic, gradually (and permanently) loosening the same perceptual constraints that psychedelics dissolve rapidly (and reversibly).
The 5-HT 2A Receptor and Balance in the Brain
The serotonin system has dozens of receptor types, serving a wide range of neuromodulator functions across cortical and subcortical brain regions. Why does a single receptor type, the serotonin 2A receptor, correspond to such profound distortions in visual processing? One clue is to look closely at where this receptor is located. In both human and non-human primates , the serotonin 2A receptor is most densely packed in a very small region of the early visual cortex: layer 4 of the primary visual cortex. This is the very first brain region where sensory data from the eyes enters into the cortex, the starting point of the visual processing pathway. Understanding the function of this brain region can go a long way toward untangling the dramatic visual effects of psychedelic drugs that target the serotonin 2A receptor.
What do we know about the effects of serotonin in the primary visual cortex? In awake behaving primates, applying serotonin to primary visual cortex causes cells to fire less vigorously when presented with a visual stimulus. Psychedelics have been shown to cause similar reduced visual responsiveness in human EEG and fMRI studies, and even in mouse models of visual processing. These reductions in response to visual stimuli likely correspond to reduced fidelity of sensory signals originating at the base of the visual processing pathway. A scenario where low-fidelity visual signals persistently propagate to higher-level visual processing stages is precisely one in which hallucinations can emerge.
This kind of sensory degradation, where low-fidelity signals enter a system tuned to expect clarity, is foundational to all major models of visual hallucinations. As Collerton and colleagues note in their recent unified visual hallucination framework , when incoming sensory data weakens, the brain’s higher-order interpretive machinery compensates. The brain becomes like an off-balance see-saw, like in the figure above.
In healthy perception, the two forces stay in equilibrium: stable sensory input keeps cortical activity grounded, and higher-order cortical feedback helps make sense of noisy sensory data. But when visual information degrades sufficiently, whether from retinal loss, cortical degeneration, or serotonin-driven suppression, the see-saw tilts. As the sensory side sinks and higher-order processes become more active, the brain begins to fill in the degraded sensory data with its own internally generated patterns. At later stages of visual processing beyond primary visual cortex, this hyperactivity may result in visual distortions, making objects seem to ripple, shift, or warp. As higher-order associative processes like attention and memory become hyperactive , more complex and emotionally evocative hallucinations may emerge. Ultimately, the brain doesn’t stop seeing when the signal degrades; it starts seeing from the inside out.
Despite these convergences, much remains unclear. We still don’t know whether greater numbers of serotonin 2A receptors in Lewy body patients directly causes hallucinatory activity in a way similar to psychedelic administration, or whether the increase in these receptors contributes to neurodegeneration, which subsequently leads to hallucinations. Psychedelics, however, give us a rare experimental handle on these questions. Future research can probe, in real time, how serotonergic mechanisms tip the balance between sensory signals and internal generation. For now, they offer a glimpse of how fragile that balance can be.
Heller, N. H., Barrett, F. S., Buchborn, T., Collerton, D., Dupuis, D., Halberstadt, A. L., ... & Leptourgos, P. (2025). Visual hallucinations in serotonergic psychedelics and Lewy body diseases. Schizophrenia bulletin , 51 (Supplement_3), S273-S291.
Pagonabarraga, J., Bejr-Kasem, H., Martinez-Horta, S., & Kulisevsky, J. (2024). Parkinson disease psychosis: from phenomenology to neurobiological mechanisms. Nature Reviews Neurology , 20 (3), 135-150.
Vignando, M., Ffytche, D., Lewis, S. J., Lee, P. H., Chung, S. J., Weil, R. S., ... & Mehta, M. A. (2022). Mapping brain structural differences and neuroreceptor correlates in Parkinson’s disease visual hallucinations. Nature communications , 13 (1), 519.
Burnet, P. W. J., Eastwood, S. L., Lacey, K., & Harrison, P. J. (1995). The distribution of 5-HT1A and 5-HT2A receptor mRNA in human brain. Brain research , 676 (1), 157-168.
Takahata, T., Shukla, R., Yamamori, T., & Kaas, J. H. (2012). Differential expression patterns of striate cortex-enriched genes among old world, new world, and prosimian primates. Cerebral Cortex , 22 (10), 2313-2321.
Seillier, L., Lorenz, C., Kawaguchi, K., Ott, T., Nieder, A., Pourriahi, P., & Nienborg, H. (2017). Serotonin decreases the gain of visual responses in awake macaque V1. Journal of Neuroscience , 37 (47), 11390-11405.
Michaiel, A. M., Parker, P. R., & Niell, C. M. (2019). A hallucinogenic serotonin-2A receptor agonist reduces visual response gain and alters temporal dynamics in mouse V1. Cell reports , 26 (13), 3475-3483.
Collerton, D., Barnes, J., Diederich, N. J., Dudley, R., Friston, K., Goetz, C. G., ... & Weil, R. S. (2023). Understanding visual hallucinations: A new synthesis. Neuroscience & Biobehavioral Reviews , 150 , 105208.
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Nicolas Davidenko, Ph.D. , is a Professor of Psychology at the University of California, Santa Cruz, where he teaches courses on perception, illusions, and face recognition.
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