Hallucinations are among the most mysterious and revealing phenomena in neuroscience. Whether they arise from neurodegenerative diseases like Parkinson’s or from psychedelics such as LSD or psilocybin, the underlying mechanism appears surprisingly similar. In both cases, when sensory input weakens, the brain begins to fill in the blanks, creating vivid internal images and sensations that blur the line between perception and imagination.
The Shared Mechanisms Behind Hallucinations
Neurologist Oliver Sacks once described a Parkinson’s patient who saw writhing tattoos covering people’s faces. At first, the man thought they were real, until the patterns began to pulse and glow. This same kind of perceptual distortion appears in psychedelic experiences, suggesting that Parkinson’s-related and psychedelic hallucinations share neural roots.
Research published in Schizophrenia Bulletin points to a common mechanism: disturbances in how the brain processes visual input. In Lewy body diseases such as Parkinson’s and dementia with Lewy bodies, up to 75% of patients report visual distortions, and about 40% experience complex hallucinations. These often begin subtly—seeing movement in still objects or faint figures in peripheral vision—before evolving into vivid scenes or characters.
Psychedelics compress this progression into hours rather than years. Users first see color shifts or breathing walls, which then develop into intricate patterns or lifelike imagery. Despite different causes, both conditions alter perception in ways that reveal how the brain constructs reality.
The Serotonin Connection
One key molecule bridges these two phenomena: the serotonin 2A receptor (5-HT2A). Psychedelics like LSD and psilocybin activate this receptor, while drugs that block it can prevent their hallucinogenic effects. In Parkinson’s and Lewy body diseases, these same receptors become overactive or more abundant, contributing to visual disturbances.
Medications such as pimavanserin, which dampen 2A receptor activity, often reduce hallucinations in Parkinson’s patients. Brain imaging studies show that the regions with the most 2A receptors are also those most affected by neurodegeneration—suggesting that receptor imbalance plays a direct role in hallucinations.
In essence, the overactive serotonin system in both drug-induced and disease-related conditions blurs the boundary between sensory reality and internally generated imagery. Psychedelics cause this distortion temporarily, while Parkinson’s produces it gradually and chronically—like a slow-motion psychedelic experience.
How the Brain Fills in the Gaps
The primary visual cortex (V1) is where raw visual data from the eyes first enters the brain. The serotonin 2A receptor is densely concentrated in this region, particularly in layer 4, where external sensory input arrives. When serotonin activity suppresses the responsiveness of these visual neurons, the result is low-fidelity visual signaling.
This weakened input forces the brain’s higher regions to compensate, creating a feedback loop where imagination substitutes for missing data. As one unified model of visual hallucinations suggests, perception becomes a see-saw between sensory input and internal prediction.
When that balance is healthy, external data keeps perception grounded. When it falters—due to retinal loss, cortical degradation, or serotonergic overstimulation—the brain leans heavily on its own memories and expectations. It begins “seeing from the inside out.”
- Mild disruptions cause distortions—objects appear to ripple or shift.
- Moderate disruptions produce recognizable figures or faces.
- Severe disruptions engage memory and emotion, creating full scenes or entities that feel alive.
In both Parkinson’s hallucinations and psychedelic experiences, the same dynamic unfolds: as sensory reliability drops, the brain fills in the blanks with its own predictive imagery.
Psychedelics as a Window Into Hallucination
Psychedelics offer scientists a unique tool for studying these mechanisms in real time. By temporarily inducing controlled hallucinations, researchers can observe how serotonergic networks interact with visual and associative brain regions. This helps explain not only drug-induced visions but also hallucinations in mental illness and neurodegeneration.
What remains unclear is whether the increase in serotonin receptors in Parkinson’s directly causes hallucinations, or if it’s a response to underlying degeneration. Either way, these findings illuminate how fragile perception really is—and how easily the brain’s internal world can overtake external reality.
Seeing From the Inside Out
Ultimately, hallucinations remind us that perception is an act of construction, not reflection. The brain constantly balances between receiving the world and generating it. When that balance shifts—through disease, drugs, or sensory loss—the imagination takes over.
Understanding hallucinations in the brain is more than a study of pathology; it’s a window into how all perception works. Every moment, your brain fills in countless blanks—you just usually don’t notice.
