Can Mushrooms Give You a Mind’s Eye? Aphantasia and Psychedelics

Close your eyes. Picture an apple. Red, green, whatever comes naturally. See it sitting on a table, the light catching the skin, maybe a stem and a leaf at the top.

If you just did that—if an apple appeared in your mind’s eye with any degree of visual detail—you’ve done something that roughly 1.2% of the population cannot do. Not “finds difficult.” Cannot. When they close their eyes and try to picture an apple, they get nothing. Blackness. The concept of an apple, the knowledge of its properties, the word—but no image. No visual experience whatsoever.

This is aphantasia. And for the people who have it, the discovery that other people literally see things when they imagine them tends to land somewhere between bewildering and devastating. There’s a particular kind of loneliness in learning that everyone around you has been watching movies in their heads their entire lives while you’ve been staring at a blank screen.

So when a published case report showed that a woman with lifelong aphantasia gained vivid mental imagery after taking psilocybin truffles—imagery that persisted for years—it hit the aphantasia community like a small earthquake. The r/Aphantasia thread that followed is one of the more extraordinary pieces of psychedelic discussion I’ve read online. Hope, skepticism, experimentation, and disappointment all layered on top of each other. Some people tried mushrooms and saw things for the first time. Others took heroic doses and saw nothing at all.

The science is genuinely fascinating. The conclusions are nowhere near as clean as anyone wants them to be.

What Aphantasia Actually Is (and Isn’t)

Aphantasia was named in 2015 by Adam Zeman, a neurologist at the University of Exeter, though the phenomenon had been described as early as 1880 by Francis Galton. The name comes from the Greek a- (without) + phantasia (imagination, or more precisely, the capacity to form mental images). It affects an estimated 1-4% of the population depending on how strictly you define it, with most studies converging around 1.2% for complete aphantasia—the total inability to generate voluntary mental imagery.

This isn’t a vocabulary problem. It’s not a failure of imagination in the broader sense. People with aphantasia can be wildly creative. They can write fiction, design buildings, solve spatial problems. They just do it without the internal visual display that most people take for granted. Ed Catmull, co-founder of Pixar, has aphantasia. The man who helped build the most visually sophisticated animation studio in history can’t see pictures in his own head.

And it’s measurable. A 2022 study published in eLife demonstrated that aphantasia can be objectively detected through pupillary response. When sighted people imagine a bright scene, their pupils constrict—a physiological response to the imagined brightness. When people with aphantasia imagine the same scene, their pupils don’t respond. The difference is reliable and involuntary. You can’t fake it in either direction. The body confirms what the person reports: the image isn’t there.

Aphantasia exists on a spectrum. Some people have zero imagery in all senses—no visual, no auditory, no tactile imagination (total aphantasia or multi-sensory aphantasia). Others have weak or partial imagery that sometimes flickers into existence but can’t be summoned at will. At the other end is hyperphantasia—imagery so vivid it’s almost indistinguishable from perception. Most people fall somewhere in the wide middle ground, able to conjure images with varying degrees of clarity and control.

The neurological basis isn’t fully mapped, but emerging research points to differences in top-down connectivity—the way higher-order brain regions (frontal and parietal cortex) send signals down to the visual cortex to generate imagery in the absence of actual visual input. In people with aphantasia, this top-down pathway appears to be weaker, absent, or differently organized. The visual cortex itself is typically intact. The eyes work fine. The problem is in the internal signal that says “generate an image of this.”

Which is what makes the psilocybin findings so strange and so interesting.

The Case Report That Changed the Conversation

A published case report—peer-reviewed, in an academic journal—documented a woman with congenital aphantasia (present from birth, as far as she or anyone could determine) who took psilocybin truffles and experienced mental imagery for the first time.

The measurement tool was the VVIQ—the Vividness of Visual Imagery Questionnaire, the standard instrument for assessing imagery capacity. It asks you to imagine a series of scenes (a relative’s face, a sunrise, a shop front) and rate the vividness on a scale from 1 (no image at all) to 5 (perfectly vivid, as if you were really seeing it). Scores range from 16 (no imagery on any item) to 80 (maximum vividness on every item).

Before psilocybin: her score was 16. The absolute floor. Complete aphantasia.

After psilocybin: her score was 80. The absolute ceiling. Maximum vividness.

And here’s the detail that elevates this from interesting to extraordinary: the change persisted. At 33 months post-dose—nearly three years later—her imagery scores remained elevated. This wasn’t a transient psychedelic effect. Something had shifted, durably, in her brain’s capacity to generate internal visual experience.

One person. One case report. But a swing from 16 to 80 on a validated instrument, sustained for 33 months, is the kind of result that makes researchers sit up and redesign their next study.

The Reddit Reality

The case report became a beacon. If psilocybin could give one person a mind’s eye, why not others?

The r/Aphantasia thread that followed is a document of what happens when a community of people who’ve been told their condition has no treatment encounters a single dramatic case of improvement. Some people were cautiously intrigued. Some were already planning their doses. Some had already tried and were reporting back.

The reports split roughly into three categories.

The ones who saw something. A subset of people with aphantasia described gaining some degree of mental imagery during or after psilocybin experiences. Fleeting flashes of color. Geometric patterns. In a few cases, recognizable images—faces, landscapes, objects. Some of these persisted after the acute effects wore off, at least for a while. The reports were moving to read. People describing, for the first time in their lives, the experience of seeing something that wasn’t physically in front of them. One person described it as “like a TV turning on in a room that’s been dark your whole life.”

The ones who saw nothing. Others took what they described as heroic doses—well above typical therapeutic levels—and got nothing visual at all. Still blackness. The body effects were all there: the shift in thinking, the emotional opening, the altered sense of self. But no images. No mind’s eye. One person described it as “the most emotionally intense blackness I’ve ever experienced.” The psychedelic state was fully present. The imagery was fully absent.

The one who lost something. At least one person in the thread reported the opposite trajectory. They had some degree of mental imagery before taking psychedelics and found it diminished or absent afterward. This is the kind of report that gets buried in the enthusiasm of a thread focused on gains, but it matters enormously. If psilocybin can modify the top-down visual pathways that generate imagery, there’s no a priori reason to assume the modification always goes in one direction.

The overall picture from the Reddit reports is messy, inconsistent, and completely unsurprising to anyone familiar with psychedelic research. Psychedelics produce highly variable responses across individuals, and that variability is especially pronounced for perceptual effects. Your neuroanatomy, your baseline connectivity, your receptor density, your psychological state—all of it influences what happens when psilocybin disrupts your brain’s normal operating patterns.

The case report woman may have had a neurological architecture that was, so to speak, pre-wired for imagery but inactive—a circuit that existed but had never been switched on, and psilocybin flipped the switch. Others may have aphantasia for different structural reasons that psilocybin simply can’t address. The same phenotype (no imagery) might have multiple underlying causes, only some of which are psilocybin-responsive. We don’t know. Nobody knows yet.

The Neuroscience: Psilocybin and the Visual System

A 2025 paper in Molecular Psychiatry—one of the highest-impact journals in psychiatric neuroscience—examined how psilocybin alters connectivity in the visual system. The findings are directly relevant to the aphantasia question, and they complicate the story in ways that the Reddit thread didn’t address.

The researchers found that psilocybin significantly alters top-down connectivity—the flow of information from higher-order brain regions down to the visual cortex. Under normal conditions, this top-down signal is what generates voluntary mental imagery. You decide to picture an apple, your prefrontal cortex sends instructions to your visual cortex, and the visual cortex generates a representation. In aphantasia, this pathway is weak or absent. The psilocybin findings suggest that the substance can temporarily (and possibly durably) modify how this pathway functions.

But—and this is the critical nuance—the imagery generated under psilocybin appears to work through a different mechanism than normal voluntary visualization. Psilocybin-induced visual experience isn’t the same as deliberately choosing to picture an apple and seeing one. It’s more spontaneous, less controlled, less directed by conscious intention. The visual cortex activates, but it’s being driven by a flood of disorganized serotonergic signaling, not by the precise top-down control that characterizes normal imagery.

This distinction matters because it suggests that psilocybin doesn’t simply “turn on” the normal visualization system. It may activate the visual cortex through an alternative route—one that bypasses the usual voluntary control mechanisms. For the case report woman, that alternative activation may have somehow primed or trained the normal pathway, resulting in lasting voluntary imagery. For others, the alternative route may produce psychedelic visual effects (fractals, color fields, geometric patterns) without activating the voluntary imagery system at all.

In other words: psilocybin might open a door, or it might open a window that happens to be in the same room as the door. From the inside, the light coming in looks similar. The mechanism is different, and the long-term consequences may be different too.

The Dark Twist Nobody Wants to Hear

A 2025 viewpoint published in Cortex—a journal focused on the neuroscience of cognition and perception—raised a possibility that the aphantasia community’s enthusiasm has largely skipped over. The authors pointed out that if psilocybin can “switch on” mental imagery in people who’ve never had it, this isn’t an uncomplicated gift. It comes with a shadow side.

Mental imagery isn’t just voluntary pictures of apples and sunsets. It’s also involuntary images. Nightmares. Intrusive mental images after witnessing something traumatic. The visual component of flashbacks. The images that accompany anxiety—the car crash you keep seeing, the worst-case scenario playing on loop, the face of someone you’re trying to forget.

People with aphantasia are largely protected from the visual component of these experiences. They can have nightmares with emotional and narrative content but without the vivid visual replay that makes PTSD flashbacks so devastating. They can be anxious without the intrusive images that feed anxiety loops. Their condition, in this specific sense, functions as an accidental shield.

If psilocybin switches on visual imagery, it switches on all of it. Not just the sunsets and the apples. The nightmares too. The intrusive images. The visual dimension of every emotional experience, including the ones you’d rather not see.

The Cortex authors weren’t making a definitive prediction. They were raising a concern—one grounded in what we know about the neuroscience of imagery and its relationship to psychopathology. Visual imagery is deeply implicated in PTSD, anxiety disorders, depression, and obsessive-compulsive disorder. Gaining a mind’s eye might mean gaining vulnerability to imagery-based distress that was previously inaccessible.

There’s a peculiar irony here. Aphantasia communities often frame the condition as a deficit—something missing, something lost, something they wish they had. And it genuinely is a deficit in some ways. It limits certain kinds of creative experience, makes certain kinds of memory less vivid, closes off an entire dimension of inner life that most people take for granted. But it also closes off a dimension of inner suffering. The trade isn’t as one-sided as it appears from the outside.

What We Actually Know (and the Vast Territory of What We Don’t)

Let me try to lay this out honestly.

We know that at least one person with congenital aphantasia gained vivid, lasting mental imagery after psilocybin. The case report is real, the measurement is validated, and the duration of the effect (33+ months) is remarkable.

We know that psilocybin alters top-down connectivity in the visual system in ways that are directly relevant to voluntary mental imagery. The neuroscience is plausible.

We know that the response is highly variable. Some people with aphantasia report gaining imagery after psychedelics. Others don’t. At least one person reports losing imagery. The inconsistency suggests that aphantasia is probably not a single condition with a single cause, and that psilocybin probably doesn’t do the same thing to everyone’s visual pathways.

We know that gaining imagery could come with costs. Involuntary imagery, intrusive images, and imagery-related psychological distress are real phenomena, and people who gain a mind’s eye also gain exposure to them.

We don’t know why the case report woman responded so dramatically while others didn’t. We don’t know what predicts response. We don’t know if the mechanism is the same as normal voluntary imagery or a different system that produces a similar subjective experience. We don’t know the long-term trajectory—will her imagery persist for a lifetime, or is 33 months a long plateau before a gradual fade? We don’t have controlled trials. We don’t have replication. We have a single extraordinary case, a handful of anecdotal reports, and a plausible but unconfirmed neurobiological mechanism.

That’s fascinating. It’s not a cure.

The Thing About Wanting to See

There’s something I keep thinking about when I read through that Reddit thread. The people who took mushrooms hoping to gain a mind’s eye weren’t approaching the experience the way most people approach psychedelics. They weren’t looking for insight, or therapy, or creative expansion, or spiritual experience. They were trying to fix something about themselves that they’d been told was unfixable. They were going in with a specific, concrete, deeply personal hope: let me see.

And some of them did see. Briefly, imperfectly, differently than they expected. Colors during the peak. Geometric patterns. A flash of a face. Not the full mind’s-eye cinema, usually, but something. After a lifetime of nothing, something.

I find it hard to read those accounts without being moved by them. Whatever the science eventually concludes, whatever the mechanism turns out to be, whatever the risks are—the experience of seeing an image in your mind for the first time after thirty or forty years of darkness is extraordinary. The people describing it aren’t deluded. They aren’t misinterpreting. They’re reporting a genuine perceptual event that represents a radical departure from everything they’ve known about their own inner life.

And then there are the ones who took heroic doses and saw nothing, and went home and lay in the dark feeling everything psychedelics make you feel—the emotional flood, the dissolution of ego, the sense that something profound is happening—but without the visual component that they came for. That the thing they wanted most was the thing the substance couldn’t give them.

There’s a tangent I want to follow here, and it circles back. My grandmother couldn’t carry a tune. Not “sang badly”—genuinely could not distinguish pitches well enough to reproduce a melody. The clinical term is amusia. She loved music. Listened to it constantly. But the thing she loved existed for her in a fundamentally different form than it existed for everyone else in the room. She wasn’t experiencing less. She was experiencing differently. And I think there’s something in that distinction that matters for aphantasia too. The absence of imagery isn’t the absence of imagination. It’s imagination in a different key. What psilocybin might offer isn’t a fix for something broken. It might be more like learning a second language—one that opens new rooms but doesn’t make the rooms you already had any less real.

Where This Goes Next

The aphantasia-psychedelics connection is going to attract more research. The case report is too dramatic, the neuroscience too plausible, and the affected population too eager for answers. Someone will run a small trial. Probably within the next few years. Probably at one of the institutions already doing psilocybin research.

When that trial happens, I’d watch for three things. Whether the effect replicates across multiple participants. Whether there are predictors of response (baseline brain connectivity, type of aphantasia, dose, context). And whether the gains, in participants who do gain imagery, come with any of the costs the Cortex authors warned about.

Until then, the honest position is that we have a remarkable case, a plausible mechanism, inconsistent anecdotal evidence, and a real possibility that gaining a mind’s eye is not the uncomplicated gift people imagine.