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People who can't picture anything are rewriting the science of imagination

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People Who Can’t Picture Anything Are Rewriting the Science of Imagination
Some people can't picture anything in their heads, and studying their brains is overturning a popular theory of how imagination works.

By George Semaan

Sep 14, 2026

8 mins read

In Brief

Mental pictures come from many brain regions working together, and aphantasia happens when that teamwork breaks down.
Patients whose primary visual cortex was destroyed can still imagine, so the old idea of imagination as reversed seeing fails.
Because the network can break in many ways, every person's inner life of pictures, sounds and voices is a little different.

Some people have lost a large stretch of the brain tissue that first receives what the eyes send in, and yet, when they close their eyes and try, they can still call up a picture of a face or a room. Such patients sit awkwardly beside an influential idea about how imagination works, one that treats the mind’s eye as ordinary seeing run backward through the same hardware.
A new review in the journal Consciousness and Cognition, written by Derek Arnold, Loren Bouyer, Blake Saurels and Samuel Schwarzkopf, argues that this backward-seeing picture has run out of road, and that the people best placed to show why are those who can’t form mental pictures at all. Their condition is called aphantasia, from the Greek phantasia, a piece of information drawn from the senses, and it describes a lifelong inability to imagine sights, and often sounds, smells, tastes or touch as well.
The plain answer to why some people can’t visualize, according to the review, is that a set of brain regions spread from the front of the head to the sides fails to work as a team. Two of the authors are themselves unable to picture anything, and their accounts, together with the patients whose visual cortex was destroyed, support a view in which a mental image is something many parts of the brain make together and no single region owns.
Seeing in Reverse
When you look at a cup, the signal from your eyes lands first in a patch at the very back of the brain called the primary visual cortex. In 2019, Joel Pearson described a model in which imagining a cup runs that pipeline backward. Planning areas at the front start the request, memory regions supply the details, and the picture is painted back onto the primary visual cortex, the same screen that real seeing uses, so that how strongly this back region lights up should decide how vivid your mental image feels.
Brain scanners can often tell which image a person is imagining by reading activity in this back region, and researchers have taken that as proof that the region builds the image. Arnold and his colleagues push back, writing that such interpretations “ignore the adage that correlation does not establish causation.” Paying attention to an imagined shape could nudge the back of the brain enough for a scanner to read it, even if that activity plays no part in the felt experience of a picture.
Stronger evidence came when Rebecca Keogh, Johanna Bergmann and Pearson passed a mild electrical current through the scalp to quiet the primary visual cortex, and people then reported more vivid imagery. Arnold’s team accepts that the region can turn imagery up or down, while noting that it could do so by shaping activity in other areas that do the real work, much as a dimmer switch changes a room without producing any light of its own.
The Patients Who Kept Their Mind’s Eye
The hardest evidence comes from the clinic, where several people have kept the power to visualize despite extensive damage to primary visual cortex. One patient studied by Beatrice de Gelder and colleagues was blind across his whole field of view because both sides of that region were destroyed, yet when asked to imagine an angry person, the front and side regions of his brain responded much as they do in sighted people. If the mind’s eye needed that back screen, such a person shouldn’t be able to picture anything.
Pooling the brain-scanning studies tells the same story. Alfredo Spagna, Paolo Bartolomeo and colleagues combined dozens of imagery experiments and found that imagining reliably engaged the front of the brain and a strip along the underside of the left temporal lobe called the fusiform gyrus, a region already known for recognizing faces and written words, while the primary visual cortex was often quiet. A case reported by Sandra Thorudottir and colleagues pointed the same way, since an architect lost his ability to imagine after a stroke to this left temporal strip.
Weighing all of this, Arnold and his co-authors conclude that the backward-seeing idea “has been largely discredited, at least in its original form.” They leave room for a gentler version, in which signals fed back to the rear of the brain hush stray activity and so sharpen an image assembled elsewhere, a possibility that Roger Koenig-Robert, Pearson and a colleague have recently raised. Even then, the primary visual cortex acts as a helper rather than a source.
Life Without Pictures
The modern story of aphantasia began when Adam Zeman and colleagues described a man who lost his ability to visualize, and readers wrote in to say they’d never had the ability at all. A follow-up by Zeman, Michaela Dewar and Sergio Della Sala gave the condition its name, and later work by Alexei Dawes and colleagues found that roughly a quarter of aphantasics report no imagined sensations of any kind, no inner sound, smell, taste or touch.
These reports show up in the body. When Marcus Wicken, Keogh and Pearson had people read scary stories, aphantasics’ skin didn’t sweat the way other readers’ skin did, though it reacted normally to scary pictures, which suggests that words usually reach the body’s fear response by way of an image. Inside the skull, Jianghao Liu and colleagues found weaker communication between the fusiform strip and the left front of the brain in aphantasics, and William Dupont and colleagues found that stimulating the movement area produced a fainter twitch in the finger, as if signals travel less well between distant regions.
Bouyer and Arnold describe themselves as visual aphantasics, and they insist this does not mean an empty mind. Asked what sits beside the television, they answer without hesitation, but “we experience these as an awareness of a set of spatial facts.” Arnold recalls being good at Tetris in his youth with no picture of the falling pieces, only learned knowledge of which gaps each shape fits, which is why the authors distrust questionnaires that treat Tetris skill as proof of spatial imagery.
A Picture the Whole Brain Makes
Several rival theories try to say what breaks. Juha Silvanto blames the insula, a region that monitors the body’s inner signals, arguing that imagining needs the inward attention you use to notice your own heartbeat. Liu proposes three stages, generating, integrating and then amplifying an image until it reaches awareness, with aphantasics failing only at the last step. Andrea Blomkvist treats the condition as a memory problem, since aphantasics recall fewer details of past events, with fact-based memory filling in as an imperfect substitute.
Arnold’s team argues that these accounts fit together better than they compete, and offers an emergent property framework, in which a mental image arises from coordinated activity across the prefrontal cortex, the fusiform strip and a region near the crown of the head involved in planning movements. A chord needs several strings sounding at once, and a single string plucked alone gives you a note, never the chord. Because a network can fail in many places, this explains why some aphantasics lack only pictures while others lack every inner sense, and why Arnold, Bouyer and Merlin Monzel found that some aphantasics dream in pictures while others don’t.
The framework also settles an argument about hidden images. The philosopher Bence Nanay has suggested that aphantasics form mental pictures they aren’t aware of, partly because they do fine at judging whether two rotated shapes match, but Lachlan Kay, Keogh and Pearson found that aphantasics solve those puzzles by comparing features one at a time. Since imagery means the felt experience itself, the review treats “any suggestion of subliminal imagery as a tautology,” and whatever the fragments are called, “some neurological difference(s) seem to prevent Aphantasics from having conscious imagined pictorial sensations when they recollect things.”
Why This Matters
There is still no objective test for aphantasia, and the review says the field should stop pretending otherwise. Priming tricks, pupil measurements and self-rating questionnaires have each fallen short, so, as with autism or anxiety, the condition will likely be recognized for years to come from a convergence of self-report, behavior and brain scans.
The bigger claim is that the network story applies to everyone. If mental images depend on how well brain regions talk to one another, then people who can visualize should differ too, some thinking mostly in pictures, others in an inner voice, others in smell or movement, and the authors predict these differences will show up in how often people use each kind of imagined sense in daily life.
Aphantasia is, at bottom, the absence of one kind of conscious experience, which makes it a rare chance to study how brains produce such experiences at all. The authors hold their answers loosely, admitting that “if we update this review in a couple of years’ time, we expect that some of what we think we know will prove to be wrong,” and they name the open questions, whether the condition runs in families, whether children grow into pictures or out of them, and whether anyone can be taught to see with their eyes closed.

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The study of individuals experiencing aphantasia, the lifelong inability to visualize mental imagery of sights, sounds, or other sensory experiences, is prompting a reevaluation of established theories regarding the mechanism of imagination and the role of the brain in consciousness. Traditional models suggested that imagination functions as a reversed form of visual seeing, with the primary visual cortex acting as the source for mental pictures. However, research, particularly a review by Arnold, Bouyer, Saurels, and Schwarzkopf in Consciousness and Cognition, argues that this backward-seeing concept is largely discredited in its original form. The central hypothesis advanced by this group posits that mental imagery arises not from a single region but from the coordinated activity of multiple brain regions working in concert, suggesting that the mind’s eye is a product of distributed network function.

The research explores how this network function is disrupted in aphantasics. While some patients with significant damage to the primary visual cortex retain the ability to imagine, this observation challenges the necessity of this specific region for visual imagery. Brain scanning experiments have further complicated the relationship between imagery and the visual system. Early models proposed that imagining involves signaling backward from higher planning areas to the visual cortex. However, the authors contend that this interpretation ignores causality, suggesting that the activity in the visual cortex may influence other areas rather than being the essential generator of the felt experience. Evidence from manipulating the primary visual cortex, where quietening it led to more vivid imagery in some subjects, supports the idea that the visual cortex functions as a modulator or helper in imagery generation rather than the sole source.

Empirical evidence gathered through brain scanning and patient observations points to a distributed system for mental imagery. Studies involving imagery experiments have demonstrated reliable engagement of frontal brain areas and the fusiform gyrus, a region critical for facial and word recognition, while the primary visual cortex was often quiet during these processes. This suggests that imagination involves a complex interplay between planning, memory, and recognition centers. The condition of aphantasia, as initially defined when Adam Zeman and colleagues described a man who lost his ability to visualize, has been further explored by subsequent work, which indicated that a significant portion of aphantasics report no imagined sensations of any kind.

Physiological differences are also noted in aphantasics. Reports indicate that aphantasics’ physiological responses, such as skin sweating during exposure to scary stories, differ from sighted individuals, suggesting alternative pathways through which sensory information influences the body’s fear response. Furthermore, research has found weaker communication between the fusiform strip and the front of the brain in aphantasics, and reduced signal transmission between distant regions, implying differences in how sensory information is integrated across the neural network.

Various alternative theoretical frameworks attempt to explain the absence of conscious imagery. Some theories focus on the insula, proposing that imagining requires the inward attention associated with monitoring internal bodily signals. Others conceptualize the process in distinct stages, where aphantasics may fail at the final amplification step. An alternative perspective views aphantasia as a memory problem, where fact-based memory substitutes for detailed experiential recall. The most compelling framework presented by Arnold and colleagues is an emergent property framework, which posits that a mental image arises from the coordinated activity across the prefrontal cortex, the fusiform strip, and planning regions. This network model elegantly accounts for the variability in aphantasias, explaining why some individuals lack only pictorial imagery while others lack all inner sensations, and why some dream in pictures while others do not. The authors conclude that the most meaningful contribution of this line of research is establishing that the ability to visualize is dependent on the functional connectivity and teamwork among brain regions.