If you were told to close your eyes and picture a red apple, what do you “see?” For some, the image of an apple is relatively easily conjured. For others, nothing appears at all. This inability to generate mental images is called aphantasia. People with aphantasia describe being unable to “see” images in their mind, even when trying to imagine something familiar, like a loved one’s face or their childhood home.
It’s estimated that roughly four percent of people experience aphantasia. Mental imagery is known to exist on a spectrum. Some individuals score at the opposite extreme, known as hyperphantasia, where mental pictures are unusually vivid. (If you’re curious, the Vividness of Visual Imagery Questionnaire is a classic test used to assess where someone falls on this scale – I actually scored as hyperphantasic!)
Scale of mental visual imagery ( image source )
From a neuroscience perspective, aphantasia is fascinating. It involves key processes like memory, perception, and imagination. Studies suggest that when people visualize mental images, areas such as the secondary visual cortex (V2), the parietal cortex, and other top-down control networks become active. In individuals with aphantasia, these circuits may be disrupted or underactive, limiting the brain’s ability to generate internal imagery.
Given that psychedelics are known to cause visual hallucinations and increase neural connectivity between visual regions and higher-order brain areas, it’s interesting to examine how they might compensate for this deficit.
One especially interesting case study describes a woman with severe aphantasia who reported that after taking psilocybin mushrooms, for the first time in her life, she was able to form mental images. She even dreamed in pictures – something she had never experienced before. Although the effect faded over time, her description of the experience is remarkable:
“I found it incredible because it was the first time I had images in my mind, and I realized that you can play with images, zoom in, zoom out, break down colors. The possibilities with mental images are endless… it’s an experience of pure mind. It opened up incredible possibilities for me… Being able to intensely live this experience for a day makes you want to revolutionize the world.”
A similar case was reported in a man with severe aphantasia who took ayahuasca, which is a brew containing the potent psychedelic DMT. Following the experience, he noted:
“I can now bring forth faint pictures in my mind. They fade quickly but they are there. When dreaming I now see faint, quickly fading images. It feels like this experience with ayahuasca has slightly opened up my mind’s eye and allowed me to experience internal images like I have never had before.”
These accounts highlight just how dramatically psychedelics can shift perception. Psychedelics also promote neuroplasticity and synaptic growth, which could further explain why some users experience changes in imagination and perception.
This article will look at potential neurological explanations for how psychedelics may (albeit temporarily) reverse aphantasia, as well as implications of this on psychedelic research and therapy as a whole.
Neurological perspective of aphantasia
Research examining neurobiological underpinnings of aphantasia is relatively new, but a handful of imaging studies have started to map out some consistent differences.
For example, researchers found that aphantasic participants showed greater activation in visual-perceptual cortices compared to controls, but controls, on the other hand, had stronger activation in the right posterior hippocampus. In other words, people with aphantasia seem to process incoming visual information just fine, maybe even more intensely, but the hippocampal circuitry does not engage in the same way when it comes to generating imagery from memory.
Aphantasics have greater visual-perceptual activation (C), and lower right posterior hippocampus activation (D) ( image source )
Another study compared groups of aphantasic, hyperphantasic, and control participants during tasks that involved both perception and visualization. The hyperphantasic and control groups showed much stronger activity than the aphantasic group in visual-occipital regions. This means that the more vivid someone’s mental imagery, the more “classic” vision areas light up even in the absence of actual sensory input.
Hyperphantasics (left) and control (right) both have stronger activity in visual-occipital regions ( image source )
Hyperphantasics also consistently show stronger activation in medial frontal regions and the insula during imagination tasks compared to low-vividness groups. This hints at a whole-brain network beyond the visual cortex, tying in memory, self-referential thought, and emotional salience.
Medial frontal lobe and insula are more strongly activated in hyperphantasics ( image source )
Aphantasia is less about seeing nothing and more about a rerouting of neural resources. Visual cortices may be active, but the hippocampal and frontal systems that stitch those perceptions into imagery don’t engage the same way.
Psychedelics and visual imagery
Psychedelics appear to enhance visual imagery by changing how the brain’s visual system interacts with other regions. Neuroimaging studies show that psychedelics increase connectivity between the primary visual cortex (V1) and higher-order areas, reduce top-down inhibition, and broadly reconfigure large-scale brain networks. This “network rewiring” is thought to underlie psychedelic hallucinations and, by extension, may temporarily strengthen the brain’s capacity to generate mental imagery.
For instance, LSD increases cerebral blood flow and functional connectivity in the visual cortex, correlating with reports of vivid and complex visual hallucinations.
LSD increases cerebral blood flow in the primary visual cortex ( image source )
Similarly, ayahuasca has been shown to increase visual cortex activation during imagery tasks to levels approaching those observed during actual visual perception.
Also, a recent effective connectivity study of psilocybin showed altered visual network dynamics characterized by stronger top-down feedback and self-inhibition, mechanisms thought to underlie the vivid eyes-closed imagery of psychedelic states.
As mentioned earlier, aphantasiacs have lower hippocampal activity when compared to control. Interestingly, LSD was found to disinhibit parahippocampal gyri, increasing activity in this region.
Disinhibition of parahippocampal gyri with LSD ( image source )
In addition, psychedelics increase the entropy of brain activity – a measure of complexity linked to conscious experience – which may allow imagery to emerge in individuals who normally cannot access it.
5HT2A receptors, which LSD is a specific agonist for, are associated with increased brain entropy ( image source )
These mechanisms align with findings that aphantasia is associated with abnormal long-range connectivity between visual, memory, and frontoparietal regions. By boosting communication across these circuits, psychedelics could – at least transiently – restore visual imagery ability.
This suggests that the same neurobiological mechanisms driving psychedelic hallucinations – enhanced visual cortex activation, increased cross-network connectivity, and reduced inhibitory control – may also explain why some individuals with aphantasia briefly gain the ability to generate mental imagery.
That said, psychedelics do not always function this way. While some people with aphantasia report being able to experience mental imagery for the first time after psychedelic or even cannabis use, anecdotally (forums here and here), others say that psychedelics do not induce hallucinations for them at all, even under high doses.
Implications and conclusions
While case studies and anecdotal reports highlight the possibility that psychedelics can temporarily restore visual imagery, the broader implications are more complex, and warrant caution. Not everyone might welcome the sudden ability to generate vivid internal images. Visual imagery is a powerful emotional amplifier. Strong mental imagery can intensify thoughts, both positive and negative, and in some cases may contribute to unwanted psychological experiences.
For example, research shows that individuals with stronger visual imagery are more prone to intrusive thoughts and memories, including distressing or unwanted content. This has obvious relevance for conditions like PTSD, where vivid flashbacks can exacerbate trauma. In the context of addiction, visual imagery can fuel cravings and anticipatory reward thoughts, potentially making relapse more likely. Similarly, maladaptive daydreaming appears to correlate with more vivid imagery, though this remains an area of ongoing investigation.
There are also concerns about long-term effects of psychedelics. While the acute experiences of imagery and altered perception are generally temporary, some users report lasting perceptual changes, such as hallucinogen-persisting perceptual disorder, which can involve persistent visual distortions. Although rare, these effects reveal the need for careful consideration when exploring psychedelics as a tool to enhance imagery or cognition.
While psychedelics may unlock new capacities in the mind’s eye for some individuals with aphantasia, stronger visual imagery is not universally beneficial. Enhancing the ability to visualize also carries the potential for emotional intensification, intrusive memories, or maladaptive mental patterns.
Regardless, the possibility that psychedelics could transiently restore imagery in individuals with aphantasia is fascinating. It reveals much about the neural mechanisms of perception and imagination, as well as how psychedelics alter these pathways.
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