People who lose the ability to recall visual memories after brain injury share damage that involves a single, highly specific brain region. Recent analyzes of these rare medical cases have revealed that structures called fusiform image nodes serve as important hubs for human imagination. These results were published in the journal cortexhelps explain the physical origins of our mind’s eye.
Most people can close their eyes and easily picture their childhood bedroom or the face of a loved one. This ability is known as visual mental imagery. This allows humans to relive past events, solve spatial problems, and envision future scenarios without external sensory input.
However, a small percentage of the population lacks this internal visual experience completely. This lack of mind’s eye is called aphantasia. An estimated 1-3% of people worldwide develop the disease from birth.
People with congenital aphantasia lead completely normal lives, often not realizing until adulthood that others can actually see pictures in their heads. In very rare cases, a person who previously had a vivid imagination may suddenly lose it. This acquired aphantasia usually occurs after a severe brain injury, such as a stroke.
Studying acquired aphantasia provides a unique window into the workings of human cognition. By pinpointing exactly where brain damage disrupts imagination, researchers can map the biological hardware that governs mental imagery. Medical researchers began this project to identify which specific brain regions are responsible for generating our internal visual world.
The research team was led by Julian Kutsche, a neurologist at Charité University Hospital in Berlin and Harvard Medical School. Kutsche and colleagues at Brigham and Women’s Hospital’s Brain Circuit Therapy Center wanted to solve a lingering neurological puzzle. Previous imaging scans of healthy adults have pointed to a specific location on the left side of the brain that activates when people use their imagination.
This position is known as the fusiform image node. It is located in the ventral visual pathway, a broader brain network involved in object recognition and face analysis. Functional magnetic resonance imaging scans have shown that this node lights up when healthy people imagine things, but these scans only show basic correlations.
The researchers needed to know whether this particular node was strictly necessary for the process of visual imagination. If that node is indeed the center of a visual mental image, destroying it or severing its connection should completely destroy the ability to visualize. The research team set out to test this idea using historical medical records of patients suffering from acquired aphantasia.
“Can a brain injury cause a loss of imagination?” Kutche said. “A lack of visual mental imagery called aphantasia occurs congenitally in about 3% of the general population, but the brain region responsible for visual imagination remains unknown. Rare cases of acquired aphantasia caused by brain injury may provide insight into the neuroanatomy underlying this condition and the brain basis of visual imagination.”
Kutsche and his team began by searching decades of published medical literature for cases of acquired aphantasia. They looked for patients who had lost visual mental imagery after a stroke or other physical brain trauma. The research team found 12 well-documented cases with high-quality brain scans showing the exact area of injury.
These 12 patients had brain damage, known as lesions, in various locations. Some had damage to the frontal lobe, others to the parietal, temporal, and occipital lobes. At first glance, the distributed nature of these lesions suggested that imagination may not depend on a single brain center at all.
To understand these different types of damage, the researchers used an advanced technique called damage network mapping. This method does more than just look at the exact location of dead brain tissue. Instead, it looks at how the damaged area normally communicates with the rest of the nervous system.
The research team mapped the coordinates of each patient’s lesions onto a standard computerized brain map. They then cross-referenced these locations with a large database of healthy brain connections. This database contains information from 1,000 healthy volunteers and shows exactly which parts of the brain communicate with each other during rest.
First, the researchers investigated the direct physical intersection between brain injury and fusiform imaging nodules. They found that only five of the 12 aphantasia lesions physically overlapped with this particular area. Although this overlap was greater than that seen in patients with other neurological symptoms, it could not completely explain the loss of imagination in the other seven patients.
Next, they looked at the functional connections in the brain. Now the results are clearer and easier to understand. The research team found that all 12 lesions were functionally connected to the left fusiform imaging nodule.
Even if the stroke occurred on the opposite side of the brain, the damaged tissue was part of a circuit that was directly connected to this particular node. To confirm that this association was specific to aphantasia, the researchers compared their data to a large control group. They examined 887 brain lesions that caused entirely different neurological problems, from paralysis to speech loss.
Connectivity to fusiform image nodes was highly specific for aphantasia. Lesions causing other symptoms did not show this uniform relationship with image nodes. Statistical tests confirmed that this particular network pattern did not occur randomly.
The team then performed a broader analysis, making no assumptions about where the center of imagination was. Their connectivity data highlighted the most common shared networks among the 12 patients. This unrestricted search directly pointed to the exact same location in the left inferior fusiform gyrus.
The researchers also looked at the brain’s physical wiring, known as white matter tracts. They used a separate database of structural brain scans to trace the physical cables that connect different brain regions. This structural analysis revealed a shared physical pathway running directly above and behind the spindle image node.
This pathway is called the left inferior longitudinal bundle. It serves as a major communication highway connecting various visual and memory processing centers. Damage to this white matter tract appears to disconnect the fusiform image nodules from other functional brain regions, effectively shutting off the mind’s eye.
To examine the results from multiple mathematical angles, the scientists used a statistical approach called Bayesian analysis. This method helps researchers assess the probability that a hypothesis is true based on available data. The Bayesian model confirmed the involvement of the fusiform region with very high confidence.
Equally important, this was not found in the Bayesian analysis. The model did not show involvement of frontal lobes or primary visual cortex in acquired aphantasia. These two areas have long been discussed as possible command centers for generating mental images.
The primary visual cortex is the first area of the brain that receives raw signals from the eyes. Some previous theories suggested that imagination relies on moving this visual receptive field in reverse. New data provide positive evidence for the idea that the primary visual cortex is solely responsible for the creation of conscious visual memories.
Instead, the spindle-shaped image nodes appear to function as important junction boxes for the brain. It is probably located between memory centers such as the temporal lobe and the hippocampus, which store semantic knowledge. This unique position allows a person to spontaneously recall concepts and translate them into visual representations.
If a stroke damages this junction box or cuts the wires leading to it, it will no longer be possible to translate conceptual knowledge into images. The patient is still able to use descriptive language to describe the apple. They just can’t see the physical apple in their minds.
“We mapped the location of brain damage in people who previously had visual imagination but lost it after a stroke or trauma,” Kutche explained. “We then used large-scale functional and structural brain atlases to analyze the connections disrupted by these lesions.”
“People with acquired aphantasia (loss of visual imagination) had damage to different brain regions, but 100% of cases involved the fusiform imaging nodules, a specialized visual processing area that is active during visual imagery tasks in normal subjects.”
“This research is important because a stroke or brain injury can cause a wide range of symptoms, many of which are subjective, unobservable to others, and experienced only by the individual. Imagination has real meaning and importance for people, so the fact that it can change after a stroke is an inexplicable surprise for patients. By recognizing that a brain injury can cause a purely subjective internal experience, patients can better understand their symptoms during recovery.”
Although this study provides clear causal evidence for the physical origins of imagination, it also has some limitations. The main limitation is the relatively small sample size. Acquired aphantasia is so rare that the research team was only able to analyze 12 cases in the past.
Additionally, many older medical reports lacked standardized tests to measure the exact severity of a patient’s image loss. The researchers had to rely heavily on the subjective clinical description provided by the original physician. Brain scans from these older studies were also limited to two-dimensional images, which are much less accurate than modern three-dimensional imaging techniques.
Future research should use modern high-resolution scanning methods to study new stroke patients who develop aphantasia. Scientists also want to investigate whether the brain networks responsible for acquired aphantasia are different from those involved in congenital aphantasia. Understanding these differences may explain why people born without a mind’s eye function quite well, while those who lose it often feel a deep sense of cognitive loss.
It’s also possible that researchers could one day find a way to stimulate these specific brain networks. Targeted, non-invasive brain stimulation may ultimately help stroke survivors restore mental imagery. Until then, these discoveries provide a clearer map of how the human brain constructs an invisible world of thought.
“Our results inform important discussions about the neural correlates of consciousness,” Kutsche added. “There is great debate as to whether conscious experience can emerge from a single part of the brain (organized in an integrated way) or whether widespread communication across the brain is required. This question in the neuroscience of consciousness may have implications for how we think about the possibility of AI consciousness.”
“In our study, we found that disconnection of a specific brain region can abolish visual imagination. Future studies should investigate whether this region can generate visual imagination independently, or whether it lies at a really important connection between brain regions that need to communicate in a coordinated way for visual imagination.”
The study, “Aphantasia-causing lesions are associated with fusiform image nodules,” was authored by Julian Kutsche, Calvin Howard, Alberto Castro Palacin, William Drew, Matthias Michel, Alexander L. Cohen, Michael D. Fox, and Isaiah Kletenik.
