New research on acquired aphantasia pinpoints specific brain network responsible for visual imagination

People who lose their ability to conjure visual memories after a brain injury share damage that connects to a single, highly specific brain region. A recent analysis of these rare medical cases reveals that a structure called the fusiform imagery node acts as an essential hub for the human imagination. These results, published in the journal Cortex, help explain the physical origins of our mind’s eye.

Most people can easily close their eyes and picture a childhood bedroom or the face of a loved one. This ability is known as visual mental imagery. It allows human beings to relive past events, solve spatial problems, and envision future scenarios without any external sensory input.

However, a small fraction of the population lacks this internal visual experience entirely. This absence of a mind’s eye is called aphantasia. It occurs from birth in an estimated one to three percent of people across the globe.

Individuals with congenital aphantasia live entirely normal lives, often realizing only in adulthood that other people can actually see pictures in their heads. In extremely rare instances, a person who previously possessed a vivid imagination can lose it suddenly. This acquired form of aphantasia typically follows a severe brain injury, such as a stroke.

Studying acquired aphantasia offers a unique window into the mechanics of human cognition. By pinpointing exactly where brain damage eliminates imagination, researchers can map the biological hardware responsible for mental imagery. Medical researchers initiated this project to identify which specific brain areas are causally responsible for generating our internal visual world.

The research team was led by Julian Kutsche, a neurologist affiliated with the Charite university hospital in Berlin and Harvard Medical School. Kutsche and his colleagues at the Center for Brain Circuit Therapeutics at Brigham and Women’s Hospital wanted to solve a lingering neurological puzzle. Previous imaging scans of healthy adults pointed to a specific spot in the left side of the brain that activates during imagination tasks.

This location is known as the fusiform imagery node. It sits in the ventral visual pathway, a broader brain network involved in recognizing objects and analyzing faces. While functional magnetic resonance imaging scans show this node lighting up when healthy people imagine things, these scans only demonstrate a basic correlation.

The researchers needed to know if this specific node was strictly necessary for the process of visual imagination. If the node is truly the center of visual mental imagery, destroying it or cutting off its connections should entirely eliminate the ability to visualize. The team set out to test this idea using historical medical records of patients suffering from acquired aphantasia.

“Can a brain injury make someone lose their imagination?” Kutsche said. “The absence of visual mental imagery, called aphantasia, occurs congenitally in about 3% of the general population, but the brain regions responsible for visual imagination remain uncertain. Rare cases of acquired aphantasia caused by brain injury may lend insight into the neuroanatomy responsible for 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 lost their visual mental imagery following a stroke or other physical brain trauma. The team found twelve well-documented cases that included high-quality brain scans showing the exact area of injury.

These twelve patients had suffered brain damage, known as lesions, in widely varying locations. Some injuries were in the frontal lobes, while others were in the parietal, temporal, or occipital lobes. At first glance, the scattered nature of these injuries suggested that imagination might not rely on a single brain center at all.

To make sense of these varied injuries, the researchers used an advanced technique called lesion network mapping. This method does not just look at the exact spot of dead brain tissue. Instead, it examines how the damaged area normally communicates with the rest of the nervous system.

The team mapped the coordinates of each patient’s lesion onto a standard, computerized brain atlas. They then cross-referenced these locations with a massive database of healthy brain connectivity. This database contains information from one thousand healthy volunteers, showing exactly which parts of the brain talk to each other during periods of rest.

First, the researchers looked at direct physical intersections between the brain damage and the fusiform imagery node. They found that only five of the twelve aphantasia lesions physically overlapped with this specific region. While this overlap was greater than what is seen in patients with other neurological symptoms, it did not fully explain the loss of imagination in the other seven patients.

Next, they looked at functional brain connections. This is where the results became much clearer and easier to understand. The team discovered that every single one of the twelve lesions was functionally connected to the left fusiform imagery node.

Even when a stroke occurred on the opposite side of the brain, the damaged tissue was part of a circuit that directly wired into this specific node. To ensure this connection was unique to aphantasia, the researchers compared their data against a massive control group. They examined eight hundred and eighty-seven brain lesions that caused entirely different neurological issues, ranging from paralysis to language loss.

The connectivity to the fusiform imagery node was highly specific to aphantasia. Lesions causing other symptoms did not show this uniform connection to the imagery node. Statistical testing confirmed that this specific network pattern was not a random occurrence.

The team then performed a broader analysis without making any assumptions about where the imagination center might be. They let the connectivity data highlight the most common shared network among the twelve patients. This unrestricted search pointed directly 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 connecting different brain regions. This structural analysis revealed a shared physical pathway running just above and behind the fusiform imagery node.

This pathway is called the left inferior longitudinal fasciculus. It serves as a major communication highway linking different visual and memory processing centers. Damage to this white matter tract appears to disconnect the fusiform imagery node from other functional brain regions, effectively shutting down the mind’s eye.

To verify their results from multiple mathematical angles, the scientists used a statistical approach called Bayesian analysis. This method helps researchers evaluate the probability of a hypothesis being true based on the available data. The Bayesian models confirmed the involvement of the fusiform areas with exceptionally high confidence.

Equally important was what the Bayesian analysis did not find. The models showed no involvement of the frontal lobes or the primary visual cortex in acquired aphantasia. These two regions have long been debated as possible command centers for generating mental imagery.

The primary visual cortex is the first area of the brain to receive raw signals from the eyes. Some previous theories suggested that imagination relies on running this visual reception area in reverse. The new data provides affirmative evidence against the idea that the primary visual cortex is solely responsible for creating conscious visual memories.

Instead, the fusiform imagery node seems to act as an essential junction box for the brain. It likely sits between the temporal lobes, which store semantic knowledge, and memory centers like the hippocampus. This unique position allows a person to voluntarily recall a concept and translate it into a visual representation.

If a stroke damages this junction box, or severs the wires leading to it, the conceptual knowledge cannot be translated into a picture. The patient can still describe an apple using descriptive words. They just cannot see the physical apple in their mind.

“We mapped the locations of brain injury from people who previously had visual imagination but lost it after stroke or trauma,” Kutsche explained. “Then we analyzed the connections that would be disrupted by these injuries using large functional and structural brain atlases.”

“People with acquired aphantasia (loss of visual imagination) had injuries in many different brain locations, but 100% of cases were connected to the fusiform imagery node, a specialized visual processing region that is active during visual imagery tasks in normal subjects.”

“This work is important because strokes and brain injury can cause a wide range of symptoms, many of which are subjective, not observable to others and only experienced by the person themself. Imagination is of real meaning and importance to people so the fact that this can be changed after a stroke is a puzzling surprise to patients. By recognizing that brain injuries can cause purely subjective, internal experiences it can allow patients to better understand their symptoms during recovery.”

While this research provides clear causal evidence for the physical origins of imagination, it does have a few limitations. The primary constraint is the relatively small sample size. Because acquired aphantasia is incredibly rare, the team could only analyze twelve historical cases.

Additionally, many of the older medical reports lacked standardized tests for measuring the exact severity of the patients’ imagery loss. The researchers had to rely heavily on the subjective clinical descriptions provided by the original doctors. The brain scans from these older studies were also limited to two-dimensional images, which are far less precise than modern three-dimensional imaging techniques.

Future research will need to study new stroke patients who develop aphantasia using modern, high-resolution scanning methods. Scientists also hope to investigate if the brain networks responsible for acquired aphantasia differ from those involved in congenital aphantasia. Understanding these differences could explain why people born without a mind’s eye function quite well, while those who lose it often feel a profound sense of cognitive loss.

There is also a possibility that researchers could one day find ways to stimulate these specific brain networks. Targeted, non-invasive brain stimulation might eventually help restore mental imagery in stroke survivors. Until then, these findings offer a clearer map of how the human brain constructs the invisible world of thought.

“Our results inform key discussions about the neural correlates of consciousness,” Kutsche added. “There’s a huge debate about whether conscious experience can emerge from a single part of the brain (organized in an integrated way) or if wide-spread communication across the brain is needed. This question in the neuroscience of consciousness may have implications for how we consider the possibility of AI consciousness.

“In our study, we found that disconnection of a specific brain region could extinguish visual imagination; future research needs to examine if this region can produce visual imagination independently or if it is sits at a really important nexus between brain regions which need to communicate in a coordinated way for visual imagination.”

The study, “Lesions causing aphantasia are connected to the fusiform imagery node,” was authored by Julian Kutsche, Calvin Howard, Alberto Castro Palacin, William Drew, Matthias Michel, Alexander L. Cohen, Michael D. Fox and Isaiah Kletenik.