Summary: About 3% of people are born with aphantasia—the inability to visualize images in their mind. But what happens when someone loses their imagination after a stroke or accident? A new study has pinpointed the exact brain region responsible for this internal vision.
By mapping brain lesions in rare cases of acquired aphantasia, the team discovered that while injuries occurred in various locations, 100% of cases were connected to a single nexus: the fusiform imagery node. This discovery identifies a critical biological “hub” required for mental imagery and opens new doors for understanding human consciousness and AI development.
Key Facts
- The “Fusiform Imagery Node”: Researchers identified this specific region as the mandatory “switch” for visual imagination. If it is damaged or disconnected, the mind’s eye goes dark.
- Acquired Aphantasia: The study focused on rare cases where individuals who previously had vivid imaginations lost the ability following a stroke or traumatic brain injury (TBI).
- Network Connectivity: Even if the injury wasn’t in the fusiform imagery node, it was always connected to it, suggesting imagination relies on this node as a central communications hub.
- Clinical Significance: Many patients find the loss of imagination distressing but “invisible” to doctors. This study provides a biological explanation for their symptoms, aiding in more holistic stroke and TBI recovery.
- Consciousness Debate: The findings contribute to the “lively debate” on whether consciousness is localized in one region or spread across the entire brain, with potential implications for artificial intelligence.
Source: Mass General
A recent study by Mass General Brigham researchers explored whether a stroke or traumatic brain injury can result in the loss of visual imagination, known as aphantasia, and which specific parts of the brain are necessary for this function.
Isaiah Kletenik, MD, and Julian Kutsche, of the Center for Brain Circuit Therapeutics within the Mass General Brigham Neuroscience Institute, are the senior and lead authors of a paper published in Cortex, “Lesions Causing Aphantasia are Connected to the Fusiform Imagery Node.”
Q: What challenges or unmet needs make this study important?
Visual imagination, or “seeing in the mind’s eye,” is a unique function that allows people to relive past events, solve problems and envision the future. However, about 3% of the general population is born lacking this visual mental imagery—a condition known as aphantasia. Beyond these congenital cases, it remains unclear how stroke or traumatic brain injury can impair this type of imagination.
Understanding the underlying neuroanatomy of aphantasia can advance the field of cognitive neuroscience and inform clinical practice as well. The lack of understanding surrounding this condition poses challenges for those affected as it can impact creativity, a sense of personal meaning and cognitive function.
What central question(s) were you investigating?
Our study was guided by two central questions:
- What specific parts of the brain are involved, or necessary, for visual imagination?
- Can a brain injury make someone lose their imagination?
By examining rare cases of acquired aphantasia caused by brain injury, we sought to lend insight into the neurological basis of visual imagination.
Q: What methods or approach did you use?
We systematically mapped the locations of brain injuries in individuals who previously possessed the ability for visual imagination, but lost it following a stroke or brain trauma. Specifically, we conducted a thorough literature review to identify cases of acquired aphantasia and mapped the lesion locations onto a common brain atlas. Next, to understand the impact of these injuries, we used extensive functional and structural brain atlases to analyze the connectivity patterns that may have been disrupted.
Q: What did you find?
Our findings revealed that individuals with acquired aphantasia had injuries in many different brain locations. However, 100% of cases were connected to the fusiform imagery node, a specialized region of the brain that is active during visual imagery tasks in healthy individuals. The fact that all identified cases were functionally linked to this specific brain region suggests a critical role for the fusiform imagery node in maintaining the capacity for visual imagination.
Q: What are the real-world implications, particularly for patients?
Strokes and traumatic brain injuries can lead to a wide range of symptoms, many of which are subjective and not observable to others. The capacity for imagination holds significant meaning and importance in people’s lives, making it particularly puzzling and surprising for patients when they discover that a stroke can alter this ability.
By recognizing that brain injuries can lead to changes in subjective, internal experiences, healthcare providers can help patients gain a better understanding of their symptoms during recovery. Moreover, understanding the link between brain injury and changes in imagination may inform future rehabilitation strategies, enhancing patient care and supporting a more holistic approach to recovery.
Q: What emerging trends in this field excite you right now?
Currently, there is a lively debate regarding whether conscious experience can arise from a single organized part of the brain or if widespread communication across multiple brain regions is needed. This question about the neuroscience of consciousness is particularly exciting as it may have implications for our understanding of potential AI consciousness.
Our discovery that disconnection of a specific brain region could extinguish visual imagination opens up intriguing avenues for future research—for example, exploring whether this region can produce visual imagination independently, or if it serves as a crucial nexus that requires coordinated communication with other brain regions.
Authorship: In addition to Kletenik and Kutsche, Mass General Brigham authors include Calvin Howard, William Drew, Alexander L. Cohen and Michael D. Fox. Additional authors include Alberto Castro Palacin and Matthias Michel.
Funding: Funding sources for this study include the German Academic Exchange Service’s Biomedical Education Program, the Canadian Clinician Investigator Program and the National Institutes of Health (NIH) NINDS (L30 NS134024).
Disclosures: Fox reported holding intellectual property on the use of brain connectivity imaging to analyze lesions and guide brain stimulation, as well as consulting for Magnus Medical, Soterix, Abbott, Boston Scientific and Tal Medical.
Key Questions Answered:
A: If I ask you to imagine a red apple, you might “see” it in your head. Someone with aphantasia knows what an apple is and can describe it, but they don’t “see” an image. It’s like a computer running a program without a monitor attached.
A: Yes. While we often focus on motor skills or speech after a stroke, this study shows that subjective internal experiences—like the ability to relive a memory visually or envision the future—can also be extinguished if the “fusiform imagery node” is disconnected.
A: That’s the exciting future. By identifying the exact node and circuit responsible, researchers can now explore whether brain stimulation (like TMS) could potentially activate or strengthen the “mind’s eye” in people with congenital or acquired aphantasia.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this aphantasia and visual neuroscience research news
Author: Katie Grant
Source: Mass General
Contact: Katie Grant – Mass General
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Lesions Causing Aphantasia are Connected to the Fusiform Imagery Node” by Julian Kutsche, Calvin Howard, Alberto Castro Palacin, William Drew, Matthias Michel, Alexander L. Cohen, Michael D. Fox, and Isaiah Kletenik. Cortex
DOI:10.1016/j.cortex.2026.01.009
Abstract
Lesions Causing Aphantasia are Connected to the Fusiform Imagery Node
The absence of visual mental imagery, called aphantasia, occurs congenitally in up to 3% of the general population, but the brain regions responsible for aphantasia remain uncertain.
Rare cases of acquired aphantasia caused by brain lesions may lend insight into the neuroanatomy responsible for this condition, and the neural substrate of visual mental imagery itself.
We performed a systematic literature review to identify cases of lesion-induced aphantasia and traced the lesion locations onto a common brain atlas. These locations were compared to control lesions causing other neuropsychiatric symptoms (n = 887).
First, we tested for intersection between lesion locations and an a priori region of interest termed the fusiform imagery node, active during visual mental imagery tasks. Second, we tested for connectivity between lesion locations and this region of interest, leveraging resting-state functional connectivity from a large cohort of healthy subjects (n = 1000).
Finally, we performed a data-driven analysis assessing whole-brain lesion connectivity that was sensitive (100% overlap) and specific (family-wise error p < .05) for aphantasia. We identified 12 cases of lesion-induced aphantasia, only 5 of which intersected the fusiform imagery node.
However, 100% of these lesion locations were functionally connected to the fusiform imagery node. Connectivity to this region was both sensitive (100% overlap) and specific (family-wise error p < .05) for aphantasia in a data-driven whole-brain analysis. Lesions causing acquired aphantasia occur in multiple different brain regions but are all functionally connected to the left fusiform imagery node.
This study provides causal support for the importance of this brain region in visual mental imagery.
