Neural Basis of Visual Imagination Unveiled

Brigham and Women's Hospital

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.

Paper cited: Kutsche, J. et al. "Lesions Causing Aphantasia are Connected to the Fusiform Imagery Node." Cortex. DOI: 10.1016/j.cortex.2026.01.009

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.

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