Brain Injuries in One Specific Region Erase the Ability to Visualize - Every Single Time

Close your eyes and picture a red apple. For most people, something approximating an image appears, even if it is hazy or incomplete. For roughly 3% of the population, nothing appears at all - a condition called aphantasia, usually present from birth. But for a smaller and more enigmatic group, the ability to visualize was once present and then, after a stroke or traumatic brain injury, simply vanished. Understanding why has been difficult because no single lesion location seemed to explain the loss - until now.

Every Case Points to the Same Region

Isaiah Kletenik, MD, and Julian Kutsche of the Center for Brain Circuit Therapeutics at Mass General Brigham conducted a systematic mapping study, published in the journal Cortex. They reviewed the scientific literature to identify every documented case of acquired aphantasia - the post-injury loss of visual imagination - then mapped each patient lesion location onto a common brain atlas.

The lesions were scattered. They appeared in many different brain regions, with no obvious single anatomical site. That alone was not surprising; the brain is complex and strokes are unpredictable. But when the team analyzed connectivity patterns - tracing which other brain regions each lesion site was functionally linked to - a single common thread emerged. Every single case, 100%, was connected to the fusiform imagery node.

The fusiform imagery node is a region of the brain that activates during visual imagery tasks in healthy individuals. It had been implicated in imagination before, but establishing it as a necessary hub - rather than just one participant among many - required exactly this kind of lesion mapping approach. "Understanding the underlying neuroanatomy of aphantasia can advance the field of cognitive neuroscience and inform clinical practice," Kletenik said.

A Tool for Understanding What Injury Takes Away

Strokes and traumatic brain injuries produce many kinds of loss, most of them visible to others: weakness, speech difficulty, memory gaps. But the loss of visual imagination is invisible. There is no test you can run in a clinic that straightforwardly measures it. Patients may not even realize they have lost it until someone asks them to close their eyes and picture something, and they cannot.

The clinical implication is that healthcare providers should be asking. Recognizing that brain injuries can alter subjective, internal experience - including something as fundamental as the capacity to imagine - could help patients make sense of what they are experiencing during recovery. "The capacity for imagination holds significant meaning and importance in people lives, making it particularly puzzling and surprising for patients when they discover that a stroke can alter this ability," the researchers wrote.

What This Tells Us About Consciousness

The study opens into a larger debate in neuroscience about whether conscious experience can arise from a single organized brain region or requires coordinated activity across a distributed network. If disconnecting the fusiform imagery node is sufficient to extinguish visual imagination, does that mean the node alone generates the experience? Or does it function as a necessary relay station, a hub that coordinates wider activity?

The researchers are cautious about claiming the former. The finding is that all acquired aphantasia cases are connected to this node - not that the node alone is sufficient for imagination. The distinction matters. A hub can be necessary without being sufficient, in the same way that a power line is necessary for electricity to reach a building without being the source of that electricity.

Kletenik noted that the discovery opens new directions: exploring whether the fusiform imagery node can produce visual imagination independently, or whether it serves as a nexus that requires coordinated input from multiple other regions. The tools to answer that question are becoming available as brain mapping technology improves.

The study was co-authored by Calvin Howard, William Drew, Alexander L. Cohen, Michael D. Fox, Alberto Castro Palacin, and Matthias Michel. Funding came from the German Academic Exchange Service Biomedical Education Program, the Canadian Clinician Investigator Program, and the NIH NINDS.