Summary: Approximately 3% of people are born with aphantasia—the inability to form voluntary visual images in the mind. New research now shows that people can also develop aphantasia after a stroke or traumatic brain injury, and it pinpoints a single brain region that appears to be essential for visual imagination.
Researchers mapped lesion locations from rare cases of acquired aphantasia and found that, although injuries occurred in diverse brain areas, every case was functionally connected to one specific hub: the fusiform imagery node. This identifies a biological nexus required for the “mind’s eye” and offers new insight for clinicians, cognitive neuroscientists, and those studying consciousness and artificial intelligence.
Key Facts
- Fusiform Imagery Node: The study highlights this left fusiform region as a critical switch for visual mental imagery. Damage or disconnection of this node correlates with loss of the ability to visualize internally.
- Acquired Aphantasia: The focus was on people who had previously experienced vivid mental imagery but lost it after a stroke or traumatic brain injury (TBI).
- Network Connectivity: Even when lesions were not physically located within the fusiform imagery node, every lesion was functionally connected to it, suggesting the node operates as a central communications hub for imagining images.
- Clinical Relevance: Loss of visual imagination is an often invisible and distressing symptom for patients. Demonstrating a biological basis helps clinicians validate patients’ experiences and informs more comprehensive rehabilitation strategies.
- Consciousness and AI Implications: The results feed into debates about whether conscious experiences are localized or emerge from distributed brain networks, and they may inform theoretical approaches to artificial intelligence.
Source: Mass General Brigham
New study overview
A team from the Mass General Brigham Neuroscience Institute examined whether stroke or traumatic brain injury can extinguish visual imagination, commonly called aphantasia, and which brain regions are necessary for that ability. The paper, published in the journal Cortex, is titled “Lesions Causing Aphantasia are Connected to the Fusiform Imagery Node.” Senior and lead authors include Isaiah Kletenik, MD, and Julian Kutsche of the Center for Brain Circuit Therapeutics.
Why this study matters
Visual imagination—the capacity to “see” memories, mental simulations, or imagined scenarios—supports memory recall, creative thinking, planning, and emotional meaning. While congenital aphantasia affects a small portion of the population, the possibility that acquired brain injury can remove this internal visual experience has been poorly understood. Identifying the neuroanatomy behind visual imagery helps explain patients’ subjective reports and supports targeted clinical care.
Research questions
- Which specific brain regions are necessary for visual mental imagery?
- Can brain lesions caused by stroke or trauma result in the loss of imagination?
To address these questions, the researchers collected case reports of acquired aphantasia following brain injury, traced lesion locations onto a standardized brain atlas, and analyzed functional and structural connectivity patterns using large-scale brain atlases.
Methods in brief
The study began with a systematic literature review to identify documented cases of lesion-induced aphantasia. Lesions were mapped to a common atlas and compared to a large control set of lesions linked to other neuropsychiatric symptoms (n = 887). The team tested overlap with an a priori region of interest—the fusiform imagery node—and examined resting-state functional connectivity from a cohort of healthy participants (n = 1000). A data-driven whole-brain analysis then assessed whether lesion connectivity patterns were sensitive and specific for acquired aphantasia.
Key findings
Twelve cases of acquired aphantasia were identified. Only a minority of those lesions physically overlapped the fusiform imagery node, but every lesion location was functionally connected to that node. Whole-brain connectivity analysis showed 100% overlap for connectivity to the fusiform imagery node in cases of aphantasia and produced statistically specific results (family-wise error p < .05). In short, lesions that abolish visual imagination can occur in several brain regions but are consistently linked, via network connectivity, to the left fusiform imagery node.
Clinical implications
Patients can experience profound distress when a previously intact inner visual life is lost after an injury. Because this change is subjective and not visible on basic exams, clinicians may miss or minimize the symptom. Demonstrating a causal, biological basis for acquired aphantasia helps validate patients’ experiences and suggests that recovery plans should consider internal cognitive changes, not only observable deficits. The findings also raise the possibility that neuromodulation techniques, such as targeted brain stimulation, might someday restore or enhance visual imagery in congenital or acquired cases.
Broader research context
The study contributes to ongoing debates about whether conscious experiences depend on specialized local hubs or on distributed networks. Discovering that disconnection of a single imagery hub can abolish mental imagery invites further investigation into whether the fusiform imagery node can generate imagery independently or must orchestrate distributed activity to produce the mind’s eye.
Authorship and funding
Authors from Mass General Brigham include Isaiah Kletenik, Julian Kutsche, Calvin Howard, William Drew, Alexander L. Cohen, and Michael D. Fox. Additional contributors are Alberto Castro Palacin and Matthias Michel. Funding sources included the German Academic Exchange Service’s Biomedical Education Program, the Canadian Clinician Investigator Program, and the NIH NINDS (L30 NS134024). Disclosures note that one author reported intellectual property and consulting relationships related to brain connectivity imaging and brain stimulation technologies.
Key Questions Answered:
A: A person with aphantasia understands what objects and scenes are and can describe them, but they lack a conscious visual image. Asking them to imagine a red apple will not produce a mental picture; instead, they retain knowledge about apples without an internal visual representation.
A: Yes. This research shows that if brain injury disconnects the fusiform imagery node from its network, the capacity for voluntary visual imagery can be lost, even when other cognitive functions appear preserved.
A: Identifying a specific node and circuit is an important step. It raises the possibility that targeted interventions, such as brain stimulation, could be explored to activate or strengthen the neural substrates of visual imagery in congenital or acquired aphantasia, though such treatments remain experimental.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- The journal paper was reviewed in full by the editorial team.
- Additional context and clarification were added by staff to help readers understand clinical and scientific implications.
About this aphantasia and visual neuroscience research news
Author: Katie Grant
Source: Mass General Brigham (Mass General)
Contact: Katie Grant – Mass General
Image credit: 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
Aphantasia—the absence of voluntary visual mental imagery—affects up to 3% of people congenitally, but the neural basis of this phenomenon has been unclear. Rare cases of acquired aphantasia following focal brain lesions can illuminate which brain regions and networks are necessary for visual imagery.
The authors performed a systematic review of lesion-induced aphantasia, mapped lesions to a common atlas, and compared them to a large control group of lesions associated with other neuropsychiatric outcomes (n = 887). They tested overlap with an a priori region called the fusiform imagery node and assessed lesion connectivity using resting-state functional data from healthy subjects (n = 1000). A data-driven whole-brain connectivity analysis identified patterns that were both sensitive and specific for aphantasia.
Twelve cases of acquired aphantasia were found. While only five lesions directly intersected the fusiform imagery node, every lesion location was functionally connected to that node. Connectivity to the left fusiform imagery node showed 100% overlap for aphantasia and statistical specificity in whole-brain analysis (family-wise error p < .05). These results provide causal support for the importance of the left fusiform imagery node in visual mental imagery.