New research published in JAMA Network Open has identified a common brain circuit linked to creativity across multiple domains, such as music, writing, drawing, and idea generation. The findings indicate that damage to this circuit—caused by brain injuries or neurodegenerative diseases—may sometimes enhance creative abilities. This counterintuitive result adds to growing evidence that creativity is not only supported by specific brain networks but might also be released when certain regions are disrupted.
“We wanted to answer the questions, ‘What brain regions are key for human creativity and how does this relate to the effects of brain injuries?’” said study author Isaiah Kletenik, an assistant professor at Harvard Medical School, researcher at the Center for Brain Circuit Therapeutics, and associate neurologist at Brigham and Women’s Hospital.
“As a cognitive neurologist, I take care of patients who have brain injuries or dementia which you would assume should only cause dysfunction but there are these rare situations in which people have a progressive brain disease and have new onset creativity. The first author, Julian Kutsche has a background in both neuroscience and in the study of music so this topic was a perfect combination of his research interests.”
To address this question, Kletenik and his colleagues at the Center for Brain Circuit Therapeutics at Brigham and Women’s Hospital examined data from 857 participants who had taken part in 36 brain imaging studies of creativity. Each of these studies used functional MRI to identify brain regions activated during creative tasks compared to control tasks. The researchers then applied a technique known as coordinate network mapping to analyze the functional connectivity of those brain areas using resting-state data from 1,000 healthy adults.
Although the specific brain regions activated during creativity tasks varied widely across studies, the researchers found that a large majority—86%—shared a connection to a common brain circuit. This circuit was characterized by negative functional connectivity with a particular region in the brain known as the right frontal pole. That is, when creative brain regions were active, the right frontal pole tended to be less active, suggesting a possible suppressive or regulatory role in creative thinking.
This finding was consistent across different types of creative tasks, different statistical thresholds, and different levels of data analysis, making it a robust result. To ensure their findings were not due to random chance or general brain activity, the researchers also compared their data with brain networks involved in unrelated tasks like working memory. The creativity circuit stood out as distinct.
“Many complex human behaviors such as creativity don’t map to a specific brain region but do map to specific brain circuits,” Kletenik told PsyPost. “Some people with neurologic diseases experience a new onset of creative behavior and show specific patterns of damage that align with a brain circuit associated with creativity.”
“We found that many complex human behaviors such as creativity don’t map to a specific brain region but do map to specific brain circuits,” added co-senior author Michael D. Fox, who founded and leads the Center for Brain Circuit Therapeutics, and helped develop the techniques of coordinate and lesion network mapping employed in this work.
To validate their results, the team looked at three independent lines of evidence: brain activation patterns in an additional 30 fMRI studies, data from patients with focal brain lesions, and data from patients with neurodegenerative diseases. In each case, the results supported the existence of a common creativity circuit.
One of the more intriguing validations came from examining patients with brain lesions in different parts of the frontal lobe. Patients with lesions in areas negatively connected to the right frontal pole—such as the lateral frontal lobe—tended to show reduced creativity. But those with lesions in the right frontal pole itself sometimes showed enhanced creative output, suggesting that damage to this area may reduce self-monitoring or internal censorship, allowing freer expression of creative ideas.
Similarly, the researchers found that certain neurodegenerative diseases—such as semantic variant primary progressive aphasia (svPPA) and the behavioral variant of frontotemporal dementia (bvFTD)—are associated with increased creativity. The brain atrophy patterns in these diseases aligned strongly with the identified creativity circuit, especially in regions negatively linked to the right frontal pole. In other conditions, such as Parkinson’s disease or nonfluent aphasia, where increased creativity is less commonly observed, the alignment was weaker.
The team also analyzed data from patients with frontotemporal dementia who had experienced a surprising boost in artistic abilities. These individuals showed brain atrophy in areas that overlapped with the newly defined creativity circuit, adding further evidence that disruption of this network may allow creativity to emerge in unexpected ways.
Taken together, these results suggest that the right frontal pole may act as a kind of gatekeeper, suppressing spontaneous or unconventional thinking in favor of rule-based decision-making. When that control is reduced—whether by task-induced deactivation, injury, or degeneration—creative behavior may become more prominent. This idea is consistent with previous studies that found lower activity in parts of the frontal cortex during improvisation and other free-form tasks.
“The most surprising finding was that all the different forms of creative tasks shared a specific regional reduced activity on brain imaging,” Kletenik explained. “In functional neuroimaging we often focus on areas where there’s increased activation, but in this study the key finding was that all the creative tasks seem to share reduced activation in the right frontal pole. This part of your brain is important for monitoring and rule-based behaviors. Creativity may depend on inhibiting self-censoring assessments that could then allow free association and idea generation to flow more freely.”
While the findings are compelling, the researchers stress that creativity is complex and likely involves many different brain systems. Their work focused on identifying a shared neural pathway across studies, not on capturing every possible variation. Moreover, the observed relationships are correlational; while lesion data suggest a causal role for the right frontal pole, more direct interventions—such as brain stimulation studies—are needed to confirm this.
“These findings rely on retrospective analyses and do not represent the entire neural circuitry involved in creativity – there are many different parts of the brain necessary for completing different creative tasks,” Kletenik noted.
Still, the findings open the door to new ways of thinking about the brain and its relationship to creativity. They may also help explain why some people report an increase in artistic or musical output after brain injuries or during early stages of neurological disease. This phenomenon, known as paradoxical functional facilitation, suggests that impairments in one area of the brain can sometimes lead to gains in another.
“These findings could help explain how some neurodegenerative diseases might lead to paradoxical increase in creativity,” Kletenik explained. “We are learning more about neurodiversity and how brain changes that are considered pathological may improve function in some ways
The study, “Mapping Neuroimaging Findings of Creativity and Brain Disease Onto a Common Brain Circuit,” was authored by Julian Kutsche, Joseph J. Taylor, Michael G. Erkkinen, Haya Akkad, Sanaz Khosravani, William Drew, Anna Abraham, Derek V. M. Ott, Juliana Wall, Alexander Li Cohen, Andreas Horn, Wolf-Julian Neumann, Isaiah Kletenik, and Michael D. Fox.
