For individuals with chronic back pain, routine movements such as bending to tie a shoe or lifting a grocery bag can provoke sharp flare-ups. Researchers have now discovered that these episodes may engage a brain network typically associated with self-reflection and identity.
Published October 5 in the British Journal of Anaesthesia, the study found that movement-induced chronic back pain correlates with heightened activity in the brain’s default mode network (DMN)—a collection of interconnected regions that activate during introspection, autobiographical memory retrieval, and mind-wandering. This result is striking because the DMN typically suppresses during acute pain, such as the brief sting of a burn or a bumped knee.
The findings suggest that chronic-pain flare-ups recruit neural processes extending beyond those responsible for nociceptive sensation alone.
How the Brain Responds to Chronic Pain
Chronic lower back pain, defined as persisting for at least three months, ranks among the leading causes of disability globally. Current theory holds that when chronic pain first emerges, a brain network known as the “pain neuromatrix” becomes sensitized, allowing pain to endure after the original stimulus has resolved. While scientists recognize that chronic pain alters brain activity, the neural dynamics triggered when movement suddenly intensifies that baseline pain remain poorly understood.
To investigate, researchers recruited 114 adults with chronic lower back pain and employed functional magnetic resonance imaging (fMRI) to monitor brain activity. fMRI tracks blood-flow changes as a proxy for neural activation.
Following a baseline scan, an examiner passively lifted each participant’s leg until their back pain increased, maintained the position for ten seconds, then lowered the leg. The team scanned participants’ brains immediately afterward and compared the results to the pre-movement scans. On average, the maneuver amplified self-reported pain intensity by 23 percent.
As anticipated, the leg movement drove increased blood flow in regions implicated in pain and motor processing. Unexpectedly, however, key nodes of the default mode network also showed elevated activity—regions that ordinarily engage when a person reflects on themselves or lets their mind wander.
Acute pain typically dampens DMN activity, presumably because it forces attention onto an external threat distinct from the self.
“When we saw just the first round of analysis, we’re like, ‘Did we do it right?'” study co-author Morgan Gianola, a postdoctoral scholar at the University of California, San Diego, told Live Science.
“We did not expect [the default mode network] to be involved at all,” said co-author Fadel Zeidan, a neuroscientist at UC San Diego. “We expected it to be deactivated to the point that we had to triple-check our work to make sure that the results were legit.”
For comparison, the researchers applied painful heat to participants’ calves—a standard method for studying acute pain. Unlike movement-evoked back pain, the heat stimulus reduced activity in part of the DMN, indicating a divergent neural mechanism.
When Pain Becomes Part of Our Internal Experience
Participants reporting more severe chronic back pain exhibited stronger functional connectivity between the DMN and brain regions processing sensory input from the back. This pattern suggests that chronic pain may become woven into how individuals perceive themselves and their bodies, the authors concluded.
“This pain flare has almost become a part of who they are from an egocentric perspective,” Zeidan said.
Katherine Martucci, a neuroscientist at Duke University not involved in the study, commended the experimental design. Researchers typically avoid movement during fMRI because motion degrades image quality; this study circumvented that limitation by scanning before and after the provoked movement, Martucci noted in an email to Live Science.
She cautioned, however, that the observed activity could reflect residual pain or anxiety following the leg raise. Additionally, the cross-sectional design cannot determine whether the altered brain activity contributes to chronic pain or emerges as a consequence of it.
Nevertheless, Zeidan and colleagues believe the findings could eventually inform novel treatments. Therapies might target how patients relate to their pain rather than focusing exclusively on the sensory experience. Zeidan, who coincidentally developed chronic back pain during the study, posits that repeated pain experiences and associated memories may rewire brain processes until the pain itself becomes integral to self-identity.
Zeidan’s team is now investigating whether established interventions such as mindfulness meditation or cognitive behavioral therapy for chronic pain (CBT-CP) can modulate the DMN and alleviate symptoms.
Martucci emphasized that clinical applications remain premature. Yet she underscored that the data provide robust evidence of how the brain responds to chronic-pain flare-ups.
“They do provide solid data on how people with chronic low back pain show important changes in their brain responses after a condition provoking their pain,” she said. “The brain imaging data validate their [the participants’] experience of pain in an important and very visible way.”
This article is for informational purposes only and is not meant to offer medical advice.
Gianola, M., Dean, J., Chen, C., Barrows, D., Riegner, G., Liu, T., & Zeidan, F. (2026). Brain mechanisms supporting movement-evoked chronic low back pain: An observational brain imaging study. British Journal of Anaesthesia.

