Chronic low back pain recruits the brain’s self network during movement-evoked flares
For people living with chronic low back pain, a routine bend, step, or leg lift can trigger more than a temporary jolt of discomfort. A new brain imaging study from UC San Diego shows that movement-evoked pain does something unusual: it activates the brain’s Default Mode Network, a circuit tied to self-awareness, inward reflection, and personal memory.
Ordinary acute pain usually has the opposite effect. The brain dampens this self-focused network when a threat demands attention. In chronic back pain, the system appears to flip. Pain does not just arrive as a bodily warning signal; it becomes entangled with identity, anticipation, and memory.
Brain imaging points to a different pain biology than acute injury pain
The study enrolled 114 patients with chronic low back pain and used a standard clinical leg raise test to provoke pain flares. Brain blood flow was measured with arterial spin labeling functional MRI, a technique that tracks activity without injected contrast. Participants also received a separate heat stimulus to the calf, providing a comparison with a more ordinary painful event.
The contrast between those two pain states was sharp. When movement triggered a chronic pain flare, the Default Mode Network became more active. When the heat stimulus produced acute pain, the same network became less active, matching the typical cerebral response to external threat. The finding matters because it shows chronic pain is not simply a louder version of acute pain. It is organized differently inside the brain.
Heart rate rose during the leg raise test in a way that tracked pain intensity, giving the flare a measurable autonomic signature. Stronger pain was also associated with greater activity in brain regions involved in sensation and movement. Patients with more severe chronic back pain showed stronger coupling between the Default Mode Network and the primary somatosensory cortex, the region that helps process physical input from the body, including signals from the back.
The Default Mode Network may be binding pain to identity
The Default Mode Network is often described as the brain’s “self network” because it becomes active when attention turns inward. It supports reflection on identity, memory, personal meaning, and emotional experience. In acute pain, the network tends to quiet down so attention can shift to the immediate threat. In this study, movement-evoked chronic pain did the reverse.
That inversion offers a plausible explanation for why persistent back pain can feel so invasive. The pain is not experienced only at the site of tissue strain. It can be folded into a person’s internal narrative, where previous flare-ups, fear of movement, embarrassment about lost function, and expectations of future pain all start to reinforce one another. Chronic pain becomes self-referential, and the brain may begin to treat the experience as part of who the person is rather than as a passing signal.
Fadel Zeidan, the corresponding investigator, described that shift bluntly: during a pain flare, the Default Mode Network turns on instead of off, and the patient starts to identify the experience with who they are.
Why conventional pain control often leaves patients dissatisfied
This brain pattern helps explain a familiar clinical problem. Treatments that mainly suppress pain signaling may reduce symptoms without touching the neural machinery that keeps chronic pain alive. Opioids and other analgesics target sensation, but they do not necessarily dismantle the links between pain, memory, fear, and self-perception.
Chronic pain is sustained by more than nociception. When each flare is followed by worry about the next one, a patient can enter a loop in which anticipation amplifies distress before movement even begins. Past episodes of lost work, missed family activities, or fear of being seen as unreliable can deepen the loop. In that setting, the brain is not only processing pain; it is also rehearsing it.
Mindfulness and psilocybin are being studied for a different target
The study points toward a different therapeutic strategy: rather than focusing only on eliminating pain signals, treatment may need to alter the brain’s relationship with those signals. Zeidan’s group has been studying mindfulness meditation and psilocybin as potential ways to do that.
Mindfulness aims to reduce the automatic judgment and emotional escalation that can attach to pain. By observing sensations without immediate reaction, patients may weaken the loop between pain and self-identity. Psilocybin is being studied for a different reason: it may alter the brain processes that connect pain to trauma, future worry, and prior experience. In both cases, the therapeutic goal is not necessarily total pain elimination. It is to prevent pain from colonizing the patient’s daily life.
Those approaches remain investigational, and the study does not establish clinical benefit for either treatment. Still, the neurobiology offers a rationale for why they are drawing attention in chronic pain research. If persistent pain lives partly in the brain’s self-referential circuitry, then therapies that modify self-processing may have a chance to help where conventional analgesics fall short.
The study is observational, but the signal is biologically coherent
This was an observational brain imaging study, not an interventional trial. It cannot prove that Default Mode Network activation causes chronic pain or that changing that network will relieve it. The design also does not tell clinicians which patients will respond best to a self-focused therapy or whether the same pattern holds across other chronic pain syndromes.
Even so, the findings are coherent with what pain medicine sees at the bedside. Movement-evoked pain often carries a heavy anticipatory burden, and fear of re-injury can shape function long before tissue stress occurs. A brain circuit built for self-reflection may be one reason that burden becomes so persistent.
The work was published in the British Journal of Anaesthesia on October 5, 2026. Additional study authors included Morgan Gianola, Jon Dean, Conan Chen, Daniel Barrows, Gabriel Reigner, and Thomas Liu. Funding came in part from the National Institutes of Health’s National Center for Complementary and Integrative Health and the UC San Diego Sanford Institute for Empathy and Compassion. No conflicts of interest were reported.