For people with chronic back pain, everyday movements like bending down to tie their shoes or picking up a grocery bag can trigger painful flare-ups. Now, scientists have made a surprising discovery: These episodes may activate a brain network that's associated with our sense of self.

In a new study, the researchers found that movement-induced chronic back pain was tied to increased activity in the brain's default mode network, a group of connected brain regions that lights up during self-reflection and mind wandering. This finding was unexpected because the network typically becomes less active during acute pain, such as transient pain triggered from touching a hot stove or banging your knee on a table.

The new study, published Oct. 5 in the British Journal of Anaesthesia, suggests that chronic-pain flare-ups may involve brain processes beyond those responsible for detecting painful sensations.

How the brain responds to chronic pain

Chronic lower back pain, defined as lasting at least three months, is a leading cause of disability worldwide. It's thought that when chronic pain first begins, a network of regions in the brain called the "pain neuromatrix" becomes sensitized so that the pain persists even after the painful stimulus is gone. Although scientists know that chronic pain is associated with changes in brain activity, they don't fully understand what happens when movements trigger sudden increases in that ongoing pain.

To investigate, researchers recruited 114 adults with chronic lower back pain and used functional magnetic resonance imaging (fMRI) to examine their brain activity. fMRI measures changes in blood flow, which acts as an indirect measure of brain activity.

After an initial scan, a researcher helped lift each participant's leg until their back pain increased, held it in position for 10 seconds, and then lowered it. The researchers scanned the participants' brains immediately after this pain-inducing leg movement and compared the results with scans collected beforehand. On average, the test increased the participants' reported pain intensity by 23%.

As expected, during the leg movement, the researchers observed increased blood flow in brain regions involved in processing pain and movement. But they also detected increased activity in key regions of the default mode network, which typically becomes more active when a person is thinking about themselves or their autobiographical memories or just letting their mind wander.

Acute pain lowers activity in the default mode network, studies show, presumably because it induces an awareness of something separate from yourself.

"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 study co-author Fadel Zeidan, a neuroscientist at UC San Diego, told Live Science. "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."

The researchers also exposed participants' calves to painful heat ‪—‬ a common method of studying brain activity during acute pain. Unlike the movement-induced back pain, the heat was associated with reduced activity in part of the default mode network, suggesting a different mechanism was at play.

When pain becomes part of our internal experience

Participants who reported more severe chronic back pain had stronger connectivity between the default mode network and brain regions that process sensations from the back. This suggests that chronic pain may become intertwined with how people perceive themselves and their bodies, the study 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 who wasn't involved in the study, praised the experimental design, noting that researchers typically avoid movement during brain scans because it can interfere with the clarity of the scan. This study "nicely gets around" that problem by taking scans before and after the painful motion, Martucci told Live Science in an email.

However, she noted that the observed brain activity could also reflect lingering pain or anxiety following the painful leg raise. In addition, the study couldn't determine whether the altered brain activity observed contributes to chronic pain or develops in response to it.

Nonetheless, Zeidan and colleagues think the findings could eventually inform future treatments for chronic pain. The therapies might address how people relate to their pain, rather than solely targeting the painful sensations themselves. Zeidan, who coincidentally developed chronic back pain while conducting the study, believes that people's past experiences and memories with chronic pain have influenced their brain processes to a point where the pain itself becomes part of who they are.

Zeidan's team is now investigating whether existing approaches, such as mindfulness meditation or cognitive behavioral therapy, can influence the default mode network and help relieve chronic pain. (Cognitive behavior therapy for chronic pain, or CBT-CP, is already a well-established treatment option.)

Martucci cautioned that it's too early to draw conclusions about how these results might be applied in clinical practice. But she said the current findings provide important 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.

Chemotherapy can save lives, but for many cancer patients, it leaves behind a painful legacy: damaged nerves that burn, tingle or go numb. Now, researchers report that a psychedelic compound may protect those nerves — not through its mind-bending effects, but by helping neurons keep their internal power supplies moving.

A new mouse study, published Thursday (Sept. 3) in the journal Science, suggests that psilocybin, the psychedelic compound in "magic mushrooms," may help prevent this painful and sometimes permanent side effect of chemotherapy, known as chemotherapy-induced peripheral neuropathy (CIPN).

In experiments in mice, psilocybin prevented nerve damage from CIPN that can cause pain, numbness and heightened sensitivity to cold and touch. Two doses of the drug given prior to chemotherapy garnered protection that persisted through as many as six rounds of the cancer treatment, according to the study.

CIPN affects roughly one-third to one-half of people receiving certain chemotherapies, said Dr. Thomas Strouse, a professor of clinical psychiatry and a neuropathy researcher at UCLA who was not involved in the study. In severe cases, the neuropathy can force doctors to reduce or stop chemotherapy. It can also contribute to mobility problems, which raise the risk of falls and fractures.

"It's a big deal, big problem," Strouse said. Researchers have been searching for a way to prevent it for a long time, he added.

Keeping nerve cells fueled

Initially, the researchers weren't looking for a neuropathy treatment, said study co-author Dr. Moran Amit, a cancer surgeon and researcher at The University of Texas MD Anderson Cancer Center. His team was investigating whether compounds that promote neuroplasticity — the nervous system's ability to change and adapt — might protect nerves and improve existing cancer treatments.

After testing several psychedelic compounds, they "very early on focused on psilocybin because this was the most effective one" for relieving neuropathy symptoms, Amit told Live Science. The psychedelic has been explored as a treatment for psychiatric disorders such as depression, in which it might promote "hyperconnectivity" between certain brain regions.

In the new study, protection against CIPN emerged as an unexpected effect of the drug.

To investigate how that protection worked, the researchers studied mice treated with cisplatin, a chemotherapy drug known to frequently cause neuropathy. Two doses of psilocybin — given nine days and two days before the first chemotherapy session, respectively — completely prevented the mice from developing hypersensitivity, and it also reduced cold sensitivity and preserved nerve endings in the skin.

The team then ran experiments using human sensory neurons and peripheral nerves that had been removed during surgery. These analyses pointed to a possible explanation: a process called mitochondrial trafficking.

Mitochondria generate the energy that cells need, but neurons present an unusual logistical challenge. Some peripheral nerves extend over enormous distances, so their mitochondria must be transported along structural tracks, called microtubules, to reach far-flung nerve endings. That in itself is an energy-intensive process.

Amit compared those microtubules to a railroad system: Chemotherapy can damage both the mitochondria themselves and the tracks they travel along.

In further experiments with human neurons, the team found that cisplatin depleted mitochondria and ATP (adenosine triphosphate) — cells' main energy currency — from the wires that extend from nerves. Psilocybin didn't restore the mitochondria's overall energy-producing capacity. Instead, it preserved their ability to travel and maintained their normal levels of ATP production, specifically within the nerve projections. That suggests the drug may help keep energy supplies where they're needed most.

The effect depended on the serotonin receptor 5-HT2A, which is responsible for many of psilocybin's psychedelic effects as well. Intriguingly, a compound called TBG — designed to activate 5-HT2A without causing hallucinations — also protected mice from neuropathy.

However, Amit cautioned that psilocybin's psychedelic effects may also be playing a neuroprotective role that we have yet to understand, so it's unclear if the effect should be avoided in humans.

A long way from patients

Strouse noted that mitochondrial damage in CIPN isn't a new idea. "What's novel is looking at psilocybin as a protectant," he said.

He also cautioned that different chemotherapy drugs may cause neuropathy through distinct mechanisms, so the protection demonstrated against one chemotherapy drug may not translate broadly.

Most importantly, the researchers have not shown that psilocybin prevents neuropathy in humans yet.

"The main thing is that it was never tested for this indication specifically in a systematic way in humans," Amit said. His team is now preparing a clinical trial at MD Anderson to test the approach. The research is part of MD Anderson's Cancer Neuroscience Program, a multidisciplinary effort that studies interactions between cancer and the nervous system, with an emphasis on improving patients' quality of life.

Human trials will need to establish both the effectiveness and safety of using psilocybin for this purpose, Strouse said, particularly before oncologists would consider giving a psychedelic drug alongside cancer treatment.

This article is for informational purposes only and is not meant to offer medical advice.