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Chronic pain is one of the world’s most costly medical problems and one out of every five people, and one of the most mysterious. However, over the past two decades, discoveries about the important role played by glia, a set of nervous system cells once thought to be only support for neurons, have rewritten the science of chronic pain.

These findings provided patients and physicians with a scientific explanation for the lack of chronic pain before. By doing this, this emerging science of chronic pain is starting to impact care—not by creating new things. treatments, but by legitimizing chronic pain, doctors are taking it more seriously.

Although glia are distributed throughout the nervous system and occupy almost half of its area, it has received much less scientific attention than the neurons that do most of the signaling in the brain and body. Some types of glia resemble neurons with roughly starfish-like bodies, while others look like structures built with Erector clusters whose long, straight structural pieces are joined at nodes.

When it was first discovered in the mid-1800s, glia, from the Greek word for glue, was thought to be the connective tissue that held neurons together.. They were later renamed as the name of the nervous system. cleaning staffIt was found that they feed neurons, clean their waste and remove their dead. emulated in the 1990s secretarial staff When discovered, they also help neurons communicate. However, research over the past 20 years has shown that glia not only support and respond to neuronal activity such as pain signals, but often drive them with tremendous consequences for chronic pain.

If you’re hearing this for the first time and you’re one of the billions of people in the world who suffer from chronic pain (i.e. pain that lasts for more than three to six months with no apparent cause or becomes independent of injury or the disease that causes it), you might want to say that your glia is failing the job of pain management.

And you would be right. In chronic pain, researchers now believe that glia disorganize a healthy pain network and send false and destructive pain signals that never cease. Pain then becomes a source of harm, not a warning; It’s not a symptom, it’s “his own disease,” as Stanford pain researcher Elliot Krause puts it.

How the pain system works and goes awry.

The pain system usually works in three different stages.

First, when an injury or ailment causes damage—say, you touched a hot pan—long nerve fibers in your finger sense the damage and send a pain message to your brain. In the second stage, these signals enter your spinal cord and hop to other neurons in the spinal cord in a tracked and sometimes fine-tuned transmission by nearby glia. Finally, in the third stage of this alarm system, these spinal cord neurons carry signals to a point in your cerebral cortex about your fingertip, creating a burning sensation. you curse.

The first part of this alarm system – it carries the pain signal to the central nervous system – operates largely on a highly efficient autopilot. Its main players are long pain-sensitive neurons that extend from the finger to the spinal cord, which quickly trigger a reflex that causes you to withdraw your hand.

In the second stage, things get messy when these signals reach the brain and spinal cord. Here, in the transition from the peripheral nervous system to the central nervous system, an abundance of glia greatly modulates pain signals, for example by increasing or decreasing their intensity or duration. And here things can go wrong and trigger chronic pain. as a flood recent research has shownChronic pain develops because glia accelerate the pain system into an endless inflammatory cycle that stimulates the nerves to produce a constant pain alarm.

Exactly how or why this glial mismanagement develops is still unclear. It can occur after an injury or seemingly out of nowhere. Pain from one or more injuries, such as in a car accident, normally lasts for days or weeks and then goes away. Sometimes, however, the glia’s regulatory system resumes pain signals after the tissue has healed. These can spread to other areas, causing more pain.

Glia can create a mess that is difficult to resolve.

In theory, identifying glia as the culprits of chronic pain should make it easier to find a solution. Unfortunately not, at least not yet. You can’t just knock out glia – they’re very important – and current pain relievers aren’t helping because they target neurons, not glia.

And glia are ridiculously versatile. They transmit information through dozens of communication channels. “Almost every way neurons communicate,” said Doug Fields, a glia researcher at the National Institutes of Health, “also uses glia.” In a kinder world, these pathways will offer targets for drugs or other treatments. But in the dauntingly complex systems in which glia operate, these goals have so far proven futile. No treatment has yet moved from counter to bedside.

That shouldn’t surprise us, said Dr. Fields: “Neuroscientists have been studying neurons for over a century, but trying to capture glia.”

David Clark, a Stanford pain researcher and clinician at the Palo Alto Veteran’s Affairs hospital, suspected that part of the problem lay in the built-in redundancy of the pain system. Glia have so many ways to transmit pain signals that even if one treatment blocks one, they quickly find another. Dr. Clark believes that circumventing this vast system of glial regulation may require new strategies.

“This isn’t going to present a target you can hit with just a drug or genetic switch. It may require something entirely new, like figuring out how to shut down a whole. family finding genes at some key points,” said Dr. Clark.

Your pain has a source.

Understanding over the past 20 years that glia underlie chronic pain offers two important sources of comfort.

First, scientists now at least have an idea of ​​where to look for a solution – glia. They have yet to find easily detectable biomarkers that could indicate that glia (or other elements) are causing chronic pain in a living human. But the underlying science is solid and growing.

For the sufferers, this is a welcome confirmation of their authenticity. “Learning this,” said Cindy Steinberg, director of national policy and advocacy for the US Pain Foundation and herself a chronic pain patient, “is extremely helpful for those of us who suffer from chronic pain.” She said she found great validation in a chronic pain support group led by Ms. Steinberg to learn that there is a different biology underlying people’s pain. This confirms something they’ve known for a long time but was skeptical of by doctors and friends: that their pain is as real as anyone else’s.