The unnoticed science that may one day end chronic pain

The cause of chronic pain is unknown, but it is one of the most expensive medical problems in the world, affecting one in every five people. It is also one of the most puzzling. Glia, a group of nervous system cells previously thought to be merely supports for neurons, have been discovered to play a critical role in chronic pain, and discoveries about this have transformed the science of chronic pain over the last two decades.

Because of these findings, patients and physicians now have a rationale for chronic pain that they did not have before. Chronic pain research is beginning to have an impact on patient care – not through the development of new treatments, but rather by legitimizing chronic pain and encouraging physicians to treat it as a serious medical condition.

Despite the fact that glia are found throughout the nervous system and account for nearly half of its total volume, they have received far less scientific attention in the past than neurons, which are responsible for the vast majority of signaling in the brain and throughout the body. Certain types of glia, with their roughly starfish-like bodies, resemble neurons, whereas others resemble structures constructed using Erector sets, with their long, straight structural components connected at nodes, resemble structures constructed using Erector sets.

It wasn’t until the mid-1800s that glia, which comes from the Greek word for glue, were discovered that it was realized that they were more than just connective tissue that held neurons together. The nervous system’s janitorial staff was given this moniker after it was discovered that they provided nutrients to neurons, cleaned up their waste, and removed the bodies of the dead. After it was discovered that they also assist neurons in communicating with one another in the 1990s, they were compared to secretarial staff. Researchers have discovered that glia not only support and respond to neuronal activity such as pain signals, but that they also frequently direct it. This discovery has enormous implications for chronic pain, as demonstrated by research conducted over the last two decades.

This may sound strange if you’re one of the billion or so people on Earth who suffer from chronic pain (defined as pain that lasts longer than three to six months and has no apparent cause, or that develops independence from the injury or illness that caused it), and you’re one of the millions who believe their glia are failing miserably in their efforts to manage pain.

A cure for chronic pain should be easier to find if glia are identified as the source of the problem, according to theory. Unfortunately, this has not been the case, at least not yet.

And you’d be absolutely correct. For researchers now believe that in chronic pain, glia cause a normally functioning pain network to become dysregulated, resulting in a never-ending stream of false and destructive pain signals being transmitted. As a result, pain ceases to be a warning of impending harm and instead becomes a cause of it; it ceases to be a symptom and instead becomes, in the words of Stanford pain researcher Elliot Krane, “its own disease.”

How the pain system functions – and how it fails 

In general, the pain system operates in three stages that are distinct from one another.

Beginning with an injury or illness that causes damage – such as when you touch a hot pan – long nerve fibers in your finger detect the damage and transmit a pain signal to your brain. Second, those signals travel down your spinal column and across the spinal cord, where they are monitored and tweaked by glia in the surrounding area. This is the third stage. Once this alarm system is activated, those spinal cord neurons transmit the signals to a location in your cerebral cortex associated with your fingertip, where they cause the sensation of burning pain to be felt there. You make a sneering face.

Most of the time, the first component of this alarm system, which is responsible for transmitting the pain signal to the central nervous system, operates on autopilot. Among its primary actors are the long, pain-sensitive neurons that run from the finger to the spinal cord and quickly trigger a reflex that causes you to jerk back your hand.

Things become more complicated, however, when these signals reach the brain and spinal cord in stage two. Pain signals are significantly modulated at this point, as the peripheral nervous system transitions to the central nervous system, by a profusion of glia, which can be amplified, decreased in intensity, or stopped altogether. And it is at this point that things can go wrong, resulting in long-term pain. Recent research has demonstrated that chronic pain develops when the glia accelerate the pain system into an endless inflammatory loop, causing the nerves to generate a perpetual pain alarm. This is the mechanism by which chronic pain develops.

It is still unclear how or why this type of glial mismanagement takes place. It may manifest itself as a result of an injury or appear out of nowhere at times. It is common for pain from a single or multiple injuries, such as those sustained in a car accident, to last for several days or even weeks before it is completely relieved. The glia’s regulatory system, on the other hand, may occasionally continue to signal pain even after the tissue has healed completely. There is a possibility that they will spread to other areas, causing additional discomfort.

Glia can be a difficult tangle to untangle

A cure for chronic pain should be easier to find if glia are identified as the source of the problem, according to theory. Unfortunately, this has not occurred, at least not to our knowledge. Glia cannot be eliminated because they are far too important, and current painkillers are ineffective because they target neurons rather than glia, as is the case with morphine.

Furthermore, glia are incredibly adaptable. They communicate with one another through a network of dozens of different communication channels. Dr. Doug Fields of the National Institutes of Health in the United States says that glia use “almost every mode of communication used by neurons.” Dr. Doug Fields studies glia at the National Institutes of Health in the United States. In a more compassionate world, these pathways would be used as targets for drugs or other forms of treatment to be administered to patients. Those targets, on the other hand, have proven to be fruitless so far in the terrifyingly complex systems in which glia must operate. No treatment has yet been able to successfully make the transition from the bench to the patient’s bed.

Fields points out that this isn’t surprising: “Neuroscientists have been studying neurons for more than a century, but they are only now catching up with glia.”

David Clark, a Stanford pain researcher and clinician at the Palo Alto Veterans Affairs hospital, believes that the built-in redundancy of the pain system is a contributing factor to the problem. Glandular pain signals appear to be transmitted through so many different pathways that even if one is blocked by treatment, they will quickly find another. Clark believes that developing novel strategies for circumventing this massive system of glial regulation may be necessary in order to achieve success.

“An easy target for either a drug or a genetic switch is not going to be found in this situation. It may necessitate the development of something completely novel, such as figuring out how to turn off an entire family of genes at a critical point “Clark expresses himself.

There is a reason for your discomfort

Discovering that glia are at the root of chronic pain has provided significant relief over the last 20 years, providing two significant sources of comfort.

Scientists now have a better idea of where to look for a solution, thanks to this discovery – in the glia. Currently, no easily detectable biomarkers have been identified that can be used to demonstrate in a living person that glia (or other elements) are responsible for chronic pain. The underlying science, on the other hand, is solid and improving all the time.

For those who suffer from chronic pain, this is a welcome affirmation of their situation. “Knowing this,” says Cindy Steinberg, national director of policy and advocacy for the US Pain Foundation and herself a chronic pain patient, “is enormously beneficial to those of us who suffer from chronic pain.”

Steinberg says that learning that their chronic pain is caused by a different biology is extremely reassuring to the people who attend her chronic-pain support group. Because of this, it reaffirms what they’ve known for a long time, but which is frequently challenged by doctors and friends: that their pain is just as real as anyone else’s.

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