Since up to 20 percent of Americans suffer chronic pain, some of you might find of interest an article in the November 2009 Scientific American which describes recent breakthroughs in understanding Chronic Pain. You can buy this article online below or read it at the library. http://www.scientificamerican.com/article.cfm?id=new-culprits-in-chronic-pain
It is often difficult for me to guess at how easy it will be for you to read, but I found that the article written by the editor of a journal specializing in Glia by R. Douglas Fields to be very well written, in contrast to most scientific articles. It is packed with information. Available drugs for other uses could be prescribed by your doctor or the use of Medical marijuana works directly at the pain source to quell pain.
Some drugs marketed for other uses that work on the glia to reduce pain:
Sativex: It activates cannabinoid receptors. Human efficacy tests for cancer-related and HIV related neuropathic pain and diabetic neuropathy.
AV411: Human tests for efficacy in enhancing morphine action and reducing withdraws; safety tests for pain completed.
Etanercept: Anti=Inflammatory signals quiet glia. Human tests for postsurgical neuropathic pain reduction
Glia Activation: ... "An injury that damages nerve fibers produces a barrage of pain signaling in the dorsal horn of the spine, where peripheral sensory nerves meet spinal pain neurons. An intensely firing sensory neuron generates large amounts of neurotransmitters as well as other molecules that glia interpret as signs of distress, sending the helper cells into a reactive state. Glia normally mop up excess neurotransmitters, but reactive glia reduce their neurotransmitter uptake and begin producing molecules intended to stabilize and heal the neurons. These glial factors act to either reduce inhibitory forces on neurons or to simulate them, allowing the cells to fire more easily. Neural distress also causes the glia to release cytokines which induce inflammation, a healing response that also further sensitizes neurons. ..."
Most pain goes from the source to the spine where most medications to reduce pain work. Here is an excerpt from the article which explains this process.
Glia Oppose Opiates
... "A stunning discovery made in recent years is that glia play a role in causing opiate painkillers to lose effectiveness. Linda R. Watkins of the University of Colorado at Boulder has demonstrated that morphine, methadone and probably other opiates directly activate spinal cord glia, causing glial responses that counteract the drugs painkilling effects. The activated helper cells begin behaving much as they do after nerve injury, spewing inflammatory cytokines and other factors that act to overly sensitize neurons. Watkins showed that the effect starts less than five minutes after the first drug dose.
By making neurons hyperexcitable, glial influence overcomes the normal neuron-dampening effects of the drugs, explaining why patients often require ever increasing doses to achieve pain relief. The same mechanism may also underlie the frequent failure of opiates to relieve chronic neuropathic pain when it is driven by reactive glia. ... " R. Douglas Fields
New Culprits in Chronic Pain ( Preview )
Glia are nervous system caretakers whose nurturing can go too far. Taming them holds promise for alleviating pain that current medications cannot ease
Key Concepts
- Chronic pain that persists after an injury heals is often caused by overly excited pain-sensing neurons that signal without an external stimulus.
- Traditional pain drugs that target neural cells directly rarely quiet these abnormal pain messages because the neurons’ heightened sensitivity is driven by a different type of cell called glia.
- Such cells monitor the activity of neurons and attempt to keep them healthy and functioning efficiently. But well-intentioned glial reactions to intense pain can at times prolong that pain.
More from the Magazine
- November
2009 Issue - RecommendedRecommended: A Shadow Falls
- SkepticWill E.T. Look Like Us?
- Feature ArticlesGrowing Skyscrapers: The Rise of Vertical Farms
- Buy the Digital Edition
Helen’s left foot slipped off the clutch on impact, twisting her ankle against the car’s floorboard. It felt like a minor sprain at the time, she recalls, but the pain never subsided. Instead it intensified. Eventually, the slightest touch, even the gentle brush of bed linen, shot electric flames up her leg. “I was in so much pain I could not speak, yet inside I was screaming,” wrote the young Englishwoman in an online journal of the mysterious condition that would torment her for the next three years.
Helen’s left foot slipped off the clutch on impact, twisting her ankle against the car’s floorboard. It felt like a minor sprain at the time, she recalls, but the pain never subsided. Instead it intensified. Eventually, the slightest touch, even the gentle brush of bed linen, shot electric flames up her leg. “I was in so much pain I could not speak, yet inside I was screaming,” wrote the young Englishwoman in an online journal of the mysterious condition that would torment her for the next three years.
The chronic pain suffered by people like Helen is different from the warning slap of acute pain. Acute pain is the body’s most alarming, intense sensation, whose purpose is to stop us from further injuring ourselves. This type of pain is also called pathological pain because an external cause, such as tissue damage, produces the signals that travel the nervous system to the brain, where they are perceived as pain. But imagine if the gut-wrenching agony of a real injury never stopped, even after the wound healed, or if everyday sensations became excruciating: “I was unable to shower ... the water felt like daggers,” Helen remembers. “The vibrations in a car, someone walking across floorboards, people talking, a gentle breeze … would set off the uncontrollable pain. Common painkillers ... even morphine had no effect. It was like my mind was playing tricks on me.” http://www.scientificamerican.com/article.cfm?id=new-culprits-in-chronic-pain
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