The Other Brain by Fields Ph.D. R. Douglas

Author:Fields Ph.D., R. Douglas
Language: eng
Format: epub
Publisher: Simon & Schuster
Published: 2009-12-28T16:00:00+00:00

WHEN PAIN BECOMES DISEASE: GLIA IN CHRONIC PAIN

Pain caused by injury is protective, but there is another type of pain that develops mysteriously and intensifies even after the injury has healed. This “neuropathic” pain transforms protective pain into an agonizing disease. Chronic pain develops because of changes in pain circuits in the central nervous system after injury and healing. Neuroscientists know that pain neurons in people suffering chronic pain become hyperexcitable after healing from injury. The slightest touch or change in temperature sets these neurons firing barrages of nerve impulses that signal intense pain to the brain. The neurons also fire abnormally in bursts of high intensity all on their own. Like a broken record, cycles of nerve impulses scream pain over and over again without any stimulus to trigger them.

What causes these pain neurons to spin out of control? After an injury to the body or an infection, cells involved in the body’s defense and healing release powerful chemicals called inflammatory cytokines and chemokines. Drugs like ibuprofen and aspirin bring relief by blocking the action of these cytokines. Inflammatory cytokines act in many ways, and one of the consequences for pain fibers is heightened sensitivity. This is nature’s way of telling us to take it easy until we are healed. We are all familiar with this phenomenon when we feel the region surrounding the site of injury become tender and painful. Also, we have all experienced the painful reaction to light and sounds while suffering a severe headache. Our senses become heightened to the point of pain. If the inflammatory condition does not resolve, however, pain and hyper-sensitivity will persist even after the injury has healed.

People suffering chronic pain often describe their misery as raw nerves, but the latest research suggests that chronic pain goes beyond nerve cells. For many pain sufferers, the source of their chronic, unreachable pain is glia. Linda Watkins, a pain researcher from the University of Colorado at Boulder, began to suspect microglia as the source of chronic pain that develops after nerve injury. She recognized that glia have no involvement in transmitting normal pain, but chronic pain that develops after an injury heals might be another matter. Microglial cells are well known as the immune system cells of the brain and spinal cord. They are also known as a main source of cytokines and chemokines after nervous system injury or infection. Both of these substances can cause neurons to become hyperexcited. All of this evidence points to microglia as a prime suspect in causing chronic pain. Indeed several years earlier, in 1994, Stephen T. Meller and colleagues at the University of Iowa had shown the involvement of another type of glia in chronic pain by administering a poison to animals that selectively kills astrocytes. These animals suffered far less chronic pain after nerve injury.

To test this theory that microglia may cause chronic pain, all one must do is block the normal reaction of microglia to injury and then test the animals to see whether numbing the glial response to injury brings relief from chronic pain.

Download

Copyright Disclaimer:
This site does not store any files on its server. We only index and link to content provided by other sites. Please contact the content providers to delete copyright contents if any and email us, we'll remove relevant links or contents immediately.