- 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.
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 condi-tion 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.”
This article was originally published with the title New Culprits in Chronic Pain.