Current treatments for chronic pain might have the opposite effect

Thousands of people suffering from chronic pain might have been treated with drugs that do not prevent, but actually facilitate the transition of acute to chronic pain. A team of researchers from the Alan Edwards Center for Research on Pain show that this finding appears to be a consequence of the lack in understanding chronic pain pathways.

It is one of the most fundamental, yet least understood questions in pain research: why does acute pain become chronic pain in some patients? Currently, the most prevailing idea is that inflammation is one of the causes of chronic pain. More concretely, after having an injury that caused acute pain, an inflammatory reaction can emerge and hold on even if the original injury has resolved, ultimately resulting in chronic pain.

Based on this hypothesis, chronic pain patients are often treated with anti-inflammatory drugs. Unfortunately, in many patients the drugs don’t work as expected and cause many side effects, such as nausea and dizziness. This makes the currently available drugs inadequate. Moreover, it raises the question whether we really understand chronic pain development.

To further unravel this question, the researchers from the Alan Edwards Centre studied a group of people suffering from back pain. The team divided this group into patients that only experienced acute pain and patients in which the acute pain persisted into chronic pain. Then, they compared the inflammatory responses of the two groups. What they found was very interesting: neutrophils, which are immune cells that promote inflammation, are actually important to prevent the switch from acute to chronic pain. Giving patients the currently prescribed anti-inflammatory drugs would therefore potentially inhibit these neutrophils, leading to chronic pain.

Giving patients the currently prescribed anti-inflammatory drugs would therefore potentially inhibit these neutrophils, leading to chronic pain.

Although these new insights are very important to better understand chronic pain development, the study had some limitations. For example, the research was only performed in a small group of patients. In addition, the researchers only corrected their findings for a limited number of factors that could have influenced the results, such as physiological distress or the use of antidepressants. For now, more research should be performed to figure out whether the medical prescriptions of chronic pain patients should be altered.

Overall, the study of the Alan Edwards Centre shows that the underlying mechanisms of chronic pain development are very complex. However, knowing more about the tight regulation of immune cells during chronic pain also opens a new window for optimizing pain treatment!