Pain and Inflammation May Be Linked

In the last 10 years, experts have identified one factor that might predict who will end up with chronic pain. It's a concept called catastrophizing. A catastrophizer is a person who feels helpless and tends to think the worst when in pain. They seem unable to cope, and they focus on their symptoms in detail. This may be the first study to show a link between pain and inflammation, which may explain what's happening at a physiologic level to explain the catastrophizing-pain response.

Participants in the study were all healthy adults. A nurse pre-evaluated everyone to make sure there were no hidden health concerns. Everyone filled out a medical history form, Beck Depression Inventory (BDI), and Pain Catastrophizing Scale (PCS).

Previous studies have shown that by using these tools, it is possible to predict who will be a high pain catastrophizer. And these folks are at risk for persistent or chronic pain associated with low back pain or prolonged pain after surgery. What makes these people more likely to experience this type of response? That's the focus of this study.

Other researchers have suggested a variety of ways catastrophizing might enhance or turn up the pain barometer. There may be social or emotional factors. There might be a specific neural (nerve) pathway that gets turned on. Or, as the results of this study showed, there could be an inflammatory process at the heart of the problem.

In this study, participants were subjected to pain testing. Pain was created using several different techniques. Three sites were chosen and tested on both sides of the body: 1) the belly of the trapezius (neck) muscle, 2) the thumb joint, and 3) the quadriceps muscle where it inserts (connects) to the knee).

First, the end of a probe was placed next to each of these three areas. Mechanical pressure was applied until the person felt pain. Second, a heat probe was applied to the same areas. Two temperatures were applied, and the subject rated how painful the stimulus felt from zero (no pain) to 100 (most intense pain possible). And last, the right hand was dunked in a bath of cold water a number of times until the hand was finally left in the tank until pain was perceived by the person being tested.

Blood samples drawn before and after the testing were analyzed for levels of cortisol and interleukin-6 (IL-6). Cortisol (also known as cortisone) is a stress hormone. It is released in the body in response to stress. It increases blood pressure and blood sugar, and reduces immune responses. IL-6 is a chemical messenger that signals the immune system to launch a response. The end result is tissue inflammation causing joint and muscle pain.

Results showed that both cortisol and IL-6 were elevated for the first 30 minutes after the pain-inducing procedures. Cortisol levels were back down to normal at the end of one hour. IL-6 remained elevated.

People who catastrophized had higher levels of IL-6. The results suggest that mental and emotional responses during pain experiences can lead to inflammatory immune responses. And using scores from the Pain Catastrophizing Scale might be a way to predict IL-6 reactivity.

The authors conclude that in some people, pain appears to cause a release of extra proinflammatory messengers that turn up the nervous system's sensitivity. The result is an amplified (louder) broadcast of pain messages to the brain. So, we know there may be an inflammatory response as the main mechanism by which catastrophizing shapes pain responses. But we still don't know the exact way in which catastrophizing turns on the cascade of steps leading to inflammation.

Clearly, there is a link between psychologic processes and central pain processing. Screening patients for catastrophizing might help identify patients at risk for this immune-based pain response. The next step is finding a way to turn it down or off to prevent a chronic pain response from developing.

Robert R. Edwards, et al. Association of Catastrophizing with Interleukin-6 Responses to Acute Pain. In PAIN. November 15, 2008. Vol. 140. No. 1. Pp. 135-144.

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