Science has almost adopted the idea that pain ought to be all in the brain. There is sophisticated research showing that some brain areas light up more when we are in pain. When we recover, these areas stop lighting up. There are even therapies directed at “retraining” the brain, which can sometimes reduce, or even occasionally cure chronic pain.
So scientists have developed the following concept: after injury or operation our tissues will heal, and normally all goes well - unless we are “vulnerable”. There is some evidence suggesting that when we are poor, smoke, are depressed, stressed, or have had chronic pain in the past, we may be more likely to develop chronic pain.
The idea is that the vulnerable brain retains memory of the trauma with its associated pain: it develops “abnormal neuroplasticity”. A good example is phantom limb pain. Following amputation many people develop pain the non-existing limb; they are more likely to do so if they had experienced a lot of pain before the amputation, so clearly the brain must be involved. Science 2.0
It makes a lot of sense. A lot of new treatments take this theory into account as well. Retrain the brain.
As with other chronic pains, many of us experts have been assuming the main problem for these patients is in the brain. But it recently emerged that the blood of patients with this condition (Complex Regional Pain Syndrome) carries specific immune substances, termed “autoantibodies”. These substances can probably cause pain by binding to peripheral tissues, prompting sensory nerves to misfire – although the exact pathway is not understood. Misfiring of sensory nerves results in a state where the central nervous system, including the brain, has become “wound up”.This is pretty fascinating for trauma related research into chronic pain. Understanding the nature of pain and chronic pain goes a long way into developing treatments. Chronic pain is after all a lot more complicated than people tend to thing in the body.
In CRPS, peripheral nerves may thus play a role comparable to electronic transistors: with very low abnormal peripheral input generated by the autoantibodies, the nerves steer a massive central abnormality. Without trauma these newly discovered antibodies are probable harmless; the trauma-induced inflammation is required to render them harmful.
In fact, these antibodies may only be present for a limited time, during a “window of vulnerability”, in sufficiently high concentration to cause harm after trauma; the same trauma sustained either earlier or later may not trigger CRPS. The good news is that there are treatment methods, originally established for the treatment of other diseases designed to reduce or remove auto-antibodies, which can now been tried. Science 2.0