Advances in pain relief

Pain, unfortunately, is a horrible necessity of life. It protects people by alerting them to things that might injure them. But some long-term pain has nothing to do with any obvious injury. One estimate suggests that one in six adults suffer from a “chronic pain” condition.

Steve McMahon, a pain researcher at King’s College, London, says that if skin is damaged — for instance with a hot iron — an area of sensitivity develops around the outside of the burn, where although untouched and undamaged by the iron, the behaviour of the nerve fibres is disrupted. As a result, heightened sensitivity and abnormal pain sensations occur in the surrounding skin. Chronic pain, he says, may similarly be caused not by damage to the body, but because weak pain signals become amplified.

This would also help explain why chronic pains such as lower-back pain and osteoarthritis fail to respond well to traditional pain therapies.

But now an entirely new kind of drug, called Tanezumab, has been developed. It is an antibody for a protein called nerve growth factor (NGF), which is vital for new nerve growth during development. NGF, it turns out, is also crucial in the regulation of the sensitisation of pain in chronic conditions.

Kenneth Verburg, one of the researchers involved in the development of Tanezumab at Pfizer, says it is not exactly clear what role NGF plays in normal physiology, but after an injury which involves tissue damage and inflammation, levels of NGF increase dramatically. The NGF seems to be involved in transmitting the pain signal. As a consequence, blocking NGF reduces chronic pain.

Tanezumab must still complete the final stages of clinical trials before it can become a weapon in the toolkit for reducing human suffering.

But unexpected pains do not always come from the body.

According to Irene Tracey, a pain researcher at the University of Oxford, how pain is experienced also depends upon a person’s state of mind. If successive patients suffer the same burn, the extent to which it hurts will depend on whether one is anxious, depressed, happy or distracted.

Such ideas are being explored with brain scans which suggest that even if a low level of pain is being sent to the brain, the signal can be turned up by the “mind” itself. Indeed, patients can even be tricked into feeling pain.

In one experiment volunteers were given a powerful analgesic and subjected to a painful stimulus — which, because of the analgesic, they could not feel. Then they were told the drug had worn off (although it had not), and subsequently complained that the stimulus hurt.

People can, therefore, feel pain simply because it is expected. They can fail to feel pain for exactly the same reasons, for example when they are given placebos or are distracted. But although pain may be subjective, that does not mean the final experience is controlled solely by the mind.

A recent paper in Proceedings of the National Academy of Sciences has shown that genes play a role in determining sensitivity to pain.

One gene, known as SCN9A, codes for a protein that allows the channels along which nerve signals are transmitted, to remain active for longer, and thus transmit more pain signals. It seems likely that this protein will attract a great deal more analgesic research. Variations in SCN9A may also explain why some patients prefer different classes of painkillers.

Although pain may be a horrible necessity, there is no doubt that humanity could cope with far less of the chronic sort. Understanding how the mind, the body and people’s genes interact to cause pain should bring more relief.