Killing pain
Damage to our tissues causes mechanical and chemical changes that activate pain-sensing neurons. The neurons send signals to the spinal cord, which relays them to the brain. Painkillers try to block this process by interfering with it at different stages. The most common over-the-counter painkillers attack the very start of the pain-sensing chain. Non-steroidal anti-inflammatory drugs (NSAIDS) – like ibuprofen – try to remove some of the chemical signals that activate pain-sensing neurons. They do this by interfering with an enzyme called cyclooxygenase (COX). COX makes chemical messengers called prostaglandins, which promote inflammation. Blocking COX dampens the inflammatory response, relieving the pain. The next step in the pathway is the transmission of pain signals towards the spinal cord. Local anaesthetics work here. For nerve cells to fire they need to transport sodium ions across their membranes. These carry a charge, which sets up the electrical signal. Local anaesthetics block the channels that transport the ions, stopping pain signals in their tracks. The strongest painkillers, the opioids, work on the next part of the pathway: preventing signals getting to the brain. This group includes codeine, morphine and the illegal drug heroin. They act on the spinal cord and brainstem to stop pain messages passing through. Finally, there are the general anaesthetics, which work on the very last link in the chain. They stop the brain being aware of pain by interfering with the way that nerve cells pass signals to each other. Each kind of painkiller has advantages and disadvantages for different situations.