Most painkillers (or analgesics, from the Greek term for the absence of pain) work on the central nervous systemthe brain and the spinal cordand the peripheral nervous system, which connects the rest of the body to them, sending signals back and forth.
Painkillers are generally broken down into three categories: opioid (narcotic) analgesics, non-narcotic analgesics (which include NSAIDs), and adjuvant therapies such as anticonvulsants, muscle relaxants, and antidepressants. We'll deal with NSAIDs here.
How NSAIDs work
The granddaddy of NSAIDs is aspirin (acetylsalicylic acid), made from a compound found in willow bark and introduced into modern medicine in 1899. Ibuprofen, a non-aspirin analgesic, was introduced in 1974 and is best known as Advil or Motrin. Naproxen was first marketed in 1976, and is best known as Aleve.
Prostaglandins are created at the sites of injury or inflammation and cause the pain receptors in the surrounding area to become more sensitive. By decreasing prostaglandin production, NSAIDs lessen the sensation of pain and reduce inflammation.
The problem is that the COX-1 enzyme has an important job to do: It helps produce the prostaglandins that protect the stomach lining from the corrosive effects of stomach acid. When COX-1 is blocked, stomach upset, bleeding, and ulcers can occur. These are well-known side effects of all NSAIDs.
Reye's syndrome, a potentially life-threatening illness.)