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Analgesia

Mechanism Of Nonaddictive Analgesics



Pain that is caused by trauma (injury) in the body sets off the creation of a chemical called prostaglandin. The initial pain is caused by the nerve impulse that relays the injury message to the brain. According to the prostaglandin theory, the pain that is felt afterward is due to the prostaglandin at the site of the injury sending pain messages to the spinal cord, which then transmits these messages to the brain.



In 1971, a Nobel prize-winning pharmacologist, Sir John R. Vane, theorized that by blocking the formation of certain prostaglandins, aspirin was able to relieve the inflammation and pain that accompanies the trauma of damaged cells. Even though analgesics like aspirin had been used for centuries, Vane's discovery was the first real breakthrough in understanding how they work, and interest in prostaglandin research grew rapidly.

How over-the-counter medicines like aspirin, acetaminophen, and ibuprofen are able to temporarily relieve mild to moderate pain and even some severe pain is not completely understood. The blocking of prostaglandin production throughout the body, not just at the site of the pain, is the major theory that is currently accepted among medical scientists, although there are other theories to explain how these drugs work. Recent research suggests that aspirin has the ability to shut off communication of pain-transmitting nerves in the spinal cord.

The effectiveness of over-the-counter pain medicine depends on the kind of pain being experienced. Some pain originates in the skin and mucous areas of the body, while other pain comes from the smooth muscles and organs within the body. This latter type of pain is often difficult to pinpoint; it may feel like a generalized dull ache or throb, or may be referred pain, meaning pain that is felt in a part of the body away from its actual source.

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