Without the ability to feel pain, life is more dangerous. To avoid injury, pain tells us to use the hammer more gently, wait for the soup to cool, or wear gloves in a snowball fight. People with rare inherited disorders that leave them without the ability to feel pain are unable to protect themselves from environmental hazards, leading to broken bones, damaged skin, infections, and eventually a shortened life span.
In these contexts, pain is much more than a sensation: it is a protective call to action. But pain that is very intense or long-lasting can be debilitating. So how does modern medicine soften the call?
As a neurobiologist and an anesthesiologist who studies pain, this is a question we and other researchers have attempted to answer. Over the past several years the understanding of science about how the body senses tissue damage and perceives it as pain has increased significantly. It has become clear that there are several pathways that signal tissue damage to the brain and trigger pain bells.
Interestingly, while the brain uses different pain signaling pathways depending on the type of damage, there is also redundancy in these pathways. Even more intriguing, these nerve pathways shape and amplify signals in the case of chronic pain and pain, which are caused by conditions affecting the nerves themselves, even though the protective function of pain is no longer needed.
Pain relievers work by tackling different parts of these pathways. However, not every pain reliever works for every type of pain. Because of the multitude and redundancy of pain pathways, an ideal pain reliever remains elusive. But in the meantime, understanding how existing pain relievers work helps medical providers and patients use them for the best results.
anti inflammatory pain reliever
Injuries, sprains, or broken bones due to injury all cause tissue inflammation, an immune response that can cause swelling and redness as the body tries to heal. Specialized nerve cells in the area of injury called nociceptors sense inflammatory chemicals produced by the body and send pain signals to the brain.
Common over-the-counter anti-inflammatory pain relievers work by reducing swelling in the injured area. These are especially useful for musculoskeletal injuries or other pain problems caused by inflammation such as arthritis.
Nonsteroidal anti-inflammatory drugs such as ibuprofen (Advil, Motrin), naproxen (Aleve) and aspirin do this by blocking an enzyme called COX that plays a key role in a biochemical cascade that produces inflammatory chemicals. Blocking the cascade reduces the amount of inflammatory chemicals, and thereby reduces pain signals sent to the brain. While acetaminophen (Tylenol), also known as paracetamol, does not reduce inflammation like NSAIDs, it also inhibits COX enzymes and has similar pain-reducing effects.
Prescription anti-inflammatory pain relievers include other COX inhibitors, corticosteroids, and more recently, drugs that target and inactivate the inflammatory chemicals themselves.
Because inflammatory chemicals are involved in other important bodily functions beyond sounding the pain alarm, drugs that block them will have side effects and potential health risks, including irritating the stomach lining and affecting kidney function. Over-the-counter medicines are generally safe if the directions on the bottle are followed strictly.
Corticosteroids such as prednisone inhibit the inflammatory cascade at the beginning of the process, which is probably why they are so powerful at reducing inflammation. However, because all chemicals in the cascade are present in nearly every organ system, long-term use of steroids can pose a number of health risks, which need to be discussed with a physician before starting a treatment plan.
Many topical medications target nociceptors, specialized nerves that detect tissue damage. Local anesthetics, such as lidocaine, block these nerves from sending electrical signals to the brain.
Protein sensors at the tips of other sensory neurons in the skin are also targets for topical pain relievers. Activating these proteins can elicit specific sensations that may reduce pain by reducing the activity of damage-sensing nerves, such as the cooling sensation of menthol or the burning sensation of capsaicin.
Since these topical medications act on the small nerves of the skin, they are used for pain affecting the skin directly. For example, a herpes infection can damage nerves in the skin, causing them to become overactive and send persistent pain signals to the brain. Calming those nerves with excessive doses of topical lidocaine or capsaicin can reduce these pain signals.