Without the ability to feel pain, life is more dangerous. To avoid injury, pain prompts us to use a hammer more carefully, wait for the soup to cool, or put on gloves during a snowball fight. this with rare hereditary diseases that rob them of their ability to feel pain are unable to protect themselves from the environment, leading to broken bones, skin damage, infection and ultimately a shorter lifespan.
In these contexts, pain is much more than a sensation: it is a protective call to action. But pain that is too severe or prolonged can be debilitating. So how does modern medicine mitigate the reputation?
As a neurobiologist and a anesthetist studying pain, this is a question that we and other researchers have tried to answer. The scientific understanding of how the body perceives tissue damage and perceives it as pain has advanced tremendously in recent years. It has become clear that there are several ways that signal tissue damage to the brain and sound the pain alarm bell.
Interestingly, while the brain uses different pain signaling pathways depending on the type of damage, these pathways are also redundant. Even more fascinating is that these neural pathways transform and amplify signals in the case of chronic pain and pain caused by Conditions affecting the nerves themselvesalthough the protective function of pain is no longer needed.
Pain relievers work by attacking different parts of these pathways. However, not every pain reliever works for every type of pain. Due to the multitude and redundancy of pain pathways, a perfect pain reliever can be difficult to find. But in the meantime, understanding how existing pain relievers work helps medical providers and patients use them for the best results.
A bruise, sprain, or broken bone from an injury all lead to tissue inflammation, an immune response that can cause swelling and redness as the body tries to heal. Specialized nerve cells called in the area of injury nociceptors sense the inflammatory chemicals the body is producing and send pain signals to the brain.
Common on the open market anti-inflammatory painkillers work by reducing inflammation in the injured area. These are especially useful for musculoskeletal injuries or other pain problems caused by inflammation like arthritis.
Nonsteroidal anti-inflammatory drugs like ibuprofen (Advil, Motrin), naproxen (Aleve), and aspirin do this by blocking something called an enzyme COX which plays a key role in a biochemical cascade that produces flammable chemicals. Blocking the cascade decreases the amount of inflammatory chemicals, thereby reducing pain signals sent to the brain. While acetaminophen (Tylenol), also known as acetaminophen, does not reduce inflammation like NSAIDs, it also inhibits COX enzymes and has similar pain-relieving effects.
Prescription anti-inflammatory pain relievers include other COX inhibitors, corticosteroids, and more recently, drugs that target and target inactivate the flammable chemicals itself.
Because inflammatory chemicals are involved in other important physiological functions beyond just triggering the pain alarm, drugs that block them have side effects and potential health risks, including irritation and disruption to the stomach lining kidney function. Over-the-counter medicines are generally safe if the directions on the bottle are followed carefully.
corticosteroids like prednisone block the inflammatory cascade early in the process, which is probably why they reduce inflammation so much. However, because all of the chemicals in the cascade are present in almost every organ system, long-term steroid use can pose many health risks that need to be discussed with a doctor before beginning a treatment plan.
Many topical medications Target nociceptors, the specialized nerves that detect tissue damage. Local anesthetics like lidocaine block these nerves from sending electrical signals to the brain.
The protein sensors at the tips of other sensory neurons in the skin are also targets for topical pain relievers. Activation of these proteins can produce certain sensations that can relieve pain by reducing the activity of nerves sensitive to damage, such as the cooling sensation of menthol or the burning sensation of capsaicin.
Because these topical medications act on the tiny nerves in the skin, they are best used for pain that directly affects the skin. For example a shingles infection can damage the nerves in the skin, causing them to become overactive and sending persistent pain signals to the brain. Calming these nerves with topical lidocaine or an overwhelming dose of capsaicin can reduce these pain signals.
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