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In order to understand how pain is categorised – and managed in terms of how the various drug classes used for analgesia exert their action – it is necessary to grasp what causes pain in the first place.
When an area of the body is damaged, sensory receptors called nociceptors send signals via the spinal cord to the brain, which then uses neurotransmitters to communicate back to the affected site: this is felt as pain. Reducing the transmission of nociceptive impulses decreases the brain’s perception of pain and is how opioids bring to bear their analgesic effect.
An individual’s emotional state influences the quantities of neurotransmitters present in the body, which are necessary to communicate from the brain to the part of the body that is out of kilter.
Someone who is depressed, for example, has lower levels of noradrenaline and serotonin, which normally help block the pain signal, so higher discomfort levels are experienced. This is the reason that antidepressants are sometimes used in pain management.
At the same time that nociceptors start firing, tissues near the affected site start releasing prostaglandins, which amplify the pain signal and force the sufferer to restrict themselves from doing anything that could exacerbate the problem. Blocking this prostaglandin release reduces pain and is the rationale behind analgesics such as paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs).[1,2,3]
The location of the nociceptors that inform the brain of a problem dictates how pain is experienced:
Pain is further categorised by how long it lasts.
According to the British Pain Society, there are three classifications for pain: