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Pain has been defined by the International Association for the Study of Pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage."

Pain has both a reactive, or emotional, and a sensory component. It is not just a sensation because it involves a degree of perception. The perception is real in that you feel the pain whether or not the message that damage has occurred is still relevant. This perception develops based on cognitive elements which are linked to the behavioural and emotional response to pain. Pain is often accompanied by feelings of anxiety and distress. It is because it is a complicated psychological and physiological phenomenon that pain is so hard to categorise.

The perception of pain and our response to it are determined by four distinct processes. The first of these is transduction. This is when damage occurs to tissue, affecting the peripheral sensory nerve endings and triggering the initial electrical impulse. Secondly, transduction involving the spinothalamic tract occurs. This incorporates the subsequent neural events that transport the impulse through the nervous system. The third part of the process is called modulation. Pain transmission neurons that originate from the peripheral and central nervous system are controlled by neural activity modulation. The final part of the process is perception. This is how pain actually feels to someone rather than pain as a physiological process. Perception encompasses complex behavioural, psychological, and emotional factors.

Strong emotional states, including extreme fear or excitement, can sometimes temporarily block the sensation of pain. This is why people who sustain an injury while playing sports are often able to ignore a painful injury during the game but notice it more once the game is over.

People have different pain thresholds and our perception of pain is influenced by past experience. The way you coped with pain in the past will affect how you are affected by subsequent episodes of pain. Individuals who are already suffering from an illness, or experience depression or insomnia, are more likely to have a lower pain threshold than healthy people.

Pain functions as part of the body's protection from further injury. The pain you feel from a sprained ankle lets you know that damage has been done and that this body part should not used without risking additional injury. Initially, there a sharp pain followed by a deeper, more enduring, pain. Nerve endings called nociceptors in the skin and the tendons become stimulated. The impulse carrying the information about the harmful stimuli is transmitted through the spinal cord to the brain. Prostaglandins and other chemicals are released by the damaged cells, causing the ankle to swell up, becoming red and painful.

The prostaglandins that are released increase the blood flow to the affected area, increase its temperature, and cause leakage in the blood vessels. The area of injury swells up because blood is directed to this area as part of the repair process. Prostaglandin also increases the sensitivity of nociceptors to the chemicals that actually produce pain. Most nociceptors are present in the skin but they can also be found in the tendons, the blood vessels and even internal organs. Some only respond to extreme stimuli such as burning or cutting, while others are more sensitive and respond to changes in temperature or pressure.

Pain is sensed in the brain. There are sensors in the surface of the skin and in other tissue that react to sensations like hot and cold or extreme pressure. This activates nerve impulses that are transmitted down the nerves, through the spinal cord and to the brain. In the case of protective pain, the brain then sends a message back to the affected area so that the body can deal with the situation, such as moving the hand away from whatever was burning it.

The sharp pain experienced just after you suffer an injury is known as protective pain. This is a physiological sensation that is an important part of the body's early warning system. It is enacted when the nerve endings detect something that is severe enough to cause damage to the body. It typically triggers a reflex motion that removes the endangered part of the body from the detected threat. We learn to anticipate pain responses to certain events, such as coming into contact with fire or bumping our head, and we can predict the familiar sensory outcome produced by these events. Some scientists believe that pain hypersensitivity represents an early form of neurons having some sort of memory based on past experience.

The nociceptors, pain-sensitive neurons at the end of nerve cells, react to noxious stimuli. They send electrical impulses up the spinal cord to the brain resulting in a clearly defined, localized sensation of pain. This process, known as peripheral sensation, involves the local release of chemicals such as prostaglandin and causes the nociceptors in the damaged area to become more sensitive.

Central sensitisation, however, can also increase the sensitivity of the neurons in the spinal cord, which carries this extreme sensitivity far beyond the area of the damaged tissue. Central sensitisation means that the very active nociceptors trigger the spinal neurons. This is why the damaged tissue becomes tender to the touch. Long-acting chemical messengers called neurotransmitters are released across the synapse, the junction across which nerve impulses pass. The neurotransmitters initiate an increase in the activity of the spinal neurons and inputs that would normally be inconsequential will now elicit a vigorous response resulting in feelings of pain.

There are a number of ways to categorise the type of pain that someone is experiencing. Pain can be categorised verbally in an effect to describe the level of discomfort experienced. A frequently used four-point scale is used to measure the intensity of pain, running from no pain to severe pain. "Mild", "Moderate" and "Severe" are all words commonly used to describe the amount of pain someone is in. Mild pain is usually treated with non-steroidal anti-inflammatory drugs (NSAIDs) like Aspirin, ibuprofen, diclofenac, and ketoprofen or analgesics like paracetamol and codeine. Moderate pain generally requires stronger narcotic analgesics. High efficacy narcotic analgesics like morphine or pethidine are used to treat patients with severe pain.

Another distinction is made between acute and chronic pain. Acute pain is a type of pain that only lasts for the duration of the injury stimulating it. The cause of the pain is usually well known and defined so it is easier to diagnose and treat. It may cause sweating or an increased heart rate. Acute pain lets us know that the injury has occurred and that the damaged area needs to be given special attention. The level of pain generally corresponds to the degree of injury. Once the injury has healed, due to treatment or the body's own recuperative powers, the pain improves until it goes away. Tension headaches, toothache, post-operative pain, and musculoskeletal pain usually come under this category.

Chronic pain and its debilitating effects, on the other hand, can continue for months or years, even after the damage has been repaired. It persists beyond the expected recovery time from a particular injury or illness. By this time, it no longer serves the useful purpose of alerting the body that damage has occurred. It is a more subjective type of pain than acute pain and is more difficult to treat. Individuals often show pain beyond what can be explained by their physical causes. The pain may no longer be related to the original site of the injury and can even occur in an unrelated part of the body. Conditions such as osteoarthritis, rheumatoid arthritis, lower back pain, neuropathic pain, and cancer pain are often included under the category of chronic pain.

Pain can also be categorized as nociceptive or neuropathic. Although somatic and visceral pain are easier to manage than neuropathic pain, they can all be experienced by an individual at the same time.

Nociceptive pain relates to ongoing tissue injury. Nociception is the term used to describe the complex series of electrochemical events that is the interaction between the site of the tissue damage and the perception of pain. This is because it involves the nociceptors, the special nerve fibres that are sensitive to noxious stimuli and can distinguish them from harmless stimuli. It is the stimulation of the nociceptors that results in the pain signal being transmitted to the brain.

Nociceptive pain can be either somatic or visceral. Somatic pain is typically a dull or aching pain if it is deep but with a localized focal point. The activation of pain receptors called nociceptors in the skin or deep tissues cause somatic pain. Deep somatic pain occurs in the musculoskeletal tissues, such as in metastasis in the bone. Surface somatic pain is frequently sharper and more akin to a stinging sensation, like post-surgical pain from a surgical incision.

Visceral pain, on the other hand, is usually much harder to locate. It comes from the word "viscera" which describes the internal parts of the body encased within a cavity. Visceral pain results from the activation of pain receptors in the thoracic, abdominal or pelvic viscera and noxious stimuli in the organs or the smooth muscles of the body. It often occurs at sites removed from its point of origin and is a deeper pain that is analogous to squeezing or pressure.

Neuropathic pain can be a severe burning or a tingling sensation, especially if it results from nerve damage to the peripheral or central nervous system (CNS). An example of neuropathic pain would be a tumour compressing neural structures. It generally results from damage to the nervous system itself and is much more severe and potentially long term. If the nerve damage is severe, spinal neurons will become abnormally hypersensitive and other nerves will rewire themselves to pain-registering nerve fibres. This occurs when sensory fibres that would normally deal with touch sensations grow away from their normal location and erroneously establish new connections with the neurons that receive inputs from the nociceptors. This means that neuropathic pain can be evoked by non-noxious stimuli. The rewiring of the circuitry of the sensory pathway may not be reversible.
Reparative pain is another term used for a dull, aching sort of pain that is more prolonged than protective pain. The trauma experienced by the damaged region is more than the body's protective systems can handle. If the damage provokes inflammation of the region, the body allows the nerve fibres in the area to become increasingly sensitive. The result is a persistent pain that is caused by sensory hypersensitivity and persists while the area heals.

Other categories of pain include psychogenic, idiopathic, and referred. Psychogenic pain is largely psychological and is not caused by an actual injury, although this does not make it any less real to the sufferer. Idiopathic pain is pain that persists despite the absence of any psychological or physical causes. Referred pain is felt in a part of the body that is far removed from the actual site of the pain.