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Hyperalgesia (/ ˌ h aɪ p ər æ l ˈ dʒ iː z i ə / or /-s i ə /; hyper from Greek ὑπέρ (huper) 'over' + -algesia from Greek ἄλγος (algos) 'pain') is an abnormally increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves and can cause hypersensitivity to stimulus.
Hypoalgesia or hypalgesia denotes a decreased sensitivity to painful stimuli. Hypoalgesia occurs when nociceptive (painful) stimuli are interrupted or decreased somewhere along the path between the input (nociceptors), and the places where they are processed and recognized as pain in the conscious mind. Hypoalgesic effects can be mild, such as ...
Opioid-induced hyperalgesia (OIH) or opioid-induced abnormal pain sensitivity, also called paradoxical hyperalgesia, is an uncommon condition of generalized pain caused by the long-term use of high dosages of opioids [1] such as morphine, [2] oxycodone, [3] and methadone. [4] [5] OIH is not necessarily confined to the original affected site. [6]
Congenital insensitivity to pain (CIP), also known as congenital analgesia, is one or more extraordinarily rare conditions in which a person cannot feel (and has never felt) physical pain. [1] The conditions described here are separate from the HSAN group of disorders, which have more specific signs and cause.
Increased touch sensitivity is referred to as "tactile hyperesthesia", and increased sound sensitivity is called "auditory hyperesthesia". In the context of pain, hyperaesthesia can refer to an increase in sensitivity where there is both allodynia and hyperalgesia .
Most pain resolves once the noxious stimulus is removed and the body has healed, but it may persist despite removal of the stimulus and apparent healing of the body. Sometimes pain arises in the absence of any detectable stimulus, damage or disease. [3] Pain is the most common reason for physician consultation in most developed countries.
Nociplastic pain is a longterm complex pain, one of three mechanisms of pain, defined by the International Association for the Study of Pain as "pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain". [2]
The intensity of pain reported is consistently reduced in response to touch. [5] [6] [7] This occurs whether the touch is at the same time as the pain, or even if the touch occurs before the pain. [8] Touch also reduces the activation of cortical areas that respond to painful stimuli. [9]