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Heike Fallago
Pain is a distressing feeling often caused by intense or damaging stimuli. The International Association for the Study of Pain defines pain as "an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage."[1]
Pain motivates organisms to withdraw from damaging situations, to protect a damaged body part while it heals, and to avoid similar experiences in the future.[2] 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.[4][5] It is a major symptom in many medical conditions, and can interfere with a person's quality of life and general functioning.[6] People in pain experience impaired concentration, working memory, mental flexibility, problem solving and information processing speed, and are more likely to experience irritability, depression, and anxiety.
Simple pain medications are useful in 20% to 70% of cases.[7] Psychological factors such as social support, cognitive behavioral therapy, excitement, or distraction can affect pain's intensity or unpleasantness.[8][9]
Allodynia is pain experienced in response to a normally painless stimulus.[18] It has no biological function and is classified by characteristics of the stimuli as cold, heat, touch, pressure or pinprick.[18][19]
Breakthrough pain is transitory pain that comes on suddenly and is not alleviated by the patient's regular pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.[25][26]
The ability to experience pain is essential for protection from injury, and recognition of the presence of injury. Episodic analgesia may occur under special circumstances, such as in the excitement of sport or war: a soldier on the battlefield may feel no pain for many hours from a traumatic amputation or other severe injury.[27]
Although unpleasantness is an essential part of the IASP definition of pain,[28] it is possible in some patients to induce a state known as pain asymbolia, described as intense pain devoid of unpleasantness, with morphine injection or psychosurgery.[29] Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all.[30] Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.[31]
Insensitivity to pain may also result from abnormalities in the nervous system. This is usually the result of acquired damage to the nerves, such as spinal cord injury, diabetes mellitus (diabetic neuropathy), or leprosy in countries where that disease is prevalent.[32] These individuals are at risk of tissue damage and infection due to undiscovered injuries. People with diabetes-related nerve damage, for instance, sustain poorly-healing foot ulcers as a result of decreased sensation.[33]
A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain".[31] Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis).[34] These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system.[31][34] A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.[35]
Experimental subjects challenged by acute pain and patients in chronic pain experience impairments in attention control, working memory capacity, mental flexibility, problem solving, and information processing speed.[36] Pain is also associated with increased depression, anxiety, fear, and anger.[37]
Although pain is considered to be aversive and unpleasant and is therefore usually avoided, a meta-analysis which summarized and evaluated numerous studies from various psychological disciplines, found a reduction in negative affect. Across studies, participants that were subjected to acute physical pain in the laboratory subsequently reported feeling better than those in non-painful control conditions, a finding which was also reflected in physiological parameters.[39] A potential mechanism to explain this effect is provided by the opponent-process theory.
Before the relatively recent discovery of neurons and their role in pain, various different body functions were proposed to account for pain. There were several competing early theories of pain among the ancient Greeks: Hippocrates believed that it was due to an imbalance in vital fluids.[40] In the 11th century, Avicenna theorized that there were a number of feeling senses including touch, pain and titillation.[41]
In 1644, Ren Descartes theorized that pain was a disturbance that passed along nerve fibers until the disturbance reached the brain.[40][42] Descartes' work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses".[43] Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature.[44] By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.[41][43]
Some sensory fibers do not differentiate between noxious and non-noxious stimuli, while others, nociceptors, respond only to noxious, high intensity stimuli. At the peripheral end of the nociceptor, noxious stimuli generate currents that, above a given threshold, send signals along the nerve fiber to the spinal cord. The "specificity" (whether it responds to thermal, chemical or mechanical features of its environment) of a nociceptor is determined by which ion channels it expresses at its peripheral end. Dozens of different types of nociceptor ion channels have so far been identified, and their exact functions are still being determined.[45]
Pain-related activity in the thalamus spreads to the insular cortex (thought to embody, among other things, the feeling that distinguishes pain from other homeostatic emotions such as itch and nausea) and anterior cingulate cortex (thought to embody, among other things, the affective/motivational element, the unpleasantness of pain),[49] and pain that is distinctly located also activates primary and secondary somatosensory cortex.[50]
Spinal cord fibers dedicated to carrying A-delta fiber pain signals, and others that carry both A-delta and C fiber pain signals to the thalamus have been identified. Other spinal cord fibers, known as wide dynamic range neurons, respond to A-delta and C fibers, but also to the much larger, more heavily myelinated A-beta fibers that carry touch, pressure and vibration signals.[46]
Ronald Melzack and Patrick Wall introduced their gate control theory in the 1965 Science article "Pain Mechanisms: A New Theory".[51] The authors proposed that the thin C and A-delta (pain) and large diameter A-beta (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that A-beta fiber signals acting on inhibitory cells in the dorsal horn can reduce the intensity of pain signals sent to the brain.[42]
They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both the sensory-discriminative and affective-motivational dimensions of pain, while suggestion and placebos may modulate only the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed.[52] (p. 432)
The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well."[52] (p. 435)
Pain is part of the body's defense system, producing a reflexive retraction from the painful stimulus, and tendencies to protect the affected body part while it heals, and avoid that harmful situation in the future.[53][54] It is an important part of animal life, vital to healthy survival. People with congenital insensitivity to pain have reduced life expectancy.[31]
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