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The word "pain" comes from the latin meaning punishment, a fine, a penalty. Pain is an unpleasant sensation; nociception[1] or nociperception[2] is a measurable physiological event of a type usually associated with pain and agony and suffering. A sensation of pain can exist in the absence of nociception: it can occur in response to both external perceived events (for example, seeing something) or internal cognitive events (for example, the phantom limb pain of an amputee). Pain is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” - International Association for the Study of Pain (IASP). Scientifically, pain (a subjective experience) is separate and distinct from nociception, the system which carries information, about inflammation, damage or near-damage in tissue, to the spinal cord and brain. Nociception frequently occurs without pain being felt and is below the level of consciousness. Despite it triggering pain and suffering, nociception is a critical component of the body's defense system. It is part of a rapid warning relay instructing the central nervous system to initiate motor neurons in order to minimize detected physical harm. Pain too is part of the body's defense system; it triggers mental problem solving strategies that seek to end the painful experience, and it promotes learning, making repetition of the painful situation less likely. The two most common forms of pain reported in the United States are headache and back pain.


In 1994, responding to the need for a more useful system for describing chronic pain, the International Association for the Study of Pain (IASP) classified pain according to specific characteristics: (1) region of the body involved (e.g. abdomen, lower limbs), (2) system whose dysfunction may be causing the pain (e.g., nervous, gastrointestinal), (3) duration and pattern of occurrence, (4) intensity and time since onset, and (5) etiology.[3] This system has been criticized by Clifford J. Woolf and others as inadequate for guiding research and treatment.[4] According to Woolf, there are three classes of pain : nociceptive pain (see hereunder), inflammatory pain which is associated with tissue damage and the infiltration of immune cells, and pathological pain which is a disease state caused by damage to the nervous system (neuropathic pain, see hereunder) or by its abnormal function (dysfunctional pain, like in fibromyalgia, irritable bowel syndrome, tension type headache, etc.).[5]


Main article: Chronic pain

Pain is usually transitory, lasting only until the noxious stimulus is removed or the underlying damage or pathology has healed, but some painful conditions, such as rheumatoid arthritis, peripheral neuropathy, cancer and idiopathic pain, may persist for years. Pain that lasts a long time is called chronic, and pain that resolves quickly is called acute. Traditionally, the distinction between acute and chronic pain has relied upon an arbitrary interval of time from onset; the two most commonly used markers being 3 months and 6 months since the onset of pain,[6] though some theorists and researchers have placed the transition from acute to chronic pain at 12 months.[7] Others apply acute to pain that lasts less than 30 days, chronic to pain of more than six months duration, and subacute to pain that lasts from one to six months.[8] A popular alternative definition of chronic pain, involving no arbitrarily fixed durations is "pain that extends beyond the expected period of healing".[6] Chronic pain may be classified as cancer pain or benign.[8]


Main article: Nociception

Nociceptive pain is caused by stimulation of peripheral nerve fibers that respond only to stimuli approaching or exceeding harmful intensity (nociceptors), and may be classified according to the mode of noxious stimulation; the most common categories being "thermal" (heat or cold), "mechanical" (crushing, tearing, etc.) and "chemical" (iodine in a cut, chili powder in the eyes).

Nociceptive pain may also be divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull.[9] Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly localized pain. Examples include sprains and broken bones. Superficial pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.[7]


Main article: Neuropathic pain

Neuropathic pain is caused by damage or disease affecting any part of the nervous system involved in bodily feelings (the somatosensory system).[10] Peripheral neuropathic pain is often described as "burning", "tingling", "electrical", "stabbing", or "pins and needles".[11] Bumping the "funny bone" elicits acute peripheral neuropathic pain.


Main article: Phantom pain

Phantom pain is pain felt in a part of the body that has been lost or from which the brain no longer receives signals. It is a type of neuropathic pain. Phantom limb pain is a common experience of amputees.[12]

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%.[12] One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it.[13][14] Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.[15]

Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks or, sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord all produce relief in some patients.[15]

Work by Vilayanur S. Ramachandran using mirror box therapy allows for illusions of movement and touch in a phantom limb which in turn cause a reduction in pain.[16]

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, fire running down the legs, or a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.[15]


Main article: Psychogenic pain

Psychogenic pain, also called psychalgia or somatoform pain, is pain caused, increased, or prolonged by mental, emotional, or behavioral factors.[17] Headache, back pain, and stomach pain are sometimes diagnosed as psychogenic.[18] Sufferers are often stigmatized, because both medical professionals and the general public tend to think that pain from a psychological source is not "real". However, specialists consider that it is no less actual or hurtful than pain from any other source.[19]

People with long term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.[20]

"The term 'psychogenic' assumes that medical diagnosis is so perfect that all organic causes of pain can be detected; regrettably, we are far from such infallibility... All too often, the diagnosis of neurosis as the cause of pain hides our ignorance of many aspects of pain medicine."

Breakthrough pain

Breakthrough pain is pain that comes on suddenly for short periods of time [citation needed] and is not alleviated by the patients' normal pain management. It is common in cancer patients who often have a background level of pain controlled by medications, but whose pain periodically "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause.

Incident pain

Incident pain is pain that arises as a result of activity, such as movement of an arthritic joint, stretching a wound, etc.

Pain asymbolia and insensitivity

Main article: Pain asymbolia

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.[21]

Although unpleasantness is an essential part of the IASP definition of pain,[22] it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery.[19] 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.[23] 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.[24]

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 this is prevalent.[25] These individuals are at risk of tissue damage due to undiscovered injury. People with diabetes-related nerve damage, for instance, sustain poorly healing foot ulcers as a result of decreased sensation.[26]

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".[24] Children with this condition incur carelessly repeated damage to their tongue, 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).[27] These conditions feature decreased sensitivity to pain together with other neurological abnormalties, particularly of the autonomic nervous system.[24][27] 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.[28]

The experience of physiological pain can be grouped according to the source and related nociceptors (pain detecting neurons).

  • Cutaneous pain is caused by injury to the skin or superficial tissues. Cutaneous nociceptors terminate just below the skin, and due to the high concentration of nerve endings, produce a well-defined, localized pain of short duration. Examples of injuries that produce cutaneous pain include paper cuts, minor cuts, minor (first degree) burns and lacerations.
  • Somatic pain originates from ligaments, tendons, bones, blood vessels, and even nerves themselves. It is detected with somatic nociceptors. The scarcity of pain receptors in these areas produces a dull, poorly-localized pain of longer duration than cutaneous pain; examples include sprains and broken bones. Myofascial pain usually is caused by trigger points in muscles, tendons and fascia, and may be local or referred.
  • Visceral pain originates from body's viscera, or organs. Visceral nociceptors are located within body organs and internal cavities. The even greater scarcity of nociceptors in these areas produces pain that is usually more aching and of a longer duration than somatic pain. Visceral pain is extremely difficult to localize, and several injuries to visceral tissue exhibit "referred" pain, where the sensation is localized to an area completely unrelated to the site of injury. Myocardial ischaemia (the loss of blood flow to a part of the heart muscle tissue) is possibly the best known example of referred pain; the sensation can occur in the upper chest as a restricted feeling, or as an ache in the left shoulder, arm or even hand. "The brain freeze" is another example of referred pain, in which the vagus nerve is cooled by cold inside the throat. Referred pain can be explained by the findings that pain receptors in the viscera also excite spinal cord neurons that are excited by cutaneous tissue. Since the brain normally associates firing of these spinal cord neurons with stimulation of somatic tissues in skin or muscle, pain signals arising from the viscera are interpreted by the brain as originating from the skin. The theory that visceral and somatic pain receptors converge and form synapses on the same spinal cord pain-transmitting neurons is called "Ruch's Hypothesis".
  • Phantom limb pain, a type of referred pain, is the sensation of pain from a limb that has been lost or from which a person no longer receives physical signals. It is an experience almost universally reported by amputees and quadriplegics.
  • Neuropathic pain, or "neuralgia", can occur as a result of injury or disease to the nerve tissue itself. This can disrupt the ability of the sensory nerves to transmit correct information to the thalamus, and hence the brain interprets painful stimuli even though there is no obvious or known physiologic cause for the pain. Neuropathic pain is, as stated above, the disease of pain. It is not the sole definition for chronic pain, but does meet its criteria.

Radicular pain, or radiculitis, is pain "radiated" along the dermatome (sensory distribution) of a nerve due to inflammation or other irritation of the nerve root (radiculopathy) at its connection to the spinal column. A common form of radiculitis is sciatica – radicular pain that radiates along the sciatic nerve from the lower spine to the lower back, gluteal muscles, back of the upper thigh, calf, and foot as often secondary to nerve root irritation from a spinal disc herniation or from osteophytes in the lumbar region of the spine.

Insensitivity to pain

Inability to experience pain, as in the rare condition congenital insensitivity to pain or congenital analgesia, can cause various health problems.

Selected common and serious causes of pain by region

It should be noted that visceral pain sensation is often referred by the CNS to a dermatome region which may be far away from the originating organ. These correlate to the position of the organ in the embryo. Examples of this include the heart which originates in the neck, thus producing the classical pain and arm pain experienced during acute cardiac pain.

Head and neck




  • Back - MSK (muscle strain), cancer, spinal disc herniation, degenerative disc disease, coccyx (coccydynia), also see joints section



Physiology of nociception (commonly Physiology of pain)

  • This section, except in the paragraph on pain in consciousness, for historical reasons uses pain to refer to nociception. Where both a historical pain term and a modern nociception term are common, a bracketed pain term is included. e.g. Nociceptors (Pain receptors)

"Nociception is the term introduced almost 100 years ago by the great physiologist Sherrington (1906) to make clear the distinction between detection of a noxious event or a potentially harmful event and the psychological and other responses to it.[29]"

Nociception is the system which carries information about noxious stimilus, usually associated with tissue damgage to the spinal cord and brain[30].

Nociception is also known as nociperception and physiological pain. Nociception is separate to, and distinct from, psychological pain.

Nociceptors (Pain receptors)

All nociceptors are free nerve endings that have their cell bodies outside the spinal column in the dorsal root ganglion and are named based upon their appearance at their sensory ends. These sensory endings look like the branches of small bushes. There are mechanical, thermal, and chemical nociceptors. They are found in skin and on internal surfaces such as periosteum and joint surfaces. Deep internal surfaces are only weakly supplied with pain receptors and will propagate sensations of chronic, aching pain if tissue damage in these areas occurs.

Two main types of nociceptor, and C fibres, mediate fast and slow pain respectively. Thinly myelinated type Aδ fibres, which transmit signals at rates of between 6 to 30 meters per second mediate fast pain. This type of pain is felt within a tenth of a second of application of the pain stimulus. It can be described as sharp, acute, pricking pain and includes mechanical and thermal pain. Slow pain, mediated by slower, unmyelinated ("bare") type C pain fibers that send signals at rates between 0.5 and 2 meters per second, is an aching, throbbing, burning pain. Chemical pain is an example of slow pain. Nociceptors do not adapt to stimulus. In some conditions, excitation of pain fibers becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia.

Transmission of nociception (pain) signals in the central nervous system

There are 2 pathways for transmission of nociception in the central nervous system. These are the neospinothalamic tract (for fast pain) and the paleospinothalamic tract (for slow pain).

  • Fast pain travels via type Aδ fibers to terminate on lamina I (lamina marginalis) of the dorsal horn of the spinal cord. Second order neurons of the neospinothalamic tract then take off and give rise to long fibres which cross the midline through the grey commisure and pass upwards in the contralateral anterolateral columns. These fibres then terminate on the reticular formation,Ventrobasal Complex (VBC) of the thalamus. From here, third order neurons communicate with the somatosensory cortex. Fast pain can be localised easily if Aδ fibres are stimulated together with tactile receptors.
  • Slow pain is transmitted via slower type C fibres to laminae II and III of the dorsal horns, together known as the substantia gelatinosa. Second order neurons take off and terminate in lamina V, also in the dorsal horn. Third order neurons then join fibers from the fast pathway, crossing to the opposite side via the grey commisure, and traveling upwards through the anterolateral pathway. These neurons terminate widely in the brain stem, with one tenth of fibres stopping in the thalamus, and the rest stopping in the medulla, pons and tectum of midbrain mesencephalon, periaqueductal grey. Slow pain is poorly localized.

Consequences of nociception

When the nociceptors are stimulated they transmit signals through sensory neurons in the spinal cord. These neurons release glutamate, a major exicitory neurotransmitter that relays signals from one neuron to another.

If the signals are sent to the reticular formation of brain stem, thalamus, then pain enters consciousness, but in a dull poorly localised manner. From the thalamus, the signal can travel to the somatosensory cortex in the cerebrum, when the pain is experienced as localised and having more specific qualities.

Feinstein and colleagues found that nociception could also, "activate generalized autonomic responses independently of the relay of pain to conscious levels" causing "pallor, sweating, bradycardia, a drop in blood pressure, subjective "faintness," nausea and syncope" [31].


The gate control theory of pain, proposed by Patrick Wall and Ron Melzack, postulates that nociception (pain) is "gated" by non-nociception stimuli such as vibration. Thus, rubbing a bumped knee seems to relieve pain by preventing its transmission to the brain. Pain is also "gated" by signals that descend from the brain to the spinal cord to suppress (and in other cases enhance) incoming nociception (pain) information.

The analgesia system is mediated by 3 major components : the periaquaductal grey matter (in the midbrain), the nucleus raphe magnus (in the medulla), and the nociception (pain) inhibitory neurons within the dorsal horns of the spinal cord, which act to inhibit nociception(pain)-transmitting neurons also located in the spinal dorsal horn.

The body has several different types of opioid receptors that are activated in response to the binding of the body's endorphins. These receptors, which exist in a variety of areas in the body, inhibit firing of neurons that would otherwise be stimulated to do so by nociceptors.

Phenotype and pain

Pain may be experienced differently depending on phenotype. A study by Liem et al. suggests that redheads are more susceptible to thermal pain. [32]

Gene SCN9A has been identified as a major factor in the development of the pain-perception systems within the body. A rare genetic mutation in this area causes non-functional development of certain sodium channels in the nervous system, which prevents the brain from receiving messages of physical damage. People having this disorder are completely ignorant to pain, and can perform without pain any kinds of self mutilation or damage. In the families studied, this has ranged from biting of the person's own tongue leading to damage, through to street acts with knives, to death from injuries due to a failure to have learned limits on injury through experience of pain. The same gene also appears to mediate a form of hyper-sensitivity to pain, with other mutations seeming to be "at the root of paroxysmal extreme pain disorder" according to a 2006 report in Neurone. Various other forms of somatic sensitivity are unaffected. [1]

Pain and alternative medicine

A recent survey by NCCAM (part of the NIH) found pain was the most common reason that people use complementary and alternative medicine (CAM). Among American adults who used CAM in 2002, 16.8% used CAM to treat back pain; 6.6% for neck pain; 4.9% for arthritis; 4.9% for joint pain; 3.1% for headache; and 2.4% used CAM to treat recurring pain. (Some survey respondents may have used CAM to treat more than one of these pain conditions.)

One such alternative, traditional Chinese medicine, views pain as a qi "blockage" equivalent to electrical resistance, or as "stagnation of blood" – theorized as dehydration inhibiting metabolism. Traditional Chinese treatments such as acupuncture are said to be more effective for nontraumatic pain than traumatic pain. Although these claims have not found broad scientific acceptance, research into both the mechanism and clinical efficacy of acupuncture supports that it can have a role in pain reduction for both humans and animals. Although the mechanism is not fully understood, it is likely that acupuncture stimulates the release of large quantities of endogenous opioids.[33] A 2004 NCCAM-funded study showed that acupuncture provides pain relief and improved function in patients with osteoarthritis of the knee, causing some managed care organizations to support acupuncture as adjunctive therapy for this purpose.[34] The NIH's 1997 Consensus Statement on Acupunture notes that research has been mixed, partly due to difficulties with designing clinical studies with the proper controls.[35]

Another common alternative treatment for chronic pain is use of nutritional supplements such as:

  • Curcumin, a polyphenol found in turmeric (Curcuma Longa) and said to be a natural cox-2 inhibitor[36]
  • Glucosamine
  • Chondroitin
  • Bromelain (a digestive enzyme from pineapple core)
  • Omega-3 fatty acids.

The efficacy of Glucosamine and Chondroitin, popular supplements for patients with arthritis, were examinied in the GAIT study, a $12 million trial funded by the NIH which showed statistical evidence for the treatment's positive effect only amongst patients with moderate to severe pain, a small subsection of the study.[37]

Philosophy of pain

Main article: Pain (philosophy)

The concept of pain has played an important part in the study of philosophy, particularly in the philosophy of mind. The question of what pain actually consists in is still open since any evaluation is dependent upon what subject one approaches the question from. Identity theorists assert that the mental state of pain is completely identical with some physical state caused by various physiological causes. Functionalists consider pain to be defined completely by its causal role (ie in the role it has in bringing about various effects) and nothing else. Theologians and other spiritual traditions have much to say about the nature of pain and its various spiritual consequences, especially its role in growth, understanding, compassion, and in providing an aspect of life to be overcome..

Survival benefit

Despite its unpleasantness, pain is an important part of the existence of humans and other animals; in fact, it is vital to survival. Pain encourages an organism to disengage from the noxious stimulus associated with the pain. Preliminary pain can serve to indicate that an injury is imminent, such as the ache from a soon-to-be-broken bone. Pain may also promote the healing process, since most organisms will protect an injured region in order to avoid further pain. People born with congenital insensitivity to pain usually have short life spans, and suffer numerous ailments such as broken bones, bed sores, and chronic infection.

The study of pain has in recent years diverged into many different fields from pharmacology to psychology and neurobiology. It was even proposed that fruit flies may be used as an animal model for pharmacological pain research [2]. Pain is also of interest in the search for the neural correlates of consciousness, as pain has many subjective psychological aspects besides the physiological nociception.

Interestingly, the brain itself is devoid of nociceptive tissue, and hence cannot experience pain. Thus, a headache is not due to stimulation of pain fibers in the brain itself. Rather, the membrane surrounding the brain and spinal cord, called the dura mater, is innervated with pain receptors, and stimulation of these dural nociceptors (pain receptors) is thought to be involved to some extent in producing headache pain. Some evolutionary biologists have speculated that this lack of nociceptive tissue in the brain might be because any injury of sufficient magnitude to cause pain in the brain has a sufficiently high probability of being fatal that development of nociceptive tissue therein would have little to no survival benefit.

Chronic pain, in which the pain becomes pathological rather than beneficial, is an exception to the idea that pain is helpful to survival. Furthermore, it is not clear what the survival benefit of sometimes extreme forms of pain (e.g. toothache) might be; and the intensity of some forms of pain (for example as a result of injury to fingernails or toenails) seem to be out of all proportion to any survival benefits.

Pain and nociception in other species


Pain is defined as a subjective conscious experience. The presence or absence of pain even in another human is only verifiable by their report; "Pain is whatever the experiencing person says it is, and exists whenever he says it does."[38]. It is not scientifically possible to prove whether an animal is in pain or not.

To determine if an animal is likely to be able to experience pain, two tests are used.

  • The first is; does the animal respond to noxious stimulus? "Most, if not all, invertebrates have the capacity to detect and respond to noxious or aversive stimuli. That is, like vertebrates, they are capable of nociception".[39]". Both vertebrates and non-vertebrates respond to noxious stimuli and are capable of modifying their response to such stimuli. However noxious stimuli will cause complex, though automatic, responses in animals who have had the higher regions of their brains destroyed and are thus incapable of experiencing pain. Which leads to;
  • the second question; does noxious stimulus have longer lasting effects that indicate that pain has been experienced. The reasoning behind this question is that the likely evolutionary benefit of experiencing pain is that learning to withdraw from the noxious stimulus, and avoid similar situations in future, is enhanced and therefore the animal is more likely to survive and breed. From this line of reasoning, if no learning from noxious stimulus is seen, then pain was not experienced.

From these lines of questioning the following groups have been identified;

  • Most invertebrates — including lobsters, crabs, worms, snails, slugs and clams- reaction to noxious stimulus does occur but no reports of longer term learning from pain — probably don't have the capacity to feel pain. [40]
  • Insects; possibly don't experience pain. Sometimes no response to noxious stimulus. No sign of longer term avoidance. Possible do not feel pain. [39]
  • Cephalopods (octopus, squid); long term withdrawal from possibly painful stimuli observed - possibly do experience pain[39].
  • Fish; respond to noxious stimuli - reports of long term learning from noxious stimulus - possibly do experience pain.[41]
  • Other non-human vertebrates (mammals, birds and reptiles); vocalizations and physiological responses (e.g. the release of stress hormones) are similar to our own when we are in pain, learned long term avoidance from noxious stimulus observed - suggesting these animals do experience pain [42].

In veterinary science this uncertainty is overcome by assuming that if something would be painful for a human then it would be painful for an animal[43]. Where possible, analgesics are used preemptively if there is any likelihood of pain being caused to an animal.

See also


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  2. The American Heritage Stedman's Medical Dictionary, 2nd Edition, Houghton Mifflin, 2004. Cited online at
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  5. Woolf CJ. What is this thing called pain?. Journal of Clinical Investigation. 2010;120(11):3742–4. doi:10.1172/JCI45178. PMID 21041955.
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  10. Treede RD, Jensen TS, Campbell JN, Cruccu G, Dostrovsky JO, Griffin JW, Hansson P, Hughes R, Nurmikko T, Serra J. Neuropathic pain: redefinition and a grading system for clinical and research purposes. Neurology. 2008;70(18):1630–5. doi:10.1212/01.wnl.0000282763.29778.59. PMID 18003941.
  11. Paice JA. Mechanisms and management of neuropathic pain in cancer. J. Support Oncol.. 2003;1(2):107–20. PMID 15352654.
  12. 12.0 12.1 Kooijman CM, Dijkstra PU, Geertzen JH, Elzinga A, van der Schans CP. Phantom pain and phantom sensations in upper limb amputees: an epidemiological study. Pain. 2000;87(1):33–41. doi:10.1016/S0304-3959(00)00264-5. PMID 10863043.
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  14. Jensen TS, Krebs B, Nielsen J, Rasmussen P. Immediate and long-term phantom limb pain in amputees: incidence, clinical characteristics and relationship to pre-amputation limb pain. Pain. 1985;21(3):267–78. doi:10.1016/0304-3959(85)90090-9. PMID 3991231.
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  16. Ramachandran VS, Rogers-Ramachandran D. Synaesthesia in phantom limbs induced with mirrors. Proc. Biol. Sci.. 1996;263(1369):377–86. doi:10.1098/rspb.1996.0058. PMID 8637922.
  17. Cleveland Clinic, Health information

    ^ "Psychogenic pain - definition from" Retrieved 2008-11-05.

  18. Cleveland Clinic, Health information
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  21. Beecher, HK (1959). Measurement of subjective responses. New York: Oxford University Press. cited in Melzack, R; Wall, PD (1996). The challenge of pain (2 ed.). London: Penguin. p. 7. ISBN 978-0-14-025670-3.
  22. International Association for the Study of Pain: Pain Definitions [Retrieved 10 Sep 2011]. "Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage" Derived from Bonica JJ. The need of a taxonomy. Pain. 1979;6(3):247–8. doi:10.1016/0304-3959(79)90046-0. PMID 460931.
  23. Nikola Grahek, Feeling pain and being in pain, Oldenburg, 2001. ISBN 3-8142-0780-7.
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  30. Section B 2. from NP(Nurse Practitioner)Central
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  33. Robert Sapolsky, Why zebras don't get ulcers, pp 196-197: "Scientists noted that Chinese veterinarians used acupuncture to do surgery on animals, thereby refuting the argument that the painkilling characteristics of acupuncture was one big placebo effect ascribable to cultural conditioning (no cow on earth will go along with unanaesthetized surgery just because it has a heavy investment in the cultural mores of the society in which it dwells. [...] Acupuncture stimulates the release of large quantities of endogenous opioids, for reasons no one really understands. The best demonstration of this is what is called a subtraction experiment: block the activity of endogenous opioids by using a drug that blocks the opiate receptor... acupuncture no longer effectively dulls the perception of pain."
  34. Berman BM, Lao L, Langenberg P, Lee WL, Gilpin AM, Hochberg MC. "Effectiveness of acupuncture as adjunctive therapy in osteoarthritis of the knee: a randomized, controlled trial." Annals of Internal Medicine 2004 Dec 21; 141(12): 901-10.
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Nervous system - Sensory system - edit
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