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As long as humans have experienced pain, they have given explanations for its existence and sought soothing agents to dull or cease the painful sensation. Archaeologists have uncovered clay tablets dating back as far as 5,000 BC which reference the cultivation and use of the opium poppy to bring joy and cease pain. In 800 BC, the Greek writer Homer wrote in his epic, The Odyssey, of Telemachus, a man who used opium to soothe his pain and forget his worries.[1] While some cultures researched analgesics and allowed or encouraged their use, others perceived pain to be a necessary, integral sensation. Physicians of the 19th century used pain as a diagnostic tool, theorizing that a greater amount of personally perceived pain was correlated to a greater internal vitality, and as a treatment in and of itself, inflicting pain on their patients to rid the patient of evil and unbalanced humors.[2] This article focuses both on the history of how pain has been perceived across time and culture, but also how malleable an individual's perception of pain can be due to factors like situation, their visual perception of the pain, and previous history with pain.
Because of the only relatively recent discovery of neurons and how they conduct and interpret signals, including sensations such as pain, within the body, various theories have been proposed as to the causes of pain and its role or function. Even within seemingly limited groups, such as the ancient Greeks, there were competing theories as to the root cause of pain. Aristotle did not include a sense of pain when he enumerated the five senses; he, like Plato before him, saw pain and pleasure not as sensations but as emotions ("passions of the soul").[3] Alternatively, Hippocrates believed that pain was caused by an imbalance in the vital fluids of a human. At this time, neither Aristotle nor Hippocrates believed that the brain had any role to play in pain processing but rather implicated the heart as the central organ for the sensation of pain.[4]
Middle ages
In the 11th century, Avicenna theorized that there were a number of feeling senses including touch, pain and titillation.[3]
Pain during the Renaissance
Portrait of René Descartes
Even just prior to the scientific Renaissance in Europe, pain was not well understood and it was theorized that pain existed outside of the body, perhaps as a punishment from God, with the only management treatment being prayer.[2] Again, even within the confined group of religious, practicing Christians, more than one theory arose. Alternatively, pain was also theorized to exist as a test or trial on a person. In this case, pain was inflicted by God onto person to reaffirm their faith, or in the example of Jesus, to lend legitimacy and purpose to a trial through suffering.
In his 1664 Treatise of Man, René Descartes theorized that the body was more similar to a machine, and that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain.[4][5] This theory transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation meaning that a cure for such pain could be found by researching and locating pain fibers within the bodies rather than searching for an appeasement for god. This also moved the center of pain sensation and perception from the heart to the brain. Descartes proposed his theory by presenting an image of a man's hand being struck by a hammer. In between the hand and the brain, Descartes described a hollow tube with a cord beginning at the hand and ending at a bell located in the brain. The blow of the hammer would induce pain in the hand, which would pull the cord in the hand and cause the bell located in the brain to ring, indicating that the brain had received the painful message. Researchers began to pursue physical treatments such as cutting specific pain fibers to prevent the painful signal from cascading to the brain.
Specificity theory
Descartes' pain pathway: "Particles of heat"(A) activate a spot of skin(B) attached by a fine thread(cc) to a valve in the brain(de) where this activity opens the valve, allowing the animal spirits to flow from a cavity(F) into the muscles causing them to flinch from the stimulus, turn the head and eyes toward the affected body part, and move the hand and turn the body protectively.
The specificity theory, which states that pain is "a specific sensation, with its own sensory apparatus independent of touch and other senses,"[6] emerged in the nineteenth century, but had been prefigured by the work of Avicenna and Descartes.[3][5]
Scottish anatomist Charles Bell proposed in 1811 that there exist different kinds of sensory receptor, each adapted to respond to only one stimulus type.[7] In 1839 Johannes Müller, having established that a single stimulus type (e.g., a blow, electric current) can produce different sensations depending on the type of nerve stimulated, hypothesized that there is a specific energy, peculiar to each of five nerve types that serve Aristotle's five senses, and that it is the type of energy that determines the type of sensation each nerve produces.[8] He considered feelings such as itching, pleasure, pain, heat, cold and touch to be varieties of the single sense he called "feeling and touch."[9] Müller's doctrine killed off the ancient idea that nerves carry actual properties or incorporeal copies of the perceived object, marking the beginning of the modern era of sensory psychology, and prompted others to ask, do the nerves that evoke the different qualities of touch and feeling have specific characteristics?[3]
Filippo Pacini had isolated receptors in the nervous system which detect pressure and vibrations in 1831. Georg Meissner and Rudolf Wagner described receptors sensitive to light touch in 1852; and Wilhelm Krause found a receptor that responds to gentle vibration in 1860.[10]Moritz Schiff was first to definitively formulate the specificity theory of pain when, in 1858, he demonstrated that touch and pain sensations traveled to the brain along separate spinal cord pathways.[3] In 1882 Magnus Blix reported that specific spots on the skin elicit sensations of either cold or heat when stimulated, and proposed that "the different sensations of cool and warm are caused by stimulation of different, specific receptors in the skin."[10]Max von Frey found and described these heat and cold receptors and, in 1896, reported finding "pain spots" on the skin of human subjects.[8] Von Frey proposed there are low threshold cutaneous spots that elicit the feeling of touch, and high threshold spots that elicit pain, and that pain is a distinct cutaneous sensation, independent of touch, heat and cold, and associated with free nerve endings.[10]
Intensive theory
In the first volume of his 1794 Zoonomia; or the Laws of Organic Life,[11]Erasmus Darwin supported the idea advanced in Plato'sTimaeus, that pain is not a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature.[12]Wilhelm Erb, in 1874, also argued that pain can be generated by any sensory stimulus, provided it is intense enough, and his formulation of the hypothesis became known as the intensive theory.[3]
Alfred Goldscheider (1884) confirmed the existence of distinct heat and cold sensors, by evoking heat and cold sensations using a fine needle to penetrate to and electrically stimulate different nerve trunks, bypassing their receptors. Though he failed to find specific pain sensitive spots on the skin, Goldscheider concluded in 1895 that the available evidence supported pain specificity, and held the view until a series of experiments were conducted in 1889 by Bernhard Naunyn.[13] Naunyn had rapidly (60–600 times/second) prodded the skin of tabes dorsalis patients, below their touch threshold (e.g., with a hair), and in 6–20 seconds produced unbearable pain. He obtained similar results using other stimuli including electricity to produce rapid, sub-threshold stimulation, and concluded pain is the product of summation. In 1894 Goldscheider extended the intensive theory, proposing that each tactile nerve fiber can evoke three distinct qualities of sensation – tickle, touch and pain – the quality depending on the intensity of stimulation; and extended Naunyn's summation idea, proposing that, over time, activity from peripheral fibers may accumulate in the dorsal horn of the spinal cord, and "spill over" from the peripheral fiber to a pain-signalling spinal cord fiber once a threshold of activity has been crossed.[3][10] The British psychologist, Edward Titchener, pronounced in his 1896 textbook, "excessive stimulation of any sense organ or direct injury to any sensory nerve occasions the common sensation of pain."[3]
Competing theories
By the mid-1890s, specificity was mainly backed by physiologists (prominently by von Frey) and clinicians; and the intensive theory received most support from psychologists. But after Henry Head in England published a series of clinical observations between 1893 and 1896, and von Frey's experiments between 1894 and 1897, 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, with Titchener in 1898 now placing "the sensation of pain" alongside that of pressure, heat and cold. Though the intensive theory no longer featured prominently in textbooks, Goldscheider's elaboration of it nevertheless stood its ground in opposition to von Frey's specificity at the frontiers of research, and was supported by some influential theorists well into the mid-twentieth century.[3][6]
William Kenneth Livingston advanced a summation theory in 1943, proposing that high intensity signals, arriving at the spinal cord from damage to nerve or tissue, set up a reverberating, self-exciting loop of activity in a pool of interneurons, and once a threshold of activity is crossed, these interneurons then activate "transmission" cells which carry the signal to the brain's pain mechanism; that the reverberating interneuron activity also spreads to other spinal cord cells that trigger a sympathetic nervous system and somatic motor system response; and these responses, as well as fear and other emotions elicited by pain, feed into and perpetuate the reverberating interneuron activity. A similar proposal was made by RW Gerard in 1951, who proposed also that intense peripheral nerve signalling may cause temporary failure of inhibition in spinal cord neurons, allowing them to fire as synchronized pools, with signal volleys strong enough to activate the pain mechanism.[6]
Pattern theory
Building on John Paul Nafe's 1934 suggestion that different cutaneous qualities are the product of different temporal and spatial patterns of stimulation, and ignoring a large body of strong evidence for receptor fiber specificity, DC Sinclair and G Weddell's 1955 "peripheral pattern theory" proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers.[6] In 1953, Willem Noordenbos had observed that a signal carried from the area of injury along large diameter "touch, pressure or vibration" fibers may inhibit the signal carried by the thinner "pain" fibers — the ratio of large fiber signal to thin fiber signal determining pain intensity; hence, we rub a smack. This was taken as a demonstration that pattern of stimulation (of large and thin fibers in this instance) modulates pain intensity.[14]
Ronald Melzack and Patrick Wall introduced their "gate control" theory of pain in the 1965 Science article "Pain Mechanisms: A New Theory".[15] The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord: transmission cells that carry the pain signal up to the brain, and inhibitory interneurons that impede transmission cell activity. Activity in both thin and large diameter fibers excites transmission cells. Thin fiber activity impedes the inhibitory cells (tending to allow the transmission cell to fire) and large diameter fiber activity excites the inhibitory cells (tending to inhibit transmission cell activity). So, the more large fiber (touch, pressure, vibration) activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. The authors had drawn a neural "circuit diagram" to explain why we rub a smack.[5] They pictured not only a signal traveling from the site of injury to the inhibitory and transmission cells and up the spinal cord to the brain, but also a signal traveling from the site of injury directly up the cord to the brain (bypassing the inhibitory and transmission cells) where, depending on the state of the brain, it may trigger a signal back down the spinal cord to modulate inhibitory cell activity (and so pain intensity). The theory offered a physiological explanation for the previously observed effect of psychology on pain perception.[16]
Modern theories
Physical explanation
In 1975, well after the time of Descartes, the International Association for the Study of Pain sought a consensus definition for pain, finalizing "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage" as the final definition.[17] It is clear from this definition that while it is understood that pain is a physical phenomenon, the emotional state of a person, as well as the context or situation associated with the pain also impacts the perception of the nociceptive or noxious event. For example, if a human experiences a painful event associated with any form of trauma (an accident, disease, etc.), a reoccurrence of similar physical pain will not only inflict physical trauma but also the emotional and mental trauma first associated with the painful event. Research has shown that should a similar injury occur to two people, one person who associates large emotional consequence to the pain and the other person who does not, the person who associates a large consequence on the pain event will feel a more intense physical pain that the person who does not associate a large emotional consequence with the pain.
Sun Dance of the Shoshone Indians
Modern research has gathered considerable amounts of evidence that support the theory that pain is not only a physical phenomenon but rather a biopsychosocial phenomenon, encompassing culture, nociceptive stimuli, and the environment in the experience and perception of pain. For example, the Sun Dance is a ritual performed by traditional groups of Native Americans. In this ritual, cuts are made into the chest of a young man. Strips of leather are slipped through the cuts, and poles are tied to the leather. This ritual lasts for hours and undoubtedly generates large amounts of nociceptive signaling, however the pain may not be perceived as noxious or even perceived at all. The ritual is designed around overcoming and transcending the effects of pain, where pain is either welcomed or simply not perceived.[4]
Visual input and pain perception
Additional research has shown that the experience of pain is shaped by a plethora of contextual factors, including vision. Researchers have found that when a subject views the area of their body that is being stimulated, the subject will report a lowered amount of perceived pain.[18] For example, one research study used a heat stimulation on their subjects' hands. When the subject was directed to look at their hand when the painful heat stimulus was applied, the subject experienced an analgesic effect and reported a higher temperature pain threshold. Additionally, when the view of their hand was increased, the analgesic effect also increased and vice versa. This research demonstrated how the perception of pain relies on visual input.
The use of fMRI to study brain activity confirms the link between visual perception and pain perception. It has been found that the brain regions that convey the perception of pain are the same regions that encode the size of visual inputs.[19] One specific area, the magnitude-related insula of the insular cortex, functions to perceive the size of a visual stimulation and integrate the concept of that size across various sensory systems, including the perception of pain. This area also overlaps with the nociceptive-specific insula, part of the insula that selectively processes nociception, leading to the conclusion that there is an interaction and interface between the two areas. This interaction tells the individual how much relative pain they are experiencing, leading to the subjective perception of pain based on the current visual stimulus.
Humans have always sought to understand why they experience pain and how that pain comes about. While pain was previously thought to be the work of evil spirits, it is now understood to be a neurological signal. However, the perception of pain is not absolute and can be impacted by various factors in including the context surrounding the painful stimulus, the visual perception of the stimulus, and an individual's personal history with pain.
1 2 3 4 Melzack R, Katz J.The Gate Control Theory: Reaching for the Brain.In:Craig KD, Hadjistavropoulos T.Pain: psychological perspectives.Mahwah, N.J:Lawrence Erlbaum Associates, Publishers;2004. ISBN0-8058-4299-3.
1 2 3 4 Bonica JJ.The management of pain.2 ed.Vol. 1.London:Lea & Febiger;1990.History of pain concepts and therapies.p. 7.
↑ Bell C.Idea of a new anatomy of the brain; submitted for the observation of his friends. 1811.In:Cranefield PF.The way in and the way out: François Magendie, Charles Bell and the roots of the spinal nerves.New York:Futura;1974. Online reprint:
1 2 Cope DK.Bonica's management of pain.4 ed.Philadelphia:Wolters Kluwer / Lippincott Williams & Wilkins;2010. ISBN978-0-7817-6827-6.Intellectual milestones in our understanding and treatment of pain.p. 1–13.
↑ Finger S.Origins of neuroscience: a history of explorations into brain function.USA:Oxford University Press;2001. ISBN0-19-514694-8.
↑ Naunyn B (1889). "Ueber die Auslösung von Schmerzempfindung durch Summation sich zeitlich folgender sensibler Erregungen". Naunyn-Schmiedeberg's Archives of Pharmacology. 25 (3–4): 272–305. doi:10.1007/BF01833969.
↑ Todd EM, Kucharski A. Pain: Historical Perspectives.In:Bajwa ZH, Warfield CA.Principles and practice of pain medicine.2nd ed.New York:McGraw-Hill, Medical Publishing Division;2004. ISBN0-07-144349-5.
↑ Baliki, M. N. . "Parsing Pain Perception Between Nociceptive Representation and Magnitude Estimation." Journal of Neurophysiology. 101.2 (2008): 875-87. Print.
Related Research Articles
Nociception is the sensory nervous system's response to certain harmful or potentially harmful stimuli. In nociception, intense chemical, mechanical, or thermal stimulation of sensory nerve cells called nociceptors produces a signal that travels along a chain of nerve fibers via the spinal cord to the brain. Nociception triggers a variety of physiological and behavioral responses and usually results in a subjective experience of pain in sentient beings.
The trigeminal nerve (the fifth cranial nerve, or simply CN V) is a nerve responsible for sensation in the face and motor functions such as biting and chewing; it is the largest of the cranial nerves. Its name ("trigeminal" = tri-, or three, and - geminus, or twin: thrice-twinned) derives from the fact that each of the two nerves (one on each side of the pons) has three major branches: the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). The ophthalmic and maxillary nerves are purely sensory, whereas the mandibular nerve supplies motor as well as sensory (or "cutaneous") functions.
The somatic nervous system is the part of the peripheral nervous system associated with the voluntary control of body movements via skeletal muscles.
Afferent nerve fibers refer to axonal projections that arrive at a particular brain region, as opposed to efferent projections that exit the region. These terms have a slightly different meaning in the context of the peripheral nervous system (PNS) and central nervous system (CNS).
The grey column refers to a somewhat ridge-shaped mass of grey matter in the spinal cord. This presents as three columns: the anterior grey column, the posterior grey column, and the lateral grey column, all of which are visible in cross-section of the spinal cord.
In physiology, a stimulus is a detectable change in the physical or chemical structure of an organism's internal or external environment. The ability of an organism or organ to respond to external stimuli is called sensitivity. When a stimulus is applied to a sensory receptor, it normally elicits or influences a reflex via stimulus transduction. These sensory receptors can receive information from outside the body, as in touch receptors found in the skin or light receptors in the eye, as well as from inside the body, as in chemoreceptors and mechanoreceptors. An internal stimulus is often the first component of a homeostatic control system. External stimuli are capable of producing systemic responses throughout the body, as in the fight-or-flight response. In order for a stimulus to be detected with high probability, its level must exceed the absolute threshold; if a signal does reach threshold, the information is transmitted to the central nervous system (CNS), where it is integrated and a decision on how to react is made. Although stimuli commonly cause the body to respond, it is the CNS that finally determines whether a signal causes a reaction or not.
A reflex arc is a neural pathway that controls a reflex. In vertebrates, most sensory neurons do not pass directly into the brain, but synapse in the spinal cord. This allows for faster reflex actions to occur by activating spinal motor neurons without the delay of routing signals through the brain. However, the brain will receive the sensory input while the reflex is being carried out and the analysis of the signal takes place after the reflex action.
Stimulus modality, also called sensory modality, is one aspect of a stimulus or what is perceived after a stimulus. For example, the temperature modality is registered after heat or cold stimulate a receptor. Some sensory modalities include: light, sound, temperature, taste, pressure, and smell. The type and location of the sensory receptor activated by the stimulus plays the primary role in coding the sensation. All sensory modalities work together to heighten stimuli sensation when necessary.
A mechanoreceptor is a sensory receptor that responds to mechanical pressure or distortion. Normally there are four main types in glabrous, or hairless, mammalian skin: lamellar corpuscles, tactile corpuscles, Merkel nerve endings, and bulbous corpuscles. There are also mechanoreceptors in hairy skin, and the hair cells in thoreceptors of primates like rhesus monkeys and other mammals are similar to those of humans and also studied even in early 20th century anatomically and neurophysiologically.
A nociceptor is a sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals to the spinal cord and the brain. If the brain perceives the threat as credible, it creates the sensation of pain to direct attention to the body part, so the threat can hopefully be mitigated; this process is called nociception.
The spinothalamic tract is a sensory pathway from the skin to the thalamus. From the ventral posterolateral nucleus in the thalamus, sensory information is relayed upward to the somatosensory cortex of the postcentral gyrus.
Sensory neurons, also known as afferent neurons, are neurons in the central nervous system, that convert a specific type of stimulus, via their receptors, into action potentials or graded potentials. This process is called sensory transduction. The cell bodies of the sensory neurons are located in the dorsal ganglia of the spinal cord.
The withdrawal reflex is a spinal reflex intended to protect the body from damaging stimuli. The reflex rapidly coordinates the contractions of all the flexor muscles and the relaxations of the extensors in that limb causing sudden withdrawal from the potentially damaging stimulus. Spinal reflexes are often monosynaptic and are mediated by a simple reflex arc. A withdrawal reflex is mediated by a polysynaptic reflex resulting in the stimulation of many motor neurons in order to give a quick response.
The gate control theory of pain asserts that non-painful input closes the nerve "gates" to painful input, which prevents pain sensation from traveling to the central nervous system.
Allodynia refers to central pain sensitization following normally non-painful, often repetitive, stimulation. Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain. Temperature or physical stimuli can provoke allodynia, which may feel like a burning sensation, and it often occurs after injury to a site. Allodynia is different from hyperalgesia, an extreme, exaggerated reaction to a stimulus which is normally painful. The term is from Ancient Greek άλλοςállos "other" and οδύνηodúnē "pain".
Group C nerve fibers are one of three classes of nerve fiber in the central nervous system (CNS) and peripheral nervous system (PNS). The C group fibers are unmyelinated and have a small diameter and low conduction velocity, whereas Groups A and B are myelinated. Group C fibers include postganglionic fibers in the autonomic nervous system (ANS), and nerve fibers at the dorsal roots. These fibers carry sensory information.
The ventrobasal complex (VB) is a relay nucleus of the thalamus for nociceptive stimuli received from nociceptive nerves. The VB consists of the ventral posteromedial nucleus (VPM) and the ventral posterolateral nucleus (VPL). In some species the ventral posterolateral nucleus, pars caudalis is also a part of the VB. The VB gets inputs from the spinothalamic tract, medial lemniscus, and corticothalamic tract. The main output of the VB is the primary somatosensory cortex.
The wide dynamic range neuron(WDR) was first discovered by Mendell in 1966. Early studies of this neuron established what is known as the gate control theory of pain. The basic concept is that non-painful stimuli block the pathways for painful stimuli, inhibiting possible painful responses. This theory was supported by the fact that WDR neurons are responsible for responses to both painful and non-painful stimuli, and the idea that these neurons couldn't produce more than one of these responses simultaneously. WDR neurons respond to all types of somatosensory stimuli, make up the majority of the neurons found in the posterior grey column, and have the ability to produce long range responses including those responsible for pain and itch.
A spinal interneuron, found in the spinal cord, relays signals between (afferent) sensory neurons, and (efferent) motor neurons. Different classes of spinal interneurons are involved in the process of sensory-motor integration. Most interneurons are found in the grey column, a region of grey matter in the spinal cord.
Tactile induced analgesia is the phenomenon where concurrent touch and pain on the skin reduces the intensity of pain that is felt.
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