Books: 'Hyperalgesia'

1

Jianren, Mao, ed. Opioid-induced hyperalgesia. New York: Informa Healthcare USA, 2010.

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2

Jianren, Mao, ed. Opioid-induced hyperalgesia. New York: Informa Healthcare USA, 2009.

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3

Lars, Lundberg. Pain and hyperalgesia in the human skin. Uppsala: Uppsala Universitet, 1992.

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4

Leonardo, Vecchiet, Albe-Fessard Denise G, and Lindblom Ulf, eds. New trends in referred pain and hyperalgesia. Amsterdam: Elsevier, 1993.

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5

Bristol-Myers Squibb Symposium on Pain Research (2nd 1991 Galveston, Tex.). Hyperalgesia and allodynia: The Bristol-Myers Squibb Symposium on Pain Research. Edited by Willis William D. 1934-. New York: Raven Press, 1992.

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6

universitet, Aalborg, ed. Fundamentals of muscle pain, referred pain and deep tissue hyperalgesia. Oslo: Taylor & Francis, 2006.

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7

1934-, Willis William D., ed. Hyperalgesia and allodynia: The Bristol-Myers Squibb Symposium on Pain Research. New York: Raven Press, 1992.

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8

1966-, Malmberg Annika B., and Chaplan Sandra R, eds. Mechanisms and mediators of neuropathic pain. Basel: Birkhäuser Verlag, 2002.

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9

Ziegler, Esther Anja. Die Bedeutung nozizeptiver A- und C-Fasern für die Mechanismen der sekundären Hyperalgesie. [s.l.]: [s.n.], 1999.

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10

Bannister, Kirsty. Opioid-induced hyperalgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0061.

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The landmark paper discussed in this chapter is ‘Opioid-induced hyperalgesia: Abnormal or normal pain?’, published by Simonnet and Rivat in 2003. Morphine remains the analgesic of choice for those patients suffering moderate-to-severe pain, but it is increasingly recognized that worsening pain can be associated with chronic opioid consumption—the so-called phenomenon of opioid-induced hyperalgesia (OIH). This paper combined knowledge from clinical studies and experimental evidence from animal research in order to delve deeper into the workings of OIH and ask whether it represented normal or abnormal pain. The authors, intrigued by evidence indicating that exogenous opioids could activate both inhibitory and facilitatory pain systems, looked to reassess the role of such enhancement in pain sensitivity. As the debate regarding the very existence of OIH rages on, we pain specialists can take comfort in the knowledge that for many before us, over a decade ago, the reality of OIH was never in question.

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11

Opioid-Induced Hyperalgesia. Taylor & Francis Group, 2017.

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12

Mao, Jianren. Opioid-Induced Hyperalgesia. Taylor & Francis Group, 2016.

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13

Mao, Jianren. Opioid-Induced Hyperalgesia. Taylor & Francis Group, 2016.

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14

Schutzer-Weissmann, John. Cytokines as central to peripheral sensitization and hyperalgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0030.

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The landmark study discussed in this chapter, published in a letter to Nature in 1988 by Ferreira et al., marked the beginning of a new era of pain research. It demonstrated elegantly and for the first time that cytokines are central to peripheral sensitization and the phenomenon of hyperalgesia. The authors first injected various cytokines into rats’ paws and then tested for hyperalgesic activity using a modified Randall–Sellito rat-paw pressure test. They found that interleukin-1β‎ evoked a dose-dependent hyperalgesic response in the injected paw. The investigators then tried to isolate the peptide domains that were responsible for interleukin-1β‎s hyperalgesic activity and identified two tripeptide sequences which had hyperalgesic activity. Since then, after almost three decades of inquiry into their role in the induction and maintenance of hyperalgesia and other phenomenon such as allodynia, the first human trials of interleukin-1β‎ antagonists for the treatment of pain have begun.

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15

Nagy, Istvan. VR1 in inflammatory thermal hyperalgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0028.

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The landmark paper discussed in this chapter, published by Davis et al. in 2000, describes the role of the capsaicin receptor, which is called transient receptor potential cation channel subfamily vanilloid member 1 (TRPV1), in inflammatory thermal hyperalgesia. Capsaicin, the pungent agent found in hot peppers, has been linked to pain for centuries because it induces a burning pain sensation which, after prolonged application of the agent, turns into analgesia. Because of this, capsaicin has been used to relieve pain, most likely since prehistoric times. The elucidation of the role of TRPV1 in nociceptive processing was heralded as the starting point for the development of agents which would revolutionize pain management. Unfortunately, that promise is yet to be realized and apparently we need a more detailed understanding of the role of TRPV1 in physiological and pathological processes in order to fulfil the analgesic potential of drugs acting on this receptor.

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16

Klein, Amanda H., and Matthias Ringkamp. Peripheral neural mechanisms of cutaneous heat hyperalgesia and heat pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0024.

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In the landmark paper discussed in this chapter, published in 1982, LaMotte et al. investigated the contribution of different cutaneous nerve fibres to heat pain and heat hyperalgesia in both psychophysical (humans) and electrophysiological studies (human and primates), using identical thermal test and conditioning stimuli; the findings from the two sets of experiments were then correlated. In non-human primates, neuronal activity was recorded from mechanoheat-sensitive A- and C-fibres (AMHs and CMHs, respectively) and warm and cold fibres, whereas, in conscious human volunteers, activity from CMHs was recorded. The authors found that pain is mediated by activity in CMHs and that sensitization of CMHs after a mild burn injury accounts for the increased heat pain after such injury. The combination of psychophysical experiments in human and correlative electrophysiological studies in non-human primates provides an important experimental approach for unravelling the contribution of different classes of afferents to pain.

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17

Tsagareli, Merab G. Hyperalgesia and Allodynia: A Closer Look. Symptoms, Mechanisms and Treatment. Nova Science Publishers, Incorporated, 2019.

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18

Elmofty, Dalia H. Opioid-Induced Hyperalgesia, Tolerance, and Chronic Postsurgical Pain: A Dilemma Complicating Postoperative Pain Management. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0037.

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Perioperative pain management continues to be a challenge for physicians. Postoperative pain can compromise patient progress and lead to poor outcomes or chronic pain. Opioid medications, the mainstay of treatment for perioperative pain, can cause opioid-induced hyperalgesia and opioid tolerance. Attempts should be made to modify factors that increase the risk for chronic postsurgical pain. Certain patient factors and anesthetic and surgical techniques have been implicated. Incorporating multimodal methods for perioperative pain management using nonconventional opioids, such as methadone, cyclooxygenase inhibitors, NMDA antagonists, and regional techniques can improve outcomes and prevent opioid-induced hyperalgesia, opioid tolerance, and chronic postsurgical pain in patients on long-term opioid therapy.

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19

(Editor), Kay Brune, and Hermann O., M.D. Handwerker (Editor), eds. Hyperalgesia: Molecular Mechanisms And Clinical Implications (Progress in Pain Research and Management, Volume 30). IASP Press, 2004.

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20

(Editor), Kay Brune, and Hermann O., M.D. Handwerker (Editor), eds. Hyperalgesia: Molecular Mechanisms And Clinical Implications (Progress in Pain Research and Management, Volume 30). IASP Press, 2004.

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21

(Editor), Kay Brune, and Hermann O., M.D. Handwerker (Editor), eds. Hyperalgesia: Molecular Mechanisms And Clinical Implications (Progress in Pain Research and Management, Volume 30). IASP Press, 2004.

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22

Lazar, Alina. Chronic Abdominal Pain in Children. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0019.

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Abdominal pain in the pediatric population is mostly functional. Patients with chronic abdominal pain (typically young females) have a high risk of anxiety, depression, and dysfunctional coping, which are also risk factors for postoperative pain and persistent postsurgical pain. In these patients, peripheral and central sensitization contribute to possible visceral hyperalgesia. When patients with chronic abdominal pain and visceral hyperalgesia undergo surgical procedures, perioperative pain can be difficult to treat. To manage the chronic pain of such patients, their complex biopsychosocial make-up should be considered. A comprehensive plan includes preventive and aggressive multimodal analgesia, adequate patient and parent education, realistic expectations, cognitive-behavioral therapy, and distraction and relaxation techniques.

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23

Szabova, Alexandra, and Kenneth R. Goldschneider. Opioid-Tolerant Patient. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0043.

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Caring for patients who are taking chronic opioids may present several challenges for clinicians in the operating room and in the immediate postoperative period. Factors such as tolerance and opioid-induced hyperalgesia can complicate perioperative pain management.

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24

Wainger, Brian J. Drug Discovery and Neuropathic Pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0117.

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Pain is one of the most common causes of physician visits and disability. Pain has been classified into specific subtypes. We refer to baseline or nociceptive pain as pain that results from an ongoing, high-threshold stimulus acting on an unenhanced somatosensory system. Inflammatory pain refers to pain in the setting of tissue damage and specifically the release of inflammatory molecules that activate and sensitize the nociceptive machinery. Hyperalgesia, or increased pain in response to a noxious stimulus, results from nociceptor sensitization whereas neuropathic pain results from a lesion or disease of the somatosensory system. Pain can have spontaneous, stimulus-independent components as well as evoked components such as hyperalgesia or allodynia, pain that is elicited by a normally innocuous stimulus. This chapter describes the research strategy for discovering new drugs to relieve these different kinds of pain.

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25

Hain, Richard D. W., and Satbir Singh Jassal. Gastrointestinal symptoms. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198745457.003.0009.

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A number of gastrointestinal symptoms are encountered in paediatric palliative care. This chapter covers commonly occurring symptoms, including constipation, diarrhoea, sialorrhoea, visceral hyperalgesia, anorexia, cachexia, and hiccough. Details on definitions, causes, and management are covered in most instances, and a section on blended feeds is also included.

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26

Zelisko, Michael Blaine. The Opioid-Tolerant Patient. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0036.

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Caring for the opioid-tolerant patient presents several challenges in the perioperative period, including a higher incidence of anxiety, pain, and unanticipated hospital admission. The goal of the anesthesiologist is to provide sufficient analgesia while preventing withdrawal symptoms. This chapter reviews multimodal analgesia techniques, and addresses opioid tolerance, opioid-induced hyperalgesia, opioid rotation, and the use of methadone during the perioperative period.

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27

Pak, Daniel J., and Neel Mehta. Pain Anatomy and Physiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190217518.003.0001.

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This chapter focuses on pain anatomy and physiology to provide a comprehensive review of the mechanisms of nociception for preparation for the ABA Pain Medicine (PM) Examination. It reviews the anatomy of pain pathways (particularly the spinothalamic sensory tract), and the process of pain conduction from peripheral nociceptors to the cerebral cortex. It also reviews the different mechanisms of sensitization and inhibition at peripheral nociceptors (manifested as primary and secondary hyperalgesia), the spinal cord (wind-up and sensitization of second-order neurons) and supraspinal structures, which all affect the processing of nociceptive signals in the nervous system and ultimately, the perception of pain.

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28

Qureshi, M. A., J. H. Gan, S. Kunnumpurath, Clara Pau, Alice Kai, Zachariah Mirsky, William Park, and Nalini Vadivelu. Preventive Analgesia for the Management of General Surgical Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0002.

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Pain created by surgery has the ability to produce both structural and functional changes in pain pathways. These changes may be reduced if timely and adequate pain relief is delivered to the patient. Poor control of pain can result in remodeling of the “hardwired” pathways involved in pain transmission, which can result in central sensitization and hyperalgesia. Furthermore, poorly controlled pain and delay in its recognition may lead to a chronic pain state, further complicating the patient’s recovery and quality of life. A multimodal approach taking into account psychosocial aspects of the patient is more likely to mitigate the development of chronic postsurgical pain (CPSP).

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29

Conklin, Jeffrey L., Frederick C. Johlin, Joseph A. Murray, Konrad S. Schulze, and Satish S. C. Rao. Gastrointestinal Motility: Tests and Problem-Oriented Approach. Springer London, Limited, 2012.

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30

Badiola, Ignacio, Tulsi Singh, Jiabin Liu, and Nabil Elkassabany. Acute Pain in the Opioid-Tolerant Patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0045.

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The number of people addicted to prescription and illicit opioids continues to increase, and many of these patients present to the hospital or pain center with acute pain issues. The matter is further complicated by the increasing number of patients with legitimately painful conditions treated with chronic opioid therapy. Typically, these patients are difficult to manage during any acute pain episode due to their opioid tolerance and opioid-induced hyperalgesia. This difficulty often leads to inadequate pain management, increased suffering, and delayed hospital discharge. Increased awareness is needed among pain management physicians and other clinicians who care for opioid-tolerant patients, yet there is a lack of evidence-based medicine regarding the optimal treatment of this population.

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31

Williams, Amanda. The understanding of social effects in pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0077.

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The landmark paper discussed in this chapter is ‘Social modulation of pain as evidence for empathy in mice’, published in 2006 by Langford et al. in Mogil’s lab at McGill University, Montreal. It elegantly demonstrated (1) that mice observed and responded to one another’s pain—effectively, socially mediated hyperalgesia; (2) that this was modulated by the nature of the social relationship, occurring between cagemates but not strangers; (3) that the mechanism in the observing mouse involved central sensitization, not local effects. The interactive behaviour met requirements for empathic responding; neither imitation nor emotional contagion could account for these effects. The findings have implications for lab pain research using rodents, for understanding of empathic responses in animals, and for understanding animal social behaviour more widely.

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32

Gordon-Williams, Richard M., and Anthony H. Dickenson. Pathophysiology of pain in cancer and other terminal illnesses. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0092.

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Cancer pain involves a myriad of peripheral changes in the function of tissue and nerves, at the site of the tumour growth, as well as a number of consequent changes in the processing of pain messages at the spinal cord level with implications for the pain experience at higher centres. This chapter reviews the changes in peripheral pain signalling, notes the likely prevalence of both inflammatory and neuropathic components, and describes the altered events at spinal levels that can come some way towards explaining ongoing pain, hyperalgesia, and allodynias that patients with cancer and other terminal illnesses such as HIV/AIDs experience. Finally, changes induced by cancer at the level of the brain are discussed. The mechanisms of action of therapies, both existing and potential novel approaches, are included at peripheral and central levels.

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33

Malmberg, Annika B., and Sandra R. Chaplan. Mechanisms and Mediators of Neuropathic Pain. Springer Basel AG, 2012.

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34

Malmberg, Annika B., and Sandra R. Chaplan. Mechanisms and Mediators of Neuropathic Pain. Birkhauser Verlag, 2012.

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35

Richebé, Philippe, and Cyril Rivat. The effects of morphine on the CNS. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0017.

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The 1973 paper by Jacquet and Lajtha, was a pivotal report in understanding the effects of opioids on nociception, as it investigated the effects of morphine on different brain structures. To do this, the authors used a microinjection technique that allowed them to specifically target subcortical sites. The animals used in this study were rats, and evaluation of the nociceptive threshold was based on the behavioural reaction to electrical shock. Two reactions were evaluated: flinch or jump responses. The main result was that, depending on the dose and the site of injection, morphine produced either an increase in nociceptive threshold (analgesia), or a decrease in the nociceptive threshold (hyperalgesia). The authors also reported severe effects characterized by hyper-reactivity and violent uncontrolled jumping in stereotyped circular leaps when morphine was administered in the periaqueductal grey matter.

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36

Trigo Blanco, Paula, Maricarmen Roche Rodriguez, and Nalini Vadivelu. Pathophysiology of Pain and Pain Pathways. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0001.

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Pain is a distressing experience and an important cause of suffering and disability. Pain usually signals the presence of injury or disease and generates a complex physiologic and emotional response. It has a protective function in order to restore homeostasis at the autonomic and psychological levels. This chapter reviews the physiology and mechanisms of pain, as well as the pathways in the central and peripheral nervous system that transmit nociceptive information. The chapter divides the pain anatomical pathways into the peripheral nervous system, the spinal cord with the medullary dorsal horn system, and the ascending and supraspinal system. The authors explain the pain pathways as a three-neuron pathway that carries noxious information from the periphery to the cerebral cortex. This chapter defines important concepts such as sensitization, hyperalgesia, and allodynia, as well as describes the modulation process of nociception.

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37

Stoneley, Sarah, and Simon Rinald. Sensory loss. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0047.

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Sensory disturbance can either be a complete loss (anaesthesia) or a reduction (hypoaesthesia) in the ability to perceive the sensory input. Dysaesthesia is an abnormal increase in the perception of normal sensory stimuli. Hyperalgesia is an increased sensitivity to normally painful stimuli, and allodynia is the perception of usually innocuous stimuli as painful. A complete loss of sensation is likely to be due to a central nervous system problem, while a tingling/paraesthesia (large fibre) or burning/temperature (small fibre) sensation is likely due to an acquired peripheral nervous system problem. Shooting, electric-shock-like pains suggest radicular pathology, a tight-band spinal cord dysfunction. Positive sensory symptoms are usually absent in inherited neuropathies, even in the context of significant deficits on examination. This chapter describes the clinical approach to patients with sensory symptoms. Common patterns of sensory loss and their causes are described.

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38

Bird, Mark F., and David G. Lambert. Deorphanization of ORL-1/LC132 by reverse pharmacology in two landmark studies. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0026.

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Deorphanization of ORL-1/LC132 in 1995 by reverse pharmacology in two simultaneously published landmark studies added a new member to the opioid family of G-protein coupled receptors. Meunier and Reinscheid used cells expressing recombinant ORL-1 (human) or LC132 (rat) and the presumed intracellular inhibition of cyclic AMP formation to ‘fish’ for endogenous peptide ligands in rat whole-brain and pig hypothalamic extracts. Both studies reported the isolation of a 17-amino-acid peptide, which was named nociceptin and orphanin FQ by the two authors, respectively. The behaviour of the isolated peptide was a complete surprise, as a general hyperalgesia was observed when the peptide was administered at supraspinal sites. We now know that this peptide has, in fact, anti-opioid action, particularly in the medulla. The endogenous peptide exerts a multitude of effects both in the nervous system and, unlike classical opioids, has efficacy in neuropathic pain.

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39

Brown, Matthew. The chronic constriction injury model of neuropathic pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0067.

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The landmark paper discussed in this chapter is ‘A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man’, published by Bennett and Xie in 1988. This paper, in which the unilateral sciatic nerve chronic constriction injury (CCI) model was first presented, is one of the earliest and most comprehensive descriptions of a specific animal paradigm that was designed to model human neuropathic pain. The authors realized that human neuropathic pain rarely involves nerve transection but instead involves evoked changes in damaged and preserved nerve fibres. Furthermore, they systematically applied a barrage of sensory testing that demonstrated quantifiable hyperalgesia and cold allodynia reflecting some of the clinical observations of human neuropathic pain phenotype. CCI provided a high-quality template for the development of neuropathic pain models that impelled the subsequent development of other animal models striving to replicate the human condition faithfully and accurately.

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40

Stogicza, Agnes, Bartha Peter Tohotom, Edit Racz, Andrea Trescot, and Alan Berkman. Complex Regional Pain Syndrome of the Upper and Lower Extremity. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0011.

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Complex regional pain syndrome (CRPS) is a chronic debilitating pain condition of the extremities; it can affect, less commonly, other areas of the body (face, pelvis, abdomen). Its early presentation—pain disproportionate to the injury, skin temperature changes, hyperalgesia, allodynia—is often not recognized, delaying treatment. In later phases, with sympathetic nervous system involvement, it presents with skin and muscle atrophy, hair loss, allodynia, loss of function, and decreased range of motion. In severe cases, it can spread from one area to the other. Imaging findings (X-ray, MRI, bone scintigraphy) are nonspecific. They are used to support the diagnosis, and to exclude conditions that can present similarly. Treatment is challenging and includes physical therapy, psychologic support, medication management, and minimally invasive interventions to decrease pain, to positively influence the sympathetic nervous system, and to preserve function. A multidisciplinary approach is likely to be the most beneficial.

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41

Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.

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Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ‎ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.

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42

Orr, William C. Gastrointestinal functioning during sleep. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0042.

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Sleep is associated with substantial changes in gastrointestinal functioning that have considerable clinical relevance Symptoms of sleep-related dysfunction are common and are primarily related to sleep-related heartburn and regurgitation. Sleep disturbances accompany several other gastrointestinal disorders, such as irritable bowel syndrome (IBS). Sleep-related gastroesophageal reflux (GER) has been shown to plan a major role in the pathogenesis of more complicated gastroesophageal reflux disease (GERD), notably via a prolongation of acid contact. Mucosal damage has been shown to be more closely associated with this pattern of reflux in comparison with waking reflux, which is associated with more frequent but very short reflux events. Sleep disturbance is also associated with a visceral hyperalgesia that enhances pain responses associated with acid–mucosal contact. Sleep does influence intestinal motility, but further research is needed to confirm the details of exactly how intestinal motility is modulated by sleep.

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43

Riley, Bobbie, and Navil Sethna. Pediatric Complex Regional Pain Syndrome Type 1. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0054.

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Complex regional pain syndrome type 1 (CRPS-1) is a condition that affects adolescents and children under the age of 7. It usually follows minor injury and rarely occurs spontaneously. The pain is usually out of proportion to the inciting injury. Pain, allodynia, and/or hyperalgesia are severe enough to inhibit use of the affected limb. Delay in diagnosis and self and/or iatrogenic immobilization of the affected limb may lead to worsening pain, skin hypersensitivity and discoloration, swelling, and vasomotor and dystrophic abnormalities. The diagnosis of CRPS-1 and 2 is based on symptoms. There are no diagnostic tests that can confirm the presence or absence of CRPS-1. CRPS-2 diagnosis is established by nerve conduction test and electromyography. Clinical practice neuropathic guidelines are most effective for CRPS-2 treatment. Pharmacological and interventional treatment options for CRPS-1 are limited and usually ineffective because the underlying mechanism(s) are yet to be determined.

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44

Bonnet, Francis, Marc E. Gentili, and Christophe Aveline. Post-surgical analgesia and acute pain management. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0046.

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Postoperative and acute pain remains uncontrolled in many instances, leading to the risk of development of chronic pain syndromes. After tissue damage, activation of postsynaptic NMDA receptors, also induced by opioid administration, plays a key role in postoperative pain sensitization, allodynia, and hyperalgesia. Pain intensity may depend on sex, age, anxiety, and genetic factors but in clinical practice, surgical procedure is the main determinant of pain, although pain may vary from one patient to one another. Serial pain measurements are mandatory to assess pain intensity and to guide pain treatment. They are based on unidimensional simple pain scales. Multimodal analgesia combining opioid and non-opioid agent and regional block or infiltration is the rule postoperatively, although evidence is sometimes lacking to support all the combinations commonly used. Opioids should be used on demand while other agents are administered systematically. Non-steroidal anti-inflammatory drugs decrease opioid demand as well as paracetamol although to a less extend. Antihyperalgesic agents including NMDA blockers (ketamine) and α‎2-δ‎ ligands (gabapentin, pregabalin) have an opioid-sparing effect and may prevent the occurrence of chronic pain syndrome after surgery. Regional blocks and infiltration provide good quality analgesia but the balance between advantages and drawbacks of central block need to be evaluated carefully for each surgical procedure.

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45

Donkin, S. Representations of the Hyperalgebra of a Semisimple Group. Cambridge University Press, 2008.

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46

Mease, Philip. Neurobiology of pain in osteoarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0013.

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Significant advances in our understanding of the neurobiology of pain in osteoarthritis (OA) have occurred in the last decade and are herein summarized. Pain is the predominant symptom of OA and occurs at multiple levels from non-cartilage peripheral tissues to spinal cord, and brain and back. At each level, nerve function is regulated by complex ionic channels, neuropeptide expression, and cytokine and chemokine activity. Previously considered a non-inflammatory condition, it is now recognized that cell proliferation and inflammatory cytokine production occurs in OA synovium, contributing to peripheral sensitization. Genetic profile influences nociceptive neuropeptide expression and thus, pain perception. Both peripheral and central sensitizing factors, including increased neuropeptide and microglial activity, lead to pain augmentation and persistence. Pain processing in brain centres such as the somatosensory cortex and insula are influenced by affective areas such as the amygdala. Descending receptor pathways through the midbrain to the dorsal horn, such as norepinephrine, serotonin, opioid, and cannabinoid, normally provide pain inhibitory function but this function may be diminished in chronic pain states such as OA, leading to allodynia and hyperalgesia. Functional neuroimaging has contributed to our understanding of the complex interplay of peripheral and central mechanisms. Recent evidence that grey matter volume decrease in chronic pain states may be reversible (e.g. after pain relief post OA hip arthroplasty) illuminates the potential for central neuroplasticity. Greater understanding of the neurobiology of OA pain provides evidence for therapeutic approaches that address peripheral and/or central pain mechanisms and provides a guide for future targeted pain therapeutics.

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47

Fuchs, Oliver. Modulation experimentell induzierter Algesie, Hyperalgesie und Allodynie mit repetitiver transkranieller Magnetstimulation des posterioren parietalen Kortex. 2011.

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48

Fuchs, Oliver. Modulation experimentell induzierter Algesie, Hyperalgesie und Allodynie mit repetitiver transkranieller Magnetstimulation des posterioren parietalen Kortex. 2011.

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49

Bruns, Mechthild Ellen. Die Beeinflussung der Primären und Sekundären Hyperalgesie nach Vorfussosteotomie durch eine präoder postoperative periphere Nervenblockade. 2001.

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Books on the topic 'Hyperalgesia'

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