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Books on the topic 'Pain sensitization'

Author: Grafiati

Published: 25 January 2025

Last updated: 31 July 2025

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1

Veldhuijzen, Dieuwke S., Henriët van Middendorp, and Andrea W. M. Evers. Stress and Sensitization in Chronic Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190627898.003.0005.

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Stress and sensitization are central concepts in chronic pain. Both can be a consequence and a contributor to the pain experience. This chapter describes the psychobiology of stress and sensitization within a multilevel perspective, indicating the impact of various forms of stress and sensitization on multiple psychoneurobiological processes (i.e., autonomic, endocrine, immune, and central processes) related to chronic pain. As a result of disordered stress regulation, sensitization may occur as a mechanism that explains how acute pain problems can become chronic and how acute pain problems ca

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2

Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.

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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for m

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3

Sandkühler, Jürgen. Making the link from “central sensitization” to clinical pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0047.

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The landmark paper discussed in this chapter is ‘Central sensitization: Implications for the diagnosis and treatment of pain’, published by C. J. Woolf in 2011. The phrase ‘central sensitization’ is often used as an umbrella term for all kinds of central nervous system (CNS) mechanisms contributing to pain hypersensitivity. The International Association for the Study of Pain (IASP) defines ‘central sensitization’ as the ‘increased responsiveness of nociceptive neurons in the CNS’. In the CNS, highly distinct mechanisms contribute to pain hypersensitivity depending upon pain aetiology and disea

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4

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,

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5

Goudie, A. J., and M. W. Emmett-Oglesby. Psychoactive Drugs: Tolerance and Sensitization. Humana Press, 2013.

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6

Goudie, A. J., and M. W. Emmett-Oglesby. Psychoactive Drugs: Tolerance and Sensitization. Humana Press, 1989.

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7

Welechew, Edward. Treatment of pain in burns patients. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199234721.003.0009.

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Pain from burns has three components: background, breakthrough, and procedural pain. Central sensitization is an important component of the ongoing pain. Early management of pain, prior to the arrival at hospital is essential. Multimodal treatment including opiates will be necessary and psychological support is key. Procedural pain is of high intensity and short duration, and will require a combination of pharmacological and non-pharmacological methods of analgesia. Central sensitization and opiate tolerance are common problems in burns patients.

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8

Jarrell, John F. History of Gynecological Treatment of Women's Pelvic Pain and the Recent Emergence of Pain Sensitization. Elsevier Science & Technology, 2024.

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9

Jarrell, John F. History of Gynecological Treatment of Women's Pelvic Pain and the Recent Emergence of Pain Sensitization. Elsevier Science & Technology Books, 2024.

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10

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,

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11

Caballero-Manrique, Esther, and Carlos A. Pino. Head and Neck Cancer Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0026.

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In the United States, there are 48,000 new cases of head and neck cancer (HNC) annually. Although HNC used to be associated mainly with smoking and drinking, it is now found in many nonsmokers and nondrinkers in their 50s due to the spread of HPV. Pain is typically present at the time of diagnosis. Treatment usually includes radiation, chemotherapy, and/or surgery, which address the mass effect and pain. Yet, patients continue to experience pain during and after treatment, because the treatment modalities can cause significant inflammation and neuropathy and can lead to central sensitization.

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12

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 h

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13

Goudie, A. J., and M. W. Emmett-Oglesby. Psychoactive Drugs: Tolerance and Sensitization (Contemporary Neuroscience). Humana Press, 1989.

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14

Chang, Victor T. Visceral pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0134.

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Visceral pain is pain that arises from, in, or around internal organs. Common examples include chest pain and functional abdominal pain. In palliative medicine, well-known visceral pain syndromes include pain from pancreatic cancer and bowel obstruction. Recent advances have increased our understanding of the diagnostic challenges and therapeutic possibilities for patients with visceral pain syndromes. Understanding the basis of referred pain is a key component of patient assessment. The complexity of visceral nociception and pain signalling is being unravelled through anatomical, immunohistoc

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15

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

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16

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

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17

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 o

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18

Vlaeyen, Johan W. S. Learning and Conditioning in Chronic Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190627898.003.0004.

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This chapter highlights the ways that individuals learn to adapt to changes due to painful experiences. Learning is the observable change in behavior due to events in the internal and external environment, and it includes non-associative (habituation and sensitization) and associative learning (Pavlovian and operant conditioning). Once acquired, new knowledge representations remain stored in memory and may generalize to perceptually or functionally similar events. Moreover, these processes are not just a consequence of pain; they may also modulate the perception of pain. In contrast to the rap

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19

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 respond

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20

Qureshi, M. A., J. H. Gan, S. Kunnumpurath, et al. 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

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21

Colvin, Lesley A., and Marie T. Fallon. Pain physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0009.

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The International Association for the Study of Pain defines pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’. A good understanding of the physiology of pain processing is important, with recent advances in basic science, functional neuroimaging, and clinical pain syndromes contributing to our understanding. It is also important to differentiate between nociception, the process of detecting noxious stimuli, and pain perception, which is a much more complex process, integrating biological, psychologic

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22

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

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23

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

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24

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

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25

Tick, Heather, and Eric B. Schoomaker. Transforming Pain Management Through the Integration of Complementary and Conventional Care. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190241254.003.0021.

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This chapter discusses some of the assumptions behind the evolution of the current program of pain care and explores different strategies that could inform transformative changes to the system. It addresses the role of self-care, nutrition, mind-body strategies, and movement in improving function. The emerging scientific literature on neuroplasticity, central and peripheral sensitization, energy generation, and mitochondrial dysfunction, and the functional role of fascia is explored. Health providers in a transformed system will potentially work in more diverse settings, collaborate more broad

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26

McDougall, Jason J., and Joel A. Vilensky. The innervation of the joint and its role in osteoarthritis pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0007.

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Diarthrodial joints possess an extensive network of sensory and sympathetic nerve fibres whose physiological functions are varied and complex. Nerves are primarily located in the synovium but also innervate the subchondral bone, the outer third of menisci, and the superficial surface of tendons and ligaments. Large-diameter, myelinated neurons are involved in joint position sense while small-diameter neurons with thin or no myelin typically sense pain. The small-diameter nerves in conjunction with sympathetic fibres control synovial blood flow and maintain joint homeostasis. In patients with o

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27

Chang, Daniel, Mia Castro, Vineetha S. Ratnamma, Alessandra Verzelloni, Dionne Rudison, and Nalini Vadivelu. Preemptive, Preventive, and Multimodal Analgesia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0004.

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Preemptive analgesia focuses on postoperative pain control and the prevention of central sensitization and chronic neuropathic pain by providing analgesia administered preoperatively. Preventive analgesia reduces postoperative pain and consumption of analgesics, and this appears to be the most effective means of decreasing postoperative pain. Preventive analgesia, which includes multimodal preoperative and postoperative analgesic therapies, results in decreased postoperative pain and less postoperative consumption of analgesics. Several advances have been made in our understanding of pain sign

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28

Charlson, Robert W., and Matthew S. Robbins. Migraine and Other Headache Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0047.

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In recent years, the characterization of the neurobiology of migraine and other headache disorders has been driven by the search to better understand several key factors: genetics, the role of neuromodulators such as calcitonin gene-related peptide (CGRP), processes including central and peripheral sensitization, neurogenic inflammation, central pain networks, and areas of activation demonstrated by advancing functional neuroimaging techniques. Yet the ultimate causes of migraine remain unknown. Nonetheless, recent work has advanced our understanding of this complex disorder, and pointed towar

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29

Tullett, William. Smell in Eighteenth-Century England. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198844136.001.0001.

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In England during the period between the 1670s and the 1820s a transformation took place in how smell and the senses were viewed. This book traces that transformation. The role of smell in creating medical and scientific knowledge came under intense scrutiny and the equation of smell with disease was actively questioned. Yet a new interest in smell’s emotive and idiosyncratic dimensions offered odours a new power in the sociable spaces of eighteenth-century England. Using a wide range of sources from diaries, letters, and sanitary records to satirical prints, consumer objects, and magazines, W

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