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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 can extend or generalize to other body parts or modalities. The evidence for stress and sensitization as consequences of or as contributors to chronic pain is reviewed, and possible underlying mechanisms are discussed. Next, strategies to reduce stress and sensitization and foster desensitization processes are described. The chapter concludes by introducing a motivational account of chronic pain informed by the stress and sensitization literature.
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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 mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.
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 disease stage. These include modification of synaptic strength, inhibitory tone, and membrane excitability and often involve components of neuroinflammation. It is thus recommended to avoid using the phrase ‘central sensitization’ in the scientific literature all together and replace it with unambiguous technical terms such as ‘CNS mechanisms of pain hypersensitivity’ or with the specific mechanism(s) and CNS location(s) in mind.
4
Goudie, A. J., and M. W. Emmett-Oglesby. Psychoactive Drugs: Tolerance and Sensitization. Humana Press, 2013.
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5
Goudie, A. J., and M. W. Emmett-Oglesby. Psychoactive Drugs: Tolerance and Sensitization. Humana Press, 1989.
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6
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.
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.
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, 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.
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. Painful mucositis is a complication of chemotherapy and radiation treatment; it can become severe, impacting patients’ ability to speak and eat, and sometimes limiting treatment. Pain treatment for HNC is multimodal, and includes preemptive approaches to prevent neuropathy and central sensitization with antiepileptics, such as gabapentin and pregabalin. Mucositis pain is treated using a stepwise protocol.
12
Goudie, A. J., and M. W. Emmett-Oglesby. Psychoactive Drugs: Tolerance and Sensitization (Contemporary Neuroscience). Humana Press, 1989.
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13
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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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, immunohistochemical, and functional studies. On a molecular level, families of receptors and signalling proteins have now been described that will lead to a future with innovative therapies. This knowledge has developed within the paradigms of pain pathways, peripheral activation and peripheral and central sensitization, thereby linking and distinguishing visceral pain from somatic and neuropathic pain. Treatment options for visceral pain in palliative care encompass a wide variety of medical, interventional, and psychological approaches. With appropriate diagnostic measures and careful consideration of therapeutic options, most patients can achieve satisfactory relief.
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 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.
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 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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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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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 rapid acquisition of learned responses, their extinction is slow, fragile, and context-dependent, and it only occurs through inhibitory processes. The chapter reviews features of associative forms of learning in humans that contribute to pain, pain-related distress, and disability. It concludes with a discussion of promising future directions.
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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.
20
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).
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, psychological, and social factors. The somatosensory nervous system, from peripheral nociceptors, to sensory nerves and spinal cord synapses has many potential sites for modulation, with ascending pathways to the brain, balanced by ‘top-down’ control from higher centres. Under certain circumstances, for example, after tissue injury from trauma or surgery, there will be continued nociceptive input, with resultant changes in the whole somatosensory nervous system that lead to development of chronic pain syndromes. In such cases, even when the original injury has healed, the pathophysiological changes in the nervous system itself lead to ongoing pain, with peripheral or central sensitization, or both. Additionally, in some chronic pain syndromes, for example, chronic widespread pain, it has been postulated that abnormalities in central processing may be the initiating factor, with some evidence for this from neuroimaging studies. Further work is needed to fully understand pain neurobiology in order to advance our management.
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 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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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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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.
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 broadly, and engage patients in conversations driven by patient priorities and emerging evidence-based modalities. The Veterans Health Administration and the Military Health System, acting on alarming increases in the incidence of chronic pain and associated comorbidities, have become the early adopters of transformative policies. Since pain is the most common cause for a healthcare visit, this chapter should be of interest to all healthcare providers, complementary, integrative, and conventional.
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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 osteoarthritis (OA), the sensory nerves become sensitized and increase their firing rate in response to normal movement. This peripheral sensitization is mediated by numerous algogenic agents released into the OA knee including neuropeptides, eicosanoids, and proteinases. A portion of joint afferents fire in the absence of mechanical stimuli and encode pain at rest. Interestingly, the firing rate of joint afferents does not correlate with OA severity, indicating that pain is a poor predictor of joint pathology. Evidence is accumulating to suggest that a subpopulation of OA patients who are unresponsive to classical non-steroidal anti-inflammatory drugs may be suffering from neuropathic pain in which there is damage to the joint nerves themselves. Better understanding of the biology of joint nerves could help in the development of patient-targeted therapies to alleviate OA pain and inflammation.
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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 signaling pathways, which have since enabled caregivers to treat pain using a multimodal (or “balanced”) approach to providing adequate pain relief while minimizing side effects. This allows for a reduction in the doses of individual drugs and thus a lower incidence of adverse effects from any particular medication used for analgesia.
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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 toward a future where these modalities may provide an integrated understanding of its pathophysiology and provide specific treatment targets.
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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, William Tullett traces how individuals and communities perceived the smells around them. From paint and perfume to onions and farts, this book highlights the smells that were good for eighteenth-century writers to think with. In doing so, the study challenges a popular, influential, and often cited narrative. Smell in Eighteenth-Century England is not a tale of the medicalization and deodorization of English olfactory culture. Instead, the book demonstrates that it was a new recognition of smell’s asocial-sociability, its capacity to create atmospheres of uncomfortable intimacy, that transformed the relationship between the senses and society. To trace this shift, the book also breaks new methodological ground. Smell in Eighteenth-Century England makes the case for new ways of thinking about the history of the senses, experience, and the body. Understanding the way past peoples perceived their world involves tracing processes of habituation, sensitization, and attention. These processes help explain which odours entered the archive and why they did so. They force us to recognise that the past was, for those who lived there, not just a place of unmitigated stench