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Article

Exercise is known to exert an influence on pain. Specifically, sensitivity to pain decreases both during and following a single bout of exercise—a phenomenon that has been termed exercise-induced hypoalgesia (EIH). EIH has been shown to occur following a variety of types of exercise including aerobic, dynamic resistance, as well as intermittent and continuous isometric exercise, and with a variety of types of pain stimuli including pressure, thermal, and electrical, among others. Depending upon the type of exercise, the intensity and duration of the exercise bout may affect the magnitude of EIH observed. EIH also may be influenced by presence of chronic pain. In individuals with chronic pain conditions, exercise can have both hypo- and hyperalgesic effects, again depending on the specifics of the exercise stimulus itself. The mechanisms underlying EIH have not been definitively established. However, a number of potentially viable mechanisms have been examined including: release of stress mediators such as adrenocorticotrophic hormone and growth hormone (GH), stimulation of the endogenous opioid system, interactions between the pain modulatory system and the cardiovascular system resulting from shared neurological pathways, activation of the endocannabinoid (eCB) system, and engagement of supraspinal pain inhibitory mechanisms via conditioned pain modulation (CPM). There is also some evidence that psychosocial factors, including pain-related beliefs like catastrophizing and expectation, may influence EIH. Research in EIH has several important implications for research and practice. In healthy adults, reduced sensitivity to pain is a salient benefit of exercise and EIH responses may play a role in exercise adherence. For chronic pain patients, research on EIH has the potential to uncover mechanisms related to maintenance of chronic pain. Improving our understanding of how and why hyperalgesia occurs following exercise in these patients can aid in understanding central nervous system mechanisms of disease maintenance and ultimately may help to avoid symptom exacerbation with exercise. However, there remain practical and mechanistic questions to be examined. Translating reductions in pain sensitivity that occur with exercise under controlled laboratory conditions to situations that are more naturalistic will be an important next step for promoting physical activity as a treatment for pain.

Article

Edgar T. Walters

Chronic pain lasting months or longer is very common, poorly treated, and sometimes devastating. Nociceptors are sensory neurons that usually are silent unless activated by tissue damage or inflammation. In humans their peripheral activation evokes conscious pain, and their spontaneous activity is highly correlated with spontaneous pain. Persistently hyperactive nociceptors mediate increased responses to normally painful stimuli (hyperalgesia) in chronic conditions and promote the sensitization of central pain pathways that allows low-threshold mechanoreceptors to elicit painful responses to innocuous stimuli (allodynia). Investigations of rodent models of neuropathic pain and hyperalgesic priming have revealed many alterations in nociceptors and associated cells that are implicated in the development and maintenance of chronic pain. These include chronic nociceptor hyperexcitability and spontaneous activity, sprouting, synaptic plasticity, changes in intracellular signaling, and modified responses to opioids, along with alterations in the expression and translation of thousands of genes in nociceptors and closely linked cells.

Article

Dayna L. Averitt, Rebecca S. Hornung, and Anne Z. Murphy

The modulatory influence of sex hormones on acute pain, chronic pain disorders, and pain management has been reported for over seven decades. The effect of hormones on pain is clearly evidenced by the multitude of chronic pain disorders that are more common in women, such as headache and migraine, temporomandibular joint disorder, irritable bowel syndrome, chronic pelvic pain, fibromyalgia, rheumatoid arthritis, and osteoarthritis. Several of these pain disorders also fluctuate in pain intensity over the menstrual cycle, including headache and migraine and temporomandibular joint disorder. The sex steroid hormones (estrogen, progesterone, and testosterone) as well as some peptide hormones (prolactin, oxytocin, and vasopressin) have been linked to pain by both clinical and preclinical research. Progesterone and testosterone are widely accepted as having protective effects against pain, while the literature on estrogen reports both exacerbation and attenuation of pain. Prolactin is reported to trigger pain, while oxytocin and vasopressin have analgesic properties in both sexes. Only in the last two decades have neuroscientists begun to unravel the complex anatomical and molecular mechanisms underlying the direct effects of sex hormones and mechanisms have been reported in both the central and peripheral nervous systems. Mechanisms include directly or indirectly targeting receptors and ion channels on sensory neurons, activating pain excitatory or pain inhibitory centers in the brain, and reducing inflammatory mediators. Despite recent progress, there remains significant controversy and challenges in the field and the seemingly pleiotropic role estrogen plays on pain remains ambiguous. Current knowledge of the effects of sex hormones on pain has led to the burgeoning of gender-based medicine, and gaining further insight will lead to much needed improvement in pain management in women.

Article

Tamar Makin and London Plasticity Lab

Phantom sensations are experienced by almost every person who has lost their hand in adulthood. This mysterious phenomenon spans the full range of bodily sensations, including the sense of touch, temperature, movement, and even the sense of wetness. For a majority of upper-limb amputees, these sensations will also be at times unpleasant, painful, and for some even excruciating to the point of debilitating, causing a serious clinical problem, termed phantom limb pain (PLP). Considering the sensory organs (the receptors in the skin, muscle or tendon) are physically missing, in order to understand the origins of phantom sensations and pain the potential causes must be studied at the level of the nervous system, and the brain in particular. This raises the question of what happens to a fully developed part of the brain that becomes functionally redundant (e.g. the sensorimotor hand area after arm amputation). Relatedly, what happens to the brain representation of a body part that becomes overused (e.g. the intact hand, on which most amputees heavily rely for completing daily tasks)? Classical studies in animals show that the brain territory in primary somatosensory cortex (S1) that was “freed up” due to input loss (hereafter deprivation) becomes activated by other body part representations, those neighboring the deprived cortex. If neural resources in the deprived hand area get redistributed to facilitate the representation of other body parts following amputation, how does this process relate to persistent phantom sensation arising from the amputated hand? Subsequent work in humans, mostly with noninvasive neuroimaging and brain stimulation techniques, have expanded on the initial observations of cortical remapping in two important ways. First, research with humans allows us to study the perceptual consequence of remapping, particularly with regards to phantom sensations and pain. Second, by considering the various compensatory strategies amputees adopt in order to account for their disability, including overuse of their intact hand and learning to use an artificial limb, use-dependent plasticity can also be studied in amputees, as well as its relationship to deprivation-triggered plasticity. Both of these topics are of great clinical value, as these could inform clinicians how to treat PLP, and how to facilitate rehabilitation and prosthesis usage in particular. Moreover, research in humans provides new insight into the role of remapping and persistent representation in facilitating (or hindering) the realization of emerging technologies for artificial limb devices, with special emphasis on the role of embodiment. Together, this research affords a more comprehensive outlook at the functional consequences of cortical remapping in amputees’ primary sensorimotor cortex.

Article

Pain  

Terry Altilio and Maris Pasquale Doran

Pain is a multidimensional, subjective experience that embodies the complex relationship of body, mind, emotions, and spirit. Assessment begins with the patient’s report and is enhanced by diagnostic tools, skilled inquiry and observation of behavioral, physical, cognitive and emotional responses. Pain may be acute, chronic, intermittent, or persistent and can be related to a chronic condition or progressive life-threatening illness—all of which may lead to significant psychological, spiritual, functional, and socioeconomic consequences. The undertreatment of pain is well documented and ubiquitous, especially in vulnerable populations, including the elderly, infants and children, and ethnic minorities. Inadequate management of pain has been the focus of national and international research and policy and relates to many variables, including the controversy and concerns about the use of opioids which are classified as controlled substances. This classification creates a unique environment of legislative, regulatory, and law enforcement scrutiny most recently exacerbated by the public health focus on the abuse of prescription medications. Pain is a clinical, ethical, policy, and advocacy issue. Advocating for state of the art pain management is a shared responsibility of professionals whose ethical codes include social justice, beneficence, and commitment to vulnerable populations.

Article

This article examines the way that the hurting body enhances, deepens, and informs religious experience. It begins by examining the contested category of religious experience, contrasting the essentialist with the constructivist approaches. Both are complicated by consideration of embodiment—specifically, of the body in pain. Two concrete cases of religious pain, or sharp discomfort, are discussed as illustrations of a qualitative approach to studying pain and religious experience. This method is evaluated against two examples of a quantitative method. The article concludes that a qualitative interpretation of the meaning, rather than the analysis of causes, of religious hurting are superior, within specified parameters. Finally, the qualitative method requires an exposition that takes the form of a narrative in which the researcher acts as a close observer–participant.

Article

Tipu Aziz and Holly Roy

Deep brain stimulation (DBS) is a neurosurgical technology that allows the manipulation of activity within specific brain regions through delivery of electrical stimulation via implanted electrodes. The growth of DBS has led to research around the development of novel interventions for a wide range of neurological and neuropsychiatric conditions, including Parkinson’s disease, dystonia, chronic pain, Tourette’s syndrome, treatment-resistant depression, anorexia nervosa, and Alzheimer’s disease. Some of these treatment approaches have a high level of efficacy as well as an established place in the clinical armamentarium for the diseases in question, such as DBS for movement disorders, including Parkinson’s disease. Other interventions are at a more developmental stage, such as DBS for depression and Alzheimer’s disease. Success both in clinical aspects of DBS and new innovations depends on a close-knit multidisciplinary team incorporating experts in the underlying condition (often neurologists and psychiatrists); neurosurgeons; nurse specialists, who may be involved in device programming and other aspects of patient care; and researchers including neuroscientists, imaging specialists, engineers, and signal analysts. Directly linked to the growth of DBS as a specialty is allied research around neural signals analysis and device development, which feed directly back into further clinical progress. The close links between clinical DBS and basic and translational research make it an exciting and fast-moving area of neuroscience.

Article

M. Aryana Bryan, Valerie Hruschak, Cory Dennis, Daniel Rosen, and Gerald Cochran

Opioid-related deaths by overdoses quadrupled in the United States from the years 1999 to 2015. This rise in mortality predominately occurred in the wake of historic changes in pain management practices and aggressive marketing of opioid medications such as oxycontin. Prescription opioid misuse and subsequent addiction spilled over to heroin and fentanyl for many. This drug epidemic differed from others in its impact among non-Hispanic whites, leading to drastic changes in how the United States views addiction and chooses to respond. This article offers an overview of opioid use disorder (OUD), its treatment and its relationship with pain. It also discusses special populations affected and provides insight into future directions for research and social work practice surrounding opioid management in the United States. Because of the profession’s emphasis on the person and social environment as well as its focus on vulnerable and oppressed populations, social work plays a critical role in addressing the crisis.

Article

Few practitioners or researchers in psychology would think of the 17th-century French philosopher, René Descartes, as the founding father of their discipline. Yet, it is difficult to see how psychology could have emerged as a discipline in its own right without the contributions of Descartes. Descartes’ theoretical and experimental contributions to our understanding of rationality, consciousness, sensation, feeling, attention, psychological self-regulation and voluntary action, and indeed the very concept of mind that lies at the heart of his philosophy, have been pivotal to the evolution of psychology since its emergence as a special science in the 19th-century. These contributions tend to get overshadowed by the unpalatable aspects of his dualism of mind and body and his denial of animal consciousness, doctrines for which he was and still is much pilloried. However, both doctrines are relevant to understanding how from its inception the subject matter and scope of psychological investigation was framed, for underlying the Cartesian concept of mind is not one dualism but two: a dualism of mind and body and a dualism of life and mind. The mind, for Descartes, could not be theorized on its own terms without conceiving of it at least to some extent independently of the physiological processes of the human body, on the one hand, and the life functions of biological organisms, on the other. Descartes’ legacy for psychology as a discipline is thus twofold. It created the conceptual space for the concept of mind to emerge as a threshold concept in its own right, distinct from the concept of matter that defined mechanics, and it demarcated those uniquely human capacities that enabled psychology to differentiate itself from the newly emerging evolutionary biology of the 19th-century, even though it would remain more closely aligned with biology than physics thenceforth. Without both dualisms of mind and body and life and mind, it is difficult to envisage how psychology as a special science distinct from anatomy and the life sciences could have emerged, and for this the discipline of psychology owes Monsieur Descartes a considerable debt.

Article

Taylor Follansbee, Mirela Iodi Carstens, and E. Carstens

Pain is defined as “An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage,” while itch can be defined as “an unpleasant sensation that evokes the desire to scratch.” These sensations are normally elicited by noxious or pruritic stimuli that excite peripheral sensory neurons connected to spinal circuits and ascending pathways involved in sensory discrimination, emotional aversiveness, and respective motor responses. Specialized molecular receptors expressed by cutaneous nerve endings transduce stimuli into action potentials conducted by C- and Aδ-fiber nociceptors and pruriceptors into the outer lamina of the dorsal horn of the spinal cord. Here, neurons selectively activated by nociceptors, or by convergent input from nociceptors, pruriceptors, and often mechanoreceptors, transmit signals to ascending spinothalamic and spinoparabrachial pathways. The spinal circuitry for itch requires interneurons expressing gastrin-releasing peptide and its receptor, while spinal pain circuitry involves other excitatory neuropeptides; both itch and pain are transmitted by ascending pathways that express the receptor for substance P. Spinal itch- and pain-transmitting circuitry is segmentally modulated by inhibitory interneurons expressing dynorphin, GABA, and glycine, which mediate the antinociceptive and antipruritic effects of noxious counterstimulation. Spinal circuits are also under descending modulation from the brainstem rostral ventromedial medulla. Opioids like morphine inhibit spinal pain-transmitting circuits segmentally and via descending inhibitory pathways, while having the opposite effect on itch. The supraspinal targets of ascending pain and itch pathways exhibit extensive overlap and include the somatosensory thalamus, parabrachial nucleus, amygdala, periaqueductal gray, and somatosensory, anterior cingulate, insular, and supplementary motor cortical areas. Following tissue injury, enhanced pain is evoked near the injury (primary hyperalgesia) due to release of inflammatory mediators that sensitize nociceptors. Within a larger surrounding area of secondary hyperalgesia, innocuous mechanical stimuli elicit pain (allodynia) due to central sensitization of pain pathways. Pruriceptors can also become sensitized in pathophysiological conditions, such as dermatitis. Under chronic itch conditions, low-threshold tactile stimulation can elicit itch (alloknesis), presumably due to central sensitization of itch pathways, although this has not been extensively studied. There is considerable overlap in pain- and itch-signaling pathways and it remains unclear how these sensations are discriminated. Specificity theory states that itch and pain are separate sensations with their own distinct pathways (“labeled lines”). Selectivity theory is similar but incorporates the observation that pruriceptive neurons are also excited by algogenic stimuli that inhibit spinal itch transmission. In contrast, intensity theory states that itch is signaled by low firing rates, and pain by high firing rates, in a common sensory pathway. Finally, the spatial contrast theory proposes that itch is elicited by focal activation of a few nociceptors while activation of more nociceptors over a larger area elicits pain. There is evidence supporting each theory, and it remains to be determined how the nervous system distinguishes between pain and itch.

Article

Ashley van Niekerk

A burn occurs when cells in the skin or other tissues are destroyed by hot liquids (scalds), hot solids (contact burns), or flames (flame burns). Injuries to the skin or other organic tissue due to radiation, radioactivity, electricity, friction or contact with chemicals are also identified as burns. Globally, burns have been in decline, but are still a major cause of injury, disability, death and disruption in some regions, with about 120,000 deaths and 9 million injuries estimated in 2017. Low-to-middle-income countries carry the bulk of this burden with the majority of all burn injuries occurring in the African and Southeast Asia regions. Thermal injuries are physically painful and may leave disabling scars not only to the skin or the body, but also impair psychological wellbeing. Severe injuries often impose significant psychological, but also educational consequences and social stigmatization, with the consequent adjustments exacerbated by a range of factors, including the circumstances of the burn incident, the severity and site of the injury, the qualities of the affected individual’s personality, and the access to supportive interpersonal and social relationships. The contributions of: economic progress, enhanced environmental and home structures, energy technology, and safety education interventions have been reported as significant for burn prevention. Similarly, legislative and policy frameworks that support access to modern energies such as electricity, govern domestic appliances and heating technology, and control storage and decanting of fossil fuels are important in energy impoverished settings. The recovery of burn survivors is affected by the availability of specialized treatment, physical rehabilitation and psychosocial support to burn victims and families, but which is still limited especially in resource constrained settings.

Article

Understanding of the various types of plasticity that occur in the spinal cord, as well as understanding of spinal cord functions, has vastly improved over the past 50 years, mainly due to an increase in the number of research studies and review articles on the subject. It is now understood that the spinal cord is not merely a passive conduit of neural impulses. Instead, the spinal cord can independently execute complex functions. Numerous experimental approaches have been utilized for more targeted exploration of spinal cord functions. For example, isolating the spinal cord from supraspinal influences has been used to demonstrate that simple forms of learning can be performed by spinal neuronal networks. Moreover, reduced preparations, such as acute spinal cord slices, have been used to show that spinal neurons undergo different types of modulation, including activity-dependent synaptic modification. Most spinal cord processes, ranging from integration of incoming sensory input to execution of locomotor outputs, involve plasticity. Nociceptive processing that leads to pain and spinal learning is an example of plasticity that is well-studied in the spinal cord. At the neural level, both processes involve an interplay of cellular mediators, which include glutamate receptors, protein kinases, and growth factors. The neurotrophin brain-derived neurotrophic factor (BDNF) has also been implicated in these processes, specifically as a promoter of both pro-nociception and spinal learning mechanisms. Interestingly, the role of BDNF in mediating spinal plasticity can be altered by injury. The literature spanning approximately 5 decades is reviewed and the role of BDNF is discussed in mediating cellular plasticity underlying pain processing and learning within the spinal cord.

Article

Utilitarianism is inextricably linked to international ethics. The roots of the principle of utility can be traced to the 18th and 19th centuries, when it was employed by thinkers such as David Hume. However, Jeremy Bentham first formulated utilitarianism in detail and carefully studied its implications. According to Bentham, happiness is a condition in which an individual enjoys more pleasure than pain. Because utilitarianism is focused on the welfare of the individual, state boundaries are of little consequence. Its reach is inherently global. There are different varieties of utilitarianism. What sets them apart from other ethical theories is their stipulation that whatever is of value should be maximized for all and whatever of disvalue should be minimized for all. For Bentham, pleasure is the ultimate value. Later, John Stuart Mill distinguished between higher and lower pleasures and argued that higher pleasures should be given greater weight. In the 20th century, authors such as R. M. Hare determined that maximal satisfaction of preferences is the value to be sought. The utilitarian emphasis on maximization of value and its choice of values have generated much criticism from those who espoused human rights theories, such as John Rawls and those influenced by his work. At present, the scholarly literature dealing with issues related to international ethics mostly comes from those who are committed to human rights theory or who are committed to equality of outcomes for human beings.

Article

Much progress has been made in unraveling the mechanisms that underlie the transition from acute to chronic pain. Traditional beliefs are being replaced by novel, more powerful concepts that consider the mutual interplay of neuronal and non-neuronal cells in the nervous system during the pathogenesis of chronic pain. The new focus is on the role of neuroinflammation for neuroplasticity in nociceptive pathways and for the generation, amplification, and mislocation of pain. The latest insights are reviewed here and provide a basis for understanding the interdependence of chronic pain and its comorbidities. The new concepts will guide the search for future therapies to prevent and reverse chronic pain. Long-term changes in the properties and functions of nerve cells, including changes in synaptic strength, membrane excitability, and the effects of inhibitory neurotransmitters, can result from a wide variety of conditions. In the nociceptive system, painful stimuli, peripheral inflammation, nerve injuries, the use of or withdrawal from opioids—all can lead to enhanced pain sensitivity, to the generation of pain, and/or to the spread of pain to unaffected sites of the body. Non-neuronal cells, especially microglia and astrocytes, contribute to changes in nociceptive processing. Recent studies revealed not only that glial cells support neuroplasticity but also that their activation can trigger long-term changes in the nociceptive system.

Article

Robert Fuller

The relationship between religion and the body can be viewed from two very different perspectives. The first perspective emphasizes culture’s role in constructing human thought and behavior. This approach illuminates the diverse ways that religious traditions shape human attitudes toward the nature and meaning of their physical bodies. Scholars guided by this perspective have helped us better understand religion’s complicity in such otherwise mysterious phenomena as mandated celibacy, restrictive diets, circumcision, genital mutilation, self-flagellation, or the specification of particular forms of clothing. Newly emerging information about the biological body has given rise to a second approach to the body’s relationship to religion. Rather than exploring how religion influences attitudes toward our bodies, these new studies investigate how our biological bodies exert identifiable influences on our religious thoughts, feelings, and behaviors. Neural chemistry, emotions, sensory modalities, pain responses, mating strategies, sexual arousal systems, and genetic personality predispositions all influence the personal salience of religious beliefs or behavior. Attention to the biological body unravels many of the enigmas that formerly accompanied the study of such things as the appeal of apocalyptic beliefs, the frequent connection between religion and systems of healing, devotional piety aiming toward union with a beloved deity, the specific practices entailed in ascetic spirituality, or the mechanisms triggering ecstatic emotional states.

Article

The traditional view of central nervous system function presumed that learning is the province of the brain. From this perspective, the spinal cord functions primarily as a conduit for incoming/outgoing neural impulses, capable of organizing simple reflexes but incapable of learning. Research has challenged this view, demonstrating that neurons within the spinal cord, isolated from the brain by means of a spinal cut (transection), can encode environmental relations and that this experience can have a lasting effect on function. The exploration of this issue has been informed by work in the learning literature that establishes the behavioral criteria and work within the pain literature that has shed light on the underlying neurobiological mechanisms. Studies have shown that spinal systems can exhibit single stimulus learning (habituation and sensitization) and are sensitive to both stimulus–stimulus (Pavlovian) and response–outcome (instrumental) relations. Regular environmental relations can both bring about an alteration in the performance of a spinally mediated response and impact the capacity to learn in future situations. The latter represents a form of behavioral metaplasticity. At the neurobiological level, neurons within the central gray matter of the spinal cord induce lasting alterations by engaging the NMDA receptor and signal pathways implicated in brain-dependent learning and memory. Of particular clinical importance, uncontrollable/unpredictable pain (nociceptive) input can induce a form of neural over-excitation within the dorsal horn (central sensitization) that impairs adaptive learning. Pain input after a contusion injury can increase tissue loss and undermines long-term recovery.