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Compared to other systems, little is known about the mechanisms of placebo and placebo-related effects in both the cardiovascular and the respiratory system. Side effects in placebo groups of cardiovascular clinical trials are common and might represent the basis of nocebo effects. Heart activity can be conditioned and can also be affected during a placebo analgesic response by the activation of the endogenous opioid systems. Not only may placebo-activated endogenous opioids act on pain transmission and the heart, but on the respiratory centres as well, inducing respiratory depression. Other conditions, like asthma and cough, are powerfully affected by placebos, but the underlying mechanisms are virtually unknown.

This chapter summarizes studies examining the link between drugs of abuse and the behavioral neurobiology of aggressive behavior in animal models. It considers studies examining how drug abuse affects the aggressive response patterns of animals, as well as the development, activity, and function of neural systems implicated in aggression control. It shows that the effects of many commonly abused drugs, illegal and prescribed, on aggression are dependent upon the sex and species of the animal, the dosing and treatment regimen, and the behavioral testing paradigm. Although very few drugs, or drug classes, have been shown to consistently influence aggressive behavior regardless of the aforementioned factors (i.e., species, age, sex, dosing, testing paradigm), there are notable exceptions, including some anabolic androgenic steroids (AAS), nicotine, 3,4-methylenedioxymethamphetamine (MDMA), and mescaline. The administration of various types of AAS has consistently increased aggression in various animal species of varying ages regardless of experimental paradigm, whereas nicotine, MDMA, and mescaline have been shown to consistently decrease aggressive responding.

This chapter discusses opioid-induced pruritus, a common and adverse effect of spinal opioid administration. It discusses pruritus caused by spinal and systemic opioids. The first half focuses on the pathogenesis and treatment of pruritus caused by spinal opioids. The second half centres on the treatment and pathogenesis of pruritus caused by systemic opioids.

When dealing with respiratory symptoms, this chapter suggests that one must not panic. Breathing symptoms are frightening for everyone. Mostly, one has more time than he thinks, and symptoms tend to respond well to treatment. One should hope for the best and prepare for the worst: There are two life-threatening situations in this area: acute airway obstruction and massive haemoptysis. Both need forward planning to ensure that, if they happen, the team can be calm, efficient and effective. They should have rapid access to drugs to enable rapid and complete sedation. Non-pharmacological methods are very effective. Meanwhile, the most distressing respiratory symptoms usually respond to low dose opioids and/or benzodiazepines.

This chapter provides a formulary for children's palliative care (CPC) in Africa. It discusses notes on drug treatment in children; principles of effective morphine prescribing; equivalent dose of opioids; children's palliative care (CPC) formulary; and formula for making oral morphine from powder.

This chapter examines the use of analgesics for the control of terminal pain. Though there is no need to resort automatically to strong analgesics when a patient approaches the terminal stages of his illness, pain must be relieved as soon as it becomes a matter of complaint. The criteria for giving analgesia, particularly opioids, should be the presence of pain and not the expected length of life. The chapter provides recommended treatment for different levels of terminal pain.

Opioids, which have long been abused, are capable of producing euphoria and other “positive” subjective effects. Although the relationship between positive subjective effects and abuse of a drug is not necessarily causal, there is a predictive relationship between those drugs that produce a positive spectrum of subjective effects and their likelihood of functioning as reinforcers and being abused. A host of factors influence the subjective effects of opioids (and subsequently their abuse liability); some of the more salient ones are covered in this chapter. It first describes how subjective effects of opioids are measured and then discusses how such factors as dose, route of administration, rate of onset of drug effects, tolerance and dependence, and drug use history can all influence an opioid's subjective effects.

This chapter discusses the pharmacological management of breathlessness. Opioids have demonstrated benefit without documented respiratory toxicity. Several psychotropic agents and nebulized furosemide have sufficient promise to warrant rigorous prospective studies. Ultimately, reducing the frightening sensation of breathlessness is something that can be achieved predictably with medications currently available.

This chapter presents a case study to illustrate the desired skills, attitudes, and knowledge required for pain assessment and management. It examines several questions such as: How to assess the patient's pain? How to choose the most appropriate treatment regimen for the patient's pain syndromes? How to initiate an oral opioid? What is incident pain and how to manage it?

This chapter discusses reflex autonomic regulation of the cardiovascular system by input from finely myelinated and unmyelinated sensory nerve fibers. The focus is on abdominal and cardiac visceral afferent activation during ischemia, somatic afferent stimulation with exercise and interactions between both afferent systems during electroacupuncture. Important mechanical and chemical stimuli are identified as well as interactions between chemical stimuli, that together provide input to cardiovascular regions in the central nervous system that process this information. For example, acupuncture-evoked modulation of visceral sympathoexcitatory reflex activity is processed in the spinal cord and hypothalamus [arcuate nucleus], midbrain [ventrolateral periaqueductal gray], and medulla [raphé nuclei and rostral ventrolateral medulla (RVLM)]. Both excitatory and inhibitory neurotransmitters, including among others, glutamate, opioids, endocannabinoids, GABA, nociceptin, and serotonin, are involved. The role of individual neurotransmitters varies by nucleus, but in concert they modulate reflex increases in blood pressure through their action on presympathetic RVLM neurons.

This chapter discusses pharmacological strategies to alleviate dyspnoea or breathlessness in patients with advanced disease. Although significant improvements have been made in the administration of pharmacological approaches in terminally ill patients suffering from dyspnoea, careful considerations should be made. In easing symptomatic breathlessness, considerations on the validity and generalizability of pharmacotherapy should be discussed and considered. This is because the palliative population is composed of heterogeneous people with various clinical situations, breathlessness problems, and responses to therapy. The main concern of the chapter is breathlessness that is refractory. Discussed in it are: the clinical data and functions of opioids in managing dyspnoea; the functions of other opioids and other medications such as indomethacin, inhaled local anaesthetics, theophylline, and buspirone; and other clinical causes of dyspnoea.

This chapter examines chronic pain. Pain starts as a symptom—associated, for example, with arthritis or neuropathy—and, for one in five Americans, this symptom becomes “chronic,” that is, it lasts for weeks, or months, or even years. Chronic pain has its own reliable neurobiology and its own brain activation signature—although it cannot be localized in any specific “pain area” like other sensory perceptions, such as smell or sight. Still, pain changes the brain’s structure, its neuronal configurations. Moreover, pain’s significance in a person’s life is highly individualized. The experience of chronic pain can be altered by mood, sleep quality, distraction, suggestion, or even anticipation of new pain. This implies that pain may be exacerbated by social conditions—by violence, by anxiety. Living in poverty, for example, increases the odds of living with chronic pain. Although pain is real, it is still doubted and disputed. In the legal system, it is the subject of arguments over payment for disability claims and personal injury suits. The lack of an objective measure of pain means that some who might deserve compensation miss out because they cannot “prove” their discomfort. Assessing and treating pain, recognizing the pain of others, coping with its presence, and limiting its ruinous effects without misusing opioids or taking one’s own life remain central tests of people’s empathy and their efforts to promote health.

This chapter focuses on the opioid crisis. There has been substantial attention devoted—appropriately—to this issue. However, there are three areas that receive far less attention than they should. First, while opioids have attracted most of the headlines, two other drugs are being misused in America at newly alarming rates, their rise paralleling that of opioids. These are cocaine and its prescription-based stimulant cousins, such as Adderall and Ritalin. Then there is the issue of who is affected by opioids. This opioid crisis has presented countless news stories about the toll on white, middle-class, suburban, and rural users. While there have indeed been dramatic increases in opioid deaths in these groups, the opioid-related deaths of black Americans have doubled in the past 15 years. Thus, people must remind themselves that this is not just a white epidemic. Finally, because access to treatment for opioid addiction remains fragile, with national treatment rates low, people should keep in mind that Medicaid remains a key source of coverage for many people who use drugs. As Americans shore up a treatment system for opioid, cocaine, and stimulant misuse that has been woefully inadequate, threats to Medicaid’s structure and funding need ongoing attention, or the consequences of drug use will continue to grow.

This chapter addresses the pharmaceutical industry’s direct-to-physician marketing of opioids, a factor that has fueled the current addiction epidemic. A 2019 study sought to understand the relationship between mortality from opioid overdose and the pharmaceutical industry’s direct marketing of opioids to physicians. The study analyzed the association between three factors in every US county: the amount of marketing payments pharmaceutical companies made to physicians, opioid prescribing rates, and the number of overdose deaths. Researchers found that direct marketing of opioids to physicians was associated with increased opioid prescribing rates and increased overdose mortality 1 year after marketing engagements. As such, the national response to the opioid epidemic has focused in part on reducing the number of opioids prescribed by physicians. Additionally, the Physician Payments Sunshine Act promotes financial transparency between pharmaceutical companies and health care providers. By increasing regulation around pharmaceutical direct-to-physician marketing, and by making reports of pharmaceutical company payments to physicians available to the public, states have the potential to reduce overdose mortality.

This chapter focuses on the management of pain, particularly neuropathic pain. Pain is experienced approximately by 75 per cent of cancer patients with advanced-stage disease. The neuropathic mechanisms are generally involved in almost 40 per cent of cancer pain syndromes. These pains are either disease or treatment related. In patients with metastatic solid tumours, neuropathic pain is generally disease related, while in patients with haematological malignancies, overall pain is less; however, neuropathic pain is prevalent in these patients. Neuropathic pain is a challenging symptom to many healthcare professionals. Although it may respond to opioids, it is less responsive to such treatment compared to other pain caused by pathophysiologies. In patients with haematological malignancies, management of neuropathic pain is more difficult, as non-steroidal anti-inflammatory drugs and intra-spinal catheters are problematic in these populations. Drugs discussed in the chapter that may be an alternative to opiods and which may alleviate neuropathic pain that is unresponsive to opiods include: adjuvant analgesics, corticosteroids, anti-convulsants, anti-depressants, local anaesthetics, and N-methyl-D-aspartate (NMDA) receptor antagonists. Other alternatives included herein are: topical analgesics therapies, intra-spinal therapies, and neural blockade.

This chapter examines dyspnoea associated with amyotrophic lateral sclerosis (AML). It explains that dyspnoea is a common symptom in motor neurone diseases. Opioids have been found effective in reducing the distress of dyspnoea but non-pharmacological measures can also relieve symptoms in many cases. Non-invasive ventilation may also be considered for some patients but careful discussion with patient and family is essential.

This chapter examines different types of drugs used in the management of dyspnoea. It describes palliative drug therapies that are usually turned to when disease-orientated strategies are exhausted. The chapter explains that appropriate management of breathlessness requires the careful and individualised use of both non-drug and drug measures and suggests that nebulised opioids should not be considered part of standard practice, and that corticosteroids should only be used for a specific reason. Benzodiazepines and opioids are the main classes of drugs used in the palliation of breathlessness.

This chapter introduces narcotics that have been derived from chemical compounds in poppies and part of the American pharmacopeia since the early nineteenth century. It talks about the United States' first opiate-addiction epidemic that developed in the context of an extensively unregulated market for new compounds, which physicians prescribed for ailments from menstrual cramps to the common cold. It also references how researchers synthesized new opioids, such as hydrocodone and oxycodone, with the expectation that these new molecules would prove less habit-forming as federal and state governments cracked down on the runaway market in the early 1900s. The chapter recounts the production of Percocet and Vicodin in the 1970s by combining semisynthetic opiates with acetaminophen, which was considered an elusive quest for a non-addictive painkiller. It mentions how the norm started to shift in the 1980s and 1990s, wherein pain was increasingly described not only as a symptom but as an illness in itself.

This chapter reviews clinical studies of naltrexone in alcoholism and pharmacogenetic studies of naltrexone clinical trials for alcohol addiction. There is growing interest in the association between μ-opioid receptors and addiction. Extensive data, across species, suggest that the 118G form of the μ-opioid receptor is characterized by decreased transcription and translation. Murine, primate, and human laboratory studies show that the 118G (or its species-specific homologue) variant permits alcohol to have a greater rewarding valence, leading to increased alcohol consumption. The human and rhesus data are equally convincing that naltrexone is able to blunt this greater rewarding signal.