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Most of the knowledge about the neurobiological mechanisms of the placebo effect comes from the field of pain and analgesia. Expectation of pain reduction plays a crucial role in placebo analgesia, and this is shown by the reduced effectiveness of painkillers when administered covertly, i.e., unexpectedly. The placebo analgesic effect is mediated by the endogenous opioid systems and antagonized by cholecystokinin in some circumstances. Many brain imaging studies indicate that several areas are involved in placebo analgesia, e.g., those involved in dopaminergic reward mechanisms. The nocebo hyperalgesic effect is mediated by anxiety which activates a cholecystokinin system that, in turn, facilitates pain transmission. The endogenous pain modulatory descending circuits represent the biological substrate for the action of placebos on pain.

This chapter shows that analgesia evoked from the periaqueductal grey matter (PAG) is best viewed as a component of one or more complex adaptive emotional coping responses. The PAG is organized functionally into four longitudinal columns of neurons. Two distinct forms of analgesia arise from activation specifically of the dorsolateral/lateral PAG columns or the ventrolateral PAG column. A long-acting, opioid-mediated analgesia is a component of a vlPAG-mediated passive coping or conservation-withdrawal reaction that promotes recovery and healing, typically as a response to extreme, inescapable physical stress, including traumatic injury. In contrast, a short-acting, non-opioid-mediated analgesia represents a component of a dlPAG- or lPAG-mediated active coping or defensive reaction to an escapable threat or stress, including acute pain. Anatomical data indicate that each PAG column lies embedded within a distinct forebrain circuit that includes select medial and orbital PFC, hypothalamic and amygdaloid areas.

This chapter discusses the basic mechanisms of pain transmission and analgesia, and shows that hyperexcitability can be set up both peripherally and centrally. The latter means that minor peripheral inputs may cause severe pain. The impact of peripheral changes after nerve injury on systems at many levels of the central nervous system are discussed.

Error correction has played an important role in the development of theories of Pavlovian conditioning, and it continues to be a central force driving research on the processes underlying learning and memory. This chapter highlights some of the key aspects of error correction—from the original groundwork that helped formulate the way we think about error correction to recent work looking at some of the physiological mechanisms that comprise error correction. In particular, this chapter focuses on the perceptual-defensive-recuperative and negative-feedback models for Pavlovian conditioning, as well as the role of conditional analgesia, attention, and dopamine in error-correction-based processes. This chapter discusses specific applications of error-correction principles in conditioning, but this chapter also tries to stress a comprehensive role for error correction, particularly in the selection of appropriate brain circuits for specific functions.

This chapter discusses electrical stimulation techniques, which include acupuncture and transcutaneous electrical nerve stimulation (TENS). The administration techniques, contraindications, and possible effects of these electrical stimulation techniques are also presented. These techniques are used to provide analgesia in various forms, and have been used by medical practitioners for centuries.

Chapter Three surveys narrative techniques for rejecting pain as a locus of meaning in martyrdom. A number of texts explicitly deny the experience of pain altogether by employing the language of analgesia or anesthesia in their descriptions of the martyrs’ experiences of torture; other texts employ typical terms for pain but negate them; some narratives differentiate the experiences of the martyrs’ bodies from those of their spirits. Often texts attribute Christian impassibility to the presence and support of the divine. Finally, many texts thwart the audience’s visual imagination by preparing listeners to envision a grotesque murder, but then unexpectedly describing, instead, a beautiful body unharmed by torture. In these stories, torture does not harm Christians but, rather, it heals them.

A 56-year-old man was receiving palliative chemotherapy with cisplatin and pemetrexed for right-sided malignant mesothelioma. He presented to the emergency department with worsening right-sided chest pain. The pain was 8/10 in severity and on further questioning there was a sensation of burning associated with it. A chest X-ray showed thickening of the pleura in the right hemithorax consistent with the known diagnosis of mesothelioma. He was taking two tablets of co-codamol 30/500 every six hours to relieve the pain. His eGFR was 90 mL/min.

This chapter presents a brief history of the use of methadone for analgesia and discusses the need for universal access to methadone for pain management where appropriate. The mechanisms of action, side-effects, drug interactions, and special considerations that are different to other opioids are discussed, with particular attention to QT interval prolongation and cytochrome P450 enzyme metabolism. Methods of methadone initiation and switching are described and compared. Use of non-oral routes of administration are presented for use in patients in whom the oral route is not possible.

This chapter explores the use of interventional analgesic modalities for the treatment of pain related to visceral tumours. Using case studies, it reviews the underlying mechanisms responsible for the pain, as well as the role of coeliac plexus neurolysis (CPN) in the management of pain related to upper gastrointestinal malignancies. The chapter also reviews the use of neuraxial techniques, both epidural and intrathecal, in the management of cancer pain, including the relevant anatomy and the pharmacokinetics of commonly used medications, as well as the clinical considerations in deciding when and how to initiate a patient on neuraxial medications. Indications and contraindications to, as well as logistic and financial considerations for interventional techniques are discussed.

Most of the knowledge about the neurobiological mechanisms of the placebo effect comes from the field of pain and analgesia. Expectation of pain reduction plays a crucial role in placebo analgesia, and this is shown by the reduced effectiveness of painkillers when administered covertly, i.e., unexpectedly. The placebo analgesic effect is mediated by the endogenous opioid and endocannabinoid systems and antagonized by cholecystokinin in some circumstances. Many brain imaging studies indicate that several areas are involved in placebo analgesia, e.g., those involved in dopaminergic reward mechanisms. The nocebo hyperalgesic effect is mediated by anxiety which activates a cholecystokinin system that, in turn, facilitates pain transmission. The endogenous pain modulatory descending circuits represent the biological substrate for the action of placebos on pain.

This chapter is dedicated to pain and analgesia, the area where most of the knowledge about the mechanisms of the placebo effect comes from. Expectation of pain reduction plays a crucial role in placebo analgesia. The placebo analgesic effect is mediated by the endogenous opioid systems and antagonized by cholecystokinin (CCK) in some circumstances. In other conditions, the endocannabinoid system is involved. Many brain imaging studies indicate that several areas are involved in placebo analgesia, including the dorsolateral prefrontal cortex and those regions involved in dopaminergic reward mechanisms. The prefrontal lobes are fundamental for a placebo response to occur: if there is no prefrontal control, there is no placebo response. The nocebo hyperalgesic effect is mediated by anxiety, which activates a CCK system that, in turn, facilitates pain transmission. The endogenous pain modulatory descending circuits represent the biological substrate for the action of placebos on pain.

This chapter addresses all preclinical evidence supporting the potential of phytocannabinoids for the treatment of pain. Findings are reviewed with an emphasis on chronic pain since it is still often refractory to conventional pharmacotherapies and since there is mounting evidence that phytocannabinoids may be more efficacious in the treatment of chronic pain conditions rather than acute pain. The aim is to provide a summative review not only of the antinociceptive efficacy of the main phytocannabinoids when given alone but also of the preclinical data now available on these agents when they are administered in combination. In fact emerging evidence highlights greater beneficial effects of whole cannabis extracts than of single components of these extracts, justifying further exploration both of the therapeutic potential of cannabis-based medicines and of pharmacological interactions between some of its constituents. Finally, the molecular mechanisms that could explain phytocannabinoids-induced relief of chronic pain are fully discussed.

We will consider just two drugs in this chapter. They are phencyclidine and ketamine. Both are widely used as anesthetic agents, ketamine in humans and phencyclidine in animals. The acronym for phencyclidine that we will use, PCP, comes from its chemical name 1-(1-PhenylCyclohexyl)-Piperidine. In addition to their medical use, both ketamine and PCP have gained roles as recreational drugs or, as others would put it, drugs of abuse. While sharing some of the properties of the depressant drugs we met in the preceding chapter, PCP and ketamine are pharmacologically and therapeutically unique. On March 26, 1956, V. Harold Maddox, a chemist working at the research laboratories of Parke, Davis & Company in Detroit, synthesized a novel compound later to be called phencyclidine. PCP was submitted in the autumn of that year for testing in animals. Pigeons, mice, rats, Guinea pigs, rabbits, dogs, cats, and monkeys all had their turn. Depending on the dose employed and the species in which it was tested, the effects ranged from excitement and stimulation to taming and quieting. Analgesia, that is, absence of pain without loss of consciousness, and anesthesia were common but, unlike the depressant drugs we met in the previous chapter, the anesthesia was not accompanied by depression of breathing. Studies in human subjects began in May 1957 at the Department of Anesthesiology of the Detroit Receiving Hospital. By this time, PCP had been given the trade name Sernyl. The drug initially was administered to seven volunteers. As had previously been noted in animals, there was no suppression of breathing or disturbance of cardiac rhythm, highly desirable qualities in an anesthetic agent. The investigators then moved on to 64 patients ranging in age from 18 to 78, 47 of whom were women, who were to undergo various surgical procedures, including breast biopsy, dilation and curettage, skin grafts, hysterectomy, and hernia repair. Immediately after the intravenous administration of PCP, there was what the anesthesiologists called “a profound state of analgesia” permitting surgical incision and, in many cases, completion of the operation without the use of other drugs.

Medication administration is a key skill and it is vital that you are able to demonstrate safety in all aspects of the medication administration process in order to avoid harm or death to your patient. The NMC (2004, 2010) reiterates this point, highlighting that the administration of medicines is an important aspect of a nurse’s professional practice. They argue that it is not simply a mechanistic task, but one that requires thought, exercise and professional judgement. Studies suggest that medicine administration is one of the highest risk processes that a nurse will undertake in clinical practice (NPSA 2007b; Elliot and Lui 2010). Medication administration errors are one of the most common errors reported to the National Patient Safety Agency (NPSA). Indeed in a 12-month period in 2007, 72,482 medication errors were reported with 100 of these causing either death or severe harm to the patient (NPSA 2009). The frequency of these errors has led to a number of changes in the medication administration process. Alongside these important recommendations, most higher education establishments will want to ensure safety of medicine administration and may test this vital skill using an OSCE to ensure that you are adequately prepared for safe administration of medication in practice. There are a number of important laws and key documents that relate to the administration of medication and it is important that you understand these as they all impact upon your practice when administering medication to a patient. You may also be tested on your knowledge in relation to these areas so it is important that you have read these. Important documents you will need to know include: ● The laws that relate to medication in the UK, ● NMC Standards for Medicines Management (2010) (www.nmc-uk.org), ● Local policies related to hospital/Primary Care Trust (PCT) regulation of medication (refer to local guidance). There are a number of laws that influence the manufacturing, prescription, supply, storage and administration of medication. Whilst you will not need to study the intricacies of these laws you will need to understand the main issues each law covers.

Questions

In the CT-based description of pilon fractures which of the following is the commonest variety of coronal-based pattern [coronal = parallel to trans-malleolar axis]?

Select the single most appropriate answer.

Anterior split

Coronal split with die punch

Posterior split

V type

Y type...

A child’s future perceptions and expectations are likely to be conditioned by early experiences of dental treatment. Just under half of all children report low to moderate general dental anxiety, and 10–20% report high levels of dental anxiety. Montiero et al. (2014) indicate that the prevalence of needle phobia may be as high as 19% in 4- to 6-year-olds. Davidovich et al. (2015) reflected that, for general practitioners and specialists alike, Local anaesthetic (LA) injection for an anxious child was the most stressful procedure regardless of the operator’s age, gender, or years of professional experience. Despite impressive reductions in caries in children in recent years, there still exists a social gradient with inequalities in experience of dental disease, and there remains a significant cohort of children for whom extractions and restoration of teeth are necessary. Aside from emerging restorative strategies that do not require LA (e.g. atraumatic restorative technique or placement of preformed metal crowns using the Hall technique), effective and acceptable delivery of LA remains an important tool to enable successful operative dental treatment to be carried out comfortably for child patients. Effective surface anaesthesia prior to injection is very important as a child’s initial experience of LA techniques may influence their future perceptions and help in establishing trust. Cooling tissues prior to injection has been described but is rarely used, and surface anaesthesia is generally achieved with intra-oral topical agents. Although the main use of topical agents is as a pre-injection treatment, they have been used as the sole means of anaesthesia for some procedures including the extraction of mobile primary teeth. It is possible to achieve a depth of 2–3mm of anaesthesia if topical agents are used correctly: • the area of application should be dried • topical anaesthetic agent should be applied over a limited area • the anaesthetic agent should be applied for sufficient time. In the UK 5% lidocaine (lignocaine) and 18–20% (17.9%) benzocaine gels are the most commonly used agents. Benzocaine topical anaesthetic gel is not recommended for use on children under 2 years old because of an increased risk of methaemoglobinaemia.