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Many of the studies exploring dopamine (DA) function in depression have produced inconsistent findings. Contributors to this inconsistency include the diagnostic heterogeneity of major depressive disorder (MDD); failure to control for age, bipolar disorder, and comorbid diagnoses; and variation in patient medication treatment status at the time of the study. Despite this variability, there is now a convergence of data from animal models, genetics, neuroimaging, and human clinical trials that strengthens the case for DA dysfunction in the pathophysiology of major depression, at least in a significant subgroup of patients. This chapter comprehensively reviews the current evidence, with subsequent recommendations for future studies of dopaminergic signaling in depression and its treatment.

Dopamine (DA) has received substantial attention due to its involvement in a wide array of neurological and psychiatric disorders, ranging from Parkinson's disease to affective disorders and schizophrenia. As a result, this system has been studied extensively at many levels of analysis. This is an exciting time for research into psychiatric disorders and the DA system, as evidenced by the convergence of basic neuroscience and clinical research studies on common pathophysiological targets. Dopamine itself has been described as involved in reward and addiction, in attention and compulsions, and in cognition and affect. However, recent studies suggest that the DA system may act to coordinate integration of information via selective potentiation of circuits or pathways. This suggests that DA is acting as a “glue” that holds together plastic relationships among diverse brain structures. This chapter focuses on the system physiology of the DA system in intact animals, how the DA system is regulated, and how dysregulation of this system may contribute to the pathophysiology of major psychiatric disorders.

This chapter looks at the natural course diseases that have a transient autistic phase take, using Rett syndrome (RTT) as an example. Topics discussed include the autistic features of RTT, autistic features of RTT compared to Kanner's autism, neurological findings in the early stage of RTT, differences in the morphology of the brain of RTT and autistic patients, pathophysiological considerations of autistic features in RTT, and the causative gene of RTT (methyl-CPG-binding protein 2).

Expectoration — the removal of secretions from the chest — is a symptom which may be triggered by a wide range of respiratory conditions. Because of this diversity, an extensive armamentarium of therapeutic options may be used which are specifically directed at individual causal agents. In general this strategy has a high success rate. Alternatively, therapy can be given to improve the act of expectoration itself or to suppress the desire to expectorate. This chapter discusses the pathophysiology of expectoration, the clinical approach to expectorant therapy, and physiotherapy for expectoration.

This chapter explains via a case study the desired skills, attitudes, and knowledge necessary to diagnose and manage malignant bowel obstruction (MBO). It addresses several questions such as: What is the likelihood that the patient will develop bowel obstruction at some time during her cancer journey? What is the pathophysiology of MBO? What are the common symptoms of MBO? What are the indications for and outcomes of surgery in patients with MBO?

This chapter contains case studies to show the desired skills, attitudes, and knowledge required to diagnose and manage cardiac disease. It includes a variety of questions such as: How to approach the patient's heart failure and what role would the palliative care physician play in his ongoing care? How does the pathophysiology of heart failure relate to the progression of disease and the symptom experience of the patient? What validated clinical test can be used to assess heart failure symptoms? From the palliative care perspective, how to manage a patient with symptomatic end-stage heart failure?

Anabolic-androgenic steroids (AASs) can be used to increase muscle mass and strength in adult males. Despite successful detection and convictions by sporting anti-doping agencies, they are still being used to increase physical performance and improve appearance. The adverse side effects and potential dangers of AAS use are well documented. Recent epidemiological research has identified that the designer drugs growth hormone (GH) and insulin are also being used because of the belief that they improve sporting performance. This chapter summarizes the classification of AASs, GH, and insulin as well as their prevalence and patterns of use. The physiology of GH and its pathophysiology in the disease states of deficiency and excess and in catabolic states are discussed and a distinction is made on the different effects between therapeutic use in replacement and abuse in a sporting context. The history, physiology, and pathophysiology of insulin in therapeutic replacement and its abuse in a sporting context are also described. A suggestion is made on potential mechanisms of the effects of GH and insulin.

In North America, as elsewhere in the Western world, dying was a routine part of life until the mid-20th century when it became medicalized, i.e. it was primarily seen as a product of pathophysiology and the responsibility of health care professionals rather than as part of the human condition and the responsibility of family and friends. The care of the dying as a special focus of activity was carried to North America by those who observed the care in France, Ireland, Scotland, and England. Palliative care education in North America still has a long way to go before it is a reliable part of the education of health professionals producing a reliable product. Nevertheless, the last ten years have produced significant calls for reform, educational curricula, and the creation of a new specialty.

The problem of designing educational systems to teach methods is complicated by the fact that the kind of knowledge by which physicians know disease and the output of technology is different from and often in conflict with the kind of knowledge by which persons are known. Knowing the history of this conflict, as well as how it is expressed in medical practice is important to educators if students and physicians-in-training are not to be constantly subverted by the lure of “hard data”. Many of the functions people want primary care physicians to perform are contradicted by medical science as it is still taught to students and house officers. Physicians have great difficulty discovering the necessary information about the sick person and entering it into the calculus of their medical judgments so that it has equal weight with information about disease, pathophysiology, and technology.

The clinical method is the means by which physicians discover facts about the sick or well patient and enter them into the diagnostic and therapeutic process in equal partnership with information about disease, pathophysiology, and technology. The inadequacy of the clinical method as currently taught and practiced creates problems for physicians, patients, and the health care system — especially primary care medicine. There are three problems. First, knowledge of persons, generally absent from the method, is just as important as knowledge of disease as a foundation of primary care. Second, much of the information required for diagnostic and therapeutic decisions in primary care must still be obtained from communicating with and examining patients. Finally, the clinical judgment of individual physicians is also a component of the clinical method that is insufficiently stressed, and yet the health and well-being of patients are directly dependent on it.

dyspnoea is a subjective experience that includes interactions of various physical, psychological, social, and environmental factors that influence the person's perception of the symptom. This chapter focuses on the multidimensional assessment of dyspnoea. Assessment of this symptom involves clinical assessment and measurement of the different factors that influence the perception of breathlessness and which impact on the breathing mechanisms of a person. Clinical assessments are designed to determine the underlying pathophysiology to pinpoint appropriate treatment and to evaluate response to therapy. Measurement tools meanwhile are used to bring objectivity and accuracy to the evaluation of the clinical assessments, interventions, and clinical researches. Among the clinical assessment methods discussed herein are: clinical history of the symptom; physical examination; laboratory examinations; and determining the qualitative dimensions of dyspnoea. Measurement of dyspnoea includes: unidimensional scales (Borg scale, numeric rating scale, Breathlessness, Cough and Sputum Scale (BCSS)); multidimensional indirect scales (Baseline/Transitional dyspnoea Index (BDI/TDI), Pulmonary Functional Status Scale (PFSS)); and disease specific scales (chronic respiratory questionnaire (CRQ), Saint George Respiratory Questionnaire (SGRQ)).

Respiratory discomfort or dyspnoea is the primary symptom of chronic obstructive pulmonary disorder (COPD) and is a prime contributor to the poor quality of life of patients diagnosed with this disease. This chapter examines the pathophysiology of COPD during rest and exercise to determine the origin of the symptom. It examines the relationship between dyspnoea and the ventilatory mechanisms and gas exchange in COPD, and also considers the possible neurophysiological underpinnings of this symptom.

Dyspnoea is a common symptom in patients with cancer, but it is often overlooked. Breathlessness can significantly increase morbidity in patients with advanced diseases. Dyspnoea is chronic with cancer patients experiencing heightened shortness of breath, which is usually accompanied by fear, panic, anxiety, and a sensation of impending death. Generally, discomfort in breathing is aggravated by emotions and activities, resulting in a reduction in the activities of patients in order to cope with the symptom. In addition, dyspnoea also affects the mood, relationships, and outlook of the patient towards life. Patients experiencing shortness of breath often exhibit a reduced will to live. This chapter discusses the epidemiology, pathophysiology, and syndromes of breathlessness prevalent in patients with advanced cancer. Determination of these factors is crucial in the development of management methods for this symptom. In this chapter, the four common causes of dyspnoea in cancer patients are examined. These are: direct tumour effects (pleural effusion, pericardial effusion, super vena cava syndrome), indirect tumour effects (muscle weakness, pulmonary eboli, infection), treatment-related effects (surgery, radiation therapy, systematic therapy), and problems unrelated to cancer (pre-existing diseases such as COPD, asthma, chest-wall deformity, obesity).

This chapter considers the state of knowledge in the pathophysiology of heart failure (HF). In particular, it reviews the pathophysiological characteristics of HF, and describes the link between these features and recent advances in the molecular basis of HF. The features of HF can be classified into several categories according to their pathophysiological characteristics: acute or chronic HF; systolic or diastolic failure; right-sided or left-sided HF; and high output or low output failure. These characteristics are discussed in detail. Factors that aggravate HF include increased uptake of water or sodium, infection, stress, poor blood pressure control, non-compliance with oral medication, transient cardiac arrhythmia including atrial fibrillation and tachycardia, anemia, and renal dysfunction, advanced aging, sleep apnea syndrome, lethal cardiac arrhythmia, and myocardial disease secondary to systemic disease such as amyloidosis or sarcoidosis. Finally, the future clinical and research implications are highlighted.

This chapter discusses the management of non-pain symptoms in terminally ill patients. These symptoms include nausea and vomiting, constipation, bowel obstruction, dyspnea, and cachexia. The chapter explains the pathophysiology, principles of therapy and recommended treatment for each of these symptoms. It also suggests that palliative care should not be so much about what the practitioners do as about why they do it.

This chapter concentrates on the pathophysiology of cardiac cachexia. It also discusses the possible clinical implications, and outlines the potential future development of therapeutic strategies. In particular, it explores the epidemiology and aetiology of cardiac cachexia. It then evaluates the alterations of body composition and the pathogenesis of cardiac cachexia. The therapeutic options include pharmacological treatment, nutritional support, and physical training. With improved knowledge of the underlying pathophysiology, a number of emerging treatment strategies for prevention and treatment are being developed and tested. Although no specific treatment is currently available, several approaches with the use of neurohormonal drugs, nutritional support, ghrelin, and physical training appear to show potential benefits and the results of ongoing clinical trials in cardiac cachexia are awaited.

Fatigue is a highly prevalent and complex symptom in populations with chronic illness. Although there have been significant advances in the methodologies to measure fatigue, few scientific investigations have focused on the nature of the problem and its management in clinical settings. In many ways, fatigue research is now at a point similar to pain research a quarter-century ago. Valid and reliable measurement is possible, and a growing number of epidemiological studies have established the seriousness of the clinical problem. The field is primed for studies that may illuminate the pathophysiology of the disorder in varied patient populations and provide an evidence base for treatment selection. However, studies are needed to clarify the mechanisms that underlie various types of fatigue, understand the epidemiology of the symptom, and provide an evidence base for management decisions.

For any hypothesis to be truly satisfying, it must be compatible with all the known facts. The manifestations of migraine are so diverse that one must resist the temptation to seize on some and reject others in an attempt to justify a tenuous theory. Certain symptoms that can be recognized within the conceptual framework of migraine may be present in some episodes and not others, and may recur in certain phases of each attack but not in others. Each of these symptoms or groups of symptoms may have a different neurovascular basis.