A towering stump of basalt second only to the Rock of Gibraltar, Beacon Rock rises 848 feet from the Washington shore of the Columbia River, about 40 miles east of my home on the Oregon side, up a dead-end street in a woodsy hilltop neighborhood in Portland. The river feels like my second home, carrying years of memories and the promise of more good times spent on the water, first with my kids when they were kids, and now with my grandchildren. This is where they learned some lessons in resourcefulness and practical skills for life and where I learned some of the ropes myself.

Those days are numbered now, though the timeline is imprecise. Ordinarily, this would be maddening for me as a former research scientist and neurologist for whom precision is second nature.

This chapter provides an overview of what anxiety problems are, and why the perinatal period features all the key ingredients that can lead to problemmatic anxiety. Nurturing and caring for a baby is not easy for anyone and involves large emotional and physical demands, managing uncertainty and avoiding harm. All in the context of disturbed sleep and a major life change. The cognitive-behavioural model of anxiety states that it is not just the situation we find ourselves in, but the particular meaning we give to our experiences that drive and make sense of our emotions and other responses. In pregnancy and the postnatal period these meanings may be influenced by a complicated and sometimes traumatic journey to pregnancy and birth, beliefs about the importance of thoughts or physical sensations, and how we respond to the responsibility of being pregnant or in charge of a baby, as well as other personal and historical factors. There are many common factors across anxiety problems. In the rest of the book we explain how to apply this basic understanding to overcome particular forms of maternal anxiety.

Peter, a 35-year-old stockbroker, has been advised by his supervisor to come and see you, the company mental health consultant. His supervisor is complaining that he often comes to appointments late, is inappropriately fidgety, interrupts people during meetings, has been offensive towards coworkers, and has been known to party excessively on weeknights. Peter asserts that he is just fine; he has a lot of projects on his mind and is simply standing up for himself when speaking with others. He likes to go out in the evenings to unwind. Recognizing probable attention deficit hyperactivity disorder (ADHD), you interview both the patient and his work buddy, who is a longtime friend. How would you start your questions?

Cognitive failure and the fear of losing control over one’s life has occupied mankind for centuries. In our chapter we describe the conceptual history of dementia starting with the first written traces from the twenty-fourth century BCE, relating the story of an Egyptian officer who not only developed the inability to remember yesterday but also became more and more childish. Subsequently, we summarize medical discoveries that have allowed cognitive, psychological and behavioral symptoms of dementia to be viewed as a result of brain disease rather than, for instance, witchcraft or ill will. In the context of growing awareness of neuro-pathophysiological mechanisms underlying dementia, associated with postmortem brain research in the late ninettenth century, Alzheimer’s disease became the ‘face’ of dementia for some time. We discuss further developments in the discovery and in the treatment of different types of dementia, also focusing on psychosocial aspects of the disease. These became an important topic of research as pharmacological treatments aimed at curing the neurodegenerative causes of dementia as yet do not exist. AWe compare how different cultures and societies deal with dementia. Finally, the political and societal attempts to promote social inclusion and empowerment of individuals with dementia are summarized.

John agreed to an evaluation of his cannabis use to appease his mother. The 10th grader cautiously acknowledged experimenting with cannabis after his best friend had been given some pot by his older brother. John asked his friend for a joint and they had smoked together half a dozen times over the past 4 months. He sheepishly admitted liking marijuana, but he also knew pot carried some vague risk for people his age. His mother was terrified when she saw her son looking at websites about cannabis, but when confronted, he was honest with his parents about his use. After talking with John, I wasn’t concerned that he was in any real danger. I taught him the signs of using cannabis too frequently, and we reviewed the reasons why he should delay use until he was a few years older.

Alzheimer’s disease (AD) drug development is a complex process that proceeds from identification of a biological target; to testing of candidate therapies in in vitro assays; assessment of efficacy in animal models and assessment of safety in several animal species; clinical testing in humans in Phase1, Phase 2, and Phase 3 clinical trials; regulatory review by agencies in all countries in which the drug might be marketed; and eventual commercialization. This process requires more than a decade to accomplish. The process involves substantial infrastructure resources; multiple stakeholders; and funding from a variety sources along the developmental pathway. This is the complex ecosystem that supports AD drug development.

Which evidence-based treatment is recommended for severe anxiety in the pediatric population?

Once thought to be an immune-privileged site, we now know that there is a complex and essential bidirectional interplay between the central nervous system (CNS) and the immune system (1). Technological advances in imaging, genomic medicine and immunology have resulted in major revisions to some of the most fundamental and long-held assumptions in neuroscience, and we now understand that the immune system is critically involved not only in brain pathology, but also in the normal processes of brain development and homeostasis.

Antipsychotics have numerous evidence-based uses in the twenty-first century, including schizophrenia spectrum and other psychotic disorders, bipolar disorder, unipolar major depression, behavioral disturbances of autism, tic disorders, and obsessive compulsive disorder [1]. The application of antipsychotic therapy in many of these conditions is adjunctive, and it may be withdrawn during less active phases of the illness. For patients with schizophrenia spectrum disorders, antipsychotics are the foundation of treatment without which the patient is at risk for relapse, and the attendant psychiatric, social, and legal consequences [2, 3]. Given the level of disability often encountered with the onset of illness, the care and management of individuals with schizophrenia exerts a significant economic toll on society [4–6]; moreover, this burden accrues most directly to families and direct caregivers in the form of financial loss compounded by stress and decreased quality of life [7, 8]. Of particular concern are the disproportionate direct and indirect costs associated with treatment-resistant schizophrenia (TRS) [4] (see Figure 0.1).

Modern psychopharmacology is largely the story of chemical neurotransmission. To understand the actions of drugs on the brain, to grasp the impact of diseases upon the central nervous system, and to interpret the behavioral consequences of psychiatric medicines, one must be fluent in the language and principles of chemical neurotransmission. The importance of this fact cannot be overstated for the student of psychopharmacology. This chapter forms the foundation for the entire book, and the roadmap for one’s journey through one of the most exciting topics in science today, namely the neuroscience of how disorders and drugs act upon the central nervous system.

The science of suicide risk and prevention is growing, making one thing very clear. While suicide risk involves a complex set of risk factors, the end common pathway is a life-threatening health crisis. As is the case with all health-related causes of death, a robust public health strategy can reduce mortality. This chapter provides a framework for understanding the public health approach to preventing suicide. Examples of effective public health suicide prevention strategies at national and regional levels are provided.

Diagnostic systems such as the DSM have long struggled over whether to organize psychiatric disorders as black-and-white categories defined by operational criteria (where “casehood” is unambiguously either present or absent) versus dimensions of psychopathology (where certain clinical elements are present but insufficient in number or duration to meet minimum criteria that define a particular clinical condition). Clinicians, meanwhile, often tend to identify and treat prominent symptoms, with varying degrees of awareness and concern about their broader context for defining the presence or absence of a distinct syndrome. In this chapter we will examine when pharmacological treatment targets can or should be thought of as unambiguous disease categories as opposed to dimensions of psychopathology that may not always be so clear-cut.

Diagnoses are clusters of signs and symptoms that should form a coherent constellation based on their inter-relationships.

The history of serious mental illness (SMI) is grim, from a cultural as well as a treatment perspective. The conditions of individuals with psychotic disorders have swung, like a pendulum, from institutional neglect to community neglect and back again over the past several hundred years. At the core of treatment failure is a failure in mental health policy and funding, with the result usually framed as the degree of human institutionalization in jails, prisons and asylums. In the middle of the nineteenth century, institutions designed to deliver moral treatment were considered the humane answer to care properly for the SMI population. By the mid-twentieth century, those same, now overcrowded, institutions were blamed for the horrible conditions of mistreatment of individuals with SMI.

Plants have been a plentiful source of useful drugs and remedies throughout human history. In the early nineteenth century Friedrich Sertürner isolated morphine from the opium plant. By 1827, morphine was marketed by Merck in Germany and the origins of the modern pharmaceutical industry began. Over the remainder of the nineteenth century further advances in organic chemistry led to identification of other drugs from plant material. Examples of important medicines developed from plants included quinine from the bark of the cinchona tree for the treatment of malaria and salicylic acid from the willow tree that eventually led to the development of aspirin (Anderson, 2005).

The year 2018 marked the 60th anniversary of clozapine’s synthesis, and the 30th anniversary of the September 1988 Archives of General Psychiatry paper by Kane and colleagues documenting clozapine’s superior efficacy in treatment-resistant schizophrenia. The peer view literature since 1988 demonstrates ongoing interest in clozapine, with 350–450 papers per year listed in PubMed (see Figure 1). The ensuing decades have also seen other evidence-based uses for clozapine (e.g. schizophrenia patients with suicidality or aggression, Parkinson’s disease psychosis, treatment-resistant mania), but treatment-resistant schizophrenia spectrum disorders remain the most common indication. Lamentably, clozapine remains significantly underutilized for treatment-resistant schizophrenia despite compelling evidence of efficacy in this population, and the enormous individual and societal benefits that can accrue from effective management of treatment-resistant patients.

Although a disease-altering treatment has yet to be found, our understanding of Alzheimer's disease (AD) genetics and neurobiology has increased exponentially over the past few decades, as has our ability to detect Alzheimer's pathology using various biomarkers. In this chapter, we will review the genetic, pathological, and behavioral features of Alzheimer's disease and discuss how the use of biomarkers for the detection of AD has potentially opened up new avenues for the prevention (or possible reversal) of AD. Given the current absence of an effective pharmacological treatment, we will also describe how lifestyle may impact one's risk for developing AD and review potential strategies for reducing AD risk as well as reviewing currently available treatments aimed at ameliorating some of the symptoms of AD. For strategies to ameliorate some of the secondary behavioral symptoms often associated with Alzheimer's disease and other dementias, the reader is directed to Chapter 5.