• Information travels through the brain as electrical signals along a complex network of interconnecting nerve cells called neurons.

• Neurons connect to each other at synapses, small gaps where chemicals called neurotransmitters amplify or muffle the electrical signals.

• The reward pathway determines our experience of pleasure and many psychoactive drugs work by over-stimulating this pathway.

• After using psychoactive drugs, the brain needs time to recover. This is often experienced as a psychological ‘crash’ or ‘come down’.

• If a drug is used regularly, the desired effects become harder to achieve – a process called tolerance.

• People who use drugs often increase the amount of drug they take over time in an attempt to overcome tolerance. This increases the risk of drug-related harm.

• Regular psychoactive drug user ends up altering brain functioning, making it much harder to enjoy non-drug experiences. The world can become joyless.

• Adolescence is the period between the onset of puberty and the point at which adult roles are assumed and involves rapid physical, psychological and social change.

• In adolescence, learning takes place as the brain establishes neural networks. These networks are constantly modified by new experiences.

• The adolescent brain develops in stages. One of the last areas to develop are the frontal lobes, the part of the brain responsible for decision-making and assessing risk.

• Just when the adolescent brain is at this delicate developmental phase, it is also most impulsive and drug use is most likely.

• Drug use in adolescence disrupts brain development, which can lead to long-term damage to brain function and increase the risk of further drug use.

• Many adolescents are surprisingly poorly informed about drugs, their effects and the harms they can cause.

• Adolescents tend to seek information about drugs from the internet or friends.

• Accurate information is available and should be highlighted to adolescents.

This chapter starts by summarising an experiment showing how the brain’s emotion circuitry responds to a set of words signalling threat. The main emotion activated in Brexitspeak is fear; the triggers are both linguistic and visual. They include representation of alarming scenarios, and factual misrepresentations capable of causing various negative emotions. The chapter analyses three well-known cases that illustrate such effects. The first is Vote Leave’s propaganda displayed on the side of a red bus: the slogan was an inaccurate statement that could evoke feelings of attachment, resentment and anger. This is also analysed in terms of speech acts, ambiguous and deniable assertions, and lying. The second case, the rightly controversial ‘breaking point’ poster displayed by Leave.EU had the avowed goal of emotion arousal. The visual element is analysed with reference to cognitive image schemas, and their potential for activating fear reactions. The third case, the most effective of the Vote Leave campaign, was crafted in order to prompt the fear of losing agency. This, too, likely activated the brain’s fear circuitry.

The Automatic Selective Perception (ASP) model posits that listeners make use of selective perceptual routines (SPRs) that are fast and efficient for recovering lexical meaning. These SPRs serve as filters to accentuate relevant cues and minimize irrelevant information. Years of experience with the first language (L1) lead to fairly automatic L1 SPRs; consequently, few attentional resources are needed in processing L1 speech. In contrast, L2 SPRs are less automatic. Under difficult task or stimulus conditions, listeners fall back on more automatic processes, specifically L1 SPRs. And L2 speech perception suffers where there is a mismatch between the L1 and the L2 phonetics because L1 SPRs may not extract the important cues needed for identifying L2 phonemes. This chapter will present behavioral and neurophysiology evidence that supports the ASP model, but which also indicates the need for some modification. We offer suggestions for future directions in extending this model.

Humans have the ability to recognize that when they perform actions, they produce effects in the external world. Even though humans are not the only animalsl with this mental capacity, their ability to perform actions is accompanied by a feeling of authorship, a feeling that “I” am the one who did it. This is what academics have called the sense of agency. When individuals claim reduced responsibility because they were “only obeying orders”, this defense is often viewed with skepticism, because the defendant has a clear motive of avoiding punishment. However, scientific methods can now be used to investigate the experience of receiving orders and how it influences how the brain processes information. As this chapter shows, obeying orders impacts the sense of agency and the feeling of responsibility at the brain level. Further, working and living in some highly hierarchical and sometimes coercive social structures, such as the military, can also impact the sense of agency when people make decisions. It thus appears that hierarchies provide a powerful ground to obtain a reduced feeling of responsibility and agency in individuals.

When we witness another person experiencing pain, be it emotional or physical, we have an empathic reaction. And even if we commit a harmful action against another person, we most of the time experience guilt in the aftermath, which prevents us from performing the same action in the future. Guilt and empathy are critical moral emotions that together usually prevent us from harming others. However, as this chapter shows, systematic processes of classification and dehumanization at play before a genocide can alter moral emotions towards another part of the population. Activity in empathy-related brain regions is generally reduced towards individuals that we consider as outgroup or towards dehumanized individuals. Neuroscience studies have further shown that when obeying orders to hurt another person, neural activity in empathy- and guilt-related brain regions is reduced compared to acting freely. Such results show how obeying orders diminishes our aversion to harming others.

Epilepsy is one of the most common neurological disorders, affecting people of all ages. This chapter focusses on what has been learnt about the microRNA system in this important disease. Starting with an overview of epilepsy, it addresses what causes seizures to occur and some of the underlying mechanisms, including gene mutations and brain injuries. It explores how and which microRNAs drive complex gene changes that underpin but also oppose the enduring hyperexcitability of the epileptic brain. This includes by regulating amounts of neurotransmitter receptors, structural components of synapses, metabolic processes and inflammation. It also covers some of the earliest studies linking microRNAs to epilepsy as well as recent large-scale efforts to map every microRNA and its target in the epileptic brain. Finally, it highlights ways to model epilepsies and use of experimental tools such as antisense oligonucleotides to understand the contributions of individual microRNAs. Collectively, these studies reveal how microRNAs contribute to the molecular landscape that underlies this disease and offer the exciting possibility of targeting microRNAs to treat genetic and acquired epilepsies.

MicroRNAs were discovered during experiments designed to learn how genes coordinate animal development. This chapter begins with the early studies that taught us the importance of microRNAs for mammalian development by studying what happened when key genes were deleted in mice. It ranges from studies that knocked out genes from the entire organism towards refined approaches that removed microRNAs at defined moments from specific tissues, including the heart and the visual system. A detailed review is taken of the genes that microRNAs regulate during brain development and their contribution to the diversity of cell types. These studies reveal the essential role for the microRNA system broadly, as well as how certain developmental events are more or less tolerant of disruption to the microRNA system. This chapter also reviews which microRNAs are the first to control gene activity after fertilisation and how environmental and parental experience can change microRNA activity. The chapter also includes explanations of the scientific toolkit needed to delete or deliver biogenesis components and microRNA genes, and how microRNAs have been used as tools in stem cell research.

The genome is the totality of information that directs the making and the maintenance of you and every other living organism. Scattered among the familiar genes that code for the proteins of life are other genes. This is a book about the genes we call microRNA. It is 30 years since their discovery. They are gene regulators, every bit as vital as their more famous gene cousins. MicroRNAs fine-tune how much protein is made in our cells, each one coordinating the activity of hundreds of genes and bringing precision to the ‘noise’ of gene expression. Without them, life is virtually impossible. This introduction provides a personal account of what fascinated the author about these genes enough to make him redirect his research to microRNAs. The journey from studying pharmacology in the UK, to the USA where his interest in the brain disease epilepsy began, and later to Dublin, to work at the Royal College of Surgeons in Ireland. It lays out the contents and style of the book, which is part history of science, describing what we know and the experiments that underpin our understanding, and part memoir of the author’s own research, and the applications of microRNAs in medicine.

The brain contains a greater diversity and abundance of microRNAs than any other organ in the body. MicroRNAs stay busy long after they’ve coordinated brain development, but doing what? In the brain, microRNAs serve two somewhat contradictory roles: enforcing the stable patterns of genes that define mature circuits while at the same time conferring the same cells with the flexibility to adapt to changing information. This chapter begins with the basic principles of brain function and some early discoveries on microRNAs in the brain. It explores how the microRNA system influences learning, memory and emotions. It also looks at the evidence that a rich and diverse pool of microRNAs contributed to evolved intelligence. It explains the molecular cues that signpost microRNAs to go to synapses, and how the amount of microRNA activity is linked to the incoming strength of signals. It then looks in depth at some specific microRNAs and their targets and how their competing actions adjust the strength of contacts between neurones. Finally, it looks at how genetic variation and erroneous amounts of certain microRNAs may contribute to risk of neuromuscular and psychiatric disease.

Fluid administration is one of the basic components in the management of neurosurgical patients. However, there is still debate on the ideal fluid. Issues related to adequate volume replacement and effects on the intracranial pressure persist. Studies have demonstrated the harmful effects of colloids over crystalloids. Normal saline has remained a fluid of choice but there is now emerging evidence that it, too, is not free of its harmful effects. Hypertonic saline has also been accepted by many practitioners, but its use and administration require close monitoring. There is now growing evidence on the use of balanced solutions for neurosurgical patients. However, this evidence comes from a small number of studies. Hemodynamic monitoring for fluid therapy in these patients is prudent as these patients are prone to hypovolemia. Dynamic parameters like stroke volume variance and pulse pressure variance are considered more reliable to monitor fluid therapy in comparison to static parameters. This chapter briefly covers various clinical situations in neurosciences with respect to fluid therapy and use of hemodynamic monitoring while providing fluid therapy and its effect on patient outcome.

This chapter focuses on the variety of different EEG patterns that can be seen after hypoxic ischemic brain injury, which often produces some of the most severe encephalopathies. Common post–cardiac arrest findings include discontinuity, burst suppression, background voltage attenuation and suppression, lack of EEG reactivity, seizures, myoclonus, and status epilepticus. The prognostic significance of these findings is discussed. Finally, the topic of using EEG as a confirmatory tool in brain death protocols is introduced.

Some people talk of their metabolism like they might talk of the performance of a motor car – slow or fast. Many people carrying excess weight might like to attribute it to their slow metabolism, but there’s no evidence that it works that way. In fact, there is evidence that metabolism is neither slow nor fast, but varies across a gradient both within and between populations. A small number of people are at the upper end of this gradient and are much less likely to gain excess weight than the small number of people who are at the lower end. There are also some people who do have genuinely very slow metabolism, but this is usually down to them having an endocrine or metabolic disorder. But driving on life’s metabolic freeway, most people are neither crawling in the slow lane nor cruising in the fast lane, but changing lanes according to circumstance. Like freeway driving, metabolism is dynamic, flexible, and adaptable.

Longstanding evidence finds that healthy older adults tend to experience greater positivity, equanimity, and well-being in daily life. Prominent psychological theories of emotional aging tend to focus on cognitive pathways such as shifting motivations and accumulated cognitive resources (e.g., attentional control, expertise) to explain observed emotional aging effects. In this chapter, we introduce the physiological hypothesis of emotional aging (PHEA). At its core, the PHEA proposes that physiological aging contributes to emotional aging, wherein age-related changes to the peripheral body and how the brain represents and regulates the peripheral body (e.g., interoception) should result in age-related changes to emotional experience and associated socioemotional perceptions and behaviors, i.e., emotion communication. Importantly, the PHEA argues that the dynamics of physiological aging (e.g., increased dysfunction, greater afferent noise from the viscera and peripheral transmission pathways, reduced interoception) may in turn facilitate the increased importance of cognitive pathways in late life emotional outcomes and functions. As such, the PHEA provides an integrative neuroscience approach to emotional aging that highlights the importance of physiological health and aging across the body and brain while providing an interpretive framework that complements existing cognitive theories of late life emotion. This chapter introduces core arguments of the PHEA, unifies existing evidence on physiological, interoceptive, and related neural aging as relevant for emotional aging, and forecasts new directions and implications for late life socioemotional functioning and interpersonal behaviors.