In addition to the international classification systems such as DSM-5 and ICD-11 discussed in earlier chapters of this book, we will now introduce three further diagnostic steps essential for diagnosing catatonia: (1) clinical rating scales, (2) the lorazepam challenge test, and (3) laboratory and neuroimaging work-up. This chapter will first present the widely used clinical rating scales for assessing catatonia, highlighting their advantages, limitations, and their role in scientific studies. While these scales are valuable tools, it is important to emphasize that clinical judgment remains crucial, as some catatonic symptoms may not be fully captured by these scales. Following this, we will explore the lorazepam challenge test, evaluating its diagnostic utility in light of current evidence. Lastly, the chapter will discuss the importance of laboratory and neuroimaging work-ups, including blood tests, lumbar puncture to examine cerebrospinal fluid, electroencephalogram, and magnetic resonance imaging, for both diagnosing catatonia and guiding therapeutic decisions.

Chapter 3.2 covers biological signals monitored during anaesthesia. We begin by focussing on the basic physics of biological signals including electro-cardiogram, electro-myelogram and electro-encephalograms. There is then detail on the monitoring of these signals and basic standards required for anaesthesia. We include a structured approach to the evaluation of an electrocardiogram which is a common exam question.

This chapter describes the many methods of Cognitive Neuroscience that are revealing the neural processes underlying complex cognitive processes in the brain. The benefits and limitations of each method are discussed, highlighting how there is no single “best” method and how the choice of method in any experiment should be motivated by the hypothesis being evaluated. Neuropsychology provides novel insights into the neural bases of cognitive processes but is limited because it relies on naturally occurring lesions. Neuroimaging methods (fMRI, PET, fNIRS) provide excellent spatial resolution but cannot assess the temporal order of neural activity across regions. Electroencephalography (EEG) and magnetoencephalography (MEG) can track neural activity in real time, but their spatial precision is limited because they are recorded from outside the head. Neurostimulation methods (TMS, tDCS, tACS) can uniquely assess causality by testing if, and when, a brain area is necessary for a particular function. Methods using non-human animals (e.g., single-unit recordings) can provide the highest levels of spatial and temporal precision, but they are limited to mental processes that the non-human animals can be trained to do. This chapter ends with a comparison of methods that includes portability, spatial precision, and temporal resolution.

This chapter introduces the methods used in cognitive neuroscience to study language processing in the human brain. It begins by explaining the basics of neural signaling (such as the action potential) and then delves into various brain imaging techniques. Structural imaging methods like MRI and diffusion tensor imaging are covered, which reveal the brain’s anatomy. The chapter then explores functional imaging approaches that measure brain activity, including EEG, MEG, and fMRI. Each method’s spatial and temporal resolution are discussed. The text also touches on non-invasive brain stimulation techniques like TMS and tES. Throughout, the chapter emphasizes the importance of converging evidence from multiple methods to draw robust conclusions about brain function. Methodological considerations such as the need for proper statistical comparisons are highlighted. The chapter concludes with a discussion of how neurodegenerative diseases have informed our understanding of language in the brain. Overall, this comprehensive overview equips readers with the foundational knowledge needed to critically evaluate neuroscience research on language processing.

In the human body, the brain is the organ that underpins mental processing. Mental processes use the interconnected structures of the brain to synthesize the experience of the internal and external environment. Psychiatric symptoms reflect dysfunctional mental processing. These abnormalities in mental processes could arise from any combination of functional or structural changes in the brain. Neuroimaging technology provides us with methods to study these abnormal functions and structures of the brain.

Neurobiological theories draw on neurobiological evidence from fMRI but also plenty of other neuroscientific methods for theory development: On a fundamental level, neurobiological theories are neurobiological explanations about the nature of the brain-behavior link.

Movement disorders arise from dysfunctional physiology within the motor and movement systems of the nervous system, and can involve multiple anatomic locations. A myriad of electrophysiologic manifestations can be detected in electromyography (EMG), electroencephalography (EEG), and other methods. Technical factors must be carefully considered and technical quality should be monitored throughout. Surface EMG provides the basis for the electrophysiologic examination of movement disorders. EEG is important for establishing cortical genesis as well as consciousness state determination during the movement disorder. Tremors of different etiologies may have different frequencies and activation characteristics that are best discovered on analysis of surface EMG characteristics. Also, classification of myoclonus physiology needs electrophysiologic testing. Proper myoclonus classification forms the best approach to symptomatic treatment strategy. Results from this testing provide important supplemental information, which can be used for a more exact diagnosis that leads to treatment.

Working memory refers to actively holding information in mind during a relatively short period of time, typically seconds. During working memory paradigms, information is actively kept in mind during the delay period. Working memory has been associated with activity in the lateral prefrontal cortex, the parietal cortex, and sensory processing regions. Section 8.1 details the brain regions that store the contents of working memory during the delay period. In Section 8.2, the evidence is evaluated that claims to link working memory with the hippocampus. Section 8.3 considers the brain timing commonly associated with working memory. In Section 8.4, brain activity associated with working memory that oscillates at particular frequencies is considered, which primarily includes alpha activity and gamma activity. In Section 8.5, changes in brain activity are highlighted that have been linked to training-related increases in working memory capacity.

This chapter focuses on the timing of brain activity associated with long-term memory. The chapter begins by introducing ERP activations that have been associated with familiarity and recollection. Familiarity has been associated with activity in frontal brain regions 300–500 milliseconds after stimulus onset, while recollection has been associated with activity in parietal brain regions 500–800 milliseconds after stimulus onset. In Section 4.2, a scientific debate that has focused on the ERP activity associated with familiarity is discussed. In Section 4.3, it is shown that synchronous activity in two different brain regions (i.e., activation time courses that increase and decrease together) indicates that these regions interact. Such synchronous activity between regions during long-term memory typically occurs within the theta frequency band, the alpha frequency band, and the gamma frequency band. Section 4.4 details some intriguing intracranial EEG findings based on recording activity in the hippocampus and the parahippocampal gyrus.

This chapter provides a cross-sectional overview of current neuroimaging techniques and signals used to investigate the processing of linguistically relevant speech units in the bilingual brain. These techniques are reviewed in the light of important contributions to the understanding of perceptual and production processes in different bilingual populations. The chapter is structured as follows. First, we discuss several non-invasive technologies that provide unique insights in the study of bilingual phonetics and phonology. This introductory section is followed by a brief review of the key brain regions and pathways that support the perception and production of speech units. Next, we discuss the neuromodulatory effects of different bilingual experiences on these brain regions from shorter to longer neural latencies and timescales. As we will show, bilingualism can significantly alter the time course, strength, and nature of the neural responses to speech, when compared with monolinguals.

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.