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Functional magnetic resonance imaging (fMRI) and other non-invasive imaging methods have greatly expanded our knowledge of human brain function. Although MRI was invented in the early 1970s and has been used clinically since the mid-1980s, its use in cognitive neuroscience expanded greatly with the advent of blood oxygenation level dependent (BOLD) functional imaging, and by now, fMRI is a mainstay of neuroscience research. This chapter gives an overview of the relation between the BOLD signal and the underlying neural signals. It focuses on intracortically recorded neural signals, recorded with microelectrodes.

This chapter considers the significance of the Ediacaran Fauna. Until the late 1980s, the Ediacaran Fauna were usually thought to represent ancient, primitive animal forms. Debate was sparked when leading paleontologist Dolf Seilacher from Tubingen, Germany, reinterpreted these fossils as something completely different. He argued that, instead of animals, they were long-extinct varieties of living organisms, a result of failed lineages with no successors. The rocks on the Avalon Peninsula of southeastern Newfoundland house the oldest known representatives of the Ediacaran Fauna. These so-called rangeomorphs date back to 575 million ago and appear relatively soon after the end of the Gaskiers glaciation some 580 million years ago. Evidence suggests that Ediacaran Fauna of the Avalon Peninsula emerged into an ocean undergoing oxygenation.

This chapter first summarizes data on the neural correlate of the initial step of declarative memory formation, i.e., of encoding which either leads to a feeling of familiarity or to conscious recollection. It summarizes evidence showing that the relationship between the blood oxygenation level-dependent (BOLD) signal (recorded with fMRI) and the underlying neural activity appears to be particularly ambiguous in the medial temporal lobe (MTL); in particular, the BOLD signal does not convey clear information about the level of excitation or inhibition in this brain region. The chapter focuses on electrophysiological recordings in animals and intracranial EEG data from epilepsy patients. It argues that memory formation relies on an inhibitory signal in the medial temporal lobe, which renders hippocampal and neocortical stimulus representations sparser, and on oscillatory activity in the gamma and theta frequency ranges. The second part of the chapter discusses the relationship of these phenomena to epileptiform activity and to memory impairments in epilepsy patients. It gives a brief overview on the neural patterns underlying the second step of memory formation, consolidation. It then describes overlapping neural phenomena during consolidation and epilepsy, such as sharp waves and ripples/fast ripples.

This chapter provides an overview of functional magnetic resonance imaging (fMRI) methods and applications, highlighting key concepts and strategies, and includes the full range of techniques by which physiological changes accompanying brain activity are defined. It focuses on the changes in blood oxygenation and flow that have been used for the functional magnetic resonance imaging methods. Direct imaging of the blood flow response using perfusion MRI is also discussed. The study furthermore deals with elegant methods that have been developed and allow an extension of this simple concept for one-dimensional imaging into methods for multi-slice two-dimensional or three-dimensional imaging. It outlines the major issues in statistical analysis for fMRI and addresses ways in which the data can be prepared for analysis to minimize artefacts and maximize sensitivity for the detection of activation changes. Finally, the chapter discusses the various applications of fMRI in neuroscience.

Brain activation is known to lead to enhanced perfusion which, together with other physiological changes, results in a decreased deoxyhaemoglobin concentration in regions of neuronal activity. This effect is referred to as the blood oxygenation level dependent (BOLD) effect. The main purpose of this chapter is to outline the acquisition methods for ultra-fast BOLD functional magnetic resonance imaging (fMRI). It helps to explain the basics of echo planar imaging and alternative ultra-fast imaging techniques, discusses possible artefacts and pitfalls, and also studies the requirements for BOLD fMRI acquisition methods, focusing on echo planar imaging (EPI). The chapter discusses the two basic types of spin echo sequences that have been employed for fMRI studies, namely multiple echo sequences and spin echo EPI. The methods discussed traverse k-space in a rectilinear fashion. Moreover, the chapter also describes promising recent developments and mentions that ultra-fast 3D methods are under development which will potentially provide better signal-to-noise ratio and BOLD contrast per unit time than EPI, and which are also less sensitive to inflow effects.

Since most fibromyalgia patients complain of aching and spasm in their muscles, common sense suggests that there must be something wrong with the muscle. This is easier said than agreed upon. For the last 80 years, researchers have been looking for the key to muscle pathology in fibromyalgia. As of this writing, there are highly respected investigators who feel that there is little if anything wrong with fibromyalgia muscles. However, other equally regarded researchers have presented evidence that abnormal muscle metabolism is the linchpin for what goes awry in the disorder. Why are there such discrepancies? Let’s explore what goes on in our muscles. Our body has 640 different muscles, which constitute as much as 40 percent of our weight. When physicians look at muscles of fibromyalgia patients under a simple microscope, they generally appear normal. In fact, muscles must be looked at under an electron microscope (which magnifies the tissue thousands of times) in order to find any consistent abnormalities. In this setting there are subtle alterations, including the deposition of a chemical, glycogen, swollen and abnormal cell organelles known as mitochondria, increased DNA fragmentation ragged red fibers, and smeared muscle cell membranes. Some investigators have shown that magnesium levels are low in the muscles of fibromyalgia patients. So where are the disagreements? Fibromyalgia patients are generally deconditioned. In other words, they are out of shape. Of course, many more people are out of shape than have fibromyalgia, but studies of muscles from out-of-shape people also show some of these alterations. If fibromyalgia muscles don’t look very different from normal muscles under themicroscope, where else can we look for muscle pathology? Muscle strength can be decreased or normal in fibromyalgia, and published studies conflict as to whether or not muscle fatigue is present. Nevertheless, people who are out of shape also have decreased muscle strength. Let’s look at blood flow to muscles. Muscles are fueled by oxygen, which is supplied and carried by arteries. Some muscles in fibromyalgia do not get enough oxygen. “Angina” of the muscles can develop, producing pain if the oxygen supply is decreased.

This chapter talks about the central insect respiratory problem – their capability of regulating oxygen delivery to tissues under variable internal and external conditions – pinpointing in particular which physiological mechanisms insects use to regulate oxygen, and how their bodies do so. It also covers the consequences of oxygen deprivation and of oxygen surplus, taking into account a few selected topics that highlight recent progress, rather than aiming for an encyclopedic scope of the subject. The first part of the chapter narrows in on the problems of tissue hypoxia, which is when insects encounter a decreased supply of oxygen. Oftentimes, the reason that tissue oxygenation turns problematic is because there is gross mismatch between supply and demand. This insufficient tissue oxygenation often occurs when an insect transitions from rest to vigorous activity, or when their environment itself contains a decreased supply of oxygen.

Congenital heart disease (CHD) has been defined as “. . . a gross structural abnormality of the heart or intrathoracic great vessels that is actually or potentially of functional significance” (Mitchell, Korones, and Berendes 1971). Congenital heart disease is the most common single group of congenital abnormalities, accounting for about 30% of the total. The incidence is reported as varying between 0.3% and 1% of all live births. Ten to 15% of children with congenital heart defects have more than one cardiac abnormality; up to one-third also have one or more associated noncardiac congenital abnormalities (Wernovsky 2006). Although some forms of CHD are minor and do not require any medical or surgical intervention, others are very complex and may necessitate a series of staged surgical procedures and/or require life-long medications. Significant improvements in medical and surgical techniques have resulted in increasing numbers of children and adults living with CHD, and it is currently anticipated that 80%–85% of children born with CHD today will survive into adulthood (British Cardiac Society 2002). However, although survival rates have improved dramatically over the last 40 years or so, morbidity remains a concern. Congenital heart defects can be broadly subdivided into two groups, based on changes in the circulation. Acyanotic defects may be due to either a left-to-right shunt or to an obstructive lesion; there is no mixing of desaturated blood in the systemic arterial circulation. With cyanotic defects, there may be either increased or diminished pulmonary flow, and desaturated blood enters the systemic arterial circulation, regardless of whether cyanosis is clinically evident. Unsaturated venous blood bypassing the lungs can result in secondary polycythemia, which is a compensatory mechanism to carry more oxygen to the tissues. This causes increased viscosity, which in turn results in sluggish blood circulation and impeded blood flow, particularly in the capillaries. Poor peripheral blood flow and clubbing of the fingers and toes can result, breathlessness and fatigue often result in a reduced exercise tolerance, and growth may be affected.

The perioperative period can be a life-changing event for many patients, the effects of which can be lifelong for better or worse. The anaesthetist’s communication at this time can have a profound impact on the care of their patients in the matter of both short-term cooperation and long-term perceptions of their hospital experience. Induction of anaesthesia is a stressful time for many patients, young and old. There is an inevitable loss of control when the patient hands this over temporarily to the anaesthetist. In order to enhance cooperation, anaesthetists will reap unexpected benefits by avoiding the use of negative language. Well-meaning staff may, however, sabotage an otherwise smooth induction by telling patients, ‘There is nothing to worry about’ with the implicit suggestion that there is ‘something to worry about’. Unfortunately such well-meaning statements, even when directed at children, tend to yield the opposite effect of what is intended. Patient stress at this time increases suggestibility such that comments frequently function as inadvertent suggestions—be they positive or negative. This can be utilized to enhance the anaesthetist’s ability to provide a smooth, safe and stress-free induction. A typical series of pre-induction communications may go something like, … ‘Don’t worry we won’t drop you’. As the patient is transferred from a trolley to the operating table. ‘The blood pressure cuff gets really tight and may hurt and try not to move while it’s pumping up’. ‘That noise over there is just the nurse checking the drill!’… Explaining what is happening in simple straightforward non-technical language, and at the same time communicating in a positive way, is invariably the more useful approach. For example, …‘Welcome to the operating room Mr P ’. ‘You can relax as we move you to this other bed—you are quite safe’. ‘We will place some monitoring leads on so we can keep you safe and comfortable. A pulse monitor gently placed on your finger, an ECG on your chest and a blood pressure cuff on your arm. As the blood pressure cuff tightens and we take its reading this often allows patients to relax knowing how closely we are looking after them’. …