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Traumatic brain injury (TBI) remains a significant source of death and permanent disability, contributing to nearly one-third of all injury related deaths in the United States and exacting a profound personal and economic toll. Despite the increased resources that have recently been brought to bear to improve our understanding of TBI, the developme
Neuronal Networks in Brain Function, CNS Disorders, and Therapeutics, edited by two leaders in the field, offers a current and complete review of what we know about neural networks. How the brain accomplishes many of its more complex tasks can only be understood via study of neuronal network control and network interactions. Large networks can undergo major functional changes, resulting in substantially different brain function and affecting everything from learning to the potential for epilepsy. With chapters authored by experts in each topic, this book advances the understanding of: - How the brain carries out important tasks via networks - How these networks interact in normal brain function - Major mechanisms that control network function - The interaction of the normal networks to produce more complex behaviors - How brain disorders can result from abnormal interactions - How therapy of disorders can be advanced through this network approach This book will benefit neuroscience researchers and graduate students with an interest in networks, as well as clinicians in neuroscience, pharmacology, and psychiatry dealing with neurobiological disorders. - Utilizes perspectives and tools from various neuroscience subdisciplines (cellular, systems, physiologic), making the volume broadly relevant - Chapters explore normal network function and control mechanisms, with an eye to improving therapies for brain disorders - Reflects predominant disciplinary shift from an anatomical to a functional perspective of the brain - Edited work with chapters authored by leaders in the field around the globe – the broadest, most expert coverage available
Work on the human brainstem has been impeded by the unavailability of a comprehensive diagrammatic and photographic atlas. In the authors' preliminary work on the morphology of the human brainstem (The Human Nervous System, 1990), Paxinos et al demonstrated that it is possible to use chemoarchitecture to establish a number of human homologs in structures known to exist in the rat, the most extensively studied species. Now, with the first detailed atlas on the human brainstem in more than forty years, the authors present an accurate, comprehensive, and convenient reference for students, researchers, and pathologists. Key Features * The first detailed atlas on the human brainstem in more than forty years * Delineated as accurately as The Rat Brain in Stereotaxic Coordinates, Second Edition (Paxinos/Watson, 1986), the most cited book in neuroscience * Based on a single brain from a 59-year-old male with no medical history of neurological or psychiatric illness * Represents all areas of the medulla, pons, and midbrain in the plane transverse to the longitudinal axis of the brainstem * Consists of 64 plates and 64 accompanying diagrams with an interplate distance of half a millimeter * The photographs are of Nissl and acetylcholinesterase (AChE) stained sections at alternate levels * Establishes systematically the human homologs to nuclei identified in the brainstem of the rat Reviewed by leading neuroanatomists * An accurate and convenient guide for students, researchers, and pathologists
Based on advances in biotechnology and neuroscience, non-invasive neuromodulation devices are poised to gain clinical importance in the coming years and to be of increasing interest to patients, clinicians,health systems, payers, and industry. Evidence suggests that both therapeutic and non-therapeutic applications of non-invasive neuromodulation will continue to expand in coming years, particularly for indications where treatments are currently insufficient, such as drug-resistant depression. Given the growing interest in non-invasive neuromodulation technologies, the Institute of Medicine's Forum on Neuroscience and Nervous System Disorders convened a workshop, inviting a range of stakeholders - including developers of devices and new technologies, researchers, clinicians, ethicists, regulators, and payers - to explore the opportunities, challenges, and ethical questions surrounding the development, regulation, and reimbursement of these devices for the treatment of nervous system disorders as well as for non-therapeutic uses, including cognitive and functional enhancement. This report highlights the presentation and discussion of the workshop.
The first report that rapid eye movements occur in sleep in humans was published in 1953. The research journey from this point to the realization that sleep consists of two entirely independent states of being (eventually labeled REM sleep and non-REM sleep) was convoluted, but by 1960 the fundamental duality of sleep was well established including the description of REM sleep in cats associated with “wide awake” EEG patterns and EMG suppression. The first report linking REM sleep to a pathology occurred in 1961 and a clear association of sleep onset REM periods, cataplexy, hypnagogic hallucinations and sleep paralysis was fully established by 1966. When a naïve individual happens to observe a full-blown cataplexy attack, it is both dramatic and unnerving. Usually the observer assumes that the loss of muscle tone represents syncope or seizure. In order to educate health professionals and the general public, Christian Guilleminault and I made movies of full-blown cataplectic episodes (not an easy task). We showed these movies of cataplexy attacks to a number of professional audiences, and were eventually rewarded with the report of a similar abrupt loss of muscle tone in a dog. We were able to bring the dog to Stanford University and with this as the trigger, we were able to develop the Stanford Canine Narcolepsy Colony. Breeding studies revealed the genetic determinants of canine narcolepsy, an autosomal recessive gene we termed canarc1. Emmanuel Mignot took over the colony in 1986 and began sequencing DNA, finally isolating canarc1 in 1999.
GABA (gamma-aminobutyric acid) is the main neurotransmitter regulating sleep. The majority of drugs presently in use for the treatment of sleep disorders act by enhancing GABAergic neuronal inhibition. The GABA system is, therefore, of prime clinical relevance for the therapy of insomnia. The focus of this volume is on the neuropsychopharmacology and the clinical impact of the GABA system in regulating sleep and wakefulness. It presents molecular, neuropharmacological, systems-biological and clinical approaches to the understanding of the mechanism of action of GABA and GABAergic drugs. It also explores the role of GABA in the basic drives that affect sleep, and the influences that adapt sleep and wakefulness to external events.