Jasper's Basic Mechanisms, Fourth Edition, is the newest most ambitious and now clinically relevant publishing project to build on the four-decade legacy of the Jasper's series. In keeping with the original goal of searching for "a better understanding of the epilepsies and rational methods of prevention and treatment.", the book represents an encyclopedic compendium neurobiological mechanisms of seizures, epileptogenesis, epilepsy genetics and comordid conditions. Of practical importance to the clinician, and new to this edition are disease mechanisms of genetic epilepsies and therapeutic approaches, ranging from novel antiepileptic drug targets to cell and gene therapies.

As a truly translational area of biomedical investigation, epilepsy research spans an extraordinary breadth of subjects and involves virtually every tool that modern neuroscience has at its disposal. The Encyclopedia of Basic Epilepsy Research provides an up to date, comprehensive reference for all epilepsy researchers. With an expert list of authors, the encyclopedia covers the full spectrum of research activities from genes and molecules to animal models and human patients. The encyclopedia's electronic format also provides unparalleled access to frequent updates and additions, while the limited edition print version provides another option for owning this content. The Encyclopedia of Basic Epilepsy Research is an essential resource for researchers of all levels and clinicians who study epilepsy. The only comprehensive reference for basic research and current activities in epilepsy Electronic format provides fast and easy access to updates and additions, with limited print version available as well Contains over 85 articles, all written by experts in epilepsy research

Written and edited by world-renowned authorities, this three-volume work is, to quote a reviewer, "the definitive textbook about seizures and epilepsy". This Second Edition is thoroughly updated and gives you a complete print and multimedia package: the three-volume set plus access to an integrated content Website. More than 300 chapters cover the spectrum of biology, physiology, and clinical information, from molecular biology to public health concerns in developing countries. Included are detailed discussions of seizure types and epilepsy syndromes; relationships between physiology and clinical events; psychiatric and medical comorbidity; conditions that could be mistaken for epilepsy; and an increasing range of pharmacologic, surgical, and alternative therapies, including vagus nerve stimulation and deep brain stimulation. This edition describes many new antiepileptic drugs, major advances in surgical treatment, and state-of-the-art neuroimaging, EEG, and other technologies for diagnosis and seizure prediction. A companion Website offers instant access to the complete, fully searchable text, plus an image bank of additional figures, video footage, and annual updates to selected chapters.

Includes bibliographical references and index.

Basic Neurochemistry: Molecular, Cellular and Medical Aspects, a comprehensive text on neurochemistry, is now updated and revised in its Seventh Edition. This well-established text has been recognized worldwide as a resource for postgraduate trainees and teachers in neurology, psychiatry, and basic neuroscience, as well as for graduate and postgraduate students and instructors in the neurosciences. It is an excellent source of information on basic biochemical processes in brain function and disease for qualifying examinations and continuing medical education. - Completely updated with 60% new authors and material, and entirely new chapters - Over 400 fully revised figures in splendid color

This book summarizes current evidence of astrocyte dysfunction in epilepsy and discusses presumed underlying mechanisms. Epilepsy is characterized by the periodic occurrence of seizures. Currently available anticonvulsant drugs and therapies are insufficient to controlling seizures in about one third of patients. Thus, there is an urgent need for new therapies that prevent generation of the disorder and improve seizure control in individuals already afflicted. The vast majority of epileptic cases are of idiopathic origin with their underlying mechanisms being unclear. Neurosurgical specimens from patients presenting with mesial temporal lobe epilepsy (MTLE) demonstrate marked reactive gliosis. Since recent studies have implicated astrocytes in important physiological roles in the CNS, such as synchronization of neuronal firing, it is plausible that they may also have a role in seizure generation and/or seizure spread. In support of this view, various membrane channels, receptors, and transporters in astrocytic membranes are altered in the epileptic brain. Excitingly, recent evidence suggests that in the course of the pathogenesis of MTLE, these glial changes alter homeostatic network functions and temporally precede the alterations in neurons. These findings might eventually classify MTLE as a glial rather than a neuronal disorder, and identify astrocytes as promising new targets for the development of more specific antiepileptogenic therapeutic strategies. Although research on astrocytes in epilepsy is still in its infancy, this book clearly demonstrates a critical role of astrocytes in the disturbance of K+ and transmitter homeostasis and its impact on seizure generation.

Emerging data suggest a link between Alzheimer’s disease (AD) and epilepsy. AD and other dementias pose increased risk for seizures, with seizure incidence in AD up to ten times greater than in age-matched controls. Mouse models of AD also demonstrate seizures and abnormal spikes or sharp wave discharges (“interictal epileptiform discharges” [IEDs]) on electroencephalography (EEG). Seizures and IEDs may underlie fluctuating cognitive abilities in AD, with the impact of antiseizure medication (ASM) requiring further investigation. Many epilepsy patients have memory and other cognitive deficits, due to multiple factors. Most adult-onset epilepsy occurs in people =60 years of age, and epilepsy patients are at increased risk of developing dementia. Hyperphosphorylated tau and amyloid deposits were found in resected temporal lobe tissue of epilepsy patients, similar to AD, and increased total and phosphorylated tau levels in the cerebrospinal fluid may predict the onset of AD and other dementias. The mechanisms underlying the associations between AD, epilepsy, tau deposition, and beta amyloid plaques, and their relationships to clinical features, are unknown. Some epilepsy patients develop dementia, and some AD patients develop seizures, while others do not. Analyses of resected tissue in epilepsy patients also suggest variable amyloid and tau deposition across patients and studies. Who is at risk? What does shared pathology indicate regarding disease development, progression, and treatment? Better understanding of the associations between epilepsy and dementia with respect to epidemiology, pathophysiology, genetics, clinical presentations, and treatment approaches based on animal models and human studies is needed to optimize patient care. Insight into the relationship between epilepsy and AD requires various approaches, including tissue analysis, imaging, genetic techniques, cognitive testing, and electroencephalography in animals and humans. We welcome manuscripts that span these approaches, including original research articles, brief research articles, clinical trials, case reports, reviews, systematic reviews, mini-reviews, methods articles, hypothesis and theory articles, perspectives, and opinions. Themes may include: • Diagnosis (e.g., seizure or interictal discharge detection in dementia patients, distinguishing comorbid dementia from epilepsy-related cognitive dysfunction) • Epidemiology (e.g., incidence and prevalence of comorbid AD and epilepsy, occurrence of epilepsy in other dementias, seizure types, age or stage of onset) • Genetic risk factors • Pathophysiology underlying seizure generation in AD and cognitive decline in epilepsy • Treatment approaches (e.g., effects of ASMs on cognitive decline, impact of disease modifying AD treatments on seizures, neurostimulation) • What can be learned from other disorders in which cognitive deficits and seizures are common (i.e., traumatic brain injury)