A distinguished international panel of authors define our current understanding of neuronal damage after ischemia and critically review the significant recent developments and progress in cerebrovascular accident (CVA) drug trials, both in animal models and in the clinical setting. These leading basic and fundamental authorities survey such important new drugs as calcium-influx inhibitors, free-radical scavenging drugs, glutamate and glycinergic antagonists, and immune suppressors. They also evaluate all the latest findings concerning calcium homeostasis, glutamate toxicity, gene activation, and the role of free radicals, glycine, and hormones. Chapters devoted to the neuroimaging of stroke, clinical trials, and the role of cerebral immune activation complete this informative collection of cutting-edge reviews.

In this volume, one of a series of monographs devoted to the problems of cerebral ischemia and related topics, we present the proceedings of an international conference on Cerebral Ischemia and Basic Mechanisms held in Bad Schachen/Lake Constance, Germany in June 1992. The enormous progress in research recently on the basic mechanisms associated with cerebral ischemia has provided greater insight into the pathophysiological mechanisms of reduced brain perfusion and decreased cerebral metabolism. The high technology instrumentation used to unravel the intricacies of cerebral blood flow and metabolism includes positron emission tomography and magnetic resonance imaging. A description of sophisticated neurophysiological techniques will give the reader insight into new models of reversible and irreversible tissue damage and changes at the molecular level have been described. The therapeutic approaches which have developed from this re search have been or will be used in clinical trials and will open new avenues in the treatment of stroke. The organizers of the meeting would like to thank the advisory board for its helpful suggestions and the Deutsche Forschungsgemeinschaft and other sponsors for their important support.

In this timely volume, eminent researchers provide detailed coverage of the relevant function of neurochemical correlates to cerebral ischemia as well as their pathophysiological significance.

First multi-year cumulation covers six years: 1965-70.

In contrast to dementia of the Alzheimer type, the subject of dementia subsequent to cerebral ischemia has been discussed rather rarely. Now this book provides a summary of the brain morphology, neurochemistry and clinical aspects of dementia subsequent to cerebral ischemia. The contributions discuss the similarities and differences between the two predominant dementia types. The broad range of aspects cover 1) the morphology and morphobiology of brain tissue during aging and under the two pathological condi- tions, 2) the neuropathochemistry of post mortem brain tissue of patients as well as brain tissue from experimental animals, 3) CSF changes during aging and in dementia states and 4) clinical research, mainly using brain imaging tech- niques to differentiate between dementia types and to find a basis for rational therapeutic approaches.

In the eight years since the publication of Volume 63 of Progress in Brain Research, on this subject, developments in the research field have been very fast. For example, receptor physiology and pharmacology is now an intensively studied field, and the excitotoxic hypothesis of cell death is commonly accepted. Furthermore, it is recognized that ischemia and other insults give rise to a sustained depression of overall protein synthesis, yet lead to the expression of dormant genes and to synthesis of new proteins.In view of this development, this volume focusses on the cellular and molecular aspects of ischemic brain damage. The book will be of great value to all those interested in the pathophysiology of ischemic and traumatic brain damage.

It has been well recognized that following an ischemic insult many nerve cells of the brain are not killed outright, but may suffer a "delayed neuronal death" or even recover. This led to the concept of "maturation phenomenon" with its main implication that the maturation of ischemic lesions may provide a "window of opportunity" i.e. a period of time when the injury to neuronal elements is still reversible, and during which an application of proper therapeutic measures might be successful. The symposium on Maturation Phenomenon in Cerebral Ischemia was the first international meeting focussed primarily on this subject and the resulting publication contains presentations and discussionsby prominent researchers engaged in this field. This book should stimulate further research on potential of brain tissue for recovery, and particularly with regard to a functional recovery of neurons suffering from chronic ischemic injury.

It is increasingly evident that polyunsaturated fatty acids (PUFA), which in the past were often believed to be mere components of cellular membranes of neural tissue, are actually major determinants of the functional properties of neural cells and are intimately involved in brain disease processes. The two families of PUF A, which are derived from the essential polyenes, linoleic (18:26) and a-linolenic (18:33) acids, constitute a major proportion (-30%) of the total fatty acids esterified to brain phospholipids. Each family is distributed in membranes in a highly specific manner with respect to brain region, cell type, and position within each of the phosphoglycerides. Unlike their behavior in other organs, the PUF A components of brain turn over slowly and are relatively resistant to dietary modification. Their unique distribution and stability suggest that they play an important role in determining the functional properties of neural cells. However, until recently very little was known regarding the precise nature of their involvement.