The Maturation Phenomenon, described by Ito et al. in 1975 [3) on the basis of his to logical observations in the hippocampus as well as other portions of the cerebral hemisphere, refers to the hours or days of delay in the development of pathological changes in various parameters of ischemic injury following the restoration of blood flow to the ischemic brain. There is a direct relationship between the intensity of ischemic insult and the speed and rate of maturation of ischemic injury, a lesser intensity being associated with slower and less severe development of the lesions. The delayed neuronal death of CAl pyramidal cells of the hippocampus [8) is a classic example. In the cerebral cortex, with increasing intensity of the ischemic insult, the maturation phenomenon of ischemic injuries intensifies, seamlessly, from less exten sive to more extensive disseminated selective neuronal necrosis (DSNN), and then further to cerebral infarction upon reaching a critical threshold [1,2,4,6,7). We also have found that following ischemic insults just under the threshold level required to induce infarction, only disseminated selective neuronal necrosis (DSNN) progresses, while following ischemic insults at the threshold level, initially only DSNN develops, followed by the evolution of a gradually enlarging infarcted focus [5, 7). The reporting of this phenomenon boosted research in the field, as it became evi dent that ischemic damage is not a sudden event, but a process potentially susceptible to therapeutic intervention.

The maturation phenomenon, first described by Ito et al. in 1975, refers to postischemic changes that develop hours or days after an ischemic insult. The delayed neuronal death of CA1 pyramidal cells of the hippocampus is a classic example. The report of the phenomenon boosted research in the field, as it became evident that ischemic damage is not a sudden event, but a process potentially susceptible to therapeutic intervention. Since then a growing number of studies have improved our knowledge on mechanisms of cell death and recovery. This volume contains the presentations of the 4th international symposium, held in New Orleans in October/November 1999, grouped in sections covering apoptosis and/or necrosis, neuronal recovery vs. death, and protection against infarction. It outlines the present status of investigations and provides further stimulation for research in this field.

Many nerve cells of the brain which are not killed outright may suffer delayed death or recovery after ischemic insult. This fact has led to the concept of "maturation phenomenon" of neuronal injuries. Since the 1st International Symposium on Maturation Phenomenon in 1990, new developments, particularly in molecular biology, have been rapidly bringing new information about molecular nature and mechanisms of cell death. This book contains the presentations of the 2nd International Symposium held in Tokyo in April 1996. The latest developments in maturation phenomenon and the present status of investigation are described and further stimulation of research in this field is provided.

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.

Brain edema is a simple phenomenon – an abnormal increase of brain tissue volume by the increase of brain tissue water content. However the etiology is not simple and relating to a wide variety of neurological disorders including ischemia, trauma, tumor, hemorrhage and hydrocephalus. It is still a major cause of death in the neurological/neurosurgical ward. This volume is an up-to-date report on progress in brain edema research, diagnosis and treatment, including papers presented at the 12th International Symposium on Brain Edema and Brain Tissue Injury in 2002. Major topics include molecular biology and blood-brain barrier disorders, ischemic and traumatic brain edema, imaging and diagnosis of brain edema, treatment and radiation effect. Various papers in the rapidly growing fields of neuroimaging and molecular medicine are also included.

Brain edema is found in a wide variety of clinical disorders including stroke, intracerebral haemorrhage, subarachnoid haemorrhage, head injury, brain tumors and hydrocephalus. This volume brings together clinical and basic scientists from all over the world. Their expertise in the understanding of brain edema and shifts in brain water compartments has led to a further significant step in our understanding of those diseases characterized by brain edema. This book has also drawn on the expertise of the International Advisory Board of the Brain Edema Society, who have carefully summarized each section, thus providing an easy-to-read summary of the latest advances in each subject. The book is therefore much more than a collection of papers: it represents a critical appraisal and puts each paper into modern scientific context. The greatest advances have come from the rapid development of modern imaging techniques, especially with magnetic resonance imaging (MRI). Imaging can now produce "water maps” and "metabolic profiles” that bring brain metabolism and water content right into every clinic with access to MRI. This book provides the background knowledge to understand these pathophysiological changes.

Because stroke is essentially a disease of the vessels and blood flow, the most fundamental aspects of ischemic blood flow in the brain are under investigation by researchers. Their work was the focus of the sixth in the series of Keio University International Symposia for Life Sciences and Medicine, held in Tokyo in 1999. Selected here are 55 papers from the symposium, covering the buffy coat (glycocalyx) of endothelial cells, the blood-brain barrier and permeability, gene expression, vascular reactivity, dysregulation, inflammatory deterioration, cortical spreading depression, edema, microvascular derangement, and pathology, in ten major sections. The book includes the thought-provoking discussions that followed the presentations, thus providing an invaluable source of up-to-date information not only for researchers investigating microcirculation but also for clinicians implementing the most effective treatment for stroke patients.

This volume contains 93 papers from internationally recognized experts in the field of brain edema and brain injury. The papers include human and animal studies on edema following stroke, cerebral hemorrhage, traumatic brain injury, spinal cord injury and hydrocephalus. Papers also address fluid dynamics in the brain (including the role of aquaporins).

Leading neuroscience researchers offer a fresh perspective on neuronal function by examining all its many components-including their pertubation during major disease states-and relate each element to neuronal demands. Topics range from the dependency of neurons on metabolic supply, as well as on both ion and transmitter homeostasis, to their close interaction with the myelin sheath. Also addressed are the astrocytic signaling system that controls synaptic transmission, the extracellular matrix and space as communication systems, the role of blood flow regulation in neuronal demand and in blood-brain barrier function, and inflammation and the neuroimmune system. Insightful and integrative, The Neuronal Environment: Brain Homeostasis in Health and Disease demonstrates a clear new understanding that neurons do not work in isolation, that they need constant interactions with other brain components to process information, and that they are not the only information processing system in the brain.

Covering neuroscience and rehabilitation strategies, an essential handbook and reference for multidisciplinary stroke rehabilitation teams.