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A distinction between primary and secondary brain damage of vari
ous origin, particularly in acute lesions, such as head injury and
ische mia is not entirely new. The concept is of practical
significance, be cause it is the foremost intention of all clinical
efforts to prevent, or at least attenuate the development of
secondary sequelae. Primary dam age to nervous elements usually
cannot be influenced by treatment. Its prevention is the objective
of prophylactic measures. The current volume gathered prominent
scientists and clinicians from various fields to pro vide a
competent introduction and survey of the various aspects involved
in secondary brain damage. It was attempted to provide criteria for
the distinction between the primary and secondary phenomena on a
morpho logical and functional level, on the basis of the kinetics
involved and, most importantly, regarding the different specific
manifestations, such as disturbances of microcirculation, aspects
of the blood-brain barrier, and of cellular structure and function
at a molecular level. Although it was not expected that a grand
unifying hypothesis will be reached recon cilable with the many,
occasionally opposing views on such a complex subject,
nevertheless, the present volume attains an appropriate result. It
can best be described as a mosaic of many different pieces which
only as an ensemble reflect the current state of the art."
Information is provided from the basic and clinical sciences on the
mechanisms damaging the brain from trauma or ischemia. New aspects
involve the endoplasmic reticulum, mitochondrial failure,
pathobiology of axonal injury, molecular signals activating glial
elements, or the emerging therapeutical role of neurotrophins.
Experimental issues involve a better analysis of the ischemic
penumbra, the salvagable tissue. Therapeutic contributions reach
from the environmental influence to gene expression, including
neuroprotection, such as hibernation - mother nature's experiment -
or hypothermia which is reported to induce cell swelling. Treatment
issues deal also with thrombolysis and combination therapies, or
with the clearance of adverse blood components - LDL/fibrinogen -
by a novel procedure using heparin. Other highlights are discussing
the specificities of pediatric vs. adult brain trauma, or the
evolving role of the Apolipoprotein-E e4 gene in severe head
injury. An update is also provided on an online assessment of the
patient management during the pre- and early hospital phase in
Southern Bavaria. The empirical observation of neuroworsening is
analyzed in further details, whether this is a specificity
autonomously driving the posttraumatic course. Finally, the
unsolved question why drug trials in severe head injury have failed
so far in view of the promising evidence from the laboratory is
subjected to an expert analysis.
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Brain Edema XII - Proceedings of the 12th International Symposium, Hakone, Japan, November 10-13, 2002 (Paperback, Softcover reprint of the original 1st ed. 2003)
T. Kuroiwa, A. Baethmann, Z. Czernicki, J.T. Hoff, U Ito, …
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Discovery Miles 59 870
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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.
The international interdisciplinary gathering of top of secondary
brain damage in brain trauma, as ac- level clinical and laboratory
scientists in Mauls, Italy knowledged from the beginning of these
workshops in has developed from its beginning in 1984into a
fruitful Mauls, the significance of inflammation is all but clear.
tradition where worldwide experts active and knowl- Although
inflammatory phenomena are seen in trauma edgeable in cerebral
ischemia and trauma convene for and ischemia ofthe brain, as
activation ofwhite blood update and exchanges of their most recent
clinical and cells with emigration into the tissue presumably en-
experimental findings and concepts. These meetings hancing damage,
inflammatory cells may have benefi- have, of course, experienced
shifts in emphasis from cial properties as well. Thechapter on the
Janus-faceof the past until now, corresponding to the most actual
inflammation isanalyzing this ambiguity. developments, which were
fascinating clinicians and The exploration of novel cell-biological
mechanisms laboratory scientists alike. The current Supplement of
on a molecular or more systemic basis causing apop- Acta
Neurochirurgica is an example in case. Its virtue totic cell death,
inflammation, or regeneration, provide as before is that authors
contribute articles in a review- useful objectives for
therapeutical interventions ex- like manner on their own field of
research, according pected to be more specific than the present
treatment to the platform presentations at the meeting as indis-
modalities.
Contrary to the neurological manifestations of arterial cerebral
blood flow disturbances, respective conditions resulting fram
obstruction of the cerebro-venous system are far less well
understood. Hence, cerebral sinus vein thrombosis (CSVT) ranks
prominently among the group of neglected diseases of the brain.
This might be attributable (a) to the diagnostic difficulties of
the disorder and (b) to the fact that CSVT is associated with a
host of heterogeneous neurological symptoms which often are not
specific for the underlying venous flow disorder. Another
complicating aspect is that CSVT is a consequence of other diseases
as disparate as focal infection, trauma, neoplasia, or a thrombosis
disposition caused by oral contraceptive use. Although progress has
been made in establishing the correct diagnosis of the syndrome,
many problems remain as the discussions contained within this
volume vividly demonstrate. The same is true for the present
understanding of the pathophysiological basis of the disease, eg,
concerning the cerebro-venous circulation, the hemodynamic and
neuropathological consequences in particular. Part of these
deficits may be attributed to a scarcity of solid experimental data
due to the limited availability of animal models. However, relevant
experimental models are required for an in-depth analysis of the
pathophysiological mechanisms, eg, causing brain tissue damage in
relationship with the topographical distribution of the venous flow
obstruction and, most importantly, for the testing of specific
methods of treatment.
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Brain Edema X - Proceedings of the Tenth International Symposium San Diego, California, October 20-23, 1996 (Paperback, Softcover reprint of the original 1st ed. 1997)
H.E. James, L. F. Marshall, H.-J. Reulen, A. Baethmann, A. Marmarou, …
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R1,628
Discovery Miles 16 280
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This volume is a compilation of papers presented at the Tenth
International Symposium on Brain Edema held on October 20-23, 1996,
in San Diego, California. This follows the sequence of meetings
that was initiated 31 years ago in the First International
Symposium held in Vienna. Subsequent symposiums were held in Mainz,
Montreal, Berlin, Groningen, Tokyo, Baltimore, Bern, and Tokyo CY
okohama). A considerable number of papers was chosen from over 100
papers that were received. The organizers wish to thank the
Advisory Committee for the excellent work done in selection of the
papers. We also wish to thank all the persons who contributed to
the success of the Tenth International Symposium, especially the
staff who worked behind the scenes. These papers were reviewed,
edited, approved or disapproved by the Editorial Board. Those
manuscripts that were felt not pertinent to this publication were
not accepted by the Editorial Board. Therefore, the excellent
quality of those that are in the book are a reflection of the
authors' dedication and work and that of those of the Editorial
Board in their review process. For the reader's convenience, the
papers are structured according to the various disease processes
which are associated with the primary topic: hypertension,
hydrocephalus, infection, ischemia, tumor, etc. We do hope that the
reader will enjoy the articles and that they will provide an
impetus and insight for future work.
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Brain Edema XI - Proceedings of the 11th International Symposium, Newcastle-upon-Tyne, United Kingdom, June 6-10, 1999 (Paperback, Softcover reprint of the original 1st ed. 2000)
A.D. Mendelow, A. Baethmann, Z. Czernicki, J.T. Hoff, U Ito, …
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R6,116
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Discovery Miles 57 030
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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.
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