: Zbigniew Czernicki, Alexander Baethmann, Umeo Ito, Yoichi Katayama, Toshihiko Kuroiwa, David Mendelo
: Zbigniew Czernicki, Alexander Baethmann, Umeo Ito, Yoichi Katayama, Toshihiko Kuroiwa, Alexander Dav
: Brain Edema XIV
: Springer-Verlag
: 9783211988114
: 1
: CHF 189.80
:
: Klinische Fächer
: English
: 403
: Wasserzeichen/DRM
: PC/MAC/eReader/Tablet
: PDF
The XIV International Symposium on Brain Edema and Brain Tissue Injury took place in Warsaw, Poland, on 11-14 June 2008. Two prominent members of the International Society for Brain Edema: Dr. Igor Klatzo and Dr. Julien Hoff have passed away after the last 2005 Symposium in Ann Arbor, USA. Dr. Igor Klatzo was actually the founder of the Society, and the Advisory Board decided to commemorate Dr. Igor Klatzo by introducing a lecture named after him to be given at the Symposium. Prof. Dr. Hans-Jürgen Reulen has been honored to give the frst Igor Klatzo lecture entitled 'Bulk Flow and Diffusion revisited, and Clinical Applications'. This volume contains 65 out of the 104 papers presented at the Symposium as lectures or posters. The topics of the Symposium were similar to those discussed at the previous ones. Many discussions focused on clinical work especially diagnosis, subarachnoid hemorrhage, hydrocephalus, and traumatic brain injury. Diagnosis and therapy, including surgical methods, have also been verifed. Much attention was drawn to the application of decompressive craniectomy in the treatment of posttr- matic intracranial hypertension. The pathomechanisms of brain edema and tissue injury studied in experimental models have been also presented.
Substance P Immunoreactivity Increases Following Human Traumatic Brain Injury (p. 211)

Andrew C. Zacest, Robert Vink, Jim Manavis, Ghafar T. Sarvestani, and Peter C. Blumbergs

Abstract Recent experimental evidence suggests that neuropeptides, and in particular substance P (SP), are released following traumatic brain injury (TBI) and may play a significant role in the aetiology of cerebral edema and increased intracranial pressure. Whether SP may play a similar role in clinical TBI remains unknown and was investigated in the current study. Archival post-mortem material was selected from patients who had sustained TBI, had died and had undergone post-mortem and detailed neuropathological examination (n = 13). A second cohort of patients who had died, but who showed no neuropathological abnormality (n = 10), served as case controls. Changes in SP immunoreactivity were examined in the cerebral cortex directly beneath the subdural haematoma in 7 TBI cases and in proximity to contusions in the other 6 cases. Increased SP perivascular immunoreactivity was observed after TBI in 10/13 cases, cortical neurones in 12/13 and astrocytes in 10/13 cases. Perivascular axonal injury was observed by amyloid precursor protein (APP) immunoreactivity in 6/13 TBI cases. Co-localization of SP and APP in a small subset of perivascular fibres suggests perivascular axonal injury could be a mechanism of release of this neuropeptide. The abundance of SP fibres around the human cerebral microvasculature, particularly post capillary venules, together with the changes observed following TBI in perivascular axons, cortical neurones and astrocytes suggest a potentially important role for substance P in neurogenic inflammation following human TBI.

Keywords Neurotrauma • edema • brain swelling • neurogenic inflammation • tachykinin • substance P

Introduction

A number of studies have now demonstrated that much of the mortality and morbidity in survivors following traumatic brain injury (TBI) is associated with the development of a secondary injury cascade that occurs between hours and days after the insult (23). While a number of factors have been identified as participating in this secondary injury, it has been recognised that edema formation is a critical determinant of outcome after TBI. Our recent experimental studies have shown that neurogenic inflammation may play an important role in edema formation following CNS insults (9,21,26).

Neurogenic inflammation is a neurally elicited reaction that has typical characteristics of an inflammatory reaction including vasodilation, protein extravasation and tissue swelling. Studies of peripheral nerves have demonstrated that neurogenic inflammation is the result of the stimulation of C-fibres, which causes the release of neuropeptides (1).

These neuropeptides cause plasma protein extravasation from blood vessels and associated edema formation. Although a number of neuropeptides have been implicated in this process, it is generally accepted that substance P (SP) increases microvascular permeability leading to edema formation whilst calcitonin gene related peptide (CGRP) is an extremely potent vasodilator (17). Substance P has been shown to be primarily associated with the formation of vasogenic edema by numerous potential interactions with target cells that produce vasoactive mediators (20,22), and with the endothelium (19,28) which leads to changes in vascular ultrastructure (8,11).
Preface6
Contents7
Igor Klatzo Lecture14
Bulk Flow and Diffusion Revisited, and Clinical Applications15
Ischemia and the Blood-Brain Barrier Disorders26
Experimental Cerebral Ischemia: The Contribution of the Bethesda Group27
Past and Recent BBB Studies with Particular Emphasis on Changes in Ischemic Brain Edema30
Increase in Activity of Neutrophils and Proinflammatory Mediators in Rats Following Acute and Prolonged Focal Cerebral Ischemia and Reperfusion37
Factors in Creepy Delayed Neuronal Death in Hippocampus Following Brain Ischemia– Reperfusion Injury with Long- Term Survival44
Endogenous Pituitary Adenylate Cyclase Activating Polypeptide Is Involved in Suppression of Edema in the Ischemic Brain49
Reduced Matrix Metalloproteinase-9 Activity and Cell Death After Global Ischemia in the Brain Preconditioned with Hyperbaric Oxygen53
Radiation Exposure Prior to Ischemia Decreases Lesion Volume, Brain Edema and Cell Death56
Effects of VEGF Administration or Neutralization on the BBB of Developing Rat Brain59
Alterations in Blood–Brain Barrier Function and Brain Pathology by Morphine in the Rat. Neuroprotective Effects of Antioxidant H- 290/ 5164
Hydrocephalus70
Clinical Proof of the Importance of Compliance for Hydrocephalus Pathophysiology71
An Algorithm to Assess the Rehabilitation Potential in Patients with Chronic Hydrocephalus76
What Can Be Found Inside Shunt Catheters81
Glue Instead of Stitches: A Minor Change of the Operative Technique with a Serious Impact on the Shunt Infection Rate86
Animal Experiments to Evaluate Complications of Foreign Materials on Silicone with Shunt Catheters: Preliminary Results89
Huge Thrombosis as a Consequence of VA-Shunts92
Does Idiopathic Normal Pressure Hydrocephalus Always Mean a Poor Prognosis?97
Gravitational Shunt Complications After a Five-Year Follow-Up103
Is It Possible to Minimize Overdrainage Complications with Gravitational Units in Patients with Idiopathic Normal Pressure Hydrocephalus? Protocol of the Randomized Controlled SVASONA Trial ( ISRCTN51046698)109
Early Shunting Using the Parallel Shunt System in Hemorrhagic Hydrocephalus: In Vitro Testing of Handling, Technical Complications and Clogging Rate112
Intracranial Irregularities Beside Hydrocephalus in H-Tx Rats115
Co-morbidity as a Predictor of Outcome in Patients with Idiopathic Normal- Pressure Hydrocephalus121
Subarachnoid Hemorrhage and Intracerebral Hemorrhage125
Effects of Magnesium Sulfate Infusion on Cerebral Perfusion in Patients After Aneurysmal SAH126
Timing of Serum Active MMP-9 and MMP-2 Levels in Acute and Subacute Phases After Spontaneous Intracerebral Hemorrhage129
Timing of Serum Soluble HLA-G Levels in Acute and Subacute Phases After Spontaneous Intracerebral Hemorrhage133
Minocycline Attenuates Brain Edema, Brain Atrophy and Neurological Deficits After Intracerebral Hemorrhage138
Myocardial Dysfunction in Subarachnoid Hemorrhage: Prognostication by Echo Cardiography and Cardiac Enzymes. A Prospective Study142
The Effects of Tetrahydrobiopterin on Intracerebral Hemorrhage- Induced Brain Injury in Mice146
Estrogen Reduces Iron-Mediated Brain Edema and Neuronal Death149
Imaging and Diagnosis153
Improving Diagnostic Value of CT Examinations in Hyperacute Ischemic Stroke154
Pattern Recognition Methods in 1H MRS Monitoring In Vivo of Normal Appearing Cerebellar Tissue After Treatment of Posterior Fossa Tumors160
Metabolic Changes in Rat Brain Following Intracerebroventricular Injections of Streptozotocin: A Model of Sporadic Alzheimer’s Disease165
MR Spectroscopic Evaluation of Brain Tissue Damage After Treatment for Pediatric Brain Tumors170
The Incidence of Imaging Abnormalities after Stereotactic Radiosurgery for Cerebral Arteriovenous and Cavernous Malformations174
Magnetic Resonance Spectroscopic Evaluation of Brain Tissue Metabolism After Irradiation for Pediatric Brain Tumors in Long- Term Survivors: A Report of Two Cases178
Evaluation of the Late Effects of CNS Prophylactic Treatment in Childhood Acute Lymphoblastic Leukemia ( ALL) Using Magnetic Resonance Spectroscopy182
A Non-invasive Assessment of Intracranial Volume Reserve by Measuring Cerebrospinal Fluid Volume with the Aid of CT Imaging185
Is Neuroradiological Imaging Sufficient for Exclusion of Intracranial Hypertension in Children? Intracranial Hypertension Syndrome Without Evident Radiological Symptoms189
Trauma and Brain Tissue Injury195
Substance P Immunoreactivity Increases Following Human Traumatic Brain Injury196