Czernicki / Baethmann / Ito Brain Edema XIV

1. Auflage 2009
ISBN: 978-3-211-98811-4
Verlag: Springer Wien
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, Band 106, 403 Seiten, eBook

Reihe: Acta Neurochirurgica Supplementum

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.

Zielgruppe

Research

Autoren/Hrsg.

Czernicki, Zbigniew

Baethmann, Alexander

Ito, Umeo

Katayama, Yoichi

Kuroiwa, Toshihiko

Mendelo, David

Mendelow, Alexander David

Dav, Alexander

Inhaltsverzeichnis

Igor Klatzo Lecture.- Ischemia and the Blood-Brain Barrier Disorders.- Hydrocephalus.- Subarachnoid Hemorrhage and Intracerebral Hemorrhage.- Imaging and Diagnosis.- Trauma and Brain Tissue Injury.- Tumor.- Treatment.- Nanoparticles and Brain Edema.

Leseproben

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).