Brain Edema XIV (eBook)

Preface 6
Contents 7
Igor Klatzo Lecture 14
Bulk Flow and Diffusion Revisited, and Clinical Applications 15
Ischemia and the Blood-Brain Barrier Disorders 26
Experimental Cerebral Ischemia: The Contribution of the Bethesda Group 27
Past and Recent BBB Studies with Particular Emphasis on Changes in Ischemic Brain Edema 30
Increase in Activity of Neutrophils and Proinflammatory Mediators in Rats Following Acute and Prolonged Focal Cerebral Ischemia and Reperfusion 37
Factors in Creepy Delayed Neuronal Death in Hippocampus Following Brain Ischemia– Reperfusion Injury with Long- Term Survival 44
Endogenous Pituitary Adenylate Cyclase Activating Polypeptide Is Involved in Suppression of Edema in the Ischemic Brain 49
Reduced Matrix Metalloproteinase-9 Activity and Cell Death After Global Ischemia in the Brain Preconditioned with Hyperbaric Oxygen 53
Radiation Exposure Prior to Ischemia Decreases Lesion Volume, Brain Edema and Cell Death 56
Effects of VEGF Administration or Neutralization on the BBB of Developing Rat Brain 59
Alterations in Blood–Brain Barrier Function and Brain Pathology by Morphine in the Rat. Neuroprotective Effects of Antioxidant H- 290/ 51 64
Hydrocephalus 70
Clinical Proof of the Importance of Compliance for Hydrocephalus Pathophysiology 71
An Algorithm to Assess the Rehabilitation Potential in Patients with Chronic Hydrocephalus 76
What Can Be Found Inside Shunt Catheters 81
Glue Instead of Stitches: A Minor Change of the Operative Technique with a Serious Impact on the Shunt Infection Rate 86
Animal Experiments to Evaluate Complications of Foreign Materials on Silicone with Shunt Catheters: Preliminary Results 89
Huge Thrombosis as a Consequence of VA-Shunts 92
Does Idiopathic Normal Pressure Hydrocephalus Always Mean a Poor Prognosis? 97
Gravitational Shunt Complications After a Five-Year Follow-Up 103
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 Rate 112
Intracranial Irregularities Beside Hydrocephalus in H-Tx Rats 115
Co-morbidity as a Predictor of Outcome in Patients with Idiopathic Normal- Pressure Hydrocephalus 121
Subarachnoid Hemorrhage and Intracerebral Hemorrhage 125
Effects of Magnesium Sulfate Infusion on Cerebral Perfusion in Patients After Aneurysmal SAH 126
Timing of Serum Active MMP-9 and MMP-2 Levels in Acute and Subacute Phases After Spontaneous Intracerebral Hemorrhage 129
Timing of Serum Soluble HLA-G Levels in Acute and Subacute Phases After Spontaneous Intracerebral Hemorrhage 133
Minocycline Attenuates Brain Edema, Brain Atrophy and Neurological Deficits After Intracerebral Hemorrhage 138
Myocardial Dysfunction in Subarachnoid Hemorrhage: Prognostication by Echo Cardiography and Cardiac Enzymes. A Prospective Study 142
The Effects of Tetrahydrobiopterin on Intracerebral Hemorrhage- Induced Brain Injury in Mice 146
Estrogen Reduces Iron-Mediated Brain Edema and Neuronal Death 149
Imaging and Diagnosis 153
Improving Diagnostic Value of CT Examinations in Hyperacute Ischemic Stroke 154
Pattern Recognition Methods in 1H MRS Monitoring In Vivo of Normal Appearing Cerebellar Tissue After Treatment of Posterior Fossa Tumors 160
Metabolic Changes in Rat Brain Following Intracerebroventricular Injections of Streptozotocin: A Model of Sporadic Alzheimer’s Disease 165
MR Spectroscopic Evaluation of Brain Tissue Damage After Treatment for Pediatric Brain Tumors 170
The Incidence of Imaging Abnormalities after Stereotactic Radiosurgery for Cerebral Arteriovenous and Cavernous Malformations 174
Magnetic Resonance Spectroscopic Evaluation of Brain Tissue Metabolism After Irradiation for Pediatric Brain Tumors in Long- Term Survivors: A Report of Two Cases 178
Evaluation of the Late Effects of CNS Prophylactic Treatment in Childhood Acute Lymphoblastic Leukemia ( ALL) Using Magnetic Resonance Spectroscopy 182
A Non-invasive Assessment of Intracranial Volume Reserve by Measuring Cerebrospinal Fluid Volume with the Aid of CT Imaging 185
Is Neuroradiological Imaging Sufficient for Exclusion of Intracranial Hypertension in Children? Intracranial Hypertension Syndrome Without Evident Radiological Symptoms 189
Trauma and Brain Tissue Injury 195
Substance P Immunoreactivity Increases Following Human Traumatic Brain Injury 196
Hyperbaric Oxygen Preconditioning Reduces Postoperative Brain Edema and Improves Neurological Outcomes After Surgical Brain Injury 202
Following Brain Trauma, Copeptin, a Stable Peptide Derived from the AVP Precusor, Does Not Reflect Osmoregulation but Correlates with Injury Severity 206
The Effects of Selective Brain Hypothermia and Decompressive Craniectomy on Brain Edema After Closed Head Injury in Mice 210
Outcome of Patients with Severe Head Injury After Decompressive Craniectomy 215
Assessing the Neurological Outcome of Traumatic Acute Subdural Hematoma Patients with and without Primary Decompressive Craniectomies 218
Changes in the Blood–CSF Barrier in Experimental Traumatic Brain Injury 221
Dynamics of S100B Release into Serum and Cerebrospinal Fluid Following Acute Brain Injury 228
Ultrastructural and Immunochemical Studies of Glial Scar Formation in Diabetic Rats 232
Significance of Monitoring the Initial Intracranial Pressure on Hematoma Irrigation with Trephination Therapy for Acute Subdural Hematomas in Critical Conditions 237
Surgical Outcome Following a Decompressive Craniectomy for Acute Epidural Hematoma Patients Presenting with Associated Massive Brain Swelling 241
Prognosis for Severe Traumatic Brain Injury Patients Treated with Bilateral Decompressive Craniectomy 245
Posterior Fossa Brain Tissue Injury: Developmental, Neuropsychological, and Neurological Consequences of Brain Tumors in Children 251
Tumor 255
The Role of eNOS in Vascular Permeability in ENU-Induced Gliomas 256
Potential Role of CT Perfusion Parameters in the Identification of Solitary Intra- axial Brain Tumor Grading 262
Treatment 267
Neuromodulation with Pleiotropic and Multimodal Drugs – Future Approaches to Treatment of Neurological Disorders 268
Selected Combination of Neurotrophins Potentiate Neuroprotection and Functional Recovery Following Spinal Cord Injury in the Rat 272
Antibodies to Dynorphin A (1–17) Attenuate Closed Head Injury Induced Blood– Brain Barrier Disruption, Brain Edema Formation and Brain Pathology in the Rat 278
Serine Protease Inhibitor Attenuates Intracerebral Hemorrhage- Induced Brain Injury and Edema Formation in Rat 284
State-of-the-Art management and Monitoring of Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure. A Proposed Algorithm 288
Novel Free Radical Monitoring in Patients with Neurological Emergency Diseases 292
Cerebrolysin Attenuates Blood–Brain Barrier and Brain Pathology Following Whole Body Hyperthermia in the Rat 297
Chronic Hypertension Aggravates Heat Stress-Induced Brain Damage: Possible Neuroprotection by Cerebrolysin 302
Nanoparticles and Brain Edema 309
Carbon Nanotubes in Neuroscience 310
Nanowired-Drug Delivery Enhances Neuroprotective Efficacy of Compounds and Reduces Spinal Cord Edema Formation and Improves Functional Outcome Following Spinal Cord Injury in the Rat 315
A New Antioxidant Compound H-290/51 Attenuates Nanoparticle Induced Neurotoxicity and Enhances Neurorepair in Hyperthermia 323
Influence of Nanoparticles on Blood–Brain Barrier Permeability and Brain Edema Formation in Rats 330
Author Index 336
Subject Index 367

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).