Brain Injuries - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

BRAIN INJURIES A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES J AM...

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BRAIN

INJURIES A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES

J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS

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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2003 by ICON Group International, Inc. Copyright 2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1

Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Brain Injuries: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83798-8 1. Brain Injuries-Popular works. I. Title.

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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.

Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail: [email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.

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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on brain injuries. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.

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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.

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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes & Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health

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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON BRAIN INJURIES ......................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Brain Injuries................................................................................ 4 E-Journals: PubMed Central ....................................................................................................... 34 The National Library of Medicine: PubMed ................................................................................ 36 CHAPTER 2. NUTRITION AND BRAIN INJURIES ............................................................................... 61 Overview...................................................................................................................................... 61 Finding Nutrition Studies on Brain Injuries............................................................................... 61 Federal Resources on Nutrition ................................................................................................... 66 Additional Web Resources ........................................................................................................... 66 CHAPTER 3. ALTERNATIVE MEDICINE AND BRAIN INJURIES......................................................... 67 Overview...................................................................................................................................... 67 National Center for Complementary and Alternative Medicine.................................................. 67 Additional Web Resources ........................................................................................................... 74 General References ....................................................................................................................... 75 CHAPTER 4. DISSERTATIONS ON BRAIN INJURIES........................................................................... 77 Overview...................................................................................................................................... 77 Dissertations on Brain Injuries.................................................................................................... 77 Keeping Current .......................................................................................................................... 79 CHAPTER 5. CLINICAL TRIALS AND BRAIN INJURIES ..................................................................... 81 Overview...................................................................................................................................... 81 Recent Trials on Brain Injuries.................................................................................................... 81 Keeping Current on Clinical Trials ............................................................................................. 85 CHAPTER 6. PATENTS ON BRAIN INJURIES ..................................................................................... 87 Overview...................................................................................................................................... 87 Patents on Brain Injuries............................................................................................................. 87 Patent Applications on Brain Injuries ......................................................................................... 95 Keeping Current ........................................................................................................................ 106 CHAPTER 7. BOOKS ON BRAIN INJURIES ....................................................................................... 109 Overview.................................................................................................................................... 109 Book Summaries: Federal Agencies............................................................................................ 109 Book Summaries: Online Booksellers......................................................................................... 111 The National Library of Medicine Book Index ........................................................................... 118 Chapters on Brain Injuries......................................................................................................... 119 CHAPTER 8. MULTIMEDIA ON BRAIN INJURIES ............................................................................ 121 Overview.................................................................................................................................... 121 Video Recordings ....................................................................................................................... 121 Bibliography: Multimedia on Brain Injuries ............................................................................. 122 CHAPTER 9. PERIODICALS AND NEWS ON BRAIN INJURIES ......................................................... 123 Overview.................................................................................................................................... 123 News Services and Press Releases.............................................................................................. 123 Academic Periodicals covering Brain Injuries ........................................................................... 127 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 129 Overview.................................................................................................................................... 129 U.S. Pharmacopeia..................................................................................................................... 129 Commercial Databases ............................................................................................................... 130 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 133 Overview.................................................................................................................................... 133 NIH Guidelines.......................................................................................................................... 133

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NIH Databases........................................................................................................................... 135 Other Commercial Databases..................................................................................................... 139 APPENDIX B. PATIENT RESOURCES ............................................................................................... 141 Overview.................................................................................................................................... 141 Patient Guideline Sources.......................................................................................................... 141 Associations and Brain Injuries................................................................................................. 148 Finding Associations.................................................................................................................. 149 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 151 Overview.................................................................................................................................... 151 Preparation................................................................................................................................. 151 Finding a Local Medical Library................................................................................................ 151 Medical Libraries in the U.S. and Canada ................................................................................. 151 ONLINE GLOSSARIES................................................................................................................ 157 Online Dictionary Directories ................................................................................................... 157 BRAIN INJURIES DICTIONARY .............................................................................................. 159 INDEX .............................................................................................................................................. 217

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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with brain injuries is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about brain injuries, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to brain injuries, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on brain injuries. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to brain injuries, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on brain injuries. The Editors

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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.

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CHAPTER 1. STUDIES ON BRAIN INJURIES Overview In this chapter, we will show you how to locate peer-reviewed references and studies on brain injuries.

The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and brain injuries, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “brain injuries” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •

Brain Injury in Sports Related to Trauma to the Lower Jaw Source: Dentistry Today. 21(12): 74-77. December 2002. Contact: Available from Dentistry Today Inc. 26 Park Street, Montclair, NJ 07042. (973) 783-3935. Summary: Concussions and traumatic brain injuries in sports are the consequence of transfer of the energy of an impact, including impact to the lower jaw, to the brain. As intraoral appliance design evolves beyond the role of protecting only the teeth and periodontal tissues to assume a role of risk reduction for brain and TMJ injury in sports, the dental professional must have a thorough understanding of the nature and consequences of lower jaw impacts. This article reviews this subject, discussing the classification of traumatic brain injuries (TBIs) and concussions, the physiology of TBI,

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mechanisms of energy transfer in brain injury, understanding the problems that result from lower jaw impacts, intraoral guards to reduce lower jaw impact trauma, a new classification for intraoral sports appliances, and appliance design requirements for minimization of concussion risk. 6 figures. 29 references. •

Comparisons of Agitation Associated With Alzheimer's Disease and Acquired Brain Injury Source: American Journal of Alzheimer's Disease. 10(6): 20-24. November-December 1996. Summary: This article reviews whether behavioral components of agitation are expressed differently in people with post-traumatic agitation compared to those with dementia and agitation due to Alzheimer's disease (AD). Participants were 19 agitated older adults with dementia due to AD, 19 agitated older adults with recently acquired brain injury, and 19 agitated younger adults with recently acquired brain injury. Agitation was measured using the Agitated Behavior Scale (ABS), with observations selected to assure that overall agitation level in each group was comparable. An analysis of variance indicated that total ABS scores did not differ among the three groups. Differences between groups were not significant for either disinhibition or lability subscale scores. However, a significant difference was evident for aggression. AD and young brain injury groups differed in aggression, but neither differed from the older brain injury group. The findings provide initial support for the hypothesis that the manifestation of agitation may be similar across affected populations. 1 figure, 22 references. (AA-M).

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Informal Caregiver Responsible for Home Care of the Individual With Cognitive Dysfunction Following Brain Injury Source: Journal of Neuroscience Nursing. 21(1): 42-45. February 1989. Summary: This journal article discusses the preparation of informal caregivers who are responsible for the home care of individuals with cognitive impairment following brain injury. These caregivers and caregivers of people with Alzheimer's disease share many of the same characteristics and problems. The first portion of the article describes the characteristics of informal caregivers and the effects of factors such as stress, role fatigue, and support. The second portion presents the AFFIRM model to assist nurses in preparing family members for their caregiving roles. The model includes five steps of nursing intervention to promote role mastery and reduce the perceived stress of caregiving. These steps are: 1) clarify the availability of resources in the patient's home environment; 2) develop a home plan of care and schedule of daily activities; 3) provide factual information and instructions for care; 4) prepare a list of resources outside the home setting; and 5) monitor the progress of both the patient and the caregiver. A case study is included which illustrates the use of this model. 22 references.

Federally Funded Research on Brain Injuries The U.S. Government supports a variety of research studies relating to brain injuries. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable 2

Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration

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database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to brain injuries. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore brain injuries. The following is typical of the type of information found when searching the CRISP database for brain injuries: •

Project Title: ABERRANT REGULATION OF COX2 AFTER TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Strauss, Kenneth I.; Neurosurgery; Temple University 406 Usb, 083-45 Philadelphia, Pa 19122 Timing: Fiscal Year 2001; Project Start 10-DEC-1999; Project End 30-NOV-2003 Summary: (adapted from applicant's abstract) After traumatic brain injury (TBI) prostaglandin synthesis rises acutely. While this may result in selective beneficial responses, we propose that chronic prostaglandin production contribute to free radical mediated cellular damage, vascular dysfunction, alterations in cellular metabolism, and apoptosis. These may result in secondary injuries to the brain, promote neuropathology, and worsen behavioral outcome. Cyclooxygenase-2 (COX2) is a primary inflammatory mediator that catalyzes the conversion of arachidonic acid from damaged membranes into vasoactive prostaglandins, producing reactive oxygen free radicals in the process. Under normal conditions this enzyme is not detectable, except in the brain. Its role there is not known, but the brain and its vasculature have unique regulatory pathways and metabolic requirements that differ from other organs. We have recently established that cerebral COX2 induction is an immediate early response in two models of TBI. In addition, histochemical and mRNA analyses have revealed prolonged elevations in COX2 expression in the cortex and hippocampus. Using novel techniques developed in our lab, we have confirmed a prolonged increase in COX2 protein and prostaglandin levels, as well. Improvements in postinjury behavioral recovery have been observed after treatment with a dehydroepiandrosterone (DHEA) analog that attenuates cytokinemediated COX2 induction in vitro. Using in vivo model systems we will determine the time course and neuroanatomical localization of changes in COX2 mRNA, protein, and prostaglandin concentrations. We will begin to elucidate the mechanism(s) of action of COX2 following TBI by treating injured animals with agents that improve behavioral recovery via attenuating COX2 expression, inhibiting COX2 activity, or blocking receptor binding of the prostaglandins produced after TBI. Knowledge of these events will serve as the rational basis for pharmacological interventions to ameliorate the secondary pathologies that lead to worsening neurological and cognitive deficits in human victims of TBI. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: AGING AND NEURONAL 5 LIPOXYGENASE Principal Investigator & Institution: Manev, Hari; Professor; Psychiatry; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612

(FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).

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Timing: Fiscal Year 2001; Project Start 01-DEC-1998; Project End 30-NOV-2002 Summary: Aging is associated with chronic neurodegenerative diseases and increased brain vulnerability that may lead to a worse outcome from brain insults in elderly than in young subjects. Inflammation is one of the pathophysiological mechanisms of both chronic and acute neurodegeneration. Leukotrienes are inflammatory lipid mediators whose formation from arachidonic acid is initiated by 5-lipoxygenase (5-LO). 5-LO is also expressed in neurons and can be activated by brain injuries, whereas 5-LO inhibitors can provide neuroprotection. The expression of the 5-LO gene appears to be inhibited by the pineal hormone, melatonin, which also is a potent neuroprotective agent. Melatonin deficiency normally develops with aging. We found that old or pinealectomized, i.e., melatonin-deficient, rats are more susceptible to kainate-triggered excitotoxic limbic brain injury than the corresponding young or sham-pinealectomized controls, and that pinealectomy or aging result in an enhanced expression of 5-LO in limbic structures. We hypothesize that an aging brain is at a higher risk of neurodegeneration via aging-suppressed melatonin secretion and the resultant upregulation of 5-LO expression, and that suppressing the 5-LO expression and/or activity will increase the brain's resistance to injury. These hypotheses will be tested in the following AIMS: (1) Characterize in aging rats (i.e., at 2, 6, 12, and 24 months of age): the neuronal expression of mRNAs and proteins of 5-LO and its activating protein FLAP; the effect of kainate on leukotriene formation and neuronal damage in the hippocampus and the entorhinal cortex; blood and brain melatonin levels (2) Characterize in limbic structures of young and old rats the effects of the nuclear melatonin receptor agonist CGP-52608 or melatonin on 5-L0 expression and kainateinduced leukotriene formation and neuronal damage; (3) Investigate the action of different classes of 5-LO inhibitors on kainate-induced leukotriene formation and neuronal damage; and (4) Investigate whether kainate is less neurotoxic in 5-LOdeficient (i.e., knockout) mice, and whether aging equally affects the vulnerability to kainate of 5-LO-deficient and age-matched wild mice. Techniques to be used include: quantitative reverse transcription/polymerase chain reaction for 5-LO and FLAP mRNAs, 5-LO and FLAP immunocytochemistry/immonobloting, enzyme- or radioimmunoassays, gas chromatography/mass spectrometry, TUNEL/Nissl stainings, and computer-assisted quantitative morphometry. The results are expected to elucidate the role of 5-LO in aging and neurodegeneration and to indicate neuroprotective therapies that would target the 5-LO pathway. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: AN ORGANOTYPIC MODEL OF TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Bottlang, Michael; Emanuel Hospital and Health Center 2801 N Gantenbein Ave Portland, or 97227 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2005 Summary: The past decade has witnessed intense scientific activity to investigate molecular mechanisms of traumatic brain injury, driven by overwhelming evidence that neuropotection by pharmacological inhibition of apoptosis has the potential to dramatically reduce the effects of brain trauma. Key requisite for the systematic investigation of neuroprotective agents is an accurately characterized, clinically relevant in vitro brain injury model. Despite this obvious need, the ability to deliver such defined, realistic trauma to specimens in vitrolags far behind the sophistication of molecular and biochemical assays used to measure the response. In a collaborative effort between neurobiologists and bioengineers, we therefore developed an in vitrobrain injury model which subjects organotypic brain cultures to angular acceleration-induced

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shear injury. In this model, organotypic brain cultures realistically model the in vivoapparent heterogeneous cell population in a three-dimensional cellular matrix, while angular acceleration-induced shear strain delivers a scalable, defined, and clinically relevant mechanical insult. We hypothesize that our acceleration model of organotypic brain cultures can realistically reproduce traumatic brain injury, where the delivered shear strain magnitude can be quantified on a cellular level. Exercising our model, we will be able to determine cell type specific injury vulnerability, and to determine if caspase-8 and caspase-9 affect cell death following brain trauma. We propose to complete a formal experimental characterization of our novel brain injury system, including assessment of the delivered angular acceleration magnitude and determination of the constitutive properties of the organotypic specimen (Aim 1). The resulting experimental source data will be directly applicable to formulate a realistic analytical model that allows computational simulation of the shear injury throughout the brain specimen for any point in time during the primary mechanical insult (Aim 2). Based on and concomitant to this rigorous system characterization, we will exercise the brain injury model to establish a dose/response history (Aim 3), and we will delineate the effects of hypoxic brain injury (Aim 4), secondary to the mechanical insult. Finally, we will employ our arganotypic trauma model to determine the neuroprotective potential of caspase-8 and caspase-9 (Aim 5). Upon successful completion, the results of this integrative research approach will yield a well-characterized, scalable, reproducible and clinically relevant brain injury model. Considering the vast interest in therapeutic interventions now under development aimed at inhibiting the cascade of secondary effects of primarily mechanical brain injuries, our organotypic trauma model will directly address the rapidly increasing demand for a well characterized, experimental system to deliver a clinically relevant traumatic insult - and may prove crucial for the discovery of caspase-based neuroprotective mechanisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BEHAVIORAL & NEUROENDOCRINE MODULATION IN SPINAL INJURY Principal Investigator & Institution: Whitacre, Caroline C.; Professor and Chair; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2001; Project Start 25-SEP-1999; Project End 31-AUG-2004 Summary: (adapted from investigator's abstract): Psychological and behavioral states are known to exert a profound impact on the immune system, and can delay the onset of acute inflammation and healing of injured tissues. Previous research from our group and others has shown that psychological influences on immune functions can be highly subtle and diverse. Personality factors, attitudes and beliefs can lead to a downregulation of immune function, and likely do so by an overlapping set of common mechanisms. While animal models may not approximate the intricacies of human psychology, they afford an important and necessary approach to understanding the mechanistic links between psychological states and health outcomes. Other projects of this proposal focus on healing of peripheral wounds, but from the vantage of psychological processes, a highly relevant issue is the impact of behavioral states on healing of brain injuries. After spinal cord injury, repair and regeneration of damaged tissues, both CNS and peripheral, is dependent on inflammatory processes. Life expectancy of spinal injured individuals has increased to a level that is consistent with the able bodied population. SCI survivors must learn to cope with the psychological stress of disability as well as the physiological challenges of rehabilitation, and these latter factors likely impact on recovery. In the present proposal, we will address the

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interrelationship between psychological stress, and wound healing in a clinically relevant model of SCI. A major hypothesis of this proposal is that physiological and psychological factors associated with SCI, and damage to sympathetic outflow will suppress inflammatory processes resulting in slowed or incomplete wound healing of both CNS and peripheral tissues. We will identify the time course of hypothalamicpituitary-adrenal and sympathetic-adrenal medullary activation after SCI injuries in mice, which can then be correlated with measures of acute inflammation in wounds of the skin and spinal cord. Morphometric analysis of immunohistochemically-stained skin (above and below the level of SCI) and injured spinal cord sections will allow us to determine how altered immunological processes affect wound healing in the periphery and CNS. The addition of a psychological stressor (restraint stress), will further illuminate how stress may impact on wound healing and inflammation, especially under conditions where the immune system and CNS are uncoupled, as in spinal injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BIOMECHANICS OF PEDIATRIC HEAD INJURY Principal Investigator & Institution: Margulies, Susan S.; Associate Professor; Bioengineering; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2001; Project Start 15-MAY-2001; Project End 30-APR-2006 Summary: Head injury is a leading cause of death and acquired disability in childhood. However, the biomechanics of pediatric head injury are poorly understood, primarily due to, the paucity of age-specific data regarding mechanical properties of immature tissue and its response to specific loads. The interdisciplinary proposed research plan is designed to answer the following question: What mechanisms cause what injuries in children of what age? The long-term objectives of the proposed research plan are to determine mechanical properties of the skull and brain, the loads they can withstand safely, and unique mechanisms for primary brain injury in infants (less than 3 months) and young children (1-3 years). In so doing, the long term impact of proposed research plan will be to open pathways for enhanced traumatic head injury prevention, detection, and treatment strategies specific to infants and toddlers. Both contact and non-contact mechanisms of brain injury will be investigated. The research plan uses an integrated bioengineering approach consisting of animal experiments, human and animal tissue tests, clinical studies, and anthropomorphic surrogates, all complemented by mathematical models to: A) measure pediatric tissue injury thresholds for acute neural, vascular, and blood-brain barrier damage B) measure pediatric skull and brain tissue mechanical properties C) create computational models for infant and toddler head injury using (A) and (B) D) qualitatively validate the computational model predictions with witnessed accidental head injuries in children E) measure loads experienced anthropomorphic surrogates during falls, shakes, and inflicted impacts F) determine the relative roles of impact forces and inertial loads in the etiology of primary brain injuries G) compare the computational simulations with acute clinical data to infer potential mechanisms of injury in non-accidental head injury. The overall hypotheses of the proposed research program are that 1) thresholds for skull fracture and tissue injury and mechanical properties of the brain and skull vary with age, such that both contribute to differences in primary head injuries between infants and toddlers, and 2) the increased compliance of the infant skull results in greater brain tissue injury from impact trauma; and 3) a valid computational model can be created to predict specific primary injuries resulting from a given reported mechanism. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CASPASE MECHANISMS AFTER BRAIN INJURY Principal Investigator & Institution: Moskowitz, Michael A.; Professor; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2002; Project Start 15-DEC-1997; Project End 31-DEC-2006 Summary: Adapted from applicant's abstract): Stroke and brain injury are major causes of morbidity and mortality and significant economic loss. This competitive renewal application will explore novel hypotheses relating to regulation of death receptors as mediators of cell death in vivo and in vitro. Preliminary evidence suggests that a Death Inducing Signaling Complex (DISC) assembles after acute brain injury and initiates caspase activation leading to cell death. Five aims are proposed to contrast mechanisms relating to the death receptor Fas, death effector proteins, and initiator caspase-8 and -10 in vivo after acute brain injury (cerebral ischemia and brain trauma). In experimental models, caspase-8 cleavage and DISC assembly was significantly greater in trauma than ischemia, suggesting differences in cell death mechanisms between acute brain injuries. To explain these differences, we propose a novel hypothesis that TYPE I (mitochondriaindependent) may be more typical of head trauma and TYPE II (mitochondriadependent) cell death may predominate in ischemia, and this hypothesis will be tested in Bid-/- null mice. To dissect mechanisms regulating DISC assembly, we propose in vitro studies using enriched cortical neurons and oxygen-glucose deprivation (OGD). Our preliminary data indicate that adding FasL kills neurons during OGD, and cell death after OGD is reduced by caspase inhibitors. We propose to determine whether both OGD and FasL cell death can be regulated by c-FLIP, an inhibitor of caspase-8 activation, using viral vectors to overexpress the c-FLIP gene. In vitro studies will explore regulation of FasL expression by determining whether inhibition of Forkhead transcription factor (FKHRLI), which promotes FasL synthesis, reduces OGD-mediated neuronal cell death. We also propose to establish the functional relevance of Fas/FasL signaling in vivo using Fas-/- mice, antisense treatment, gld mice and overexpression of c-FLIP using HSV-I amplicon viral transfer. Finally, we will expand upon preliminary data detecting DISC assembly in human brain following acute injury and thereby validate the importance of cell surface death receptors in acute injury. Together these experiments will explore death receptor-mediated acute cell killing within brain in order to identify mechanisms and potential targets of ischemic and traumatic brain injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CHILD AND FAMILY FUNCTIONING AFTER PEDIATRIC HEAD TRAUMA Principal Investigator & Institution: Youngblut, Joanne M.; Professor of Nursing; School of Nursing; Florida International University Division of Sponsored Research and Training Miami, Fl 33199 Timing: Fiscal Year 2001; Project Start 01-JUL-1997; Project End 31-MAR-2004 Summary: (Adapted from the Investigator's Abstract): When a child suffers an accidental injury, families are suddenly faced with fears about the child's survival and uncertainty about the child's future. Even school-age children with mild traumatic brain injuries (TBI) experience deficits in attention and memory that affect every aspect of their lives. Effects of the stress of parenting a child with continuing but subtle deficits on parent mental health, parent-child, and family relationships are unknown. The purpose of this longitudinal nursing study is to describe the impact of TBI severity, resistance resources, and parental appraisal on adaptation of preschool children with TBI and their parent(s) and on quality of parent-child and family relationships during the first year.

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Families (N=420) with a 3- to 6-year-old hospitalized child with an injury where a blow to the head was likely and either a history of loss of consciousness, symptoms of head injury in children, x-ray or CT scan suggestive of TBI will be recruited. Other inclusion criteria are child living with at least one parent before the accident, and parent(s) able to understand spoken English. Exclusion criteria are: severe pre-existing cognitive deficits, pre-existing chronic illness, previous hospitalization other than at birth, living in a foster home before admission, being evaluated with brain criteria, injury suspected to be due to child abuse, parent(s) hospitalized concurrently or death of a parent in the accident. A conceptual model based on the Resiliency Model of Family stress, Adjustment, and Adaptation guides the study's design and analysis. Data will be collected in the hospital at 24 hours after admission, within 24 hours before hospital discharge, and in the family's home at 2 weeks, 3, 6, and 12 months after discharge. The proposed study will provide data on behavioral, cognitive, memory, motor, and functional outcomes for preschoolers and effects of the child's injury and outcomes on parental mental health and indirectly on parent-child and family relationships in the first year after hospital discharge. Describing the frequency of problems and identifying factors that affect the rate of change in child, parent, and family outcomes is the first step toward successfully guiding families through the early recovery period in a way that promotes optimal child functioning, parent mental health, and family stability. If nursing research and care can facilitate achieving these objectives, burden on health care, educational, and family systems will be reduced. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CHILD AND FAMILY SEQUELAE OF PRESCHOOL BRAIN INJURY Principal Investigator & Institution: Wade, Shari L.; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2002; Project Start 10-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Traumatic brain injury (TBI) in younger children results in more severe and persistent sequelae than TBI in older children, affecting emerging skills most. Yet, little is known regarding the effects of early TBI on the family or the factors that facilitate or hinder recovery among children in this age group. Research suggests that family and social factors play an important role in determining longer-term outcome following TBI in school-aged children. The current investigation uses a prospective cohort design to examine family adaptation following TBI in young children and the relationship between the social environment and child recovery over time. Children aged 3 to 6 with moderate to severe TBI will be compared to a matched group of children hospitalized for orthopedic injuries not involving the CNS. Children in both groups will be assessed shortly after the injury and at 6, 12, and 24 months post injury. Child outcomes of interest include emerging skills in the domains of language, social competence, and executive functions that are likely to have important implications for later functioning. Family outcomes include injury-related burden, caregiver and family functioning, and parent-child interactions. We hypothesize that families of young children with TEI will exhibit more burden and caregiver distress, poorer family functioning, and higher levels of directiveness and restrictiveness in interactions with their children than families of children with orthopedic injuries. Further, we hypothesize that both the pre-injury social environment and changes in the family brought about by the injury will be related to the child's recovery, and that these associations will be moderated by injury severity, such that the environment has a stronger influence among children with more severe TBI. We anticipate that certain aspects of the environment (e.g., maternal maintaining behaviors) will accelerate

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recovery, whereas others (e.g., maternal directiveness) will retard growth following TBI. Understanding the relevance of the environment to the child's recovery following TBI will allow us to develop interventions to improve outcomes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CLINICAL PERFORMANCE MEASURE FOR PEDIATRIC BRAIN INJURY Principal Investigator & Institution: Smith, Kevin W.; New England Research Institutes, Inc. 9 Galen St Watertown, Ma 02472 Timing: Fiscal Year 2001; Project Start 01-SEP-1998; Project End 31-MAY-2003 Summary: Children with acquired brain injuries comprise the largest diagnostic group requiring in patient care in specialized rehabilitation hospitals. For accreditation purposes, these hospitals are now required to collect performance measure data for high-volume patient groups. This mandate presents a serious dilemma, since current performance measures in pediatric rehabilitation are inadequate to guide internal improvements or to evaluate comparative performance. After conducting an extensive literature review and consulting experts in the field, in Phase I we designed a 44-item prototype performance instrument. The instrument focuses on three critical content areas for brain-injured children: 1) daily activities, 2) social and behavioral competence, and 3)community readiness skills. In Phase II of the research project, we will conduct a prospective survey of patients in 8 randomly selected facilities, revise the item content, conduct reliability and validity analyses, and develop risk-adjusted benchmarks for expected levels of functioning. The risk adjustment methodology is designed to meet the Joint Commission for the Accreditation of Health Organization's (JCAHO) requirements for approving new instruments. The final product of Phase II will be a marketable performance measurement system for children with acquired brain injury that will meet content and measurement requirements of accreditation and contracting agencies. PROPOSED COMMERCIAL APPLICATIONS: The product of this SBIR project will be a marketable Performance Measurement System for children with Pediatric Brain Injury. As of 1998, all JCAHO accredited hospitals need to contract with a data system to provide comparative data for high-volume patient groups. This Performance Measure meets all the JCAHO requirements and will fill a critical void for in patient pediatric rehabilitation programs. Many acute care children's hospitals may also find this measure helpful in comparing performance of trauma care for children who are directly discharged home. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CNS STEM CELL THERAPY AFTER TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Dietrich, W. Dalton.; Professor; University of Miami Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2002; Project Start 19-JUL-2002; Project End 30-JUN-2007 Summary: Recent data indicate that after a variety of acute CNS injuries, there is a massive proliferation of stem/progenitor cells. Identification of the origin and fate of these cells is an area of intensive investigation. Whether these proliferative cells are stem cells that are capable of differentiation to neurons, glia, or other cell types that may repopulate damaged brain regions and enhance recovery remains to be determined. The provision of new cells from exogenous sources is an alternative approach to enhance recovery of function and may be necessary when neuronal loss and axonal injury are severe. Stem cell-like transplants from various sources have been shown to improve

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function in several models of brain and spinal cord injury. This project will utilize established animal models and histopathological and immunocytochemical techniques to characterize the temporal and regional cellular response to traumatic brain injury (TBI) and determine the consequences of stem cell transplantation in the post-injured brain. Indicators of cellular proliferation, mitotic divisions, cellular phenotypes, and apoptotic cell death will be specifically assessed. Preliminary data presented in this proposal indicative a massive proliferation of cells in the first several days after TBI, with many of these cells becoming astrocytes. Proposed studies in Specific Aim 1 will first characterize the temporal and regional cellular response to moderate TBI. In Specific Aim 2, the effects of growth factor treatment on cellular proliferation and differentiation and differentiation and/or cell death will be assessed. Quantitative sensorimotor and cognitive endpoints will be used to document behavioral deficits and treatment strategies after TBI. Prior to stem cell transplantation, Specific Aim 3 will determine effectors that may control embryonic rat neutral in vitro. Finally, in Specific Aim 4, the assessment of whether growth factor treatment can alter the cellular response to injury or induce neuronal and/or oligodendrocyte stem cell graft differentiation and result in improved functional outcome will be tested. Together, these studies emphasize endogenous as well as exogenous reparative processes and should provide novel information concerning strategies to enhance recovery of function following TBI. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CORE--SCIENTIFIC BEHAVIORAL Principal Investigator & Institution: Almli, Charles R.; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2002; Project Start 25-SEP-2002; Project End 31-AUG-2007 Summary: The overall function of the Behavioral Core is to provide neurobehavioral testing (learning-memory, sensory-motor, and behavior) of rodents (rats and mice) in support of the experiments initiated by the Program Project Grant (PPG) investigators. The specific aims of the behavioral core are: 1. To conduct long-term learning-memory, sensory-motor, and behavioral testing of rodents for in vivo and in vitro experimental protocols proposed by PPG investigations (e.g., neonatal hypoxia-ischemia, transient focal ischemia [middle cerebral artery occlusion], perinatal infection, and knockout [caspase-3, clusterin, HIF1a] preparations). 2. To conduct long-term learning-memory, sensory-motor, and behavioral testing of rodents for in vivo and in vitro experimental protocols proposed by PPG investigations that combine various neonatal treatments (e.g., hypoxia-ischemia in clusterin, caspase-3, or HIF1a knockout mice, infection pretreatment with neonatal hypoxia-ischemia). 3. To conduct long-term learningmemory, sensory-motor, and behavioral testing of rodents for promising therapeutic agents and strategies identified by PPG investigators in their in vitro and in vivo models of perinatal brain injuries (e.g., brain-derived neurotrophic factor, caspase-3 inhibitors, cobalt chloride and iron chelator desferoxamine, pharmacological inhibition of iNOS, and neutrophil depletion). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CORTICAL EXCITABILITY AFTER TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Golarai, Golijeh; Neurosciences; University of New Mexico Albuquerque Controller's Office Albuquerque, Nm 87131 Timing: Fiscal Year 2002; Project Start 01-APR-1999; Project End 31-MAR-2004

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Summary: (Applicant's abstract) Traumatic brain injury (TBI) leads to severe and lasting disabilities in sensorimotor and cognitive functions in 30,000 to 50,000 people in the United States each year. Approximately one third of individuals with serious head injuries eventually develop epilepsy. As TBI largely afflicts young people, health care and lost income are more costly than for stroke or degenerative diseases that typically affect the elderly. Clearly, interventions to prevent epilepsy, while promoting recovery from primary deficits after TBI, would be of great social value. Accordingly, this proposal examines the development of epileptogenic cellular physiology in rat sensorimotor cortex after a controlled injury, using a combination of extra-and intracellular electrophysiolgy, voltage- and calcium imaging, and histological methods. The experiments will also include an examination of the neuromodulatory role of noradrenaline (NA) after TBI for two reasons. First, NA plays a complex role in both suppressing and promoting epileptogenesis. Second, NA with physical therapy (NA/PT) is the only pharmacotherapy that has enhanced functional recovery in doubleblind studies of patients with well-established brain injury. This proposal represents a synthesis of my ongoing interest in basic mechanisms of epilepsy (which I have explored in hippocampus) and my career goal of expanding my area of research to include the neocortex, intracellular electro-and calcium physiology, and pathophysiology of head trauma. This project, including the mentorship of J.A. Connor and the collaboration of D.M. Feeney and R.C. S. Lin, will allow me to establish myself in these new areas, wile drawing on my experience with the kindling and kainate models of epilepsy, with various histological methods, with electrophysiolgy in vivo, and with the voltage-imaging techniques that I have learned with J.A. Connor. I will work with three senior scientists who have made major contributions to the fields of neuronal calcium and electrophysiology (Connor), TBI and NA/PT (Feeney) and anatomical correlates of neuopathophysiology (Lin). This rare interdisciplinary research opportunity will allow me to contribute to the understanding of post-traumatic epilepsy while increasing my breadth and depth as a scientist. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EFFECTS OF DIHYDROEPIANDROSTERONE ON BRAIN INJURY Principal Investigator & Institution: Hoffman, Stuart W.; Emergency Medicine; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2003 Summary: (provided by applicant): At present, there is no effective pharmacological agent to enhance neurobehavioral recovery after traumatic brain injury (TBI). The longterm objective of this research is to develop a safe and effective treatment that would enhance neurorehabilitation after traumatic injuries to the central nervous system. After the initial cascade of destructive events occurs, the brain is in a state of dysfunction due to injured neurons, disrupted synapses, continuing inflammatory responses, and decreased neuronal activity. However, the brain has the capability to recover significantly from this post-injury state, if proper behavioral or pharmacological therapies are administered. In this proposal, it is the investigators'goal to demonstrate that dihydroepiandrosterone (DHEA) will significantly increase recovery of function. DHEA is a special type of steroid hormone that is synthesized both inside and outside of the nervous system in both males and females. DHEA, a known neurosteroid, can stimulate the formation of new synapses, modulate the immune system, and increase neuronal activity involved in cognitive function. These same characteristics make DHEA worth considering as potential therapy to facilitate recovery of cognitive function after brain injury. In addition, long-term administration of DHEA has shown that it produces

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no adverse side-effects in rodents or humans. In this proposal, the investigators will investigate whether DHEA can promote a more complete recovery of function after experimental TBI. The investigators will use a controlled cortical impactor to create bilateral medial frontal contusions in rats to model TBI. The investigators goals will be to: (1) determine whether DHEA can promote functional recovery in both males and females, a subject that has received virtually no attention in the experimental literature; (2) determine the most effective dose of DHEA; (3) determine whether treatment with DHEA can affect the morphology and survival of neurons as well as the proliferation of glial cells; and (4) determine if the effects of DHEA on recovery of function can produce a dose dependent causal effect on histological measures. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EFFECTS OF VITAMIN B3 ON TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Hoane, Michael R.; Psychology; East Carolina University 1000 E 5Th St Greenville, Nc 27858 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-JAN-2005 Summary: (provided by applicant): Annually, approximately 2 million Americans suffer a moderate to severe traumatic brain injury (TBI). These injuries produce enduring disabilities that include cognitive, sensory, motor, and emotional impairments. The associated health care costs from these injuries are staggering. Confounding this major public health issue is the fact that currently there are very few pharmacological treatment options for patients who have suffered TBI. In part, this occurs because many newly synthesized drugs fail in various stages of efficacy testing. Given the fact that newly synthesized drugs fail in clinical trials it seems reasonable to begin to examine the potential efficacy of more natural substances. It has recently been demonstrated that administration of vitamin B3 (B3) following experimentally induced stroke reduces the size of the infarct and can improve behavioral outcome in rats. In addition, the preclinical efficacy of magnesium pharmacotherapy has been well established. The proposed research will investigate the potential preclinical efficacy of B3 to lessen the physiological consequences of brain injury and improve behavioral outcome. We will use the rodent bilateral frontal cortical contusion injury model, which is similar to a frontal head injury sustained in a car accident. The specific aims of this study are to: 1) determine if administration of B3 following injury can significantly reduce the cognitive and sensorimotor impairments seen following TBI; 2) determine the best injections parameters (i.e., window of opportunity and dose response) for B3 pharmacotherapy following TBI; 3) determine if administration of B3 following injury can significantly decrease the amount of injury-induced edema and injury-induced magnesium depletion; 4) determine the effect of B3 pharmacotherapy on apoptosis and reactive gliosis following TBI. The research proposed here will determine if B3 holds any preclinical efficacy for the treatment of TBI and begin to define the parameters for the development of B3 as a clinical treatment for TBI. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ENRICHMENT EFFECTS & BRAIN INJURY IN MALE & FEMALE RATS Principal Investigator & Institution: Elliott, Brenda M.; Henry M. Jackson Fdn for the Adv Mil/Med Rockville, Md 20852 Timing: Fiscal Year 2003; Project Start 01-JAN-2003

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Summary: (provided by applicant): One and a half Americans are brain injured each year. Of those, approximately 50,000 of the people will die and 80,000 will suffer longterm disabilities. The proposed research will use an animal model of closed head injury to study whether enriched environments affect recovery. The project includes two experiments and 240 male and female Sprague-Dawley rats. The proposed work will compare effects of no enrichment, social enrichment, physical enrichment, combined social and physical enrichment on behavioral responses in neurologically-intact and brain-injured rats. Experiment 1 is a 2 (no social enrichment or social enrichment) x 2 (no enrichment or physical enriched environment) x 2 (male or female) in neurologicallyintact animals. Experiment 2 follows the same experimental design but will study animals that have been brain injured using a fluid percussion device to model closed head injury. The behavioral dependent variables are locomotor activity, acoustic startle reflex responses and pre-pulse inhibition of acoustic startle responses, and performance in the Morris water maze. The proposed work is designed to determine the extent to the specific contributions of social or physical enrichment enhance recovery from head injury and whether there are gender differences in these effects. The long-term goal of this project is to improve treatment programs for rehabilitation and recovery from head injuries. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EPO AS A RESCUE AGENT FOR PERINATAL HYPOXIA-ISCHEMIA Principal Investigator & Institution: Juul, Sandra E.; Pediatrics; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2005 Summary: (provided by applicant): Injury to the brain during the perinatal period is a leading cause of death and disability in children. We currently do not have successful therapeutic regimens for the treatment of brain injury in children. However, recent research has shown that erythropoietin (Epo) may be of therapeutic benefit. Recombinant Epo (rEpo) has been shown to provide significant neuroprotection in many adult animal models of brain injury, including hypoxia-ischemia and trauma. Indeed, when rodents are subjected to a variety of experimental brain injuries, rEpo administration, even up to 6 hr after the event, reduces subsequent brain injury by 5070 percent. Although the mechanism of rEpo action is not fully understood, it is known to decrease apoptotic cell death in neurons; it has direct antioxidant effects, and it may also reduce peri-neuronal inflammation. rEpo was previously thought to have limited clinical applicability, as it was not thought to cross the blood brain barrier (BBB) due to its large size (37 kD) and highly glycosylated structure. Recently, however, it has been shown that when very high dose rEpo (5000 U/kg) is given systemically, it protects the brain from a variety of mechanisms of injury. This suggests that a proportion of systemically administered rEpo crosses the BBB, or that systemically administered rEpo is neuroprotective through secondary mechanisms. No studies have applied this therapy to a neonatal model of injury. rEpo is commonly used in premature infants to stimulate erythropoiesis and reduce erythrocyte transfusions (200-400 U/kg/dose), but the dose of rEpo required for neuroprotective effects (5000 U/kg/dose) is much higher than those traditionally used for erythropoiesis. We hypothesize that neonatal hypoxicischemic brain injury can be ameliorated by the early administration of systemic (intravenous) high dose rEpo, and furthermore, that it will be safe both in the short and long-term. We will use the well-established model of perinatal hypoxia-ischemia developed by Vannucci (unilateral carotid artery ligation followed by hypoxia) to test these hypotheses. The specific aims of the current proposal are to determine: 1) the time

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course and degree of rEpo penetration across the BBB of neonatal rats, 2) the optimal rEpo treatment parameters for neuroprotection following hypoxia-ischemia, 3) mechanism(s) by which rEpo decreases neuronal injury, and 4) the short and long-term safety of systemically administered high dose rEpo in the neonatal rat. If high dose rEpo treatment of human neonates following birth asphyxia indeed resulted in a 50 percent reduction in brain damage (as it does in laboratory animals) this treatment could annually save up to 1 million lives world wide while substantially lessening the financial and emotional consequences of birth asphyxia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FOCAL CEREBRAL ISCHEMIA IN ACUTE BRAIN INJURY Principal Investigator & Institution: Diringer, Michael N.; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001 Summary: Each year approximately 2 million people suffer traumatic brain injuries (TBI) in the U.S. of these about 100,000 die and 90,000 are left with long-term disabilities. Advances in the management of these patients have reduced mortality but done little to ameliorate brain injury. Recent studies in severe TBI patients have suggested that reduced regional cerebral blood flow (rCBF) in the first few hours after injury contributes to secondary brain injury. in order to determine the role of cerebral ischemia in the pathophysiology of TBI, it is important to determine if the reduction in rCBF seen in TBI patients is due to a primary reduction in supply causing ischemia or merely represents a decline in rCBF secondary to reduced metabolic demands of injured brain tissue. Positron emission tomography (PET) is the only technology currently available that can quantify CBF and CMRO2 regionally in humans, and provide indices of the balance between CBF and CMRO2; oxygen extraction fraction OEF, differences in arteriovenous O2 content (A-VDO2), and cerebrovenous oxygen content (CvO2). Barnes-Jewish Hospital at Washington University Medical Center is a Level I trauma center which admits approximately 120 TB1 patients each year. A new Siemens ECAT EXACT HR 47 PET scanner has been installed in the Neurology/Neurosurgery Intensive Care Unit (NNICU) and is currently being used to study TBI patients. The presence of a PET scanner in the NNICU, combined with our extensive experience with the use of PET to detect ischemia, our expertise in the clinical management of TBI patients, and the large available patient patient population gives us a unique opportunity to address these issues. We propose to investigate the prevalence, severity, and duration of cerebral ischemia in severe TBI. Specifically we will measure regional CBF. CMRO2, CvO2, A-VDO2 and OEF using PET in 60 patients with severe head injury (GCS less then or equal to 8) within the first 12 hours after injury and again 24-72 hours latter. These investigations are critical to optimize treatment for these patients. If ischemia is a significant problem in TBI, then management of arterial hypertension and cerebral perfusion pressure will need to modified accordingly. In addition neuroprotective agents currently being studied in ischemic stroke may be useful in TBI as well. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GUIDANCE MOLECULES IN SPINAL CORD REGENERATION Principal Investigator & Institution: Selzer, Michael E.; Professor; Neurology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2001; Project Start 03-JUL-2000; Project End 30-JUN-2005

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Summary: (Adapted from the Investigator's Abstract): This is a proposal to determine if regeneration of spinal cord axons is guided or otherwise modulated by the actions of netrins and semaphorins, molecules that guide axons during development and are present in the CNS of mature vertebrates. Following spinal cord transection, mammalian axons ordinarily do not regenerate, which complicates the study of molecular mechanisms of regeneration. By contrast, lampreys recover from complete spinal transection and axons regenerate selectively in their correct paths. Other advantages of the lamprey for regeneration research include: 1) Identified giant reticulospinal neurons differ from one another in their regenerative abilities, which have been determined previously. 2) These neurons can be visualized in vivo and in CNS wholemounts. 3) Molecular expression patterns can be correlated with regenerative abilities in individual neurons and identified neuron types. 4) In vivo transfection of neurons with Gene Gun results in long-lasting transgene expression. We already have partial sequences for two semaphorins, one netrin and two netrin receptors in lamprey. We have localized expression of three of these by in situ hybridization and have evidence that their expression is modulated by spinal cord transection. We now propose to determine whether overexpression or underexpression of netrin and semaphorin receptors in reticulospinal neurons alters the probability and/or pathway specificity of their regeneration. We will complete the full length cloning of the proposed guidance molecules and their receptors, and localize their expression in uninjured and spinal cord transected animals. The expression of receptors will then be enhanced or inhibited in reticulospinal neurons by Gene Gun transfection with the sense or antisense (alternatively, a truncated dominant negative) cDNA for netrin and semaphorin receptors. Cotransfection with the reporter Green Fluorescent Protein will distinguish transfected from untransfected cells. The probability of regeneration will be determined by retrograde transport of HRP, while the directional specificity of regeneration will be determined by intracellular injection of HRP and observation of the regenerated axons in spinal cord wholemounts. If developmental guidance molecules influence the effectiveness of axon regeneration in CNS, their manipulation could form the basis for therapies to improve regeneration of interrupted axons in patients with spinal cord injuries, traumatic brain injuries and stroke. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HIGH DOSE ERYTHROPOIETIN FOR NEONATES WITH ASPHYXIA Principal Investigator & Institution: Christensen, Robert D.; Professor; Pediatrics; University of South Florida 4202 E Fowler Ave Tampa, Fl 33620 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 30-MAR-2005 Summary: (provided by applicant): Damage to the central nervous system as a result of hypoxic-ischemic injury at birth is a major cause of life-long mental and neurodevelopmental handicap. Unfortunately, no therapeutics have yet been identified which, when administered to neonates following birth asphyxia, significantly lessen the extent of brain damage or improve outcome. Recent studies in the investigators' laboratories, and in many others, indicate that erythropoietin (Epo) is a "natural" neuroprotectant. During hypoxemia Epo is produced rapidly and abundantly by the microglia, and in a paracrine fashion this Epo binds to specific Epo receptors on neurons. This binding has at least three salutary actions; 1) it induces antiapoptotic factors that preserve neurons which would otherwise undergo apoptosis, 2) it reduces perineuronal inflammation, and 3) it has direct antioxidant effects. An improved understanding of the biology of Epo during human neuronal development has led to experiments where recombinant Epo (rEpo) was administered in an attempt to reduce

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post-hypoxic-ischemic brain damage. Indeed, when rodents were subjected to a variety of experimental brain injuries, rEpo administration, even up to six hour after the event, reduced subsequent brain injury by 50-70%. However, the doses of rEpo required were considerably higher (5,000 U/kg/dose) than those traditionally used by neonatologists to stimulate erythropoiesis and reduce erythrocyte transfusions (100 to 200 U/kg/dose). Before a clinical trial can be designed to test the efficacy of very-high-dose rEpo administration in reducing post-asphyxic brain injury, basic Phase I/II information on pharmacokinetics, biologic effect, and safety must be obtained. Therefore, the investigators designed a multi-centered, open-labeled, dose-escillation trial of veryhigh-dose rEpo administration to neonates who have had birth asphyxia. The study will be performed using the consortium known as the Florida Collaborative Neonatology Trials Group and the follow-up will be accomplished using the State of Florida Early Intervention Program (EIP), in which all study patients will be enrolled. Within three hours of birth, each eligible patient will receive one dose of rEpo intravenously (n=5 will receive 1,000 U/kg; the subsequent n=5 will receive 2,500 U/kg; the final n=5 will receive 5,000 U/kg). The doses will be increased to the next highest group if such is sanctioned after review by the Data Safety Monitoring Board. Any patient who has a lumbar puncture performed during the first week of life will have natural Epo and rEpo in their spinal fluid determined to assess the degree of penetration of rEpo across the blood brain barrier. They will also have free iron and total isoprostanes in the spinal fluid quantified as measures of oxidative stress and oxidative damage. The effect of rEpo on plasma free iron and plasma total Isoprostanes following hypoxia will be assessed at intervals following rEpo treatment. Pharmacokinetics of rEpo in this population will be determined and safety parameters evaluated. To aid the design of a subsequent Phase III trial, neurodevelopmental outcome will be measured in the EIP program clinics at six and 12 months or life. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMPACT OF A LITTERMATE ON PSYCHOLOGICAL STRESS IN RATS Principal Investigator & Institution: Wilson, Janie H.; Psychology; Georgia Southern University Statesboro, Ga 30458 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2004 Summary: (provided by applicant): Generally known for its reproductive role, the hormone prolactin is now known to be released in response to stress. Acute psychological stress reliably increases prolactin and affects behaviors in adult male rats; however, responses of adult females and juvenile males and females remain to be explored. In the proposed experiments, four psychological stressors will be examined: novel open field, noise, the conditioned-emotional- response (CER) paradigm, and nonpainful exposure to a cat. As a second component, the present slate of experiments will examine the impact of a conspecific on responses to psychological stressors by testing animals in the presence of a same-sex littermate. A third component, pretreatment with 1 mg/kg i.p. injection of the oxytocin antagonist 1-deamino-2-D-Try(Oet)-4-Thr-8-Om-oxytocith will examine the possible role of oxytocin in social buffering as measured by prolactin levels. Prolactin and individual as well as social behaviors in the stressful environments will be recorded. It is hypothesized that adult male and female rats tested alone in the chamber will have lower levels of prolactin than those tested alone in the chamber with a stressor. Low levels of prolactin are also expected in females exposed to a stressor in the presence of a conspecific, and the oxytocin antagonist is expected to block oxytocin in the pre-treated conspecific females, resulting

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in high levels of prolactin comparable to those found in animals tested alone with a stressor. Conversely, adult males may not experience social buffering and are expected to have high levels of prolactin in the social condition; therefore, pre-treatment with an oxytocin antagonist will not cause higher levels of prolactin as compared with the nontreated social animal. Among juvenile males and females, no such sex X treatment condition interaction is expected. Juveniles are expected to respond to stress, social buffering, and the oxytocin antagonist in a pattern similar to adult females (above). Each animal model will serve as a foundation to build an understanding of responses to stress and social buffering, particularly in nonverbal populations such as children, the aged, and adults with brain injuries. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LOCAL INTERACTIONS BETWEEN HIPPOCAMPAL NEURONS Principal Investigator & Institution: Dudek, Francis Edward.; Professor; Anatomy and Neurobiology; Colorado State University Fort Collins, Co 80523 Timing: Fiscal Year 2001; Project Start 01-DEC-1987; Project End 31-JAN-2003 Summary: (from applicant's abstract) The long-term consequences of brain injury are a critical problem in clinical neuroscience. One important example is how excitotoxic neurodegenerative lesions, such as damage to hippocampal neurons that occurs with prolonged status epilepticus, can ultimately lead to chronic epilepsy. The proposed studies use acute hippocampal slices from kainate-treated rats to determine how status epilepticus leads to the reorganization of local synaptic circuits in the dentate gyrus and CA1 areas of the hippocampus. Whole cell patch clamp analyses of synaptic currents, focal microstimulation of hippocampal neurons with photolysis of caged glutamate, and dual recordings will be combined with anatomic techniques to test specific hypotheses about changes in recurrent excitation and inhibition. We aim to determine whether status epilepticus is followed by a progressive development of new abnormal synaptic circuits that contribute to changes in hippocampal seizure susceptibility. Although our primary focus will be to evaluate more rigorously whether new recurrent excitatory circuits are formed in the hippocampus after status epilepticus, and to understand how the putative increase in density of these circuits alters the properties of hippocampal networks, the applicants will also examine hypothetical changes in local inhibitory circuits. The applicants aim to focus on the progressive nature of the synaptic reorganization of the hippocampus as a model for time-dependent changes in cortical networks that may occur throughout the temporal lobe and other neocortical areas after neurodegenerative brain injuries. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MAGNESIUM SULFATE FOR NEUROPROTECTION AFTER BRAIN TRAUMA Principal Investigator & Institution: Winn, H Richard.; Professor and Chairman; Neurological Surgery; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-JUL-1983; Project End 31-JUL-2002 Summary: (Adapted from Applicant's Abstract): Traumatic brain injuries represent an important health problem; they occur with high frequency, the population affected contains many previously healthy young people, and they are associated with high mortality and morbidity. The proposed study continues on our 16 years of experience in conducting clinical trials evaluating treatments for preventing seizures following head injury (Dilantin Prophylaxis of Post-traumatic Seizures, Valproate for Prophylaxis of

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Post-traumatic Seizures) and in examining neurobehavioral outcome after head injury. Our previous trials showed that Dilantin prevents early seizures but is ineffective in preventing epilepsy following head trauma and that Valproate is possibly associated with higher mortality that short-term Dilantin. The trials and outcome studies found that epileptic seizures, serious cognitive difficulties, high unemployment, and inability to live independently are common among survivors of moderate or severe head injury. Using a randomized, double-blind design, the present study will evaluate magnesium sulfate as a neuroprotectant and anti-epileptogenic agent following head injury. Magnesium sulfate is a widely used, well-tolerated compound that has been shown in the laboratory to be effective in reducing seizures and also in limiting neuronal damage and in improving functional outcome following experimental head injury. Specifically, the study will test the hypothesis that magnesium sulfate, when given within 8 hours of a moderate or severe head injury, a) increases survival, b) decreases seizures, and c) improves neurobehavioral functioning. Additionally, the study will: assess the effects of timing of dosage (e.g. <4 hours vs. 4-8 hours), gender, and race; determine the rate of adverse events: and evaluate the time course and correlates of total and ionized magnesium concentrations. Patients with moderate or severe head injury (postresuscitation Glasgow Coma Scale 3-12) will be randomized to receive high doses of magnesium sulfate or placebo. Treatment will be started as soon as possible, and definitely within 8 hours of injury. The initial bolus of magnesium sulfate will be followed by a 7 day infusion to keep magnesium levels high during the period when secondary damage from the head injury is most likely. Patients will be closely monitored for survival and seizures over the first six months after injury and will have a comprehensive neurobehavioral assessment at six months after injury. In summary, this placebo-controlled, randomized clinical trial will determine the effects of magnesium sulfate on survival, post-traumatic seizures, and the patients behavioral functioning following head injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MAGNESIUM SULFATE FOR NEUROPROTECTION AFTER BRAIN TRAUMA Principal Investigator & Institution: Temkin, Nancy R.; Associate Professor; Neurological Surgery; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2002; Project Start 01-JUL-1983; Project End 31-AUG-2005 Summary: (provided by applicant): Traumatic brain injuries represent an important health problem: they occur with high frequency, the population affected contains many previously healthy young people, and they are associated with high mortality and morbidity. This study continues on our 20 years of experience in conducting clinical trials evaluating treatments for preventing seizures following head injury (Dilantin Prophylaxis of Post-traumatic Seizures. Valproate for Prophylaxis of Post-traumatic Seizures) and in examining neurobehavioral outcome after head injury. The trials and outcome studies found that epileptic seizures, serious cognitive difficulties, high unemployment, and inability to live independently are common among survivors of moderate or severe head injury the ongoing trial tests whether these consequence can be ameliorated by magnesium sulfate. Using a randomized, double-blind design, the present study evaluates magnesium sulfate as a neuroprotectant and anti-epileptogenic agent following head injury. Magnesium sulfate is a widely used, well tolerated compound that has been shown in the laboratory to be effective in reducing seizures and also in limiting neuronal damage and in improving functional outcome following experimental head injury. Specifically, the study will test the hypothesis that

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21

magnesium sulfate, when given 8 hours of a moderate or severe head injury, a) increases survival b) decreases seizures, and c) improves neurobehavioral functioning. Additionally, the study will: assess the effects of timing of dosage (e.g. <4 hours vs. 4-8 hours), gender, and race; determine the rate of adverse events; and evaluate the time course and correlates of total and ionized magnesium concentrations. Patients with moderate or severe head injury (post-resuscitation Glasgow Coma Scale 3-12 or having an early craniotomy) are randomized to receive moderate doses of magnesium sulfate or placebo. Treatment is started as soon as possible, and definitely within 8 hours of injury. The initial bolus of magnesium sulfate is followed by a 5 day infusion to keep the magnesium levels elevated during the period when secondary damage from the head injury is most likely. Patients are closely monitored for survival and seizures over the first six months after injury and have a brief neurobehavioral assessment at I and 3 months and a comprehensive neurobehavioral assessment at six months after injury. In summary, this placebo-controlled, randomized double-masked clinical trial will determine the effects of magnesium sulfate on survival, post-traumatic seizures, and the patients' functional status and neurobehavioral functioning following traumatic brain injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISM OF MOSSY FIBER SYNAPTIC PLASTICITY Principal Investigator & Institution: Calakos, Nicole; Pathology; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2006 Summary: (Applicant's Abstract): The candidate proposes to undertake a program of research which will involve extensive training in the fields of electrophysiology and synaptic plasticity. The addition of expertise in these fields will complement the candidate's already extensive background in the molecular biology and biochemistry of synaptic vesicle function. Specifically, the goals of the research are to understand the basis of long-term potentiation (LTP) in the mossy fiber synapses of the hippocampus, an area that relies on presynaptic mechanisms for this plasticity. Two proteins, rab3a and protein kinase A (PKA), whose essential role at mossy fiber LTP (mfLTP) has already been established will be the focus of investigation. To determine the downstream effectors of rab3a which mediate mfLTP, extensive electrophysiologic analysis of a null mouse strain for the candidate rab3a effector protein, rim, will be undertaken. Once the basis of the rim (-/-) mutant phenotype on mfLTP is characterized, rescue experiments in primary cultures of hippocampal granule cells using transient expression systems will be performed. This approach will further be used to identify the specific domains of rim required for mfLTP. A second line of study will be the pursuit of targets of PKA phosphorylation required to establish mfLTP. In addition to standard techniques of studying phosphoproteins, a specific analysis of proteins important for synaptic vesicle docking and fusion will be performed as there is evidence that suggests they may be targets of PKA. The final area of investigation will return to the role of rim in mfLTP and seek to understand the molecular basis of this effect by identifying interacting proteins. In the long term, using such approaches to study synaptic plasticity, the candidate hopes to understand the role of plasticity in memory, recovery from brain injuries such as stroke, and neurodegenerative diseases such as Alzheimer's with the goal of improving therapy in disease states. The candidate's background of graduate study in Neuroscience and residency training in Neurology is particularly suited to make basic science discoveries and apply them to areas of clinical relevance. The mentor, Dr. Robert Malenka is also a physician-scientist

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Brain Injuries

and serves as an ideal role model for excellence in research. The research environment at Stanford University School of Medicine is well suited both in its physical plant and intellectual resources to embark upon these studies. Lastly, in addition to acquiring new research skills, the candidate will be active in a variety of relevant scientific meetings (journal clubs, lecture series, national meetings) and the Department of Neurology to prepare for a career in academic medicine with both research and clinical responsibilities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISMS OF CAM KINASE II SIGNAL TRANSDUCTION Principal Investigator & Institution: Colbran, Roger J.; Associate Professor; Molecular Physiol & Biophysics; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 15-MAY-2001; Project End 31-MAR-2006 Summary: From applicant's abstract): Detailed characterizations of neuronal signal transduction and protein phosphorylation/dephosphorylation are critical for understanding many brain functions. For example, activation of NMDA-type glutamate receptors stimulates both protein kinases and protein phosphatases, which feedback to modulate AMPA- and NMDA-type glutamate receptors. Ca-+/calmodulin-dependent protein kinase II (CaMKII) is a major dendritic kinase activated by NMDA receptor stimulation, resulting in Thr286-autophosphorylation and phosphorylation of AMPAand NMDA-receptors and several other proteins including densin-180, an Osialoglycoprotein with a PDZ domain. We showed that CaMKII autophosphorylation promotes its translocation to postsynaptic densities (PSDs), submembranous cytoskeletal specializations, and identified the NR2B subunit of NMDA receptors and densin- 180 as two proteins that likely contribute to translocation. Five Specific Aims address our hypothesis that binding to NR2B and densin-180 modulates CaMKII, resulting in synapse-specific regulation of glutamate receptors. 1. Neuronal interaction of CaMKII and dens in- 180 will be verified by colocalization using immunofluorescent confocal microscopy and by coimmunoprecipitation assays. Relative contributions of NR2B and densin- 180 to CaMKII binding activities in PSDs will be determined. 2. Interaction domains in NR2B, densin-180 and CaMKII will be identified in vitro by truncation/deletion and site-directed mutagenesis, and their importance will be confirmed in HEK293 cells and neurons. This information will be used to develop reagents that specifically manipulate CaMKII localization in cells. 3. Dynamics of CaMKII.densin-180 and CaMKII.NR2B interactions, and regulatory roles of phosphorylation/dephosphorylation of densin-180, NR2B and CaMKII, as well as NMDA receptor activation, will be examined in vitro and in intact cells. 4. Effects of interaction with NR2B or densin-180 on CaMKJI autophosphorylation will be investigated in vitro and in intact cells. AMPA receptor phosphorylation and potentiation in HEK293 cells and neurons will be compared under conditions where NR2B and densin-180 are used to differentially target CaMKJI. 5. Roles of CaMKIIbinding and CaMKII-mediated NR2B phosphorylation in regulation of NMDA receptors will be determined. More long-range goals are to establish the roles of CaMKII targeting by NR2B and densin-180 in regulation of synaptic transmission and synapse-specific synaptic plasticity. These studies will provide fundamental insights into signal transduction mechanisms underlying normal brain functions such as learning and memory. Reagents that block these protein.protein interactions also have potential for development as therapeutic compounds to treat mental disorders, such as schizophrenia or depression, and possibly brain injuries.

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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISMS OF GROWTH CONE TURNING IN DIFFUSIBLE GRADIENT Principal Investigator & Institution: Zheng, James Q.; Associate Professor; Neuroscience and Cell Biology; Univ of Med/Dent Nj-R W Johnson Med Sch Robert Wood Johnson Medical Sch Piscataway, Nj 08854 Timing: Fiscal Year 2003; Project Start 20-AUG-1998; Project End 30-APR-2007 Summary: (provided by applicant): Formation of specific neuronal connections requires accurate guidance of developing axons to their correct targets by a variety of surfacebound and diffusible guidance cues. Axon guidance is also critically important for functional repair of damaged neuronal connections after brain injuries and diseases. During guidance, the motile growth cone at the tip of the axon senses direction from extracellular space and steers the axon through the complex environment of developing embryos to reach its specific target. Significant progress has been made in recent years towards the molecular identification of a variety of surface-bound and diffusible guidance molecules. However, the cellular mechanisms underlying directional sensing and steering of the growth cone remain largely unknown. The proposed study aims to understand how the growth cone responds to different types of diffusible guidance molecules to steer in a particular direction. The working hypothesis to be tested is as follow: different extracellular cues can act through different signaling pathways, but they all elicit localized signaling cascades that target the cytoskeleton in a spatially and temporally restricted fashion to cause the growth cone to steer in a specific direction. Taking advantage of the large size of Xenopus growth cones, an in vitro system for rigorous assay of growth cone turning, and a combination of high-resolution digital imaging and intracellular manipulation techniques, the research team plans to thoroughly investigate the cellular components associated with and, particularly, responsible for specific steering behaviors (attractive or repulsive) of the growth cone. The proposed project has four specific aims: (1) to determine the asymmetric motile activities associated with and/or responsible for growth cone attractive and repulsive turning, respectively, (2) to examine the local cytoskeletal events associated with attraction and repulsion respectively, (3) to elucidate the precise role of the microtubules and actin cytoskeleton, as well as their interactions, in steering the growth cone, and (4) to determine whether and how spatially- and temporally-regulated membrane recycling contributes to guided growth cone steering. The long-term goal is to identify the cellular events that are common as well as specific for attractive and repulsive turning, respectively, thus achieving a better understanding towards the cellular mechanisms underlying axon guidance for the generation of highly ordered brain architecture. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: PERCEPTION

MECHANISMS

OF

INTERMEDIATE

DISTANCE

SPACE

Principal Investigator & Institution: He, Zijiang; Associate Professor; Psychological and Brain Sciences; University of Louisville University of Louisville Louisville, Ky 40292 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): A significant proportion of human activities involving space orientation, locomotion and action occur over a critical span of space of about 2 to 25m from the observer. Yet, the mechanisms underlying the abilities to flawlessly perform these activities in the intermediate distance range are not well

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Brain Injuries

understood, though appreciated whenever the abilities are impaired due to brain injuries. How is space perception impaired? A key to answering this question is to understand how human perception in the intermediate distance range is referenced relative to the physical space. An early theoretical answer to this question was provided by Gibson (1950), who proposed that space perception in the intermediate distance range is highly influenced by the structure of the ground surface. The current proposal presents some empirical evidence to support the ground reference idea, in addition to presenting new hypotheses to uncover the perceptual mechanisms underlying space perception in the intermediate distance range. Three broadly defined issues will be addressed. These are: 1. How does the visual system define the ground surface reference frame for distance judgment? 2. How is the eye level determined and calibrated? 3. How is an object above the ground surface localized? This research will be conducted both in the real and virtual reality environments. The latter not only provides for a controlled stimulus environment, but will also provide valuable insights into designing virtual reality systems with high immersion quality, which will be of benefit to those interested in the vocational and therapeutic usage of the virtual reality systems. Above all, this research will advance the knowledge of how the ground surface is represented by the brain, and how it is employed as a reference frame for localizing objects, which is an important step to understanding space perception and cognition. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MULTIDISCIPLINARY ASSESSMENT OF SEVERE BRAIN INJURY Principal Investigator & Institution: Plum, Fred; Chairman; Neurology Neuroscience; Weill Medical College of Cornell Univ New York, Ny 10021

and

Timing: Fiscal Year 2001; Project Start 19-SEP-2001; Project End 31-JUL-2004 Summary: A recent NIH Consensus Statement (JAMA 1999 282:974) noted that 70-90,000 Americans each year incur long-term substantial loss of function from traumatic brain injury (TBI). The panel further noted that "the more problematic consequences involve the individual's cognition, emotional function, and behavior." The present studies are aimed at developing pilot data to guide a controlled trial for the use of deep brain stimulation technologies in selected TBI patients: those with recovery limited to regained consciousness, minimal self-awareness, and minimal interpersonal communication. Study patients will either be in a minimally conscious state (MCS) or have emerged from a MCS but remain incapable of independent activities of daily living as measured by the Disability Rating Scale. Emergence from MCS is suggested by reliable and consistent demonstration of functional interaction. Many of these patients demonstrate preserved, but fluctuating, capacities for basic communication, memory, attention, intention, and awareness of self and environment. These observations provide clinical evidence that their limited functional capacities do not represent entirely irreversible damage. The immediate goals of the proposed studies are to define appropriate clinical and imaging criteria and outcome measures to evaluate patients for selection into deep brain stimulation studies, and to evaluate physiological measures that can aid the design of stimulation parameters. We present preliminary neuroimaging data both from patients in chronic vegetative states, and from patients with other neurological conditions with implanted deep brain stimulators that demonstrate selective functional brain activations during neurostimulation. We detail potential strategies for selection of patients and for choosing targets within the thalamic intralaminar nuclei of these patients for electrical stimulation. The strategy of selection of patients for neuromodulation of impaired cognitive function will be evaluated via neuroimaging tools and neuropsychologic evaluation. The proposal combines the

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unique clinical expertise and experience of neurological, functional stereotactic neurosurgical, and neurorehabilitation investigators. To achieve these goals we will develop a strong multi- disciplinary team with recognized expertise in both investigational and therapeutic studies of brain injured patient populations. The longrange goal of the studies proposed here is to provide a foundation for rational therapies for chronic cognitive disabilities following complex brain injuries. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DISORDERS

NEUROCOGNITIVE

IMPAIRMENT

AND

ALCOHOL

USE

Principal Investigator & Institution: Bates, Marsha E.; Research Professor; Center of Alcohol Studies; Rutgers the St Univ of Nj New Brunswick Asb Iii New Brunswick, Nj 08901 Timing: Fiscal Year 2001; Project Start 01-SEP-1997; Project End 30-APR-2004 Summary: Neurocognitive impairment is believed to affect alcoholism treatment process and outcome. However, alcohol researchers have had difficulty empirically validating this relationship between impairment and outcome, often finding weak and inconsistent support. This competitive renewal application seeks to extend a Rutgers CAS research program studying neurocognitive impairment in persons treated for alcohol use disorders. The unmet need to examine neurocognitive moderation models has often been highlighted by alcohol researchers and is strongly supported by the literature on the relation of neuropsychological impairment to behavioral outcomes following treatment for brain injuries of multiple etiologies. We have found support for a hypothesized model wherein neurocognitive impairment moderated the relation of robust change processes to intensity of alcohol and other drug use 6 months after treatment. Self-efficacy, commitment to abstinence, and AA affiliation were strong predictors of outcome in unimpaired persons, but only weak predictors of outcome in those who were impaired. Results supported a threshold model of impairment which suggests that only severe neurocognitive impairments may affect moderation. The goal of this competitive renewal application is to develop heuristic models of brain-behavior relations that adequately characterize the effect of alcohol-related neurocognitive impairment on treatment outcome through secondary analysis of three existing longitudinal data bases which overlap substantively in constructs and measures. We will use two convergent analytic methods to contrast direct effect, mediation, and moderation models of neurocognitive influences on alcohol- and drug-specific, and psychosocial outcomes within a conceptual framework informed by the traumatic brain injury rehabilitation literature. By examining the generality of results across different addictions treatment populations, we can provide a more robust test of putative neurocognitive models of treatment outcome than otherwise would be possible without costly collection of new longitudinal data. Results will advance understanding of mechanisms which support good outcomes in neurocognitively impaired individuals and will have theoretical implications for cognitive models of relapse. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEURONAL SOMATIC RESPONSE TO TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Povlishock, John T.; Professor and Chair; Anatomy and Neurobiology; Virginia Commonwealth University Richmond, Va 232980568 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-MAY-2007

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Brain Injuries

Summary: (provided by applicant): This amended application seeks to explore a relatively unchartered area in the pathobiology of traumatic brain injury (TBI) focusing on those injuries involving diffuse damage to the brain. Unlike the majority of contemporary TBI literature which focuses on focal change, most of which entails large destructive lesions such as contusion and hematoma formation, this application explores the potential that diffuse TBI, not complicated by focal lesions or secondary insult, evokes diffuse changes in either the neuronal somatic plasma membrane or perisomatic axonal appendages. Specifically, we posit that the forces of injury are capable of mechanically porating the intact plasma membrane causing either enduring or transient membrane perturbations that can respectively participate in progressive damage leading to cell death or membrane resealing and cell recovery. The same forces of injury are also envisioned to evoke, in other populations of neurons, perisomatic axotomy. It is posited that this TBI-induced damage translates into neuronal somatic perturbation. However, in contrast to published literature, we posit that most neurons do not die. Rather they undergo a reparative attempt. These premises will be explored in two well characterized models of TBI, fluid percussion and impact acceleration TBI. The potential for plasma membrane poration and resealing will be assessed via different molecular in weight/size tracers administered intrathecally at various time points pre and post injury. Companion quantitative studies using the principles of modern stereology will assess the numbers of neurons involved in this complex pathobiology within specific domains of the neocortex. Parallel LM immunocytochemical and ultrastructural analyses will provide for the direct assessment of membrane integrity and related cytoskeletal, organelle or nuclear changes that correlate either with cell recovery or a progression of damage leading to death. Intrathecal tracers will be used in those neurons sustaining perisomatic axotomy to exclude the potential for plasma membrane potation, while using parallel immunocytochemical approaches to understand if such axotomized neurons progress to cell death or rather undergo transient perturbation with reorganization and repair. Collectively, these studies should reshape our appreciation of the complex pathobiology of TBI. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEUROPSYCHOLOGICAL OUTCOMES IN NEONATAL BRAIN INJURIES Principal Investigator & Institution: Durkin, Maureen; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2001 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: NEUROREHABILITATION PREGNENOLONE

WITH

PROGESTERONE

&

Principal Investigator & Institution: Wright, David W.; Emergency Medicine; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2006 Summary: (provided by applicant): There are about 5.3 million people in this country living with a range of disabilities caused by traumatic brain injury, and about 25-30% of those people are unable to return to work one year later. At present, there are no effective clinical treatments currently available to the victims of traumatic brain injuries that can repair the primary and secondary damage caused by the cascade of cytotoxic

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damage unleashed by the initial insult. Obviously, a safe, low cost and effective treatment for such a significant health problem is worth addressing. Numerous reports have documented the role of neurosteroids in immediate post-injury neuroprotection. However, few studies have examined the effect of these steroids as a treatment after the acute phase. We are particularly interested in the effect of progesterone long-term because it is currently being tested in a human clinical trial as an acute phase neuroprotectant. Extensive preclinical trials have shown that progesterone is neuroprotective when administered shortly after injury. However, at least two of the potential mechanisms (inhibition of NMDA transmission and stimulation of GABAA receptors), by which progesterone exhibits neuroprotection, could potentially worsen subacute rehabilitation and subsequent long-term recovery. Conversely, pregnenolone, the precursor of progesterone, exhibits opposite effects with respect to NMDA and GABAA modulation and could enhance neurorehahilitation. We propose to determine the effects of progesterone and pregnenolone when treatment is delayed after injury in animals. The data gathered would provide information regarding the potential utility of these neurosteroids in subacute or long-term treatment conditions. In addition, should progesterone prove to be an effective neuroprotectant in the human clinical trial, it will be necessary to know how long treatment should be maintained and whether long-term treatment enhances or deters post-injury rehabilitation. There is a growing body of evidence that both progesterone and pregnenolone can also stimulate remyelination of damaged nerve cells and that they also have the potential to stimulate neuronal repair after the initial injury cascade has long subsided. This means that these steroids, both of which are synthesized in the brain, may be beneficial as adjunct therapies for long-term rehabilitation. We propose to investigate the role of the neurosteroids progesterone (PROG) and pregnenolone-sulfate (PREGS) as putative treatment for traumatic brain injury during the rehabilitation phase of recovery in both male and female subjects. Therefore, we will examine two delayed treatment paradigms (7 days & 28 days post injury) on the recovery process at the behavioral and morphological levels of analysis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OUPATIONAL SURVEILLANCE MODULES FOR PREVENTION Principal Investigator & Institution: Bonauto, David; Washington State Dept Lab/Indust of Labor and Industries Olympia, Wa 98504 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2005 Summary: Through surveillance of several National Occupational Research Agenda (NORA), Healthy People, and Washington State Department of Labor and Industries priority conditions including occupational asthma (OA), adult lead poisoning, musculoskeletal disorders of the upper extremity, low back disorders, dermatitis, hospitalized burns, traumatic head and brain injuries (THBI) as well as assaults, the Safety and Health Assessment and Research for Prevention (SHARP) program will demonstrate the application of a comprehensive, occupational surveillance program. Through demonstration of the proposed surveillance program, SHARP will create a systematic model for adoption by other states. To allow for adaptability, SHARP proposes development of a modular approach which demonstrates several approaches to outcome based surveillance, hazard based surveillance, and subsequent prevention activities. The proposed project will address the following aims: 1) Conduct a survey of state based occupational surveillance programs to determine currently employed approaches to surveillance and prevention, program capabilities, and program opinion leaders. 2) Demonstrate a modular approach to occupational surveillance. This modular approach should encompass the use of different data sources for priority conditions

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Brain Injuries

selected by an individual program. 3) Develop modules for the creation, dissemination, and evaluation of prevention efforts. 4) Conduct an employer/employee survey to further identify etiologic agents or practices in one identified industry. 5) Develop an Internet based library of surveillance modules and prevention materials. 6) Produce and disseminate three surveillance reports for WA State priority conditions per year. 7) Produce and disseminate two prevention reports to employers or employees per year. Through the proposed project, SHARP will demonstrate the utilization of several data sources for the surveillance of occupational diseases and hazards. Further, SHARP will demonstrate the analysis of such data, the creation of simple public health interventions using surveillance data, the implementation of interventions, and the evaluation of interventions using surveillance data. Finally, SHARP will produce a web accessible library of materials detailing the methodology of the various components of the surveillance program including prevention materials that may be modified and disseminated in other states. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OUTCOMES OF TRAUMATIC BRAIN INJURY IN CHILDREN Principal Investigator & Institution: Yeates, Keith O.; Associate Professor; Children's Research Institute 700 Children's Dr Columbus, Oh 43205 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): The applicant is seeking a K02 (Independent Scientist Award) to continue building a program of research focusing on the outcomes of childhood traumatic brain injury (TBI). His objectives are (1) to investigate how children's development following TBI is related to severity of injury, age at injury, and time since injury; (2) to examine the role of environmental factors as moderators of recovery from TBI; and (3) to study the relationships between focal brain lesions, cognitive and social problem-solving skills, and "real world" social functioning following TBI. He has been a Co-Investigator on a prospective, longitudinal study of moderate to severe TBI in school-age children, and currently is Principal Investigator on an NICHD-funded research grant to study the outcomes of mild closed head injuries (CHI) in children and adolescents (see below). His future research efforts will include studies of TBI in preschool children and of the effects of TBI on children's social development. His proposed career development plan will enhance his skills in statistical methods pertinent to his research, including (a) analysis of longitudinal data, (b) treatment of missing data, and (c) robust statistical methods. He also will obtain additional training in the responsible conduct of research. The specific aims of the research are to examine the (1) natural history, (2) prediction, and (3) consequences of post-concussive symptoms in children with mild CHI. The study will involve 200 8 to 15 year old children with mild CHI and 100 with mild orthopedic injuries not involving the head in a concurrent cohort/prospective research design. The children and their families are assessed four times during the first year post injury (i.e., at 1 week, 1 month, 3 months, and 12 months post-injury). Post-concussive symptoms are assessed using rating scales and interviews, with both children and parents as informants. Predictors of post-concussive symptoms include injury characteristics, cognitive abilities, and noninjury related child and family variables. Outcomes include school performance, health utilization, and other aspects of child and family functioning. The study will examine three major hypotheses: (1) Children with mild CHI display more post-concussive symptoms than children with mild orthopedic injuries. (2) The incidence of postconcussive symptoms is related to (a) injury characteristics, (b) impairments in cognitive skills, and (c) non-injury related child and family factors. (3) Severe post-concussive

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symptoms are associated with more child disability. The findings will help resolve the scientific controversy regarding the outcomes associated with mild CHI, and will assist physicians and other health care providers in identifying and managing the sequelae of mild CHI. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PERSISTENT TRAUMATIC BRAIN INJURY

NEUROPSCHIATRIC

DISORDERS

IN

MILD

Principal Investigator & Institution: Strickland, Tony L.; Professor; Charles R. Drew University of Med & Sci 1621 E 120Th St Los Angeles, Ca 90059 Timing: Fiscal Year 2002; Project Start 25-SEP-2002; Project End 31-JUL-2005 Summary: The primary goal of this project is to determine if the presence of substantial abuse is associated with differential patterns of sustained neuropsychiatric disorders in mild traumatic brain injury (MTBI) patients. Traumatic brain injury (TBI) represents a major pubic health concern in the United States and worldwide. Neurocognitive and neuropsychiatric sequelae secondary to MTBI usually resolve within 90 days, however, for a significant minority of patients symptoms persist and can be severe. Incidence estimates of TBI based on U.S. studies are about 200 per 100,000 per year, thus yielding approximately 470,000 cases of brain injury annually. The most common causes of TBI include motor vehicle accidents, falls, assaults, firearm injuries, and sports. The majority of TBI is classified as mild. Toxicology studies of TBI patients reveal that they were often under the influence at the time of their acquired brain traumas. However, importantly, the relative contribution of acquired brain trauma versus substance-induced persistent neuropsychiatric pathology is incompletely understood. Understanding differential patterns of neuropsychiatric outcomes in minority patients is particularly important, because of the increased prevalence of intentional and unintentional injuries in the groups. Due to a dramatic surge in alcohol and other drugs in the past decade, there is a pressing need to study the associated neuropsychiatric aspects, particularly when substance abuse is combined with acquired brain trauma. It is now well-established that substance abuse, especially the abuse of alcohol and stimulants, can lead to hypertensive encephalopathy and ischemic brain hemorrhage, and that depression and other neuropsychiatric symptomatology are common (Bigler, 2001; Pulse Watch, 2000; Strickland, et al., 1998). Despite that alcohol and stimulants can induce significant cerebral pathology, little is known about differences in the magnitude of neuropsychiatric impairment, duration of symptoms, or the specific brain region(s) adversely impacted when substance abuse co-occurs with MTBI. Existing information is even less complete regarding differences in neurobehavioral outcomes secondary to ethnic, cultural, and socioeconomic influences. To strengthen our understanding of differences in neuropsychiatric and quality of life (QOL) outcomes in MTBI patients, this proposed project utilizes a five-year, between- and within-subject, repeated-measures design to investigate these parameters in a sample of 200 subjects. Fifty MTBI subjects positive for substance abuse will be evaluated within thirty days of injury (Time 1), and three months later (Time 2). Fifty non-MBTI and non-substance abusing subjects will be evaluated (Time 1), and three months later (Time 2). The proposed study has the following specific aims: 1. To determine if severity and duration of neuropsychiatric impairment in MTBI is associated with the presence of substance abuse. 2. To compare severity of neuropsychiatric and neuropsychological functioning between MTBI and substance abuse subjects over time (three months after initial assessment). 3. To identify and describe factors that are associated with improvement in neuropsychiatric

30

Brain Injuries

symptoms via evaluation of primary or secondary analyses (such as interventions, demographics, or socioeconomics). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PRESYNAPTIC MECHANISMS AT RIBBON-CLASS SYNAPSES Principal Investigator & Institution: Roberts, William M.; Institute of Neuroscience; University of Oregon Eugene, or 97403 Timing: Fiscal Year 2004; Project Start 01-JAN-1990; Project End 31-DEC-2008 Summary: (provided by applicant): The long-term objective of this work is to understand the mechanism of synaptic transmission in sensory receptor cells in the ear, eye and other sensory systems that use graded transmission at ribbon-class synapses. This specialized form of chemical signaling appears to be an adaptation to allow the transmission of information about small changes in sensory input that would be lost during conventional synaptic transmission that uses action potentials. The proposed experiments will investigate the physiology, anatomy and biochemistry of these synapses. The work on sensory receptors (hair cells) in the ear will use frogs and zebrafish as model species. The zebrafish work will also study photoreceptors and bipolar cells in the retina, and hair cells in the lateral line organs. All of these calls have ribbon-class synapses. These species were chosen for study because of the cellular and molecular tools that are available to answer fundamental questions in synaptic physiology. In the case of frogs, there is also a wealth of information already available upon which to build. During the past 10 years, several laboratories have developed techniques that allow detailed electrophysiological analysis of synaptic transmission using tight-seal voltage clamp to measure small changes in membrane capacitance to observe synaptic transmission on a millisecond time scale. This physiological method will be used in conjunction with electron tomography and recently developed membrane tracer dyes to study the ultra structure of the synaptic vesicle cycle ribbon synapses. The goal is to test several key hypotheses concerning the function of the synaptic "ribbon", the prominent anatomical feature for which these synapses are named. The project will also focus on two major proteins (calretinin and parvalbumin 3) that are believed to serve central roles in synaptic transmission in these cells by capturing and transporting calcium ions away from the synapses. The project will investigate the important biochemical properties that determine how fast these proteins bind calcium, how much calcium they can sequester, and how fast they can diffuse within the cell. These properties are central to understanding synaptic transmission in hair cells, and have a wider relevance to the proposed function of these and related calcium-binding proteins in protection from calcium overload during strokes and other brain injuries. The genetic and molecular tools developed by zebrafish researchers during the past decade will allow a direct test the function of a protein (Ribeye) that has recently been identified as a major component of the ribbon. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: RETICULAR FORMATION CONTROL OF REACHING Principal Investigator & Institution: Buford, John A.; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001 Summary: The primary aim of this study is to investigate the role of the reticular formation in the control of reaching. Neurons in the reticular formation project to the spinal cord and ultimately contribute to the activation of muscles. Indeed, the

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reticulospinal system is one of the major descending pathways from the brain to the spinal cord. In most accounts, the role ascribed to the reticular formation is control of posture and other support-related roles, with "more advanced" systems supplying the details required, for example, to control the hand. Consistent with this view, studies to date have focused on the role of reticulospinal systems in locomotion, a movement with complex postural demands. The anatomical connections, however, suggest a role for reticulospinal systems in skilled movements, especially those requiring preparation to "set-up in advance" of anticipated movements. The present project has identified activity in the reticular formation related to skille d reaching. In some reticular formation cells, activity starts well in advance of movement, suggesting a role in movement preparation. This function had not previously been ascribed to this part of the brain. A new grant proposal stemming from this work has been submitted to investigate the role of preparatory activity in governing spinal reflexes. A more complete understanding of the normal role of the reticulospinal system in the control of skilled movement will lead to better strategies for rehabilitation after strokes and other brain injuries. FUNDING NIH grants RR00166, NS01767, and NS15017. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SHORT TERM MEMORY DEFICITS IN FOCAL LESION PATIENTS Principal Investigator & Institution: Baldo, Juliana V.; East Bay Institute for Research and Educ and Education Martinez, Ca 945534668 Timing: Fiscal Year 2001; Project Start 10-JUN-2001 Summary: The aim of this research proposal is to study the neurobiological substrates of short-term memory by comparing two groups of neuropsychological patients. Both patients with anterior (prefrontal cortex) lesions and conduction aphasics with posterior (temporo-parietal cortex) lesions exhibit short-term memory deficits. It is hypothesized that the two groups' deficits arise from impairment in different components of shortterm memory. To assess this hypothesis, the two patient groups and elderly controls will be administered a series of tasks requiring short-term memory. These tasks will vary along several dimensions, such as the domain of the task (verbal versus spatial). Findings from this research will illuminate understanding of normal short-term memory processes as well as identify the brain regions mediating those processes. In addition, this research has implications for treatment (e.g., cognitive rehabilitation) of patients with similar brain injuries and cognitive deficits. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: STUDIES ON CHILDREN WITH EARLY FOCAL BRAIN INJURY Principal Investigator & Institution: Bates, Elizabeth A.; Professor; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2001; Project Start 16-SEP-1985; Project End 31-JUL-2006 Summary: Over the past 15 years, we have made significant progress in the study lf language and affective development in children with congenital injuries to one side of the brain (FL). In each behavioral , we have covered evidence of initial deficits, and specific effects of lesion side and site, but these initial deficits are followed by substantial recovery and development, providing strong evidence for behavioral and neural plasticity in this population. Furthermore, we have shown that trajectories of deficit and recovery differ across domains. In language, lesion- symptom correlations exist in the first years of life, but they do not resemble the patterns observed in adults; by 5-7 years of age, specific effects of lesion side and site seem to have disappeared altogether. In

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spatial cognition, lesion-symptom correlations persist across childhood and adolescence, albeit in a mild form, and continue to resemble the correlations observed in adults. These results are compatible with a large literature on plasticity and reorganization in animals, supporting the view that brain development is a dynamic, responsive and selforganizing system. But they also offer a unique perspective on plasticity and brain organization in humans. We are now well-positioned to take a historic new steps, with convergent use of functional magnetic resonance imaging (fMRI), event-related brain potentials(ERP), combined with analogous "on-line" (timed" behavioral studies of language, spatial cognition and spatial attention. These convergent methods will yield unprecedented information about the "alternative brain plans" that have emerged across the course of development in children with FL. E will also continue to chart language and cognitive development into adolescence, using benchmark "off-line" (untimed" measures of language (including aspects of discourse that re critical to success in school and work), visual-spatial cognition, memory and executive function. On all measures, results for children with FL will be compared systematically to findings for children in other populations, including Specific Language Impairment, Williams Syndrome, Down Syndrome, and new project studying other forms of FL. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: THERMOREGULATORY SEQUELA OF TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Thompson, Hilaire J.; None; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2001; Project Start 01-JUN-2001 Summary: (provided by applicant) The goal of this experiment is to characterize an animal model of post-traumatic hyperthermia (PTH) in order that future interventional studies may be undertaken and then translated to patient care. PTH is a condition that affects up to 37% of patients with moderate-severe traumatic brain injuries (TBI). It has been well documented that hyperthermia post-injury worsens outcome in animal models of ischemia and TBI. Hyperthermia increases metabolic expenditure, resulting in the inability of patients to maintain muscle or fat stores. Muscle loss can significantly extend the time required to return to maximal function. Additionally, PTH is a diagnosis of exclusion, requiring the patient to be subjected to multiple costly and painful diagnostic tests. This delay in diagnosis also delays initiation of appropriate treatment as traditional interventions for fever are ineffective, and can delay transfer to rehabilitation. To date, studies have been aimed solely at determining incidence, thus very little is known about the phenomenon of PTH. The development of an animal model of PTH using lateral fluid percussion injury would provide needed knowledge about this sequela, particularly regarding the effect of temperature in the immediate post injury phase on inducing the subsequent development of PTH. The effect of PTH on behavior and cognition will also be examined in this exploratory study. Additionally, the findings of this study will provide information on the relationship of three acute phase reactants, copper, zinc, and alpha-1 antitrypsin, to PTH to determine their potential use as biological markers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CHILDREN

TRAINING

IN

TREATMENT

OUTCOME

RESEARCH

FOR

Principal Investigator & Institution: Boggs, Stephen; University of Florida Gainesville, Fl 32611

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Timing: Fiscal Year 2003; Project Start 01-MAY-1999; Project End 30-APR-2008 Summary: (provided by applicant): This is a revision of a competing renewal for T32 HD07524 titled, "Training in Treatment Outcome Research for Children." This competitive application represents an extension of the prior postdoctoral training program to include predoctoral training, and shifts the focus of the training grant to treatment outcome research with children. This training program has been designed to address three critical issues in the field of clinical psychology: 1) the need to develop and evaluate psychological interventions for children that have empirical support, 2) the shortage of clinical researchers emerging from doctoral and postdoctoral training programs who are prepared to advance the science of psychology, and 3) the need to include children and adolescents in medical and psychological research. Funds are requested to train five predoctoral research fellows (for 3 years each) and four postdoctoral fellows (for two years each). Key features of the proposed training program include: 1) a skills-based approach to providing research training that includes a specialized curriculum (grant writing, program evaluation, advanced statistics), 2) mentorship by core training faculty who all have current, funded treatment outcome research, 3) a longstanding history of multidisciplinary research with physicians, biostatisticians, and health economists, and 4) opportunities to conduct research with diverse child populations. Seven Core Training Faculty, all of whom have current, external funding for treatment outcome research with children and adolescents will be the primary research mentors. Their treatment outcome research is being conducted with diverse populations, including children with chronic conditions, such as cystic fibrosis, diabetes, and epilepsy, children with attention-deficit disorder, children recovering from traumatic brain injuries, children with conduct-disorders, and children exposed prenatally to drugs, such as cocaine. Seventeen Affiliate Faculty, from the Schools of Medicine, Pharmacy, Dentistry, and Education will also participate in this training program. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VASC MECHS OF SECONDARY INSULTS IN SEVERE BRAIN INJURY Principal Investigator & Institution: Robertson, Claudia S.; Professor; Neurology; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 26-JUL-1999; Project End 30-JUN-2004 Summary: The overall hypothesis of this proposal is that traumatic brain injury (TBI) causes a reduction in CBF in the early post-injury period that contributes to the brain damage by 2-mechanisms: 1-if the reduction in CBF is severe enough and lasts long enough, ischemic injury (primary ischemia; occurs 2- if the reduction is CBF is more modest, ischemic injury may not occur, but the brain is more susceptible to secondary insults (secondary ischemia). Global reductions in CBF severe enough to result in ischemic injury (CBF,18 ml/100g/min) occur with very severe injuries and this finding is associated with a high mortality rate. Regional reductions in CBF severe enough to result in ischemic injury (rCBF<18 ml/100g/min) occur more commonly and are typically found in areas of brain contusion and underlying evacuated extracerebral hematomas. Even more commonly, a moderate reduction in CBF which is compensated by increased cerebral oxygen extraction occurs during the first few hours after TBI. This program projects will approach the problem of vascular changes after traumatic brain injury with both clinical and laboratory studies. There are 3 projects and 3 cores in the program project. Project 1. Regulation of Cerebral Blood Flow after Traumatic Brain Injury. Project 2. Increased Vascular Resistance after Traumatic Brain Injury. Project 3.

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L-arginine Treatment of a Reduced CBF after Traumatic Brain Injury. Core A. Administrative Core Core B. Statistical and Modeling Core Core C. Analytical Lab Core Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VISUAL PATTERN MEMORY: NEURAL BASIS IN HUMANS Principal Investigator & Institution: Muller, James R.; Psychology; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 26-MAR-2003; Project End 30-SEP-2005 Summary: (provided by applicant): The broad goal of this proposal is to understand how certain aspects of working memory performance depend on neural activity in specific areas of the human brain, measured with functional magnetic resonance imaging (fMRI). There are three specific aims: to relate behavior to neural activity, to make topographic maps of the brain regions, and to determine whether striate cortex (V1) is active at any stage during a working memory task. Working memory activity has been reported throughout the brain. The first specific aim is to identify the parietal, temporal, and prefrontal areas that exhibit activity during a threshold-difficulty working memory task; test the hypothesis that working memory activity is greater when observers perform well; and test the hypothesis that intervening stimuli (task-relevant or otherwise), when presented during a working memory delay, alter working memory in the parietal lobe while leaving prefrontal working memory unchanged. The second specific aim is to test the hypothesis that complex patterns made of random elements have to be remembered in an image-like representation, and thus are topographically organized. We will test separately for retinotopic and head-centered organizations. The third specific aim is to explore the discrepancy between imagery tasks that have been reported to evoke fMRI activity in V1 and similar working memory tasks that have not. We will test the hypotheses that this can be explained by differences in the stimuli, the tasks, or the time during the task when brain activity is measured. The proposed work, by allowing us to understand working memory in normals, is meant ultimately to contribute to better characterization of cognitive deficits due to acquired brain injuries. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “brain injuries” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for brain injuries in the PubMed Central database:

3 4

Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.

With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.

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A population-based study of potential brain injuries requiring emergency care. by Pickett W, Ardern C, Brison RJ.; 2001 Aug 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=81328

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Advancing toward a modern death: the path from severe brain injury to neurological determination of death. by Shemie SD, Doig C, Belitsky P.; 2003 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=152683

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Calpain Inhibitor AK295 Attenuates Motor and Cognitive Deficits Following Experimental Brain Injury in the Rat. by Saatman KE, Murai H, Bartus RT, Smith DH, Hayward NJ, Perri BR, McIntosh TK.; 1996 Apr 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39625

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Catecholamine-induced interleukin-10 release: a key mechanism in systemic immunodepression after brain injury. by Woiciechowsky C, Schoning B, Lanksch WR, Volk HD, Docke WD.; 1999; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=137244

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Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury. by Scherbel U, Raghupathi R, Nakamura M, Saatman KE, Trojanowski JQ, Neugebauer E, Marino MW, McIntosh TK.; 1999 Jul 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17583

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Enhanced Expression of the Developmentally Regulated Extracellular Matrix Molecule Tenascin Following Adult Brain Injury. by Laywell ED, Dorries U, Bartsch U, Faissner A, Schachner M, Steindler DA.; 1992 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48716

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Erythropoietin crosses the blood --brain barrier to protect against experimental brain injury. by Brines ML, Ghezzi P, Keenan S, Agnello D, de Lanerolle NC, Cerami C, Itri LM, Cerami A.; 2000 Sep 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27058

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Estrogen receptor [alpha], not [beta], is a critical link in estradiol-mediated protection against brain injury. by Dubal DB, Zhu H, Yu J, Rau SW, Shughrue PJ, Merchenthaler I, Kindy MS, Wise PM.; 2001 Feb 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=29363

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FGF-2 regulates neurogenesis and degeneration in the dentate gyrus after traumatic brain injury in mice. by Yoshimura S, Teramoto T, Whalen MJ, Irizarry MC, Takagi Y, Qiu J, Harada J, Waeber C, Breakefield XO, Moskowitz MA.; 2003 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=213483

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FGF-2 regulation of neurogenesis in adult hippocampus after brain injury. by Yoshimura S, Takagi Y, Harada J, Teramoto T, Thomas SS, Waeber C, Bakowska JC, Breakefield XO, Moskowitz MA.; 2001 May 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33306

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Functional Magnetic Resonance Studies of the Reorganization of the Human Hand Sensorimotor Area After Unilateral Brain Injury in the Perinatal Period. by Cao Y, Vikingstad EM, Huttenlocher PR, Towle VL, Levin DN.; 1994 Sep 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=44863

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Impairments in verb morphology after brain injury: A connectionist model. by Joanisse MF, Seidenberg MS.; 1999 Jun 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22131

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Traumatic brain injury information database: a user survey. by Peters AV.; 1994 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=225887

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Virulence Factors of Escherichia coli Isolates From Patients with Symptomatic and Asymptomatic Bacteriuria and Neuropathic Bladders Due to Spinal Cord and Brain Injuries. by Hull RA, Rudy DC, Wieser IE, Donovan WH.; 1998 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124819

The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with brain injuries, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “brain injuries” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for brain injuries (hyperlinks lead to article summaries): •

“Loss of self” in the narratives of people with traumatic brain injuries: a qualitative analysis. Author(s): Nochi M. Source: Social Science & Medicine (1982). 1998 April; 46(7): 869-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9541072&dopt=Abstract

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“Silent” brain injuries and their complications. Author(s): Arnold LC. Source: Med Trial Tech Q. 1978; 25(2): 149-60. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=732545&dopt=Abstract

6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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A decision rule for identifying children at low risk for brain injuries after blunt head trauma. Author(s): Palchak MJ, Holmes JF, Vance CW, Gelber RE, Schauer BA, Harrison MJ, Willis-Shore J, Wootton-Gorges SL, Derlet RW, Kuppermann N. Source: Annals of Emergency Medicine. 2003 October; 42(4): 492-506. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520320&dopt=Abstract

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A population-based study of potential brain injuries requiring emergency care. Author(s): Pickett W, Ardern C, Brison RJ. Source: Cmaj : Canadian Medical Association Journal = Journal De L'association Medicale Canadienne. 2001 August 7; 165(3): 288-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11517644&dopt=Abstract

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A population-based study of seizures after traumatic brain injuries. Author(s): Annegers JF, Hauser WA, Coan SP, Rocca WA. Source: The New England Journal of Medicine. 1998 January 1; 338(1): 20-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9414327&dopt=Abstract

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A review of the scientific evidence on the treatment of traumatic brain injuries and strokes with hyperbaric oxygen. Author(s): Alternative Therapy Evaluation Committee for the Insurance Corporation of British Columbia. Source: Brain Injury : [bi]. 2003 March; 17(3): 225-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623499&dopt=Abstract

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A supported relationships intervention to increase the social integration of persons with traumatic brain injuries. Author(s): Johnson K, Davis PK. Source: Behavior Modification. 1998 October; 22(4): 502-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9755649&dopt=Abstract

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A transitional living environment for persons with brain injuries: staff and client perceptions. Author(s): Minnes P, Harrick L, Carlson P, Johnston J. Source: Brain Injury : [bi]. 1998 November; 12(11): 987-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9839031&dopt=Abstract

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Acquired brain injuries--demanding nursing excellence. Author(s): Costello M, Pedersen C, Tan M, Devaux R, Tan S, Dixon P, Lee L, Cahuya E. Source: Australian Nursing Journal (July 1993). 1997 August; 5(2): 24-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9325708&dopt=Abstract

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Acute care management of severe traumatic brain injuries. Author(s): Yanko JR, Mitcho K. Source: Critical Care Nursing Quarterly. 2001 February; 23(4): 1-23; Quiz 2 P Following 66. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11852947&dopt=Abstract

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Acute psychosocial impact of pediatric orthopedic trauma with and without accompanying brain injuries. Author(s): Stancin T, Taylor HG, Thompson GH, Wade S, Drotar D, Yeates KO. Source: The Journal of Trauma. 1998 December; 45(6): 1031-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9867044&dopt=Abstract

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Aerobic and neuromuscular training: effect on the capacity, efficiency, and fatigability of patients with traumatic brain injuries. Author(s): Jankowski LW, Sullivan SJ. Source: Archives of Physical Medicine and Rehabilitation. 1990 June; 71(7): 500-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2350220&dopt=Abstract

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After hospital: working with schools and families to support the long term needs of children with brain injuries. Author(s): Savage RC, Pearson S, McDonald H, Potoczny-Gray A, Marchese N. Source: Neurorehabilitation. 2001; 16(1): 49-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11455103&dopt=Abstract

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Alterations of cerebral metabolism in cases with acute brain injuries during spontaneous respiration of air, oxygen and hyperbaric oxygen. Author(s): Holbach KH, Schroder FK, Koster S. Source: European Neurology. 1972; 8(1): 158-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5052137&dopt=Abstract

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Ambulatory care for traumatic brain injuries in the US, 1995-1997. Author(s): Schootman M, Fuortes LJ. Source: Brain Injury : [bi]. 2000 April; 14(4): 373-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10815845&dopt=Abstract

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Analysis of 127 war inflicted missile brain injuries sustained in north-eastern Croatia. Author(s): Vrankovic D, Splavski B, Hecimovic I, Glavina K, Dmitrovic B, Mursic B. Source: Journal of Neurosurgical Sciences. 1996 June; 40(2): 107-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9049892&dopt=Abstract

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Anxiety disorders associated with traumatic brain injuries. Author(s): Hiott DW, Labbate L. Source: Neurorehabilitation. 2002; 17(4): 345-55. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12547982&dopt=Abstract

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Anxiety in patients with brain injuries--rooming-in with close relatives as a therapeutic approach. Author(s): Werner GT, Gadomski M. Source: International Journal of Rehabilitation Research. Internationale Zeitschrift Fur Rehabilitationsforschung. Revue Internationale De Recherches De Readaptation. 1987; 10(4 Suppl 5): 232-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3503849&dopt=Abstract

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Are brain injuries a significant problem in soccer? Author(s): Green GA, Jordan SE. Source: Clinics in Sports Medicine. 1998 October; 17(4): 795-809, Viii. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9922903&dopt=Abstract

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Behavioural differences between psychiatric patients with confirmed versus nonconfirmed traumatic brain injuries. Author(s): Holtzer R, Burright RG, Lynn SJ, Donovick PJ. Source: Brain Injury : [bi]. 2000 November; 14(11): 959-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11104136&dopt=Abstract

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Brain injuries among infants, children, adolescents, and young adults. Author(s): Kraus JF, Rock A, Hemyari P. Source: Am J Dis Child. 1990 June; 144(6): 684-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2346150&dopt=Abstract

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Brain injuries in athletics. Assessment and management to prevent a catastrophic outcome. Author(s): Scholl DJ. Source: Jaapa. 1999 December; 12(12): 40-2, 45-6, 49-52 Passim. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11010082&dopt=Abstract

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Brain injuries in early foetal life: consequences for brain development. Author(s): Mancini J, Lethel V, Hugonenq C, Chabrol B. Source: Developmental Medicine and Child Neurology. 2001 January; 43(1): 52-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11201424&dopt=Abstract

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Brain injuries in polytrauma. Author(s): Bakay L. Source: World Journal of Surgery. 1983 January; 7(1): 42-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6837065&dopt=Abstract

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Brain injuries in sports: guidelines for managing concussions. Author(s): Weiner HR. Source: Compr Ther. 2001 Winter; 27(4): 330-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11765691&dopt=Abstract

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Brain injuries--causes of death, and life expectancy. Author(s): Sekulovic N, Ceramilac A. Source: Acta Neurochir Suppl (Wien). 1979; 28(1): 203-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=290150&dopt=Abstract

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Can modern therapy influence the prognosis of brain injuries in childhood? Author(s): Kloti J. Source: Z Kinderchir. 1985 June; 40(3): 131-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4036363&dopt=Abstract

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Caring for patients with brain injuries.and neuropsychiatrists. Author(s): Bird JM. Source: Bmj (Clinical Research Ed.). 1993 July 3; 307(6895): 58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8343677&dopt=Abstract

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Caring for patients with brain injuries. The role of rehabilitation specialists. Author(s): McLellan DL. Source: Bmj (Clinical Research Ed.). 1993 July 3; 307(6895): 58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8343678&dopt=Abstract

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Caring for patients with brain injuries. Towards a better service. Author(s): Rose MJ. Source: Bmj (Clinical Research Ed.). 1993 July 3; 307(6895): 58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8343679&dopt=Abstract

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Catecholamine functioning in children with traumatic brain injuries and children with attention-deficit/hyperactivity disorder. Author(s): Konrad K, Gauggel S, Schurek J. Source: Brain Research. Cognitive Brain Research. 2003 May; 16(3): 425-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706222&dopt=Abstract

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Cisternal and lumbar acid-base balance in patients with acute brain injuries: its association with respiratory alkalosis. Author(s): Posner JB, Plum F, Shapiro WR. Source: Scand J Clin Lab Invest Suppl. 1968; 102: Ix: B. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5714656&dopt=Abstract

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Clinical and pathological studies of brain injuries in horse-riding accidents: a description of cases and review with a warning to the unhelmeted. Author(s): Ilgren EB, Teddy PJ, Vafadis J, Briggs M, Gardiner NG. Source: Clin Neuropathol. 1984 November-December; 3(6): 253-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6518686&dopt=Abstract

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Clinical application of tentorium cerebelli hiatus incision in treatment of severe and most severe brain injuries. Author(s): Cai X, Wang Y, Chen Z, Hu K, Fang W, Shi Z, Liu B, Dong J. Source: Chinese Journal of Traumatology = Chung-Hua Ch'uang Shang Tsa Chih / Chinese Medical Association. 2001 May; 4(2): 82-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11834150&dopt=Abstract

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Cognitive screening in mild traumatic brain injuries: analysis of the neurobehavioral cognitive status examination when utilized during initial trauma hospitalization. Author(s): Blostein PA, Jones SJ, Buechler CM, Vandongen S. Source: Journal of Neurotrauma. 1997 March; 14(3): 171-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9104934&dopt=Abstract

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Cold caloric test for prognosis of brain injuries. Author(s): Tarkkanen J, Troupp H. Source: The Laryngoscope. 1971 November; 81(11): 1741. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5117716&dopt=Abstract

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Comments on nonoperative treatment of severe brain injuries. Importance of controlled ventilation and hyperventilation. Author(s): Gordon E. Source: Acta Neurochir Suppl (Wien). 1986; 36: 146. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3467547&dopt=Abstract

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Comparison of remedial and compensatory interventions for adults with acquired brain injuries. Author(s): Dirette DK, Hinojosa J, Carnevale GJ. Source: The Journal of Head Trauma Rehabilitation. 1999 December; 14(6): 595-601. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10671705&dopt=Abstract

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Concurrent validity of the Functional Independence Measure for Children (WeeFIM) and the Pediatric Evaluation of Disabilities Inventory in children with developmental disabilities and acquired brain injuries. Author(s): Ziviani J, Ottenbacher KJ, Shephard K, Foreman S, Astbury W, Ireland P. Source: Physical & Occupational Therapy in Pediatrics. 2001; 21(2-3): 91-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12029858&dopt=Abstract

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Constraint-induced movement therapy for hemiplegic children with acquired brain injuries. Author(s): Karman N, Maryles J, Baker RW, Simpser E, Berger-Gross P. Source: The Journal of Head Trauma Rehabilitation. 2003 May-June; 18(3): 259-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802168&dopt=Abstract

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Continuous monitoring of cerebral substrate delivery and clearance: initial experience in 24 patients with severe acute brain injuries. Author(s): Zauner A, Doppenberg EM, Woodward JJ, Choi SC, Young HF, Bullock R. Source: Neurosurgery. 1997 November; 41(5): 1082-91; Discussion 1091-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9361062&dopt=Abstract

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Controlled respiration in the management of patients with traumatic brain injuries. Author(s): Gordon E. Source: Acta Anaesthesiologica Scandinavica. 1971; 15(3): 193-208. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5120955&dopt=Abstract

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Coping and stress in Canadian family caregivers of persons with traumatic brain injuries. Author(s): Minnes P, Graffi S, Nolte ML, Carlson P, Harrick L. Source: Brain Injury : [bi]. 2000 August; 14(8): 737-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10969892&dopt=Abstract

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Correlations between brain injuries and mechanical response of the head at impact. Author(s): Lindgren SO, Rinder L, Stalhammar D, Asberg A. Source: Injury. 1973 August; 5(1): 31-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4742523&dopt=Abstract

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Courageous kids: children with traumatic brain injuries. Author(s): O'Sullivan C. Source: Nurs Spectr (Wash D C). 1996 December 16; 6(26): 6-7, 12. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9433321&dopt=Abstract

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Craniofacial fractures and brain injuries. Author(s): Bracard S, Marchal JC, Auque J, Picard L, Stricker M, Lepoire J. Source: Journal of Neuroradiology. Journal De Neuroradiologie. 1986; 13(4): 265-77. English, French. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3585488&dopt=Abstract

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Defining community integration of persons with brain injuries as acculturation: a Canadian perspective. Author(s): Minnes P, Buell K, Nolte ML, McColl MA, Carlson P, Johnston J. Source: Neurorehabilitation. 2001; 16(1): 3-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11455098&dopt=Abstract

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Detection and treatment of cerebral hypoxia key to avoiding intraoperative brain injuries. Author(s): Edmonds HL Jr. Source: Journal of Clinical Monitoring and Computing. 2000 January; 16(1): 69-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12578096&dopt=Abstract

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Detection of an intense resonance at 2.4 ppm in 1H MR spectra of patients with severe late-delayed, radiation-induced brain injuries. Author(s): Yeung DK, Chan Y, Leung S, Poon PM, Pang C. Source: Magnetic Resonance in Medicine : Official Journal of the Society of Magnetic Resonance in Medicine / Society of Magnetic Resonance in Medicine. 2001 June; 45(6): 994-1000. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11378876&dopt=Abstract

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Developing a suicide prevention strategy based on the perspectives of people with brain injuries. Author(s): Kuipers P, Lancaster A. Source: The Journal of Head Trauma Rehabilitation. 2000 December; 15(6): 1275-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11056408&dopt=Abstract

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Developing brain injuries: a new pediatric focus. Author(s): Hung KL. Source: Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1996 November-December; 37(6): 399-400. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9074273&dopt=Abstract

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Developing prosthetics to treat cognitive disabilities resulting from acquired brain injuries. Author(s): Schiff ND, Plum F, Rezai AR. Source: Neurological Research. 2002 March; 24(2): 116-24. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11877893&dopt=Abstract

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Development of epilepsy in children with perinatal brain injuries: relationship to other neuropsychiatric deficits and EEG features. Author(s): Otani K, Tagawa T, Futagi Y. Source: Jpn J Psychiatry Neurol. 1992 June; 46(2): 417-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1434171&dopt=Abstract

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Diagnosis, physiology, pathology and rehabilitation of traumatic brain injuries. Author(s): Berker E. Source: The International Journal of Neuroscience. 1996 April; 85(3-4): 195-220. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8734559&dopt=Abstract

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Early clinical signs and prognosis in children with brain injuries. Author(s): Vapalahti M, Luukkonen M, Puranen M, Hernesniemi J, Tapaninaho A. Source: Ann Clin Res. 1986; 18 Suppl 47: 37-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3101575&dopt=Abstract

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Early ischaemia after severe head injury. Preliminary results in patients with diffuse brain injuries. Author(s): Sahuquillo J, Poca MA, Garnacho A, Robles A, Coello F, Godet C, Triginer C, Rubio E. Source: Acta Neurochirurgica. 1993; 122(3-4): 204-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8372709&dopt=Abstract

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Early monitoring of P(ti)O(2), P(ti)CO(2), pH and brain temperature in patients with brain injuries and the clinical significance. Author(s): Li W, Cai X, Wang J, Chen G, Chai Z. Source: Chinese Journal of Traumatology = Chung-Hua Ch'uang Shang Tsa Chih / Chinese Medical Association. 2001 February; 4(1): 20-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11835703&dopt=Abstract

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Effect of hyperventilation associated with administration of central nervous depressants in brain injuries. Author(s): Escuret E, Roquefeuil B, Frerebeau P, Baldy-Moulinier M. Source: Acta Neurologica Scandinavica. Supplementum. 1977; 64: 154-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=268767&dopt=Abstract

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Effect of Italy's motorcycle helmet law on traumatic brain injuries. Author(s): Servadei F, Begliomini C, Gardini E, Giustini M, Taggi F, Kraus J. Source: Injury Prevention : Journal of the International Society for Child and Adolescent Injury Prevention. 2003 September; 9(3): 257-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966016&dopt=Abstract

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Effects of changes in Pa CO2 on rCBF, cerebral oxygenation and EEG in severe brain injuries. Author(s): Rossanda M, Boselli L, Casteli A, Corona C, Erminio F, Nardini M, Porta M, Villa C. Source: European Neurology. 1972; 8(1): 169-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5052140&dopt=Abstract

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Efficiency of the Glasgow Outcome Scale (GOS)-Score for the long-term follow-up after severe brain injuries. Author(s): Woischneck D, Firsching R. Source: Acta Neurochir Suppl (Wien). 1998; 71: 138-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9779167&dopt=Abstract

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Electron microscopic analysis of cortical biopsies in patients with traumatic brain injuries and dysfunction of neurobehavioural system. Author(s): Castejon OJ. Source: J Submicrosc Cytol Pathol. 1998 January; 30(1): 145-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9530862&dopt=Abstract

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Elevated initial blood glucose levels and poor outcome following severe brain injuries in children. Author(s): Michaud LJ, Rivara FP, Longstreth WT Jr, Grady MS. Source: The Journal of Trauma. 1991 October; 31(10): 1356-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1942143&dopt=Abstract

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Environment effect of functional task performance in adults with acquired brain injuries: use of the assessment of motor and process skills. Author(s): Darragh AR, Sample PL, Fisher AG. Source: Archives of Physical Medicine and Rehabilitation. 1998 April; 79(4): 418-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9552108&dopt=Abstract

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Epidemiology of severe brain injuries: a prospective population-based study. Author(s): Masson F, Thicoipe M, Aye P, Mokni T, Senjean P, Schmitt V, Dessalles PH, Cazaugade M, Labadens P; Aquitaine Group for Severe Brain Injuries Study. Source: The Journal of Trauma. 2001 September; 51(3): 481-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11535895&dopt=Abstract

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Epidemiology of traumatic brain injuries: Indian scenario. Author(s): Gururaj G. Source: Neurological Research. 2002 January; 24(1): 24-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11783750&dopt=Abstract

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Estrogen and progesterone as neuroprotective agents in the treatment of acute brain injuries. Author(s): Stein DG, Hoffman SW. Source: Pediatric Rehabilitation. 2003 January-March; 6(1): 13-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745891&dopt=Abstract

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Excessive daytime sleepiness in adults with brain injuries. Author(s): Masel BE, Scheibel RS, Kimbark T, Kuna ST. Source: Archives of Physical Medicine and Rehabilitation. 2001 November; 82(11): 152632. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11689971&dopt=Abstract

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Explaining quality of life for persons with traumatic brain injuries 2 years after injury. Author(s): Webb CR, Wrigley M, Yoels W, Fine PR. Source: Archives of Physical Medicine and Rehabilitation. 1995 December; 76(12): 11139. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8540786&dopt=Abstract

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Expression of the plasminogen activator system and the inhibitors PAI-1 and PAI-2 in posttraumatic lesions of the CNS and brain injuries following dramatic circulatory arrests: an immunohistochemical study. Author(s): Dietzmann K, von Bossanyi P, Krause D, Wittig H, Mawrin C, Kirches E. Source: Pathology, Research and Practice. 2000; 196(1): 15-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10674268&dopt=Abstract

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Football brain injuries draw increased scrutiny. Author(s): Vastag B. Source: Jama : the Journal of the American Medical Association. 2002 January 23-30; 287(4): 437-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11798345&dopt=Abstract

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Forensic-neuropathological aspects of brain injuries in child abuse. Author(s): Bratzke H. Source: Neuropathology and Applied Neurobiology. 1996 December; 22(6): 513-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9004239&dopt=Abstract

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Functional status following traumatic brain injuries: population-based rural-urban differences. Author(s): Schootman M, Fuortes L. Source: Brain Injury : [bi]. 1999 December; 13(12): 995-1004. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10628504&dopt=Abstract

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How safe are childcare products, toys and playground equipment? A Swedish analysis of mild brain injuries at home and during leisure time 1998-1999. Author(s): Emanuelson I. Source: Injury Control and Safety Promotion. 2003 September; 10(3): 139-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861912&dopt=Abstract

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Humans with traumatic brain injuries show place-learning deficits in computergenerated virtual space. Author(s): Skelton RW, Bukach CM, Laurance HE, Thomas KG, Jacobs JW. Source: J Clin Exp Neuropsychol. 2000 April; 22(2): 157-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10779831&dopt=Abstract

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Impairment of short-term memory in left hemispheric traumatic brain injuries. Author(s): Maeshima S, Uematsu Y, Ozaki F, Fujita K, Nakai K, Itakura T, Komai N. Source: Brain Injury : [bi]. 1997 April; 11(4): 279-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9134202&dopt=Abstract

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Incidence, external causes, and outcomes of work-related brain injuries in males. Author(s): Kraus JF, Fife D. Source: J Occup Med. 1985 October; 27(10): 757-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4067679&dopt=Abstract

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Incidence, severity, and outcomes of brain injuries involving bicycles. Author(s): Kraus JF, Fife D, Conroy C. Source: American Journal of Public Health. 1987 January; 77(1): 76-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3789243&dopt=Abstract

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Interaction between systemic circulation and brain injuries in newborns. Author(s): Bauer R, Zwiener U, Buchenau W, Bergmann R, Beyer R, Beyer GJ, Hoyer D, Lampe V. Source: Exp Pathol. 1991; 42(4): 197-203. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1959579&dopt=Abstract

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International symposium on cerebral blood flow regulation, acid-base and energy metabolism in acute brain injuries. Author(s): Severinghaus JW. Source: Anesthesiology. 1972 April; 36(4): 414-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5020653&dopt=Abstract

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Intracranial haemodynamics in diffuse and focal brain injuries. Evaluation with transcranial Doppler (TCD) ultrasound. Author(s): Shigemori M, Moriyama T, Harada K, Kikuchi N, Tokutomi T, Kuramoto S. Source: Acta Neurochirurgica. 1990; 107(1-2): 5-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2096609&dopt=Abstract

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Intraindividual variability in physical and emotional functioning: comparison of adults with traumatic brain injuries and healthy adults. Author(s): Burton CL, Hultsch DF, Strauss E, Hunter MA. Source: Clin Neuropsychol. 2002 August; 16(3): 264-79. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12607140&dopt=Abstract

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Intramuscular midazolam for treatment of acute seizures or behavioral episodes in patients with brain injuries. Author(s): Wroblewski BA, Joseph AB. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1992 April; 55(4): 328-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1583523&dopt=Abstract

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Intrathecal and serum interleukin-6 and the acute-phase response in patients with severe traumatic brain injuries. Author(s): Kossmann T, Hans VH, Imhof HG, Stocker R, Grob P, Trentz O, MorgantiKossmann C. Source: Shock (Augusta, Ga.). 1995 November; 4(5): 311-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8595516&dopt=Abstract

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Intravenous sodium lactate administration in respiratory alkalosis secondary to severe brain injuries. Author(s): Bondoli A, Scrascia E, Magalini SI, Barbi S, Rocchi C, Cavaliere F. Source: Resuscitation. 1978; 6(4): 279-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=755270&dopt=Abstract

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Intraventricular pressure in patients with severe brain injuries. II. Author(s): Troupp H. Source: The Journal of Trauma. 1967 November; 7(6): 875-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6053794&dopt=Abstract

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Lack of correlation between ventricular fluid pressure and arterial blood pressure in severe brain injuries. Author(s): Troupp H, Kuurne T, Valtonen S. Source: Acta Neurochirurgica. 1973; 28(3): 193-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4746540&dopt=Abstract

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Late improvements in mobility after acquired brain injuries in children. Author(s): Vander Schaaf PJ, Kriel RL, Krach LE, Luxenberg MG. Source: Pediatric Neurology. 1997 May; 16(4): 306-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9258963&dopt=Abstract

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Letter: Brain injuries. Author(s): Feindel W. Source: Surgical Neurology. 1975 May; 3(5): 269. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1154250&dopt=Abstract

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Long-term executive function deficits in children with traumatic brain injuries: assessment using the Behavior Rating Inventory of Executive Function (BRIEF). Author(s): Mangeot S, Armstrong K, Colvin AN, Yeates KO, Taylor HG. Source: Neuropsychology, Development, and Cognition. Section C, Child Neuropsychology : a Journal on Normal and Abnormal Development in Childhood and Adolescence. 2002 December; 8(4): 271-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759824&dopt=Abstract

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Long-term multi-dimensional outcome following isolated traumatic brain injuries and traumatic brain injuries associated with multiple trauma. Author(s): Moore AD, Stambrook M, Peters LC, Cardoso ER, Kassum DA. Source: Brain Injury : [bi]. 1990 October-December; 4(4): 379-89. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2252970&dopt=Abstract

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Microembolic brain injuries from cardiac surgery: are they seeds of future Alzheimer's disease? Author(s): Brown WR, Moody DM, Tytell M, Ghazi-Birry HS, Challa VR. Source: Annals of the New York Academy of Sciences. 1997 September 26; 826: 386-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9329709&dopt=Abstract

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Mild traumatic brain injuries in low-risk trauma patients. Author(s): Chambers J, Cohen SS, Hemminger L, Prall JA, Nichols JS. Source: The Journal of Trauma. 1996 December; 41(6): 976-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8970549&dopt=Abstract

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Mothering children who survive brain injuries: playing the hand you're dealt. Author(s): Guerriere D, McKeever P. Source: Journal of the Society of Pediatric Nurses : Jspn. 1997 July-September; 2(3): 10515. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9292853&dopt=Abstract

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Movement disorders after status epilepticus and other brain injuries. Author(s): Fowler WE, Kriel RL, Krach LE. Source: Pediatric Neurology. 1992 July-August; 8(4): 281-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1388417&dopt=Abstract

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Neurological deterioration as a potential alternative endpoint in human clinical trials of experimental pharmacological agents for treatment of severe traumatic brain injuries. Executive Committee of the International Selfotel Trial. Author(s): Morris GF, Juul N, Marshall SB, Benedict B, Marshall LF. Source: Neurosurgery. 1998 December; 43(6): 1369-72; Discussion 1372-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9848851&dopt=Abstract

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Neuropsychological results versus prognosis factors--64 patients with diffuse brain injuries. Author(s): Sichez-Auclair N, Sichez JP. Source: Neurosurgical Review. 1989; 12 Suppl 1: 474-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2812419&dopt=Abstract

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North Star Project: reality orientation in an acute care setting for patients with traumatic brain injuries. Author(s): Thomas H, Feyz M, LeBlanc J, Brosseau J, Champoux MC, Christopher A, Desormeaux N, Dorais L, Lin H. Source: The Journal of Head Trauma Rehabilitation. 2003 May-June; 18(3): 292-302. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802171&dopt=Abstract

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Ossifications and fracture-healing in paraplegia and brain injuries. Author(s): Benassy J. Source: Proc Annu Clin Spinal Cord Inj Conf. 1966 November 7; 15: 55-60. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4993940&dopt=Abstract

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Ossifications and fracture-healing in paraplegia and brain injuries. Author(s): Benassy J. Source: Proc Annu Clin Spinal Cord Inj Conf. 1966; 15: 55-60. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4975471&dopt=Abstract

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Outcome of traumatic brain injuries in 1,508 patients: impact of prehospital care. Author(s): Rudehill A, Bellander BM, Weitzberg E, Bredbacka S, Backheden M, Gordon E. Source: Journal of Neurotrauma. 2002 July; 19(7): 855-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12184855&dopt=Abstract

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Parkinson's disease and exposure to infectious agents and pesticides and the occurrence of brain injuries: role of neuroinflammation. Author(s): Liu B, Gao HM, Hong JS. Source: Environmental Health Perspectives. 2003 June; 111(8): 1065-73. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826478&dopt=Abstract

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Participation readiness at discharge from inpatient rehabilitation in children and adolescents with acquired brain injuries. Author(s): Bedell GM, Haley SM, Coster WJ, Smith KW. Source: Pediatric Rehabilitation. 2002 April-June; 5(2): 107-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490054&dopt=Abstract

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Patients with brain injuries. Author(s): Sumners D, Lewin J. Source: Bmj (Clinical Research Ed.). 1993 May 8; 306(6887): 1220-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8499847&dopt=Abstract

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Pediatric brain injuries: the nature, clinical course, and early outcomes in a defined United States' population. Author(s): Kraus JF, Fife D, Conroy C. Source: Pediatrics. 1987 April; 79(4): 501-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3822667&dopt=Abstract

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Performance of healthy adults versus individuals with brain injuries on the supplemental measures of the WAIS-R NI. Author(s): Mercer WN, Harrell EH, Miller DC, Childs HW, Rockers DM, Deldotto JE. Source: Brain Injury : [bi]. 1998 September; 12(9): 753-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9755366&dopt=Abstract

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Persons with traumatic brain injuries and their families: living arrangements and well-being post injury. Author(s): Brzuzy S, Speziale BA. Source: Social Work in Health Care. 1997; 26(1): 77-88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9406340&dopt=Abstract

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Post-traumatic and postoperative treatment of severe brain injuries with controlled hyperventilation. Author(s): Gordon E. Source: Acta Anaesthesiol Belg. 1976; 27 Suppl: 291-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1015232&dopt=Abstract

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Preinjury family environment as a determinant of recovery from traumatic brain injuries in school-age children. Author(s): Yeates KO, Taylor HG, Drotar D, Wade SL, Klein S, Stancin T, Schatschneider C. Source: Journal of the International Neuropsychological Society : Jins. 1997 November; 3(6): 617-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9448375&dopt=Abstract

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Prevalence and correlates of depressive symptoms following traumatic brain injuries in children. Author(s): Kirkwood M, Janusz J, Yeates KO, Taylor HG, Wade SL, Stancin T, Drotar D. Source: Neuropsychology, Development, and Cognition. Section C, Child Neuropsychology : a Journal on Normal and Abnormal Development in Childhood and Adolescence. 2000 September; 6(3): 195-208. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11402397&dopt=Abstract

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Preventing secondary brain injuries. Author(s): Cunning S, Houdek DL. Source: Dimensions of Critical Care Nursing : Dccn. 1999 September-October; 18(5): 202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10640037&dopt=Abstract

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Prognosis for patients with severe brain injuries. Author(s): Vapalahti M, Troupp H. Source: British Medical Journal. 1971 August 14; 3(771): 404-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5571262&dopt=Abstract

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Prognostic factors in children with severe diffuse brain injuries: a study of 74 patients. Author(s): Pillai S, Praharaj SS, Mohanty A, Kolluri VR. Source: Pediatric Neurosurgery. 2001 February; 34(2): 98-103. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11287810&dopt=Abstract

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Prognostic problems in patients with severe brain injuries. Author(s): af Bjorkesten G. Source: Ann Chir Gynaecol Fenn. 1971; 60(1): 3-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5549689&dopt=Abstract

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Prolonged hyperventilation in treatment of unconscious patients with severe brain injuries. Author(s): Rossanda M. Source: Scand J Clin Lab Invest Suppl. 1968; 102: Xiii: E. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5249717&dopt=Abstract

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Protective role of cerebrospinal fluid in brain injuries. Author(s): Hodgson DC, Shippen JM, Sunderland R. Source: Archives of Disease in Childhood. 2001 February; 84(2): 187. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11273570&dopt=Abstract

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Psychiatric disorders and functional disability in outpatients with traumatic brain injuries. Author(s): Fann JR, Katon WJ, Uomoto JM, Esselman PC. Source: The American Journal of Psychiatry. 1995 October; 152(10): 1493-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7573589&dopt=Abstract

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Psychopathology of children with minimal brain injuries. Author(s): Kucera O. Source: Psychiatr Neurol Med Psychol Beih. 1968; 8-9: 32-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5006384&dopt=Abstract

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Psychoses following war brain injuries. Author(s): Achte KA, Hillbom E, Aalberg V. Source: Acta Psychiatrica Scandinavica. 1969; 45(1): 1-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5345563&dopt=Abstract

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Regional cerebral blood flow and intraventricular pressure in acute brain injuries. Author(s): Fieschi C, Beduschi A, Agnoli A, Battistini N, Collice M, Prencipe M, Risso M. Source: European Neurology. 1972; 8(1): 192-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4340695&dopt=Abstract

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Relative effects of brain and non-brain injuries on neuropsychological and psychosocial outcome. Author(s): Dacey R, Dikmen S, Temkin N, McLean A, Armsden G, Winn HR. Source: The Journal of Trauma. 1991 February; 31(2): 217-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1994081&dopt=Abstract

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Remote memory in patients with acute brain injuries. Author(s): Leplow B, Dierks CH, Lehnung M, Kenkel S, Behrens C, Frank G, Mehdorn M. Source: Neuropsychologia. 1997 June; 35(6): 881-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9204492&dopt=Abstract

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Retrieval of long-term memory in patients with brain injuries. Author(s): Thone AI, Zysset SD, von Cramon DY. Source: J Clin Exp Neuropsychol. 1999 December; 21(6): 798-815. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10649535&dopt=Abstract

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Screening patients with traumatic brain injuries for substance abuse. Author(s): Fuller MG, Fishman E, Taylor CA, Wood RB. Source: The Journal of Neuropsychiatry and Clinical Neurosciences. 1994 Spring; 6(2): 143-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8044035&dopt=Abstract

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Seizures in the de-institutionalized patients with early brain injuries. Author(s): DeToledo JC. Source: Brain Injury : [bi]. 1998 August; 12(8): 715-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9724843&dopt=Abstract

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Self-administered written prompts to teach home accident prevention skills to adults with brain injuries. Author(s): O'Reilly MF, Green G, Braunling-McMorrow D. Source: J Appl Behav Anal. 1990 Winter; 23(4): 431-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2074235&dopt=Abstract

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Social and physical factors in the referral of people with traumatic brain injuries to rehabilitation. Author(s): Wrigley JM, Yoels WC, Webb CR, Fine PR. Source: Archives of Physical Medicine and Rehabilitation. 1994 February; 75(2): 149-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8311670&dopt=Abstract

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Social problem solving in children with acquired brain injuries. Author(s): Lewis JK, Morris MK, Morris RD, Krawiecki N, Foster MA. Source: The Journal of Head Trauma Rehabilitation. 2000 June; 15(3): 930-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10785623&dopt=Abstract

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Spinal fluid and blood serum enzyme activity in brain injuries. Author(s): Klun B. Source: Journal of Neurosurgery. 1974 August; 41(2): 224-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4841877&dopt=Abstract

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Statistical studies on the brain injuries, their occurrence, treatment, and prognosis. Author(s): Kondo S, Hamano K, Sakai A. Source: Bull Osaka Med Sch. 1966 April; 12(1): 48-58. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5960876&dopt=Abstract

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Struggling with the labeled self: people with traumatic brain injuries in social settings. Author(s): Nochi M. Source: Qualitative Health Research. 1998 September; 8(5): 665-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10621567&dopt=Abstract

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Subjective improvement following treatment with carbamazepine (Tegretol) for a subpopulation of patients with traumatic brain injuries. Author(s): Persinger MA. Source: Percept Mot Skills. 2000 February; 90(1): 37-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10769880&dopt=Abstract

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Surveillance of traumatic brain injuries in Utah. Author(s): Thurman DJ, Jeppson L, Burnett CL, Beaudoin DE, Rheinberger MM, Sniezek JE. Source: The Western Journal of Medicine. 1996 October; 165(4): 192-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8987423&dopt=Abstract

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Test/retest reliability and inter-rater agreement of the Quality of Upper Extremities Skills Test (QUEST) for older children with acquired brain injuries. Author(s): Sakzewski L, Ziviani J, Van Eldik N. Source: Physical & Occupational Therapy in Pediatrics. 2001; 21(2-3): 59-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12029854&dopt=Abstract

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TGF-beta is elevated in the CSF of patients with severe traumatic brain injuries and parallels blood-brain barrier function. Author(s): Morganti-Kossmann MC, Hans VH, Lenzlinger PM, Dubs R, Ludwig E, Trentz O, Kossmann T. Source: Journal of Neurotrauma. 1999 July; 16(7): 617-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10447073&dopt=Abstract

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The anatomical localization of brain injuries sustained in traffic accidents. Author(s): Dubrzy A, Raszeja S. Source: J Forensic Med. 1970 July-September; 17(3): 99-102. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5506296&dopt=Abstract

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The clinical picture of brain death after serious brain injuries. Author(s): Lucking CH, Gerstenbrand F. Source: Electroencephalography and Clinical Neurophysiology. 1971 March; 30(3): 272. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4103237&dopt=Abstract

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The costs of traumatic spinal cord and brain injuries in Wisconsin. Author(s): Chudy NE, Remington PL, Blustein JN. Source: Wis Med J. 1995; 94(3): 147-50. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7778333&dopt=Abstract

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The definition of community integration: perspectives of people with brain injuries. Author(s): McColl MA, Carlson P, Johnston J, Minnes P, Shue K, Davies D, Karlovits T. Source: Brain Injury : [bi]. 1998 January; 12(1): 15-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9483334&dopt=Abstract

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The epidemiology of sports-related traumatic brain injuries in the United States: recent developments. Author(s): Thurman DJ, Branche CM, Sniezek JE. Source: The Journal of Head Trauma Rehabilitation. 1998 April; 13(2): 1-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9575252&dopt=Abstract

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The evidence for brain injury in whiplash injuries. Author(s): Alexander MP. Source: Pain Res Manag. 2003 Spring; 8(1): 19-23. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12717473&dopt=Abstract

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The pathology of traumatic brain injuries. Author(s): Hardman JM. Source: Adv Neurol. 1979; 22: 15-50. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=384769&dopt=Abstract

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The surgical management of severe open brain injuries with consideration of the long-term results. Author(s): McDonald JV. Source: The Journal of Trauma. 1980 October; 20(10): 842-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7420494&dopt=Abstract

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The use of EEG spectral analysis after thiopental bolus in the prognostic evaluation of comatose patients with brain injuries. Author(s): Klein HJ, Rath SA, Goppel F. Source: Acta Neurochir Suppl (Wien). 1988; 42: 31-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3189018&dopt=Abstract

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'They never told us anything': postdischarge instruction for families of persons with brain injuries. Author(s): Paterson B, Kieloch B, Gmiterek J. Source: Rehabilitation Nursing : the Official Journal of the Association of Rehabilitation Nurses. 2001 March-April; 26(2): 48-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12035699&dopt=Abstract

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Touch-screen computerized education for patients with brain injuries. Author(s): Patyk M, Gaynor S, Kelly J, Ott V. Source: Rehabilitation Nursing : the Official Journal of the Association of Rehabilitation Nurses. 1998 March-April; 23(2): 84-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9668870&dopt=Abstract

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Transcranial brain injuries caused by metal rods and pipes over the past 150 years. Author(s): Stone JL. Source: Journal of the History of the Neurosciences. 1999 December; 8(3): 227-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11624154&dopt=Abstract

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Transcranial Doppler sonography and intracranial pressure monitoring in children and juveniles with acute brain injuries or hydrocephalus. Author(s): Sanker P, Richard KE, Weigl HC, Klug N, van Leyen K. Source: Child's Nervous System : Chns : Official Journal of the International Society for Pediatric Neurosurgery. 1991 November; 7(7): 391-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1794119&dopt=Abstract

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Traumatic brain injuries evaluated in U.S. emergency departments, 1992-1994. Author(s): Jager TE, Weiss HB, Coben JH, Pepe PE. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 2000 February; 7(2): 134-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10691071&dopt=Abstract

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Traumatic brain injuries in Alaska, 1996-1998. Author(s): Sallee D, Moore M, Johnson M. Source: Alaska Med. 2000 April-June; 42(2): 37-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10916856&dopt=Abstract

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Traumatic brain injuries. Author(s): Ponten U. Source: Acta Anaesthesiologica Scandinavica. Supplementum. 1971; 45: 123-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5290066&dopt=Abstract

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Traumatic brain injuries: predictive usefulness of CT. Author(s): Kido DK, Cox C, Hamill RW, Rothenberg BM, Woolf PD. Source: Radiology. 1992 March; 182(3): 777-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1535893&dopt=Abstract

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Traumatic brain injuries: structural changes. Author(s): Cervos-Navarro J, Lafuente JV. Source: Journal of the Neurological Sciences. 1991 July; 103 Suppl: S3-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1940963&dopt=Abstract

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Urban and rural traumatic brain injuries in Colorado. Author(s): Gabella B, Hoffman RE, Marine WW, Stallones L. Source: Annals of Epidemiology. 1997 April; 7(3): 207-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9141644&dopt=Abstract

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Using stimulus equivalence procedures to teach name-face matching to adults with brain injuries. Author(s): Cowley BJ, Green G, Braunling-McMorrow D. Source: J Appl Behav Anal. 1992 Summer; 25(2): 461-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1634433&dopt=Abstract

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Using the spectral analysis of the EEG for prognosis of severe brain injuries in the first post-traumatic week. Author(s): Steudel WI, Kruger J. Source: Acta Neurochir Suppl (Wien). 1979; 28(1): 40-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=290184&dopt=Abstract

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Ventricular fluid pressure recording after severe brain injuries. Author(s): Troupp H. Source: European Neurology. 1974; 11(4): 227-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4855386&dopt=Abstract

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Violent brain injuries by gunshot in Duval County, Florida, 1989-1991. Author(s): Deshmukh VD, Laneve L, Fallon WF Jr. Source: Archives of Neurology. 1992 June; 49(6): 588. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1596193&dopt=Abstract

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Virulence factors of Escherichia coli isolates from patients with symptomatic and asymptomatic bacteriuria and neuropathic bladders due to spinal cord and brain injuries. Author(s): Hull RA, Rudy DC, Wieser IE, Donovan WH. Source: Journal of Clinical Microbiology. 1998 January; 36(1): 115-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9431932&dopt=Abstract

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Visual evoked potentials (VEP) evaluating treatment for post-trauma vision syndrome (PTVS) in patients with traumatic brain injuries (TBI) Author(s): Padula WV, Argyris S, Ray J. Source: Brain Injury : [bi]. 1994 February-March; 8(2): 125-33. Erratum In: Brain Inj 1994 May-June; 8(4): 393. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8193632&dopt=Abstract

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What factors should be considered in rehabilitation: are anger, social desirability, and forgiveness related in adults with traumatic brain injuries? Author(s): Gisi TM, D'Amato RC. Source: The International Journal of Neuroscience. 2000 November; 105(1-4): 121-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11069052&dopt=Abstract

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CHAPTER 2. NUTRITION AND BRAIN INJURIES Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and brain injuries.

Finding Nutrition Studies on Brain Injuries The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail: [email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “brain injuries” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.

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Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.

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The following information is typical of that found when using the “Full IBIDS Database” to search for “brain injuries” (or a synonym): •

Agitated symptom response to divalproex following acute brain injury. Author(s): Department of Brain Injury Rehabilitation,Good Shepherd Rehabilitation Hospital, Allentown, PA 18103-3296, USA. Source: Chatham Showalter, P E Kimmel, D N J-Neuropsychiatry-Clin-Neurosci. 2000 Summer; 12(3): 395-7 0895-0172

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Alcohol consumption in traumatic brain injury: attenuation of TBI-induced hyperthermia and neurocognitive deficits. Author(s): Department of Neurobiology and Brain Research Institute, UCLA School of Medicine, Los Angeles, California 90095-1763, USA. [email protected] Source: Taylor, A N Romeo, H E Beylin, A V Tio, D L Rahman, S U Hovda, D A JNeurotrauma. 2002 December; 19(12): 1597-608 0897-7151

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Altered cellular anatomy and physiology of acute brain injury and spinal cord injury. Author(s): School of Nursing and Health Studies, Department of Cell Biology, School of Medicine, Georgetown University, Washington, DC, USA. Source: Zuccarelli, L A Crit-Care-Nurs-Clin-North-Am. 2000 December; 12(4): 403-11 0899-5885

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Altered cellular metabolism following traumatic brain injury: a magnetic resonance spectroscopy study. Author(s): Department of Biochemistry, University of Oxford, United Kingdom. [email protected] Source: Garnett, M R Corkill, R G Blamire, A M Rajagopalan, B Manners, D N Young, J D Styles, P Cadoux Hudson, T A J-Neurotrauma. 2001 March; 18(3): 231-40 0897-7151

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Antenatal brain injury: aetiology and possibilities of prevention. Author(s): Perinatal Center Dept of Obstetrics, Institute for the Health of Women and Children and Dept of Physiology, Sahlgrenska University Hospital/Ostra, Goteborg, 416 85, Sweden. [email protected] Source: Hagberg, H Mallard, C Semin-Neonatol. 2000 February; 5(1): 41-51 1084-2756

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Attenuation of working memory and spatial acquisition deficits after a delayed and chronic bromocriptine treatment regimen in rats subjected to traumatic brain injury by controlled cortical impact. Author(s): The Brain Trauma Research Center, Department of Neurosurgery, University of Pittsburgh, Pennsylvania 15260, USA. Source: Kline, A E Massucci, J L Marion, D W Dixon, C E J-Neurotrauma. 2002 April; 19(4): 415-25 0897-7151

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Behavioral and neurochemical effects of dopaminergic drugs in models of brain injury. Author(s): Department of Experimental and Clinical Pharmacology, University of Catania, Catania, Italy. Source: Medico, M De Vivo, S Tomasello, C Grech, M Nicosia, A Castorina, M D'Agata, M A Rampello, L Lempereur, L Drago, F Eur-Neuropsychopharmacol. 2002 June; 12(3): 187-94 0924-977X

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Brain injury: the uncertainties of using complementary therapies. Author(s): Institute of Health & Community Studies, Bournemouth University, Dorset, UK. [email protected] Source: Heidari, F Dumbrell, A Galvin, K Holloway, I Complement-Ther-NursMidwifery. 2001 May; 7(2): 66-71 1353-6117

Nutrition

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Cannabinoids and brain injury: therapeutic implications. Author(s): Dept of Medicinal Chemistry and Natural Products, Medical Faculty, Hebrew University, Jerusalem 91120, Israel. [email protected] Source: Mechoulam, Raphael Panikashvili, David Shohami, Esther Trends-Mol-Med. 2002 February; 8(2): 58-61 1471-4914

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Changes of cerebral energy metabolism and lipid peroxidation in mitochondrial dysfunction after diffuse brain injury. Author(s): Department of Neuroscience, University of Rome Tor [email protected] Source: Vagnozzi, R Marmarou, A Tavazzi, B Signoretti, S Di Pierro, Amorini, A M Fazzina, G Sherkat, S Lazzarino, G J-Neurotrauma. 1999 903-13 0897-7151

rats leading to Vergata, Italy. D del Bolgia, F October; 16(10):

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Clinical efficacy of stimulation programs aimed at reversing coma or vegetative state (VS) following traumatic brain injury. Author(s): Universite de Montreal, Montreal, Quebec, Canada. Source: Vanier, M Lamoureux, J Dutil, E Houde, S Acta-Neurochir-Suppl. 2002; 79: 53-7 0065-1419

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Divalproex in the management of neuropsychiatric complications of remote acquired brain injury. Author(s): Department of Psychiatry, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, 671 Hoes Lane, Piscataway, NJ 08855-1392, USA. [email protected] Source: Kim, Edward Humaran, Teresa J J-Neuropsychiatry-Clin-Neurosci. 2002 Spring; 14(2): 202-5 0895-0172

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Early polyneuropharmacologic intervention in brain injury agitation. Author(s): Department of Emergency Medicine, Traumatology, and Rehabilitation, Hartford Hospital, Hartford, Connecticut, USA. Source: Rosati, D L Am-J-Phys-Med-Rehabil. 2002 February; 81(2): 90-3 0894-9115

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Effect of posttraumatic hyperglycemia on contusion volume and neutrophil accumulation after moderate fluid-percussion brain injury in rats. Author(s): Department of Neurological Surgery, University of Miami School of Medicine, Miami, Florida 33101, USA. Source: Kinoshita, K Kraydieh, S Alonso, O Hayashi, N Dietrich, W D J-Neurotrauma. 2002 June; 19(6): 681-92 0897-7151

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Effects of olfactory stimulation on the vigilance performance of individuals with brain injury. Author(s): University of Cincinnati, USA. [email protected] Source: Sullivan, T E Warm, J S Schefft, B K Dember, W N O'Dell, M W Peterson, S J JClin-Exp-Neuropsychol. 1998 April; 20(2): 227-36 0168-8634

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Effects of six weeks of chronic ethanol administration on the behavioral outcome of rats after lateral fluid percussion brain injury. Author(s): Department of Surgery, University of Kentucky Chandler Medical Center, Lexington 40536-0084, USA. Source: Zhang, L Maki, A Dhillon, H S Barron, S Clerici, W J Hicks, R Kraemer, P J Butcher, J Prasad, R M J-Neurotrauma. 1999 March; 16(3): 243-54 0897-7151

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Hypomania induced by herbal and pharmaceutical psychotropic medicines following mild traumatic brain injury. Author(s): Division of Social and Behavioral Sciences, Richard Stockton College of New Jersey, Pomona 08240-0195, USA. [email protected] Source: Spinella, Marcello Eaton, Lisa A Brain-Inj. 2002 April; 16(4): 359-67 0269-9052

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Mitochondrial dysfunction after experimental traumatic brain injury: combined efficacy of SNX-111 and U-101033E. Author(s): Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA. Source: Xiong, Y Peterson, P L Verweij, B H Vinas, F C Muizelaar, J P Lee, C P JNeurotrauma. 1998 July; 15(7): 531-44 0897-7151

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Moderate zinc deficiency increases cell death after brain injury in the rat. Author(s): Department of Nutrition, Food and Exercise Sciences, Florida State University, Tallahassee 32306-4340, USA. Source: Yeiser, E C Vanlandingham, J W Levenson, C W Nutr-Neurosci. 2002 October; 5(5): 345-52 1028-415X

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Neurochemical characterization of traumatic brain injury in humans. Author(s): Department of Biochemistry of the Federal University of Rio Grande do Sul, Porto Alegre, Brazil. [email protected] Source: Regner, A Alves, L B Chemale, I Costa, M S Friedman, G Achaval, M Leal, L Emanuelli, T J-Neurotrauma. 2001 August; 18(8): 783-92 0897-7151

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Novel pharmacologic strategies in the treatment of experimental traumatic brain injury: 1998. Author(s): Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104-6316, USA. Source: McIntosh, T K Juhler, M Wieloch, T J-Neurotrauma. 1998 October; 15(10): 731-69 0897-7151

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Persistent accumulation of cyclooxygenase-1-expressing microglial cells and macrophages and transient upregulation by endothelium in human brain injury. Author(s): Institute of Brain Research, University of Tubingen, Medical School, Germany. [email protected] Source: Schwab, J M Beschorner, R Meyermann, R Gozalan, F Schluesener, H J JNeurosurg. 2002 May; 96(5): 892-9 0022-3085

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Prostaglandins contribute to impaired angiotensin II-induced cerebral vasodilation after brain injury. Author(s): Department of Anesthesia and Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. Source: BaraNovember, D Armstead, W M J-Neurotrauma. 2002 Nov; 19(11): 1457-66 0897-7151

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Protective effect of anisodamine on respiratory function after severe brain injury. Author(s): Neurosurgery Department, People's Hospital of Quzhou City, Quzhou 324000, China. Source: Huang, Q Dai, W Jie, Y Yu, G Chin-J-Traumatol. 2002 December; 5(6): 352-4 1008-1275

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Relationship between NOC/oFQ, dynorphin, and COX-2 activation in impaired NMDA cerebrovasodilation after brain injury. Author(s): Department of Anesthesia, University of Pennsylvania, Philadelphia, Pennsylvania, 19104, USA.

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Source: Kulkarni, M Armstead, W M J-Neurotrauma. 2002 August; 19(8): 965-73 08977151 •

Reversal of attenuation of cerebrovascular reactivity to hypercapnia by a nitric oxide donor after controlled cortical impact in a rat model of traumatic brain injury. Author(s): Department of Surgery, University of Texas Health Science Center, San Antonio 78229-3900, USA. [email protected] Source: Zhang, F Sprague, S M Farrokhi, F Henry, M N Son, M G Vollmer, D G JNeurosurg. 2002 October; 97(4): 963-9 0022-3085

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Selective activation of central subtypes of the nicotinic acetylcholine receptor has opposite effects on neonatal excitotoxic brain injuries. Author(s): Laboratoire de Neurologie du Developpement, INSERM E9935, Hopital Robert Debre, Paris, France. [email protected] Source: Laudenbach, Vincent Medja, Fadia Zoli, Michele Rossi, Francesco M Evrard, Philippe Changeux, Jean Pierre Gressens, Pierre FASEB-J. 2002 March; 16(3): 423-5 15306860

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Stilbazulenyl nitrone, a novel azulenyl nitrone antioxidant: improved neurological deficit and reduced contusion size after traumatic brain injury in rats. Author(s): Department of Neurology, Cerebral Vascular Disease Research Center, University of Miami School of Medicine, Florida 33101, USA. Source: Belayev, Ludmila Becker, David A Alonso, Ofelia F Liu, Yitao Busto, Raul Ley, James J Ginsberg, Myron D J-Neurosurg. 2002 June; 96(6): 1077-83 0022-3085

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The type 1 interleukin-1 receptor is essential for the efficient activation of microglia and the induction of multiple proinflammatory mediators in response to brain injury. Author(s): Department of Neuroscience and Anatomy, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA. Source: Basu, Anirban Krady, J Kyle O'Malley, Mark Styren, Scott D DeKosky, Steven T Levison, Steven W J-Neurosci. 2002 July 15; 22(14): 6071-82 1529-2401

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Three months of chronic ethanol administration and the behavioral outcome of rats after lateral fluid percussion brain injury. Author(s): Department of Surgery, University of Kentucky Chandler Medical Center, University of Kentucky, Lexington 40536-0084, USA. Source: Masse, J Billings, B Dhillon, H S Mace, D Hicks, R Barron, S Kraemer, P J Dendle, P Prasad, R M J-Neurotrauma. 2000 May; 17(5): 421-30 0897-7151

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Traumatic brain injury and subarachnoid hemorrhage: in vivo occult pathology demonstrated by magnetic resonance spectroscopy may not be “ischaemic”. A primary study and review of the literature. Author(s): Department of Clinical Neurosciences, University of Edinburgh, Western General Hospital, Edinburgh, UK. Source: Macmillan, C S Wild, J M Wardlaw, J M Andrews, P J Marshall, I Easton, V J Acta-Neurochir-(Wien). 2002 September; 144(9): 853-62; discussion 862 0001-6268

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Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •

healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0

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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov

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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov

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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/

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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/

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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/

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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/

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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/

Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats

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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html

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Google: http://directory.google.com/Top/Health/Nutrition/

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Healthnotes: http://www.healthnotes.com/

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Open Directory Project: http://dmoz.org/Health/Nutrition/

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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/

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WebMDHealth: http://my.webmd.com/nutrition

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

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CHAPTER INJURIES

3.

ALTERNATIVE

MEDICINE

AND

BRAIN

Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to brain injuries. At the conclusion of this chapter, we will provide additional sources.

National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to brain injuries and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “brain injuries” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to brain injuries: •

A review of the use of single-photon emission computerized tomography as a diagnostic tool in mild traumatic brain injury. Author(s): Davalos DB, Bennett TL. Source: Applied Neuropsychology. 2002; 9(2): 92-105. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12214827&dopt=Abstract

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A structured approach to family intervention after brain injury. Author(s): Kreutzer JS, Kolakowsky-Hayner SA, Demm SR, Meade MA. Source: The Journal of Head Trauma Rehabilitation. 2002 August; 17(4): 349-67. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12106003&dopt=Abstract

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A typology of alcohol use patterns among persons with recent traumatic brain injury or spinal cord injury: implications for treatment matching. Author(s): Turner AP, Bombardier CH, Rimmele CT. Source: Archives of Physical Medicine and Rehabilitation. 2003 March; 84(3): 358-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12638103&dopt=Abstract

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Assessment of P3a and P3b after moderate to severe brain injury. Author(s): Solbakk AK, Reinvang I, Andersson S. Source: Clin Electroencephalogr. 2002 July; 33(3): 102-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12192659&dopt=Abstract

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Auditory evoked potentials to spectro-temporal modulation of complex tones in normal subjects and patients with severe brain injury. Author(s): Jones SJ, Vaz Pato M, Sprague L, Stokes M, Munday R, Haque N. Source: Brain; a Journal of Neurology. 2000 May; 123 ( Pt 5): 1007-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10775545&dopt=Abstract

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Brain injury: the uncertainties of using complementary therapies. Author(s): Heidari F, Dumbrell A, Galvin K, Holloway I. Source: Complementary Therapies in Nursing & Midwifery. 2001 May; 7(2): 66-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11855774&dopt=Abstract

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Cognitive and histopathological outcome after weight-drop brain injury in the rat: influence of systemic administration of monoclonal antibodies to ICAM-1. Author(s): Isaksson J, Hillered L, Olsson Y. Source: Acta Neuropathologica. 2001 September; 102(3): 246-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11585249&dopt=Abstract

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Combined motor disturbances following severe traumatic brain injury: an integrative long-term treatment approach. Author(s): Keren O, Reznik J, Groswasser Z. Source: Brain Injury : [bi]. 2001 July; 15(7): 633-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11429091&dopt=Abstract

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Congenital and acquired brain injury. 4. New frontiers: neuroimaging, neuroprotective agents, cognitive-enhancing agents, new technology, and complementary medicine. Author(s): McEligott JM, Greenwald BD, Watanabe TK. Source: Archives of Physical Medicine and Rehabilitation. 2003 March; 84(3 Suppl 1): S18-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12708554&dopt=Abstract

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Defining community integration of persons with brain injuries as acculturation: a Canadian perspective. Author(s): Minnes P, Buell K, Nolte ML, McColl MA, Carlson P, Johnston J. Source: Neurorehabilitation. 2001; 16(1): 3-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11455098&dopt=Abstract

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Dietary supplement creatine protects against traumatic brain injury. Author(s): Sullivan PG, Geiger JD, Mattson MP, Scheff SW. Source: Annals of Neurology. 2000 November; 48(5): 723-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11079535&dopt=Abstract

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Diminution of metabolism/blood flow uncoupling following traumatic brain injury in rats in response to high-dose human albumin treatment. Author(s): Ginsberg MD, Zhao W, Belayev L, Alonso OF, Liu Y, Loor JY, Busto R. Source: Journal of Neurosurgery. 2001 March; 94(3): 499-509. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11235957&dopt=Abstract

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Distribution of services and supports for people with traumatic brain injury in rural and urban Missouri. Author(s): Johnstone B, Nossaman LD, Schopp LH, Holmquist L, Rupright SJ. Source: The Journal of Rural Health : Official Journal of the American Rural Health Association and the National Rural Health Care Association. 2002 Winter; 18(1): 109-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12043749&dopt=Abstract

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Driving plasticity in human adult motor cortex is associated with improved motor function after brain injury. Author(s): Fraser C, Power M, Hamdy S, Rothwell J, Hobday D, Hollander I, Tyrell P, Hobson A, Williams S, Thompson D. Source: Neuron. 2002 May 30; 34(5): 831-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12062028&dopt=Abstract

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EEG operant conditioning (biofeedback) and traumatic brain injury. Author(s): Thatcher RW. Source: Clin Electroencephalogr. 2000 January; 31(1): 38-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10638351&dopt=Abstract

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Effect of training frequency on face-name recall by adults with traumatic brain injury. Author(s): Hux K, Manasse N, Wright S, Snell J. Source: Brain Injury : [bi]. 2000 October; 14(10): 907-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11076136&dopt=Abstract

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Effects of lecithinized superoxide dismutase on neuronal cell loss in CA3 hippocampus after traumatic brain injury in rats. Author(s): Yunoki M, Kawauchi M, Ukita N, Sugiura T, Ohmoto T. Source: Surgical Neurology. 2003 March; 59(3): 156-60; Discussion 160-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12681536&dopt=Abstract

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Evaluation of a specific balance and coordination programme for individuals with a traumatic brain injury. Author(s): Dault MC, Dugas C. Source: Brain Injury : [bi]. 2002 March; 16(3): 231-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11908477&dopt=Abstract

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Evidence that synaptically-released zinc contributes to neuronal injury after traumatic brain injury. Author(s): Suh SW, Chen JW, Motamedi M, Bell B, Listiak K, Pons NF, Danscher G, Frederickson CJ. Source: Brain Research. 2000 January 10; 852(2): 268-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10678752&dopt=Abstract

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Flexyx Neurotherapy System in the treatment of traumatic brain injury: an initial evaluation. Author(s): Schoenberger NE, Shif SC, Esty ML, Ochs L, Matheis RJ. Source: The Journal of Head Trauma Rehabilitation. 2001 June; 16(3): 260-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11346448&dopt=Abstract

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Free fatty acids in cerebrospinal fluids from patients with traumatic brain injury. Author(s): Pilitsis JG, Coplin WM, O'Regan MH, Wellwood JM, Diaz FG, Fairfax MR, Michael DB, Phillis JW. Source: Neuroscience Letters. 2003 October 2; 349(2): 136-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12946571&dopt=Abstract

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Ginkgo biloba: applications in traumatic brain injury. Author(s): Elovic EP, Zafonte RD. Source: The Journal of Head Trauma Rehabilitation. 2001 December; 16(6): 603-7. Review. Erratum In: J Head Trauma Rehabil 2002 February; 17(1): Viii. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11732975&dopt=Abstract

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Homeopathic treatment of mild traumatic brain injury: A randomized, double-blind, placebo-controlled clinical trial. Author(s): Chapman EH, Weintraub RJ, Milburn MA, Pirozzi TO, Woo E. Source: The Journal of Head Trauma Rehabilitation. 1999 December; 14(6): 521-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10671699&dopt=Abstract

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Hypomania induced by herbal and pharmaceutical psychotropic medicines following mild traumatic brain injury. Author(s): Spinella M, Eaton LA. Source: Brain Injury : [bi]. 2002 April; 16(4): 359-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11953006&dopt=Abstract

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Impaired dopaminergic neurotransmission in patients with traumatic brain injury: a SPECT study using 123I-beta-CIT and 123I-IBZM. Author(s): Donnemiller E, Brenneis C, Wissel J, Scherfler C, Poewe W, Riccabona G, Wenning GK. Source: European Journal of Nuclear Medicine. 2000 September; 27(9): 1410-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11007526&dopt=Abstract

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Improvement in cerebral metabolism in chronic brain injury after hyperbaric oxygen therapy. Author(s): Golden ZL, Neubauer R, Golden CJ, Greene L, Marsh J, Mleko A. Source: The International Journal of Neuroscience. 2002 February; 112(2): 119-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12325401&dopt=Abstract

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Improving outcome after traumatic brain injury--progress and challenges. Author(s): Gentleman D. Source: British Medical Bulletin. 1999; 55(4): 910-26. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10746339&dopt=Abstract

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Low-dose prostacyclin improves cortical perfusion following experimental brain injury in the rat. Author(s): Bentzer P, Venturoli D, Carlsson O, Grande PO. Source: Journal of Neurotrauma. 2003 May; 20(5): 447-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803977&dopt=Abstract

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Metabolic recovery following human traumatic brain injury based on FDG-PET: time course and relationship to neurological disability. Author(s): Bergsneider M, Hovda DA, McArthur DL, Etchepare M, Huang SC, Sehati N, Satz P, Phelps ME, Becker DP. Source: The Journal of Head Trauma Rehabilitation. 2001 April; 16(2): 135-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11275575&dopt=Abstract

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Peer support in the community: initial findings of a mentoring program for individuals with traumatic brain injury and their families. Author(s): Hibbard MR, Cantor J, Charatz H, Rosenthal R, Ashman T, Gundersen N, Ireland-Knight L, Gordon W, Avner J, Gartner A.

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Source: The Journal of Head Trauma Rehabilitation. 2002 April; 17(2): 112-31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11909510&dopt=Abstract •

Pilot evaluation of a mindfulness-based intervention to improve quality of life among individuals who sustained traumatic brain injuries. Author(s): Bedard M, Felteau M, Mazmanian D, Fedyk K, Klein R, Richardson J, Parkinson W, Minthorn-Biggs MB. Source: Disability and Rehabilitation. 2003 July 8; 25(13): 722-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791557&dopt=Abstract

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Postconcussional disorder following mild to moderate traumatic brain injury: anxiety, depression, and social support as risk factors and comorbidities. Author(s): McCauley SR, Boake C, Levin HS, Contant CF, Song JX. Source: J Clin Exp Neuropsychol. 2001 December; 23(6): 792-808. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11910545&dopt=Abstract

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Protein tyrosine kinase and mitogen-activated protein kinase activation contribute to K(ATP) and K(ca) channel impairment after brain injury. Author(s): Armstead WM. Source: Brain Research. 2002 July 12; 943(2): 276-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12101050&dopt=Abstract

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Regional cerebrovascular and metabolic effects of hyperventilation after severe traumatic brain injury. Author(s): Diringer MN, Videen TO, Yundt K, Zazulia AR, Aiyagari V, Dacey RG Jr, Grubb RL, Powers WJ. Source: Journal of Neurosurgery. 2002 January; 96(1): 103-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11794590&dopt=Abstract

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Rehabilitation of a person with severe traumatic brain injury. Author(s): Burke D, Alexander K, Baxter M, Baker F, Connell K, Diggles S, Feldman K, Horny A, Kokinos M, Moloney D, Withers J. Source: Brain Injury : [bi]. 2000 May; 14(5): 463-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10834341&dopt=Abstract

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Restoration of vasodilation and CBF autoregulation by genistein in rat pial artery after brain injury. Author(s): Hong KW, Shin HK, Kim CD, Lee WS, Rhim BY. Source: American Journal of Physiology. Heart and Circulatory Physiology. 2001 July; 281(1): H308-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11406498&dopt=Abstract

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Role of nitric oxide in blood-brain barrier permeability, brain edema and cell damage following hyperthermic brain injury. An experimental study using EGB-761 and Gingkolide B pretreatment in the rat. Author(s): Sharma HS, Drieu K, Alm P, Westman J. Source: Acta Neurochir Suppl. 2000; 76: 81-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11450097&dopt=Abstract

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Satisfaction of life and late psycho-social outcome after severe brain injury: a nineyear follow-up study in Aquitaine. Author(s): Mazaux JM, Croze P, Quintard B, Rouxel L, Joseph PA, Richer E, Debelleix X, Barat M. Source: Acta Neurochir Suppl. 2002; 79: 49-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11974987&dopt=Abstract

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Sleep disturbances and their management in patients with brain injury. Author(s): Thaxton L, Myers MA. Source: The Journal of Head Trauma Rehabilitation. 2002 August; 17(4): 335-48. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12106002&dopt=Abstract

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Stress as a diagnostic challenge for postconcussive symptoms: sequelae of mild traumatic brain injury or physiological stress response. Author(s): Hanna-Pladdy B, Berry ZM, Bennett T, Phillips HL, Gouvier WD. Source: Clin Neuropsychol. 2001 August; 15(3): 289-304. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11778766&dopt=Abstract

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The immunophilin ligand FK506 attenuates axonal injury in an impact-acceleration model of traumatic brain injury. Author(s): Singleton RH, Stone JR, Okonkwo DO, Pellicane AJ, Povlishock JT. Source: Journal of Neurotrauma. 2001 June; 18(6): 607-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11437083&dopt=Abstract

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The magnitude and correlates of alcohol and drug use before traumatic brain injury. Author(s): Bombardier CH, Rimmele CT, Zintel H. Source: Archives of Physical Medicine and Rehabilitation. 2002 December; 83(12): 176573. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12474184&dopt=Abstract

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Towards the development of brain injury specialists. Author(s): Jackson H, Manchester D. Source: Neurorehabilitation. 2001; 16(1): 27-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11455101&dopt=Abstract

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Traumatic brain injury in older adults. Author(s): Ferrell RB, Tanev KS. Source: Current Psychiatry Reports. 2002 October; 4(5): 354-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12230964&dopt=Abstract

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Traumatic brain injury. State of the state. Author(s): Hooper SR, Callahan B. Source: N C Med J. 2001 November-December; 62(6): 336-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11729461&dopt=Abstract

Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •

Alternative Medicine Foundation, Inc.: http://www.herbmed.org/

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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats

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Chinese Medicine: http://www.newcenturynutrition.com/

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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html

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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm

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Google: http://directory.google.com/Top/Health/Alternative/

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Healthnotes: http://www.healthnotes.com/

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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine

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Open Directory Project: http://dmoz.org/Health/Alternative/

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HealthGate: http://www.tnp.com/

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WebMDHealth: http://my.webmd.com/drugs_and_herbs

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/

The following is a specific Web list relating to brain injuries; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •

General Overview Hypothermia Source: Integrative Medicine Communications; www.drkoop.com Meningitis Source: Integrative Medicine Communications; www.drkoop.com

Alternative Medicine 75

Obesity Source: Integrative Medicine Communications; www.drkoop.com •

Alternative Therapy Dance Therapy Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,687,00.html

General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.

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CHAPTER 4. DISSERTATIONS ON BRAIN INJURIES Overview In this chapter, we will give you a bibliography on recent dissertations relating to brain injuries. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “brain injuries” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on brain injuries, we have not necessarily excluded nonmedical dissertations in this bibliography.

Dissertations on Brain Injuries ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to brain injuries. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •

A Prospective Randomized Study to Assess the Effects of a Community-based Socialization Program for Individuals with Severe Traumatic Brain Injuries by Morton, Mary Virginia, Phd from Virginia Commonwealth University, 1992, 139 pages http://wwwlib.umi.com/dissertations/fullcit/9235058

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An Analysis of the Process of Educational Recovery for Children and Youth with Violent and Nonviolent Brain Injuries: a Multiple Case Study Replication Design by Krankowski, Theresa; Edd from The George Washington University, 1999, 573 pages http://wwwlib.umi.com/dissertations/fullcit/9949344

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Brain Injury, Memory and Learning by Thurston, Roy John; Phd from University of Calgary (canada), 2000, 146 pages http://wwwlib.umi.com/dissertations/fullcit/NQ49543

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Correlates of Codependency in Families of People with Traumatic Brain Injuries by Templeton, S. Mark, Phd from The University of Alabama, 1993, 164 pages http://wwwlib.umi.com/dissertations/fullcit/9417171

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Ecological Validity of Neuropsychological Performance As a Predictor of Work Outcome Following Mild Traumatic Brain Injury by Crean, Rebecca Dawn; Phd from California School of Professional Psychology - San Diego, 2003, 150 pages http://wwwlib.umi.com/dissertations/fullcit/3080411

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Extending Independent Living to Persons with Brain Injuries by Williams, Janet Marie, Phd from University of Kansas, 1997, 183 pages http://wwwlib.umi.com/dissertations/fullcit/9830124

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Frontal Lobe Functioning in Children with Focal Frontal Brain Injury, Non-focal Brain Injury and Matched Controls (lurian Tasks, Wisconsin Card Sorting Test) by Couch, Kathy Watkins, Phd from University of Georgia, 1985, 105 pages http://wwwlib.umi.com/dissertations/fullcit/8606032

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Posttraumatic Stress Disorder Symptomatology in Family Caregivers of Persons with Recent Traumatic Brain Injuries: an Exploratory Study by Courtney, Linda Jean, Phd from University of Houston, 1997, 229 pages http://wwwlib.umi.com/dissertations/fullcit/9734906

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Prospective Memory Performance and Self-report in a Traumatic Brain Injury Sample by Magdalinski, Michael; Phd from Saint Louis University, 2002, 80 pages http://wwwlib.umi.com/dissertations/fullcit/3051815

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Returning to Productive Activities: Perspectives of Individuals with Longstanding Acquired Brain Injuries by Petrella, Lina; Msc from Queen's University at Kingston (canada), 2002, 173 pages http://wwwlib.umi.com/dissertations/fullcit/MQ73075

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Risk Factors to School-aged Traumatic Brain Injury Survivor's Academic Success by Leuenberger, Sharon Lynn, Phd from State University of New York at Buffalo, 1998, 97 pages http://wwwlib.umi.com/dissertations/fullcit/9822165

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Silent Impact: Adult Siblings of Persons with Traumatic Brain Injuries by Degeneffe, Charles Edmund; Phd from The University of Wisconsin - Madison, 2002, 195 pages http://wwwlib.umi.com/dissertations/fullcit/3060410

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The Associations between Categorization, Deductive Reasoning, Self-awareness and Instrumental Activities of Daily Living among Individuals with Acute Brain Injury by Goverover, Yael; Phd from New York University, 2002, 150 pages http://wwwlib.umi.com/dissertations/fullcit/3060293

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The Relationship between the Wechsler Intelligence Scale for Children-third Edition and the Test of Memory and Learning in a Pediatric Traumatic Brain Injury Population by Schmidt, Mark Edward; Phd from Texas Woman's University, 2003, 74 pages http://wwwlib.umi.com/dissertations/fullcit/3084186

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The Transition of Students with Traumatic Brain Injuries from Hospital to School: a Nationwide Survey (rehabilitation) by Beard, Gene Huntley, Edd from University of South Carolina, 1992, 106 pages http://wwwlib.umi.com/dissertations/fullcit/9239012

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Word Retrieval Strategies by Individuals with Traumatic Brain Injury by Burke, Rebecca Dail; Phd from The University of Nebraska - Lincoln, 2002, 105 pages http://wwwlib.umi.com/dissertations/fullcit/3055263

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Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.

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CHAPTER 5. CLINICAL TRIALS AND BRAIN INJURIES Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning brain injuries.

Recent Trials on Brain Injuries The following is a list of recent trials dedicated to brain injuries.8 Further information on a trial is available at the Web site indicated. •

Genotype Influence on Recovery After Traumatic Brain Injury Condition(s): Brain Injury Study Status: This study is currently recruiting patients. Sponsor(s): Department of Veterans Affairs Medical Research Service Purpose - Excerpt: Genetic differences in response to brain injury may reasonably be expected to play a role in the initial consequences of traumatic brain injury and in the rate of recovery from such injury. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00018499

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Hypothermia to Treat Severe Brain Injury Condition(s): Brain Injuries; Hypothermia Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Neurological Disorders and Stroke (NINDS) Purpose - Excerpt: The purpose of this trial is to determine if hypothermia (body cooling), administered very soon after a severe brain injury in patients who are hypothermic on admission, improves functional outcome.

8

These are listed at www.ClinicalTrials.gov.

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Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00040339 •

Magnesium Sulfate For Brain Injury Condition(s): Brain Injuries; Head Injury; Brain Concussion Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Neurological Disorders and Stroke (NINDS) Purpose - Excerpt: The purpose of the study is to determine whether magnesium sulfate, given within 8 hours of a moderate or severe traumatic brain injury improves survival, decreases the number of people developing seizures, improves the survivors' mental and psychological functioning, including the ability to return to daily life, live independently, and return to work or school. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004730

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Measuring Head Impacts in Sports Condition(s): Brain Injuries; Brain Concussion Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: Head impacts in sports can lead to brain injury even when the participant is wearing a helmet. The forces that contribute to brain injury from sportsrelated head impacts are not well understood. This study will test a new device to measure the speed of head impacts among football players. Phase(s): Phase II Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00060827

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Neuropsychiatric Evaluation of Healthy Volunteers and Adults with Schizophrenia Condition(s): Brain Injury; Dementia; Healthy; Mental Disorder; Schizophrenia Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Mental Health (NIMH) Purpose - Excerpt: The purpose of this study is to evaluate the cognitive processes of participants with schizophrenia, participants with nervous system and mental disorders, and healthy volunteers. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001323

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Pediatric Traumatic Brain Injury: Methylphenidate Effects on Early Recovery Condition(s): Brain Injuries Study Status: This study is currently recruiting patients. Sponsor(s): National Center for Research Resources (NCRR); Murray Fellowship Purpose - Excerpt: Traumatic Brain Injury (TBI) is the leading cause of acquired long term disability among children and young adults. Deficits in attention and memory are common and persist for years after moderate or severe TBI. The similarity between these symptoms and those of children with AD/HD, the efficacy of methylphenidate in the treatment of AD/HD, and the efficacy of methylphenidate in improving recovery of animals with brain injuries, support the need to study methylphenidate effects in children with TBI. This investigation of methylphenidate in children with moderate to severe TBI aims to: (1) Assess the acute effects of 2 different dosages of methylphenidate on attention and reaction time when the medication is administered to children early in recovery; (2) Assess the ability of 8 weeks of methylphenidate to improve the rate of recovery of cognitive, memory, and attentional skills in children with TBI; (3) Identify the frequency of common methylphenidate side effects in children with TBI. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00035139

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Phase I/II Study of Neuroendocrine Dysfunction in Patients With Closed Head Injuries Condition(s): Brain Injury Study Status: This study is currently recruiting patients. Sponsor(s): National Center for Research Resources (NCRR); University of Texas Purpose - Excerpt: Objectives: I. Determine the incidence of neuroendocrine dysfunction in patients with closed head injuries admitted to the Transitional Learning Community in Galveston, Texas, for rehabilitation. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006271

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Progesterone Treatment of Blunt Traumatic Brain Injury Condition(s): Traumatic Brain Injury Study Status: This study is currently recruiting patients. Sponsor(s): Emory University; National Institutes of Health (NIH) Purpose - Excerpt: The purpose of this study is to determine if progesterone treatment safely reduces brain swelling and damage after injury. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00048646

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Prospective Memory in Children with Traumatic Brain Injury Condition(s): Traumatic Brain Injury Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: Prospective memory (PM) is memory to complete future tasks, such as recalling to give a note to someone when you next see them, pick up milk on the way home, or remembering to keep an appointment. This study will evaluate PM in children with traumatic brain injury (TBI). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061399

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Safety testing of AVP-923 in the Treatment of Emotional Lability (Uncontrolled Laughter & Crying) Condition(s): Amyotrophic Lateral Sclerosis; Multiple Sclerosis; Alzheimer's Disease; Stroke; Traumatic Brain Injury Study Status: This study is currently recruiting patients. Sponsor(s): Avanir Pharmaceuticals Purpose - Excerpt: The purpose of this study is to evaluate the safety of AVP-923 for the treatment of emotional lability. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00056524

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Study of the Approximate Entropy of Adrenocorticotropic Hormone and Cortisol Secretion in Patients With Head Injury Condition(s): Brain Injury; Craniocerebral Trauma Study Status: This study is currently recruiting patients. Sponsor(s): National Center for Research Resources (NCRR); University of Texas Purpose - Excerpt: Objectives: I. Determine the randomness of adrenocorticotropic hormone (ACTH) and cortisol secretion using approximate entropy in patients who have sustained a head injury. II. Determine the correlation between randomness of ACTH and cortisol secretion and stages of sleep in these patients. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006270

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Therapy for Reading Problems in Adults After Brain Injury Condition(s): Dyslexia, Acquired; Brain Injuries; Cerebrovascular Accident Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD)

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Purpose - Excerpt: Adults who sustain brain damage due to stroke, head injury, or traumatic surgery may develop difficulty reading. This study examines the effectiveness of behavior-based programs to improve reading ability in these individuals. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00064805

Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “brain injuries” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •

For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/

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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html

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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/

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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm

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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm

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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm

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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp

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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm

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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/

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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm

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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm

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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm

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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm

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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm

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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials

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CHAPTER 6. PATENTS ON BRAIN INJURIES Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “brain injuries” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on brain injuries, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Brain Injuries By performing a patent search focusing on brain injuries, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an 9Adapted

from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.

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example of the type of information that you can expect to obtain from a patent search on brain injuries: •

2,3-dihydro-5-(3-oxo-2-cyclohexen-1-yl)-2-benzofurancarboxylic acids, and their salts useful in the treatment of brain injury Inventor(s): Cragoe, Jr.; Edward J. (Lansdale, PA), Woltersdorf, Jr.; Otto W. (Chalfont, PA) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 4,654,365 Date filed: September 26, 1985 Abstract: The invention relates to novel substituted 2,3-dihydro-5-(3-oxo-2-cyclohexen1-yl)-2-benzofurancarboxylic acids, their derivatives and their salts. The compounds are useful for the treatment and prevention of injury to the brain and of edema due to head trauma, stroke (particularly ischemic), arrested breathing, cardiac arrest, Reye's syndrome, cerebral thrombosis, cerebral embolism, cerebral hemorrhage, cerebral tumors, encephalomyelitis, spinal cord injury, hydrocephalus, post-operative brain injury trauma, edema due to cerebral infections and various brain concussions. Excerpt(s): Trauma to the brain or spinal cord caused by physical forces acting on the skull or spinal column, by ischemic stroke, arrested breathing, cardiac arrest, Reye's syndrome, cerebral thrombosis, cerebral embolism, cerebral hemorrhage, encephalomyelitis, hydrocephalus, post-operative brain injury, cerebral infections and various concussions results in edema and swelling of the affected tissues. This is followed by ischemia, hypoxia, necrosis, temporary or permanent brain and/or spinal cord injury and may result in death. The tissue mainly affected are classified as grey matter, more specifically astroglial cells. The specific therapy currently used for the treatment of the medical problems described include various kinds of diuretics (particularly osmotic diuretics), steroids (such as, 6-.alpha.-methylprednisolone succinate) and barbiturates. The usefulness of these agents is questionable and they are associated with a variety of untoward complications and side effects. Thus, the compounds of this invention comprise a novel and specific treatment of medical problems where no specific therapy is available. A recent publication entitled "Agents for the Treatment of Brain Injury" 1. (Aryloxy)alkanoic Acids, Cragoe et al, J. Med. Chem., (1982) 25, 567 -79, reports on recent experimental testing of agents for treatment of brain injury and reviews the current status of treatment of brain injury. Some 2benzofurancarboxylic acids have been reported to be diuretic and saluretic agents in U.S. Pat. Nos. 3,843,797; 3,761,494; 3,751,436; 3,751,430, 3,726,904; 3,723,619; 3,709,909; 3,682,961; 3,681,502; 3,676,560; 3,674,810; 3,651,094; 3,627,785; 3,580,931; 3,574,208 and 3,557,152 of Habicht et al. Additionally, E. J. Cragoe, Jr., Diuretics: Chemistry, Pharmacology and Medicine (1983) p. 220 as well as, U.S. Pat. Nos. 4,085,117; 4,087,542; 4,100,294; 4,154,742; 4,163,794; 4,181,727; 4,237,144; 4,296,122 and 4,401,669 of E. J. Cragoe, Jr. et al. disclosed that the 6,7-dichloro derivatives of these compounds also have activity as diuretics. There is, however, no suggestion in the patents or publication that any of the compounds disclosed therein would be of use in the treatment of brain injury. Web site: http://www.delphion.com/details?pn=US04654365__

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•

Apparatus and method for adjunct (add-on) treatment of coma and traumatic brain injury with neuromodulation using an external stimulator Inventor(s): Boveja; Birinder R. (P.O. Box 210095, Milwaukee, WI 53221) Assignee(s): none reported Patent Number: 6,564,102 Date filed: April 19, 2001 Abstract: A system and method of neuromodulation adjunct (add-on) therapy for coma and traumatic brain injury, comprises an implantable lead-receiver and an external stimulator. Neuromodulation is performed using a pulsed electrical stimulation. The external stimulator contains a power source, controlling circuitry, a primary coil, and predetermined programs. The primary coil of the external stimulator inductively transfers electrical signals to the lead-receiver, which is also in electrical contact with a vagus nerve. The external stimulator emits electrical pulses to stimulate the vagus nerve according to a predetermined program. The predetermined programs have different levels of control, which is password protected. The external stimulator may also be equipped with a telecommunications module to control the predetermined programs remotely. Excerpt(s): This invention relates generally to a medical device for the treatment of coma and brain injury, more specifically a medical device for adjunct (add-on) treatment of coma and traumatic brain injury by electrical stimulation neuromodulation of a selected nerve or nerve bundle utilizing an implanted lead-receiver and an external stimulator. Coma is an abnormally deep state of unconsciousness with an absence of voluntary response to stimuli and with varying degrees of reflex activity. It represents the extreme of a graded continuum of impairment of consciousness, at the opposite pole of the spectrum from full alertness and awareness of the environment. It is not a single uniform disorder, but may stem from different causes such as trauma, disease, or their condition, and which may be characterized by different levels of consciousness. There are degrees of coma, but no varieties. Coma differs from both sleep and syncope (temporary suspension of consciousness due to generalized cerebral ischemia). Cerebral oxygen uptake is normal in sleep or actually increases during the rapid eye movement stage, but cerebral oxygen uptake is abnormally reduced in coma. The patient is incapable of sensing or responding adequately to external stimuli or inner needs, shows little or no spontaneous movement apart from respiration, and no evidence whatever of mental activity. At the deepest state of coma there is no reaction to stimuli of any intensity, and corneal, pupillary, pharyngeal, tendon and plantar reflexes are absent. Respiration is slow and sometimes periodic (Cheyne-Stokes respiration) and cardiovascular regulating processes may show signs of failure. Lighter degrees of coma (`semicoma`) allow partial response to stimulation, though this is imcomplete, mostly nonpurposive and usually consists of ineffectual movements or rubbing and scratching of the stimulated area. Bladder distension may call forth groaning or ill-coordinated motor stirring but the patient is still incontinent. Tendon refexes may or may not be obtainable, and the plantars may be either flexor or extensor. The Glasgow Coma Scale has proved its usefulness for the grading of depth of coma. Web site: http://www.delphion.com/details?pn=US06564102__

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Apparatus for simulating traumatic brain injury and method for inducing spinal cord injury Inventor(s): Eleftheriou; Evangelos (Hoover, AL), Meythaler; Jay M. (Birmingham, AL), Peduzzi; Jean (Chelsea, AL) Assignee(s): UAB Research Foundation (Birmingham, AL) Patent Number: 6,588,431 Date filed: September 28, 2001 Abstract: An apparatus for simulating human traumatic brain injury in an animal, said apparatus comprising a support having an aperture having end walls and side walls disposed therein; a sliding element slidingly engaged with said side walls of said aperture, said sliding element having a retainer disposed thereon for receiving an animal holder therein; and a crank arm operatively connected to both said sliding element and an actuator mechanism. There is also disclosed a method of simulating human traumatic brain injury in an animal which includes the steps of providing an animal and repeatedly laterally displacing the animal in a reciprocal manner in order to cause acceleration and deceleration of the animal laterally to cause the animal's brain to be correspondingly accelerated and decelerated thereby causing traumatic brain injury. A method of simulating human spinal cord injury in an animal, said method comprising the steps of providing a vertebrate animal having an invertebral space and a spinal cord; causing an opening in the animal at the invertebral space to the interior surface of the spinal cord; inserting a deflated balloon embolectomy catheter into the opening, and rapidly inflating the balloon catheter to cause the balloon catheter to expand and contact the spinal cord whereby the contact causes injury to the spinal cord. Excerpt(s): The subject invention relates to an apparatus and method for simulating human central nervous system injuries and, more particularly, the subject invention relates to an apparatus and method for animal simulation of human traumatic brain injury and spinal cord injury. The predominant mechanism in most cases of traumatic brain injury (TBI) is diffuse axonal injury (Whyte and Rosenthal, 1993). While axonal injury is common in all TBI regardless of severity (Povlishock et al., 1992; Mittl, 1994), a shearing of the axons occurs in human diffuse axonal injury (DAI) leading to progressive changes that ultimately may result in the loss of connections between nerve cells. The slow progression of events in DAI continues for up to several weeks after injury creating a window of opportunity for therapeutic intervention. Up to now, there are no consistently reproducible small animal models for DAI which closely mimic the changes associated with DAI in humans (Maxwell et al., 1997; Povlishock, 1993). Without such a model to study the mechanism of injury, it is difficult to develop prevention and/or interventional methodologies to limit the extent of injury. In part, this may explain the lack of efficacy of the clinical trials to assess various medications to limit injury in TBI. There are approximately 500,000 new cases of TBI in the U.S. each year (Frankowski, 1985), and the incidence requiring hospitalization is estimated to be approximately 200-225/100,000 population (Frankowski, 1986; Carus, 1993). Currently, it is estimated that brain injuries account for 12% of all hospital admissions in the United States (Sandel, 1993). When compared to spinal cord injury, which accounts for less than 1% of hospital admissions, it is clear that TBI is a medical care problem which has a significant impact financially within the United States. Approximately 30,00044,000 people will survive a severe TBI with GCS score<9 (Glasgow Coma Score Scale, Jennett, 1981) in the U.S. each year and more than 70,000 will be significantly disabled from moderate to severe TBI (GCS.ltoreq.10) (Whyte & Rosenthal, 1988). Yet with new medical management techniques, less than 10% will remain in a persistent vegetative

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state (Whyte, 1993; Rosner, 1992; Rosner, 1990). A GCS score of eight or less generally reflects a state of unconsciousness in which the patient demonstrates no eye opening, does not follow simple commands to move muscles, and has vocalizations which are limited to sounds. Such signs are indicative of severe brain injury (Whyte, 1993; Jennett, 1975, Jennett, 1981). Web site: http://www.delphion.com/details?pn=US06588431__ •

Method of treatment of traumatic brain injury Inventor(s): Scheiner; Stuart L. (East Brunswick, NJ) Assignee(s): Forest Laboratories, Inc. (New York, NY) Patent Number: 5,527,822 Date filed: December 29, 1993 Abstract: A method of treatment of a mammal, including humans, suffering from traumatic brain injury, which comprises administering to the sufferer a therapeutically effective amount of a butyrolactone derivative. Excerpt(s): The present invention is directed to a method of treatment of traumatic brain injuries. It is widely accepted that severe traumatic brain injuries (TBI) initiate a cascade of events that lead to dramatic elevation of intracranial pressure (ICP) and dysfunction of cerebrovascular regulatory mechanisms essential for survival. Indeed, ischemic brain injury is seen universally in those patients who die following severe TBI. Intracranial hypertension (IH) following traumatic brain injury is associated with direct effects on cerebral perfusion which may be responsible for secondary ischemia. The contributions of both post-traumatic cerebral edema and alteration in cerebral blood volume to ICP appear to vary based on the length of time after the primary mechanical insult. This combination of vasomotor dysfunction and abnormalities in vascular permeability is characteristic of acute inflammation. Y is O or S. Web site: http://www.delphion.com/details?pn=US05527822__

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Methods of treating traumatic brain injury by vagus nerve stimulation Inventor(s): Browning; Ronald A. (Carbondale, IL), Clark; Kevin B. (Murphysboro, IL), Jensen; Robert A. (Carbondale, IL), Naritoku; Dean K. (Springfield, IL), Smith; Douglas C. (Carbondale, IL), Terry, Jr.; Reese S. (Houston, TX) Assignee(s): Board of Trustees of Southern Illinois University (Springfield, IL) Patent Number: 6,104,956 Date filed: May 30, 1997 Abstract: Methods of modulating brain neural plasticity, improving memory and learning, improving recovery from traumatic brain injury, preventing epilepsy, treating memory disorders and chronic memory impairment, and treating persistent impairment of consciousness in humans and animals by vagus nerve stimulation are provided. These methods comprise selecting an appropriate human or animal subject and applying to the subject's vagus nerve an electrical stimulation signal having parameter values effective in modulating the electrical activity of the vagus nerve in a manner so as to modulate the activity of preselected portions of the brain.

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Excerpt(s): The present invention relates to methods and apparatus for modulating neural plasticity in the nervous system. Neural plasticity includes phenomena such as memory and learning consolidation processes, as well as recovery of function following traumatic brain injury. The methods of the present invention are directed to modulating neural plasticity, improving memory and learning consolidation processes, cognitive processing, and motor and perceptual skills in both normal subjects and subjects suffering from chronic memory impairment, alleviating symptoms and improving outcome in subjects suffering from traumatic brain injury, preventing the development of epilepsy in subjects prone to developing this condition, and treating persistent impairment of consciousness. These methods employ electrical stimulation of the vagus nerve in human or animal subjects via application of modulating electrical signals to the vagus nerve by use of a neurostimulating device. The vagus nerve comprises both somatic and visceral afferents (inward conducting nerve fibers that convey impulses toward a nerve center such as the brain or spinal cord) and efferents (outward conducting nerve fibers that convey impulses to an effector to stimulate the same and produce activity). The vast majority of vagal nerve fibers are C fibers, and a majority are visceral afferents having cell bodies lying in masses or ganglia in the neck. For the most part, the central projections terminate in the nucleus of the solitary tract, which sends fibers to various regions of the brain such as the hypothalamus, thalamus, and amygdala. Other projections continue to the medial reticular formation of the medulla, the cerebellum, the nucleus cuneatus, and other regions. The solitary nucleus has important pathways to brain regulatory networks, including the serotonergic nuclei and the noradrenergic nuclei. These neurotransmitter systems are crucial for memory, learning, cognitive and sensory/perceptual processing, and motor skills. These neurotransmitters also prevent the development of epilepsy, i.e., they are antiepileptogenic, and are important for the processes that subserve brain recovery following traumatic injury. The majority of vagus nerve fibers are viscerosensory afferents originating from receptors located in the lungs, aorta, heart, and gastrointestinal tract, and convey, among other things, cardiopulmonary and nocicepive information to various forebrain and brainstem structures (Cechetto, D. F. (1987) Federation Proceedings 46:17-23). Three populations of vasal afferents are known to exist: the vastly abundant unmyelinated C fibers involved in pain mediation, and small myelinated B fibers and large A fibers which subserve autonomic reflexes and probably more complex visceroendocrine responses, such as glucose metabolism and fluid homeostasis (Barraco, I.R.A. (1994) Nucleus of the Solitary Tract, CRC Press, Boca Raton). Nearly all vagal afferents terminate in the nucleus of the solitary tract (NTS), where the information they carry is first integrated before being divergently projected to each rostral level of the neuroaxis. Because NTS neurons impinge on a number of CNS structures and regions, including the hypothalamus, hippocampus, amygdaloid complex, dorsal raphe nucleus, and mesencephalic reticular formation (Rutecki, P. (1990). Epilepsia 31 (Suppl. 2):51-56), an equally large number of cognitive, somatic, and visceral operations can be initiated or coordinated with autonomic information. Thus, as one might expect, neural signals sent via vagal afferents have a profound impact on CNS function that, in turn, influence general behaviors and arousal. For instance, electrical stimulation of the cervical vagus can modify the electrophysiological profile of neocortical, thalamic, and cerebellar neurons. These and other changes in supramedullary circuits are thought to precipitate overt changes in, for example, sleep, feeding behavior, responsiveness to noxious stimuli, and monosynaptic muscular reflexes (Rutecki, supra). Web site: http://www.delphion.com/details?pn=US06104956__

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Traumatic and ischemic brain injury treatment with opiate-receptor antagonists Inventor(s): Faden; Alan I. (406 Wendy Way, Mill Valley, CA 94941) Assignee(s): none reported Patent Number: 4,906,637 Date filed: December 21, 1988 Abstract: The present invention involves methods of inducing opiate-receptor antagonistic activity in a patient suffering from ischemic or traumatic brain injury by administering to said patient an effective amount of an opiate-receptor antagonist having enhanced activity at the kappa-opiate receptor suitable to permit the induction of opiate-receptor antagonistic activity. Excerpt(s): Endogenous opioids may be released following traumatic or ischemic injury of the central nervous system. These opioids may serve as secondary pathophysiologic factors contributing to the neurological disorder which stems from the injury to the central nervous system. Opiate receptor antagonists, such as naloxone, have been used to treat brain or spinal cord injury at dosages in the range of 1 to 10 mg/kg of body weight of the patient. However, naloxone is neither completely selective nor a pure opiate antagonist in all situations. At low dosages, naloxone has considerable selectivity for the mu-opiate receptor. At higher dosages, naloxone acts on other opiate receptors, including the delta and kappa receptors. Further at higher dosages, naloxone may have effects that are not mediated by opiate receptors. In order to simplify and enhance the safety of central nervous system protocols, opiate receptor antagonists which exhibit a high degree of specificity for or enhanced activity at a specific opiate receptor are being sought. Also, opiate receptor antagonists which act exclusively as such without producing any undesirable side reactions within the body are preferred. Web site: http://www.delphion.com/details?pn=US04906637__

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Treatment of ischemic brain injuries with brain targeted anti oxidant compounds Inventor(s): Atlas; Daphne (Jerusalem, IL), Melamed; Eldad (Tel Aviv, IL), Offen; Daniel (Ha Roe, IL) Assignee(s): Mor-Research Applications Ltd. (Petach Tikua, IL), Ramot University Authority for Applied Research & Industrial Development (Tel-Aviv, IL), Yissum Research Development Company of the Hebrew University of Jerusalem (Jerusalem, IL) Patent Number: 6,369,106 Date filed: December 27, 1999 Abstract: A method of reducing oxidative stress in the brain of an organism having a blood brain barrier and suffering an ischemic brain injury, the method comprising the step of administering a compound to the organism, the compound having (a) a combination of molecular weight and membrane miscibility properties for permitting the compound to cross the blood brain barrier of the organism; (b) a readily oxidizable chemical group for exerting antioxidation properties; and (c) a chemical make-up for permitting the compound or its intracellular derivative to accumulate within the cytoplasm of cells. Excerpt(s): The present invention relates, in general to the use of antioxidant compounds, also referred herein as antioxidants, for the treatment of ischemic head injuries. More particularly, the present invention relates to novel brain targeted low

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molecular weight, hydrophobic antioxidants and their use in treatment of ischemic head injuries, such as, but not limited to stroke and head trauma. In the last few years evidences have accumulated which connect oxidative stress (OS) with the pathogenesis of Parkinson's, Alzheimer's Creutzfeldt-Jakob's diseases and other human neurodegenerative disorders (Olanow, 1990, 1993; Fahn and Cohen, 1992; Cafe et al., 1996, Brown et al., 1996; Thomas et al., 1996). These studies were initiated (i) since outooxidation of levodopa and dopamine is known to produce oxygen free radicals, H.sub.2 O.sub.2, quinones and semiquinones, the later two are high molecular weight polymers possessing an aromatic structure and are therefore potentially toxic and (ii) since postmortem studies in Parkinson's disease patients showed a dramatic decline in the levels of endogenous reduced glutathione (GSH), which is, as is further delineated hereinbelow, essential for maintaining the oxidative state of the cells. The decrease in reduced glutathione levels progresses from the pre symptomatic Parkinson's disease condition to the advanced clinical Parkinson's disease condition. Web site: http://www.delphion.com/details?pn=US06369106__ •

Treatment or prevention of anoxic or ischemic brain injury with melatonincontaining compositions Inventor(s): Fahy; Gregory M. (Gaithersburg, MD), Federowicz; Michael G. (Riverside, CA), Wood; Lawrence E. (Wrightwood, CA) Assignee(s): Life Resuscitation Technologies, Inc. (Chicago, IL) Patent Number: 5,700,828 Date filed: December 7, 1995 Abstract: A method for treating or preventing anoxic or ischemic brain injury that includes administering melatonin to a person who is suffering from or has a high risk of suffering from an anoxic or ischemic insult or injury. The method may also include administering complementary agents. Excerpt(s): The present invention relates generally to treating or preventing ischemic and anoxic brain injuries, particularly those associated with normothermic cardiac arrest. More particularly, the present invention provides a composition and method for resuscitation of the brain and maintenance of viability during or after trauma or other periods of decreased blood flow, allowing the health professional extra time to restore blood circulation and body functions. Hundreds of thousands of people suffer from sudden cardiac arrest each year in the United States alone. During cardiac arrest, the heart ceases to pump blood. Subsequently, there is no circulation, and the brain fails to receive freshly oxygenated blood. Without a steady supply of oxygenated blood, the brain will cease to function. Current resuscitation techniques for cardiac arrest victims have been directed almost exclusively towards the heart. However, even with methods such as cardiopulmonary resuscitation (CPR), patient survival rates are low. In hospitals and clinics with advanced CPR and advanced life support (ALS) systems, the survival rate is normally around 14%. Outside of hospital settings, the survival rate is about 5%. Among cardiac arrest victims overall, less than 10% survive neurologically intact and without significant brain damage. The other approximately 90% either die or sustain some neurologic injury from ischemia (i.e., lack of blood flow to the brain), or anoxia (i.e., lack of oxygen to the brain). Web site: http://www.delphion.com/details?pn=US05700828__

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Patent Applications on Brain Injuries As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to brain injuries: •

1-Diphenylmethyl-pyrazole derivatives as opioid receptor ligands Inventor(s): Mchardy, Stanton F.; (Coventry, RI), Vetelino, Michael G.; (North Stonington, CT) Correspondence: PFIZER INC; 150 EAST 42ND STREET; 5TH FLOOR - STOP 49; NEW YORK; NY; 10017-5612; US Patent Application Number: 20030069241 Date filed: July 23, 2002 Abstract: This invention relates to 1-diphenylmethyl-pyrazole derivatives of formula (I): 1and pharmaceutically acceptable salts thereof; wherein R.sup.1, R.sup.2, R.sup.3, R.sup.4 and R.sup.5 are defined herein, as ligands for opioid receptors, particularly the delta opioid receptor. The compounds of the invention have a broad range of therapeutic uses in the area of addictions, analgesia, immunotherapy, shock and brain injuries, neurological dysfunction, gastrointestinal dysfunction, among others. Excerpt(s): and pharmaceutically acceptable salts thereof; wherein R.sup.1, R.sup.2, R.sup.3, R.sup.4 and R.sup.5 are defined herein, as ligands for opioid receptors, particularly the delta opioid receptor. The compounds of the invention have a broad range of therapeutic uses in the area of addictions, analgesia, immunotherapy, shock and brain injuries, neurological dysfunction, gastrointestinal dysfunction, among others. Significant research has focused on understanding the mechanism of action of identified endogenous and non-endogenous opioid compounds, particularly as in the context of cellular and differentiated tissue opioid receptors. Opioid compounds are typically classified by their binding selectivity with respect of these cellular and differentiated tissue receptors to which a specific drug species binds as a ligand. These receptors include the three subtypes of opioid receptors, mu (.mu.), delta (.delta.) and kappa (.kappa.) receptors, which are described and documented in the scientific literature. All three receptors are present in the central and peripheral nervous systems of many species, including man. Activation of delta receptors produces antinociception in rodents and can induce analgesia in man, in addition to influencing motility of the gastrointestinal tract. (see, T. F. Burks in The Pharmacology Of Opioid Peptides, Ed. L. F. Tseng (Harwood Academic Publishers 1995)). The well-known narcotic opioid compounds, such as morphine and its analogs, are selective for the opioid mu receptor. Mu receptors mediate analgesia, respiratory depression, and inhibition of gastrointestinal transit. Kappa receptors mediate analgesia and sedation. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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This has been a common practice outside the United States prior to December 2000.

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Administration of noncompetitive AMPA receptor antagonist for neuroprotection after traumatic brain injury Inventor(s): Belayev, Ludmila; (Miami, FL), Ginsburg, Myron D.; (Coconut Grove, FL) Correspondence: IVAX CORPORATION; 4400 Biscayne Boulevard; Miami; FL; 33137; US Patent Application Number: 20030073683 Date filed: September 18, 2002 Abstract: The invention provides compositions and methods for treating traumatic brain injury by the administration of a noncompetitive AMPA receptor antagonist. In certain embodiments, the noncompetitive AMPA receptor antagonist is a 2,3benzodiazepine derivative. Illustrative 2,3-benzodiazepine derivatives useful according to the invention include (R)-7-acetyl-5(4-aminophenyl)-8,9-dihydro-8-methyl-7H-1,3dioxolo[4,5-h][- 2,3]benzodiazepine. Excerpt(s): This application claims priority to United States Provisional Patent Application Serial No. 60/323,012, filed on Sep. 18, 2001. The present invention relates to the field.alpha.-amino-3-hydroxy-- 5-methyl-4-isoxazoic propionic acid (AMPA) receptor agonists. Traumatic brain injury ("TBI") represents one of the most tragic, common, and costly of all neurological disorders. Traumatic brain injury is associated with a large number of physical or behavioral disabilities. Each year in the United States, nearly 2 million people suffer from head injuries of sufficient severity to result in brain trauma (see Thurman et. al., J. Head Trauma Rehabil. 14: 602-615 (1999)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Brain injury diagnostic system Inventor(s): Ziejewski, Mariusz; (Fargo, ND) Correspondence: Michael S. Neustel; Suite No. 4; 2534 South University Drive; Fargo; ND; 58103; US Patent Application Number: 20020028987 Date filed: January 17, 2001 Abstract: A brain injury diagnostic system for providing a quick and accurate assessment of various accident scenarios for providing an accurate brain injury diagnosis. The invention includes the process of collecting data at the accident site or from an emergency room, entering the collected data into a computer, transferring the collected data to a central computing facility through a communication system, conducting a biomechanical analysis of the collected data at the central computing facility, determining the results of the biomechanical analysis, transferring the results to the computer, and displaying the results upon a computer monitor of the computer preferably prior to the patient's arrival at the emergency room. Based upon the displayed results, health care providers can then make an informed decision regarding the proper treatment for the patient. Excerpt(s): I hereby claim benefit under Title 35, United States Code, Section 119(e) of U.S. provisional patent application Ser. No. 60/176,524 filed Jan. 18, 2000. This application is a continuation of the 60/176,524 application. The 60/176,524 application is currently pending. The 60/176,524 application is hereby incorporated by reference into this application. The present invention relates generally to diagnostic systems and more

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specifically it relates to a brain injury diagnostic system for providing a quick and accurate assessment of various accident scenarios and an accurate brain injury diagnosis. Individuals in the medical profession encounter patients that have suffered injuries as a result of vehicle accidents, slip and falls, falling objects and various other scenarios. These individuals often incur mild traumatic brain injury that may not immediately demonstrate any physical symptoms noticeable to the physician or patient. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Brain rescue instrument and method Inventor(s): Gunning, Mark I.; (Auckland, NZ), Williams, Christopher E.; (Auckland, NZ) Correspondence: NIXON & VANDERHYE P.C.; 8th Floor; 1100 North Glebe Road; Arlington; VA; 22201-4714; US Patent Application Number: 20020082514 Date filed: January 23, 2002 Abstract: An intelligent brain rescue instrument for identifying, monitoring, and guiding the application of brain therapies to patients with evolving brain injuries, comprises input means (101-103) for acquiring a multiple number of signals each indicative of a different biochemical or biophysical parameter of a patient, computing means (104-107) to continuously sample each of the acquired signals and display to a user on a monitor (109) at least some of the parameters, the displayed parameters being selected by system software embodying expert analytical rules as the most significant parameters, or as parameters having values indicative, or predictive at any time of actual, or potential future deterioration of the brain state of the patient. Excerpt(s): This invention relates particularly to data evaluation equipment and procedures for the monitoring and management of brain injuries in mammals. The brain can be compromised by a number of adverse influences during all stages of life including perinatal asphyxial and hypoperfusion insults, strokes, traumatic brain injuries, cardiac arrest, cardiac bypass surgery, poisoning, and subarachnoid haemorrhages. Considerable variation occurs in the degree and distribution of neuronal loss depending on the type and severity of the injury to the brain. Recent studies suggest that it is possible to interfere with these mechanisms and thereby rescue susceptible neurons. Biophysical measures of the pathophysiologic processes preceding and during the phases of neuronal death are likely to prove useful for identifying those patients who may benefit from neuronal rescue therapies. Several clinically relevant factors such as pre-existing injuries, hypotension or metabolic status may sensitise and alter the response of the brain to injury. Several biophysical parameters recorded during and after an insult are generally needed to reliably discriminate the present phase of injury and periods of cytotoxic activity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Chemokine Inventor(s): Lesslauer, Werner; (Riehen, CH), Utans-Schneitz, Ulrike; (Basle, CH) Correspondence: HOFFMANN-LA ROCHE INC.; PATENT LAW DEPARTMENT; 340 KINGSLAND STREET; NUTLEY; NJ; 07110 Patent Application Number: 20030175895 Date filed: January 16, 2003 Abstract: The present invention relates to the discovery of novel genes and proteins, which function in pathways involved in brain pathogenesis. In particular, the novel genes and proteins relate to inflammatory tissue responses caused by brain injuries such trauma, ischemia or autoimmune-inflammation or other diseases or processes related to neuroinflammation. The compounds disclosed in the present invention are useful as therapeutics, diagnostics and in screening assays. Excerpt(s): This is a divisional of copending application Ser. No. 09/426,321, filed Oct. 25, 1999, which is a divisional of application Ser. No. 09/071,353, filed Apr. 30, 1998, now U.S. Pat. No. 6,057,426, issued May 2, 2000. The present invention relates to proinflammatory and anti-inflammatory proteins. Brain injury such as trauma, ischemia or autoimmune-inflammation leads to an inflammatory tissue response involving both activated, resident and infiltrating cells. In brain ischemia this inflammatory reaction is characterized by an early influx of polymorphonuclear leukocytes, primarily neutrophils, into the zone of injury followed by a late infiltration of activated microglia and blood monocyte/macrophages (Dereski et al. (1992) Neurosci. Res. Commun. 11:179-186; Ramsay et al. (1992) Lancet 339:1054-1055). Infiltrating leukocytes as well as activated resident glial cells may exert a cytotoxic effector function by releasing reactive oxygen species, nitric oxide, proteinases, inflammatory cytokines or excitotoxins such as glutamate or quinolinic acid and, therefore, have been implicated in the pathogenesis of cerebral ischemia and stroke. (Kochanik & Hallenbeck (1992) Stroke 23:1367-1379; Lees (1993) J. Neurol. Sci. 114:119-122; Wood (1995) Neurol. Res. 17:242:248). The specific mechanisms responsible for the initiation and propagation of the inflammatory reaction in response to focal and transient brain ischemia are not fully elucidated. Studies showing a very early and sustained upregulation of the pro-inflammatory cytokines TNF alpha and IL-1 in the ischemic area and a more delayed increase for mediators such as IL-6, MCP-1 or MIP-1 alpha provide evidence for a specific role of brain cytokines in this process (Buttini et al. (1994) Mol. Brain Res. 23:126-134; Kim et al. (1995) J. Neuroimmunol. 56:127-134; Wang et al. (1995) Stroke 26:661-666; Buttini et al. (1996) Neurosci. 71:1-16; Yoshimoto et al. (1997) Acta Neuropathol. 93:154-158). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Identification, diagnosis, and treatment of neuropathologies, neurotoxicities, tumors, and brain and spinal cord injuries using microelectrodes with microvoltammetry Inventor(s): Broderick, Patricia A.; (Bronx, NY), Pacia, Steven V.; (New York, NY) Correspondence: BAKER & BOTTS; 30 ROCKEFELLER PLAZA; NEW YORK; NY; 10112 Patent Application Number: 20030032001 Date filed: April 8, 2002

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Abstract: The present invention relates to devices and methods of use thereof for making semiderivative voltammetric and chronoamperometric measurements of chemicals, e.g. neurotransmitters, precursors, and metabolites, in vitro, in vivo, or in situ. The invention relates to methods of diagnosing and/or treating a subject as having or being at risk of developing a disease or condition that is associated with abnormal levels of one or more neurotransmitters including, inter alia, epilepsy, diseases of the basal ganglia, athetoid, dystonic diseases, neoplasms, Parkinson's disease, brain injuries, spinal cord injuries, and cancer. The invention provides methods of differentiating white matter from grey matter using microvoltammetry. In some embodiments, regions of the brain to be resected or targeted for pharmaceutical therapy are identified using Broderick probes. The invention further provides methods of measuring the neurotoxicity of a material by comparing Broderick probe microvoltammograms of a neural tissue in the presence and absence of the material. Excerpt(s): This application claims priority to U.S. application Ser. Nos. 60/282,004 filed on Apr. 6, 2001, 60/297,276 filed on Jun. 11, 2001, and 60/326,407 filed on Oct. 1, 2001, all of which are incorporated herein in their entirety by reference. This invention was made, in part, with government support. The government has certain rights in the invention. The present invention relates to devices and methods of use thereof for determining the presence and concentration of chemicals in a cell, tissue, organ or organism. The invention relates to, inter alia, semiderivative voltammetric measurements and chronoamperometric measurements of chemicals, e.g. neurotransmitters, precursors and metabolites, to identify, diagnose, and/or treat neuropathologies, neurotoxicities, tumors, and brain and spinal cord injuries. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method for diagnosing and distinguishing traumatic brain injury and diagnostic devices for use therein Inventor(s): Davey, Michelle; (Mississauga, CA), Jackowski, George; (Kettleby, CA), Stanton, Eric B.; (Burlington, CA), Takahashi, Miyoko; (North York, CA) Correspondence: MCHALE & SLAVIN; 4440 PGA BLVD; SUITE 402; PALM BEACH GARDENS; FL; 33410 Patent Application Number: 20030040660 Date filed: August 27, 2001 Abstract: Methods of implementing rapid assessment of patients presenting with brain trauma injury in humans are provided. These methods comprise presenting a subject possibly suffering from traumatic brain injury, selecting one or more markers to detect injury, tracking evolution of injury by tracking marker concentration over time, and determining repetitive injury by the correlation of molecular weight markers appearing over the course of time. Excerpt(s): The present invention relates to methods for rapid assessment of subjects suffering from traumatic brain injury. The invention particularly relates to a process and device for one or more markers indicative of cellular damage, and further relates to tracking the concentration of those markers to accurately assess severity of injury. The present invention additionally relates to the diagnosis of repeated injury associated with traumatic brain injury. Damage to the brain by a physical force is broadly termed traumatic brain injury (TBI) The resulting effect of TBI causes alteration of normal brain processes attributable to changes in brain structure and/or function. There are two basic

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types of brain injury, open head injury and closed head injury. In an open head injury, an object, such as a bullet, penetrates the skull and damages the brain tissue. Closed head injury is usually caused by a rapid movement of the head during which the brain is whipped back and forth, bouncing off the inside of the skull. Closed head injuries are the most common of the two, which often results from motor vehicle crashes or falls. In a closed head injury, brute force or forceful shaking injures the brain. The stress of this rapid movement pulls apart and stretches nerve fibers or axons, breaking connections between different parts of the brain. In most cases, a resulting blood clot, or hematoma, may push on the brain or around it, raising the pressure inside the head. Both open and closed head injuries can cause severe damage to the brain, resulting in the need for immediate medical attention. Depending on the type of force that hits the head, varying injuries such as any of the following can result: jarring of the brain within the skull, concussion, skull fracture, contusion, subdural hematoma, or diffuse axonal injury. Though each person's experience is different, there are common problems that many people with TBI face. Possibilities documented include difficulty in concentrating, ineffective problem solving, short and long-term memory problems, and impaired motor or sensory skills; to the point of an inability to perform daily living skills independently such as eating, dressing, or bathing. The most widely accepted concept of brain injury divides the process into primary and secondary events. Primary brain injury is considered to be more or less complete at the time of impact, while secondary injury evolves over a period of hours to days following trauma. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method of treating traumatic brain injury and other neuronal disorders Inventor(s): Deford, S. Michelle; (Richmond, VA), Hamm, Robert; (Crozier, VA), Shiotani, Tadashi; (Tokyo, JP) Correspondence: OBLON SPIVAK MCCLELLAND MAIER & NEUSTADT PC; FOURTH FLOOR; 1755 JEFFERSON DAVIS HIGHWAY; ARLINGTON; VA; 22202; US Patent Application Number: 20010041734 Date filed: June 22, 2001 Abstract: A method for treatment of neuronal disorders and traumatic brain injury is provided which involves timely administration to a subject in need thereof of an effective amount of nefiracetam. Excerpt(s): The present invention relates to a method for treatment of brain injury and neuronal disorders, such as epilepsy, by administration of an effective amount of nefiracetam. Traumatic brain injury, as well as neuronal disorders with common pathological features, such as stroke and epilepsy, can have devastating effects on a person, both short-term and long-term. Traumatic brain injury is often associated with cerebral concussion. Cerebral concussion is a traumatically induced derangement of the nervous system, characterized clinically by immediate and transient impairment of consciousness and is generally not associated with remarkable gross anatomical changes. Even moderate levels of concussive human head injury, not requiring prolonged hospitalization, can result in persistent neurological disturbances often lasting for months. These disturbances often include dizziness and balance problems, and fine motor skill dysfunction. Lyeth et al, Brain Research, 452, 39-48 (1988). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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METHOD OF TREATING, PREVENTING OR INHIBITING CENTRAL NERVOUS SYSTEM INJURIES AND DISEASES Inventor(s): Koenig, Michael L.; (Silver Spring, MD), Meyerhoff, James L.; (Silver Spring, MD), Yourick, Debra L.; (Linthicum Heights, MD) Correspondence: Office of the Staff Judge Advocate; U.S. Army Medical Research and Materiel Command; ATTN: MCMR-JA (Ms. Elizabeth Arwine); 504 Scott Street; Fort Detrick; MD; 21702-5012; US Patent Application Number: 20020177558 Date filed: April 20, 2001 Abstract: Methods of preventing, treating, or both preventing and treating CNS injury, disease, neurotoxicity or memory deficit in a subject by the administration of at least one lipoic acid compound to the subject are disclosed. Examples of CNS injuries or disease include traumatic brain injury (TBI), posttraumatic epilepsy (PTE), stroke, cerebral ischemia, neurodegenerative diseases of the brain such as Parkinson's disease, Dementia Pugilistica, Huntington's disease and Alzheimer's disease, brain injuries secondary to seizures which are induced by radiation, exposure to ionizing or iron plasma, nerve agents, cyanide, toxic concentrations of oxygen, neurotoxicity due to CNS malaria or treatment with anti-malaria agents, and other CNS traumas. Examples of lipoic acid compounds include alpha-lipoic acid (ALA), dihydrolipoic acid (DHLA), 2-(N,Ndimethylamine) ethylamido lipoate-HCL (LA-plus), the oxidized or reduced R- or Sisomers thereof, the metabolites of alpha-lipoic acid such as 6,8-bisnorlipoic acid and tetranorlipoic acid and analogs thereof. Also disclosed are pharmaceutical compositions and kits comprising at least one lipoic acid compound. Excerpt(s): This application claims the benefit of U.S. Provisional Patent Application No. 60/198,958, filed Apr. 21, 2000, naming James L. Meyerhoff, Debra L. Yourick and Michael L. Koenig as inventors, which is herein incorporated by reference. 1. Field of the Invention. The invention relates to a method of treating, preventing or inhibiting central nervous system (CNS) injuries and diseases. In particular, the invention relates to a method of treating, preventing or inhibiting a CNS injury or disease in a subject by the administration of at least one lipoic acid compound to the subject. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Methods and compositions for producing neural progenitor cells Inventor(s): Agoston, Denes V.; (Bethesda, MD) Correspondence: MORRISON & FOERSTER LLP; 1650 TYSONS BOULEVARD; SUITE 300; MCLEAN; VA; 22102; US Patent Application Number: 20030170736 Date filed: January 31, 2002 Abstract: The invention relates generally to methods and compositions for altering the differentiation status of cells such as stem and progenitor cells, and producing these cells for transplantation into mammals. The differentiation status of cells can be altered by contacting a nucleic acid decoy molecule to a mammalian cells and culturing the cell, whereby the differentiation status of the cell is altered. Pharmaceutical compositions of the invention are capable of entering a cell and binding to a protein in the cell and thereby altering a septamer function, a septamer-downstream function or a septamer-

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related function. The methods disclosed herein can be used in treating diseases by providing new cells to ameliorate symptoms of the disorder. Preferably, methods of the invention create homogeneous populations of progenitor and other cells, that can be administered to patients by transplantation. Diseases and disorders that can be treated in this fashion include, but are not limited to, CNS disorders, disorders of the lymphatic system, endothelial cell disorders, epithelial cell disorders, erythropoietic and hematopoietic diseases and disorders, neuro-degenerative disease, and traumatic brain injuries. Excerpt(s): This application claims priority to U.S. provisional patent application Serial No. 60/265,113, filed Jan. 31, 2001, the entirety of which is hereby incorporated by reference. The present invention generally relates to methods and compositions comprising nucleic acid decoys for altering the differentiation of cells, and in particular, stem and progenitor cells. The invention also relates to methods of treating diseases and to pharmaceutical compositions used in diagnosis and therapy of diseases such as neurological diseases and disorders of the CNS. Neurons and glial cells of the adult mammalian CNS are derived from multipotent progenitors that develop into neurons and glial cells (Brustle and McKay, 1996; Lillien, 1998; Pincus et al., 1998). At the level of transcriptional control, neurodifferentiation is envisaged as a cascade of spatiotemporally coordinated and cooperative interactions between regulatory DNA elements of neuron- or glial-specific genes and transcription factors that are differentially expressed in developing cells at progressive stages of neural development (Lemke, 1993). However, the identity of these transcription factors, as well as their coordinated interactions that must occur during development, is poorly understood because of the enormous complexity of the mammalian CNS. One approach to overcome this complexity is to search for mammalian homologs of genes identified in Drosophila or Caenorhabditis elegans (He and Rosenfeld, 1991). Despite some setbacks, for example, gcm (Kim et al., 1998), this strategy has been successful (Rubenstein and Beachy, 1998). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Methods for treating cognitive impairments caused by traumatic brain injuries Inventor(s): Pratt, Raymond; (Leonia, NJ) Correspondence: Edward D. Grieff, Esq.; Hale and Dorr LLP; 1455 Pennsylvania Avenue, NW; Washington; DC; 20004; US Patent Application Number: 20020035129 Date filed: September 4, 2001 Excerpt(s): This application claims priority to PCT Application No. PCT/US01/07027 filed Mar. 5, 2001, which claims priority to U.S. Provisional Application No. 60/259,226 filed Jan. 3, 2001, U.S. Provisional Application No. 60/220,783 filed Jul. 25, 2000, U.S. Provisional Application No. 60/197,610 filed Apr. 18, 2000, and U.S. Provisional Application No. 60/186,744 filed Mar. 3, 2000. The invention describes novel methods for treating and preventing cognitive impairments caused by traumatic brain injuries by administering a therapeutically effective amount of at least one of the cholinesterase inhibitor compounds described herein. A preferred cholinesterase inhibitor for use in the methods of the invention is donepezil hydrochloride or ARICEPT.RTM. Novel cholinesterase inhibitors are described in U.S. Pat. No. 4,895,841 and WO 98/39000, the disclosures of which are incorporated by reference herein in their entirety. The cholinesterase inhibitors described in U.S. Pat. No. 4,895,841 include donepezil

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hydrochloride or ARICEPT.RTM., which has proven to be a highly successful drug for the treatment of Alzheimer's disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Pharmaceutical combinations for the treatment of stroke and traumatic brain injury Inventor(s): Chenard, Bertrand L.; (Waterford, CT), Menniti, Frank S.; (Mystic, CT), Saltarelli, Mario D.; (Mystic, CT) Correspondence: PFIZER INC; 150 EAST 42ND STREET; 5TH FLOOR - STOP 49; NEW YORK; NY; 10017-5612; US Patent Application Number: 20020045656 Date filed: September 6, 2001 Abstract: This invention relates to methods of treating traumatic brain injury (TBI) or hypoxic or ischemic stroke, comprising administering to a patient in need of such treatment an NR2B subtype selective N-methyl-D-aspartate (NMDA) receptor antagonist in combination with either: (a) a neutrophil inhibitory factor (NIF); (b) a sodium channel antagonist; (c) a nitric oxide synthase (NOS) inhibitor; (d) a glycine site antagonist; (e) a potassium channel opener; (f) an AMPA/kainate receptor antagonist; (g) a calcium channel antagonist; (h) a GABA-A receptor modulator (e.g., a GABA-A receptor agonist); or (i) an antiinflammatory agent. Excerpt(s): This application claims priority under 35 U.S.C. 119(e) of U.S. Provisional Application No. 60/230,944, filed Sep. 6, 2000. This invention relates to methods of treating traumatic brain injury (TBI), ischemic stroke, or hypoxic brain injury, comprising administering to a patient in need of such treatment an NR2B subtype selective N-methyl-D-aspartate (NMDA) receptor antagonist in combination with one or more other compounds that protect neurons from toxic insult, inhibit the inflammatory reaction after brain damage or promote cerebral reperfusion. More specifically, this invention relates to methods of treating traumatic brain injury (TBI) or hypoxic or ischemic stroke, comprising administering to a patient in need of such treatment an NR2B subtype selective N-methyl-D-aspartate (NMDA) receptor antagonist in combination with either: (a) a neutrophil inhibitory factor (NIF); (b) a sodium channel antagonist; (c) a nitric oxide synthase (NOS) inhibitor; (d) a glycine site antagonist; (e) a potassium channel opener; (f) an AMPA/kainate receptor antagonist; (g) a calcium channel antagonist; (h) a GABA-A receptor modulator (e.g., a GABA-A receptor agonist); (i) an antiinflammatory agent; or (j) a matrix metalloprotease (MMP) inhibitor. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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System method for reducing brain injury particularly in newborn infants Inventor(s): Coldham, Dlana Katrina; (Auckland, NZ), Gunn, Alistair; (Auckland, NZ), Gunn, Alistair Jan; (Auckland, NZ), Gunn, Bernard Maurice; (Auckland, NZ), Gunn, Christopher Bernard; (Auckland, NZ), Gunn, Derek Ivan; (Auckland, NZ), Gunn, Tania R.; (Auckland, NZ) Correspondence: NIXON & VANDERHYE P.C.; 1100 North Glebe Road, 8th Floor; Arlington; VA; 22201-4714; US Patent Application Number: 20020091431 Date filed: October 25, 2001 Abstract: A method for preventing or reducing the development of delayed brain damage in a patient, comprises applying headwear (1) to the patient's head and circulating a fluid coolant through conduits (3) or passages in the headwear to cool the brain and thermostatically controlling the coolant temperature within a predetermined range to maintain the brain at a temperature sufficiently below normal for an extended period sufficient to prevent the death of neurons, glial or other cells that would otherwise die as a consequence of direct injury to the brain or other injury to the patient likely to cause injury to the brain. Excerpt(s): The invention comprises apparatus and a method for preventing or reducing delayed brain damage in a patient, and headwear for fitting to a patient's head for use with the apparatus and method of the invention. During brain injury, the brain is deprived of freshly oxygenated blood. Following this, neurons in the brain die soon after or at a later stage occurring hours to days after the insult and are not capable of regeneration. Glial cells, which are non-neuronal cells essential for normal brain functioning, also die. Permanent loss of function is a likely outcome of a severe injury to the brain. Perinatal hypoxic-ischemic injury continues to be a major cause of death or later neurodevelopmental sequelae. This type of head injury in the neonate occurs during asphyxial, traumatic, toxic, infectious, metabolic, ischemic or hypoxic insults to the brain. Specifically, perinatal asphyxia caused by cord occlusion or associated with intrauterine growth retardation; perinatal asphyxia associated with failure of adequate resuscitation or respiration; near miss drowning, near miss cot death, carbon monoxide poisoning, ammonia or other gaseous intoxication, coma, hypoglycaemia and status epileptics; stroke; cerebral trauma. Experimental and clinical studies have shown that hypoxic ischemic encephalopathy (HIE) is an evolving process. Following the primary phase of energy failure during asphyxia cerebral metabolism may initially recover in a latent phase, but then deteriorate in a secondary phase of brain injury 6 to 15 hours later. In the human infant the severity of delayed energy failure after asphyxia is correlated with adverse neurodevelopmental outcome at one and four years of age. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Treatment of ischemic brain injuries with brain targeted antioxidant compounds Inventor(s): Atlas, Daphne; (Jerusalem, IL), Melamed, Eldad; (Tel Aviv, IL), Offen, Daniel; (Ha'roe, IL) Correspondence: Anthony Castorina; G E Ehrlich; Suite 207; 2001 Jefferson Davis Highway; Arlington; VA; 22202; US Patent Application Number: 20030083266 Date filed: September 24, 2002

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Abstract: A method of reducing oxidative stress in the brain of an organism having a blood brain barrier and suffering an ischemic brain injury, the method comprising the step of administering a compound to the organism, the compound having (a) a combination of molecular weight and membrane miscibility properties for permitting the compound to cross the blood brain barrier of the organism; (b) a readily oxidizable chemical group for exerting antioxidation properties; and (c) a chemical make-up for permitting the compound or its intracellular derivative to accumulate within the cytoplasm of cells. Excerpt(s): The present invention relates, in general to the use of antioxidant compounds, also referred herein as antioxidants, for the treatment of ischemic head injuries. More particularly, the present invention relates to novel brain targeted low molecular weight, hydrophobic antioxidants and their use in treatment of ischemic head injuries, such as, but not limited to stroke and head trauma. In the last few years evidences have accumulated which connect oxidative stress (OS) with the pathogenesis of Parkinson's, Alzheimer's Creutzfeldt-Jakob's diseases and other human neurodegenerative disorders (Olanow, 1990, 1993; Fahn and Cohen, 1992; Cafe et al., 1996, Brown et al., 1996; Thomas et al., 1996). These studies were initiated (i) since outooxidation of levodopa and dopamine is known to produce oxygen free radicals, H.sub.2O.sub.2, quinones and semiquinones, the later two are high molecular weight polymers possessing an aromatic structure and are therefore potentially toxic and (ii) since post-mortem studies in Parkinson's disease patients showed a dramatic decline in the levels of endogenous reduced glutathione (GSH), which is, as is further delineated hereinbelow, essential for maintaining the oxidative state of the cells. The decrease in reduced glutathione levels progresses from the pre symptomatic Parkinson's disease condition to the advanced clinical Parkinson's disease condition. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Treatment of ischemic brain injury Inventor(s): Aronowski, Jaroslaw A.; (Houston, TX), Grotta, James C.; (Bellaire, TX), Strong, Roger A.; (Humble, TX) Correspondence: Edwin S. Flores; Gardere Wynne Sewell LLP; Suite 3000; 1601 Elm Street; Dallas; TX; 75201; US Patent Application Number: 20020169179 Date filed: May 17, 2002 Abstract: A composition and method adapted for the treatment of ischemic brain injury is disclosed, which includes applying hypothermic conditions to a subject within 5 hours after onset of brain injury and administering to the subject in need thereof a dose of a pharmaceutically effective amount of caffeine and at least a pharmaceutically effective amount of an alcohol or mixtures thereof adapted for the treatment of cerebral ischemia under hypothermic conditions. Excerpt(s): This is a Continuation-In-Part of U.S. Ser. No. 09/552,924 filed Apr. 20, 2000, which claims priority to U.S. Provisional Patent Application Serial No. 60/131,116, filed Apr. 27, 1999. The present invention relates in general to the field of ischemic brain injury, and more particularly, to a neuroprotective method and composition adapted for the treatment of cerebral ischemia. Without limiting the scope of the invention, its background is described in connection with the treatment of Ischemic brain injury such

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as a stroke or a secondary ischemic injury after a brain trauma, with stroke as an example. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Use of amino-isoxazolidone compounds for treatment of memory impairment following traumatic brain injury Inventor(s): Fakouhi, Daniel T.; (Wilmette, IL), Herting, Robert L.; (Park Ridge, IL), Williams, J. Michael; (Philadelphia, PA) Correspondence: J. Timothy Keane; PHARMACIA CORPORATION; Corporate Patent Department; 800 North Lindbergh Blvd. - O4E; St. Louis; MO; 63167; US Patent Application Number: 20030073730 Date filed: October 16, 2002 Abstract: A class of amino-isoxazolidone compounds is described for use in treatment of memory impairment associated with Traumatic Brain Injury ("TBI"). Preferred compounds of this class are D-cycloserine and its prodrugs. Excerpt(s): This invention is in the field of clinical neurology and relates specifically to compounds, formulations and methods for treatment of memory impairment or deficit following or associated with Traumatic Brain Injury ("TBI"). In a summary of epidemiology of Traumatic Brain Injury ("TBI") in the United States, an overall incidence of 200 per 100,000 people was reported [J. F. Kraus, In: Neuroepidemiology, 335-357, D. W. Anderson & D. H. Schoenberg, eds., CRC Press, Boca Raton, Fla., (1991)]. TBI patients may develop a number of neuropsychological disorders, including severe memory impairment. Epidemiological studies of cognitive impairment following Traumatic Brain Injury have not been reported. However, outcome studies using consecutive admissions to trauma centers suggest that the incidence rate leading to cognitive impairment is approximately 40-80% of all cases of Traumatic Brain Injury in which the patient was in a coma for at least one-half hour [J. M Williams et al, J. Neurosurg., 61, 581-585 (1984); M. R. Bond et al, Scand. J. of Rehab. Med., 8, 127-133 (1976); G. S. Carlsson et al, J. of Neurosurgery, 67, 507-513 (1986); S. Dikmen et al, Arch. Physical Medicine and Rehabilitation, 67, 507-513 (1986); S. Dikmen et al, J. Neurology, Neurosurgery and Psychiatry, 50, 1613-1618 (1987); H. S. Levin et al, J. Neurosurgery, 50, 412-422, (1979)] Post-traumatic memory impairment persists through the patient's physical recovery and may become the permanent sequelae of the injury [G. S. Carlsson et al, J. of Neurosurgery, 67, 507-513 (1986); S. Dikmen et al, Arch. Physical Medicine and Rehabilitation, 67, 507-513 (1986); S. Dikmen et al, J. Neurology, Neurosurgery and Psychiatry, 50, 1613-1618 (1987); H. S. Levin et al, J. Neurosurgery, 50, 412-422, (1979)). Traumatic injury of the brain produces mechanical injury of neurons, axonal stretching and neuronal degeneration. Compression injury of neural tissues may also result from increased intracranial pressure due to hematoma and diffuse swelling. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

Keeping Current In order to stay informed about patents and patent applications dealing with brain injuries, you can access the U.S. Patent Office archive via the Internet at the following Web address:

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http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “brain injuries” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on brain injuries. You can also use this procedure to view pending patent applications concerning brain injuries. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

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CHAPTER 7. BOOKS ON BRAIN INJURIES Overview This chapter provides bibliographic book references relating to brain injuries. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on brain injuries include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.

Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “brain injuries” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on brain injuries: •

Mild Traumatic Brain Injury: A Therapy and Resource Manual Source: San Diego, CA: Singular Publishing Group, Inc. 1998. 260 p. Contact: Available from Singular Publishing Group, Inc. 401 West 'A' Street, Suite 325, San Diego, CA 92101-7904. (800) 521-8545 or (619) 238-6777. Fax (800) 774-8398 or (619) 238-6789. E-mail: [email protected]. Website: www.singpub.com. PRICE: $49.95 plus shipping and handling. ISBN: 1565938275. Summary: This book is a therapy and reference manual created in response to the unique needs of adolescents and adults who have sustained mild to moderate traumatic brain injuries (MTBI). The authors focus on providing practical suggestions for developing individualized therapy tasks to promote a client's successful return to the demands of the home, school, or work environment. Nine chapters cover the diversified roles of the speech language pathologist, the assessment of MTBI, treatment options (including establishing a positive therapeutic relationship), treating complex attention

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impairments, treating functional and prospective memory impairments, treating word retrieval and thought formulation impairments, treating information processing impairments (auditory and visual), treating executive functioning impairments, and therapy documentation, transition, and discharge. Each chapter includes therapy tasks, home practice tasks, and suggestions for families (including patient and family handouts). The text concludes with a reference list and subject index. 26 references. •

Children with traumatic brain injury: A parent's guide Source: Bethesda, MD: Woodbine House. 2001. 482 pp. Contact: Available from Woodbine House, 6510 Bells Mill Road, Bethesda, MD 20817. Telephone: (800) 843-7323 or (301) 897-3570 / fax: (301) 897- 5838 / e-mail: [email protected] / Web site: http://www.woodbinehouse.com. $17.95; plus shipping and handling. Summary: This book is written for parents of children who have suffered traumatic brain injury (TBI) to help them navigate the medical and educational systems and to find additional information and support for the family and the child. Chapter topics include defining TBI; rehabilitation and medical concerns; coping as a family; helping the child adjust; how TBI affects learning and thinking, speech and language, and behavior; strategies for managing behavior; the educational needs of children with TBI; and legal issues for families. An appendix provides scales used to assess patients with TBI. The book also contains a glossary, reading list, resource guide, notes, and an index.

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Coping with Mild Traumatic Brain Injury Source: Garden City Park, NY: Avery Publishing Group, Inc. 1998. 352 p. Contact: Available from Avery Publishing Group, Inc. 120 Old Broadway, Garden City Park, NY 11040. (800) 548-5757. PRICE: $14.95 (retail price); bulk rates available. ISBN: 0895297914. Summary: This book presents a guide to coping with mild traumatic brain injury (MTBI), a problem resulting from car accidents, falls, sports injuries, work-related accidents, and physical assault. The authors note that MTBI is commonly misdiagnosed because the symptoms are unpredictable and can be mistaken for those of many other conditions. The authors first review how the brain works and how it can be injured, the procedures used to diagnose brain injury, and the different treatments available. They then examine the most common physical, mental, and psychological symptoms of brain injury, explaining why each occurs and what can be done about it, and offering practical suggestions for coping with the problem. Also covered are financial, insurance, and family issues; the rehabilitation process; and eventual outcomes. Most of the chapters deal with one particular aftereffect of MTBI and provide a real-life story, an explanation of why the symptom or problem occurs, information about treatment, and practical suggestions for coping with the problem. Chapters cover specific problems including fatigue, headaches, dizziness, problems with sexuality, vision problems, hearing problems, sensory and metabolic disturbances, muscular and motor problems, and seizures. Other problems relate to attention and concentration, memory, reasoning and understanding, speech and language, academic performance, moods and behaviors, psychiatric disorders, and grieving. The book concludes with an extensive resource section that provides additional guidance and sources of support.

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Pediatric Brain Injury: A Practical Resource Source: San Antonio, TX: Communication Skill Builders, Inc. 1993. 192 p. Contact: Available from Communication Skill Builders. Psychological Corporation, Order Service Center, P.O. Box 839954, San Antonio, TX 78283-3954. Voice (800) 2118378; TTY (800) 723-1318; Fax (800) 232-1223. PRICE: $52.00 plus shipping and handling. ISBN: 0884506436. Summary: This book, intended for speech-language pathologists, parents, teachers, and students, presents information on treatment of children who experience brain injury after a history of normal development. The authors discuss the nature and incidence of brain injury in children, the philosophy of therapy, suggestions for working with parents and family members, and current research on brain injury in children. Factors in the prevention of injury to children are also discussed. Specific topics include closed head injury, open head injury, anoxia, infection, the structure of the brain, diagnostic tests used to confirm or classify brain injuries, the neuropathology of brain injury in children, the implications of normal development stages in recovery, coma, the multidisciplinary care team involved in treating patients with brain injury, the family's role, philosophies of therapy, the functionally comatose child, the structure-dependent child, the concrete processor, issues of feeding, the continuum of care, and caring for the caregivers. For each of classification of brain injury, the authors discuss symptoms and specific therapeutic recommendations. The book concludes with a bibliography and appendices on levels of consciousness, suggested tests and assessment tools, and suggested language and cognitive activities. 73 references. (AA-M).

Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “brain injuries” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “brain injuries” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “brain injuries” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •

An Educational Challenge: Meeting the Needs of Students With Brain Injury by Dana S. Deboskey (1996); ISBN: 188285537X; http://www.amazon.com/exec/obidos/ASIN/188285537X/icongroupinterna

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An Educator's Manual: What Educators Need to Know About Students With Brain Injury by Ronald C. Savage (Editor), et al (1995); ISBN: 0927093030; http://www.amazon.com/exec/obidos/ASIN/0927093030/icongroupinterna

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Analysis, Understanding, and Presentation of Cases Involving Traumatic Brain Injury by Charles N. Simkins (1994); ISBN: 0927093014; http://www.amazon.com/exec/obidos/ASIN/0927093014/icongroupinterna

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Assisting Survivors of Traumatic Brain Injury: The Role of Speech-Language Pathologists by Karen Hux (Editor), Victoria Sutton (2003); ISBN: 0890798958; http://www.amazon.com/exec/obidos/ASIN/0890798958/icongroupinterna

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Awareness of Deficit After Brain Injury: Clinical and Theoretical Issues by George P. Prigatano (Editor), Daniel L. Schacter (Editor) (1991); ISBN: 0195059417; http://www.amazon.com/exec/obidos/ASIN/0195059417/icongroupinterna

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Behind the Shadows in Silent Screams: Success Stories of Traumatic Brain Injury Cases by Maria A. Hernandez (2002); ISBN: 1401061133; http://www.amazon.com/exec/obidos/ASIN/1401061133/icongroupinterna

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Brain Hypothermia: Pathology, Pharmacology and Treatment of Severe Brain Injury by N. Hayashi (Editor) (2000); ISBN: 4431702776; http://www.amazon.com/exec/obidos/ASIN/4431702776/icongroupinterna

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Brain Injury and After : Towards Improved Outcome by F. D. Rose (Editor), D. A. Johnson (Editor) (1996); ISBN: 0471952761; http://www.amazon.com/exec/obidos/ASIN/0471952761/icongroupinterna

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Brain Injury and Gender Role Strain: Rebuilding Adult Lifestyles After Injury by Sharon A., Phd, Otr Gutman (2001); ISBN: 0789011867; http://www.amazon.com/exec/obidos/ASIN/0789011867/icongroupinterna

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Brain Injury and Pediatric Cardiac Surgery by Richard A. Jonas (Editor), et al (1996); ISBN: 0750695676; http://www.amazon.com/exec/obidos/ASIN/0750695676/icongroupinterna

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Brain Injury Pathway by McDermott (1998); ISBN: 0127850651; http://www.amazon.com/exec/obidos/ASIN/0127850651/icongroupinterna

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Brain Injury Rehabilitation: An Overview by William Burke (Editor) (1999); ISBN: 1882855663; http://www.amazon.com/exec/obidos/ASIN/1882855663/icongroupinterna

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Brain Injury Rehabilitation: Brain Injury Rehab With Children and Adolescents (Professional Series, Vol 12) by Mark Ylvisaker, William H. Burke (Editor) (1996); ISBN: 1882855507; http://www.amazon.com/exec/obidos/ASIN/1882855507/icongroupinterna

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Brain Injury Rehabilitation: Developing Adaptive Work Behaviors (Professional Series , Vol 17) by Frank D. Lewis (1997); ISBN: 1882855647; http://www.amazon.com/exec/obidos/ASIN/1882855647/icongroupinterna

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Brain Injury Rehabilitation: Developing Social Skills (The Hdi Professional Series on Traumatic Brain Injury) by William H. Burke (Editor) (1997); ISBN: 1882855574; http://www.amazon.com/exec/obidos/ASIN/1882855574/icongroupinterna

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Brain Injury Rehabilitation: Developing the Tbi Rehab Plan by William Burke (1997); ISBN: 1882855612; http://www.amazon.com/exec/obidos/ASIN/1882855612/icongroupinterna

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Brain Injury Rehabilitation: Increasing Self-Awareness by Mark L. Guth, et al (1999); ISBN: 1882855620; http://www.amazon.com/exec/obidos/ASIN/1882855620/icongroupinterna

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Brain Injury Rehabilitation: Management of Communication and Language Deficits (Professional Series, No 20) by Mark Ylvisaker (1997); ISBN: 1882855604; http://www.amazon.com/exec/obidos/ASIN/1882855604/icongroupinterna

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Brain Injury Rehabilitation: Management of Memory Disorders (The Professional Series , Vol 8) by Amy Weinstein, et al (1995); ISBN: 1882855396; http://www.amazon.com/exec/obidos/ASIN/1882855396/icongroupinterna

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Brain Injury Rehabilitation: Managing Anger & Aggression (Professional Series on Traumatic Brain Injury Volume 6) by Burke William H. (Editor) (1996); ISBN: 1882855531; http://www.amazon.com/exec/obidos/ASIN/1882855531/icongroupinterna

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Brain Injury Rehabilitation: Managing Anger and Aggression (Hdi Professional Series on Traumatic Brain Injury, Vol 6) by Michael D. Wesolowski (Editor), William H. Burke (Editor) (1996); ISBN: 1882855132; http://www.amazon.com/exec/obidos/ASIN/1882855132/icongroupinterna

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Brain Injury Rehabilitation: Managing Attention Deficits (Hdi Professional Series on Traumatic Brain Injury, No 7) by Richard Guare, William H. Burke (Editor) (1996); ISBN: 1882855493; http://www.amazon.com/exec/obidos/ASIN/1882855493/icongroupinterna

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Brain Injury Rehabilitation: Sexuality After Tbi (Professional Series , Vol 10) by William Burke (Editor), William Blackerby (Editor) (1994); ISBN: 1882855418; http://www.amazon.com/exec/obidos/ASIN/1882855418/icongroupinterna

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Brain Injury Rehabilitation: Supported Employment and Tbi (Professional Series , Vol 18) by William H. Burke (Editor), et al (1996); ISBN: 1882855256; http://www.amazon.com/exec/obidos/ASIN/1882855256/icongroupinterna

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Brain Injury Rehabilitation: Teaching Job Seeking Skills by Michael D. Wesolowski, et al (1998); ISBN: 1882855639; http://www.amazon.com/exec/obidos/ASIN/1882855639/icongroupinterna

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Brain Injury Survivor and Caregiver Education Manual by Aspen Reference Group, et al (1996); ISBN: 0834207443; http://www.amazon.com/exec/obidos/ASIN/0834207443/icongroupinterna

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Brain Injury: A Family Tragedy by Patt Abrahamson, et al (1997); ISBN: 1882855566; http://www.amazon.com/exec/obidos/ASIN/1882855566/icongroupinterna

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Brain Injury: A Home Based Cognitive Rehabilitation Program by Staff of the Tampa General Rehabilitation Center (1996); ISBN: 1882855582; http://www.amazon.com/exec/obidos/ASIN/1882855582/icongroupinterna

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Careers of Care: Survivors of Traumatic Brain Injury and the Response of Health and Social Care by P. E. Higham, Kay Phelps (1998); ISBN: 1857424255; http://www.amazon.com/exec/obidos/ASIN/1857424255/icongroupinterna

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Catastrophic Brain Injury by Harvey S. Levin (Editor), et al (1996); ISBN: 0195085337; http://www.amazon.com/exec/obidos/ASIN/0195085337/icongroupinterna

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Children With Traumatic Brain Injury: A Parent's Guide (The Special Needs Collection) by Lisa Schoenbrodt (Editor) (2003); ISBN: 0933149999; http://www.amazon.com/exec/obidos/ASIN/0933149999/icongroupinterna

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Clinical Management of Communication Problems in Adults With Traumatic Brain Injury (The Rehabilitation Institute of Chicago Publication Series) by Anita S. Halper, et al (2004); ISBN: 0944480144; http://www.amazon.com/exec/obidos/ASIN/0944480144/icongroupinterna

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Cognitive Effects of Early Brain Injury by Casey Dorman, Bilha Katzir (1994); ISBN: 0801848563; http://www.amazon.com/exec/obidos/ASIN/0801848563/icongroupinterna

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Cognitive Rehabilitation for Persons With Traumatic Brain Injury by Jeffrey S. Kreutzer (Editor), Paul Wehman (Editor) (1996); ISBN: 1883315158; http://www.amazon.com/exec/obidos/ASIN/1883315158/icongroupinterna

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Coming Home: A Discharge Manual for Families of Persons With a Brain Injury by Dana S., Phd Deboskey (Editor) (1996); ISBN: 1882855345; http://www.amazon.com/exec/obidos/ASIN/1882855345/icongroupinterna

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Communication Disorders Following Traumatic Brain Injury: Management of Cognitive, Language, and Motor Impairments by David R. Beukelman, Kathryn M. Yorkston (Editor) (1991); ISBN: 089079295X; http://www.amazon.com/exec/obidos/ASIN/089079295X/icongroupinterna

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Communication Problems After a Brain Injury or Stroke by Pritchett & Hull Associates (1996); ISBN: 0939838443; http://www.amazon.com/exec/obidos/ASIN/0939838443/icongroupinterna

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Confronting Traumatic Brain Injury : Devastation, Hope, and Healing by William J. Winslade, James S. Brady (1999); ISBN: 0300079427; http://www.amazon.com/exec/obidos/ASIN/0300079427/icongroupinterna

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Conquering the Darkness : One Woman's Story of Recovering from a Brain Injury by Deborah A. Quinn (1998); ISBN: 1557787638; http://www.amazon.com/exec/obidos/ASIN/1557787638/icongroupinterna

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Coping With Mild Traumatic Brain Injury (Coping With.) by Diane Roberts Stoler, et al (1998); ISBN: 0895297914; http://www.amazon.com/exec/obidos/ASIN/0895297914/icongroupinterna

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Cracked: Recovering after Traumatic Brain Injury by Lynsey Calderwood (2003); ISBN: 1843100657; http://www.amazon.com/exec/obidos/ASIN/1843100657/icongroupinterna

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Developing and Implementing Critical Paths in Rehabilitation: Brain Injury Pathway by Michael T., Phd McDermott, et al (1998); ISBN: 0761624724; http://www.amazon.com/exec/obidos/ASIN/0761624724/icongroupinterna

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Developmental Brain Injury by S. J. Vannucci (Editor), et al (2003); ISBN: 3805575726; http://www.amazon.com/exec/obidos/ASIN/3805575726/icongroupinterna

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Educational Dimensions of Acquired Brain Injuries by Ronald C. Savage (Editor), Gary F. Wolcott (Editor) (1994); ISBN: 0890795983; http://www.amazon.com/exec/obidos/ASIN/0890795983/icongroupinterna

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Family Support Programs and Rehabilitation: A Cognitive-Behavioral Approach to Traumatic Brain Injury by Hamish P.D. Godfrey, Louise Margaret Smith (1995); ISBN: 0306449323; http://www.amazon.com/exec/obidos/ASIN/0306449323/icongroupinterna

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Group Activities for Adults with Brain Injury by Cindy Drolet (Editor), et al (1998); ISBN: 1883315336; http://www.amazon.com/exec/obidos/ASIN/1883315336/icongroupinterna

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Heading for Better Care: Commissioning and Providing Mental Health Services for People with Huntington's Disease, Acquired Brain Injury and Early Onset Dementia (An NHS Health Advisory Service Thematic Review) by Richard Williams, et al (1997); ISBN: 0113219377; http://www.amazon.com/exec/obidos/ASIN/0113219377/icongroupinterna

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Hiring the Person With a Brain Injury: What to Expect (1999); ISBN: 1882855655; http://www.amazon.com/exec/obidos/ASIN/1882855655/icongroupinterna

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I'll Carry the Fork!: Recovering a Life After Brain Injury by Kara L. Swanson, Mike Chrumka (Illustrator) (1999); ISBN: 0933670044; http://www.amazon.com/exec/obidos/ASIN/0933670044/icongroupinterna

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Intracranial Pressure and Neuromonitoring in Brain Injury: Proceedings of the Tenth International Icp Symposium, Williamsburg, May 25-29, 1997 by Va.)/ Marmarou, Anthony International Icp Symposium 1997 Williamsburg, et al (1998); ISBN: 3211830944; http://www.amazon.com/exec/obidos/ASIN/3211830944/icongroupinterna

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Life After Brain Injury: Who Am I? (Coping Series , Vol 4) by Tampa General Rehabilitation Center Staf (1996); ISBN: 1882855477; http://www.amazon.com/exec/obidos/ASIN/1882855477/icongroupinterna

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Listening in the Silence, Seeing in the Dark: Reconstructing Life After Brain Injury by Ruthann Knechel Johansen (2002); ISBN: 0520231147; http://www.amazon.com/exec/obidos/ASIN/0520231147/icongroupinterna

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Living on Equal Terms: Supporting People With Aquired Brain Injury in Their Own Homes (1998); ISBN: 1861341105; http://www.amazon.com/exec/obidos/ASIN/1861341105/icongroupinterna

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Living with Brain Injury by Philip L. Fairclough (2002); ISBN: 1843100592; http://www.amazon.com/exec/obidos/ASIN/1843100592/icongroupinterna

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Living With Brain Injury: A Guide for Families and Caregivers by Sonia Griffin Acorn (Editor), Penny Offer (Editor) (1998); ISBN: 0802081037; http://www.amazon.com/exec/obidos/ASIN/0802081037/icongroupinterna

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Management and Prognosis of Severe Traumatic Brain Injury (Book ) with CDROM by Brain Trauma Foundation, American Association of Neurological Sur (2000); ISBN: 097031440X; http://www.amazon.com/exec/obidos/ASIN/097031440X/icongroupinterna

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Management of Communication & Language Deficits (Professional Series on Traumatic Brain Injury Series, Vol 20) by William H. Burke (Editor) (1996); ISBN: 1882855272; http://www.amazon.com/exec/obidos/ASIN/1882855272/icongroupinterna

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Maximizing Brain Injury Recovery: Integrating Critical Care and Early Rehabilitation by Linda E. Mackay, et al (2004); ISBN: 0944480624; http://www.amazon.com/exec/obidos/ASIN/0944480624/icongroupinterna

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Mild Brain Injury: An Overview (Applied Neuropsychology, Vol 4, No 1, 1997) by Thomas L. Bennett (Editor), Michael J. Raymond (Editor) (1997); ISBN: 0805898689; http://www.amazon.com/exec/obidos/ASIN/0805898689/icongroupinterna

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Mild Traumatic Brain Injury: A Clinician's Guide by Michael J. Raymond (Editor), et al (1999); ISBN: 0890798095; http://www.amazon.com/exec/obidos/ASIN/0890798095/icongroupinterna

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Neuromonitoring in Brain Injury (Acta Neurochirurgica. Supplement 75) by Ross Bullock (Editor), et al (2000); ISBN: 321183379X; http://www.amazon.com/exec/obidos/ASIN/321183379X/icongroupinterna

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Neuropsychiatry of Traumatic Brain Injury by Stuart C. Yudofsky (Editor), et al (1994); ISBN: 0880485388; http://www.amazon.com/exec/obidos/ASIN/0880485388/icongroupinterna

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Normal Again: Redefining Life With Brain Injury by Dennis P. Swiercinsky (2002); ISBN: 0595237169; http://www.amazon.com/exec/obidos/ASIN/0595237169/icongroupinterna

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Objects in Mirror Are Closer Than They Appear: Inside Brain Injury by Sol Mogerman (2001); ISBN: 0595209424; http://www.amazon.com/exec/obidos/ASIN/0595209424/icongroupinterna

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Occupational Therapy Approaches to Traumatic Brain Injury by Jerry A. Johnson (Editor), Laura Krefting (Editor) (1990); ISBN: 1560240644; http://www.amazon.com/exec/obidos/ASIN/1560240644/icongroupinterna

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Our FAScinating Journey: Keys to Brain Potential Along the Path of Prenatal Brain Injury by Jodee Kulp (2002); ISBN: 0963707248; http://www.amazon.com/exec/obidos/ASIN/0963707248/icongroupinterna

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Parenting a Child With Traumatic Brain Injury by Barry Kent Hughes (1990); ISBN: 0398056463; http://www.amazon.com/exec/obidos/ASIN/0398056463/icongroupinterna

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Patients With Brain Injury: A Family Guide to Assisting in Speech, Language, and Cognitive Rehabilitation by Roselyn M. Cera (1995); ISBN: 9997725581; http://www.amazon.com/exec/obidos/ASIN/9997725581/icongroupinterna

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Pediatric Brain Injury: A Practical Resource by Carole Wedel Sellars, Candace Hill Vegter (2000); ISBN: 0761678123; http://www.amazon.com/exec/obidos/ASIN/0761678123/icongroupinterna

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Pediatric Traumatic Brain Injury by Stephen R. Hooper (Author), Jeffrey H. Snow (Author) (1994); ISBN: 0803951817; http://www.amazon.com/exec/obidos/ASIN/0803951817/icongroupinterna

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Perinatal Brain Injury: Proceedings and Abstracts of the Second Hershey Conference on Developmental Cerebral Blood Flow and Metabolism, Hershey, Pa., June 8-11, 2000 by S. J. Vannucci (Editor), et al (2001); ISBN: 3805572808; http://www.amazon.com/exec/obidos/ASIN/3805572808/icongroupinterna

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Physical Therapy for Traumatic Brain Injury (Clinics in Physical Therapy) by Jacqueline Montgomery (Editor) (1995); ISBN: 0443089086; http://www.amazon.com/exec/obidos/ASIN/0443089086/icongroupinterna

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Psychotherapeutic Interventions for Adults with Brain Injury or Stroke: A Clinician's Treatment Resource by Karen G. Langer (Editor), et al (1999); ISBN: 1887841237; http://www.amazon.com/exec/obidos/ASIN/1887841237/icongroupinterna

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Recovery After Traumatic Brain Injury (Institute for Research in Behavioral Neuroscience) by Barbara P. Uzzell (Editor), Henry H. Stonnington (Editor) (1996); ISBN: 0805818243; http://www.amazon.com/exec/obidos/ASIN/0805818243/icongroupinterna

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Rehabilitation of Persons With Traumatic Brain Injury: Nih Consensus Statement by Kristjan T. Ragnarsson (Editor) (1998); ISBN: 0756725518; http://www.amazon.com/exec/obidos/ASIN/0756725518/icongroupinterna

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Rehabilitation of the Adult and Child With Traumatic Brain Injury by Mitchell Rosenthal (Editor), et al (1999); ISBN: 0803603916; http://www.amazon.com/exec/obidos/ASIN/0803603916/icongroupinterna

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Rehabilitation of Visual Deficits After Brain Injury (Neuropsychological Rehabilitation: A Modular Handbook) by Josef Zihl (2000); ISBN: 0863778984; http://www.amazon.com/exec/obidos/ASIN/0863778984/icongroupinterna

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Role of Reactive Oxygen Species in Traumatic Brain Injury: Experimental Studies in the Rat (Comprehensive Summaries of Uppsala Dissertations from the Faculty of mediciNe, 1048) by Niklas Marklund (2001); ISBN: 9155450539; http://www.amazon.com/exec/obidos/ASIN/9155450539/icongroupinterna

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Sexual Difficulties After Traumatic Brain Injury and Ways to Deal With It by Ronit Aloni, Shlomo Katz (2003); ISBN: 0398073678; http://www.amazon.com/exec/obidos/ASIN/0398073678/icongroupinterna

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Shock, Sepsis, and Organ Failure: I Brain Damage Secondary to HemorrhagicTraumatic Shock: II Brain Damage Secondary to Sepsis: III Brain Damage Secondary to Traumatic Brain Injury by Austria)/ Schlag, Gunther/ Traber, D. Wiggers Bernard Conference 1996 Krumbach (1997); ISBN: 0387624198; http://www.amazon.com/exec/obidos/ASIN/0387624198/icongroupinterna

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Signs and Strategies for Educating Students With Brain Injuries: A Practical Guide for Teachers and Schools by Marilyn Lash, et al (1995); ISBN: 1882855337; http://www.amazon.com/exec/obidos/ASIN/1882855337/icongroupinterna

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Students With Acquired Brain Injury: The School's Response by Ann Glang (Editor), et al (1997); ISBN: 1557662851; http://www.amazon.com/exec/obidos/ASIN/1557662851/icongroupinterna

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Teaching Persons With a Brain Injury: What to Expect (Hdi Coping Series on Brain Injury, Vol 5) by Tampa General Rehabilitation Center (1996); ISBN: 1882855000; http://www.amazon.com/exec/obidos/ASIN/1882855000/icongroupinterna

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The Brain Injury Glossary by L. Don Lehmkuhl (Editor) (1993); ISBN: 1882855329; http://www.amazon.com/exec/obidos/ASIN/1882855329/icongroupinterna

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The Cognitive Rehabilitation Workbook: A Dynamic Assessment Approach for Adults With Brain Injury by Pamela M. Dougherty, Mary Vining Radomski (2004); ISBN: 0944480233; http://www.amazon.com/exec/obidos/ASIN/0944480233/icongroupinterna

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The Evaluation and Treatment of Mild Traumatic Brain Injury by Nils R. Varney (Editor), Richard J. Roberts (Editor) (1999); ISBN: 0805823948; http://www.amazon.com/exec/obidos/ASIN/0805823948/icongroupinterna

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The Mild Traumatic Brain Injury Workbook: Your Program for Regaining Cognitive Function and Overcoming Emotional Pain by Douglas J. Mason (2004); ISBN: 1572243619; http://www.amazon.com/exec/obidos/ASIN/1572243619/icongroupinterna

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The Official Patient's Sourcebook on Traumatic Brain Injury: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2003); ISBN: 0597835373; http://www.amazon.com/exec/obidos/ASIN/0597835373/icongroupinterna

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The Role of Neurotransmitters in Brain Injury by Mordecai Y.-T Globus, W. Dalton Dietrich (Editor) (1992); ISBN: 0306442558; http://www.amazon.com/exec/obidos/ASIN/0306442558/icongroupinterna

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The Role of the Family in Tbi Rehab (Professional Series on Traumatic Brain Injury; Vol 19) by William H. Burke (Editor) (1996); ISBN: 1882855469; http://www.amazon.com/exec/obidos/ASIN/1882855469/icongroupinterna

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The Traumatic Brain Injury Handbook by Camilia Anne Czubaj (2002); ISBN: 0972123806; http://www.amazon.com/exec/obidos/ASIN/0972123806/icongroupinterna

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Traumatic Brain Injury Activities: Back into Life (Functional Communication Series) by Andrew K. Gruen, Lynn S. Gruen (1994); ISBN: 0930599950; http://www.amazon.com/exec/obidos/ASIN/0930599950/icongroupinterna

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Traumatic Brain Injury and Neuorpsychological Impairment: Sensorimotor, Cognitive, Emotional and Adaptive Problems of Children and Adults by Rolland S. Parker (1990); ISBN: 0387972390; http://www.amazon.com/exec/obidos/ASIN/0387972390/icongroupinterna

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Traumatic Brain Injury: Rehabilitation for Everyday Adaptive Living by Jennie Ponsford, et al (1997); ISBN: 086377377X; http://www.amazon.com/exec/obidos/ASIN/086377377X/icongroupinterna

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Visual & Vestibular Consequences of Acquired Brain Injuries by Irwin B. Suchoff (Editor), et al (2001); ISBN: 0943599423; http://www.amazon.com/exec/obidos/ASIN/0943599423/icongroupinterna

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Vocational Evaluation & Traumatic Brain Injury: A Procedural Manual by Stephen W. Thomas (1991); ISBN: 0916671941; http://www.amazon.com/exec/obidos/ASIN/0916671941/icongroupinterna

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Vocational Rehabilitation: For Persons With Traumatic Brain Injury by Paul Wehman, et al (1990); ISBN: 0834201356; http://www.amazon.com/exec/obidos/ASIN/0834201356/icongroupinterna

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Waiting to Clear: Brain Injury: Early Stages of Recovery/Book and Notebook by Mary M. Castiglione, Cynthia C. Johnson (1994); ISBN: 0939838354; http://www.amazon.com/exec/obidos/ASIN/0939838354/icongroupinterna

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What Legislators Need to Know About Traumatic Brain Injuries by Barbara Wright (1993); ISBN: 1555166601; http://www.amazon.com/exec/obidos/ASIN/1555166601/icongroupinterna

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Working After Brain Injury: What Can I Do? by Dana S., Ph.D. Deboskey (Editor), et al (1996); ISBN: 1882855353; http://www.amazon.com/exec/obidos/ASIN/1882855353/icongroupinterna

The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “brain injuries” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 11

In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed

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A study of the effect of evipan on the flicker fusion intensity in brain injuries. Author: Berg, Ole.; Year: 1964; Copenhagen, Munksgaard, 1949

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Experimental brain injury Author: Persson, Lennart.; Year: 1966; Göteborg: [s.n.], 1976

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Korsakoff-like amnesic syndrome in penetrating brain injury; a study of Finnish war veterans. [Translated from the Finnish]. Author: Jarho, Leo.; Year: 1949; Copenhagen, Munksgaard, 1973; ISBN: 8716010949 http://www.amazon.com/exec/obidos/ASIN/8716010949/icongroupinterna

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The child's book about brain injury with an introduction for parents. Author: Gardner, Richard A.; Year: 1964; New York, [New York] Assn. for

Chapters on Brain Injuries In order to find chapters that specifically relate to brain injuries, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and brain injuries using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “brain injuries” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on brain injuries: •

Assessment of Mild-to-Moderate Traumatic Brain Injury Source: in Green, B.S.; Sevens, K.M.; Wolfe, T.D.W. Mild Traumatic Brain Injury: A Therapy and Resource Manual. San Diego, CA: Singular Publishing Group, Inc. 1998. p. 19-60. Contact: Available from Singular Publishing Group, Inc. 401 West 'A' Street, Suite 325, San Diego, CA 92101-7904. (800) 521-8545 or (619) 238-6777. Fax (800) 774-8398 or (619) 238-6789. E-mail: [email protected]. Website: www.singpub.com. PRICE: $49.95 plus shipping and handling. ISBN: 1565938275. Summary: This chapter is from a therapy and reference manual created in response to the unique needs of adolescents and adults who have sustained mild to moderate traumatic brain injuries (MTBI). The authors focus on providing practical suggestions for developing individualized therapy tasks to promote a client's successful return to the demands of the home, school, or work environment. This chapter addresses the assessment of MTBI. Topics include neuropsychological evaluation and assessment considerations, the importance of an integrated assessment, test administration, complex attention, memory skills, verbal communication skills, written communication skills, verbal information processing skills, written information processing skills, executive functioning skills, reasoning skills, and mathematical skills. A final section covers preparing the cognitive language evaluation report, including analyzing test scores, interpreting supplemental information, and sharing assessment results. The chapter

in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.

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concludes with extensive appendices, including client interview questionnaires, sample evaluation segments, vocational recommendations, and publisher and purchasing information for standardized tests. 10 references. •

Traumatic Brain Injury Source: in Vinson, B.P. Essentials for Speech-Language Pathologists. San Diego, CA: Singular Publishing Group. 2001. p. 397-407. Contact: Available from Thomson Learning Group. P.O. Box 6904, Florence, KY 41022. (800) 842-3636. Fax (606) 647-5963. Website: www.singpub.com. PRICE: $49.95 plus shipping and handling. ISBN: 0769300715. Summary: Traumatic brain injury (TBI) is often referred to as a closed head injury and is typically classified as mild, moderate, or severe. The Individuals With Disabilities Education Act (IDEA) calls for the reintegration of children with TBI into the classroom, and teachers report that language disabilities are the factors that cause the greatest interference with success in school. This chapter on TBI is from a textbook that is designed to help new professionals with the transition to clinical practice in speech language pathology. The author first defines TBI, then reports the types of injuries that may be involved, the underlying complications, the effects (initial effects, acute recovery period, and residual effects), and pediatric versus adult aphasia (impairment of language comprehension). The author then discusses assessment considerations (including specific assessment instruments) and treatment strategies. The author concludes by emphasizing the importance of following children with TBI closely throughout their academic careers to monitor possible residual deficits that may play a role in a child's educational and social progress. In addition, the speech language pathologist should track the patient's progress and maintenance of skills once the client has been discharged from active therapy. Cognitive and communicative demands will increase as the client explores reentering different social and vocational aspects of life, and the need for additional therapy may become apparent. 3 tables.

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CHAPTER 8. MULTIMEDIA ON BRAIN INJURIES Overview In this chapter, we show you how to keep current on multimedia sources of information on brain injuries. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.

Video Recordings An excellent source of multimedia information on brain injuries is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “brain injuries” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “brain injuries” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on brain injuries: •

Breaking the Silence Barrier Source: Princeton, NJ: Films for the Humanities and Sciences. 1996. (videocassette). Contact: Available from Films for the Humanities and Sciences. P.O. Box 2053, Princeton, NJ 08543-2053. (800) 257-5126 or (609) 275-1400. Fax (609) 275-3767. E-mail: [email protected]. Website: www.films.com. PRICE: $99.00 plus shipping and handling. Item number BVL6244. Summary: Stereotypes and misconceptions can often create the most daunting obstacles for people with disabilities. This videotape program is one in a series of programs demonstrating how technology is reshaping the lives of people with disabilities and transforming society's attitudes about who they are and what they can do. This videotape program reports on creative technologies that are being used to help people with autism, traumatic brain injuries, and learning and speech disabilities. Temple Grandin, an autistic woman with a Ph.D. in animal science, explains her 'squeeze machine' which uses deep pressure therapy to help ease the hyperacute sensory

122 Brain Injuries

dysfunction that often accompanies autism. Neurologist Oliver Sacks shares his views on how people with autism can find meaning in their own distinctive way. Also profiled is Bob Williams, who is the first person with a significant speech disability to hold a major Federal office, and several people with learning disabilities and traumatic brain injuries who have improved their lives by using multimedia software programs.

Bibliography: Multimedia on Brain Injuries The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in brain injuries (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on brain injuries: •

Helping the patient with brain injury to learn [videorecording]: self-feeding as a place to begin Source: produced by the Drucker Brain Injury Center of Moss Rehabilitation Hospital; Year: 1987; Format: Videorecording; Philadelphia, PA: The Hospital, c1987

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Patterns of brain injury: on rounds in neurology [filmstrip] Source: Trainex Corporation; Year: 1978; Format: Filmstrip; Garden Grove, Calif.: Trainex, c1978

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The Brain: vital and protected; Brain injury and intracranial pressure [filmstrip] Source: Trainex Corporation; Year: 1978; Format: Filmstrip; Garden Grove, Calif.: Trainex, c1978

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Traumatic brain injury overview [videorecording]. Year: 1985; Videorecording; Sacramento, Calif.: Head Trauma Support Project, c1985

Format:

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CHAPTER 9. PERIODICALS AND NEWS ON BRAIN INJURIES Overview In this chapter, we suggest a number of news sources and present various periodicals that cover brain injuries.

News Services and Press Releases One of the simplest ways of tracking press releases on brain injuries is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “brain injuries” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to brain injuries. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “brain injuries” (or synonyms). The following was recently listed in this archive for brain injuries: •

Recovery time increases with multiple sports-related traumatic brain injuries Source: Reuters Medical News Date: November 18, 2003

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Alzheimer gene ups seizure risk after brain injury Source: Reuters Health eLine Date: June 17, 2003

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APOE-e4 genotype increases seizure risk after brain injury Source: Reuters Medical News Date: June 16, 2003

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Prematurity, infection behind newborn brain injury Source: Reuters Health eLine Date: June 11, 2003

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Hypothermia may improve outcome of traumatic brain injury Source: Reuters Industry Breifing Date: June 10, 2003

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Cooling the body may help treat severe brain injury Source: Reuters Health eLine Date: June 10, 2003

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New guidelines address management of severe brain injuries in children Source: Reuters Medical News Date: June 06, 2003

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Fewer football players dying of brain injury Source: Reuters Health eLine Date: April 18, 2003

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Baby brain injury often occurs before labor: report Source: Reuters Health eLine Date: January 31, 2003

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Crash victim's face injury may signal brain injury Source: Reuters Health eLine Date: January 20, 2003

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Study questions whether cycle helmets prevent brain injury Source: Reuters Medical News Date: January 07, 2003

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Cycle helmets may not prevent brain injury: group Source: Reuters Health eLine Date: January 07, 2003

•

Post-fall brain injury deaths rise among elderly: CDC Source: Reuters Health eLine Date: December 06, 2002

•

Fall-related traumatic brain injury deaths up in the elderly Source: Reuters Medical News Date: December 06, 2002

•

Full bed rest after mild traumatic brain injury not recommended Source: Reuters Medical News Date: August 16, 2002

•

Area of brain injury linked with PTSD symptoms in children Source: Reuters Medical News Date: August 02, 2002

•

IL-1 leads to inflammatory response that exacerbates damage after brain injury Source: Reuters Medical News Date: July 31, 2002

Periodicals and News

•

Minocycline protects the neonatal rats from hypoxic-ischemic brain injury Source: Reuters Industry Breifing Date: July 29, 2002

•

Low-level falls can cause greater pediatric brain injury than previously thought Source: Reuters Medical News Date: April 09, 2002

•

Community rehabilitation beneficial after severe traumatic brain injury Source: Reuters Medical News Date: February 14, 2002

•

Against guidelines, hyperventilation continues for traumatic brain injury Source: Reuters Medical News Date: February 14, 2002

•

Rear seat passengers at higher brain injury risk Source: Reuters Health eLine Date: January 28, 2002

•

Young men most likely to survive brain injury Source: Reuters Health eLine Date: November 12, 2001

•

Tizanidine improves spastic hypertonia after brain injury Source: Reuters Industry Breifing Date: September 20, 2001

•

Clinical pathways improve care of patients with traumatic brain injury Source: Reuters Medical News Date: September 04, 2001

•

Brain injury group to study rollercoaster rides Source: Reuters Health eLine Date: August 24, 2001

•

Disney settles brain injury lawsuit over park ride Source: Reuters Health eLine Date: June 22, 2001

•

Disney says it will hand over brain injury records Source: Reuters Health eLine Date: June 11, 2001

•

Brain injury reality scares young felons straight Source: Reuters Health eLine Date: April 25, 2001

•

Skills training after brain injury shows promise Source: Reuters Health eLine Date: April 09, 2001

•

Skills training after brain injury shows performance benefit Source: Reuters Medical News Date: April 09, 2001

•

Therapeutic target for newborn brain injury found Source: Reuters Health eLine Date: March 01, 2001

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•

Cooling body does not prevent brain injury Source: Reuters Health eLine Date: February 22, 2001

•

Induced hypothermia not effective in patients with severe brain injury Source: Reuters Medical News Date: February 21, 2001

•

Creatine supplementation may be neuroprotective in traumatic brain injury Source: Reuters Industry Breifing Date: November 21, 2000

•

Glucocorticoids influence BDNF expression after brain injury Source: Reuters Medical News Date: November 10, 2000

•

Women have poorer outcomes than men after traumatic brain injury Source: Reuters Medical News Date: November 06, 2000

•

Blood alcohol level at time of traumatic brain injury predicts long-term mortality Source: Reuters Medical News Date: November 03, 2000

•

Guitar player loses his music due to brain injury Source: Reuters Health eLine Date: September 25, 2000

•

Home rehabilitation as good as in-hospital treatment for traumatic brain injury Source: Reuters Medical News Date: June 21, 2000

•

Three-month Glasgow Outcome score predicts long-term outcome of brain injury Source: Reuters Medical News Date: April 13, 2000

•

Brain injury from ischemic stroke can be reversed Source: Reuters Medical News Date: April 11, 2000 The NIH

Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name.

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Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “brain injuries” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “brain injuries” (or synonyms). If you know the name of a company that is relevant to brain injuries, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “brain injuries” (or synonyms).

Academic Periodicals covering Brain Injuries Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to brain injuries. In addition to these sources, you can search for articles covering brain injuries that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”

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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.

U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for brain injuries. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with brain injuries. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The

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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to brain injuries: Botulinum Toxin Type A •

Parenteral-Local - U.S. Brands: Botox http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202608.html

Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.

Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.

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APPENDICES

133

APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.

NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: •

Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm

•

National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/

•

National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html

•

National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25

•

National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm

•

National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm

•

National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375

•

National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/

12

These publications are typically written by one or more of the various NIH Institutes.

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•

National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm

•

National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/

•

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm

•

National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm

•

National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/

•

National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/

•

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm

•

National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html

•

National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm

•

National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm

•

National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm

•

National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html

•

National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm

•

Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp

•

National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/

•

National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp

•

Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html

•

Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm

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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 •

Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html

•

HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html

•

NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html

•

Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/

•

Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html

•

Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html

•

Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/

•

Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html

•

Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html

•

Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html

•

MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html

13

Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.

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•

Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html

•

Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database

A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “brain injuries” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “brain injuries” (or synonyms) into the “For these words:” box. The following is a sample result: •

Funding traumatic brain injury services Source: Denver, CO: National Conference of State Legislatures. 2001. 33 pp. Contact: Available from National Conference of State Legislatures, 1560 Broadway, Suite 700, Denver, CO 80202. Telephone: (303) 830-2200 or (303) 830-2054 book order line / fax: (303) 863-8003 / e-mail: [email protected] / Web site: http://www.ncsl.org. $15.00, plus shipping and handling. Summary: This brief offers an overview of traumatic brain injury (TBI) and its effect on individuals and society, particularly in the need for and use of a variety of health and assistive services. It is designed to serve as a guide for states to identify resources and funding streams to help address the range of associated issues. Topics discussed include defining TBI; outlining legislative concerns; determining how prevalent TBI is in the United States in relation to other chronic illnesses and conditions; and identifying legislation and funding sources covering TBI. The appendix contains state-by-state information about federal and state spending on TBI, data collected in a study conducted by the Brain Injury Association of America Inc. in 1999. Statistical information is presented in charts, graphs, and tables throughout the report. [Funded by the Maternal and Child Health Bureau].

•

Report of the NIH Consensus Development Conference on the Rehabilitation of Persons With Traumatic Brain Injury Source: Rockville, MD: National Institute of Child Health and Human Development. 1999. 530 pp. Contact: Available from National Institute of Child Health and Human Development Clearinghouse, P.O. Box 3006, Rockville, MD 20847. Telephone: (800) 370-2943 TTY: (888) 320-6942 / fax: (301) 984-1473 / e-mail: [email protected] / Web site: http://www.nichd.nih.gov/publications/info.htm. Available at no charge. Summary: This consensus development statement is meant to inform the biomedical research and clinical practice communities of the results of the National Institutes of Health Consensus Development Conference on Rehabilitation of Persons with Traumatic Brain Injury, held October 26- 28, 1998 in Bethesda, Maryland. The statement

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provides information on effective rehabilitation measures for persons who have suffered a traumatic brain injury as well as conclusions and recommendations of the consensus panel. Additional topics include epidemiology of brain injury, hospitalization trends, family consequences, the economics of rehabilitation, research in cognitive rehabilitation, models of care, access to services, and ethical considerations in traumatic brain injury research. Report sections include the consensus statement, a list of consensus development panel, speakers, planning committee, the conference abstracts, and the consensus panel report. Also included is a listing of acronyms/abbreviations and three appendices containing three studies on traumatic brain injury. •

TBI: Traumatic Brain Injury State Demonstration Grant Program: Project abstracts, FY__ Source: Silver Spring, MD: TBI Technical Assistance Center. 1998. annual. Contact: Available from TBI Technical Assistance Center, 8737 Colesville Road, Suite 950, Silver Spring, MD 20910. Telephone: (301) 650-8080 / fax: (301) 650-8045. Summary: This report begins with background information on the Traumatic Brain Injury State Demonstration Grant Program. Part II of the report is a tabular state-bystate summary of objectives. Part III contains project abstracts for planning grants and implementation grants, each section arranged alphabetically by state name. Part IV is the grantee contact list. [Funded by the Maternal and Child Health Bureau].

•

Traumatic brain injury in Massachusetts: Incidence and prevention Source: Boston, MA: Injury Prevention and Control Program, Massachusetts Department of Public Health. 1994. 44 pp. Contact: Available from Cindy Rodgers, Massachusetts Department of Public Health, Injury Prevention and Control Program, 250 Washington Street, Fourth Floor, Boston, MA 02108-4619. Telephone: (617) 624-5070 / fax: (617) 624-5075 / e-mail: [email protected]. Available at no charge. Summary: This report describes the extent of traumatic brain injury in Massachusetts, including the frequency of brain injury by cause, and estimates the lifetime costs of health care and lost earnings. Clinical patterns of these injuries, sample cases from one emergency department, and prevention strategies targeted at the three leading causes of brain injuries: motor vehicles, falls and firearms, are also described.

•

Traumatic brain injury in the United States: Assessing outcomes in children: Summary and recommendations from the Expert Working Group, Atlanta, GA, October 26-27, 2000 Source: [Atlanta, GA]: National Center for Injury Prevention and Control. [2001]. 50 pp. Contact: Available from HRSA Information Center, 2070 Chain Bridge Road, Suite 450, Vienna, VA 22182-2536. Telephone: (888) ASK-HRSA or (877) 474-4772 TTY / fax: (703) 821-2098 / e-mail: [email protected] / Web site: http://www.ask.hrsa.gov. Summary: This report is intended for researchers, public health professional including those from state health departments, and advocates interested in furthering research on outcomes of traumatic brain injury (TBI) in children. This report summarizes the comments, suggestions, and recommendations of a working group convened by the Centers for Disease Control and Prevention (CDC) on assessment of TBI outcomes in children and youth. Meeting participants identified (1) key research topics and variables

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to measure in assessing longer-term outcomes; (2) reviewed conceptual models of disability that could provide a framework for designing appropriate studies of TBI outcomes; (3) discussed the advantages and shortcomings for assessing these outcomes; and (4) described the challenges in designing and implementing studies on TBI and recommended ways to address those challenges. The appendices include an overview of available outcome assessments; presentation slides; surveillance data from South Carolina; resources to guide selection of research topics; and an overview of TBI surveillance activities funded by the CDC.

The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “brain injuries” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total

Items Found 25254 983 915 23 30 27205

HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “brain injuries” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

15

Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.

16

The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 17 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 18 19

The HSTAT URL is http://hstat.nlm.nih.gov/.

Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community

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Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.

Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •

CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.

•

Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.

Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 20 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 21

The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.

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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on brain injuries can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.

Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to brain injuries. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to brain injuries. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “brain injuries”:

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•

Other guides Brain Cancer http://www.nlm.nih.gov/medlineplus/braincancer.html Head and Brain Injuries http://www.nlm.nih.gov/medlineplus/headandbraininjuries.html Peripheral Nerve Disorders http://www.nlm.nih.gov/medlineplus/peripheralnervedisorders.html Spinal Cord Injuries http://www.nlm.nih.gov/medlineplus/spinalcordinjuries.html Spinal Cord Injury http://www.nlm.nih.gov/medlineplus/tutorials/spinalcordinjuryloader.html Sports Injuries http://www.nlm.nih.gov/medlineplus/sportsinjuries.html

Within the health topic page dedicated to brain injuries, the following was listed: •

General/Overviews Facts about Concussion and Brain Injury and Where to Get Help http://www.cdc.gov/ncipc/tbi/tbibook.pdf Head Injuries: What to Watch for Afterward Source: American Academy of Family Physicians http://familydoctor.org/healthfacts/084/

•

Diagnosis/Symptoms Computed Tomography (CT)-Head Source: American College of Radiology, Radiological Society of North America http://www.radiologyinfo.org/content/ct_of_the_head.htm Functional MR Imaging (fMRI) - Brain Source: American College of Radiology, Radiological Society of North America http://www.radiologyinfo.org/content/functional_mr.htm Head Trauma Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=FA00008

•

Treatment First Aid for Head Injuries Source: National Institute for Occupational Safety and Health http://www.cdc.gov/nasd/docs/d000801-d000900/d000815/d000815.html What Is Neurosurgery? http://www.nlm.nih.gov/medlineplus/tutorials/whatisneurosurgeryloader.html

Patient Resources

•

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Specific Conditions/Aspects Brain Injuries and Mass Trauma Events Source: National Center for Injury Prevention and Control http://www.cdc.gov/masstrauma/factsheets/public/brain_injuries.htm Brain Pain: Recognizing a Subdural Hematoma Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=BN00015 Cerebral Hypoxia (Anoxia) Source: National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/health_and_medical/disorders/anoxia_doc.htm Coma, Including Persistent Vegetative State Source: National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/health_and_medical/disorders/coma_doc.htm Concussion Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00320 Intracranial Hematoma Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00330 Traumatic Brain Injury: Cognitive and Communication Disorders Source: National Institute on Deafness and Other Communication Disorders http://www.nidcd.nih.gov/health/voice/tbrain.asp Traumatic Brain Injury: No One Pathway to Recovery Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=BN00005

•

Children Bump on the Head: When Is It Serious? Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=HQ00763 Concussions Source: Nemours Foundation http://kidshealth.org/kid/ill_injure/aches/concussion.html Head Injuries Source: Nemours Foundation http://kidshealth.org/parent/firstaid_safe/emergencies/head_injury.html JAMA Patient Page: Inflicted Brain Injury in Children Source: American Medical Association http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZ4SS4F0JD&s ub_cat=187 Shaken Baby Syndrome Source: National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/health_and_medical/disorders/shakenbaby.htm

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Traumatic Brain Injury Source: National Information Center for Children and Youth with Disabilities http://www.nichcy.org/pubs/factshe/fs18txt.htm •

From the National Institutes of Health Traumatic Brain Injury Source: National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/health_and_medical/disorders/tbi_doc.htm Traumatic Brain Injury: Hope Through Research Source: National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/health_and_medical/pubs/TBI.htm

•

Latest News Concussions Need at Least a Week to Heal Source: 11/18/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14732 .html

•

Law and Policy Bicycle Helmet Use Laws Source: National Highway Traffic Safety Administration http://www.nhtsa.dot.gov/people/injury/New-factsheet03/BicycleHelmetUse.pdf

•

Organizations Brain Injury Association http://www.biausa.org/Pages/home.html National Center for Injury Prevention and Control http://www.cdc.gov/ncipc/ National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/

•

Pictures/Diagrams Atlas of the Body: The Brain -- Lobes Source: American Medical Association http://www.medem.com/MedLB/article_detaillb.cfm?article_ID=ZZZR9WH46JC &sub_cat=185 Atlas of the Body: The Brain -- Side View Source: American Medical Association http://www.medem.com/MedLB/article_detaillb.cfm?article_ID=ZZZYUAM46JC &sub_cat=185 Atlas of the Body: The Skull Source: American Medical Association http://www.medem.com/MedLB/article_detaillb.cfm?article_ID=ZZZCIHWBGJC &sub_cat=523

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Prevention/Screening Heads Up: Preventing Brain Injuries Source: National Center for Injury Prevention and Control http://www.cdc.gov/ncipc/pub-res/tbi_toolkit/patients/preventing.htm JAMA Patient Page: Protecting against Head Injuries Source: American Medical Association http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZ8ZI10NAC& sub_cat=366

•

Research Knocking Noggins Source: Society for Neuroscience http://web.sfn.org/content/Publications/BrainBriefings/knocking.html Life and Death of a Neuron Source: National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/health_and_medical/pubs/NINDS_Neuron.htm

•

Statistics Traumatic Brain Injury: The Problem Source: National Center for Injury Prevention and Control http://www.cdc.gov/ncipc/factsheets/tbi.htm

•

Teenagers Concussions Source: Nemours Foundation http://kidshealth.org/teen/safety/first_aid/concussions.html Pre-Season Testing Can Lead to Better Management of Injured High School Athletes Source: American Association of Neurological Surgeons http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZPT89GR9C& sub_cat=405

You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on brain injuries. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to

146 Brain Injuries

http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •

Facts About Concussion and Brain Injury Source: Atlanta, GA: National Center for Injury Prevention and Control. 199x. 18 p. Contact: Available from National Center for Injury Prevention and Control. Mailstop F41, 4770 Buford Highway, Atlanta, GA 30341. (770) 488-4642. Also available from www.cdc.gov/ncipc.tbi. PRICE: Single copy free. Summary: A blow or jolt to the head can disrupt the normal function of the brain. Doctors often call this type of brain injury a concussion or closed head injury. This brochure explains what can happen after a concussion, how to get better, and where to go for more information and help when needed. The brochure was written to help people who are treated for less severe brain injuries, either in hospital emergency departments or with brief hospital admission. The brochure reviews the health care provided to people with concussion, the danger signs of concussion in adults and in children, the symptoms of brain injury in adults, children, and in older adults, tips for healing (for adults and for children), and where to get help, including help for families and caregivers. Symptoms of brain injury related to communication disorders can include having trouble remembering things, experiencing slowness in thinking, acting, speaking or reading, having trouble with balance or feeling dizzy, or experiencing a ringing in the ears (tinnitus). The brochure concludes with a list of resources for additional information, including the help line and web site of the Brain Injury Association (BIA).

•

Prevalence of Traumatic Brain Injury in the United States Source: Rockville, MD: American Speech-Language-Hearing Association (ASHA), Science and Research Department. 1995. 1 p. Contact: Available from American Speech-Language-Hearing Association (ASHA). Science and Research Department. 10801 Rockville Pike, Rockville, MD 20852. (301) 8975700. PRICE: Single copy free. Summary: This fact sheet from the American Speech-Language Hearing Association (ASHA) provides information on the prevalence of traumatic brain injury in the United States. Topics covered include communication disorders resulting from traumatic brain injury, statistics on head trauma, the most common causes of head injuries and the most common victims, survival rates, language function and brain hemisphere, hematomas, and prognostic considerations. 5 references.

•

Traumatic Brain Injury: Cognitive and Communication Disorders Source: Bethesda, MD: National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health (NIH). July 1998. [4 p.]. Contact: Available from NIDCD Information Clearinghouse. 1 Communication Avenue, Bethesda, MD 20892-3456. Voice (800) 241-1044. TTY (800) 241-1055. Fax (301) 907-8830. E-mail: [email protected]. Website: www.nidcd.nih.gov. PRICE: Single copy free. NIH Publication Number 98-4315. Summary: This fact sheet provides basic information about traumatic brain injury (TBI), defined as sudden physical damage to the brain. The fact sheet outlines the possible

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causes of TBI, and the resulting brain injuries. The author notes that major speech and language areas often receive damage in TBI, resulting in communication difficulties. Other problems due to TBI can be voice, swallowing, walking, balance, and coordination difficulties, as well as changes in the ability to smell and in memory and cognitive (thinking) skills. The fact sheet reports some statistics about who suffers from TBI, and outlines more specifically the cognitive and communication problems that can result from TBI. The fact sheet also briefly considers assessment of these cognitive and communication problems, as well as treatment options. Therapy usually focuses on regaining lost skills as well as on learning ways to compensate for abilities that have been permanently changed because of the brain injury. The fact sheet concludes with a brief description of current research efforts in this area, and a listing of organizations through which readers can get additional information. 1 figure. The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “brain injuries” (or synonyms). The following was recently posted: •

Guidelines for prehospital management of traumatic brain injury Source: Brain Trauma Foundation - Disease Specific Society; 2000; 81 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3288&nbr=2514&a mp;string=brain+AND+injuries

•

Part I. Guidelines for the management of severe traumatic brain injury. In: Management and prognosis of severe traumatic brain injury Source: American Association of Neurological Surgeons - Medical Specialty Society; 2000; 165 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3121&nbr=2347&a mp;string=brain+AND+injuries

•

Part II. Early indicators of prognosis in severe traumatic brain injury. In: Management and prognosis of severe traumatic brain injury Source: American Association of Neurological Surgeons - Medical Specialty Society; 2000; 116 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3122&nbr=2348&a mp;string=brain+AND+injuries

•

Practice management guidelines for the management of mild traumatic brain injury Source: Eastern Association for the Surgery of Trauma - Professional Association; 2000; 29 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2793&nbr=2019&a mp;string=brain+AND+injuries

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•

Rehabilitation of persons with traumatic brain injury Source: National Institutes of Health (NIH) Consensus Development Panel on Rehabilitation of Persons With Traumatic Brain Injury - Independent Expert Panel; 1998 October; 30 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2104&nbr=1330&a mp;string=brain+AND+injuries The NIH Search Utility

The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to brain injuries. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats

•

Family Village: http://www.familyvillage.wisc.edu/specific.htm

•

Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/

•

Med Help International: http://www.medhelp.org/HealthTopics/A.html

•

Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/

•

Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/

•

WebMDHealth: http://my.webmd.com/health_topics

Associations and Brain Injuries The following is a list of associations that provide information on and resources relating to brain injuries: •

Brain Injury Association, Inc Telephone: (703) 236-6000 Toll-free: (800) 444-6443 Fax: (703) 236-6001 Email: [email protected] Web Site: http://www.biausa.org

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Background: The Brain Injury Association of America is a national health organization dedicated to creating a better future through brain injury prevention, research, education and advocacy. Established in 1980, the Brain Injury Association provides information, assistance, and a variety of programs and services to people with brain injuries and their families, health care professionals, and the general public. The BIAA networks with and provides guidance to state associations as well as hundreds of chapters and support groups that offer a range of services including care/case management, respite care, recreational opportunities, and, in some cases, housing, transportation, and emergency financial assistance. The BIAA also lobbies before Congress and the Administration; encourages state agencies to develop and fund appropriate services for people with brain injuries; offers a toll-free Family Helpline; provides emergency financial assistance through its 'Thumbs Up Fund'; and offers the 'Brain Injury Resource Center,' an interactive multimedia computer system with comprehensive brain injury information that is available at rehabilitation facilities, trauma centers, and hospitals across the country. The BIAA publishes manuals, directories, magazines, and books. Relevant area(s) of interest: Brain Injury •

Brain Injury Resource Center Telephone: (206) 621-8558 Fax: (206) 329-0912 Email: [email protected] Web Site: http://www.headinjury.com/ Background: Brain Injury Resource Center is a nonprofit clearinghouse founded and operated by head injury activists in1985. Visitors get information, join a discussion group, build advocacy skills, and self-care skills. Catalogues resources from diverse organizations including support groups, rehabilitation, and research sites, as well as lay and professional journals and more.

Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to brain injuries. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with brain injuries. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about brain injuries. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797.

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Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “brain injuries” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “brain injuries”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “brain injuries” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “brain injuries” (or a synonym) into the search box, and click “Submit Query.”

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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.

Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.23

Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.

Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of

23

Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.

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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)24: •

Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/

•

Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)

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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm

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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html

•

California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html

•

California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html

•

California: Gateway Health Library (Sutter Gould Medical Foundation)

•

California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/

•

California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp

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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html

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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/

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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/

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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/

•

California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html

•

California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/

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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/

•

Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/

•

Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/

24

Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.

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•

Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml

•

Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm

•

Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html

•

Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm

•

Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp

•

Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/

•

Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm

•

Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html

•

Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/

•

Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm

•

Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/

•

Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/

•

Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/

•

Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm

•

Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html

•

Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm

•

Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/

•

Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/

•

Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10

•

Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/

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•

Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html

•

Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp

•

Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp

•

Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/

•

Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html

•

Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm

•

Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

•

Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

•

Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

•

Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

•

Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

•

Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/

•

Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html

•

Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm

•

Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330

•

Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)

•

National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html

•

National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/

•

National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/

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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm

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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/

•

New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm

•

New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm

•

New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/

•

New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html

•

New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/

•

New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html

•

New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/

•

Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm

•

Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp

•

Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/

•

Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/

•

Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml

•

Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html

•

Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html

•

Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml

•

Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp

•

Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm

•

Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/

156 Brain Injuries

•

South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp

•

Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/

•

Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/

•

Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72

157

ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •

ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html

•

MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp

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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/

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Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html

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On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/

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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp

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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm

Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).

Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •

Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical

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MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html

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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

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BRAIN INJURIES DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acculturation: Process of cultural change in which one group or members of a group assimilates various cultural patterns from another. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acoustic: Having to do with sound or hearing. [NIH] Actin: Essential component of the cell skeleton. [NIH] Action Potentials: The electric response of a nerve or muscle to its stimulation. [NIH] Activities of Daily Living: The performance of the basic activities of self care, such as dressing, ambulation, eating, etc., in rehabilitation. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a

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synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Advanced Life Support: The medical care given by medical doctors and nurses trained in critical care medicine with the use of specialized technical equipment, infusion of fluids and drugs aimed to stabilize or restore vital functions. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aetiology: Study of the causes of disease. [EU] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Alertness: A state of readiness to detect and respond to certain specified small changes occurring at random intervals in the environment. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alkalosis: A pathological condition that removes acid or adds base to the body fluids. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [NIH] Alternative medicine: Practices not generally recognized by the medical community as

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standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Ambulatory Care: Health care services provided to patients on an ambulatory basis, rather than by admission to a hospital or other health care facility. The services may be a part of a hospital, augmenting its inpatient services, or may be provided at a free-standing facility. [NIH]

Ameliorated: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amenorrhea: Absence of menstruation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amnestic: Nominal aphasia; a difficulty in finding the right name for an object. [NIH] Amphetamines: Analogs or derivatives of amphetamine. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopression, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation. [NIH] Amygdala: Almond-shaped group of basal nuclei anterior to the inferior horn of the lateral ventricle of the brain, within the temporal lobe. The amygdala is part of the limbic system. [NIH]

Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable. [NIH] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local

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inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaplasia: Loss of structural differentiation and useful function of neoplastic cells. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Anesthetics: Agents that are capable of inducing a total or partial loss of sensation, especially tactile sensation and pain. They may act to induce general anesthesia, in which an unconscious state is achieved, or may act locally to induce numbness or lack of sensation at a targeted site. [NIH] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angiopathy: Disease of the blood vessels (arteries, veins, and capillaries) that occurs when someone has diabetes for a long time. There are two types of angiopathy: macroangiopathy and microangiopathy. In macroangiopathy, fat and blood clots build up in the large blood vessels, stick to the vessel walls, and block the flow of blood. In microangiopathy, the walls of the smaller blood vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood through the body. Then the cells, for example, the ones in the center of the eye, do not get enough blood and may be damaged. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]

Anoxia: Clinical manifestation of respiratory distress consisting of a relatively complete absence of oxygen. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Anterior Cerebral Artery: Artery formed by the bifurcation of the internal carotid artery. Branches of the anterior cerebral artery supply the caudate nucleus, internal capsule, putamen, septal nuclei, gyrus cinguli, and surfaces of the frontal lobe and parietal lobe. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]

Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this

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binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Anxiolytic: An anxiolytic or antianxiety agent. [EU] Aorta: The main trunk of the systemic arteries. [NIH] Aperture: A natural hole of perforation, especially one in a bone. [NIH] Aphasia: A cognitive disorder marked by an impaired ability to comprehend or express language in its written or spoken form. This condition is caused by diseases which affect the language areas of the dominant hemisphere. Clinical features are used to classify the various subtypes of this condition. General categories include receptive, expressive, and mixed forms of aphasia. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Approximate: Approximal [EU] Aqueous: Having to do with water. [NIH] Arachidonate 12-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in platelets. EC 1.13.11.31. [NIH]

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Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Aspartate: A synthetic amino acid. [NIH] Asphyxia: A pathological condition caused by lack of oxygen, manifested in impending or actual cessation of life. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atmospheric Pressure: The pressure at any point in an atmosphere due solely to the weight of the atmospheric gases above the point concerned. [NIH] ATP: ATP an abbreviation for adenosine triphosphate, a compound which serves as a carrier of energy for cells. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH]

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Auditory: Pertaining to the sense of hearing. [EU] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Axonal: Condition associated with metabolic derangement of the entire neuron and is manifest by degeneration of the distal portion of the nerve fiber. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Axotomy: Transection or severing of an axon. This type of denervation is used often in experimental studies on neuronal physiology and neuronal death or survival, toward an understanding of nervous system disease. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriuria: The presence of bacteria in the urine with or without consequent urinary tract infection. Since bacteriuria is a clinical entity, the term does not preclude the use of urine/microbiology for technical discussions on the isolation and segregation of bacteria in the urine. [NIH] Barbiturates: A class of chemicals derived from barbituric acid or thiobarbituric acid. Many of these are medically important as sedatives and hypnotics (sedatives, barbiturate), as anesthetics, or as anticonvulsants. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Bed Rest: Confinement of an individual to bed for therapeutic or experimental reasons. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]

Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its

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composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Bioengineering: The application of engineering principles to the solution of biological problems, for example, remote-handling devices, life-support systems, controls, and displays. [NIH] Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc. [NIH] Biomechanics: The study of the application of mechanical laws and the action of forces to living structures. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Body Burden: The total amount of a chemical, metal or radioactive substance present at any

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time after absorption in the body of man or animal. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Bolus: A single dose of drug usually injected into a blood vessel over a short period of time. Also called bolus infusion. [NIH] Bolus infusion: A single dose of drug usually injected into a blood vessel over a short period of time. Also called bolus. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Diseases: Pathologic conditions affecting the brain, which is composed of the intracranial components of the central nervous system. This includes (but is not limited to) the cerebral cortex; intracranial white matter; basal ganglia; thalamus; hypothalamus; brain stem; and cerebellum. [NIH] Brain Hypoxia: Lack of oxygen leading to unconsciousness. [NIH] Brain Infarction: The formation of an area of necrosis in the brain, including the cerebral hemispheres (cerebral infarction), thalami, basal ganglia, brain stem (brain stem infarctions), or cerebellum secondary to an insufficiency of arterial or venous blood flow. [NIH] Brain Injuries: Acute and chronic injuries to the brain, including the cerebral hemispheres, cerebellum, and brain stem. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with diffuse axonal injury or coma, posttraumatic. Localized injuries may be associated with neurobehavioral manifestations; hemiparesis, or other focal neurologic deficits. [NIH] Brain Ischemia: Localized reduction of blood flow to brain tissue due to arterial obtruction or systemic hypoperfusion. This frequently occurs in conjuction with brain hypoxia. Prolonged ischemia is associated with brain infarction. [NIH] Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]

Breakdown: A physical, metal, or nervous collapse. [NIH]

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Bromocriptine: A semisynthetic ergot alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion and is used to treat amenorrhea, galactorrhea, and female infertility, and has been proposed for Parkinson disease. [NIH] Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge of electricity. [NIH] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium-Binding Proteins: Proteins to which calcium ions are bound. They can act as transport proteins, regulator proteins or activator proteins. [NIH] Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels. [NIH] Carbamazepine: An anticonvulsant used to control grand mal and psychomotor or focal seizures. Its mode of action is not fully understood, but some of its actions resemble those of phenytoin; although there is little chemical resemblance between the two compounds, their three-dimensional structure is similar. [NIH] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carbon Monoxide Poisoning: Toxic asphyxiation due to the displacement of oxygen from oxyhemoglobin by carbon monoxide. [NIH] Carcinogenic: Producing carcinoma. [EU] Cardiac: Having to do with the heart. [NIH] Cardiac arrest: A sudden stop of heart function. [NIH] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiopulmonary Resuscitation: The artificial substitution of heart and lung action as indicated for heart arrest resulting from electric shock, drowning, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation and closed-chest cardiac massage. [NIH] Cardiopulmonary Resuscitation: The artificial substitution of heart and lung action as

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indicated for heart arrest resulting from electric shock, drowning, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation and closed-chest cardiac massage. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Cellular metabolism: The sum of all chemical changes that take place in a cell through which energy and basic components are provided for essential processes, including the synthesis of new molecules and the breakdown and removal of others. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebellum: Part of the metencephalon that lies in the posterior cranial fossa behind the brain stem. It is concerned with the coordination of movement. [NIH]

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Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Arteries: The arteries supplying the cerebral cortex. [NIH] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebral Hemorrhage: Bleeding into a cerebral hemisphere of the brain, including lobar, subcortical white matter, and basal ganglia hemorrhages. Commonly associated conditions include hypertension; intracranial arteriosclerosis; intracranial aneurysm; craniocerebral trauma; intracranial arteriovenous malformations; cerebral amyloid angiopathy; and cerebral infarction. [NIH] Cerebral Infarction: The formation of an area of necrosis in the cerebrum caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., infarction, anterior cerebral artery), and etiology (e.g., embolic infarction). [NIH]

Cerebral Palsy: Refers to a motor disability caused by a brain dysfunction. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Cholinesterase Inhibitors: Drugs that inhibit cholinesterases. The neurotransmitter acetylcholine is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system. [NIH]

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Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]

Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis. [NIH] Coca: Any of several South American shrubs of the Erythroxylon genus (and family) that yield cocaine; the leaves are chewed with alum for CNS stimulation. [NIH] Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. [NIH] Cochlear: Of or pertaining to the cochlea. [EU] Cochlear Diseases: Diseases of the cochlea, the part of the inner ear that is concerned with hearing. [NIH] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH] Colloidal: Of the nature of a colloid. [EU] Comatose: Pertaining to or affected with coma. [EU] Communication Disorders: Disorders of verbal and nonverbal communication caused by receptive or expressive language disorders, cognitive dysfunction (e.g., mental retardation), psychiatric conditions, and hearing disorders. [NIH]

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Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH]

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Concomitant: Accompanying; accessory; joined with another. [EU] Conduction: The transfer of sound waves, heat, nervous impulses, or electricity. [EU] Cone: One of the special retinal receptor elements which are presumed to be primarily concerned with perception of light and color stimuli when the eye is adapted to light. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Consolidation: The healing process of a bone fracture. [NIH] Constriction: The act of constricting. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Continuum: An area over which the vegetation or animal population is of constantly changing composition so that homogeneous, separate communities cannot be distinguished. [NIH]

Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contralateral: Having to do with the opposite side of the body. [NIH] Controlled clinical trial: A clinical study that includes a comparison (control) group. The comparison group receives a placebo, another treatment, or no treatment at all. [NIH] Contusion: A bruise; an injury of a part without a break in the skin. [EU] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that has ruptured and discharged its ovum. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial

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structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Craniotomy: An operation in which an opening is made in the skull. [NIH] Creatine: An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. [NIH]

Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Critical Care: Health care provided to a critically ill patient during a medical emergency or crisis. [NIH] Cues: Signals for an action; that specific portion of a perceptual field or pattern of stimuli to which a subject has learned to respond. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cyanide: An extremely toxic class of compounds that can be lethal on inhaling of ingesting in minute quantities. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cycloserine: Antibiotic substance produced by Streptomyces garyphalus. It may be used in the treatment of resistant tuberculosis as part of a multi-drug regimen. It has also been used in urinary tract infections. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydroepiandrosterone: DHEA. A substance that is being studied as a cancer prevention drug. It belongs to the family of drugs called steroids. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline

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is usually progressive, and initially spares the level of consciousness. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dentate Gyrus: Gray matter situated above the gyrus hippocampi. It is composed of three layers. The molecular layer is continuous with the hippocampus in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called granule cells, whose axons pass through the polymorphic layer ending on the dendrites of pyramidal cells in the hippocampus. [NIH] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Dermatitis: Any inflammation of the skin. [NIH] Dextroamphetamine: The d-form of amphetamine. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diastolic blood pressure: The minimum pressure that remains within the artery when the heart is at rest. [NIH] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Diffuse Axonal Injury: A relatively common sequela of blunt head injury, characterized by a global disruption of axons throughout the brain. Associated clinical features may include neurobehavioral manifestations; persistent vegetative state; dementia; and other disorders. [NIH]

Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Dilatation: The act of dilating. [NIH] Dilatation, Pathologic: The condition of an anatomical structure's being dilated beyond normal dimensions. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH]

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Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Diuretic: A drug that increases the production of urine. [NIH] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] DNA Topoisomerase: An enzyme catalyzing ATP-independent breakage of single-stranded DNA, followed by passage and rejoining of another single-stranded DNA. This enzyme class brings about the conversion of one topological isomer of DNA into another, e.g., the relaxation of superhelical turns in DNA, the interconversion of simple and knotted rings of single-stranded DNA, and the intertwisting of single-stranded rings of complementary sequences. (From Enzyme Nomenclature, 1992) EC 5.99.1.2. [NIH] Donepezil: A drug used in the treatment of Alzheimer's disease. It belongs to the family of drugs called cholinesterase inhibitors. It is being studied as a treatment for side effects caused by radiation therapy to the brain. [NIH] Dopa: The racemic or DL form of DOPA, an amino acid found in various legumes. The dextro form has little physiologic activity but the levo form (levodopa) is a very important physiologic mediator and precursor and pharmacological agent. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dorsum: A plate of bone which forms the posterior boundary of the sella turcica. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service

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produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Electric shock: A dangerous patho-physiological effect resulting from an electric current passing through the body of a human or animal. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophysiological: Pertaining to electrophysiology, that is a branch of physiology that is concerned with the electric phenomena associated with living bodies and involved in their functional activity. [EU] Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e., radiation. [NIH] Embolectomy: Surgical removal of an obstructing clot or foreign material which has been transported from a distant vessel by the bloodstream. Removal of a clot at its original site is called thrombectomy. [NIH] Embolism: Blocking of a blood vessel by a blood clot or foreign matter that has been transported from a distant site by the blood stream. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emesis: Vomiting; an act of vomiting. Also used as a word termination, as in haematemesis. [EU]

Empirical: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] Encephalomyelitis: A general term indicating inflammation of the brain and spinal cord, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and encephalitis in the literature. [NIH] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endoscopic: A technique where a lateral-view endoscope is passed orally to the duodenum for visualization of the ampulla of Vater. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph

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vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] Entorhinal Cortex: Cortex where the signals are combined with those from other sensory systems. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]

Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Eosinophils: Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. [NIH] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epilepticus: Repeated and prolonged epileptic seizures without recovery of consciousness between attacks. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Ergot: Cataract due to ergot poisoning caused by eating of rye cereals contaminated by a fungus. [NIH] Erythrocyte Transfusion: The transfer of erythrocytes from a donor to a recipient or reinfusion to the donor. [NIH] Erythrocyte Volume: Volume of circulating erythrocytes. It is usually measured by

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radioisotope dilution technique. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythropoiesis: The production of erythrocytes. [EU] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]

Estradiol: The most potent mammalian estrogenic hormone. It is produced in the ovary, placenta, testis, and possibly the adrenal cortex. [NIH] Estrogen: One of the two female sex hormones. [NIH] Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Evoked Potentials: The electric response evoked in the central nervous system by stimulation of sensory receptors or some point on the sensory pathway leading from the receptor to the cortex. The evoked stimulus can be auditory, somatosensory, or visual, although other modalities have been reported. Event-related potentials is sometimes used synonymously with evoked potentials but is often associated with the execution of a motor, cognitive, or psychophysiological task, as well as with the response to a stimulus. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Excitatory Amino Acids: Endogenous amino acids released by neurons as excitatory neurotransmitters. Glutamic acid is the most common excitatory neurotransmitter in the brain. Aspartic acid has been regarded as an excitatory transmitter for many years, but the extent of its role as a transmitter is unclear. [NIH] Exhaustion: The feeling of weariness of mind and body. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Expiration: The act of breathing out, or expelling air from the lungs. [EU] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]

Extracellular: Outside a cell or cells. [EU] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extravasation: A discharge or escape, as of blood, from a vessel into the tissues. [EU]

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Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Facial: Of or pertaining to the face. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Family Relations: Behavioral, psychological, and social relations among various members of the nuclear family and the extended family. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]

Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Feeding Behavior: Behavioral responses or sequences associated with eating including modes of feeding, rhythmic patterns of eating, and time intervals. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Firearms: Small-arms weapons, including handguns, pistols, revolvers, rifles, shotguns, etc. [NIH]

Fissure: Any cleft or groove, normal or otherwise; especially a deep fold in the cerebral cortex which involves the entire thickness of the brain wall. [EU] Flatus: Gas passed through the rectum. [NIH] Flexor: Muscles which flex a joint. [NIH] Flicker Fusion: The point or frequency at which all flicker of an intermittent light stimulus disappears. [NIH] Foetal: Of or pertaining to a fetus; pertaining to in utero development after the embryonic period. [EU] Forearm: The part between the elbow and the wrist. [NIH] Fossa: A cavity, depression, or pit. [NIH] Frontal Lobe: The anterior part of the cerebral hemisphere. [NIH] Functional magnetic resonance imaging: A noninvasive tool used to observe functioning in the brain or other organs by detecting changes in chemical composition, blood flow, or both. [NIH]

Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH]

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Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gastrointestinal Transit: Passage of food (sometimes in the form of a test meal) through the gastrointestinal tract as measured in minutes or hours. The rate of passage through the intestine is an indicator of small bowel function. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]

Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genistein: An isoflavonoid derived from soy products. It inhibits protein-tyrosine kinase and topoisomerase-ii (dna topoisomerase (atp-hydrolysing)) activity and is used as an antineoplastic and antitumor agent. Experimentally, it has been shown to induce G2 phase arrest in human and murine cell lines. [NIH] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Gliosis: The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion. [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH]

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Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Gonadal: Pertaining to a gonad. [EU] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grading: A system for classifying cancer cells in terms of how abnormal they appear when examined under a microscope. The objective of a grading system is to provide information about the probable growth rate of the tumor and its tendency to spread. The systems used to grade tumors vary with each type of cancer. Grading plays a role in treatment decisions. [NIH]

Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Granule: A small pill made from sucrose. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth Cones: Bulbous enlargement of the growing tip of nerve axons and dendrites. They are crucial to neuronal development because of their pathfinding ability and their role in synaptogenesis. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Hair Cells: Mechanoreceptors located in the organ of Corti that are sensitive to auditory stimuli and in the vestibular apparatus that are sensitive to movement of the head. In each case the accessory sensory structures are arranged so that appropriate stimuli cause movement of the hair-like projections (stereocilia and kinocilia) which relay the information centrally in the nervous system. [NIH] Handicap: A handicap occurs as a result of disability, but disability does not always constitute a handicap. A handicap may be said to exist when a disability causes a substantial and continuing reduction in a person's capacity to function socially and vocationally. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Care Costs: The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from

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health expenditures, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost. [NIH] Health Expenditures: The amounts spent by individuals, groups, nations, or private or public organizations for total health care and/or its various components. These amounts may or may not be equivalent to the actual costs (health care costs) and may or may not be shared among the patient, insurers, and/or employers. [NIH] Hearing Disorders: Conditions that impair the transmission or perception of auditory impulses and information from the level of the ear to the temporal cortices, including the sensorineural pathways. [NIH] Heart Arrest: Sudden and usually momentary cessation of the heart beat. This sudden cessation may, but not usually, lead to death, sudden, cardiac. [NIH] Hematoma: An extravasation of blood localized in an organ, space, or tissue. [NIH] Hemiparesis: The weakness or paralysis affecting one side of the body. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hepatic: Refers to the liver. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Human Activities: Activities performed by humans. [NIH] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydrocephalus: Excessive accumulation of cerebrospinal fluid within the cranium which may be associated with dilation of cerebral ventricles, intracranial hypertension; headache; lethargy; urinary incontinence; and ataxia (and in infants macrocephaly). This condition may be caused by obstruction of cerebrospinal fluid pathways due to neurologic abnormalities, intracranial hemorrhages; central nervous system infections; brain neoplasms; craniocerebral trauma; and other conditions. Impaired resorption of cerebrospinal fluid from the arachnoid villi results in a communicating form of hydrocephalus. Hydrocephalus ex-vacuo refers to ventricular dilation that occurs as a result of brain substance loss from cerebral infarction and other conditions. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H,

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atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hyperbaric: Characterized by greater than normal pressure or weight; applied to gases under greater than atmospheric pressure, as hyperbaric oxygen, or to a solution of greater specific gravity than another taken as a standard of reference. [EU] Hyperbaric oxygen: Oxygen that is at an atmospheric pressure higher than the pressure at sea level. Breathing hyperbaric oxygen to enhance the effectiveness of radiation therapy is being studied. [NIH] Hypercapnia: A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertensive Encephalopathy: Brain dysfunction or damage resulting from malignant hypertension, usually associated with a diastolic blood pressure in excess of 125 mmHg. Clinical manifestations include headache, nausea, emesis, seizures, altered mental status (in some cases progressing to coma), papilledema, and retinal hemorrhage. Focal neurologic signs may develop. Pathologically, this condition may be associated with the formation of ischemic lesions in the brain (brain ischemia). [NIH] Hyperthermia: A type of treatment in which body tissue is exposed to high temperatures to damage and kill cancer cells or to make cancer cells more sensitive to the effects of radiation and certain anticancer drugs. [NIH] Hypertonia: Or hypertony n, pl. hypertonias or hypertonies : hypertonicity. n. Pathology: increased rigidity, tension and spasticity of the muscles. [EU] Hyperventilation: A pulmonary ventilation rate faster than is metabolically necessary for the exchange of gases. It is the result of an increased frequency of breathing, an increased tidal volume, or a combination of both. It causes an excess intake of oxygen and the blowing off of carbon dioxide. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] Hypoglycaemia: An abnormally diminished concentration of glucose in the blood, which may lead to tremulousness, cold sweat, piloerection, hypothermia, and headache, accompanied by irritability, confusion, hallucinations, bizarre behaviour, and ultimately, convulsions and coma. [EU] Hypotension: Abnormally low blood pressure. [NIH] Hypothalamic: Of or involving the hypothalamus. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals;

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in man usually accidental or unintentional. [NIH] Hypoxemia: Deficient oxygenation of the blood; hypoxia. [EU] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Imaging procedures: Methods of producing pictures of areas inside the body. [NIH] Immersion: The placing of a body or a part thereof into a liquid. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]

Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunophilin: A drug for the treatment of Parkinson's disease. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an

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area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]

Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate a carcinogenic process. [NIH] Inotropic: Affecting the force or energy of muscular contractions. [EU] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-10: Factor that is a coregulator of mast cell growth. It is produced by T-cells and B-cells and shows extensive homology with the Epstein-Barr virus BCRFI gene. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Capsule: White matter pathway, flanked by nuclear masses, consisting of both afferent and efferent fibers projecting between the cerebral cortex and the brainstem. It consists of three distinct parts: an anterior limb, posterior limb, and genu. [NIH]

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Interpersonal Relations: The reciprocal interaction of two or more persons. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracranial Aneurysm: A saclike dilatation of the walls of a blood vessel, usually an artery. [NIH]

Intracranial Arteriosclerosis: Vascular diseases characterized by thickening, hardening, and remodeling of the walls of intracranial arteries. There are three subtypes: (1) atherosclerosis, marked by fatty depositions in the innermost layer of the arterial walls, (2) Monckeberg's sclerosis, which features calcium deposition in the media and (3) arteriolosclerosis, which refers to sclerosis of small caliber arteries. Clinically, this process may be associated with transient ischemic attack, brain infarction, intracranial embolism and thrombosis, or intracranial aneurysm. [NIH] Intracranial Hemorrhages: Bleeding within the intracranial cavity, including hemorrhages in the brain and within the cranial epidural, subdural, and subarachnoid spaces. [NIH] Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Intracranial Pressure: Pressure within the cranial cavity. It is influenced by brain mass, the circulatory system, CSF dynamics, and skull rigidity. [NIH] Intravenous: IV. Into a vein. [NIH] Involuntary: Reaction occurring without intention or volition. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic stroke: A condition in which the blood supply to part of the brain is cut off. Also called "plug-type" strokes. Blocked arteries starve areas of the brain controlling sight, speech, sensation, and movement so that these functions are partially or completely lost. Ischemic stroke is the most common type of stroke, accounting for 80 percent of all strokes. Most ischemic strokes are caused by a blood clot called a thrombus, which blocks blood flow in the arteries feeding the brain, usually the carotid artery in the neck, the major vessel bringing blood to the brain. When it becomes blocked, the risk of stroke is very high. [NIH] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH]

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Kainate: Glutamate receptor. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lactation: The period of the secretion of milk. [EU] Language Disorders: Conditions characterized by deficiencies of comprehension or expression of written and spoken forms of language. These include acquired and developmental disorders. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lead Poisoning: Disease caused by the gradual accumulation of a significant body burden of lead. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]

Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Levodopa: The naturally occurring form of dopa and the immediate precursor of dopamine. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to dopamine. It is used for the treatment of parkinsonism and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]

Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [NIH] Ligands: A RNA simulation method developed by the MIT. [NIH]

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Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Limbic: Pertaining to a limbus, or margin; forming a border around. [EU] Limbic System: A set of forebrain structures common to all mammals that is defined functionally and anatomically. It is implicated in the higher integration of visceral, olfactory, and somatic information as well as homeostatic responses including fundamental survival behaviors (feeding, mating, emotion). For most authors, it includes the amygdala, epithalamus, gyrus cinguli, hippocampal formation (see hippocampus), hypothalamus, parahippocampal gyrus, septal nuclei, anterior nuclear group of thalamus, and portions of the basal ganglia. (Parent, Carpenter's Human Neuroanatomy, 9th ed, p744; NeuroNames, http://rprcsgi.rprc.washington.edu/neuronames/index.html (September 2, 1998)). [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Locomotor: Of or pertaining to locomotion; pertaining to or affecting the locomotive apparatus of the body. [EU] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Long-Term Potentiation: A persistent increase in synaptic efficacy, usually induced by appropriate activation of the same synapses. The phenomenological properties of long-term potentiation suggest that it may be a cellular mechanism of learning and memory. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lumbar puncture: A procedure in which a needle is put into the lower part of the spinal column to collect cerebrospinal fluid or to give anticancer drugs intrathecally. Also called a spinal tap. [NIH] Lutein Cells: The cells of the corpus luteum which are derived from the granulosa cells and the theca cells of the Graafian follicle. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH]

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Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]

Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Magnetic Resonance Spectroscopy: Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (magnetic resonance imaging). [NIH] Malaria: A protozoan disease caused in humans by four species of the genus Plasmodium (P. falciparum (malaria, falciparum), P. vivax (malaria, vivax), P. ovale, and P. malariae) and transmitted by the bite of an infected female mosquito of the genus Anopheles. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high fever, sweating, shaking chills, and anemia. Malaria in animals is caused by other species of plasmodia. [NIH] Malaria, Falciparum: Malaria caused by Plasmodium falciparum. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations. [NIH] Malaria, Vivax: Malaria caused by Plasmodium vivax. This form of malaria is less severe than malaria, falciparum, but there is a higher probability for relapses to occur. Febrile paroxysms often occur every other day. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Meatus: A canal running from the internal auditory foramen through the petrous portion of the temporal bone. It gives passage to the facial and auditory nerves together with the auditory branch of the basilar artery and the internal auditory veins. [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU]

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Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Memory Disorders: Disturbances in registering an impression, in the retention of an acquired impression, or in the recall of an impression. Memory impairments are associated with dementia; craniocerebraltrauma; encephalitis; alcoholism (see also alcohol amnestic disorder); schizophrenia; and other conditions. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Menstrual Cycle: The period of the regularly recurring physiologic changes in the endometrium occurring during the reproductive period in human females and some primates and culminating in partial sloughing of the endometrium (menstruation). [NIH] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mental Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH]

Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mesencephalic: Ipsilateral oculomotor paralysis and contralateral tremor, spasm. or choreic movements of the face and limbs. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Methylphenidate: A central nervous system stimulant used most commonly in the treatment of attention-deficit disorders in children and for narcolepsy. Its mechanisms appear to be similar to those of dextroamphetamine. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of

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the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Midazolam: A short-acting compound, water-soluble at pH less than 4 and lipid-soluble at physiological pH. It is a hypnotic-sedative drug with anxiolytic and amnestic properties. It is used for sedation in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. Because of its short duration and cardiorespiratory stability, it is particularly useful in poor-risk, elderly, and cardiac patients. [NIH]

Middle Cerebral Artery: The largest and most complex of the cerebral arteries. Branches of the middle cerebral artery supply the insular region, motor and premotor areas, and large regions of the association cortex. [NIH] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mitotic: Cell resulting from mitosis. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]

Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer

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detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motor Cortex: Area of the frontal lobe concerned with primary motor control. It lies anterior to the central sulcus. [NIH] Motor Skills: Performance of complex motor acts. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multiple Trauma: Physical insults or injuries occurring simultaneously in several parts of the body. [NIH] Muscular Diseases: Acquired, familial, and congenital disorders of skeletal muscle and smooth muscle. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors. [NIH] Narcolepsy: A condition of unknown cause characterized by a periodic uncontrollable tendency to fall asleep. [NIH] Narcosis: A general and nonspecific reversible depression of neuronal excitability, produced by a number of physical and chemical aspects, usually resulting in stupor. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial

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swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neocortex: The largest portion of the cerebral cortex. It is composed of neurons arranged in six layers. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nerve Fibers: Slender processes of neurons, especially the prolonged axons that conduct nerve impulses. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neurobehavioral Manifestations: Signs and symptoms of higher cortical dysfunction caused by organic conditions. These include certain behavioral alterations and impairments of skills involved in the acquisition, processing, and utilization of knowledge or information. [NIH]

Neurodegenerative Diseases: Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures. [NIH] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to stimulation of the nervous system. [NIH] Neuroglia: The non-neuronal cells of the nervous system. They are divided into macroglia (astrocytes, oligodendroglia, and schwann cells) and microglia. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the blood-brain and blood-retina barriers, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH] Neurology: A medical specialty concerned with the study of the structures, functions, and diseases of the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH]

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Neuroprotective Agents: Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotoxicity: The tendency of some treatments to cause damage to the nervous system. [NIH]

Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutrophil: A type of white blood cell. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]

Nonverbal Communication: Transmission of emotions, ideas, and attitudes between individuals in ways other than the spoken language. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclear Family: A family composed of spouses and their children. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Occult: Obscure; concealed from observation, difficult to understand. [EU]

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Oculomotor: Cranial nerve III. It originate from the lower ventral surface of the midbrain and is classified as a motor nerve. [NIH] Odour: A volatile emanation that is perceived by the sense of smell. [EU] On-line: A sexually-reproducing population derived from a common parentage. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Opium: The air-dried exudate from the unripe seed capsule of the opium poppy, Papaver somniferum, or its variant, P. album. It contains a number of alkaloids, but only a few morphine, codeine, and papaverine - have clinical significance. Opium has been used as an analgesic, antitussive, antidiarrheal, and antispasmodic. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]

Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Osmosis: Tendency of fluids (e.g., water) to move from the less concentrated to the more concentrated side of a semipermeable membrane. [NIH] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]

Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH]

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Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Oxytocin: A nonapeptide posterior pituitary hormone that causes uterine contractions and stimulates lactation. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Papilledema: Swelling around the optic disk. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Paraplegia: Severe or complete loss of motor function in the lower extremities and lower portions of the trunk. This condition is most often associated with spinal cord diseases, although brain diseases; peripheral nervous system diseases; neuromuscular diseases; and muscular diseases may also cause bilateral leg weakness. [NIH] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Parietal Lobe: Upper central part of the cerebral hemisphere. [NIH] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] Partial response: A decrease in the size of a tumor, or in the extent of cancer in the body, in response to treatment. [NIH] Particle: A tiny mass of material. [EU] Parturition: The act or process of given birth to a child. [EU] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]

Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]

Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perception: The ability quickly and accurately to recognize similarities and differences among presented objects, whether these be pairs of words, pairs of number series, or multiple sets of these or other symbols such as geometric figures. [NIH] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of

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the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Nervous System Diseases: Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves. [NIH] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photoreceptors: Cells specialized to detect and transduce light. [NIH]

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Physical Therapy: The restoration of function and the prevention of disability following disease or injury with the use of light, heat, cold, water, electricity, ultrasound, and exercise. [NIH]

Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]

Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigments: Any normal or abnormal coloring matter in plants, animals, or micro-organisms. [NIH]

Piloerection: Involuntary erection or bristling of hairs. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasma Volume: Volume of plasma in the circulation. It is usually measured by indicator dilution techniques. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together

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can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Pons: The part of the central nervous system lying between the medulla oblongata and the mesencephalon, ventral to the cerebellum, and consisting of a pars dorsalis and a pars ventralis. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postoperative: After surgery. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-traumatic: Occurring as a result of or after injury. [EU] Postural: Pertaining to posture or position. [EU] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for

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the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Prefrontal Cortex: The rostral part of the frontal lobe, bounded by the inferior precentral fissure in humans, which receives projection fibers from the mediodorsal nucleus of the thalamus. The prefrontal cortex receives afferent fibers from numerous structures of the diencephalon, mesencephalon, and limbic system as well as cortical afferents of visual, auditory, and somatic origin. [NIH] Pregnenolone: Steroid hormone. [NIH] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Problem Solving: A learning situation involving more than one alternative from which a selection is made in order to attain a specific goal. [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Program Evaluation: Studies designed to assess the efficacy of programs. They may include the evaluation of cost-effectiveness, the extent to which objectives are met, or impact. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Prolactin: Pituitary lactogenic hormone. A polypeptide hormone with a molecular weight of about 23,000. It is essential in the induction of lactation in mammals at parturition and is synergistic with estrogen. The hormone also brings about the release of progesterone from lutein cells, which renders the uterine mucosa suited for the embedding of the ovum should fertilization occur. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH]

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Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Protein-Tyrosine Kinase: An enzyme that catalyzes the phosphorylation of tyrosine residues in proteins with ATP or other nucleotides as phosphate donors. EC 2.7.1.112. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and

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treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychomotor: Pertaining to motor effects of cerebral or psychic activity. [EU] Psychotropic: Exerting an effect upon the mind; capable of modifying mental activity; usually applied to drugs that effect the mental state. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]

Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]

Pyramidal Cells: Projection neurons in the cerebral cortex and the hippocampus. Pyramidal cells have a pyramid-shaped soma with the apex and an apical dendrite pointed toward the pial surface and other dendrites and an axon emerging from the base. The axons may have local collaterals but also project outside their cortical region. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quinolinic: It is produced by immune cells and slowly infiltrates the brain tissues after an injury. [NIH] Quinolinic Acid: 2,3-Pyridinedicarboxylic acid. A metabolite of tryptophan with a possible role in neurodegenerative disorders. Elevated CSF levels of quinolinic acid are significantly correlated with the severity of neuropsychological deficits in patients who have AIDS. [NIH] Quinones: Hydrocarbon rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from

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radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Reaction Time: The time from the onset of a stimulus until the organism responds. [NIH] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recovery of Function: A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflex: An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [NIH]

Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH]

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Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Resected: Surgical removal of part of an organ. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory Physiology: Functions and activities of the respiratory tract as a whole or of any of its parts. [NIH] Respite Care: Patient care provided in the home or institution intermittently in order to provide temporary relief to the family home care giver. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Reticular: Coarse-fibered, netlike dermis layer. [NIH] Reticular Formation: A region extending from the pons & medulla oblongata through the mesencephalon, characterized by a diversity of neurons of various sizes and shapes, arranged in different aggregations and enmeshed in a complicated fiber network. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Hemorrhage: Bleeding from the vessels of the retina. [NIH] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rodenticides: Substances used to destroy or inhibit the action of rats, mice, or other rodents. [NIH]

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Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Second Messenger Systems: Systems in which an intracellular signal is generated in response to an intercellular primary messenger such as a hormone or neurotransmitter. They are intermediate signals in cellular processes such as metabolism, secretion, contraction, phototransduction, and cell growth. Examples of second messenger systems are the adenyl cyclase-cyclic AMP system, the phosphatidylinositol diphosphate-inositol triphosphate system, and the cyclic GMP system. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] Sedatives, Barbiturate: Those derivatives of barbituric or thiobarbituric acid that are used as hypnotics or sedatives. The structural class of all such derivatives, regardless of use, is barbiturates. [NIH] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Self Care: Performance of activities or tasks traditionally performed by professional health care providers. The concept includes care of oneself or one's family and friends. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Sequela: Any lesion or affection following or caused by an attack of disease. [EU] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Sequester: A portion of dead bone which has become detached from the healthy bone tissue, as occurs in necrosis. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins

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have been removed. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]

Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]

Social Behavior: Any behavior caused by or affecting another individual, usually of the same species. [NIH] Social Desirability: A personality trait rendering the individual acceptable in social or interpersonal relations. It is related to social acceptance, social approval, popularity, social status, leadership qualities, or any quality making him a socially desirable companion. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH]

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Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Lactate: The sodium salt of racemic or inactive lactic acid. It is a hygroscopic agent used intravenously as a systemic and urinary alkalizer. [NIH] Solitary Nucleus: Gray matter located in the dorsomedial part of the medulla oblongata associated with the solitary tract. The solitary nucleus receives inputs from most organ systems including the terminations of the facial, glossopharyngeal, and vagus nerves. It is a major coordinator of autonomic nervous system regulation of cardiovascular, respiratory, gustatory, gastrointestinal, and chemoreceptive aspects of homeostasis. The solitary nucleus is also notable for the large number of neurotransmitters which are found therein. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Space Perception: The awareness of the spatial properties of objects; includes physical space. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Spastic: 1. Of the nature of or characterized by spasms. 2. Hypertonic, so that the muscles are stiff and the movements awkward. 3. A person exhibiting spasticity, such as occurs in spastic paralysis or in cerebral palsy. [EU] Spasticity: A state of hypertonicity, or increase over the normal tone of a muscle, with heightened deep tendon reflexes. [EU] Spatial disorientation: Loss of orientation in space where person does not know which way is up. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU]

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Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinal Cord Diseases: Pathologic conditions which feature spinal cord damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord. [NIH] Spinal Cord Injuries: Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., wounds, gunshot; whiplash injuries; etc.). [NIH] Spinal Nerves: The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [NIH] Spinal tap: A procedure in which a needle is put into the lower part of the spinal column to collect cerebrospinal fluid or to give anticancer drugs intrathecally. Also called a lumbar puncture. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Status Epilepticus: Repeated and prolonged epileptic seizures without recovery of consciousness between attacks. [NIH] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [NIH] Stem cell transplantation: A method of replacing immature blood-forming cells that were destroyed by cancer treatment. The stem cells are given to the person after treatment to help the bone marrow recover and continue producing healthy blood cells. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Stereotactic: Radiotherapy that treats brain tumors by using a special frame affixed directly to the patient's cranium. By aiming the X-ray source with respect to the rigid frame, technicians can position the beam extremely precisely during each treatment. [NIH] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]

Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH]

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Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Striate: Recurrent branch of the anterior cerebral artery which supplies the anterior limb of the internal capsule. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stupor: Partial or nearly complete unconsciousness, manifested by the subject's responding only to vigorous stimulation. Also, in psychiatry, a disorder marked by reduced responsiveness. [EU] Subacute: Somewhat acute; between acute and chronic. [EU] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subiculum: A region of the hippocampus that projects to other areas of the brain. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Substrate: A substance upon which an enzyme acts. [EU] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Symptomatology: 1. That branch of medicine with treats of symptoms; the systematic discussion of symptoms. 2. The combined symptoms of a disease. [EU]

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Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate through direct electrical connections which are sometimes called electrical synapses; these are not included here but rather in gap junctions. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synaptic Vesicles: Membrane-bound compartments which contain transmitter molecules. Synaptic vesicles are concentrated at presynaptic terminals. They actively sequester transmitter molecules from the cytoplasm. In at least some synapses, transmitter release occurs by fusion of these vesicles with the presynaptic membrane, followed by exocytosis of their contents. [NIH] Syncope: A temporary suspension of consciousness due to generalized cerebral schemia, a faint or swoon. [EU] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Telecommunications: Transmission of information over distances via electronic means. [NIH]

Telencephalon: Paired anteriolateral evaginations of the prosencephalon plus the lamina terminalis. The cerebral hemispheres are derived from it. Many authors consider cerebrum a synonymous term to telencephalon, though a minority include diencephalon as part of the cerebrum (Anthoney, 1994). [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Temporal Lobe: Lower lateral part of the cerebral hemisphere. [NIH] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamus: Paired bodies containing mostly gray substance and forming part of the lateral wall of the third ventricle of the brain. The thalamus represents the major portion of the diencephalon and is commonly divided into cellular aggregates known as nuclear groups. [NIH]

212 Brain Injuries

Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Third Ventricle: A narrow cleft inferior to the corpus callosum, within the diencephalon, between the paired thalami. Its floor is formed by the hypothalamus, its anterior wall by the lamina terminalis, and its roof by ependyma. It communicates with the fourth ventricle by the cerebral aqueduct, and with the lateral ventricles by the interventricular foramina. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombectomy: Surgical removal of an obstructing clot or foreign material from a blood vessel at the point of its formation. Removal of a clot arising from a distant site is called embolectomy. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tidal Volume: The volume of air inspired or expired during each normal, quiet respiratory cycle. Common abbreviations are TV or V with subscript T. [NIH] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH]

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Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicokinetics: Study of the absorption, distribution, metabolism, and excretion of test substances. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Tracer: A substance (such as a radioisotope) used in imaging procedures. [NIH] Traction: The act of pulling. [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Trauma Centers: Specialized hospital facilities which provide diagnostic and therapeutic services for trauma patients. [NIH] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]

Tremor: Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of cerebellar diseases, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of Parkinson disease. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for

214 Brain Injuries

nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tubulin: A microtubule subunit protein found in large quantities in mammalian brain. It has also been isolated from sperm flagella, cilia, and other sources. Structurally, the protein is a dimer with a molecular weight of approximately 120,000 and a sedimentation coefficient of 5.8S. It binds to colchicine, vincristine, and vinblastine. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [NIH]

Urinate: To release urine from the bladder to the outside. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Uterine Contraction: Contraction of the uterine muscle. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vagal: Pertaining to the vagus nerve. [EU] Vagus Nerve: The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx). [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasoactive: Exerting an effect upon the calibre of blood vessels. [EU] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vasomotor: 1. Affecting the calibre of a vessel, especially of a blood vessel. 2. Any element or agent that effects the calibre of a blood vessel. [EU] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vegetative: 1. Concerned with growth and with nutrition. 2. Functioning involuntarily or unconsciously, as the vegetative nervous system. 3. Resting; denoting the portion of a cell

Dictionary 215

cycle during which the cell is not involved in replication. 4. Of, pertaining to, or characteristic of plants. [EU] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vestibular: Pertaining to or toward a vestibule. In dental anatomy, used to refer to the tooth surface directed toward the vestibule of the mouth. [EU] Vestibulocochlear Nerve: The 8th cranial nerve. The vestibulocochlear nerve has a cochlear part (cochlear nerve) which is concerned with hearing and a vestibular part (vestibular nerve) which mediates the sense of balance and head position. The fibers of the cochlear nerve originate from neurons of the spiral ganglion and project to the cochlear nuclei (cochlear nucleus). The fibers of the vestibular nerve arise from neurons of Scarpa's ganglion and project to the vestibular nuclei. [NIH] Vestibulocochlear Nerve Diseases: Diseases of the vestibular and/or cochlear (acoustic) nerves, which join to form the vestibulocochlear nerve. Vestibular neuritis, cochlear neuritis, and acoustic neuromas are relatively common conditions that affect these nerves. Clinical manifestations vary with which nerve is primarily affected, and include hearing loss, vertigo, and tinnitus. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral Afferents: The sensory fibers innervating the viscera. [NIH] Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the crystalline lens of the eye and in front of the retina. It is contained in a thin hyoid membrane

216 Brain Injuries

and forms about four fifths of the optic globe. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Void: To urinate, empty the bladder. [NIH] War: Hostile conflict between organized groups of people. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]

Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Wounds, Gunshot: Disruption of structural continuity of the body as a result of the discharge of firearms. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH]

217

INDEX A Abdomen, 159, 167, 187, 189, 209, 212, 214, 215 Acceptor, 159, 189, 196 Acculturation, 43, 69, 159 Acetylcholine, 65, 159, 170, 195 Acoustic, 15, 159, 215 Actin, 23, 159 Action Potentials, 30, 159 Activities of Daily Living, 24, 78, 159 Adaptability, 27, 159, 169 Adaptation, 9, 10, 30, 159, 199 Adenosine, 159, 164, 168, 198 Adjustment, 10, 11, 159 Adolescence, 32, 49, 52, 159 Adrenal Cortex, 159, 173, 179, 201 Adrenal Medulla, 8, 159, 169, 178, 195 Adrenergic, 159, 176, 178, 210 Advanced Life Support, 94, 160 Adverse Effect, 160, 207 Aerobic, 38, 160, 192 Aetiology, 62, 160 Afferent, 160, 186, 201 Affinity, 160, 164, 194, 208 Agonist, 6, 103, 160, 168, 176, 193 Albumin, 69, 160, 199 Alertness, 89, 160, 168 Algorithms, 160, 166 Alkaline, 160, 161, 168 Alkaloid, 160, 168, 171, 193 Alkalosis, 41, 48, 160 Alpha Particles, 160, 203 Alpha-1, 32, 160 Alternative medicine, 127, 160 Alveoli, 161, 215 Ambulatory Care, 161 Ameliorated, 15, 20, 161 Amenorrhea, 161, 168 Amino Acids, 161, 179, 181, 197, 200, 202 Ammonia, 104, 161, 210 Amnestic, 161, 191, 192 Amphetamines, 161, 171 Amygdala, 92, 161, 189, 211 Amyloid, 161, 170 Anaesthesia, 161, 185 Anal, 25, 54, 58, 161, 178, 189 Analgesic, 161, 193, 196 Analog, 5, 161

Analogous, 32, 161, 213 Analysis of Variance, 4, 161 Anaphylatoxins, 161, 172 Anaplasia, 162, 194 Anatomical, 13, 30, 31, 55, 100, 162, 175, 185 Anemia, 162, 171, 190 Anesthesia, 64, 162, 192 Anesthetics, 162, 165, 178 Aneurysm, 162, 214 Angiopathy, 162, 170 Animal model, 7, 12, 15, 19, 32, 90, 162 Anions, 160, 162, 187, 210 Annealing, 162, 200 Anoxia, 94, 111, 143, 162 Antagonism, 162, 168 Anterior Cerebral Artery, 162, 170, 210 Antibacterial, 162, 208 Antibiotic, 162, 174, 208 Antibodies, 162, 163, 183, 190, 192 Antibody, 160, 162, 163, 172, 183, 185, 186, 191, 192, 204, 208 Anticonvulsant, 163, 168 Antigen, 160, 162, 163, 172, 183, 186, 191 Antigen-Antibody Complex, 163, 172 Anti-inflammatory, 98, 163 Antineoplastic, 163, 181 Antioxidant, 15, 17, 65, 93, 104, 105, 163, 196 Anus, 161, 163, 167 Anxiety, 39, 72, 163 Anxiolytic, 163, 192 Aorta, 92, 163, 215 Aperture, 90, 163 Aphasia, 120, 161, 163 Apoptosis, 5, 6, 14, 17, 163, 169 Applicability, 15, 163 Approximate, 7, 84, 163 Aqueous, 163, 165, 174, 184 Arachidonate 12-Lipoxygenase, 163, 189 Arachidonate 15-Lipoxygenase, 164, 189 Arachidonate Lipoxygenases, 164, 189 Arachidonic Acid, 5, 6, 163, 164, 188, 202 Arginine, 34, 161, 164, 195 Aromatic, 94, 105, 164, 198 Arterial, 16, 48, 164, 167, 170, 184, 187, 202, 211

218 Brain Injuries

Arteries, 162, 163, 164, 166, 170, 173, 187, 192, 212 Arteriovenous, 16, 164, 170 Aspartate, 103, 164 Asphyxia, 16, 17, 104, 164 Assay, 23, 164 Astrocytes, 12, 164, 181, 194 Asymptomatic, 36, 59, 164 Ataxia, 164, 183 Atmospheric Pressure, 164, 184 ATP, 72, 164, 176, 181, 198, 202 Atrophy, 164, 194 Attenuation, 62, 65, 164 Auditory, 68, 110, 165, 179, 182, 183, 190, 201, 214 Autonomic, 92, 159, 165, 195, 198, 208 Autonomic Nervous System, 165, 198, 208 Axonal, 11, 26, 73, 90, 106, 165 Axons, 17, 23, 90, 100, 165, 175, 182, 194, 196, 203 Axotomy, 26, 165 B Bacteria, 162, 163, 165, 178, 192, 204, 208, 213, 214 Bacterial Physiology, 159, 165 Bactericidal, 165, 179 Bacteriophage, 165, 213 Bacteriuria, 36, 59, 165 Barbiturates, 88, 165, 206 Basal Ganglia, 99, 164, 165, 167, 170, 189 Base, 41, 47, 160, 165, 175, 181, 188, 203, 211 Basophils, 165, 182, 188 Bed Rest, 124, 165 Benign, 165, 167, 182, 194 Bilateral, 14, 165, 197 Bile, 165, 166, 180, 189, 209 Bilirubin, 160, 166 Biochemical, 6, 30, 97, 166, 206 Bioengineering, 8, 134, 166 Biological Markers, 32, 166 Biomechanics, 8, 166 Biosynthesis, 164, 166 Biotechnology, 34, 36, 118, 127, 135, 166 Biotransformation, 166 Bladder, 89, 166, 170, 185, 214, 216 Blood Coagulation, 166, 168 Blood Glucose, 45, 166 Blood pressure, 48, 166, 184, 192, 208 Blood vessel, 162, 166, 167, 169, 170, 171, 177, 178, 187, 190, 198, 207, 210, 212, 214 Blood Volume, 91, 166

Blood-Brain Barrier, 8, 55, 73, 166, 188 Body Burden, 166, 188 Body Fluids, 160, 167, 168, 208 Bolus, 20, 21, 56, 167 Bolus infusion, 167 Bone Marrow, 167, 179, 185, 190, 209 Bowel, 161, 167, 175, 181, 187 Bowel Movement, 167, 175 Bradykinin, 167, 195, 199 Brain Diseases, 167, 197 Brain Hypoxia, 167 Brain Infarction, 167, 187 Brain Ischemia, 98, 167, 184 Brain Neoplasms, 167, 183 Brain Stem, 167, 169 Branch, 155, 167, 177, 190, 197, 203, 208, 210, 212 Breakdown, 167, 169, 181 Bromocriptine, 62, 168 Burns, 27, 168 Burns, Electric, 168 Bypass, 97, 168 C Caffeine, 105, 168 Calcium, 13, 30, 103, 168, 172, 187, 207 Calcium-Binding Proteins, 30, 168 Calmodulin, 22, 168 Carbamazepine, 55, 168 Carbon Dioxide, 168, 181, 184, 199, 205 Carbon Monoxide Poisoning, 104, 168 Carcinogenic, 168, 186, 209 Cardiac, 49, 88, 94, 97, 112, 168, 169, 178, 183, 192, 193, 205, 209 Cardiac arrest, 88, 94, 97, 168 Cardiopulmonary, 92, 94, 168 Cardiopulmonary Resuscitation, 94, 168 Cardiorespiratory, 169, 192 Cardiovascular, 89, 169, 188, 206, 208 Caspase, 7, 9, 12, 169 Catecholamine, 35, 40, 169, 176, 198 Cations, 169, 187 Caudal, 169, 175, 184, 200 Causal, 14, 169, 178 Cause of Death, 8, 15, 104, 169 Cell Cycle, 169, 215 Cell Death, 7, 9, 12, 15, 26, 64, 163, 169, 194 Cell Differentiation, 169, 207 Cell proliferation, 169, 207 Cell Respiration, 169, 192, 205 Cell Transplantation, 12, 169 Cellular metabolism, 5, 62, 169

Index 219

Central Nervous System Infections, 169, 182, 183 Cerebellar, 92, 164, 169, 213 Cerebellum, 92, 167, 169, 200 Cerebral Arteries, 170, 192 Cerebral hemispheres, 165, 167, 170, 211 Cerebral Hemorrhage, 88, 170 Cerebral Infarction, 167, 170, 183 Cerebral Palsy, 170, 208 Cerebrospinal, 53, 70, 170, 183, 189, 209 Cerebrospinal fluid, 53, 70, 170, 183, 189, 209 Cerebrovascular, 65, 72, 84, 91, 170 Cerebrum, 170, 211 Cervical, 92, 170 Cervix, 170 Character, 170, 174 Chemotactic Factors, 170, 172 Cholesterol, 166, 170, 209 Cholinergic, 170 Cholinesterase Inhibitors, 102, 170, 176 Choroid, 171, 205 Chromatin, 163, 171, 178 Chronic, 5, 6, 10, 19, 24, 33, 35, 62, 63, 65, 71, 91, 92, 136, 167, 171, 186, 210 Circulatory system, 171, 177, 187 Clamp, 19, 30, 171 Clinical Medicine, 171, 201 Clinical study, 171, 173 Clinical trial, 5, 14, 18, 19, 20, 27, 50, 81, 85, 90, 135, 171, 204 Cloning, 17, 166, 171 Cobalt, 12, 171 Coca, 171 Cocaine, 33, 171 Cochlear, 171, 212, 215 Cochlear Diseases, 171, 212 Cofactor, 171, 202 Cognition, 24, 32, 49, 52, 171 Colloidal, 160, 171 Comatose, 56, 111, 171 Communication Disorders, 86, 114, 134, 143, 146, 171 Complement, 21, 62, 161, 172, 181, 199 Complementary and alternative medicine, 67, 75, 172 Complementary medicine, 67, 68, 172 Computational Biology, 135, 172 Computed tomography, 172 Computerized axial tomography, 172 Computerized tomography, 67, 172 Concomitant, 7, 173

Conduction, 31, 173 Cone, 23, 173 Confusion, 173, 184 Connective Tissue, 167, 173, 180, 181, 190 Consciousness, 10, 24, 89, 91, 92, 100, 111, 161, 173, 175, 178, 205, 209, 211 Consolidation, 92, 173 Constriction, 173, 187 Consumption, 62, 173, 196 Continuum, 89, 111, 173 Contraindications, ii, 173 Contralateral, 173, 191, 196 Controlled clinical trial, 70, 173 Contusion, 14, 26, 33, 63, 65, 100, 173 Convulsions, 163, 173, 184, 195 Coordination, 70, 147, 169, 173 Coronary, 173, 192 Coronary Thrombosis, 173, 192 Corpus, 173, 189, 201, 212 Corpus Luteum, 173, 189, 201 Cortex, 5, 13, 31, 34, 164, 167, 170, 173, 178, 179, 180, 186, 192, 194, 201, 203 Cortical, 9, 14, 19, 45, 62, 65, 71, 173, 179, 194, 201, 203, 206 Cortisol, 84, 160, 173 Cranial, 169, 173, 174, 182, 187, 196, 198, 214, 215 Craniocerebral Trauma, 84, 170, 173, 182, 183, 212 Craniotomy, 21, 174 Creatine, 69, 126, 174 Creatinine, 174 Critical Care, 38, 52, 115, 160, 174 Cues, 23, 174 Curative, 174, 212 Cyanide, 101, 174 Cyclic, 168, 174, 182, 195, 202, 206 Cycloserine, 106, 174 Cytokine, 5, 174 Cytoplasm, 93, 105, 163, 165, 174, 178, 182, 211 Cytoskeleton, 23, 174, 192 Cytotoxic, 26, 97, 98, 174, 207 D Databases, Bibliographic, 135, 174 Degenerative, 13, 102, 174, 181 Dehydroepiandrosterone, 5, 174 Deletion, 22, 163, 174 Delivery of Health Care, 174, 182 Dementia, 4, 82, 101, 114, 174, 175, 191 Denaturation, 175, 200 Dendrites, 175, 182, 194, 203

220 Brain Injuries

Dendritic, 22, 175 Density, 19, 175, 196, 208 Dentate Gyrus, 19, 35, 175, 183 Depolarization, 175, 207 Deprivation, 9, 175 Dermatitis, 27, 175 Dextroamphetamine, 175, 191 Diagnostic procedure, 87, 127, 175 Diastolic, 175, 184 Diastolic blood pressure, 175, 184 Diencephalon, 175, 184, 201, 211, 212 Diffuse Axonal Injury, 90, 100, 167, 175 Diffusion, 175, 186 Digestive system, 86, 175 Dilatation, 162, 175, 187, 201, 214 Dilatation, Pathologic, 175, 214 Dilation, 167, 175, 183, 214 Dimethyl, 101, 176 Direct, iii, 15, 17, 25, 26, 30, 91, 104, 129, 171, 176, 204, 211 Disinfectant, 176, 179 Distal, 165, 176, 202 Diuresis, 168, 176 Diuretic, 88, 176 Dizziness, 100, 110, 176 DNA Topoisomerase, 176, 181 Donepezil, 102, 176 Dopa, 176, 188 Dopamine, 94, 105, 168, 171, 175, 176, 188, 198 Dorsal, 92, 176, 200, 209 Dorsum, 176 Drug Interactions, 130, 176 Dyes, 30, 161, 165, 176 E Edema, 14, 73, 88, 91, 176, 187 Effector, 9, 21, 92, 98, 159, 172, 176, 195 Effector cell, 176, 195 Efficacy, 14, 18, 25, 63, 64, 83, 90, 176, 189, 201, 213 Electric shock, 168, 169, 177 Electrolyte, 177, 200, 208 Electrons, 163, 165, 177, 187, 190, 196, 203 Electrophysiological, 30, 92, 177 Elementary Particles, 177, 190, 195, 202 Embolectomy, 90, 177, 212 Embolism, 88, 177, 187 Embryo, 169, 177, 185 Emesis, 177, 184 Empirical, 24, 33, 177 Encephalitis, 177, 191 Encephalomyelitis, 88, 177

Encephalopathy, 104, 177 Endemic, 177, 190, 209 Endocrine System, 177, 194 Endoscopic, 177, 192 Endothelial cell, 102, 166, 177 Endothelium, 64, 178, 195, 199 Endothelium, Lymphatic, 178 Endothelium, Vascular, 178 Endothelium-derived, 178, 195 Endotoxin, 178, 214 Entorhinal Cortex, 6, 178, 183 Environmental Exposure, 166, 178 Environmental Health, 51, 134, 136, 178 Enzymatic, 168, 172, 178, 200, 205 Enzyme, 5, 6, 54, 163, 164, 166, 169, 176, 178, 182, 189, 199, 200, 202, 207, 210, 216 Eosinophils, 178, 182, 188 Epidemiologic Studies, 166, 178 Epilepticus, 19, 178 Epinephrine, 159, 176, 178, 195, 214 Epithelial, 102, 178 Epithelium, 178 Ergot, 168, 178 Erythrocyte Transfusion, 15, 18, 178 Erythrocyte Volume, 166, 178 Erythrocytes, 162, 167, 178, 179 Erythropoiesis, 15, 18, 179 Erythropoietin, 15, 17, 35, 179 Esophagus, 175, 179, 198, 209 Estradiol, 35, 179 Estrogen, 35, 46, 179, 201 Ethanol, 63, 65, 179 Eukaryotic Cells, 179, 185, 196 Evoke, 26, 34, 179, 209 Evoked Potentials, 59, 68, 179 Excitation, 19, 161, 179 Excitatory, 19, 179, 182, 195 Excitatory Amino Acids, 179, 195 Exhaustion, 162, 179, 190 Exogenous, 11, 166, 179 Expiration, 179, 205 Extensor, 89, 179 Extracellular, 23, 35, 161, 164, 173, 179, 180, 194, 208 Extracellular Space, 23, 179 Extraction, 16, 33, 179 Extrapyramidal, 176, 179 Extravasation, 179, 183 Extremity, 27, 180 F Facial, 180, 190, 208 Family Planning, 135, 180

Index 221

Family Relations, 9, 180 Fat, 32, 162, 164, 167, 180, 189 Fatigue, 4, 110, 180 Fatty acids, 70, 160, 180, 189, 202, 212 Feeding Behavior, 92, 180 Fetus, 179, 180, 199, 214 Fibrinogen, 180, 199 Fibroblasts, 180, 186 Fibrosis, 33, 180 Firearms, 137, 180, 216 Fissure, 175, 180, 201 Flatus, 180, 181 Flexor, 89, 179, 180 Flicker Fusion, 119, 180 Foetal, 39, 180 Forearm, 166, 180 Fossa, 169, 180 Frontal Lobe, 78, 162, 170, 180, 193, 201 Functional magnetic resonance imaging, 32, 34, 180 G Gallbladder, 175, 180 Ganglia, 92, 159, 180, 194, 198 Gap Junctions, 181, 211 Gas, 6, 161, 168, 175, 180, 181, 184, 195, 203, 214, 215 Gas exchange, 181, 215 Gastrin, 181, 183 Gastrointestinal, 92, 95, 167, 170, 178, 179, 181, 188, 190, 206, 208, 210 Gastrointestinal tract, 92, 95, 170, 179, 181, 188, 206 Gastrointestinal Transit, 95, 181 Gelatin, 181, 182 Gene, 6, 9, 17, 78, 118, 123, 166, 181, 186, 199, 206 Genetic Code, 181, 195 Genetic Engineering, 166, 171, 181 Genetic testing, 181, 200 Genistein, 72, 181 Genotype, 81, 124, 181, 198 Gestation, 181, 198, 199 Gland, 159, 181, 190, 197, 206, 209, 212 Gliosis, 14, 181 Glucose, 9, 92, 166, 181, 184, 206 Glutamate, 19, 22, 98, 182, 188 Glycine, 103, 182 Glycoprotein, 179, 180, 182, 214 Gonadal, 182, 209 Governing Board, 182, 201 Grade, 182 Grading, 89, 182

Graft, 12, 182, 183, 185 Graft Rejection, 182, 185 Granule, 21, 175, 182 Granulocytes, 182, 188, 207, 216 Growth, 11, 12, 23, 104, 159, 162, 163, 169, 182, 186, 190, 194, 199, 206, 212, 213, 214 Growth Cones, 23, 182 Guanylate Cyclase, 182, 195 H Hair Cells, 30, 182 Handicap, 17, 182 Headache, 168, 182, 183, 184 Health Care Costs, 14, 182, 183 Health Expenditures, 183 Hearing Disorders, 171, 183 Heart Arrest, 168, 169, 183 Hematoma, 26, 100, 106, 143, 183 Hemiparesis, 167, 183 Hemorrhage, 29, 65, 174, 182, 183, 210 Hepatic, 160, 183 Heredity, 181, 183 Hippocampus, 5, 6, 13, 19, 21, 35, 70, 92, 175, 183, 189, 203, 210 Homeostasis, 92, 183, 208 Homogeneous, 102, 173, 183 Homologous, 183, 206, 211 Hormone, 6, 13, 18, 84, 166, 173, 178, 179, 181, 183, 197, 201, 206, 207, 212 Host, 165, 183, 185, 188 Human Activities, 23, 183 Hybridomas, 183, 186 Hydrocephalus, 57, 88, 183, 187 Hydrogen, 159, 165, 175, 183, 184, 189, 192, 195, 196, 198, 202, 210 Hydrogen Peroxide, 184, 189, 210 Hydrophobic, 94, 105, 184 Hyperbaric, 37, 38, 71, 184 Hyperbaric oxygen, 37, 38, 71, 184 Hypercapnia, 65, 184 Hyperglycemia, 63, 184 Hypertension, 16, 91, 170, 184, 187 Hypertensive Encephalopathy, 29, 184 Hyperthermia, 32, 62, 184 Hypertonia, 125, 184 Hyperventilation, 41, 44, 51, 52, 72, 125, 184 Hypnotic, 184, 192 Hypoglycaemia, 104, 184 Hypotension, 97, 173, 184 Hypothalamic, 8, 184 Hypothalamus, 92, 165, 167, 175, 184, 189, 212

222 Brain Injuries

Hypothermia, 74, 81, 112, 124, 126, 184 Hypoxemia, 17, 185 Hypoxia, 12, 15, 18, 43, 88, 143, 185 I Id, 66, 74, 142, 143, 147, 148, 154, 156, 185 Imaging procedures, 185, 213 Immersion, 24, 185 Immune function, 7, 185 Immune response, 163, 182, 185, 210, 215 Immune system, 7, 13, 176, 185, 188, 190, 216 Immunization, 185 Immunoglobulin, 162, 185, 192 Immunophilin, 73, 185 Immunosuppressive, 185 Immunosuppressive therapy, 185 Immunotherapy, 95, 185 Impairment, 4, 25, 29, 31, 32, 47, 72, 89, 91, 92, 100, 106, 118, 120, 164, 185, 191 In situ, 17, 99, 185 In Situ Hybridization, 17, 185 In vitro, 5, 6, 9, 12, 22, 23, 99, 185, 200 In vivo, 5, 7, 9, 12, 13, 17, 65, 99, 185, 212 Incision, 41, 185 Incontinence, 183, 185 Indicative, 12, 91, 97, 99, 111, 185, 197, 214 Induction, 5, 65, 93, 185, 201 Infarction, 170, 173, 185, 191, 204 Infection, 12, 111, 124, 170, 177, 185, 186, 189, 190, 210, 216 Infertility, 168, 186 Infiltration, 98, 186 Inflammation, 6, 7, 15, 17, 91, 98, 160, 163, 175, 177, 180, 186, 188 Infusion, 20, 21, 160, 186 Ingestion, 186, 200 Inhalation, 186, 200 Initiation, 32, 98, 186, 213 Initiator, 9, 186 Inotropic, 176, 186 Insecticides, 186, 198 Interleukin-1, 35, 65, 186 Interleukin-10, 35, 186 Interleukin-2, 186 Interleukin-6, 48, 186 Intermittent, 180, 186 Internal Capsule, 162, 186, 210 Interpersonal Relations, 187, 207 Intestine, 167, 181, 187, 188 Intoxication, 104, 187 Intracellular, 13, 17, 23, 93, 105, 168, 186, 187, 195, 200, 202, 206, 207

Intracranial Aneurysm, 170, 187 Intracranial Arteriosclerosis, 170, 187 Intracranial Hemorrhages, 183, 187 Intracranial Hypertension, 182, 183, 187, 212 Intracranial Pressure, 57, 91, 106, 115, 122, 187 Intravenous, 15, 48, 186, 187 Involuntary, 187, 193, 199, 204, 208 Ion Channels, 164, 187, 194, 195, 211 Ionization, 187 Ionizing, 101, 160, 178, 187 Ions, 30, 165, 168, 177, 184, 187 Ischemia, 9, 12, 15, 16, 32, 33, 88, 89, 91, 94, 98, 101, 105, 164, 167, 187, 195, 204 Ischemic stroke, 16, 88, 103, 126, 187 J Joint, 11, 180, 187 K Kainate, 6, 13, 19, 103, 188 Kb, 134, 188 Kinetic, 187, 188 L Labile, 172, 188 Lactation, 188, 197, 201 Language Disorders, 171, 188 Large Intestine, 175, 187, 188, 204, 207 Larynx, 188, 214 Latent, 104, 188 Lead Poisoning, 27, 188 Lesion, 31, 181, 188, 189, 206 Lethal, 165, 174, 188 Lethargy, 183, 188 Leucocyte, 160, 188 Leukocytes, 98, 165, 167, 170, 178, 182, 188, 214 Leukotrienes, 6, 164, 188 Levodopa, 94, 105, 176, 188 Library Services, 154, 188 Life Expectancy, 40, 188 Ligands, 95, 188 Ligation, 15, 189 Limbic, 6, 161, 189, 201 Limbic System, 161, 189, 201 Lipid, 6, 63, 189, 192, 196 Lipid Peroxidation, 63, 189, 196 Lipoxygenase, 6, 164, 188, 189 Liver, 160, 164, 165, 175, 179, 180, 183, 189 Localization, 5, 22, 55, 189 Localized, 17, 23, 24, 167, 183, 186, 189, 199 Locomotion, 23, 31, 189, 199

Index 223

Locomotor, 15, 189 Longitudinal study, 28, 189 Long-Term Potentiation, 21, 189 Lumbar, 18, 41, 189, 209 Lumbar puncture, 18, 189, 209 Lutein Cells, 189, 201 Lymph, 170, 171, 177, 178, 189, 190 Lymph node, 170, 190 Lymphatic, 102, 178, 186, 189, 190, 209, 212 Lymphatic system, 102, 189, 190, 209, 212 Lymphocyte, 163, 190, 191 M Macrophage, 186, 190 Magnetic Resonance Imaging, 190 Magnetic Resonance Spectroscopy, 62, 65, 190 Malaria, 101, 190 Malaria, Falciparum, 190 Malaria, Vivax, 190 Malignant, 163, 167, 184, 190, 194 Malnutrition, 160, 164, 190 Manifest, 165, 190 Meatus, 190, 214 Medial, 14, 92, 190, 196 Mediate, 21, 95, 176, 190 Mediator, 5, 176, 186, 191, 206 MEDLINE, 135, 191 Meiosis, 191, 211 Melanin, 191, 198, 214 Membrane, 23, 26, 30, 93, 105, 164, 171, 172, 175, 179, 187, 188, 191, 193, 196, 198, 205, 207, 211, 215 Memory Disorders, 91, 112, 191 Meninges, 169, 174, 191, 209 Menstrual Cycle, 191, 201 Mental Disorders, 22, 82, 86, 191, 203 Mental Health, iv, 4, 9, 82, 86, 114, 134, 138, 191, 203 Mental Processes, 191, 203 Mental Retardation, 171, 191 Mentors, 33, 191 Mesencephalic, 92, 191 Metabolite, 166, 176, 191, 201, 203 Metastasis, 191, 194 Methionine, 176, 191 Methylphenidate, 83, 191 MI, 157, 191 Microbiology, 59, 159, 165, 192 Microorganism, 171, 192, 216 Microscopy, 22, 192 Microtubules, 23, 192

Midazolam, 48, 192 Middle Cerebral Artery, 12, 192 Mitochondria, 9, 192, 196 Mitochondrial Swelling, 192, 194 Mitosis, 163, 192 Mitotic, 12, 192 Mobility, 49, 192 Modification, 37, 181, 192, 203 Modulator, 103, 192 Molecule, 35, 101, 163, 165, 172, 176, 178, 179, 192, 196, 204, 207, 214 Monitor, 4, 96, 97, 120, 174, 192, 195 Monoclonal, 68, 183, 192, 204 Monoclonal antibodies, 68, 192 Monocyte, 98, 193 Mononuclear, 193, 214 Morphine, 95, 193, 196 Morphological, 27, 177, 193 Morphology, 14, 36, 193 Motility, 95, 193, 206 Motor Cortex, 69, 193 Motor Skills, 92, 193 Mucosa, 193, 201 Multiple Trauma, 49, 193 Muscular Diseases, 193, 197 Mutagenesis, 22, 193 Mutagens, 193 Myocardium, 191, 193 N Naloxone, 93, 193 Narcolepsy, 175, 191, 193 Narcosis, 193 Narcotic, 95, 193 Nausea, 184, 193 NCI, 1, 85, 133, 193 Necrosis, 88, 163, 167, 170, 186, 191, 193, 204, 205, 206 Neocortex, 13, 26, 194 Neonatal, 12, 15, 65, 125, 194 Neoplasms, 99, 163, 167, 194 Nerve Fibers, 92, 100, 194 Nervous System, 13, 17, 57, 82, 90, 92, 93, 100, 101, 159, 160, 161, 165, 167, 168, 169, 170, 171, 175, 179, 180, 182, 188, 191, 193, 194, 195, 196, 198, 200, 206, 210, 211, 214 Networks, 19, 92, 149, 194 Neural, 8, 31, 34, 91, 92, 99, 101, 102, 106, 160, 161, 194 Neurobehavioral Manifestations, 167, 175, 194

224 Brain Injuries

Neurodegenerative Diseases, 6, 21, 101, 194 Neuroendocrine, 83, 194 Neuroglia, 181, 194 Neurologic, 94, 167, 183, 184, 194 Neurology, 16, 21, 24, 33, 38, 39, 45, 48, 49, 50, 53, 58, 65, 68, 69, 70, 106, 122, 194 Neuromuscular, 38, 159, 194, 197 Neuromuscular Junction, 159, 194 Neuronal, 6, 9, 11, 13, 15, 17, 20, 22, 23, 26, 27, 70, 97, 100, 104, 106, 165, 182, 193, 194 Neuroprotective Agents, 6, 16, 46, 68, 195 Neurotoxic, 6, 195 Neurotoxicity, 99, 101, 195 Neurotransmitters, 92, 99, 117, 179, 195, 208 Neutrons, 160, 195, 203 Neutrophil, 12, 63, 103, 195 Nitric Oxide, 65, 73, 98, 103, 195 Nonverbal Communication, 171, 195 Norepinephrine, 159, 176, 195 Nuclear, 6, 26, 71, 165, 171, 177, 179, 180, 186, 189, 194, 195, 211 Nuclear Family, 180, 195 Nuclei, 24, 92, 160, 161, 162, 177, 181, 189, 190, 192, 195, 196, 202, 215 Nucleic acid, 101, 102, 181, 185, 193, 195 O Occult, 65, 195 Oculomotor, 191, 196 Odour, 164, 196 On-line, 32, 157, 196 Opacity, 175, 196 Opium, 193, 196 Optic Chiasm, 184, 196 Optic Nerve, 196, 205 Organelles, 174, 196 Osmosis, 196 Osmotic, 88, 160, 192, 196 Outpatient, 196 Ovary, 173, 179, 196 Overexpress, 9, 196 Ovum, 173, 181, 196, 201 Oxidation, 94, 105, 159, 163, 164, 166, 189, 196 Oxidative Stress, 18, 93, 94, 105, 196 Oxygen Consumption, 196, 205 Oxygenation, 45, 185, 197 Oxytocin, 18, 197 P Palliative, 197, 212

Pancreas, 175, 197 Papilledema, 184, 197 Paralysis, 183, 191, 197, 208 Paraplegia, 50, 197 Parietal, 31, 34, 162, 197 Parietal Lobe, 34, 162, 197 Parkinsonism, 188, 197 Partial response, 89, 197 Particle, 197, 208, 213 Parturition, 197, 201 Patch, 19, 197 Pathogenesis, 94, 98, 105, 197 Pathologic, 163, 167, 173, 197, 205, 209 Pathologic Processes, 163, 197 Pathologies, 5, 197 Pathophysiology, 13, 16, 197 Patient Education, 145, 152, 154, 157, 197 Peptide, 197, 200, 202 Perception, 24, 173, 183, 197 Perforation, 163, 197 Perfusion, 16, 71, 91, 185, 197 Perinatal, 12, 15, 35, 44, 62, 97, 104, 116, 198 Peripheral Nervous System, 95, 194, 197, 198, 210 Peripheral Nervous System Diseases, 197, 198 Pesticides, 51, 186, 198 PH, 45, 67, 198 Pharmacokinetic, 198 Pharmacologic, 64, 162, 198, 213 Pharmacotherapy, 13, 14, 198 Pharynx, 198, 214 Phenotype, 21, 166, 198 Phenylalanine, 198, 214 Phospholipases, 198, 207 Phospholipids, 180, 198 Phosphorus, 168, 198 Phosphorylation, 21, 22, 198, 202 Photoreceptors, 30, 198 Physical Therapy, 13, 116, 199 Physiologic, 160, 166, 176, 191, 199, 202, 204, 205, 213 Physiology, 3, 13, 30, 44, 62, 72, 165, 166, 177, 199 Pigments, 171, 199, 205 Piloerection, 184, 199 Placenta, 179, 199, 201 Plants, 160, 168, 171, 181, 193, 195, 199, 206, 213, 215 Plasma, 18, 26, 101, 160, 162, 166, 178, 180, 181, 199

Index 225

Plasma protein, 160, 178, 199 Plasma Volume, 166, 199 Plasmin, 199 Plasminogen, 46, 199 Plasminogen Activators, 199 Plasticity, 21, 22, 31, 69, 91, 92, 199 Platelet Activation, 199, 207 Platelet Aggregation, 161, 195, 199, 212 Platelets, 163, 195, 199, 200, 206, 212 Poisoning, 97, 178, 187, 193, 200 Polymerase, 6, 200 Polymerase Chain Reaction, 6, 200 Polymers, 94, 105, 200, 202 Polymorphic, 175, 200 Polypeptide, 180, 199, 200, 201 Pons, 70, 167, 200, 205 Posterior, 31, 161, 164, 169, 171, 176, 186, 197, 200 Postnatal, 200, 209 Postoperative, 51, 200 Postsynaptic, 22, 200, 207, 211 Post-traumatic, 4, 13, 19, 20, 32, 51, 58, 91, 106, 167, 200 Postural, 31, 200 Potassium, 103, 200 Potentiates, 186, 200 Potentiation, 22, 170, 189, 200, 207 Practicability, 200, 213 Practice Guidelines, 138, 147, 200 Preclinical, 14, 27, 201 Precursor, 27, 164, 176, 178, 188, 195, 198, 199, 201, 214 Prefrontal Cortex, 31, 201 Pregnenolone, 27, 201 Presynaptic, 21, 201, 211 Prevalence, 16, 29, 52, 146, 201 Probe, 99, 201 Problem Solving, 54, 100, 201 Prodrug, 201 Progesterone, 27, 46, 83, 201, 209 Program Evaluation, 33, 201 Progression, 26, 90, 162, 201 Progressive, 19, 26, 90, 102, 169, 175, 182, 193, 194, 199, 201 Projection, 195, 196, 201, 203 Prolactin, 18, 168, 201 Prone, 92, 201 Prophase, 201, 211 Prospective study, 189, 202 Prostaglandin, 5, 202, 212 Prostaglandins A, 202 Protein C, 160, 165, 202

Protein Kinases, 22, 202 Protein S, 118, 166, 181, 202 Protein-Tyrosine Kinase, 181, 202 Proteolytic, 160, 172, 180, 199, 202 Protons, 160, 184, 187, 190, 202, 203 Proximal, 176, 201, 202 Psychiatric, 39, 53, 110, 166, 171, 191, 202 Psychiatry, 5, 44, 48, 53, 63, 74, 106, 202, 210, 215 Psychic, 203, 206 Psychology, 7, 14, 18, 33, 34, 78, 203 Psychomotor, 168, 203 Psychotropic, 64, 71, 203 Public Health, 14, 28, 47, 137, 138, 203 Public Policy, 135, 203 Publishing, 34, 109, 110, 119, 120, 203 Pulmonary, 166, 173, 184, 188, 203, 215 Pulmonary Artery, 166, 203, 215 Pulmonary Ventilation, 184, 203 Pulse, 15, 29, 192, 203 Pyramidal Cells, 175, 203 Q Quality of Life, 29, 46, 72, 203 Quinolinic, 98, 203 Quinolinic Acid, 98, 203 Quinones, 94, 105, 203 R Race, 20, 21, 176, 203, 208 Radiation, 43, 101, 176, 177, 178, 184, 187, 203, 204, 216 Radiation therapy, 176, 184, 203 Radioactive, 166, 184, 187, 193, 195, 204 Radioisotope, 179, 204, 213 Randomized, 20, 70, 77, 177, 204 Randomized clinical trial, 20, 204 Reaction Time, 83, 204 Reactive Oxygen Species, 98, 117, 204 Receptor, 5, 6, 9, 22, 30, 35, 65, 93, 95, 96, 103, 159, 163, 173, 176, 179, 188, 204, 206, 207 Recombinant, 15, 17, 204, 214 Recovery of Function, 11, 13, 92, 204 Rectum, 163, 167, 175, 180, 181, 185, 188, 204 Refer, 1, 172, 176, 189, 195, 204, 215 Reflex, 15, 89, 204 Refraction, 204, 208 Regeneration, 7, 17, 104, 204 Regimen, 62, 174, 176, 198, 204 Relapse, 25, 204 Reliability, 11, 55, 204 Reperfusion, 103, 204, 205

226 Brain Injuries

Reperfusion Injury, 204, 205 Research Design, 28, 205 Resected, 99, 205 Resorption, 183, 205 Respiration, 38, 42, 89, 104, 168, 192, 205 Respiratory Physiology, 205, 215 Respite Care, 149, 205 Restoration, 72, 199, 204, 205, 216 Resuscitation, 20, 21, 48, 94, 104, 168, 169, 205 Reticular, 30, 92, 205 Reticular Formation, 30, 92, 205 Retina, 30, 171, 194, 196, 205, 215 Retinal, 173, 184, 196, 205 Retinal Hemorrhage, 184, 205 Retrograde, 17, 205 Rigidity, 184, 187, 197, 199, 205 Risk factor, 72, 178, 202, 205 Rod, 171, 205 Rodenticides, 198, 205 S Salivary, 175, 206 Salivary glands, 175, 206 Saponins, 206, 209 Schizophrenia, 22, 82, 191, 206 Screening, 41, 54, 98, 171, 206 Second Messenger Systems, 195, 206 Secretion, 6, 84, 168, 188, 206 Secretory, 206, 211 Sedative, 192, 206 Sedatives, Barbiturate, 165, 206 Segregation, 165, 206 Seizures, 19, 20, 37, 48, 54, 82, 101, 110, 168, 178, 184, 206, 209 Self Care, 159, 206 Semisynthetic, 168, 206 Sequela, 32, 175, 206 Sequencing, 200, 206 Sequester, 30, 206, 211 Serotonin, 198, 206, 214 Serous, 178, 206 Serum, 48, 54, 160, 161, 172, 206, 214 Sex Characteristics, 159, 207 Shock, 48, 95, 117, 207, 213 Side effect, 83, 88, 129, 160, 176, 207, 213 Signal Transduction, 22, 207 Signs and Symptoms, 204, 207 Skeletal, 170, 171, 193, 207, 208 Skeleton, 159, 187, 202, 207 Skull, 8, 88, 100, 144, 174, 187, 207, 211 Small intestine, 183, 187, 207, 215

Smooth muscle, 161, 168, 193, 207, 208, 210 Social Behavior, 18, 207 Social Desirability, 59, 207 Social Environment, 10, 203, 207 Social Support, 72, 207 Sodium, 48, 103, 208, 210 Sodium Lactate, 48, 208 Solitary Nucleus, 92, 165, 208 Solvent, 179, 196, 208 Soma, 203, 208 Somatic, 26, 92, 159, 189, 191, 192, 198, 201, 208, 214 Sound wave, 173, 208 Space Perception, 24, 208 Spasm, 191, 208 Spastic, 125, 208 Spasticity, 184, 208 Spatial disorientation, 176, 208 Specialist, 149, 175, 208 Species, 30, 95, 169, 178, 190, 191, 192, 203, 204, 207, 208, 210, 213, 214, 216 Specificity, 17, 93, 160, 164, 208 Spectrum, 89, 208 Spinal Cord Diseases, 197, 209 Spinal Cord Injuries, 17, 98, 99, 142, 209 Spinal Nerves, 198, 209 Spinal tap, 189, 209 Spleen, 190, 209 Sporadic, 194, 209 Status Epilepticus, 19, 50, 209 Steel, 171, 209 Stem cell transplantation, 12, 209 Stem Cells, 11, 179, 209 Stereotactic, 25, 209 Steroid, 13, 173, 201, 206, 209 Stimulant, 168, 175, 191, 209 Stimulus, 24, 58, 176, 179, 180, 187, 204, 209, 212 Stomach, 175, 179, 181, 183, 193, 198, 207, 209 Strand, 200, 209 Stress, 4, 7, 9, 18, 42, 73, 78, 100, 165, 169, 173, 193, 196, 210 Striate, 34, 210 Stupor, 188, 193, 210 Subacute, 27, 186, 210 Subarachnoid, 65, 97, 182, 187, 210 Subclinical, 186, 206, 210 Subcutaneous, 176, 210 Subiculum, 183, 210 Subspecies, 208, 210

Index 227

Substance P, 166, 174, 191, 206, 210 Substrate, 42, 210 Superoxide, 70, 210 Superoxide Dismutase, 70, 210 Supplementation, 126, 210 Support group, 149, 210 Survival Rate, 94, 146, 210 Sweat, 184, 210 Sympathomimetic, 175, 176, 178, 195, 210 Symptomatic, 36, 59, 94, 105, 210 Symptomatology, 29, 78, 210 Synapses, 13, 21, 30, 170, 189, 195, 211 Synapsis, 211 Synaptic, 19, 21, 22, 30, 189, 207, 211 Synaptic Transmission, 22, 30, 211 Synaptic Vesicles, 211 Syncope, 89, 211 Synergistic, 201, 211 Systemic, 15, 35, 47, 68, 163, 166, 167, 178, 186, 187, 204, 208, 211 Systolic, 184, 211 T Telecommunications, 89, 211 Telencephalon, 165, 211 Temporal, 12, 19, 34, 68, 161, 183, 190, 211 Temporal Lobe, 19, 161, 211 Testis, 179, 211 Thalamic, 24, 92, 164, 211 Thalamus, 92, 167, 175, 189, 201, 211 Therapeutics, 17, 98, 130, 212 Thermal, 195, 200, 212 Third Ventricle, 184, 211, 212 Thorax, 159, 189, 212, 214 Threshold, 25, 34, 184, 212 Thrombectomy, 177, 212 Thrombolytic, 199, 212 Thrombosis, 88, 187, 202, 210, 212 Thromboxanes, 164, 212 Thrombus, 173, 186, 187, 200, 212 Thymus, 185, 190, 212 Thyroid, 212, 214 Thyroxine, 160, 198, 212 Tidal Volume, 184, 212 Tinnitus, 146, 212, 215 Tolerance, 159, 212 Tomography, 16, 30, 142, 190, 212 Tooth Preparation, 159, 213 Topical, 179, 184, 213 Toxic, iv, 94, 101, 103, 104, 105, 168, 174, 177, 178, 213 Toxicity, 176, 213 Toxicokinetics, 213

Toxicology, 29, 136, 213 Toxins, 163, 177, 186, 193, 213 Trace element, 171, 213 Tracer, 30, 213 Traction, 171, 213 Transcription Factors, 102, 213 Transduction, 22, 207, 213 Transfection, 17, 166, 213 Translocation, 22, 213 Transmitter, 159, 164, 176, 179, 187, 191, 194, 195, 211, 213 Transplantation, 101, 185, 213 Trauma Centers, 106, 149, 213 Treatment Outcome, 25, 33, 213 Tremor, 191, 197, 213 Tryptophan, 203, 206, 213 Tuberculosis, 173, 174, 214 Tubulin, 192, 214 Tumor Necrosis Factor, 35, 214 Tyrosine, 72, 176, 202, 214 U Unconscious, 52, 162, 185, 214 Urinary, 165, 170, 174, 183, 185, 208, 214 Urinary tract, 165, 174, 214 Urinary tract infection, 165, 174, 214 Urinate, 214, 216 Urine, 165, 166, 174, 176, 185, 214 Uterine Contraction, 197, 214 Uterus, 170, 173, 201, 214 V Vagal, 92, 214 Vagus Nerve, 89, 91, 92, 208, 214 Vascular, 5, 8, 33, 65, 91, 171, 178, 186, 187, 195, 199, 209, 212, 214 Vasoactive, 5, 214 Vasodilation, 64, 72, 214 Vasodilator, 167, 176, 214 Vasomotor, 91, 214 VE, 119, 214 Vector, 213, 214 Vegetative, 24, 63, 90, 143, 175, 214 Vein, 162, 164, 187, 195, 215 Venous, 164, 167, 170, 202, 215 Ventilation, 41, 168, 169, 215 Ventricle, 161, 183, 203, 211, 212, 215 Ventricular, 48, 58, 183, 215 Vertebrae, 209, 215 Vestibular, 118, 182, 215 Vestibulocochlear Nerve, 212, 215 Vestibulocochlear Nerve Diseases, 212, 215 Veterinary Medicine, 135, 215

228 Brain Injuries

Villi, 183, 215 Viral, 9, 177, 213, 215 Viral vector, 9, 215 Virus, 165, 169, 181, 186, 213, 215 Viscera, 208, 215 Visceral, 92, 165, 189, 214, 215 Visceral Afferents, 92, 165, 214, 215 Vitreous Body, 205, 215 Vitro, 6, 9, 12, 22, 216 Vivo, 9, 12, 17, 62, 216 Void, 11, 216

W War, 38, 53, 119, 216 White blood cell, 162, 188, 190, 193, 195, 216 Wound Healing, 8, 216 Wounds, Gunshot, 209, 216 X Xenograft, 162, 216 X-ray, 10, 172, 195, 203, 209, 216 Y Yeasts, 198, 216

Index 229

230 Brain Injuries

Index 231

232 Brain Injuries

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