Head Trauma - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

HEAD TRAUMA 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 2004 by ICON Group International, Inc. Copyright 2004 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., 1960Head Trauma: 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: 0-497-00512-3 1. Head Trauma-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 head trauma. 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 HEAD TRAUMA......................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Head Trauma ................................................................................ 6 E-Journals: PubMed Central ....................................................................................................... 40 The National Library of Medicine: PubMed ................................................................................ 41 CHAPTER 2. NUTRITION AND HEAD TRAUMA ............................................................................... 85 Overview...................................................................................................................................... 85 Finding Nutrition Studies on Head Trauma ............................................................................... 85 Federal Resources on Nutrition ................................................................................................... 86 Additional Web Resources ........................................................................................................... 87 CHAPTER 3. ALTERNATIVE MEDICINE AND HEAD TRAUMA ........................................................ 89 Overview...................................................................................................................................... 89 National Center for Complementary and Alternative Medicine.................................................. 89 Additional Web Resources ........................................................................................................... 90 General References ....................................................................................................................... 91 CHAPTER 4. DISSERTATIONS ON HEAD TRAUMA .......................................................................... 93 Overview...................................................................................................................................... 93 Dissertations on Head Trauma .................................................................................................... 93 Keeping Current .......................................................................................................................... 93 CHAPTER 5. PATENTS ON HEAD TRAUMA ..................................................................................... 95 Overview...................................................................................................................................... 95 Patents on Head Trauma ............................................................................................................. 95 Patent Applications on Head Trauma ....................................................................................... 100 Keeping Current ........................................................................................................................ 106 CHAPTER 6. BOOKS ON HEAD TRAUMA ....................................................................................... 109 Overview.................................................................................................................................... 109 Book Summaries: Federal Agencies............................................................................................ 109 Book Summaries: Online Booksellers......................................................................................... 110 Chapters on Head Trauma ......................................................................................................... 111 CHAPTER 7. MULTIMEDIA ON HEAD TRAUMA ............................................................................ 119 Overview.................................................................................................................................... 119 Video Recordings ....................................................................................................................... 119 CHAPTER 8. PERIODICALS AND NEWS ON HEAD TRAUMA ......................................................... 121 Overview.................................................................................................................................... 121 News Services and Press Releases.............................................................................................. 121 Newsletter Articles .................................................................................................................... 123 Academic Periodicals covering Head Trauma............................................................................ 124 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 127 Overview.................................................................................................................................... 127 NIH Guidelines.......................................................................................................................... 127 NIH Databases........................................................................................................................... 129 Other Commercial Databases..................................................................................................... 131 APPENDIX B. PATIENT RESOURCES ............................................................................................... 133 Overview.................................................................................................................................... 133 Patient Guideline Sources.......................................................................................................... 133 Finding Associations.................................................................................................................. 138 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 141 Overview.................................................................................................................................... 141 Preparation................................................................................................................................. 141

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Finding a Local Medical Library................................................................................................ 141 Medical Libraries in the U.S. and Canada ................................................................................. 141 ONLINE GLOSSARIES................................................................................................................ 147 Online Dictionary Directories ................................................................................................... 147 HEAD TRAUMA DICTIONARY ............................................................................................... 149 INDEX .............................................................................................................................................. 221

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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 head trauma 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 head trauma, 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 head trauma, 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 head trauma. 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 head trauma, 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 head trauma. 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 HEAD TRAUMA Overview In this chapter, we will show you how to locate peer-reviewed references and studies on head trauma.

The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and head trauma, 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 “head trauma” (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: •

Head Trauma and Mid-Frequency Hearing Loss Source: American Journal of Audiology. 8(2): 101-105. December 1999. Contact: Available from American Speech-Language-Hearing Association (ASHA). Product Sales, 10801 Rockville Pike, Rockville, MD 20852. (888) 498-6699. TTY (301) 8970157. Website: www.asha.org. Summary: Numerous reports in the literature associate head trauma with high frequency hearing losses, often mimicking '4K notches' attributed to noise exposure. In this article, the authors discuss their observations of some patients with a positive history for head trauma who instead show midfrequency single and double sensorineural notches in their audiometric configurations. They offer two case studies that illustrate these notch audiograms following serious head injury. Case 1 reveals two

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distinct audiometric configurations postinjury: one ear had a marked notch pattern at 2000 Hz, whereas the opposite ear showed a gently sloping high frequency sensorineural loss. Case 2 data are intriguing in that the hearing sensitivity for the involved ear gradually improved over a 30 month period. The authors conclude by noting that it is appropriate to make inquiries regarding head trauma when attempting to establish possible causative factors of a hearing loss for individuals who have a sensorineural hearing loss with a midfrequency notch configuration. 3 figures. 16 references. •

Olfactory Dysfunction in Patients with Head Trauma Source: Archives of Neurology. 54(9): 1131-1140. September 1997. Summary: The ability to smell is commonly altered by head trauma (HT). However, the nature, prevalence, prognosis, and etiology of such alterations are poorly understood. This article reports on a study undertaken to quantitatively determine the degree of olfactory function in patients with HT-related chemosensory complaints and to examine the influence of age, sex, HT severity, time since HT, and other variables on such function. The study also investigated the use of magnetic resonance imaging (MRI) to establish whether and to what degree damage occurs to the olfactory bulbs and tracts, frontal lobes, and temporal lobes. Two hundred sixty-eight (268) patients with HT were administered a quantitative odor identification test, a depression inventory, and a medical history questionnaire; 66 were retested after 1 month to 13 years. The volume of olfactory-related brain structures was determined in 15 patients and 15 controls using MRI. One hundred seventy-nine (179) patients (66.8 percent) had anosmia (absence of the sense of smell), 55 (20.5 percent) had microsomia (limited sense of smell), and 34 (12.7 percent) had normosmia (normal sense of smell). Frontal impacts produced less dysfunction than back or side impacts. Of the 66 retested patients, 24 (36 percent) improved slightly, 30 (45 percent) had no change, and 12 (18 percent) worsened; only 3 patients, none of whom initially had anosmia, regained normal olfactory function. Trauma severity was related to olfactory test scores in patients with microsomia. Parosmia prevalence decreased from 41.1 percent to 15.4 percent over an 8 year posttrauma period. Olfactory bulb and tract volumes of male patients with HT were greatly reduced relative to volumes of controls. 6 figures. 1 table. 36 references. (AA-M).

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Long-term Follow-up of Olfactory Loss Secondary to Head Trauma and Upper Respiratory Tract Infection Source: Archives of Otolaryngology Head and Neck Surgery. 121(10): 1183-1187. October 1995. Summary: This article reports on a study undertaken to determine the extent to which olfactory function can improve after loss induced by head trauma or a previous upper respiratory tract infection (URI) and the time for this improvement for more effective patient counseling. Forty-one patients with olfactory loss induced by head trauma (n=20) or previous URI (n=21) were evaluated with the University of Pennsylvania Smell Identification Test 1 to 5 years after initial testing at the University of Cincinnati Taste and Smell Center. Seven (35 percent) of the patients with head trauma improved on the smell test by 4 points or more. Fourteen (67 percent) patients with previous URI had improved scores of this magnitude or more. A statistically significant correlation was noted between the amount of improvement and length of follow-up for URI patients. Thirteen of these patients also reported improved olfactory function. 2 figures. 2 tables. 22 references. (AA-M).

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Neurological Assessment of the Child with Head Trauma Source: Journal of Dentistry for Children. 62(2): 93-96. March-April 1995. Summary: This article, written for dentists, reviews the neurological assessment of the child with head trauma. The authors note that, since dental trauma is a subset of head trauma, the emergency appearance of a child in the dental office may present as a true medical emergency. A force that is strong enough to fracture, intrude, or avulse a tooth in a child is clearly strong enough to result in cervical spine or intracranial injury. The dental practitioner must be particularly alert to a number of difficult to diagnose problems associated with head trauma. The article discusses epidemiology of head trauma in children, closed-head injury, office neurological assessment, posttreatment precautions, and legal aspects. The authors reiterate that it is essential for the dentist to be able to assess the gross neurological status of the child presenting with head injury and to recognize acute and delayed signs of nerve injury. 1 table. 16 references. (AA-M).

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Head Trauma and the Risk of Alzheimer's Disease Source: American Journal of Epidemiology. 135(7): 775-782. April 11, 1992. Summary: This journal article describes a population based study of the association between head trauma and risk of Alzheimer's disease. The study was conducted in the Netherlands between 1980 and 1987 and included 198 patients with a diagnosis of early onset Alzheimer's disease and 198 controls matched for age and sex. After adjusting for age, sex, education, and family history of dementia, the odds ratio for a history of head trauma with loss of consciousness was 1.6. The odds ratio for men was 2.5 and that for women was 0.9. The association between Alzheimer's disease and head trauma with loss of consciousness was confined to head trauma that occurred within the 10 year period before the onset of dementia. The association was not modified by family history of dementia as measured on a multiplicative scale. The findings are compatible with a role of head trauma in Alzheimer's disease, but the authors caution that the suspected association needs to be confirmed in a prospective follow up study. 35 references.

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Head Trauma and Risk of Dementia and Alzheimer's Disease: The Rotterdam Study Source: Neurology. 53: 1959-1962. December 1999. Summary: This journal article describes a study that investigated the relation between head trauma and incidence of dementia. The study population consisted of 6,645 participants of the prospective, population-based Rotterdam Study, aged 55 years or older, who were free of dementia at baseline. Information was collected by self-report about number of head traumas, time since head trauma, and duration of loss of consciousness. Participants were followed for an average of 2.1 years, and incident dementia was diagnosed according to international criteria. After adjusting for age, gender, and education, no increased risk of dementia or Alzheimer's disease (AD) was found for participants with a history of head trauma and loss of consciousness (relative risk for dementia = 1.0; relative risk for AD = 0.8). Risk of dementia was not influenced by multiple head traumas, time since head trauma, or duration of unconsciousness, or by the presence of an apolipoprotein E4 allele. The results suggest that mild head trauma is not a major risk factor for dementia or AD in the elderly. In addition, they do not concur with previous findings suggesting an interaction with the apoE genotype. 4 tables, 32 references. (AA-M).

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Federally Funded Research on Head Trauma The U.S. Government supports a variety of research studies relating to head trauma. 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 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 head trauma. 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 head trauma. The following is typical of the type of information found when searching the CRISP database for head trauma: •

Project Title: A NEW SCINTILLATOR FOR RADIONUCLIDE IMAGING Principal Investigator & Institution: Shah, Kanai S.; Radiation Monitoring Devices, Inc. 44 Hunt St Watertown, Ma 02472 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2003 Summary: (provided by applicant):Single Photon Emission Computed Tomography (SPECT) is a powerful, non-invasive medical imaging technique which provides an image of the three-dimensional distribution of radionuclide in any slice through an organ under study in the body. These images allow investigation of metabolism in the region being studied and are also a useful tool for understanding the functioning of the organs, as well as diagnosing symptoms of diseases such as cancer, myocardial ischemia, Alzheimer's disease, head trauma, and stroke. Scintillation crystals (such as NaI:TI) coupled to photomultiplier tubes are typically used as detectors in SPECT systems and the imaging performance of the system is often limited by the characteristics of the available scintillation materials. In order to overcome the limitations in the existing detectors, the goal of the proposed research is to investigate a promising new scintillation material which shows higher light output, faster response, and higher stopping efficiency compared to NaI(T1) crystals. The Phase I project will be aimed at demonstrating the feasibility of producing large crystals of the new scintillation material and applying such crystals to radionuclide imaging. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ACUTE BRAIN INJURY, MECHANISMS AND CONSEQUENCES Principal Investigator & Institution: Olney, John W.; Professor; Psychiatry; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 21-FEB-2002; Project End 31-JAN-2007 Summary: (Adapted from applicant's abstract): This is an application to support studies aimed at clarifying the role(s) of excitotoxic and /or apoptotic cell death mechanisms in developmental (perinatal) brain injury associated with head trauma and

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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 (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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hypoxia/ischemia. In addition to addressing these aims during the application period, the investigator has made the unanticipated discovery that during the synaptogenesis period of development transient ethanol intoxication triggers a massive wave of apoptotic neurodegeneration, deleting millions of neurons from many different regions of the developing rat, mouse, or guinea pig brain. Our findings document that ethanol triggers apoptosis by a dual mechanism - blockade of NMDA glutamate receptors and excessive activation of GABAA receptors. We propose that our findings can help explain the reduced brain mass and lifelong neurobehavioral disturbances associated with the human fetal alcohol syndrome (FAS). Significance of this discovery is broadened by accompanying evidence that ethanol's neurotoxic properties are shared by numerous other agents that either block NMDA glutamate receptors or activate GABAA receptors, and many of these agents are drugs of abuse and/or are used regularly in obstetric and pediatric medicine. An important feature of our findings is that within the synaptogenesis period (first 2 weeks after birth for rats and mice, but third trimester and first several years after birth for humans) different neuronal populations have different temporal patterns for responding to the apoptosis-inducing effects of these drugs. Thus, depending on the timing of exposure, different combinations of neuronal groups will be deleted. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ALTERED CA2+ HOMEOSTASIS IN POST-ISCHEMIC NEURON DEATH Principal Investigator & Institution: Connor, John A.; Research Professor; Neurosciences; University of New Mexico Albuquerque Controller's Office Albuquerque, Nm 87131 Timing: Fiscal Year 2002; Project Start 01-MAY-1997; Project End 31-MAR-2005 Summary: (Applicant's Abstract) Specific and important populations of neurons in the brain are subject to delayed death following short periods of blood flow disruption as occurs in stroke, head trauma, or cardiac arrest. While many neurons are killed outright by the ischemic insult, many populations suffer attrition over a period of several days, retaining many of their normal signaling functions during that time. Some of these populations vulnerable to the delayed death, such as CA1 pyramidal neurons of the hippocampus, are vital parts of learning and memory circuitry of the brain. It is possible that these neurons could be rescued given an understanding of the drawn out death program they undergo. If so, the increasing financial and social costs of rehabilitation and support of survivors of brain injury, an ever-increasing number in an aging population, might be reduced. Many lines of evidence, converge to indicate that severe disruptions in intracellular Ca2+ levels during and shortly after an insult are the immediate trigger for delayed neuronal death, however the drawn out chain of subsequent events, that might be interrupted by suitable interventions, is poorly understood. Our research, using an in vivo model of ischemia has shown that there is a delayed depression of Ca2+ signaling activity in neurons destined to die. This body of data suggests clearly different mechanisms of cell death from currently held views, derived largely from in vitro, culture experiments, that increased Ca2+ burdens on the neurons after insult cause the delayed death. It is proposed here, 1) to investigate further the depression of Ca2+ signaling in post-ischemic CA1 neurons, 2) to investigate whether this depression is responsible for disrupting vital cellular functions that result in delayed death of neurons, and 3) to determine whether certain procedures and drugs that have proven effective in preventing neuronal death are acting by preventing the depression of Ca2+ signaling. If successful this research would suggest new modes of

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treatment, or give scientific basis for existing experimental treatments, of stroke or trauma that could prove to be effective when begun after significant delay. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ANTIAPOPTOTIC ACTIONS OF CONNEXIN Principal Investigator & Institution: Nedergaard, Maiken; Professor; Cell Biology and Anatomy; New York Medical College Valhalla, Ny 10595 Timing: Fiscal Year 2002; Project Start 15-JUN-1992; Project End 30-JUN-2005 Summary: (Provided by applicant): The aim of this application is to establish by which mechanisms Cx-proteins improve cellular survival following injury. We have in preliminary observations established that Cx-expression antagonizes cell death indicating that the connexin proteins have death-inhibitory or anti-apoptotic activity. In specific we will ask: Does an adaptive remodeling and reorganization of Cx43 contribute to the high resistance to injury of Cx43 expressing cells? A Cx43-eGFP fusion protein has been stably expressed in C6 cells and time-lapse analysis has revealed that Cx43-eGFP undergo major structural reorganization after injury. We will here test the preposition that Cx43 reorganization represents an adaptive response that improves survival and that the lower resistance of Cx-deficient cells results from their limited ability to initiate the same process after injury on a single cell level. The analysis will be extended to include primary astrocytes transfected with an adenoviral vector encoding Cx43-GFP. By which mechanisms do connexin proteins increase cellular resistance to injury? Is formation of functional gap junction channels a prerequisite for their anti-apoptotic action? Alternatively, do mutant Cx's with deficient channel function also provide injury-resistance indicating that yet undefined actions of Cx.proteins are responsible for the increased survival? We have established several cell lines with stable expression of either wildtype Cx43, or Cx-mutants with deficiencies in either channel function or membrane localization. These clones represent a powerful tool to establish at which level the Cx-proteins antagonize cell death. Is the increase in cellular resistance associated with Cx-expression dictated by the phenotypic transformation? Does loss of cytoskeletal organization increase cellular sensitivity to injury? We will in these studies test the preposition that the Cx-induced phenotypic transformation observed, in part, may contribute to the increased cellular resistance. Does the death-inhibitory activity of Cx require ATP secretion? Do purinergic receptor blockers antagonize the Cx-induced increase in cellular resistance? It is here postulated that ATP secreted from Cxexpressing cells acts as an autocoid differentiation factor that increases the cellular resistance to injury. The effects on cellular resistance of long-term treatment with purinergic-receptor agonist and antagonists will here be analyzed. Defining the pathways, by which connexin proteins increase cellular resistance to injury, may provide a potential new therapeutic target for preventing cell death in acute pathologies as stroke and head trauma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ANTIAPOPTOTIC ACTIVITY OF ALZHEIMER ABETA Principal Investigator & Institution: Atwood, Craig Stephen.; Professor; Pathology; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 01-JUN-2001; Project End 31-MAY-2003 Summary: Alzheimer's disease (AD) is a debilitating neurodegenerative disease that is characterized by neuronal cell loss and the deposition of protein aggregates. These neuropathological parameters are correlated with the presence of numerous markers of

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oxidative stress in the cell bodies of neurons suggesting the involvement of oxidative mechanisms in neuronal cell loss and/or protein deposition. Although the sources of the reactive oxygen species (ROS) leading to this oxidative stress have not been clarified, the brain responds to this chronic oxidative challenge by upregulating antioxidant defense systems (eg. increasing SOD1 and glutathione peroxidase expression). We now have three lines of evidence indicating that the increased generation of Abeta in AD also may be a compensatory response to oxidative stress that prevents neuronal apoptosis. Firstly, we have determined from in vitro studies that Abeta has significant antioxidant (superoxide dismutase) activity, secondly, that nanomolar concentrations of Abeta block apoptosis of neurons following trophic factor withdrawal, and thirdly that the Abeta amyloid burden of the AD-affected brain is significantly negatively correlated with oxidative stress markers. In support of these findings, we find fewer oxidative modifications in amyloid deposits and neurofibrillary tangles compared with the cell bodies of the neurons of AD-affected brains. Together, these compelling data provide a plausible physiological explanation for the increased generation of Abeta in AD and following head trauma. We hypothesize that as the disease progresses, the chronic overproduction of hydrogen peroxide by neuronal cells, microglia and Abeta amyloid deposits may overwhelm the antioxidant defense systems of the aging brain with the end result that ROS promote the apoptotic demise. Thus, the novel aspect of our hypothesis is the recognition that Abeta generation may be a form of pleiotrophic antagonism, whereby Abeta may be physiologically purposive under "normal" conditions (i.e. moderately increased concentrations of superoxide and/or high reducing equivalents), but may promote neuronal cell death under abnormal conditions (i.e. high concentrations of superoxide and Abeta that lead to excess hydrogen peroxide/low reducing equivalents). The proposed studies will therefore examine the generation of Abeta as a compensatory mechanism to oxidative stress that is both antioxidant and anti-apoptotic in nature while testing whether overwhelming oxidative challenges promote apoptosis. We also will test whether oxidative stress induces neurons to re-enter the cell cycle as a mechanism leading to cell death. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ANTIEPILEPTOGENIC & DISEASE MODIFYING EFFECTS OF AEDS Principal Investigator & Institution: Pitkanen, Asla Sl.; University of Kuopio Box 6, Sf70211 Kuopio, Timing: Fiscal Year 2004; Project Start 03-AUG-2004; Project End 30-MAY-2006 Summary: (provided by applicant): Each year about 140,000 Americans and 280,000 Europeans are diagnosed with epilepsy. Epidemiological studies suggest that symptomatic and presumed symptomatic etiologies comprise about 60% of the cases. These data suggest that about 250,000 individuals undergo epileptogenesis each year in the two continents. Even though the elevated risk of epileptogenesis after epileptogenic insult like head trauma, stroke, or status epilepticus (SE)) is readily identifiable, there is no evidence-based treatment that can be offered to patients at risk of epileptogenesis. Aim of the present study is to investigate whether administration of 3 standard antiepileptic drugs (carbamazepine, valproate, levetiracetam) as monotherapy during epileptogenic phase (1) prevents the development of epilepsy, and if not, (2) has a disease modifying effect. The compounds were chosen based on their different mechanism of action and variable effects on the development of kindling, a model considered to predict the antiepileptogenic effects in humans. To mimic clinical situation, administration of compounds (carbamazepine 120 mg/kg/d, valproate 600 mg/kg/d, levetiracetam 150 mg/kg/d, or vehicle) will be started 24 h after the

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beginning of SE (SE is stopped at 4 h with diazepam) induced by electrical stimulation of the amygdala in adult male Sprague-Dawley rats (n=10-20 per group). Treatment will be continued for 1 wk that corresponds to 20-25% of the latency period. The first 2-wk continuous video-EEG monitoring will be started 10 wk after SE. To confirm antiepileptogenesis or disease modification, the second 2-wk continuous video-EEG will be started 14 wk after SE. Thereafter, animals will undergo behavioral testing (Morris water-maze and fear-conditioning). Finally, animals will be perfused for histology. As outcome measures we use (1) development of epilepsy (yes/no), (2) severity of epilepsy (frequency, duration, behavioral severity of seizures), (3) spatial and emotional learning and memory, and (4) pathology (cell death, mossy fiber sprouting). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BCL-2 FAMILY GENES AND TBI Principal Investigator & Institution: Graham, Steven H.; Professor & Vice Chairman; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002 Summary: Bcl-2 family genes have a key role in controlling programmed cell death in neurons. We have found evidence that bcl-2 family genes are dysregulated and PCD occurs in both animal models and TBI in humans. The hypothesis of this proposal is that altered expression of bcl-2 family gene occurs after brain trauma and contributes to programmed cell death, oxidative stress, neuronal death, and adverse behavioral outcome. Specific aims are as follows: 1. Characterize alterations in expression of the bcl2 family genes (including bcl-2, bcl-x, Bax) that occur after CCI in mice. 2. Test whether bcl-2 expression inhibits PCD, oxidative stress and improves histological and behavioral outcome after CCI by use of a transgenic mouse that over-expresses bcl-2. 3. Test whether Bax expression is necessary to trigger PCD after CCI, and whether Bax expression mediates oxidative stress, adverse histological and behavioral outcome by use of Bax-disrupted transgenic mice subjected to CCI. 4. Test whether over-expression of bcl-x-1 by replication deficient herpes simplex viral vectors can protect hippocampal neurons against CCI. 5. Determine if similar alterations in bcl-2 family expression occur in human TBI by examining expression of bcl-2 and Bax in human tissue removed during decompressive craniotomies and CSF from ventriculostomies. Furthermore, determine if there is evidence of apoptosis in CSF (nucleosomes). Correlate these findings with long term outcome as determined by the Glasgow outcome score (GOS) and other measures. The proposed experiments address the key issues regarding the alteration of bcl-2 family genes in traumatic brain injury: Do bcl-2 family genes regulate cell death after trauma or is their altered expression an epiphenomena in cells already destined to live or die, and are these changes relevant to human head trauma? If these experiments support the hypothesis that bcl-2 family genes regulate cell death after trauma, alteration of expression of these genes or mimicking or inhibiting their effects could provide new strategies for treatment of traumatic brain injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: BIOMARKER OF NEURONAL DAMAGE IN TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Zemlan, Frank P.; Ceo; Phase 2 Discovery, Inc. 3130 Highland Ave, 3Rd Fl Cincinnati, Oh 452192374 Timing: Fiscal Year 2002; Project Start 20-SEP-2001; Project End 31-AUG-2004

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Summary: (provided by applicant): The pharmaceutical industry has spent $200 million on drug trials for treating head trauma, all have failed, Identified problems include inappropriate selection of drug candidates, and failure to use prognostic indicators and surrogate biomarkers in clinical trials. Proposed Phase II studies assess the utility of our newly developed biomarker of neuronal damage as a surrogate biomarker and prognostic indicator in clinical drugs trials of neuroprotectant agents. Our Phase I studies developed a biomarker of neuronal damage. After head trauma, neuronal MAPtau is proteolytically cleaved (C-tau) and gains access to cerebrospinal fluid (CSF) and serum where levels are elevated 30,000 fold and 300 fold respectively compared to controls. Further, patient C-tau levels were highly predictive of clinical outcome. Proposed Phase II studies will assess serial CSF and serum C-tau levels as surrogate biomarkers of clinical outcome in severe head injury patients (N=70). Serial CSF and serum C-tau levels will be measured at 24-hour periods after injury and their ability to predict patient outcome at 3 months determined (Specific Aims 2 and 4). The ability of initial CSF and serum C-tau levels to serve as screening biomarkers to identify head injured patients thought unlikely to respond to drug treatment (dead before end of study) will be determined and compared to the currently employed industry marker, initial Glasgow Coma Scores (N=70). PROPOSED COMMERCIAL APPLICATION: The C-tau ELISA will be utilized by the pharmaceutical industry in clinical drug trials as a purchased inhouse assay. Proposed Phase II studies put in place the foundation for a Phase III program which will develop our C-tau ELISA as an FDA approved in vitro diagnostic test for head trauma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BLOOD-BRAIN-CSF BARRIERS, CNS HOMEOSTASIS, DRUG DELIVERY Principal Investigator & Institution: O'donnell, Martha E.; Gordon Research Conferences Box 984, 512 Liberty Ln West Kingston, Ri 028920984 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2003 Summary: This proposal is a request for funds toward the support of a Gordon Research Conference to be held in July 2002. The intended meeting is the second Gordon Research Conference on Barriers of the Central Nervous System. This Gordon Research Conference was initiated as a catalyst for interaction among researchers from a variety f disciplines working on issues of blood-brain- and blood-CSF barriers in health disease. Research in this area is already leading to development of new therapeutic approaches for th treatment of stroke, head trauma, neurodegeneration, brain inflammation and brain tumors, to name a fe3w. Although portions of these areas of investigation are represented at several national and international research meetings, there have been few opportunities for scientists working in the field to come together with a specific concentrated focus on issues related to barriers of the CNS. The subtitle of the upcoming second Barriers of the CNS Gordon Research Conference is "Blood-Brain CSF barriers, CNS Homeostasis and Drug Delivery to the Brain". The specific focus of this conference will include discussion of a number of the problems and tissues faced by the Pharmaceutical industry in targeting therapeutic drugs to the CNS as well as discussion of broader current major developments of the blood- brain-barrier and blood-CSF barrier field. Most of these problems concern overcoming the blood-brain barrier to drugs. To this end a number of eminent scientists from academia and from the pharmaceutical industry, are being brought together for an exciting "leading edge" meeting. The intention is to foster the development of new ideas and their application to fundamental knowledge and the treatment of human and animal disease. Speakers have

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Head Trauma

been selected on the basis of their eminence in the field and their communication skills. TO this end they are drawn from a wide geographical background. Chairs of the sessions have been selected on the basis of their considerable eminence and experience in the field and a known ability to communicate and debate well. In addition the presentation of posters is being vigorously encouraged especially by young postdoctoral and research students. It is expected that a considerable proportion of any NIH grant will be used to fund the attendance of young scientists and chairs. It is also intended to have three open workshops/debates during the meeting. One is already in place on "Microdialysis". The maximum permitted attendance at this meeting is 150 scientists. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: APOPTOSIS

CASPASE

CLEAVAGE

OF

MEF2

MEDIATES

NEURONAL

Principal Investigator & Institution: Lipton, Stuart A.; Professor and Director; Burnham Institute 10901 N Torrey Pines Rd La Jolla, Ca 920371005 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Apoptotic neuronal cell death may play a role in many acute and chronic neurologic disorders. These disorders range from acute stroke, head trauma and epilepsy to more chronic states, such as Huntington's disease, Alzheimer's disease, amyotrophic lateral sclerosis, HIV-associated dementia, and glaucoma. Moreover, a contributing factor to such damage is excessive excitation of glutamate receptors, particularly (but not exclusively) the N-methyI-D-aspartate (NMDA) subtype of glutamate receptor because of its high permeability to Ca 2+ and subsequent free radical generation. The aim of this proposed research project is to uncover the role of myocyte enhancer factor-2 (MEF2) transcription factors in this excitotoxic/apoptotic process in neurons during ischemic stroke in vivo. MEF2 transcription factors are activated by p38 mitogen-activated protein kinase during neuronal and myogenic differentiation. Recent work has shown that stimulation of this pathway is anti-apoptotic in stem cells but pro-apoptotic in mature neurons exposed to mild excitotoxic or other stresses. Here, preliminary data in vitro show that mild excitotoxic (NMDA) insults to mature cerebrocortical neurons activate caspases-3, -7, in turn cleaving MEF2A, C and D isoforms. Endogenous MEF2 cleavage fragments containing a truncated transactivation domain but preserved DNA binding domain are shown to block MEF2 transcriptional activity via dominant interference. In vitro transfection of constitutively-active/uncleavable MEF2 (MEF2-CA) rescues MEF2 transcriptional activity following NMDA insult and prevents neuronal apoptosis. Conversely, dominant-interfering MEF2 (MEF2-DN) abrogates neuroprotection by MEF2C-CA. Our underlying hypothesis is that these results obtained in vitro can now be applied in vivo using tetracycline (or doxycycline, "dox")-controlled transgenic mice expressing these MEF2-CA and MEF2-DN transgenes. This grant will define a novel pathway to neuronal apoptosis in ischemia via caspase-catalyzed cleavage of MEF2. The Specific Aims are as follows: 1. To characterize anti-apoptotic effects of MEF2-CA in stroke using dox-controlled transgenic mice. 2. To characterize the effect of caspase cleavage fragments of MEF2 as dominant interfering forms that contribute to stroke damage using dox-controlled transgenic mice that express doxycycline-controlled, MEF2 cleavage products. 3. To characterize MEF2 transcriptional activity in vivo after an hypoxic/ischemic (stroke) insult but prior to cell loss using a MEF2-indicator mouse that has been engineered to activate the LacZ gene in accord with the degree of MEF2 transcriptional activity (designated des-mef2-LacZ). 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-2005 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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Head Trauma

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: CLINIC PATHOPHYSIOLOGY OF ACUTE BRAIN INJURY Principal Investigator & Institution: Powers, William J.; Professor; Neurology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 01-SEP-1997; Project End 31-MAY-2008 Summary: (provided by applicant): The overall goal of this Program Project is to investigate the pathophysiological changes that occur during injury and treatment in human subjects with acute brain damage. We will investigate three types of acute brain injury: intracerebral hemorrhage, ischemic stroke and head trauma. In Project 1, Dr. Allyson Zazutia will investigate the mechanism, extent and clinical importance of edema following intracerebral hemorrhage. In Project 2, Drs. William Powers and Venkatesh Aiyagari will use PET to determine the effect of pharmacologic reduction of systemic arterial pressure on regional cerebral blood flow in acute ischemic stroke. In Project 3, Drs. Michael Diringer and Robert Grubb will investigate the pathophysiological effects of mannitol and hypertonic saline on brain edema due to ischemic stroke and head trauma. The Imaging Core will perform acquisition, reconstruction, processing and archiving of the PET, MR and CT data for Projects 1,2 and 3 as well as validate recently developed MR methods of CBF and OEF estimation against gold-standard techniques. The Radiochemistry Core will provide radiopharmaceuticals for Projects 1,2 and 3 as well as construct a steady state oxygen-15 gas inhalation system to permit PET studies in subjects who are not endotracheally intubated or who cannot actively inhale. This Program Project draws on a combination of facilities and expertise at Washington University that is unique. It combines state-ofthe art quantitative neuroimaging, expertise in the care of critically ill neurological patients and many years experience in studying cerebral blood flow and metabolism. This research will provide fundamentally important pathophysiological information to guide future research toward the most fruitful approaches for ameliorating the devastating impact of acute brain injury.

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

Project Title: COGNITIVE DYSFUNCTION AFTER TBI: ROLE OF ALPHA7 NACHRS Principal Investigator & Institution: Pauly, James R.; Assistant Professor; Pharmacol & Exper Therapeutics; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2006 Summary: Trauma to the CNS initiates acute and secondary cascades of biochemical and metabolic changes often results in a state of persistent neurological dysfunction. Understanding the neurochemical alterations that occur following damage to the CNS is critical for the development of therapeutic strategies that can prevent and/or remediate the detrimental effects of trauma. The neurobiological basis for the protracted memory deficit that commonly occurs following traumatic brain injury (TBI) is not clearly understood although a number of studies have suggested that deficits in the CNS cholinergic system play a prominent role. However, most of the previous studies have focused on muscarinic, rather than nicotinic cholinergic receptor mechanisms. This is surprising since deficits in the nicotinic receptor system have been repeatedly associated with the cognitive deficit that occurs to neurodegenerative conditions such as Alzheimer's disease and Parkinson's disease. Our initial studies clearly demonstrate that a cortical contusion injury (CCI) causes significant and widespread defects in hippocampal and cortical alpha 7 nicotinic receptor (nAChr) expression. The working hypothesis of the proposed studies is that changes in the CNS alpha7 nAChr's contribute significantly to head trauma- induced cognitive dysfunction. Furthermore, we predict that pharmacological modulation of alpha7 neuronal nicotinic receptors will have neuroprotective and cognitive-enhancing properties in head-injured rats. The Specific Aims of this proposal will evaluate: 1) the time course of changes in alpha7 protein and message expression following TBI 2) neuroprotective actions of nicotinic receptor antagonists administered in the acute phase of TBI, 3) cognitive enhancing properties of nicotine and selective alpha7 agonists administered acutely (or chronically) in the delayed phase of TBI 4) the effects of TBI on deficits in auditory sensory gating and 5) restoration of sensory gating following treatment with nicotine and other selective alpha7 agonists. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: COMPLEX NEUROPROTECTION

ISOPATHIC

DRUG

DEVELOPMENT

FOR

Principal Investigator & Institution: Jonas, Wayne B.; Director; Henry M. Jackson Fdn for the Adv Mil/Med Rockville, Md 20852 Timing: Fiscal Year 2002; Project Start 15-FEB-2002; Project End 30-APR-2004 Summary: (provided by applicant): Stroke is the third leading cause of death in the United States and the leading cause of disability. Diseases of neurodegeneration and brain damage from non-missile head trauma account for nearly 500,000 hospital admissions in the U.S. annually. Although the etiology may differ, the same anatomic and physiologic substrates are involved in these conditions, including ischemia and hypoxic injury and the release of excitatory amino acids, especially glutamate from diseased or damaged cells. We have been using in vitro and in vivo models of experimental ischemia and cellular models of glutamate toxicity to examine these mechanisms of neuronal injury, and to target early intervention treatment strategies for neurodegeneration. One promising strategy that has not been explored is the use of low

16

Head Trauma

doses of chemicals to enhance cell tolerance and recovery. High doses of toxic chemicals will inhibit and kill biological systems, while low doses frequently stimulate those systems. Stimulation of cell function by exposure to low doses of chemicals can often mitigate the adverse effects produced by high doses. This phenomenon has been extensively studied in the area of toxicology called "hormesis" and is the theoretical basis for the observed effects in some types of homeopathy (specifically isopathy). While paradoxical dose effects have been demonstrated across multiple cell types and phyla they have not yet been examined in neurodegeneration. In preliminary research we have demonstrated that protective effects occur in neuronal cells exposed to low and ultralow doses of glutamate and NMDA and that certain doses of glutamate/potassium combinations protect against stroke in vivo. The objective of this project is to use neuronal culture systems to identify the optimal protective doses and of four neurotoxins that work by different mechanisms - a glutamate/potassium preparation, NMDA, cycloheximide, MPPepsilon, a combination of these. We will also begin preliminary examination of selected mechanisms of the optimal protective combination and dose. This project will, for the first time, have produced a systematic approach for use of protective hormesis and will lay the foundation for the scientific development of homeopathic and isopathic drugs in neurodegeneration and brain injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

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 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

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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: COURSE SCHIZOPHRENIA

OF

FUNCTIONAL

DEFICITS

IN

LATE-LIFE

Principal Investigator & Institution: Harvey, Philip D.; Professor; Psychiatry; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): This is a collaborative study of the course and antecedents of functional decline in geriatric patients with schizophrenia. Functional (i.e., social, occupational, self-care, and independent living) impairment is one of the primary factors that influences both quality of life and societal cost of schizophrenia, with some evidence suggesting that some older patients with schizophrenia experience functional decline in later life. While in other illnesses such as dementia and head trauma it is clear that cognitive decline is an antecedent to functional decline, evidence regarding the correlates of functional status in schizophrenia is largely cross-sectional. The present study adopts a longitudinal approach to determine if the cross-sectional relationships between cognitive and functional deficits are the result of cognitive decline being an antecedent of functional decline. The results of previous studies regarding cognitive and functional decline are contradictory, with the Mt. Sinai group studying older and sicker patients finding decline and the UCSD group finding no evidence of decline in similar time periods. In order to determine if these discrepancies are due to differences in subject samples or the methods employed, the Mt. Sinai group will employ both their previous methods and those of the UCSD group in this study. Samples of healthy controls and ambulatory older schizophrenia patients who vary in their lifetime history of course of illness will be followed for 5 years and examined with performance-based measures of functional skills, assessments of cognitive functioning, and clinical symptom ratings. Sophisticated data analytic techniques will be employed to determine the course of functional changes, their temporal relationships with changes in cognitive and functional status, and their association with lifetime illness history. Findings from this study will clarify the course of functional status in schizophrenia and the timing of cognitive and functional changes. The results will also inform research on the biological basis of functional change in schizophrenia, as well as research on treatment of the illness. In a much-neglected area, the study of schizophrenia in late life, this research will focus on an aspect of the illness (the course of functional status) that has been studied for 100 years, but is still not well understood. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DIFFUSION TENSOR IMAGING IN SEXUALLY ABUSED CHILDREN Principal Investigator & Institution: De Bellis, Michael D.; Professor; Psychiatry; Duke University Durham, Nc 27710 Timing: Fiscal Year 2004; Project Start 09-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): This application, Diffusion Tensor Imaging in Sexually Abused Children (SAC)is a proposal to supplement the NIMH funded study, "PTSD & Childhood Sexual Abuse: Psychobiology," RO1-MH63407. The parent proposal is a 5-year cross-sectional investigation with a one-year prospective follow-up to noninvasively examine the psychobiology of childhood posttraumatic stress disorder (PTSD) secondary to sexual abuse. In the parent study, we are examining the diagnosis

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Head Trauma

and severity of PTSD on outcomes of biological stress system regulation and brain maturation. We will study 3 groups of 70 children (35 males/35 females) aged 6 to 12 years: children with PTSD secondary to sexual abuse, SAC without PTSD, and nontraumatized age and sociodemograghically comparable controls. Biological stress system regulation will be assessed by 24-hour urinary catecholamine and free cortisol levels. Brain maturation will be assessed by: magnetic resonance spectroscopy-based brain N-acetylaspartate concentrations, which reflect neuronal integrity, magnetic resonance imaging-based brain morphometry (cerebral, and amygdala/hippocampal volumes and corpus callosum (CC) area), and cognitive function. Although the parent grant examines cortical myelination through MRI-based morphometry, the present grant supplement proposes to enhance our measurements of cortical myelination and other microstructural aspects of brain development by adding an additional MRI acquisition protocol to our existing morphometric MRI scan, diffusion-weighted imaging (DWI). DWl is a functional neuroimaging mode which measures brain waterdiffusion characteristics reflecting axon density and myelin abnormalities. It also permits enhanced discrimination of brain injuries involving sheering, contusion, and other manifestations of head trauma. DWl will assist in determining which SAC may have had other reasons than sexual abuse for adverse brain development. We hypothesize that compared with controls, SAC will show water-diffusion characteristics on DWl consistent with (1) decreased myelination and (2) slower age-related growth of the CCo We also hypothesize that (3) SAC with PTSD will show DWl characteristics reflecting decreased myelination and slower CC growth compared with SAC without PTSD. The study will enhance our knowledge of neuroanatomical/neuropsychological concomitants of sexual abuse in exchange for additional image analysis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DISINHIBITION FOLLOWING NEOCORTICAL TRAUMA Principal Investigator & Institution: Benardo, Larry S.; Professor and Vice Chairman; Neurology; Suny Downstate Medical Center 450 Clarkson Ave New York, Ny 11203 Timing: Fiscal Year 2002; Project Start 01-JUL-1999; Project End 30-JUN-2005 Summary: (Verbatim from the Applicant's Abstract) Acute seizures develop in up to 80 pecent of cases of moderate to severe head trauma, indicating serious cortical damage. The majority of these individuals will have chronic seizures (epilepsy). Concepts regarding the mechanisms underlying epileptogenesis and cell damage have focused on excitotoxicity. Excitotoxicity consists of a cascade of events triggered by excitatory amino acid transmitters, calcium influx via transmitter-gated and voltage-dependent channels, and intracellular calcium release, which then activate autodestructive processes ending in membrane damage and cell death. Epileptogenesis, signaling the dominance of excitation over inhibition can occur at any stage in the excitotoxic process. Such inhibitory failure following trauma cona only be understood by studying local neuronal circuits. A model of traumatic neocortical injury has been developed in order to investigate the mechanisms of excitotoxicity and epileptogenesis. This model utilizes rat in vitro somatosensory cortical slices, wherein after removal of the superficial third of coronal slices, over half the isolated deep segments express epileptiform activity. Preliminary findings postulate that hyperexcitability results from GABAergic disinhibition owing to physical removal of superficial inhibitory circuits and glutamatetriggered increases in intracellular calcium. Experiments will be performed in order to test this hypotheses with regarded to these issues: 1) Strength of glutamatergic excitation and fast GABAergic inhibition in deep neurons from intact versus damaged preparations, 2) Properties of monosynaptic fast GABAergic inhibition in intact versus

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damage preparations, 3) Intracellular calcium concentration in pyramidal cells after damage, 4) Whether increased intracellular calcium concentration leads to fast GABAergic disinhibition in deep pyramidal neurons, and 5) Testing whether lowering the intracellular calcium concentration in damaged preparations restores fat inhibition. Experiments will utilize standard intracellular or patch clamp recordings of deep pyramidal cells and videoimaging of calcium-sensitive dyes to allow correlation of inhibitory strength with intracellular calcium concentration. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DOES NITRIC OXIDE CONTROL SYNAPTIC ZINC RELEASE? Principal Investigator & Institution: Frederickson, Christopher J.; Chief Executive Officer; Neurobiotex, Inc. 101 Christopher Columbus Blvd Galveston, Tx 77550 Timing: Fiscal Year 2002; Project Start 23-JUL-2002; Project End 31-MAY-2004 Summary: (provided by applicant): Synaptically-released zinc has toxic impact in seizure, ischemia, and trauma, contributing to neuronal injury in all three conditions. Conversely, blockade of the excitotoxic synaptic zinc flux with zinc chelators can reduce neuronal degeneration markers by as much as 80%. We have recently discovered evidence indicating that Nitric Oxide (NO) may control the synaptic release of zinc. Should NO prove to be the controlling factor, this would open completely new avenues for management of zinc-induced brain damage in stroke, ischemia, trauma, and seizure. Moreover, prophylactic control of the Zn2+ toxicity via NO modulation could be used as therapeutic pretreatment in cardiac bypass and carotid endarterectomy procedures. Our pilot data indicate that NO infused into the brain simultaneously depletes presynaptic boutons of their zinc while releasing zinc into dialysates, and we have complementary data from brain slice preparations indicating that NO causes the release of Zn2+ into the bath. Perhaps more compelling, additional data suggest that zinc-induced neuronal injury after head trauma is decreased by up to 50% after blockade of NO* synthesis. The objective of the present proposal is to establish with certainty whether, in fact, NO controls Zn2+ release during excitotoxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DYNAMIC NEUROIMAGING WITH HIGH-RESOLUTION SSVEPS Principal Investigator & Institution: Srinivasan, Ramesh; Cognitive Science; University of California Irvine Irvine, Ca 926977600 Timing: Fiscal Year 2004; Project Start 01-JAN-2004; Project End 31-DEC-2006 Summary: The proposed experimental, simulation, and theoretical EEG studies will develop modern engineering tools for future use by cognitive and medical scientists. These tools are potentially applicable to a wide variety of disease states, including mental disorders (ADHD, depression, schizophrenia, depression, sleep disorders, etc.) and neurological conditions (epilepsies, head trauma, strokes, coma, Alzheimer's disease, etc.). The proposed tools combine high-resolution EEG with MEG and new methods to quantify dynamic (spatial-temporal) properties of EEG and steady-state visually evoked potentials (SSVEP). Experimental studies will apply high-resolution SSVEP dynamic measures to investigate conscious perception, selective attention, perceptual organization, and working memory. Methods to identify genuine measures of functional integration between cortical areas will be developed and tested with highresolution SSVEP. SSVEP provides robust measures of neocortical dynamic and cognitive function that are largely artifact-free. SSVEP measures of the "competition" between functional localization and integration will include coherence and other phase

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Head Trauma

locking measures in various frequency bands. The experimental SSVEP data will be interpreted in the context of cell assembly formation embedded within a background of "synaptic action fields" using theoretical models of neocortical dynamic function based on genuine physiology and anatomy. The synaptic action fields are defined as the number densities of active excitatory and inhibitory synapses at any time, independent of function. This theoretical construct provides the necessary connection between physiology and EEG/SSVEP data. In this manner, a triple correspondence between EEG dynamics, cognitive processes, and theoretical models will be obtained. The EEG and SSVEP tools developed in these studies should provide firm foundations for later studies applied to a wide range of specific cognitive or medical conditions. These tools will be freely distributed as software for high-resolution EEG, SSVEP, and MEG analysis with a supporting manual and examples Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FUNCTIONAL ULTRASONIC TISSUE PULSATILITY: BRAIN IMAGING Principal Investigator & Institution: Beach, Kirk W.; Research Professor; Surgery; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): We will create a low cost portable instrument for functional imaging of brain that can be used outside the hospital for emergency evaluation of stroke patients and in the classroom for monitoring the learning and mastery of tasks. Imaging of brain physiology has become a valuable tool in research and in the evaluation of clinical brain diseases. Both functional Magnetic Resonance Imaging (fMRI) and Evoked Response Potentials (ERP) (functional electroencephalography (fEEG)) have revealed the regional dynamics of brain function in response to mental activity and challenges. Both methods have limitations. Although MR methods can reveal functional chemical details about anatomic regions of the brain, the temporal resolution of these MR methods is limited and the environmental conditions of the magnet restrict the kinds of mental and physical tasks that can be performed by the patient under study. Although EEG methods have a time resolution much better than a second, the spatial information about brain function from EEG data must be inferred by indirect methods. In this project, we will develop an ultrasonic method of displaying cortical pulsatility, which is a surrogate of brain cortex perfusion. This system will be designed to provide brain perfusion maps that differentiate areas of normal, hyper- and hypo- pulsatility using a conspicuous contrast method. The temporal resolution of the method is near one second and the spatial resolution is near 1 cm. This brain cortex perfusion imaging system has applications in functional brain research, in stroke diagnosis and management and in the management of head trauma. It can be used on ambulatory patients and research subjects for prolonged periods. In addition to clinical applications, we plan to use this instrumentation to support research in learning and in mental disability research. This new ultrasonic method holds the promise of extremely low cost. Currently, ultrasound instruments with similar complexity can be purchased at prices affordable by primary care clinics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GENETIC DISSECTION OF GLUTAMATE RECEPTOR FUNCTION Principal Investigator & Institution: Heinemann, Stephen F.; Professor; Salk Institute for Biological Studies 10010 N Torrey Pines Rd La Jolla, Ca 920371099

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Timing: Fiscal Year 2002; Project Start 01-JUL-1990; Project End 29-SEP-2003 Summary: Most theories of nervous system function depend heavily on the properties of the synapse and for this reason the synapse has been a focus of neuroscience research for many decades. The synapse is also the focus of medical and pharmaceutical research because in general the drugs that have proven useful for the treatment of mental illness and neurological disease act on various aspects of synaptic function, i.e. transmitter uptake and metabolism, ion channels and receptors. It is also likely that synaptic changes underlie the long term or permanent changes that take place in memory formation and learning. Recently there are suggestions that similar long term changes in synaptic transmission take place as part of the mechanism of many neurological diseases such as epilepsy, drug addiction and long term intractable pain. Long term alterations in synaptic function may explain the symptoms of withdrawal experienced by addicts when drug administration is terminated. Inappropriate activation of glutamate receptors is thought to contribute to the nerve cell death which occurs after brain injury due to stroke, epilepsy, head trauma and perhaps other neurological diseases such as ALS, Parkinson's and Alzheimer's disease. Little is known about the function of the kainate glutamate receptor subtype which is a major focus of this grant application made possible by the recent cloning of the kainate receptor genes. The structure of the glutamate binding site will be studied. A search for glutamate receptor modulatory and accessory proteins will be undertaken using a new molecular genetic approach. The calcium permeability and function of the glutamate receptors are regulated by a novel mechanism of RNA editing which will be studied and altered in mutant mice. The role of kainate receptors will be studied making use of a battery of mutant mice that we have engineered to alter the kainate receptor system and synaptic transmission. Results from these studies will provide insight into the role that specific glutamate receptor subtypes play in the nervous system. This should make it possible by using recombinant DNA technology to develop new drugs and therapies to treat epilepsy, pain, stroke, mental illness, degenerative diseases and drug addiction. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETICS OF ALZHEIMER'S DISEASE IN ISRAELI ARABS Principal Investigator & Institution: Friedland, Robert P.; Associate Professor and Chief; Neurology; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-AUG-2004 Summary: (Adapted from the Applicant's Abstract): In a population based study of AD, we have screened all elderly residents of Wadi Ara, an Arab community near Tel Aviv in northern Israel, and observed an unusually high prevalence (20.5% of those >60 years, 60.5% of those >85 years). This prevalence is higher than that found anywhere else in the world, even after adjustment for age, education and gender, and apparently is not due to increased frequency of the APOE epsilon-4 allele. We hypothesize that the increased prevalence of AD in this genetic isolate is caused by the presence of AD susceptibility alleles which are over-represented because of mating patterns in this closed population which has few founders. In this application we propose to study extensively all persons residing in this community ages 60 and older (numbering 855 at the time of the last survey including 168 persons meeting NINDS/ADRDA criteria for AD). We will obtain from each subject risk/protective factor data (including smoking, blood pressure, head trauma, education, diet, physical and mental activity levels, occupation and medication history) and blood samples for biochemical and DNA studies. Family informants will be used to construct detailed pedigrees. Our scientific aims are: (1) Estimate the life-time risk of AD in first-degree relatives of prevalent cases using survival techniques and

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Head Trauma

compare these estimates to those obtained for relatives of cognitively normal subjects and for relatives of AD cases in other populations; (2) Localize the gene(s) causing AD in this population using a homozygosity mapping approach. In order to rapidly screen for markers linked to the disease, one AD affected and one elderly nondemented from each of several families from the same tribal group (hamula) will be genotyped with 400 polymorphic microsatellite markers spaced less than 10 cM apart. Suspect chromosomal regions will be pursued by genotyping all subjects individually with markers spaced at 2 cM intervals. A variety of analytical techniques including both parametric (lod score) and non-parametric (affected relative, sib-transmission-disequilibrium and allelefrequency-dependent homozygosity mapping) approaches will be employed to assess the marker data for linkage to AD; (3) Examine genes from candidate regions identified in aim 2 by SSCP/CSGE; and direct sequencing for polymorphisms which may directly influence AD susceptibility; (4) Analyze the effects of non-genetic factors (singly and in combination with each other and with linked genetic markers or candidate gene polymorphisms) on risk of AD. Identifying specific genes and elucidating their mechanisms and the nature of gene/environment interactions will be a major achievement. Results from this study may have immediate impact on the development of new treatment or prevention strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HIPPOCAMPAL NETWORK STRUCTURE AND FUNCTION IN EPILEPSY Principal Investigator & Institution: Sloviter, Robert S.; Professor; Pharmacology; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2002; Project Start 01-DEC-1984; Project End 31-JUL-2003 Summary: (Adapted from Investigator's Abstract): Although complex partial seizures of temporal lobe origin can occur as the apparent result of tumors, arteriovenous malformations, and disorders of cortical development, they often occur "spontaneously," in the absence of any obvious cause. In these "cryptogenic" patients, an antecedent episode of prolonged febrile seizures, infection, or head trauma is often reported, but of unproved causation. This clinical history led to the hypothesis that an initial injury alters the temporal lobe/hippocampal network in such a way that it ultimately becomes a source of seizure discharges. Experimental studies on this subject can be extrapolated to the human condition because the structural and functional properties of the mammalian temporal lobe have been highly conserved phylogenetically. This application describes experiments designed to test the hypothes:is that post-injury non-principal cell (interneuron) death or dysfunction causes hippocampal principal cell disinhibition and. hyperexcitability. The proposed experiments have been designed to: 1) continue to elucidate the normal structural and functional organization of the hippocampal formation with particular reference to the identification of the interneuron populations that have distant axonal projections necessary for establishing "lateral'' inbibition; 2) determine whether parvalbumin-positive inhibitory basket cells die as a consequence of prolonged seizures, or simply stop expressing parvalbumin; 3) determine if interneuron loss per se induces principal cell disinhibition and hyperexcitability, and; 4) utilize experimental epilepsy models to elucidate the structural and functional changes that follow injury, and precede and follow synaptic reorganization and the development of spontaneous seizures. The first experiments involve the characterization of normal hippocampal interneuron populations in terms of their longitudinal/associational and commissural projections, as well as the neuroactive substances they contain. These studies utilize retrograde and anterograde tracer injections and double fluorescence

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immunocytochemistry. The second experiments utilize electron nucroscopy and colocalization immunocytochemistry to determine if a subset of basket cells dies or survives after seizures. The third set of experiments involve saporin-based neurotoxins that target different interneuron populations relatively selectively. These studies directly address the "interneuron loss" and "lateral inhibition't' hypotheses proposed previous,ly by the applicant. The f inal set of experiments utilizes the perforant path stimulation-, and pilocarpine models to deterrrune which structural network defects may give rise to abnorrnal network excitability and spontaneous seizures. These studies involve both anesthetized and awake recording, as well as anatomical and irnmunocytochernical methods designed to elucidate the functional and structural basis of epileptogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IL-1 INDUCED MEDIATORS OF CNS INFLAMMATION AND AD-COXPrincipal Investigator & Institution: O'banion, Michael Kerry.; Associate Professor; Neurology; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 28-APR-2000; Project End 31-JUL-2003 Summary: (adapted from applicant's abstract): Inflammation-related changes are a prominent part of the CNS response to acute injury, infection, and chronic neurodegenerative disease. Numerous studies indicate that attenuation of CNS inflammation may be beneficial in treating CNS disorders, including Alzheimer's disease (AD). Microglia and astrocytes play a significant role in the initiation and maintenance of CNS inflammation by producing a wide-range of inflammation-related gene products. Elaboration of inflammatory responses elicited by both acute and chronic stimuli depends on key molecular players that drive interactions among cells. One of these players is IL-1 beta proinflammatory cytokine strongly implicated in acute CNS inflammation as well as AD. Based on studies of peripheral inflammation, another key player is likely to be prostaglandin E2 (PGE2) produced by the inflammation-responsive protein, cyclooxygenase-2 (COX-2), one of two isoforms of the obligate enzyme for prostaglandin biosynthesis. COX-2 is made in brain and can be induced by IL-1 beta and other proinflammatory cytokines in astrocytes and microglia. Moreover, preliminary studies indicate that selective inhibition of COX-2 attenuates the expression of inflammation-related genes following acute CNS injury. Based on these findings and epidemiological evidence that inhibitors of cyclooxygenase may be beneficial in AD, this competitive renewal focuses on the role of COX-2 in CNS inflammation. The hypothesis that COX-2 derived prostaglandins are required for elaboration of acute as well as chronic local inflammatory responses in the central nervous system will be tested in three different model systems. The first specific aim will characterize direct influences of COX-2 and PGE2 on expression of IL-1 beta responsive genes in primary cultures of human and murine astrocytes. In the second specific aim, the contributions of COX-2 and PGE2 to an acute inflammatory cascade elicited by cortical injection of IL-1 beta will be established. In the third and fmal specific aim, COX-2 specific inhibitors will be employed in double transgenic PS-1/APP mice to ascertain the role of COX-2 in chronic CNS inflammation secondary to Abeta deposition. Together, these studies examine the role of COX-2 and increased prostaglandin production in CNS inflammation and a model of Alzheimer's disease. This work will provide a clearer understanding of the mechanisms by which anti-inflammatory drugs influence AD and may reveal new avenues for therapeutic intervention. Moreover, these studies have relevance to pathological processes occurring in head trauma, stroke, and other neurodegenerative diseases where gliosis and inflammation-related changes take place.

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

Project Title: INTRACRANIAL STRAIN IN MILD TRAUMATIC HEAD INJURY Principal Investigator & Institution: Bayly, Philip V.; Mechanical Engineering; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2005 Summary: (provided by applicant): The goal of this project is to develop the technology needed to measure deformation and strain fields in the brain of the mouse or rat during mild traumatic closed-head injury. The project addresses the need for information on neuronal strain in closed-head trauma and its relationship to subsequent injury and impairment. The technology will be applied to the immature rat; it also is applicable to the mouse and mature rat. Our long-term objectives are to: (1) determine the strain fields within the brain that result from impacts or skull accelerations; (2) characterize the response of the intact brain to high strains. Measurement of brain deformation will increase our understanding of brain injury and will advance trauma therapy and prevention. Injury and degeneration can be studied with respect to the fundamental parameter: strain. Results for the immature rat are relevant to brain injury in young children. Specific aims are: AIM 1: Develop instrumentation and MR tagging procedures to obtain images of deformation in the immature rat brain during mild head injury: An MR-compatible system to deliver calibrated impacts will be developed. MR images of deformed tag lines in the brain of a prone, anesthetized, immature rat will be acquired during delivery of light, sub-concussive impacts to the head. Impact energy and velocity will be prescribed within a range based on prior published studies and on pilot studies using euthanized animals. Motion will be repeated to acquire resolved images of the deformed tag lines. The imaging procedure will be directly analogous to that used in cardiac MRI cine studies in the rat and mouse heart. In vivo studies will provide fundamental data on brain deformation in this trauma model. AIM 2: Develop software to estimate strain fields, quantify strain, and compare to overall levels of neuronal degeneration. Software developed for analysis of cardiac strain will be adapted to compute strain fields in the brain and to characterize strain as a function of location and impact characteristics (amplitude, duration). Histopathological studies will be performed post-trauma in rats that receive multiple light impacts during imaging, and in rats receiving a single larger impact, to determine total neuronal degeneration. Hypotheses: Strain will increase predictably with impact energy. In both groups, total neuronal degeneration is expected to increase with peak strain and the area of high strain in a manner characterized by sigmoid "dose-response" curves. This is an interdisciplinary project involving impact mechanics, MR tagging, histopathology, and brain injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: AWARENESS

INTRALAMINAR

THALAMIC

INFLUENCES

ON

VISUAL

Principal Investigator & Institution: Schiff, Nicholas D.; Assistant Professor; Neurology and Neuroscience; Weill Medical College of Cornell Univ New York, Ny 10021 Timing: Fiscal Year 2002; Project Start 11-SEP-2000; Project End 31-AUG-2005 Summary: (Adapted From The Applicant's Abstract):The immediate aim of the proposed research is to develop an awake behaving primate model to investigate the role of the intralaminar and associated paralaminar thalamic nuclei in visual awareness. The long-range goal is to develop a neurophysiological basis for remediation of acquired

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cognitive disabilities, including deep brain stimulation in the intralaminar thalamus. Direct injury or functional impairment of the intralaminar thalamic nuclei (ILN) leads to disturbances of attention, working memory, and other cognitive processes. It is proposed that the ELN play a critical role in facilitating specific longrange corticocortical communications that link attention, working memory, and gaze control in support of visual awareness. The precise cellular mechanisms of interaction between the ILN and the cortical regions that support these functions are only beginning to be understood. This is the focus of the present proposal. Two research paradigms will be developed: pharmacological inactivation and electrical stimulation of the intralaminar nuclei during a visuospatial attention task. Impaired cognition resulting from head trauma or stroke remains a growing problem for which little intervention is currently available. Several experimental and clinical studies suggest that deep brain stimulation and other approaches aimed at improving cognitive function may be possible. While these are long-range goals, and the studies proposed here do not represent direct investigations of these possibilities, completion of these experiments is necessary and logical step toward these goals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ISOLATION AND USE OF ADULT HUMAN OLIGODENDROCYTE PROGENI Principal Investigator & Institution: Goldman, Steven A.; Nathan Cummings Professor; Neurology and Neuroscience; Weill Medical College of Cornell Univ New York, Ny 10021 Timing: Fiscal Year 2002; Project Start 01-DEC-1999; Project End 30-NOV-2003 Summary: Demyelination in the setting of oligodendrocytic loss is a significant contributor to neurological dysfunction in a variety of subcortical pathologies, including posthypoxic leukoencephalopathy, capsular stroke, and head trauma, as well as in the inflammatory, hereditary and degenerative leukoencephalopathies. We have found that a distinct and separate pool of mitotically-competent oligodendrocyte (oligo) progenitor cells resides in the adult human capsular white matter. This glial progenitor does not appear to be uncommon; it may comprise as many as 4 percent of the cells of the mature white matter. Although the existence of an analogous cell-type has been postulated in rats, its presence in humans had remained controversial, in part because of the difficulty in specifically identifying or obtaining these cells. We therefore developed a means of isolating these cells from adult human patients, by transfecting dissociates of resected white matter with plasmids that selectively identify oligo progenitors, by their expression of fluorescent transgenes controlled by early oligodendrocyte promoters. Specifically, we use the early promoter (P2) for cyclic nucleotide phosphodiesterase (CNP), which is preferentially active in mitotic oligo progenitors, to direct expression of green fluorescence protein (GFP) to these cells. This approach has allowed us not only to identify live oligo progenitors in vitro, but to enrich them by fluorescence-activated cell sorting (FACS). As a result, we can use FACS based upon CNP2:hGFP expression to purify oligodendrocyte progenitor cells from the adult human white matter, in highyield, and with retained mitotic potential, differentiation competence and in vitro survival. In this application, I will capitalize upon our acquisition of these purified adult human oligodendrocyte progenitor cells, with experiments designed to assess their capacity for structural remyelination. To this end, I plan to define several therapeutically-relevant aspects of the biology of these cells, including 1) their lineage potential and capacity for myelination, and the humoral control thereof, and 2) the humoral regulation of their clonal expansion, and 3) their capacity for oligodendrocytic

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maturation and myelination upon engraftment. To these ends, I plan to transplant P/CNP2:hGFP-defined, FACS-purified populations of adult human oligo progenitors into a rodent model of focal demyelination. These latter studies would serve as a prelude to preclinical analysis of this cell type's response to implantation in nonhuman primates, in models of both chemical and radiation-induced demyelination. This application is intended to develop oligodendrocyte precursor implants, as well as induced oligoneogenesis from endogenous progenitors, as feasible therapeutic options for the structural repair of demyelinated brain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LARGE SCALE DATA ANALYSIS FOR BRAIN IMAGES Principal Investigator & Institution: Megalooikonomou, Vasileios; Computer and Information Sciences; Temple University 406 Usb, 083-45 Philadelphia, Pa 19122 Timing: Fiscal Year 2004; Project Start 22-JAN-2004; Project End 31-DEC-2007 Summary: (provided by applicant): The goal of this project is to address a great need for developing efficient brain informatics tools for the analysis and management of large collections of brain images (from various imaging modalities) and associated clinical data. These automated tools will enable interoperable brain image data representation that is easy to search while focusing on the management of the spatial regions of interest (ROIs) under a general unified framework regardless of whether these are lesions, tumors, areas of brain activation, or regions of (normal/abnormal) morphological variability of a variety of brain structures. We envision this brain informatics system as a platform for the effective and efficient analysis of a large number of epidemiological studies. Towards these ends we propose four specific aims: (a) development of efficient methods for the quantitative characterization and classification of ROIs, (b) development of fast and effective database techniques supporting efficient retrieval of similar regions of interest in large brain image databases as well as spatial data mining tools for discovering associations between anatomic and other variables such as function, pathology, or response to drugs, (c) integration of the above techniques with morphological analysis tools to correlate morphological changes to changes of other measurements such as functional, physiological, etc, (d) evaluation of the proposed techniques using real and simulated data. We will demonstrate the utility of the proposed techniques in the analysis of large data sets from a number of epidemiological studies of brain morphology and function. The data sets we propose to analyze are (a) MR spectroscopy and anatomic MRI correlation representing disease states such as multiple sclerosis, stroke, tumors and neurologic disease states (2,400 participants), (b) structural MR data on Schizophrenia (more than 500 participants), (c) structural and functional MR data from normal volunteers and patients with stroke, head trauma, and epilepsy (an ongoing study with over 150 participants), (d) structural and functional MR data on Alzheimer disease (an ongoing study with over 30 participants), (e) structural and functional MR data from a study on aging (an ongoing study with over 45 participants) and (f) an Alzheimer structural MR data from a diverse group of 40 participants. Through large-scale data analysis we will provide new insight into the relation of brain structure and function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: LOCALIZATION AND ACTIVATION OF PROTEASE RECEPTOR PAR1 Principal Investigator & Institution: Junge, Candice E.; Pharmacology; Emory University 1784 North Decatur Road Atlanta, Ga 30322

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Timing: Fiscal Year 2002; Project Start 01-SEP-2002 Summary: Provided by applicant): It is increasingly evident that serine proteases such as plasmin and tissue plasminogen activator (tPA) as well as protease activated receptors (PARs) have a role in the central nervous system (CNS). Recent findings suggest a role for serine proteases and their receptors in normal brain function as well as a potential role in pathological situations such as stroke or head trauma in which the blood brain barrier is compromised. In addition, the brain expresses several unique serine proteases, but their physiological role and substrates in the CNS are unknown. The overall goalof the experiments outlined in this proposal is to expand our understanding of serine protease signaling cascades inthe CNS, and to explore the mechanism by which the blood serine protease, plasmin, may influenceneurodegenerabon when the blood brain barrier is compromised. To accomplish this, three separate lines ofinvestigabon will be initiated. First, immunocytochemistry will be performed in rat brain bssue to determine theprotease activated receptor 1 (PAR1) protein distribution as well as subcellular localization. Second, heterologousexpression systems as well as mouse brain tissue from wild type and PAR1-/- mice will be employed to determine ifthe CNS produces endogenous actvators/inactivators of PAR1. The third goal is to determine the mechanism ofplasmin-mediated potentiation of NMDA receptor responses using electrophysiological and biochemical techniques.The rationale for the proposed studies is that serine proteases and their receptors may participate in a signalingcascade that mediates neurodegeneration in situations where the blood brain barrier is compromised and thus mayprovide a potential therapeutic target. Because tPA is currently approved for stroke, these studies may lead to a possible adjunct therapy that enhances tPA?s beneficial effects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISMS & TREATMENT OF PROGRESSIVE DAMAGE AFTER TBI Principal Investigator & Institution: Bramlett, Helen Marie.; University of MiamiMedical Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2002; Project Start 19-JUL-2002; Project End 30-JUN-2007 Summary: Several laboratories using focal and diffuse models of traumatic brain injury (TBI) have reported the progressive nature of histopathological damage that can continue in rodent models up to one year. Evidence for progressive damage has previously been reported in humans following head trauma. Preliminary data in this application presented for the first time provides quantitative data for chronic white matter pathology following moderate fluid-percussion brain injury. The overall goal of the proposed studies is to assess the importance of moderate and severe TBI on longterm vulnerability patterns after trauma. In Specific Aim 1, regional patterns of gray and white matter pathology and their associated neurobehavioral alterations will be assessed. Histopathological techniques along with magnetic resonance imaging (MRI) strategies will be used to assess temporal and regional patterns of progressive damage in order to correlate these changes with behavioral outcomes. In Specific Aim 2, immunocytochemical markers of axonal damage, demyelination, cell atrophy, and cell death will be utilized to assess cellular injury progression. To begin to determine the pathomechanisms underlying progressive white matter injury, the role of prolonged hypoperfusion and abnormal protein aggregation on these structural changes will be regionally and temporally assessed. Finally, therapeutic strategies targeting excitotoxic processes as well as abnormal protein aggregation will be evaluated to reduce progression of advancing atrophy. It is felt that these experiments are necessary to

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understand the pathogenesis of progressive injury as well as to develop therapeutic strategies to promote recovery of function following TBI. Established animal models and behavioral, MRI, immunocytochemical, autoradiography, and molecular techniques will be utilized. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISMS OF NEUROPROTECTION IN HIBERNATION AND AROUSAL Principal Investigator & Institution: Drew, Kelly L.; Associate Professor; University of Alaska Fairbanks 109 Admin Services Center Fairbanks, Ak 997757880 Timing: Fiscal Year 2002 Summary: Incidence of stroke is the #1 cause of disability in America and is disproportionately high in Alaskan Native populations. Hibernating mammals provide an animal model of natural tolerance to profound (up to 90%) reductions in cerebral blood flow. The long term goal of this project is to elucidate mechanisms of neuroprotection during hibernation and arousal from hibernation. Anti-oxidants defense mechanisms and suppression of CNS activity via adenosine release or changes in ion channel densities provide hibernating brain tissue enhanced protection from oxidative stress and neuronal cell death. Aim 1 is to test the hypothesis that release of adenosine, an inhibitory neuromodulator, is associated with entrance into and exit from hibernation. This hypothesis will be tested by sampling interstitial adenosine during entrance, maintenance and exit from hibernation using quantitative microdialysis in brains of arctic ground squirrels. Our second aim is to test the hypotheses that a) voltage gated sodium channel density is decreased during hibernation, and, b) ATP regulated potassium channel density is increased during hibernation. Studies will focus on changes in the quantity of channel protein using radioligand binding and western blotting and mRNA using quantitative PCR. Aim 3 examines mechanisms responsible for neuroprotection using 3 models of stress or trauma, i) arousal from hibernation, ii) traumatic brain injury induced by insertion of a microdialysis probe and ii) an in vitro brain slice model of oxidative stress and excytotoxicity. Our final aim is to add a comparative dimension to experiments proposes in Aims 1 to 3 to investigate speciesspecific aspects of neuroprotection using hypoxia as a model of arousal from hibernation, traumatic brain injury and our in vitro slice model. The project will be conducted as an integrated and coordinated collaboration between investigators at the University of Alaska Fairbanks (UAF) and Case Western Reserve University (CWRU). The UAF component of the project will focus on animal studies utilizing UAF's unique access to arctic ground squirrels. The CWRU component will provide expertise and training in immunocytochemistry and molecular technique which will ultimately be transferred to UAF. The hypothesis to be tested through the integration of both components will allow the complementary expertise in hibernation physiology, neurochemistry, immunocytochemistry and molecular biology to be applied in a maximally productive and mutually beneficial way. The collaboration will also provide opportunities for students and fellows at UAF to obtain training in immunocytochemical techniques and molecular biology at CWRU. The results of the proposed research will lead to a better understanding of mechanisms of neuroprotection during hibernation. Hibernation offers an excellent mammalian model of tolerance to reduced cerebral blood flow and neurodegeneration. Better understanding of mechanisms of neuroprotection may lead to improved therapies for stroke and head trauma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MEDICATION DEVELOPMENT FOR COCAINE ABUSE--CDP CHOLINE Principal Investigator & Institution: Lukas, Scott E.; Professor of Psychiatry (Pharmacology) a; Mc Lean Hospital (Belmont, Ma) Belmont, Ma 02478 Timing: Fiscal Year 2001; Project Start 10-APR-1999; Project End 30-NOV-2004 Summary: (Applicant's Abstract) This is a revised application that focuses on the development of a novel medication for cocaine dependence--CDP-choline. This naturally occurring nucleotide is a major component in phospholipid metabolism and is an integral ingredient in membrane synthesis. It is approved for use in Europe to treat head trauma and a variety of neurological degenerative disorders. Interestingly, it also enhances dopamine activity. Thus, CDP-choline's efficacy as a treatment for cocaine dependence may be high because it repairs two putative consequences of chronic cocaine abuse: 1) membrane damage, and 2) depleted dopamine levels. Two experiments are proposed in this three year study. The first is a challenge study designed to assess the acute effects of cocaine administration in CDP-choline treated non-dependent, casual cocaine users. A multidisciplinary assessment battery including EEG, physiologic, subjective responses and plasma cocaine and metabolite levels will be conducted after cocaine or placebo challenge. This experiment will be conducted in the first six months of the project and will provide basic information on how cocaine's effects are altered by this medication. Study 2 is a 6-week placebo-controlled clinical trial of CDP-choline in cocaine dependent men and women. Follow-up assessments will be made at 8, 12 and 26 weeks. In an attempt to gain insight into the possible mechanism of CDP- choline's effects, two different assessments of CNS function will be conducted at baseline, after 6 weeks of treatment and at the 12 week follow-up visit. The first is a cue reactivity challenge using subjective reports of craving, physiologic and EEG activity after neutral, emotionally laden and cocaine-related stimuli. The second assessment is Magnetic Resonance Spectroscopy (MRS), which will be used to measure changes in brain chemistry that reflect neuronal damage. One of the major appeals of CDP-choline is its low inherent toxicity. Large doses have been given for relatively long periods of time with no adverse effects. The implication of this is that CDP-choline may be safe enough to treat cocaine dependence in pregnant women and adolescents and may even be useful for treating infants who are born to cocaine-dependent mothers. Although we have collected very encouraging preliminary data on CDP-choline's effects in cocainedependent male and female subjects, we recognize that it is not a "magic bullet" and that CDP-choline may serve as an important adjunct to other psychotherapy or pharmacotherapy programs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MUSCARINIC RECEPTOR COUPLING TO INOSITIDES IN CNS Principal Investigator & Institution: Fisher, Stephen K.; Professor; Pharmacology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2003; Project Start 01-SEP-1986; Project End 30-JUN-2007 Summary: (provided by applicant): The regulation of cell volume is of critical importance to the CNS due to the restrictions of the skull. Brain swelling, which may occur in response to a lowering of plasma osmolarity or during cytotoxic edema, is associated with a number of clinical conditions, including congestive heart failure, hepatic encephalopathy, ischemic stroke, or head trauma. To counteract the increased volume, cells release Kv, CI-, and "non-perturbing" organic osmolytes, a major

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component of which is myo-inositol. Efflux of the osmolytes occurs via a volumesensitive organic anion channel (VSOAC), which primarily gates CI'. Although most attention has been focused on the role played by glia in the process of volume regulation, cultured neuronal cells have also been recently shown to exhibit similar properties. Moreover, recent results from this laboratory indicate that high concentrations of myo-inositol are present in some neuronal populations and that the polyol can be released in a volume-dependent manner. Although the electrophysiological and pharmacological characteristics of VSOAC have been well documented, relatively little is known of the cell signaling pathways that regulate osmolyte efflux through this channel. A central tenet of this proposal is that, in the face of hypoosmotic challenge, the capacity of neural cells to restore their volume via the efflux of inositol and other osmolytes can be regulated by extracellular agonists operating via phosphoinositide-linked receptors, such as the muscarinic cholinergic receptor. Thus we plan to examine the characteristics of myo-inositol efflux from human SH-SY5Y neuroblastoma cells under hypoosmotic conditions and evaluate the relationship between effiux of the polyol and changes in cell volume. In addition, we will test the hypothesis that activation of muscarinic cholinergic and other phosphoinositide-linked receptors leads to an increase in the effiux of inositol, and other osmolytes, from these cells. Furthermore, the possibility that individual osmolytes exit the cell via multiple VSOACs will be explored via a comparison of the effiux characteristics of inositol, taurine, and D-aspartate, all of which can be released from these cells. The ability to manipulate osmolyte effiux could be of potential benefit for a number of clinically relevant conditions. Accordingly, knowledge of the signal transduction pathways that regulate VSOAC is an essential prerequisite for the rational design of therapeutic agents. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OXYGEN METABOLISM AND RATE OF BLOOD FLOW Principal Investigator & Institution: Fiat, Daniel; Professor; Physiology and Biophysics; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2002; Project Start 03-JUL-1998; Project End 30-JUN-2003 Summary: (Adapted from Applicant's Abstract): The long-term objectives are to develop 17O magnetic resonance imaging (OMRI) and spectroscopy (OMRS) to a stage that 17O then may be used: 1) in physiological research and 2) for clinical diagnostic purposes. MRI may be very useful in studying physiological processes in which oxygen plays a major metabolic role. It can noninvasively measure the regional metabolic rate of oxygen (rMR02) and regional blood flow (rBF) in many body organs, particularly, brain. There is no radiation exposure. The specific aims of the current application are to develop the hardware and software for 170 MRI imaging in a whole body clinical imager and to test the method by: 1) using phantoms of water at physiological pH. 2) imaging the baboon brain, 3) imaging the human brain, 4) in-vivo measurements of brain pH 5) measuring cerebral metabolism rate of oxygen (CMRO2) and cerebral blood flow (CBF) in the baboon, 6) studying the effects of anesthetics on CMR02 and CBF in the baboon, and 7) measuring CMRO, and CBF in man. 17O MRI offers an additional means to conventional proton MRI of brain water. 17O MRI is more sensitive to slower molecular motions than 1H MRI. This may allow earlier diagnosis of tissue pathology. 17O nuclear relaxation times are two to three orders of magnitude shorter than 1H, opening the way to study faster bio-molecular physiological processes. The proposed methodology is unique in being noninvasive, in utilizing a stable (non-radioactive) isotope and in being carried out in-vivo utilizing conventional MRI scanners. 17O MRI methodology may

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have great potential for both physiological and pathophysiological studies in man and for improving our understanding of numerous disease processes including dementia, stroke, head trauma, cancer and epilepsy. Cerebral ischemia, dementia, pseudotumor cerebri and low grade brain tumors all of which are difficult to detect on conventional proton MRI, may be better delineated and studied. Tissue perfusion can be noninvasively measured in brain and other organs, perhaps providing a means to detect early microvascular changes characteristic of such diseases processes as diabetes mellitus and hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PLASTICITY OF GABAERGIC INHIBITION FOLLOWING HEAD INJURY Principal Investigator & Institution: Soltesz, Ivan; Assistant Professorr; Anatomy and Neurobiology; University of California Irvine Irvine, Ca 926977600 Timing: Fiscal Year 2002; Project Start 01-JUN-1997; Project End 31-MAY-2005 Summary: (Adapted from applicant's abstract): Previous studies have suggested that mossy cells are lost from the neuronal circuit of the dentate gyrus after various epiletogenic insults, and has given rise to the widely accepted, although often questioned, so called "dormant basket cell" hypothesis of epileptogenesis. In the previous award made to Dr. Soltesz he has set out to comprehensive challenge and explore at a cellular and synaptic level each element of the dentate-gyrus-hippocampal circuit to explore what elements are directly and indirectly impacted in a model of fluid percussion head trauma. This competitive renewal turns the focus of the study to the principal hilar neuron the "mossy cell" and proposes a rather straightforward set of experiments to disprove the "dormant basket cell hypothesis" and demonstrate that instead of being lost in models of epileptogenesis, significant numbers of mossy cells persist following percussive head trauma and contribute to an increased hyperexcitability by entering into a increased recurrent excitation of dentate gyrus granule cells which in turn feedback to both inhibitory interneurons and hilar mossy cells to increase hippocampal excitability and the resultant epileptogenic activity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PLASTICITY OF LANGUAGE NETWORKS IN CHILDHOOD EPILEPSY Principal Investigator & Institution: Gaillard, William D.; Associate Professor; Children's National Medical Center Washington, D.C., Dc 20010 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): This study will examine the effects of seizures on the functional anatomy of language skills in children with both early onset and chronic epilepsy. This population provides an opportunity to gain insight into the effect of chronic neuronal dysfunction on the development of human language abilities and their brain representation. We hypothesize that seizures cause neuronal injury and force reorganization of the representation of essential cognitive skills, such as language. Patients with early epilepsy onset are expected to have greater variation in fMRI language activation patterns than those with later onset; these changes are expected to occur only after several years of epilepsy. Children will be evaluated with high resolution structural 1.5 Tesla MR.1, and functional MRI. Image data will also be transformed into a standard brain atlas to facilitate intra-subject regional comparison, as well as to account for inter-subject variability of language activation patterns. Three

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Head Trauma

groups will be compared: 1) children within one year after localization related seizure onset 2) children with chronic localization related epilepsy (>3 years duration) 3) a normal control population. As a result of this study a greater understanding of the anatomic organization of language during critical periods of cognitive development and neuronal plasticity will be gained. We will determine whether seizures themselves or a common brain pathology is the driving force behind brain plasticity. Such information is important to plan intervention strategies to mitigate the sequelae of epilepsy at disease onset and in the most vulnerable children to its effects. Unlike acute and limited neuronal insults, such as head trauma and stroke, epilepsy is a chronic process with continuing but paroxysmal neuronal sequelae. Furthermore, patients may be identified and evaluated at the outset of the disease process so that the neuronal response and degree of plasticity may be assessed and monitored. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PREVALENCE /INCIDENCE /RISK FACTORS FOR DEMENTIA ON GUAM Principal Investigator & Institution: Galasko, Douglas R.; Associate Professor; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2002; Project Start 01-MAR-1997; Project End 31-MAR-2007 Summary: (provided by applicant): An extraordinarily high incidence rate of amyotrophic lateral sclerosis (ALS) and Parkinson's Dementia Complex (PDC) was documented in the 1950's among Chamorros living on Guam. ALS has declined markedly on Guam over the following 50 years but PDC has declined to a lesser degree. Among older Chamorros, late-life dementia clinically resembling Alzheimer's disease (AD) is now at least as common as PDC. We aim to carry out a population-based study to characterize the rates of dementia and PDC among Chamorros on Guam. Our overall hypothesis is that interactions between genetic and environmental factors and aging explain the complex pattern of neurodegenerative disorders seen on Guam and the rapid changes in patterns of disease. We hypothesize that the Chamorros have a genetic predisposition to form neurofibrillary tangles (NFT). When this predisposition is combined with a strong exposure to factors in the environment, ALS and PDC may result. When Chamorros escape these two disorders, factors associated with aging and the brain, particularly oxidative stress, may result in tangle formation and late-life dementia. Specific aims of project 1 of this renewal are: 1) To determine the prevalence of dementia ('pure' dementia, PDC and other causes) among Chamorros on Guam aged 65 and older; 2) To determine the age- and sex-specific incidence of dementia among Chamorros on Guam; 3) To examine the effect of putative risk factors on the prevalence and incidence of dementia and PDC. Potential risk factors include environment: (traditional Chamorro diet and lifestyle; sources of water); genetics (family history of ALS or PDC; ApoE e4 allele; tau polymorphisms and other candidate genes); risk factors for AD (education, head trauma, head circumference and others); biological measures (plasma levels of F-2-isoprostanes; cholesterol levels); 4) To characterize neuropathologic changes among elderly Chamorros who are cognitively normal and those who have clinical syndromes of dementia or AD. This project will draw on the Clinical core on Guam; Neurologists and a neuropsychologist at UCSD and OHSU; a Neuropathology core at Mt Sinai Hospital, New York, and Neuroepidemiologists at University of South Florida. The project is planned for 5 years. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PREVENTION OF NEURONAL APOPTOSIS BY HEAT SHOCK PROTEIN Principal Investigator & Institution: Jardine, David S.; Anesthesiology; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 30-SEP-1999; Project End 29-SEP-2004 Summary: Hypoxic-ischemic injury (HII) to the brain is a serious, commonly encountered medical problem that results in permanent severe disability. It occurs after injuries such as stroke, cardiac arrest and often occurs in head trauma. It has been well demonstrated that although some brain cells die shortly after HII, others undergo a delayed form of cell death 24-36 hours later. The cells undergoing delayed death show characteristics of apoptotic cell death, suggesting that the cell is intact following HII, but that the injury has activated the apoptotic program. Recent evidence indicates that the inducible, 70 kilodalton heat shock protein (HSP70), may reduce cell death in some cell types following a stimulus that normally causes apoptosis. It is not known if HSP70 will reduce apoptosis in neuronal cells following apoptotic stimuli such as HII. If HSP70 is effective in this role, it may be useful as a medical therapy. Because HSP70 is inducible by a variety of stimuli, not just by hyperthermia, it is possible that its synthesis could be induced immediately following an HII to reduce apoptotic neuronal loss. The initial phases of this investigation will be carried out using the PC6-3 cell line, a neuronal cell line that undergoes maturation and terminal differentiation in the presence of nerve growth factor (NGF). After terminal differentiation, withdrawal of NGF results in extensive apoptosis. This cell line will be stably transfected with vectors that can be induced to overexpress HSP70, in order to determine if HSP70 can reduce apoptosis following withdrawal of NGF. Because there is a small body of literature that suggests that persistent overexpression of HSP70 may be harmful, another goal is to determine if long-term over-expression of HSP70 is toxic to cultured neuronal cells. The final goal is to create a transgenic mouse model that will inducibly overexpress HSP70 to determine if HSP70 can ameliorate apoptotic neuronal loss following middle cerebral artery occlusion. This project will provide an opportunity for the principal investigator to expand his experience in molecular biology and to gain experience with transgenic animals. He will also broaden his knowledge in the basic biological sciences through laboratory meetings and seminars. These measures will provide the skills and background necessary for his planned career an independent investigator in translational research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PREVENTION EPILEPTOGENESIS

OF

POSTTRAUMATIC

NEOCORTICAL

Principal Investigator & Institution: Graber, Kevin D.; Neurology & Neurological Scis; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 01-JUL-2000; Project End 31-MAR-2004 Summary: (Adapted From The Applicant's Abstract): Epilepsy following head trauma often appears after a quiescent period of months or years. In the rat "undercut" model of posttraumatic epileptogenesis, tetrodotoxin (TTX) treatment will prevent epileptogenesis, allowing comparison of epileptogenic and nonepileptogenic injured neocortex. More information about changes in cortical circuitry and changes in receptor fimction following epileptogenic injuries is fundamental to progress in developing prophylaxis or new treatments suitable for humans. This project focuses on the function and critical role of ionotropic glutamatergic receptor-mediated excitation in the

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undercut model. Patch clamp techniques will be used to evaluate miniature, spontaneous and evoked excitatory currents and unitary responses of synaptically coupled pairs of pyramidal neurons in epileptogenic and nonepileptogenic injured neocortical slices from rats several weeks following surgical cortical isolations. Each of these indices will be quantified to provide complementary information about the state of functional excitation in chronically epileptogenic cortex. The project will be carried out in the fully equipped and well supported epilepsy research laboratory of the Department of Neurology and Neurological Sciences at Stanford University. The sponsor has trained numerous students and fellows, many of whom are now prominent in the field of neurophysiology and epilepsy. An outstanding neuroscience faculty, a critical mass of postdoctoral fellows in the Stanford Epilepsy Training Program, numerous seminars and courses are available to enrich and supplement the laboratory training. This fellowship is an important step in the acquisition of technical acumen and research experience that will be crucial in developing a successful academic career as a clinician/scientist and independent investigator in epilepsy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF EXTRACELLULAR EXCITOTOXINS Principal Investigator & Institution: Robinson, Michael B.; Associate Professor; Children's Hospital of Philadelphia 34Th St and Civic Ctr Blvd Philadelphia, Pa 191044399 Timing: Fiscal Year 2002; Project Start 01-JAN-1993; Project End 30-NOV-2006 Summary: (provided by applicant): The acidic amino acids, glutamate and aspartate, are the predominant excitatory neurotransmitters in the mammalian CNS. An extracellular accumulation of these excitatory amino acids (EAAs) causes neuronal cell death. This process known as 'excitotoxicity' contributes to the neurodegeneration that accompanies acute insults to the brain, including stroke, hypoglycemia, and head trauma. Normally, the extracellular concentrations of glutamate and aspartate are maintained in the low micromolar range by a family of Na+-dependent high-affinity glutamate transporters. It is generally thought that both failure and reversed operation of these transporters contribute to the rise in extracellular EAAs during the acute insults. We have recently found that activation of protein kinase C (PKC) rapidly (within min) changes both the activity and cell surface expression of the three forebrain glutamate transporters, EAAC1, GLT-1, and GLAST. PKC increases the activity and cell surface expression of EAAC1, a neuronal transporter that is enriched in brain areas that are exquisitely sensitive to excitotoxic insults. It has the opposite effect on the cell surface expression of the glial transporters. In fact, individual PKC isozymes appear to have different effects on a single transporter. These data imply that activation of PKC can dramatically shift the balance of glial and neuronal EAA clearance. Our data also suggest that EAAC1 couples to the functional antagonist of PKC, protein phosphatase. In our first two aims, we propose using biochemical, cell biological, pharmacological, and molecular biological techniques to study this regulation using both primary cultures derived from neuronal tissue and clonal cell lines. In our final aim, we wish to determine if this PKCdependent regulation contributes to altered transporter function and activity that is observed during and after an acute insult. Several studies have demonstrated that PKC is activated by hypoxic/ischemic insults. Our preliminary data have prompted the hypothesis that hypoxic/ischemic insults activate PKC-dependent regulation of these transporters. By exploring this hypothesis, we will determine if these signaling pathways contribute to the failure or loss of these transporters. An understanding of

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these events should lead to the development of alternative strategies that will protect the brain from excitotoxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: RISK FACTORS FOR MSA Principal Investigator & Institution: Tanner, Caroline M.; Director of Clinical Research; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 30-JUN-2008 Summary: Few studies have explored the determinants of MSA. Apart from age, no risk factor has been definitively identified. The goal of this proposal will be to take the first step in identifying factors associated with MSA, using a case-control method. Our hypotheses will be determined not only by an investigation of current understandings about MSA, but also by current theories regarding the determinants and the pathogenesis of other late-life neurodegenerative diseases, particularly Parkinson's disease (PD), which, like MSA, has alpha-synuclein-containing inclusions. In addition, risk factors for neurodegenerative disorders sharing the more general finding of protein aggregation will be investigated. A unique advantage of this application is the use of a well-characterized population with clinically Probable MSA, who will be followed clinically and for some studied at autopsy. All cases (n = 175) and controls (n = 350) enrolled in Core A will participate in Project I. Four specific aims will be addressed: SA 1: To test the hypothesis that exposure to specific occupational or a vocational chemical exposure is associated with an increased risk of MSA; SA 2: To test the hypothesis that specific dietary factors have a direct effect on the risk of MSA; SA 3: To test the hypotheses that certain risk factors associated with PD or Alzheimer's disease (AD) alter the risk of MSA. Risk factors of interest include: use of tobacco, caffeine, alcohol, antiinflammatory drugs (lower risk); head trauma, stimulant use (higher risk); SA 4:To determine whether there is familial aggregation of MSA or the symptoms of MSA, or of MSA and other neurodegenerative diseases (PD, AD, motor neuron disease). For each hypothesis, exposures believed to be causally associated with MSA are expected to be more common in persons with MSA than in controls. Hypothesis testing will use classical methods for univariate and multivariate analysis of case-control studies. We stress that these investigations constitute a necessary exploratory step in attempting to characterize the determinants of MSA. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ROLE NEURODEGENERATION

OF

APOE4

DOMAIN

INTERACTION

IN

Principal Investigator & Institution: Weisgraber, Karl; Deputy Director/Senior Investigator; J. David Gladstone Institutes Box 419100, 365 Vermont St San Francisco, Ca 94103 Timing: Fiscal Year 2002; Project Start 01-FEB-2002; Project End 31-JAN-2007 Summary: (provided by the applicant): Apolipoprotein (apo) E4 is an established risk factor for neurodegenerative disease, including Alzheimer's disease (AD), and for poor outcome from head trauma and stroke. However, the mechanism underlying this increased risk remains elusive. Since protein function is directly related to protein structure, we have focused on determining the structural features that distinguish the apoE isoforms to gain insight into how these differences relate to the mechanism for the different effects of the isoforms in neurodegeneration. Our structural and mutagenesis studies established that apoE contains two structural domains. In apoE4, but not apoE3

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and apoE2, the two domains interact. Our working hypothesis is that this unique structural property of apoE4 has a major influence on its functional properties, including lipid transport, metabolism, and mechanisms by which apoE4 contributes to neurodegeneration and heart disease. The aims in this application are designed to test this hypothesis in the context of neurodegeneration and AD using in vitro model systems and a novel apoE mouse model, in which domain interaction was engineered into mouse apoE in by gene targeting (Arg-6 1 mouse apoE). In Specific Aim 1, we will test the hypothesis that domain interaction determines the lipid-binding properties of Arg-6 1 mouse apoE and human apoE4. In Specific Aim 2, we will test the hypothesis that domain interaction in Arg-61 mouse apoE influences the type and composition of lipoprotein particles secreted by cultured primary astrocytes. In Specific Aim 3, we will test the hypothesis that domain interaction in Arg-6 1 mouse apoE decreases neuronal outgrowth in cell and organ culture systems. In Specific Aim 4, we will test the hypothesis that domain interaction in Arg-6 1 mouse apoE4 contributes to neurodegeneration. The results from these studies have the potential to provide clues into the mechanism by which apoE4 contributes to neurodegeneration and to identify therapeutic targets based on isoform-specific effects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SECONDARY BRAIN INJURY IN INTRACEREBRAL HEMORRHAGE Principal Investigator & Institution: Hemphill, Jesse C.; Neurology; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 15-JUL-2001; Project End 30-JUN-2006 Summary: (provided by applicant): Acute primary non-traumatic intracerebral hemorrhage (ICH) is a common disorder for which there is currently no therapy of proven benefit in improving mortality and functional outcome. In fact, there remains controversy regarding the mechanisms by which ICH creates primary and secondary brain injury. The overall objective of this proposal is to produce a program which combines didactic teaching, mentoring, and clinical research to build upon Dr. Hemphill's training in neurologic critical care, thereby allowing him to develop into an independent clinical investigator studying mechanisms of injury and treatment of ICH. While management decisions in ischemic stroke, head trauma, and subarachnoid hemorrhage may be made based on clinical and diagnostic monitoring for secondary brain injury, the usefulness of this in ICH is not known. The overall hypothesis for this project is that secondary brain injury adversely effects outcome after ICH and that approaches that decrease secondary brain injury after ICH will improve outcome. This will be investigated through a series of studies related to clinical, neuromonitoring, and neuroimaging evaluation of secondary brain injury in ICH, culminating in a pilot clinical trial of ICH treatment. Studies will address: 1) the impact of clinical secondary brain insults (systemic hypoxia, hypotension, fever, and seizures) on outcome, 2) the influence of brain tissue hypoxia (measured through direct monitoring of brain tissue oxygen tension in the neurologic intensive care unit) on outcome, 3) the correlation between brain tissue hypoxia and ischemia on dynamic CT perfusion and MR diffusionweighted imaging, and 4) the feasibility of targeting secondary brain injury in a pilot study of ICH treatment. This research should provide new and important information about the role of secondary brain injury in ICH. In conjunction with the didactic training and mentoring undertaken, this program will foster Dr. Hemphill's development into an independent researcher in neurologic critical care, specifically focusing on intracerebral hemorrhage. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SPONTANEOUS ACTIVITY OF MITRAL CELLS Principal Investigator & Institution: Griff, Edwin R.; Biological Sciences; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2005 Summary: (provided by applicant): The long-term objective of this project is to understand how the olfactory system encodes information about odors. The olfactory system has a major role in regulating body hormonal state, emotional disposition, hunger, reproductive and social behavior. The work proposed here will advance understanding of the physiological processes, which subserve sensory function. Odors are received by olfactory receptor neurons in the olfactory epithelium of the nose and these receptor neurons convey the information to the main olfactory bulb in the brain, where they synapse onto mitral cells. The mitral cells process this information via neural circuits in the bulb and relay it to the primary olfactory or piriform cortex. The specific aims of this project are to measure the spontaneous activity of mitral cells, analyze temporal patterns and respiratory modulation of spontaneous action potentials, to correlate spontaneous activity with the impulse conduction velocity of mitral cells, and to investigate to what extent spontaneous activity in mitral cells is controlled by spontaneous activity in olfactory receptor neurons. Loss of the sense of smell is a common and debilitating problem. Acute loss may follow head trauma or environmental insult, while gradual loss often accompanies aging. Impaired olfaction compromises a person's ability to detect potential hazards such as smoke, gas leaks, and rancid food. Quality of life is also affected since most of the pleasure of food and drink comes from the nose. Increased knowledge of the normal and basic physiology of olfactory neurons is essential for developing strategies to treat olfactory deficits. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: THERAPEUTIC PROCESSES/FUNCTIONS

EFFECT

OF

EMFS

ON

NEURAL

Principal Investigator & Institution: Tuttle, Jeremy B.; Professor; Neuroscience; University of Virginia Charlottesville Box 400195 Charlottesville, Va 22904 Timing: Fiscal Year 2002; Project Start 01-JUN-2000; Project End 31-MAR-2005 Summary: Magnetic devices and therapies are gaining rapid acceptance among some groups, even in the absence of reliable outcome data. This Center is focused upon the potential treatment with electromagnetic fields (EMFs) of fibromyalgia and the sequelae to CVA and closed head trauma. Despite considerable effort, it is still not clear how biological systems might be responding to therapeutically applied EMFs. The development and refinement of this potential new mode of therapy will be advanced considerably by a more explicit understanding of what basic biological processes are responsible for the desired therapeutic effects. This project will examine the effect of therapeutic magnetic fields upon specific neural processes and functions, in the effort to outline potential biosensors for EMFs in the nervous system. The tests will be conducted in vitro upon reasonable cellular reductionist models of events in the nervous system. In each case, EMF effects under basal and stressed conditions will be examined. Specific aims will measure magnetic field effects upon: l) Fiber regeneration by peripheral and central neurons. Primary neurons in culture will be used and the rate of regeneration of neurites measured. 2) Synapse formation and maturation. Cultures of peripheral neurons and muscle, as well as central neurons, will be examined for synapse formation and function at various times after isolation. 3) Calcium signaling via cytosolic transients in nerve and muscle cells. Fura-2 imaging will be used to examine EMF effects

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on IP3-mediated calcium signaling in primary cultures of muscle and human neuroblastoma cells. 4) Synthesis and release of neurotrophins. The production of NGF at the cellular level by muscle, neuroblastoma and glial cells will be examined. 5) Cell death and neuroprotective gene expression. EMF effects on induction of apoptosis and expression of free-radical scavengers and bcl-2 will be tested. Each of these test areas relates to a biological process involved in the response of the nervous system to injury or disorder and thus may be involved in the therapeutic efficacy of magnetic fields. The results of these largely exploratory experiments will outline likely basic biological processes capable of responding to EMF with a desirable therapeutic effect. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: TRAUMATIC BRAIN INJURY AND ALZHEIMERS DISEASE Principal Investigator & Institution: Trojanowski, John Q.; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002 Summary: Alzheimer's disease (AD) is a heterogeneous neurodegenerative disorder that may be caused by epigenetic and/or genetic factors. For example, the epsilon allele encoded by the apolipoprotein E (APOE) gene on chromosome 19 increases the risk of sporadic AD, while head trauma is an environment risk factor for sporadic AD. Further familial, AD (FAD) is caused by autosomal dominant mutations in the amyloid precursor protein (APP) gene on chromosomal 21, as well as in genes encoding two different membrane spanning proteins known as Presenilin 1 (PS-1) and Presenilin 2 (PS-2) on chromosome 14 and 1, respectively, while trisomy 21 (Down's syndrome) patients developed extensive AD-like pathology by age 40. However, other AD genes and epigenetic risk factors undoubtedly exist. Despite the genotypic and phenotypic heterogeneity of AD, elderly patients with a progressive dementia are assigned a diagnosis of AD when postmortem examination reveals numerous telencephalic Abetarich senile plaques (SPs) and tau-rich neurofibrillary tangles (NFTs). Thus, we hypothesize that SPs and NFTs represent part of a final common pathway leading to neuron loss and dementia in AD, and that head trauma augments this process. Indeed, head trauma could increase the risk for AD by acting synergistically (i.e. as a "second hit" with AD pathologies. Since animal models that recapitulate AD-like SPs and NFTs enable rigorous tests of the hypothesis, the Aims of Project 4 are designed to accomplish this goal by: 1) Inducing or augmenting the formation of AD-like SPs in existing transgenic mice that over-express mutant human APP and develop age-related SP-like lesions by subjecting young and aged mice to traumatic brain injury (TBI); 2) Developing transgenic mice that over-express human tau and accumulate tau in neuronal perikarya; 3) Cross-breeding human tau transgenic mice with mutant human APP transgenic mice described above in Aim 1; 4) Inducing or augmenting the formation of AD-like SPs, perikaryal tau accumulations and NFTs in the tau and crossed transgenic mice described above in Aim 3 by subjecting young and aged mice to TBI; 5) Determining modes of neuron degeneration in regions of the brain with and without AD-like SPs, perikaryal tau accumulations and NFTs before and after TBI or sham treatment of the transgenic mice described in Aims 1-3 using biochemical, morphological and "single cell mRNA profiling" methods. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TRAUMATIC BRAIN INJURY AND MARROW STROMAL CELLS Principal Investigator & Institution: Mahmood, Asim; Neurological Surgery; Case Western Reserve Univ-Henry Ford Hsc Research Administraion Cfp-046 Detroit, Mi 48202 Timing: Fiscal Year 2002; Project Start 01-MAR-2002; Project End 28-FEB-2006 Summary: (Verbatim from applicant's abstract) This project is designed to investigate the effects of intravenous transplantation of bone marrow stromal cells on the rat brain after traumatic brain injury. Traumatic brain injury continues to be an important cause of human morbidity and as many as 50,000 Americans are killed and an equal number are disabled by head trauma each year. Currently, we have no therapeutic intervention to repair the biostructural neuronal damage and treatment consists of evacuating mass lesions and providing an optimal milieu for the brain to recover. In this application, we will transplant marrow stromal cells intravenously in the adult female Wistar rat after head injury with the intention of improving brain function. Adult female Wistar rats will be injured using the controlled cortical impact model of head trauma. After injury, bone marrow stromal cells harvested from the tibia and femur of normal male adult rats will be injected into the tail vein of the female rat. The marrow stromal cells will be identified by Y chromosomes. Following transplantation, the animals will be sacrificed at different time points and brain sections will be stained for immunohistochemistry to examine for proliferation of the marrow stromal cells and the phenotypes of newly generated cells. Using immunohistochemistry and enzyme-linked immunosorbent assay (ELISA), the expression of neurotrophic factors following marrow stromal cell transplantation will also be studied. The safety of marrow stromal cell treatment of traumatic brain injury will be evaluated and a battery of functional outcome measurements will be performed to test for enhanced recovery resulting from treatment. If intravenous transplantation of marrow stromal cells succeeds in improving functional outcome, a new avenue will be opened for further development of therapeutic interventions to improve outcome of traumatic brain injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: USING BIOCHEMICAL MARKERS TO DETECT ABUSIVE HEAD TRAUMA Principal Investigator & Institution: Berger, Rachel P.; Professor; Children's Hosp Pittsburgh/Upmc Hlth Sys of Upmc Health Systems Pittsburgh, Pa 152132583 Timing: Fiscal Year 2003; Project Start 14-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Child abuse is a leading cause of serious traumatic brain injury (TBI) in infants and young children. Proper diagnosis of abusive head trauma (AHT) is difficult even for experienced, astute physicians. Misdiagnosis is common and can have catastrophic medical consequences for patients. Aside from increased awareness, there are currently no established strategies or diagnostic tests to help physicians properly identify AHT. A screening test that could alert physicians to the possibility of AHT and thereby aid in proper and timely diagnosis, could have an enormous impact. Biochemical markers of brain injury are released from the brain after TBI and diffuse into cerebrospinal fluid (CSF) and/or serum, where their concentrations can be measured. CSF and serum concentrations of three of these biochemical markers -neuron-specific enolase (NSE), S100B, and myelin-basic protein (MBP) - are sensitive indicators of mild, moderate and severe TBI in adults and children. These markers may therefore have the potential to act as diagnostic adjuncts to complement physician acumen in properly diagnosing AHT. Specific Aim 1 is to determine the sensitivity and

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specificity of serum NSE concentrations for detecting AHT in infants at increased risk of AHT and to determine whether the use of a panel of NSE, S100B and MBP improves sensitivity or specificity when compared with NSE as a single marker. Specific Aim 2 is to determine whether increases in CSF and serum NSE, S100B and/or MBP are specific to TBI or whether their concentrations can be affected by four non-traumatic neurological insults: hypoxic-ischemic encephalopathy, meningitis, progressive encephalopathy and seizures. The candidate is a pediatrician at Children's Hospital of Pittsburgh (CHP). This Mentored Career Development Award will allow the candidate to pursue a unique and highly integrated mentored program in pediatric neurotrauma and child abuse. Pittsburgh is an ideal environment for this type of program because of the resources of CHP, the Safar Center for Resuscitation Research and The Child Advocacy Center. Dr. Patrick Kochanek, the primary mentor for this award, is internationally recognized for his work in the field of pediatric TBI, has served as a mentor on multiple K awards and is the PI of an NICHD-funded training grant (T32) in pediatric neurointensive care. 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 “head trauma” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for head trauma in the PubMed Central database: •

Increased mRNA Levels for Components of the Lysosomal, Ca2+-activated, and ATPubiquitin-Dependent Proteolytic Pathways in Skeletal Muscle from Head Trauma Patients. by Mansoor O, Beaufrere B, Boirie Y, Ralliere C, Taillandier D, Aurousseau E, Schoeffler P, Arnal M, Attaix D.; 1996 Apr 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39696

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N-Methyl-d-aspartate antagonists and apoptotic cell death triggered by head trauma in developing rat brain. by Pohl D, Bittigau P, Ishimaru MJ, Stadthaus D, Hubner C, Olney JW, Turski L, Ikonomidou C.; 1999 Mar 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26815

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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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 head trauma, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “head trauma” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for head trauma (hyperlinks lead to article summaries): •

A 37-year-old man with severe head trauma, and a "hot nose" sign on brain flow study. Author(s): Baron M, Brasfield J. Source: Chest. 1999 November; 116(5): 1468-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10559115

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A case of penetrating head trauma in an 8-month-old. Author(s): O'Loughlin M, Criddle L. Source: Journal of Emergency Nursing: Jen : Official Publication of the Emergency Department Nurses Association. 2003 April; 29(2): 189-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12660711

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A case of pneumocephalus secondary to blunt head trauma. Author(s): McRae A, Amankwa K, Sirsi S. Source: The Journal of Emergency Medicine. 2001 October; 21(3): 277-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11604284

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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/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14520320

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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 practical method for the evaluation of symptom exaggeration in minor head trauma among civil litigants. Author(s): Sreenivasan S, Eth S, Kirkish P, Garrick T. Source: J Am Acad Psychiatry Law. 2003; 31(2): 220-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12875501

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A study of persistent post-concussion symptoms in mild head trauma using positron emission tomography. Author(s): Chen SH, Kareken DA, Fastenau PS, Trexler LE, Hutchins GD. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 2003 March; 74(3): 326-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12588917

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A useful tool for predicting outcome for the pediatric head trauma patient. Author(s): Heard C, Li V, Heard A. Source: Critical Care Medicine. 2002 June; 30(6): 1403-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12072714

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Abducens nerve palsy and ipsilateral Horner syndrome: a predicting sign of intracranial carotid injury in a head trauma patient. Author(s): Fujisawa H, Marukawa K, Kida S, Hasegawa M, Yamashita J, Matsui O. Source: The Journal of Trauma. 2001 March; 50(3): 554-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11265039

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Abusive head trauma in Maine infants: medical, child protective, and law enforcement analysis. Author(s): Ricci L, Giantris A, Merriam P, Hodge S, Doyle T. Source: Child Abuse & Neglect. 2003 March; 27(3): 271-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12654325

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Acinetobacter meningitis following head trauma. Author(s): Venkataraman S, George V, Jesudason M, Ganesh A. Source: J Assoc Physicians India. 1999 October; 47(10): 1020-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10778700

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Admission perfusion CT: prognostic value in patients with severe head trauma. Author(s): Wintermark M, van Melle G, Schnyder P, Revelly JP, Porchet F, Regli L, Meuli R, Maeder P, Chiolero R. Source: Radiology. 2004 July; 232(1): 211-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15220504

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An audit of head trauma care and mortality. Author(s): Siddiqui AA, Zafar H, Bashir SH. Source: J Coll Physicians Surg Pak. 2004 March; 14(3): 173-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15228853

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An infant who has head trauma. Author(s): Zenel JA. Source: Pediatrics in Review / American Academy of Pediatrics. 2000 June; 21(6): 210-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10854318

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Analysis of missed cases of abusive head trauma. Author(s): Jenny C, Hymel KP, Ritzen A, Reinert SE, Hay TC. Source: Jama : the Journal of the American Medical Association. 1999 February 17; 281(7): 621-6. Erratum In: Jama 1999 July 7; 282(1): 29. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10029123

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Application of guidelines for severe head trauma: data from an Italian database. Author(s): Citerio G, Stocchetti N, Cormio M, Beretta L, Galli D, Pesenti A. Source: European Journal of Emergency Medicine : Official Journal of the European Society for Emergency Medicine. 2003 March; 10(1): 68-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12637868

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Assessment and remediation of an auditory processing disorder associated with head trauma. Author(s): Musiek FE, Baran JA, Shinn J. Source: Journal of the American Academy of Audiology. 2004 February; 15(2): 117-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15112839

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Assessment of cognitive recovery following sports related head trauma in boxers. Author(s): Ravdin LD, Barr WB, Jordan B, Lathan WE, Relkin NR. Source: Clinical Journal of Sport Medicine : Official Journal of the Canadian Academy of Sport Medicine. 2003 January; 13(1): 21-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12544160

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Assessment of speed of processing after paediatric head trauma: need for better norms. Author(s): Kizilbash A, Warschausky S, Donders J. Source: Pediatric Rehabilitation. 2000 April-June; 4(2): 71-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11469744

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Association of head trauma with cervical spine injury, spinal cord injury, or both. Author(s): Iida H, Tachibana S, Kitahara T, Horiike S, Ohwada T, Fujii K. Source: The Journal of Trauma. 1999 March; 46(3): 450-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10088849

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Avoiding secondary brain injury after severe head trauma: monitoring and management. Author(s): Verweij BH, Muizelaar JP. Source: J Craniomaxillofac Trauma. 1996 Fall; 2(3): 8-17. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11951458

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Bedside measurement of the third ventricle's diameter during episodes of arising intracranial pressure after head trauma. Using transcranial real-time sonography for a non-invasive examination of intracranial compensation mechanisms. Author(s): Mursch K, Vogelsang JP, Zimmerer B, Ludwig HC, Behnke J, Markakis E. Source: Acta Neurochirurgica. 1995; 137(1-2): 19-23; Discussion 23-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8748862

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Behavioral and cognitive sequelae of head trauma. Author(s): Hilton G. Source: Orthopaedic Nursing / National Association of Orthopaedic Nurses. 1994 JulyAugust; 13(4): 25-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7831081

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Behavioral management of the agitated head trauma client. Author(s): Patterson TS, Sargent M. Source: Rehabilitation Nursing : the Official Journal of the Association of Rehabilitation Nurses. 1990 September-October; 15(5): 248-9, 253. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2399358

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Benign focal epileptiform discharges in children after severe head trauma: prognostic value and clinical course. Author(s): Wohlrab G, Schmitt B, Boltshauser E. Source: Epilepsia. 1997 March; 38(3): 275-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9070588

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beta A4 amyloid protein deposition in brain after head trauma. Author(s): Roberts GW, Gentleman SM, Lynch A, Graham DI. Source: Lancet. 1991 December 7; 338(8780): 1422-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1683421

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Bilateral craniotomies for blunt head trauma. Author(s): Razack N, Singh RV, Petrin D, Villanueva P, Green BA. Source: The Journal of Trauma. 1997 November; 43(5): 840-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9390498

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Bilateral internuclear ophthalmoplegia due to acute cervical hyperextension without head trauma. Author(s): Jammes JL. Source: J Clin Neuroophthalmol. 1989 June; 9(2): 112-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2526155

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Bilateral internuclear ophthalmoplegia following minor head trauma. Author(s): Walsh WP, Hafner JW Jr, Kattah JC. Source: The Journal of Emergency Medicine. 2003 January; 24(1): 19-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12554035

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Bilateral sixth nerve palsy after head trauma. Author(s): Advani RM, Baumann MR. Source: Annals of Emergency Medicine. 2003 January; 41(1): 27-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12514679

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Biochemical markers of cerebral injury in patients with minor head trauma and ethanol intoxication. Author(s): Levitt MA, Cook LA, Simon BC, Williams V. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 1995 August; 2(8): 675-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7584744

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Bipolar and pure mania disorders precipitated by head trauma. Author(s): Burstein A. Source: Psychosomatics. 1993 March-April; 34(2): 194-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8456169

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Blindness following minor head trauma in children: a report of two cases with a review of the literature. Author(s): Harrison DW, Walls RM. Source: The Journal of Emergency Medicine. 1990 January-February; 8(1): 21-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2191027

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Blood flow velocities in the basal cerebral vein after head trauma: a prospective study in 82 patients. Author(s): Mursch K, Muller CA, Buhre W, Lang JK, Vatter H, Behnke-Mursch J. Source: Journal of Neuroimaging : Official Journal of the American Society of Neuroimaging. 2002 October; 12(4): 325-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12380479

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Blunt basal head trauma: aspects of unconsciousness. Author(s): Bostrom K, Helander CG, Lindgren S. Source: Acta Neurochir Suppl (Wien). 1992; 55: 25-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1414539

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Blunt basal head trauma: rupture of posterior inferior cerebellar artery. Author(s): Bostrom K, Helander CG, Lindgren SO. Source: Forensic Science International. 1992 February; 53(1): 61-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1568681

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Blunt head trauma: comparison of various weapons with intracranial injury and neurologic outcome. Author(s): Alcantara AL, Roszler MH, Guyot AM, Peterson PL. Source: The Journal of Trauma. 1994 October; 37(4): 521-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7932879

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Blunt pediatric head trauma requiring neurosurgical intervention: how subtle can it be? Author(s): Brown L, Moynihan JA, Denmark TK. Source: The American Journal of Emergency Medicine. 2003 October; 21(6): 467-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14574653

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Brain SPECT evaluation of amnestic ED patients after mild head trauma. Author(s): Lorberboym M, Lampl Y, Gerzon I, Sadeh M. Source: The American Journal of Emergency Medicine. 2002 July; 20(4): 310-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12098178

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Brainstem auditory evoked potential with increased stimulus rate in minor head trauma. Author(s): Podoshin L, Ben-David Y, Fradis M, Pratt H, Sharf B, Schwartz M. Source: The Journal of Laryngology and Otology. 1990 March; 104(3): 191-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2341771

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CART for prediction of function after head trauma. Author(s): Germanson T, Lanzino G, Kassell NF. Source: Journal of Neurosurgery. 1995 November; 83(5): 941-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7472572

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Cerebellar contusion associated with type I Chiari malformation following supratentorial head trauma: case report. Author(s): Couldwell WT, Zhang W, Allen R, Arce D, Stillerman CB. Source: Neurological Research. 1998 January; 20(1): 93-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9471110

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Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm. Author(s): Martin NA, Patwardhan RV, Alexander MJ, Africk CZ, Lee JH, Shalmon E, Hovda DA, Becker DP. Source: Journal of Neurosurgery. 1997 July; 87(1): 9-19. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9202259

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Characterizing and treating dizziness after mild head trauma. Author(s): Hoffer ME, Gottshall KR, Moore R, Balough BJ, Wester D. Source: Otology & Neurotology : Official Publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology. 2004 March; 25(2): 135-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15021772

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Clinical case conference: alcoholism and head trauma. Author(s): Sticco SL. Source: Crna. 1995 November; 6(4): 183-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8680348

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Clinical evaluation of extracellular amino acids in severe head trauma by intracerebral in vivo microdialysis. Author(s): Kanthan R, Shuaib A. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1995 September; 59(3): 326-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7673969

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Clinical evaluation of patients with head trauma. Author(s): Ko DY. Source: Neuroimaging Clin N Am. 2002 May; 12(2): 165-74. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12391629

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Clinical review 113: Hypopituitarism secondary to head trauma. Author(s): Benvenga S, Campenni A, Ruggeri RM, Trimarchi F. Source: The Journal of Clinical Endocrinology and Metabolism. 2000 April; 85(4): 135361. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10770165

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Coagulopathy in pediatric abusive head trauma. Author(s): Hymel KP, Abshire TC, Luckey DW, Jenny C. Source: Pediatrics. 1997 March; 99(3): 371-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9041291

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Cognitive structure of executive deficits in frontally lesioned head trauma patients performing activities of daily living. Author(s): Fortin S, Godbout L, Braun CM. Source: Cortex. 2003 April; 39(2): 273-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12784889

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Communication and ethics: cardiopulmonary resuscitation in head trauma rehabilitation. Author(s): Phipps EJ. Source: The Journal of Head Trauma Rehabilitation. 1998 October; 13(5): 95-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9753540

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Comparison of intracranial computed tomographic (CT) findings in pediatric abusive and accidental head trauma. Author(s): Hymel KP, Rumack CM, Hay TC, Strain JD, Jenny C. Source: Pediatric Radiology. 1997 September; 27(9): 743-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9285736

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Comparison of quantitative methods for brain single photon emission computed tomography analysis in head trauma and stroke. Author(s): Loutfi I, Singh A. Source: Investigative Radiology. 1995 October; 30(10): 588-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8557498

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Confusional migraine precipitated by mild head trauma. Author(s): Soriani S, Cavaliere B, Faggioli R, Scarpa P, Borgna-Pignatti C. Source: Archives of Pediatrics & Adolescent Medicine. 2000 January; 154(1): 90-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10632261

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Cranial computed tomography in the emergency evaluation of adult patients without a recent history of head trauma: a prospective analysis. Author(s): Rothrock SG, Buchanan C, Green SM, Bullard T, Falk JL, Langen M. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 1997 July; 4(7): 654-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9223687

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Cranial nerve II-VII injuries in fatal closed head trauma. Author(s): Mariak Z, Mariak Z, Stankiewicz A. Source: Eur J Ophthalmol. 1997 January-March; 7(1): 68-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9101199

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Critical care management of head trauma in children. Author(s): Mazzola CA, Adelson PD. Source: Critical Care Medicine. 2002 November; 30(11 Suppl): S393-401. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12528780

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CT and MR imaging of nonaccidental pediatric head trauma. Author(s): Petitti N, Williams DW 3rd. Source: Academic Radiology. 1998 March; 5(3): 215-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9522889

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CT of head trauma. Author(s): Zee CS, Go JL. Source: Neuroimaging Clin N Am. 1998 August; 8(3): 525-39. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9673311

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CT scan findings in mild head trauma: a series of 2,000 patients. Author(s): Bordignon KC, Arruda WO. Source: Arquivos De Neuro-Psiquiatria. 2002 June; 60(2-A): 204-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12068346

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Death following minor head trauma in two adult individuals with the Chiari I deformity. Author(s): Wolf DA, Veasey SP 3rd, Wilson SK, Adame J, Korndorffer WE. Source: J Forensic Sci. 1998 November; 43(6): 1241-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9846405

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Decisionmaking in pediatric minor head trauma. Author(s): Greenes DS. Source: Annals of Emergency Medicine. 2003 October; 42(4): 515-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14520322

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Decreased plasma protein binding of valproate in patients with acute head trauma. Author(s): Anderson GD, Gidal BE, Hendryx RJ, Awan AB, Temkin NR, Wilensky AJ, Winn HR. Source: British Journal of Clinical Pharmacology. 1994 June; 37(6): 559-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7917774

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Delayed and progressive brain injury in children and adolescents with head trauma. Author(s): Stein SC, Spettell CM. Source: Pediatric Neurosurgery. 1995; 23(6): 299-304. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8743998

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Delayed cerebral edema and fatal coma after minor head trauma: role of the CACNA1A calcium channel subunit gene and relationship with familial hemiplegic migraine. Author(s): Kors EE, Terwindt GM, Vermeulen FL, Fitzsimons RB, Jardine PE, Heywood P, Love S, van den Maagdenberg AM, Haan J, Frants RR, Ferrari MD. Source: Annals of Neurology. 2001 June; 49(6): 753-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11409427

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Delayed deterioration after head trauma due to traumatic aneurysm. Author(s): Voelker JL, Ortiz O. Source: W V Med J. 1997 November-December; 93(6): 317-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9439194

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Delayed upper airway obstruction following a retropharyngeal haematoma after minor head trauma. Author(s): Kette F, Mergoni P, Girardis M, Sabbadini D, Zauli M, Sussi L, Pasetto A. Source: European Journal of Emergency Medicine : Official Journal of the European Society for Emergency Medicine. 2000 December; 7(4): 301-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11764141

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Dementia Due to Head Trauma: An obscure name for a clear neurocognitive syndrome. Author(s): Leon-Carrion J. Source: Neurorehabilitation. 2002; 17(2): 115-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12082238

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Determining cerebral perfusion pressure thresholds in severe head trauma. Author(s): Lewis S, Wong M, Myburgh J, Reilly P. Source: Acta Neurochir Suppl (Wien). 1998; 71: 174-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9779177

Studies

51

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Developing a clinical decision instrument to rule out intracranial injuries in patients with minor head trauma: methodology of the NEXUS II investigation. Author(s): Mower WR, Hoffman JR, Herbert M, Wolfson AB, Pollack CV Jr, Zucker MI; NEXUS II Investigators. National Emergency X-Radiography Utilization Study. Source: Annals of Emergency Medicine. 2002 November; 40(5): 505-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12399794

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Development of a novel method to predict disability after head trauma in children. Author(s): Cassidy LD, Potoka DA, Adelson PD, Ford HR. Source: Journal of Pediatric Surgery. 2003 March; 38(3): 482-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12632372

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Development of anterior cranial fossa dural arteriovenous malformation following head trauma. Case report. Author(s): Ishikawa T, Houkin K, Tokuda K, Kawaguchi S, Kashiwaba T. Source: Journal of Neurosurgery. 1997 February; 86(2): 291-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9010433

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Diffuse axonal injury after head trauma. A review. Author(s): Sahuquillo J, Poca MA. Source: Adv Tech Stand Neurosurg. 2002; 27: 23-86. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11887581

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Diffuse axonal injury without direct head trauma and with delayed onset of coma. Author(s): Gieron MA, Korthals JK, Riggs CD. Source: Pediatric Neurology. 1998 November; 19(5): 382-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9880145

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Diffusion imaging shows abnormalities after blunt head trauma when conventional magnetic resonance imaging is normal. Author(s): Rugg-Gunn FJ, Symms MR, Barker GJ, Greenwood R, Duncan JS. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 2001 April; 70(4): 530-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11254782

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Diffusion-weighted imaging: basic concepts and application in cerebral stroke and head trauma. Author(s): Huisman TA. Source: European Radiology. 2003 October; 13(10): 2283-97. Epub 2003 March 06. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14534804

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Disorders of ocular motility following head trauma. Author(s): Lepore FE. Source: Archives of Neurology. 1995 September; 52(9): 924-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7661732

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Dynamics of sensorineural hearing loss after head trauma. Author(s): Segal S, Eviatar E, Berenholz L, Kessler A, Shlamkovitch N. Source: Otology & Neurotology : Official Publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology. 2002 May; 23(3): 312-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11981387

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Dysphagia after head trauma: the effect of cognitive-communicative impairments on functional outcomes. Author(s): Halper AS, Cherney LR, Cichowski K, Zhang M. Source: The Journal of Head Trauma Rehabilitation. 1999 October; 14(5): 486-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10653944

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Dystonia after head trauma. Author(s): Lee MS, Rinne JO, Ceballos-Baumann A, Thompson PD, Marsden CD. Source: Neurology. 1994 August; 44(8): 1374-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8058132

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Early cellular brain damage and systemic inflammatory response after cardiopulmonary resuscitation or isolated severe head trauma: a comparative pilot study on common pathomechanisms. Author(s): Mussack T, Biberthaler P, Gippner-Steppert C, Kanz KG, Wiedemann E, Mutschler W, Jochum M. Source: Resuscitation. 2001 May; 49(2): 193-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11382526

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Early hypotension worsens neurological outcome in pediatric patients with moderately severe head trauma. Author(s): Kokoska ER, Smith GS, Pittman T, Weber TR. Source: Journal of Pediatric Surgery. 1998 February; 33(2): 333-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9498412

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Early onset pneumonia: risk factors and consequences in head trauma patients. Author(s): Bronchard R, Albaladejo P, Brezac G, Geffroy A, Seince PF, Morris W, Branger C, Marty J. Source: Anesthesiology. 2004 February; 100(2): 234-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14739794

Studies

53

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Edema fluid accumulation within necrotic brain tissue as a cause of the mass effect of cerebral contusion in head trauma patients. Author(s): Katayama Y, Kawamata T. Source: Acta Neurochir Suppl. 2003; 86: 323-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14753461

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Effects of pediatric head trauma for children, parents, and families. Author(s): Youngblut JM, Singer LT, Boyer C, Wheatley MA, Cohen AR, Grisoni ER. Source: Critical Care Nursing Clinics of North America. 2000 June; 12(2): 227-35. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11249368

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Elder patients with closed head trauma: a comparison with nonelder patients. Author(s): Nagurney JT, Borczuk P, Thomas SH. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 1998 July; 5(7): 678-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9678391

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Elderly patients with closed head trauma after a fall: mechanisms and outcomes. Author(s): Nagurney JT, Borczuk P, Thomas SH. Source: The Journal of Emergency Medicine. 1998 September-October; 16(5): 709-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9752942

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Electroencephalogram silence ratio for early outcome prognosis in severe head trauma. Author(s): Theilen HJ, Ragaller M, Tscho U, May SA, Schackert G, Albrecht MD. Source: Critical Care Medicine. 2000 October; 28(10): 3522-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11057811

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Electroencephalography in primary diagnosis of mild head trauma. Author(s): Pointinger H, Sarahrudi K, Poeschl G, Munk P. Source: Brain Injury : [bi]. 2002 September; 16(9): 799-805. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12217205

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Elevated intracranial pressure associated with hypermetabolism in isolated head trauma. Author(s): Bucci MN, Dechert RE, Arnoldi DK, Campbell J, McGillicuddy JE, Bartlett RH. Source: Acta Neurochirurgica. 1988; 93(3-4): 133-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3177029

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Elevated serum levels of S-100B reflect the extent of brain injury in alcohol intoxicated patients after mild head trauma. Author(s): Biberthaler P, Mussack T, Wiedemann E, Gilg T, Soyka M, Koller G, Pfeifer KJ, Linsenmaier U, Mutschler W, Gippner-Steppert C, Jochum M. Source: Shock (Augusta, Ga.). 2001 August; 16(2): 97-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11508872

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Endogenous neuropeptides in patients with acute traumatic head injury. II: Changes in the levels of cerebrospinal fluid substance P, serotonin and lipid peroxidation products in patients with head trauma. Author(s): Karakucuk EI, Pasaoglu H, Pasaoglu A, Oktem S. Source: Neuropeptides. 1997 June; 31(3): 259-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9243523

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Evaluation and management of children younger than two years old with apparently minor head trauma: proposed guidelines. Author(s): Schutzman SA, Barnes P, Duhaime AC, Greenes D, Homer C, Jaffe D, Lewis RJ, Luerssen TG, Schunk J. Source: Pediatrics. 2001 May; 107(5): 983-93. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11331675

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Evaluation of computed tomograms in paediatric head trauma. Author(s): Magu S, Mishra DS, Gandhi SB. Source: J Indian Med Assoc. 1998 January; 96(1): 13-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9601184

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Evaluation of minimally invasive percutaneous CT-controlled ventriculostomy in patients with severe head trauma. Author(s): Krotz M, Linsenmaier U, Kanz KG, Pfeifer KJ, Mutschler W, Reiser M. Source: European Radiology. 2004 February; 14(2): 227-33. Epub 2003 November 06. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14605843

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Evaluation of S-100b as a specific marker for neuronal damage due to minor head trauma. Author(s): Biberthaler P, Mussack T, Wiedemann E, Kanz KG, Koelsch M, GippnerSteppert C, Jochum M. Source: World Journal of Surgery. 2001 January; 25(1): 93-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11213162

Studies

55

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Evaluation of the patient with closed head trauma: an evidence based approach. Author(s): Cheung DS, Kharasch M. Source: Emergency Medicine Clinics of North America. 1999 February; 17(1): 9-23, Vii. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10101338

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Evidence for integrity of the growth hormone/insulin-like growth factor-1 axis in patients with severe head trauma during rehabilitation. Author(s): Bondanelli M, Ambrosio MR, Margutti A, Boldrini P, Basaglia N, Franceschetti P, Zatelli MC, Degli Uberti EC. Source: Metabolism: Clinical and Experimental. 2002 October; 51(10): 1363-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12370860

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Experimental models of head trauma. Author(s): Leker RR, Shohami E, Constantini S. Source: Acta Neurochir Suppl. 2002; 83: 49-54. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12442621

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Exsanguination from impact head trauma; the explanation for the "empty heart" sign. Author(s): Contostavlos DL. Source: Forensic Science International. 1998 August 12; 95(3): 201-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9800356

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Failure of the Miller criteria to predict significant intracranial injury in patients with a Glasgow Coma Scale score of 14 after minor head trauma. Author(s): Holmes JF, Baier ME, Derlet RW. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 1997 August; 4(8): 788-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9262697

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Fatal carotid dissection after blunt head trauma. Author(s): Tartara F, Regolo P, Servadei F, Versari PP, Giovanelli M. Source: Journal of Neurosurgical Sciences. 2000 June; 44(2): 103-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11105840

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Fatal head trauma from tree related injuries. Author(s): Escoffery CT, Shirley SE. Source: Med Sci Law. 2001 October; 41(4): 298-300. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11693223

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Fentanyl and sufentanil increase intracranial pressure in head trauma patients. Author(s): Weinstabl C, Spiss CK. Source: Anesthesiology. 1993 March; 78(3): 622-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8457074

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Fentanyl and sufentanil increase intracranial pressure in head trauma patients. Author(s): Sperry RJ, Bailey PL, Reichman MV, Peterson JC, Petersen PB, Pace NL. Source: Anesthesiology. 1992 September; 77(3): 416-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1306051

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Fetal head trauma without maternal uterine injury. Author(s): Watts CC, Clark K, McConnell TH. Source: American Journal of Obstetrics and Gynecology. 1967 September 15; 99(2): 28990. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6039072

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Fluctuating hypoxemia and pulmonary shunting following fatal head trauma: a case report. Author(s): Pace NL. Source: Anesthesia and Analgesia. 1977 January-February; 56(1): 129-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=556902

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Frequency of occurrence of a WAIS dementia profile in male head trauma patients. Author(s): Heinrichs RW, Celinski MJ. Source: J Clin Exp Neuropsychol. 1987 April; 9(2): 187-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3558751

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Frequency of primary brain stem lesions after head injuries. A CT scan analysis from 186 cases of severe head trauma. Author(s): George B, Thurel C, Pierron D, Ragueneau JL. Source: Acta Neurochirurgica. 1981; 59(1-2): 35-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7315559

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Frontal lobe abscess secondary to head trauma and nasal polyposis. Author(s): Bizakis JG, Prassopoulos P, Doxas P, Papadakis CE, Skoulakis CE, Kyrmizakis DE, Helidonis ES. Source: Auris, Nasus, Larynx. 2000 October; 27(4): 367-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10996499

Studies

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Frontal lobe personality syndromes. Ominous sequelae of head trauma. Author(s): Massey EW, Coffey CE. Source: Postgraduate Medicine. 1983 May; 73(5): 99-101, 104-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6844181

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Further experience with contrast-enhanced CT in head trauma. Author(s): Tsai FY, Huprich JE. Source: Neuroradiology. 1978; 16: 314-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=745700

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Gangrene and renal failure caused by dihydroergotamine used to treat raised intracranial pressure following head trauma. Author(s): Gupta VL, Mjorndal TO. Source: Acta Anaesthesiologica Scandinavica. 1996 March; 40(3): 389-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8721476

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Gastric secretory and mucosal injury response to severe head trauma. Author(s): Gudeman SK, Wheeler CB, Miller JD, Halloran LG, Becker DP. Source: Neurosurgery. 1983 February; 12(2): 175-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6835500

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Genetics of migraine without aura, migraine with aura, migrainous disorder, head trauma migraine without aura and tension-type headache. Author(s): Russell MB. Source: Cephalalgia : an International Journal of Headache. 2001 September; 21(7): 77880. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11595012

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Giant cervical epidural veins after craniectomy for head trauma. Author(s): Caruso RD, Smith MV, Chang JK, Wasenko JJ, Rosenbaum AE. Source: Ajnr. American Journal of Neuroradiology. 1998 May; 19(5): 903-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9613509

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Glasgow Coma Score versus severity systems in head trauma. Author(s): Chesnut RM. Source: Critical Care Medicine. 1998 January; 26(1): 10-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9428535

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Globe tenting as a result of head trauma. Author(s): Hrach CJ, Quint DJ. Source: Ajnr. American Journal of Neuroradiology. 1997 May; 18(5): 980-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9159381

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Gross pulmonary embolization with cerebral tissue following head trauma. Case report. Author(s): Legier J, Rinaldi I. Source: Journal of Neurosurgery. 1973 July; 39(1): 109-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4717134

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Guidelines for the treatment of adults with severe head trauma (part I). Initial assessment; evaluation and pre-hospital treatment; current criteria for hospital admission; systemic and cerebral monitoring. Author(s): Procaccio F, Stocchetti N, Citerio G, Berardino M, Beretta L, Della Corte F, D'Avella D, Brambilla GL, Delfini R, Servadei F, Tomei G. Source: Journal of Neurosurgical Sciences. 2000 March; 44(1): 1-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10961490

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Guidelines for the treatment of adults with severe head trauma (part II). Criteria for medical treatment. Author(s): Procaccio F, Stocchetti N, Citerio G, Berardino M, Beretta L, Della Corte F, D'Avella D, Brambilla GL, Delfini R, Servadei F, Tomei G. Source: Journal of Neurosurgical Sciences. 2000 March; 44(1): 11-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10961491

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Guidelines for the treatment of adults with severe head trauma (part III). Criteria for surgical treatment. Author(s): Davella D, Brambilla GL, Delfini R, Servadei F, Tomei G, Procaccio F, Stocchetti N, Citerio G, Berardino M, Beretta L, Della Corte F. Source: Journal of Neurosurgical Sciences. 2000 March; 44(1): 19-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10961492

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Guillain-Barre syndrome and head trauma. Case report. Author(s): De Freitas GR, De Freitas MR, Ferreira MC. Source: Arquivos De Neuro-Psiquiatria. 1997 June; 55(2): 315-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9629394

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Guillain-Barre syndrome following acute head trauma. Author(s): Duncan R, Kennedy PG. Source: Postgraduate Medical Journal. 1987 June; 63(740): 479-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3432176

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Haemorrhage into an arachnoid cyst: a serious complication of minor head trauma. Author(s): De K, Berry K, Denniston S. Source: Emergency Medicine Journal : Emj. 2002 July; 19(4): 365-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12101165

Studies

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Head trauma and Alzheimer's disease. Author(s): Nandoe RD, Scheltens P, Eikelenboom P. Source: Journal of Alzheimer's Disease : Jad. 2002 August; 4(4): 303-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12446932

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Head trauma and brain tumours revisited. Author(s): Henderson RD, Campbell SF. Source: Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia. 2000 May; 7(3): 262-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10833628

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Head trauma and epilepsy. Author(s): Ruggles KH, Hansotia PL, Ahmann PA. Source: Wis Med J. 1988 February; 87(2): 16-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3279711

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Head trauma and intellectual status: relation to quantitative magnetic resonance imaging findings. Author(s): Bigler ED, Johnson SC, Blatter DD. Source: Applied Neuropsychology. 1999; 6(4): 217-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10635436

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Head trauma and mid-frequency hearing loss. Author(s): Scott AM, Bauch CD, Olsen WO. Source: American Journal of Audiology. 1999 December; 8(2): 101-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10646193

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Head trauma and neuroprotection. Author(s): Stelmasiak Z, Dudkowska-Konopa A, Rejdak K. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2000 March-April; 6(2): 426-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11208350

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Head trauma and risk of dementia and Alzheimer's disease: The Rotterdam Study. Author(s): Mehta KM, Ott A, Kalmijn S, Slooter AJ, van Duijn CM, Hofman A, Breteler MM. Source: Neurology. 1999 December 10; 53(9): 1959-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10599765

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Head trauma discharge instructions. Author(s): Waseem M, Ryan MT. Source: Southern Medical Journal. 2003 March; 96(3): 327. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12659380

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Head trauma due to child abuse: serial computerized tomography in diagnosis and management. Author(s): Sinal SH, Ball MR. Source: Southern Medical Journal. 1987 December; 80(12): 1505-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3423894

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Head trauma in children younger than 2 years: are there predictors for complications? Author(s): Gruskin KD, Schutzman SA. Source: Archives of Pediatrics & Adolescent Medicine. 1999 January; 153(1): 15-20. Erratum In: Arch Pediatr Adolesc Med 1999 May; 153(5): 453. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9894994

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Head trauma in the child. Author(s): Pascucci RC. Source: Intensive Care Medicine. 1988; 14(3): 185-95. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3288659

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Head trauma in the older adult population. Author(s): Neatherlin JS. Source: Critical Care Nursing Quarterly. 2000 November; 23(3): 49-57. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11852938

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Head trauma preceding PD: a case-control study. Author(s): Bower JH, Maraganore DM, Peterson BJ, McDonnell SK, Ahlskog JE, Rocca WA. Source: Neurology. 2003 May 27; 60(10): 1610-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12771250

•

Head trauma. American College of Radiology. ACR Appropriateness Criteria. Author(s): Davis PC, Drayer BP, Anderson RE, Braffman B, Deck MD, Hasso AN, Johnson BA, Masaryk T, Pomeranz SJ, Seidenwurm D, Tanenbaum L, Masdeu JC. Source: Radiology. 2000 June; 215 Suppl: 507-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11037462

Studies

61

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Head trauma: comparison of infection rates for different methods of intracranial pressure monitoring. Author(s): Smith KA. Source: The Journal of Neuroscience Nursing : Journal of the American Association of Neuroscience Nurses. 1987 December; 19(6): 310-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2961824

•

Head trauma: CT scan interpretation by radiology residents versus staff radiologists. Author(s): Wysoki MG, Nassar CJ, Koenigsberg RA, Novelline RA, Faro SH, Faerber EN. Source: Radiology. 1998 July; 208(1): 125-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9646802

•

Heterotopic ossifications in patients after severe blunt trauma with and without head trauma: incidence and patterns of distribution. Author(s): Pape HC, Lehmann U, van Griensven M, Gansslen A, von Glinski S, Krettek C. Source: Journal of Orthopaedic Trauma. 2001 May; 15(4): 229-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11371787

•

History of head trauma and risk of intracranial meningioma: population-based casecontrol study. Author(s): Phillips LE, Koepsell TD, van Belle G, Kukull WA, Gehrels JA, Longstreth WT Jr. Source: Neurology. 2002 June 25; 58(12): 1849-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12084890

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Hypothalamic-pituitary-adrenal axis and interleukin-6 activity in children with head trauma and syndrome of inappropriate secretion of antidiuretic hormone. Author(s): Gionis D, Ilias I, Moustaki M, Mantzos E, Papadatos I, Koutras DA, Mastorakos G. Source: J Pediatr Endocrinol Metab. 2003 January; 16(1): 49-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12585340

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Idiopathic cholangiopathy in a biliary cast syndrome necessitating liver transplantation following head trauma. Author(s): Byrne MF, Chong HI, O'Donovan D, Sheehan KM, Leader MB, Kay E, McCormick PA, Broe P, Murray FE, McCormack A. Source: European Journal of Gastroenterology & Hepatology. 2003 April; 15(4): 415-7. Erratum In: Eur J Gastroenterol Hepatol. 2003 August; 15(8): 939. Mccormack Aiden [corrected to Mccormick P Aiden]. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12655263

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Imaging findings in diffuse axonal injury after closed head trauma. Author(s): Parizel PM, Ozsarlak, Van Goethem JW, van den Hauwe L, Dillen C, Verlooy J, Cosyns P, De Schepper AM. Source: European Radiology. 1998; 8(6): 960-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9683701

•

Imaging of head trauma in infancy and childhood. Author(s): Woodcock RJ, Davis PC, Hopkins KL. Source: Semin Ultrasound Ct Mr. 2001 April; 22(2): 162-82. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11327530

•

Imaging of nonaccidental head trauma in children. Author(s): Griscom NT. Source: Academic Radiology. 1999 January; 6(1): 81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9891158

•

Imaging of pediatric head trauma. Author(s): Poussaint TY, Moeller KK. Source: Neuroimaging Clin N Am. 2002 May; 12(2): 271-94, Ix. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12391636

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Imaging of sequelae of head trauma. Author(s): Zee CS, Hovanessian A, Go JL, Kim PE. Source: Neuroimaging Clin N Am. 2002 May; 12(2): 325-38, Ix. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12391639

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Improved documentation of retinal hemorrhages using a wide-field digital ophthalmic camera in patients who experienced abusive head trauma. Author(s): Nakagawa TA, Skrinska R. Source: Archives of Pediatrics & Adolescent Medicine. 2001 October; 155(10): 1149-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11576011

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Increased interleukin-12 levels in human cerebrospinal fluid following severe head trauma. Author(s): Stahel PF, Kossmann T, Joller H, Trentz O, Morganti-Kossmann MC. Source: Neuroscience Letters. 1998 June 19; 249(2-3): 123-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9682832

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Influence of head trauma on outcome following anterior temporal lobectomy. Author(s): Schuh LA, Henry TR, Fromes G, Blaivas M, Ross DA, Drury I. Source: Archives of Neurology. 1998 October; 55(10): 1325-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9779660

Studies

63

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Influence on outcome of ventilator-associated pneumonia in multiple trauma patients with head trauma treated with selected digestive decontamination. Author(s): Leone M, Bourgoin A, Giuly E, Antonini F, Dubuc M, Viviand X, Albanese J, Martin C. Source: Critical Care Medicine. 2002 August; 30(8): 1741-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12163786

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Injury biomechanics for aiding in the diagnosis of abusive head trauma. Author(s): Pierce MC, Bertocci GE, Berger R, Vogeley E. Source: Neurosurg Clin N Am. 2002 April; 13(2): 155-68. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12391701

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Injury of the vertebral artery after closed head trauma. Author(s): Della Corte F, Caricato A, Pennisi Mariano A, Pappalardo F, Piazza O, Rollo M. Source: European Journal of Emergency Medicine : Official Journal of the European Society for Emergency Medicine. 1999 September; 6(3): 255-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10622393

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Intercenter variance in clinical trials of head trauma--experience of the National Acute Brain Injury Study: Hypothermia. Author(s): Clifton GL, Choi SC, Miller ER, Levin HS, Smith KR Jr, Muizelaar JP, Wagner FC Jr, Marion DW, Luerssen TG. Source: Journal of Neurosurgery. 2001 November; 95(5): 751-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11702863

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Interhemispheric pressure gradients in severe head trauma in humans. Author(s): Mindermann T, Gratzl O. Source: Acta Neurochir Suppl (Wien). 1998; 71: 56-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9779144

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Intracranial hemorrhage and rebleeding in suspected victims of abusive head trauma: addressing the forensic controversies. Author(s): Hymel KP, Jenny C, Block RW. Source: Child Maltreatment. 2002 November; 7(4): 329-48. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12408245

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Intracranial insertion of a nasogastric tube in a case of homicidal head trauma. Author(s): Gianelli Castiglione A, Bruzzone E, Burrello C, Pisani R, Ventura F, Canale M. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 1998 December; 19(4): 329-34. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9885926

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Is SjvO2 monitoring useful in the management of head trauma patients? Author(s): Latronico N, Rasulo FA, Beindorf EA, Stefini R. Source: Intensive Care Medicine. 1999 December; 25(12): 1476-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10660862

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Isolated basilar artery occlusion by parietal dissection after severe chest and minor head trauma. Author(s): Gallerani M, Veronesi V, Ceruti S, Mantovani G, Ghadirpour R. Source: The American Journal of Emergency Medicine. 1998 October; 16(6): 614-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9786550

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Isolated unilateral hypoglossal nerve palsy after minor head trauma. Author(s): Kaushik V, Kelly G, Richards SD, Saeed SR. Source: Clinical Neurology and Neurosurgery. 2002 December; 105(1): 42-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12445924

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Isolated vestibular areflexia after blunt head trauma. Author(s): Guyot JP, Liard P, Thielen K, Kos I. Source: The Annals of Otology, Rhinology, and Laryngology. 2001 June; 110(6): 562-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11407848

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Juvenile head trauma syndromes and their relationship to migraine. Author(s): Haas DC, Pineda GS, Lourie H. Source: Archives of Neurology. 1975 November; 32(11): 727-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1180741

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Kleine-Levin syndrome: report of two cases with onset of symptoms precipitated by head trauma. Author(s): Will RG, Young JP, Thomas DJ. Source: The British Journal of Psychiatry; the Journal of Mental Science. 1988 March; 152: 410-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3139128

Studies

65

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Kluver-Bucy syndrome as a result of minor head trauma. Author(s): Asensio JA. Source: Southern Medical Journal. 2003 July; 96(7): 726. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12940334

•

Kluver-Bucy syndrome as a result of minor head trauma. Author(s): Olson DA. Source: Southern Medical Journal. 2003 March; 96(3): 323. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12659375

•

Kluver-Bucy syndrome as a result of minor head trauma. Author(s): Salim A, Kim KA, Kimbrell BJ, Petrone P, Roldan G, Asensio JA. Source: Southern Medical Journal. 2002 August; 95(8): 929-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12190235

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Language and memory disorders following closed head trauma. Author(s): Groher M. Source: Journal of Speech and Hearing Research. 1977 June; 20(2): 212-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=895093

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Late neuropsychologic status after childhood head trauma. Author(s): Costeff H, Abraham E, Brenner T, Horowitz I, Apter N, Sadan N, Najenson T. Source: Brain & Development. 1988; 10(6): 371-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3218710

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Late outcome of very severe blunt head trauma: a 10-15 year second follow-up. Author(s): Thomsen IV. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1984 March; 47(3): 260-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6707671

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Late psychosocial outcome in severe blunt head trauma. Author(s): Thomsen IV. Source: Brain Injury : [bi]. 1987 October-December; 1(2): 131-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3454678

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Letter: Defibrination after head trauma. Author(s): Anzil AP. Source: The New England Journal of Medicine. 1974 September 19; 291(12): 632-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4852747

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Limits of intermittent jugular bulb oxygen saturation monitoring in the management of severe head trauma patients. Author(s): Latronico N, Beindorf AE, Rasulo FA, Febbrari P, Stefini R, Cornali C, Candiani A. Source: Neurosurgery. 2000 May; 46(5): 1131-8; Discussion 1138-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10807245

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Limits of intermittent jugular bulb oxygen saturation monitoring in the management of severe head trauma patients. Author(s): Stocchetti N, Rossi S. Source: Neurosurgery. 2001 February; 48(2): 454-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11220398

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Long-term enteral nutrition support in a pregnant patient following head trauma. Author(s): Brown RO, Vehe KL, Kaufman PA, Rogers R, Kudsk KA, Luther RW. Source: Nutr Clin Pract. 1989 June; 4(3): 101-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2499751

•

Long-term follow-up of olfactory loss secondary to head trauma and upper respiratory tract infection. Author(s): Duncan HJ, Seiden AM. Source: Archives of Otolaryngology--Head & Neck Surgery. 1995 October; 121(10): 11837. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7546588

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Long-term follow-up review of 31 children with severe closed head trauma. Author(s): Costeff H, Groswasser Z, Goldstein R. Source: Journal of Neurosurgery. 1990 November; 73(5): 684-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2145403

•

Long-term hyperexcitability in the hippocampus after experimental head trauma. Author(s): Santhakumar V, Ratzliff AD, Jeng J, Toth Z, Soltesz I. Source: Annals of Neurology. 2001 December; 50(6): 708-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11761468

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Long-term outcome of children with severe head trauma and prolonged coma. Author(s): Mahoney WJ, D'Souza BJ, Haller JA, Rogers MC, Epstein MH, Freeman JM. Source: Pediatrics. 1983 May; 71(5): 756-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6835758

Studies

67

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Low-load, prolonged stretch in treatment of elbow flexion contractures secondary to head trauma: a case report. Author(s): MacKay-Lyons M. Source: Physical Therapy. 1989 April; 69(4): 292-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2928396

•

Lucid interval in infantile fatal head trauma. Author(s): Plunkett J. Source: Child Abuse & Neglect. 1998 October; 22(10): 943-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9793717

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Lumbar subarachnoid air after head trauma. Author(s): Power N, Ryan S, Glane P, Hamilton P. Source: Ajr. American Journal of Roentgenology. 2004 March; 182(3): 827. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14975999

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Magnetization transfer imaging in the detection of injury associated with mild head trauma. Author(s): McGowan JC, Yang JH, Plotkin RC, Grossman RI, Umile EM, Cecil KM, Bagley LJ. Source: Ajnr. American Journal of Neuroradiology. 2000 May; 21(5): 875-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10815663

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Major depressive disorder with psychotic features in an aviator after head trauma. Author(s): McLay RN, Drake A, Santiago PN, Kim CH. Source: Aviation, Space, and Environmental Medicine. 2004 February; 75(2): 175-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14960056

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Management of head trauma. Author(s): Marik PE, Varon J, Trask T. Source: Chest. 2002 August; 122(2): 699-711. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12171853

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Management of TMD caused by temporal head trauma. Author(s): Yustin D, Neff P. Source: Ont Dent. 1994 June; 71(5): 33-4, 36-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9468917

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Massive ketonuria during sedation with propofol in a 12 year old girl with severe head trauma. Author(s): Canivet JL, Gustad K, Leclercq P, Damas P, Lamy M. Source: Acta Anaesthesiol Belg. 1994; 45(1): 19-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8209621

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Massive pneumocephalus after minimal head trauma. Author(s): Sherman SC, Bokhari F. Source: The Journal of Emergency Medicine. 2003 October; 25(3): 319-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14585462

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Maternal head trauma during pregnancy. Author(s): Jordan BD. Source: Adv Neurol. 1994; 64: 131-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8291462

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Maternal head trauma. Author(s): Rabadi MH, Jordan BD. Source: Adv Neurol. 2002; 90: 75-85. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12068466

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Melanotic neuroectodermal tumor of infancy discovered after head trauma. Author(s): Paueksakon P, Parker JR, Fan X, Miles G, Ruiz H, Wushensky C, Johnson MD. Source: Pediatric Neurosurgery. 2002 January; 36(1): 33-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11818744

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Metabolic rate in severe head trauma. Author(s): Raurich JM, Ibanez J. Source: Jpen. Journal of Parenteral and Enteral Nutrition. 1994 November-December; 18(6): 521-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7602727

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Middle cerebral artery thrombosis following blunt head trauma. Author(s): De Caro R, Munari PF, Parenti A. Source: Clin Neuropathol. 1998 January-February; 17(1): 1-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9496532

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Migraine and childhood head trauma. Author(s): Friedrichs ES. Source: Headache. 1995 March; 35(3): 169. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7721580

Studies

69

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Mild head trauma. Author(s): Borczuk P. Source: Emergency Medicine Clinics of North America. 1997 August; 15(3): 563-79. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9255133

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Minimal head trauma in children revisited: is routine hospitalization required? Author(s): Roddy SP, Cohn SM, Moller BA, Duncan CC, Gosche JR, Seashore JH, Touloukian RJ. Source: Pediatrics. 1998 April; 101(4 Pt 1): 575-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9521936

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Minor head trauma in anticoagulated patients. Author(s): Garra G, Nashed AH, Capobianco L. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 1999 February; 6(2): 121-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10051903

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Minor head trauma unmasking asymptomatic lesions. Author(s): Wolf P. Source: Epilepsia. 2001 April; 42(4): 573. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11440356

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Minor head trauma. Author(s): Weight DG. Source: The Psychiatric Clinics of North America. 1998 September; 21(3): 609-24. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9774799

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Mortality prediction in head trauma patients: performance of Glasgow Coma Score and general severity systems. Author(s): Alvarez M, Nava JM, Rue M, Quintana S. Source: Critical Care Medicine. 1998 January; 26(1): 142-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9428557

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Mycoplasma hominis meningitis complicating head trauma: case report and review. Author(s): Cohen M, Kubak B. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1997 February; 24(2): 272-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9114165

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Necessity for ICP monitoring to supplement GCS in head trauma cases. Author(s): Hara M, Kadowaki C, Watanabe H, Shiogai T, Numoto M, Takeuchi K. Source: Neurochirurgia (Stuttg). 1988 March; 31(2): 39-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3380237

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Nephrogenic diabetes insipidus presenting after head trauma. Author(s): Trivedi HS, Nolph KD. Source: American Journal of Nephrology. 1994; 14(2): 145-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8080007

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Neurobehavioral recovery after pediatric head trauma: injury, pre-injury, and postinjury issues. Author(s): Donders J, Strom D. Source: The Journal of Head Trauma Rehabilitation. 2000 April; 15(2): 792-803. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10739968

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Neuroleptic malignant syndrome in an adolescent head trauma patient. Author(s): Trasmonte J, Dayner J, Barron TF. Source: Clinical Pediatrics. 1999 October; 38(10): 611-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10544869

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Neurological assessment of the child with head trauma. Author(s): Davis MJ, Vogel L. Source: Asdc J Dent Child. 1995 March-April; 62(2): 93-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7608377

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Neuromagnetic assessment of pathophysiologic brain activity induced by minor head trauma. Author(s): Lewine JD, Davis JT, Sloan JH, Kodituwakku PW, Orrison WW Jr. Source: Ajnr. American Journal of Neuroradiology. 1999 May; 20(5): 857-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10369357

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Neuro-ophthalmic manifestations of head trauma. Author(s): Van Stavern GP, Biousse V, Lynn MJ, Simon DJ, Newman NJ. Source: Journal of Neuro-Ophthalmology : the Official Journal of the North American Neuro-Ophthalmology Society. 2001 June; 21(2): 112-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11450900

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Neuro-ophthalmological findings in closed head trauma. Author(s): Sabates NR, Gonce MA, Farris BK. Source: J Clin Neuroophthalmol. 1991 December; 11(4): 273-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1838548

Studies

71

•

Neuropeptide Y-like immunoreactivity in lumbar cerebrospinal fluid of patients after severe head trauma. Author(s): Stachura Z, Obuchowicz E, Herman ZS. Source: Neuropeptides. 1997 February; 31(1): 12-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9574830

•

Neuropsychological treatment and longtime follow-up in an aphasic patient with very severe head trauma. Author(s): Thomsen IV. Source: J Clin Neuropsychol. 1981 May; 3(1): 43-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6168658

•

Neutrophil-rich anaplastic large cell lymphoma of the skull presenting after head trauma. Author(s): Parker JR, Lopez-Terrada D, Gresik MV, Vogel H, Baumgartner JE, Finegold MJ. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 2001 July-August; 4(4): 397401. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11441342

•

New phenomenon of abnormal auditory perception associated with emotional and head trauma: pathological confirmation by SPECT scan. Author(s): Stephane M, Hill T, Matthew E, Folstein M. Source: Brain and Language. 2004 June; 89(3): 503-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15120541

•

New therapeutic strategies in head trauma. Author(s): Latronico N, Candiani A. Source: Intensive Care Medicine. 1995 May; 21(5): 464-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7665761

•

Non space-occupying sequelae of head trauma. Author(s): Bergeron RT, Rumbaugh CL. Source: Radiologic Clinics of North America. 1974 August; 12(2): 315-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4414832

•

Nonfluent aphasia after closed head trauma: report of a case. Author(s): Stein M, Cantrell SB. Source: Journal of Oral and Maxillofacial Surgery : Official Journal of the American Association of Oral and Maxillofacial Surgeons. 1999 June; 57(6): 745-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10368104

72

Head Trauma

•

Nonhemorrhagic pontine infarct in a child following mild head trauma. Author(s): Tannebaum RD, Sloan EP. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 1995 June; 2(6): 523-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7497054

•

Non-target visual event-related potentials in evaluation of children with minor head trauma. Author(s): Gorke W, Schmidt U. Source: Neuropediatrics. 1991 May; 22(2): 79-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1857498

•

Nursing rehabilitation after severe head trauma. Author(s): Norsworthy E. Source: The American Journal of Nursing. 1974 July; 74(7): 1246-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4495006

•

Nutritional assessments and immunological responses in head trauma: a critical review of early nutritional support and its metabolic response with and without steroid usage. Author(s): Hu SH, Lin CN, Chang FT, Liu WJ, Howng SL. Source: Gaoxiong Yi Xue Ke Xue Za Zhi. 1987 September; 3(9): 591-604. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3133491

•

Nutritional support and head trauma. Author(s): Varella LD. Source: Critical Care Nurse. 1989 June; 9(6): 28-9, 32-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2509138

•

Objective indications for early tracheostomy after blunt head trauma. Author(s): Major KM, Hui T, Wilson MT, Gaon MD, Shabot MM, Margulies DR. Source: American Journal of Surgery. 2003 December; 186(6): 615-9; Discussion 619. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14672767

•

Observation of head trauma patients at home: a prospective study of compliance in the rural south. Author(s): Cline DM, Whitley TW. Source: Annals of Emergency Medicine. 1988 February; 17(2): 127-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3337430

Studies

73

•

Occult head trauma in young suspected victims of physical abuse. Author(s): Laskey AL, Holsti M, Runyan DK, Socolar RR. Source: The Journal of Pediatrics. 2004 June; 144(6): 719-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15192615

•

Ocular complications of head trauma in children. Author(s): Levin AV. Source: Pediatric Emergency Care. 1991 April; 7(2): 129-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2047311

•

Ocular motor abnormalities from head trauma. Author(s): Baker RS, Epstein AD. Source: Survey of Ophthalmology. 1991 January-February; 35(4): 245-67. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2011819

•

Oculomotor palsy from minor head trauma: initial sign of intracranial aneurysm. Author(s): Walter KA, Newman NJ, Lessell S. Source: Neurology. 1994 January; 44(1): 148-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8290050

•

Olfactory dysfunction in patients with head trauma. Author(s): Fujii M, Fukazawa K, Takayasu S, Sakagami M. Source: Auris, Nasus, Larynx. 2002 January; 29(1): 35-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11772488

•

Olfactory dysfunction in patients with head trauma. Author(s): Doty RL, Yousem DM, Pham LT, Kreshak AA, Geckle R, Lee WW. Source: Archives of Neurology. 1997 September; 54(9): 1131-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9311357

•

Olfactory mucosa of patients with olfactory disturbance following head trauma. Author(s): Yamagishi M, Okazoe R, Ishizuka Y. Source: The Annals of Otology, Rhinology, and Laryngology. 1994 April; 103(4 Pt 1): 279-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8154769

•

Optic disc haemorrhage following frontal head trauma. Author(s): Varma D, Chang BY, Das A. Source: Eye (London, England). 2004 February; 18(2): 216-7; Discussion 217-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14762429

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Head Trauma

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Optic nerve damage in head trauma: clinical and experimental studies. Author(s): Matsuzaki H, Kunita M, Kawai K. Source: Japanese Journal of Ophthalmology. 1982; 26(4): 447-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6820094

•

Optometric management of binocular dysfunctions secondary to head trauma: case reports. Author(s): Cohen AH. Source: J Am Optom Assoc. 1992 August; 63(8): 569-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1512408

•

Orthostatic tremor: delayed onset following head trauma. Author(s): Sanitate SS, Meerschaert JR. Source: Archives of Physical Medicine and Rehabilitation. 1993 August; 74(8): 886-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8347075

•

Outcome of severe closed head injury in the Midwest. A review and comparison with other major head trauma studies. Author(s): Bergman TA, Rockswold GL, Haines SJ, Ford SE. Source: Minn Med. 1987 July; 70(7): 397-401. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3614179

•

Perimacular retinal folds from childhood head trauma. Author(s): Lantz PE, Sinal SH, Stanton CA, Weaver RG Jr. Source: Bmj (Clinical Research Ed.). 2004 March 27; 328(7442): 754-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15044292

•

Perpetrators of abusive head trauma: a comparison of two geographic populations. Author(s): Starling SP, Holden JR. Source: Southern Medical Journal. 2000 May; 93(5): 463-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10832941

•

Pharmacology in the mild head trauma patient. Author(s): Rosenberg NM, Furnival RA, Luria JW, Harley JR. Source: Pediatric Emergency Care. 2000 August; 16(4): 299-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10966356

•

Phenoprocoumon, head trauma and delayed intracerebral haemorrhage. Author(s): Halatsch ME, Markakis E. Source: Funct Neurol. 1999 July-September; 14(3): 155-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10568216

Studies

75

•

Prevalence of head trauma in patients with difficult headache: the North Norway Headache Study. Author(s): Bekkelund SI, Salvesen R. Source: Headache. 2003 January; 43(1): 59-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12864760

•

Preventing bicycle-related head trauma in children. Author(s): Marsh E, Connor S, Wesolowski K, Grisoni E. Source: International Journal of Trauma Nursing. 2000 October-December; 6(4): 117-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11035854

•

Prevention of abusive head trauma in infants. Author(s): Barron CC. Source: Medicine and Health, Rhode Island. 2003 December; 86(12): 383-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14983538

•

Prevention of epilepsy after head trauma: do we need new drugs or a new approach? Author(s): Benardo LS. Source: Epilepsia. 2003; 44 Suppl 10: 27-33. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14511392

•

Promising strategies to minimize secondary brain injury after head trauma. Author(s): Bayir H, Clark RS, Kochanek PM. Source: Critical Care Medicine. 2003 January; 31(1 Suppl): S112-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12544985

•

Pulmonary contusion in severe head trauma patients: impact on gas exchange and outcome. Author(s): Leone M, Albanese J, Rousseau S, Antonini F, Dubuc M, Alliez B, Martin C. Source: Chest. 2003 December; 124(6): 2261-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14665509

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Radiological evaluation of head trauma by computer tomography in Ibadan, Nigeria. Author(s): Ogunseyinde AO, Obajimi MO, Ogundare SM. Source: West Afr J Med. 1999 January-March; 18(1): 33-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10876730

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Rapid identification of high-risk patients after minor head trauma (MHT) by assessment of S-100B: ascertainment of a cut-off level. Author(s): Biberthaler P, Mussack T, Wiedemann E, Kanz KG, Mutschler W, Linsenmaier U, Pfeifer KJ, Gippner-Steppert C, Jochum M. Source: European Journal of Medical Research. 2002 April 30; 7(4): 164-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12010651

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Rapid neurological deterioration associated with minor head trauma in chronic hydrocephalus. Author(s): Dickerman RD, McConathy WJ, Lustrin E, Schneider SJ. Source: Child's Nervous System : Chns : Official Journal of the International Society for Pediatric Neurosurgery. 2003 April; 19(4): 249-51; Discussion 252-3. Epub 2003 March 20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12715191

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Recognizing abusive head trauma in children. Author(s): Plunkett J. Source: Jama : the Journal of the American Medical Association. 1999 October 20; 282(15): 1421-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10535427

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Recognizing abusive head trauma in children. Author(s): Becker H, Gupta BK. Source: Jama : the Journal of the American Medical Association. 1999 October 20; 282(15): 1421; Author Reply 1422. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10535426

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Recognizing abusive head trauma in children. Author(s): Lavin A. Source: Jama : the Journal of the American Medical Association. 1999 October 20; 282(15): 1421; Author Reply 1422. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10535425

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Relationship between brain perfusion computed tomography variables and cerebral perfusion pressure in severe head trauma patients. Author(s): Wintermark M, Chiolero R, van Melle G, Revelly JP, Porchet F, Regli L, Meuli R, Schnyder P, Maeder P. Source: Critical Care Medicine. 2004 July; 32(7): 1579-87. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15241105

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Research ethics in head trauma rehabilitation. Author(s): Phipps EJ. Source: The Journal of Head Trauma Rehabilitation. 2000 June; 15(3): 965-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10785627

Studies

77

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Retropharyngeal haematoma leading to airway obstruction in a child with closed head trauma. Author(s): Cox RG. Source: Paediatric Anaesthesia. 1998; 8(4): 353-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9672937

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Routinely repeated computed tomography after blunt head trauma: does it benefit patients? Author(s): Kaups KL, Davis JW, Parks SN. Source: The Journal of Trauma. 2004 March; 56(3): 475-80; Discussion 480-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15128116

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Self-inflicted head trauma using a captive bolt pistol: report of three cases. Author(s): Caird J, Roberts G, Farrell M, Allcutt D. Source: British Journal of Neurosurgery. 2000 August; 14(4): 349-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11045203

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Serum neuron-specific enolase as a predictor of intracranial lesions in children with head trauma: a pilot study. Author(s): Fridriksson T, Kini N, Walsh-Kelly C, Hennes H. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 2000 July; 7(7): 816-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10917333

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Severe head trauma in children: cranial computer tomography and clinical consequences. Author(s): Hirsch W, Schobess A, Eichler G, Zumkeller W, Teichler H, Schluter A. Source: Paediatric Anaesthesia. 2002 May; 12(4): 337-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11982842

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Severe head trauma in patients with unexplained central hypothyroidism. Author(s): Benvenga S, Vigo T, Ruggeri RM, Lapa D, Almoto B, LoGiudice F, Longo M, Blandino A, Campenni A, Cannavo S, Trimarchi F. Source: The American Journal of Medicine. 2004 June 1; 116(11): 767-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15144914

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Severity of cervical spine ligamentous injury correlates with mechanism of injury, not with severity of blunt head trauma. Author(s): Albrecht RM, Malik S, Kingsley DD, Hart B. Source: The American Surgeon. 2003 March; 69(3): 261-5; Discussion 265. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12678485

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Should transient loss of consciousness in blunt head trauma be a pre-hospital trauma triage criterion? Author(s): Horowitz BZ, Earle OJ. Source: The Journal of Emergency Medicine. 2001 November; 21(4): 381-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11728764

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Spasm of accommodation associated with closed head trauma. Author(s): Chan RV, Trobe JD. Source: Journal of Neuro-Ophthalmology : the Official Journal of the North American Neuro-Ophthalmology Society. 2002 March; 22(1): 15-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11937900

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Strategic sequence planning and prospective memory impairments in frontally lesioned head trauma patients performing activities of daily living. Author(s): Fortin S, Godbout L, Braun CM. Source: Brain and Cognition. 2002 March-April; 48(2-3): 361-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12030468

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Sufentanil, fentanyl, and alfentanil in head trauma patients: a study on cerebral hemodynamics. Author(s): Albanese J, Viviand X, Potie F, Rey M, Alliez B, Martin C. Source: Critical Care Medicine. 1999 February; 27(2): 407-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10075068

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Surgical management of head trauma. Author(s): Gruen P. Source: Neuroimaging Clin N Am. 2002 May; 12(2): 339-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12391640

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The child welfare response to serious nonaccidental head trauma. Author(s): Jaudes PK, Bilaver LA. Source: Child Welfare. 2004 January-February; 83(1): 27-48. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15002911

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The critical care nurse's role in preventing secondary brain injury in severe head trauma: achieving the balance. Author(s): Chamberlain DJ. Source: Aust Crit Care. 1998 December; 11(4): 123-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10188409

Studies

79

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The mechanism of injury of the abducens nerve in severe head trauma: a postmortem study. Author(s): Sam B, Ozveren MF, Akdemir I, Topsakal C, Cobanoglu B, Baydar CL, Ulukan O. Source: Forensic Science International. 2004 February 10; 140(1): 25-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15013163

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The neuropsychology of heading and head trauma in Association Football (soccer): a review. Author(s): Rutherford A, Stephens R, Potter D. Source: Neuropsychology Review. 2003 September; 13(3): 153-79. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14584910

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The postconcussion syndrome after mild head trauma part II: is migraine underdiagnosed? Author(s): Margulies S. Source: Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia. 2000 November; 7(6): 495-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11029228

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The postconcussion syndrome after mild head trauma: is brain damage overdiagnosed? Part 1. Author(s): Margulies S. Source: Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia. 2000 September; 7(5): 400-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10942660

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The relationship of blunt head trauma, subarachnoid hemorrhage, and rupture of preexisting intracranial saccular aneurysms. Author(s): Cummings TJ, Johnson RR, Diaz FG, Michael DB. Source: Neurological Research. 2000 March; 22(2): 165-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10763504

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The role of ultrasonography in imaging of paediatric head trauma. Author(s): Decarie JC, Mercier C. Source: Child's Nervous System : Chns : Official Journal of the International Society for Pediatric Neurosurgery. 1999 November; 15(11-12): 740-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10603015

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The role of visual evoked potentials in the diagnosis of optic nerve injury as a result of mild head trauma. Author(s): Cerovski B, Sikic J, Juri J, Petrovic J. Source: Coll Antropol. 2001; 25 Suppl: 47-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11817014

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The use of head computed tomography in elderly patients sustaining minor head trauma. Author(s): Mack LR, Chan SB, Silva JC, Hogan TM. Source: The Journal of Emergency Medicine. 2003 February; 24(2): 157-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12609645

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Unilateral internuclear ophthalmoplegia after head trauma. Author(s): Catalano RA, Sax RD, Krohel GB. Source: American Journal of Ophthalmology. 1986 April 15; 101(4): 491-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3963114

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Unsuspected upper cervical spine fractures associated with significant head trauma: role of CT. Author(s): Kirshenbaum KJ, Nadimpalli SR, Fantus R, Cavallino RP. Source: The Journal of Emergency Medicine. 1990 March-April; 8(2): 183-98. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2362121

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Unusual accessory cranial sutures in pediatric head trauma--case report. Author(s): Nakahara K, Miyasaka Y, Takagi H, Kan S, Fujii K. Source: Neurol Med Chir (Tokyo). 2003 February; 43(2): 80-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12627884

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Unusually late onset of cerebrospinal fluid rhinorrhea after head trauma. Author(s): Okada J, Tsuda T, Takasugi S, Nishida K, Toth Z, Matsumoto K. Source: Surgical Neurology. 1991 March; 35(3): 213-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1996450

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Use of decompressive craniectomy after severe head trauma. Author(s): Wick J, Wade J, Rohrer D, O'Neill O. Source: Aorn Journal. 1999 March; 69(3): 517-25, 527, 529. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11957449

Studies

81

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Use of hypertonic saline/acetate infusion in treatment of cerebral edema in patients with head trauma: experience at a single center. Author(s): Qureshi AI, Suarez JI, Castro A, Bhardwaj A. Source: The Journal of Trauma. 1999 October; 47(4): 659-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10528599

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Using CT of the cervical spine for early evaluation of pediatric patients with head trauma. Author(s): Keenan HT, Hollingshead MC, Chung CJ, Ziglar MK. Source: Ajr. American Journal of Roentgenology. 2001 December; 177(6): 1405-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11717095

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Using dependency/association rules to find indications for computed tomography in a head trauma dataset. Author(s): Imberman SP, Domanski B, Thompson HW. Source: Artificial Intelligence in Medicine. 2002 September-October; 26(1-2): 55-68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12234717

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Utilizing clinical factors to reduce head CT scan ordering for minor head trauma patients. Author(s): Miller EC, Holmes JF, Derlet RW. Source: The Journal of Emergency Medicine. 1997 July-August; 15(4): 453-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9279694

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Utilizing neuropsychological measures to predict vocational outcome in a head trauma population. Author(s): Ryan TV, Sautter SW, Capps CF, Meneese W, Barth JT. Source: Brain Injury : [bi]. 1992 March-April; 6(2): 175-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1571722

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Variability in brain death declaration practices in pediatric head trauma patients. Author(s): Chang MY, McBride LA, Ferguson MA. Source: Pediatric Neurosurgery. 2003 July; 39(1): 7-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12784069

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Variation in therapy and outcome for pediatric head trauma patients. Author(s): Tilford JM, Simpson PM, Yeh TS, Lensing S, Aitken ME, Green JW, Harr J, Fiser DH. Source: Critical Care Medicine. 2001 May; 29(5): 1056-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11378621

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Variation in utilization of computed tomography scanning for the investigation of minor head trauma in children: a Canadian experience. Author(s): Klassen TP, Reed MH, Stiell IG, Nijssen-Jordan C, Tenenbein M, Joubert G, Jarvis A, Baldwin G, St-Vil D, Pitters C, Belanger F, McConnell D, Vandemheen K, Hamilton MG, Sutcliffe T, Colbourne M. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 2000 July; 7(7): 739-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10917321

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Vasopressin levels and pediatric head trauma. Author(s): Padilla G, Leake JA, Castro R, Ervin MG, Ross MG, Leake RD. Source: Pediatrics. 1989 May; 83(5): 700-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2717286

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Venous air embolism in homicidal blunt impact head trauma. Case reports. Author(s): Adams V, Guidi C. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 2001 September; 22(3): 322-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11563750

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Ventilatory support for pulmonary failure of the head trauma patient. Author(s): Hemmer M. Source: Bull Eur Physiopathol Respir. 1985 May-June; 21(3): 287-93. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3890990

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Ventriculosubgaleal shunting for acute head trauma. Author(s): Savitz MH, Katz SS. Source: Critical Care Medicine. 1983 April; 11(4): 290-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6600995

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Vestibular neurectomy for dizziness after head trauma. A review of 28 patients. Author(s): Sanna M, Ylikosky J. Source: Orl; Journal for Oto-Rhino-Laryngology and Its Related Specialties. 1983; 45(4): 216-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6877799

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Vietnam head injury study. Preliminary analysis of the functional and anatomical sequelae of penetrating head trauma. Author(s): Sweeney JK, Smutok MA. Source: Physical Therapy. 1983 December; 63(12): 2018-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6647558

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Visual evoked response in head trauma: pattern-shift stimulus. Author(s): Gupta NK, Verma NP, Guidice MA, Kooi KA. Source: Neurology. 1986 April; 36(4): 578-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3960337

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War on the road. Prevention of the head trauma. Author(s): Pertuiset B, Mahdi M. Source: Acta Neurochirurgica. 1990; 107(1-2): 1-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2096601

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Woman with COPD and fixed and dilated pupil following head trauma. Author(s): Hodder RV. Source: Chest. 2004 January; 125(1): 305-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14718457

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CHAPTER 2. NUTRITION AND HEAD TRAUMA Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and head trauma.

Finding Nutrition Studies on Head Trauma 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 “head trauma” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.

7 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 “head trauma” (or a synonym): •

0.45% saline and 5% dextrose in water, but not 0.9% saline or 5% dextrose in 0.9% saline, worsen brain edema two hours after closed head trauma in rats. Author(s): Division of Anesthesiology, Soroka Medical Center and the Faculty of Health Science, Beer-Sheva, Israel. Source: Talmor, D Shapira, Y Artru, A A Gurevich, B Merkind, V Katchko, L Reichenthal, E Anesth-Analg. 1998 June; 86(6): 1225-9 0003-2999

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Effect of magnesium given 1 hour after head trauma on brain edema and neurological outcome. Author(s): Department of Neurosurgery, Soroka Medical Center, Ben-Gurion University, Beer-Sheva, Israel. Source: Feldman, Z Gurevitch, B Artru, A A Oppenheim, A Shohami, E Reichenthal, E Shapira, Y J-Neurosurg. 1996 July; 85(1): 131-7 0022-3085

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Long-chain versus medium and long-chain triglyceride-based fat emulsion in parental nutrition of severe head trauma patients. Author(s): Service d'Anesthesie et de Reanimation Chirurgicale, Hopital de Hautepierre, Strasbourg, France. Source: Calon, B Pottecher, T Frey, A Ravanello, J Otteni, J C Bach, A C Infusionstherapie. 1990 October; 17(5): 246-8 1011-6966

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The metabolic needs of head trauma victims. Author(s): Stevens Hall Convalescent Home, North Andover, MA 01845. Source: Anderson, B J J-Neurosci-Nurs. 1987 August; 19(4): 211-5 0888-0395

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/

Nutrition

•

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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 3. ALTERNATIVE MEDICINE AND HEAD TRAUMA Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to head trauma. 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 head trauma 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 “head trauma” (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 head trauma: •

Behavioral treatment of dizziness secondary to benign positional vertigo following head trauma. Author(s): Shutty MS Jr, Dawdy L, McMahon M, Buckelew SP. Source: Archives of Physical Medicine and Rehabilitation. 1991 June; 72(7): 473-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1676257

•

Chiropractic diagnosis and treatment of closed head trauma. Author(s): Dalby BJ. Source: Journal of Manipulative and Physiological Therapeutics. 1993 July-August; 16(6): 392-400. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8409787

•

Long-chain versus medium and long-chain triglyceride-based fat emulsion in parental nutrition of severe head trauma patients. Author(s): Calon B, Pottecher T, Frey A, Ravanello J, Otteni JC, Bach AC.

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Source: Infusionstherapie. 1990 October; 17(5): 246-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2127044 •

Monocular visual loss after closed head trauma: immediate resolution associated with spinal manipulation. Author(s): Gorman RF. Source: Journal of Manipulative and Physiological Therapeutics. 1995 June; 18(5): 308-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7673798

•

Tai Chi Chuan practice as a tool for rehabilitation of severe head trauma: 3 case reports. Author(s): Shapira MY, Chelouche M, Yanai R, Kaner C, Szold A. Source: Archives of Physical Medicine and Rehabilitation. 2001 September; 82(9): 1283-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11552205

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/

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The following is a specific Web list relating to head trauma; 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 Alzheimer's Disease Source: Integrative Medicine Communications; www.drkoop.com Epilepsy Source: Integrative Medicine Communications; www.drkoop.com Ménière's Disease Source: Healthnotes, Inc.; www.healthnotes.com Seizure Disorders Source: Integrative Medicine Communications; www.drkoop.com Vertigo Source: Healthnotes, Inc.; www.healthnotes.com

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 HEAD TRAUMA Overview In this chapter, we will give you a bibliography on recent dissertations relating to head trauma. 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 “head trauma” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on head trauma, we have not necessarily excluded nonmedical dissertations in this bibliography.

Dissertations on Head Trauma 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 head trauma. 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: •

Severe head trauma and the reestablishment of intimacy: Perspectives of survivors by Diefenthaler, Linda Reineck, PhD from University of Virginia, 1991, 217 pages http://wwwlib.umi.com/dissertations/fullcit/9219267

•

The effectiveness of social group work with head trauma rehabilitation patients by Futeral, Susan Todd, PhD from University of Maryland, Baltimore, 1993, 170 pages http://wwwlib.umi.com/dissertations/fullcit/9328952

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. PATENTS ON HEAD TRAUMA 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.8 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 “head trauma” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on head trauma, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Head Trauma By performing a patent search focusing on head trauma, 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 8Adapted

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 head trauma: •

Assay for detecting damage to the central nervous system Inventor(s): Cornell-Bell; Ann H. (Westbrook, CT), Madden; Kathleen S. (Bethesda, MD), Riblet; Leslie A. (Killingworth, CT) Assignee(s): Viatech Imagin, LLC (Ivoryton, CT) Patent Number: 6,268,223 Date filed: August 27, 1999 Abstract: A method is disclosed for the rapid diagnosis of disorders characterized by an ischemic event, such as stroke, transient ischemic attack, head trauma, myocardial infarction or other insults resulting in interrupted cranial blood flow. The method involves detection of the presence of the gamma isoform of protein kinase C (PKCg) in peripheral blood, which signals damage to central nervous system tissue and at least transient breakdown of the blood brain barrier. The assay may be performed, e.g., by emergency medical personnel, in a time frame that allows treatment of the patient before permanent damage to the central nervous system occurs. Excerpt(s): The present invention discloses a method for the rapid and accurate detection of damage to the central nervous system (CNS) caused by an ischemic event such as stroke or head trauma. The method focuses on detecting the release of the gamma isoform of protein kinase c (PKCg) into the bloodstream, e.g., as a result of the breakdown of the blood-brain barrier. The current invention provides a diagnostic method and a diagnostic kit that is useful for the early diagnosis and treatment of an ischemic event. Such methods and kits may be advantageously used, e.g., by emergency medical personnel, to obtain an early indication of an ischemic event within a time period following the event where permanent CNS damage may be avoided. The methods and kits may also be used to monitor patient progress and recovery following an ischemic event. Brain ischemia resulting from stroke, head trauma or other events that interfere with blood flow to the brain is a leading cause of death and disability in industrialized nations. Stroke, for example, affects 0. 1-0.2% of the North American and European population. Approximately 500,000 people in the United States have a new or recurrent stroke each year, with a significant number resulting in death. An estimated 3,000,000 people in the United States have survived a stroke, however many of these survivors are considered to be at risk for recurrent episodes. There are no specific neuroprotective drugs on the market to treat ischemic stroke, and consequently this condition represents a major clinical problem with 25-35% fatality for acute strokes within the first three weeks. Of the survivors, 25-50% will be totally dependent on family or institutional care for the rest of their lives. Web site: http://www.delphion.com/details?pn=US06268223__

•

Cytokine suppressive anti-inflammatory drug binding protein Inventor(s): Kumar; Sanjay (King of Prussia, PA) Assignee(s): SmithKline Beecham Corporation (Philadelphia, PA) Patent Number: 6,350,856 Date filed: March 24, 1998

Patents 97

Abstract: p38beta2 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing p38beta2 polypeptides and polynucleotides in the design of protocols for the treatment of central nervous system disorder such as senile dementia of the Alzheimer's type (SDAT), multiple sclerosis, cerebral malaria, stroke, head trauma and spinal cord injury; cardiovascular diseases such as restenosis and atherosclerosis; inflammatory diseases such as Adult Respiratory Disease Syndrome (ARDS), Rheumatoid arthritis, Osteoarthritis, Inflammatory Bowel Disease (IBD), psoriasis, dermatitis, asthma; and other such diseases or conditions associated with dysregulated or excess cytokines such as osteporosis, sepsis due to surgical or traumatic incident, chronic renal failure, AIDs, cachexia and autoimmune conditions such as lupus erthyromatosis, host graft rejection and graft versus host disease, among others, and diagnostic assays for such conditions. Excerpt(s): This invention relates to newly identified polynucleotides, polypeptides encoded by them and to the use of such polynucleotides and polypeptides, and to their production. More particularly, the polynucleotides and polypeptides of the present invention relate to CSBP/p38 MAP Kinases family, hereinafter referred to as p38beta2. The invention also relates to inhibiting or activating the action of such polynucleotides and polypeptides. Cytokines play an important role in regulating the cellular response during inflammation and other immune functions. Of particular interest are the cytokines interleukin-1 (IL-1,.alpha. and.beta.) and tumor necrosis factor (TNF,.alpha. and.beta.), which are the intercellular proteins involved in the initial step of the inflammatory response cascade (Arai, et al., Ann. Rev. Biochem. 59: 783-836 (1990). Thus, there has been a substantial amount of research recently devoted to interfering with the production of IL-1 and TNR in response to an inflammatory stimulus. One therapeutic approach involves suppressing the production of IL-1 and TNF at the level of transcription and/or translation and/or secretion. The activities associated with certain of pyridinyl imidazoles led to a class of compounds referred to as "CSAIDs", or Cytokine Suppressing Anti-Inflammatory Drugs. These compounds appear to arrest the expression of IL-1 and TNF predominantly at the translational level, although a lesser effect on transcription has also been observed but effects on other steps cannot be ruled out. Web site: http://www.delphion.com/details?pn=US06350856__ •

Perfusion shunt apparatus and method Inventor(s): Esch; Brady D. (San Jose, CA), Leary; James J. (Sunnyvale, CA), Macoviak; John A. (La Jolla, CA), Samson; Wilfred J. (Saratoga, CA) Assignee(s): Cardeon Corporation (Cupertino, CA) Patent Number: 6,254,563 Date filed: March 20, 2000 Abstract: A perfusion shunt apparatus and methods are described for isolating and selectively perfusing a segment of a patient's cardiovascular system and for directly circulatory flow around the isolated segment. An aortic perfusion shunt apparatus is configured for deployment within a patient's aortic arch and methods are described for isolating the aortic arch vessels from the aortic lumen, for selectively perfusing the arch vessels with a fluid and for directly blood flow within the aortic lumen through a shunt past the isolated arch vessels. The perfusion shunt apparatus may be mounted on a catheter or cannula for percutaneous introduction or for direct insertion into a circulatory vessel, such as the aorta. The perfusion shunt apparatus has application for

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protecting a patient from embolic stroke or hypoperfusion during cardiopulmonary bypass or cardiac surgery and also for selectively perfusing the cerebrovascular circulation with oxygenated blood or with neuroprotective fluids in the presence of risk factors, such as head trauma or cardiac insufficiency. The perfusion shunt apparatus will also find application for selective perfusion of other organ systems within the body. Excerpt(s): The perfusion shunt apparatus of the present invention may be mounted on a catheter or cannula for percutaneous introduction or for direct insertion into a circulatory vessel, such as the aorta. The perfusion shunt apparatus has application for protecting a patient from embolic stroke or hypoperfusion during cardiopulmonary bypass or cardiac surgery and also for selectively perfusing the cerebrovascular circulation with oxygenated blood or with neuroprotective fluids in the presence of risk factors, such as head trauma or cardiac insufficiency. The perfusion shunt apparatus will also find application for selective perfusion of other organ systems within the body. Over the past decades tremendous advances have been made in the area of heart surgery, including such life saving surgical procedures as coronary artery bypass grafting (CABG) and cardiac valve repair or replacement surgery. Cardiopulmonary bypass (CPB) is an important enabling technology that has helped to make these advances possible. Recently, however, there has been a growing awareness within the medical community and among the patient population of the potential sequelae or adverse affects of heart surgery and of cardiopulmonary bypass. Chief among these concerns is the potential for stroke or neurologic deficit associated with heart surgery and with cardiopulmonary bypass. One of the likely causes of stroke and of neurologic deficit is the release of emboli into the blood stream during heart surgery. Potential embolic materials include atherosclerotic plaques or calcific plaques from within the ascending aorta or cardiac valves and thrombus or clots from within the chambers of the heart. These potential emboli may be dislodged during surgical manipulation of the heart and the ascending aorta or due to high velocity jetting (sometimes called the "sandblasting effect") from the aortic perfusion cannula. Air that enters the heart chambers or the blood stream during surgery through open incisions or through the aortic perfusion cannula is another source of potential emboli. Emboli that lodge in the brain may cause a stroke or other neurologic deficit. Clinical studies have shown a correlation between the number and size of emboli passing through the carotid arteries and the frequency and severity of neurologic damage. At least one study has found that frank strokes seem to be associated with macroemboli larger than approximately 100 micrometers in size, whereas more subtle neurologic deficits seem to be associated with multiple microemboli smaller than approximately 100 micrometers in size. In order to improve the outcome of cardiac surgery and to avoid adverse neurological effects it would be very beneficial to eliminate or reduce the potential of such cerebral embolic events. Several medical journal articles have been published relating to cerebral embolization and adverse cerebral outcomes associated with cardiac surgery, e.g.: Determination or Size of Aortic Emboli and Embolic Load During Coronary Artery Bypass Grafting; Barbut et al.; Ann Thorac Surg 1997; 63; 1262-7; Aortic Atheromatosis and Risks of Cerebral Embolization; Barbut et al.; J Card & Vasc Anesth, Vol 10, No 1, 1996; pp 24-30; Aortic Atheroma is Related to Outcome but not Numbers of Emboli During Coronary Bypass; Barbut et al.; Ann Thorac Surg 1997; 64; 454-9; Adverse Cerebral Outcomes After Coronary Artery Bypass Surgery; Roach et al.; New England J of Med, Vol 335, No 25, 1996; pp 1857-1863; Signs of Brain Cell Injury During Open Heart Operations; Past and Present;.ANG.berg; Ann Thorac Surg 1995; 59; 1312-5; The Role of CPB Management in Neurobehavioral Outcomes After Cardiac Surgery; Murkin; Ann Thorac Surg 1995; 59; 1308-11; Risk Factors for Cerebral Injury and Cardiac Surgery; Mills; Ann Thorac Surg 1995; 59; 1296-9; Brain Microemboli Associated with

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Cardiopulmonary Bypass; A Histologic and Magnetic Resonance Imaging Study; Moody et al.; Ann Thorac Surg 1995; 59; 1304-7; CNS Dysfunction After Cardiac Surgery; Defining the Problem; Murkin; Ann Thorac Surg 1995; 59; 1287+; Statement of Consensus on Assessment of Neurobehavioral Outcomes After Cardiac Surgery; Murkin et al.; Ann Thorac Surg 1995; 59; 1289-95; Heart-Brain Interactions; Neurocardiology Comes of Age; Sherman et al.; Mayo Clin Proc 62: 1158-1160, 1987; Cerebral Hemodynamics After Low-Flow Versus No-Flow Procedures; van der Linden; Ann Thorac Surg 1995; 59; 1321-5; Predictors of Cognitive Decline After Cardiac Operation; Newman et al.; Ann Thorac Surg 1995; 59; 1326-30; Cardiopulmonary Bypass; Perioperative Cerebral Blood Flow and Postoperative Cognitive Deficit; Venn et al.; Ann Thorac Surg 1995; 59; 1331-5; Long-Term Neurologic Outcome After Cardiac Operations; Sotaniemi; Ann Thorac Surg 1995; 59; 1336-9; Macroemboli and Microemboli During Cardiopulmonary Bypass; Blauth; Ann Thorac Surg 1995; 59; 13003. Web site: http://www.delphion.com/details?pn=US06254563__ •

Pharmaceutical compositions comprising S-(-)-N-propargyl-1-aminoindan Inventor(s): Cohen; Sasson (Tel-Aviv, IL), Finberg; John P. M. (Keryat Tivon, IL), Levy; Ruth (Tel-Aviv, IL), Sterling; Jeff (Jerusalem, IL), Youdim; Moussa B. H. (Haif, IL) Assignee(s): Technion Research and Development Foundation, Ltd. (Technion City, IL), Teva Pharmaceutical Industries, Ltd. (Jerusalem, IL) Patent Number: 6,277,886 Date filed: January 11, 1999 Abstract: Pharmaceutical compositions for the treatment of a neurological disorder of neurotrauma or for improving memory in a patient comprising a therapeutically effective amount of S-(-)-N-proparygl-1-aminoindan or a pharmaceutically acceptable salt thereof as active ingredient, and a pharmaceutically active carrier. The pharmaceutical compositions are adapted, in particular for treating a neurological hypoxia or anoxia, neurodegenerative diseases. Parkinson's Disease, Alzheimer's Disease, neurotoxic injury, head trauma injury, spinal trauma injury or any other form of nerve damage. Excerpt(s): The present invention concerns the novel therapeutical use of S-(-)-Npropargyl-1-aminoindan and pharmaccutically acceptable salts thereof for the treatment of neurological disorders or neurotrauma and for improving memory in a patient. As used herein, the term "neurotrauma" is meant to refer to damage caused to the central and/or peripheral nervous system as a result of ischemic damage such as a stroke, hypoxia or anoxia, neurodegenerative diseases, Parkinson's Disease, Alzheimer's Disease, neurotoxic injury, head trauma injury, spinal trauma injury or any other form of nerve damage. R(-) deprenyl (also known as L-deprenyl), N,.alpha.-dimethyl-N2propenylphenethylamine) is a well-known inhibitor of the B-form of monoamine oxidase enzyme (hereinafter "MAO-B"). Web site: http://www.delphion.com/details?pn=US06277886__

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Patent Applications on Head Trauma As of December 2000, U.S. patent applications are open to public viewing.9 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 head trauma: •

Brain retraction sensor Inventor(s): Ayad, Michael; (Washington, DC) Correspondence: Daryl A. Basham; Roylance Abrams Berdo & Goodman; 1300 19th Street, N.W.; Washington; DC; 20036; US Patent Application Number: 20040010208 Date filed: July 9, 2002 Abstract: An electrode grid device is disclosed comprising a deformable envelope, further comprising non-polarizable electrodes and a pressure recording port. The device is designed to allow for monitoring of brain retraction pressure and local cortical electrical activity including DC potential, as well as to redistribute the force applied during retraction and thereby diminish the chance of focal brain injury during surgery. Retraction pressure recorded is equal over the full area of contact, providing a more meaningful measurement than simply at one point on the retractor. A means is disclosed for evacuation of air from the system to improve accuracy and fidelity of the pressure measurements. It is a further aspect of the device to allow for measurement of intracranial pressure, DC potential and EEG in epileptic and severe head trauma patients for management of edema and injury, respectively. Excerpt(s): This invention is related generally to intracranial sensors for prevention of retractor blade injury (i.e., "retraction injury") of the brain, and subdural monitoring devices. A retractor is an instrument used during surgery for, among other things, holding back structures adjacent to the immediate operative field (See, e.g., U.S. Pat. No. 5,769,781). During neurosurgical operations for aneurysms, tumors or other lesions located in the skull base, the surgeon must employ retracting devices in order to displace one or more lobes of the brain enough to gain adequate surgical exposure to the lesion. These retractors are adjusted by hand to optimize exposure. Unfortunately, it is very difficult for the surgeon to accurately gauge the amount of pressure actually applied to the brain during such placement of the retractor (see, e.g., Hongo et al., J Neurosurg 1987; 66:270-275). Moreover, it is also possible to inadvertently position the blade of the retractor such that a focal pressure point occurs at one particular area of the retractor blade pressing against the brain. Thus, injury to the brain can occur as a result of brain retraction when either the force applied is excessive or when the pressure is not adequately distributed to a large enough area of brain. This injury is thought to be the result of ischemia (inadequate blood flow) caused by the retraction, local trauma, or a combination of both. It has been estimated that brain retraction injury occurs in approximately 10% of major cranial base tumor procedures and 5% of intracranial aneurysm surgeries (Andrews et al., Neurosurgery 1993; 33:1052-64). Various attempts have been made to develop technology to help minimize the incidence of this type of injury, with limited success. For example, a strain gauge or gauges attached to the retractor blade has been employed (Hongo et al., 1987; Rosenorn J., Acta Neurochir (Wein) 1987; 85:17-22). This approach has limited utility because pressure can only be

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

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measured from the point or points where the strain gauges are situated. As mentioned above, sometimes the brunt of the force occurs at the tip of the retractor blade where no strain gauge is present. Certainly this technique does little, if anything, to distribute force on the brain more evenly. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Calcium channel blockers Inventor(s): Hu, Lain-Yen; (Ann Arbor, MI), Rafferty, Michael Francis; (Ann Arbor, MI), Ryder, Todd Robert; (Ann Arbor, MI) Correspondence: Warner-Lambert Company; 2800 Plymouth Road; Ann Arbor; MI; 48105; US Patent Application Number: 20010023249 Date filed: January 25, 2001 Abstract: The present invention provides compounds that block calcium channels having the Formula I shown below. 1The present invention also provides methods of using the compounds of Formula I to treat stroke, cerebral ischemia, head trauma, or epilepsy and to pharmaceutical compositions that contain the compounds of Formula I. Excerpt(s): The present invention relates to compounds that act to block calcium channels; methods of using the compounds to treat stroke, cerebral ischemia, pain, head trauma or epilepsy; and to pharmaceutical compositions that contain the compounds of the present invention. The entry of excessive amounts of calcium ions into neurons following an ischemic episode or other neuronal trauma has been well documented. Uncontrolled high concentrations of calcium in neurons initiates a cascade of biochemical events that disrupts normal cellular processes. Among these events are the activation of proteases and lipases, breakdown of neuronal membranes and the formation of free radicals, which may ultimately lead to cell death. Several types of calcium channels have been discovered and called the L, N, P, Q, R, and T types. Each type possesses distinct structural features, functional properties and cellular/subcellular distributions. Type selective calcium channel blockers have been identified. For example, SNX-111 has been shown to be a selective N-type calcium channel blocker and has demonstrated activity in a number of models of ischemia and pain (Bowersox S. S., et al., Drug News and Perspective, 1994:7:261-268 and references cited therein). The compounds of the present invention are calcium channel blockers that can block N-type calcium channels and can be used to treat stroke, pain, cerebral ischemia, head trauma, and epilepsy. and the pharmaceutically acceptable salts, esters, amides, and prodrugs thereof. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Interleukin converting enzyme (ICE) and central nervous system damage Inventor(s): Friedlander, Robert M.; (Cambridge, MA), Yuan, Junying; (Newton, MA) Correspondence: Sterne, Kessler, Goldstein & Fox Pllc; 1100 New York Avenue, N.W., Suite 600; Washington; DC; 20005-3934; US Patent Application Number: 20030105046 Date filed: April 17, 2002

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Abstract: The invention relates to methods of treating central nervous system damage. This includes methods of treating ALS using a mutant ICE gene and methods of treating head trauma injuries by ICE inhibition. The invention also relates to transgenic nonhuman animals comprising a mutant ICE gene and a mutant SOD gene. These transgenic animals exhibit attenuated symptoms of ALS. This invention also relates to methods of using the transgenic animals to screen for compounds to treat ALS. Excerpt(s): This application claims the benefit of the filing date of U.S. Provisional Application No. 60/050,242 filed Jun. 19, 1997 and said provisional application is incorporated herein by reference. The invention is generally in the field of molecular biology as related to the control of programmed cell death and treatment of disease. The invention further relates to treatment of amyotrophic lateral sclerosis and head trauma injury. ALS is characterized by neuronal cell death. Little is known about the triggering mechanism responsible for executing this cell death in ALS. Although ALS has been included in a list of diseases associated with increased apoptosis (Thompson, C. B., Science 267:1456-1462 (1995), there has been no direct evidence in the art to indicate that such is actually the case. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

L-DOPA ethyl ester salts and uses thereof Inventor(s): Frenkel, Anton; (Modiin, IL), Lidor-Hadas, Ramy; (Kfar Saba, IL) Correspondence: Cooper & Dunham Llp; 1185 Avenue OF The Americas; New York; NY; 10036; US Patent Application Number: 20030162832 Date filed: November 12, 2002 Abstract: The present invention provides non-hygroscopic, crystalline salts of levodopa ethyl ester (LDEE), wherein the salt is the octanoate salt, the myristate salt, the succinate salt, the succinate dihydrate salt, the fumarate salt or the fumarate dihydrate salt of levodopa ethyl ester. The subject invention also encompasses compositions comprising a levodopa ethyl ester salt and a carrier and processes for making these compositions. In addition, the subject invention concerns pharmaceutical compositions comprising a levodopa ethyl ester salt and a pharmaceutically acceptable carrier, as well as processes for making these pharmaceutical compositions. Furthermore, the subject invention includes methods of treating a subject afflicted with Parkinson's disease, senile dementia, dementia of the Alzheimer's type, a memory disorder, depression, hyperactive syndrome, an affective illness, a neurodegenerative disease, a neurotoxic injury, brain ischemia, a head trauma injury, a spinal trauma injury, schizophrenia, an attention deficit disorder, multiple sclerosis and seizures by the administration of levodopa ethyl ester salts. Excerpt(s): This application claims benefit of U.S. Provisional Application No. 60/350,477, filed Nov. 13, 2001, the contents of which are hereby incorporated by reference. Throughout this application, various references are cited, using arabic numbers within parentheses. Full citations for these references can be found at the end of the specification, immediately preceding the claims. These publications, in their entireties, are hereby incorporated by reference into the application to more fully describe the state of the art to which the invention pertains. The present invention concerns the use of levodopa ethyl ester (LDEE) salts to treat Parkinson's disease, senile dementia, dementia of the Alzheimer's type, a memory disorder, depression,

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hyperactive syndrome, an affective illness, a neurodegenerative disease, a neurotoxic injury, brain ischemia, a head trauma injury, a spinal trauma injury, schizophrenia, an attention deficit disorder, multiple sclerosis, withdrawal symptoms, epilepsy, convulsions or seizures. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method and apparatus for cerebral embolic protection Inventor(s): Esch, Brady D.; (San Jose, CA), Leary, James J.; (Sunnyvale, CA), Macoviak, John A.; (La Jolla, CA), Samson, Wilfred J.; (Saratoga, CA) Correspondence: Gunther Hanke; Fulwider Patton Lee & Utecht; P.O. Box 22615; Long Beach; CA; 90801-5615; US Patent Application Number: 20020010411 Date filed: July 3, 2001 Abstract: An aortic shunt apparatus and methods for cerebral embolic protection are described for isolating the aortic arch vessels from the aortic lumen, for selectively perfusing the arch vessels with a fluid and for redirecting blood flow within the aortic lumen and any potential embolic materials carried in the blood through a shunt past the isolated arch vessels. The perfusion shunt apparatus may be mounted on a catheter or cannula for percutaneous introduction or for direct insertion into the aorta. The perfusion shunt apparatus has application for protecting a patient from embolic stroke and hypoperfusion during cardiopulmonary bypass or cardiac surgery and also for selectively perfusing the cerebrovascular circulation with oxygenated blood or with neuroprotective fluids in the presence of risk factors, such as head trauma or cardiac insufficiency. The perfusion shunt apparatus will also find application for selective perfusion of other organ systems within the body. Excerpt(s): This application is a continuation of application Ser. No. 09/532,660, filed Mar. 20, 2000, now U.S, Pat. No. 6,254,563, which is a continuation of application Ser. No. 09/212,580, filed Dec. 14, 1998, now U.S. Pat. No. 6,139,517, which claims the benefit of U.S. Provisional application Ser. No. 60/069,470, filed Dec. 15, 1997, which are hereby incorporated by reference in their entirety. The present invention relates to an aortic shunt apparatus and methods for cerebral embolic protection by isolating the aortic arch vessels from the aortic lumen, selectively perfusing the arch vessels with a fluid and directing blood flow within the aortic lumen and any potential embolic materials carried in the blood through a shunt past the isolated arch vessels. The perfusion shunt apparatus of the present invention may be mounted on a catheter or cannula for percutaneous introduction or for direct insertion into a circulatory vessel, such as the aorta. The perfusion shunt apparatus has application for protecting a patient from embolic stroke or hypoperfusion during cardiopulmonary bypass or cardiac surgery and also for selectively perfusing the cerebrovascular circulation with oxygenated blood or with neuroprotective fluids in the presence of risk factors, such as head trauma or cardiac insufficiency. The perfusion shunt apparatus will also find application for selective perfusion of other organ systems within the body. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Non-sedating barbituric acid derivatives Inventor(s): Gutman, Daniella; (Rishon, IL), Moros, Daniel A.; (Larchmont, NY) Correspondence: Venable, Baetjer, Howard And Civiletti, Llp; P.O. Box 34385; Washington; DC; 20043-9998; US Patent Application Number: 20030187005 Date filed: January 30, 2003 Excerpt(s): This Application is a CIP of the U.S. application (application number not yet received), filed Jan. 27, 2003, a National Stage of International Application No. PCT/US01/23420, filed Jul. 26, 2001, which claims priority to U.S. provisional application No. 60/221,672 filed Jul. 26, 2000. This Application also claims the benefit of U.S. provisional application No. 60/352,273, filed Jan. 30, 2002. Each of these applications is incorporated herein by reference in its entirety. The present invention relates to novel non-sedating barbituric acid derivatives, pharmaceutical compositions containing them and methods of neuroprotection in cases of cerebral ischemia, head trauma and other acute neurologic injuries, and prevention of resulting neuronal damage. The invention also relates to the use of non-sedating barbituric acid derivatives given in a manner and dosage effective to produce blood levels and brain levels of these drugs and/or their active metabolites sufficient to provide a therapeutic effect. Barbituric acid and its derivatives have been known since the turn of the century to possess pharmacological properties and some of them serve as active ingredients in widely used drugs. Barbituric acid derivatives are known to act mainly as sedatives, hypnotics and anaesthetics. Certain derivatives also have an anticonvulsive effect and are therefore employed in the treatment of epilepsy. Thus, pharmaceutical compositions containing 5-ethyl-5-phenyl barbituric acid (phenobarbital) are at present most widely used as drugs employed in the treatment of epilepsy. However, like other barbituric acid derivatives, phenobarbital has sedative and hypnotic effects, which are a disadvantage in the treatment of epilepsy. Therefore, a great effort has been devoted to the search for compounds which have anticonvulsant properties and at the same time are devoid of sedative and hypnotic effects. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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The use of scopolamine salts Inventor(s): De Moraes Mello, Luiz E.A.; (Sao Paulo, BR), Goncalves Massant, Christina C; (Sao Paulo, BR), Kastropil Benassi, Simone; (Sao Paulo, BR) Correspondence: Larson & Taylor, Plc; 1199 North Fairfax Street; Suite 900; Alexandria; VA; 22314; US Patent Application Number: 20030060481 Date filed: September 12, 2002 Abstract: The use of scopolamine salts for preventing the onset of epilepsy that might ensue after the condition of status epileticus, major head trauma, including those occasioned by neurosurgical trauma, and acute lesional events to the brain. Excerpt(s): The current invention relates to a preventive treatment based on the administration of scopolamine as a means to prevent the onset of epilepsy that might ensue after an episode of status epilepticus, head trauma, including those caused by neurosurgical procedures as well as by acute lesional events in general. Epilepsy is

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defined as a condition where motor or non-motor seizures recur even in the absence of a toxic-metabolic or febrile background. The above definition clearly distinguishes between a non-epileptic seizure, which is often a single isolated event associated to a metabolic disturbance or intoxication from the true epilepsies. Even though both epileptic and non-epileptic seizures might have a similar clinical manifestation; a convulsive fit, epilepsy implies a permanently altered background condition. In this manner, the nervous system of persons with epilepsy is in some way different in its anatomy, physiology, and pharmacology from that of persons without epilepsy. Epilepsy has a high prevalence with an annual incidence ranging from 11 to 131/100,000 and a prevalence of 1.5% in the general population (Guerreiro and Guerreiro, 1993). The etiology of this condition, even though unknown in most cases, can sometimes be clearly linked to a previous lesional event. As such, the incidence of epilepsy as a consequence of severe head trauma ranges from 15 to 80% depending on the extent, location and severity of the injured brain area (Gumnit R J. Epilepsy and brain injury. In: Epilepsy updated: Causes and treatment, P. Robb (Ed.), Symposia Specialists, Chicago, pp. 177-183, 1980). Indeed the risk for developing epilepsy after severe head trauma is 13 times higher than that of the general population. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Use of r-enantiomer of N-propargyl-1-aminoindan, salts, and compositions thereof Inventor(s): Finberg, John P.M.; (Tivon, IL), Levy, Ruth; (Tel Aviv, IL), Sterling, Jeffrey; (Jerusalem, IL), Youdim, Moussa B.H.; (Haifa, IL) Correspondence: John P. White; Cooper & Dunham Llp; 1185 Avenue OF The Americas; New York; NY; 10036; US Patent Application Number: 20030065038 Date filed: October 26, 2001 Abstract: The subject invention provides R(+)-N-propargyl-1-aminoindan and pharmaceutically acceptable salts thereof, as well as pharmaceutical compositions containing same. The subject invention also provides methods of treating a subject afflicted with Parkinson's disease, a memory disorder, dementia, depression, hyperactive syndrome, an affective illness, a neurodegenerative disease, a neurotoxic injury, stroke, brain ischemia, a head trauma injury, a spinal trauma injury, neurotrauma, schizophrenia, an attention deficit disorder, multiple sclerosis, or withdrawal symptoms, using R(+)-N-propargy-1-aminoindan, or the pharmaceutically acceptable salt of the subject invention. The subject invention further provides a method of preventing nerve damage in a subject. Finally, the subject invention provides methods of preparing R(+)-N-propargyl-1-aminoindan, a salt thereof, and racemic Npropargyl-1-aminoindan Excerpt(s): Throughout this application, various references are referred to. Disclosures of these publications in their entireties are hereby incorporated by reference into this application to more fully describe the state of the art to which this invention pertains. I. The subject invention is in the field of selective irreversible inhibitors of the enzyme monoamine oxidase (hereinafter MAO) and provides the R(+) enantiomer of Npropargyl-1-aminoindan (also referred to herein as PAI) which is a selective irreversible inhibitor of the B-form of monoamine oxidase enzyme (hereinafter MAO-B). The subject invention also provides pharmaceutical compositions containing R(+)PAI which are particularly useful for the treatment of Parkinson's disease, a memory disorder, dementia, depression, hyperactive syndrome, an affective illness, a neurodegenerative

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disease, a neurotoxic injury, stroke, brain ischemia, a head trauma injury, a spinal trauma injury, neurotrauma, schizophrenia, an attention deficit disorder, multiple sclerosis, and withdrawal symptoms. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

USE OF SERINE PROTEASE INHIBITORS TO INHIBIT PATHOPHYSIOLOGY AND NEUROPATHOLOGY IN A HOST Inventor(s): HOFFMAN, KEITH B; (SAN DIEGO, CA), LYNCH, GARY; (IRVINE, CA) Correspondence: Bozicevic, Field & Francis Llp; 200 Middlefield RD; Suite 200; Menlo Park; CA; 94025; US Patent Application Number: 20030144212 Date filed: July 6, 2000 Abstract: Methods are provided for inhibiting cell adhesion molecule cleavage in brain tissue of a host. In the subject methods, an effective amount of a protease inhibitor, particularly serine protease inhibitors, such as those that inhibit tPA and related proteases, is administered to the host. The subject methods find use in the treatment and prevention of pathophysiology and neuropathology in a host, such as the treatment of a variety of pathological conditions resulting from pathophysiology and/or excitotoxicity. Specific pathological conditions in which the subject methods find use include epilepsy (and related seizure states) and neuronal damage associated with excessive glutamate activity, e.g. resulting from an acute event such as hypoxia, head trauma or stroke. Excerpt(s): The field of the invention is methods of treating seizures and related neurological disorders. Synaptic plasticity is natural physiological process that is associated with memory and learning. See Wang et al., J. Clin. Neurophysiology (July 1997) 14: 264-293. It has been found that activity-dependent short- and long-term changes in the strength of synaptic transmission, such as long-term potentiation, are important for memory processes, and that such changes can result from synaptic plasticity. Thus, some synaptic plasticity is normal and does not lead to neuropathological conditions. However, where the magnitude of synaptic plasticity deviates from that required for normal physiological purposes, such as memory and learning, neuropathological conditions or diseases can arise. For example, synaptic plasticity can lead to the consolidation of excessive long-term potentiation and a concomitant increase in neuronal excitability. Ben Ari & Represa, Trends in Neuroscience (August 1990) 13:312-318. Such changes can, in turn, render the host more susceptible to seizures. 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 head trauma, you can access the U.S. Patent Office archive via the Internet at the following Web address: 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 “head trauma” (or synonyms) into

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the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on head trauma. You can also use this procedure to view pending patent applications concerning head trauma. 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 6. BOOKS ON HEAD TRAUMA Overview This chapter provides bibliographic book references relating to head trauma. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on head trauma 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 “head trauma” (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 head trauma: •

Disorders of Taste and Smell. 2nd ed Source: Alexandria, VA: American Academy of Otolaryngology-Head and Neck Surgery, Inc. 1996. 62 p. Contact: Available from American Academy of Head and Neck Surgery, Inc. (AAOHNS). One Prince Street, Alexandria, VA 22314. (703) 836-4444. Fax (703) 683-5100. Website: www.entnet.org. PRICE: $20.00 for members; $30.00 for non-members, plus shipping and handling. ISBN: 1567720242. Summary: The special senses of smell and taste, collectively known as chemosensation, are now amenable to identification, classification, and in certain instances, treatment. This self instruction packet is designed to serve as an up to date clinical reference on disorders of taste and smell. Topics include the anatomy of the olfaction (smell) system, including primary olfactory neuroepithelium, olfactory nerve fibers, vomeronasal system, trigeminal system, central olfactory pathway, and embryology; the physiology

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of the olfactory system, including odorant access to the receptor site, receptor cell neurophysiology, and neurotransmitters; the pathology of the olfactory system, including age, upper respiratory tract infection, rhinosinusitis, head trauma, surgery, chemical injury, endocrine metabolic abnormalities, neurodegenerative disorders, neoplasia (growth of new cells, including cancers), and congenital anosmia (lack of smell); determination of olfactory function; medical evaluation of the patient with an olfactory disorder; treatment of olfactory dysfunction; the anatomy of gustation (taste), including peripheral gustatory receptors, innervation of the taste buds, and central gustatory pathways; development of the gustatory apparatus; gustatory physiology, including chemosensory transduction and the role of saliva; pathology of the gustatory system, including drug effects, trauma, metabolic disturbances, infections, electrochemical taste, malnutrition, age, and cancer; the interaction of tastes among themselves and olfaction (smell); clinical assessment of gustatory function; evaluation of the patient with a taste complaint; and treatment of gustatory dysfunction. The information packet includes a pretest and posttest, interim quizzes for self evaluation, a list of references, and a form with which readers can qualify for continuing education credits. 5 figures. 3 tables. 82 references. •

Neurobiology of Primary Dementia Source: Washington, DC: American Psychiatric Press, Inc. 1998. 418 p. Contact: American Psychiatric Press, Inc. 1400 K Street, NW, Washington, DC 20005. (800) 368-5777; (202) 682-6262. Internet access: http://www.appi.org. PRICE: $61.50. ISBN: 0880489154. Summary: This book for health care practitioners, service providers, and policy makers, presents findings from recent research into the neurobiology of Alzheimer's disease (AD) and other primary dementias. One chapter reviews the epidemiology of dementia, using data from an ethnically diverse registry of older people who use communitybased services. Chapters focusing on AD discuss such topics as the genetics of familial AD, the cellular production of amyloid beta-protein in AD, the regulation of betaamyloid metabolism in AD, beta-amyloid amyloidogenesis in model systems of AD, head trauma as a risk factor for AD, brain imaging in AD, and diagnostic markers for AD. Other dementias are addressed in chapters on prion diseases, dementia associated with poststroke major depression, vascular dementia, dementia pugilistica, and the acquired immunodeficiency syndrome dementia complex. The book also discusses potential pharmacological treatments for AD, the practical management of AD, genetic counseling in AD and Huntington's disease, ethical issues in dementia, and the prospects for health care reform.

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 “head trauma” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “head trauma” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “head

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trauma” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •

Abusive Head Trauma In Infants And Children by Kay , MD. Rauth-Farley, et al; ISBN: 1878060740; http://www.amazon.com/exec/obidos/ASIN/1878060740/icongroupinterna

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Abusive Head Trauma in Infants and Children, 2-Volume Set: Medical Legal and Forensic Issues by Kay Rauth-Farley, et al; ISBN: 1878060406; http://www.amazon.com/exec/obidos/ASIN/1878060406/icongroupinterna

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Assessment of the Behavioral Consequences of Head Trauma (Frontiers of Clinical Neuroscience, Vol 7) by Muriel D. Lezak; ISBN: 0845145061; http://www.amazon.com/exec/obidos/ASIN/0845145061/icongroupinterna

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Families of the Brain Injured (Journal of Head Trauma Rehab 3.4) by Mi. Bond; ISBN: 9991238867; http://www.amazon.com/exec/obidos/ASIN/9991238867/icongroupinterna

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Litigating Head Trauma Cases (Personal Injury Library) by AC Roberts; ISBN: 0471554235; http://www.amazon.com/exec/obidos/ASIN/0471554235/icongroupinterna

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Litigating Head Trauma Cases, 1993 Supplement (Personal Injury Library) by Arthur C. Roberts; ISBN: 0471591505; http://www.amazon.com/exec/obidos/ASIN/0471591505/icongroupinterna

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Litigating Head Trauma Cases, 1994 Supplement (Loose Leaf) by Arthur C Roberts; ISBN: 0471023698; http://www.amazon.com/exec/obidos/ASIN/0471023698/icongroupinterna

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Management of Behavior Disorders (Journal of Head Trauma Rehab 3.3) by Eames; ISBN: 9991238662; http://www.amazon.com/exec/obidos/ASIN/9991238662/icongroupinterna

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Neurological Assessment: Head Trauma (Windows CD-ROM Single User) by Rybowiak; ISBN: 0683400312; http://www.amazon.com/exec/obidos/ASIN/0683400312/icongroupinterna

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Proving or defending repetitive stress injury, medical device, lead, pharmaceutical, and closed head trauma cases: A satellite program (Commercial law and practice course handbook series); ISBN: 0872242021; http://www.amazon.com/exec/obidos/ASIN/0872242021/icongroupinterna

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The Journal of Head Trauma Rehabilitation: Volume 6, Nos 1-4, 1991 by Sheldon, Md. Berrol, Mitchell, Phd. Rosenthal; ISBN: 9992722622; http://www.amazon.com/exec/obidos/ASIN/9992722622/icongroupinterna

Chapters on Head Trauma In order to find chapters that specifically relate to head trauma, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and head trauma 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 “head trauma” (or

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synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on head trauma: •

Alzheimer's Disease Source: in Howells, J.G. Modern Perspectives in Clinical Psychiatry. New York, NY: Brunner/Mazel, Inc. 1988. p. 261-285. Contact: This publication may be available from your local medical library. Call for information. ISBN: 0876304994. Summary: During the past two decades, Alzheimer's disease (AD) has become known as a prevalent severe psychiatric condition in the elderly. Difficulties of diagnosis are a significant stumbling block to progress in understanding AD. This chapter reviews and discusses approaches to diagnosis and diagnostic criteria and the nature of brain abnormalities (plaques and tangles; neurotransmitter deficits; neuronal loss; analysis via brain imaging; AD subtypes). Attention also is given to the epidemiology of AD, including its prevalence and risk factors (old age, family history of dementia, Down's syndrome and family, and head trauma), and to etiological theories that attempt to account for the neuropathological and neurochemical changes associated with AD and its confirmed risk factors (including the genetic theory, the toxic-exposure theory, and the virus-like particle theory). The author concludes with a discussion of the management of AD, concerning detection of dementia, community and residential care options, drug and psychological interventions, and trends in the need for AD services. 111 references.

•

Evaluation of Olfactory Deficits by Medical Imaging Source: in Doty, R.L., ed. Handbook of Olfaction and Gustation. New York, NY: Marcel Dekker, Inc. 1995. p. 395-419. Contact: Available from Marcel Dekker, Inc. 270 Madison Avenue, New York, NY 10016. (800) 228-1160 or (212) 696-9000; Fax (212) 685-4540. PRICE: $225.00 plus shipping and handling. ISBN: 0824792521. Summary: In this chapter, from a medical text on olfaction and gustation, the authors review the literature on the evaluation of olfactory deficits by medical imaging. Topics covered include imaging modalities and techniques, including plain radiographs, conventional tomography, computer tomography, magnetic resonance imaging, nuclear medicine, and angiography; the basic anatomy and physiology of the olfactory system; peripheral causes of olfactory disturbance, including sinonasal infectious disease, tumors of the nasal cavity and paranasal sinuses, allergic rhinitis, congenital or developmental abnormalities, and substance abuse; and central causes of olfactory diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, Korsakoff's psychosis, schizophrenia, congenital anosmia, head trauma, brain tumors, and AIDS. The authors conclude that in assessing the peripheral causes of olfactory deficits, medical imaging studies can reveal anatomical information and structural changes, suggest differential diagnosis, and provide guidelines for surgical intervention. In the evaluation of central causes, imaging studies can provide information elucidating the links between olfactory dysfunction and the structural or functional changes in the living brain. 5 figures. 152 references. (AA-M).

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Clinical Disorders of Olfaction: A Review Source: in Doty, R.L., ed. Handbook of Olfaction and Gustation. New York, NY: Marcel Dekker, Inc. 1995. p. 345-365. Contact: Available from Marcel Dekker, Inc. 270 Madison Avenue, New York, NY 10016. (800) 228-1160 or (212) 696-9000; Fax (212) 685-4540. PRICE: $225.00 plus shipping and handling. ISBN: 0824792521. Summary: In this lengthy chapter, from a medical text on olfaction and gustation, the authors provide an overview of the clinical disorders of olfaction. Topics covered include the evaluation of smell complaints, including the medical history, diagnostic classification and terminology, and psychophysical measurement in a clinical setting; common types of olfactory dysfunction, including nasal and/or sinus disease, prior upper respiratory infection, head trauma, and idiopathic smell dysfunction; other, less common, etiologies for olfactory disorders; and smell dyfunction secondary to other diseases, including endocrine, neurological, psychiatric, and nutritional disorders. 4 figures. 173 references.

•

Nongenetic Sensorineural Hearing Loss in Children Source: in Canalis, R.F. and Lambert, P.R., eds. Ear: Comprehensive Otology. Philadelphia, PA: Lippincott Williams and Wilkins. 2000. p. 489-510. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-3030. Fax (301) 223-2300. Website: www.lww.com. PRICE: $179.00 plus shipping and handling. ISBN: 078171558X. Summary: Persistent, bilateral congenital or early onset hearing loss in the moderate to profound range (41 to 100 dB) distorts the speech perception of a developing child. This chapter on nongenetic sensorineural hearing loss in children is from a textbook that offers complete coverage of the field of clinical otology (study of the ear). The book is oriented to serve both the otolaryngology resident as a practical learning tool and the practicing otolaryngologist as an updated reference source of clinical and basic information. Topics include the evaluation of a young child with a hearing loss, including history and physical examination, laboratory testing, and audiometric testing; and specific causes of nongenetic sensorineural hearing loss, including congenital and early onset infections, late onset infections, ototoxic drugs and chemicals, hyperbilirubinemia, prematurity and term low birth weight, ear and head trauma, and noise induced hearing loss. The authors stress that comprehensive evaluation of a child with educationally significant hearing impairment is best accomplished by a team of specialists. Rehabilitative advances such as cochlear implants and improved hearing aid technology have improved the prospects for children with marked sensorineural hearing loss (SNHL). 2 figures. 3 tables. 68 references.

•

Risk Factors for Alzheimer's Disease Source: in Jorm, A.F. Understanding Senile Dementia. Kent, England: Croom Helm Ltd. 1987. p. 49-58. Contact: This publication may be available from your local medical library. Call fro information. ISBN: 0412437406 (paperback). Summary: This chapter discusses risk factors for Alzheimer's disease that have been confirmed in at least two or more independent studies. To date, only five such risk factors have been identified: old age; family history of Alzheimer's disease; head

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trauma; Down's syndrome; and family history of Down's syndrome. Evidence supporting and illustrating each of these five risk factors is presented and discussed. The importance of being aware of valid risk factors for preventive measures is emphasized. •

Auditory Processing Disorders Source: in Mencher, G.T.; Gerber, S.E.; McCombe, A. Audiology and Auditory Dysfunction. Needham Heights, MA: Allyn and Bacon. 1997. p. 220-232. Contact: Available from Allyn and Bacon. 160 Gould Street, Needham Heights, MA 02194-2310. (800) 278-3525; Fax (617) 455-7024; E-mail: [email protected]; http://www.abacon.com. PRICE: $46.95 plus shipping and handling. ISBN: 0205161014. Summary: This chapter on auditory processing disorders is from an audiology textbook on auditory dysfunction, a term used to label those kinds of situations in which the patient seems to sense the auditory signal adequately, but is unable to process it. The author discusses pathology and etiology; prelingual disorders, including those relating to auditory discrimination, auditory association, auditory closure, auditory memory, auditory localization, and auditory figure-ground perception; postlingual disorders, including those relating to neoplasms, diseases, vascular events (cerebrovascular accidents or stroke), head trauma, and iatrogenesis (physician or treatment induced); identifying central auditory pathology; and the treatment and management of central processing disorders. A treatment regimen in which other avenues of input are employed and special teaching devices and methods are used is necessary to compensate for the impaired auditory channel. Educational approaches include use of alternate sensory modes (visual versus auditory), drug therapy, reduction of motor activities during communication, limited expectations and educational goals (sometimes in spite of above average intelligence), repetition of messages via recorded programs, and other similar methods. 2 figures.

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Taste and Smell Source: in Jafek, B.W.; Stark, A.K., eds. ENT Secrets: Questions You Will Be Asked On Rounds, In the Clinic, In the OR, On Exams. Philadelphia, PA: Hanley and Belfus. 1996. p. 345-349. Contact: Available from Hanley and Belfus. Medical Publishers, 210 South 13th Street, Philadelphia, PA 19107. (800) 962-1892 or (215) 546-7293. Fax (215) 790-9330. PRICE: $35.95 plus shipping and handling. ISBN: 1560531592. Summary: This chapter on taste and smell is from a book that utilizes a question and answer format to review details of the specialty of otorhinolaryngology (ear, nose and throat, or ENT). Topics discussed include the different types of taste papillae, innervation of taste buds, trigeminal nerves and their role in taste and smell disorders, anosmia (inability to smell) and hyposmia (decreased sensitivity to odorants), dysgeusia (alteration in taste perception), major causes of smell disorders, diseases associated with smell disorders, Kallman's syndrome, major causes of taste disorders, head trauma, diseases associated with taste disorders, burning mouth syndrome (BMS), taste disorders associated with mouthwash use, taste and smell effects of cardiovascular drugs, evaluation of a patient with a potential taste or smell disorder, differentiating between taste and smell disorders, additional laboratory tests that may be indicated, etiologies of sinus disease and upper respiratory infection and how they impact taste and smell, three anatomic categories for loss of olfactory and gustatory sensitivity (transport losses, sensory losses, and neural losses), and role of the psyche in taste and

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smell disorders. The chapter focuses on helping readers acquire the vocabulary required to discuss disorders of smell and taste. 7 references. •

Auditory System and Related Disorders Source: in Gelfand, S.A. Essentials of Audiology. 2nd ed. New York, NY: Thieme Medical Publishers, Inc. 2001. p. 173-218. Contact: Available from Thieme Medical Publishers, Inc. 333 Seventh Avenue, New York, NY 10001. (800) 782-3488. Fax (212) 947-0108. E-mail: [email protected]. PRICE: $49.00 plus shipping and handling. ISBN: 1588900177. Summary: This chapter on the auditory (hearing) system and related disorders is from an undergraduate textbook that deals with audiology and related topics in speech language pathology. The author addresses the nature of various pathologies (problems or diseases), where and when they occur, their major signs and symptoms, how hearing is affected, and the ways they are treated. The author first explains the importance of the case history in diagnosis and patient care. The chapter then covers conductive, sensorineural, and mixed hearing impairments; tinnitus (ringing or buzzing sounds in the ears); congenital and hereditary disorders; maternal infections, including syphilis, toxoplasmosis, rubella, cytomegalovirus (CMV); other influences in the maternal environment; congenital anomalies of the ear, including dysplasia (abnormal development in the anatomical structure); syndromes involving the ear and hearing; acquired disorders, including head trauma; outer ear disorders, including impacted cerumen (earwax), foreign bodies, growths and tumors, and infections; middle ear disorders, including bullus myringitis, tympanosclerosis, perforations of the tympanic membrane (eardrum), otitis media (middle ear infection), and otosclerosis (bone disease); surgery to improve or restore hearing, including otosclerosis surgery, tympanoplasy (repair and reconstruction of the eardrum), and surgery for growths and tumors; cochlear disorders, including noise induced hearing loss (NIHL), Meniere's disease, ototoxicity (chemical damage to the ear), infections, perilymphatic fistulas; retrocochlear disorders; auditory neuropathy; central disorders; sudden hearing loss; presbycusis (hearing loss related to aging); Paget's disease (osteitis deformans, a progressive bone disease); obscure auditory dysfunction; and nonorganic hearing loss. 19 figures. 2 tables. 138 references.

•

Vertigo of Central Origin Source: in Canalis, R.F. and Lambert, P.R., eds. Ear: Comprehensive Otology. Philadelphia, PA: Lippincott Williams and Wilkins. 2000. p. 665-679. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-3030. Fax (301) 223-2300. Website: www.lww.com. PRICE: $179.00 plus shipping and handling. ISBN: 078171558X. Summary: This chapter on vertigo of central origin is from a textbook that offers complete coverage of the field of clinical otology (study of the ear). The book is oriented to serve both the otolaryngology resident as a practical learning tool and the practicing otolaryngologist as an updated reference source of clinical and basic information. Topics include differentiating central and peripheral causes of vertigo; the neurologic complications of ear infections, including epidural abscess and brain abscess; vascular disease, including vertebrobasilar insufficiency, infarction of the brainstem and cerebellum, hemorrhage into the brainstem and cerebellum, and the diagnosis of vascular causes of vertigo; migraine, including the clinical profile, migraine equivalents, and the mechanism of vertigo with migraine; tumors, including tumors of the

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cerebellopontine angle, and brain tumors; brain trauma, including the mechanism of brain injury, brainstem contusion, postconcussion syndrome, and the diagnosis of persistent dizziness after head trauma; cerebellar degeneration syndromes, including alcohol cerebellar degeneration and familial ataxia syndromes; disorders of the cranial vertebral junction, including the mechanism of brain damage, basilar impression, atlantoaxial dislocation, and Chiari malformation; multiple sclerosis; and vertigo and focal seizure disorders. For each disorder, the author discusses diagnosis, diagnostic tests, and treatment options. 3 figures. 2 tables. 74 references. •

Bodily Injuries and Their Effects on the Voice Source: in Sataloff, R.T., ed. Professional Voice: The Science and Art of Clinical Care. 2nd ed. San Diego, CA: Singular Publishing Group, Inc. 1997. p. 355-357. 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: $325.00 plus shipping and handling. ISBN: 1565937287. Summary: This chapter, from a book on the clinical care of the professional voice, discusses bodily injuries and their effects on the voice. Such maladies may affect the voice by altering abdominal support, introducing excess tension, distracting the person through pain, or by other means that throw the vocal mechanism out of balance. The author stresses that recognizing the potential hazard of injuries throughout the body often allows a singer or actor to compensate for them safely, preventing vocal stress and injury. The author discusses anterior neck trauma, posterior neck trauma, head trauma, injury to the supraglottic vocal tract, chest and abdominal injuries, injuries to the lower extremities, and injury to the upper extremities. The author concludes by reiterating that the voice mechanism is extremely sensitive to minor alterations anywhere in the body.

•

Rapid Gastric Emptying Source: in Snape, W.J., ed. Consultations in Gastroenterology. Philadelphia, PA: W.B. Saunders Company. 1996. p. 259-263. Contact: Available from W.B. Saunders Company. Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 545-2522. Fax (800) 874-6418 or (407) 352-3445. PRICE: $125.00. ISBN: 0721646700. Summary: This chapter, from a gastroenterology yearbook, covers rapid gastric emptying. Rapid gastric emptying has been demonstrated in a myriad of medical conditions, and has been a well-recognized problem following gastric surgery. After a section outlining postgastrectomy dumping, the authors consider other causes of rapid gastric emptying and the interplay of gastric emptying and other diseases, including duodenal ulcer disease, gastric ulcers, achalasia, obesity, pancreatic insufficiency, bulimia, portal hypertension, diabetes mellitus, dumping syndrome in children, severe head trauma, thyroid disease, and Zollinger-Ellison syndrome. Treatment of symptomatic rapid gastric emptying remains less than satisfactory. Diet is important. Small, frequent meals without accompanying liquids, and decreased simple carbohydrate ingestion are the basics of therapy directed at diminishing dumping symptoms. Patients with dumping syndrome frequently find that lying down after eating helps with reducing their symptomatology, possibly by reducing gravitational forces that may facilitate gastric emptying. Other treatment options include the use of high-viscosity meals, pectin, alteration of gastrointestinal peptides, medications, and surgery. 46 references. (AA-M).

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Chronic Tinnitus Following Electroconvulsive Therapy Source: in Hazell, J., ed. Proceedings of the Sixth International Tinnitus Seminar. London, England: Tinnitus and Hyperacusis Centre. 1999. p. 243-245. Contact: Available from Tinnitus and Hyperacusis Centre. 32 Devonshire Place, London, W1N 1PE, United Kingdom. Fax 44 + (0) 207 486 2218. E-mail: [email protected]. Website: www.tinnitus.org. PRICE: Contact publisher for price. ISBN: 0953695700. Also available on CD-ROM. Summary: Tinnitus can be caused by almost any pathology involving the auditory system and can also result from head trauma, a variety of medications, and electrical shock, including lightning strikes. This article is from a lengthy document that reprints the proceedings of the Sixth International Tinnitus Seminar, held in Cambridge, United Kingdom, in September 1999 and hosted by the British Society of Audiology. In this article, the authors report a case study of chronic tinnitus that began immediately following electroconvulsive therapy (ECT). A 43 year old female with a 27 year history of obsessive compulsive disorder and major depression had previously been treated with psychotherapy, antidepressant and antipsychotic medications. Because these treatments were minimally effective and because the frequency and duration of her depressive episodes continued to increase, the patient was scheduled to undergo a series of ECT procedures. The patient received four ECT treatments during one week. Stimulating current was delivered through a unilateral electrode to the right frontotemporal region of the head. EEG seizures occurred during each of the ECT procedures. After the patient recovered from anesthesia, she complained of headaches, muscle pain, amnesia, and, after the fourth ECT, she reported a ringing sound in her right ear. Audiometric testing the day after the fourth ECT revealed a slight increase in threshold for 8000 Hz tones in her right ear. The authors conclude that it is likely that current delivered during the fourth ECT treatment triggered the perception of tinnitus for this patient. The unique organization of this patient's central nervous and auditory systems combined with her particular pharmacological history might have predisposed her to developing this symptom.

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CHAPTER 7. MULTIMEDIA ON HEAD TRAUMA Overview In this chapter, we show you how to keep current on multimedia sources of information on head trauma. 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 head trauma is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “head trauma” 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 “head trauma” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on head trauma: •

Understanding the Symptoms and Causes of Dementia Source: Tuscaloosa, AL: Dementia Education and Training Program. 1993. (videocassette). Contact: Alabama Department of Public Health. Bureau of Geriatric Psychology. Dementia Education and Training Program. 200 University Boulevard, Tuscaloosa, AL 35401. (800) 457-5679; (205) 759-0820; FAX (205) 759-0891. PRICE: $15.00. Summary: In this videotape, Dr. Richard Powers gives a basic overview of dementia. The video is one of a series directed to home health nurses. However, it may be useful to a variety of professionals. Among the topics discussed are historical perspectives of dementia, 'hardening of the arteries,' cognitive and psychiatric clinical manifestations, current theories of etiology, and methods of treatment. Also included are descriptions of the risk factors for vascular dementia, syndromes associated with head trauma, and organic mental disorders related to alcohol abuse.

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CHAPTER 8. PERIODICALS AND NEWS ON HEAD TRAUMA Overview In this chapter, we suggest a number of news sources and present various periodicals that cover head trauma.

News Services and Press Releases One of the simplest ways of tracking press releases on head trauma 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 “head trauma” (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 head trauma. 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 “head trauma” (or synonyms). The following was recently listed in this archive for head trauma: •

High-dose mannitol therapy may improve survival of head trauma patients Source: Reuters Industry Breifing Date: September 06, 2002

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Mild head trauma not a major risk factor for dementia or Alzheimer's disease Source: Reuters Medical News Date: January 18, 2000

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Subset of children at low risk of complication from head trauma identified Source: Reuters Medical News Date: January 28, 1999

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Urban Pediatric Head Trauma A Costly Health Burden Source: Reuters Medical News Date: February 09, 1998

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Neurex Halts Enrollment In Trial Of Severe Head Trauma Drug Source: Reuters Medical News Date: July 30, 1997

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Risk Of Dementia High In Parkinson Disease Patients And Low In Epilepsy and Severe Head Trauma Patients Source: Reuters Medical News Date: January 09, 1996 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. 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 “head trauma” (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 “head trauma” (or synonyms). If you know the name of a company that is relevant to head

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trauma, 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 “head trauma” (or synonyms).

Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “head trauma” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on head trauma: •

Introduction to Taste and Smell Dysfunction Source: Renal Nutrition Forum. 20(1): 1, 3-8. Winter 2001. Summary: Sensory and perceptual changes in taste and smell function have long been documented in patients with renal (kidney) failure and the dysfunction is attributed to the renal disease and its sequalae (consequences). These problems can affect the ways patients manage (or fail to manage) appetite and diet, adding to problems of compliance with dietary restrictions, decreasing the enjoyment from foods eaten, and in general decreasing the overall quality of life. This article reviews taste and smell dysfunction in the renal population. The author first describes smell (olfactory) and taste (gustatory) dysfunction when it occurs as the primary disease, in order for readers to better understand these dysfunctions outside the context of kidney disease. Olfactory dysfunction can be caused by head trauma, nasal or sinus disease, or prior upper respiratory infection (a 'cold'); aging also can cause taste or smell problems. Whatever the cause of the olfactory problem, the effects on safety (natural gas, smoke, spoiled food) and nutrition must not be overlooked, especially for the patient with dietary restrictions. Decreased taste sensation (hypogeusia) is less common than olfactory dysfunction, but it does occur. The major causes of taste deficits are taste nerve damage, medications, oral disease, or metabolic conditions. The author then summarizes smell and taste dysfunction associated with renal disease and the possible therapies that may be used to address these problems. The author concludes that even normal taste and smell may be altered by dialysis and other renal disease treatments. For example, salt preferences can be altered by changes in dietary salt, and a recent study found that renal patients have increased salt appetite. Dialysis itself may alter taste perception and preferences; preferences for salt have been reported to change with dialysis, perhaps decreasing immediately after dialysis and increasing 24 hours later. And the complex interactions among tastes, taste and smell stimuli, and even color and odor all determine food flavor and will determine palatability and preferences. 80 references.

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Smell Disorders: Loss of Sense of Smell Can Impair Quality of Life Source: From Your Shoulders Up. 4(1): 2. Winter 1994-95. Contact: Available from American Academy of Otolaryngology-Head and Neck Surgery, Inc. (AAOHNS). One Prince Street, Alexandria, VA 22314. (703) 836-4444. Fax (703) 683-5100. Website: www.ent.org. Summary: This brief article, from a patient education newsletter, discusses smell disorders. Topics covered include the prevalence of smell and taste disorders; the impact of smell disorders on one's quality of life, most notably on taste; aging and how it affects the sense of smell; five categories of olfactory or smell complaints, classified as obstructive nasal or sinus disease, prior upper respiratory infection, head trauma, aging, and unknown. The article concludes with a brief discussion of diagnostic tests that might be used to investigate loss of smell and taste, and treatment options for the different categories.

Academic Periodicals covering Head Trauma Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to head trauma. In addition to these sources, you can search for articles covering head trauma 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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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 Institute10: •

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

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

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

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

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

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

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

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

10

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

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

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

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

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

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

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

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

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

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

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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

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

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

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

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

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

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

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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.11 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:12 •

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

11

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). 12 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 NLM Gateway13 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.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “head trauma” (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 73897 450 922 26 82 75377

HSTAT15 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.16 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.17 Simply search by “head trauma” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

13

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

14

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). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17

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 Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.

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Coffee Break: Tutorials for Biologists18 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.19 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.20 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/.

18 Adapted 19

from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.

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. 20 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 head trauma 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 head trauma. 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 head trauma. 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 “head trauma”:

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Disasters and Emergency Preparedness http://www.nlm.nih.gov/medlineplus/disastersandemergencypreparedness.html Head and Brain Injuries http://www.nlm.nih.gov/medlineplus/headandbraininjuries.html Neck Disorders and Injuries http://www.nlm.nih.gov/medlineplus/neckdisordersandinjuries.html Seniors' Health Issues http://www.nlm.nih.gov/medlineplus/seniorshealthissues.html 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 head trauma. 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 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: •

Alzheimer's Disease: A Status Report Source: New York, NY: American Council on Science and Health. 1990. 31 p. Contact: Available from American Council on Science and Health. 1995 Broadway, 2nd Floor, New York, NY 10023-5860. (212) 362-7044; (FAX) (212) 362-4919. PRICE: $3.85. Summary: This booklet summarizes for the general reader the current state of knowledge on Alzheimer's disease, its prevalence, symptoms, diagnosis, and possible causes. Initial sections provide an overview of the disease, and discuss diagnosis, disease progression, and the loss of nerve cells, damage to neurons, and deficiencies of neurotransmitters that occur in Alzheimer's disease. Research on Alzheimer's disease and current research hypotheses are then reviewed in a discussion that covers abnormal proteins, possible genetic predisposition, the influence of gender, head trauma, insufficient cellular energy, pathologically accelerated aging, infectious agents, lack of neurotransmitters, overstimulation of nerve cells, environmental toxins, defective membranes, and malnutrition. A glossary and a list of recommended readings are included.

•

Hearing and Hearing Loss: How the Ear Functions and Possible Causes of Hearing Loss Source: Naperville, IL: Phonak, Inc. 1998. [6 p.].

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Contact: Available from Phonak, Inc. P.O. Box 3017, Naperville, IL 60566. (800) 777-7333 or (708) 505-7007. Fax (630) 505-2830. E-mail: [email protected]. PRICE: Single copy free. Summary: This booklet, one in a series describing the role of hearing in one's quality of life, reviews the anatomy and physiology (including function) of the ears and the hearing system. Topics include the parts of the outer, middle, and inner ear, and what each part does; the possible causes of hearing loss arising in each part of the ear; and the impact of hearing loss on speech perception. Typical problems in the middle ear include perforation of the eardrum, infection (otitis media) and otosclerosis (a calcification around the stapes, limiting its ability to move). Many outer and middle ear problems can be treated medically or surgically. When this is not possible, a remaining conductive hearing loss can be assisted by using hearing aids. The vast majority of hearing losses are a result of damage to the inner ear structures. Typical problems include the natural aging process (the most frequent cause of hearing loss), excessive exposure to noise, intake of medication which is toxic to the auditory system, head trauma, and hereditary factors. In these cases, the tiny hair cells in the cochlea are damaged, usually permanently. This damage cannot be corrected medically but most of sensorineural hearing losses can be alleviated by the use of hearing instruments. 6 figures. •

Selecting Hearing Aids That Are Right for You Source: McLean, VA: American Academy of Audiology. 2001. [4 p.]. Contact: Available from American Academy of Audiology. 8300 Greensboro Drive, Suite 750, McLean, VA 22102-3611. (800) 222-2336 or (703) 790-8466. Fax (703) 790-8631. Website: www.audiology.org. PRICE: $40.00 for 100 for members; $50.00 for 100 for non-members, plus shipping and handling. Summary: This brochure helps readers obtain appropriate hearing aids. The brochure reminds readers that hearing loss is not only associated with aging, but can also occur from exposures to loud noise, from illness and infections, from head trauma, birth defects, certain drugs, or even the mumps or measles. Hearing aids can provide a substantial benefit to users in both quiet and noisy situations, and add much to improve the quality of life for persons with hearing loss. The brochure describes the professional role and training of the audiologist, emphasizing that the majority of hearing aids are dispensed by licensed audiologists. The brochure includes full color pictures of four types of hearing aids: behind the ear (BTE), in the ear (ITE), in the canal (ITC), and completely in the canal (CIC). The brochure explains recent advances in hearing aid technology and the differences between conventional hearing aids, programmable hearing aids, and digital hearing aids. The brochures emphasizes that the hearing aid selection process begins with a comprehensive diagnostic hearing assessment, followed by a hearing aid evaluation. The back side of the brochure reprints the pre purchase assessment guideline for amplification devices, as outlined by the American Academy of Audiology. 2 figures.

•

Genetics of Alzheimer's Disease and Related Risk Factors Source: Houston, TX: Baylor College of Medicine Alzheimer's Disease Research Center. 200X. 4 p. Contact: Available from Baylor College of Medicine Alzheimer's Disease Research Center. 6550 Fannin Street, Smith Tower, #1801, Houston, TX 77030. (713) 798-6660; FAX: (713) 798-5326. Internet: http://www.bcm.tmc.edu/neurol/struct/adrc/adrc1.html. PRICE: Free.

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Summary: This document discusses genetic causes of Alzheimer's disease (AD) and related risk factors. It is designed to address questions relatives may have about the inheritability of AD. Research has so far identified two distinct forms of AD: Early Onset Familial AD (FAD) and Sporadic AD. Early onset FAD refers to the form of the disease known to be caused by specific genetic mutations. Early Onset FAD is rare, accounting for less than five percent of all AD cases. Late onset FAD has been linked to inheriting a risk factor rather than an AD gene. The presence of the E4 type of apolipoprotein E appears to increase the risk of AD but is not a definitive cause. Other risk factors for AD include aging, family history, head trauma, educational experiences, and environmental factors. The report concludes with a discussion of the ethical issues involved in genetic testing. •

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.

•

Perilymph Fistula Source: Portland, OR: Vestibular Disorders Association. 1991. 2 p. Contact: Available from Vestibular Disorders Association (VEDA). P.O. Box 4467, Portland, OR 97208-4467. (503) 229-7705. Fax (503) 229-8064. E-mail: [email protected]. Website: www.vestibular.org. PRICE: $0.50 plus shipping and handling. Order number F-3. Summary: This fact sheet from the Vestibular Disorders Association presents information on perilymph fistulas. Topics covered include the anatomy of the ear; the symptoms of perilymph fistula; the causes of these fistulas, notably head trauma; diagnostic tests used to confirm a fistula; treatment options, including bed rest and surgical repair; coping with dizziness; and changes to make in the home environment while coping with a perilymph fistula. The fact sheet concludes with a reminder that learning to cope with an illness that causes persistent dizziness takes time and patience.

•

Benign Paroxysmal Positional Vertigo Source: Portland, OR: Vestibular Disorders Association (VEDA). 1997. 4 p. Contact: Available from Vestibular Disorders Association (VEDA). P.O. Box 4467, Portland, OR 97208-4467. (503) 229-7705. Fax (503) 229-8064. E-mail: [email protected]. Website: www.vestibular.org. PRICE: $0.50 per copy. Order number R-5. Summary: This fact sheet provides detailed information on benign paroxysmal positional vertigo (BPPV), which causes dizziness due to debris that has collected within

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a part of the inner ear. Topics covered include the symptoms of BPPV; the causes of BPPV, including head trauma, viral infection, and Meniere's disease; diagnostic considerations; the office treatment of BPPV, including the Semont maneuver and the Elpey maneuver; post-procedure instructions for patients; home treatment using BrandtDaroff exercises, including a recommended schedule; the surgical treatment of BPPV; and the impact of BPPV on one's daily life. The fact sheet lists physicians in various regions of the U.S. (as well as one in Canada and two in France) who are known for treating BPPV. 2 figures. 11 references. •

Impact of Aphasia on Patients and Family: Results of a Needs Survey Source: New York, NY: National Aphasia Association. 199x. 4 p. Contact: National Aphasia Association. Distribution Center, 351 Butternut Court, Millersville, MD 21108. (800) 922-4622; http://www.aphasia.org. PRICE: $0.50 each. Summary: This fact sheet provides general information about aphasia and its impact on patients and family. Aphasia is a speech and language disorder that can result from a stroke, head trauma, or other neurological condition. All people with aphasia experience some degree of difficulty talking and comprehending spoken language. Many with aphasia have problems reading, writing, and calculating. The fact sheet answers common questions about the impact of aphasia on the patient and family. Topics include the prevalence of the condition, the causes and outcome of aphasia, common emotional responses to having aphasia, ways to alleviate the isolation for both patient and family members, how to get information that is helpful but not too technical, and the role of the National Aphasia Association. (AA-M).

•

Vocal Cord Paralysis Source: Bethesda, MD: National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health (NIH). June 1999. [3 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 99-4306. Summary: Vocal cord paralysis is a voice disorder that occurs when one or both of the vocal cords (vocal folds) do not open or close properly. Vocal cord paralysis is a common disorder, and symptoms can range from mild to life threatening. This fact sheet describes vocal cord paralysis and its management. Written in a question and answer format, the fact sheet covers the physiology and anatomy of the vocal cords; the causes of vocal cord paralysis, including head trauma, stroke, neck injury, lung or thyroid cancer, or viral infections; the symptoms of vocal cord paralysis; diagnostic tests used to determine the presence of paralysis; treatment options, including voice therapy and surgery; and research studies that are being conducted on vocal cord paralysis. The fact sheet concludes with a list of resource organizations through which readers can obtain additional information. 1 figure. 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

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in some way to head trauma. 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

Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to head trauma. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with head trauma. 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 head trauma. 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. 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.

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To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “head trauma” (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 “head trauma”. 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 “head trauma” (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 “head trauma” (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.21

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

21

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)22: •

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)

•

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

•

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

•

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

•

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

•

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

•

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/

•

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/

22

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

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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/

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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html

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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

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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330

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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)

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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html

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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/

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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/

Finding Medical Libraries

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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/

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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm

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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm

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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/

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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html

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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/

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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html

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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/

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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm

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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp

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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/

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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/

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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml

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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html

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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html

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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml

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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp

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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm

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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/

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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp

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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/

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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/

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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72

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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

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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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HEAD TRAUMA DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Injuries: General or unspecified injuries involving organs in the abdominal cavity. [NIH] Abducens: A striated, extrinsic muscle of the eyeball that originates from the annulus of Zinn. [NIH] Abducens Nerve: The 6th cranial nerve. The abducens nerve originates in the abducens nucleus of the pons and sends motor fibers to the lateral rectus muscles of the eye. Damage to the nerve or its nucleus disrupts horizontal eye movement control. [NIH] Abscess: A localized, circumscribed collection of pus. [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] Accommodation: Adjustment, especially that of the eye for various distances. [EU] 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] Acidity: The quality of being acid or sour; containing acid (hydrogen ions). [EU] Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [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]

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Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] 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] 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 synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] 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] 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] Air Embolism: Occurs when the lungs over expand to the point that air bubbles are forced through the air sacs of the lungs into the circulatory system. [NIH] Air Sacs: Thin-walled sacs or spaces which function as a part of the respiratory system in birds, fishes, insects, and mammals. [NIH] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Akathisia: 1. A condition of motor restlessness in which there is a feeling of muscular quivering, an urge to move about constantly, and an inability to sit still, a common extrapyramidal side effect of neuroleptic drugs. 2. An inability to sit down because of intense anxiety at the thought of doing so. [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

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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] Alfentanil: A short-acting opioid anesthetic and analgesic derivative of fentanyl. It produces an early peak analgesic effect and fast recovery of consciousness. Alfentanil is effective as an anesthetic during surgery, for supplementation of analgesia during surgical procedures, and as an analgesic for critically ill patients. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] 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] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergic Rhinitis: Inflammation of the nasal mucous membrane associated with hay fever; fits may be provoked by substances in the working environment. [NIH] Allogeneic: Taken from different individuals of the same species. [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] Alternative medicine: Practices not generally recognized by the medical community as 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] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amnesia: Lack or loss of memory; inability to remember past experiences. [EU] 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] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH]

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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] Amyloid beta-Protein: A 4 kD protein, 39-43 amino acids long, expressed by a gene located on chromosome 21. It is the major protein subunit of the vascular and plaque amyloid filaments in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (Down syndrome). The protein is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue. [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] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] 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 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] Anaplastic: A term used to describe cancer cells that divide rapidly and bear little or no resemblance to normal cells. [NIH] Anaplastic large cell lymphoma: A rare agressive form of lymphoma (cancer that begins in cells of the lymphatic system) that is usually of T-cell origin. [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] Angiography: Radiography of blood vessels after injection of a contrast medium. [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]

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Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Anomalies: Birth defects; abnormalities. [NIH] Anosmia: Absence of the sense of smell; called also anosphrasia and olfactory anaesthesia. [EU]

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] Antecedent: Existing or occurring before in time or order often with consequential effects. [EU]

Anterograde: Moving or extending forward; called also antegrade. [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 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] Anticonvulsive: An agent that prevents or relieves convulsions. [NIH] Antidiuretic: Suppressing the rate of urine formation. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]

Antiepileptic: An agent that combats epilepsy. [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-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [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] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also

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neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antispasmodic: An agent that relieves spasm. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Aorta: The main trunk of the systemic arteries. [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] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [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] Aqueous: Having to do with water. [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] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Aspartate: A synthetic amino acid. [NIH]

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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] Atherectomy: Endovascular procedure in which atheromatous plaque is excised by a cutting or rotating catheter. It differs from balloon and laser angioplasty procedures which enlarge vessels by dilation but frequently do not remove much plaque. If the plaque is removed by surgical excision under general anesthesia rather than by an endovascular procedure through a catheter, it is called endarterectomy. [NIH] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] 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] Atropine: A toxic alkaloid, originally from Atropa belladonna, but found in other plants, mainly Solanaceae. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Audiologist: Study of hearing including treatment of persons with hearing defects. [NIH] Audiology: The study of hearing and hearing impairment. [NIH] Auditory: Pertaining to the sense of hearing. [EU] Auditory Perception: The process whereby auditory stimuli are selected, organized and interpreted by the organism; includes speech discrimination. [NIH] Aura: A subjective sensation or motor phenomenon that precedes and marks the of a paroxysmal attack, such as an epileptic attack on set. [EU] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] 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

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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] Autopsy: Postmortem examination of the body. [NIH] Autoradiography: A process in which radioactive material within an object produces an image when it is in close proximity to a radiation sensitive emulsion. [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] 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] Basal cells: Small, round cells found in the lower part (or base) of the epidermis, the outer layer of the skin. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Basilar Artery: The artery formed by the union of the right and left vertebral arteries; it runs from the lower to the upper border of the pons, where it bifurcates into the two posterior cerebral arteries. [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]

Beta-pleated: Particular three-dimensional pattern of amyloidoses. [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 composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [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]

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Biological Sciences: All of the divisions of the natural sciences dealing with the various aspects of the phenomena of life and vital processes. The concept includes anatomy and physiology, biochemistry and biophysics, and the biology of animals, plants, and microorganisms. It should be differentiated from biology, one of its subdivisions, concerned specifically with the origin and life processes of living organisms. [NIH] Biological Transport: The movement of materials (including biochemical substances and drugs) across cell membranes and epithelial layers, usually by passive diffusion. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biomechanics: The study of the application of mechanical laws and the action of forces to living structures. [NIH] Biophysics: The science of physical phenomena and processes in living organisms. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [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] 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 Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [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-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 Fluids: Liquid components of living organisms. [NIH] Bone Conduction: Sound transmission through the bones of the skull to the inner ear. [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]

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Bone metastases: Cancer that has spread from the original (primary) tumor to the bone. [NIH]

Bone Resorption: Bone loss due to osteoclastic activity. [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] 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] Brain Stem Infarctions: Infarctions that occur in the brain stem which is comprised of the midbrain, pons, and medulla. There are several named syndromes characterized by their distinctive clinical manifestations and specific sites of ischemic injury. [NIH] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Burning Mouth Syndrome: A group of painful oral symptoms associated with a burning or similar sensation. There is usually a significant organic component with a degree of functional overlay; it is not limited to the psychophysiologic group of disorders. [NIH]

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Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Cachexia: General ill health, malnutrition, and weight loss, usually associated with chronic disease. [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] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [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 channel blocker: A drug used to relax the blood vessel and heart muscle, causing pressure inside blood vessels to drop. It also can regulate heart rhythm. [NIH] Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cell membranes or on the release and binding of calcium in intracellular pools. Since they are inducers of vascular and other smooth muscle relaxation, they are used in the drug therapy of hypertension and cerebrovascular spasms, as myocardial protective agents, and in the relaxation of uterine spasms. [NIH] Calcium Channels: Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue. [NIH] Calcium Signaling: Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins. [NIH]

Cannula: A tube for insertion into a duct or cavity; during insertion its lumen is usually occupied by a trocar. [EU] Capsular: Cataract which is initiated by an opacification at the surface of the lens. [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]

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Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] 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] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] 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 Bypass: Diversion of the flow of blood from the entrance of the right atrium directly to the aorta (or femoral artery) via an oxygenator thus bypassing both 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 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] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carotid Arteries: Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery. [NIH] Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship

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of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group. [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] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [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] 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 Adhesion: Adherence of cells to surfaces or to other 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 Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] 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] 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] Cerebellar Diseases: Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, gait ataxia, and muscle hypotonia. [NIH] Cerebellopontine: Going from the cerebellum (the part of the brain responsible for coordinating movement) to the pons (part of the central nervous system located near the base of the brain.) [NIH] Cerebellopontine Angle: Junction between the cerebellum and the pons. [NIH]

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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] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Arteries: The arteries supplying the cerebral cortex. [NIH] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [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] 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] Cerebrovascular Circulation: The circulation of blood through the vessels of the brain. [NIH] 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] Cerumen: The yellow or brown waxy secretions produced by vestigial apocrine sweat glands in the external ear canal. [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] Chemical Warfare: Tactical warfare using incendiary mixtures, smokes, or irritant, burning, or asphyxiating gases. [NIH] Chemical Warfare Agents: Chemicals that are used to cause the disturbance, disease, or death of humans during war. [NIH] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] 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] Child Welfare: Organized efforts by communities or organizations to improve the health and well-being of the child. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for

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the passage of blood vessels and a nerve. [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] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Choline: A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chorda Tympani Nerve: A branch of the facial (7th cranial) nerve which passes through the middle ear and continues through the petrotympanic fissure. The chorda tympani nerve carries taste sensation from the anterior two-thirds of the tongue and conveys parasympathetic efferents to the salivary glands. [NIH] Chorea: Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as choreatic disorders. Chorea is also a frequent manifestation of basal ganglia diseases. [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] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [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] Cirrhosis: A type of chronic, progressive liver disease. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Clear cell carcinoma: A rare type of tumor of the female genital tract in which the inside of the cells looks clear when viewed under a microscope. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient.

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[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] Clot Retraction: Retraction of a clot resulting from contraction of platelet pseudopods attached to fibrin strands that is dependent on the contractile protein thrombosthenin. Used as a measure of platelet function. [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] Cochlea: The part of the internal ear that is concerned with hearing. It forms the anterior part of the labyrinth, is conical, and is placed almost horizontally anterior to the vestibule. [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] Cochlear Implants: Electronic devices implanted beneath the skin with electrodes to the cochlear nerve to create sound sensation in persons with sensorineural deafness. [NIH] Cochlear Nerve: The cochlear part of the 8th cranial nerve (vestibulocochlear nerve). The cochlear nerve fibers originate from neurons of the spiral ganglion and project peripherally to cochlear hair cells and centrally to the cochlear nuclei (cochlear nucleus) of the brain stem. They mediate the sense of 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] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] 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] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [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.

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Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Concomitant: Accompanying; accessory; joined with another. [EU] Conduction: The transfer of sound waves, heat, nervous impulses, or electricity. [EU] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [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] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constriction: The act of constricting. [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] Contrast medium: A substance that is introduced into or around a structure and, because of the difference in absorption of x-rays by the contrast medium and the surrounding tissues, allows radiographic visualization of the structure. [EU] 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] Convulsive: Relating or referring to spasm; affected with spasm; characterized by a spasm or spasms. [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 Arteriosclerosis: Thickening and loss of elasticity of the coronary arteries. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a

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myocardial infarction. [NIH] Corpus: The body of the uterus. [NIH] Corpus Callosum: Broad plate of dense myelinated fibers that reciprocally interconnect regions of the cortex in all lobes with corresponding regions of the opposite hemisphere. The corpus callosum is located deep in the longitudinal fissure. [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] Cranial Sutures: A type of fibrous joint between bones of the head. [NIH] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial 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] Cribriform: Pierced with small holes as in a sieve. Refers to the appearance of a tumor when viewed under a microscope. The tumor appears to have open spaces or small holes inside. [NIH]

Criterion: A standard by which something may be judged. [EU] Critical Care: Health care provided to a critically ill patient during a medical emergency or crisis. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [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] Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis. [NIH] Cyst: A sac or capsule filled with fluid. [NIH] Cytogenetics: A branch of genetics which deals with the cytological and molecular behavior of genes and chromosomes during cell division. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [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] Cytotoxic: Cell-killing. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decontamination: The removal of contaminating material, such as radioactive materials,

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biological materials, or chemical warfare agents, from a person or object. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delirium: (DSM III-R) an acute, reversible organic mental disorder characterized by reduced ability to maintain attention to external stimuli and disorganized thinking as manifested by rambling, irrelevant, or incoherent speech; there are also a reduced level of consciousness, sensory misperceptions, disturbance of the sleep-wakefulness cycle and level of psychomotor activity, disorientation to time, place, or person, and memory impairment. Delirium may be caused by a large number of conditions resulting in derangement of cerebral metabolism, including systemic infection, poisoning, drug intoxication or withdrawal, seizures or head trauma, and metabolic disturbances such as hypoxia, hypoglycaemia, fluid, electrolyte, or acid-base imbalances, or hepatic or renal failure. Called also acute confusional state and acute brain syndrome. [EU] Delusions: A false belief regarding the self or persons or objects outside the self that persists despite the facts, and is not considered tenable by one's associates. [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 is usually progressive, and initially spares the level of consciousness. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] 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] Dentists: Individuals licensed to practice dentistry. [NIH] Deprenyl: Substance that blocks the breakdown of dopamine, thus preserving its availability in the striatum. [NIH] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Dermatitis: Any inflammation of the skin. [NIH] DES: Diethylstilbestrol. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [NIH] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Diabetes Insipidus: A metabolic disorder due to disorders in the production or release of vasopressin. It is characterized by the chronic excretion of large amounts of low specific

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gravity urine and great thirst. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Ketoacidosis: Complication of diabetes resulting from severe insulin deficiency coupled with an absolute or relative increase in glucagon concentration. The metabolic acidosis is caused by the breakdown of adipose stores and resulting increased levels of free fatty acids. Glucagon accelerates the oxidation of the free fatty acids producing excess ketone bodies (ketosis). [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diastolic: Of or pertaining to the diastole. [EU] 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] Digestion: The process of breakdown of food for metabolism and use by the body. [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] Dihydroergotamine: A derivative of ergotamine prepared by the catalytic hydrogenation of ergotamine. It is used as a vasoconstrictor, specifically for the therapy of migraine. [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] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrimination: The act of qualitative and/or quantitative differentiation between two or more stimuli. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Dislocation: The displacement of any part, more especially of a bone. Called also luxation. [EU]

Disposition: A tendency either physical or mental toward certain diseases. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is

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roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [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] Dominance: In genetics, the full phenotypic expression of a gene in both heterozygotes and homozygotes. [EU] 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] Double-blind: Pertaining to a clinical trial or other experiment in which neither the subject nor the person administering treatment knows which treatment any particular subject is receiving. [EU] Doxycycline: A synthetic tetracycline derivative with a range of antimicrobial activity and mode of action similar to that of tetracycline, but more effective against many species. Animal studies suggest that it may cause less tooth staining than other tetracyclines. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Drug Toxicity: Manifestations of the adverse effects of drugs administered therapeutically or in the course of diagnostic techniques. It does not include accidental or intentional poisoning for which specific headings are available. [NIH] Duct: A tube through which body fluids pass. [NIH] Dumping Syndrome: Gastrointestinal nonfunctioning pylorus. [NIH]

symptoms

resulting

from

an

absent

or

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Duodenal Ulcer: An ulcer in the lining of the first part of the small intestine (duodenum). [NIH]

Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] 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] Dysgeusia: A condition characterized by alterations of the sense of taste which may range from mild to severe, including gross distortions of taste quality. [NIH] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dysphoric: A feeling of unpleasantness and discomfort. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Eardrum: A thin, tense membrane forming the greater part of the outer wall of the tympanic cavity and separating it from the external auditory meatus; it constitutes the boundary between the external and middle ear. [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] Efficacy: The extent to which a specific intervention, procedure, regimen, or service 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] Electroconvulsive Therapy: Electrically induced convulsions primarily used in the treatment of severe affective disorders and schizophrenia. [NIH] Electrode: Component of the pacing system which is at the distal end of the lead. It is the interface with living cardiac tissue across which the stimulus is transmitted. [NIH] Electroencephalography: Recording of electric currents developed in the brain by means of electrodes applied to the scalp, to the surface of the brain, or placed within the substance of the brain. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electromagnetic Fields: Fields representing the joint interplay of electric and magnetic forces. [NIH] 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]

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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] Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH] Emboli: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embolization: The blocking of an artery by a clot or foreign material. Embolization can be done as treatment to block the flow of blood to a tumor. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryology: The study of the development of an organism during the embryonic and fetal stages of life. [NIH] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] 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] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endarterectomy: Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called atherectomy. [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] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH] Endorphins: One of the three major groups of endogenous opioid peptides. They are large peptides derived from the pro-opiomelanocortin precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; opioid peptides is used

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for the broader group. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Enkephalins: One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla. [NIH] Enteral Nutrition: Nutritional support given via the alimentary canal or any route connected to the gastrointestinal system (i.e., the enteral route). This includes oral feeding, sip feeding, and tube feeding using nasogastric, gastrostomy, and jejunostomy tubes. [NIH] Entorhinal Cortex: Cortex where the signals are combined with those from other sensory systems. [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] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiological: Relating to, or involving epidemiology. [EU] Epidural: The space between the wall of the spinal canal and the covering of the spinal cord. An epidural injection is given into this space. [NIH] Epidural Space: Space between the dura mater and the walls of the vertebral canal. [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] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH]

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Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Ergotamine: A vasoconstrictor found in ergot of Central Europe. It is an alpha-1 selective adrenergic agonist and is commonly used in the treatment of migraine headaches. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [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] Ethmoid: An unpaired cranial bone which helps form the medial walls of the orbits and contains the themoidal air cells which drain into the nose. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evacuation: An emptying, as of the bowels. [EU] 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] Excitability: Property of a cardiac cell whereby, when the cell is depolarized to a critical level (called threshold), the membrane becomes permeable and a regenerative inward current causes an action potential. [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] Excitotoxicity: Excessive exposure to glutamate or related compounds can kill brain neurons, presumably by overstimulating them. [NIH] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [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]

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Extrapyramidal: Outside of the pyramidal tracts. [EU] Facial: Of or pertaining to the face. [EU] Facial Nerve: The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and salivary glands, and convey afferent information for taste from the anterior two-thirds of the tongue and for touch from the external ear. [NIH] Facial Nerve Diseases: Diseases of the facial nerve or nuclei. Pontine disorders may affect the facial nuclei or nerve fascicle. The nerve may be involved intracranially, along its course through the petrous portion of the temporal bone, or along its extracranial course. Clinical manifestations include facial muscle weakness, loss of taste from the anterior tongue, hyperacusis, and decreased lacrimation. [NIH] 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] Febrile: Pertaining to or characterized by fever. [EU] Femoral: Pertaining to the femur, or to the thigh. [EU] Femoral Artery: The main artery of the thigh, a continuation of the external iliac artery. [NIH] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fentanyl: A narcotic opioid drug that is used in the treatment of pain. [NIH] Fetal Alcohol Syndrome: A disorder occurring in children born to alcoholic women who continue to drink heavily during pregnancy. Common abnormalities are growth deficiency (prenatal and postnatal), altered morphogenesis, mental deficiency, and characteristic facies - small eyes and flattened nasal bridge. Fine motor dysfunction and tremulousness are observed in the newborn. [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] Fibula: The bone of the lower leg lateral to and smaller than the tibia. In proportion to its length, it is the most slender of the long bones. [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] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flatus: Gas passed through the rectum. [NIH] Fluid Therapy: Therapy whose basic objective is to restore the volume and composition of

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the body fluids to normal with respect to water-electrolyte balance. Fluids may be administered intravenously, orally, by intermittent gavage, or by hypodermoclysis. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fossa: A cavity, depression, or pit. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Frontal Lobe: The anterior part of the cerebral hemisphere. [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] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] 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] Gastric: Having to do with the stomach. [NIH] Gastric Emptying: The evacuation of food from the stomach into the duodenum. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas). [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gastrostomy: Creation of an artificial external opening into the stomach for nutritional support or gastrointestinal compression. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes

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are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]

Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Targeting: The integration of exogenous DNA into the genome of an organism at sites where its expression can be suitably controlled. This integration occurs as a result of homologous recombination. [NIH] Genetic Counseling: Advising families of the risks involved pertaining to birth defects, in order that they may make an informed decision on current or future pregnancies. [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 Markers: A phenotypically recognizable genetic trait which can be used to identify a genetic locus, a linkage group, or a recombination event. [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] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Geriatric: Pertaining to the treatment of the aged. [EU] 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] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]

Glomerular Filtration Rate: The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to inulin clearance. [NIH] Glomeruli: Plural of glomerulus. [NIH] Glossopharyngeal Nerve: The 9th cranial nerve. The glossopharyngeal nerve is a mixed motor and sensory nerve; it conveys somatic and autonomic efferents as well as general, special, and visceral afferents. Among the connections are motor fibers to the stylopharyngeus muscle, parasympathetic fibers to the parotid glands, general and taste afferents from the posterior third of the tongue, the nasopharynx, and the palate, and afferents from baroreceptors and chemoreceptors of the carotid sinus. [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] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH]

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Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]

Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [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] 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] Grafting: The operation of transfer of tissue from one site to another. [NIH] Granule: A small pill made from sucrose. [EU] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Haematoma: A localized collection of blood, usually clotted, in an organ, space, or tissue, due to a break in the wall of a blood vessel. [EU] Haemorrhage: The escape of blood from the vessels; bleeding. Small haemorrhages are classified according to size as petechiae (very small), purpura (up to 1 cm), and ecchymoses (larger). The massive accumulation of blood within a tissue is called a haematoma. [EU] 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] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Hay Fever: A seasonal variety of allergic rhinitis, marked by acute conjunctivitis with lacrimation and itching, regarded as an allergic condition triggered by specific allergens. [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

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disease process are referred to as headache disorders (e.g., migraine). [NIH] Headache Disorders: Common conditions characterized by persistent or recurrent headaches. Headache syndrome classification systems may be based on etiology (e.g., vascular headache, post-traumatic headaches, etc.), temporal pattern (e.g., cluster headache, paroxysmal hemicrania, etc.), and precipitating factors (e.g., cough headache). [NIH] Health Care Reform: Innovation and improvement of the health care system by reappraisal, amendment of services, and removal of faults and abuses in providing and distributing health services to patients. It includes a re-alignment of health services and health insurance to maximum demographic elements (the unemployed, indigent, uninsured, elderly, inner cities, rural areas) with reference to coverage, hospitalization, pricing and cost containment, insurers' and employers' costs, pre-existing medical conditions, prescribed drugs, equipment, and services. [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [NIH] Hearing aid: A miniature, portable sound amplifier for persons with impaired hearing, consisting of a microphone, audio amplifier, earphone, and battery. [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] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Hemiparesis: The weakness or paralysis affecting one side of the body. [NIH] Hemodynamics: The movements of the blood and the forces involved in systemic or regional blood circulation. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]

Hepatic: Refers to the liver. [NIH] Hepatic Encephalopathy: A condition that may cause loss of consciousness and coma. It is usually the result of advanced liver disease. Also called hepatic coma. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes simplex or to herpes zoster. [EU] Herpes Zoster: Acute vesicular inflammation. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]

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Heterozygotes: Having unlike alleles at one or more corresponding loci on homologous chromosomes. [NIH] Hibernation: The dormant state in which some animal species pass the winter. It is characterized by narcosis and by sharp reduction in body temperature and metabolic activity and by a depression of vital signs. It is a natural physiological process in many warm-blooded animals. [NIH] 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] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Histones: Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each. [NIH] 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] Homozygotes: An individual having a homozygous gene pair. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [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] Horseradish Peroxidase: An enzyme isolated from horseradish which is able to act as an antigen. It is frequently used as a histochemical tracer for light and electron microscopy. Its antigenicity has permitted its use as a combined antigen and marker in experimental immunology. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] 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]

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Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, 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] Hydrogenation: Specific method of reduction in which hydrogen is added to a substance by the direct use of gaseous hydrogen. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [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] Hypnotic: A drug that acts to induce sleep. [EU] Hypoglossal Nerve: The 12th cranial nerve. The hypoglossal nerve originates in the hypoglossal nucleus of the medulla and supplies motor innervation to all of the muscles of the tongue except the palatoglossus (which is supplied by the vagus). This nerve also contains proprioceptive afferents from the tongue muscles. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypotension: Abnormally low blood pressure. [NIH] 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] Hypothyroidism: Deficiency of thyroid activity. In adults, it is most common in women and is characterized by decrease in basal metabolic rate, tiredness and lethargy, sensitivity to cold, and menstrual disturbances. If untreated, it progresses to full-blown myxoedema. In infants, severe hypothyroidism leads to cretinism. In juveniles, the manifestations are intermediate, with less severe mental and developmental retardation and only mild symptoms of the adult form. When due to pituitary deficiency of thyrotropin secretion it is called secondary hypothyroidism. [EU] 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] Hypoxic: Having too little oxygen. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Illusion: A false interpretation of a genuine percept. [NIH] Imaging procedures: Methods of producing pictures of areas inside the body. [NIH]

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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]

Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunoglobulins: Glycoproteins present in the blood (antibodies) and in other tissue. They are classified by structure and activity into five classes (IgA, IgD, IgE, IgG, IgM). [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunology: The study of the body's immune system. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] 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] Incus: One of three ossicles of the middle ear. It conducts sound vibrations from the malleus to the stapes. [NIH] 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] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infantile: Pertaining to an infant or to infancy. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an 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]

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]

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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] Inner ear: The labyrinth, comprising the vestibule, cochlea, and semicircular canals. [NIH] Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH] Inotropic: Affecting the force or energy of muscular contractions. [EU] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Intensive Care: Advanced and highly specialized care provided to medical or surgical patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [NIH]

Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [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-12: A heterodimeric cytokine that stimulates the production of interferon gamma from T-cells and natural killer cells, and also induces differentiation of Th1 helper cells. It is an initiator of cell-mediated immunity. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which

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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] Intermediate Filaments: Cytoplasmic filaments intermediate in diameter (about 10 nanometers) between the microfilaments and the microtubules. They may be composed of any of a number of different proteins and form a ring around the cell nucleus. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Interneurons: Most generally any neurons which are not motor or sensory. Interneurons may also refer to neurons whose axons remain within a particular brain region as contrasted with projection neurons which have axons projecting to other brain regions. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestines: The section of the alimentary canal from the stomach to the anus. It includes the large intestine and small intestine. [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 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] Intralaminar Thalamic Nuclei: Cell groups within the internal medullary lamina of the thalamus. They include a rostral division comprising the paracentral, central lateral, central dorsal, and central medial nuclei, and a caudal division composed of the centromedian and parafascicular nuclei. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]

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] 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] Ipsilateral: Having to do with the same side of the body. [NIH] Iris: The most anterior portion of the uveal layer, separating the anterior chamber from the posterior. It consists of two layers - the stroma and the pigmented epithelium. Color of the iris depends on the amount of melanin in the stroma on reflection from the pigmented

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epithelium. [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] Isozymes: The multiple forms of a single enzyme. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]

Jejunostomy: Surgical formation of an opening through the abdominal wall into the jejunum, usually for enteral hyperalimentation. [NIH] 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] Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Ketonuria: Having ketone bodies in the urine; a warning sign of diabetic ketoacidosis (DKA). [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kinetics: The study of rate dynamics in chemical or physical systems. [NIH] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Labyrinth: The internal ear; the essential part of the organ of hearing. It consists of an osseous and a membranous portion. [NIH] Language Disorders: Conditions characterized by deficiencies of comprehension or expression of written and spoken forms of language. These include acquired and developmental disorders. [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

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secondarily as the organ of voice. [NIH] Latency: The period of apparent inactivity between the time when a stimulus is presented and the moment a response occurs. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukoencephalopathy: A condition with spongy holes in the brain's white matter. [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] Ligaments: Shiny, flexible bands of fibrous tissue connecting together articular extremities of bones. They are pliant, tough, and inextensile. [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] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]

Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH]

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Lobe: A portion of an organ such as the liver, lung, breast, or brain. [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] Lod: The lowest analyte content which, if actually present, will be detected with reasonable statistical certainty and can be identified according to the identification criteria of the method. If both accuracy and precision are constant over a concentration range. [NIH] Lod Score: The total relative probability, expressed on a logarithmic scale, that a linkage relationship exists among selected loci. Lod is an acronym for "logarithmic odds." [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] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Luxation: The displacement of the particular surface of a bone from its normal joint, without fracture. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] 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] Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Macroglia: A type of neuroglia composed of astrocytes. [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]

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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] Malformation: A morphologic developmental process. [EU]

defect

resulting

from

an

intrinsically

abnormal

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]

Mammogram: An x-ray of the breast. [NIH] Mania: Excitement of psychotic proportions manifested by mental and physical hyperactivity, disorganization of behaviour, and elevation of mood. [EU] Manic: Affected with mania. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mannitol: A diuretic and renal diagnostic aid related to sorbitol. It has little significant energy value as it is largely eliminated from the body before any metabolism can take place. It can be used to treat oliguria associated with kidney failure or other manifestations of inadequate renal function and has been used for determination of glomerular filtration rate. Mannitol is also commonly used as a research tool in cell biological studies, usually to control osmolarity. [NIH] Mastication: The act and process of chewing and grinding food in the mouth. [NIH] Maxillary: Pertaining to the maxilla : the irregularly shaped bone that with its fellow forms the upper jaw. [EU] Maxillary Nerve: The intermediate sensory division of the trigeminal (5th cranial) nerve. The maxillary nerve carries general afferents from the intermediate region of the face including the lower eyelid, nose and upper lip, the maxillary teeth, and parts of the dura. [NIH]

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] Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] 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] 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] Meningioma: A type of tumor that occurs in the meninges, the membranes that cover and protect the brain and spinal cord. Meningiomas usually grow slowly. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental deficiency: A condition of arrested or incomplete development of mind from inherent causes or induced by disease or injury. [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 Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH]

Mesolimbic: Inner brain region governing emotion and drives. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [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] 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] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcalcifications: Tiny deposits of calcium in the breast that cannot be felt but can be detected on a mammogram. A cluster of these very small specks of calcium may indicate that cancer is present. [NIH] Microdialysis: A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane. [NIH] Microglia: The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling. [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] Microtubule-Associated Proteins: High molecular weight proteins found in the microtubules of the cytoskeletal system. Under certain conditions they are required for tubulin assembly into the microtubules and stabilize the assembled microtubules. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [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] Miotic: 1. Pertaining to, characterized by, or producing miosis : contraction of the pupil. 2. An agent that causes the pupil to contract. 3. Meiotic: characterized by cell division. [EU] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [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] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH]

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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] Monoamine: Enzyme that breaks down dopamine in the astrocytes and microglia. [NIH] Monoamine Oxidase: An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4. [NIH] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH] Mononuclear: A cell with one nucleus. [NIH] Monotherapy: A therapy which uses only one drug. [EU] 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] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Motor Activity: The physical activity of an organism as a behavioral phenomenon. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multiple Trauma: Physical insults or injuries occurring simultaneously in several parts of the body. [NIH] Multivariate Analysis: A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH]

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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] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of 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] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myristate: Pharmacological activator of protein kinase C. [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] Nasal Cavity: The proximal portion of the respiratory passages on either side of the nasal septum, lined with ciliated mucosa, extending from the nares to the pharynx. [NIH] Nasal Septum: The partition separating the two nasal cavities in the midplane, composed of cartilaginous, membranous and bony parts. [NIH] Nasogastric: The process of passing a small, flexible plastic tube through the nose or mouth into the stomach or small intestine. [NIH] Natural killer cells: NK cells. A type of white blood cell that contains granules with enzymes that can kill tumor cells or microbial cells. Also called large granular lymphocytes (LGL). [NIH] 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] 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 swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Neocortex: The largest portion of the cerebral cortex. It is composed of neurons arranged in six layers. [NIH] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] 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] Nephropathy: Disease of the kidneys. [EU] 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]

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Nerve Growth Factor: Nerve growth factor is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [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] Neurites: In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell. [NIH] 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]

Neuroblastoma: Cancer that arises in immature nerve cells and affects mostly infants and children. [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] Neuroectodermal tumor: A tumor of the central or peripheral nervous system. [NIH] Neurofibrillary Tangles: Abnormal structures located in various parts of the brain and composed of dense arrays of paired helical filaments (neurofilaments and microtubules). These double helical stacks of transverse subunits are twisted into left-handed ribbon-like filaments that likely incorporate the following proteins: (1) the intermediate filaments: medium- and high-molecular-weight neurofilaments; (2) the microtubule-associated proteins map-2 and tau; (3) actin; and (4) ubiquitin. As one of the hallmarks of Alzheimer disease, the neurofibrillary tangles eventually occupy the whole of the cytoplasm in certain classes of cell in the neocortex, hippocampus, brain stem, and diencephalon. The number of these tangles, as seen in post mortem histology, correlates with the degree of dementia during life. Some studies suggest that tangle antigens leak into the systemic circulation both in the course of normal aging and in cases of Alzheimer disease. [NIH] Neurofilaments: Bundle of neuronal fibers. [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] Neuroleptic: A term coined to refer to the effects on cognition and behaviour of antipsychotic drugs, which produce a state of apathy, lack of initiative, and limited range of emotion and in psychotic patients cause a reduction in confusion and agitation and normalization of psychomotor activity. [EU] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU]

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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] Neuronal Plasticity: The capacity of the nervous system to change its reactivity as the result of successive activations. [NIH] 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] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropeptides: Peptides released by neurons as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells. [NIH] Neurophysiology: The scientific discipline concerned with the physiology of the nervous system. [NIH] Neuropsychology: A branch of psychology which investigates the correlation between experience or behavior and the basic neurophysiological processes. The term neuropsychology stresses the dominant role of the nervous system. It is a more narrowly defined field than physiological psychology or psychophysiology. [NIH] Neurosurgical Procedures: Surgery performed on the nervous system or its parts. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotoxins: Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept. [NIH] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neurotrophins: A nerve growth factor. [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] Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH] Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [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

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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] Nuclear Medicine: A specialty field of radiology concerned with diagnostic, therapeutic, and investigative use of radioactive compounds in a pharmaceutical form. [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] Nucleosomes: The repeating structural units of chromatin, each consisting of approximately 200 base pairs of DNA wound around a protein core. This core is composed of the histones H2A, H2B, H3, and H4. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nursing Research: Research carried out by nurses, generally in clinical settings, in the areas of clinical practice, evaluation, nursing education, nursing administration, and methodology. [NIH] Nutritional Support: The administration of nutrients for assimilation and utilization by a patient by means other than normal eating. It does not include fluid therapy which normalizes body fluids to restore water-electrolyte balance. [NIH] Occipital Lobe: Posterior part of the cerebral hemisphere. [NIH] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Olfaction: Function of the olfactory apparatus to perceive and discriminate between the molecules that reach it, in gas form from an external environment, directly or indirectly via the nose. [NIH] Olfaction Disorders: Loss of or impaired ability to smell. This may be caused by olfactory nerve diseases; paranasal sinus diseases; viral respiratory tract infections; craniocerebral trauma; smoking; and other conditions. [NIH] Olfactory Bulb: Ovoid body resting on the cribriform plate of the ethmoid bone where the olfactory nerve terminates. The olfactory bulb contains several types of nerve cells including the mitral cells, on whose dendrites the olfactory nerve synapses, forming the olfactory glomeruli. The accessory olfactory bulb, which receives the projection from the vomeronasal organ via the vomeronasal nerve, is also included here. [NIH] Olfactory Nerve: The 1st cranial nerve. The olfactory nerve conveys the sense of smell. It is formed by the axons of olfactory receptor neurons which project from the olfactory

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epithelium (in the nasal epithelium) to the olfactory bulb. [NIH] Olfactory Receptor Neurons: Neurons in the olfactory epithelium with proteins (receptors, odorant) that bind, and thus detect, odorants. Olfactory receptor neurons are bipolar. They send to the surface of the epithelium apical dendrites with non-motile cilia from which project odorant receptor molecules. Their unmyelinated axons synapse in the olfactory bulb of the brain. Unlike other neurons, they can be generated from precursor cells in adults. [NIH]

Oligo: Chemical and mineral elements that exist in minimal (oligo) quantities in the body, in foods, in the air, in soil; name applied to any element observed as a microconstituent of plant or animal tissue and of beneficial, harmful, or even doubtful significance. [NIH] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Ophthalmic: Pertaining to the eye. [EU] Ophthalmoplegia: Paralysis of one or more of the ocular muscles due to disorders of the eye muscles, neuromuscular junction, supporting soft tissue, tendons, or innervation to the muscles. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [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] Optic Nerve Diseases: Conditions which produce injury or dysfunction of the second cranial or optic nerve, which is generally considered a component of the central nervous system. Damage to optic nerve fibers may occur at or near their origin in the retina, at the optic disk, or in the nerve, optic chiasm, optic tract, or lateral geniculate nuclei. Clinical manifestations may include decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Orthostatic: Pertaining to or caused by standing erect. [EU] Osmolarity: The concentration of osmotically active particles expressed in terms of osmoles of solute per litre of solution. [EU] Osmoles: The standard unit of osmotic pressure. [NIH] Ossicles: The hammer, anvil and stirrup, the small bones of the middle ear, which transmit the vibrations from the tympanic membrane to the oval window. [NIH]

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Osteitis Deformans: A disease marked by repeated episodes of increased bone resorption followed by excessive attempts at repair, resulting in weakened, deformed bones of increased mass. The resultant architecture of the bone assumes a mosaic pattern in which the fibers take on a haphazard pattern instead of the normal parallel symmetry. [NIH] Otitis: Inflammation of the ear, which may be marked by pain, fever, abnormalities of hearing, hearing loss, tinnitus, and vertigo. [EU] Otitis Media: Inflammation of the middle ear. [NIH] Otolaryngology: A surgical specialty concerned with the study and treatment of disorders of the ear, nose, and throat. [NIH] Otology: The branch of medicine which deals with the diagnosis and treatment of the disorders and diseases of the ear. [NIH] Otorhinolaryngology: That branch of medicine concerned with medical and surgical treatment of the head and neck, including the ears, nose and throat. [EU] Otosclerosis: The formation of spongy bone in the labyrinth capsule. The ossicles can become fixed and unable to transmit sound vibrations, thereby causing deafness. [NIH] Ototoxic: Having a deleterious effect upon the eighth nerve, or upon the organs of hearing and balance. [EU] Outer ear: The pinna and external meatus of the ear. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [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] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [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]

Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] 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] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU]

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Oxygenator: An apparatus by which oxygen is introduced into the blood during circulation outside the body, as during open heart surgery. [NIH] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Paediatric: Of or relating to the care and medical treatment of children; belonging to or concerned with paediatrics. [EU] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate and the posterior soft palate. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Palsy: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] 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] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic Insufficiency: Absence of or reduced pancreatic exocrine secretion into the duodenum and resultant poor digestion of lipids, vitamins, nitrogen, and carbohydrates. [NIH]

Papilledema: Swelling around the optic disk. [NIH] Paradoxical: Occurring at variance with the normal rule. [EU] Paralysis: Loss of ability to move all or part of the body. [NIH] Paresthesia: Subjective cutaneous sensations (e.g., cold, warmth, tingling, pressure, etc.) that are experienced spontaneously in the absence of stimulation. [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] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Particle: A tiny mass of material. [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]

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Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penicillin: An antibiotic drug used to treat infection. [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] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] 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 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] Perilymph: The fluid contained within the space separating the membranous from the osseous labyrinth of the ear. [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 blood: Blood circulating throughout the body. [NIH] 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] Perivascular: Situated around a vessel. [EU] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [NIH] Petechiae: Pinpoint, unraised, round red spots under the skin caused by bleeding. [NIH] Petrolatum: A colloidal system of semisolid hydrocarbons obtained from petroleum. It is used as an ointment base, topical protectant, and lubricant. [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] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [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

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of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It promotes binding to inhibitory GABA subtype receptors, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations. [NIH] Phenolphthalein: An acid-base indicator which is colorless in acid solution, but turns pink to red as the solution becomes alkaline. It is used medicinally as a cathartic. [NIH] Phenotypes: An organism as observed, i. e. as judged by its visually perceptible characters resulting from the interaction of its genotype with the environment. [NIH] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phenytoin: An anticonvulsant that is used in a wide variety of seizures. It is also an antiarrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs. [NIH] Phorbol: Class of chemicals that promotes the development of tumors. [NIH] Phorbol Esters: Tumor-promoting compounds obtained from croton oil (Croton tiglium). Some of these are used in cell biological experiments as activators of protein kinase C. [NIH] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [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] Phosphorylates: Attached to a phosphate group. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] 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]

Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH]

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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] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [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] Plasmids: Any extrachromosomal hereditary determinant. Plasmids are self-replicating circular molecules of DNA that are found in a variety of bacterial, archaeal, fungal, algal, and plant species. [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] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pneumocephalus: Presence of air or gas within the intracranial cavity (e.g., epidural space, subdural space, intracerebral, etc.) which may result from traumatic injuries, fistulous tract formation, erosions of the skull from neoplasms or infection, neurosurgical procedures, and other conditions. [NIH] Pneumonia: Inflammation of the lungs. [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] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] 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

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ventralis. [NIH] Port: An implanted device through which blood may be withdrawn and drugs may be infused without repeated needle sticks. Also called a port-a-cath. [NIH] Port-a-cath: An implanted device through which blood may be withdrawn and drugs may be infused without repeated needle sticks. Also called a port. [NIH] Portal Hypertension: High blood pressure in the portal vein. This vein carries blood into the liver. Portal hypertension is caused by a blood clot. This is a common complication of cirrhosis. [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] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-traumatic: Occurring as a result of or after injury. [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] Practice Guidelines: Directions or principles presenting current or future rules of policy for 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] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Premedication: Preliminary administration of a drug preceding a diagnostic, therapeutic, or surgical procedure. The commonest types of premedication are antibiotics (antibiotic prophylaxis) and anti-anxiety agents. It does not include preanesthetic medication. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Presbycusis: Progressive bilateral loss of hearing that occurs in the aged. Syn: senile deafness. [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] Prion: Small proteinaceous infectious particles that resist inactivation by procedures modifying nucleic acids and contain an abnormal isoform of a cellular protein which is a

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major and necessary component. [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] 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] 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] Promoter: A chemical substance that increases the activity of a carcinogenic process. [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] Prophylaxis: An attempt to prevent disease. [NIH] Propofol: A widely used anesthetic. [NIH] 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] Prostaglandins: A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes. [NIH] 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] Prostaglandins D: Physiologically active prostaglandins found in many tissues and organs. They show pressor activity, are mediators of inflammation, and have potential antithrombotic effects. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH] Protective Agents: Synthetic or natural substances which are given to prevent a disease or

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disorder or are used in the process of treating a disease or injury due to a poisonous agent. [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 Kinase C: An enzyme that phosphorylates proteins on serine or threonine residues in the presence of physiological concentrations of calcium and membrane phospholipids. The additional presence of diacylglycerols markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by phorbol esters and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters. EC 2.7.1.-. [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] 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] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] 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] Protozoan: 1. Any individual of the protozoa; protozoon. 2. Of or pertaining to the protozoa; protozoal. [EU] Pseudotumor Cerebri: A condition marked by raised intracranial pressure and characterized clinically by headaches; nausea; papilledema, peripheral constriction of the visual fields, transient visual obscurations, and pulsatile tinnitus. Obesity is frequently associated with this condition, which primarily affects women between 20 and 44 years of age. Chronic papilledema may lead to optic nerve injury (optic nerve diseases) and visual loss (blindness). [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] 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]

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Psychophysiology: The study of the physiological basis of human and animal behavior. [NIH]

Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Psychotherapy: A generic term for the treatment of mental illness or emotional disturbances primarily by verbal or nonverbal communication. [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] 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]

Pupil: The aperture in the iris through which light passes. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Pylorus: The opening in a vertebrate from the stomach into the intestine. [EU] 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] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and uracil) and form the basic structure of the barbiturates. [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] Quaternary: 1. Fourth in order. 2. Containing four elements or groups. [EU] Quiescent: Marked by a state of inactivity or repose. [EU] 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]

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Racemic: Optically inactive but resolvable in the way of all racemic compounds. [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] 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] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radionuclide Imaging: Process whereby a radionuclide is injected or measured (through tissue) from an external source, and a display is obtained from any one of several rectilinear scanner or gamma camera systems. The image obtained from a moving detector is called a scan, while the image obtained from a stationary camera device is called a scintiphotograph. [NIH]

Radiopharmaceuticals: Drugs containing a radioactive substance that are used in the diagnosis and treatment of cancer and in pain management of bone metastases. Also called radioactive drugs. [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] 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] Reality Testing: The individual's objective evaluation of the external world and the ability to differentiate adequately between it and the internal world; considered to be a primary ego function. [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] Receptors, Odorant: Proteins, usually projecting from the cilia of olfactory receptor neurons, that specifically bind odorant molecules and trigger responses in the neurons. The large number of different odorant receptors appears to arise from several gene families or subfamilies rather than from DNA rearrangement. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [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] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] 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]

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Recur: To occur again. Recurrence is the return of cancer, at the same site as the original (primary) tumor or in another location, after the tumor had disappeared. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [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] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [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] 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 Ganglion Cells: Cells of the innermost nuclear layer of the retina, the ganglion cell layer, which project axons through the optic nerve to the brain. They are quite variable in size and in the shapes of their dendritic arbors, which are generally confined to the inner plexiform layer. [NIH] Retinal Hemorrhage: Bleeding from the vessels of the retina. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH]

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Retraction: 1. The act of drawing back; the condition of being drawn back. 2. Distal movement of teeth, usually accomplished with an orthodontic appliance. [EU] Retractor: An instrument designed for pulling aside tissues to improve exposure at operation; an instrument for drawing back the edge of a wound. [NIH] Retrocochlear: Hearing loss in which the air conduction threshold and the bone conduction threshold have risen almost equally with no gap between them. In such cases the defect is usually either in the cochlea of the inner ear or in the central pathways. [NIH] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU] Rheumatoid: Resembling rheumatism. [EU] Rhinorrhea: The free discharge of a thin nasal mucus. [EU] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Risk patient: Patient who is at risk, because of his/her behaviour or because of the type of person he/she is. [EU] Rod: A reception for vision, located in the retina. [NIH] Rubella: An acute, usually benign, infectious disease caused by a togavirus and most often affecting children and nonimmune young adults, in which the virus enters the respiratory tract via droplet nuclei and spreads to the lymphatic system. It is characterized by a slight cold, sore throat, and fever, followed by enlargement of the postauricular, suboccipital, and cervical lymph nodes, and the appearances of a fine pink rash that begins on the head and spreads to become generalized. Called also German measles, roetln, röteln, and three-day measles, and rubeola in French and Spanish. [EU] Saline: A solution of salt and water. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] 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] Satellite: Applied to a vein which closely accompanies an artery for some distance; in cytogenetics, a chromosomal agent separated by a secondary constriction from the main body of the chromosome. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a

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person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Scopolamine: An alkaloid from Solanaceae, especially Datura metel L. and Scopola carniolica. Scopolamine and its quaternary derivatives act as antimuscarinics like atropine, but may have more central nervous system effects. Among the many uses are as an anesthetic premedication, in urinary incontinence, in motion sickness, as an antispasmodic, and as a mydriatic and cycloplegic. [NIH] Screening: Checking for disease when there are no symptoms. [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] 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] Semicircular canal: Three long canals of the bony labyrinth of the ear, forming loops and opening into the vestibule by five openings. [NIH] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Senile Plaques: Spherical masses consisting of amyloid fibrils and neuronal processes. [NIH] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH] Sensory loss: A disease of the nerves whereby the myelin or insulating sheath of myelin on the nerves does not stay intact and the messages from the brain to the muscles through the nerves are not carried properly. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] 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] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino

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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] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [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]

Shunt: A surgically created diversion of fluid (e.g., blood or cerebrospinal fluid) from one area of the body to another area of the body. [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] Sigmoid: 1. Shaped like the letter S or the letter C. 2. The sigmoid colon. [EU] Sigmoid Colon: The lower part of the colon that empties into the rectum. [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] Skull Base: The inferior region of the skull consisting of an internal (cerebral), and an external (basilar) surface. [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 Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] 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] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [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]

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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] Sorbitol: A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications. [NIH] 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] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] 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] Speech Perception: The process whereby an utterance is decoded into a representation in terms of linguistic units (sequences of phonetic segments which combine to form lexical and grammatical morphemes). [NIH] Sperm: The fecundating fluid of the male. [NIH] 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 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] Spirochete: Lyme disease. [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] Stapes: One of the three ossicles of the middle ear. It transmits sound vibrations from the incus to the internal ear. [NIH]

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Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be expected to happen by chance alone. [NIH] Status Epilepticus: Repeated and prolonged epileptic seizures without recovery of consciousness between attacks. [NIH] Steady state: Dynamic equilibrium. [EU] 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 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] 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] Streptomycin: O-2-Deoxy-2-(methylamino)-alpha-L-glucopyranosyl-(1-2)-O-5- deoxy-3-Cformyl-alpha-L-lyxofuranosyl-(1-4)-N,N'-bis(aminoiminomethyl)-D-streptamine. Antibiotic substance produced by the soil actinomycete Streptomyces griseus. It acts by inhibiting the initiation and elongation processes during protein synthesis. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Striatum: A higher brain's domain thus called because of its stripes. [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] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [EU] Subclavian: The direct continuation of the axillary vein at the lateral border of the first rib. It passes medially to join the internal jugular vein and form the brachiocephalic vein on each side. [NIH] Subclavian Artery: Artery arising from the brachiocephalic trunk on the right side and from the arch of the aorta on the left side. It distributes to the neck, thoracic wall, spinal cord, brain, meninges, and upper limb. [NIH] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other

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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] Sufentanil: An opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent. [NIH] 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] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppressive: Tending to suppress : effecting suppression; specifically : serving to suppress activity, function, symptoms. [EU] Supratentorial: Located in the upper part of the brain. [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] Sweat Glands: Sweat-producing structures that are embedded in the dermis. Each gland consists of a single tube, a coiled body, and a superficial duct. [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] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [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

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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] Syncope: A temporary suspension of consciousness due to generalized cerebral schemia, a faint or swoon. [EU] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]

Systemic: Affecting the entire body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Talus: The second largest of the tarsal bones and occupies the middle and upper part of the tarsus. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late in appearing. [EU] Taste Buds: Small sensory organs which contain gustatory receptor cells, basal cells, and supporting cells. Taste buds in humans are found in the epithelia of the tongue, palate, and pharynx. They are innervated by the chorda tympani nerve (a branch of the facial nerve) and the glossopharyngeal nerve. [NIH] Taste Disorders: Conditions characterized by an alteration in gustatory function or perception. Taste disorders are frequently associated with olfaction disorders. Additional potential etiologies include metabolic diseases; drug toxicity; and taste pathway disorders (e.g., taste bud diseases; facial nerve diseases; glossopharyngeal nerve diseases; and brain stem diseases). [NIH] Taurine: 2-Aminoethanesulfonic acid. A conditionally essential nutrient, important during mammalian development. It is present in milk but is isolated mostly from ox bile and strongly conjugates bile acids. [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] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Tetrodotoxin: Octahydro-12-(hydroxymethyl)-2-imino-5,9:7,10a-dimethano10aH(1,3)dioxocino(6,5-a)pyrimidine-4,7,10,11,12-pentol. An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order Tetradontiformes (pufferfish, globefish, toadfish), which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of

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neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalamic Nuclei: Several groups of nuclei in the thalamus that serve as the major relay centers for sensory impulses in the brain. [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]

Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [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] Thrombosis: The formation or presence of a blood clot inside a blood vessel. [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] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [NIH] Tibia: The second longest bone of the skeleton. It is located on the medial side of the lower leg, articulating with the fibula laterally, the talus distally, and the femur proximally. [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] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts plasminogen to plasmin. It has fibrin-binding activity and is immunologically different from urinary plasminogen activator. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases. EC 3.4.21.68. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired

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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] 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] Torsion: A twisting or rotation of a bodily part or member on its axis. [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] 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] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Tracer: A substance (such as a radioisotope) used in imaging procedures. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Tracheostomy: Surgical formation of an opening into the trachea through the neck, or the opening so created. [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] Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]

Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [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]

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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] Triage: The sorting out and classification of patients or casualties to determine priority of need and proper place of treatment. [NIH] Trigeminal: Cranial nerve V. It is sensory for the eyeball, the conjunctiva, the eyebrow, the skin of face and scalp, the teeth, the mucous membranes in the mouth and nose, and is motor to the muscles of mastication. [NIH] Trigeminal Nerve: The 5th and largest cranial nerve. The trigeminal nerve is a mixed motor and sensory nerve. The larger sensory part forms the ophthalmic, mandibular, and maxillary nerves which carry afferents sensitive to external or internal stimuli from the skin, muscles, and joints of the face and mouth and from the teeth. Most of these fibers originate from cells of the trigeminal ganglion and project to the trigeminal nucleus of the brain stem. The smaller motor part arises from the brain stem trigeminal motor nucleus and innervates the muscles of mastication. [NIH] Trigger zone: Dolorogenic zone (= producing or causing pain). [EU] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Trisomy: The possession of a third chromosome of any one type in an otherwise diploid cell. [NIH]

Trophic: Of or pertaining to nutrition. [EU] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for 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] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [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] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]

Tunica Intima: The innermost coat of blood vessels, consisting of a thin lining of endothelial cells longitudinally oriented and continuous with the endothelium of capillaries on the one hand and the endocardium of the heart on the other. [NIH] Tympanic membrane: A thin, tense membrane forming the greater part of the outer wall of the tympanic cavity and separating it from the external auditory meatus; it constitutes the boundary between the external and middle ear. [NIH] Tyramine: An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine

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oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems. [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] Ubiquitin: A highly conserved 76 amino acid-protein found in all eukaryotic cells. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Plasminogen Activator: A proteolytic enzyme that converts plasminogen to plasmin where the preferential cleavage is between arginine and valine. It was isolated originally from human urine, but is found in most tissues of most vertebrates. EC 3.4.21.73. [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] 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] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi, protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [NIH]

Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Valves: Flap-like structures that control the direction of blood flow through the heart. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasodilator: An agent that widens blood vessels. [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 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] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling

Dictionary 219

prey or predator. [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] Ventriculostomy: Surgical creation of an opening in a cerebral ventricle. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertebral: Of or pertaining to a vertebra. [EU] Vertebral Artery: The first branch of the subclavian artery with distribution to muscles of the neck, vertebrae, spinal cord, cerebellum and interior of the cerebrum. [NIH] Vertebrobasilar Insufficiency: Localized or diffuse reduction in blood flow through the vertebrobasilar arterial system, which supplies the brain stem; cerebellum; occipital lobe; medial temporal lobe; and thalamus. Characteristic clinical features include syncope; lightheadedness; visual disturbances; and vertigo. brain stem infarctions or other brain infarction may be associated. [NIH] Vertigo: An illusion of movement; a sensation as if the external world were revolving around the patient (objective vertigo) or as if he himself were revolving in space (subjective vertigo). The term is sometimes erroneously used to mean any form of dizziness. [EU] 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] Vestibule: A small, oval, bony chamber of the labyrinth. The vestibule contains the utricle and saccule, organs which are part of the balancing apparatus of the ear. [NIH] 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

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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] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [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] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Visual field: The entire area that can be seen when the eye is forward, including peripheral vision. [NIH] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [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] Vocal cord: The vocal folds of the larynx. [NIH] Vomeronasal Organ: A specialized part of the olfactory system located anteriorly in the nasal cavity within the nasal septum. Chemosensitive cells of the vomeronasal organ project via the vomeronasal nerve to the accessory olfactory bulb. The primary function of this organ appears to be in sensing pheromones which regulate reproductive and other social behaviors. While the structure has been thought absent in higher primate adults, data now suggests it may be present in adult humans. [NIH] Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] 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]

221

INDEX A Abdominal, 116, 149, 185, 198 Abdominal Injuries, 116, 149 Abducens, 42, 79, 149 Abducens Nerve, 79, 149 Abscess, 56, 115, 149 Acceptor, 149, 186, 197 Accommodation, 78, 149 Acetylcholine, 149, 163, 194 Acidity, 149, 199 Acquired Immunodeficiency Syndrome, 110, 149 Actin, 149, 193 Action Potentials, 37, 149 Activities of Daily Living, 48, 78, 149 Adaptability, 149, 161 Adaptation, 13, 149, 201 Adenine, 150, 205 Adenosine, 28, 150, 159, 200 Adjustment, 14, 21, 149, 150 Adrenal Cortex, 150, 167, 203 Adrenal Medulla, 150, 161, 173, 194 Adrenergic, 150, 154, 170, 173, 174, 213, 217 Adverse Effect, 16, 29, 150, 170, 200, 210 Aerobic, 150, 190 Affinity, 34, 150, 155, 193, 210 Agonist, 8, 150, 170, 174, 194, 200 Air Embolism, 82, 150 Air Sacs, 150 Airway, 50, 77, 150 Akathisia, 150, 154 Albumin, 150, 201 Alertness, 151, 159 Alfentanil, 78, 151 Algorithms, 151, 157 Alimentary, 151, 173, 184 Alkaline, 151, 159, 200 Alkaloid, 151, 155, 164, 194, 209 Alleles, 21, 151, 180 Allergic Rhinitis, 112, 151, 178 Allogeneic, 151, 178 Alpha Particles, 151, 206 Alternative medicine, 122, 151 Ameliorating, 14, 151 Amnesia, 117, 151 Amnestic, 46, 151, 189 Amphetamines, 151, 164

Amplification, 135, 151 Amygdala, 10, 18, 152, 156, 186, 214 Amyloid, 9, 38, 44, 110, 152, 209 Amyloid beta-Protein, 110, 152 Anaesthesia, 77, 152, 153, 182 Anal, 17, 152, 191 Analgesic, 151, 152, 213 Analogous, 24, 25, 152, 216 Anaphylatoxins, 152, 165 Anaplasia, 152, 192 Anaplastic, 71, 152 Anaplastic large cell lymphoma, 71, 152 Anatomical, 16, 23, 82, 112, 115, 152, 155, 162, 182, 190, 209 Anemia, 152, 188 Anesthesia, 56, 117, 150, 152, 155, 172, 213 Anesthetics, 30, 152, 173 Aneurysm, 50, 152 Angiography, 112, 152 Animal model, 10, 28, 38, 152 Anions, 150, 153, 184, 213 Anomalies, 115, 153 Anosmia, 4, 110, 112, 114, 153 Anoxia, 99, 153 Antagonism, 9, 153, 159 Antecedent, 17, 22, 153 Anterograde, 22, 153 Antibiotic, 153, 167, 199, 202, 211, 212, 214 Antibodies, 153, 178, 180, 182, 187 Antibody, 150, 153, 165, 173, 178, 180, 182, 189, 211 Anticonvulsant, 104, 153, 159, 200 Anticonvulsive, 104, 153 Antidiuretic, 61, 153 Antiemetic, 153, 154 Antiepileptic, 9, 153 Antigen, 150, 153, 165, 173, 180, 182, 189, 190 Antigen-Antibody Complex, 153, 165 Anti-infective, 153, 181 Anti-inflammatory, 23, 35, 96, 153 Antimicrobial, 153, 170 Antioxidant, 9, 153, 197 Antipsychotic, 117, 153, 193 Antispasmodic, 154, 209 Anus, 152, 154, 184 Aorta, 97, 98, 103, 154, 160, 212, 219 Aphasia, 71, 137, 151, 154

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Apolipoproteins, 154, 186 Apoptosis, 7, 9, 10, 12, 33, 38, 102, 154, 161 Aqueous, 154, 167, 172, 181, 186 Arachidonic Acid, 154, 203 Arterial, 14, 154, 158, 163, 181, 204, 214, 219 Arteries, 119, 154, 156, 157, 160, 162, 166, 185, 187, 190, 192 Arterioles, 154, 157, 192 Arteriovenous, 22, 51, 154 Artery, 46, 68, 98, 152, 154, 156, 160, 166, 172, 175, 184, 185, 190, 205, 208, 212 Aseptic, 154, 196 Aspartate, 12, 30, 34, 40, 154 Assay, 11, 96, 155, 182 Astrocytes, 8, 23, 36, 155, 177, 187, 190, 191, 193 Asymptomatic, 69, 155 Ataxia, 116, 155, 161, 180, 214 Atherectomy, 155, 172 Atrium, 155, 160, 219 Atrophy, 27, 155, 193 Atropine, 155, 209 Attenuated, 102, 155, 218 Attenuation, 23, 155 Audiologist, 135, 155 Audiology, 3, 43, 59, 114, 115, 117, 135, 155 Auditory, 15, 43, 46, 71, 114, 115, 117, 135, 155, 171, 174, 178, 179, 188, 217 Auditory Perception, 71, 155 Aura, 57, 155 Autoimmune disease, 155, 191 Autonomic, 149, 154, 155, 177, 194, 199 Autonomic Nervous System, 155, 199 Autopsy, 35, 156 Autoradiography, 28, 156 Axonal, 22, 27, 51, 156 Axons, 156, 168, 169, 184, 195, 196, 205, 207 B Bacteria, 153, 156, 172, 190, 206, 209, 211, 216, 218 Bacterial Physiology, 149, 156 Bactericidal, 156, 174 Bacteriophage, 156, 201, 216 Basal cells, 156, 214 Basal Ganglia, 154, 155, 156, 158, 163, 176, 186 Basal Ganglia Diseases, 155, 156, 163 Basilar Artery, 64, 156, 188 Bed Rest, 136, 156

Benign, 44, 89, 136, 156, 158, 176, 178, 192, 208 Beta-pleated, 152, 156 Bilateral, 45, 113, 156, 202 Bile, 156, 176, 180, 185, 186, 212, 214 Bile Acids, 156, 212, 214 Bile duct, 156 Biliary, 61, 156 Bilirubin, 150, 156, 181 Biochemical, 15, 21, 27, 34, 38, 39, 45, 101, 151, 156, 157, 209 Biological Sciences, 33, 37, 157 Biological Transport, 157, 169 Biomarkers, 11, 157 Biomechanics, 63, 157 Biophysics, 30, 157 Biopsy, 157, 199 Biosynthesis, 23, 154, 157, 203, 209 Biotechnology, 40, 41, 122, 129, 157 Bladder, 157, 165, 182, 191, 203, 218 Blood Coagulation, 157, 159 Blood Platelets, 157, 210 Blood pressure, 21, 157, 160, 162, 181, 191, 202, 210 Blood-Brain Barrier, 11, 96, 157, 186 Body Fluids, 157, 159, 170, 176, 195, 210, 217 Bone Conduction, 157, 208 Bone Marrow, 39, 157, 187, 191, 212 Bone metastases, 158, 206 Bone Resorption, 158, 197 Bowel, 97, 152, 158, 169 Bradykinin, 158, 201 Brain Diseases, 20, 158 Brain Hypoxia, 158, 215 Brain Infarction, 158, 219 Brain Injuries, 13, 18, 41, 134, 158 Brain Ischemia, 102, 103, 105, 106, 158 Brain Neoplasms, 158, 180, 215 Brain Stem, 56, 158, 162, 164, 193, 214, 217, 219 Brain Stem Infarctions, 158, 219 Breeding, 38, 158 Buccal, 158, 187 Bulimia, 116, 158 Burning Mouth Syndrome, 114, 158 Bypass, 19, 98, 159 C Cachexia, 97, 159 Caffeine, 35, 159, 205 Calcification, 135, 159

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Calcium, 16, 18, 21, 37, 50, 101, 159, 165, 190, 204 Calcium channel blocker, 101, 159 Calcium Channel Blockers, 101, 159 Calcium Channels, 101, 159 Calcium Signaling, 38, 159 Cannula, 97, 98, 103, 159 Capsular, 25, 159 Carbamazepine, 9, 159 Carbohydrate, 116, 160 Carbon Dioxide, 160, 176, 207 Carcinogenic, 160, 183, 203, 212 Carcinogens, 160, 197 Cardiac, 7, 19, 24, 33, 98, 103, 159, 160, 171, 173, 174, 179, 192, 212 Cardiac arrest, 7, 33, 160 Cardiopulmonary, 48, 52, 98, 103, 160 Cardiopulmonary Bypass, 98, 103, 160 Cardiopulmonary Resuscitation, 48, 52, 160 Cardiovascular, 97, 114, 159, 160, 210 Cardiovascular disease, 97, 160 Cardiovascular System, 97, 160 Carotene, 160, 207 Carotid Arteries, 98, 160 Carrier Proteins, 160, 201 Case report, 47, 51, 56, 58, 67, 69, 74, 80, 82, 90, 160, 164 Case-Control Studies, 35, 160 Caspase, 12, 13, 161 Catecholamine, 18, 161, 170, 199 Catheter, 97, 98, 103, 155, 161, 172 Cations, 161, 184 Caudal, 161, 169, 181, 184, 202 Cause of Death, 15, 96, 161 Cell Adhesion, 106, 161 Cell Cycle, 9, 161, 218 Cell Death, 6, 7, 8, 9, 10, 12, 13, 18, 21, 27, 28, 33, 34, 40, 101, 102, 154, 161, 192 Cell Division, 156, 161, 167, 178, 189, 190, 201, 203 Cell membrane, 157, 159, 160, 161, 176, 200 Cell Respiration, 161, 190, 207 Cell Transplantation, 39, 161 Central Nervous System Infections, 161, 178, 180 Cerebellar, 46, 47, 116, 155, 161, 207, 217 Cerebellar Diseases, 155, 161, 217 Cerebellopontine, 116, 161 Cerebellopontine Angle, 116, 161

Cerebellum, 115, 158, 161, 162, 201, 207, 219 Cerebral Arteries, 156, 162, 190 Cerebral Cortex, 155, 158, 162, 174, 175, 192, 205 Cerebral hemispheres, 156, 158, 162 Cerebrospinal, 11, 39, 54, 62, 71, 80, 162, 180, 210 Cerebrospinal fluid, 11, 39, 54, 62, 71, 80, 162, 180, 210 Cerebrovascular, 98, 103, 114, 156, 159, 160, 162, 215 Cerebrovascular Circulation, 98, 103, 162 Cerebrum, 162, 219 Cerumen, 115, 162 Cervical, 5, 44, 45, 57, 77, 80, 81, 162, 208 Cervix, 162 Character, 162, 168 Chemical Warfare, 162, 168 Chemical Warfare Agents, 162, 168 Chemoreceptor, 154, 162 Chemotactic Factors, 162, 165 Child Welfare, 78, 162 Chin, 162, 189 Cholesterol, 32, 156, 163, 166, 186, 187, 212 Cholesterol Esters, 163, 186 Choline, 29, 163 Cholinergic, 15, 30, 154, 163, 194 Chorda Tympani Nerve, 163, 214 Chorea, 154, 163 Chromatin, 154, 163, 195 Chromosomal, 22, 38, 151, 163, 180, 208 Chromosome, 38, 152, 163, 186, 208, 217 Chronic, 9, 12, 14, 18, 23, 27, 29, 31, 76, 97, 117, 158, 159, 163, 168, 173, 182, 185, 204, 212 Chronic Disease, 159, 163 Chronic renal, 97, 163 Chylomicrons, 163, 186 Circulatory system, 150, 163, 184 Cirrhosis, 163, 202 CIS, 163, 207 Clamp, 19, 34, 163 Clear cell carcinoma, 163, 168 Clinical Medicine, 163, 202 Clinical study, 164, 166 Clinical trial, 6, 11, 36, 63, 129, 164, 170, 204, 206 Cloning, 21, 157, 164 Clot Retraction, 164, 201 Coca, 164 Cocaine, 29, 164

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Cochlea, 135, 164, 183, 208 Cochlear, 113, 115, 164, 215, 219 Cochlear Diseases, 164, 215 Cochlear Implants, 113, 164 Cochlear Nerve, 164, 219 Cofactor, 164, 204 Cognition, 25, 78, 164, 193 Collagen, 151, 164, 175 Communication Disorders, 128, 136, 137, 164 Complement, 39, 152, 165, 177, 201 Complementary and alternative medicine, 89, 91, 165 Complementary medicine, 89, 165 Compliance, 72, 123, 165 Computational Biology, 129, 165 Computed tomography, 48, 49, 76, 77, 80, 81, 82, 165, 166 Computerized axial tomography, 165, 166 Computerized tomography, 60, 165 Concomitant, 106, 166 Conduction, 37, 166, 208, 214 Cones, 166, 207 Congestion, 154, 166 Congestive heart failure, 29, 166 Conjunctiva, 166, 217 Connective Tissue, 157, 164, 166, 175, 176, 187, 212 Consciousness, 5, 14, 78, 151, 152, 166, 168, 170, 179, 204, 212, 214 Consolidation, 106, 166 Constipation, 154, 166 Constriction, 166, 185, 204, 208 Contraindications, ii, 166 Contrast medium, 152, 166 Controlled clinical trial, 29, 166 Contusion, 15, 18, 47, 53, 75, 116, 166 Convulsions, 103, 153, 166, 171 Convulsive, 105, 166 Coordination, 162, 166, 191 Coronary, 98, 160, 166, 190, 192 Coronary Arteriosclerosis, 166, 192 Coronary heart disease, 160, 166 Coronary Thrombosis, 166, 190, 192 Corpus, 18, 167, 203 Corpus Callosum, 18, 167 Cortex, 16, 20, 34, 37, 48, 167, 173, 174, 190, 207 Cortical, 13, 15, 18, 19, 20, 22, 23, 25, 33, 39, 100, 167, 174, 193, 205, 209, 214 Cortisol, 18, 150, 167

Cranial, 49, 51, 77, 80, 96, 100, 116, 149, 162, 163, 164, 167, 174, 175, 177, 178, 181, 184, 188, 195, 196, 199, 217, 219 Cranial Sutures, 80, 167 Craniocerebral Trauma, 156, 167, 178, 180, 195, 215 Cribriform, 167, 195 Criterion, 78, 167 Critical Care, 36, 42, 49, 53, 57, 60, 63, 69, 72, 75, 76, 78, 81, 82, 167 Curative, 167, 215 Cutaneous, 167, 187, 198 Cyclic, 25, 159, 167, 200 Cycloheximide, 16, 167 Cyst, 58, 167 Cytogenetics, 167, 208 Cytokine, 23, 96, 97, 167, 183 Cytomegalovirus, 115, 167 Cytoplasm, 154, 159, 161, 167, 173, 191, 193, 208 Cytotoxic, 29, 167 D Deamination, 167, 191 Decontamination, 63, 167 Degenerative, 16, 21, 25, 29, 168, 177 Deletion, 154, 168 Delirium, 154, 168 Delusions, 168, 205 Dendrites, 168, 193, 194, 195, 196, 205 Density, 18, 28, 168, 186, 196, 211 Dentate Gyrus, 31, 168, 180 Dentists, 5, 168 Deprenyl, 99, 168 Depressive Disorder, 67, 168, 186 Deprivation, 13, 168 Dermatitis, 97, 168 DES, 12, 152, 168 Deuterium, 168, 181 Diabetes Insipidus, 70, 168 Diabetes Mellitus, 31, 116, 169, 177 Diabetic Ketoacidosis, 169, 185 Diagnostic procedure, 95, 122, 169 Diastolic, 169, 181 Diencephalon, 169, 181, 193, 215 Diffuse Axonal Injury, 62, 158, 169 Diffusion, 17, 36, 51, 157, 169 Digestion, 151, 156, 158, 169, 186, 198, 212 Digestive system, 169, 176 Dihydroergotamine, 57, 169 Dilation, 155, 158, 169, 180 Dimethyl, 99, 169 Diploid, 169, 201, 217

225

Direct, iii, 22, 23, 25, 35, 36, 51, 97, 98, 102, 103, 163, 169, 170, 181, 207, 212, 213 Discrimination, 18, 114, 155, 169 Disinfectant, 169, 174 Dislocation, 116, 169 Disposition, 37, 169 Dissection, 55, 64, 169 Dissociation, 150, 169 Distal, 156, 170, 171, 208 Diuresis, 159, 170 Diuretic, 170, 188, 211 Dizziness, 47, 82, 89, 116, 136, 170, 219 Dominance, 18, 170 Dopa, 170, 186 Dopamine, 29, 154, 164, 168, 170, 186, 191, 194 Dorsal, 170, 184, 202, 211 Double-blind, 16, 170 Doxycycline, 12, 170 Drive, ii, vi, 23, 85, 116, 135, 170 Drug Interactions, 170 Drug Tolerance, 170, 216 Drug Toxicity, 170, 214 Duct, 159, 170, 174, 208, 213 Dumping Syndrome, 116, 170 Duodenal Ulcer, 116, 171 Duodenum, 156, 171, 176, 198, 212 Dura mater, 171, 173, 189, 198 Dyes, 19, 152, 171 Dysgeusia, 114, 171 Dyskinesia, 154, 171 Dysphoric, 168, 171 Dysplasia, 115, 171 E Eardrum, 115, 135, 171 Edema, 14, 29, 50, 53, 81, 86, 100, 171, 184, 185 Effector, 13, 149, 165, 171, 200 Efficacy, 29, 38, 171, 187 Electric shock, 160, 171 Electroconvulsive Therapy, 117, 171 Electrode, 100, 117, 171 Electroencephalography, 20, 53, 171 Electrolyte, 168, 171, 176, 195, 202, 210 Electromagnetic Fields, 37, 171 Electrons, 153, 171, 184, 188, 197, 206 Electrophysiological, 27, 30, 171 Elementary Particles, 171, 172, 188, 194, 204 Emaciation, 149, 172 Emboli, 58, 98, 172 Embolization, 58, 98, 172

Embolus, 172, 182 Embryo, 172, 182 Embryology, 109, 172 Emulsion, 86, 89, 156, 172 Encephalitis, 172, 189 Encephalopathy, 40, 172 Endarterectomy, 19, 155, 172 Endemic, 172, 188, 211 Endogenous, 12, 26, 27, 54, 170, 172, 173, 174, 197, 216 Endopeptidases, 172, 203 Endorphins, 172, 194 Endothelial cell, 157, 173, 217 Endotoxins, 165, 173 End-stage renal, 163, 173 Enhancer, 12, 173 Enkephalins, 173, 194 Enteral Nutrition, 66, 68, 173 Entorhinal Cortex, 173, 180 Environmental Health, 128, 130, 173 Enzymatic, 151, 159, 160, 165, 173, 180, 207 Enzyme Inhibitors, 173, 201 Enzyme-Linked Immunosorbent Assay, 39, 173 Epidemic, 173, 211 Epidemiological, 9, 23, 26, 173 Epidural, 57, 115, 173, 184, 201 Epidural Space, 173, 201 Epinephrine, 150, 170, 173, 194, 218 Epithelial, 157, 173, 174 Epithelial Cells, 173, 174 Epithelium, 37, 174, 184, 196 Ergotamine, 169, 174 Erythrocytes, 152, 157, 174 Esophagus, 169, 174, 176, 200, 212 Ethanol, 7, 45, 174 Ethmoid, 174, 195 Eukaryotic Cells, 174, 218 Evacuation, 100, 166, 174, 176 Evoke, 174, 212 Evoked Potentials, 19, 80, 174 Excitability, 23, 31, 106, 174, 192 Excitation, 12, 18, 31, 33, 151, 162, 174, 194 Excitatory, 15, 18, 20, 34, 174, 178 Excitatory Amino Acids, 15, 34, 174 Excitotoxicity, 18, 19, 34, 106, 174 Exhaustion, 153, 174, 188 Exocrine, 174, 198 Exogenous, 172, 174, 177 Extensor, 174, 204 Extracellular, 30, 34, 47, 152, 155, 166, 174, 175, 190, 193, 210

226

Head Trauma

Extracellular Space, 174, 190 Extrapyramidal, 150, 154, 170, 175 F Facial, 163, 175, 188, 214 Facial Nerve, 175, 214 Facial Nerve Diseases, 175, 214 Family Planning, 129, 175 Family Relations, 13, 175 Fat, 19, 86, 89, 154, 157, 160, 166, 172, 175, 185, 186, 191, 210, 217 Febrile, 22, 105, 175, 188 Femoral, 160, 175 Femoral Artery, 160, 175 Femur, 39, 175, 215 Fentanyl, 56, 78, 151, 175 Fetal Alcohol Syndrome, 7, 175 Fibrinogen, 175, 201 Fibroblasts, 175, 184 Fibrosis, 175, 209 Fibula, 175, 215 Fissure, 163, 167, 168, 175 Fistula, 136, 175 Flatus, 175, 176 Fluid Therapy, 175, 195 Fluorescence, 22, 25, 176 Fold, 11, 175, 176 Forearm, 157, 176 Fossa, 51, 162, 176 Free Radicals, 101, 153, 169, 176 Frontal Lobe, 4, 176 G Gallbladder, 149, 156, 169, 176 Ganglia, 149, 156, 176, 193, 199 Ganglion, 164, 176, 207, 217, 219 Gap Junctions, 176, 214 Gas, 14, 37, 75, 123, 160, 169, 175, 176, 181, 194, 195, 201, 219 Gas exchange, 75, 176, 219 Gastric, 57, 116, 176, 180 Gastric Emptying, 116, 176 Gastrin, 176, 180 Gastroenterology, 61, 116, 176 Gastrointestinal, 116, 158, 170, 173, 174, 176, 188, 210, 213, 217 Gastrointestinal tract, 174, 176, 210, 217 Gastrostomy, 173, 176 Gene, 10, 12, 13, 22, 23, 36, 38, 50, 102, 136, 151, 152, 157, 170, 176, 177, 180, 201, 206, 216 Gene Expression, 38, 177 Gene Targeting, 36, 177 Genetic Counseling, 110, 177

Genetic Engineering, 157, 164, 177 Genetic Markers, 22, 177 Genetic testing, 136, 177 Genetics, 32, 57, 110, 135, 167, 170, 177 Genotype, 5, 177, 200 Geriatric, 17, 119, 177 Gestation, 177, 199 Gland, 150, 177, 187, 198, 203, 209, 212, 213, 215 Gliosis, 23, 177 Glomerular, 177, 188, 207 Glomerular Filtration Rate, 177, 188 Glomeruli, 177, 195 Glossopharyngeal Nerve, 177, 214 Glucose, 13, 169, 177, 183, 208, 211 Glucose Intolerance, 169, 177 Glutamate, 7, 12, 15, 18, 21, 34, 106, 174, 178, 185, 200 Glutamic Acid, 178, 194 Glutathione Peroxidase, 9, 178 Glycine, 151, 178, 194, 209 Glycoprotein, 175, 178, 217 Gonadal, 178, 212 Governing Board, 178, 202 Grade, 31, 178 Graft, 97, 178 Graft Rejection, 97, 178 Grafting, 98, 178, 182 Granule, 31, 168, 178, 208 Growth factors, 178, 190, 193 H Haematoma, 50, 77, 178 Haemorrhage, 58, 73, 74, 178 Hair Cells, 135, 164, 178 Haptens, 150, 178 Hay Fever, 151, 178 Headache, 57, 68, 75, 159, 178, 179, 180 Headache Disorders, 179 Health Care Reform, 110, 179 Health Services, 179 Hearing aid, 113, 135, 179 Hearing Disorders, 164, 179 Heart Arrest, 160, 179 Heart attack, 160, 179 Heart failure, 179 Hemiparesis, 158, 179 Hemodynamics, 78, 99, 179 Hemorrhage, 14, 36, 63, 79, 115, 167, 178, 179, 205, 212 Hemostasis, 179, 210 Hepatic, 29, 151, 168, 179, 191 Hepatic Encephalopathy, 29, 179

227

Hereditary, 25, 115, 135, 179, 193, 201 Heredity, 176, 177, 179 Herpes, 10, 179 Herpes Zoster, 179 Heterogeneity, 38, 150, 179 Heterozygotes, 170, 180 Hibernation, 28, 180 Hippocampus, 7, 16, 66, 168, 180, 186, 193, 205, 213 Histamine, 152, 154, 180 Histology, 10, 180, 193 Histones, 163, 180, 195 Homologous, 151, 177, 180, 214 Homozygotes, 170, 180 Hormonal, 37, 155, 180 Hormone, 55, 61, 167, 168, 173, 176, 180, 183, 203, 215 Horseradish Peroxidase, 173, 180 Humoral, 25, 178, 180 Humour, 180 Hybridomas, 180, 184 Hydrocephalus, 76, 180, 184 Hydrogen, 9, 149, 160, 168, 178, 181, 186, 191, 194, 197, 199, 204, 213 Hydrogen Peroxide, 9, 178, 181, 186, 213 Hydrogenation, 169, 181 Hydrophobic, 181, 186 Hydroxyproline, 151, 164, 181 Hyperbilirubinemia, 113, 181, 185 Hypertension, 31, 159, 160, 181, 184, 202 Hyperthermia, 33, 181 Hypnotic, 104, 181 Hypoglossal Nerve, 64, 181 Hypoglycemia, 34, 181 Hypotension, 36, 52, 154, 166, 181 Hypothalamus, 156, 158, 169, 181, 186 Hypothyroidism, 77, 181 Hypoxemia, 56, 181 Hypoxia, 7, 28, 36, 99, 106, 168, 181 Hypoxic, 12, 15, 33, 34, 40, 181 I Idiopathic, 61, 113, 181 Illusion, 181, 219 Imaging procedures, 181, 216 Immune function, 97, 182 Immune response, 153, 155, 178, 182, 213, 220 Immunoassay, 173, 182 Immunodeficiency, 149, 182 Immunoglobulins, 182, 201 Immunohistochemistry, 39, 182 Immunology, 150, 180, 182

Impairment, 17, 24, 25, 113, 155, 168, 171, 182, 189, 205 Implantation, 26, 182 In situ, 27, 182 In vitro, 7, 9, 11, 12, 13, 15, 18, 25, 28, 36, 37, 182, 215 In vivo, 7, 12, 13, 15, 16, 24, 47, 182, 190, 197 Incision, 182, 184 Incontinence, 180, 182, 209 Incus, 182, 211 Induction, 38, 154, 182 Infancy, 62, 68, 182 Infantile, 67, 182 Infarction, 115, 158, 180, 182 Inflammation, 11, 23, 97, 151, 153, 168, 172, 175, 179, 182, 189, 197, 198, 201, 203 Infusion, 81, 183 Ingestion, 116, 183 Inhalation, 14, 183 Initiation, 23, 183, 212, 216 Initiator, 13, 183 Inner ear, 135, 137, 157, 164, 183, 208 Innervation, 110, 114, 175, 181, 183, 196 Inositol, 30, 183 Inotropic, 170, 183 Insight, 21, 26, 29, 31, 35, 183 Insulator, 183, 191 Insulin, 55, 169, 183, 185 Insulin-dependent diabetes mellitus, 183 Insulin-like, 55, 183 Intensive Care, 36, 60, 64, 71, 183 Interferon, 183 Interleukin-1, 62, 97, 183 Interleukin-12, 62, 183 Interleukin-2, 183 Interleukin-6, 61, 184 Intermediate Filaments, 184, 193 Intermittent, 66, 176, 184 Interneurons, 31, 184 Interstitial, 28, 174, 184, 207 Intestines, 149, 169, 176, 184 Intoxication, 7, 45, 105, 168, 184, 220 Intracellular, 7, 16, 18, 159, 182, 184, 202, 206 Intracranial Aneurysm, 73, 100, 184 Intracranial Hemorrhages, 180, 184, 215 Intracranial Hypertension, 178, 180, 184, 215 Intracranial Pressure, 44, 53, 56, 57, 61, 100, 184, 204 Intralaminar Thalamic Nuclei, 25, 184

228

Head Trauma

Intravenous, 39, 183, 184 Intrinsic, 150, 184 Invasive, 6, 44, 54, 184, 187 Ion Channels, 21, 155, 184, 193, 200, 214 Ions, 101, 149, 159, 169, 171, 181, 184 Ipsilateral, 42, 184, 207 Iris, 184, 205 Ischemia, 7, 12, 13, 15, 19, 31, 36, 96, 100, 101, 104, 155, 158, 185 Ischemic stroke, 12, 14, 29, 36, 96, 185 Isozymes, 34, 185 J Jaundice, 181, 185 Jejunostomy, 173, 185 K Kainate, 16, 21, 185 Kb, 128, 185 Ketone Bodies, 169, 185 Ketonuria, 68, 185 Kidney Disease, 123, 128, 185 Kidney Failure, 173, 185, 188 Kinetics, 159, 185 L Labile, 165, 185 Labyrinth, 164, 183, 185, 197, 199, 209, 219 Language Disorders, 164, 185 Larynx, 56, 73, 185, 216, 220 Latency, 10, 186 Latent, 186, 202 Lens, 159, 186 Lesion, 100, 177, 186, 187, 209, 214, 218 Lethargy, 180, 181, 186 Leukocytes, 157, 162, 186, 191, 217 Leukoencephalopathy, 25, 186 Levodopa, 102, 170, 186 Ligaments, 166, 186 Limbic, 152, 186 Limbic System, 152, 186 Linkage, 22, 177, 186, 187 Lipid, 36, 54, 154, 163, 183, 186, 191, 197, 217 Lipid Peroxidation, 54, 186, 197 Lipoprotein, 36, 186, 187 Lithium, 154, 186 Liver, 61, 149, 150, 154, 156, 163, 167, 169, 172, 176, 179, 186, 187, 191, 202, 214 Liver Transplantation, 61, 186 Lobe, 22, 56, 57, 187 Localization, 8, 19, 27, 32, 114, 182, 187 Localized, 149, 158, 178, 182, 187, 191, 201, 218, 219 Lod, 22, 187

Lod Score, 22, 187 Long-Term Potentiation, 106, 187 Low-density lipoprotein, 186, 187 Lumbar, 67, 71, 187 Lupus, 97, 187 Luxation, 169, 187 Lymph, 162, 163, 173, 180, 187, 208 Lymph node, 162, 187, 208 Lymphatic, 152, 182, 187, 208, 211 Lymphatic system, 152, 187, 208, 211 Lymphocyte, 149, 153, 187, 189 Lymphocyte Count, 149, 187 Lymphoma, 152, 187 M Macroglia, 187, 190, 193 Macrophage, 183, 187 Magnetic Resonance Imaging, 4, 18, 20, 27, 30, 51, 59, 99, 112, 187, 188 Magnetic Resonance Spectroscopy, 18, 29, 188 Malaria, 97, 188 Malaria, Falciparum, 188 Malaria, Vivax, 188 Malformation, 47, 51, 116, 188 Malignant, 70, 149, 158, 188, 192 Malnutrition, 110, 134, 151, 155, 159, 188 Mammogram, 159, 188, 190 Mania, 45, 188 Manic, 154, 186, 188, 205 Manifest, 156, 188 Mannitol, 14, 121, 188 Mastication, 188, 217 Maxillary, 188, 217 Maxillary Nerve, 188, 217 Meatus, 171, 188, 197, 217 Medial, 174, 184, 188, 196, 215, 219 Mediate, 164, 170, 188 Mediator, 170, 183, 189, 210 MEDLINE, 129, 189 Medullary, 184, 189 Meiosis, 189, 214 Memory, 7, 10, 13, 15, 19, 21, 25, 65, 78, 99, 102, 105, 106, 114, 151, 168, 187, 189 Memory Disorders, 65, 189 Meninges, 161, 167, 171, 189, 212 Meningioma, 61, 189 Meningitis, 40, 42, 69, 189 Mental deficiency, 175, 189 Mental Disorders, 19, 119, 189, 204, 205 Mental Health, iv, 6, 13, 128, 130, 189 Mental Retardation, 164, 189 Mesolimbic, 154, 189

229

Metabolic disorder, 168, 189 Metabolite, 29, 169, 189, 203 Metastasis, 189, 192 Methionine, 169, 189 MI, 51, 101, 147, 189 Microbe, 190, 216 Microbiology, 149, 190 Microcalcifications, 159, 190 Microdialysis, 12, 28, 47, 190 Microglia, 9, 23, 155, 190, 191, 193 Microorganism, 164, 190, 220 Microtubule-Associated Proteins, 190, 193 Microtubules, 184, 190, 193 Middle Cerebral Artery, 33, 190 Miotic, 190, 200 Mitochondria, 13, 190 Mitosis, 154, 190 Mitotic, 25, 190 Mobilization, 159, 190 Modification, 10, 151, 177, 190, 205 Molecule, 106, 153, 165, 169, 171, 174, 191, 197, 206, 218 Monitor, 59, 96, 191, 195 Monoamine, 99, 105, 191, 217 Monoamine Oxidase, 99, 105, 191, 218 Monocytes, 183, 184, 186, 191 Mononuclear, 191, 217 Monotherapy, 9, 191 Morphological, 26, 38, 172, 191 Morphology, 26, 191 Motility, 52, 191, 210 Motion Sickness, 191, 192, 209 Motor Activity, 166, 191 Mucins, 191, 208 Mucosa, 73, 187, 191, 192, 212 Mucus, 191, 208 Multiple sclerosis, 26, 97, 102, 103, 105, 106, 116, 191 Multiple Trauma, 63, 191 Multivariate Analysis, 35, 191 Mutagenesis, 35, 191 Mutagens, 191, 192 Mydriatic, 169, 192, 209 Myelin, 18, 39, 191, 192, 193, 209 Myocardial infarction, 96, 167, 189, 192 Myocardial Ischemia, 6, 192 Myocardium, 189, 192 Myristate, 102, 192 N Narcosis, 180, 192 Narcotic, 175, 192 Nasal Cavity, 112, 192, 220

Nasal Septum, 192, 220 Nasogastric, 64, 173, 192 Natural killer cells, 183, 192 Nausea, 153, 154, 192, 204, 218 Necrosis, 154, 158, 182, 189, 192 Neocortex, 16, 33, 192, 193 Neoplasia, 110, 192 Neoplasms, 114, 149, 158, 160, 192, 201 Nephropathy, 185, 192 Nerve Growth Factor, 33, 193, 194 Nervous System, 11, 21, 23, 27, 37, 76, 79, 96, 97, 101, 102, 105, 149, 151, 152, 155, 158, 159, 161, 164, 174, 176, 178, 186, 189, 190, 191, 192, 193, 194, 196, 199, 200, 201, 209, 210, 213, 214, 218 Neural, 30, 37, 114, 152, 180, 190, 191, 193 Neurites, 37, 193 Neurobehavioral Manifestations, 158, 169, 193 Neuroblastoma, 30, 38, 193 Neurodegenerative Diseases, 23, 35, 99, 156, 193 Neuroectodermal tumor, 68, 193 Neurofibrillary Tangles, 9, 32, 38, 193 Neurofilaments, 193 Neuroglia, 177, 187, 193 Neuroleptic, 70, 150, 154, 193 Neurologic, 12, 26, 36, 46, 98, 104, 115, 158, 180, 193 Neuromuscular, 149, 193, 194, 196, 214 Neuromuscular Junction, 149, 194, 196 Neuronal Plasticity, 32, 194 Neuropathy, 115, 194 Neuropeptides, 54, 71, 194 Neurophysiology, 34, 106, 110, 194 Neuropsychology, 59, 79, 194 Neurosurgical Procedures, 104, 194, 201 Neurotoxic, 7, 99, 102, 103, 105, 106, 194 Neurotoxins, 16, 23, 194 Neurotransmitter, 112, 149, 150, 151, 158, 170, 174, 178, 180, 184, 194, 213, 214, 218 Neurotrophins, 38, 194 Neutrons, 151, 194, 206 Nicotine, 15, 194 Nitrogen, 151, 194, 198, 217 Nonverbal Communication, 164, 194, 205 Norepinephrine, 150, 170, 194 Nuclear, 30, 112, 156, 171, 174, 175, 176, 186, 192, 195, 207, 215 Nuclear Family, 175, 195 Nuclear Medicine, 112, 195 Nucleic acid, 192, 194, 195, 202, 205

230

Head Trauma

Nucleosomes, 10, 195 Nursing Research, 14, 128, 195 Nutritional Support, 72, 176, 195 O Occipital Lobe, 195, 219 Ocular, 52, 73, 195, 196 Odds Ratio, 5, 195, 207 Olfaction, 37, 109, 112, 113, 195, 214 Olfaction Disorders, 195, 214 Olfactory Bulb, 4, 37, 195, 196, 220 Olfactory Nerve, 109, 195 Olfactory Receptor Neurons, 37, 195, 196, 206 Oligo, 25, 196 Oliguria, 185, 188, 196 Opacity, 168, 196 Ophthalmic, 62, 70, 196, 217 Ophthalmoplegia, 45, 80, 196 Opportunistic Infections, 149, 196 Opsin, 196, 207, 208 Optic Chiasm, 181, 196 Optic Nerve, 80, 196, 198, 204, 207 Optic Nerve Diseases, 196, 204 Organ Culture, 36, 196, 215 Orthostatic, 74, 154, 196 Osmolarity, 29, 188, 196 Osmoles, 196 Ossicles, 182, 196, 197, 211 Osteitis Deformans, 115, 197 Otitis, 115, 135, 197 Otitis Media, 115, 135, 197 Otolaryngology, 4, 66, 109, 113, 115, 124, 197 Otology, 46, 47, 52, 64, 73, 113, 115, 197 Otorhinolaryngology, 114, 197 Otosclerosis, 115, 135, 197 Ototoxic, 113, 197 Outer ear, 115, 197 Ovaries, 197, 214 Ovary, 197, 212 Overexpress, 13, 33, 197 Oxidants, 28, 197 Oxidation, 149, 153, 169, 178, 186, 197 Oxidation-Reduction, 197 Oxidative Stress, 9, 10, 28, 32, 197 Oxygenation, 181, 197 Oxygenator, 160, 198 P Pachymeningitis, 189, 198 Paediatric, 43, 54, 71, 77, 79, 198 Palate, 177, 198, 214 Palliative, 198, 215

Palsy, 42, 45, 64, 73, 198 Pancreas, 149, 157, 169, 176, 183, 198, 217 Pancreatic, 116, 198 Pancreatic Insufficiency, 116, 198 Papilledema, 198, 204 Paradoxical, 16, 198 Paralysis, 137, 179, 196, 198, 214 Paresthesia, 198, 214 Parietal, 64, 198 Parietal Lobe, 198 Parkinsonism, 154, 186, 198 Paroxysmal, 32, 136, 155, 179, 198 Particle, 112, 198, 211, 216 Patch, 19, 34, 198 Pathogenesis, 28, 35, 198 Pathologic, 154, 157, 158, 166, 181, 198, 204, 207 Pathologic Processes, 154, 198 Pathologies, 8, 25, 38, 115, 198 Pathophysiology, 16, 106, 198 Patient Education, 124, 134, 142, 144, 147, 198 Pelvis, 187, 197, 199, 218 Penicillin, 153, 199 Peptide, 151, 172, 199, 201, 203, 204, 215 Perception, 19, 114, 117, 123, 179, 199, 209, 214 Percutaneous, 54, 97, 98, 103, 199 Perforation, 135, 199 Perfusion, 20, 31, 36, 42, 50, 76, 97, 98, 103, 181, 199 Perilymph, 136, 199 Perinatal, 6, 199 Peripheral blood, 96, 199 Peripheral Nervous System, 99, 173, 193, 194, 198, 199, 213 Perivascular, 190, 199 Peroxide, 9, 199 Petechiae, 178, 199 Petrolatum, 172, 199 PH, 48, 199 Phagocyte, 197, 199 Phagocytosis, 190, 199 Pharmacologic, 14, 152, 199, 216 Pharmacotherapy, 16, 29, 199 Pharynx, 192, 199, 214 Phenobarbital, 104, 200 Phenolphthalein, 172, 200 Phenotypes, 39, 200 Phenyl, 104, 200 Phenytoin, 159, 200 Phorbol, 200, 204

231

Phorbol Esters, 200, 204 Phosphodiesterase, 25, 200 Phospholipids, 175, 183, 186, 200, 204 Phosphorus, 159, 200 Phosphorylates, 200, 204 Physical Examination, 113, 200 Physical Therapy, 16, 67, 82, 200 Physiologic, 15, 29, 150, 157, 170, 200, 206, 207, 217 Physiology, 16, 20, 28, 30, 37, 105, 109, 112, 135, 137, 157, 171, 176, 194, 200, 219 Pigments, 160, 185, 200, 207 Pilocarpine, 23, 200 Pilot study, 36, 52, 77, 200 Plants, 151, 155, 157, 158, 160, 163, 164, 177, 191, 194, 195, 200, 201, 208, 216, 218 Plaque, 152, 155, 201 Plasma, 29, 32, 50, 150, 153, 161, 163, 175, 177, 179, 185, 201 Plasma protein, 50, 150, 201 Plasmids, 25, 201 Plasmin, 27, 201, 215, 218 Plasminogen, 201, 215, 218 Plasminogen Activators, 201 Plasticity, 32, 106, 201 Platelets, 201, 215 Pneumocephalus, 41, 68, 201 Pneumonia, 52, 63, 166, 201 Polymorphic, 22, 168, 201 Polypeptide, 151, 164, 175, 201 Polyposis, 56, 201 Pons, 149, 156, 158, 161, 201 Port, 100, 202 Port-a-cath, 202 Portal Hypertension, 116, 202 Posterior, 46, 116, 152, 155, 156, 162, 170, 177, 184, 195, 198, 202 Postnatal, 175, 202, 212 Postsynaptic, 202, 214 Post-traumatic, 17, 158, 179, 202 Potassium, 16, 28, 202 Potentiates, 183, 202 Potentiation, 27, 106, 187, 202 Practice Guidelines, 130, 202 Preclinical, 26, 202 Precursor, 26, 38, 154, 163, 170, 171, 172, 173, 186, 194, 196, 201, 202, 203, 217, 218 Predisposition, 32, 134, 202 Premedication, 202, 209 Prenatal, 172, 175, 202 Presbycusis, 115, 202 Presynaptic, 19, 194, 202, 214

Prevalence, 4, 21, 32, 75, 105, 112, 124, 134, 136, 137, 195, 202 Prion, 110, 161, 202 Probe, 28, 190, 203 Prodrug, 203 Progesterone, 203, 212 Progression, 27, 134, 152, 203 Progressive, 27, 38, 40, 50, 115, 163, 168, 170, 192, 193, 202, 203, 207 Projection, 184, 194, 195, 196, 203, 205, 207 Promoter, 25, 203 Prone, 24, 203 Prophase, 203, 214 Prophylaxis, 33, 202, 203 Propofol, 68, 203 Prospective study, 46, 72, 203 Prostaglandins, 23, 154, 203 Prostaglandins A, 23, 203 Prostaglandins D, 203 Prostate, 157, 203, 217 Protease, 27, 106, 203, 215 Protease Inhibitors, 106, 203 Protective Agents, 159, 203 Protein C, 150, 154, 156, 186, 195, 204 Protein Kinase C, 96, 204 Protein S, 35, 152, 157, 167, 204, 208, 212, 214 Proteolytic, 40, 165, 175, 201, 204, 215, 218 Protocol, 18, 204 Protons, 151, 181, 188, 204, 206 Protozoan, 161, 188, 204 Pseudotumor Cerebri, 31, 184, 204 Psoriasis, 97, 204 Psychiatric, 69, 110, 112, 113, 119, 164, 189, 204 Psychiatry, 6, 17, 29, 42, 47, 51, 64, 65, 112, 204, 219 Psychic, 189, 204, 209 Psychoactive, 204, 220 Psychology, 119, 169, 194, 204 Psychomotor, 159, 168, 193, 204 Psychophysiology, 194, 205 Psychosis, 112, 153, 205 Psychotherapy, 29, 117, 205 Public Policy, 129, 205 Publishing, 40, 116, 205 Pulmonary, 56, 58, 75, 82, 157, 185, 205, 219 Pulmonary Artery, 157, 205, 219 Pulse, 191, 205 Pupil, 83, 169, 190, 192, 205 Purines, 205, 209

232

Head Trauma

Purpura, 178, 205 Pylorus, 170, 205 Pyramidal Cells, 19, 168, 205 Pyrimidines, 205, 209 Q Quality of Life, 17, 123, 124, 135, 205 Quaternary, 205, 209 Quiescent, 33, 205 R Race, 105, 170, 205, 206 Racemic, 105, 170, 206 Radiation, 6, 26, 30, 156, 172, 176, 181, 206, 220 Radioactive, 30, 156, 167, 181, 182, 195, 206 Radioisotope, 206, 216 Radiological, 75, 199, 206 Radiology, 42, 48, 49, 51, 54, 60, 61, 62, 195, 206 Radionuclide Imaging, 6, 206 Radiopharmaceuticals, 14, 206 Randomized, 171, 206 Reactive Oxygen Species, 9, 206 Reality Testing, 205, 206 Receptors, Odorant, 196, 206 Receptors, Serotonin, 206, 210 Recombinant, 21, 97, 206, 218 Recombination, 177, 206 Recovery of Function, 28, 206 Rectum, 154, 169, 175, 176, 182, 203, 206, 210 Recur, 105, 207 Red Nucleus, 155, 207 Refer, 1, 99, 158, 165, 170, 172, 179, 184, 187, 193, 194, 205, 207, 216, 219 Regeneration, 37, 207 Regimen, 114, 171, 199, 207 Relative risk, 5, 207 Renal failure, 57, 168, 207 Resected, 25, 207 Resorption, 180, 207 Respiration, 160, 162, 191, 207 Retina, 166, 186, 193, 196, 207, 208 Retinal, 62, 74, 196, 207, 208 Retinal Ganglion Cells, 196, 207 Retinal Hemorrhage, 62, 207 Retinol, 207, 208 Retraction, 100, 164, 208 Retractor, 100, 208 Retrocochlear, 115, 208 Retrograde, 22, 208 Rheumatoid, 97, 197, 208

Rhinorrhea, 80, 208 Rhodopsin, 196, 207, 208 Ribose, 150, 208 Ribosome, 208, 216 Risk factor, 5, 32, 35, 38, 52, 98, 103, 110, 112, 113, 119, 121, 136, 203, 207, 208 Risk patient, 76, 208 Rod, 163, 208 Rubella, 115, 208 S Saline, 14, 81, 86, 208 Saliva, 110, 208 Salivary, 163, 167, 169, 175, 208 Salivary glands, 163, 167, 169, 175, 208 Saponins, 208, 212 Satellite, 111, 208 Schizoid, 208, 220 Schizophrenia, 17, 19, 26, 102, 103, 105, 106, 112, 171, 189, 209, 220 Schizotypal Personality Disorder, 209, 220 Sclerosis, 12, 32, 102, 191, 209 Scopolamine, 104, 209 Screening, 11, 39, 164, 209 Secretion, 8, 61, 97, 180, 181, 183, 190, 191, 198, 209 Secretory, 57, 209, 214 Sedative, 104, 209 Seizures, 10, 18, 22, 31, 36, 40, 102, 103, 105, 106, 117, 159, 168, 198, 200, 209, 212 Self Care, 149, 209 Semicircular canal, 183, 209 Senile, 38, 97, 102, 113, 202, 209 Senile Plaques, 38, 209 Sensor, 100, 209 Sensory loss, 114, 209, 214 Sepsis, 97, 209 Sequela, 169, 209 Sequencing, 22, 209 Serine, 27, 106, 172, 204, 209, 215 Serotonin, 54, 154, 191, 194, 199, 206, 209, 217 Serum, 11, 39, 54, 77, 150, 152, 165, 187, 210, 217 Shock, 33, 54, 117, 210, 216 Shunt, 97, 98, 103, 210 Side effect, 150, 154, 210, 216 Sigmoid, 24, 210 Sigmoid Colon, 210 Signs and Symptoms, 115, 210 Skeletal, 40, 163, 210, 211 Skeleton, 149, 175, 210, 215

233

Skull, 24, 29, 71, 100, 157, 167, 184, 201, 210, 214 Skull Base, 100, 210 Small intestine, 163, 171, 180, 184, 192, 210, 219 Smooth muscle, 151, 152, 159, 180, 210, 211, 213 Social Behavior, 37, 210, 220 Social Environment, 205, 210 Sodium, 28, 210, 213 Soft tissue, 157, 196, 210 Solvent, 174, 210 Soma, 205, 211 Somatic, 177, 180, 186, 189, 190, 199, 211 Sorbitol, 188, 211 Sound wave, 166, 211 Spasm, 78, 154, 166, 211 Spatial disorientation, 170, 211 Specialist, 138, 169, 211 Species, 28, 151, 161, 170, 173, 180, 188, 189, 190, 201, 205, 206, 210, 211, 213, 216, 217, 220 Specificity, 40, 150, 159, 172, 211 Spectrum, 190, 211 Speech Perception, 113, 135, 211 Sperm, 163, 211 Spinal Nerves, 199, 211 Spirochete, 211, 214 Spleen, 167, 187, 211 Sporadic, 38, 136, 193, 211 Stapes, 135, 182, 211 Statistically significant, 4, 212 Status Epilepticus, 9, 104, 212 Steady state, 14, 212 Steel, 163, 212 Stem Cells, 12, 212 Steroid, 72, 167, 208, 212 Stimulant, 35, 159, 180, 212 Stimulus, 33, 46, 83, 97, 170, 171, 174, 183, 184, 186, 212, 215 Stomach, 149, 169, 174, 176, 180, 184, 192, 200, 205, 210, 211, 212 Streptomycin, 167, 212 Stress, 9, 10, 13, 17, 28, 35, 111, 113, 116, 155, 161, 167, 192, 197, 202, 212 Striatum, 168, 212 Stromal, 39, 212 Stromal Cells, 39, 212 Subacute, 182, 212 Subarachnoid, 36, 67, 79, 178, 184, 212 Subclavian, 212, 219 Subclavian Artery, 212, 219

Subclinical, 182, 209, 212 Subcutaneous, 171, 213 Subiculum, 180, 213 Subspecies, 211, 213 Substance P, 189, 209, 212, 213 Substrate, 173, 213, 217 Sufentanil, 56, 78, 213 Superoxide, 9, 213 Superoxide Dismutase, 9, 213 Supplementation, 151, 213 Suppression, 28, 213 Suppressive, 96, 213 Supratentorial, 47, 213 Survival Rate, 136, 213 Sweat, 162, 213 Sweat Glands, 162, 213 Sympathomimetic, 170, 173, 195, 213, 217 Symptomatic, 9, 116, 213 Symptomatology, 116, 213 Synapse, 21, 37, 150, 194, 196, 202, 213, 214, 216 Synaptic, 19, 20, 21, 22, 31, 106, 187, 194, 213, 214 Synaptic Transmission, 21, 106, 194, 214 Syncope, 214, 219 Syphilis, 115, 214 Systemic, 14, 36, 52, 58, 154, 157, 158, 168, 173, 179, 182, 184, 193, 214 Systolic, 181, 214 T Talus, 214, 215 Tardive, 154, 214 Taste Buds, 110, 114, 214 Taste Disorders, 114, 124, 214 Taurine, 30, 214 Temporal, 4, 7, 17, 19, 20, 22, 27, 37, 62, 67, 152, 175, 179, 180, 188, 214, 219 Temporal Lobe, 4, 22, 62, 152, 214, 219 Tetracycline, 12, 170, 214 Tetrodotoxin, 33, 214 Thalamic, 24, 155, 214, 215 Thalamic Diseases, 155, 214 Thalamic Nuclei, 24, 215 Thalamus, 25, 158, 169, 184, 186, 214, 215, 219 Therapeutics, 15, 89, 90, 191, 215 Thorax, 187, 215 Threonine, 204, 209, 215 Threshold, 117, 174, 181, 208, 215 Thrombosis, 68, 204, 212, 215 Thrombus, 98, 166, 182, 185, 192, 215 Thyroid, 116, 137, 181, 215, 218

234

Head Trauma

Thyrotropin, 181, 215 Tibia, 39, 175, 215 Tinnitus, 115, 117, 197, 204, 215, 219 Tissue Culture, 193, 215 Tissue Plasminogen Activator, 27, 215 Tolerance, 16, 28, 149, 177, 215 Tomography, 6, 42, 75, 77, 112, 188, 216 Tooth Preparation, 149, 216 Topical, 174, 181, 199, 216 Torsion, 182, 216 Toxic, iv, 16, 19, 33, 105, 112, 135, 155, 194, 216 Toxicity, 15, 19, 29, 170, 216 Toxicology, 16, 130, 216 Toxin, 214, 215, 216 Tracer, 22, 180, 216 Trachea, 185, 200, 215, 216 Tracheostomy, 72, 216 Traction, 163, 216 Transcription Factors, 12, 216 Transduction, 30, 110, 159, 183, 216 Transfection, 12, 157, 216 Transgenes, 12, 25, 216 Translation, 97, 151, 216 Translational, 33, 97, 216 Transmitter, 18, 21, 149, 155, 170, 174, 184, 189, 193, 194, 216, 218 Transplantation, 39, 163, 216 Tremor, 74, 198, 217 Triage, 78, 217 Trigeminal, 109, 114, 188, 217 Trigeminal Nerve, 114, 217 Trigger zone, 154, 217 Triglyceride, 86, 89, 217 Trisomy, 38, 152, 217 Trophic, 9, 217 Tryptophan, 164, 210, 217 Tuberculosis, 187, 217 Tumor marker, 157, 217 Tumor Necrosis Factor, 97, 217 Tunica, 172, 191, 217 Tunica Intima, 172, 217 Tympanic membrane, 115, 196, 217 Tyramine, 191, 217 Tyrosine, 170, 218 U Ubiquitin, 40, 193, 218 Ulcer, 171, 218 Ultrasonography, 79, 218 Unconscious, 152, 218 Uremia, 185, 207, 218 Urinary, 18, 180, 182, 196, 209, 215, 218

Urinary Plasminogen Activator, 215, 218 Urine, 153, 157, 169, 170, 182, 185, 196, 218 Uterus, 162, 167, 197, 203, 218 V Vaccines, 218, 220 Vagina, 162, 168, 218 Valves, 98, 218 Vascular, 110, 114, 115, 119, 152, 159, 179, 182, 201, 215, 218 Vasodilator, 158, 170, 180, 218 Vector, 8, 216, 218 Vegetative, 169, 218 Vein, 39, 46, 152, 154, 184, 195, 202, 208, 212, 218 Venereal, 214, 218 Venoms, 194, 218 Venous, 82, 154, 158, 204, 219 Ventilation, 160, 219 Ventricle, 44, 152, 180, 181, 205, 214, 215, 219 Ventricular, 180, 219 Ventriculostomy, 54, 219 Vertebrae, 211, 219 Vertebral, 63, 116, 156, 173, 219 Vertebral Artery, 63, 219 Vertebrobasilar Insufficiency, 115, 219 Vertigo, 89, 91, 115, 136, 197, 219 Vestibular, 64, 82, 136, 178, 219 Vestibule, 164, 183, 209, 219 Vestibulocochlear Nerve, 164, 215, 219 Vestibulocochlear Nerve Diseases, 215, 219 Veterinary Medicine, 129, 219 Villi, 180, 219 Viral, 10, 13, 137, 172, 195, 216, 219 Viral vector, 10, 13, 219 Virulence, 155, 216, 220 Virus, 112, 149, 156, 161, 173, 177, 201, 208, 216, 219, 220 Viscosity, 116, 220 Visual field, 196, 204, 220 Vitamin A, 183, 207, 220 Vitro, 12, 13, 25, 28, 220 Vivo, 12, 13, 16, 30, 220 Vocal cord, 137, 220 Vomeronasal Organ, 195, 220 W Windpipe, 200, 215, 220 Withdrawal, 9, 21, 33, 103, 105, 106, 168, 220 X Xenograft, 152, 220

235

X-ray, 14, 165, 166, 176, 188, 195, 206, 220

236

Head Trauma