DOCSLIB.ORG

Greenberg, Michael J

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Greenberg, Michael J Clinical Neurology 5th edition (February 9, 2002): by David A. Greenberg, Michael J. Aminoff, Roger P. Simon By McGraw-Hill/Appleton & Lange By OkDoKeY Clinical Neurology Contents Editors Dedication Preface Chapter 1: Disorders of Consciousness Chapter 2: Headache & Facial Pain Chapter 3: Disorders of Equilibrium Chapter 4: Disturbances of Vision Chapter 5: Motor Deficits Chapter 6: Disorders of Somatic Sensation Chapter 7: Movement Disorders Chapter 8: Seizures & Syncope Chapter 9: Stroke Chapter 10: Coma Chapter 11: Neurologic Investigations Appendices A: The Neurologic Examination B: A Brief Examination of the Nervous System C: Clinical Examination of Common Isolated Peripheral Nerve Disorders Frequently Used Neurological Drugs Selected Neurogenetic Disorders Dedication To Our Families Editors David A. Greenberg, MD, PhD Professor and Vice-President for Special Research Programs Buck Institute for Age Research Novato, California Michael J. Aminoff, MD, DSc, FRCP Professor of Neurology Department of Neurology School of Medicine University of California, San Francisco Roger P. Simon, MD Robert Stone Dow Chair of Neurology Director of Neurobiology Research Legacy Health Systems Portland, Oregon Frequently Used Neurological Drugs Drug Brand Use Sizes (mg)1 Usual dose2 Alteplase (rt-PA) Activase Stroke — 0.9 mg/kg IV Amantadine Symmetrel Parkinsonism 100 100 mg bid Amitriptyline Elavil Headache, pain 10,25,50,75,100,150 10–150 mg qd Aspirin Ecotrin TIA/stroke, headache 81,325,500,650,975 81 mg qd–650 mg q4–6h Baclofen Lioresal Spasticity 10,20 5 mg tid–20 mg qid Benztropine Cogentin Movement disorders 0.5,1,2 1–2 mg qd–bid Bromocriptine Parlodel Parkinsonism 2.5,5 1.5–20 mg bid Carbamazepine Tegretol Seizures, pain 100,200,400 200–600 mg bid Carbidopa/levodopa Sinemet Parkinsonism 10/100,25/100,25/250, 50/200 25/250 mg tid–qid Clonazepam Klonopin Seizures, myoclonus 0.125,0.25,0.5, 1,2 0.5–6.5 mg tid Clopidogrel Plavix TIA/stroke 75 75 mg qd Cyclobenzaprine Flexeril Pain 10 10–20 mg tid Dihydroergotamine Migranal Headache 4 4 mg IN Donepezil Aricept Alzheimer's disease 5, 10 5–10 mg qhs Entacapone Comtan Parkinsonism 200 200 mg up to 5 times daily Ethosuximide Zarontin Seizures 250 250–500 mg qd Fosphenytoin Cerebyx Seizures 150,750 22.5–30 mg/kg IV Gabapentin Neurontin Seizures, pain 100,300,400 300–1200 mg tid Glatiramer Copaxone Multiple sclerosis 20 20 mg SC qd Haloperidol Haldol Movement disorders 0.5, 1,2,5,10,20 1–5 mg tid Heparin — TIA/stroke — 1000 U/hr3 Ibuprofen Motrin Headache, pain 200,300,400,600,800 200–800 mg qid Indomethacin Indocin Headache, pain 25,50,75 25–50 mg tid Interferon beta-1A Avonex Multiple sclerosis 0.003 0.003 mg IM q week Interferon beta-1b Betaseron Multiple sclerosis 0.25 0.25 mg Lamotrigine Lamictal Seizures 25,100,150,200 150–250 mg bid Meclizine Antivert Vertigo 12.5, 25, 50 25 mg q6h Metoclopramide Reglan Headache 5,10 10–30 mg qid Naproxen Naprosyn Headache, pain 200,250,375,500 250–500 mg bid Naratriptan Amerge Headache 1,2.5 2.5 mg q4h × 1–2 Nimodipine Nimotop Subarachnoid hemorrhage 30 60 mg q4h Nortriptyline Pamelor Headache, pain 10,25,50,75 10–150 mg qhs Pergolide Permax Parkinsonism 0.05,0.25,1 1–5 mg tid Phenobarbital Luminal Seizures 15,30,60,100 60 mg bid–tid Phenytoin Dilantin Seizures, pain 30,50,100 300–400 mg qd Pramipexole Mirapex Parkinsonism 0.125,0.25,1,1.5 0.5–1.5 mg tid Primidone Mysoline Seizures, tremor 50,250 250 mg tid–qid Prochlorperazine Compazine Headache 5,10,25 5–10 mg tid–qid Propranolol Inderal Headache, tremor 10,20,40,80,90,120,160 20–120 mg bid Pyridostigmine Mestinon Myasthenia gravis 60,180 6–120 mg tid Riluzole Rilutek ALS 50 50 mg q12h Ropinirole Requip Parkinsonism 0.25,0.5,1 0.25–8 mg tid Selegiline Eldepryl Parkinsonism 5 5 mg bid Sumatriptan Imitrex Headache 25,50,100 PO; 6 SC; 5,20 nasal spray 25–100 mg × 1–3; 6 mg SC × 1–2; 20 mg IN × 1–2 Tacrine Cognex Alzheimer's disease 10,20,30,40 10–20 mg qid Tiagabine Gabitril Seizures 4,12,16,20 8–28 mg bid Ticlopidine Ticlid TIA/stroke 250 250 mg bid Tolcapone Tasmar Parkinsonism 100,200 100–200 mg tid Topiramate Topamax Seizures 25,100,200 200 mg bid Trihexyphenidyl Artane Movement disorders 2,5 1 mg qd–5 mg tid Valproic acid Depakote Seizures, headache 125,250,500 250–650 mg tid Verapamil Calan Headache 40,80,120,180,240 80 mg tid Vigabatrin Sabril Seizures 500 1–4 g/d Warfarin Coumadin TIA/stroke 1,2,2.5,3,4,5,6,7.5,10 5 mg qd4 Zolmitriptan Zomig Headache 2.5,5 2.5 mg q2h × 1–4 Zonisamide Zonegran Seizures 100 100–400 mg/d 1 Includes extended- or sustained-release preparations, but not liquid formulations. 2 Typical maintenance doses in adults, given orally unless stated otherwise (IM = intramuscular; IN = intranasal, IV = intravenous, SC = subcutaneous). Consult prescribing information for indications and contraindications, drug interactions, adverse drug effects, safety in pregnancy and breastfeeding, doses in hepatic or renal failure, and recommended initial doses. 3 Adjusted according to partial thromboplastin time (PTT) or international normalized ratio (INR). 4 Adjusted according to prothrombin time (PT) or international normalized ratio (INR). Preface The fifth edition of Clinical Neurology, like its predecessors, offers a problem-oriented approach to neurology based on the authors' experience in teaching medical students and house staff at the University of California, San Francisco. Chapters are organized according to problems such as headache, seizures, stroke, and coma, because these are the conditions for which patients usually seek medical care. Careful history taking and neurologic examination are emphasized, as these remain the cornerstones of neurologic diagnosis, even in an era of technologic diagnostic advances. The need to update this book arises from two main sources: rapid expansion of knowledge about the molecular basis of neurologic diseases and recent innovations in the treatment of disorders such as headache, epilepsy, stroke, Parkinson's disease, and multiple sclerosis. Accordingly, increased prominence has been given to molecular mechanisms of diseases—for example, Alzheimer's disease and the polyglutamine disorders, including Huntington's disease. Sections on treatment have been updated and expanded to reflect the introduction of new therapies for neurological disorders. The summary tables of therapeutic drugs and genetic disorders inside the front and back covers, which were introduced in the last edition, have been revised to maintain currency. Key Concepts is a new feature that has been introduced in this issue. In the beginning of each chapter, some of the major concepts are presented with numbered icons. These same numbered icons appear within the text to indicate where these specific points are discussed in the chapter. We thank our colleagues, who have contributed their expert advice to the preparation of this new edition of Clinical Neurology, especially Lydia Bayne, Megan Burns, Chadwick Christine, Paul Garcia, Alisa Gean, Cheryl Jay, Catherine Lomen-Hoerth, Neil Raskin, Tom Shults, and Norman So. The staff at McGraw-Hill have been enormously helpful in moving this book through editing and production. We hope our efforts will help to demystify clinical neurology for students and practitioners and contribute to providing patients better and more focused diagnosis and treatment. David A. Greenberg Michael J. Aminoff Roger P. Simon Novato, San Francisco, and Portland February 2002 Selected Neurogenetic Disorders Disorder Gene Locus Protein Inh1 PRE2 Alzheimer's disease, familial APP 21q21.3–q22.05 Amyloid b A4 precursor protein AD Alzheimer's disease, familial PS1 14q24.3 Presenilin-1 AD Alzheimer's disease, familial PS2 1q31–q42 Presenilin-2 AD Alzheimer's disease, susceptibility APOE 19q13.2 Apolipoprotein E AD Amyotrophic lateral sclerosis, familial SOD1 21q22.1 Superoxide dismutase-1 AD Ataxia-telangiectasia ATM 11q22.3 Unknown AR Benign neonatal epilepsy 1 KCNQ2 20q13.2 Voltage-gated K channel AD Benign neonatal epilepsy 2 KCNQ3 8q24 Voltage-gated K channel AD CADASIL3 NOTCH3 19p13.2–p13.1 Notch-3 AD Centronuclear myopathy MYF6 12q21 Myogenic factor-6 AD Cerebral amyloid angiopathy CST3 20p11 Cystatin C AD Charcot-Marie-Tooth disease, type IA PMP22 17p11.2–p12 Peripheral myelin protein-22 AD Charcot-Marie-Tooth disease, type IB MPZ 1q22 Myelin protein zero AD Charcot-Marie-Tooth disease, X-linked CX32 Xq13.1 Connexin-32 XLR Choreoacanthocytosis CHAC 9q21 Chorein AR Creutzfeldt-Jakob disease, familial PRNP 20pter-p12 Prion protein AD Dentatorubral-pallidoluysian atrophy DRPLA 12p13.31 Atrophin-1 AD CAG Duchenne/Becker dystrophy DMD Xp21.2 Dystrophin XLR Emery-Dreifuss muscular dystrophy LMNA 1q21.2 Lamin A/C AD/AR Episodic ataxia 1 KCNA1 12p13 Shaker-related K channel AD Episodic ataxia 2 CACNL1A4 19p13 Ca channel a 1A subunit AD Familial hemiplegic migraine 1 CACNL1A4 19p13 Ca channel a 1A subunit AD Friedreich's ataxia FRDA1 9q13–q21.1 Frataxin AR GAA Generalized epilepsy with febrile seizures plus 1 SCN1B 19q13 Na channel type 1, b1 subunit AD Generalized epilepsy with febrile seizures plus 2 SCN1A 2q24 Na channel type 1, a subunit AD Generalized epilepsy with febrile seizures plus 3 GABRG2 5q31.1–q33.1 GABAA receptor, g2 subunit AD Hereditary spastic paraplegia SPG7 16q24.3 Paraplegin AR Huntington's disease HD 4p16.3 Huntingtin AD CAG Hyperkalemic periodic paralysis SCN4A 17q23.1–q25.3 Na channel type IV, a subunit AD Hypokalemic periodic paralysis CACNL1A3 1q32 Ca channel a1S subunit AD Limb-girdle dystrophy 1A TTID 5q31 Myotilin AD Limb-girdle dystrophy
Load more

Recommended publications
  • Understanding Icd-10-Cm and Icd-10-Pcs 3Rd Edition Download Free
    UNDERSTANDING ICD-10-CM AND ICD-10-PCS 3RD EDITION DOWNLOAD FREE Mary Jo Bowie | 9781305446410 | | | | | International Classification of Diseases, (ICD-10-CM/PCS) Transition - Background Palmer B. Manual placenta removal. A: Understanding ICD-10-CM and ICD-10-PCS 3rd edition International Classification of Diseases ICD is a common framework and language to report, compile, use and compare health information. Psychoanalysis Adlerian therapy Analytical therapy Mentalization-based treatment Transference focused psychotherapy. Hysteroscopy Vacuum aspiration. Every code begins with an alpha character, which is indicative of the chapter to which the code is classified. Search Compliance Understanding BC, resilience standards and how to comply Follow these nine steps to first identify relevant business continuity and resilience standards and, second, launch a successful While many coders use ICD lookup software to help them, referring to an ICD code book is invaluable to build an understanding of the classification system. Pregnancy test Leopold's maneuvers Prenatal testing. Endoscopy : Colonoscopy Anoscopy Capsule endoscopy Enteroscopy Proctoscopy Sigmoidoscopy Abdominal ultrasonography Defecography Double-contrast barium enema Endoanal ultrasound Enteroclysis Lower gastrointestinal series Small-bowel follow-through Transrectal ultrasonography Virtual colonoscopy. Psychosurgery Lobotomy Bilateral cingulotomy Multiple subpial transection Hemispherectomy Corpus callosotomy Anterior temporal lobectomy. While codes in sections are structured similarly to the Medical and Surgical section, there are a few exceptions. Send Feedback Do you have Understanding ICD-10-CM and ICD-10-PCS 3rd edition on the new website? Help Learn to edit Community portal Recent changes Upload file. D Radiation oncology. Stem cell transplantation Hematopoietic stem cell transplantation. The primary distinctions are:. Palmer Joseph C.
    [Show full text]
  • Perception of Facial Expressions in Social Anxiety and Gaze Anxiety
    The Pegasus Review: UCF Undergraduate Research Journal (URJ) Volume 9 Issue 1 Article 6 2016 Perception of Facial Expressions in Social Anxiety and Gaze Anxiety Aaron Necaise University of Central Florida, [email protected] Part of the Psychology Commons Find similar works at: https://stars.library.ucf.edu/urj University of Central Florida Libraries http://library.ucf.edu This Article is brought to you for free and open access by the Office of Undergraduate Research at STARS. It has been accepted for inclusion in The Pegasus Review: UCF Undergraduate Research Journal (URJ) by an authorized editor of STARS. For more information, please contact [email protected]. Recommended Citation Necaise, Aaron (2016) "Perception of Facial Expressions in Social Anxiety and Gaze Anxiety," The Pegasus Review: UCF Undergraduate Research Journal (URJ): Vol. 9 : Iss. 1 , Article 6. Available at: https://stars.library.ucf.edu/urj/vol9/iss1/6 Necaise: Perception of Facial Expressions Social Anxiety & Gaze Anxiety Published Vol. 9.1: 40-47 October 19th, 2017 THE UNIVERSITY OF CENTRAL FLORIDA UNDERGRADUATE RESEARCH JOURNAL Analysis of the Pathomechanism and Treatment of Migraines Related to the Role of the Neuropeptide CGRP By: Marvi S. Qureshi Faculty Mentor: Dr. Mohtashem Samsam UCF Burnett School of Biomedical Sciences ABSTRACT: Migraines are a type of headache that specifically act on only one side of the head, although about 30% of patients with migraines may experience a bilateral headache. Migraines are brain disorders that typically involve issues of sensory processing taking place in the brainstem. Possible causation has been linked to blood vessels, blood flow, and oxygen levels in the brain.
    [Show full text]
  • Potential Mechanisms of Prospective Antimigraine Drugs: a Focus on Vascular (Side) Effects
    CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector Pharmacology & Therapeutics 129 (2011) 332–351 Contents lists available at ScienceDirect Pharmacology & Therapeutics journal homepage: www.elsevier.com/locate/pharmthera Associate Editor: John Fozard Potential mechanisms of prospective antimigraine drugs: A focus on vascular (side) effects Kayi Y. Chan a, Steve Vermeersch b, Jan de Hoon b, Carlos M. Villalón c, Antoinette MaassenVanDenBrink a,⁎ a Division of Vascular Medicine and Pharmacology, Department of Internal Medicine, Erasmus Medical Center, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands b Center for Clinical Pharmacology, University Hospitals Leuven, Campus Gasthuisberg, (K.U. Leuven), Leuven, Belgium c Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Deleg. Tlalpan, C.P. 14330, México D.F., Mexico article info abstract Available online 2 December 2010 Currently available drugs for the acute treatment of migraine, i.e. ergot alkaloids and triptans, are cranial vasoconstrictors. Although cranial vasoconstriction is likely to mediate—at least a part of—their therapeutic Keywords: effects, this property also causes vascular side-effects. Indeed, the ergot alkaloids and the triptans have been Antimigraine drugs reported to induce myocardial ischemia and stroke, albeit in extremely rare cases, and are contraindicated in Neuropeptides patients with known cardiovascular risk factors. In view of these limitations, novel antimigraine drugs
    [Show full text]
  • Current and Prospective Pharmacological Targets in Relation to Antimigraine Action
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Erasmus University Digital Repository Naunyn-Schmiedeberg’s Arch Pharmacol (2008) 378:371–394 DOI 10.1007/s00210-008-0322-7 REVIEW Current and prospective pharmacological targets in relation to antimigraine action Suneet Mehrotra & Saurabh Gupta & Kayi Y. Chan & Carlos M. Villalón & David Centurión & Pramod R. Saxena & Antoinette MaassenVanDenBrink Received: 8 January 2008 /Accepted: 6 June 2008 /Published online: 15 July 2008 # The Author(s) 2008 Abstract Migraine is a recurrent incapacitating neuro- (CGRP1 and CGRP2), adenosine (A1,A2,andA3), glutamate vascular disorder characterized by unilateral and throbbing (NMDA, AMPA, kainate, and metabotropic), dopamine, headaches associated with photophobia, phonophobia, endothelin, and female hormone (estrogen and progesterone) nausea, and vomiting. Current specific drugs used in the receptors. In addition, we have considered some other acute treatment of migraine interact with vascular receptors, targets, including gamma-aminobutyric acid, angiotensin, a fact that has raised concerns about their cardiovascular bradykinin, histamine, and ionotropic receptors, in relation to safety. In the past, α-adrenoceptor agonists (ergotamine, antimigraine therapy. Finally, the cardiovascular safety of dihydroergotamine, isometheptene) were used. The last two current and prospective antimigraine therapies is touched decades have witnessed the advent of 5-HT1B/1D receptor upon. agonists (sumatriptan and second-generation triptans), which have a well-established efficacy in the acute Keywords 5-HT. Antimigraine drugs . CGRP. treatment of migraine. Moreover, current prophylactic Noradrenaline . Migraine . Receptors treatments of migraine include 5-HT2 receptor antagonists, Ca2+ channel blockers, and β-adrenoceptor antagonists. Despite the progress in migraine research and in view of its Introduction complex etiology, this disease still remains underdiagnosed, and available therapies are underused.
    [Show full text]
  • Serotonin Receptor Knockouts: a Moody Subject David Julius* Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143-0450
    Proc. Natl. Acad. Sci. USA Vol. 95, pp. 15153–15154, December 1998 Commentary Serotonin receptor knockouts: A moody subject David Julius* Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143-0450 The neurotransmitter serotonin (5-hydroxytryptamine; 5-HT) receptors are expressed in a number of brain regions to which is believed to play a significant role in determining one’s serotonergic neurons project, including the hippocampus, ce- emotional state. Indeed, serotonergic synapses are sites of rebral cortex, and amygdala (11, 12). As in the case of action for a number of mood-altering drugs, including the presynaptic autoreceptors, activation of postsynaptic 5-HT1A now-legendary antidepressant Prozac (fluoxetine) (1). As a receptors leads to hyperpolarization of the neuron and the result, there has been tremendous interest in identifying consequent inhibition of neurotransmitter release. This effect molecular components of the serotonergic system, including appears to be mediated through a biochemical signaling path- cell surface receptors and transporters, and understanding way in which 5-HT1A receptors activate a G protein (Gi)- whether and how these proteins contribute to the regulation of coupled inwardly rectifying potassium channel (13, 14). mood and emotion. This quest is driven, in part, by the In light of the pharmacological evidence that 5-HT1A re- possibility that behavioral disorders, such as depression or ceptors exert negative ‘‘feedback’’ control on serotonergic anxiety, may be linked to deficits in one or more components neurons, one would predict that mice lacking this receptor of this signaling system. Such information could, in turn, focus should show elevated levels of extraneuronal serotonin, or an attention on specific targets for the development of novel increase in the amount of serotonin released after nerve drugs with which to treat psychiatric disorders.
    [Show full text]
  • Does Sumatriptan Cross the Blood–Brain Barrier in Animals and Man?
    J Headache Pain (2010) 11:5–12 DOI 10.1007/s10194-009-0170-y REVIEW ARTICLE Does sumatriptan cross the blood–brain barrier in animals and man? Peer Carsten Tfelt-Hansen Received: 24 August 2009 / Accepted: 27 October 2009 / Published online: 10 December 2009 Ó Springer-Verlag 2009 Abstract Sumatriptan, a relatively hydrophilic triptan, development [6, 7] or an effect on trigeminovascular nerves based on several animal studies has been regarded to be [6]. A peripheral effect on trigeminal vascular nerves was unable to cross the blood–brain barrier (BBB). In more indicated by the blocking effect of sumatriptan of neuro- recent animal studies there are strong indications that genically mediated plasma extravasation [8]. Inhibitors of sumatriptan to some extent can cross the BBB. The CNS neurogenic inflammation (NI) were, however, ineffective in adverse events of sumatriptan in migraine patients and the treatment of migraine [9] and it is thus difficult to normal volunteers also indicate a more general effect of ascribe a pivotal role for NI in migraine. In 1996 it was, sumatriptan on CNS indicating that the drug can cross the based on the effect of zolmitriptan, suggested that inhibition BBB in man. It has been discussed whether a defect in the of trigeminal neurons in the brain stem by lipophilic triptans BBB during migraine attacks could be responsible for a may play a role in the anti-migraine effect of these drugs possible central effect of sumatriptan in migraine. This and that these results offered the prospect of a third path- review suggests that there is no need for a breakdown in the ophysiological target site for triptans [10].
    [Show full text]
  • Study Guide Medical Terminology by Thea Liza Batan About the Author
    Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails ­proficiency­in­communicating­with­healthcare­professionals­such­as­physicians,­nurses,­ or dentists.
    [Show full text]
  • Histamine and Antihistaminics Chapter 11
    Histamine and Antihistaminics Chapter 11 HISTAMINE Histamine, meaning ‘tissue amine’ (histos—tissue) is almost ubiquitously present in animal tissues and in certain plants, e.g. stinging nettle. Its pharmacology was studied in detail by Dale in the beginning of the 20th century when close parallelism was noted between its actions and the manifestations of certain allergic reactions. It was implicated as a mediator of hypersensitivity Fig. 11.1: Synthesis and degradation of histamine phenomena and tissue injury reactions. It is now MAO-Monoamine oxidase known to play important physiological roles. Histamine is present mostly within storage by Asch and Schild (1966) into H1 and H2 : those granules of mast cells. Tissues rich in histamine blocked by then available antihistamines were are skin, gastric and intestinal mucosa, lungs, liver labelled H1. Sir James Black (1972) developed and placenta. Nonmast cell histamine occurs in the first H2 blocker burimamide and confirmed brain, epidermis, gastric mucosa and growing this classification. A third H3 receptor, which regions. Turnover of mast cell histamine is slow, serves primarily as an autoreceptor controlling while that of nonmast cell histamine is fast. histamine release from neurones in brain was Histamine is also present in blood, most body identified in 1983. Though some selective H3 secretions, venoms and pathological fluids. agonists and antagonists have been produced, none has found any clinical application. Features of Synthesis, storage and destruction these 3 types of histaminergic receptor are Histamine is β imidazolylethylamine. It is compared in Table 11.1. synthesized locally from the amino acid histidine Molecular cloning has revealed yet another (H4) receptor and degraded rapidly by oxidation and methylation in 2001.
    [Show full text]
  • Current Awareness in Clinical Toxicology Editors: Damian Ballam Msc and Allister Vale MD
    Current Awareness in Clinical Toxicology Editors: Damian Ballam MSc and Allister Vale MD January 2017 CONTENTS General Toxicology 11 Metals 38 Management 21 Pesticides 39 Drugs 23 Chemical Warfare 41 Chemical Incidents & 33 Plants 41 Pollution Chemicals 33 Animals 42 CURRENT AWARENESS PAPERS OF THE MONTH 2015 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 33rd Annual Report Mowry JB, Spyker DA, Brooks DE, Zimmerman A, Schauben JL. Clin Toxicol 2016; 54: 924-1109. Introduction This is the 33rd Annual Report of the American Association of Poison Control Centers' (AAPCC) National Poison Data System (NPDS). As of 1 January 2015, 55 of the nation's poison centers (PCs) uploaded case data automatically to NPDS. The upload interval was 9.52 [7.40, 13.6] (median [25%, 75%]) minutes, creating a near real-time national exposure and information database and surveillance system. Methods We analyzed the case data tabulating specific indices from NPDS. The methodology was similar to that of previous years. Where changes were introduced, the differences are identified. Poison center cases with medical outcomes of death were evaluated by a team of medical and clinical toxicologist reviewers using an ordinal scale of 1-6 to assess the Relative Contribution to Fatality (RCF) of the exposure. Results In 2015, 2,792,130 closed encounters were logged by NPDS: 2,168,371 human exposures, 55,516 animal exposures, 560,467 information calls, 7657 human confirmed nonexposures, Current Awareness in Clinical Toxicology is produced monthly for the American Academy of Clinical Toxicology by the Birmingham Unit of the UK National Poisons Information Service, with contributions from the Cardiff, Edinburgh, and Newcastle Units.
    [Show full text]
  • Spontaneous CSF Leaks Low CSF Volume Syndromes
    Spontaneous CSF Leaks Low CSF Volume Syndromes Bahram Mokri, MD KEYWORDS Spontaneous CSF leak Spontaneous intracranial hypotension (SIH) CSF hypovolemia Orthostatic headaches Diffuse patchy meningeal enhancement Acquired Chiari malformation Epidural blood patch Radioisotope cisternography KEY POINTS Spontaneous intracranial hypotension nearly always results from spontaneous cerebro- spinal fluid (CSF) leaks, typically at the spine level and only rarely from the skull base. The triad of orthostatic headaches, diffuse patchy meningeal enhancement, and low CSF pressure, although a diagnostic hallmark, may or may not be encountered because the variability in clinical presentations, imaging observations, and CSF findings is indeed substantial. The core pathogenetic factor is a decreased volume of CSF rather than its pressure. The anatomy of the leak may be complex. A preexisting dural weakness, usually in connection with an abnormality of the connective tissue matrix sometimes along with triv- ial traumas, may play an etiologic role. Slow-flow and fast-flow CSF leaks each present challenges on locating the actual site of the leak. Epidural blood patch (EBP) has emerged as the treatment of choice when conservative measures have failed. However, expect considerable variability in response to this treat- ment, and recall that the efficacy of EBP in spontaneous CSF leaks is substantially less than its efficacy in postlumbar puncture leaks. Surgery may be helpful in well-selected cases, when less invasive measures have failed and when the site of the leak has been definitely identified. INTRODUCTION About 2 decades ago, the first report on pachymeningeal gadolinium enhancement in spontaneous intracranial hypotension (SIH) appeared in the literature.1 This relatively short interval has witnessed enormous progress while a much larger number of pa- tients are now identified and a far broader clinical spectrum is recognized.2 Funding Source: None.
    [Show full text]
  • Meningeal Sarcoidosis, Pseudo-Meningioma, and J Neurol Neurosurg Psychiatry: First Published As 10.1136/Jnnp.55.4.300 on 1 April 1992
    30030ournal ofNeurology, Neurosurgery, and Psychiatry 1992;55:300-303 Meningeal sarcoidosis, pseudo-meningioma, and J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.300 on 1 April 1992. Downloaded from pachymeningitis of the convexity D Ranoux, B Devaux, C Lamy, J Y Mear, F X Roux, J L Mas Abstract lb) and was enhanced on TI-weighted gado- Two cases of meningeal sarcoidosis with linium MRI (fig 1c). Carotid angiography unusual and misleading presentations are showed a slight stenosis of the C5 segment of reported. In the first case, CT scan, the left internal carotid artery. Selective left angiographic, and MRI findings were external carotid angiography showed a vas- indistinguishable from those ofmeningio- cular lesion lateral to the carotid siphon, ma. CSF pleiocytosis may help in diag- supplied by the middle meningeal artery (fig nosing sarcoid pseudo-meningioma. The id). Cerebrospinal fluid was normal except for second patient had transient focal deficits elevated proteins (0-85 g/l). A diagnosis of and pachymeningitis ofthe convexity. The meningioma was made, and the patient was transient deficits were probably of epi- treated with carbamazepine. leptic origin based on their response to She was readmitted 16 months later because antiepileptic treatment. The diagnosis of of worsening headaches and diplopia. Exam- neurosarcoidosis was made only after ination showed trigeminal hypesthesia, ptosis meningeal biopsy, despite thorough and paresis ofthe medial rectus on the left. CT investigations. scans and MRI showed an increase in the size of the lesion. A craniotomy revealed a firm, whitish tissue which was adherent to the dura, Neurological symptoms, including cranial extended to the cavernous sinus, and reached neuropathies, aseptic meningitis, hydrocepha- the sphenoid wing.
    [Show full text]
  • Cerebrospinal Fluid Dissemination and Neoplastic Meningitis in Primary Brain Tumors Sajeel Chowdhary, MD, Sherri Damlo, and Marc C
    Special Report Cerebrospinal Fluid Dissemination and Neoplastic Meningitis in Primary Brain Tumors Sajeel Chowdhary, MD, Sherri Damlo, and Marc C. Chamberlain, MD Background: Neoplastic meningitis, also known as leptomeningeal disease, affects the entire neuraxis. The clinical manifestations of the disease may affect the cranial nerves, cerebral hemispheres, or the spine. Because of the extent of disease involvement, treatment options and disease staging should involve all compartments of the cerebrospinal fluid (CSF) and subarachnoid space. Few studies of patients with primary brain tumors have specifically addressed treatment for the secondary complication of neoplastic meningitis. Therapy for neoplastic meningitis is palliative in nature and, rarely, may have a curative intent. Methods: A review of the medical literature pertinent to neoplastic meningitis in primary brain tumors was performed. The complication of neoplastic meningitis is described in detail for the various types of primary brain tumors. Results: Treatment of neoplastic meningitis is complicated because determining who should receive ag- gressive, central nervous system (CNS)–directed therapy is difficult. In general, the therapeutic response of neoplastic meningitis is a function of CSF cytology and, secondarily, of the clinical improvement in neuro- logical manifestations related to the disease. CSF cytology may manifest a rostrocaudal disassociation; thus, consecutive, negative findings require that both lumbar and ventricular cytological testing are performed to confirm the complete response. Based on data from several prospective, randomized trials extrapolated to primary brain tumors, the median rate of survival for neoplastic meningitis is several months. Oftentimes, therapy directed at palliation may improve quality of life by protecting patients from experiencing continued neurological deterioration.
    [Show full text]