Daniel Kondziella · Gunhild Waldemar Neurology at the Bedside

Total Page:16

File Type:pdf, Size:1020Kb

Daniel Kondziella · Gunhild Waldemar Neurology at the Bedside Daniel Kondziella · Gunhild Waldemar Neurology at the Bedside 123 Neurology at the Bedside Daniel Kondziella • Gunhild Waldemar Neurology at the Bedside Daniel Kondziella, MD, PhD, FEBN Gunhild Waldemar, MD, DMSC Department of Neurology Department of Neurology Rigshospitalet Rigshospitalet Copenhagen University Hospital Copenhagen University Hospital Copenhagen Copenhagen Denmark Denmark ISBN 978-1-4471-5250-7 ISBN 978-1-4471-5251-4 (eBook) DOI 10.1007/978-1-4471-5251-4 Springer London Heidelberg New York Dordrecht Library of Congress Control Number: 2013944580 © Springer-Verlag London 2013 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifi cally the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfi lms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. Exempted from this legal reservation are brief excerpts in connection with reviews or scholarly analysis or material supplied specifi cally for the purpose of being entered and executed on a computer system, for exclusive use by the purchaser of the work. Duplication of this publication or parts thereof is permitted only under the provisions of the Copyright Law of the Publisher's location, in its current version, and permission for use must always be obtained from Springer. Permissions for use may be obtained through RightsLink at the Copyright Clearance Center. Violations are liable to prosecution under the respective Copyright Law. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specifi c statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. While the advice and information in this book are believed to be true and accurate at the date of publication, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) Foreword The days of textbooks are numbered but not for this one. In the modern computer age, most of our knowledge is gained online and the need for weighty textbooks is over. Much of our learning comes from clinical experience and seeing our col- leagues, senior and junior, at work. During the early stages of a neurologists’ career, there is a tremendous need for a reasonably short book which enables the beginner to grasp the whole span of the subject, a book which will provide a framework on which to graft their growing bedside experience. This is that book. It takes its stance at the bedside, be that the outpatient clinic couch or the hospital bed. The winning combination of junior neu- rologist Daniel Kondziella and senior professor Gunhild Waldemar covers the spec- trum from anatomy and physiology, through history and examination, to differential diagnosis, investigation, and treatment. Concise, clear, and written in impeccable English, each chapter could be consumed in an evening, leaving the reader with a sound basis for their clinical practice, further enquiry, and lifelong learning. Each generation needs its own text to tackle the problems of the modern era. This text is modern and full of wisdom. I warmly recommend it to the neurologist in training and the more senior neurologist who wants to match their knowledge against an authoritative template. London, 2013 Richard Hughes, MD, FRCP, FMedSci v Discl aimer Medicine, including neurology, is an ever-changing fi eld. As new research and clin- ical experience extends our knowledge, revisions of diagnostic procedures, treat- ment protocols, and drug therapy may become necessary. While the authors have made considerable efforts to describe generally accepted practices and to confi rm the accuracy of the data, they are not responsible for errors or omissions or for any consequences from application of the information in this publication. To the fullest extent of the law, neither the authors nor the publisher assumes any liability for any damage and/or injury to persons or property arising from this book. The application of the information in this book remains the professional responsibility of the practi- tioner. In particular, the reader is urged to confi rm the accuracy of the information relating to drug therapy by checking the most current product information provided by the drug manufacturer and by consulting other pharmaceutical literature to verify the recommended dose, the method and duration of administration, as well as pos- sible contraindications and drug side effects. The treating physician is responsible for the decision on dosages and the best available treatment for each individual patient. vii Acknowledgments The authors are grateful for the invaluable suggestions and comments to the manu- script made by Poul Brodersen, Siska Frahm-Falkenberg (Copenhagen), Fredrik Asztely (Gothenburg), and Lawrence A. Zeidman (Chicago). Further, the authors would like to thank Vibeke Andrée Larsen and Annika Reynberg Langkilde (Copenhagen) for their excellent help in providing many of the neuroimaging fi gures. The authors wish also to express their gratitude for the support and help they have received from their families during the writing of this book. Finally, the authors would like to thank all their patients and colleagues – you have taught us neurology, it is a pleasure working with you! Copenhagen, Denmark Daniel Kondziella Gunhild Waldemar ix Contents 1 What to Expect from This Book (and What Not to) . 1 2 Clinical History and Neuroanatomy: “Where Is the Lesion?” . 5 2.1 Muscle . 8 2.2 Neuromuscular Junction . 10 2.3 Peripheral Nerves, the Plexus, and Spinal Nerve Roots . 12 2.3.1 Peripheral Nerves . 14 2.3.2 Brachial Plexus and Lumbosacral Plexus . 23 2.3.3 Spinal Nerve Roots . 25 2.4 Spinal Cord . 27 2.4.1 Complete or Near-Complete Transection of the Spinal Cord . 29 2.4.2 Brown-Séquard Syndrome . 31 2.4.3 Anterior Cord Syndrome . 32 2.4.4 Dorsal Cord Syndrome . 33 2.4.5 Syringomyelia . 34 2.4.6 Central Cord Syndrome . 35 2.4.7 Conus Medullaris Syndrome . 35 2.5 Brainstem . 36 2.6 Cranial Nerves . 38 2.6.1 Olfactory Nerve . 38 2.6.2 Optic Nerve . 38 2.6.3 Oculomotor Nerve, Trochlear Nerve, Abducens Nerve . 41 2.6.4 Trigeminal Nerve . 48 2.6.5 Facial Nerve . 50 2.6.6 Vestibulocochlear Nerve . 53 2.6.7 Glossopharyngeal Nerve . 54 2.6.8 Vagus Nerve . 55 2.6.9 Spinal Accessory Nerve . 56 2.6.10 Hypoglossal Nerve . 57 2.7 Cerebellum . 57 xi xii Contents 2.8 Subcortical Gray Matter . 58 2.8.1 Basal Ganglia . 58 2.8.2 Diencephalon . 60 2.9 Subcortical White Matter . 61 2.10 Cortex. 65 2.10.1 Frontal Lobes . 66 2.10.2 Temporal Lobes . 68 2.10.3 Parietal Lobes . 70 2.10.4 Occipital Lobes . 72 2.11 Cerebrovascular System. 74 2.11.1 Anterior Circulation . 76 2.11.2 Posterior Circulation . 77 2.12 The Healthy Brain . 80 References and Suggested Reading . 81 3 Neurological Bedside Examination: “Can I Confi rm My Anatomical Hypothesis?” . 83 3.1 Cognitive and Mental Functions . 86 3.1.1 The History as Part of the Cognitive Examination . 86 3.1.2 Bedside Examination of Mental and Cognitive Functions . 90 3.1.3 General Neurological Examination in the Cognitively Impaired Patient . 93 3.2 Cranial Nerves . 94 3.3 Motor Function . 102 3.4 Sensory Function . 108 3.5 Cerebellar Function . 109 3.6 Gait . 110 3.7 System Overview . 112 3.8 Examination of the Comatose Patient . 116 3.8.1 Verifi cation and Quantifi cation of Unconsciousness . 117 3.8.2 Assessment of Neurological Defi cits, in Particular Signs of Brainstem Injury . 118 3.8.3 Neurological Causes for Coma . 120 3.8.4 Prognostication of Neurological Outcome Following Cardiac Arrest . 123 3.8.5 Diagnosis of Brain Death . 124 3.9 Examination of the Patient with an Acute Ischemic Stroke . 126 3.10 Examination of the Patient with an Epileptic Seizure . 127 3.10.1 Taking the History of a Patient with a Seizure . 127 3.10.2 The Examination and Management of a Patient with a Seizure . 129 3.11 Examination of the Patient with Functional/Nonorganic Defi cits . .130 References and Suggested Reading . 135 Contents xiii 4 Differential Diagnosis: “What Is the Lesion?” . 137 4.1 The Differential Diagnosis of Coma . 138 4.1.1 Structural Causes of Coma . 140 4.1.2 Non-structural Causes of Coma . 142 4.2 The Differential Diagnosis of Traumatic Brain Injury . 143 4.2.1 Assessing the Need for Observation and Imaging in Closed Head Injury . 144 4.3 The Differential Diagnosis of Headache . 146 4.3.1 Primary Headache Syndromes . 146 4.3.2 Symptomatic Headaches . 149 4.4 The Differential Diagnosis of Cognitive Impairment and Dementia . 152 4.4.1 Potentially Reversible Conditions . ..
Recommended publications
  • Inherited Cerebellar Ataxia in Childhood: a Pattern-Recognition Approach Using Brain MRI
    REVIEW ARTICLE Inherited Cerebellar Ataxia in Childhood: A Pattern-Recognition Approach Using Brain MRI L. Vedolin, G. Gonzalez, C.F. Souza, C. Lourenc¸o, and A.J. Barkovich ABSTRACT SUMMARY: Ataxia is the principal symptom of many common neurologic diseases in childhood. Ataxias caused by dysfunction of the cerebellum occur in acute, intermittent, and progressive disorders. Most of the chronic progressive processes are secondary to degen- erative and metabolic diseases. In addition, congenital malformation of the midbrain and hindbrain can also be present, with posterior fossa symptoms related to ataxia. Brain MR imaging is the most accurate imaging technique to investigate these patients, and imaging abnormalities include size, shape, and/or signal of the brain stem and/or cerebellum. Supratentorial and cord lesions are also common. This review will discuss a pattern-recognition approach to inherited cerebellar ataxia in childhood. The purpose is to provide a comprehensive discussion that ultimately could help neuroradiologists better manage this important topic in pediatric neurology. ABBREVIATIONS: AR ϭ autosomal recessive; CAC ϭ cerebellar ataxia in childhood; 4H ϭ hypomyelination with hypogonadotropic hypogonadism and hypodon- tia; JSRD ϭ Joubert syndrome and related disorders; OPHN1 ϭ oligophrenin-1 taxia is an inability to coordinate voluntary muscle move- plastic/paraneoplastic disorders, immune-mediated/demyelinat- Aments that cannot be attributed to weakness or involuntary ing disorders, and drugs/toxins (antiepileptic medications,
    [Show full text]
  • Radiculopathy Vs. Spinal Stenosis: Evocative Electrodiagnosis Identifies the Main Pain Generator
    Functional Electromyography Loren M. Fishman · Allen N. Wilkins Functional Electromyography Provocative Maneuvers in Electrodiagnosis 123 Loren M. Fishman, MD Allen N. Wilkins, MD College of Physicians & Surgeons Manhattan Physical Medicine Columbia University and Rehabilitation New York, NY 10028, USA New York, NY 10013, USA [email protected] ISBN 978-1-60761-019-9 e-ISBN 978-1-60761-020-5 DOI 10.1007/978-1-60761-020-5 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2010935087 © Springer Science+Business Media, LLC 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein.
    [Show full text]
  • 7/19/2018 1 Falls and Movement Disorders
    7/19/2018 Falls and Movement Disorders Victor Sung, MD AL Medical Directors Association Annual Conference July 28, 2018 Falls and Movement Disorders • Gait Disorders and Falls • Movement Disorders Primer • Hypokinetic Movement Disorders • Hyperkinetic Movement Disorders • Other Neurologic Contributors to Falls • Non‐Neurologic Contributors to Falls • Pearls/Pitfalls Physiology/Epidemiology of Gait Disorders • 3 Key Subsystems for Maintaining Balance • Visual • Vestibular • Somatosensory / Proprioception • Gait disorders are common • 15% of people age 65 • 25% of people age 85 • Increases risk of falls by 2.5‐3 X • >80% of gait disorders in patients >65 are multifactorial • Most common are orthopedic and neurologic factors 1 7/19/2018 Epidemiology of Gait Disorders Frequency of Etiologies for Patients Referred to Neurology for Gait D/O Etiology Percent Sensory deficits 18.3% Myelopathy 16.7% Multiple infarcts 15.0% Unknown 14.2% Parkinsonism 11.7% Cerebellar degeneration / ataxia 6.7% Hydrocephalus 6.7% Psychogenic 3.3% Other* 7.5% *Other = metabolic encephalopathy, sedative drugs, toxic disorders, brain tumor, subdural hematoma Evaluation of Gait Disorders • Start with history • Do they have falls? If so, what type/setting? • In general, what setting does the gait disorder occur? • What other medical problems may be contributing? • Exam • Abnormalities on motor/sensory/cerebellar exam • What does the gait look like? Anatomy of the Motor System Overview • Localize the Lesion!! • Motor Cortex • Subcortical Corticospinal tract • Modulators
    [Show full text]
  • Possibilities of Automated Diagnostics of Odontogenic Sinusitis According to the Computer Tomography Data
    sensors Article Possibilities of Automated Diagnostics of Odontogenic Sinusitis According to the Computer Tomography Data Oleg G. Avrunin 1, Yana V. Nosova 1 , Ibrahim Younouss Abdelhamid 1, Sergii V. Pavlov 2 , Natalia O. Shushliapina 3, Waldemar Wójcik 4, Piotr Kisała 4,* and Aliya Kalizhanova 5,6 1 Department of Biomedical Engineering, Faculty of Electronic and Biomedical Engineering Kharkiv National University of Radio Electronics, 61166 Kharkiv, Ukraine; [email protected] (O.G.A.); [email protected] (Y.V.N.); [email protected] (I.Y.A.) 2 Department of Biomedical Engineering, Vinnytsia National Technical University, 21021 Vinnytsia, Ukraine; [email protected] 3 Department of Otorhinolaryngology, Stomatological Faculty Kharkiv National Medical University, 61022 Kharkiv, Ukraine; [email protected] 4 Institute of Electronic and Information Technologies, Faculty Electrical Engineering and Computer Science, Lublin University of Technology, 20-618 Lublin, Poland; [email protected] 5 Institute of Information and Computational Technologies CS MES RK, 050010 Almaty, Kazakhstan; [email protected] 6 University of Power Engineering and Telecommunications, 050013 Almaty, Kazakhstan * Correspondence: [email protected]; Tel.: +34-815-384-309 Abstract: Individual anatomical features of the paranasal sinuses and dentoalveolar system, the complexity of physiological and pathophysiological processes in this area, and the absence of actual standards of the norm and typical pathologies lead to the fact that differential diagnosis Citation: Avrunin, O.G.; Nosova, and assessment of the severity of the course of odontogenic sinusitis significantly depend on the Y.V.; Abdelhamid, I.Y.; Pavlov, S.V.; measurement methods of significant indicators and have significant variability. Therefore, an urgent Shushliapina, N.O.; Wójcik, W.; task is to expand the diagnostic capabilities of existing research methods, study the significance of Kisała, P.; Kalizhanova, A.
    [Show full text]
  • CT, MRI and Ultrasound of the Orbit
    6/15/2018 CT, MRI and Ultrasound of the Orbit GABRIELA S SEILER DR.MED.VET. DECVDI, DACVR PROFESSOR OF RADIOLOGY NORTH CAROLINA STATE UNIVERSITY 1 6/15/2018 Orbital imaging Principles and Indications of Computed Tomography and Magnetic Resonance Imaging Relevant Imaging Parameters Imaging of Orbital Diseases with Case Examples www.intechopen.com 2 6/15/2018 Tomographic Benefit Exopthalmos, OS Squamous cell carcinoma 148533M 3 6/15/2018 Mixbreed dog, 1 year history of nasal and ocular discharge, initially responded to antibiotics radiograph CT image 4 6/15/2018 5 6/15/2018 Cross‐Sectional Imaging Computed Tomography Magnetic Resonance Imaging Voxel Diagnostic Ultrasound Pixel Pixel ‐ picture element Voxel ‐ volume element 6 6/15/2018 Principles of Cross‐ sectional imaging SPATIAL CONTRAST MODALITY RESOLUTION RESOLUTION Radiography <1 mm Good Ultrasound 1-2mm Better CT 0.4 mm Even better MRI 1-3 mm Best! 7 6/15/2018 Computed Tomography “Cat Scan” 8 6/15/2018 Computed Tomography First CT scanner was built by Sir Godfrey Hounsfield at the EMI Research Laboratories in 1972 9 6/15/2018 Anatomy of a CT scanner X‐ray detectors X‐ray tube 10 6/15/2018 Most CTs are helical or spiral CTs X‐ray tube and an array of receptors rotate around the patient 11 6/15/2018 Image Reconstruction Images acquired by rapid rotation of X‐ray tube 360°around patient as couch moves. The transmitted radiation is then measured by a ring of radiation sensitive ceramic detectors. An image is generated from these measurements 12 6/15/2018 Image Reconstruction Complex mathematical algorithms allow each voxel to be assigned a numerical value based on the x ray attenuation within that volume of tissue.
    [Show full text]
  • Neuropathology Category Code List
    Neuropathology Page 1 of 27 Neuropathology Major Category Code Headings Revised 10/2018 1 General neuroanatomy, pathology, and staining 65000 2 Developmental neuropathology, NOS 65400 3 Epilepsy 66230 4 Vascular disorders 66300 5 Trauma 66600 6 Infectious/inflammatory disease 66750 7 Demyelinating diseases 67200 8 Complications of systemic disorders 67300 9 Aging and neurodegenerative diseases 68000 10 Prion diseases 68400 11 Neoplasms 68500 12 Skeletal Muscle 69500 13 Peripheral Nerve 69800 14 Ophthalmic pathology 69910 Neuropathology Page 2 of 27 Neuropathology 1 General neuroanatomy, pathology, and staining 65000 A Neuroanatomy, NOS 65010 1 Neocortex 65011 2 White matter 65012 3 Entorhinal cortex/hippocampus 65013 4 Deep (basal) nuclei 65014 5 Brain stem 65015 6 Cerebellum 65016 7 Spinal cord 65017 8 Pituitary 65018 9 Pineal 65019 10 Tracts 65020 11 Vascular supply 65021 12 Notochord 65022 B Cell types 65030 1 Neurons 65031 2 Astrocytes 65032 3 Oligodendroglia 65033 4 Ependyma 65034 5 Microglia and mononuclear cells 65035 6 Choroid plexus 65036 7 Meninges 65037 8 Blood vessels 65038 C Cerebrospinal fluid 65045 D Pathologic responses in neurons and axons 65050 1 Axonal degeneration/spheroid/reaction 65051 2 Central chromatolysis 65052 3 Tract degeneration 65053 4 Swollen/ballooned neurons 65054 5 Trans-synaptic neuronal degeneration 65055 6 Olivary hypertrophy 65056 7 Acute ischemic (hypoxic) cell change 65057 8 Apoptosis 65058 9 Protein aggregation 65059 10 Protein degradation/ubiquitin pathway 65060 E Neuronal nuclear inclusions 65100
    [Show full text]
  • GENETIC TESTING REQUISITION Please Ship All
    GENETIC TESTING REQUISITION 1-844-363-4357· [email protected] Schillingallee 68 · 18057 Rostock Germany Attention Patient: Please visit your nearest LifeLabs or CML Healthcare Patient Service Centre for sample collection LL: K012-01/ CML: CEN CONTRACT # Report to Physician Billing # LifeLabs Demographic Ordering Physician Name Label Physician Signature: Ordering Physician Address: Tel: Fax: Address & Contact Info: Copy to (name & contact info): Name: Contact: Bill to Contract # K012-01 (patient does not pay at time of collection) Patient Gender: (M/F) Patient Name (Last, First): Patient DOB: (YYYY/MM/DD) Patient Address: Patient Health Card: Patient Telephone: Please ship all NON-PRENATAL samples to: LifeLabs · Attn CDS Department • 100 International Boulevard• Toronto ON• M9W6J6 TEST REQUESTED LL TR # / CML TC# □ Genetic Test - Blood Sample 2 x 4mL EDTA 4005 □ Genetic Test (Pediatric) - Blood Sample 1 x 2mL EDTA 4008 □ Genetic Test - Other Sample Type 4014 PRENATAL SAMPLES: Please ship directly to CENTOGENE. Date Blood Collected (YYYY/MM/DD): ___________ Time Blood Collected (HH:MM)) :________ Collector Name: ___________________ GENETIC TESTING CONSENT I understand that a DNA specimen will be sent to LifeLabs for genetic testing. My physician has told me about the condition(s) being tested and its genetic basis. I am aware that correct information about the relationships between my family members is important. I agree that my specimen and personal health information may be sent to Centogene AG at their lab in Germany (address below). To ensure accurate testing, I agree that the results of any genetic testing that I have had previously completed by Centogene AG may be shared with LifeLabs.
    [Show full text]
  • Vol. 13 No. 2 December 2020 Eissn 2508-1349 Vol
    eISSN 2508-1349 Vol. 13 No. 2 December 2020 eISSN 2508-1349 Vol. 13 No. 2 December 2020 pages 69 - 136 I I www.e-jnc.org eISSN 2508-1349 Vol. 13, No. 2, 31 December 2020 Aims and Scope Journal of Neurocritical Care (JNC) aims to improve the quality of diagnoses and management of neurocritically ill patients by sharing practical knowledge and professional experience with our reader. Although JNC publishes papers on a variety of neurological disorders, it focuses on cerebrovascular diseases, epileptic seizures and status epilepticus, infectious and inflammatory diseases of the nervous system, neuromuscular diseases, and neurotrauma. We are also interested in research on neurological manifestations of general medical illnesses as well as general critical care of neurological diseases. Open Access This is an Open Access article distributed under the terms of the Creative Commons Attribution Non- Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non- commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Publisher The Korean Neurocritical Care Society Editor-in-Chief Sang-Beom Jeon Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, 88 Oylimpic-ro 43-gil, Songpa-gu, Seoul 05505, Korea Tel: +82-2-3010-3440, Fax: +82-2-474-4691, E-mail: [email protected] Correspondence The Korean Neurocritical Care Society Department of Neurology, The Catholic University College of Medicine, 222 Banpo-Daero, Seocho-Gu, Seoul 06591, Korea Tel: +82-2-2258-2816, Fax: +82-2-599-9686, E-mail: [email protected] Website: http://www.neurocriticalcare.or.kr Printing Office M2community Co.
    [Show full text]
  • Atypical Development of the Cerebellum : Impact on Language Function Lynette M
    University of New Mexico UNM Digital Repository Psychology ETDs Electronic Theses and Dissertations 8-28-2012 Atypical development of the cerebellum : impact on language function Lynette M. Silva Follow this and additional works at: https://digitalrepository.unm.edu/psy_etds Recommended Citation Silva, Lynette M.. "Atypical development of the cerebellum : impact on language function." (2012). https://digitalrepository.unm.edu/psy_etds/129 This Dissertation is brought to you for free and open access by the Electronic Theses and Dissertations at UNM Digital Repository. It has been accepted for inclusion in Psychology ETDs by an authorized administrator of UNM Digital Repository. For more information, please contact [email protected]. Lynette M. Silva Candidate Psychology Department This dissertation is approved, and it is acceptable in quality and form for publication: Approved by the Dissertation Committee: Steven Verney, Co-Chairperson Ron Yeo, Co-Chairperson Robert Thoma Jean Lowe ATYPICAL DEVELOPMENT OF THE CEREBELLUM: IMPACT ON LANGUAGE FUNCTION By LYNETTE M. SILVA B.A., English, Stanford University, 1996 M.S., Psychology, University of New Mexico, 2009 DISSERTATION Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Psychology The University of New Mexico Albuquerque, New Mexico July 2012 iii Dedication For my parents, extended family, and valued friends, because it took a village. And for Martin Rodriguez, who served as my Virgil, and showed me the way. iv Acknowledgements I would like to thank Drs. Steven Verney, Ron Yeo, Robert Thoma, and Jean Lowe for their guidance and support as members of my dissertation committee. I am very thankful for the encouragement and supervision I continue to receive from Dr.
    [Show full text]
  • Diagnosing and Managing Common Adrenal Disorders
    Diagnosing and Managing Common Adrenal Disorders Veronica Piziak MD, PhD Emeritus Director of Endocrinology Scott & White Fellowship Director Endocrinology Baylor S&W [email protected] Disclosures: None Objectives Discuss the Management of Incidental Adrenal Masses Discuss the management of common Adrenal Disorders Incidental Adrenal Masses What do you need to know? Is it cancer? What is the a potential for morbidity or mortality? Does it produce hormones that Is it functional? can cause problems? Is it growing? What vital Is there a mass effect? structures could be compromised? About 80+ % of the time the nodules of the adrenal are just warts! Adrenal Mass > 1.0 cm Is it malignant? Very rarely Is it functional? Rarely it can make hormones that cause hypertension, weight gain and diabetes Is there a mass effect? Rarely adrenal tumors can destroy the normal tissue and cause the gland to fail Adrenal Incidentalomas Prevalence of incidentally discovered adrenal Masses: 4.4%- 10% of patients undergoing CT scan Terzolo M et al Eur J Endo 2011;164:851 nonfunctioning benign lesion 82.5% cortisol-secreting adenoma 5.3% pheochromocytoma 5.1% adrenocortical carcinoma 4.7% metastatic lesion 2.5% aldosteronoma 1 % Malignant overall 8% Musella et al. BMC Surgery 2013; 13:57 Goals: Find adrenal carcinoma Identify all adrenal non-functioning lesions suspicious for adrenocortical cancer (imaging) Identify functional pheochromocytomas Identify cortisol or aldosterone secreting lesion Identify benign adenomas You should perform biochemical testing Obtain adequate imaging - CT or MRI adrenal protocol Indications for Surgery Functioning nodules: Unilateral aldosterone producing masses Hormonally active pheochromocytomas Overt Cushing’s Syndrome Non functioning lesions larger than 4 cm 93% of the adrenal carcinomas were >/= 4 cm when found.
    [Show full text]
  • Gait Disorders in Older Adults
    ISSN: 2469-5858 Nnodim et al. J Geriatr Med Gerontol 2020, 6:101 DOI: 10.23937/2469-5858/1510101 Volume 6 | Issue 4 Journal of Open Access Geriatric Medicine and Gerontology STRUCTURED REVIEW Gait Disorders in Older Adults - A Structured Review and Approach to Clinical Assessment Joseph O Nnodim, MD, PhD, FACP, AGSF1*, Chinomso V Nwagwu, MD1 and Ijeoma Nnodim Opara, MD, FAAP2 1Division of Geriatric and Palliative Medicine, Department of Internal Medicine, University of Michigan Medical School, USA Check for 2Department of Internal Medicine and Pediatrics, Wayne State University School of Medicine, USA updates *Corresponding author: Joseph O Nnodim, MD, PhD, FACP, AGSF, Division of Geriatric and Palliative Medicine, Department of Internal Medicine, University of Michigan Medical School, 4260 Plymouth Road, Ann Arbor, MI 48109, USA Abstract has occurred. Gait disorders are classified on a phenom- enological scheme and their defining clinical presentations Background: Human beings propel themselves through are described. An approach to the older adult patient with a their environment primarily by walking. This activity is a gait disorder comprising standard (history and physical ex- sensitive indicator of overall health and self-efficacy. Impair- amination) and specific gait evaluations, is presented. The ments in gait lead to loss of functional independence and specific gait assessment has qualitative and quantitative are associated with increased fall risk. components. Not only is the gait disorder recognized, it en- Purpose: This structured review examines the basic biolo- ables its characterization in terms of severity and associated gy of gait in term of its kinematic properties and control. It fall risk. describes the common gait disorders in advanced age and Conclusion: Gait is the most fundamental mobility task and proposes a scheme for their recognition and evaluation in a key requirement for independence.
    [Show full text]
  • Arthrogryposis and Congenital Myasthenic Syndrome Precision Panel
    Arthrogryposis and Congenital Myasthenic Syndrome Precision Panel Overview Arthrogryposis or arthrogryposis multiplex congenita (AMC) is a group of nonprogressive conditions characterized by multiple joint contractures found throughout the body at birth. It usually appears as a feature of other neuromuscular conditions or part of systemic diseases. Primary cases may present prenatally with decreased fetal movements associated with joint contractures as well as brain abnormalities, decreased muscle bulk and polyhydramnios whereas secondary causes may present with isolated contractures. Congenital Myasthenic Syndromes (CMS) are a clinically and genetically heterogeneous group of disorders characterized by impaired neuromuscular transmission. Clinically they usually present with abnormal fatigability upon exertion, transient weakness of extra-ocular, facial, bulbar, truncal or limb muscles. Severity ranges from mild, phasic weakness, to disabling permanent weakness with respiratory difficulties and ultimately death. The mode of inheritance of these diseases typically follows and autosomal recessive pattern, although dominant forms can be seen. The Igenomix Arthrogryposis and Congenital Myasthenic Syndrome Precision Panel can be as a tool for an accurate diagnosis ultimately leading to a better management and prognosis of the disease. It provides a comprehensive analysis of the genes involved in this disease using next-generation sequencing (NGS) to fully understand the spectrum of relevant genes involved, and their high or intermediate penetrance.
    [Show full text]