DOCSLIB.ORG

Parkinson's Disease

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Parkinson's Disease BRITISH MEDICAL JOURNAL VOLUME 293 9 AUGUST 1986 379 Br Med J (Clin Res Ed): first published as 10.1136/bmj.293.6543.379 on 9 August 1986. Downloaded from Clinical Algorithm Parkinson's disease N P QUINN, F A HUSAIN Idiopathic Parkinson's disease is a degenerative neurological dis- importance of oculogyric crises occurring in a patient with Parkinson's order classically presenting in old or late middle age. The brain disease receiving dopaminergic treatment is unknown. shows characteristic cell loss and depigmentation in pigmented Huntington's disease-Most patients with akinetic-rigid Huntington's disease are young (onset before age 20), 90% inheriting their "Westphal brain stem nuclei. The presence of rounded eosinophilic intra- variant" from an affected father. Additional dystonic features are common cytoplasmic inclusions, known as Lewy bodies, in some of the and mental changes profound. Older subjects with Huntington's disease neurons qua non affected is a sine for definitive pathological rarely present with an akinetic-rigid syndrome, but in many adult patients diagnosis. In life, however, the diagnosis of idiopathic Parkinson's parkinsonian features develop as the disease progresses, even without disease rests entirely on clinical features and is primarily one of neuroleptic treatment.3 The family history and the mental changes point exclusion. towards the diagnosis. A paucity of a rhythm on the electroencephalogram and caudate atrophy on computed tomography may provide additional clues. A gene specific test on DNA harvested from whole blood may become available. Parkinsonism Wilson's disease-Young subjects with parkinsonism (onset before age 40) should have blood and urine tests of copper metabolism and slit lamp The first prerequisite is the recognition of parkinsonism, which comprises examination for Kayser-Fleischer rings. Traditional teaching holds that two or more of the following signs: tremor, rigidity, akinesia, and postural neurological Wilson's disease never begins after the age of 40, is never abnormality (either flexed posture or impaired postural reflexes). From then diagnosed after the age of 50, and is always associated with Kayser-Fleischer onwards unusual clinical features, with or without the results of ancillary rings. Despite two recently reported, and hotly debated, possible exceptions investigations, may point to alternative causes of the syndrome. Many of to these rules,4 for practical purposes Kayser-Fleischer rings are always these atypical features may be evident only with time, so that a clinical found in neurological Wilson's disease (but not hepatic Wilson's disease' so diagnosis ofidiopathic Parkinson's disease must be continually re-evaluated. long as slit lamp examination is performed by an experienced ophthalmolo- Progress down the algorithm therefore resembles an upside down version of gist. Other family members may be affected, and a history of parental snakes and ladders: the appearance of an unusual feature at any time in the consanguinity may be elicited. course of the disease may call for the whole case of differential diagnosis to be is common and, like idiopathic Parkinson's reopened. Here we briefly consider the important features of the different Drug induced parkinsonism disease, the incidence increases with age. It can result from treatment with diagnostic possibilities in the boxes across the middle of the algorithm in a any receptor drug of the phenothiazine, more conventional manner. This background information provides the neuroleptic (dopamine blocking) rationale underlying the algorithm. butyrophenone, thioxanthene, or benzamide class and also from treatment http://www.bmj.com/ Benign essential tremor-This monosymptomatic disorder, dominantly with dopamine depleting agents such as reserpine and tetrabenazine. overlooked are metoclopramide (Maxolon), inherited but with variable penetrance, is commoner than Parkinson's Causative drugs commonly (Stemetil), and various antidepressant-anxiolytic-neuro- disease and shows a similar rising prevalence with increasing age. It is often prochlorperazine temporarily relieved by alcohol, improved by blockers, and exacerbated by leptic combinations, such as Motival. It is also surprising how often a history of depot injections is not picked up. If the condition is due to drugs alone Pl agonist drugs. It is probably the most frequent cause of misdiagnosis. Although cogwheeling of affected limbs due to the tremor is allowable, such patients usually recover after six months without medication, although months to two years may occasionally be necessary. When parkinsonism classical rigidity, akinesia, and other parkinsonian features are lacking. 18 period the patient may have been destined to develop Some patients with idiopathic Parkinson's disease may display a fast postural persists after this anyway. Several patients whose first parkin- on 26 September 2021 by guest. Protected copyright. tremor as well as, or sometimes instead of, a classic slow resting tremor. idiopathic Parkinson's disease symptom is a vague complaint of unsteadiness or "dizziness" may in Also, many patients with akinetic-rigid parkinsonism may never develop sonian tremor. fact be given prochlorperazine, thus hastening the appearance of other Postencephalitic Parkinson's disease-Enecephalitis lethargica is the only features of the disease. The reason some patients treated with antidopa- whereas others ofthe same age treated frequently accepted encephalitic cause of persisting Parkinson's disease.' minergic drugs develop parkinsonism same do not unknown but may well be related to the extent Cases are extremely rare. Although the typical patient gives a history of with the doses is encephalitis and oculogyric crises followed by the development of parkin- oftheir basal gangliar "dopamine reserve" (in idiopathic Parkinson's disease reserve Those with sonism at a relatively young age, diagnosis is confounded on the one hand by 80% of dopamine is lost before clinical signs appear). may at increased risk of developing the fact that patients without a preceding history of oculogyric crises or drug induced parkinsonism be evidence for this is encephalitis have been described (one of the latter showing at necropsy the idiopathic Parkinson's disease later, but epidemiological classical sequelae ofencephalitis lethargica2) and on the other by the fact that lacking. recently many papers referred several patients with the changes ofidiopathic Parkinson's disease may give a Arteriosclerotic pseudoparkinsonismn-Until to as an Now, history of some unrelated encephalitic illness. Persisting signs ofpupillary or arteriosclerotic Parkinson's disease aetiological subgroup. to no part Parkinson's oculomotor disturbance or of associated dystonia and extremely slow however, cerebrovascular disease is recognised play in now progression of the disease may be useful clinical clues. The diagnostic disease and the condition is dubbed arteriosclerotic pseudoparkin- sonism. Most patients display neither classical rest tremor nor true akinesia and usually walk with an erect "military," albeit shuffling, gait (the term "marche a petit pas" was originally coined for these subjects). Those affected are most often elderly and hypertensive and may have other vascular risk factors, suffer additional dementia, and show lacunar infarcts in basal ganglia, larger multiple infarcts elsewhere, or extensive symmetrical white College School of Medicine and Dentistry, London SE5 9RS King's matter lucency ("Binswanger change") on computed tomography. Matters N P QUINN, MB, MRCP, lecturer in neurology are complicated by the fact that the infarcts may be too small to be F A HUSAIN, medical student demonstrable on computed tomography and also that idiopathic Parkinson's Correspondence to: Dr Quinn. disease and lacunar infarction are often associated since both conditions are common among the elderly. Only in the minority with coincidental 380 380 ~~~~~~~~~~~~~~BRITISHMEDICAL JOURNAL VOLUME 293 9 AUGUST 1986 Br Med J (Clin Res Ed): first published as 10.1136/bmj.293.6543.379 on 9 August 1986. Downloaded from ;., :-,. .,. '. .. -1 .. I Potralt-anorrity Akitn '?. " , I U-' Two .out of four -signs present 7t.. EMMF. Takig neurolept.ic, A .- .,. Per-sistn perkftisoniijm aftr'6-'months with,nio Yet drug ttreatment.e r 4p~ ~~~Ye No1 Positive faily -history ? >.OA* POSTENCEPI{ALITIC Yes PAR KiCNONDS .DRUG.INDUCIPARKj'JON SD Conside nderlying * 7 e~meni X demeibtift :I NoO http://www.bmj.com/ drijO Wittm*.Airad* Sornpbrgzeply vi Md~~~~~~~~~~~~~~N~~~~~~~~~~~7 0 Tretmen Persists after~~~~~~~~~~~~~~~i drug withdrawal? dF(I~~~~r& L'IbyoddptWn' N o ,.',., .. Y es~~~~~~~~~~~~~~~~~~~3 on 26 September 2021 by guest. Protected copyright. -ffi. N . I'- .'. -1 ~~~~~~~~~~~~~~~~~~~~~~~~~~~f'' O- .. I, . ..:. -.. 4. I Symtv ai osuiyes .u- . ..:' hypot~~~~~0nsloiiwtho No *5%mwoprmpnton ..l. ..-- .. a.- :,.. OWIN G .* ,. adequfl4 iopamine -I., * .34. RI~NSO!, DSEASE . '5,, --l NoLewy bodies found. -at ner o .: .., .. I BRITISH MEDICAL JOURNAL VOLUME 293 9 AUGUST 1986 381 Br Med J (Clin Res Ed): first published as 10.1136/bmj.293.6543.379 on 9 August 1986. Downloaded from Parkinson's disease I lm~ o http://www.bmj.com/ on 26 September 2021 by guest. Protected copyright. 0 0* d.0 0 Indicates that these features, while not characteristic of * - .- idiopathic Parkinson's disease, may nevertheless be present in some cases 382 BRITISH MEDICAL JOURNAL VOLUME 293 9 AUGUST 1986 Br Med J (Clin Res Ed): first published as 10.1136/bmj.293.6543.379
Load more

Recommended publications
  • Level Diagnosis of Cervical Compressive Myelopathy: Signs, Symptoms, and Lesions Levels
    Elmer Press Original Article J Neurol Res • 2013;3(5):135-141 Level Diagnosis of Cervical Compressive Myelopathy: Signs, Symptoms, and Lesions Levels Naoki Kasahata ficult to accurately localize the lesion before radiographic Abstract diagnosis. However, neurological level diagnosis of spinal cord is important for accurate lesion-specific level diagnosis, Background: To elucidate signs and symptoms corresponding to patients’ treatment, avoiding diagnostic error, differential di- each vertebral level for level-specific diagnoses. agnosis, and especially for accurate level diagnosis of other nonsurgical myelopathies. Moreover, level diagnosis should Methods: We studied 106 patients with cervical compressive my- be considered from multiple viewpoints. Therefore, we in- elopathy. Patients who showed a single compressive site on mag- tend to make level diagnosis of myelopathy more accurate. netic resonance imaging (MRI) were selected, and signs, symp- Previously, lesion-specific level diagnoses by determin- toms, and the levels of the MRI lesions were studied. ing a sensory disturbance area or location of numbness in Results: Five of 12 patients (41.7%) with C4-5 intervertebral level the hands had the highest accuracy [1, 2]. Previous stud- lesions showed decreased or absent biceps and brachioradialis re- ies reported that C3-4 intervertebral level lesions showed flexes, while 4 of these patients (33.3%) showed generalized hyper- increased or decreased biceps reflexes, deltoid weakness, reflexia. In comparison, 5 of 24 patients (20.8%) with C5-6 inter- and sensory disturbance of arms or forearms [1, 3, 4], while vertebral level lesions showed decreased or absent triceps reflexes; C4-5 intervertebral level lesions showed decreased biceps however, 9 of these patients (37.5%) showed decreased or absent reflexes, biceps weakness, and sensory disturbance of hands biceps and brachioradialis reflexes.
    [Show full text]
  • Clinical Assessment
    ID Canadian Study of Health and Aging - 3 CLINICAL ASSESSMENT CONSENSUS DIAGNOSTIC OPINION English: 1 To reach 'Part 1 - Final Diagnosis' the following are reviewed: Screening Questionnaire Informant or Caregiver Interview Clinical Assessment, Section 1: Clinician's Evaluation Clinical Assessment, Section 2: Clinician's Preliminary Diagnostic Opinion Neuropsychological Assessment, including Score Sheets and Evaluation Complete 1 Incomplete 2 YES NO Edited 1 2 Editor's # www.csha.ca C-i CONSENSUS DIAGNOSTIC OPINION ID Date of consensus conference / / dd mm yyyy NOTE: Circle only one of the diagnostic categories A to F. Fill in more detail where appropriate. Diagnoses must be made. Confidence in the diagnoses can be recorded for each diagnosis. PART 1 FINAL DIAGNOSIS 1 A. No cognitive impairment B1. Cognitive impairment but no dementia (CIND) (circle one or more of the subcategories below) 1 delirium 6 age-associated memory impairment 15 epilepsy 2 chronic alcohol abuse 7 mental retardation 16 socio-cultural 3 chronic drug intoxication 10 cerebral vascular, stroke 17 social isolation 4 depression 11 general vascular 18 blind/deaf 5 psychiatric disease 12 Parkinson's disease 19 unknown (other than depression) 13 brain tumour 8 other, specify: 14 multiple sclerosis B2. Specify most important of those listed in B.1 C. Alzheimer's Disease (circle only one of 1 or 2): 1 probable 2 possible (circle only one of 2.1 to 2.4): 2.1 atypical presentation/course (e.g. major aphasia, apraxia) specify: 2.2 with vascular components 2.3 with Parkinsonism (EP signs) 2.4 with coexisting disease D. Vascular dementia [ischemic score ] (circle only one of 1 to 4) 1 of acute onset 2 multiple cortical infarct 3 subcortical 4 mixed cortical and subcortical E.
    [Show full text]
  • MW S Rationales Files/Brain Rationale.Pdf
    A RATIONALE FOR THE BRAIN A RATIONALE FOR the BRAIN Assoc. Prof. Warwick Carter MB.BS; FRACGP; FAMA A guide to the diagnosis of diseases that may cause neurological symptoms. 1 A RATIONALE FOR THE BRAIN CONTENTS Introduction SECTION ONE Headache Diagnostic Chart A chart that leads the user through the headache symptoms to possible diagnoses. SECTION TWO Diagnostic Algorithm for Neurological Symptoms Symptoms involving the brain and the conditions that may be responsible SECTION THREE Neurological Conditions The symptoms, signs, investigation and treatment of medical conditions that may cause neurological symptoms. Appendices Mini-Mental Test Glasgow Coma Scale 2 A RATIONALE FOR THE BRAIN INTRODUCTION This book is designed for both the medical student and the doctor who is not a specialist in neurology. It will take the user through a logical rationale in order to diagnose, and then treat, virtually every neurological condition likely to be encountered outside a specialist practice. There are two ways to reach a diagnosis, using the chart in Section One, or the Diagnostic Algorithms in Section Two. In Section One, the chart will guide the user through headcahe symptoms to a selection of possible diagnoses. In Section Two the algorithms will indicate the diagnoses possible with a variety of neurological presenting symptoms. Once a diagnosis has, or number of differential diagnoses have been made, a detailed explanation of the various diagnoses can be found in the largest part of the book, Section Three. This has been written in a style that should be easy to understand by even junior medical students, with technical terms explained in each monograph, but should still be useful to the non-specialist doctor.
    [Show full text]
  • เวชศาสตร์ฟื้นฟูทันสมัยในผู้ป่วยพาร์กินสัน 103 March-April 2010
    บทความพเศษิ Chula Med J Vol. 54 No. 2 March - April 2010 เวชศาสตรฟ์ นฟ้ื ทู นสมั ยในผั ปู้ วยพาร่ ก์ นสิ นั อารรี ตนั ์ สพุ ทธุ ธาดาิ * Suputtitada A. Up-to-date rehabilitation in Parkinson’s patients. Chula Med J 2010 Mar - Apr; 54(2): 101 - 10 Parkinson’s disease is a degenerative brain disease. The dopamine producing cells in substantia nigra of basal ganglia are progressively degenerate. This causes patients unable to control their movements. Symptoms usually show up with bradykinesia, or slowness of movement and one or more of three following symptoms: (1) tremor, or trembling in hands, arms, legs, jaw, and face, (2) rigidity, or stiffness of limbs and trunk (3) postural instability. In addition, abnormal autonomic nervous system, pain sensation, swallowing, bowel and bladder, sexual, emotion can present. At present, research and clinical evidences reveal that rehabilitation treatment can help the patients improve walking and movement abilities, have better balance, decrease fall risk, increase activities of daily living, and improve quality of life. Keywords: Parkinson’s disease, Walk, Balance, Rehabilitation. Reprint request: Suputtitada A. Department of Rehabilitation Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. Received for publication. September 15, 2009. *ภาควิชาเวชศาสตร์ฟื้นฟ ู คณะแพทยศาสตร์ จุฬาลงกรณ์มหาวทยาลิ ยั 102 อารรี ตนั ์ สพุ ทธุ ธาดาิ Chula Med J อารรี ตนั ์ สพุ ทธุ ธาดาิ . เวชศาสตรฟ์ นฟ้ื ทู นสมั ยในผั ปู้ วยพาร่ ก์ นสิ นั . จฬาลงกรณุ เวชสาร์ 2553 ม.ี ค. - เม.ย.; 54(2): 101 - 10
    [Show full text]
  • Handbook on Clinical Neurology and Neurosurgery
    Alekseenko YU.V. HANDBOOK ON CLINICAL NEUROLOGY AND NEUROSURGERY FOR STUDENTS OF MEDICAL FACULTY Vitebsk - 2005 УДК 616.8+616.8-089(042.3/;4) ~ А 47 Алексеенко Ю.В. А47 Пособие по неврологии и нейрохирургии для студентов факуль­ тета подготовки иностранных граждан: пособие / составитель Ю.В. Алексеенко. - Витебск: ВГМ У, 2005,- 495 с. ISBN 985-466-119-9 Учебное пособие по неврологии и нейрохирургии подготовлено в соответствии с типовой учебной программой по неврологии и нейрохирургии для студентов лечебного факультетов медицинских университетов, утвержденной Министерством здравоохра­ нения Республики Беларусь в 1998 году В учебном пособии представлены ключевые разделы общей и частной клиниче­ ской неврологии, а также нейрохирургии, которые имеют большое значение в работе врачей общей медицинской практики и системе неотложной медицинской помощи: за­ болевания периферической нервной системы, нарушения мозгового кровообращения, инфекционно-воспалительные поражения нервной системы, эпилепсия и судорожные синдромы, демиелинизирующие и дегенеративные поражения нервной системы, опу­ холи головного мозга и черепно-мозговые повреждения. Учебное пособие предназначено для студентов медицинского университета и врачей-стажеров, проходящих подготовку по неврологии и нейрохирургии. if' \ * /’ L ^ ' i L " / УДК 616.8+616.8-089(042.3/.4) ББК 56.1я7 б.:: удгритний I ISBN 985-466-119-9 2 CONTENTS Abbreviations 4 Motor System and Movement Disorders 5 Motor Deficit 12 Movement (Extrapyramidal) Disorders 25 Ataxia 36 Sensory System and Disorders of Sensation
    [Show full text]
  • Medical Management of Parkinson's Disease
    3 Differential Diagnosis of Parkinsonism and Tremor Dr D Grosset Consultant Neurologist and Honorary Professor, Institute of Neurological Sciences, Queen Elizabeth University Hospital, Glasgow When Do Symptoms Develop? In PD, symptoms develop after the reserve capacity of dopaminergic neurones is exhausted. 18F- fluorodopa PET studies suggest that this probably occurs after at least 50% of dopaminergic neurones have degenerated, lower than previous estimates of 60 to 80%. However, enhanced synthesis of dopamine in surviving neurones (upregulation of striatal dopa decarboxylase activity) and increased dopaminergic stimulation of the striatum may underestimate the true proportion of cell loss. Symptoms may be present for some time (occasionally years) before the diagnosis is made, particularly in younger patients. Abnormalities in pre-synaptic dopamine turnover or dopamine transporter levels are detectable on functional imaging. Patients lose their sense of smell in the pre-clinical phase of PD. Olfactory dysfunction is found in 70- 80% of PD patients and is therefore as common as tremor, but loss of sense of smell occurs with aging and most hyposmic people do not get PD: Olfactory dysfunction also occurs in dementia with Lewy bodies Olfaction remains normal in PSP, corticobasal degeneration and vascular parkinsonism In MSA, spinocerebellar syndromes and essential tremor, any olfactory disturbance is mild Olfactory loss is usually not volunteered by the patient, who may only realise it once asked or with testing Olfactory loss tends not to occur in one of the genetic types of PD (Parkin). A higher rate of PD is reported in patients with essential tremor, and in families with essential tremor, but quantifying the relationship is difficult: Functional imaging studies suggests two separate entities As essential tremor is relatively common, is it inevitable that some patients with essential tremor will later develop PD Rarely, familial essential tremor occurs in conjunction with familial PD A subset of patients present temporally with ET and PD.
    [Show full text]
  • Dementia – Etiology and Epidemiology
    Dementia – Etiology and Epidemiology A Systematic Review Volume 1 June 2008 The Swedish Council on Technology Assessment in Health Care SBU • Statens beredning för medicinsk utvärdering SBU Evaluates Healthcare Technology SBU (the Swedish Council on Technology Assessment in Health Care) is a government agency that assesses the methods employed by medical professionals and institutions. In addition to analyzing the costs and benefits of various health care measures, the agency weighs Swedish clinical practice against the findings of medical research. The objective of SBU’s activities is to provide everyone who is involved in decisions about the conduct of health care with more complete and accurate information. We welcome you to visit our homepage on the Internet at www.sbu.se. SBU issues three series of reports. The first series, which appears in a yellow binding, presents assessments that have been carried out by the agency’s project groups. A lengthy summary, as well as a synopsis of measures proposed by the SBU Board of Directors and Scientific Advisory Committee, accompanies every assessment. Each report in the second, white-cover series focuses on current research in a parti- cular healthcare area for which assessments may be needed. The Alert Reports, the third series, focus on initial assessments of new healthcare measures. To order this report (No 172E/1) please contact: SBU Mailing Address: Box 5650, SE-114 86 Stockholm, Sweden Street Address: Tyrgatan 7 Tel: +46 8 412 32 00 Fax: +46 8 411 32 60 Internet: www.sbu.se E-mail: [email protected]
    [Show full text]
  • 395 ABCC6, 300 ABCD2 Score, 98 Abetaliproteinemia, 349 Abscess
    Cambridge University Press 978-0-521-86622-4 - Toole’s Cerebrovascular Disorders, Sixth Edition E. Steve Roach, Kerstin Bettermann and Jose Biller Index More information Index ABCC6, 300 AFO. See ankle-foot orthosis ANCA. See antineutrophilic cytoplasmic ABCD2 score, 98 age antibodies abetaliproteinemia, 349 CBF and, 204 ancrod, 364 abscess, 39, 304 hypoxia and, 71–72 Anderson-Fabry disease. See Fabry disease liver, 350 ischemia and, 71–72 anemia, 19, 111, 162, 164 abulia, 38 progeria, 302–303 aplastic, 163 ACA. See anterior cerebral artery subdural hematoma and, 275 Fanconi’s, 184, 306 ACAS. See Asymptomatic Carotid agenesis, 30 anesthesia, 66 Atherosclerosis Study AICA. See anterior inferior cerebellar artery anesthesia dolorosa, 51 ACE. See angiotensin converting enzyme AIDS. See acquired immune deficiency aneurysms, 238–247. See also specific types acetaminophen, 171 syndrome associated conditions with, 242–259 acetazolamide, 61 air embolism, 127, 128–129, 349 with AVM, 261 for moyamoya disease, 185 Alagille syndrome, 319 distribution of, 239–243 TCD and, 87 alcohol, 19 pregnancy and, 337 for venous thrombosis, 290 atherosclerosis and, 114 screening for, 249–250 acetylcholinesterase inhibitors, 212 dilated cardiomyopathy and, 121 TIA and, 100 Achilles tendon, 379 hypertension and, 139 unruptured, 252 achromatopsia, 51 subdural hematoma and, 276 vaginal delivery and, 338 acquired immune deficiency syndrome TIA and, 100 angiokeratoma corporis diffusum. See Fabry (AIDS), 322 alexia, 51 disease acquired thrombophilia, 336 alpa-amino-3-hydroxy-5-methyl-4-isoxazole
    [Show full text]
  • Freezing of Gait in Parkinson's Disease
    PDF hosted at the Radboud Repository of the Radboud University Nijmegen The following full text is a publisher's version. For additional information about this publication click this link. http://hdl.handle.net/2066/93606 Please be advised that this information was generated on 2021-10-05 and may be subject to change. Tackling freezing of gait in Parkinson’s disease freezing of gait in Parkinson’s Tackling Tackling freezing of gait in Parkinson’s disease Anke H. Snijders ANKE H. SNIJDERS ISBN 978-94-91027-33-8 90 Tackling freezing of gait in Parkinson’s disease Anke H. Snijders ‘like the wheels of a locomotive failing to bite the rails when they are slippery with frost and making, in consequence, ineffective revolutions’ William W describing his gait disorder, according to Thomas Buzzard, neurologist National Hospital Queen Square, London, 1882 The studies presented in this thesis were carried out at the Donders Institute for Brain, Cognition and Behaviour, Centre for Neuroscience and Centre for Cognitive Neuroimaging, Radboud University Medical Centre, Nijmegen, the Netherlands, with financial support of the Prinses Beatrix Fonds, the Radboud University Medical Centre and the Netherlands Organization for Scientific Research (NWO), grant numbers 92003490 (A.H.Snijders) and 016076352 (B.R.Bloem). Cover design and layout by: In Zicht Grafisch Ontwerp, Arnhem Printed by: Ipskamp Drukkers, Enschede DVD layout and production by: Mimumedia, Nijmegen ISBN: 978-94-91027-33-8 ©2012 A.H. Snijders Tackling freezing of gait in Parkinson’s disease Proefschrift ter verkrijging van de graad van doctor aan de Radboud Universiteit Nijmegen op gezag van de rector magnificus prof.
    [Show full text]
  • MW Secret Files/DC 2 Signs.Pdf
    Dr. Warwick Carter DOCTOR’S COMPANION Section Two - Signs SECTION TWO SIGNS Clinical Signs and their Interpretation SIGN: Objective evidence of disease or deformity Butterworths Medical Dictionary FORMAT Sign (Alternate Name) [Abbreviation] Exp: An explanation of the sign, with its methodology described in sufficient detail to enable the practitioner to perform the test. Int: The interpretation of the sign. (+) The diseases, syndromes etc. that should be considered if the test is positive (++) The interpretation of an exaggerated or grossly positive test (–) Ditto for a negative test result (AB) Ditto for an abnormal test result Phys: The pathophysiology of the sign to enable its significance to be better understood See also Other Signs of Significance Alternate Name See Sign Name © Warwick Carter Signs - 1 DOCTOR’S COMPANION Section Two - Signs EXAMINATION Abdominal Mass Exp: Palpation of an abnormal structure in or around the abdominal cavity Int: (+ Superficial) - Lipoma, sebaceous cyst, umbilical hernia, inguinal hernia, incisional hernia, post-traumatic scarring, rectus sheath haematoma, divarication of the recti (+ Deep) - Carcinoma of bowel or stomach, Crohn's disease, Hodgkin's disease, other lymphomas, metastatic carcinoma, appendiceal abscess, pancreatic tumour, aortic aneurysm, pregnancy, uterine fibroid or tumour, ovarian tumour or cyst, hydatid cyst, distended gall bladder, enlarged liver (see Hepatomegaly), enlarged spleen (see Splenomegaly), enlarged kidney (see Kidney, Large), pyloric stenosis, bladder carcinoma, vertebral
    [Show full text]
  • MW Secret Files/Medical Miscellany.Pdf
    Carter’s Medical Miscellany Carter’s MEDICAL MISCELLANY Dr. Warwick Carter MB.BS., FRACGP, FAMA Miscellany - noun - Separate articles or studies on a subject, or compositions of various kinds, collected into one volume. A literary work or production containing miscellaneous pieces on various subjects. (OED) 1 Carter’s Medical Miscellany These egregiously piquant peccadilloes of allopathic and homeopathic epistemology offer some chthonic edification extra mural to the canonical modes of the medical quidnunc. They are of inestimable significance to the virtuosity and animus of the therapist. These profoundly sagacious enunciations have been serendipitously gleaned from a wide amplitude of unerringly reliable provenances including my therial janizzaries. 2 Carter’s Medical Miscellany INTRODUCTION Doctors encounter some extraordinary and unusual facts during their training and careers, some of which are totally useless to the practice of medicine, but never the less interesting. This is a collection of just such information. This is not a dictionary, guide book, encyclopaedia or vademecum, just a miscellany of fascinating facts gleaned from a more than 30 year career in medicine, and the research necessary to write twenty other books that cover everything from postgraduate pathology texts to simple question and answer collections for lay people. In no way can the veracity of the facts within be vouched for, but to the best of my limited knowledge, they are true. As a result, no action should be taken on the basis of this information unless a doctor’s opinion is sought. This collection is designed primarily to intrigue, secondly to entertain, and rarely to educate. Please enjoy.
    [Show full text]
  • Examination of Gait
    PACES (CNS- Gait) Adel Hasanin Ahmed CNS - GAIT STEPS OF EXAMINATION Step 1: Approach the patient Read the instructions carefully for clues Shake hands, introduce yourself Ask few questions “Could you tell me your name please? Are you right- or left-handed? Are you quite comfortable? Do you feel pain anywhere?” Ask permission to examine him Step 2: General inspection: Bedside: walking stick, shoes-callipers, built-up heels General appearance: scan the patient quickly looking for: . Nutritional status (under/average built or overweight) . Abnormal movement or posture (rest or intention tremors, dystonia, choreoathetosis, hemiballismus, Myoclonic jerks, tics, pyramidal posture) . Abnormal facial movements (hemifacial spasm, facial myokymia, blepharospasm, oro-facial dyskinesia) . Facial asymmetry (hemiplegia) . Nystagmus (cerebellar syndrome) . Facial wasting (muscular dystrophy) . Sad, immobile, unblinking facies (Parkinson’s disease) . Peroneal wasting (Charcot-Marie-Tooth disease) . Pes cavus (Friedreich’s ataxia, Charcot-Marie-Tooth disease) Hands: tell the patient “outstretch your hands like this (palms facing downwards)”… then “like this (palms facing upwards)” . Check for wasted hands (MND, Charcot-Marie-Tooth disease, syringomyelia) . feel the radial pulse (AF → thromboembolism) Step 3: Ask the patient “Can you walk without help? I will stay with you in case of any problems”. Notice any cerebellar dysarthria during his reply. Step 4: Ask him to walk to a defined point, turn and walk back. Look at the patient from behind,
    [Show full text]