DOCSLIB.ORG

Neurological Board Examination 2010 09 25 B-Type: for Each Numbered

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Neurological Board Examination 2010 09 25 B-Type: for Each Numbered Neurological Board Examination 2010 09 25 B-type: For each numbered item, select the heading most closely associated with it. Each heading may be selected once, more than once, or not at all Part 1 (1-4) Please match the term below: ( ) 1 Progressive supranuclear palsy ( ) 2 Dementia with Lewy body ( ) 3 Creutzfeldt-Jakob disease (CJD) ( ) 4 ALS with dementia A. Prionopathy B. β-Amyloidopathy C.α-synucleinopthy D. Tauopathy E. TDP-43 proteinopathy 解答：( D ) ( C ) ( A ) (E ) 題目之出處：Merritt’s Neurology, 12th edition, P710-722 題目屬性：Degenerative, genetic disease and pediatric neurology 題目難易：中 Part 2 (5-8) What is the specific neurological manifestation in heavy metal intoxication? ( ) 5 Lead ( ) 6 Manganese ( ) 7 Mercury ( ) 8 Aluminum A. Parkinsonism B. Tremor C. Radial palsy D. myelopathy E. Dementia 解答：( C ) (A ) ( B ) ( E ) 題目之出處：Merritt’s Textbook of Neurology 12th Edition 2010 p. 1093-1096 1 題目屬性：Metabolic & toxic disease, 題目難易：中等 Part 3 (9-12) Polyneuropathy type and its clinical/electrophysiologic pattern ( ) 9 Porphyria ( ) 10 Vasculitis ( ) 11 Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) ( ) 12 Organophosphate toxicity A. Sensorimotor, axonal, acute B. Sensorimotor, axonal, subacute or chronic C. Predominantly motor axonal, acute D. Predominantly motor axonal, subacute or chronic E. Sensory only, axonal 解答：( C ) ( A ) ( E ) ( B ) 題目之出處：Office Practice of Neurology, 2th, p571 題目屬性：Metabolic & toxic disease, 題目難易：中等 Part 4 (13-16) Myopathic syndrome and corresponding drug or toxin ( ) 13 Necrotizing myopathy ( ) 14 Hypokalemic myopathy ( ) 15 Antimicrotubular myopathy ( ) 16 Mitochondrial myopathy A. Licorice B. Zidovudine C. Statin drug D. Colchicine E. D-Penicilamine 解答：( C ) ( A ) ( D ) ( B ) 題目之出處： Principles of Neurology 9th 2009, p1394, table 51-2 題目屬性：Metabolic & toxic disease, 題目難易：中等 Part 5 (17-20) Please match the agent and its related clinical manifestation. ( ) 17 Carbon disulfide ( ) 18 Thallium ( ) 19 n-Hexane ( ) 20 Lead A. Giant axonal swellings B. Sacral sensory loss C. Parkinsonism D. Wrist drop E. Dysesthesia with alopecia 解答：(C) (E) (A) (D) 題目之出處：Neurology in Clinical Practice5th Edition, p. 1658-1662 題目屬性：Metabolic & toxic disease, 題目難易：易 Part 6 (21-24) About nutrition deficiency or toxicity: ( ) 21 Pellagra ( ) 22 Pseudotumor cerebri ( ) 23 A-ß lipoproteinemia ( ) 24 Wernike-Korsakoff syndrome A. Vitamin A B. Vitamin B1 C. Vitamin B6 D. Vitamin E E. Niacin 解答：( E ) ( A ) ( D ) (B ) 題目之出處：Merritt’s 12th p1035~1049 題目屬性：Metabolic & toxic disease, 題目難易：中 Part 7 (25-28) Select the appropriate term to match each disease ( ) 25 Lewy body dementia 3 ( ) 26 Cortical-basal ganglionic degeneration ( ) 27 Parkinsonism-dementia-ALS ( ) 28 Wilson’s disease A. Guamanian B. Eye-of-the-tigger signs C. Alien limb phenomena D. Formed visual hallucinations E. Kayser-Fleischer ring 解答：( D ) ( C ) ( A ) ( E ) 題目之出處：Merritt’s Neurology 12th p721, 773-774, 657 題目屬性：Movement disorder, 題目難易：中等 Part 8 (29-32) Side effects of anti-parkinsonian agents ( ) 29 Livedo reticularis ( ) 30 Fibrotic valvulopathy ( ) 31 Forgetfulness and psychosis ( ) 32 Impulse control problem A. Amantadine B. Anti-cholinergic drug C. Dopamine agonist D. Levodopa 解答：( A ) ( C ) ( B ) ( C ) 題目之出處：Merritt’s Neurology, twelfth edition, p. 761-763 題目屬性：Movement disorder, 題目難易：易 Part 9 (33-36) Please choose medication for involuntary movement disorders. ( ) 33 Segawa disease ( ) 34 Rapid-onset Dystonia-Parkinsonism ( ) 35 Paroxysmal kinesigenic dyskinesias ( ) 36 Paroxysmal nonkinesigenic dyskinesias A. Beta-Blockers B. Anti-convulsants C. Levodopa D. Clonazepam, benzodiazepins, acetazolamide, antimuscarinics E. No effect treatment 解答：(C ) (E ) (B ) (D ) 題目之出處：Merritt's Neurology 12th edition, p. 743,775 題目屬性：Movement disorder, 題目難易：中等 Part 10 (37-40) The side effects of medications used to treat neuropathic pain ( ) 37 Amitriptyline (TCA) ( ) 38 Venlafaxine (SNRI) ( ) 39 Gabapentine ( ) 40 Tramadol A. Hypertension, sexual dysfunction B. Arrhythmia, urinary retention C. Seizure, nausea, constipation D. Steven-Johnson rash E. Pedal edema, Somnolence 解答：( B ) ( A ) ( E ) ( C ) 題目之：Merritt’s Neurol0gy 12 edition P842 Table 135.1 題目屬性：Miscellaneous, 題目難易：中等 Part 11 (41-44) Match the adverse effects with medications used to treat neuropathic pain. ( ) 41 Amitriptyline ( ) 42 Gabapentin ( ) 43 Topiramate ( ) 44 Lidocaine patch A. Kidney stone B. Application site reactions. C. Pedal edema 5 D. Urinary retention E. Diarrhea 解答：( D ) ( C ) ( A ) ( B ) 題目之出處：Merritt’s Neurology 12th edition, p 842 題目屬性：Headache & pain, 題目難易：易 Part 12 (45-48) Predominant mechanism of the drugs for treating neuropathic pain ( ) 45 Amitriptyline ( ) 46 Carbamazepine ( ) 47 Gabapentin ( ) 48 Lamotrigine A. Blocking voltage-gated sodium channels B. Blocking voltage-gated sodium and calcium channels C. Balanced monoamine reuptake inhibitor D. Binding to voltage-dependent calcium channels E. Pre-synaptically blocking sodium channels and inhibiting release of glutamate 解答：(C ) (A ) (D ) (E ) 題目之出處：Neurology in Clinical Practice 5th, p2260 題目屬性：Headache & pain, 題目難易：難 Part 13 (49-52) Which is the MOST proper description for each headache: ( ) 49 Unilateral lacrimation and rhinorrhea ( ) 50 Plasma interleukin-6 (IL-6) measurement may be the marker of disease activity ( ) 51 Meningeal enhancement on MRI ( ) 52 The progression of headache for weeks or months A. Spontaneous intracranial hypotension B. Brain tumor headache C. Cluster headache D. Giant cell arteritis 解答：( C )( D )( A )( B ) 題目之出處：Merritt’s Neurology, 12th edition, p.959 題目屬性：Headache & pain, 題目難易：易 Part 14 (53-56) Match the headache type and its lasting time ( ) 53 Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing SUNCT ( ) 54 Cluster headache ( ) 55 Tension type headache ( ) 56 Migraine without aura A. 15~180 minutes B. 2 ~ 30 minutes C. 30 minutes~7 days D. 4~72 hours E. 5~240 seconds 解答：( E ) ( A ) ( C ) ( D ) 題目之出處：ICHD-2 2004 題目屬性：Headache & pain, 題目難易：中等 Part 15 (57-60) Gait. ( ) 57 Muscular dystrophy ( ) 58 Unilateral cerebellar hemisphere lesion ( ) 59 Normal pressure hydrocephalus ( ) 60 Hereditary spastic paraplegia A. Ataxic gait and deviation to the lesion side B. Steppage gait C. Waddling gait D. Apraxic gait E. Scissor gait 解答：( C ) ( A ) ( D ) ( E ) 題目之出處：Merritt’s neurology, 12th edition (p. 58~61) 題目屬性：Laboratory & NE, 題目難易：易 Part 16 (61-64) Localization ( ) 61 Word deafness (auditory verbal agnosia) ( ) 62 Dysnomia or amnesic aphasia ( ) 63 Asomatognosia ( ) 64 Achromatopsia 7 A. frontal lobe B. left temporal lobe C. parietal lobe D. occipital lobe E. non-dominant temporal lobe 解答：( B ) ( B ) ( C ) ( D ) 題目之出處：Adams 9ed, p443-456 題目屬性：Laboratory & NE, 題目難易：中等 Part 17 (65-68) ( ) 65 Symptom suggestive of carotid transient ischemic attacks ( ) 66 Symptom suggestive of vertebrobasilar transient ischemic attacks ( ) 67 Symptom suggestive of bilateral ACA-MCA watershed infarction ( ) 68 Symptom suggestive of anterior thalamic infarction A. Binocular vision loss B. Amaurosis fugax C. Neuropsychiatrical disturbances D. Man-in-a-barrel 解答：( B ) ( A ) ( D ) ( C ) 題目之出處：Neurology in Clinical Practice 5th, p1171, 1177,1178 題目屬性：Stroke, 題目難易：中等 Part 18 (69-72) ( ) 69 Hypsarrhythmia ( ) 70 Slow generalized spike and wave (< 2 cps) ( ) 71 Focal centrotemporal epileptiform discharge ( ) 72 Generalized polyspike wave (often >3 cps) A. Absence seizure B. Benign rolandic epilepsy C. Juvenile myoclonic epilepsy D. Lennox-Gastuat syndrome E. West syndrome 解答：( E ) ( D ) ( B ) ( C ) 題目之出處：From Merritt’s 12th Chapter 15 p 77 題目屬性：Epilepsy, 題目難易：易 Part 19 (73-76) The adverse effects of antiepileptic drugs ( ) 73 Phenytoin. ( ) 74 Valproic acid. ( ) 75 Carbamazepine. ( ) 76 Topiramate. A. Impotence B. Acute pancreatitis C. Cognitive dysfunction D. Hyponatremia E. Megaloblastic anemia 解答：( E ) ( B ) ( D ) ( C ) 題目之出處：Adams, 8th ed, p.295 題目屬性：Epilepsy, 題目難易：易 Part 20 (77-80) The pharmacological mechanism of the following antiepileptic drugs ( ) 77 Oxcarbazepine ( ) 78 Vigabatrin ( ) 79 Tiagabin ( ) 80 Ethosuximide A. Blocking voltage-gated calcium channel B. Enhancing release of GABA C. Decreasing GABA reuptake D. Inhibition of GABA transaminase E. Blocking voltage-gated sodium channel 解答：(E) (D) (C) (A) 題目之出處：Neurology in Clinical Practice P.1935-1942 題目屬性：Epilepsy, 題目難易：中等 9 .
Load more

Recommended publications
  • Categorization of Functional Impairments in Human Locomotion
    University of Texas at El Paso DigitalCommons@UTEP Open Access Theses & Dissertations 2010-01-01 Categorization of Functional Impairments in Human Locomotion using the Methods of the Fusion of Multiple Sensors and Computational Intelligence Huiying Yu University of Texas at El Paso, [email protected] Follow this and additional works at: https://digitalcommons.utep.edu/open_etd Part of the Biomedical Commons, and the Electrical and Electronics Commons Recommended Citation Yu, Huiying, "Categorization of Functional Impairments in Human Locomotion using the Methods of the Fusion of Multiple Sensors and Computational Intelligence" (2010). Open Access Theses & Dissertations. 2814. https://digitalcommons.utep.edu/open_etd/2814 This is brought to you for free and open access by DigitalCommons@UTEP. It has been accepted for inclusion in Open Access Theses & Dissertations by an authorized administrator of DigitalCommons@UTEP. For more information, please contact [email protected]. CATEGORIZATION OF FUNCTIONAL IMPAIRMENTS IN HUMAN LOCOMOTION USING THE METHODS OF THE FUSION OF MULTIPLE SENSORS AND COMPUTATIONAL INTELLIGENCE HUIYING YU Department of Electrical and Computer Engineering APPROVED: ________________________________ Thompson Sarkodie-Gyan, Ph.D., Chair ________________________________ Scott Starks, Ph.D. ________________________________ Richard Brower, M.D. ________________________________ Bill Tseng, Ph.D. ________________________________ Eric Spier, M.D. __________________________________ Patricia D. Witherspoon, Ph.D. Dean of the Graduate
    [Show full text]
  • Neurological History and Physical Examination
    emedicine.medscape.com eMedicine Specialties > Clinical Procedures > none Neurological History and Physical Examination Kalarickal J Oommen, MD, FAAN, Professor and Crofoot Chair of Epilepsy, Department of Neurology, Chief, Section of Epilepsy, Texas Tech University Health Sciences Center; Medical Director, Texas Tech University Health Sciences Center (TTUHSC) Covenant Comprehensive Epilepsy Center Updated: Nov 25, 2009 Neurological History "From the brain and the brain only arise our pleasures, joys, laughter and jests, as well as our sorrows, pains, griefs, and tears.... These things we suffer all come from the brain, when it is not healthy, but becomes abnormally hot, cold, moist or dry." —Hippocrates The Sacred Disease, Section XVII Taking the patient's history is traditionally the first step in virtually every clinical encounter. A thorough neurologic history allows the clinician to define the patient's problem and, along with the result of physical examination, assists in formulating an etiologic and/or pathologic diagnosis in most cases.[1 ] Solid knowledge of the basic principles of the various disease processes is essential for obtaining a good history. As Goethe stated, "The eyes see what the mind knows." To this end, the reader is referred to the literature about the natural history of diseases. The purpose of this article is to highlight the process of the examination rather than to provide details about the clinical and pathologic features of specific diseases. The history of the presenting illness or chief complaint should
    [Show full text]
  • Equinus Deformity in the Pediatric Patient: Causes, Evaluation, and Management
    Equinus Deformity in the Pediatric Patient: Causes, Evaluation, and Management a,b,c Monique C. Gourdine-Shaw, DPM, LCDR, MSC, USN , c, c Bradley M. Lamm, DPM *, John E. Herzenberg, MD, FRCSC , d,e Anil Bhave, PT KEYWORDS Equinus Pediatric External fixation Achilles tendon lengthening Gastrocnemius recession Tendo-Achillis lengthening Different body and limb segments grow at different rates, inducing varying muscle tensions during growth.1 In addition, boys and girls grow at different rates.1 The rate of growth for girls spikes at ages 5, 7, 10, and 13 years.1 The estrogen-induced pubertal growth spurt in girls is one of the earliest manifestations of puberty. Growth of the legs and feet accelerates first, so that many girls have longer legs in proportion to their torso during the first year of puberty. The overall rate of growth tends to reach a peak velocity (as much as 7.5 to 10 cm) midway between thelarche and menarche and declines by the time menarche occurs.1 In the 2 years after menarche, most girls grow approximately 5 cm before growth ceases at maximal adult height.1 The rate of growth for boys spikes at ages 6, 11, and 14 years.1 Compared with girls’ early growth spurt, growth accelerates more slowly in boys and lasts longer, resulting in taller adult stature among men than women (on average, approximately 10 cm).1 The difference is attributed to the much greater potency of estradiol compared with testosterone in Two authors (BML and JEH) host an international teaching conference supported by Smith & Nephew.
    [Show full text]
  • Conversive Gait Disorder: You Cannot Miss This Diagnosis
    DOI: 10.1590/0004-282X20140022 ARTICLE Conversive gait disorder: you cannot miss this diagnosis Distúrbio conversivo da marcha: você não pode deixar de fazer esse diagnóstico Péricles Maranhão-Filho1,2, Carlos Eduardo da Rocha e Silva3, Maurice Borges Vincent1 ABSTRACT Bizarre, purposeless movements and inconsistent findings are typical of conversive gaits. The objective of the present paper is to review some phenomenological aspects of twenty-five consecutive conversive gait disorder patients. Some variants are typical – knees give way-and-recover presentation, monoparetic, tremulous, and slow motion – allowing clinical diagnosis with high precision. Keywords: somatic symptom, conversive gait, neurological examination. RESUMO Movimentos bizarros, sem finalidade e inconsistentes são típicos das marchas conversivas. O objetivo deste artigo é descrever os aspectos fenomenológicos de vinte e cinco pacientes com distúrbio conversivo da marcha, salientando que algumas variantes são tão típicas – dobrando os joelhos e recuperando, monoparética, trêmula e em câmara lenta – que praticamente não possuem diagnóstico diferencial. Palavras-chave: sintoma somático, marcha conversiva, exame neurológico. The neurological examination as we know today, disorders”, which replaced the previous so-called “somato- emerged by the end of the 19th century, when signs that form disorders”9. would trustfully discriminate weakness due to structural The cases presented herein suggest that objective land- damage from hysteria became crucial1. Conversion disorder, marks do provide the neurologist with sturdy evidence for which may affect 11-300/100,000 individuals, remains a trustworthy conversive gait diagnosis. largely underdiagnosed, partially because its mechanisms are still unknown2,3. Conversive gait disorders correspond to approximately 3% (0-7%) of the movements’ disorders METHOD in specialized centres4,5.
    [Show full text]
  • OUTPATIENT PHYSICAL THERAPY for a TODDLER with CEREBRAL PALSY PRESENTING with DEVELOPMENTAL DELAYS a Doctoral Project a Comprehe
    OUTPATIENT PHYSICAL THERAPY FOR A TODDLER WITH CEREBRAL PALSY PRESENTING WITH DEVELOPMENTAL DELAYS A Doctoral Project A Comprehensive Case Analysis Presented to the faculty of the Department of Physical Therapy California State University, Sacramento Submitted in partial satisfaction of the requirements for the degree of DOCTOR OF PHYSICAL THERAPY by Amy K. Holthaus SUMMER 2015 © 2015 Amy K. Holthaus ALL RIGHTS RESERVED ii OUTPATIENT PHYSICAL THERAPY FOR A TODDLER WITH CEREBRAL PALSY PRESENTING WITH DEVELOPMENTAL DELAYS A Doctoral Project by Amy K. Holthaus Approved by: __________________________________, Committee Chair Katrin Mattern-Baxter, PT, DPT, PCS __________________________________, First Reader Brad Stockert, PT, PhD __________________________________, Second Reader Edward Barakatt, PT, PhD ____________________________ Date iii Student: Amy K. Holthaus I certify that this student has met the requirements for format contained in the University format manual, and that this project is suitable for shelving in the Library and credit is to be awarded for the project. __________________________________, Department Chair ____________ Edward Barakatt, PT, PhD Date Department of Physical Therapy iv Abstract of OUTPATIENT PHYSICAL THERAPY FOR A TODDLER WITH CEREBRAL PALSY PRESENTING WITH DEVELOPMENTAL DELAYS by Amy K. Holthaus A pediatric patient with cerebral palsy was seen for physical therapy treatment provided by a student for ten sessions from February 2014 to May 2014 at a university setting under the supervision of a licensed physical therapist. The patient was evaluated at the initial encounter with Gross Motor Function Measurement-66, Peabody Developmental Motor Scale-2 and Pediatric Evaluation of Disability Inventory, and a plan of care was established. Main goals for the patient were to improve development motor functions through increasing independent ambulation, functional balance and strength.
    [Show full text]
  • Gait Abnormalities in Functional Problems of the Lower Extremities and in Neurological Diseases
    48 Review articles GAIT ABNORMALITIES IN FUNCTIONAL PROBLEMS OF THE LOWER EXTREMITIES AND IN NEUROLOGICAL DISEASES M. Becheva, PhD Medical University- Plovdiv, Medical College, Bulgaria, 120Buxton Bros. 4004 Plovdiv Abstract: Gait is a complex, automated and stereotyped motor activity that allows for movement of the body in an upright position. The investigation of gait is an integral part of the pathokinesiological study of the functional problems in any of the segments of the lower limbs. As the stereotype of walking changes at departure, stopping, turning, walking alongside another one, gait should be examined in different situations. In functional problems of the lower limbs and in some neurological diseases, the follow- ing abnormal gaits are detected: arthrogenic gait in extensional contractures of the hip or knee, walking in flexion contractures, "Gluteus maximus" gait, "Gluteus medius"gait, ataxic gait, hemiparetic (hemiplegic) gait, gait in parkinsonism, gait in paresis of plantar flexor, lameness in spasm of m. psoas major, gait in insufficiency of m. quadriceps femo- ris, gait in shortening of a lower limb, steppage gait and scissor gait. Adjusting abnormal gait is especially important to improve the functional condition of the patients in view of procuring a better quality of life. Keywords: abnormal gait, functional problems, neurological diseases. Introduction ground and allows the body to move forward. Gait is a complex stereotyped and auto- Gait is a conscious and volitional motor activity mated motor activity, which allows for move- [3]. ment of the body in an upright position. It 3. A complex coordination action during consists of several components: body movements, to maintain the center of grav- 1.
    [Show full text]
  • Oculodentodigital Dysplasia Presenting As Spastic Paraparesis: the First Genetically Confirmed Korean Case and a Literature Review
    JMD https://doi.org/10.14802/jmd.17050 / J Mov Disord 2017;10(3):149-153 pISSN 2005-940X / eISSN 2093-4939 CASE REPORT Oculodentodigital Dysplasia Presenting as Spastic Paraparesis: The First Genetically Confirmed Korean Case and a Literature Review Kye Won Park,1 Ho-Sung Ryu,1 Juyeon Kim,2 Sun Ju Chung1 1Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea 2Department of Neurology, Metro Hospital, Anyang, Korea ABSTRACT Oculodentodigital dysplasia (ODDD) is a rare autosomal dominant inherited disease caused by mutations of the human gap junction alpha 1 gene, which encodes the protein Connexin-43. Patients with ODDD may present with neurological deficits with a typical pleiotropic combination of characteristic craniofacial, ophthalmological, phalangeal, and dental anomalies. In this report, we describe the first genetically confirmed Korean ODDD patient, who presented with spastic paraparesis. We will also review the neurological aspects of ODDD as reported in the literature. Key Wordsaa Oculodentodigital dysplasia; gap junction alpha 1; Connexin-43. Oculodentodigital dysplasia (ODDD, OMIM #164200) is a She began to feel stiffness in her legs in her mid-30s. She also rare autosomal dominant inherited disorder. ODDD is caused suffered from urinary frequency and incomplete voiding of by the mutation of the human gap junction alpha 1 (GJA1) gene, urine. These symptoms worsened over the following five years. which encodes the protein, Connexin-43 (Cx43).1 ODDD pa- Her father had suffered intracerebral hemorrhage 2 years prior tients present with heterogeneous phenotypic combinations of but did not manifest with any gait problems. She was married craniofacial, ophthalmological, phalangeal, dental, and neuro- and had two children, but none of her siblings, children, or neph- logical symptoms.1-4 Neurological manifestations have been re- ews had a gait problem (Figure 1A).
    [Show full text]
  • Habitual Toe Walking
    MedicalContinuing Education CLINICAL PODIATRY Objectives HabitualHabitual ToeToe After reading this article the pod- iatric physician should be able to: WWalkingalking 1) Recognize a pediatric patient that exhibits habitual toe walking 2) Take a proper medical and family history of a child suspected of toe walking 3) Understand other medical conditions that may cause a child to toe walk 4) Perform an appropriate phys- ical examination to rule out non idiopathic toe walking etiologies Learn to evaluate and treat this idiopathic 5) Develop a treatment plan for a child that is determined to be a childhood condition. habitual (idiopathic) toe walker Welcome to Podiatry Management’s CME Instructional program. Our journal has been approved as a sponsor of Continu- ing Medical Education by the Council on Podiatric Medical Education. You may enroll: 1) on a per issue basis (at $15 per topic) or 2) per year, for the special introductory rate of $99 (you save $51). You may submit the answer sheet, along with the other information requested, via mail, fax, or phone. In the near future, you may be able to submit via the Internet. If you correctly answer seventy (70%) of the questions correctly, you will receive a certificate attesting to your earned credits. You will also receive a record of any incorrectly answered questions. If you score less than 70%, you can retake the test at no additional cost. A list of states currently honoring CPME approved credits is listed on pg. 176. Other than those entities currently accepting CPME-approved credit, Podiatry Management cannot guarantee that these CME credits will be acceptable by any state licensing agency, hospital, man- aged care organization or other entity.
    [Show full text]
  • Spastic Cerebral Palsy
    Spastic Cerebral Palsy What is Spastic Cerebral Palsy? Spastic cerebral palsy is a subtype of cerebral palsy characterized by stiffness in the muscles and overall difficulty in bodily movements. It is a type of hypertonia, or increased muscle tone. Spastic cerebral palsy is the most common form of cerebral palsy, accounting for about 75% of cases (those including spastic CP and mixed CP). Causes of Spastic Cerebral Palsy Spastic cerebral palsy is often caused by a birth injury that affects the part of the motor cortex (the part of the brain involved in planning, control, and execution of movement). A birth injury may take the form of an injury to the developing brain before, during, or after birth. For many babies, cerebral palsy is caused by: Hypoxic-ischemic encephalopathy (HIE) or another oxygen-depriving birth injury Maternal infection that travels from mother to baby at birth, causing meningitis or sepsis Brain hemorrhage at birth caused by traumatic or prolonged labor or the use of vacuum extractors or forceps during delivery Spastic Cerebral Palsy | 1 Spastic Cerebral Palsy Spastic Cerebral Palsy Signs and Symptoms Early signs of cerebral palsy include: Abnormal head position Low Apgar scores Seizures Breathing difficulty right after delivery Muscular stiffness or jerkiness (hypertonia) Muscular weakness or floppiness (hypotonia) Specific Signs of Spastic Cerebral Palsy The evolution of the upper motor neuron syndrome can take any amount of time following damage or injury to the motor cortex. Therefore, the presentation of spasticity in every patient, even those who have similar injuries, varies. Some forms of spasticity will be hardly- noticeable, while others will require a cane or wheelchair.
    [Show full text]
  • 2020-10-01 ERN-RND Webinar
    01.10.20 The Natural History of Hereditary Spastic Paraplegias Rebecca Schüle Center for Neurology and Hertie Institute for Clinical Brain Research, Tübingen 1 Webinar outline • Phenotypic spectrum of HSPs: core symptoms and additional features • Typical gait patterns in HSP • Age of onset • Disease progression 2 1 01.10.20 Learning objectives • recognize typical signs and symptoms of HSP • recognize typical gait patterns in HSP • distinguish HSP from other motoneuron diseases and movement disorders • monitor disease progression in clinical practice 3 What is your professional background? a) Adult neurologist b) Pediatric neurologist c) Resident (Neurology) d) Resident (Pediatrics) e) Geneticist f) Researcher g) Rehabilitation specialist h) Nurse i) Patient / family member / patient advocate single choice 4 2 01.10.20 How much experience do you have with HSP? a) I consider myself a specialist for HSPs b) I routinely see HSP patients as part of my clinical practice c) I have seen some HSP patients and would like to learn more d) I do not have any practical experience with HSP (have never (knowingly) seen a patient) e) I am a researcher working on HSP and am interested in learning about the clinical aspects of HSP f) I or a friend/family member is affected by HSP and I would like to learn more multiple choice 5 Core symptoms of HSP 6 3 01.10.20 Heterogeneity > 150 known HSP genes phenotype core features SPG 1 – 82 maintained by omim (www.omim.org) Challenges: facultative complicating many HSP genes without SPG number or signs and symptoms part of different classification (e.g.
    [Show full text]
  • PDF Download Walking Stumbling Limping Falling
    WALKING STUMBLING LIMPING FALLING : A CONVERSATION PDF, EPUB, EBOOK Alyson Hallett | 104 pages | 13 Jul 2017 | Triarchy Press | 9781911193067 | English | Bridport, United Kingdom Walking Stumbling Limping Falling : A Conversation PDF Book Growing pain is present only at night; it is present in both legs; and by definition it does not cause a limp. Other differential diagnoses include frontal gait and secondary parkinsonian syndromes, in particular vascular parkinsonism. Examples include spinocerebellar ataxias that are associated with polyneuropathy. This site uses cookies to ensure you get the best experience. Multiple system atrophy MSA. Understanding Parkinson's There is a lot to know about Parkinson's disease. Age Ageing. Greater trochanteric pain syndrome, also called trochanteric bursitis or GTPS, is an inflammation of the bursa of the greater trochanter. Postgrad Med. International Some freezing happens when you are due for the next dose of dopaminergic medication. Tribute Gift. Remember to consider hypophosphataemic rickets in children with bow legs or knock knees, particularly if the child is also short less than 25th centile for age. The role of cognition for gait is revealed in the multitask paradigm where persons are asked to perform mental tasks while walking. Depending on the diagnosis, he or she may recommend the following. Left Arrow Icon. In spastic paraparetic gait, each leg appears to be dragged forward. Dimensions xx6. These postural habits can produce knock-on problems themselves. Prevention and treatment of iatrogenic, especially medication-induced, gait disorders are important measures to reduce the burden of falls in the geriatric population. References 1. Analysis of gait in cervical myelopathy.
    [Show full text]
  • Ferezy's MSR's
    Presented By: Joseph S. Ferezy, D.C. 1 Examination Components I. History and mental status II. Cranial nerve (special senses) III.Somatic motor IV.Somatic sensory V. Reflex VI.Tone, posture, station and movement 2 Ferezy’s MSR’S Motor Reflex STV Deep Strength Superficial Tone Visceral Volume Pathologic Sensory Serebellar Deep Station Superficial Movement 3 1 Basic Exam Organization Sitting (Chair) History of Present Illness Observe Mental Status ‐ Include Cleanliness Stream of Talk Mood Content of Thought Intelligence Sensorium (Cognitive) 4 Basic Exam Organization Standing Free, Heel/toe, Tandem Walking/Hopping/Knee Bend Romberg Posture (observe –tremor, asymmetry, atrophy, Etc.) T & L ROM’s 5 Basic Exam Organization • Sitting (Exam Table) ▫ Cranial Nerve Examination. ▫ Motor Tests ‐ Strength, Tone, and Volume (most other then spinal extensors). ▫ Coordination Tests (Drift, Finger To Finger/Nose, Heel to Shin, Rapid Alternating Movements, Etc.). ▫ Intrathecal Tests. ▫ Orthopedic Tests (Most). ▫ Muscle stretch reflexes. 6 2 The Examination of Station, Movement and Gait Station ‐ The place at which someone is positioned or is assigned to remain, the act or manner of standing. Gait ‐ a manner of walking or moving on foot. Station and gait disorders are among the most common reasons patients seek outpatient neurologic consultation. A careful assessment of station and gait provides a quick, reliable snapshot of the integrated function of the patient's motor and sensory systems of both the central and peripheral nervous systems. Often involved in both somatoform (psychogenic) disorders as well as mistaken as psychogenic in etiology. 7 The Examination of Station, Movement and Gait A normal examination requires nervous system function at the highest level, integration and performance.
    [Show full text]