DOCSLIB.ORG

The Clinical Significance of Fasciculations In

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Clinical Significance of Fasciculations In BRrnM JULY 28, 1951 FASCICULATIONS IN VOLUNTARY MUSCLEO MEDICAL JOURNAL 209 fasciculation can involve part or all of a fasciculus-that THE CLINICAL SIGNIFICANCE OF is, from one to all of its motor units. We were interested FASCICULATIONS IN VOLUNTARY in the possible correlation between the extent and duration of such fasciculation and its significance in MUSCLE clinical terms. On the eiectromyograph the duration oi: BY fasciculation varies between 8 and 12 milliseconds, its amplitude between 0.5 and 1 millivolt. M.D. ROBERT S. SCHWAB, Fibrillation, on the other hand, is produced by the DAVID STAFFORD-CLARK, M.D., M.R.C.P. contraction of individual muscle fibres no longer under - AND the control of a motor nerve: it is seen only in con- of the nerve JOHN STOBO PRICHARD, M.R.C.P. ditions involving severance or degeneration supply. Such individual contractions are so small that (From the Departments of Electrophysiology and Neuiro- although hundreds are probably occurring together at psychiatry, Massachusetts General Hospital, Boston, Mass.) any one instant, they remain invisible under ordinary they can be seen by the of the voluntary muscles has skin. In the tongue, however, Spontaneous twitching aid of a lens and careful lighting. On the electro- aroused the interest of clinicians and neurophysiologists myograph they last 0.5 to 1 millisecond and are no more for many years. Despite the classical paper of Denny- They are not other valuable than 30 to 60 microvolts in amplitude. Brown and Pennybacker in 1938, and usually recordable on an ink-writing oscillograph, requir- contributions by Ayer et al. though less well-known ing special electromyographic techniques with the use of (1934), Ford (1939), Odom et al. (1943), Denny-Bro-%n screen for their of needle electrodes and a cathode-ray and Foley (1948), and the earlier observations demonstration, though we were able to overcome this Duchenne (1855), of Kny (1888), and of Schultze (1894) difficulty without needle electrodes for clinical purposes, on view is still videly heli, both in the myokymia, the as will be seen. The problem here was to record both United States and in Great Britain, that such spon- fibrillation and fasciculation at the same time if both occurs repeatedly in taneous involuntary flickering, if it were present, and again to correlate this with the clinical eyelids or periorbital muscles other than those of the state. area, and particularly if it occurs in the small muscles of the hand, is indicative of progressive muscular atrophy Method (P.M.A.). The normal full clinical history and examination of The terms " fasciculation " and " fibrillation " are still the nervous system formed the basis of our approach sometimes used synonymously to describe these visible to patients: the mental state and psychiatric history were twitchings, and their appearance in the hands, arms, or carefully evaluated. Subsequent follow-up extended feet of doctors or medical students may strike terror into from a minimum of seven months to a maximum of these patients' hearts, whereas in the layman the pheno- six years from the time when the fasciculations were menon may be scarcely noticed, and even if observed is first observed. unlikely to provoke alarm in the absence of other com- Electromyographic studies were made with surface plaint. During the past five years we have collected 16 electrodes and an ink-writing oscillograph, storing the ,cases, of which no fewer than 10 were in doctors or electromyographic discharge on to a wire recorder and senior medical students. In all these cases spontaneous playing it back at one-fifth normal speed into the ink- fasciculation was occurring repeatedly and was often writer when the presence or absence of fibrillation was widespread, and none were in fact suffering from under investigation. The findings in the 16 benign cases P.M.A. It is of some interest, however, that in every were compared with a number of established cases of one of the 10 medically trained patients the presenting progressive muscular atrophy or amyotrophic lateral complaint was of fasciculation, and the overwhelming sclerosis. anxiety thereby aroused concerning the possible diag- Results presence of nosis dominated the picture, whereas the been stated, all 16 cases forming the subjectively by only one As has already fasciculation had been noticed subject of this report displayed continuous and often of the six non-medical patients. widespread fasciculations; none suffered from any form It has seemed worthwhile to record our observations of P.M.A. The medical patients showed a number of on this group if only to clarify further a benign syndrome features in common: in nine out of ten the fasciculations already described, but still apparently too little known had occurred in the small muscles of the hands as well and appre- to prevent considerable unnecessary distress as elsewhere, and had been accompanied by tension, hension. anxiety, fatigue, and some insomnia. In complaining The Problem of this the patients stressed their own conviction that were to was to identify, measure, and record their undeniable tension and distress secondary Our first concern with all that true fasciculations, as distinct from fibrillation, and- to apprehension of the diagnosis of P.M.A., with clinical diagnosis. We this implied: but in every case objective consideration correlate these records situation revealed accepted, and were able subsequently to confirm, the of their recently preceding history and clear -differentiation made by Denny-Brown and Penny- other and important sources of emotional disturbance. backer between these terms. F-asciculations are the In every case the fasciculations had been noticed by a source gross visible and often palpable and subjectively sensible the doctor or student concerned and had been contractions of a number of muscle fibres supplied by a of great anxiety and misery for some weeks or months single motor-nerve filament; in other words, contrac- before he had been able to bring himself to seek the tions of motor units. Whereas the motor unit is a advice of a colleague. In several cases an electromyo- physiological whole, a fasciculus or muscle bundle is graphic examination with an ominous or equivocal re- composed of a number of separate motor units loosely port-for example, " diphasic spontaneous action poten- knit together on a purely anatomical basis. Clinical tials . consistent with P.M.A."-had added to the BRrnSH 210 JULY 28, 1951 FASCICULATIONS IN VOLUNTARY MUSCLE MDICAL JOURNAL patient's tribulation before the diagnosis had been ques- Case 13.-A 36-year-old university professor first noticed fasciculation in the muscles of his hand tioned or the case came under our observation. right following, pro- longed writing three years before coming under our observa- With the exception of a case (No. 4) in which there tion. He was at this time overseas with the U.S. Army. was radiological evidence of arthritis of the cervical A civilian physician in- the area proffered the diagnosis of spine, none of the medical patients displayed any evi- " creeping paralysis" and set the stage for a long-continued dence of structural abnormality, nor of weakness or state of anxiety and apprehension. Fasciculations were wasting, whatever. Apart from the fasciculations their intermittent, sometimes a month going by without their clinical picture included the tension, apprehension, and appearance. Eighteen months later he consulted another but noted the visible anxiety already mentioned, a tendency to cramps and physician, who found no atrophy which at times were brisk to move hyperhidrosis especially of the palms and axillae, some fasciculations, enough a finger. The remainder of the neurological examination loss of appetite, disturbance of sleep, and tremor of the the doctor ordered classical was normal. To settle the diagnosis, outstretched hands. They displayed, in fact, the an electromyogram of the muscles, putting on the referral syndrome of myokymia as originally described by Kny slip, " ? possibility of P.M.A." The report read: " Diphasic and by Schultze. spontaneous action potentials seen in the muscles of the calf One only of the non-medical group of six patients and occasionally in the abductor digiti quinti. Consistent complained primarily of fasciculation. He was a 36-year- with the diagnosis of P.M.A." On the strength of this old university professor (Case 13, below). By the time the diagnosis of P.M.A. was accepted, but eventually a further was and we saw him the ominously guarded nature of the medical electromyographic investigation requested, in this way he came to us. By this time it was perfectly had received, reinforced by his own amateur opinions he apparent that he was not suffering from P.M.A., there being but highly intelligent researches into the medical litera- no atrophy despite the occasional fasciculations, nor any ture, had reduced him to a state of iatrogenic alarm and abnormal neurological findings. He recovered his morale despondency comparable to that of his medical fellow- with appropriate reassurance and has remained well. sufferers. Like them, his was a case of myokymia. The other five patients included four women between the ages of 26 and 40 currently under treatment for anxiety Electromyographic Studies state or mixed affective disorder at the Department of The nature of these has already been indicated. They Psychiatry of the Massachusetts General Hospital, and are further illustrated by Figs. 1, 2, and 3. While the a young man of 22, an engineer, who actually had simultaneous occurrence of fibrillation and fasciculation muscular dystrophy of the distal type described by Gowers. Three brief illustrative case histories are appended. FIBRILLATION FASCICULATION MYOKYMIA VOLUNTARY Illustrative Cases CON TRACTION Case 2.--A 22-year-old medical student noted fascicula- tions in the small muscles of the left hand. Six months later he noted the same thing in the right hand during the writing of an examination.
Load more

Recommended publications
  • New Observations Letters Familial Spinocerebellar Ataxia Type 2 Parkinsonism Presenting As Intractable Oromandibular Dystonia
    Freely available online New Observations Letters Familial Spinocerebellar Ataxia Type 2 Parkinsonism Presenting as Intractable Oromandibular Dystonia 1,2 2,3 1,3* Kyung Ah Woo , Jee-Young Lee & Beomseok Jeon 1 Department of Neurology, Seoul National University Hospital, Seoul, KR, 2 Department of Neurology, Seoul National University Boramae Hospital, Seoul, KR, 3 Seoul National University College of Medicine, Seoul, KR Keywords: Dystonia, spinocerebellar ataxia type 2, Parkinson’s disease Citation: Woo KA, Lee JY, Jeon B. Familial spinocerebellar ataxia type 2 parkinsonism presenting as intractable oromandibular dystonia. Tremor Other Hyperkinet Mov. 2019; 9. doi: 10.7916/D8087PB6 * To whom correspondence should be addressed. E-mail: [email protected] Editor: Elan D. Louis, Yale University, USA Received: October 20, 2018 Accepted: December 10, 2018 Published: February 21, 2019 Copyright: ’ 2019 Woo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution–Noncommercial–No Derivatives License, which permits the user to copy, distribute, and transmit the work provided that the original authors and source are credited; that no commercial use is made of the work; and that the work is not altered or transformed. Funding: None. Financial Disclosures: None. Conflicts of Interest: The authors report no conflict of interest. Ethics Statement: This study was reviewed by the authors’ institutional ethics committee and was considered exempted from further review. We have previously described a Korean family afflicted with reflex, mildly stooped posture, and parkinsonian gait. There was spinocerebellar ataxia type 2 (SCA2) parkinsonism in which genetic no sign of lower motor lesion, including weakness, muscle atrophy, analysis revealed CAG expansion of 40 repeats in the ATXN2 gene.1 or fasciculation.
    [Show full text]
  • Cramp Fasciculation Syndrome: a Peripheral Nerve Hyperexcitability Disorder Bhojo A
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by eCommons@AKU Pakistan Journal of Neurological Sciences (PJNS) Volume 9 | Issue 3 Article 7 7-2014 Cramp fasciculation syndrome: a peripheral nerve hyperexcitability disorder Bhojo A. Khealani Aga Khan University Hospital, Follow this and additional works at: http://ecommons.aku.edu/pjns Part of the Neurology Commons Recommended Citation Khealani, Bhojo A. (2014) "Cramp fasciculation syndrome: a peripheral nerve hyperexcitability disorder," Pakistan Journal of Neurological Sciences (PJNS): Vol. 9: Iss. 3, Article 7. Available at: http://ecommons.aku.edu/pjns/vol9/iss3/7 CASE REPORT CRAMP FASCICULATION SYNDROME: A PERIPHERAL NERVE HYPEREXCITABILITY DISORDER Bhojo A. Khealani Assistant professor, Neurology section, Aga khan University, Karachi Correspondence to: Bhojo A Khealani, Department of Medicine (Neurology), Aga Khan University, Karachi. Email: [email protected] Date of submission: June 28, 2014, Date of revision: August 5, 2014, Date of acceptance:September 1, 2014 ABSTRACT Cramp fasciculation syndrome is mildest among all the peripheral nerve hyperexcitability disorders, which typically presents with cramps, body ache and fasciculations. The diagnosis is based on clinical grounds supported by electrodi- agnostic study. We report a case of young male with two months’ history of body ache, rippling, movements over calves and other body parts, and occasional cramps. His metabolic workup was suggestive of impaired fasting glucose, radio- logic work up (chest X-ray and ultrasound abdomen) was normal, and electrodiagnostic study was significant for fascicu- lation and myokymic discharges. He was started on pregablin and analgesics. To the best of our knowledge this is report first of cramp fasciculation syndrome from Pakistan.
    [Show full text]
  • Cerebellar Ataxia with Neuropathy and Vestibular Areflexia Syndrome
    n e u r o l o g i a i n e u r o c h i r u r g i a p o l s k a 4 8 ( 2 0 1 4 ) 3 6 8 – 3 7 2 Available online at www.sciencedirect.com ScienceDirect journal homepage: http://www.elsevier.com/locate/pjnns Case report Cerebellar ataxia with neuropathy and vestibular areflexia syndrome (CANVAS) – A case report and review of literature a a b a, Monika Figura , Małgorzata Gaweł , Anna Kolasa , Piotr Janik * a Department of Neurology, Medical University of Warsaw, Warsaw, Poland b 2nd Department of Clinical Radiology, Medical University of Warsaw, Warsaw, Poland a r t i c l e i n f o a b s t r a c t Article history: CANVAS (cerebellar ataxia with neuropathy and vestibular areflexia syndrome) is a rare Received 19 March 2014 neurological syndrome of unknown etiology. The main clinical features include bilateral Accepted 27 August 2014 vestibulopathy, cerebellar ataxia and sensory neuropathy. An abnormal visually enhanced Available online 6 September 2014 vestibulo-ocular reflex is the hallmark of the disease. We present a case of 58-year-old male patient who has demonstrated gait disturbance, imbalance and paresthesia of feet for 2 fl Keywords: years. On examination ataxia of gait, diminished knee and ankle re exes, absence of plantar reflexes, fasciculations of thigh muscles, gaze-evoked downbeat nystagmus and abnormal Cerebellar ataxia with neuropathy visually enhanced vestibulo-ocular reflex were found. Brain magnetic resonance imaging and vestibular areflexia syndrome revealed cerebellar atrophy. Vestibular function testing showed severely reduced horizontal Cerebellar ataxia nystagmus in response to bithermal caloric stimulation.
    [Show full text]
  • Facial Myokymia: a Clinicopathological Study
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.37.6.745 on 1 June 1974. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry, 1974, 37, 745-749 Facial myokymia: a clinicopathological study P. K. SETHI1, BERNARD H. SMITH, AND K. KALYANARAMAN From the Department of Neurology, Edward J. Meyer Memorial Hospital anid School of Medicine, State University of New York at Buffalo, N. Y., U.S.A. SYNOPSIS Clinicopathological correlations are presented in a case of facial myokymia with facial palsy. The causative lesions were considered to be metastatic tumours to the pons and it was con- cluded that both the facial palsy and the myokymia were due to interruption of supranuclear path- ways impinging on the facial nucleus. Oppenheim (1916) described a patient with con- CASE REPORT tinuous undulation and fasciculation in the right A 57 year old white man was admitted to hospital on facial muscles. The movements had started in the 30 December 1971, suffering from productive cough, infraorbital region and progressed to involve the haemoptysis, and weight loss of some months' dura- entire territory of the facial nerve. He called the tion. He had been a heavy smoker for many years. Protected by copyright. condition facial myokymia, commented on its There was no history of fever or of pains around the association with sustained facial contraction, face. and expressed the view that, like facial palsy, it He was oriented as to time, place, and person but might be an early sign of multiple sclerosis. Kino confused and lethargic and unable to describe his (1928) reported three patients with undulating symptoms well.
    [Show full text]
  • Abadie's Sign Abadie's Sign Is the Absence Or Diminution of Pain Sensation When Exerting Deep Pressure on the Achilles Tendo
    A.qxd 9/29/05 04:02 PM Page 1 A Abadie’s Sign Abadie’s sign is the absence or diminution of pain sensation when exerting deep pressure on the Achilles tendon by squeezing. This is a frequent finding in the tabes dorsalis variant of neurosyphilis (i.e., with dorsal column disease). Cross References Argyll Robertson pupil Abdominal Paradox - see PARADOXICAL BREATHING Abdominal Reflexes Both superficial and deep abdominal reflexes are described, of which the superficial (cutaneous) reflexes are the more commonly tested in clinical practice. A wooden stick or pin is used to scratch the abdomi- nal wall, from the flank to the midline, parallel to the line of the der- matomal strips, in upper (supraumbilical), middle (umbilical), and lower (infraumbilical) areas. The maneuver is best performed at the end of expiration when the abdominal muscles are relaxed, since the reflexes may be lost with muscle tensing; to avoid this, patients should lie supine with their arms by their sides. Superficial abdominal reflexes are lost in a number of circum- stances: normal old age obesity after abdominal surgery after multiple pregnancies in acute abdominal disorders (Rosenbach’s sign). However, absence of all superficial abdominal reflexes may be of localizing value for corticospinal pathway damage (upper motor neu- rone lesions) above T6. Lesions at or below T10 lead to selective loss of the lower reflexes with the upper and middle reflexes intact, in which case Beevor’s sign may also be present. All abdominal reflexes are preserved with lesions below T12. Abdominal reflexes are said to be lost early in multiple sclerosis, but late in motor neurone disease, an observation of possible clinical use, particularly when differentiating the primary lateral sclerosis vari- ant of motor neurone disease from multiple sclerosis.
    [Show full text]
  • Motor Neurone Disease
    Neurology Motor neurone disease Margaret Zoing Matthew Kiernan Caring for the patient in general practice Motor neurone disease (MND) is a progressive Background neurodegenerative disease. It is characterised by motor Motor neurone disease is a neurodegenerative disease that systems failure that results in the death of nerves responsible leads to progressive disability – and eventually death – for all voluntary movements, leading to limb paralysis, within 2–3 years. weakness of the muscles of speech and swallowing, and Objective ultimately respiratory failure. Typically MND strikes patients This article describes the role of the general practitioner in at the prime of adult life, usually in the fifth to sixth decades, caring for patients with motor neurone disease. and has a short trajectory from diagnosis with an average life Discussion expectancy of less than 3 years.1 Current estimates are that The diagnosis of motor neurone disease relies on the 1400 people are living with MND in Australia at any time, presence of upper and lower motor neurone features. There with 370 newly diagnosed patients each year.2 More than one is currently no pathognomic test for motor neurone disease Australian dies every day from this most pernicious disease. and it largely remains a diagnosis of exclusion following an accurate clinical history, combined with basic screening The cause of MND remains unknown but appears heterogeneous. blood investigations and structural imaging of the brain Environmental factors may trigger an underlying susceptibility – toxins, and spinal cord. Neuro-physiological studies may be useful chemicals, metals and trauma have all been proposed.1 Most cases as an ancillary diagnostic tool.
    [Show full text]
  • By : Ali Younes Ali Dr : Mehdi Delrobaei
    K.N.Toosi University of Technology By : Ali younes ali Dr : Mehdi Delrobaei Contents 1-Introduction and general description 2-Signs and symptoms 3-Risk factors 4-Causes 5-Ways of detection 6-Treatment 7-References 1-Introduction and General description Fasciculations (muscle twitch): is a small, local, involuntary muscle contraction and relaxation which may be visible under the skin Deeper areas can be detected by electromyography (EMG) testing, though they can happen in any skeletal muscle in the body Fasciculations can often by visualized and take the form of a muscle twitch or dimpling under the skin, but usually do not generate sufficient force to move a limb Fasciculations arise as a result of spontaneous depolarization of a lower motor neuron leading to the synchronous contraction of all the skeletal muscle fibers within a single motor unit Usually, intentional movement of the involved muscle causes fasciculations to cease immediately, but they may return once the muscle is at rest again. Fasciculations have a variety of causes, the majority of which are benign, but can also be due to disease of the motor neurons They are encountered by virtually all healthy people, though for most, it is quite infrequent In some cases, the presence of fasciculations can be annoying and interfere with quality of life If a neurological examination is otherwise normal and EMG testing does not indicate any additional pathology, a diagnosis of benign fasciculation syndrome is usually made 2-Signs and symptoms The main symptom of fasciculation is focal or widespread involuntary muscle activity (twitching), which can occur at random or specific times (or places).
    [Show full text]
  • Part Ii – Neurological Disorders
    Part ii – Neurological Disorders CHAPTER 14 MOVEMENT DISORDERS AND MOTOR NEURONE DISEASE Dr William P. Howlett 2012 Kilimanjaro Christian Medical Centre, Moshi, Kilimanjaro, Tanzania BRIC 2012 University of Bergen PO Box 7800 NO-5020 Bergen Norway NEUROLOGY IN AFRICA William Howlett Illustrations: Ellinor Moldeklev Hoff, Department of Photos and Drawings, UiB Cover: Tor Vegard Tobiassen Layout: Christian Bakke, Division of Communication, University of Bergen E JØM RKE IL T M 2 Printed by Bodoni, Bergen, Norway 4 9 1 9 6 Trykksak Copyright © 2012 William Howlett NEUROLOGY IN AFRICA is freely available to download at Bergen Open Research Archive (https://bora.uib.no) www.uib.no/cih/en/resources/neurology-in-africa ISBN 978-82-7453-085-0 Notice/Disclaimer This publication is intended to give accurate information with regard to the subject matter covered. However medical knowledge is constantly changing and information may alter. It is the responsibility of the practitioner to determine the best treatment for the patient and readers are therefore obliged to check and verify information contained within the book. This recommendation is most important with regard to drugs used, their dose, route and duration of administration, indications and contraindications and side effects. The author and the publisher waive any and all liability for damages, injury or death to persons or property incurred, directly or indirectly by this publication. CONTENTS MOVEMENT DISORDERS AND MOTOR NEURONE DISEASE 329 PARKINSON’S DISEASE (PD) � � � � � � � � � � �
    [Show full text]
  • Paraneoplastic Neurological and Muscular Syndromes
    Paraneoplastic neurological and muscular syndromes Short compendium Version 4.5, April 2016 By Finn E. Somnier, M.D., D.Sc. (Med.), copyright ® Department of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark 30/01/2016, Copyright, Finn E. Somnier, MD., D.S. (Med.) Table of contents PARANEOPLASTIC NEUROLOGICAL SYNDROMES .................................................... 4 DEFINITION, SPECIAL FEATURES, IMMUNE MECHANISMS ................................................................ 4 SHORT INTRODUCTION TO THE IMMUNE SYSTEM .................................................. 7 DIAGNOSTIC STRATEGY ..................................................................................................... 12 THERAPEUTIC CONSIDERATIONS .................................................................................. 18 SYNDROMES OF THE CENTRAL NERVOUS SYSTEM ................................................ 22 MORVAN’S FIBRILLARY CHOREA ................................................................................................ 22 PARANEOPLASTIC CEREBELLAR DEGENERATION (PCD) ...................................................... 24 Anti-Hu syndrome .................................................................................................................. 25 Anti-Yo syndrome ................................................................................................................... 26 Anti-CV2 / CRMP5 syndrome ............................................................................................
    [Show full text]
  • Wasting with Fasciculations—Differentiating Peripheral Nerve
    WASTING WITH FASCICULATIONS – Differentiating Peripheral Nerve Injuries form ALS Tim S ch oonover DO, FACN Dayton Center for Neurological Disorders OCT 2010 1 OVERVIEW DEFINITION AMYOTROPHIC LATERAL SCLEROSIS DIFFERENTIAL DIAGNOSIS WORK UP OCT 2010 2 FASCICULATIONS Spontaneous, involuntary, irregular and painless twitching (contractions) of part of a muscle Visually apparent Percussion may bring out Creates concern because of its association with ALS OCT 2010 3 FASCICULATIONS - EMG Spontaneous discharge of single motor unit Fire irregularly Relative slow pattern 2-3 ppyer second to one every several seconds “corn popping” OCT 2010 4 FASCICULATIONS - benign OFTEN BENIGN Eyelids Thumb Gastrocnemius Tend to fire faster than malignant form Tend to continue in same muscle OCT 2010 5 FASCICULATIONS -benign 70% of medical personal have occasionally 2% have daily Majority who present with fasciculations have NO associated neurological disease OCT 2010 6 FASCICULATIONS - malignant Tend to fire slower Varying muscles Associated with Atroppyhy Weakness Reflex abnormalities More complex wave form on EMG OCT 2010 7 FASCICULATIONS Pathogenesis Neural in origin Impulses generated in peripheral nerve TiltifthTerminal portion of the axon Hyperexcitable distal motor axons Stretching the muscle = decreased fascics Seen in virtually all ALS patients May be generated at multiple points along diseased motor neuron If no fasciculations need to reconsider dx OCT 2010 8 FASCICULATIONS benign causes: not usually associated
    [Show full text]
  • Neuro Vignettes Psychiatry Board Exam Preparation Resource
    Neuro Vignettes Psychiatry Board Exam Preparation Resource www.BeatTheBoards.com 1 of 69 877-225-8384 Table of Contents 1. Parkinson’s Disease 2. Wilson’s Disease 3. Huntington’s Disease 4. Alzheimer’s Disease 5. Frontal-Temporal Dementia 6. Dementia with Lewy Bodies 7. Binswanger’s Dementia 8. New Variant Creutzfeldt-Jakob Disease 9. Tay Sach’s Disease 10. Friedrich’s Ataxia 11. Metachromatic Leukodystrophy 12. Coma 13. Subdural Hematoma 14. Epidural Hematoma 15. Cortical Ischemic Stroke 16. Brainstem Ischemic Stroke 17. Hemorrhagic Stroke 18. Status Epilepticus 19. Partial Complex Seizure 20. Grand Mal Seizure 21. Multiple Sclerosis 22. Amyotrophic Lateral Sclerosis 23. Guillain-Barre Syndrome 24. Myasthenia Gravis 25. Duchenne Muscular Dystrophy 26. High Grade Glioma 27. Astrocytoma 28. Medulloblastoma 29. Brain Death Evaluation Copyright Notice: Copyright © 2008-2010 American Physician Institute for Advanced Professional Studies, LLC. All rights reserved. This manuscript may not be transmitted, copied, reprinted, in whole or in part, without the express written permission of the copyright holder. Requests for permission or further information should be addressed to Jack Krasuski at: [email protected] or American Physician Institute for Advanced Professional Studies, LLC, 125 Windsor Dr., Suite 111, Oak Brook, IL 60523 Disclaimer Notice: This publication is designed to provide general educational advice. It is provided to the reader with the understanding that Jack Krasuski and American Physician Institute for Advanced Professional Studies LLC are not rendering medical services and are not affiliated with the American Board of Psychiatry and Neurology. If medical or other expert assistance is required, the services of a medical or other consultant should be obtained.
    [Show full text]
  • 1997 Documentation Guidelines for Evaluation and Management Services
    1997 DOCUMENTATION GUIDELINES FOR EVALUATION AND MANAGEMENT SERVICES TABLE OF CONTENTS Introduction ....................................................................................................…… 2 What Is Documentation and Why Is it Important?............................………. 2 What Do Payers Want and Why? .......................................................……… 2 General Principles of Medical Record Documentation ..................................... 3 Documentation of E/M Services........................................................................... 4 Documentation of History .................................................................................... 5 Chief Complaint (CC) ..................................................................................... 6 History of Present Illness (HPI) ..................................................................... 7 Review of Systems (ROS) .............................................................................. 8 Past, Family and/or Social History (PFSH) ................................................... 9 Documentation of Examination ........................................................................... 10 General Multi-System Examinations ............................................................ 11 Single Organ System Examinations ............................................................ 12 Content and Documentation Requirements ................................................ 13 General Multi-System Examination ………..............................................
    [Show full text]