DOCSLIB.ORG

Facial Myokymia: a Clinicopathological Study

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

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. There was a palsy of the left face, fascicular twitching of the face which he inde- involving both upper and lower portions, with lagophthalmos and Bell's phenomenon. There were pendently termed facial myokymia. All three involuntary movements of the left facial muscles, patients were diagnosed as suffering from mul- most marked around the mouth and in the platysma, tiple sclerosis. Andermann et al. (1961) reviewed but also seen in the zygomatic region around the the literature, discussed seven previously reported lower lid. The movements were continuous, worm- cases, and added four of their own. They postu- like, and undulating; varying in location and not lated that the myokymia resulted from a central affecting all areas at the same time; undisturbing to excitatory focus of demyelination within or near the patient; and unaffected by sleep or emotional or the facial nucleus. However, they had no histo- volitional movements of the face, jaw, or eyes, or by http://jnnp.bmj.com/ pathological studies to substantiate their postula- patting or pulling of the skin of the face. There were tion. no percussion myotonia or myoedema, and no ab- normal synkineses or associated movements. There In earlier literature there are rare references to was no tenderness around the external ear or mastoid neoplastic and vascular lesions within the pons and no hearing loss, and the external acoustic being responsible for what was probably facial meatuses were normal. myokymia but referred to as continuous rhyth- There was also a left partial homonymous hemi- mic fascicular contraction of the facial muscles, anopia, affecting the lower visual fields more than on September 27, 2021 by guest. but in these cases histopathological data are the upper and sparing the macular area. Otherwise meagre. cranial nerve functions were intact and the power, The present case is reported because of the tone, coordination, and sensory functions in the rarity of previous reports, because the facial limbs were good and equal on the two sides. The myokymia was associated with facial palsy, and deep reflexes in the limbs were present and equal and because postmortem studies made clinicopatho- the plantar responses normal. The blood pressure was 120/80 mmHg, the pulse logical correlations possible. 100 per minute and regular. His right upper chest 1 Present address: Command Hospital, Lucknow, India. moved poorly on respiration and auscultation re- 745a e J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.37.6.745 on 1 June 1974. Downloaded from 746 P. K. Sethi, Bernard H. Smith, and K. Kalyanaraman vealed rhonchi in the underlying lung and radio- left than on the right and there was on the left an ill- graphy showed a right upper lobe cavity. sustained ankle clonus and a Babinski plantar response. Pin-prick appreciation in the face and LABORATORY DATA The sputum was repeatedly corneal sensitivity were depressed on the left. The negative for acid-fast bacilli and malignant cells, and visual field defect had not changed. no definite pathogenic organisms were grown. Other Bronchoscopy showed, coming mainly from the routine laboratory tests on urine and blood, includ- right bronchial trees, abundant purulent sero- ing those for syphilis, were normal. sanguineous secretion, specimens of which failed to Nerve conduction studies showed normal conduc- reveal tumour tissue. tion times in the facial nerve (left orbicularis oculi- On the electroencephalogram there was depression 3 ms, conduction distance being 8 cm; left orbicu- of background rhythm on the right hemisphere and laris oculi-2 ms, conduction distance being 6 cm. mild to moderately severe slowing over the central Electromyography using fine monopolar needle and parietal areas on the right. No epileptiform dis- electrodes showed a suggestion of rhythmic spon- charges were seen. taneous discharge in the platysma, and in all other areas only spontaneous continuous low amplitude Brain scan revealed independent areas of increased potentials, hardly distinguishable from normal uptake in the right posterior frontal and right motor unit action potentials except for their low parietal region; and a right carotid arteriogram amplitude. showed avascularity in the posterior frontal region and a small 'blush' in the right parietal area. There HOSPITAL COURSE The patient became more and was no evidence of displacement of midline vessels or more lethargic and confused. Two weeks after of uncal herniation. admission he had a further bout of haemoptysis and On 16 January 1972, a large frontoparietal crani- about the same time an episode of dizziness with fall- otomy revealed evidence of what to the naked eye Protected by copyright. ing. He was disoriented as to time and place and appeared to be two tumours, one on the right inferior exhibited motor impersistence in that he had to be frontal area, and the other in the right lateral repeatedly reminded to keep his eyes closed during parietal area. Biopsy from these areas showed frag- sensory testing. The left facial weakness persisted but ments of cerebral cortex, extensive areas of necrosis, the myokymia was now limited to the platysma and 'nests' of tumour cells which the pathologist muscle. There was also mild weakness of the left thought to be of metastatic origin and probably limbs and some suggestion of his neglecting the left adenocarcinomatous. Postoperatively the patient half of the body on bilateral simultaneous stimula- remained disoriented and lethargic and over the tion. The knee and ankle jerks were brisker on the ensuing week deteriorated and died. http://jnnp.bmj.com/ FIG. 1. Section ofpons showing the two metastases, one median, the other in the on September 27, 2021 by guest. left tegmentum. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.37.6.745 on 1 June 1974. Downloaded from Facial myokymia: a clinicopathological study 747 PATHOLOGICAL FINDINGS At necropsy, broncho- In the upper and mid pons, two well-circumscribed genic carcinoma in the upper lobe of the right lung metastases were noted, corresponding to the areas of was confirmed, with metastases to lymph nodes, greyish discolouration in the gross specimen (Fig. 1). liver, kidneys, and adrenal glands. The brain was One of the metastases was in the left tegmentum, somewhat swollen and its convolutions flattened and and the other in the basis pontis with greater exten- the pia-arachnoid membranes over the right lateral sion to the right than the left side. These metastases frontal convexity were opaque. The arteries at the appeared to be rostral to and not to involve the base showed spotty atheromatosis without luminal facial nucleus or its intramedullary fibres-the level occlusion. of the lesion is indicated in Fig. 2 where the section is On coronal sections, a slight general brain swelling just above the facial colliculus. was confirmed. In the white matter of the right posterior frontal and inferior parietal areas there were several small fine cystic areas of encephalomalacia DISCUSSION and there was softening in the right parietal sub- The facial musculature may be involved in cortical area and in the right superior temporal A gyrus. various types of involuntary movements. care- Fairly sharply delimited areas of pale grey dis- ful clinical examination combined with relevant colouration were found in the tegmentum of the left ancillary investigations can give much help in mid pons and in the upper and mid pons on the right differentiating them. in the region of the medial lemniscus. No lesions Facial myokymia is one of the rare facial were noted in the midbrain, cerebellum, or medulla, dyskinesias but stands out as a distinct clinical and no lesions of the facial nerve or its nucleus were entity. It is usually easily distinguished from detected. fasciculations, which appear as brief, irregularly Protected by copyright. Histologically no cancer cells were obvious in the occurring twitches in different parts of the facial necrotic tissue in the right hemisphere, but several of muscles; whereas myokymia is a slower contrac- the pial arteries were packed with cancer cells. No gross atheromatous lesions were encountered, and tion involving small bands or strips of muscles the large arteries at the base were unoccluded. The and occurs more continuously, transmitting a cancer cell stasis in the local leptomeningeal arterioles ripple (like a 'bag of worms') to the overlying was thought to have contributed to the underlying skin.
Recommended publications
  • New Observations Letters Familial Spinocerebellar Ataxia Type 2 Parkinsonism Presenting As Intractable Oromandibular Dystonia

    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.
  • Cramp Fasciculation Syndrome: a Peripheral Nerve Hyperexcitability Disorder Bhojo A

    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.
  • Drug-Induced Movement Disorders

    Drug-Induced Movement Disorders

    Expert Opinion on Drug Safety ISSN: 1474-0338 (Print) 1744-764X (Online) Journal homepage: https://www.tandfonline.com/loi/ieds20 Drug-induced movement disorders Dénes Zádori, Gábor Veres, Levente Szalárdy, Péter Klivényi & László Vécsei To cite this article: Dénes Zádori, Gábor Veres, Levente Szalárdy, Péter Klivényi & László Vécsei (2015) Drug-induced movement disorders, Expert Opinion on Drug Safety, 14:6, 877-890, DOI: 10.1517/14740338.2015.1032244 To link to this article: https://doi.org/10.1517/14740338.2015.1032244 Published online: 16 May 2015. Submit your article to this journal Article views: 544 View Crossmark data Citing articles: 4 View citing articles Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=ieds20 Review Drug-induced movement disorders Denes Za´dori, Ga´bor Veres, Levente Szala´rdy, Peter Klivenyi & † 1. Introduction La´szlo´ Vecsei † University of Szeged, Albert Szent-Gyorgyi€ Clinical Center, Department of Neurology, Faculty of 2. Methods Medicine, Szeged, Hungary 3. Drug-induced movement disorders Introduction: Drug-induced movement disorders (DIMDs) can be elicited by 4. Conclusions several kinds of pharmaceutical agents. The major groups of offending drugs include antidepressants, antipsychotics, antiepileptics, antimicrobials, antiar- 5. Expert opinion rhythmics, mood stabilisers and gastrointestinal drugs among others. Areas covered: This paper reviews literature covering each movement disor- der induced by commercially available pharmaceuticals. Considering the mag- nitude of the topic, only the most prominent examples of offending agents were reported in each paragraph paying a special attention to the brief description of the pathomechanism and therapeutic options if available. Expert opinion: As the treatment of some DIMDs is quite challenging, a pre- ventive approach is preferable.
  • Cerebellar Ataxia with Neuropathy and Vestibular Areflexia Syndrome

    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.
  • TWITCH, JERK Or SPASM Movement Disorders Seen in Family Practice

    TWITCH, JERK Or SPASM Movement Disorders Seen in Family Practice

    TWITCH, JERK or SPASM Movement Disorders Seen in Family Practice J. Antonelle de Marcaida, M.D. Medical Director Chase Family Movement Disorders Center Hartford HealthCare Ayer Neuroscience Institute DEFINITION OF TERMS • Movement Disorders – neurological syndromes in which there is either an excess of movement or a paucity of voluntary and automatic movements, unrelated to weakness or spasticity • Hyperkinesias – excess of movements • Dyskinesias – unnatural movements • Abnormal Involuntary Movements – non-suppressible or only partially suppressible • Hypokinesia – decreased amplitude of movement • Bradykinesia – slowness of movement • Akinesia – loss of movement CLASSES OF MOVEMENTS • Automatic movements – learned motor behaviors performed without conscious effort, e.g. walking, speaking, swinging of arms while walking • Voluntary movements – intentional (planned or self-initiated) or externally triggered (in response to external stimulus, e.g. turn head toward loud noise, withdraw hand from hot stove) • Semi-voluntary/“unvoluntary” – induced by inner sensory stimulus (e.g. need to stretch body part or scratch an itch) or by an unwanted feeling or compulsion (e.g. compulsive touching, restless legs syndrome) • Involuntary movements – often non-suppressible (hemifacial spasms, myoclonus) or only partially suppressible (tremors, chorea, tics) HYPERKINESIAS: major categories • CHOREA • DYSTONIA • MYOCLONUS • TICS • TREMORS HYPERKINESIAS: subtypes Abdominal dyskinesias Jumpy stumps Akathisic movements Moving toes/fingers Asynergia/ataxia
  • Abadie's Sign Abadie's Sign Is the Absence Or Diminution of Pain Sensation When Exerting Deep Pressure on the Achilles Tendo

    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.
  • Motor Neurone Disease

    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.
  • ADCY5 Mutations Are Another Cause of Benign Hereditary Chorea

    ADCY5 Mutations Are Another Cause of Benign Hereditary Chorea

    Published Ahead of Print on June 17, 2015 as 10.1212/WNL.0000000000001720 ADCY5 mutations are another cause of benign hereditary chorea Niccolo E. Mencacci, ABSTRACT * MD Objective: To determine the contribution of ADCY5 mutations in cases with genetically undefined * Roberto Erro, MD benign hereditary chorea (BHC). Sarah Wiethoff, MD Methods: We studied 18 unrelated cases with BHC (7 familial, 11 sporadic) who were negative for Joshua Hersheson, NKX2-1 mutations. The diagnosis of BHC was based on the presence of a childhood-onset move- MRCP ment disorder, predominantly characterized by chorea and no other major neurologic features. Mina Ryten, MRCP, ADCY5 analysis was performed by whole-exome sequencing or Sanger sequencing. ADCY5 and PhD NKX2-1 expression during brain development and in the adult human brain was assessed using Bettina Balint, MD microarray analysis of postmortem brain tissue. Christos Ganos, MD . Maria Stamelou, MD, Results: The c.1252C T; p.R418W mutation was identified in 2 cases (1 familial, 1 sporadic). PhD The familial case inherited the mutation from the affected father, who had a much milder presen- Niall Quinn, MD, FRCP tation, likely due to low-grade somatic mosaicism. The mutation was de novo in the sporadic case. Henry Houlden, PhD, The clinical presentation of these cases featured nonparoxysmal generalized chorea, as well as FRCP dystonia in the most severely affected, but no facial myokymia. We observed significant progres- ADCY5 NKX2-1 Nicholas W. Wood, PhD, sion of symptoms in mutation carriers, in contrast to BHC secondary to muta- FRCP, FMedSci tions. The difference in the clinical course is mirrored by the brain expression data, showing ADCY5 NKX2-1 Kailash P.
  • By : Ali Younes Ali Dr : Mehdi Delrobaei

    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).
  • Part Ii – Neurological Disorders

    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) � � � � � � � � � � �
  • Paraneoplastic Neurological and Muscular Syndromes

    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 ............................................................................................
  • Facial Myokymia

    Facial Myokymia

    23 July 1966 Leading Articles MEDICAL JOURNAL 189 2 to 6% calcium oxide in commercial talcs. When the talc intermittent and irregular twitching of the muscles around is wetted the boric acid reacts with the calcium hydroxide to one eye, and later may spread to those around the so mouth, Br Med J: first published as 10.1136/bmj.2.5507.189 on 23 July 1966. Downloaded from produce the highly insoluble calcium borate. Absorption that intermittent sharp and momentary contractions of the from dusting powder when the surface of the skin is intact is entire facial musculature on one side may ensue. The negligible and harmless, but if the surface is broken a dusting probable cause is compression or irritation of the facial nerve powder is probably not the best treatment anyway. within its bony canal, but regrettably there is no certain It should be recognized that there is no single blunderbuss method of determining the site of the lesion, so that operations method of treating napkin rashes, because they are not all of designed to decompress the affected nerve are rarely success- the same type or due to the same cause. The common ful. A similar type of intermittent twitching may be seen ammonia dermatitis, with its diffuse erythema where the wet following a severe Bell's palsy in association with the facial napkin was in contact with the skin, leaving the-creases clear, contracture which can occur as a result of partial regeneration is due to the liberation of ammonia from the urine by in the facial nerve.