Conversion Motor Paralysis Disorder: Analysis of 34 Consecutive Referrals
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A Syndrome-Based Clinical Approach for Clerkship Students General Comments 1. This Is Not an All-Inclusive “Cookbook” for Ev
A Syndrome-Based Clinical Approach for Clerkship Students General Comments 1. This is not an all-inclusive “cookbook” for every Neurology patient, but a set of guidelines to help you rationally approach patients with certain syndromes (sets of signs and symptoms which suggest a lesion in particular parts of the nervous system). 2. As you obtain a history and perform a neurological physical exam, try initially to localize all the patient’s signs and symptoms to one, single lesion in the nervous system. It may be surprising that a variety of signs and symptoms, at first glance apparently unrelated, on second thought can localize accurately to a single lesion. If this approach fails, then consider multiple, separate lesions for the patient’s signs and symptoms. 3. The tempo or rate at which signs and symptoms develop or occur often suggests the underlying pathological process. a. sudden onset---favors stroke (ischemia or hemorrhage), seizure, migraine (or other headache syndromes), and trauma b. subacute onset---favors inflammatory, infectious or immune-mediated disorders c. chronic onset---favors degenerative disorders, tumors Toximetabolic disorders, potentially treatable and reversible, may mimic lesions in the nervous system, and can evolve at variable tempos. Hereditary conditions may be congenital (present at birth) and nonprogressive or static, or develop later in life, with variable rates of progression. Family members affected by the same genetic disorder may be remarkably similar with regards to onset and clinical severity, while some genetic disorders vary widely regarding when and how severely family members are affected. 4. In the central nervous system, “positive symptoms or phenomena,” such as flashes of light, or a tingling sensation, suggest “excitation” or increased activity in the nervous system: migraine or seizure. -
Child Neurology: Hereditary Spastic Paraplegia in Children S.T
RESIDENT & FELLOW SECTION Child Neurology: Section Editor Hereditary spastic paraplegia in children Mitchell S.V. Elkind, MD, MS S.T. de Bot, MD Because the medical literature on hereditary spastic clinical feature is progressive lower limb spasticity B.P.C. van de paraplegia (HSP) is dominated by descriptions of secondary to pyramidal tract dysfunction. HSP is Warrenburg, MD, adult case series, there is less emphasis on the genetic classified as pure if neurologic signs are limited to the PhD evaluation in suspected pediatric cases of HSP. The lower limbs (although urinary urgency and mild im- H.P.H. Kremer, differential diagnosis of progressive spastic paraplegia pairment of vibration perception in the distal lower MD, PhD strongly depends on the age at onset, as well as the ac- extremities may occur). In contrast, complicated M.A.A.P. Willemsen, companying clinical features, possible abnormalities on forms of HSP display additional neurologic and MRI abnormalities such as ataxia, more significant periph- MD, PhD MRI, and family history. In order to develop a rational eral neuropathy, mental retardation, or a thin corpus diagnostic strategy for pediatric HSP cases, we per- callosum. HSP may be inherited as an autosomal formed a literature search focusing on presenting signs Address correspondence and dominant, autosomal recessive, or X-linked disease. reprint requests to Dr. S.T. de and symptoms, age at onset, and genotype. We present Over 40 loci and nearly 20 genes have already been Bot, Radboud University a case of a young boy with a REEP1 (SPG31) mutation. Nijmegen Medical Centre, identified.1 Autosomal dominant transmission is ob- Department of Neurology, PO served in 70% to 80% of all cases and typically re- Box 9101, 6500 HB, Nijmegen, CASE REPORT A 4-year-old boy presented with 2 the Netherlands progressive walking difficulties from the time he sults in pure HSP. -
Outcomes Following Unilateral Selective Dorsal Rhizotomy In
Outcomes and Perioperative Considerations for Unilateral Selective Dorsal Rhizotomy in Children with Spastic Hemiplegia with Pre- and Postoperative Quantitative Gait Analysis Christine Hunt, D.O.1, Nicholas Wetjen, M.D.2, Kenton Kaufman, Ph.D.3, Krista Coleman Wood, P.T., Ph.D.3, Joline Brandenburg, M.D.1, Bradford Landry, D.O.1 1Department of Physical Medicine & Rehabilitation, 2Department of Neurologic Surgery, 3Department of Orthopedic Surgery Mayo Clinic, Rochester, MN Abstract Background & Objectives Methods Results: Postoperative Gait Analysis Discussion Background: Selective dorsal rhizotomy (SDR) is a Background Preoperative Baseline Characteristics Patient 1: Right SDR December 2013 • Pre-SDR, patients undergo an in-depth review of their medical procedure used to improve function, decrease pain and • Several human trials examining outcomes in SDR in children • Patient 1: 6 year old male, spastic right hemiplegia • 62.5% of sensory dorsal rootlets sectioned ( L2 to S1) history and imaging studies, consultation with a physiatrist, reduce spasticity in children and adults with cerebral palsy or neurosurgeon, and orthopedic surgeon, and evaluation with PT with spastic diplegia have been conducted, but there is a • GMFCS Level II • Normalized velocity and stride length stroke. Positive outcomes have been reported by numerous and OT. Testing includes QGA, MRI lumbar spine and brain, paucity of data describing outcomes following SDR for • 12 series of botulinum toxin • Improved hip and knee kinematics and kinetics authors but pediatric -
Study Guide Medical Terminology by Thea Liza Batan About the Author
Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails proficiencyincommunicatingwithhealthcareprofessionalssuchasphysicians,nurses, or dentists. -
Hereditary Spastic Paraplegia
8 Hereditary Spastic Paraplegia Notes and questions Hereditary Spastic Paraplegia What is Hereditary Spastic Paraplegia? Hereditary Spastic Paraplegia (HSP) is a medical term for a condition that affects muscle function. The terms spastic and paraplegia comes from several words in Greek: • ‘spastic’ means afflicted with spasms (an alteration in muscle tone that results in affected movements) • ‘paraplegia’ meaning an impairment in motor or sensory function of the lower extremities (from the hips down) What are the signs and symptoms of HSP? Muscular spasticity • Individuals with HSP commonly will have lower extremity weakness, spasticity, and muscle stiffness. • This can cause difficulty with walking or a “scissoring” gait. We are grateful to an anonymous donor for making a kind and Other common signs or symptoms include: generous donation to the Neuromuscular and Neurometabolic Centre. • urinary urgency • overactive or over responsive “brisk” reflexes © Hamilton Health Sciences, 2019 PD 9983 – 01/2019 Dpc/pted/HereditarySpasticParaplegia-trh.docx dt/January 15, 2019 ____________________________________________________________________________ 2 7 Hereditary Spastic Paraplegia Hereditary Spastic Paraplegia HSP is usually a chronic or life-long disease that affects If you have any questions about DM1, please speak with your people in different ways. doctor, genetic counsellor, or nurse at the Neuromuscular and Neurometabolic Centre. HSP can be classified as either “Uncomplicated HSP” or “Complicated HSP”. Notes and questions Types of Hereditary Spastic Paraplegia 1. Uncomplicated HSP: • Individuals often experience difficulty walking as the first symptom. • Onset of symptoms can begin at any age, from early childhood through late adulthood. • Symptoms may be non-progressive, or they may worsen slowly over many years. -
Functional Neurologic Disorders and Related Disorders Victor W Mark MD ( Dr
Functional neurologic disorders and related disorders Victor W Mark MD ( Dr. Mark of the University of Alabama at Birmingham has no relevant financial relationships to disclose. ) Originally released April 18, 2001; last updated December 13, 2018; expires December 13, 2021 Introduction This article includes discussion of psychogenic neurologic disorders, functional neurologic disorder, functional movement disorder, conversion disorder, and hysteria. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations. Overview Several behavioral disorders are related by (1) their resemblance to other, more familiar neurologic disorders; (2) lack of well-established biomarkers (eg, structural lesions on brain imaging studies, seizure waveforms on EEGs); and (3) aggravation of symptoms with the patient s attention to the disorder. However, the features and causes for these disorders are very different among themselves. This topic reviews functional neurologic disorder, Munchausen syndrome, Munchausen syndrome by proxy, and Ganser syndrome. Key points • Functional neurologic disorders are commonly encountered in general neurologic practices and, hence, knowing their manifestations and treatment is crucial for clinical care. • The disturbance is involuntary, yet at the same time it can be controlled by the patient intermittently. • Despite being self-controllable, the disturbance is generally disabling unless expert professional care is provided. • There is no consistent association between functional neurologic disorder and either posttraumatic emotional stress or sexual abuse. • Functional neurologic disturbances disorder responds best to empathetic concern by the clinician; demonstration that the disorder lacks a structural or permanent etiology; explanation that it can be improved with distraction; and guided attempts to reduce triggers of onset. Cognitive behavioral therapy, combined with physical therapy when warranted, is emerging as a successful intervention. -
Approach to a Patient with Hemiplegia and Monoplegia
CHAPTER Approach to a Patient with Hemiplegia and Monoplegia 27 Sudhir Kumar, Subhash Kaul INTRODUCTION 4. Injury to multiple cervical nerve roots. Monoplegia and hemiplegia are common neurological 5. Functional or psychogenic. symptoms in patients presenting to the emergency department as well as outpatient department. Insidious onset, gradually progressive monoplegia affecting lower limb can be caused by the following Monoplegia refers to weakness of one limb (either arm or conditions: leg) and hemiplegia refers to weakness of one arm and leg on the same side of body (either left or right side). 1. Tumor of the contralateral frontal lobe. There are a variety of underlying causes for monoplegia 2. Tumor of spinal cord at thoracic or lumbar level. and hemiplegia. The causes differ in different age groups. 3. Chronic infection of brain (frontal lobe) or spinal The causes also differ depending on the onset, progression cord (thoracic or lumbar level), such as tuberculous. and duration of weakness. Therefore, one needs to adopt a systematic approach during history taking and 4. Lumbosacral-plexopathy, due to diabetes mellitus. examination in order to arrive at the correct diagnosis. Insidious onset, gradually progressive monoplegia, Appropriate investigations after these would confirm the affecting upper limb, can be caused by one of the following diagnosis. conditions: The aim of this chapter is to systematically look at the 1. Tumor of the contralateral parietal lobe. differential diagnosis of monoplegia and hemiplegia and outline the approach needed to pinpoint the exact 2. Compressive lesion (tumor, large disc, etc) in underlying cause. cervical cord region. 3. Chronic infection of the brain (parietal lobe) or APPROACH TO THE DIAGNOSIS OF MONOPLEGIA spinal cord (cervical region), such as tuberculous. -
Changes Caused by Stroke
Recovery Frontal lobe Parietal lobe let’s talk about controls personality, controls speech and reasoning, parts of sensation (touch and Changes speech, and muscles pressure) Caused by Stroke Your brain controls how you move, feel, communicate, think and act. Brain injury from a stroke may affect any of these abilities. Some changes are common no matter which side of the brain the injury is on. Others Temporal lobe are based on which side of the brain Occipital lobe controls hearing, the stroke injures. speech, and short- controls vision term memory What are the most common general What are common changes with a effects of stroke? right-brain injury? • Hemiparesis (weakness on one side of the body) or • Paralysis or weakness on the left side of the body. hemiplegia (paralysis on one side of the body) • One-sided neglect, which is a lack of awareness of the • Dysarthria (difficulty speaking or slurred speech), or left side of the body. It may also be a lack of awareness dysphagia (trouble swallowing) of what is going on to the survivor’s left. For example, • Fatigue they may only eat from the right side of their plate, ignoring the left side of the plate. • Loss of emotional control and changes in mood • Behavior may be more impulsive and less cautious • Cognitive changes (problems with memory, judgment, than before. problem-solving or a combination of these) • It may be harder for the survivor to understand facial • Behavior changes (personality changes, improper expressions and tone of voice. They also may have less language or actions) expression in their own face and tone of voice when • Decreased field of vision (inability to see peripheral communicating. -
Myelopathy—Paresis and Paralysis in Cats
Myelopathy—Paresis and Paralysis in Cats (Disorder of the Spinal Cord Leading to Weakness and Paralysis in Cats) Basics OVERVIEW • “Myelopathy”—any disorder or disease affecting the spinal cord; a myelopathy can cause weakness or partial paralysis (known as “paresis”) or complete loss of voluntary movements (known as “paralysis”) • Paresis or paralysis may affect all four limbs (known as “tetraparesis” or “tetraplegia,” respectively), may affect only the rear legs (known as “paraparesis” or “paraplegia,” respectively), the front and rear leg on the same side (known as “hemiparesis” or “hemiplegia,” respectively) or only one limb (known as “monoparesis” or “monoplegia,” respectively) • Paresis and paralysis also can be caused by disorders of the nerves and/or muscles to the legs (known as “peripheral neuromuscular disorders”) • The spine is composed of multiple bones with disks (intervertebral disks) located in between adjacent bones (vertebrae); the disks act as shock absorbers and allow movement of the spine; the vertebrae are named according to their location—cervical vertebrae are located in the neck and are numbered as cervical vertebrae one through seven or C1–C7; thoracic vertebrae are located from the area of the shoulders to the end of the ribs and are numbered as thoracic vertebrae one through thirteen or T1–T13; lumbar vertebrae start at the end of the ribs and continue to the pelvis and are numbered as lumbar vertebrae one through seven or L1–L7; the remaining vertebrae are the sacral and coccygeal (tail) vertebrae • The brain -
Non-Ketotic Hyperglycaemia and the Hemichorea- Hemiballismus
This open-access article is distributed under ARTICLE Creative Commons licence CC-BY-NC 4.0. Non-ketotic hyperglycaemia and the hemichorea- hemiballismus syndrome – a rare paediatric presentation M P K Hauptfleisch, MB BCh, MMed Paeds, FCPaed (SA), Cert Paed Neuro (SA); J L Rodda, MB BCh, FCPaed (SA) Department of Paediatrics, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa and Chris Hani Baragwanath Academic Hospital, Johannesburg, Africa Corresponding author: M P K Hauptfleisch ([email protected]) Hemichorea-hemiballismus may be due to non-ketotic hyperglycaemia, but this condition has rarely been described in paediatrics. We describe the case of a 13-year-old girl with newly diagnosed type 1 diabetes and acute onset of left-sided choreoathetoid movements. Neuroimaging revealed an area of hyperintensity in the right basal ganglia. Her blood glucose level at the time was 19 mmol/L, and there was no ketonuria. The hemiballismus improved with risperidone and glycaemic control. Repeat neuroimaging 4 months later showed complete resolution of the hyperintensities seen. S Afr J Child Health 2018;12(4):134-136. DOI:10.7196/SAJCH.2018.v12i4.1535 Non-ketotic hyperglycaemic hemichorea-hemiballismus (NKHHC) is a rare, reversible condition, with the clinical and radiological signs usually resolving within 6 months, following correction of hyperglycaemia.[1] The condition has previously been described as specifically affecting the elderly, with very few cases described in children and adolescents.[2] We describe a paediatric patient presenting with the classic clinical and radiological findings of NKHHC. Case A 13-year-old female presented to hospital with severe cramps in her left hand. -
Absence of Neurobehavioral Disturbance in a Focal Lesion of the Left Paracentral Lobule
Behavioural Neurology (1992), 5,189-191 ICASE REPORTI Absence of neurobehavioral disturbance in a focal lesion of the left paracentral lobule T. Imamura and K. Tsuburaya Department of Neurology, Tohoku Kohseinenkin Hospital, Sendai, Japan Correspondence to: T. Imamura, Department of Neurology, Institute of Brain Diseases, Tohoku University School of Medicine, 1-1, Seiryo-machi, Aoba-Ku, Sendai 980, Japan The case of a right-handed woman with an infarcation confined to the left paracentral lobule and sparing the supplementary motor area (SMA) is reported. She presented with a right leg monoplegia and displayed no mutism. The absence of any associ ated neurobehavioral disturbances (mutism, forced grasping, reduced spontaneous arm activity or aphasia raises the possi bility that the left SMA has discrete neurobehavioral functions. Keywords: Medial frontal lobe - Precentral gyrus - Supplementary motor area - Transcortical motor aphasia INTRODUCTION Various kinds of neurobehavioral disturbances associated medial part of the left precentral gyrus, which is adjacent with left medial frontal lesions involving the supplemen to the SMA, to evaluate its possible neurobehavioral tary motor area (SMA) have been reported. Aphasia due to functions. damage of the left medial frontal lobe is characterized by an initial period of mutism followed by a stage of CASE REPORT decreased verbal output and spontaneous initiation with normal articulation (Stuss and Benson, 1986). Forced A 73-year-old right-handed woman with a history of grasping, compulsive manipulation of tools and decreased hypertension and diabetes mellitus suddenly developed a spontaneous limb movements have also been described gait disturbance. On examination, 24 h later, she was alert (Wise, 1984; Feinberg et al., 1992). -
ICD9 & ICD10 Neuromuscular Codes
ICD-9-CM and ICD-10-CM NEUROMUSCULAR DIAGNOSIS CODES ICD-9-CM ICD-10-CM Focal Neuropathy Mononeuropathy G56.00 Carpal tunnel syndrome, unspecified Carpal tunnel syndrome 354.00 G56.00 upper limb Other lesions of median nerve, Other median nerve lesion 354.10 G56.10 unspecified upper limb Lesion of ulnar nerve, unspecified Lesion of ulnar nerve 354.20 G56.20 upper limb Lesion of radial nerve, unspecified Lesion of radial nerve 354.30 G56.30 upper limb Lesion of sciatic nerve, unspecified Sciatic nerve lesion (Piriformis syndrome) 355.00 G57.00 lower limb Meralgia paresthetica, unspecified Meralgia paresthetica 355.10 G57.10 lower limb Lesion of lateral popiteal nerve, Peroneal nerve (lesion of lateral popiteal nerve) 355.30 G57.30 unspecified lower limb Tarsal tunnel syndrome, unspecified Tarsal tunnel syndrome 355.50 G57.50 lower limb Plexus Brachial plexus lesion 353.00 Brachial plexus disorders G54.0 Brachial neuralgia (or radiculitis NOS) 723.40 Radiculopathy, cervical region M54.12 Radiculopathy, cervicothoracic region M54.13 Thoracic outlet syndrome (Thoracic root Thoracic root disorders, not elsewhere 353.00 G54.3 lesions, not elsewhere classified) classified Lumbosacral plexus lesion 353.10 Lumbosacral plexus disorders G54.1 Neuralgic amyotrophy 353.50 Neuralgic amyotrophy G54.5 Root Cervical radiculopathy (Intervertebral disc Cervical disc disorder with myelopathy, 722.71 M50.00 disorder with myelopathy, cervical region) unspecified cervical region Lumbosacral root lesions (Degeneration of Other intervertebral disc degeneration,