Abnormal Movements in Critical Care Patients with Brain Injury: a Diagnostic Approach
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Cp-Research-News-2014-06-23
Monday 23 June 2014 Cerebral Palsy Alliance is delighted to bring you this free weekly bulletin of the latest published research into cerebral palsy. Our organisation is committed to supporting cerebral palsy research worldwide - through information, education, collaboration and funding. Find out more at www.cpresearch.org.au Professor Nadia Badawi Macquarie Group Foundation Chair of Cerebral Palsy PO Box 560, Darlinghurst, New South Wales 2010 Australia Subscribe at www.cpresearch.org/subscribe/researchnews Unsubscribe at www.cpresearch.org/unsubscribe Interventions and Management 1. Iran J Child Neurol. 2014 Spring;8(2):45-52. Associations between Manual Abilities, Gross Motor Function, Epilepsy, and Mental Capacity in Children with Cerebral Palsy. Gajewska E, Sobieska M, Samborski W. OBJECTIVE: This study aimed to evaluate gross motor function and hand function in children with cerebral palsy to explore their association with epilepsy and mental capacity. MATERIAL & METHODS: The research investigating the association between gross and fine motor function and the presence of epilepsy and/or mental impairment was conducted on a group of 83 children (45 girls, 38 boys). Among them, 41 were diagnosed with quadriplegia, 14 hemiplegia, 18 diplegia, 7 mixed form, and 3 athetosis. A neurologist assessed each child in terms of possible epilepsy and confirmed diagnosis in 35 children. A psychologist assessed the mental level (according to Wechsler) and found 13 children within intellectual norm, 3 children with mild mental impairment, 18 with moderate, 27 with severe, and 22 with profound. Children were then classified based on Gross Motor Function Classification System and Manual Ability Classification Scale. RESULTS: The gross motor function and manual performance were analysed in relation to mental impairment and the presence of epilepsy. -
Dystonia and Chorea in Acquired Systemic Disorders
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.4.436 on 1 October 1998. Downloaded from 436 J Neurol Neurosurg Psychiatry 1998;65:436–445 NEUROLOGY AND MEDICINE Dystonia and chorea in acquired systemic disorders Jina L Janavs, Michael J AminoV Dystonia and chorea are uncommon abnormal Associated neurotransmitter abnormalities in- movements which can be seen in a wide array clude deficient striatal GABA-ergic function of disorders. One quarter of dystonias and and striatal cholinergic interneuron activity, essentially all choreas are symptomatic or and dopaminergic hyperactivity in the nigros- secondary, the underlying cause being an iden- triatal pathway. Dystonia has been correlated tifiable neurodegenerative disorder, hereditary with lesions of the contralateral putamen, metabolic defect, or acquired systemic medical external globus pallidus, posterior and poste- disorder. Dystonia and chorea associated with rior lateral thalamus, red nucleus, or subtha- neurodegenerative or heritable metabolic dis- lamic nucleus, or a combination of these struc- orders have been reviewed frequently.1 Here we tures. The result is decreased activity in the review the underlying pathogenesis of chorea pathways from the medial pallidus to the and dystonia in acquired general medical ventral anterior and ventrolateral thalamus, disorders (table 1), and discuss diagnostic and and from the substantia nigra reticulata to the therapeutic approaches. The most common brainstem, culminating in cortical disinhibi- aetiologies are hypoxia-ischaemia and tion. Altered sensory input from the periphery 2–4 may also produce cortical motor overactivity medications. Infections and autoimmune 8 and metabolic disorders are less frequent and dystonia in some cases. To date, the causes. Not uncommonly, a given systemic dis- changes found in striatal neurotransmitter order may induce more than one type of dyski- concentrations in dystonia include an increase nesia by more than one mechanism. -
PPCO Twist System
PEER REVIEWED The NEUROLOGICNEUROLOGIC EXAMINATIONEXAMINATION in Companion Animals In the January/February issue of Part 2: Interpreting Today’s Veterinary Practice, Part 1 of this article discussed performing Abnormal Findings a neurologic examination; Part 2 will address interpretation of Helena Rylander, DVM, Diplomate ACVIM (Neurology) abnormal findings. complete neurologic examination should be THE BRAIN done in all animals presenting with suspected Lesions in the brain can be localized to the: Aneurologic disease. Abnormalities found during t Cerebrum and thalamus (ie, prosencephalon) the neurologic examination can reflect the location of t Brainstem the lesion, but not the cause, requiring further tests, t Cerebellum. such as blood analysis, electrodiagnostic tests, and In order to localize the lesion to a specific part of advanced imaging, to determine a diagnosis. the brain, an understanding of the anatomy and func- The neurologic examination evaluates different parts tion of the brain is necessary (see Brain Anatomy & of the nervous system; the findings from the examina- Related Functions). tion help localize the lesion to the: t Brain Ataxia t Spinal cord A patient with ataxia may have a lesion in the proprio- t Peripheral nervous system ceptive pathways (peripheral nerves, spinal cord, or t Cauda equina. cerebrum), vestibular system, or cerebellum. Ataxia A fundic examination is recommended, especially in can be described as an uncoordinated gait, with cross- patients with brain disorders. Repeat neurologic exami- ing of the limbs and, sometimes, listing or falling to 1 nations are helpful to discover subtle abnormalities and or both sides. Ataxia can be further characterized as: assess progression of disease. -
The Rostrocaudal Gradient for Somatosensory Perception in The
692 J Neurol Neurosurg Psychiatry 2000;69:692–709 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.69.5.692 on 1 November 2000. Downloaded from A 49 year old right handed man suddenly shape, and texture weighing 50, 60, 70, 80, developed dysaesthesia in the right hand. 90, and 100 g. For texture perception, we LETTERS TO This recovered gradually, but 1 month later prepared six wooden plates of an identical he still had an impaired tactile recognition for size and shape, on which one of six diVerent THE EDITOR objects. His voluntary movements were skill- textures (sandpaper, felt, wood, wool, fine ful. Deep tendon reflex was slightly exagger- grain, synthetic rubber) were mounted. The ated in his right arm. Babinski’s sign was patient palpated one texture by either hand absent. His language was normal. Brain MRI with his eyes closed. Then he was asked to on the 35th day after the onset showed a select tactually a correct one among the six The rostrocaudal gradient for laminar necrosis on the caudal edge of the textures. For shape perception (three somatosensory perception in the human lateral portion of the left postcentral gyrus dimensional figures) the patient palpated one postcentral gyrus (figure). of the five wooden objects (cylinder, cube, Somaesthetic assessment was done during sphere, prism, and cone) with his eyes closed. Anatomical organisation of the primate post- the 21–28th days of the illness. Then he was asked to explain the shape ver- central gyrus has been described in terms of Elementary somatosensory functions were bally. -
History-Of-Movement-Disorders.Pdf
Comp. by: NJayamalathiProof0000876237 Date:20/11/08 Time:10:08:14 Stage:First Proof File Path://spiina1001z/Womat/Production/PRODENV/0000000001/0000011393/0000000016/ 0000876237.3D Proof by: QC by: ProjectAcronym:BS:FINGER Volume:02133 Handbook of Clinical Neurology, Vol. 95 (3rd series) History of Neurology S. Finger, F. Boller, K.L. Tyler, Editors # 2009 Elsevier B.V. All rights reserved Chapter 33 The history of movement disorders DOUGLAS J. LANSKA* Veterans Affairs Medical Center, Tomah, WI, USA, and University of Wisconsin School of Medicine and Public Health, Madison, WI, USA THE BASAL GANGLIA AND DISORDERS Eduard Hitzig (1838–1907) on the cerebral cortex of dogs OF MOVEMENT (Fritsch and Hitzig, 1870/1960), British physiologist Distinction between cortex, white matter, David Ferrier’s (1843–1928) stimulation and ablation and subcortical nuclei experiments on rabbits, cats, dogs and primates begun in 1873 (Ferrier, 1876), and Jackson’s careful clinical The distinction between cortex, white matter, and sub- and clinical-pathologic studies in people (late 1860s cortical nuclei was appreciated by Andreas Vesalius and early 1870s) that the role of the motor cortex was (1514–1564) and Francisco Piccolomini (1520–1604) in appreciated, so that by 1876 Jackson could consider the the 16th century (Vesalius, 1542; Piccolomini, 1630; “motor centers in Hitzig and Ferrier’s region ...higher Goetz et al., 2001a), and a century later British physician in degree of evolution that the corpus striatum” Thomas Willis (1621–1675) implicated the corpus -
Post Stroke Focal Aware Seizures Presenting As Delayed Onset Choreoathetosis
Lehigh Valley Health Network LVHN Scholarly Works Department of Medicine Post Stroke Focal Aware Seizures Presenting as Delayed Onset Choreoathetosis Artish Patel USF MCOM - LVHN Campus, [email protected] Patrick Davis USF MCOM - LVHN Campus, [email protected] Beth Stepanczuk MD Lehigh Valley Health Network, [email protected] Follow this and additional works at: https://scholarlyworks.lvhn.org/medicine Part of the Medicine and Health Sciences Commons Published In/Presented At Patel, A., Davis, P., & Stepanczuk, B. (2021, February 9-13). Post Stroke Focal Aware Seizures Presenting as Delayed Onset Choreoathetosis. [Poster presentation]. Association of Academic Physiatrists Annual Meeting, Virtual. This Poster is brought to you for free and open access by LVHN Scholarly Works. It has been accepted for inclusion in LVHN Scholarly Works by an authorized administrator. For more information, please contact [email protected]. Post Stroke Focal Aware Seizures Presenting as Delayed Onset Choreoathetosis Artish Patel, MD, BS, Patrick Davis, MD, BS, and Beth Stepanczuk, MD Lehigh Valley Health Network; Allentown, Pa. Setting Case Description Discussion Outpatient follow-up office She initially presented with acute onset confusion, nausea, This patient offered a rare case of focal aware seizures vomiting, and aphasia. Imaging revealed acute left parietal presenting as delayed onset choreoathetosis of the right Patient temporal intraparenchymal hemorrhage with surrounding upper extremity secondary to acute left parietal temporal 39-year-old female with history of migraines and recent left parietal edema and restricted diffusion consistent with infarction intraparenchymal hemorrhage. It has been documented that temporal intraparenchymal hemorrhage presenting at three- secondary to superior sagittal sinus thrombosis. -
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 ............................................................................................ -
EMERGENCY CARE AID for ALTERNATING HEMIPLEGIA of CHILDHOOD (AHC) PATIENTS a Reference Guide for Medical Professionals
EMERGENCY CARE AID FOR ALTERNATING HEMIPLEGIA OF CHILDHOOD (AHC) PATIENTS A Reference Guide for Medical Professionals AHC DEFINITION: (Handb Clin Neurol. 2013; 112:821-6) Alternating hemiplegia of childhood (AHC) is a very rare disease characterized by recurrent attacks of loss of muscular tone resulting in hypomobility of one side of the body. The etiology of the disease is due to ATP1A3 gene mutations in the majority of patients. AHC has an onset in the first few months of life. Hemiplegic episodes are often accompanied by other paroxysmal manifestations, such as lateral eyes and head deviation toward the hemiplegic side and a very peculiar monocular nystagmus. Movement disorders such as dystonia and abnormal movements are frequent. Cognitive delay of variable degree is a common feature. Epilepsy has been reported in 50% of the cases, but seizure onset is usually during the third or fourth year of life. Many drugs have been used in AHC with very few results. Flunarizine has the most supportive anecdotal evidence regarding efficacy. AHC RISK FACTORS: TREATMENT: (Neurol Genet. 2017 Apr; 3(2): e139) There is no specific treatment for AHC. There is no approved medication or device that alters the underlying deficit in the Na+/K+ pump (see Flunarizine next page). NEUROLOGICAL: (Neurology. 2019 Sep 24;93(13)) Epilepsy is present in over 50% of AHC patients. Epilepsy in AHC can be focal or generalized seizures. Dystonia is also a common feature that affects the majority of patients dealing with AHC. Patients with AHC can deteriorate either abruptly or gradually at the motor and intellectual function level, depending on the severity of their disease. -
Botulinum Neurotoxin Injections in Childhood Opisthotonus
toxins Article Botulinum Neurotoxin Injections in Childhood Opisthotonus Mariam Hull 1,2,* , Mered Parnes 1,2 and Joseph Jankovic 2 1 Section of Pediatric Neurology and Developmental Neuroscience, Texas Children’s Hospital and Baylor College of Medicine, Houston, TX 77030, USA; [email protected] 2 Parkinson’s Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA; [email protected] * Correspondence: [email protected] Abstract: Opisthotonus refers to abnormal axial extension and arching of the trunk produced by excessive contractions of the paraspinal muscles. In childhood, the abnormal posture is most often related to dystonia in the setting of hypoxic injury or a number of other acquired and genetic etiologies. The condition is often painful, interferes with ambulation and quality of life, and is challenging to treat. Therapeutic options include oral benzodiazepines, oral and intrathecal baclofen, botulinum neurotoxin injections, and deep brain stimulation. Management of opisthotonus within the pediatric population has not been systematically reviewed. Here, we describe a series of seven children who presented to our institution with opisthotonus in whom symptom relief was achieved following administration of botulinum neurotoxin injections. Keywords: opisthotonus; opisthotonos; axial dystonia; botulinum toxin Key Contribution: This is the first series of pediatric patients with opisthotonus treated with bo- tulinum neurotoxin injections. Botulinum neurotoxin injections should be added to the armamentar- ium of treatment options in children with axial dystonia, including opisthotonos. Citation: Hull, M.; Parnes, M.; 1. Introduction Jankovic, J. Botulinum Neurotoxin Injections in Childhood Opisthotonus. Opisthotonus, derived from the Greek “opistho” meaning behind and “tonos” mean- Toxins 2021, 13, 137. -
Neurological Emergencies Natasha Olby Vetmb, Phd, MRCVS, DACVIM (Neurology) College of Veterinary Medicine, NCSU, Raleigh, NC In
Neurological Emergencies Natasha Olby VetMB, PhD, MRCVS, DACVIM (Neurology) College of Veterinary Medicine, NCSU, Raleigh, NC Introduction Neurological emergencies are common and require a cool head, careful patient assessment and prompt action! While there are many instances when an owner perceives their patient to be in a crisis when in fact they are not, any rapidly changing neurological dysfunction should be considered an emergency and the patient evaluated immediately. This presentation will give an overview of alterations in mentation, seizures and paralysis using case examples. An important general point is that you should have emergency protocols available as they improve outcomes in any emergency situation. Altered Mentation: Stupor and Coma Terms used to describe mental status include terms that describe level of consciousness (e.g. stupor, coma) and terms that describe behavior (e.g. dementia, hysteria). Level of consciousness is controlled by the ascending reticular activating system (ARAS). This mass of neurons extends through the brainstem to project to the thalamus and from there to the cortex. The ability to interact appropriately with the surrounding environment depends on the ability to process and integrate sensory information and to combine this information with learned information. The forebrain, and in particular the cerebrum and limbic system, is vital for normal behavior. Stupor is defined as decreased consciousness, but responsive to strong stimuli: these patients tend to be in sternal or lateral recumbency and are difficult to rouse. Coma is defined as unresponsive to stimuli. Stupor and coma are considered to be emergencies. Causes of changes in mental status There are numerous different causes of changes in mental status. -
Neurodegeneration with Brain Iron Accumulation: Two Additional Cases with Dystonic Opisthotonus
Freely available online Case report Neurodegeneration with Brain Iron Accumulation: Two Additional Cases with Dystonic Opisthotonus Sahil Mehta* & Vivek Lal Department of Neurology, Post Graduate Institute of Medical Education and Research, Chandigarh, IN Abstract Background: Specific phenomenology and pattern of involvement in movement disorders point toward a probable clinical diagnosis. For example, forehead chorea usually suggests Huntington’s disease; feeding dystonia suggests neuroacanthocytosis and risus sardonicus is commonly seen in Wilson’s disease. Dystonic opisthotonus has been described as a characteristic feature of neurodegeneration with brain iron accumulation (NBIA) related to PANK2 and PLA2G6 mutations. Case report: We describe two additional patients in their 30s with severe extensor truncal dystonia causing opisthotonic posturing in whom evaluation revealed the diagnosis of NBIA confirmed by genetic testing. Discussion: Dystonic opisthotonus may be more common in NBIA than it is reported and its presence especially in a young patient should alert the neurologists to a possibility of probable NBIA. Keywords: Opisthotonus, dystonia, neurodegeneration with brain iron accumulation, secondary, phenomenology, genetics, botulinum toxin Citation: Mehta S, Lal V. Neurodegeneration with brain iron accumulation: Two additional cases with dystonic opisthotonus. Tremor Other Hyperkinet Mov. 2019; 9. doi: 10.7916/tohm.v0.683 *To whom correspondence should be addressed. E-mail: [email protected] Editor: Elan D. Louis, Yale University, USA Received: June 14, 2019 Accepted: July 24, 2019 Published: August 21, 2019 Copyright © 2019 Mehta S, Lal V. 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. -
Dem11. Leukodystrophies.Pdf
LEUKODYSTROPHIES Dem11 (1) Leukodystrophies Last updated: September 5, 2017 ADRENOLEUKODYSTROPHY .................................................................................................................... 2 METACHROMATIC LEUKODYSTROPHIES (S. SULFATIDE LIPIDOSES) ..................................................... 3 GLOBOID CELL LEUKODYSTROPHY (S. KRABBE DISEASE) .................................................................... 4 PELIZAEUS-MERZBACHER DISEASE ........................................................................................................ 4 CANAVAN DISEASE (S. SPONGY DEGENERATION OF NERVOUS SYSTEM)................................................ 5 COCKAYNE SYNDROME............................................................................................................................ 5 ALEXANDER DISEASE ............................................................................................................................... 5 LEUKODYSTROPHIES - uncommon genetic biochemical defects of: a) myelin formation (synthesis) → DYSMYELINATION (→ loss of defective myelin); abnormal lipids incorporated into defective myelin are metachromatic. b) myelin maintenance (turnover) → DEMYELINATION (e.g. many sudanophilic leukodystrophies). N.B. sudanophilia is produced when Sudan black reacts with neutral fat breakdown products of myelin; since myelin breakdown is result of variety of metabolic or acquired insults, sudanophilia provides no useful information about pathogenesis! it is very difficult to distinguish