DOCSLIB.ORG

13 Spasticity, Rigidity, and Other Motor Symptoms

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
13 Spasticity, Rigidity, and Other Motor Symptoms Spasticity, Rigidity, and Other Motor Symptoms in Neurodegenerative Disorders Zoltan Mari, MD Ruvo Family Chair & Director, Parkinson’s & Movement Disorders Program Clinical Professor of Neurology, University of Nevada Adjunct Associate Professor of Neurology, Johns Hopkins University Hypertonias OUTLINE Definitions and classifications of increased muscle tone (hypertonias) Evaluation and management of hypertonias: Properly identify and diagnose the etiology/nature of hypertonia – a vignette Physical therapy Pharmacotherapy Chemodenervation: Phenol/ethanol Botulinum toxins Surgery DISCLOSURES No speaker bureau activity in the past 12 months Institutionally awarded research support from: NIH, PF, MJFF, Eli Lilly, Cerevel, Amneal, NeuroDerm Consulting fees from: GB Sciences, Biogen, GKC, Acadia, Elsevier Hypertonias 1 Definitions • Spasticity: Caused by lesions in the pyramidal tract (i.e. upper motor neurons) such the corticospinal tract MS MSA (MSA may cause cerebellar pathology [MSA-C] leading to hypo-, not hypertonia, but it may well cause pathology affecting long tracts [corticospinal included] leading to spasticity Stroke Spinal cord compression Motor neuron disease Weakness usually present More resistance in one direction the other direction More tone in initial part of movement – “Clasp knife spasticity” It is velocity dependent (i.e. more noticeable with fast movements) • Rigidity: Seen in extrapyramidal disorders (i.e. Parkinson’s), often implicating the rubrospinal or vestibulospinal tracts Subtypes include: Cog wheel rigidity (Parkinson’s) – Tremor superimposed on this hypertonia that results in intermittent increase in tone during the movement. Lead pipe rigidity (neuroleptic malignant syndrome, Parkinsonism-hyperpyrexia syndrome or less commonly stiff man syndrome) – Uniform increase in tone Same resistance in all directions Not velocity dependent – does not vary with speed of movement of muscle groups involved • Dystonia: Sustained or repetitive involuntary muscle contractions resulting in twisting and repetitive movements or abnormal fixed postures – common in PD • Paratonia (Gegenhalten): Inability to relax muscles during muscle tone assessment Oppositional paratonia ("gegenhalten"): subjects involuntarily resist to passive movements – usually seen in cases of dementing disorders and/or frontal pathology Facilitatory paratonia ("mitgehen"): subjects involuntary assist passive movements (does not represent hypertonia – only mentioned here for completeness) Hypertonias Vignette • 70 years old gentleman • History significant for advanced PD (diagnosed in 2013, DaTscan in 2018 showed profound ioflupane uptake loss, taking 250 mg levodopa 7x/day), severe spinal stenosis (multiple surgeries, significant spinal cord impingement with signal changes) • In addition, his PD presentation included what was believed to be dystonias • Currently c/o of episodic, extremely severe stiffening of muscles in both LEs, as well as lumbar paraspinal musculature These contractions are reported to be “extremely painful” No clear relationship between C/L dosing and the timing of these episodes The episodes are getting worse over the years Hypertonias 2 Personal kinetograph (PKG) analysis performed, to identify C/L response While there is C/L response, the patient remains under-medicated Increased PTI signals significant immobility Lack of dyskinesias rules out the possibility of ON-dystonias as a possible source of hypertonia, but OFF-dystonia remains possible While the patient seems under- treated, a pure OFF-rigidity or dystonia cause is unlikely Hypertonias Vignette Summary • Multiple contributors to hypertonia simultaneously possible • Timing to C/L dosing can inform about dopaminergic mechanisms – OFF dystonia is often painful, whereas rigidity usually isn’t • Spasticity is probably a contributor, however, unlikely to be prominently episodic • PKG analysis confirmed some C/L related variation in motor speed • Further effort may include: Additional C/L could confirm a primarily dopaminergic source – if episodes improve – a deterrent is the already very high daily C/L dose + the lack of a clear result from previous similar attempts to increase C/L A (diagnostically) even better alternative is the use of “rescue” (rapid acting parenteral) dopamine options BoNT injections – a limitation being the overall size of affected muscles PT may be limited due to the prominently episodic nature of the hypertonia SPS may be considered (anti-GAD65 testing) Hypertonias 3 Negative Clinical Aspects of Hypertonia • Interferes with mobility, exercise, and joint range of motion • Interferes with activities of daily living • Causes pain (see Vignette) • Makes patient care more difficult, including ADLs, transfers, basic care • Causes sleep disturbance • As demonstrated in the vignette, the exact source/etiology of hypertonia may be confusing, ambiguous, and/or multi-factorial • Interference with ambulatory abilities Hypertonias Positive Clinical Aspects of Hypertonia • Maintains muscle tone • May counter (flaccid) weakness • Helps support circulatory function • May prevent formation of deep vein thrombosis • May assist in activities of daily living • May assist in maintaining erect posture • May assist in gait Hypertonias 4 Mechanical Contracture vs Hypertonia Mechanical (not active muscle) Hypertonia (active muscle) • Fixed • Dynamic • Tendon and/or ligament • Slow stretch • Charcot joint • Palpable antagonistic • Heterotopic ossification muscle action • Increased reflexes Most often, both mechanical and muscle factors Hypertonias Assessing Hypertonia • History • Neurological examination • Measurement tools Hypertonias 5 Key Questions in History • Location? • Time of day, aggravating/alleviating factors? (diary) • Painful spasms? • Functional limitations? • Need for extensor tone in legs for standing? Hypertonias Neurological Examination • Standard musculoskeletal examination including range of motion (may be measured with a goniometer) • Detailed neurologic examination • Clonus • Tone measures (eg, Ashworth scale) Hypertonias 6 Modified Ashworth Scale (MAS) • 0 = Normal tone • 1 = Slight “catch” • 1+ = Significant “catch” • 2 = Mild, limb moves easily • 3 = Moderate, passive range of movement difficult • 4 = Severe, rigid limb Hypertonias Quantitative Evaluation • Gait lab with surface electromyography (mostly research use) • Fugl-Meyer test for upper-limb dexterity Hypertonias For educational purposes only. 7 What Is Meaningful Function? Passive Function Active Function • Increased ROM • Improved upper limb use: • Improved positioning Reaching, grasping, releasing • Increased ease of hygiene • Improved mobility • Improved cosmesis • Improved gait • Decreased spasm frequency • Decreased energy • Improved orthotic fit expenditure • Decreased pain ROM = range of motion. Brin M. Muscle Nerve. 1997;20:s208. Hypertonias Goal Attainment Scales (GAS) • Select 2 SMART (specific, measurable, achievable, realistic, time-frame) goals with patient -2 did not achieve by a lot -1 did not achieve by a little 0 achieved +1 exceeded by a little +2 exceeded by a lot Hypertonias 8 Spectrum of Care for Management of Hypertonias Intrathecal Prevent Baclofen Nociception Therapy Rehabilitation Oral Therapy Drugs Patient Orthopedic Injection Treatment Therapy Neurosurgery Hypertonias Treatment Paradigms “Old School” “New School” • Stepwise approach • Generalized vs localized • • Modalities Acute vs chronic • Patient-specific analysis of • Medications side effects • Injections • Mix and match therapies • Tendon surgery early • Nerve ablation • Consider multiple simultaneous etiologies and localizations Hypertonias 9 Simplified Treatment Algorithm for Hypertonias Treat Underlying Disease/Specific Etiology PT/OT Medical Treatments Surgical Treatments Stretch/Splint Oral Medications Myelotomy Dorsal Rhizotomy Positioning Chemodenervation: -BoNT Injections Other Surgeries Other Modalities -Phenol/Ethanol (Tendon Transposition, etc) Intrathecal Baclofen Hypertonias Oral Medications (1) • Baclofen Binds GABA-b receptors Side effects—weakness, lethargy, rebound seizures—if stopped abruptly GABA = gamma-aminobutyric acid. Hypertonias 10 Oral Medications (2) • Dantrolene Blocks Ca++ channels in muscle No CNS effects, but causes significant weakness Hepatic dysfunction rare CNS = central nervous system. Hypertonias Oral Medications (3) • Tizanidine (TIZ) Alpha-2 agonist Side effects: Lethargy, orthostasis, dry mouth Inferior to BoNT in head-to-head placebo- controlled trial (Simpson) BoNT = botulinum toxin. Simpson et al. J Neurol Neurosurg Psych. 2009;80:380-385. Hypertonias 11 Oral Medications (4) • Diazepam Enhances GABA through benzodiazepine receptors in brain Rapid development of tolerance Side effects: Drowsiness, delirium, abuse potential, withdrawal seizures Hypertonias Cannabinoids • THC and CBD • Cochrane analysis reviewed 38 papers—only 6 were RCTs. • Nonsignificant improvements in 6-minute walk and MAS scores, but significant subject improvement. • Med legalization CBD = cannabidiol; THC = tetrahydrocannabinol; RCT = randomized controlled trial. Lakhand S, et al. BMC Neurol. 2009;9:1-6. Hypertonias 12 Intrathecal Baclofen • Generalized spasticity • Not controlled or side effects from oral medications • Delivers approximately 1/50 dose baclofen direct to cerebrospinal fluid • Infinitely programmable • Refill every 3 to 12 months • Mechanical complications Hypertonias Phenol and Alcohol . Causes degeneration of both motor
Load more

Recommended publications
  • Joint Contractures and Acquired Deforming Hypertonia in Older People
    Annals of Physical and Rehabilitation Medicine 62 (2019) 435–441 Available online at ScienceDirect www.sciencedirect.com Review Joint contractures and acquired deforming hypertonia in older people: Which determinants? a,b, c d,e a Patrick Dehail *, Nathaly Gaudreault , Haodong Zhou , Ve´ronique Cressot , a,f g h Anne Martineau , Julie Kirouac-Laplante , Guy Trudel a Service de me´decine physique et re´adaptation, poˆle de neurosciences cliniques, CHU de Bordeaux, 33000 Bordeaux, France b Universite´ de Bordeaux, EA 4136, 33000 Bordeaux, France c E´cole de re´adaptation, faculte´ de me´decine et des sciences de la sante´, universite´ de Sherbrooke, Sherbrooke, Canada d Department of Biology, Faculty of Science, University of Ottawa, Ottawa, ON, Canada e Bone and Joint Research Laboratory, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada f De´partement de me´decine, division de physiatrie, universite´ Laval, Que´bec, QC, Canada g De´partement de me´decine, division de ge´riatrie, universite´ Laval, Que´bec, QC, Canada h Department of Medicine, Division of Physical Medicine and Rehabilitation, University of Ottawa, Bone and Joint Research Laboratory, The Ottawa Hospital Research Institute, Ottawa, ON, Canada A R T I C L E I N F O A B S T R A C T Article history: Joint contractures and acquired deforming hypertonia are frequent in dependent older people. The Received 29 March 2018 consequences of these conditions can be significant for activities of daily living as well as comfort and Accepted 29 October 2018 quality of life. They can also negatively affect the burden of care and care costs.
    [Show full text]
  • Neurovascular Anatomy (1): Anterior Circulation Anatomy
    Neurovascular Anatomy (1): Anterior Circulation Anatomy Natthapon Rattanathamsakul, MD. December 14th, 2017 Contents: Neurovascular Anatomy Arterial supply of the brain . Anterior circulation . Posterior circulation Arterial supply of the spinal cord Venous system of the brain Neurovascular Anatomy (1): Anatomy of the Anterior Circulation Carotid artery system Ophthalmic artery Arterial circle of Willis Arterial territories of the cerebrum Cerebral Vasculature • Anterior circulation: Internal carotid artery • Posterior circulation: Vertebrobasilar system • All originates at the arch of aorta Flemming KD, Jones LK. Mayo Clinic neurology board review: Basic science and psychiatry for initial certification. 2015 Common Carotid Artery • Carotid bifurcation at the level of C3-4 vertebra or superior border of thyroid cartilage External carotid artery Supply the head & neck, except for the brain the eyes Internal carotid artery • Supply the brain the eyes • Enter the skull via the carotid canal Netter FH. Atlas of human anatomy, 6th ed. 2014 Angiographic Correlation Uflacker R. Atlas of vascular anatomy: an angiographic approach, 2007 External Carotid Artery External carotid artery • Superior thyroid artery • Lingual artery • Facial artery • Ascending pharyngeal artery • Posterior auricular artery • Occipital artery • Maxillary artery • Superficial temporal artery • Middle meningeal artery – epidural hemorrhage Netter FH. Atlas of human anatomy, 6th ed. 2014 Middle meningeal artery Epidural hematoma http://www.jrlawfirm.com/library/subdural-epidural-hematoma
    [Show full text]
  • Diagnosing Dementia: Signs, Symptoms and Meaning
    Université de Montréal Diagnosing Dementia: Signs, Symptoms and Meaning Pa= Janice Elizabeth Graham Département d'anthropologie Faculté des arts et des sciences Thèse présentée à la Faculté des études supérieures en vue de l'obtention du grade de Philosophia Doctor 0h.D.) en anthropologie Janice E.Graharn, 1996 National Library Bibliothèque nationale I*I of Canada du Canada Acquisitions and Acquisitions et Bibtiographic Services services bibliographiques 395 Wellington Street 395, rue Wellington Ottawa ON K1A ON4 Ottawa ON KIA ON4 Canada Canada Vour fik Vorre réference Our file Notre refdrence The author has granted a non- L'auteur a accordé une licence non exclusive licence dowing the exdusive permettant à la National Library of Canada to Bibliothèque nationde du Canada de reproduce, loan, distribute or sell reproduire, prêter, distribuer ou copies of this thesis in microform, vendre des copies de cette thèse sous paper or electronic formats. la fome de microfiche/nlm, de reproduction sur papier ou sur format électroniq2e. The author retains ownership of the L'auteur conserve la propriété du copyright in this thesis. Neither the droit d'auteur qui protège cette thèse. thesis nor substantial extracts f?om it Ni la thèse ni des extraits substantiels may be printed or othenvise de celle-ci ne doivent être imprimés reproduced without the author's ou autrement reproduits sans son permission. autorisation. Université de Montréal Faculte des Btudes superieures Cette thèse ultitulee: Diagnosing Dementia: Signs, Symptoms and Meaning presentée
    [Show full text]
  • (Post-Tenure) Abbott PW, Gumusoglu SB, Bittle J, Beversdorf DQ, Stevens HE
    RESEARCH PUBLICATIONS - UNIVERSITY OF MISSOURI: SINCE LAST REVIEW (Post-Tenure) Abbott PW, Gumusoglu SB, Bittle J, Beversdorf DQ, Stevens HE. (2018). Prenatal stress and genetic risk: how prenatal stress interacts witH genetics to alter risk for psycHiatric illness. PsycHoneuroendocrinology 90:9-21. Matsui F, HecHt P, YosHimoto K, Watanabe Y, Morimoto M, FritscHe K, Will M, Beversdorf D. (2017). DHA Mitigates Autistic BeHaviors Accompanied by Dopaminergic CHange in a Gene/Prenatal Stress Mouse Model. Neurosci 371:407-419. Sun GY, Simonyi A, FritscHe, KL, CHuang DY, Hannick M, Gu Z, Greenlief CM, Yao JK, Lee JC, Beversdorf DQ. DocosaHexaenoic acid (DHA): an essential nutrient and a nutraceutical for brain HealtH and diseases. Prostaglandins, Leukitrienes and Essential Fatty Acids (PLEFA). 2017, DOI: 10.1016/j.plefa.2017.03.006 [Epub aHead of print] Sjaarda CP, HecHt P, McNaugHton AJM, ZHou A, Hudson ML, Will MJ, SmitH G, Ayub M, Liang P, CHen N, Beversdorf D, Liu X. Interplay between maternal Slc6a4 mutation and prenatal stress: a possible mecHanism for autistic beHavior development. Sci Rep. 2017 Aug 18;7(1):8735.12 Marler S, Ferguson BJ, Lee EB, Peters B, Williams KC, McDonnell E, Macklin EA, Levitt P, Margolis KG Beversdorf DQ, Veenstra-VanderWeele. J. Association of rigid-compulsive beHavior witH functional constipation in autism spectrum disorder. J Autism Devel Disord 47:1673-1681. Davis DJ, HecHt PM, Jasarevic E, Beversdorf DQ, Will MJ, FritscHe F, Gillespie CH. Sex-specific effects of docosahexaenoic acid (DHA) on the microbiome and beHavior of socially-isolated mice. Brain BeHav Immun 2017;59:38-48. BelencHia AM, Jones KL, Will M, Beversdorf DQ, Vieira-Potter V, Rosenfeld CS, Peterson CA.
    [Show full text]
  • Motor Function, Paratonia and Glycation Cross-Linked in Older People
    Hans Dretnh Motor function, paratonia UITNODIGING voor het bijwonen van de openbare verdediging van mijn proefschrift and glycation cross-linked in older people Motor function, paratonia and glycation cross-linked Motor function decline and paratonia in older people and their relation with Advanced Glycation End-Products Maandag 24 september om 12.45 in de aula van het Academiegebouw van de Rijksuniversiteit Groningen, Broerstraat 5 te Groningen Aansluitend bent u van harte welkom op de receptie ter plaatse Motor Function, Paratonia and Glycation Cross-linked in Older People Cross-linked and Glycation Paratonia Function, Motor Tevens bent u tussen 16.00 en 18.00 welkom voor een borrel in ZuidOostZorg/Sunenz, Burgemeester Wuiteweg 140, Drachten. Graag aanmelden voor de borrel via [email protected] voor 17 september. Hans Drenth [email protected] [email protected] Paranimfen: Sjoukje Drenth Fransisca Spa Contact [email protected] Hans Drenth Motor Function, Paratonia and Glycation Cross-linked in Older People Motor function decline and paratonia and their relation with Advanced Glycation End-Products Hans Drenth The work presented in this thesis was performed at the Research Group Healthy Ageing, Allied Health Care and Nursing, Hanze University of Applied Sciences, Groningen, the Netherlands, at the Research Institute SHARE of the Groningen Graduate School of Medical Sciences of the University Medical Center Groningen, University of Groningen, The Netherlands and at the Frailty in Ageing research group, Vrije Universiteit Brussel, Brussels, Belgium. The work described in this thesis was sponsored by Alzheimer Nederland (the Dutch Alzheimer Organisation) and ZuidOostZorg, organisation for Elderly Care, Drachten, the Netherlands.
    [Show full text]
  • Pseudoparkinsonism: a Review of a Common Nonparkinsonian Hypokinetic Movement Disorder
    Vol.2, No.4, 108-112 (2013) Advances in Parkinson’s Disease http://dx.doi.org/10.4236/apd.2013.24020 Pseudoparkinsonism: A review of a common nonparkinsonian hypokinetic movement disorder Roger Kurlan*, Marcie L. Rabin Atlantic Neuroscience Institute, Overlook Medical Center, Summit, USA; *Corresponding Author: [email protected] Received 16 September 2013; revised 16 October 2013; accepted 24 October 2013 Copyright © 2013 Roger Kurlan, Marcie L. Rabin. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT [2-4]. Over time, clinicians learned that a variety of entities This article reviews the syndrome pseudopark- besides neuroleptic drugs can similarly cause a clinical insonism, a movement disorder described in the picture resembling that of PD. The notion that a parkin- literature that resembles parkinsonism but dif- sonian syndrome could be caused by cerebrovascular fers qualitatively. Patients with this disorder disease became popularized in the 1980’s and 1990’s. have apraxic slowness, paratonic rigidity, frontal Some publications referred to the condition as “vascular gait disorder and elements of akinesia that, pseudoparkinsonism” [5,6], similar to the term used for taken together, may be mistaken for true park- neuroleptic drugs. Other articles, in contrast, used the insonism. Pseudoparkinsonism appears to be term “vascular parkinsonism” to describe features with a common and is most often due to Alzheimer’s vascular etiology that are reminiscent of, but distinct disease or vascular dementia. It seems that pa- from, those found in PD.
    [Show full text]
  • Assessment of Cognitive Complaints Toolkit for Alzheimer’S Disease
    Assessment of Cognitive Complaints Toolkit for Alzheimer’s Disease PRODUCED BY THE CALIFORNIA ALZHEIMER’S DISEASE CENTERS AND FUNDED BY THE CALIFORNIA DEPARTMENT OF PUBLIC HEALTH, ALZHEIMER’S ACCT-AD 1 DISEASE PROGRAM CONTENTS Wellness Visit Interview 1 Instructions 1 Patient Questions (Section A) 2 Informant Questions (Section B) 6 Full Clinical Assessment 10 Instructions 10 Open Questioning and History of Present Illness 11 History for Full Evaluation 15 History of Motor Symptoms 27 Family History 33 Daily Function 34 Physical and Neurological Examination 36 Cognitive Scores 40 Labs and Imaging 41 Diagnostic Disclosure and Counseling 43 Discussing the Diagnosis of Dementia 43 Driving Scripts 45 Medication for Treatment Scripts 48 Script for Discussion of Dementia-Related Behavioral Symptoms 51 Script To Discuss Possible Participation In Research 53 Guidance on Making a Referral 54 Guidance on Billing 55 Evaluating a Concern 55 After Diagnosis 57 WELLNESS VISIT INTERVIEW Ask 3 questions about memory, language & personality in Section A, Part 1 If all answers “green,” If any answers are confirm with informant orange, proceed to using questions in-depth patient questions in Section B, Part 1 in Section A, Part 2 If informant available If informant expresses If any answers are and confirms concern, proceed to If no informant, yellow, proceed to no concerns, in-depth questions in do Mini-Cog Full Clinical Assessment stop assessment Section B, Part 2 (pg. 10) If Mini-Cog is not If any answers are If Mini-Cog is normal, normal, proceed to yellow, proceed to stop assessment and Full Clinical Assessment Full Clinical Assessment reassure patient (pg.
    [Show full text]
  • Treatment of Ballism and Pseudobulbar Affect with Sertraline
    OBSERVATION Treatment of Ballism and Pseudobulbar Affect With Sertraline Michael S. Okun, MD; Alonso R. Riestra, MD; Stephen E. Nadeau, MD Background: The pathogenesis of ballism is uncertain Results: Complete remission of symptoms within 48 and may involve more than one mechanism; treatment hours of each drug trial. is not always efficacious. Objective: To provide evidence of a nondopaminergic Conclusion: Sertraline may offer an alternative with a mechanism and the potential for a prompt and nearly com- better adverse effect profile than dopamine receptor plete response to a serotonergic agent. blockers in the treatment of patients with ballism. Methods: Report of 2 separate trials of sertraline hy- drochloride in a single patient. Arch Neurol. 2001;58:1682-1684 HE MECHANISM of ballism is not smoked in 25 years. He was a former uncertain, and its re- railroad worker now practicing television sponse to treatment with evangelism. neuroleptics is frequently Although the patient’s vital signs were slow, fraught with adverse normal, he had an irregularly irregular Teffects, and occasionally so unsatisfac- heartbeat. He recalled none of 3 objects af- tory as to motivate surgical treatment. We ter several minutes of distraction, and he report a case that suggests that an alter- had an anomic aphasia. He had a de- native treatment, sertraline hydrochlo- pressed mood and flattened affect, and he ride, may be rapidly effective and associ- frequently exhibited pseudobulbar cry- ated with few adverse effects. This and ing. When asked, he denied that he was sad other reported cases also suggest that the on these occasions. Cranial nerve exami- mechanism of ballism may be complex and nation results were normal with the excep- susceptible to different treatments in dif- tion of an incongruous right homony- ferent patients.
    [Show full text]
  • A Dictionary of Neurological Signs.Pdf
    A DICTIONARY OF NEUROLOGICAL SIGNS THIRD EDITION A DICTIONARY OF NEUROLOGICAL SIGNS THIRD EDITION A.J. LARNER MA, MD, MRCP (UK), DHMSA Consultant Neurologist Walton Centre for Neurology and Neurosurgery, Liverpool Honorary Lecturer in Neuroscience, University of Liverpool Society of Apothecaries’ Honorary Lecturer in the History of Medicine, University of Liverpool Liverpool, U.K. 123 Andrew J. Larner MA MD MRCP (UK) DHMSA Walton Centre for Neurology & Neurosurgery Lower Lane L9 7LJ Liverpool, UK ISBN 978-1-4419-7094-7 e-ISBN 978-1-4419-7095-4 DOI 10.1007/978-1-4419-7095-4 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2010937226 © Springer Science+Business Media, LLC 2001, 2006, 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made.
    [Show full text]
  • RES11078 CONTROL PATIENTS Book: Blank Case Report
    Blank Case Report Form for Study: RES11078 Book: CONTROL PATIENTS Page 1 Blank Case Report Form for Study RES11078 PT: _ _ INVSITE:: INV: Visit_Name : CSA Visit_Date: COMMON SUBJECT ASSESSMENT (CSA) Date of completion ___________ Participant: (CASE= Case, CNTL= Control, FAM= Family Member) CRF Version _ Complete by site staff before handing to study participant for Items 1-15 Page 2 Blank Case Report Form for Study RES11078 PT: ____________________ INVSITE: INV: Visit_Name : CSA Visit_Date: COMMON SUBJECT ASSESSMENT Continued Medical and Family History These questions are about you and your health. There are no right or wrong answers. You can put 'Don't Know'. Most people take 5 to 15 minutes to complete, but take as much time as you need. Feel free to ask the study staff if you need help or have questions. Section 1 - Your Information Please fill in boxes: 1. Date of birth ___________ 2. Please put your sex. __ (M= Male , F= Female) 3. Are you adopted? __ (Y= Yes, N= No, K= Don't know) Page 3 Blank Case Report Form for Study RES11078 PT: ____________ INVSITE: INV: Visit_Name : CSA Visit_Date: COMMON SUBJECT ASSESSMENT Continued Section 2 - You and Your Family's Origins The following is about you, your parents and grandparents if related by blood (for example, your biological parents, but NOT your step-parents). 4. For You SL SELF Race _ (W= White, B= Black, A= Asian, X= Other). Other, specify ____________________ Your first Language(s) 1. __ ____________________ (EN= English, FR= French, GE= German, 2. __ ____________________ HL= Dutch, IT= Italian, X= Other).
    [Show full text]
  • University of Groningen Motor Function, Paratonia and Glycation Cross
    University of Groningen Motor function, paratonia and glycation cross-linked in older people Drenth, Hans IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2018 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Drenth, H. (2018). Motor function, paratonia and glycation cross-linked in older people: Motor function decline and paratonia and their relation with Advanced Glycation End-products. [Groningen]: University of Groningen. Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date: 21-05-2019 Chapter 4 Advanced Glycation End-Products are Associated with the Presence and Severity of Paratonia in Early Stage Alzheimer Disease Hans Drenth, Sytse U. Zuidema, Wim P. Krijnen, Ivan Bautmans, Cees van der Schans, Hans Hobbelen JAMDA 2017, Jul 1; 18(7): 636.e7-636.e12.
    [Show full text]
  • Temporal Lobe Epilepsy and Alzheimer's Disease
    Journal of Alzheimer’s Disease Reports 5 (2021) 243–261 243 DOI 10.3233/ADR-200286 IOS Press Review Temporal Lobe Epilepsy and Alzheimer’s Disease: From Preclinical to Clinical Evidence of a Strong Association Mario Tombini∗, Giovanni Assenza, Lorenzo Ricci, Jacopo Lanzone, Marilisa Boscarino, Carlo Vico, Alessandro Magliozzi and Vincenzo Di Lazzaro Unit of Neurology, Neurophysiology, Neurobiology, Department of Medicine, University Campus Bio-Medico, Rome, Italy Accepted 5 March 2021 Pre-press 30 March 2021 Abstract. Increasing evidence coming from both experimental and humans’ studies strongly suggest the existence of a link between epilepsy, in particular temporal lobe epilepsy (TLE), and Alzheimer’s disease (AD). Patients with mild cognitive impairment and AD are more prone to have seizures, and seizures seem to facilitate amyloid-␤ and tau deposits, thus promoting neurodegenerative processes. Consistent with this view, long-lasting drug-resistant TLE and AD have been shown to share several pathological and neuroimaging features. Even if studies addressing prevalence of interictal and subclinical epileptiform activity in these patients are not yet conclusive, their findings raise the possibility that epileptiform activity might negatively impact memory and hasten cognitive decline, either directly or by association with unrecognized silent seizures. In addition, data about detrimental effect of network hyperexcitability in temporal regions in the premorbid and early stages of AD open up new therapeutic opportunities for antiseizure medications and/or antiepileptic strategies that might complement or enhance existing therapies, and potentially modify disease progression. Here we provide a review of evidence linking epileptiform activity, network hyperexcitability, and AD, and their role promoting and accelerating neurodegenerative process.
    [Show full text]