Textbook of Neural Repair and Rehabilitation

In two freestanding volumes, Textbook of Neural Repair and Rehabilitation provides comprehensive coverage of the science and practice of neurological rehabilitation. This volume, Medical Neurorehabilitation, can stand alone as a clinical handbook for neurorehabilitation. It covers the practical applications of the basic science principles presented in Volume I, provides authoritative guidelines on the management of disabling symptoms, and describes comprehensive rehabilitation approaches for the major categories of disabling neurological disorders. Emphasizing the integration of basic and clinical knowledge, this book and its companion are edited and written by leading international authorities. Together they are an essential resource for neuroscientists and provide a foundation for the work of clinical neurorehabilitation professionals.

Michael E. Selzer is Professor of Neurology at the University of Pennsylvania and Research Director in the Department of Physical Medicine Rehabilitation. He is editor-in-chief of Neurorehabilitation and Neural Repair, the official Journal of the American Society of Neurorehabilitation and the World Federation of Neurorehabilitation. Leonardo G. Cohen is Chief of the Human Cortical Physiology Section and the Stroke Rehabilitation Clinic at the National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Bethesda. Stephanie Clarke is Professor and Head of Neuropsychology at the University Hospital, Lausanne and President of the Swiss Society of Neurorehabilitation. Pamela W. Duncan is Professor of Health Services Administration and Physical Therapy, and Director

of the Brooks Center for Rehabilitation Studies, University of Florida.

Fred H. Gage is Professor in the Laboratory of
Genetics at the Salk Institute, and served as President of the Society for Neuroscience, 2001–2002. He is a fellow of the American Association for the Advancement of Science and a member of the National Academy of Sciences and the Institute of Medicine.

Textbook of Neural Repair and Rehabilitation
Volume II Medical Neurorehabilitation
EDITED BY

Michael E. Selzer
University of Pennsylvania

Stephanie Clarke
University of Lausanne

Leonardo G. Cohen
National Institutes of Health

Pamela W. Duncan
University of Florida

Fred H. Gage
The Salk Institute

cambridge university press Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo Cambridge University Press The Edinburgh Building, Cambridge cb2 2ru, UK Published in the United States of America by Cambridge University Press, New York www.cambridge.org Information on this title: www.cambridge.org/9780521856423 © Cambridge University Press 2006 This publication is in copyright. Subject to statutory exception and to the provision of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. First published in print format 2006 isbn-13 isbn-10 isbn-13 isbn-10 978-0-511-16919-9 eBook (NetLibrary) 0-511-16919-1 eBook (NetLibrary) 978-0-521-85642-3 hardback 0-521-85642-6 hardback

Cambridge University Press has no responsibility for the persistence or accuracy of urls for external or third-party internet websites referred to in this publication, and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Every effort has been made in preparing this book to provide accurate and up-to-date information which is in accord with accepted standards and practice at the time of publication. Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved. Nevertheless, the authors editors and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation. The authors, editors and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this book. Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use.

Contents (contents of Volume II)

Preface Contributors Neural repair and rehabilitation: an introduction Section A:

xiii xv xxvii

Technology of neurorehabilitation 1

Section A1: Outcomes measurement and diagnostic technology 1 Outcomes measurement: basic principles and applications in stroke rehabilitation Carol L. Richards, Sharon Wood-Dauphinee, Francine Malouin Human voluntary motor control and dysfunction Catherine E. Lang, Karen T. Reilly, Marc H. Schieber Assessments, interventions, and outcome measures for walking Bruce H. Dobkin Electromyography in neurorehabilitation Austin J. Sumner, Amparo Gutierrez Functional neuroimaging Nick S. Ward, Richard S.J. Frackowiak

3

5

2

24

3

37

4

48

5

56

v

vi

Contents

Section A2:

Therapeutic technology

69

Section B: Symptom-specific neurorehabilitation Section B1: Sensory and motor dysfunctions 15 Chronic pain Herta Flor, Frank Andrasik Loss of somatic sensation Leeanne Carey Management of spasticity David A. Gelber Arm and hand weakness Sarah Blanton, Steven L. Wolf Gait disorders and rehabilitation Volker Dietz Balance, vestibular and oculomotor dysfunction Courtrey D. Hall, Susan J. Herdman Deconditioning and energy expenditure Marilyn MacKay-Lyons

215

6

Cell transplantation therapy for Parkinson’s disease Brian J. Snyder, C. Warren Olanow

71

217 219

7

Conditions of task practice for individuals with neurologic impairments Carolee J. Winstein, Jill Campbell Stewart

89 16 103 17

231

8

Balance training Gammon M. Earhart, Fay B. Horak

248

9

Functional electrical stimulation in neurorehabilitation Peter H. Gorman, Gad Alon, P. Hunter Peckham

119

18

265

19 10 Environmental control and assistive devices Jessica Johnson, William C. Mann 136 20

283

298

11

Wheelchair design and seating technology Rory A. Cooper, Rosemarie Cooper, Michael L. Boninger

147 21 315

12

Rehabilitation robotics, orthotics, and prosthetics Hermongo Igo Krebs, Neville Hogan, William K. Durfee, Hugh M. Herr

165

Section B2: Vegetative and autonomic dysfunctions 22 Rehabilitation of the comatose patient Francesco Lombardi, Antonio De Tanti Plasticity in the neural pathways for swallowing: role in rehabilitation of dysphagia John C. Rosenbek, Neila J. Donovan Autonomic dysfunction Brenda S. Mallory

337 339

13

Virtual reality in neurorehabilitation Patrice L. Weiss, Rachel Kizony, Uri Feintuch, Noomi Katz

182

23

356

14

Communication devices Cheryl Y. Trepagnier, Beth Mineo Mollica, Sheela Stuart, Carole W. Brown

198 24 368

Contents

vii

25

Sexual neurorehabilitation Mindy L. Aisen, Danielle M. Kerkovich Cognitive neurorehabilitation

400

34

Neurorehabilitation in epilepsy Andres M. Kanner, Antoaneta Balabanov

542

Section B3: 26

411 413

35

Rehabilitation for aphasia Stefano F. Cappa Apraxia Thomas Platz Unilateral neglect and anosognosia Stephanie Clarke, Claire Bindschaedler Memory dysfunction Jonathan Evans Neurorehabilitation of executive function Mark D’Esposito, Adam Gazzaley Rehabilitation of dementia Keith M. Robinson, Murray Grossman

Parkinson’s disease and other movement disorders 560 Georg Ebersbach, Jörg Wissel, Werner Poewe Neurorehabilitation of the stroke survivor Richard D. Zorowitz Rehabilitation in spinal cord injury Diana D. Cardenas, Catherine Warms Multiple sclerosis Serafin Beer, Jürg Kesselring Cerebral palsy and paediatric neurorehabilitation Peter J. Flett, H. Kerr Graham

36 27 424

579

28

444

37

593

29

461

38

616

30

39 475

636

31

488

40

Section C: Disease-specific neurorehabilitation systems 32

Neuromuscular rehabilitation: diseases of the motor neuron, peripheral nerve and neuromuscular junction 657 Hubertus Köller, Hans-Peter Hartung Muscular dystrophy and other myopathies James S. Lieberman, Nancy E. Strauss

513 41 677

The organization of neurorehabilitation services: the rehabilitation team and the economics of neurorehabilitation 515 Richard D. Zorowitz Traumatic brain injury Michael P. Barnes 527

Index

699

33

Contents (contents of Volume I)

Preface Contributors Neural repair and rehabilitation: an introduction

xiii xv xxvii

Section A:

Neural plasticity

1 3

Section A1: Cellular and molecular mechanisms of neural plasticity 1 Anatomical and biochemical plasticity of neurons: regenerative growth of axons, sprouting, pruning, and denervation supersensitivity Oswald Steward Learning and memory: basic principles and model systems Kimberly M. Christian, Andrew M. Poulos, Richard F. Thompson Short-term plasticity: facilitation and post-tetanic potentiation Ralf Schneggenburger Long-term potentiation and long-term depression Zafir I. Bashir, Peter V. Massey Cellular and molecular mechanisms of associative and nonassociative learning John H. Byrne, Diasinou Fioravante, Evangelos G. Antzoulatos

5

2

26

3

44

4

60

5

79

ix

x

Contents

Section A2: Functional plasticity in CNS system 6 Plasticity of mature and developing somatosensory systems Jon H. Kaas, Tim P. Pons Activity-dependent plasticity in the intact spinal cord Jonathan R. Wolpaw

95

Section B: Section B1: processes

Neural repair Basic cellular and molecular

267 269

97

16

7

Neuronal death and rescue: neurotrophic factors and anti-apoptotic mechanisms 271 Thomas W. Gould, Ronald W. Oppenheim Axon degeneration and rescue John W. Griffin, Ahmet Höke, Thien T. Nguyen 293

109 17

8

Plasticity of cerebral motor functions: implications for repair and rehabilitation 126 Catherine L. Ojakangas, John P. Donoghue Plasticity in visual connections: retinal ganglion cell axonal development and regeneration Kurt Haas, Hollis T. Cline Plasticity in auditory functions Josef P. Rauschecker Cross-modal plasticity in sensory systems Krishnankutty Sathian Attentional modulation of cortical plasticity Bharathi Jagadeesh

18

9

Adult neurogenesis and neural precursors, progenitors, and stem cells in the adult CNS 303 Jeffrey D. Macklis, Gerd Kempermann Axon guidance during development and regeneration Simon W. Moore, Timothy E. Kennedy Synaptogenesis Matthew S. Kayser, Matthew B. Dalva

147

19

326

10

162 20 346

11

180 Section B2: Determinants of regeneration in the injured nervous system 194 21 Inhibitors of axonal regeneration Tim Spencer, Marco Domeniconi, Marie T. Filbin Effects of the glial scar and extracellular matrix molecules on axon regeneration Jared H. Miller, Jerry Silver
Trophic factors and their influence on regeneration

363

12

365

Section A3: 13

Plasticity after injury to the CNS 207 209 22

Plasticity in the injured spinal cord Serge Rossignol Plasticity after brain lesions Randolph J. Nudo, Ines Eisner-Janowicz, Ann M. Stowe From bench to bedside: influence of theories of plasticity on human neurorehabilitation Agnes Floel, Leonardo G. Cohen

390

14

228
23 405

Joel M. Levine, Lorne M. Mendell 15 24 248 Intraneuronal determinants of regeneration Lisa J. McKerracher, Michael E. Selzer

421

Contents

xi

Section B3: Promotion of regeneration in the injured nervous system 25 Cell replacement in spinal cord injury Itzhak Fischer, Angelo C. Lepne, Steve Sang Woo Han, Alan R. Tessler

443

30

445

Assessment of sensorimotor function after spinal cord injury and repair Ronaldo M. Ichiyama, Roland R. Roy, V. Reggie Edgerton

548

Section B4: Translational research: application to human neural injury 31

563

26

Dysfunction and recovery in demyelinated and dysmyelinated axons 468 Stephen G. Waxman

Alzheimer’s disease, model systems and experimental therapeutics 565 Donald L. Price, Tong Li, Huaibin Caj, Philip C. Wong Biomimetic design of neural prostheses Gerald E. Loeb, Cesar E. Blasco
Brain–computer interfaces for communication and control

27

Role of Schwann cells in peripheral nerve regeneration Wesley J. Thompson

487

32

587

33

28

Transplantation of Schwann cells and olfactory ensheathing cells to promote regeneration in the CNS Mary B. Bunge, Patrick M. Wood

602

Jonathan R. Wolpaw and Niels Birbaumer 513 34 Status of neural repair clinical trials in brain diseases Olle F. Lindvall, Peter Hagell

615

29

Trophic factor delivery by gene therapy Ken Nakamura, Un Jung Kang

532 Index 633

Preface

Neurorehabilitation is a medical specialty that is growing rapidly because medical advances have extended life expectancy and saved the lives of persons who previously would not have survived neurological injury. It is now urgent to develop a rigorous scientific basis for the field. The basic science relevant to functional recovery from neural injury is perhaps the most exciting and compelling of all the medical sciences. It encompasses areas of plasticity, regeneration and transplantation in the nervous system that individually have been the subjects of many monographs. With the Textbook of Neural Repair and Rehabilitation, these areas are integrated with each other and with the clinical topics to which they apply. The Textbook of Neural Repair and Rehabilitation is organized into two volumes. Volume I, Neural Repair and Plasticity can stand alone as a textbook for graduate or advanced undergraduate level courses on recovery from neural injury. It is subdivided into two sections: Section A, Neural Plasticity and Section B, Neural Repair. Following an injury to the nervous system, most patients partially regain function. Section A, Plasticity, addresses the mechanisms that underlie spontaneous recovery as well as the added recovery induced by therapies based on use, retraining and pharmacological manipulations. The chapters cover the anatomical and physiological responses of neurons to injury, mechanisms of learning and memory, and plasticity in specific areas of the nervous system consequent to intense use, disuse and injury. Ultimately, interventions aimed at repairing the damaged neural circuitry will

xiii

xiv

Preface

be required if full function is to be restored. Thus Section B, Neural Repair, covers topics on neuronal death, trophic factors, axonal regeneration and the molecules that inhibit it, stem cell biology, and cell transplantation. Section B builds on Section A because the mechanisms of plasticity will have to be invoked to translate restored neuronal connections into useful function. Volume II, Medical Neurorehabilitation can stand alone as a clinical handbook for physicians, therapists, rehabilitation nurses and other neurorehabilitation professionals. It is organized into three sections. Section A, The Technology of Neurorehabilitation, is a direct transition from Volume I, emphasizing the applications of basic scientific principles to the practice of neurorehabilitation. This section includes material on functional imaging, motor control, gait and balance assessment, electrodiagnosis, virtual

reality, and bioengineering and robotic applications to prosthetics and orthotics. Section B, SymptomSpecific Neurorehabilitation, provides guidelines to managing spasticity, gait disorders, autonomic and sexual dysfunction, cognitive deficits and other disabling neurological symptoms that are common to many disorders. Section C, Disease-Specific Neurorehabilitation, describes comprehensive approaches to the rehabilitation of persons suffering from the major categories of disabling neurological disorders, such as spinal cord injury, multiple sclerosis, stroke and neurodegenerative diseases. Wherever possible, the chapters in this book refer the reader back to chapters that deal with relevant material at a different level. It is hoped that by stressing the integration of clinical and basic scientific knowledge, this book will help to advance the quality and scientific rigor of neurorehabilitation.

Contributors (contributors of Volume II)

Mindy L. Aisen, MD
United Cerebral Palsy Research and Education Foundation Department of Neurology and Neuroscience, Georgetown University

Gad Alon, PT, PhD
Department of Physical Therapy and Rehabilitation Science University of Maryland School of Medicine Baltimore, MD, USA

Frank Andrasik, PhD
Institute for Human and Machine Cognition University of West Florida Pensacola, FL, USA

Antoaneta Balabanov, MD
Department of Neurological Sciences Rush Medical College Chicago, IL, USA

Michael P. Barnes, MD, FRCP
Department of Neurological Rehabilitation Hunters Moor Regional Neurological Rehabilitation Centre Newcastle upon Tyne, UK

Serafin Beer, MD
Department of Neurology and Neurorehabilitation Rehabilitation Centre Valens, Switzerland

xv

USA Michael L. PA. PA. USA . MPT. MN. USA Neila J. Switzerland Gammon M. Berkeley Berkeley. WA. Italy Bruce H. Louis. DC. EdD Department of Education The Catholic University of America Washington. PhD Program in Physical Therapy Washington University School of Medicine St. MD. USA Volker Dietz. Switzerland Stefano F. MD Department of Rehabilitation Science & Technology University of Pittsburgh School of Health and Rehabilitation Sciences Pittsburgh. Switzerland Rory A. NCS Department of Rehabilitation Medicine Emory University Atlanta. Earhart. Durfee. USA Sarah Blanton. FRCP Spinal Cord Injury Center University Hospital Balgrist Forchstr.xvi Contributors Claire Bindschaedler. MD. Australia William K. Cardenas. MD Division de Neuropsychologie Centre Hospitalier Universitaire Vaudois Lausanne. MD Departments of Neuroscience and Psychology Helen Wills Neuroscience Institute University of California. FRCP Department of Neurology David Geffen School of Medicine. Cooper. DPT. GA. PhD Division de Neuropsychologie Centre Hospitalier Universitaire Vaudois Lausanne. MHA Department of Rehabilitation Medicine University of Washington Seattle. PhD Department of Rehabilitation Science & Technology University of Pittsburgh School of Health and Rehabilitation Sciences Pittsburgh. USA Stephanie Clarke. Donovan. Cappa. USA Mark D’Esposito. Dobkin. Brown. ATP Department of Rehabilitation Science & Technology University of Pittsburgh School of Health and Rehabilitation Sciences Pittsburgh. PhD School of Occupational Therapy Faculty of Health Sciences LaTrobe University Bundoora. CA. FL. BAppSc(OT). UCLA Los Angeles. Boninger. PA. USA Carole W. MD Department of Neuroscience Vita-Salute University and San Raffaele Scientific Institute Milano. Zurich. Victoria. PT. CA. USA Leeanne Carey. MO. MA Department of Communicative Disorders VA RR&D Brain Rehabilitation Research Center University of Florida Gainesville. USA Rosemarie Cooper. PhD Department of Mechanical Engineering University of Minnesota Minneapolis. USA Diana D. MD.

PhD Wellcome Department of Imaging Neuroscience Institute of Neurology University College London London. UK Hans-Peter Hartung. Decatur . Germany University of California. PhD Section of Psychological Medicine Gartnavel Royal Hospital Glasgow. USA Herta Flor. Germany Courtney D. MD. MD Department of Child and Adolescent Development. Decatur Department of Rehabilitation Medicine Emory University Atlanta. University of Haifa Haifa. Hall. Neurology and Rehabilitation. PT.J. MD. Calvary Rehabilitation Services. USA Amparo Gutierrez. PhD. Philadelphia. IL. Israel Caesarea-Rothschild Institute for Interdisciplinary Applications of Computer Science. MD. MD Department of Orthopaedics. LA. Frackowiak. Israel Baltimore. MD Department of Neurology Heinrich-Heine-University Düsseldorf. GA. Gelber. MD Springfield Clinic Neuroscience Institute Springfield. Gorman. Kerr Graham. Victoria. USA David A. MD Neurologisches Fachkrankenhaus für Bewegungsstörungen/Parkinson Beelitz-Heilstätten. UK Peter H. PhD School of Occupational Therapy Hadassah-Hebrew University Jerusalem. USA Richard S. Germany Adam Gazzaley Helen Wills Neuroscience Institute and Department of Psychology Susan J. Hobart. PA. MD Department of Neurology Louisiana State University Medical Center New Orleans. Berkeley Berkeley.Contributors xvii Georg Ebersbach. Herdman. Tasmania Murray Grossman. MD Department of Neurology and Rehabilitation The James Lawrence Kernan Hospital Uri Feintuch. EdD Department of Neurology University of Pennsylvania School of Medicine. Australia Peter J. Victoria. USA H. Australia Present Address: Paediatric Rehabilitation. CA. PhD Atlanta Veterans Administration Rehabilitation Research and Development. University of Melbourne The Royal Children’s Hospital Parkville. PT FAPTA Atlanta Veterans Administration Rehabilitation Research and Development. Women’s and Children’s Hospital North Adelaide Melbourne. USA Jonathan Evans. PhD Department of Clinical and Cognitive Neuroscience University of Heidelberg Central Institute of Mental Health Mannheim. Flett.

MD Riabilitazione Intensiva Neurologica Ospedale di Correggio Correggio. PhD Department of Mechanical Engineering Massachusetts Institute of Technology. MD Department of Neurology and Neurorehabilitation Rehabilitation Centre Valens. Israel Danielle M. GA. PhD School of Physiotherapy Dalhousie University Halifax. Jerusalem. Kanner. USA Noomi Katz. PhD Rehabilitation Research and Development Service Department of Veterans Affairs Washington. OTR Department of Occupational Therapy University of Florida Gainesville. Emilia. USA Department of Neuroscience The Winifred Masterson Burke Medical Research Institute Weill Medical College of Cornell University New York. MSc School of Occupational Therapy Hadassah-Hebrew University. NY. Israel Hugh M. MO. Horak. DC. Germany Neville Hogan. Cambridge. USA Hubertus Köller. MD School of Occupational Therapy Hadassah-Hebrew University. MD Department of Neurological Sciences Rush Medical College Chicago. NY. Kerkovich. Israel Department of Occupational Therapy University of Haifa Haifa.xviii Contributors Departments of Rehabilitation Medicine and Otolaryngology-Head and Neck Surgery Emory University Atlanta. USA Hermano Igo Krebs. USA Fay B. and Brain and Cognitive Sciences Massachusetts Institute of Technology Cambridge. Nova Scotia. PT Neurological Sciences Institute Oregon Health & Science University Beaverton. MD Department of Neurology Heinrich-Heine-University Düsseldorf. MA. PhD The Media Laboratory and The Harvard/MIT Division of Health Sciences and Technology Cambridge. USA Andres M. Herr. Jerusalem. Canada . USA Rachel Kizony. USA Catherine E. Louis. MA. USA Francesco Lombardi. Lieberman. Italy Jürg Kesselring. PhD Program in Physical Therapy Washington University School of Medicine St. Switzerland Marilyn MacKay-Lyons. FL. Reggio. MA. IL. PhD Departments of Mechanical Engineering. OR. MD Department of Rehabilitation Medicine Columbia University College of Physicians and Surgeons New York. USA Jessica Johnson. Lang. USA James S. PhD. PT.

DE. Mann. PT. USA Marc H. Quebec. Hunter Peckham. USA Beth Mineo Mollica.Contributors xix Brenda S. USA Francine Malouin. MD Department of Neurological Rehabilitation Free University Berlin Berlin. MD Department of Neurology Medical University Innsbruck Innsbruck. USA Keith M. NY. FL. Schieber. PhD Department of Rehabilitation and Centre for Interdisciplinary Research in Rehabilitation and Social Integration Laval University Quebec City. PhD Department of Occupational Therapy University of Florida Gainesville. MD Department of Physical Medicine and Rehabilitation University of Pennsylvania School of Medicine Philadelphia. PhD Department of Communicative Disorders VA RR&D Brain Rehabilitation Research Center University of Florida Gainesville. NY. OTR. USA Thomas Platz. Quebec. Canada William C. MD Werner Poewe. NY. Warren Olanow. NCS Department of Biokinesiology and Physical Therapy University of Southern California Los Angeles. PT Department of Rehabilitation and Centre for Interdisciplinary Research in Rehabilitation and Social Integration Laval University Quebec City. Richards. PhD Center for Applied Science & Engineering and Department of Linguistics University of Delaware Wilimington. PA. USA John C. NY. Mallory. FL. Rosenbek. MD. NY. Robinson. NY. Germany Nancy E. PhD Department of Biomedical Engineering Case Western Reserve University and FES Center of Excellence Cleveland VA Medical Center Cleveland. MD Departments of Neurology Mount Sinai School of Medicine New York. USA C. CA. Reilly. MS. MD Department of Rehabilitation Medicine Columbia University College of Physicians & Surgeons New York. USA Jill Campbell Stewart. Snyder. Germany Department of Rehabilitation Medicine Columbia University College of Physicians and Surgeons New York. USA . Strauss. PhD Department of Neurology University of Rochester School of Medicine & Dentistry Rochester. USA Brian J. USA P. PhD Department of Neurobiology and Anatomy University of Rochester School of Medicine & Dentistry Rochester. Canada Carol L. OH. USA Karen T. MD Department of Neurosurgery Mount Sinai School of Medicine New York. PhD.

Germany Antonio De Tanti. Quebec. Zorowitz. PT. Winstein.O. LA. ARNP. Gravi Cerebrolesioni e Disturbi Cognitivi Centro Riabilitativo “Villa Beretta” Costamasnaga. DC. PhD. RN. PhD. PhD Department of Occupational Therapy University of Haifa Haifa. MD. DC. CRRN Department of Rehabilitation Medicine University of Washington Seattle. USA Jörg Wissel. Weiss. Israel . PhD Children’s Hearing and Speech Center Children’s National Medical Center Washington. FAPTA Department of Rehabilitation Medicine Emory University Atlanta. USA Carolee J. USA Cheryl Y. UK Richard D. PhD Department of Psychology The Catholic University of America Washington. GA. Ward. PA. MD Department of Physical Medicine and Rehabilitation University of Pennsylvania School of Medicine Philadelphia. Wolf.xx Contributors Sheela Stuart. USA Austin J. CA. Trepagnier. PhD. PT. USA Sharon Wood-Dauphinee. Sumner. PhD. USA Patrice L. PT School of Physical and Occupational Therapy McGill University Montreal. Lecco. MRCP Wellcome Department of Imaging Neuroscience Institute of Neurology University College London London. MD Department of Neurology Louisiana State University Medical Center New Orleans. FAPTA Department of Biokinesiology and Physical Therapy University of Southern California Los Angeles. MD Responsabile U. Italy Steven L. USA Catherine Warms. Canada Nick S. MD Neurologische Rehabilitationsklinik Kliniken Beelitz GmbH Beelitz-Heilstätten. WA.

PhD Department of Neurobiology and Anatomy University of Texas Health Science Center at Houston Houston. FL. UK Niels Birbaumer. PhD Department of Biomedical Engineering A. Blanco. USA John H. USA xxi .E.Contributors (contributors of Volume I) Evangelos G. TX. Bashir. PhD Department of Anatomy MRC Centre for Synaptic Plasticity University of Bristol Bristol. PhD The Miami Project to Cure Paralysis University of Miami School of Medicine Miami. Germany Cesar E. Byrne. PhD Institute of Behavioural Neurosciences Eberhard-Karls-University Tubingen. TX. USA Zafar I. Mann Institute for Biomedical Engineering University of Southern California Los Angeles. CA. USA Mary Bartlett Bunge. Antzoulatos Department of Neurobiology and Anatomy University of Texas Health Science Center at Houston Houston.

PhD Cold Spring Harbor Laboratory Cold Spring Harbor. PhD Department of Neurobiology and Anatomy Drexel University College of Medicine Philadelphia. USA Thomas W. NC. MD. NIA National Institutes of Health Bethesda. USA Agnes Floel. Griffin. Filbin. Dalva. USA Matthew B. Reggie Edgerton. MD Departments of Neurology and Neuroscience Johns Hopkins University School of Medicine Baltimore. NY. MD Human Cortical Physiology Section National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda. RI. MD. USA John P. CA. Los Angeles Los Angeles. PA. USA John W. USA Ines Eisner-Janowicz Department of Molecular and Integrative Physiology University of Kansas Medical Center Kansas City. Christian Neuroscience Program University of Southern California Los Angeles. USA Marco Domeniconi Department of Biological Sciences Hunter College City University of New York New York. USA V. USA Kimberly M. NY. USA Diasinou Fioravante Department of Neurobiology and Anatomy University of Texas Health Science Center at Houston Houston.xxii Contributors Huaibin Cai. KS. PhD Department of Neuroscience Brown University Providence. MD. USA Leonardo G. PhD Department of Physiological Science and Neurobiology University of California. PhD Department of Biology Hunter College City University of New York New York. Cline. PA. USA . USA Itzhak Fischer. NY. PhD Computational Biology Section Laboratory of Neurogenetics. MD. TX. MD Human Cortical Physiology Section National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda. Cohen. USA Hollis T. Donoghue. CA. PhD Department of Neuroscience University of Pennsylvania School of Medicine Philadelphia. Gould Department of Neurobiology and Anatomy and the Neuroscience Program Wake Forest University School of Medicine Winston-Salem. USA Marie T.

WA. MD. British Columbia. Canada Ahmet Höke. PhD Steve Sang Woo Han. USA Angelo C. USA Department of Pathology Johns Hopkins University School of Medicine Baltimore. Quebec. MD Department of Neurology University of Chicago Chicago. Canada Matthew S. MD.Contributors xxiii Kurt Haas. Lepore Department of Neurobiology and Anatomy Drexel University College of Medicine Philadelphia. PhD Department of Anatomy and Cell Biology University of British Columbia Vancouver. PhD Department of Neurology Johns Hopkins University School of Medicine Baltimore. Ichiyama. MD Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch. CA. Lindvall. USA Peter Hagell. PA. CA. Sweden Gerald E. USA Department of Biomedical Engineering A. RN PhD Department of Nursing Faculty of Medicine Lund University Lund. MD. NY. MD. USA Tong Li Bharathi Jagadeesh. USA Joel M. PhD Department of Psychology Vanderbilt University Nashville. USA . PhD Department of Neurobiology and Anatomy Drexel University College of Medicine Philadelphia. Levine. Los Angeles Los Angeles. Kayser Department of Neuroscience University of Pennsylvania School of Medicine Philadelphia. MD. USA Department of Neurobiology and Behavior State University of New York at Stony Brook Stony Brook. Kaas.E. PA. Loeb. PhD Ronaldo M. Germany Timothy E. USA Department of Neurology and Neurosurgery Montreal Neurological Institute McGill University Montreal. MD Un Jung Kang. PhD Department of Physiology and Biophysics University of Washington Seattle. TN. PhD Department of Physiological Science University of California. USA Olle F. PhD Jon H. Mann Institute for Biomedical Engineering University of Southern California Los Angeles. PA. USA Section of Restorative Neurology Wallenberg Neuroscience Center/BMC A11 Lund University Hospital Lund. Sweden Gerd Kempermann. Kennedy. IL.

PhD Department of Neurobiology and Behavior State University of New York at Stony Brook Stony Brook. PhD Departments of Neurology and Neuroscience Johns Hopkins University. Canada Josef P. PhD Department of Neurosurgery Wake Forest University School of Medicine Winston-Salem. DHST Department of Neurology MGH–HMS Center for Nervous System Repair Harvard Medical School Boston. MD. USA Randolph J. USA Andrew M. NY. PhD Department of Anatomy MRC Centre for Synaptic Plasticity University of Bristol Bristol. PhD Department of Neurology University of California. Macklis. PhD Department of Neurobiology and Anatomy Wake Forest University Winston-Salem. McKerracher. Quebec. Moore Department of Neurology and Neurosurgery Center for Neuronal Survival Montreal Neurological Institute McGill University Montreal.xxiv Contributors Jeffrey D. Nudo. MD. Ojakangas. Miller Department of Neurosciences Case Western Reserve University School of Medicine Cleveland. MD. DC. PhD Department of Physiology and Biophysics Georgetown Institute for Cognitive and Computational Sciences Georgetown University Medical Center Washington. USA Ken Nakamura. Quebec. MD. Roy. PhD Départment de Pathologie et Biologie Cellulaire Université de Montreal Montreal. CA. PhD Department of Molecular and Integrative Physiology University of Kansas Medical Center Kansas City. USA Lisa J. Los Angeles Los Angeles. OH. MD Division of Neuropathology Johns Hopkins University School of Medicine Baltimore. Poulos Neuroscience Program University of Southern California Los Angeles. USA . RI. Canada Thien Nguyen. Canada Tim P. CA. NC. PhD Brain Research Institute University of California. USA Ronald W. Pons. School of Medicine Baltimore. KS. USA Donald L. USA Catherine L. USA Serge Rossignol. Oppenheim. Mendell. San Francisco San Francisco. USA Roland R. Price. USA Simon W. CA. Rauschecker. USA Lorne M. MA. Massey. PhD Peter V. MD. Quebec. NC. USA Jared H. MD. PhD du centre de rechercher en sciences University de Montreal Montreal. UK Department of Neuroscience Brown University Providence. MD.

Tessler. KS. PhD Department of Neurology University of Pennsylvania School of Medicine Philadelphia. USA Patrick M. PhD Department of Neurosciences School of Medicine Case Western Reserve University Cleveland. OH. PA. USA . CA. PhD The Miami Project to Cure Paralysis Department of Neurological Surgery University of Miami School of Medicine Miami. MD Department of Neurobiology and Anatomy Drexel University College of Medicine Philadelphia. USA Jonathan R. FL. USA Stephen G. PhD Department of Pathology Johns Hopkins University School of Medicine Baltimore. USA Tim Spencer Department of Biological Sciences Hunter College City University of New York New York. PhD Department fo Psychology and Biological Sciences University of Southern California Keck School of Medicine Los Angeles. USA Michael E. PhD Section of Neurobiology University of Texas Austin. MD Laboratory of Nervous System Disorders Wadsworth Center. Wolpaw. Selzer. GA. USA Alan R. USA Philip C. TX. MD. and Neurosurgery Reeve-Irvine Research Center College of Medicine University of California. MD. PhD Department of Neurology Emory University Atlanta. Thompson. Irvine Irvine. Neurobiology and Behavior. State University of New York at Albany Albany.Contributors xxv Krishnankutty (Krish) Sathian. PhD Department of Neurology Yale University School of Medicine New Haven. NY. CT. USA Ann M. USA Wesley J. PhD Departments of Anatomy and Neurobiology. Wong. Wood. MD. USA Jerry Silver. MD. PhD Abteilung Membranbiophysik and AG synaptische Max-Planck Institut für Biophysikalische Chemie Gottingen. NYS Department of Health Department of Biomedical Sciences. Waxman. USA Ralf Schneggenburger. Thompson. CA. PA. USA Oswald Steward. Germany Richard F. Stowe Department of Molecular and Integrative Physiology University of Kansas Medical Center Kansas City. NY.

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Philadelphia. In that classification. the field of rehabilitation medicine. In order to improve healthcare data reporting by the nations of the world. FL. 1999. the editors have devoted equal space and emphasis to the clinical practice of neurorehabilitation and to its basic science underpinnings. La Jolla. Cohen3. each with two components: • Part 1: Functioning and disability: (a) body functions and structures. “impairment” referred to a biological condition: for example. The reasons for this relate in part to the urgent need for clinical service and the dearth of experienced practitioners in the field during its formative years. the WHO replaced ICIDH with an International Classification of Functioning. Practice PPoE-B. Bethesda. In this respect. 2University of Lausanne. spinal cord injury. Ottenbacher and Maas. that the perceived lack of a scientific basis be reversed in order for rehabilitation medicine to achieve its full academic recognition and fulfill its great potential for relieving human suffering. 1999. political.” whereas “… ‘disability’ denotes the collective economic. 4University of Florida. xxvii . National Institutes of Health. cultural. Disability and Health (ICF) in 2001. According to the social model of disability adopted by the World Health Organization (WHO). rehabilitation has been one of the slowest to develop a basic science framework and to establish evidence-based practices as its norms. These definitions have collapsed older distinctions of the WHOs 1980 International Classification of Impairments. 2001). Gage5 1 3 University of Pennsylvania. “‘ impairment’ refers to an individual’s biological condition …. USA. However. “disability” referred to the loss of a specific function: for example. The chapters in the clinical sections of this book stress those therapies for which evidence exists based on controlled clinical trials. two areas of basic science are highlighted – neuroplasticity and neural repair. MD. consequent to the disability. CA. and social disadvantage encountered by people with impairments” (Barnes. In particular. Disabilities and Handicap (ICIDH) (Thuriaux. Switzerland. Leonardo G. Duncan4 and Fred H. USA Among medical specialties. 2001). 5The Salk Institute. loss of locomotor ability consequent to the impairment. ICF has two parts. Precisely because the need and the potential are so great. Lausanne. 1995).Neural repair and rehabilitation: an introduction Michael E. the book differs from most clinical textbooks. USA.. has begun to put great emphasis on the development of evidence-based medical practices (DeLisa et al. the professional neurorehabilitation community has been especially supportive of this direction and has taken very active steps to further the development of a basic scientific underpinning for its field. 1 Definitions Neurorehabilitation Neurorehabilitation is the clinical subspecialty that is devoted to the restoration and maximization of functions that have been lost due to impairments caused by injury or disease of the nervous system. (b) activities and participation. inability to work as a postman. Selzer1. Stephanie Clarke2. Gainesville. and in particular neurorehabilitation. This book represents an attempt to place the practice of neurorehabilitation in a rigorous scientific framework. and “handicap” referred to the loss of functioning in society: for example. Similarly. Pamela W. It is imperative now. PA. USA.

xxviii Michael E. electrical and magnetic event-related potentials (including electroencephalogram (EEG). and magneto-encephalography (MEG)) and noninvasive brain stimulation in the form of transcranial magnetic or electrical stimulation (TMS and trancranial direct current stimulation. the transplantation of a variety of tissues and cells to replace lost neurons. cfm.int/ icf/icftemplate. and the use of prosthetic neuronal circuits to bridge parts of the nervous system that have become functionally separated by injury or disease. but because of its widespread use. concepts of neural plasticity have been accepted as important elements in the scientific understanding of functional recovery. • Part 2: Contextual factors: (c) environmental factors. The term encompasses diverse processes. The term is useful as part of the basic science of neurorehabilitation because it encompasses more than “regeneration” or “transplantation” alone. the older classification is more useful in understanding the level of interventions and research performed by the rehabilitation community. interest in understanding the mechanisms underlying recovery of function has increased. rehabilitation medicine has concerned itself with disabilities and handicaps but very little with the level of impairment and even less with the molecular and cellular mechanisms that underlie impairments. Neurorehabilitation has come to represent the application of this continuum to neurologically impaired individuals. Once considered overused and trite. By focusing on components of health. Traditionally. sprouting in response to injury. It is not possible to review the entire classification here. to dendritic pruning and axonal . An expression of this interest has been the substantial increment in basic science and translational studies geared to characterize the extent to which the central nervous system (CNS) can reorganize to sustain clinical rehabilitation. whereas the ICIDH focused on consequences of disease and thus had a narrower usefulness.who.” the term “neural repair” generally refers to processes that do not occur spontaneously in humans to a degree sufficient to result in functional recovery. (d) personal factors. “Neural repair” has been used in the title of this textbook in order to convey the breadth of subject matter that it covers and is now considered relevant to neurorehabilitation. Included in this term are means to enhance axonal regeneration. evoked potentials (Eps). Neural repair The term “neural repair” has been introduced in the past several years to describe the range of interventions by which neuronal circuits lost to injury or disease can be restored. However. Selzer et al. In recent years. Although there is overlap with aspects of “neuroplasticity. including some of the chapters in this book. Thus therapeutic intervention is necessary to promote repair. the term “neuroplasticity” has regained currency in the neurorehabilitation community as a concise way to refer to hypothetical mechanisms that may underlie spontaneous or coaxed functional recovery after neural injury and can now be studied in humans through such techniques as functional imaging (including positronemission tomography (PET) and functional magnetic resonance imaging (fMRI)). Over the last 30 years. a brief summary is presented in Chapter 32 of volume II. this state of affairs has begun to change as rehabilitation professionals have come to recognize the continuity that exists from molecular pathophysiology to impairments to disabilities and handicaps. The rehabilitation community has been slower to embrace repair as a relevant therapeutic goal. ICF can be used to describe both healthy and disabled populations. Neuroplasticity The term “neuroplasticity” is used to describe the ability of neurons and neuron aggregates to adjust their activity and even their morphology to alterations in their environment or patterns of use. The complete version can be found at http://www3. tDCS). In recent years. as from learning and memory in the execution of normal activities of life.

the term “Rehabilitation Medicine” has replaced “Physical Medicine and Rehabilitation” in the naming of some hospital and university departments. management of pain syndromes and other medical aspects of the treatment of chronically ill patients. A concomitant of the broadening of the focus of rehabilitation has been a trend toward specialization. interest developed in the possibility that then exotic forms of energy. changing its name to the American Congress of Physical Therapy in 1925. such as bone fractures and limb amputations. medical specialists outside of physical medicine and rehabilitation (PM&R) became more interested in the rehabilitation of patients whom they might have treated during the acute phase of their illness. More recently. members of that section formed the American Society for Neurorehabilitation. Training programs for physical therapy technicians were started in the 1920s and an American Medical Association (AMA) Council on Physical Therapy (later the Council on Physical Medicine) was started in 1926.. This organization merged with the American Physical Therapy Association in 1933 and in 1945. By 1938. X-ray treatments and radiology were closely linked to electrotherapy (Nelson. With the large number of injuries to soldiers in World War I. electro-stimulation. Epidemiology of neurological disabilities For many years. gait disorder) and signs (e. designating Neurorehabilitation and Neural Repair as its official journal. the practice of rehabilitation medicine was dominated by orthopedic problems. since the latter term is associated with limitations to specific therapeutic modalities. the need for therapists to attend to their retraining and reintroduction to productive life created a new specialty that was based on physical modalities of treatment..Neural repair and rehabilitation: an introduction xxix 2 History of neurorehabilitation as a medical subspecialty Origins of rehabilitation medicine In late 19th century America. the American College of Radiology and Physiotherapy was formed. could help to heal patients with diseases and disabilities. 1973) and in 1923. 1969). Previously. that is. autonomic instability and urinary tract infections. In particular. it adopted the name American Congress of Physical Medicine. then American Congress of Physical Medicine and Rehabilitation. rather than to a target patient population or therapeutic goal. Gradually. these national societies confederated officially as the World Federation of Neurorehabilitation. the tendency was to approach disabilities generically. This was especially true among neurologists. But with a growing conviction that the rehabilitation of patients requires knowledge of the pathophysiological basis of their disorders.. the focus of rehabilitation has broadened to include the social and psychological adjustment to disability. such as physical therapy. regardless of the cause. parallel developments have occurred in many countries throughout the world. With variations. including physical and occupational therapy. diathermy. the American Congress of Rehabilitation Medicine (ACRM). electricity. In 2003. National societies of neurorehabilitation were also formed in Europe and more recently in other parts of the world. the American Academy of Physical Medicine and Rehabilitation (AAPM&R) was formed and in 1947. and finally in 1966. restoration of function. high-frequency electrical stimuli were applied to generate deep heat in tissues (diathermy) and some physicians adopted this treatment modality as a specialty. As with the name of the ACRM. This is a multidisciplinary organization with membership open to physicians from many specialties and to nonphysician rehabilitation specialists. i. based on their symptoms (e.g.g. including organ system-specific specialization.e. spasticity). the Academy sponsored a specialty board with a residency requirement and qualifying examination (Krusen. These modalities were expanded during World War II. heat and massage. treatment of medical complications such as bedsores. progress in keeping severely neurologically injured . The American Academy of Neurology formed a section on rehabilitation and in 1990. and especially during the two world wars. a medical specialty organization. In the early days.

Practice PPoE-B. and social problems of the medically disabled patient population. traumatic injuries of the brain and spinal cord. To date.047. neck. As practiced in most countries. bronchus. The resulting sophistication of outcomes measurement has had an important impact on all of medicine. 2003. intestine. and other neurological conditions) accounted for 80% (Deutsch et al. Selzer et al. while neurological conditions (stroke. complete and partial paralysis of extremities (60. The five conditions causing the most limitations are: heart disease (7. see Chapter 18 Volume II). knee. This also was difficult to assess with the limited instruments available only one generation ago. multiple sclerosis (69. only two large-scale.932.000).000). 2000). in terms of roles in work. In the USA. of whom over 70% live in the developing countries. the evaluation of outcomes for specific physical therapy treatments has lagged. involving combinations of treatment modalities administered by multiple therapists.592. so the prevalence of neurological disabilities may have been underestimated.3%). spinal cord injury. arthritis (5. multicenter. hip replacements) accounted for 20% of rehabilitation admissions. The WHO estimates that more than 300 million people worldwide are physically disabled. In order to catch up to other fields in the practice of evidence-based medicine. which developed a structured and rigorous methodology to improve formulation of evidence-based clinical practice guidelines (EBCPGs. process. colon. 2003. see Chapter 3 of volume II) and the trial of constraint-induced movement therapy for upper extremity dysfunction after stroke (Winstein et al. and community. In a recent survey. A consensus conference was held in 2002. approximately 300.6%). and the complexity of the treatment regimens. and to make recommendations for randomized clinical trials. and diabetes (2.000 times each year (Kraus et al. chronic health conditions cause activity limitations 61. amputations. stroke. These are the trial of body weightsupported treadmill training for spinal cord injury (Dobkin et al. malignant neoplasm of the stomach. and shoulder pain. 1996).000).672. asthma (2. which now routinely considers quality of life in the evaluation of effectiveness in clinical trials. orthopedic conditions (hip and limb fractures.. and rectum (62. and other respiratory sites (60. while outcomes measurement has begun to have an important impact on the evaluation of systems of rehabilitation. 2001).. Evidence that amphetamines combined with physical therapy can enhance recovery in several animal models of stroke 3 Outcomes measurement in rehabilitation medicine The complex medical. back problems (7. The survey excluded Guillain–Barré syndrome. traumatic brain injury.000 people are admitted to inpatient rehabilitation facilities each year. Moreover.. rehabilitation is a multidisciplinary . It is estimated that in the USA. has made assessing outcomes difficult. the most important outcome of the rehabilitation process is the degree of reintegration of the patient in society.000). patients alive has shifted the emphasis toward rehabilitation of patients with developmental neurological disorders.xxx Michael E.4%). and other chronic disabling diseases. This was used to develop EBCPGs based on the literature for selected rehabilitation interventions in the management of low back. prospective. family.721. polyneuropathy. and blindness in both eyes (60. the conditions causing people to have major activity limitations most often are: mental retardation (87.1%). malignant neoplasm of the lung.7%). 4 Impact of evidence-based medicine on neurorehabilitation Ironically. the rehabilitation field has been forced to become extremely resourceful in designing outcomes measures to evaluate the efficacy of its treatments (Stineman. Thus disorders of the nervous system are those most often requiring intensive rehabilitation interventions.569. randomized clinical trials have been carried out to test-specific physical therapy treatments. emotional.5% of people with the condition have a limitation). 2001). However. and on complex aspects of rehabilitation outcomes.000)..

controlled clinical trials were applied to test the effectiveness of those treatments in patients.6-fold. In order to estimate research in medical rehabilitation. and in particular. their coincidence increased 25. Similarly. to interest in the rehabilitation of patients disabled by neurological disorders. Thus there is a correlation between the use of the term “neurorehabilitation” and acceleration in the application of basic science and evidence-based medicine to rehabilitation research. These have suggested a tendency toward effect in human patients with ischemic stroke (Long and Young. Parallel growth of research in medical rehabilitation and in neural plasticity and repair over the past 25 years. the trend toward specialization in the field of rehabilitation medicine carried with it recognition of the need to develop a basic science research underpinning and to become more rigorous in the evaluation of its therapies and clinical practices. 2003). the combination of “rehabilitation” and either “neuroplasticity” or “regeneration” did not appear until after the term “neurorehabilitation” became current. the term “neurorehabilitation” was used less than 10 times/year in Medlineindexed articles until 1994. a PubMed search was conducted using the term “physical rehabilitation.8-fold increase in annual publications in the field of rehabilitation medicine (best searched on Medline using the term “physical rehabilitation”). 1).” In order to estimate research on neuroplasticity. A larger clinical trial is underway. In the first phase. From then until 2003. However. the term “neuroplasticity” was sufficient.8-fold increase during the same time (Fig. in which therapy is directed not only at maximizing function based on the post-injury residual anatomical substrate. but incorporates attempts at repairing that substrate. A Medline search using the terms “neuroplasticity” or “nerve regeneration” showed a steady or slightly accelerating 7. the terms “rehabilitation” and “evidencebased medicine” did not appear in the same article until 1994.Neural repair and rehabilitation: an introduction xxxi Number of references and traumatic brain injury has led to several smallscale randomized clinical trials. This can be ascribed to the accelerated interest in organ-specific rehabilitation. In order to estimate research on regeneration in the nervous system. As in other fields of medicine. there was a relatively constant 3. the enormous need for clinical service was met by reliance on the experience and a priori reasoning of medical clinicians and therapists in devising methods to maximize function.” From the above. scientific exploration in animal models was used to buttress the rationale for these therapies. From then until 2003.” and “rehabilitation medicine.5-fold. This second phase is still very active. which replicates the pattern seen in other specialties. it can be seen that the maturation of neurorehabilitation as a clinical specialty has experienced two phases. 1985 1990 Year 1995 2000 Figure 1.” which yielded the highest combination of sensitivity and specificity among such terms as “medical rehabilitation.4-fold. During that same period. As indicated in Fig. the annual number of articles on “neurorehabilitation” increased 9. In the second phase. the best combination of specificity and sensitivity was achieved by searching for the term “nerve regeneration.” “rehabilitation. As with clinical trials of neuroprotective agents in human stroke and trauma. 2. but we are already witnessing the beginning of a third phase. while the rigors of prospective. 2500 2000 1500 1000 500 0 1980 Neuroplasticity or nerve regeneration Physical rehabilitation 5 Impact of the revolution in the science of neuroplasticity and regeneration on neurorehabilitation Between 1980 and 2003. the number of articles on (“neuroplasticity” or “regeneration”) and “physical rehabilitation” increased 7. early results of cell and gene therapies for .

. attempts to replace dopaminergic cells in human patients have been carried out for more than a decade. sham operated controlled clinical trials have not suggested major benefits in idiopathic Parkinson’s disease (Olanow et al. and especially cognitive functions. Based on results in animal models. The subspecialization represented by the term “neurorehabilitation” has followed closely the application to rehabilitation medicine of basic research on neural plasticity and repair. and epidural injection of a rho-A antagonist for spinal cord injury. How do you convince patients to undergo a neurosurgical procedure that might be a sham operation? Should a clinical trial be performed on only the most severely disabled patients. The US Food and Drug Administration has approved small-scale clinical trials of intracerebral transplantation of tumor-derived neuronal progenitors for stroke. Yet despite promising results in small-scale studies on special populations (Lindvall.. the most disabling aspects of injury to the nervous system often relate to impairments in other domains. the best combination of sensitivity and specificity was obtained with the terms “rehabilitation. highly invasive therapies are matched by ethical concerns. larger double-blind. In order to estimate the frequency with which research on neuroplasticity and neural repair is applied to rehabilitation medicine. 100 90 80 Number of references 70 60 50 40 30 20 10 0 1980 1985 1990 1995 Year 2000 Neurorehabilitation Neuroplasticity or nerve regeneration and rehabilitation Rehabilitation and evidence-based medicine Figure 2. intraventricular infusions of glial cell line-derived neurotrophic factor (GDNF) also failed to provide improvement in human Parkinson’s disease.” “neuroplasticity. nerve growth factor-secreting fibroblasts for Alzheimer’s disease. A multicenter clinical trial of autologous macrophages activated by exposure to skin and injected into the spinal cord (Bomstein et al. Selzer et al.xxxii Michael E. Most major neuropsychological syndromes. and has closely led evidence-based clinical research. Chapter 6 of Volume II).” and “nerve regeneration. in the absence of evidence for effectiveness or experimental controls. The technical difficulties of carrying out controlled trials of these novel. who may have less to lose? Or should they be done on less disabled patients. Despite favorable results in animals.. many patients have received transplants of stem cells and other highly invasive treatments for a variety of disabling neurological disorders. human injuries and diseases of the CNS have highlighted the need for caution in translating animal studies into human therapies. Chapter 34 of Volume I). is planned. Thus a small-scale clinical trial of intraputamenal GDNF injections has been reported (Gill et al. . In countries where clinical research is less stringently regulated. 1998. It turns out that because of the large size of the human brain. 6 Rehabilitation of cognitive functions Although rehabilitation is commonly thought of as relating primarily to motor retraining. 2003. sensory. knowing that a failed trial might make it difficult to mount a subsequent one on a more favorable patient population. 2003) is currently under way. using an adeno-associated virus vector containing the gene for neurturin. who might have a better chance of responding favorably to an effective treatment. 2003). A multicenter trial of in vivo gene therapy. such as autonomic. a GDNF-related peptide that has similar biological activity. the GDNF failed to penetrate far enough into the brain parenchyma. The most notable example is Parkinson’s disease.” Similarly the term “evidence-based medicine” was best paired with “rehabilitation” rather than other terms pairing “rehabilitation” with modifiers. These and other questions are under intensive discussion and guidelines for the application of these advanced therapies to human patients are needed.

and physiotherapists and occupational therapists. have been identified in the second half of the 19th and the first half of the 20th century. the goal should be full restoration of function by any means necessary. Most of the studies published in the early 1980s concerned aphasia. why write a separate textbook of neurorehabilitation rather than incorporating it with the rest of rehabilitation medicine into a general rehabilitation textbook? The editors believe that it is time for rehabilitation medicine to go beyond optimizing function based on what is left to the body after an injury or illness. This current expansion of rehabilitation studies of specific syndromes is linked to the application of cognitive models to rehabilitation and to a better understanding of post-lesional plasticity as apparent in functional imaging studies. Increase in publications on neuropsychological rehabilitation. and in particular large-scale multicenter investigations. with close interactions between physicians. degenerative diseases such as Parkison’s disease or progressive diseases such as multiple sclerosis are increasingly investigated in their own rights. The annual number of publications concerning neuropsychological rehabilitation. such as aphasia. have started accumulating this type of evidence. tumors. and neglect rehabilitation. are needed and should be carried out during the next decade. Specific fields. has increased from about 100 in 1980 to over 500 in 2004. By focusing on the nervous system. including actual repair of the injured tissues and organs. However. apraxia. During the last 25 years the field of rehabilitation of cognitive functions has expanded rapidly. aphasia (therapy OR rehabilitation). based on principles and professional interactions that have a deep vertical penetration. Thus. 3). visual agnosia. The titles of the included publications were then checked for appropriateness. such as aphasia and neglect rehabilitation. witnessed a 10-fold increase by 2004. The chapters on rehabilitation of cognitive functions and on disease-specific rehabilitation demonstrate the necessity and the putative strength of evidence-based approaches. This type of research requires more than ever a multidisciplinary approach to neuropsychological rehabilitation. A PubMed search was conducted to identify articles published between 1980 and 2004 on rehabilitation of cognitive functions key words: (neuropsychological OR aphasia) AND (rehabilitation OR therapy). Many of the original reports described the course of spontaneous recovery and proposed specific rehabilitative measures. we can present a cogent and intellectually rigorous approach to restoration of function. In recent years. neuropsychologists. However. speech therapists. or neglect. 7 Purpose and organization of this book If most severely disabling disorders are neurological. which continued to be investigated and experienced a 2-fold increase between 1980 and 2004. Rather. A small but important part of this increase can be accounted for by studies of specific neuropsychological syndromes. with a steep increase beginning around 1987 (Fig. research in other cognitive syndromes has grown even faster. Unilateral neglect. very little investigated in the 1980s. rehabilitation of traumatic brain injury. many more studies.Neural repair and rehabilitation: an introduction xxxiii 600 500 Number of citations 400 300 200 100 0 1980 Rehabilitation of cognitive functions Aphasia therapy or rehabilitation Neglect rehabilitation 1985 1990 Year 1995 2000 Figure 3. stroke. including aphasia therapy. Although we need to understand the mechanisms underlying recovery from cognitive deficits. most of the impressive increase in studies of neuropsychological rehabilitation was due to studies of disease-specific rehabilitation. we also must have proof of the efficacy of our interventions. This requires two additions to .

and adapt to injury. Ultimately. and Yoles.. S. traumatic brain injury. and translational research.. apart from the specific disease processes that underlay them. contains chapters on outcomes measurement. 78. Butovsky. applying animal experimental results to human patients. Marder. The volume is divided into three sections.. D. C.xxxiv Michael E. (2001). the molecular mechanisms inhibiting and promoting axon regeneration in the CNS. spasticity and other motor dysfunctions. Granger.. and to cross-reference relevant chapters where the integration is supported. for example. At the same time clinicians and clinical scientists in the various fields of rehabilitation medicine will be encouraged to enhance their curiosity and understanding of the mechanisms underlying their practice. Elashoff. Dobkin.H.F. C. Neural repair. L. Methods for . 133–142. 81.B.. Y. This book is presented in two volumes. designed to be used either separately or as an integrated whole.A. (2003). Volume I. Features of skin-coincubated macrophages that promote recovery from spinal cord injury. the design of prosthetic neural circuitry.. Basso. includes chapters on the neuronal responses to injury. and cognitive dysfunctions.. K. A. DeLisa.. Section A. WHO. The uniform data system for medical rehabilitation report of patients discharged from comprehensive medical rehabilitation programs in 1999. will be of greatest interest to clinical rehabilitation specialists. H.. M. Throughout the two volumes. Fiedler. C. M. R. Neural Plasticity and Repair. and Scott. Evidence-based medicine in physiatry: the experience of one department’s faculty and trainees. includes chapters on the morphological and physiological plasticity of neurons that underlie the ability of the nervous system to learn. we hope to stimulate basic scientists to broaden their understanding of the clinical relevance of their work. Lisaey. J Neuroimmunol. neurodegenerative diseases.. Volume II. Medical Neurorehabilitation. we hope that encouraging communication between basic and clinical scientists in relevant areas of research will help to accelerate the translation of basic research into effective clinical treatments that will expand the degree of functional recovery of neurologically disabled persons. diagnostic techniques such as functional imaging and clinical electrophysiology. rehabilitation engineering and prosthetics design. multiple sclerosis. the traditional rehabilitation approach. (2000). S. S. and Christodoulou.. 228–232. First. Kirshblum. Section C. I. Saulino. REFERENCES Barnes... E. Harkema.V. stroke. which had considered disabilities and handicaps in the abstract.. World Health Organization – Disability and Rehabilitation Team Conference Report and Recommendations. Am J Phys Med Rehabil. but will be useful to basic scientists who need to understand the clinical implications of their work. Selzer et al.. Vitner.. Am J Phys Med Rehabil. 142. Behrman. Ditunno. Jain. Technology of neurorehabilitation. (2003).. Section B. Second. 10–16. C. M. etc. there is a need to understand the pathophysiological bases of disabling neurological disorders. Section B. J. A. Oslo. D. there is a need to apply basic scientific knowledge about the plastic properties of the nervous system in order to effect anatomical repair and physiological restoration of lost functions.. explores the basic science underpinnings of neurorehabilitation and can be used as a textbook for graduate level courses in recovery of function after neural injury. It is divided into two sections.. Fulga. and Russell. Dudley. V. Norway. B.S. Apple. efforts have been made to relate the basic science to the clinical material. sensory disturbances including chronic pain. Neural plasticity. and special therapeutic techniques. J.. (1999). Section A. In: Rethinking Care from the Perspective of Disabled People. and sexual dysfunctions. stem cells and neurogenesis in the adult CNS. considers rehabilitation approaches to neurological symptoms that are common to many types of neurological disorders. autonomic. In this way. and strategies to promote cell replacement and axon regeneration after injury. Deforge. Bomstein. Deutsch. accommodate to altered patterns of use. Smirnov. G. Symptom-specific rehabilitation. considers the integrated approaches that have been developed to address the rehabilitation of patients with specific diseases and disease categories.C. J. Barbeau.. Fugate. G. O. Disease-specific neurorehabilitation systems. R.

(1996)... 54(Suppl. Phys Ther. History of the once close relationship between electrotherapeutics and radiology. E. C. (1969).. and Gilmartin.F.J. Stoddard. Methods for a multisite randomized trial to investigate the effect of constraint-induced movement therapy in improving upper extremity function among adults recovering from a cerebrovascular stroke. and Heywood. and outcomes of interest: reconciling the rules of biology with meaningfulness. Shannon. Nat Med. status. Uswatte. Ann Neurol. O. (1999). How to detect effects: statistical power and evidence-based practice in occupational therapy research. 96. 13.. Ottenbacher.). Hotton.B. (2001). 83–87. and prospects. 589–595. (2003). (1973). S. P. DC. Direct brain infusion of glial cell line-derived neurotrophic factor in Parkinson disease. (2003). Disabil Rehabil. Thuriaux.H. A. J. Arch Phys Med Rehabil.P. treatments. Patel. Olanow. K. 9. Neurorehabil Neural Repair.K. (2003). F.Neural repair and rehabilitation: an introduction xxxv a randomized trial of weight-supported treadmill training versus conventional training for walking during inpatient rehabilitation after incomplete traumatic spinal cord injury. Dexamphetamine treatment in stroke. Blanton.. Stoessl. and Young.R. The ICIDH: evolution.M. Am J Occup Ther. and Wolf. 608–640. Bunnage. Washington...J.G. M. Section 3: Causes of disabilities. Zeiter Lecture.H. Sossi. Brooks.. C.C. R. V.M. M.. S. Svendsen. G. 147–159. Am J Phys Med Rehabil. 137–152.G. S. Brin. 81.. Lindvall. G.. Quart J Nuclear Med. G.. U. 1–5. 80. Nelson. J.. Morris. 1629–1640. . K. Update on fetal transplantation: the Swedish experience. and Freeman. D. In: Chartbook on Disability in the United States. and Maas.J. 53. Neurorehabil Neural Repair. Kordower.. Kraus. A double-blind controlled trial of bilateral fetal nigral transplantation in Parkinson’s disease. S. Stineman.A. C. (1998). J. Winstein.. 112–118. P.J. Krusen. Miller. D. (1995). National Institute on Disability and Rehabilitation Research. N. Philadelphia panel evidence-based clinical practice guidelines on selected rehabilitation interventions: overview and methodology. L. 50. Practice PPoE-B (2001). D. J. 17. O’Sullivan. 17. 17.N. F.W. Arch Phys Med Rehabil. Long.. Gill. M. D. D. Perl.S..P Godbold. C. Historical development in physical medicine and rehabilitation during the last forty years.S. Walter J. K.. Nichols. D. M. Taub. Nauert. 153–167. 181–188. Goetz. T. 54. 403–414. (2003).. Defining the population. 673–685. . Mov Disord... An InfoUse Report... McCarter.

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Therapeutic technology 3 69 1 .SECTION A Technology of neurorehabilitation CONTENTS A1. Outcomes measurement and diagnostic technology A2.

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Frackowiak 5 24 37 48 56 3 . Karen T. Schieber 3. Lang.SECTION A1 Outcomes measurement and diagnostic technology CONTENTS 1. Dobkin 4. Sharon Wood-Dauphinee and Francine Malouin 2. Richards. and outcome measures for walking Bruce H. Outcomes measurement: basic principles and applications in stroke rehabilitation Carol L. Electromyography in neurorehabilitation Austin J. interventions. Functional neuroimaging Nick S. Sumner and Amparo Gutierrez 5. Ward and Richard S. Reilly and Marc H. Assessments. Human voluntary motor control and dysfunction Catherine E.J.

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This information will enable the reader to critique published scales when selecting them for clinical practice or research. a section on how to create an evaluative scale that measures “participation” is provided. McGill University. the first section includes a theoretical discussion of reliability. psychologic or social characteristics of people. Montreal. cure or rehabilitation” (Brook et al. This discussion is based on classical test theory.. performance-based ratings and laboratory assessments. and demonstrates their applications in stroke rehabilitation. Future trends related to computer-adapted testing (CAT) are also briefly described. and how to approach interpretation. the evaluation of “walking competency” after stroke is used as an example to illustrate the selection of appropriate outcome measures for this population as well as their relation to participation. 1976). In the second section. Quebec. Richards1. Laval University. 1994. control of illness. Measures used to evaluate the outcomes of rehabilitation for individuals with stroke generally reflect physical.1 Outcomes measurement: basic principles and applications in stroke rehabilitation Carol L. Sharon Wood-Dauphinee2 and Francine Malouin1 1 Department of Rehabilitation and Centre for Interdisciplinary Research in Rehabilitation and Social Integration. Quebec City and 2School of Physical and Occupational Therapy. This chapter starts by introducing basic concepts related to the development of outcome measures.3 Developing and testing measures 1. This chapter introduces basic concepts related to the development of outcome measures and demonstrates their applications in stroke rehabilitation. These measures include self-reported scales. This chapter concludes with examples of how laboratory-based gait assessments and measures of brain reorganization help explain changes in clinical scales and performance-based measures.1 Summary The objective of this chapter is to give an overview of basic principles guiding the development and application of outcome measures. Canada 1.2 Introduction “Outcomes are the end results of medical care: what happened to the patient in terms of palliation. mobility and quality of life. the evaluation of “walking competency” after stroke is used to illustrate the selection of appropriate outcome measures for this population. Finch et al. 2002). They 5 . This chapter ends with discussions as to how laboratory-based gait assessments and measures of brain reorganization help explain changes in clinical scales and performance-based measures. and measures of brain plasticity... In the second part. To avoid a redundant review of traditional scales (Wood-Dauphinee et al. For each property the theory is applied to development of a measure of “participation”. validity and responsiveness. Outcome measures used in stroke rehabilitation can be divided into three categories: scales that assess constructs such as function. Physical attributes or abilities are most easily assessed as they are observed directly. Specifically. 1. performance-based measures that evaluate such areas as gait speed and upper limb dexterity. as well as their relation to “participation”.

Development and testing of evaluative scales Generating the items A series of well-defined steps is necessary for the development and testing of a standardized scale (Juniper et al. fitness. Psychologic and social characteristics are more difficult to evaluate because they are concepts and often cannot be observed directly. 2000). traveling. The items are then administered to a convenience sample of approximately 100 people who reflect the characteristics of the individuals who will be using the scale (Juniper et al. one would begin with a conceptual framework such as the International Classification of Functioning. or even in addition to it. and adds to its interpretability. and the response options may be dichotomous (yes/no). communicating and interacting with family. one might solicit issues related to caring for oneself or one’s home. community mobility. for instance. we must make inferences from what we observe and decide if. body functions and structures. 2003). motivated. Other constructs we might want to assess include impairment. In the absence of a theoretical framework. Richards et al. they are termed constructs (Portney and Watkins.. participation or quality of life. It also provides a guide to evaluating the validity of the measure. 2001). the past week. which proposes multiple interactions between the health condition. environmental and personal factors. A categorical scale needs descriptors for each choice and a VAS needs descriptive anchors at each end. Decisions are then made about the response options and the time frame of the questions. Such constructs are evaluated using standardized scales. These data provide information useful for further item reduction. self-efficacy. If possible. Item frequency distributions tell us about the spread of responses across the sample. 1996). depressed. friends and colleagues. etc. We are interested in creating an evaluative scale (Kirshner and Guyatt. To assess a concept. an individual is independent. the time frame may refer to today. receiving sufficient support or coping with life’s challenges. Each item is initially judged qualitatively to eliminate those that are unclear. participation in life. Ideas are also obtained from patients. principally to determine if change has occurred. pertinent information is obtained from a review of literature to identify existing instruments assessing similar constructs that may incorporate useful items. In optimal circumstances. For example. First one must decide what the instrument is to measure and the type of measure to be developed. can be evaluated using electromechanical devices or functional status scales. Streiner and Norman. Reducing the number of items The goal of this step is to select the items that are the most suitable for the scale. Disability and Health (ICF) (World Health Organization. The overall goal of this step is to amass a large number of ideas that will form the basis for writing many items that represent the construct of interest. 1985) to assess “participation” of an individual or a group at baseline. a subset of this group (30–40 people) can be asked to complete the items a second time. Such a framework names broad categories. Items that are highly correlated with another item . For the “participation” example. and provide the first hint as to whether or not the item will be responsive. When one cannot directly observe these concepts or behaviors.. and again at one or more points later on. and engaging in work and leisure activities as well as about factors in the social or physical environments that impede or assist “participation”. suggests relationships among categories and anchors a measure to an extensive body of knowledge. 1996. ability/disability. moving around the home or the community. activities. preferably. have not been involved in their creation must carefully review all items. significant others in their lives and involved health professionals. Knowledgeable individuals who. may contain several ordinal categories or may be a visual analog scale (VAS). Individual un.or semi-structured interviews and/or focus groups are conducted with these persons to gather information that is sufficiently specific to provide the basis for scale items. health status.6 Carol L.

Reliability coefficients range between 0 and 1. 2002). This process may need to be repeated until no further changes are necessary. Coefficient alpha (Cronbach. 1952). Items with similar means and standard deviations (SD) can be summed to provide subscale or total scores (Likert. or to the format of the measure. Two administrations of the scale are required. how well the items are inter-correlated or measure the same characteristic. 1951) is the test statistic most often used. one administration of the scale to an appropriate sample of subjects is needed. or in other words. 2003).70 for use with groups and 0. stability of a scale is examined over time (test–retest and intra-rater (including the situation in which the subject self-completes the scale twice)) or between raters.. Item reliabilities may also be estimated using data from the group that completed the items twice. 1957) is the preferred test statistic as it assesses agreement. 2002). For “participation” internal consistency and test–retest reliability would be assessed. 1996) is conducted to reduce problems related to understanding the content. Testing the reliability. If criteria for excluding items are set a priori. and items with very low correlations to other items may not belong in the scale. Commonly accepted minimal standards for reliability coefficients are 0. Following completion of the scale. Validity is defined as the extent to which a scale measures what it claims to measure.90 for use with individuals as in the clinical setting. reflecting different test situations. It should be completed by five to ten subjects using the same mode of administration as intended for routine use. subjects should be debriefed. To examine internal consistency. The interval between administrations should be sufficiently short to minimize changes in the subjects but far enough apart to avoid the effects of learning memory or fatigue. Internal consistency denotes precision. rater training prior to testing is usually provided. and are interpreted by their closeness to 1. Reliability reflects the degree to which a measure is free from random error. these data allow a quantitative approach to reducing the number of items. reliability has been categorized as either reflecting internal consistency or stability. using estimates of variance obtained from an analysis of variance (ANOVA). . for example through the use of videotapes. The intra-class correlation coefficient (Cronbach. Traditionally. For intra. This process ensures that respondents really understand the item and that all respondents understand it in the same way. Different versions. Lower coefficients yield confidence intervals that are too wide for monitoring an individual over time (Scientific Advisory Committee. validity and responsiveness of the new scale The measurement properties of the scale need to be examined on a new sample of subjects with stroke. by assessing the correlation between the scale and another hypothetical scale selected from the same group of items at the same time.00. Inter-rater reliability is most easily assessed if all raters can observe the subject simultaneously but independently. It is currently advocated that each item be examined using cognitive testing procedures (Collins. and it can be divided into three main types: content.Outcomes measurement: basic principles and applications 7 may be redundant.85 tells us that the data contain 85% true variance and 15% error variance.00. Scales that require interactions between the subject and the rater may not lend themselves to this approach and multiple tests need to be conducted. Kappa statistics are often used for this purpose (Cohen. A coefficient of 0. In this situation issues related to the testing intervals are again important. Pre-testing the scale A pre-test on a small sample that reflects the characteristics of subjects in the target population (Juniper et al. 2000). Items with missing data may indicate that the content was unclear or offensive to the respondent. In general. It provides an estimate of the amount of error that is due to the sampling of items.and interrater reliability tests. 1960). are available (Portney and Watkins. the degree to which the observed score is different from the true score (Scientific Advisory Committee.

1992. One must always ask if a measure is valid for a certain population or in a specific setting. Predictive-criterion validity attempts to demonstrate that a new measure can successfully predict a future criterion. one might expect that stroke survivors living (1) at home with a willing and able caregiver. By collecting “participation” data on each of the groups and comparing mean scores across the groups via ANOVA one can determine if the measure can discriminate as hypothesized. One might hypothesize that “participation” among community-dwelling stroke survivors was positively and moderately correlated with the ability to drive a car. as could the relationships between “activities” or “body structures and functions” and “participation”. Content validity signifies that the items contained in the measure provide a representative sample of the universe of content of the construct being measured.. The new scale and one of the existing measures would be administered at the same time to an appropriate sample of community-dwelling individuals with stroke and the scores would be correlated to assess the strength of the association. a month after discharge could predict the living situation over the next 2 years. Criterion-related validity is based on the relationship between a new scale and a criterion measure. Finally. a measure of “participation” should contain items reflecting each of the domains listed earlier in this chapter. (2) at home with paid assistance or (3) in an institution would demonstrate different levels of “participation”. 1996. For instance. This type of validation would use regression to determine if the “participation” scores obtained. For instance. a measure of “participation” could be tested in the stroke sample noted earlier to determine if it would predict institutionalization over time. A subjective judgment is required as there is no statistical test to assess this type of validity.8 Carol L. When developing a new measure most investigators select a few tests of validity according to available time and resources. Nonetheless. .. which scores are to be contrasted. Construct validity examines evidence that a measure performs according to theoretical expectations by examining relationships to different constructs. that incorporates three axes (who is to be studied. Known groups. because the “participation” measure is to be based on the ICF framework. but one might choose the reintegration to normal living index (Wood-Dauphinee et al. These hypotheses would be tested on appropriate samples of stroke survivors by evaluating both “participation” and the other constructs at the same point in time. another form of construct validation. 2000. In fact. A gold standard for “participation” is probably not available.. criterion-related and construct (Portney and Watkins. For example. a “gold standard”. Environmental or personal factors that assist or limit the stroke survivor in terms of participating could be explored. 2002) as measures tapping a similar construct to evaluate concurrentcriterion validity. Terwee et al. validity could also be evaluated by testing hypotheses that support the conceptual framework.. a taxonomy for responsiveness. While reliability and validity are traditional psychometric properties with a long history in the social sciences. 1988) or the impact on participation and autonomy questionnaire (Cardol et al. To finish this brief section on validity it is important to note that validation is never completed. there has been considerable discussion as to whether it is simply another aspect of validity (Hays and Hadorn. Content validity is usually judged by the thoroughness of the item generation and reduction processes previously described. 2003). and what type of change is to be assessed). Stratford et al. responsiveness is a relative newcomer. The most difficult aspect of this type of validation is finding a “gold standard” that reflects the same criterion and is measurable. which is examined at the same point in time or in the future. Richards et al. Scientific Advisory Committee. It might also be negatively correlated with the absence of a significant other who was willing to plan and execute activities with the stroke survivor (convergent construct validity). examines the performance of a new measure through the use of existing external reference groups. 2002). for example. One could also hypothesize that the extent of functional recovery following the stroke would be more highly correlated with “participation” than would the presence of shoulder pain (divergent construct validity).

For example.. For testing responsiveness of the measure of “participation” one could enroll subjects upon return to their home setting and monitor them for a defined number of months. 1993). clinically important change and real change in the concept being measured (Terwee et al. associated with the measure being tested and clinically meaningful .. These have been grouped as the ability to detect change in general. 1983. usually an effect size as calculated from the magnitude of change and the variability of the subjects at baseline or over time. calculations of effect size. and those based on measurement precision such as the index of reliable change and the standard error of measurement. Most depend on assessing patients longitudinally over time during a period of anticipated change... 1995). 1991. however. Examples include the use of a paired t-test to test the hypothesis that a measure has not changed over time. Following a stroke we expect considerable recovery during the first 6 weeks (Richards et al. 1992. A protocol to evaluate responsiveness is strengthened when one can collect data on both: a group that is expected to change as well as one not expected to change (Guyatt et al.. As noted above. 1997) because it encompasses all types of change (Beaton et al. The developer needs to choose one or more approaches based on the data collection protocol. In addition to many definitions there are also many approaches to measuring responsiveness. 2001). The term effect size.. patients and their caregivers should independently be asked if they are “better. The various statistical approaches to quantifying responsiveness. that because of the different methods of calculation they are not interchangeable for interpretative purposes.8 represent small medium and large effects. termed anchor based.2. Limitations of this approach include differing variability across groups being tested and the meaning of the values obtained. One should be aware. Two basic approaches have been proposed to help interpret scalar data (Lydick and Epstein. after which time the gradient flattens somewhat but there is considerable improvement until around 6 months from the index event. 2003). The different types of change being assessed have served to categorize various definitions of responsiveness. is a standardized. Given sufficient subjects this will allow like responders to be grouped for analysis. At each evaluation point. Interpretability means the capacity to assign a qualitative meaning to a quantitative score (Ware and Keller. 2001). Terwee et al. 2002). 2003. To date. the same or worse” since the previous evaluation. As clinicians and researchers have only a short history of trying to interpret the meaning of scale scores as compared to clinical tests. coined by Cohen (1988).. Crosby et al. In addition. At that time recovery tends to plateau although further gains are clearly possible.. as well as others that are based on sample variation. a person with mild stroke returning home would be expected to gradually resume participation in former activities and roles.. these values are somewhat arbitrary (Guyatt et al. The first. While Cohen suggested that 0. respectively. People saying they are better form a positive response group and those who report being worse make up a deteriorating group. 1996). examines the relationship between the change score on the instrument being tested.Outcomes measurement: basic principles and applications 9 has been proposed (Beaton et al. a distribution-based approach. 1987. in addition to descriptive data. 0. relies on the statistical distributions of the results of a study.. For this chapter we have selected a definition from the third group – “the accurate detection of change when it has occurred” (De Bruin et al. along with their strengths and weaknesses. patients who perceive positive or negative changes need to be separated from those who report no change. to that of an independent measure that is well known. in addition to completing the scale. Skilbeck et al. Jorgensen et al. the different versions of the effect size based on sample variation are most commonly found in the literature. standardized response mean (SRM) or Guyatt’s responsiveness statistic.5 and 0. have been extensively presented in recent literature (Husted et al. Scientific Advisory Committee. 2002). unitless measure of change in a group... there are many statistical approaches from which to choose. 2000. The second approach. contextual relationships are required to facilitate understanding. 2003). Tuley et al.. particularly in the functional and social realms.

For the scale developer. 2002) has recommended that several types of information would be useful in interpreting scale scores. 1999. Hays. global ratings of change by patients or physicians. 1992a. to normal living index (Wood-Dauphinee et al. 1988). severity classifications. 1995... If the measure is to be used with stroke survivors. the balance scale (Berg et al. to develop and test a number of measures for use with individuals who have sustained a stroke: the reintegration . a statistical disadvantage is that only an overall reliability estimate is possible Applications During the past 25 years the authors of this chapter have used these steps.. 1997). Finally. there is some empirical evidence that in certain situations the distribution.. scores of the test sample determine how much of the trait is present and this.and anchor-based approaches provide similar information (Norman et al.. Dynamic assessments The prior paragraphs outlined the development of a scale based on classical test theory as advocated by many psychometricians during the last century. This will increase familiarity with the measure and thus. and eventually. 2003) and the preference-based stroke index (Poissant et al. their significant others or their clinicians. Bjorner and Ware. 1998). 2003). the known psychometric properties of a test apply only to those in the testing sample. considering that they range from having extremely severe limitations to only minor limitations and a high level of functioning.. primarily because a number of limitations to the psychometric approach were known. Wyrwich et al.10 Carol L. 1989.. 2001. assist interpretation.. b. Investigators have proposed several methods of calculating MIDs (Jaeschke et al.. 1996. In the 1990s. Indeed. 1997). Population norms. 1996.. possibilities include data on the relationship of scores or change scores to ratings of the MID by those with stroke. The MID is defined as “the smallest difference in score in the domain of interest which patients perceive as beneficial and which would mandate. 1997) recognized the need for a new approach to creating health scales. 1997. Redelmeier et al.. This scale would be time consuming and perhaps distressing for persons to complete as they are faced with items far beyond or below their capabilities (Cleary. a group of psychometric experts (Scientific Advisory Committee. In addition. 2003). Revicki and Cella.. Wood-Dauphinee et al. is related to test norms (Streiner and Norman. a scale with a very large number of items would be needed to encompass the entire continuum of activities for people with stroke. 2003). Richards et al. discussions of which are beyond the scope of this chapter.. in the absence of troublesome side effects and excessive costs. 1997). 1991. Theoretically at least. comparative data on the distribution of scores from population groups. (Guyatt et al.. 1998. 2002). Foremost was the difficulty of any one scale covering the entire spectrum of a construct such as physical functioning (Revicki and Cella. several health researchers (Fisher. Ahmed et al. 1993. with modifications. 2002). information on the relationship of scores on the new measure to other measures used with people who have had a stroke. symptom scores. McCorney. the psychometric properties need to be reexamined. It is sufficient to say that the magnitude of MIDs tend to vary across measures. In other words. a change in the patient’s management” (Jaeschke et al. the stroke rehabilitation assessment of movement (STREAM) (Daley et al. and the minimum important difference (MID) have all been used. 1997. in turn. McHorney. results from multiple studies that have used the instrument and reported findings. 1989. Guyatt et al. 2002). This means that if the measure is to be used with others who are different. a fluidity scale for evaluating the motor strategy of the rise-to-walk test (Malouin et al. Neither of these approaches is without limitations but each provides a framework for investigation and contributes information important for understanding scale scores. 1989).. traditional scaling techniques do not allow one to separate the properties of the items from the subject’s abilities (Hambleton et al. On a more positive note.

Nonetheless. Thus. This curve depicts the relationship between the actual response to the item and the underlying ability. physical function) is unrelated to the probability of answering any other item positively for subjects with the same amount of the trait (Streiner and Norman.e. It is based on two assumptions: that the items tap only one construct. Given the current stage of development as well as the large numbers of subjects and technical support needed to create the new scales. All items undergo careful analyses to examine dimensionality and item fit. but results can be compared across subjects using IRT. it should be noted that the review criteria (Scientific Advisory Committee. called an item characteristic curve. and that the probability of answering in a manner that reflects an increasing amount of the trait (i. A subject’s response to each item is described by a curve.Outcomes measurement: basic principles and applications 11 with a traditionally developed scale. 2004). 2002). the computer algorithm adapts the third series of items to reflect the subject’s level of performance. Items are further analyzed to determine if the construct is adequately represented. To start. For example. IRT places each subject on the continuum underlying the construct of interest. most often from existing measures. a measure of item effectiveness. Before finishing this section of this chapter.e.. both statistically and clinically (Cella et al. statistical and technical methods. it is predicted that scales developed according to the methods of classical test theory will be used well beyond the next decade. but we know that measurement precision changes according to the level of the subject’s ability (Hays. One is from the National Institute of Neurological Disorders and Stroke. the US National Institutes of Health has announced two initiatives related to IRT. have been combined to create a modern approach to scale construction and delivery. . 1998). were expanded from a previous version to reflect modern test theory principles and methods. Information describing the inter-item relationships as well as the relationships of responses to the various items is available. After confirming this classification in a second series of items of similar difficulty. a person with stroke may be classified as having a low level of functional performance. 1993). dynamic testing is being developed in several areas and we can expect to read more and more about it in the near future. allowing the comparison across subjects noted previously. Already. It is important that researchers in rehabilitation are involved with research teams creating dynamic measures so that constructs useful in rehabilitation are included. Additional validation. and then they are calibrated onto a common ruler to create a measure with one metric. namely item response theory (IRT). A framework for developing an item bank has been described by Cella and colleagues (2004). and it is expected to create item banks for use in clinical research for people with neurologic conditions. a data bank is a group of items that is able to define and quantify one construct (Revicki and Cella. To address these issues and others. subjects are presented only with items close to their level of ability. referenced frequently in the paragraphs related to classical scale development. according to his or her level of performance. 1997). the subject responds to a series of items and an initial classification of performance is made. field testing and analyses lead to the creation of a “data bank” of items relating to one domain. all known items that assess the same underlying construct (i. and this process continues until his or her performance stabilizes. It also means that different subjects take different versions of the same test. and is thus. 2003). To use CAT with an individual patient. Stroke researchers should benefit from the new technology. New items reflecting missing areas may also be written. computer adapted testing (CAT) and computer-assisted scale administration. and how this performance is associated with the abilities assessed by test items (Hambleton and Jones. At the beginning of the test. mobility or self-care or physical activities outside the home) are collected. This means that the time to complete the test is usually shortened because after determining the general level of performance. a computer algorithm is employed to select the items for the subject. IRT is a statistical framework related to a subject’s performance on individual items and on the test as a whole.

. for example cross a busy street (Nakamura et al.. negotiate sidewalk curbs independently. For the sake of argument. Bohannon and Walsh. 1987) and test–retest reliability (Holden et al. Thus walking competency is linked to the accomplishment of basic every-day tasks. 1986). data from the sub-acute stroke subjects in the Richards et al.. Richards et al. Perry et al.. 1987. followed by the balance scale and the TUG... Moreover. data. Hsu et al.. and negatively correlated to spasticity of the lower extremity (Norton et al. To further examine the relation between stroke severity. Lamontagne et al. 1992a. 10 or 30 m) are easy to carry out and when standardized instructions are used. Richards et al. Reliability. 1984. Brandstater et al. 1997) of measures of walking speed in persons with stroke are high. subjects who walk faster tend to have a better walking pattern (Wade et al. see Volume II. 1975. walking speed was less sensitive. Richards et al. one with subjects in the early (Salbach et al.. walk far enough to accomplish activities of daily living (LernerFrankiel et al. In persons with stroke. 2003). 2004) is used to describe an ensemble of abilities related to walking that enables the individual to navigate the community proficiently and safely. the 5mW was more responsive than the timed up and go (TUG) (Podsiadlo and Richardson. In this group of subjects. 1990. tested an average of 8 and 38 days after stroke. 1995).. but is it always the most responsive measure? For example. 1992). in terms of reliability and validity. 1988. Table 1.. 1995). and responsiveness. to functional mobility (r 0. to motor recovery (r 0. the 10-min walk (10mW) test at natural or free pace is a very good measure. should maximum gait speed also be tested to assess the capacity of persons with stroke to have a burst of speed to. 1995).62. 1992). Others believe measuring gait speed over 5 m is enough. validity and responsiveness of gait speed Gait speed at a comfortable pace is likely the bestknown measure of walking performance (Wade. chapter 3)..25–0.. As demonstrated by the Salbach et al.67) of the lower extremity (Bohannon. Bohannon and Walsh. are comparable between groups at both evaluations and the SRMs indicate that it is the second most responsive measure for both groups.4 Principles guiding the selection of outcomes to measure walking competency after stroke The term walking competency (Salbach et al. in the Richards et al. 1954) ambulation subscore was the most sensitive measure. Evans et al. 1991). comfortable walking speed has been shown to be positively correlated to strength (r 0.61. Responsiveness of a measure of physical performance cannot be generalized because it is related to stroke severity.. data. The balance scale scores. the 10mW comfortable and the 10mW maximum pace... Salbach et al. Suzuki et al. Wade et al. 1988. turn the head while walking without losing balance. Thus. the inter-rater (Holden et al. Timed walking tests (over 5. (2001) examined the responsiveness of four different timed gait tests in 50 persons. however. 1983). 2004) post-stroke.60. The construct validity of walking speed is also very good. 1991) or the balance scale (Berg et al. leisure activities and participation in life. let us define “measure of choice” as the measure that is most responsive to change as determined by the SRM. as gauged by walking speed. 1986. 2001.. 2001) and the other in a subacute phase (Richards et al. It gives estimates of the magnitude of change that can be expected in clinical measures over 8 weeks. react to unexpected perturbations while walking without loss of stability.1 compares data from two studies. 1.. On the other hand. Podsiadlo and Richardson. and demonstrate anticipatory strategies to avoid or accommodate obstacles in the travel path (Shumway-Cook and Woollacott. b. likely due to the more severe disability as indicated by the walking speed and TUG time. the Barthel index (Mahoney and Barthel. 1995). (2004) study were subdivided . 1989.. 1995). They found the 5-min walk (5mW) at comfortable pace test was most responsive followed by the 5mW maximum pace. 1992.. Elements of walking competency include being able to: walk fast enough to cross the street safely (Robinett and Vondran.12 Carol L. to balance (r 0. 1984.

Outcomes measurement: basic principles and applications 13 Table 1.89 19.5 38 55 36 47 1. Thereafter. Figure 1. 1992.5 8.2 8.6 24.31 1.88 1. *Comfortable walking speed measured over 5. Jorgensen et al.5 7. recovery has been documented up to 2-year poststroke (Richards et al. were evaluated on average 52-days post-stroke and 8 weeks later. . a number of intervention studies in persons with chronic stroke have confirmed that recovery of function (Dean et al. Teixeira-Salmela et al. Maximum (max.8 7. 1975) subscale and the balance scale which rate the achievement of movement tasks.74 Baseline Sub-acute stroke (n Post-therapy 62) Change (%) SRM Post-therapy 88 18 Change Data for subjects with acute stroke obtained from Salbach et al.0 3. These results are similar to those reported by Salbach et al.3 9.3 7.3 or 0.04 0. (2001) and Richards et al. Richards et al. (2001). score) STREAM (100) FM-L (34) FM-A (66) Barthel index (100) Barthel ambulation (47) Balance scale (56) TUG (time..2 37. We must now question the classical recovery curve that has been defined by plotting change over time in clinical measures that have a ceiling effect. subjects. s) 5mWcom (cm/s) 5mWmax (cm/s) 10mWcom (cm/s) 10mWmax (cm/s) 37 32.14 1. Thus. Tangeman et al.5 18. recovery slows but continues up to about 6-month post-stroke (Skilbeck et al.9 2. 1999).) score for each measure shown in first column.3 14. SRM that represents the average change score over a set period of time divided by the SD of that change.8 22.1 34 50 34 47 47 19. Data for subjects with sub-acute stroke taken from Richards et al. the balance scale is more responsive in the slower walking group.. 10 or 30 m.. Moreover. walking speed can have a floor effect when evaluating subjects who walk at very slow speeds and require assistance (Richards et al. 2000. 2000) occur beyond 6 months post-stroke.1* 57 35. 2001.7 25. 1995).92 0. Although the Barthel ambulation subscore remains the most responsive. 2004) and changes in brain organization (Liepert et al. 1999...00 0... Salbach et al.22 1. (2004). When selecting a locomotor-related outcome measure it is important to consider the locomotor abilities of the persons to be evaluated.3 120 38 40 86 46 22 2.1. The TUG also has a floor effect because many subjects cannot complete the test 2 months after stroke (Richards et al.0 127 130 1. Magnitude of change over 8-week period in persons with acute and sub-acute stroke.4 36. Conversely..8 20 25 29 36 0.9 31.4 21.8 19. (1995).. have a ceiling effect when evaluating higherperforming subjects.16 84 105 11 17.83 26.06 75 26 90 17 0.22 Baseline 77 25 50) SRM 0.5 30.7 29.8 22.9 18.6 6. Such results illustrate how floor and ceiling effects relate to responsiveness.8 5. the SRM is closer to the TUG and gait speed values in the faster walking group and conversely..8 30. 1983. The Fugl-Meyer leg (FM-L) (Fugl-Meyer et al. 1990.1 compares the SRM values of the different measures in the two groups.7 45. it is generally accepted that most recovery occurs in the first 6-week post-stroke when the effects of rehabilitation augment natural recovery. Acute stroke (n Measure (max.6 6.7 6.6 17. values give mean or mean 1 SD..1 53. 1995). 1995).77 0. subjects who received task-oriented physical therapy.6 10.6 88 1.3 59 83 59 79 18 29.99 19.. however.3 m/s at baseline. according to whether the subjects walked 0. With a continuous measure such as gait speed. undergoing regular rehabilitation were evaluated 1-week post-stroke and 8 weeks later. in persons with acute stroke.

walking speed alone will not evaluate aspects of walking competency related to endurance.. FM-A: Fugl-Meyer arm subscale. When examining change in outcome measures..8 1. walking initiation and walking. 1997).30) Gait speed (m/s) BA BB TUG FM-L FM-A Speed Figure 1. largely ignored in clinical practice. 2003) combines the sit-to-rise test with walking initiation.30 m/s) at baseline.. stair climbing will reveal the impairment. in part because the affected leg supports less than 50% of the body weight (Engardt and Olsson.4 0. Once it is established if the change is greater than the error estimation. A mobility test like the TUG thus also assesses the ability to perform the sub-tasks of rising and sitting. as measured by the percent maximum muscle activation level (PMAL) of the vastus medialis. Malouin et al.30 m/s) or moderate speeds ( 0. it is important to question whether the amount of change is larger than the measurement error. has been . 2003). 1997). 2003). 1995. Stair ascent and descent of a flight of 14 stairs can be added to the TUG to create the more difficult stair test (Perron et al.1.4 2.0 Standardized response mean 1.6 1. For continuous measures.. not easy tasks for persons with stroke.8 0. has become the focus of much research and the 6 MINW test. 2001).6 0. systematic and random error in repeated measures (measurement error) can be mathematically derived (Evans et al. 2003).30) ( 0. Although persons with a dynamic strength deficit of about 25% in the knee extensors (Moffet et al. 2004)...4 1. Richards et al.. one usually must rise from a bed or a chair before beginning to walk..0 0.2 1. It is also possible to calculate the standard error of the mean of scale scores from published reliability studies (Stratford.0 Slow Moderate ( 0. that measures functional endurance. Data from Richards et al.14 Carol L. 1992. 1999). Richards et al. 1997) and for the Stroke Impact Scale it is 10–15 points on a subscale (Duncan et al. Malouin et al. Macko et al. This decreased fluidity of task merging can be evaluated in the laboratory (Dion et al. b) can walk without apparent disability. another is the value one-half an SD of baseline scores (Norman et al.... One suggested MID for scale scores is a change of about 11% (Iyer et al. it becomes important to decide the MID. b). 2005). for the 6-min walk (6 MINW) test it is 54 m (Redelmeier et al. 2003. 2004a. 2. 1989). For example. or by a recently validated clinical method (Malouin et al. 1985. The physical demands of rising from a chair. In real life. are more than triple the approximately 25% PMAL needed for walking.2 0.6 2. and larger than the 65% PMAL required for stair ascent in healthy subjects (Richards.. 2003).. The recently developed rise-to-walk test (Dion et al. BA: Barthel index ambulation subscale. Comparison of responsiveness for six outcome measures as determined by the SRM (y-axis) in subjects (n 62) with sub-acute stroke who walked at slow ( 0. or navigate in different terrains under various environmental conditions (Malouin and Richards. 2003. 2003).. Clearly. the MID of the balance scale is 6 points (Stevenson. the ability to ascend or descend stairs. thus combining two different motor programs while remaining an easier test than the TUG because it does not require the subject to walk 3 m. 1993a.2 2. (2004)... Poor endurance (Potempa et al. Subjects with more severe stroke are less able to smoothly transfer from one activity to another and tend to perform first one task and then the second (Dion et al. 2003). such as walking speed. speed: walking speed at comfortable pace. BB: balance scale.

b. While analysis of gait movements and muscle activations recorded concomitantly during a laboratory gait study allow for the differentiation of the salient motor disturbance (Knutsson and Richards. excessive coactivation of antagonist muscles and hypoextensibility of muscles and tendons (Knutsson and Richards. in persons with chronic stroke. Winter. 1996). although the reliability of certain items has been questioned in this population (Wrisley et al. particularly those aspects related to cognitive processes such as anticipatory control and navigational skills. 1991. Moreover. . 2000). From studies of moments of force and mechanical power produced by the muscle activations during walking. 2003). It is able to predict falls in the elderly (Shumway-Cook et al. The dynamic gait index evaluates the ability to modify gait in response to changing task demands. 2001). 2001). These laboratory results point to the ankle plantarflexors and hip flexors as muscles to be targeted in therapy to promote better walking speed (Olney et al.. 1997. It has been validated to assess many aspects of life participation of people with disabilities. based on the handicap creation process model (Fougeyrollas et al. Olney et al. develop new measures. housing and mobility categories of the assessment of life habits (Life-H) instrument.. 1979) to guide therapy. 2000.. 1995) to promote social integration after stroke.. 1981. Clinicians and researchers alike are grappling to develop new approaches for both therapy and evaluation. Nilsson et al... 2000a. 2003. regardless of the type of underlying impairment (Fougeyrollas and Noreau. 2001. we know that the main propulsive force comes from the “push-off” contraction of the ankle plantarflexors (generation of power) at the end of the stance phase aided by the “pull-off” contraction of the hip flexors (generation of power) at swing initiation and the contraction of the hip extensors in early stance (Olney et al. guide therapy. Others have investigated the dimensions of the physical environment that might impact on mobility. Duncan et al. supporting the importance of mobility and gait speed (Perry et al. 1991. 2001. explain the results of clinical outcomes. Moreover... It is not surprising that Desrosiers et al.. hyperactive stretch reflexes. personal care. 2004). Salbach et al... 1999). 2002). 1998. Understanding the relationship of environment to mobility is crucial to both prevention and rehabilitation of mobility problems in older adults (Shumway-Cook et al.5 The use of laboratory-based gait assessments and measures of brain reorganization help explain changes in clinical scales and performance-based measures Laboratory outcome measures This section will briefly illustrate how laboratory outcome measures can be used to: 1 2 3 4 validate clinical measures. In-depth gait studies (see Volume II. (2003) have reported high correlations between participation (handicap situations) measured by the Life-H. Even persons with chronic stroke who walk at near-normal speed (122–142 cm/s) may require functional endurance training (Richards et al. such analyses are not available to usual clinical practice. Dietz et al. Dean et al. 1979.Outcomes measurement: basic principles and applications 15 selected as an outcome measure in a number of stroke trials (Visintin et al.. 1. Lamontagne et al. One can argue that the best test of walking competency is to be able to participate in daily routines such as evaluated by the fitness. 2002) may be present to a different extent across subjects. chapter 19) have elucidated the disturbed motor control during gait in persons after chronic stroke. and impairment and disability measures of the leg.. Olney and Richards. highlighting the importance of using tests with increasing physical demands. 1998). (1994) found the power generated by the hip flexors and ankle plantarflexors of the paretic lower extremity to be the best predictors of walking speed. the practice of calculating the distance walked in 6 min from the walking speed over 10 m overestimates the actual distance (Dean et al. 1997) and in persons with vestibular problems (Whitney et al..... Low muscle activations (paresis). “Walking competency” as a goal of therapy is relatively new.

Both studies found that. 1991. 2003). 2003)... 2002). Gérin-Lajoie et al. An analysis of gait kinetics (muscle activations. powers. 2000. 2004). 2002) and PET (Nelles et al. Similar correlations between changes in brain activation patterns and motor recovery have also been reported after a single dose of fluoxetine (Pariente et al.. chapter 5). 2003) provide further evidence of a relationship between traininginduced cerebral changes and motor recovery. the effects of taskoriented training for the upper limb on brain activation patterns were studied using fMRI (Carey et al. Numerous studies have looked at the predictive value of TMS (Hendricks et al.. Virtual reality technology is now being applied to the development of training paradigms to enable persons with stroke to practice navigational skills safely in changing contextual environments (Comeau et al. for example.. Richards et al. 2003).. The clinical fluidity scale of the rise-to-walk test was validated by comparing clinical decisions to the smoothness of the momentum curve derived from a biomechanical analysis made in the laboratory (Dion et al. It provides important prognostic information in the early stage after stroke... in a recent trial evaluating the effects of task-oriented physical therapy. Volume I. it does not explain why the person walks faster. 2003) and led to the development of a fluidity scale (Malouin et al. 2001. 2002) and persons with stroke (Said et al. it has been proposed that the early bilateral activation of the motor networks seen in patients with rapid and good recovery may be a prerequisite to regain motor function rapidly.. For example. For example. 1999. the persistence of motor evoked potentials (MEPs) in paretic muscles has been correlated with good motor recovery. 2002. 2001).. For instance. moments. whereas the lack of TMS responses is predictive of poor motor recovery. Richards et al. Richards et al.. in two rigorously controlled studies. Based on findings from a study combining fMRI and TMS.. Much work. In these studies. may be predictive of motor recovery (Foltys et al.. 1998. has been done on obstacle avoidance in healthy persons (McFadyen and Winter. 2004). An example of the use of laboratory data to validate a clinical measure is recent work related to the rise-to-walk test. work) is needed to pinpoint the source of the increased speed.. Chapter 15). In a longitudinal fMRI study. Many new therapeutic approaches and outcome measures are first developed in the laboratory. the early recruitment and high activation of the supplementary motor area (SMA) was correlated with faster or better recovery (Loubinoux et al. 2003).. 2003). Neuroimaging techniques for studying changes in brain activation patterns and their relationship with functional recovery With the rapid development of neuroimaging techniques (Volume II. . Functional imaging and electrophysiologic brain imaging techniques have provided substantial information about adaptive changes of cerebral networks associated with recovery from brain damage (Calautti and Baron. Richards et al. functional magnetic resonance imaging (fMRI) and transcranial magnetic stimulations (TMS. (2004) were able to attribute 27% of the improvement in walking speed to a better plantarflexor power burst.. in contrast to patients in control groups whose brain activation patterns remained unchanged. Patterns of brain activation can also be used early after stroke for predicting functional outcomes. Dean et al.. 2003. TMS was used to map the motor output area (motor representation) of targeted muscles. where hand motor scores were compared to the whole sensorimotor network activation. Increased cortical excitability and a shift in the motor maps after active rehabilitation (Traversa et al.. Liepert. 2001).16 Carol L. TMS mapping studies (Liepert. McFadyen et al. it has become possible to study neural organization associated with motor recovery after brain damage. 1997) or constraint-induced therapy (Liepert et al. TeixeiraSalmela et al. such as positronemitted tomography (PET). While gait speed can be used to discern a change in functional status. and thus. patients in the treatment groups displayed enhanced activations in the lesioned sensorimotor cortex in parallel with improved motor function.

50 0. These LIs are generally lower in patients.00 20 30 40 50 60 TMS (%) 70 80 90 i/o contralateral i/o ipsilateral Figure 1.2. Dynamic changes in LI values over time have also been reported in a longitudinal study (Marshall et al. suggesting that the LI is a good marker of brain reorganization. Each symbol normal curves from a (c) healthy subject (LI (Schneider and Malouin.. In contrast. steeper slope and higher plateau of MEP amplitude) compared to the ipsilateral motor cortex and resembles the pattern seen in a healthy individual (LI of motor threshold 1. The i/o curves. LI values range from 1 (activation exclusively ipsilesional or affected hemisphere) to 1 (activation exclusively contralesional or unaffected hemisphere).2). the laterality index (LI) has been proposed to quantify changes of brain activation patterns observed in functional neuroimaging studies of recovery post-stroke (Cramer et al.50 0.50 MEPs from paretic TA (mV) 1.25 1.00 0.. provide a reliable measure (Carroll et al.0)..00 20 30 40 50 60 TMS (%) 70 80 90 i/o contralateral i/o ipsilateral (c) 1.75 0.75 0. 2000. represents the mean of 4 MEPs ( 1 SD). inter-hemispheric motor reorganization can be quantified using TMS input/output (i/o) curves. indicate that in a patient with good motor recovery.50 MEPs from paretic TA (mV) 1.50 1. 2001) of the increase of MEP amplitudes against incrementing levels of TMS intensity (Devanne et al. the excitability of the motor cortex contralateral to the paretic tibialis anterior (TA) muscle (LI of motor threshold 0. 2000). Examples of the contralateral and ipsilateral i/o curves of the paretic TA in a patient with (a) poor motor recovery (LI: 0.25 0. 2001).Outcomes measurement: basic principles and applications 17 2000) are associated with improved motor function suggesting treatment-induced reorganization in the affected hemisphere (Liepert et al.28) and (b) good recovery (LI 0.25 0. 1997).50 0.25 1.25 TA MEPs (mV) 1.. (a) 1. Recently. See text for more details .75 0. (2002) found increases in LI values corresponding to a switch of activation to the affected hemisphere to be related to improved hand function.. indicating a relatively greater activation of the unaffected hemisphere consistent with the aforementioned general patterns of changes (Calautti and Baron. Calautti et al. 1. 2003). After specific finger-tracking training.25 0. unpublished data). Likewise.0).78) is greater (lower motor threshold. LI provides an estimate of the relative hemispheric activation in motor cortices. 1997)..00 50 55 60 65 70 75 80 TMS (%) 85 90 95 100 Motor threshold Slope Plateau i/o contralateral i/o ipsilateral (b) 1.00 0. Carey et al. Comparisons of the excitability of the motor cortex of the two hemispheres (Fig. especially in poorly recovered chronic patients.00 0.78) compared to 1.

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Three important points provide evidence for this current. which can be traced to Gowers (Phillips and Landau. 1990). the current view indicates . First. the concept of motor somatotopy. down to the level of a different region for each finger of the hand. has been interpreted to mean that different segments of the body are controlled from spatially separate regions of M1. neurons distributed over a wide cortical region are active during the movement of a given body segment. 1950). Karen T. 2001) such that different spinal motoneuron pools receive input from broad.1 The M1 The current view of M1 organization Our thinking about M1 has been shaped largely by the oversimplification of two related concepts.2 Human voluntary motor control and dysfunction Catherine E. The current view of M1 is quite different (Schieber. The concluding section of this chapter discusses how. Schieber2. and discusses how the current view indicates that M1 is a flexible control system with an inherent capacity for plastic reorganization after brain injury. in addition to lesion size and lesion location. in part from the network of connections among areas. Primary motor cortical (M1) areas and non-primary motor cortical areas (NPMAs) are presented as a flexible control system for voluntary movement. and many M1 neurons have projections that diverge to more than one motoneuron pool (Fig. and in part from the availability of more than one descending pathway. 2. the concept of the upper motor neuron. Rochester. In part. with an inherent capacity for reorganization. Penfield and Rasmussen. 1937. Louis. M1 has previously been viewed as a somatotopically organized sheet of separate groups of upper motor neurons.1(b)). Reilly2 and Marc H. more complex view of M1. this capacity for flexible reorganization arises from the intrinsic organization of cortical areas.1(a)). each of which controls a pool of spinal motoneurons. territories and tracts that are spared after a lesion can affect the capacity for functional recovery of movement. has been interpreted to mean that cortical neurons are simply higher order neurons whose physiologic behavior is essentially like that of lower motoneurons. This section reviews evidence that supports the current. In the current view. whereas the prior view of M1 suggested that stimulation of different regions of M1 should elicit movement of different body segments. overlapping cortical territories. which was carried farthest by the work of Penfield and his memorable cartoon.3 1 2 Program in Physical Therapy. USA The ability to promote functional recovery after nervous system injury depends in part on understanding how the normal brain works and how the damaged brain reorganizes itself. and thereby moves a particular body segment (illustrated schematically in Fig. Following these two concepts. Lang1. the homunculus (Penfield and 24 Boldrey. more complex view of M1. First. Second. St. MO. University of Rochester. NY. 2. Washington University School of Medicine. USA and Departments of Neurobiology and Anatomy and 3Neurology. This chapter discusses the current understanding of how areas of the cerebral cortex and their descending pathways contribute to voluntary motor control in humans in the context of how these areas may provide compensatory control for each other in the damaged brain. 2.

whereas the prior view of M1 suggested that each M1 neuron with corticospinal output influences just one muscle. Buys et al. Intracortical microstimulation shows a broadly overlapping mosaic of points where stimulation elicits movements of different body segments (Sato and Tanji. 1986) and that some single M1 neurons connect to both proximal and distal muscles (McKiernan et al. 1937. horseradish peroxidase staining has shown that some single corticospinal axons have terminal arbors in multiple spinal motoneuron pools (Shinoda et al. 2001). these studies support the view that output from a broad cortical territory converges on the spinal motoneuron pool for a given muscle and that the cortical territories for different muscles overlap extensively. arm region. Despite the development of more focal stimulation of the cortex over the past few decades. 1975). Evidence that single M1 neurons provide output to multiple muscles has been obtained using spike-triggered averaging.. 1917. 1993). the current view indicates that neurons in overlapping M1 territories will be active during movements of different body segments.1. show that within the face region. many others diverge to multiple muscles... 1980. Third. Second.. that focal stimulation can elicit movement of the same body part from multiple sites in a broad region. or leg region. Park et al. Reversible inactivation studies in similarly trained monkeys show that small amounts of muscimol injected into the hand area disrupt some . although some corticospinal neurons may influence only one muscle. Classical view (a) and current view (b) of the manner in which M1 neurons connect to the spinal motoneuron pools and their muscles.. the spatial resolution of motor maps has not become finer. 1952). 1981).. Penfield and Boldrey. Evidence supporting the current view has been found in monkeys and in humans. Woolsey et al. Thus. Recording the activity of single M1 hand area neurons in monkeys trained to flex and extend each of their fingers revealed that (1) a given neuron could be active with movement of several different fingers and (2) the region of M1 where active neurons were found during movement of a given digit was co-extensive with the region where active neurons were found during the movement of any other digit (Schieber and Hibbard. whereas the prior view of M1 suggested that neurons in one region of M1 would be active during movement of one body segment and neurons in another region of M1 would be active during movement of another body segment. 1989. 1998). the current view indicates that a given M1 neuron may influence the motoneuron pools of several muscles. the territories from which stimulation can elicit movement of different segments overlap considerably (Leyton and Sherrington. an analysis technique that is used to detect and quantify relatively direct relationships between a cortical neuron and a spinal motoneuron pool.. Thus. Moreover large cortical territories have projections that converge on single spinal motoneurons (Andersen et al. Early studies of electrical stimulation of the cortical surface. Waters et al.Human voluntary motor control and dysfunction 25 (a) A B C M1 (b) X Y Z A B C Spinal motoneuron pools A B C 1 2 3 Muscles 1 2 3 Figure 2. Taken together. Anatomically. Spike-triggered averaging studies in awake monkeys have shown that single M1 neurons usually connect to two or more muscles (Fetz and Cheney. regions where stimulation elicits movements of different body segments must overlap extensively. including those of Penfield. 1990.

then when part of M1 is injured. 1998) lesions to the M1 hand area have documented impairment in movements of body segments proximal to the hand. Redistribution of function within M1 may be capable of occurring over greater cortical distances and faster than previously thought. but weakness is not confined to one small body segment. 1993. see also Volume I. Implications of M1 organization for recovery after brain injury What implications do these advances in our understanding of M1 have for functional recovery and neurorehabilitation after brain injury? First. these patterns do not occur because the physiologic boundaries do not exist.. spared regions of M1 may be able to restore function. The weakness may be greater in the thumb and index than in the ulnar fingers. 2001. and shoulder likely does not exist. or of the more proximal arm segments (Grafton et al. any lesion affecting M1 that is large enough to produce clinical findings produces simultaneous weakness of multiple contiguous body segments. Kim. but strong fingers. the areas of M1 devoted to control of the fingers have been shown to enlarge when a normal subject practices a complex finger movement task (Karni et al. 2001). such enlargement . physiatrists. Thus. the entire hand. part of the functional recovery seen after brain injury may arise from the inherent flexibility of the remaining M1 territory. For example.. now produced contractions in hand muscles (Nudo et al. Beisteiner et al. Sanes et al. 1998. This may explain. several fingers. why after small experimental lesions to the M1 hand territory in monkeys with subsequent forced use of the affected hand. Similarly. Chapter 8 on Plasticity in motor functions and Chapter 14. extensively overlapping M1 regions are activated during movements of a single finger. In humans. Indovina and Sanes. 1995). other reports of small reversible (Brochier et al. 1999. The entire face on one side. in part. such that impairments in motor control can be detected only during kinematic testing of independent finger movements (Lang and Schieber. although a small somatotopic shift for the center of activation can be identified. Taken together. Enlargement of the M1 hand area over several weeks has been observed with intracortical microstimulation mapping in monkeys (Nudo et al. Similarly. 2003)... regional cerebral blood flow studies have shown that.. this evidence shows that natural movements of different body parts involve activation of M1 in broad. Hlustik et al. if some M1 territory is spared. Kleinschmidt et al. If any one region of M1 normally participates in the control of many body parts. Rather. but a strong thumb.. or the entire foot becomes weak from a cortical lesion. But if this were the reason. finger movements more than others. or just the little finger. 1997. cases of small lesions to the M1 hand territory suggest that although there is a general somatotopic gradient in human M1 (Lee et al. 2001.. One never sees a cortical lesion produce weakness of just the thumb. 1996b). 1998). some patients should have a weak face and thumb... note that the current view suggests that any region of M1 normally participates in the control of many body parts. a strict mediolateral somatotopy with discrete regions for each finger and for the wrist.. not because they have assumed entirely new functions. Schieber. or a weak leg and little finger. 1997). Neurologists. elbow. 2001). and studies employing transcranial magnetic stimulation suggest that in humans. 1995. and rehabilitation professionals witness this in clinical practice daily. Likewise.26 Catherine E. Lang et al. in people with small lesions of the hand knob area of M1 (Yousry et al. 1999) and permanent (Friel and Nudo. but because they were participating in those functions before the injury. but the movements that are disrupted were unrelated to the mediolateral location of the inactivation along the central sulcus (Schieber and Poliakov. recovery may be nearly complete.. Plasticity after Brain Lesions). intracortical microstimulation in the territory surrounding the lesion that had originally represented more proximal muscles. overlapping territories. This observation is customarily ascribed to the fact that disease processes do not respect physiologic boundaries. or greater distally than proximally in an extremity. or just the upper lip. Instead. as well as in the hand itself. 1996a.

NPMAs and M1 areas are engaged together in generating the motor plan and controlling spinal motoneurons. the parallel. distributed model. These NPMAs can be distinguished from one another because they have: (1) different cytoarchitechtonic features.Human voluntary motor control and dysfunction 27 can occur within minutes (Pascual-Leone et al. Corticospinal projections arise not only from . we speculate that neurorehabilitation will eventually be able to make use of M1’s ability to flexibly redistribute its function. PMv and PMd can be further subdivided into a ventrorostral premotor area (PMvr). 1990.. dorsorostral premotor area (PMdr). Giraux et al.2).. Area 24 in the superior and inferior banks of the cingulate sulcus contains at least dorsal (CMAd). hierarchical model of voluntary motor control is inaccurate and should be replaced with a more parallel. and potentially result in improved hand function in people with chronic stroke (Muellbacher et al. with M1 and/or with one another. rostral (CMAr). 2. the frontal association areas pass a command to the “premotor” cortical areas. and that many NPMAs have significant corticospinal projections themselves.. 2. see Volume I. Evidence has emerged over the past few decades suggesting that this sequential. distributed model.3 shows our current road map of the interconnections between these areas. which in turn select a motor plan and pass it to M1. For example. and (4) different features of physiologic activity (for reviews see Rizzolatti et al. Permanent changes in the human M1’s neural connections with the periphery. by identifying the injured regions and then designing specific rehabilitative strategies that make maximal use of nearby uninjured regions. 1993). 2002.. other centers may be able to take over. What evidence is there that voluntary motor control should be viewed as a parallel. distributed model implies that if one center is destroyed. 1994). (3) separate reciprocal interconnections with the thalamus. Dum and Strick. and the supplementary motor area (SMA) on the medial surface. Rostral to the SMA. Primate studies have identified multiple NPMAs in the frontal lobe (Fig. and caudal (CMAc) cingulate motor areas. Whereas the sequential. area 6 contains a ventral premotor area (PMv). An important and rapidly developing topic in neurorehabilitation research is how this capacity for flexible reorganization of M1 might be exploited in humans with brain injury to enhance functional recovery. such as those occurring with spinal cord injury or amputation. 2001). hierarchical model suggested that destruction of any single area in the hierarchy would prevent voluntary movement. area 6 also contains the pre-supplementary motor area (pre-SMA). M1 can thus reorganize extensively and promptly. Muellbacher and colleagues are exploring how afferent input from proximal versus distal upper extremity segments may be manipulated to increase the M1 representation of the hand. Figure 2. Likewise.2 NPMAs The current view of NPMA organization The classical view of voluntary motor control was that. and dorsocaudal premotor area (PMdc).. ventrocaudal premotor area (PMvc). 1998. Chapter 15 on Influence of theories of plasticity on humans). (2) separate microstimulation maps.. While it could be many years until these novel approaches might be proven efficacious enough to be used routinely in clinical practice.. and a dorsal premotor area (PMd) on the lateral surface of the hemisphere. 2002). have been shown to alter the M1 map (Levy et al. distributed process? It is now known that there are many more frontal cortical motor areas than formerly thought. when an action is willed. M1 executes the movement via direct and indirect commands to the spinal motoneurons. temporary ischemic anesthesia of the forearm for 30 min produces greater activation of proximal arm muscles by a constant transcranial magnetic stimulus compared to before the ischemic anesthetic (BrasilNeto et al. 1992). Simply repositioning the forelimb in rodents has been shown to shift the boundary between the forelimb and vibrissae (whisker) representations in M1 (Sanes et al. that these areas are extensively interconnected with M1 and with one another. Anterior to the M1 in area 4. In a parallel.

and CMAc. SMA. PMd. but also from PMv. human reaction times. Note that the various NPMAs are defined based on research in the non-human primate and that the human parcellation is currently under investigation. CMAd. M1. 1989).3. Further evidence supporting a parallel. See text for definitions of abbreviations. Lang et al. 2002). The thick line from M1 to the spinal cord indicates that this corticospinal projection is stronger than corticospinal projections from other areas. Diagram of a macaque (a) and a human brain (b) showing current parcellation of cortical motor areas in the frontal lobe. distributed model of motor control and not a sequential. CMAr. M1 SMA Pre-SMA C MAv C MAr C MAd (a) (b) M1 SMA Pre-SMA C MAd C MAv C MAr M1 PMdr PMdc M1 PMdc PMdr PMvr PMvr PMvc PMvc Figure 2.28 Catherine E. allow sufficient time for information sharing within and between multiple cortical and subcortical areas prior to a motor response. Given that conduction times from M1 to spinal motoneurons and then to hand muscles require only 20–30 ms. approximately 200 ms for visual cues.2. Most corticocortical connections are reciprocal. . and 100 ms for somatosensory cues (Cordo and Flanders. Connections of the cortical motor areas. in a distribution that is quantitatively less but qualitatively similar to axonal projections from M1 (for review see Dum and Strick. hierarchical model comes from reaction time and neuronal firing time data. C MAr C MAv C MAd Pre-SMA PMdr PMvr PMvc PMdc SMA M1 Spinal cord Figure 2. Corticospinal axons from the NPMAs terminate in the intermediate zone and the ventral horn of the spinal cord.

guided by remembered internal cues. 1991). where the surgical resection leaves M1 intact. whereas SMA neurons on average were more active during internally-cued movements. Mushiake et al. the distributions of onset times are broadly overlapping. Though this work cannot be reviewed thoroughly here. CMAr. bilateral SMA lesions produce a deficit in internally-cued movements but not in visually-cued choices.e. 1992). Conversely. resections of NPMAs such as the SMA. Krainik et al. 1988. internally-cued movements (Passingham.. a new sequence was cued to the monkey by illuminating the buttons one at a time on each trial. allowing for the exchange of information between multiple cortical and subcortical areas related to the planning and execution of the intended movement. So although the PMv may play a greater role in visually-cued movements. (1991) trained monkeys to press three buttons in sequence.. 20 mm anterior to the precentral gyrus) produces motor effects in humans (Uematsu et al. a parallel. Studies of regional cerebral blood flow showing activation of NPMAs – including SMA. physiologic recordings show some overlap of function. Though the PMv and SMA both contained neurons that were active during both visually-cued and internally-cued movements. CMAc – during various motor tasks suggests that the human brain contains NPMAs that are homologous to the NPMAs identified in non-human primates (see Picard and Strick. Once the monkey had practiced the sequence enough. current research suggests that different NPMAs may have overlapping but partially separate functions.. Motor related cortical potentials derived from electroencephalography suggest that both the SMA and M1 are normally involved in self-paced movements (Tarkka and Hallett. and internally-cued movements only by the SMA. 1987). At first. all the above evidence indicates that human voluntary movement control normally requires NPMAs along with M1 and that voluntary movement is controlled via a parallel. Shima et al.. With their individual loosely somatotopic . 1977. 1991.. Although the average onset of increased task-related neuronal firing in the NPMAs slightly precedes the average onset of firing in M1. there is now a considerable amount of evidence indicating that humans have multiple NPMAs similar to those identified in monkeys (Fig. making it unlikely that a motor command would progress in a sequential. 2. task-related M1 neurons and NPMA neurons increase their firing approximately 50–200 ms prior to the onset of movement (Tanji et al. produces an initial hemiparesis that almost completely resolves (Laplane et al. PMd. but these same lesions do not impair the ability to generate self-paced. Though one might conclude that visually-cued movements are controlled only by the PMv. PMv.Human voluntary motor control and dysfunction 29 Likewise in non-human primates. distributed process. these are quantitative differences and there is some overlap of function between PMv and SMA. 2001 for review).. Understanding the roles played by these NPMAs in voluntary motor control is a focus of ongoing research. he could continue performing it for several trials without having the buttons illuminated. Although the majority of studies investigating NPMAs have been done with animals. The NPMAs are therefore well-suited to provide compensatory control of voluntary movement after damage to M1. 1992). Cortical surface stimulation via implanted subdural electrode grids up to 30 mm anterior to the Rolandic fissure (i. and the SMA in internally-cued movements. distributed control process would allow for better recovery after damage to one part of the system. hierarchical manner. Ikeda et al. And finally. A good example is the difference between the PMv and the SMA during visually-cued versus self-paced movements. Passingham and his coworkers have shown that bilateral lesions of the premotor cortex (which include PMv) produce profound deficits in a monkey’s ability to choose which movement to make based on visual cues. Implications of NPMA organization for recovery after brain injury Compared with a hierarchical control process.2(b)). PMv neurons on average were more active during visually-cued movements. Though the correspondence between particular activated regions in humans and those more precisely defined in monkeys has yet to be fully understood. CMAd. 2001)..

. Electrical stimulation in patients with structural cortical lesions. . 1998). In this way. 1992). thick line). Furthermore. movements made in response to visual cues might be most severely impaired.4. For example. Shima et al. Boudreau et al. 1991.. Pathway of the corticospinal tract (green. Although each NMPA has its own unique inputs and neural activation patterns in relation to various aspect of movement control. suggesting that NPMAs have developed more output to motoneurons (Levy et al. each patient’s neurorehabilitation might be better tailored to their particular brain injury. and the rubrospinal tract (red. dashed line). 2. subsets of neurons in each area have activation patterns that are similar to M1 neurons (Tanji and Kurata. and magnetic stimulation in patients with traumatic quadriplegia. 1997. or teach the patient compensatory strategies to substitute internal cues in situations where visual cues normally suffice. Thus NPMAs.. 2001). We speculate that as the particular situations that maximally engage each NPMA are better understood. 1990. 1982. Lang et al. 2.. many imaging studies after stroke show increased activity not only in the NPMAs described above. both have been found to evoke muscle contractions from a much wider area of cortex than just M1. but also in parietal regions and in ipsilateral M1.4). thinner line). Interestingly. Cadoret and Smith. The corticospinal tract is the most Cortex Midbrain Pons Medulla Cervical spinal cord Figure 2.. which play a role in generating normal voluntary movements. suggesting that these NPMAs are providing compensatory control of voluntary movements after damage to M1. Uematsu et al. whereas internally generated movements that are mediated in part by the SMA might be relatively spared. Seitz et al. Imaging studies indicate that PM and SMA are more active during finger movements in hemiparetic subjects compared to control subjects (Weiller et al. reticulospinal tract (blue.30 Catherine E. The most effective rehabilitative approach might then primarily employ internally generated movements.3 The corticospinal tract Motor control signals from M1 and the NPMAs travel to the spinal cord via several descending tracts (Fig. 1993. neurons in NPMAs could provide compensatory control of spinal motoneurons after damage to the M1. representations and corticospinal projections.. take on an increasingly important role after brain injury. neurons in NPMAs are more frequently related to bilateral movements than neurons in M1 (Tanji et al.. rehabilitation professionals will be better able to promote functional recovery. if a particular patient has a lesion that affects M1 and the human equivalent of PMv but spares the SMA. and thus may be able to exert control over spinal motor neurons via both corticospinal pathways. 1988). 1992.

3. the corticospinal axons are found in the posterior limb. The axons leave the cortex. the greatest proportion of axons originates from M1 (approximately 30% of the total corticospinal tract). synapsing on interneurons in the intermediate zone and synapsing directly on motoneurons in the ventral horn. In man. 2. whereas axons traveling in the uncrossed ventral corticospinal tract tend to synapse on motoneurons and interneurons involved in the control of axial and more proximal limb muscles. Axer and Keyserlingk. 2002). In humans. concentrating in its middle third. resulting in hemiparesis. A small number of corticospinal axons recross the midline in the spinal cord and terminate in the ventral horn ipsilateral to their origin. The corticospinal tract originates from multiple areas in the frontal and parietal lobes. 2000. as well as other structures.4 Other descending motor tracts Descending motor tracts such as the reticulospinal tract and the rubrospinal tract may contribute to voluntary movement and may assist in recovery of function after damage to the motor cortex or to the corticospinal tract (Fig. the majority of corticospinal axons cross the midline and form the lateral corticospinal tract on the opposite side of the spinal cord. strokes affecting the white matter in the territory of the middle cerebral artery frequently damage the corticospinal tract. In the medulla. axons carried in the uncrossed ventral corticospinal tract from the opposite hemisphere may be able to exert compensatory control over muscles on the affected side of the body (Fisher. 2. At the spinomedullary junction. 1964. and the cingulate motor areas (Dum and Strick. The reticulospinal tract arises from the pontine and medullary reticular formation and descends in the ventral and ventrolateral columns of the spinal cord. 1970). Corticospinal axons arise from the large pyramidshaped cell bodies in cortical layer V. and enter the internal capsule. the corticospinal tract forms the medullary pyramid. 1991). pass through the corona radiata. Relatively isolated lesions of the corticospinal tract can occur in humans when a small ischemic lesion is located in the posterior limb of the internal capsule or in the basis pontis. 1993. along with many other corticofugal projections. corticospinal axons originate from Brodmann’s areas 1. 2. The remaining corticospinal axons descend uncrossed as the ventral corticospinal tract near the ventral midline of the spinal cord. Morecraft et al. This spared ventromedial input to spinal motoneurons controlling the affected side of the body may therefore account for the relative preservation of axial and proximal motor control seen after stroke (Colebatch and Gandevia. and 7 (approximately 40% of the total corticospinal tract) and project to the dorsal horn of the spinal cord to regulate sensory inflow. 1998). In the parietal lobe.. The corticospinal tract then descends through the cerebral peduncle of the midbrain. and axons from parietal areas pass through just posterior to the primary motor axons (Fries et al. 2000) and pass below the thalamus. In the internal capsule. Axons traveling in the crossed lateral corticospinal tract tend to synapse on motoneurons and interneurons involved in the control of more distal musculature.4). axons from M1 pass through the middle third of the posterior limb. where axons from the NPMAs pass through the genu and anterior third of the posterior limb. After damage to the corticospinal tract. resulting in the clinical syndrome of pure motor hemiparesis (Fisher and Curry.Human voluntary motor control and dysfunction 31 direct pathway from the cerebral cortex to the spinal motoneurons. with the remaining frontal lobe axons (another 30% of the total corticospinal tract) originating from the SMA. In the frontal lobe of primates. In the pons. the corticospinal axons branch and enter the spinal gray matter.. 1992. These uncrossed axons terminate in the ventromedial portion of the ventral horn and are likely to exert more control over proximal and axial rather than distal musculature (Kuypers and Brinkman. the reticulospinal tract exists as scattered bundles of fibers that terminate primarily in the ventromedial portion . As the axons descend through the internal capsule. Fisher. In the spinal cord. Cao et al. the corticospinal axons pass around the nuclei in the base of the pons (basis pontis). they shift posteriorly (Axer and Keyserlingk. 5. 1989). the premotor areas.. 1979).

Only a small proportion of the fibers continue into the thoracic. exerts control chiefly over axial and proximal limb musculature to assist with postural control and orientation (Lawrence and Kuypers. In man. the rubrospinal tract exerts control over proximal and distal limb motoneurons and can provide some degree of compensatory control after damage to the corticospinal tract (Lawrence and Kuypers. and motor function. and sacral levels of the spinal cord (Nathan et al. motor impairments and potential for functional recovery can be better predicted by determining what percentage of the corticospinal system is affected (Pineiro et al. In man. and descending pathways appear to be a relatively flexible system. 1967). Belhaj-Saif and Cheney. the reticular formation. The rubrospinal tract arises from the magnocellular red nucleus. the reticulospinal tract has been cited as an anatomical substrate for the recovery of function. after partial cordotomy (Nathan and Smith. receives input from a variety of sources. Rather. For example.. 2000). and is heavily interconnected with other brainstem structures such as the vestibular nuclei (Kuypers. of the spinal gray matter at or above the cervical enlargement (Nathan et al. 1991). Kuypers. This final section discusses how. Cheney et al. just anterior to and somewhat intermingled with the corticospinal tract. lumbar. researchers have examined the relationships between lesion size. 1968a. Two lesions of comparable size but in different locations can produce differing degrees of motor impairments and differing prognoses for functional recovery. 2001). 1982). crosses directly to the opposite side in the anterior tegmental decussation.. If the rubrospinal tract were to provide compensatory control of motoneurons in man. In contrast to the bilateral motor cortical input to the reticular formation. yet within a few . via the reticulospinal tract. this relationship is confounded by lesion location and by what territory or tracts are spared. 1991.. Axons from the rubrospinal tract terminate in dorsal and lateral parts of the intermediate zone of the spinal cord. the rubrospinal tract is considerably smaller and only a minimal number of axons likely extend down into the upper cervical cord (Nathan and Smith. b. Binkofski et al. 2001). in addition to lesion size and location. 1982). including bilateral motor cortical areas (Kuypers and Lawrence. Kuypers. With the development of imaging techniques such as computed tomography (CT) and magnetic resonance (MR). this compensatory control would be greatest over the axial and proximal upper limb muscles. If the reticulospinal tract provides compensatory control over spinal motoneurons after damage to the motor cortex or the corticospinal tract. a small lesion relatively confined to the M1 hand knob results in initial paresis of only the hand and arm (Kim. The M1 areas. 1982. 1996). the red nucleus receives input from the ipsilateral cerebral cortex (Kuypers and Lawrence. Although we intuitively think that larger lesions will produce more severe motor impairments with less potential for recovery. In non-human primates..5 The importance of spared territory for reorganization and functional recovery The previous sections in this chapter have discussed how various cortical areas and descending pathways contribute to voluntary movement in the context of how these areas might provide compensatory control for each other after brain injury. along with the ipsilateral corticospinal tract. The reticular formation. controlling movement through parallel. spared territories and tracts might affect the capacity for functional recovery of movement. 2000. Although the extent and relative importance of the rubrospinal tract in man remains unclear.32 Catherine E. 1996).. Lang et al. and descends in the lateral column of the spinal cord. The degree of motor impairment and recovery of function cannot be predicted by just lesion size or just lesion location (Chen et al. 2000)... 1967). the possibility exists that the rubrospinal tract could provide some compensatory control of voluntary movement after damage to the motor cortex or corticospinal tract in humans. NPMAs. The origin of the reticulospinal tract. 1982). 1973) and after capsular stroke (Fries et al. distributed processes. 2. lesion location. 1968b. then this control would have to be exerted primarily through the most rostral cervical segments.

reorganization occurred in the contralateral M1 and NPMAs. 83..G. In the case of small to moderate lesions that affected the entire M1 territory.. In summary. the patient typically can use the hand and arm well except for activities requiring fine independent finger movements. Gartus. 2001). J Neurophysiol. A. better functional recovery is associated with less activation in the NPMAs of the same hemisphere and with less activation in the contralateral M1 and NPMAs (Ward et al. (1975). (2000). J. Activity in ventral and dorsal premotor cortex in response to predictable force-pulse perturbations in a precision grip task. Similarly in humans after stroke. Mapping by microstimulation of overlapping projections from area 4 to motor units of the baboon’s hand. Edward. T. Pawelec. T.. Cerebrovasc Dis.. Neuroimage. P. F.. Erdler.G. V. and Deecke. reorganization occurred primarily in NPMAs in the same hemisphere. so that compensatory control from the intact M1 and NPMAs can reach the spinal cord only through alternate descending pathways. R. Plasticity in the distribu. arm. 273–281. and thus promote greater functional recovery. A better understanding of the anatomy and physiology of the spared components of the nervous system and their capacity for reorganization may improve the ability to design and implement effective individualized rehabilitative strategies. but compensatory control for functional recovery can arise from both spared M1 territory and the NPMAs. Mapping of fiber orientation in human internal capsule by means of polarized light and confocal scanning laser microscopy. M. (2001).Human voluntary motor control and dysfunction 33 months. The first lesion damages M1 territory controlling the hand and arm. B. Patients with more complete recovery were likely to have near normal brain activation patterns. and although much of the initial deficit typically improves over time. 13. Moser. H. C. L. Belhaj-Saif. Thus. Proc R Soc Lond B Biol Sci.J.P. Recovery of motor functions following hemiparetic stroke: a clinical and magnetic resonancemorphometric study.J. P (2000). Cunnington. R. D. Hacklander. 86. Windischberger. 1999). R. (2001). 1982). these data suggest that spared territories and tracts can control voluntary movement in humans after brain injury. Pare. R. as well as assessing lesion location. D. lesion size. Lanzenberger. Brochier.J... Differences in functional recovery reflect both the structures affected by the lesion and the structures that remain intact. a lesion of comparable size on one side of the basis pontis. such as typing... M. E. J Neurosci Methods.D. Streibl. Phillips.. 31–36. and size. . and spared territories interact in a complex manner to affect not only motor impairments.M.. the probability of recovery of upper extremity function is greatest after lesions relatively isolated to M1 and decreases progressively with descending lesions affecting the descending corticospinal axons (Shelton and Reding. 1016–1026. lesion location. and leg (Fisher. 3147–3153. but that the spared territories and tracts cannot fully compensate for the highly selective control provided by M1 and the crossed corticospinal system. and leg. reorganization was observed primarily in the spared territory within M1. P. 11.. Furthermore. Lesion size and location may also influence which cortical motor areas undergo plastic reorganization after brain injury (Liu and Rouiller. reaching the spinal cord over an otherwise intact corticospinal tract.. The latter lesion damages the entire corticospinal tract. results in initial paresis affecting the face. and Freund.. and Keyserlingk. 1067–1078. hand. REFERENCES Andersen. T. And in the case of large lesions that affected M1 and NPMAs.. Boudreau.J. J Neurophysiol.. H. Hagan. 165–175. Axer. but the capacity for plastic reorganization and the resulting recovery of function. In contrast. A. In the case of very small experimental lesions that affect only a portion of monkey M1. tion of the red nucleus output to forearm muscles after unilateral lesions of the pyramidal tract. 2003). and Powell. arm. 188. Mau. the patient often is left with permanent residual deficits in the hand. A. Finger somatotopy in human motor cortex. affecting the entire corticospinal tract. Beisteiner. while patients with poor recovery were more likely to activate additional motor areas in the same and in the contralateral hemispheres. and Smith. Binkofski. Taken together. Seitz. M. rehabilitation professionals should evaluate what areas and tracts remain intact after each patient’s brain injury. 94. C. and Cheney.. (2001).

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2 Rationales for gait retraining Interneuron-linked oscillators within the lumbar cord for flexion and extension of the hindlimbs. 75% with sensorimotor loss. Greenlund et al. Indeed. This circuitry may be driven by the timing of cutaneous and weight-bearing inputs from the soles and by proprioceptive and load information from joints.. 2004). and outcome measures for walking Bruce H. The rehabilitation of walking poses some common questions about the services provided by clinicians (Dobkin. walking speeds greater than 80 cm/s make it more likely that a person can participate in the community (Perry et al. and 44% a wheelchair. Neurologic Rehabilitation and Research Program. More functional walking may also reduce risk factors for cardiovascular disease.. 28% use a walker... 2003a). 2001. 85% of patients with a pure motor impairment. 25% receive some physical therapy during the year of major difficulty walking. 30% of those graded ASIA B (motor complete). interventions. By report. The push for faster. Dobkin Professor of Neurology. and 94% graded ASIA C (Geisler et al. Musculoskeletal and joint diseases account for 24% of causes of major difficulty. These levels of gains do not necessarily lead to walking well enough to navigate outside of the home. especially 37 . Six months after a traumatic spinal cord injury (SCI). 2001). They are unable to walk or climb stairs or stand. called central pattern generators (CPGs). Reed Neurologic Research Center. Los Angeles. Successful approaches to improve these walking outcomes would lead to greater participation. Director. 2% of subjects graded by the American Spinal Injury Association (ASIA) scale as ASIA A (sensorimotor complete) at 24 h after onset are able to walk at least 25 ft. 1995. USA 3.. have become a target for both locomotor training interventions and for neural repair (Chapter 13 of Volume I). 48% with stroke use a cane. recurrent stroke. stroke for 5%. 2002. The most rapid rates of increase occur after ages 54 and 74 years old. 2003).. CA. Six months after stroke. and frailty by permitting more opportunity for exercise and fitness (Chapter 21 of Volume II) (Macko et al. half of those who are walking do so at less than 50 cm/s (about 1 mph). 2000). One-third report major difficulty. Kurl et al. Lord et al. Falls affect 41% of these people yearly. back pain for 8%.. At this level of difficulty. and 35% with sensorimotor and hemianopsia deficits will recover the ability to walk at least 150 ft without physical assistance (Patel et al. more functional walking speeds and longer distances walked is an underplayed goal in rehabilitation. Eleven percent never leave their homes and only 32% get out of the home daily. In general. How do we know when our patients have received enough goal-directed therapy for their level of motor control? What measures should we use to rate progress? What do we really mean when we say that a patient has reached a plateau in recovery and will no longer benefit from therapy? Do outside-the-box therapies exist that might augment gains? 3. Gill et al. 2003).3 Assessments. 2002.1 When walking fails Difficulty walking is reported by 10% of Americans (Iezzoni.. University of California Los Angeles. Only 40% of patients who recover walking ability after stroke achieve community-walking velocities. and multiple sclerosis for 2%.

Subcort: subcortical nodes. Cing: cingulate motor Z 3 (red) to 9 (yellow) cortex.5 mph wearing bilateral solid ankle–foot orthoses with a cane in each hand for balance. Following a low thoracic spinal cord transection. are responsible for locomotion in man. However. insula. .1(a)) reveals significantly greater recruitment compared to control subjects. R Toes: right toes. Studies in patients with clinically complete SCI reveal similar responses to limb loading and hip inputs as were found in spinal transected cats (Chapter 30 Volume II). however. Figure 3. He dorsiflexed his right ankle a maximum of 5° and could not offer resistance. beyond the CPGs. Cereb: cerebellum. 1998). 3. act at many levels of the neuroaxis. Right ankle (b) R Knee dorsiflexion and right quadriceps contraction during fMRI of a subject with a SCI at the conus. the supplementary motor area.. cats and rats have been trained to step with their hindlimbs on a moving treadmill belt with support for the sagging trunk. SMA: supplementary motor area. along with other forms of spinal organization (Lemay and Grill. during the practice of stepping.1. He had no movement or sensation below L3 on the left and L4 on the right.1 shows the extent of cortical reorganization induced by a conus/cauda equina SCI followed by gait training. R Knee: right knee. He was able to extend each knee against gravity and minimal resistance. Review articles may overstate the evidence for the case that spinal networks. These sensory inputs. The subject walked modest distances with a reciprocal gait at 1. The animals are not as successful walking over ground. The fMRI study of voluntary right ankle dorsiflexion (Fig.38 Bruce H. Traininginduced adaptations within the cord in these animal models point to the potential of plasticity induced by rehabilitation to lead to behavioral gains. Dobkin the hips. and dorsolateral prefrontal cortex (dlpf) activity also significantly (a) M1/S1 & SMA Cing S2 Subcort & d1pfc Cereb. plasticity within the cord may be no more important than plasticity induced within cortical and subcortical nodes of the sensorimotor network for walking in patients who have residual descending supraspinal input to the lumbosacral motor pools. involving the contralateral thoracolumbar representation in primary sensorimotor cortex (M1S1) and in bilateral M1S1 that represents the whole leg. It seems likely that a network of locomotor spinal motoneurons and interneurons has been conserved in humans (Dimitrijevic et al. R Toes Figure 3. Contralateral cingulate motor cortex and premotor area activation and bilateral parietal. Rationales for gait retraining in patients can draw from animal models about specific sensory inputs that aid the timing and efficacy of the step cycle. Pulling down on their tails or a noxious input enhances hindlimb loading in extension. 2004) that increase the flexibility of supraspinal regions to control hindlimb and lower extremity movements. in concert with specific sensory information. This 52-year-old subject suffered a burst fracture of the first lumbar vertebral body 8 years prior to the functional magnetic resonance imaging (fMRI) study. and cerebellar hemispheres. basal ganglia.

and initial contact with the whole foot or forefoot rather than heel contact followed by a rocker motion onto the forefoot that provides forward momentum. and the joint angles at the hip. computerized video analysis with joint markers. Kinetics are measured by a force plate in the ground or embedded in a treadmill.Assessments. and peak dorsiflexion in swing during inpatient rehabilitation for stroke (Mulroy et al. Electrogoniometers. knee. knee extension in terminal stance. In this subject.2b). explanatory variables of impairment were velocity. a portion of the CPG network is likely damaged. Surface and wire electrodes are used for EMG data. time. a broad range of strategies for gait training suggest themselves for further evaluation. the ground reaction forces elicited (3. midstance. interventions. foot flat. Nielsen.3 Assessments Analysis of gait Figure 3. and paraparetic subjects does help inform an observational analysis of a new patient. mechanisms for declarative and procedural learning. Knowledge of the typical patterns revealed by analyses in normal. and electromagnetic field motion analysis will reveal the kinematics in two or three dimensions. which may lead to circumduction of the affected leg or vaulting off the unaffected one to clear the affected foot. knee extension in terminal 3. less knee flexion and ankle dorsiflexion during swing. and through drugs and electrical stimulation procedures. a hemiparetic gait often reveals temporal differences – a shorter step length for the unaffected leg because the affected leg is impaired as it supports single-limb stance. and outcome measures for walking 39 exceeded that of healthy subjects. Using cluster analysis. 2003. and end of swing heel contact). and equipment to perform and analyze. Grasso et al. 2003a). The evoked activity for contraction of the quadriceps. the clinician can look for temporal as well as kinematic asymmetries between the phase components for each leg. hemiparetic. as well as by a load cell embedded in a shoe.2 shows a quantitative gait analysis in a normal subject for the timing and amplitude of electromyographic (EMG) activation of muscle groups (3.2a). was similar to that of control subjects (Fig. By combining a visual assessment of the stance (initial heel contact. For example. visuoperception.1(b)). Of clinical importance. mostly from less time spent in single-limb stance on the affected leg.. greater double-limb support time compared to healthy persons. however. 3. but residual cortical control and practice led to useful motor control for gait. 2004). planning. In human subjects who are healthy or have had a stroke or incomplete SCI. 2003). Kinematic differences include excessive flexion at the hip during midstance which. At 6 months. midswing. Common gait deviations The gait cycle can be assessed by educated observational skills and knowledge of the disease and its resulting symptoms and impairments. These procedures take considerable expertise. and shorter duration of swing for each leg. formal gait studies characterized differences among patients based on walking velocity. Dobkin. walking velocity correlates with many of the measured temporal parameters of the gait cycle. and ankle (3. By better defining supraspinal components and the means to engage them by voluntary action. 2000b. 2001. heel off ) and swing phases (toe off. decreased lateral shift to the paretic side during single-limb stance. 2003c. functional neuroimaging and other neurophysiological studies of walking reveal considerable contributions from supraspinal nodes of the distributed locomotor network for effective bipedal walking (Dobkin. Formal gait studies are best reserved for a research laboratory and for presurgical evaluations of orthopedic and neurosurgical procedures. Miyai et al.. by moving the center of gravity forward. The numerous variables collected and their interactions demand special statistical and . modeling approaches. Energy cost is also measurable by oxygen consumption studies.2c) during the step cycle (Dobkin.. increases the knee extensor moment. with the exception of recruitment of the bilateral secondary sensory (SII) area and the trunk representation within M1S1.

Normal gait cycle: EMG. pelvic drop with compensatory lateral shift of the trunk to the stance leg. loss of coordination of muscle firing patterns. courtesy of Oxford University Press. Treatment approaches could address each of these patterns. As in children with spastic diplegia from cerebral palsy. excessive hip and knee flexion and plantar flexion. and poor plantar flexor force for push off. hypertonicity . and knee flexion in pre-swing. use of synergistic movements.40 Bruce H. 2003a). motor control of paraparetic gait is complicated by variations in residual selective strength. Dobkin (a) Hip adductors Gluteus maximus Iliopsoas Hamstrings Quadricep Tibialis anterior Triceps surae Erector spinae 50 0 50 150 100 0 100 150 Force 800 700 600 500 400 300 200 100 0 30 20 10 0 10 20 70 60 50 40 30 20 10 0 10 0 10 20 0 10 Stance phase Swing phase Lateral Medial Aft Fore Right (b) Left Body weight Vertical (c) Hip Midswing Hip Toe off Degrees Heel contact Foot flat Midstance Heel off Knee Knee Heel contact Figure 3. Paraparetic gait (Chapter 30 of Volume II) during the stance phase may include absent heel strike. 20 30 40 50 60 Percent of gait cycle 70 80 90 stance.2. Ankle Ankle ground reaction force. The pelvis may drop on the swing side from weakness and overactive hip adductors may narrow the base of support. and kinematic data starting at heel strike (taken from Dobkin. During the swing phase. excessive plantar flexion and insufficient hip or knee flexion may impair foot clearance.

canes. then proceed to sitting and standing balance (Chapter 8 of Volume II). Anti-spasticity agents and intramuscular botulinum toxin may improve aspects of the gait cycle. 2002) • Task-specific shaping of more selective movements (Taub et al. et al.. 2002. however.1. tissue changes in muscles and across joints. Only one trial with clinically meaningful outcome measures obtained by blinded . as well as confounders such as hemi-inattention. Reviews and some initial reports of BWSTT after SCI often suggest that the beneficial effect of locomotor training in incomplete SCI patients is “well established” and that “even chronic SCI patients who underwent locomotor training had greater mobility compared with a control group with conventional rehabilitation” (Dietz and Harkema. Walkers. 2003) • Pharmacological adjuncts for learning or neuromodulation • Biofeedback – kinematic or EMG • Practice in virtual environments • Imagery (Lafleur et al. Several of the approaches in Table 3... 2003). but few comparisons have been made... It also provides task-oriented. 2003) or they employed “historical” controls (Wernig et al.. 2001. 2002) • Treadmill training body weight support • Circuit training (Dean et al. Herman et al. no particular style of care has been shown to be better than another. transcranial magnetic or direct motor cortex stimulation induced muscle stimulation (Moreland et al. primarily in patients with excessive plantar flexion/inversion. 1995). 2002).Assessments. Practice paradigms ought to include a clear schedule and form of reinforcement (Chapter 7 of Volume II). 2000).. For step-training per se. 2002). 2001. truncal ataxia. • Bobath... Sinkjaer et al. 2000. included control subjects at all (Field-Fote.. Table 3. balance. Locomotor interventions are limited only by the imagination of the rehabilitation team. and Parkinson’s disease (Miyai et al. 2000) Task-oriented training Body weight-supported treadmill training (BWSTT) is partially derived from treadmill training experiments on spinal transected animals and CPGs (Barbeau. NDT. stance • Progression from parallel bars. gait apraxia. 2002) • Robotic and electromechanical assists for stepping (Hesse et al. Forms of BWSTT have been employed after SCI. 1999. and extrapyramidal features. and aid foot clearance and knee control..1 are being tested in randomized clinical trials (RCTs). 2003) • Increase walking speed and distance • Reverse deconditioning (Teixeira-Salmela et al. • Braces and assistive devices • Increase muscle strength (Moreland et al. to improve head and trunk control.. 1998. stroke. knee–ankle– foot braces are used to improve balance. Rehabilitation approaches for walking are listed in Table 3. multiple sclerosis (Lord et al. 2003b) – peripheral nerve. 1998). The studies that are usually quoted have not.. limitations in range of motion.. interventions. Loeb and Richmond.. lateral pulsion (pusher syndrome). and outcome measures for walking 41 that is state dependent. and on occasion. massed practice under more optimal conditions for managing weight bearing and walking speed (Dobkin. cerebral palsy (Schindl et al. ankle–foot orthoses. An eclectic problem-solving approach is taken by most therapists. Malouin et al. 1999. correct qualitative gait deviations • Massed practice of walking 3. 2004). A trial-and-error approach for fitting and employing these aids and a reassessment over the time of improved motor control is usually needed. MacKay-Lyons and Makrides. Barbeau. General approaches for retraining walking. 2000) • Functional electrical stimulation for reflexive flexion or to fire a critical muscle group during the step cycle (Daly and Ruff. and truncal and multi-joint interactions during stance and swing phases. 2004) • Increase cortical excitation during practice (Dobkin.1.4 Interventions for retraining gait Strategies for retraining gait start with interventions to improve control of the head and trunk when necessary. lessen the need for full lower extremity weight support. Sullivan et al.

6 41 2. bear some weight in the legs. 1995. Such trials will need to establish training scenarios for the manipulation of BWS and treadmill speeds. Trophic substances produced by activity can increase peripheral axon regeneration to re-innervate muscle. the patient whose fMRI is shown in Fig. as is typically required for drug studies. the outcomes were statistically significant for walking speed. 2003).5 3. For example. RCTs are needed to determine if BWSTT ought to be offered to patients who cannot walk over ground with a reciprocal gait or to those who still walk too slowly to ambulate outside of the home ( 50 cm/s) more than 6 months after onset of hemiplegic stroke or SCI in ASIA C subjects.1 was enabled to stand upright.2 is an overview of the results for ASIA C and D subjects with upper motor neuron impairments.8 43 1..2 10 CONV 5.. 3. LEMS: lower extremity motor score. Subjects received 12 weeks of BWSTT complemented by over ground training when feasible or an equal amount of conventional over ground training. 2003a). and a demonstration of the reproducibility of training techniques will require considerable pilot data (Dobkin. 1998. 2003). Six-month outcomes for a clinical trial of BWSTT versus conventional mobility training for 60 ASIA C and D subjects randomized within 8 weeks of SCI. The SCI Locomotor Trial (SCILT) randomized 145 subjects with incomplete SCI who could not walk on admission to six regional SCI facilities.42 Bruce H. Table 3.. BWSTT may enable some loading and foster rhythmic stepping. when he could not stand or step after routine rehabilitation. Dose–response studies for the amount of training. and pharmacological interventions (Norman et al.3 85 1125 15 18 44 52 19 5 15 618 1.2. 2002)... the same result may have been possible using more aggressive conventional therapies. 2004). 2000. and that revealed no benefit of BWSTT over conventional care in incomplete subjects. but not clinically significant. No benefit of the intervention was found for ASIA B subjects. most of whom did not recover any ability to walk. Chaplin. .9 12 CONV: conventional physical therapy. functional electrical stimulation (Hesse et al. in addition to usual inpatient and outpatient therapies (Dobkin et al. and activate the iliopsoas and quadriceps muscles reciprocally 3 months after the SCI. Barbeau and Visintin. This comparison is of interest. along with justifying the duration and intensity of treatment. 1996. 2002). 2004). Dobkin. Also. Barbeau et al. 2002. most of whom did walk at remarkably functional speeds and distances (Dobkin et al.. Even greater attention will be necessary for the design of RCTs of BWSTT augmented by robotic assistive devices (Colombo et al. 2003). In patients who cannot stand and yet have some proximal motor control that may be brought out by an upright posture. BWSTT FIM walking score (0–7) LEMS (0–50) Walking speed (ft/s) Median FIM total motor score 6-min walk (ft) WISCI (0–20) Median Berg balance (0–58) Median 5. or to ASIA C and D subjects.. (Dobkin and Havton. graded at time of admission for rehabilitation. As interesting as this recovery seems. Other RCTs of BWSTT during acute inpatient rehabilitation after stroke revealed no clinical benefits for walking independence or speed (Nilsson et al. but not a clinically useful distinction for evidencebased practices.9 3. The upright posture and leg assistance allowed him to concentrate on finding some motor control over residual descending pathways to surviving motoneurons that still innervated these muscles. BWSTT when instituted a mean of 70 days after acute hemiparetic stroke revealed statistically significant gains in gait when compared to treadmill training without BWS (Visintin et al. 2004).. Werner et al. 1998. Lennihan et al.8 86 1197 14 18 43 55 19 7 17 564 1.. Training and neuromuscular activity may then drive cerebral control for gait over various surfaces and speeds.. observers has been reported. Dobkin Table 3.

independent) offer insight into the need for assistance and thus the burden of . Duncan et al. are of no value as an outcome measure. changes over time of gait training can be shown after SCI. Dobkin et al. 2000b. or recondition a patient to lessen disability.. and practice walking on uneven surfaces and stairs. Duncan et al. accelerometers placed on the trunk. Sullivan et al. 2002. specified goals for progressive gains in walking distance or walking speed.5 Outcome measures for clinical care Whether an individual patient is in rehabilitation as an inpatient or outpatient or participating in a clinical trial.3 was calculated from gait cycle data recording from bilateral foot and thigh accelerometers. sensitive and reliable outcome measures help determine the success of an intervention for walking. 2. a timed stand up and walk task. de Bode et al. 2003b). 2002. Time spent walking can be measured using an accelerometer that records activity (Coleman et al. Fresno. Functional neuroimaging may serve to reveal the nodes of the supraspinal networks that are engaged over the course of a training intervention. CA).. 2005).or 6-min walking distance and heart rate change from rest.3 shows the step cycle from one foot accelerometer obtained using a commercial device. modest resistance exercises with weights or latex bands. near-infrared spectroscopy has assessed changes in M1S1 and premotor cortex that contribute to improved motor control during walking on a treadmill (Miyai et al. strengthen leg muscles. the Intelligent Device for Energy Expenditure and Physical Activity (IDEEA) system (MiniSun.. Physiological measures Walking speed over 10 m or 50 ft. 2003b) and other chronically disabling neurological diseases. 2000). Figure 3. Using an ankle dorsiflexion fMRI activation paradigm. each thigh. partial squats while braced against a wall. 2003). pool exercise. Fugl-Meyer motor assessment. with its other two measures. These techniques may provide insight into the optimal duration of an intervention and the effects of medications on cortical representational plasticity.. stroke. and ASIA motor score provide quick and reliable measures relevant to walking after stroke or SCI (Steffen et al.. need help.. and in children after hemispherectomy for epilepsy (Dobkin. and outcome measures for walking 43 Pulse therapies The efficacy of a pulse of various training strategies for walking has been demonstrated in well-designed trials from months to years after stroke (Hesse et al. A homebased program might include sets of practice in sit-to-stand. and under each foot reveal both temporal aspects of the gait cycle and acceleration forces at key points in the step cycle. such as the Ashworth scale. With well-designed software. 1999. For example. interventions. These measures may be more sensitive to changes during a subacute intervention compared to a treatment in chronically disabled subjects. Scales for spasticity. Zhang et al.... Serial monitoring of walking speed can serve as both a measure and an incentive for progress during formal rehabilitation and for practice at home. such as at toe off and initial swing. 3. 2003). Ankle dorsiflexion or other active and passive leg movements may also be of value in discerning the completeness of a SCI and in determining the functional effects of a subcortical or spinal neural repair strategy.Assessments. supine and prone leg lifts.. The duration of effect will be limited in progressive diseases. Resistance to movement tested at a single joint while supine cannot be correlated with hypertonicity and impaired motor control during walking. treadmill walking. Table 3. 2004. That should not dissuade the clinician from attempting to maintain functional walking through a home-based exercise program and a brief course of goal-directed therapy to improve the gait pattern. 2003... and measures of impairment such as the Berg balance scale. Functional measures The locomotor score (0–7) of the Functional Independence Measure (FIM) and of the Barthel Index (dependent. Ada et al. The Multiple Sclerosis Functional Composite scale includes a 25-foot timed walk that. 1994. has proven valuable for clinical trials (Kalkers et al.

45 2.1 265.2 168.9 170.278 7.057 0.3 18.4 618.2 19.056 Right leg 281 2 min.51 0.23 0.5 68.4 27.1 1. the locomotor FIM and the WISCI correlated with lower extremity strength and walking speed.037 0.55 2.051 0.3.3 0.041 0. In the SCILT trial.88 79.1 445. 3.1 25.41 SD 19.90 87.2 4. Dobkin Right D Acceleration (Gs) Left B A C AB B BC BD CD D DE DB AA E Time (s) A Terminal stance Heel off Toe off Swing duration Swing Initial contact or heel strike Loading (DA AB) Stance duration Step duration care related to walking.4 167.7 0. The Stroke Impact Scale and the physical activity portion of the SF-36 for any neurological disease may reveal how patients assess themselves for mobility tasks in everyday activities. 1992.7 68. braces and assistive devices needed and reflects.41 SD 16.099 0.44 Bruce H.071 0.3 266.705 1.7 26.345 0.0 26.46 7.518 0.8 26. 2000.056 SDL/DLS: single-limb support/double-limb support.7 265.6 Neural repair strategies and gait training A well-defined approach for the retraining of walking will be needed to engage and incorporate new neurons.2 0.271 11.3. 54 s 0.22 4.1 17.13 0.754 1. axons. 46 s 0. 1995.265 12.089 0.565 0.7 1. Healthy subject walking with IDEEA system foot accelerometers.759 1.24 0.37 0.542 SD 18.396 Mean 448.7 96.8 4.9 68. functional limitations (Ditunno and Ditunno.094 0.054 0. 51 s 0.50 2. . A measure such as the Walking Index for SCI (WISCI) takes into account the physical help..103 0. and networks created by Figure 3.7 97.047 0.89 83. which reflects health-related quality of life (Ware and Sherbourne.5 0.710 1.4 17. in part.41 0.7 448.40 4.0 17. 2001).326 0.4 1.3 450. Duncan et al. 2003a).8 1.24 0. Gait cycle defined by accelerometry of each foot.032 0.2 616.048 0.197 Mean Single support (ms) Double support (ms) SLS/DLS (%) Swing duration (ms) Step duration (ms) Cycle duration (ms) Pulling acceleration foot (Gs) Pulling acceleration thigh (Gs) Swing power (Gs) Ground impact (Gs) Foot fall (G) deceleration Push-off (°) angle at B Speed (m/min) Cadence (steps/min) Step length (m) Stride length (m) 450. Table 3.9 0.9 615.6 98.9 25. Vickrey et al.51 9.046 0.750 1.9 16.364 0.376 0.054 Bilateral 562 5 min..4 0. Statistics Steps Duration Distance (km) Left leg 281 2 min.297 0.200 Mean 445. synapses.

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The EMG study can be tailored in such a fashion as to specifically localize the lesion to the nerve roots. Nerve conduction studies (NCs) and needle electromyography (EMG). the nerve root.. plexus. electrodiagnostic testing serves as an important diagnostic and prognostic tool when applied within the context of the clinical neurologic examination. the dorsal root ganglia. Lesions with mixed pathology will recover in an intermediate time frame.1 Introduction One of the fundamental principles of electrodiagnostic medicine is the assessment of the peripheral nervous system’s ability to conduct an electrical impulse (Dumitru et al. USA 4. Additionally.. are commonly referred to as electrodiagnostic or EMG studies. Electrodiagnostic studies can also identify disturbances at the level of the neuromuscular junction and in the muscle. demyelination or if the underlying disorder is secondary to muscle disease or neuromuscular dysfunction.4 Electromyography in neurorehabilitation Amparo Gutierrez and Austin J. The EMG study can provide data on the temporal course and rate of recovery of a lesion. Sumner Department of Neurology. This differentiation between pathologic processes allows for a narrowing of the differential diagnosis. and assess the temporal course of the disorder (Preston et al. focused history and neurologic examination should serve as the template upon which one designs and performs the EMG study.2 Basic principles in EMG The primary goals of the EMG study are to localize the lesion. LA. Abnormalities seen on the EMG can separate lesions into hyperacute . Thus. The EMG study can also assess the degree or extent of axonal loss versus demyelination. A lesion that is the result of demyelination can be expected to recover fully when given the required time for remyelination. The clinician designing the EMG study must have intimate knowledge of the anatomy of the peripheral nervous system for precise lesion localization. New Orleans. 4. characterize the underlying nerve 48 pathophysiology. EMG studies can provide useful information in disorders involving the upper motor neurons or disorders of volition as well as evaluating gait. or the anterior horn cell. or individual peripheral nerves. Data acquired during the EMG study must always be interpreted within the clinical context because the same data may have very different interpretations depending on the clinical situation. Louisiana State University Medical Center. quantitate the severity of the lesion. The EMG study can determine whether the pathology leading to the clinical deficit is secondary to axonal loss. A detailed. Electrodiagnostic studies play a crucial role in identifying disorders that affect the peripheral nerve. 2002). which then allows the clinician to predict the extent of recovery from a particular lesion and the expected time frame in which this recovery should take place. Localizing a lesion within the peripheral nervous system is best determined with the use of an EMG study. An EMG study performed in isolation of the clinical context may provide little useful information. 1998). trunks. EMG studies can often identify the underlying pathologic process involving a nerve lesion. A lesion that primarily involves axonal loss will carry a worse prognosis and therefore a less complete recovery would be expected.

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(less than 1 week), acute (less than a few weeks), or chronic. The electromyographer must therefore be aware of the patient’s clinical time course to accurately interpret the abnormalities observed during the study.

(Dewald et al., 1999). Additional discussion of upper motor lesions are found in several chapters of this volume (e.g., Volume II, Chapters 17, 18, 36, and 38).

Lower motor lesions
In a patient undergoing rehabilitation, there is the potential for the patient to be immobilized for protracted periods of time. These patients may consequently develop superimposed patterns of weakness, due to deconditioning, development of contractures and joint problems. Additionally, they may develop a lower motor neuron lesion secondary to either a compressive neuropathy or a polyneuropathy (see Volume II, Chapter 40). Being able to distinguish between these varying patterns of weakness is important. NCs are extremely useful in assessing these types of patients. Compressive and entrapment neuropathies usually lead to numbness and weakness in the area of the involved nerve. Although the terms compression and entrapment are often used interchangeably, it is important to recognize the distinction between a nerve entrapped in a fibroosseous tunnel where chronic low pressure and ischemia are the major mechanisms of nerve injury and external compression where, in acute situations, high mechanical pressures can result in a unique structural deformation of the nerve producing a focal demyelination (a neuropraxia). Certain forms of compression, with moderately high external pressure for limited time periods, result in a failure of action potential propagation (conduction block) but not in Wallerian degeneration (Fowler et al., 1972). If the compression is more prolonged, even with relatively low pressures there is a mixed lesion with both action potential blockade and Wallerian degeneration. These histologic findings can be anticipated from careful electrodiagnostic studies. Electrodiagnostic studies performed on a nerve with a compressive lesion should reveal that the conduction velocity above and below the region of the segmental demyelination are normal (McDonald, 1962). However, across the demyelinated region of the nerve, the velocity of action potential propagation is significantly slowed. Conduction block is defined as

4.3 Assessment of weakness
A motor deficit can result as a consequence of a lesion that lies within various places in the neuraxis. Weakness can be secondary to a lesion in the upper motor neuron pool (corticospinal tracts) or within the lower motor neuron pool (anterior horn cell and its peripheral process). Weakness may also be secondary to neuromuscular junction dysfunction. Finally, weakness can be due to muscle disease. Differentiating between these various etiologic factors in the clinical setting can be quite challenging. The EMG study provides an excellent tool for determining the cause of weakness. In a study performed by Nardin et al. (2002), the diagnostic accuracy of electrodiagnostic testing in the evaluation of patient weakness had an overall accuracy of 91%.

Upper motor lesions
Clinically, patients with lesions of the brain and/or spinal cord present with weakness and most often also have numbness. These patients usually have increased deep tendon reflexes, extensor plantar responses, and increased muscle tone that marks the lesion site. Assessment of a lesion that involves the upper motor neuron pool is done during the EMG portion of the study. These patients have a delayed onset of EMG activity and a decreased ability to recruit motor unit potentials. Several studies have documented that there is a delay of initiation and prolonged termination of muscle contraction in paretic muscles from upper motor impairment (Chae et al., 2002). Following a stroke, changes in descending input may modify interneuronal excitability throughout the cord (Grimby, 1963). The loss of excitability at the level of the spinal interneurons may account for the delayed onset of EMG activity observed in paretic limbs in an upper motor neuron lesion

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5 ms

A1 A2 A3 A4 A5

100 mA 5 mV 100 mA 5 mV 100 mA 5 mV 100 mA 5 mV 5 mV

Figure 4.1. Conduction block.

a normal motor response when stimulating the affected nerve distal to the lesion, but either a reduced or absent response is elicited when stimulating proximal to the lesion. (Fig. 4.1) Neuropraxic lesions, (conduction block), may take up to 6 months to resolve, although typically block reverses over 2 weeks to 3 months. The presence of Wallerian degeneration can be especially observed during EMG. In this situation of axon loss, one can see fibrillation potentials of the involved muscles. These patients usually have an incomplete recovery. When a diagnosis of a compressive neuropathy is made, the patient’s caretakers can then be given specific instructions for positioning of the patient or other equipment utilized in the care of the patient. Therefore, early recognition of this pattern of weakness is important. Frequently distal weakness is secondary to a polyneuropathy. Patients commonly develop this neuropathy insidiously. The most common neuropathy is a generalized axonal sensorimotor polyneuropathy. Etiologic causes can be varied: metabolic, nutritional, secondary to a systemic disorder, infectious, or cryptogenic. The most common etiology of a generalized distal axonal sensorimotor polyneuropathy is diabetes mellitus (Melton and Dyck, 1987). The risk of developing a diabetic peripheral neuropathy

correlates with the duration of the diabetes, the control of hyperglycemia, and the presence of retinopathy and nephropathy (Dyck et al., 1993). Other causes of axonal polyneuropathy are shown in Table 4.1. Patients with an axonal polyneuropathy first develop a distal pattern of sensory loss followed by distal weakness. The reflexes, when lost, are in a length-dependent fashion. Electrodiagnostic studies reveal reduced amplitudes of sensory and motor action potentials. Conduction velocities are minimally affected (Oh, 1993). EMG reveals a pattern compatible with denervation mostly affecting the distal muscles. Motor unit potentials are usually large with an increased recruitment and decreased interference pattern (Brown and Bolton, 1987). Spontaneous activity is usually sparse. Identifying the underlying etiology can lead to improvement or at least a stabilization of the polyneuropathy. Occasionally, patients develop another pattern of weakness that involves both proximal and distal muscles. This pattern of weakness is most consistently seen in a demyelinating polyneuropathy. Demyelinating neuropathies may be divided into acute or chronic presentations. Guillain–Barre syndrome (GBS) or acute inflammatory demyelinating polyradiculoneuropathy (AIDP) has become the most

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Table 4.1. Causes of axonal polyneuropathies. Nutritional deficiencies Thiamine Pyridoxine (B6) Cobalamin (B12) Folate Vitamin E Strachan syndrome Toxins Alcohol Drugs Chloramphenicol Chloroquine Dapsone Metronidazole Nitrofurantoin Zalcitabine and other nucleoside analogs Cisplatinum Paclitaxel Misonidazole Thalidomide Heavy metals Hexacarbons Acrylamide Carbon disulfide Ethylene glycol Organophosphates Hydralazine Aminodarone Propafenone FK 506 (Prograf) Colchicine Vincristine Disulfiram Glutethimide Simivastin and other statins

common cause of acute paralysis in Western countries since the virtual elimination of poliomyelitis with vaccination programs (Parry, 1993). GBS is clinically a predominant motor neuropathy affecting the patient in a symmetrical fashion. At the nadir of the illness there is approximately equal weakness of proximal and distal muscles in about 50% of cases (Ropper and Shahani, 1984). Roughly 60–70% of patients with AIDP note some form of acute illness (e.g., a viral syndrome) 1–3 weeks before the onset of neurologic symptoms. In a recent case control study of 154 patients with GBS, serologic evidence of recent infections with Campylobacter jejuni (32%), cytomegalovirus (13%), Epstein–Barr virus (10%), and Mycoplasma pneumoniae (5%) were more frequent than in the control population (Jacobs et al., 1998).

The early and accurate diagnosis of GBS depends primarily on NCs. Carefully performed NCs of multiple nerves, including cranial nerves and proximal segments of spinal nerves, if indicated, are almost always abnormal even when the cerebrospinal fluid protein is normal. The electrophysiologic diagnosis of GBS requires the demonstration of the characteristic changes associated with acute demyelination (Gilliatt, 1966). The most studied aspects in AIDP are motor nerves; distal latencies, compound action potentials, conduction velocities, waveform duration and morphology, and F-waves. The electrophysiologic hallmarks include prolongation of the distal latencies, slow conduction velocities, temporal dispersion, conduction block, and prolonged F-waves. Another electrodiagnostic finding often seen in GBS is superimposed axonal degeneration (Ensurd and Krivickas, 2001). The degree of axonal loss has been shown to correlate with both acute mortality and long-term disability in patients with GBS (Chio et al., 2003). Nearly 40% of patients hospitalized with GBS will require inpatient rehabilation (Meythaler et al., 1994). The electrodiagnostic study aids in identifying these patients. Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired demyelinating polyradiculoneuropathy that shares a similar pathology and presumed autoimmune etiology with AIDP but differs primarily in the time course of presentation and evolution of clinical signs. In typical CIDP , motor and sensory symptoms develop slowly over the course of weeks to months, or even years. The clinical course may be relapsing, with variable periods of remission, or stepwise and chronically progressive. The diagnosis of CIDP is based on a combination of clinical and electrophysiologic findings as well as evaluation of the cerebrospinal fluid. The patient with CIDP has variable weakness in proximal and distal muscles. Sensory impairment is common, and tendon reflexes are either reduced or absent (McCombe et al., 1987). Electrodiagnostic studies usually reveal absent sensory responses. Motor conduction velocities are very slow, usually below 80% of normal values, and distal latencies may be prolonged.

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Table 4.2. Concurrent diseases with CIDP . HIV infection Diabetes mellitus Chronic active hepatitis Inflammatory bowel disease Connective tissue disease Nephrotic syndrome Melanoma Monoclonal gammopathy Lyme disease Lymphoma

Table 4.3. Drugs that may cause a myopathy. Amiodarone Anesthetics Cytarbine Cyclosporine Cyclophosphamide Cholesterol-lowering agent Colchicine Corticosteroids Diazepam Diuretics Gemfibrozil Interferon alpha Isoniazid Neuroleptics Penicillamine Steroids Tacrolimus Vasopressin Zidovudine

If the pathology is concentrated proximally, the F-wave latencies are markedly abnormal (Nicolas et al., 2002; Scarlato and Comi, 2002). Some patients with CIDP may have a concurrent illness (Table 4.2).

Muscle disease
Some patients may, in the course of their rehabilitation, develop a pattern of proximal weakness. This weakness usually begins in the lower extremities and then progresses to involve the proximal arms. There may or may not be associated muscle pain. In this setting, the most common etiology would be a toxic or iatrogenic myopathy. Certain drugs are known to cause an immunologic reaction directed against muscle (Scarlato and Comi, 2002) (Table 4.3). Electrolyte imbalances have also been associated with vacuolar muscle damage (Saleh and Seidman, 2003). Prompt recognition of this clinical picture is important because toxic or iatrogenic myopathies are potentially reversible, thus reducing their damaging effect. Inflammatory myopathies are another cause of proximal weakness. The inflammatory myopathies are a diverse group, ranging from focal varieties to widespread skeletal involvement. Etiologic factors are mainly immune-mediated or infectious agents. The most common immune-related varieties in clinical practice are dermatomyositis and polymyositis, each of which have distinctive clinical and histopathological features, and may occur in isolation or associated with a systemic connective tissue disease (Amato and Barohn, 1997). Human immunodeficiency virus

(HIV) causes a myopathy in almost a third of infected patients (Dalakas et al., 1986). Another infectious agent is human T-cell lymphotropic virus 1 (HTLV-1). Electrodiagnostically, patients with a myopathy should have normal nerve conductions. EMG in these patients demonstrates short duration, small amplitude, polyphasic motor unit potentials with early recruitment (Mastaglia et al., 2003). For additional discussion of myopathies, see Volume II, Chapter 41.

Neuromuscular transmission defect
Infrequent causes of muscle weakness are the diseases of the neuromuscular junction (Volume II, Chapter 40). Neuromuscular transmission defect can be a result an autoimmune disease like Myasthenia gravis (MG) or Eaton– Lambert syndrome (LEMS), or toxins that block neuromuscular transmission. MG occurs with a prevalence of 20 per 100,000 (Phillips, 2003). Like other autoimmune disorders, it is characterized by periods of relapses and remissions (Richman and Agius, 2003). The target of the autoimmune attack in MG is the nicotinic acetylcholine receptor, which is located on the postsynaptic muscle endplate membrane (Tzartos and Lindstrom, 1980). Patients present with weakness of the ocular and or bulbar musculature that over time may generalize to involve proximal limb muscles. An important characteristic of patients with neuromuscular transmission defect is fatigability. Additionally, these patients can present with unexplained respiratory failure.

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Repetitive nerve stimulation is a useful electrophysiologic test in the evaluation of patients with suspected neuromuscular junction disorders. In patients with MG, there is a decremental response seen on the compound motor action potential (CMAP) with slow rates of stimulation. In patients with LEMS, fast rates of repetitive stimulation produce a marked increase in the CMAP (Kimura, 1989).

4.4 EMG in movement
Surface EMG (SEMG) can provide a simple, noninvasive method to assess the activation of muscles involved in performing specific tasks. Likewise SEMG can aid in determining the timing and intensity of muscular activation and contraction during task specific performance. Thus, SEMG analysis has been widely employed in the field of ergonomics, biomechanics, sports science, and kinesiology (McGill, 2004). SEMG can serve as a useful tool specifically in gait analysis, the origins of which date back to Europe in the 17th century. Vern Inman, and colleagues moved the science of gait analysis dramatically forward by adding kinesiologic EMG, 3-D force, and energy measurements in the study of walking in normal subjects and amputees (1944–1947) (Sutherland, 2001). Kinesiologic EMG is a technique which is used to determine the relationship of muscle activation to joint movement and to the gait (see Volume II, Chapter 19). These techniques of dynamic EMG have been employed to evaluate varies disease states, such as children with cerebral palsy, stroke patients and in patients with prosthetic devices. The use of gait analysis in children with cerebral palsy has allowed for better surgical intervention to influence gait function. Finally, electromyographic biofeedback has been used to improve lower extremity function after stroke (Moreland et al., 1998).

Clear identification of the clinical question allows the electromyographer to design the appropriate electrical tests. Most EMG reports should include various sections: chief complaint, history, physical examination, nerve conductions, needle EMG, summary of findings, and impression. Likewise it is important to understand the limitations of electrodiagnostic testing. NCs and EMG display a limited repertoire of abnormalities that include loss of myelinated motor or sensory nerve fibers, or both, abnormalities in myelin that affect conduction properties and membrane characteristics, compensatory changes associated with reinnervation of muscle fibers, and changes that are consistent with acute or chronic lesions (Krarup, 2003). Routine nerve conductions only assess the large myelinated fibers usually in their more distal distribution. Symptoms that are as a result of pathology of the small myelinated or unmyelinated fibers require alternative methods of evaluation. The timing of the electrodiagnostic evaluation is important, as there is an orderly sequence of electrophysiologic changes that follow nerve injury. Knowledge of these changes is necessary for proper interpretation of results.

4.6 Use of the EMG as an outcome measure
The ability to predict a patient’s eventual prognosis is an important part of the overall treatment plan. Unfortunately the current literature dealing with electrodiagnostic prognostication is meager. There are only a few areas that electrophysiologic testing provides important outcome data. One of these areas is the evaluation of traumatic peripheral nerve injury. Traumatic nerve injuries can result in different grades of injuries as outlined by Seddon; neuropraxic, axonotmesis, and neurotmesis. They are based on morphologic criteria and the presence of Wallerian degeneration. The electromyographer is frequently asked to participate in the clinical evaluation and therapeutic decision-making of patients with peripheral nerve injury. Careful EMG evaluation can identify a lesion that is a result of neuropraxia versus

4.5 Interpreting the EMG report
An electrodiagnostic consultation is best interpreted within the context of a specific clinical question.

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axonotmesis and neurotmesis. In the latter case there is varying degrees of Wallerian degeneration. The timing of the EMG study is important and is guided by experimental studies of sensory and motor nerve regeneration (Gilchrist and Sachs, 2004). Nerves have been shown to regenerate at an average rate of 1–2 mm/day (Seddon et al., 1943). Knowing when the lesion occurred allows the evaluator a time course in which one can predict the course of regeneration and likewise when a nerve is not regenerating as one would anticipate. For most nerve lesions in continuity, surgical exploration is generally recommended if there is no evidence of axonal regeneration by 3–6 months post injury. Prognostically, lesions with the least amount of Wallerian degeneration recover best (Cros, 2001). NCs are useful in mapping the recovery from a compression neuropathy or a neuropraxic lesion. Neuropraxic lesions result from a disruption of myelin with intact axons and stroma. This type of lesion can also be seen in traumatic brachial plexus injuries. In this situation the large myelinated fibers are more susceptible. Thus motor fibers are usually more affected than sensory fibers, resulting in motor paralysis. Motor paralysis from, a neuropraxic lesion, is expected to last from 1 to 6 months, although most resolve by 3 months (Rudge, 1974). Nerve conductions serve to document and outline the recovery of this type of injury. Electrodiagnostic testing is perhaps the most important predictor of outcome in patients with GBS (Katirji et al., 2002). Patients with severe axonal loss have poorer outcomes. The amplitude of the CMAP is the most reliable measure of axonal loss: low CMAP amplitude (less than 10–20% of normal) has been correlated with poor outcomes (McKhann et al., 1985). NCs can be used in assessing the response of diabetic neuropathy to various therapeutic interventions. Early studies revealed improvement in conduction velocity following glycemic control in newly diagnosed diabetics (Fraser et al., 1977). Lastly, electrophysiologic testing has played an important role in determining the extent of facial nerve injury when there is early, complete paralysis of the facial muscles. Testing is best performed on

the 5th day after onset or within 2 weeks (Gutierrez and Sumner, 2003). The facial nerve conduction is the most useful. CMAP side-to-side comparisons seem to hold the best prognostic values. May demonstrated that a 25% or greater sparing of CMAP amplitude when compared to the unaffected side had a 98% chance of satisfactory recovery (May et al., 1983).

REFERENCES
Amato, A. and Barohn, R.J. (1997). Idiopathic inflammatory myopathies. Neurol Clin N Amer, 15, 615–641. Brown, W.F. and Bolton, C.F. (1987). Clinical Electromyography, Butterworth, Boston, pp. 379–381. Chae, J., Yang, G., Park, B.K. and Labatia, I. (2002). Delay initiation and termination of muscle contraction, motor impairment, and physical disability in upper limb hemiparesis. Muscle Nerve, 25, 568–575. Chio, A., Cocito, D., Leone, M., et al. (2003). Guillain–Barre syndrome: a prospective, population-based incidence and outcome survey. Neurology, 60, 1146–1150. Cros, D. (2001). Peripher Neuropath: A Practical Approach to Diagnosis and Management, Lippincott Williams & Wilkins, Boston. Dalakas, M.C., Pezeshkpour, G.H., Gravell, M., et al. (1986). Polymyositis associated with AIDS retrovirus. J Am Med Assoc, 256, 2381. Dewald, J.P Beer, R.F., Given, J.D., et al. (1999). Reorganization .A., of flexion reflexes in the upper extremity of hemiparetic subjects. Muscle Nerve, 22, 1209–1221. Dumitru, D., Amato, A.A. and Zwarts, M.J. (2002). Electrodiagnostic Medicine, 2nd edn., Hanley & Belfus Inc., Philadelphia. Dyck, P.J., Kratz, K.M., Litchy, W.J., et al. (1993). The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: the Rochechester diabetic neuropathy study. Neurology, 43, 817–824. Ensurd, E.R. and Krivickas, L.S. (2001). Acquired inflammatory demyelinating neuropathies. Phys Med Rehabil Clin N Am, 12, 321–324. Fowler, T.J., Danta, G. and Gilliatt, R.W. (1972). Recovery of nerve conduction after a pneumatic tourniquet: observations on the hind-limb of the baboon. J Neurol Neurosurg Psychiatr, 35, 638–647. Fraser, D.M., Campbell, I.W., Ewing, D.J., et al. (1977). Peripheral and autonomic nerve function in newly diagnosed diabetes mellitus. Diabetes, 26, 546–550.

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Gilchrist, J.M. and Sachs, G.M. (2004). Electrodiagnostic studies in the management and prognosis of neuromuscular disorders. Muscle Nerve, 29, 165–190. Gilliatt, R.W. (1966). Nerve conductions in human and experimental neuropathies. Proc Roy Soc Med, 59, 989–993. Grimby, L. (1963). Pathological plantar response: disturbances of the normal integration of flexor and extensor reflex components. J Neurol Neurosurg Psychiatr, 26, 314–321. Gutierrez, A. and Sumner, A.J. (2003). Idiopathic (Bell’s) Facial Palsy. Neurological Disorders Course and Treatment, Academic Press, Boston (Chapter 14). Jacobs, B.C., Rothbarth, P .H., Vander Meche, N., et al. (1998). The spectrum of antecedent infections in Guillain– Barre syndrome. A case control study. Neurology, 51, 1110–1115. Katirji, B., Kaminski, H.J., Preston, D., et al. (2002). Neuromuscular Disorders in Clinical Practice, Butterworth Heinemann, Boston (Chapter 41). Kimura, J. (1989). Electrodiagnosis in Diseases of Nerve and Muscle, Davis, Philadelphia. Krarup, C. (2003). An update on electrophysiological studies in neuropathy. Curr Opin Neurol, 16, 603–612. Mastaglia, F.L., Garlep, M.J., Philips, B.A., et al. (2003). Inflammatory myopathies: clinical, diagnostic, and therapeutic aspects. Muscle Nerve, 27, 407–425. May, M., Blumenthal, F. and Klein, S.R. (1983). Acute Bell’s P5falsy: prognostic value of evoked electromyography, maximal stimulation and other electrical test. Am J Otol, 5, 1–7. McCombe, P.A., Pollard, J.D. and McLeod, J.G. (1987). Chronic inflammatory demyelinating polyradiculoneuropathy: a clinical and electrophysiological study of 92 case. Brain, 110, 1617–1630. McDonald, W.I. (1962). Conduction in muscle afferent fibres during experimental demyelination in cat nerve. Acta Neuropath, 1, 425–432. McGill, K.C. (2004). Surface electromyography signal modeling. Med Biol Eng Comput, 42, 446–454. McKhann, G.M., Griffin, J.W., Cornblath, D.R., et al. (1985). Prognosis in Guillain–Barre syndrome. Lancet, 1, 1202–1203. Melton, L.J. and Dyck, P.J. (1987). Clinical features of diabetic neuropathies. In: Diabetic Neuropathy (eds Dyck, P.J., Thomas, P and Asbury, A.K.), W.B. Saunders, Philadelphia, .K. pp. 27–35. Meythaler, J., DeVivo, M., Clausen, G., et al. (1994). Prediction of outcome in Guillain–Barre syndrome patients admitted to rehabilitation. Arch Phys Med Rehabil, 75, 1027.

Moreland, J.D., Thomson, M.A. and Fuoco, A.R. (1998). Electromyographic biofeedback to improve lower extremity function after stroke: a meta-analysis. Arch Phys Med Rehabil, 79, 134–140. Nardin, R.A., Rutkove, S.B. and Raynor, E.M. (2002). Diagnostic accuracy of electrodiagnostic testing. In: Neuromuscular Disorders in Clinical Practice, (eds Katirji, B., Kaminski, H.J., Preston, D., et al.), Butterworth Heinemann, Boston (Chapter 41). Nicolas, G., Maisonobe, T., Le Forestier, N., et al. (2002). Proposed revised electrophysiological criteria for chronic inflammatory demyelinating polyradiculoneuropathy. Muscle Nerve, 25, 26–30. Oh, S.J. (1993). Clinical Electromyography Nerve Conductions Studies, 2nd edn., Williams & Wilkens, Baltimore, MD, pp. 482–485. Parry, G.J. (1993). Guillain–Barre Syndrome., Thieme Medical Publishers Inc., New York, p. 10. Phillips, L.H. (2003). The epidemiology of myasthenia gravis. Ann New York Acad Sci, 998, pp. 407–412. Preston, D.C., Shapiro, B.E. and Katirji, B. (1998). Electromyography and Neuromuscular Disorders: Clinical–Electrophysiologic Correlations, Butterworth-Heinemann, Boston (Chapter 7). Richman, D.P. and Agius, M.A. (2003). Treatment of autoimmune myasthenia gravis. Neurology, 61, 1652–1661. Ropper, A.H. and Shahani, B.T. (1984). Diagnosis and management of areflexic paralysis with emphasis on Guillain–Barre syndrome. In: Peripheral Nerve Disorders (eds Asbury, A.K. and Gilliatt, R.W.), Butterworth, London, pp. 21–45. Rudge, P. (1974). Tourniquey paralysis with prolonged conduction block. An electrophysiological study. J Bone Joint Surg, 56B, 716–720. Saleh, F.G. and Seidman, R.J. (2003). Drug-induced myopathy and neuropathy. J Clin Neuromusc Dis, 5, 81–92. Scarlato, G. and Comi, G.P. (2002). Metabolic and drug-induced muscle disorders. Curr Opin Neurol, 15, 533–538. Seddon, H.J., Medawar, P.B. and Smith, H. (1943). Rate of regeneration of peripheral nerves in man. J Physiol, 102, 191–215. Sutherland, D.H. (2001). Gait and Posture, 14, 61–70. Tzartos, S.J. and Lindstrom, J.M. (1980). Monoclonal antibodies used to probe acetylcholine receptor structure: localization of the main immunogenic region and detection of similarities between subunits. Proc Natl Acad Sci, 77, 755–759.

5 Functional neuroimaging
Nick S. Ward and Richard S.J. Frackowiak
Wellcome Department of Imaging Neuroscience, Institute of Neurology, University College London, London, UK

5.1 Introduction
Patients who survive focal brain injury for example stroke, undergo complete or more commonly partial recovery of function (Twitchell, 1951). The management of patients with incomplete recovery draws on specific rehabilitation interventions aimed at assisting adaptation to impairment. However there is a growing interest in designing therapeutic strategies to promote cerebral reorganisation as a way of reducing rather than compensating for impairment. This interest stems largely from experiments in animal models, which have unequivocally demonstrated post-lesional changes in cerebral organisation related to recovery. In addition, it is clear that focal cortical damage in adult brains renders widespread surviving cortical regions more able to change structure and function in response to afferent signals in a way normally only seen in the developing brain (Schallert et al., 2000; Bury and Jones, 2002) (see Chapter 14 of Volume I, pp. 21–28 for a more extensive discussion of these changes). Activity-driven changes in these regions may be enhanced by experiential (Nudo et al., 1996) or pharmacological (Feeney, 1997) context, and correlate with functional recovery. These findings are clearly very exciting for clinicians. It has been suggested that similar injury-induced changes occur in the human brain, and that their manipulation will provide a means of promoting functional recovery in patients with focal brain damage. One crucial aspect of developing such strategies involves building an empirical understanding of how the brain responds to injury and how such changes may be manipulated in a way that promotes functional
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recovery. The investigation of cerebral reorganisation after focal brain injury in humans is less well advanced than similar work in animal models. There are clearly greater limitations in studying the human brain, but functional imaging, a technique that allows measurement of task-related brain activation, provides an opportunity to do so. Furthermore, one must consider that the findings from animals apply almost exclusively to cortical damage, whereas much of the work in humans to date has been performed in patients with deep subcortical infarcts. Nevertheless, both approaches have yielded important results from which a clearer picture of functional cerebral reorganisation is beginning to emerge.

5.2 Functional imaging techniques
The detailed theoretical background to the techniques positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) are beyond the scope of this chapter. In brief however, both techniques rely on the assumption that neuronal activity is closely coupled to a local increase in cerebral blood flow (CBF) secondary to an increase in metabolism. PET relies on mapping the distribution of inert, freely diffusible radioactive tracers deposited in tissue as a function of regional perfusion (rCBF). Functional MRI comprises different methods, but the studies described below use blood oxygen level-dependent (BOLD) imaging techniques. During an increase in neuronal activation there is an increase in local CBF, but only a small proportion of the greater amount of oxygen delivered locally to the tissue is

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used. There is a resultant net increase in the tissue concentration of oxyhaemoglobin and a net reduction in paramagnetic deoxyhaemoglobin in the local capillary bed and draining venules. The magnetic properties of haemoglobin depend on its level of oxygenation so that this change results in an increase in local tissue derived signal intensity on T2*weighted MR images.

5.3 Methodological considerations
The study of patients with motor impairment requires careful consideration. Many early studies were performed in fully recovered patients so that comparisons with healthy controls could be made. However, to address the issue of whether differences between stroke patients and controls are related to recovery, patients with a wide range of outcomes must be studied. In this way, correlations between task-related brain activation and outcome can be identified. There are two consequences of this consideration. Firstly, outcome must be characterised in a detailed and appropriate way. Secondly, patients must perform the same task during the acquisition of fMRI data so that a meaningful comparison can be made across subjects or scanning sessions. Equality of task may be interpreted in a number of ways. In patients with different abilities a task may be the same in terms of absolute or relative parameters. For example a simple motor paradigm can be equated in terms of absolute parameters of force and rate of task performance across subjects, or in terms of how effortful the task is. The experimenter is interested in different states of cerebral reorganisation. However depending on paradigm selection, changes in brain activation patterns across subjects may also be attributable to differences in absolute performance parameters (if effort is equated) or differences in effort (if absolute task parameters are equated). Most studies have used finger tapping as the motor task. This task is problematic as many stroke patients with poor outcome are unable to perform fractionated finger movements adequately. As a result neither effort nor absolute task parameters can be controlled

for. The return of fractionated finger movements represents an excellent outcome and is therefore of clinical interest but this does not mean that it is the best paradigm to use, for the reasons described above. An important concept in experimental design is that it is not possible to scan patients in order to determine the neural correlates of something they cannot do (Price and Friston, 1999). An experimenter must find alternative ways to probe the system of interest. An alternative task is dynamic hand grip which is used in several studies described in this chapter (Ward and Frackowiak, 2003; Ward et al., 2003a,b). Hand grip can be performed by patients with even minimal recovery and its performance correlates well with other measures of upper limb recovery (Heller et al., 1987; Sunderland et al., 1989). In order to control as much as possible for the effort involved in performing a hand grip task subjects (controls and patients) can be set target forces that are a fixed percentage of their own maximum hand grip. This is therefore a task that all can perform. In our series of experiments all patients were able to perform repetitive hand grips at 10%, 20%, 40%, etc. of their own maximum exertable force. The results of these studies pertain to how a damaged motor system is able to perform this task. Thus by using a motor task (hand grip) that reflects intrinsic motor recovery more than adaptation (Sunderland et al., 1989) and by controlling for motor effort as much as possible, the results within known motor-related regions are then more likely to reflect cerebral reorganisation rather than change of strategy after focal brain damage. The interpretation of results from all functional imaging studies involving patients with differing abilities needs to take these factors into consideration (Poldrack, 2001).

5.4 Cerebral reorganisation in chronic stroke
Early functional imaging studies were performed in recovered chronic subcortical stroke patients. These patients demonstrated relative overactivations in a number of motor-related brain regions when performing a motor task compared to control subjects.

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In particular, overactivations were seen in dorsolateral premotor cortex (PMd), ventrolateral premotor cortex (PMv), supplementary motor area (SMA), cingulate motor areas (CMA), parietal cortex, and insula cortex (Chollet et al., 1991; Weiller et al., 1992, 1993; Cramer et al., 1997; Seitz et al., 1998). Such findings contributed to the notion that recruitment of these brain regions, particularly those in the unaffected hemisphere, might be responsible for recovery. However, in order to make inferences about the mechanisms underlying functional recovery it is necessary to study patients with different degrees of recovery. If one studies patients with a range of late post-stroke outcomes, it appears that those patients with the best outcome have a “normal” activation pattern when compared to normal controls, whereas

those with poorer outcome show excessive activation of the primary and non-primary motor areas in both hemispheres (Ward et al., 2003a). These relative overactivations are often bilateral, involving sensorimotor, premotor, posterior parietal, prefrontal and insular cortices, SMA, CMA, and cerebellum. When this relationship is explored formally, a significant negative linear correlation is found between the size of brain activation and outcome in a number of brain regions (Fig. 5.1). This result does not initially seem to support the notion that recruitment of these regions facilitates recovery. A key determinant of motor recovery is the integrity of fast direct motor output pathways from primary motor cortex (M1) to spinal cord motor neurons (Heald et al., 1993; Cruz et al., 1999; Pennisi et al., 1999).

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Thus it is likely that those patients with poorer outcome have greater disruption to this corticomotoneuronal (CMN) pathway. The work of Strick (1988) and others suggests that in primates at least, the non-primary motor system is organised as a number of neural networks or loops involving premotor (both lateral and medial wall), parietal and subcortical regions (see also Chapter 14 of Volume I, p. 12). These motor loops are independent of those involving M1 but crucially they are interconnected at the level of the cortex (Strick, 1988; Dum and Strick, 1991). Furthermore, each has its own direct projection to spinal cord motor neurons. In the face of disruption to the CMN pathway the generation of an output to the musculature requires an increase in signals to spinal cord motor neurons via alternative pathways. The non-primary motor loops described by Strick provide an ideal substrate. The implication is that damage in one of these networks could be compensated for by activity in another, thus explaining the recruitment of regions seen in recovered stroke patients. These projections are unlikely to completely substitute for projections from M1 as they are less numerous and less efficient at exciting spinal cord motor neurons (Maier et al., 2002). Thus patients who rely on these alternative pathways to augment or substitute for CMN pathways are unlikely to fully regain dextrous finger movements. In attempting to reconcile these results with those from early studies it seems likely that patients in many previous studies may not have been fully recovered. Some patients found the finger tapping task more effortful to perform (Chollet et al., 1991) and results in those patients were similar to results in patients with residual motor deficit in a later study (Ward et al., 2003a). The question of the functional relevance of these additionally recruited regions remains. If one could explain differential recovery in a group of patients with identical anatomical damage by the degree to which certain areas are recruited, that would constitute direct evidence of their functional significance in relation to recovery. Due to the heterogeneous nature of infarcts such a result is very difficult to achieve. An alternative approach is to study the same chronic

stroke patients before and after a therapeutical intervention. In chronic stroke patients there should be no change in anatomical connections as a result of treatment, but differences in brain activation seen in relation to improved functional status might suggest that certain regions were causally involved. Increased activity in ipsilesional (IL) PMd has been associated with therapy-induced improvement in both upper limb function (Johansen-Berg et al., 2002a) and gait (Miyai et al., 2003). There is also evidence to suggest that disruption of IL PMd (Fridman et al., 2004) and contralesional (CL) PMd (Johansen-Berg et al., 2002b) by transcranial magnetic stimulation (TMS) impairs performance of a simple motor task in chronic stroke patients but not controls. Fridman et al. (2004) however failed to find any behavioural effect from disruption of CL PMd. It is possible that the patients studied by Johansen-Berg et al. (2002b) had greater impairment, and thus were more reliant on CL PMd, but outcomes were not well characterised in either study so it is difficult to make a comparison. Thus “alternative” brain regions appear to be recruited after focal damage in those patients with greatest need. In addition, there is evidence that IL PMd takes on an executive motor role, such that task-related BOLD signal increases linearly as a function of hand grip force in chronic stroke patients with significant impairment, but not in good recoverers or in controls. Thus it is unlikely that the response to focal injury involves the simple substitution of one cortical region for another, as nodes within a remaining motor network may take on new roles, that is there is true lesion-induced reprogramming in the human central nervous system. The studies discussed so far have been on chronic stroke patients. It appears that the relationship between size of brain activation and outcome in the late post-stroke phase holds true for patients in the early post-stroke phase also, at least when considering the primary and non-primary motor regions discussed above (Ward et al., 2004). Thus patients with greater initial deficit recruited more of the primary and non-primary motor network during hand grip. This result suggests that rather than slowly being recruited over time, brain regions in non-primary

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motor loops can participate in motor action very early after stroke in those patients that have the greatest need. Such rapid cerebral reorganisation can also be seen in normal people after repetitive TMS (rTMS) to the hand area of M1, which reduces M1 cortical excitability without altering task performance. Lee et al. (2003) demonstrated an immediate increase in recruitment of ipsilateral PMd following rTMS to M1 suggesting that this compensation allowed maintenance of task performance. In other brain regions there is an interaction between outcome and time after stroke. In CL middle intraparietal sulcus, CL cerebellum, and IL rostral premotor cortex there is a negative correlation between size of activation and outcome in the early but not late post-stroke phase (Fig. 5.2) (Ward et al., 2004). In other words patients with poorer outcome scores recruit these areas only in the early and not in the late post-stroke phase suggesting that those with greater deficit engage attentional networks more in

the early compared to late post-stroke phase. Attention may no longer be a useful tool for optimising motor performance in the late post-stroke phase. Alternatively, increasing the degree to which a motor task is attended to by chronic stroke patients might facilitate performance by enhancing detection of discrepancies between predicted and actual consequences of any action. These findings need to be explored further, but in those patients with most to gain from rehabilitation, different therapeutical approaches may be required at different stages after stroke. The role of CL (ipsilateral to the affected hand) M1 in recovery of motor function after stroke remains controversial. Anatomical studies suggest that both direct (corticospinal) and indirect (corticoreticulospinal) pathways from ipsilateral M1 end in projections to axial and proximal stabilising muscles rather than hand muscles (Brinkman and Kuypers, 1973; Carr et al., 1994). However, repetitive TMS to

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Figure 5.2. A plot of task-related signal change in posterior contralesional (CL) intraparietal sulcus versus outcome/recovery score for a group of early phase patients (10–14 days post stroke) and a group of late phase stroke patients (over 3 months post stroke). The peak voxel in intraparietal sulcus is shown on canonical coronal T1-weighted brain slice (P comparisons across whole brain). 0.05, corrected for multiple

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M1 results in errors in both complex and simple motor tasks with the ipsilateral hand (Chen et al., 1997) suggesting that ipsilateral M1 may play a role in planning and organisation of normal hand movement. CL M1 recruitment not present in normal controls has been described in some chronic stroke patients (see Calautti and Baron, 2003, for review), but its contribution to functional recovery remains controversial. A negative correlation between size of activation and outcome, similar to that described in non-primary motor regions, has been demonstrated for CL posterior M1 (Brodmann area, BA 4p) but not anterior M1 (BA 4a) (Ward et al., 2003a). Studies using TMS to disrupt local cortical function have failed to find any functional significance of increased CL M1 activation after stroke (JohansenBerg et al., 2002b; Werhahn et al., 2003). TMS to the motor hot spot for hand muscles (corresponding to M1) may affect predominantly BA 4a, rather than BA 4p, and so it remains plausible that parts of CL M1 can generate a motor output to an affected hand in patients with a significant deficit, in whom a dependency on alternative motor projections has developed. For chronic stroke patients with preserved IL M1 shifts in the peak IL sensorimotor activations have been found by comparison to control subjects (Weiller et al., 1993; Pineiro et al., 2001). As with other motor regions, this recruitment depends on the final outcome of the patient. A negative correlation between size of brain activation and outcome is seen in IL BA 4p and in BA 4a, ventral to the peak hand region of M1 (Ward et al., 2003a). Overall, these data suggest that there is a certain amount of remapping of hand representation in M1, even though undamaged, which may result from functionally relevant changes in both its afferent and efferent connections. Changes in somatotopical representation in non-primary motor regions might result in stronger connections with different (e.g. more ventral or caudal) regions of M1 in order to facilitate access to intact portions of the direct corticospinal pathway. Shifts in somatotopic representation in non-primary motor regions might also facilitate recruitment of surviving ischaemia-resistant small diameter myelinated

corticospinal fibres, such as those arising from premotor cortex, to compensate for loss of large diameter fibres. In our studies, parts of SMA, CMA, and PMd that were outside regions normally activated by the task in the control group, were recruited by chronic patients with poorer outcome (Ward et al., 2003a). Thus shifts in the hand representation in M1 as well as in non-primary motor regions occurred primarily in patients with greatest deficit and presumably with the most significant damage to CMN pathways. Support for lesion-induced changes in connectivity comes from the observation that rTMS to M1 leads to the stimulated part of M1 becoming less responsive to input from PMd and SMA, as well as increased coupling between an inferomedial portion of M1 and anterior motor areas (Lee et al., 2003).

5.5 The evolution of cerebral reorganisation after stroke
It appears that in the chronic setting a damaged brain will utilise those remaining structures and networks that can generate some form of motor signal to spinal cord motor neurons, and that in addition some areas such as PMd take on a new role in motor performance. What such studies do not tell us is how this reorganised state evolved from the time of infarction. Two early longitudinal studies with early and late time points demonstrated initial task-related overactivations in motor-related brain regions followed by a reduction over time in patients said to recover fully (Marshall et al., 2000; Calautti et al., 2001). Feydy and co-workers (2002), found no relationship between longitudinal changes and recovery scores and another study found no correlates of functional improvement outside the ipsilateral (CL) cerebellum, in which increases in task-related activation were seen with recovery (Small et al., 2002). A more detailed longitudinal fMRI study of patients with infarcts not involving M1 indicated an initial overactivation in many primary and non-primary motor regions that was more extensive in those with greatest clinical deficit (Ward et al., 2003b). The subsequent longitudinal

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changes were predictably different in each patient but there were changes common to all. After early overactivation, a negative correlation between size of activation and recovery scores was observed in all patients throughout IL M1, and in inferior CL M1, as well as in anterior and posterior PMd, bilaterally (BA 6 and BA 8), CL PMv, and IL SMA-proper, pre-SMA, prefrontal cortex (superior frontal sulcus), and caudal cingulate sulcus (Fig. 5.3). A positive correlation between size of activation and recovery across sessions was seen in some brain regions in four patients (including IL M1 in one patient), but there were no consistent increases in a group analysis (Ward et al., 2003b). These longitudinal recovery-related changes are reminiscent of those seen during motor learning experiments in normal people. One model of motor learning suggests that during early motor learning movements are encoded in terms of spatial coordinates, a process requiring high levels of attention (Hikosaka et al., 2002). Encoding is performed within a frontoparietal network and in parts of the basal ganglia and cerebellum. Once learning has occurred and a task has become automatic, movement is encoded in terms of a kinematic system of joints, muscles, limb trajectories, etc., by a network involving primary motor cortex, and parts of the basal ganglia and cerebellum that are different from those involved in early learning (Hikosaka et al., 2002). Interaction between these parallel systems and the transfer of reliance from one to the other, occurs not only in cerebellum and basal ganglia but also via intracortical connections involving particularly premotor cortex and pre-SMA (Hikosaka et al., 1999, 2002). An important aspect of any motor learning model is the generation of an error signal. Attempted movements by hemiparetic patients will result in significant discrepancies between predicted and actual performance. The error signals thus generated in normal subjects are used by the cerebellum to optimise subsequent sensorimotor accuracy (Blakemore et al., 2001). Thus the longitudinal recovery-related changes described above are in part similar to those seen when normal subjects learn a motor sequence. The need to re-learn simple motor

tasks after stroke is likely to engage such a mechanism, but the degree to which this is successful will depend on the degree of overall damage to the motor network. The role of error signal generation in a damaged motor system is clearly of interest, particularly as it may diminish with chronicity of impairment (Ward et al., in press Ward et al 2004). These important issues remain to be explored, and may have significant implications for rehabilitative interventions. In summary, the goal of cerebral reorganisation after focal damage to the motor system appears to be to re-establish a connection between IL M1 and spinal cord motor neurons via fast direct CMN pathways if possible. This allows recovery of fractionated finger movements. In the face of partial CMN damage, one potential strategy is to re-map the somatotopic representations in M1 and in those parts of the motor system that project to M1. If CMN pathways are completely lost then parallel motor loops become useful only for their projections to spinal cord, not by virtue of their projections to M1. Studies in adults with damage to the entire middle cerebral artery territory are scarce. However, data from young adults who suffer unilateral brain damage in the perinatal period suggest that the ipsilateral hemisphere becomes the main source of motor output in these circumstances (Cao et al., 1998). A process such as cerebral reorganisation during motor learning occurs in the normal brain and is a reflection of changes occurring at synaptic and systems levels. The degree to which such “normal processes” are successfully employed in the recovery process will depend on a number of variables, not least the precise amount and site of anatomical damage caused by an infarct and the amount of retraining available to the patient. However, the evidence from animal models suggests that the lesioned brain has an increased capacity for plastic change, at least early after damage. For example, widespread areas of cortical hyperexcitability appear immediately after cerebral infarction in animal brains, changes which subside over subsequent months (Buchkremer-Ratzmann et al., 1996). These changes occur in regions structurally connected to the lesion in both hemispheres as a consequence of

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Figure 5.3. Results of single subject longitudinal analysis examining for linear changes in task-related brain activations over sessions as a function of recovery. The patient suffered from a left sided pontine infarct resulting in right hemiparesis. (a) Results are surface rendered onto a canonical brain; red areas represent recovery-related decreases in task-related activation across sessions, and green areas represent the equivalent recovery related increases. All voxels are significant at P 0.001 (uncorrected for multiple comparisons) for display purposes. The brain is shown (from left to right) from the left ipsilesional (IL) side, from above (left hemisphere on the left), and from the right contralesional (CL). (b) Results are displayed on patients own normalised T1-weighted anatomical images (voxels significant at P 0.05, corrected for multiple comparisons across the whole brain), with corresponding 26, y 84, z 22) 28, plots of size of effect against overall recovery score (normalised), for selected brain regions. Coordinates of peak voxel in each region are followed by the correlation coefficient and the associated P value: (1) ipsilesional (IL) cerebellum (x (r2 y (x 0.77, P 14, z 30, y 0.01), (2) contralesional (CL) PMd (x 70) (r2 14, z 0.74, P 58) (r2 0.80, P 38, y 0, z 58) (r2 2, y 0.85, P 2, z 0.01), (4) ipsilesional (IL) SMA (x 60) (r2 18, y 0.53, P 10, z 0.01), (3) contralesional (CL) M1 (x 74) (r2 0.63, P

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downregulation of the 1-gamma-aminobutyric acid (GABA) receptor subunit and a decrease in GABAergic inhibition (Neumann-Haefelin et al., 1998) (see Chapter 14 of Volume I, pp. 18–21 for further discussion of these phenomena). This would be of particular interest to clinicians as it is easier to induce long-term potentiation (LTP) in hyperexcitable cortex, that is the cortex is more responsive to afferent input. In humans, acute limb deafferentation leads to reduced levels of GABA within minutes (Levy et al., 2002). It is tempting to think that the same thing may happen in areas of partially disconnected cortex after stroke. There is evidence of hyperexcitability in the CL motor cortex after both cortical and subcortical stroke in humans with at least moderate recovery (Bütefisch et al., 2003). Such hyperexcitability decreases with time after infarction, in keeping with data from animals (BuchkremerRatzmann et al., 1996; Witte, 1998; Shimizu et al., 2002). This window of opportunity, if therapeutically useful, may last only for a limited time. One final caveat should be mentioned. After injury-induced reorganisation of the brain the capacity for subsequent adaptive change is reduced (Kolb et al., 1998). Adaptive changes in older brains have been described (Ward and Frackowiak, 2003) and these may themselves limit the capacity for further reorganisation after injury in older patients. This may have implications for what can be expected from therapy designed to promote cerebral reorganisation after stroke in older subjects. Cerebral reorganisation undoubtedly contributes to functional recovery after stroke, but it is clear that a more detailed understanding of the natural history of these processes is required, together with the factors that influence them, before they can be utilised to rationalise therapeutical strategies in individual patients or groups.

et al., 2001; Carey et al., 2002; Schaechter et al., 2002; Johansen-Berg et al., 2002a; Jang et al., 2003; Miyai et al., 2003). Each study uses functional imaging before and after a particular therapeutical intervention. In general these studies have shown increased task-related activation in affected hemispheres (e.g. in PMd) and reduced activation in unaffected hemispheres after a period of treatment. Although of interest as discussed earlier in this chapter, these are likely to represent the consequences of functional improvement rather than the mechanism. However, this approach has limitations. Functional imaging is unlikely to be useful purely as a marker of clinical improvement, something that is measurable with simple outcome scores. Functional imaging will become a useful marker of the potential for change in damaged brain. Furthermore, it is to be hoped that the potential of different therapeutical interventions can be assessed, both in groups and individuals. Functional imaging, in conjunction with other techniques such as TMS, electro-encephalography (EEG), and magneto-EEG, has the potential to achieve these aims.

5.7 Other imaging modalities
The interpretation of functional imaging data from patients with brain lesions will be influenced by the site and extent of lesions. Two separate imaging techniques can provide accurate objective anatomical data that can be used to address hypotheses about the structure–function relationships of surviving brain regions. Voxel-based morphometry (VBM) and diffusion tensor imaging (DTI) are both MRI-dependent techniques. VBM is used to characterise grey and white matter differences in structural MRI scans (Ashburner and Friston, 2000) thus providing objective anatomical data about which regions of the brain have been damaged. A number of studies have validated VBM techniques against more traditional region of interest volumetric approaches (Good et al., 2002; Maguire et al., 2003). In stroke patients VBM has been used to identify structural changes in peri-lesional tissue and

5.6 Therapeutic interventions
A number of studies have appeared recently that have attempted to evaluate therapeutically driven change with functional imaging techniques (Pariente

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Rachel Kizony. Trepagnier. Cooper. Herr 13. Warren Olanow 7. Gorman. and prosthetics H. orthotics. Winstein and Jill Campbell Stewart 8. Communication devices Cheryl Y. W.SECTION A2 Therapeutic technology CONTENTS 6. Snyder and C. Virtual reality in neurorehabilitation Patrice L. Functional electrical stimulation in neurorehabilitation Peter H. Durfee and H. Earhart and Fay B. Mann 11.I. Rosemarie Cooper and Michael L. Hogan. Krebs.K. Hunter Peckham 10. Cell transplantation therapy for Parkinson’s disease Brian J. N. Wheelchair design and seating technology Rory A. Boninger 12. Weiss. Sheela Stuart and Carole Brown 71 89 103 119 136 147 165 182 198 69 . Uri Feintuch and Noomi Katz 14. Conditions of task practice for individuals with neurologic impairments Carolee J. Gad Alon and P.M. Rehabilitation robotics. Horak 9. Environmental control and assistive devices Jessica Johnson and William C. Balance training Gammon M. Beth Mineo Mollica.

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serotonin neurons of the dorsal raphe. Importantly. Pathologically the hallmark of PD is degeneration of the substantia nigra pars compacta (SNc) with the loss of midbrain dopaminergic neurons combined with the presence of intraneuronal inclusion (Lewy) bodies. there is a theoretical concern that exogenous administration of levodopa may be toxic to dopamine neurons based on its oxidative metabolism and its capacity to damage dopamine neurons in tissue culture. It is characterized by bradykinesia. While the drug has not been shown to be toxic in the in vivo experiments (Olanow et al. postural instability and tremor (Lang and Lozano. which likely reflect degeneration of non-dopaminergic neurons (Lang and Lozano. Warren Olanow2 Departments of 1Neurosurgery and 2Neurology. cholinergic neurons of the nucleus basalis of Meynert. 1998. the pedunculopontine nucleus. the implantation system and stimulation (2001). Deep brain stimulation (DBS) of the subthalamic nucleus (STN) or globus pallidus pars interna (GPi) is now widely used to reduce the incidence and severity of levodopa-induced dyskinesias. treatment of PD is primarily based on a dopamine replacement strategy. and nerve cells in the dorsal motor nucleus of the vagus. urinary and sexual dysfunction). Dopamine agonists are associated with reduced motor complications. however. 1976. 2001). autonomic impairment (orthostatic hypotension and gastrointestinal. 1998. NY. speech difficulties. 2004). Treatment with levodopa is extremely effective in the early stages of the disease. and “off” periods in which they do not respond to the drug and suffer features of parkinsonism. Mount Sinai School of Medicine. It is converted to dopamine within the brain by an aromatic acid decarboxylase (AADC). Chapter 35).. Ahlskog and Muenter. Finally. dysphagia. New York.. and dementia.. the imaging component of the recently completed 71 . Olanow et al. Indeed. sleep disturbances. depression. but patients eventually require levodopa treatment with the risk of motor complications (Olanow. These include freezing of gait. chronic levodopa treatment is associated with the development of motor complications (motor fluctuations and dyskinesias) which affect as many as 80% of patients after 5–10 years of treatment (Marsden and Parkes. USA 6. degeneration also occurs in nondopaminergic regions including epinephrine neurons of the locus coeruleus. 2003). Snyder1 and C. Olanow et al. Despite the involvement of multiple brain regions and multiple transmitter systems. 2001. but this treatment is associated with side-effects related to the surgery. 2004). Motor complications can be an important source of disability for many patients who cycle between “on” periods in which they respond to levodopa but have complicating dyskinesia.6 Cell transplantation therapy for Parkinson’s disease Brian J. Levodopa is the most widely employed and most effective symptomatic agent. the disease continues to progress despite levodopa treatment. postural instability. PD is also associated with features that do not respond to levodopa or other available treatments. Olanow. rigidity. 2001).1 Introduction Parkinson’s disease (PD) is an age-related progressive neurodegenerative disorder that affects approximately 1–2% of the population (see Volume II. and peripheral autonomic system.

Improvement was observed in a variety of measures of motor function including motor score on the unified Parkinson’s disease rating scale (UPDRS) performed in the practically defined off state (approximately 12 h after the 6. In the clinic. The specificity of the transplant procedure is illustrated by the observation that benefits are not detected if the right tissue (fetal mesencephalon) is implanted into the wrong part of the brain (cerebellum). Brundin et al. At present. Much attention has focused on transplantation strategies as a treatment option because of the potential of transplanted dopamine nerve cells to replace degenerating dopamine neurons.. Transplantation using fetal nigral dopamine cells derived from human ventral mesencephalon provides superior results in the laboratory (Dunnett and Annett. 1994.... It is also theoretically possible that early and physiologic replacement of dopamine might prevent degeneration in non-dopaminergic regions that occurs secondary to dopamine loss (Rodriguez et al.. 1988). 1979). Snyder and C. 1991.. to form normal appearing synapses. Freeman et al. Restoration of dopamine in a more physiologic manner might provide the benefits of levodopa with a reduced risk of motor complications..72 Brian J. no treatment intervention has been demonstrated to provide such an effect in PD. 6. but these were not confirmed in subsequent studies (Lindvall et al. successful transplantation could obviate the need for levodopa therapy and protect against the potentially toxic effects of exogenously administered levodopa. 1996). 1990) and few if any surviving cells were detected at autopsy (Peterson et al. 1990. 1989). Dramatic benefits were reported in a small group of patients (Madrazo et al. While transplantation of dopaminergic cells may not address all of the problems in PD. Autopsy studies in these animals showed that transplantation was associated with significant increases in striatal tyrosine hydroxylase (TH) immunoreactive staining and dopamine levels (Nikkhah et al.. dopamine cell loss is primarily responsible for the motor features of the disease. 1987). 2004). illustrating the importance of striatal dopamine innervation for motor function (Dunnett et al. Further.. Olanow et al. Olanow et al. Implanted cells have been shown to manufacture and release dopamine. 1982..3 Open label human trials The first studies of transplantation in humans utilized autologous adrenomedullary cells implanted into the caudate nucleus.. 1994). 1987. 1992.. Transplantation of dopamine neurons into the SNc failed to produce similar benefits unless axons extended to the . Peschanski et al. several open label studies reported benefit following fetal nigral transplantation (Lindvall et al. 1995. Motor improvement in this model was proportional to the number of transplanted fetal ventral mesencephalic cells (Brundin et al. and to be capable of autoregulation (Wuerthele et al. 1981. numerous studies have demonstrated motor benefits following transplantation of fetal nigral dopamine cells into the striatum of both the 6-OHDA lesioned rodent and the MPTP-lesioned primate (Dunnett and Annett. It is thus clear that PD patients can suffer intolerable disability despite currently available therapies. and a treatment that slows disease progression and/or restores function is an urgent priority.. 1991. Bjorklund et al.. Goetz et al. striatum.. 1988). to have normal electrical firing patterns.. 1989.. Freed et al. Schmidt et al. 1983. Importantly. 2002).. The procedure was associated with substantial morbidity and this treatment approach has been abandoned. Collier et al..2 Early transplant studies Studies in the late 1970s first reported that transplantation of fetal ventral mesencephalic tissue into the striatum could improve motor function in the 6-hydroxy dopamine (6-OHDA) lesioned rat model of PD (Bjorklund and Stenevi.. 1971. Perlow et al. 2003). 1992. Olanow et al. 1998). 1986). or if the wrong tissue (nondopaminergic cells) is implanted into the right place (striatum) (Dunnett et al. 1996).. Warren Olanow ELLDOPA study noted a faster rate of decline in an imaging biomarker of the nigrostriatal system in levodopa compared to placebo-treated patients consistent with a toxic effect of levodopa (Fahn et al...

2005). The authors noted further improvement during the course of follow-up (38% at 3 years).. 1999). 1999. individual implanted cells express a normal dopamine phenotype. donor age (ontogeny studies suggest age 6.. 1996. The rationale for considering these various transplant variables is discussed in detail in reference (Olanow et al. On the other hand. and the use of embryonic tissue as a source of dopamine cells remains a controversial topic (Cohen. 1994. placebo-controlled trials. and the use of immunosuppression.. Benefits have been reported to be long-lasting (Lindvall et al. and solid grafts derived from two donors per side were implanted longitudinally into the putamen using two deposits or “noodles”. The first of these studies was a 1 year trial in which 40 advanced PD patients were randomized to receive bilateral transplantation or a sham placebo operation (Freed et al. Kordower et al.. The sham procedure consists of a burr hole without needle penetration of the brain. some patients did not improve following transplant.. the National Institutes of Health in the USA supported two double-blind. 1994.000 transplanted cells per side (Kordower et al. or both). 2001).1 on UPDRS in the transplant group and 0. These studies were not without controversy. grafted regions stained positively for cytochrome oxidase indicating increased metabolism. Mendez et al. 1994). 1996).Cell transplantation therapy for Parkinson’s disease 73 last evening dose of levodopa) and in percent on time without dyskinesia based on home diary assessments. Hauser et al.. others argued against the use of sham controls for a surgical procedure. TH positive processes extended from the graft into the striatum providing continuous dopamine innervation between graft deposits with a patch-matrix pattern. 1995.. The primary endpoint of the study was the change from baseline to final visit in a measure of quality of life. 1996).4 1. possibly reflecting differences in patient selection and the transplant variables employed (reviewed in Olanow et al. Ventral mesencephalic tissue was stored for up to 4 weeks. but not in older patients. Variables that must be considered in developing a transplant protocol include method of tissue storage prior to surgery. type of transplant (cell suspension or solid graft)..0 2. Macklin. and some transplanted patients no longer required levodopa. 1995).. although there was increased expression of immune markers in grafted regions (Kordower et al. Post-mortem studies on transplanted patients have shown healthy appearing graft deposit with survival of more than 100. electron microscopy demonstrated normal appearing synaptic connections. In these studies. 1994. caudate. The study failed to meet its primary endpoint. 1997). and increased striatal FD uptake has been interpreted to represent an index of the survival of transplanted dopamine neurons (Lindvall et al. and expressed TH mRNA consistent with functional activity..5–9 weeks post conception is the optimal time)... 6. site of transplantation (putamen. although it should be noted that these later evaluations were performed by unblinded investigators. as transplanted patients were not improved in comparison to those in the placebo group (0.. Immunosuppression was not employed. Freeman et al.1).7 in the sham surgery group). A pre-specified analysis demonstrated a significant benefit of transplantation in younger patients ( 60 years) in UPDRS motor score performed in the practically defined off state (P 0. no host-derived sprouting was observed. number of donors implanted (most studies have chosen 1–4 donors per side). Clinical improvement in PD features following fetal nigral transplantation has been associated with a significant and progressive increase in striatal fluorodopa (FD) uptake on positron emission tomography (PET) in some studies (Lindvall et al. Remy et al. FD–PET is a surrogate biomarker of dopamine terminal function. A subsequent analysis by the authors suggested that baseline response to levodopa rather than patient’s age . Some felt it was premature to carry out a double-blind clinical trial. and no overt graft rejection was detected.4 Double-blind controlled studies to assess fetal nigral transplantation in PD To better define the safety and efficacy of fetal nigral transplantation as a treatment for PD. 1995. 1999).

although a paired comparison of the four donor versus placebo group just failed to meet significance (P 0.. Neurophysiologic assessments of reaction time (RT) and movement time (MT) noted significant improvement in transplanted patients in comparison to patients in the sham group. . involuntary movements that predominantly affected the lower extremities and were associated with parkinsonism in other body regions.74 Brian J. 2004). The primary endpoint was the change in UPDRS motor score during the practically defined off state. Patients in the placebocontrol group received bilateral partial burr holes which did not penetrate the inner table of the skull. The surgical procedure was also well tolerated in this study. and the authors considered the findings indicative of graft survival in 17/20 transplanted patients.096).000 TH cells in each striatum and extensive reinnervation of the striatum.244). and upper extremities to an equal or greater degree than the lower extremities. Autopsy in two patients confirmed survival of TH neurons in each of the transplant tracks with fibers extending approximately 2–3 mms into the striatum.1). 6.05) and deteriorated afterwards (Fig. 2004). Off-medication dyskinesias in this study were characterized by stereotypic. 5 transplanted patients developed severe and disabling dyskinesias that were not alleviated by a reduction or cessation in the dose of levodopa (see discussion below). No difference between younger and older patients or in baseline response to levodopa was observed in patients who did or did not respond to transplantation. and differed from classical on period levodopa-related dyskinesias which typically are more choreiform in nature and affect the head.. In the second double-blind. bilateral transplantation of fetal mesencephalic tissue derived from one donor per side (11 patients). post-mortem studies did show increased CD45 immunostaining in the region of graft deposits. raising the possibility that immune rejection might have compromised continued benefit. but were sufficiently severe in three to warrant surgical intervention. off-medication dyskinesias were generally mild. who in contrast demonstrated significant worsening over time (Gordon et al.2).01). Cell counting noted survival of approximately 7000–40.01 compared to controls) (Fig. bilateral transplantation of fetal mesencephalic tissue derived from four donors per side (12 patients) or sham surgery (11 patients) (Olanow et al. 2003). Warren Olanow best predicted a good response to transplantation (Bjorklund et al. The procedure itself was well tolerated. 34 patients were randomized to one of three treatment groups. In this study. torso. However. similar to what we have seen in open label studies (Fig. 2003. In support of this concept. Off-medication dyskinesias thus resembled diphasic dyskinesias. 6. FD–PET studies showed improvement in striatal FD uptake. It is noteworthy that transplanted patients in both the one and four donor groups did show improvement at 6 and 9 months (P 0. placebo-controlled study. Fetal mesencephalic tissue was stored for no more than 48 h in cool hibernation media and was not cultured. This problem was not observed in any patient in the control group. Transplanted patients had a significant increase in striatal FD uptake on PET (P 0..3).000 cells per side. Post hoc analysis of the data in this study demonstrated that transplanted patients with milder disease in both the one and four donor groups were significantly improved in comparison to the placebo group despite the small sample size (P 0. neck. this study also failed to meet its primary endpoint (P 0. Solid grafts were implanted exclusively into the post-commissural putamen with deposits placed no more than 5 mm apart in an attempt to achieve continuous reinnervation of the striatum. Some evidence of inflammation was observed in transplanted regions based on immunostaining for CD3 and HLA class II antigen. but a blinded and randomized review of videotapes obtained during visits conducted in the practically defined off state noted that 13/23 transplanted patients developed off-medication dyskinesia. Freed et al. All patients received cyclosporine beginning 2 weeks prior to surgery and continuing for 6 months following the operation. this time period corresponds with the discontinuation of cyclosporine.. 6. Snyder and C. rhythmic. Interestingly. however. Post-mortem studies demonstrated robust graft survival with more than 100.

TH immunostaining of striatum in patients receiving treatment with bilateral grafts using four donors per side (left panel). Figure 6. Note also that grafts in the four donor group are larger and have a cylindric appearance whereas in the one donor group they are smaller.. 2003). Scans were obtained at baseline (left panels). 1 year (middle panels) and 2 years (right panels). 2003).2. more concentric. and more densely packed (Olanow et al.. one donor per side (middle panel).Cell transplantation therapy for Parkinson’s disease 75 Figure 6. and a sham placebo procedure (right panel). . Note the progressive increase in striatal FD uptake in the transplanted patient in comparison to the progressive loss of striatal FD uptake consistent with continued disease progression in the placebo treated patient (Olanow et al. FD–PET studies in a representative patient receiving bilateral transplantation with four donors per side (top panels) and a patient receiving a sham procedure (lower panels).1. Note healthy appearing graft deposits and extensive striatal TH innervation with both four and one donors per side.

did not find an age effect. Snyder and C. possibly reflecting the same phenomenon (Olanow et al. several studies have reported that patients who do best following transplantation are receiving relatively lower doses of levodopa than those who do poorly (Wenning et al.5 42. 2000a).. or a sham placebo procedure. and that transplant-related benefit disappears after approximately 9 months coincident with the cessation of cyclosporine treatment (Olanow et al. There is no evidence to suggest that fetal nigral transplantation will benefit patients with atypical Parkinsonism where degeneration occurs in the striatum and pallidum and likely precludes any benefit from restoration of the nigrostriatal system. these studies provide some clues that might permit better results to be obtained with a variety of protocol modifications (Winkler et al. and most groups utilize the UK brain bank criteria in order to minimize the risk of an atypical Parkinsonism. but observed significant benefits with transplantation in the subset of patients with milder disease. It is not certain why benefits were observed in open label studies but not in two double-blind studies. Brundin et al.5 UPDRS motor off score 57. This observation is consistent with the notion that the patients who do best with transplantation have relatively mild disease. 2001)...76 Brian J. Insight into the cause of this complication and the development of methods to prevent this complication from occurring are required before further trials of fetal nigral transplantation or other forms of cell-based therapy can be resumed. suggest that transplantation is more effective in younger patients who respond well to levodopa. 2003). 6. possibly because there is less degeneration of non-dopaminergic systems and transplant has a better chance of improving patient disability (Freed et al. possibly because of involvement of non-dopaminergic regions (Lang and Obeso.5 0 6 12 Months 18 24 Placebo 1 donor 4 donors Figure 6. 6. 1997. Freed et al. 2005). 2003). It is obviously important to ensure the correct diagnosis. Interestingly. It is also not certain why transplanted patients developed offmedication dyskinesias. 2004a).5 Commentary It is clear that fetal nigral transplantation remains an experimental procedure and cannot be presently recommended as a therapy for PD. While these results are disappointing. four donors per side.3. Olanow et al.... To this point.5 52. Note that transplantation is associated with improvement for 6–9 months.5 47. Warren Olanow Fetal nigral transplant study mean UPDRS motor off score by visit 62.5 37. These are discussed below. Hagell et al.. Mean UPDRS scores in patients receiving bilateral transplantation with one donor per side. 1999. It is certainly possible that benefits observed in open label studies were exaggerated by placebo effect or bias. More advanced patients who require higher levodopa doses may benefit less. despite using similar protocols and evidence of graft survival on both PET studies and post-mortem examination. studies .6 Patient selection Patient selection is an important factor in the design of transplantation studies.

did not use immunosuppression and had much less survival of transplanted cells than did Olanow et al.. 1993. T-cells. who employed cyclosporine for 6 months (Kordower et al. 6. but immune rejection can still occur even following transplantation of autografts (Fisher and Gage. and reported long-lasting benefits with the ability to stop levodopa in some patients (Wenning et al.. 6. we have previously demonstrated dense HLA-DR immunostaining and numerous pan macrophages. Indeed. differences in the expression of major and minor histocompatability antigens between graft and host can result in a long-term inflammatory response with macrophage and microglial activation and upregulation of immunological markers (Duan et al. 1996.. and B-cells in otherwise normal appearing graft deposits. Shinoda et al. Gordon et al. Freed et al.. Transplantation of functioning dopamine neurons and terminals might thus be expected to provide dopamine to the striatum in a more continuous and physiologic manner than regular oral formulations of levodopa and so reduce rather than increase the risk of dyskinesia.. these observations suggest that the best candidates for fetal nigral transplantation and other cell-based therapies might be younger PD patients with relatively mild disease who respond well to levodopa and have minimal or no evidence of non-dopaminergic lesions. although observations during the last 2 years were unblinded. Freed et al. evidence of some degree of an immune response was seen in post-mortem studies of patients in each of the double-blind trials.. Thus. . in the latter group it was suggested that an immune response may have limited the clinical benefit of fetal nigral transplantation. In this regard. 2000). In addition. 2004). Olanow et al. Further.. late improvement in physiologic measures of motor performance and a delay in recovery in movement-related cortical function have been reported (Brundin et al.. Such immune reactions could be detrimental to graft survival and function.. 1996). Piccini et al. Collectively. Indeed.. 18 months following fetal nigral transplantation (Kordower et al. Freed et al. 1996). Indeed.. 1996. 1997. 1993. current evidence suggests that long-term immunosuppression might be desirable in future transplant regimens. 2003). as benefits deteriorated following withdrawal of cyclosporine and there was evidence of increased CD45 staining in grafter regions at post-mortem (Olanow et al. 2004). The precise cause of off-medication dyskinesia is not known. the Lund group used suspension grafts and a “cocktail” of three immunosuppressive agents. 1995. 2000). 1995. Baker-Cairns et al.7 Immunosuppression A fundamental question in transplantation is whether immunosuppression is necessary in order to permit host tolerance of the graft. and are likely relevant to human transplantation.. noted continued improvement over 3 years..8 Off-medication dyskinesia Off-medication dyskinesia is an important and potentially disabling side-effect of transplantation that currently represents a major obstacle to future studies of fetal nigral transplantation and other cell-based therapies in PD. Drucker-Colin and Verdugo-Diaz.. Longer periods of follow-up may also be required to see the full benefits of transplantation. The brain has been considered to be an immunologically privileged site. 1997). Current evidence indicates that levodopa-induced on-medication dyskinesias are related to abnormal intermittent or pulsatile stimulation of denervated dopamine receptors (Obeso et al. While intracerebral grafts can survive in the absence of immunosuppression. 2001).. 2001. 2003). These studies each used solid tissue grafts.Cell transplantation therapy for Parkinson’s disease 77 in the 6-OHDA model in the rat similarly note greater benefits with intrastriatal transplantation in animals that have lesions confined to the striatum in comparison to those with lesions involving both striatal and non-striatal forebrain dopaminergic projections (Kirik et al. Additionally. 2000a. and it has been suggested that solid grafts are more likely to generate an immune response as the blood vessels within the graft are of donor origin and likely to express major histocompatability type 1 antigens which are intensely immunogenic (Baker-Cairns et al.

Further.. 1993.. Sortwell et al. Sortwell et al. The authors suggested that dopamine released from innervated regions of the striatum or “hot spots” could stimulate upregulated. PET scans in other transplant studies have not shown inhomogeneities (Olanow et al. and noted a correlation in their studies with the severity of on-medication dyskinesia at baseline (Hagell et al... 1994. 2000a) and another 60–70% of cells die during the first week post-transplantation (Barker et al. Studer et al... 2000).9 Attempts to enhance survival of transplanted dopamine neurons Only about 5% of neurons in the SNc are dopaminergic. 2003).. while increased in comparison to baseline. 2003). Approximately 20–30% of mesencephalic cells die during preparation of the tissue for transplantation probably due to ischemia or trauma associated with dissection and dissociation of the cells (Fawcett et al... found a reduction in levodopa-induced dyskinesia following transplantation of dopamine neurons in a rodent model of PD (Lee et al. Brundin et al. reinnervation of the striatum. However. and only about 5–20% of grafted dopamine neurons survive transplantation (Kordower et al. Nikkhah et al. This hypothesis raises the intriguing possibility that transplantation of increased numbers of functioning dopamine neurons might both enhance efficacy and eliminate off-medication dyskinesia.. we have reported reduced dyskinesia with survival of larger numbers of implanted dopaminergic neurons (Kordower et al. Enhanced survival of transplanted cells would facilitate the logistics of performing a fetal nigral transplant procedure and could potentially yield enhanced clinical results.. patchy reinnervation of the striatum or abnormal synaptic connectivity such as could occur with an immune reaction. Indeed.. 1998. Further insight into the cause of off-medication dyskinesia and the development of methods that prevent their occurrence are crucial before studies of fetal nigral transplantation can be resumed in PD patients. Freed et al. did not return to the lower limits of normal in any patient (Olanow et al. Hagell et al. 1993. A variety of other hypotheses have been put forward. and that striatal FD uptake. and found no correlation between off-medication dyskinesia and the number of implanted donor cells (Olanow et al. 6.. In contrast to these findings.. regional areas of increased FD uptake on PET were observed in one study (Ma et al. in a larger double-blind study. Neurotrophic factors promote the survival of dopaminergic neurons in vitro and in vivo (Lin et al. a form of dyskinesia that is seen with suboptimal dopaminergic levels. 2003). 2002). Snyder and C.. off-medication dyskinesia were observed with freshly transplanted cells that were not cultured and there was no correlation with on-medication dyskinesia scores at baseline or at any other time point during the trial (Olanow et al. it has been observed that off-medication dyskinesia resemble diphasic dyskinesia. hypersensitive receptors in denervated neighboring areas leading to dyskinesia. 1996. However.. suggested that offmedication dyskinesia might relate to long-term storage of cells in tissue culture prior to transplantation.. 2001). proposed that off-medication dyskinesia might be due to excessive dopamine release from grafts (Freed et al. It remains uncertain whether this sideeffect will prove to be a problem with other cell-based therapies such as stem cells and laboratory studies to assess grafts in animals who have been exposed to levodopa and who experience levodopa-related dyskinesia must be performed prior to commencing clinical trials.78 Brian J. 1995) and might therefore be expected to . although this does not exclude this possibility. Finally. These observations suggest that off-medication may be due to partial. 1995). 2000). but there is no evidence of excess dopaminergic activity on PET or postmortem examination in any of the studies performed to date. Considerable research has focused on ways of trying to improve this yield. 1998)... but incomplete. 1995. could lead to regional pulsatility and consequent dyskinesia.. Altar et al. 2002). 2003). Warren Olanow Lee et al. 2004). Mesencephalic cell graft aggregates can be maintained in culture and exposed to agents such as antioxidants and trophic factors that promote their survival that promote their survival following transplantation (Meyer et al.

suggesting that co-administration of GDNF might be a way to enhance the clinical effects associated with fetal nigral grafts. GDNF infusion in MPTP lesioned primates enhances survival of nigral neurons. 2004).. increases TH staining in the striatum. Increased expression or co-administration of antiapoptotic and antioxidant agents is another approach that has been tried in an attempt to increase the survival of transplanted dopamine neurons.. 1999). 2004).. 1998). 1997. 2001) and mixed lineage kinase (MLK) activation is a critical event in this sequence of events (Xu et al.. 1994). through co-transplantation of cells that manufacture and secrete neurotrophic factors. 2000). as well as brain derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3). The carotid body contains DA rich chromaffin cells which release neurotrophic factors such as GDNF. 1995... 1996. Antioxidants also improve graft survival. 6.. and improves behavioral features even when delivered weeks after the insult (Gash et al.. Trophic factors can be administered by direct infusion into the striatum... 2002. Winkler et al. MLK inhibitors have been shown to protect against dopaminergic cell death in culture systems (Harris et al. Approximately 94% of melanized neurons within the SNc normally contain fibroblast growth factor 2 (FGF-2) receptors suggesting this might be an important trophic factor for dopamine neurons (Tooyama et al. 2004). striatal TH immunoreactivity and dopamine levels. This approach theoretically provides for dopamine reinnervation of the striatum as well as regions of the basal ganglia and the cerebral cortex that receive dopaminergic inputs from the SNc. and functional recovery in 6-OHDA lesioned rats (Shukla et al.. but have not been tested in conjunction with transplanted dopamine cells (Yasuhara et al. Caspase inhibitors also reduce apoptosis in many model systems and increase the survival of dopaminergic grafts in the 6-OHDA rat model (Schierle et al. Indeed.. 2000b). GDNF has been shown to improve survival of grafted dopamine neurons and to increase striatal reinnervation in the 6-OHDA rat (Granholm et al. and by gene therapy approaches.Cell transplantation therapy for Parkinson’s disease 79 enhance survival and functional effects of dopamine cell transplants.10 Combined striatal and SNc grafts Combined striatal and SNc grafts are reported to provide enhanced behavioral benefits in complex tasks in animal models of PD in comparison to intrastriatal grafts alone (Baker et al. Encapsulated cells that constitutively express high levels of VEGF have also been reported to improve behavior and decrease TH cell loss in a rat model of PD. striatal TH-immunoreactivity and behavioral function when co-administered with ventral mesencephalic grafts (Agrawal et al.. 2001). Mendez and colleagues transplanted fetal ventral mesencephalic tissue into both the striatum and the SNc in a small numbers of PD patients and reported clinical benefits along with increased striatal FD uptake on . Zawada et al. Lentivirus delivery of GDNF similarly is associated with marked behavioral and anatomic benefits in both the 6-OHDA rodent and the MPTP monkey (Bensadoun et al. 2002). Gearan et al.. 2000). 2004).. Kordower et al. Murakata et al. Co-transplantation of carotid body cells has been shown to enhance the survival of grafted fetal ventral mesencephalic dopaminergic cells. Co-administration of lazaroids with fetal nigral transplantation has now been attempted in PD patients with good clinical results (Brundin et al.. and to improve long-term survival. The Jun-N-terminal kinase (JNK) stress pathway is central to apoptotic neuronal death in several model systems (Chun et al.... 2000. Glial derived neurotrophic factor (GDNF) is a member of the transforming growth factor family and appears to have the greatest capacity amongst trophic factors to protect dopaminergic neurons both in culture and in vivo. 2004). graft size and fiber outgrowth following transplantation of rat ventral mesenecephalic cells (Boll et al.. but it is not possible to say with any certainty how much the lazaroids contributed to the observed benefit based on this anecdotal report. 2001. 1996). co-transplantation of Schwann cells that express FGF-2 enhances the survival of intrastriatal dopamine grafts and promotes striatal reinnervation and functional recovery in the rat model of PD (Timmer et al.

Stem cells are pluripotent cells that have the potential to differentiate into all of the different cell types of the body. 2003). ES cells are harvested from the inner cell membrane of the blastocyst and offer the potential of being expanded to provide a renewable source of dopamine neurons. 2003) were reported to provide some benefits to a small number of PD patients (Arjona et al. ES cells are the most promising as approximately 50% spontaneously differentiate into a neuronal phenotype. 2002). Most optimism for the treatment of PD with a cellbased therapy rests on stem cells as a source of dopamine neurons for transplantation. Mouse ES cells have been shown to spontaneously differentiate into neurons following transplantation. 1999.. adrenomedullary tissue has been abandoned as patients did not maintain longterm benefit and the procedure was associated with considerable morbidity.11 Other cell-based approaches to transplantation in PD The limited clinical benefits obtained with fetal nigral transplantation to date coupled with the societal and logistic issues involved in the use of human embryonic tissue. However. As previously discussed. Transplantation of autologous carotid body cells improved motor function in Parkinsonian rodents and (Luquin et al.. Extra-adrenal chromaffin tissue has attracted some attention. although there are still many hurdles that must be overcome.. and no benefit was detected in double-blind studies (unpublished studies).. 6.. The procedure was well tolerated with no side-effects related to implantation into the midbrain.. The magnitude of clinical improvement and degree of survival of implanted neurons was similar to that reported in previously reported studies. ToledoAral et al. None of these procedures has been studied in double-blind placebo-controlled trials. Spheramine transplantation has been reported to provide anti-Parkinson effects when transplanted into the striatum of the MPTP monkey and in open label trials in PD patients (Watts et al. 1982). are relatively resistant to immune rejection and survive following transplantation when implanted attached to gelatin microcarriers (Spheramine®) (Subramanian et al. 2001). Off-medication dyskinesias were not recorded.. No serious adverse events related to the microcarrier system have been noted and no patient has yet been reported with off-medication dyskinesia. Warren Olanow PET in an open label study (Mendez et al. and calbindin. Carotid body tissue undergoes atrophy with increasing age and it has been suggested that any improvement seen in these experiments was due to the release of trophic factors and not from restoration of the nigrostriatal system (Toledo-Aral et al. 2000). post-mortem studies demonstrated no evidence of graft integration into the brain nor evidence that they secreted dopamine. Autologous sympathetic ganglia cells have been tested in small groups of patients with advanced PD. Several types of stem cells have been studied: embryonic stem cells (ES cells). 2002). Transplant of this tissue has been reported to induce functional improvement in Parkinsonian rats (Espejo et al.. At autopsy. A doubleblind placebo-controlled study to test this approach in PD patients is currently under way. and primitive cells that are found in the bone marrow and umbilical cord. with a few showing phenotypic features of dopamine neurons . Human retinal epithelial cells secrete levodopa. 2003).. patients were reported to have a decrease in “off” time (Nakao et al. 1997). In the laboratory. 2001)..80 Brian J. However. 1997). has led to a search for alternate sources of dopaminergic cell types for transplantation in PD. In one study... while another found amelioration of bradykinesia and gait dysfunction in half of transplanted patients (Itakura et al. Transplantation of porcine fetal nigral cells has been reported to provide some benefit in open label studies in PD patients (Schumacher et al. Snyder and C. neural stem cells (NSCs) that are found within the fetal and adult brain. surviving transplanted cells were detected in both the striatum and the SNc and stained positively for TH. Doubleblind trials are required to confirm these results.. there were only a few surviving transplanted dopaminergic cells at post-mortem (Deacon et al. G-protein-coupled inward rectifying current potassium channel type 2 (Girk2). 2003). The organ of Zuckerkandl is a paired organ located adjacent to the abdominal aorta which represents a source of GDNF (Bohn et al.

Park et al. The yield can be increased by inducing ES cells to differentiate into dopamine neurons while in culture using agents such as Nurr-1. There are numerous examples of surgical procedures that were adopted into general practice based on . Transplantation of pluripotential stem cells carries with it the risk of unregulated growth and tumor formation.12 Need for double-blind controlled trials and sham surgery While there has been some resistance to the use of double-blind placebo-controlled trials to assess new surgical therapies. However. Importantly. 2004). and if so how to prevent them.. 2004). trophic factors.. Neural stem cells initially generated considerable enthusiasm because they already have a neuronal lineage. 2001. Behavioral effects can be observed following transplantation into the rat model of PD. 2004). Wang et al.. Stem cells will also need to be proven to be more effective than just pharmacologic replacement of lost dopamine. Transplanted dopamine neurons derived from ES cells have now been shown to be able to survive and to provide behavioral improvement in the 6-OHDA rat model (Bjorklund et al. and the optimal type of stem cell and method of inducing them to differentiate into dopamine neurons remain to be determined... 2005).. extensive laboratory testing will have to be performed to exclude unanticipated side-effects. it is by no means assured that even complete and physiologic restoration of the nigrostriatal dopamine system will eliminate disability in PD patients caused by degeneration of nondopaminergic neurons (see below).. It has not yet proven easy to routinely generate large numbers of dopamine neurons for transplantation. Indeed. 5 of 17 rats transplanted with stem cells had teratomas at post-mortem examination (Bjorklund et al. but only a few TH positive cells are found at post-mortem.. More recently. they also default to glial cells and to date it has proven difficult to generate large numbers of dopamine neurons suitable for transplantation.. and they can be induced to differentiate into midbrain dopaminergic neurons by exposure to agents such as cytokines and trophic factors (Carvey et al. 2004... Placebo and bias effects can be powerful and seriously distort the results of a trial (McRae et al. A higher yield of TH cells for transplantation can be accomplished by using a cell sorter to identify dopaminergic cells that have been transfected with a green fluorescent protein reporter (Yoshizaki et al. Storch et al.. 2004). 2001. 2004). 1999). A few cells spontaneously differentiate into dopamine phenotypes following transplantation (Yang et al. Stem cells offer the theoretical advantage of providing a source of virtually unlimited and optimized dopamine neurons for transplantation in PD. studies have demonstrated that human ES cells can also be induced to differentiate into dopamine neurons (Perrier et al. 6. prior to entering into clinical trial. 2002). In addition. 2002). Placebo therapy can also be associated with dopamine release with possible clinical consequences (de la Fuente-Fernandez et al. 2002). Finally. we believe that it is essential to employ this study design in evaluating the safety and efficacy of cell-based therapies for PD (Freeman et al. 2004). to the extent possible... 2001). and following transplantation they have been shown to produce behavioral improvement in the 6-OHDA rat (Dezawa et al.. Magavi and Macklis. 2000. and ascorbate (Kim et al. Bcl-XL. Studies will also have to be conducted to determine if stem cells are associated with offmedication dyskinesia. Burnstein et al. In vitro treatment with GDNF increase TH positivity in bone marrow stromal cells. 2003. 2005). ES cells have also been reported to improve motor features and to increase striatal FD uptake on PET in MPTP-lesioned monkeys (Takagi et al. but results have been disappointing as they primarily differentiate into astroglia (Gage. 2002). Autologous stem cells derived from the umbilical cord or bone marrow are also of great interest because they can avoid the immunological and societal issues associated with embryonic stem cells.Cell transplantation therapy for Parkinson’s disease 81 (Bjorklund et al. There are however many issues that remain to be resolved. sonic hedgehog. The adverse event profile must be defined.. which to date have not been confirmed to yield significant results in PD patients in double-blind trials. Studies in models of PD show limited cell survival and do not provide benefits superior to fetal nigral transplants..

. While a sham procedure is not fully without risk. it has been postulated that dopamine depletion-induced increased firing of glutamatergic neurons in the STN could cause excitotoxic damage in target neurons such as the globus pallidus. Snyder and C. 6. report the best results in patients whose clinical features can be best controlled with levodopa. For additional discussion of . Post hoc analyses in the double-blind transplant studies suggest that improved clinical results might be obtained with protocols that employ younger patients with milder disease and long-term use of immunosuppression. porcine fetal nigral transplantation. However. It is also possible that enhanced benefit can be derived by transplantation of other dopaminergic cell types such as stem cells. and dementia presumably because they result from degeneration of nondopaminergic neurons. Indeed. as well as the SNc (Rodriguez et al. Post-mortem studies reveal histologic evidence of robust graft survival with extensive and organotypic striatal reinnervation. Further. Indeed. reinnervate the striatum and provide benefit in animal models of PD. and GDNF infusion were not confirmed in double-blind trials. substantia nigra pars reticulata. autonomic dysfunction. It is possible that early replacement of dopaminergic tone will have downstream effects that prevent damage to non-dopaminergic regions. Thus. Levodopa does not improve potentially disabling features of PD such as sleep disturbances. It is also possible that degeneration of dopaminergic pathways to cerebral cortex and other brain regions might contribute to the gait. Laboratory studies have demonstrated that transplanted dopamine cells can survive. we have recently seen that positive results in open label trials of human fetal nigral transplantation.. It is by no means clear. Open label studies of fetal nigral transplantation showed positive clinical benefits associated with increased striatal FD uptake on PET. Lindvall et al. and whose safety and efficacy profile has not been fully defined. distribution. delayed response. the pedunculopontine nucleus.82 Brian J. 2005). and cognitive dysfunction that occurs in PD. Transplantation therapies in PD are particularly appropriate for evaluation in double-blind trials as the intervention is relatively standardized and the treatment has much in common with drug therapies. transplantation of fetal mesencephalic dopamine neurons was associated with a potentially disabling off-medication dyskinesia. the alternative is to expose patients to a procedure that might not work. Warren Olanow anecdotal observations that were discarded after negative results in more formal clinical trials (Freeman et al. postural instability.. Early restoration of dopamine might prevent these non-dopaminergic consequences. It remains to be determined if transplantation of larger numbers of cells or co-administration of agents that enhance cell survival will influence outcome. however.13 Conclusion The future of mesencephalic cell transplantation for PD is uncertain at this time. It is still possible that transplantation using different transplant protocols or different dopaminergic cells will prove helpful for PD patients. 1999). release dopamine. 2005). that transplantation of dopamine neurons into the striatum will have any effect on these non-dopaminergic systems and that these types of disability that occur in PD will persist despite complete restoration of the nigrostriatal dopamine system. a recent survey showed that 97% of PD investigators would insist on a doubleblind placebo-controlled trial before accepting that a cell-based or gene therapy procedure was efficacious. and suggest that these are the optimal candidates for a transplant procedure. and immune reactivity must all be considered (Olanow. freezing of gait. In PD. For example. two double-blind studies failed to demonstrate that transplanted patients were superior to placebo with respect to their primary endpoints. It is not clear that transplanted dopamine cells will provide better results. autonomic. fetal nigral transplantation can not be currently recommended as a treatment for PD. It is also important to question whether transplantation of dopaminergic cells can provide benefits any greater than can be achieved with levodopa (Lang and Obeso. metabolism/degeneration. despite the need for a sham control (Kim et al. issues such as dose. 2004b). 1998).

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the majority of published protocols in neurologic rehabilitation lack an explicit scientific rationale for the intensity. approximately 700.7 Conditions of task practice for individuals with neurologic impairments Carolee J. LOS Angeles. revising the parameters of training to fit patient characteristics and rehabilitation goals. 2001) and the recovery of upper extremity (UE) use after strokehemiparesis (Taub and Uswatte. More importantly. 2002).000 people suffer a stroke and the estimated economic 1 It is perhaps no accident that most behavior modification programs that are based on traditional operant-conditioning methods are 2 weeks in duration. refining patient selection criteria. Stroke is the leading cause of disability among American adults. 2004). Whitall. 2004). However. This process undermines scientific enquiry and in some cases tends to hinder the development of alternative and innovative approaches. objective treatment protocols will become a necessary component of valid efficacy and effectiveness research (Whyte and Hart. At present. 2004. duration. Why is the signature constraint-induced therapy (CIT) protocol of 6 h/day (60 h total) with one-onone supervised training for no less than a 2-week period (10 days) “optimal” for achieving an effect (Taub and Uswatte. its practitioners must heed the temptation to simply adopt these protocols without questioning their rationale. 2001) and chronic stroke (Sullivan et al. 2003)?1 How important is the “constraint” within a CIT training protocol? Why is a typical bout of step training with body weight support during treadmill walking 20 min in duration.. and developing reliable prognostic indicators of outcome (Dobkin.g. defining rehabilitation treatments is necessary for this field to advance.. Winstein and Jill Campbell Stewart Department of Biokinesiology and Physical Therapy. 2003). and content (e. Recently. University of Southern California.. for example. On one hand. task-specific versus muscle-specific) of training used within the rehabilitation treatments. 2003). 89 . The development of specific and objective rehabilitation treatment protocols will be a clear signal of progress in the field of rehabilitation medicine. For example. CA 7. research in rehabilitation has witnessed the application of the scientific method to specific functional problems such as the recovery of walking in neurologic populations (Barbeau and Fung. 2003). but on the other hand. and lead to “blind” following at best (Dromerick. 2003). to enhance walking in individuals with spinal cord injury (Field-Fote. Nearly 3 million of Americans are stroke affected.. the precise parameters of training for a given rehabilitation treatment can take on a mythical quality with hidden meaning at worst. if rehabilitation medicine is to join the ranks of other evidence-based medical and pharmaceutical practices. 3 times/week for 4 weeks (Sullivan et al. Without an explicit rationale (or even hypothesis).1 Introduction Significant growth and interest in the field of rehabilitation medicine has been fueled in part by advances in rehabilitation science within an interdisciplinary research model (DeLisa. and to enable use of the hemiparetic UE in adults with sub-acute stroke (Winstein et al. 2002)? These rhetorical questions suggest that the field of rehabilitation medicine is at a critical cross-road in its development. each year. this translational research has spawned various protocolbased treatments.

There is an extensive literature in . patients typically spend 70% of the day in activities largely unrelated to physical outcome and less than 20% of the day in activities that could potentially contribute to their recovery (Mackey et al. Residual burden of care is significant with 44% of community-based individuals post-stroke in a National Survey reporting difficulty with at least five to six activities of daily life (Chan et al. Winstein and Jill Campbell Stewart burden from stroke-related disability is 35 billion dollars annually in direct costs (American Heart Association. Chapter 36 of Volume II).. sub-maximal torque levels for a given duration) in the latter. Previous work that has invoked performance improvements and/or experience-dependent neuroplasticity shows that large amounts of practice (consisting of 1000s sometimes 10. Lincoln et al. maximum torque) or muscle endurance (e.. we distinguish between exercise and task-specific training in neurorehabilitation.. 1997). More effective acute management of stroke has resulted in declining mortality while the number of stroke survivors who need long-term care or rehabilitation is expected to greatly increase. is considered the most crucial component for recovery (Butefisch et al. For these reasons. 1993. a critical goal of rehabilitation science is to understand the parameters of training and conditions of task practice that will optimize functional outcomes from rehabilitation programs (Whitall. Nudo et al.. despite these impressive statistics. These large amounts of practice are a dramatic contrast to the limited time that patients post-stroke spend in therapeutic activities: on average between 30 and 40 min/day (Keith and Cowell. more importantly. imposing an enormous economic burden on individuals and society (Rundek et al. there has been little principled and systematic research to determine the most effective and efficient parameters of training or conditions of task practice for the rehabilitation of the motor skills that constitute a significant portion of daily life. Surprisingly. 2000. 2005). (2) cardiovascular endurance. Future advances in rehabilitation science will depend on the development of hypothesis-driven clinical trials that are designed to test relevant and innovative ideas about exercise training (Dobkin.. 2003). without a sound theoretical framework for exercise parameter selection. 2004).g. Karni. See Chapters 8 and 14 in Volume I for details about cortical re-organization and learningdependent changes associated with task practice. Doyon et al. 2004. Further. The term “exercise training” in the classical sense refers to cardiovascular fitness training (aerobic and anaerobic) or muscle strength training. 2002). 2002). Weinrich et al.g. intensity (within session attributes for training goal and progression). Perhaps. 1995.. 7. current medical “practice” models in stroke rehabilitation are not designed to enhance recovery and maximize functional outcomes.90 Carolee J. 1996). an approach that will not survive the rigors of scientific review (Verville and DeLisa. The goal for these exercise training protocols is either cardiovascular conditioning as evidenced by various performance-based tests including VO2 peak in the former or targeted levels of voluntary muscle force (e. 1999. 2005). intense task practice. or (4) motor skill acquisition? We ask this rhetorical question to emphasize the point that without explicit discussion of the goals of exercise training for individuals with neurologic impairments... In sum. (3) reversal of “learnednon-use”. 1987. 1995. Thus..000s of trials) are needed (Pavlides et al. Kwakkel et al. 1996. and duration (total number of sessions or hours). future clinical trials in this field will be limited to a purely empirical approach. Wolf et al. 1996). if the goals were specific for: (1) muscle strengthening.2 Parameters of exercise training depend on the goal Would you choose different parameters of exercise training... the selection of precise parameters will have undefined rationale. including frequency (number of training sessions in a given period).. In cases where movement deficits result from a stroke.. defined as repeated attempts to produce motor behaviors beyond present capabilities.

impairment. we define a motor skill as one in which the task is performed effectively.Conditions of task practice for individuals with neurologic impairments 91 both of these areas that can be used to develop appropriate exercise parameters for the desired goal. coordination. efficiently. including: pathology. endurance. Next. Next. we review the literature pertaining to two important conditions of practice known to be critical for motor skill learning: (1) augmented feedback and explicit information and (2) task scheduling. 1998. Then. and disability. skills and the disablement model A 1997 research agenda that emanated from a workshop focused on facilitating patient learning during medical rehabilitation proposed that “the effectiveness and efficiency of learning-oriented practices will likely be enhanced by well-formulated investigations grounded in available learning theory and research” (Fuhrer and Keith. A program that focuses on the learning of motor skills can take a “top-down approach” whereby the inability to perform a personal or societal role is identified first. First. motor control. 2005. 560). the appropriate resources such as strength. For purposes of this chapter. we discuss the differences between “use” and “skill” as these terms apply to UE and manual actions. and coordination provide the foundation that supports task practice. including in individuals with neurologic impairments. We argue that this distinction becomes important for choosing the appropriate conditions of practice for individuals post-stroke. further evaluation and analysis determines the functional skills required to meet those roles and the impairments (strength.) that are interfering with an individual’s ability to perform these skills (Gordon.3 Motor learning. Task-specific training focused on improving the skill with which an individual performs motor tasks draws heavily upon the principles of learning derived from the cognitive neuroscience and movement science literature. focuses on improving the performance of functional tasks through repetition and goal-oriented practice. Task-specific training.. stroke-hemiparesis). taskspecific training can be quite limited without a foundation grounded in the rubric of skill learning. have fundamentally different goals. etc. Given this specific therapeutic goal.. Emphasis on the underlying impairments. A task-specific training program and a generic exercise program. Further. functional limitation. therefore. Three key terms/phrases that are critical for determining optimal parameters and conditions of training are . 2000). in the top-down model allows the development of more efficient and flexible movement strategies that can be used in a variety of task and environmental contexts. we define skill and motor learning within the context of neurorehabilitation. in contrast to a generic exercise program. termed resources.g. the purpose of this chapter is to provide a scientific rationale for choosing the conditions of practice that best promote skill learning in the context of task-specific training for diminished functional ability in the neurologically impaired patient. p. 2000). 7. 2003). the underlying impairments require attention if functional ability is to improve (Sunderland and Tuke. More recently others have argued for the need to investigate and better explain the specific ingredients of rehabilitation protocols including the conditions of practice that optimize learning and recovery (Whyte and Hart. 2005). Motor learning is a set of processes associated with “practice” or experience leading to relatively permanent changes in the capability for responding (Schmidt and Lee. The reader is referred to Chapter 21 by MacKay-Lyons in this volume for an excellent discussion of cardiovascular fitness and training in neurorehabilitation and Chapter 18 by Blanton and Wolf for a review of UE muscle weakness following stroke. When the goal of rehabilitation is to enhance skilled task performance. endurance. Such a model takes into account the levels of Nagi’s model of disablement. For each we outline how these conditions might be manipulated to promote recovery of functional skills in the neurologically impaired patient. 2005). For neurologic disorders in which motor control deficits are marked (e. and within a variety of environmental contexts (Gordon. Wolf et al.

while a skill-learning model treats “augmented feedback” as information about performance for cognitive processing (e. 2001) such as those reviewed in Chapter 2 of Volume I. Gordon.g. does not address the known resource impairments of motor control. 1994. For example. “relatively permanent”.4 Spontaneous use versus skilled performance in arm and hand rehabilitation training Programs that employ task-specific training can do so for a variety of reasons.92 Carolee J.. however. 1994. Winstein and Jill Campbell Stewart “practice”. In fact. 2003). pigeon in this case) is relatively passive in this process while performance is progressively “shaped” towards the behavioral objective (task goal) in small steps through reinforcement or reward (positive feedback).. Taub et al. the pigeon is not aware that this is a game-like. referred to as “learned-non-use” (Taub et al. Simple repetition of a task is not sufficient to increase skill or promote the associated cortical re-organization (Plautz et al. practice is designed to reverse the sub-acute conditioning that leads to decreased spontaneous use of an extremity. The shaping procedure stands in sharp contrast to the procedures employed when designing task practice to optimize motor skill learning in the context of neurorehabilitation. the pigeon. 2005). 7. 2000). Obviously.. the learner practices under a set of active learning principles that are derived from more modern theories of learning and memory (Cahill et al. 2000). The shaping procedure is designed around the elicitation of behavior and not the acquisition of a voluntary skill. 1997. With shaping. In fact.. and environmental conditions that require him/her to generate successful motor solutions. In contrast to a motor-learning-based approach. 2005).. For skill acquisition. Equally important. can be shaped without knowing or ever understanding the goal behavior. a training program for patients with diminished motor control and impaired functional ability is designed to promote skilled performance (Dean and Shepherd. strength and coordination (Sunderland and Tuke. a behavior is progressively modified towards the goal through successive approximation and positive reinforcement. Skinner (1968) taught us that shaping was a form of operant conditioning in which the probability of experimenter determined behaviors are “elicited” through reinforcement (reward or punishment). the “shaping” procedure as described within the context of CIT (Morris et al. It is this ability to adapt that provides the individual with the capability to perform a task over time (relatively permanent change). problem-solving) relevant to the preparation for the next practice trial. the conditions of practice are designed directly from operantconditioning principles and include the “shaping” procedure. an operant-conditioning model treats “augmented feedback” as a form of “reinforcement” or reward. Since the goal of CIT is to promote spontaneous hand use and not necessarily to develop skilled use. Amount of practice is the most important variable for motor skill learning (Schmidt and Lee. Sunderland and Tuke. goal-oriented behavior.. The learner must perform the task under conditions that require variations in speed. CIT protocols grew out of the behavioral model put forth by Taub and colleagues (1994) in which it is proposed that during the early post-injury phase (e. or any animal. Using this procedure he shaped pigeons to peck a ping-pong ball over a net. 1997. The design of CIT protocols is therefore directed towards the reversal of learned-non-use and the increase of spontaneous use of the hemiparetic limb in individuals post-stroke.. deafferentation). timing. If the learner is challenged to assess task conditions and to prepare and generate an appropriate response over practice trials. is that the learner be actively involved in solving the motor problem during practice (Lee and Maraj. use of the limb is suppressed when spontaneous attempts to move it are unsuccessful (negative reinforcement).. . and “capability”. 2003). the learner (i. In the context of CIT. 2005. Winstein and Prettyman.e. the probability is greater that an ability is acquired to adapt those responses to the ever-changing circumstances of daily life.g. 2005). By contrast. This conditioned response is “learned” and ultimately results in diminished spontaneous use.

intensity. • These progression techniques are recommended especially for the lower or beginning levels of skill acquisition. Task progression is learning based and depends on an analysis of underlying motor control deficits (strength. etc. or schema formation and the development of internal representations for action explain the increased functional use of the affected limb for purposeful. we review the literature and expand the discussion of two of Table 7.) . • The optimal duration. • The term “massed” practice is contrasted with “distributed” practice where within a bout of practice the distribution of practice-rest is manipulated. motor program. Practice variable Operant-conditioning training principles Lifting of learned suppression explains the increased use of the affected limb in real-world activities: • Learned-non-use develops from negative reinforcement during the acute stage where non-reinforced behavior becomes suppressed. should enhance learning within a motor-learning-based approach. where feedback is provided on progressively fewer trials. Table 7.): • Progression can be accomplished by manipulating a variety of variables depending on individual needs (e. ROM. Motor-learning training principles Skill acquisition. designing practice with frequent rewards should enhance learning within an operantconditioning-based approach.Conditions of task practice for individuals with neurologic impairments 93 If augmented feedback operates like positive reinforcement.g. Task progression Shaping of motor behavior is essential especially for patients with limited ability: • Shaping is based on the idea of successive approximations. • Task complexity and parameterization within a class of actions are important components of task progression.1 compares and contrasts training principles derived from each of these two learning models (operant conditioning and voluntary skill) as they apply to the choice of task practice variables to enhance recovery. part-whole task practice). Comparison of training principles between operant-conditioning and motor-learning-based interventions. In contrast. In “massed” practice. Amount and scheduling of practice Massed practice is essential for cortical re-organization and reversal of learned-non-use: • “Massed” practice in CIT is the term used to mean intense or extensive practice that is necessary to reverse learned-non-use and leads to cortical re-organization. speed.. or challenge (level of difficulty) of practice for enhancing functional recovery has not been determined. designing practice with a faded feedback schedule. In the remaining sections of this chapter. Physical practice is the most important variable for motor learning: • Practice that challenges the learner is motivating and optimal for learning-dependent cortical re-organization.1. this manifests as skill develops. volitional activities: • Automatic and implicit procedural knowledge develops with practice of motor tasks. there is little to no rest and performance decrements due to fatigue are generally not considered detrimental to learning. • Tasks are controlled more automatically and with less cognitive effort. adding or freeing degrees of freedom. • Guidelines for progression are performance based and not learning based. coordination. (Cont. if augmented feedback operates like post-response information that elicits cognitive processing and problem-solving. • Successful performance and positive reinforcement are necessary to lift the suppression allowing the behavior to be expressed in a real-world environment.

is provided by an external source. such as a trainer or therapist.5 Conditions of practice to promote functional recovery of motor skills Augmented feedback and explicit information It is well known that augmented feedback provided during or after trial completion can be manipulated to enhance motor learning. Role of errors Errors during performance are ignored: • Error feedback serves as negative reinforcement and is detrimental to the reversal of learned suppression of behavior. The development of skill through practice is by nature embedded into a meaningful and social context: • The choice of tasks to practice and the development of self-efficacy as performance improves are intertwined with this approach and are recognized mediators for self-management and maintenance after training ends. intrinsic feedback provided through the perceptual and sensory systems. Knowledge of results (KR) is one form of augmented feedback and is defined as “verbal (or verbalizable). the learner is able to evaluate performance based on internally generated. ROM: range of motion. Social-cognitive factors Behaviors are “elicited” in this model. (Cont. Motor-learning training principles Contextual variety enhances problem-solving and retention of skills: • The task practice schedule is designed to challenge the cognitive operations important for future capability in variable contexts. and provides error information that can be used in addition to the learner’s own intrinsic error signals. Winstein and Jill Campbell Stewart Table 7. Following a movement. augmented feedback and task scheduling. as they relate to motor skill acquisition in neurorehabilitation. Augmented feedback Constant and frequent feedback is necessary for optimal lifting of learned suppression: • The informational content of feedback is de-emphasized while reinforcement and encouragement are emphasized. KP) frequency and faded schedules that promote problem-solving and the development of internal error-detection capabilities are more beneficial for learning than constant and frequent feedback: • The informational content of feedback is emphasized and is distinct from the encouragement provided during practice. 7. • Movement problems are effectively solved partially through the provision of error information (feedback).1.. terminal (i. post-movement) feedback about the outcome of the movement in terms of the environmental goal” .e. no more than two sets of 10 trials of a given task should be practiced in a single day.94 Carolee J. KP: knowledge of performance. Errors during performance are beneficial to learning and therefore should be provided as information feedback to the performer: • Errors are viewed as information that can be useful for planning the next trial.) Operant-conditioning training principles Practice variability Diversity of tasks leads to a more generalized benefit of practice: • During shaping. These behaviors can be shaped through successive approximations during practice with positive reinforcement: • Collaboration with the patient for task selection or engagement for self-management and development of self-efficacy are not directly addressed in this model. • Errors are viewed as punishment that leads to avoidance of the behavior. Reduced augmented feedback (KR. these practice variables. Augmented feedback. in contrast.

1995). 1992. In essence. 100% KR performed better on a retention test than did the 50% KR group. it seems that there is something different about learning a complex task compared with a simple task. such as 50% (half of the trials) or 25% (one-quarter of the trials). Wulf and Schmidt. promotes the development of intrinsic error-detection capabilities. It may also be achieved by use of a faded schedule whereby an average relative frequency of 50% is obtained by providing more frequent KR during early practice (say 100%) and progressively reducing the frequency over trials (e. Guadagnoli and Lee. Wulf et al. 1992) except in one study where a reduced frequency KR schedule did not benefit either younger or older subjects (Wishart and Lee. therefore. 1997). In this case. patients must be able to perform tasks once they leave the sheltered rehabilitation setting. then we might imagine that the aggregate processing demands could be quite large for the learning of a complex task under conditions of reduced KR frequency. 1993. an optimal schedule of KR provides an opportunity for practice that attenuates dependence on the extrinsic KR.g. Goodwin et al. While several studies found no benefit of a decreased KR frequency on learning a linear positioning task (Sparrow and Summers. or when performance falls outside a pre-determined acceptable range. called bandwidth KR. Additionally. 1991). the processing demands may be too high resulting in . it is imperative for the learner to be able to perform a given task without augmented feedback as this is how tasks are performed in the “real world”. Why might reducing the frequency of augmented feedback benefit learning? KR is beneficial in that it provides useful information that leads to improved performance on the next trial and.. suggested that more frequent feedback may be needed when practicing a complex motor skill (Wulf and Shea.. Relative frequency of KR refers to the percentage of total practice trials for which KR is provided. 2005). 1999. it is yet unclear if such a KR schedule also benefits learning more complex real-world skills that may require several days to learn and involve multiple degrees of freedom (Wulf and Shea. If feedback is provided after every trial or at high relative frequencies though. p. a 50% relative frequency schedule may be achieved by providing KR on every other trial. 1984.. KR can be provided after every practice trial. where a summary of performance is provided after a specified number of trials.. 1992. This is an important point when discussing feedback in rehabilitation. In fact. The prescribed relative frequency or scheduling can be accomplished in different ways.Conditions of task practice for individuals with neurologic impairments 95 (Schmidt and Lee. Research that used summary KR. This benefit seen when KR is provided only after a percentage of practice trials has also been demonstrated in older. Schmidt. healthy adults (Behrman et al.. 1998. 1989. 1990. 2002). 2001). the group that practiced the task while receiving continuous. termed reduced relative frequency of KR. 2002). and allows active engagement in information processing activities required for future skillful action (Salmoni et al.. multiple studies have found a beneficial effect on the learning of other motor tasks in healthy young adults (Ho and Shea. 2002.. 325). retention test) and actually degrade learning. Lai and Shea. Conditions of practice that promote the development of intrinsic error-detection capabilities are important for self-maintenance and persistence of skilled performance in the future. Lee et al. Additionally. Swanson and Lee. Sparrow. facilitates learning of the motor task. 1993. Here we review the effect of reducing the relative frequency of KR as an example of how manipulating augmented feedback can impact motor skill learning. One hypothesis is that the cognitive processing demands may be inherently greater for the learning of a complex task (Wulf and Shea. Wulf et al. Winstein and Schmidt. If a reduced KR frequency schedule requires more processing by the learner compared to one with feedback after every trial.e. to 25%) (Winstein and Schmidt. 1990. 1990.. Therefore. For example. 1994. 1978. While a reduced KR frequency may benefit learning of relatively simple laboratory tasks. the learner may become dependent on the KR such that it can be detrimental to performance on trials without KR (i. 1994. Winstein et al.. 2004). after only a portion of trials. Schmidt and Lee. Vander Linden et al. (1998) found that reducing KR frequency did not benefit the learning of a complex ski simulation task.

Dempster. While their performance was not as accurate as age-matched controls. 1999). There is a great deal yet to be learned about the interaction of task complexity and augmented feedback scheduling to enhance motor learning. this research needs to be replicated and expanded to include other tasks. Donovan and Radosevich.1(a)). performance and learning was disrupted. The information provided. 1999). Brady. 2000). Pohl and Winstein. Several studies have demonstrated that individuals post-stroke have the ability to learn a new motor task (Platz et al. an arrangement that can persist for . This was not the case for age-matched control subjects who actually demonstrated better learning across days when explicit information was provided than when it was not. 1990. It is hoped that these ideas will invoke new approaches and hypotheses for rehabilitation science as researchers from multiple disciplines including psychologic and physiologic science collaborate to gain a better understanding of the neural correlates of motor learning (Miller and Keller. While the faded schedule of KR did not enhance learning.. Winstein and Jill Campbell Stewart diminished learning. 2000). In a massed practice schedule. 1996... Both control and stroke Participants that practiced the task under a faded feedback schedule (67% average KR frequency) condition demonstrated similar learning when compared to their peers who received KR after every trial (100% KR frequency). the subjects with stroke were able to demonstrate learning of the task as measured by a delayed retention test. this work in general suggests that there may be differences in the way in which motor skills are learned between individuals post-stroke and age-matched controls. 7. the subjects with stroke demonstrated very similar performance curves to control subjects when compared across feedback conditions. Winstein et al. 2004) for the learning of motor skills in healthy adults. While there is limited research about how these principles apply to individuals post-stroke. Additionally.96 Carolee J. Therefore. Further work is needed to better understand the benefits of augmented feedback for motor learning in individuals with central nervous system pathology. Optimal scheduling of to-be-learned items has been the subject of considerable behavioral research since early in the 20th century. 1994. (1999) study suggests that individuals with stroke benefit from feedback similarly to controls. Winstein et al. 1991. there is typically little to no time between presentations of the same task (Fig. it was not detrimental either. 2004) found that when individuals post-stroke were provided with explicit information during practice of an implicit lever task. Druckman and Bjork. Task scheduling Individuals post-stroke generally need to learn or re-learn numerous tasks during rehabilitation. 1999) and (2) a random task practice schedule is better than a blocked task practice schedule (for reviews see Magill and Hall. the inter-trial interval between task presentations is longer than in a massed schedule. 1996. the findings from these lines of research can be used to provide some guidance for clinicians and researchers as to the best way to structure practice for motor learning (Marley et al.. In a distributed practice schedule. Only one study to date has directly investigated the effect of reducing the relative frequency of KR on learning in individuals post-stroke. the results of this study suggest that the literature on relative frequency of KR with healthy control subjects may be applicable to individuals with stroke (Winstein et al. One of the most robust finding in this domain of study is the so-called “spacing effect” according to which distributed presentation of an item strongly increases the retention of learned material compared to massed presentations. While the Winstein et al. Although explicit prescriptive information about the movement strategy is distinctly different from post-response augmented feedback. Recent work that manipulated explicit instructions (Boyd and Winstein. Hanlon. may be processed in different ways after brain damage. The literature emphasizes two key principles of task scheduling: (1) spacing of trials is better than massing trials (for reviews see Lee and Genovese. 1999. including augmented feedback or explicit task information. 1988. (1999) used a lever task that required subjects to learn a series of elbow flexion–extension movements with specific amplitude and timing requirements using the less-involved UE.

found that a distributed practice schedule did not benefit learning of a discrete tapping task compared to a massed schedule. Wright and Shea. 1978). It is important to note that a random practice schedule also provides space between repeated trials of the same task. however. 1983. 412). Contextual interference (CI) is “the interference effects in performance and learning that arise from practicing one task in the context of other tasks” (Schmidt and Lee. others have suggested that a distributed practice schedule may not always be optimal and that boundary conditions likely exist related to task type. 1999). Examples of the micro-scheduling of practice for motor-learning studies. 1990. An alternative would be to insert other tasks within the vacant “space” so that multiple tasks could be practiced simultaneously. Shea et al. 2001). 1996. It is well accepted that a random practice schedule (Fig. p.. For example. overall task complexity.1(b)) provides greater CI than a blocked schedule and is generally thought to be better for learning motor skills in healthy adults (Shea and Morgan. Lee and Genovese (1989).1. a blocked schedule for the practice of three tasks would provide 0 intervening items between presentations of the same task. . T2: Task 2. (b) Practice of three different tasks for eight trials each in schedules with varying levels of contextual variety. would be extremely time consuming if the inter-trial interval contained only empty time. Distributing practice of several items during a rehabilitation session. (a) Practice of five trials of a single task in a massed and distributed schedule. 1956) to typing (Baddeley and Longman. and the length of the inter-trial interval (Donovan and Radosevich.Conditions of task practice for individuals with neurologic impairments 97 (a) Massed schedule Trial 1 Trial 2 Trial 3 Trial 4 Trial 5 Inter-trial interval Distributed schedule Trial 1 Trial 2 2s Trial 3 Trial 4 Trial 5 Inter-trial interval 20 s (b) Blocked schedule T1 T1 T1 T1 T1 T1 T1 T1 T2 T2 T2 T2 T2 T2 T2 T2 T3 T3 T3 T3 T3 T3 T3 T3 Serial schedule T1 T2 T3 T1 T2 T3 T1 T2 T3 T1 T2 T3 T1 T2 T3 T1 T2 T3 T1 T2 T3 T1 T2 T3 Random schedule (for each block of three trials) T1 T3 T2 T3 T2 T1 T1 T2 T3 T2 T1 T3 T2 T1 T3 T1 T3 T2 T2 T3 T1 T1 T2 T3 Figure 7.. dozens of seconds to weeks in duration. 1994. In addition. Sekiya et al. T1: Task 1. 7. however. and T3: Task 3. A benefit for distributed practice has been shown in a variety of motor tasks from pursuit rotor (Bourne and Archer. 1999. Lee and Magill. 1979.

because the functional task used was a complex fivestep sequential task that involved grasping and moving a cup. success of the task was only measured by the cup not being dropped. Winstein and Jill Campbell Stewart A random schedule. The skill level of the learner is another variable that may play a role in designing optimal practice schedules for learning. was equivalent in effect to that of a random schedule. and shoulder abduction) with the hemiparetic UE. However. This analysis suggests that it is the engagement in information processing surrounding task performance and not just the task performance itself that is critical for effective motor learning. In the blocked and random practice groups. In a blocked schedule. 2004). While there was no significant difference between the two practice groups for the number of trials to reach criterion (three consecutive successful trials). Lee and Magill (1983) showed that a serial schedule. the learner knows which item will be presented on the next trial. subjects post-stroke performed three different movements (wrist/finger extension. Subjects were assigned to either a blocked practice. Random practice was better for learning the easy version but not the more difficult version of the task. what is learned enables the individual to perform the task with skill effectively with differing speeds and directions and under a variety of environmental contexts. It has been suggested that novices may benefit from a blocked schedule while those who have more experience may benefit from a random schedule (Guadagnoli and Lee. In this case. It is not clear if random practice is always better for learning more difficult.. Therefore. a random schedule is thought to require greater attention and deeper processing (Shea and Zimny. 1994). and no kinematics or force measures were taken.98 Carolee J. or no practice control group. Brady. than a blocked schedule. though. Thus. a random practice schedule provides greater spacing. Recently. 2004). Some have supported this idea (Shea et al. 2002). the random practice group practiced additional movements with the hemiparetic UE between presentations of the criterion task giving subjects in that group overall more practice in moving the arm. Lee and Maraj. would provide a range from 0 to 4 intervening items between presentations of a single item. or number of intervening items.. A control group performed the same movements without stimulation. Lee and Magill. Therefore. thus confounding a precise interpretation of the results. In a study by Cauraugh and Kim (2003). After four sessions lasting 90 min each over a . it is hard to know which motor control parameters benefited from the random schedule. Applying a more difficult practice schedule to an already difficult task may make the processing demands too high for adequate learning (Wulf and Shea. the random group had a significantly greater number of successful trials on the 2. 1990) while others have not (Ollis et al. In a random schedule. Why might a random practice schedule be better for learning than a blocked practice schedule? One hypothesis is that the processing demands for learning are different for these two practice schedules. 1983. and preparing and generating a new solution with each trial. The predictability of the next task was not the critical factor in this study. Furthermore. but rather the process of determining the movement requirements. in comparison. real-world tasks (Wulf and Shea.and 7-day retention tests compared to the blocked group. Albaret and Thon (1998) found such an effect when studying the learning of a drawing task. the learner does not know which item will be presented next. 2005). random practice. This process required the learner to be more actively engaged in the practice session under random or serial task schedules compared with the blocked task schedule. elbow extension. some authors have questioned whether the CI effect generalizes to all tasks and conditions. this study provides some evidence that random practice may be more beneficial than blocked practice to improve function of the paretic limb in patients with stroke. Only two studies have examined the effect of practice schedules on neural recovery from stroke. movements were completed with a combination of active muscle activity and neuromuscular stimulation. 1985. 2002. Hanlon (1996) investigated the effect of practice schedules on learning a functional reaching task with the hemiparetic UE in individuals post-stroke. However. where the task schedule was predictable but not blocked.

enhance neurorecovery and rehabilitation. The 1997 call for “well-formulated investigations grounded in available learning theory and research” (Fuhrer and Keith. 7. More research is needed to determine if differences in motor learning exist for individuals with specific stroke locations and levels of severity. REFERENCES Albaret.. 9–24. which was more a force production task than a functional task (see Winstein et al. The effect of lesion location on motor skill learning is not well understood either. but one that warrants a careful. Differential effects of task complexity on contextual interference in a drawing task. 627–635. American Heart Association (2005). More importantly. the optimal practice schedule may need to be tailored differently to accommodate individuals with more severe motor impairments compared with those with less severe deficits. Some work has suggested that individuals with more severe motor impairments may not demonstrate the same degree of short-term performance change (Dancause et al. For example. subjects in both experimental groups performed better than controls on several behavioral measures but there was no difference in performance between the blocked and random groups. We have reviewed the literature relevant to a motor-learningtheory-based design of training that emphasizes the acquisition of skilled functional behaviors and contrasted this with an operant-conditioning approach that focuses on elicited behaviors and spontaneous use. D. For the purposes of this chapter. We are at an exciting time in rehabilitation medicine.A. B. (1978). Further research is needed to better determine the optimal conditions of practice for motor skill learning in individuals with neurologic impairments. J.. 1998. 2004) and did not require the demands of skill acquisition. ACKNOWLEDGEMENT The authors wish to thank Nicolas Schweighofer for valuable discussions of scientifically derived and optimal task practice schedules and funding support to CJW from the NIH. 21. Recent work has shown that if the primary locus of the stroke-affected area is the basal ganglia. theory-based analysis as we proceed to develop a scientific rationale for our interventions to promote recovery and rehabilitation.. concomitant motor control deficits. Dallas.H. we distinguish between exercise training and task-specific training designed for skill acquisition. Cirstea et al. in order to effectively incorporate motor-learning principles into rehabilitation treatments and to design effective protocols. lesion location. This is a relatively open area for additional research to better understand the relationship between stroke severity. The emergent principles of training from these two learning theories have tremendous implications for future developments in the area of neurorehabilitation. 2004). tremendous advances have been made in developing effective programs to . The lack of difference between groups practicing under different schedules is partially explained by the nature of the task. and Longman.Conditions of task practice for individuals with neurologic impairments 99 2-week period. and conditions of practice will need a concentrated and focused research program. and Thon. Heart Disease and Stroke Statistics – 2005 Update. 2001) as individuals with less severe symptoms. Acta Psychol. the interaction of stroke severity. 100. this is only a beginning. NS 45485 and the Foundation for Physical Therapy.J.M. Texas. However. 2002.. p. Ergonomics.6 Conclusions Over the past decade. Baddeley. 560) has only just begun to be addressed. The influence of length and frequency on training sessions on the rate of learning to type. A. American Heart Association. there is more difficulty using explicit information to benefit implicit motor learning than age-matched controls (Boyd and Winstein. (1998). We discussed the top-down model of rehabilitation that focuses on the skills necessary for rehabilitation. 2003) or learning (Pohl et al. Stroke severity and lesion location are important factors to consider when discussing motor learning in this population. and motor learning.

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2002). 2000. Balance performance is a very sensitive measure of health.4 billion by 2020. It may not be immediately obvious that these tasks also require active balance control and practice. The total cost of all fall injuries in people age 65 or older in the USA was over $20. In fact. standing on one leg. Given the high personal and economic cost of falls and the high incidence of balance problems in patients seen for rehabilitation. In addition..1 Why balance matters Introduction Consider riding a bicycle. In fact. This cost is expected to increase to $32.. standing quietly. such as stroke and Parkinson disease (PD). In fact. 2001). or walking along a narrow beam. and the falls that result.2 Balance control Basic terminology Balance. balance skills can be compromised by a variety of central neurologic pathologies. assessment. Next consider sitting on a stool. all of the tasks mentioned above and most other tasks that we perform on a daily basis require the ability to maintain balance. All of these tasks require active control of balance. Murphy.. damage or pathology to almost any part of the body may affect balance because it is a complex skill requiring many resources. Earhart1 and Fay B. 1996). Neurological Sciences Institute 8. more than onethird of community-dwelling elderly and 60% of nursing home residents fall each year (Hornbrook et al. although it is often not a very specific diagnostic indicator of particular diseases. as these tasks can often be performed without devoting attention specifically to the maintenance of an upright posture. complex skill for successful movement within our changing environments. Although all age groups are subject to falls. has both orientation and stability components.8 Balance training Gammon M. Fuller. the risk of falling increases exponentially with age (Samelson et al. a basic understanding of balance control. 1994. In order to successfully complete these tasks one may have to make a conscious effort to keep from falling and practice may be necessary to improve performance.2 billion in 1994 (Englander et al. are serious problems. However. and rehabilitation is essential for effective treatment. 103 . Horak2 1 Washington University School of Medicine. Whether consciously or more automatically controlled. 1992. Statistics on the incidence and cost of falls Loss of balance. lack of independence. balance is a key. as the elderly population grows. Although balance is generally viewed as a function of the cerebellum and the vestibular system. Hausdorff et al. 2000). or walking across the floor. 8.. Program in Physical Therapy and 2Oregon Health and Science University. and even death.. Falls are often the precursor to immobility. falls are the leading cause of death in people over 85 years and the leading cause of injuries in people over 65 years (Alexander et al. the incidence of falls in people with neurologic pathology such as PD may be more than double that of age-matched healthy subjects. a skill required to maintain upright posture. and by peripheral pathologies such as sensory loss or musculoskeletal injuries.

Horak (a) (b) CoM CoM CoM must be kept over the BoS. the CoM must be controlled both within and outside a changing BoS (Winter..1). 1994).. 1997. The boundaries of the region in which the CoM can be moved safely without changing the BoS are referred to as the limits of stability. For dynamic equilibrium. 1990). the visual environment. the environment. as well as the position. CoM refers to the point at which the entire mass of the body may be considered to be concentrated (Winter. and the next postural strategy modified BoS Figure 8. 1990).. Earhart and Fay B. the support surface. Successful accomplishment of the desired task depends on processing and integrating multiple sensory inputs to determine the relative orientation among body segments and body position relative to the environment. during unsupported stance. the BoS includes the combined area under both the assistive device and the feet (Fig. BoS is the region bounded by the points of contact between body segments and the support surface. For example. the model is changed. and internal representations.1. 2003). Postural stability.. This information is used to plan and execute movements that allow maintenance of balance during task performance. the limits of stability depend on the momentum. The body may be aligned using several references. Systems model of balance control Control of body orientation and stability results from complex interactions among the individual. For static equilibrium.104 Gammon M. Figure 8. A postural control strategy is selected to achieve the desired body orientation and a copy of the control strategy is fed to the internal models to yield estimated orientation and expected sensory afferent signals. Illustration of the CoM and BoS in normal standing (a) and when using an assistive device (b). is relayed to the internal model of body dynamics. or equilibrium. Orientation involves interpreting sensory information and using it to maintain the appropriate alignment of the body with respect to the environment and the task. involves controlling the center of body mass (CoM) relative to the base of support (BoS) to resist perturbations or allow functional movement. the BoS consists of an area under the base of foot support and when the subject is using an assistive device. These expected afferent signals are then compared to actual sensory afferent signals that result from the postural movement performed.2 shows a contemporary model of postural control (adapted from Merfeld et al. including gravity. and the task being performed. the central nervous system uses sensory inputs in combination with knowledge of biomechanical constraints to form internal models of body and sensory dynamics. Older models of postural control as parallel sensory reflexes (such as visual. such as during walking. During dynamic tasks such as locomotion or arising from a chair. or difference between expected and actual afferent signals. A sensory conflict. Mergner et al. In this model. the . 8. vestibular. of the body CoM (Pai et al. and proprioceptive righting responses) are no longer considered useful (Horak et al. 1993) that outlines how the process of selection and adaptation of balance responses may occur.

both of which are covered in more detail in the following sections. and . Abnormal perception of spatial orientation relative to the environment can skew the internal model of the body. such as proactive modifications in order to avoid or accommodate obstacles. and a basic understanding of these functional systems is necessary in order to diagnose balance disorders and design treatments Sensory integration and weighting Multiple sources of sensory information are required for postural stability and orientation (Fig. and somewhat stereotyped. drive change in the internal model of body dynamics. that focus specifically on the affected systems. and/or make it difficult to improve postural control based on prior experience. Two additional resources that are crucial for balance control are sensory strategies and movement strategies. This type of model explains how postural strategies can be rapid. See text for details (adapted from Merfeld et al. Disruptions of cognitive control may make balance difficult in dual-task situations where attention is divided. Dynamic control is essential for challenges to balance that occur during gait. although they are constantly being improved based on prior experience and knowledge of results.. Contemporary model of postural control that outlines how balance responses may be selected and adapted.Balance training 105 External disturbances Biological noise Actual orientation Efferent signals Body dynamics Sensory dynamics Sensory afferent signals Sensory conflict Efferent copy Internal model of body dynamics Estimated orientation Internal model of sensory dynamics Expected sensory afferent signals Control strategy Desired orientation Central nervous system Figure 8. Biomechanical constraints. 8. External. 8.2. 1993). play an important role in balance control. as well as self-initiated postural disturbances cause changes in afferent signals and these. Multiple resources required for postural stability and orientation Multiple resources are required for postural stability and orientation (Fig.3).. such as muscle strength and range of motion. Sensory contributions to balance control come from three major sensory systems: visual. too. resulting in implementation of a more efficient and effective postural control strategy to regain the desired orientation. such that estimated orientation more closely approaches actual orientation. as they can limit the strategies available for use. 2003).3). This model also assumes that sensory information is integrated by the nervous system to form an internal representation of the body and world that is used for both perception of postural orientation as well as for automatic control of posture (Mergner et al. vestibular.

3.g. somatosensory Postural stability and orientation Spatial orientation • Perception • Verticality • Gravity. This information can be used to determine the orientation of the body with respect to the environment and to adapt movements to meet environmental conditions. including the constant acceleration due to gravity. the otoliths are sensitive to changes in orientation (e. Forward motion of the neighboring car results in an illusion of self-motion backwards.106 Gammon M. As such.5 m away cannot be used to effectively control sway during quiet stance (Paulus et al. whereas yaw movements are detected by the horizontal canals. The visual system also detects relative motion of the self with respect to the environment. surfaces. as the nearer an object the greater angular displacement of its image on the retina with body movement. visual acuity. vision Movement strategies • Reactive • Anticipatory • Voluntary CoM movement Cognitive control • Attention • Learning Figure 8. such as during locomotion. Earhart and Fay B. avoiding an obstacle in one’s path during locomotion. Pitch (sagittal) and roll (frontal) movements of the head are detected by the anterior and posterior canals. somatosensory. Objects at about arm’s length away allow for more effective balance control than objects at a great distance. 2001). in contrast to the low-frequency sensitive otoliths that are suited to control static postural . the anterior and posterior semicircular canals are particularly important for control of postural sway. The system can detect both linear and rotational accelerations of the head in space. 1984) and sway increases for many subjects in the absence of vision (Romberg. vestibular. Chiari et al. objects in the environment. The influence that vision has on postural control varies with changes in lighting conditions. An example of this phenomenon that many of us have experienced is the sensation of movement that is briefly felt when sitting in a parked car as the neighboring car starts to move. Resources required for balance control. and the location and size of a visual stimulus within the visual field (Leibowitz et al.. vision can induce illusions of movement when the visual scene moves slowly with respect to a stationary individual. such as postural sway during standing or progression during locomotion. Horak Biomechanical constraints • Degrees of freedom • Range of motion • Strength • Limits of stability Control of dynamics • Gait and transfers • Proactive • Head/trunk in space • Obstacle avoidance Sensory strategies • Sensory integration • Sensory reweighting • Visual. the semicircular canals sense angular head accelerations. Objects greater than 2. As the visual system cannot differentiate self-motion from environmental motion. The otoliths sense all of the linear accelerations acting on the head. 1972). and detection of orientation and movement of. tilt) with respect to gravity and provide an important source of information for the perception of verticality.. for example. In contrast. The visual system allows recognition of. The semicircular canals are most sensitive to highfrequency head movements.. Since pitch and roll movements move the body CoM toward its limits of stability. The vestibular system is specialized for the control of postural orientation and balance (see Chapter 20 of Volume II). 1851.

and joint receptors. This important information comes from somatosensors. which moves independently from the body. which provides evidence of an increased weighting of visual information in conditions where the support surface is unstable or compliant (Soechting and Berthoz.. obviously an essential component of successful balance. However. movement of a visual surround has a stronger influence when the support surface is also moving. sensory reweighting occurs not only in response to the context in which a task in being performed. 1989. 1969. 1999). 2002). Dickstein et al. that are distributed throughout the body. Without vestibular and/or proprioceptive information to use in addition to the visual input. such as muscle spindles. Horak and Hlavacka. Thus. But information from each of these sources alone would not be sufficient to allow selection of an appropriate postural response. Lestienne et al. the nervous system can increase the weight placed on the intact sensory systems to compensate for the damage (Nashner et al. Balance strategies Postural movement strategies take advantage of body biomechanics to allow for effective and efficient .. Thus. This may explain why the use of a cane as a sensory substitution device. 1977. Golgi tendon organs. Mittelstaedt. For example. 1994). For example. 1985). if an image moves across the retina this could be interpreted as body movement with respect to the object being viewed or as movement of the object relative to a stationary body. even more powerful than the effects of vision (Jeka and Lackner. Marchand and Amblard.Balance training 107 alignment (Nashner. 1992). The processing and integration of information from the three systems. 2002). that same person will gradually increase dependence on vestibular information (and vision. without important somatosensory information from the neck and trunk. Nashner et al. vestibular. 1979. Peterka and Benolken. but also in response to injury to one of the sensory systems. these two systems do not provide direct information about body orientation in space. Sensory channel reweighting refers to the ability of the nervous system to modify the relative contributions of the three sensory systems to balance control based on the context in which balance is to be maintained.. For example.. 1984. as evidenced by the fact that stimulation of each of the three systems can induce body sway (Coats and Stoltz. if available) in proportion to the amplitude of random surface orientations (Peterka.. Horak et al. pressure receptors. cutaneous mechanoreceptors. 2001. the somatosensory system also provides information about the support surface and the forces exerted by the body against those surfaces. 1992). rather than as a mechanical support. and somatosensory systems all contribute to balance control. Recent studies have established that a healthy subject standing on a stable surface in a well-lit room relies primarily upon somatosensory information for postural orientation (Peterka and Benolken. Both the visual and the vestibular systems are located in the head. visual and vestibular information alone cannot help the nervous system distinguish between: (1) head movements on a stable body and head movements accompanied by movement of the body CoM that may result in postural instability and (2) forward head movements when the body CoM moves backward via hip flexion and forward head movements when the body CoM moves forward via ankle dorsiflexion. Hlavacka and Nijiokiktjien. When one of the sensory systems is damaged. cutaneous and deep mechanoreceptors on the soles of the feet are activated in relation to forces under the feet. Light haptic touch from a single finger on a stable support can also provide a powerful sensory reference. 1997. is so effective in improving balance and reducing falls in patients with sensory deficits (Jeka. In addition to relaying information about body configuration. 2002). 2001). relies on sensory integration and sensory channel reweighting (Peterka. 1982. Studies have shown that patients with loss of somatosensory or vestibular information can increase the sensitivity of their other senses for balance control and particularly benefit from substituting light touch for their missing sensory information for postural stability. In fact. the retinal slip signal cannot be successfully interpreted. It has been clear for some time that the visual. 1972.

1997). hip. Although postural strategies are rather stereotyped. 1982). calf muscles are activated to stabilize the body and prevent a forward fall during the pull (Cordo and Nashner. the ankle strategy. 1987. 8. or at the same time as.. consist of a continuum of strategies that may or may not involve changes in the BoS (Horak et al. Fixed support strategies are those where the BoS is not altered (Fig. For example. Anticipatory postural adjustments are dependent on predictive. Responses to external perturbations. Patients with injuries affecting the cerebellum or parts of frontal cortex may have poor control of anticipatory postural adjustments. Illustration of ankle. they are constantly being shaped. However. 1980). is generated in response to small perturbations experienced when standing Ankle (a) (b) Hip (c) Stepping (d) (e) (f) Figure 8. feedforward control.4. as the postural muscles are activated prior to. and stepping strategies used in response to backward (a–c) and lateral (d–f) perturbations (reprinted with permission from Horak and Shumway-Cook.4). sensory feedback control is important for postural responses to unexpected external perturbations. 1987). One fixed support strategy. Oddsson and Thorstensson. sensory feedback is not available to trigger anticipatory postural adjustments. which can be elicited by movement of the support surface or of the body. . Thus. prior to pulling on a handle to open a door. or adapted. Anticipatory postural adjustments are those that occur prior to a voluntary movement. the muscles that are the prime movers for the voluntary movement (Crenna et al.. based on prior experience and knowledge of results. Horak control of body CoM. These anticipatory postural adjustments are specific to each particular voluntary movement pattern and do not consist of simple stiffening of the body (Horak and Anderson. Earhart and Fay B.108 Gammon M. 1990).

. allowing upright orientation of the body during motion of the body CoM (Henry et al. Pathology Interruption or interference with normal processes and efforts to regain normal state Impairment Anatomic. Change in support strategies are those that involve an alteration in the BoS (Maki and McIlroy. 1997). the hip strategy. The ankle and hip strategies both have muscle activation latencies of 75–100 ms and represent the two extremes of the continuum of fixed support strategies.Balance training 109 on a firm. but they are not simply used as a last resort when fixed support strategies are unsuccessful (Maki and McIlroy.5) is a helpful model to use in approaching balance assessment. Assessment may identify the underlying pathology causing the balance problem (such as PD. resulting in hip torque that rotates the trunk opposite the legs to more rapidly move the body CoM (Runge et al. 1965). Another fixed support strategy. etc. physiologic.5. The hip strategy in response to forward or backward perturbations is characterized by proximal-to-distal activation of muscles.). For example. elderly subjects who are prone to falls or who fear falling are more likely to use a stepping or arm reaching strategy than a fixed support strategy. mental or emotional limit Strategy Methods or tactics used to accomplish tasks Disability Limitation in roles or tasks in sociocultural and physical environments Functional limitation Reduced capacity to perform a task or activity Figure 8. 1999). increasing the size of the BoS. the first step in balance rehabilitation. 1998). 1986). expectations based on prior experience. Use of a similar strategy in response to lateral perturbations involves hip abduction/adduction and loading/ unloading of the limbs.3 Assessment and treatment of balance disorders Framework/goal of assessment and treatment Nagi’s (1965) disablement scheme (Fig. 1998). 1997). . Use of a similar strategy that involves lateral flexion of the trunk in response to lateral perturbations involves activation of trunk paraspinal muscles (Henry et al. A second change in support strategy is to grasp a nearby object. and the environmental context in which the perturbation is experienced. Nagi’s disablement model (adapted from Nagi.. Different combinations of the ankle and hip strategies can be used depending on the characteristics of the perturbation. is generated in response to larger perturbations or perturbations experienced on support surfaces that do not allow use of ankle torque. wide surface (Horak and Nashner. vestibular loss. These strategies are more complex than the hip and ankle strategies in that they involve anticipatory unloading of the stepping leg and longer latencies than the ankle and hip strategies. Stepping is one example of a change in support strategy that is used for very large or fast perturbations.. 8. Use of the ankle strategy in response to forward or backward perturbations is characterized by distalto-proximal activation of muscles on the side of the body opposite the direction of sway with torque generated primarily around the ankles. 8.

voluntary movements. or both deteriorate significantly. A therapist must decide if the individual is using the most effective and efficient strategy possible given their particular impairments and pathology. Measures of sway during quiet stance are not necessarily good predictors of instability or fall risk for some neurologic conditions. Biomechanical constraints at the feet. Sensory organization is quantified by measuring increases in postural sway when visual and/or surface information is no longer providing adequate postural feedback (Nashner et al. The strategy level is located between the impairment and functional levels and represents the tactics or methods by which a subject accomplishes a task. and/or electromyography (EMG) to quantify sway. For example. and cognitive limitations (Fig. in anticipation of voluntary movements. one should consider the adaptation of these strategies to different environmental contexts. in PD sway is markedly reduced during stance in people who are actually quite unstable (Horak et al. motor coordination for static and dynamic tasks.. or by the push and release test (Horak et al. are particularly important. motion analysis. strength. The ultimate goal of assessment is to make a differential diagnosis of a postural disorder that allows for development of an intervention that is patient-specific and targets the particular impairments and functional limitations identified. Dynamic posturography is more effective than vestibulo-ocular reflex testing in identifying dizziness (Stewart et al.. Nagi’s disablement scheme does not include another level that therapists should consider in their assessment and treatment of balance and movement disorders. Horak but the clinician should be aware that diagnosis of pathology itself is not sufficient. gait. 1997). and sensory organization. body kinematics.. sensory orientation. and during voluntary movements of the whole body is also essential (Horak. In addition.110 Gammon M.. Assessment of a person’s ability to select and coordinate appropriate postural movement strategies in response to external perturbations. 1997 review). Responses to external perturbations may be evaluated by examining responses to a tug at the shoulders or hips. For example. and postural alignment during standing and sitting.. and difficulties with sensorimotor integration (Horak et al. 1997). If either the cognitive task or the balancing task.3). Earhart and Fay B. 2004). Reactions to movements of the support surface can discriminate among problems with force scaling. the use of an instrumented movable platform. 1992). flexibility. 1999). correlates with fall . 1997 or Monsell et al. reactions to movements of the support surface. and muscle activation patterns (see Horak et al. which provide the BoS for standing and walking. Motor coordination is also central to balance control. The same pathology may affect individuals quite differently. Biomechanical factors include range of motion. Balance assessment A complete assessment includes evaluation of both intrinsic and extrinsic factors that may influence balance. 8. strategy selection. the strategies by which individuals accomplish a functional task given their impairments. One means of quantifying postural control is through dynamic posturography. so an assessment must also identify specific impairments and functional limitations that stem from the pathology. Anticipatory postural adjustments may be examined by asking a patient to rapidly raise both arms to shoulder level or to place one foot on a step. 2002). this may suggest either that the balancing task has not become automatic or that the patient lacks sufficient attentional resources to safely and accurately perform both a cognitive and a balancing task (Woollacott and Shumway-Cook. how long does it take for a patient to use a hip strategy to balance with a narrow BoS or to take an effective compensatory step in response to a large perturbation? The effects of cognitive processing on postural control may be evaluated by asking subjects to perform a secondary cognitive task while they are also doing a balance task. Intrinsic factors that could limit balance ability include biomechanical factors. response latency.. sense of vertical.. For example. Posturography can be used to evaluate stance. therapists may ask a subject to count backwards from 100 in increments of 3 while they are walking or trying to stand on one foot. 1982).

Visual information is eliminated by closing the eyes or is rendered inaccurate by having the person wear a paper lantern over his head such that as the head moves the visual surround moves with it. People with somatosensory loss as a result of spinal cord injury.. despite the usefulness of dynamic posturography. a paper lantern. requires only a piece of foam. The eyes are closed in condition two. Illustration of the six conditions of the CTSIB (a). or other conditions have difficulty on condition two (Allison. and stroke. Figure 8.Balance training 111 history of elderly persons (Topp et al. and somatosensory) are available and accurate in condition one. The CTSIB has six different conditions in which the accuracy or availability of visual and somatosensory information is altered.6. 1982). These conditions test the ability to suppress inaccurate visual information and rely on other sources for balance control.6 shows the six CTSIB conditions. it is not always feasible to include dynamic posturography in a balance assessment. and some patients with vestibular pathology leading to increased visual dependence may have difficulty with these conditions. In condition four. Those with central nervous system (a) Sensory condition 1 (b) Fall 100 2 3 4 5 6 Vestibular loss pattern 50 0 Sway as % of maximum Visually dependent pattern 100 50 0 Sensory selection pattern 100 50 0 Surface dependent pattern Figure 8. modeled after a dynamic posturography sensory organization protocol (Nashner et al. 1988). the subject stands on foam to reduce the accuracy of somatosensory information from the feet and ankles. and a stopwatch. In condition five. As such.6 (adapted from Black et al. the eyes are closed and the person stands on the foam. In this case only vestibular information is accurate. and differentiates between diabetics with and without neuropathy (Simmons et al. lesions such as multiple sclerosis (MS). and sensory selection problems (black bars) are shown in (b) (adapted from Black et al. Figure 8. One inexpensive alternative for clinical assessment of sensory organization is the clinical test for sensory integration in balance (CTSIB) (ShumwayCook and Horak.. head injury. three and six. vestibular. All three senses (visual. it is expensive and requires sophisticated equipment. 1988) shows the patterns . For each condition. In the remaining conditions. OH) of medium density. subjects are asked to stand quietly for 30 s... peripheral neuropathy. 1995). Patterns of sway in healthy subjects (open bars) and subjects with vestibular loss. People with visual deficits may have difficulty with condition four. 1997). visual dependence. Not surprisingly. 1998).. Somatosensory information is altered by having the person stand on 4-in. 1986). people with vestibular loss have difficulty in condition five. the person wears the lantern on his head. thick Temper foam (Kees Goebel Medical Specialties. This test. However. leaving only vestibular and somatosensory information. Hamilton.

training of postural strategies. 2001). for example. elderly individuals who are taking psychoactive medications. 1997. it does not reduce. 1997). Shumway-Cook et al. Strength training of the leg muscles. Although Tai Chi improves balance and functional mobility. 2002).112 Gammon M. as improper or inadequate lighting can reduce the usefulness of visual inputs (Birge. 1998). Clinical assessment of sensory organization should also include evaluation of the person’s perceived limits of stability (by asking them to lean in all directions without moving their feet) and postural vertical (by assessing their standing and sitting postural alignment with respect to gravity with and without vision and on an unstable surface). 1990. Balance rehabilitation: approaches and efficacy Just as assessment of balance is multifactorial. 1995. Review of these balance instruments is beyond the scope of this chapter (see Allison. Taggart. but appears to increase. Patients with somatosensory loss in the feet show reduced limits of stability in standing whereas patients after some strokes or unilateral vestibular loss may show asymmetrical limits of stability (as well as a tilted postural verticality). reduced range of motion.. There are several ways that one can train motor strategies for balance. 1989). Zwick et al. 1993). Shumway-Cook et al. 1998. Nelson et al. 1995. a Chinese conditioning exercise known for its slow. 1997). It is important to recognize that people must balance in a variety of environments in the community and the home. Treatment of the musculoskeletal system is imperative to address balance constraints including weakness. Earhart and Fay B.. has a beneficial effect on balance. postural sway in stance (Wolf et al. Current clinical instruments have been developed to predict whether patients are at risk for falls rather than to determine the underlying reason for the balance problems. Many different approaches have been used to treat balance disorders... multidimensional exercise programs are more effective than generic exercises for improving balance (Shepard and Telian. and improper postural alignment. 2002 for review). For example. Balance assessment is complex because balance control is multifactorial. biofeedback. wet. can improve dynamic balance and walking speed (Fiatarone et al. scaling. Several studies have shown that Tai Chi training can improve balance (see Lan et al. or more than four medications. and appropriate selection and adaptation of motor strategies. there are many others. are twice as likely to fall when compared to those not taking these medications (Cumming.. Tai Chi reduces the risk of falls in the elderly (Li et al. such as aerobics and strength training. Increase of postural sway may indicate larger limits of stability. The most effective balance retraining programs are customized for the particular constraints on balance control in each individual patient (Tinetti et al. Tai Chi. Postural stability and strategies may be affected similarly whether a patient’s perceived or actual limits of stability are small or distorted. neuromuscular constraints must also be addressed. For example. balance-specific exercises. In conjunction with treatment of musculoskeletal constraints. Customized. do not improve balance or postural stability. Whitney et al.. and environmental modifications paired with education.. likely because subjects differ in their underlying balance problems (Lichtenstein et al. uneven. 2000. sensory organization training. Lighting can also greatly influence balance. reduced flexibility. In addition to the factors mentioned above. One should also consider the role of extrinsic factors in balance control. 1994). Other generalized exercise programs. Horak of sway in control subjects and patients with various sensory organization problems. relative timing of muscle activity.. postural responses should be practiced on a broad. for more information). These treatments should address problems with response latency. to promote the ankle strategy.... and cluttered surfaces and stairs. Extrinsic factors that may contribute to balance problems include slippery. including generalized exercise programs. 1994. which improves postural stability. so too is treatment of balance disorders. controlled movements. stable surface and movement at the ankles without movement at the hips or knees .

sensory prostheses are being developed that can reduce postural sway in subjects with vestibulopathy (Dozza et al. For those with complete loss of a sense. 1999). If. EMG biofeedback can also be used in balance rehabilitation. To promote the hip strategy. For subjects with excessive or unwanted postural muscle activity. a person is overly dependent on somatosensory inputs for balance control. the use of moving visual stimuli to create sensory conflict. called tactors. Following optokinetic stimulation. The stepping strategy can be encouraged by practicing unweighting of the stepping leg during gait initiation and moving the CoM outside the BoS. tactors on different parts of the torso vibrate or the subject hears tone changes correlated with body sway and direction. 1994). postural responses should be practiced on narrow surfaces where the ability to generate ankle torque is reduced. Virtual reality allows a person to interact with a complex and realistic environment in a manner that is safe and can be adapted to suit individual needs. thus challenging the subject to rely on somatosensory and vestibular information to remain upright and stable. 1992. They key to successful sensory organization training is to first identify which senses are being used effectively and which are not.. Optokinetic stimulation is particularly useful because nervous system adaptation to deficits is more efficient when the person must actively deal with complex and natural sensory conflicts. Several tools are available to assist with sensory retraining for balance control. 2002).. Whitney et al. 1994). is one such tool. 1988. 2002). Duckett . in press. and introduction of movement of the visual surround to create sensory conflict situations where the appropriate sense must be relied upon in order to maintain balance. the after-effects on postural stability are mild and short lived (Cobb and Nichols. this can be discouraged by practicing standing and walking on a variety of surfaces such as carpet. 1998. The devices consist of an accelerometer that provide signals used to estimate the fore/aft tilt angle of the subject. Wall and Weinberg. Recent work has also focused on promoting sensory substitution. and grass. visual biofeedback of muscle activity can be used to assist healthy people and people with neurologic injuries to relax overactive muscles (Poppen et al. Balance during dynamic gait exercise should also be practiced in a variety of environments. people with vestibular loss tend to rely heavily on visual inputs for balance control and as a result are unstable in situations where visual information is not accurate or is not available. Virtual reality can be used to induce movement of the visual environment relative to a stationary subject. Progressive reduction of information from the overused sense will promote increased utilization of the underused source(s) of information. Preliminary studies of virtual reality for balance training in subjects with traumatic brain injury and vestibular loss are promising (McComas and Sveistrup. as attention must be diverted to the secondary task rather than being focused on keeping balance (Woollacott and Shumway-Cook. on the other hand. As the subject leans forward. For example. another approach has been the use of prosthetic devices to provide information that would normally be provided by the impaired sensory system. sand.. 2002. Vitte et al. Sensory organization training based on the six conditions of the CTSIB is an effective means of rehabilitation (Hu and Woollacott.. gravel. This tilt estimate is fed into a digital controller which activates either a series of vibrotactile devices.Balance training 113 should be facilitated. that are in contact with the subject’s skin or a set of earphones that provides audio biofeedback. Visual over-dependence can be discouraged by provision of accurate and secure somatosensory inputs. Another means of inducing sensory conflicts is through the use of virtual reality. Use of a dual-task paradigm may also help to make balance a more automatic process. Although some subjects experience motion sickness as a result of virtual environment immersion.. For example. and then have the person practice balance tasks in contexts where sensory information is reduced or eliminated. 2003). 2003. Optokinetic stimulation. Cobb. patients with vestibular loss and presbyastasia demonstrate less postural sway (Sémont et al. gradual reduction of availability and complexity of visual inputs.

Despite their usefulness. 1997.. however. evidence suggests that improvements in quiet stance stability following biofeedback training do not translate to improvements in dynamic balance during gait (Winstein et al.. Furthermore. surface substantially stabilizes postural sway in healthy people and people with peripheral neuropathy or vestibular loss (Jeka. Most research indicates that postural instability in PD stems from insufficient and slow force production such that responses are not adequate to counteract Environment and education Just as assessment of balance must consider both intrinsic and extrinsic factors.. about the use of force platform biofeedback. the situations they should avoid or use caution in given their particular problems. and the measures they can take to make their environment safer. People with PD often have disordered postural alignment characterized by thoracic kyphosis and reduced lumbar lordosis accompanied by a narrow base of support. In fact. force platform biofeedback may not confer an added benefit (Walker et al.. Postural instability in PD frequently leads to gait difficulties and falls. too. 1997. 2003). Dickstein et al. using a rubber mat or a shower seat when bathing. Earhart and Fay B. 1996). Chong et al. For example. Muscles important for control of posture (such as the ankle strategy muscles) can also be activated with surface electrodes based on feedback from force sensors under the feet. 1997. so. however. 1999).. 1994). those using assistive devices need to practice allocating attention during walking with the device and may need to refrain from performing other tasks while walking. Postural responses to perturbations as well as anticipatory postural adjustments prior to a voluntary movement in patients with PD are normal in latency. assistive devices can increase the attentional demands associated with walking (Wright and Kemp. When used in conjunction with conventional balance rehabilitation. but reduced in amplitude with excessive muscle co-contraction (Horak et al. Measures to be taken include: removing throw rugs or securing them to the floor with double-sided tape. and people with peripheral neuropathy are less likely to fall while standing on an unstable surface when using a cane (Ashton-Miller et al. and a monitor that provides visual feedback about weight distribution during standing. People with PD show inflexibility of postural set as evidenced by difficulty modifying postural strategies based on environmental context (Bloem.. Nichols. must treatment of balance. 2001). Patients must be educated regarding the nature of their particular balance deficits. Simmons et al. all of which contribute to reduced limits of stability. 2001).. Force platform biofeedback is an effective means of reducing the number of falls in patients with peripheral neuropathy (Wu. Horak and Kramer. 1993. 1997). Both standard and quad canes reduce postural sway in people with hemiparesis (Milczarek et al. Chong et al. Another treatment option is to prescribe an assistive device. Force platform biofeedback systems consist of two force platforms. Laufer.. 2003). There is controversy.114 Gammon M. Sackley and Lincoln.. Modification of the home environment to reduce or eliminate fall hazards is advisable. 1996. using adequate lighting. such as a cane or a walker. 1989). patients with PD have difficulty suppressing unnecessary leg muscle activity in response to postural perturbations when sitting or when holding onto a stable support (Chong et al. 1997). and can be used to train a more symmetrical weight distribution and reduce postural sway during quiet stance following stroke (Lee et al. 2000). 1992. 2001). 1996. As such.. and installing handrails on stairways. Synthesis of principles: balance in PD Postural instability is one of the hallmark features of PD and often does not respond well to medications or surgical treatments that ameliorate other symptoms (McAuley. 1998). wearing supportive shoes with non-skid soles.. 1992) and prevent patients from effectively grabbing onto a stable support in response to external perturbation (Maki and McIlroy. Force platform biofeedback training is another methodology used to treat balance disorders. 1992. even light fingertip touch on a stable . a computer.

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If depolarization occurs with sufficient intensity and speed. University of Maryland School of Medicine and Spinal Cord Injury Service. USA 9. The number of nerve fibers activated during applied stimulation will be related to the amount of phase charge delivered with each pulse (Adams et al. 1974). Therefore for practical purposes. FES-stimulated muscles will change morphologically and physiologically. This phenomenon is associated with changes in vascular supply and increased fatigue resistance (Munsat et al. The term neuroprosthesis refers to devices that use electrical stimulation to activate the nervous system in order to perform a specific functional task. although NMES typically refers to using surface electrodes.. 2Department of Physical Therapy and Rehabilitation Science. Case Western Reserve University and FES Center of Excellence. or terminal motor nerve branches. The number and type of motor units activated depends on motor unit size. Similar to muscles undergoing voluntary exercise. 2002). depolarization of the axon will occur. There has been some literature on electrical stimulation of denervated muscle. Motor units are activated electrically by depolarization of motor axons. Hunter Peckham3 1 Department of Neurology and Rehabilitation. 1999. 1993).1 Introduction Functional electrical stimulation (FES).. Kernan Orthopaedics and Rehabilitation Hospital. Electrical current can directly depolarize muscle fibers. This chapter will examine both the therapeutic aspects of FES as well as the direct functional applications as it is applied to individuals with neurologic injury. The terms FES. Baltimore MD. the membrane will reach threshold and an action potential will fire and propagate bidirectionally. but the amount of current necessary for this to occur is considerably greater than that for depolarization of nerve axons (Crago et al. 1990). Gad Alon2 and P. USA and 3Department of Biomedical Engineering. depending on the intensity and frequency of stimulation.2 Mechanism of FES activation of nervous tissue Peripheral effects When a sufficiently strong external electric field is applied to a nerve via a pair of electrodes.. and the relative impedance of intervening tissues (Knaflitz et al. FES systems stimulate nerves. Baltimore MD. It is still not clear 119 . 1976).9 Functional electrical stimulation in neurorehabilitation Peter H. Cleveland. Cleveland VA Medical Center. Tetanic contraction can be achieved in denervated muscle so long as long duration and high amplitude stimulation is used via very large surface electrodes (Kern et al. Unlike the normal physiological recruitment order of motor units that follows the size principle. but clinical applicability remains controversial. not muscles. electrically induced recruitment order is neither reversed nor predictable. FNS. Type II glycolytic fibers will convert to Type I oxidative fibers over weeks to months. and NMES are often used interchangeably. University of Maryland School of Medicine. also known as functional neuromuscular stimulation (FNS) or neuromuscular electrical stimulation (NMES) is the method of applying safe levels of electric current to activate the damaged or disabled neuromuscular system.. the distance of each motor unit from the stimulating electrode. 9. Gorman1.. USA. OH.

These electrodes will be discussed separately. epimysial. Surface electrodes Surface electrodes vary in composition. Conduction through the entire electrode surface and the contact pressure should be as uniform as possible. Central nervous system effects Recent evidence affirms the rationale of applying NMES to paralyzed or paretic muscles in order modulate central nervous system (CNS) plasticity. which may be external or implanted. Most portable FES neuroprostheses are built around a microprocessor controller. Electronic stimulators are usually battery powered. For subject-controlled FES systems (i. Third.. As part of this ongoing adaptation process there seems to be competition among body segments for territorial representation in the sensorimotor cortex (Muellbacher et al. NMES treatment groups have shown at least a 50% improvement over controls in Fugl-Meyer (Chae et al. which may allow for software modification of the stimulator output. In open loop control. (2003) and Smith et al. how much FES “exercise” is adequate to achieve fiber changes and allow for functional use. and configuration.120 Peter H. Non-uniformity of the conductive medium can generate loci of high current density that can cause discomfort. percutaneous intramuscular. etc. the electrical output of the FES system is not dependent on the muscular force or joint movement produced by the stimulation.3 Components of FES systems FES systems typically consist of three major components. Second. Cabling or other technologies such as radio-frequency coupled telemetry allow for communication between these three components. 2003) in various populations. In closed loop control. and nerve cuff electrodes. Different types that have been used include surface. A potential role for NMES in promoting recovery following damage to the brain is derived from the hypothesis of territorial competition. control can come in the form of switches. (2003) have presented evidence of increased excitability in the contralateral hemisphere following excitation of selected peripheral nerves of both stroke survivors and healthy subjects (see Volume I. implantable intramuscular. there are electrodes that allow for interface between the stimulator and . thus helping those segments compete for territorial representation. Artificial alteration of afferent inputs can be achieved with NMES via amplification and sustaining of afferent vollies from the more deprived distal segments. or even burns. switches.. The hypothesis is based on evidence that the cortical representation of body segments is continuously modulated in response to activity. NMES induces transmission of afferent inputs along sensory pathways originating from both muscular and non-contractile structures. voice activated controls. (2004) Han et al. and skill acquisition. Gorman et al. inactivity. Subject control of an FES system can be either “open loop” or “closed loop”.. joysticks.. sip and puff devices. Kimberley et al. Electrodes provide the interface between the electrical stimulator and the nervous system. Channels can be activated sequentially or in unison to allow for orchestration of complex movements. and upper limb advanced distributed learning tests (Popovic et al. 1999). 1998) action research arm (ARA) test scores (Powell et al. 9. 1991). there is a control mechanism. joint position sensors. Control systems for therapist-operated FES systems consist of dials and switches.. Chapters 6. First. 14 and 15). neuroprostheses). there is an electronic stimulator. 2002). real time information on muscle force and/or joint position or movement is fed back into the FES system to allow for modification of its output (Crago et al. the nervous system. skin irritation.. electromyography (EMG) electrodes. Stimulators range in sophistication and number of channels. Electrode materials that dominate in clinical practice are carbon–silicon and stainless steel or silver fibers–fabric mesh. buttons.e. size.. The number of stimulator channels can vary with the application.

1996. Electrodes that travel across the skin to insert into muscle are percutaneous intramuscular electrodes. nerve cuff. and bipolar epimysial electrodes. Small muscles require considerably smaller electrode sizes than larger muscles. There are also implantable intramuscular electrodes that are more robust than the percutaneous versions. 1996). They typically have a conductive metallic alloy core or disc and a surrounding silicone elastomer skirt. Their long-term survival has not been as great as that for implanted electrodes (Memberg et al. Both are likely to change over time and with repeated electrode reuse. Burridge et al.1. Epimysial electrodes are surgically sewn onto the epimysial surface of muscles. the increased size is relative to the contractile mass of the target muscle. Alon et al. intramuscular.Functional electrical stimulation in neurorehabilitation 121 Electrode size should be considered a major factor that can help minimize electrode–skin interface impedance and current density. Implanted cables link the stimulator and the stimulating electrodes and are complex in design to Figure 9. Implantable electrodes Implantable electrodes fall into several subcategories.. mainly because of their thicker lead wires. Clinicians must be aware of the need to continually ascertain the adequacy of the surface electrode–skin interface. 1985. However. Larger electrode size enables stronger muscle force generation and less perceived stimulation discomfort (Alon. 1994. 1997b). . Nerve cuff electrodes directly stimulate nerves by surrounding them circumferentially. The following electrodes are pictured (from left to right): monopolar epimysial. and have a barbed end to ensure stability once inside the muscle.. Percutaneous electrodes have been used primarily in developmental research protocols or temporary applications. Kantor et al.. Failure to do so may jeopardize treatment effectiveness. They are usually inserted using a hypodermic needle. The relationship between electrode size and impedance is non-linear.. increase skin irritation and possibly cause skin burns (Hasan et al.. Implantable electrodes used in FES applications. 1993). Actual effective size of surface electrodes is not determined by simply measuring the diameter of the electrode because the effective size is influenced by the uniformity of conduction and pressure.

Frijns et al. Increasing pulse rate is known to cause a greater degree of muscle fatigue during tetanic contractions (Binder-Macleod and Guerin. minimize skin–electrode interface impedance. Laufer et al. 1984. 1988.4 Stimulation parameters There are several important parameters that can be adjusted during FES application. Cestari et al.. 9.122 Peter H. The product of the amplitude and pulse duration represents the net charge injected into the tissue. and modulations (Baker et al. Monophasic stimulation is also less desirable for longterm implanted FES use. Individual parameters will be discussed below. For any biphasic waveform there are two peaks.. In contrast. biphasic waveforms are characterized by very rapid reversal of stimulus polarity. Also termed pulse width. 1975. 1997. Bennie et al. There is considerable inter-subject variability with regard to fusion frequency. Gold and Shorofsky. Pulse rate is also associated with stimulation comfort during tetanic contractions (Naaman et al. Mulcahey et al. duration. 2003). Knowing the root mean squared (RMS) current is important in order to determine the safety of stimulation because current density (RMS current divided by electrode surface area) may be closely associated with the risk of skin irritation and the risk . Phase duration 9. This relationship is important to be aware of when attempting gradual proportional recruitment of motor strength. 2000)..1.. frequency. 1985. Constant current waveforms are used primarily (although not exclusively) in FES systems. 1981). Stimulus waveform Stimulators with a pulsatile current (PC) output typically deliver either monophasic or biphasic waveforms. 2002). 1990. Wesselink et al. Binder-Macleod and Lee... 2001. Alon et al... For most applications it is desirable to have a tetanic contraction of muscle.. Gorman et al.. 1994a.. The absence of charged ion movement makes the symmetric biphasic waveform preferred because it minimizes skin irritation and is perceived as being more comfortable (Baker et al. 1996). 1994... phase duration indicates how long each phase lasts. amplitude. Photographs of several implanted electrodes are found in Fig. Waveforms can be either constant voltage or constant current (Kantor et al. Panescu et al. of burns (Alon. Kantor et al. since it can cause electrode and tissue breakdown (Mortimer. 1978. 1993). spatial recruitment of additional motor units will occur. Peak and root mean square current amplitude Peak current refers to the highest amplitude of each phase. It usually ranges between 5 and 400 s. 1995. 1996. b. charge. Monophasic waveforms produce unidirectional current flow and thus cause a net movement of charged ions across the electrode/tissue interface. The charge injected and the force output of the muscle being stimulated is related by an S-shaped curve within which a portion of the curve has a very high gain.. Pulse rate (frequency) Pulse rate or frequency determines the rate of nerve depolarization. 1994. Faster pulse rates (15–25 pps) induce incomplete tetanic contractions and pulse rates higher than 45–50 pps typically induce fused tetanic contraction. 1988. Baker et al. 1999). including pulse waveform. 1994. and reduce the chance of electrochemical skin irritation (the latter in the case of monophasic waveforms only) (Rollman. Henkin et al. As either pulse amplitude or duration is increased above threshold.. withstand bending stresses and the body’s saline environment.. Short durations minimize the stimulation discomfort. 1999. 1994. A pulse rate that ranges between 1 and 10 pulses per second (pps) induces twitch contractions of skeletal muscles. Alon et al. Increasing pulse frequency provides for temporal summation of force output. Friedli and Meyer. Iggo.

more nerve fibers are excited leading to stronger perception (sensory excitation) and stronger muscle contraction (Fig. Modulation of the inter-pulse interval simultaneously modulates pulse (rate) frequency. and edema. Alon et al. The option of interrupted pulses is mandatory in most neurorehabilitation clinical applications. 1993. pain.88481 2. loss of motor control. As the amount of phase charge increases. 1994). One is termed interpulse interval.. The greater the duty cycle. A number of clinical .5 Applications of FES systems Management of musculoskeletal impairments Impairments that dominate the difficulties in neurorehabilitation of CNS mediated paralysis/paresis are muscle weakness/atrophy. The perception of discomfort was determined by a visual-analog scale from 0% to 100%. Phase charge has been closely associated with the ability of a stimulus to depolarize the nerve membrane and initiate action potential propagation (Gracanin and Trnkoczy.. limited passive and active joint range of motion. Each stimulation program for different clinical applications is likely to require somewhat different contraction (on) and relaxation (off ) times. Galea..2. 1999. the tradeoff as stimulating frequency is increased (in order to obtain a smoother contraction) is more rapid muscle fatigue.. 1994). spasticity. 20 Perception 25 30 35 40 Russ and Binder-Macleod. Russ and Binder-Macleod.31706 * ln(X) Figure 9. Having a burst of three pulses decreases the amplitude of peak current at a given level of excitation while concurrently causing a threefold increase in RMS current amplitude compared to a single biphasic pulse (Kantor et al. Vanderthommen et al..Functional electrical stimulation in neurorehabilitation 123 Data 14 12 10 Phase charge 8 6 4 2 0 2 0 5 10 15 Y 3. the more profound the problem with muscle fatigue. 9. 1983. Consequently the use of burst of pulses can be justified only if it makes the stimulation more comfortable. 2000). Binder-Macleod and colleagues identified a pattern of modulation termed catch-like property of human muscle where manipulation of the inter-pulse 9. Kantor et al. the second “burst of pulses” and the third “interrupted pulses” (or “ON and OFF” modes).2) (Adams et al. Phase charge (charge per phase) Phase charge is defined as the current-time integral over the phase duration period. 1996. intervals resulted in greater force production and less muscle fatigue compared to using constant pulse rate (Binder-Macleod and Lee. 2001). 1975. Logarithmic relationship between phase charge and perception of stimulus discomfort in a single healthy volunteer. also known as the duty cycle. 1999). For FES. since the time of rest is reduced. Stimulus time modulations Three basic modulations are common in commercially available stimulators.

Alon et al. The second approach elicits muscle contraction in the antagonist muscle group for strengthening and simultaneous stretch of the spastic muscles.. Chae et al. 2005).. 1998.. Kimberley et al. 2002. see Volume II. Alon et al. Chantraine et al. 1994. Berner et al. Alon et al. 2000.. Gorman et al. More recent clinical trials have combined the NMES with task-specific training of the paretic upper limb (Alon.. 1998. Most studies that tested true upper limb function and not just impairments enrolled only patients with chronic stroke. This training is insufficient to yield meaningful reduction if the NMES is delayed for 6–12 months post-subluxation (Wang et al. 2004)..7–1 notch on the 0–5 Ashworth scale. Recent studies have begun to test the contribution of NMES particularly to hand function (Cauraugh et al. 1998. Alon et al. Four clinical investigations synchronized clearly described task-specific activities with stimulation. 2003. 2004). 1994. (2003) recently used a comprehensive test battery that included many ADLs that depend on the upper limb collectively termed upper extremity functioning test (UEFT) as well as hand drawing test and patients testimonial statements regarding reduced upper extremity motor activity long (MAL) tests. Upper limb function in hemiparesis The value of NMES to the training of upper limb function remains controversial. 2002.. Alon and Ring. 2003a. Pandyan et al. 2003a. 2002. 1994. Popovic et al.. 2000). For additional information on the mechanisms and management of spasticity.... (Faghri et al. The first approach uses sensory stimulation over the spastic muscle group. 2003. c). 2003. c.124 Peter H. 2003). Hazlewood et al. Francisco et al. Chapter 36 on stroke rehabilitation). Cauraugh and Kim... Cauraugh et al. 2004. 2003. Diversity of training programs and the delay of training initiation have contributed to the reluctance of the clinical community to accept FES as a valuable intervention. It should be noted that these studies used reduction of subluxation as an outcome and not upper limb functional activities. 1999). b. however. Cauraugh and Kim. 1999. 1999. The third. Ring et al. Linn et al. Popovic et al. All three approaches have been statistically equally beneficial.. The authors added a cautionary note Spasticity Over 50 clinical studies are published on the application of stimulation for modification of spasticity.. Improved functional ability was limited to improvement in performance speed or increasing number of blocks transferred but not re-learning of hand function or ability lost due to paralysis. most recent approach has been to stimulate alternately both agonists and antagonists (Alon et al... a problem in 20–40% of stroke survivors (see Volume II. b. Powell et al. 2002. 2003a. Many patients are likely to experience a long-term reduction in spasticity of about 0. 2003... Wang et al. Outcome measures used in hand function evaluation vary considerably. 1997. Significant improvement in motor control as documented by Fugl-Meyer score or EMG has been reported by a number of investigators (Faghri et al. 1999. studies in chronic stroke have demonstrated that a daily or three times per week stimulation program over 3–6 weeks strengthens the stimulated muscles and restores some degree of active and passive range of motion of the mobilized joints (Smith. Three approaches have been used.. c. Cauraugh and colleagues only use the box and blocks test while others also use the Jebsen-Taylor and the nine-hole peg (Alon and Ring. Alon et al. Cauraugh and Kim. Such synchronization resulted in upper limb functional improvement in 70–80% of participants (Alon and Ring... a rather modest effect that may not justify prescribing NMES for the sole purpose of spasticity management. Powell et al. 2000).. 2003). Kimberley et al. 1990.. 1998. Stroke Shoulder subluxation Four clinical trials have been performed investigating whether early initiation of NMES could minimize .. shoulder subluxation. 2003. Chapter 17. b. The impairments of subluxation and shoulder pain can be minimized in the majority of patients while improving passive joint range and volitional deltoid activation after 4–6 weeks of training. 2003. 2000.

These applications will be discussed separately. gait velocity improved 36% and cadence by 19% (Alon and Ring. especially in those with lesions above T5. Walking speed after the training period without the stimulator only improves 10–14% if the stimulation was limited to the dorsiflexors. Ambulation in hemiparesis Gait performance has been enhanced by FES during ambulation (Malezic et al. Some subjects can train with FES ergometry up to a similar aerobic metabolic rate (measured by peak VO2) as those achieved in the able-bodied population (Glaser. The stimulation is typically synchronized with the gait cycle. so that the dorsiflexors are active during the swing phase. Inc. Some systems also include the capacity for simultaneous voluntary arm crank exercise by paraplegics. The most common target muscle for stimulation has been the dorsiflexors of hemiparetic patients. thereby permitting hybrid exercise. and electroejaculation. Training involved increasing speed of ambulation as well as stair climbing and walking on different terrains. walking. 1987). 1991). hand grasp. FL). 2003). respiratory assist. Table 9. There are limits to the cardiovascular benefits of FES ergometry. The most common commercially available ergometer is the ERGYS Clinical Rehabilitation System (Therapeutic Technologies. Electrical exercise also increases peripheral venous return and fibrinolysis. Therapeutic exercise The most common system for lower extremity FES exercise is the bicycle ergometer (Glenn and Phelps. bladder and bowel function. however (Burridge et al. 1997b.. 1985).. 2005). The main outcome measures that improve after 4–5 months of use are walking speed (20–27%) and physiological cost index (PCI).. Ergys) Yes (Avery Mark IV) (IDE: Atrotech) Yes (Freehand and Handmaster) No Yes (Parastep) Yes (Vocare) Yes that while the gains of hand functions were both statistically and clinically meaningful.1 lists the applications and indicates for each one the current stage of development. however. Cardiac capacity and muscle oxidative capacity (see Volume II. Yan et al. which represents an improvement from the results with dorsiflexors stimulation alone. which in turn 9.. In those patients. there is loss of supraspinal sympathetic control. Tampa.6 Spinal cord injury Functional uses for FES after spinal cord injury (SCI) include applications in standing. Chapter 21) have both been shown to improve with FES ergometry. Clinical research Type of system Cardiovascular exercise Breathing assist Hand grasp Standing Walking Bladder/bowel Electroejaculation √ √ √ Basic research Feasibility √ √ √ √ √ √ Completed √ Completed √ √ Multicenter FDA regulatory approval Yes (Regys.. . This computer controlled ergometer uses six channels and surface electrodes to sequentially stimulate quadriceps. the vast majority of patients improve the time of performance but did not re-learn functional ability. hamstrings and glutei bilaterally. 1999. Development stages of FES systems for use in spinal cord injury. Using this paradigm. Taylor et al.1.Functional electrical stimulation in neurorehabilitation 125 Table 9. Each of these technologies have been developed and implemented to various degrees over the course of the past few decades. multisegment stimulation of both plantar flexors and dorsiflexors has been used in stroke.

Most patients using electrophrenic respiration maintain their tracheostomy stoma to be used at night and for suctioning. slow-twitch Type I fibers (Oda et al. 1981). limits the body’s ability to increase heart rate. four have sufficient ventilation for breathing without other aids (e. and the leads are tunneled through the third or fourth inter-costal space. Breathing assistance in high tetraplegia Phrenic nerve pacing was developed in the early 1960s by Glenn and colleagues (Glenn and Phelps. and then is reduced to 6–12 breaths/min later on. The implanted components of neuroprosthetic systems for phrenic nerve pacing consist of nerve electrodes placed around or adjacent to the phrenic nerves. The possible complications of phrenic nerve pacing include infection. amplitude. 2001). The external components are the radio-frequency transmitter and the antenna. The Atrotech has a more sophisticated four-pole electrode system. and MedImplant. All of these systems allow for changes in stimulus frequency. Recent advances for respiratory pacing have been contributed by the work of DiMarco and colleagues.. Atrotech. The Avery and Atrotech devices are available in the USA. as well as to reduce anxiety and the volume of respiratory secretions. and is the one most widely used. Low-frequency stimulation (7–12 Hz) is required to help convert the diaphragm to primarily oxidative. The receiver is placed in a subcutaneous pocket on the anterior chest wall. There are currently three manufactures of these devices: Avery. although many of them can plug the sites during the day. the electrodes are placed on or around the phrenic nerve in the neck or thorax. stroke volume and cardiac output (Ragnarsson. which is thought to reduce the chance for fatigue. This technique significantly reduces the surgical procedure required. respirator) for many hours per day. 1997). the bone mineral density reverted to pre-training levels (Mohr et al. upper airway obstruction. Electrodes are placed bilaterally near the motor points to activate the muscles simultaneously for inspiration. The Atrotech system is available under an FDA Investigational Device Exemption. and cabling. bone mineral density of the proximal tibia increased 10%. and reduce required nursing care in ventilator dependent tetraplegic individuals (DiMarco. 3 days per week. speech. and technical malfunctions. reduction in ventilation due to altered respiratory system mechanics. 1985).. and overall health. Stimulation is initiated approximately 2 weeks post-operatively. In one study of 10 spinal cord injured individuals who underwent 12 months of FES cycling 30 min per day. Gorman et al. improve the level of comfort. Subjects also report the return of smell as a result of the procedure (DiMarco.. FES for standing and walking in paraplegia There have been over 24 centers worldwide that have participated over the years in investigation of the . 2001). Evidence is mixed as to whether FES ergometry can retard or reverse the osteoporosis seen in patients with SCI. after a further 6 months of exercise but at a frequency of only one session per week. and train rate. 1981). mechanical injury to the phrenic nerve.g. In appropriate candidates (see Volume II. phrenic nerve pacing has the potential to improve mobility. radio-frequency receivers. Surgically. Unfortunately. expiration is due to passive relaxation. who have demonstrated the use of a minimally invasive approach for introducing electrodes into the diaphragm with a laparoscope. Reconditioning is then required to improve the fatigue resistance of the diaphragm. Confirmation of phrenic nerve function via nerve conduction studies or observation of diaphragm movement under fluoroscopy is necessary before considering phrenic nerve stimulation and diaphragmatic pacing (MacLean and Mattioni. 1991). Of five subjects who have been entered into a clinical protocol and are through the exercise period.126 Peter H. Chapter 37 on Rehabilitation in Spinal Cord Injury). The respiratory rate usually lies within 8–14 breaths/min during initiation of therapy. The Avery device has received pre-market approval by the food and drug administration (FDA).

bowel and bladder function. the Parastep system is a four. patients with injuries between T4 and T12 with upper body strength and stability as well as intact lower motor neurons are appropriate candidates for consideration.Functional electrical stimulation in neurorehabilitation 127 use of FES for lower extremity standing and walking in paraplegia (Peckham. Several different approaches have been used in helping paraplegics walk.or six-channel surface stimulation device for ambulation with the aide of a walker.. The patient controls the gait with switches integrated into a rolling walker. 1990). although higher-level patients have been involved in some protocols. and improved transfer between surfaces. Implantable lower extremity FES has also been developed. such as standing. rotator cuff. All of the above mentioned pure FES systems require use of a walker for stability and safety. The energy expenditures required for continuous FES walking using any system is at least twice (if not more) than that for normal upright ambulation. It is not anticipated that FES for walking in paraplegia will replace the wheelchair as the primary mobility aide. transfer assistance. Implanted systems. The considerable effort required for maintenance of percutaneous electrodes has made that type of system impractical for widespread use. Those with C4 level injury have also participated in limited laboratory-based investigations of FES systems (Nathan and Ohry. deltoid. These individuals have adequate voluntary strength in the proximal muscles (i.. Future directions for lower extremity FES for paraplegia would be to achieve more modest goals than originally envisioned. 1992). biceps) to move their hand in a functional space. 1987. and possibly short distance (e.g. thereby increasing independence in performance of functional tasks.. Tetraplegic hand grasp systems have focused on the C5 and C6 level SCI patient populations. use both mechanical bracing and surface FES. home) mobility. In general. 1996). however. The muscles usually stimulated to provide for standing function are the quadriceps and hip extensors. 1997). hold and release. Specifically. also employ trunk extension for greater postural stability (Triolo et al. 1996). such as the reciprocating gait orthosis (RGO) originally developed at Louisiana State University. Hybrid approaches. 1998). the Centers for Medicare and Medicaid Services (CMS) started to provide insurance coverage for the purchase of and training with the Parastep. Standing alone is a goal of some systems. FES hip extension on one side provides contralateral leg swing through the RGO mechanism (Solomonow et al. Peckham and Creasey. Made by Sigmetics Inc. FES for hand grasp and release Technology for the restoration of hand function in tetraplegic individuals has been under development for over three decades (Billian and Gorman. The Parastep System and other similar systems have been used by paraplegics not only for functional standing and walking but also for aerobic exercise (Graupe and Kohn. The percutaneous system developed in Cleveland used up to 48 different electrodes to provide reciprocal gait.e. and modified at Wright State University. The potential physiologic benefits of standing include a beneficial effect on digestion.. There are also functional standing goals of reaching for high objects and face-to-face interaction with other people. which provide activation of eight separate muscle groups.. In April. but the results of these studies have been limited. The Parastep system uses the triple-flexion response elicited by peroneal nerve stimulation as well as knee and hip extensor surface stimulation to construct the gait cycle.. . There is one FDA approved class III surface FES walking system available for use in the USA.. 2001). Patients injured at the C7 and lower levels have multiple voluntarily active forearm muscles which can be used to motor new functions by means of tendon transfer surgery (Keith et al. The objective of the use of FES in hands of tetraplegic individuals is to restore grasp. 1992) and has now entered the clinical environment (Peckham et al. 2003. The electronic controller is housed in a cassette-sized box mounted on the patient’s belt. which provide for knee and hip extension and joint stability in a locked position in a similar biomechanical way as do knee-ankle-foot orthoses. Implantable eight-channel systems with the more limited goals of standing and transfer are also under investigation.

. 1997). On the left of the diagram are the implanted components. All of the patients had one or more concurrent surgical procedures to augment hand function. which is located in a surgical pocket in the upper chest. is through radiofrequency coupling.. and in some cases a sensory electrode to provide a form of sensory feedback. epimysial electrodes. a rechargeable programmable external control unit (ECU) and an implantable eight-channel stimulator/receiver attached via flexible wires to epimysial disc electrodes (Fig. The joint position transducer is typically mounted on the skin from sternum to contralateral shoulder or across the ipsilateral wrist.3. which include a shoulder position External control unit controller incorporating the device’s on/off switch. A grasp and release test was used to evaluate each subject’s ability to grasp. move. electrode leads. The system can be programmed through a personal computer interface to individualize the grasps as well as the shoulder control (Kilgore et al. .128 Peter H. Summary pinch force measurements with and without the neuroprosthesis are shown in Fig. On the right are the external components of the neuroprosthesis. 9. which include the implant stimulator. Communication between the ECU and the implantable stimulator. Implanted components Sensor feedback electrode Implantable receiver stimulator In-line connectors External components Transmitting coil Shoulder controller Figure 9. Freehand system The Freehand System® consists of an external joint position transducer/controller. One of them is a surface system and one is implanted. The small improvement seen post-operatively with the neuroprosthesis turned off can be attributed to tendon synchronization. These devices will be discussed separately. Not shown are implantable intramuscular electrodes which are an available option. Gorman et al.3). 2001). This is helpful in handling either large objects or small objects respectively. The number of completed moves in 30 s achieved by subjects increased significantly for the heavier objects with the neuroprosthesis. and release six standardized objects. Components of an implantable upper extremity neuroprosthesis. 9. The current system is intended to provide unilateral hand grasp only. All patients realized some improvement in pinch force measurement in at least one grasp pattern with the neuroprosthesis. Electrodes Triceps electrode PC Laptop er mm progra Two commercially available FDA approved upper extremity neuroprostheses have been developed. Sixty-one C5 or C6 patients were enrolled. Results from the multicenter trial that led to FDA approval in 1997 are discussed below (Peckham et al. Individuals can choose to use either a palmar or lateral prehension grasp pattern. an ECU. and a transmitting coil. The ECU uses this signal to power proportional control of hand grasp and release. Pinch force in both lateral and palmar prehension improved with the neuroprosthesis. A total of 128 cumulative implant years were evaluated.4. The user controls the system through small movements of either the shoulder or wrist.

manufactured by NESS Limited. An ADL abilities test evaluated whether the neuroprosthesis decreased the amount of assistance required to perform various ADLs. Surface electrodes are built into the shell and stimulate the finger flexors and extensors and the thenar musculature. No improvement was seen in manipulation of the lightest objects. This is probably related to the increase in tone produced by surgical tightening of the flexor tendons.4. Across all patients and tasks. skin openings. which contains a trigger button to start stimulation and a mode button to choose between pre-programmed patterns of muscle activation. palmar grasp is on the right. the company has recently produced a proximal arm segment Figure 9. indicated that it had a positive impact on their lives. . The Handmaster System external orthoses. irritation from incisions or sutures and skin irritation from splints or casts. The subject controls the device through a controller box. The major non-surgical adverse events included swelling or discomfort over the implantable components. In addition. and provided them with less dependence on other adaptive equipment. The forearm device incorporates three surface stimulation electrodes into the molded orthosis to provide pinch grip. Pinch force for lateral and palmar prehension with and without the Freehand® neuroprosthesis. skin irritation from external products. 50% showed an improvement in independence score.4 Figure 9.. and 78% preferred to use the neuroprosthesis to perform the activities. infection requiring electrode removal or system explant and tendon adhesion. An additional arm segment and a lower leg segment using the same surface stimulation technology.3 Lateral 12 Pre-op Post-op wo/NP Post-op w/NP 6. 1996). Through a survey instrument. electrode breakage. Handmaster The Handmaster. which is produced by the NESS Corporation in Israel (Jjzerman et al. is composed of a hinged shell with a spiral splint that stabilizes the wrist. patients reported overall satisfaction with the performance of the system.7 Palmar off.Functional electrical stimulation in neurorehabilitation 129 14 Pinch force (Newtons) 12 10 8 6 4 2 0 1. As of January 2004. There is some increase in force produced postoperatively even with the neuroprosthesis turned 0 0. Adverse events requiring surgical management included receiver repositioning or replacement. there are over 200 patients in the world who have received this device.6 0. is also available. The histogram family on the left represents lateral grasp. Force represented in Newtons.5.

one has to abolish reflex incontinence caused by activation of the sensory reflex pathway. which couples to an external stimulator/transmitter. Over 1500 sacral anterior root stimulators have been implanted. is loss of perineal sensation in sensory incomplete individuals and loss of reflex erection and ejaculation if present. This produces short spurts of urination that result in nearly complete bladder emptying. improvements in grip strength. In the USA. however. Alon and McBride. The downside of this procedure. In addition. finger motion. Ultimately. thereby avoiding the chance of autonomic dysreflexia. Potential candidates for the Vocare implant need to have intact parasympathetic efferent neurons to the detrusor musculature (see Volume II. Gorman et al. A separate mode button allows the user to choose different pre-programmed patterns of muscle activation. A significant reduction in the number of . 1993). the FDA approved the implantation of the device in 1998 under the trade name Vocare™. Pulsed stimulation is used to take advantage of the differences between activation of the slow response smooth musculature of the detrusor (bladder) and activation of the fast twitch striated sphincter musculature (Fig. and Fugl-Meyer scores were documented. and myoelectric EMG control. In a study of 20 patients. The device is designed to be used with C5 and C6 tetraplegic individuals as well as individuals with hemiplegia. A trigger button mounted on a separate control unit allows the user to start the stimulation sequence. A case study of seven patients with C5 or C6 tetraplegia has been completed. use of implantable controllers (Johnson et al. This procedure abolishes uninhibited reflex bladder contractions and restores bladder compliance. This has been done by performance of a sacral posterior rhizotomy. and relative ease of application. The overall objective of these developments is to simplify the control functions by making them more natural. provide enhanced movement of the hand and stronger control of the proximal musculature. This can be ascertained by cysometrogram recording of bladder pressure (Creasey. 1998. proximal muscle control. Stimulation at various levels of the neurourologic axis has been attempted. 1999). while sphincter pressure rapidly falls after the end of each stimulation pulse. closed loop feedback with improved sensor technology. and a leg segment using the same technology (Fig. Brindley and Rushton (1990) has had the most experience and success with S2 through S4 anterior sacral nerve root stimulation in combination with posterior rhizotomy. bilateral implementation. The advantages of the Handmaster are its non-invasiveness. 9. Bladder pressure gradually increases in a tetanic fashion.130 Peter H. In Great Britain.. as external splinting is required and the fact that the device is less customizable than the Freehand system. Disadvantages include its cosmesis. Of those approximately 90% are in regular use 4–6 times per day. 2003).. control of the prontation/supination axis. and three ADL activities that could not be performed without the Handmaster were performed successfully with the neuroprosthesis. post-void residual volumes were reduced on average from 212 to 22 ml with the Vocare system (Van Kerrebroeck et al.5). and reduce the donning process. In order to provide continence of urine with this device. Detrusor-sphincter dyssynergia is also reduced. addition of finger intrinsics to improve finger extension (Lauer et al. 1999). Future directions for hand grasp neuroprostheses Future developments and improvements in tetraplegic hand grasp systems include increasing the number of channels.. This system is surgically implanted through lumbar laminectomy and employs either epidural or intradural electrodes. 9. Electrodes are connected via cable to an implanted radio receiver. The NESS device has been studied clinically in pilot investigations (Weingarden et al.6).. cost. Chapter 24). technologies such as the development of injectable electrodes and cortical control of movement may impact as well on these devices. Control of micturition with FES Electrical stimulation to control bladder function after supra-sacral SCI has been under investigation for several decades. 1999).

.. Physiology of micturition produced by the Vocare® sacral nerve stimulator as identified by cystometrogram recording. (c) Cumulated volume of urine voided in ml with the scale from 0 to 600 ml. Electroejaculation Originally developed within veterinary medicine. the amount of time spent in bowel evacuation has been shown to be considerably less (MacDonagh et al.e. As the coordination required to achieve successful pregnancies with this technique. 2001). 1990). 1 (b) 13 1 0 40 Flow 0 13º ml/s 0 600 Volume 16 435º ml 0 (c) 4 247 431 (d) symptomatic urinary tract infections has been seen. (b) Urine flow rate in ml/s with the scale from 0 to 40 ml/s. About half of implant recipients can use the stimulator to defecate. Electrically stimulated rectal probes are used to produce seminal emission. medical resources etc.7 Future directions and challenges The intense scientific research and developmental work in the field of FES that has occurred over the last half century has realized meaningful clinical applications to ameliorate functional deficiencies of . Chapter 25. Economic analysis of the long-term cost savings due to the decreased use of catheters. 1995). Long-term follow-up from Europe has documented the safety of this implant device and procedure. multidisciplinary expertise is required (Ohl. antibiotics. Even in those patients that cannot. Continence has been achieved in more than 85% of implant recipients. see Volume II. reduced constipation). probably due to the concurrent posterior rhizotomy (Brindley. 2000).6. (a) Intravesicular pressure in mm water from 0 to 150.Functional electrical stimulation in neurorehabilitation 131 0 30 V Ur 108 1:00 V 1:30 Pe 108 2:00 2:30 Ur V 69 Laborie 433 min 150 Pves 1 132º cm H20 (a) Figure 9. X-axis represents time in minutes and seconds with the total tracing lasting approximately 3 min. the quality of the semen produced generally improves to the point where artificial insemination or in-vitro fertilization is possible. The sacral anterior root stimulators have also been shown to improve bowel care (i. increased defecation. Approximately 60% of men can also produce penile erection with the device. electroejaculation now provides a mechanism by which spinal cord injured men can father children. 1993). After serial electroejaculation procedures. Improved health of the upper urinary tracts has been demonstrated by a decreased incidence of bladder trabeculation and hydronephrosis (Peckham et al. 9. indicate that the implant would pay for itself within 5–7 years (Creasey et al. For additional discussion of rehabilitation for sexual dysfunction.. (d) Approximate timing of the sacral nerve stimulation used to produce this intermittent voiding pattern..

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radio. maintain. Fourthly. and microwave oven to more specialized devices such as walkers. Thirdly. walking/mobility. 10. and assistive technology device are used synonymously. or air conditioner. AT device refers to “any item. Mann Department of Occupational Therapy. and/or psychosocial. Environmental control devices can be set up to remotely operate electronic devices in the home (Mann. The assessment must consider the individual’s physical deficits and strengths.1 AT intervention Prior to recommending assistive devices. Finally. or dressing sticks. The AT increases a person’s level of independence in performing tasks. assistive device. FL. This is an adaptive utensil that allows people to cut food with one hand. television. furnace. piece of equipment. we will cover AT by categories of activities of daily living (ADL) including: bathing. who shows her how to use a rocker knife. Gainesville. sensory . modified. or improve functional capabilities of individuals with disabilities” (Assistive Technology Act. after having a stroke. assistive listening devices. we will discuss AT for neuromotor impairments. Secondly. phone. whether acquired commercially. toileting. she no longer needs to rely on her husband. we will address AT for sensory-perceptual impairments. With the rocker knife. 2004). or product system. or customized. a woman experiences hemiplegia and becomes dependent on her husband for cutting food. a thorough assessment of the individual should be performed. Her newly acquired independence makes her feel more self-reliant. are simple environmental control devices that turn lights on and off at pre-set times of day. the chapter will outline considerations for intervening with AT following a neurologic condition resultant from injury or disease. 1998). telephone use. The deficits may be physical. the chapter will end with a discussion about future AT. Environmental control devices provide another example of assistive devices. eating/drinking. a person may have residual deficits even after completing a therapeutic program designed to regain function. and higher-technology devices such as computers with special interfaces. Assistive devices range from basic consumer products like a television remote. The terms assistive technology. While we recognize psychosocial issues may have an impact on the person’s life and their response to AT. dressing. cognitive. To overcome the dependency. that is used to increase. shopping. including lights. and it may also have a positive impact on self-esteem. medication management. For example. Firstly. Light timers. use of AT for physical and cognitive deficits is emphasized. and leisure. cordless phone.10 Environmental control and assistive devices Jessica Johnson and William C. USA Following a stroke or traumatic brain injury (TBI). To overcome these deficits. food preparation. Assistive devices include both low-technology items such as a long-handled shoehorn. University of Florida. cognitive status. This chapter focuses on use of AT to address residual deficits resultant from a brain injury. This 136 dependency may make her feel more like a child than a wife. people frequently use assistive technology (AT). we will present AT for cognitive impairments. the woman works with an occupational therapist. for example. grooming. Then.

and work well for individuals with both mobility and memory impairment. but be an inappropriate intervention given his living situation. but the task could take 40 min and result in fatigue. Grab bars are placed in critical locations in the home. Cognition is also very important in being able to use assistive devices effectively. or may forget that they have the device. different devices accomplish the same thing. gross and fine motor coordination. Wander alerts help caregivers supervise people with impaired cognition by alerting them when the person moves beyond a prescribed environment. AT for balance and gait impairments Patients with balance and gait impairments are at risk for falling (Volume II. The individual may rush through a transfer without using the assistive device appropriately and safely. the dressing stick would allow the patient to be independent. the tasks the person performs or would like to participate in. Sensory deficits. a stroke survivor may be able to put on his pants independently with a dressing stick. 1998). shower. in using a reacher one must be able to sense how much force is being applied to ensure objects are adequately grasped. and unilateral weakness or paralysis (National Institute of Neurological Disorders and Stroke (NINDS). For some tasks. using an adapted nail clipper that can be pressed with a gross motor movement of the left hand. Functional status relates to how much assistance an individual requires to complete tasks and activities. While recognizing deficits. who assists as a primary caregiver. are also important to consider in recommending assistive devices. When AT is prescribed inappropriately. Consider a person who is unable to squeeze a fingernail clipper with her left hand to trim the nails on her right hand.2 AT for motor impairments Common motor deficits resultant from neurologic conditions include impairments in balance. 10. remaining abilities must be considered in recommending AT. such as near the toilet. and others living in the person’s environment (Mann. which are often not obvious. Functional status alone is not enough to decide where to intervene with AT. During AT intervention for falls. caregivers. For instance. On the other hand. 2002). But if he lives with his wife.Environmental control and assistive devices 137 status. which further increases the person’s risk of falling. Chapter 8). When an individual initially obtains an assistive device. For example. they are still likely to have a fear of falling. They are usually made from metal but may be covered in a more attractive material. he or she may not remember how to use a device. Automatic braking systems on wheelchairs lock when an individual moves from sitting to standing without applying the brakes manually. A person with decreased sensation may not be able to determine the applied force. but each device may offer unique features and a distinctive design. and bed (Fig. The type of AT to recommend will also depend on what activities the client wishes to accomplish and what device features are important to the client. functional status. Grab bars are simple yet important devices that assist with impaired balance. The assessment must also address the role and needs of informal caregivers. 2003). and become quickly frustrated in trying to use a reacher to grasp objects. an increase in the frequency and duration of education can positively impact the safe and effective use of the device (Mann et al. this risk may decrease. With training in the use of assistive devices. it often ends up unused. In this example. Simply moving from place to place within their residence may provoke anxiety. . Intact sensation is important in using many assistive devices safely and effectively. bathtub. environment. Professional training is essential for safe and effective use of balance and mobility devices. With the remaining strength in her left arm. assistive devices may be used to increase the safety of people with cognitive deficits. gait.1). 10.. Physical status is also important in prescription of AT. April 21. If a patient has impaired cognition. her assistance with donning his pants could save him time and energy. she is able to trim her own nails on her right hand.

unilateral neglect. using a walker. April 21. Chapter 36). or weakness on one side of the body. handrails should be placed on both sides of the staircase. Moreover. In some instances. Handrails are also important in compensating for balance impairments. To compensate for lowerextremity weakness. a perpendicular arm extends from the vertical pole to facilitate grasping. a half-bed rail may be helpful in Following a brain injury. devices such as an ankle-foot orthosis provide extra stability to the affected limb and allow for a safer gait pattern. 2003. and where the support is needed. grab bars may be floor mounted. some individuals use both handrails for added stability while climbing up and down stairs. 2003). These devices enable a person to use one hand to complete tasks that typically require two hands. and during pericare.138 Jessica Johnson and William C. buttoning a shirt. or difficulty completing tasks from start to finish and following instructions (NINDS. Assistive devices can compensate for the functional loss of the impaired limb. The vertical pole extends from floor to ceiling. or bed rail. Grab bars in the shower or by the bathtub assist a person with a balance impairment in transferring safely in and out of the shower. Mann Figure 10. Grab bars can be attached to the shower wall or clamped to the side of the bathtub with a rubber-covered clamp (Abledata. Stairs leading into the house or between floors should have at least one handrail. impaired short-term memory. These systems provide support during transferring on and off the toilet. or moving from sitting to standing. 2004). preparing food. such as a stroke. wall to floor mounted. An individual with balance or gait impairment may benefit from a variety of devices when transferring in and out of bed including: a vertical pole. tying a shoe. Finally. during clothing management. A toilet seat with armrests may be installed to offer support (Abledata. A trapeze bar can assist a person in moving from a prone to sitting position. and is usually attached to the bed frame. For a person with hemiparesis.3 AT for cognitive impairments A person who has survived a stroke or TBI may have residual cognitive impairments that include: language impairments. shortened attention span. Similarly. or attached to the toilet itself. 2004).1. flossing teeth. Grab bars installed around toilet to assist with impaired balance. . and provide support while standing in the shower. an upper extremity may be weak or paralyzed. and using a wheelchair. wall mounted. poor insight to the extent of deficits. trapeze bar. Depending on the individual’s needs. A variety of devices available to accomplish these tasks using one hand are discussed later in this chapter. such as cutting food with a knife. handrails assist on one side when ascending a staircase and on the opposite side when descending the staircase. grab bars may be installed in several different configurations inside and outside of the shower/tub area. April 21. many individuals experience residual weakness or paralysis on one side of the body (NINDS. AT for hemiparesis/hemiplegia There are several types of bathroom grab bar systems. 10. Volume II. brushing dentures. sitting up. assisting people with rolling onto their side. The number and placement of grab bars will depend on how much support a person requires. For use by the toilet. Often.

2005). This suggests that some of the participants were able to use the device for a short time and continue to meet daily demands without its use. (2003) reported that the four most common memory interventions for people with brain injury are a wall calendar/chart. However. Typically. list. Often someone who is diagnosed with one form of aphasia will have mild symptoms of the other. People who do not possess these characteristics may require more support in learning to use memory aids. which can be updated as needed. Chapter 29). Group A was 74% successful in remembering daily tasks compared to 48% for Group B. With expressive aphasia the person has difficulty communicating their thoughts to a listener. or date book. such as stroke or TBI (Volume II. a medical alert tag may be beneficial so that others understand the individual has a language impairment. (1997) studied the use of electronic devices to help people with brain injuries remember appointments. Wilson et al. and other daily events. This suggests that the paging system allowed the participants to perform more tasks than they did without the paging system. and appointment diary. Expressive and receptive aphasia do not exist in isolation. having a more recent injury. 1995). The user may set the paging system to alert with a beep and/or vibration when a text message is delivered. notebook. Four factors associated with memory-aid usage were found: being less than age 30 at time of injury. some individuals required long-term use of the electronic device.” which means “a device that supports weakened. 2003). at the end of the last 7 weeks. these methods were considered not as effective as less-used electronic systems. expressive aphasia. Wilson et al.Environmental control and assistive devices 139 AT for language and cognition At least 25% of stroke survivors have some form of aphasia (American Speech–Language–Hearing Association (ASHA). An example of a paging system for persons with memory impairment is the NeuroPage (Oliver Zangwell Centre. April 21. There are three major types of aphasia: receptive aphasia. higher current intellectual ability. and having better attention skills. The use of AT to compensate for memory deficits may require that the individual remember to use the memory device. However. The caregiver provides NeuroPage with the appropriate messages and delivery times. Half of the participants (Group A) received the paging system for the first 7 weeks of the study and then discontinued use of the paging system the last 7 weeks. When the paging system was discontinued for 2–4 weeks. With the use of an electronic paging system. such as a calendar. the system pages the person when a certain task needs to be performed. People with expressive aphasia may use communication boards and computer systems to communicate with others (Mann and Lane. The other group (Group B) did not use the paging system until the last 7 weeks of the study. After receiving the information from the caregiver. The prompt displayed on the screen can be worded so that it is meaningful to the user. . Evans et al. Group B was 76% successful compared to 62% for Group A. aberrant. These symptoms may range from mild to severe depending on the location and extent of brain damage. With receptive aphasia a person has difficulty understanding what is said to them.” Currently. or deficient cognitive functions” (Bergman. 2004) (NINDS. Assistive devices for memory are commonly called “cognitive orthotics. Paging systems appear to work well for people with brain injury. medications. memory journal. participants continued to be 76% successful. However. there are no assistive devices to help persons with receptive aphasia understand what is being said to them. 2002). AT for memory Memory impairment is one of the most common residual deficits following a brain injury. Chapter 26). (2001) conducted a 14-week randomized controlled cross-over trial with 143 participants. and global aphasia (Volume II. In a follow-up study of electronic paging systems. Similarly. it is called “global aphasia. When both types of aphasia are severe. Wilson found that participants’ rate of success in remembering tasks increased from 37% to 86% in 12 weeks. At the end of the first 7 weeks. notebook.

no scald shower/bath faucets should be installed. If the person does not feel pain. The individual presses one button and reads the message. they could get their hand caught in the wheel of a wheelchair. The tag may also provide the person’s name and phone number. Other devices used by people with memory impairments include medical alert tags and personal emergency response systems. 1997). 2005). 2004). ADLs AT for bathing Most homes in the US have a bathtub/shower combination either with glass doors or with a shower curtain (Mann. temperature. 10. which is useful if he or she becomes disoriented and lost. As a result. Like a paging system. provide reassurance. A personal emergency response system provides a quick link to help for a person with limited memory or problem solving abilities (Federal Trade Commission for the Consumer and American Association of Retired Persons. checklists. resulting in a burn. Inc. Current applications and devices that can be used to assist people with a brain injury in completing daily activities have been reviewed recently (LoPresti. text. and a console that is connected to the person’s telephone. This device has a pressure sensitive screen that the user touches when a message is delivered. ISAAC is an example of another cognitive orthosis (Cogent Systems.5 AT for ADL and instrumental ADL ADL refers to basic self-care tasks. PEAT comes up with a best plan to complete all steps. pain. use of sensors and switches to detect the task the person is performing and providing cues to assist the person in its completion. April 21. temperature gauges may be employed. To decrease the risk of injury due to sensory impairments. taking into consideration alternative steps in completing tasks. pain. Chapter 16). a call is placed to a response center. they may experience odd sensations (paresthesias) like numbness.140 Jessica Johnson and William C. The user tells PEAT when a step has been completed or if the user requires more time. The planning and execution assistant and trainer (PEAT) uses artificial intelligence on a PDA to help people with brain injury function independently (Levinson. For example. Then PEAT provides cues to the user assisting them to complete the steps. and the individual should be trained to visually inspect the affected body part often.4 AT for sensory perceptual impairments People who have a neurologic condition resulting from injury or disease may have sensory impairments (NINDS. such as allergies. The medical alert tag conveys information. Furthermore. 2004). the person may not be able to determine that their hand is on something hot. When the button is pressed. This is often a difficult setup for someone with a physical impairment. Loss of sensation can cause safety problems. when the individual is unable to remember the information. 10. The response center operator can answer questions. Mann NeuroPage automatically sends messages to the individual’s pager at the appropriate times. or in an emergency. and paging systems. Instrumental ADLs (IADLs) refer to more complex tasks. Some of the devices and systems include: customized computer systems adapted to the individual’s needs. send help. equipment for improved positioning can be used. or tingling in the affected limbs. or graphics to the user at the appropriate time of day. such as using a phone or cooking a meal. The ISAAC device is wearable and battery powered. PEAT alters the plan based on the user’s input. and can be affected in less severely impaired individuals than ADLs. 2003). ISAAC delivers prompts in the forms of auditory speech. These impairments may include diminished or absent tactile. The program helps the individual plan their day. such as dressing or eating. 1998). or proprioceptive (position of the limb or body in space) sensations (Volume II. These systems typically include a button on a necklace or bracelet that the individual wears. Getting .

Dressing can be challenging when one side of the body is weak and balance is impaired. AT for dressing Dressing requires body movement and the use of both hands. some back brushes can also be used to wash the lower legs. Some have backs that assist people with compromised sitting balance and some have armrests for additional stability. A variety of brushes and sponges can assist with bathing (Abledata. A soap swing can turn any bar of soap into “soap on a rope. A person with decreased balance should have a sturdy chair to sit on while dressing.Environmental control and assistive devices 141 down into the tub and out again may not be possible due to decreased balance and hemiparesis. To put on socks and shoes. Several water temperature control devices are available. foot brushes attach to the bathtub to clean feet and toes. Many assistive devices are available for soap and shampoo dispensing. 10.” Soap is placed in the soft mesh bag that doubles as a bathing sponge. other options include showering or sponge bathing. For hands-free use. a shower chair or bath bench is recommended. Shower chair with backrest. However. Finally. These are available in several styles. People who are unable to press buttons could use hands-free motion-activated dispensers. Finally. One consideration when using a transfer bench is the amount of space in the bathroom as they require space outside of the tub. the person turns toward the front of the tub and swings one leg and then the other into the tub. 2004).2. A push button dispenser is useful for an individual who is unable to use both hands to open a shampoo bottle and pour it into the other hand. as listed at www. a shower curtain must be used rather than glass doors because glass doors do not allow enough room to sit and swing the legs into the tub. These devices are important for people with sensation deficits and can prevent burns. Furthermore. 1998). To shower safely.com (Abledata. but the arms may interfere with putting on a shirt. hand-held showers with an on/off control are relatively inexpensive. A foot sponge is much like the long-handled sponge but narrower for cleaning toes and feet. A chair with arms may be helpful for transferring. The use of a hand-held shower may also help keep water in the tub when using a transfer bench. Grab bars are an option. tying shoes involves the use of two hands and fine motor coordination. A hand-held shower is useful for rinsing when seated on a bath bench or shower chair.abledata. the hand-held shower can be set down into the tub while the person washes. but are unable to remain standing while showering. A transfer bench allows a person to perform a seating transfer into the tub (Mann. The shower curtain must be positioned so that water does not spill out of the shower and onto the floor creating a safety hazard. If a person has the use of only one-hand and the showerhead does not have an on/off button. For people who can safely perform a standing transfer. The mesh bag is attached to a long nylon rope that is mounted to the wall. After sitting. a person must have good trunk flexion and be able to maintain balance (Mann. Beds are not an Figure 10. as discussed earlier in this chapter. Again. as well as in the tub. Also. several types of device can be used.2). . the weight of the chair must be considered if it has to be removed for others to use the bathtub (Fig. A long-handled sponge can help a person with impaired balance or range of motion wash their lower legs. 2004). Devices that control the water temperature can be installed. 1998). If tub bathing is not feasible. the weight of the bench should be considered if it will be removed when others use the tub/shower.

Also. Velcro can also be substituted for hard-to-close fasteners. A toothpaste dispenser is available that has a slot for the toothbrush: the device dispenses the appropriate amount of paste when the person presses the dispenser lever. Button extenders enable a person to pull a button-up shirt over the head (Abledata. September). emery boards. Fingernail clippers for operation with one hand are available. 2004).142 Jessica Johnson and William C. Elastic laces can be placed in shoes. An emery board with a suction cup allows one-handed use for filing nails. jewelry can also be challenging to don. The laces come in different colors. zipper pulls can be added to zippers and allow a person with use of only one hand to zip a garment. AT for grooming Typically. Devices are available to assist in fastening clothes that have buttons. pull-on pants and pullover shirts are easier because there are no closures. Likewise. For many people with these impairments. Elastic cuff links allow a person to slip their hand through cuffs without unbuttoning them. and laces. the end of a dressing stick can act as a long-handled shoehorn. A few items that make nail care easier for people with hemiplegia or hemiparesis include adapted nail clippers. A foot-operated nail clipper is also available (Abledata.3). Sometimes the affected leg will have an ankle-foot orthosis. Necklaces and bracelets with magnetic clasps may be easier than other traditional jewelry clasps (Abledata. Long-handled shoehorn. which make donning them similar to slip on shoes. Figure 10. This may be especially helpful for a person who shaves with the non-dominant hand due to hemiplegia. Other devices to fasten shoes include Velcro and shoelace fasteners that can be used to lock shoelaces in position. For an individual with decreased fine motor coordination. Brushing dentures also requires two hands. and snaps are often difficult to manipulate due to hemiparesis or decreased fine motor coordination..3. and nail brushes. zippers. and styles. 10. but a disposable or non-disposable dental floss holder can make flossing with one hand possible (Mann et al. However. zippers. Nailbrushes with suction bases can be used to clean under nails for people with hemiplegia. sport bras in an extra size may be easier for women to pull over than using a rear closure bra with hooks or even a front closure bra. Mann ideal platform for dressing as they are often too soft for an individual to maintain an upright posture. 2004). widths. an electric shaver may prevent cuts. flossing is a two-hand task. Clip-on earrings or earrings with hooks rather than posts are easier to put on with one hand. 2004). . For garments with buttons. For a person with diminished fine motor control or hemiplegia. The dressing stick can also assist in getting pants over feet and pulling them up to the knees where the hand can take over. The person has to point their toe into the shoe and get the shoehorn behind the heel before they begin to push down into the shoe. button aids can compensate for fine motor impairment and can be used by one hand. A long-handled shoehorn may help in putting on shoes (Fig. Fasteners like buttons. Reachers can also be used for donning pants. 1995b. denture brushes with a suction cup make it possible to clean dentures using one hand (Abledata. although for some individuals it may still be difficult to clip the nails on the unaffected hand. or AFO. 2004). Similarly. They are larger than the typical zipper lever so people with fine motor impairments can grasp the pull as well. which is already in the shoe and acts like a shoehorn.

10. Four-wheeled walkers have a seat that allows the user to rest when needed. front-wheeled. raised toilet seats with armrests can be used. Canes are usually single-end or have multiple feet. Roller knives look similar to a small pizza cutter. 2004). Walker accessories can help the user transport items while walking. Some of the adaptive utensils that make cutting food with one hand easier include rocker knives. The Toilevator adds a section between the floor and the bottom of the toilet. Add-on washing devices serve the same purpose as a bidet at much lower cost. Pre-moistened wipes make it easier to cleanse after toileting if hygiene is difficult (Mann. To avoid an accident on the way to the bathroom. Hemi-walkers are used by people with hemiplegia. Finally. To prevent spilling. Canes support up to 25% of a person’s weight (Mann. 2004). The Toilevator is a device that raises the toilet from the bottom up. such as a quad cane. 1998). The weight of the urinal after it has been used should also be considered.4). Bags are useful to transport items that do not have to stay upright. and are still used with one hand. Also. four-wheeled walkers provide some support and are able to move faster than standard and two-wheeled walkers. a person with hemiplegia or impaired balance may require a significant amount of time to get from bed to the bathroom to use the toilet. A commode with a seat lift helps the person move from sitting to standing. Bedside commode. or stationary arms (Abledata. 1998). Rocker utensils have an edge the shape of a semi-circle that is used to cut food. At night. A platform walker allows the person to put the affected hand and forearm in a trough on the walker and then bear weight through the upper arm to push the walker forward. These are available in many different styles. . 1998). and trays. Walkers can support up to 50% of a person’s body weight (Mann. swing away arms. Some four-wheeled walkers have a bin under the seat for carrying objects. rocker fork-knife combinations. Quad canes offer more support than single-end canes. The weight of the urinal is important for a person with hemiplegia or hemiparesis. and fourwheeled. 1998). Standard walkers and front-wheeled walkers provide support to people with impaired balance. so the person is still sitting on his or her own toilet seat. a person with poor coordination or decreased cognition may use bowls and plates with built up edges. AT for eating and drinking Assistive devices are available that make eating with one hand easier. including commodes with removable arms. baskets. Baskets allow Figure 10. but the person must grasp both sides of the walker to use it properly. Another option is a bedside commode. They include walker bags. standard. plate guards.4. and cups with lids. AT for walking and mobility A variety of mobility devices are available for people with impaired balance or gait. A consideration when prescribing a bedside commode is how the indi- vidual transfers. but are heavier. dishes with non-skid bottoms. Raised toilet seats may make it easier for someone with hemiparesis or hemiplegia to get on and off the toilet. and roller knives (Abledata. use of a bidet rather than toilet paper can be beneficial for people who are unable to maintain balance while wiping themselves. the individual may use a urinal or a bedside commode (Fig. Urinals may be gender specific or unisex (Mann. These walkers offer more support than a quad cane. platform. Types of walkers include hemiwalkers.Environmental control and assistive devices 143 AT for toileting Several options for hygiene assistance are available. If the person requires extra support or something to push on when transferring.

but may interfere with the individual approximating counters and cabinets. a brake extension on the affected side allows the individual to reach with the unaffected hand to lock the opposite brake. just one foot and one hand. An answering machine can also limit the need for rising to answer the phone by screening out unwanted calls. Several items can be helpful in the kitchen for someone with a neurologic injury or disease.144 Jessica Johnson and William C. half tray. a less expensive foam cushion may be appropriate. A pan holder holds . hands-free headsets. 2004). power wheelchairs. which is very difficult). vehicles. and power assisted wheelchairs. IADLs Telephone AT Cordless telephones allow people with impaired mobility to carry their phone at all times. Additionally. Another consideration when positioning someone is the type of wheelchair cushion they should use. the person may need lateral support to maintain an upright posture in the wheelchair. Trays are another alternative for carrying objects and allow the user to approach counters and cabinets closely. Many people who use these devices use wheelchair ramps and lifts. In positioning someone post-stroke in a wheelchair there are several important considerations. 1998). Often motorized scooters have baskets to allow transportation of objects. Initially. Pull-out racks in lower cabinets can make it easier to get the items stored there (Mann. including manual wheelchairs. or speakerphones. Mann transportation of items in an upright position. People who have difficulty holding the receiver can use voice-activated phones. Lazy Susans can make it easier to get to items that would normally be stored in the rear of cabinets. 10. If the person has residual memory impairment. Phones with large buttons are easier to dial for people with impaired fine motor coordination (Mann. Cutting boards with pins and clamps to hold food in place are helpful for those who need to prepare food with one hand (Abledata. Many stores carry motorized scooters with baskets. a pressure-relieving cushion would be best. then the person needs a wheelchair that can be maneuvered on one side. AT for medications For people who have mild memory impairment. an automatic braking system may help prevent falls. The individual may need a seat alarm or seat belt if he or she does not have good insight into the deficits present and is at risk of trying to walk.5). Wheelchairs are another category of mobility device (Chapter 11 of Volume II). but do not allow the person to use a walker seat to rest. so they do not have to get up to answer the phone. People who have a neurologic condition and use a wheelchair or scooter have to consider how they will get around their home. If the person is not very mobile and is at risk of developing pressure sores. 1998) (Fig. the memory dial feature of a phone or a list of frequently called numbers can be especially beneficial for people with impaired memory. Scooters are a less expensive alternative to power wheelchairs. Lastly. Some watches can also be set to sound an alarm at appropriate times to remind the person to take their medication. A tray table. how will the person propel the chair? Will they use their hands and feet. Telephones have many features today that can be helpful to someone with physical and cognitive impairments. medication organizers can be helpful. Paging systems may be used to remind the person to take a specific medication at a certain time. no feet and two hands? If they are going to use one hand and one foot (or one hand. but they offer less support (Mann. 1998). Finally. There are many different types of wheelchairs. Food preparation Items that will be used for food preparation should be within easy reach. The person with hemiplegia may have to request medications be put in an easy to open container. something other than a childproof container that can be opened with one hand. But if the person is able to shift in the seat and transfers often. and community. or arm trough may be used to keep the patient’s arm in a safe position.

Countertop devices may be helpful such as: a toaster oven. open doors. Often store-bought frozen foods come in a dish that is microwaveable. and battery power are making it possible to design electronic devices that will serve multiple functions: operate appliances. or a toaster. An automatic dishwasher will help prevent fatigue from standing and doing dishes by hand. Lightweight dishes facilitate transporting dishes. the Internet. some of their shopping can be done over the phone or with a computer. Microwave ovens can be used to ease food preparation. The article points out that these are all leisure activities and often leisure is not a focus of intervention.6 Future assistive devices Advances in computing power. and long walks. Multi-use containers make food preparation and storage easier by allowing the individual to use the same container for cooking and refrigerating leftovers. close and open drapes. 10. This is especially important for a person with decreased sensation. At the University of Florida. Cooking time in a microwave is significantly less than with a conventional oven or stove. Figure 10. (1995a. scooters with baskets or walkers with baskets and seats are helpful (Mann. discussed the case of a man who survived a stroke and used a computer for word processing to compensate for difficulty formulating thoughts and putting them on paper. or forget to turn the stove off. crafts. an automatic shut off coffeepot. High-intensity lighting can help people who are having difficulty seeing their project. the Rehabilitation Engineering Research AT for shopping For people with impaired mobility. 1998). or who are only able to use one hand (Abledata. a computer may be used for word processing. burns from cooking are not as likely with a microwave oven. Electric can openers and power-operated corkscrews make it easier to open cans and bottles with one hand. provide reminders for medications. Card holders and card shufflers are available for people with decreased fine motor coordination. wireless technologies. A television remote with large buttons is easier to use for someone with decreased fine motor coordination or visual disturbances.Environmental control and assistive devices 145 When the individual travels to a store. Many devices are available to assist people with leisure activities following a brain injury. Burner guards also help keep pans from sliding off burners. March) found the types of activities most missed by older stroke survivors living at home were sports. a hot pan in place while the cook stirs with one hand. 2004). which may be beneficial for someone with diminished activity tolerance. (1999). Also. Many computer interfaces can be used if a standard keyboard is not feasible. Crochet and knitting aids are also available to allow for one-handed work. A sewing machine with an attached magnifier may help people with visual disturbances. . They may be a better option for those with mild memory impairment who may forget about foods they were cooking on the stove. 2004). Pull out racks. If writing with a pen or pencil is too difficult or impossible. and much more (Mann. Several types of writing aids are available for people who have difficulty grasping or controlling a pen. using a cart or backpack may be helpful in carrying items home from the store.5. AT for leisure Mann et al. Schweitzer et al. Also. A variety of jar openers make it possible to open a jar using one hand.

Nochajski. P and Brentnall. M. (2004) Smart Technology: Aging.d.. Goodall. Bergman.. and Charavat. Evaluation of NeuroPage: a new memory aid.C. The American Occupational therapy Association. Mann. Aspen Publishers. 130–139.gov/health_ and_medical/pubs/poststrokerehab. J. March. For with the neurologically disabled. The planning and execution assistant and trainer (PEAT).C. 431–445. 113–115... Assistive technology for cognitive rehabilitation: state of the art. MD. http://www. Aspen Publishers. 52–66. J.. Hoboken. J. Assistive Technology for Persons .J. American Speech–Language–Hearing Association Aphasia.M. Neuropsychol Rehabil.J. W. W. or doors are left unlocked. (1997).. W. Bethesda. from http://www. In: Topics in Geriatric Rehabilitation. Neurosurg. (1999). from http://www. Mann Center on Technology for Successful Aging (www. Quirk.. .org/public/speech/disorders/Aphasia_info. Mann.C. Retrieved REFERENCES Abledata Database. Retrieved March 30. from March 22. Federal Trade Commission for the Consumer & American Association of Retired Persons (2004). M. The State of the Science. Post-Stroke Rehabilitation Fact Sheet. B.htm Assistive Technology Act of 2004. pp. B. LoPresti. Products or applications such as these will be available in the very near future. J Head Trauma Rehabil. htm Levinson. had a sleepless night. Retrieved March 22.. reminders to drink. Retrieved March 22. or had not eaten – all of which could trigger an alert to a family member or a formal care provider. B. Inc. Suite 930.C.abledata. asha. The benefits of a cognitive orthotic in brain injury rehabilitation. such as when mail is delivered. Assessment and Management of Arthritis in Rehabilitation (Chapter 16. with Disabilities. For information.P (1995).D. Gaithersburg. S. W. and Tomita. Disability and Independence. M.. N. 70. and to take meals or medications. D.htm. Hurren. 2004.nhs. 369–392). Patterns of engagement in Leisure activity by older adults using assistive devices.edu) is developing voice activated computer applications as well as auditory and visual alerts that accomplish all of these tasks and provide alerts.gov/bcp/conline/pubs/services/ pers. J.. Mann. NeroPage. 5–39. 10(3). W. Assistive technology for persons with arthritis. (1995b). M. MD. cannot be overly stressed. Selection of appropriate devices. R. 925–935. 11(1). M.S. V. M.C. (2001). Combining these advanced technologies in a home setting provides even more potential applications.. typically by an occupational therapist.A. B. NJ (in preparation). National Institute of Neurological Disorders and Stroke (2003).htm Schweitzer. J Int Neuropsychol Soc.). Emsile. MD. and Lane. Retrieved March (n. Mann. S. training in their use. MD. Psychiatr. (2004). September. J. telephone 800-227-0216 or write Abledata. Technol Disabil. 63(1). Hurren. 8630 Fenton Street. J Head Trauma Rehabil. J Neurol. (1995a). Silver spring. and Tomita. (1997). While the future promises a new generation of assistive devices.C. 12(2). Assist Technol.. D. §3002 (2004).C.ufl. Wilson. 477–482. 14(1–2). and Evans. (1998). Mann. 29 U. Smart homes such as these will also help a person with a cognitive impairment by providing prompts through everyday activities.” the basic assistive devices we have described in this chapter can make a very large difference for a person who has a neurologic injury or disease – helping them maintain their independence and quality of life. Wiley. Inc...A. B. Mann.C. In: Topics in Geriatric Rehabilitation. Justiss. Evans. and Charavat. Bethesda. H. Evans.. behavior could be tracked by adding sensors throughout the home. H. Assistive devices for home-based older stroke survivors. (2003). Tomita. The Oliver Zangwell Centre (2005). 2004. 85–91. A. 9. Tomita.F. K.J. and Malinek. Mann. rerc. 17(5)... (2002). Sensors and “intelligence” programmed into the home will make it possible to determine if the occupant had not risen from bed. pp. April 21. American Occupational Therapy Association. The need for careful assessment.ftc.A. 75–86. pp. Psychiatr.ninds. Facts for Consumers: Personal Emergency Response Systems.com/Site_2/prod_type. and continued follow-up are essential. J Neurol. 14.A.. 11. 2004. Neurosurg.neuropage. E. 2003 from http://www. 103–117. Who makes good use of memory aids? Results of a survey of . 11. A follow-up study of older stroke survivors living at home.uk Wilson. 2004. Wilson. and Kirsch. 2nd edn.nih. from http://www.. Mihailidis. Gaithersburg. Dissatisfaction and nonuse of assistive devices among frail elders. In: Rheumatologic Rehabilitation Series: Volume 1. W. MD 20910..C. (2002). Inc.146 Jessica Johnson and William C. Reducing everyday memory and planning problems by means of a paging system: a randomized control crossover study. Needham. Emsile. S. Inc. people with acquired brain injury. W. and “assistive environments.

Upper extremity repetitive strain injuries Studies have shown that manual wheelchair propulsion efficiency is between 5% and 18% depending upon the style of the wheelchair and the fit to the user (Bayley et al... repetitive strain injuries). 1997b. 1987. Robertson et al. injuries from wheelchair tips and falls. Changes can be made to the wheelchair that alter the biomechanics 147 . 2002). The SMARTWheel kinetic measurement system was developed to study wheelchair propulsion and to improve clinical assessment of manual wheelchair propulsion (Cooper et al. 11. The low efficiency of manual wheelchairs make them ineffective for some individuals to use during activities of daily living.2 Prevention of secondary conditions Wheelchair and seating biomechanics research includes studies to prevent secondary conditions due to wheelchair and seating use (e.g. 2002. 1997)... 1996).. The risk of injury tends to increase with age. Boninger et al. Pittsburgh. 1998b. Worldwide. Of particular importance was that the body mass of the wheelchair user was significantly correlated with NCS. 1995. and Rehabilitation and VA Pittsburgh Healthcare System Human Engineering Research Laboratories.11 Wheelchair design and seating technology Rory A.000 people injured or killed by landmines each year (Department of Veterans Affairs.. Upper extremity models have been created in order to determine motion as well as net joint forces and moments (Koontz et al. Manual wheelchair users also experience a high incidence of upper extremity pain and joint degeneration.. Between 25% and 80% of long-term manual wheelchair users are reported to have injuries to the wrist.2 million people currently use wheelchairs for their daily mobility (Americans with Disabilities. 2001). Boninger Departments of Rehabilitation Science and Technology Physical Medicine. 2000).. PA. 2002). This study found that when controlling for subject weight. while cardiovascular fitness tends to decrease (Boninger et al. It has been shown that wheelchair pushrim forces are related to nerve conduction studies (NCS) variables (Boninger et al. Cooper.... adverse changes in posture. particularly in developing nations.. 1994. Shalala et al. Nichols et al. USA 11. NCS are used to diagnose carpal tunnel syndrome (CTS) a common condition that causes pain for wheelchair users.g. 1997c. 1999. NCS was correlated with the cadence of propulsion and the rate of rise of the resultant force.. Curtis et al. and to reduce the incidence of accidental injuries (e. leading to 26. While these numbers are staggering. Rosemarie Cooper and Michael L. injuries from motor vehicle accidents).. The leading cause of disabilities in the world can be attributed to landmines. 2003a). experts predict that the number of people who need wheelchairs will increase by 22% over the next 10 years (Department of Veterans Affairs. 1979). 1998b. 2001)..1 Introduction In the USA an estimated 2. elbow or shoulder (Boninger et al. The SMARTWheels provides a method for analyzing pushrim force that has proven critical to assess injury mechanisms (Cooper. Boninger et al. pressure ulcers. 1993). an estimated 100–130 million people with disabilities need wheelchairs. though less than 10% own or have access to one (New Freedom Initiative Act. It is likely that more than twice that number use wheelchairs at any given time to augment their mobility. 1999. Asato et al. 1996).

(2001) concluded that. and offer the potential for intervention (Boninger et al. Cooper et al. 2000). 2002). curb descents. recorded the forces when using the American National Standards Institute (ANSI)/Rehabilitation Engineering and Assistive Technology Society of North America (RESNA) standards double drum and curb drop tests and compared them to the road loads during ordinary propulsion (VanSickle et al.. showing differences in how seating systems transmit or dampen vibrations. Shock and vibration induced discomfort and fatigue may also lead to poor body mechanics leading to secondary disability. which through extended exposure can cause low back pain. (2000) showed that users prefer ultralight wheelchairs to lightweight wheelchairs while traversing a simulated road course with higher comfort level and better ergonomics.. To date. This could be related to wheelchair set up or other gender differences (Boninger et al. 1999). possibly due to the orientation of the suspension elements. Boninger et al.. both of which likely protect against injury. on average. Wolf et al. The way an individual with paraplegia propels a wheelchair at baseline can predict progression of MRI findings 2 years later. and uneven driving surfaces. 2001). (2002) have shown that suspension manual wheelchairs are approaching significance in reducing the amount of shock vibrations transmitted to wheelchair users during curb descents. Vibration exposure injuries and prevention While propelling a wheelchair.. but are not yet optimal in their design. Whole-body vibration experienced during wheelchair mobility can decrease an individual’s comfort and increase the rate of fatigue (Boninger et al. 1998. DiGiovine et al. (2002) revealed that although suspension manual wheelchairs reduce shock vibrations the chairs are not yet ideal. Investigations of the propulsive stroke concluded that the recovery phase is an important and modifiable parameter that can impact injurious biomechanics (Shimada et al. a high prevalence of osteolysis of the distal clavicle was revealed (Boninger et al. Cooper et al. also showed that wheelchair propulsion produces vibration loads that exceed the ISO 2631-1 standards at the seat of the wheelchair as well as the head of the user (VanSickle et al. Typically. Women use a larger radial force and are at greater risk of injury... DiGiovine et al. Interestingly. These obstacles cause vibrations on the wheelchair and in turn. Research has shown that individuals who sit low and behind the rear wheels had lower propulsive forces and stroke frequency. little research has been conducted to assess the vibrations experienced by wheelchair users (Tai et al. 1998).... both shown to be associated with CTS (Cooper and Boninger. (2003b) have shown that in the natural frequency of humans (4–15 Hz) the addition of suspension caster forks do reduce the amount of vibrations transferred to the user. In a series of magnetic resonance imaging (MRI) and X-ray imaging results for people with paraplegia. Kwarciak et al. DiGiovine et al. 1986). seating systems are prescribed by clinicians based on the ability of the cushion to reduce pressure and provide proper positioning (Cooper et al. Wolf et al. almost all of the individuals with progression of MRI findings were women. 2000). 2000). 2001). Foam and captured air cushions are best at attenuating the peak and average shocks and vibrations seen during actual wheelchair use. .. The primary goals being to reduce the risk of developing an ulcer and ensure adequate seated posture. 2003b. Specifically.148 Rory A. suspension manual wheelchairs do reduce the transmission of shock vibrations to wheelchair users. disc degeneration and other harmful effects to the body (Seidel et al. VanSickle et al. a large force directed towards the hub (radial force) was correlated with a higher MRI change score over time. 1996.. The ability of a seating system to minimize impact (shock) and repetitive vibrations that an individual experiences is commonly not considered.. This may adversely affect the physical performance of the individual. It may also lead to social inactivity. (2003) examined the relationship between the seating systems for manual wheelchairs and the vibrations experienced. VanSickle et al. users encounter obstacles such as bumps. 1996). 2003a). A propulsion stroke during which the hand drops below the pushrim results in a greater push angle and lower stroke frequency. the wheelchair user.

000 serious wheelchair accidents annually. 2001). Characterized by chronicity and relapse... and chronically swollen limbs are examples of common. A video-based analysis of tips and falls shows that proper legrest adjustment and seat belt use offers wheelchair users greater safety when traversing common obstacles (Corfman et al. In 1991 alone there were 50. Wheelchairs accidents are often attributed to improper use or installation of safety systems and/or poor adjustment of the wheelchair (Van Roosmalen et al. Only wheelchairs that meet safety criteria should be used regularly as seats in a motor vehicle (Bertocci et al..Wheelchair design and seating technology 149 Dobson et al. injury or lowering the speed while driving without legrests may also decrease risk of injury. 30 mph at 30 times gravity acceleration frontal collision. 1999a). The method of braking affects the braking distance. 1999b). 770 wheelchairs-related deaths were reported to the United States Consumer Product Safety Commission (USCPSC). 1999). Recent work has resulted in significant findings and developments. Unmat and Kirby (1994) reported that there are about 36. In a randomized control trial pressure-reducing seat cushions for elderly wheelchair users were found to reduce the incidence and severity of pressure ulcers (Geyer et al.. and to provide independent mobility for others it raises an entire set of safety issues.. Injury depends on the duration and intensity of tissue loading as well as the characteristics of both the tissue and the interfacing support surface. and should be considered acceptable as a pedestrian access route for wheelchair users.000 wheelchair-related accidents that required emergency room treatment (Kirby et al. Between 1973 and 1987.. (1996b) developed a system for the analysis of seat support surfaces using shape control and simultaneous measurement of applied pressures. Their results indicate that all surfaces with an 8 mm gap or less between components surfaces yielded results that were similar to the poured concrete sidewalk. early detection. and management of soft tissue injuries. Brienza et al.. The system has been used to investigate the biomechanical factors for predicting pressure ulcer risk (Wang et al. 2001).. The results indicate that using a seat belt and properly adjusted legrests reduces risk of Prevention of pressure ulcers The loss of tissue integrity evidenced by pressure ulcers. 2003b). 1990). diabetic foot ulcers. While this is necessary to transport some individuals. Cooper.5% of which were attributed to falls and tips (Calder and Kirby. In an investigation of the relationship between pressure ulcer incidence and buttock-seat cushion interface pressure in at-risk elderly wheelchair users showed that lower interface pressures corresponded to fewer pressure ulcers (Brienza et al. venous stasis ulcers. as been shown by both simulation and testing (Bertocci et al. these conditions are among the most costly. Prevention of accidental injuries while using wheelchairs Wheelchair-related driving accidents occur frequently and can have devastating effects. chronic medical conditions (Brienza et al. . (2003) and Wolf et al. Excessive. braking time. 1996a). 1996). 1998. A study of power wheelchair driving revealed that the obstacles most likely to induce a fall or loss of control were ascending a curb cut. and braking acceleration (Cooper et al.. In some cases. 68. Injuries are more likely to occur in wheelchairs that are unable to fail gracefully during crash loads (Bertocci et al. yet preventable of soft tissue injuries.. (2003) conducted evaluations of the vibration exposure during electric-powered wheelchair driving and manual wheelchair propulsion over selected sidewalk surfaces. Serious injury may occur under typical test conditions. people use their wheelchairs as seats in motor vehicles. In-depth knowledge of the interaction between externally applied pressure and the soft tissue is crucial to the prevention. 2000). and descending a 5-degree ramp. Bertocci et al. 2001. 1994). 2002. ascending a curb (50 mm) at a 45-degree angle. unevenly applied or repetitive tissue loading is a common contributory factor in all of these conditions. 1998a)..

g.. Lightweight manual wheelchairs are minimally adjustable or non-adjustable manual wheelchairs intended for an individual or for institutional use.1(c).. All manual wheelchairs are not alike. and adjustable wheelchair is best (Cooper and Cooper. 1999a. 2001).. 2003.. However. It is important for clinicians to realize the benefits of a proper wheelchair prescription.. 2001a). and appropriate for in home use (CMS. hospitals) and are generally not appropriate as a long-term mobility device. 2003). 1997a). 11. Cooper et al. Ultralight manual wheelchairs are moderately adjustable or selectable manual wheelchairs intended to be used by a single individual.3 Manual wheelchairs Design characteristics The Centers for Medicare and Medicaid Services (CMS) is one of the nation’s largest purchasers of wheelchairs (CMS. 11. Shalala et al. For most firsttime wheelchair users. Wheelchairs are considered by CMS to be durable medical equipment (DME) and must meet the following criteria: capable of withstanding repeated use. The obvious attraction of depot wheelchairs is their low purchase price... 11. see Fig.g. 2003c). Adjustment and fitting Ultralight wheelchairs offer to most flexibility in selecting or setting the fit to the user (Cooper. 1991. 1998a). b. Cooper et al. and (c) depot manual wheelchairs. Pictures of (a) ultralight. There are variations in the quality and performance of manual wheelchairs (Cooper et al. The last criterion is often interpreted by Durable Medical Equipment Regional Carriers (DMERC’s) to exclude payment of wheelchairs that would provide community mobility and improve function outside the home (Fitzgerald et al.150 Rory A. 1995. 1994a. 1996. 1996). 11. neither CMS’s coverage nor payment of wheelchairs is always in the best interest of the patients who need them (Collins et al. 2003c. see Fig.1. not useful to person in absence of illness or injury. Lightweight and ultralight wheelchairs provide clinicians and consumers greater ability to select and adjust the wheelchair to the user and accommodate the consumer’s functional needs. Fitzgerald et al. For anyone who will be self-propelling a wheelchair for more then a few months.. (b) lightweight.1(b). see Fig. and ultralight wheelchair should be recommended. not only for the consumer’s comfort and mobility needs but also in the quality of the wheelchair that will last with minimal repairs (Cooper and Cooper. Depot wheelchairs represent wheelchairs that are essentially designed for depot (e. 1999b. . primarily used to serve a medical purpose. for experienced and highly skilled wheelchair users more features may be selected and set by the manufacturer (a) (b) (c) Figure 11. amusement park) or temporary institutional use (e. 2002).1(a). airport. However.

A larger caster requires a lower legrest angle. start/stop quickly. can effect seat height as well. however. an assistant can tilt the user and wheelchair backwards to find the balance point. also known as seat dump. Whitman et al. There are two basic rules of thumb for determining seat height. a balance must be struck between the caster size and legrest angle. so that there is 40–75 mm space between the front edge of the seat and the popliteal area behind the knees. research shows that placing the rear axle as close as possible to the CoM is best.. Simple method for setting the rear axle position is to set it slightly forward (anterior) for the rearmost position and ask the use to balance on the rear wheels. Casters under 100 mm should only be recommended for users who can balance their wheelchair on its rear wheels.g. the user should be able to comfortably touch the rear axle with his/her arms at the side. home. Otherwise. About 5 degrees of posterior tilt is common. than a higher legrest angle is recommended. The legrest angle will bring the footrests closer or further from the front casters. Rear anti-tip wheels can be used to assist the operator from becoming more comfortable with the wheelchair set-up and to help prevent rearward falls. Bringing the rear wheels in close to the user facilitates propulsion as well as negotiation of the built environment (e. However. The seat should be high enough to perform typical activities of daily living. The axle should continue to be moved forwards so that the front casters are between 50–100 mm above the ground while balancing. Typically. Casters are readily available from most manufacturers in sizes ranging from 50–200 mm in diameter. the maximum legrest angle that can accommodate the user’s range of motion should be specified. Probably the most critical feature to set is the axle position with respect to the center of mass (CoM) of the user and wheelchair combination. it tends to make a larger portion of the pushrim accessible for propulsion. The backrest angle should be set at 90 degrees.g. balance on rear wheels). A larger seat dump helps to increase stability by pushing the . While there is no agreed upon method of optimizing the rear axle position. The angle of the seat with respect to horizontal.Wheelchair design and seating technology 151 to reduce the overall mass and increase reliability (Cooper. Legrest angles commonly vary from 70 to 95 degrees. If the person is unable to balance on the rear wheels. larger angles are desirable for some wheelchair users who require more trunk support. but low enough to fit under desks and tables and to efficiently propel the wheelchair. A simple rule to follow is that one finger should be between the sides of the wheelchair and the greater trochantors of the user. A backrest that is too high may interfere with the arms when propelling the wheelchair. The best approach is to start with an adjustable tension backrest or a rigid padded backrest. In addition. 1996.. 1998). and then it can be reclined to improve balance. work). ascend/descend ramps. Therefore.. A tight legrest angle provides smaller maneuvering space for the wheelchair. the backrest height may be lower than standard upholstery as they tend to provide greater support for the pelvis and lumber spine. Rear axle position near the CoM reduces the efforts required for propulsion. which makes it easier to get around indoors. The seat depth and the seat width are often the best starting points when selecting the wheelchair dimensions. and at the same time the elbow angle should be 90–120 degrees with the upper arm along the trunk and the hand at top dead center on the pushrim. Clothing guards are most useful for allowing the chair to remain narrow and to keep clothing out of the wheels. If the user feels uncomfortable in this position. The backrest height and angle effect both balance and the ability to propel the wheelchair. In order the set the seat height. the seat width should be as narrow as possible. The optimal angle is best found having the user attempt a few different driving tasks (e. the rear axles can be moved rearwards a few millimeters. and decreases the tendency to veer of course on a cross slope. Most backrests offer some adjustment. school. if the backrest is not high enough it will not provide adequate support for the user. With rigid backrests. The seat depth should be selected. Often the rear wheel size can be selected to provide a wider range of positions. If the user has good flexibility and low tone. for turning. Either of these designs offers some adjustment for the user.

Active indoor/ outdoor wheelchairs may be best suited for these individuals. provides another option that may be most appropriate for some clients. people with cerebral palsy.. Individuals with spinal cord injury or dysfunction. travel long distances. 2001). The power base consists of the .g. 1998a). Individuals who experience pain or fatigue negotiating ramps. This allows them to be maneuverable in confined spaces. but who have difficulty negotiating ramps.152 Rory A. The pushrim activated powerassisted wheelchairs (PAPAW). Indoor/outdoor powered wheelchairs are used by people who wish to have mobility at home.g. 2001). Indoor wheelchairs have a small footprint (i. it is not difficult for an assistant. and elderly people may benefit from a PAPAW. protrusion rims. flooring). to lower the stroke frequency. and to reduce the range of motion required for efficient propulsion (Corfman et al. Transferring out of the wheelchair becomes more difficult as seat dump increases. driveways.. pelvis into the backrest. 11. A convenient grouping by intended use is primarily indoor. soft surfaces (e. These individuals may have impaired upper extremities or their limitation could be due to disease or injury-related reduction in cardiorespiratory capacity. school.. PAPAWs have been shown to reduce the amount of force required for propulsion. 1995a. carpets or outdoor surfaces are ideal candidates for a PAPAW. There are a variety of pushrims available. 2002c). sidewalks.e. There are also clients who desire a manual wheelchair. Some wheelchair users want to drive over unstructured environments. and in the community. The most common types are standard anodized aluminum tubing.. 2002b).. the individual must have the coordination and strength to propel a manual wheelchair over a smooth hard floor with at least one arm. A PAPAW can provide mobility similar to a manual wheelchair with less stress on the arm joints. People who have severe difficulty walking or who have the inability to walk should be evaluated for a PAPAW.. Both indoor and indoor/outdoor wheelchairs conserve weight by using smaller batteries. they may not have the stability or power to negotiate obstacles outdoors. Some people cannot functionally propel a manual wheelchair while at the same time they may have barriers to be able to use an electric powered wheelchair effectively (Buning et al. work. Cooper et al. while at the same time offering some of the aerobic exercise benefits of manual wheelchair propulsion (Arva et al. 2003a). 11. carpet) and other mobility barriers. and to move fast (Cooper et al. although one must be cautious not to promote pressure sore on the back. but who stay on finished surfaces (e. The PAPAW is beneficial for reducing the stress on the upper extremities. both indoor/outdoor..4 Pushrim activated power assisted wheelchairs A pushrim activated power assisted wheelchair uses motors and batteries to augment the power applied by the users to one or both pushrims during propulsion or braking (Cooper et al. and to provide a more natural fit for the hand. area connecting the wheels). However. The active indoor/outdoor-use wheelchairs include those with suspension and use of a power-base design. It may be difficult for the wheelchair user to load a PAPAW into a car or van that is not equipped with a lift or ramp.. increasing propulsion efficiency. The PAPAW novel control technology amplifies the force applied to the pushrim to propel or brake the wheelchair (Cooper et al. and ergonomic rims.5 Electric powered mobility Electric powered wheelchair designs Powered wheelchairs can be grouped into several classes or categories (Cooper. which in turn reduces the range for travel. 2001).. vinyl coated aluminum tubing. neoprene coated aluminum tubing. Most people should use ergonomic rims designed to help reduce the loading on the upper extremity joints. and lowering the cardiopulmonary demand of wheelchair propulsion. side slopes. In order to use a PAPAW effectively. and active indoor/outdoor.

2. 1998a). drive wheels. A potential drawback to a RWD system is its low maneuverability in tight areas due to a larger turning radius. When transitioning from a steep slope to a level surface (like coming off a curb cut). armrests. backrest. 11. In RWD power bases the drive wheels are behind the user’s CoG and the casters are in the front. The drive wheel position defines the basic handling characteristic of any power wheelchair. Most scooter seats swivel to ease ingress and egress. handle bar) steering system.2(c). (b) mid wheel.. seat. In MWD power bases the drive wheels are directly below the user’s CoG and generally have a set of casters or anti-tippers in front and rear of the drive wheels. castors. see Fig. RWD systems are the traditional design and therefore many long-term power wheelchairs are familiar with their performance and prefer them to other designs.2(b). see Fig.Wheelchair design and seating technology 153 (a) (b) (c) Figure 11. legrests. Picture of (a) rear wheel. and frame. see Fig. mid wheel drive (MWD).. The advantage of the MWD system is a smaller turning radius to maneuver in tight spaces. 11. A major advantage of RWD systems is its predictable driving characteristics and stability. or front wheel drive (FWD) (Cooper. Power wheelchair bases can be classified as rear wheel drive (RWD). All three systems have unique driving and handling characteristics.. Often.g. A disadvantage is that a FWD system has more rearward CoG. The seating system (e. The seats are often removable to simplify transport in a personal automobile. Scooters Scooters are designed for people with limited walking ability and substantial body control (Cooper.3. FWD systems may climb obstacles or curbs more easily as the large front wheels hit the obstacle first. Scooters are primarily characterized by the captain’s seat. A disadvantage is a tendency to rock or pitch forward especially with sudden stops or fast turns. The classification of these three drive systems is based on the drive wheel location relative to the systems center of gravity (CoG). controllers. seating systems from one manufacturer are used on a power base from another manufacturer. 1998a). footrests) is a separate integrated unit. 2004). see Fig. One of the most important distinguishing features of a scooter is that speed is controlled electronically and . 11. A FWD power base has the drive wheels in front of the user’s CoG and it tends to be quite stable and provides a tight turning radius.2(a). and (c) front wheel drive electric-powered wheelchairs. motors. therefore the system may tend to fishtail and be difficult to drive in a straight line especially on uneven surfaces (Guo et al. batteries. They are power bases with a mounted seat and usually a tiller (e. 11.g. the front and rear casters can hang up leaving less traction on the drive wheels in the middle.

Most scooters allow the steering column to fold or be removed without tools in order to make the scooter easier to transport in a personal motor vehicle. Simpson et al. Their device was intended to assist with climbing curbs and uneven terrain. traversing outdoor surfaces (e. “man/ machine interface” or “access method”. Use assessment. 1998). fitting. (1996) and Levine et al. 11. (1999) have reported on combing obstacle detection and avoidance with an electric powered wheelchair. all refer to a combination of a technology and a communication paradigm that allows a consumer to independently access and operate a useful system. They use a combination of ultrasound and infrared sensors to map the environment and provide assistance with guidance and control of an electric powered wheelchair for people who have visual as well as lower limb impairments. There are three main elements when examining the usage of an assistive device.. There are products that use electronic steering by using a motor to change the direction of one or both front wheels. Figure 11. Figure 11. subjects reported using the IBOT to perform a variety of activities including holding eye-level discussions with colleagues and shopping by balancing on two wheels. (2003a). going up and down steep ramps. activities of daily living. Robotic wheelchairs The Independence 3000 IBOT Transporter (IBOT) has probably garnered the most attention for its innovations in dynamic stabilization that provide it with a unique combination of capabilities. employment and community integration (Spaeth et al. Fig. (2002). Critical for the success of these devices is the link between the consumer and the machine.3.154 Rory A.. In a study by Cooper et al. The IBOT incorporates a variety of sensors and actuators for dynamic stabilization of the device. Other stairclimbing and curb-negotiating devices have also been investigated. Cooper et al. An IBOT in balance function. grass. (1995) described the investigation into combing the use of robotic legs with a wheeled device to provide increased mobility to people with disabilities.g. speed control. 2003a). and training The mastery and functional use of electric powered wheelchair can be instrumental to self-esteem. and for changing operational functions (Cooper et al. Wellman et al. Yoder et al.4.. self-diagnosis. Future advances in controls may benefit from learning from nature and how insects negotiate rough terrain (Jindrich and Full.4. 1998. Photograph of a three-wheeled scooter. Jones and Cooper. dirt trails) and climbing curbs. (2001) reported on an electric powered wheeled mobility device that can negotiate stairs and ingress/egress into a motor vehicle. direction is controlled manually. 2002). Interchangeably referred to as the “interface”. Lawn et al. The first element is the person who .

c). In addition. the third element is often simply referred to as the interface.g. Based on these arguments tilt-in-space and recline are widely prescribe accessories on power wheelchairs. physical output devices and information processing capabilities. 2000a. which has certain physical input devices. the joints of the body maintain their seated position) Fig. The return spring tension of the stick.. and changes circulation. 1989). sensory. Individuals with movement disorders are often the most underserved population.g. 11. because sensory impairments. Manufacturers provide gain adjustments at the motor control power stage but these provide little improvement in a consumer’s control capability. Nachemson (1975) found decreased inter-vertebral disc pressure by reclining the back from 80 to 130 degrees. the commercial control options fall off precipitously to devices such as keyguards. If an individual has partial or complete paralysis but has residual fine motor control either in the affected limb or at an alternative motor site.. Others purported advantages of tilt and recline system include better swallowing and decreased leg edema (Schunkewitz et al. using recline and tilt-in-space can allow for a change in position in the wheelchair and thus improve comfort. a technology for control access is commercially available.. However. joystick is the traditional method of control for electric powered wheelchairs (Cooper et al. The commercial offerings have almost no options for personalization (Cooper et al. Fehr et al. transfer information and affect each other. This is the most dynamic.. Elevating the legs while lowering the torso can improve venous return. It is through the interface that the person and machine actually interact. tremor or other unintentional movement pattern. The maximum speed forward and reverse can be set.6 Specialized seating and mobility Pressure ulcers. see Fig. if the consumer has a movement disorder. . e. and cognitive abilities. (2000) describe the result of a clinical survey of 65 practicing clinicians in a variety of rehabilitation services from 29 states. template shape.6. There are some difficulties with tilt-in-space wheelchairs. Finally. as well as acceleration in the fore–aft directions and while turning. The analog.Wheelchair design and seating technology 155 has certain physical. 11. The second is the machine or technology. The clinicians reported that between 10% and 40% of their clients who desired powered mobility could not be fitted with electric powered wheelchairs.. a key ingredient in the development of pressure sores. alters the load on postural musculature. Changing seating position redistributes pressure on weight-bearing surfaces. and possibility the most complex element of the system.5. and decrease fluid pooling in the lower extremities.. Changing position can also facilitate respiration. Sprigle and Sposato (1997) and Hobson (1992) studied the effects of various seated positions and found that pressure was reduced significantly with 120 degrees of recline. axis alignment. Changing seating posture can extend the amount of time a person can safely remain seated without damaging tissue or becoming fatigued. armrest mounted. Reclining wheelchairs allow the user to change sitting posture through the use of a simple interface (e. expanded keyboards and single switch scanning interfaces. switch). 2002a). poor motor function or cognitive deficits made it impossible for them to safely drive a power wheelchair with any of the existing commercial controls. Tilt-in-space and recline seating functions may be of benefit for ameliorating these conditions. Tilt-in-space systems allow the person to change position with respect to gravity without changing their seated posture (i. clinicians only have simple adjustments in the electronic controls to accommodate their clients for electric-powered wheelchairs (Cooper. In 2000. 1998a). and damping factor are non-adjustable-one size fits all. Currently. 11.e. Gain adjustments simply slow the chair down (to a crawl if necessary) so that the consumer can obtain a minimal level of mobility. Reclining wheelchairs assist in performing pressure relief. pain management and postural accommodation are critical issues for many individuals with neurological impairments. Tilt-in-space can significantly reduce static seating pressure.

Example of an electric-powered wheelchair with powered seat elevation function. Increasing seat height tends to decrease the stability of the wheelchair. Tasks such as cooking and washing can be simplified with an elevated seat height. 11. Picking up objects from the floor can also be assisted by an adjustable seat height. Many activities can be promoted by using a variable seat height wheelchair. Sliding or stretching during reclining or tilting in some individuals may produce undesirable shear forces. Some seat lowering mechanisms alter the legrest angle in order to get closer to the ground. Access to the floor is an important feature for promoting the cognitive and social development of children. As the person is lowered to the floor by the wheelchair stability is affected. Cooper et al.156 Rory A. Picture of an electric-powered wheelchair with power seat tilt function. It is important to assure that the rider has suitable range of motion to safely use this feature. Most wheelchair manufacturers do not recommend elevating the seat on a slope or uneven terrain. and bunch clothing. Children who use wheelchairs can benefit from being able to access the ground. and interact with other children at ground level. Picture of an electric-powered wheelchair with a power seat recline. Items on high shelves or in high cabinets can be obtained by using an elevating seat. Lowering the seat makes access to desks and tables easier. Children often play. and can require greater turning diameter when reclined. Lowering the seat height tends to make the wheelchair more stable. Figure 11. Lowering seat height can make it simpler to get under tables and desks.7. These wheelchairs are heavier than standard wheelchairs. Many powered wheelchair controllers cause the speed of the wheelchair to decrease as the seat height is raised. Raising the seat height also offers several benefits. they are less stable. A potential problem with tilt-in-space and reclining seating systems is that the body may not remain in a stable position after transitioning through several seating orientations.6.5. . excite spasticity. Fig. A lower seat position can be helpful when maneuvering the wheelchair on steep ramps or slopes. Figure 11. The added stability of being able to lower the seat height can be of considerable benefit on cross slopes. Figure 11.7. explore the environment. Elevating the seat height is helpful for viewing people at eye level.

e. contouring. cooking.7 Seating and positioning hardware Seat cushions Various densities and types (Polyurethane. This is because the viscous fluid moves to come to a constant pressure within its container. 2000b). Example of an electric-powered stand-up wheelchair.. 11. The pressure distribution can be altered by using a stiff base (e. shelves. washing dishes. specialized technology provides greater flexibility when making individual accommodations (Troy et al. Stand-up wheelchairs offer a variety of advantages over standard wheelchairs.8.. counters. Manually powered stand-up wheelchairs are heavier than lightweight manual wheelchairs. and baffling. Stand-up wheelchairs are being produced that are lightweight and transportable. Stand-up features are integrated into some power wheelchairs with minimal trade-offs (i. sinks. However. Figure 11.. The ability to perform some occupations can be enhanced by using a stand-up wheelchair. Many activities around the home are easier to accomplish by using a stand-up wheelchair. Urethane. foam has a tendency to deteriorate at an undesirable rate.. see Fig. T-Foam. The rehabilitation team must work with the individual to determine if the stand-up wheelchair should have an electric powered base or Positioning hardware With some care and properly adjusted and maintained postural support system can promote good . If one were to simply sit on a balloon full of air.Wheelchair design and seating technology 157 whether it should be manually propelled (Cooper et al.8. 2001b). Viscous fluid cushions use an electrolyte fluid mixture in a closed plastic or latex pocket. Baffles can be used to control to flow of the viscous fluid just as with air cushions. accessing copiers. and many windows. The viscous fluid conforms to the body and provides a nearly even pressure distribution. Foam has been shown to offer the lowest maximum pressure over the seating surface when the appropriate densities and contours are used. Stand-up wheelchairs can reduce the need for significant home modifications. the pressure over the entire seating surface would be equal.g. 1997). 11. Viscous fluid cushions work much like air to equalize pressure over the entire seating surface. In the workplace. Sun-Mate) of foam are commonly used in linear seating systems. Air floatation cushions do an excellent job of distributing the pressure over the entire seating area. They provide easy access to cabinets. and interacting with colleagues. plastic or foam) to provide some contouring. A foam cushion may be sculpted or contoured in order to make foam more effective for pressure relief. machine operators or machinists can perform normal job functions with minimal modifications to the worksite and physicians and surgeons can examine patients and perform procedures safely and effectively. no additional weight or size). for example. However. For example.. stand-up wheelchairs may help when making presentations using a “white board”. In order to better control interface pressure many air floatation cushions use multiple compartments. Air floatation cushions provide an excellent example of cushion design based upon the interface pressure theory (Fitzgerald et al. and ironing clothes.

These devices can help to prevent or correct a slouching posture with an unacceptable postural pelvic tilt. If an anti-thrust seat is used. The width and height of the back base should be determined based upon the users mode of mobility (e. Cooper.. foam in place. Most systems are available with a variety of covers (e. The pelvic belt or subasis bar should prevent the person from sliding forward on the seat even when the occupant wiggles or squirms. power) and postural support needs. lycre-spandex. All wheelchair users require some degree of postural support. 1991). spina Bifida. The pelvic belt or subasis bar must be positioned snugly (e. The ability to use the hands and arms to perform activities of daily living may be increased through positioning. The simplest form of postural support uses a linear sling back and a linear sling seat. Greater postural control can be obtained by using off-the-shelf products for most cases. lap belt. Backrests may also be contoured to provide additional support for those people who need it. stroke.g. 1998a). Postural support systems can be customized to meet individual needs. If attached to the wheelchair. the higher the degree of impairment the taller the backrest must be to provide adequate support. The latch on the pelvic belt must be selected to meet the physical and cognitive abilities of the user. Plastic.. Proper positioning can help to improve pulmonary function. increasing function. For people who use manual wheelchairs the backrest should follow the individuals frontal contour and the height should not extend above 4 cm below the scapula. or advanced muscular dystrophy primarily use postural supports and positioning hardware. health and maximal function (Engel. attendant propelled. or antithrust cushion. Positioning helps to orient the skeleton and the distribution of stresses within soft tissues. subasis bar. the child may slump in the seat such that the thoracic supports can bruise or abrade the underarms. People with cerebral palsy. and preventing some of the debilitating effects associated with long-term wheelchair use. . There are a wide variety of products which are used to promote good seating posture and functional seating for wheelchair users. and to prevent pressure sores. For some people linear systems provide adequate support. If the pelvic belt or subasis bar is not adjusted properly with the pelvis against the backrest. Cooper et al. More recently. lower limb amputations. 1998a. the pelvic belt or subasis bar should be used whenever the person is sitting in the wheelchair. The pelvis should be maintained in a neutral position against the backrest. bare). The pelvic belt should not slip or become unlatched inadvertently. However. people who have spinal cord injury. Special mounting hardware can be provided by manufacturers upon request or developed by local rehabilitation engineers. Contour can be added to backrests via carved foam. In a few cases. In some cases choking may occur which can lead to death. The anti-thrust seat helps to maintain posture by positioning the ischial tuberosities. manual. Two common approaches used are a flat back base with additional supports or a back base with curved sides. severe multiple sclerosis.158 Rory A. traumatic brain injury. In some cases combinations of these devices must be used. arthritis. This can be used to help prevent or control pelvic and spinal deformities. postural control has gained greater attention among active wheelchair users as a means of improving comfort. about two adult fingers should be able to fit between the belt and abdomen). or some severely impaired elderly persons can benefit from postural supports (Boninger et al. The height should be sufficient to provide comfortable support. Pelvic support and positioning can be achieved using a pelvic belt.. custom fabricated postural support systems are necessary. vinyl. and to provide a base to push against.g. Generally. wood or metal can be used to reinforce areas for additional support and control. For some people the pelvic belt or subasis bar works in concert with thoracic supports..g. Other people who are more severely impaired or who are at risk for developing postural deformities require greater postural support. the step in the seat must be positioned in front of the ischial tuberosities such that the proper pelvic angle is maintained. osteogenesis imperfecta. arthrogyposis. Pelvic support for minor cases can be provided by using a seat belt and an anti-thrust seat cushion.

A good seating and head support system is unlikely to be a solutions to all of a person’s functional limitations.e. and the person should be isolated from all fasteners. For people who require minimal head and neck support a simple flat headrest is sufficient.. Lumbar support can improve balance with added comfort and mobility. In most case. or custom molded/carved contours. Scoliosis support systems can provide additional support for proper positioning for greater comfort and better control over the wheelchair. Head supports should not apply pressure to the temporal area. Unfortunately. or cam lock) to aid in transferring in and out of the wheelchair. For many wheelchair users a standard sling seat induces sacral seating.Wheelchair design and seating technology 159 standard contours.g. The clinicians must work with the person to develop a plan for how the person will ultimately sit and function. A skilled clinician must determine the direction and the amount of force required to place the head in the desired position. and may include a strap which wraps around the trunk for greatest support. This can be corrected with a lumbar support. Spinal extension can be achieved with some people. quick release pin. 11. typically 8–25 mm is sufficient depending upon the applied force). A lumbar support can be added to the backrest or a rigid backrest can be used on many wheelchairs for people who have difficulty maintaining the natural curvature of the spine. some functional tests with the head support hardware are required to verify improved function.. the desired support is duplicated by selecting head support hardware. A properly placed lumbar support can position the head squarely over the shoulders.g. Most systems attempt to bring the head to a neutral position. After determining the amount of force and direction of force required. which is especially important if the seating system is tilted or reclined. Extensions are designed and added to the backrest structure which support the head and neck. Rehabilitation technology suppliers can be an important part of the wheelchair and seating selection and fitting process. Custom devices and systems can be designed for people with unusual postural support needs. Rigid backrest for lumbar support is becoming widely used among wheelchair users. there are few suppliers who are trained in AT or who have . RESNA offers three levels of credentials. Head and neck supports often provide the necessary stability required to control a power wheelchair. or communication device. Head control is difficult to evaluate and requires specialized knowledge. fore–aft. ring lock. Scoliosis supports should be prescribed or designed to be independently adjustable (i. Velcro. the RESNA developed a credentialing program in AT. A depth between 125 and 200 mm is sufficient for most people.8 Applying evidence-based practice to wheelchairs and seating Credentialing In response to the needs of clinicians with specialized knowledge of and experience with assistive technology (AT). The clinician should be cautious to avoid placing excessive force while positioning the head. The degree of support required determines the type of head and neck support employed.. Supports can be designed or prescribed to wrap around the trunk anteriorly. Often the wrap around Scoliosis supports incorporate a quick adjust mechanism (e. and improve pelvic alignment. the mastoid process. or the mandible. inferior–superior. This type of headrest prevents the head from extending beyond the plane of the backrest. The height and width depends on the individual’s anatomy. When using lateral supports many backrest plates require reinforcement.. People with significant loss of lateral stability may benefit from fixed or adjustable lateral trunk supports.e. Many people who can benefit from head positioning systems can exert active muscle forces in addition to gravitational and passive connective tissue forces. Lateral and Scoliosis supports require padding (i. medial–lateral). knob head bolt) and a simply operated strap locking mechanism (e. A 25–100 mm thick piece of contoured foam the width of the back is placed in the lumbar area. environmental control unit. Curvature can be added to the headrest to keep the user’s head within the confines of the headrest.

or speech therapy. US Department of Commerce. nurses. For example. Unfortunately. audiology. needs and goals of the client. (Cooper. the team will have ready access to a variety of assistive devices for the client to evaluate during his/her clinic visit and if necessary to try at home. however. 1998a). personal care assistants and other similar professionals can also make important contributions to the AT service delivery team. Team approach Medical rehabilitation is a profession that is best practiced as part of a team. these individuals typically have a clinical degree and license in occupational therapy. It is absolutely critical for the team to thoroughly discuss each client’s circumstances and to prepare detailed documentation supported by scientific and clinical literature. and consumers. The best AT clinics include a team consisting of a therapist. individuals are eligible to sit for the ATP examination and the supplemental RET examination. These individuals work with cooperatively with the client to attain the client’s rehabilitation goals. an individual must demonstrate compensated employment in the field of AT and pass an examination that consists of fundamental elements and case-based scenarios. current abilities. Cooper et al. rehabilitation engineer. the standards do not require disclosure of most of the results in manufacturer’s product literature (Cooper. This has led to wide discrepancies in the quality of the services provided by rehabilitation technology suppliers. For years engineers and technicians have been supporting AT clinics. engineers. SB/94-1. In order to identify clinicians whom have specialized in AT service provision. 2003). (1994). Improving products can increase the reliability of wheelchairs and reduce the risk to users. Bureau of Census Statistical Brief. 1998a). 1998b) For these individuals. RESNA created the Assistive Technology Supplier (ATS) credential. Wheelchair standards attempt to provide quantitative data to clinicians. RESNA created the Rehabilitation Engineering Technologist (RET) credential which requires an individual to hold and engineering or technology degree. . Rehabilitation counselors. manufacturers can improve their products. Suppliers with the ATS credential have demonstrated a minimum level of knowledge and experience in with AT. 1998. AT is an area of healthcare that receives undue scrutiny and hence extra diligence is required in ensure that each client’s needs are met (HCFA. but this is tedious and makes comparisons difficult. Hence. there was no appropriate clinical credential for these individuals. particularly because consumers are demanding higher quality products and competition between manufacturers is growing. These credentials help consumers to identify individuals who have acquired specialized knowledge of AT and who are committed to providing high-quality services. Clinics should give careful consideration to encouraging the suppliers who work with them to demonstrate that their employees hold the ATS credential. and a physician. a credentialed supplier. Schmeler. Other professionals may also be consulted depending on the REFERENCES Americans with Disabilities. RESNA created the Assistive Technology Provider (ATP) credential. physical therapy. Some therapists and other licensed clinicians choose to specialize in the delivery of AT services. Unfortunately.160 Rory A. A means of demonstrating safety and efficacy is to use the ANSI and RESNA wheelchair standards (Cooper. ANSI-RESNA and International Based on the results of wheelchair standards testing. and availability of resources (Cooper. After a suitable period of clinical AT service delivery experience. Ideally. During an AT assessment the team must work with the client to assess the client’s goals. 1995b). In order to attain the ATS credential. Consumers or clinicians can obtain the information if requested. AT standards When developing a new mobility device for people with disabilities it is a requirement of the US Food and Drug Administration that the device be both safe and effective. formal rehabilitation training or experience. January.

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In this chapter. Durfee reviews pioneering developments in orthotics. rehabilitation robotics. clinical devices designed to evaluate patients and. 2003 and 2005). USA 12. discuss the growing pains of forging a novel technology. Herr4 1 Department of Mechanical Engineering. and prosthetics. Durfee3 and H. fashions a new class of interactive and user-friendly robots that enhance the clinicians’ goal of facilitating recovery by not only evaluating but also by delivering measured therapy to patients. Krebs1. USA and 4 The Media Lab and The Harvard/MIT Division of Health Science and Technology. by contrast. orthotics. and Brain and Cognitive Sciences. Cambridge. The new focus on mechanisms of recovery and evidence-based treatment together with developments facilitating safe human–machine interaction has paved the way for the surge in academic research. Previously. New York. 37(6) of Nov/Dec 2000. Massachusetts Institute of Technology. which started in early 1990s. Rehabilitation robotics.1 Overview One overarching goal drives our research and development activities: to revolutionize rehabilitation medicine with robotics. 12. also deliver therapy. We will also discuss some emerging developments that could render some science fictions into reality.12 Rehabilitation robotics. 3 Department of Mechanical Engineering. In fact. USA. mechatronics. 2 Departments of Mechanical Engineering. has grown significantly in the last 10 years (cf. Orthotics and prosthetics may be considered as a category of assistive robotics. and prosthetics H. we will limit our discussion to mechatronic systems. special issue of the Journal of Rehabilitation Research and Development. and neuroconnectivity (neuro-prostheses) have reinvigorated research in this field.2 Rehabilitation robotics Rehabilitation robotics encompasses an emerging class of interactive. USA. University of Minnesota. the lack of equivalent advances in realm of energy storage represents the only major hurdle preventing the realization of practical versions of Hollywood’s fancies such as Star Trek’s Commander Data or the Terminator. Massachusetts Institute of Technology and Adjunct Assistant Research Professor of Neuroscience. thereby facilitating a disabled individual’s functional recovery. and Herr reviews lower extremity prostheses. Hogan2. and outline the potential for a brilliant future.I. Cambridge. Krebs and Hogan review pioneering clinical results in the field. The Winifred Masterson Burke Medical Research Institute. Robots and computers are being harnessed to support and enhance clinicians’ productivity. Krebs and Hogan review upper-limb prostheses. 165 . N. While the previous high water mark for mechatronic assistive technology occurred during the Vietnam War decades of 1960s and 1970s. International Conference on Rehabilitation Robotics – ICORR 2001. W. and information technologies that can assist movement. robotics were incorporated into assistive devices to help the physically challenged accommodate their impairment. Weill Medical College of Cornell University.K. enhance treatment and quantify outcomes. Of the other two activities. This development represents a shift from earlier uses of robotics as an assistive technology for the disabled. we present three fronts of this revolution: rehabilitation robotics. user-friendly. computers. The first and newest approach. orthotics. recent advancements in materials. Minnesota.M.

2000. Evolving lower extremity devices are inspired mainly by gym machines and orthoses rather than by re-configured industrial robots. 2004. While attempts to adapt or re-configure industrial robots for use in rehabilitation robotics appears to be a reasonable approach it suffers from a critical drawback: some 20 years of experience with industrial robots shows that low impedance comparable to the human arm cannot practically be achieved with these machines (intrinsically high impedance machines). arthritic conditions. in whole or in part... Reinkensmeyer et al. Accompanying the vigorous development of rehabilitation robotic devices is an equivalent growth in clinical evaluations of device performance. 2002. and into the rehabilitation techniques that best engage those mechanisms. 2002). Harwin et al. 1990). extremity. 2002.I. (1990) described a patented robotic “smart exercise partner” in which the recovering stroke patient executes general spatial motions specified by the robot. 2000).. Other upper extremity robotic tools differ insofar as they do not require patients to be capable of independent movement. Krebs et al. 2003. Ferraro et al. 2002. Lum et al.. The best examples are Hesse’s Elliptical Gait Trainer. the MIT-MANUS robot developed in the Newman Laboratory for Biomechanics and Human Rehabilitation was specifically designed for clinical neurologic applications and ensures a gentle compliant behavior (Hogan et al. Areas of research focus include not only stroke. Hesse and Uhlenbrock.g. 1998. 1998. 1995) described the design and application of robotic assistive devices focused on bi-manual tasks to promote motor recovery.. see Volume II. Lum et al. 2002). 2000. 2000.. A number of studies demonstrated the exciting opportunities and benefits of integrating robotic technology into patients’ daily rehabilitation program (e. but also motor deficits associated with diverse neurologic. Operationally. Chapters 3 and 19). orthopedic. 2001. Rahman’s functional upper limb orthosis (Rahman et al. 2000. However. Not unlike their upper-extremity industrial robot counterparts. 1995). Reinkensmeyer et al. Reinkensmeyer et al. Colombo et al. Results include new insights into the recovery mechanisms for a variety of conditions. Burgar et al. They can therefore be programmed to allow the recovering stroke survivor to express movement.. stable and compliant operation in close physical contact with humans. Fasoli et al.. 2000. rigidity or muscle tone. Aisen et al. even when the attempts are weak or uncoordinated. and the Lokomat (Sakaki et al. Krebs et al. in which the robot moves the impaired limb to mirror movements of the contralateral limb. Rohrer et al. 1999a.. Volpe et al. and Burdea’s pneumatically actuated glove (Merians et al. these robots can “get out of the way” as needed.. Most are presently being re-designed to modulate their impedance and to afford an interactive experience similar to the lowimpedance lower extremities devices under development at MIT in the Newman Laboratory and at University of California Irvine. Lum et al. (Burgar et al. 2000. (2001) is using another commercial robot (Fokker) to move the impaired arm in the recently initiated European Union sponsored project. 1999. Other low-impedance rehabilitation devices are Reinkensmeyer’s ARM Guide (2000) and Furusho’s EMUL (2003). 1995). however. 2000. 1997.. 1999... Positive results using that system in a clinical setting were reported (Erlandson. 2000.166 H. Hesse and Uhlenbrock. patients had to be capable of moving independently or using the contralateral limb to move and guide the impaired limb (self-ranging). Lum et al. Colombo et al. Independent movement is also essential to use of Rosen’s 3-D controllable brake device (Maxwell. More recently. 2000. Whether this feature is crucial for effective therapy remains unproven but its importance for obtaining uncorrupted measurements of a patient’s sensorimotor function has been established unequivocally (Krebs et al. these designs suffer from a high impedance drawback.. controlled forces can be exerted to move the patient or to measure aspects of motor status such as spasticity. In contrast to these approaches other groups have developed robotic technology configured for safe.. For example.. Erlandson et al. 2003). 2002) used a commercial PUMA robot augmented by improved sensors to implement the Mirror Image Movement Enabler (MIME) system. For upper. Yaskawa’s therapeutic exercise machine (TEM).. (1993.. 2000a... We can group devices into two main categories for the upper and lower extremity. ..

a strength grade of 3/5 or less in muscle groups of the proximal arm) as assessed with the standardized Medical Research Council battery. and prosthetics 167 (a) (b) (c) Figure 12.. NY). To date. Rhode Island (RI) Rehabilitation Hospitals. NY) who met inclusion criteria and consented to participate.1. 12. (a) and (b) show the shoulder and elbow robot (MIT-MANUS) and the wrist robot. and the Baltimore (MD) and Cleveland (OH) Veterans Administration Medical Centers. If the patient could not perform the task. wrist.Rehabilitation robotics. Volpe (2001) reported results of robotic training with 96 consecutive inpatients admitted to Burke Rehabilitation Hospital (White Plains. This chapter presents only our own results to delineate the potential of the technology and future directions for rehabilitation robotics. the ability to understand and follow simple directions. the robot-trained group demonstrated significantly greater motor . and spatial movements (Fig. The sensorimotor training group received an additional 4–5 h per week of robotaided therapy while the control group received an hour of weekly robot exposure. the robot assisted and guided the patient’s hand. Helen Hayes (NY). orthotics. and upper limb weakness in the hemiparetic arm (i. Patients were randomly assigned to either an experimental or control group. 1 Hospitals presently operating one or more MIT-MANUS class robots include Burke (NY). Rehabilitation robot modules during clinical trials at the Burke Rehabilitation Hospital (White Plains.e. Inclusion criteria were diagnosis of a single unilateral stroke within 4 weeks of admission to the study. and (c) the anti-gravity spatial module.1). we have deployed three distinct robot modules in collaborating clinical institutions1 for shoulder and elbow. Spaulding (MA). Although patient groups were comparable on all initial clinical evaluation measures. The sensorimotor training for the experimental group consisted of a set of “video games” in which patients were required to move the robot endeffector according to the game’s goals.

.5 NS 6.1 4.. NS: not significant. Krebs et al.9 2. although there was a trend favoring the robot group.1 1. 2004). indicating the stability of chronic motor impairments in this subject group (Fasoli et al. Long after stroke.5 2. patients still suffer a variety of impairments dependent on the size and location of their individual stroke.7 4. For all evaluations higher scores indicate better performance. Use of the FIM to indicate changes in the level of disability that may be associated with robotic therapy is not without limitations. Fasoli et al.2. 1993).6 4. increased motor function.01 0..I.01 NS Robot-trained (n 55) Control (n 41) P-value improvement (higher mean interval change SEM) than the control group on the impairment scales (see Table 12. These gains were specific to motions of the shoulder and elbow. used to indicate changes in the level of disability. Between group comparisons: final evaluation minus initial evaluation Impairment measures ( SEM) Fugl Meyer shoulder/elbow (FM-se) max/42 MP max/40 Motor Status shoulder/elbow (MS-se) max/40 2.1 1.01 0. There were no significant between group differences in the mean change scores for wrist and hand function. For all evaluations higher scores indicate better performance. MP was only evaluated for shoulder and elbow movements. Comparison of mean interval change for outpatients at Spaulding Rehabilitation Hospital (n 42.0 0. Therefore.1). and the Motor Power (MP) score. Table 12. reliable.0 5. and reduction in disability is not possible with the FIM. the focus of the robot training. Mean interval change in impairment and disability measure for inpatients (significance P 0.0 0. However. a definitive conclusion about the relationship between changes in upper limb motor impairment.7 0.1.4 0.4 1.5 6. These patients received the same sensorimotor robotic training used with inpatients (see above). Granger et al. sensorimotor protocol).8 2. Prior to engaging in robotic therapy.2 3. MP was only evaluated for shoulder and elbow movements.1 8.0 0.6 0.05). Likewise there were no significant differences in functional independence measure (FIM) performance.8 1.168 H. 2004) reported results of robotic training described at Spaulding Rehabilitation Hospital (Boston. 2003.4 4. MA) with 42 consecutive community dwelling volunteers with stroke. Although the FIM is a wellestablished. many of the self-care tasks that comprise the motor subscale of the FIM can be independently accomplished by using only the “unaffected” upper limb (Dodds et al. The primary outcome measures were the Fugl Meyer.8 NS 0. these patients were assessed on three separate occasions to determine baseline function and to establish a within subject control. after robotic training we found . Motor Status Scale for the shoulder and elbow.01 3.3 0. and valid measure of basic activities of daily living. 1993. Our baseline analyses revealed no statistically significant differences among any of the pre-treatment clinical evaluations. (2003. Between group comparisons: final evaluation minus initial evaluation Impairment measures ( SEM) Fugl Meyer shoulder/elbow (FM-se) max/42 MP max/20 Motor Status shoulder/elbow (MS-se) max/40 Motor Status wrist/hand (MS/wh) max/42 Disability evaluation FIM (upper) max/42 MP: Motor Power. 32. who responded to information they had Table 12.0 25.5 0.01 Robot-trained (n 42) P-value obtained from media sources about the robotic training experiments.

In prior work Hogan (Flash and Hogan. and the MP Clinically. mean interval changes in performance were calculated between the initial and final evaluations. (2003. This approach appears particularly suitable when considering that different stroke lesions can lead to quite different kinematic behavior during reach. To exemplify the potential of delivering different kinds of therapy.. Shor et al. . In fact. For all evaluations higher scores indicate better performance.6 0. The parameters of these minimum-jerk reference trajectories were obtained from therapists performing the same task at comfortable speed for training.3. 2002. For Table 12. on average. 1999. 2005 manuscript in preparation). 2003). 2000. subjects reported greater comfort when attempting to move their hemiparetic limb. Effect of robot training on impairment and disability measures. Between group comparisons: final evaluation minus initial evaluation Impairment measures ( SEM) Fugl Meyer shoulder/elbow (FM-se) max/42 MP max/40 Motor Status shoulder/elbow (MS-se) max/40 Disability Evaluation: FIM upper max/42 ( SEM) All patients (n strokes (n 29) 16) 0. Results indicated statistically significant increases in each primary measure: Fugl Meyer test. 1985) has shown that normal reaching movements may be accurately described as “optimally smooth” in the sense of minimizing meansquared jerk. 2004). orthotics. persons with moderate stroke receiving the performance-based protocol improved twice as much as the ones receiving the sensorimotor protocol for both impairment and disability measures (Krebs et al. Reinkensmeyer et al.Rehabilitation robotics. Burgar et al.2 with those from an innovative robotic therapy modality developed in our laboratory based on motor-learning models.01 Patients with moderate 3.2.7 0. Motor Status Score for shoulder and elbow. the robot controller uses this minimum-jerk profile as the reference hand path.. Kahn et al. 2003). During sensorimotor training. who responded to information they had obtained from media sources about the robotic training experiments (Ferraro et al.3 2. The novel feature of the performancebased progressive algorithm is that it can guide the hand of the patient that aims poorly without holding him/her back and assist the slow patient in making faster movements. 1993. A critical aspect of low-impedance rehabilitation robots that often escapes clinicians is that these devices can be programmed to deliver a vast range of different kinds of therapy. 6 months after stroke.. 2001).7 0.3).9 0. For 29 outpatients at Burke Rehabilitation Hospital.7 0. For example. the sensorimotor training mentioned earlier can be described in lay terms as a “hand-over-hand” approach. and were better able to actively coordinate shoulder and elbow movements when reaching toward visual targets during robotic therapy. and prosthetics 169 significant reductions in motor impairment of the hemiparetic upper limbs shown in Table 12. Others have obtained similar results (Lum et al. but the outcome of the performance-based protocol represent a significant improvement over the sensorimotor one (see Table 12.6 NS 0...0 0. . While executing point-to-point movements. Ferraro reported results of performance-based robotic training at Burke Rehabilitation Hospital with consecutive community dwelling volunteers with stroke. the robot uses a fixed impedance controller while following this fixed minimum-jerk reference trajectory..01 5.. 2001. one patient might make rapid but poorly aimed movements.01 0. This protocol has the same enrollment criteria and lasted the same amount of time and number of sessions as the one reported by Fasoli et al.01 Robot-trained (n 29) P-value NS: not significant. let us compare the results of Table 12.9 3. 2000. while another might aim well but move slowly. example.6 0. if we exclude the severe strokes from the analysis of both protocols. It applies a performancebased progressive algorithm and modulates the parameters of an impedance controller according to patient’s performance (Krebs et al. MP was only evaluated for shoulder and elbow movements.. This result has demonstrated that task specific robotic therapy can improve upper limb motor abilities and reduce chronic motor impairments.

Trunk and neck orthoses include thoracolumbosacral orthoses (TLSO) for correcting scoliosis. 2002). and the common cervical orthoses (neck braces) for whiplash injuries or muscle spasms. For example. Other orthoses transfer motion. and wrist–hand orthoses to position the joints or assist in activities of daily living. In these cases. align body structures. lubrosacral orthoses (LSO) for stabilizing low back fractures. Krebs et al. While movement-based therapy may lack the glamor of cure. Foot orthoses are carefully designed to shift load bearing forces on the bottom of the foot from one area to another. Unlike prostheses that replace a body part.I. functional knee orthoses (KO) for athletic injuries. Extension of the wrist causes the fingers to close enabling patients with spinal cord . the next step is to determine how to tailor therapy to particular patient needs and maximize the stroke survivor’s motor outcome.170 H. bear weight.3 Orthoses Orthoses are passive or powered external devices that support loads. thus enhancing a strengthening program following stroke (Fess and Philips. upper limb. long leg knee–ankle–foot orthosis (KAFO). research in rehabilitation robotics has so vibrantly evolved during the last decade that it is now feasible to mingle robots with humans. and for over-ground walking. protect joints or correct deformities. It is not far-fetched to predict that by decade’s end. balanced forearm orthoses (BFO) for feeding assist. Common types of lower limb orthoses include foot orthosis (FO) shoe inserts for correcting ankle and foot deformities. 1987). single strap shoulder sling off loads the weight of the arm from the ipsilateral shoulder joint and applies it to the contralateral scapula and clavicle. neuro-regeneration or tissue-regeneration agents to achieve results equivalent to a “cure”. Upper limb devices include shoulder and elbow slings for weight support during fracture healing. a knee brace restricts motion to the sagittal plane to protect a knee from off-axis forces following surgery or injury (Edelstein and Bruckner. typically to reduce pain or to off load pressure ulcers. We envision a short-term future with a range of natural extensions of the existing rehabilitation robots including novel modules suitable to provide therapy for the fingers. and either control or assist movement. A sling orthosis transfers loads from one part of the body to another. Results to date are statistically strong and reproducible by different groups in different clinical settings. For the near-term future. and lower limb that are designed to guide motion. or assist or restrict relative motion between body segments. A hand orthosis can be constructed to provide elastic resistance to finger extension. we will have a range of rehabilitation robots at home and in the clinic. elastic trunk supports for preventing back injuries during lifting. orthoses act very much like mechanical bearings whose purpose is to restrict motion in some dimensions and allow frictionless motion in others. a simple. operating much like a gym. Orthoses apply forces to resist or transfer motions and loads. but the reported results are also arguably functionally modest. and full length hip–knee–ankle–foot orthoses (HKAFO) for standing and gait stability. thus preventing ipsilateral shoulder subluxation in those with rotator cuff injuries or paralysis. Orthotics plays an important role in the rehabilitation of patients with motor impairments. Seymor. we envision a range of clinical and neuroscience-based training paradigms addressing both functional abilities and impairment. and an array of wrist. In conclusion. The word orthosis is derived from Greek for making or setting straight. supporting or participating in therapy activities. for the long-term future we envision the combination of rehabilitation robotics working synergistically with novel pharmacological. Plaster casts and wrist immobilization splints are orthoses that restrict all motion. for the ankle. harnessing the patient’s potential to its limits with just movement-based therapy. Orthotics include devices for the neck. orthoses are designed to work in cooperation with the intact body. hand. For example. ankle–foot orthoses (AFO) for correcting foot drop. Since it appears that we can influence impairment and disability. 12. trunk. 2002. and is a general term that encompasses bracing and splints. A prehension orthosis contains a linkage that couples the wrist to the fingers. hip abduction orthoses for limiting range of motion.

Popovic et al. Nene and Jennings. 1989. Of particular concern is excess pressure. The fit of orthosis is critical as they must carry loads without interfering with normal skin and tissue function (Fess and Philips. 1990.. 1991). Orthopedic impairments result from chronic musculoskeletal disorders or acute musculoskeletal injuries. Functional electrical stimulation (FES) is another means of providing assisted gait to those with spinal cord injury (see Volume II.. powered orthoses are designed for use by individuals with spinal cord injury to restore modest function to a paralyzed extremity. In an attempt to overcome the limitations of FES and orthotic walking systems alone. while gait velocity is about one-third normal. more efficient means of travel. Others have combined stimulation with the HGO (McClelland et al. The most common neurologic impairments where orthotic approaches are considered include traumatic brain injury. The first is the hip guidance orthosis (HGO) that locks the knee joint but has freely moving hip and ankle joints (Major et al. 1989). This brings out an inherent tradeoff that continually challenges orthosis designers. Several HKAFOs have been developed as paraplegic walking systems (Miller.. weight and unwieldiness of the hardware has resulted in limited use (Stallard et al. wheelchairs are generally the device of choice for those with severe neurologic impairments. Orthotic interventions are prescribed for patients with orthopedic or neurologic impairments (Nawoczenski. 1997). Simple AFOs are used to correct the foot drop that is a common byproduct of stroke. The challenge with designing and prescribing more involved orthotics is to generate an energy-efficient gait (Waters and Yakura. 1990). particularly over bony prominences. 1991. Greene and Granat. The ideal orthosis should be rigidly anchored to the skeleton. Solomonow et al. custom fit orthosis to limit motion in the subtalar joint (Hemsley. 2002). 1997). the Hybrid Assistive System (Popovic et al. 1989). hybrid systems that combine FES and orthotics have been developed. 1992. The second is the reciprocating gait orthosis (RGO) that links opposite joints so that extension of the hip on one side leads to flexion on the contralateral side (Jefferson and Whittle. the energy cost. including athletic injuries..2 (Goldfarb and Durfee 1996. Goldfarb et al. 1997). while KAFOs can improve gait for those with progressive quadriceps weakness. 1990). and the size. 1997).. to control the speed or direction of limb motion. This is a particular problem when fitting patients with neuropathies or spinal cord injury who lack conscious sensation. that can lead to pressure ischemia and eventually skin ulcers. starting from the . 1997. and the Controlled Brake Orthosis shown in Fig.. and spinal cord injury (Zablotny. Whittle et al. Lower limb orthotics prescribed for those with neurologic impairments have the function of restoring or improving gait (Zablotny. the Case Western Hybrid System (Ferguson et al. 1981. 2003). 1999.. Chapter 9). Walking with bi-lateral KAFOs and crutches requires five times the energy per meter as normal gait. The addition of power to an orthosis enables the external device to move a limb actively. while practical orthoses have considerable motion with respect to the skeleton because of the soft tissue that lies between. Powered exoskeletons have a long and rich history.. 1987). 1997).. Ankle taping for athletes is a simple.Rehabilitation robotics. A basic principle for the design and fitting of an orthosis is to spread the load over as large an area as possible. Hirokawa et al. Marsolais et al. 1989). 1997).. Avoiding bony prominences means the body attachment point for an orthosis is largely over soft tissue.. 2003)... 12.. and prosthetics 171 injury at C6 to grasp objects (Edelstein and Bruckner. There are two major walking systems. Most commonly. the Strathclyde Hybrid System (Yang et al.. Petrofsky and Smith. an enhanced AFO (Andrews et al.. Typical objectives for walking orthotics are to establish stable weight bearing. 1984. Butler et al. Stallard et al.. Popovic 1990. 1987. and with the recent explosion in mobility device design and improved accessibility of buildings. stroke. 2000). Isakov et al. 1989. Several studies have shown improved gait speeds and lower energy consumption when FES and the RGO are combined (Solomonow et al. or to reduce the energy required to ambulate. orthotics. Wheelchairs are a faster. 1989. Although these systems can restore rudimentary gait for some people with spinal cord injury. 1988).

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Powered lower limb walking systems have also been designed. Popovic developed a powered knee joint (Popovic et al., 1990), as did Beard (Beard et al., 1991). A hydraulic powered, 5 degree of freedom walking assist device was developed by Seireg and colleagues in the 1970s (Grundman, 1981). More recently, Beleforte et al. have created the pneumatic active gait orthosis (Belforte et al., 2001) and Hiroaki and Yoshiyuki have developed the Hybrid Assistive Leg, a battery and direct current (DC) motor driven powered exoskeleton (Kawamoto, 2002). Laboratory-based powered exoskeletons have been developed for non-rehabilitation, human power amplification applications. The most famous is the 1965 Hardiman whole-body exoskeleton developed at the General Electric Research and Development Center in Schenectady, NY (Rosheim, 1994). Since then, a variety of human amplification systems have been developed for civilian and military applications, but none have made it out of the laboratory (Kazerooni and Mahoney, 1991; Rosheim, 1994; Kazerooni, 1996; Jansen et al., 2000; Neuhaus and Kazerooni, 2001).

12.4 Prosthetics
Upper-limb amputation prostheses
Figure 12.2. Laboratory version of a hybrid orthotic/FES system to enable rudimentary gait for some individuals with complete spinal cord injury at the thoracic level. The controlled brake orthosis combines surface electrical stimulation of the lower limb muscles with an orthotic structure containing computer-controlled brakes that regulate stance and swing phase trajectories (Goldfarb and Durfee, 1996; Goldfarb et al., 2003).

first robotics arm built in the 1960s at Case Western Reserve University, and the early powered walking machines pioneered by Tomovic and colleagues (Tomovic et al., 1973). For example, an electromyogram (EMG) controlled battery powered hand orthosis can provide grasp for C5 quadriplegics (Benjuya and Kenney, 1990), while more ambitious multi-degree of freedom, upper extremity exoskeletons have been tested in the laboratory (Johnson et al., 2001).

Despite advances in technology, progress in the development of effective upper-limb amputation prostheses has been modest. This may be partly due to irregular interest in their development, which tends to correlate with major wars. Mann (1981) shows an 1866 Civil War era below-elbow prosthesis with eating utensils and a hook. World War II saw the development by Northrop Aircraft cable-operated “body-powered” arm prosthesis. Mechatronic or “externally powered”2 prostheses were introduced in the Vietnam War decades. Unfortunately, the resulting devices offer limited benefits. Studies suggested that as few as 50% of upper-limb amputees
2 A “body-powered” prosthesis is powered by the amputee, for example, bi-scapular abduction (shoulder rounding) for elbow flexion; mechatronic prostheses are typically powered by batteries “external” to the amputee.

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use any prosthesis at all, versus 75% for lower-limb amputees (LeBlanc, 1973). Unilateral amputees (with one sound arm) overwhelmingly find that a prosthesis offers too little cosmetic or functional benefit to offset its discomfort and inconvenience. LeBlanc (1991) estimated that only 10% of prosthesis users in the USA (5% of the upper-limb amputee population) operate externally powered devices. Thus half of all upper-limb amputees do not use a prosthesis and nine-tenths of those who do use the body-powered type, whose basic design is essentially unchanged in over half a century. Yet mechatronic prostheses hold substantial promise. It is difficult to transmit significant power from the body to the prosthesis without severely compromising comfort; externally powered devices avoid this problem. It is difficult to control multiple degrees of freedom (e.g., elbow, wrist, thumb, fingers) by recruiting other body motions; mechatronic prostheses may be controlled by bioelectric signals, which can be obtained from a large number of nerves or muscles including, in principle, those originally responsible for controlling the functions of the lost limb. The concept of using bioelectric signals to control a mechatronic device is due to MIT’s Norbert Wiener who proposed it in his well-known work cybernetics (Wiener, 1948). In founding cybernetics, the “study of automatic control systems formed by the nervous system and brain and by mechanical–electrical communication systems” he had “the idea several years ago to take an amputated muscle, pick up the action potentials, amplify this and make motion of it”. Mann implemented this idea in an above-elbow amputation prosthesis controlled by EMG3 from muscles in the residual limb (Rothchild and Mann, 1966; Mann, 1968), which led to commercial products including the Boston Arm (Jerard et al., 1974; Liberty Mutual, Inc.; Liberating Technologies, Inc.) and the Utah Arm (Jacobsen et al., 1982; Sarcos, Inc.; Motion Control, Inc.). EMG control has been applied to other upperextremity motions including wrist rotation and grasp and methods for simultaneous control of many
3

degrees of freedom have been proposed (Jerard and Jacobsen, 1980). Given the potential advantages of EMG control, the continued overwhelming preference for the body-powered system is remarkable. Although generally lighter and less expensive, a body-powered prosthesis is also considerably less comfortable, mostly due to the harness needed to transmit body motion the prosthesis; its lifting ability is extremely limited; it is less cosmetic than mechatronic models as it requires unnatural body motions for its operation; and independent operation of multiple degrees of freedom is difficult to impossible (LeBlanc, 1991). A clue to this puzzle may be found by studying how an arm amputation prosthesis is used.

Motion control and sensory feedback
One abiding concern is that EMG control may restore “forward path” communication between the central nervous system and the peripheral (bio-)mechanical system but does not restore “feedback” sensory communication from periphery to center. However, whether continuous feedback is essential for unimpaired movement control remains unclear with recent evidence suggesting that neural commands are substantially “pre-computed” from learned internal models (Shadmehr and Mussa-Ivaldi, 1994). Furthermore, substantial feedback information is available through mechanical interaction with the socket and harness that secure the prosthesis to the amputee. Doeringer and Hogan (1995) compared motor performance of unilateral amputees using a body-powered prosthesis with their performance using their unimpaired arm on a series of elbow motion tasks. Motion control with the prosthesis was remarkably good. For the more active and experienced prosthesis users, eyes-closed positioning ability was indistinguishable from unimpaired arm performance.

Interaction control
Most functional tasks for an upper-limb prosthesis are contact tasks involving kinematically constrained motions (e.g., opening a drawer, wiping a surface,

“EMG” refers to the ElectroMyoGram, more correctly “myoelectric activity”.

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etc.) or mechanical interaction (e.g., wielding a tool, cooperating with the other arm, etc.). For unilateral amputees (who constitute about 95% of the arm amputee population) a prosthesis will mostly serve as the non-dominant arm, for example, holding or steadying objects while they are manipulated by the unimpaired limb. Controlling interaction is thus a fundamental requirement for arm prosthesis function. However, most mechatronic prostheses have been designed using motion control technology (Klopsteg and Wilson, 1968; Mason, 1972; Jerard et al., 1974; Jacobsen et al., 1982). Unfortunately, robotic experience has shown that motion controllers are poorly suited to controlling interaction. A comparison with natural motor behavior is informative. Natural arms are compliant, yielding on contact with objects, which makes them less sensitive to the disturbances caused by contact (see Hogan, 2002 for a review). In contrast, a typical mechatronic prosthesis responds little, if at all, to external forces. Furthermore, the natural arm’s compliance is under voluntary control (Billian and Zahalak 1983; Humphrey and Reed 1983). Tensing muscles makes the arm less compliant and serves to stabilize it against disturbances. Relaxing the muscles makes the arm more compliant and allows it to accommodate external constraints. The advantages of the natural arm’s behavior may be conferred on a machine using impedance control (Hogan, 1979, 1985), which has proven effective for robot control, especially for contact tasks (see Hogan and Buerger, 2004 for a brief review). Impedance control has been applied to an EMG-controlled mechatronic arm prosthesis, partially mimicking the natural arm’s behavior (Abul-Haj and Hogan, 1990): the response to external forces varies with co-activation of agonist and antagonist muscles while differential activation generates motion.

Figure 12.3. Prosthesis emulator.

Amputee performance of contact tasks
A study of amputees performing simple contact tasks showed the importance of interaction control. A computer-controlled arm amputation prosthesis (see Abul-Haj and Hogan, 1987; Fig. 12.3) was programmed

to emulate (1) a body-powered prostheses in freeswing mode; (2) the Boston elbow; and (3) the New York elbow (two mechatronic prostheses which control elbow velocity from the difference between EMG of remnant arm muscles); and (4) an impedance-controlled prosthesis. The main difference between these cases is that the velocity-controlled prostheses, (2) and (3), are unresponsive to external forces whereas the other two, (1) and (4), move easily under external forces. Unilateral amputee subjects used each prosthesis to turn a crank mounted in a vertical plane at three speeds (low, medium and fast, approximately 2, 4 and 6 rad/s). In almost all cases, motions of prosthesis and crank were similar, the crank handle moving with a smooth, unimodal speed profile, indicating that all prostheses provided comparable motion control. In contrast, the forces exerted on the crank were significantly different in each case. Computation of the power produced by the prosthesis motor showed that for the impedance control system, prosthesis output power was always positive. For the body-powered prosthesis in free-swing mode power was zero. For the Boston elbow and the New York elbow control systems, output power was negative for a significant portion of the task. Positive output power from the impedance control system means that it always assisted motion; amputees consistently rated this prosthesis easiest to control. Negative output power means that the Boston elbow and New York elbow prosthesis were behaving as brakes and impeding performance of the task, not assisting it (Mansfield et al., 1992; Krebs et al., 1999b).

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Control and communication are the barriers
The way a mechatronic prosthesis responds to forces (its mechanical impedance) is clearly an important factor determining its usefulness. Unfortunately, most available mechatronic prostheses are unresponsive (they typically have high impedance) and this may be the main reason why, after decades of development, most amputees prefer not to use them, despite their apparent functional advantages such as independent control of different motions (e.g., elbow and terminal device). Providing an amputee with the ability to adjust impedance (as in the natural limb) yielded superior performance and seems a promising way to improve upper-limb prostheses. However, it requires additional control signals to assess the user’s intent (e.g., both reciprocal and co-contraction of antagonist muscles). For limited motions EMG may be suitable; activity of two muscles such as the remnant biceps and triceps may be used to command the elbow. However, the ideal mechatronic arm, assuming that one could be built, is not limited to elbow movement, but must also assess the user’s intent to drive the wrist and fingers. Recent work on brain-machine interfaces (Nicolelis et al., 1995) shows that in principle the required information may be obtainable directly from the brain (see Chapter 33 of Volume I), though advances in technology for implantable neuro-electric recording in the periphery may be more practical (e.g., Bions, Chapter 32 of Volume I). New ways to communicate and more natural control strategies could reinvigorate research and open a plethora of possibilities to turn Hollywood’s mechatronic fancies into reality.

extended, resulting in a knee torque that increases with increasing knee angular rate. To control knee damping, the size of the fluid orifice is adjusted. Although for most commercial knees the orifice size is controlled passively when weight is applied to the prosthesis, some contemporary knee systems use a motor to actively modulate orifice size. For example, in the Otto Bock C-Leg, hydraulic valves are under microprocessor control using knee position and axial force sensory information (James et al., 1990). Actively controlled knee dampers such as the C-Leg offer considerable advantages over passive knee systems, enabling amputees to walk with greater ease and confidence (Dietl and Bargehr, 1997; Kastner et al., 1998). Today’s prosthetic ankle–foot systems typically employ elastomeric bumper springs or carbon composite leaf springs to store and release energy throughout each walking or running step (Popovic and Sinkjaer, 2000). For example, in the Flex-Foot Vertical Shock Pylon System, carbon composite leaf springs offer considerable heel, toe, and vertical compliance to the below-knee prosthesis, enabling leg amputees to move with greater comfort and speed. Although considerable progress has been made in materials and methods, commercially available ankle–foot devices are passive, and consequently, their stiffnesses are fixed and do not change with walking speed or terrain.

Patient-adaptive prosthetic knee system
Using state-of-the-art prosthetic knee technology such as the C-Leg, a prosthetist must pre-program knee damping levels until a knee is comfortable, moves naturally, and is safe (James et al., 1990; Dietl and Bargehr, 1997; Kastner et al., 1998). However, these adjustments are not guided by biological gait data, and therefore, knee damping may not be set to ideal values, resulting in the possibility of undesirable gait movements. Still further, knee-damping levels in such a system may not adapt properly in response to environmental disturbances. Recently, an external knee prosthesis was developed that automatically adapts knee damping values to match the amputee’s gait requirements, accounting for variations in both

Lower-limb amputation prostheses Dissipative knees and energy-storing prosthetic feet
Today’s prosthetic knees typically comprise a hydraulic and/or pneumatic damper that dissipates mechanical energy under joint rotation (Popovic and Sinkjaer, 2000). In these devices, fluid is pushed through an orifice when the knee is flexed or

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forward speed and body size (Herr et al., 2001; Herr and Wilkenfeld, 2003). With this technology, knee damping is modulated about a single rotary axis using magnetorheologic (MR) fluid in the shear mode, and only local mechanical sensing of axial force, sagittal plane torque, and knee position are employed as control inputs (see Fig. 12.4). With every step, the controller, using axial force information, automatically adjusts early stance damping. When an amputee lifts a suitcase or carries a backpack, damping levels are increased to compensate for the added load on the prosthesis. With measurements of foot contact time, the controller also estimates forward speed and modulates swing phase flexion and extension damping profiles to achieve biologically realistic lower-limb dynamics. For example, the maximum flexion angle during early swing typically does not exceed 70 degrees in normal walking (Inman et al., 1981). Hence, to achieve a gait cycle that appears

natural or biological, the knee controller automatically adjusts the knee damping levels until the swinging leg falls below the biologic threshold of 70 degrees for each foot contact time or forward walking speed. To assess the clinical effects of the patient-adaptive knee prosthesis, kinematic gait data were collected on unilateral trans-femoral amputees. Using both the patient-adaptive knee and a conventional, nonadaptive knee, gait kinematics were evaluated on both affected and unaffected sides. Results were compared to the kinematics of age, weight and height-matched normals. The study showed that the patient-adaptive knee successfully controlled early stance damping, enabling amputee to undergo biologically realistic, early stance knee flexion. Additionally, the knee constrained the maximum swing flexion angle to an acceptable biologic limit. In Fig. 12.4, the maximum flexion angle during the swing phase is plotted versus walking speed for a unilateral

(a)

(b) Angle (degrees)

90 60 30 0 0.0 90 0.5 1.0 1.5 Speed (m/s) 2.0 2.5

Angle (degrees)

60 30 0 0.0 0.5 1.0 1.5 Speed (m/s) 2.0 2.5

Figure 12.4. An external knee prosthesis for trans-femoral amputees. The damping of the knee joint is modulated to control the movement of the prosthesis throughout each walking cycle. (a) The prosthesis shown on the left comprises MR brake (1), potentiometerangle sensor (2), force sensors (3), and battery and electronic board (4). (b) The right plots show the maximum flexion angle during the swing phase versus walking speed. The patient-adaptive knee affords a greater symmetry between affected and unaffected sides.

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trans-femoral amputee using the non-adaptive, mechanical knee (top plot, filled diamonds) and the patient-adaptive knee (bottom plot, filled diamonds). In both plots, the subject’s sound side leg is shown (open squares), along with reference data from unimpaired walkers (standard error bars). For the amputee participant, the non-adaptive, mechanical knee produced a maximum flexion angle that increased with increasing speed, far exceeding 70 degrees at the fastest forward walking speed, whereas the patientadaptive knee gave a maximum flexion angle that was less than 70 degrees and agreed well with the unimpaired, biologic data. These results indicate that a patient-adaptive control scheme and local mechanical sensing are all that is required for amputees to walk with an increased level of biologic realism compared to mechanically passive prosthetic systems.

or local mechanical sensors were employed in prosthetics imposes dramatic limitations in the system’s ability to assess user intent. In the advancement of prosthetic systems, we feel that distributed sensory architectures are research areas of critical importance.

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New horizons for lower-limb prosthetic technology: merging body and machine
Society is at the threshold of a new age when prostheses will no longer be separate, lifeless mechanisms, but will instead be intimate extensions of the human body, structurally, neurologically, and dynamically. Such a merging of body and machine will not only increase the acceptance of the physically challenged into society, but will also enable individuals suffering from leg amputation to more readily accept their new artificial appendage as part of their own body. Several scientific and technological advances will accelerate this mergence. An area of research of considerable importance is the development of improved power supplies and more efficient prosthetic actuator designs where both joint impedance and mechanical power generation can be effectively controlled in the context of a low-mass, high cycle-life, commercially viable prosthesis. Another critical area of research will be to combine local mechanical sensing about an external prosthetic joint with peripheral and/or central neural sensors positioned within the body. Neural prostheses such as the Bion (Loeb, 2001, see Chapter 32 of Volume I), combined with external biomimetic prosthetic systems, may offer important functional advantages to amputees. The fact that only EMG

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13 Virtual reality in neurorehabilitation
Patrice L. Weiss1, Rachel Kizony1,2, Uri Feintuch2,3 and Noomi Katz2
1

Department of Occupational Therapy, University of Haifa, Haifa; 2School of Occupational Therapy,

Hadassah-Hebrew University, Jerusalem and 3Caesarea-Rothschild Institute for Interdisciplinary Applications of Computer Science, University of Haifa, Haifa, Israel

Imagine the following scenario. Stuck in traffic, you have your digital agent make contact with the secretary at the Rehabilitation Center via your wireless palmtop. You are immediately provided with a verbal listing of your daily schedule. It is clear that you will have a tight timetable, and already anticipate a hectic day filled with clinical rounds, research meetings and an afternoon lecture for third year medical students. You request your digital agent to retrieve last year’s lecture presentation on the rehabilitation of patients with Parkinson’s disease, and to locate abstracts of the latest research on this topic. These files will be waiting for you on your office computer when you arrive at the Rehabilitation Center. Finally traffic starts to move, and you make it to your office. Clinical rounds have been delayed and you use the opportunity to complete your daily exercise routine on your stationary bike which is facing an omnisurround screen.Viewing a virtual mountain path winding through the Swiss Alps, you are inspired to cycle uphill for a full 15 min. Your digital agent calls you just as you warm down to notify you that ward rounds are about to begin. The first patient is a 45-year-old businessman who is at the Center for intensive rehabilitation following knee arthroscopy. The patient is anxious to return home so you ask your intelligent agent to contact the agents of the surgeon, physiotherapist and occupational therapist who are not currently at the Center. All team members gather around an interactive, collaborative workspace to examine the X-rays, digital probe and ultrasound as well as other clinical outcome measures. The decision is to discharge with a course of telerehabilitation; the patient will sign on daily to a remotely supervised exercise program. You then ask the surgeon
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to demonstrate the procedure he used to the ward resident via a virtual knee arthroscopy simulator. The manipulation is somewhat complex but with some practice the resident gains a good sense of what the procedure entails. Upon your return to your office, you log onto your synchronous distance learning platform to connect up with the third year students who are in their classroom on campus. They can each see your slide presentation on their personal tablets and hear you lecture. They each activate emoticons to indicate their response to your lecture as it unfolds. After reviewing the basic concepts of the disease etiology, prevalence and clinical signs and symptoms, you ask them to each don a cyberglove in order to feel the difference between Parkinsonian rigidity and upper motor neuron spasticity. They next put on a miniature liquid crystal display (LCD) lens while you run through a series of simulations that enable them to evaluate the improvement in Parkinsonian gait experienced by these patients when provided with virtual overground cues. The students use their own microphones to participate in an interactive discussion about the advantages and limitations of these and other recent non-invasive interventions. As you complete the class and prepare for the intake of a new patient you reflect in amazement that not a single student fell asleep! This is a certainly different from the days when you went to medical school.

13.1 Introduction
Not so very long ago the “high tech” gadgets of the type used by Dr. McCoy of Star Trek fame were

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considered to be intriguing but far from attainable. Beaming through space, scanning medical diagnostic “tricorders” and “genetronic replicators” came from the creative imaginations of the hit television shows creators. Although the future has not yet arrived, recent developments in technology have succeeded in changing the practice of today’s clinician. Indeed, technology has enhanced a variety of clinical, administrative, academic and personal tasks facing the clinician of the new millennium. Virtual reality (VR) is one of the most innovative and promising of these developments and promises to have a considerable impact on neurorehabilitation over the next 10 years (Schultheis and Rizzo, 2001). VR typically refers to the use of interactive simulations created with computer hardware and software to present users with opportunities to engage in environments that appear and feel similar to real world objects and events (Sheridan, 1992; Weiss and Jessel, 1998). Users interact with displayed images, move and manipulate virtual objects and perform other actions in a way that attempts to “immerse” them within the simulated environment thereby engendering a feeling of “presence” in the virtual world. One way to achieve a stronger feeling of presence, users are provided with different feedback modalities including visual and audio feedback and, less often, haptic and vestibular feedback of their performance. Depending on the characteristics of hardware, software and task complexity, VR aims to provide users with more than just an engaging experience, and is hence quite different in both scope and intensity than traditional computer simulation games. The purpose of this chapter is to provide an overview of applications of VR to rehabilitation.

13.2 Key concepts related to VR
Presence is widely considered to be the subjective feeling of being present in a simulated environment. Sheridan (1992) has defined it as being “… experienced by a person when sensory information generated only by and within a computer compels a feeling of being present in an environment other than the

one the person is actually in” (Sheridan, 1992, p. 6). Presence is believed to be a major phenomenon characterizing a person’s interaction within a virtual environment, but the term is used inconsistently by different researchers (Slater, 2003). Slater (1999) suggested that presence includes three aspects – the sense of “being there”, domination of the virtual environment over the real world and the user’s memory of visiting an actual location rather than a compilation of computer-generated images and sounds. Witmer and Singer (1998) related presence to the concept of selective attention. Despite the numerous studies that have attempted to merge the various definitions of presence, it continues to be viewed as a complex concept that may be influenced by numerous interdependent factors (Schuemie et al., 2001; Mantovani and Castelnuovo, 2003). One set of factors relates to characteristics of the system that presents the virtual environment (see Fig. 13.1). These include the extent to which the user is encumbered with sensors, the way in which the user is represented within the virtual environment (Nash et al., 2000), whether the platform supports two- (2-D) or three-dimensional (3-D) interactions, and the number and quality of feedback modalities (e.g., Durfee, 2001). Another set of factors relates to a given user’s characteristics. These include age, gender, immersive tendencies, prior VR experience and disability (e.g., Stanney et al., 1998). Finally, a third set of factors relates to characteristics of the virtual environment and the task that is being performed within it (Nash et al., 2000). These include the meaningfulness of the task (Hoffman et al., 1998), how realistic it is and the intuitiveness of the interaction (Rand et al., 2005). A second key concept related to VR is immersion. Immersion relates to the extent to which the VR system succeeds in delivering an environment which refocuses a user’s sensations from the real world to a virtual world (Slater, 1999, 2003). Whereas immersion is an objective measure referring to the VR platform, it does not immediately correspond to the level of presence (which is a subjective measure), produced by the system. Immersion is thus dependent, in large part, upon the quality of the technologies used with

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VR system characteristics Dimensionality Representation Multimodality Encumbrance User characteristics Age Gender Immersive tendencies Prior experience Disability VR task characteristics Meaningfulness Realism Interaction

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Figure 13.1. Factors contributing to the user’s sense of presence.

the VR system (e.g., their resolution and speed of response) (Slater, 2003). Virtual environments may be delivered to the user via a variety of different technologies that differ in the extent to which they are able to “immerse” a user. In contrast to past references to immersive versus non-immersive VR systems, it is preferable to regard immersion as a continuum, ranging from lower to higher degrees of immersion. The relationship between the sense of presence, immersion and performance within the virtual environments is still not fully understood (Mania and Chalmers, 2001; Nash et al., 2000). Nevertheless, there is considerable evidence indicating that a high sense of presence may lead to deeper emotional response, increased motivation and, in some cases, enhanced performance (Schuemie et al., 2001). The use of a more immersive system does not necessarily generate a higher level of presence (Rand et al., 2005) nor does it guarantee clinical effectiveness. Taken together, there are many interwined issues involved in building a successful VR rehabilitation tool. A third issue is cybersickness which refers to the fact that some users experience side effects during and following exposure to virtual environments delivered by some of the more immersive VR systems, a factor that may limit its usability for all

patients under all circumstances (Kennedy and Stanney, 1996; Kennedy et al., 1997). Effects noted while using some VR systems can include nausea, eyestrain and other ocular disturbances, postural instability, headaches and drowsiness. Effects noted up to 12 h after using VR include disorientation, flashbacks and disturbances in hand–eye coordination and balance (e.g., Kennedy and Stanney, 1996; Stanney et al., 1998). Many of these effects appear to be caused by incongruities between information received from different sensory modalities (Lewis and Griffin, 1998). Other factors that may influence the occurrence and severity of side effects include characteristics of the user and the display, the user’s ability to control simulated motions and interactivity with the task via movement of the head, trunk or whole body (Lewis and Griffin, 1998). VR systems which include the use of a head mounted display (HMD), have a greater potential of causing short-term side effects, mainly oculomotor symptoms (Lo Priore et al., 2003). The potential hazard of side effects for patients with different neurologic deficits has not been sufficiently explored although there is increasing evidence that their prevalence is minimal with video-capture VR systems (see below) that are growing in popularity for clinical applications (Rand et al., 2005).

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13.3 Instrumentation
Virtual environments are usually experienced with the aid of special hardware and software for input (transfer of information from the user to the system) and output (transfer of information from the system to the user). The selection of appropriate hardware is important since its characteristics may greatly influence the way users respond to a virtual environment (Rand et al., 2005). The output to the user can be delivered by different modalities including visual, auditory, haptic, vestibular and olfactory stimuli, although, to date, most VR systems deliver primarily visual auditory feedback. Visual information is commonly displayed by HMDs, projection systems or flat screens of varying size. An HMD, such as Fifth Dimension Technologies (www.5dt.com) unit shown in Fig. 13.2, is essentially composed of two small screens positioned at eye level within special goggles or a helmet. Thus users view the virtual environment in very close proximity. Advanced HMDs even provide stereoscopic 3-D displays of the environment and usually are referred to as more immersive systems. Other VR applications use projection systems whereby the virtual environment is projected onto a large screen located in front of the user. VividGroup’s Gesture Xtreme (GX)-VR system (www.vividgroup. com), shown in Fig. 13.3, is an example of a videocapture projection system. The user sees him or herself within the simulated environment, and is able to interact with virtual objects that are presented. Some expensive projection systems, such as the CAVE (http://evlweb.eecs.uic.edu/info/index.php3), are composed of several large screens surrounding users from all sides such that the virtual environment may be viewed no matter where they gaze. A third way of displaying visual information is based on simple desktop monitors, used singly or sometimes in clusters of screens positioned around the user providing a quasi-panoramic view of the virtual environment (Schultheis and Mourant, 2001). This method is the least immersive but its low cost supports wider distribution to clinics and even to patients’ homes.

Figure 13.2. Fifth Dimension Technologies (www.5dt.com) HMD.

Sophisticated VR systems employ more than specialized visual displays. Engaging the user in the virtual environment may be enhanced via audio display, either ambient or directed to specific stimuli (Västfjäll, 2003). In recent years, haptic display has been introduced to the field of VR. Haptic feedback enables users to experience the sensation of touch, making the systems more immersive and closer to the real world experience. Haptic gloves, such as the Rutgers Master II shown in Fig. 13.4, may provide force feedback while manipulating virtual objects (Jack et al., 2001) or for strength training (Deutsch et al., 2002). Haptic information may also be conveyed by simpler means such as a force-feedback joystick (Reinkensmeyer et al., 2003) or a force-feedback steering wheel (Kline-Schoder, 2004). Other, less frequently used ways of making the virtual environment more life-like are by letting the user stand on a platform capable of perturbations and thereby providing vestibular stimuli such as that available with Motek’s CAREN multisensory system (http://www. e-motek.com/medical/index.htm). Still more rare is the provision of olfactory feedback to add odor to a virtual environment, a feedback channel whose potential is now being investigated (Harel et al., 2003; Bordnick et al., 2005).

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Figure 13.3. VividGroup’s GX-VR system (www.vividgroup.com) video-capture projection VR system.

Figure 13.4. Rutgers Master II force-feedback glove.

The technologies mentioned above address only the output aspect of the VR experience. Equally important to achieving a realistic experience within a virtual environment is the ability of the user to navigate and manipulate objects within it. Thus the user must be able to interact (directly or indirectly) with the environment via a wide array of input technologies. One class of input technologies may be considered as direct methods since users behave in a natural way, and the system tracks their actions and

responds accordingly. Generally, this is achieved by using special sensors or by visual tracking. With the sensor approach, such as used by Intersense’s (www. isense.com) InterTrax2, a three degree of freedom, inertial orientation tracker used to track pitch, roll and yaw movements, the user wears a tracking device that transmits position and orientation data to the VR system. With the visual tracking approach, such as used by VividGroup’s video-capture VR system, the user’s motion is recorded by video cameras, where special software processes the video image, extracts the user’s figure from the background in real-time, and identifies any motion of the body. A second class consists of indirect ways for users to manipulate and navigate within a virtual environment. These include activation of computer keyboard keys, a mouse or a joystick or even virtual buttons appearing as part of the environment (Rand et al., 2005). In addition to specialized hardware, application software is also necessary. In recent years, off-theshelf, ready-for-clinical-use VR software has become available for purchase. However, more frequently, special software development tools are required in order to design and code an interactive simulated environment that will achieve a desired rehabilitation goal. In many cases, innovative intervention ideas may entail customized programming to construct a virtual environment from scratch, using traditional programming languages. VR hardware that facilitates the input and output of information, in combination with programmed virtual environments provide the tools for designing tasks that enable users to perform in ways that help them achieve established rehabilitation goals. When creating a specific virtual rehabilitation tool the clinician and technical team face the challenge of choosing and integrating the software and hardware, and the input and the output methods. For example, should one use an HMD, attach to it an orientation tracker and move around the virtual environment with a joystick? Or, should the user be positioned in front of a virtual environment projected onto a large screen and employ visual tracking to capture the user’s responses? Such decisions have to take many

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factors into account including budget, physical space, mobility of the system, the nature of the patient population, the complexity of the task with respect to the patient population and the extent of immersion desired from the system.

13.4 VR attributes for rehabilitation
In recent years, VR technologies have begun to be used as an assessment and treatment tool in rehabilitation. The rationale for using VR in rehabilitation is based on a number of unique attributes of this technology (Riva et al., 1999; Schultheis and Rizzo, 2001). These include the opportunity for experiential, active learning which encourages and motivates the participant (Mantovani and Castelnuovo, 2003). In addition, there is the ability to objectively measure behavior in challenging but safe and ecologically valid environments, while maintaining strict experimental control over stimulus delivery and measurement (Rizzo et al., 2002b). VR also

offers the capacity to individualize treatment needs, while providing increased standardization of assessment and retraining protocols. Virtual environments provide the opportunity for repeated learning trials and offer the capacity to gradually increase the complexity of tasks while decreasing the support and feedback provided by the therapist (Schultheis and Rizzo, 2001). Moreover, the automated nature of stimulus delivery within virtual environments enables a therapist to focus on the provision of maximum physical support when needed without detracting from the complexity of the task. For example, several objects can be displayed simultaneously from different directions while the therapist supports the patient’s paretic shoulder. Finally, the ability to change the virtual environments relatively easily enables clinicians to assess more efficiently different environmental modifications, which endeavor to enhance clients’ accessibility. A summary of these attributes are listed in Table 13.1 together with some applications taken from the literature.

Table 13.1. VR attributes and some applications taken from the literature. Attributes Safe and ecologically valid environments Examples Training patients with neglect to safely cross the street (Naveh et al., 2000; Weiss et al., 2003a) Assessment of driving with patients following traumatic brain injury (Schultheis and Rizzo, 2001) Control over delivery of stimuli via adaptation of the environment and task to elicit various levels of performance Gradual changes in task complexity while changing extent of therapist intervention Increased standardization of assessment and treatment protocols Objective measurement of behavior and performance Using video-based VR system with patients following spinal cord injury (Kizony et al., 2003b) Assessment of cognitive function using a virtual kitchen (Christiansen et al., 1998) Documenting hand function (e.g., range of motion of fingers) after stroke ( Jack et al., 2001) Analyzing behavior (movements of body parts as well as success in virtual task) of children with ADHD (Rizzo, 2000, 2002a) Provision of enjoyable and motivating experiences Providing leisure opportunities using video-based VR with young adults with physical and intellectual disabilities (Weiss et al., 2003) ADHD: attention deficits hyperacture disorder. Adaptation of the GX-VR system in terms of color, direction, speed and amount of stimulus (Kizony et al., 2003a)

For example.and post-testing of standard cognitive measures such as digit span.. a town and countryside and snowy mountain with ski runs) that were linked to a cycle ergometer and displayed on a screen while steering within the virtual course. six stroke patients and six matched controls (Naveh et al. 1999). 2000). as well as pre. the program is being used in a controlled clinical trial to train patients with right hemisphere stroke and unilateral spatial neglect (USN) in order to improve their attention and ability to scan to the left. Rizzo et al. memory. sequencing and executive functioning (Pugnetti et al. run on a desktop VR system. such as visual perception. trail making and memory (auditory.188 Patrice L. 13. Currently. The control group consisted of 12 patients from the same hospital who did not receive this treatment but were matched for other variables. suggesting that learning may have been facilitated by an increase in arousal activation level (Grealy et al.. the VR group completed the tests in less time which may also be an indicator of improvement. meta-cognitive and motor deficits Cognitive deficits VR has been used as a medium for the assessment and rehabilitation of cognitive processes. Measures included standard paper and pencil cancellation tests. visual and logic). 2003a). while the control group needed longer time to perform (Katz et al.. a street crossing virtual environment. however.. 1998). logic sequence and speed of responding. participants with brain injury showed significantly worse performance when compared to healthy volunteers (Zhang et al. An experimental group included 13 patients with traumatic brain injury (TBI) who were treated for 4 weeks with pre. Results showed significant improvement in auditory and visual learning following the VR treatment but not in complex figure and logic memory tasks. Weiss et al.5 VR applications in neurologic populations VR applications in rehabilitation are expanding at a rapid pace and a large variety of platforms and programs are currently being used and developed. (1999) combined a bicycle exercise program with three virtual environments (a Caribbean Island.. 1998. as all patients improved in looking to the left and most of them had fewer accidents during the virtual street crossing at post-test. The GX video-capture VR system has recently been investigated to determine its potential for remediation of cognitive and motor deficits (Kizony et al... Grealy et al. 1987). in all components. . attention. Weiss et al. Results showed that the program is suitable for patients with neurologic deficits in both its cognitive and motor demands. 2001)..and post-performance within the virtual environment and during actual street crossing. Initial results from 11 patients who used the virtual environment (VR street test) versus a control group of eight patients who used non-VR computer-based scanning tasks showed that both groups improved in their scores.to post-test on the VR street test. with successively graded levels of difficulty was developed to provide users’ with an opportunity to decide when it is safe to cross a virtual street. Assessment and remediation of cognitive. 1987) and Mesulam symbol cancellation test (Weintraub and Mesulam. The performance of the VR group in the VR street test showed training effects. Speed of information processing was also enhanced.. 2005). Due to limitations in space this review is by no means comprehensive. problem solving. 2000. It was initially tested on 12 subjects. namely the number of correctly canceled items on the star cancellation from the behavioral inattention test (BIT) (Wilson et al. while the majority of the control group did not change their performance from pre. a meal preparation task in a virtual kitchen viewed via an HMD examined the sequencing of 30 steps during a soup preparation task.. The study aimed to improve cognitive abilities via exercise within different virtual environments. The evaluation was found to be reliable and valid for the assessment of cognitive functioning of 30 patients with closed head injury (Christiansen et al. In a different series of studies. In a second study with the same VR scenario the subtasks were categorized into information processing.

2004) and to provide recreational opportunities for people with severe disabilities (Weiss et al. For example. tables. fire hydrant). performs various tasks of selective. memory was also tested (Rizzo et al. 2003a)..g. The desktop VR system focuses mainly on visual scanning whereas the video-capture system combines visual scanning with motor activation both of which have been shown to be important rehabilitation goals.g.Virtual reality in neurorehabilitation 189 2002.g. and received immediate visual and auditory feedback to help him improve his performance.. and a Virtual Office was developed for assessment of memory processes in patients with TBI. A virtual classroom was developed for the assessment and training of attention in children with attention deficits hyperactive disorder (ADHD). The user is asked to scan the office via an HMD for 1 min and then to recall the objects from memory.. The patient expressed enjoyment and motivation to continue with this kind of treatment. an ability that is critical for . in addition to attention.g. Hyperactive motor movements tracked from the head. Schultheis and Rizzo. blackboard. This is an example of where off-the-shelf software has been adapted to make it more applicable for clinical use. number and color of stimuli and by adding distracters to the scenario (Kizony et al. The adaptations applied to these VR environments enable the treatment of visual spatial attention and USN common symptoms following brain damage. 2002a). paper airplane flying above the classroom) and auditory (e. clock) whereas eight would not be (e. Both the street crossing environment as well as the video-capture games (such as soccer) are examples of the use of VR technology as applied to the treatment of stroke patients with attention deficits and USN. 2002a). Results showed that the children with ADHD had slower and more variable reaction times. The virtual classroom contains the basic objects (e. In a recent review of the use of VR in memory rehabilitation. 2000.. he played the role of a soccer goalkeeper whose task was to deflect balls that came towards him from all directions. Sixteen objects are placed in the environment. The child’s performance is measured in terms of reaction time. by controlling the direction.. During VR treatment he was required to pay attention to the entire visual space as well as moving his affected arm in the neglected space. he saw himself within the virtual environment. (2003a) described an example of a patient following a right hemisphere stroke with attention deficits 6 months after the event. 2002.. as a child who wears an HMD to view the environment. windows) and subjects (e.g. Rizzo et al. Kizony et al. A study is now underway in which the effect of training with this VR system to remediate attention and USN deficits of patients with right hemisphere stroke is being evaluated.g... 2002a). chairs. steps in the hallway) distracters inside and outside the classroom randomly appear.. Sveistrup et al. however. car outside the window. made more omission and commission errors and showed higher overall body movements than did the control children (Rizzo et al.. An initial clinical trial compared eight children aged 6–12 years with ADHD and 10 control children on standard tests and VR performance. 2003b). similar to real world settings. Another approach for the assessment and rehabilitation of attention and memory processes is one that makes use of HMD-delivered virtual environments such as the applications developed by Rizzo and colleagues (Rizzo et al. eight of the objects would typically be found in an office environment (e. The Virtual Office is modeled on the same principles as the virtual classroom.. Brooks and Rose (2003) discussed one example of a virtual four-room bungalow which runs on a desktop computer for the assessment of prospective memory.. pupils) found in a typical classroom.. as for example. but still controlled with the possibility of systematic and precise measurement. a phenomenon described more fully in Chapters 28 and 36 of this volume.. female teacher. Both the classroom and office virtual environments have considerable potential to train individuals to improve their attention and memory abilities within a task that is relevant. 2003. Weiss et al. 2001. Both visual (e. Reid. arms and legs were greater for the children with ADHD and more pronounced when distractions were presented. During the game. Behavioral factors such as head turning and gross motor movement related to distractibility and hyperactivity are also recorded. sustained and divided attention.

. (2002) developed the V-store. In another study. virtual environments appear to offer a way to systematically assess and rehabilitate executive functions. was highly correlated. They defined components of strategy formations. (2002) used a haptic device for the assessment and training of motor coordination. Performance in both the real and virtual environments.. Twenty-two patients with stroke and a control group were requested to perform a furniture removal task (using a mouse or a joystick) while they were required to remember certain conditions of cue.. since they have ecologic validity and can be readily designed to simulate the demands found in everyday tasks as noted above (Rizzo et al. (2002). Their results showed that the VR test procedure was successful in differentiating between the groups on all measures. and Jack et al. 2002). neuropsychologic and presence measures showed no major differences between the VR systems. defined as the number of errands completed in a 20-min period. emphasizing the echologic validity of the VR. (2001) and Merians et al. 1998) was one of the first groups to assess executive functions via VR. a desktop VR-based tool for the rehabilitation of executive functions for patients with TBI. Weiss et al. Initial evidence points to the value of VR technology for the rehabilitation of executive functions in TBI. Lo Priore et al. The video taped performance of subjects was coded and compared while performing a series of errands in the University of Aberdeen Psychology Department (real world) and within a flat screen VR scenario modeled after this environment. problem solving. This finding suggests that performance in the real and virtual worlds was functionally similar. rule breaking and prospective memory for 35 patients with focal prefrontal neurosurgical lesions as compared to 35 matched controls. 2002b). Moreover. This environment requires the patient to choose and place different pieces of fruit in a basket in accordance with verbal commands. measures of both real and virtual world performance showed concordance with staff observations of planning skills (Rizzo et al. categorical abstraction. Outcomes including physiologic. activity and timed-based tasks. Executive functions deficits VR environments have the potential to enhance cognitive neuropsychologic tests of executive function since they generate a better subjective perception of presence and immersion than do artificial laboratory tests (Lo Priore et al. (2001) used a virtual environment to train reaching movements. McGeorge et al. (2002) have developed a force-feedback glove to improve hand strength and a non-haptic glove to improve the range of motion and speed of hand movement. memory and attention. 2003). Finally. (1995. behavioral control. (2001) compared real world and virtual world “errand running” performance in five patients with TBI who had poor planning skills and in five normal control subjects. The four-room bungalow environment described above was successfully used to test executive functions by Morris et al. Background material on executive functions and TBI are presented in Chapters 30 and 33 of this volume.190 Patrice L. Broeren et al. Based on the results of the latter study. Six tasks are graded in complexity with the aim of eliciting the need for executive functions.. An initial study of control subjects who used the V-store environment via an immersive HMD display as well as via a non-immersive flat screen display was carried out (Lo Priore et al. which included three patients .. Piron et al. They developed an HMD-delivered virtual environment that embodied the cognitive challenges that characterize the Wisconsin card sorting test (WCST). 2002). 2004). A series of distracting elements are included to generate time pressure and elicit management strategies. multitasking. Motor deficits The majority of VR-based interventions used to train motor deficits have been used with patients who have had a stroke. The differences between the groups indicated that using VR as a rehabilitation intervention enabled a more comprehensive and controlled assessment of prospective memory than did standard memory tests (Brooks et al. Pugnetti et al.

.Virtual reality in neurorehabilitation 191 who had a stroke. The VividGroup’s GX system was used to develop an exercise program for balance retraining in which users see their own mirror image. they were able to maintain balance under the very dynamic conditions available within the virtual environment (Kizony et al.. 2003b). However. This was most notable given that prior to training the patient had resided on the unit for 2 months and was still unable to find her way around. were highly motivated to participate and asked to have repeated sessions with the VR system. (1999).. digit or ankle movements as illustrated above. For example. Davies et al. Since many of the VR applications for rehabilitation have used desktop VR systems wherein the user interacts within the virtual environment via a keyboard. The findings showed that the system is suitable for use with elderly patients who have motor and cognitive deficits. controlled and stimulating for patients with stroke and TBI. (2004) presented results of 13 patients who had a stroke and who used a number of virtual games via the GX-VR system. 2002) developed three desktop applications for rehabilitation of daily tasks – a virtual kitchen. topics that are presented in Chapters 20 and 37 of this volume. a patient with stroke and with severe amnesia showed significant improvements in her ability to find her way around a rehabilitation unit following training within a virtual environment modeled on the unit. (2000) to enable practice that is safe. 2003b). thus enabling training without having to travel which is difficult for many patients. individuals with acquired brain injury have been trained to perform specific arm movements within a virtual environment and have then been able to generalize this ability and engage in daily functional use of the affected arm (Holden et al. This preliminary evidence demonstrates the value of VR technology for balance training and SCI. Following 6 weeks of training at an intensity of three sessions per week. . In this report. mouse or joystick.. Results showed that for all patients virtual training was found to be as successful as real training (Brooks and Rose. 2002). prior to practice within an actual kitchen. 2003b). improvement was found for all 14 participants in both the VR and control groups (Sveistrup et al. it appears that training within a virtual environment may lead to improvements in upper extremity function in this population even when at a chronic stage (Merians et al. Initial results from a usability study of nine patients showed that they enjoyed doing the tasks. meta-cognitive or functional or limited to wrist. 2002) and appeared to make considerably more effort than during conventional therapy (Kizony et al. Initial support for the ecological value of VR “route finding training” can be found in a case study by Brooks et al. namely remediation of motor deficits via compensatory strategies to maintain balance.... The functional tasks and the 3-D way finding within the virtual environment were carried out using an adapted keyboard or a touch screen. In addition all participants expressed their enjoyment from the experience. even to places that she visited regularly. 2001). A virtual kitchen was also developed by Gourlay et al. Such training for these patients is essential in order to help them achieve maximal independence. More recently the use of other methods of interaction has enabled applications that can also be used for the improvement of motor deficits. It was also evident that the task was highly motivating for him (Kizony et al. These researchers developed a “telerehabilitation” system for use at home under supervision by practitioners from a clinic. who have cognitive deficits. the VR group reported more confidence in their ability to “not fall” and to “not shuffle while walking”. 2003). The same VR system has been used to explore its potential to train balance for patients with spinal cord injury (SCI) (Kizony et al. More importantly. Kizony et al. (1999. Four additional patients were trained on this system using four different routes. a service and vending machine and a hospital and university way-finding environment. 2003). Functional evaluation and training Instrumental activities of daily living VR shows promise for training activities of daily living with different populations. the focus of intervention has often been cognitive.

both cognitive variables which may explain the difficulty of performing the actual task (crossing streets or driving) and the functional evaluation and training for transfer and generalization to the daily tasks are combined. The client interacts within the virtual environment. The results on the divided attention task were highly correlated with neuropsychologic tests..5.. Next. meaning and actual performance). Naveh et al.192 Patrice L.e. Within the “interaction space” sensations and perceptions related to the virtual experience take place (sense of presence.. The first of these factors relates to the user’s personal characteristics (body functions and structures). 2001) terminology (Kizony et al. Application of VR to driving assessment and training has had. performing functional or game-like tasks of varying levels of difficulty. The ultimate goal of VR-based intervention is to enable clients to become more able to participate in their own real environments in as independent manner as possible.6 A model of VR-based rehabilitation The VR experience is multidimensional and appears to be influenced by many parameters whose interactions remain to be clarified. and found comparable results for the two approaches (Schultheis and Rizzo. night driving) (Schultheis and Mourant. the current “gold standard”. . two primary factors within the “interaction space” influence the nature of the interaction between the user and the virtual environment. Thus. 2000. The comparison of three patients with TBI to matched healthy controls showed that speed of driving was consistent and similar for the two groups. straight. but the patients failed to call the digits. Safe street crossing is a major concern for many patients with neurologic deficits as well as for elderly people. A VR-based driving assessment system using an HMD was developed and tested at Kessler Medical Rehabilitation. 2001). The first study compared the VR-based driving system with the behind the wheel (BTW) evaluation. crowded. 13. 2002) and consists of three nested circles. 13. non-populated roads) and gradually progress to more challenging situations (i. In contrast to real world settings. This enables the therapist to determine the optimal environmental factors for the client. The characteristics of the virtual environment may be either barriers or enablers to performance. 2003a) aimed at testing the effectiveness of virtual training for patients with stroke who had USN or other deficits of spatial perception. The VR desktop system of street crossing described above (Katz et al. an analysis of the demands for safe driving was carried out. while the healthy performed this task significantly better than the patients. 2001). to date. 2005. highway roads.e. and is thus an important goal in rehabilitation. Another activity of daily living is street crossing.. validating the method of testing during VR driving. This model was developed within the context of the International Classification of Functioning. described above. and to determine whether these skills transferred to performance in the real world. and the issue of divided attention was studied by adding a task of calling out digits appearing on the screen while maintaining driving at differing speed levels. the patients with TBI showed a serious problem in dual tasking. Disability and Health (ICF) (World Health Organization. As represented schematically in Fig. 13. As in the case of the street crossing program. 2001). the virtual environment can be adapted with relative ease to the needs and characteristics of the clients under our care. the intermediate “transfer phase” and the outer “real world”. very promising results (Schultheis and Rizzo. The second factor relates to characteristics of the virtual environment including both the type of VR platform and its underlying technology and the nature and demands of the task to be performed within the virtual environment.5.. the inner “interaction space”.. An extensive research project is underway to test the system for different neurologic populations. This provides for ecologic validity of VR systems which is missing in traditional standard measures. Weiss et al. When using VR in rehabilitation we construct a virtual environment that aims to simulate real world environments. A proposed model for VR in rehabilitation is presented in Fig. Weiss et al. The rehabilitation of driving skills following TBI is one example where individuals may begin at a simple level (i.

Finally. In addition to the many exciting rehabilitation applications presented above.. From the interaction space (inner circle) we move to the transfer phase (intermediate circle) since our goal in rehabilitation is to improve daily function in the real world and this requires transfer of the trained skills or tasks as well as environmental modifications from the virtual environment to the real world. 2002) cues for individuals with severe visual impairment via interactive virtual environments. VR has also been shown to be highly effective as a means for providing alternate modes of feedback in cases of sensory impairment such as the substitution of auditory (Sanchez et al. The cost of equipment is decreasing and the availability of off-the-shelf software is growing such that it is now feasible for many clinical facilities to embrace this new technology. The entire process is facilitated by the clinician whose expertise helps to actualize the potential of VR as a rehabilitation tool. 13.. As presented above. 2000) and venipuncture (Reger et al.5.. 2003).7 Conclusions It is clear from the above review that the future holds great promise for the further development of applications of VR to rehabilitation. adapting to or minimizing the environmental barriers. 2001) and to reduce of pain during burn care (Hoffman et al. A model of VRbased rehabilitation within the context of terminology from the ICF (indicated in bold)..Virtual reality in neurorehabilitation 193 Occupational performance in real world – Participation Transfer phase Interaction space “Presence” Meaning Virtual environment Environmental factors System characteristics User characteristics Personal factors Body functions and structures in VR space in real world Task performance within virtual environment Clinician Activity Side effects Environmental factors Real world Figure 13. VR-based therapy has been very effective in other realms of medicine such as in the treatment of phobias (Hodges et al. the literature to date strongly suggests that these . the large. 2000) and/or haptic (Yu and Brewster. outer circle represents real world environments illustrating that the ultimate goal is to help the client achieve participation in the real world environment by overcoming.

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Perring et al. Even when residual motor control is very limited. 2001.. 3Children’s Hearing and Speech Center. Beth Mineo Mollica2. Newark. but vital. 2001). 2002). Communication devices can make an important difference in the quality of life of people affected by disorders that result in impaired speech or writing (Tolley et al. Children’s National Medical Center. DC. since devices and techniques to support communication are generally affordable. 2004). 2001). DC. Techniques also exist to help most persons with cognitive. and begin to progress in social and communicative skills (Cress and Marvin. There are also devices to facilitate computer access for individuals who have impaired ability to write or keyboard. Diener and Bischof-Rosarioz. Patients in 198 critical care need not be deprived of a means of interaction with their family members and care providers (Happ. very young children for whom development of speech and/or language are at risk can gain a foothold in the communicative world. The Catholic University of America. 2Center for Applied Science and Engineering and Department of Linguistics. or when there are sensory impairments or parasite movements. Patients with amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) can continue to communicate with their family.1 Introduction Among the most disabling impairments in patients with neural injuries are those affecting communication. Nor is cost a major barrier. It is not only possible. Sheela Stuart3 and Carole W. educators. consumers. 2001). Gragnani. Higdon. the . 1990. Happ. Delaware. Neither cognitive disabilities. advances in the technology of communication devices and communication training have greatly expanded the proportion of affected individuals who can reacquire the ability to communicate. 1996. for example persons with high-level spinal cord injury that reduces their upper limb control (Hurlburt and Ottenbacher. People with significant core language impairments coupled with severe developmental disabilities can interact socially. Washington. and third-party reimbursement has become increasingly available (Smith. language or behavioral challenges to enhance their level of participation and control (Trepagnier. 2003).. nor very young or old age. Washington. nor absence of literacy skills.. Kubota et al. technology exists to translate something that the would-be communicator can comfortably do into a means of operating a communication device (e. Unawareness of the fact that there are means to support communication by people with severe impairments is also not an acceptable justification.. 2003). 1992).g. become active rather than passive agents. friends and colleagues when they can no longer speak (Doyle and Phillips. USA 14. is sufficient justification for any individual to be deprived of a means of communication. Youngsters with severe movement disorder from cerebral palsy can pursue educational and career goals (McNaughton and Bryen. 1996. Brown4 1 Department of Psychology. USA. Finally. nor being on school vacation. Gryfe. nor the temporary nature of the impairment. communicate preferences.14 Communication devices Cheryl Y. 1998. University of Delaware.. Neurobehavioral Sciences Department. family members and the general public know about supports for people with severe communication impairments. express feelings and conduct their own lives with the help of carefully selected augmentative techniques (Trepagnier. Washington. The Catholic University of America.. Trepagnier1. for people across the lifespan to gain the capacity to interact effectively with the people around them. Gorman et al. 2000. USA. USA and 4Department of Education. 1996. 2002). DC. Fortunately. 1995. The more that healthcare providers. Hadjistavropoulos et al. 2003).

their goals and the contexts in which they will be participating (Beukelman and Ball. or other professions. The community is often a good information source. a speech pathologist who is experienced in AAC will be the one to provide the overall guidance of the process of assessment. While AAC specialists may come from occupational therapy..Communication devices 199 more apt they will be to identify the need when it is present. there is no central registry of AAC specialists. and the symptomatology and prognosis of the disabling condition all need to be taken into account. it is necessary to obtain an evaluation and recommendation from a speech-language pathologist (an SLP) in order to acquire funding for purchase of a device. for convenience. as well as educators and human services and healthcare providers (Granlund et al.. The people served are often referred to as “augmentative communicators”. Just as one would not ask a salesperson at a General Motors dealership for advice on what make of car to purchase. This includes the individual’s family. It is of particular importance that whoever manages the evaluation process be independent. The family’s awareness of the individual’s activities and communication partners will be important in deciding on the particular features the techniques will need to incorporate. such as an occupational or physical therapist and/or a rehabilitation engineer. including associations of individuals with the same disabling condition. educator or healthcare provider seeking these services needs to review the human and information resources available in order to meet the communicator’s needs as effectively as possible. for example. as they may be able to arrange for a loaner device. for (relative) brevity. The best route to obtaining financial help with purchase of communication supports may depend on the individual’s circumstances. . 1998). The challenge of evaluating the potential communicator’s needs and putting together an optimal means of addressing them is complex. or. 1989. conversation partners will need to modify their interactive style in order to foster participation by device-users (Russel. the individual’s needs and abilities. rehabilitation engineering. and everyone who exerts influence on the communication context. Manufacturers can also help navigate funding issues. are important to the success of the aided communication. McEwen and Karlan. The family member. the communicator may wish to “test-drive” a potential purchase. The people who will communicate with the device-using individual. and recognize that it can be addressed. In order to select the most useful techniques. 1984). and can provide the necessary technical support for getting started. 2002). Accordingly it is very important to involve someone with depth and breadth of experience and up-to-date knowledge in the AAC domain. and will be referred to here. The growing body of knowledge and clinical experience related to supporting communication by means of assistive devices and techniques is known as “augmentative and alternative communication”. Manufacturers’ representatives can be of great help at this point. 1990). Once recommendations have been made. the school system may provide devices for school-aged children and adolescents. to resolve questions of seating and positioning for maximum stability and function (Goossens’ et al. Ideally. The SLP may work with other health professionals. and the state vocational rehabilitation system may be a source of funding for people who wish to work (Smith. the characteristics of the living and working context. recommendations and integration of the techniques into the communicator’s daily life. Once the devices and techniques are acquired. The physician’s information regarding expected disease course will affect the selection of control modalities. as they have acquired considerable experience in dealing with third-party payers. friends and colleagues. and to identify the best control options within the individual’s repertoire. 1998). it is wise to obtain evaluation and recommendation services from professionals who have no financial connection with a particular device manufacturer. as “communicators”. 2001). The SLP will also be concerned with communicators’ cognitive and language status. “augmentative communication” or “AAC” (Beukelman and Mirenda. Appendix 1 lists some additional resources. Unfortunately.

Of necessity. Of course the output of a computerized device need not be limited to just speech and/or text. as illustrated in Fig.200 Cheryl Y. Control parameter values may be adjustable to fit the communicator’s abilities. from hitting a large.. Control input.1.words-plus. to changes in direction of gaze sensed by an infrared eye tracking system. keystroke or equivalent can produce. difficult to obtain funding to support training.com Inc. Figure 14. can be wholly independent of each other. 2003. Havstam et al. any longer. The communicator and family members may need help with technical aspects of device operation.2 Control and display There are many kinds of actions that can be sensed and converted into the equivalent of a switch closure or a computer keystroke. People also communicate with electronic and computer-aided devices.. 14. That has been replaced in most devices either by digitally recordable and re-recordable spoken messages. so that accidental bumping would not close them. Trepagnier et al. the cost of this service will already have been folded into the purchase price of the device. 1992. Even dysarthric speech can be a viable control option in some cases (Goodenough-Trepagnier et al. Some individuals with aphasic impairments of written expression have been able to use their residual speech as a control mode. how to maintain calibration when using a device operated by direction of gaze.1. for example. There are switches that require sustained force. in order to control electrical . and output. or it may go out to untold numbers of people who access a web site. or by sophisticated text-to-speech software and a variety of more natural-sounding artificial voices. Bruce et al. 2001). robotic-sounding synthetic speech. but also to persons who will receive the communication at a future date. Training is needed for communicators and for their frequent communication partners. Communication may be directed not only to persons in the immediate environment. Training of this type is usually provided by the manufacturer’s representatives Parents and teachers may be offered guidance for using the device to support development of a child’s language and communication. Output is seldom. and the gap is often filled by manufacturers’ representatives. and there are switches that require no force at all. Simply acquiring a communication device does not in itself equip the individual to be a competent communicator. so that the communicator can choose an age.. Control inputs can range from tongue contact with switches to a “sip-and-puff” switch. to almost imperceptibly contracting a muscle in the forearm or slightly raising an eyebrow (Soderholm et al. robust switch by extending a limb or inclining the head. from an eye-blink. there are many types of effects that a switch closure. unfortunately. generally by an SLP or educational specialist (Pebly and Koppenhaver. Courtesy of Words www. It is. on the one hand. on the other. 2001). by means of mass-market speech recognition software. Similarly. 2003). or who are a few miles or a continent away. 14. merely contact.and gender-appropriate one.. An infrared blink switch.

14. It is a misperception that devices that incorporate technology inevitably entail complexity for the people who will use these devices. which have for the most part come to involve computers of one type or another. there are electronic devices. It can be helpful to think of AAC techniques and devices in terms of three categories. for example by reciting the alphabet until the communicator indicates which letter is intended. Difficulty of learning or use is in most cases an indication of poor design or. people who do not have deficits in motor control. While a device may get left behind. 2002). Goodenough-Trepagnier. and can be used in combination with speech (Konstantareas. and are indeed preferred in some (Doyle and Phillips. 1987). there are advantages and disadvantages to be considered in the context of individual communicators and their activities and communication partners. These are sometimes called “no-tech” and “low-tech”. 1981. but also plays the role that a device would fulfill. In no-tech scanning. and it is often the case that more than one technique is needed. the conversation partner not only speaks both parts of the conversation. language-impaired communicators with mental retardation. and they will undoubtedly use computers in the near future to carry out other activities that most of us have not yet imagined. 2001). and techniques that involve non-electronic ones. communication depends on the conversation partner. as long as a knowledgeable communication partner is present. Signs (borrowed from American Sign Language. poor fit to the consumer’s abilities (Norman. listen to music. With this caveat. 1982. or for one adult with acquired neuromotor impairment. or both. This is a useful starting point. a young adult with brain injury that impairs speech . the following portion of the chapter will point out considerations that are often of special concern for particular disability groups. A device that proves helpful for one individual with autism. if not more than. Norman. there are language boards that offer letters. With a skilled familiar conversation partner. it is important to recognize the diversity within any clinical category.Communication devices 201 devices in their environment. Individuals with motor impairment An adult who can no longer speak intelligibly. Finally. edit photos. Goodenough-Trepagnier et al. a no-tech method is always available. and are sometimes referred to as “hi-tech”. Musselwhite and Ruscello. chunks of words. In the domain of “low-tech”. seek information. Whatever the technique. language or cognition. Low-tech and no-tech have in common that there is no explicit output entirely under the communicator’s control. These are represented by regular or phonetically adapted spelling. however. the native language of many deaf people in this country) are another notech method. shop. There is some evidence that using gesture at the same time as speech is helpful to the speaker (Clibbens. manage finances. at the least.. these techniques provide more rapid spontaneous communication than current devices. 1993. 2001). whole words and messages. Instead. because the familiar partner can use special knowledge of the communicator and the context to guess ahead. respectively. At the same time. The individual with communicative impairment needs access to these capabilities as least as much as. autism.3 Communicative needs of particular clinical populations Just as devices can be categorized. These methods can be highly effective in many circumstances. device-users are often considered in terms of the disability that is at the root of their need for communication support. They have been useful for some hearing. perhaps by a facial movement or eye movement. may be wholly unsuitable for others who happen to share the same diagnostic labels. at the same time. pictures and/or symbols of various types (Goodenough-Trepagnier and Prather. and it can offer greater privacy and intimacy within a conversation dyad. There are techniques that do not require any props. 1984). only an electronic device offers independent communication. play games or take courses. The language board never runs out of batteries. 1994.

www. as a prerequisite to effective use of a communication device. and the communicator does not need to exert as much effort. Retrieval of such pre-constructed messages usually involves some variant of a shift-key strategy. then the “h. to produce half a dozen words of real-time output. as illustrated in Fig. a phrase that will capture the listener’s attention while a novel message is slowly composed (a “floorholder”) or a slogan in support of a favorite team may be stored whole on the device. no communicator should be required to spend a long period as a trainee. and communicators whose device does not provide easy access to a spelling mode of some type. most users of augmentative devices require as much as 3 minutes and others may take longer still.2. education and employment.com Inc. or part of a code) and Figure 14. 2003). is to compose phrases in advance and store them for quick retrieval. the ability to interject “How about them Redsox” at the socially appropriate moment does not suffice (Bedrosian et al. However. and a young student with severe cerebral palsy who has acquired basic literacy skills are some of the people to whom this category applies. Despite many ingenious attempts to improve this situation. by means of which the software anticipates intended words based on letters already typed. and makes new learning difficult.202 Cheryl Y. While it is to be expected that one would make gains in skill and speed with experience. Since these are largely people who do not have serious problems understanding language. or who do not have the skills to utilize spelling. Communicators with preserved cognitive and language skills rightfully expect to be able to utilize their device right from the start. sometimes implemented in mass-market computers. if the communicator cannot accomplish the precise verbal task she or he wishes to carry out.. whether it is a question of augmentative devices. the problem that shows up here in particularly stark relief is the issue of impoverished communication rate. Courtesy of Words words-plus. Usability is important in all cases. With expertise. a drawback that is common across all AAC. generally by means of the rather complex way of representing speech sounds that standard English spelling provides. individual preference and acceptance is key. the user might first hit a designated shift key (usually called a “level” key. For example. One such technique is “prediction”. . This requires combining the sounds of speech. instead of just hitting the “h” key (to produce the letter “h”). prediction becomes equivalent to a practised shorthand.” to call up a message that had been constructed in advance. 14. As is the case for any group. intended to accelerate and support communication.2. Communicators whose impairment is primarily motor in nature need a communication device with which they can express whatever message they intend. Another approach. of which there are numerous variants. Spelling of individual words does not preclude use of software techniques. the problem remains a major stumbling block to the successful integration of augmentative communicators in conversation. are at a disadvantage. Using an orthographical system implemented on a laptop computer. While English speakers may converse at rates of 200 and even more words per minute. one’s phone number. Trepagnier et al. glasses or orthopedic shoes. Entire jokes or speeches.

. Current understanding of how language typically develops can usefully inform the facilitation of language development in children with SSPI (Gerber and Kraat. Young children with cerebral palsy In the first years of life. actions and attributes in the environment (Pinker. Typically-developing children’s intensive vocal exploration is not available to children with significant physical limitations. 1997. Woolfe et al. then. or whose early exposure to sign is sporadic. young children with SSPI may experience their prime language-development years in a suboptimal manner. 1987). Clearly. and progress to word combination by 18 months of age. Once they have some knowledge of syntax. 1992). 1990.. Chapter 39). Mineo and Goldstein. and accrue impairments in development of grammar. 1979. when the proportion of actions increases (Benedict. has been found to result in language impairments and failure to acquire “native-speaker” level skills (whether in signed or oral language) (Mayberry and Eichen. Although there is great variability among children regarding rate of lexical acquisition. 1991). and their amenability to intervention. the new emphasis given to literacy as a metric of schools’ educational success and the implementation of novel instructional and assistive technologies. Delayed access to language. rather than resort to the more intelligible channel offered by augmentative technology. 1994). 1990). children’s first words tend to be about things and events in the “here and now. the consequences of delay and suboptimality of exposure to language and communication experienced by deaf infants. Children initially learn from experience and interaction how to map words to objects. While comparable studies of individuals with motor limitations have not been carried out.. the additional limitations of reading and writing impairments (Berninger and Gans. The unfortunate sequelae of SSPI will. begin to produce words at around the time of their first birthday. maximizing the SSPI child’s opportunities for interaction and providing a means to address lexical and syntactic development are important considerations in the design of AAC interventions. and there is evidence of negative effects on other aspects of cognitive development (Mayberry and Eichen. however difficult it is to understand. 1992). may be instructive here. the emergence of grammar coincides with mastery of sufficient vocabulary to facilitate word combination. 1991. 2003). Long-term effects on the representation of language in the brain have been documented (Kral et al. 2001. 1994). For example. Koppenhaver and Yoder. To these individuals’ deficits in mobility and opportunities to engage with their environment are added. the entitlements provided in the Individuals with Disabilities Education Act. with the help of early intervention. it is hoped. prefer to use speech. and a given individual may. Leybaert and D’Hondt. who are unable to orchestrate the complex movements of the articulators needed to create differentiated word forms and build a basic expressive vocabulary. phonological awareness and metalinguistic skills that will undermine their literacy development (Wagner and Torgesen. Absence of intelligible speech often has the secondary effect of relegating children with significant speech and physical impairments (SSPI) to a passive role in social interaction (see Volume II. for a number of reasons. typically-developing children use their oral mechanisms to engage in sound play. Golinkoff et al. they can use the information derived from syntactic relationships to intuit the meaning of unfamiliar words (Gleitman. which offer new ways for children to participate and learn. 1984. . as happens with deaf infants who are not taught sign. Function words remain relatively infrequent until the child has passed the 400-word mark..” with nouns predominating until the vocabulary reaches about 100 words. Bates et al. Augmentative techniques need to be applied to acquisition of morphological and syntactic structures as well as metalinguistic awareness (Paul. be minimized in children now growing up. 1986.Communication devices 203 The potentially most useful device will not do much good if the individual does not wish to use it. As a result of the direct and second-order effects of their deficit. 2002). AAC can scaffold early language learning and provide the means to engage in language practice and experimentation that otherwise would be unattainable.

small size and long battery-life). It is also the case that many existing devices and techniques are a poor fit to the needs of people with significant mental retardation. and that can help introduce to persons with severe cognitive involvement the concept of indicating their preferences and thereby gaining a desirable outcome. Pittsburgh. Trepagnier et al. Severe motor impairment from cerebral palsy does not entail severe cognitive impairment. Often training with assistive technology can enable the capacities for independent expression that will in turn make it possible to assess. or they may be unable or unwilling to explore the range of technology options available. who also experience cognitive impairments. Photo courtesy of DynaVox Systems LLC. Paul. have the numerous characteristics that make them practical (including light weight. Devices that are hardened to survive everyday use. may be considered for a variety of populations. In part this stems from the complexity of diagnosing and addressing communication disturbances that are secondary to cognitive deficits (Beukelman and Mirenda. . including children with impairments in motor control as well as individuals. too. discussed below. 2002). 1994. they do not become advocates for the inclusion of these services in program planning. such as the one illustrated in Fig. devices that primarily offer these strategies do not provide children with expressive language experiences that parallel those of their typically-developing peers.3. 14. there may be little left to meet the demands of message formulation and partner engagement. and to train individuals and their circles of supports in how to operate the devices or techniques and how to utilize them in the context of real-world exchanges. When device operation demands a disproportionate share of the user’s cognitive resources. Individuals with mental retardation and other developmental cognitive disabilities Not so long ago individuals with developmental disabilities whose communicative intent was hard to discern were not offered augmentative techniques. an effect that might be amplified by incorporating rhyming games and other tasks designed for building phonological awareness. and the flexibility and power of a computer. PA (1800-344-1778). Mollica. It is unfortunately the case that knowledge and skill barriers still preclude many from accessing augmentative services and supports. and this population continues to be seriously underserved.3.204 Cheryl Y. 1998. Sutton et al. While parents and service providers may find it appealing to offer devices that yield complete sentences from single selections. Voice output may facilitate the development of phonological awareness (Blischak. An augmented communicative interaction using a large-vocabulary graphical display on a dedicated device. often hinder access to communication technology by individuals with Figure 14. the child’s potential. 1997). Many clinicians lack the confidence and/or expertise necessary to exploit the potential of AAC tools for maximum consumer benefit: they may not understand how to assess communication skills at a pre-intentional or emerging intentional level. to customize the device to meet consumer needs. Since many families are not aware that their loved ones could benefit from communication technologies.. Policy and practice barriers. There are nevertheless AAC techniques and devices available that can support expression of communicative intent. A large number of speech language pathologists have had neither academic coursework nor practicum experience in supporting communication development and use by individuals with significant cognitive limitations. Indeed it can co-exist with superior intellectual abilities. 1999). and thus better serve.

Linebarger et al. as well as time after stroke or injury.. In fact. and visual support may help some individuals with aphasia to engage in conversation and transmit information (Goodenough-Trepagnier. At the other extreme is chronic severe “global” aphasia. In between the extremes there is a broad range that is not linear. someone with severely limited speech may be able to convey specific words by pointing to words on a list. 1997. voice output and flexible language organization may facilitate language development and communication in ways not possible through other means such as sign language or static picture cards. however. In practice. the availability of dynamic language representations (increasingly in portable and wearable form). 2000. Many individuals who experience aphasia in the period immediately after their stroke recover fully or recover with minor residual deficits. or subcategories of words.. and these factors. Historically. are the main factors determining the type and severity of the aphasia (Pedersen et al. 2003). also affect its course (Pradat-Diehl et al. many third-party payers. 1995). typically from a cerebrovascular accident or stroke. 2001. While gains can be achieved years after onset.. for reading or writing. have denied requests on behalf of individuals with mental retardation for communication devices. it can be a helpful component of a communication system. violates recommended practice principles by precluding consideration of individual needs (National Joint Committee for the Communication Needs of Persons with Severe Disabilities. Kiran and Thompson. such as Medicaid and school districts. and who is cognizant of therapeutic and augmentative techniques that have been of help to individuals with aphasic disorders. extent and type of lesion.Communication devices 205 cognitive limitations (Mollica. 1999). 1998. such as chronological age. 2002). the growing body of research documenting the efficacy of AAC in enhancing both language development and use (Sevcik and Romski. such as names or common nouns. in most cases on the left side of the brain (see Chapter 26 of Volume II). is preserved. Augmentative approaches must accordingly be tailored to their users’ profile of preserved and impaired abilities. While computerized systems that enable users to select and string together pictures standing for concepts are useful for some individuals with aphasia both for communication and as therapy (Weinrich. in general aphasia that persists after 1 year is considered chronic. 1995. In addition to reports by neurology and rehabilitation medical specialists.. in conjunction with treatment. Residual aphasia may be as mild as a difficulty in retrieving names or other precise words in as timely a fashion as one would like. Written language. Persons with relatively preserved speech but impaired writing may be able to use augmentative technology in the form of speech recognition. and may be unable to assign verb and preposition meanings to graphical . Garrett and Huth. to accomplish writing tasks (Wade et al. The location. Similarly. 2003). is also globally impaired in these severe cases. 2001. If the ability to recall the initial letters of words. diagnosis or the absence of cognitive or other skills purported to be prerequisites. The recent position statement of the National Joint Committee for the Communication Needs of Persons with Disabilities clarifies that reliance on a priori eligibility criteria. 2001. Linebarger Schwartz et al.. Rowland and Schweigert. Bruce et al. it is helpful to have a thorough evaluation of expressive and receptive written and auditory language carried out by a speech language pathologist who specializes in aphasia. Some individuals may have specific impairments in the context of an otherwise high level of preserved language ability. 2004). Others may have some preserved skills that are the more remarkable compared with the severity of their overall level of language impairment.. Aphasia Aphasia is the blanket term used for the myriad speech and language disorders that can result from injury to the adult brain. 2000) reinforces that such discriminatory practices are unjustified. Individuals with aphasia of this type can make little sense of what people say to them and their attempts to speak may yield only a couple or at best a few “frozen phrases”. persons with global language impairment may not be able to relate spatial order of pictures or words to grammatical function. 2003). presuming that such individuals would derive only limited benefits.

and who is also familiar with AAC techniques. 1987). or a device developed for young children with cerebral palsy.206 Cheryl Y. While there are movement and motor control anomalies associated with autism. The pace of autism-related research has increased rapidly in recent years. children with autism share with SSPI children a key secondary consequence of their disability: exclusion from communicative interaction. and clinicians and investigators have long advocated .. who have not had the benefit of typical socialization. and the need for a repertoire of techniques in keeping with the demands of different situations should be considered (Cress and King. It should also be remembered that unlike the primarily motor-impaired population. Rimland. Accordingly. 1976. the range of contexts in which they might benefit from communicative supports can be large.. Scientific study of this spectrum of disorders began to gather momentum as general agreement was reached on diagnostic criteria around 1994 (American Psychiatric Association. Directional skills are also generally retained. and to support efforts to foster their language development. they are also profoundly impaired in understanding nonverbal communication: how to interpret the facial expressions. tones of voice and gestures of the people around them (Trepagnier. 1989. While it is possible that a communication device designed for an adult with acquired neuromotor disability. 2001) whose signal feature is a profound disturbance of social relations (Wing.. Children with autism who have not developed speech are not only verbally impaired.. 1943. with the help of appropriate training (Rayner and Marshall. 2002). It is estimated that as many as half of people with autism do not develop speech that is adequate to meet their communication needs (Sigman and Capps. can be of great help in this regard. however. these are minor in relation to the overall picture of profound deficits. that can in no way be assumed. 1999). Children whose speech is not emerging at the expected time need augmentative support in order to begin to gain social interaction experience. As with other populations who use augmentative techniques. many individuals with aphasia retain the ability to read social situations and extract information from non-language cues. and has yielded improved methods of detection and intervention that can make a major difference in the individual’s potential to live a satisfying life (Eikeseth et al. 1994). 2003). 2003). The beginning of modern understanding of autism dates back to the mid-20th century (Kanner. conversation partners can take steps to improve communicators’ participation. Preserved social and spatial abilities may be put to use for communication via gestures. however. and can improve with training (Sacchett et al. which are helpful for some individuals. many people with aphasic communication difficulties are ambulatory and some may continue to drive a personal vehicle. is present to some degree in most individuals on the spectrum (Rapin and Dunn. representations at all (Goodenough-Trepagnier. 2004). 1964). 1998). mime and drawing. About 70% have mental retardation (La Malfa et al. could be useful for someone with aphasia. directions of gaze. There is. 1997). Beukelman and Mirenda. Autism Autism is a lifelong disability with complex genetic origins (Folstein and Rosen-Sheidley. 1996). 1987. and indeed the fact that these individuals are almost all ambulatory and that many children are especially active puts its own sorts of constraints on augmentative choices. in addition to the evident pragmatics deficits (Wing and Atwood. being able to provide verbal directions. such that someone may be an effective navigator without. 1996). Many people with autism demonstrate strengths in the area of visuo-spatial and visual memory skills. no cure. Shelton et al. Their limited and idiosyncratic social and communicative repertoire results in their failing to participate in most of the play-based learning in which typically-developing children constantly engage. Motor impairments do not limit the AAC options for most people with autism. Trepagnier et al. 1999). Despite their mobility. Volkmar. Unlike individuals with congenital disabilities. A speech-language therapist specializing in aphasia. and language impairment.

be produced at a normal conversational rate. and the more important if speech impairment is severe. management and treatment of their child and in regard to the particular issues involved in communication support. Dawson and Osterling. (Bondy and Frost. and there is some evidence that its use can have beneficial effects on the child’s development (Bondy and Frost. They must make life-affecting decisions on the basis of woefully inadequate information. these have included populating the device’s vocabulary. 1987. both in regard to the education. support for communication. using transitional probabilities of letters to “guess” the word once an initial letter or letters have been entered (Koester and Levine. 1985) and a variety of attempts at mnemonic storage and retrieval schemes. 1995. so that the augmentative technique .Communication devices 207 multimodal. the reason for storing pre-constructed messages. the inherent flaw remains. communicating by means of augmentative techniques is terribly slow relative to speech. 1981. Printed materials too can appeal even to very young communicativelyimpaired children with autism. Hunnicutt. Besides choosing what items should be offered in the device’s “selection set”. 2001) makes use of the autistic child’s mobility to build interaction into the use of the technique. 2003). The descriptively-named Picture Exchange Communication System or PECS. While the disparity is perhaps most acutely felt by individuals who have had to turn to AAC because of the deterioration of their own motor capabilities.. attention is also given to where they should be placed. 1990). 14. Investigators recognize and are striving to address the need to minimize demands on working memory and attention.. Charlop-Christy et al. since such messages can. and pays special attention to generalization across partners and settings (Beukelman and Mirenda. 2003).4 Ongoing and emerging issues Unmet needs Communication rate: As noted above. A useful analogy might be that of speaking a language one does not know very well. This is. similar to the guidelines for autism treatment in general (Simeonsson et al. in principle. using multi-letter keys such that the software “disambiguates” by referring to transitional probabilities and a dictionary look-up (Minneman. Goodenough-Trepagnier et al. Families of children with autism face a myriad of divergent information. involves the family. Helms Tillery et al. 2001). Mental load: The additional cognitive demands that device operation places on the communicator are a problem not only for people with cognitive disabilities but for all augmentative users. that communicators are being asked to use their residual. 2003). 1997). include intensive intervention that begins as early as possible. 1982).. or “selection set” with items chosen for their frequency of occurrence in combination with each other (Goodenough-Trepagnier and Prather. 1998). 1995. 2002). and especially visual. Literacy is important. Recommended guidelines for augmentative support. Todman and Rzepecka. as it is to any individual. as is frequently used in the TEAACH program (Mesibov. it is a problem for anyone who is attempting to join the flow of human social and communicative interaction by means of a communication device (Goodenough-Trepagnier et al. with positive effects on development of literacy skills (Koppenhaver. of course. in order to make operation of the device as easy and rapid as possible (Levine and GoodenoughTrepagnier. 1994. 1984. motor control to compensate for their motor speech impairment. meeting a new colleague or communicating in an emotionally fraught interaction would be all the more difficult if one had to do so using a language one does not know well. since it opens the door to spelling-based communication.. It is not difficult to imagine that passing an interview. often impaired.. Whatever the technique. The challenge of finding some way around this problem in order to achieve responsive communication at conversationally acceptable rates still stands. The desperate nature of the problem and the paucity of research have combined to create a vacuum into which many unsubstantiated “treatments” have flowed. Investigators have developed numerous strategies for accelerating communication.

5 Conclusion Recognition of the human right to communication and the many ways in which communication can be supported. Helms Tillery et al. less ultimately useful techniques. Non-disabled keyboard users have resisted the relatively minor alteration of replacing the QWERTY keyboard arrangement (designed to prevent tangling the typewriter’s keys) with the potentially more rapid Dvorak system. signal processing is required to extract the pertinent information. there are stages: first augmentative systems tend to be picture-based. Furthermore. Lifelong use: In the communication history of most children and adults with persistent severe speech impairment. whatever the nature of the individual’s . despite the training. Trepagnier et al. then. and later ones alphabet-based. Unlearning is undesirable.. 2003). 2000) will bring added power to this intriguing interface approach. in which trained monkeys have rapidly attained the ability to control events on a monitor using a brain interface. which was then supplanted by Japanese and later still by English. it is the interface of the user to the device that continues to be problematic. Questions remain as to the extent to which individuals with movement disorders of various types would be capable of controlling signals from somatosensory areas of the brain. 2002) describe. To use again the analogy of second language. recent animal work. since it is so much more powerful and economical than pictures. including individuals who are not disabled. Mind over matter It is conceivable that by the time these words are published there will be a communication device on the market that the communicator can operate by means of electrical events in his or her own brain. a challenge that is perhaps the area of greatest need. the brain activity of interest is sensed by electrodes in contact with the communicator’s scalp. While at present there are usually more easily acquired techniques with similar power to which a person with severe motor disability can have recourse. strongly suggest that we will have significantly improved interfaces to offer to people with disabilities in the not-too-distant future (Wolpaw et al. This work encompasses several different types of brain signals. Since the electrodes receive innumerable signals simultaneously.. can become “second nature” to the communicator (Goodenough-Trepagnier.. Hunnicutt. Typically. Even this level of capability can entail large amounts of training. Indeed it is the case that the individual who can use written language should have the opportunity to do so. 2000. The limiting factor here is not computing power and speed: the signal processing is carried out in real time. 1994. Not surprisingly. as Wolpaw and colleagues (Wolpaw et al. a far from satisfactory means of device operation. 14. including evoked potentials in response to the appearance of significant events (e. This goal also implies providing more powerful and effective communication media for the earliest stages of communicative life.. control is by means of a two-state switch. and brain rhythms that change as a function of preparation for movement. In virtually all current brain interfaces. some individuals.. adequate only for scanning of some kind. 2001).208 Cheryl Y. Yet children with severe communication disorders are as a matter of standard practice asked to give up their communication techniques to move on to techniques that are presumed to be better. with possibly intervening stages using symbols and combinations of all three. At present several groups of investigators around the world are pursuing this goal. it is as if the child’s education were begun in Chinese.g. is to meet the need for conversational rate and transparency and add to it the goal of continuity: devise a way to meet the child’s need for more powerful communication and at the same time reduce and ideally obviate the need to learn and then give up earlier. It may be that combining information about the type of signal with information about the time relationship between device events and brain events (Schalk et al. The challenge here. are unsuccessful. the illumination of an intended letter on a letter matrix). since our failure to meet it deprives the individual of developmental opportunities that will not recur.

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is the professional organization of Speech Pathologists and Audiologists.htm . with its American chapter. manufacturers and people who use the techniques.ussAAC.abledata.org/index.asha.Communication devices 213 Appendix: web resources ABLEDATA is an on-line database project funded by the National Institute on Disability and Rehabilitation Research (NIDRR). Hearing and Language Association. http://www. is an interdisciplinary association of people with an interest in technology and disability that sponsors conferences and certifies assistive technology providers.org/index.AACproducts.lasso RESNA. is an AAC research and development center also funded by NIDRR and competitively renewed every 5 years.org/ pages/membership. http://www. the Rehabilitation Engineering and Assistive Technology Society of North America.com/ The Rehabilitation Engineering Research Center (RERC) on Communication Enhancement. http://www. the United States Society for Alternative and Augmentative communication (USSAC) is an organization of AAC service providers.php The International Society for Augmentative and Alternative Communication (ISAAC).org/default.AAC-rerc. and their families. http://www. The American Speech. http://www.com/ The Communication Aid Manufacturers Association (CAMA) is a non-profit organization representing manufacturers of AAC software and hardware technology that provides information workshops in locations that rotate around the country. This society provides educational and networking opportunities.html ASHA. part of the Office of Special Education and Rehabilitative Services (OSERS) of the US Department of Education to provide information on assistive technology. http://www.resna.

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Vegetative and autonomic dysfunctions B3. Cognitive neurorehabilitation 217 337 411 215 . Sensory and motor dysfunctions B2.SECTION B Symptom-specific neurorehabilitation CONTENTS B1.

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SECTION B1 Sensory and motor dysfunctions CONTENTS 15. Chronic pain Herta Flor and Frank Andrasik 16. Dietz 20. Gait disorders and rehabilitation V. Gelber 18.J. Hall and S.D. Deconditioning and energy expenditure Marilyn Mackay-Lyons 219 231 248 265 283 298 315 217 . Herdman 21. Wolf 19. vestibular and oculomotor dysfunction C. Balance. Management of spasticity David A. Arm and hand weakness Sarah Blanton and Steven L. Loss of somatic sensation Leeanne Carey 17.

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Animal models have shown that long-lasting and/or intense states of pain (e. Germany and 2Institute for Human and Machine Cognition. Chronic forms of tension-type headache consistently reveal evidence of central sensitization to thermal.. they show steeper increases in perceived pain intensity with repetitive painful stimulation. One major factor that seems to contribute to chronicity are memory traces that occur as a consequence of ongoing and/or very intense pain and that are enhanced by learning processes designed to imprint and consolidate these painrelated memory traces. when an inflammation is present) lead to the sensitization of spinal cord neurons (e. In fibromyalgia syndrome. 1999). In addition.g.1 Introduction Despite the many advances in the pathophysiology and treatment of pain. hypervigilance and exaggerated perception of both painful and non-painful tactile stimuli has been reported (Staud et al. University of West Florida. 1993. Pensacola. whereas patient groupings whose diagnoses are episodic or episodic mixed with chronic do not (Bovim. 2004). 1996). Mannheim. the lower the threshold) (Flor et al. and these thresholds varied as a function of chronicity (the more chronic pain.. 2000). perception and pain thresholds as well as pain tolerance levels were found to be significantly lower in patients with chronic back pain compared to persons with episodic headaches and healthy controls.. this sensitivity has not been observed with respect to auditory stimuli (Lorenz.. 2003). 15... 2000) as well as an altered representation of the painful area in the brainstem (Tinazzi et al.. that is. FL. 2001). 1989. 2000. Jensen. For example.2 Pain and plasticity Chronic musculoskeletal pain In the last two decades our understanding of the modifiability of the primary sensory and motor areas of the brain has greatly changed (see Chapters 6–8 of Volume 1). Ji et al. Kleinböhl et al. peripheral factors seem to loose their importance and central changes become much more important (Sandkühler.. 1998). In chronic pain patients both perceptual and cerebral hyperreactivity to tactile or noxious stimuli have been observed. Jensen et al. thalamus (Vos et al. Bendtsen et al.15 Chronic pain Herta Flor1 and Frank Andrasik2 1 Department of Clinical and Cognitive Neuroscience. Central Institute of Mental Health.. This chronicity distinction is particularly important when considering tension-type headache. (1999) showed that patients with back pain as well as patients with tension headache sensitize more than healthy controls.. chronic pain still remains elusive to treat. Schoenen et al. however.. 1991. USA 15. Sandkühler.. Elevated responses to painful and non-painful tactile stimulation as assessed by magnetoencephalography were reported in chronic back pain 219 . electrical and pressure stimulation (Langemark et al. 1996). 1992.g. Once the pain problem has exceeded the acute and subacute stage. 2000) and cortex (Benoist et al. University of Heidelberg. In this chapter we will review the evidence on plastic changes along the neuraxis and their relationship to pain in humans and then delineate treatment approaches that are designed less towards analgesia but more towards reversing maladaptive plasticity with the hypothesis that this would consequently also reduce chronic pain and extinguish pain memories.

spouses who habitually reinforced pain behaviors caused a 2. . The accompanying fMRI measurements revealed enhanced activation in somatosensory cortex but reduced activation in anterior cingulate cortex compared to the healthy controls (see Fig. 1984). At the finger no difference for the presence or the absence of the spouse was observed nor was there a difference for the healthy controls (see Fig. Although they referred mainly to explicit memories. This type of memory trace may lead to pain perception in the absence of peripheral stimulation since an expansion of a representational zone is related to higher acuity in the perception of tactile input (Merzenich et al.. a spouse who habitually reinforces pain can also influence the pain-related cortical response.220 H. The cerebral activation was also site-specific in the back pain patients but generalized in the fibromyalgia patients. In patients with chronic upper back pain it was shown that the stimulation of the trapezius but not the flexor digitorum muscle showed sensitization. For example. It is therefore impossible for the patient to counteract these pain memories. 15. 1997).5-fold increase in the patients’ brain response to pain applied to the back. The main difference between these conditions was observed in an area that corresponds to the location of the anterior cingulate cortex that has been shown to be involved in the processing of the emotional aspects of pain (Rainville et al.. somatosensory memories can also be implicit as already stated by them. Whereas the spouses who habitually ignored the pain or punished their partners for expressing pain had no effect. These data suggest that chronic pain leads to an expansion of the cortical representation zone related to nociceptive input much like the expansions of cortical representations that have been documented to occur with other types of behaviorally relevant stimulation (Braun et al.1). 2000). the patients’ recollection that the phantom pain was similar to previously experienced pains. it was shown to originate from primary somatosensory cortex (SI).. This type of central alteration may correspond to what Katz and Melzack (1990) have termed a somatosensory pain memory in patients with phantom limb pain. When chronic back pain patients were stimulated with electric impulses at either the finger of the back in either the presence or absence of the spouse. suggesting site-specificity. Implicit pain memories are based on changes in the brain that are not open to conscious awareness but lead to behavioral and perceptual changes – such as hyperalgesia and allodynia – the patient is not aware of.. 1997). The amount of expansion of the back region was positively correlated with chronicity suggesting that this pain-related cortical reorganization develops over time. (2002) reported a similar hyperreactivity to painful stimulation in a number of brain regions including SI cortex in fibromyalgia patients. Implicit pain memories can be established and altered by learning processes such as habituation and sensitization. that is. This was true for both the affected (trapezius muscle) and the noneffected body part (finger muscle). There is now ample evidence that learning not only affects pain behaviors and the subjective experience of pain but also the physiologic processing of painful stimulation. Nociceptive input is of high relevance for the organism and it might be useful to enhance the representation of this type of stimulation to prepare the organism for the adequate response. Stimulation at the affected back but not at the finger led to a significantly higher magnetic field in the time window 100 ms whereas both types of stimulation caused higher fields in the later time windows ( 200 ms) in the patients compared to the controls. Whereas the localization of the fingers was not significantly different between patients and controls. When the source of this early activity was localized. In a continuous pain rating in the scanner it was shown that patients with fibromyalgia displayed an increasing level of pain across several stimulation trials and failed to return to baseline. 15. Andrasik patients (Flor et al. the localization of the back was more inferior and medial in the patients indicating a shift and expansion toward the cortical representation of the leg.2). operant and classical conditioning or priming. spouse presence influenced the electroencephalographic potentials that were recorded from the patients’ skull. Flor and F. Using functional magnetic resonance imaging (fMRI). Gracely et al.

000 8.171 0.00 R 4. The numbers to the right give the slope. When patients and healthy controls were reinforced for increasing or decreasing their verbal pain responses both groups learned this task equally well.1283 m m 0.000066 Figure 15. The patients were stimulated in blocks of 20s with 20-s rest intervals. the late event-related responses ( 200 ms) were unaltered and showed mainly habituation. The top right (b) panel shows the same ratings for the healthy controls. Direct verbal reinforcement of pain has been identified as an additional important modulator of the pain response. The top left panel (a) shows the pain ratings (visual analogue scale (VAS) 0–100) of the fibromyalgia patients to the stimulation of the back (black) or the finger (grey).) 1.1. The straight lines show the slope of the ratings.00 8. the early response (N150) was affected by the conditioning procedure and remained high in the chronic pain group that had been reinforced for higher pain ratings thus indicating a direct effect of verbal reinforcement on the early cortical processing of nociceptive information (Flor et al.000066 Finger P 4.00 t(1968) 0. However.00 P Back 4. The brain activity was computed as the global field power related to the EEG gathered with 90 surface electrodes.1053 0. A negative slope indicates a reduction in pain rating and thus habituation and a positive slope indicates sensitization and increased pain ratings.. the patients showed a delay in the extinction of the response.00 C OR P (cor.00 t(1968) 0. This figure shows the enhanced brain response in the chronic back pain patients with solicitous spouses to the back but not the finger stimulation. however.) 1. When the somatosensory evoked potentials to the pain stimuli were examined.2.129 (c) C OR P (cor. 4 3 GFP ratio 2 1 0 Punishing Healthy controls Solicitous Finger Back Figure 15.00 8. . Note that the FMS patients show more activation both during the back and finger stimulation.00 R 4.000 8. 2002b).Chronic pain 221 (a) 100 90 80 70 60 50 40 30 20 10 0 FMS m m 0.0863 0. The bottom panel (c) shows the difference in activation between the fibromyalgia patients (FMS) and the healthy controls related to the secondary somatosensory cortex.0312 (b) C ontrols 100 90 80 70 60 50 40 30 20 10 0 1 11 21 31 41 51 61 71 81 91 101 111 121 Echo planar image Back Finger VAS (0–100) VAS (0–100) m m 1 11 21 31 41 51 61 71 81 91 101 111 121 Echo planar image 0.

however. (1992) that phantom sensation could be elicited in upper extremity amputees when they were stimulated in the face. The invasion of the cortical hand or arm area by the mouth representation might lead to activity in the cortical amputation zone which would be projected into the no longer present limb. (1994) and Yang et al. Flor et al. 2002a). Andrasik This lack of extinction in the cortical domain suggests that learning processes related to verbal and behavioral conditioning may exert long-lasting influences on the cortical response to pain-related stimuli and form implicit pain memories. Subsequently. Flor et al. Patients with phantom limb pain displayed a significant shift of the mouth into the hand representation . for example warmth was perceived as a warm phantom sensation. To what extent deficient descending pain inhibition is involved in chronic pain has not yet been established nor do we know enough about the role of learning and memory process in the inhibition of pain.222 H. 1989). Flor and F. 1999). chronic pain states lead to the development of somatosensory pain memories that manifest themselves in alterations in the somatotopic map in somatosensory cortex as well as other brain areas related to the processing of pain. 2003) used pain as an conditioned and affective pictures as unconditioned stimuli (US) and showed that a classical conditioning procedure modified the pain ratings to a more or less intense perception depending on the nature of the US (aversive versus appetitive). In summary.. not only enduring nociceptive input but also the loss of input. These studies were instigated by the report of Ramachandran et al. for example. There was a point-to-point correspondence between stimulation sites in the face and the localization of sensation in the phantom. Wunsch and colleagues (Wunsch et al. the sensations in the phantom matched the modality of the stimulation. In addition to operant. 1999. classical conditioning has been identified as an important modulator of painrelated responses. They observed a significant shift of the mouth representation into the zone that formerly represented the now amputated hand or arm. This effect pertains not only to the ascending nociceptive system but also to descending pain-modulatory systems (Dubner and Ren. Paininhibitory systems are also influenced by learning and memory processes and may be altered in chronic pain. These plastic changes may contribute to hyperalgesic and allodynic states in the absence of or the presence of only minor peripheral nociceptive stimulation. The fact that stress positively influences the pain response and activates the descending paininhibitory system has commonly been described by the term stress-induced analgesia or hypoalgesia. Moreover. subsequent to amputation or nerve injury.. Animal studies have shown that stress analgesia can be conditioned and that some forms of both conditioned and unconditioned stress analgesia are mediated by the endogenous opioid system (Maier. can alter the cortical map. (1995) showed that phantom limb pain rather than referred sensation was the perceptual correlate of these cortical reorganizational changes. In an elegant study. this shift occurred in patients with and without phantom sensation referred from the mouth. chronic states of pain are associated with increased cortical excitation that may significantly contribute to cortical reorganization. Neuropathic pain As noted above. In addition to local representational changes. These pain memories can be influenced by psychologic processes such as operant and classical conditioning that may establish additional and potentially more widespread implicit memories and may enhance existing memories. (1994) used a combination of magnetoencephalographic recordings and structural magnetic resonance imaging – neuromagnetic source imaging – to test this hypothesis. Several studies examined cortical reorganization after amputation in humans. Elbert et al. The authors assumed that this phenomenon might be the perceptual correlate of the type of reorganization previously described in animal experiments. It was recently shown that stress analgesia can also be classically conditioned in humans and that this conditioned analgesia is mediated by the release of endogenous opioids (Flor and Grüsser. painful touch was perceived as pain.

it was concluded that alterations in the organization of SI. Grüsser et al. The magnitude of this shift was also highly significantly correlated with the amount of phantom limb pain experienced by the patients thus suggesting parallel processes in the somatosensory and motor system. The patients had to Amputated side Intact side Amputated side Intact side puck their lips. Reorganization in the motor cortex related to chronic phantom limb pain. It was later shown that referred sensations as those described by Ramachandran et al. The importance of pain experiences prior to amputation was confirmed by a study of Nikolajsen et al. Note the more medial/superior and more widespread activation in the phantom limb pain patients. Therefore. anesthesia of the brachial plexus lead to the elimination of phantom limb pain in about 50% of the amputees whereas phantom limb pain remained unchanged in the other half.3). . Similar results were obtained when the motor cortex was investigated.Chronic pain 223 whereas this was not the case in patients without phantom limb pain. The close association between cortical alterations and phantom limb pain was further underscored in a study by Birbaumer et al. 15. These data suggest that in some patients peripheral factors might be important in the maintenance of phantom limb pain whereas in others pain and reorganizational processes might have become independent of peripheral input. Patients who continued to have phantom limb pain during the elimination of sensory input from the residual limb had an even more reorganized mouth representation. (1992) can also be elicited from areas far removed from the amputated limb (e. an fMRI study where upper extremity amputees had to perform pucking lip movements showed that the representation of the lip in primary motor cortex had also shifted into the area that formerly occupied the amputated hand (Lotze et al. 2001. Neuroelectric source imaging revealed that cortical reorganization was also reversed in those amputees that showed a reduction of phantom limb pain. see Fig. 2004).g. The intensity of phantom limb pain was significantly positively correlated with the amount of displacement of the mouth representation. A high concordance of changes in the somatosensory and the motor system was reported by Karl et al.. In upper limb amputees. This close interconnection of changes in the somatosensory and motor system suggests that rehabilitative efforts directed at one modality may also affect the other..3. 1998.. (1997). (2001) who used transcranial magnetic stimulation to map the motor cortex and neuroelectric source imaging (that combines the determination of cortical sources by evoked potential recordings with structural magnetic resonance imaging) to map the somatosensory cortex. from the foot in arm amputees). where arm and foot are represented far apart. (2000a) who reported a close association between mechanical sensitivity Phantom limb pain No phantom limb pain Figure 15. 2001. are most likely not the neuronal substrate of referred phantom sensations (Borsook et al. For example..

In addition.. a consistent feature has been an inability to habituate to various types of sensory stimulation in the pain-free interval. the dorsal horn. a larger representation was found to be associated with more pain. They also observed altered activity in the motor cortex suggesting a change of inhibition. Initial evidence from a longitudinal study (Huse et al. Based on these findings and the results obtained on somatosensory memories in chronic back pain it can be assumed that prior pain memories might also be important in the development of phantom limb pain although they are surely not the only factors. Longstanding states of chronic pain prior to the amputation may be instrumental in the formation of these pain memories by inducing representational and excitability changes. As Devor and Seltzer (1998). somatosensory pain memories represented by alterations in the topographic map of SI cortex may underlie the development of phantom limb pain and may contribute to other neuropathic pain syndromes such as CRPS. when pain has occurred prior to the amputation. Similarly.. We do not yet fully understand the mechanisms underlying these types of relationship. 2002). however. (2002) showed that in patients with CRPS the localization of the fingers of the affected hand had shifted closer together and that the magnitude of the magnetic response on the affected side was positively correlated with the amount of pain experienced by the patients.224 H. For example. Willoch et al. Thus. Spitzer et al. Thus. Andrasik prior to amputation and early phantom limb pain. Deafferentation does not alter the original assignment of cortical representation zones to peripheral input zones but leads to double coding. Similar alterations in the cortical processing of sensory information have recently also been reported in patients with complex regional pain syndromes (CRPS). The amount of hemispheric asymmetry was positively correlated with the amount of pain they experienced. In a magnetoencephalographic investigation. spontaneous activity from neuroma or psychophysiologic activation may also influence the cortical representational changes (Calford and Tweedale. In migraine headache. in press) suggests that chronic pain before the amputation is a much more important predictor of later phantom limb pain than acute pain at the time of the amputation thus supporting this assumption. Further research is needed to better clarify these relationships. Juottonen et al. and others have pointed out it is to date not clear on which level of the neuraxis the cortical changes that have been observed in imaging studies originate. Several imaging studies (e. alterations in somatosensory cortex and other brain areas might have occurred that would later – when activated by neighboring input subsequent to the amputation – lead to the sensation of phantom limb pain (Flor. 1991. Pleger et al. Learning processes are instrumental in the development and maintenance of these cerebral changes. peripheral changes related to the amputation may contribute to enhanced cortical reorganization and phantom limb pain. Peripheral factors such as loss of C-fiber activity. migraine headache and cluster headache are distinct categories of pain with different etiologies.. 1995). (2004) found that CRPS patients revealed a marked hemispheric difference in the representation of the hand with the affected hand also being smaller in extent than the intact hand. 2000) have also shown that not only the primary and secondary somatosensory cortex and the posterior parietal cortex but also regions such as the insula and the anterior cingulate cortex are involved in the processing of phantom phenomena. the brain stem or the thalamus. In addition to intracortical changes alterations might be present in the dorsal root ganglion. the amount of use of the limb as well as the type of input from the limb or adjacent territory might play an important modulatory role. the authors only tested thresholds and not sensitization. However. both in phantom limb pain and in CRPS a smaller representation of the affected and completely or partially deafferented body part was associated with more pain whereas in chronic musculoskeletal pain. Migraine and cluster headache Whereas tension headache seems to have some similarity to musculoskeletal pain disorders. in migraine headache a lack of . To summarize.. Flor and F.g.

In this case the provision of correlated input into the amputation zone might be an effective method to influence phantom limb pain. Patients who systematically used a myoelectric prosthesis that provides sensory and visual as well as motor feedback to the brain showed much less phantom limb pain and cortical reorganization than patients who used either a cosmetic or no prosthesis. 2001). 2002). 1997) or by employing a sensory stimulation protocol that provides relevant correlated sensory input to the respective brain region. which was not found in migraine headache. The training was conducted for 90 min per day and was spread over a time of 2 weeks (10 days of training).. These studies were performed in chronic phantom limb pain patients. In phantom limb pain. This could be achieved by altering the peripheral input that enters the brain region that coded a pain memory. When it was partialled out from the correlation. for a review). In cluster headache. The patients were trained to discriminate the location or the frequency of the stimulation (alternating trials) of the stimulation and received feedback on the correct responses. An early fitting and training with a myoelectric prosthesis would probably be of great value not only in the rehabilitation of amputees but also in preventing or reversing phantom limb pain. multiple presentations of the S1–S2 stimuli lead to habituation of the CNV. 1999... several functional and structural imaging studies have identified a cluster headache-specific alteration in the hypothalamus (May et al. 1999. see Ambrosini et al. it was assumed that the pain is maintained by cortical alterations fed by peripheral random input. 2003. Flor et al. a slow cortical potential that is typically present in an S1–S2 task where S1 signals the occurrence of a second signal. Alternatively. however. 1998.. It would also be possible to directly alter the brain response to pain by providing feedback of event-related potential components or electroencephalogram (EEG) rhythms (Kropp et al. pharmacologic interventions could be used that prevent or reverse the establishment of central memory traces. 1992. 15. The relationship between phantom limb pain and use of a myoelectric prosthesis was entirely mediated by cortical reorganization.. fMRI was used to investigate the effects of prosthesis use on phantom limb pain and cortical reorganization (Lotze et al. This was assessed either by visual evoked potentials or by changes in the contingent negative variation. 2003. S2 that is the sign for a response to be made by the subject. for a review see Goadsby et al. 2004. 2002). Eight electrodes were attached to the residual limb and provided high-intensity nonpainful electric stimulation of varying intensity and location that led to the experience of intense phantoms. 1998. 2004). a brainstem migraine generator has been proposed because alterations in brain stem activity have repeatedly been found during migraine attacks (Weiller et al.. not clear to what extent these changes are a cause or a consequence or merely an epiphenomenon of the pain that is experienced. Usually. It is. for a review see Sanchez del Rio and Linera. phantom limb pain and prosthesis use were no longer associated. 1999).3 Influencing chronic pain and brain plasticity Behavioral interventions The discussion in the preceding sections suggests that the alteration of somatosensory pain memories might be an influential method to reduce both chronic musculoskeletal and neuropathic pain. This suggests that sensory input to the brain region that formerly represented the now absent limb may be beneficial in reducing phantom limb pain.. Evers et al.Chronic pain 225 habituation to auditory or visual stimuli was observed for the pain-free interval (Gerber and Schoenen. These assumptions were further confirmed in an intervention study where the patients received feedback on sensory discrimination of the residual limb (Flor et al. for example by using electromyogram (EMG) or temperature biofeedback or other types of standard behavioral interventions (for reviews see Andrasik. Sherman.. Most of these methods have not yet been tested in a systematic manner and their effects on cortical reorganization are so far unknown. In addition.. 1995. Compared to a medically .

Changes in cortical reorganization (distance of the hand and lip representation in millimeter) during the discrimination training (electrode montage is depicted on the left side). 2001b) asynchronous tactile stimulation of the mouth and hand region was used over a time period of several weeks. gamma amino butyric acid (GABA) agonists. 2001. pain and cortical reorganization were highly significantly correlated (see Fig.4. 15. Andrasik Mouth pre Mouth post Thumb pre Thumb post Figure 15. a well-controlled study by Nikolajsen et al. (1997) showed no effect of preemptive analgesia on phantom limb pain. The alterations in discrimination ability..4). A recent double-blind placebo-controlled study that used the NMDA receptor antagonist memantine in the perioperative phase in acute amputations reported a decrease of the incidence of phantom limb pain from 72% to 20% 1 year after the amputation (Wiech et al. that eliminates afferent barrage in the perioperative phase but will not alter previously formed neuronal changes may be ineffective. Among these substances. N-methyl-D-aspartate (NMDA) and alpha-amino-3hydroxy-5methyl-4-isoxazole propionic acid (AMPA) receptor antagonists and anticholinergic substances seem to be the most promising. 15. They also experienced a more than 60% reduction of phantom limb pain and a significant reversal of cortical reorganization with a shift of the mouth representation back to its original location. This training was based on the idea that synchronous stimulation leads to fusion and asynchronous stimulation leads to a separation of cortical representation zones. pharmacologic interventions may also be useful in the treatment of both chronic musculoskeletal and neuropathic pain.226 H. In this case it was postulated that input from the mouth representation that would now activate the region that formerly represented the now amputated hand and arm would be eliminated and with it the phantom phenomena that would be projected to the amputated limb. the use of preemptive analgesia. The prevention of pain memories might be possible by using pharmacologic agents that are known to also prevent or reverse cortical reorganization. Treatment of chronic phantom limb pain with pharmacologic agents has also yielded inconsistent . This study could explain why the results of different controlled prospective studies about the effect of preemptive analgesia initiated at least 24 h before the amputation on the incidence of phantom limb pain are inconsistent. If a preexisting pain memory is important in the development of phantom limb pain. Pharmacologic interventions In addition to behavior. The pharmacologic intervention was most effective in those patients where treatment had begun before or immediately after the amputation.5). This intervention also showed a reduction in phantom limb pain and cortical reorganization. see Fig. Flor and F. For example.. treated control group that received an equal amount of attention the trained patients showed significantly better discrimination ability on the stump. In a related study (Huse et al.

These central alterations may be viewed as pain memories that alter the processing of both painful and non-painful input to the somatosensory system as well as its effects on the motor system. 2000b. in phantom limb pain and other neuropathic pain syndromes cortical reorganization is correlated with the amount of pain. A complicating factor is that in chronic pain syndromes lack of use of an affected body part may contribute to the central changes that are observed. Maier et al. We found positive effects of both opioids (Huse et al.Chronic pain 227 Incidence of phantom limb pain 100 90 80 % of patients 70 60 50 40 30 20 10 0 Baseline Figure 15.. 2001a).. 1992).. Pharmacologic interventions include a host of agents and although tricyclic antidepressants and sodium channel blockers have been indicated as treatments of choice for neuropathic pain (see Sindrup and Jensen. was. 2003. 2001a) and memantine (Koeppe et al.. It is so far not clear to what extent changes in the spinal cord.. In chronic low back pain and fibromyalgia patients the amount of reorganizational change increases with chronicity.4 Conclusions and summary The empiric evidence discussed above suggests that neuroplastic changes in the central nervous system play an important role in the development and maintenance of chronic pain. there are few controlled studies for phantom limb pain. Antidepressants yielded no pain relief (Robinson et al.. 1999 for a review). an NMDA receptor antagonist like ketamine. Cortical plasticity related to chronic pain can be modified by behavioral interventions that provide feedback to the brain areas that were altered by somatosensory pain memories or by pharmacologic agents that prevent or reverse maladaptive memory . Functional reorganization in both the somatosensory and the motor system was observed in neuropathic and musculoskeletal pain. ketamine (Nikolajsen et al.. results. Wiech et al. 2002) all of which were found to effectively reduce phantom limb pain. 1996) and gabapentin (Bone et al. Note the significantly lower incidence of Memantine Placebo After 7 days After 28 days After 6 months After 12 months phantom limb pain at the 12-month follow-up in the memantine condition. however. 2003) on both chronic phantom limb pain and cortical reorganization suggesting that more work is necessary to determine under which circumstances which pharmacologic agents can effectively reverse the maladaptive plastic changes that are a consequence of amputation and chronic pain. Memantine.5. calcitonin (Jaeger and Maier.. Here the results of the NMDA receptor antagonist memantine on acute phantom limb pain are shown in amputees who participated in a doubleblind randomized study with either memantine or placebo. Longitudinal studies and controlled outcome studies would also be needed to elucidate in greater detail the efficacy and mechanisms of feedback-based interventions designed to alter cortical pain memories. not effective in three studies (Nikolajsen et al. the brain stem or the thalamus contribute to the changes in cortical reorganization and to what extent cortical reorganization affects the lower levels. 2004). Controlled studies have been performed for opioids (Huse et al. 15. 2004)..

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1 Nature of impairment and functional implications of loss Definition and processing within the somatosensory system Somatosensory function is the ability to interpret bodily sensation (Puce. Two features of the structure and function of the system have particular implication for understanding the nature of impairment and neurorehabilitation. This may result from disease or trauma associated with a wide range of conditions (see Section E Disease-specific Neurorehabilitation Systems of Volume II). as well as the presence of distributed sensory networks and multiple somatotopic representation (Gardner and Kandel. 2003). (Gardner and Martin. Schwartz and Jessell (Gardner and Martin. 2000). pain and itch are identified. Australia Evidence of behavioral recovery of somatic sensations following peripheral and central nervous system lesions challenges therapists to not only understand the nature and extent of the change. Detailed description of the system involved in sensory processing is provided in seminal texts Loss of somatic sensation following interruption to central and peripheral nervous systems Loss of somatic sensations can be sustained due to damage at various levels of the sensory system. Second. treatments currently available to address this problem. modality-specific line of communication (Gardner and Martin. specific columnar organization and sub-modality-specific neurons in primary (SI) and secondary (SII) somatosensory areas (Mountcastle. Comparisons will also be made in relation to loss following peripheral nervous system (PNS) lesions. This challenge requires input from basic sciences and rehabilitation fields.. proprioception. but the conditions under which the recovery can be maximized and the mechanisms underlying. First is the high degree of specificity in the organization and processing of information. Within the somatosensory system submodalities of touch. The focus of this chapter will be on loss of somatic sensations. with particular reference to stroke. Integration of these fields will provide direction for the development and testing of scientific-based interventions designed to maximize recovery by driving and shaping neural reorganization. for example from receptors to peripheral nerves.16 Loss of somatic sensation Leeanne Carey School of Occupational Therapy Faculty of Health Sciences. 2000). 16. impact on the scope for neural plastic changes (Volume I. 1997) support this specificity. Chapter 6) and rehabilitation outcome. 1998). brainstem and cerebral cortex. 2000). More detail will be given to therapies following central nervous system (CNS) lesions. Specialized sensory receptors. LaTrobe University. Further. Somatosensory impairment may be in the form of anesthesia (total loss of one or more sensory submodalities 231 . process and transmit information obtained from the periphery to the cerebral cortex. such as Kandel. temperature sense. neuroimaging studies are complementing and extending information gained from animal and lesion studies in humans (Schnitzler et al. the opportunity for convergence of somatosensory information within the CNS (Mesulam. Bundoora. and the potential application of theories of perceptual learning and neural plasticity. Victoria. spinal cord. 2000). 2000). Sensory systems are organized to receive.

. Typically the loss is contralateral to the injury.. Kim and Choi-Kwon. 1997). sharp or blunt. Bassetti et al. capable of crushing objects with one’s grip yet incapable of letting go or throwing off even the lightest objects (e.. 1993) are observed. 1995. the affected limb may not be used spontaneously.. as a rough surface (Wing et al. ability to sustain and adapt appropriate force without vision (Jeannerod et al. There are differences in the nature of the loss following peripheral and CNS lesions. These activity limitations impact on life roles. despite adequate movement abilities. 1997). Clinical description of loss should include identification of body part and submodalities affected as well as the level of processing impairment.g. restraint of moving objects (Johansson et al. qualitative alterations. maintaining the grip of an object without crushing or dropping it. 1988). 1987. and adjustment to sensory conflict conditions such. 1995. How does one trust a foot that “feels” as though it has no real connection with the earth? It is difficult to pick up or hold a pair of glasses or a sheet of paper when one’s right hand/fingers feel uncontrollably strong and very big and clumsy. 1911–1912). … better to feel something-however bizarre-than nothing. 1993. as indicated in a review of stroke outcome studies (Carey. motor function. 1992). personal safety. from complete hemianaesthesia of multiple modalities to dissociated loss of sub-modality specificity in a particular body location (see Carey. 1995) and dissociated sensory loss (Roland. heavy or light. 1996). injury to the PNS involves well-defined loss of specific modalities that can be mapped relative to the nerve distribution or receptor location. safety and participation in personal and domestic activities of daily living as well as sexual and leisure activities (Carey. social communication. The important role of sensation in motor function is particularly evident in: control of pinch grip (Johansson and Westling. relative sparing and redundancy within the distributed sensory system and neural plastic changes that may occur with recovery. thresholds for primary sensory qualities (e. discrimination and integration of information across submodalities.” Loss of somatic sensations also negatively impacts on rehabilitative and functional outcomes. It cannot tell whether that which touches it as hand or tennis racket…it is frustratingly difficult to control or feel relaxed about any right-sided movement … . This may contribute to a learned non-use of the limb and further deterioration of motor function after stroke (Dannenbaum and Dykes. 1995). for example detection. Everyday tasks such as searching for a coin in a pocket. feeling if a plate is clean when washing dishes. 1990). Functional implications of loss Impairment of body sensations poses a significant loss in its own right and has a negative impact on effective exploration of the environment. 1996). and quality of life (Rothwell et al. object manipulation (Johansson. Loss of discriminative sensibilities is most characteristic (Bassetti et al. writing and walking on uneven ground become difficult and often frustrating (Carey. 1982. response variability (Carey. 1995). including poor localization. paraesthesia or causalgia). In comparison. discrimination of surfaces at end of handheld objects (Chan and Turvey. Carey. fastening buttons.. Moreover. 1996). It has a cumulative impact on functional . combining component parts of movement such as transport and grasp (Gentilucci et al. 1995).232 Leeanne Carey in the region). 1984). 1991).g. Carey. loss following CNS lesions such as stroke can result in very different patterns of deficit. although ipsilateral deficits are also reported (Carey.. touch) are often indefinable (Head and Holmes. 1995). using cutlery.. 1984).. smooth. The personal and functional implications of sensory loss are highlighted in the words of a client who experienced sensory loss after stroke: “… my right side cannot discriminate rough. discrimination and integration). 1995 for review). The early and chronic pattern of deficit may be influenced by the site of lesion. and hypersensitivity may be present initially or develop over time (Holmgren et al. For example. hyposensitivity (reduced ability to perceive sensations. a tissue). rigid or malleable. or hypersensitivity (non-noxious stimuli become irritating.. Kim and Choi-Kwon. for example dyesthesia.

Loss of somatic sensation 233 deficits beyond severity of motor deficits alone (Patel et al. for example discrimination. postural control and ambulation (Reding and Potes. A test of sustained touch-pressure.. 1980) and perception of the grid surfaces has been associated with cerebral activation in multiple somatosensory areas in unimpaired (Burton et al. 1997) and impaired (Carey et al. Over the past decade new measures have been developed for use post-stroke. It has been suggested that sensory reorganization may precede motor reorganization and may. 1986. 1984).. 1991. Intra and inter-rater reliability are variable. but also on the ability to make accurate discriminations and recognize objects with multiple sensory attributes. proprioception and tactual object recognition (Carey. use gross scales such as “normal”.2 Assessment of somatic sensation Guidelines for the selection of measures for use in clinical settings The directive to follow evidence-based practice demands that clinicians employ quantitative measures that are valid and reliable. Lincoln et al.. 2002). trigger the latter (Weiller. good reliability and age-appropriate normative standards. and are often insensitive or inaccurate (Carey et al. 1998). quantitative measurement. was developed and impairment demonstrated in six patients with severe sensory deficit (Dannenbaum and Dykes. “impaired” or “absent” (Wade.. but are more detailed and standardized. The revised NSA reports acceptable (k 0. 1998) and the Rivermead Assessment of Somatosensory Performance (RASP) (Winward et al. neurotemp and two-point neurodiscriminator. with most tests showing relatively poor agreement across raters. Measures commonly used are largely subjective. 1990). 1988).92). In clinical settings we need information not only on thresholds of detection. The need for standardized measures for use following stroke has been highlighted (Carey. no defined criterion of abnormality... 16. Morley. 1992).00 for the stereognosis component (Gaubert and Mockett. lack standardized protocol (Lincoln et al. 1998).. 1995.. The NSA employs methods consistent with clinical practice.). Selection of suitable measures should be based on the following criteria: valid measurement of the sensory outcome of interest.6) agreement in only 12 of 86 items (Lincoln et al. 1997) and proprioceptive (Carey et al. 1995. 1999). 1996). uses seven quantifiable subtests of touch and proprioceptive discrimination and includes three new instruments. 2000) and negatively impacts on reacquisition of skilled movements of the upper limb (Kusoffsky et al. 2002a) . Dellon (2000) and Winward et al. have variable reliability (Winward et al. in fact. 1999). 1991. and inter-rater reliability of 0. The importance of the sensory system as an early indicator of motor recovery after stroke has been suggested in neuroimaging (Weiller. For a critique of routine clinical and quantitative measures refer to Carey (1995).... Clinical test batteries developed are the Nottingham Sensory Assessment (NSA) (Lincoln et al.38–1. Empirical foundations for the test are required. Carey... 1998) and clinical (Kusoffsky et al. control for test bias and other clinical deficits. The RASP is standardized. including touch. based on the need to appreciate sustained contact of an object in the hand during daily manual tasks.. objectively defined stimuli. 2000). 1996) discrimination provide quantitative measurement of the characteristic discriminative loss post-stroke. New measures of tactile (Carey et al. 1982. 2000). adequate scale resolution to monitor change. 1980. pressure.. 2002c). They are founded on strong neurophysiological and psychophysical evidence (Clark and Horch. New tests of specific sensory functions commonly impaired post-stroke have also been achieved. temperature. 1995. Numerous tests have been developed to evaluate the various qualities of sensibility. 1982) studies. (1999). Intra and inter-rater reliability are high (r 0. Kim and Choi-Kwon found that discriminative sensation remained in only 3 of 25 stroke patients who were reported as having no sensory impairment on the basis of conventional sensory tests (Kim and Choi-Kwon. Winward et al. Dellon. Darian-Smith and Oke.. the neurometer. pain. Jeannerod et al. standardized protocol.

The temporal aspects of recovery are also relatively unknown. 16. ranging from lasting deficits (Wadell et al. 2000) and CNS (Carey. 2000). 1987) to “quite remarkable” improvement in capacities such as stereognosis (Schwartzman. Tests of fabric discrimination and discrimination of finger and elbow position sense have also been developed (Carey. 1972).. In addition to quantitative measures of sensibility. although ongoing recovery has been observed at 6 months and later (Kusoffsky. see also Chapters 12. extent of injury. 1995. As yet there is no standardized test of the impact of sensory loss on daily activities. task-specific and generalized training effects have been observed across tactile. following lesions to peripheral (Dellon.g. 1996. Improvements have been reported across a range of measures including touch detection. the extent of recovery is varied (Kusoffsky et al. it is important to evaluate the presence and impact of the impairment in daily activities. 1970). This may involve structured interview and/or observation of occupational performance difficulties in tasks relevant to the patient. under quasi-experimental and controlled conditions (see Section Review of documented programs in relation to basic science and empirical foundations of documented of this chapter for review).. Tasks with varying sensory demands may be structured to systematically assess the impact of sensory loss. 1990). age. proprioceptive and object recognition tasks. 2000). 1972). and 27 of Volume I). It has been suggested that persistent deficit may be associated with particular lesion site (Corkin et al. 1995) and are being empirically tested by us. progression of disease. 1982). 1995 for review). have empirically demonstrated ability to differentiate impaired performance relative to normative standards (Carey et al. comparison. prior and intervening experience (Callahan.. Similarly following stroke. Moreover. after the period of expected nerve regeneration (Dellon. Dellon.. few studies have systematically investigated the natural history of spontaneous recovery of somatosensations post-stroke. standardized. In Neural plastic changes associated with recovery of somatic sensations Neural plastic changes occur in response to injury. Recovery appears most marked within the first 3 months (Newman. 1995) nervous systems under both spontaneous and training-induced recovery conditions. Dellon (2000) asserts that results of sensory rehabilitation must be due to higher CNS functions and that cortical plasticity is the underlying mechanism. The measures are quantitative.234 Leeanne Carey humans. 13. but also as part of normal learning and development (refer . measure small changes in ability.3 Potential for recovery The potential for recovery of somatosensory abilities has been demonstrated. The natural history of recovery The potential for recovery depends on regeneration of structures within the somatosensory system as well as the capacity for neural plasticity and reinterpretation of altered stimuli. These factors are further influenced by the level at which the system is interrupted. nature of difficulties (e. 2000) and central (Carey. 2002c). texture and proprioceptive discrimination and object recognition (see Carey. 2000. 1997) and advance current clinical assessment (Carey et al.. Regeneration and recovery following damage to PNS has been relatively well described (Callahan. 1995) lesions. Neural plastic changes have also been proposed as the likely mechanism underlying these improvements. improvements have been observed months and years post-injury. Focus of observations may include impact of loss on unilateral and bilateral tasks. 1995. level of independence. Carey. 1995. Evidence of training-induced recovery Evidence of training-induced sensory improvements further highlights the potential for recovery following PNS (Dellon.. reliable. However. clumsy) and use of compensatory techniques. Dellon. In most instances the improvements have been observed after the period of expected spontaneous recovery.

1998). 2000).. SII (Carey et al. suggestive of neural reorganization.. 2002. Chapter 11). et al. 1996b. 2002).. Patient 1. Patient 2). Changes can occur immediately postlesion or months and years later and can involve multiple levels of the somatosensory system (Jones and Pons. are providing new insights into the mechanisms underlying stroke recovery (Weiller.1. 1998. In serial pilot functional magnetic resonance imaging (fMRI) studies we found re-emergence of activation in ipsilesional SI and bilateral SII in a stroke patient who had marked sensory loss followed by good recovery (Fig. In comparison. Small et al. we have recently demonstrated good clinical recovery and changes in ipsilesional SI. 2000. Changes in SI (Rossini et al.. Longer-term stable changes. 1998. Some of the most influential programs are those developed by Wynn Parry and Salter (1976) and expanded by Dellon (1981. 2000. 2001) have been reported in the few studies of somatosensory recovery post-stroke... verbalization of sensations and comparison of sensations experienced across hands. introduction to this text). Carey et al.. In addition. repeated sensory practice. Investigation of changes in brain activation associated with training-induced recovery of somatosensations under randomized control conditions is now required.R. bilateral SII and premotor areas following somatosensory training in a patient who showed poor spontaneous recovery in the 6 months prior (see Fig. 14 and 15 of Volume I). 16. 2002a). Ward et al. 1994) and injury to the PNS (Merzenich and Jenkins. 2000.. Nelles et al. As yet little is known about neural mechanisms underlying functional recovery associated with specific training post-stroke in humans. 2002a. Whilst some programs are directed to localized somatosensory deficits and regeneration of specific nerve fibers. 2002a) and thalamus (Ohara and Lenz. 16.Loss of somatic sensation 235 to Section A on Neural plasticity in Volume I). Sensory re-education has been an integral part of the rehabilitation of patients with peripheral nerve disorders for many years.. Findings indicate involvement of cortical and subcortical sites primarily within the pre-existing motor network and include recruitment of sites not typically used for the task and return to a more “normal” pattern of activation. Dellon (2000) highlights the need to focus on interpretation of altered stimuli at a cortical level based on evidence of neural plasticity.. Carey J. The cellular.. are the most relevant for rehabilitation. Controlled studies in primates suggest that both positive and negative patterns of brain reorganization can occur and that these can be “strongly influenced by appropriate rehabilitation programs after brain damage” (Nudo et al. 2001.. only very limited recruitment in nonprimary sensory areas was observed in the second patient who showed poor spontaneous recovery. see also Chapter 5 of Volume II). 1993). feedback through vision. 1993) and CNS (Carey et al. subjective grading of stimuli such as texture and objects. 2000). 1999).4 Approaches to retraining impaired sensory function Review of documented programs in relation to basic science and empirical foundations Neurorehabilitation needs to be founded on a rigorous basic and clinical science platform and include cure in its mission (Seltzer. 2005. Investigations in humans confirm reorganization in somatosensory regions following extensive use (Pascual-Leone and Torres. Nudo. 16. Brain plasticity related to treatment-induced motor recovery has been suggested in the sensorimotor system of humans post-stroke (Liepert et al. 2003). Carey et al. Evolution of change over time and a potential relationship with recovery has been demonstrated in the motor system (e. Wikström et al.. Evidence for the effectiveness of sensory training following peripheral lesions is reviewed in (Dellon. Studies of change in human brain activation.. Wikström et al. likely linked with change in synaptic connections and learning. see also Chapters 6. Animal models highlight the benefit of experience in facilitating brain reorganization within motor and sensory systems. transient anesthesia (Rossini et al. There are a relatively limited number of documented sensory retraining programs designed for ..1. physiological and behavioral mechanisms operating in adaptive brain plasticity are discussed in this section. These programs employ principles of direct.g.

The only early study with a controlled design (Van Deusen Fox. Serial fMRI pilot studies of touch discrimination during the interval of spontaneous recovery (non-specific rehabilitation) and following specific sensory retraining post-stroke. that is primary somatosensory cortex (SI) posterior to the central sulcus (CS). Subjects were encouraged to attend to the input and given reinforcement. Yekutiel and Guttman (1993) reported significant gains following sensory retraining in 20 stroke patients with chronic sensory impairment under . Electric stimulation and velcro were used in the early stages. Early studies suggesting improvement of sensory abilities (Vinograd et al. and secondary somatosensory cortex (SII). Significant brain activation (Puncorrected the affected hand is circled. 0. 1964) also did not employ current theories of perceptual learning and neurophysiology and failed to obtain a therapeutic effect (see Carey. Improvement was reported in the case study presented. 1995 for review). De Jersey. 1995).0001) in ipsilesional SI and bilateral SII observed during stimulation of use with stroke patients (Carey. 1962. Their program involved stimulation of “important sensory surfaces” at an intensity sufficient for appreciation and in a task that was motivating to the patient. In comparison. exploration of velcro shapes and use of utensils taped with velcro. involved repeated exposure to test stimuli with 3D feedback from a box lined with mirrors while DeJersey used bombardment with multiple sensory stimuli. The functional echoplanar axial slices shown sample two brain regions of interest. followed by finger localization. 1979) have lacked controls and a sound theoretical basis. The program by Vinograd et al.236 Leeanne Carey Stroke Spontaneous recovery Patient 1 R hand 2 weeks 3 months 6 months CS SI SII Spontaneous recovery Training Patient 2 L hand 5 weeks SI 3 months 6 months 7.1.5 months CS SII Left Figure 16.. Dannenbaum and Dykes (1988) described a therapeutic rationale based on neurophysiologic concepts and “rules governing somatosensory cortical reorganization after trauma”.

as shown in Fig. 1993) and Stimulus Generalization Training (SGT) (Carey and Matyas. with contributions from psychology (Yekutiel. SST effects were specific to the trained sensory perceptual dimension (tactile or proprioceptive) and stimulus type (e. Improvement in sensory and motor outcomes. feedback on performance and progression in difficulty.0001) and SGT effects (tactile z 5. 1993. In comparison. blindfolded motor tasks involving reach and grasp of different objects. Finally.7. we have also applied the SGT approach to training friction discrimination and investigated its effect on the fundamental pinch grip task in pilot studies.0001. The program involved graded exercises. intermittent feedback and tuition of training principles (Carey and Matyas. Gibson. included: matching tasks to ability of the subject. the method used – although aimed at higher brain centers – may still be too “peripheral” (Yekutiel and Guttman. SST effects were replicated in 37 of 41 time-series across 30 single-case experiments. attention.3. 1991. employ principles consistent with perceptual learning and neural plasticity and focus on training sensory and motor functions. to within normal performance standards. Carey et al.2.6. repetition. Principles of training were derived initially from peripheral nerve injury training programs (Wynn Parry and Salter. The findings confirm that sensory discriminations are trainable after stroke and suggest a potential for generalized sensory gains. that is untrained fabric surfaces. proprioception z 4.Loss of somatic sensation 237 controlled conditions.. with positive results (Carey et al. weight discrimination. 2005. Schmidt and Lee. the SGT approach was designed to facilitate transfer of training effects to untrained. as well as practice of seven daily life activities. Stimulus Generalization effects were found in 8 of 11 time-series across 11 subjects. feedback on accuracy. Exercises focused on tactile discrimination using different textured surfaces. recovery following brain damage (Bach-yRita. use of anticipation trials. attention and motivation.. 2002b) Two further retraining programs have been documented recently. P 0.0001) supports the overall conclusion that tactile and proprioceptive discriminations are retrainable following stroke and that both modes of training are effective.. was reported in the four cases studied. The essential principles included focus on the hand. 1980. P 0. Carey et al. 16. 1976). suggesting a longterm therapeutic effect. 2000). The programs employ principles derived from theories of perceptual learning (Gibson. Byl et al. were achieved by the program deliberately oriented to enhance transfer (Carey and Matyas. (2003) described a program aimed to improve accuracy and speed in sensory discrimination and sensorimotor feedback. 1991. 2005). method of exploration and salient features of the stimuli. novel stimuli and included additional principles of variation in stimulus and practice conditions. SST was designed to maximize improvement in specific stimuli trained. Meta-analysis of SST effects (tactile z 8. progression from easy to more difficult discriminations. 1999). P 0. 243). (2003) describe a program of sensory and motor exercises for patients with pure sensory stroke. and feedback on accuracy and execution of task for each trial. It involves repeated presentation of targeted discrimination tasks. 2005). reported to be challenging for the patient. object recognition. The authors reported variation in results across patients and noted that.. 1993) (p. Generalized improvements in touch discrimination. These programs are in part derived from earlier programs. derived from studies of neural adaptation. attentive exploration of stimuli with vision occluded. and use of vision to facilitate calibration of sensory information (Carey. 1998) and neurophysiology of somatosensory processing (Gardner and Kandel. were achieved within ten or fewer training sessions and maintained over follow-up periods of 3–5 months. texture gratings or fabrics). 1993. Weiller. 1998). Sensory training focused on improving .g. Smania et al. We have developed and investigated the effectiveness of two different approaches to training sensory discrimination: Stimulus Specific Training (SST) (Carey. 2000). Marked improvements. Principles. as well as increased use of the affected arm in daily activities. guided exploration of the tactics of perception and use of the “good” hand. Goldstone. 1993). joint position sense.

01) confirm the training effects shown for 16.5 3 2. A more detailed discussion of principles of training related to perceptual learning and neural plasticity follows with suggestions for their application. mental rehearsal to reinforce learning and tasks to quiet the nervous system were also used. Gains were hemispheric and training specific. The criterion of normality for the Grid Matching Test is 0.5 3 2. These include: attention to the sensory stimulus. both in acute and chronic phases.5 2 1.61 z score 2. graded progression of tasks and feedback on accuracy and execution. In summary.5 Principles of neural plasticity and learning as they apply to rehabilitation of sensation Identification and application of principles to optimize perceptual learning and brain adaptation Evidence of neural plasticity provides a strong foundation for restorative sensory retraining post-injury. stereognosis and kinesthesia.5 0 3. Patients were educated regarding the potential for improvement in neural processing and the unaffected hand was constrained through wearing of a glove. repetitive stimulation with and without vision. .5 0 0.5 1 3. use of tasks that are challenging and motivating. Statistical time-series analyses of trend and 0. Higher scores represent an improvement in texture matching ability.5 2 1.5 3 2.5 1 0.62 z score (mean (mean 1. level effects (P this subject. 30 Untrained fabric matching score Z Untrained grid matching score Z 15 Session 20 25 Figure 16. Improvements in sensory discrimination. Improvement in untrained fabric discriminations is evident only following introduction of the program designed to enhance generalization.2.47) and for the Fabric Matching Test is 1. use of velcro on objects. although no placebo intervention period was employed. fine motor function and musculoskeletal measurements of the upper limb were reported following sensory training.238 Leeanne Carey Phase 1 Trained grid matching score Z 4 3. Example single-subject case chart demonstrating SST effects on trained grids and untrained grids. focus on the hand. Training was investigated in 21 subjects with order of sensory or motor training crossed.46). Review of theories of perceptual learning and the conditions under which neural plastic changes occur suggests a number of principles that have potential application in retraining somatosensations following PNS or CNS injury. localization.5 1 0. recent training programs with successful outcomes have included a number of common principles consistent with theories of learning and neural plasticity.5 1 0.5 2 1. The raw time-series data ( ) and predicted timeseries models ( ) are shown. Baseline conditions of repeated exposure to the stimuli were not sufficient to effect clinically significant improvement.5 0 0 5 10 Extended baseline Baseline Phase 2 Phase 3 Stimulus specific training Stimulus generalization training sensory discriminations through games and fine motor activities. retrieving objects from a box filled with rice and exercises in graphesthesia. Movements of the hand.

Loss of somatic sensation 239 Table 16.1. 1995). 2002).1. 1996a) and the system is competitive (Merzenich and Jenkins. intermittent feedback and tuition of training principles required for learning within and across sensory dimensions improved performance and retention facilitates transfer of training effects forced use.. Forced use of the system. competitive use progressively challenge system improved perception cross-modal plasticity pre-existing connections within system extrinsic and summary feedback may enhance learning link with attention. Rather changes are associated with specific skill learning. are discussed below. or have potential for application. Derived from and/or consistent with theories of Principle of training Repeated stimulation of specific stimuli Attentive exploration Vision occluded Motivating/ meaningful task Use of anticipation trials (and imagery) Feedback on – accuracy – method of exploration and summary feedback Calibration of sensation: within and across modalities Progression from easy to more difficult discriminations Intensive training Variation in stimuli.R.. repetitive use alone may not be sufficient to effect changes in cortical representation. enhance new connections consistent with normal processing Physiology specificity of processing within the system component of sensory processing vision may dominate Most of the principles identified from these fields are complementary. Weinreich and Armentrout. More recent sensory retraining approaches have begun to base their training on these principles (see Section Review of documented programs in relation to basic science and empirical foundations of this chapter for review). et al. Even less intensive programs based on principles of motor learning found training-induced changes (Carey J.. neural plasticity and physiology of the somatosensory system. consistent with the knowledge that neural plasticity underlies learning and recovery following injury. consistent with a . Summary of principles of sensory training derived from theories of perceptual learning. Functional reorganization has been demonstrated after behaviorally controlled tactile stimulation in intact animals (Recanzone et al. for example using constraint induced movement therapy. Key principles that have been successfully applied. Nudo et al. the physiology of processing somatosensory information must be considered in application to the sensory system. 1992). Their application is summarized in Table 16. 2000). 1993. has also been associated with neural plastic changes in post-stroke motor recovery (Liepert et al. In addition. Importantly.. Neural plastic changes are experience-dependent (see Section A on Neural plasticity in Volume I. learning and success Perceptual learning improvement maximal for specific stimulus attention important in learning Neural plasticity modification of sensory map is task-dependent modulation of neural plasticity force use of somatosensory system brain responds to meaningful goals activation of similar sites as for direct stimulation.

. Yekutiel. 1995. Attention is also important in the modulation of cortical plasticity (see Chapter 12 of Volume I). 1993). 1996b). 1998). 1999) and may enhance perceptual learning (Gibson.. Attention is crucial in perceptual learning. 1998. as vision may dominate tactile and proprioceptive senses in some instances (Clark and Horch. 1997). Yekutiel. 1993). and the brain responds to meaningful goals (Nudo et al. 2000. prior and subjective experience can influence early stages of information processing and facilitate stimulus differentiation (Goldstone. Learning is reported to be maximal for the specific task trained (Gibson. Anticipation trials. 1969). 1991). Plautz et al. Augmented feedback on accuracy of response outcome and on performance is important in skill acquisition (Schmidt and Lee. 1993). Repetition over time with an increasing number of coincident events serves to strengthen synaptic connections (Byl and Merzenich. 2000). interesting and demanding if it is to tap into the brain’s potential for functional reorganization (Byl and Merzenich.. based on evidence that haptic (tactile and proprioceptive) information is represented through imagery (Klatzky et al. practice with correction can enhance learning .. may tap into this capacity and encourage new neural connections. However.. Training of important sites normally responsible for the sensation. Further. 1993).240 Leeanne Carey “learning-dependent” hypothesis of neural plasticity (Karni et al. 1988. 1989) and perception becomes adapted to tasks by increasing the attention paid to important features (with less noticing of irrelevancies) (Gibson. 2000). Sensory neurorehabilitation should therefore challenge the sensory system using repeated stimulation of targeted sensory tasks coupled with an intensive perceptual-learning based training program. 1995). Further. 1989). 1981). 1998) and neurophysiological (Johnson and Hsiao. Goldstone. particularly in early stages of plastic changes and learning (Karni et al.. and discriminations characteristically impaired and important for daily function (Carey et al. 1992) evidence propose that “distinctive features of difference” are learned and form the basis of transfer of training. Similar brain sites are active under direct stimulation and anticipated stimulation conditions (Roland. 1992). Perceptual learning (Goldstone. Sathian and Zangaladze.. 1969.. 1998).. Lederman et al. 1980). competition between afferent inputs for connections in the sensory cortex (Merzenich and Jenkins. Consequently to maximize task-specific learning. 1993).. 1986. 1993) suggests the need for caution with overstimulation of a specific site at the expense of related areas.... 2000). 1998) and recovery after brain injury (Bach-y-Rita. This may be facilitated through requiring a response and guiding the patient to search for distinctive features (Carey et al. in which the patient is informed that a limited set of previously experienced stimuli will be used (Carey et al. with reinforcement to encourage motivation and participation (Carey. training stimuli and the method of processing the information should match targeted discrimination tasks (Carey et al. Attentive exploration of stimuli allows purposeful feedback within the sensory-perceptual system (Epstein et al. It should provide regular opportunities for success. 1986). 1969. A patient may also be encouraged to imagine what a stimulus should feel like. for example the hand (Dannenbaum and Dykes. Training should therefore be goal directed. 1993) have been recommended. Anticipation may facilitate recruitment of existing or new sensory sites in the brain. Thus patients should actively (where possible) and purposively explore sensory stimuli with attention directed to distinctive features of difference. consistent with highly specific organization of the system (see Section Definition and processing within the somatosensory system of this chapter for review) and evidence that functional reorganization is directly linked with changes in cortical regions engaged by these inputs (Recanzone et al. exploration of stimuli with vision occluded should be included to allow subjects to focus specifically on the somatic sensations (Carey et al. 1993. Motivation is important in learning (Goldstone. Goldstone.. Although improvement in perceptual discriminations may be experienced in unimpaired subjects without extrinsic feedback in some cases (Epstein et al. Yekutiel and Guttman. 2000).

However. 1993). 1969). Moreover. there are limits on the generality of perceptual learning. 2005). especially of complex stimuli. 1997). Similarity between original and transfer tasks is an important factor influencing the degree of transfer (Gibson. 1991). 1990) and specific instruction on principles of training and how these apply ... Similarly. 1987). a higher level of performance is possible than if they remained independent (Becker. 1998). Carey and Matyas. should be provided. 1989. We found that repeated exposure alone was insufficient to effect a positive training outcome in the majority of cases post-stroke (Carey et al. Transfer of training effects is more effective when variation in stimuli is employed (Gibson. 1969). Schmidt and Lee. 2005). Goldstone. receptor location and method of processing (Sathian and Zangaladze. Finer perceptual differences are able to be distinguished through exposure to a series of graded stimuli (Ahissar and Hochstein. 1991. 1998). Goldstone. 1993. 2005).. Thus feedback on accuracy of response and performance. progressive difficulty should be defined across stimuli sets as well as within sets (Carey and Matyas. 1986). 1999). Goldstone. 1984). sub-modality (grid or fabric textures) and body location (fingertip or wrist) with SST post-stroke (Carey et al. consistent with activity in visual cortical regions during tactile perception (Zangaladze et al. 1990. 1997). perceptual transfer is possible in some instances with unimpaired subjects (Epstein et al. In addition. 1997. Graded progression facilitates perceptual differentiation.. This further suggests the need for repetition and intensive training.. for example method of exploration (Lederman and Klatzky. Transfer across body sites has also been reported in unimpaired systems (Sathian and Zangaladze. Intermittent feedback on accuracy of response (Winstein and Schmidt. 2005). transfer from one stimulus to another within a unidimensional sensory quality requires presentation in a graded manner (Gibson. Thus training should progress from easy to more difficult discriminations across stimuli and within a unidimensional sensory quality. 1999). cross-modal plasticity in sensory systems (see Chapter 11 of Volume I) may facilitate alternate and new neural connections. 1984) and should be provided at the end of each training session. Carey and Matyas. as well as variation in tasks and environments (Carey and Matyas. best available evidence suggests that training should continue for some time after “mastery” to increase retention (Lane. Feedback should be immediate. 1998).Loss of somatic sensation 241 (Gibson. as presentation of an easy discrimination first allows the subject to allocate attention to the relevant dimension (Goldstone. 1993. To achieve grading. Computational neural models indicate that when two modalities are trained at the same time and provide feedback for each other. 1969) and use of vision to facilitate cross-modal calibration (Lederman et al. 1998). Further. Goldstone. Perceptual learning is usually highly specific to the task.. 1997.. 1998. for example roughness characteristics. 1997). 1969). It has been suggested that transfer should be more prominent where the stimuli are more complex and potentially share a number of distinctive features (Gibson. Performance is better on frequently presented items than rare items (Allen and Brooks. Spengler et al. Principles of learning that facilitate transfer of training effects in unimpaired subjects have potential application following injury. and may be influenced by the attention demands and complexity of the task (Ahissar and Hochstein. 1996). Spengler et al. Ettlinger and Wilson. precise and quantitative to maximize acquisition (Salmoni et al. 1997. This may involve comparison of the sensation with the other hand (Gibson.. Optimally this should include training across a variety of stimuli with a wide range of distinctive features.. Summary feedback also enhances learning (Salmoni et al. we found highly specific training effects in tasks employing the same sensory dimension (tactile or proprioceptive). Calibration of perceptions would also appear to be important. Specificity of learning and principles to facilitate learning transfer Whilst the above principles have been associated with positive perceptual learning. 1991.

Confirmation of the prediction that neural plastic changes occur primarily within the pre-existing somatosensory system (Weinreich and Armentrout.. the characteristic learning curve was only achieved under supervised training conditions (Carey et al. 1993. possibly suggestive of different behavioral strategies. as applied to neurorehabilitation of somatic sensation Brain networks may reorganize to optimize stroke recovery. an important part of learning transfer tasks is acquiring the capacity to cope with novel situations (Schmidt and Lee.. 16. in contrast to unimpaired subjects (Epstein et al. 1996b). provided a program designed to enhance transfer is used (Carey and Matyas. 2003. Epstein et al.6 Future directions for the integration of basic science in clinical practice. 2005). Yekutiel and Guttman. Systematic investigation of the conditions under which behavioral improvement and neural repair is most effectively achieved is required to provide ongoing direction for the development of science-based interventions. that is stimulus specific versus generalization optimized. However.. compared to nonspecific exposure. different principles of training (e. Similarly. the timing (post-injury) and intensity of training requires investigation. Further. despite evidence of behavioral improvement.. derived from theories of perceptual learning and recovery following brain damage. such as attention (see Chapter 12 of Volume I) and visual (see Chapters 9 and 11 of Volume I) systems. Other programs that have employed training across a variety of tasks have also found generalized training effects (Byl et al. Evidence of a learning phenomenon associated with sensory retraining post-stroke has been quantified in the intervention time-series data of our patients (Carey. Evidence of recruitment of different sites may identify involvement of other systems important in recovery. Smania et al.. 1999). see also Fig. 2003.. the nature of training. 16..g. This suggests the need to provide exposure to novel stimuli with opportunity to get feedback on the act of generalization (Carey and Matyas. 1987. will highlight the importance of sparing and dynamic adaptation within pre-existing sensory sites. given evidence of possible maladaptive changes (Merzenich and Jenkins. and the neural outcomes of learning transfer (Spengler et al. 1997) will help elucidate the mechanisms and brain regions involved in different training methods. it is not known to what extent training-induced recovery is associated with changes in the functional neuroanatomy of sensation in humans. appears crucial to outcome.. For example. The improvement curve was consistent with that described in the learning literature (Lane. may be used to test for outcomes related to brain adaptation. The potential for generalization of training within a sensory dimension has also been demonstrated post-stroke.242 Leeanne Carey across tasks (Cormier and Hagman. 1993. In summary. Investigation of the need for specific training. cross-modality matching and feedback on accuracy) require systematic investigation of their contribution as they may involve different neural structures and mechanisms. 1989). 1993). 1992).2). Paradigms that permit investigation of component stages in neural processing need to be conducted and interpreted . 1995). 1987) have also been associated with enhanced transfer and retention. Further. Comparison with motor recovery findings will help determine if there is a common model of neural plasticity associated with motor and somatosensory recovery. Nudo et al. 2005). 1993). In particular it is unknown whether sites different to those typically used are involved in the recovery process. positive findings from studies of sensory retraining (see section Review of documented programs in relation to basic science and empirical foundations of this chapter for review) support the application of principles of training derived from literature on perceptual learning and neural plasticity. 1989) and in studies of neural plasticity (Recanzone et al.. However. Clinically effective sensory training programs. This will advance our understanding of whether training is operating at a level of restitution or substitution within the system and provide insight into behavioral strategies associated with training.

Ongoing clinical studies are being conducted also in collaboration with Prof Derek Wade and Dr Richard Macdonnell... Bach-y-Rita. level of task difficulty and relative body location on learning transfer is needed to guide clinical training programs and clarify the nature of what is being learnt. Multiple foci in parietal and frontal cortex activated by rubbing embossed grating patterns across fingerpads: a positron emission tomography study in humans. Allen. (1993). S. J. In particular Ass/Prof Thomas Matyas and Ms Lin Oke have collaborated on the clinical studies investigating methods of assessing and training somatosensations post-stroke. Finally. 2005). G. Bach-y-Rita. Cereb Cortex. 1999). N... detection versus discrimination versus multisensory integration).. M. Burton.. 225–263. Bassetti. (1997). regulation of pressure during grasp and spontaneous use of the limb. S. Programs reviewed (see Section Review of documented programs in relation to basic science and empirical foundations of this chapter for review) have incorporated principles consistent with perceptual learning and neural plasticity. O. method of information processing. and Hochstein. detection of slip when holding objects.. H. M. 1993. individual features of the training protocols have not been dissected. Neurology. Prof Aina Puce and Prof Rüdiger Seitz.. P. (1991). Dr David Abbott. Task difficulty and the specificity of perceptual learning.E. 401–406. Systematic investigation of these is indicated. and Regli. 1942–1949. Vienna. C.M. Investigation of neural outcomes associated with motor and sensory recovery under spontaneous and training-induced recovery conditions is being conducted in collaboration with a number of researchers including Prof Geoffrey Donnan. The most optimal combination of principles may also vary with individual patient characteristics including the nature of loss (e. The focus of training could also be expanded to include training in discrimination of size.). Byl. Potential explanations for individual differences in the nature and extent of recovery may relate to lesion site (Zemke et al. Previous studies have provided some insight into the boundaries of spontaneous and facilitated transfer with stroke patients (Carey et al. S. Roderick.R... M. 3–19. Bogousslavsky. F. Network Comp Neural Syst. shape and weight of objects. pp.. (1996). P. Dr Gary Egan. 120. Further development of current training programs is also indicated. and the effect of improving sensation on motor function and activities of daily living. This is necessary to identify the critically important elements associated with successful learning and transfer. 7–31. Becker. Hanny. L. In: Recovery of function: theoretical considerations for brain injury rehabilitation (ed. M. Brain plasticity as a basis for therapeutic procedures. A. Effectiveness of sensory .. Hans Huber. MacLeod. 387. T. 2003) and remote changes in structure. the ability to modify sensory abilities experimentally opens up an experimental paradigm for future investigations of the relationship between sensation and other abilities. Mutual information maximization: models of cortical self-organization. Nature. 7.Loss of somatic sensation 243 using models of analysis that focus on connectivity within the system. (1997). including diaschisis (Seitz et al. Investigation of similarity of trained and transfer tasks. ACKNOWLEDGEMENTS I wish to acknowledge the contribution of collaborators who have worked with me on various aspects of research related to sensory recovery and retraining following stroke. Kotler. Sensory syndromes in parietal stroke. and Brooks. 43. A. Specializing the operation of an explicit rule. and Raichle. Videen. 7. Knowledge of the relationship between brain activation and recovery will have predictive significance in relation to identifying patients who are likely to show spontaneous recovery and/or who are able to benefit from training. Mohamed. J. Tang. (1980).g. (2003).O. such as pinch grip. Investigation of the association between structural brain changes and the brain’s capacity for reorganization is indicated.. REFERENCES Ahissar. Smith. Carey and Matyas. and Abrams. J Exp Psychol Gen. However. 3–17. J. the phase of recovery (acute versus chronic) and the site of lesion (PNS versus CNS or specific location within these).W.

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