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Visit This Book’s Web Page / Buy Now / Request an Exam/Review CopyThis is a sample from Spasticity: Diagnosis and Management, Second Edition

© Demos Medical Publishing

Spasticity

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Spasticity

Diagnosis and Management

SECOND EDITION

EditorAllison Brashear, MD, MBAWalter C. Teagle ProfessorProfessor and ChairDepartment of NeurologyWake Forest University School of MedicineWake Forest Baptist Medical CenterWinston-Salem, North Carolina

Associate Editor

Elie Elovic, MDDirector, Traumatic Brain Injury ProgramRenown Rehabilitation HospitalRenown HealthReno, Nevada

New York

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Visit our website at www.demosmedical.com

ISBN: 9781620700723e-book ISBN: 9781617052422

Acquisitions Editor: Beth BarryCompositor: Newgen KnowledgeWorks

© 2016 Demos Medical Publishing, LLC. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publisher.

Medicine is an ever-changing science. Research and clinical experience are continually expanding our knowl-edge, in particular our understanding of proper treatment and drug therapy. The authors, editors, and publisher have made every effort to ensure that all information in this book is in accordance with the state of knowledge at the time of production of the book. Nevertheless, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the contents of the publication. Every reader should examine carefully the package inserts accompanying each drug and should carefully check whether the dosage schedules mentioned therein or the contraindications stated by the manufacturer differ from the statements made in this book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market.

Library of Congress Cataloging-in-Publication DataSpasticity (Brashear) Spasticity : diagnosis and management / editor, Allison Brashear ; associate editor, Elie Elovic.—Second edition. p. ; cm. Includes bibliographical references and index. ISBN 978-1-62070-072-3—ISBN 978-1-61705-242-2 (e-book) I. Brashear, Allison, editor. II. Elovic, Elie, editor. III. Title. [DNLM: 1. Muscle Spasticity—diagnosis. 2. Muscle Spasticity—therapy. 3. Botulinum Toxins—therapeutic use. 4. Extremities—physiopathology. 5. Motor Neuron Disease. WE 550] RC935.S64 616.8’56—dc23 2015031221

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We dedicate this book to our families for their unconditional support, and to our professors, colleagues, students and patients

who continue to humble us with their strength and challenge us to improve the care of those with spasticity.

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Contributors ixPreface xiiiAcknowledgments xv

PART I. GENERAL OVERVIEW

1. Why Is Spasticity Treatment Important? 3 Allison Brashear and Elie Elovic

2. Epidemiology of Spasticity in the Adult and Child 5 John R. McGuire

3. Spasticity and Other Signs of the Upper Motor Neuron Syndrome 17 Nathaniel H. Mayer

4. Ancillary Findings Associated With Spasticity 33 Cindy B. Ivanhoe and Ana V. Durand Sanchez

PART II. ASSESSMENT TOOLS

5. Measurement Tools and Treatment Outcomes in Patients With Spasticity 51 Elie Elovic

6. Techniques and Scales for Measuring Spastic Paresis 73 Marjolaine Baude and Jean-Michel Gracies

7. Assessment of Spasticity in the Upper Extremity 81 Thomas Watanabe

8. Assessment of Lower Limb Spasticity and Other Consequences of the Upper Motor Neuron Syndrome 91

Alberto Esquenazi

9. Setting Realistic and Meaningful Goals for Treatment 101 Elie Elovic and Allison Brashear

PART III. TREATMENT OF SPASTICITY

10. Chemoneurolysis With Phenol and Alcohol: A “Dying Art” That Merits Revival 111 Lawrence J. Horn, Gurtej Singh, and Edward R. Dabrowski

11. Botulinum Toxin in the Treatment of Lower Limb Spasticity 129 Alberto Esquenazi

12. Botulinum Toxin in the Treatment of Upper Limb Spasticity 141 Allison Brashear

13. Guidance Techniques for Botulinum Toxin Injections: A Comparison 153 Katharine E. Alter

Contents

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viii ■ CONTENTS

14. Anatomical Correlation of Common Patterns of Spasticity 181 Mayank Pathak and Daniel Truong

15. The Role of Physical and Occupational Therapy in the Evaluation and Management of Spasticity 193

Susan Reeves and Kelly Lambeth

16. Emerging Technologies in the Management of Upper Motor Neuron Syndromes 219 Ira G. Rashbaum and Steven R. Flanagan

17. Effects of Noninvasive Neuromodulation in Spasticity 239 Lumy Sawaki

18. Pharmacologic Management of Spasticity: Oral Medications 251 Jay M. Meythaler and Riley M. Smith

19. Intrathecal Baclofen for Spasticity 287 Gerard E. Francisco and Michael Saulino

20. Surgery in the Management of Spasticity 299 David A. Fuller

PART IV. EVALUATION AND MANAGEMENT OF DISEASES WITH SPASTICITY

21. Diagnostic Evaluation of Adult Patients With Spasticity 329 Geoffrey Sheean

22. Overview of Genetic Causes of Spasticity in Adults and Children 339 Rebecca Schüle and Stephan Züchner

23. Spasticity Due to Disease of the Spinal Cord: Pathophysiology, Epidemiology, and Treatment 351

Heather W. Walker, Alice J. Hon, and Steven Kirshblum

24. Spasticity Due to Multiple Sclerosis: Epidemiology, Pathophysiology, and Treatment 383 Anjali Shah and Ian Maitin

25. Poststroke Spasticity Management With Botulinum Toxins and Intrathecal Baclofen 401 Anthony B. Ward and Poornashree Holavanahalli Ramamurthy

26. Management of Brain Injury Related Spasticity 413 Mary Alexis Iaccarino, Saurabha Bhatnagar, and Ross Zafonte

27. Management of the Cancer Patient With Spasticity 429 Adrienne R. Hill, Vishwa S. Raj, and Heather W. Walker

28. Evaluation, Treatment Planning, and Nonsurgical Treatment of Cerebral Palsy 439 Ann Tilton and Daniella Miller

29. Surgical Management of Spasticity in the Child With Cerebral Palsy 449 Kat Kolaski, John Frino, and L. Andrew Koman

30. Spasticity Management in Long-Term Care Facilities 471 Amanda Currie and David Charles

31. Economic Impact of Spasticity and Its Treatment 477 Michael Saulino

Index 483

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Edward R. Dabrowski, MDSystem Medical Director, Pediatric Physical Medicine

and RehabilitationDepartments of Physical Medicine and Rehabilitation

and PediatricsBeaumont Health; andAssociate ProfessorDepartments of Physical Medicine and Rehabilitation

and PediatricsOakland University Medical SchoolRoyal Oak, Michigan

Ana V. Durand Sanchez, MDAssistant ProfessorDepartment of Physical Medicine and

RehabilitationIndiana UniversityIndianapolis, Indiana

Elie Elovic, MDDirector, Traumatic Brain Injury ProgramRenown Rehabilitation HospitalRenown HealthReno, Nevada

Alberto Esquenazi, MDJohn Otto Haas Chair and ProfessorDirector, Gait and Motion Analysis LaboratoryDepartment of Physical Medicine and

Rehabilitation MossRehab/Einstein Healthcare NetworkElkins Park, Pennsylvania

Steven R. Flanagan, MDHoward A. Rusk Professor of Rehabilitation

MedicineChair of the Department of Rehabilitation

MedicineNYU Langone Medical CenterNew York, New York

Katharine E. Alter, MDSenior Clinician, National Institute of Child Health

and Human Development; andMedical Director, Functional and Applied

Biomechanics Section, Rehabilitation Medicine, National Institutes of Health; and

Staff Physiatrist, Rehabilitation Programs, Mount Washington Pediatric Hospital

Baltimore, Maryland

Marjolaine Baude, MDClinical FellowDepartment of NeurorehabilitationHenri Mondor University Hospitals; andUniversité Paris-Est CréteilCréteil, France

Saurabha Bhatnagar, MDAssociate Director, Physical Medicine and

Rehabilitation Residency ProgramDepartment of Physical Medicine and RehabilitationHarvard Medical School, Massachusetts General

Hospital; andSpaulding Rehabilitation HospitalBoston, Massachusetts

Allison Brashear, MD, MBAWalter C. Teagle ProfessorProfessor and Chair, Department of NeurologyWake Forest University School of MedicineWake Forest Baptist Medical CenterWinston-Salem, North Carolina

David Charles, MDProfessor and Vice-Chairman of NeurologyDirector, Movement Disorders ClinicDepartment of NeurologyVanderbilt University Medical CenterNashville, Tennessee

Amanda Currie, BAClinical Trials SpecialistDepartment of NeurologyVanderbilt University Medical CenterNashville, Tennessee

Contributors

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x ■ CONTRIBUTORS

Cindy B. Ivanhoe, MDProfessorDepartment of Physical Medicine and

RehabilitationBaylor College of MedicineHouston, Texas

Steven Kirshblum, MDProfessorDepartment of Physical Medicine and RehabilitationRutgers New Jersey Medical SchoolNewark, New Jersey; andMedical DirectorKessler Institute for RehabilitationWest Orange, New Jersey

Kat Kolaski, MDAssociate Professor of Orthopedics

and PediatricsWake Forest University School of MedicineWinston-Salem, North Carolina

L. Andrew Koman, MDProfessor and ChairDepartment of Orthopedic Surgery Wake Forest School of MedicineWake Forest Baptist Medical CenterWinston-Salem, North Carolina

Kelly Lambeth, MPH, OTR/LClinical Coordinator, NeurorehabilitationDepartment of Physical and Occupational TherapyWake Forest Baptist Medical CenterWinston-Salem, North Carolina

Ian Maitin, MD, MBAChairperson, Physical Medicine and RehabilitationProfessor, Physical Medicine and RehabilitationTemple University School of MedicinePhiladelphia, Pennsylvania

Nathaniel H. Mayer, MDDirector, Motor Control Analysis LaboratoryMossRehab/Einstein Healthcare NetworkElkins Park, Pennsylvania; andEmeritus Professor of Physical Medicine and

RehabilitationDepartment of Physical Medicine and RehabilitationTemple University School of MedicinePhiladelphia, Pennsylvania

John R. McGuire, MDAssociate ProfessorDepartment of Physical Medicine and RehabilitationMedical College of WisconsinMilwaukee, Wisconsin

Gerard E. Francisco, MDProfessor and ChairmanDepartment of Physical Medicine and RehabilitationUniversity of Texas Health Science Center at

Houston (UTHealth); andChief Medical Offi cer and DirectorNeuroRecovery Research CenterTIRR Memorial HermannHouston, Texas

John Frino, MDAssociate ProfessorOrthopedics and PediatricsWake Forest School of MedicineWake Forest Baptist Medical CenterWinston-Salem, North Carolina

David A. Fuller, MDAssociate Professor of Surgery and Program DirectorDepartment of Orthopaedic SurgeryCooper Medical School of Rowan UniversityCamden, New Jersey

Jean-Michel Gracies, MD, PhDProfessorDepartment of NeurorehabilitationHenri Mondor University Hospitals; andUniversité Paris-Est CréteilCréteil, France

Adrienne R. Hill, DOAssistant ProfessorDepartment of Physical Medicine and

RehabilitationWake Forest Baptist HealthWinston-Salem, North Carolina

Alice J. Hon, MDDepartment of Spinal Cord Injury and DisordersVA Long Beach Healthcare SystemLong Beach, California

Lawrence J. Horn, MDProfessor and ChairDepartment of Physical Medicine and RehabilitationWayne State University School of Medicine/

Rehabilitation Institute of MichiganDetroit, Michigan

Mary Alexis Iaccarino, MDBrain Injury Medicine FellowDepartment of Physical Medicine and

RehabilitationHarvard Medical School; andSpaulding Rehabilitation HospitalBoston, Massachusetts

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CONTRIBUTORS ■ xi

Michael Saulino, MD, PhDPhysiatristDepartment of Physical Medicine and RehabilitationMossRehab/Einstein Healthcare NetworkElkins Park, Pennsylvania; and Assistant ProfessorDepartment of Rehabilitation MedicineSydney Kimmel College of MedicinePhiladelphia, Pennsylvania

Lumy Sawaki, MD, PhDAssociate ProfessorDepartment of Physical Medicine and

RehabilitationUniversity of Kentucky College of Medicine and

Cardinal Hill Rehabilitation HospitalLexington, Kentucky

Rebecca Schüle, MDHertie Institute for Clinical Brain ResearchEberhard Karls University TübingenTübingen, Germany

Anjali Shah, MDAssociate ProfessorDepartment of Physical Medicine and RehabilitationUniversity of Texas Southwestern Medical CenterDallas, Texas

Geoffrey SheeanDirector of Electromyography and

Neuromuscular ServicesDivision of NeurologyScripps Clinic Torrey PinesLa Jolla, California

Gurtej Singh, MDInterventional Pain and Rehabilitation

Medicine SpecialistDepartment of SurgeryGreater Baltimore Medical CenterBaltimore, Maryland

Riley M. Smith, MDAssistant ProfessorDepartment of Physical Medicine and

RehabilitationWayne State UniversityDearborn, Michigan

Ann Tilton, MDProfessor of Neurology and PediatricsDepartment of Neurology—Child NeurologyLouisiana State UniversityNew Orleans, Louisiana

Jay M. Meythaler, MD, JDProfessor–ChairDepartment of Physical Medicine

and RehabilitationWayne State UniversityDearborn, Michigan

Daniella Miller, MD, MPHChief ResidentDepartment of Neurology—Child NeurologyLouisiana State UniversityNew Orleans, Louisiana

Mayank Pathak, MDParkinson’s and Movement Disorder InstituteOrange Coast Memorial Medical CenterFountain Valley, California

Vishwa S. Raj, MDDirector of Oncology RehabilitationDepartment of Physical Medicine

and RehabilitationCarolinas Rehabilitation and the Levine Cancer

Institute; andVice-Chairperson, Associate Medical DirectorDepartment of Physical Medicine

and RehabilitationCarolinas RehabilitationCharlotte, North Carolina

Poornashree Holavanahalli Ramamurthy, MDSpecialist Registrar in Rehabilitation MedicineMidland Spinal Injuries CentreRobert Jones and Agnes Hunt

Orthopaedic HospitalOswestry, United Kingdom

Ira G. Rashbaum, MDClinical Professor of Rehabilitation MedicineDepartment of Rehabilitation MedicineMedical Director, Stroke RehabilitationNYU Langone Medical CenterNew York, New York

Susan Reeves, MPT, DPTClinical DirectorDepartment of Physical and

Occupational TherapyWake Forest Baptist Medical CenterWinston-Salem, North Carolina

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xii ■ CONTRIBUTORS

Thomas Watanabe, MDClinical Director, Drucker Brain Injury CenterDepartment of Physical Medicine and RehabilitationMossRehab/Einstein Healthcare NetworkElkins Park, Pennsylvania

Ross Zafonte, DOEarle P. and Ida S. Charlton Professor

and ChairmanDepartment of Physical Medicine

and RehabilitationHarvard Medical School, Massachusetts General

Hospital; andSpaulding Rehabilitation HospitalBoston, Massachusetts

Stephan Züchner, MDAssociate Professor for Human Genetics and NeurologyUniversity of Miami Miller School of MedicineMiami Institute for Human GenomicsMiami, Florida

Daniel Truong, MDParkinson’s and Movement Disorder InstituteOrange Coast Memorial Medical CenterFountain Valley, California

Heather W. Walker, MDClinical Associate ProfessorDepartment of NeurosciencesMedical University of South Carolina; andProgram Director of Neuroscience ServicesHealthSouth Rehabilitation Hospital of CharlestonCharleston, South Carolina

Anthony B. Ward, BSc, MBChB, FRCPEd, FRCPProfessorNorth Staffordshire Rehabilitation CentreHaywood Hospital; andProfessorFaculty of Health SciencesStaffordshire UniversityBurslem, Stoke-on-Trent, United Kingdom

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Preface

Spasticity: Diagnosis and Management is the fi rst book solely dedicated to the diagnosis and treat-ment of spasticity. This second edition has been sub-stantially revised to refl ect the signifi cant advances in the treatment of spasticity since the fi rst edition. Our objectives in the development of this second edi-tion were to outline the still-evolving process for the diagnosis of spasticity and the basic science behind its pathophysiology, and to provide updated informa-tion on both the measurement tools used for spas-ticity evaluation and the newest available treatment options. This book remains the most comprehensive guide to diagnosis and management of spasticity.

Over the past 5 years, the focus of spasticity man-agement has moved from interventions on tone to the impact of the spasticity on the lives of patients and caregivers. Additional drugs, including new forms of botulinum toxin, have been reported in large clinical trials and are changing or will, in the future, change treatment paradigms. Comprehensive programs in spasticity management increasingly focus on special populations including children, cancer survivors, and patients in long-term care programs. As a result, this edition addresses new treatment pathways, out-comes, and economics of spasticity care within the larger context of the rapidly changing health care environment.

Divided into four sections, this book is intended to provide both clinicians and researchers up-to-date access on the latest comprehensive treatment of spas-ticity. Part I includes a general overview with four chapters highlighting why spasticity is important, epi-demiology of spasticity and other signs of the upper motor neuron syndrome, and fi nally ancillary fi ndings associated with caring for the patient with spasticity.

Part II focuses on the assessment tools in diagnosis and management of spasticity. Five chapters include an outline of general overview measurement tools, specifi c techniques and scales, assessment of the upper and lower extremity, and setting realistic goals for treatment. The revised chapter, “Measurement Tools

and Treatment Outcomes in Patients With Spasticity,” includes the Goal Attainment Scale, which is specifi -cally designed to focus on patient-specifi c outcomes. The newly added chapter, “Techniques and Scales for Measuring Spastic Paresis,” details the use of scales such as the Tardieu. The use of such scales is more common in both patient care and clinical trials. These chapters provide details on the administration of these scales. Taken together, these fi ve chapters provide a comprehensive review of assessment and measurement of spasticity.

Part III provides 11 comprehensive chapters on treatment of spasticity. New chapters include the role of the physical and occupational therapist in spastic-ity management, the use of ultrasound in guidance of botulinum toxin management, and emerging technol-ogies in the treatment of spasticity. Part III is designed to highlight the changes in the fi eld in the past 5 years.

The fi nal section, Part IV, is devoted to individual diseases involving spasticity and treatment within the context of these conditions. In addition to updated chapters on evaluation, genetics, and spasticity in adults and children with spinal cord injury, multiple sclerosis, stroke, traumatic brain injury, and cerebral palsy, we have added new chapters on more special-ized areas including spasticity in patients with cancer, treatment of spasticity in patients in long-term care facilities, and the economics of spasticity treatment.

With the development of effective therapies for spasticity, we originally sought to address the diagno-sis and treatment of spasticity in an integrated, clini-cally useful text. This revised second edition builds on that foundation and integrates recent advances in the fi eld for diagnosis, treatment, and outcomes. The real focus of this book is on providing the most up-to-date, effective, comprehensive, and economi-cal therapy for patients with spasticity. We invite you to explore these pages and join us in our mission to improve the care for our patients with spasticity.

Allison Brashear, MD, MBA

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Acknowledgments

Thank you to our patients, their families, our col-leagues and staff, and our families for their many contributions to this text. This second edition chal-lenges us to improve the diagnosis and care of spastic-ity in our patients. Thank you to you, the reader, for

joining us on this journey. We hope this book inspires you to continue to improve the diagnosis and man-agement of spasticity.

Allison Brashear, MD, MBA

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General Overview

IP A R T






Why Is Spasticity Treatment Important?Allison Brashear and Elie Elovic

Spasticity treatment is important because the increased tone may interfere with the physical func-tioning of patients. The overarching goal of spastic-ity management should be to improve the ability of patients to perform active and passive ranges of motion and improve the ability of caregivers to assist patients with disabilities. Increased tone or spasticity is the tightness that patients and/or caregivers report with passive movement of the limb. In more scientifi c language, spasticity is a motor disorder characterized by a velocity-dependent increase in the tonic stretch refl ex. A clinical fi nding on the neurologic examina-tion, spasticity, together with increased tone, brisk refl exes with incoordination, and weakness, repre-sents the upper motor neuron syndrome.

Regardless of the cause, spasticity causes signifi -cant disability. An estimated 4 million individuals are stroke survivors in the United States, and as many as one third may have spasticity with suffi cient disabil-ity to require treatment. According to the Centers for Disease Control and Prevention, 1.4 million people in the United States sustain a traumatic brain injury each year, and additional patients develop spasticity after spinal cord injury. The result of any brain or spinal cord injury is a variable pattern of increased tone with weakness and discoordination that leads to signifi cant disability in many patients.

The treatment of spasticity relies on the physician’s assessment of the individual together with conversa-tions with the caregiver. Patients’ inability to perform simple activities of daily living for themselves and the adverse effects on the caregiver drive physicians to fi nd ways to decrease tone, build strength, and improve coordination. The team approach is a cor-nerstone of a successful treatment, and interaction of the patient, the caregiver, the therapist, and the physi-cians works best to provide a care plan that addresses functional impairment and plots a course to treat the problems.

Spasticity is a clinically relevant medical problem when it interferes with function or care of patients. The evolution of upper motor neuron syndrome may take days to months after a central nervous system injury. Moreover, the presentation in one patient may differ from that of another despite both hav-ing similar central nervous system lesions. The lesion alone does not predict the amount or impact of the spasticity. Other factors such as medications, stress, medical illness, timing of therapy, and so on impact the clinical presentation. As a result, each patient must be assessed individually with his or her care-giver, noting the concerns that impair the perfor-mance of activities of daily living or other defi cits. No matter how much we learn about stroke, trau-matic brain injury, multiple sclerosis, and spinal cord injury, the assessment of spasticity and the effect of tone on function will remain unique to each individ-ual patient’s circumstance.

Although neurologic examination is essential for the diagnosis of spasticity, the management of spas-ticity has many paths for treatment depending on the disability and goals of the patient and caregiver. One patient may benefi t from a combination of tools for spasticity, including interventions such as botulinum toxin injections and intrathecal baclofen, whereas others may require a more conservative route such as splinting or oral medications. The informed physician should know how to assess the amount of spasticity, determine the functional limitations it creates, and then be able to develop a management plan for that individual patient.

How to assess the complicated picture of spasticity and when to intervene are the focus of this text. Our coauthors defi ne for you why spasticity is important and detail the diagnosis and management options, but the goal is to provide the reader with the best options for the physician’s individual patient. As editors, we aim to explore the diagnosis and management of the

1C H A P T E R






4 ■ I GENERAL OVERVIEW

So why is spasticity important? The answer is because it often causes disability and impairs function in our patients. The goal of this book is to provide the foundation for excellent care of our patients facing these disabilities.

many different types of patients with spasticity and to open the door to the different treatment paradigms for patients with spasticity. This second edition has been updated to refl ect the newest assessments and treatments.






Botulinum Toxin in the Treatment of Lower Limb SpasticityAlberto Esquenazi

Approximately 700,000 people are affected by a stroke each year in the United States, and there are more than 1,100,000 Americans surviving with residual functional impairment after stroke (1,2). Traumatic brain injury (TBI) is another form of acquired brain injury and continues to be an enor-mous public health problem in the 21st century even with modern medicine. Most patients with TBI (75%–80%) have mild head injuries; the remaining injuries are divided equally between moderate and severe categories. The cost to society of TBI is stag-gering, both from an economic and an emotional standpoint. Almost 100% of persons with severe head injury and as many as two thirds of those with moderate head injury will be permanently disabled in some fashion and will not return to their premor-bid level of function. In the United States, the direct cost of care for patients with TBI, excluding inpatient care, is estimated at more than $25 billion annually. The impact is even greater when one considers that most severe head injuries occur in adolescents and young adults with long survival rates.

Acquired brain injury affects a person’s cognitive, language, perceptual, sensory, and motor functions (3). Recovery is a long process that continues beyond the hospital stay and into the home setting. The reha-bilitation process is guided by clinical assessment of motor abilities. Accurate assessment of the motor abilities is important in selecting the different treat-ment interventions available to a patient.

Spasticity is a term that is often used by clinicians, and although used frequently, it can have differ-ent meanings in its interpretation and presentation. Spasticity is just one of the many positive signs of the upper motor neuron syndrome (UMNS), yet, under the heading of “spasticity,” clinicians often group all positive signs together and sometimes include negative signs as well. Many of these frequently misidentifi ed

phenomena fall under the broader heading of the UMNS—a condition that has classically been parti-tioned into a syndrome of positive and negative signs, including weakness, loss of dexterity, increased pha-sic and tonic stretch refl exes, clonus, cocontraction, released fl exor refl exes, spastic dystonia, and associ-ated reactions or synkinesias.

The issue of terminology is more than seman-tics and of great clinical importance because, for example, treatment of cocontraction, a phenom-enon likely to be of supraspinal origin, will differ from treatment of clonus, a phenomenon of the segmental stretch refl ex loop. If clinicians desire a concise, descriptive, utilitarian term that captures the essence of positive UMN phenomena, “muscle overactivity” may be a more suitable term than “spasticity,” especially because the phrase “muscle overactivity” evokes an image of dynamic muscle contraction, the general hallmark of all positive signs of UMNS (4).

Spasticity has classically meant increased excit-ability of skeletal muscle stretch refl exes, both phasic and tonic, that are typically present in most patients with a UMN lesion. After a UMN lesion, a net loss of inhibition impairs direct descending control over motor neurons. There is also a loss of inhibitory con-trol over interneuronal pathways of the cord that ordinarily regulate segmental spinal refl exes, includ-ing stretch refl exes, especially those concerned with antigravity muscles.

Lance characterized spasticity as an increase in velocity-dependent tonic stretch refl exes with exag-gerated tendon jerks (5). In Lance’s consensus defi -nition, tonic stretch refl exes referred to the output response of a muscle group that was stretched at dif-ferent velocities. “Exaggerated tendon jerks” were examples of “phasic” stretch refl exes. In routine prac-tice at the bedside, the two ways of assessing phasic

11C H A P T E R






130 ■ III TREATMENT OF SPASTICITY

serve as a rational basis for interventions that focus on specifi c muscles, including chemodenervation with botulinum toxin (BoNT); neurolysis with phenol; and surgical lengthening, transfers, and releases of indi-vidual muscles.

This concept, namely, identifying which muscles contribute dynamically and statically to upper motor neuron dysfunction, serves as a conceptual basis for this text. Simply put, identifying muscles that pro-duce deforming maladaptive joint movements and postures statically and dynamically is an important endeavor in aiding clinical interpretation of gait dys-function and in rationalizing subsequent treatment interventions (12,13).

Dynamic EMG, gait, motion analysis, and diag-nostic nerve blocks frequently provide the necessary detailed information about specifi c muscle groups that will guide decision making for treatment. Before selecting treatment interventions, the clinical team and the patient should explicitly develop functional goals. Functional goals may be classifi ed as symptom-atic, passive, or active in nature (9). A symptomatic goal refers to the intent to address clonus, fl exor, or extensor spasms, and pain, among others, as some of the targeted goals. Active functions refer to a patient’s direct use of the limb to carry out a functional activ-ity. Passive function has a different context and refers to the passive manipulation of limbs to achieve func-tional ends, typically through patients’ passive manip-ulation of the affected limb with the noninvolved limbs or having their caregivers perform the manipu-lation. Identifying muscles with volitional capacity is important to the achievement of this goal. In broad terms, clinical evaluation focuses on the identifi cation of several factors: Is there selective voluntary control of a given muscle? Is the muscle activated dyssynergi-cally (ie, as an antagonist in movement)? Is the muscle resistive to passive stretch? Does the muscle have fi xed shortening (contracture)? In the Gait and Motion Analysis Laboratories, dynamic EMG is acquired and examined in reference to simultaneous measure-ments of joint motion (kinematics) and ground reac-tion forces (kinetics) obtained from force platforms. Kinetic, kinematic, and dynamic EMG data augment the clinician’s ability to interpret whether voluntary function is present in a given muscle and whether that muscle’s behavior is also dyssynergic (Figure 11.1). Combined with clinical information, the laboratory measurements of muscle function often provide the degree of detail and confi dence necessary to select, aim, and optimize the rehabilitation interventions. In addition, evaluation under the effect of temporary diagnostic nerve or motor point blocks can help the clinician distinguish between obligatory and compen-satory limb postures and gait patterns (14).

and tonic stretch refl exes are tendon taps and passive stretch of a muscle group at different velocities (6,7).

Although positive signs are a common source of clinical concern and are frequently treated, negative signs may be at times more functionally disabling and diffi cult to address. Negative signs signify loss or impairment of voluntary movement assembly and production, a kind of “muscle underactivity” that, in effect, can be described as phenomena of absence (5,8).

The clinical picture is made more complex by another phenomenon that has not been classically positioned among the positive signs, namely, con-tracture or what is better described as the physical changes in the rheologic properties of muscle tissue. Contracture is well recognized by rehabilitation clini-cians as a major source of disability for patients with UMNS. Ironically, phenomena of absence and phe-nomena of presence can both provide a context for the development of contracture (9).

FUNCTIONAL IMPLICATIONS OF SPASTICITY

Fifty years ago, Nikolai A. Bernstein suggested that the basic problem of motor control relates to over-coming redundant degrees of freedom in our multi-jointed skeletal system, the multijointed limb segments that allow us to interact with the three-dimensional (3-D) world we live in. Commonly, there are multiple “agonists” and “antagonists” for virtually any move-ment direction. To match a required joint torque even across a single joint, the question regarding which muscles should be activated and at what levels of activity is likely to have a very variable answer with-out a unique solution. For a given patient, however, there may be a “unique” solution in that equinovarus deformity may be solely attributable to an overactive tibialis anterior in one patient, whereas in another, it may be an overactive tibialis posterior (9).

Patterns of limb dysfunction in the UMNS have an impact on the limb utilization for gait or other functional use. A number of muscles typically cross major joints of the extremities, and identifying the actual muscles that contribute dynamically and stati-cally to a UMNS deformity is an important key to clinical management of the resulting gait or upper limb dysfunctions (10,11). Clinical evaluation is use-ful to the analysis of movement dysfunction, but gait and motor control assessment laboratory evaluation using dynamic electromyography (EMG) and other assessment techniques is often necessary to identify the particular contributions of offending muscles with confi dence. The correct selection of target muscles that contribute to any one pattern of dysfunction may






11 BOTULINUM TOXIN IN THE TREATMENT OF LOWER LIMB SPASTICITY ■ 131

muscle strength, Ashworth, and Tardeau are exam-ples of such techniques that are frequently used.

For more information, the reader is encouraged to review Chapter 7 of this text. Passive range of motion can be used to determine the available movement for each joint but does not provide information on the cause of limitations if present. Spasticity, muscle overactivity, contracture, or pain can all play a role in limited joint passive range of motion.

Manual muscle testing allows grading of available strength if normal control is present; the grading is done using a 6-point scale, where 5 is a normal rating with ability to resist signifi cant force and 0 is unable to move. In the UMNS, testing of strength may be affected by impaired motor control, the presence of synergistic patterns, and cognitive defi cits.

The Ashworth Scale allows assessment of muscle tone; in the Modifi ed Ashworth, the rating uses a 5-point scale. The scale has only been validated for the elbow and requires the movement of the joint through its available range in 1 second. Ideally, the test should always be done in the same position and under similar conditions (15). One disadvantage is that this test does not take into consideration the presence of contracture or other factors that may limit joint motion.

The Tardeau Test was developed in the pediatric population in the mid-1960s. It attempts to assess spasticity by varying the speed of joint motion avail-able from very slow (V1) to as fast as possible (V3). The difference between the parameters permits an esti-mation of the effect of spasticity (16) (Figure 11.2).

Unfortunately, none of these assessments provides a functional perspective, such as during walking, and cannot precisely determine the source of the problem. Based on our clinical experience, methods based on a functional perspective such as those described in the following can be more helpful in this regard.

The Impact of Gait

Gait is a functional task performed by most humans. The three main functional goals of ambulation are to move from one place to another, to move safely, and to move effi ciently. These three goals are frequently compromised in the patient with residual UMNS. Most patients will be able to perform limited ambu-lation, but they will often have problems because of ineffi cient movement strategies, the presence of insta-bility or pain due to abnormal limb postures, and decreased safety. Some generalizations can be made about the gait of patients with acquired brain injury. These include a decrease in walking velocity with a reduction in the duration of stance phase and impair-ment of weight bearing in the affected limb with an

CLINICAL ASSESSMENT OF SPASTICITY

There are many assessment techniques used in rou-tine clinical examination of the patient with spastic-ity. Motor control, passive range of motion, manual

FIGURE 11.1 Subject instrumented for gait analysis data collec-tion including dynamic EMG and CODA 3-D motion sensors.

EMG, electromyography; 3-D, three-dimensional.







problematic throughout the gait cycle, meaning that they may interfere with both swing and stance phases. Stiff knee and adducted thigh are predominantly deviations of the swing phase, and both can interfere with limb clearance and advancement. The fl exed hip is considered a primary stance phase deviation.

Equinovarus. Equinovarus foot is the most preva-lent UMN posture affecting walking and requiring intervention after an acquired brain injury. The foot and ankle are turned down (Figure 11.3A), and toe curling or toe clawing may coexist. The lat-eral border of the foot is the main weight-bearing surface. Skin breakdown over the metatarsal head may develop from concentrated pressure particu-larly over the fi fth metatarsal head; weight bearing typically occurs when walking but may take place against the footrest of a wheelchair in the nonam-bulatory population. In walking, equinovarus is frequently maintained throughout stance phase and inversion may increase, causing ankle instability during weight bearing. Limited ankle dorsifl exion during early and midstance prevents the appropriate forward advancement of the tibia over the station-ary foot, promoting knee hyperextension. Impair-ment in dorsifl exion range of motion in the late stance and preswing phases interferes with push-off and forward propulsion of the center of mass, and, combined with reduce walking velocity, results in marked reduction in joint power generation. During the swing phase, the equinus posture of the foot may result in limb clearance problem, whereas the lack of appropriate posture of the foot in the stance phase may result in instability of the whole body. Under the latter presentation, correction of this problem is essential even for limited ambulation or those per-forming standing transfers.

A number of muscles may generate the abnor-mal forces with respect to the equinovarus pattern (19). Muscles that can potentially contribute to the equinovarus deformity include the tibialis anterior, tibialis posterior, long toe fl exors, gastrocnemius, soleus, extensor hallucis longus (EHL), and the weakness of the peroneus longus, peroneus brevis, and the long toe extensors. As mentioned, dynamic polyelectromyographic (poly-EMG) recordings of the aforementioned muscles in combination with clinical examination provide a more detailed understanding of the genesis of this deformity. Dynamic poly-EMG recordings often demonstrate prolonged activation of the gastrocnemius and soleus complex, as well as the long toe fl exors as the most common cause of plantar fl exion. Occasionally, the gastrocnemius and soleus may activate differentially, and treatment interventions must take this into consideration. Ankle

increase in the duration of stance time of the less affected limb (17). Ochi et al (18) reported on dif-ferences in temporo-spatial parameters of locomotion among patients with residual stroke and TBI. From a functional perspective, gait defi ciencies can be cat-egorized with respect to the gait cycle. In the stance phase, an abnormal base of support can be caused by equinovarus, toe fl exion, or ankle valgus. Limb instability can occur due to knee buckling (sudden fl exion) or hyperextension, which may result in knee joint pain or lack of trunk control. This may result in unsafe, ineffi cient, or painful walking.

During the swing phase, inadequate limb clearance caused, for example, by a stiff knee and inadequate limb advancement caused by limited hip fl exion or knee extension may interfere with the safety and energy effi ciency of walking. To identify the potential source of the problem and to focus more appropri-ately on the essence of multifactorial gait dysfunc-tion, formal gait analysis in a laboratory may be required. Combining clinical evaluation with labora-tory measurements will increase the degree of resolu-tion needed to understand the common patterns of gait dysfunction in the UMNS (17).

Patterns of UMN Dysfunction

Because of scope and space limitations, only the most common patterns of UMN dysfunction in the lower limb that affect walking have been selected for review in this chapter, and they include: (a) equin-ovarus foot, (b) hyperextended great toe, (c) stiff knee, (d) adducted (scissoring) thighs, and (e) fl exed hip (9,12). The fi rst two patterns are considered to be

FIGURE 11.2 Demonstrating the Tardeau measurement using superimposed images of very slow and very fast PROM. A dif-ference of approximately 20° can be seen between the two measures and indicative of the degree of spasticity.

PROM, passive range of motion.







fi rst one is to use the EMG data and the joint pow-ers obtained as part of the kinematic data in routine gait analysis. The second possibility is a diagnostic tibial nerve block with a short-acting anesthetic. One has to be mindful that reducing the activation of the gastrocnemius–soleus complex will tend to increase ankle dorsifl exion and that tightness of the toe fl ex-ors usually becomes more apparent as a result of the

inversion is the result of the overactivation of the tibi-alis posterior and anterior in combination with the gastrocnemius and soleus and, at times, the EHL (Figure 11.3B). If the tibialis posterior and anterior are both suspect of contributing to the ankle varus deformity, a decision has to be made about which one of the two muscles is the main contributor. Two approaches are possible for this differentiation. The

AB

FIGURE 11.3 (A) Equinovarus left foot posture after cerebrovascular accident. Patient has a large bursa under the base of the fi fth metatarsal with complaints of pain and instability during the stance phase. (B) Dynamic EMG data of the subject seen in panel (A) with equinovarus foot posture after cerebrovascular accident. Data are normalized, and vertical line at 62% indicates the initiation of the swing phase. Note overactive tibialis anterior, EHL, and gastrocnemius and soleus complex during the swing phase.

EHL, extensor hallucis longus; EMG, electromyography.







during normal walking is primarily generated by the inertial forces produced by hip fl exion. Reduction in swing phase hip fl exion may result in decreased knee fl exion. The limb appears to be functionally longer because it remains extended at the knee through-out the swing phase, resulting in toe drag that may cause tripping and falling. To achieve compensated foot clearance for this relative leg length discrepancy, the patient may attempt contralateral vaulting (early heel rise), ipsilateral circumduction, or hip hiking. All of these compensations increase energy consump-tion and can result in diminished walking capacity. EMG recordings frequently demonstrate a reduc-tion in the activation of iliopsoas (a hip fl exor) along with excessive activation of the rectus femoris, vas-tus intermedius, vastus medialis, and vastus latera-lis. An overactive gluteus maximus (a hip extensor) in the swing phase may act to restrain hip fl exion and impair swing limb advancement resulting in an extended knee pattern, and at times, excessive activa-tion or out-of-phase activation of the hamstrings may also be seen. If ankle equinus is also present, a reduc-tion in joint power generation and plantar fl exion moment may further reduce swing phase knee fl exion (14,20).

Based on clinical and laboratory fi ndings, che-modenervation with BoNT to individual heads of the quadriceps may be considered; caution in dos-ing is suggested to avoid overweakening of the knee extensor mechanism that may result in stance phase knee instability. If there is uncertainty of the quad-riceps’ force-generating capacity during walking, it may be advisable to perform a diagnostic block of the motor branch of the femoral nerve to the knee extensors with a short-acting anesthetic to better determine it. If involvement of the gluteus maximus is evident, this can also be treated with chemode-nervation with BoNT (Figure 11.5B). Treatment should also incorporate marching exercises to strengthen hip fl exors and stretch quads, and if the patient exhibits an abnormal ankle posture, appro-priate interventions for this problem should be implemented.

Adducted (Scissoring) Thigh. This deformity is char-acterized by adduction of the hip during the swing phase of locomotion. Hip adduction posturing at the end of the swing phase generates a narrow base of support during stance, ultimately making upright balance uncertain. It can also interfere with limb advancement because the adducting swing phase limb may collide with the contralateral stance limb. When adductor spasticity is complicated by hip fl exion, other functional activities such as toileting and perineal access can be affected and posture in a

toe fl exor tenodesis effect brought on by the allowed increased dorsifl exion.

Hyperextended Great Toe. Hyperextended great toe is a deformity that is characterized by toe exten-sion throughout the gait cycle, sometimes referred to as striated toe or “hitchhiker’s toe.” Ankle equi-nus and varus may accompany this foot deformity (Figure 11.4). When wearing shoes, the patient may complain of pain at the tip of the big toe, and dur-ing stance phase, abnormal concentration of forces under the fi rst metatarsal head can also produce pain. Toe extension during early and midstance affects weight bearing and can impair gait due to ineffi cient translation of the center of pressure dur-ing late stance phase. It also has an impact on center of gravity stability during stance phase single limb support. EHL hyperactivity is the main deforming force causing great toe hyperextension. A weak fl exor hallucis longus may not be able to compen-sate and offset the extension force of EHL. When equinovarus is also present, analysis of the contri-butions of tibialis anterior, tibialis posterior, gas-trocnemius, soleus, and the long toe fl exors needs to be taken into consideration as well. Chemode-nervation with BoNT or motor point injection of EHL with phenol can easily be achieved to alleviate these problems.

Stiff Knee. The stiff knee, as previously mentioned, is a swing phase deformity by defi nition. The knee is kept extended during preswing and initial swing, resulting in a reduction of the knee arc of motion with its peak less than 40° at mid-swing (normal refer-ence approximately 60° [14]). In addition, there may be delay in the timing of fl exion and a concomitant reduction in hip fl exion (Figure 11.5A). Knee fl exion

FIGURE 11.4 Hyperextended hallux after cerebrovascular accident. The patient complains of pain at the tip of the big toe and pressure under the fi rst metatarsal base.







helpful to differentiate the role of hip adduction in an obligatory-versus-compensatory pattern. Longer term interventions, such as chemodenervation with botulinum neurotoxin (BoNT), can be easily car-ried out after that. Other treatment options, such as a percutaneous phenol obturator nerve block, exist. After the intervention, aggressive stretching of the hip adductors and exercises to strengthen the hip fl exors and abductors should be implemented. Electrical stimulation to the hip abductors may be used to pro-mote strengthening (14,20).

Flexed Hip. The patient with excessive hip fl exion potentially experiences diffi culty during walking with negative impact during both phases of the

chair requires frequent repositioning of the patient (Figure 11.6). Dynamic poly-EMG recordings will frequently demonstrate overactivation of the hip adductors, medial hamstrings, and pectineus. Weak-ness of the hip abductors and the iliopsoas may also contribute to this deformity because the patient may be attempting to use the hip adductors during walk-ing in a compensatory manner to advance the limb forward during the swing phase.

For the patient with walking capacity, it is essen-tial to ascertain if the hip adductor deformity is obligatory (the result of adductor overactivity) or compensatory (the result of weak hip fl exors) because treatment will differ. If the clinician is uncertain, a diagnostic temporary obturator nerve block can be

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FIGURE 11.5 (A) Stiff knee gait evident in the swing phase in a patient with residual UMNS from TBI. Note the lack of knee fl exion during the swing phase possibly forcing the patient to use compensatory mechanisms for limb clearance, such as circumduction and hip hiking. (B) CODA 3-D kinematic data before (top) and after (bottom) treatment of stiff knee gait in the patient depicted in Figure 11.5A. Note marked improvement in left knee (solid line) peck fl exion and hip fl exion. The dashed line represents right leg and the dotted line represents normative data that are velocity matched. Data are normalized; the vertical line at 65% to 75% indicates the beginning of the swing phase. Based on dynamic EMG and gait analysis, the patient was treated with 200 U of BoNT-A (BOTOX®) injected to the right rectus femoris (100 U), vastus medialis (50 U), lateralis (50 U), and gluteus maximus (50).

3-D, three-dimensional; BoNT-A, botulinum toxin A; EMG, electromyography; TBI, traumatic brain injury; UMNS, upper motor neuron syndrome.







gait cycle (Figure 11.7). In normal gait, the hip is fl exed 30° at initial contact but thereafter extends throughout stance phase to about 10°. This defor-mity can also interfere when standing up from a seated position and during perineal care and sexual intimacy. The UMN pattern of hip fl exion is defi ned as persistent hip fl exion throughout stance. Knee fl exion deformity may develop as a consequence of severe hip fl exion deformity, because in the supine position, the knee fl exes to allow the heel to touch the bed. During walking, a shortened contralateral step results from stance phase excessive hip fl exion. Excessive hip fl exion may also affect single limb support stability of the center of gravity. Dynamic poly-EMG recordings during walking may identify overactive iliopsoas, rectus femoris, hip adduc-tors, or lack of activation of the hip extensors and paraspinals. Interventions to reduce overactive hip fl exors (iliopsoas and rectus femoris), chemode-nervation with BoNT, to these two muscles can be easily performed guided by electrical stimula-tion or ultrasound and followed by appropriate rehabilitation techniques including the implemen-tation of hip stretching and attempting long step walking (14).

THE ROLE OF BoNT IN THE TREATMENT OF SPASTICITY

Intramuscular injection of BoNT inhibits the release of acetylcholine at the neuromuscular junc-tion causing muscle weakness. Three steps are involved in the toxin-mediated paralysis: (a) inter-nalization, (b) disulfi de reduction and transloca-tion, and (c) inhibition of neurotransmitter release. The toxin must enter the nerve ending to exert its effect. OnabotulinumtoxinA injection is currently approved by the U.S. Food and Drug Administration (FDA) for the treatment of blepharospasm, facial spasm, strabismus, cervical dystonia, hyperhidro-sis, and upper limb spasticity. AbobotulinumtoxinA is approved for cervical dystonia and upper limb spasticity by the FDA and IncobotulinumtoxinA is only approved by the U.S. FDA for the treatment of cervical dystonia and blepharospasm. In Europe, Canada, and several countries in Latin America, BOTOX, Dysport, and Xeomin are also approved for the management of cerebral palsy-related and stroke-related spasticity. BoNT-B (formulated as MyoBloc® in the United States and NeuroBloc® else-where) is approved by the U.S. FDA only for the treatment of cervical dystonia. The reader is encour-aged to read other chapters of this text for further information on the topic (21,22).

FIGURE 11.6 Adducted hips in a nonambulatory patient with UMNS caused by TBI. Passive function is impaired for position-ing, dressing, and hygiene.

TBI, traumatic brain injury; UMNS, upper motor neuron syndrome.

FIGURE 11.7 Flexed hip in a patient with UMNS caused by TBI. Note short left step length caused by limitation in right hip extension.

TBI, traumatic brain injury; UMNS, upper motor neuron syndrome.







of muscle selection, dose, and effects is encouraged to allow for dose or muscle selection adjustment in future treatment cycles if necessary. In our practice, if multiple large muscles are to be injected, we try to concentrate the available dose to a few of them and we may increase dilution and use electrical stimula-tion before the treatment to enhance the effect and consider using other agents such as phenol injected to other muscles or motor nerves to achieve a com-plete treatment strategy. With the currently available information, we recommend not injecting BoNT in patients who are pregnant or lactating or have sig-nifi cant medical comorbidities (22,25,26).

Before using BoNT for the clinical management of spasticity, the physician should be knowledge-able about the diagnosis and medical management of the condition producing the UMNS. The physi-cian should be profi cient in the relevant anatomy and kinesiology and have a clear understanding of the potential benefi ts of unmasking function and of the limitations of this therapeutic intervention. Unlike the patient with dystonia where voluntary capacity is not an issue, spastic muscles may very well have evidence or potential for voluntary capac-ity, which the clinician would like to preserve or unmask, and, therefore, titration of the paralytic effect of the toxin becomes a much more critical factor in its administration (5). The duration of toxin effectiveness ranges between 10 weeks and 4 months. In our experience, patients have received doses greater than 600 U of BOTOX or 1,500 U of Dysport at 3-month intervals for more than 3 years without evidence of loss of effectiveness of the medication. Esquenazi et al (26) have reported an increase in duration of effect over time under a similar treatment paradigm.

The toxin might be an effective tool to “simulate” the effects of surgery to the benefi t of the surgeon and patient alike (24).

The strategy of performing a BoNT-A injection is as follows: the skin is prepared by cleaning it with alcohol before insertion of a Tefl on-coated, 25-gauge stimulating injecting needle. The electri-cally conductive inner core of the tip of the needle is used to pass current to the tissues or to record EMG activity; alternatively ultrasound can be used to locate the needle position within the desired muscle. Before or soon after injection, muscle acti-vation should be encouraged to increase the avail-ability of Synaptobrevin 2, a major factor in the uptake and internalization of BoNT-A. As the paralytic effect appears evident, aggressive stretch-ing, muscle reeducation, and functional training are important parts of the treatment protocol (17) (Table 11.1).

The purpose of BoNT injections in the manage-ment of the UMNS is to reduce force produced by a contracting overactive muscle or muscle group. A reduction in muscle tension can lead to improvement in passive and active range of motion and allows for more successful stretching of tight musculature. More subtly, and more importantly as well, improved motor control and posture may provide the patient with the opportunity to develop compensatory behaviors dur-ing functional activities (9). A reduction in muscle overactivity in one muscle or muscle group may have consequences for tone in other muscle groups of the limb through a reduction in the overall effort required to perform movement and/or through changes in sen-sory information going to the central nervous system from that limb, and may infl uence more distant mus-cles or benefi t function (21). Finally, the application of external devices such as braces, splints, casts, and even shoes can be facilitated by interventions with chemodenervation.

BoNT is injected directly into an offending mus-cle. The major advantages in its use are the ease of application that permits its injection without anes-thesia and its predictable effect. The most common adverse effect is excessive weakness of injected mus-cles, which occasionally spreads to nontarget mus-cles. Given suffi cient time, when the patient has a strong response to the paralytic effect of the toxin with excessive weakening, strength will gradually return. No adverse effect on the sensory system are evident with botulinum toxin A (BoNT-A), but pain relief when pain is present has been reported in some patients (22,23). In rare cases, nausea, headache, and fatigue have also been reported. No anaphylac-tic response has ever been reported due to BoNT-A injection. Depending on the size of the muscle being injected, therapeutic doses of BOTOX have ranged between 10 and 400 U. Because of the potential risk of migration out of the muscle and the possibility of antibody formation, usually doses not greater than 600 U of BOTOX and Xeomin or 1,500 U of Dysport are administered in a single-treatment ses-sion (24). This may be suffi cient, however, to treat a number of muscles in that one session (22,25). In cases of accidental poisoning, an antitoxin is avail-able. Based on clinical experience and prospective randomize trials, the development of resistance to BoNT-A therapy does not impact the management of patients with muscle overactivity. However, to minimize the risk of immunoresistance, it is rec-ommended that clinicians use the smallest possible effective dose, extend the interval between treat-ments for at least 3 months or longer, and avoid the use of booster injections in between treatment or mix different toxin brands. Careful documentation







are well recognized by rehabilitation clinicians as a major source of disability for patients with UMNS. This syndrome produces upper and lower limb pat-terns of dysfunction that commonly affect more than one joint at a time and that need to be correlated with their clinical presentation and resulting impair-ment. Identifying the specifi c possible source of the deforming force is of the essence for proper treatment planning and intervention. Dynamic poly-EMG and motion analysis can be used to identify the contribu-tors to the specifi c pattern, and when the technology is not available, thorough careful clinical assessment and selected use of diagnostic nerve blocks can be used to develop a successful BoNT chemodenerva-tion management strategy for this patient population.

CONCLUSION

This chapter reviewed the most salient points related to the clinical presentation of UMNS in the lower limb especially as it affects walking. Negative signs of the UMNS include weakness and loss of dexter-ity. Positive fi ndings such as spasticity, increased pha-sic and tonic stretch refl exes, clonus, cocontraction, released fl exor refl exes, spastic dystonia, and associ-ated reactions or synkinesias can all be summed up in the term “muscle overactivity,” with resulting gait impairment. The clinical picture is made more complex by changes in the viscoelastic properties of muscle and other soft tissues in the form of a con-tracture. The combined effects of these phenomena

TABLE 11.1

SUGGESTED BOTOX DOSING FOR ADULTS

Clinical Pattern Potential Muscle Involved BOTOX Dose U/Session

Dysport Dose U/Session

No. of Injection Sites

Equinovarus foot Gastrocnemius 50–250 150–300 2–4

Soleus 50–200 150–300 2–4

Tibialis posterior 25–150 50–250 1–2

Flexor halucis longus 25–75 50–150 1–2

Flexor digitorum longus 25–100 50–200 1–2

Flexor digitorum brevis 20–40 50–100 1

Tibialis anterior 20–120 50–200 1–3

Flexed hip Iliacus 50–150 150–250 2

Psoas 50–150 150–250 2

Rectus femoris 75–200 200–450 2–4

Flexed knee Medial hamstrings 50–200 150–450 2–3

Lateral hamstrings 50–200 150–450 2–3

Gastrocnemius (as knee flexors) 50–150 150–250 2–4

Extended (stiff) knee Rectus femoris 50–200 150–450 2–4

Vasti 50–150 150–250 2–4

Hyperextended toe (striatal)

EHL 20–100 50–200 1–2

Adducted thigh Adductor longus/magnus/brevis 75–300 200–500 4–6

EHL, extensor hallucis longus.

Source: Modifi ed from Ref. (26). Esquenazi A, Albanese A, Chancellor MB, et al. Evidence-based review and assessment of botulinum neurotoxin for the treatment of adult spasticity in the upper motor neuron syndrome. Toxicon. 2013;67:115–128.







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