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(BQ) Part 1 book “Neurological rehabilitation - Spasticity and contractures in clinical practice and research” has contents: Definition and measurement of spasticity and contracture, pathophysiology of spasticity, the clinical management of spasticity and contractures in cerebral palsy, clinical management of spasticity and contractures in stroke,… and other contents.
Neurological Rehabilitation Spasticity and Contractures in Clinical Practice and Research Rehabilitation Science in Practice Series Series Editors Marcia J Scherer, PhD President, Institute for Matching Person and Technology Professor, Physical Medicine & Rehabilitation, University of Rochester Medical Center Dave Muller, PhD Visiting Professor, University of Suffolk Past and Founding Chair of Chamber of Commerce Editor-in-Chief, Disability and Rehabilitation Director, Ipswich Central Ltd Paediatric Rehabilitation Engineering: From Disability to Possibility, edited by Tom Chau and Jillian Fairley Quality of Life Technology Handbook, Richard Schultz Computer Access for People with Disabilities: A Human Factors Approach, Richard C Simpson Computer Systems Experiences of Users with and Without Disabilities: An Evaluation Guide for Professionals, Simone Borsci, Maria Laura Mele, Masaaki Kurosu, and Stefano Federici Rethinking Rehabilitation: Theory and Practice, edited by Kathryn McPherson, Barbara E Gibson, and Alain Leplège Human-Computer Interface Technologies for the Motor Impaired, edited by Dinesh K Kumar and Sridhar Poosapadi Arjunan Rehabilitation: A Post-Critical Approach, Barbara E Gibson Wheelchair Skills Assessment and Training, R Lee Kirby Robotic Assistive Technologies: Principles and Practice, edited by Pedro Encarnỗóo and Albert M Cook Geriatric Rehabilitation: From Bedside to Curbside, edited by K Rao Poduri, MD, FAAPMR Devices for Mobility and Manipulation for People with Reduced Abilities, Teodiano Bastos-Filho, Dinesh Kumar, and Sridhar Poosapadi Arjunan Multiple Sclerosis Rehabilitation: From Impairment to Participation, edited by Marcia Finlayson Neuroprosthetics: Principles and Applications, edited by Justin Sanchez Ambient Assisted Living, Nuno M Garcia and Joel J.P.C Rodrigues Assistive Technology for Blindness and Low Vision, Roberto Manduchi and Sri Kurniawan Rehabilitation Goal Setting: Theory, Practice and Evidence, edited by Richard J Siegert and William M M Levack Assistive Technology Assessment Handbook, Second Edition, edited by Stefano Federici and Marcia Scherer Neurological Rehabilitation: Spasticity and Contractures in Clinical Practice and Research, edited by Anand D Pandyan, Hermie J Hermens, Bernard A Conway Neurological Rehabilitation Spasticity and Contractures in Clinical Practice and Research Edited by Anand D Pandyan Hermie J Hermens Bernard A Conway CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2018 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S Government works Printed on acid-free paper International Standard Book Number-13: 978-1-4665-6544-9 (Hardback) International Standard Book Number-13: 978-1-315-37436-9 (eBook) This book contains information obtained from authentic and highly regarded sources Reasonable efforts have been made to publish reliable data and information, but the author and publisher cannot assume responsibility for the validity of all materials or the consequences of their use The authors and publishers have attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint Except as permitted under U.S Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers For permission to photocopy or use material electronically from this work, please access www.copyright com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400 CCC is a not-for-profit organization that provides licenses and registration for a variety of users For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe Library of Congress Cataloging‑in‑Publication Data Names: Pandyan, Anand, editor | Hermens, Hermie J., editor | Conway, Bernard A., editor Title: Neurological rehabilitation : spasticity and contractures in clinical practice and research / [edited by] Anand Pandyan, Hermie J Hermens, and Bernard A Conway Other titles: Neurological rehabilitation (Pandyan) | Rehabilitation science in practice series Description: Boca Raton, FL : CRC Press/Taylor & Francis Group, 2018 | Series: Rehabilitation science in practice series | Includes bibliographical references and index Identifiers: LCCN 2017058710| ISBN 9781466565449 (hardback : alk paper) | ISBN 9781315374369 (ebook) Subjects: | MESH: Muscle Spasticity therapy | Contracture therapy | Neurological Rehabilitation Classification: LCC RC935.S64 | NLM WE 550 | DDC 616.85/6 dc23 LC record available at https://lccn.loc.gov/2017058710 Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com Contents Editors vii Contributors ix Definition and Measurement of Spasticity and Contracture .1 Anand D Pandyan, Bernard A Conway, Hermie J Hermens and Garth R Johnson Pathophysiology of Spasticity 25 Jens Bo Nielsen, Maria Willerslev-Olsen and Jakob Lorentzen Functional Problems in Spastic Patients Are Not Caused by Spasticity but by Disordered Motor Control 59 Jakob Lorentzen, Maria Willerslev-Olsen, Thomas Sinkjær and Jens Bo Nielsen The Clinical Management of Spasticity and Contractures in Cerebral Palsy 79 Andrew Roberts Clinical Management of Spasticity and Contractures in Stroke 101 Judith F M Fleuren, Jaap H Buurke and Alexander C H Geurts Clinical Management of Spasticity and Contractures in Spinal Cord Injury 135 Martin Schubert and Volker Dietz Clinical Management of Spasticity and Contractures in Multiple Sclerosis 175 Lorna Paul and Paul Mattison Clinical Assessment and Management of Spasticity and Contractures in Traumatic Brain Injury 203 Gerard E Francisco and Sheng Li Hereditary Spastic Paraparesis and Other Hereditary Myelopathies 235 Jon Marsden, Lisa Bunn, Amanda Denton and Krishnan Padmakumari Sivaraman Nair Index 289 v http://taylorandfrancis.com Editors Anand D Pandyan, PhD, is Professor for Rehabilitation Technology and Head of the School of Health & Rehabilitation at Keele University He originally trained as a bioengineer and has a special interest in neurological rehabilitation, clinically usable measurement and applied clinical research His interest in spasticity started during his PhD study (Bioengineering Unit, University of Strathclyde, Glasgow) and he completed a five-year postdoctoral training period at the Centre for Rehabilitation and Engineering Studies (CREST), Newcastle upon Tyne (with Professors Garth Johnson and Michael [Mike] Barnes) exploring the phenomenon of spasticity in stroke His current portfolio of research projects, carried out in partnership with therapists and local clinicians, is aimed at: developing a better understanding of the pathophysiological basis of spasticity and its impact on people with upper motor neurone lesions; identifying the therapeutic benefits (and mechanisms of action) associated with treatment involving electrical stimulation; and exploring the effects of early antispasticity treatment and studying their long-term impacts Much of his current research is focussed on neurological patients with severe levels of disability Hermie J Hermens, PhD, earned his master’s in Biomedical Engineering at the University of Twente His PhD, on surface EMG modelling, processing and clinical applications, was also undertaken at the University of Twente, and he subsequently became Professor of Neuromuscular Control at the same institution He was the initiator and coordinator of the SENIAM project, which resulted in a broadly accepted worldwide standard on surface EMG electrode properties and their placement on the muscles He was, together with Anand D Pandyan, actively involved in the European SPASM project, which resulted in important new insights into the definition of spasticity and procedures and methods for assessing spasticity in a quantitative way Dr Hermens was co-founder of Roessingh Research and Development (RRD), originating from the Roessingh Rehabilitation Centre, which has now grown into the largest institute in the area of rehabilitation technology and telemedicine in the Netherlands He gradually switched his research area from rehabilitation technology towards combining biomedical engineering with ICT to enable remote monitoring and telemedicine In 2008, he became Professor of Telemedicine and Head of the Telemedicine Research Group, at UTwente; in 2010 Director of Telemedicine at RRD and, in 2012, Director of Technology at the Centre for Care Technology Research (CCTR) and Visiting Professor at the Caledonian University in Glasgow vii viii Editors Bernard A Conway, PhD, is Professor in Biomedical Engineering at the University of Strathclyde, where he co-directs the Centre for Excellence in Rehabilitation Research He earned his PhD in Neurophysiology from the University of Glasgow and since then has focussed his research interests on problems related to the loss of control of movement in patients with neurological conditions including spinal cord injury, movement disorders, and limb loss Over his career he has enjoyed close collaboration with clinical colleagues, giving his research a translational perspective The multidisciplinary nature of his research has led to its publication in a diversified group of journals He has also been actively involved in supporting funding agencies in various advisory capacities linked to bioengineering, rehabilitation, health technologies, and ageing He currently is a trustee of the Institute of Physics and Engineering in Medicine and Medical Research Scotland Contributors Lisa Bunn School of Health Professions Faculty of Health and Human Sciences University of Plymouth Plymouth, United Kingdom Jaap H Buurke Roessingh Research and Development University of Twente Enschede, Netherlands Bernard A Conway Department of Biomedical Engineering University of Strathclyde Scotland, United Kingdom Volker Dietz Spinal Cord Injury Center University Hospital Balgrist Zürich, Switzerland Amanda Denton School of Health Professions Faculty of Health and Human Sciences University of Plymouth Plymouth, United Kingdom Judith F M Fleuren Roessingh Rehabilitation Centre Roessingh Research and Development Enschede, Netherlands Gerard E Francisco Department of Physical Medicine and Rehabilitation University of Texas Health Science Center and NeuroRecovery Research Center TIRR Memorial Hermann Hospital Houston, Texas Alexander C H Geurts Radboud University Medical Centre Department of Rehabilitation Nijmegen, Netherlands Hermie J Hermens Roessingh Research and Development University of Twente Enschede, Netherlands Garth Johnson ADL Smartcare Ltd Newcastle University Newcastle, United Kingdom Sheng Li Department of Physical Medicine and Rehabilitation University of Texas Health Science Center and NeuroRecovery Research Center TIRR Memorial Hermann Hospital Houston, Texas ix 120 Neurological Rehabilitation The Ashworth Scale and its modified version are still common practice in the clinical setting and are widely used in scientific research as well They are both ordinal scales that aim to score spasticity However, to be a measure of spasticity, a scale can only be valid when the increase in resistance to passive movement is caused by an increase in neural, stretch-related reflex activity (Vattanasilp and Ada, 1999; Pandyan et al., 2003) This is probably not the case, as the resistance to passive movement is a sum total of reflex muscle activity and non-neural mechanical characteristics (Pandyan et al., 1999; Fleuren et al., 2010) Therefore, adjusting the measured construct into the resistance to passive movement of a limb, as perceived by the clinician, would be more consistent with what is actually being rated (Table 5.2) Although the methodological value of the adapted scale might be questioned, it completes the clinical examination without the misconception of measuring true spasticity Biomechanical measurement methods assess muscle activation indirectly, by calculation of the applied force (or moment) needed for passive rotation of a joint over a certain range This rotation can be performed manually, by instrumented displacement, or by gravity, like in the pendulum test for the knee (Vodovnik et al., 1984) Obviously, the complexity to discriminate the contributions of neural and non-neural components to the resistance to passive movement is one of the main limitations of these methods Although new techniques with application of haptic robots and advanced modelling techniques are in progress to discriminate more accurately between neural and mechanical components of velocity-dependent stiffness (De Gooijer et al., 2013, Sloot et al., 2015), these are not yet accessible for clinical use Second, agreed protocols for the tests and normative data of age-matched controls are lacking in the current literature (Wood et al., 2005) TABLE 5.2 Perceived Resistance to Passive Movement (PRPM) Test Perceived Resistance to Passive Movement No increased resistance Slightly increased resistance (a catch) when the limb is moved in flexion or extension More marked increase in resistance, but limb easily moved Considerable increase in resistance, passive movement is difficult Limb is rigid in flexion or extension Technique: Patient in relaxed position (document position of the patient) Instruct the patient not to assist or oppose the movement First, test the passive range of motion of the joint by slow flexion or extension Subsequently, perceived resistance is assessed within the entire range with a faster movement, covering the whole range within second The movement can be repeated maximally times (note the lowest score) Source: With permission from Fleuren J, Voerman G, Nene A, Snoek G, Hermens H Protocol for spasticity assessment in patients with complex spasticity Roessingh Rehabilitation Centre and Roessingh Research and Development, Enschede, 2012 (not published) Clinical Management of Spasticity and Contractures in Stroke 121 With neurophysiological measurement methods, electrical activity of involved muscles is measured The use of the Hoffmann reflex, the electrical equivalent of the mechanical tendon reflex, has been studied extensively (Voerman et al., 2005) The same accounts for some other electrically elicited reflexes However, their clinical relevance is limited The use of surface electromyography (sEMG) for the recording of (reflex) muscle activity during functional tasks or during passive movement can be a valuable addition, when applied in a standardised way The construct validity is potentially good, as it comes close to the definition of spasticity However, due to large inter- and intra-subject variability, parameters related to intensity of muscle activity cannot be used reliably Interpretation of data is mainly dependent on timing parameters, which can be compared to available datasets of healthy subjects during a standardised task, such as walking Timing errors represent any inappropriate phasing of muscle activity The activity of any muscle may be prolonged or shortened, continuous or absent Its onset and cessation may be premature or delayed Each of these phasing errors may alter the pattern of sequential movements during gait (Perry and Burnsfield, 2010) In the case of “overactivity,” the inappropriate timing may be related to altered reflex threshold values, but it can also be related to abnormal efferent drive (De Niet et al., 2011) 5.6.2 Assessment of Spasticity: Activity and Participation When the goal of treatment is to improve daily functioning, other methods should be considered to assess (the functional consequences of) spasticity In general, the association between a decrease in spasticity and an improvement of functioning is rather weak (Ada et al., 1998) However, an individual patient may benefit from spasticity treatment when it allows less effort for the performance of a specific activity For example, a decrease in spasticity of the elbow flexor muscles can increase the reaching distance and, consequently, improve the utility of the hand In general, detailed history-taking of the patients’ perception and needs is an essential first step Self-report instruments, such as the Canadian Occupational Performance Measure, the Goal Attainment Scale, or Visual Analogue Scaling (using a well-defined construct), may be helpful in this process When treatment aims to improve arm or hand capacity in a stroke patient, the Action Research Arm Test (Lyle, 1981) or the Stroke Upper Limb Capacity Scale (Houwink et al., 2011) can be chosen to evaluate the effects of treatment For the improvement of gait, timed walking tests, e.g., the 10-meter Walking Test (Collen et al., 1990), 6-minute Walking Test (Eng et al., 2002), and Timed Up and Go Test (Podsiadlo et al., 1991) are easily applicable For more accurate diagnostics of spasticity during gait, for example, when neuromuscular blocks or ankle-foot surgery is considered, instrumented gait analysis with kinematic recording and dynamic EMG is required 122 Neurological Rehabilitation Example: Patient W Mrs W is a 57-year-old patient who suffered a left-sided stroke years ago, which led to right-sided hemiplegia and mild cognitive impairments She can walk approximately 100 meters outside with a wheeled walker, but starts toe-dragging when walking longer distances Because of hyperextension of the right knee during stance phase she underwent phenol blocks of the right tibial nerve several times, with fairly good results However, during swing phase stiff knee gait is observed Mrs W hopes to be able to walk longer distances without tripping Her physiatrist suggests instrumented gait analysis The clinical question is whether the reduced foot clearance is related to decreased knee flexion in swing phase and – if so – to assess the cause Is the stiff knee a result of a lack of propulsion force from the calf muscles, is it caused by overactivity of the rectus femoris muscle during swing, or both? For this analysis measurement of joint angles, ground reaction force and dynamic electromyography of gastrocnemius and/or soleus muscle, rectus femoris, and vastii is needed 5.7 Management of Spasticity after Stroke As emphasised in earlier paragraphs, spasticity treatment is indicated only when its presence is considered problematic Decision-making is based on the patients’ needs and characteristics, such as the distribution of spasticity, the perceived degree of discomfort, and the secondary risks of spasticity On the other hand, clinical decisions depend on the available treatment options, their invasiveness and reversibility (Table 5.3) It can be helpful to distinguish between focal, regional, multifocal, or generalised spasticity Focal spasticity is limited to one or a few muscles TABLE 5.3 Overview of Treatment Methods in Terms of Invasiveness and Reversibility I Noninvasive methods • Elimination of provocative factors • Physical therapy • Oral medication II Invasive, reversible methods • Nerve blocks • Neuromuscular blocks • Intrathecal medication III Invasive, permanent methods • Neurosurgical procedures • Orthopedic procedures Clinical Management of Spasticity and Contractures in Stroke 123 acting at the same joint, e.g., elbow flexors Regional spasticity includes a group of muscles innervated by the same (e.g., the tibial) nerve Generalised spasticity is seen when spasticity is not limited to a muscle group of muscle synergy 5.7.1 Noninvasive Methods Noninvasive treatment options with temporary effect are usually a first step in spasticity treatment A decrease in spasticity provides new information about the actual impact of spasticity and its contribution to the clinical problem First, spasticity-provoking factors need to be identified and eliminated Suddenly increasing spasticity can be a response to a certain internal or external stimulus A variety of factors can provoke this increase (Phadke et al., 2013) Any physical stimulus is a possible provoking factor, such as pressure sores, infection, constipation, or pain Clinicians should routinely examine for spasticity-triggering factors, e.g., by evaluation of proper positioning, by regular skin inspection, and adequate management of bladder and bowel function In addition, psychological factors may affect the degree of spasticity Emotional stress, anxiety, and being rushed to perform an activity are described to increase self-reported spasticity (Phadke et al., 2013) Education of the patient and their carers is highly relevant in this respect Physical therapy is not primarily aimed at spasticity reduction In stroke patients, physical therapy is commonly applied to facilitate active muscle control and to maintain the joints’ range of motion and muscle length There are some techniques that can reduce spasticity, but only for a short time period, such as application of heat, stretching of the muscles, and hippotherapy Surface neuromuscular electrical stimulation is used, but spasticity treatment is usually not the main goal Although the intervention may have a short-term inhibiting effect on spasticity, possibly via reciprocal inhibition by stimulation of the (non-spastic) antagonist or by exhausting the stimulated spastic muscle, a long-term effect on upper limb spasticity in stroke patients without functional arm movement has not been shown (Malhotra et al., 2013) Post-stroke, orthotic devices are often applied to the wrist and hand Although it is controversial as to whether orthotic treatment is effective in the reduction of muscular contracture (Tyson and Kent, 2011), it is suggested that in combination with botulinum toxin treatment, prescription of an orthotic device may aid in the preservation of muscle length Oral spasmolytic drugs are usually considered in more generalised spasticity Baclofen, a gamma-aminobutyric acid (GABA) agonist, is often used as the first-choice drug in patients with spasticity It reduces the motor output of spastic muscles, as GABA is one of the main inhibiting neurotransmitters in the central nervous system, leading to hyperpolarisation of the post-synaptic membrane of the 1a afferent The optimal dosage must be individually evaluated Sedation is a common side effect in stroke patients, potentially leading to (increase in) attention and memory deficits, ataxia, 124 Neurological Rehabilitation and confusion Benzodiazepines enhance the inhibiting effect of GABA, but obviously a sedative effect may be present Tizanidine, an alpha-2-adrenerge agonist, has an indirectly inhibiting effect on polysynaptic reflexes, probably via facilitation of glycine, another important inhibitory neurotransmitter in the central nervous system Dantrolene sodium is a postsynaptic muscle relaxant that lessens excitation-contraction coupling in muscle cells, probably by interfering with the calcium release from the sarcoplasmic reticulum An advantage of this peripherally acting drug is a lower risk of central side effects However, both dantrolene sodium and tizanidine have a potential for hepatotoxicity, so liver function examination should be performed at regular intervals Despite the widespread use, the evidence for the efficacy of orally administered antispastic agents is scarse and weak (Montane et al., 2004) In placebo- controlled trials with dantrolene, tizanidine, baclofen, or diazepam, the experimental drug was significantly better than placebo in patients with stroke, but the therapeutic effect was modest Adverse effects were generally more frequent in the active treatment groups than in the placebo groups, up to 64% in a dantrolene group (Ketel and Kolb, 1984; Katrak et al., 1992) Drowsiness, weakness, and fatigue were most often reported Therefore, generally speaking, these drugs should be applied cautiously for spasticity treatment after stroke Particularly when the aim is to improve function, their effect is often disappointing Nonetheless, specific indications such as symptom reduction, especially during the night, or presence of otherwiseintractable spasticity may justify their use 5.7.2 Invasive, Reversible Methods For the treatment of focal or regional spasticity, different types of neuromodulation can be useful options Neurolysis of well-accessible motor branches of peripheral nerves impairs the conduction along that nerve The most frequently used agents for this procedure are phenol and alcohol The effect is not permanent and the duration is highly variable, on average about months In stroke patients, a nerve block of the tibial nerve, a mixed motor and sensory nerve to the calf muscles, tibialis posterior, and toe flexors, with phenol 5–7% solution is the most commonly applied The proper indication is the presence of hindering clonus of the ankle plantar flexors, interfering with stance stability Other well-accessible nerves are the musculocutaneous nerve (which innervates a.o elbow flexors) and obturator nerve (for disabling hip adductor spasticity) However, blocks of mixed nerves with phenol, such as the tibial nerve, carry the risk of neuropathic pain in the sensory region of the nerve Since botulinum toxin has appeared on the market and was licensed for spasticity treatment, the use of nerve blocks has decreased In particular the more difficult procedures have become less popular Nevertheless, some clinicians claim greater clinical efficacy of phenol for specific indications (Manca et al., 2010) Clinical Management of Spasticity and Contractures in Stroke 125 Nowadays, intramuscular injection of botulinum toxin is an established, well-tolerated, but relatively expensive treatment for focal spasticity Botulinum toxin prevents the release of acetylcholine from the pre-synaptic nerve terminals, thus blocking the peripheral cholinergic transmission at the neuromuscular junction This results in reduced muscle contraction The clinical effects are dose-dependent and temporary Usually, the effects taper off after to months Botulinum toxin is injected in the muscle belly of specifically selected muscles As it diffuses within the muscles, the injections not have to be placed precisely in the region of motor endplate (of which the exact location is usually unknown), which makes the procedure fairly easy Nevertheless, ultrasound guided injections are recommended for proper muscle targeting Adequate dosages and concentrations for spasticity treatment with intramuscular injections of botulinum toxin are extensively described in different guidelines There is a substantial body of evidence for the effectiveness of botulinum toxin in the management of upper and lower limb spasticity in stroke patients However, its contribution to the improvement of upper limb function has not been clearly established (Shaw et al., 2011) In general, the focus of botulinum toxin treatment in the upper limb is on improving posture and passive function of the non-functional arm and hand, with the aim to support hygiene and the independent performance of various activities of daily life, such as grooming, dressing, etc The effects of botulinum toxin injections on active function of the upper limb are less strongly supported by the literature As for the lower limb, focal spasticity interfering with the prerequisites of gait, as described in paragraphs 5.4.1 and 5.4.2, can effectively be treated with botulinum toxin Particularly the triceps surae, posterior tibial, rectus femoris, extensor hallucis and toe flexor muscles are fairly easily accessible with ultrasound guidance or electrical stimulation If spasticity causes multifocal problems, e.g., both in the affected upper and lower limb, botulinum toxin can be helpful as well, but dose limitations may reduce its applicability Therefore, additional strategies must be considered Due to its reversibility, repeated treatment may be required over several years Botulinum toxin has shown sustained activity with repeated use However, a lack of response can occur, possibly due to inaccurate selection of the correct muscle, inadequate injection technique, increasing non-neural contribution to the muscle stiffness, or – rarely – the presence of neutralising antibodies (Wissel et al., 2009) For some patients, repeated injections may be undesirable Therefore, an alternative approach is to use botulinum toxin treatment as a diagnostic procedure prior to surgical techniques (see next paragraph) The reversibility gives the opportunity to evaluate the effect without permanent consequences Intrathecal baclofen (ITB) might be an attractive option in case of more generalised spasticity Unlike oral baclofen, the intrathecal route bypasses the blood-brain barrier, thereby dramatically reducing the required dose and minimising the occurrence of side effects In the literature on ITB in stroke, 126 Neurological Rehabilitation significant reduction of spastic hypertonia in upper and lower limbs has been described (Meythaler et al., 2001; Ivanhoe et al., 2006) without affecting the strength of the unaffected side In addition, improvement of hemiplegic gait was reported Catheter tip placement and dose adjustments after ITB pump implantation have a significant influence on clinical outcomes ITB distribution can be influenced by the location of the catheter tip and by changing the infusion mode When only spasticity in the leg is aimed to treat, catheter tip location in the lower thoracic region will suffice It is subject of discussion whether, in case spasticity in the upper limb must be reduced as well, the catheter tip should be located more cranially in the high thoracic region or at the cervical level (Heetla et al., 2014) In ambulatory stroke patients, a test phase with an external pump, prior to definitive pump implantation, is highly recommended, to make sure that walking ability is preserved during treatment (Bleyenheuft et al., 2007) 5.7.3 Invasive, Permanent Methods Nonsurgical management of spasticity provides temporary relief of symptoms and does not interfere with spontaneous recovery after stroke Surgical intervention should be avoided during this time In the chronic phase of stroke, roughly starting after months when the clinical condition has stabilised, surgical management can be valuable In the nonfunctional upper limb, problems with cosmetics and hygiene are addressed mostly Persistent stiffness in the arm or a clenched fist may be difficult and painful to handle during washing and dressing In addition, patients may have objections against repeated botulinum toxin injections In a functional hand, surgeons tend to hold back due to the risk of loss of active function In the lower limb, functional goals are easier to pursue When the aim is to improve gait, surgical intervention should be based on instrumented gait analysis Neurosurgical procedures are uncommon in stroke patients Selective neurotomy of the tibial nerve is described in a Belgian study (Bollens et al., 2013) as an alternative treatment for overactivity of the calf muscles In this study, triceps surae, tibialis posterior, and flexor hallucis longus muscles were denervated selectively and permanently, which resulted in a long-lasting effect On gait parameters, such as ankle kinematics during stance and swing phase, tibial nerve neurotomy and botulinum toxin treatment showed similar effect Orthopedic or plastic surgery (tendon lengthening and/or transfer) is indicated in the case of fixed muscle contracture or to adjust imbalanced muscle activity Treatment of spasticity is usually not the primary goal, although reduction of spasticity may be a desired secondary effect, considered a result of an altered threshold for stretch reflex activity due to the increased length In the spastic lower limb, several surgical techniques can be performed for correction of deformities (Kamath et al., 2009) Some procedures address the negative consequences of spasticity on gait In general, these options should be preserved for patients with at least a fair prognosis with respect to regaining Clinical Management of Spasticity and Contractures in Stroke 127 walking ability For example, a commonly performed procedure is the percutaneous Achilles tendon lengthening, during which three small incisions are made at the back of the ankle along the Achilles tendon, one laterally and two medially The tendon stretches as the fibres are cut and the ankle is dorsiflexed to the desired angle (Canale and Beaty, 2008) In the case of a structural pes equinovarus, lengthening of spastic soleus and/or gastrocnemius can be performed in combination with release of posterior tibial muscle to improve ankle-foot stability during the stance phase as well as to provide proper prepositioning of the foot for loading Prior to surgery, the effect of weakening of the muscles can be evaluated by performing a neuromuscular block If a dynamic pes varus deformity is present during swing phase, a split anterior tibial tendon transfer can be performed, provided that the tibialis anterior shows sufficient muscle strength The lateral half of the anterior tibial tendon is released from its insertion and transferred to the cuboid bone (Canale and Beaty, 2008) If the tibialis anterior is too weak, an alternative may be to transfer the tendon of an overactive posterior tibial muscle to the cuboid bone to support a balanced dorsiflexion of the foot An arthrodesis of the talonavicular joint may also support a balanced ankle dorsiflexion when the lateral foot elevators (long toe extensors and peroneus tertius) are paretic Extensor hallucis longus transfer to the mid-dorsum of the foot can be performed to treat a troubling striatal toe, but may also provide additional dorsiflexion force for the ankle Spasticity of the long toe flexor muscles often leads to clawing of the toes and contributes to equinus deformity of the foot Particularly after Achilles tendon lengthening, as the foot is brought into a more plantigrade position, shortening of the long toe flexors might be revealed In that case, concomitant correction of claw toes is advised, e.g by tenotomy of the long toe flexors In the case of forefoot equinus, release of the short toe flexors (intrinsics) should be considered as well (Canale and Beaty, 2008) In the thigh, tendon transfer of rectus femoris can be considered in a patient with stiff knee gait When dynamic EMG analysis reveals a rectus femoris muscle that is abnormally active during swing phase, a diagnostic neuromuscular block of the rectus femoris can be performed, to assess whether it leads to improvement on peak knee flexion during swing (Tenniglo et al., 2014) For a medial transfer, the rectus femoris is separated from the vastii The rectus tendon is then dissected and transferred through the medial intermuscular septum to the semimembranosus (Canale and Beaty, 2008) In the upper extremity, spasticity reduction is observed after release of elbow flexors (brachioradialis, biceps brachii, and/or brachialis muscles), pronator teres, and wrist flexors (flexor carpi ulnaris and radialis, and the palmaris longus) Muscles that contribute to finger flexion deformities are flexor digitorum superficialis and profundus, which can be fractionally lengthened by incising the tendon fibres obliquely at the musculotendinous junction However, superficialis to profundus transfer will provide more lengthening and opening of the hand After release of the extrinsic finger flexors, persisting intrinsic muscle spasticity may be revealed, leading to an intrinsic-plus 128 Neurological Rehabilitation deformity In that case, surgical tendon release of the intrinsic muscles must be performed as well Tendon transfers, for example, transfer of the flexor carpi ulnaris tendon to the extensor carpi radialis brevis tendon to provide for stronger wrist extension, are uncommon in stroke patients Generally, patients lack active wrist extension, and – if present – wrist flexor lengthening is believed to provide sufficient wrist extension (Tafti et al., 2008) 5.7.4 Management Strategy for Stroke Patients with Spasticity When an indication for treatment of problematic spasticity is assessed, a stepwise approach is recommended Potential provoking factors of spasticity must always be identified and eliminated if present In the early phase after stroke reversible treatment options are preferred Depending on the distribution of spasticity, focal spasmolysis is often the first choice, because of its effectiveness and reversibility Focal injections have the drawback of being invasive, but debilitating side effects, as observed frequently after oral medication, are much less common Oral medication can be prescribed when more generalised spasticity is present, but its use is mostly restricted to symptom reduction, especially during the night More permanent treatment options become relevant in the chronic phase, roughly from months post-stroke onwards, as an alternative to repeated focal injections Selective neurotomy of the tibial nerve may be an effective substitute, but it is rarely performed to treat spastic pes equinovarus up till now Otherwise, tendon lengthening and release procedures, possibly in combination with tendon transfer to enhance active function, are available treatment options for both upper and lower limb spasticity However, much more adequately conducted research is necessary to build on sufficient evidence and to support treatment algorithms References Ada L, Vattanasilp W, O’Dwyer NJ, Crosbie J Does spasticity contribute to walking dysfunction after stroke? 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Standard Book Number -1 3 : 97 8 -1 -4 66 5-6 54 4-9 (Hardback) International Standard Book Number -1 3 : 97 8 -1 - 31 5-3 743 6-9 (eBook) This book contains information obtained from authentic and highly regarded... [2002]); Kumar Definition and Measurement of Spasticity and Contracture 70 70 Force (N) 10 0 Force (N) 10 0 40 10 –20 20 38 56 74 92 11 0 12 8 14 6 16 4 18 2 200 10 20 38 56 74 92 11 0 12 8 14 6 16 4 18 2 200 –20... originally trained as a bioengineer and has a special interest in neurological rehabilitation, clinically usable measurement and applied clinical research His interest in spasticity started during