Ebook Neurological rehabilitation - Spasticity and contractures in clinical practice and research: Part 1

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
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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 


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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 />Visit the Taylor & Francis Web site at

and the CRC Press Web site at



Contents
Editors..................................................................................................................... vii
Contributors.............................................................................................................ix
1. Definition and Measurement of Spasticity and Contracture.................1
Anand D. Pandyan, Bernard A. Conway, Hermie J. Hermens
and Garth R. Johnson
2. Pathophysiology of Spasticity..................................................................... 25

Jens Bo Nielsen, Maria Willerslev-Olsen and Jakob Lorentzen
3. 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
4. The Clinical Management of Spasticity and Contractures
in Cerebral Palsy............................................................................................ 79
Andrew Roberts
5. Clinical Management of Spasticity and Contractures in Stroke....... 101
Judith F. M. Fleuren, Jaap H. Buurke and Alexander C. H. Geurts
6. Clinical Management of Spasticity and Contractures in Spinal
Cord Injury................................................................................................... 135
Martin Schubert and Volker Dietz
7. Clinical Management of Spasticity and Contractures
in Multiple Sclerosis................................................................................... 175
Lorna Paul and Paul Mattison
8. Clinical Assessment and Management of Spasticity
and Contractures in Traumatic Brain Injury......................................... 203
Gerard E. Francisco and Sheng Li
9. Hereditary Spastic Paraparesis and Other Hereditary
Myelopathies................................................................................................ 235
Jon Marsden, Lisa Bunn, Amanda Denton
and Krishnan Padmakumari Sivaraman Nair
Index...................................................................................................................... 289
v

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

x

Jakob Lorentzen
Institute of Neuroscience
University of Copenhagen
and
Elsass Institute
Charlottenlund, Denmark
Jon Marsden
School of Health Professions
Faculty of Health and Human
Sciences
University of Plymouth
Plymouth, United Kingdom
Paul Mattison
Ayrshire Multiple Sclerosis Service
Douglas Grant Rehabilitation Centre
Ayrshire Central Hospital
Irvine, United Kingdom
Krishnan Padmakumari
Sivaraman Nair
Department of Neurology
Royal Hallamshire Hospital
Sheffield Teaching Hospitals NHS
Foundation Trust
Sheffield, United Kingdom
Jens Bo Nielsen
Institute of Neuroscience
University of Copenhagen

and
Elsass Institute
Charlottenlund, Denmark

Contributors

Anand D. Pandyan
School of Health and Rehabilitation
Keele University
Keele, United Kingdom
Lorna Paul
School of Health and Life Sciences
Glasgow Caledonian University
Glasgow, United Kingdom
Andrew Roberts
Orthotic Research and Locomotor
Assessment Unit
Robert Jones and Agnes Hunt
Hospital Oswestry
United Kingdom
Martin Schubert
Spinal Cord Injury Center
University Hospital Balgrist
Zürich, Switzerland
Thomas Sinkjær
Department of Health Science and
Technology
Aalborg University
Aalborg, Denmark
Maria Willerslev-Olsen

Elsass Institute
Charlottenlund, Denmark


1
Definition and Measurement
of Spasticity and Contracture
Anand D. Pandyan, Bernard A. Conway,
Hermie J. Hermens and Garth R. Johnson
CONTENTS
1.1Introduction.....................................................................................................1
1.2 Definition of Spasticity...................................................................................2
1.2.1 Can the Words Increased Tone/Hypertonia and Spasticity
Be Used Interchangeably?.................................................................3
1.2.2 Developing the Framework for Defining Spasticity.......................6
1.2.2.1 Increased (Hyper-Excitable/Exaggerated) Reflexes........8
1.2.2.2 Spasms and Clonus..............................................................8
1.2.2.3 Altered Tone or the Response of a Relaxed Muscle
to an Externally Imposed Stretch......................................9
1.2.2.4 Abnormal Movement Patterns and Co-Contraction..... 12
1.2.3 The Classification and Definition of Spasticity in Upper
Motoneuron Syndrome.................................................................... 13
1.2.4 Contractures in Patients with Upper Motoneuron Syndrome......14
1.2.5 The Measurement of Spasticity and Contracture........................ 17
1.2.6 Concluding Thoughts....................................................................... 19
References................................................................................................................ 21

1.1 Introduction
Spasticity is a clinical condition that is expected to develop following a lesion
in the descending tracts of the central nervous system (CNS), at any level (i.e.,

cortex, internal capsule, brain stem, or spinal cord) (Burke [1988]). It is a common neurological impairment with a reported prevalence of between 20%
and 80% (this will depend on the population under study and the method
of measurement), which is considered clinically important (see subsequent
chapters for disease-specific data). Not all spasticity is considered troublesome to patients; however, a significant number of patients with spasticity
will require treatment. Treatment of spasticity is often driven by goals aimed

1


2

Neurological Rehabilitation

at improving function or preventing significant secondary complication such
as pain, pressure sores, limb deformities, etc.
At a pathophysiological level this condition has been studied in reasonable
detail since the 1880s and our current understanding of the pathophysiological basis of this condition and its impact on function has been summarised in
Chapters 2 and 3. Unfortunately, the literature related to treatment is scanty
and the quality is predominantly poor (and the team found this to be a significant challenge in the compilation of this book). The two main barriers to
good science have been the lack of a proper definition of the term spasticity
and the use of invalid methods of measurement.
Attempting to provide a universally acceptable definition that is both scientifically valid and clinically usable is probably too much of a challenge
for now; however, an attempt will be made to present a framework that may
help in this process. It may help for readers to have an understanding of
this framework before reading the individual disease-specific chapters. The
measurement of spasticity is a much easier problem to deal with as there
are a range of valid measures that are available. This chapter will, therefore,
summarise the state-of-the-art approaches to the measurement of spasticity,
both directly or indirectly.

1.2 Definition of Spasticity
The observations of Landau (1974) that the term spasticity has become such
a habitual part of neurological jargon that no one is expected to define it remains
true today in practice (Landau [1974]). What is more challenging is that this
behaviour appears also to have permeated the published research! In his
editorial, Landau (1974) provides six variations to the definition of spasticity
found in the literature. Unfortunately, since then, many more have appeared
(e.g. Lance [1980a,b,c]; Sanger et al. [2003]; Pandyan et al. [2005]; Malhotra et
al. [2009]).
Currently, there is agreement that spasticity is a condition that can develop
following an upper motoneuron lesion. Most texts would suggest that the
sensory motor problems following an upper motoneuron lesion, of any
origin, can be classified as having positive features and negative features
(Pandyan et al. [2009]). This particular approach to classification can be traced
back to the work of Hughlings Jackson (York and Steinberg [2007]), who considered that the positive features were associated the exposure of activity
that was previously inhibited by the nervous system and the negative features result from the loss of higher-level excitatory control. This classification
was based on Jackson’s thinking of the nervous system as being hierarchical,
with the higher levels having modulatory control over the lower levels. Table
1.1 summarises the features of the upper motor syndrome as commonly


Definition and Measurement of Spasticity and Contracture

3

TABLE 1.1
A Summary of the Positive and Negative Features Associated with the Upper
Motoneuron Syndrome, as Commonly Reported in the Literature
Positive Features
Increased reflexes

Spasticity
Altered tone
Spasm & clonus
Abnormal movement patterns & co-contraction

Negative Features
Weakness
Fatigueability
Loss of dexterity (motor control)

reported in the literature and the text, and it is important to note that spasticity was only considered as one feature of the upper motoneuron syndrome.
Spasticity is derived from the Greek root word spastikos, which means drawing or tugging. If one reads the literature from the time of 1830 (see Chapter 4),
it appears that the term spasticity is often associated with a ‘resistance one feels
when passively moving/mobilising a limb segment’ and was also associated
with the terms tone and rigidity (Siegel [1988]). Although a variety of descriptions exist in the literature, the first formal definition appears in the works of
Denny Brown, where he defines spasticity in capsular hemiplegia as the presence of a soft yielding resistance that appears only towards the end of a passive stretch,
and is associated with increased amplitude stretch reflex (Denny-Brown [1966]). Two
decades later, in a series of post-conference discussions and a presentation,
Lance (1980a,b,c) put forward a series of definitions for the term spasticity. Of
the three definitions, the one that is most commonly cited defines spasticity as
a motor disorder characterised by a velocity dependent increase in tonic stretch reflexes
(muscle tone) and increased tendon jerks resulting from disinhibition of the stretch
reflex, as one component of an upper motoneuron lesion (Lance [1980b]).
However, the literature still appears not to have any form of consensus
with respect to a definition (Pandyan et al. [2005]; Malhotra et al. [2009]).
When the literature was last reviewed, approximately a third of the literature equated spasticity with increased or altered muscle tone or hypertonia
(and this will be discussed in Section 1.2.1). A third of the literature defined
spasticity according to the Lance (1980b) definition (as cited above) or some
minor variation. A third of the literature did not define the term spasticity at
all, suggesting that not much has been learnt since Landau (1974) or the more

recent article from Thilmann (1993). Accordingly, and before we progress to
discussing a framework for defining spasticity, it is important to first deal
with use of the term (high) tone as a synonym for spasticity.
1.2.1 Can the Words Increased Tone/Hypertonia
and Spasticity Be Used Interchangeably?
The term tonus was originally introduced in 1838 to describe the slight contractile tension in the muscles when at rest (Rushworth [1960] citing Mueller


4

Neurological Rehabilitation

[1838]). It is fascinating to read the summary of Cobb and Wolf (1932) following the First International Congress of Neurology:
Confusion of thought has occurred throughout the diverse use of the
term tonus. However carefully defined it now carries with an incubus
of vague connotation which seems to cloud the issue. Its place as term
applied to striated muscle can be more accurately taken over by such
specific terms as ‘standing reflex’, ‘postural reflex’, and ‘righting reflex’.
The state of the striated muscle at any moment can be described by
adjectives such as slack or taut. Better still the amount of tension can
be measured and stated in quantitative terms. We make a plea that the
term tone be either discarded or returned to its former home in smooth
muscle and kept there.

It is frustrating that we appear not to have learnt very much from the precision in the literature of the past. There is now clear evidence that in a state
of rest skeletal muscles are electrically silent and that there is good reason to
believe that the advice of Cobb and Wolf (1932) is just as appropriate today
as it was then. However, asking for people to change entrenched behaviour
is unlikely.
There are currently two separate definitions of the term tone that are

acknowledged:
• The first equates tone with the resistance one feels when passively
moving a limb segment about a joint.
• The second equates tone with the readiness to act.
The term hypertonia (or high tone) is related to the first definition of tone (i.e.,
an increased resistance that one encounters during passive limb displacement).
The assumption being made is that any resistance encountered to an externally imposed passive movement is due to an increased activation of muscles
(e.g. Sanger et al. [2003]). There is now ample evidence that such an assumption
cannot be made (Malhotra et al. [2008]). The resistance that one encounters is
often associated with changes in the biomechanical properties of soft tissues
and joint structures (Figure 1.1). In certain circumstances, increased muscle
activity can contribute to this increased resistance in the absence of any form
of soft tissue and joint changes, but this is rare (Figure 1.1).
The term hypotonia is often related to both definitions of tone. If one
considers the argument in support of a condition of hypotonia against the
first definition of tone then the hypothesis one has to consider is that the
resistance to passive movement in people with hypotonia is lower than normal. This does make the assumption there is ‘normal tone’. The evidence is
clear: in a relaxed state there is no electrical activity in muscles. The stiffness
measured in patients with a dense flaccid paralysis is also not very different
to people who have no neurological deficits (Barnaby et al. [2002]); Kumar


5

Definition and Measurement of Spasticity and Contracture

70

70
Force (N)

100

Force (N)

100

40
10

–20

20 38 56 74 92 110 128 146 164 182 200

10

20 38 56 74 92 110 128 146 164 182 200
–20
–50

–50
Pre
Lin. reg pre
Post

(a)

40

Angle (degrees)

Linear reg post

Pre
Lin. reg pre
Post

(b)

Angle (degrees)

Linear reg post

FIGURE 1.1
Recording of stiffness at the elbow (the slope of the force angle curve) measured before and
after injection of Botulinum Toxin – A (BoNT-A). The trace in gray is before injections and
the trace in black is four weeks after injections. Both patients are responders to treatment of
botulinum toxin, i.e., the injections suppressed the stretch-induced activation of muscles. In
the patient with no contractures (left-hand pane [a]; discussed in Section 2.3) the stiffness was
influenced by the abnormal muscle activity associated with spasticity (stiffness pre-injection
was 0.4 N/deg and post-injection was 0.2 N/deg). Note also that in this patient a catch followed by a release can be seen. However, in the patient with the established contractures
(b) there was no change in stiffness, suggesting that the spasticity had no contribution to the
resistance to passive movement (stiffness pre-injection was 1.1 N/deg and post-injection was
1.0 N/deg). (With permission from Pandyan AD et al. [2009] Spasticity, The New Encyclopedia
of Neuroscience. Squire LR, ed. Vol 9. Oxford: Academic Press, pp. 153–163.)

et al. [2006]). In the circumstances, the argument that people with low tone
have lower-than-normal resistance to an externally imposed movement is
untenable. The other argument links the definition of hypotonia to the second definition of tone (i.e., the muscles can be activated with a smaller-thannormal ­stimulus or the muscle is not in a state of readiness to act). This is a
more complex problem to deal with. In some patients with an upper motoneuron lesion there is evidence that a smaller-than-normal stimulus (proprioceptive, cutaneous, etc.) can trigger the activation of an involuntary response

of either an isolated muscle or a group of muscles (see Chapter 2). However,
such patients are often treated, contradictorily, as hypertonic not hypotonic.
One then has to consider whether patients with hypotonia have a lower-thannormal ‘readiness to act’ and the only interpretation left is that such a person
does not have an ability to act, i.e., they are paralyzed. It is important to highlight that the original articles on rigidity and spasticity use two specific terms:
hypertonic paralysis and hypertonicity in paralysis. The former term is used to
describe patients who were unable to voluntarily activate muscles (paralysis)
and whose muscles are in a state of contraction. The latter term is used to
describe patients who are unable to activate muscles voluntarily (paralysis) but
an examiner is able to elicit or observe reflex muscle activation (Bennett [1887]).


6

Neurological Rehabilitation

In summary, the words hypertonia and spasticity cannot be used interchangeably. From a first-principles argument, if there was a choice the authors
would probably want to support the position taken by Cobb and Wolf (1932)
and Rushworth (1960), i.e., not to use these terms within the context of neurological rehabilitation. These terms, however, have been extensively used
already and such a recommendation would not be adopted. However, it is
important that readers reflect on this discussion when they interpret the
term tone, both within this book and in the general literature. Furthermore,
for the future, if people choose to use the word tone then it is important that
the term is explicitly defined whenever it is used. The challenges of not providing such definitions can be seen with the chapters of this book, in particular the chapters on cerebral palsy and multiple sclerosis (Chapters 4 and 7,
respectively), where the authors have struggled to interpret the term tone as
the literature has not defined this for them.
1.2.2 Developing the Framework for Defining Spasticity
Having accepted that the term spasticity is likely to remain in common use,
one then needs to consider a framework that will help with articulating a
clinically meaningful definition of this term for routine clinical and research
use. More importantly, a valid definition and description is an essential first

step in measurement. The remainder of this section will therefore focus on
developing a framework for the definition and description of the term spasticity. Two teams, in the early part of 2000, explored ways to develop a universally acceptable definition for spasticity. The first of these teams, the Task
Force on Childhood Motor Disorders, took the approach of splitting existing definitions to provide a series of sub-definitions. The second of these teams, A
European Thematic Network to Develop Standardised Measures of Spasticity, took
a diametrically opposite approach of lumping existing definitions into a universal definition. The two approaches are chronologically described below.
Sanger et al. (2003) provide a series of definition linked to both spasticity
and hypertonia. Their definition for hypertonia will not be discussed further
in this section as the arguments as to why such a definition will not work
have already been presented in Section 2.1. Sanger et al. (2003) defined hypertonia as a case in which one or both of the following signs are present: (1) resistance
to externally imposed movement increase with increasing speed of stretch and varies
with the direction of joint movement and/or (2) resistance to externally imposed movement rises rapidly above a threshold speed or joint angle. Such a definition does not
add much clarity to the definition originally proposed by Lance (1980b); in
fact, one could argue that it confuses the measurement a lot more. At a fundamental level, there are two major problems with the above definition: (i) a
velocity-dependent increase in resistance to passive movement is an inherent
viscoelastic behaviour of muscles and tendons (Figure 1.2); and (ii) the threshold speed or joint angle are not defined per se. Under these circumstances one
would argue that the approach to splitting lacks adequate precision.


7

Definition and Measurement of Spasticity and Contracture

20

–10º
PF

10º
DF

Torque (N.m)

16
12

Affected
limb

8

25º.s–1

5º.s–1

4
0
FIGURE 1.2
Stiffness measured at the knee joint using two different velocities. The authors Singer et al.
(2003) have clearly demonstrated that changes in velocity-dependent stiffness can be independent of spasticity. (With permission from Singer B et al. [2003] Velocity dependent passive
flexor resistive torque in patients with acquired brain injury. Clinical Biomechanics 18:157–165.)

The SPASM Consortium (Pandyan et al. [2005]), after reviewing the literature came to the conclusion that the term spasticity was being used to refer
to a range of signs and symptoms associated with the upper motoneuron
lesion. This is probably true of clinical practice too, and anecdotal evidence
from discussions with students, researchers and clinical practitioners confirms that this is the case. If one were to ensure that all of the relevant literature associated with the term spasticity was to be reviewed, then there
was a need to develop a definition that was sufficiently broad so as to be
inclusive of all of the clinical manifestation but adequately specific to focus
on the neurological basis of the phenomenon. The consensus definition that
was agreed defined spasticity as disordered sensori-motor control, resulting from
an upper motoneuron lesion, presenting as intermittent or sustained involuntary

activation of muscles. This definition then meant that spasticity was no longer
a term used to denote one component of the upper motoneuron syndrome
(as described in Table 1.1) but all of the positive features upper motoneuron
syndrome (Table 1.2).
TABLE 1.2
The Redefining of Spasticity by the Spasm Consortium Resulted in a Definition
That Was a Reflection of Both the Literature and Clinical Practice
Positive Features
Increased reflexes
Spasticity
Spasm and clonus
Altered tone
Abnormal movement patterns & co-contraction

Spasticity as Defined by SPASM
Consortium
Increased reflexes
Spasm and clonus
Altered tone
Abnormal movement patterns
and co-contraction


8

Neurological Rehabilitation

Whilst such an all-encompassing definition has some benefit, it is of limited clinical and research value as this does not provide an unambiguous
framework to inform the measurement process. In order to develop this definition further it is important the lumped definition can be split or stratified
in a way that could inform the measurement process. This would require the

examination of the individual components and explore if the components
could be classified as spasticity. This process is described below. It is important to note that pathophysiology is discussed comprehensively in Chapter 2,
so this chapter will not review pathophysiology.
1.2.2.1 Increased (Hyper-Excitable/Exaggerated) Reflexes
The term increased reflexes will very specifically be equated to the response
observed following a clinical testing of reflexes, i.e., where an examiner taps a
tendon to produce a transient stretch of the muscle that then leads to a subsequent
contraction. Although not formally studied, the literature seems to suggest that
the sensitivity* and specificity† of the stretch reflex response as currently measured is a poor indicator of spasticity in both acute and chronic populations. The
literature also remains unclear on what constitutes the signature of an increased
reflex: do these terms mean the reflex has a lower threshold, greater magnitude,
longer duration or a combination of all. The reflex response, when tested clinically using a tendon tap, normally will involve mono- and­­polysynaptic pathways, meaning that the observation of a change in reflex cannot in itself be a
sub-classification of spasticity but rather is a reflection of changed excitability.
Furthermore, as this discussion develops (Sections 1.2.2.2 and 1.2.2.3) it will
become more apparent that many of the other signs and symptoms that can be
classified under the umbrella definition of spasticity is predominantly associated with changes in excitability within a variety of motor pathways.
1.2.2.2 Spasms and Clonus
A spasm can be defined as a transient but continuous muscular contraction which
can be triggered by a combination of cutaneous and/or visceral triggers and a clonus is defined as a transient but intermittent rhythmic muscle contraction with
proprioceptive and/or cutaneous triggers. Both of these signs are commonly
reported in patients with spasticity. Both of these phenomena are common
in patients with upper motoneuron lesions. Exact prevalence and incidence
cannot be reported as these are not systematically documented. Spasms
can affect both the flexor and extensor muscle groups of patients and can
be influenced by changes in ambient temperature. Anecdotal reports suggest that an increase in spasms is normally associated with a decrease in
temperature. Cutaneous stimuli that are noxious can trigger spasms. There
* Sensitivity: the ability to accurately identify those with spasticity.
† Specificity: the ability to accurately identify those without spasticity.

Definition and Measurement of Spasticity and Contracture

9

is some anecdotal evidence that spasms can be influenced by changes in
activity within the autonomic nervous system. However, this association has
not been systematically studied in any depth. It is important to note that
spasms can occur due to reasons other than spasticity, i.e., there is a lack
of specificity. Despite this, if a person has spasms subsequent to the upper
motoneuron lesion one could conclude that this is an indicator of spasticity.
Clonus is also documented to occur, predominantly at the ankle joint, in the
later stages following an upper motoneuron lesion. In studies conducted on
stroke patients, upper limb clonus is very rarely observed at the elbow joint
(<1%) and its prevalence in the lower limb is most likely a consequence of
excitability changes facilitating interactions between neurogenic networks,
reflex loops, and the biomechanics of the muscle/joint system. At this stage,
there is adequate theoretical evidence to consider both spasms and clonus as
sub-classifications under the umbrella term of spasticity.
1.2.2.3 Altered Tone or the Response of a Relaxed Muscle
to an Externally Imposed Stretch
The research underpinning the response of a relaxed muscle to an externally
imposed stretch has probably been studied the most extensively in the literature. Some of the earliest clinicians and researchers measured spasticity by
studying the muscle response to an externally imposed stretch using either
fine wire or surface electromyography (EMG). It is a pity that somewhere
along the way this approach to studying spasticity has for all practical purposes disappeared in clinical practice.
In neurologically healthy subjects, when a relaxed muscle is passively
stretched no EMG responses are normally observed below velocities of 200
deg/s. However, in patients with an upper motoneuron syndrome a range
of EMG responses can be seen (Figure 1.3). These can be classified as (a) a
velocity-dependent response, (b) a position-dependent response, a combination of (a) and (b), and (c) a clasp-knife-type response.

Whilst the muscles of most patients will be in a state of rest prior to the start
of the test, there are some patients in whom residual EMG activity at rest is
observed. The literature describes these patients as having ‘spastic dystonia’‡
(Figure 1.4). However, what is important to also note in such patients is the
phenomenon of position dependency, and possibly a combination of velocity
and position dependency can be observed.
Recordings such as those above have been widely observed (by, e.g.,
Tardieu et al. [1954]; Lance [1980a,b,c] and Rymer and Katz [1994]). Readers
are encouraged (after reading Chapter 2 of this publication) to explore the
literature produced by notable authors such as Sherrington, Matthews,
Denny-Brown, Tardieu, Pierrot-Deseilligny, Hultborn, Burke, Lance, etc.,
‡

Although we are not comfortable with this term it will be used until a suitable alternative can
be found (this is unlikely to happen!).


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Neurological Rehabilitation

Slow vs fast (Vel & EMG)
0.1

Velocity during
fast movement

400

EMG during 0.08

fast movement

Velocity (deg/s)

300
S_Vel

0.06

200

F_Vel

Velocity during
slow movement

100
0
–1.818

0.04

EMG during slow movement

–100
–80

–60

–64.139

–40

0

–20

F_FEMG

0.02
0
40

20

S_Angle, F_Angle, S_Angle, F_Angle,

S_FEMG

EMG (mV)

500

402.48

4.406 × 10–3

36.153

Angle (deg)

Slow velocity
Fast velocity
Slow_flexor EMG
Fast_flexor EMG

(a)

0.29
Velocity during
fast movement

60
S_Vel
F_Vel

Velocity during
slow movement

40

0.2
S_FEMG

EMG during
fast movement

F_FEMG

20

0.1

0
–5.31

EMG (mV)

Velocity (deg/s)

99.189

Slow vs fast (Vel & EMG)

100

–20
–100

–80

–97.38

–60

EMG during
slow movement
–40
–20

S_Angle, F_Angle, S_Angle, F_Angle,

0
0

4.309 × 10–3

–10.003

Angle (deg)

(b)

Slow velocity
Fast velocity
Slow_flexor EMG
Fast_flexor EMG

FIGURE 1.3
Images recorded from the Biceps Brachii muscle of stroke patients. The elbow joint was fully flexed
and then extended using a ‘ramp and hold’ method (Rymer and Katz [1994]). The hold was <5 seconds in duration. Two velocities were used to stretch the joint (an uncontrolled slow velocity and
an uncontrolled fast velocity as annotated on the respective graphs). The EMG during movement
was also collected and the corresponding EMG traces are annotated on the respective graphs. The
EMG activity was notch-filtered (50 Hz) and then smoothed using an RMS procedure as described
in the source article. (a) This graph shows a velocity-dependent response to an externally imposed
movement. There is very little EMG activity during the slow movement; however, there is a large
burst of activity during the fast movement. The EMG activity starts to drop off towards zero at the
end of the stretching movement. (b) This graph shows a position-dependent response to an externally imposed movement. The EMG activity increase as the muscle is stretched and the activity
remains elevated during the hold phase. It is also important to note the EMG activity during the
quick stretch starts earlier in the range of movement.
(Continued)

11

Definition and Measurement of Spasticity and Contracture

Slow vs fast (Vel & EMG)

294.345

EMG during
fast movement
Velocity during
fast movement

Velocity (deg/s)

200
S_Vel
F_Vel

0.269
0.25
0.2

Velocity during
slow movement

100

0.15

S_FEMG
F_FEMG

EMG (mV)

300

0.1
0
–5.04

–100
–60

0.05

EMG during
slow movement
–40

–48.161

–20

0

20

S_Angle, F_Angle, S_Angle, F_Angle,

0
60

40

9.557 × 10–3

40.704

Angle (deg)
Slow velocity
Fast velocity
Slow_flexor EMG
Fast_flexor EMG

158.085

200

Slow vs fast (Vel & EMG)
EMG during fast
movement

Velocity (deg/s)

F_Vel

Velocity during

fast movement

100

Velocity during
slow movement

50

0.06
0.04

S_FEMG
F_FEMG

0.02

0
–7.425

0.084

0.08

150

S_Vel

0.1

EMG (mV)

(c)

EMG during fast
movement

0
–50
–140
–120
–100
–80
–60
–40
–20
–122.589 S_Angle, F_Angle, S_Angle, F_Angle,
–27.948

0.012

Angle (deg)

(d)

Slow velocity
Fast velocity
Slow_flexor EMG
Fast_flexor EMG

FIGURE 1.3 (CONTINUED)
Images recorded from the Biceps Brachii muscle of stroke patients. The elbow joint was fully flexed
and then extended using a ‘ramp and hold’ method (Rymer and Katz [1994]). The hold was <5 sec­­
onds in duration. Two velocities were used to stretch the joint (a uncontrolled slow velocity and an
uncontrolled fast velocity as annotated on the respective graphs). The EMG during the movement
was also collected and the corresponding EMG traces are annotated on the respective graphs. The
EMG activity was notch-filtered (50 Hz) and then smoothed using an RMS procedure as described
in the source article. (c) This graph shows a combination of velocity- and position-dependent
responses to an externally imposed movement. The EMG activity increase as the muscle is
stretched and the activity remains elevated during the hold phase. It is also important to note the
EMG activity during the quick stretch starts earlier in the range of movement and is of a greater
magnitude. (d) This graph shows the clasp-knife response to an externally imposed movement.
The EMG activity increases rapidly as the muscle is stretched and this slows the movement down.
If the examiner continues with the stretch the EMG activity then reduces. This response occurs
during both the slow and fast stretch and is triggered at relatively slow velocities.


12

Neurological Rehabilitation

150
100

Angle
EMG triceps brachii

50
0
–50

0

EMG biceps brachii
2000

4000

6000

Force
8000 1 · 104 1.2 · 104 1.4 · 104

Angle
Force
EMG(Flexors)
EMG(Extensors)
FIGURE 1.4
A figure illustrating the phenomenon of spastic dystonia. A patient demonstrating EMG of the
Biceps Brachii at rest. When the muscle is stretched the EMG activity increases as the stretch on
the muscle is increased and as the stretch is carried out using a quicker speed the magnitude
of the activity increases. It is important to note that in this patient stretching of the extensors
lead to activation of the Triceps Brachii. When the Triceps were active the activity in the Biceps
reduced.

all of whom employed direct measures of muscle electrical activity to gain
an understanding of spasticity.
What is obvious is that the stretch-induced response (i.e., velocity-dependent
response, position-dependent response, the velocity- and position-dependent
response and the ‘clasp-knife’ phenomenon) results from an afferent input
to the central nervous system. However, the abnormal muscle activity at

rest (i.e., spastic dystonia) appears to be independent of an afferent input to
the CNS (e.g., loss of cortical inhibition to the brainstem pathways/nuclei).
Within the context of a SPASM definition all of these conditions can be considered a sub-classification of spasticity.
1.2.2.4 Abnormal Movement Patterns and Co-Contraction
The abnormal movement patterns and co-contractions that are commonly
seen after an upper motoneuron lesion are currently classified under the
term spasticity. However, it is possible that the abnormal patterns of movement and co-contraction one observes during voluntary movement may
result from the compensation to the weakness that co-exists (Chapters 2
and 3 discuss this possibility in greater detail). Furthermore, if one were to
test individuals with no known impairments, enhanced tremor-like oscillations and co-contractions can be provoked in cases of fatigue or peripheral


Definition and Measurement of Spasticity and Contracture

13

loading, the latter being the interia-sensitive mechanical-reflex oscillation
component of tremor (Elble and Koller [1990]). In normal movement, patterns
of co-contraction and the synergetic activation and de-activation of muscles
are the norm and are an essential feature of successful movement execution in both simple and complex actions. For example, the ability to grip and
transport an object will be severely compromised if one is unable to stabilise
the wrist and simultaneously coordinate the co-contraction of muscles of the
shoulder and elbow joint during this action. Under these conditions classifying abnormal movement patterns and co-contraction as a sub-classification
of spasticity is not appropriate and, collectively, more appropriately reflects
a deficit of control.
1.2.3 The Classification and Definition of Spasticity
in Upper Motoneuron Syndrome
Based on our current understanding, and extending the work of the SPASM
consortium, it is possible to first define spasticity as an emergent feature of
disordered sensori-motor control, resulting from an upper motoneuron lesion, presenting as intermittent or sustained involuntary activation of muscles. Spasticity

can present as:
• Spasms (A transient but continuous muscular contraction which can be
triggered by a combination of cutaneous and/or visceral triggers).
• Clonus (A transient but intermittent rhythmic muscle contraction with
proprioceptive and/or cutaneous triggers).
• Abnormal activation of muscles to an externally imposed stretch,
which can present as a combination of:
• velocity-dependent response;
• position-dependent response;
• ‘clasp-knife’ response.
• A continuous activation of muscles even in a state of rest (spastic
dystonia).
The clinical presentations of spasticity can be modulated by ambient afferent inputs (e.g., touch, temperature, etc.); however, at this stage it is not possible to expand. Further, the time course of the development of spasticity
has not been well documented. What is clear is that immediately following
a lesion the central nervous system goes into a period of shock and recovery
during which time the system will start to present with varying responses
and time delays. The time course of development of spasticity is likely to be
disease-specific. In stroke, traumatic/hypoxic brain injury, and spinal cord
injury the evidence is that spasticity onset can be rapid (i.e., within 48 hours
or earlier) but often the onset time course is highly variable. The natural


14

Neurological Rehabilitation

history and time course of onset in many disease populations needs to be
established.
A significant limitation to the proposed definition is the narrow focus on
patients with an acquired upper motoneuron lesion. There are large population of patients with acquired/degenerative disease of the nervous system

who present with signs that are similar to those described under spasticity
or spastic dystonia. In particular, patients with Parkinsonism who present
with rigidity and/or cog-wheel rigidity, patients with movement disorders
such as Huntington’s disease, Blepharospasm, and Cervical Dystonia, all of
whom can present with spasms (often termed dystonia) affecting different
parts of the body, and patients with motoneuron disease. Maybe discussion
of this is for a second edition; however, there is much work that needs to be
done to produce such a unifying framework for definition and measurement.
1.2.4 Contractures in Patients with Upper Motoneuron Syndrome
A contracture has been defined as a pathological condition of soft tissues
characterised by stiffness and is usually associated with loss of elasticity and
fixed shortening of the involved tissues (muscle, tendon, ligament, subcutaneous tissue, skin, blood vessels, and nerves) and results in loss of movement
around a joint (Botte et al. [1988]; Lehmann et al. [1989]; Harburn and Potter
[1993]; Teasell and Gillen [1993]). Contractures normally occur as a result of
a joint being fixed in a shortened position with a lack of loading to the soft
tissue structures. In the following paragraphs, we will briefly discuss factors
that can contribute to contractures following an upper motoneuron lesion.
Following an upper motoneuron lesion a patient will present with
paralysis or paresis and as a result the muscle and joint structures of the
affected periphery become unloaded. In particular, if a patient does not
regain functionally useful movement then the patient will present with
muscle atrophy, i.e., a decrease in the size of the muscle fibres and therefore the muscle itself, a decrease in the force generation capacity within
the muscle, and an increase in the fatiguability of muscles. The increase
in fatiguability probably arises from decreasing glycogen stores and ATP
levels within a muscle (Lieber [2009]). The loss of muscle mass could in
part be explained by an increase in the catabolic enzyme levels within
these muscles that have been paralyzed (Lieber [2009]). The loss of loading, on the soft tissues, may also contribute to an increase in the collagen
crosslinks that occur within the tendon and soft tissue structures and this
can contribute to an increase in stiffness. However, it is important to note
that a patient presenting with no symptoms other than paralysis rarely

presents with contractures in the acute and subacute stages following the
neurological injury (Figure 1.5).
If a patient were to develop contractures, as defined above, in addition to
the lack of loading and motion, the joints should also be held in a shortened
position. Based on the evidence collected by Pandyan and co-workers there