Current Challenges to Clinical Assessment of Spasticity
Chetan
P Phadke, Farooq Ismail, Chris Boulias
Chetan P Phadke, Farooq Ismail, Chris Boulias, Spasticity
Research Program, West Park Healthcare Centre, Toronto, Canada
Chetan P Phadke, Farooq Ismail, Chris Boulias, Faculty of
Medicine, University of Toronto, Toronto, Canada
Chetan P Phadke, Faculty of Health, York University,
Toronto, Canada
Correspondence to: Chetan P Phadke, Spasticity
Research Program, 82 Buttonwood Ave., Toronto, ON, Canada.
Email: chetan.phadke@westpark.org
Telephone: +1-416-243-3600 x 2716
Fax: +1-416-243-3747
Received: January 2,
2015
Revised: January 23, 2015
Accepted: January 24, 2015
Published online: February 2, 2015
ABSTRACT
A high prevalence
of spasticity in patients with a variety of upper motor neuron lesions has been
reported and spasticity assessments and treatments have been the focus of
several recent research articles. It is important for researchers based in
non-clinical settings, who are designing scales to measure spasticity, to
understand the nuances of the challenges facing clinicians involved in
spasticity management. Likewise, it is also important for clinicians to
understand the need for objectivity and systematic approach to measuring
spasticity that is at once valid and reliable. This paper summarizes the
challenges clinicians face when using clinical tools for spasticity
assessments, presents variety of lab-based measures available to clinicians,
and describes the pros and cons of each approach. Finally, information on
devices to measure spasticity that can satisfy both clinical as well as
research demands are presented with areas for future work.
© 2015 ACT. All
rights reserved.
Key words: Muscle spasticity; Botulinum toxin; Spinal reflexes
Phadke CP, Ismail
F, Boulias C. Current Challenges to Clinical Assessment of Spasticity. International Journal of Neurology Research 2015; 1(1): 1-4 Available from: URL:
http://www.ghrnet.org/index.php/ijnr/article/view/1005
INTRODUCTION
Spasticity is a positive sign of upper motor neuron lesions
characterized by an increase in resistance to movement perceived when a
clinician quickly moves the limb through the available passive range of motion.
Spasticity has been classically defined by Lance (1980) as “a
velocity-dependent increase in resistance” as a result of “hyperexcitable
stretch reflexes”[1]. More recently, an updated and more
comprehensive definition of spasticity described as “disordered sensori-motor
control, resulting from an upper motor neuron lesion, presenting as
intermittent or sustained involuntary activation of muscles” has been proposed[2].
For the purposes of this paper, we discuss assessments of spasticity based on
the classic definition of Lance. Spasticity requiring treatment is most
commonly seen in conditions such as stroke, multiple sclerosis, and cerebral
palsy[3]. Spasticity and the resulting tightening of muscles has a
multi-dimensional impact in areas such as reduced range of motion in arms and
legs, potential for contractures if left untreated, hygiene issues specifically
in areas of hip and shoulder adductor and finger flexor spasticity, poor body
image, mobility, pain, balance, and walking variability[4,5]. Treatments
are available to help manage spasticity which can present an ongoing and
long-term problem[4].
Choice of
treatment options is dependent on the underlying mechanisms that result in an
increased resistance to movement. There are two mechanisms to explain the
increased resistance: (1) hyperexcitable spinal reflexes (neural)[1]
and (2) secondary tightening of soft tissue structures around the joints
(musculotendinous)[6]. The neural or reflex component can be teased
apart by assessing the muscle response to manipulation of movement speed,
whereas, the musculotendinous or non-reflex component can be isolated by
measuring the end range or resistance to slow passive movement of the joint[6].
The neural component can be managed using physical means such as rhythmic
repetitive motion exercises[7-9] or using pharmaceutical agents
delivered either orally or using targeted delivery such as in the case of
Baclofen pumps[4] or intramuscular interventions[10].
Botulinum toxin (BoNTA) intramuscular injections chemically denervate parts of
the muscle and are also used to target the neural component of spasticity[10].
The musculotendinous component can also be managed by active as well as passive
exercise involving systematic stretching and joint positioning using orthosis[4].
Irrespective
of the choice of treatment, accurate assessment of spasticity level is critical
to the success of the treatment. Spasticity is commonly seen in several muscles
in arms and legs either unilaterally such as in stroke or bilaterally as in the
case of MS[3]. Muscle groups typically requiring treatment for
spasticity are elbow, wrist, and finger flexors, hip adductors, knee flexors,
ankle plantar flexors, and toe flexors[3]. Thus, clinicians face the
pressure of completing and recording spasticity assessment on multiple limb
muscle groups (or individual muscles) in an accurate and a timely manner. There
are several tests available to assess spasticity. Based on the feasibility of
the tests in a clinical environment, spasticity assessment techniques can be
divided into two groups: (1) clinic-based and (2) lab-based. There are other
tests that measure impact of spasticity on function and quality of life in
patients with spasticity[4]; however, this review purely focuses on
tools specifically used to assess level of spasticity only.
There are
number of clinic based tests for spasticity assessments such as Modified
Ashworth Scale (MAS), Modified Tardieu Scale (MTS), Wartenberg Knee Pendulum
Test (WKPT), Numerical Rating Scale (NRS), Penn Spasm Frequency Scale (PSFS),
time taken for muscle to relax, and Range of Motion (ROM; resting, passive, and
active available ROM). These assessments have been described in detail
elsewhere[4]. Common elements in all spasticity assessments are passive
movement of the limb and perception and rating of the increased resistance to
movement sometimes described as a catch. Among these scales, clinicians
perceive MAS to be the most feasible test in terms of time requirements and
ease of testing in multiple muscles. There are indications from research
studies in patients with spinal cord injury that MAS is correlated with reflex
hyperexcitability[11] as well as in patients with stroke where
changes in MAS are correlated with changes in muscle spindle sensitivity[10].
Unfortunately, MAS has limited reliability and poor validity leading to appeals
for clinicians to stop using it in its current form[12,13]. There
have also been efforts to further modify the MAS and have shown promising
improvements in intrarater reliability[13].
One of the
criticisms of the MAS is that it does not provide spasticity rating in response
to different movement speeds, which has been shown to be a sensitive way of
assessing the reflex hyperexcitability (neural component) underlying spasticity[14].
On the other hand, MTS is performed both at slow and fast velocities and
inherently has better validity than MAS considering Lance’s definition of
spasticity. In the MTS, slow movement velocity is used to determine if there is
a contracture or loss of range of motion and the fast movement speed is used to
trigger the stretch reflex. In addition to the qualitative rating of spasticity
similar to the MAS (examiner’s perception of resistance), MTS also incorporates
measurement of the spasticity angle. Spasticity angle is the angle of catch at
fast speed and as spasticity decreases, it is conceivable that the spasticity
angle would also decrease. Thus, MTS is more promising scale because it is able
to discriminate the neural component better by using two movement speeds[15];
however, MTS requires use of a goniometer which is difficult to align with the
joint during limb movements and may be a factor affecting reliability of the
MTS[16-18].
Among other
tests to assess spasticity, WKPT is only useful for spasticity in knee muscles
and cannot be readily used for other joints in the arm and leg because it
relies heavily upon the long lever and gravity to provide consistent repeatable
limb movement to produce muscle stretch and elicit spasticity. Specifically
ankle plantar flexors spasticity which is commonly treated with BoNTA[3]
cannot be tested using WKPT because of a very small lever arm (foot). NRS and
PSFS are useful measures to assess patient perception of spasticity[4,19];
however, they cannot be solely relied upon because patient perception of
spasticity only partially represents the neural component of spasticity[20].
Time taken by the muscle to relax in response to a stretch may be an important
and readily testable measure that reflects muscle spindle sensitivity and
reflex hyperexcitability underlying spasticity and clonus[21], but
no research has been done on this measure. ROM measurements are useful in
assessing the end range, but do not discriminate between neural or
musculotendinous changes. Additionally, goniometry method to assess ROM has
validity and repeatability concerns due to variability in placement, force
application, and alignment of the goniometer arms[22] and is thus, non-sensitive
to small changes.
In contrast to
the clinic-based measures, in the lab-based spasticity assessments limb
movement and perception of increased movement resistance are both automated and
objectified; thus, requiring specialized equipment. A motor drives the passive
limb movement and force transducers quantify speed of movement and increased
resistance or surface electromyography (EMG) sensors quantify output from the
muscle being stretched[23]. A good working knowledge of
biomechanical principles is necessary to conduct lab-based tests of spasticity.
Force entities such as torque (measured in Newton–N), stiffness (damping), or
elasticity (viscosity) are estimated using equations[24] and
measured using length of the lever arm and joint angle[23]. For
example, tonic stretch reflex threshold measurement (TSRT-a lab-based measure)
more accurately reflects spasticity as defined by Lance[1] than
other clinical tests of spasticity[23]. TSRT is measured using a
combination of joint movement speeds and is velocity-dependent in evoking a
muscle response[23].
Although TSRT
incorporates velocity-dependence, a hallmark of Lance’s definition, it is worth
noting that both neural as well as non-neural structures such as the connective
tissues surrounding the joint contribute towards the velocity-dependent
increase in resistance[2,24]. Thus, a velocity-dependent increased
resistance to movement could be attributed to reflex (neural) or viscoelastic
properties of joints and muscles (non-neural)[2]. To counter this
velocity-dependent behavior of both neural as well as non-neural structures,
Gaverth et al (2013) have used an elegant biomechanical model to isolate
the neural from the non-neural components of increased resistance to movement[25].
Their method involves isokinetic wrist extension using a NeuroFlexor device
that moves the joint at different velocities and is thus limited only to the
wrist and finger joints[25]. They define the neural component (after
removing the elastic and viscous components) as an estimate of true spasticity
which has been shown to be a sensitive method to assess changes in spasticity
after botulinum toxin injections[26].
Among the
spasticity measurements available, the lab-based measures appear to be the most
robust assessments. These approaches have been routinely used in animal[27]
as well as human[14,26] spasticity research. Although these
motor-driven assessments are robust and provide a consistent and accurate
assessment of spasticity, they require specialized equipment run by a computer
software, which is also required for data analysis[28]. This process
can be time intensive requiring a special facility and personnel to collect and
process the data and does not provide point-of-care (POC) spasticity assessment.
POC assessments are valuable for timely and efficient spasticity management. To
address this issue, efforts have been made to design clinic friendly POC
equipment that balances the need for ease of testing and scoring as well as a
need for accurate and valid measurements[14,25]. These devices are
able to discriminate the neural from the musculotendinous components in a
relatively short period of time. However, this technology is in its early
stages of development and is limited to testing a single joint (elbow or
wrist/fingers) and thus, may be cost-prohibitive.
In the absence
of a better outcome measures that match the ease of testing and scoring of MAS,
clinicians continue to use MAS to assess spasticity. There is also some
evidence to support using MAS[10] and hence researchers continue to
make efforts to refine this scale to improve its validity and reliability[13].
In addition to the scoring method, another concern with MAS that needs to be
addressed in future work is the need to test increased movement resistance at
various movement speeds. A recent paper used a simple yet promising approach to
moving limbs at consistent and repeatable speeds across sessions using a
metronome[6]. Reasons why this approach is promising are that it
uses very little if any specialized equipment, assesses the neural component
using different limb movement speeds, and allows a consistent way to replicate
movement speeds before and after spasticity treatment[6].
If spasticity
assessments are time-consuming, require multiple steps, and specialized
equipment and personnel, then it will be harder for clinicians to adopt and
implement such assessments in their clinical practice. Researchers should keep
this in mind as future studies are designed to investigate the best way to
clinically assess spasticity. It is clear that MAS in its current form is not
the perfect answer and future work is being directed towards improving the
validity and reliability of MAS.
Acknowledgments
We would like to thank the clinical team in the Comprehensive
Spasticity Management Clinic in West Park Healthcare Centre, Toronto for their
input and the West Park Foundation (salary support for Dr. Phadke).
CONFLICT OF INTERESTS
Unrelated to this paper, the authors have received research grant
funding from Allergan Inc. and Merz Pharma (CP, FI, CB) and honoraria and
speaker fees from Allergan Inc. and Merz Pharma (FI, CB). No other conflicts of
interests.
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Peer reviewer: Fang Li, MD, PhD,
Department of Rehabilitation Medicine,, Huashan Hospital, Fudan University,
Shanghai, 200040, China; Arzu Yagiz On, Professor, Ege University Medical
Faculty, Department of Physical Medicine and Rehablitation, 35100, Izmir,
Turkey.
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