SPASTICITY MANAGEMENT AFTER STROCKE

Spasticity Management
After Stroke
Francois Bethoux, MD
INTRODUCTION
Spasticity is a movement disorder, defined as a velocity-dependent increase in
stretch reflexes
1
due to impaired supraspinal inhibitory signals. Recent observations
suggest, however, that decreased homosynaptic depression (ie, impaired depletion
of the release of excitatory neurotransmitters with repetitive afferent activation), rather
than decreased presynaptic inhibition, is associated with poststroke spasticity.
2
In
addition, defective supraspinal control of various spinal inhibitory and facilitatory
circuits is associated with abnormal muscle contraction during voluntary movement.
3
Finally, changes in the rheologic and contractile properties of musculoskeletal soft tis-
sue are frequently associated with chronic spasticity and in turn have been linked to
increased spasticity.
4
Cerebral-origin spasticity after a stroke differs from spinal-origin spasticity as
encountered in spinal cord injury and multiple sclerosis. Cerebral-origin spasticity is
characterized by
Mellen Center Rehabilitation Services, The Cleveland Clinic, 9500 Euclid Avenue/Desk U10,
Cleveland, OH 44195, USA
E-mail address: [email protected]
KEYWORDS
Stroke Spasticity Symptom management Outcome measures Rehabilitation
KEY POINTS
Spasticity from stroke is classified as cerebral-origin spasticity, characterized by hyperex-
citability of monosynaptic pathways, a rapid rise in excitation, and stereotypical postures
involving antigravity muscle groups.
The prevalence of spasticity after stroke can be as high as 46% in the chronic phase
(over 3 months).
Spasticity is most often associated with other neurologic impairments, in particular
paresis, which complicate its evaluation and management.
Treating spasticity after a stroke entails combining nonpharmacological and pharmaco-
logic interventions.
There is emerging evidence suggesting that some treatments for spasticity improve upper
and lower extremity functional performance.
Phys Med Rehabil Clin N Am 26 (2015) 625–639
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Hyperexcitability of monosynaptic pathways
A rapid rise in excitation
Stereotypical postures involving antigravity muscle groups. The hemiplegic
posture commonly observed after a stroke consists of
In the upper extremity: shoulder adduction; forearm pronation; and elbow,
wrist, and finger flexion
In the lower extremity: hip adduction, knee extension, ankle plantarflexion, and
often pes varus
Spasticity is only one component of the upper motor neuron (UMN) syndrome. As a
consequence, other features of the UMN syndrome most often accompany spasticity,
such as weakness, loss of dexterity, and synkinetic movements. In one study, 100%
of patients with spasticity exhibited limb weakness (vs 50% of patients without spas-
ticity) when assessed over 3 months after a stroke.
5
Because other neurologic impair-
ments are commonly seen after a stroke (eg, visual, sensory, and cognitive), it may be
difficult to isolate the specific impact of spasticity on functional limitations. It has been
stated that the functional limitations experienced by stroke survivors are mostly
related to neurologic deficits other than spasticity.
6
The prevalence of spasticity after stroke is difficult to ascertain in the absence of
rigorous population-based studies. In a survey from the National Stroke Association,
57% of 504 stroke survivors reported tight or stiff muscles, suggesting the presence of
spasticity.
7
Clinician-based determination of the prevalence of spasticity is most often
conducted in hospital stroke units, with sample sizes ranging from 50 to 200 individ-
uals. Prevalence values are between 4% and 27% in the first month after stroke and
between 17% and 46% past 3 months.
8,9
Longitudinal studies generally report higher
prevalence values at the chronic phase.
5,9,10
PATIENT EVALUATION OVERVIEW
Identifying Spasticity
The diagnosis of spasticity is based on clinical features, in the context of a central
nervous system disorder. Spasticity is usually associated with some or all of the pa-
tient complaints presented in Table 1. Even though these symptoms are suggestive
of spasticity, they are not sufficient to establish the diagnosis. For example, difficulty
moving a limb can be described as “stiffness” even when it is due to weakness. Pain
can be related to spasticity (particularly if it is associated with spasms or occurs with
passive movement), but central neuropathic pain (particularly after a thalamic stroke)
or musculoskeletal pain may also be present.
The diagnosis of spasticity is confirmed by clinical examination findings, summa-
rized in Table 1. Some of these signs are associated with passive stretch (resistance
Table 1
Patient complaints and examination findings associated with spasticity
Complaints Clinical Signs
Muscle stiffness or tightness
Muscle spasms
Clonus (shaking)
Pain
Difficulty performing voluntary
movement
Limb deformity (cosmetic or
functional concern)
Resistance to passive movement
Clonus
Spasms
Co-contraction of agonist and antagonist muscles
Spastic dystonia
Decreased passive range of motion
Abnormal posture
Limb deformity
Bethoux
626
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to passive movement, clonus); others are observed only with active movement,
such as muscle co-contraction and spastic dystonia. Therefore, spasticity needs to
be examined at rest and with voluntary movement (whenever possible) to better
understand the functional consequences of spasticity. In addition, it is useful to assess
spasticity in various positions (standing vs sitting vs supine) because position-
dependent variations in spasticity have been reported and are commonly observed
in practice.
Other signs of the UMN syndrome are almost always present, in particular paresis
and loss of dexterity but also synergistic movement patterns. In addition, other neuro-
logic impairments often increase the complexity of the clinical presentation but are
important to document, because they have an impact on goal setting and treatment
planning. Strength output is of particular importance, because increased weakness
may occur as spasticity is treated. Finally, the presence of partial or total musculo-
skeletal contractures should be documented, because they have an impact on the
treatment plan, whether or not they are directly related to spasticity.
Spasticity needs to be differentiated from other movement disorders associated
with increased tone, in particular
Dystonia, which causes abnormal sustained or intermittent muscle contrac-
tions with twisting movements and abnormal postures. Some of the features of
dystonia, however, are observed with spasticity (spastic dystonia), as discussed
previously.
Extrapyramidal hypertonia, which is characterized by cogwheeling and rigidity
Velocity-dependent resistance to passive movement is a useful clinical feature to
distinguish spasticity from these other movement disorders but may be difficult to
assess in the presence of severe hypertonia and ROM limitations. In addition, various
movement disorders may coexist, depending on the location of the stroke.
Measuring Spasticity
Once spasticity is identified, it is useful to rate its severity, particularly for monitoring
treatment outcomes. Table 2 gives examples of some of the assessment tools avail-
able to clinicians and researchers.
Most of the spasticity severity scales used in the clinic and in clinical trials mea-
sure resistance to passive movement (eg, Ashworth Scale and Tardieu Scale), despite
the aforementioned limitations of this approach. In addition, patient-reported ques-
tionnaires have been used to quantify spasm frequency and, more recently, patients’
overall assessment of their spasticity (spasticity numeric rating scale). Instrumented
tests measurements (electromyogram [EMG], dynamometry, and pendulum test) are
not routinely used in the clinic, due to time and equipment requirements and because
they do not always correlate with clinical findings.
Although functional tests and scales are increasingly used in clinical trials of treat-
ments for spasticity, none of them was specifically developed and validated for this
application, to the author’s knowledge. The appropriateness of a specific functional
test depends on the limb(s) targeted for treatment, the treatment goals, the instru-
ment’s psychometric properties, and feasibility. Among others, the Frenchay Arm
Test, the Disability Assessment Scale have been used to assess upper limb function;
timed walking tests to assess lower limb function; and the Barthel Index and Func-
tional Independence Measure for overall functional status have been used in the eval-
uation of treatments of spasticity after stroke.
Other neurologic impairments need to be documented in the initial evaluation and
taken into account for goal setting but may not need to be monitored in a quantitative
Stroke Spasticity 627
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Table 2
Assessment tools for spasticity
Name Clinical Parameter Assessed Scoring Comments
Clinical examination scales
Ashworth Scale (AS)
and Modified
Ashworth Scale
(MAS)
38
Resistance to passive
movement
AS: 1 (no increase in muscle tone) to 5 (affected part[s]
rigid in flexion or extension)
MAS: 0 (no increase in muscle tone) to 4 (affected part
[s] rigid in flexion or extension)
Includes 11rating (catch followed by minimal
resistance throughout the remainder of the range of
motion)
Pros: easy to administer; frequently used in
clinical trials
Cons: lacks sensitivity to change; inter-rater
reliability is an issue; resistance to passive
movement is not equivalent to spasticity
Tardieu Scale (TS)
39
and Modified
Tardieu Scale
(MTS)
40
Resistance to passive
movement
TS: resistance to passive movement assessed at 3 speeds:
V1 (as slow as possible), V2 (speed of the limb falling
under gravity), V3 (as fast as possible)
Two angles measured: R1 (first catch to a quick stretch)
and R2 (total passive range of motion with slow
stretch)
R2–R1 5dynamic tone
MTS: only 2 speeds (V1 and V3)
Pros: easy to administer; more detailed
assessment than AS or MAS
Cons: lacks sensitivity to change; inter-rater
reliability is an issue
Triple Spasticity
Scale
41
Change in resistance to
passive movement
between slow and fast
speed, clonus, dynamic
muscle length
Total score from 0 to 10
Three subscales: increased
resistance
between a slow
stretch and a fast
stretch (0–4), clonus (0–2), dynamic muscle length (0–4)
—
Self-report measures
Spasm Frequency
Scale
42
Spasm frequency 0 (No spasm) to 4 (more than 10 spontaneous spasms
per hour)
Pros: easy to use; frequently used in clinical trials
Cons: does not take into account fluctuations of
spasm frequency; does not assess spasm
severity or pain associated with spasms; lacks
sensitivity to change
Bethoux
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Spasm Frequency
Score
43
Spasm frequency 0 (No spasms) to 10 (10 or more spasms per day, or
continuous contraction)
Pros and cons are similar to those cited for the
Spasm Frequency Scale. Not as commonly used
in clinical trials.
Spasticity numeric
rating scale
(NRS)
44
Global severity of spasticity 0 (No spasticity) to 10 (worst possible spasticity) Pros: easy to use, good test-retest reliability,
correlates with other measures of spasticity
Clinically important difference was calculated
at 30% change in score (minimal clinically
important difference: 18% change)
Cons: validated only for multiple sclerosis–
related spasticity
Instrumented measurements
Isokinetic
dynamometry
45
Resistance to passive
movement
Torque Pros: high test-retest reliability; excellent control
of stretch velocity and amplitude;
quantification of resistance to passive
movement
Cons: equipment and time requirements;
correlation with traditional clinical measures
not always satisfactory
Pendulum test
46
Lower leg swing in patient
sitting
Amplitude of leg swing around the knee (assessed with
electrogoniometer), angle difference between start
and finish positions
Pros: simple setup; correlates well with clinical
measures of spasticity
Cons: requires equipment; only assesses
spasticity around the knee joint
EMG
47
EMG response to stretch,
tendon tap (T reflex) and
electrical stimulation of
the peripheral nerve (H-
reflex)
Threshold values
H/M ratio (H 5H-reflex threshold, M 5M-reflex
threshold)
Pros: measures reflex activity
Cons: equipment and time requirements
Poor or no correlation with clinical measures
Tonic stretch reflex
threshold (TSRT)
48
Excitability of motoneurons
without stretch (0/s
velocity) TSRT computed
from angles where the
EMG signal increases for
a given velocity of stretch
The TSRT is defined as the intercept value of the linear
regression line for dynamic stretch reflex thresholds
(at various angular velocities) with the angle axis
(dependent variable: angle; independent variable:
velocity).
Pros: portable device; moderate inter- and
intrarater reliability for moderate to high
spasticity; tested in poststroke spasticity
Cons: time consuming; did not correlate with
MAS scores in preliminary validation study
Stroke Spasticity 629
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