Special Section-Spasticity

Editor’s note: This Special Section on Spasticity is a series of 5 clinical focused review articles that was developed from the “Advanced
Assessment and Management Skills for Spasticity, Dystonia, and Related Motor Disorders” Pre-course at the 2008 AAPM&R Annual
Assembly in San Diego, CA. These articles are not an exact representation of that course nor are they designed to represent comprehensive
coverage of the field. However, these reviews do provide clinically pertinent and practical information that the clinician will hopefully be
able to incorporate into his or her practice. The authors of these articles are expert practitioners who served on the faculty for this course.
For further details, the course content can be accessed at http://me.e-aapmr.org/

Spastic Hypertonia and Movement Disorders:

Pathophysiology, Clinical Presentation, and
Quantification
Geoffrey Sheean, MD, John R. McGuire, MD

A delayed consequence of a lesion affecting the upper motor neuron pathways is the
appearance of some forms of motor overactivity, including spasticity. Many of these are
caused by hyperexcitability of spinal reflexes, such as stretch reflexes (spasticity, tendon
hyperreflexia) or flexor withdrawal reflexes (flexor spasms), and are elicited at rest by
sensory stimulation. Spastic co-contraction is probably attributable to failure of reciprocal
inhibition; it occurs only during active voluntary movement and constrains such move-
ment. The basic underlying mechanism of these changes is not clear, although a change in
the balance between the inhibitory and excitatory supraspinal upper motor neuron path-
ways toward net excitation most likely contributes. Increased intrinsic excitability of the
alpha motor neurons is another possible factor. Spastic dystonia is most often seen as the
presence of tonic muscle contraction in the absence of voluntary movement or spinal reflex
activation, and the underlying mechanisms are obscure. Prolonged shortening of tissues,
either because of weakness or muscle contraction, leads to stiffness of the soft tissues, which
contributes to hypertonia and is thus self-perpetuating, and ultimately to contracture with
fixed shortening. Some of these forms of motor overactivity produce involuntary move-
ments (hyperkinetic), eg, flexor spasms, whereas others impair movement (hypokinetic),
either voluntary movement, eg, spastic co-contraction, or passive movement, eg, spasticity.
Quantification has mostly focused on hypertonia, that is, increased resistance at rest to
passive movement. In the upper motor neuron syndrome, hypertonia could be caused by a
combination of spasticity, spastic dystonia, and soft tissue stiffness (rheologic changes).
Some measures, such as the Ashworth or Modified Ashworth Scales, quantify hypertonia
but are very poor at distinguishing between spasticity and soft tissue stiffness. Another, the
Tardieu Scale, is better at making this distinction, but quantification of the spasticity portion
of hypertonia remains difficult, at least in a clinical setting.

G.S. University of California San Diego, 402

INTRODUCTION Dickinson St, Suite 190, San Diego, CA
92103. Address correspondence to: G.S.;
After a lesion of the upper motor neurons (UMN), certain clinical deficits are immediately e-mail: gsheean@ucsd.edu
apparent—weakness and loss of dexterity. Sometime later, other features appear, which are Disclosure: 2A, Allergan, Ipsen, Solstice; 5A,
Allergan
characterized by excessive muscle contraction. The initial deficits are referred to as the
J.R.M. Medical College of Wisconsin, Mil-
negative features of the upper motor neuron syndrome (UMNS), and the various muscle
waukee, WI
overactivities are the positive features (Table 1). Spasticity or spastic hypertonia are types of Disclosure: nothing to disclose
muscle overactivity elicited by passive stretch of a muscle at rest. Spasticity and several of the Disclosure Key can be found on the Table of
other positive features can interfere with active or passive movement. Contents and at www.pmrjournal.org
This paper will review the pathophysiology, clinical features, and methods of quantifying Submitted for publication July 16, 2009;
spasticity and those other positive features that interfere with movement. accepted August 6.

PM&R © 2009 by the American Academy of Physical Medicine and Rehabilitation

1934-1482/09/$36.00 Vol. 1, 827-833, September 2009 827
Printed in U.S.A. DOI: 10.1016/j.pmrj.2009.08.002
828 Sheean and McGuire SPASTICITY: PATHOPHYSIOLOGY, CLINICAL PRESENTATION, AND QUANTIFICATION
Table 1. Upper motor neuron syndrome: negative and posi-
tive features
Negative Positive
Weakness Spasticity
Loss of dexterity Spastic dystonia
Fatigue Flexor and extensor spasms
Spastic co-contraction
Extensor plantar responses
Clonus
Exaggerated deep tendon reflexes
Associated reactions
PATHOPHYSIOLOGY AND CLINICAL
FEATURES
The UMN pathways are descending motor tracts, originating
in the cortex or brain stem, that directly or indirectly influ-
ence the excitability of the lower motor neuron or anterior
horn cell (AHC) (Figure 1) [1]. These pathways include the
corticospinal (or pyramidal tract) from the cortex, which has
direct excitatory input to the AHC. In addition, there are
descending motor pathways originating in the brain stem
that indirectly influence the excitability of the AHC, through
various spinal reflex pathways. These include the predomi-
nantly excitatory medial reticulospinal tract and lateral ves-
tibulospinal tract, and the inhibitory dorsal reticulospinal
tract (DRT), the latter receiving facilitatory input from the
cortex via corticoreticular fibers, whereas the excitatory path-
ways do not. The excitatory pathways are actually mixed in
their effects as they also inhibit flexor reflex afferents. The
DRT runs close to the corticospinal tract, so both are usually
simultaneously affected by the same pathologic condition.
The positive features of the UMNS are probably more related
to damage to these nonpyramidal or parapyramidal motor
pathways of brain stem origin than to the pyramidal tracts.
Depending on the location of the lesion, different patterns of
muscle weakness and overactivity may occur.
For a finite period after an acute lesion to the UMN
pathway, there is a loss of all spinal reflex activity, frequently
referred to as spinal shock. Gradually, reflex activity emerges
and along with it the spastic muscle overactivities. Many of
these are caused by hyperexcitability or disinhibition of spi-
nal reflexes. As defined by Lance [2]:
Spasticity is a motor disorder characterized by a velocity-
dependent increase in tonic stretch reflexes (“muscle tone”)
with exaggerated tendon jerks, resulting from hyperexcit-
ability of the stretch reflex, as one component of the upper
motor neurone syndrome.
The stretch reflex is mediated by Ia afferents and involves
the muscle spindles, whose excitability is controlled by
gamma efferents. There is no evidence of increased spindle
sensitivity as a result of increased gamma efferent drive in
spasticity. The hyperexcitability appears to arise in the spinal
cord, presumably owing to loss of inhibition from damage to
the DRT in the brain stem or spinal cord, or to the corticore-
ticular fibers that facilitate it, in the case of supratentorial
lesions. The velocity-dependence of spasticity can be attrib-
uted to the velocity sensitivity of the Ia afferents (Figure 2)
[3]. This should imply that once the stretching movement
has finished the contraction should stop; however, in some
cases there is continued contraction, possibly caused by the
more length-dependent type II muscle afferents.
Other forms of muscle overactivity are also attributable to
hyperexcitability of spinal reflexes. Flexor withdrawal re-
flexes are mediated by flexor reflex afferents, which include
touch, nociceptive, and mechanical afferents from nearly all
tissues; clinicians testing for a Babinski reflex are well aware
of this reflex. The extensor toe response is caused by disinhi-
bition of a normal reflex that becomes inhibited developmen-
tally at around 12 months of age. This is probably the only
positive feature of the UMNS that is exclusively attributable
to damage to the corticospinal tract [4]. Hyperexcitability of
the flexor withdrawal reflex is responsible for the flexor
spasms of the lower limbs, commonly seen after spinal cord
injury. Similarly, extensor spasms of the lower limbs are
attributable to exaggeration of extensor reflexes. These are
less commonly encountered in clinical practice, but they can
be elicited and studied electrophysiologically.
There is another type of motor overactivity, which is not
caused by an exaggerated spinal reflex. This is seen in two
forms. The first is with tonic contraction of a muscle or
muscle group at rest, often in the upper limb, contributing to
the so-called hemiplegic posture. Tonic contraction is seen
and can be recorded electromyographically in shoulder ad-
ductors, elbow flexors, and wrist and finger flexors. This
phenomenon, when studied in monkeys, was called spastic
dystonia by Denny-Brown [5]. He found that the contraction
persisted even when the dorsal roots were cut, indicating that
it was a phenomenon independent of spinal reflexes. Al-
Figure 1. UMN pathways (Reprinted with permission from
Sheean G, The pathophysiology of spasticity, Eur J Neurol,
Wiley-Blackwell, 2002 [1]).
PM&R
Figure 2. Velocity dependence of spasticity (Sheean 2008, reprinted with permission [3]).
though not dependent on stretch reflexes, spastic dystonia is
sensitive to stretch and length (Figure 3). It may initially
increase with stretch but tends to gradually reduce with
sustained stretch and increasing length [6].
The second type of motor overactivity is action-induced
spastic dystonia, which should be quite familiar to those
clinicians who see patients after stroke. On standing or
during walking, the affected lower limb may adopt a posture
of extension at the knee and plantarflexion of the ankle,
perhaps with inversion (Figure 4). With continued walking
there may be progressive flexion of the elbow, called an
associated reaction. This type of associated reaction can also
Vol. 1, Iss. 9, 2009 829
occur with voluntary activity in other parts of the body or
with involuntary events such as yawning or sneezing. Such
mass movements with voluntary upper limb movement re-
semble the overflow phenomenon seen in dystonia owing to
extrapyramidal or basal ganglia disorders; thus, the use of the
term spastic dystonia is unfortunate because dystonia is
usually associated with such extrapyramidal or basal ganglia
conditions.
Flexor and extensor spasms and action-induced spastic
dystonia can be classified as hyperkinetic (to borrow a term
from movement disorders) because they produce involun-
tary movement (Table 2). Conversely, spasticity and static
830 Sheean and McGuire SPASTICITY: PATHOPHYSIOLOGY, CLINICAL PRESENTATION, AND QUANTIFICATION

Figure 3. Spastic dystonia sensitive to stretch and length

(Gracies 2005, reprinted with permission of John Wiley & Sons
Inc. © 2005 [6]).

spastic dystonia (at rest) interfere with movement. By defini-

tion, spasticity occurs only at rest and can only interfere with
passive movement. Spastic dystonia can interfere with both
active and passive movements.
Active movement in the UMNS is mostly impaired by the
deficits—weakness and loss of dexterity. However, one can
also see active movement impaired by co-contraction of
agonist and antagonist muscle pairs. A common example is
the elbow extensors limited by co-contraction of the elbow
flexors, which will sometimes be so severe as to limit any
Figure 4. Hemiplegic posture
elbow extension, thus imitating severe triceps weakness. One
explanation for co-contraction is that the elbow extension
produces passive stretch of the elbow flexors, eliciting a tonic
stretch reflex, that is, spasticity. Another is that there is
limitation of extension caused by continuation of spastic lesion leaves the AHC intrinsically more excitable so that it
dystonia of the elbow flexors. However, there are instances in overreacts to reflexive input? The intrinsic excitability of
which the co-contraction occurs when there is no contraction AHCs is difficult to study. Spasticity is usually studied by
at rest and begins before movement has occurred (before testing reflex excitability electrophysiologically, but this does
stretch, see Figure 5 [7]) or when the contraction is isometric not isolate the intrinsic excitability of the AHCs, as the reflex
(no stretch). This can only occur if there is a failure of pathways themselves are modulated by supraspinal activity.
reciprocal inhibition between the two muscle groups at either Similarly, F waves are influenced by Renshaw cell activity,
the spinal cord or cortical level resulting in simultaneous which is also under supraspinal control.
activation of each group by the UMN drive. Failure of recip- One technique that can examine in vivo the intrinsic
rocal inhibition has been demonstrated electrophysiologi- excitability of the AHC is through the study of persistent
cally in the UMNS. In extreme cases, the drive to the antag- inward currents and plateau potentials. Recordings can be
onist exceeds the agonist. This results in the clinically familiar
examples of attempted extension of the fingers resulting in Table 2. Classification of the types of motor overactivity in the
flexion, or attempted ankle dorsiflexion resulting in plantar- upper motor neuron syndrome
flexion (Figure 6) [6]. Interestingly, co-contraction and fail-
Hyperkinetic Hypokinetic
ure of reciprocal inhibition are core features of dystonia as a (involuntary movements) (impairment of movement)*
result of extrapyramidal or basal ganglia disorders.
Spasms (flexor, extensor, Spasticity
adductor) Static spastic dystonia
Great toe extension Spastic co-contraction
BASIC MECHANISMS OF SPASTIC MOTOR Associated reactions
Mass movements
OVERACTIVITY
Clonus
Given that the previously described forms of flexor and Action-induced spastic
dystonia
extensor spasms and action-induced spastic dystonia are
examples of motor overactivity, could it be that the UMN *Evaluated by tone and active or passive range of movement.
PM&R
Figure 5. Co-contraction before movement. (Figure 2j from
Mayer 2002, reprinted with permission. © WeMove 1st edition;
3rd edition available at www.mdvu.org).
made directly from the AHC of rats with spinal cord lesions.
These studies show that motor neuron excitability is reduced
in the acute phase (spinal shock), but then returns and is
increased concomitantly with the emergence of spasticity.
Furthermore, reflex spasms can be induced with a brief
sensory stimulus and are associated with repetitive, sustained
firing of the motor neurons. The persistent inward currents
that underlie these phenomena are under supraspinal control
and are affected by antispasticity medications.
Although some of the spastic motor overactivities—
particularly spasticity, flexor and extensor spasms, and pos-
sibly static spastic dystonia—might be explained by this
mechanism, others such as action-induced spastic dystonia,
associated reactions, and spastic co-contraction cannot. It
Figure 6. Co-contraction causing opposite movement
(Gracies 2005, reprinted with permission of John Wiley & Sons,
Inc. © 2005 [6]).
Vol. 1, Iss. 9, 2009 831
would also fail to explain the not-too-uncommon dissocia-
tion between spasticity and exaggerated tendon reflexes.
Disruption of the inhibitory and the excitatory pathways
in a UMN lesion could result in net disinhibition of the AHCs
and associated spinal reflex networks, resulting in those types
of motor overactivity that are reflex-mediated. The failure
to appear immediately after the lesion would be expected,
possibly related to spinal shock. Alternatively, some other
changes through neural plasticity might be necessary. The
actual spinal reflex pathways responsible for hyperexcita-
bility of the tonic stretch reflex that underlies spasticity are
unknown. Many have been studied electrophysiologically,
but there has generally been poor and inconsistent correla-
tion with spasticity.
SOFT TISSUE CHANGES
Secondary soft tissue changes can occur in the UMNS. Stiff-
ness of the soft tissues reduces compliance and can con-
tribute to hypertonia; therefore, it can be hard to distinguish
from hypertonia caused by spasticity or spastic dystonia. Not
uncommonly, both are present. Fixed shortening of the soft
tissues, ie, contracture, reduces the range of movement. It is
assumed that both soft tissue stiffness and contractures result
from prolonged shortening. Such shortening can be caused
by weakness and poor positioning, as well as spasticity,
spastic dystonia, and flexor spasm.
QUANTIFICATION
From a technical standpoint, the amount of spasticity present
is affected by many extraneous factors, including ambient
temperature, anxiety, time of day, level of pain, body posi-
tion, and the amount of prior stretching, all confounding the
interpretation of serial measurements.
Hypertonia can be described clinically using well-estab-
lished rating scales, such as the Ashworth [8] or Modified
Ashworth Scales [9] (Table 3). Such scales have been criti-
cized for many reasons [10], including the inability to distin-
guish between soft tissue and neural contributions to hyper-
tonia. The Tardieu Scale (Table 3) attempts to do this by
measuring two angles, the angle (R1) at which resistance is
first encountered with a quick muscle stretch and the final
angle (R2), which reflects the maximum range of movement
with a slow muscle stretch [11]. The difference between the
two is claimed to represent the true amount of spasticity or
spasticity angle.
In the lower limbs, spasticity in the quadriceps can be
measured by the pendulum test, in which the subject is
supine and the thigh is resting on a table. The lower leg is
held up with the knee fully extended against gravity and then
allowed to fall, oscillating through a few cycles of flexion and
extension until stopping at rest. The movement of the leg can
832 Sheean and McGuire SPASTICITY: PATHOPHYSIOLOGY, CLINICAL PRESENTATION, AND QUANTIFICATION
Table 3. Clinical measurement of spasticity
Measure Ashworth Scale
0 No increased tone
1 Slight increase in muscle tone, manifested by a catch and release or by
minimal resistance at the end of the range of motion when the affected
part is moved in flexion or extension
2 More marked increase in muscle tone through most of the range of motion,
but affected part(s) easily moved
3 Considerable increase in muscle tone, passive movement difficult
4 Affected part(s) rigid in flexion or extension
be recorded with accelerometers and the pattern compared
with normal subjects (Figure 7) [12].
The only true method of measuring spasticity, as defined
by Lance [2], is to measure tonic stretch reflexes electromyo-
graphically. Simultaneous torque measurement can quantify
the resistance to passive movement, but it is still difficult to
determine how much resistance is produced by the tonic
stretch reflex and how much is produced by soft tissue
stiffness.
Flexor and extensor spasms can be measured using logs of
spasm frequency and severity. In addition, flexor withdrawal
reflexes can be elicited and recorded electromyographically,
as a means of testing the effect of certain medications.
Spastic co-contraction can also be recorded and quan-
tified electromyographically (Figure 5). Because co-con-
traction that restricts movement tends to occur in muscles
Figure 7. Pendulum test (Reprinted with permission from Ho et
al, Sensitivity of the pendulum test for assessing spasticity in
persons with cerebral palsy, Dev Med Child Neurol [11],
Wiley-Blackwell).
Tardieu Scale
No resistance
Slight resistance
Catch followed by a release
Fatigable clonus (⬍10 seconds)
Infatigable clonus (⬎10 seconds)
that are also affected by soft tissue stiffness, it can be
difficult to determine the relative contributions of soft
tissue stiffness and spastic co-contraction to the limitation
of movement.
Action-induced spastic dystonia of the lower limb can
be measured using gait analysis techniques that record
movement, electromyography, and torque forces simulta-
neously.
SUMMARY AND CONCLUSION
Many of the positive features of the UMNS are caused by
disinhibition of spinal reflexes or the failure of reciprocal
inhibition. The spinal reflex networks responsible for the
disinhibition of the tonic stretch reflex responsible for spas-
ticity are unknown. The mechanisms underlying both static
and action-induced spastic dystonia are also unknown.
Quantification of spastic hypertonia is complicated by the
coexistence of spasticity, spastic dystonia, and soft tissue
stiffness, all of which contribute to hypertonia.
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