Spasticity is defined as “a motor disorder, characterized by a velocity-dependent

STROKE CLINICAL UPDATES
POST-STROKE LOWER EXTREMITY SPASTICITY: Evidence and Opportunities
Spasticity is defined as “a motor disorder,
characterized by a velocity-dependent
increase in tonic stretch reflexes (muscle
tone) with exaggerated tendon jerks,
resulting from hyper-excitability of the
stretch reflex as one component of the upper
motor neurone syndrome."1 The
pathophysiology of spasticity is complex. It
involves not only prolonged disinhibition of
spinal reflexes under the control of
inhibitory and excitatory descending
pathways, but also may involve lesions of
premotor and supplementary motor areas.
Spasticity is part of a larger picture that
includes spastic dystonia, co-contractions
and associated reactions. Spastic dystonia
is dependent on efferent drives, and cocontraction results from an inability to
control reciprocal inhibition of agonist and
antagonist muscle groups.2
Post-stroke spasticity is a common
complication. After 2 weeks, the
prevalence of spasticity in any limb is 25%.
After 6 months, it increases to 43%, and
after one year it decreases back to 25%.3,4,5
Within the first month post-stroke, the
incidence of significant spasticity is 27%.6
For stroke survivors admitted to an
inpatient rehabilitation facility, the
prevalence of spasticity in any limb is
42%,7 and the incidence of upper limb
spasticity over the first 3 months is 33%.8
The strongest predictor of moderate-tosevere spasticity is severe proximal and
distal limb weakness on acute hospital or
rehabilitation admission.6,10 Early
development of spasticity in the shoulder
joint has been associated with poor motor
recovery.9 Spasticity is a direct cause of
limitations in mobility and activities of
daily living, and may increase the cost of
care10 and reduce quality of life11 of the
stroke survivor.
This case provides a practical example of
how clinicians manage stroke survivors
with lower extremity spasticity throughout
the continuum of care. Evidence- and
consensus-based treatments are utilized to
decrease spasticity and improve quality of
life.
CASE
Ms. Jones (not her real name) is a 60-yearold right-handed white female, with a
history of stroke in 2007 with residual left
hemiparesis, hypertension, hyperlipidemia,
and depression, who was admitted to an
acute care hospital for pain after slipping on
the floor. She was found to have an iliac
wing fracture. CT and MRI Head were
negative for new infarcts. MRI Cervical
Spine demonstrated multi-level disk disease
with no significant stenosis. She was noted
to have near occlusion of her right internal
carotid artery. Cerebral Angiogram
demonstrated diffuse intracranial right
internal carotid artery stenosis particularly
in the supraclinoid area. She did not require
surgery. For her previous stroke, she
continued atorvastatin 80 mg by mouth at
bedtime and aspirin 325 mg by mouth daily.
She was transferred to a subacute
rehabilitation unit, during which time she
was noted to have spasticity of the left
lower limb resulting in an equinovarus
deformity. She remained in the
rehabilitation unit for approximately 2
weeks, and was discharged home. She
ultimately presented to the outpatient clinic
for management of her spasticity.
The patient denies the use of tobacco,
alcohol, or illicit drug products. She is
disabled from her stroke. She is single, and
lives alone with her cat in a senior citizen’s
apartment with no steps to enter the
building. She ambulates independently
with a left molded ankle-foot orthosis
(MAFO) only.
On physical examination, her extremities
were symmetrical without cyanosis,
clubbing, or edema. Range of motion is
limited in the left ankle due to spasticity.
Her left ankle is positioned in equinovarus
deformity without toe clawing. Cognition
and speech were grossly intact. Cranial
nerves from II-XII were grossly intact
except for her right eye being abducted and
elevated due to the previous stroke.
Sensation to light touch, pinprick, and
proprioception was grossly intact in all
extremities. Muscle strength was as
follows: Right upper and lower extremities
5/5 throughout; left upper and lower
extremities Brunnstrom grade III. The
patient ambulated independently with only a
left MAFO. Without the MAFO, the left
foot was positioned in equinovarus position,
and her gait was characterized by walking
on the lateral aspect of her foot with foot
drop during swing phase. She had difficulty
donning the MAFO because of the severity
of the equinovarus deformity, but ultimately
could don it independently.
Assessment and Treatment of Lower
Limb Post-Stroke Spasticity
The assessment of spasticity includes the
identification of impairments, activities
limitations, and participation restrictions
that spasticity affects. The clinician and
stroke survivor should evaluate whether
spasticity has resulted in or will lead to
musculoskeletal deformity. If the clinician
and stroke survivor come to a mutual
decision to treat spasticity, goals of
treatment should be identified and
discussed. Goals may be as simple as
reducing tone to increase range of motion,
improve joint position, or reduce pain.
Functional objectives may include
improving transfers and ambulation, or
easing the performance of activities of daily
living. Patient preferences should be
evaluated as some tone may be required to
optimize mobility or activities of daily
living. Any source of noxious stimulus that
can increase the severity of spasticity
should be identified and treated.
The most common evaluation tool for
spasticity is the modified Ashworth scale
(Table 1).12 While the Ashworth scale
actually measures muscle tone and not
spasticity, it is the most widely used scale in
research and clinical applications. Muscle
tone should be recorded in all appropriate
pivots of each joint so that the effects of
treatment can be assessed.
A comprehensive spasticity management
program requires a multi-modal approach
that may include any combination of
physical therapy, occupational therapy, oral
medications, intrathecal medications,
intramuscular chemicals and biological
agents, and surgery. One means to
determine treatment is whether spasticity
involves a discrete location or is diffuse
throughout the body. If spasticity is
discrete, appropriate treatments include
intramuscular chemicals, such as phenol or
denatured alcohol, or biological agents,
such as the botulinum toxins. If spasticity is
more diffuse, oral or intrathecal medications
should be considered.
For this case, spasticity is limited to the left
lower limb. Assessment of lower limb
spasticity in the stroke survivor involves
evaluation of positioning in bed and
wheelchair, as well as deviations during
gait. Stroke survivors who are confined to
wheelchairs may have deformities in hip
and knee flexion. During gait, common
deviations may include scissoring gait due
to hip adductor tone, knee buckling due to
quadriceps weakness, knee hyperextension
due to hamstring weakness, foot drop due to
gastrocnemius and soleus weakness,
equinovarus deformity due to spasticity, and
toe clawing due to toe flexor tone. Table 2
lists movements and corresponding muscles
of the lower limb.
Botulinum toxins currently used for the
treatment of post-stroke spasticity include
onabotulinumtoxinA (Botox®),
abobotulinumtoxinA (Dysport®),
incobotulinumtoxinA (Xeomin®), and
rimabotulinumtoxinB (Myobloc®).i While
no botulinum toxin currently is approved by
the FDA for post-stroke lower limb
spasticity, they, along with phenol, may
play a significant role in correcting gait
deviations and positioning issues.
Scissoring gait may be treated by ablating
the anterior and posterior branches of the
obturator nerve using phenol, or with
botulinum toxin injections into each of the
hip adductor muscles. Equinovarus
deformities may be treated with botulinum
toxin injected into the ankle plantarflexor
and inverter muscles,13,14,15 and may
improve gait speed slightly.16 No studies
have been conducted to determine whether
botulinum toxin injections improve orthotic
fit.
The initial session of injections consisted of
500 units of onabotulinumtoxinA (Botox®)
were injected into the left tibialis anterior
(100 units), tibialis posterior (150 units),
extensor hallucis longus (50 units), flexor
digitorum longus (50 units), gastrocnemius
(100 units), and soleus (50 units) muscles.
The patient returned for recheck 2 weeks
after the injections to assess the initial
effects of the injections, and 6 weeks after
injections to assess the maximal effects of
the injections. It is very important to
counsel the patient that several cycles of
injections may be required to determine the
dosage for optimal management of
spasticity. Because spasticity in this patient
was so severe, the dosage of
onabotulinumtoxinA was increased several
times. At the current time, approximately 2
years after treatment was initiated, the
patient now receives a total of 500 units of
Botox injected into the left tibialis anterior
(100 units), tibialis posterior (150 units),
extensor hallucis longus (50 units), flexor
digitorum longus (50 units), gastrocnemius
(100 units), and soleus (50 units) muscles.
Despite repeated injections, the equinovarus
deformity has not significantly reduced. As
a result, the patient was referred to an
orthopedic surgeon for a splint anterior
tibialis transfer (SPLATT).17 The SPLATT
involves rerouting half of the tibialis
anterior tendon posteriorly to the cuboid
bone to address the varus deormity. It also
involves lengthening of Achilles tendon,
thus addressing the equinus deformity.
Occasionally, the tibialis posterior tendon
also must be lengthened. Prior to the
surgery, gait analysis with surface
electromyography should be performed to
confirm the hyperactive muscles that need
to be addressed.
CONCLUSION
This update has provided a definition of
spasticity, a brief synopsis of the assessment
and treatment of post-stroke spasticity, and
presented a case of lower limb post-stroke
spasticity. Post-stroke spasticity is a
common complication with a complex
pathophysiology. It affects activities and
participation, can cause pain, and can lead
to musculoskeletal deformity. The clinician
and stroke survivor mutually should decide
treatment modality and goals, and may
include physical and occupational therapies,
oral and intrathecal medications,
intramuscular injections, and surgery.
Appropriate treatment of spasticity can lead
to improved function and quality of life.
Faculty
Richard D. Zorowitz, M.D.
Associate Professor of Physical Medicine
and Rehabilitation The Johns Hopkins
University School of Medicine
Chairman, Department of Physical
Medicine and Rehabilitation
Johns Hopkins Bayview Medical Center
4940 Eastern Avenue, AA Building,
Room 1654
Baltimore, MD 21224-2735
F: 410-550-1345
V: 410-550-5299
Email: rzorowi1@jhmi.edu
Disclosure Statement
Dr. Zorowitz is a paid consultant for
Allergan, Inc., Avanir Pharmaceuticals,
and Medergy.
i
Doses among the different botulinum
toxins are not interchangeable.
TABLE 1. Modified Ashworth Scale (Bohannon and Smith 1987)
Score
Description
0
No increase in tone
1
Slight increase in tone giving a catch, release and minimal resistance at the
end of range of motion (ROM) when the limb is moved in
flexion/extension
1+
Slight increase in tone giving a catch, release and minimal resistance
throughout the remainder (less than half) of ROM
2
More marked increased in tone through most (more than half) of ROM,
but limb is easily moved
3
Considerable increase in tone – passive movement difficult
4
Limb rigid in flexion and extension
TABLE 2. Movements of the Lower Limb and their Associated Muscles
Movement
Muscle(s)
Hip Flexion
Iliopsoas
Sartorius
Rectus femoris
Hip Adduction
Adductor magnus
Adductor longus
Adductor brevis
Iliopsoas (weak)
Pectineus (weak)
Knee Extension
Rectus femoris
Vastus lateralis
Vastus medialis
Vastus intermedius
Knee Flexion
Lateral Hamstrings
Medial Hamstrings
Gastrocnemius
Equinovarus with
Flexed Toes
Medial gastrocnemius
Lateral hamstrings
Soleus
Tibialis posterior
Tibialis anterior
Flexor hallicis longus
Long toe flexors
Peroneus longus
Striatal (Hitchhiker) Toe
Extensor hallicis longus
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Lance JW. Symposium synopsis. In: Feldman RG, Young RR, Koella WP, editors.
Spasticity: Disordered control. Chicago: Yearbook Medical, 1980, pp. 485-494.
Sheehan G. The pathophysiology of spasticity. Eur J Neurol 2002; 9 (Suppl 1): 3-9.
Moura RCR, Fukujima MM, Aguiar AS, Fontes SV, Dauar RF, Prado Gf. Predictive factors
for spasticity among ischemic stroke patients. Arq Neuropsiquiatr 2009; 67: 1029-1036.
Urban PP, Wolf T, Uebele M, et al. Occurrence and clinical predictors of spasticity after
ischemic stroke. Stroke 2010; 41: 2016-2020.
Wissel J, Schelosky LD, Scott J, Christe W, Fais JH, Mueller J. Early development of
spasticity following stroke: a prospective observational trial. J Neurol 2010; 257: 1067-1072.
Lundstrom E, Smits A, Terent A, Borg J. Time-course and determinants of spasticity during
the first six months following first ever stroke. J Rehabil Med 2010; 42: 296-301.
Ryu JS, Lee JW, Lee SI, Chun MH. Factors predictive of spasticity and their effects on motor
recovery and functional outcome in stroke patients. Top Stroke Rehabil 2010; 17: 380-388.
Kong KH, Lee J, Chua KS. Occurrence and temporal evolution of upper limb spasticity in
stroke patients admitted to a rehabilitation unit. Arch Phys Med Rehabil 2012; 93:143-148.
Twitchell TE. The restoration of motor function following hemiplegia in man. Brain 1951;
74(4): 443-480.
Lundstrom E, Smits A, Borg J, Terent A. Four-fold increase in direct costs of stroke
survivors with spasticity compared with stroke survivors without spasticity: the first year
after the event. Stroke 2010; 41: 319-324.
Doan QV, Brashear A, Gillard PJ, et al. Relationship between disability and health-related
quality of life and caregiver burden in patients with upper limb poststroke spasticity. PM&R
2012; 4(1): 4-10..
Bohannon RW, Smith MB. Inter-rater reliability of a modified Ashworth scale of muscle
spasticity. Physical Therapy 67: 1987; 206-227.
Kaji R, Osako Y, Suyama K, Maeda T, Uechi Y, Iwasaki M. Botulinum toxin type A in poststroke lower limb spasticity: a multicenter, double-blind, placebo-controlled trial. J Neurol
2010;257:1330-1337.
Santamato A, Micello MF, Panza F, et al. Safety and efficacy of incobotulinum toxin type A
(NT 201-Xeomin) for the treatment of post-stroke lower limb spasticity: a prospective openlabel study. Eur J Phys Rehabil Med 2013; 49: 1-7.
Santamato A, Panza F, Ranieri M, et al. Efficacy and safety of higher doses of botulinum
toxin type A NT 201 free from complexing proteins in the upper and lower limb spasticity
after stroke. J Neural Transm 2013;120:469-476.
Foley N, Murie-Fernandez M, Speechley M, Salter K, Sequeira K, Teasell R. Does the
treatment of spastic equinovarus deformity following stroke with botulinum toxin increase
gait velocity? A systematic review and meta-analysis. Eur J Neurol 2010; 17: 1419-1427.
Hosalkar H, Goebel J, Reddy S, Pandya NK, Keenan MA. Fixation techniques for split
anterior tibialis transfer in spastic equinovarus feet. Clin Orthop Relat Res 2008; 466(10):
2500–2506.