PM R xx (2014) 1-8

www.pmrjournal.org

Analytical Review: Systematic Search

Post-stroke Spasticity: Predictors of Early Development and

Considerations for Therapeutic Intervention
Jörg Wissel, MD, FRCP, Molly Verrier, Dip (P&OT), MHSc, David M. Simpson, MD, FAAN,
David Charles, MD, Pia Guinto, PhD, Spyros Papapetropoulos, MD, PhD,
Katharina S. Sunnerhagen, MD, PhD

Abstract

Objective: The complexities of post-stroke spasticity (PSS), and the resultant difficulties in treating the disability, present a
significant challenge to patients, stroke rehabilitation teams, and caregivers. Reducing the severity of spasticity and its long-term
complications may be facilitated by early intervention, making identification of stroke patients at high risk for developing
spasticity essential. Factors that predict which patients are at risk for the development of PSS are identified.
Type: Systematic search and review
Literature Survey: A PubMed search of the following terms was conducted: predictors OR risk factors AND stroke AND spasticity.
Studies discussing predictors of early PSS development and factors predictive of motor/functional outcomes and recovery were
selected and reviewed in detail.
Synthesis: Several predictors of PSS have been proposed, based on studies conducted in patients within 6 months after stroke,
including development of increased muscle tone, greater severity of paresis, hemihypesthesia, and low Barthel Index score.
Predictors identified in later stages post-stroke (within 12 months) have also proved useful for clinicians, as has the consideration
of predictors of motor and functional outcomes and recovery; yet there is a need for additional studies in this area. An under-
standing of these and other potential predictive factorsdsuch as motor impairment, neurologic and sensory deficit, lesion volume
and location, and associated diseasesdhas not progressed to the same extent and warrants further investigation.
Conclusion: The studies discussed in this review support the notion that early identification of factors predictive of PSS should
significantly affect the course of intervention, help target individuals who would benefit most from specific types and intensities
of therapy, and possibly provide better motor and functional outcomes.

Introduction and therapeutic intervention for PSS, along with iden-

Post-stroke spasticity (PSS) is a complex disorder that
can be difficult initially to identify and treat. More than
two thirds of stroke survivors develop post-stroke
sequelae, including PSS and impaired motor function
[1,2]. Early recognition of spasticity, and identification
of predictors to assist rehabilitation professionals
recognize which stroke patients are at risk for spasticity
to develop, could result in earlier treatment and
possibly better outcomes. It would be helpful for clini-
cians and therapists to know which factors help identify
patients at high risk for developing severe PSS and for
which motor abilities, especially during the initial
admission post-stroke. Understanding more about the
pathophysiology, evolution of disease, epidemiology,
tifying PSS risk factors, should lead to better care.
Definition and Pathophysiology
Patients with stroke often experience significant im-
pairments that lead to disability. A common motor
consequence of stroke is spasticity, defined by Lance as
“a motor disorder characterized by a velocity-
dependent increase in tonic stretch reflexes (‘muscle
tone’) with exaggerated tendon jerks, resulting from
hyperexcitability of the stretch reflex, as one compo-
nent of the upper motor neuron syndrome” [3].
Although Lance’s definition is the one most frequently
cited, no gold standard definition has been accepted.
The difficulty in arriving at a universal definition may

1934-1482/$ - see front matter ª 2014 by the American Academy of Physical Medicine and Rehabilitation
http://dx.doi.org/10.1016/j.pmrj.2014.08.946
2 Post-stroke Spasticity Predictors
be due to the enormous variability in the manifestations
of spasticity, as evidenced by the many post-stroke
patients who exhibit involuntary muscle activity
typical of spasticitydand as verified by biomechanical
and neurophysiological measuresdyet who fail to ach-
ieve scores on the Modified Ashworth Scale (MAS) diag-
nostic for spasticity [4]. Other definitions of spasticity
that build on Lance’s definition have been proposed,
including Young’s, which defines the condition as “a
motor disorder characterized by a velocity-dependent
increase in tonic stretch reflexes that results from
abnormal intraspinal processing of primary afferent
input, as one component of the upper motor neuron
syndrome” [5]. Another definition, from the Task Force
on Childhood Motor Disorders, describes spasticity as a
form of hypertonia “in which one or both of the
following signs are present: (1) resistance to externally
imposed movement increases 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” [6].
Patients with spasticity comprise a clinically
and physiologically recognizable population disabled
by two or three factors of motor impairment, including
paresis, muscle overactivity, and, with time, soft
tissue contracture [7,8] (Figure 1). Paralysis or paresis
after the initial neural insult, such as stroke, is defined as
having difficulty or being completely unable to voluntarily
recruit skeletal motor units to generate torque or move-
ment. Consequently, paresis immediately leaves the
affected muscles immobilized. Immobilization of the
paretic body part, commonly imposed by the current care
Figure 1. Development of spastic paresis [8]. Solid arrows represent established causal relationships; dashed arrow represents a conjectural
connection.
environment, causes adaptive shortening of the muscles
and joint contracture (soft tissue contracture). Over time,
this immobilization and contracture leads to chronic
disuse, which further aggravates the consequences of
baseline paresis. These gradual changes result in the
progressive development of abnormal responses to mus-
cle stretch in the paretic body part, such as increases in
velocity-dependent stretch reflexes. Although these
abnormal stretch responses have been shown to manifest
in multiple ways in patients with central paresis [9,10],
the observation of increased velocity-dependent stretch
reflexes is a consistent feature [8,11,12]. Hence, patients
with spasticity present with a syndrome of muscle over-
activity. Muscle overactivity aggravates muscle contrac-
ture, which in turn enhances responses to stretch and
further aggravates spastic overactivity [7]. Preferential
cortical activation of synergistic groups of muscles also
interferes with movement and function [13]. Motor
impairment in patients with PSS can be described by a
cycle of overactivityecontractureeoveractivity evolving
in parallel with the continuum of paresisedisuseeparesis.
To optimize motor recovery and function, both cycles
must be disrupted [7,8].
Epidemiology, Disability, and Burden of Disease
The reported prevalence of PSS ranges from 4% to 27%
during the first 6 weeks after stroke [14-16]. The rate
has been reported to be 19% at 3 months, 21.7% to 42.6%
at 4 and 6 months [14-17], and 17% to 38% at 12 months
[18-20] post-stroke (Table 1). In addition to the
increased muscle tone of PSS, indirect effects, such as
 J. Wissel et al. / PM R xx (2014) 1-8 3

Table 1
Prevalence of post-stroke spasticity
Study N Time After Stroke Evaluation Method Prevalence of Spasticity
Lundström et al, 2010 [14] 49 Up to 6 mo Modified Ashworth Scale Spasticity:
(spasticity: MAS 1) At 2-10 d: 4%
At 1 mo: 27%
At 6 mo: 23%
Disabling spasticity:
At 1 mo: 2%
At 6 mo: 13%
Sommerfeld et al, 2004 [15] 95 Up to 3 mo Modified Ashworth Scale At 5.4 d: 21%
(spasticity: MAS >0) At 3 mo: 19%
Wissel et al, 2010 [16] 94 Up to 4 mo Modified Ashworth Scale Spasticity:
(spasticity: MAS >0) At 2 wk: 24.5%
At 6 wk: 26.7%
At 4 mo: 21.7%
Severe spasticity:
9.6% (MAS 3)
Urban et al, 2010 [17] 211 Up to 6 mo Modified Ashworth Scale Spasticity: 42.6%
(spasticity: MAS 1) Severe spasticity:
15.6% (MAS 3)
Watkins et al, 2002 [19] 106 Up to 12 mo Modified Ashworth Scale and Spasticity: 27%
Tone Assessment Scale Combined MAS and TAS: 38%
(spasticity: MAS >0; TAS >0)
Leathley et al, 2004 [18] 106 Up to 12 mo Tone Assessment Scale Spasticity: 36%
(spasticity: TAS >0) Severe spasticity: 20% (by lower day 7 BI score,
left-sided weakness
and ever smoked)
Lundström et al, 2008 [20] 140 Up to 12 mo Modified Ashworth Scale Spasticity: 17%
(spasticity: MAS 1); mRS; BI Disabling spasticity: 4% (by mRS score
of 2-5; and a worse BI score)
MAS ¼ Modified Ashworth Scale score; TAS ¼ Tone Assessment Scale score; BI ¼ Barthel Index; mRS ¼ modified Rankin Scale.

limitations of activities and participation due to physical
impairments, have significant impact on a patient’s
daily functioning (eg, personal hygiene, housework, and
workplace activities) and quality of life [21].
Evaluation, Clinical Course, and Therapeutic
Intervention
Studies have assessed spasticity at various time
points post-stroke, using a number of different mea-
sures (Table 1). Although a time lag may exist between
stroke and the onset of PSS, only a limited number of
studies have examined the time to onset of either PSS or
its related manifestations and complications [21]. At
baseline (mean, 5.4 days), 21% of patients with first-
ever stroke were deemed to have spasticity according
to the Modified Ashworth Scale (MAS; score >0),
whereas 19% demonstrated spasticity at 3 months post-
stroke [15]. Not all cases of spasticity require thera-
peutic intervention [22], but for those that do, early
intervention or selective prophylactic treatment (eg,
physical therapy, botulinum toxin, intrathecal baclofen)
[22] may reduce the development of spasticitydor its
severitydafter stroke [18].
Early identification of high-risk patients and early
diagnosis of spasticity are essential for optimal patient
care [21,23]. Patients with disabling spasticity scored
worse than those with mild spasticity on the modified
Rankin Scale (mRS; P ¼ .009) and the Barthel Index (BI;
P ¼ .005), suggesting that treatment needs are not the
same for all patients with spasticity, and that individuals
with disabling spasticity must be distinguished from
those with less serious deficits [20].
The consequences of PSS are important to consider
when assessing patients and deciding on appropriate
rehabilitation therapies for optimal post-stroke recov-
ery. In clinical practice, to better understand the course
of PSS and its related complications, evaluation tools
should do the following: (1) be used based on individu-
alized goals; (2) be relevant to what is being measured
(ie, symptoms, postural assessments, function, etc); (3)
account for the advantages and disadvantages of each
measure; and (4) capture more global aspects, such as
effects on quality of life [21].
The ability of a multidisciplinary team to recognize
and to better understand early the specificity and signs
of PSS types before progression to more severe spas-
ticity manifestations will aid in proper management and
intervention [24]. Specifically, an early diagnosis and
treatment plan for PSS may reduce the risk of secondary
maladaptation, impairment, and decreased level of
workplace and daily activity and social participation
[21], and potentially aid in improving long-term out-
comes for post-stroke patients.
4 Post-stroke Spasticity Predictors

Methods for Literature Search improved by using measures of early PSS, the time point
at which these measures should be taken is unclear [18].
The objective of this systematic search and review A recent study included 49 subjects with any initial
was to identify factors that predictdearly after the central paresis in the face, arm, hand, or leg after
onset of strokedwhich patients are at risk for the first-ever stroke who were examined at baseline (day
development of PSS. We reviewed literature on pre- 2-10 after stroke) and at 2 follow-up time points of 1
dictors of early PSS development and factors predictive and 6 months [14]. At all time points, muscle tone
of motor/functional outcomes and recovery. A PubMed (assessed by MAS), global disability (assessed by the
search of the following terms was used: predictors OR mRS), stroke severity, paresis severity, and sensory
risk factors AND stroke AND spasticity. The search was disturbance (all assessed by the National Institutes of
limited to human studies and publications written in Health Stroke Scale [NIHSS]) were recorded to deter-
English, with no restrictions on publication date. The mine the occurrence of and risk factors for PSS. At
results were further limited to studies focusing on the baseline, 4% of patients (2 of 49) had PSS (MAS score
first 6 months post-stroke but also, in some cases, 1). Early PSS development was further observed in
involving follow-up within 12 months post-stroke. This 27% of patients (13 of 48) at 1 month and in 23% (11 of
was accomplished by an initial abstract review, then a 47) at 6 months. Spasticity in the upper limb was noted
full-text assessment of the publication of interest. more often than in the lower limb: at 1 month, 25% of
Studies discussing predictive factors of functional out- patients had PSS in the upper limb versus 13% in the
comes and recovery were also included. The reference lower limb; and at 6 months, the rates were 22% and
lists from the publications of interest were examined for 13%, respectively. Disabling spasticity occurred in 13%
other studies that were not identified through the of patients (6 of 47) at the 6-month follow-up [14].
PubMed searches. Nine articles were selected based on Multiple logistic regression analysis found severe paresis
this methodology, and Tables 1 and 2 represent a sum- of the arm (>2 points on item 5 of the NIHSS) at
mary of the articles included and discussed in this baseline to be associated with a higher risk for spas-
review. ticity (P < .001) as early as 1 month after stroke
[14-18,25,26] (Table 2). The 6 patients displaying
disabling spasticity throughout the follow-up period had
Predictors of Early PSS Development initial severe arm paresis as well (P < .002) [14].
Similarly, 301 subjects with first-ever stroke and limb
Few studies have evaluated the onset and course of paresis were examined in the acute phase after stroke
spasticity during the first 6 months post-stroke. (within 5 days) and again 6 months later. At both time
Although the prediction of late-developing PSS is likely points, the degree and pattern of paresis and muscle
Table 2
Factors predictive* of post-stroke spasticity development
Risk Factor Time of Onset Time and Degree of Spasticity Development
Severe arm paresis [14] Baseline (2-10 d post-stroke) Spasticity by 1 mo
Increased muscle tone (MAS 1) [15,16] Baseline (1-14 d post-stroke) Spasticity by 12-24 wk post-stroke
Low BI score [16,17] Baseline (1-14 d post-stroke) Severe spasticity (MAS 3) by 12-24 wk post-stroke
Moderately increased muscle tone Baseline to 6 wk post-stroke Severe spasticity by 12-24 wk post-stroke
(MAS 2) [16]
Hemihypesthesia [17] Baseline (1-5 d post-stroke) Spasticity by 6 mo
Severe paresis [17] Baseline (1-5 d post-stroke) Spasticity by 6 mo
Low EQ-5D score [17] Baseline (1-5 d post-stroke) Spasticity by 6 mo
Paresis [16,17] Any time point post-stroke Spasticity by 6 mo
Low day 7 BI score with early arm or Baseline (7 d post-stroke) Spasticity by 12 mo
leg weakness [18]
Low day 7 BI score with left-sided weakness Baseline (7 d post-stroke) Severe spasticity by 12 mo
and positive smoking status [18]
Hemispasticity [16] 4-12 wk post-stroke Permanent spasticity
Increased muscle tone (MAS 1) in more 4-12 wk post-stroke Permanent spasticity
than 2 joints [16]
More severe degree of paresis [16] 12-24 wk post-stroke Permanent spasticity
NIHSS scores, nonsurgical treatment, and At patient admission; retrospective Spasticity by 3 mo
low Motricity Index scores [25] review
Manual activities before stroke, previous At patient admission; retrospective Spasticity by 1 y
history of stroke, and extensive lesions review
seen on tomography [26]
MAS ¼ Modified Ashworth Scale score; BI ¼ Barthel Index; EQ-5D ¼ a standardized instrument of health-related quality of life; NIHSS ¼ National
Institutes of Health Stroke Scale.
*
All risk factors in the table were shown to be significantly (P < .05) predictive of spasticity in at least 1 study.
 J. Wissel et al. / PM R xx (2014) 1-8
tone (assessed via the British Medical Research Council
[BMRC] scale and MAS), BI, and EQ-5D (a standardized
instrument of health-related quality of life) score were
evaluated [17]. Of the 211 subjects reassessed at
6 months, 42.6% (n ¼ 90) had developed PSS (MAS score
1). A more severe degree of spasticity (MAS score 3)
was observed in 15.6% of these subjects (n ¼ 33). Lo-
gistic regression analysis confirmed that subjects with a
more severe degree of paresis (BMRC grades 1 and 0) in
the proximal and distal muscles of the upper and lower
limbs during the acute stage had a higher risk of
developing PSS (P  .001). Furthermore, the develop-
ment of PSS in the upper and lower limbs was more
frequent in subjects with initial hemihypesthesia than
in subjects without sensory deficits (odds ratio [OR] ¼
2.27, P ¼ .011). Sensory examination included only
sensitivity to light touch. The study concluded that
predictors for the development of PSS included a severe
degree of paresis and hemihypesthesia at stroke onset
(Table 2). In addition, subjects with PSS at 6 months
showed lower BI (P < .001) and EQ-5D (P < .001) scores
in the acute phase compared to the group without PSS
at 6 months [17].
In another trial, a cohort of 94 subjects without pre-
existing spasticity was examined at 6 days (baseline;
range 1-14 days), 6 weeks (range 4-12 weeks), and 16
weeks (range 12-24 weeks) after stroke [16]. At all
time points, muscle tone (MAS), pain, paresis, and BI
score were recorded to identify risk factors for the
development of PSS. Similar to previous studies, early
development of PSS was observed, with 24.5% of sub-
jects (23 of 94) with stroke developing an increase in
muscle tone (MAS score >0) within 2 weeks after
stroke [16]. Spasticity was observed in 26.7% of pa-
tients (23 of 86) by the first follow-up at 6 weeks after
stroke and in 21.7% (18 of 83) by 16 weeks after stroke
(Figure 2) [16]. Among all subjects who developed PSS
at any time during the course of the study, 98%
exhibited PSS by the first follow-up (median 6 weeks)
[16]. Subjects with PSS had higher incidences of pain
(P < .001) and nursing home placement (P < .05) and
lower BI (P ¼ .035) scores than subjects with normal
muscle tone. Severe spasticity (MAS score 3) was
predicted by lower BI scores (median score 63.3,
compared to 80.6 in patients without spasticity) at
baseline, and moderate muscle tone (MAS score ¼ 2) at
baseline to 6 weeks post-stroke. Presence of hemi-
paresis correlated with PSS at first (P ¼ .02) and second
(P ¼ .005) follow-ups. Hemispasticity and increased
muscle tone (MAS score 1) in more than 2 joints at 6
weeks, and more severe degrees of paresis at 16
weeks, were risk factors for permanent spasticity [16]
(Table 2). Severity of paresis at the second follow-up
(12-24 weeks after stroke) correlated with degree of
spasticity (P ¼ .02). Lower BI at baseline predicted
development of more severe spasticity at final follow-
up (P ¼ .002). None of the baseline characteristics,
5
such as age, gender, location or type of stroke, or
smoking history, was associated with the development
of PSS in this sample [16].
One study investigated the possibility of combining
risk factors to develop models that can be used to
predict spasticity 12 months after a stroke using data
routinely recorded as part of early clinical post-stroke
care (in particular, arm or leg weakness within the
first 24 hours of stroke onset and BI score on day 7 post-
stroke) [18] (Table 2). The following variables consid-
ered for the prediction models are routinely recorded as
part of clinical care and have been used in previous
models to predict outcome after stroke: age, gender,
previous cerebrovascular disease, history of diabetes,
history of smoking, prestroke mRS score, worse level of
consciousness and arm or leg weakness (within the first
24 hours of stroke onset), side of weakness, higher
cortical dysfunction (presence of visual neglect, confu-
sion, and/or aphasia), type of stroke (determined by
computed tomography scan), Oxfordshire Community
Stroke Project (OCSP) classification, and day 7 BI score
[18]. With a univariate analysis, a low day 7 BI score (P <
.001) and early arm or leg weakness (P < .001) were
each associated with some spasticity at 12 months after
stroke. When combined as a model, these 2 predictors
had a sensitivity of 68%, a specificity of 83%, a positive
predictive value of 71%, a negative predictive value of
80%, and an efficiency of 77%. Moreover, a low day 7 BI
score, combined with arm or leg weakness, left-sided
weakness, and positive smoking status, was associated
with more severe PSS at 12 months [18]. This model had
a sensitivity of 62%, a specificity of 92%, a positive
predictive value of 68%, a negative predictive value of
89%, and an efficiency of 85%. However, these findings
have not been replicated to date [18].
Prevalence and predictors of PSS in 245 subjects with
stroke transferred to the Department of Rehabilitation
Medicine of a tertiary care hospital were evaluated.
Variables evaluated upon admission included gender,
age, stroke duration (interval between stroke onset and
admission), stroke type (cerebral infarction, cerebral
hemorrhage, or subarachnoid hemorrhage), NIHSS
score, surgical treatment, lesion location, comorbid-
ities, and Motricity Index score (assessment of motor
function) [25]. The investigators found that 42.4% of
subjects exhibited PSS; in multivariate logistic regres-
sion analysis of predictive factors, the NIHSS scores (P ¼
.029), nonsurgical treatment (P ¼ .002), and low
Motricity Index scores (P < .001) were significantly
predictive of PSS. Stroke duration, gender, and age were
not predictive of the development of PSS. The high
prevalence of PSS in one study may be due to bias
introduced by inclusion of patients specifically trans-
ferred to a rehabilitation department.25
In a recent study, predictive factorsdincluding clin-
ical, computed tomographic, demographic, epidemio-
logic, and social variablesdin 146 subjects with stroke
6 Post-stroke Spasticity Predictors
Figure 2. Development of muscle hypertonia during follow-up [16]. Number of patients with muscular hypertonia at different time points after
stroke: baseline ¼ within 2 weeks post-stroke; first follow-up ¼ 6 weeks; second follow-up ¼ 16 weeks. Total number of patients studied at each
time point: baseline ¼ 94; first follow-up ¼ 86; second follow-up ¼ 83.
were investigated to determine possible links to the
development of PSS [26]. The study investigators re-
ported that a subject’s pattern of muscle use may in-
fluence PSS development. In multivariate regression
analysis, subjects who engaged in manual activities
before their strokes had a greater relative risk for PSS
(RR ¼ 2.9; P ¼ .013). Spasticity developed more
frequently among subjects with a previous history of
stroke (RR ¼ 3.9; P ¼ .005) and those with extensive
lesions seen on tomography (RR ¼ 3.6; P ¼ .017). How-
ever, the specifics of the PSS were not reported.
Extensive lesion involvement of more than one cerebral
lobe was frequent in patients with PSS: 20 patients
(23.8%) presented extensive lesions; among these, 7
patients (35%) presented with lesions in more than one
cerebral lobe, and 13 (65%) in a single lobe [26]. Post-
stroke imaging studies implicate the motor and pre-
motor areas and the loss of strength in the development
of PSS [27,28]. However, limited data are available on
the correlation between PSS and imaging assessments,
such as stroke lesion volume and location, thus war-
ranting further investigation.
Limitations of Published Literature
Limitations of some of the studies reviewed include
their retrospective design, lack of follow-up measure-
ments for all subjects, ascertainment bias, non-
standardized examinations, and lack of detailed
assessment of the domains that comprise the syndrome
of spasticity [25,26]. The factors predictive of abnormal
muscle tone that were shown to be clinically significant
by other researchers (such as left-sided weakness,
greater degree of paresis, and low BI scores described
earlier and in Table 2) were either not significant or not
investigated in these studies. Hence, further research is
required to resolve these differences in predictors [25].
Despite evidence supporting the possibility that these
additional predictive factors may be of clinical impor-
tancedparticularly motor impairment, neurologic and
sensory deficit, associated diseases, and surrogate
markers from magnetic resonance imaging such as lesion
volume and locationdfurther investigation is warranted
to validate their correlation with PSS development [26].
Further research to determine the clinical utility of
models to predict the onset of PSS and other common
post-stroke complications is also warranted. In addition,
research to determine the specificity of how upper and
lower limb spasticity contribute to outcome and quality
of life would be welcome to this field. These findings
point out that individualized assessment of different
locations and degrees of spasticity and paresis need to
be carefully documented, particularly when treatment
approaches such as botulinum toxin need to be admin-
istered with a substantial degree of specificity.
In addition to the predictors of early development of
PSS summarized in Table 2, consideration of predictors
of motor and functional outcomes and recovery may aid
in improving therapeutic approaches. Assessing pre-
dictors of motor and functional outcomes after post-
stroke therapy may also affect treatment outcomes
and thus help to identify patients who could benefit
 J. Wissel et al. / PM R xx (2014) 1-8
from such neurorehabilitation techniques [29]. Howev-
er, studies exploring such predictors are very limited.
The relationship between motor ability and PSS requires
further investigation to help clinicians and therapists
decide on early treatments to prevent or reduce the
development of PSS and to provide better motor and
functional outcomes.
Taken together, the literature points to a number of
different predictive factors for the development of PSS,
with paresis being, perhaps, the most significant. Paresis
at any of the measured post-stroke intervals was, in
general, associated with an increased risk for PSS, and
more severe paresis conferred a higher risk. Increased
muscle tone, even moderately increased, was also pre-
dictive of PSS, and low baseline scores on measurements
of quality of life and activities of daily living were seen to
increase spasticity risk. Perhaps less surprisingly, poorer
scores on measurements of post-stroke disability were
linked with development of PSS, as was the presence of
extensive lesions in computed tomographic imaging.
Conclusion
Given the complexities of PSS and the difficulties in
treating the associated disability, preventing or
reducing the development of PSS is critical [30]. It
would be helpful for clinicians and therapists to have
standardized tools during the initial admission post-
stroke that would identify which patients are at high
risk for developing severe PSS and which motor abilities
might be affected. The PSS predictors have limitations,
as described above, but still are useful in providing some
level of understanding [15-18]. Identifying risk factors
for PSS will lead to better care. Further research on
PSSdspecifically, prospective studies with well-defined
endpoints and clearly applied spasticity definitions,
focusing on the early identification of factors influ-
encing motor and functional outcomes and recoverydis
needed to improve PSS prediction. Neuroimaging studies
may also help to identify clinical signs and surrogate
markers of PSS, and application of the NIHSS and Rankin
Scale in studies of PSS risk could affect the course of
intervention and help target individuals who would
benefit most from specific types of therapy.
Acknowledgment
The authors thank Allergan, Inc., for funding Imprint
Publication Science, New York, NY, to provide editorial
support in the preparation of this manuscript.
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Disclosure
J.W. Department of Neurology, Neurorehabilitation Unit, Vivantes Klinikum
Spandau, Neue Bergstrasse 6, D-13585, Berlin, Germany. Address correspon-
dence to: J.W.; e-mail: joerg@schwarz-wissel.de
Disclosure: nothing to disclose
M.V. Department of Physical Therapy, Faculty of Medicine, University of Tor-
onto, Toronto, ON, Canada
Disclosure: nothing to disclose
D.M.S. Clinical Neurophysiology Laboratories, Department of Neurology, Mount
Sinai Medical Center, New York, NY
Disclosure: nothing to disclose
D.C. Department of Neurology, Vanderbilt University Medical Center, Nashville,
TN
Disclosures related to this publication: Recipient of income from Allergan for
education or consulting services; employment at Vanderbilt University, which
receives income from grants or contracts with Allergan, Ipsen, Merz, and Med-
tronic for research or educational programs led by D.C.
29. Lin KC, Huang YH, Hsieh YW, Wu CY. Potential predictors of motor
and functional outcomes after distributed constraint-induced
therapy for patients with stroke. Neurorehabil Neural Repair
2009;23:336-342.
30. Gregson JM, Sharma AK. Measuring poststroke spasticity. Rev Clin
Gerontol 2000;10:69-74.
Disclosures outside this publication: Recipient of income from Ipsen, Merz, and
Medtronic for education or consulting services.
P.G. Imprint Publication Science, New York, NY
Disclosure: Employment at Imprint Publication Science (funded by Allergan).
S.P. Allergan, Inc., Irvine, CA, and University of Miami, Miller School of Medicine,
Miami, FL
Disclosure: nothing to disclose
K.S.S. Institute of Neuroscience and Physiology, Section for Clinical Neurosci-
ence and Rehabilitation, Gothenburg University, Gothenburg, Sweden
Disclosure: nothing to disclose
This review was sponsored by Allergan, Inc.
S.P. is currently with R&D Neurosciences, Pfizer, Cambridge, MA.
Submitted for publication January 8, 2013; accepted August 2, 2014.