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PM R xx (2014) 1-8

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


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-

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

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

Figure 1. Development of spastic paresis [8]. Solid arrows represent established causal relationships; dashed arrow represents a conjectural
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 worse than those with mild spasticity on the modified
impairments, have significant impact on a patient’s Rankin Scale (mRS; P ¼ .009) and the Barthel Index (BI;
daily functioning (eg, personal hygiene, housework, and P ¼ .005), suggesting that treatment needs are not the
workplace activities) and quality of life [21]. same for all patients with spasticity, and that individuals
with disabling spasticity must be distinguished from
Evaluation, Clinical Course, and Therapeutic those with less serious deficits [20].
Intervention The consequences of PSS are important to consider
when assessing patients and deciding on appropriate
Studies have assessed spasticity at various time rehabilitation therapies for optimal post-stroke recov-
points post-stroke, using a number of different mea- ery. In clinical practice, to better understand the course
sures (Table 1). Although a time lag may exist between of PSS and its related complications, evaluation tools
stroke and the onset of PSS, only a limited number of should do the following: (1) be used based on individu-
studies have examined the time to onset of either PSS or alized goals; (2) be relevant to what is being measured
its related manifestations and complications [21]. At (ie, symptoms, postural assessments, function, etc); (3)
baseline (mean, 5.4 days), 21% of patients with first- account for the advantages and disadvantages of each
ever stroke were deemed to have spasticity according measure; and (4) capture more global aspects, such as
to the Modified Ashworth Scale (MAS; score >0), effects on quality of life [21].
whereas 19% demonstrated spasticity at 3 months post- The ability of a multidisciplinary team to recognize
stroke [15]. Not all cases of spasticity require thera- and to better understand early the specificity and signs
peutic intervention [22], but for those that do, early of PSS types before progression to more severe spas-
intervention or selective prophylactic treatment (eg, ticity manifestations will aid in proper management and
physical therapy, botulinum toxin, intrathecal baclofen) intervention [24]. Specifically, an early diagnosis and
[22] may reduce the development of spasticitydor its treatment plan for PSS may reduce the risk of secondary
severitydafter stroke [18]. maladaptation, impairment, and decreased level of
Early identification of high-risk patients and early workplace and daily activity and social participation
diagnosis of spasticity are essential for optimal patient [21], and potentially aid in improving long-term out-
care [21,23]. Patients with disabling spasticity scored 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 5

tone (assessed via the British Medical Research Council such as age, gender, location or type of stroke, or
[BMRC] scale and MAS), BI, and EQ-5D (a standardized smoking history, was associated with the development
instrument of health-related quality of life) score were of PSS in this sample [16].
evaluated [17]. Of the 211 subjects reassessed at One study investigated the possibility of combining
6 months, 42.6% (n ¼ 90) had developed PSS (MAS score risk factors to develop models that can be used to
1). A more severe degree of spasticity (MAS score 3) predict spasticity 12 months after a stroke using data
was observed in 15.6% of these subjects (n ¼ 33). Lo- routinely recorded as part of early clinical post-stroke
gistic regression analysis confirmed that subjects with a care (in particular, arm or leg weakness within the
more severe degree of paresis (BMRC grades 1 and 0) in first 24 hours of stroke onset and BI score on day 7 post-
the proximal and distal muscles of the upper and lower stroke) [18] (Table 2). The following variables consid-
limbs during the acute stage had a higher risk of ered for the prediction models are routinely recorded as
developing PSS (P  .001). Furthermore, the develop- part of clinical care and have been used in previous
ment of PSS in the upper and lower limbs was more models to predict outcome after stroke: age, gender,
frequent in subjects with initial hemihypesthesia than previous cerebrovascular disease, history of diabetes,
in subjects without sensory deficits (odds ratio [OR] ¼ history of smoking, prestroke mRS score, worse level of
2.27, P ¼ .011). Sensory examination included only consciousness and arm or leg weakness (within the first
sensitivity to light touch. The study concluded that 24 hours of stroke onset), side of weakness, higher
predictors for the development of PSS included a severe cortical dysfunction (presence of visual neglect, confu-
degree of paresis and hemihypesthesia at stroke onset sion, and/or aphasia), type of stroke (determined by
(Table 2). In addition, subjects with PSS at 6 months computed tomography scan), Oxfordshire Community
showed lower BI (P < .001) and EQ-5D (P < .001) scores Stroke Project (OCSP) classification, and day 7 BI score
in the acute phase compared to the group without PSS [18]. With a univariate analysis, a low day 7 BI score (P <
at 6 months [17]. .001) and early arm or leg weakness (P < .001) were
In another trial, a cohort of 94 subjects without pre- each associated with some spasticity at 12 months after
existing spasticity was examined at 6 days (baseline; stroke. When combined as a model, these 2 predictors
range 1-14 days), 6 weeks (range 4-12 weeks), and 16 had a sensitivity of 68%, a specificity of 83%, a positive
weeks (range 12-24 weeks) after stroke [16]. At all predictive value of 71%, a negative predictive value of
time points, muscle tone (MAS), pain, paresis, and BI 80%, and an efficiency of 77%. Moreover, a low day 7 BI
score were recorded to identify risk factors for the score, combined with arm or leg weakness, left-sided
development of PSS. Similar to previous studies, early weakness, and positive smoking status, was associated
development of PSS was observed, with 24.5% of sub- with more severe PSS at 12 months [18]. This model had
jects (23 of 94) with stroke developing an increase in a sensitivity of 62%, a specificity of 92%, a positive
muscle tone (MAS score >0) within 2 weeks after predictive value of 68%, a negative predictive value of
stroke [16]. Spasticity was observed in 26.7% of pa- 89%, and an efficiency of 85%. However, these findings
tients (23 of 86) by the first follow-up at 6 weeks after have not been replicated to date [18].
stroke and in 21.7% (18 of 83) by 16 weeks after stroke Prevalence and predictors of PSS in 245 subjects with
(Figure 2) [16]. Among all subjects who developed PSS stroke transferred to the Department of Rehabilitation
at any time during the course of the study, 98% Medicine of a tertiary care hospital were evaluated.
exhibited PSS by the first follow-up (median 6 weeks) Variables evaluated upon admission included gender,
[16]. Subjects with PSS had higher incidences of pain age, stroke duration (interval between stroke onset and
(P < .001) and nursing home placement (P < .05) and admission), stroke type (cerebral infarction, cerebral
lower BI (P ¼ .035) scores than subjects with normal hemorrhage, or subarachnoid hemorrhage), NIHSS
muscle tone. Severe spasticity (MAS score 3) was score, surgical treatment, lesion location, comorbid-
predicted by lower BI scores (median score 63.3, ities, and Motricity Index score (assessment of motor
compared to 80.6 in patients without spasticity) at function) [25]. The investigators found that 42.4% of
baseline, and moderate muscle tone (MAS score ¼ 2) at subjects exhibited PSS; in multivariate logistic regres-
baseline to 6 weeks post-stroke. Presence of hemi- sion analysis of predictive factors, the NIHSS scores (P ¼
paresis correlated with PSS at first (P ¼ .02) and second .029), nonsurgical treatment (P ¼ .002), and low
(P ¼ .005) follow-ups. Hemispasticity and increased Motricity Index scores (P < .001) were significantly
muscle tone (MAS score 1) in more than 2 joints at 6 predictive of PSS. Stroke duration, gender, and age were
weeks, and more severe degrees of paresis at 16 not predictive of the development of PSS. The high
weeks, were risk factors for permanent spasticity [16] prevalence of PSS in one study may be due to bias
(Table 2). Severity of paresis at the second follow-up introduced by inclusion of patients specifically trans-
(12-24 weeks after stroke) correlated with degree of ferred to a rehabilitation department.25
spasticity (P ¼ .02). Lower BI at baseline predicted In a recent study, predictive factorsdincluding clin-
development of more severe spasticity at final follow- ical, computed tomographic, demographic, epidemio-
up (P ¼ .002). None of the baseline characteristics, 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 muscle tone that were shown to be clinically significant
development of PSS [26]. The study investigators re- by other researchers (such as left-sided weakness,
ported that a subject’s pattern of muscle use may in- greater degree of paresis, and low BI scores described
fluence PSS development. In multivariate regression earlier and in Table 2) were either not significant or not
analysis, subjects who engaged in manual activities investigated in these studies. Hence, further research is
before their strokes had a greater relative risk for PSS required to resolve these differences in predictors [25].
(RR ¼ 2.9; P ¼ .013). Spasticity developed more Despite evidence supporting the possibility that these
frequently among subjects with a previous history of additional predictive factors may be of clinical impor-
stroke (RR ¼ 3.9; P ¼ .005) and those with extensive tancedparticularly motor impairment, neurologic and
lesions seen on tomography (RR ¼ 3.6; P ¼ .017). How- sensory deficit, associated diseases, and surrogate
ever, the specifics of the PSS were not reported. markers from magnetic resonance imaging such as lesion
Extensive lesion involvement of more than one cerebral volume and locationdfurther investigation is warranted
lobe was frequent in patients with PSS: 20 patients to validate their correlation with PSS development [26].
(23.8%) presented extensive lesions; among these, 7 Further research to determine the clinical utility of
patients (35%) presented with lesions in more than one models to predict the onset of PSS and other common
cerebral lobe, and 13 (65%) in a single lobe [26]. Post- post-stroke complications is also warranted. In addition,
stroke imaging studies implicate the motor and pre- research to determine the specificity of how upper and
motor areas and the loss of strength in the development lower limb spasticity contribute to outcome and quality
of PSS [27,28]. However, limited data are available on of life would be welcome to this field. These findings
the correlation between PSS and imaging assessments, point out that individualized assessment of different
such as stroke lesion volume and location, thus war- locations and degrees of spasticity and paresis need to
ranting further investigation. be carefully documented, particularly when treatment
approaches such as botulinum toxin need to be admin-
Limitations of Published Literature istered with a substantial degree of specificity.
In addition to the predictors of early development of
Limitations of some of the studies reviewed include PSS summarized in Table 2, consideration of predictors
their retrospective design, lack of follow-up measure- of motor and functional outcomes and recovery may aid
ments for all subjects, ascertainment bias, non- in improving therapeutic approaches. Assessing pre-
standardized examinations, and lack of detailed dictors of motor and functional outcomes after post-
assessment of the domains that comprise the syndrome stroke therapy may also affect treatment outcomes
of spasticity [25,26]. The factors predictive of abnormal and thus help to identify patients who could benefit
J. Wissel et al. / PM R xx (2014) 1-8 7

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J.W. Department of Neurology, Neurorehabilitation Unit, Vivantes Klinikum Disclosures outside this publication: Recipient of income from Ipsen, Merz, and
Spandau, Neue Bergstrasse 6, D-13585, Berlin, Germany. Address correspon- Medtronic for education or consulting services.
dence to: J.W.; e-mail:
Disclosure: nothing to disclose P.G. Imprint Publication Science, New York, NY
Disclosure: Employment at Imprint Publication Science (funded by Allergan).
M.V. Department of Physical Therapy, Faculty of Medicine, University of Tor-
onto, Toronto, ON, Canada S.P. Allergan, Inc., Irvine, CA, and University of Miami, Miller School of Medicine,
Disclosure: nothing to disclose Miami, FL
Disclosure: nothing to disclose
D.M.S. Clinical Neurophysiology Laboratories, Department of Neurology, Mount
Sinai Medical Center, New York, NY K.S.S. Institute of Neuroscience and Physiology, Section for Clinical Neurosci-
Disclosure: nothing to disclose ence and Rehabilitation, Gothenburg University, Gothenburg, Sweden
Disclosure: nothing to disclose
D.C. Department of Neurology, Vanderbilt University Medical Center, Nashville,
This review was sponsored by Allergan, Inc.
S.P. is currently with R&D Neurosciences, Pfizer, Cambridge, MA.
Disclosures related to this publication: Recipient of income from Allergan for
education or consulting services; employment at Vanderbilt University, which Submitted for publication January 8, 2013; accepted August 2, 2014.
receives income from grants or contracts with Allergan, Ipsen, Merz, and Med-
tronic for research or educational programs led by D.C.