European Journal of Neurology 2012, 19: 2127 doi:10.1111/j.1468-1331.2011.03448.

REVIEW ARTICLE

A literature review of the pathophysiology and onset of post-stroke

spasticity
Anthony B. Ward
Faculty of Health, Staffordshire University, Stoke on Trent, UK

Keywords:
early intervention, spas-
ticity onset, stroke, upper
motor neuron syndrome
Received 8 December 2010
Accepted 26 April 2011
Background: Spasticity occurs after stroke and gives rise to substantial burden for
patients and caregivers. Although it has been studied for many years, its denition
continues to undergo reconsideration and revision. This partly reects the diversity of
its manifestations and that its pathophysiology, although well studied, is still debated.
Methods: A literature review was carried out to dene the pathophysiology and risk
factors for onset of post-stroke spasticity.
Results: It is clear that an acquired brain injury, including stroke, results in an
imbalance of inhibitory and excitatory impulses that leads to upper motor neuron
symptoms and that the location and extent of the lesions result in diering symptoms
and degrees of spastic severity. The onset of spasticity is highly variable and may occur
shortly or more than 1 year after stroke. The current understanding of spasticity onset is
complicated by the role of contractures, which have been assumed to arise out of
spasticity but may have a role in its cause. Other possibly predictive factors for the risk
of post-stroke spasticity have been identied, including early arm and leg weakness, left-
sided weakness, early reduction in activities of daily living, and a history of smoking.
Conclusions: Further understanding of spasticity risk factors is necessary for the
development and integration of early interventions and preventive measures to reduce
spasticity onset and severity.

work as a result of their spasticity [5]. Apart from these

Introduction
Spasticity is a common feature of the upper motor neu-
ron syndrome following stroke [1]. It can have a dis-
abling eect on the stroke survivor through pain and
reduced mobility, which may limit the potential success
of rehabilitation [2,3]. Spasticity can also aect quality of
life (QoL) and can be both diverse and highly detrimental
to daily functioning. Spasticity can result in urinary
incontinence; limit sexual intimacy; interfere with walk-
ing, sitting, and standing; and generally reduce a persons
ability to undertake activities of daily living (ADLs) [1].
The physical limitations associated with spasticity con-
fer risk for falls and consequent fractures [4].
The consequences of spasticity-related disability may
extend further to aect work and productivity. A recent
survey of patients with spasticity found that nearly 60%
stated their condition had made it impossible for them
to work at all, while an additional 29% said their
spasticity interfered with their ability to work; in all,
89% of respondents reported total or partial inability to
Correspondence: A. B. Ward, Director, North Staffordshire Reha-
bilitation Centre, University Hospital of North Staffordshire, Stoke on
Trent, UK (tel.: 0044 (0) 1782 673 693; fax: 0044 (0) 1782 673 912;
e-mail: anthony.ward@uhns.nhs.uk).
limitations on the lives of stroke suerers themselves, a
secondary eect of spasticity is often an increased
burden on caregivers [1,6].
The severity of pain and overall QoL burden asso-
ciated with the development of post-stroke spasticity
may be reduced or avoided through the initiation of
preventive approaches in patients with upper motor
neuron syndrome (UMNS). Early interventions may
prevent the onset of post-stroke spasticity or slow or
limit its progression [79]. The goal of this review is to
dene the pathophysiology and risk factors for the
onset of post-stroke spasticity. Rigorous and objective
measures of spasticity, and a clear understanding of the
factors associated with its onset and pathophysiology,
may facilitate the development and integration of pre-
ventive approaches and early interventions.
Methods
A literature review was carried out using CINAHL and
Embase databases as well as the Cochrane Collabora-
tion Library with a search on the following terms:
stroke, upper motor neuron syndrome, spasticity,
spasticity pathophysiology, spasticity onset, and early
intervention. The literature search was selected from

 2011 The Author(s)

European Journal of Neurology  2011 EFNS 21
22 A. B. Ward
more recent papers focusing on post-stroke spasticity
and none before 1990.
Results
Describing spasticity
Arriving at a formal denition of spasticity has been an
evolving project for at least half a century. Lances 1980
denition is most commonly cited and describes spas-
ticity as a motor disorder characterized by a velocity-
dependent increase in tonic stretch reexes (muscle tone)
with exaggerated tendon jerks, resulting from hyperex-
citability of the stretch reex, as one component of the
upper motor neuron syndrome [10]. A subsequent 1994
denition of spasticity was a motor disorder character-
ized by a velocity-dependent increase in tonic stretch re-
exes that results from abnormal intra-spinal processing
of primary aerent input [11]. A more recent 2005 de-
nition superseded the Lance denition and described a
disordered sensori-motor control, resulting from an up-
per motor neuron lesion, presenting as intermittent or
sustained involuntary activation of muscles [12].
There is thus no correct and universal denition, which
partly reects the fact that spasticity is not a single entity.
Post-stroke spasticity shows considerable variability and
often does not conform to any of the standard deni-
tions, particularly with regard to the role of muscle tone.
Malhotra et al.[13] found that a substantial portion of
post-stroke patients exhibiting involuntary muscle
activity consistent with spasticity, as measured by
biomechanical and neurophysiologic measures, did not
exhibit scores on the Modied Ashworth Scale (which
measures muscle tone) that were diagnostic for spastic-
ity. Eighty-seven of 100 patients were diagnosed with
abnormal muscle activity using biomechanical and neu-
rophysiologic measures. Spasticity was then measured in
the same set of patients using the six-point Modied
Ashworth Scale, and 56 of the 87 previously identied
patients scored a 0, indicating no detectable spasticity.
The Ashworth and Modied Ashworth Scales are fre-
quently used clinical methods for evaluating muscle tone.
Such incongruity between common measures of spas-
ticity and standard denitions of the condition [14] at
best complicates diagnosis and at worst results in sub-
optimal treatment of the patient with spasticity.
Pathophysiology of upper motor neuron syndrome
Spasticity arises from a dissociation or disintegration of
motor responses to sensory input co-incident with a
hyperexcitability of segmental central nervous system
(CNS) processing. Additional sensory input provokes a
greater spasticity manifestation, although the location
European Journal of Neurology  2011 EFNS European Journal of Neurology 19, 2127
of the lesion also plays a role in determining the char-
acter of the spasticity [15,16] (Fig. 3). Spasticity can
occur in muscles with high stretch sensitivity and in
those not stretch sensitive [15].
Eerent processes also contribute to positive UMNS
symptoms that are generally referred to as spastic dys-
tonia [16]. Such symptoms occur as continuous mus-
cular activity, lack volitional command, are not entirely
dependent on peripheral sensory feedback, and lack
phasic stretch. An example is the hemiplegic posture in
which a patient experiences nger, elbow, and wrist
contraction in addition to leg extension.
It would appear that pyramidal bers do not play a
major role in UMNS, but parapyramidal bers do have
an important role [16]. Inhibition of sensory impulses
for spinal reex activity occurs via the dorsal reticu-
lospinal tract, while additional inhibitory eects on the
spinal cord take place through the brain stem (Fig. 1)
[15,16]. The dorsal reticulospinal tract runs close to the
corticospinal or pyramidal tract, and it is the parapy-
ramidal dorsal reticulospinal tract that causes the main
symptoms associated with spinal reex activity. In the
brain stem, excitatory pathways that descend through
the medial reticulospinal tract, mainly through the
bulbopontine tegmentum, are also present.
The unbalancing of an otherwise stable equilibrium
between inhibitory and excitatory bers can result in
any number of complex and diverse variations of
UMNS, and lesions occurring in a given area may have
varying eects on dierent patients. The location of a
lesion may have a large eect on the type of symptoms
experienced. The three primary locations for lesions
Figure 1 Major pathways of spinal reex inhibitory (gray) and
excitatory (black) pathways. Reproduced with permission from
Wiley-Blackwell: Sheean G, The pathophysiology of spasticity,
European Journal of Neurology; 9(Suppl. 1): 39. Copyright 2002
{Ref. [16]}.
 2011 The Author(s)
 Post-stroke spasticity: pathophysiology and onset 23

into which the diering eects can be clearly catego-
rized are brain stem, cortex, and spinal cord [16].
Cortical lesions will often result in some degree of
spasticity, hyper-reexia, and in some cases clonus, but
these will usually be much less severe in nature than
those symptoms arising from spinal cord lesions. Partial
and complete lesions have diering eects. If a partial
spinal cord lesion is entirely destructive of the inhibi-
tory pathways but not of the excitatory ones, then
spinal activity will remain, although the result will be
high levels of spasticity and hyper-reexia, while a total
spinal cord lesion that destroys both inhibitory and
excitatory pathways will result in a total loss of sup-
raspinal control and lead to hyperactivity [16].
The order of events following the initial stroke-
related injury typically involves a period of shock
followed by a transitional interlude of non-hyperac-
tive reex responses. Flaccidity and hypotonia are
experienced rst [16] in a way that may be related to
the appearance of spinal shock after a spinal cord
injury [17], with a delay occurring before spasticity
sets in. The onset of spasticity is likely to be con-
tingent upon a plastic rearrangement in the CNS, and
possibly the sprouting of axonal bers [3,16]. The
result is overactivity of the muscles and exaggerated
reex responses to peripheral stimulation [15]. The
processes for this development are similar to those of
other cerebral pathologies, and the early pathophysi-

Acute care Rehabilitation unit

Damage to central motor pathways

Immediate Delayed

Figure 2 Process of muscle overactivity. Flaccid paralysis Plastic rearrangements

Disuse
Adapted with permission from Wiley
Periodicals: Gracies JM, Pathophysiology
of spastic paresis II: emergence of muscle
overactivity, Muscle & Nerve, 31: 552571. Immobilisation in Changes in spinal reactivity
shortened position and supraspinal command
Copyright 2005 {Ref. [18]}; and from
Mark Allen Healthcare: Ward AB, Botu-
linum toxin in spasticity management, Spasticity
British Journal of Therapy and Re- Contracture Spastic dystonia Overactivity
habilitation, 6: 2634. Copyright 1999 Spastic Co-contraction
Other
{Ref. [19]}.

Figure 3 Spasticity, self-reported muscle

stiffness, hyper-reexia, and clonic beats
in the plantar exors immediately*
post-stroke and at 3 months post-stroke.
*Mean follow-up 5.4 days.
Reproduced with permission from
Lippincott Williams & Wilkins:
Sommerfeld DK, Eek EU, Svensson AK,
Holmqvist LW, von Arbin MH, Spasticity
after stroke: its occurrence and association
with motor impairments and activity
limitations, Stroke, 35: 134139.
Copyright 2004 {Ref. [20]}.

 2011 The Author(s)

European Journal of Neurology  2011 EFNS European Journal of Neurology 19, 2127
24 A. B. Ward
ological pathway, shown in Fig. 2, is much the same
[18,19].
There are three possible explanations for the hyper-
active spinal reexes in positive features of UMNS:
(i) disinhibition of the normal reex activities that are
the deep tendon reexes (proprioceptive phasic stretch
reex) and exor withdrawal reexes (nociceptive
reex); (ii) release of primitive reexes, such as a
positive Babinski sign; and (iii) enhancement of spas-
ticity because of active tonic stretch reex [12,15].
What to look for in the clinical onset of spasticity
The onset of spasticity is highly variable and may occur
in the short-, medium-, or long-term post-stroke period.
There is evidence to suggest that these variations in the
time of onset of post-stroke spasticity are the reections
of dierent causes or triggers. These variations in
spasticity onset intervals undermine eorts at measur-
ing spasticity prevalence, because the varying nature
and timing of actual onsets may confound how one
counts and assesses instances of spasticity. The result is
that there is no clear consensus regarding the number of
patients who develop spasticity after stroke [20].
Early on (03 months post-stroke), the available data
point to a rate of spasticity between 19% and 28%. A
2004 study by Sommerfeld et al. [20] of 95 rst-time
stroke patients (60 women, 35 men; mean age = 78
years) measured the occurrence of spasticity immedi-
ately post-stroke (mean follow-up 5.4 days) and
3 months post-stroke, using the Modied Ashworth
Scale (Fig. 2). In the immediate post-stroke measure-
ment, 20 patients (21%) were determined to have
spasticity. After 3 months, 18 (19%) were spastic
(Table 1) [20].
A recent study examined 103 patients at 6 days,
6 weeks, and 16 weeks post-stroke for change in muscle
tone, pain, and paresis. Within 2 weeks of stroke,
24.5% of patients developed an increase in muscle tone
according to the Modied Ashworth Scale. By the rst
follow-up (median time = 6 weeks after baseline mea-
surements were recorded), spasticity had emerged in
98% of patients diagnosed with spasticity throughout
the course of the study, and the rate of spasticity at rst
follow-up had increased only slightly, up to 26.7%
(Table 1) [21].
In the medium term, Urban et al. [22] assessed 211
patients for spasticity 6 months post-stroke using the
Modied Ashworth Scale, and 90 (42.6%) were found
to have the condition (Table 1). Long-term data
which may be dened as 1 year post-strokevary. A
cohort study from the United Kingdom examined
spasticity in 106 consecutive community-dwelling
patients and found that, when measured using the
European Journal of Neurology  2011 EFNS European Journal of Neurology 19, 2127
Modied Ashworth Scale, 27% were found to have
spasticity 1 year post-stroke [23]. However, when using
the Tone Assessment Scale, which measures spasticity
at multiple joints rather than at only one (as with
Ashworth), the rate of spasticity climbed to 36%.
A Swedish study also examined spasticity at 1 year
among 140 patients who had experienced rst-time
stroke, nding a rate of 17% spasticity and estimated
disabling spasticity at 4% (Table 1) [24]. A study from
Eastern India found a much higher 46% rate of spas-
ticity among a group of 88 rst-ever stroke patients,
one-third of whom were designated as having severe
spasticity (Table 1) [25].
The 3-month study by Sommerfeld et al. [20] previ-
ously noted was extended through an 18-month follow-
up, although the original 95 patients were reduced to 66
[26]. Nineteen percent had been diagnosed with spas-
ticity at 3 months, and at 1 years, the rate was almost
the same: 20% (Table 1) [26]. Fifty-eight percent of
subjects were hemiparetic, and of these, 34% were
spastic. Four of the original subjects identied with
spasticity at 3 months who remained in the study had
ceased to be spastic, but another four, who were not
spastic at 3 months, had acquired spasticity later on. The
authors concluded that those developing later spasticity
had done so because of intrinsic muscle changes [26].
In clinical practice, signs of exaggerated tendon tap
reexes associated with muscle hypertonia are generally
thought to be responsible for spastic movement disor-
ders. Many antispastic treatments are, therefore,
directed at the reduction of reex activity. There is,
however, a discrepancy between spasticity and func-
tional spastic movement disorders, which are primarily
because of the dierent roles of reexes in passive and
active states, respectively [27]. We now know that cen-
tral motor lesions are associated with a loss of sup-
raspinal drive. This arises from altered aerent inputs,
and these changes lead to paresis and maladaptation of
the movement pattern. Secondary changes in mechan-
ical muscle ber, collagen tissue, and tendon properties
(e.g. loss of sarcomeres, subclinical contractures) result
in increased muscle tone, which in part compensates for
paresis and allows functional movements on a simpler
level of organization. By reducing this through the use
of antispastic drugs, the paresis can become more evi-
dent and clinicians should apply caution when using
them in mobile patients.
With a growing number of studies evaluating preva-
lence of spasticity among the post-stroke population, it
is clear that variability in time of onset of spasticity
impedes the determination of a universal prevalence
rate. Our understanding of the onset of spasticity is
complicated by the etiologic role of contractures. A
small study of 24 hemiparetic patients recruited within
 2011 The Author(s)
 Post-stroke spasticity: pathophysiology and onset 25

13 months of stroke (mean = 5.3 months) examined

Spasticity + no dysautonomia = 27.6%,

Spasticity + dysautonomia = 45.1%

46%, Disabling spasticity rate = 33%

Immediate = 21%, 3 months = 19%
the relationship between spasticity and contracture [28].

17%, Disabling spasticity rate = 4%

6 days = 24.5%, 6 weeks = 26.7%,
Electromyography (EMG) was employed, and subjects
were measured for spasticity both by resistance to
passive stretch and by increased tonic stretch. The
16 weeks = 21.7% investigators found only limited evidence of tonic
stretch reexes (at most ve subjects, although only one
demonstrated reexes in all measured stretching con-
Prevalence rate

ditions), but half the subjects exhibited contracture, and

the contracture was associated with resistance to pas-
42.6%

27% sive movement [28]. The authors concluded that the

20%
increased passive resistance was a result of the con-
tractures and that spasticity is not causative of con-
Upper and lower limbs

Upper and lower limbs

Upper and lower limbs

limbs
limbs
limbs
limbs tractures but rather the reverse, that contractures are,
post-acute stroke
Neurological decits

or can be, the cause of spasticity [28]. If this is the case,

lower
lower
lower
lower

then correction of contractures may reduce the occur-

dysautonomia
Affected areas

rence of spasticity.
and
and
and
and

An EMG study by Thilmann et al.[29] highlights the

Upper
Upper
Upper
Upper

diculties; primary and secondary causes of spasticity

remain poorly understood, which not only aects the
determination of prevalence rates, but more impor-
5 days post-stroke) and
Time period post-stroke

tantly can aect a physicians ability to diagnose and

3 months post-stroke

16 weeks post-stroke

6 months post-stroke
6 days, 6 weeks, and

1.5 years post-stroke

Immediate (mean =

treat properly spasticity associated with post-stroke

1 year post- stroke
1-week post-stroke

1 year post-stroke
1 year post-stroke

patients.

Potential predictors and associated risk factors of post-

stroke spasticity

An understanding of precipitating events or precondi-

100 rst-time acute stroke patients

tions for spasticity may allow for early intervention or

prophylactic treatment to reduce spasticity risk after
211 patients experiencing limb
paresis after rst-time stroke
103 post-stroke patients who
were previously non-spastic

140 rst-time stroke patients

95 rst-time stroke patients

88 rst-time stroke patients

66 rst-time stroke patients

stroke. This applies also the development of contrac-

Sommerfeld et al. [20])
106 post-stroke patients

tures. Predictive criteria for spasticity are still to be

(same study cohort as

completely determined, but they may be identied to a

degree to modify the approach to spasticity manage-
No. of patients

ment. This could then at least allow post-stroke patients

to be better informed about what potential sequelae
may occur.
The previously cited 1 year post-stroke spasticity
study from the United Kingdom also examined the
Bhattacharya et al. [25]

same group of 106 post-stroke patients to try to identify

Table 1 Studies assessing prevalence of spasticity

Sommerfeld et al. [20]

Lundstrom et al. [24]

risk factors for the onset of spasticity and found several

Diserens et al. [32]

Watkins et al. [23]

Welmer et al. [26]

Urban et al. [22]
Wissel et al. [21]

predictive factors. People with spasticity had a lower

score on the 7-day Barthel Index (an instrument for
evaluating stroke severity by evaluating ADLs at 7-day
Study

post-stroke) than those without disabling spasticity.

They also had experienced early arm or leg weakness
[7]. Predictors of more severe disability from spasticity
Medium-term studies

were the Barthel Index, evidence of left-sided weakness,

Short-term studies

Long-term studies

and a history of smoking.

A recent study from Wissel et al. [21] following
patients 6 days, 6 weeks, and 16 weeks post-stroke
found the typical patient at high risk for developing
severe spasticity to have hemispasticity, more often in

 2011 The Author(s)

European Journal of Neurology  2011 EFNS European Journal of Neurology 19, 2127
26 A. B. Ward
Figure 4 Demonstration of silent period after transcranial
magnetic stimulation. Reproduced with permission from Elsevier
Ireland Ltd: Cruz Martinez A, Munoz J, Palacios F, The muscle
inhibitory period by transcranial magnetic stimulation. Study in
stroke patients, Electromyography and clinical neurophysiology,
38: 189192. Copyright 1998 {Ref. [30]}. Demonstrates the
inhibitory period in thenar eminence muscles following motor-
evoked potential by magnetic cortical stimulation. Top Panel:
healthy individual, aged 55 years. Lower Panel: spastic stroke
patient aged 60 years. The inhibitory period is shorter in the
spastic patient.
the arm, 2 joints aected, and a modied Ashworth
Score 2 from baseline to rst follow-up (median
time = 6 weeks). Other predictive factors include a low
Barthel Index score (indicating severe disability) at
baseline and paresis at any point throughout the study.
Unlike Leathley et al. [7], a history of smoking and all
other baseline factors such as sex and age were not
associated with severe spasticity.
Transcranial magnetic stimulation (TMS) is an elec-
trophysiologic measure of central motor pathways and
has diagnostic value for neurological disorders. TMS
elicits a motor-evoked potential followed by a pause in
muscle activity. Several studies point to the silent per-
iodthe post-stroke pause in muscle activity during
tonic muscle contraction as measured by electromyog-
raphy following TMSas being prognostic for spas-
ticity, with a shorter silent period being the indicator of
increased spasticity risk. A study in 10 post-stroke and
10 healthy subjects found that the silent period after
TMS in healthy subjects was longer than in stroke
patients with spasticity [30]. The extent to which the
silent period was shortened was correlated with the
degree of spasticity. An earlier study in 49 post-stroke
hemiparetic subjects and 20 matched controls similarly
European Journal of Neurology  2011 EFNS European Journal of Neurology 19, 2127
employed TMS to evaluate silent period duration at 7
and 90 days after stroke [31]. At 90 days, a shorter
duration of silent period was associated with worse
functional outcome and higher likelihood of spasticity
[31]. These data are certainly provocative, but they are
limited (Fig. 4).
Early treatment of post-stroke spasticity
With better recognition, not only should it be easier to
treat post-stroke spasticity, but also the available
treatments may be more eective prior to progression
of severe spasticity [7]. Optimal treatment of spasticity
uses a multidisciplinary approach, which includes
physical muscle stretching regimens, oral medications,
and chemodenervation with botulinum toxin A for the
treatment of focal spasticity [9].
Conclusions
Spasticity is a major consequence of stroke with complex
neurophysiologic processes that can lead to life-threat-
ening, disabling, and costly consequences. Its onset can
vary. Its clinical presentation may represent dierent
stages of the condition (i.e. later stages may indicate
intrinsic change in muscle) and may be complicated by
the presence of contractures. Preventing spasticity and
treating emerging spasticity in a timely manner is
essential [8,9], and early interventions may prevent or
reduce the development of spasticity after stroke [7]. A
better understanding of the predictive factors for the
onset of post-stroke spasticity may help clinicians to
better identify patients at high risk and to appropriately
incorporate early interventions and preventive measures.
Acknowledgements
The author thanks Allergan, Inc., for funding Imprint
Publication Science, New York, NY, to provide edito-
rial support in the preparation and styling of this
manuscript.
Disclosure of conflict of interest
The authors declare no nancial or other conict of
interest.
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