Brain Injury, July 2009; 23(7–8): 632–638

Efficacy of therapeutic ultrasound and infrared in the management

of muscle spasticity

NOUREDDIN NAKHOSTIN ANSARI1, SOOFIA NAGHDI1, SCOTT HASSON2,

& MARYAM RASTGOO1
1
Faculty of Rehabilitation, Tehran University of Medical Sciences, Iran, and 2Physical Therapy Department, Angelo
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State University, San Angelo, TX, USA

(Received 2 January 2009; accepted 15 April 2009)

Abstract
Primary objective: This study was designed to compare the short-term effects of infrared (IR) and therapeutic ultrasound
(US) on clinical and electrophysiological measures of spasticity and range of motion (ROM) in hemiplegic patients with
For personal use only.

plantar flexor muscle spasticity.

Research design: A cross-sectional, single centre trial.
Interventions: Ultrasound and Infrared were used.
Methods and procedures: Twenty-one patients (13 males and eight females) aged 27–78 years (mean  SD: 60.4  13.2) were
randomly assigned into either the US or IR treatment groups. The IR and US were delivered for 20 and 10 minutes,
respectively. The H-reflex, Ashworth scale (AS) and ROM were collected before, immediately after and 15 minutes after the
end of the treatment.
Main outcomes and results: Both groups were statistically similar on all variables at the beginning of the study. Results
indicated that the dependent variables were not significantly different between groups at the end of study. The use of IR and
US was not associated with significant reductions of H-reflex and Ashworth scores. A significant main effect for time on
active and passive ROM was obtained.
Conclusions: It was concluded neither IR nor US reduced electrophysiological or clinical measures of spasticity in this sample
of patients.

Keywords: Spasticity, hemiplegia, ultrasound, infrared, physiotherapy

Introduction that increase in passive stiffness of a muscle to

A major disabling symptom following upper motor
neuron (UMN) syndrome is spasticity. It is com-
monly seen after conditions such as stroke, multiple
sclerosis, spinal cord injuries, traumatic brain injury
and cerebral palsy. Lance [1] defined spasticity as
a motor disorder characterized by a velocity-depen-
dent increase in the tonic stretch reflex. Therefore,
increased excitability of the stretch reflex is a central
factor contributing to spasticity [2]. Studies indicate
stretch in patients with spasticity can also be due to
changes in collagen tissue, tendons and muscle
contractures [3–5]. Evidence exists that patients
with spasticity may be disabled by a combination of
paresis, soft tissue contracture and muscle over-
activity [6]. Negative symptoms of weakness, fatig-
ability and reduced dexterity also exist and weakness
has been shown to be the main contributor to
activity limitations [7].

Correspondence: Dr Noureddin Nakhostin Ansari, Faculty of Rehabilitation, Tehran University of Medical Sciences, Enghelab Ave, Pitch-e-shemiran
Zip: 11498, PO Box: 11155-1683 Tehran, Iran. Fax: 98 21 77882009. E-mail: nakhostin@sina.tums.ac.ir
ISSN 0269–9052 print/ISSN 1362–301X online ß 2009 Informa Healthcare Ltd.
DOI: 10.1080/02699050902973939

Spasticity, if uncontrolled, can negatively influ-
ence function and activities of daily living.
Uncontrolled spasticity can cause pain and fatigue,
contractures and disturbed sleep [8, 9]. There are
a variety of options for the management of spasticity
including: anti-spasticity medication; intrathecal
baclofen; phenol and ethanol injections; administra-
tion of botulinum toxin; physical rehabilitation
modalities; and surgery [8, 10, 11]. The most
conservative procedures are utilized first, namely
rehabilitation modalities [8].
Physiotherapists as one of the members of
a rehabilitation team are involved in the manage-
ment of spasticity [12]. There are different physical
modalities currently available used by physiothera-
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pists for the treatment of muscle spasticity. In the
clinical situation, superficial and deep heat in the
form of infrared (IR) and ultrasound (US), respec-
tively, are used for reduction of spasticity. However,
the effects of these modalities on spasticity are not
thoroughly investigated [13].
There are two reports on the effect of US on
spasticity. The first preliminary study used contin-
uous thermal US to treat four adult patients with
For personal use only.
post-stroke muscle spasticity [14]. Following 15
treatment sessions, the spasticity in terms of the
Ashworth scores and Hmax/Mmax ratio, despite
improvements, did not reduce significantly. The
second study to quantify the effects of continuous
thermal US on ankle plantar flexor spasticity
included 12 patients with stroke. The patients were
treated with either US or sham US for 3 days per
week, every other day for 15 treatment sessions.
While there was a significant reduction in the Hmax/
Mmax ratio in the treatment group, it was increased
in the placebo group. The difference between groups
on the Hmax/Mmax ratio was statistically significant.
The Ashworth scores demonstrated statistically sig-
nificant changes within the US group. However,
there was no statistical difference between groups
[15]. Clinical study of IR on spasticity is scarce and
no reports exist on the short term anti-spastic
efficacy of IR and US. This study was therefore
designed to compare the short-term effects of IR and
US on plantar flexor muscle spasticity in patients
with hemiplegia.
Methods and procedures
Study design
A cross-sectional, single centre trial was used to
compare the short-term effects of IR and US in the
treatment of muscle spasticity.
Efficacy of heat in spasticity 633
Subjects
Patients diagnosed to have hemiplegia and referred
for treatment in the physiotherapy clinic, faculty of
Rehabilitation, Tehran University of Medical
Sciences participated in the study. Adult subjects
aged 18 years with first ever UMN lesion were
included. Patients were excluded from the study if
they had: botulinum toxin injection; fixed ankle
contracture; were taking anti-spasticity drugs; sen-
sory abnormalities; peripheral circulatory problems;
and any other contraindication to the use of IR or
US. The approval of the Research Council of
Rehabilitation Faculty, Tehran University of
Medical Sciences was obtained. All subjects gave
their informed consent before the start of the study.
Procedure
Initially, the rationale and procedure for the study
were explained to the subjects. Subjects who met the
inclusion criteria were then assigned to either the IR
or US treatment groups in the order of their
recruitment into the study. The first patient was
assigned by tossing a coin, however. Patient’s height
and body weight were then measured using the
height meter and weight scale, respectively.
Treatment. Patients in the IR study group received
20 minutes of IR (500 W, wavelengths in the IR-A
band) over the area of the calf muscle group. The
perpendicular distance between IR machine and the
skin was 60–90 cm based on each patient’s tolerance,
but all subjects were generally advised that they
should feel just a comfortable warmth.
Surface skin temperature was measured in the IR
group.
Patients in the US study group received continuous
thermal mode and intensity at 1.5 W cm2 for
10 minutes [US unit (Shrewsbury Medical, model
SM 3371, UK), operating at a frequency of
1.0  10% MHz]. The US was applied to the area
of the calf muscle group. Transmission gel was the
coupling medium (Sonogel, Germany). A large
treatment applicator (5 cm2) was used and moved in
a stroking technique. The effective radiation area
(ERA) was 5 cm2.
Measurements
Measurements were carried out at the beginning
of the study (before treatment), immediately after
treatment and 15 and 30 minutes after the end of the
treatment. Clinical measurements of active and
passive range of motion (ROM) and Ashworth
scale (AS) for spasticity were performed first.
 634 N.N. Ansari et al.
These measurements were followed by the electro-
myographic evaluation (Hmax/Mmax ratio). The
measurements were done by one physiotherapist.
The primary outcome measures were the Hmax/Mmax
ratio and the Ashworth Scale [16] used as measures
of spasticity. The secondary outcome measurements
were goniometry measurements of active and
passive ROM.
Electromyographic measurements. The EMG mach-
ine (Toennies, Germany) was used for electrophy-
siological (EP) evaluation to obtain the H-reflex.
Briefly, patients were placed in prone position and
the feet suspended over the end of the bed. The
H-reflex was evoked from the gastrocnemius muscle
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after stimulation of the tibial nerve in the popliteal
fossa using bipolar silver–silver chloride surface
electrodes 5 mm in diameter. The stimulus was
a single, 1-ms rectangular pulse delivered every
5 seconds. The active electrode was placed over the
medial head of the gastrocnemius halfway between
the medial malleolus and the tibial epicondyle;
ground electrode over the lateral gastrocnemius
muscle between the stimulation and the active
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electrode; and reference electrode over the Achilles
tendon.
The EMG signal was band-pass filtered set at 3 Hz
to 3 kHz. The maximum amplitudes of the H-reflex
and the M-wave were measured from the peak-
to-peak. The ratio of the Hmax/Mmax was calculated
by dividing the maximum amplitudes of the H-reflex
by that of the M-wave. The Hmax/Mmax ratio served
as an EP index of spasticity [14, 15].
Spasticity. The clinical rating of AS was used to
assess the spasticity of the ankle plantar flexors that
provided a measure of muscle hypertonia. The AS
was undertaken with the patient lying in supine
position.
Range of motion measurements. A universal goni-
ometer (A Bissell Health Care, model 7524, USA)
was used. We followed a standard method for ROM
measurements [17] used and described elsewhere
[14, 15]. The maximal PROM (passive ROM) was
evaluated in supine position with the knee in
extension. The AROM (active ROM) was measured
while the patient voluntarily dorsiflexed the ankle.
The positive and negative values from the position of
90 (zero position) indicated the ankle dorsiflexion
and plantarflexion, respectively.
In order to determine the ankle resting position,
the ankle was passively dorsiflexed and released to
reach a new resting position. The final resting
position of the ankle was measured as the resting
posture after three repetitions.
Statistical analysis
Independent sample t-tests were used to analyse
initial differences between groups for patient char-
acteristics. The change of skin temperature in the IR
group across time was analysed using paired t-test.
Descriptive statistics were calculated and percentage
of individuals increasing, decreasing or having no
change for each dependent variable was determined.
The effect of the IR vs. US group on electromyo-
graphic measurements (Hmax/Mmax ratio) and range
of motion (both passive and active) was examined
using a Group (IR and US)  Time (pre-, immedi-
ately post- and 15 minutes post-intervention) 2  3
mixed model ANOVA. Effect sizes for F-ratios were
reported as eta-squared (2).
The effect of the IR vs. US group on spasticity
(Ashworth Scale) was examined using non-
parametric statistics since the data were of ordinal
scale. Mann-Whitney U-test was used to compare
the AS scores of the patients between the two study
groups. Within-group analyses were tested with
paired Wilcoxon Signed Ranks Test to evaluate the
effectiveness of either IR or US.
The significance level was defined as p < 0.05. The
analysis was conducted using SPSS version 11.5 for
windows.
Main outcomes and results
Twenty-four patients were included. Data of two
subjects in the IR group and one subject in the US
group were excluded from final analysis because of
non-compliance with electromyography (EMG)
measurements. The remaining 21 subjects (13
men, eight women; mean age 60.4  13.2, range
27–78 years) were randomized in the IR (n ¼ 10) and
US group (n ¼ 11). Seven patients did not agree with
the measurements at time 30 minutes after treat-
ment, therefore this time point was not included in
the analysis and final outcomes. The causes for
hemiplegia were stroke (n ¼ 18), tumour (n ¼ 2) and
traumatic brain injury (n ¼ 1). Fifteen patients had
left hemiplegia and six patients had right hemiplegia.
The initial resting plantarflexion position of the
ankle joint was 21.8  6.9 .
The demographic and clinical data of subjects in
the two treatment groups are presented in Table I.
There was no significant difference between the two
groups with regards to age, duration of stroke,
height, body weight, BMI and resting ankle position.
In addition there was no significant initial difference
 Efficacy of heat in spasticity 635

between Hmax/Mmax ratio, Ashworth scores, ankle decreased significantly at post-15 minutes
joint AROM and PROM. (33.7 C  1.4, p < 0.001). The changes of skin tem-
Surface skin temperature was 32 C  1.7 at base- perature between pre- and 15 minutes after treat-
line and increased significantly (38 C  2.3) after ment was also statistically significant ( p ¼ 0.003).
treatment ( p < 0.001). The skin temperature
The Hmax/Mmax ratio
Table I. Patients characteristics (n ¼ 21).
The Hmax/Mmax ratio data are provided in Figure 1.
Groups The mixed model ANOVA on Hmax/Mmax ratio
values did not identify a statistically significant
Characteristics IR (n ¼ 10) US (n ¼ 11) p
Time, F(2, 38) ¼ 1.09, p ¼ 0.31, 2 ¼ 0.05; Group,
Age (years) 64.3  11.7 56.8  13.9 NS F(1, 19) ¼ 0.14, p ¼ 0.71, 2 ¼ 0.007; or Group 
Duration (months) 25.6  13.7 48  87.4 NS Time interaction, F(2, 38) ¼ 0.96, p ¼ 0.34,
Height (cm) 163.5  7.5 167.2  9.1 NS 2 ¼ 0.05.
Weight (kg) 71.9  11.1 70.3  13.5 NS
When comparing the two groups descriptively, the
BMI (kg m2) 27.2  2.8 25  2.6 NS
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Ankle rest posture 21.5  6.4 22  7.6 NS percentage of individuals who had decreases (moved
Hmax/Mmax ratio 0.52  0.27 0.47  0.28 NS toward a normal value) in their Hmax/Mmax ratio
Ashworth score 2  0.8 1.72  1.1 NS immediately following the intervention was equal
AROM (degree) 15.2  13.5 15.6  12.7 NS (50% in the IR group compared to 45.5% in the US
PROM (degree) 4.2  7 4.3  10.4 NS
group). Interestingly the percentage of individuals
Values are mean  SD. NS, not significant. AROM, active range who had increases (moved away from a normal
of motion; PROM, passive range of motion.
value) in their Hmax/Mmax ratio immediately

(a) 0.9 (c) 30

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0.8

0.7 20
Hmax/Mmax ratio

Passive ROM

0.6

0.5 10

0.4

0.3 0
US US
0.2
0.1 IR −10 IR
Pre Post Post 15 Pre Post Post 15
Time Time

(b) 3.5 (d) 10

3.0
0
Ashworth score

2.5
Active ROM

2.0 −10

1.5
−20
1.0

US −30 US
.5

0.0 IR −40 IR
Pre Post Post 15 Pre Post Post 15
Time Time

Figure 1. Hmax/Mmax ratio, Ashworth score, active range of motion (ROM) and passive ROM values before and after treatment within
groups IR and US.
 636 N.N. Ansari et al.
following the intervention was also equal (50% in the
IR group compared to 45.5% in the US group). One
subject in the US group Hmax/Mmax ratio remained
unchanged. The percentage of individuals who had
decreases in their Hmax/Mmax at 15 minutes post-
intervention compared to the initial baseline (again
moved toward a normal value) was 80% and 72.7%
in the IR and US group, respectively. A minority of
patients (20% and 27.3%) experienced an increase
in the Hmax/Mmax ratio in the IR and US group,
respectively.
Ashworth scale
The AS data are provided in Figure 1. The Mann-
Whitney U-test on AS scores did not identify
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a statistically significant difference between groups
(pre Z ¼ 0.48, p ¼ 0.65; immediately post
Z ¼ 0.98, p ¼ 0.35; post-15 minutes
Z ¼ 0.30, p ¼ 0.81). Within groups analysis by
using Wilcoxon Signed Ranks Test did not show
significant changes immediately after and 15 min-
utes after treatment in the IR and US groups
( p > 0.05). When comparing the two groups
descriptively, the percentage of individuals who
For personal use only.
had decreased spasticity (lower AS scores) immedi-
ately following the intervention was equal (30% in
the IR group compared to 36.4% in the US group).
The percentage of individuals who stayed the same
for their AS scores following intervention were 40%
(IR group) and 54.5% (US group). Interestingly the
percentage of individuals who had increased spasti-
city (higher AS scores) immediately following the
intervention was also equal (30% in the IR group
compared to 9.1% in the US group).
The percentage of individuals who had decreased
spasticity (lower AS scores) at 15 minutes post-
intervention compared to the initial baseline was
50% and 18.2% in the IR and US group, respec-
tively. The percentage of individuals who stayed the
same for their AS scores following at 15 minutes
post-intervention compared to the initial baseline
was 40% and 63.6% and in the IR and US group,
respectively. Finally, a small minority of patients
following at 15 minutes post-intervention compared
to the initial baseline had increased spasticity (10%
and 18.2% for IR and US, respectively).
Range of motion
Passive range of motion. The PROM data are
provided in Figure 1. The mixed model ANOVA
revealed that the main effect for Time was statisti-
cally significant for PROM, F(2, 38) ¼ 5.64,
p ¼ 0.03, 2 ¼ 0.23. Post-hoc analyses indicated
a significant difference between pre- and immedi-
ately post-treatment (PROM mean difference ¼
6.14, p ¼ 0.004); pre- and 15 minutes
post-treatment (PROM mean difference ¼
5.59, p ¼ 0.01). However, neither a significant
Group (F(1, 19) ¼ 0.04, p ¼ 0.85, 2 ¼ 0.002) nor
Time  Group interaction (F(2, 38) ¼ 0.05, p ¼
0.83, 2 ¼ 0.002) was obtained.
Descriptively, the PROM increased immediately
after treatment in both groups (IR 80% and US
81.8%). The percentage of patients who still showed
increases in PROM beyond the initial baseline
measure at 15 minutes post-treatment constituted
70% (IR group) and 54.5% (US group) of the
patients. However, a few patients in both groups
demonstrated decreased PROM at immediately post
(IR 10%) or at 15 minutes (IR 20% and US 27.3%).
Active range of motion. The AROM data are also
provided in Figure 1. The mixed model ANOVA
revealed that the main effect for Time was statisti-
cally significant for AROM, F(2, 38) ¼ 9.11,
p ¼ 0.007, 2 ¼ 0.32. Post-hoc analyses indicated
a significant difference between pre- and immedi-
ately post-treatment (AROM mean difference ¼
3.35, p ¼ 0.004); pre- and 15 minutes post-
treatment (AROM mean difference ¼ 5.31,
p ¼ 0.004). However, once again neither
a significant Group F(1, 19) ¼ 0.03, p ¼ 0.86,
2 ¼ 0.002 nor Time  Group interaction
(F(2, 38) ¼ 0.72, p ¼ 0.41, 2 ¼ 0.04) was obtained.
Descriptively, the AROM increased immediately
after treatment in both groups (IR 40% and US
63.6%). The percentage of patients who still showed
increases in AROM beyond the initial baseline
measure and at 15 minutes post-treatment consti-
tuted 40% (IR group) and 54.5% (US group) of the
patients. No patient in either group had decreases in
AROM immediately and at 15 minutes post-
intervention.
Discussion
To the authors’ knowledge, the present study is the
first investigation comparing the short-term effect of
IR and US on muscle spasticity in patients with
hemiplegia. The primary finding was that using the
IR or US did not reduce significantly electrophysio-
logical or clinical outcome measures of spasticity in
this sample of patients.
Patients in both groups had high Hmax/Mmax ratio
at baseline, indicating hyperexcitability of the stretch
reflex (normal range 0.05–0.35) and had moderate
spasticity as indicated by the Ashworth Scale.
Although changes of the EP and spasticity post-
treatment were not statistically significant across
time, a greater percentage of individuals had expe-
rienced a decline or no change as compared to
an increase immediately after intervention and

after 15 minutes post-treatment as compared to the
baseline measure. This would indicate that few
individuals have an increase in hyperexcitability
and spasticity following application of thermal heat
modalities and that in fact the majority of individuals
with hyperexcitability of the stretch reflex have
a reduction towards normal values. However it
must be duly noted, there was not a significant
difference in overall Hmax/Mmax ratio or Ashworth
Scale scores between groups or across time.
Although the changes of both EP index and
spasticity measures were not statistically significant,
any improvement may be desirable clinically.
The effect of IR and US on electrophysiological
and clinical indices of spasticity in patients with
hemiplegia might depend on the short-term vs. long-
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term use of them. One recent study reported that
a 5-week period of thermal ultrasound therapy
reduced the Hmax/Mmax ratio (pre 0.41  0.19, post
0.19  0.22) and Ashworth scores (pre median 3,
post median 2) in patients with stroke who had
spastic plantarflexor muscle groups [15]. Within the
present study, there was not a statistically significant
reduction in Hmax/Mmax ratio or AS scores after one
treatment session in patients with spastic hemiplegia.
For personal use only.
Such findings suggest that the significant effect of
US and perhaps IR on electrophysiological and
clinical indices of spasticity might be long-term in
nature.
The AROM and PROM after treatment were
significantly higher than those before treatment. The
increase in the active ROM and passive ROM
improved immediately after treatment and persisted
for 15 minutes after treatment. There were no
overall difference between groups in AROM and
PROM. Thus, it appears that the short-term use of
IR and US was not associated with a reduction in
Hmax/Mmax ratio and AS scores as indices of
spasticity. The results suggest that short-term use
of IR and US is associated with improvements in
ROM, but statistically neither improves nor worsens
spasticity.
The improvements in active and passive ROM
suggest that the heat, no matter deep or superficial,
is effective from the ROM perspective. The finding
that the PROM increased significantly in the patients
suggests that improvements of the ROM might have
been due to mechanical factors. Repeated applica-
tion of passive stretching for measurements of
PROM and Ashworth score evaluation, combined
together with heat application might have length-
ened muscle-tendon unit by viscoelastic changes in
muscle. Evidence indicates that non-reflex and
intrinsic factors contribute to spasticity [18, 19]
and passive stretch tends to reduce resistance and
cause neural modulation [20, 21]. In the earlier
study by Ansari et al. [15] using long-term
Efficacy of heat in spasticity 637
application of US for treatment of ankle plantar
flexor spasticity, despite improvement, did not pro-
duce statistically significant changes in ROM. It
follows that the effect of US and perhaps IR on
AROM and PROM might be short-term rather than
long-term, unless stretching of the musculature is
consistently provided.
In the IR group, the peak PROM was reached
immediately after treatment, thus coinciding with
the peak surface skin temperature. It was also noted
that the PROM tended to decrease at post-15 once
again coinciding with declining skin temperatures.
This implies that the effect of IR may be a function
of the surface skin temperature. The use of IR and
US prior to applying passive stretch or active
exercise may facilitate tissue extensibility.
Limitation
This study is not without limitations. First, the
measurer of all outcomes was the same individual.
Secondly, the assessor was not blinded to the
treatments. Thirdly, this study did not include the
muscle groups without contracture in the limbs.
Finally, there was a small group of patients.
Conclusion
This data suggest that IR and US did not signifi-
cantly reduce electrophysiological or clinical mea-
sures of spasticity in this sample of patients. The
authors encourage continued examination of the
physiotherapeutic heat modalities effects on spasti-
city in patients with UMN lesions.
Acknowledgement
This study was supported by research deputy,
Tehran University of Medical Sciences (TUMS).
Declaration of interest: The authors report no
conflicts of interest. The authors alone are respon-
sible for the content and writing of the paper.
References
1. Lance JW. The control of muscle tone, reflexes, and movement:
Robert Wartenberg Lecture. Neurology 1980;30:1303–1313.
2. Nielsen JB, Crone C, Hultborn H. The spinal pathophysiology
of spasticity—from a basic science point of view. Acta
Physiology 2007;189:171–180.
3. Dietz V, Sinkjaer T. Spastic movement disorder: Impaired
reflex function and altered muscle mechanics. Lancet
Neurology 2007;6:725–733.
4. Lieber RL, Steinman S, Barash LA, Chambers H. Structural
and functional changes in spastic skeletal muscle. Muscle &
Nerve 2004;29:615–627.
 638 N.N. Ansari et al.
5. Lieber RL, Friden J. Spasticity causes a fundamental
rearrangement of muscle-joint interaction. Muscle & Nerve
2002;25:265–270.
6. Gracies J. Pathophysiology of spastic paresis. I: Paresis
and soft tissue changes. Muscle & Nerve 2005;31:
535–551.
7. Ada L, O’Dwyer N, O’Neill E. Relation between spasticity,
weakness and contracture of the elbow flexors and upper limb
activity after stroke: An observational study. Disability and
Rehabilitation 2006;28:891–897.
8. Adams MM, Hicks AL. Spasticity after spinal cord injury.
Spinal Cord 2005;43:577–586.
9. Meythaler JM. Concept of spastic hypertonia. Physical
Medicine and Rehabilitation Clinics of North America
2001;12:725–732.
10. Chou R, Peterson K, Helfand M. Comparative efficacy and
safety of skeletal muscle relaxants for spasticity and muscu-
loskeletal conditions: A systematic review. Journal of Pain
and Symptom Management 2004;28:140–175.
Brain Inj Downloaded from informahealthcare.com by University of Virginia on 09/13/12
11. Abbruzzese G. The medical management of spasticity.
European Journal of Neurology 2002;9(Suppl. 1):
30–34.
12. Richardson D. Physical therapy in spasticity. European
Journal of Neurology 2002;9(Suppl. 1):17–22.
13. Gracies JM. Physical modalities other than stretch in spastic
hypertonia. Physical Medicine and Rehabilitation Clinics of
North America 2001;12:769–792.
For personal use only.
14. Ansari NN, Adelmanesh F, Naghdi S, Tabatabaei A. The
effect of physiotherapeutic ultrasound on muscle spasticity in
patients with hemiplegia. Electromyography and Clinical
Neurophysiology 2006;46:247–252.
15. Ansari NN, Naghdi S, Bagheri H, Ghassabi H. Therapeutic
ultrasound in the treatment of ankle plantarflexor spasticity in
a unilateral stroke population: A randomized, single-blind,
placebo-controlled trial. Electromyography and Clinical
Neurophysiology 2007;47:137–143.
16. Ashworth B. Preliminary trial of carisoprodol in multiple
sclerosis. Practitioner 1964;192:540–542.
17. Norkin CC, White DJ. Measurement of joint motion: A guide
to goniometry. 2nd ed. Philadelphia: FA Davis; 1995.
18. Alibiglou L, Rymer WZ, Harvey RL, Mirbagheri MM. The
relation between Ashworth scores and neuromechanical
measurements of spasticity following stroke. Journal of
NeuroEngineering and Rehabilitation 2008;5:18.
19. Mirbagheri MM, Settle K, Harvey R, Rymer WZ.
Neuromuscular abnormalities associated with spasticity of
upper extremity muscles in hemiparetic stroke. Journal of
Neurophysiology 2007;98:629–637.
20. O’Dwyer NJ, Ada L, Neilson PD. Spasticity and muscle
contracture following stroke. Brain 1996;119:1737–1749.
21. Schmit BD, Dewald JPA, Rymer WZ. Stretch reflex adap-
tation in elbow flexors during repeated passive movements in
unilateral brain-injured patients. Archives of Physical
Medicine and Rehabilitation 2000;81:269–278.