Spasticity and electrophysiologic changes after extracorporeal shock wave therapy on gastrocnemius.

Abstract

To evaluate the spasticity and electrophysiologic effects of applying extracorporeal shock wave therapy (ESWT) to the gastrocnemius by studying F wave and H-reflex.
Ten healthy adults and 10 hemiplegic stroke patients with ankle plantarflexor spasticity received one session of ESWT on the medial head of the gastrocnemius. The modified Ashworth scale (MAS), tibial nerve conduction, F wave, and H-reflex results were measured before and immediately after the treatment. The Visual Analogue Scale (VAS) was used during ESWT to measure the side effects, such as pain.
There were no significant effects of ESWT on the conduction velocity, distal latency and amplitude of tibial nerve conduction, minimal latency of tibial nerve F wave, latency, or H-M ratio of H-reflex in either the healthy or stroke group. However, the MAS of plantarflexor was significantly reduced from 2.67±1.15 to 1.22±1.03 (p<0.05) after applying ESWT in the stroke group.
After applying ESWT on the gastrocnemius in stroke patients, the spasticity of the ankle plantarflexor was significantly improved, with no changes of F wave or H-reflex parameters. Further studies are needed to evaluate the mechanisms of the antispastic effect of ESWT.

Full text

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Spasticity and Electrophysiologic
Changes after Extracorporeal Shock Wave
Th erapy on Gastrocnemius
Min Kyun Sohn, M.D., Kang Hee Cho, M.D., Young-Jae Kim, M.D., Seon Lyul Hwang, M.D.
Department of Rehabilitation Medicine, School of Medicine, Chungnam National University, Daejeon 301-172, Korea
Objective To evaluate the spasticity and electrophysiologic eff ects of applying extracorporeal shock wave therapy
(ESWT) to the gastrocnemius by studying F wave and H-refl ex.
Method Ten healthy adults and 10 hemiplegic stroke patients with ankle plantarflexor spasticity received one
session of ESWT on the medial head of the gastrocnemius. The modified Ashworth scale (MAS), tibial nerve
conduction, F wave, and H-refl ex results were measured before and immediately after the treatment. Th e Visual
Analogue Scale (VAS) was used during ESWT to measure the side eff ects, such as pain.
Results There were no significant effects of ESWT on the conduction velocity, distal latency and amplitude of
tibial nerve conduction, minimal latency of tibial nerve F wave, latency, or H-M ratio of H-reflex in either the
healthy or stroke group. However, the MAS of plantarfl exor was signifi cantly reduced from 2.67±1.15 to 1.22±1.03
(p<0.05) after applying ESWT in the stroke group.
Conclusion After applying ESWT on the gastrocnemius in stroke patients, the spasticity of the ankle plantarfl exor
was significantly improved, with no changes of F wave or H-reflex parameters. Further studies are needed to
evaluate the mechanisms of the antispastic eff ect of ESWT.
Key Words Extracorporeal shock wave therapy, Spasticity, F wave, H-refl ex
Annals of Rehabilitation Medicine
Original Article
Ann Rehabil Med 2011; 35: 599-604
pISSN: 2234-0645 • eISSN: 2234-0653
http://dx.doi.org/10.5535/arm.2011.35.5.599
INTRODUCTION
Spasticity is one of the most important causes of
disability in stroke patients; it interferes with the patients’
rehabilitation, especially regarding functional recovery.1
Received April 24, 2011; Accepted July 30, 2011
Corresponding author: Young-Jae Kim
Department of Rehabilitation Medicine, Chungnam National University
Hospital, 282, Munhwa-ro, Jung-gu, Daejeon 301-172, Korea
Tel: +82-42-280-7811, Fax: +82-42-256-6056, E-mail: yjsjk214@cnuh.
co.kr
This is an open-access article distributed under the terms of the Creative
Commons Attribution Non-Commercial License (http://creativecommons.org/
licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution,
and reproduction in any medium, provided the original work is properly cited.
Copyright © 2011 by Korean Academy of Rehabilitation Medicine
Because the primary lesion causing spasticity is located
in the central nervous system, most studies have focused
on the neural mechanisms such as excessively increased
spinal excitability as the primary cause of spasticity.2,3
In recent years, there have been several reports that
chronic spasticity itself plays a role in the increase of
joint resistance by structural and mechanical changes in
skeletal muscles through fi brosis of connective tissue.4
Recent studies have reported that intramuscular
injections of botulinum toxin type A reduces spasticity
in hypertonic muscles of the upper limb or equinovarus
deformity by lower limb spasticity, and improves
functional abilities.5-7 However, the development of
neutralizing antibodies can reduce the efficacy of

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MATERIALS AND METHODS
Subjects
Ten healthy adults (4 males and 6 females, mean age of
25.8±3.1 years) and 10 hemiplegic stroke patients with
ankle plantarflexor spasticity (6 males and 4 females,
mean age of 44.9±11.3 years) were enrolled for this study.
Two patients had ischemic stroke, and 8 patients had
hemorrhagic stroke. Two patients had cortical lesions, 3
patients had thalamic lesions, and 5 patients had basal
ganglia lesions. All patients had a spasticity greater than
grade I, by modifi ed Ashworth scale (MAS) and were in a
chronic stage for over 15 months. Patients with previous
or planned treatment of the limb with botulinum toxin,
phenol, or intrathecal baclofen pump were excluded.
All patients were receiving antispastic pharmacological
therapy and did not change the dose of antispastic
medication during the study (Table 1).
Extracorporeal shock wave therapy
Evotron® (SwiTech, Kreuzlingen, Switzerland) was used
for ESWT. Th e pressure pulses were focused at the medial
head of the gastrocnemius of the spastic side. Shots
(1,500) were given in the middle of the belly and the
intensity was 0.1 mJ/mm2. In the healthy control group,
the same methods of ESWT were applied at the right side
medial head of the gastrocnemius. R20 with the focusing
treatment for some patients. In addition, the dosage of
botulinum toxin is not always suffi cient to treat extensive
and severe hypertonia in the upper and lower limbs.
Chronic hypertonic muscles can lead to the fibrosis
of connective tissue, and should be considered in the
rehabilitation of stiff joints.8
Extracorporeal shock wave therapy (ESWT), defined
as a sequence of single sonic pulses characterized by
high peak pressure (100 MPa), fast pressure rise (<10
ns), and short duration (10 μs), is conveyed by an
appropriate generator to a specific target area with an
energy density in the range of 0.003-0.890 mJ/mm2.
ESWT was first applied to patients in 1980 to break up
kidney stones.9 Recent studies have indicated that ESWT
is effective for treatment of musculoskeletal diseases
such as pseudoarthrosis, calcific tendinitis of shoulder,
epicondylitis, plantar fasciitis, and several infl ammatory
tendon diseases.10-13 Mariotto et al.14 reported that ESWT
induced nitric oxide (NO) synthesis, and NO plays a
critical role in anti-infl ammatory responses.
The amplitude of the F wave and the F-M ratio reflect
the excitability of motor neurons and are increased
by spasticity.15-17 Many studies have reported that the
amplitude of the F wave and the F-M ratio can be used as
tools for measuring the spasticity electrophysiologically.
Latency of H-reflex and H-M ratio, which reflect the
excitability of α motor neurons, can also be used as a tool
for measuringspasticity.18,19
Manganotti and Amelio20 reported that ESWT on
the flexor hypertonic muscles of the forearm and the
interosseus muscles of the hand was effective for the
improvement of upper limb spasticity in stroke patients
for >12 weeks; 1,500 shots were used to treat flexor
muscles of the forearm and 800 shots for each interosseus
muscle of the hand with 0.030 mJ/mm2 intensity. Yoo
et al.21 reported significantly reduced spasticity on the
elbow flexor and wrist pronator for 1 to 4 weeks after
1,000 shots of ESWT with 0.069 mJ/mm2 intensity;
however, there was no report on ESWT’s therapeutic
eff ect on lower limb spasticity for stroke patients, and it’s
mechanism is still unknown. The goal of this study was
to evaluate the spasticity and electrophysiologic effects
by studying F wave and H-reflex after applying ESWT
on the gastrocnemius in stroke patients with lower limb
spasticity.
Table 1. General Characteristics of Subjects
Characteristics
Healthy controls
(n=10)
25.8 ± 3.1
4/6
Stroke patients
(n=10)
44.9 ± 11.3
6/4
Age (years)
Gender, male/female
Diagnosis
Infarction
Hemorrhage
Site of lesion
Cortex
Th alamus
Basal ganglia
Time since onset
(months)
MAS
Values are means±standard deviation
MAS: Modifi ed Ashworth scale
2
8
2
3
5
53.4±23.9
2.67±1.15

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depth of 20-30 mm was used for the head of ESWT to
minimize or avoid stimulation of the soleus.
Clinical and electrophysiologic evaluation
F wave and H-refl exes of the tibial nerve were recorded
before and immediately after the treatment to assess the
electrophysiologic eff ects of ESWT on spasticity. Medelec
Synergy® (Viasys healthcare, San Diego, USA) was used
for electrophysiologic assessment and all studies were
performed by one rehabilitation physiatrist. In the F
wave study, an active recording electrode was placed in
the abductor hallucis muscle and the reference electrode
was at the proximal interphalangeal joint of the great
toe. Supramaximal stimulation of the tibial nerve was
done 20 times on the posterior area of the ankle medial
malleolus using antidromic conduction, and the F wave’s
minimal latency was recorded. The sweep speed was
5-10 ms/div, sensitivity was 200-500 μV/div, and the fi lter
range was 20-10,000 Hz. In the H-refl ex study, the active
recording electrode was placed in the soleus muscle
and the reference electrode in the Achilles tendon. To
evoke H-refl ex, the posterior tibial nerve was stimulated
in popliteal fossa with 0.2 Hz frequency and 0.5 ms
duration. We gradually increased stimulation intensity
and recorded H-reflex latency and H-M ratio using
the maximal amplitude of H-reflex and M wave. Distal
latency, amplitude of compound muscle action potential,
and conduction velocity of the tibial nerve were recorded
to assess the peripheral nerve injury by ESWT.
Modifi ed Ashworth Scale (MAS) was used to assess the
spasticity of an ankle plantarflexor. MAS is a velocity-
independent method which manually assesses the
joint range of motion. For convenience of statistical
analysis, MAS grade 1+ was matched to point 2; grades
2, 3 and 4 were matched to 3, 4 and 5, respectively.22 To
avoid inter-rater bias, all studies were performed by one
rehabilitation physiatrist.
The Visual Analogue Scale (VAS) was used to estimate
the severity of pain produced by ESWT. A vertical line
with 10 cm length on paper was presented to the subjects
and the subjects were told that the lower end of the line
indicated “pain-free state” and the upper end indicated
“can not endure because of too severe pain.” After ESWT,
all subjects were drawing the perpendicular line on the
vertical line based on their pain experienced during
treatment. Vertical lines were divided by 10 grades with 1
cm intervals, and this indicated the degree of pain.23
Statistical analysis
MAS, F-wave minimal latency, H-reflex latency, H-M
ratio, and tibial nerve distal motor conduction study
before and immediately after ESWT were analyzed by
the Wilcoxon signed rank test using SPSS 17.0, Korean
version. A p<0.05 was considered statistically signifi cant.
RESULTS
Healthy controls
No significant changes were found in the F wave
minimal latency, H-reflex latency or H-M ratio after
ESWT in healthy controls. Likewise, changes in the
latency, amplitude of compound muscle action potential
Table 2. Eff ect of ESWT on Spasticity and Electrophysiologic Findings
Healthy controls
Before
3.33±0.39
15.83±3.4
52.80±2.44
37.63±2.82
28.27±1.66
3.74±1.64
Stroke patients
Before
3.80±0.69
13.02±3.09
50.94±3.95
41.82±3.89
30.77±1.17
5.63±2.98
2.67±1.15
AfterAfter
CMAP latency (ms)
CMAP amplitude (mV)
Tibial nerve conduction velocity (m/s)
F wave min. latency (ms)
H-refl ex latency (ms)
H-M ratio
MAS
Values are means±standard deviation
ESWT: Extracorporeal shock wave therapy, CMAP: Compound muscle action potential of tibial nerve, F wave min.
latency: F wave minimal latency of tibial nerve
*p<0.05 with Wilcoxon signed rank test
3.36±0.32
15.91±3.18
53.72±2.95
37.23±2.89
28.00±1.62
3.62±1.89
4.00±0.60
13.09±3.30
51.12±4.25
41.57±2.88
30.94±1.43
5.76±3.12
1.22±1.03*

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and conduction velocity of the tibial nerve were not
significant (Table 2). Mild pain was experienced during
ESWT, VAS 2.87±1.49.
Change of ankle plantarfl exor spasticity in stroke
patients
In stroke patients, MAS of ankle plantarflexor before
treatment was 2.67±1.15, and was significantly reduced
to 1.22±1.03 immediately after ESWT (p<0.05) (Table 2).
Also, mild pain (VAS 3.23±1.28) was produced by ESWT.
Electrophysiologic changes in stroke patients
In stroke patients, F wave minimal latency, H-reflex
latency, and H-M ratio before treatment were 41.82±3.89
ms, 30.77±1.17 ms, and 5.63±2.98, respectively.
Immediately after treatment, they were 41.57±2.88 ms,
30.94±1.44 ms, and 5.76±3.12 ms, respectively. There
were no signifi cant changes after treatment (Table 2).
In stroke patients, the latency and amplitude of tibial
nerve compound muscle action potential before
treatment were each 3.80±0.69 ms and 13.02±3.10 mA.
Immediately after treatment, these values were 4.00±0.60
ms and 13.09±3.30 mA, respectively, and no significant
changes were noted after treatment (Table 2). Also, there
was no significant change of tibial nerve conduction
velocity from 50.94±3.95 m/s before treatment to 51.12±
4.25 m/s after treatment (Table 2).

DISCUSSION
ESWT is known to be effective in musculoskeletal
diseases for treating pain, inflammation, or injury of a
ligament. ESWT produces mechanical effects such as
regeneration of degenerated tissue, neovascularization,
and resorption of calcium deposit,24,25 and also
physiological responses such as changes of epithelial
cell permeability, free radical formation, change of cell
membrane permeability, NO formation, and variable
growth factor formation.14, 20, 26
The mechanisms of ESWT on spasticity due to central
nervous system injury are still unknown. Mariotto et
al.14 stated that ESWT can induce NO synthesis and NO
is involved in improvement of variable tendon disease.
NO is involved in neuromuscular junction formation
in the peripheral nervous system27 and in physiological
functions of the central nervous system, including
neurotransmission, and synaptic plasticity.28
Likewise, variable mechanisms have been proposed,
including acting on fibrosis of chronic hypertonic
muscles,20 decreasing spinal excitability,29 and
mechanical vibratory stimulation.29 Considering the
therapeutic effects of ESWT on bones and tendons
Manganotti and Amelio20 proposed that reduction of
spasticity could be caused by improving the stiffness of
connective tissue by directly acting on fi brosis of chronic
hypertonic muscles.
In this study, we attempted to evaluate the antispastic
mechanism of ESWT by using F waves and H-reflexes
that reflect spinal excitability. Results showed no
significant changes in F wave minimal latency, H-reflex
latency, or H-M ratio after treatment. Therefore, those
factors can be eliminated as the mechanism by which
ESWT reduces spasticity by decreasing spinal excitability.
Manganotti and Amelio20 also reported that the eff ect of
ESWT on spinal excitability can be excluded as the main
mechanism, because no change of F wave latency or
amplitude after treatment was demonstrated.
Another possible mechanism was mechanical vibratory
stimulation, which reduces excitability of motor neurons
and induces the change of F wave.29 In this study, we
can rule out this theory because no significant change
of F wave or H-reflex were detected. Considering the
clinical anti-spastic effect observed up to 4 weeks after
treatment,20 mechanical vibratory stimulation, which is
transitory and short lasting, could also be excluded as a
major eff ect.
Because the latency and amplitude of compound
muscle action potential and conduction velocity of tibial
nerve were not changed in this study, we can rule out a
significant effect of ESWT on peripheral nerves and the
eff ect of botulinum toxin A on neuromuscular blockage.
Results of this study could not reveal the exact mecha-
nism of ESWT for reducing spasticity. However, we
can rule out several proposed mechanisms such as
decreased spinal excitability, peripheral nerve injury,
and mechanical vibratory stimulation by using electro-
physiologic studies. It was previously reported that
range of motion of the joint increased after ESWT;20,21
however, we did not evaluate range of motion of the joint
in the study, and therefore the mechanisms proposed
by Maganotti and Amelio20 for reducing spasticity
mediated by improving stiffness of connective tissue

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aff ecting fi brosis of chronic hypertonic muscles were not
confi rmed in this study .
Similar to previous studies performed in stroke patients
with upper limb spasticity, an immediate therapeutic
effect of ESWT in reducing spasticity was found for
stroke patients with ankle spasticity. ESWT can reduce
spasticity in stroke patients with lower limb spasticity
and prevent complications of spasticity, such as equi-
novarus deformity. This study only measured the
immediate eff ect of ESWT, but Manganotti and Amelio20
and Yoo et al.21 reported that the therapeutic effect of
ESWT on upper limb spasticity could last at least 4 weeks,
maximally 12 weeks, and that ESWT had a therapeutic
effect on reducing spasticity for a considerable time.
There were several cases where the patient complained
of pain during treatment, but the degree of pain was not
severe (< VAS 3), and not all subjects reported pain after
treatment; other side eff ects were not found in this study.
ESWT appears to be safe and noninvasive and can reduce
fi nancial burden compared to treatment using botulinum
toxin A. ESWT can be helpful in treatment of chronic
stroke patients with spasticity.
There are several limitations in this study. First, the
mechanism of ESWT for reducing spasticity was not fully
evaluated in this study. Further studies are needed to
elucidate the mechanism of ESWT for reducing spasticity
by comparing the anti-spastic effects; for example,
stiffness of connective tissue for acute stroke patients
compared with chronic stroke patients. Second, this
study used F wave minimal latency to assess the spinal
excitability instead of F wave amplitude or F-M ratio,
which are well known and widely used. Further studies
concerning the correlation between F wave minimal
latency and spinal excitability are needed. Th ird, similar
to results from previous studies conducted for upper
limb spasticity,20,21 range of motion of the joint should
be measured. Reduced eff ect of spasticity on functional
abilities such as ambulation or activities of daily living
should be assessed. Finally, further studies concerning
the most effective level of intensity, number of ESWT
treatments, and duration of therapeutic effect, need to
be conducted in a larger number of patients.
CONCLUSION
In this study, 1 session of ESWT for chronic stroke
patients with ankle plantarfl exor spasticity produced an
immediate effect. There were no significant changes in
electrophysiologic studies such as F wave, H-reflex, or
tibial nerve conduction studies after treatment. ESWT
appears to be safe and noninvasive, and can reduce
fi nancial burden compared to treatment with botulinum
toxin A. ESWT can be helpful for treatment of stroke
patients with spasticity, prevention of complications such
as equinovarus deformity, and result in a more stable gait
pattern. Further studies in larger numbers of patients on
functional changes produced by reduced spasticity, the
most eff ective treatment protocol for ESWT, and duration
of therapeutic eff ect, are warranted.
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