Does extracorporeal shock wave therapy decrease spasticity of ankle plantar flexor muscles in patients with stroke: A randomized controlled trial

Abstract

Objective:

To evaluate the effectiveness of radial extracorporeal shock wave therapy on ankle flexor spasticity in stroke survivors and to reveal changes in the fibroelastic components of muscle.

Design:

Randomized controlled trial.

Setting:

Inpatient neuro-rehabilitation clinic of a university hospital.

Participants:

Stroke patients with ankle flexor spasticity.

Interventions:

Patients were randomized to three groups; radial extracorporeal shock wave therapy, sham, or control. Active and sham therapy were administered two sessions/week for two weeks. All patients received conventional rehabilitation.

Main measures:

The primary outcome was Modified Ashworth Scale. Secondary outcomes were the Tardieu Scale and elastic properties of plantar flexor muscles assessed by elastography (strain index). All assessments were performed before, immediately after the treatment, and four weeks later at follow-up.

Results:

Fifty-one participants were enrolled (active therapy n = 17, sham n = 17, control n = 17). Modified Ashworth scores showed a significant decrease in the active therapy group (from 2.47 ± 0.72 to 1.41 ± 0.62) compared to sham (from 2.19 ± 1.05 to 2.06 ± 1.12) and control (from 2.06 ± 0.85 to 2.00 ± 0.73) groups immediately after the treatment (P < 0.001). Tardieu results were also in concordance (P < 0.001), however this effect was not preserved at follow-up. Elastic properties of the ankle flexors were improved in all groups at both assessments after the therapy showing significant decreases in strain index (P < 0.001). However, there was no difference among the groups in terms of improvement in elastography.

Conclusion:

Radial extracorporeal shock wave therapy has short-term anti-spastic effects on ankle flexor muscles when used as an adjunct to conventional rehabilitation.

Keywords

Stroke spasticity ESWT elastography ankle

Introduction

Spasticity is an important clinical problem having negative effects on the functional improvement of stroke survivors during rehabilitation.¹ Various therapeutic interventions can be used to reduce spasticity such as physical therapy.^2–5

Extracorporeal shock wave therapy is a physical therapy modality applying high-intensity pressure waves to the body. Recently, three meta-analyses have evaluated the effects of ESWT on post-stroke spasticity.^6–8 The RCTs included in these papers were limited in number and heterogeneous in terms of both type of ESWT (radial vs focal) and site of application (upper vs lower limb muscles). Especially, the effects of radial ESWT (rESWT) on ankle plantar flexor spasticity were not well-established. Furthermore, its effects on fibro-elastic properties of the muscles in terms of intrinsic component of spasticity have not been investigated. The aim of this study was to evaluate the effectiveness of rESWT for the treatment of ankle plantar flexor muscle spasticity in stroke patients and to reveal the associated changes in fibro-elastic components of the calf muscles.

Methods

Study design and participants selection

This study was planned as a prospective, double-blind randomized controlled clinical trial. One hundred and thirty-five post-stroke in-patients with ankle plantar flexor spasticity were screened to be included in the study at the Neurorehabilitation Unit of the Department of Physical Medicine and Rehabilitation, Ankara University, Faculty of Medicine. Among the patients who met the inclusion criteria, an informed consent form was signed by those who volunteered to participate in the study.

The inclusion criteria were as follows: Post-stroke patients aged between 20–80 years, with ankle plantar flexor spasticity graded more than one according to the Modified Ashworth Scale (MAS), and who were medically stable (no uncontrolled systemic disease such as hypertension, diabetes, cardiac, hepatic or renal disease). Patients with ankle contracture, malignancy, deep venous thrombosis, local inflammation/infection at the treatment site, cardiac pacemaker, bleeding diathesis, history of botulinum toxin, phenol or alcohol injections within six months, and anti-spastic surgery of the calf muscles as well as patients using oral anti-spastic drugs were excluded.

The protocol was approved by Ankara University Faculty of Medicine Clinical Research Ethics Committee and by Turkey Pharmaceuticals and Medical Devices Agency Ministry of Health (Decision No. 19-797-15 Date: December 14, 2015) and the trial was executed in accordance with the Declaration of Helsinki and International Conference on Harmonization Good Clinical Practice Guidelines. The study was registered on Clinical Trial (ANZCTR) (Trial Id: ACTRN12616001057471).

Interventions

After the screening and evaluation visit, eligible patients were randomly allocated into three groups; rESWT, sham and control. The ESWT group received rESWT plus a conventional rehabilitation program and the sham group received sham ESWT plus conventional rehabilitation. The control group received only conventional rehabilitation. The rESWT and sham ESWT were administered 2 sessions per week for two weeks (total four sessions). The conventional rehabilitation program was administered to all patients five days a week, 2–3 hours/day. The conventional program was tailored to the patient’s needs and consisted of physical and occupational therapy. Physiotherapy was based on the Bobath technique and focused on positioning, postural control, weight shifting, facilitation techniques, range of motion and progressive resistive exercises, and balance and gait training. Occupational therapy sessions included training of upper extremity and activities of daily living. Speech and language therapy was also administered for aphasic/dysphasic patients. The ESWT was applied with Intelect Radial Pressure Wave (RPW) device (Chattanooga, UK). In rESWT group 1500 shots with a pressure of 2 bar and frequency of 10 Hz were applied with D20-S D-ACTOR^® 20 mm transmitter head.⁹ Patients in the sham group were treated with V25 V-ACTOR^® 25 mm vibration transmitter of the same device. An insulating pad was placed between the muscle and the probe. The device was switched off immediately after it was switched on and the probe was kept in equal time with the active treatment on the muscle. Thus, sham ESWT was applied without energy emission. In both groups, the shock waves were applied across the calf muscles; between the most prominent mid-point of the medial and lateral heads of the affected side of gastrocnemius muscle and the musculo-tendinous junction.

Outcome measurements

All patients were examined by the same physical medicine and rehabilitation (PMR) physician (SYA), who was blinded to the randomization and the treatment procedure. Evaluations were performed at baseline before the first ESWT treatment and immediately after the last ESWT session (week 2) and then four weeks later at follow-up (week 6).

Primary outcome measure was the Modified Ashworth Scale (MAS).¹⁰ For convenience of statistical analysis, MAS grade 1+ was graded as point 2; grades 2, 3, and 4 were respectively matched to 3, 4, and 5.

The secondary outcome measures are Tardieu Scale (Tardieu X – spasticity angle, Tardieu Y – spasticity degree),⁴ ankle range of motion (ROM) of the affected side, 6-meter timed walk test, the Modified Barthel Index (lower extremity scores),^11,12 and muscle stiffness evaluated by the strain index. The strain index was calculated by ultrasonographic elastography technique.

The measurements were performed by the same radiologist (EDA) with expertise in using the GE Healthcare (GE Ultrasound Korea, Ltd 9, Sunhwan-ro, Seongnam-si) Logiq S7 Expert ultrasound system with an ML6-15 linear transducer in Ankara University Faculty of Medicine, Department of Radiology. Measurements were performed while the patients were in prone position and the knees were in full extension and leg immobilized. First, B-Mode images then elastographic images (color maps) of the gastrocnemius muscle were taken. With the guide of B-mode image, the region of interest (ROI) in muscle was determined. The defined ROI was taken from the same site in each patient at each measurement. The strain index is rated between 0–6 (0, softest; 6, hardest) and automatically calculated on the ultrasound machine.

To avoid the inter-rater bias, all outcome measurements except elastography were done by the same PMR physician (SYA).

Randomization/Blinding

After the screening and evaluation visit, the eligible patients were randomly allocated into three groups; ESWT, sham and control. Block randomization with a size of 3 was used by a computer-generated random allocation schedule (Random Allocation Software (RAS)). Concealment was provided by closed envelopes which were numbered and opened in a sequence based on the computer generated random numbers table. The physician performing the clinical evaluations, the radiologist and the patients in sham and ESWT groups were blinded to the treatment allocation.

Statistical analysis

For convenience of statistical analysis, MAS 1+ was substituted by 2; then grades 2, 3, and 4 were substituted by 3, 4, and 5, respectively. The primary outcome variable of this study was the ΔMAS (difference between time 1 and time 2). The total sample of 48 subjects achieves a power of 80.1% using the Kruskal-Wallis Test with a target significance level of 0.05 and an actual significance level of 0.04. The null and alternative hypotheses are that the standard deviation of the group means is 0.0 and 0.5 for the ΔMAS, respectively. Within group standard deviation of all groups for the ΔMAS is equal to 1.0 under the assumption of alternative hypothesis. Considering that 48 subjects is needed to reach the desired power, sample size was increased 5% for probable drop-outs in each of three groups, resulting in 51 subjects in total.

Data were expressed as mean ± standard deviation or median with interquartile range for continuous variables and as proportions (percentages) for categorical variables. The Shapiro Wilk test was used to verify normal distribution of variables. Friedman Two-Way Analysis of Variance by Ranks was used for within-group comparisons and the Kruskal Wallis variance analysis was used for between-group comparisons. Dunn test was used for pairwise post hoc tests to know which time point or group differs from which others. In this way type I error was controlled. Baseline nominal variables were compared between treatment groups using the chi-square tests of independence for categorical data. A significance level of 0.05 was used.

Results

A total of 135 patients were screened for eligibility between November 2016 and December 2017. Seventy-four patients did not meet the inclusion criteria and 10 patients did not agree to participate in the study. Consequently 51 patients were randomly assigned to 3 groups: 17 patients in the rESWT group, 17 patients in the sham group, and 17 patients in the control group. Two patients discontinued the therapy. One from the control group moved to another city and another from the sham group had an appendicitis attack during treatment. Overall 49 patients completed the study. Figure 1 shows the study flowchart.

The sociodemographic and clinical features of the patients are shown in Table 1. The baseline mean Modified Ashworth Scale scores were 2.47 ± 0.72, 2.19 ± 1.04, and 2.06 ± 0.85 in the rESWT, sham and control groups, respectively. No significant difference was found between the groups with regard to the sociodemographic characteristics and clinical features at baseline except for the lower extremity scores of Modified Barthel Index that was lower in the sham group.

Table 1.

The sociodemographic and clinical features of the patients (Data were expressed as mean ± SD and median (IQR) for continuous variables and as % for categorical variables.).

	ESWT (n = 17)	sESWT (n = 16)	Control (n = 16)
Gender n (%)
Female	8 (47)	7 (44)	7(44)
Male	9 (53)	9 (56)	9(56)
Site of hemiplegia n (%)
Right	12 (71)	7 (44)	9 (56)
Left	5 (29)	9 (56)	7 (44)
Age (year)	57.5 ± 14.3	58.8 ± 10.8	60.6 ± 9.6
Time since stroke (month)	35.5 ± 70.2	28.9 ± 76.5	3.8 ± 2.8
Time since stroke (month)	3.0 (23.0)	3.0 (21.0)	3.3 (3.0)
MAS	2.5 ± 0.7	2.2 ± 1.0	2.1 ± 0.9
MAS	2.0 (1.0)	2.0 (2.0)	2.0 (0.0)
Tardieu X	17.8 ± 3.9	14.2 ± `6.9	14.5 ± 4.7
Tardieu X	17.5 (5.0)	15.0 (10.0)	13.8 (10.0)
Tardieu Y	3.2 ± 0.7	2.9 ± 0.9	2.8 ± 0.8
Tardieu Y	3.0 (1.0)	3.0 (2.0)	3.0 (1.0)
ROM	42.9 ± 13.1	38.1 ± 10.6	41.6 ± 13.6
ROM	40 (22.5)	35.0 (18.8)	42.5 (20.0)
Barthel index	31.2 ± 8.2	17.8 ± 13.4	24.4 ± 12.1
Barthel index	30.0 (15.0)	17.5 (24.0)	27.5 (15.0)
6mTW	26.5 ± 22.7	23.3 ± 11.8*	25.3 ± 17.8**
6mTW	14.0 (26.0)	23.0 (22.0)	20.0 (15.0)
US-SI	2.8 ± 0.9	3.1 ± 0.8	2.7 ± 1.1
US-SI	2.5 (1.4)	2.9 (1.1)	2.5 (0.8)

ESWT: rESWT group; sESWT: sham ESWT group; SD: standard deviation; IQR: interquartile range; MAS: modified ashworth scale; ROM: range of motion; US-SI: ultrasound strain index; 6mTW: 6-meter timed walk test.

Eight patients were able to walk.

Thirteen patients were able to walk.

The change of outcome variables by treatment for each group is presented at Table 2. In the rESWT group, there was a significant decrease in the Modified Ashworth Scale score immediately after the treatment at week 2 (P < 0.001). In the sham group, there was a significant change in the Modified Ashworth Scale score among three periods (P = 0.002), but in the multiple comparison tests, it could not be statistically determined which period caused this significance. In the control group, there was no significant decrease in the Modified Ashworth Scale scores at both assessment times (P = 0.223). In comparison among the groups, the Modified Ashworth Scale score was significantly decreased in the rESWT group immediately after the treatment (week 2) compared to the sham and control groups (P < 0.001) (Table 3).

Table 2.

Change of outcome variables by treatment in each group.

	ESWT	sESWT	Control
	Mean ± SD Median(IQR)	Mean ± SD Median(IQR)	Mean ± SD Median(IQR)
MAS
Baseline	2.5 ± 0.7*	2.2 ± 1.1	2.1 ± 0.9
Baseline	2.0 (1.0)	2.0 (2.0)	2.0 (0.0)
Week 2	1.4 ± 0.6	2.1 ± 1.1	2.0 ± 0.7
Week 2	1.0 (1.0)	2.0 (2.0)	2.0 (0.0)
Week 6	1.8 ± 0.7	1.7 ± 1.0	1.9 ± 0.8
Week 6	2.0 (1.0)	2.0 (1.0)	2.0 (1.0)
P-value	<0.001	0.002	0.223
Tardieu X
Baseline	17.8 ± 3.9**	14.2 ± 6.9	14.5 ± 4.7
Baseline	17.5 (5.0)	15.0 (10.0)	13.8 (10.0)
Week 2	12.5 ± 2.3	14.4 ± 8.5	15.2 ± 4.5
Week 2	12.5 (5.0)	15.0 (10.0)	15.0 (8.8)
Week 6	15.1 ± 6.2	12.5 ± 5.5	14.8 ± 4.3
Week 6	15.0 (10.0)	12.5 (5.0)	15.0 (10.0)
P-value	0.002	0.527	0.607
ROM
Baseline	42.9 ± 13.1***	38.1 ± 10.6	41.6 ± 13.6
Baseline	40.0 (22.5)	35.0 (18.8)	42.5 (20.0)
Week 2	47.4 ± 13.1	40.6 ± 10.6	42.2 ± 12.8
Week 2	50.0 (20.0)	37.5 (15.0)	40.0 (22.5)
Week 6	48.2 ± 12.5	39.4 ± 9.5	43.8 ± 13.8
Week 6	50.0 (20.0)	40.0 (17.5)	42.5 (28.8)
P-value	<0.001	0.078	0.042
Barthel index
Baseline	31.2 ± 8.2^###	17.8 ± 13.4^##	24.4 ± 12.1^#
Baseline	30.0 (15.0)	17.5 (24.0)	27.5 (15.0)
Week 2	34.4 ± 7.3	20.6 ± 12.9	26.6 ± 11.7
Week 2	40.0 (10.0)	20.0 (24.0)	30.0 (15.0)
Week 6	36.5 ± 6.3	25.0 ± 11.0	31.3 ± 9.6
Week 6	40.0 (8.0)	25.0 (14.0)	35.0 (13.0)
P-value	<0.001	0.001	<0.001
6mTW
Baseline	26.5 ± 22.7^§§	13.4 ± 11.8	25.3 ± 17.8^§
Baseline	14.0 (26.0)	23.0 (22.0)	20.0 (15.0)
Week 2	19.8 ± 13.5	20.9 ± 12.0	19.5 ± 11.8
Week 2	11.0 (20.0)	16.5 (20.0)	15.0 (13.0)
Week 6	17.9 ± 14.4	20.3 ± 11.5	19.5 ± 12.6
Week 6	10.0 (21.0)	17.5 (16.0)	14.0 (12.0)
P-value	<0.001	0.576	<0.001
Strain index
Baseline	2.8 ± 0.9^ϑ	3.1 ± 0.8^ϑϑ	2.7 ± 1.1^ϑϑϑ
Baseline	2.5 (1.4)	2.9 (1.1)	2.5 (0.8)
Week 2	2.0 ± 0.8	2.1 ± 0.8	2.1 ± 0.9
Week 2	2.0 (1.1)	1.8 (1.1)	2.1 (1.2)
Week 6	1.4 ± 0.6	1.9 ± 1.0	1.4 ± 0.6
Week 6	1.3 (0.5)	1.5 (1.2)	1.4 (1.1)
P-value	<0.001	<0.001	<0.001

ESWT: rESWT group; sESWT: sham ESWT group; SD: standard deviation; IQR: interquartile range; MAS: modified ashworth scale; ROM: range of motion; 6mTW: 6-meter timed walk test.

: different from week 2 for ESWT (P < 0.001).

: different from week 2 for ESWT (P = 0.003).

***

: different from week 6 for ESWT (P = 0.018).

: different from both week 2 and week 6 for ESWT (P = 0.005 and P < 0.001, respectively).

ϑϑ

: different from both week 2 and week 6 for sESWT (P = 0.006 and P < 0.001, respectively).

ϑϑϑ

: different from week 6 for control (P < 0.001).

: different from week 6 for control (P = 0.002).

: different from week 6 for sESWT (P = 0.024).

###

: different from week 6 for ESWT (P = 0.018).

: different from both week 2 and week 6 for control (P = 0.003 and P = 0.001, respectively).

§§

: different from both week 2 and week 6 for control (P = 0.001 and P < 0.001, respectively).

Table 3.

Inter-group comparison of outcome variables by treatment.

	ESWT median (IQR) 95% CI	sESWT median (IQR) 95% CI	Control median (IQR) 95% CI	P
MAS
Week 2-baseline	–1.0 (0.0)*	0.0 (0.0)	0.0 (0.0)	<0.001
Week 2-baseline	(–1.0, –1.0)	(0.0, 0.0)	(0.0, 0.0)	<0.001
Week 6-baseline	0.0 (1.0)	0.0 (1.0)	0.0 (0.0)	0.063
Week 6-baseline	(–0.5, 0.5)	(–0.4, 0.4)	(0.0, 0.0)	0.063
Tardieu X
Week 2-baseline	–5.0 (2.5)*	0.0 (4.4)	0.0 (3.8)	<0.001
Week 2-baseline	(–6.2, –3.8)	(–1.1, 1.1)	(0.0, 0.0)	<0.001
Week 6-baseline	–5.0 (7.5)	0.0 (9.4)	0.0 (5.0)	0.345
Week 6-baseline	(–7.5, –2.5)	(–3.2, 3.2)	(–2.1, 2.1)	0.345
ROM
Week 2-baseline	5.0 (10.0)	0.0 (5.0)	0.0 (5.0)	0.118
Week 2-baseline	(0.0, 10.0)	(–2.1, 2.1)	(–2.1, 2.1)	0.118
Week 6-baseline	5.0 (10.0)	0.0 (5.0)	2.5 (5.0)	0.275
Week 6-baseline	(0.0, 10.0)	(–2.1, 2.1)	(0.4, 4.6)	0.275
Strain index
Week 2-baseline	–0.9 (1.1)	–0.9 (0.8)	–0.6 (1.1)	0.247
Week 2-baseline	(–1.5, –0.5)	(–1.1, –0.6)	(–0.9, –0.2)	0.247
Week 6-baseline	–1.2 (1.3)	–1.3 (0.9)	–1.4 (1.0)	0.999
Week 6-baseline	(–1.8, –0.7)	(–1.6, –1.0)	(–1.6, –1.2)	0.999
Barthel index
Week 2-baseline	0.0 (5.0)	0.0 (5.0)	0.0 (5.0)	0.669
Week 2-baseline	(–2.5, 2.5)	(–2.1, 2.1)	(–2.1, 2.1)	0.669
Week 6-baseline	5.0 (10.0)	5.0 (10.0)	5.0 (8.8)	0.835
Week 6-baseline	(0.0, 10.0)	(0.7, 9.3)	(2.9, 7.1)	0.835

ESWT: rESWT group; sESWT: sham ESWT group.

: different from both sESWT and Control P < 0.001, respectively.

The Tardieu X score showed a significant decrease from baseline to immediately after treatment at week 2 in the rESWT group (P = 0.003). In other groups Tardieu X score did not show significant change (Table 2). In comparison among the groups, the Tardieu X score was significantly decreased in the rESWT group at week 2 compared to the sham and the control groups (P < 0.001) (Table 3).

In the rESWT group, ROM of the ankle joint showed a significant increase from baseline to week 6 (P = 0.018) (Table 2). When compared in terms of an increase in ROM, no significant difference was found among the three groups (Table 3).

The scores of the lower extremity functioning of the Modified Barthel Index increased significantly in all groups at week 6 (P < 0.001 for all groups) compared to baseline (Table 2). However, there was no difference among the groups in terms of change from baseline to week 2 and week 6 (Table 3).

In the rESWT group 17 of 17 patients (100.0%), in the sham group 8 of 16 patients (50%) and in the control group 13 out 16 patients (81.3%) were able to walk at baseline. Therefore, the 6-meter timed walk test could be performed in 38 patients who were able to walk initially. In the rESWT and control groups, walking times were significantly decreased at week 2 and week 6 compared to the baseline whereas there was no significant change in the sham group (Table 2). When compared in terms of the change in 6-meter walking time no difference was found among the three groups (P > 0.05).

The ultrasound strain index decreased significantly in all groups at week 2 and week 6 compared to baseline (Table 2). There was no significant difference among the three groups in terms of change from baseline to weeks 2 and 6 immediately after treatment and at the fourth week (Table 3).

No significant adverse effect was observed in any patients throughout the study. During the first rESWT session, two patients had mild pain without a need for analgesia. Otherwise no other adverse effects were observed.

Discussion

In this randomized controlled study, it has been found that the rESWT is effective in decreasing plantar flexor spasticity in stroke patients immediately after the treatment. Although several studies have described the effects of ESWT on stroke-induced spasticity, there are only six clinical trials that evaluated the effects of rESWT on post-stroke lower extremity spasticity.^8,13 Two single group studies with repeated measures design found that spasticity scores were improved after a single session of rESWT.^14,15 Another study with the same design reported decreased thickness, spasticity, and pain as well as increased gait ability after three sessions of rESWT.¹⁶ Only three studies had a randomized controlled design. The first study, including eight patients, found no superiority of rESWT regarding spasticity and ROM compared with usual treatment after 3 sessions of therapy each week.¹⁷ In the second study, the effects of radial and focused ESWT were compared on 32 patients with spastic equinus and both groups yielded similar improvements in the Modified Ashworth Scale and Tardieu scale whereas rESWT was found to be superior in terms of improvements in ROM.¹⁸ The third study was a sham controlled one-session trial including 18 patients with chronic stroke. They found no difference between the groups in terms of Modified Ashworth Scale and ROM however ultrasonographic measures (muscle fascicle length, Achilles tendon length, muscle thickness and pennation angle) were significantly improved in rESWT group at the first and fourth weeks.¹⁹

In our study, four sessions of rESWT were administered and anti-spastic effect was observed immediately after the therapy. This effect was not preserved at follow-up. There are some studies reporting a long-term effect (up to 12–16 weeks) of ESWT on post-stroke upper limb spasticity.^20,21 On the contrary there are some studies which ESWT has been reported to have lost its effect in the following periods.^22,23 The difference in shock wave energy densities, number of sessions, target area size, and stroke duration in the studies may cause differences in treatment effectiveness in the medium and long term. In 2013, Moon examined the effect of focal ESWT on 30 stroke patients, applying 1500 pulses of ESWT at a dose of 0.089 mj/mm² for three sessions to the lower extremity plantar flexors, and the spasticity decreased significantly after ESWT but not at four weeks.¹⁴ As seen in these studies, a standard dose, duration and number of sessions of both focal and radial ESWT for anti-spastic therapy have not yet been fully established.⁸ Further studies are needed to determine the optimal dose and number of sessions to achieve a prolonged effect.

The mechanism of the effect of ESWT on spasticity has not yet been clearly determined in the studies conducted so far, and various mechanisms have been proposed. The lack of electrophysiological changes in studies using electrophysiological examinations among the evaluation parameters, largely excluded the theory of the reduction of spinal excitability as a possible mechanism for anti-spasticity and the theory of alpha-motor neuron inhibition through the golgi tendon organ.^1,14,21,24 As a mechanism, it is often emphasized that shock waves provide a direct effect on the rheological components and fibrosis of chronic hypertonic muscles.^1,18,21 Shock wave pressure may lead to a reduction in intrinsic stiffness of the spastic muscle by breaking the functional link between actin and myosin.²⁴ Among the elements that make up the spasticity, it is thought that the reflex mediated increase in muscle tone reaches its maximum within one to three months after stroke, then changes in intrinsic muscle structure such as atrophy, fibrosis and changes in elastic properties and stiffness, shortening of supportive soft tissues are predominantly responsible for spasticity.²⁵ Therefore, if the time since stroke is long, long-term and more frequent shock wave therapy sessions may be required as structural changes contribute more to spasticity.^23,26 In order to clarify this, further studies exploring the treatment efficacy in different periods after stroke would be helpful.

The results of ROM are similar comparing our study with studies that evaluate the changes in ROM after ESWT. ^14,21,26,27 The reduction in intrinsic stiffness and increase in extensibility with direct effect of ESWT on muscle and soft tissues may have improved the range of passive ROM.¹⁸ Increase in ROM may support the hypothesis that ESWT provides a reduction in stiffness with a direct effect, which is the most emphasized theory of anti-spasticity. Marinelli did not find any change in motor staging score in both ESWT and sham groups after single dose ESWT. However, unlike our study, a conventional rehabilitation program was not given to patients in that study.²⁴ In the current study, all three groups received the conventional rehabilitation program and consequently the increase in lower extremity scores of Modified Barthel Index which was not significant in the short term became meaningful at week 6. Marinelli et al. found no change in walking time after ESWT and explaining that it was because physiotherapy was not performed in their study. They stated that physiotherapy should be in the rehabilitation program when the target was development of functionality, such as improvement in walking time.²⁴ ESWT has been shown to provide an increase in walking speeds in patients with cerebral palsy.²⁸ In our study, it did not affect walking speed, probably because the patients who were unable to walk at baseline were dropped out and analysis has been performed with an insufficient number of patients.

In a study comparing botulinum toxin type A injection alone and botulinum toxin type A injection with ESWT in cerebral palsy, it was found that both Modified Ashworth Scale and elastography showed a significant improvement in the combined treatment group, compared to the botulinum toxin type A injection group. It has been interpreted that in addition to the neural effect of botulinum toxin type A on the neuromuscular junction, the effect of ESWT on the rheological components of the muscle provides more significant improvement both clinically and elastographically.²⁹ In our study, the elastic components of the muscle improved in all three groups. Although the reduction in elastography strain index, which examined the elastic properties and intrinsic structure of the muscle was achieved in all groups, a significant reduction in the clinical measurements of spasticity was achieved only in the ESWT group. It can be interpreted that the conventional rehabilitation methods could have provided this reduction in muscle stiffness.

In the current study, during the first ESWT session, two patients reported mild pain without the need for any treatment and no other adverse effects were observed. Pain is the most commonly reported side effect of ESWT.^1,12,16 Petechia in the application area¹⁶ and mild weakness²⁶ are the other adverse effects reported.

To the best of our knowledge, our study is the second randomized sham-controlled study that has evaluated the effect of rESWT on lower extremity post-stroke plantar flexor spasticity. In the current study, spasticity was evaluated comprehensively by both the Modified Ashworth Scale and Tardieu Scale, where Modified Ashworth Scale graded spasticity level and Tardieu assessed the velocity-dependent aspect of spasticity. Another strength of this study was that the intrinsic and elastic structures of spastic muscles were evaluated with elastography to document the intrinsic non-reflex component of muscle over-activity. There are some limitations of this study. First, ESWT was applied only in a single protocol. It is not known whether increasing the number of sessions or treatment intensity would affect the outcome as current evidence is insufficient in this respect. Another limitation of the study was the variation of time since stroke in our sample. Considering the hypothesis that the effectiveness of ESWT might vary according to the post-stroke phase (acute/post-acute/long-term), new studies controlling the factor of time since stroke should be planned. Finally, the strain index measurements used in the tension elastography technique were performed from the same region of the muscle with a heterogeneous structure. However, this is considered as the standard protocol and it would have been difficult and time-consuming to calculate measurements taken from different regions of the muscle.

Conclusion

rESWT can be an effective treatment modality in decreasing post-stroke ankle plantar flexor spasticity. Its effect seems to appear immediately after the therapy and not last for long-term. It is safe and well-tolerated, and may be used for spasticity treatment as a part of the rehabilitation program. However, further studies are needed to determine the most effective ESWT protocol for the treatment of post-stroke spasticity in terms of dose, duration, number of sessions as well the best administration phase (subacute or chronic). The strain index measurement of elastography can provide detection of any clinically undetectable decrease in spasticity and therefore may be a useful clinical assessment method for the intrinsic component of muscle over-activity.

Clinical messages

rESWT gives only a short-term reduction for post-stroke ankle plantar flexor spasticity.

It appears to be a safe and well-tolerated treatment modality.

Footnotes

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Sehim Kutlay

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