Spasticity is one of the most common complications after stroke. With
the gradual intensification of spasticity, stroke patients will have a
series of problems such as joint ankylosis and movement restriction,
which affect the daily activities and increase the burden on patients'
families, medical staff and society. There are many ways to treat
post-stroke spasticity (There is NOTHING TO CURE SPASTICITY! Survivors want cures, not treatments that don't work!)before, including physical therapy and exercise
therapy, drug therapy, surgery and so on, but not satisfied because of a
few shortcomings. In recent years, many researchers have applied
extracorporeal shock wave therapy (ESWT) for the treatment of
post-stroke spasm and achieved good clinical effect, because it is
non-invasive, safe, easy to operate, low cost and other advantages
compared with other treatment methods. This article reviews the research
progress and existing problems of ESWT in the treatment of post-stroke
spasticity.
1. Introduction
Stroke, also known as “stroke” and “cerebrovascular
accident” (CVA), is an acute cerebrovascular disease, which is a group
of diseases caused by the sudden rupture of blood vessels in the brain
or the blockage of blood vessels that prevents blood from flowing,
causing brain tissue damage (1).
Stroke is the third leading cause of human death, and its incidence is
second only to tumor and ischemic heart disease. Stroke is also one of
the leading causes of long-term disability in humans (2),
which survivors are often accompanied by varying degrees of dyskinesia,
sensory impairment, cognitive impairment, speech disorders and
swallowing disorders and other sequelae (3, 4).
Especially noticed spasticity is one of the most common
complications in stroke patients and usually occurs during the recovery
period of stroke, after 3 months following stroke (5).
About 4–42.6% of stroke patients experience spasticity after stroke
onset, and 2–13% of these patients may cause severe disability (6, 7).
Early in stroke, the presence of a spastic state means that the
patient's muscle tone improves and motor function recovers; however, as
the spastic state gradually increases, the patient may experience
problems such as pain, pressure sores, muscle weakness, joint ankylosis,
and limitation of movement (8–10),
leading to difficulties in daily activities and increasing the burden
on the patient's family, medical staff, and society. The cost of medical
care increases nearly a four-fold in patients with stroke in the
presence of spasticity compared with patients without spasticity (11).
In 1980, Lance first defined spasticity as “a movement
disorder characterized by velocity-dependent hypertonia due to stretch
hyperreflexia, and mostly associated with tendon hyperreflexia, as a
form of upper motor neuron syndrome” (12),
which is widely used and has greatly facilitated advances in the
research and management of spasticity. Young and so on combined possible
mechanisms of spasticity after stroke to define spasticity as “a
movement disorder characterized by velocity-dependent tonic stretch
hyperreflexia due to abnormal processing of primary inputs within the
spinal cord” (13).
Other definitions are descriptive, such as “hypertonia, which is
characterized by resistance to externally imposed movements that
increases with the rate of stretching and changes with the direction of
joint movement,” “sensorimotor dysregulation caused by lesions of upper
motor neurons, which manifests as intermittent or persistent involuntary
activation of muscles” and “spasticity is involuntary muscle
hyperactivity that occurs with central paralysis” (14–16).
Due to the complexity and diversity of symptoms of post-stroke
spasticity, there is no uniform definition of spasticity in the
international academic so far. Regarding the definition of spasticity
after stroke, we more recommend Lance's description of the definition of
spasticity. First, spasticity must be one of the manifestations of
upper motor neuron syndrome. The increased muscle tension without upper
motor neuron system damage cannot be described as “spasticity,” which is
one of the mistakes that many people are prone to make. Second, the
spasticity is a velocity-dependent hyperreflexia of stretch reflex,
which is the theoretical basis for our correct evaluation of
spasticity—rapid stretch.
Moderate spasm in stroke patients can reduce the
occurrence of complications, such as prevention of osteoporosis,
prevention of venous thrombosis, a certain degree of muscle tension can
also help maintain muscle capacity, slow down the degree and speed of
muscle atrophy, and spasm of knee extensor muscle groups can assist
patients to achieve standing and transfer (17, 18).
However, severe spasticity may lead to muscle contracture, abnormal
posture, pain, joint deformity, tissue contracture, etc., causing
stiffness and discomfort, affecting daily care, washing, dressing,
perineal hygiene and normal sitting posture, resulting in limited
activities of daily living and decreased quality of life (19–21). Therefore, it is necessary and important to treat severe spasticity for stroke patients in rehabilitation.
There are currently many treatments for spasticity after
stroke, including physical therapy and exercise therapy, drug therapy,
and surgical treatment (22).
Among them, physical therapy has the advantages of safety, cheapness,
non-invasiveness, and effectiveness, and is one of the most commonly
used methods for the treatment of spasticity, and is generally used as
an adjunct to other treatments, including vibration therapy,
transcutaneous electrical nerve stimulation, neuromuscular electrical
stimulation, transcranial direct current stimulation, repetitive
transcranial magnetic stimulation, biofeedback therapy, caloric
stimulation therapy, orthosis use, good limb position placement,
proprioceptive stimulation, stretching therapy, and movement therapy (23–26).
Drug therapy is the main way to treat spasm, of which oral drugs used
to treat systemic spasm affecting multiple sites include baclofen,
diazepam, dantrolene and tizanidine; while for the treatment of small
range spasm, local injection of botulinum toxin or ethanol and phenol
block are mostly used (27–30).
Because of the complexity of surgical operation and the limitation of
therapeutic effect, surgical treatment is rarely used in clinical
practice. It is mainly used for relieving severe spasm, correcting
deformity and contracture, and preventing and treating complications
when drug therapy and other interventions cannot effectively relieve
spasm and the patient's activities of daily living and functional status
are seriously affected. In fact, due to the side effects of drug
therapy, invasiveness of local therapy, and economic burden, spasm
sometimes cannot be effectively controlled even with many treatment
modalities, so it is necessary to find new, economical, non-invasive,
and effective treatment modalities to relieve spasm and improve the
quality of life of patients. In recent years, many scholars have used
extracorporeal shock wave therapy (ESWT) to treat spasticity after
stroke and achieved good clinical results (31, 32).
Because it has the advantages of non-invasive, safe, easy operation,
and low cost compared with other treatment methods, more and more
scholars have conducted in-depth studies. This article reviews the
research progress of ESWT in the treatment of upper limb spasticity
after stroke, in order to provide the basis for ESWT in the treatment of
post-stroke upper limb spasticity.
2. Mechanism of spasticity after stroke
Regarding the occurrence of spasticity, at present, the
mechanism of spasticity after stroke was divided into two categories:
hypertonia due to stretch reflex, that is, reflexively mediated
mechanism; hypertonia due to soft tissue changes, that is,
non-reflexively mediated mechanism (33).
With regard to the reflex mediated mechanism of
spasticity, neurophysiology currently believes that spasticity is the
result of enhanced stretch reflex (12).
In stroke patients with spastic hemiplegia, on the one hand, motor
cortex and its corticospinal descending tract are injured, which will
immediately lead to hemiplegia after stroke, mainly including upper and
lower limb muscles on the affected side, and trunk muscles are also
affected to some extent (34).
On the other hand, due to the damage of the cortical bulbar pathway
accompanied by the damage of the motor cortex or the corticospinal
descending tract, the supraspinal inhibition was lost, and bulbar spinal
cord overexcitation occurred (35).
This is mainly a de-inhibition phenomenon, or de-masking effect.
Reticulocyte hyperexcitability provides unopposed excitatory descending
inputs to spinal extension reflex circuits, resulting in increased
excitability of spinal motor neurons (36).
This adaptive change can explain most of the clinical manifestations of
spasticity, such as hyperreflexia, velocity dependent resistance to
stretch, excessive muscle activity, or spontaneous discharge of motor
units (37–39).
In addition to hyperreflexia, spasticity after stroke is
also associated with changes in the mechanical properties of muscles,
tendons, joints and other tissues, that is, non-reflex factor-mediated
muscle spasm mechanism (33).
Spasticity after stroke is mostly attributed to brain injury itself and
less attention is paid to muscle tissue structure, metabolism and
function. Muscle function and structure are altered following spasm,
mainly by changes in muscle fiber size and fiber type distribution;
extracellular matrix proliferation as measured morphologically and
biochemically; and increased stiffness of spastic muscle cells (40–42). Spastic muscle has poorer mechanical properties of extracellular material compared to normal muscle (43, 44).
In conclusion, the changes of muscle fiber classification, proportion
and length of spastic muscles after stroke will promote the changes of
physiological function and biomechanical characteristics of the affected
skeletal muscles, and these changes further aggravate the spastic
state.
3. Introduction to ESWT
ESWT is a series of single-pulse high-energy mechanical
waves, characterized by high pressure (100 MPa), rapid pressure increase
(< 10 ns), and short action cycle (10 μs), which can propagate in
three-dimensional space, and the propagation speed accelerates with the
increase of pressure (45).
It can be divided into two types: focused extracorporeal shock wave
therapy (fESWT) and radial extracorporeal shock wave therapy (rESWT) (46).
Focused shock wave concentrates acoustic wave energy on a certain focal
zone on target tissue, with very high energy at focal zone. According
to different pressure generating devices, it can be divided into
electrohydraulic extracorporeal shock wave, electromagnetic
extracorporeal shock wave and piezoelectric extracorporeal shock wave,
with penetration depth up to 12 cm. X-ray or ultrasound-guided precise
localization of treatment site is often required during treatment to
avoid damage to surrounding tissues (47, 48).
Dissipative shock waves transmit acoustic energy into the body in a
radially attenuated manner through contact with the skin, and there is
only one pneumatic ballistic type, which requires the coupling agent to
be applied to the surface of the treatment site during treatment, which
has a much shallower penetration depth of about 3.5 cm compared with
focused extracorporeal shock waves, and has low energy and slow
transmission speed. The treatment head can move flexibly during the
operation, has a larger therapeutic range, does not require the use of
other equipment for positioning, is safer, less expensive, and is more
suitable for the treatment of soft tissues such as muscles and ligaments
(49, 50).
At present, extracorporeal shock wave therapy is widely
used in the treatment of spasticity after stroke, doctors will select
focused or dissipated extracorporeal shock waves according to the actual
situation of patients themselves. Therefore, the adverse reactions of
patients during the treatment period were few and mild, well tolerated,
and the treatment could be repeated (51, 52).
4. Mechanisms of ESWT in treating spasticity after stroke
Currently, with the depth study on the mechanism of
extracorporeal shock wave therapy for spasticity after stroke, it
believed that there may be the following mechanisms.
4.1. ESWT induced nitric oxide synthesis
Nitric oxide (NO) is a non-classical neurotransmitter
that acts as a messenger molecule in humans and is involved in
neuromuscular junction formation as well as important physiological
functions of the central nervous system, including the transmission,
storage, and synapse-related functions of information in the nervous
system (53, 54).
Some scholars have proposed that extracorporeal shock waves can induce
NO production through enzymatic and non-enzymatic pathways, reduce
acetylcholine at the neuromuscular junction, and thus relieve muscle
spasm (55, 56).
Gotte et al. found that nitrite concentrations increased with
increasing energy levels after shock waves applied to mixed solutions
containing L-arginine and H2O2, providing a rationale for non-enzymatic pathways promoting NO production (57).
Ciampa et al. found that shock waves increased the activity of nitric
oxide synthase in the cytoplasm of rat glial cells C6 when shock waves
were applied, thereby accelerating the production of NO. It also
increases neuronal nitric oxide (nNOS) activity and NO production
induced by a mixture of lipopolysaccharides (LPS), tumor necrosis
factor-α (TNF-α), and interferon gamma (IFN-γ) (58).
It has also been suggested that shock waves may temporarily reduce
acetylcholine receptors at the neuromuscular junction, thereby affecting
neuromuscular junction function and thereby reducing spasticity (56, 59).
Shock waves can regulate NO synthesis and affect enzyme activity, so it
is speculated that ESWT alleviates limb spasticity after stroke may be
related to the regulation of NO synthesis.
4.2. Extracorporeal shock waves reduce motor neuron excitability
Some scholars believe that due to cerebral cortex damage
after stroke, upper motor neurons lose their inhibitory effect on lower
motor neurons, resulting in abnormal excitation of motor neurons (60, 61).
Extracorporeal shock waves may reduce the excitability of motor neurons
by vibratory stimulation of tendons, thereby achieving the goal of
reducing tension. Leone et al. performed shock wave therapy on the
Achilles tendon of hemiplegic patients to assess motor neuron
excitability innervating the muscle by H-reflex and showed a decrease in
H-reflex amplitude, suggesting that improving the functional status of
the contractured Achilles tendon by continuous or intermittent
compression of the Achilles tendon site may be related to regulating
motor neuron excitability, but its neurophysiological effects and
clinical effects could not be sustained (62).
Daliri et al. observed the changes in the ratio of the maximum
amplitude of H wave to the maximum amplitude of M wave (Hmax/Mmax value)
after ESWT for flexor carpi spasm after stroke and found that the
Hmax/Mmax value decreased, indicating that extracorporeal shock waves
could improve the excitability of α motor neurons and thus relieve limb
spasm (63).
4.3. ESWT modulates the process of nerve conduction
The occurrence of limb spasticity after stroke is not
only related to the high excitability of motor neurons, but also related
to the innervation and nerve conduction of muscles. Extracorporeal
shock waves can produce nerve block at free nerve endings, neuromuscular
junctions and other parts, thus regulating the conduction of nerves (64, 65).
Ohtofi et al. used shock waves to act on rats, and all epidermal
sensory nerve fibers degenerated within 1 week, and epidermal nerves
regenerated after 2 weeks (66).
Kenmoku et al. applied an extracorporeal shock wave to the right calf
muscle of rabbits and found that there was degeneration of acetylcholine
receptors in the muscle after shock wave application, causing transient
nerve conduction dysfunction at the neuromuscular junction, suggesting
that ESWT may cause transient dysfunction of nerve conduction, which in
turn affects the functional status of the muscle, but the number of
receptors that were reduced at the neuromuscular junction by shock wave
application would recover at an extremely rapid rate, which may be the
reason why shock wave treatment of spasticity is generally of short
duration (67).
4.4. Effect of extracorporeal shock waves on muscle and soft tissue
Extracorporeal shock waves, acting on human tissues, may
produce different physical stress effects in the area of action through
the human medium, namely tensile stress and shear force, thereby
causing tissue release, improving the microcirculation of muscles and
thus relieving the state of muscle spasm in patients (68–70).
A meta-analysis showed that ESWT improves passive joint mobility and
muscle properties such as stiffness, tension, and elasticity, which are
thought to be related to the rheological properties of shock waves on
spastic muscles (71).
Kim et al. found that after 2 weeks of ESWT, the range of motion
significantly increased, and supraspinatus muscle strength, thickness,
tension and stiffness were effectively restored (72).
Lee et al. showed that ESWT helps revascularization by applying ESWT to
lesions and reduces pain and improves function by stimulating or
reactivating the healing process of connective tissue, including tendons
and bones (73).
We believe that the mechanism of extracorporeal shock
wave in treating spasticity after stroke is not single, but the result
of multiple mechanisms. For different patients, a certain mechanism may
be the main one but this needs further in-depth study.
5. Clinical study of ESWT in the treatment of upper limb spasticity after stroke
Most upper limb spasms after stroke are mainly flexor
spasms, which seriously affect rehabilitation and hinder the improve of
motor function. Severe spasms may lead to shoulder pain, shoulder hand
syndrome, etc. In 2005, Manganotti et al. applied extracorporeal shock
wave to patients with spastic stroke for the first time, and observed
the effect of ESWT on upper limb dystonia in patients with stroke. They
selected 20 stroke patients with hypermyotonia of the upper limbs, and
gave 1,500 pulse shocks to the belly of the forearm flexor muscle and
3,200 pulse shocks to the hand interosseous muscle. The energy density
was 0.030 mJ/mm2. The results showed that the muscular
tension of flexor carpi and flexor digitorum could be effectively
reduced immediately after ESWT compared with that before treatment.
Among them, the flexor muscle tension of the finger was significantly
improved 1 week, 4 weeks and 12 weeks after treatment compared with that
before treatment. The flexor carpi muscle tension was significantly
improved after 1 and 4 weeks of treatment compared with that before
treatment, while it was not significantly improved after 12 weeks. In
addition, the study measured the motor nerve conduction velocity and F
wave response of the abductor digiti minimus muscle endings, and
observed the shock wave stimulation of the ulnar nerve. The results
showed that there was no indication of denervation changes such as
potential changes, which failed to explain its mechanism. This study
shows that ESWT can significantly reduce upper limb muscle spasm in
stroke patients, especially for finger flexor muscle tension, and can
maintain the effect for 12 weeks. During the study, patients had not
reported any side effects related to extracorporeal shock waves (74).
Kim et al. treated 57 stroke patients with subscapularis spasm with
five times of divergent extracorporeal shock wave therapy for 2 weeks to
observe whether this method is equally effective for subscapularis
spasm. The researchers were followed up for 6 weeks before and after
each shock wave treatment, evaluated once a week, and evaluated 11 times
in total. The results confirmed that the rESWT could relieve the
subscapular muscle spasm, relieve shoulder pain, and improve shoulder
joint range of motion in patients with stroke. There is a significant
difference between the evaluation indexes 4 weeks after treatment and
those before treatment, and there is no significant difference between
the indexes 6 weeks after treatment, but the overall trend is still
improved compared with those before treatment (75).
In recent years, more and more clinical research showed
that ESWT can reduce the upper limb flexor muscle tension of stroke
patients and effectively improve muscle spasm (76–78).
Troncati et al. observed the ESWT of 12 hemiplegic patients with upper
limb spasticity. The energy density of the abdominals of forearm flexors
was 0.105 mJ/mm2 for 1,600 pulses, and the energy density of hand interosseous muscles was 0.08 mJ/mm2
for 800 pulses. The results showed that the muscular tension of rotator
cuff, elbow flexor, wrist flexor and finger flexor decreased after
treatment. After 3 and 6 months of treatment, the muscular tension of
rotator cuff, flexor carpi and flexor digitorum decreased compared with
that before treatment, while the muscular tension of elbow flexor did
not change significantly compared with that before treatment. The
passive range of motion of upper limb joints was significantly improved
after treatment, 3 months after treatment and 6 months after treatment.
It is believed that shock wave therapy has a definite effect on upper
limb motor function, and can significantly improve upper limb motor
function, which can last for 6 months. This study shows that ESWT has a
long-term effect on upper limb spasm in stroke patients (79).
Li et al., in order to further observe the effective time of ESWT in
relieving spasticity, performed rESWT treatment on the antagonist and
agonist muscles of the upper limb elbow in stroke patients. The results
showed that rESWT could improve spasticity and pain by acting on
spasmodic antagonists or agonists. The therapeutic effect lasted at
least 4 weeks, but it could not improve the motor function of upper
limbs (80).
Park et al. randomly divided 30 stroke patients into the treatment
group and the control group. MyotonPrO muscle detector was used to
detect the upper limb muscle tension of stroke patients after ESWT
treatment. The results showed that the mechanical indexes of flexor
carpi ulnaris, flexor carpi radialis and flexor digitorum in the
treatment group were significantly higher than those in the control
group, suggesting that ESWT can effectively relieve the upper limb
flexor spasm (81).
Some scholars focus on muscle spasms of small joints of
upper limbs such as wrist joint, metacarpophalangeal joint, etc.
Gjerakaroska Savevska et al. reported that a 42 year old ischemic stroke
patient was treated with ESWT for his right hand spasm. After six times
of rESW treatment, the efficacy was evaluated according to the modified
Ashworth scale (MAS) and disability rating scale (DAS) scores before
treatment, after the sixth treatment, and 1 and 3 months after the end
of treatment respectively. The results showed that ESW could improve the
spasticity of wrist and finger flexors after stroke, and the effect was
continuous (82).
Daliri et al. observed 15 patients with wrist flexor spasm after stroke
one time of comfort treatment and one time of routine ESWT 1 week
later, and recorded the changes of motor function at each stage in the
MAS score, Hmax/Mmax value and Brunstrom evaluation method. The results
showed that the MAS scores and Hmax/Mmax values after conventional ESWT
treatment were improved compared with those after placebo treatment, but
no significant changes in motor function were observed in each stage of
Brunstrom assessment. It shows that single ESWT treatment can relieve
wrist flexor spasm after stroke, but has no significant improvement in
motor function (63).
To sum up, ESWT treatment can better relieve upper limb
spasticity after stroke, and last the effect for a long time. ESWT
treatment is effective not only for typical flexor spasms, but also for
agonists and antagonists. At present, ESWT is used in the treatment of
upper limb spasticity after stroke, and the treatment intensity mostly
is selected low energy as the treatment intensity. Although there are
two types of shock wave and the treatment methods include fESWT and
rESWT. There is no significant difference have shown in the therapeutic
effect between them these two extracorporeal shock waves.
6. Current problems
The current clinical research shows that the main adverse
reaction of ESWT in the treatment of muscle spasticity in stroke
patients is pain and ecchymosis in the local part of the action site,
but these can be disappeared in a short time (83–85).
As the known literature has not been followed up for a long time, there
may also be long-term side effects, but they have not been found yet.
In addition, there is no unified reference standard for the treatment
parameters, site, case selection, evaluation scale selection, etc. of
shock wave treatment of spastic state. Most of the existing clinical
studies are based on the experience of clinicians, lacking objectivity.
The clinical treatment scheme of shock wave needs further exploration.
6.1. Treatment site and treatment parameters
Yoon et al. compared the efficacy of extracorporeal shock
wave in the treatment of limb spasticity in different parts of stroke
patients. MAS score and modified Tardieu scale (MTS) score were the main
evaluation indicators. The results showed that the effect of
extracorporeal shock wave on muscle abdomen or the junction between
muscle abdomen and tendon was better (86).
Our recommended treatment sites are to include the muscle belly, the
tendon symphysis, and the tendon, which is the whole muscle portion of
the target muscle. Troncati et al. showed that the MAS scores of wrist
flexor, finger flexor and shoulder external rotator muscles decreased
after 3 and 6 months of treatment, but there was no significant change
in elbow flexor muscle. It was believed that the lack of sample size
might be due to factors such as different muscle locations, insufficient
shock wave dose and intensity. On the other hand, in clinical research,
the treatment time and follow-up time are inconsistent, so it is
difficult to determine the best treatment interval of EWST (79).
At present, there is no uniform standard for the therapeutic parameters
of ESWT treatment for spasticity, including the intensity, frequency,
number of pulse, duration of session, which needs more in-depth clinical
research.
6.2. Case selection
A meta-analysis by Mihai et al. (87)
shows that ESWT has long-term clinical efficacy in relieving lower limb
spasticity, reducing pain intensity and increasing range of activity in
stroke patients, but Bae et al. found that EWST has immediate efficacy (88).
It may be that the inclusion criteria of Bae et al. include patients
with mild spasticity, which is not enough to achieve lasting effects.
Another reason may be that the patient has a long course of disease,
muscle spasm lasts for a long time, and periarticular tissue sclerosis
lasts for a long time. Only repeated shock wave treatment can alleviate
the stiffness of these connective tissues. We suggest that the criteria
for inclusion should be more strictly specified in future studies to
make the research results referential and to exclude false results
caused by non-standard inclusion criteria.
6.3. Selection of evaluation scale
It is a problem worthy of discussion to evaluate the
curative effect of muscle spasm with a high credit rating scale. At
present, MAS has a high reliability (89, 90)
in the clinical evaluation scale of muscle spasm, but MAS does not take
into account the speed dependent components of muscle spasm and the
degree of muscle flexion and extension when resistance occurs. According
to the definition of Lance spasticity (12),
MAS cannot fully assess the degree of spasticity. MTS reflects the
speed dependence of spasticity by comparing the resistance of muscles
during passive stretching at slow speed and fast speed, so it is
considered to be more suitable for Lance spasticity assessment than MAS (91, 92).
On the other hand, the MAS score did not include clinical symptoms such
as pain, convulsions and effects on function, which are closely related
to muscle spasm. On the contrary, clinical symptoms such as twitching,
pain and decreased ability of daily living may occur with muscle spasm.
Therefore, other clinical scales such as visual analysis scale (VAS),
modified Barthel index and Fugl Meyer evaluation scale (93–95) should be used to observe the therapeutic effect of ESWT.
7. Conclusion and future outlook
Recent studies have confirmed that ESWT can safely,
economically and effectively treat upper limb spasticity after stroke,
reduce the use of antispasmodic drugs in patients with upper limb
spasticity after stroke, and thus reduce adverse drug reactions. The
side effects observed so far are mainly tolerable pain and ecchymosis,
but these can disappear quickly. However, at present, ESWT still has
some limitations: ① There are few basic researches on ESWT, and its
mechanism is still unclear. ② There is no uniform standard for the
treatment parameters of ESWT, and the best parameters of ESWT for muscle
spasm cannot be determined. ③ The duration of the effect of ESWT on
post-stroke spasticity is still unclear. Therefore, the mechanism of
action, treatment parameters and duration of efficacy of ESWT are the
key directions of future research, providing more basis for its further
clinical promotion, and making its application in patients with upper
limb spasms after stroke more standardized.
Haoyang Duan
Yawen Lian, 
Zhenlan Li