Abstract
Background: The use of extracorporeal shock wave therapy for the
treatment of lateral epicondylitis is controversial. The purpose of this study
was to evaluate the use of extracorporeal shock wave therapy without local
anesthesia to treat chronic lateral epicondylitis.
Methods: One hundred and fourteen patients with a minimum six-month
history of lateral epicondylitis that was unresponsive to conventional therapy
were randomized into double-blind active treatment and placebo groups. The
protocol consisted of three weekly treatments of either low-dose shock wave
therapy without anesthetic or a sham treatment. Patients had a physical
examination, including provocation testing and dynamometry, at one, four,
eight, and twelve weeks and at six and twelve months after treatment.
Radiographs, laboratory studies, and electrocardiograms were also evaluated
prior to participation and at twelve weeks. A visual analog scale was used to
evaluate pain, and an upper extremity functional scale was used to assess
function. Crossover to active treatment was initiated for nonresponsive
patients who had received the placebo and met the inclusion criteria after
twelve weeks.
Results: A total of 108 of the 114 randomized patients completed all
treatments and the twelve weeks of follow-up required by the protocol.
Sixty-one patients completed one year of follow-up, whereas thirty-four
patients crossed over to receive active treatment. A significant difference (p
= 0.001) in pain reduction was observed at twelve weeks in the intent-to-treat
cohort, with an improvement in the pain score of at least 50% seen in 61%
(thirty-four) of the fifty-six patients in the active treatment group who were
treated according to protocol compared with 29% (seventeen) of the fifty-eight
subjects in the placebo group. This improvement persisted in those followed to
one year. Functional activity scores, activity-specific evaluation, and the
overall impression of the disease state all showed significant improvement as
well (p < 0.05). Crossover patients also showed significant improvement
after twelve weeks of active treatment, with 56% (nineteen of thirty-four)
achieving an improvement in the pain score of at least 50% (p <
0.0001).
Conclusions: These results demonstrate that low-dose shock wave
therapy without anesthetic is a safe and effective treatment for chronic
lateral epicondylitis.
Level of Evidence: Therapeutic Level I. See Instructions
to Authors for a complete description of levels of evidence.
Lateral epicondylitis is a common orthopaedic symptom. Initially,
nonoperative management is effective in most patients; however, studies on the
natural history and surgical management of the disorder have shown that
surgical intervention is necessary in 4% to 11% of
patients1-3.
While surgical intervention is often successful, it carries with it pain,
risks, and costs that may be avoided with successful nonoperative
management.
Despite the widespread use of extracorporeal shock wave therapy in the
treatment of lateral epicondylitis, there is a lack of evidence-based support
of its
efficacy4-6.
The mechanism of action for shock wave therapy remains uncertain, but it
includes the possible stimulation of the healing process in damaged tendons by
disrupting avascular, damaged tissues and encouraging revascularization,
release of local growth factors, and the recruitment of appropriate stem cells
to the
area7,8.
Another proposed mechanism for its efficacy is hyper-stimulation analgesia,
where, through brief sensory stimulation, shock wave therapy can provide
long-term pain
relief9,10.
Alteration of chemical mediators of pain, modulation of the pain signal, and
disruption of cell membranes have all been proposed as possible generators of
this analgesic
effect7,8,10.
Several structured studies of the treatment of lateral epicondylitis have
failed to find a significant benefit from extracorporeal shock wave
therapy11-15.
The present study was designed to evaluate the efficacy of extracorporeal
shock wave therapy without local anesthesia in the treatment of chronic
lateral epicondylitis. To date, no double-blind, placebo-controlled,
multicenter study of shock wave therapy without local anesthesia in a general
population with lateral epicondylitis refractory to traditional conservative
management has been published as far as we know. The null hypothesis of the
present study was that shock wave therapy has no effect on lateral
epicondylitis.
A total of 114 patients from three large orthopaedic practices were
evaluated for inclusion in the study. The study design was a randomized,
multicenter, double-blind, placebo-controlled parallel treatment protocol.
Patients were initially screened for inclusion and then were randomized into
an active treatment group (fifty-six patients) or a placebo treatment group
(fifty-eight patients). At randomization, each patient was given a unique
study number and a sealed envelope with his or her study number on it. The
sealed envelope contained a randomization code (A or B), which was only opened
by the shock wave operator and was not shared with anyone else involved in the
study. All patients provided informed consent, and the study was approved by
each participant's institutional review board. Patients were not charged for
treatment during the study.
Active treatment consisted of one treatment each week with 2000 impulses at
0.06 mJ/mm2 with use of the Sonocur extracorporeal shock wave
therapy system (Siemens Medical Solutions USA, Iselin, New Jersey) for three
weeks. The treatment head of the device, which measures 11 × 12 cm and
produces a treatment area that is 6 × 6 mm and 58 mm in depth, was
directed to the point of maximal tenderness on the lateral epicondyle as
identified by physician palpation and patient report. An ultrasound coupling
gel was used. During treatment, the technique of so-called clinical focusing
was used by adjusting the shock wave focus every 200 to 400 impulses and
redirecting the shock waves to the most symptomatic site. Placebo treatment
consisted of sham treatments of 2000 impulses at 0.06 mJ/mm2 but
with use of a sound-reflecting pad between the patient and the application
head of the machine. Patients were treated in isolation by a technician, so
that no patient could view another's treatment. Both the patients and the
evaluating physicians were blinded to the treatment assignment, and only the
technician knew the treatment group. No local anesthesia or other injections
were used. Patients were evaluated prior to treatment and at follow-up
examinations at one, four, eight, and twelve weeks and at six and twelve
months after completion of treatment. Follow-up examiners were not aware of
the patient's treatment group unless the patient had become unblinded during
crossover treatment.
The primary efficacy end point was relief of pain elicited by provocative
Thomsen testing and recorded on a visual analog scale at twelve weeks compared
with baseline. Patients who did not respond to their assigned treatment with
at least a 50% reduction in pain from baseline after twelve weeks could have
their treatment group revealed to them. If the patient had received placebo
treatment and still met the inclusion criteria, he or she could be crossed
over into the active treatment group. These crossover patients were then
followed for twelve weeks after treatment to evaluate their response, but they
were considered lost to the placebo group. If the patient had been in the
active treatment group and treatment failed after twelve weeks, other standard
therapies could be considered according to the physician and standard medical
practice.
The inclusion criterion for participation in the study was a history of
lateral epicondylitis for a minimum of six months with pain that was resistant
to at least two of three conventional therapies. These included more than four
weeks of physical or occupational therapy, use of nonsteroidal
anti-inflammatory medications for more than four weeks, and corticosteroid
injections. Patients also had to have tenderness on palpation of the lateral
epicondyle and reproducible pain provoked by resisted wrist extension (the
Thomsen test) of =40 mm on the 100-mm visual analog scale.
The Thomsen test was performed with the shoulder flexed to 60°, the
elbow extended, the forearm pronated, and the wrist extended 30°. Pressure
was applied on the dorsum of the hand to stress the extensor carpi radialis
and brevis. The test was performed three times, with the patient recording the
pain on the 100-mm visual analog scale after the third test.
The exclusion criteria were an age of less than eighteen years, a history
of a lateral elbow injection within the prior six weeks, physical therapy
within the prior four weeks, and the use of nonsteroidal anti-inflammatory
medications or acetaminophen for any reason within one week prior to the
study. In addition, active bilateral epicondylitis, treatment with systemic
therapeutic anticoagulation, or a history or radiographic findings of cervical
spondylosis, upper extremity arthritis, elbow arthritis, a neurologic
abnormality, rheumatoid disease, or radial nerve entrapment were criteria for
exclusion. Patients receiving Workers' Compensation as well as those who had
prior surgery for lateral epicondylitis or those with severe systemic disease
or who were pregnant were also excluded.
The study population consisted of sixty women and fifty-four men with a
mean duration of symptoms of twenty-one months prior to participation. The
average age was forty-seven years. The right arm was affected in 67%
(seventy-six patients), and the left arm was involved in 33% (thirty-eight
patients). Of the 114 patients who met the inclusion criteria (failure of
treatment with injections, nonsteroidal anti-inflammatory medications, and
physical therapy), eighty-four (74%) had failed all three treatments. Overall,
for 92% (105) of the patients, steroid injections failed to relieve the pain.
No significant differences were detected between the placebo and active
treatment groups in terms of demographic characteristics such as age, race,
gender, body habitus, affected arm, chronicity of pain, medical diagnoses, or
prior treatments.
The initial evaluation of the patients consisted of a thorough history and
physical examination, as well as baseline studies consisting of complete
blood-cell count with differential, electrocardiogram, and anteroposterior and
lateral radiographs of the affected arm. Radiographs were reviewed by the
treating physicians to evaluate any concomitant abnormality or possible
exclusion criteria. These studies were then repeated at twelve weeks to
monitor any potential change related to treatment with the shock wave
device.
Prior to treatment and at one, four, eight, and twelve weeks and at six
months and one year after treatment, each patient had a clinical evaluation to
assess the symptoms. The evaluation consisted of Thomsen provocation testing,
functional assessment with the upper extremity functional
scale16
(Table I), and a subjective
evaluation of the disease status by the patient. In addition to the clinically
validated functional
score16 calculated
with subjective reports of the activities in
Table I, a patient-specific
activity score was determined for each patient at each follow-up visit as
well. To calculate this activity score, patients rated their ability to
perform two patient-identified activities that they found particularly
difficult to do on a scale from 1 (no difficulty) to 10 (cannot perform). Grip
strength was also evaluated with dynamometry at each follow-up visit through
twelve weeks. Patients were queried with regard to these activities and any
adverse effects at each follow-up visit.
Statistical Methods
The primary efficacy end point was a 50% reduction in the provocation in
pain on the Thomsen test. On the basis of previous experience with
extracorporeal shock wave therapy, we assumed a response rate of 80% for
patients in active treatment and 50% for patients in the placebo group. With
use of this information, it was determined that a sample size of forty-five
patients per treatment group would have an 80% power in detecting the
treatment difference with a two-sided significance level of 0.05. Assuming a
retention rate of at least 80%, a total of 114 patients were then recruited
into the study. To demonstrate a difference between the two treatments for the
primary efficacy end point, a Fisher exact test was used. Missing responses
were input as the last recorded value carried forward for intent-to-treat
calculations.
On the basis of pilot study results, the power of a sample size of
forty-five patients for the mean upper extremity functional score would be
>90%. The analysis of variance test was used for the functional score
difference and other continuous variables. Statistical significance was set
for p = 0.05 for all outcome parameters.
One hundred and fourteen patients were randomized into the placebo
group (fifty-eight patients) and the active treatment group (fifty-six
patients). In the active treatment group, fifty-three patients completed the
twelve-week protocol requirements, two patients were unable to complete the
requirements because of intolerance of the treatment, and one patient withdrew
from the study because of thrombocytopenia, which had been documented prior to
study enrollment. Fifty-five patients in the placebo group completed the
twelve-week protocol requirements, and three patients withdrew from the study
to seek alternative treatment by twelve weeks. Additionally, thirty-four
patients left the placebo group after twelve weeks to cross over into the
active treatment protocol (Fig.
1).
At twelve weeks, a significant difference between treatment groups (p =
0.001) was observed with respect to pain reduction on the Thomsen test, with
reduction in pain of at least 50% achieved in 61% (thirty-four) of the
fifty-six patients in the active treatment group who were treated according to
protocol compared with only 29% (seventeen) of the fifty-eight patients in the
placebo group. The average pain score for the active treatment group decreased
from 74 at baseline to 38 at twelve weeks on the 100-mm visual analog scale
compared with a decrease from 76 to 51, respectively, for the placebo group.
The difference between the groups with respect to the mean pain scores was
significant (p < 0.024) (Fig.
2).
The mean improvement in the upper extremity functional scores at twelve
weeks was 2.4 (from 4.7 to 2.3) for the active treatment group compared with
1.4 (from 4.6 to 3.2) for the placebo group; the difference was significant (p
< 0.01). A significant improvement in the patient activity scores was also
seen at twelve weeks, with a mean improvement of 4.2 (from 7.7 to 3.5) in the
active treatment group compared with 2.4 (from 7.4 to 5.0) in the placebo
group (p = 0.0002).
The mean improvement in grip strength was 14.6 lb (6.6 kg) (from 71 to 87.1
lb [32.2 to 38.2 kg]) in the active treatment group at twelve weeks compared
with 8.6 lb (3.9 kg) (from 72.5 to 81.5 lb [32.9 to 37.4 kg]) in the placebo
group. However, this difference was not significant (p = 0.09).
The rating of the overall impression of their disease state by the patients
in the active treatment group improved significantly from 70.3 at baseline to
32.8 at twelve weeks. Compared with the ratings of the placebo group, the
difference was significant (p = 0.0013)
(Table II).
At six months, a similar improvement was seen among the forty-seven
patients in the active treatment group, some of whom had been unblinded after
twelve weeks. Thirty-five patients in the group (twenty-eight of whom remained
blinded) had maintained at least a 50% reduction in pain at that time. With
the patients who were not evaluated included as treatment failures, the rate
of patients who maintained the level of pain relief was 63% (thirty-five) of
the fifty-six patients. When only those who remained blinded were considered,
the rate was 50% (twenty-eight patients). Only one patient who had achieved a
50% reduction in pain at twelve weeks was found not to have maintained this
level of relief at six months. The mean pain score in the active treatment
group at six months was 24, with a median score of 8. The functional scores in
the active treatment patients had also improved at six months, with a mean
improvement of 2.8 (from 4.7 to 1.9).
By six months, most patients in the placebo group had been lost to
crossover and were therefore not available for comparison. Of the sixteen
placebo patients who had not crossed over and were seen at six months,
thirteen had achieved a 50% reduction in pain. However, this represents only
22% (thirteen) of the fifty-eight patients in the intent-to-treat placebo
cohort. The mean pain score in the placebo group at six months was 18, with a
median score of 6.
At one year, forty-six patients in the active treatment group were
evaluated again. Forty-three (93%) reported at least a 50% reduction in pain.
With those from the intent-to-treat cohort who were not evaluated included as
treatment failures, the rate of patients who had achieved and maintained at
least a 50% reduction in pain was 81% (forty-three of fifty-three patients).
The mean pain score was 10, with a median score of 4. Of the fifteen patients
in the placebo group who had not crossed over and were seen at one year, all
fifteen had achieved a 50% reduction in pain. This, however, represents only
26% (fifteen) of the fifty-eight patients in the original placebo cohort.
Thirty-four patients from the placebo group crossed over after twelve weeks
to receive active treatment. All patients were nonresponsive to placebo
treatment and fulfilled the same criteria for inclusion as at the beginning of
the study. These patients were then given the same active treatment protocol
weekly for three weeks and were followed for twelve weeks, according to the
protocol previously outlined. Eight patients (24%) dropped out prior to
completing the twelve-week follow-up evaluation. The reasons for dropping out
were an inability to tolerate treatment (one patient), failure to return for
follow-up (one patient), patient request (five patients), and relocation from
the region (one patient).
The mean pain score for the crossover patients before they began active
treatment was significantly lower than it had originally been at the start of
placebo treatment (p = 0.034). During the placebo phase, the mean pain score
had changed from 78 before placebo treatment to 70 before active treatment;
whereas during active treatment, the mean pain score had decreased from 70 to
28 at twelve weeks. At all visits during active treatment, the crossover
patients had significantly lower pain scores than those during their
corresponding placebo treatments (p = 0.0339 at baseline, p = 0.0027 at week
1, and p < 0.0001 at weeks 4, 8, and 12)
(Fig. 3). For the primary
efficacy analysis, a reduction in pain of at least 50% was achieved by 56%
(nineteen) of the thirty-four crossover patients compared with 0% during the
placebo phase. The mean functional scores with active treatment also improved.
During the twelve-week placebo period, they had improved from 4.7 to 4.0, and,
after twelve weeks with active treatment, they improved from 3.9 to 1.98. The
difference between the two treatment groups (the original placebo patients and
the same patients who crossed over to active treatments) with respect to this
improvement did not reach significance (p = 0.25); however, within the active
treatment group, the change from baseline was significant (p < 0.0001).
Adverse Effects
No changes from baseline were seen in either the active treatment group or
the placebo group with respect to the hematologic, radiographic, or
electrocardiographic studies obtained at baseline and at the twelve-week
follow-up examination. No serious adverse effects from the device were found.
Twenty-eight patients (50%) in the active treatment group compared with
thirteen patients (22%) in the placebo group experienced moderate
treatment-related pain that was transient. Ten patients (18%), all in the
active treatment group, experienced nausea during treatment. Two active
treatment patients had to stop treatment sessions prior to receiving the full
2000 impulses because of these symptoms. One withdrew from the study, and one
was able to resume and tolerate the treatment later. One other active
treatment patient withdrew because of pain and a slight tremor in the treated
arm after completing the first treatment. No lasting adverse effects were
noted, and all of these effects had resolved by the final follow-up
evaluation. A full list of the adverse events probably or possibly related to
the shock wave treatment is provided in
Table III.
In this study, we found extracorporeal shock wave therapy to be
effective in the treatment of chronic lateral epicondylitis that had been
refractory to other nonoperative treatment modalities. To our knowledge, this
is the only double-blind, placebo-controlled multicenter trial of shock wave
therapy for lateral epicondylitis to show efficacy in a general population.
Active treatment resulted in significant improvement compared with placebo
with respect to the reduction of pain, functional scores, patient activity
score, and subjective rating of the disease state by the patient at twelve
weeks. While grip strength improvement with active treatment was not
significantly different from that with placebo treatment, the functional
score, a validated measure of upper extremity function that combines
activities requiring power grip and wrist and/or finger extension, showed a
significant improvement. The improvements gained by active treatment were
maintained in almost all of the patients who were followed for twelve months.
Furthermore, the placebo patients who had not responded and crossed over to
active treatment showed significant improvement compared with their own scores
during placebo treatment.
The support for the use of shock wave therapy for lateral epicondylitis in
the literature has been highly
questionable6,9,10,17-19.
In a meta-analysis of extracorporeal shock wave therapy in the musculoskeletal
system, Ogden et al. reviewed the cases of more than 8000 patients with a wide
variety of musculoskeletal
conditions5. For
lateral epicondylitis, the published and abstracted studies involved 1672
patients. Eleven prospective studies identified in that meta-analysis, which
were not blinded or did not have control groups, described success rates of
48% to 72%. In contrast, several recent high-quality, prospective, randomized
trials of extracorporeal shock wave therapy did not find similar results and
concluded that there was no benefit to treatment over
placebo11-15.
Speed et al. assessed moderate-dose shock wave therapy for patients with
lateral epicondylitis of at least three months' duration in a double-blind,
randomized, placebo-controlled trial and found that the success rates for
active shock wave treatment (35%; fourteen of forty patients) and placebo
(34%; twelve of thirty-five patients) were not significantly
different12. The
dosing protocol used in that study was moderate-dose shock wave therapy (1500
impulses at 0.12 mJ/mm2) given at monthly intervals for three
months. The dose and dosing interval are different from the weekly application
of low-dose (2000 impulses at 0.06 mJ/mm2) shock wave therapy used
in our study and in most other trials of shock wave therapy. Despite the
higher individual doses given in their monthly regimen, the total energy
delivered per month was one-half of that delivered in the current study. As
the histologic response of tissue treated with shock wave therapy is a
dose-dependent phenomenon, this may have influenced the findings of their
study8,18.
Similarly, Melikyan et al. evaluated higher-energy shock wave therapy
without local anesthesia for the treatment of lateral epicondylitis in a
randomized, double-blind
study14. The
patients were treated with a single fractionated dose of 1000
mJ/mm2 of shock wave therapy split over three sessions of 333
mJ/mm2 each. The authors found no significant benefit to shock wave
treatment over placebo in any parameter including the Disabilities of the Arm,
Shoulder and Hand score, pain, grip strength, analgesic use, or subsequent
surgical rate. That study differs from the current study in many ways. The
energy level and dosing protocol are different, and the concomitant use of
nonsteroidal anti-inflammatory medications was allowed. These medications
inhibit the efficacy of extra-corporeal shock wave
therapy9,18.
All patients in that study were already awaiting surgery, were treated at a
single institution, and had been selected for inclusion by a single surgeon,
which may have been a source of bias.
Chung and Wiley recently evaluated shock wave therapy as a primary
treatment for previously untreated lateral epicondylitis in a double-blind,
placebo-controlled
trial15. The
success rate in the active treatment group (39%; twelve of thirty-one
patients) was not significantly higher than that in the placebo group (31%;
nine of twenty-nine subjects). They used a treatment protocol that was similar
to ours, but the study group was much smaller and the patients had a shorter
duration of follow-up and had not previously been treated for epicondylitis.
The study protocol also allowed concurrent use of nonsteroidal
anti-inflammatory medications as well as a stretching program, both of which
could confound their conclusions.
Haake et al. evaluated low-dose extracorporeal shock wave therapy with
local anesthesia in a randomized, double-blind, placebo-controlled
trial13. In that
large study, no difference between shock wave therapy and sham treatment was
noted for any of the treatment efficacy end points. Both the active treatment
and placebo groups showed equal success rates at 25.8% (thirty-two of 124
patients) and 25.4% (thirty-one of 122 patients), respectively. These results
are similar to the success rate spontaneously achieved in our placebo group,
in which 29% (seventeen of fifty-eight patients) attained a 50% reduction in
pain. While that study and ours are both multi-center, randomized,
double-blind, placebo-controlled trials with similar inclusion and exclusion
criteria and dosing protocols, the study by Haake et al. used local anesthesia
injected at the treatment site. The use of a local anesthetic may alter the
tissue effect of the shock wave therapy, interfere with hyper-stimulation
analgesia, or simply inhibit the aiming of the treatment head at the point of
maximal tenderness. Regardless, this confounding factor was not used in our
study and may be a reason for the very different outcomes.
Rompe et al. recently reported the results of a treatment protocol nearly
identical to that used in the current study but limited to patients with
epicondylitis secondary to playing
tennis18. While
smaller in numbers, the results are very similar to our findings with success
in twenty-five (65%) of the thirty-eight patients in the active treatment
group compared with eleven (28%) of the forty patients in the placebo group.
Unlike our study, that study was done at a single center, was limited to
tennis-related disease, and did not use a crossover design.
The decision not to use local anesthesia in our study, while absolutely
needed to eliminate its possible influence on the effect of shock wave therapy
and to allow clinical refocusing, may have biased the efficacy of our blinding
to some extent. Although the patients were treated in isolation and did not
know whether the treatment should be uncomfortable, a sham treatment with a
reflecting pad is a slightly different experience than active treatment. This
may be inferred by the higher rate of transient local pain with active
treatment (50%) compared with placebo (22%). However, half of the active
treatment patients did not experience pain with treatment, indicating that
their experience was not radically different from that of most of the placebo
group.
Other authors have found that a substantial number of patients with lateral
epicondylitis improve with time, and this certainly occurred to a certain
extent within our placebo
group3,12,13.
In the patients who remained in the placebo cohort, high success rates were
seen at six months (81%) and one year (100%); however, this represents only
22% and 26%, respectively, of the intent-to-treat cohort, a rate that has been
seen in other
studies13. The high
success rate of those who remained in the placebo group is likely due to the
bias resulting from the fact that those who improved spontaneously did not
cross over into active treatment. In fact, of those who remained in the
placebo group after twelve weeks, only one patient had a pain score that would
have qualified for inclusion into the crossover cohort.
Extracorporeal shock wave therapy as utilized in the current study, without
the use of local anesthesia, is a safe and effective treatment of chronic
lateral epicondylitis. In patients who have had failure of conventional
treatment of lateral epicondylitis, shock wave therapy can significantly
improve the pain scores, functional scores, and the subjective impression of
the disease state. These results are contradictory to those found when
extracorporeal shock wave therapy is used with local anesthesia or with
concomitant use of nonsteroidal anti-inflammatory medications. Further
research and clinical trials may be necessary to evaluate the ideal dosing and
influence of confounding factors on the efficacy of shock wave therapy.
?
In support of their research or preparation of this manuscript, one or more
of the authors received grants or outside funding from Siemens Medical. None
of the authors received payments or other benefits or a commitment or
agreement to provide such benefits from a commercial entity. No commercial
entity paid or directed, or agreed to pay or direct, any benefits to any
research fund, foundation, educational institution, or other charitable or
nonprofit organization with which the authors are affiliated or
associated.
Boyd HB, McLeod AC Jr. Tennis elbow.
J Bone Joint Surg Am.1973;55:
1183-7.551183
1973
[PubMed]
Coonrad RW, Hooper WR. Tennis elbow: its
course, natural history, conservative and surgical management. J Bone
Joint Surg Am.1973;55:
1177-82.551177
1973
Nirschl RP, Pettrone FA. Tennis elbow.
The surgical treatment of lateral epicondylitis. J Bone Joint Surg
Am.1979;61:
832-9.61832
1979
Boddeker I, Haake M. [Extracorporal
shock wave therapy in treatment of epicondylitis humeri radialis. A current
overview]. Orthopade.2000;29: 463-9.
German.29463
2000
[PubMed][CrossRef]
Ogden JA, Alvarez RG, Levitt R, Marlow
M. Shock wave therapy (Orthotripsy) in musculoskeletal disorders. Clin
Orthop Relat Res.2001;387:
22-40.38722
2001
[CrossRef]
Vogt W, Dubs B. [The value of shockwave
therapy in treatment of humero-radial epicondylitis]. Swiss
Surg.2001;7:
110-5. German.7110
2001
[CrossRef]
Thiel M. Application of shock waves in
medicine. Clin Orthop Relat Res.2001;387:
18-21.38718
2001
[PubMed][CrossRef]
Rompe JD, Kirkpatrick CJ, Kullmer K,
Schwitalle M, Krischek O. Dose-related effects of shock waves on rabbit tendo
Achillis. A sonographic and histological study. J Bone Joint Surg
Br.1998;80:
546-52.80546
1998
[CrossRef]
Rompe JD, Hope C, Kullmer K, Heine J,
Burger R. Analgesic effect of extracorporeal shock-wave therapy on chronic
tennis elbow. J Bone Joint Surg Br.1996;78:
233-7.78233
1996
[PubMed]
Rompe JD, Hopf C, Kullmer K, Heine J,
Burger R, Nafe B. Low-energy extracorporeal shock wave therapy for persistent
tennis elbow. Int Orthop.1996;20:
23-7.2023
1996
[PubMed][CrossRef]
Crowther MA, Bannister GC, Huma H,
Rooker GD. A prospective, randomised study to compare extracorporeal
shock-wave therapy and injection of steroid for the treatment of tennis elbow.
J Bone Joint Surg Br.2002;84:
678-9.84678
2002
[PubMed][CrossRef]
Speed CA, Nichols D, Richards C,
Humphreys H, Wies JT, Burnet S, Hazleman BL. Extracorporeal shock wave therapy
for lateral epicondylitis—a double blind randomised controlled trial.
J Orthop Res.2002;20:
895-8.20895
2002
[PubMed][CrossRef]
Haake M, Konig IR, Decker T, Riedel C,
Buch M, Muller HH; Extracorporeal Shock Wave Therapy Clinical Trial Group.
Extracorporeal shock wave therapy in the treatment of lateral epicondylitis: a
randomized multicenter trial. J Bone Joint Surg Am.2002;84:
1982-91.841982
2002
[PubMed]
Melikyan EY, Shahin E, Miles J,
Bainbridge LC. Extracorporeal shock-wave treatment for tennis elbow. A
randomised double-blind study. J Bone Joint Surg Br.2003;85:
852-5.85852
2003
[PubMed]
Chung B, Wiley JP. Effectiveness of
extracorporeal shock wave therapy in the treatment of previously untreated
lateral epicondylitis: a randomized controlled trial. Am J Sports
Med.2004;32:
1660-7.321660
2004
[CrossRef]
Pransky G, Feuerstein M, Himmelstein J,
Katz JN, Vickers-Lahti M. Measuring functional outcomes in work-related upper
extremity disorders. Development and validation of the Upper Extremity
Functional Scale. J Occup Environ Med.1997;39:
1195-202.391195
1997
[PubMed][CrossRef]
Ko JY, Chen HS, Chen LM. Treatment of
lateral epicondylitis of the elbow with shock waves. Clin Orthop Relat
Res.2001;387:
60-7.38760
2001
[CrossRef]
Rompe JD, Decking J, Schoellner C, Theis
C. Repetitive low-energy shock wave treatment for chronic lateral
epicondylitis in tennis players. Am J Sports Med.2004;32:
734-43.32734
2004
[PubMed][CrossRef]
Wang CJ, Chen HS. Shock wave therapy for
patients with lateral epicondylitis of the elbow: a one- to two-year follow-up
study. Am J Sports Med.2002;30:
422-5.30422
2002
[PubMed]