I read with interest the Stasinopoulos/johnson article on ECWST for
"tennis elbow". I would like to bring to the author's attention our double
-blinded, randomized (placebo vs. active treatment groups) study
previously presented at the AAOS annual meeting 2003 with 6 month results
and at the 2004 meeting with 12 month results. This study has been
accepted for publication in the JBJS.
I read with interest the Stasinopoulos/johnson article on ECWST for
"tennis elbow". I would like to bring to the author's attention our double
-blinded, randomized (placebo vs. active treatment groups) study
previously presented at the AAOS annual meeting 2003 with 6 month results
and at the 2004 meeting with 12 month results. This study has been
accepted for publication in the JBJS.
Our study involved 114 patients non-responsive to two of three
conventional therapies including physical therapy, NSAIDS, and steriod
injections. Active treatment consisted of 3 weekly treatments of low-dose
shock wave therapy. without anaesthetic. Patients were evaluated with
radiographs and physical examination omcluding provocative testing and
dynamometry. A visual analog scale was used to evaluate pain and an upper
extremity functional scale was used to assess function. Evaluations of
patients were performed prior to treatment and at 1, 4, 8, 12 weeks, 6
months and 12 twelve months.
A stistically sighnificant difference (p=0.001) in pain reduction
was observed at 12 weeks in the active cohort with 61% (34/56) of active
treated patients showing at least 50% improvement in pain , compared to
29% (17/58) in the placebo group. This was found to persist for one year.
These results demonstrated ECSWT to be a safe and effective treatment
for chronic lateral epicondylitis. Interestingly, our results mirror those
of Rompe (AJSM 2004;32:734-43). Hence, in combination, provide additional
weight of evidence to this conclusion. Clearly, the effectiveness is dose
related and some consistency of methodology must be achieved to be able to
objectively evaluate differing studies.
I read with interest the review of Stasinopuolos and Johnson on the
“Effectiveness of extracorporeal shock wave therapy for tennis elbow” (Br
J Sports Med 2005; 39:132-139).
I acknowledge their evaluation in terms that the trials from Haake et
al. [1] and from our group [2] are by far the highest-ranking publications
in this field, while other studies show various major flaws in study
desi...
I read with interest the review of Stasinopuolos and Johnson on the
“Effectiveness of extracorporeal shock wave therapy for tennis elbow” (Br
J Sports Med 2005; 39:132-139).
I acknowledge their evaluation in terms that the trials from Haake et
al. [1] and from our group [2] are by far the highest-ranking publications
in this field, while other studies show various major flaws in study
design.
Unfortunately, Stasinopoulos and Johnson failed to provide a sensible
explanation for the different clinical outcomes of these two easily
comparable randomized controlled trials. To understand the discrepancy of
results of these two trials it is necessary to have insight into the most
recent results of experimental work on the mechanism of action of low-
energy ESWT.
The rationale for ESWT in clinical use is stimulation of soft tissue
healing and inhibition of pain receptors.
Haake et al., as usual, failed to provide any evidence for a specific
biological response when evaluating changes in the activity of local
nociceptive afferent nerve fibers or of spinal cord neurones in a rat
model after shock wave application (1000 impulses, Energy Flux Density
(EFD) = 0.13mJ/mm² - 0.33 mJ/mm²). The authors concluded that it was
unlikely that ESWT could trigger stimulation-induced analgesic response
via activation of peripheral nerves, and that analgesic effects of ESWT
were endogenous opioid – dependent. The authors further negated that ESWT
could trigger the endogenous pain control system. [3-5]
Others showed that Haake et al. were completely wrong!
Wang et al. [6] investigated the effect of low-energy shock wave
therapy on neovascularization at the tendon-bone junction in rabbits. The
results showed that low-energy shock wave treatment (500 impulses, EFD=
0.12 mJ/mm²) produced a significantly higher number of neo-vessels and
angiogenesis-related markers including endothelial nitric oxide synthase
(eNOS), vessel endothelial growth factor (VEGF) and proliferating cell
nuclear antigen (PCNA) than the control without shock wave treatment.
Chen et al. [7] reported that only an optimal ESW treatment promoted
healing of Achilles tendintis by inducing TGF-beta1 and IGF-I. Rats with
the collagenease-induced Achilles tendinitis were given a single shock
wave treatment (EFD= 0.16 mJ/mm²) with 0, 200, 500 and 1000 impulses. 200
impulses restored biomechanical and biochemical characteristics of healing
tendons 12 weeks after treatment. However, ESW treatments with 500 and
1000 impulses elicited inhibitory effects on tendinitis repair.
Histological observation demonstrated that ESW treatment resolved edema,
swelling, and inflammatory cell infiltration in injured tendons. The
proliferation of tenocytes adjunct to hypertrophied cell aggregate and
newly formed tendon tissue coincided with intensive TGF-beta1 and IGF-I
expression. Together, low-energy shock wave effectively promoted tendon
healing.
Meirer et al. [8] investigated the effect of low-energy ESWT on
compromised skin flaps. For this purpose, the epigastric skin flap model
in rats, based solely on the right inferior epigastric vessels was used.
20 rats were divided into an ESWT-group (2500 impulses, EFD= 0.15 mJ/mm²),
and a control group. Necrotic zones relative to total flap surface area
were measured and expressed as percentages. Overall, there was a
significant reduction in the surface area of the necrotic zones of the
flaps in the ESWT group compared to the control group (2.2% versus
control: 17.4%). Low-energy ESWT represented a feasible and cost effective
method to improve blood supply in ischemic tissue.
To investigate the analgesic properties of low-energy shock wave
application, Ohtori et al. [9] demonstrated that low-energy shock waves
(1000 impulses, EFD= 0.08 mJ/mm²) produced morphologic changes in
cutaneous nerve fibers. The number of sensory fibers decreased
significantly following shock wave application as indicated by the loss of
immunoreactivity for calcitonin gene related peptide (CGRP) compared to
the untreated skin. CGRP is a marker of sensory neurons, regarded as the
primary afferent peptide with the strongest evidence of a role in pain
perception, and has immunohistochemically been co-localized with substance
P. Reinnervation of the epidermis started 2 weeks after treatment. Ohtori
concluded that low-energy ESWT was able to temporarily destroy the sensory
free nerve endings in the rat skin.
When repeating shock wave application after 14 days in another
experiment, the same authors described delay of re-innervation for as long
as 42 days, significantly longer than after single shock wave
application. [10]
Takahashi et al. [11] investigated the analgesic properties of low-
energy shock wave application (1000 impulses, EFD= 0.08 mJ/mm²). They
analyzed changes in CGRP-immunoreactive (ir) neurons in the dorsal root
ganglion (DRG). In the nontreated group, 61% of fluorogold-labeled dorsal
root ganglion neurons innervating the most middle foot pad of hind paw
were CGRP-ir. However, in the shock wave-treated group, the percentage
decreased to 18%.
The described effect on CGRP-positive nociceptive nerve fibers is of
particular importance. Ljung et al. [12] studied the muscle origin in
patients suffering from tennis elbow. Immunohistochemistry and antibodies
to substance P (SP) and CGRP as well as the general nerve marker PGP 9.5
were used. Specific immunoreactions were observed in nerve bundles and as
free nerve fibers, the observations constituting a morphological correlate
for the occurrence of nerve mediated effects in this region. Their study
gave further evidence to previous suggestions that tennis elbow is not an
inflammatory process in the sense of involving inflammatory cells.
Frequent mechanical involvement obviously affected sensory innervation.
Substance P and calcitonin gene-related peptide were suggested to have
various important efferent effects in the etiology of tennis elbow.
From neurophysiological studies it is well known that nociceptive C-
fiber nerve endings release CGRP and substance P which result in protein
extravasation and vasodilation. This neurogenic inflammation has been
implicated in the pathophysiology of various human diseases with uncertain
etiology such as arthritis or tendinosis. Most important, beyond its
primarily inflammatory character neurogenic inflammation was regarded as a
mechanism that activates protective responses, thus bringing about a first
line of defence to maintain the integrity of the tissue and to contribute
to tissue repair. [13] Application of a local anesthetic effectively
inhibits this CGRP-induced healing cascade. [14]
Being aware of this fact a critical focus has to be on the use of
local anesthetics in the various trials. And the use of local anesthesia
happens to be the most decisive difference between the two highest-ranking
trials in Stasinopoulos´ analysis.
Accordingly, in the trial by Haake et al. [1] applying low-energy ESWT
under local anesthesia, the success rate was 26% in the verum group,
compared to 25% in the sham group.
In the study doing low-energy ESWT without local anesthesia, the success
rate was 65% in the verum group, compared to 33% in the sham group. [2]
And, those results have been supported by a US multicenter trial using an
identical study design. [15]
What is more, the same discrepancy of study results may be observed
when treating patients with chronic plantar fasciitis.
Again, Haake et al. [16] used a low-energy treatment under local
anesthesia, and again the results were unfavorable, with a success rate of
34% in the verum group, and of 30% in the sham group.
In the study doing low-energy ESWT without local anesthesia, the success
rate was 60% in the verum group, compared to 27% in the sham group. [17,18]
In an upcoming publication, Rompe et al. [19] evaluated the effect of local
anesthesia on the clinical outcome after repetitive low-energy ESWT for
chronic plantar fasciitis. 86 patients with chronic plantar fasciitis were
randomly assigned to receive either low-energy ESWT without local
anesthesia, given weekly for three weeks (3 x 2000 pulses, EFD= 0.09
mJ/mm2) or identical ESWT with local anesthesia. At 3 months,
significantly more patients achieved ≥ 50% reduction of pain
after low-energy ESWT without compared to low-energy ESWT with local
anesthesia (67% vs. 29%).
Together, I contradict the conclusion by Stasinopoulos and Johnson.
There are well designed trials providing meaningful evidence on the
effectiveness of ESWT for the management of tennis elbow. US and German
groups [2,15] have independently shown a treatment design leading to
successful outcome in close to 70% of patients with recalcitrant lateral
elbow tendinosis.
As always it is much easier to achieve unfavorable results with various
treatment regimes than to develop a successful treatment strategy. One
recent example is the trial by Chung and Wiley [20] who adopted the
treatment parameters of the above mentioned US and German trials, but
focused on patients with acute, not previously treated patients with a
tennis elbow, instead of chronic recalcitrant cases. As could be expected
from several other randomized controlled trials evaluating conservative
treatment methods for acute tennis elbow they found it impossible to beat
the self-limiting course of acute tendinosis at 8-week follow-up.
References
1. Haake M et al. Extracorporeal shock wave therapy in the treatment
of lateral epicondylitis. J Bone Joint Surg 2002; 84-A:1982-1991.
2. Rompe et al. Repetitive low-energy shock wave treatment for
chronic lateral epicondylitis in tennis players. Am J Sports Med 2004;
32:734-743.
3. Haake M et al. Absence of spinal response to extracorporeal shock
waves on the endogenous opioid systems in the rat. Ultrasound Med Biol
2001; 27:279-284.
4. Haake M et al. No influence of low-energy extracorporeal shock
wave therapy (ESWT) on spinal nociceptive systems. J Orthop Sci 2002; 7:97
-101.
5. Haake M et al. Unchanged c-Fos expression after extracorporeal
shock wave therapy: an experimental investigation in rats. Arch Orthop
Trauma Surg 2002; 122:518-521.
6. Chen YJ et al. Extracorporeal shock waves promote healing of
collagenase-induced Achilles tendinitis and increase TGF-beta1 and IGF-I
expression. J Orthop Res 2004; 22: 854-861.
7. Wang CJ et al. Shock wave therapy induces neovascularization at
the tendon-bone junction. A study in rabbits. J Orthop Res 2003; 21:984-
989.
8. Meirer R et al. Extracorporeal shock wave may enhance skin flap
survival in an animal model. Br J Plast Surg 2005; 58:53-57.
9. Ohtori S. et al. Shock wave application to rat skin induces
degeneration and reinnervation of sensory nerve fibres. Neurosci Lett
2001; 315:57-60.
10. Takahashi N et al. Application of shock waves to rat skin
decreases calcitonin gene-related peptide immunoreactivity in dorsal root
ganglion neurons. Auton Neurosci 2003; 107:81-84.
11. Takahashi N et al. The mechanism of pain relief in extracorporeal
shock wave therapy. Poster # 448, AAOS Annual Meeting San Francisco, 2004.
http://www.aaos.org/wordhtml/anmt2004/poster/p448.htm.
12. Ljung BO et al. Neurokinin-1 receptors and sensory neuropeptides
in tendon insertion of the medial and lateral epicondyles of the humerus.
Studies on tennis elbow and medial epicondylalgia. J Orthop Res 2004;
22:321-327.
13. Herbert MK, Holzer P. Neurogenic inflammation. II.
pathophysiology and clinical implications. Anasthesiol Intensivmed
Notfallmed Schmerzther 2002; 37:386-394.
14. Zimmermann M. Neuronal mechanism of chronic pain. Orthopade 2004;
33: 515-524.
15. Pettrone F, McCall B. Low-energy shock wave treatment for chronic
lateral epicondylitis. Journal Bone Joint Surg 2005; 87-A: in press.
16. Haake M et al. Extracorporeal shock wave therapy for plantar
fasciitis: randomised controlled multicentre trial. BMJ 2003; 327:75-85.
17. Rompe JD et al. Evaluation of low energy extracorporeal shock
wave application and treatment in chronic plantar fasciitis. J Bone Joint
Surg 2002; 84-A:335-341.
18. Rompe JD et al. Shock wave application for chronic plantar
fasciitis in running athletes - a prospective, randomized, placebo-
controlled trial. Am J Sports Med 2003; 31:268-275.
19. Rompe JD et al. Repetitive low-energy shock wave application
without local anesthesia is more efficient than repetitive low-energy
shock wave application with local anesthesia in the treatment of chronic
plantar fasciitis. J Orthop Res 2005; 23: in press (available online 7
December 2004).
20. 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; 32:1660-1667.
I read your editorial 'The power of placebo' with some relief. It
would seem that all too often, 'advances' in practice and even research
are relegating the placebo effect to the status of quackery. Certainly, I
am not a great fan of many therapies or technologies that claim
scientifically dubious healing or performance-enhancing qualities (I am to
be honest even less of a fan of those who sell them...
I read your editorial 'The power of placebo' with some relief. It
would seem that all too often, 'advances' in practice and even research
are relegating the placebo effect to the status of quackery. Certainly, I
am not a great fan of many therapies or technologies that claim
scientifically dubious healing or performance-enhancing qualities (I am to
be honest even less of a fan of those who sell them). However, by
dismissing the power of such artefacts/interventions to bring about a wide
range of positive effects, we are also dismissing the power of the mind to
bring about these very same effects.
Certainly the placebo effect, based essentially on the twin processes
of conditioning and expectancy (i.e. human beliefs), may be more easily
elicited in the more suggestible individual, and certainly may not be
powerful enough to operate in a wide range of conditions in which various
authors have made some fairly extreme claims. However, evidence, both
empirical and anecdotal, suggests that it is very much alive and well, if
hidden from view much of the time. It will remain hidden until the sports
science community adopts methodologies that allow it to demonstrate its
power. For example, the use of no-placebo control groups alongside placebo
and experimental groups (allowing not only the comparison of placebo and
experimental conditions but placebo and no-placebo conditions) might
reveal placebo effects of a far greater magnitude than one would imagine.
In fact, a recent meta analysis indicated that placebo effects may account
for up to 75% of the overall therapeutic effect of anti-depressant drugs
[1]. Certainly, such methodologies are complex and require a
high degree of control over variables, but they provide a far better
picture of what is really going on when, for example, an athlete takes a
tablet to reduce pain or sits on a treatment table.
What is all too often forgotten by practitioners is that the placebo
effect does not operate in isolation; it sits alongside many other
processes (e.g. pharmacological or biomechanical) and, if utilised
effectively, may augment many intervention significantly. On this basis
alone, it warrants far greater exploration in sport.
For those sceptics among us, or those who would like an informed
debate as opposed to the often emotional and opinionated rhetoric on this
subject, I strongly recommend Dylan Evans’ recent book on the subject [2]. Evans proposes a sound physiological basis for the placebo effect, and on
this basis, offers a strong case for a range of conditions being either
placebo responsive or not. A very useful starting point for practitioners
interested in the phenomenon.
Yours
Dr Chris Beedie
Canterbury, UK
No competing interests
References
1. Kirsch, I. Sapirstein, G., 1998, Listening to Prozac but Hearing Placebo.
A Meta-Analysis of Antidepressent Medication. Prevention and Treatment.
1(2): 1 – 15.
2. Evans, D., 2003, Placebo: The Belief Effect. London: Harper Collins.
Having worked in sport's injury prevention with children for the last
15 years and having monitored their evolution in a representative group of
about 160 adolescent girls and boys competing in various sports, I can but
express a certain amount of frustration as to the results of injury
prevention.
Having contributed to introduce and observed changes in, nutritional
and psychological counse...
Having worked in sport's injury prevention with children for the last
15 years and having monitored their evolution in a representative group of
about 160 adolescent girls and boys competing in various sports, I can but
express a certain amount of frustration as to the results of injury
prevention.
Having contributed to introduce and observed changes in, nutritional
and psychological counselling, stretching, interaction with coaches and
clubs, school timetable adaptation and physiological evaluation, I would
have expected to see at least part of the 75% injury reduction proposed by
Ekstrand in 1982 [1] even though their study only concerned football
players.
Over the last 15 years the incidence of sport injuries in our group
of adolescents has stayed constant at about 0.28 +/- .066 injuries / pupil
/ school year or 1.08 x 10-3 +/- 2.6 x10-4 injuries / pupil / 100 hours of
sport practised. The proportion of boys and girls and the type of sports
staying relatively constant through time. There was however a decrease in
overuse injuries, that seems to have been compensated by non-overuse
injuries.
Over the same period, the mean average increase in training time was
18 min./week.
Should we be finding a decrease in the incidence of injuries with
preventive measures, or does prevention merely permit athletes to practice
more and/or harder and reach higher levels of performance? Might it be
more pertinent to monitor the increase in performance (if possible)to get
an idea of the effectiveness of prevention?
To measure a change in incidence, attributable to prevention, would
imply that the training load and absolute performance objectives stay
constant through time. This, as one imagines, is contrary to the concept
of competitive sports, where the objective is to challenge our limits may
they be physical, mental or other.
I therefore believe that it might be difficult to measure the overall
efficacy of injury prevention in a constantly changing paradigm based on
performance and challenging limits. Improving records and performances
over time might confirm this.
References
1. Ekstrand J., A training program for the prevention of injuries to
reduce soccer injuries by 75 per cent. Nord Med. 1982 Jun;97(6-7):164-5
Dr P.B. Mahler,
Centre de Médecine d'Exercice,
Service de Santé de la Jeunesse,
11 Glacis de Rive, CP 3682,
1211 Genève 3,
Switzerland,
Tel: 41-22-3276157,
Fax: 41-22-3276171,
per.mahler@etat.ge.ch http://www.geneve.ch/ssj/
Huang and colleagues have prepared an estimate of the cost-
effectiveness of the Victorian, Active Script Programme, which they
conclude indicates a successful program and one suitable for wider
adoption. Confidence in a cost effectiveness estimate depends on
confidence in the evidence on effectiveness and costs.
The Active Script Program evaluation was designed to determine up-
take of the...
Huang and colleagues have prepared an estimate of the cost-
effectiveness of the Victorian, Active Script Programme, which they
conclude indicates a successful program and one suitable for wider
adoption. Confidence in a cost effectiveness estimate depends on
confidence in the evidence on effectiveness and costs.
The Active Script Program evaluation was designed to determine up-
take of the program by GPs. For the crucial evidence on patient physical
activity levels, the authors draw on the results of a different physical
activity intervention reported in a non-peer reviewed, unpublished
conference presentation by Bull (1999), which on inspection appears to
indicate a just significant 20% difference in activity levels between
control and intervention group at 6 months, which had fallen to a small
(<_5 non="non" significant="significant" difference="difference" in="in" the="the" percent="percent" active="active" between="between" intervention="intervention" and="and" control="control" groups="groups" at="at" _12="_12" months.="months." huang="huang" colleagues="colleagues" assume="assume" model="model" a="a" _20="_20" increase="increase" physical="physical" activity="activity" levels="levels" associated="associated" with="with" script="script" which="which" is="is" thus="thus" likely="likely" to="to" be="be" overstated="overstated" not="not" varied="varied" sensitivity="sensitivity" analysis.="analysis." fifty="fifty" of="of" this="this" group="group" presumed="presumed" maintain="maintain" their="their" long="long" enough="enough" accrue="accrue" health="health" benefit="benefit" unreferenced="unreferenced" consistent="consistent" data="data" by="by" bull="bull" shows="shows" that="that" months="months" there="there" has="has" been="been" _75="_75" reduction="reduction" observed="observed" _6="_6" p="p"/> Another more intensive active script type intervention demonstrated
an increase in the proportion of people physically active from baseline of
<_10 for="for" the="the" intervention="intervention" group="group" compared="compared" to="to" control="control" elley="elley" et="et" al="al" _2002="_2002" which="which" is="is" considerably="considerably" less="less" than="than" that="that" assumed="assumed" in="in" huang="huang" _2004="_2004" evaluation.="evaluation." p="p"/> The key effectiveness figure is likely to be overstated in the Huang
et al (2004) model. We find the step taken in the economic analysis from
GP awareness, knowledge and behaviour (which was measured) to patient
behaviour (which was not rigorously measured) to be beyond the scope of
the original data. It is likely that the estimates of cost effectiveness
would be higher and less certain than those presented, and that it may
have been more useful to highlight gaps in existing data.
References
(1). Bull F. Physical activity and General Practice: overview of the evidence.
Prepared for the participants of Active Australia Symposium on Physical
Activity in General Practice. Canberra, 1999.
(2). Elley CR, Kerse N, Arroll B, Robinson E. Effectiveness of counselling
patients on physical activity in general practice: cluster randomised
controlled trial. BMJ 2003;326:793.
Prompted by Lippi & Guidi [1] and their discussion that drugs
which modulate hypoxia inducible factors (HIFs) should soon be included in
antidoping legislation, is an old argument from my undergraduate days.
They state that HIFs stimulate red cell production and so could be used as
an athletic stimulant or to treat pathological conditions that involve
altered oxygen metabolism. On the flipside of...
Prompted by Lippi & Guidi [1] and their discussion that drugs
which modulate hypoxia inducible factors (HIFs) should soon be included in
antidoping legislation, is an old argument from my undergraduate days.
They state that HIFs stimulate red cell production and so could be used as
an athletic stimulant or to treat pathological conditions that involve
altered oxygen metabolism. On the flipside of the coin HIFs stimulate
genes encoding proteins involved in cell division and survival which could
ultimately promote the development of cancer [2].
This brings to mind an ongoing debate with an old lecturer.
Silicosis is a group of lung diseases that develop following the
inhalation of crystalline silica dust (SiO2)[3,4]. While for coal miners
this may simply be an occupational hazard, should the side effects of
steroids (or in this case gene manipulation) be an occupational hazard for
athletes?
Every drug is potentially toxic if administered in high enough doses
and drug use has increased in prevalence as athletes will “do anything,
take anything, short of killing themselves in order to improve
performance” [5]. In ancient Greece it was hallucinogenic mushrooms, 19th
century boxers used heroin as a painkiller, amphetamines and cocaine were
used together in the 50’s [6] and today athletes are using an even wider
range of drugs and genetic manipulation.
This historical view raises the point that drug use is not new, so we
cannot attribute it’s increase to financial rewards or increased media
scrutiny. In reality there is no justification for cheating, the
pressures and temptations are equal for all and any problem is of morality
and ethical justification. So what if the aspect of cheating was removed
and only the cost and availability limited the use of performance
enhancing techniques?
The mere seeking of an advantage is not implicitly unfair, nor is the
gaining of an advantage implicitly unfair [7]. In most cases any advantage
comes from an external source (e.g. sharkskin swimming suits), so why
should drugs or genetic manipulation be any different? So long as
athletes are informed of the risks, then why not allow (for example)
steroid use, it would certainly level the playing field. It would allow
those athletes who have to work harder to acquire an advantage through
training to easily achieve the same level as those who can gain a training
advantage with less effort.
The side-effects provide a sufficient basis for prohibition alone,
but is stopping competent adults from doing something an unwarranted
intrusion of privacy? There is in comparison little or no debate about
banning high-risk sports such as rugby or boxing and there is little
difference between athletes who risk their health by competing when
injured and those who risk their health to drugs. We admire those
competing dosed up to the eyeballs with painkillers and then condemn them
for taking other drugs to build muscle and relax after they have pushed
their bodies too far. If we are prepared to accept concern for an
athlete’s health as a basis to intervene over drug-use then logically we
should look at other aspects of certain high-risk sports. Allowing
performance-enhancing techniques may even decrease the risk for
athletes [8]. Banning them places a reliance on black market operations
(whose quality could not be guaranteed), there would be no advice on
dosages and hygiene could be compromised. If a ban is lifted then these
techniques could be controlled.
Any game is defined by its specific rules and if the rules are broken
you are not really playing that game. For example if a soccer player
picks up the ball and runs it is no longer soccer but branches off to
become rugby union, by the same token if one lone athlete takes drugs or
modifies their genes to express hypoxia tolerant characteristics then they
are playing a different game. A more effective way to ensure maximum
fairness may be to allow the free use of drugs. Consequently though, if
unrestricted access to drugs was allowed would that be fair? Inequalities
would exist between users themselves as well as users and non-users [9]. No
two people can be guaranteed to respond in the same way to the same drug
due to their individual physiology and no matter what drugs are used,
someone is always going to be first to use those that are newly developed.
Whatever route is taken to justify or oppose drug-use they all seem
to lead to a cul-de-sac of ambiguity and counter argument and therefore
the answer to the original question is not simple. It is down to the
individual athlete to consider all the risks involved and only then can
they decide if using performance enhancing techniques is just an
occupational hazard.
References
(1). Lippi, G, Guidi, G. Gene manipulation and improvement of athletic
performance: new strategies in blood doping. Br J Sports Med 2004;38: 641.
(2). Marx J. How cells endure low oxygen. Science 2004;303: 1454-6.
(3). Beckett, W, Abraham, J, Becklake, M, Christiani, D, Cowie, R,
Davis, G, Jones, R, et al. Adverse effects of crystalline silica exposure.
Am J Respir Crit Care Med 1997;155: 761-765.
(4). Mossman, B, Churg, A. Mechanisms in the pathogenesis of
asbestosis and silicosis. Am J Respir Crit Care Med 1998;157: 1666-1680.
(5). Connelly, H. cited in J.J. Coakley. Sport in Society: Issues and
Controversies. Mosby, St Louis, Missouri, USA. 1994; 151.
(6). Todd, T. Anabolic Steroids: the gremlins of sport. J Sport Hist
1987;14(1): 87-107.
(7). Fost, N.C. Ethical and Social Issues in Anti-doping Strategies in
Sport. In Landry, F., Landry M.,& Yerles, M. (eds.) Sport... The Third
Millenium. Sainte-Foy, Les Presses de l’Universite de Laval. 1991.
(8). Black, T, Pape, A. The Ban on Drugs in Sport, The Solution or the
Problem? J Sport Soc Iss 1997;21(1): 83-92.
(9). Gardner, R. On Performance-enhancing Substances and the Unfair
Advantage Argument J Phil Sport 1989;XVI: 59-73.
I recently read the article by Dadebo et al with interest [1]. I am a
little confused by their results and their take home message. First, the
correlation for SHT is reported as 0.02 (Table 6) and 0.54 (Table 8, one
predictor) when the two correlations should be equal [2].
Second, the
appropriate analysis is Poisson regression with counts of injuries as
outcome and exposure rates as a covaria...
I recently read the article by Dadebo et al with interest [1]. I am a
little confused by their results and their take home message. First, the
correlation for SHT is reported as 0.02 (Table 6) and 0.54 (Table 8, one
predictor) when the two correlations should be equal [2].
Second, the
appropriate analysis is Poisson regression with counts of injuries as
outcome and exposure rates as a covariate. Third, the authors should
report confidence intervals for the coefficients in the regression model
for an appropriate interpretation. Fourth, if assumptions behind
correlation and multiple regression statistics (e.g. linearity of
relationship, non-correlated variables) are not valid, inappropriate
interpretations are likely [2].
Stepwise regression increases the
complexity; forwards stepwise regression (adding variables one at a time)
and backwards stepwise regression (deleting variables one at a time)
usually produce different conclusions [2]. It is therefore very important
to see the actual raw data in a figure for the univariate relationship
[2]. For example, re-ordering the data of Table 5 shows that Division II
had the least number of teams stretching and the lowest hamstring injury
rate (Division II is more elite than Division III but still had lower
injury rates). What was the actual risk of injury in teams that stretched
and teams that did not (maybe produce 2 different categories for those
that stretched different amount of times)?
The correlations for
warm-up and endurance training were higher than SHT and STE (Table 6, no
correlation for strength training reported) but the injury rates were not
reported. We need to know the coding for stretching technique to
compare the three categories (add a fourth for “no stretching”). The analysis is a linear model and it is not clear why the authors suggest
that stretching be limited to 15-30 seconds.
Finally, the authors cite two studies suggesting stretching is
associated with increased injury only in studies that used multiple
interventions [3,4]. Neither study suggested this, and one [4] suggested
the opposite; stretching was beneficial in a multi-intervention study [5],
but the benefits were likely due to the other interventions.
Given the previous research in this area, the current study design
and lack of patient-level data, and the limitations noted above, it seems
premature to recommend stretching to prevent injury in soccer players.
References
(1). Dadebo B, White J, George KP. A survey of flexibility training
protocols and hamstring strains in professional football clubs in England.
Br.J.Sports Med. 2004;38:388-94.
(2). Glantz SA, Slinker BK. Primer of applied regression and analysis
of variance. New York: McGraw-Hill Inc, 1990.
(3). Gleim GW,.McHugh P. Flexibility and its effects on sports injury
and performance. Sports Med 1997;24:289-99.
(4). Shrier I. Stretching before exercise does not reduce the risk of
local muscle injury: a critical review of the clinical and basic science
literature. Clin.J.Sport Med. 1999;9:221-7.
(5). Ekstrand J, Gillquist J, Moller M, Oberg B, Liljedahl S-O.
Incidence of soccer injuries and their relation to training and team
success. Am.J.Sports Med. 1983;11:63-7.
Pseudo-scientific detection of illusory entities did not end in 1907.
Attributing physical mass to the “soul,” a man-made theological construct,
exemplifies a fallacy Gould attributed to Mill:
The tendency has always been strong to believe that whatever received
a name must be an entity or being, having an independent existence of its
own. And if no real entity answering to the name could be...
Pseudo-scientific detection of illusory entities did not end in 1907.
Attributing physical mass to the “soul,” a man-made theological construct,
exemplifies a fallacy Gould attributed to Mill:
The tendency has always been strong to believe that whatever received
a name must be an entity or being, having an independent existence of its
own. And if no real entity answering to the name could be found, men did
not for that reason suppose that none existed, but imagined that it was
something peculiarly abstruse and mysterious.[1]
Gould cited the fallacy in noting that Benet, originator of IQ, intended
none of the social elitism to which it has given rise.[1] IQ exemplifies
a related fallacy:
The test-trait fallacy begins with the assumption that test scores
are trait measures. The second assumption is that trait measures are
basic properties of the person...This sequence...converts a dependent
variable into an independent variable; hence a measurement is reified into
a causal force...the unsound logic of drawing inferences about ability on
the basis of observed performance is integral to the test-trait
fallacy[2].
Medical test-scores masquerade as traits, e.g., “board-certified
internist,” “Fellow of the Royal College of Surgeons” and the like. Under
aegis of the American Board of Medical Specialties (purveyor-in-chief of
board-certification), Sharp et al comprehensively reviewed as much
evidence from as many medical and surgical specialties as they could find,
in an effort to introduce specialty-board certification to the age of
evidence-based medicine and correlate it with superiority of clinical
outcomes. They failed, yet concluded:
Despite the lack of unequivocal evidence documenting the value of
board certification, we do not advocate removing it as a measure of
expertise.[3]
They thus violated a fundamental scientific and ethical tenet by ignoring
evidence they had adduced. Even more Americans subscribe to the bunkum of
board-certification than to alien-abduction.
References
(1). Gould SJ. The Mismeasure of Man. Norton, NY, 1981
(2). Tryon WW. The test-trait fallacy. Am Psychologist. 1979
May;34(5):402-6
(3). Sharp LK, Bashook PG, Lipsky MS, Horowitz SD, Miller SH. Specialty
board certification and clinical outcomes: the missing link. Acad Med.
2002 Jun;77(6):534-42. PMID: 12063199
I read with interest the article “Extracorporeal shock wave therapy
for plantar fasciitis: randomised controlled multicentre trial” by John
Ogden (Br J Sports Med 38: 382, 2004).
I strongly contradict his suggestion that multiple dosed, low-energy,
non-anaesthetically based treatments [9] cannot accomplish the same
clinical outcome and patient satisfaction as single dosed, high-energy,
ana...
I read with interest the article “Extracorporeal shock wave therapy
for plantar fasciitis: randomised controlled multicentre trial” by John
Ogden (Br J Sports Med 38: 382, 2004).
I strongly contradict his suggestion that multiple dosed, low-energy,
non-anaesthetically based treatments [9] cannot accomplish the same
clinical outcome and patient satisfaction as single dosed, high-energy,
anaesthetically based treatments [1,7,14].
Not a single study has been published directly comparing high-energy
with low-energy treatment protocols for chronic plantar fasciitis!
What is more the alleged efficacy of these single dosed, high-energy,
anaesthetically based treatments have already been discussed in an
exhaustive way by Buchbinder [2]:
Regarding the HealthTronics sponsored FDA trial [7] Buchbinder critizised
that the presence of plantar fasciitis was determined solely on clinical
grounds. It was uncertain whether the 2 groups in the trial were
comparable at baseline. In the “results” section none of 4 success
criteria was statistically significant in favor of the active treatment.
Regarding the Dornier sponsored FDA trial [1,14] Buchbinder wrote while a
statistical significant difference favoring the active group in
improvement of morning pain was reported to be evidence of efficacy of
ESWT, it could be argued that a difference of 0.7 on a 10-cm VAS pain
scale may not be clinically significant. And, there was no statistically
significant difference between groups in the proportion of participants
with at least 60% improvement in morning pain, AOFAS Ankle-Hindfoot-Scale,
and SF12 Health Status Questionnaire.
When discussing a possible working mechanism of shock wave
application it is important to focus not only on differences of shock wave
devices in clinical use. There are also different pathways for the effects
of high- versus low-energy shock waves.
It is important to know that the current literature [5,6,12,13]
indicates that shock waves may selectively lead to dysfunction of
peripheral sensory unmyelinated nerve fibers without affecting nerve
fibers responsible for motor function (large myelinated fibers).
For high-energy treatment with 0.9 mJ/mm², this selective destruction
of unmyelinated sensory nerve fibers within the focal zone of ESWT may
contribute to clinically evident long-term analgesia (5).
For low-energy application with 0.1 mJ/mm², analgesia may be a result
of a shock wave-induced release of neuropeptides, such as CGRP, resulting
in a local neurogenic inflammation in the focal area with subsequent
prevention of sensory nerve endings from reinnervating this area [6,12]. A
second application accentuated these inflammatory changes and therefore
prevented reinnervation [13].
Centrally, the common findings of a reduction in the number of
neurons immunoreactive to CGRP and substance P without a reduction of the
total number of neurons within the lower lumbar DRG probably are a
secondary effect following the (primarily induced) decrease of the number
of sensory nerve fibers in the focal zone of shock wave application. So
the peripheral and central nervous system may both play a pivotal role in
mediating shock wave induced long-term analgesia.
Recently, Wang [15] showed that low-energy shock wave application
resulted in increased neovascularization at the tendon-bone junction in
rabbits. Chen [4] treated rats with a collagenease-induced Achilles
tendinitis with a single low-energy shock wave treatment with 0, 200, 500
and 1000 impulses. Shock wave application with 200 impulses restored
biomechanical and biochemical characteristics of healing tendons 12 weeks
after treatment. However, shock wave treatments with 500 and 1000 impulses
elicited inhibitory effects on tendinitis repair. Together, low-energy
shock wave effectively promoted tendon healing.
In my view it is clear from these experimental data that with
increasing energy applied there is a chance of side effects that my well
inhibit healing of an already diseased fascia or tendon.
It is also clear that even low-energy shock waves may induce a
positive local reaction regarding down-regulation of pain transmitters,
and up-regulation of cell proliferation factors. I am not aware of any
such studies with regard to energy flux densities of about 0.3 mJ/mm² as
used by Ogden [7] or Theodore [14].
Accordingly, I cannot agree with Ogden´s [8] and Theodore´s [14]
statement that high energy shock waves initiate a more effective and
quicker clinical response than low-energy shock waves. I would like the
authors to support this statement with results from experimental studies
or from prospective controlled clinical trials.
I agree with Speed [11] that some regimes of ESWT are a potentially
helpful addition to the options for the management of soft-tissue
conditions such as chronic plantar fasciitis. Like Ogden [8] and Theodore
[14] I am opposed to the opinion of Buchbinder [3]. Contrary to her I
strongly recommend that these regimes of ESWT - producing virtually no
complications, allowing immediate full weight bearing without splints -
should be given priority before surgery [10].
References
(1). Buch M et al. Extracorporeal shockwave therapy in symptomatic heel
spurs. Orthopade 31:637-644, 2002.
(2). Buchbinder R et al. Ultrasound-guided extracorporeal shock wave
therapy for plantar fasciitis: a randomized controlled trial. JAMA
288:1364-1372, 2002.
(3). Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med
350:2159-2166, 2004.
(4). Chen YJ et al. Extracorporeal shock waves promote healing of
collagenase-induced Achilles tendinitis and increase TGF-beta1 and IGF-I
expression.J Orthop Res 22:854-861, 2004.
(5). Maier M et al. Substance P and prostaglandin E2 release after
shock wave application to the rabbit femur. Clin Orthop 406:237-245, 2003.
(6). Ohtori S et al. Shock wave application to rat skin induces
degeneration and reinnervation of sensory nerve fibres. Neurosci Lett
315:57-60, 2001.
(7). Ogden JA et al. Shock wave therapy for chronic proximal plantar
fasciitis.
Clin Orthop 387: 47-59, 2001.
(9). Rompe JD et al. Shock wave application for chronic plantar
fasciitis in running athletes – a prospective, randomized, placebo-
controlled trial. Am J Sports Med 31:268-275, 2003.
(10). Rompe JD. Letter to the editor. N Engl J Med 351: 834; 2004.
(11). Speed CA. Extracorporeal shock-wave therapy in the management of
chronic soft-tissue conditions. JBJS 86-B:165-171, 2004.
(12). Takahashi N et al. Application of shock waves to rat skin
decreases calcitonin gene-related peptide immunoreactivity in dorsal root
ganglion neurons. Auton Neurosci 107:81-84, 2003.
(13). Takahashi N et al. The mechanism of pain relief in extracorporeal
shock wave therapy. Poster # 448, AAOS Annual Meeting San Francisco, 2004.
http://www.aaos.org/wordhtml/anmt2004/poster/p448.htm.
(14). Theodore GH et al. Extracorporeal shock wave therapy for the
treatment of plantar fasciitis. Foot Ankle Int 25:290-297, 2004.
(15). Wang CJ. Shock wave therapy induces neovascularization at the
tendon-bone junction. A study in rabbits. J Orthop Res 21:984-989, 2003.
This a very interesting, but curious,paper.The novel theory
presented, enhanced the CNS as the more important center regulatory of
exercise fatigue, resembles all the research that occupied the minds of
clinical and experimental neuroscience people in regard of pain.
Pain is a reality, an alarm signal. Of course there are many pain
syndromes as diseases by thereselfes, as migraine, cluster h...
This a very interesting, but curious,paper.The novel theory
presented, enhanced the CNS as the more important center regulatory of
exercise fatigue, resembles all the research that occupied the minds of
clinical and experimental neuroscience people in regard of pain.
Pain is a reality, an alarm signal. Of course there are many pain
syndromes as diseases by thereselfes, as migraine, cluster headache,
trigeminal neuralgia, thalamic pain post-stroke, etc., and very important
pain due to other diseases, especially in cancer patients.
Nothing new about the typical pain neurosurgery, as cingullectomy, to
give a better quality of life in terminal oncology people: they continue
to refer pain, but without the limbic system information as these stimulus
is a nociceptive one, the suffering disappear – they points and describe
pain when questioned, but this symptom don’t cause any distress: the
emotional aspect of this form of sensibility was removed.
In another example, people with trigeminal neuralgia can survive many
years with good control of the pain with carbamazepine and perhaps (after
more controlled studies and evidence-based guidelines) gabapentin.However,
the total control of the disease is based in an anatomical question, the
vascular loop around the trigeminal pathway, and the definitive treatment
is the surgery, first performed by Janetta, from Pittsburgh, many years
ago.
After these considerations, the theory explained could reach a danger
level: fatigue is a periphery nociceptive sensation, an alarm signal.
Techniques to reduces or control the CNS role are, in thesis, something
like doping: the athlete could perform better marks, however could be
present a potential risk of damage in the muscles, bones, peripheral
nerves and even in central nervous structures.
The whole thing resembles a different way of Pavlov’s conditioning
methods, with a plausible cause of disease risk to people in good health.
Dear Editior,
I read with interest the Stasinopoulos/johnson article on ECWST for "tennis elbow". I would like to bring to the author's attention our double -blinded, randomized (placebo vs. active treatment groups) study previously presented at the AAOS annual meeting 2003 with 6 month results and at the 2004 meeting with 12 month results. This study has been accepted for publication in the JBJS.
Our s...
Dear Editor,
I read with interest the review of Stasinopuolos and Johnson on the “Effectiveness of extracorporeal shock wave therapy for tennis elbow” (Br J Sports Med 2005; 39:132-139).
I acknowledge their evaluation in terms that the trials from Haake et al. [1] and from our group [2] are by far the highest-ranking publications in this field, while other studies show various major flaws in study desi...
Dear Editor,
I read your editorial 'The power of placebo' with some relief. It would seem that all too often, 'advances' in practice and even research are relegating the placebo effect to the status of quackery. Certainly, I am not a great fan of many therapies or technologies that claim scientifically dubious healing or performance-enhancing qualities (I am to be honest even less of a fan of those who sell them...
Dear Editor,
Having worked in sport's injury prevention with children for the last 15 years and having monitored their evolution in a representative group of about 160 adolescent girls and boys competing in various sports, I can but express a certain amount of frustration as to the results of injury prevention.
Having contributed to introduce and observed changes in, nutritional and psychological counse...
Dear Editor,
Huang and colleagues have prepared an estimate of the cost- effectiveness of the Victorian, Active Script Programme, which they conclude indicates a successful program and one suitable for wider adoption. Confidence in a cost effectiveness estimate depends on confidence in the evidence on effectiveness and costs.
The Active Script Program evaluation was designed to determine up- take of the...
Dear Editor,
Prompted by Lippi & Guidi [1] and their discussion that drugs which modulate hypoxia inducible factors (HIFs) should soon be included in antidoping legislation, is an old argument from my undergraduate days. They state that HIFs stimulate red cell production and so could be used as an athletic stimulant or to treat pathological conditions that involve altered oxygen metabolism. On the flipside of...
Dear Editor,
I recently read the article by Dadebo et al with interest [1]. I am a little confused by their results and their take home message. First, the correlation for SHT is reported as 0.02 (Table 6) and 0.54 (Table 8, one predictor) when the two correlations should be equal [2]. Second, the appropriate analysis is Poisson regression with counts of injuries as outcome and exposure rates as a covaria...
Dear Editor
Pseudo-scientific detection of illusory entities did not end in 1907. Attributing physical mass to the “soul,” a man-made theological construct, exemplifies a fallacy Gould attributed to Mill:
The tendency has always been strong to believe that whatever received a name must be an entity or being, having an independent existence of its own. And if no real entity answering to the name could be...
Dear Editor,
I read with interest the article “Extracorporeal shock wave therapy for plantar fasciitis: randomised controlled multicentre trial” by John Ogden (Br J Sports Med 38: 382, 2004).
I strongly contradict his suggestion that multiple dosed, low-energy, non-anaesthetically based treatments [9] cannot accomplish the same clinical outcome and patient satisfaction as single dosed, high-energy, ana...
Dear Editor,
This a very interesting, but curious,paper.The novel theory presented, enhanced the CNS as the more important center regulatory of exercise fatigue, resembles all the research that occupied the minds of clinical and experimental neuroscience people in regard of pain.
Pain is a reality, an alarm signal. Of course there are many pain syndromes as diseases by thereselfes, as migraine, cluster h...
Pages