Author’s note: If you haven’t read the original post (The Magic Show), you may wish to before continuing on. The post will provide a background and basis for this series on passive modalities.
Part 4 of the passive modalities discussion will cover instrument assisted soft tissue mobilization (IASTM). This is the modality that the after effects are often displayed as a badge of honor on social media, but leaves us wondering if the person was a trauma victim or merely a trauma recipient. Clinicians today discuss the modality based on its ability to scrape, break-up, emulsify, release – almost any verb imaginable related to fascia, muscles, or other soft tissues. But does this modality really do anything? In this blog we will dive into the history and research of IASTM to find out.
IASTM isn’t new. Like most things, there are no new ideas – just rebranded and repackaged marketing ploys. Utilizing tools on soft tissues has historically been prevalent in East Asian medicine via the technique known as Gua Sha. The tools have been updated, and a bit more radical, but the premise is the same – expel blood stasis. Typically composed of various materials, the tools are placed on lubricated skin and then dragged across an area in several passes.
The original thought process was to treat issues by eliciting petechia and ecchymosis thus improving blood stasis. This is a nod to the homeopathic roots of treatment where like treats like. If “bad blood” is what causes the issue then “new blood” should cure it. This is grossly unsubstantiated in the literature. Gua Sha was advertised to treat a variety of issues, such as: pain, colds/flu, respiratory problems (asthma/bronchitis), musculoskeletal issues, and other internal organ related functional problems. Recently, the focus has narrowed to only musculoskeletal issues, but any support for its efficacy there is still lacking.
There are a plethora of case studies arguing for the efficacy of IASTM. But when we consider stronger level evidence (RCTs and systematic reviews) the modality’s ineffectiveness becomes more apparent. Much of the research originated from rat studies in the 90s focusing on tendinopathies.
3 studies in particular (Davidson, Gehlsen, and Sevier) form the foundation of IASTM research.
Davidson et al and Gehlsen et al both studied the effects of IASTM on rat tendons after inducing achilles tenindopathy. At the time, their results were promising – indicating increased presence of fibroblasts (indicative of remodeling the tendon). But newer research elucidating the topic shows their premise (fibroblast proliferation) was based on a false pretense from the outset. Articles like this one by Xu Y et al., demonstrate the hallmark sign of tendinopathy is increased presence of fibroblasts. Any study using increased fibroblasts as an outcome measure for healing in tendinopathy research is most likely flawed due to the physiological principles we now know about tendinopathy.
Gehlsen also attempted to identify various pressure effects of IASTM on healing parameters. They identified extreme pressure (1.5 N·mm−2) as having the greatest increase in fibroblasts. But 1.5 N·mm−2 equates to 217.557 pound-force per square inch and based on what we know from Chaudhry et al – this is nowhere close enough force to effect human tissue. It is also drastically more pressure than the average force applied by a clinician when utilizing the technique.
Sevier et al – attempted to compare IASTM to “traditional” physical therapy in the treatment of lateral epicondylitis. Two groups were studied: traditional PT group of phonorphoresis with hydrocortisone + cross friction massage vs non-traditional IASTM group. As a relevant aside, phonophoresis’s ability to disseminate hydrocrotisone was later debunked as not actually improving absorption when compared to sham (see Gurney et al.).
Several issues cause concern with this study:
- Both groups received multiple interventions in addition to their assigned group interventions (cold pack, stretches, progressive resistive exercises, and HEP)
- The authors delivered both protocols (risk of personal bias)
- Allowed for a crossover of treatment groups
- Both groups improved – more support for almost anything works in short term.
Given the knowledge we had at the time, some of the IASTM research appeared promising in its infancy stage. Unfortunately, before the research could progress to adulthood, special interest groups began manufacturing tools and teaching continuing ed courses. Now 20 years later we are beginning to debunk the modality – slowly.
Newer RCTs are emerging like Crothers et al , demonstrating IASTM to not be better than sham.
And most recently, a systematic review by Cheatham et al stated IASTM lacked efficacy for certain musculoskeletal issues. The authors discussed the gap between current research and clinical practice stating,
“The current evidence seems to lack the methodological rigours necessary to validate the efficacy of IASTM itself or any of the IASTM protocols.”
Overall, the evidence is lacking for the use of IASTM in clinical practice.
To better understand why the modality is still being used today, we must examine the rationale for its use.
Often our own desire to set ourselves apart as clinicians, to offer a unique experience to our patients, drives us to seek what is different. Ultimately, what should drive treatment is not our desires but those of the patient to get better.
Citing the use of IASTM for pain, performance, myofascial trigger points, scar tissue, adhesions, and inflammation provide elaborate narratives, but these explanations of physiological effects and proposed mechanisms for improving function while decreasing pain remain unsubstantiated in the research literature.
When we examine the rationale little to no substance is provided for these narratives.
We can’t even decide if MFTP actually exist (Quintner et al) or are a pathology when they apparently are readily identifiable in asymptomatic populations. Even if they do exist, evidence shows poor reproducibility to identify them (Myburgh et al & Wolfe et al). Adhesions have yet to be substantiated in the musculoskeletal world. Admittedly they are a cause for concern in automimmune issues, abdominal surgery, and pelvic surgery. But those scenarios exceed most of our scopes. Inflammation is an odd duck as most can’t decide if they wish to increase it or decrease it. Either way, a 2015 study by Vardiman et al discovered via biopsy that IASTM has no intramuscular effect. The authors biopsied healthy subjects 24, 48, and 72 hours post-IASTM for Interleukin-6 and Tumor Necrosis Factor – alpha (pro-inflammatory markers) and found no significant difference. They go on to demonstrate IASTM does not improve functional abilities either. Performance doesn’t seem to be effected either per a study by MacDonald et al.
On to the most fun discussion of all – pain reduction. As cited above, IASTM doesn’t appear to be better than sham. More importantly, research continues to elucidate pain is a multifactorial issue that can be altered by many methods such as setting patient expectations, as discussed by Schwarz et al, Freeman et al, and Peerdeman et al. Most likely the case studies reporting reduction of pain and improved function are due to the clinician priming the patient the intervention will help (setting expectations) and regression to the mean.
Lee et al attempted to examine the effects of Graston on chronic low back pain and is a good example of the illusionary healing effects a modality can have on chronic pain management without consideration for regression to the mean or dependency created on a clinician.
Regression to the mean is discussed quite a bit today but it warrants a brief overview.
An old but good paper by Whitney et al discusses the topic nicely. The authors reference temporomandibular disorder as it relates to chronic pain.
“Like many other pain conditions, the course of temporomandibular disorder (TMD) pain is episodic. Thus, the level of pain at any single point in time does not indicate where individuals are in relation to their characteristic level of pain (or across-time central tendency). The present status of a person in their cycle of pain, along with the variability and central tendency of their cycle, determines the potential magnitude of change in the level of pain between the present and some future point in time. The likelihood of a change of a particular magnitude is determined by the proximity of the initial measurement to its characteristic level. The closer the level of pain is to an extreme of an individual’s across-time distribution of pain, the greater the likelihood of the next measurement being less extreme. In statistical terms, this phenomenon is known as ‘regression to the mean’.”
In case that wasn’t crystal clear, they elaborate:
“That is, a variable that is extreme when it is measured will tend, by chance alone to be closer to its central tendency on a subsequent measure. Studies which base subject selection on the outcome variable of interest, in this case pain, are at risk of inducing this phenomenon. As a consequence, if someone seeks treatment when their level of pain is at its peak, then pain can be expected to decrease towards its characteristic level whether or not treatments are given. Similarly, if someone is experiencing the lowest level of pain in their cycle, then an increase in pain would be expected.”
How does this apply to clinical practice?
Patients who seek out treatment for a painful issue typically do so when they are having an episode/flare-up or when the pain exceeds their subjective tolerance level. If a patient’s pain level and behavior (seeking treatment) are correlated then the patient and clinician’s observation of treatment efficacy may exceed the treatment’s true effect. In other words – the treatment may have an out of proportion representation of its effects if applied at a particular point in the pain cycle that would lead to a natural regression of pain anyways (think of this as a typical day in the clinic). Things become even more convoluted when we make baseline measurements of various performance based tasks and attempt to pin any deficit to a perceived structural abnormality (like MFTRP or adhesion). Most likely these subjective – objective measurements would improve on their own but we tend to think our intervention (in this case IASTM) improved our baseline measurements. This rationale is the number 1 reason we require RCTs – otherwise we think everything we do has an effect. The RCTs help identify what treatment is actually reducing pain/improving function and what is simply due to cyclical variation of pain.
Keep in mind the body is constantly fighting for homeostasis i.e. regression to the mean, and since we can’t expedite the healing process we can simply foster it while ensuring patients remain calm. Preventing catastrophizing and altering patients’ beliefs are some of the biggest components of our jobs..
Back to Whitney’s experiment. The authors decided to measure the magnitude of regression to the mean. They devised a RCT where patients seeking treatment for TMD pain were placed in one group and compared to patients surveyed for the same pain but not seeking treatment. The two groups were followed-up 1 year later. At this point, most can expect what the authors found:
“Thus, an appreciable reduction in pain intensity occurred in patients not seeking treatment when they were sampled on the same basis as patients entering treatment.”
The authors conclude how clinicians can use the regression to the mean phenomenon to patients’ advantage:
“Among patient groups in whom significant regression to the mean occurs, the natural process of improvement may provide opportunities to reinforce patient self-care behaviors and enhance patient beliefs in their own abilities to control pain, rather than reinforcing patient beliefs in the efficacy of medical care for chronic pain. If so, the phenomenon of regression to the mean may have the potential to enhance patient autonomy in managing chronic pain just as it may now contribute to the dependence of pain patients on health care providers.”
Applicable even 25 years later, and yet we still struggle to heed their words of wisdom.
Oddly enough, when IASTM is done on healthy individuals (like in Vardiman – referenced above) pain increased post-IASTM and function decreased for 10 days.
Poorly designed and executed randomized studies singing the praises of IASTM are not lacking either – for example Sevier & McMorack. Many either fail to use a true control group (not receive an intervention), utilize too short of a study design, small sample sizes, don’t account for regression to the mean, and overinflate their conclusions and effectiveness of IASTM.
Overall, a butter knife is best used to spread butter, jam, or (my favorite) peanut butter on some tasty treat. We have far better evidentially supported options to choose for our patients, such as education and therapeutic exercise.
Without valid understanding of the intervention’s premise and capabilities to treat a patient’s issue, the clinician is left stabbing in the dark with their IASTM tool of choice all the while increasing patient cost for treatment while possibly driving a nocebo effect and unnecessary dependency on an inefficacious modality. We can do better.
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