Reflection on IASTM/scraping theory

Background:

With gentle pressure, the skin should glide in all directions with varying amount of give (I like to compare affected side to unaffected side when assessing skin mobility). During this assessment, is important to completely relax the underlying muscles, because muscular contraction has been shown to significantly decrease skin glide (studied in the spine1.) The most common causes of decreased skin mobility I see in an orthopedic setting are scars, wounds, and swelling. Even when the swelling decreases and the incisions heal, decreased skin mobility can persist, accompanied by patient reports of tightness when trying to move nearby joints.

Anatomy:

Skin sits on top of fat cells, and deep to these cells is a layer called the superficial fascia which is loosely connected to the skin by little ligaments called the retinaculum cutis superficialis. These structures form a latticework for small nerves, blood vessels, and fat cells.

Scraping:

One of my favorite treatments for increasing skin mobility is instrument-assisted soft tissue mobilization (IASTM) or "scraping." A variety of companies sell smooth metal tools for this technique, but I have applied these techniques on my family members with a rounded silverware handle in a pinch.

IASTM has been a treatment I've subscribed to since my first clinical instructor had me feel a before- and after- anterior tibia that he treated with a scraping tool. If you've used an IASTM tool before you probably know the transformation I am referring to-- from the beginning to the end of the treatment, the tissue feels less "lumpy" as the tool glides over it. It's super satisfying, and the patient usually feels less focal tightness after. This was all the clinical reasoning I needed to use this method for a while. The palpable tissue quality completely changes after a few minutes of gentle pressure.

More recently, my biggest challenge had been wrapping my head around what exactly is happening physiologically with scraping-- especially as PT myth-busters on social medial speak out against these techniques, citing the strength of cadaver fascia as a reason that traditional "myofascial mobilization" explanations fall short. If I understand correctly, the main findings cited are that fascia is very difficult to passively deform (although in-vivo fascial stretching/ changes in neuro reactivity are concepts I would love to learn more about before I completely dismiss the concept).

If I concede that I am not stretching the fascia to gain this mobility, I would hypothesize that IASTM is instead increasing the capacity for independent movement between the dermis and the subcutaeous/superficial fascia layer.

But what are the lumps I feel with the tool? Going into upper extremity dissection (an awesome perk of my residency program) last week, that was one of the big questions I wanted an answer to.

My proposed answer-- especially after looking at the relatively fresh cadaver on Friday -- is that those lumps are fat pearls. "Fat pearl" is a term I am borrowing from the literature about liposuction, and is defined as the units of subcutaneous fat visible on dissection. Looking at the tissue layers beneath the skin, the small fat deposits were the size and shape of the lumpy tissue I have been feeling.

Because there is little chance I am playing any role in the "breaking up" of fat beneath the skin, perhaps that is the terminology we need to ditch. Those lumps are there before IASTM, and they are there after. What we can feel is that IASTM tools are pushing on these structures, and that little by little the tool no longer bumps over them. So here's my IASTM theory:

(1) the tool "bumps" over subcutaneous fat pearls

(2) in many parts of the body, subcutaneous fat is mobile enough that gentle scraping will push it through space independently of the skin above it

(3) in areas of inflammation or history of injury/immobility, the connective tissue scaffolding holds the subcutaneous fat more firmly in place in relation to the skin (as compared to the unaffected side)

(4) the superficial fascia - fat - skin layers move with some independence from each other when our joints move; increased adherence of these layers can contribute to feelings of tightness with gross movements

Beyond the above tenants, the actual source of "adhesion" could involve decreased mobility between any of the following structures:

• the collagenous membrane that encases fat pearls

• the retinaculum cutis superficialis (skin ligaments connecting the superficial fascia to the dermis, hypothesized in the dermatology world as playing a role in wrinkle formation)

• the connective tissue of the dermis

• the superficial fascia itself

• other structures that I have not considered

Clinically, the exact cause doesn't make too much of a difference to me, except to increase the evidence behind a tool that I find clinically useful. Browsing through the literature, it looks like we have ways of generating stress/strain curves for skin mobility with a vacuum pump1 -- or even with measurement of skin glide of a marked point. If anyone knows any labs/schools doing this type of research, I feel like an IASTM before- and after- skin mobility (and adjacent joint mobility) would be interesting to look into.

Is it possible that IASTM affects deeper tissues as well? Sure! Might muscles move better if there are more layers of mobile tissue above them? Sounds reasonable. As I briefly alluded to above, there are definitely clinicians out there that propose a neuro-modulatory connections as well. This article is really conglomeration of my anatomy understanding and my clinical ponderings. If you are reading this and have a clarification, objection or question, feel free to comment below! I am very open to learning more about these structures and tools. I also haven't tracked back to the companies that sell these tools, I imagine they have more to add to my understanding!

1. Hirschberg GG, Fatt I, Brown RD. Measurement of skin mobility in the upper back. Scandinavian Journal of Rehabilitation Medicine. 1986 Jan 1;18(4):173-175.