How can trauma be stored in the body’s tissues (Part 1)?

On Rolfing sites and in books on structural integration, you’ll find countless claims about “trauma being stored in our tissues.” For some, this can be a hard pill to swallow – it was for me – but neurobiological investigations bear out this metaphorical claim. New tools to investigate the mechanisms involved in the experience of pain are yielding some surprising (or perhaps not so surprising) insights.

In Part 1 of this investigation, we’ll look at how simple physical trauma can be stored in the body. In Part 2, we’ll look at the emotional side (though from the perspective of monism, there really is not much of a difference…).

The processes by which physical insults can be stored have been painstakingly mapped out in recent years by neurobiological researchers. (I’ll spare you the chemical details, but for those looking for the chemistry involved, please click through to the studies referenced at the end the of this post.)

There is a kind of specialized nerve ending known as a “nociceptor.” Nociceptors are found in cutaneous (skin), muscular, and visceral tissues, and are responsible for reporting high threshold “noxious” stimuli. Nociceptors are sensitive to both thermal and mechanical forces. They come in two primary types, A∂ (A-delta) and C fibers.¹

When A∂ fibers are triggered, you feel sharp, incapacitating pain (known as “first pain”). A∂ fibers are myelinated, meaning they have a coat around them that helps their electrical signal travel faster to the brain. They require high threshold input to be activated (pinching, strong pushing, pulling).

When C fibers are triggered, you feel aching and burning (known as “second pain” or perhaps as the pain you feel chronically in your lower back or your shoulder). C fibers are unmyelinated and have large receptive fields (they collect information from larger surface areas than A∂ fibers), so their electrical signals take a much longer time to arrive and the specificity of the information they report is fuzzier. They also outnumber A∂ fibers in the skin.¹

Dr. James Giordano of the Georgetown University Medical Center wrote in the Pain Physician in 2005, “Traumatically acute and prolonged durable pain can produce functional changes in peripheral and central nociceptive neurons that may lead to sensitization, structural modification, and long-term potentiation.”²

Basically, if it hurts bad enough and/or long enough, it can leave a lasting mark and make it easier to get worse!

How does it happen?

Since Rolfers don’t use blowtorches or liquid hydrogen in sessions and most people generally have impact-related trauma, let’s talk about the mechanical forces with relation to nociceptors and not the kind of pain triggered by thermal input.

High threshold (strong) mechanical input distorts collagenous elements that connect the nociceptor nerve endings and the surrounding tissue matrix. When that happens, it produces a cascade of chemical reactions that results in the firing off of a signal of “pain” and can lead to sensitization of the C-fibers in the affected area (i.e. the threshold before the nociceptors signal pain is lowered).²

Sensitization results from the chemical products of the inflammatory response, and more pain signaling from the C fibers results. This encourages a chemical chain reaction in which more pro-inflammatory products are released into the affected area which leads to the signaling of pain. This is a perpetual loop of pain signaling and tissue inflammation. The threshold for pain signaling through the C fibers is continuously lowered, causing an inflammation response, and the products of the inflammation response cause further sensitization of the C fibers which means more pain signaling.^{2, 3}

The injured tissue, in a constant state of sensitized inflammation, cannot heal properly, and — voila! — you have a physical trauma “stored” and recapitulating itself in the body’s tissues. You feel the aching and burning (those C fibers at work!), and your Rolfer feels the inflammation in the tissues. When your Rolfer contacts those tissues — even gently — you might feel intense pain because the nociceptors have been hypersensitized.

Luckily, the hypersensitivity isn’t permanent and can be deprogrammed. I’ve helped clients with this, and I know others do too, but there isn’t any research out there that I know of that exactly explains how it works on a cellular or molecular level…yet.

Update: I got your mechanism for breaking the inflammation chain right here (at least part of it)! Dr. Paul Standley, PhD. of the University of Arizona College of Medicine studied the effects of myofascial release techniques (those used typically in Rolfing and osteopathy) on a cellular level and found that modeled myofascial release techniques decrease inflammatory cytokine secretion and increase anti-inflammatory cytokine secretion.⁴

¹Biology and therapy of fibromyalgia. Functional magnetic resonance imaging findings in fibromyalgia

²The Neurobiology of Nociceptive and Anti-nociceptive Systems

³Marked attenuation of inflammatory mediator-induced C-fiber sensitization for mechanical and hypotonic stimuli in TRPV4-/- mice

⁴Development of an in vitro biophysical strain model of tissue injury and osteopathic manipulative treatment. J. Am. Osteopathic. Assoc. 106(3):157-66, 2006