Inflammation, Arborization and a Little Heresy

Inflammation is likely the only process that is absolutely essential to our continued existence and, at the same time, a serious source of debility and death. As a culture we spend billions combatting this evil that we couldn’t live without.

In the classes I teach I’m often surprised at the level of understanding that practitioners have (or don’t have) about the nature of inflammation. I don’t know why I’m surprised. I had worked for 26 years largely uninformed about what was happening beneath my fingers. As my awareness has increased, inflammation and its effects have come to represent the largest single obstacle to balanced and fully functioning bodies.

 

The Forces of Inflammation

Inflammation in our everyday awareness is perceived as an event — a sprained ankle, a bout of hay-fever. You fight an infection. It happens for a while, you take some Advil, and then it’s gone. We seldom think of inflammation as an on-going process — that is, until we must deal with sinusitis that won’t resolve or a persistent arthritis. It may be more accurate to view inflammation as a kind of underlying state — controlled at any moment by the balance between the pro- and anti-inflammatory forces at work in the body. The “forces” are actually molecules and their effect is to drive the process forward or to inhibit it.

For many of us the “anti” forces hold sway - keeping the flames at bay - until a time of threat to the body. But that is hardly the case for others. For them the pro-inflammatory processes hold a slight edge, so trivial insults cause a reaction. The role that inflammation plays in the body is something like that of a bouncer in a beer-hall - not very discriminating but able to deliver quite a punch.

There are basically three sentinels which keep track of environmental threats - both external and internal - and which, in coordination with the central nervous system, govern the inflammatory response. They are the immune system, the stress mechanism and the nociceptive fibers of the nervous system. My point is not to inform you of something you may already know, but to identify the players in what is a hugely complex game of the molecular excitation and inhibition that keep our bodies alive long enough to reproduce.

Immune System

The immune system response is the most straightforward. Immune cells encounter a molecule or organism which doesn’t belong and mounts an attack. Several of the immune cells are capable of launching an inflammatory cascade.

Nociceptors

Nociceptive fibers — small unmyelinated fibers which are triggered by noxious stimuli that often is experienced as pain — secrete inflammatory neurotransmitters when the noxious stimulus is noxious enough and prolonged enough. So “pain” causes neurogenic inflammation. And neurogenic inflammation can cause pain. It sometimes seems to be a self-perpetuating loop.

Stress Response

The stress apparatus is more complex. The immune and nociceptive systems activate the inflammatory process. But the primary hormone released by the stress axis, suppresses inflammation, at least in short-term stress. With long-term arousal the picture becomes more cloudy. In long-term stimulation of cortisol receptors, they become desensitized, and cortisol may then promote the inflammatory response instead of inhibiting it.

When there is a breakdown, such as occurs in prolonged stress, we get to see the preemptive nature of these systems. They are each likely to respond first and ask questions later. They provide the possibility of our engaging agents in our environment - external and internal - that threaten well-being. At their most proficient they themselves sometimes can threaten life.

The Mechanism of Inflammation

How does inflammation work? We can talk about systems and mechanisms, but what we’re really watching is a dance of cells

and molecules - excitable tissue getting excited. The cells include white blood cells, the endocrine cells of the hypothalamus, pituitary and adrenal tissues (the stress pathway), the neural tissue of the nociceptors, and the cells that make up the walls of arterioles and capillaries. Cells secrete molecules which target receptors on other cells, which continue the signaling chain.

The first step in the inflammatory process occurs when the appropriate molecules dock with the necessary receptors in the muscles of arterioles, causing them to dilate and the venuoles to constrict - thus pooling the blood in the capillaries. So the first step is a vascular one. The pooling blood, which necessarily slows as it pools, allows white blood cells (immune tissue) to attach themselves to the capillary walls in preparation for leaving the blood supply for the injured tissue. Then capillaries get “leaky”; the cell junctions soften so lymphocytes and the various molecules that make the inflammatory cascade can escape into the extra-cellular space. As smaller protein molecules migrate from the capillary to the extracellular space, they pull fluid with them. As fluid accumulates, particularly in an enclosed space, pressure builds. Pressure build-up in a joint capsule causes problems; in a nerve trunk, it can cause havoc.

The problem with inflammation is not really encountered in the acute inflammatory patterns that we notice when we have an injury. It’s in the long term, often hidden, processes that drag on for years. As an example, periodontitis goes on hidden from any outward manifestation until suddenly the ligaments lack stability. The difficulty in this and countless other examples is the degradation of collagen that takes place as a result of the inflammatory attack. Many cell types release enzymes that in an acute process help clean up debris and damaged collagen. In long-term, low-grade inflammation those enzymes degrade and destroy healthy tissue.

 

Neurogenic Inflammation

In the 1980's research began on what was then a new discovery — that neurotransmitters were causing inflammation at the site of pain. Nerves (in particular the nociceptors or “pain fibers”) are among the major players in producing pro-inflammatory substances and are involved in many of the low-grade inflammatory states that are so prevalent in the population. Immune cells and nerve tissue exchange molecular information continually.

Neurogenic inflammation has been investigated in a wide variety of degenerative conditions from arthritis to inflammatory lung problems to headaches. In the inflammatory process, neurotransmitters are secreted at the distal end of nociceptors. All nerves have the capability of transmitting action potentials in both directions, but only nociceptors make a habit of it. When the spinal cord has been bombarded with nociceptive input for a period of time, it responds by creating a reflex loop which excites the proximal end (the “wrong” end) of the nociceptor. This excitation causes the release of excitatory neuropeptides in the tissue that was injured.

The evolutionary value of increasing inflammation at sites of pain is unclear. The reflex which sends the action potential back down the nociceptor is not very discriminating. Often the signal is sent down fibers on the opposite side of the body or on different levels of the spinal cord. This creates inflammation at sites that were not originally injured. The inflammatory neuropeptides trigger mast cells at the site where they are released, causing the release of a molecule called Nerve Growth Factor (NGF). NGF causes more pain and, it has been shown, causes nerves to grow or “arborize”.

 

Arborization and structural work

Of all the effects of neurogenic inflammation, arborization is one of the more profound. What follows is the result of my own findings and is not supported by independent research that I’m familiar with (mostly because pain researchers don’t actually touch people, and it would likely be hard to palpate nerves on a rat). It is possible to follow the growth of nerve fibers into territory where most people have no palpable nerves. Small cutaneous nerves seem to be the biggest offenders.

It has been well-studied since the early ‘80’s that NGF causes nerves - in particular sensory and sympathetic nerves - to arborize. They’ve even demonstrated that NGF antagonists decrease the sensitivity of nociceptors. So the neural effects of the process are well known. What has not been examined are the mechanical effects of nerve fibers entering new territory.

I began this informal investigation shortly after I had read about the phenomenon of arborization. I had clients with pain patterns that didn’t fit any nerve pathways I knew of. Soon I was able to connect the new patterns to existing nerves. In the first case a tiny nerve from the dorsal ramus of the sacrum had arborized around my client’s hip, over her iliac crest and past the midline in the front. (Imagine a nerve which is typically palpable for 2-3 inches that has grown to 2-3 feet.) Each movement of the trunk caused severe pain along the iliac crest. Excepting trauma, I’d never seen such a pattern. The pain over the ilium decreased and eventually disappeared as I worked the tiny nerve endings on the opposite side of the midline on her lower abdomen.

The second phenomenon I found was that arborized nerves don’t glide. They appear to become anchored in the new area effectively tethering the nerve. This become a problem when nerves cross a joint. Then the tethering creates a strain at the joint whenever the joint is flexed.

 

Neurogenic inflammation and nervi nervorum

The nervi nervorum are the tiny fibers that innervate nerve trunks. Nerve bundles have their own vascular and nerve supply which are sequestered from other tissues by the perineurium (a fascial sheath that creates a water-tight barrier). Several authors have noted that some fibers of the nervi nervorum are nociceptors, which give them the potential for creating neurogenic inflammation inside the nerve bundle. From a practitioner’s perspective that is clearly what happens. Flare-ups with nerve bundles happen with almost trivial insult — like bending down to see what’s in the refrigerator. Such incidents cause a stretch or compression of the nerve bundle and an almost immediate inflammatory response.

In my experience intraneural inflammation is the most obvious and prevalent demonstration of the inflammatory process. I now look for neural inflammation whenever a client complains of a pain without a traumatic origin. And more importantly, work on the nerves confirms this suspicion by providing a reduction in symptoms. The symptom relief follows a somewhat unpredictable pattern but it is a definite phenomenon.

I’m aware that reports of this work strain the credulity of seasoned SI practitioners. I’ve questioned my own findings on a number of occasions. Given what we’ve been taught about nerves as passive conductors, it doesn’t seem realistic that they would have such an active role.

 

The effect on posture

It’s typical to speak about posture as if it were something static. Of course, it’s not static — with the possible exception of lying unconscious. When we speak about posture we’re really talking about the freedom to move and the ability to find equilibrium as we move. The ability to approach equilibrium requires an intact central nervous system,

peripheral nerve tracts and proprioceptive receptors. The freedom to move ultimately hinges on the mobility of joints and thus on the flexibility and responsiveness of tissues crossing the joints.

While the tissues that can inhibit joint movement include muscle, tendons, ligaments, fascia, cartilage and bone, it is the nerves with their layers of fascial sheathing that are the most interesting to me. Nerves have several distinct effects on joints behavior:

Mechanical effect - inflamed nerves resist stretching

Mechanical effect - nerve sheaths become tethered in other collagenous tissue

Mechanical effect - arborization anchors nerves in ways that restrict joint flexion

Neurological effect - stretching or compression causes inflamed nerves to fire and excite muscles controlling the joint.

Nociceptive effect - nociception causes changes at the dorsal root of the spinal cord including inhibition of motor output.

[Note: Regarding arborization and the nociceptive effect, I’ve not seen research support of these points, but the effects are easily demonstrable.]

It’s possible to see that inflammation creates, on the one hand, a hardening and densifying effect in the neural tissue and, on the other, a contractile response in muscles that are innervated by inflamed nerves. The contraction of muscle is caused by ectopic firing (activation of the nerve cell along its axon) and is triggered by inflammatory mediators present within the nerve bundle. The densifying of the nerve limits its stretchability, which limits mechanically but also by creating pain when joint movement pulls it beyond its limits. This is often subtle. People will unconsciously avoid even slight pain if there is a way of changing the movement pattern to relieve it. They’ll change their gait patterns or their way of holding their bodies.

A touch of heresy

The most significant discovery I’ve made recently is the effect of nerves, particularly arborized nerves, on the larger postural patterns we deal with. I’ve been tracking arborization for some time now. I’m continually surprised. It sometimes takes great care to be certain the tissue that I’m following is continuous, because in some cases there are numerous other fibers to differentiate. An example is the nerves behind the knee. Other times an easily palpable nerve will pass through an area where no major nerves are known to travel. The posterior medial border of the calf is such an example. But arborization in this area has a major effect of pelvic torsion.

In the anatomy texts there are no nerves that travel down the posterior surface of the achilles tendon. There is, however, an arborization that occurs there, a tiny cutaneous nerve that extends down the leg from the pelvis and is often responsible for pelvic and back pain — not neurologically responsible, but mechanically. That constant tug can create problems in the sacral plexus and in the balance of the inominates and the sacrum. That one nerve creates an abnormal pull with every step that is taken.

Bold statement:

I’ve not found a pelvic/sacral distortion pattern which could not be relieved by freeing the neural restrictions. I understand that mine is a very small universe. Yet I work with a variety of traumatic and other injuries, and I offer my “bold statement” as an incentive to those who may have become complacent in their understanding.

We’ve been taught that myofascial restriction is the primary mechanical determinant of posture. I think it is time for re-evaluating that assumption. This is not to question the role of the ECM and fascia in the organization of the body, or even to suggest that myofascial strains are not important in the search for postural balance. It is, however, a recommendation that we pay more attention to what tissues that are actually responsible for postural distortion, that we narrow our focus from the broad sheets to those tubes of excitable gel which play a much larger role than we previously thought.

You change structure by either improving the ability to move or by reducing the restrictions to movement. Pretty simple strategy! Working with neuro-fascial tissue the two are accomplished by the same intervention. The intervention, the treatment - so to speak - frees the tethering that limits neural glide and joint motion, and - by reducing extraneous neural input to the muscles - enables them to relax and thus control the joints more effectively.

The technique is simple. You use light pressure and movement to both assess and treat. The light pressure assists in reducing inflammatory pressure and movement helps free the nerve from its tethering. All that is left to understand is where and how much.