Jan Sultan: How did you first become interested in the nerve work?
Don Hazen: Probably my first “niblet” was Robert Becker’s Body Electric, which opened the notion for me that more was happening than our models of neural function explained. A decade later, in chiropractic school there was a lot of buzz about a chiropractor and Ph.D. neurophysiologist named Ted Carrick, who had developed an extraordinary technique for using ordinary environmental stimuli – light, sound, joint manipulation, etc. – to resolve severe neurological problems that the medical neurologists were often unable to handle. I studied his work over a period of four to five years and several hundred classroom hours.
The amount of study required to attain the level of mastery to use Carrick’s work fulltime was beyond me, but I was profoundly influenced by his underlying model: that imbalance in the firing rates of the brain’s hemispheres sometimes produced pathological effects throughout the body. Applying this model led me to a greater understanding of structural imbalances that structural integration (SI) practitioners face everyday. Things like pelvic rotations and many of the left-right imbalances we find are more easily explained and reduced. Brain imbalance, because of the complexities of cortical inhibition of motor output, causes muscles on opposites sides of the body to be excited differentially.
Then in 2004 I discovered, serendipitously, that Jean-Pierre Barral was teaching a class for the American Academy of Osteopathy on peripheral and cranial nerves. I managed to enroll. I discovered, to my surprise, that nerves were palpable and that they were treatable. I wasn’t sure how I would use my new information in my Rolfing practice—except in those obvious cases where people had pain from inflamed nerves. One of my first clients [after the class] had a hallux rigidus (rigid first toe), which resolved easily when I released the plantar nerve. I was hooked.
JS: What would you say are the fundamental concepts that underlie working with nerves in a structural context?
DH: Stretch and glide. Healthy nerves have a couple of properties that are essential to normal movement: the ability to stretch and the ability to glide through surrounding tissue. As joints approach their end ranges, stress is placed on the nerves that cross them – the closer to the surface the more the stress. To appreciate this, consider that the path of a cutaneous nerve traveling over the gluteus must stretch when the hip is in flexion compared to the sciatic nerve that runs beneath it. The mass of the gluteus creates a greater arc.
Tethering: This is often called “entrapment.” I like the term “tethering” because we’re often talking about relative restriction of glide and the summation of several restrictions. A nearby scar can impede a nerve’s glide and can add to other sources restricting it.
Inflammation: Neurogenic inflammation was first examined in the ’80s and has been shown to have a role in everything from headaches to plantar fascitis. Inflammation is the genesis of nerve arborization (growth of inflamed nerves) and neuropathic pain.
Arborization: This is an absolutely key concept, and yet I doubt if there is much or any clinical data to support its existence. It’s a well-known term in laboratory research into nerve behavior, but I’ve never seen it used to refer to nerves in vivo. In the lab, inflamed nerves grow because inflammatory neurotransmitters cause the release of nerve growth factor from local mast cells. I consistently find inflamed nerves that have grown beyond their “usual” length – sometimes by several feet. I constantly test my assumption because it is such a novel idea; and, by extension, the arborized branch will not appear in an anatomy book. Arborization is an important concept because when a growing nerve crosses a joint it is instantly more vulnerable. Each joint it crosses represents an additional demand for the nerve to stretch. Additionally, joints are typically sites for tethering because they often sustain low-grade injuries and the resultant inflammation.
Dorsal Root Reflex: This is the process by which neurogenic inflammation occurs and is perpetuated. It’s important to the understanding of the whole process, though not especially relevant to structural problems.
JS: What is the difference between nerves as transmitters and nerves as structural elements?
DH: Our everyday understanding of the nervous system reflects what I call the USB-cable model of neurology. Nerves hook up various input and output devices to the central processor. They even use binary code. If we want to continue our analogy to structural matters, you can think of what happens when you go to move your computer and the keyboard and printer USB-cables are under a large pile of books. The computer doesn’t budge. If a nerve bundle is trapped in a pile of scar tissue, the joint won’t bend and the limb won’t move.
We’ll have to leave our analogy to see the other structural effects on nerves. For instance, certain nerves, when stimulated by the CNS [central nervous system], produce neurogenic inflammation, which, among other things, causes nerves to be highly sensitized to stretching or compression. (Thankfully, USB cables don’t share that trait.) Stretching the inflamed nerve causes pain, which makes you unconsciously adjust your posture or your movement to minimize even slightly annoying input. (It’s much more persuasive than an error message on your screen.)
In spite of the appearance that computer cables seem to multiply, they don’t actually grow. Inflamed nerves do. In growing longer, they often cross joints, which adds to the possibility of stretching, pain and structural compensation. The joint flexion produces both stretching and compression, which excites the axons in the nerve bundle; thereby generating pain, aberrant sensation, and muscle spasm – hence structural compensation.
JS: What is the function of nerve inflammation?
DH: Nerve inflammation is an unfortunate by-product of neurogenic inflammation, which appears to have a function in the pinpoint delivery of pro-inflammatory agents to an area of pain. But the same neurotransmitters that initiate inflammation in the painful area also trigger an inflammatory response within the nerve bundles themselves. That response is not so useful. Most of the literature deals more with the undesirable effects – effects which include most of the major health threats we face, not to mention the pain that is produced.
JS: What is the physiology of nerve inflammation?
DH: Neurogenic inflammation – of which “nerve inflammation” is a subset – is a process orchestrated by the central nervous system as a response to prolonged nociception (think pain input) from the peripheral nerves. You sprain your ankle. If it doesn’t heal quickly, changes start to occur in your spinal cord, where nociceptors from the ankle synapse with the nerves that carry the signal to the brain.
These spinal cord centers cause a signal to be sent back down the fibers that brought the signal in. This is an example of the dorsal root reflex. The fibers secrete neurotransmitters in the tissue where the signal originated, causing an inflammatory response. That’s annoying enough, but the inflammatory neurotransmitter also gets released in the nerve bundle itself. This is nerve inflammation. In the way the body works, one molecule triggers a cellular response which causes the release of another molecule, which causes another cell to respond.
The inflammatory neurotransmitter causes an immune cell to release a molecule (interleukin 2 beta, if you’re interested) that vastly increases the sensitivity of all the nerve axons in the nerve bundle. All the axons can now fire more easily when stretched or compressed, enabling you to have more pain and increased spasm.
JS: Why does it persist when no longer necessary?
DH: Once nerve inflammation gets started, it tends to be self-perpetuating unless it’s interrupted. The inflammatory process promotes pain, and pain causes more inflammation. Nice process.
JS: What actually happens to an inflamed nerve that makes it important to structural integration?
DH: Nerves get inflamed all the time. This usually resolves spontaneously. On practically any client on any day, it’s possible to find nerves that are inflamed and tender to palpation. The client may not even be aware of the area until some movement causes stretch or compression that fires the nerve. But here is one very innocuous piece in the puzzle of human structure. Bodies try to minimize pain – even pain which is below the threshold of consciousness.
At the most elementary level. this behavior is important in SI because it often leads to compensatory patterns. There’s more. As inflamed nerves swell, they lose their ability to stretch. This restricts the range of motion at joints. While nerve fibers themselves are microscopic, gel-filled tubules, each fiber is loosely wrapped in fascia, and each bundle of nerves is sheathed in a denser, water-tight fascial layer called the perineurium. The perineurial layer protects the nerve from ions, immune cells and organisms that populate the extra-cellular matrix. It also contains the inflammatory fluid. Under normal circumstances nerves stretch and glide through the muscles and around bone. When inflamed they are limited. Therefore, the joints they cross are limited.
But the biggest problem I encounter comes from the fact that inflamed nerves grow and then become tethered in scar tissue particularly in areas of high mechanical activity – like joints. Whenever nerves are tethered, the motion at the adjacent joints then becomes restricted. An example is what is commonly thought of as tight hamstrings. It is more often a tight posterior femoral cutaneous nerve which has become tethered behind the knee. Where the nerve crosses the ishial tuberosity it gets compressed, generating pain. One of the hallmarks of integration has to be joint mobility. That hallmark is lost in a body with extensive neural inflammation.
JS: What are the properties of nerves that you have found to be important enough to devote your practice to studying them?
DH: This has been a process of “un-covery.” The first stage was surprise and excitement to find the ease with which structure and function changed with work on nerves. I set about to find out the limits of this way of working and would sometimes have three anatomy books on the stool next to me. Then I began to find nerves that weren’t in the anatomy books and which had even more profound effects. Large diameter nerves began to show up in areas where no large nerves were listed. They would interconnect with other nerves in ways I hadn’t anticipated.
I spent essentially two years evolving a technique. I was aware that I was leaving behind the nuance and subtlety that I had learned in the previous twenty-five years as I struggled to get some mastery over this unruly subject. I worried that I was becoming a technician – that nerves were becoming my answer to every condition.
Slowly, I began to bring my earlier way of working back into my work with nerves. In the process was a delightful “re-covery.” I’ve long had the ability to sense, with my own body, areas of difficulty in clients’ bodies. They’ve mostly been vague and ill-defined. Suddenly I noticed I was picking up sensations with much more clarity and precision, and that I could tell before even touching the client which nerve was involved and how far it went. Perhaps nerves have a more defined electromagnetic field. I don’t know, but it leads to surprising accuracy.
I have little idea where this will lead. After five years of immersion, I’m now looking to find places of integration with other modalities I’ve used, e.g. cranial and visceral work, and points of contact with the work of others, such as Peter Schwind’s book.1 I am perpetually looking for conditions where nerves are not the primary source of distortions. Thus far, osseous malformations and traumatic and surgical disruptions of the fascia seem to be the only ones. Even scars, where the myofascial mobility has been compromised, appear to have most of their effect because of nerves that are entrapped.
JS: What is the value of symptom relief in the context of Rolfing?
DH: Here I will suggest that not only is the symptom no longer something to ignore, the symptom becomes critical to the process of unraveling the biomechanics. I am also getting close to suggesting that chronic pain generally is caused by, or related to, inflamed nerves. I know! It sounds that way to me, too!
This, of course, is an incredibly complex question. We’ve been warned, over the years, about treating symptoms and “chasing the devil” and been admonished to “go where it ain’t.” This makes perfect sense if the model you choose is one where symptoms are the result of strains in the myofascial system. Most likely they are sometimes. If the reign of pain comes mainly from the strain, it is useful to look at the larger structure for biomechanical imbalance.
If, however, the source of the symptom is the same tissue as the biomechanical restriction, we need to draw different conclusions. Now the symptom is a piece of information at the same level of usefulness as the visible biomechanical imbalance is in the former system. In this model, what causes the pain is the result of intraneural inflammation within a particular nerve bundle and the heightened sensitivity that inflammation causes in axons within that bundle. If you follow the course of the nerve, you will typically find the nerve tethered at a joint sometimes three joints removed from the site of the pain. It is a nerve that has lost its ability to stretch and glide, and the pain comes from compression at the site of the bony or ligamentous ridge, which causes it to fire. Accordingly, low back pains may have their origin in a tethered nerve in the knee or even the ankle. This inverts the typical clinical relationship where injuries in the back produce symptoms in the feet. Obviously, these also occur though not nearly as frequently.
Pelvic rotations and sacral misalignments also follow this pattern. There are two or three nerves that are always involved in pelvic distortions, and releasing them levels the pelvis every time. I have not worked with a single SI [sacroiliac] joint problem since I began working this way. This is not to say that clients don’t have pain around the SI joint nor that sacral distortions aren’t problematic. Thus far, the distortions at the SI joint have been directly related to neural tension; and the pains more often are the result of inflamed nerves descending from the back. It used to be that I was working on sacral problems several times a week, which I would resolve with osseous manipulation. Sometimes the pain comes from dorsal sacral nerve roots, which are stretched by sacral malposition, but that malposition itself is relieved by addressing nerves that innervate pelvic floor muscles.
I realize I haven’t quite answered the question. The symptom isn’t important because it hurts – except, of course, to the owner of the body. It’s important because it is indicative of an inflamed nerve, and the inflamed nerve is typically also a tethered nerve. The tethered nerve more than likely has biomechanical sequellae – either by direct mechanical restriction of neurofascia, by firing motor neurons that excite muscles that cause the joint to flex, or by generating pain, which causes avoidance behavior.
The inflamed nerves, by themselves, cause significant postural distortions. I’ve been working with a number of scoliosis sufferers. I’m perpetually surprised and delighted by the results of working only on nerves – in this case the dorsal rami of individual vertebrae. The dorsal rami (the tiny nerves that innervate the posterior area of the spine) at the apex of scoliotic curves and at the transition of the curves are always “hot.” Reducing the inflammation in these tiny nerves affects the segment in a way that it reduces the sidebend. Don’t ask me “how come?”
JS: Traditional Rolfing is known as a very direct method of intervention, stressing fascial differentiation and education. Over the years, the system has been informed by studies in parallel disciplines, like craniosacral therapy, visceral manipulation, deepening understanding of biomechanics, and ligament function. Where does neural manipulation fit into the technologies that support the basic concepts and goals of Rolfing?
DH: As I approach it, I don’t think of neural work as a parallel discipline to Rolfing. At times I think that what Rolfers have been doing over the years has been neural work without being aware of it. I know I don’t have widespread support in that point of view. Many of the places that are popular for creating change in Rolfing are the habitat of important nerves. The TFL [tensor fascia lata] is home to the lateral femoral cutaneous nerve. The medial border of the ischial ramus houses the pudendal nerve, which is vitally important to pelvic floor tone and balance. The list goes on.
I use the neural approach to accomplish the goals of Rolfing as I’ve understood them. I find I am much more effective approaching the structure from the model I’ve outlined in this interview than I was before I began this journey. Of course, I was never tested to see “how good a Rolfer” I was before I started “nerve futzing” (as one of my clients calls it), so this is a subjective perspective.
For me this is not, in any sense, a “nerves versus fascia” debate. Nerves live in the extracellular matrix. They are sheathed in several layers of fascia. Nerves, like all the cells of the body, are in perpetual participation with the matrix. You mention fascial differentiation in your question. A large part of the neural work is to differentiate neural fascia from surrounding myofascia, periosteum, peritoneum, and so on. That said I think that in the current fascination with fascia, some writers have assigned to fascia functions which may better belong to neural tissue.
If you would like more detailed information, I recommend you visit my web site where I have several articles addressing these subjects, at http://dhazen.com/Articles/AbouttheArticles.html
The Neurology of Posture[:]