Hip and foot pain and the link between hyperpronation and sciatic pain
THE TERM “SCIATICA” IS A DESCRIPTION OF A SET OF SYMPTOMS, NOT A DIAGNOSIS, as Janet Travell, MD, the creator of trigger-point therapy, pointed out in her seminal Trigger Point Manual. Unfortunately, a web search of the term “sciatica diagnosis” will reveal a confusing array of conflicting viewpoints among medical professionals, in addition to the connection between hip and foot pain. Most promote the assumption that sciatica implies a compromise of the sciatic nerve in the form of a radiculopathy or entrapment — in other words, a diagnosis of disease or injury.
My term for this pervasive worldview is “injury-centric” thinking. This view assumes that pain originates with injury or disease within physiological structures such as joints, nerves, tendons or bursa, usually near the site of the perceived pain.
Radiating pain as seen in sciatica is commonly ascribed to impingement or entrapment of the sciatic nerve, or possibly an injury to the IT band or other structures. The assumption is that pain originates in the injury, and pain signals travel from the injury as an input to the brain — in other words, pain is an “outside-in” experience.
Modern neuroscience has thoroughly debunked this model, yet it persists throughout our medical system and popular culture. V.S. Ramachandran’s work with phantom limb pain is very instructive for understanding the origins of pain. Phantom limb pain is felt as if it is within a limb that has been removed. He found that by introducing a mirror box, which reflects the existing limb on the other side of the body, the visual evidence of the missing limb still being present stops the pain in many cases. In Ramachandran’s words, pain is an output, not an input.
Lorimer Mosely, PhD, worked with Ramachandran during his phantom limb research, and has become a major voice in modern neuroscience. Mosely points out that “soft tissue damage is neither necessary nor sufficient for the experience of pain.” The brain doesn’t receive pain signals; it monitors nociceptive (danger) signals from the periphery and then decides “is this dangerous, really?”
Pain can be seen as a warning signal from the brain that some attention must be paid to a perceived injury. And in some cases, there is a real injury or physiological disturbance setting up nociception — but these cases are in the minority, and a far more frequent nociceptive source is trigger points in muscles.
Trigger points and nociception
Travell’s work presented numerous examples of muscles that commonly develop trigger points and whose referral patterns mimic virtually all of the symptoms ascribed to the sciatic nerve. Our work has shown us that most sciatic pain finds its origins in muscles with trigger points.
Jay Shah, MD, of the National Institutes of Health has shown convincingly that trigger points are potent sources of nociception. He introduced microtubules into the trigger point area and withdrew ambient fluid, finding that it contained many of the same nociceptive compounds as would be seen at the site of actual tissue damage. Yet trigger points are not injuries and can be resolved relatively easily. They tend to develop under conditions of acute or chronic overuse, which can tax local metabolic and vascular exchange, resulting in trigger point development.
Pain referral is a confusing phenomenon that is seen when trigger points are sufficiently active to rise above a threshold, producing an experience of pain that is frequently far from the site of the trigger point. In their work, Travell and Simons documented the direct referral patterns of a wide array of muscles. As a relevant example, trigger points in the gluteus minimus can produce all or part of a pain pattern that includes gluteal and sacral pain, often radiating down the posterior or lateral leg as far as the foot and ankle. Because of its resemblance to the dermatomal distribution of the sciatic nerve, this referral pattern of hip and foot pain is often assumed to be radiculopathy or entrapment of the nerve.
However, gluteus minimus sciatic referral is such a common phenomenon that Travell and Simons nicknamed this muscle “Pseudo-sciatica.” Gluteus medius is commonly co-involved, potentially adding low back referral to the mix.
Hip and foot pain: chains of muscle pain
Simple direct referral from a single muscle is quite rare — more often, a pain report involves many muscles. Some of them operate silently, contributing to patterns of satellite referral, in which one muscle’s referral pattern overlays the trigger point area of another muscle, causing it to develop its own trigger points. These chains can be several muscles long. The patient may experience only the referral of the last muscle in the chain.
While satellite referral sounds mysterious and confusing, it is a real phenomenon that we have found to be extremely important in 20 years of clinical experience. Satellite chains were sparsely documented in the original trigger point literature, but the authors did observe and mention it in isolated cases. We have also documented many recurring patterns that set up many of the most common pain complaints seen in a clinical practice.
Sciatic pain is a prime example. The gluteus minimus pattern crosses many muscles as it proceeds down the leg, including the quadriceps, hamstrings, adductor magnus and many muscles of the lower leg. While it is tempting for a practitioner to focus on tender areas in one of the terminal muscles such as vastus lateralis, this can be a profound waste of clinical time if the vastus lateralis is being set up by satellite referral from the gluteus minimus.
In addition to satellite chains, functional relationships between muscles must also be considered in finding the true source of pain. The CNS is constantly monitoring the relationships of muscles to their antagonists so that it can produce smooth, coordinated motion at each joint. Due to this close coordination, trigger point dysfunction in a muscle often encourages dysfunction in its antagonists.
Author and physiotherapist Leon Chaitow pointed out that the taut fibers seen in muscles with trigger points could have a useful role in that taut fibers are full contractures of individual fiber bundles and can simulate the stabilization ideally provided by ligaments and other connective tissue. It is my premise that the CNS may introduce taut fibers as a means of adding stability to a joint perceived to be unstable, due to factors such as hypermobility or muscular imbalance.
For this reason, one of our clinical approaches is to “hack the CNS,” downregulating it via various methods of neurological distraction and providing an experience of pain-free motion in an area that has been splinted by taut fibers in opposing muscle groups.
Hyperpronation and leg length
Hyperpronation at the ankle is essentially a failure to provide adequate stability in the ankle and foot due to lax ligaments. We have observed this condition to be widespread in 20 years of clinical practice, particularly in sciatic pain patients.
A hypermobile subtalar joint will tend to allow the femur and knee to drift valgus due to collapse at the arch. The leg abductors, including the gluteals and TFL, are a primary means of preventing the valgus drift by bracing the leg with abduction. Chronic over-engagement of these muscles during gait is an ideal environment for creating trigger points, resulting in a composite referral pattern that can include many of the symptoms of sciatica: low back, sacral and gluteal pain and radiation down the leg.
Effective leg length discrepancies often occur in tandem with hyperpronation, particularly if the degree of pronation is different on the two sides. The quadratus lumborum and iliocostalis muscles are extremely sensitive to effective LLD. A tilted sacrum results in different resting lengths between the two QLs, and the CNS abhors this sort of imbalance.
The result is likely to be trigger point development in one or both QLs in an attempt to stabilize a potentially dangerous situation. The QL has an extensive referral pattern with gluteal, abdominal, sacral and radiating components, which is a potent recipe for a chain of satellite referral from QL to glutes to the leg. Unilateral sciatica is a common result.
A protocol for sciatic pain
Our protocol for treating sciatic pain consists of movement-oriented bodywork to reset the muscles along the satellite referral and functional hip and foot pain chains, followed by assessment and correction of hyperpronation via midfoot and forefoot support.
If an effective LLD is present, an appropriate lift should be added to the short side after correcting hyperpronation. These gait correction steps are necessary to provide lasting relief. We have found this strategy to have a high rate of success with what can be a serious and debilitating pain syndrome.
CHUCK DUFF founded the Coaching The Body® (CTB) Institute in 2001, and has taught thousands of students highly effective techniques for resolving pain. CTB integrates trigger-point therapy, movement-based techniques derived from traditional Thai bodywork and other approaches along with insights from modern neuroscience. His book, Ending Pain: Coaching the Body with Neuroscience, Movement, and Trigger Point Therapy, is due to be released in late September 2022. For more information go to coachingthebody.com.
 Travell and Simons, Myofascial Pain and Dysfunction, 172.
 Doidge, The Brain That Changes Itself, 142.
 “50 Shades of Pain with Prof. Lorimer Moseley | Trust Me, I’m a Physiotherapist.”
 Duff, Charles, Ending Pain, 223.
 Shah et al., “Biochemicals Associated With Pain and Inflammation Are Elevated in Sites Near to and Remote From Active Myofascial Trigger Points.”
 Travell and Simons, Myofascial Pain and Dysfunction, 186.
 Chaitow, “Might Trigger Points Sometimes Be Useful? – Leon Chaitow.”
 Duff, Charles, Ending Pain, 127.