Slide Matters and Other Fascial Significant Paradigm Shifting Considerations

Slide Matters and Other Fascial Significant Paradigm Shifting Considerations

– Interview with Antonio Stecco, MD, on Fascial Manipulation Courses

According to Hankinson & Hankinson (2012) Musculoskeletal Disorders are more prevalent than all chronic disease types, making musculoskeletal [soft-tissue] pain and dysfunction the most pervasive health afflition.

Myofascial pain is estimated to be the most commonly experienced musculoskeletal pain (Srbely 2010). Meaning, that although the condition is often termed/diagnosed as musculoskeletal – fascia, this may be [at least in part] the pain generating tissue in such cases.

85% of patients receiving care at specialized pain management centres are experiencing myofascial pain (Gerwin 2001) and Myofascial pain syndrome (MPS – aka fibositis and myofibositis) is one of the most common disorders encountered by physicians in clinical practice (Rachlin 1994). Yet, given all of this, no standard, universally accepted biochemical, electro-diagnostic, diagnostic-imaging, or physical examination criteria exist for a diagnosis of MPS (Annaswamy et al. 2011) and therefore it is most often an under-diagnosed or misdiagnosed condition (Cummings 2007).

Recovery following musculoskeletal injuries has traditionally focused on restoration of strength [muscular force generation and tendon/ligament tensile capabilities] and joint range of motion.

Until recently, little attention has been given to restoration of “glide” within the fascial system’s sliding mechanism, likely because up until recently little was known about the sliding mechanism. And indeed fascia in general, has been largely overlooked within the sphere of conventional diagnostics and treatment interventions.

Throughout my massage therapy career, fascia has fascinated me, understandably a career highlight has been attending the Fascia Research Congresses (FRCs). Dr. Antonio Stecco’s presentation at the 1st FRC was a principal accelerant for my fascial obsession that has exponentially heightened since then. A Stecco FRC3 highlight was the fascial system’s sliding mechanism.

In the human body, available movement and coordination of movement involves more than “the joint(s)” and the central nervous system. Although traditionally, “synchronisationof movement was exclusively attributed to the nervous system components, at a certain point, neurophysiologists began to question how the brain alone was able to control all of the variables involved in a motor gestures. The control of movements in the periphery had to be more complex than initially thought” (L. Stecco). Glide between the interfascial planes, endofascial fiber, endomuscular fiber all factor into movement potential and any impediment in the gliding of the fascia could impact available movement and alter afferent input resulting in incoherent movement.

A primary aim of Fascial Manipulation (FM) [aka: the Stecco Method] is to restore unimpeded gliding within the fascial  system’s sliding mechanism. We will explore this topic with renowned fascia expert, Dr. Antonio Stecco.

Hello Dr. Stecco, thank you for taking the time to speak with us and welcome to Massage Matters Canada.

AS: Thank you for inviting me.

CR: Dr. Stecco, can you provide us with a general anatomical/physiological overview of the deep fascia (DF) and the fascial system’s sliding mechanism?

AS: Throughout much of  the body the DF is a multi-layer presentation consisting of 2-3 layers of dense connective tissue (CT) and 1-2 layers of loose CT (e.g. fascia lata, brachial, & antebrachial fascia). A loose CT layer is also often present between the deepest most layer of the DF and the underlying layer of epimysium. The dense layers are constructed of parallel bundles of collagen fibers(type I & III). In the loose layers we findcollagen, adipose cells, glycosaminoglycans (GAGs) and a rich supply of Hyaluronan (HA). The dense layers transmit force and the loose layers augment gliding/slide between the layers [i.e. constitute the sliding mechanism].

CR: Can you provide us with a general pathophysiolgical overview? What goes wrong and why?

AS: Pathophysiological processes [within the sliding layer] are not completely understood. Current hypotheses suggest that increased resistance within the sliding layer — likely due to changes in viscosity — warrants valid consideration.

It is known that ground substance (GS) can change its viscosity and that HA, a component of GS, plays a significat role in viscosity changes. HA is a primary component of the loose CT/sliding layer. Mechanical stimulation (e.g. exercise, movement) triggers increased production of HA in the various sliding layers. If over-stimulation of abnormally high volumes of HA occurs, HA will tend to aggregate a transformation into a super-molecular structure that changes its ‘normal’ configuation. Aggregation results in increased viscosity, which in turn increases friction or resistance in the sliding layer. Another consideration is that a shift in pH toward acidity tends to instigate HA aggregation as well (e.g. 6.6 – 6.9 pH; possibly associated with an increase in lactic acid following hard exercise or overuse).

CR: What types of impairment/dysfunction can be attributed to ‘slide mechanism’ interference or dysfunction? What might the patient experience?

AS: As the sliding mechanism plays a significat role in movement potential; conversely interference with sliding can impact available range of motion (ROM), so a patient might present with movement difficultie (e.g. quantity and quality of available movement, stiffness). Additionally, slide/glide resistance incites friction, which in turn can provoke neural hyperstimulation (irritation). Neural-irritation can lead to hypersensitization of mechano and nociceptors and as such correlates with a patient’s experience of pain, allodynia, paresthesia and abnormal proprioception and subsequently altered movement/postural patterns. Generally speaking, pain is the most common reason for a patient to seek treatment and pain can occur with or without ROM limitations/difficulties

CR: Regarding glide interference, what kind of observations/indicators might the clinician note?

AS: The patient’s account of pain — location and referral pattern — is a key indicator: this is furthered by palpation and movement verifiction. In the FM model specificlocalized areas — approximately a 1 inch segment — of densifiction increased viscosity and fibosis correlate with the patient’s pain presentation – however, the sites of densifiction are not located at the site of pain. From a biomechanical point of view, these specificpoints — referred to in FM as centre’s of coordination (CC), centre’s of fusion (CF) — are of greater significane than say that of adjacent or other areas within the sliding layer. It is the clinician’s palpation of resistance to glide/slide and the patient’s notable increase in CC/CF point tenderness that denotes a malfunctioning/densifiedCC or CF. The FM model movement assessment differs from traditional ROM testing – this model takes into consideration myokinetic chain/sequences of movement. To recap, location of the patient’s pain, observable movement limitations and the clinician’s verifiction of painful points are the key diagnostic indicators of interference/dysfunction within the sliding layers.

CR: The advancement in Massage/Manual Therapy research is being aided by various imaging and measurement tools that can be used to identify biomarkers and denote differences in normal\abnormal tissue presentations, and thereby track pre\post treatment changes.

What kind of imaging/diagnostic tools are you currently using in practice and research, and what are some significat pre/post FM treatment changes you are seeing?

AS: Ultrasound is one commonly used diagnostic tool in practice and research. Changes in viscosity/tissue thickness can be viewed via ultrasound in some regions of the body. The region of the SCM and Medial Scalene are one of the more ‘viewable’ areas and thicker than normal areas in the correlating DF can be seen in patients presenting with chronic neck pain. Subsequently, thickness changes following FM treatment can also be viewed. Ultrasound is also being used to look at glide/slide differences (e.g. Langevin’s research comparing LBP sufferers to a non-pain group). The use of ultrasound to view moving tissue still presents some limitations (e.g. complexity and expense of computer software, resolution quality and depth of the tissue). There is currently no ‘gold standard’ in this area of diagnostics and research. EMG, DynaPort and robotics (providing computer generated movement animations) are also being explored as means by which to better understand fascia’s biomechanical role, monitor/measure tissue changes, identify normal and abnormal presentations and denote changes post treatment.

CR: On the topic of alignment: I am not an anti-structuralist, but I am not a predominantly structural-istic driven clinician [meaning, perfect alignment is the key to pain free functioning]. The scoliosis case that you shared at the Level I course in Vancouver last fall comes to mind. The  X ray image you showed us was of a dramatic spinal deviation (87 degrees), yet following FM treatment your patient has been able to function by returning to work, resumption of activities of daily living and sport/recreational activities with significatly less pain.

Dr. Stecco, how much did the actual curvature of her spine change post FM treatment? And from your perspective how imperative is ‘perfect’ alignment with regard to pain-free functioning?

AS: There was no significat change in the degree of her scoliosis following treatment. Scoliosis [spinal deviation] is not necessarily correlated with pain.

With this patient, there are three important components to look at: the scoliosis, hyperkyphosis and hyperlordosis. The impact of the spinal deviations essentially present as ‘overuse’ type syndromes in the paraspinal and other associated musculature’s sliding mechanism, which appears to be the predominant source of the presenting musculoskeletal pain and dysfunction. This patient still experiences some low back pain but not at the debilitating degree she experienced prior to FM treatment (e.g. missing time at work, stopping all activity). Occasional use of paracetamol (mild analgesic) (2-3 times a month) manages her back pain well, while FM treatment 2-3 times a year effectively addresses her compensatory neck pain. Following treatment she experiences no neck pain between treatments and her episodes of neck pain are occurring less frequently and are quicker to resolve.

CR: Regarding a couple of dosage considerations – Direction and Duration:

CR: Are there specific direction considerations and if so what are considerations for determining the direction of the FM technique? Cyriax (fractioning) for example is applied cross-fiberin reference to the underlying muscle/tendon – but articulating fascial layers are not parallel (oblique arrangement at a 78 degree angle). Does this arrangement have any bearing on the direction of FM application? Or are there other factors within the sliding layer that are taken into consideration?

AS: Direction of the FM technique is not specificto underlying fiberorientation. Where you feel the restriction is the most significat determinate factor pertaining to the direction the technique is applied, which sometimes can be multi-directional. There are some site-specificconsiderations (e.g. accessibility and proximity of sensitive anatomical structures; limited space between bones or anterior neck muscles and close proximity of vascular structures).

CR: What about duration? How long is FM technique applied for and why? What are the changes that you are listening for or  feeling for — indicating a productive change in the sliding layer?

AS: Knowing when to stop the technique is a combination of patient feedback and what the clinician is feeling. It takes an average of 3.14 minutes for a patient to report a 50% reduction in what was their initial level of tenderness/pain (e.g. if the patient reported that upon initial contact with the site [CC or CF] their pain level was a 7 on the NRS, it would take approximately 3.14 minutes for their pain to drop to 3.5).  What the clinician is feeling for is a decreased resistance to glide in the direction where resistance was initially strongly felt.

From a treatment perspective there are three important factors to consider: disengagement of collagen cross-links, restoration of normal HA presentation and restoration of normal GS/HA fluidit. Our hypothesis is that FM, a provocation-type technique, catalyzes a sequence of chemical events culminating in the restoration of normal quality/quantity of ground substance (GS) constituents (e.g. HA) within the dense collagen layers of deep fascia. Tracking changes poses some difficult, as post-treatment tissue biopsy is not reasonable. However biochemical measurements can track inflammtory mediated changes, which typically occur over a 48-hour period.

CR: What research are you currently working on? What might we expect to see you presenting on at the FRC4 in 2015? AS: Current studies include FM efficacyrelated to Spasticity associated with neurological disorders and Musculoskeletal Pain and Dysfunction. We are conducting various clinical trials: neck, shoulder, carpal tunnel syndrome and using various instruments/diagnostic technologies (e.g. EMG, DynaPort, Robotics) to assist with these studies and further our understanding of sliding layer pathophysiology and effective treatment interventions. We are also exploring a new pharmascopic track.

by Cathy Ryan RMT
Source: MTO:

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