FASCIAL DYSFUNCTION: CONNECTIVE TISSUE CONNECTIONS

In the late 1 970s, Stephen Levin, an orthopedic surgeon, conceived of a model for the structure of organic tissue that could account for many physical and clinical characteris· tics. Through a process of systematic evaluation of the basic physical properties of tissue, he arrived at the conclusion that all organic tissue must be composed of a type of truss (triangular form) and that the essential building block of all tis ue must be the tension icosohedron.17.19 This model, also referred to as the <emegriry model anJ the myofascial skeletol truss, has gradually emerged as a viable explanation for the nature of organic tissue. Recendy, this model has been con· firmed by electron-microscopic methods and through phys­

ical stress extrapolation experiments.19,S1 This model accounts for the concept of the kinecic chain , which recog� nizes that lesions transmit tensions throughout the body and that symptoms can be traced back to their source and treated indirectly by aligning fascial lines of force in rela­ tion to the primary focus of restriction { Fig. 2-4). "·)4

The implications of Levin's model, from a clinical per· spective, are that all tissues share cerrain fundamental char· actcristics. Indeed, this model confirms that all tisslles are alike at the molecular and ultrastructural level. The tension icosohedron helps clarify the properties of the tissues and may be predictive of the effects of any therapeutic system. The tensegrity model delineates the following properties of somatic tissue: the forces maintaining the structure of the body are tension and compression and have no bending momentS (such as in the hinge mechanism ascribed to joints); the structural integrity of the body is gravity inde­ pendent and is stable with flexible joints; the tissues of the body have a nonlinear stress/strain response to external forces; and the body is a functional lInit, in that forces applied to it at one point are transmitted uniformly and instantaneously throughout the entire organism.

This model implies that a perceived condition in one area of the body may have its origin in another area and that therapeutic action at the source of the dysfunction will have an immediate, corrective effect on all secondary areas, including the site of symptom manifestation. It also may account for some of the physiologic effects that produce the release phenomenon. I

Because of this interconnectedness of the entire fascial system, restriction in one area may result in a reduced range of morion in a distal stnlcture.J•10,14 The area of perception of pain by the patient, especially in chronic cases, may often be remore from the area of the most sensitive tender points. Because the tender points represent areas of relative fixa� tion, these areas are, in essence, splinted, and this results in lines of tension that extend to peripheral structures. As we move peripherally from the primary foclls of restriction, the

The Rauonnle

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Fig. 2-4 Represenuuion of fascial [erui(m pauems.

[cn�l'gnty �HuCtlirC of the tisslies transmits these forces, without any Imi� of intensity, to an area of the body which interfaces with external mechanical influences.

TI'lC hoJy anempts to create a full range of gross motion by compenS3nng for arca� of relative fixation. This results in excessive morton in regions of the hoJy that extend from the focus of dysfunction. Excessl\'c force, Jue to strain or repetitive motion against thc restriction barrier, may cause local mflammation amI pam. The mcreaseu mechanical deformation anJ strccch wlthu) these tissues may result in the release of pain-producing chemical mediacors. Thus pam may be exprc!lScJ within WiSUCS, which are, III fact, secondary areas of Involvemem. The goal of treatment of these hypermobile tissues (joints, ligaments, etc.) is [0

reduce the exceSSive tissue ph.1Y and range of motion. Ther# apies such as fusion or prolotherapy create relative fixation of tI"�ues.1l The reduced mechanical strain and the cnnse· quent diminishment in the release of nociceptive mediators

result In reduced pain. These approaches may, however, also produce secondary lesions and an increase in aherrant biomechanics.

It is hypothesized that PRT, hy reducing the tension on the myofascial system, also engages the fascial componems of the dysfunction. TIle reduction in tension on the collagenow, crOS!).llnkages appears [Q induce a dic;engagemenr of (he elec· trochemical bonds and a conversion back to the sol state. This fascial component of release during the roc appears to require a maintenance of the positionmg for several mmures. The 90 seconJ mterval espouoed by Jones theoretically addresses only the neuromuscular aspect of thc dysfunction.

Some of the effects of the POC may be (brecdy attrihutable to the changes in the condition of the fascial matnx Itself. Othcrs may be due to aumnomic and electro· chemical associations betwecn the myofascial structures and othcr systems."! The resulting reduction in tension at the level of the pnmary lesion would, III accordance With the tensegnty m<.xlel, create an equilibration of tension throughout the orgaOism. The previous discrepancy between hypomobile and hyperrnobde arcas woulJ be resolveJ, anJ there would be a reduction in the abnormal hlOmechanical stresses associated with the stimulation of pain receprors.

Positional release therapy thus appears to be capable of initiating a release of tension patterns both at the neufU# muscular level and at the f'lscial levcl. The determining fac# tors are the preCision and skill exercised by the practitioner In maintaining thc ideal position and the length of time requireJ for the completion of the release prt'lCCSS.

, SUMMARY

New paradigms are emerging that are morc coru,I':otcnt with clinical observation in the field of musculoskeletal dysfunc# [Ion. Current m(K.lels recognizc the Intrinsic properties of the tissues and how these arc affectcd at thc ultrastructural Icvcl. Somatic dysfunction may manifest within <-lny of the tissues of the body. Each of these tissues expresses trauma and dysfunction In unique ways and is interconnected With

,)11 of the tissues of the body a� part of a kinctic challl. Thus trauma to one part of the body may result III pe"l>ting dys' function in any other pan.

The render poilU is a clinically recognized exprcs.o;ion of somatic dysfunction and is used in PRT a� a diagnn'tlc indicator.

Several pathophysiologic mechanisms may he respon· sible for the development of the c1mical manifesrations associated with somatic dysfunction. Ncuromuscular responses, mediated by monosynaptic reflexes and musculo· tendinous proprioceprors, can alter the length/tenSion rela# tionship of the muscular component of the dysfunction. Tissue injury results in the release of proinflamm�ltory