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Journal of Bodywork & Movement Therapies (2015) xx, 1e18

Available online at www.sciencedirect.com 61


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9 FASCIA SCIENCE AND CLINICAL APPLICATIONS: EXTENSIVE REVIEW 71
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12 A unifying neuro-fasciagenic model of 73
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14 somatic dysfunction e Underlying 75
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mechanisms and treatment e Part II
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Q5 Paolo Tozzi, MSc Ost, DO, PT a,b,* 80
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School of Osteopathy C.R.O.M.O.N., Rome, Italy 83
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C.O.ME. Collaboration, Pescara, Italy 84
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Received 3 October 2014; received in revised form 20 February 2015; accepted 24 February 2015
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29 Summary This paper offers an extensive review of the main fascia-mediated mechanisms un-
KEYWORDS 91
30 derlying various therapeutic processes of clinical relevance for manual therapy. The concept of
Fascia; 92
31 somatic dysfunction is revisited in light of the several fascial influences that may come into
Somatic dysfunction; 93
32 play during and after manual treatment. A change in perspective is thus proposed: from a noci-
Fascial dysfunction; 94
33 ceptive model that for decades has viewed somatic dysfunction as a neurologically-mediated
Fascial mechanisms; 95
34 phenomenon, to a unifying neuro-fascial model that integrates neural influences into a multi-
Osteopathic 96
35 factorial and multidimensional interpretation of manual therapeutic effects as being partially,
manipulative 97
36 if not entirely, mediated by the fascia. By taking into consideration a wide spectrum of fascia-
treatment; 98
37 related factors e from cell-based mechanisms to cognitive and behavioural influences e a
Osteopathic models; 99
38 model emerges suggesting, amongst other results, a multidisciplinary-approach to the inter-
Fascial treatment; 100
39 vention of somatic dysfunction. Finally, it is proposed that a sixth osteopathic ‘meta-model’
Fascial release; 101
40 e the connective tissue-fascial model e be added to the existing five models in osteopathic
Manual therapy 102
41 philosophy as the main interface between all body systems, thus providing a structural and 103
42 functional framework for the body’s homoeostatic potential and its inherent abilities to heal. 104
43 ª 2015 Published by Elsevier Ltd. 105
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restrictive barrier, described as a “functional limit that 111
50 Introduction 112
51 abnormally diminishes the normal physiologic range”
(E.C.O.P., 2011a). This is maintained until tensions modify; 113
52 In osteopathic practice there are three main manual ap-
2) indirect approach e tissues are brought away from the 114
53 proaches that are directed towards the fascia: 1) direct
restrictive barrier while a position of ease (a balanced 115
54 approach e the affected tissue is brought against the 116
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* School of Osteopathy C.R.O.M.O.N., Rome, Italy. 118
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E-mail address: pt_osteopathy@yahoo.it. 119
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http://dx.doi.org/10.1016/j.jbmt.2015.03.002 121
60 1360-8592/ª 2015 Published by Elsevier Ltd. 122

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
YJBMT1216_proof ■ 17 March 2015 ■ 2/18

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2 P. Tozzi

1 tension in all planes and directions) is found and main- A static load may also break abnormal tissue collagen 63
2 tained up to a release; 3) combined approach e both the crosslinking and stimulate fibroblast differentiation under 64
3 point of ease and the restrictive barrier are consecutively the influence of IL-6, with a potential role in tissue repair 65
4 engaged in an interactive fashion (Ward, 2003). Although and remodelling (Hicks et al., 2012; Khan and Scott, 2009). 66
5 myofascial and fascial-ligamentous release techniques are In addition, the duration of the load appears to be a sig- 67
6 the most commonly applied fascial approaches amongst nificant factor. It seems that brief periods of stretching may 68
7 American osteopathic physicians (Johnson and Kurtz, 2003), decrease the effects of TGF-b1 production of additional 69
8 there are a multitude of fascia related techniques that collagen, thus reducing the risk of fibrosis or scarring 70
9 utilize various levels of aggressiveness (Sergueef and (Langevin et al., 2006). Scars may generate pain syndromes 71
10 Nelson, 2014), from balanced ligamentous tension tech- that can be relieved by a direct manual approach to the 72
11 nique to counterstrain, from articulatory to cranial and involved connective tissue (Kobesova and Lewit, 2000), and 73
12 visceral techniques, including soft tissue work from inhibi- this could be applied in the first 12 h following surgery to 74
13 tory pressure to effleurage manoeuvres. reduce inflammatory reactions and the risk of adhesion 75
14 Osteopathic treatment of fascia has shown to be effec- formation (Chapelle and Bove, 2013). 76
15 tive for a wide variety of conditions, from local musculo- 77
16 skeletal causes, such as acute joint injury (Eisenhart et al., 78
17 2003) to general mood disorders such as depression (Plotkin Cell-based mechanisms 79
18 et al., 2001). Other non-osteopathic manual modalities 80
19 have shown similar results, possibly because of the common As will be described in this section, various forms of manual 81
20 therapeutic influence and stimulation of the myofascial loading, whether sustained or cyclical, that differ in di- 82
21 complex (Simmonds et al., 2012). rection, speed, magnitude and frequency, appear to exert a 83
22 Several mechanisms may underlie therapeutic changes strong impact on cell behaviour, gene expression and tissue 84
23 in the fascia. remodelling through growth factors and enzyme activation. 85
24 Several cell-based mechanisms may potentially repre- 86
25 sent crucial factors in the achievement of a palpable 87
Fascia-related mechanisms involved in the
26 release during manual fascial work. Some of these are 88
27 treatment of somatic dysfunction described in Table 1. 89
28 Fibroblasts in vitro and in vivo have shown an almost im- 90
29 Structural changes mediate response to traction, pressure and shear forces, 91
30 followed by a series of changes in chemical signalling path- 92
31 Structural modifications in the connective tissue may occur ways and gene activation, ATP release, actin polymeriza- 93
32 immediately or just after treatment and may account for the tion, and also differential stretch-activated calcium channel 94
33 palpable changes following manipulation. Myofascial release signalling (Wall and Banes, 2005; Stoltz et al., 2000). 95
34 of the thoracolumbar fascia in patients with chronic low back Although most of the proposed mechanisms may require 96
35 pain has shown an increase in thickness of fascial layers that hours or even days before producing desirable effects on 97
36 remained for at least 24 h (Blanquet et al., 2010). This sug- tissue texture and function, some of them may take place 98
37 gests a sustained change in the architecture and/or hydra- within minutes from the starting point of a therapeutic 99
38 tion of the fascia being worked on. In addition, US manouver. Langevin et al. (2013) note that in response to 100
39 measurements applied immediately before and after manual sustained changes in tissue length, fibroblasts may rapidly 101
40 intervention, showed highly significant differences in modulate such tension by remodelling their cytoskeleton 102
41 collagen fibre density and orientation in the structure of the and changing their contractile apparatus. Within minutes 103
42 matrix in the dermis, reflecting palpable differences in ten- they could remodel their cell-matrix contacts (focal adhe- 104
43 sion and regularity (Pohl, 2010). These findings are consistent sions) along the direction of tissue stretch (Ciobanasu et al., 105
44 with the re-organization and remodelling of collagen fibres, 2013; Geiger et al., 2009), or expand microtubule network 106
45 which have been suggested to result from myofascial work and actomyosin activation so as to maintain tensional 107
46 (Martin, 2009) through a breakdown of abnormal collagen homoeostasis through an equal counter-tension (Eastwood 108
47 cross-links and an increased matrix hydration. et al., 1998). This may produce a counterforce in the ma- 109
48 Since abnormal palpable findings (such as altered trix tension that might be palpable. Tensional load appears 110
49 texture) in connective tissue might be related to abnormal to be perceived by the cell at a nuclear level too. Ex vivo and 111
50 cross-links between collagen fibres, it has been shown that in vivo studies demonstrate that fibroblasts respond within 112
51 human fibroblasts respond better to cyclical (3 min stress-3 minutes to mechanical stretching by dynamically remodel- 113
52 minutes relaxation, of about 7% of their length) rather than ling their cytoskeleton with perinuclear redistribution of 114
53 static stretch by increasing the production of collagenase alpha-actin (Langevin et al., 2005, 2006; 2010). Although this 115
54 by 200% (Carano and Siciliani, 1996). property of rapidly responding to mechanical stress appears 116
55 This enzyme has a potential role in collagen remodelling to be specific to areolar connective tissues only, it remains 117
56 in dysfunctional tissue by breaking cross-linking peptide significant for fascial work because loose connective tissues 118
57 bonds, thus preventing excessive connective tissue forma- form the interface between subcutaneous and perimuscular 119
58 tion, as occurs during wound healing. However, the repet- layers, and are potentially engaged in manual interventions. 120
59 itive mechanical stretch-induced collagenase activity can However, cytoskeletal remodelling failed to occur when 121
60 also be suppressed by hormonal (oestradiol and progester- distinct matrix properties were produced in gel, as for 122
61 one) influences (Zong et al., 2010), as might occur during denser and stiffer connective tissue with increased cross- 123
62 the menstrual cycle or in hormonal therapy. linked collagen (Abbott et al., 2013). This shows the 124

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
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Q1 A unifying neuro-fasciagenic model of somatic dysfunction 3

1 63
Table 1 Cellular mechanisms that may be involved in the manual fascial treatment of somatic dysfunction.
2 64
3 Fibroblast response Strain direction, frequency and duration of a (therapeutic) load may influence fibroblast 65
4 morphology, function and behaviour (Grinnell, 2003; Wang et al., 2004). When equi-radially 66
5 applied, it may lead to reduction of proinflammatory mediators and decrease of fibroblast 67
6 proliferation, possibly linked to clinical improvements in range of motion and reduction of 68
7 pain/inflammation (Standley and Meltzer, 2008). 69
8 Collagen response Collagen synthesis and architecture responds to mechanical loading (Kjaer et al., 2009; 70
9 Thomopoulos, 2006), hence a therapeutic load may stimulate connective tissue remodelling 71
10 and repair. 72
11 Mechano-coupling Physical load produces a transduction into various chemical signals, leading to a modulation of 73
12 cell metabolism and response, changes in intracellular biochemistry and gene expression 74
13 (Ingber et al., 2014; Chiquet et al., 2009), depending on the type, duration, amplitude and 75
14 frequency of the load being applied (Lavagnigno et al., 2003). 76
15 Cellecell communication Stimulus in one location leads to a perturbation of distant cells, although these have not 77
16 received any direct mechanical stimulus (Lu and Thomopoulos, 2013; Wall and Banes, 2005). 78
17 Therefore a therapeutic load may produce beneficial effects even at distance to where it is 79
18 applied. 80
19 Effector cell response Appropriate mechanical loading stimulates protein synthesis at the cellular level, promoting 81
20 tissue repair and remodelling (Hardmeier et al., 2010; Wang et al., 2012) as well as cell 82
21 proliferation and migration in wound healing, by sensitizing fibroblasts to nitric oxide (Cao 83
22 et al., 2013b) 84
23 85
24 86
25 intrinsic interdependence between matrix and cell proper- increased (occasionally reduced) fibroblast proliferation, 87
26 ties on determining the tissue response to a mechanical load. whereas a completely reversed pattern was observed with 88
27 During manual fascial techniques, the operator may feel equibiaxial or acyclic long-duration strains. In the latter, 89
28 various tissue responses to the applied load that are even a normalization of the apoptotic rate was found 90
29 described as ‘resistance’ or ‘give’ to the stretch. Interest- (Meltzer et al., 2010). This means the fascial tissue may 91
30 ingly, the mechanical loading of fascia causes changes respond better to balanced and sustained stretch rather 92
31 through activation of fibroblast response and the different than intermittent and unequal loads. 93
32 receptors present in the fascial tissue, leading to modulation The force and duration of tension applied may also be 94
33 of myofascial contraction (Hicks et al., 2014). Spontaneous relevant. It has been shown that high magnitude (thera- 95
34 contractions in fascia suggest the existence of an intrinsic peutic) load (from 9% to 12% elongation) can produce an up- 96
35 tension or pre-stress in the collagen scaffold (Staubesand regulation of ECM proteins, while increasing magnitude and 97
36 et al., 1997); and when an additional load alters this duration (1e5 min) loads induce cytokine and growth fac- 98
37 tensional balance, so that the fascia is distended, the myo- tors secretions (Cao et al., 2013a). These results are 99
38 fibroblasts contract and resist this (Tomasek et al., 2002). consistent with those obtained by Yang et al. (2005), where 100
39 Various studies in vitro have demonstrated different cell large-magnitude loads caused pro-inflammatory responses, 101
40 behaviours depending on the type, magnitude and fre- and cyclic (0.5 Hz per 4 h), uniaxial, small-magnitude 102
41 quency of the artificial load being applied, and may be stretching produced anti-inflammatory reactions in human 103
42 clinically relevant to understand how tissues respond to tendon fibroblasts. Similarly, brief, moderate amplitude 104
43 different modalities of intervention. (20e30% strain), static stretching of connective tissue 105
44 Fibroblasts and myofibroblasts are both highly respon- in vivo and ex vivo has been shown to decrease TGF-b1and 106
45 sive to magnitude (Cao et al., 2013a), direction (Eagan collagen synthesis, thus preventing soft tissue adhesions 107
46 et al., 2007), frequency and duration (Meltzer and (Bouffard et al., 2008). 108
47 Standley, 2007) of a (therapeutic) load, and can regulate In conclusion, brief, light/moderate, balanced, static or 109
48 cell activity, proliferation or apoptosis (Meltzer et al., slow cyclic strains appropriately applied to fascia may be 110
49 2010), mainly by influencing ion conductance, gene sensed at the cellular level and transduced in normalizing 111
50 expression and secretion of inflammatory mediators. In tissue structure and function. 112
51 particular, the secretion of IL-6 and IL-1 by fibroblasts It is worth noting that while fibroblast cell orientation, 113
52 under equibiaxial stretch can exert powerful pro or anti including cell shape and cytoskeleton, changes in a non 114
53 inflammatory responses, potentially leading towards linear fashion according to different magnitudes of applied 115
54 beneficial or detrimental matrix remodelling and cell cyclic load (Faust et al., 2011), the response of fibroblasts 116
55 behaviour (Tsuzaki et al., 2003). A concomitant autocrine to mechanical loading is also dependent on cell orientation. 117
56 and paracrine release of ATP may also serve as a negative In cells oriented parallel to a given cyclic stretch, higher 118
57 feedback mechanism to limit activation of destructive levels of alpha-smooth muscle actin were found to be 119
58 pathways (Tsuzaki et al., 2003); and all of these factors may expressed; whereas fibroblasts that were perpendicular to 120
59 influence the clinical efficacy of fascial treatment. this showed higher activity levels of secretory phospholi- 121
60 Although there were differences in degree and form, pase A(2) which has a potential inflammatory role (Wang 122
61 most studies showed that heterobiaxial or cyclic short et al., 2004). This indicates that therapeutic loads 123
62 duration strains can produce inflammatory reactions and applied differently with respect to tissue tension (that 124

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
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4 P. Tozzi

1 presumably corresponds to cell orientation) may produce and serve to optimize transmission and control of forces. 63
2 different cell and tissue responses. Finally, secretion of IL-6 Thus, “because of the architecture, receptors can also be 64
3 was significantly induced by 15 min of cyclic biaxial me- stimulated by changes in muscle tension without skeletal 65
4 chanical stretching after 4 and 8 h in human tendon fibro- movement, or by skeletal movement without change in 66
5 blasts, suggesting that inflammatory reactions following muscle tension.” (Van der Wal, 2009). A similar concept of 67
6 manual intervention may be partially caused by IL-6 inter-tissue continuity has been advanced by Benjamin 68
7 secretion (Skutek et al., 2001). et al. (2008), who re-elaborated the existence of the so- 69
8 called ‘supertendons’. This term refers to the tendon 70
9 network formed by the anatomically intrinsic interrelation 71
10 Neuromuscular interaction of fascia, tendon sheaths, joint capsules, retinacula, fat 72
11 pads and bursae, “in which the function of the whole is 73
12 Fascial oriented work may produce beneficial effects by greater than that of its individual parts” (Benjamin et al., 74
13 activating various receptors in the connective tissues that 2008). Such supertendinous structures may be critical for 75
14 elicit a series of neuromuscular reflexes. According to the understanding of neuromuscular control. In fact, 76
15 Schleip’s neurobiological model (2003), these types of cadaveric experiments and computer simulations have 77
16 events occur together with concomitant autonomic and shown that the distribution of tensions through these 78
17 viscoelastic changes, and are more likely to explain the fast ‘super-structures’ regulates how force is distributed 79
18 tissue responses that a therapist perceives during fascial distally, acting as a ‘switching function of a logic gate that 80
19 techniques. nonlinearly enables different torque production capabil- 81
20 Although the dermis is the first tissue to be loaded during ities’ (Valero-Cuevas et al., 2007). This would demonstrate 82
21 manual treatment, evidence suggests that therapeutic ef- the existence of a “non-neural somatic logic” that is able to 83
22 fects such as inhibition on hypertonic muscle and presum- elaborate information at a macroscopic scale without 84
23 ably on the myofascial complex, do not originate from requiring neural processes. Therefore it is plausible that an 85
24 mechanical stimulation of superficial cutaneous mechano- interaction of afferent impulses might come at different 86
25 receptors (Merkel, Meissner receptors) during manual frequencies and modalities from such a connective tissue 87
26 therapy (Morelli et al., 1999). Similarly, deep receptors such complex, including ligaments. The latter are apparently 88
27 as Golgi tendon organs mainly exist in the myofascia, joint capable of eliciting inhibitory ligament-muscular reflexes 89
28 capsules and myotendinous junctions (Jami, 1992), and are with consequent inhibitory effects on related joint muscles 90
29 unlikely to come into play during fascial treatment because (Solomonow, 2009; Voigt et al., 1998), although this has not 91
30 they have a high threshold that makes them respond to yet been demonstrated to occur during manual therapy. 92
31 strong and fast manual stimulus, to which they quickly adapt According to Schleip’s neurobiological model, the im- 93
32 (Pickar and Wheeler, 2001). This is why Golgi organs have mediate effects that occur during fascial release are 94
33 been mostly implied as being involved in neurophysiological mediated through Ruffini’s endings and interstitial mecha- 95
34 explanations that underlie the efficacy of spinal manipula- noreceptors that are abundant in fascia. The latter are 96
35 tion (Pickar, 2002) and not of fascial treatment. In contrast, polymodal receptors (responsive to different kinds of 97
36 Pacinian corpuscles are present in dense connective tissue stimulation): some of them are very low threshold and 98
37 and deep fascia (Benjamin, 2009) and tend to quickly adapt respond more to light tissue stretching, while others are 99
38 to stimuli, hence they respond better to rapid or intermit- more sensitive to rapid pressure (Sandkühler, 2009). They 100
39 tent compression and vibrations (Bell et al., 1994) applied to may also account for haptic perception (the sense of touch 101
40 the myofascia, myotendinous junctions and deep capsular through proprioception and somatosensory perception) in 102
41 layers. They are thought to respond to such stimuli by the whole body (Schleip et al., 2014). It has been suggested 103
42 enhancing proprioceptive feedback and by maintaining that they may exert an influence on autonomic activity (by 104
43 muscle tone (Zimny and Wink, 1991). The type of thera- decreasing sympathetic activity) and on the central nervous 105
44 peutic force needed to activate Pacinian corpuscles may be system, producing an indirect effect on haemodynamics 106
45 applied in some manual interventions such as in high- (vasodilation and plasma extrusion) and tissue viscoelas- 107
46 velocity manipulation or vibratory techniques. ticity together with a descending inhibition of muscular 108
47 Finally, Ruffini’s endings are mainly located in joint tone (Schleip, 2003). 109
48 capsules and in the dense connective tissue (Halata et al., Some of the free nerve endings present in the interstitial 110
49 1985), including fascia (Yahia et al., 1992). They have a myofascial tissue have been defined as interoceptors, since 111
50 slow adaptation to the stimuli being applied, and are thus they inform the brain about physiological tissue conditions 112
51 generally sensitive to slow, sustained or rhythmic deep such as temperature, pH and visceral changes (Craig, 2002). 113
52 pressures, and in particular to lateral (perpendicular) tissue In particular, ‘tactile C-fibres’ have been recently discov- 114
53 stretches (Van der Wal, 2012). These kind of forces are ered in the human subcutaneous connective tissue. How- 115
54 normally applied in most fascial techniques, such as myo- ever, whereas classically C-fibres are described as 116
55 fascial release. nociceptors or chemoreceptors, these ‘tactile C-fibres’ are 117
56 Although these receptors have traditionally been low-threshold mechanoreceptive receptors accounting for 118
57 described as being organized in parallel arrangements, they an alternative and distinctive system signalling touch in 119
58 have more recently been shown to be functionally related humans (Björnsdotter et al., 2010). It appears that activa- 120
59 within a musculoskeletal and connective tissue continuum tion of these unmyelinated sensory fibres, for example 121
60 that is in series (Van der Wal, 2009). Mechanoreceptors are during gentle touch therapy, relay signals to the insular 122
61 mainly concentrated in the transitional areas within the cortex, the medial prefrontal cortex, the dorso-anterior 123
62 continuum of the muscle-connective tissue-skeletal unit, cingulate cortex (but not to the somatosensory areas) 124

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
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A unifying neuro-fasciagenic model of somatic dysfunction 5

1 (McGlone et al., 2014), where sensory and affective infor- the elastic potential of tissues is exceeded and a plastic 63
2 mation are integrated giving rise to limbic touch, with deformation occurs (Jäger, 2005). 64
3 resultant downstream effects on interpersonal touch, Traditionally, it has been suggested that most of the 65
4 affiliative behaviour, psycho-endocrine function, immune immediate tissue changes following manual fascial work 66
5 system, autonomic regulation and pain modulation may be the result of a colloidal change in the fascia, which 67
6 (Olausson et al., 2010). means a transformation of the ground substance from a 68
7 The classical nociceptive model, instead, proposes that dense solid-like state (gel) to a more fluid (sol) state (Rolf, 69
8 indirect fascial techniques may modulate muscle tone and 1962). However, a 3D mathematical model for fascial 70
9 related fascial tension by decreasing mechanical stress and deformation has rejected the idea that palpable sensa- 71
10 neural inputs (Van Buskirk, 1990). This may in turn reduce tions of tissue release following manual therapy may be 72
11 the activity of nociceptors and of the correspondent facil- due to plastic deformations of firm type of fascia, such as 73
12 itated spinal level that by neurological reflex may produce the fascia lata and plantar fascia, whereas this may be 74
13 a consequent modulation of autonomic activity on blood possible in thin and more elastic types of fasciae 75
14 and lymphatic flow. Finally, in response to the proprio- (Chaudhry et al., 2008). Schleip’s neurobiological model 76
15 ceptive input, the central nervous system may change has instead proposed that following proprioceptive stim- 77
16 muscle tone, allowing the therapist to follow myofascial ulation the Ruffini’s endings and interstitial fascia mech- 78
17 paths of least resistance until a palpable release is anoreceptors may be involved in efferent control of the 79
18 perceived (Minasny, 2009). vasodilation and increase of plasma extravasation via 80
19 autonomic activation (Schleip, 2003). This would initiate 81
20 Autonomic influence ECM viscosity changes. Nevertheless, there is evidence 82
21 that a similar phenomenon may take place within minutes 83
22 of a tensional load being applied and as the result of cell- 84
Somatic dysfunction has been traditionally related to
23 matrix-induced regulation of fluid flow that is independent 85
correspondent facilitated spinal levels and aberrant auto-
24 of neurological activation. Langevin et al. (2011) have 86
nomic activity that in turn influences various visceral
25 demonstrated that static tissue stretch of areolar con- 87
functions (Korr, 1979; Beal, 1985). Interestingly, autonomic
26 nective tissue (w20e25 %) causes fibroblast cytoskeletal 88
adrenergic fibres have been found in fascia (Tanaka and Ito,
27 remodelling via activation of focal adhesion complexes 89
1977), with a plausible major role on vasomotor control of
28 and initiate signalling pathways mediated by Rho kinase. 90
intrafascial blood vessels (Tesarz et al., 2011). It has been
29 This in turn leads to remodelling of the cell’s focal adhe- 91
suggested that therapeutic touch may produce stimulation
30 sions and actomyosin activation that develops counter- 92
of pressure-sensitive mechanoreceptors in the fascia (Ruf-
31 tension. The latter process allows surrounding tissue to 93
fini’s and interstitial receptors), followed by a para-
32 relax further and achieve a lower level of resting tension. 94
sympathetic response (Schleip, 2003). This in turn may
33 The study has shown that by changing shape, fibroblasts 95
induce a change in local vasodilatation and tissue viscosity,
34 can dynamically modulate the viscoelastic behaviour of 96
together with a lowered tonus of intrafascial smooth mus-
35 areolar connective tissue through Rho-dependent cyto- 97
cle cells, and such a response has been partially demon-
36 skeletal mechanisms. 98
strated. Both massage therapy and myofascial osteopathic
37 99
treatment have been shown to produce an increase in vagal
38 100
efferent activity, as shown by changes in heart rate (Field Fluid dynamics
39 101
et al., 2010), even in healthy subjects (Giles et al., 2013);
40 102
while other forms of fascia oriented manual therapy (Danis
41 The mechanism described above may also potentially 103
Bois method) may produce an upregulation of para-
42 regulate extracellular fluid flow into the tissue and protect 104
sympathetics with an influence on blood shear rate and
43 against osmotically-driven swelling when the matrix is 105
blood flow turbulence (Queré et al., 2009). At the same
44 stretched (Langevin et al., 2013). The flow of water in the 106
time, a modulation of hypersympathetic activity may take
45 ECM depends on the opposing forces between the osmotic 107
place (Henley et al., 2008), normalizing various haemody-
46 pull of under-hydrated glycosaminoglycans and the active 108
namic parameters, with improvement of endothelial func-
47 restraint of the tensioned collagenous network as the result 109
tion (Lombardini et al., 2009), and anxiety levels
48 of fibroblast activity. Therefore, as long as the tension in 110
(Fernandez-Perez et al., 2008). However, reduced psycho-
49 the matrix is maintained by fibroblasts, water is prevented 111
logical distress, anger status, anxiety levels and perceived
50 from entering the tissue (Reed et al., 2010). During the 112
pain have also been associated with an increase of sym-
51 acute onset of inflammation, however, the matrix swells as 113
pathetic activity and heart rate following manual therapy
52 inflammatory mediators disrupt the cell-matrix contacts, 114
(Hatayama et al., 2008; Toro-Velasco et al., 2009).
53 causing a drop in matrix tension and interstitial fluid pres- 115
54 sure, and allowing water to be ‘sucked into’ the matrix 116
55 Viscolelastic changes (Reed and Rubin, 2010). A (therapeutic) stretch lasting for a 117
56 few minutes could then e potentially e un-restrain the 118
57 Biological structures exhibit viscoelastic properties and matrix and promote transcapillary fluid flow and temporary 119
58 responses under mechanical loads (Kucharová et al., 2007), matrix swelling. Fibroblasts, in turn, can either release 120
59 with significant changes depending on chronological age their matrix contacts e resulting in a further drop of 121
60 (Doubal and Klemera, 2002). Generally, the stronger and interstitial fluid pressure e or remodel the contractile 122
61 more rapidly that a load is applied to organic materials, the cytoskeleton and adhesive matrix contacts, so as to develop 123
62 more rigidly will the tissue respond, up to the point when a counter-tension sufficient to restore tension equilibrium 124

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
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+ MODEL
6 P. Tozzi

1 (Langevin et al., 2013). This model would also fit with the in circulating lymphocyte markers and cytokine expression, 63
2 fascial hydrodynamic response reported by Schleip et al. while twice-weekly sessions increased oxytocin levels and 64
3 (2012). In response to mechanical stimuli, such as production of pro-inflammatory cytokines, together with 65
4 compression and stretch, fascia may exhibit a sponge-like decreased arginine vasopressine and cortisol levels 66
5 behaviour, showing a squeezing and refilling response (Rapaport et al., 2012). Hormonal changes were sustained 67
6 under the opposing forces of the restraint of collagen for up to four days, while cyotokines changes persisted for 68
7 network and the osmotic pull of proteoglycans complex. up to eight days. In another study, the increase of oxytocin 69
8 Interestingly, the fluid pressure might increase more was also correlated with a decrease in adrenocorticotropin 70
9 during tangential oscillation (2e4 Hz) and perpendicular hormone following manual work (Morhenn et al., 2012). 71
10 vibration (15e60 Hz) with respect to the fascial layer than Oxytocin, in particular, could play a role as an endogenous 72
11 during constant sliding or back-and-forth motion, as pre- pain controlling system. It has been demonstrated that, 73
12 dicted by 3D mathematical modelling methods (Roman following manual intervention, increased levels of this 74
13 et al., 2013; Chaudhry et al., 2013). This would cause the hormone have been found in plasma and periaqueductal 75
14 flow to occur more around the edges of the area under grey matter, exhibiting anti-nociceptive effects possibly 76
15 manipulation e due to an increased pressure gradient e through interaction with the opioid system (Lund et al., 77
16 producing an enhanced lubrication and an improved sliding 2002). Furthermore, oxytocin appears to be strongly 78
17 potential between fascial layers and muscle tissue. Thus, related to the formation of social bonds as well as of 79
18 the use of vibratory and oscillatory techniques e and not interpersonal bonding involving trust (Lieberwirth and 80
19 just constant sliding motions e should be considered, Wang, 2014), thus influencing the psychosocial dimension 81
20 especially when interstitial fluid dynamics need to be of the individual. 82
21 improved such as in the case of fibrotic tissue. The benefits of osteopathic manipulation, including 83
22 Interstitial flow also induces fibroblast-to-myofibroblast myofascial work, have also been related to a remarkable 84
23 differentiation as well as collagen alignment and fibroblast increase in nitric oxide (NO) concentration in the blood 85
24 proliferation, playing an important role in fibrogenesis and following therapeutic intervention (Salamon et al., 2004). 86
25 tissue repair (Ng et al., 2005). Furthermore, it appears to This has been demonstrated to occur in equal amounts to 87
26 affect intracellular processes (calcium signalling, protein that released during moderate physical exercise 88
27 secretion) and influence fibroblast activities such as (Overberger et al., 2009). Similarly, results obtained from 89
28 growth, proliferation, differentiation, alignment, adhesion, in vitro studies have confirmed this possibility. For 90
29 migration (Dan et al., 2010), including tissue morphogen- instance, acyclic biophysical strain on normal human 91
30 esis, remodelling and embryonic development (Rutkowski dermal fibroblasts has shown a three-fold increase in NO 92
31 and Swartz, 2007) through mechanisms such as direct when applied at 10% magnitude for 72 h (Dodd et al., 93
32 shear stress, matrix-cell transduction and autologous 2006). In addition, an increased sensitivity to NO via 94
33 gradient formation. Interstitial flow may also be enhanced phosphokinase signalling, together with a 12.2% increase in 95
34 by the interplay of calcium ion concentration and unbound NO secretion, were found in fibroblasts following modelled 96
35 water oscillations (Lee, 2008), whose respective electric myofascial release (Cao et al., 2013b). This suggests a po- 97
36 and pressure gradients improve the transport of oxygena- tential clinical role for NO in wound healing by promoting 98
37 tion and nutrients in the tissues. Since fluid flow in the ECM cell proliferation and migration. NO is an important sig- 99
38 is likely to transport metabolic and messenger substances nalling molecule whose known beneficial effects (Tota and 100
39 (Meert, 2012), it may indeed play a role in restoring Trimmer, 2011), may explain some of the therapeutic re- 101
40 homoeostasis where it has been compromised. For sults following fascial work. It may be involved in promot- 102
41 instance, it could improve drainage of inflammatory medi- ing tissue repair and collagen synthesis, improving clinical 103
42 ators, so decreasing chemical irritation and nociceptive symptoms and functions following injury (Bokhari and 104
43 stimuli to nerve endings, hence leading to a reset of aber- Murrell, 2012); in smooth muscle relaxation and angiogen- 105
44 rant reflexes underlying somatic dysfunction. esis (Ziche and Morbidelli, 2000); in neurotransmission 106
45 (Garthwaite, 2008) as well as in the response to immuno- 107
46 gens (Wink et al., 2011). 108
47 Endocrine-immunity response There is a strong possibility that the physiological effects 109
48 of myofascial work may be in part due to stimulation of the 110
49 The evidence suggests that manual therapy focussed on endocannabinoid system (McPartland et al., 2005). This 111
50 myofascial tissues could cause hormonally mediated effects system affects fibroblast remodelling and may play a role in 112
51 that persist for several days and modulate the fascial reorganisation by diminishing nociception and 113
52 hypothalamic-pituitary-adrenal axis and immune function reducing inflammation in myofascial tissue (McPartland, 114
53 (Rapaport et al., 2012, 2010; Morhenn et al., 2012). How- 2008). Osteopathic treatment, including myofascial work 115
54 ever, such hormonal response does not occur following to specific sites of somatic dysfunction, has demonstrated a 116
55 isolated articulatory techniques such as the osteopathic change in the concentration of several circulatory noci- 117
56 technique known as rib raising directed towards enhanced ceptive biomarkers in patients with chronic low back pain 118
57 thoracic mobility, respiration efficiency and lymph-flow (Degenhardt et al., 2007). Amongst other results, the in- 119
58 (Henderson et al., 2010). Interestingly, the response to crease in N-palmitoylethanolamide (an endogenous fatty 120
59 myofascial treatment can differ quite profoundly depend- acid amide with potent analgesic and anti-inflammatory 121
60 ing on the frequency of therapeutic sessions. Consistently properties) was found 30 min after intervention, at a con- 122
61 with results from a previous study (Rapaport et al., 2010), a centration two times greater than that observed in control 123
62 once-a-week intervention demonstrated patterns of change subjects. 124

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
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+ MODEL
A unifying neuro-fasciagenic model of somatic dysfunction 7

1 Finally, it has been proposed that fascial work may together with peripheral blood flow and therefore body 63
2 enhance cytokine pools from actively proliferating fascial temperature (Ahmed et al., 1982). All these interactions 64
3 fibroblasts (Willard et al., 2010), which may be delivered appear to be centrally coupled, interconnected and 65
4 beyond the sites being treated via intrafascial blood flow modulated (Dick et al., 2009, 2014), hence suggesting 66
5 (Bhattacharya et al., 2005). pulmonary respiration as an entry point for the homoeo- 67
6 static potential of the body during treatment. 68
7 Epigenetics 69
8 70
9 Vibratory and oscillatory activating forces 71
Mechanical forces seem to be crucial regulators of cell
10 72
behaviour and tissue differentiation by affecting gene
11 Oscillations and vibrations are frequently applied as acti- 73
regulation at the epigenetic level, therefore producing an
12 vating forces in many fascial manoeuvres. Sutherland 74
heritable reduction of DNA methylation (Arnsdorf et al.,
13 (1990) suggested the benefits of vibration applied to the 75
2010). In other words, “mechanical stimulation can pro-
14 lymphatics, while Mitchell (1999) proposed vibrations as a 76
duce durable alterations in gene expression during cell
15 way to counteract the myotactic reflex in hypertonic 77
lineage commitment” (Arnsdorf et al., 2010). It can be
16 muscles. Fulford’s percussion hammer, in particular, is 78
speculated that a therapeutic mechanical load might pro-
17 proposed as an effective tool to treat fascial dysfunctions 79
duce the same sort of effects. These epigenetic changes
18 by applying beneficial vibrational frequencies to the 80
may also regulate extracellular matrix composition,
19 affected tissue (Fulford and Stone, 1997). Interestingly, 81
inflammation, angiogenesis and fibroblast activity involved
20 fascial tissue seems to display a physiological oscillatory 82
in tissue repair and function (Bavan et al., 2011). Mechan-
21 behaviour at a cellular level. Castella et al. (2010) have 83
ical signals applied in the form of vibration to hydrogel-
22 shown that myofibroblastic contractions exhibit periodic 84
encapsulated fibroblasts in culture have also been demon-
23 oscillation periods of approximately 100 s (1 c.p. 100 s), 85
strated to be a critical epigenetic factor in regulating the
24 modulated by periodic intracellular calcium oscillations. 86
microenvironment of the ECM. In particular, they produce
25 These in turn are mediated via cell adherence junctions 87
significant increases in glycosaminoglycans and decreases in
26 (Follonier Castella et al., 2010) that could explain the in- 88
collagen, thus providing a basis for reducing tissue adhe-
27 crease of calcium oscillation frequencies in myofibroblasts 89
sions and improving connective tissue function (Kutty and
28 when an increased mechanical load is applied and trans- 90
Webb, 2010).
29 mitted through such intercellular junctions. In turn, this 91
30 also induces reactive changes in the contractile cell 92
31 Respiration behaviour (Godbout et al., 2013). 93
32 Research suggests that vibration and oscillation of 94
33 Traditionally, patient respiratory cooperation has been different amplitude, forces or frequencies (from 8 to 95
34 used in osteopathic practice to assess and treat vertebral, 110 Hz), applied from seconds to 45 min, and whether 96
35 appendicular, cranial, visceral and soft tissue dysfunc- manually or artificially induced, may have an influence on a 97
36 tions, including myofascial ones, especially in acute pre- variety of body functions, such as: modulating spinal 98
37 sentations (Kimberly, 1949). It has also been used to excitability (Kipp et al., 2011) and pain perception in both 99
38 promote patient relaxation, or divert his/her attention. healthy and chronic patients (Kosek and Hansson, 1997); 100
39 Most osteopathic fascial techniques may require a respi- increasing tissue blood perfusion with the increase of 101
40 ratory co-operation when holding tissues at the barrier vibratory load (Fuller et al., 2013); enhancing fascial 102
41 point, or while keeping them at a balance point. Suther- interstitial fluid flow, as suggested by a mathematical 103
42 land, in particular, proposed it as a specific tool to exag- model (Roman et al., 2013); increasing oxygen saturation 104
43 gerate dysfunction and induce correction: “. the and improving pulmonary mechanism and perfusion 105
44 respiratory movement picks up the abnormally related (Doering et al., 1999); modulating blood flow in different 106
45 parts and swings them into motion in unison with contig- cerebral areas (Coghill et al., 1994); improving joint range 107
46 uous parts” (In Hoover, 1945). Such respiratory contribu- of motion (Bakhtiary et al., 2011) and reducing muscle 108
47 tion may play a role in relaxation of the myofascia and stiffness (Peer et al., 2009); enhancing wound healing 109
48 improvement in joint mobility, indeed breathing fre- processes and regeneration of vessels by also reducing local 110
49 quency seems to be synchronized with cerebral electrical oedema and general congestion (Leduc et al., 1981); 111
50 activity (Busek and Kemlink, 2005) and to produce both a regulating the microenvironment of the ECM at an epige- 112
51 mechanical effect on resting myofascial tissue (Cummings netic level, when applied to fibroblasts in vitro (Kutty and 113
52 and Howell, 1990) and to have a neurological influence on Webb, 2010); and improving cognitive performance in 114
53 non-respiratory muscles (Kisselkova and Georgiev, 1979). both healthy and pathological conditions (Fuermaier et al., 115
54 This shows the interaction of respiration with the muscu- 2014). Furthermore, manual low frequency oscillations may 116
55 loskeletal system. Furthermore, breathing frequency has induce myofascial relaxation by influencing motoneuron 117
56 the ability to be synchronised with oscillations in blood excitability (Newham and Lederman, 1997), or by producing 118
57 pressure (De Burgh Daly, 1986), heart rate (Song and an inhibitory effect on vestibular nuclei, hence inducing a 119
58 Lehrer, 2003) and lymphatic flow (Zawieja, 2009), psychogenic relaxation (Ayres, 1979). As Littlejohn stated 120
59 together with being amplified due to resonance effects (1902): “There is no function of the body that does not 121
60 between these systems (Courtney, 2009). Through fre- have peristaltic or rhythmic vibrations . the power of 122
61 quency entrainment, pulmonary respiration may also osteopathic treatment occurs from its effect upon physio- 123
62 potentially modulate autonomic activity (Gilbey, 2007), logic oscillations”. 124

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
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+ MODEL
8 P. Tozzi

1 Bioenergetic interactions be the balancing of resonant vibratory circuits. Osteopathic 63


2 manipulative treatment may entrain such physiological 64
3 All cells appear to generate and detect electromagnetic phenomena, restoring harmonic resonance where disso- 65
4 fields, ranging from kHz to the visible part of the electro- nance is present (McPartland and Mein, 1997). 66
5 magnetic spectrum (400e790 THz) (Cifra et al., 2011). 67
6 These fields may be forms of non-chemical cell signalling Finally, the human body has been demonstrated to emit 68
7 able to influence cell proliferation rate and morphology ultra-weak photons in the visible part of the electromag- 69
8 (Rossi et al., 2011). In addition, such electromagnetic sig- netic spectrum (380e780 nm) and in the range from 1 to 70
9 nals may be amplified by ion channels, with ionic flow 1000 photons  s 1  cm 2 (Schwabi and Klima, 2005). This 71
10 oscillating at various coherent frequencies as an intracel- property is the result of cellular metabolic activities and 72
11 lular sensing system (Galvanovskis and Sandblom, 1997). appears to be enhanced by increased oxidative processes 73
12 Furthermore, ion channels and pumps seem to modulate (Rastogi and Pospı́sil, 2010). The quantum state of photons 74
13 endogenous transmembrane resting voltage potential that, emitted by a subject could be in a coherent state and un- 75
14 in turn, may regulate cell proliferation, migration and dif- dergoing constant variations (Van Wijk et al., 2008), dis- 76
15 ferentiation, serving as an informational signalling pathway playing a typical anatomic percentage distribution pattern, 77
16 (Adams and Levin, 2013). Importantly, this is a mediator of depending on the individuals’ condition and vitality. Photon 78
17 large-scale anatomical polarity with an effect on gene emissions may be used by cells and tissues as a modality of 79
18 regulation pathways, hence influencing tissue morphogen- communication, independently from chemical and cell-to- 80
19 esis, development and regeneration (Levin, 2014). Inter- cell contact signalling (Scholkmann et al., 2013). They 81
20 estingly, endogenous electrical potentials may promote may also represent an informational and regulatory system 82
21 epithelial cell migration and wound healing (Zhao, 2009), as (Kucera and Cifra, 2013) affecting at least energy uptake, 83
22 well as angiogenic responses in endothelial cells (Zhao cell division rate and growth correlation (Fels, 2009). This 84
23 et al., 2004). This phenomenon is mediated by polarized property may be deregulated or altered in case of 85
24 activation of multiple signalling pathways that include ki- dysfunction or disease e including those affecting connec- 86
25 nases, membrane growth factor receptors and integrins. tive tissue e and related to a generally high oxidative status 87
26 Fibroblasts in particular have shown to be highly responsive of the organism (Popp, 2009). Interestingly, the emissions 88
27 to endogenous electrical fields, by aligning themselves intensity decreases with a reduction in body temperature 89
28 perpendicular to the electrical current and consequently and oxygen concentration (Nakamura and Hiramatsu, 90
29 modulating their motility (Guo et al., 2010). They also seem 2005), while it reduces in long-term practitioners of medi- 91
30 to respond to exogenous electricity; exposure to electrical tation, as a probable reflection of different free radical 92
31 stimulation of 50 or 200 mV/mm promotes wound healing reactions in the organism (Van Wijk et al., 2006). This ev- 93
32 by enhancing growth factor secretion, skin fibroblast idence suggests the integrative use of additional strategies 94
33 migration and fibroblast to myofibroblast differentiation such as nutritional care, appropriate physical activity, 95
34 (Rouabhia et al., 2013). ‘mind-body’ therapy to enhance therapeutic effects of 96
35 Therefore, electromagnetic fields appear to be strictly manual treatment of somatic dysfunction by reducing the 97
36 related to ionic flow and oscillations, and these in turn are general oxidative status in patients. 98
37 highly responsive to mechanical tension via stretch- 99
38 activated calcium channels (Follonier Castella et al., 100
39 2010). (Therapeutic) mechanical pressure or electrical Additional strategies 101
40 stimulation may be amplified and propagated by proton 102
41 currents or coherent oscillations and polarization waves - Physical Exercise 103
42 throughout the organism (Pang, 2012). Such proton con- 104
43 duction may be coupled with electron transfer (Cukier and Specific physical training programs for fascial tissue may be 105
44 Nocera, 1998) and with hydrogen-atom translocation along applied (Schleip and Müller, 2013), implying elastic recoil, 106
45 the watereproteins complex (Cukier, 2004). In this sense, it slow and dynamic stretching, rehydration practices and 107
46 can be speculated that fascia combines the property of a proprioceptive refinement. It has been demonstrated that 108
47 sol-liquid conductor and of a crystal generator system due the elastic storage capacity and subsequent recoil of the 109
48 to the liquid crystal continuum of the matrix, which can elastic energy in tendons may significantly increase, with a 110
49 generate and conduct direct currents as well as vibrations. decrease in stiffness, following physical exercise programs 111
50 (Ishikawa and Komi, 2004; Reeves, 2006), without affecting 112
51 Hypothesis. A yet more interesting possibility is that the fascial thickness (Uzel et al., 2006). Furthermore, fascia- 113
52 liquid crystalline continuum of the body matrix may function specific stretching protocols may produce long-term bene- 114
53 as a quantum holographic medium, recording patterns of fits where there is chronic fascial pain and improve physi- 115
54 local activities interacting with a globally coherent field. ological function and patient satisfaction (Digiovanni et al., 116
55 During bodywork an interaction of vibrational, biomagnetic 2006). 117
56 and bioelectric fields between therapist and client may take 118
57 place. This would allow an exchange of information about - Nutrition 119
58 the history and the present status of the living matrix, which 120
59 is encoded in cell and tissue structure, and which is A tryptophan or atherogenic diet may increase oxidative 121
60 accessable holographically by tuning to the appropriate damage in muscles, with infiltration of inflammatory cells in 122
61 frequencies (Oschman and Oschman, 1994). The result may muscular fascia (Ronen et al., 1999). Instead, an anti- 123
62 124

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
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+ MODEL
A unifying neuro-fasciagenic model of somatic dysfunction 9

1 inflammatory diet may provide a natural approach to mean not only the narrow effect of an imitation intervention 63
2 reduce inflammation, also in the case of musculoskeletal but also the broad amalgam of nonspecific effects present in 64
3 conditions (Marcason, 2010). It mainly implies a reduction any patientepractitioner relationship, including attention; 65
4 of intake of saturated fatty acids, with an increase of plant- communication of concern; intense monitoring; diagnostic 66
5 based food (Pomari et al., 2014), beverages rich in poly- procedures; labelling of complaint; and alterations pro- 67
6 phenolic catechins (such as green tea), cold water fish duced in a patient’s expectancy, anxiety, and relationship to 68
7 (Kris-Etherton et al., 2002), culinary herbs and spices with the illness” (Kaptchuk, 2002). Traditionally, placebo is 69
8 anti-inflammatory effects e such as ginger and turmeric e thought of as a nuisance in clinical and pharmacological 70
9 (Tapsell et al., 2006). In particular, a group of aromatic research, and controls are employed to filter out non- 71
10 ketones, called chalcones, present in several plants such as specific, undesired and psychological effects that may 72
11 licorice and mulberry, have been linked with immunomo- interfere with the results from a particular therapeutic 73
12 dulation, anti-inflammatory and anti-oxidant activities intervention. However, it is likely that an individual’s un- 74
13 (Yadav et al., 2011). For example: avocado and soybean derstanding of the intervention influences the effects of any 75
14 oils, etc, contain biologically active compounds that are given therapeutic approach, showing the importance of 76
15 able to produce long-term beneficial effects in the symp- placebo in clinical, scientific and physiological fields 77
16 toms of osteoarthritis (Ragle and Sawitzke, 2012); devil’s (Oeltjenbruns and Schäfer, 2008). This then drives research 78
17 claw has been used to treat degenerative disorders of the to further our understanding of the underlying mechanisms, 79
18 musculoskeletal system, and for its pain-relieving, anti-in- which is needed in order to maximize therapeutic results in 80
19 flammatory and anti-oxidant actions (Akhtar and Haggi, clinical practice (Walach and Jonas, 2004). Placebo anal- 81
20 2012); crude extract of blueberries, rich in phenolic acids gesia is now considered as a biological phenomenon, 82
21 and flavonoids, have anti-nociceptive and anti- implying both opioid and non-opioid mechanisms (Carlino 83
22 inflammatory properties (Torri et al., 2007); and extracts et al., 2011) that are measurable through brain imaging 84
23 from plants such as Phyllanthus corcovadensis have technologies and that can be pharmacologically blocked and 85
24 demonstrated potent anti-nociceptive effects (Gorski behaviourally enhanced (Greene et al., 2009). It seems to be 86
25 et al., 1993). Finally, the balance in the omega 6/omega dependent on frontal cortical areas that generate and 87
26 3 ratio in dietary patterns is crucial for the maintenance of maintain cognitive expectancies, which in turn may be 88
27 health (Gómez Candela et al., 2011), as well as for the reinforced by dopaminergic reward pathways (Faria et al., 89
28 prevention and management of inflammatory conditions 2008). Finally, the ability of placebo to modulate periph- 90
29 (Simopoulos, 2009), or as an adjunct treatment for chronic eral immune reactivity is plausible (Pacheco-López et al., 91
30 arthritis (James and Cleland, 1997). 2006), although “other placebo responses result from less 92
31 conscious processes, such as classical conditioning in the 93
32 - Meditation case of immune, hormonal, and respiratory functions” (Price 94
33 et al., 2008). Recent research on placebo response, placebo 95
34 Mindfulness meditation and breath therapy seem to play analgesia and nocebo has shown how the psychosocial 96
35 a role in improving quality of life and sense of coherence in aspect of every treatment is crucial in determining the na- 97
36 people who start with a low health assessment (Fernros ture and degree of a placebo effect, affecting both research 98
37 et al., 2008). In particular, mindfulness-based treatment and clinical practice (Koshi and Short, 2007; Marchand and 99
38 may reduce cortisol level, proinflamatory cytokines and Gaumond, 2013). ‘Alternative and complementary’ medi- 100
39 blood pressure (Carlson et al., 2007), with enhanced out- cine may also have an enhanced placebo effect, compared 101
40 comes for health and quality of life in chronic disease, with mainstream medicine, through a ritual-based “perfor- 102
41 including musculoskeletal disorders (Merkes, 2010). mative efficacy” (Kaptchuk, 2002). 103
42 Furthermore, when associated with home meditation prac- 104
43 tice, it may ameliorate pain intensity and functional limi- 105
44 tations in chronic musculoskeletal conditions (Rosenzweig Cognitive-behavioural factors and multidisciplinary 106
45 et al., 2010). Breath therapy integrating body awareness, approach 107
46 breathing, meditation and movement appears to produce 108
47 significant improvement in chronic low back pain and coping Manual therapeutic intervention should never be focused 109
48 skills (Mehling et al., 2005). Finally, yoga intervention may on the dysfunctional or symptomatic area exclusively, apart 110
49 reduce pain and catastrophizing, increase acceptance of the from in some presentations such as time-limited emergency 111
50 condition and alter total cortisol levels in people with situations. Instead, the multidimensional aspect of pain 112
51 chronic disorders (Curtis et al., 2011). Even more, it may should be considered, especially for chronic patients (Lima 113
52 improve functional disability in people with chronic low back et al., 2014), with respect to the tenet of the body, mind 114
53 pain (Holtzman and Beggs, 2013), with both short and long- and spirit unity (Rogers et al., 2002). Therefore, in order to 115
54 term effectiveness (Cramer et al., 2013). approach the totality of an individual (not just ‘a pain’), 116
55 including his/her social environment, it is necessary to 117
56 wisely apply biopsychosocial models (Flor and Herman, 118
57 Placebo 2004) e considered as congruous with osteopathic princi- 119
58 ples (Penney, 2010) e as well as interdisciplinary paradigms 120
59 Placebo effects are complex phenomena, possibly mediated (Gatchel, 2005), which resonate with osteopathic philoso- 121
60 by specific physiological and neural mechanisms, but these phy (Mackintosh et al., 2011). Instead of just treating a 122
61 are currently poorly understood (Miller et al., 2013). In the dysfunction, health should be promoted through a saluto- 123
62 field of manual therapy, “the term placebo effect is taken to genic process (Antonovsky, 1979) that is guiding the patient 124

Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
YJBMT1216_proof ■ 17 March 2015 ■ 10/18

+ MODEL
10 P. Tozzi

1 from the cure of the disease to the protection and poten- status) may also be included, if appropriate, since it ap- 63
2 tiation of their own health and quality of life. Information pears to have a strong impact on the rehabilitation process 64
3 and education are the key tools to guide the patient and of those with chronic musculoskeletal disorders (Hamberg 65
4 his/her social environment through such a process, where et al., 1997), and improve immune function and cardio- 66
5 the operator may just be a catalyst for the change to take vascular health (Kiecolt-Glaser and Newton, 2001; Kiecolt- 67
6 place (Gafni et al., 1998). In addition, the social coherence Glaser et al., 2010). 68
7 of interdisciplinary and inter-sectorial action is crucial to The interaction between mind, body, behaviour, and the 69
8 support health-related quality of life (Drageset et al., 2009) environment is thus a crucial factor affecting the patients 70
9 as well as the process of health through the course of life physical and psychological health, and is used in ‘mind- 71
10 (Eriksson and Lindström, 2008). body’ medicine clinics to treat stress-related or chronic 72
11 Maladaptive behaviours, fears and emotional experience conditions by improving disease coping strategies and the 73
12 of pain, catastrophism, helplessness, expectations, thrust, overall quality of life (Gimpel et al., 2014). 74
13 cognitive factors, faith, beliefs and personality all need to 75
14 be addressed in a comprehensive and integrative concep- 76
15 tual model that is applied to the clinical assessment, Conclusion 77
16 treatment and management of patients with pain, and in 78
17 particular when pain is persistent (Keefe et al., 2004; It is evident that various factors may interplay with myo- 79
18 Nicholas et al., 2011). These factors should be identified fascial structure and function as well as with its ability to 80
19 and managed as far as reasonably possible in order to respond to treatment. The effects of manual fascial in- 81
20 support and promote active coping strategies (Jensen terventions can be local (as tissue texture changes), 82
21 et al., 1991), mechanisms of self-efficacy (Bandura, 1982) segmental (as via neurological response) and global (as 83
22 and an empowerment process (Haldeman et al., 2008). through hormonal effects) in extent, and may occur at 84
23 These mechanisms may increase tolerance for pain through different intervals e ranging from minutes to weeks e after 85
24 endogenous opioid activation, when confronted with a a given input, with many interacting mechanisms influ- 86
25 painful stimulus (Bandura et al., 1987). Conversely, pa- encing tissue properties and behaviours, including placebo 87
26 tients with chronic pain and high levels of depression tend (Fig. 1). Some of these factors are strongly supported by the 88
27 to experience and rate their pain as more severe (Parmelee available evidence whereas others need further investiga- 89
28 et al., 1991). Probably through a similar process, a patient’s tion. Nevertheless, connective tissue may serve as a trait 90
29 attitude may strongly influence the effect of myofascial d’union of all these elements, potentially representing a 91
30 treatment. For instance, patients with cancer-related fa- meta-system (Langevin, 2006) that coherently influences 92
31 tigue who had a positive attitude towards manual therapy structure and function of the whole organism and the 93
32 showed a significant (p > .05) increase of immune response interaction between its constituents. 94
33 (IgA), compared to the control group, following myofascial In the light of what has been presented in this work, the 95
34 release (although no difference was found in the pressure author suggests an integration of the existing five osteo- 96
35 pain threshold) (Fernández-Lao et al., 2012a). Further- pathic models e structural, respiratory-circulatory, meta- 97
36 more, a positive patient attitude may positively modulate bolic, neurologic and behavioural (E.C.O.P., 2011b). These 98
37 the impact of manual therapy compared to a placebo group are conceptual models of assessing, treating and caring for 99
38 (Fernández-Lao et al., 2012b). patients in osteopathic practice. They are all based on 100
39 A multidisciplinary approach is paramount to achieve anatomy, physiology, biochemistry and psychology princi- 101
40 the most desirable clinical outcomes, especially in chronic ples, providing five specific lenses through which osteo- 102
41 patients (Pergolizzi et al., 2013), also those with musculo- paths may interpret and approach patients. In other words, 103
42 skeletal pain (Hildebrandt et al., 1996) and even in a pri- they provide five different relations of structure and func- 104
43 mary care setting (Kim et al., 2010). Multidisciplinary tion, reflecting five different physiological modalities of 105
44 rehabilitation programs have been demonstrated to be body adaptation to inner and outer stressors. They are 106
45 more effective than the care given by independent physi- normally used in integration in osteopathic practice to 107
46 cians in patients with chronic low back pain, when orga- release dysfunctional patterns, restore function and pro- 108
47 nized with the cooperation of local health-care providers in mote health (Seffinger et al., 2011). In particular, the 109
48 the community (Lang et al., 2003). Its clinical imple- musculoskeletal system has traditionally been presented as 110
49 mentation may extend to include relaxation training, the main interface of these models (Hruby, 1992), by 111
50 biofeedback, hypnosis, imagery, cognitive-behavioural influencing and maintaining communication with all the 112
51 therapy (Golden, 2002), social reinforcement and time- other body functions. Korr (1976) defined it as the “primary 113
52 contingent medications, but it may also require the inter- machinery of life”, indicating the musculoskeletal system 114
53 action of rehabilitative, occupational, pharmaceutical, as more than just a framework which supports and contains 115
54 surgical, orthesic, psychological and nutritional care. Group the viscera of the body, but as the main dynamic compo- 116
55 therapy programs also seem to produce good results. For nent of the living body through which we function, live, 117
56 instance, patients with chronic musculoskeletal pain move, interact and express ourselves. However, the major 118
57 improve their self-awareness and active coping strategies, element through which the musculoskeletal system in- 119
58 with a decreased pain experience, when participating in fluences the body’s response in health and disease has been 120
59 group sessions of experience-oriented learning programmes traditionally indicated as the nervous system. As an alter- 121
60 (Steen and Haugli, 2001). native, this paper suggests that fascia might be the over- 122
61 Psychological support that deals with the patient’s looked somatic component interplaying between the 123
62 relationship difficulties (such as those related to marital musculoskeletal system and its function as the ‘primary 124

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Figure 1 Fasciagenic treatment effects. The diagram shows the possible effects of manual fascial treatment, reinforced by
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activating forces to prompt release. These effects may occur at different times, ranging from minutes during or after intervention,
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to days and week, producing several tissue responses and changes that normalize somatic dysfunction features (tissue texture
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changes, asymmetry, restriction of motion, tenderness). Additional strategies may reinforce the therapeutic effects of manual
36 98
work to fascia. The psychosocial-behavioural aspect could also ultimately influence and be influenced by these processes.
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39 machinery of life’ also because of the shared embryologic laying between and playing within the other models; by 101
40 origin. As suggested by the work of Blechschmidt and integrating and coordinating their activity; by pervading 102
41 Gasser (2012), each connective tissue in the body pre- their essence, but also transcending their contingent na- 103
42 sents a functional and anatomical continuity, due to their ture; and finally by providing a structural and functional 104
43 common embryologic origins in the mesoderm, although framework for the body’s homoeostatic potential and its 105
44 loading demands acting through and upon tissues can inherent abilities to heal. By its nature, it is the only model 106
45 determine their differentiation by influencing fibre that resonates with A.T. Still’s original intention: “. this 107
46 arrangement, length, and density. philosophy (of Osteopathy) has chosen the fascia as a 108
47 In addition, due to the multi-functional nature and foundation of which to stand .” (Still, 1899). 109
48 ubiquitous structure of fascial tissue e that makes it a In conclusion, rather than defining bits and pieces of this 110
49 unique component in the musculoskeletal apparatus e the body wide fascial structure (Stecco, 2014) e as if it is just a 111
50 author suggests the addition of a sixth ‘meta-model’ that dead tissue to be surgically dissected and named in its single 112
51 integrates but also transcends the musculoskeletal system components, and separated from surrounding tissues e the 113
52 itself, the connective tissue-fascial model. This is the only author recalls Hollinshead (1974): “descriptions of fascia 114
53 tissue providing intracellular and extracellular connection tend to be confusing . all connective tissue in the body is 115
54 as well as communication at all levels between each body continuous with all other connective tissue. Thus, in one 116
55 system; it offers various mechanisms for information sig- sense, a fascia has no beginning and no end, and any 117
56 nalling together with several forms of transducing infor- description of fascias is necessarily somewhat arbitrary”. 118
57 mation; it is an embodying structure that expresses This concept of intrinsic multi-tissue continuity has been 119
58 coherent functions from molecular to macroscopic scales, advanced by various authors, who highlighted the structural 120
59 allowing their constant interdependence in health as well and functional interrelationship between muscular, fascial, 121
60 as in disease e all features that no other musculo-skeletal ligamentous, capsular and articular components. Such 122
61 element can display to this extent. This sixth osteopathic whole-body connection has been referred to as ‘ectoskele- 123
62 model is the true interface between all body systems, by ton’ (Wood Jones, 1944), ‘ligamentous complex system’ 124

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12 P. Tozzi

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Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
treatment e Part II, Journal of Bodywork & Movement Therapies (2015), http://dx.doi.org/10.1016/j.jbmt.2015.03.002
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Please cite this article in press as: Tozzi, P., A unifying neuro-fasciagenic model of somatic dysfunction e Underlying mechanisms and
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