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Clinical Relevance of Fascial Tissue and Dysfunctions

Article  in  Current Pain and Headache Reports · August 2014

DOI: 10.1007/s11916-014-0439-y · Source: PubMed

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Curr Pain Headache Rep (2014) 18:439

DOI 10.1007/s11916-014-0439-y
1
3 MYOFASCIAL PAIN (R GERWIN, SECTION EDITOR)
2

4 Clinical Relevance of Fascial Tissue and Dysfunctions

8
6 W. Klingler & M. Velders & K. Hoppe & M. Pedro &
7 R. Schleip
9

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10
# Springer Science+Business Media New York 2014

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11

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12 Abstract Fascia is composed of collagenous connective tis- Imbalance of this regulatory mechanism results in increased or 26
13 sue surrounding and interpenetrating skeletal muscle, joints, decreased myofascial tonus, or diminished neuromuscular co- 27
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14 organs, nerves, and vascular beds. Fascial tissue forms a ordination, which are key contributors to the pathomechanisms 28
15 whole-body, continuous three-dimensional viscoelastic matrix of several musculoskeletal pathologies and pain syndromes. 29
16 of structural support. The classical concept of its mere passive Here, we summarize anatomical and biomechanical properties 30
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17 role in force transmission has recently been disproven. Fascial of fascial tissue with a special focus on fascial dysfunctions 31
tissue contains contractile elements enabling a modulating and resulting clinical manifestations. Finally, we discuss cur-
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18 32
19 role in force generation and also mechanosensory fine- rent and future potential treatment options that can influence 33
20 tuning. This hypothesis is supported by in vitro studies dem- clinical manifestations of pain syndromes associated with 34
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21 onstrating an autonomous contraction of human lumbar fascia fascial tissues. 35

22 and a pharmacological induction of temporary contraction in
23 rat fascial tissue. The ability of spontaneous regulation of
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24 fascial stiffness over a time period ranging from minutes to Keywords Myofascial pain . Fascia . Lumbar fascia . 36
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25 hours contributes more actively to musculoskeletal dynamics. Dysfunction 37

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W.K. and M.V. contributed equally to this paper.

This article is part of the Topical Collection on Myofascial Pain Introduction
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38
W. Klingler : R. Schleip (*)
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Q1 =Q2 Fascia Research Group, Division of Neurophysiology, Ulm In recent years, fascia has aroused increasing interest for both 39
University, Albert-Einstein-Allee 11, 89081 Ulm, Germany biomedical scientists and manual body therapists [1]. This is, 40
Q3 e-mail: robert.schleip@uni-ulm.de
at least in part, a result of recent developments in tissue 41
W. Klingler : R. Schleip imaging and advanced assessment technologies: high- 42
Department of Neuroanaesthesiology, Neurosurgical University resolution ultrasound to assess the efficacy of manual therapy; 43
Hospital, Guenzburg, Germany in vivo measurement of fascial behavior using myometry or 44
bioelectrical impedance; and digital analysis of the fascial 45
W. Klingler : K. Hoppe
Department of Anaesthesia, Ulm University, Ulm, Germany tissue throughout the body [2–4]. International research net- 46
works were founded, which now hold regular meetings (e.g., 47
M. Velders fasciaresearchsociety.org). At the first fascia research confer- 48
Division of Sports Medicine, Ulm University, Ulm, Germany
ence (Boston, MA, USA), definitions of fascial tissue were 49
K. Hoppe determined, which comprise connective tissue sheets such as 50
Department of Anaesthesia, University of Frankfurt, Frankfurt, aponeuroses; joint and organ capsules; and also muscular 51
Germany connective tissue. The components are interconnected 52
throughout the whole body, making up a three-dimensional 53
M. Pedro
Department of Neurosurgery, Neurosurgical University Hospital, architecture that is a multilayer system of interconnected 54
Guenzburg, Germany sheets [2, 5, 6•]. 55
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56 Anatomy of Human Fascial Tissue phenomenon of “stitch” is possibly related to a painful disten- 105
sion of the fascial liver and/or kidney organ capsule: unbal- 106
57 Muscular fascia is composed of three structures: superficial anced compensatory mechanisms during athletic endeavors 107
58 fascia, more dense deep fascia; and muscle-related layers may cause a precardial venous congestion followed by stasis 108
59 (epimysium, perimysium, and endomysium) [7]. The superfi- of the venous vasculature and, owing to the low resistance, 109
60 cial fascia is a macroscopically well organized membranous particularly within the liver and spleen, finally results in 110
61 fibroelastic tissue that is, with the exception of the face, the tensional pain of the organ capsule. 111
62 soles of the feet and the palms of the hands, found ubiqui-
63 tously throughout the human body [5]. Microscopically, its
64 structure has been described as being like a tightly packed
Matrix Remodeling in Fascial Tissue 112
65 honeycomb [8]. The deep fascia is a membrane that extends
66 throughout the whole body and is kept under basal tension via
The extracellular matrix (ECM) has been considered to be an 113
67 numerous muscular expansions [6•]. Based on this anatomical
amorphous scaffolding that provides long-term mechanical 114
68 composition, fascial expansions transmit the tension generat-
support. However, recent insights have revealed that this 115

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69 ed by muscle contraction to the neighboring areas, resulting
matrix is a very dynamic structure that modifies mechanical 116
70 in stimulation of the proprioceptors within this area [9].

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and viscoelastic properties, decreases stress susceptibility, and 117
71 Histologically, the deep fascia is formed of a single layer of
may increase load resistance [14]. The skeletal muscle ECM 118

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72 undulated collagen fibers intermixed with elastin fibers, and
consists of noncollagenous glycoproteins and is reinforced by 119
73 independent of the underlying muscle, separated by the epi-

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stiffer fibrous proteins. By building a supramolecular net- 120
74 mysium and a layer of loose connective tissue [6•].
working system, this matrix can transmit contractile muscle 121
forces while maintaining tissue integrity. The ECM provides 122

75
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Biomechanical Properties of Fascial Tissue
intramuscular continuations of neuromuscular tracts in which
blood vessel and nerve branches are embedded [14, 15•]. The
123
124
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viscoelasticity of fascial tissue can alter activation of the nerve 125
76 Fascial tissue exhibits a regulative function during mechanical
receptors within fascia: mechanoreceptors respond to sur- 126
77 force transmission, bypassing mechanical forces via lateral
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rounding tissue viscoelasticity and participate in their re- 127

78 cross-links, buffering energy, and strengthening movements
sponse [16•]. Moreover, molecules of the ECM interact with 128
79 in a way similar to a servomechanism steering a car. Recently,
the sarcolemmal, cytoskeletal, and nuclear elements to main- 129
80 functional ultrasonic investigations of the musculus gastroc-
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tain skeletal muscle integrity [14]. Growing insights into the 130
81 nemius and soleus provided exciting findings: contrary to the
importance of the ECM have revealed that defects or deficien- 131
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82 classical point of view, these muscles operate in an almost

cies in these proteins can result in myopathies like Bethlem 132
isometric manner [10]. The main shortening and elongation is
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83
myopathy or congenital muscular dystrophies [17]. 133
84 mediated by fascial tissue, which is, moreover, enhanced with
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85 movement frequency toward a greater use of the tendon elastic

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86 energy at higher frequencies. In particular, the Achilles tendon

87 operates like an elastic spring, which is able to absorb, store, Inflammation, Myofibroblasts, and Fibrosis 134
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88 and release kinetic energy. The fascia thoracolumbalis func-

89 tions as an energy reserve, which is discharged or recharged Repair of damaged tissue generally begins with a regenerative 135
90 during every single step. Biomechanical investigations with phase, consisting of inflammation and proliferation of stem 136
91 working women of the African Kikuyu clan revealed that cells [18, 19]. Early after injury, innate immune cells invade 137
92 these women are able to carry 70 % of their own body weight damaged skeletal muscle areas to phagocytose tissue debris 138
93 on their head, with only minimally increased energy expendi- and to release signaling molecules to attract further immune 139
94 ture [10, 11]. The effectiveness of energy storage in fascial cells (Fig. 1.). There is a complex interaction between 140
95 tissue is reinforced by several animal examples: gazelles and fibroblasts and skeletal muscle stem cells (satellite 141
96 kangaroos use connective tissue as an elastic spring, utilizing cells). Ablation of fibroblasts in a genetic mouse model 142
97 this mechanism in their primary methods of locomotion [12]. has been shown to deplete the satellite cell pool and reduce the 143
98 A totally different but no less intelligent mechanism is pro- size of regenerating muscle fibers [20]. Release of cytokines 144
99 vided by the fascia of the spleen: racehorses are able to store and chemokines from inflammatory cells contributes to satel- 145
100 30 % of their erythrocytes within the spleen, which can be lite cell and fibroblast activation during the early stages of 146
101 released by contraction of the spleen organ capsule. This regeneration [21, 22]. However, chronic inflammation and 147
102 autotransfusion results in increased physical capacity owing fibroblast activation, for example during chronic tissue dam- 148
103 to an increased capacity to transport oxygen [13]. This age and regeneration in muscular dystrophies, attenuates the 149
104 mechanism is currently unverified in humans; however, the regenerative capacity of satellite cells [23]. 150
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excessive collagen production by cardiac myofibroblasts con- 188

tributes to myocardial stiffness, which compromises ventric- 189
ular function [35]. To date, there are only limited therapeutic 190
options for progressive fibrotic diseases. Use of systemic 191
antifibrotic agents, such as inhibitors of TGF-β1 [36], remains 192
controversial because global inhibition of TGF-β1 could im- 193
pair tumor suppression and stimulate chronic inflammation. 194
Modern therapeutic approaches to treat fibrosis include antag- 195
onism of fibrotic factors in a tissue-specific manner or target 196
molecules that are expressed only in diseased tissues [37]. 197

Fig. 1 Hematoxylin/eosin stained rat skeletal muscle cross-section after

toxin-induced injury. Mononuclear immune cells (dark blue) invade
injured skeletal muscle areas 12 h after injury [18] Increase of Fascial Stiffness 198

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Increased matrix stiffness can lead to, or contribute to,

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199
151 Use of nonsteroidal anti-inflammatory medication myofascial pain. Most notably, painful contractures are mostly 200

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152 (NSAIDs) is widespread in the sporting community to associated with an increase in fascial tissue (Table 1). Global 201
153 reduce pain prior to or after intense or unaccustomed conditions include spastic palsy, for example after stroke; 202

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154 exercise. However, chronic use of NSAIDs has been shown neuromuscular disease; or autoimmune diseases, such as rheu- 203
155 to impact negatively on satellite cell activation and prolifera- matoid arthritis or scleroderma. Focal increase of fascial stiff- 204
156 tion during recovery from endurance and strength exercise
D ness is found in several contractures that are characterized by a 205
157 [24, 25]. In contrast to skeletal muscle regeneration, no in- dense connective tissue rich of myofibroblasts, which are 206
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158 flammatory response could be observed after acute exercise in often associated with past or present inflammatory processes. 207
159 tendinopathic human tendon. Consequently, treatment with Table 1 presents an overview of related pathologies. The 208
160 NSAIDs had no effects on inflammatory gene expression in following sections highlight only a few of these conditions. 209
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161 tendinopathic Achilles tendon [26].

162 Chronic inflammation can lead to the development of scar
163 tissue formation (fibrosis). Fibrosis is the leading cause of
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164 deaths in the USA, where 45 % of deaths can be attributed Hypermobility 210
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165 to some type of fibroproliferative disease, such as pulmonary

fibrosis, systemic sclerosis, liver cirrhosis, cardiovascular dis- A lack of tissue stiffness can lead to soft tissue pain. One of the
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166 211
167 ease, progressive kidney disease, and macular degeneration most frequent conditions in this respect is general joint 212
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168 [27]. Fibrosis occurs owing to the excessive production of hypermobilty. When associated with symptoms it is referred 213
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169 ECM components such as collagen and fibronectin by con- to as hypermobility syndrome (Table 1). This condition is 214
170 tractile myofibroblasts, which are characterized by the expres- characterized by an excessive range of joint movement, taking 215
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171 sion of α-smooth muscle actin [28, 29]. Myofibroblasts orig- age, sex, and ethnicity into consideration. It is considered a 216
172 inate from different cellular sources depending on the pathol- hereditary multisystemic connective tissue disorder. 217
173 ogy or physiological situation, including locally residing mes- Prevalence in European populations is reported as 10 %; in 218
174 enchymal cells such as fibroblasts and bone marrow-derived other ethnic groups it is 25 %. It is more frequent in women, 219
175 fibrocytes [30]. Mechanical stress, as well as the presence of and an association of this condition has been confirmed with 220
176 transforming growth factor (TGF)-β1, is essential to convert fibromyalgia, mitral valve prolapse, and panic disorder [38]. 221
177 fibroblasts to myofibroblasts [31]. Contractile activity of The soft tissue pain associated with this condition tends to 222
178 myofibroblasts increases in response to extracellular mechan- be widespread without conforming to anatomical details, and 223
179 ical challenges due to increased calcium oscillation frequen- tends to be resistant to even strong analgesics, including 224
180 cies [32]. Furthermore, cytokines and growth factors released opiates. Pain is often aggravated by active movement, and 225
181 from immune cells during the inflammatory response stimu- therefore the condition is frequently associated with 226
182 late the migration of fibroblasts into damaged tissue regions kinesiophobia. Current therapeutic strategies include exercises 227
183 and trigger the phenotypic switch towards myofibroblasts for core and joint stabilizing, proprioception enhancement, 228
184 [33]. Mesenchymal cells from the vasculature, such as coupled with pain management training based on cognitive 229
185 pericytes and smooth muscle cells, serve as myofibroblast behavioral therapy, as well as with a general fitness program 230
186 precursors during blood vessel repair and are also involved aimed at reversing the inevitable muscle conditioning that 231
187 in the development of systemic sclerosis [34]. In the heart, results from pain inhibition and kinesiophobia. 232
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t1:1 Table 1 Comparison of fascial

t1:2 dysfunctions affecting biome- Lack of stiffness Increase of stiffness Decreased shearing ability
chanical tissue properties
t1:3 Local • Inguinal hernia • Dupuytren contracture • Nerve compression syndromes
• Abdominal hernia • Frozen shoulder • Postsurgical abdominal adhesions
• Lumbar hernia • Morbus Ledderhose • Chronic low back pain
• Hypertrophic scars
• Peyronie’s disease
• Plantar fasciosis
t1:4 Global • Ehlers-Danlos syndrome • Sclerodermia
• Marfan syndrome • Duchenne dystrophy
• Hypermobility syndrome • Spastic paresis
Major organ fibrosis

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233 Nociception, Neuroplasticity, and Pain Mediators compartment syndrome, the so-called runners’ knee, tennis/ 268
234 golfer elbow, frozen shoulder, and fasciitis. Histological in-

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in Fascial Tissue 269
vestigations show accumulations of fibroblasts or contractile 270

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235 Sensory feedback of myofascial tissue is critical in directed myofibroblasts. Whether these cells are contributors to the 271
236 neuromuscular control of coordination and movement pat- pathogenesis of connective tissue induced contractures is cur- 272

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237 terns. Functional neurophysiological, as well as histopatho- rently still under investigation. Moreover, recent data have 273
238 logical, investigations have suggested that fascial connective revealed that fascial epimysium is a central participant in the 274
239 tissue is a potential source of pain. Within fascial tissue,
D pathogenesis of the sport induced “muscle ache” [42]. 275
240 so-called “wide dynamic range” neurons were found to Unspecific back pain was also suggested to be medi- 276
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241 predominate, which can detect multiple sensory signals. ated, at least in part, by fascial structures, especially the 277
242 Electrophysiological investigations have revealed that the im- thoracolumbar fascia. This fascia receives a large part of the 278
243 pulse activity and the number of spinal cord neurons after mechanical force transmission during lumbar flexion and is 279
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244 stimulation of fascia is very variable. Artificial inflammation rich in nociceptive nerve endings [41]. Cracks in the 280
245 of the lumbar fascia causes a significant increase of posterior thoracolumbar fascia, muscle hernias, microlesions, and me- 281
246 horn neurons receiving afferent signals from fascial tissue, as chanical irritations can result in malfunctions and painful 282
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247 well as a significant increase of posterior horn neurons with contractures. Interestingly, a tendency towards an increase in 283
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248 converged impulsion from different tissues. Finally, the cen- thickness (of about 25 %) is found in men with chronic back 284
tral nervous system is very sensitive to received fascial infor- pain. Additionally, a reduction in shear motion (i.e., sliding
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249 285
250 mation caused by pathological changes in the lumbar area of ability during passive lumbar flexion) of this fascial structure 286
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251 the back [39]. Recently, Schilder et al. [40••] found support in in relation to the underlying musculature has been document- 287
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252 humans for this theory: pain effects evoked by ultrasound- ed for both sexes [43]. Injection of nerve growth factor (NGF) 288
253 guided bolus injection of hypertonic saline in fascial tissue within the thoracolumbar fascia caused hyperalgesia. This 289
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254 exceeded those of muscle. Interestingly, pain after fascia in- finding may open a new and promising method of treatment 290
255 jection, was described by the patients in rather extreme terms for low back pain the inhibition of NGF using monoclonal 291
256 like “torturous”, “exhausting”, “and agonizing”, which sug- antibody (Tanezumab) caused analgesic effects in those suf- 292
257 gests innervation by both A- and C-fiber nociceptors. In fering from back pain syndromes [39]. 293
258 contrast, muscle-derived pain was predominantly attributed These cells are known to be either contractile smooth 294
259 to sensory qualities like “stinging”, “numbness”, and “throb- muscle cells or fibroblast with smooth muscle like features, 295
260 bing” [40••]. Apart from biogenic amines, interleukins, for example myofibroblasts [44]. In vitro investigation re- 296
261 growth factors, and additions humoral factors, Tesarz et al. vealed contractile properties of myofibroblasts, which are 297
262 [41] also detected substance P and calcitonin gene-related regulated by inactivation of the myosin light chain phosphor- 298
263 peptide-dependent neurons in fascial tissue. Both substances ylation via the Rho-associated kinase ROCK, leading to inac- 299
264 are known mediators in chronic pain [41]. tivation of myosin light chain phosphatase, and, finally, con- 300
tinued contraction [45, 46]. In vivo experimentation using rat 301
fascial tissue confirmed these results: suspended thin strips in 302
265 Collagen Tissue as a Source of Pain a superfusion system yielded clear and reversible tissue con- 303
tractions in response to pharmacological drugs [47]. Isometric 304
266 Stiffening of connective tissue accompanies several pain stretching of strips of human lumbar fascia tissue (1.5 mm× 305
267 syndromes, which include exercise-induced lower leg 1.0 mm×30 mm) resulted in a maximal measured force 306
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307 increase of up to 1.5 N. Application of this ratio to whole pain aspect, although it may reappear as the stiffness 357
308 fascial tissue sheets revealed substantial force in active con- eases (duration of this phase is 5–12 months). 358
309 tractions within a range at which a lumbar paraspinal com-
310 partment syndrome could be triggered [48]. In contrast, de-
311 creased fascial tonus can result in spinal segmental instability, Chronic Neck Pain 359
312 and a total loss of fascial tone can contribute to hypermobility,
313 as frequently occurs during pregnancy [49, 50]. A recent ultrasound examination of patients with chronic neck 360
314 Recently, the critical role of connective tissue was proven pain revealed that they tend to have a greater fascial thickness 361
315 regarding the understanding and treatment of spastic pareses in at the sternal endings of the sternocleidomastoid, as well as at 362
316 children: apart from targeting the main pathological mecha- the lower and upper side of the medial scalene muscle. In 363
317 nism, for example the neuromuscular interaction, investigations particular, a measurement of 0.15 cm (the mean value of two 364
318 revealed that the clinical behavior of these children is often SDs of controls) of the sternocleidomastoid fascia was con- 365
319 more crucially influenced by additional changes observed in sidered to be a cut-off value, which enables clinicians to make 366
320 muscular connective tissue. The recognition of increased a diagnosis of myofascial pathology—rather than of a primary 367

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321 epimuscular force transmission to antagonistic muscles (via neuromuscular dysfunction—in a patient with chronic neck 368
322 increased endomysial and perimysial cross-links) has now lead pain. The increase in thickness was associated with an accom-

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369
323 to encouraging surgical advances in this field [15•, 51, 52]. panying reduction in active, as well as passive, cervical range 370

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of motion in the pain group. Taken together—the increase in 371
thickness and the reduced mobility—the authors postulated an 372

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324 Frozen Shoulder increased stiffness of related muscular fasciae. 373
Following a series of fascial manipulation sessions a sig- 374
325 One of the most common syndromes is frozen shoulder. The
D nificant decrease in the thickness of the fasciae were found 375
326 condition expresses as symptoms of shoulder pain and accompanied by a reduction in pain, as well as increased range 376
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327 discomfort that are slow in onset and located around the of motion [53••]. 377
328 deltoid insertion. Patients commonly express reduced
329 glenohumeral abduction and external rotation, accompa-
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330 nied by unremarkable radiographic findings. Upon pal- Nerve Compression Syndromes 378
331 pation of the glenohumeral joint, tenderness is often felt
332 at this location. The condition mainly affects patients aged 40– Peripheral nerve compression syndromes can be detected at 379
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333 60 years, with a female predominance. Prevalence is increased different locations throughout the human body, which 380
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334 in patients with diabetes, cardiovascular disease, hyper- and depend, at least in part, on the kind of sport activities. 381
hypothyroidism, and Parkinson’s disease. In addition, prote-
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335
336 ase inhibitors used for antiretroviral therapy have been asso-
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337 ciated with the development of this condition. It remains

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338 unclear why the contracture limits abduction and external

339 rotation despite a global capsular fibroplasia. Biopsies obtain-
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340 ed during surgery have revealed a thickened capsule and

341 coracohumeral ligament. Immunohistochemical examinations
342 have revealed a dense matrix of type III collagen populated
343 with fibroblasts and myofibroblasts in the capsule. In addition,
344 there are varied and sometimes contradictory reports about
345 increased vascularity, fibrosis, hyalinization, vascular villous
346 synovitis, and the presence of mature scar tissue. However,
347 little evidence of an acute inflammatory process is found.
348 Generally, frozen shoulder is a regarded as a self-limiting
349 condition. The pathology then usually progresses through
350 three clinical phases: (1) a painful phase with a gradual onset,
Fig. 2 Nerve entrapment syndrome. The figure shows an endoscopic
351 usually worse at night and when lying on the affected side, photograph of the ulnaris nerve in the cubital tunnel distal to the Osborne
352 with a duration of 2–9 months; (2) stiffening phase with fascia. Abnormal thickenings of perineural fascial tissue compress the
353 usually no change in the pain level—the stiffness progresses nerve and lead to a long-segment stenosis. Irritation of the nerve leads to a
partial or total loss of function characterized by pain, decreased haptic
354 and may lead to muscle atrophy due to disuse, with a duration perception and loss of muscle force, and muscle atrophy. Pain is typically
355 of 4–12 months; (3) thawing phase, in which the patient shows referred to the ulnar part of the wrist. However, retrograde transmission of
356 a gradual improvement in rage of movement, as well as in the pain predominantly at night-time can mimic a cervical spine stenosis
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382 Nerve compression syndromes are always associated Compliance with Ethics Guidelines 430
383 with a fascial pathology. Pressure, traction, and repeti- 431
Conflict of Interest The authors each declare no potential conflicts of 432
384 tive irritation may trigger relocating disturbances and interest. 433
385 increased thickness of fascial tissue, which restrict the 434
386 corresponding nerve. Consequently, the nerves swell at Human and Animal Rights and Informed Consent This article does 435
387 the restriction and the endoneural fluid pressure in- not contain any studies with human or animal subjects performed by any 436
388 creases, resulting in an insufficient blood supply of the of the authors. 437
389 corresponding nerve segment. Finally, a painful function
390 restriction in the innervated area occurs.
391 The Osborne fascia between the epicondylus medialis References 438
392 and the olecranon represents an anatomical narrowing
393 that can compress the nervus ulnaris within the cubital
Papers of particular interest, published recently, have been 439
394 channel. This painful compression is treated with the
highlighted as: 440
395 surgical separation of the Osborne fascia. However,
• Of importance 441

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396 recent investigations have revealed that increased fascial
•• Of major importance 442
397 thickness might also compress the nerve at regions other

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398 than the cubital channel (Fig. 2). This has resulted in
443

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400 gates the whole course of the nerve endoscopically.

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