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The new edition of Clinical Application of Neuromuscular Techniques are described within the context of normal anatomy and

t of normal anatomy and physiology


Volume 1 - The Upper Body updates and expands on the theories, of the structures, as well as the common dysfunctions that may arise.
validation and techniques for the manual treatment of chronic and Indications for treatments and guidance on making the appropriate
acute neuromuscular pain and somatic dysfunction. Over 600 pages treatment choice are given for 'each muscle to be addressed, and
of highly illustrated material from the two leaders in the field of particular attention is paid to the treatment of trigger points. Clinical
manual therapy ensure the anatomy and techniques involved in the insights stem from many years of clinical and teaching experience of
application of neuromuscular techniques are easier to follow than both authors.
ever before. This new edition of Clinical Application of Neuromuscular Techniques
New to this edition is a CD-ROM containing fully searchable and Volume 1 - The Upper Body continues to combine and integrate key
referenced book text complete with the illustrations and bonus information from several sources. The result is a textbook which will
illustrative material. do much to ensure the safe and effective application of soft tissue

The content covers NMT (neuromuscular techniques), MET (muscle techniques and provide an invaluable source of reference to all students

energy techniques). PR (positional release) and many other bodywork and practitioners in the field of manual therapy.

techniques for neuromusculoskeletal disorders. The text is arranged This updated volume is accompanied by Volume 2 - The Lower Body,
by regions in a muscle-by-muscle approach with templated headings which addresses the problems of the lower body (lumbar spine, sacrum,
making important information easy to locate. The theory and practice pelvis, hip, leg, and foot).

Key Features About the Authors

Comprehensive 'one-stop' text on care of somatic pain and dysfunction Leon Chaitow NO DO is an internationally known and respected osteopathic
Foundations, theories, and current research perspectives as to causes of and naturopathic practitioner and teacher of soft tissue manipulation methods
myofascial pain of treatment. He is author of over 60 books, including a series on Advanced Soft
All muscles covered from the perspective of assessment and treatment of
Tissue Manipulation (Muscle Energy Techniques, Positional Release Techniques,
myofascial pain
Modern Neuromuscular Techniques) and also Palpation Skills; Cranial
Describes the normal anatomy and physiology as well as the common
Manipulation: Theory and Practice; Fibromyalgio Syndrome: A Practitioner's
dysfunctions
Provides indications for treatments and guidance on making the appropriate Guide to Treatment, and many more. He is editor of the peer reviewed Journal of

treatment choice for each patient Bodywork and Movement Therapies, that offers a multidisciplinary perspective on
Practical step-by-step technique descriptions for each treatment physical methods of patient care. Leon Chaitow was for many years senior lecturer
Describes the different neuromuscular techniques (NMn in relation to the on the Therapeutic Bodywork degree courses which he helped to design at the
joint anatomy involved School of Integrated Health, University of Westminster London, where is he now

Includes muscle energy, myofascial release, and positional release techniques, an Honorary Fellow. He continues to teach and practice part-time in London, when
as well as NMT to offer a variety of treatment options not in Corfu, Greece where he focuses on his writing.
Includes location and treatment of trigger points
Covers manual and complementary techniques.
Judith Delany LMT has spent two decades developing neuromuscular
New to this edition
therapy techniques and course curricula for manual practitioners as well
Expanded text includes additions on the 'internal environment' (biochemistry),
as for massage schools and other educational venues. Her ongoing private
connective tissue, updated research, and many new illustrations
trainings with the Tampa Bay Devil Rays athletic trainers (professional
Illustrations demonstrating the bony anatomy under the treating fingers
enhance aid to the reader in visualizing what is under palpation baseball) as well as customized trainings for noteworthy US-based spas show
Fully searchable text on CD-ROM incorporation of NMT into diverse settings. She has contributed a chapter
Additional, full-colour illustrations on CD-ROM to Modern uromusular Techniques and co-authored a contribution to
Evolve website with downloadable image collection for lecturers. Principles and Practices of Manual Therapeutics. As an international instructor
of NMT American version, co-author of three NMT textbooks, and associate
Reader reviews from the first edition editor for Journal af Bodywark and Movement Therapies, her professional
-As the massoge profession embraces the knowledge base that is the foundation focus aims to advance education in all healthcare professions to include
for the work that we do, there is a need for texts and reference bootes that provide myofascial therapies for acute and chronic pain syndromes. She resides in
concrete, researched, and integrated information free from the influence of St. Petersburg, Florida where she is the director of and primary curriculum
personal sty/e. This text has accomplished the task by expertly weaving the sciences developer for NMT Center.
with the skills, and blending methods for physiologic outcomes
Sandy Fritz BS NCTMB

"This book mosterfully integrates the biomechanical biopsychosocial and


biomechanicol approoches of monogement of the soft tissue dysfunction:
Craig Liebenson DC

"This book is destined to become a classic and a 'must have' in every seriaus
manual therapist's library for years to come ... I, for one, will be recommending it
to everyone I con becouse it is without a doubt the most well thought out ond well
orgonized presentation of soft tissue manual therapy thot I have seen to date
Whitney W Lowe LMT

ISBN 978-0-443-07448-6

CHURCHILL
LIVINGSTONE
ELSEVIER
9780443074486
www.elsevierhealth.com
Clinical Application of Neuromuscular .Techniques
For Elsevier:

Senior Commissioning Editor: Sarena Wolfaard


Associate Editor: Claire Wilson
Project Manager: Gail Wright
Designer: Eric Drewery
Illustration Manager: Bruce Hogarth
lIlustrators: Graeme Chambers, Peter Cox, Bruce Hogarth, Paul Richardson,
Richard Tibbitts
Clinical Application of
Neuromuscular Techniques
Volume 1 - The Upper Body
Second Edition

leon Chaitow ND DO
Consultant Naturopath and Osteopath. Honorary Fellow, University of Westminster, London, UK

Judith Delany LMT


Lecturer in Neuromuscular Therapy, Director of NMT Center, St Petersburg, Florida, USA

Foreword by

Diane lee BSR FCAMT CGIMS

Director, Diane Lee Et Associates, Consultants in Physiotherapy,

White Rock, BC, Canada

CHURCHILL
LIVINGSTONE

ELSEVIER

EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS SYDNEY TORONTO 2008
CHURCHILL
LIVINGSTONE
ELSEVlER

Elsevier Limited 2000. All rights reserved.


Elsevier Ltd, 2008. All rights reserved.

The right of Leon Chaitow and Judith DeLany to be identified as authors of this work has been
asserted by them in accordance with the Copy right, Designs and Patents Act 1988.

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You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com).
by selecting 'Support and contact' and then 'Copyright and Permission'.

First edition 2000


Second edition 2008

ISBN 978-0-443-07448-6

British Library Cataloguing in Publication Data


A catalogue record for this book is available from the British Library

Library of Congress Cataloging in Publication Data


A catalog record for this book is avaUabJe from the Library of Congress

Notice
Neither the Publisher nor the authors assume any responsibility for any loss or injury and/or
damage to persons or property arising out of or related to any use of the material contained in
this book. It is the responsibility of the treating practitioner, relying on independent expertise and
knowledge of the patient, to determine the best treatment and method of application for the
patient.
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vii

Contents

List of boxes xv Major types of voluntary contraction 33


Foreword xvii Terminology 33
Preface to the Second Edition xix Muscle tone and contraction 33
Vulnerable areas 34
Acknowledgments xxi
Muscle types 34
Cooperative muscle activity 35
Connective tissue and the fascial system 1
Muscle spasm, tension, atrophy 37
The fascial network 2 Contraction (tension with EMG elevation,
Fascia and proprioception 2 voluntary) 38
Fascia: collagenous continuity 2 Spasm (tension with EMG elevation,
Further fascial considerations 2 involuntary) 38
Elasticity 3 Contracture [tension of muscles without
Plastic and elastic features 3 EMG elevation, involuntary) 38
Connective tissue as a 'sponge' 6 Increased stretch sensitivity 38
Deformation characteristics 6 Viscoelastic influence 39
Hypermobility and connective tissue 7 Atrophy and chronic back pain 39
Trigger points, fascia and the nervous system 8 What is weakness? 39
The importance of Langevin's research 9 Trick patterns 39
Summary of fascial and connective tissue function 13 Joint implications 40
Fascial dysfunction 16 When should pain and dysfunction be
Restoring gel to sol 17 left alone? 40
A different model linking trauma and connective tissue 17 Beneficially overactive muscles 41
Therapeutic sequencing 1 9 Somatization - mind and muscles 41
But how is one to know? 41
2 Muscles 23
3 Reporting stations and the brain 45
Dynamic forces - the 'structural continuum' 23
Signals 25 Proprioception 45
Essential information about muscles 25 Fascia and proprioception 46
Types of muscle 25 Reflex mechanisms 47
Energy production in normal tissues 27 Local reflexes 50
Energy production in the deconditioned Central influences 50
individual 28 Neuromuscular dysfunction following injury 51
Muscles and blood supply 28 Mechanisms that alter proprioception 52
Motor control and respiratory alkalosis 31 An example of proprioceptive dysfunction 52
Two key definitions 32 Rectus capitis posterior minor (RCPMin)
The Bohr effect 32 research evidence 52
Core stability, transversus abdominis, the Neural influences 53
diaphragm and BP D 32 Effect of contradictory proprioceptive information 53
Summary 32 Neural overload, entrapment and crosstalk 57
viii CONTENTS

Manipulating the reporting stations 58 Scapulohumeral rhythm test 91


Therapeutic rehabilitation using reflex systems 59 Neck flexion test 92
Conclusion 60 Push-up test 92
Breathing pattern assessments 92
4 Causes of m usculoskeletal d ysfunction 63 Seated assessment 92
Supine assessment 93
Adaptation - GAS and LAS 63
Sidelying assessment 93
Posture, respiratory function and the adaptation
Prone assessment 93
phenomenon 64
Trigger point chains 94
An example of 'slow' adaptation 66
What of adaptation to trauma? 67
6 Trigger points 97
What of adaptation to habits of use? 67
Making sense of the picture 67 Ischemia and muscle pain 101
Example 68 Ischemia and trigger point evolution 102
Postural and emotional influences on Trigger point connection 102
musculoskeletal dysfunction 69 Microanalysis of trigger point tissues 103
Postura I interpretations 69 Ischemia and fibromyalgia syndrome (FMS) 1 03
Contraction patterns 69 FMS and myofascial pain 105
Emotional contractions 69 Facilitation - segmental and local 105
'Middle fist' functions 70 Trigger points and organ dysfunction 106
'Upper fist' functions 70 How to recognize a facilitated spinal area 108
Behavior and personality issues 71 Local facilitation in muscles 1 08
Cautions and questions 72 Lowering the neural threshold 109
Postural imbalance and the diaphragm 73 Varying viewpoints on trigger points 109
Balance 74 Awad's analysis of trigger points 109
Respiratory influences 75 Nimmo's receptor-tonus techniques 109
Effects of respiratory alkalosis in a Improved oxygenation and reduced trigger
deconditioned individual 75 point pain - an example 110
Respiratory entrainment and core stability issues 75 Pain-spasm-pain cycle 110
Summary of effects of hyperventilation 76 Fibrotic scar tissue hypothesis 110
Neural repercussions 77 Muscle spindle hypothesis 110
Tetany 77 Radiculopathic model for muscular pain 111
Biomechanical changes in response to upper Simons' current perspective: an integrated hypothesis 111
chest breathing 77 Central and attachment trigger points 112
Additional emotional factors and musculoskeletal Primary, key and satellite trigger points 112
dysfunction 78 Active and latent trigger points 113
Selective motor unit involvement 78 Essential and spillover target zones 114
Conclusion 79 Trigger points and joint restriction 1 1 4
Trigger points associated with shoulder restriction 114
5 Patterns of dysfunction 81 Other trigger point sites 114
Testing and measuring trigger points 114
Upper crossed syndrome 82
Basic skill requirements 115
Lower crossed syndrome 82
Needle electromyography 116
Layer (stratification) syndrome 83
Ultrasound 116
Chain reaction leading to facial and jaw pain:
Surface electromyography 116
an example 84
Algometer use for research and clinical training 117
Patterns from habits of use 84
Thermography and trigger points 117
The big picture and the local event 85
Clinical features of myofascial trigger points 118
Janda's 'primary and secondary' responses 85
Developing skills for TrP palpation 1 1 9
Recognizing dysfunctional patterns 86
Which method i s more effective? 121
Excessive muscular tone 86
Simple functional tests for assessing excess
7 The internal environment 125
muscular tone 87
Functional screening sequence 88 Local myofascial inflammatory influences 125
Prone hip (leg) extension (PLE) test 89 Pain progression 126
Trunk flexion test 90 Sensitization 126
Hip abduction test 90 Mechanisms of chronic pain 126
Contents ix

Glutamate: a contrary view of the cause of Psychosocial factors in pain management: the
tendon pain 127 cognitive dimension 170
Acute (lag) phase of the inflammatory response 128 Guidelines for pain management 171
Regeneration (repair) phase 128 Group pain management 171
Remodeling phase 128 The litigation factor 171
Difference between degenerative and Other barriers to progress in pain management 171
inflammatory processes 129 Stages of change in behavior modification 171
Antiinflammatory nutrients and herbs 129 Wellness education 172
What about antiinflammatory medication7 130 Goal setting and pacing 172
Controlled scarring - friction and prolotherapy 130 Low back pain rehabilitation 172
When inflammation becomes global 131 The biopsychosocial model of rehabilitation 172
Hormonal influences 131 Concordance 173
Muscles, joints and pain 140 Patient advice and concordance (compliance) issues 173
Reflex effects of muscular pain 141
Source of pain 142 9 Modern neuromuscular techniques 177
Is it reflex or local? 142
Neuromuscular therapy - American version 177
Radicular pain 142
Biomechanical factors 178
Are the reflexes normal? What is the source of
Biochemica I factors 179
the pain? 142
Psychosocial factors 180
Differentiating between soft tissue and joint pain 143
Biomechanical, biochemical and psychosocial
Neuropathic pain 143
interaction 180
Neurotoxic elements and neuropathic pain 144
NMT techniques contraindicated in initial
Effects of pH changes through breathing 149
stages of acute injury 181
Alkalosis and the Bohr effect 149
NMT for chronic pain 182
Deconditioning and unbalanced breathing 149
Palpation and treatment 182
Caffeine in its various forms 150
Treatment and assessment tools 189
When should pain and dysfunction be left alone? 151
Pain rating tools 190
Somatization 152
Treatment tools 190
How is one to know? 152
European (Lief's) neuromuscular technique (NMT) 191
Pain management 154
NMT thumb technique 192
Gunn's view 154
Lief's NMT finger technique 193
Questions 154
Use of lubricant 194
Pain control 154
Variations 194
8 Assessment, treatment and rehabilitation 161 Variable ischemic compression 194
A framework for assessment 195
Numerous influences 162
Some limited NMT research 196
A biomechanical example 162
Integrated neuromuscular inhibition technique 197
'Looseness and tightness' as part of the
biomechanical model 163
10 Associated therapeutic modalities and techniques 205
Lewit (1996) and 'loose-tight' thinking 164
Soft tissue treatment and barriers 164 Hydrotherapy and cryotherapy 206
Pain and the tight-loose concept - and the How water works on the body 206
trigger point controversy 164 Warming compress 206
Three-dimensional patterns 165 Alternate heat and cold: constitutional
Methods for restoration of 'three-dimensionally hydrotherapy (home application) 208
patterned functional symmetry' 165 Neutral bath 209
Neuromuscular management of soft tissue dysfunction 166 Alternate bathing 209
Manipulating tissues 166 Alternating sitz baths 210
Nutrition and pain: a biochemical perspective 167 Ice pack 210
Nutritional treatment strategies 167 Integrated neuromuscular inhibition technique (lNIT) 210
Specific nutrients and myofascial pain 167 INIT method 1 210
Allergy and intolerance: additional biochemical INIT rationale 211
influences on pain 168 Ruddy's reciprocal antagonist facilitation (RRAF) 212
What causes this increase in permeability? 169 Lymphatic drainage techniques 212
Treatment for 'allergic myalgia' 169 McKenzie Method 213
Antiinflammatory nutritional (biochemical) strategies 169 Massage 215
x CONTENTS

Petrissage 215 Landmarks 255


Kneading 215 Functional features of the cervical spine 255
Inhibition 215 Muscular and fascial features 256
Effleurage (stroking) 215 Neurological features 256
Vibration and friction 216 Circulatory features and thoracic outlet syndrome 256
Transverse friction 216 Cervical spinal dysfunction 259
Effects explained 216 Assessments 259
Mobilization and articulation 217 Assessment becomes treatment 266
Notes on sustained natural apophyseal Assessment and treatment of
glides (SI'JAGs) 217 occipitoatlantal restriction (CO-C'I) 268
Muscle energy techniques (MET) and variations 218 Functional release of atlantooccipital joint 269
l'Jeurological explanation for MET effects 218 Translation assessment for cervical spine (C2-7) 269
Use of breathing cooperation 218 Treatment choices 270
Muscle energy technique variations 219 Alternative positional release approach 271
Myofascial release techniques (MFR) 221 SCS cervical flexion restriction method 271
Exercise 1 Longitudinal paraspinal myofascial release 222 SCS cervical extension restriction method 271
Exercise 2 Freeing subscapularis from serratus Stiles' (1984) general procedure using MET
anterior fascia 223 for cervical restriction 272
Myofascial release of scar tissue 223 Harakal's (1975) cooperative isometric
Neural mobilization of adverse mechanical or technique (MET) 272
neural tension 223 Cervical treatment: sequencing 273
Adverse mechanical tension (AMT) and pain sites Cervical planes and layers 274
are not necessarily the same 224 Posterior cervical region 275
Types of symptoms 224 NMT for upper trapezius in supine position 277
Neural tension testing 224 MET treatment of upper trapezius 278
Positional release techniques (PRT) 225 Positional release of upper trapezius 279
The proprioceptive hypothesis 225 Myofascial release of upper trapezius 280
The nociceptive hypothesis 226 Variation of myofascial release 280
Resolving restrictions using PRT 226 NMT: cervical lamina gliding techniques - supine 281
Circulatory hypothesis 227 Semispinalis capitis 282
Variations of PRT 227 Semispinalis cervicis 283
Rehabilitation 230 Splenii 283
Relaxation methods 231 NMT techniques for splenii tendons 284
Rhythmic (oscillatory, vibrational, harmonic) methods 231 Spinalis capitis and cervicis 285
What's happening? 231 NMT for spinalis muscles 286
Application exercise for the spine 232 Longissimus capitis 286
Trager exercise 233 Longissimus cervi cis 286
Spray and stretch for trigger point treatment 233 Iliocostalis cervicis 286
Additional stretching techniques 235 Multifidi 287
Facilitated stretching 235 Rotatores longus and brevis 287
Proprioceptive neuromuscular facilitation Interspinales 287
(PNF) variations 235 NMT for interspinales 289
Active isolated stretching (AIS) 236 Intertransversarii 289
Yoga stretching (and static stretching) 236 Levator scapula 289
Ballistic stretching 236 NMT for levator scapula 290
Using multiple therapies 236 MET treatment of levator scapula 291
Positional release of levator scapula 291
Suboccipital region 292
11 The cervical region 243
Rectus capitis posterior minor 294
The vertebral column: a structural wonder 244 Rectus capitis posterior major 295
Cervical vertebral structure 246 Obliquus capitis superior 295
The upper and lower cervical functional units 248 Obliquus capitis inferior 295
Movements of the cervical spine 250 NMT for suboccipital group - supine 296
Upper cervical (occipitocervical) ligaments 251 Platysma 298
Lower cervical ligaments 253 NMT for platysma 299
Assessment of the cervical region 253 General anterior neck muscle stretch utilizing MET 299
Contents xi

Sternocleidomastoid 300 Muscles of mastication 358


NMT for SCM 301 Neck pain and TMD 359
Treatment of shortened SCM using MET 303 External palpation and treatment of
Positional release of sternocleidomastoid 304 craniomandibular muscles 365
Suprahyoid muscles 304 I'JMT for temporalis 366
Infrahyoid muscles 304 NMT for masseter 367
Sternohyoid 305 Massage/myofascial stretch treatment of masseter 368
Sternothyroid 306 Positional release for masseter 368
Thyrohyoid 306 NMT for lateral pterygoid 369
Omohyoid 306 NMT for medial pterygoid 369
NMT for infrahyoid muscles 307 Stylohyoid 369
Soft tissue technique derived from External palpation and treatment of styloid and
osteopathic methodology 308 mastoid processes 371
Longus colli 308 Intraoral palpation and treatment of
Longus capitis 309 craniomandibular muscles 372
NMT for longus colli and capitis 311 Intraoral NMT applications 372
MET stretch of longus capitis 31 2 Temporalis 372
Rectus capitis anterior 312 NMT for intraoral temporalis tendon 373
Rectus capitis lateralis 313 Masseter 373
NMT for rectus capitis lateralis 31 3 NMT for intraoral masseter 375
Scalenii 314 Lateral pterygoid 375
NMT for scalenii 316 NMT for intraoral lateral pterygoid 378
Treatment of short scalenii by MET 318 Medial pterygoid 379
Positional release of scalenii 319 NMT for intraoral medial pterygoid 380
Cervical lamina - prone 319 Musculature of the soft palate 380
NMT for posterior cervical lamina - prone position 320 NMT for soft palate 382
NMT for posterior cranial attachments 320 Muscles of the tongue 382
NMT for muscles of the tongue 383
Suprahyoid muscles - the floor of the mouth 384
12 The cranium 3 25
NMT for intraoral floor of mouth 385
Cranial structure 326 Cranial treatment and the infant 387
Occiput 328 The craniocervical link 388
Sphenoid 332 Sleeping position and cranial deformity 389
Ethmoid 335 What other factors do medical authorities
Vomer 336 think cause serious cranial distortion in infants? 389
Mandible 337 What are the long-term effects of deformational
Frontal 340 plagiocephaly? 389
Parietals 343 Different cranial approaches 390
Temporals 344 Ear disease and cranial care 390
Zygomae 347 Summary 392
Maxillae 349
Palatines 350
13 Shoulder. arm and hand 3 99
NMT treatment techniques for the cranium 351
Muscles of expression 351 Shoulder 401
Mimetic muscles of the epicranium 352 Structure 40 1
Occipitofrontalis 352 Key joints affecting the shoulder 401
Temporoparietalis and auricular muscles 352 Pivotal soft tissue structures and the shoulder 404
NMT for epicranium 354 Assessment 407
Positional release method for occipitofrontalis 355 Repetitions are important 408
Mimetic muscles of the circumorbital and Janda's perspective 41 0
palpebral region 355 Observation 41 0
NMT for palpebral region 355 Palpation of superficial soft tissues 41 1
Mimetic muscles of the nasal region 356 Range of motion of shoulder structures 41 1
NMT for nasal region 356 Active and passive tests for shoulder girdle motion
Mimetic muscles of the buccolabial region 356 (standing or seated) 41 2
NMT for buccolabial region 357 Strength tests for shoulder movements 41 3
xii CONTENTS

Muscular relationships 41 3 NMT for anconeus 453


Spinal and scapular effects of excessive tone 415 Teres minor 453
Shoulder pain and associated structures 415 Assessment for teres minor weakness 453
Therapeutic choices 416 NMT for teres minor 454
Specific shoulder dysfunctions 417 PRT for teres minor (most suitable for
Specific muscle evaluations 420 acute problems) 455
Infraspinatus 420 Teres major 456
Levator scapula 420 NMT for teres major 457
Latissimus dorsi 420 PRT for teres major (most suitable for
Pectoralis major and minor 421 acute problems) 457
Supraspinatus 421 Latissimus dorsi 458
Subscapularis 421 Assessment for latissimus dorsi shortness/dysfunction 458
Upper trapezius 421 NMT for latissimus dorsi 459
Is the patient's pain a soft tissue or a joint problem? 422 MET treatment of latissimus dorsi 460
The Spencer sequence 422 PRT for latissimus dorsi (most suitable for
Treatment 429 acute problems) 460
Trapezius 429 Subscapularis 460
Assessment of upper trapezius for shortness 431 Assessment of subscapularis dysfunction/shortness 462
NMT for upper trapezius 432 Observation of subscapularis dysfunction/shortness 462
NMT for middle trapezius 433 Assessment of weakness in subscapularis 463
NMT for lower trapezius 433 NMT for subscapularis 463
NMT for trapezius attachments 434 MET for subscapularis 463
Lief's NMT for upper trapezius area 434 PRT for subscapularis (most suitable for
MET treatment of upper trapezius 435 acute problems) 464
Myofascial release of upper trapezius 435 Serratus anterior 464
Levator scapula 435 Assessment for weakness of serratus anterior 465
Assessment for shortness of levator scapula 436 NMT for serratus anterior 465
NMT for levator scapula 436 Facilitation of tone in serratus anterior using
MET treatment of levator scapula 438 pulsed MET 466
Rhomboid minor and major 438 Pectoralis major 467
Assessment for weakness of rhomboids 439 Assessment for shortness in pectoralis major 470
Assessment for shortness of rhomboids 439 Assessment for strength of pectoralis major 470
NMT for rhomboids 439 NMT for pectoralis major 471
MET for rhomboids 440 MET for pectoralis major 472
Deltoid 441 Alternative MET for pectoralis major 473
NMT for deltoid 443 MFR for pectoralis major 474
Supraspinatus 443 Pectoralis minor 474
Assessment for supraspinatus dysfunction 446 NMT for pectoralis minor 476
Assessment for supraspinatus weakness 446 Direct (bilateral) myofascial stretch of shortened
NMT treatment of supraspinatus 446 pectoralis minor 477
MET treatment of supraspinatus 446 Subclavius 477
MFR for supraspinatus 447 MFR for subclavius 477
Infraspinatus 447 Sternalis 479
Assessment for infraspinatus shortness/dysfunction 447 Coracobrachialis 479
Assessment for infraspinatus weakness 448 Assessment for strength of coracobrachialis 479
NMT for infraspinatus 448 NMT for coracobrachialis 481
MET treatment of short infraspinatus MFR for coracobrachialis 481
(and teres minor) 448 PRT for coracobrachialis 481
MFR treatment of short infraspinatus 449 Biceps brachii 482
PRT treatment of infraspinatus (most suitable for acute Assessment for strength of biceps brachii 483
problems) 449 Assessment for shortness and MET treatment of biceps
Triceps and anconeus 449 brachii 483
Assessment for triceps weakness 452 NMT for biceps brachii 483
NMT for triceps 452 MET for painful biceps brachii tendon (long head) 484
MET treatment of triceps (to enhance shoulder flexion PRT for biceps brachii 485
with elbow flexed) 452 Elbow 485
Contents xiii

Introduction to elbow treatment 485 Carpal tunnel syndrome 507


Structure and function 485 Phalanges' 508
Humeroulnar joint 486 Carpometacarpal ligaments (2nd, 3rd, 4th, 5th) 509
Humeroradial joint 486 Metacarpophalangeal ligaments 510
Radioulnar joint 486 Range of motion 510
Assessment of bony alignment of the epicondyles 486 Thumb 511
The ligaments of the elbow 486 Thumb ligaments 511
Assessment for ligamentous stability 487 Range of motion at the joints of the thumb 511
Evaluation 487 Testing thumb movement 511
Biceps reflex 487 Dysfunction and evaluation 511
Brachioradialis reflex 487 Preparing for treatment 511
Triceps reflex 488 Terminology 512
Ranges of motion of the elbow 488 Neural entrapment 513
Range of motion and strength tests 488 Distant influences 513
Elbow stress tests 488 Anterior forearm treatment 513
Strains or sprains 489 Palmaris longus 513
Indications for treatment (dysfunctions/syndromes) 489 Flexor carpi radialis 515
Median nerve entrapment 489 Flexor carpi ulnaris 515
Carpal tunnel syndrome 489 Flexor digitorum superficialis 515
Ulnar nerve entrapment 489 Flexor digitorum profundus 51 6
Radial nerve entrapment 492 Flexor pollicis longus 516
,
Tenosynovitis ( tennis elbow' and/or 'golfer's elbow') 492 NMT for anterior forearm 518
Assessments for tenosynovitis and epicondylitis 492 Assessment and MET treatment of shortness in the
Elbow surgery and manual techniques 492 forearm flexors 519
Treatment 493 MET for shortness in extensors of the wrist and hand 521
Brachialis 493 PRT for wrist dysfunction (including carpal tunnel
NMT for brachialis 493 syndrome) 521
Triceps and anconeus 493 MFR for areas of fibrosis or hypertonicity 521
NMT for triceps (alternative supine position) 494 Posterior forearm treatment 522
NMT for anconeus 494 Superficial layer 522
Brachioradialis 494 Extensor carpi radialis longus 523
Assessment for strength of brachioradialis 494 Extensor carpi radialis brevis 523
NMT for brachioradialis 495 Extensor carpi ulnaris 524
MFR for brachioradialis 495 Extensor digitorum 524
Supinator 495 Extensor digiti minimi 525
Assessment for strength of supinator 496 NMT for superficial posterior forearm 525
NMT for supinator 496 Deep layer 527
MET for supinator shortness 496 Abductor pollicis longus 527
MFR for supinator 496 Extensor pollicis brevis 528
Pronator teres 496 Extensor pollicis longus 528
Assessment for strength of pronator teres 497 Extensor indicis 528
NMT for pronator teres 497 NMT for deep posterior forearm 528
MFR for pronator teres 498 Intrinsic hand muscle treatment 529
PRT for pronator teres 498 Thenar muscles and adductor pollicis 530
Pronator quadratus 498 Hypothenar eminence 532
NMT for pronator quadratus 498 Metacarpal muscles 532
Forearm, wrist and hand 498 NMT for palmar and dorsal hand 533
Forearm 499
Wrist and hand 499
14 The thorax 53 9
Capsule and ligaments of the wrist 501
Ligaments of the hand 502 Structure 540
Key (osteopathic) principles for care of elbow, Structural features of the thoracic spine 540
forearm and wrist dysfunction 503 Structural features of the ribs 541
Active and passive tests for wrist motion 503 Structural features of the sternum 541
Reflex and strength tests 506 Posterior thorax 541
Ganglion 506 Identification of spinal levels 542
xiv CONTENTS

The sternosymphyseal syndrome 542 Thoracic treatment techniques 557


Spinal segments 543 Posterior superficial thoracic muscles 557
Palpation method for upper thoracic NMT: posterior thoracic gliding techniques 560
segmental facilitation 544 NMT for muscles of the thoracic lamina groove 562
How accurate are commonly used palpation Spinalis thoracis 563
methods? 544 Semispinalis thoracis 563
Red reflex assessment (reactive hyperemia) 545 Multifidi 563
Biomechanics of rotation in the thoracic spine 546 Rotatores longus and brevis 564
Coupling test 547 NMT for thoracic (and lumbar) lamina
Observation of restriction patterns in thoracic spine groove muscles 565
(C-curve observation test) 547 PR method for paraspinal musculature:
Breathing wave assessment 547 induration technique 566
Breathing wave - evaluation of spinal motion Muscles of respiration 567
during inhalation/exhalation 548 Serratus posterior superior 567
Passive motion testing for the thoracic spine 548 Serratus posterior inferior 568
Flexion and extension assessment of Tl-4 548 Levatores costarum longus and brevis 568
Flexion and extension assessment of T5-12 548 Intercostals 570
Sideflexion palpation of thoracic spine 549 NMT for intercostals 571
Rotation palpation of thoracic spine 549 Influences of abdominal muscles 571
Prone segmental testing for rotation 550 NMT assessment 571
Anterior thorax 550 PR of diaphragm 572
Respiratory function assessment 550 MET release for diaphragm 572
Palpation for trigger point activity 554 Interior thorax 572
Alternative categorization of muscles 554 Diaphragm 572
Rib palpation 554 NMT for diaphragm 573
Specific 1st rib palpation 554 Transversus thoracis 574
Test and treatment for elevated and depressed ribs 554 Thoracic mobilization with movement - SNAGs
Rib motion 554 method 575
Tests for rib motion restrictions 554
Discussion 556 Index 579
xv

List of boxes

1.1 Definitions 1 7.3 Leptin and other chemical influences in


1.2 Biomechanical terms relating to fascia 3 systemic inflammation 134
1.3 Biomechanical laws 2 7.4 Key concepts in the relation between adipose
1.4 Connective tissue 4 tissue and inflammation 140
1.5 Myers' fascial trains 11 7.5 Mercury - is there a 'safe' level? 145
1.6 Tensegrity 14 7.6 Umami 1 47
1.7 Postural (fascial) patterns 18 7.7 Health influences of tea, coffee, and other beverages 1 50
7.8 Placebo power 153
2.1 Muscle contractile mechanics and the
sliding filament theory 26 8.1 Tight-loose palpation exercise 164
2.2 The lymphatic system 29
9.1 The roots of modern neuromuscular techniques 178
2.3 Alternative categorization of muscles 36
9.2 Semantic confusion 178
2.4 Muscle strength testing 39
9.3 Summary of rehabilitation sequencing 182
2.5 Two-joint muscle testing 39
9.4 Effects of applied compression 183
3.1 Neurotrophic influences 47 9.5 Two important rules of hydrotherapy 185
3.2 Reporting stations 51 9.6 The general principles of hot and cold applications 185
3.3 Co-contraction and strain 54 9.7 Compression definitions 187
3.4 Biochemistry, the mind and 9.8 Summary of American NMT assessment protocols 189
neurosomatic disorders 55 9.9 Positional release techniques (PRT) 198
3.5 Centralization mechanisms including 9.10 Muscle energy techniques 199
wind-up and long-term potentiation [LTP] 58 9.11 Notes on synkinesis 201
9.12 Ruddy's pulsed muscle energy technique 201
4.1 Partial pressure symbols 76
4.2 Hyperventilation in context 76 1 0.1 Acupuncture and trigger points 207
10.2 A summary of soft tissue approaches to FMS and CFS 211
5.1 Hooke's law 85
5.2 Trigger point chains 94 11.1 Water imbibition by the nucleus 247
11.2 Important questions to ask 254
6.1 Historical research into chronic referred
11.3 How acute is a problem? 254
muscle pain 98
11.4 Posttrauma fibromyalgia 256
6.2 Fibromyalgia and myofascial pain 105
11.5 Tests for circulatory dysfunction 257
6.3 Trigger point activating factors 113
11.6 Tests for cervical spinal dysfunction 257
6.4 Active and latent features 114
11.7 Whiplash 261
6.5 Trigger point incidence and location 11 6
11.8 Lief's NMT for upper trapezius area 278
6.6 Trigger point and referred inhibition 117
11.9 Summary of American NMT assessment protocols 281
6.7 Trigger point perpetuating factors 119
11.10 Spinal mobilization using mobilization
6.8 What are taut bands? 1 1 9
with movement (MWM) 288
6.9 Clinical symptoms 120
11 .11 Cranial base release 296
6.10 Lymphatic dysfunction and trigger point activity 120
11.1 2 Lief's NMT for the suboccipital region 297
7.1 The endocrine system 132 11.1 3 PRT (strain-counterstrain) for any painful areas
7.2 Underactive thyroid 133 located in the posterior cervical musculature 298
xvi LIST OF BOXES

11.14 Balancing of the head on the cervical column 302 13.8 Acromioclavicular and sternoclavicular MET
11.15 Sidelying position repose 316 approaches 426
13.9 Spencer's assessment sequence including MET and
12.1 Cranial terminology and associated motion patterns
PRT treatment 427
based on traditional osteopathic methodology 326
13.10 MFR 466
12.2 The meaning of 'release' 327
13.11 Shoulder and arm pain due to neural impingement 475
12.3 Cranial bone groupings 328
13.12 Modified PNF spiral stretch techniques 478
12.4 Temporomandibular joint structure, function and
13.13 Sternalis and chest pain 479
dysfunction 359
1 3.1 4 Definition of enthesitis 492
12.5 Temporal arteritis 366
13.15 Focal hand dystonia (FHd) - 'repetitive strain injury' 503
1 2.6 Notes on the ear 370
13.16 Nerve entrapment possibilities 507
12.7 How do we maintain equilibrium? 370
13.17 Mulligan's mobilization techniques 520
12.8 Muscles producing movements of mandible 371
13.18 Arthritis 529
12.9 Latex allergy alert 371
12.10 Tinnitus: the TMD and trigger point connection 374 14.1 Identification of spinal level from spinous process 546
12.11 Deglutition 386 14.2 Liefs NMT of the upper thoracic area 549
12.12 Muscles of the eye 392 14.3 Respiratory muscles 550
14.4 Respiratory mechanics 551
13.1 Ligaments of the shoulder girdle 405
14.5 Some effects of hyperventilation 553
13.2 Caution: Scope of practice 409
14.6 Upper ribs and shoulder pain 556
13.3 Reflex tests (always compare both sides) 411
14.7 Pressure bars 566
13.4 What is normal range of arms? 411
14.8 Liefs NMT of the intercostal muscles 569
13.5 Neutralizers 413
14.9 McConnell and the diaphragm 572
1 3.6 Spencer's assessment sequence 423
13.7 Clavicular assessment 425
xvii

Foreword

Headache, TMJ, neck/shoulder pain and tennis elbow are evidence-based and I think it is worthwhile defining exactly
all common complai nts of patients seeking help from vari what evidence-based practice is. According to Sackett et al
ous hea lth practitioners. The source of the impairment (2000),
and/or the pain is often found in the neuromyofascial sys
Evidence-based practice is the integration of best research
tem. As a novice, a cli nician will approach the problem
evidence, clinical expertise and patient values. External
based on the paradigm taught in their formal training such
clinical evidence can inform, but can never replace individ
as physiotherapy, osteopathy, massage therapy, Rolfing,
ual clinical expertise, and it is this expertise that decides
acupuncture or chiropractic. Thus we see the advocacy of
whether the external evidence applies to the patient at all,
many different traditional treatments for myofascial pain
and if so, how it should be integrated into a clinical decision.
such as:
W hat is expertise? Expertise has been defined as the abil-
Physiotherapy - thermal agents followed by stretching
ity to do the right thing at the right time (Ericsson & Smith
exercises
1991). Indeed, I believe that this monumental text is evi
Osteopathy - strain/counterstrain, positional release,
dence-based since it includes the best a vailable research evi
functional and muscle energy techniques
dence and integrates it with the multi-disciplinary clinical
Massage therapy - deep pressure on tender points,
expertise that has accumulated over the last 100 years.
stroking, lymphatic massage techniques
As mentioned earlier, this text is a bout more than neuro
Rolfi ng - deep fascial release/stretching tec hniques
muscular techniques. It begins with an o verview of the
Acupunc ture - dry needling of 'An Shi' pOints
anatomy and function of connective tissue, fascia, muscles
Chiropractic - manipulation (high velocity, low amphtude
and the nervous systems (peripheral and central). The
thrust techni ques) of the spinal segment which correlates
anatomical illustrations are clear, weU-labeled and perti
to the segmental nerve supply of the affected muscle.
nent. Many of the current hypotheses regarding the ca uses
At this point, you may be thinking 'Wait a mi nute! I do of musculoskeletal dysfunction and the various patterns of
more than tha t (or all of that, or some of tha t) for my presentation are outlined . There is an extensive discussion
patients with myofascial pain'. This is true enough, since on the current theories and evidence pertaining to the
over time most clinicians gain expertise and are exposed to cause, effect and cli nical presentation of myofascial trigger
the paradigms of other disciplines and thus their 'tool box' points. While ultima tely the text turns to the detailed trea t
grows. l11is book is a wonderful representation of all the ment of every possible muscle you could think of i n the
paradigms of the many discipl ines that ha ve ever consid upper half of the body, prior to this the a uthors discuss
ered how to rela x/release a muscle or a trigger point in a where, when and how the neuromuscular techniques fit
muscle. Yet, this book is way more than this and even more into the entire treatment protocol. This ensures tha t the
than the title Clinical Application of Neuromuscular Techniques reader is not left with the impression that neuromuscular
alludes to. release is all that is needed for treating a patient. Once into
While this text relies heavily on the clinical expertise of trea tment, consideration is given to the role of non-manual
both the authors and the historical leaders in both their pro therapies such as thermal modal ities, spray and stretch and
fessions and others, it also refers and draws on the current exercise, and then the use of the manual techni ques is
scientific evidence where it is available. Some may say that explained in great detail. Following this, the upper half of
the techniques and suggested protocols in this text are not the body is divided and each section begins with a review of
xviii FOREWORD

the regional anatomy and biomechanics and a Hsting of the Neuromuscular Techniques, a text which is applicable to the
muscles in which trigger p oints are commonly found. Each novice and the expert of any discipline that deals with
manual tecl mique is illustrated and described in explicit patients p resenting with i mp airments of the neuromyofas
detail. This is easy for the novice to follow and often con ciaI system.
tains 'pearls of clinical wisdom' for the expert clinician.
Leon C haitow and Judith DeLany are to be congratu
lated for the second editi on of Clinical Application of White Rock, Be C anada 2007 Diane Lee

References

Ericsson KA, Smith J 1991 Towards a general theory of expertise: Sackett DL, Strauss SE, Richardson WS, et al 2000 How to practice
prospects and limits. Cambridge University Press, New York & teach evidence-based medicine. Elsevier Science, New York
xix

Preface to the Second Ed ition

The clinical utilization of soft tissue manipulation has logically the main focus for the p atient. However, we believe
increased dramatically in recent years in all areas of manual it is vital that loc al problems should be commonly seen by
health-care provision. A text that integrates the safe and the p ractitioner to form p art of a larger picture of compensa
proficient application of some of the most effective soft tis tion, adaptation and/or decompensation and that the back
sue tedmiques is both timely and necessary. The decision to ground causes (of local myofascial pain, for example) be
write this book was therefore based on a growing aware sought and, where possible, removed or at least m odified.
ness of the need for a text that describes, in some detail, the We also take the position t hat it is the p ractitioner's role
clinical applications of neuromuscular techniques in p artic to take account of biochemical (nutriti onal and hormonal
ular, and soft tissue manipulation in general, on each and influences, allergy, etc.), biomec hanical (posture, b reathing
every area of the musculoskeletal system. p atterns, habits of use, etc.) and/or psychosocial (anxiety,
There are n umerous texts c ommunicating the features of depression, stress factors, etc.) influences that might be
different manual therapy systems (osteopathy, chiropractic, involved, as far as this is p ossible. If appropriate, suitable
physical therapy, manual medicine, massage the rapy, etc.) advice or treatment c an then be offe red. However, if the
and of modalities employed with i. n these health-care deliv p ractitioner is not trained and licensed to do so, profes
ery systems (high-velocity thrust techniques, muscle energy sional referral becomes the obvious choice. In this way, the
tedmiques, myofascial release and many, many more). focus of health care goes beyond treatment of local condi
There are also excellent texts that describe regional p rob tions and moves toward holism, to the benefit of the patient.
lems (say of the pelvic region, temporomandibular j oint or In this volume, the person applying the techniques i s
the spine) with protocols for assessment and treatment, referred t o as the 'practitioner' so as to include all the ra
often presented from a p articular perspective. Increasingly, pists, physicians, nurses or others who apply manual tech
edited texts incorporate a variety of perspectives when niques. To ease confusion, the practitioner is depicted as
focusing on particular regions, offering the reader a broad male and t he recipient of the treatment modalities (the
view as well as detailed informati on on the topic. And t hen patient) is depicted as female so that gender references (he,
there are wonderfully crafted volumes, such as those p ro his, she, hers) used within the text are n ot ambiguous. In
duced by Travell and Simons, covering the spectrum of Volume 2, the roles are reversed with the female p racti
'myofascial pain and dysfu nction' and incorporating a tioner treating the male p atient.
deeply researched and evolving model of care. The protocols described in this text fall largely within the
We adopted Travell and Simons' view of the human b ody, biomechanical arena, with the main emphasis being the first
which offers a valuable regional approach model on which comprehensive, detailed description of the clinical applica
to base our own perspectives. To this practical and intellec tion of NMT (neuromuscular therapy in the USA, neuro
tually satisfying model, we have added detailed anatomical muscular technique in Europe). The desc riptions of NMT are
and physiological descripti ons, coupled with clinically prac mainly of the modern American version, as described by
tical 'bodywork' solutions to t he problems located in each Judith DeLany, whose many years of involvement with
region. In this first vol ume of the text, the upper b ody is cov NMT, both clinically and academically, make her a leading
ered; in Volume 2, the region from the waist down is sur authority on the subject.
veyed in the same way. As authors, we have attempted to Additional therapeutic choices, including nutri tional and
place in context the relative importance and significance of hydrotherapeutic, as well as complementary bodywork
local conditions, pain and/or dysfu nction, which are quite methods, such as muscle energy, positional release and
xx PREFACE TO THE SECOND EDITION

variations of myofascial release teclmiques, and the especially if they have had previous training in soft tissue
European version of NMT, are largely the contribution of palpation and treatment. The text of this book is therefore
Leon Chaitow, as are, to a large extent, the opening chapters intended as a framework for the clinical application of NMT
regarding the physiology of pain and dysfunction. for those already quali fied (and, where appropriate,
In addition to the practical application sections of the licensed to practice), as well as being a learning tool for
book, a nwnber of chapters offer a wide-ranging overview those in training. It is definitely not meant to be a substitute
of current think ing and research into the background of the for hands-on training with skilled in structors.
dysfunctional sta tes for which solutions a nd suggestions To this volume is married the companion text for the
are provided in la ter chapters. The overview, 'big picture' lower body, the layout and style of which is very similar. Its
chapters cover the latest research findings a nd information foundational chapters cover posture, gait, balance, influ
relevant to understanding fascia, muscles, neurological fac ences of the close environment surrounding the body, adap
tors, pa tterns of dysflmction, pain and inflammation , tations from sport and other repetitious use, and other
myofascial trigger points, emotional and nutritional influ contextual material that influences clinical thinking.
ences a nd much more. It is our assertion tha t the combina Additionally, Clinical Application of Neuromuscular
tion of the 'big picture', together with the detailed NMT Techniques - Practical Case Study Exercises is now available to
protocols, offers a foundation on which to build the excep support the practitioner in developing a model by which to
tional palpation and treatment skills necessary for finding apply the protocols to clinical cases. The use of the study
effective, practical solutions to chronic pain conditions. guide cases is enhanced with the addition of key words
Some chapters, such as Chapters 6 and 7, have evolved printed in red that may be found in the indices of the larger
substantially since the first edition, based on integration of texts. We trust that these tools, together with practitioner's
our diverse viewpoints, with the occasional result being skills and training, will assure that NMT remains a power
paradigm shifts that altered therapeutic platforms. We ful tool in the manual therapy fields.
believe that this integration of new i rtforma tion and
research, in ta ndem with our combined clinical experience,
offers an expanded perspective. Readers can use these con London 2007 LC
cepts to assist in safe application of the methods described, Florida 2007 JD
xxi

Acknowl ed g m ents

In the first edition of this text and its companion volume for support is threaded through these pages in remarkable yet
the lower body, a substantial number of people dedica ted indiscernible ways.
many hours of time to assure clarity and accuracy of the
final text. Their contribution was not lost in the second edi
AC K N O W L E D G E M E N TS F R O M T H E
tion. Instead, it served as a solid foundation to be built upon
F I RST E D IT I O N
with the contributions of revised and added material.
The authors once again express sincere gratitude to the Books are wri tten by the efforts of numerous people,
original team who help formulate this project many years a l though most of the support team is invisible to the reader.
ago and to the various authors and illustrators whose work We humbly express our appreciation to our friends and col
was cited, quoted and borrowed. Addi tionally, contribu leagues who assisted in this project and who enrich our
tions, support and inspiration for this revised edition were lives simply by being themselves.
given by William Ellio tt, Donald Kelley, Ken Crenshaw, Ron From the long list of staff members and practitioners who
Porterfield, Nathan Shaw, Mary-Beth Wagner, Andrew and dedicated time and effort to read and comment on this text,
Kaila DeLany, and Adam Cunliffe. we are especially grateful to Jamie Alagna, Paula Bergs,
In the second edition of this book, a new team of talented Bruno Chikly, Renee Evers, Jose Fernandez, Gretchen Fiery,
staff members at Elsevier offered insightful ideas, patient Barbara Ingram-Rice, Donald Kelley, Leslie Lynch, Aaron
support to achieve deadlines, and a variety of professional Mattes, Chama Rosenholtz, Cindy Scifres, Alex Spassoff,
services in order for the work to evolve. Among those who Bonnie Thompson and Paul Witt for reviewing pages of
made this second edition possible, the a uthors especially material, often at a moment's notice. And to those whose
acknowledge and appreciate the efforts of Claire Wilson, work has inspired segments of this text, such as John
Gail Wright, Claire Bonnett and the illustration team who Hannon, Tom Myers, David Simons, Janet Travell and
gave visual life to the pages of text. others, we offer our heartfelt appreciation for their many
To Sarena Wolfaard , we express deep apprecia tion for her contributions to myofascial therapies.
steady na ture and for her ability to juggle the assorted John and Lois Ermatinger spent many hours as models for
deadlines and the many phases of the project so as to keep the photographs in the book, some of which eventually
it close to its production schedule. She has proven herself as became line art, while Mary Beth Wagner dedicated her time
capable of filling the extraordinary shoes of Mary Law, who coordinating each photo session. The enthusiastic attitudes
served as the editorial director of the first edition. As to and tremendous pa tience shown by each of them turned
Mary, her contributions will last forever and her presence is what could have been tedious tasks into pleasant events.
continually missed. Many people offered personal support so tha t quality
And, most endearingly, we offer our deepest gratitude to time to write was available, including Lois Allison, Jan
our families for their pa tience, support, and inspiration, all Carter, Linda Condon, Andrew DeLany, Valerie Fox,
of which fills an ever-present and deep well from which we Patricia Guillote, Alissa Miller, and Trish Solito. Special
can draw to sustain and nurture ourselves. Their loving appreciation is given to Mary Beth Wagner and Andrea
xxii ACKNOWLED G M ENTS

Conley for juggling many, many ongoing tasks which serve worldwide. Mary's ability to foster organization amidst
to enhance and fortify this work. chaos, to find solutions to enormous challenges and to sim
Jane Shanks, Katrina Mather, and Valerie Dearing each put ply provide a listening ear when one is needed has
forth exceptional dedication to find clarity, organization and endeared her to our hearts.
balance within this text, which was exceeded only by their And finally, to each of our families, we offer our deepest
patience. The illustration team as well as the many authors, gratitude for their inspiration, patience, and ever present
artists and publishers who l oaned artwork from other books understanding. Thei r supporting l ove made this project
have added visual impact to help the material come alive. possible.
To Mary Law, we express our deepest app reciation for
her vision and commitment to complementary medicine
Chapter 1

Connective tissue and the fascial system

Connective tissue forms the single largest tissue component


CHAPTER CONTENTS of the body. The material we know as fascia is one of the
many forms of connective tissue.
The fascial network 2
In this chapter we will examine some of the key features
Fascia and proprioception 2
and functions of fascia in particular, and connective tissue
Fascia: collagenous continuity 2
in general, with specific focus on the ways in which:
Further fascial considerations 2
Elasticity 3 these tissues influence myofascial pain and dysfunction
Plastic and elastic features 3 their unique characteristics determine how they respond
Connective tissue as a 'sponge' 6 to therapeutic interventions, as well as to adaptive stresses
Deformation characteristics 6 imposed on them.
Hypermobility and connective tissue 7
In order to understand myofascial dysfunction, it is impor
Trigger points, fascia and the nervous system 8
tant to have a clear picture of this single network that
The importance of Langevin's research 9
enfolds and embraces all other soft tissues and organs of the
Summary of fascial and connective tissue function 13
body, the fascial web. In the treatment focus in subsequent
Fascial dysfunction 1 6
chapters, a great deal of reductionist thinking will be called
Restoring gel to sol 17
for as we identify focal points of dysfunction, local trigger
A different model linking trauma and
points, individual muscular stresses and attachment prob
connective tissue 17
lems, with appropriate local and general treatment descrip
Therapeutic sequencing 19
tions flowing from these identified areas and structures.

Box 1.1 Definitions

Stedman's Medical Dictionary (2004) says fascia is:


A sheet of fibrous tissue that envelops the body beneath the skin; it
also encloses muscles and groups of muscles, and separates their
several layers or groups

and that con nective tissue is:


The supporting or framework tissue of the . . . body. formed of
fibraus and graund substance with more or less numerous cells of
various kinds; it is derived fram the mesenchyme, and this in turn
from the mesoderm; the varieties of connective tissue are: areolar
or loose; adipose; dense, regular or irregular, white fibrous; elastic;
mucous; and lymphoid tissue; cartilage; and bone; the blood and
lymph may be regarded as connective tissues, the ground sub
stance of which is a liquid.

Fascia, therefore, is one form of con nective tissue.


2 CLI N I CA L A P P L I CATIO N OF N E U R O M U SC U LA R TECH N I Q U E S : T H E U P P E R B O DY

The truth, of course, is that no tissue exists in isolation but fascia moves in response to complex muscular activities
acts - is bound to and is interwoven - with other structures, to acting on bone, joints, ligaments, tendons and fascia
the extent that a fallen arch can directly be shown to influence fascia, according to Bonica (1990), is critically involved in
TMJ dysfunction (Janda 1986). In contrast, loss of occlusal proprioception, which is, of course, essential for postural
supporting zone can change weight distribution on the feet integrity (see Chapter 3)
and alter overall body posture (Yoshino et aI 2003a,b) When . research by Staubesand (using electron microscope stud
we work on a local area, we need to keep a constant aware ies) shows that 'numerous myelinated sensory neural
ness of the fact that we are influencing the whole body. structures exist in fascia, relating to both proprioception
Remarkable research (see Box 1.5 in particular) is adding and pain reception' (Staubesand 1996)
to our understanding of just how important connective tis after joint and muscle spindle input is taken into account,
sues are in relation to musculoskeletal function, and to pain the majority of remaining proprioception occurs in fas
management (Chen & Ingber 1999, Langevin et al 2001, cial sheaths (Earl 1965, Wilson 1966)
2004, 2005, Schleip et al 2004). As a foundation of under new research by Langevin et al (2001, 2004, 2005), described
standing of connective tissue is built within this chapter, later in this chapter, suggests that a great deal of commu
this and other research evidence is presented that alters pre nication occurs by means of fascial cellular structures
vious concepts of this extraordinary matrix. (integrins).

THE FASCIAL NETWORK FASCIA: COLLAGENOUS CONTINUITY

Fascia comprises one integrated and totally connected net Fascia is one form of connective tissue, formed from colla
work, from the attachments on the inner aspects of the skull gen, which is ubiquitous. The human framework depends
to the fascia in the soles of the feet. If any part of this net upon fascia to provide form, cohesion, separation and sup
work becomes deformed or distorted, there will be com port and to allow movement between neighboring structures
pensating adaptive stresses imposed on other parts of the without irritation. Since fascia comprises a single structure,
connective tissue web, as well as on the structures that it from the soles of the feet (plantar fascia) to the inside of the
divides, envelopes, enmeshes, supports and with which it cranium (dura and meninges), the implications for body
connects. There is ample evidence that Wolff's law (Wolff wide repercussions of distortions in that structure are clear.
1870) applies, in that fascia accommodates to chronic stress An example is found in the fascial divisions within the cra
patterns and deforms itself (Cailliet 1996), something which nium, the tentorium cerebelli and falx cerebri, which are
often precedes deformity of osseous and cartilaginous struc commonly warped during birthing difficulties (too long or
tures in chronic diseases (see Box 1.3). As fascia, ligaments too short a time in the birth canal, forceps delivery, etc.).
and tendons deform when accommodating to chronic stress They are noted in craniosacral therapy to affect total body
(Dorman 1997, Lederman 1997), this might disrupt the home mechanics via their influence on fascia (and therefore the
ostasis of the body (Keeffe 1999, Kochno 2001) and certainly musculature) throughout the body (Brookes 1984, Carreiro
interferes with normal function. 2003, Von Piekartz & Bryden 2001).
Visualize a complex, interrelated, symbiotically function Dr Leon Page (1952) discusses the cranial continuity of
ing assortment of tissues comprising skin, muscles, ligaments, fascia:
tendons and bones, as well as the neural structures, blood
The cervical fascia extends from the base of the skull to the
and lymph channels and vessels which bisect and invest
mediastinum and forms compartments enclosing the esoph
these tissues - all given shape, cohesion and functional abil
agus, trachea and carotid vessels and provides support for
ity by the fascia. Now imagine removing from this all that is
the pharynx, larynx and thyroid gland. There is direct con
not connective tissue. What remains would still demon
tinuity of fascia from the apex of the diaphragm to the base
strate the total form of the body, from the shape of the eye
of the skull. Extending through the fibrous pericardium
ball to the hollow voids for organ placement.
upward through the deep cervical fascia the continuity
extends not only to the outer surface of the sphenoid, occip
ital and temporal bones but proceeds further through the
FASCIA AND PROPRIOCEPTION foramina in the base of the skull around the vessels and
nerves to join the dura.
Research has shown that:

muscle and fascia are anatomically inseparable


fascia and other connective tissues form a mechanical con FURTHER FASCIAL CONSIDERATIONS
tinuum that extends throughout the body that includes
even the innermost parts of each cell - the cytoskeleton Fascia is colloidal, as is most of the soft tissue of the body (a
(Chen & Ingber 1999, Oschman 2000) colloid is defined as comprising particles of solid material
-----------..
------------

1 Connective tissue a n d the fascial system J

stick or spoon. A slowly moving stick or spoon will travel


smoothly thlough the paste, whereas any attempt to move
Creep Continued deformation (i ncreasing strai n) of a viscoelastic it rapidly will be met with a semirigid resistance (known as
material with time under constant load (traction, compression, 'drag'). This makes a gentle touch a fundamental require
twist) ment if viscous drag and resistance are to be avoided when
Hysteresis Process of energy loss due to friction when tissues are attempting to produce a change in, or release of, restricted
loaded and unloaded fascial structures, which are all colloidal in their behavior.
Load The degree of force (stress) applied to an area or an
organism as a whole
Strain Change in shape as a result of stress (external force)
Stress Force (load) normalized over the area on which it acts ELASTICITY
(all tissues exh ibit stress-stra in responses)
Thixotropy A qua lity of colloids in wh ich the more rapidly force Soft tissues, and other biological structures, have an innate,
is applied ( load), the more rig id the tissue response and to variable degree of elasticity, springiness, resilience or 'give',
become less viscous when shaken or subjected to shearing forces which allows them to withstand deformation when force
and to return to the original viscosity upon standing. or pressure is applied. This provides the potential for sub
Viscoelastic The potential to deform elastica lly when load is sequent recovery of tissue to which force has been applied, so
applied and to return to the original non-deformed state when
that it returns to its starting shape and size. This quality of
load is removed
elasticity derives from these tissues' (soft or osseous) ability
Viscoplastic A perma nent deformation resulting from the elastic
to store some of the mechanical energy applied to them and
potential having been exceeded or pressure forces susta i ned for
too great a period of time to utilize this in their movement back to their original sta
tus. This is a process known as hysteresiS (see below).
The stability and movement characteristics of each body
part - whether this involves organs, vessels, nerves, mus
cles or bones - is defined by a fibrin matrix combined with
Mecha nical princi ples i nfluencing the body neurologica l ly and other elements. For example, bone incorporates calcium
anatom ica l ly are governed by basic laws. phosphate to lend rigidity, while muscle contains neurore
Wolffs law states that biological systems (including soft and sponsive proteins that enable changes in shape. Each ele
hard tissues) deform in relation to the l ines of force imposed ment in connective tissue contributes to its strength, resilience
on them. and compliance, with elastin allowing controlled, reversible
Hooke's law states that deformation (resulting from strain) deformation under strain, and fibrin, laid out along the lines
imposed on an elastic body is in proportion to the stress
of the local axis of motion, serving as a check on the extent
(force/load) placed on it.
Newton's third law states that when two bodies interact, the of this deformation.
force exerted by the first on the second is equa l in magnitude Although a certain amount of deformation is physiologi
and opposite in di rection to the force exerted by the second cally necessary, trauma may cause deformation beyond the
on the fi rst. elastic limit of the tissues, thereby causing permanent dam
Ardnt-Schultz's law states that weak stimuli excite age or possibly resulting in a semipermanent distortion of
physiological activity, moderately strong ones favor it, strong
ones retard it and very strong ones a rrest it. the connective tissue matrix if the damage is not too severe.
Hilton's l aw states that the nerve su pplying a joint a lso Return to normal is then sometimes possible, but only with
supplies the muscles that move the joint and the skin covering the reintroduction of sufficient energy to allow a reversal of
the a rticular insertion of those muscles. the deformation process - for example, by means of manual
Head's law states that when a painful stimulus is a pplied to a therapy ('soft tissue manipulation'). Appropriately applied
body part of low sensitivity (such as a n organ) that is in close
central connection (the same segmenta l supply) with an area 'force' (i.e. slowly) can assist in resolving the deformation
of higher sensitivity (such as a part of the soma), pain will be results of strain. In such processes energy is both absorbed
felt at the point of higher sensitivity rather than where the and released. This energy transfer feature, known as hystere
stimulus was appl ied. sis, is described further below (Becker 1997, Comeaux 2002).

suspended in fluid - for example, wallpaper paste or,


PLASTIC AND ELASTIC FEATURES
indeed, much of the human body). Scariati (1991) points out
that colloids are not rigid - they conform to the shape of Greenman (1989) describes how fascia responds to loads and
their container and respond to pressure even though they stresses in both a plastic and an elastic manner, its response
are not compressible. The amount of resistance colloids offer depending, among other factors, upon the type, duration
increases proportionally to the velocity of force applied to and amount of the load. When stressful forces (undesirable
them. A simple example that gives a sense of colloidal behav or therapeutic) are gradually applied to fascia (or other bio
ior is available when flour and water are stirred together logical material), there is at first an elastic reaction in which
with the resulting colloid being mixed into a paste, using a the degree of slack is reduced. If the force persists, this is
4 C L I N I CAL APP LICAT I O N O F N E U R O M USCU LAR TECH N I QU ES: T H E UPPER B O DY

Box 1.4 Connective tissue

Connective tissue is composed of cells (including fibroblasts and abnorma l crossbridges which prevent normal movement. Fol lowing
chond rocytes) and an extrace l l ular matrix of collagen and elastic tissue i nju ry, it is important that activity be introduced as soon as
fibers surrounded by a g round substance made primarily of acid the healing process will allow in order to prevent maturation of the
glycosam inoglycans (AGAGs) and water (Gray's Anatomy 2005, sca r tissue and development of adhesive crossl inks (Lederman 1 997).
Lederman 1997). Its patterns of deposition change from location to Lederman ( 1 997) tel ls us:
location, depending upon its role and the stresses applied to it.
The pattern of collagen deposition varies in different types of
The collagen component is com posed of three polypeptide cha ins
connective tissue. It is an adaptive process related to the direction
wound around each other to form triple hel ixes. These microfi la ments
of forces imposed on the tissue. In tendon, collagen fibers ore
are arranged in parallel manner and bound together by crossl inking
organized in parallel orrangement; th is gives the tendon stiffness and
hydrogen bonds, which 'glue' the e lements together to provide
strength under unidirectional loads. In ligaments, the organization of
strength and stabil ity when mecha nical stress is applied. Movement
the fibers is looser. groups of fibers lying in different directions. This
encourages the col lagen fibers to a l ign themselves a long the l ines of
reflects the multidirectional forces that ligaments are subjected to,
structural stress as well as improving the ba lance of
for example during complex movements of a joint such as flexion
glycosami noglycans and water, therefore lubricating and hydrating
combined with rotation ond shearing . . . Elostin has an arrongement
the connective tissue (Lederman 1997).
similar to that of collagen in the extracellular matrix, and its
While these bonding crossbridges do provide structu ra l support,
deposition is also dependent on the mechanical stresses imposed on
injury, chronic stress and immobility cause excessive bonding,
the tissue.
leading to the formation of scars and adhesions wh ich limit the
movement of these u sually resil ient tissues (Juhan 1 998). The loss of Elastin provides an elastic-l ike quality that allows the connective
tissue lengthening potential would then not be due to the volume of tissue to stretch to the limit of the collagen fiber's length, while
collagen but to the random pattern in which it is laid down and the absorbing tensile force. If this elastic quality is stretched over time,
it may lose its abil ity to recoil (as seen in the stretch marks of
preg nancy). When stress is applied, the tissue can be stretched
to the limit of the collagen fiber length with flexibility being
dependent upon elastic quality (and quantity) as well as the
Procollagen F i broblast extent of crossbridging that has occurred between the col lagen
fibers. Additional ly, if heavy pressure is suddenly appl ied, the
connective tissue may respond as brittle and may tea r more easily
(Ku rz 1 986).
Surrounding the col lagen and elastic fibers is a viscous, gel-l ike
------- g round substance, composed of proteoglycans and hyaluronan
\ \
/O-TropOCOllagen
(formerly called hyaluronic acid), which l ubricates these fibers and
allows them to sl ide over one another (Barnes 1 990, Ca illiet 1 996,
Gray's Anatomy 2005, Jackson et al 2001 ).

Ground substance provides the immediate envi ron ment for every
cell in the body.
The protein component is hydrophilic (draws water into the tis
sue), producing a cushion effect as well as maintaining space
between the collagen fibers (Jackson et al 200 1 ).
Ground substance provides the med ium through which other ele
ments are exchanged, such as gases, nutrients, hormones, cel l ular
'------Collagen microfibril waste, antibodies and white blood cells (Juhan 1998).
L The condition of the g round substance ca n then affect the rate of
diffusion and therefore the health of the cel l s it su rrounds.

The consistency of the connective tissue varies from tissue to tissue.


Where fewer fibers and more liquid is found, an ideal environment
for metabolic activities abounds. With less fluid and more fibers, a
soft, flexible lattice is achieved that can hold skin cel ls, nerve cells or
organ tissue in place. With little fluid and many fibers, a tough,
Fibroblasts
stringy material forms for use in muscle sacs, tendons and ligaments.
When chondroblasts (ca rtilage-producing cel ls) and their hya l ine
Fascicle
secretions are added, a more solid substance occurs, a nd when
mineral salts are added to achieve a rock-like hardness, bones a re
formed (Juhan 1998).
Unless i rreversible fibrotic changes have occurred or other
pathologies exist, connective tissue's state ca n be changed from a
Tendon gelatinous-like substance to a more solute (watery) state by the
i ntroduction of energy through muscu lar activity (active or passive
movement provided by activity or stretching), soft tissue manipulation
(as provided by massage) or heat (as in hydrotherapies). Th is
Figure 1.1 Col lagen is p rod uced locally for repa i r of d a maged characteristic, cal led thixotropy, is a 'property of certain gels of
connective tissue. After Lederm a n 1997. becoming less viscous when shaken or subjected to shea ring forces

box continues
1 Connective tissue and the fascial system 5

Box 1 .4 (continued)

Elongation

Toe Elastic
region region

Pre-elastic Elastic rangel Initially, molecular


range physiological displacement
Slack range range leading to microtears
Intramolecular and complete
crosslinks rupture

Figure 1.2 Collagen's triple helices are bound together by inter Loss of mechanical
properties
and intramolecular crosslinking bonds. After Lederman (1997).

and returning to the original viscosity upon standing' (Stedman's


Medical Dictionary 2004). Without th i x otropic properties, movement
would eventually cease due to solid ification of synovium and
connective tissue. Figure 1.3 Schematic represe n tatio n of the stress-strain cu rve.
Oschman states (1997): After Lederman (1 997).
If stress, disuse and lack of movement cause the gel to deh ydrate,
contract and harden (an idea that is supported both by scientific con ten t and in its ability to conduct energy and movement. The
evidence and by the experiences of many somato therapists) the ground substance becomes more porous, a better medium for the
application of pressure seems to bring about a rapid solation and diffusion of nutrien ts, oxygen, waste products of metabolism and the
rehydration. Removal of the pressure allows the system to rapidly enzymes and building blocks involved in the 'metabolic regenera tion '
re-gel, but in the pracess the tissue is transformed, both in its water process ..

followed by what is colloquially referred to as creep a vari - fracture when rapid force meets the resistance of bone. If
able degree of resistance (depending upon the state of the tis force is applied gradually, 'energy' is absorbed by and stored
sues). This gradual change in shape is due to the viscoelastic in the tissues. The usefulness of this in tendon function is
property of corulective tissue. obvious and its implications in therapeutic terms profound
Creep, then, is a term that accurately describes the slow, (Binkley 1989).
delayed, yet continuous deformation that occurs in Hysteresis is the term used to describe the process of energy
response to a sustained, slowly applied load, as long as this loss due to friction and to minute structural damage that
is gentle enough not to provoke the resistance of colloidal occurs when tissues are loaded and unloaded. Heat will be
'drag'. During creep, tissues lengthen or distort ('deflect') produced during such a sequence, which can be illustrated
until a point of balance is achieved. An example often used by the way intervertebral discs absorb force transmitted
of creep is that which occurs in intervertebral discs as they through them as a person jumps up and down. During
gradually compress during periods of upright stance. treatment (tensing and relaxing of tissues, for example, or
Stiffness of any tissue relates to its viscoelastic properties on-and-off pressure application), hysteresis induction reduces
and, therefore, to the thixotropic colloidal nature of colla stiffness and improves the way the tissue responds to sub
gen/ fascia. Thixotropy reIates to the quality of colloids in sequent demands. The properties of hysteresis and creep
which the more rapidly force is applied (load), the more provide much of the rationale for myofascial release tech
rigid the tissue response will be - hence the likelihood of niques, as well as aspects of neuromuscular therapy, and
6 CLINICAL A PPLICATION OF NEUROMUSCULAR TECHN IQUES: THE U P PER BODY
L

need to be taken into account during technigue applica


tions. Especially important are the facts that:

rapidly applied force to collagen structures leads to defen


sive tightening
slowly applied load is accepted by collagen structures
and allows for lengthening or distortion processes to
commence.

When tissues (cartilage, for example) that are behaving vis


coelastically are loaded for any length of time, they first
deform elastically. Subseguently, there is an actual volume
change, as water is forced from the tissue as they become
less sol-like and more gel-like . Ultimately, when the applied
force ceases, there should be a return to the original non
deformed state. However, if the elastic potential has been
exceeded, or pressure forces are sustained, a viscoplastic
response develops and deformation can become perma
nent. When the applied force ceases, the time taken for tis
sues to return to normal, via elastic recoil, depends upon the
uptake of water by the tissues. This relates directly to osmotic Figure 1 .4 Electron photomicroscopy of a typical smooth muscle
pressure, and to whether the viscoelastic potential of the tis cell within the fascia cruris. Above it is the terminal portion of a
sues has been exceeded, which can result in a viscoplastic type IV (unmyelated) sensory neuron. ( Photo reproduced with the
(permanent deformation) response. kind permission of Springer Verlag, first published in Staubesand
1 996.) Reproduced with permission from Journal of Bodywork and
Movement Therapies 2003; 7(2) :104-11 6.

CONNECTIVE TISSUE AS A 'SPONGE'

Schleip et al (2004) have shown that when an isometric con to sponge-like squeezing and refilling effects in the semi-liquid
traction takes place - as in sustained effort, or therapeuti ground substance, with its intricate scrub-like arrangement
cally with methods such as muscle energy technigue (MET), of water binding glycosaminoglycans and proteoglycans.
proprioceptive neuromuscular facilitation (PNF) or other
Schleip et al (2004) have presented evidence that derives from
similar techin gues
the same German research, showing that the thoracolumbar
simultaneously loses some of its stability, making it easier to
fascia has the ability to contract, suggesting that the 'fascia
stretch.
may play an active role in joint dynamics and regulation'.
It behaves like a sponge, and if the contraction is long
Schleip et al also suggest that this research 'offers new insights
and strong enough, and if no movement occurs after the
into understanding low back instability, compartment syn
contraction, the fascia reabsorbs water, becoming stiffer as it
drome, and my ofascial release therapies'.
does so. Research into this phenomenon is in its early stages
but at this time the researchers (Schleip et a12004) have been
able to report:
DE FORMATION CHARACTERISTICS
By carefully measuring the wet weight of our fascial strips,
at different experimental stages, plus the final dry weight Cantu & Grodin (1992) describe what they see as the 'unigue'
(after later drying the strips in an oven), we found the fol feature of connective tissue as its 'deformation characteris
lowing pattern: During the isometric stretch period, water tics'. This refers to the combined viscous (permanent, plastic)
is extruded, which is then refilled in the following rest period. deformation characteristic, as well as an elastic (temporary )
Interestingly if the stretch is strong enough, and the following deformation status discussed above. The fact that cOIUlective
rest period long enough, more water soaks into the ground tissues respond to applied mechanical force by first chang
substance than before. The water content then increases to a ing in length, followed by some of the change being lost
higher level than before the stretch. Fascia seems to adapt in while some remains, has implications in the application of
very complex and dynamic ways to mechanical stimuli, to stretching technigues to such tissues. It also helps us to
the degree that the matrix reacts in smooth-muscle-like con understand how and why soft tissues respond as they do to
traction and relaxation responses of the whole tissue. It seems postural and other repetitive insults that exert load on them,
likely that much of what we do with our hands in Structural often over long periods of time.
Integration and the tissue response we experience, may not It is worth emphasizing that although viscoplastic changes
be related to cellular or collagen arrangement changes, but are described as 'permanent', this is a relative term. Such
1 Connective tissue a nd the fascial system 7

changes are not necessarily absolutely permanent since col


lagen (the raw material of fascia/connective tissue) has a
limited (300-500 day) half-life and, just as bone adapts to
stresses imposed upon it, so will fascia.
If negative stresses (e.g. poor posture, use, etc.) are mod
ified for the better and/or positive (therapeutic) 'stresses'
are imposed by means of appropriate manipulation and/or
exercise, apparently 'permanent' changes can modify for the
better. Dysfunctional connective tissue changes can usually
be improved, if not quickly then certainly over time (Brown
2000, Carter & Soper 2000, Neuberger 1 953). However, some
connective tissue changes are more permanent.
Schleip et al (2004) have observed many examples of tis
sue contractions caused by connective tissue cells called
myofibroblasts (see Box 1 .5):
This happens naturally in wound healing, but also in sev
eral chronic fascial contractures. In the hand, it presents as
palmar fibromatosis, also known as Dupuytren's contrac
ture, or as a pad-like thickening of the knuckles. In the foot
the same process is called plantarfibromatosis, while in club
foot contraction of the myofibroblasts is focused on the
medial side. In frozen shoulder, the contraction occurs in the
shoulder capsule . . . considering the existence of pathologi
cal faSCial contractu res, it seems likely that there may be
lesser degrees offascial contractions, which may influence
biomechanical behavior.

Important features of the response of tissue to load include:


the degree of the load
the amount of surface area to which force is applied B
the rate, uniformity and speed at which it is applied
how long load is maintained
the configuration of the collagen fibers (i.e. are they par
allel to or differently oriented from the direction of force,
offering greater or lesser degrees of resistance?)
the permeability of the tissues (to water)
the relative degree of hydration or dehydration of the indi
vidual and of the tissues involved
the status and age of the individual, since elastic and
plastic qualities diminish with age
another factor (apart from the nature of the stress load)
that inl1uences the way fascia responds to application of
a stress load, and what the individual feels regarding the
process, relates to the number of collagen and elastic
fibers contained in any given region.

HYPERMOBILITY AND CONNECTIVE TISSUE

Ligamentous laxity and general increased mobility of the


connective tissues creates a background of instability.
Hypermobility is usually genetically acquired. Kerr &
Grahame (2003) describe the sequence that leads to this C
as follows: 'Genetic aberrations affecting fibrous proteins Fig u re 1.5 A-C: Examples of hypermobility. Reproduced with
give rise to biochemical variations, then in turn to permission from Kerr Et Grahame (2003).
8 CLI N I CA L A P P L I CATI O N O F N E U R O M USCULAR TECH N I QUES: TH E U P P E R B O DY

at the cost of stability (Simons 2002, Thompson 2001).


Simons (2002) concurs:
In this case it is wise to correct the u nderlying cause of
ins tability before releasing the MTrP tension. In fact, cor
recting the underlying instability often results in sponta
neous resolution of the M TrP. It is important to identify
and remove or modify as many etiological and perpetuat
Mechanical failure
ing influences as can be found, however, without creating
further distress or a requirement for excessive adaptation.
Figure 1 .6 Pathophysiology of heritable connective tissue disorders. It is also important to consider that, at times, apparent
Reproduced with permission from Kerr Et Grahame (2003). symptoms may represent a desirable physiological
response (Thompson 2001).

A safer alternative is to encourage fitness training,


impairments of tensile strength, resulting in enhanced along with the self-use of ice, hydrotherapy and gentle
mobility but at a cost of increased fragility, ultimately risk stretching and toning exercises (Goldman 1991). It might
ing mechanical tissue failure.' also be helpful to selectively deactivate the most painful
A number of disorders derive from connective tissue MTrPs before movement therapies can begin; active
pathophysiology, including Marfan syndrome, Ehlers movement and, therefore, toning can then be part of the
Danlos syndrome, osteogenesis imperfecta and joint immediate therapy session when the MTrPs are suffi
hypermobility syndrome. ciently reduced.
The commonality of these different syndromes, all result
ing from variations of connective tissue laxity, is a ten
dency toward hypermobility, arthralgia, tendency to TRIGGER POINTS. FASCIA AND THE NERVOUS
dislocation (and possible fracture), osteoporosis, thin SYSTEM
skin (and stretch marks), varicose veins, prolapse (rectal,
uterine, mitral valve), hernia and diverticulae. Changes that occur in connective tissue, and which result in
Hypermobility has been shown to be a major risk factor alterations such as thickening, shortening, calcification and
in the evolution of back pain (Muller et aI2003). erosion, may be a painful result of sudden or sustained ten
Hypermobile individuals often present with chronic pain sion or traction. Cathie (1 974) points out that many trigger
syndromes and an increased tendency to anxiety and points (he calls them trigger 'spots') correspond to points
panic attacks (Bulbena et al 1 993, Martin-Santos et al where nerves pierce fascial investments. Hence, sustained
1998). tension or traction on the fascia may lead to varying degrees
Hypermobility is more common in people of African, of fascial entrapment of neural structures and consequently
Asian and Arab origin where rates can exceed 30% (as a wide range of symptoms and dysfunctions. Neural recep
compared with Caucasians 6%), as well as being more tors within the fascia report to the central nervous system as
frequently identified in the young compared with the part of any adaptation process, with the pacinian corpuscles
elderly, and in females compared with males (Hakim & being particularly important (these inform the CNS about
Grahame 2003). the rate of acceleration of movement taking place in the
When joints are vulnerable because of hypermobility, pas area) in terms of their involvement in reflex responses.
sive stretches and end-range positions seem to be able to Other neural input into the pool of activity and responses to
trigger musculoskeletal symptoms (Russek 2000). biomechanical stress involve fascial structures, such as ten
Patient care requires that patients modify their ergonom dons and ligaments which contain highly specialized and
ics and body mechanics (avoiding overuse and extreme sensitive mechanoreceptors, and proprioceptive reporting
posi tions) to avoid stretching their joints past end-range stations (see reporting stations, Chapter 3).
during activities of daily living (Russek 2000). Additionally:
Trigger point evolution in associated muscles is a com
mon result of the relative laxity of joints (Kerr & Grahame German research has shown that fascia is 'regularly' pen
2003). The authors of this text hypothesize that these energy etrated (via 'perforations') by a triad of venous, arterial
efficient (if painful) entities may offer an efficient means and neural structures (Heine 1995, Staubesand 1996)
of achieving short-term stability in unstable areas (Chaitow these seem to correspond with fascial perforations previ
2000, Chaitow & DeLany 2002, DeLany 2000). ously identified by Heine, which have been correlated
The implications of this possibility are clear. If myofascial (82% correlation) with known acupuncture points (Heine
trigger points (MTrPs) are serving functional roles, such 1 995). Further, Bauer & Heine (1998) showed that the
as in stabilization of hypermobile joints, deactivation of triad of pedora ting neurovascular structures was regu
potentially stabilizing trigger points may ease pain but larly 'strangulated' by an excessive amount of collagen
1 Connective tissue and the fascial system 9

Fig u re 1 .7 Location of acupuncture points and meridians


in serial gross anatomical sections through a human arm.
Reproduced from Langevin H M , Yandow J A Relationship
of acupuncture points and meridians to connective tissue
planes. Anatomical Record 269(6):257-265, 2002.
Copyright 2002, Wiley-Liss, Inc. Reprinted with permission
SJ1 of Wiley-Liss, Inc., a subsidiary of John Wiley Et Sons, Inc.

P2

Meridians
Yin Yang @ acupunclure
H= heart pOint
p= pencarolum SJ triple heat"r meridian
L= lung SI= small intestine intersection

fibers around these openings in most of the acupoints of THE IMPORTANCE OF LANGEVIN'S RESEARCH
the painful region. When those strangulated areas were
Ongoing research at the University of Vermont has pro
surgically opened a little, most of the patients experi
duced remarkable new information regarding the function
enced significant improvements (i.e. less pain)
of fascial connective tissue (Langevin et al 2001, 2004, 2005).
many of these fascial neural structures are sensory and
In evaluating the importance of the research information
capable of being involved in pain syndromes.
(below) it is important to recall that approximately 80% of
Staubesand states: common trigger point sites have been claimed to lie pre
cisely where traditional acupuncture points are situated on
The receptors we found in the lower leg fascia in humans meridian maps (Wall & Melzack 1 990). Indeed, many
could be responsible for several types of myofascial pain experts believe that trigger points and acupuncture points
sensations . . . Another and more specific aspect is the inner are the same phenomenon (Kawakita et al 2002, Melzack
vation and direct connection of fascia with the autonomic et al 1 977, Plummer 1 980).
nervous system. It now appears that the fascial tonus might Others, however, take a different view. For example,
be influenced and regulated by the state of the autonomic Birch (2003) and Hong (2000) have revisited the original
nervous system . . . intervention in the fascial system might work of Wall & Melzack (1 990) and have both found this
have an effect on the autonomic nervous system, in general, to be flawed, particularly when the acupuncture points
and upon the organs which are directly effected from it. referred to as correlating with trigger points are seen to be
(Schleip 1998) 'fixed' anatomically, as on myofascial meridian maps. Both
10 CLINICAL APPLICATION O F NEUROMUSCULAR TECHNIQUES: THE UPPER BODY

Birch and Hong agree, however, that so-called 'Ah shi' tissue matrix (e.g. fibroblasts, sensory afferents, immune
acupW1cture points may well represent the same phenome and vascular cells)'.
non as trigger points. Ah shi points do not appear on the The key elements of Langevin's research can best be sum
classical acupW1cture meridian maps, but refer to 'sponta marized as follows:
neously tender ' points which, when pressed, create a Acupuncture points, and many of the effects of acupW1c
response in the patient of, 'Oh yes' ('Ah shi'). In Chinese ture, seem to relate to the fact that most of these localized
medicine Ah shi points are treated as 'honorary acupuncture 'points' lie directly over areas where there is fascial cleav
points' and are needled or receive acupressure in the same age; where sheets of fascia diverge to separate, surround
way as regular acupW1cture points, if/when they are ten and support different muscle blmdles (Langevin et al
der/painful. This would seem to make them, in all but in 2001).
name, identical to trigger points. COlU1ective tissue is a commW1ication system of as yet
It is clearly important therefore, in attempting to under unknown potential. The tiny projections emerging from
stand trigger points more fully, to pay attention to current each cell are called 'integrins'. Ingber demonstrated
research into acupuncture points and cOlU1ective tissue in (Ingber 1993b, Ingber & Folkman 1 989; see Box 1.6) inte
general, as noted in the following research. grins to be a cellular signaling system that modify their
Langevin & Yandow (2002) have presented evidence that fW1ction depending on the relative normality of the shape
links the network of acupW1cture points and meridians to a of cells. The structural integrity (shape) of cells depends
network formed by interstitial cOlU1ective tissue. Using a on the overall state of normality (deformed, stretched, etc.)
unique dissection and charting method for location of of the fascia as a whole. As Langevin et al (2004) report:
cOlU1ective tissue (fascial) planes, acupW1cture points and
acupuncture meridians of the arm, they note that: 'Overall, 'Loose' connective tissue forms a network extending
more than 80% of acupuncture points and 50% of meridian throughout the body inc/uding subcutaneous and intersti
intersections of the arm appeared to coincide with inter tial connective tissues. The existence of a cellular network
muscular or intramuscular cOlU1ective tissue planes.' of fibroblasts within loose connective tissue may have
Langevin & Yandow's research further shows microscopic considerable significance as it may support yet unknown
evidence that when an acupuncture needle is inserted and body-wide cellular signaling systems . . . Our findings
rotated (as is classically performed in acupW1cture treatment), indicate that soft tissue fibroblasts form an extensively
a 'whorl' of cOlU1ective tissue forms around the needle, interconnected cellular network, suggesting they may
thereby creating a tight mechanical coupling between the have important, and so far unsuspected integrative func
tissue and the needle. The tension placed on the cOlU1ective tions at the level of the whole body.
tissue as a result of further movements of the needle delivers Perhaps the most fascinating research in this remarkable
a mechanical stimulus at the cellular level. They note that series of discoveries is that cells change their shape and
changes in the extracellular matrix ' . . . may, in turn, influ behavior following stretching (and crowding/deforma
ence the various cell populations sharing this connective tion) . The observation of these researchers is that: 'The

Figure 1 .8 Formation of a connective tissue 'whorl' when an acupuncture needle was inserted through the tissue and progressively rotated.
Reproduced from Langevin H M, Yandow J A Relationship of acupuncture points and meridians to connective tissue planes. Anatomical Record
269(6): 257-265, 2002. Copyright 2002, Wiley-Liss, Inc. Reprinted with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.
1 Connective tissue and the fascial system 11

dynamic, cytoskeleton-dependent responses of fibrob when gravity is removed or reduced. The behavior of cells
lasts to changes in tissue length demonstrated in this changes to the extent that, irrespective of how good the
study have important implications for our understand overall nutritional state is, or how much exercise (static
ing of normal movement and posture, as well as thera cycling in space) is taking place, individual cells cannot
pies using mechanical stimulation of connective tissue, process nutrients normally, and problems such as decalcifi
including physical therapy, massage and acupuncture' cation emerge.
(Langevin et aI2005). The importance we give to this information should be
As will become clear, changes in the shape of cells also alter tied to the awareness that, as we age, adaptive forces cause
their ability to function normally, even in regard to how changes in the structures of the body, with the occurrence of
they handle nutrients. Ingber conducted research (Ingber shortening, crowding and distortion. With this, we are see
1993a,b, 2003, Ingber & Folkman 1989), much of it for ing in real terms, in our own bodies and those of our
NASA, into the reasons that astronauts lose bone density patients, the environment in which cells change shape. As
after a few months in space. He showed that cells deform they do so they change their potential for normal genetic

Box 1 . 5 Myers' fascial tra i n s (Myers 1 997. 2001 )

Tom Myers, a distinguished teacher of structural i ntegration, has subcutaneous ligament, linking the ischial tuberosities to sacrum
described a number of clinically useful sets of myofascial chai ns. The l u mbosacra l fascia, erector spinae and nuchal ligament, linking
connections between different structures ('long functional the sacrum to the occiput
continuities') that these insights a l low will be drawn on and referred sca lp fascia, linking the occiput to the brow ridge.
to when treatment protocols are discussed in this text. They a re of
particu lar importance in helping draw attention to (for example) The superficial front line (Fig. 1 .1 0) i nvolves a chain that starts
dysfu nctional patterns in the lower limb which impact d i rectly (via with:
these chains) on structures in the upper body.
the anterior compartment and the periostium of the tibia, linking
the dorsal surface of the toes to the tibial tuberosity
The five major fascial ch a i ns
rectus femoris, linking the tibial tuberosity to the anterior i nferior
The superficial back line (Fig. 1 .9) involves a chain that starts with:
iliac spine and pubic tubercle
the plantar fascia, linking the plantar su rface of the toes to the rectus abdominis as well as pectora lis and sternalis fascia, linking
calcaneus the pubic tubercle and the anterior i nferior iliac spine with the
gastrocnem ius, linking calcaneus to the femoral condyles manubrium
hamstrings, l inking the femoral condyles to the ischial sternocleidomastoid, linking the manubri um with the mastoid
tuberosities process of the tempora l bone.

Figure 1 .9 Myers' superficial fascial back


l i n e. Reproduced with permission fro m t h e
Journal o f Bodywork and Movement
Therapies 1 997; 1 (2):95.

The superficial back line (SBl)

box con tinues


12 C LI N I CAL A P P LI CAT I O N O F N E U R O M U S CU LAR TECH N I Q U E S : T H E U P P ER B O DY
c::

the sacrotuberous ligament li nks the ischial tuberosity to the


sacrum
the sacral fascia and the erector spinae link the sacrum to the
occipital ridge.
The deep front line describes several a lternative chains i nvolving the
structures anterior to the spine (internally, for example) :
the anterior longitud inal l iga ment. diaph rag m, pericardium,
med iastinum, parietal pleura, fascia prevertebra lis and the
scalene fascia, which connect the lumbar spine (bodies and
transverse processes) to the cervical tra nsverse processes and via
longus ca pitis to the basilar portion of the occiput
other l inks in this chain might involve a connection between the
posterior manubrium and the hyoid bone via the subhyoid
muscles a nd
the fascia pretrachea lis between the hyoid and the
cranium/mandible, involving suprahyoid muscles
the muscles of the jaw li nking the mandible to the face and
cranium.
Myers includes in his cha in description structures of the lower limbs
that connect the tarsum of the foot to the lower l u mbar spine,
making the li nkage complete. Additional smaller chains involving the
a rms are described as follows.

Back of the a rm l i nes


The superficial front line (SFL)
The broad sweep of trapezius links the occipital ridge and the
Fig u re 1 . 1 0 Myers' su perficial fascial front l i ne. Reproduced with cervical spinous processes to the spine of the scapula and the
perm ission from the Journal of Bodywork a n d Movement clavicle.
The deltoid, together with the latera l intermuscu lar septum,
Therapies 1 997 ; 1 (2) :97.
connects the scapula and clavicle with the lateral epicondyle.
The latera l epicondyle is joined to the hand and fi ngers by the
com mon extensor tendon.
Another track on the back of the arm can arise from the
The lateral line involves a cha i n that starts with: rhomboids, which link the thoracic tra nsverse processes to the
peroneal muscles, linking the 1 st and 5th metatarsal bases with medial border of the sca pula.
the fibular head The sca pula in turn is linked to the olecranon of the u l na by
ilioti bial tract, tensor fascia latae and g luteus maximus, linking infraspinatus and the triceps.
the fibu lar head with the iliac crest The olecranon of the ulna connects to the sma l l fi nger via the
external obliques, internal obliques and (deeper) quadratus lum periostium of the u l na.
borum, linking the iliac crest with the lower ribs A 'stabil ization' feature in the back of the arm i nvolves
externa l i ntercostals and internal intercostals, linking the lower latissimus dorsi and the thoracolumbar fascia, which connects
ribs with the remaining ribs the a rm with the spinous processes, the contra lateral sacral
splenius cervicis, i liocostal is cervicis, sternocleidomastoid and fascia and gluteus maximus, wh ich in tu rn attaches to the shaft
(deeper) sca lenes, linking the ribs with the mastoid process of the of the femur.
temporal bone. Vastus latera lis connects the femur shaft to the tibial tuberosity
and (via this) to the periostium of the tibia.
The spiral line involves a chain that starts with:
splenius capitis, which wraps across from one side to the other, Front of the arm l i nes
linking the occipital ridge (say, on the rig ht) with the spinous Latissimus dorsi, teres major and pectoralis major attach to the
processes of the lower cervical and u pper thoracic spine on the left humerus close to the medial i ntram uscular septum, connecting it
continuing in this direction, the rhomboids (on the l eft) link via to the back of the trunk.
the medial border of the scapula with serratus anterior and the The medial i ntramuscu lar septum connects the humerus to the
ribs (stil l on the left), wrapping around the tru nk via the external medial epicondyle which con nects with the palmar hand and
obliques and the abdom inal a poneurosis on the left, to connect fi ngers by means of the common flexor tendon.
with the internal obliques on the right and then to a strong An additional line on the front of the arm involves pectora lis
anchor point on the anterior superior i l iac spine (ASIS) (right side) mi nor, the costocoracoid ligament, the brachial neurovascular
from the ASIS, the tensor fascia latae and the il iotibial tract link bundle and the fascia clavi pectoral is, which attach to the
to the lateral tibial condyle coracoid process.
tibialis anterior links the lateral tibial condyle with the 1 st The coracoid process also provides the attachment for biceps
metatarsal and cuneiform brachii (and coracobrachialis), linking this to the radius and the
from this a pparent endpoint of the chain ( 1 st metatarsal and thumb via the flexor compartment of the forearm.
cuneiform), peroneus longus rises to link with the fibular head A 'stabil ization' line on the front of the arm involves pectora lis
biceps femoris connects the fibu lar head to the isch ial tu berosity major attaching to the ribs, as do the external obliques, which

box continues
1 Con nective tissue a n d the fascial system 13

then run to the pubic tubercle, where a con nection is made to


the contralateral adductor longus, graci lis, pes anserinus and the
tibial periosti um.
In the following chapters' discussions of local dysfu nctional patterns
i nvolving the cervical, thoracic, shoulder and a rm regions, it will be
useful to hold in mind the direct muscular and fascia l connections
that Myers highlig hts, so that the possibil ity of d istant infl uences is
never forgotten.
Di ssection confirm ation of fasci a l conti n u ity (Fig. 1 . 1 1 )
Barker Et Briggs ( 1 999) have shown the lu mbodorsal fascia to extend
from the pelvis to the cervical area and base of the cranium, in a n
unbroken sweep: 'Both superficial a n d deep laminae o f the posterior
layer are more extensive superiorly than previously thoug ht:
There is fibrous continuity throughout the lumbar, thoracic and
cervical spine and with the tendons of the splenius muscles superiorly.
There is a lso growing i nterest in the possible effects that
contractile smooth muscle cells (SMC) may have in the many
fascial/connective tissue sites in which their presence has now been
identified, including cartilage, ligamen ts, spinal discs and the
lu mbodorsal fascia (Ah luwalia et a l 2001 , Hastreiter et a l 200 1 ,
Meiss 1 993, Murray Et Spector 1 999).
For example, Yahia et a l (1 993) have observed that: 'H istologic
studies indicate that the posterior layer of the (Iumbodorsal) fascia is
able to contract as if it were infiltrated with muscular tissue:
Schleip and col leagues (2006) report that: 'Morphological
considerations, as well as histological observations in our laboratory,
suggest that the perimysium is characterized by a high density of
myofibroblasts, a class of fibroblasts with smooth muscle-like
contractile kinetics:
Analysis of 39 tissue samples from the thoracolumbar fascia of 1 1
human donors (aged 1 9-76 years) by Schleip e t al (2004) demonstrated
the widespread presence of myofibroblasts in all samples, with an
average density of 79 cells/mm2 i n the longitudi na l sections.
Schleip et al (2006) suggest that: 'These fi ndings confirm that
fascial tissues can actively contract, and that their contractility
appears to be driven by myofibroblasts. The q uestion as to whether
or not these active fascial contractions could be strong enough to
exert any sig nifican t impact on musculoskeletal dynamics has
previously been addressed in this journal (Schleip et al 2005) the
fol lowing way: taking the g reatest measu red force of in vitro fascial
contractions and extra polating that to an average size of the A B
superficial layer of the thoracolumbar fascia in humans the resulting
Fig u re 1 . 1 1 AEtB: The cont i n u ity of vertical a n d spira l myofascia l
contraction force can amount to 3 8 N, which may be a force strong
enough to infl uence biomechanical behaviour, such as in a l i n es i m plies a mechanical con nection from head to toe.
contribution to paraspinal compartment syndrome or in the R eproduced with permission from Myers (2001 ).
prevention of spinal segmental instability:

expression, as well as their abilities to communicate and to changes that follow the application of manual techniques
handle nutrients efficiently. that offer pain relief and improve function is sorely needed.
Reversing or slowing these undesirable processes is
the potential of appropriate bodywork and movement
approaches. It is yet to be precisely established to what
SUMMARY OF FASCIAL AND CONNECTIVE
degree cellular function can be modified by soft tissue tech
TISSUE FUNCTION
niques, such as those used in neuromuscular therapy.
However, the normalizing of structural and functional fea
Fascia is involved in numerous complex biochemical
tures of connective tissue by means of addressing myofas
activities.
cial trigger points, chronic muscle shortening and fibrosis,
as well as perpetuating factors such as habits of use, has Connective tissue contains a subtle, bodywide signaling
clear implications. Well-designed research to assess cellular system with as yet unknown potentials.
14 CLI N I CA L A PPLICATI O N O F N EU R O M USCU LAR TECH N I Q U E S : T H E U P P E R B O DY
L

The fascial cleavage planes appear to be sites of unique Many of the neural structures in fascia are sensory in
sensit ivity and of great importance in manual (and nature.
acupuncture) therapeutic focus. Fascia supplies restraining mechanisms by the differenti
Connective tissue provides a supporting matrix for more ation of retention bands, fibrous pulley s and check liga
highly organized s tructures and attaches extensively to ments as well as assist ing in the harmonious production
and invests into muscles. and control of movement.
Individual muscle fibers are enveloped by endomysium, Where connective tissue is loose in texture it allows move
which is connec ted to the stronger perimy sium that sur ment between adjacent structures and, by the formation of
rounds the fasciculi. bursal sacs, i t reduces the effects of pressure and friction .
The perimysium's fibers attach to the even stronger Deep fascia ensheaths and preserves the characteristic
epimy sium that surrounds the muscle as a whole and contours of the limbs and promotes the circulation in the
attaches to fascial tissues nearby. veins and lymphatic vessels.
Because it contains mesenchymal cells of an embry onic The superficial fascia, which forms the panniculus adipo
type, connective tissue provides a generalized tissue sis, allows for the storage of fat and also provides a sur
capable of giving rise, under certain circumstances, to face covering that aids in the conservation of body heat.
more specialized elements. By virtue of its fibroblastic activity, connective tissue aids
It provides (by its fascial planes) pathway s for nerves, in the repair of injuries by the deposition of collagenous
blood and lymphatic vessels and structures. fibers (scar tissue).

Box 1 . 6 Tensegrity

Tensegrity, a term coined by architect/eng ineer Buckmi nster Fuller,


represents a system characterized by a discontinuous set of
compressional elements (struts) which are held together, u prighted
and/or moved by a continuous tensional network (Myers 1 999, 2001 ,
Oschman 1 997, 2000). Fu l ler, one of the most original thinkers of the
20th centu ry, developed a system of geometry based on tetrahedral
(four-sided) shapes found i n nature which maximize strength while
occupying minima l space (maxi mum stabil ity with a minimum of
materials) (Juhan 1 998). From these concepts he designed the
geodesic dome, including the US Pavilion at Expo '67 in Montreal.
Tensegrity structures actually become stronger when they are
stressed as the load a ppl ied is distributed not only to the area being
A
directly loaded but a lso throughout the structure (Barnes 1 990).
They employ both compressional and tensional elements. When
applying the principles of tensegrity to the human body, one ca n
readily see the bones and i ntervertebral discs as the disconti nuous
compressional u n its and the myofascial tissues (muscles, tendons,
l igament, fascia and to some degree the discs) as the tensiona l
elements. When load is applied (as in lifting) both the osseous and
myofascial tissues distribute the stress incu rred.
Ingber ( 1 999) concurs with this concept and then adds to it:

I n reality. our bodies are composed of 206 compression-resistant


bones that are pulled up against the force of gravity and stabilized
through interconnection with a continuous series of tensile muscles,
tendons, and ligaments . . . cells may sense mechanical stresses, includ
ing those due to gravity. through changes in the balance of forces that
are tronsmitted across transmembrane adhesion receptors that link
the cytoskeleton to the extracellular matrix ond to the other cells (e.g.
in tegrins, cadherins, selectins). The mechanism by which these Figure 1 . 1 2 ARB: Tenseg rity-based structures. Reproduced w ith
mechanical signals are transduced and converted into a biochemical perm ission from the Jaurnal of Bodywork a n d Movement
response appears to be based, in part, on the finding that living cells Therapies 1 99 7 ; 1 (5) :300-302.
use a tension-dependent form of architecture, known as tensegrity. to
organize and stabilize their cytoske/etons.

Oschman (2000) suggests that bones fit in both the strut and tensile the point of impact and to be absorbed throughout the structure.
categories, argu ing that: 'Bones contai n both compressive and 'The more flexible and balanced the network (the better the
tensile fibres, and are therefore tensegrity systems unto themselves: tensiona l integ rity), the more readily it absorbs shocks and converts
Tensegrity a l lows mecha nica l energy to be transmitted away from them to information rather than damage:

box con tinues


1 Connective tissue a n d the fascial system 15

Regarding Ingber's work, Oschman (2000) points out that the Osch man ( 1 997) concurs, adding another element:
living tensegrity network is not only a mechanical system, but a lso a Robbie (1977) reaches the remarkable conclusion that the soft tissues
vibratory continuum. When a part of a tensegrity structure is araund the spine, when under apprapriate tension, can actually lift
plucked, the vibration produced travels throughout the entire each vertebra off the one below it. He views the spine as a tensegrity
structure: mast. The various ligaments form 'slings ' that are capable of support
Restrictions in one part have both structural and energetic ing the weight of the body without applying compressive forces to the
consequences for the en tire organism. Structural integrity, vibratory vertebrae and intervertebral discs. In other words, the vertebral col
integrity, and energetic or information integrity go hand in hand. umn is not, as it is usually portrayed, a simple stack of blocks, each
One cannot influence the structural system without influencing cushioned b y an intervertebral disc.
the energetic/informational system, and vice versa. Ingber's work
These views are also suggested by Myers (200 1 ) in his enlightening
shows how these systems also interdigitate with biochemical
book, Anatomy Trains: Myofascial Meridians for Manual and
poth ways.
Movemen t Therapists (see a lso Box 1 .4).
Of tensegrity, Juhan (1 998) tells us: Later Oschman continues:
Besides this hydrostatic pressure (which is exerted by every fascial Cells and nuclei are tensegrity systems (Coffey 1 985, Ingber Et
compartment, not just the outer wrapping), the connective tissue Folkman 1989, Ingber Et Jamieson 1985). Elegant research has docu
framework - in conjunction with active muscles - provides another mented how the gravity system connects, via a family of molecules
kind of tensional force that is crucial to the upright structure of the known as in tegrins, to the cytoskeletons of cells throughout the body.
skeleton. We are not made up of stacks of building blocks resting Integrins 'glue' every cell in the body to neighbouring cells and to the
securely upon one another, but rather of poles and guy-wires, whose surrounding connective tissue matrix. An important study by Wang
stability relies not upon flat stacked surfaces, but upon praper angles et al (1 993) documents that integrin molecules carry tension from the
of the poles and balanced tensions on the wires. . . . There is not a extracellular ma trix, across the cell surface, to the cytoskeleton,
single horizontal surface anywhere in the skeleton that pravides a which behaves as a tensegrity matrix. Ingber (1 993a,b) has shown
stable base for anything to be stacked upon it. Our design was not how cell shape and function are regulated by an interacting tension
conceived by a stone-mason. Weight applied to any bone would and compression system within the cytoskeleton.
cause it to slide right off itsjoints if it were not for the tensional
Levin (1 997) informs us that once spherica l shapes involving
balances that hold it in place and contral its pivoting. Like
tensegrity structures occur (as in the cells of the body), a many-sided
the beams in a simple tensegrity structure, our bones act more
framework evolves which has 20 triangular faces. This is the
as spacers than as compressional members; more weigh t is
hierarchica lly constructed tensegrity icosahedron ( icosa is 20 in
actually borne by the connective system of cables than by the bony
Greek) which a re stacked together to form an infinite n u mber of
beams.
tissues.
Levin ( 1 997) further explains a rchitectural aspects of tensegrity
as it relates to the human body. He discusses the work of Wh ite Et
Panjabi ( 1 978) who have shown that any part of the body wh ich is
free to move in any direction has 1 2 degrees of freedom: the abil ity
to rotate around three axes, in each direction (six degrees of
freedom) as well as the ability to translate on three planes in either
direction (a further six degrees of freedom). He then asks, how is this
stabil ized?
To fix in space a body thot has 12 degrees of freedom it seems logical
that there need to be 12 restraints. Fuller (1975) proves this ... This

Fig u re 1 . 1 4 Cycle wheel structure a l l ows com pressive load to be


Fig u re 1 . 1 3 Tensegrity-based structures. distributed to rim t h rough tension network.

box con tinues


16 CLI N ICAL A P P L I CATI O N O F N E U RO M USCU LA R TECH N I Q U E S : T H E U P P E R B O DY
L

Box 1 . 6 (tott t{ntled)

Fig u re 1 . 1 5 A : Dehydration of g round


su bstance may ca use kinking of collagen
fibers. B: Sustained pressure may result
i n tempora ry solation of g round
substance, a l lowing kinked collagen
fibers to lengthen, thereby redu cing
m uscular stra i n. Reproduced with
permission from the Journal of Bodywork
and Movemen t Therapies 1 997; 1 (5) :309.

A B

principle is demonstrated in a wire-spoked bicycle wheel. A minimum distributes evenly around the rim and the bicycle frame and its load
of 12 tension spokes rigidly fixes the hub in space (anything more hangs from the hubs l i ke a ham mock between trees'.
than 12 is a fail safe mechanism). Other examples of tensegrity in common use include a tent and a
crane. In the body this architectural principle is seen in many tissues,
Levin points out that the tension-loaded spokes transmit
most specifica lly in the way the sacrum is suspended between
compressive loads from the fra me to the ground while the hub
the il ia.
remains suspended in its tensegrity network of spokes: 'the load

The ensheathing lay er of deep fascia, as well as inter ubiquitous, tenacious, living tissue that is deeply
muscular septa and interosseous membranes, provides involved in almost all of the fundamental processes of
vast surface areas used for muscular attachment. the body 's structure, function and metabolism.
The meshes of loose connective tissue contain the 'tissue In therapeutic terms, there can be little logic in try ing to
fluid' and provide an essential medium through which consider muscle as a separate structure from fascia since
the cellular elements of other tissues are brought into they are so intimately related.
functional relation with blood and ly mph. Remove connective tissue from the scene and any muscle
This occurs partly by diffusion and partly by means of left would be a jelly -like structure without form or func
hy drokinetic transportation encouraged by alterations in tional ability.
pressure gradients - for example, between the thorax and
the abdominal cavity during inhalation and exhalation.
Connective tissue has a nutritive function and houses
FASCIAL DYS FUNCTION
nearly a quarter of all body fluids.
Fascia is a major arena of inflammatory processes (Cathie
Mark Barnes (1997) states:
1 974) (see Chapter 7).
Fluids and infectious processes often travel along fascial
Fascial restrictions can create abnormal strain patterns that
planes (Cathie 1 974).
can crowd, or pull the osseous structures out of proper
Chemical (nutritional) factors influence fascial behavior
alignment, resulting in compression of joints, producing
directly. Pauling (1976) showed that 'Many of the results
pain and/or dysfunction. Neural and vascular structures
of deprivation of ascorbic acid [vitamin C] involve a defi
can also become entrapped in these restrictions, causing
ciency in connective tissue which is largely responsible
neurological or ischemic conditions. Shortening of the
for the strength of bones, teeth, and skin of the body and
myofascial fascicle can limit its functional length - reducing
which consists of the fibrous protein collagen'.
its strength, contractile potential and deceleration capacity.
The histiocytes of connective tissue comprise part of an
Facilitating positive change in this system [by therapeutic
important defense mechanism against bacterial invasion
intervention] would be a clinically relevant event.
by their phagocytic activity.
They also play a part as scavengers in removing cell
Cantu & Grodin (1992) have stated that 'The response of
debris and foreign material.
normal connective tissue [fascia] to immobilization pro
Connective tissue represents an important 'neutralizer'
vides a basis for understanding traumatized conditions'.
or detoxicator to both endogenous toxins (those produced
A sequence of dy sfunction has been demonstrated as
under phy siological conditions) and exogenous toxins.
follows (Akeson & Amiel 1977, Amiel & Akeson 1983,
The mechanical barrier presented by fascia has important
Evans 1960).
defensive functions in cases of infection and toxemia.
Fascia, then, is not just a background structure with little The longer the immobilization, the greater the amount of
function apart from its obvious supporting role, but is an infiltrate there will be.
1 Connective tissue and the fascial system 17

If immobilization continues beyond about 12 weeks, colla To achieve this, he says:


gen loss is noted; however, in the early days of any restric
Most important is the change in the ground substance from
tion, a significant degree of grolU1d substance loss occurs,
a gel to a sol. T his occurs with a state phase realignment of
particularly glycosarninoglycans and water. Loss of (47%
crystals exposed to electromagnetic fields. This may occur as
of) muscle strength due to immobilization has been shown
a piezoelectric event (changing a mechanical force to electric
to occur in as little as 3 weeks (Hortobagyi et al 2000).
energy) which changes the electrical charge of collagen and
Since one of the primary purposes of ground substance is
proteoglycans within the extracellular matrix.
the lubrication of the tissues it separates (collagen fibers),
its loss leads inevitably to the distance between these In offering this opinion Barnes is basing his comments on
fibers being reduced. the research evidence relating to connective tissue behavior
Loss of interfiber distance impedes the ability of collagen which takes the properties of fascia into an area of study
to glide smoothly, encouraging adhesion development. involving liquid crystal and piezoelectric events
This allows crosslinkage between collagen fibers and (Athenstaedt 1 974, Pischinger 199 1). Appropriately applied
newly formed connective tissue, which reduces the manual therapy can, Barnes suggests, often achieve such
degree of fascial extensibility as adjacent fibers become changes, whether this involves stretching, direct pressure,
more and more closely bound. myofascial release or other approaches. As noted earlier,
Because of immobility, these new fiber connections will much that changes can be seen to possibly involve the
not have a stress load to guide them into a directional for 'sponge-like' behavior of connective tissues as they extrude
mat and they will be laid down randomly. and absorb water. All these elements form part of neuro
Similar responses are observed in ligamentous as well as muscular therapy interventions.
periarticular connective tissues.
Mobilization of the restricted tissues can reverse the
effects of immobilization as long as this has not been for A DIFFERENT MODEL LINKING TRAUMA AND
an excessive period. CONNECTIVE TISSUE
If, due to injury, inflammatory processes occur as well as
immobilization, a more serious evolution occurs, as Discussion of trauma and connective tissue has focused
inflammatory exudate triggers the process of contrac thus far on the physical changes that evolve, and the adap
ture, resulting in shortening of connective tissue. tations and compensations that are often amenable to soft
This means that, following injury, two separate processes tissue therapeutic interventions.
may be occurring simultaneously: there may be a process Oschman (2006) offers a different perspective, which
of scar tissue development in the traumatized tissues and may be seen to build on the observations above on the work
also fibrosis in the surrolU1ding tissues (as a result of the of Langevin, since both conceive connective tissue as
presence of inflammatory exudate). (amongst other things) a communication network. Oschman
Cantu & Grodin ( 1992) give an example: 'A shoulder may summarizes this hypothesis as follows:
be frozen due to macroscopic scar adhesion in the folds The hypothesis is that the connective tissue matrix and its
of the inferior capsule . . . a frozen shoulder may also be extensions reaching into every cell and nucleus in the body
caused by capsulitis, where the entire capsule shrinks.' is a whole-person physical system that senses and a bsorbs
Capsulitis could therefore be the result of fibrosis involv the physical and emotional impact in any traumatic experi
ing the entire fabric of the capsule, rather than a localized ence. T he matrix is also the physical material that is influ
scar formation at the site of injury. enced by virtually all hands-on, energetic and movement
Noted author Rene Cailliet (2004) points out that the vis therapies. It is suggested that the living [connective tissue]
coelastic properties of collagen are influence by tempera matrix is the physical substrate where traumatic memories
ture, 'which, when added to the equation of force and speed are stored and resolved.
of stress, may cause irrecoverable damage'. Prolonged immo Oschman continues:
bilization results in a number of alterations in tissue, includ
ing failure of collagen fibers to physiologically elongate and The living matrix is a pervasive system, consisting of both
loss of collagen strength in as little as 4 weeks. the nerves and the connective tissues and cytoskeletons of
every neural and non-neural cell in the body. On the basis of
the known biophysical properties of this system, we can
RESTORING GEL TO SOL visualize this as a high-speed solid-state information proces
sor with capabilities that far exceed the brightest minds and
Mark Barnes ( 1997) insists that therapeutic methods that try fastest computers. Intuition can therefore be described as an
to deal with this sort of fascial, connective tissue change emergent property of a very sophisticated semiconducting
(summarized above in relation to trauma or immobilization) liquid crystalline molecular matrix that is capable of stor
would be to 'elongate and soften the connective tissue, cre ing, processing and communicating a vast amount of sub
ating permanent three-dimensional depth and width'. liminal information that never reaches the nervous system
18 C L I N I CA L A P P LI CAT I O N O F N EU R O M U S C U LA R TECH N I Q U E S : T H E U PPER B ODY

link Et Lawson have described patterns of postural patterning link Et Lawson observed that the 20% of people whose compen
determ ined by fascial compensation and decompensation. satory pattern d id not a lternate had poor health h istories.
Treatment of either CCP or uncompensated fascial patterns has
Fascial compensation is seen as a usefu l, beneficia l and, above all,
the objective of trying, as far as is possible, to create a sym metri
functional adaptation (i.e. no obvious symptoms) on the part of
cal degree of rotatory motion at the key crossover sites.
the musculoskeleta l system, for exa mple, in response to anom
The treatment methods used to ach ieve this ra nge from direct
a l ies such as a short leg, or to overuse.
muscle energy approaches to indirect positional release techniques.
Decompensation describes the same phenomenon but only in
relation to a situation in which adaptive changes are seen to be Assessment of tissue preference
dysfunctional, to produce symptoms, evidencing a failure of
homeostatic adaptation. Occipitoatl antal area (Fig. 1 . 1 6)
Patient is supine.
By testing the tissue 'preferences' in different areas it is possible to Practitioner sits at head, and cradles upper cervical region.
classify patterns i n clin ically useful ways: The neck is fu l ly flexed.

ideal (minimal ada ptive load transferred to other regions) The occiput is rotated on the atlas to eva luate tissue preference

compensa ted patterns which alternate in direction from area to as the head is slowly rotated left and then right.
area (e.g. atla ntoocci pital, cervicothoracic, thoracolumbar, lum Cervi cothoracic area (Fig. 1 . 1 7)
bosacral) and which a re commonly adaptive in nature Patient is seated in relaxed posture with practitioner behind, with
uncompensated patterns which do not a lternate and which are
hands placed to cover medial aspects of upper trapezius so that
commonly the result of trauma. fingers rest over the clavicles.
Functi o n a l eva l u ation of fasci a l postural patterns
link Et Lawson ( 1 979) have described methods for testing tissue
preference.
There a re fou r crossover sites where fascial tensions can be
noted : occipitoatiantal (OA), cervicothoracic (CT), thoracolu mbar
(TL) and lumbosacral (LS). A
These sites a re tested for their rotation and side-bending
preferences.
link Et Lawson's research showed that most people display alter
nating patterns of rotatory preference with about 800/0 of people
showing a common pattern of left-right-Ieft-right (termed the
common compensatory pattern or CCP) 'reading' from the occipi
toatlantal region downwards.

Fig u re 1 . 1 6 Alternative hand positions for assessment of u pper F i gu re 1 . 1 7 AEtB: Hand positions for assessment of u pper
cervical region tissue d i rection prefe rence. cervicothoracic reg ion tissue di rection preference.
box continues
1 Connective tissue and the fascial system 19

Box 1 . 7 (conin ued) .


'
. '

The hands assess the area being palpated for its 'tightness/loose NOTE: By holding tissues in their 'loose' or ease positions, by holding
ness' preferences as a slight degree of rotation left and then right tissues in their 'tight' or bind positions and introd ucing an isometric
is introduced at the level of the cervicothoracic junction. contraction or just by holding tissues at their barrier, waiting
for a release, changes ca n be encouraged. The latter a pproach would
Thoraco l u m b a r area be i nducing the myofascial release in response to lig ht, sustained
Patient is supine, practitioner stands at waist level facing cepha load.
lad and places hands over lower thoracic structures, fingers a long
lower rib shafts lateral ly. Questions following assessment exercise:
Treating the structure being pal pated as a cyl inder, the hands test
the preference the lower thorax has to rotate a round its central 1 . Was there an 'a lternating' pattern to the tissue preferences?
axis, one way and then the other. 2. Or was there a tendency for the tissue preference to be the same
i n all or most of the four a reas assessed?
Lumbosacral a rea 3 . If the latter was the case, was this in an i ndividual whose health
Patient is supine, practitioner stands below waist level facing is more compromised than average - in line with Zink & Lawson's
cepha lad and places ha nds on anterior pelvic structu res, using the suggestion?
contact as a 'steering wheel' to eval uate tissue preference as the 4. By means of any of the methods suggested in the 'Note' above,
pelvis is rotated around its central axis while seeking information are you able to produce a more balanced degree of tissue
as to its 'tightness/looseness' preferences. preference?

and consciousness directly. A computer, with its software superficial tissues (involving autonomic responses) as well as
programs and memory and information storage capacities deeper tissues (influencing the mechanical components of
pales to insignificance in comparison with the evolutionar the musculoskeletal system) and that also address the factor
ily ancient solid-state system that is expressed within every of mobility (movement) meet with the requirements of the
cell and sinew of the body. body when dysfunctional problems are being treated. NMT,
Since the primary channels of this informational system as presented in this text, adopts this comprehensive approach
are the acupuncture meridians, it is not surprising that and achieves at least some of its beneficial effects because of
there are energy psychology methods that involve tapping its influence on fascia.
on key paints on the meridian system. Such tapping will In the upcoming chapters we will see how influences
introduce electrical fields into the meridian system because from the nervous system, inflarrunatory processes and pat
of the piezoelectric or pressure-electricity effect (e.g. terns of use affect (and are affected by) the fascial network.
Lapinski 1977, MacGinitie 1995). Such currents, then, will In the second volume of this text, the principles of tenseg
be transduced into signals that will be propagated through rity, thixotropy and postural balance will be seen to form an
the meridian/living matrix system for a certain distance, intricate part of the foundations of whole-body structural
since the meridians are low resistance pathways to the flow integri ty. As will become clear in the next chapter, Ingber
of electricity (e.g. Reichmanis et aI 1975). (2003) now tends to use the term 'structural continuum' as
an advance on the tensegrity model, wherein the entire
body and all its myriad structures are seen to be interde
THERAPEUTIC SEQUENCING pendently enmeshed. The authors of this text believe that
an understanding of these different ways of appreciating
Cantu & Grodin (1992) conclude that therapeutic approaches the structures of the body is a foundation for the use of ther
which sequence their treahuent protocols to involve the apeutic bodywork methods.

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I
23
I
Chapter 2 I

Muscles

In this chapter our focus of a ttention is placed on the prime


CHAPTER CONTENTS movers and stabilizers of the body, the muscles. It is neces
sary to understand those aspects of muscle struc ture, func
Dynamic forces - the 'structural continuum' 23
tion and dysfunction that can help to make selection and
Signals 25
applica tion of therapeutic interventions as suitable and
Essential information about muscles 25
effective as possible. Unless otherwise noted, the general
Types of muscle 25
muscle discussions in this chapter refer to skeletal muscles.
Energy production in normal tissues 27
The skeleton provides the body with an appropria tely
Energy production in the deconditioned individual 28
semlflgld framework that has facility for movement a t its
Muscles and blood supply 28
junctions a d joints. However, it is the muscular system,
Motor control and respiratory alkalosis 31
given coheslOn by the fascia (see Chapter 1), that both sup
Two key definitions 32
ports and propels this framework, providing us with the
The Bohr effect 32
ability to express ourselves through movement, in activities
Core stability, transversus abdominis, the
ranging from c opping wood to brain surgery, climbing
diaphragm and BPD 32 .
mo untams to glvmg a massage. Almost everything, from
Summary 32 . .
faCIal expresslOn to the beating of the heart, is dependent on
Major types of voluntary contraction 33
muscular function.
Terminology 33
Synchronized and coordinated movement depends on
Muscle tone and contraction 33
structural integra tion, in which the form of the body parts,
Vulnerable areas 34
and how they interrelate spatially, from the smallest to the
Muscle types 34
largest, determines the efficiency of function. It is in this
Cooperative muscle activity 35
complex setting that muscle function (and dysfunction)
Muscle spasm, tension, atrophy 37
should be seen.
Contraction (tension with EMG elevation,
voluntary) 38
Spasm (tension with EMG elevation, involuntary) 38
DYNAMIC FORCES - THE 'STRUCTURAL
Contracture (tension of muscles without EMG elevation'
CONTINUUM'
involuntary) 38
Increased stretch sensitivity 38
It may be useful to qualify the description above, in which a
Viscoelastic influence 39
division is suggested between the semirigid skeleton and
Atrophy and chronic back pain 39
the attaching elastic soft tissues that propel and move it. In
What is weakness? 39
fact, the integrated systems of the body are better described
Trick patterns 39
as representing a series of interrelated tensegrity structures .
Joint implications 40
It as Fuller (1975) who used the term tensegrity to
When should pain and dysfunction be left alone? 40
desc lbe structures whose stability, or tensionaL integrity,
Beneficially overactive muscles 41
reqUired a dynamic balance betvveen discontinuous com
Somatization - mind and muscles 41
pression elements (such as bones) connected (and moved)
But how is one to know? 41
by continuous tension cables (such as the soft tissues of the
body, e.g. ligaments, tendons, muscle and fascia). There
24 C L I N ICAL A P P LICAT I O N OF N E U RO M U SCULAR T E C H N I QU E S : TH E U P P E R B O DY

-- Upper trapezius

-- Spine of scapula

----Infraspinatus
Site of vertebral
malrotation---L-- '----- Teres minor

---- Thoracolumbar junction

----- Piriformis
Iliopsoas-----t---'

TFUITB------1
t------ Biceps femoris

Gastrocnemius and
soleus-------t

Figure 2.2 Typical sites of increased muscle/ tendon tension and


tenderness resulting from malalignment. The drawing also indicates
the typical lateralization; if the structure is involved bilaterally, the
one indicated here is usually affected more severely. TFL/ ITB, tensor
fascia lata/ iliotibial band. Redrawn with permission from
Schamberger (2002).

misuse (poor posture, for example) leads to structural mod


ifications, and that once such structural rearrangements
Figure 2.1 The miraculous possibilities of human balance. have occurred, normal (or at least optimal) function may
Reproduced with permission from Gray's Anatomy (1 995). become impossible.
The interlocking elements of structure, function and dys
was, in this construct, the implied balance created between function are the territory of the manual therapist, as we
tension and compression, involving all tissues, from an intra evaluate in our patients these processes of 'coordinated
and extracellular level, to the gross skeletal and muscular structural rearrangement' that are capable of affecting all
structures of the physical body (Ingber 1993, 2003). tissues, including neural, fascial and muscular. The end
Ingber (2003) has, in fact, moved beyond the tensegrity results of such 'rearrangement' will be noted when a muscle
model in his descriptions, having more recently discussed is found to be shortened, fibrotic or to contain trigger points.
what he terms a 'structural continuum', in which every These symptom-producing changes (reduced range of
thing from the macro (skeleton, muscles, organs, etc.) to the motion, tense, tight and /or indurated muscles that may
micro (intra- and extracellular structures) are interdepend be housing trigger points) are the manifestation of rearrange
ently enmeshed. Ingber summarizes this when he states: ment of the structural continuum. An example of a
'Mechanical deformation of whole tissues [the outcome of 'rearranged' structure is given by Schamberger (2002) who
the interaction between tensional, shear and compression describes an example of what he terms a 'malalignment
forces] results in coordinated structural re-arrangements on syndrome' (Fig. 2.2). In this example rotational and other
many different size scales.' malalignments are seen to cause increased muscular ten
He uses the word mechanotransduction to summarize the sions and corresponding adaptations.
effects of shear and other forces on cells, which change Fortunately, 'coordinated structural rearrangement' in a
their shape and function, including gene expression. These positive direction is also possible, when appropriate thera
processes occur in tissues that have been, or are being, peutic measures are initiated to help restore the 'structural
over- or underused, or abused. This implies that functional continuum', offering the chance for function to improve, or
2 Muscles 25

it will be possible to commence explora tion of the many


dysfunctiomll patterns that can interfere with the quality of
life and create painful
leading to degenerative changes.
Because the ana tomy and physiology of muscles are ade
quately covered elsewhere, the information in this chapter
will be presented largely in summary form. Some specific
topics (muscle type, for example) receive a fuller discussion
due to the significance they have in regard to neuromuscu
lar therapy.

ESSENTIAL IN FORMATION ABOUT MUSCLES


Triad --HI- (Fritz 1998, Jacob a Falls 1997, Lederman 1997,
Liebenson 1996, Macintosh et al 2006, Schafer 1987)
Z disc ----"'I

Skeletal muscles are derived embryologically from mes


enchyme and possess a particular ability to contract
when neurologically stimulated.
Skeletal muscle fibers comprise a single cell with hun
dreds of nuclei.
The fibers are arranged into bundles (fasciculi) contain
ing approxima tely 100 fibers, with connective tissue fill
ing the spaces between the fibers (the endomysium) as
well as surrounding the fasciculi (the perimysium).
Entire muscles are surrounded by denser connective tis
sue (fascia, see Chapter 1 ) where it is known as the
epimysium.
Figure 2.3 Details of the intricate organization of skeletal muscle. The epimysium is continuous with the connective tissue
Reproduced with permission from Gray's Anatomy (2005). of surrounding structures.
Individual muscle fibers, which are bundles of 1000-2000
myofibrils, can vary in length from a few millimeters to
about 12 cm. When a muscle appears to be longer than
this, it has fibers a rranged in series, separated into com
normalize. It is within this context that you should consider partments by inscriptions. The sartorius, for instance, has
our survey of fascia (Chapter 1) and muscles (this chapter) three such inscriptions (four compartments), with each
and the dysfunctions that are described and the treatments compartment having its own nerve supply (Macintosh
proposed throughout the book. et aI2006).
IndividuC{1 muscle fibers can vary in diameter from 10 to
60m, with most adult fibers being a round 50m.
Individual myofibrils are composed of a series of sarcom
SIGNALS
eres, the basic contractile units of a skeletal muscle, con
nected end to end. Actin and myosin filaments overlap
Healthy, well-coordinated muscles receive and respond to a
within the sarcomere and slide in rela tion to one another
multitude of signals from the nervous system, providing
to produce shortening of the muscle (see Box 2.1).
the opportunity for coherent movement. When, through
overuse, misuse, abuse, disuse, disease or trauma, the
smooth interaction between the nervous, circulatory and
TYPES OF MUSCLE
the musculoskeletal systems is disturbed, movement
becomes difficult, restricted, commonly painful and, some
Muscle fibers can be broadly grouped into those that are:
times, impossible. Dysfunctional patterns affecting the
musculoskeletal system (see Chapter 5) which emerge from longitudinal (or strap or parallel or fusiform), which have
such a background lead to compensatory adaptations and a lengthy fascicles, largely oriented with the longitudinal
need for therapeutic, rehabilitation and / or educational axis of the body or its parts. These fascicles favor speedy
interven tions. This chapter will highlight some of the action and are usually involved in range of movement
unique qualities of the muscular system. On this founda tion (sartorius, for example, or biceps brachii)
26 CL I N I CAL A P P L I CAT I O N OF N E U R O M U SC ULAR TECH N I Q U E S : T H E U P P E R B O DY

Striated (skeletal) muscles are com posed of fasciculi, the nu mber of filaments). it partially hydrolyzes them to produce an energized (pre
which is dependent upon the size of the muscle. Each fascicle is made cocked) myosin head. This preloaded thick filament has a high
up of bundles of (approximately) 1 00 fibers with each fiber containing affinity for the thinner actin component. When a muscle is at rest,
up to around 2000 myofibrils (Macintosh et al 2006, Simons et a l binding of the two filaments m ust be blocked or else continual
1 999). Each myofibri l is composed of a series of sarcomeres laid end to contraction will resu lt, such as seen in rigor mortis. The tropomyosin
end; these conta in two primary types of protein filament, actin a nd filament overlies the myosin binding sites on the actin molecule,
myosin, as well as a stabi lizing filament (titin) a nd other proteins, such thereby preventing coupling of the two fi la ments.
as troponin, tropomyosin and nebulin. In most a natomy books the As an action potential spreads across the muscle fiber, signaling
reader can easily find illustrations and d iscussions regarding the contraction, it travels down the transverse tubu les, which lie close to
distinct bands and shadings, such as the Z-line, H-zone and M-region, the term inal cisternae (lateral sacs), the storage site for Ca2+. As the
which are created by the myofibri l components. action potential progresses, it causes a depolarization of the
The sliding fi lament theory, first proposed by biophysicist Jea n membrane, an opening of the calcium cha n nels and the release of
Hanson and physiologist H ugh Esmor H uxley in 1 954, offers a n Ca2+ from the sarcoplasmic reticu lum.
explanation of how m uscles shorten during contraction. Although The release of Ca2+ cata lyzes tropon in to cha nge its sha pe,
scientists have fa iled to fu l ly explain the biomechanics of movement, thereby moving tropomyosin aside. This process exposes the binding
the sl iding fila ment theory remains today as the foundational sites on the actin molecule and allows myosin to attach itself to the
platform. The fol lowing i l l u strates the basis of this theory. actin fi la ments. This occurs to many filaments sim u l taneously, not
Figure 2.4 i l l u strates the relationsh ip of acti n, myosin and other just the one described here. The myosin heads (and possibly shafts)
components of the m u scle cell during contraction. As ATP binds to flex, causing nu merous myosin and actin fi la ments to slide past each
the myosin heads (which form the crossbridges between the two other, resulting in muscle contraction.

Tropinin Actin Tropomyosin Z band


At rest, ATP binds to myosin head

Thin filament ---iM88Jii;is1liiiijePSi;,iIi1 I groups and is partially hydrolyzed to


I produce a high-affinity binding site
I

II for actin on the myosin head group.

-r=I!=I=I" i;!i
However, the head group cannot
bind because of the blocking of the
Thick (myosin) filament I actin binding sites by tropomyosin.
, Note: Reactions shown occurring in
only one crossbridge, but same
process takes place at all or most
A new molecule of ATP binds to crossbridges.
the myosin head, causing it to I
release from the actin molecule.
Partial hydrolysis of this ATP
(ATP- Pi) will 'recock' the
myosin head and produce a
high-affinity binding site for actin.
: If Ca2+levels are still elevated,
a8;i;lgat r Ca2+ released from sarcoplasmic
, reticulum in response to action

,, reform,
the crossbridge will quickly , potential binds to troponin, causing
causing further sliding of I tropomyosin to move and expose
I the actin and myosin filaments I
I
the myosin binding site on the actin
past each other. If Ca2+ is no molecule, The crossbridge is

I longer elevated, the muscle ormed.


relaxes.

ATP

f -

I
ADP-Pi ADP and Pi are released, the myosin I
head nexes, and the myosin and ,
I actin filaments slide past each other. I
I _ _ _ I

Figure 2.4 The contraction of the myofilaments resu lts from the interaction of actin and myosin. Redrawn after Hansen Et Koeppen (2002).

box continues
2 M uscles 27

Box 2.1 (continued)

Once this occurs, the myosin loses its energy a nd remains bonded
to the actin until it is re-energized with AlP. In other words, the AlP
unlocks the myosin head and preloads it for the next cycle. However,
the absence of adequate AlP and the presence of Ca2+ ca n cause the
fi laments to remain in a shortened position for a n indefinite period
of time.
After the contraction is completed, if adequate AlP is avai lable,
the myosin can be detached, the Ca2+ can be actively transported
back into the term inal cisternae of the sarcoplasmic reticulum,
thereby allowing the tropomyosin to slide back into place and cover
the actin-reactive sites. Muscle fiber relaxation occurs.
For best results (maximal force output and fu nctional shorten i ng)
the fi la ments should beg in at normal resting length, neither
overapproximated nor overstretched. This will a l low the maximal
number of myosin heads to be used. Adequate AlP is needed for
myosin energy and Ca2+ must be avai lable as a catalyst to tropon in.
A functional calcium pump will a llow for removal of the molecule.
AlP is also needed for this step since the calcium requires active
transportation, which requires energy.
When ischemia reduces the availability of elements used by the
local mitochondria to produce AlP, a local energy crisis develops.
When this is taken into account with the above description, one can
readily understand how persistent muscle fiber shortening
(contractu res) might form. Due to the unavai labil ity of AlP to d rive
the ca lcium pump, the conti nual presence of Ca2+ in the immed iate
vicinity of the filaments wou ld add to the conti nuity of muscle
shortening. It is also easily apparent that these would be chemically
induced by local factors rather than neurona lly d riven.
In Chapter 6 we will explore what occurs when some of these
steps are altered from their n ormal process (by trauma, overuse,
strain, etc.) and how these filaments produce some of the most
vicious, un relenting, pain-producing elements - myofascial trigger
points.

Thin filaments

Figure 2.5 From whole muscle to the sarcomere's actin and myosin
elements. Reproduced with pe rm i ss ion from Gray's Anatomy (2005).

pennate, which have fascicles running at an angle to the energy from chemically bound energy (in the form of
muscle's central tendon (its longitudinal axis). These fasci adenosine triphosphate ATP).-

cles favor strong movement and are divided into unipennate This process of energy production depends on an ade
(flexor pollicis longus), bipennate, which has a feather-like quate supply of oxygen, something that will be normal in
appearance (rectus femoris, peroneus longus) and multi aerobically fit tissues, but not in the tissues of the decon
pennate (deltoid) forms, depending on the configuration of ditioned individual (see below).
their fibers in relation to their tendinous attadunents Some of the energy so produced is stored in contractile
circular, as in the sphincters tissues for subsequent use when activity occurs. The force
triangular or convergent, where a broad origin ends with a that skeletal muscles generate is used to produce or pre
narrow attachment, as in pectoralis major vent movement, to induce motion or to ensure stability.
spiral or twisted, as in latissimus dorsi or levator scapulae. Muscular contractions can be described in rela tion to
what has been termed a strength continuum, varying from
a small degree of force, capable of lengthy maintenance,
ENERGY PRO DUCTION IN NORMAL TISSUES to a full-strength contraction, which can be sustained for
very short periods.
Muscles are the body's force generators. In order to When a contraction involves more than 70% of available
achieve this function, they require a source of power, strength, blood flow is reduced and oxygen availability
which they derive from their ability to produce mechanical diminishes.
28 CLINICAL APPLICATION OF NEUROMUSCULAR TECHNIQUES: THE UPPER BODY

Strap Strap with tendinous Tricipital Triangular


intersections

Quadrilateral

Bipennate Radial Multipennate

Figure 2.6 Types of muscle fiber arrangement. Reproduced with permission from Gray's Anatomy (2005).

ENERGY PRO DUCTION IN THE MUSCLES AND BLOOD SUPPLY


DECONDITIONE D INDIVI DUAL
Gray's Anatomy (2005, p. 118) explains the intricacy of blood
When anaerobic energy (ATP) pathways are activated in supply to skeletal muscle as follows:
the tissues of deconditioned individuals, the result is In most muscles the major source artery enters on the deep
accumulation of incompletely oxidized metabolic prod surface, frequently in close association with the principal
ucts, such as lactic acid and pyruvic acid (Fried 1987, vein and nerve, which together form a neurovascular hilum.
Nixon & Andrews 1996). The vessels course and branch within the connective tissue
The effects of this are described by Nixon & Andrews framework of the muscle. The smaller arteries and arterioles
(1996) as leading to: 'Muscular aching at low levels of ramify in the perimysial septa and give off capillaries which
effort; restlessness and heightened sympathetic activity; run in the endomysium. Although the smaller vessels lie
increased neuronal sensitivity; constriction of smooth mainly parallel to the muscle fibres, the1j also branch and
muscle tubes [e.g. vascular, respiratory and gastrointesti anastomose around the fibres, forming an elongated mesh.
nal], accompanying the basic symptom of inability to
make and sustain normal levels of effort.' Gray's also tells us that the capillary bed of predominantly
Aerobic activity, if at all possible, is the solution to such red muscle (type I postural, see below) is far denser than
problems. that of white (type II phasic) muscle.
As outlined later in this chapter, another feature that can Research has shown tha t there are two distinct circula
result in anaerobic glycolysis is a disturbed breathing tions in skeletal muscle (Grant & Payling Wright 1968).
pattern, where excessive levels of CO2 are exhaled (as in Nutritive circulation derives from arteriolar branches of
h yperven tila hon). arteries entering by way of the neurovascular hilus. These
2 M uscles 29

penetrate to the endomysium where all the blood passes site) will diffuse elsewhere until pressure is released, at
through to the capillary bed before collection into venules which time a 'flushing' of the previously ischemic tissues
and veins to leave again through the hilus. Alternatively, will occur. A blanching/ flushing combination repeated sev
some of the blood passes into the arterioles of the epi- and eral times can act as a local 'irrigation pump' to significantly
perimysium in which few capillaries are present. Arteriove increase blood flow to localized ischemia.
nous anastomosis [a coupling of blood vessels] are abundant As explained below, when a situation of increased alka
here, and most of the blood returns to the veins without linity (respiratory a lkalosis) leads to the smooth muscles
passing through the capillaries; this circuit therefore consti around blood vessels constricting, blood supply w ill be
tutes a non-nutritive [collateral} pathway through which diminished. In addition, oxygen release to the tissues will
blood may pass when the flow in the endomysia I capillary also be reduced in such a setting due to the Bohr effect
bed is impeded, e.g. during contraction. (Pryor & Prasad 2002).
Some a reas of the body have relatively inefficient anasto
In this way blood would keep moving but would not be moses and are termed hypovascular. These are particularly
nourishing the tissues it was destined for, if access to the prone to injury and dysfunction. Examples include the
capillary bed was blocked for any reason. This includes supraspinatus tendon, which corresponds with 'the most
when ischemia is present in the tissues due to overuse, pro common site of rotator cuff tendinitis, calcification and
longed shortening due to postural positioning, and tight spontaneous rupture' (Cailliet 1991, Tulos & Bennett 1984).
clothing, such as an elastic waistband in pants applying Other hypovascular sites include the insertion of the infra
pressure to the lower back tissues. spinatus tendon and the intrascapular aspect of the biceps
This is also particularly relevant to deep pressure tech tendon (Brewer 1979).
niques, designed to create 'ischemic compression' - for The lymphatic drainage of muscles occurs via lymphatic
example, when treating myofascial trigger points. When capillaries that lie in the epi- and perimysial sheaths. They
ischemic compression is applied, the blood destined for the converge into larger lymphatic vessels that travel close to
tissues being obstructed by this pressure ( the trigger point the veins as they leave the muscle.

Box 2.2 The lymphatic system

Coming in contact with lymph is to connect with the liquid 1813-1878) in which the cells are immersed, receive their nutritive
dimension of the organ ism. (Ch ikly 1 996) substances and reject damaging by-products. Lymph is a fluid which
The lymphatic system serves as a collecting and filtering system originates in the connective tissue spaces of the body. Once it has
for the body's interstitial fluids, while removing the body's cellular entered the first lymph capillaries ... this fluid is called lymph.
debris. It is able to process the waste materials from cel l u lar
Col lection beg ins in the interstitial spaces as a portion of the
metabolism and provide a strong line of defense agai nst foreign
circu lating blood is picked up by the lymphatic system. This fl uid is
invaders while reca pturing the protein elements and water content
comprised primarily of large waste particles, debris and other material
for recycling by the body. Through 'immunolog ica l memory',
from which protein might need to be recovered or that may need to
lymphocyte cells, which reside in the lymph and blood a n d are part
be disposed. Foreign particulate matter and pathogenic bacteria are
of the general immune system , recognize invaders (antigens) a nd
screened out by the lymph nodes, which a re interposed a long the
rapidly act to neutra l ize these. This system of defending during
course of the vessels. Nodes a lso produce lymphocytes, which makes
invasion and then clea ning up the battleground makes the lymphatic
their location at various points a long the transportation pathway
system essential to the health of the organism.
convenient should infectious material be encountered.
Organization of the lymph system Lym ph nodes (Chikly 200 1 ):
The lymphatic system comprises an extensive network of lymphatic
filter and purify
capilla ries, a series of collecting vessels and lymph nodes. It is
capture and destroy toxins
associated with the lymphoid system (lymph nodes, spleen, thymus,
reabsorb a bout 40 0/0 of the lymphatic liq uids, so concentrating
tonsi ls, appendix, mucosal-associated lym phoid tissue such as
the lymph while recycling the removed water
Peyer's patches and bone ma rrow), which is pri marily responsible for
produce mature lymphocytes - white blood cells that destroy
the immune response (Braem 1 994, Chikly 1 996, 2001 ). The
bacteria, virus-infected cel ls, foreign matter and waste
lym phatic system is:
materia ls.
an essential defensive component of the immune system
a carrier of (especially heavy and large) debris on behalf of the Production of lymphocytes increases (in nodes) when lym phatic flow
circulatory system is increased (e.g. with lymphatic d ra i nage techniques).
a transporter of fat-soluble nutrients (and fat itself) from the A lymphatic ca pillary network made of vessels slightly larger than
digestive tract to the bloodstream . blood ca pil laries d rains tissue fl uid from nearly a l l tissues and organs
that have a blood vascularization. The blood circu latory system is a
Chikly (2001) notes: closed system, whereas the lymphatic system is an open-end system,
The lymphatic system is therefore a second pathway back to the beginning blind in the interstitial spaces. The moment the fluid
heart, parollel to the blood system. The interstitial fluid is a very enters a lymph capillary, a fla p valve prevents it from returning into
important fluid. It is the real 'interior milieu' (Claude Bernard, the interstitia l spaces. The fluids, now cal led 'lymph', continue

box continues
30 CL I N I CA L A P PL I CATI O N OF N E U RO M U S C U LAR T EC H NIQU ES: T H E U P P E R B ODY

Box 2.2 (continued)

coursing th rough these 'precollector' vessels which empty into lymph the head and neck and right side of the thorax and empties in a
col lectors. similar manner to that of the l eft side.
The collectors have valves every 6-20 mm that occur directly Stimulation of Iymphangions (and therefore lymph movement)
between two to th ree layers of spira l muscles, the unit being occurs as a result of automotoricity of the Iymphangions (electrical
ca lled a Iymphangian (Fig. 2.7). The alternation of valves and potentials from the autonomic nervous system) (Kurz 1 986). As the
muscles gives a characteristic 'monil iform' shape to these vessels, spiral muscles of the vessels contract, they force the lymph through
like pearls on a string. The Iymphangions contract in a peristaltic the flap valve, which prevents its return. Additionally, stretching of the
man ner that assists in pressing the fluids through the va lved system. muscle fibers of the next Iymphangion (by increased fluid volume of
When stimulated, the muscles can substantially increase (up to the segment) leads to reflex muscle contraction (internally stimulated),
20-30 ti mes) the capacity of the whole lymphatic system (Chikly thereby producing peristaltic waves along the lymphatic vessel. There
2001). are a lso external stretch receptors that may be activated by manual
The la rgest of the lymphatic vessels is the thoracic duct, wh ich methods of lymph drainage which create a similar peristalsis.
begins at the cisterna chyli, a large sac-like structure withi n the Lymph movement is also augmented by respiration as the altering
abdominal cavity located at approximately the level of the 2nd intrathoracic pressure produces a suction on the thoracic duct and
lumbar vertebra. The thoracic duct, containing lymph fluids from cisterna chyli and thereby increases lymph movement in the duct
both of the lower extremities and a l l abdominal viscera except part and presses it toward the venous arch (Kurz 1 986, 1 987). Skeletal
of the liver, runs posterior to the stomach a n d intestines. Lymph muscle contractions, movement of l imbs, peristalsis of smooth
fluids from the left upper extremity, left thorax and the left side of muscles, the speed of blood movement in the veins into which the
cranium and neck may join it just before it empties into the left ducts empty and the pulsing of nearby arteries a l l contribute to
subclavian vein or may empty nearby into the internal jugular vein, lymph movement (Wittl inger & Wittl inger 1 982). Exposure to cold,
brachiocepha l ic junction or directly into the subclavian vein. The tight cloth ing, lack of exercise and excess protein consumption can
right lymphatic duct d rains the right upper extrem ity, right side of hinder lymphatic flow (Kurz 1 986, Wittlinger & Wittlinger 1 982).

White pulp

Spleen

Afferent
lymphatic
vessels

via Lymphatic

efferent drainage
lymphatic
vessels

marrow

tissue:
including:
connective tissue,
epithelia, non-encapsulated
lymphoid tissue of gut, elc.

Figure 2.7 Lymph pathway (a Iymphangion is shown in insert).

box continues
2 M uscles 31

Box 2.2 (continued)

Contraction of neighboring muscles compresses lymph vessels, mov significantly increases lymph movement by crosswise and lengthwise
ing lymph in the directions determined by their valves; extremely little stretching of the anchoring filaments that open the lymph
lymph flows in an immobilized limb, whereas flow is increased by capillaries, thus allowing the i n terstitial fluid to enter the lymphatic
either active or passive movements. This fact has been used clinically system. However, shearing forces (like those created by deep
to diminish dissemination of toxins from infected tissues by immobi pressure gliding techniques) can lead to temporary i n hibition of
lization of the relevant regions. Conversely, massage aids the flow of lymph flow by inducing spasms of lymphatic muscles (Kurz 1 986).
lymph from oedematous regions. (Gray's Anatomy 1995) Unless the vessels are d amaged, lymphatic movement can then be
reactivated by use of manual tech niques that sti mulate the
By recovering up to 20% of the interstitial fluids, the lymphatic
Iymphangions.
system rel ieves the venous system (and therefore the heart) of the
While each case has to be considered individual ly, numerous
responsibility of transporting the large molecules of protein and
conditions, ranging from postoperative edema to premenstrual fluid
debris back to the general circulation. Additional ly, the lymphocytes
retention, may benefit from lymphatic d rainage. There are, however,
remove particulate matter by means of phagocytosis, that is, the
conditions for which lymphatic d rainage would be contrai ndicated or
process of ingestion and digestion by cel ls of solid substances (other
precautions exercised. Some of the more serious of these conditions
cells, bacteria, bits of necrosed tissue, foreign particles). By the time
include:
the fluid has been returned to the veins, it is ultrafiltered, condensed
and hig hly concentrated. acute infections and acute inflammation (generalized and local)
thrombosis
In effect, if the lymphatic system did not regain the 2-20% of the
circulatory problems
protein-rich liquid that escaped in the interstitium (a large part of
cardiac conditions
which the venous system cannot recover), the body would probably
hemorrhage
develop major edemas and autointoxication and die within 24-48
malignant cancers
hours. (Chikly 2001, Guyton 1986)
thyroid problems
Conversely, when applying lymph d rainage techniques, care must be acute phlebitis.
taken to avoid excessive increases in the volume of lymph flow in
Conditions that might benefit from lymphatic d rainage but for which
people who have heart conditions as the venous system must
precautions are indicated include:
accom modate the load once the fluid has been delivered to the
subclavian veins. Significantly increasing the load could place certain edemas, depending upon their cause, such as cardiac
excessive strain on the heart. insufficiency
Lymphatic circulation is separated i n to two layers. The superficial carotid stenosis
circulation, which constitutes approxi mately 70% of all lymph flow bronchial asthma
(Chikly 2001 1. is located just under the dermoepidermic junction. The burns, scars, bruises, moles
deep muscular and visceral circulation, below the fascia, is activated abdom i nal surgery, radiation or undetermined bleeding or pain
by muscular contraction; however, the superficial circulation is not removed spleen
directly sti mulated by exercise. Additional ly, lymph capi l l aries major kidney problems or insufficiency
(Iacteals) in the jejunum and i l eum of the digestive tract absorb fat menstruation (drain prior to menses)
and fat-soluble nutrients that ultimately reach the liver through the gynecological infections, fibromas or cysts
blood ci rculation (Braem 1 994). some pregnancies (especially in the first 3 months)
Manual or mechanical lymphatic d rainage tech niques are chronic infections or inflammation
effective ways to increase lymph removal from stag nant or edemic low blood pressure.
tissue. The manual techn iques use extremely light pressure, which

MOTOR CONTROL AND RESPIRATORY below), which interferes with the first tvvo of those three ele
ALKALOSIS ments - the CNS as well as muscle function.
People who 'overbreathe', or who have marked upper
Motor control is a key component in injury prevention. Loss chest breathing patterns ('brea thing pattern disorders' or
of motor control involves failure to con trol joints, com BPD), automatically exhale more carbon dioxide (C02) than
monly because of incoordination of agonist-antagonist is appropriate for their current metabolic needs. Exhaled
muscle coactivation. According to Panjabi (1992), three sub CO2 derives from carbonic acid in the bloodstream, and an
systems work together to maintain joint and spinal stability: excessive reduction of this leads to a situation known as res
piratory alkalosis, where the pH of the blood becomes more
1. The central nervous subsystem (control)
alkaline than its normal of ::'::7 .4 (Lum 1987, Pryor & Prasad
2. The muscle subsystem (active)
2002).
3. The osteoligamentous subsystem (passive).
There are a number of major consequences of increased
Anything that interferes with any aspect of these features of alkalinity, one of which is a contrac tion of smooth muscle
normal motor control may contribute to dysfunction and cells (SMC) . This reduces the diameter of all struc tures sur
pain. This includes a condition in which the bloodstream rounded by smooth muscles, such as the blood vessels and
increases in alkalinity because of overbreathing (for exam intestinal structures. Reduced diameter of blood vessels
ple hyperventilation, the extreme of overbreathing, see limits blood supply to the tissues and the brain, thereby
32 C L I N I CA L A P P L I CATI O N OF N E U RO M USCULAR TEC H N I Q U ES: TH E U P P E R B ODY

resulting in a variety of symptoms (see below), one of which motor discharges, muscular tension and spasm, speeding of
is increased fatigability. It is postulated that SMC contrac spinal reflexes, heightened perception (pain, photophobia,
tion may also influence fascial tone (Schleip et aI 2004). (See hyperacusis) and other sensory disturbances. ' Muscles
Chapter 1 for information regarding smooth muscle cells affected in this way inevitably become prone to fatigue,
and their location and behavior in connective tissues.) altered function, cramp and trigger point evolution (George
et al 1964, Levitzky 1995, Macefield & Burke 199 1).
TWO KEY DEFINITIONS

Hypocapnia: Deficiency of CO2 in the blood, possibly CORE STABILITY, TRANSVERSUS ABDOMINIS,
resul ting from hyperventilation, leading to respiratory THE DIAPHRAGM AND BPD
alkalosis. It is well established that the tone of both the diaphragm
Hypoxia: Reduction of O2 supply to tissue, below physio and transversus abdominis hold the key to maintenance of
logical levels despite adequate perfusion of the tissue by core stability (Panjabi 1992) .
blood. McGill et al (1995) have observed a reduction in spinal
Lum (1987) reports that research indica tes that not less than support if there is both a load challenge to the low back,
10% of patients attending general internal medicine practice combined with a demand for increased breathing (imagine
in the US have such breathing pattern disorders as their pri shoveling snow!). 'Modulation of muscle activity needed to
mary diagnosis. Newton (2001) agrees with this assessment. facilitate breathing may compromise the margin of safety of
The authors of this text suggest that there exists a large tissues that depend on constant muscle activity for support.'
patient population with BPDs who do not meet the criteria Hodges & Gandevia (2000) reported that after approxi
for hyperventilation, but whose breathing patterns may mately 60 seconds of overbreathing, the postural (tonic) and
contribute markedly to their symptom picture, and whose phasic functions of both the diaphragm and transversus
mo tor control is likely to be negatively affected as a result abdominis are reduced or absent.
(Chaitow 2004).

Breathing pattern disorders are female dominated, rang SUMMARY


ing from a ratio of 2:1 to 7:1 (Lum 1994).
BPDs alter blood pH, thereby creating respiratory
Women are more at risk, possibly because progesterone
alkalosis.
is a respiratory accelerator (Damas-Mora et aI 1980).
This induces increased sympathetic arousal, which
Progesterone is known to cause hyperventilation and
affects neuronal function (including motor control).
hypercapnia in the luteal phase of a normal menstrual
There will be an increased sense of apprehension and
cycle (Brown 1998, Rajesh et a l 2000, Stahl et aI 1985).
anxiety. As a result, the person's balance may be compro
During post ovulation phase, CO2 levels drop ::+::25%
mised (Winters & Crago 2000).
(Lum 1994) .
Depletion of Ca and Mg ions enhances neural sensitiza
Additional stress then, 'increases ventilation when CO2
tion, encouraging spasm and reducing pain thresholds.
levels are already low' (Lum 1994).
As pH rises, smooth muscle cells constrict, leading to
vasoconstriction that reduces blood supply to the brain
THE BOHR EFFECT (Fried 1987, Pryor Et and tissues (particularly the muscles) and possibly alters
Prasad 2002) fascial tone.
Reduced oxygen release to cells, tissues and brain (Bohr
The Bohr effect states that a rise in alkalinity (due to a
effect) leads to ischemia, fatigue and pain, and the evolu
decrease in CO2) increases the affinity of hemoglobin (Hb)
tion of myofascial trigger points.
for oxygen (02). This means that when tissues, and the
If the individual is deconditioned, not involved in aero
bloodstream, increase in alkalinity the Hb molecule binds
bic activity, this sequence will trigger release of acid
more firmly to the oxygen it is carrying, releasing it less effi
wastes when tissues a ttempt to produce ATP in a rela
ciently, which leads to hypoxia. Increased OrHb affinity
tively anaerobic environment (as discussed earlier in this
also leads to changes in serum calcium and red cell phos
chapter).
phate levels which both reduce.
Biomechanical overuse stresses emerge along with com-
Additionally, there is a loss of intracellular Mg2+ as part
promised core stability and postural decay.
of the renal compensation mechanism for correcting alkalo
sis. The function of motor and sensory axons will be signif What this (overbreathing) scenario illustrates is that when
icantly affected by lower levels of calcium ions and these pain and dysfunction involving neuromuscular imbalance
sensi tive neural structures will tend toward hyperirritabil are evident in a patient, any therapeutic intervention that
ity, negatively affecting motor control (Seyal et a11998). fails to pay attention to breathing patterns is less likely to be
Lum (1994) explains: 'Loss of CO2 ions from neurons successful than if this receives appropriate clinical evalua
stimulates neuronal activity, causing increased sensory and tion and rehabilitation, if necessary (see Chapter 4).
2 M uscles 33

MAJOR TYPES OF VOLUNTARY CONTRACTION

Muscle contractions can be:

isometric (with no movement resulting)


isotonic concentric (where shortening of the muscle pro
duces approximation of its attachments and the struc
Epimysium
tures to which the muscle attaches) or
isotonic eccentric (in which the muscle lengthens during w-;_-- Perimysium
its contraction, therefore the attachments separate during
contraction of the muscle) .

TERMINOLOGY Basement

The terms origin and insertion are somewhat inaccurate,


Thin filament
with attachments being more appropriate. Attachments
can be further classified as proximal or distal (in the Thick filament Crossbridge
extremities) or by location, such as sternal, clavicular, Cross-sections show
costal or humeral attachments of pectoralis major. relationships of
In many instances, muscular attachments can adaptively myofilaments within
reverse their roles, depending on what action is involved myofibril at levels
indicated
and therefore which attachment is fixed. As an example,
psoas can flex the hip when its lumbar attachment is 'the
H
Q)
E
origin' (fixed point) or it can flex the spine when the A 0 -,
u

femoral attachment becomes 'the origin', i.e. the pOint ,,"""VI'VO' ro


(/)

toward which motion is taking place.

z ----- - - - /
Myofilaments
MUSCLE TONE AND CONTRACTION 11\.I/1\L'!V111 _

Muscles display excitability - the ability to respond to stimuli Figure 2.8 Organization of skeletal muscle. Redrawn after Hansen
& Koeppen (2002).
and, by means of a stimulus, to be able to actively contract,
extend (lengthen) or to elastically recoil from a distended posi
tion, as well as to be able to passively relax when stimulus
A motor nerve fiber will always activate more than one
ceases.
muscle fiber and the collection of fibers it innervates i s
Lederman (1997) suggests that muscle tone in a resting
called a motor unit. The greater the degree o f fine control a
muscle relates to biomechanical elements - a mix of fascial
muscle is required to produce, the fewer muscle fibers a
and connective tissue tension together with intramuscular
nerve fiber will innervate in that muscle. This can range
fluid pressure, with no neurological input (therefore, not
from 10 muscle fibers being innervated by a single motor
measurable by EMG). If a muscle has altered morphologi
neuron in the extrinsic eye muscles to one motor neuron
cally, due to chronic shortening, for example, or to compart
innervating several hundred fibers in major limb muscles
ment syndrome, then muscle tone, even at rest, will be
(Gray's Anatomy 2005, p. 121).
altered and palpable.
Because there is a diffuse spread of influence from a sin
He differentiates this from motor tone, which is measura
gle motor neuron throughout a muscle (i.e. neural influence
ble by means of EMG and which is present in a resting mus
does not necessarily correspond to fascicular divisions)
cle only under abnormal circumstances - for example,
only a few need to be active to influence the entire muscle.
when psychological stress or protective activity is involved .
The functional contractile unit of a muscle fiber is its sar
Motor tone is either phasic or tonic, depending upon the
comere, which contains filaments of actin and myosin. These
nature of the activity being demanded of the muscle - to
myofilaments (actin and myosin) interact in order to
move something (phasic) or to stabilize it (tonic). In normal
shorten the muscle fiber. Gray's Anatomy (2005) describes
muscles, both activities vanish when gravitational and
the process as follows:
activity demands are absent.
Contraction occurs in response to a motor nerve impulse At higher power, sarcomeres are seen to consist of two types
acting on muscle fibers. of filament, thick and thin, organized into regular arrays.
34 CLI N I CAL A P PL I CAT I O N OF N E U RO M U S C U LA R TEC H N I Q U E S : T H E U P P E R B O DY

The thick filaments, which are c. 15 nm in diameter, are There are also several phasiC (type II) fiber forms, notably:
composed mainly of myosin. The thin filaments, which are
type IIa (fast-twitch fibers) which contract more speedily
8 nm in diameter, are composed mainly of actin. The arrays
than type I and are moderately resistant to fatigue with
of thick and thin filaments form a partially overlapping
relatively high concentrations of mitochondria and myo
structure . . . The A-band consists of the thick filaments,
globulin
together with links of thin filaments that interdigitate with,
type IIb (fast-twitch glycolytic fibers) which are less
and thus overlap, the thick filaments at either end . . . The
fatigue resistant and depend more on glycolytic sources of
I-band consists of the adjacent portions of two neighbouring
energy, with low levels of mitochondria and myoglobulin
sarcomeres in which the thin filaments are not overlapped
type lIm (superfast fibers) which depend upon a unique
by thickfilaments. It is bisected by the Z-disc, into which the
myosin structure that, along with a high glycogen con
thin filaments of the adjacent sarcomeres are anchored. In
tent, differentia tes them from the other type II fibers
addition to the thick and thin filaments, there is a third type
(Rowlerson 1981). These are found mainly in the jaw
of filament composed of the elastic protein, titin . . . The
muscles.
banded appearance of the individual myofibrils is thus
attributable to the regular alteration of the thick and thin fil As mentioned above, long-term stress involving type I mus
aments arrays. cle fibers leads to them shortening, whereas type II fibers,
undergOing similar stress, will weaken without shortening
over their whole length (they may, however, develop local
ized areas of sarcomere contracture, for example where trig
VULNERABLE AREAS
ger points evolve without shortening the muscle overall).
Shortness/ tightness of a postural muscle does not neces
In order to transfer force to its attachment site, contractile
sarily imply strength. Such muscles may test as strong or
units merge with the collagen fibers of the tendon which
weak. However, a weak phasic muscle will not shorten
attaches the muscle to bone.
overall and will always test as weak.
At the transition area, between muscle and tendon, these
Fiber type is not totally fixed, in that evidence exists as to
structures virtually 'fold' together, increasing strength
the potential for adaptability of muscles, so that committed
while reducing the elastic quality.
muscle fibers can be transformed from slow twitch to fast
This increased ability to handle shear forces is achieved
twitch, and vice versa (Lin 1994).
at the expense of the tissue's capacity to handle tensile
An example of this potential, which has profound clinical
forces.
significance, involves the scalene muscles. Lewit (1985) con
The chance of injury increases at those locations where
firms that they can be classified as either a postural or a pha
elastic muscle tissue transitions to less elastic tendon and
sic muscle. The scalenes, which are largely phasic (type II)
finally to non-elastic bone - the attachment sites of the
and dedicated to movement, can have postural functions
body.
thrust upon them, as with forward head postures, or when
chronically contracted to maintain a virtually permanently
elevated status of the upper chest, as in asthma. If these pos
MUSCLE TYPES tural demands are prolonged, more postural (type I) fibers
may develop to meet the situation. If overuse continues (as
Muscle fibers exist in various motor unit types - basically in upper chest breathing involving the upper ribs being reg
type I slow red tonic and type II fast white phasic (see ularly elevated during inhalation), these now postural mus
below). Type I are fatigue resistant while type II are more cles will shorten, as would any type I muscle when
easily fatigued. chronically stressed (Janda 1982, Liebenson 2006).
All m uscles have a mixture of fiber types (both I and II), The following findings, relating to the scalene muscles,
although in most there is a predominance of one or the were reported in a study that evaluated the link between
other, depending on the primary tasks of the muscle (pos these and inappropriate breathing patterns, in this instance,
tural stabilizer or phasic mover). mainly asthma.
Those which contract slowly (slow-twitch fibers) are clas
sified as type I (Engel 1986, Woo 1987) . These have very low The incidence of scalene muscle pathology was assessed in
stores of energy-supplying glycogen, but carry high con 46 consecutively hospitalized patients with bronchial
centrations of myoglobulin and mitochondria. These fibers asthma and irritable cough diagnoses. Three tests described
fatigue slowly and a re mainly involved in postural and sta by Travell & Simons were used in patient evaluation,
bilizing tasks. The effect of overuse, misuse, abuse or disuse including palpation for scalene trigger points and the use of
on postural muscles (see Chapters 4 and 5) is that, over Adson's test. Breathing patterns were also evaluated in all
time, they will shorten. This tendency to shorten is a clini patients for the presence of paradoxical breathing patterns.
cally important distinction between the response to 'stress' Scalene muscle pathologtj [dysfunction] was identified in 20
of type I and type II muscle fibers (see below). of the 38 bronchial asthma patients (52%), and in 5 of the
2 M uscles 35

Sternocleidomastoid -----e.\ l'+------ Upper trapezius


Levator scapula ----".
----- Deltoid
Pectoralis major --- --+.......
Sacrospinalis ---+--It-----111 -\--- Latissimus dorsi
B..":++-+-Quadratus lumborum
External oblique ---h
..\----\- Quadratus lumborum
Flexors -----r.J +--+---+-+--- Iliopsoas
Tensor fascia lata -----;;f-J'III'--IH Piriformis ---+--f--j"

lY----l---\-i*\-- Add uctor long us


Adductor magnus ----t-_III :+-/'----- Biceps femoris
Rectus femoris -------\:\-H
Semimembranosus ---1-jIJF--J<----+
1Ift------- Semitendinosus

A.Jf----- Gastrocnemius

11:...f/----Tibialis posterior

A B
Figure 2 .. 9 Major postural muscles. A : Anter ior. B : Posterior. Reproduced with permission from Chaitow ( 1 996).

8 irritable cough syndrome patients (62%). Postisometric abdominal (or lower) aspects of pectoralis major, middle
relaxation technique [muscle energJj] was used in those with and lower aspects of trapezius, the rhomboids, serratus
scalene dysfunction. Self-administered stretching tech anterior, rectus abdominis, gluteals, the peroneal muscles,
niques for home use were also taught. One patient with par vasti and the extensors of the arms.
adoxical breathing pattern was taught an alternative Some muscle groups, such as the scalenii, are equivocal.
breathing pattern. The authors are of the opinion that Although commonly listed as phasic muscles, this is how
bronchial asthma and irritable cough syndrome patients they start life but they can end up as postural ones if suffi
should be examined and evaluated by Rehabilitation cient demands are made on them (see above) .
Medicine Department stafffor functional pathology of the
scalene muscles. They are also of the opinion that examina
tion, treatment and self-administered stretching techniques COOPERATIVE MUSCLE ACTIVITY
should be a par t of routine management of bronchial asthma
patients. (Pleidelova et al 2002) Few, if any, muscles work in isolation, with most move
ments involving the combined effort of two or more, with
Among the more important postural muscles that become one or more acting as the 'prime mover ' or agonist.
hypertonic in response to dysfunction are: Almost every skeletal muscle has an antagonist that per
forms the opposite action, with one of the most obvious
trapezius (upper), sternocleidomastoid, levator scapula
and upper aspects of pectoralis major in the upper trunk examples being the elbow flexors (biceps brachii) and
extensors (triceps brachii).
and the flexors of the arms
quadratus lumborum, erector spinae, oblique abdomi Prime movers usually have synergistic muscles that
nals and iliopsoas in the lower trunk assist them and which contract at almost the same time. An
tensor fascia latae, rectus femoris, biceps femoris, add uc example of these roles would be hip abduction, in which
tors (longus, brevis and magnus), piriformis, semimem gluteus medius is the prime mover, with tensor fascia latae
and gluteus minimus acting synergistically and the hip
branosus and semitendinosus in the pelvic and lower
adductors acting as antagonists, being reciprocally inhibited
extremity region.
(RI) by the action of the agonists if movement is to occur. RI
Phasic muscles, which weaken in response to dysfunction is the physiological phenomenon in which there is an auto
(i.e. are inhibited), include the paravertebral muscles (not matic inhibition of a muscle when its antagonist contracts,
erector spinae), scalenii and deep neck flexors, deltoid, the also known as Sherrington's law II.
36 CL I N I CA L A P PL I CATION OF N E U RO M USCULAR TECH N I Q U E S : T H E U P P E R BODY

Box 2.3 Alternative catt on of musc:l

It is general ly accepted that muscles respond to overuse, misuse or result in postural adaptations. Treatment would aim to nor
disuse by either shortening or weaken ing (and possibly lengtheni ng). ma lize the tissues and lengthen the fibers.
As Kolar has explained (in Liebenson 2006, p. 533) : 'There is clinical
and experi mental evidence that some muscles are incli ned to Many of these categories interface - for instance, overused tight
inh ibition (hypotonus, weakness, inactivity), while other muscle muscles tend to create joint pressure leading to interneuron
groups are likely to be hyperactive with a tendency to become short: responses. Psychological stress might result in muscle tightening and
It was Janda (1 969, 1 983a) who first showed that these cha nges trigger point formation. Al though the body has a number of response
fol lowed certa in rules, and who named them as phasic (those choices that it can make to cope with the load to which it is
tending to inh ibition) and postura l (those tending to shortening). A adapting (biochemical, biomechan ical and psychosocial), the
plethora of different descriptors have been used to l abel these two practitioner a lso has a wide range of choices i n the way of
muscle groups, including stabil izer, mobil iz er; global, local ; i nterventions. Chapters 9 a nd 10 carry a ful l discussion of some of
superficial, deep, etc. (Norris 1 995a,b), adding a sense o f potential those options.
disagreement and confusion to the understa nding of what is in In sum mary, whatever the causes, there are two main responses
essence relatively simple: some muscles fol low one pathway toward by muscles when chronically stressed :
dysfunction, while others fol low a different pathway - whatever
names they are ascribed. In the interest of simpl icity, the authors of 1 . They are inh ibited and show evidence of hypotonus and weakness
this text have continued to designate these different muscle types as (phasic). or
postura I a nd phasic. 2. They develop hypertonus, and possibly spasm and rigidity
Liebenson (2006, p. 4 1 1 ) d iscusses Janda's classification of tense (postural).
and tight muscles and further separates muscle dysfunction into a
va riety of different treatment-specific categories that are either
neuromuscular or connective tissue related. These cha nges appear to involve mainly the contractile elements of
These classifications are as fol lows: muscles. However, i n some i nstances, connective tissue may a lso be
involved, resulting in contracture (Ja nda 1 99 1 ) .
There is quite natura l ly n o t only a functional but a lso a structural
Neuromuscular: aspect to these differences, and these have been identified by
1. Reflex spasm: As a response to n ociception, this often acts as physiologists. As Kolar expla ins (Liebenson 2006, p. 533) :
a spl inting mechan ism. Treatment would aim toward removal
of the cause of pa in, such an infla med appendix.
Differences are found in the nervous structure in control of these [dif
2. Interneuron: This del icate part of the reflex arc can become
ferent] muscles, for it is the type of neurons that determines the type
involved when afferent information is sent from spinal or
of muscle fibre. It is therefore better to speak of tonic and phasic
peripheral joints. Treatment would a i m to normalize the
motor units. Tonic motorneurons, i.e. small alpha motor cells, inner
involved joints.
vate red muscle fibres, whereas phasic motorneurons (large alpha
3. Trigger point: This is thought to be associated with loca lized
cells) innervate white muscle fibres. In humans, both types of motor
congestion within the muscle stem m i n g from short muscle
units are present in every muscle, in different proportions.
fibers. A variety of treatments are offered in this book to nor
malize myofascial tissue.
4. Limbic: This is associated with psychological stress. It can be Examples of patterns of imbalance which emerge as som e muscles
treated with counseling, stress management and a variety of weaken and lengthen and their synergists become overworked, while
relaxation methods including yoga and meditation. their antagonists shorten, ca n be summarized as follows.

Connective tissue:
1 . Overuse muscle tightness: This stems from muscle imba la nces,
overuse, faulty movement patterns and other stresses that

Len gthened or underactive stabi l izer Overactive synergist Shortened a ntagonist


1 . Gluteus medius TFL, QL, piriformis Thigh adductors
2. Gluteus maximus Iliocostalis lumborum Et hamstrin gs Il iopsoas, rectus femoris
3. Transversus abdominis Rectus abdom i n is Il iocostalis lumborum
4 . Lower trapezius Levator scapulae/Upper trapezius Pectora lis major
5. Deep neck flexors SCM Suboccipita ls
6. Serratus anterior Pectora lis major/minor Rhomboids
7. Diaphragm Scalenes, pectora lis major/minor

Observation
Observation can often provide evidence of a n imbalan.ce involving muscle l ength tests, movement patterns and inner holding
cross patterns of weakness/lengtheni n g and shortness. A number of endurance times. Posture is valuable because it provides a quick
tests can be used to assess muscle i mbalance: postural i n spection, screen.
box continues
2 M u scles 37

M uscle i n h i bition/weakness/lengthening Observable sign


Transversus abdom inis Protru d i ng umbi licus
Serratus a nterior Winged scapula
Lower trapezius Elevated shoulder gi rd le ('gothic' shoulders)
Deep neck flexors Chin 'poking'
Gluteus medius Un level pelvis o n one-legged standing
Gluteus maximus Sagging buttock

Inner range endurance tests Gluteus maximus: Patient is prone. Practitioner lifts one leg into
'I nner holding isometric endura nce' tests can be performed for extension at the hip (knee flexed to 90') and the patient is asked
muscles that have a tendency to lengthen, in order to assess their to hold this position.
abil ity to maintain joint alignment in a neutral zone. Usually a Posterior fibers of gluteus medius: Patient is sidelying with lower
lengthened muscle will demonstrate a loss of endura nce, when leg straight and uppermost leg flexed at hip and knee so that the
tested in a shortened position. This ca n be tested by the practitioner m edial aspect of both the knee and foot are resting on the
passively prepositioning the muscle in a shortened position and floor/surface. Practitioner places the flexed leg into a position of
assessing the d u ration of time that the patient can hold the muscle maximal unforced externa l rotation at the hip, so that sole of
in this position. There a re various methods used, including 10 foot is in contact with the floor su rface, and the patient is asked
repetitions of the holding position for 1 0 seconds at a time. to maintain this position.
Alternatively, a single 30-second hold can be requested. If the Norris states:
patient ca nnot hold the position actively from the moment of
passive prepositioning, this is a sign of ina ppropriate antagon ist Optimal endurance is indicated when the full inner range position can
muscle shortening. be held for 10 to 20 seconds. Muscle lengthening is present if the limb
Norris (1 999) describes an exa mple of inner range holding tests. falls away from the inner range position immediately.

Iliopsoas: Patient is seated. Practitioner lifts one leg i nto greater


hip flexion so that foot is well clear of floor and the patient is
asked to hold this position.

Movement can only take place normally if there is coor even within the same muscle, changes dependent upon the
dination of all the interacting muscular elements. With desired effect.
many habitual complex movements, such as how to rise The ways in which skeletal muscles produce or deny
from a sitting position, a great number of involuntary, movement in the body, or in part of it, can be classified as:
largely unconscious reflex activities are involved. In many
postural, where stability is induced. If this relates to
cases, patterns of dysfunction, including muscle substitu
standing still, it is worth noting that the maintenance of
tion and changes in firing sequence, develop and often add
the body's center of gravity over its base of support
undesirable consequences. Altering such patterns has to
requires constant fine tuning of a multitude of muscles,
involve a relearning or repatterning process (see Chapters 4
with continuous tiny shifts back and forth and from side
and 5).
to side
The most important action of an antagonist occurs at the
ballistic, in which the momentum of an action carries on
outset of a movement, where its function is to facilita te a
beyond the activation produced by muscular activity
smooth, controlled initiation of movement by the agonist
(the act of throwing, for example)
and its synergists, those muscles that share in and support
tension movement, where fine control requires constant
the movement. When agonist and antagonist muscles con
muscular activity (playing a musical instrument, such as
tract simultaneously they act in a stabilizing fixator role,
the violin, for example, or giving a massage).
which results in virtually no movement.
Sometimes a muscle has the ability to have one part act
ing as an antagonist to other parts of the same muscle, a
phenomenon seen in the deltoid, where its anterior fibers MUSCLE SPASM, TENSION, ATROPHY
are antagonistic to its posterior fibers during internal and (Liebenson 1996, Walsh 1 992)
external rotation of the humerus. Interestingly, these same
fibers become synergists in the movement of lateral abduc Muscles are often said to be short, tight, tense or in spasm;
tion of the humerus. Hence the role that various fibers play, however, these terms are often used very loosely.
38 C L I N I C A L A P P LI CATI O N O F N E U R O M U S C U LA R TEC H N I Q U E S : T H E U P PER B O DY

Muscles experience either neuromuscular, viscoelastic or Muscle fibers housing trigger points have been shown to
connective tissue alterations or combinations of these. A have different levels of EMG activity within the same
tight muscle could have either increased neuromuscular functional muscle unit.
tension or connective tissue modification (for example, Hyperexcitability, as shown by EMG readings, has been
fibrosis) that results in it palpating as tight. demonstrated in the nidus of the trigger point, which is
It is worthwhile differentiating between three commonly situated in a taut band (that shows no increased EMG
used terms: contraction, spasm and contracture. With activity) and has a characteristic pattern of reproducible
regards to skeletal muscles, each of these produces a short referred pain (Hubbard & Berkoff 1993, Simons et aI 1999).
ening or increase in tension of a muscle. However, they are When pressure is applied to an active trigger point, EMG
unique in many ways. activity is found to increase in the muscles to which sen
sations are being referred ('target area') (Simons 1994).
A contracture differs from a contraction in that it is invol
CONTRACTION (TENSION WITH EMG E LEVATION , untary and that activation of the myofibrils is prolonged
VOLUN TARY) in the absence of ac tion potential activity (MacIntosh et al
Muscle tension, usually with shortening, that denotes the 2006, Simons et aI 1999).
These types of 'physiologic' contractures are differenti
normal function of a muscle.
Electromyographic (EMG) activity is increased in these a ted from the 'pathologic' contractu res associated with
cases. permanent shortening of muscles produced by excessive
Contraction is voluntary, not obligatory, i.e. one can vol growth of fibrous tissue, such as seen in Duchenne mus
untarily relax a contraction if desired. cular dystrophy (MacIntosh et aI 2006).
While contraction usually produces movement of the
joint(s) on which the muscle acts, it can also contract to INCREASED STR E TCH SENSITIVITY
produce stability in a moving joint, as a result of anxiety
Increased sensitivity to stretch can lead to increased mus
or for postural purposes.
cle tension.
This can occur under conditions of local ischemia, which
SPASM (TENSION WITH E MG ELEVATION, have also been demonstrated in the nidus of trigger
INVOLUN TARY) points, as part of the 'energy crisis' "vhich, it is hypothe
sized, produces them (Mense 1993, Mense et al 2001,
Muscle spasm is a neuromuscular phenomenon relating Simons 1994) (see Chapter 6) .
either to an upper motor neuron disease or an acute reac Many free nerve endings in group III (smallest myeli
tion to pain or tissue injury. nated) and IV (non-myelinated) afferent fibers are sensi
Electromyographic (EMG) activity is increased in these tive to pressure or stretch (MacIntosh et al 2006) and
cases. would likely be affected by the degree of ischemia within
Spasm is involuntary, i.e. one cannot voluntarily relax a the muscle.
spasm. These same afferents also become sensitized in response
Examples include spinal cord injury, reflex spasm (such as to a build-up of metabolites (MacIntosh et al 2006) when
in a case of appendicitis) or acute Iwnbar antalgia with sustained mild contractions occur, such as occurs in pro
loss of flexion relaxation response (Triano & Schultz 1987). longed slumped sitting (Johansson 1991).
Long-lasting noxious (pain) stimulation has been shown Mense (1993) and Mense et al (2001) suggest that a range
to activate the flexion withdrawal reflex (Dahl et aI 1992) . of dysfunctional events emerge from the production of
Using electromyographic evidence Simons (1994) has local ischemia that can occur as a result of venous con
shown that myofascial trigger points can 'cause reflex gestion, local contracture and tonic activation of muscles
spasm and reflex inhibition in other muscles, and can by descending motor pathways.
cause motor incoordination in the muscle with the trig Sensitization (which, in all but name, is the same phenom
ger point'. enon as facilitation, as discussed more fully in Chapter 6)
involves a change in the stimulus-response profile of neu
rons (Mense et aI 2001), leading to a decreased threshold as
CONTRACTUR E (TENSION OF MUSCLES
well as increased spontaneous activity of types III and IV
WITHOUT EMG E LE VATION , INVOLUN TARY)
primary afferents.
Increased muscle tension can occur without a consis Schiable & Grubb (1993) have implicated reflex dis
tently elevated EMG. charges from (dysfunctional) joints in the production of
Contracture is involuntary, i.e. one cannot voluntarily such neuromuscular tension. Liebenson (2006) notes that
relax a contracture. 'joint inflammation or pathology initiates a complex neu
An example is trigger points, in which muscle fibers fail romuscular response in the dorsal horn of the spinal cord,
to relax properly. resulting in flexor facilitation and extensor inhibition' .
2 M uscles 39

According to Janda (199 1 ), and agreed to by Liebenson Type I (postural or aerobic) fibers hypertrophy on the
(2006), neuromuscular tension can also be increased by symptomatic side and type II (phasic or anaerobic) fibers
central influences due to limbic dysfunction. atrophy bila terally in chronic back pain patients
(Fitzmaurice et aI 1992) .
VISCOELASTI C INFLU ENCE

Muscle stiffness is a viscoelastic phenomenon that has to WHAT IS WEA KNESS?


do with fluid mechanics and viscosity (so-called sol or
gel) of tissue (Liebenson 2006, Walsh 1992), which is True muscle weakness is a result of lower motor neuron dis
explained more fully in Chapter 1 . ease (e.g. nerve root compression or myofascial entrap
Fibrosis occurs gradually in muscle or fascia and is typi ment) or disuse atrophy. In chronic back pain patients,
cally related to post trauma adhesion formation (see generalized atrophy has been demonstra ted. This atrophy
notes on fibrotic change in Chapter 1, p. 16) . is selective in the type II (phasic) muscle fibers bila terally.
Fibroblasts proliferate i n inj ured tissue during the Muscle weakness is another term tha t is used loosely. A
inflammatory phase (Lehto et aI 1986). muscle may simply be inhibited, meaning that it has not
If the inflammatory phase is prolonged then a connective suffered disuse atrophy but is weak due to a reflex phe
tissue scar will form as the fibrosis is not absorbed. nomenon. Inhibited muscles are capable of spontaneous
strengthening when the inhibitory reflex is identified and
remedied (commonly achieved through soft tissue or joint
.AT RO PHY AND CHRONIC BACK PAIN
manipulation). A typical example is reflex inhibition from
In chronic back pain patients, generalized atrophy has an antagonist muscle due to Sherrington's law of reciprocal
been observed and to a greater extent on the symp to inhibition, which declares that a muscle will be inhibited
matic side (Stokes et aI 1992) . when its antagonist contracts.
Reflex inhibition of the vastus medialis oblique (VMO)
Box 2.4 Muscle strength testing muscle after knee inflammation/injury has been repeat
edly demonstrated (DeAndrade et al 1965, Spencer et al
For efficient m uscle strength testing it is necessa ry to ensure 1984).
that:
Hides et al (1994) found unilateral, segmental wasting of
the patient builds force slowly after engaging the barrier of the multifidus in acute back pain patients. This occurred
resista nce offered by the practitioner rapidly and thus was not considered to be disuse atrophy.
the patient uses maximum control led effort to move in the
In 1994, Hallgren et al found tha t some individuals with
prescribed direction
the practitioner ensures that the point of m uscle origin is effi chronic neck pain exhibited fatty degeneration and atro
ciently stabilized phy of the rectus capitis posterior major and minor muscles
care is taken to avoid use by the patient of 'tricks' in which as visualized by MR!. Atrophy of these small suboccipital
synergists are recruited. muscles oblitera tes their important proprioceptive output,
Muscle strength is most usua l ly graded as follows.
G rade 5 is normal, demonstrating a complete ( 1 00%) ra nge of which may destabilize postural balance (McPartland et al
movement against gravi ty, with firm resistance offered by the 1997) (see Chapter 3 for more detail on these muscles).
practitioner.
Grade 4 is 75% efficiency in achieving ra nge of motion Various pathological situa tions have been listed that can
against g ravity with slight resistance. affect either the flexibility or the strength of muscles. The
Grade 3 is 50% efficiency in achievi ng ra nge of motion result is muscular imbalance involving increased tension or
agai nst gravity without resista nce. tigh tness in postural muscles, coincidental with inhibition
Grade 2 is 25% efficiency in achieving range of motion with or weakness of phasic muscles.
gravity eliminated.
Grade 1 shows slight contractility without joint motion.
G rade 0 shows no evidence of contractility.
TRICK PATTERNS

Al tered muscular movement pa tterns were first recognized


Box 2.5 Two-joint muscle testing
clinically by Janda (1982) when it was noticed that classic
As a rule when testing a two-joint muscle good fixation is muscle-testing methods did not differentiate between nor
essentia l. The same applies to a l l m uscles in children and in mal recruitment of muscles and 'trick' patterns of substitu
adults whose cooperation is poor and whose movements a re tion during an action. So-called trick movements (see
u ncoord inated and weak. The better the extremity is stead ied, the below) are uneconomical and place unusual strain on joints.
less the stabilizers are activated and the better and more They involve muscles that function in uncoordinated ways
accu rate are the results of the muscle function test. (Janda
1 983b) and are related to both altered motor control and poor
endurance.
40 C L I N I CA L A P P L I CATI O N OF N EU R O M U S C U LA R TEC H N I Q U E S : T H E U P P E R B O DY

In a traditional test of prone hip extension it is difficult to This was in contrast to subjects without low back pain
identify overactivity of the lumbar erector spinae or ham who showed that contraction of transversus abdominis
strings as substitutes for an inhibited gluteus maximus. precedes contraction of the muscles involved in limb
Tests developed by Janda are far more sensitive and allow movement (Hodges & Richardson 1996) .
us to iden tify muscle imbalances, faulty (trick) movement The upper and deep cervical flexor muscles (type II, pha
patterns and joint overstrain by observing or palpating sic) have been shown to lose their endurance capacity in
abnormal substitution during muscle-testing protocols. For subjects with neck pain and headache (Watson & Trott
example, in a prone position, hip extension should be initi 1993) .
ated by gluteus maxim us. If the hamstrings undertake the When testing for activity in these deep flexor muscles, it
role of prime mover and gluteus maximus is inhibited, this has been found that patients w i th neck pain tend to sub
is easily noted by palpating activity wi thin each of them as stitute with the superficial flexor muscles (sternocleido
movement is initiated. mastoid and scalenes) to achieve the desired position of
Similar imbalances can be palpated and observed in the the neck (Ju1l 2000).
shoulder region where the upper fixators dominate the The posterior suboccipital muscles, which control the
lower fixa tors by inhibiting them, which results in major position of the head, have been shown to atrophy in
neck and shoulder stress. These patterns have major reper patients with chronic neck pain (McPartland et al 1997).
cussions, as will become clear when crossed syndromes, The synergistic function of these muscles may be lost so
and Janda's functional assessment methods, are outlined in that other muscles, such as upper trapezius and levator
Chapter 5 (Janda 1978) . scapulae, substitute for the suboccipital muscles during
As Sterling et al (2001) explain: functional movements. This is confirmed by studies that
have reported increased activity in these muscles in
Musculoskeletal pain potentially produces many changes in
people with neck pain (Bansevicius & Sjaastad 1996) .
motor activity. Some of these changes can be explained by
peripheral mechanisms in the muscles themselves and by These examples offer insights into the adaptive capacity of
mechanisms within the central nervous system. Certainly, the musculoskeletal system when faced with problems of
pain has a potent effect on motor activity and control. pain, overuse and disuse. There is clear evidence that some
The dysfunction that occurs in the neuromuscular sys muscles respond by becoming inhibited and/or by losing
tem in the presence of pain is extremely complex. In addition stamina, while others shorten.
to the more obvious changes, such as increased muscle activ
ity in some muscle groups, and inhibition of others, more JOINT IM PLICATIONS
subtle anomalous patterns of neuromuscular activation
seem to occur . . . Loss of selective activation and inhibition When a movement pattern is altered, the activation
of certain muscles that perform key synergistic functions, sequence, or firing order of different muscles involved in a
leading to altered patterns of neuromuscular activation, and specific movement, is disturbed. The prime mover may be
the ensuing loss of joint stability and control, are initiated slow to activate while synergists or stabilizers substitute
with acute pain and tissue injury. However, these phenom and become overactive. When this is the case, new joint
ena persist into the period of chronicity and could be one stresses will be encountered. Sometimes the timing
reason for ongoing symptoms. sequence is normal yet the overall range may be limited due
to joint stiffness or antagonist muscle shortening. Pain may
well be a feature of such dysfunctional patterns.
Exa m p l es

Pain may lead to inhibition or delayed activation of spe WHEN SHOUL D PAIN AND DYSFUNCTION
cific muscles or muscle groups involved in key synergis BE LEFT ALONE?
tic functions. This seems to most commonly occur in the
deep local muscles that perform a synergistic function to Splinting (spasm) can occur as a defensive, protective,
control joint stability (Cholewicki et aI 1997). involuntary phenomenon associated with trauma (fracture)
EMG has been used to detect selective fatigue of lumbar or pathology (osteoporosis, secondary bone tumors, neuro
multifidus, as opposed to other erector spinae muscles genic influences, etc.). Splinting-type spasm commonly dif
(Roy et aI 1989). fers from more common forms of contraction and
U1trasonography was used by Hides et al (1994) to identify hypertonicity because it often releases when the tissues that
a marked atrophy of lumbar multifidus ipsilateral to the it is protecting, or immobilizing, are placed at rest.
patients' symptoms. These changes remained even after When splinting remains long term, secondary problems
the patients had ceased to report pain (Hides et aI 1996). may arise in associated joints (e.g. contractures) and bone
A delay of contraction of transversus abdominis was (e.g. osteoporosis) . Travell & Simons (1983) note that,
noted in subjects with low back pain when they per 'Muscle-splinting pain is usually part of a complex process.
formed limb movements (Hodges & Richardson 1999) . Hemiplegic and brain-injured patients do identify pain that
2 M uscles 41

depends on muscle spasm'. They also note 'a degree of mas it is tight and consider that, in some circums tances, it is
seteric spasm which may develop to relieve strain in trigger offering beneficial support to the 51} or that it is reducing
points in its parallel muscle, the temporalis'. low back stress (Simons 2002, Thompson 2001). It is possible
Travell & Simons (1983) note a similar phenomenon in to conceive similar supportive responses in a v ariety of set
the lower back: tings, including the shoulder joint when lower scapular fix
a tors have weakened, thus throwing the load onto other
In patients with low back pain and with tenderness to pal muscles (see discussion of upper crossed syndrome in
pation of the paraspinal muscles, the superficial layer tended Chap ter 5).
to show less than a normal amount of EMC activity until
the test movement became painful. Then these muscles
showed increased motor unit activity or 'splinting' . . . This
SOMATIZATION - MIND AND MUSCLES
observation fits the concept of normal muscles 'taking over'
(protective spasm) to unload and protect a parallel muscle
It is entirely possible for musculoskeletal symptoms to
that is the site of significant trigger point activity.
represent an unconscious attempt by the patient to entomb
their emotional distress. As most cogently expressed by
Recognition of this degree of spasm in soft tissues is a mat
Philip Latey (1996), pain and dysfunction may have psy
ter of training and intuition. Whether attempts should be
chological distress as their root cause. The patient may be
made to release, or relieve, what appears to be protective
somatizing the distress and presenting with apparently
spasm depends on understanding the reasons for its exis
somatic problems (see Chapter 4).
tence. If splinting is the result of a cooperative a ttempt to
unload a painful but not pathologically compromised struc
ture, in an injured knee or shoulder for example, then treat
BUT HOW IS ONE TO KNOW?
ment is obviously appropriate to ease the cause of the
original need to protect and support. If, on the other hand, Karel Lewit (1992) suggests that, 'In doubtful cases, the
spasm or splinting is indeed protecting the struc ture it sur physical and psychological components will be distin
rounds (or supports) from movement and further (possibly) guished during the treatment, when repeated comparison
serious damage, as in a case of advanced osteoporosis for of (changing) physical signs and the pa tient's own assess
example, then it should clearly be left alone. ment of them will provide objective criteria'. In the main, he
suggests, if the patient is able to give a fairly p recise
description and localization of his pain, we should be reluc
BENEFICIALLY OVERACTIVE MUSC L E S
tant to regard it as 'merely psychological'.
Van Wingerden et al (1997) report that both intrinsic and In masked depression, Lewit suggests, the reported
extrinsic support for the sacroiliac joint (51]) derives, in part, symptoms may well be of vertebral pain, particularly
from hamstring (biceps femoris) status. Intrinsically, the involving the cervical region, with associated muscle ten
influence is via the close anatomic and physiological rela sion and 'cramped' posture. As well as being alerted by
tionship between biceps femoris and the sacrotuberous lig abnormal responses during the course of treatment to the
ament (they frequently attach via a strong tendinous link). fact that there may be something other than biomechanical
They state: 'Force from the biceps femoris muscle can lead causes of the problem, the history should provide clues. If
to increased tension of the sacrotuberous ligament in vari the masked depression is treated appropriately, the verte
ous ways. Since increased tension of the sacrotuberous liga brogenic pain will clear up rapidly, he states.
ment diminishes the range of sacroiliac joint motion, the In particular, Lewit notes, 'The most important symp tom
,
biceps femoris can play a role in stabilization of the SI} (Van is disturbed sleep. Characteristically, the patient falls asleep
Wingerden et al 1997; see also Vleeming 1 989). normally but wakes within a few hours and cannot get back
Van Wingerden et al (1997) also note that in low back to sleep'. Pain and dysfunction can be masking major psy
pain patients forward flexion is often painful as the load on chological distress and awareness of it, how and when to
the spine increases. This happens whether flexion occurs in cross-refer should be part of the responsible practitioner's
the spine or via the hip joints (tilting of the pelvis). If the skills base.
hamstrings are tight and short, they effectively prevent Muscles cannot be separated, in reality or intellectually,
pelvic tilting. 'In this respect, an increase in hamstring ten from the fascia that envelops and supports them. Whenever
sion might well be part of a defensive arthrokinematic it appears we have done so in this book, it is meant to high
reflex mechanism of the body to diminish spinal load.' light and reinforce particular characteristics of each. When
If such a state of affairs is long standing, the hamstrings it comes to clinical applications, these structures have to be
(biceps femoris) will shorten (see discussion of the effects of considered as integrated units. As muscular dysfunction is
stress on postural muscles, p. 25), possibly influencing being modified and corrected it is almost impossible to con
sacroiliac and lumbar spine dysfunction. The decision to ceive that fascial structures are not also being remodeled.
treat a tight hamstring should therefore take account of why Some of the quite amazingly varied functions of fascia are
42 CLI N I CA L A P P L I CATI O N O F N E U R O M U S C U L A R TECH N I Q U E S : TH E U P P E R B O DY

detailed in Chapter 1 . In this chap ter we have reviewed In the next chapter, as we review the myriad reporting
some of the important features of muscles themselves, their sta tions embedded in the soft tissues in general and the
structure, function and at least some of the influences that muscles in particular, it becomes clear that muscles are as
cause them to become dysfunctional, in unique ways, much an organ of sense as they are agents of movement and
depending in part on their fiber type. stability.

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45

Chapter 3

Reporting stations and the brain

Irwin Korr (1970), osteopathy's premier researcher into the


CHAPTER CONTENTS physiology of the musculoskeletal system, has described it
as 'the primary machinery of life'.
Proprioception 45
The musculoskeletal system (not our digestive or our
Fascia and proprioception 46
immune system) is the largest energy consumer in the body.
Reflex mechanisms 47
It allows us to perform tasks, play games and musical instru
Local reflexes 50
ments, make love, give treatment, paint and, in a multitude
Central influences 50
of other ways, engage in life. Korr stated that the parts of the
Neuro muscular dysfunction following injury 51
body act together 'to transmit and modify force and motion
Mechanisms that alter proprioception 52
through which man acts out his life'. This coordinated inte
An example of proprioceptive dysfunction 52
gration takes place under the control of the central nervous
Rectus capitis posterior minor (RCPMin) research
system as it responds to a huge amount of sensory input
evidence 52
from both the internal and the external environment.
Neural influences 53
Our journey through the structures that make up these
Effect of contradictory proprioceptive information 53
communica tion pathways incl udes an overview of the
Neural overload, entrapment and crosstalk 57
ways in which information, most notably from the soft tis
Manipulating the reporting stations 58
sues, reaches the higher centers. The neural reporting sta
Therapeutic rehabilitation using reflex systems 59
tions represent 'the first line of contact between the
Conclusion 60
environment and the human system' (Boucher 1996).

PROPR I O CEPTIO N

Information that is fed into the central control systems of the


body relating to the external environment flows from extero
ceptors (mainly involving data relating to things we see, hear
and smell). A wide variety of internal reporting stations also
transmit data on everything from the tone of muscles to the
pOSition and movement of every part of the body. The vol
ume of information entering the central nervous system for
processing almost defies comprehension and it is little won
der that, at times, the mechanisms providing the information,
or the way it is transmitted, or received, or the way it is
processed and responded to, become dysfunctional.
Proprioception can be described as the process of deliv
ering information to the central nervous system as to the
position and motion of the body relative to other neighbor
ing parts of the body. In contrast to six exteroception human
senses that advise us of the outside world (sight, smell,
46 CLI N I CA L A PPLICA TI O N O F N EU R O MU S C U LAR TEC HN IQUES: THE U PPER B O DY

taste, hearing, touch and balance), proprioception provides Butler and Moseley (2003) seek to clarify the concept of
information solely on the status of the internal body. The nociceptors (pain sensors) when they say:
information is derived from neural reporting stations (affer
We don't actually have 'pain receptors', or 'pain pathways'
ent receptors) in the muscles, the skin, other soft tissues and
or 'pain centers'. However, there are some neurons that
joints, independent of vision, and is combined with input
respond to all manner of stimuli, if those stimuli are suffi
from the vestibular apparatus. The term 'proprioception'
cient to be dangerous to the tissue. Activation of these spe
was first used by Sherrington in 1907 to describe the sense
cial neurons sends a prioritized alarm signal to [the] spinal
of position, posture and movement. Janda (1996) states that
cord, which may send it towards the brain.
it is now used ('not quite correctly') in a broader way, 'to
describe the function of the entire afferent system'. Whether a message sent by a nociceptor is actually per
Schafer (1987) describes proprioception as 'kinesthetic ceived as pain depends on many factors, perhaps the most
awareness' relating to 'body posture, position, movement, important being the interpretation given to the message by
weight, pressure, tension, changes in equilibrium, resistance the brain. This is discussed further in Chapter 7 where we
of external objects, and associated stereotyped response pat examine the phenomenon of pain.
tems'. In addition to the unconscious data being transmitted Lewit has shown that altered function can produce
from the proprioceptors, Schafer lists the sensory receptors as: increased pain perception, and that this is a far more com
mon occurrence than pain resulting from direct compres
Mechanoreceptors, which detect deformation of adjacent sion of neural structures, such as that which produces
tissues. These are excited by mechanical pressures or dis radicular pain when the sciatic nerve is compressed.
tortions and so would respond to touch or to muscular Lewit (1985) suggests that there is seldom a need to explain
movement. Mechanoreceptors can become sensitized fol pain by actual mechanical irritation of nervous structures, as in
lowing what is termed a 'nociceptive barrage' so that they the root-compression model. It would be a peculiar conception
start to behave as though they are pain receptors. This of the nervous system (a system dealing with information)
would lead to pain being sensed (reported) centrally in that would have it reacting, as a rule, not to stimulation of its
response to what would normally have been reported as receptors but to mechanical damage to its own structures.
movement or touch (Schaible & Grubb 1993, Willis 1993). Lewit offers as examples of the reflex nature of much pain
chemoreceptors, which report on obvious information perception: referred pain from deeper structures (organs or
such as taste (gustation) and smell (olfaction), as well as ligaments) which produce radiating pain, altered skin sensi
local biochemical changes such as CO2 and O2 levels. tivity (hyperalgesia) and sometimes muscle spasm. These
Taste buds and olfactory epithelium, rich with receptor reflex referrals are discussed later in this chapter in the con
cells, allow distinction among a wide range of chemical text of somatosomatic and viscerosomatic reflexes. Even true
stimuli. Information obtained is transmitted to the limbic radicular pain (for example, resulting from disc prolapse)
system, a portion of the brain that can respond to emo usually involves stimulation of nociceptors that are present
tion and thought (Butler & Moseley 2003). in profusion in the dural sheaths and the dura rather than
thermoreceptors, which detect modifications in tempera direct compression that would produce paresis and anesthe
ture, such as when something hot or cold is applied to the sia (loss of motor power and numbness) but not pain.
skin, as well as changes in the immediate climate. These Pain derives from irritation of pain receptors, and where
are also used in palpation of tissue temperature varia this results from functional changes (such as inappropriate
tions and are most dense on the hands and forearms (and degrees of maintained tension in muscles), Lewit suggests
the tongue). the most appropriate descriptive term would be 'functional
electromagnetic receptors, which respond to light entering pathology of the motor system'.
the retina.
nociceptors, which register pain. The word nociception
FASCIA AND PROPRIOCEPTION
actually means 'danger reception'. These receptors can
become sensitized when chronically stimulated, leading Bonica (1990) suggests that fascia is critically involved in
to a drop in their threshold (see notes on facilitation, proprioception and that, after joint and muscle spindle
Chapter 6, p. 105). This is thought by some to be a process input is taken into account, the majority of remaining pro
associated with trigger point evolution (Korr 1976). prioception occurs in fascial sheaths (Earl 1965, Wilson
polymodal receptor (PMR), a type of nociceptor responsive 1966). Staubesand (1996) confirms this and has demon
to mechanical (e.g. acup uncture), thermal (moxibustion) strated that myelinated sensory neural structures exist in
and chemical stimuli. Its sensory terminals are free nerve fascia, relating to both proprioception and pain reception.
endings and exist in various tissues throughout the body. The various neural reporting organs in the body provide a
Research suggests that these pain receptors may play a constant source of information feedback to the central nerv
significant part in the evolution of trigger points, and are ous system, and higher centers, as to the current state of
also capable of being used to modify pain (Kawakita et al tone, tension, movement, etc. of the tissues housing them
2002). PMR is discussed further in Chapter 6. (Travell & Simons 1983, 1992, Wall & Melzack 1991). It is
3 Reporting stations and the brain 47

Box 3.1 Neurotrophic influences t"vo-way traffic along neural pathways, is arguably at least as
important as the passage of impulses with which we usually
I rvin Korr (Korr 1 967, 1 986) spent half a century investigating the associate nerve function.
scientific backg round to osteopathic methodology and theory.
Some of his most im portant work related to the role of neu ral
structures in the delivery of trophic substances. The various REFLEX MECHAN ISMS
patterns of stress that are covered in the next chapter are
capable of d rastically affecting this axoplasmic transportation.
Korr states: As Schafer (1987) points out, 'The human body exhibits an
astonishingly complex array of neural circuitry'. Among
These 'trophic' proteins are thought to exert long-term influences
on the developmental, morphologic, metabolic and functional
these are receptors, reflex arcs and mechanisms that com
qualities of the tissues - even on their viability. Biomechanical municate from outside the muscular system.
abnormalities in the musculoskele tal system can cause trophic A receptor (proprioceptor, mechanoreceptor, etc.) resides
disturbances in ot least two ways: (7) by mechanical deformation on the cell surface or within the cytoplasm and is composed of
(compression, stretching, angUla tion, torsion) of the nerves, which
structural protein molecules. It binds to a specific factor, such
impedes axonal transport; and (2) by sustained hyperactivity of
neurons in facilitated segments of the spinal cord [see discussion
as a neurotransmitter, by which it is stimulated as follows.
of this phenomenon in Chap ter 6J which slows axonal transport
An afferent impulse travels, via the central nervous system,
and which, because of metabolic changes, may affect protein
synthesis by the neurons. It appears that manipula tive treatment
to a part of the brain that we can call an integrative center.
would alleviate such impairments of neurotrophic function. This integrative center evaluates the message and, with
influences from higher centers, sends an efferent response.
The manufactu ring process of macromolecules for transportation
This travels to an effector unit, perhaps a motor endplate,
takes place in nerve cells, is packaged by the Golgi apparatus and
transported along the neural axon to the target neurons (Ochs Et and a response occurs.
Ranish 1 969). The speed of transportation along axons is
sometimes remarkably swift at the rate of up to half a meter per
Additionally, the basic reflex arcs, which control much of
day (although m uch slower than the 1 20 meters per second of the body's 'immediate reaction' responses, can be summa
actual neural transmission) (Ochs 1 9 75). rized as follows (Sato 1992).
Once the macromolecu les reach their destination, where they
influence the development and maintenance of the tissues being A sensory receptor (or proprioceptor, mechanoreceptor,
supplied, a return transportation of materials for reprocessing etc.) is stimulated.
com mences. When there is interference in axonal flow (because An afferent impulse travels via a sensory neuron to the
of com pression, etc.) the tissues not receivin g the trophic spinal cord.
material degenerate and a build-up of axoplasm occu rs, forming
The sensory neuron synapses with an interneuron, which,
a swel ling (Schwartz 1 980).
Korr ( 1 98 1 ) has shown that w h en a m uscle is denervated by in turn, synapses with the motor neuron to send an effer
injury and atrophies, it is the interruption of trophic substances ent response, without any intervention by the brain.
which causes this rather than loss of neural impulses (see This travels to an effector unit, perhaps a motor endplate,
notes on rectus capitis posterior minor denervation following and a response occurs (see Box 3.2).
whiplash, p. 294).
Research has shown that when the neural supply to a postural Reflex mechanisms extend beyond the musculoskeletal sys
(predominantly red fiber) m uscle is su rgically altered, so that it tem. It is possible to further characterize the reflex mecha
receives neurotrophic material originally destined for a phasic nisms that operate as part of involuntary nervous system
(white fiber) muscle, there is a transformation in which the
postural muscle can become a phasic m u scle (and vice versa)
function as follows.
based on the trophic material it receives. This suggests that Somatosomatic reflexes, which may involve stimuli from
genetic expression can be neurally mediated. The axoplasm tells
sensory receptors in the skin, subcutaneous tissue, fascia,
the muscle what its function is going to be (Guth 1 968).
striated muscle, tendon, ligament or joints, producing
reflex responses in segmentally related somatic struc
tures - for example, from one such site on the body to
important to realize that the traffic between the center and the another segmentally related site on the body. Such
periphery in this dynamic mechanism operates in both direc reflexes are commonly triggered by manual therapy tech
tions along efferent (away from the CNS and brain) and affer niques (during application of compression, vibration,
ent (toward the CNS and brain) pathways. Any alteration in massage, manipulation, application of heat or cold, etc.).
normal function at the periphery (such as a proprioceptive Somatovisceral reflexes, which involve a localized somatic
source of information) leads to adaptive mechanisms being stimulation (from cutaneous, subcutaneous or muscu
initiated in the central nervous system, and vice versa loskeletal sites) producing a reflex response in a segmen
(Freeman 1967). tally related visceral structure (internal organ or gland)
It is also important to reahze that it is not only neural (Simons et aI1999). Such reflexes are also commonly trig
impulses that are transmitted along nerve pathways, in both gered by manual therapy techniques (during application
directions, but also a host of important trophic substances. of compression, vibration, massage, manipulation, appli
This process of the transmission of trophic substances, in a cation of heat or cold, etc.).
48 CLI N ICAL A PPLI CATIO N O F N EU RO M U S C U LA R TEC H N IQ U ES : TH E U PPER B O DY

.
@y Lacrimal gland

. ... .
- .. .... . . . . . ,
..

.. ..

Eye
Gray rami
communicantes

.. . .
C1
.. .
. . . ... . 1.........
. .

..
. . . ...
Parotid gland

. . .
..

. ... .. Submandibular gland

.
.

. .
..
.
. .
Sublingual gland

--
Larynx
Trachea
Bronchi
Lungs

T1

Heart


.
:: -o>;r-
::.::: --
_-: G re
;;;
::: a ter thora . Sl'h
Innervation to arrector -.:::.::::.::.:::.::.::.:
-- C/c $pl.
___
pili muscles,vascular
-....
--- q"f]lc
...
smooth musde and

.. . . fI7
sweat glands of skin
--...;::..."c9I)...c9
.
.

..
.

: . : .: : t
Iadder

. .b
..
Gray ramus communicans
.U Bile ducts

"
.
Pancreas

. .... .
While ramus communicans Aortiroreoal


. . t' . ,
. Kidneys

-.:.::.:===,
v--.;;;:=---+---<.., .. .
.

.:..:: : . :)!/
Intestines

;.
..
Descending colon
. ... -..,./ Sigmoid colon

.
mesenlenc

.
.
.
9i Rectum

---- P9'"::,:'b
.
Inlener S:
::
S1 --

..., :7.;': "dd"

Preganglionic fibres

..................... Posiganglionic fibres

hy :::
plexus
nc ":: : 1UJ Extemal genitalia

F ig u re 3.1 A EtB : Co rd level of organ i n n ervation via (A ) sympathetic nervous system an d (B) parasympathetic nervous system. Drawn after
N etter (2006) .

Viscerosomatic reflexes, in which a localized visceral (inter the intensity of the visceral stimulus. Obvious examples of
nal organ or gland) stimulus produces a reflex response in this include right shoulder pain in gallbladder disease and
a segmentally related somatic structure (cutaneous, subcu cardiac ischemia producing the typical angina distribution
taneous or musculoskeletal) (Fig. 3.1). It has been sug of left arm and thoracic pain. Giamberardino (2005) notes
gested that such reflexes, feeding into the superficial that visceral pain can affect the somatic tissues in the area
structures of the body, can give rise to trigger points of referral for months or even years, and long after the vis
and/or dysfunction in the somatic tissues (De Sterno 1977, ceral problem has been resolved .
Giamberardino 2005, Simons et al 1999). Balduc (1983) Viscerocutaneous reflex, in which organ dysfunction stim
reports that these reflexes are intensity oriented, which is uli produce superficial effects involving the skin (includ
to say that the degree of reflex response relates directly to ing pain, tenderness, heightened sensitivity to heat,
3 R eporting stations and the brain 49

Medulla
. Lacrimal gland

oblongala -'-
. :::: (
:::
.
'

.
..
/
Eye
.

..
..

Parotid gland

Submandibular gland

Sublingual gland

Larynx
Trachea
Bronchi

Lungs
Pulmonary plexus
T1 --

Heart

Stomach

Liver


Gallbladder
Bile ducts
Pancreas

Kidneys

L1 --


Intestines

Descending colon


Sigmoid colon
Inferior Rectum
hypogastric

1
S1 -_
S2
Urinary bladder
S3 Prostate
---- Preganglionic fibres

..................... Postganglionic fibres


M--------
Pelvic splanchnic nerves

External genitalia

B
Fig u re 3.1 (Continued)

touch or pinprick, etc.) Examples of this include itch pat coronary heart disease plus gallbladder calculosis, for
.
terns and heightened skin sensitivity associated with the instance, may experience more frequent attacks of angina
referral pattern of an organ. and biliary colic than patients with a single condition,
Viscerovisceral reflex in which a stimulus in an internal organ based upon the partially overlapping (T5) afferent path
or gland produces a reflex response in another segmentally ways from the heart and gallbladder. Women with both
related internal organ or gland Giamberardino (2005) dysmenorrhea and irritable bowel syndrome (IBS) tend to
.
places particular importance on 'visceroviscero hyperalge complain of more intense menstrual pain, intestinal pain
sia, an augmentation of pain symptoms due to the sensory and referred abdominal/pelvic hyperalgesia than do
interaction between two different internal organs that women with only one of these conditions. She suggests
share at least part of the afferent circuitry. Patients with that treatment of one visceral condition may improve
50 CLINICAL A PP LICATIO N OF N EU RO MU S C U LAR TEC H N IQ U ES : THE U PPER B O DY

symptoms from another. It should be noted, however, that Afferent messages are received centrally from somatic,
such pathologies, layered one over the other, often present vestibular (ears) and visual sources, all reporting new
a complex symptomatology and are difficult to diagnosis data and providing feedback for requested information.
a clear cause for each symptom may never be proven. To If all or any of this information is excessive, noxious or
compound the situation, prolonged visceral afferent bar inappropriately prolonged, sensitization (see notes on
rage into the CNS may produce long-term sensitization facilitation, Chapter 6, p. 108) can occur in aspects of the
that results in hyperalgesia, trophic changes and somatic central control mechanisms, which results in dysfunc
pain that is deceptive, and may delay appropriate treat tional and inappropriate output (Mense et al 2001,
ment, unless the viscera are fully considered. Russell 2001).
The limbic system of the brain can also become dysfunc
Whether such reflexes have bidirectional potential is tional and inappropriately process incoming data, leading
debated. Some research suggests that a visceral problem to complex problems, such as fibromyalgia (Goldstein
can exhjbit in a specific dermatomal segment via a viscero 1996) (see Box 3.4).
cutaneous reflex (Giamberardino 2005) and that stimulation The entire suprasegmental motor system, including the
of the skin could have a distinct effect on related visceral cortex, basal ganglia, cerebellum, etc., responds to the
areas via a cutaneovisceral reflex. afferent data input with efferent motor instructions to
Schafer (1987) makes the very important observation the body parts, with skeletal activity receiving its input
that, 'The difference between somatovisceral and visceroso from alpha and gamma motor neurons, as well as the
matic reflexes appears to be only quantitative and to be motor aspects of cranial nerves.
accounted for by the lesser density of nociceptive receptors As noted in Chapter 2, any alteration in pH, for example
in the viscera'. This can best be understood by means of when respiratory alkalosis follows overbreathing, modi
Head's law, which states that when a painful stimulus is fies neural function, which can include speeding reflexes,
applied to a body part of low sensitivity (such as an organ) reducing thresholds (such as pain) and allowing sensiti
that is in close central connection (the same segmental sup zation to occur more easily (Chaitow et aI2002).
ply) with an area of higher sensitivity (such as a part of the
soma), pain will be felt at the point of higher sensitivity Schafer (1987) sums up the process:
rather than where the stimulus was applied.
Whether a person is awake or asleep, the brain is constantly
bombarded by input from all skin and internal receptors.
LOCAL RE FLEXES
This barrage of incoming messages is examined, valued, and
translated relative to a framework composed of instincts,
A number of mechanisms exist in which reflexes are stimu experiences and psychic conditioning. In some yet to be dis
lated by sensory impulses from a muscle leading to a covered manner, an appropriate decision is arrived at that is
response being transmitted to the same muscle. Examples transmitted to all pertinent muscles necessary for the
include the stretch reflexes, myotatic reflexes and the deep response desired. By means of varying synaptic facilitation
tendon reflexes. and restraints within the appropriate circuits, an almost
The stretch reflex is a protective mechanism in which a limitless variety of neural integrntion and signal transmis
contraction is triggered when the annulospiral receptors in sion is possible.
a muscle spindle are rapidly elongated. Concurrently there
are inhibitory messages transmitted to the motor neurons of The sum of proprioceptive information results in specific
the antagonist muscles inducing reciprocal inhibition, with responses.
simultaneous facilitating impulses to the synergists.
Motor activity is refined and reflex corrections of move
If enough fibers are involved the threshold of the Golgi
tendon organs will be breached, leading to the muscle 'giv ment patterns occur almost instantly.
A conscious awareness occurs of the position of the body
ing way'. This is a reflex process known as autogenic inhibi
tion (Ng 1980). and the part in space.
This body awareness in the brain relates to the presence
there of a 'virtual body', a homunculus ('little man'), a
'sensory map' of the brain, that is aware of the spatial
CENTRAL INFLUENCES
location of the parts, and that responds to messages of
Sensory information received by the central nervous system distress (danger) that may be interpreted as pain (Butler
can be modulated and modified both by the influence of the & Moseley 2003).
mind and changes in blood chemistry, to which the sympa The more neurons a particular part of the body has to
thetic nervous system is sensitive (see notes on carbon dioxide represent it in the brain, the more attention the message
influences on neural sensitivity, Chapter 4, p. 77). Whatever receives, with the hands, face, tongue and genitals being
local biochemical influences may be operating, the ultimate highly represented, compared, for example, with the rest
overriding control on the response to any neural input of the head or the chest. This is discussed in more detail
derives from the brain itself. in Chapter 7, particularly in relation to phantom pain.
3 Reporting stations and the brai n 51

Over time, learned processes can be modified in response


to altered proprioceptive information and new move
ment patterns can be learned and stored.
It is this latter aspect, the possibility of learning new pat
terns of use, that makes proprioceptive influence so
important in rehabilitation.

N E U R OMUSCULAR DYSFU N CTIO N


FOLLOWI N G INJU RY (Ryan 1994)

Functional instability may result from altered proprio


ception following trauma, e.g. the ankle 'gives way'
(functional instability) during walking when no appar
ent structural reason exists (Lederman 1997).
Proprioceptive loss following injury has been demon
strated in spine, knee, ankle and TMJ (following trauma,
surgery, etc.) (Spencer 1984).
These changes contribute to progressive degenerative
joint disease and muscular atrophy (Fitzmaurice 1992).
The motor system will have lost feedback information for
refinement of movement, leading to abnormal mechanical
stresses of muscles/joints. Such effects of proprioceptive
Fig u re 3.2 The h o m u nc u l u s represents the a m o u n t of cerebral
cortex designated to p rocess 'touch receptors'. Rep rod uced with
deficit may not be evident for many months after trauma.
permission from BrainCo n nection.

Box 3.2 Reporting stations -j. .

Some important structures involved in this i nternal information The pacinian corpuscle. This is found in periarticu lar connective
highway, which may under given circumstances be involved in the tissue and adapts rapidly. It triggers discharges, and then ceases
production or maintenance of pain (LaMotte 1992), are listed below. reporting in a very short space of time. These messages occur
Ruffini end-organs. Found within the joint capsu le, around the successively, d u ring motion, and the CNS can, therefore, be aware of
joints, so that each is responsible for describing what is happening the rate of acceleration of movement taking place in the area. It is
over an angle of approximately 15' with a deg ree of overlap sometimes called an acceleration receptor.
between it and the adjacent end-organ. These organs are not easily Skin receptors are responsive to touch, pressure and pain and are
fatigued and are progressively recruited as the joint moves, so that involved in primitive responses such as withdrawal and g rasp
movement is smooth and not jerky. The prime concern of Ruffini reflexes.
end-organs is a steady position. They are also to some extent Cervical receptors, especially relative to the suboccipital
concerned with reporting the direction of movement. m usculature (see notes on rectus capitis posterior minor, p. 292),
Golgi end-organs. These, too, adapt slowly and continue to in teract with the labyrinthine (ear) receptors to maintain balance
discharge over a lengthy period. They are fou nd in the ligaments and an appropriate positioning of the head in space.
associated with the joint. Unlike the Ruffin i end-organs, which respond There are other end-organs, but those described above can be seen
to muscular contraction that alters tension in the joint capsule, Golgi to provide information on the present status, position, direction and
end-organs can deliver information independently of the state of rate of movement of any muscle or joint and of the body as a whole.
muscular contraction. This helps the body to know just where the joint Muscle spindle. This receptor is sensitive and complex (Macintosh
is at any given moment, irrespective of muscular activity. et al 2006).
Slow-adapting joint receptors (above) have a powerful
It detects, evaluates, reports and adjusts the length of the muscle
modu lating influence on reflex responses (for example, in the
in which it lies, setting its tone.
sacroiliac joint) and seem to have the ability to produce long-lasting
Acting with the Golgi tendon organ, most of the information as
influences, either in maintaining dysfunction or in helping in its
to m uscle tone and movement is reported.
resolution (if pressure/stress on them can be normalized). Direct joint
Spindles lie paral lel to the m uscle fibers and are attached to
manipulation (Lefebvre et al 1993) can have just such an effect or, as
either skeletal m uscle or the tendinous portion of the m uscle.
Lewit has shown, so can normalization of joint function by less
Inside the spind le are fibers that may be one of two types. One is
direct means. Lewit (1985) emphasizes this by saying :
described as a 'nuclear bag' fiber and the other as a chain fiber.
The basic [soft tissue] techniques . . . are very gentle and are also very In different muscles, the ratio of these internal spindle fibers differs.
effective for mobilization, using muscular facilitation and inhibition, In the center of the spindle is a receptor called the annu lospiral
i.e. the inherent forces of the patient. It is most unfortunate that in receptor (or primary ending) and on each side of this lies a 'flower
the minds of most people, physicians and laymen alike, manipula tion spray receptor' (secondary ending).
is tantamount to thrusting techniques - techniques that should The primary ending discharges rapid ly and this occurs in response
rather be the exception. to even small changes in muscle length.

box continues
52 C L I N ICAL A P P L I CAT I ON OF N EU R OM U SCULA R TEC H N I QUES: TH E UPPER B ODY

Box 3.2 (continued)

The secondary ending compensates for this, because it fires The activities of the spindle appear to provide information as to
messages only when l a rger changes in m uscle length have length, velocity of contraction and changes in velocity (Gray's
occurred. Anatomy 2005). How long is the m uscle, how quickly is it changing
The spind le is a 'length comparator' (a lso called a 'stretch recep length and what is happening to this rate of change of length?
tor') and it may discharge for long periods at a time.
Within the spind l e there a re fine, intrafusal fibers which a lter the Go/gi tendon receptors. These structures indicate how hard the
sensitivity of the spind le. These can be a l tered without any actual m uscle is working ( whether contracting or stretching ) since they
change taking place in the length of the m uscl e itself, via a n reflect the tension of the m uscle, rather than its length. If the
independent g a m m a efferent supply t o t h e intrafusal fibers. This tendon organ detects excessive overload it may cause cessation of
has im plications in a variety of acute and ch ronic problems. fu nction of the m uscle to prevent damage. This produces relaxation.

MECHANISMS THAT ALTER PROPRIOCEPTION


head translation, this space nearly vanishes (Penning
(Lederman 1997) 1989).
Hack et al (1995) noted that a fascial bridge between the
RCPMin and the dura is oriented perpendicularly, resist
Ischemic or inflammatory events at receptor sites may pro
ing movement of the dura toward the spinal cord with
duce diminished proprioceptive sensitivity due to the
head translation.
build-up of metabolic by-products that stimulate group III
The attachment of the ligamentum nuchae into the dura
and IV, mainly pain afferents (this also occurs in muscle
between the atlas and axis serves a complementary func
fatigue).
tion with the RCPMins (Mitchell et aI1998).
Physical trauma can directly affect receptor axons (artic
Through the ligamentum nuchae, other posterior mus
ular receptors, muscle spindles and their innervations).
cles may also be acting indirectly with the RCPMin to
1. In direct trauma to muscle, spindle damage can lead
coordinate dural position with head movement.
to denervation (e.g. following whiplash) (Hallgren
EMG studies suggest RCPMin does not fire during exten
et aI1993).
sion, but rather does so when the head translates for
2. Structural changes in parent tissue lead to atrophy
wards (Greenman 1997, personal communication).
and loss of sensitivity in detecting movement, as well
The high density of muscle spindles found in the RCPMs
as altered firing rate (e.g. during stretching).
suggests the value of these muscles lie not in their motor
Loss of muscle force (and possibly wasting) may result
function but in their role as 'proprioceptive monitors' of
when a reduced afferent pattern leads to central reflexo
the cervical spine and head.
genic inhibition of motor neurons supplying the affected
Observations linking the suboccipital and cervical mus
muscle.
cles with equilibrium are not new (Longet 1845).
Psychomotor influences (e.g. feeling of insecurity) can
In 1955, the importance of proprioceptors in this region
alter patterns of muscle recruitment at local level and
was recognized and the term 'cervical vertigo' was
may result in disuse and muscle weakness.
coined (Ryan & Cope 1955).
The combination of muscular inhibition, joint restriction
Cervical proprioception currently is recognized as an
and trigger point activity is, according to Liebenson
essential component in maintaining balance. This is par
(1996), 'the key peripheral component of the functional
ticularly true in the elderly, in whom there is a shift in
pathology of the motor system'.
emphasis from vestibular reflexes to cervical reflexes in
maintaining balance (Wyke 1985).
AN EXAMPLE OF PROPRIOCEPTIVE
DYSFUNCTION

In order to appreciate some of the profound influences that Proprioception and pain
proprioceptive function offers and the devastating effect
Proprioceptive signals from these suboccipital mus
disturbance of this function can produce in terms of pos
tural stability and pain, a particular example is summarized cles may also serve as a 'gate' that blocks nocicep
below involving rectus capitis posterior minor. tor (pain fiber) transmission into the spinal cord
and higher centers of the central nervous system (Wall
1989).
RECTUS CAPITIS POSTERIOR MINOR (RCPMin)
According to the gate theory of pain, large-diameter
RESEARCH EVIDENCE
(A-beta) fibers from proprioceptors and mechanorecep
In head extension, the posterior atlas arch maintains a tors enter the spinal cord and synapse on interneurons in
mid-position between the occiput and the axis. In forward the dorsal horn of the spinal cord.
3 R eporting stations and th e brain 53

Occipital bone RCPMin evluation and treatment

Dura McPartland (1997) palpated individuals with RCPMin


atrophy and found they had twice as many areas of cer
Rectus capitis posterior minor muscle
vical somatic dysfunctions as control subjects.

'------r.:onnprlii'vp tissues
Somatic dysfunctions were identified by tenderness of
paraspinal muscles, asymmetry of joints, restriction in
First cervicat vertebra ROM and tissue texture abnormalities.
Janda (1978) screened for proprioceptive dysfunction by
First cervical nerve root testing standing balance with eyes closed. Bohannon et al
(1984) suggest that between the ages of 20 and 49 a main
tained balance time of between approximately 25 and 29
seconds is normal. Between ages 49 and 59, 21 seconds is
Fig u re 3.3 Lateral view of the upper cervical joint complex. normal, while between 60 and 69 just over 10 seconds is
Redrawn with permission from the Journol ofMonipulative and
acceptable. After 70 years of age 4 seconds is normal.
Physiological Therapeutics 1999; 22(8):534-539.
Anything less than this is regarded as indicating degrees
of proprioceptive dysfunction. Patients with propriocep
tive dysfunction are treated with 'sensory motor retrain
Interneurons inhibit nociceptor transmission, specifically
ing' - balance retraining with the eyes closed. (See
nociceptors that synapse in lamina V of the dorsal
Volume 2, Chapter 2 for more on balance retraining.)
horn.
In Chapter 2 of this text there is a description of respiratory
Chronic postural stress (slouching or 'chin poking') or
alkalosis resulting from common overbreathing patterns.
trauma may lead to hypertonic suboccipital muscles.
It is worth noting that a common feature of respiratory
Hallgren et al (1994) found that some individuals with
alkalosis is a disturbance in the individual's ability to
chronic neck pain exhibited fatty degeneration and atro
maintain balance, suggesting that in any attempt to restore
phy of the RCPMin and RCPMaj, as visualized by MRl.
normal balance, breathing retraining should form a part of
Atrophy of the RCPMin reduces its proprioceptive output
the protocol (Balaban & Theyer 2001).
and this may destabilize poshual balance (McPartland
1997).
Subjects with chronic neck pain (and RCPMin atrophy as
N E U RAL I N FLUEN CES
seen by MRl) showed a decrease in standing balance
when compared to control subjects.
EFFECT OF CONTRAD ICTORY PROPRIOCEPTIVE
Reduced proprioceptive input facilitates the transmis
II\IFORMATIOI\I
sion of impulses from a wide dynamic range of nocicep
tors, which can develop into a chronic pain syndrome. Korr (1976) reminds us:
When muscle pain increases in intensity referral of the
The spinal cord is the keyboard on which the brain plays
pain sensation to remote sites occurs, such as to other
when it calls for activity or for change in activity. But each
muscles, fascia, tendons, joints and ligaments (Mense &
'key' in the console sounds, not an individual 'tone', such as
Skeppar 1991).
the contraction of a particular group of muscle fibers, but a
Noxious stimulation of the rectus capitus posterior
whole 'melody' of activity, even a 'symphony' of motion, In
muscles causes reflex EMG activity in distal muscles,
other words, built into the cord is a large repertoire of pat
including the trapezius and the masseter muscles (Hu
terns of activity, each involving the complex, harmonious,
et aI1993). Hu and colleagues (1995) showed that irrita
delicately balanced orchestration of the contractions and
tion of the dural vasculature in the upper cervical spine
relaxations of many muscles. The brain 'thinks' in terms of
leads to reflexive EMG activity of the neck and jaw
whole motions, not individual muscles. It calls selectively,
muscles.
for the preprogrammed patterns in the cord and brain stem,
Injury or dysfunction of the RCPMin may irritate the C1
modifying them in countless ways and combining them in
nerve, which, if chronic, may lead to facilitation of sym
an infinite variety of still more complex patterns. Each
pathetic fibers associated with Ct resulting in a chronic
activity is also subject to further modulation, refinement,
pain syndrome.
and adjustment by the afferent feedback continually stream
Alternatively, chronic C1 irritation may refer pain to the
ing in from the participating muscles, tendons, and joints,
neck and face, via C1's connections with C2 and cranial
nerve V. This means that the pattern of information fed back to the CNS
Conclusion: RCPMin dysfunction (atrophy) leads to and brain reflects, at any given time, the steady state of joints,
increased pain perception and reduced proprioceptive the direction as well as speed of alteration in position of joints,
input, reflexively affecting, for example, other cervical together with data on the length of muscle fibers, the degree of
and jaw muscles (Hack et aI1995). load that is being borne and the tension this involves. It is a
54 C LI NICA L A PP LI C AT I O N OF N E U R O M U SC U LA R TECH N I Q U E S : T H E U P P E R B O DY

Box 3.3 Co-contraction and strain

The work of Laurence Jones DO ( 1 995) in developing his treatment


method of strain and cou nterstrain (see Chapter 9) led him to
research the mechanisms that might occur u nder conditions of acute
strain. His concept is based on the predictable physiological
responses of m uscles in given situations.
Jones describes how in a ba lanced state the proprioceptive
functions of the va rious muscles su pporting a joint will be feeding a
flow of information derived from the neural receptors in those
m uscles and their tendons. For exa mple, the Golgi tendon organs will A
be reporting on tone, while the various receptors in the spind les wil l
b e firing a consta nt stream o f information (slowly or rapidly,
depending u pon the demands being placed on the tissues) regarding
their resting length and any cha nges which mig ht be occurring in
that length (Korr 1 947, 1 974, Mathews 1981 ) .
Jones (1964) first observed t h e phenomenon o f spontaneous
release when he 'accidental ly' placed a patient who was in
considerable pain and some degree of compensatory distortion into a
position of comfort (ease) on a treatment table. Despite no other
treatment being given, after just 20 minutes resting in a position of
relative ease the patient was able to stan d upright and was free of
pain. The pain-free position of ease into which Jones had hel ped the
patient was one that exaggerated the deg ree of distortion in which
his body was being held. He had taken the patient into the
direction of ease (rather than toward tension or 'bind') since any B
attempt to correct or straighten the body wou ld have been
met by both resista nce and pain. In contrast, moving the body
further into distortion was acceptable and easy and seemed to
al low operation of the physiological processes involved in resolution
of spasm.
The events that occur at the moment of strain provide the key to
understa nding the mecha nisms of neurological ly induced positional
release. For exam ple, consider an a l l too common exa mple of
someone bending forwa rd. At this time the tru nk flexors would be
t
short of their resting length and their muscle spindles wou ld be
firing slowly, indicating little or no activity and no change of length
taking place. At the sa me time the spinal erector g roup wou ld be
stretched, or stretching, and firing rapidly. Any stretch affecting a
m uscle (and therefore its spindles) will increase the rate of reporting, c
which will reflexively induce further contraction (myotatic stretch
A B C
reflex) and an increase in tone in that muscle. This prod uces a n

I":'t': '" : ",,1""':":'''' ': ::':


insta nt reciprocal inhibition o f t h e function a l a ntagonists to it
(flexors), reducing even further the a l ready limited deg ree of Brachialis
reporting from their muscle spindles.
This feedback link with the central nervous system is the primary II II ! ! II ! l! III! I J!JI!! 1 Triceps
muscle spindle afferent response, modulated by an additional muscle
spindle function, the gamma efferent system, which is controlled from
higher (brain) centers. In simple terms, the gamma efferent system Fi g u re 3.4 A: Arm flexor (brach i al is) and extensor ( triceps brachii)
influences the primary afferent system, for example when a muscle is in in e asy normal rel ationsh i p i n dicated by rate of firing on the scale
a quiescent state. When it is relaxed and short with little information for each muscle. B: When sudden force is appl ied, the flexors are
coming from the primary receptors, the gamma efferent system might
stretche d an d the extensors protect the joi n t by rapidly shortening.
fine-tune and increase ('turn up') the sensitivity of the primary
C: Stretch receptors i n the flexors continue to fi re as though
afferents to ensure a continued information flow (Mathews 1 98 1 ).
stretch conti n u es. Firing of both flexors and extensors con ti n ues at
i n appropri ately h i g h rates, producing the effect noted in a strai ned
/! Crisis joint where restriction exists w i th i n the join t's physiolog i cal range
Now imagine an emergency situation in which im mediate demands of motion. Reproduced w i th permission from Chaitow (2007).
for stabilization a re made on both sets of muscles (the short,
relatively 'quiet' flexors and the stretched, relatively actively firing
extensors) even though they a re in q uite different states of some of which ensures that the relaxed flexor muscles remain even
prepared ness for action. more relaxed due to inhibitory activity.
The flexors would be 'unloaded', relaxed and providing minimal The central nervous system wou ld at this time have minimal
feedback to the control centers, while the spinal extesors would be information as to the status of the relaxed flexors and, at the
at stretch, providing a rapid outflow of spind le-derived information, moment when the crisis demand for stabilization occurred, these

box continues
3 Reporting stations a n d the brain 55

Box 3.3 (tonti'W:


.
shortened and relaxed flexors would be obliged to stretch quickly to function. One would be shorter and one longer than its normal resting
a length which would balance the a l ready stretched extensors - length.
which would be contracting rapidly to stabilize the a rea. At this time any attempt to extend the a rea/joint(s) would be
As this ha ppened the a n n u l ospiral receptors in the short (flexor) strongly resisted by the tonically shortened flexor group. The
muscles would respond to the sudden stretch demand by contracting individual wou l d be locked into a forward-bending distortion. i n this
even more. as the stretch reflex was triggered. The neural reporting example. The joints involved would not have been taken beyond their
stations in these shortened muscles would be firing impulses as if normal physiological range and yet the normal range wou ld be
the m uscles were being stretched - even when the muscle remained u navailable due to the shortened status of the flexor group (in this
well short of its normal resting length. At the same time the extensor particular exa mple). Going further into flexion. however. would
muscles. which had been at stretch and which in the alarm situation present no problems or pain.
were obliged to rapidly shorten. wou ld remain l onger than their Walther ( 1 988) summarizes the situation as fol l ows.
normal resting length as they were attempting to stabilize the
When proprioceptors send conflicting information there may be
situation.
simul taneous contraction of the antagonists . . . without an tagonis t
Korr has described what happens in the abdomina l m uscles
muscle inhibition joint and o ther strain results . . . a reflex pa ttern
(flexors) in such a situation. He says that. because of their relaxed
develops which causes muscle or o ther tissue to main tain this contin
status short of their resting length. a silencing of the spindles
uing strain. It [strain dysfunction] often rela tes to the inappropriate
occurs. However. due to the sudden demand for information by the
signaling from muscle proprioceptors that have been strained from
higher centers. gamma gain is increased so that. as the muscle
rapid change that does not allow proper adaptation.
contracts rapidly to stabilize the situation and demands for
information are received from the central nervous system. the muscle This situation wou ld be u nlikely to resolve itself spontaneously and is
reports back that it is being stretched when it is actually short of its the 'strain' position in Jones' strain/counterstrain method. We can
normal resting length. This results in co-contraction of both sets recognize it in an acute setting in torticol lis as wel l as in acute
of muscles. agonists and antagonists. In effect. the muscles wou ld 'Iumbago: It is a lso recognizable as a feature of many types of chronic
have adopted a restricted position as a result of ina ppropriate somatic dysfu nction in which joints remain restricted due to muscular
proprioceptive reporti ng (Korr 1 976). The two opposi ng sets of muscles imba lances of this type. This is a time of intense neurological and
become locked into positions of imbalance in relation to their normal proprioceptive confusion. This is the moment of 'strain:

Box 3.4 Biochemistry. the mind and neurosom atic disorders

Goldstein ( 1 996) has described many chronic health conditions. 3. Genetica lly predetermined susceptibility to viral infection
including chronic fatigue and fibromyalgia syndromes (CFS. FMS). as affecting the neurons and g lia. 'Persistent CNS viral infections
neurosomatic disorders. q uoting Yu nus ( 1 994) who says they are . . . the
cou ld a lter production of transmitters as well as cel l ular
commonest grou p of il l nesses for which patients consult physicians: mechanisms:
Neurosomatic disorders are ill nesses which Goldstein suggests are 4. Increased susceptibility to environmental stressors due to reduction
caused by 'a complex interaction of genetic. developmental and in neural plasticity (resulting from all or any of the causes listed in
environmenta l factors'. often involving the possibility of early 1 -3 above). This might include deficiency in glutamate or nitric
physical. sexual or psychological abuse (Fry 1 993). Symptoms emerge oxide (NO) secretions, which results in encoding new memory.
as a result of 'impaired sensory information processing' by the neural 'Neural plasticity' capacity may be easily overtaxed in such individu
network (including the bra i n). Examples given a re of light touch als which. Goldstein suggests, is why neurosomatic patients often
being painful. mild odors producing nausea. walking a short distance develop their problems after a degree of increased exposure to envi
being exhausting. climbing stairs being like going u p a mou ntain. ronmental stressors such as acute infection. sustained attention.
reading something lig ht ca using cog nitive impairment - all of which exercise. immunization. emergence from anesthesia. trauma. etc.
examples a re true for many people with CFS/FMS.
Goldstein is critical of psychological approaches to treatment of Goldstein ( 1 996) describes the limbic system and its dysreg ulation
such conditions. apart from cog nitive behaviour therapy. which he thus.
.
suggests ... may be more appropriate. since coping with the
vicissitudes of these ill nesses. which wax and wane u n predictably. is 1 . The limbic system acts as a regu lator (integrative processing) i n
a major problem for most of those afflicted'. He claims that most t h e b ra i n with effects on fatigue, pain. sleep. memory. attention.
major medical journals concerned with psychosomatic medicine weight. appetite. libido, respiration. temperatu re, blood pressure.
rarely discuss neu robiology and 'apply the concept of somatization mood. immune and endocrine function.
to virtually every topic between their covers' (Hudson 1 992. Yunus 2. Limbic function dysreg u lation influences a l l or any of these fu nc
1 994). tions and systems.
The four basic influences on neurosomatic i l lness are. he believes. 3. Regulation of autonomic control of respiration derives from the
as follows. limbic system and major abnormalities (hyperventilation tenden
cies. irregu l a rity in tida l volu me, etc.) in breathing function a re
1 . Genetic susceptibility, which can be strong or weak. If only a noted in people with chronic fatigue syndrome. along with abnor
weak tendency exists. other factors a re needed to influence the mal responses to exercise (including failure to find expected lev
trait. els of cortisol increase. catecholamines. g rowth hormone,
2. If a child feels unsafe between birth and puberty. hypervigila nce somatostatin. increased core temperatu re, etc.) (Gerra 1 993,
may develop and interpretation of sensory input will a lter. Goldstein Et Daly 1 993. G riep 1 993, M u nschauer 1 99 1 ) .

box continues
56 C LI N I CA L A P P L I CATI O N O F N E U R O M U SC U LA R TECH N I QU E S : T H E U P PE R B O DY

Box 3.4

4. Dysfu nction of the l i m bic system ca n resu l t from centra l or


peripheral i nfl uences ('stress').
5. Sensory gating (the weight given to sensory inputs) has been
shown to be less effectively i n h ibited i n women than in men Early intense
(Swerdlow 1 993). psychosocial
6. Many biochemical i m balances are i nvolved i n l imbic dysfunction stress (abuse,
and no attempt will be made in this summary to deta i l etc.)
t h e m all.
7. The trigeminal nerve, states Goldstein, modulates l imbic regula Additional
tion. 'The trigeminal nerve may produce expansion of the recep mu lti ple
tive field zones of wide dynamic-ra nge neurons and environ mental
nociceptive-specific neurons under certai n cond itions, perhaps stressors
i nvolving increased secretion of substance P, so that a greater
n u m ber of neurons w i l l be activated by sti m u lation of a receptive
zone, causi ng innocuous sti m u l i to be perceived as painful'
(Dubner 1 992). Allostasis = modified homeostasis (genetically or via early experience)
which produces exaggerated or insufficient responses, for example:
8. Goldstein reports that nitrous oxide, which is a primary vasod ila
stress-hormone elevation
tor i n the brain, has profound infl u ences on glutamate secretion

behavioral and neuroimmunoendocrine disorders


and the neurotransm itters which infl uence short-term memory

physiological regulation of abnormal states (out of balance)


(Sandman 1 993), anxiety (Jones 1 994), dopamine release

glucocorticoid elevation
(Hanbauer 1 992) (so affecting fatigue), descending pain inh ibi
various key sites in the brain produce neurohumoral changes
tion processes, sleep induction and even m enstrual problems.
potentially influencing almost any part of the body or its
' Female patients with CFS/FMS usually have premenstru a l exacer functions.
bations of their symptoms. Most of the symptoms of late luteal
phase dysphoric diso rder [premenstrual syndrome) a re sim ilar to
those of CFS, and it is l i kely that this d isorder has a l imbic etiol Figure 3.5 Schematic representation of a l l ostasis. Reprodu ce d
ogy sim ilar to CFS/FMS' (Iadecola 1 993). w i t h permission from Chaitow (2003a).

Allostasis is a major feature of Goldstein's model. He reports the


fol lowing.

Approximately 40% of CFS/FMS patients screened have been


shown to have been physical ly, psychologica l ly or sexua l ly abused Allostatic load, in contrast to homeostatic mechan isms which
i n child hood. By testing for brain electricity imbala nces, using stabilize deviations in normal variables, is 'the price the body pays
brain electricity activity mapping (BEAM) techniques, Goldstein for containing the effects of a rousing stimuli and the expectation
has been able to demonstrate abnorm a l ities in the left tempora l of negative consequences' (Schul kin 1 994).
area, a feature of people who have been physica l ly, psychologi Chronic negative expectations and subsequent a rousal seem to
cally or sexually abused in childhood (as compared with non increase allostatic load. This is cha racterized by a nxiety and
abused controls) (Teicher 1 993). anticipation of adversity lead ing to elevated stress hormone levels
Major child hood stress, he reports, i ncreases cortisol levels (Sterling Et Eyer 1 98 1 ) .
which can affect h i ppocampal function and structure Goldstein attempts t o explain t h e imme nsely complex biochemi
(McEwan 1 994, Sa polsky 1 990). It seems that early experience cal and neural i nteractions which are involved i n this scenario,
and envi ronmental sti m u l i i nteracting with undeveloped biolog i embracin g a reas of the brain such a s the a mygdala, the pre
c a l systems l e a d t o altered homeostatic responses: 'For frontal cortex, the lower brainstem and other sites, as well as
exam ple, exaggerated or i nsufficient H PA axis responses to myriad secretions including hormones (includi n g g lucocorticoids),
defend a homeostatic state i n a stressful situation cou ld resu lt in neurotransmitters, substance P, dopamine a nd nitric oxide.
behavioural and neuroi m munoendocrine diso rders i n adulthood, Final ly, he states, prefrontal cortex function can be alte red by
particula rly if sti m u l i that shou l d be non-stressful were n u m erou s triggering agents in the predisposed individual (possibly
evaluated ... ina ppropriately by the prefrontal cortex .. .' (Meaney i nvolving genetic featu res or early trau ma) includ ing:
1 994).
Sa polsky ( 1 990) has studied this area of 'a l l ostasis' (regu lation of 1. viral infections that a lter neuronal function
internal m i l ieu through dynam ic change in a number of hormonal 2. immunizations that deplete biogenic amines (Gardier 1 994)
and physical variables that a re not i n a steady-state condition) 3. orga nophosphate or hydrocarbon exposure
a nd identifies as a primary feature a sense of lack of control. 4. head i nj u ry
Sapolsky a l so identifies a sense of lack of predictability and vari 5. childbirth
ous other stressors which infl u ence the H PA axis and which are 6. electromag netic fields
less balanced i n i ndividuals with CFS/FMS; all these stressors 7. sleep deprivation
involve 'ma rked absence of control, predictabil ity, or outlets for 8. general a nesthesia
frustration'. 9. 'stress', e.g. physica l, such a s marathon running , or mental or
In studies of this topic CFS/FMS patients are found to predomi emotional.
nantly attribute their symptoms to external factors (virus, etc.)
while control subjects (depressives) usually experience i nward What Goldstein is reporting is a n a l tered neurohumoral response in
attribution (Powell 1 990). individuals whose defense and repair systems a re predisposed to this
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -

box continues
3 Reporting stations a n d the bra i n 57

Box 3.4 (continued) .

happening, either because of i nherited tendencies or because of nutritional approaches. Goldstein h a s offered us insights and his own
early developmental (physical or psychological) insul t(s), to which solutions. Not everyone w i l l necessarily accept these sol u tions but
additional multiple stressors have been added. His sol ution is a the i l l u mination of the highly com plicated mechanisms i nvolved,
biochemical (drug) modification of the i m balances he iden tifies as which he offers, is to be commended.
key features of this situation. It is also worth reflecting on the possible effects, on predisposed
Alternative approaches might attempt to modify behavior or to mechanisms, of whiplash-type i nj u ries, as d iscussed in this cha pter.
a lter other aspects of the complex d isturbances, possibly using

totality of information that is received, rather than individual papers offering glimpses of what may be going on in the
pieces of information from particular reporting stations. apparently never-ending pain states.
Should any of this mass of information be contradictory and Dommerholt (2004a,b) has examined one such syndrome
actually conflict with other information being received, what CRPS (chronic regional pain syndrome, previously known
then? If conflicting reports reach the cord from a variety of as reflex sympathetic dystrophy). He notes that, 'It is
sources simultaneously, no discernible pattern may be recog likely that CRPS is a disease of the central nervous sys
nized by the CNS (see Korr 's discussion below and Box 3.3). In tem, but at the same time there are numerous indications
such a case no adequate response would be forthcoming and that point to peripheral inflammatory processes, abnor
it is probable that activity would be stopped and a protective mal sympathetic-afferent coupling, and adrenoreceptor
co-contraction ('freezing', splinting) spasm could be the result. pathology. It is plausible that there are multiple simulta
neous processes that contribute to the development of
Sensitization CRPS' (Dommerholt 2004a) .
Dommerholt (2004b) acknowledges that when attempt
W hen pain persists past the time that an injury should
ing to treat such conditions, while physical (manual)
have healed, a process of central sensitization may have
therapy may be useful, there is no research evidence to
occurred.
validate its efficacy. There is certainly no general prescrip
Similarly, if pain, instead of reducing in the area involved
tion as to what will help most in any of the widespread
over time, gradually spreads, sensitization is a probable
pain conditions listed above. However, Dommerholt sug
cause.
gests that (and the authors of this text agree) : 'Therapy [of
Sensitization is also the likely mechanism if pain inten
CRPS] should include at least general range of motion
sity increases for no apparent reason.
exercises, inactivation of myofascial trigger points, desen
The process of sensitization involves the dorsal horn of
sitization interventions, aquatic physical therapy, posture
the spinal cord and/or the brain becoming increasingly
training and movement retraining.'
easily irritated, with its threshold reduced.
A process known as wind-up, and another known as long
In later chapters all of these options will be explored, along
term potentiation (see Box 3 .5) may result in a degree of
with nutrition, stress management and emotional well
sensitization and chronic pain, such as allodynia, where
being, all of which can also be influential to these conditions.
even a light stimulus provokes extreme pain (Kandel
et al 2000, Van Griensven 2005).
Commonly, when central sensitization occurs, move
NEURAL OVERLOAD , ENTRAPMENT AND
ments become limited because of the pain and a degree
CROSSTAL K
of anxiety and 'pain behavior' starts, in which activities
are reduced to avoid an increase in pain. Korr (1976) discusses a variety of insults that may result in
The sorts of conditions that might have these characteris increased neural excitability, including the triggering of a
tic may carry labels such as fibromyalgia, chronic fatigue barrage of supernumerary impulses to and from the cord
syndrome, somatoform pain disorder, myofascial pain that can result in 'crosstalk', in which axons may overload
syndrome, non-specific neuropathic pain . . . and many and pass impulses to one another directly. Muscle contrac
others, depending on who made the diagnosis, who tion disturbances, vasomotion, pain impulses, reflex mech
offered the 'label' . anisms and disturbances in sympathetic activity may aU
Aspects of the mechanisms described i n Box 3.4, a s well as result from such behavior, due to what might be relatively
in Box 3.5, may be involved in central sensitization, with slight tissue changes (in the intervertebral foramina, for
altered biochemistry as a feature, possibly relating to early example), possibly involving neural compression or actual
childhood stresses (biochemical and/or psychological). entrapment.
The fact is that complex chronic pain syndromes appear In addition, Korr states that normal patterned transmis
to have multiple possible causes, and the processes sion from the periphery can be jammed when any tissue is
involved remain unclear - despite mountains of research disturbed, whether bone, joint, ligament or muscle. These
58 C LI N I CA L A P P L I CATI O N OF N E U R O M U SC U LA R T E C H N I Q U E S : T H E U P P E R B O DY

factors, combined with any mechanical alterations in the tis debated. Some take a pOSition that this is a minimal effect
sues, are the background to much somatic dysfunction. (Lederman 1997), while others suggest a strong, if tempo
Korr summarizes the picture as follows: rary, influence that allows for an easier stretch of previ
These are the somatic insults, the sources of incoherent and ously shortened structures (Lewit 1985). In Chapter 9 new
meaningless feedback, that cause the spinal cord to halt nor research evidence is described that helps to explain just
mal operations and to freeze the status quo in the offending what does happen following an isometric contraction as
and offended tissues. It is these phenomena that are used in MET and other soft tissue manipulation tech
detectable at the body surface and are reflected in disorders niques such as 'hold-relax' and 'contract-relax-antagonist
of muscle tension, tissue texture, visceral and circulatory contract'.
Positional release techniques (PRT) - muscle spindles are
function, and even secretory junction; the elements that are
so much a part of osteopathic diagnosis. influenced by methods which take them into an 'ease'
state and which theoretically allow them an opportunity
Goldstein (1996) offers a more complex scenario in which the to 'reset' and reduce hypertonic status. Jones' (1995) 'strain
brain itself (or at least part of it) becomes hyperreactive and and counterstrain' and other positional release methods
starts to miSinterpret incoming information (see Box 3.4). use the slow and controlled return of distressed tissues to
the position of strain as a means of offering spindles a
MANIPULATING THE REPORTING STATIONS chance to reset and so normalize function. This is particu
larly effective if they have inappropriately held an area in
There exist various ways of 'manipulating' the neural
just such protective splinting.
reporting stations to produce physiological modifications in
Direct inf luences can be achieved, for example, by means
soft tissues.
of pressure applied to the spindles or Golgi tendon
Muscle energy technique (MET) - isometric contractions uti organs (sometimes termed 'ischemic compression' or
lized in MET affect the Golgi tendon organs, although the 'inhibitory pressure', equivalent to acupressure method
degree of subsequent inh ibition of muscle tone is strongly ology) (Stiles 1984).
Proprioceptive manipulation (applied kinesiology) is possi
STRENGTHEN ble (Walther 1988). For example, kinesiological muscle
tone correction utilizes two key receptors in muscles to
achieve its effects. A muscle in spasm may be helped to
relax by the application of direct pressure (using approx
imately 2 1bs or 0.5 kilos of pressure) away from the belly
of the muscle, in the area of the Golgi tendon organs,
and/or by the application of the same amount of pres
sure toward the belly of the muscle, in the area of the
muscle spindle cells (Fig. 3.6).
c WEAKEN
The precise opposite effect (i.e. temporary toning or
strengthening of the muscle) is achieved by applying
pressure away from the belly, in the muscle spindle
region, or toward the belly of the muscle in the tendon
A = Golgi tendon organs B = belly of muscle C = muscle spindle
organ region.
F ig u re 3.6 Proprioceptive m a n i pu l a t i o n of m u scles as described i n The mechanoreceptors in the skin are very responSive to
the text. Reproduced with pe rmission from Ch aitow (2003b). stretching or pressure and are, therefore , easily influenced

Box 3:5

Van Griensven (2005, p . 64) explains t h e processes th at occur It is in teresting to note that wind-up develops whether a person is
in the dorsal horn that can lead to central sensitization and extreme conscious or not. A person undergoing surgery may develop long
pain : lasting sensitization of the dorsal horns supplying the operation
site with sensory nerves, even though they are under general
Wind-up is a phenamenon that has been observed in laboratory anaesthetic.
settings. When a C fibre is stimulated repeatedly at a relatively high Long-term potentiation is thought to be the result of wind-up and
frequency. it continues to depolarize even when stimulation has other forms of persistent nociceptive stimulation. The bombardment
ceased. The spontaneous firing can take a lang time to fizzle out and of the secondary neuron with glutamate opens more ion channels in
it can be main tained by successive stimulatian. In ather wards, its membrane than when stimulation is of shorter duration and lower
although it takes in tense and high frequency stimula tion for a C intensity. The result is an ever-increasing calcium influx into the sec
fibre to go in to a state of wind up, it requires much less to main tain . . . ondary cell, which makes it even more exitable.

box continues
3 R eporting stations and t h e brain 59

Box 3.5 (contin ued)

Presynaptic

Dorsal
horn

Tissue

Presynaptic

Dorsal
horn
receptors
opened

Postsynaptic Tissue

F i g u re 3.7 The ro l e of N M DA c h a n nels. A: Nociceptive


sti m u l ation leads to the release of g l utamate, w h i c h opens A M PA
channels. The N M DA c h a n n e l s rema i n b l ocked by m a g nesi u m F i g u re 3.8 State dependent processing. A: Control state.
(Mg2+). B : Pe rsistent sti m u lation causes the ej ection o f M g 2 + , Mech a n ical sti m u l i affect low t h reshold affe rents and noxious
creati ng a n infl ux o f ca l c i u m (Ca2 + ) . As long as the channels sti m u l i affect high thresho ld affe rents. The signals a re passed
rema i n u n blocked, a s m a l l a m o u nt of g l u tam ate has a greater o n u n c h a nged. B : Sensitized state. Sti m u l i a re a m p l ified . I n put
effect than when only the AM PA c h a n n e l s a re opened. I n creased from high t h reshold a fferents generates hyperalgesia. I n p u t
levels of i n tracel l u l a r calci u m trigger processes i nside the from low th reshold afferents i s felt a s i ntense (hyperaesthesia)
postsyna ptic ce l l , leading to a greater response. They a lso trigger or even pai nfu l (a l lodynia). C: Supp ressed state. All i n p ut is
the release of retrog rade messengers that fac i l itate the release of reduced i n i n tensity. Reproduced w ith permission from van
'
g l utamate from the presy n a ptic mem bra ne. Reproduced with Griensven (2005).
permission from van Gri ensven (2005).

NMDA, N-methyl d-aspartate; AMPA, alpha-amina-3-hydroxy-5-methyl-4-isaxazo/e propionic acid

Note: It may be useful to refer to the discussion of facititation in Chapter 6 to compare the similarities and d i ffere nc es between t h i s phenomenon a n d centra l
faci l i tation.

by methods which rub them (e.g. massage), apply pres reprogramming proprioceptive information (Chaitow &
sure to them (NMT, reflexology, acupressure, shiatsu, DeLany 2002, Liebenson 2006).
etc.), stretch them or 'ease' them (as in osteopathic func
tional technique, see Chapter 9).
The mechanoreceptors in the joints, tendons and liga THERAPEUTI C REHABI LITATI O N U SING
ments are influenced to varying degrees by active or pas REFLEX SYSTEMS
sive movement including articulation, mobilization,
adjustment and exercise (Lederman 1997). V ladimir Janda has researched and developed ways in which
Sensory motor stimulation, using a variety of tools (see reeducation of dysfunctional patterns of use can best be
below), may activate afferent pathways as a means of achieved, using our knowledge of neural reporting stations - a
60 C L I N I C A L A P P L I CAT I O N OF N E U R O M U SC U LA R TECH N I QU E S : T H E U P P E R B O DY

'sensory motor' approach Ganda 1996). There are, he states, trampolines and many others, including balance exercises,
two stages to the process of learning new motor skills or such as Tai Chi (see Volume 2, Chapter 2) . The principles of
relearning old ones. this approach are based on the work of Bobath & Bobath
(1964) who developed motor education programs for chjJ
1. The first is characterized by the learning of new ways of dren w i th cerebral pa lsy. A program of reeducation of sen
performing particular functions. This involves the cortex sory motor function can apparently double the speed of
of the brain in conscious participation in the process of muscle contraction, significantly improving general and
skill acquisition. As this process proceeds, Janda says, 'the postural function (Bullock-Saxton et aI 1993) .
brain tries to minimize the pathways and to simplify the
regulatory circuits', speeding up this relatively slow
means of rehabiJita tion. However, he warns, 'If such a
motor program has become fixed once, i t is difficult, if not C O N C LU S I O N
impossible, to change it. This calls for other approaches'.
2. The speedier approach to motor learning involves bal A n appreciation o f the roles o f the neural reporting stations
ance exercises tha t a ttempt to assist the proprioceptive helps us in our understanding of the ways in which dys
system and associated pa thways relating to posture and functional adaptive responses progress, as they evolve out
equilibrium. Janda (1996) informs us that, 'From the of patterns of overuse, misuse, abuse and disuse.
pOint of view of afference, recep tors in the sole of the Compensatory changes that emerge over time or as a result
foot, from the neck muscles, and in the sacroiliac area of adapta tion to a single tra uma tic event are seen to have a
have the main proprioceptive influence' (Abrahams logical progression. We will focus on these pa tterns in the
1977, Freeman et a1 1965, Hinoki & Ushio 1975). next chapter. There we will take both a broad and a local
view of compensations and adaptations to the normal
Aids to stimulating the proprioceptors in these areas (gravity) and abnormal (use patterns or trauma) stresses of
include wobble boards, rocker boards, balance shoes, mini life and how these impact our remarkably resilient bodies.

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63
::::::oJ
Chapter 4

Causes of musculoskeletal dysfunction

The struggle with gravity is a lifelong battle, often compli


CHAPTER CONTENTS cated by the sheer range of adaptive stresses to which we
subject our bodies throughout life. Adaptation and com
Adaptation - GAS and LAS 63
pensation are the processes by which our functions re
Posture, respiratory function and the adaptation
gradually compromised as we respond to an endless senes
phenomenon 64
of demands, ranging from postural repositioning in our
An example of 'slow' adaptation 66
work and leisure activities to habitual patterns (such as how
What of adaptation to trauma? 67
we choose to sit, walk, stand or breathe). There are local
What of adaptation to habits of use? 67
tissue changes as well as whole body compensations to
Making sense of the picture 67
short- and long-term insults imposed on the body. A sum
Example 68
mary discussion of the adaptive mechanisms involved,
Postural and emotional influences on musculoskeletal
together with a deeper examination of key features m the
dysfunction 69
evolution of musculoskeletal dysfunction, will support an
PosturaI interpretations 69
understanding of how the body adapts, how it may be
Contraction patterns 69
assisted and when it might be appropriate to leave the
Emotional contractions 69
adaptation alone.
'Middle fist' functions 70
'Upper fist' functions 70
Behavior and personality issues 71
ADAPTATION - GAS AND LAS
Cautions and questions 72
Postural imbalance and the diaphragm 73
When we examine musculoskeletal function and dysfunc
Balance 74
tion we become aware of a system that can become compro
Respiratory influences 75
mised as a result of adaptive demands exceeding its capacity
Effects of respiratory alkalosis in a deconditioned
to absorb the load, while attempting to maintain something
individual 75
Respiratory entrainment and core stability issues 75
approaching normal function. Elastic limits ay at tim: be
exceeded, resulting in structural and functlOnal modlfIca
Summary of effects of hyperventilation 76
tions. Assessing these dysfunctional patterns - making sense
Neural repercussions 77
of what can be observed, palpated, demonstrated - allows
Tetany 77
for detection of causes and guidance toward remedial
Biomechanical changes in response to upper chest
action.
breathing 77
The demands that lead to dysfunction can either be violent,
Additional emotional factors and musculoskeletal
forceful, single events or they can be the cumulative influence
dysfunction 78
of numerous minor events (microtrauma). Each such event is
Selective motor unit involvement 78
a form of stress and provides its own load demand on the
Conclusion 79
local area as well as the body as a whole. To better understand
these processes it is useful to refer back to the principal
researcher of this phenomenon, Hans Selye.
Selye (1956) called stress the 'non-specific element' in
disease production. He described the general adaptatzon
64 C L I N I CA L A P P LICAT I O N O F N E U R O M U S C U LA R T E C H N I Q U E S : TH E U P P E R B O DY

ADAPTING TO STRESS
Alarm phase Aching muscles

Different activities
place the body under
different kinds of
stress. It is how we Postural changes, shoulders slumped,
adapt to the stresses Strengthening muscles in dominant arm head pushed forwards
Changes
that determines how Increased heart strength Possible changes to eyesight as eye muscles
we are affected by adapt to long periods focused on screen
them. These two
examples show the
two paths taken during
Regular movement
the adaptation phase - Adaptation Lack of awareness
and postural
the planned adaptation phase of changes
path leads to recovery
without injury or
damage; unplanned
adaptation leads to Improvement of
breakdown and the strength and
Recovery or Injury or strain, No long-term Repetitive strain
development of coordination
breakdown e.g. tennis elbow damage injury
particular problems. No injury or tissue
damage

Figure 4.1 Examples of appropriate and inapp ropriate responses to stress. Redrawn after Peters (2005).

syndrome (GAS) as being composed of three distinct changes that occur when particular load is applied to, or par
stages: ticular demands are made of, body areas (Norris 2000a,b).
Selye demonstrated that stress results in a pattern of adap
the alarm reaction when initial defense responses occur
tation, individual to each organism. He also showed that
('fight or flight')
when an individual is acutely alarmed, stressed or aroused,
the resistance (adaptation) phase (which can last for
homeostatic (self-normalizing) mechanisms are activated.
many years, as long as homeostatic - self-regulating -
However, if the alarm status is prolonged or if adaptive
mechanisms can maintain function)
demands are excessive, long-term, chronic changes occur and
the exhaustion phase (when adaptation fails) where
these are almost always at the expense of optimal functional
frank disease emerges.
integrity.
GAS affects the organism as a whole, while the local adaptation When assessing or palpating a patient or a dysfunctional
syndrome (LAS) goes through the same stages but affects area, neuromusculoskeletal changes can often be seen to
localized areas of the body. For example, imagine the tissue represent a record of the body's attempts to adapt and adjust
response to digging the garden, chopping wood or playing to the multiple and varied stresses that have been imposed
tennis after a period of relative inactivity - an 'acute adap upon it over time. The results of repeated postural and trau
tive response' would result with accompanying stiffness and matic insults over a lifetime, combined with the somatic
aching, followed by resolution of the stress effects after a few effects of emotional and psychological origin, will often
days. Imagine the same activity repeated over and over present a confusing pattern of tense, shortened, bunched,
again, in which adaptive ('training') responses would result, fatigued and, ultimately, fibrous tissue (Chaitow 1989).
leading to chronic tissue responses involving hypertrophy,
possible shortening, strengthening and so on. Anyone who
regularly trains by running or lifting weights will recognize POSTURE, RESPIRATORY FUNCTION AND
this seguence. The body, or part of the body, responds to THE ADAPTATION PHENOMENON
the repetitive stress (running, lifting, etc.) by adapting to the
needs imposed on it. It gets stronger or fitter, unless the Some of the many forms of soft tissue stress responses that
adaptive demands are excessive, in which case it would affect the body include the following (Barlow 1959,
ultimately break down or become dysfunctional (see Basmajian 1974, Dvorak & Dvorak 1984, Janda 1982, 1983,
Fig. 4.1). The acronym SAID (specific adaptation to imposed Korr 1978, Lewit 1985, Simons et a11999, Travell & Simons
demand) has been coined to illustrate this process of the 1992).
4 Causes of musculoskeletal dysfunction 65
]

Ischemia itself has not been considered to be a producer of


Adaptation Shrinking of
Immobilization pain; however, an ischemic muscle that contracts rapidly
to non-use capsular tissues
does produce pain (Lewis 1942, Liebenson 1996, Mense
et al 2001).
However, it is now hypothesized (Ost et al 2006) that
local hypoxia/ischemia creates pain via venous congestion
or temporized arterial perfusion. For example, pelvic
venous microvascular dysfunction and congestion has
been speculated to be a contributing factor in women
Trauma or with chronic pelvic pain (Foong et al 2002). In addition,
repeated Inflammation hypoxia may increase the rate of muscle fatigue and dis
microtrauma comfort. On a cellular level, alterations in oxygen supply
may alter the regulation of cellular respiration, affecting
the onset of impaired Ca2+ handling associated with
such fatigue (Hepple 2002).
Increased tone might also lead to a degree of edema.
Elevated An environment of ischemia results in local energy crisis,
Pain Degeneration compression of which is associated with trigger point formation (Simons
articular cartilage
et aI1999).
Figure 4.2 Changes in biochemistry associated with reduced These factors (retention of wastes/ischemia/edema/trig
physical activity. Redrawn with permission after Liebenson (2006). ger point formation) can all contribute to discomfort
or pain.
Discomfort or pain reinforces hypertonicity.
1. Congenital and inborn factors, such as short or long leg, Inflammation or, at least, chronic irritation may result.
small hemipelvis, fascial influences (e.g. cranial distor Neurological reporting stations in these distressed hyper
tions involving the reciprocal tension membranes due to tonic tissues \vill bombard the CNS with information
birthing difficulties, such as forceps delivery), or tendency regarding their status, leading, in time, to a degree of sensi
to hypermobility (see Chapter 1). tization of neural structures and the evolution of facilita
2. Overuse, misuse and abuse factors, such as injury or tion and its accompanying hyperreactivity.
inappropriate or repetitive patterns of use involved in Macrophages are activated, as is increased vascularity
work, sport or regular activities. and fibroblastic activity (see Chapter 6).
3. Immobilization, disuse (can result in loss of muscles Connective tissue production increases with cross
strength at the rate of 10% per week) (Liebenson 2006) linkage, leading to shortened fascia.
(see Chapter 7). Chronic muscular stress (a combination of the load/'stress
4. Postural stress patterns (see below). and strain' involved, and the number of repetitions or the
5. Inappropriate breathing patterns (see below). degree of sustained influence) results in the gradual
6. Chronic negative emotional states such as depression, development of hysteresis, in which collagen fibers and
anxiety, etc. (see below). proteoglycans are rearranged to produce an altered
7. Reflexive influences (trigger points, facilitated spinal structural pattern (see Chapter 1).
regions) (see Chapter 6). This results in tissues that are far more easily fatigued
and prone to frank damage, if strained.
As a result of these influences, which affect each and every
Since all fascia and other connective tissue is continuous
one of us to some degree, acute and painful adaptive changes
throughout the body, any distortions or contractions that
can occur, thereby producing the dysfunctional patterns and
develop in one region can potentially create fascial defor
events on which neuromuscular therapies focus.
mations elsewhere, resulting in negative influences on
When the musculoskeletal system is 'stressed', by these
structures that are supported by or attached to the fascia,
or other means, a sequence of events occurs as follows.
including nerves, muscles, lymph structures and blood
'Something' (see list above) occurs that leads to increased vessels (Myers 2001).
muscular tone. Hypertonicity in a normal muscle will usually produce
If this increased tone is anything but short term, retention inhibition of its antagonist(s) and aberrant behavior in its
of metabolic wastes may occur, particularly in a decondi synergist(s).
tioned person who is not aerobically fit (Nixon & Chain reactions evolve in which some muscles
Andrews 1996). (postural - type I) shorten while others (phasic - type II)
Increased tone simultaneously leads to a degree of weaken.
hypoxia, localized oxygen deficiency (relative to the tis Because of sustained increased muscle tension, ischemia
sue needs), and the development of ischemia. in tendinous structures occurs, as it does in localized
66 C L I N I CA L A P P L I CATI O N O F N EU R O M U S C U LA R TEC H N I Q U ES : T H E U P PER B O DY

areas of muscles, leading to tendon and attaclunent inflam The chronic adaptive changes that develop in such a sce
mation and the development of periosteal pain. nario lead to the increased likelihood of future acute exacer
Compensatory adaptations evolve, leading to habituaL bations as the increasingly chronic, less supple and less
'built-in' patterns of use emerging, as the CNS learns to resilient biomechanical structures attempt to cope with
compensate for modifications in muscle strength, length additional stress factors resulting from the normal demands
and functional behavior. of modern living.
Abnormal biomechanics result, involving malcoordination For example, Bakker et al (2003) have reported that not
of movement (with antagonistic muscle groups being only do musculoskeletal tissues weaken from overuse or
either hypertonic or weak - for example, erector spinae disuse, but also that the actual shape of the vertebrae and
tightens while rectus abdorninis is inhibited and weakens). the intervertebral discs, as well as the ligaments, adapt and
The normal firing sequence of muscles involved in par adjust to the type of load imposed. This is clearly an exam
ticular movements alters, resulting in muscle substitu ple of a specific adaptation to imposed demand (Conroy &
tion and additional strain (Janda 1982, 1983). Earle 2000) and is supported by Wolff's law (see Chapter 1).
Joint biomechanics are directly influenced by the accu The degree of physiological musculoskeletal adaptation -
mulated influences of such soft tissue changes and can that causes changes to both function and structure - is largely
themselves become significant sources of referred and determined by the magnitude of the load, as well as the use,
local pain, reinforcing soft tissue dysfunctional patterns or misuse, to which the spine is put.
(DeFranca 2006, Schaible & Grubb 1993). Wall den (2000) has described such adaptation sequences
Deconditioning of the soft tissues becomes progressive as a in slightly different terms, identifying both the rate of tissue
result of the combination of simultaneous events involved damage (micro trauma) and the rate of tissue repair as key fea
in soft tissue pain, 'spasm' (hypertonic guarding), jOint tures in the rate of advance toward adaptation exhaustion:
stiffness, antagonist weakness, overactive synergists, etc.
Across the life-span of an organism, or of a tissue, the rate of
Progressive evolution of localized areas of hyperreactivity
repair slowly declines, whilst the rate of cumulative micro
of neural structures occurs (facilitated areas) in paraspinal
trauma to the organism/tissue increases. The point at which
regions or within muscles (myofascial trigger points) (see
the rate of trauma exceeds the rate of repair is the point at
Chapter 6).
which the organism/tissue fails. If repair mechanisms are
In the region of these trigger points (see discussion of
optimal, the organism or tissue should realize its genetic
myofascial triggers, p. 97) a great deal of increased neu
potential. If repair mechanisms are impaired or overloaded,
rological activity occurs (for which there is EMG evi
potential is not realized, and adaptation will fail.
dence) that is capable of adversely influencing distant
tissues (Hubbard 1993, Simons 1993, Simons et aI1999). This observation highlights a need to focus on both reduction
Energy wastage, due to unnecessarily sustained hyper of microtrauma as well as enhancement of repair potentials
tonicity and excessively active musculature, leads to gen (nutrition, etc.).
eralized fatigue as well as to a local 'energy crisis' in the
local tissues (see trigger point discussion, p. 97).
AN EXAMPLE OF 'SLOW' ADAPTATION
More widespread functional changes develop - for exam
ple, affecting respiratory function and body posture - with Consider the cumulative effects of a leg-length imbalance.
repercussions on the total economy of the body. Using data on leg-length inequality, obtained by accurate
Induction of muscle hypertonicity is part of the alarm and reliable x-ray methods, Knutson (2005) fOlmd the preva
reaction of the flight/fight alarm response. In the pres lence of anatomic leg length inequality to be 90%. The evi
ence of a constant neurological feedback of impulses to dence suggested that, for most people, anatomic leg-length
the CNS/brain from neural reporting stations indicating inequality does not appear to be clinically significant until the
heightened arousaL there will be increased levels of psy magnitude reaches approximately 20mm (74").
chological arousal and a reduction in the ability of the Janda (1988) has described the sequence of adaptive
individual, or the local hypertonic tissues, to relax effec changes, resulting from the presence of a significant degree of
tively. This will consequently result in reinforcement of leg shortness, that culminate in back, head, neck and facial
hypertonicity. pain. This is summarized in Chapter 5 (p. 84).
Functional patterns of use of a biologically unsustainable Over time, adaptational modifications may progress from
nature will emerge, probably involving chronic muscu the production of soft tissue changes to evidence of dysfunc
loskeletal problems and pain. tion (e.g. low back pain) and the evolution of actual patho
logical changes. For example, Gofton & Trueman (1971)
At this stage, restoration of normal function requires thera found a strong association between leg length and unilat
peutic input which addresses both the multiple changes eral osteoarthritis (OA) on the side of the anatomically long
that have occurred, and the need for a reeducation of the leg. They noted that all subjects with this type of OA 'had
individual as to how to use his body, to breathe and to carry led healthy active lives prior to the onset of hip pain' and
himself in more sustainable ways. few subjects were aware of any difference in leg length.
4 Causes of musculoskeletal dysfunction 67

They also point out that this form of OA has its onset picture of health. From the shoes we wear to the seats we sit
around the age of 53, but acknowledge that many people upon, to the awkward positions we assume in the work
with precisely this anatomic asymmetry failed to develop environment, daily activities have perhaps the most pro
an arthritic hip, suggesting that factors other than the leg found impact. Further discussion of the myriad of static and
length disparity are also important. dynamic influences is found in Volume 2 of this text.
This underscores the importance of the context in which
these mechanical adaptations are being processed by the tis
sues under stress - with some joints becoming arthritic and
MAKING SENSE OF THE PIC TURE
others not.
It may be useful to ask what the other variables were that
Motor control is a key component in injury prevention and
allowed some people with significant leg length discrepan
loss of motor control involves failure to control joints, com
cies to avoid arthritic changes and others to develop
monly due to incoordination of the agonist/antagonist mus
them: Nutritional? Genetic? Gender? Weight? Occupation?
cle coactivation (McGill 1998).
Other?
According to Panjabi (1992), three subsystems work
together to maintain spinal stability:

WHAT OF ADAPTATION TO TRAUMA?


the central nervous subsystem (control). This subsystem is
Slow adaptation to overuse, misuse and factors such as an capable of becoming dysfunctional due to anything that
anatomic short leg can be contrasted with the adaptations interferes with nerve function, and can be enhanced by
that occur in response to injury. exercises that focus on improving proprioception (Norris
Lederman (1997) points out that following actual trau 2000b).
matically induced structural damage, tissue repair may lead the osteoligamentous subsystem (passive). The efficiency

to compensating patterns of use, with reduction in muscle of this subsystem can be reduced by injury (or by
force and possible wasting, often observed in backache hypermobility).
patients. If uncorrected, such altered patterns of use inevitably the muscle subsystem (active). This subsystem can be
lead to the development of habitual motor patterns and even impaired by deconditioning and inhibition (for example, by
tually to structural modifications. overactive antagonists, or the presence of trigger points),
The possible adaptational sequelae to trauma may include: and can be enhanced by strength training.

modified proprioceptive function due to alteration in Anything that interferes with any aspect of these features
mechanoreceptor behavior of normal motor control may contribute to dysfunction
inhibition of joint afferents influencing local muscle func and pain.
tion, possibly involving the build-up of metabolic In the discussion below, attention will be given to various
by-products, if joint damage has occurred core elements of the evolution of musculoskeletal dysfunc
altered motor patterns resulting from higher center res tion - including musculoskeletal stress resulting from pos
ponses to injury, possibly involving a sense of insecurity tural, emotional and respiratory causes. These three factors
and the development of protective behavior patterns, interface with each other and reinforce any resulting dys
resulting in actual structural modification, such as mus functions. As will become clear in these descriptions, there
cle wasting is a constant merging and mixing of fundamental influences
associated non-painful reflexogenic responses to pain, on health and ill health. In trying to make sense of a
and also to injury (Hurley 1991). patient's problems, it is frequently clinically valuable to
cluster etiological factors. One model that the authors find
useful divides negative influences into:
WHAT OF ADAPTATION TO HABITS OF USE?
biomechanical (congenital, overuse, misuse, trauma, dis
Habits of use, as well as the close environment that comes in use, etc.)
intimate contact with the body, can have profound effects biochemical (toxicity, endocrine imbalance, nutritional
on tissue tone, flexibility and behavior. Prolonged periods of deficiency, ischemia, inflammation, hydration)
distorted or strained positioning that is often involved in psychosocial (anxiety, depression, unresolved emotional
professional or leisure activities may produce shortened states, somatization, etc.).
and/or weakened, fibrotic, indurated or, in some other way,
dysfunctional tissues. Stresses being loaded onto these Obviously some of these features are inborn, while others are
already compromised tissues that would not have been acquired. Some are easily modified and some are extremely
harmful to normal tissue may result in injury. difficult to change.
Everything that comes in contact with the body, or to Part of the practitioner/ therapist'S role is to help to identify
which the body must conform, is important in the overall what can be most easily modified by treatment or altered
68 C L I N I CA L A P P L I CATI O N OF N E U R O M U S C U LA R TE C H N I Q U E S : THE U P P E R B O DY

behavior - say inhibited or overtight muscles - and the rea result of the CO2 imbalance caused by this breathing
sons for these changes, as well as helping to improve func pattern, or might possibly be breathing in this way because
tion so that the stress load can be better handled (postural of a predisposing anxiety (Chaitow et al 2002, Timmons
and breathing rehabilitation, balance training, etc.). 1994).
The usefulness of this approach is that it allows a focus to
be brought to factors that are amenable to change via (for Interventions that reduce anxiety will help all associated
example): symptoms and these could involve biochemical modifi
cation (herbs, drugs), stress coping approaches (includ
manual methods, rehabilitation, reeducation and exer ing breathing rehabilitation) or psychotherapy.
cise, all of which influence biomechanical factors Interventions that improve breathing function, probably
nutritional or pharmaceutical tactics, which modify bio involving easing of soft tissue distress (including deacti
chemical influences, and vation of trigger points) and/or joint restrictions, as well
psychological approaches, which deal with psychOSOCial as breathing retraining, should significantly help to
influences. reduce symptoms associated with musculoskeletal dys
function.
In truth, the overlap between these causative categories is
so great that in many cases interventions can be randomly The most appropriate approach will be the one that most
selected since, if effective, all will (to some degree) modify closely deals with causes rather than effects and which
the adaptation demands, or will enhance self-regulatory allows for long-term changes that will reduce the likelihood
functions sufficiently for benefit to be noted. of recurrence. Biochemistry, biomechanics and the mind are
seen in this example to be inextricably melded to each other.
In other examples, etiological influences may not always be
EXAMPLE
as clearly defined; however, they will almost always impact
Consider someone who is habitually breathing in an upper on each other.
chest mode, the stress of which will place adaptive The theme of respiratory influence on musculoskeletal
demands on the accessory breathing muscles, with conse dysfunction is explored further, later in this chapter. Before
quent stiffness, pain, trigger point activity (particularly in that, a summary of postural and emotional influences will
the scalenes) and joint involvement. This individual will prepare us for a more comprehensive understanding of one
probably display evidence of anxiety (see below) as a direct of the most important body processes - respiration.

Psychosocial influences - including


depression, anxiety traits, poor stress
I
....I-
.. -------i coping abilities, loneliness, fear,
M
consequences of childhood abuse, etc.
M
U
N
E
Biochemical influences -
including acquired or self-generated S
toxicity, nutrient deficiencies, infectious, r------:=--7'il y
endocrine, allergic and other factors
S Biomechanical influences - including
T structural (congenital, e.g. short leg or
E hyper mobility features, postural or
M traumatically induced characteristics)
....-:--
.. 7-------i or functionally induced changes

The interacting influences of a bio che mical, biomechanical and psychosocial nature (overuse, misuse, e.g. hyperventilation

do not produce single changes. For example: stresses on respiratory mechanisms

a negative emotional state (e.g. depression) produces specific biochemical changes, and structures)

impairs immune function and leads to altered muscle tone.


hyperventilalion modifies blood pH, alters neural reporting (initially hyper and
then hypo), creates feelings of anxiety/apprehension and directly impacts on the
structural components of the thoracic and cervical region - muscles and joints.
altered chemistry affects mood; altered mood changes blood chemistry; altered
structure (posture for example) modifies function and therefore impacts on chemistry
(e.g. liver function) and potentially on mood.
Within these categories - biochemical, biomechanical and psych9social- are to be
found most major influences on health.

Figure 4-3 Biochemical, biomechanical and psychosocial influences on health. Reproduced with permission from Chaitow (2003).
4 Causes of musculoskeletal dysfunction 69

which to accompany more mechanistic interpretations of


POSTURAL AND EMOTIONA L INFLUENCES ON
what may be happening in any given dysfunctional pattern.
MUSCULOSKELETA L DYSFUNCTION
Below is a brief discussion of his work insofar as this relates
to the main theme of this book.
An insightful Charlie Brown cartoon depicts him standing
in a pronounced stooping posture, while he philosophizes
to Lucy that it is only possible to get the most out of being POSTURAL INTERPRETATIONS
depressed if you stand this way. Standing up straight, he
asserts, removes all sense of being depressed. Latey describes the patient entering the consulting room as
Once again, as in the breathing dysfunction example displaying an image posture, which is the impression the
above, we can see how emotions and biomechanics are patient subconsciously wishes you to see.
closely linked. Anything that relieved the depressed state If the patient is requested to relax as far as possible, the
would almost certainly result in a change of body language next image noted is that of slump pasture, in which gravity
and, if Charlie is correct, standing tall should impact (to acts on the body as it responds according to its unique
some extent at least) on his state of mind. attributes, tensions and weakness. Here it is common to
Australian-based British osteopath Philip Latey (1996) observe overactive muscle groups coming into operation -
has found a useful metaphor to describe observable and hands, feet, jaw and facial muscle may writhe and clench or
palpable patterns of distortion that coincide with particular twitch.
clinical problems. He uses the analogy of 'clenched fists' Finally, when the patient lies down and relaxes we come
because, he says, the unclenching of a fist correlates with to the deeper image, the residual posture. Here are to be
physiological relaxation, while the clenched fist indicates found the tensions the patient cannot release. These are pal
fixity. rigidity, overcontracted muscles, emotional turmoil, pable and, says Latey, leaving aside sweat, skin and circula
withdrawal from communication and so on. tion, represent the deepest 'layer of the onion' available to
Latey states: examination.

The 'lower fist' is centered entirely on pelvic function. When


I describe the 'upper fist' I will include the head, neck, shoul CONTRACTION PATTERNS
ders and arms with the upper chest, throat and jaw. The Wha t is seen varies from person to person according to their
'middle fist' will be focused mainly on the lower chest and state of mind and wellbeing. Apparent is a record or psy
upper abdomen. chophysical pattern of the patient's responses, actions,
We find Latey's manner of describing the emotional back transactions and interactions with their environment. The
ground to physical responses a meaningful vehicle with patterns of contraction that are observed and palpated often
have a direct relationship with the patient's unconscious
and provide a reliable avenue for discovery and treatment.
One of Latey's concepts involves a mechanism that leads
to muscular contraction as a means of disguising a sensory
barrage resulting from an emotional state. Thus Latey
describes:

a sensation which might arise from the pit of the stomach


being hidden, masked, by contraction of the muscles
attached to the lower ribs, upper abdomen and the junc
tion between the chest and lower spine
genital and anal sensations which might be drowned out
by contraction of hip, leg and low back musculature
throat sensations which might be concealed with con
traction of the shoulder girdle, neck, arms and hands.

EMOTIONAL CONTRACTIONS

A restrained expression of emotion itself results in suppres


sion of activity and, ultimately, chronic contraction of the
muscles which would be used were these emotions to be
expressed (such as rage, fear, angel joy, frustration, sorrow
Figure 4.4 Cartoon showing Latey's 'middle fist' concept. or anything else). Latey points out that all areas of the body
Reproduced with permission from the Journal of Bodywork and producing sensations that arouse emotional excitement may
Movement Therapies 1996; 1 (1):50. have their blood supply reduced by muscular contraction.
70 CLI N I CAL A P PLI CATI O N OF N E U R O M U SCULA R T E C H N I Q U ES : THE U P P E R B O DY

Also sphincters and hollow organs can be held tight until whereas, in vomiting, it remains in total contraction through
numb. He gives as examples the muscles that surround the out each eliminative wave. Between waves of vomiting the
genitals and anus as well as the mouth, nose, throat, lungs, breathing remains in the inspiratory phase, with upper chest
stomach and bowel. panting. Transversus is slack in this phase. Latey suggests
When considering the 'middle fist', Latey concentrates that often it is only muscle fatigue that breaks cycles of
his attention on respiratory and diaphragm function and laughter/weeping/vomiting.
the many emotional inputs which affect this region. He dis The clinical problems associated with 'middle fist' dys
counts as a popular misconception the idea that breathing is function relate to distortions of blood vessels, internal organs,
produced by contraction of the diaphragm and the muscles autonomic nervous system involvement and alteration in
that raise the rib cage, with exhalation being simply a relax the neuroendocrine balance. Diarrhea, constipation and colitis
ation of these muscles. He states, 'The even flow of easy may be involved, but more direct results relate to lung and
breathing should be produced by dynamic interaction of ... stomach problems. Thus, bronchial asthma is an obvious
two sets of muscles'. example of 'middle fist' fixation.
The active exhalation phase of breathing is instigated, he There is a typical associated posture with the shoulder
suggests, by the following muscles. girdle raised and expanded as if any letting go would pre
cipitate a crisis. Compensatory changes usually include very
1. Transversus thoracis which lies inside the front of the taut, deep neck and shoulder muscles (see Janda's upper
chest and attaches to the back of the sternum, \vhile fan crossed syndrome description, discussed in Chapter 5)
ning out inside the rib cage and then continuing to the (Janda 1983).
lower ribs where the fibers separate. This forms an inverted In treating such a problem, Latey starts by encouraging
'V' below the chest. This muscle, Latey says, has direct function of the 'middle fist' itself, then extending into the
intrinsic abilities to generate all manner of uniquely pow neck and shoulder muscles, while encouraging them to relax
erful sensations, with even light contact sometimes pro and drop. He then goes back to the 'middle fist'. Dramatic
ducing reflex contractions of the whole body or of the expressions of alarm, unease and panic may be seen. The
abdomen or chest. Feelings of nausea and choking and patient, on discussing what they feel, might report sensa
all types of anxiety, fear, anger, laughter, sadness, weep tions of being smothered, drowned, choked, engulfed or
ing and other emotions may be displayed. He discounts crushed.
the idea that the muscle's sensitivity is related to the
'solar plexus', suggesting that its closeness to the internal
'UPPER FIST' FUN CTION S
thoracic artery is probably more significant since, when it
is contracted, it can exert direct pressure on the artery. He The 'upper fist' involves muscles which extend from the
believes that physiological brea thing has, as its central thorax to the back of the head, where the skull and spine
event, a rhythmical relaxation and contraction of this join, and extends sideways to include the muscles of the
muscle. Rigidity is often seen in the patient with 'middle shoulder girdle. These muscles therefore set the relative
fist' problems, where 'control' dampens the emotions positions of the head, neck, jaw, shoulders and upper chest
that relate to it. and, to a large extent, the rest of the body follows this lead (it
2. The other main exhalation muscle is serratus posterior was F.M. Alexander (1932) who showed that the head-neck
inferior, which runs from the lower thoracic and upper relationship is the primary postural control mechanism). This
lumbar spine and fans upwards and outwards over the region, says Latey, is 'the center, par excellence, of anxieties, ten
lower ribs, which it grasps from behind to pull them sions and other amorphous expressions of unease'.
down and inwards on exhalation. These two muscles In chronic states of disturbed 'upper fist' function, he
mirror each other and work together. Latey states that it asserts, the main physical impression is one of a restrained,
is common to find a static overcontracture of serratus overcontrolled, damped down expression. The feeling of the
posterior inferior, with the underlying back muscles in a muscles is that they are controlling an 'explosion of affect'.
state of fibrous shortening and degeneration, reflecting Those experiences that are not allowed free play on the face
'the fixity of the transversus, and the extent of the emo are expressed in the muscles of the skull and the base of the
tional blockage'. skull. This is, he believes, of central importance in problems of
headache, especially migraine. Says Latey, 'I have never seen
a migraine sufferer who has not lost complete ranges of facial
'MIDDLE FIST' FUN CTIONS
expression, at least temporarily'.
Latey reports that laughing, weeping and vomiting are three
emotional 'safety valve' functions of 'middle fist' function,
Effects of 'upper fist' patterns
used by the body to help resolve internal imbalance. Anything
stored internally that cannot be contained emerges explo The mechanical consequences of 'upper fist' fixations are
sively via this route. In laughing and weeping, there is a many and varied, ranging from stiff neck to compression fac
definite rhythm of contraction/relaxation of transversus tors leading to disc degeneration and facet wear. Swallowing
4 Causes of musculoskeletal dysfunction 71

and speech difficulties are common, as are shoulder dys the scope of this text. However, it is important to consider
functions including brachial neuritis, Reynaud's syndrome emotional influences, particularly those that are most
and carpal tunnel problems. impacting.
Latey states: What are the backgrounds to feelings that Latey conjures
up in his 'clenched fist' model of physical contraction and
The medical significance of 'upper fist' contracture is mainly
congestion - of being stressed, pressured, tense, anxious?
circulatory. Just as 'lower fist' contraction contributes to
Without doubt, there are probably as many different back
circulatory stasis in the legs, pelvis, perineum and lower
grounds as there are people affected. However, some common
abdomen, so may 'upper fist' contracture have an even more
elements seem likely, and most of these have become familiar
profound effect. The blood supply to the head, face, special
to us through the popular media - with 'life events' and
senses, the mucosa of the nose, mouth, upper respiratory
'type A personality' being among the most obvious.
tract, the heart itself and the main blood vessels are con
trolled by the sympathetic nervous system and its main
'junction boxes' (ganglia) lie just to the front of the verte Life events
brae at the base of the neck.
Holmes & Rahe (1967) studied some 5000 people who had
Thus, headaches, eye pain, ear problems, nose and throat as recently been ill, inquiring into the 'events' that had taken
well as many cardiovascular troubles may contain strong place over the previous 12 months. Using questionnaires that
mechanical elements relating to 'upper fist' muscle contrac listed both major events, such as 'death of a spouse' (100
tions. Latey reminds us that it is not uncommon for cardio points or 'life crisis units'), 'divorce' (60 points), as well as
vascular problems to manifest at the same time as chronic minor ones such as 'moving house' (15 points) and 'taking a
muscular shoulder pain (such as avascular necrosis of the minor loan' (10 points), they were able to demonsh'ate a
rotator cuff tendons) and that the longus colli muscles are cumulative effect.
often centrally involved in such states. If the 'score' resulting from the 50 or so questions totaled
He looks to the nose, mouth, lips, tongue, teeth, jaws and 250 or more, an 80% risk of serious illness within 2 years
throat for evidence of functional change related to 'upper was suggested. Different scores carried with them varying
fist' dysfunction, with relatively simple psychosomatic percentages of risk, although it was recognized that people
disturbances underlying these. Sniffing, sucking, biting, had different degrees of stress susceptibility, meaning that
cheWing, tearing, swallowing, gulping, spitting, dribbling, for some people a far lower score than 250 might suggest
burping, vomiting, sound making and so on are all signifi significant risk.
cant functions which might be disturbed acutely or chroni The attractiveness of the model constructed by Rahe &
cally. These patterns of use can all be approached via Holmes was that it illustrated the cumulative effect of a
breathing function. number of minor stresses as having the same potential to
When all the components of the 'upper fist' are relaxed, the cause harm (if not adequately adapted to) as major events.
act of expiration produces a noticeable rhythmical move This is a concept that Selye (1956) had identified in his
ment. The neck lengthens, the jaw rises slightly (rocking the model of the general adaptation syndrome. It also allowed
whole head), the face fills out, the upper chest drops. When a rough and ready picture of vulnerability. However, a
the patient is in difficulty [ may try to encourage these number of provisos need to be made in relation to the accu
movements by manual work on the muscles and gentle racy of the 'life event' model.
direction to assist relaxed expiration. Again, by asking the 1. Correlation does not prove cause. In other words, because
patient to let go and let feelings happen, I encourage resolu many people had become ill within a certain time of a
tion. Specific elements often emerge quite readily, especially major, or a number of minor, stress events, this did not
those mentioned with the 'middle fist', the need to vomit, prove that the stresses caused the illness, only that there
cry, scream, etc.
was a probable link.
Note: More detail of Latey's perspective regarding 'lower 2. The way the scale was created did not allow for individ
fist' function is presented in Volume 2 of this book, which ual variations in the way people respond to the stresses
deals with the lower body. affecting them.
3. Nevertheless the questionnaire and scale offers a relatively
simple way of scoring the amount of stress people are
BEHAVIOR AN D PERSON ALITY ISSUES
suffering, suggesting their current risk of becoming ill.
In this segment, focus will be on the everyday contributory
states ('anxiety', 'tension' and 'stress') that add to muscu
Type-A personality
loskeletal distress, arising from a background of what may
be termed exaggerated emotional states. The authors have Within the framework of behavior and personality, as it
deliberately avoided discussion of the potential biomechani relates to how stress is handled, the now (in)famous Type-A
cal influences of true psychological illness as they lie beyond personality is a major feature.
72 C L I N I CAL A P P L I CATI O N OF N E U R O M USCU LAR TECHN I Q U ES : THE U P P E R B O DY

Alarm reaction is perceived as challenging rather than threatening, then


he/ she is more likely to cope successfully with stress. The
person without hardiness characteristics tends to have poor
self-image and commitment; feels vulnerable to the vicissi
tudes of life, as though at the mercy of fate; and feels threat
ened rather than challenged.
The hardy individual recognizes that while we cannot
always control events in our external world, we have the
ability to control how we view these events and the emo
tional response we choose to have to them.
Minor stress events - Among the main features of hardiness are:
individually incapable of
an internal sense of control
triggering alarm reaction
action orientation (not passive)
high levels of self-esteem
A combination of minor stresses, each incapable of
having a life plan with established priorities.
triggering an alarm reaction in the general adaptation
syndrome can, when combined or sustained, produce The important aspect of knowledge of hardiness is that it can
sufficient adaptive demand to initiate that alarm.
be acquired. It is possible, by a process of awareness and
In fibromyalgia a combination of major and minor adoption of new ways of viewing and dealing with life
biochemical, biomechanical and psychosocial stressors
events, that a vulnerable individual can begin to 'stress
commonly seem to be simutaneously active.
proof him/herself and can become 'hardy' (Wooten 1996).
Figure 4.5 Schematic representation of multiple minor stressors The importance of these simple concepts is as important
producing similar effect to sing le major stress event. in the context of musculoskeletal dysfunction as it is in rela
Reproduced with permission from Chaitow (2003). tion to general health concerns.

Type A has been defined as a person with an 'action


CAUTIONS AN D QUESTION S
emotion complex' with a 'tendency to aggressively struggle --

to achieve more and more in less and less time' (Booth There is (justifiably) intense debate regarding the question
Kewley & Friedman 1987). This is the 'workaholic' individual, of the intentional induction of 'emotional release' in clinical
feverishly working to deadlines, often - as Norman Cousins settings in which the therapist is relatively untrained in
(1979) showed - with a tendency to cardiac disease (Booth psychotherapy.
Kewley & Friedman 1987).
If the most appropriate response an individual can cur
There is unlikely to be an easy ability to relax, and if exer
rently make to the turmoil of their life is the 'locking
cise is taken it is also likely to be with great intensity. A car
away' of the resulting emotions into their musculoskele
toon of a patient speaking to his doctor sums up the nature
tal system, what is the advisability of unlocking the emo
of the true Type-A individual: 'I am learning to relax doctor,
tions that the tensions and contractions hold, especially
but I want to relax better and faster ... in fact I want to be at
when the practitioner has no training and the patient has
the cutting edge of relaxation as quickly as possible. '
no skills with which to handle those emotions?
The bodyworker attempting t o relax the muscles o f a
If there exists no current ability to mentally process the
Type-A patient is fighting an uphill battle, unless an internal
pain that these somatic areas are holding, are they not
awareness of the problem is achieved, accompanied by
best left where they are until counseling or psychother
behavior modification.
apy or self-awareness leads to the individual's ability to
reflect, handle, deal with and eventually work through
Hard iness the issues and memories?
What are the advantages of triggering a release of emo
But there are healthy Type-As, just as there are people who
tions, manifested by crying, laughing, vomiting or what
cope adequately and actually seem to suffer little ill-effect
ever - as described by Latey and others - if neither the
physically or mentally, even though they endure severe
individual nor the therapist can then take the process to a
overload of 'life events'. This appears to be because they
healthier position?
carry the attributes of what has been termed 'hardiness'
(Kobassa 1983, Maddi & Kobassa 1984). In the experience of one of the authors (LC) there are indeed
The key 'hardiness factors' that increase a person's patients whose musculoskeletal and other symptoms are
resilience to stress and prevent burnout are commitment, patently linked to devastating life events (torture, abuse,
control and challenge. If an individual has a strong commit witness to genocide, refugee status and so on) to the extent
ment to him/ herself; and believes that he /she is in control that extreme caution is called for in addressing obvious
of the choices in life (internal locus of control); and if change symptoms for the reasons suggested above.
4 Causes of musculoskeletal dysfu nction 73

What would emerge from a 'release'? How would the stress can hav on associated tissues, starting with diaphrag
person handle it? The truth is that there are many examples matic weakness.
in modern times of people whose symptoms represent the
The main factors which determine the maintenance of the
end result of appalling social conditions and life experiences.
abdominal viscera in position are the diaphragm and the
Healing may require a changed life (often impossible to envis
abdominal m uscles, both of which are relaxed and cease to
age) or many years of work with psychological rehabilitation,
support in faulty posture. The disturbances of circulation
and not interventions that address apparent symptoms,
resulting from a low diaphragm and ptosis may give rise to
which may be the merest tips of large icebergs.
chronic passive congestion in one or all of the organs of the
The contradictory perspective to these questions suggests
abdomen and pelvis, since the local as well as general
that there would not be a 'spontaneous' release of 'emotional
venous drainage may be impeded by the failure of the
baggage' unless the person was able to intellectually and
diaphragmatic pump to do its full work in the drooped body.
emotionally handle whatever emerged from the process.
Furthermore, the drag of these congested organs on their
This is indeed a debate without obvious resolution. The
nerve supply, as well as the pressure on the sympathetic
authors feel it worthy of exposure in this context but cannot
ganglia and plexuses, probably causes many irregularities
offer definitive answers. These questions are intended to be
in their function, varying from partial paralysis to over
thought-provoking. It is suggested that each patient and
stimulation. All these organs receive fibers from both the
each therapist/practitioner should reflect on these issues
vagus and sympathetic systems, either one of which may be
before removing (however gently and however temporarily)
disturbed. It is probable that one or all of these factors are
the defensive armoring that life may have obliged vulnera
active at various times in both the stocky and the slender
ble individuals (almost all of us at one time or another) to
anatomic types, and are responsible for many functional
erect and maintain. It may be that, in some circumstances, an
digestive disturbances. These disturbances, if continued
individual's 'physical tensions' may be all that are prevent
long enough, may lead to diseases later in life. Faulty body
ing him/her from fragmenting emotionally.
mechanics in early life, then, becomes a vital factor in the
It is important to differentiate between the skill to pro
production of the vicious cycle of chronic diseases and pres
voke an emotional release and the skill to adequately
ents a chief point of attack in its prevention . . . In this
process the resulting emotional instability. Many trainings
u pright position, as one becomes older, the tendency is for
teach the skills to provoke emotional release, but few offer
the abdomen to relax and sag more and more, allowing a
any training whatsoever in appropriate steps to resolution.
ptosic condition of the abdominal and pelvic organs unless
Practitioners who practice 'emotional release' techniques
the supporting lower abdominal muscles are taught to con
are responsible for also acquiring training, skills and proper
tract properly. As the abdomen relaxes, there is a great ten
licensure to ensure safe handling of the patient's emotional
dency towards a drooped chest, with narrow rib angle,
state, regardless of whether the emotional release courses
forward shoulders, prominent shoulder blades, a forward
provided those skills as part of the training.
position of the head, and probably pronated feet. When
At the very least we should all learn skills that allow the
the human machine is out of balance, physiological func
safe handling of 'emotional releases' that may occur with
tion cannot be perfect; muscles and ligaments are in an
out deliberate efforts to induce them. And we should have a
abnormal state of tension and strain. A well-poised body
referral process in place to direct the person for further pro
means a machine working perfectly, with the least amount
fessional help.
of muscular effort, and therefore better health and strength
As a first-aid approach, should such an event occur dur
for daily life.
ing or following treatment, emphasis should be on initiat
ing calm, and this may best be achieved through slow Note how closely Goldthwaite mirrors the picture Janda
breathing, focusing on the outbreath. The patient should be paints in his upper and lower crossed syndrome and 'pos
allowed to talk if he/she wishes but, unless adequately ture and facial pain' descriptions (see Chapter 5, p. 84).
h'ained, the practitioner should avoid any attempt to advise Also note the descriptions of faulty body mechanics, a.nd
or to try to 'sort out' the patient's problems. The focus should try to imagine that same individual standing in a balanced
be on helping the patient through the crisis to a state of calm manner while breathing in a slow, deep, relaxed way. The
before offering an appropriate referral. idea of normal postural or respiratory (or almost any other
physiologic) function emerging from an unbalanced and
crowded, anatomically compromised structure, is far-fetched
POSTURAL IM B A LANC E AND THE at best.
DIAPHRAGM (Goldthwa ite 1 945) Goldthwaite, in his description above, speaks of 'the fail
ure of the diaphragmatic pump' being able to do its work in
Goldthwaite, in his classic 1930s discussion of posture, links a 'drooped body'. This highlights one of the key elements
a wide array of health problems to the absence of balanced required to normalize posture and breathing pattern disor
posture. Clearly, some of what he hypothesized remains ders. There is a need not only to encourage (and teach if
conjecture but we can see j ust how much impact postural possible) better brea thing and postural habits, but also to
74 C L I N I CA L A P P L I CAT I O N O F N E U R O M U S C U LA R TE C H N I Q U E S : T H E U P P E R B O DY

focus attention on the drooped and crowded structures that upon neural circuits that are shared by pathways that medi
will, over time, have become compromised - and which will, ate autonomic control, vestibuloautonomic interactions and
unless appropriately treated (loosened, stretched, mobilized, anxiety:
etc.), be virtually unable to improve their function.
A key measure of good posture is optimal balance. The core of this circuitry is a parabrachial nucleus network,
consisting of the parabrachial nucleus . . . a site of conver
BALAN CE gence of vestibular information processing, and somatic and
visceral sensory information processing, in pathways that
Maintaining body balance and equilibrium is a primary role appear to be involved in avoidance conditioning, anxiety,
of functionally coordinated muscles, acting in task-specific and conditioned fear.
patterns, and this is primarily dependent on normal motor
control (Winters & Crago 2000). At its simplest, balance depends on optimal motor control,
Without doubt, balance largely depends on adequate and motor control depends on coordinated neurological
proprioceptive input, as discussed in Volume 2, Chapter 2. direction. Feelings of anxiety - such as can be triggered by
Without a steady flow of proprioceptive information (deriv breathing pattern disorders - or imbalances such as those
ing from the eyes, inner ear, muscles and joints of the entire described above (also see notes on deconditioning below),
body) reaching the higher centers, balance is going to be result in poor motor control, unbalanced body function, and
compromised. the likelihood of malcoordinated use patterns. Resultant
Balaban & Theyer (2001) have examined the neurological adaptations lead to shortening of postural muscles, inhibi
basis for links between balance control and anxiety, based tion of phasic muscles and the evolution of trigger points.

Body goes on
alert (the 'fight
or flight' response)

Symptoms Rapid pulse, Upper body


are frightening sweating, tension; breathing
butterflies in the becomes more
Psychological effects: stomach, rapid
tiredness, sensory tense muscles,
disturbance, dizziness Nociceptors 'twitchiness'
Physical effects: exhaustion, more sensitive Aching shoulders,
tingling, cramps, weakness, - increases head and
etc. pain perception neck pain

Increased dioxide lost


swallowing rate through
and bloating overbreathing
Low calcium
causes nerves and
muscles to
Blood pH
function poorly Calcium
becomes more
lost in urine
alkaline as carbonic
acid is mobilized

Smooth muscles constrict,


reducing arterial blood supply
to the brain and tissues,
leading to fatigue and
'brain fog'

4.6 Negative health infl uences of a dysfunctional breathing pattern such as hyperventilation. Reproduced with permission from
F i g u re
Peters et a I (2002).
4 Causes of musculoskeletal dysfunction 75

These thoughts offer an example of the meeting poin t of The products of this process, which is more extreme in
mind and body - where biochemistry, biomechanics and deconditioned individuals, include the b uild-up of acids,
the mind interact seamlessly. Here we can see emotions such as lactic and pyruvic acids (Fried 1987) . As lactate
(anxiety, for example) influencing function (brea thing), aCCLUTIulates in muscle cells and the bloodstream, pH reduces
while at the same time being aware tha t the reverse is also and this triggers a homeostatic retention of bicarbonate
true, that an habitual breathing pa ttern can trigger anxiety. (part of renal function) in an attempt to balance the increasing
Whichever way round this cause-and-effect cycle goes, the acidity. This, in turn, stimula tes the brea thing rate, causing
end result is - a series of disturbed neurological and func CO2 levels to drop again, resulting in symp toms of brea th
tional patterns, operating in a biochemically compromised lessness (dyspnea) and fatigue. And the fluctua ting cycle
system, where pH is unbalanced and calcium and magne continues to repeat i tself (Lum 198 1 ) .
sium reserves are seriously affected. Out of this environment According t o Nixon & Andrews ( 1996) the outcomes of
emerges the likelihood (virtual certainty) of disturbed bal these events in a decondi tioned individual include:
ance, increased sympa thetic arousal, sensitized neurons,
loss of muscle mass (due partly to poor protein synthesis)
muscular distress, trigger point activity, fatigue and pain
decreased ability to use energy substra tes efficiently
(Chaitow et al 2002).
decreased neurom uscular transmission
These complications from respiratory influences are wor
decreased efficiency in m uscle fiber recrui tment, with
thy of the following deeper investigation.
indications of disruption of normal motor con trol being
apparent (Wittink & Michel 2002).

RESPIRATORY IN F LUENCES Nixon & Andrews (1996) summa rized the emerging symp
toms tha t result from overbrea thing in a decondi tioned
Breathing dysfunction is seen to be at least an associated individual as follows:
factor in most chronically fatigued and anxious people, and
Muscular aching at low levels of effort
almost aU people subject to panic a ttacks and phobic behavior,
Restlessness and heightened sympathetic activity
many of whom also display multiple musculoskeletal symp
Increased neuronal sensitivity
toms. In modern inner cities in particular and early 21st
Constriction of smooth muscle tubes (e.g. vascular, respi
century existence in general, there exists a vast expression
ratory and gastrointestinal) tha t can accompany the basic
of respiratory imbalance, as seen in paradoxical brea thing,
symptom of inability to make and sustain normal levels
upper chest breathing and chronic hyperventilation (Aust &
of effort.
Fischer 1997, Cholewicki & McGill 1996, Hodges et aI 200 1 ) .
A s a tendency toward upper chest brea thing becomes In practice this means tha t pa tients who are not aerobically
more pronounced, biochemical imbalances occur when fi t are the most likely individuals whose motor con trol will
excessive amounts of carbon dioxide (C02) are exhaled, be impaired, and who will be most vulnerable to muscle
leading to relative alkalosis, which automatically produces and joint - particularly the spine - dysfunction (Panjabi
a sense of apprehension and anxiety. This condition of res 1992).
piratory al kalosis frequently leads to panic a ttacks and pho
bic behavior, from which recovery is possible only when
RESP I RATORY EN TRAIN MEN T AN D CORE
breathing is normalized (King 1988, Lum 198 1 ) .
STABILITY ISSU ES
Since carbon dioxide is one of the major regulators of
cerebral vascular tone, any reduction due to hyperventilation Diaphragm and transversus abdominis tone are well estab
patterns leads to vasoconstriction and cerebral oxygen defi lished as key features in the provision of core stability (Panjabi
ciency. Whatever oxygen there is in the bloodstream then 1992). There is evidence tha t increased intraabdominal pres
has a tendency to become more tightly bound to its hemo sure (lAP), even with limited participa tion of the abdominal
globin carrier molecule, leading to decreased oxygenation or back muscles, augments the stability of the spine (Hodges
of tissues. All this is accompanied by a decreased threshold et al 2001, 2005).
of peripheral nerve firing. Recent data confirm that the activity of the diaphragm
occurs in association with tasks tha t challenge the stabi lity
of the spine (Hodges & Gandevia 2000a,b, Hodges et al
E F FECTS OF RESPIRATORY AL KALOSIS IN A
1997). When, however, a challenge occurs that ma kes pos
DECON DITION ED IN DIVIDUAL
tural/stabilizing demands on the diaphragm at the same
Oxygen is a necessary ingredient of ATP (energy) production time that respiratory demands are occurring, it is the stability
in normal tissues. However, when respiratory alkalosis occurs, element that s uffers.
the activation of anaerobic energy pathways starts (anaero Using a 1 0% CO2 gas mixture to elevate breathing, McGill
bic glycolysis - the p roduction of energy in the relative et al (1995) demonstrated that reduction in the support offered
absence of oxygen), leading to an accumulation of incom to the spine by the muscles of the torso may occur if there is a
pletely oxidized products of metabolism (Fried 1987). load challenge to the low back combined with a breathing
76 C L I N I CA L A P P L I CAT I O N O F N E U R O M U S C U LA R TE C H N I Q U E S : TH E U P P E R B O DY

challenge (shovelling snow is given as an easily understood


Box 4. 1 Partial pressure symbols
example in real-life ra ther than under research conditions) .
'Modula tion of muscle activity needed to facilitate breath Partial pressure was formerly symbolized by p, followed by the
ing may compromise the margin of safety of tissues that chemical symbol in capital letters (e.g. pC02, p02)' Curre ntly, in
depend on constant muscle activity for support: respiratory physiology, P, followed by subscripts, denotes location
and/or chem ical species (e.g. PC02, P02, PaC02).
McGill et al offer the dramatic example of an individual
shovelling snow, placing enormous torsional and shear PC02 = partial p ressure of carbon d ioxide
forces onto the spine, while breathing rapidly. Other exam P02 = p a rtial pressure of oxygen
PaC02 = arterial carbon dioxide tension (where a = arterial)
ples come to mind in both work and leisure settings, but
wha tever the particular scenario, spinal stress, combined
with rapid brea thing, presents the control mechanisms of
the body with choices, and survival (i.e. breathing) clearly
Box 4.2 Hyperventilation in context
takes precedence over stability in that contest.
To amplify McGill's message, Hodges et al (2001) noted The sim plest d efinition of hyperve ntilation is that it represents a
tha t after approximately 60 seconds of overbreathing, both pattern of (over)breathing which is in excess of metabolic requ ire
the postural (tonic) and phasic functions of the diaphragm ments. It is normal to hyperventilate ('puffing and panting') in
and transversus abdominis are reduced or absent. 'The association w ith physical exertion, such as running, or if there
exists a heig htened degree of acid in the bloodstream (acidosis),
present data suggest tha t increased central respira tory d rive
possibly a result of kidney or liver d isease. I n these examples the
may a ttenuate the postural commands reaching motoneu rapid breathing p attern produces a reduction i n acid ity v i a
rons. This a ttenuation can affect the key inspiratory and exh a l ation o f CO2 and i s therefore seen to b e help ing to resto re
expira tory muscles, and is likely to be co-ordinated at a pre normal acid - a l k a l ine balance (pH 7.4).
motoneuronal site.' It is when a p attern of overbre ath ing occurs without an
associated acidosis that problems arise, as this leads to alkalosis
Hodges et al further hypothesize:
and all the sym ptoms w h ich flow from t h at state (see m a in text
Although investigation of spinal mechanics is required to for details).
There are m a ny ind ividuals whose blood g as profile would not
confirm the extent to which spinal control is compromised by
categorize them as h aving reached a state of true hyperventila
increases in respiratory demand, it is hypothesised that such a tion, but who are clearly prog ressing toward that state. It is such
compromise may lead to increased potential for injury to individu als who often display many of the e a rly signs of chronic
spinal structures and reduced postural control. During stren unwellness, ranging from fatigue to chronic muscular pains and
llOUS exercise, when the physical stresses to the spine are
loss of concentration. These individuals may well benefit from a
combination of stress m a n agement, musculoskeletal norm aliza
greater, the physiological vulnerability of the spine to injury is
tion and breathing retraining approaches.
likely to be increased.

Clearly other spinal support is required to take over when


this sort of reduction occurs in primary stabilizing muscles;
individual performing regular arm or leg movement in
however, whether the additional stability is in fact available
work or leisure activity, is obvious.
will depend on the overall level of fitness and tone.
Leaving aside all other considerations outlined in this
Studies by O'Su llivan et al (2002) have also indica ted that
chapter, the influence of upper chest (non-diaphragmatic)
people with sacroiliac pain have impaired recruitment of
overbreathing alone can be seen to be capable of compro
the diaphragm and pelvic floor.
mising spinal stability.
Hodges et al (2001) also investiga ted respiratory and pos
tural diaphragm function during repetitive upper limb
movement and showed a virtual entrainment between limb
SUMMARY OF EFFECTS OF HYPERVEN TILAT I ON
movement and respiratory rate. 'Results indicate tha t activ
ity of human phrenic motoneurones is organised such tha t Reduction in PC02 (tension or partial pressure of carbon
it contributes to both posture and respiration during a task dioxide) causes respiratory alkalosis via reduction in arte
which repetitively challenges trunk posture.' rial carbonic acid, which leads to abnormally decreased
Peper (2004) has recorded the effect on breathing rate (as arterial carbon dioxide tension (hypocapnia) and major
well as on the EMG activity of the scalenes and forearm systemic repercussions (see Figs 4.6 and 4.7,.
extensors) of an individual sitting with hands on Jap, mov The first and most direct response to hyperventilation is
ing the hands to the keyboard, and then starting to type. cerebral vascular constriction, reducing oxygen availability
The breathing rate goes from a slow rhythm to rapid as the by about 50%.
EMG activity increases during the stages mentioned, and Of aU body tissues, the cerebral cortex is the most vulnera
reverses as the person stops typing with hands still on the ble to hypoxia, which depresses cortical activity and causes
keyboard, and then returns to the initial calm state when dizziness, vasomotor instability, blurred consciousness
hands return to the lap. The implications, relative to the respi ('foggy brain') and visual disturbances.
ratory rate and all that th.is means relative to the health of an Loss of cortical inhibition results in emotional lability.
4 Causes of musculoskeletal dysfunction 77

1 . Upper fixator overactivity


Breathing in shor tening of accessory
excess of breathing muscles
Reduced PC02
metabolic 2. Painful nodules in nape of
= respiratory alkalosis
requirements neck, anterior chest and

I shoulder girdle


3. Temporal headaches
4. Painful legs
5. Whole body expresses
'Tetany, muscle spasm, 'Sympathetic dominance - dilated 'Increased neuronal activity
tension - cannot relax in
paresthesia pupils, dry mouth, sweaty palms, gut speeding spinal reflexes as well
any position
Increased neuronal irritability and digestive dysfunction, abdominal (initially) as heightened pain
Reduced blood flow to brain, bloating, tachycardia perception + photophobia,
limbs and heart + hyperacusis

Dizziness, light headedness,

'foggy brain'
Cold extremities
'all these symptoms are increased during progesterone phase of menstrual cycle ..... Chest pain
Anxiety, apprehension (sense
of mild panic)
Depressed cortical activity
Vasomotor instability, blurring
Increased circulating histamines of consciousness and vision
make allergic reaction more Loss of cortical inhibition results
violent and possibly more likely in emotional lability

Figure 4.7 Negative health infl uences of a dysfunctional breathing pattern such as hyperventilation.

N EURAL REPERCUSSI ON S most likely to be affected and these are also common sites for
active myofascial trigger points (Timmons 1994).
Loss of CO2 ions from neurons during moderate hyperven
tilation stimulates neuronal activity, while producing mus Painful muscular contractions (,nodules') develop and

cular tension and spasm, speeding spinal reflexes as well as are easily felt in the nape of the neck, anterior chest and
producing heightened perception (pain, photophobia, hyper shoulder girdle.
acusis) - all of which are of major importance in chronic pain Temporal headaches centered on painful nodules in the
conditions. \A/hen hypocapnia is more severe or prolonged parietal region are common.
it depresses neural activity until the nerve cell becomes Sympathetic dominance is evident by virtue of dilated
inert. pupils, dry mouth, sweaty palms, gut and digestive dys
What seems to occur in advanced or extreme hyperventi function, abdominal bloating and tachycardia.
lation is a change in neuronal metabolism; anaerobic glycol Allergies and food intolerances are common due to
ysis produces lactic acid in nerve cells, while lowering pH. increased circulating histamines.
Neuronal activity is then diminished so that in extreme
hypocapnia (reduced levels of CO2), neurons become inert.
BIOMECHAN ICAL CHAN GES IN RESPONSE TO
Thus, in the extremes of this clinical condition, initial hyper
UPPER CHEST BREATHI N G
activity gives way to exhaustion, stupor and coma (Lum
1981). \"ihereas Goldthwaite (1945), Janda ( 1 982) and others point
to the collapse of normal posture leading inevitably to
changes which preclude normal breathing function, Garland
TETANY (1994) presents the picture in reverse, suggesting that it is the
functional change of inappropriate breathing (e.g. hyper
According to Stedman's Medical Dictionary (2004) tetany is
ventilation or upper chest patterns of breathing) that ulti
characterized by muscle twitches, cramps and cramping of
mately modifies structure. It was Garland who coined the
the hands and feet and, if severe, may include laryngospasm
memorable phrase 'where psychology overwhelms physi
and seizures. These findings reflect irritability of the central
ology' to describe the changes which occur.
and peripheral nervous systems, which may result from
Garland describes the somatic changes that follow from a
low serum levels of ionized calcium or, rarely, magnesium.
pattern of hyperventilation and upper chest breathing:
A reduced degree of CO2 resulting in excessive alkalinity
can also produce this effect. A degree of visceral stasis and pelvic floor weakness will
In tetany that is secondary to alkalosis (excessive alkalin develop, as will an imbalance between increasingly weak
ity), muscles which maintain 'attack-defense' mode (hunched abdominal muscles and increasingly tight erector spinae
shoulders, jutting head, clenched teeth, scowling) are those muscles.
78 C L I N I C A L A P P L I CAT I O N OF N E U R O M U S C U LA R T E C H N I Q U E S : T H E U P P E R B O DY

Fascial restriction from the central tendon of the Remember that thefunctional status of the diaphragm is prob
diaphragm via the pericardial fascia, all the way up to the ably the most powerful mechanism of the whole body. It not
basiocciput, will be noted. only mechanically engages the tissues of the pharynx to the
The upper ribs will be elevated and there will be sensi perineum, several times per minute, but is physiologically
tive costal cartilage tension. indispensable to the activity of every cell in the body. A work
The thoracic spine will be disturbed by virtue of the lack ing knowledge of the crura, tendon, and the extensive ramifi
of normal motion of the articulation with the ribs and cation of the diaphragmatic tissues, graphically depicts the
sympa thetic outflow from this area may be affected. significance of structural continuity and functional unity. The
Accessory muscle hypertonia, notably affecting the sca le wealth of soft tissue work centering in the powerful mecha
nes, upper trapezius and levator scapulae, will be palpa nism is beyond compute, and clinically it is very practical.
ble and observable.
Fibrosis will develop in these muscles as will myofascial
trigger points (see pp. 65-66). The cen1ical spine will ADDITIONAL EMOTIONAL FACTORS AND
become progressively more rigid, with a fixed lordosis MUSCULOSKELETA L DYS FUNCTION
being a common feature in the lower cervical spine.
A reduction in the mobility of the 2nd cervical segment Use of electromyographic techniques has shown a statis
and disturbance of vagal ou tflow from this region is tical correlation between unconscious hostility and arm
likely. tension as well as leg muscle tension and sexual distur
bances (Shagass & Malmo 1954).
Although not noted in Garland's list of dysfunctions, the Wolff (1948) proved that the majority of patients with
other changes which Janda has listed in his upper crossed headache showed 'marked contraction in the muscles of
syndrome (see p. 82) are likely consequences, including the the neck . . . most commonly due to sustained contrac
potentially devasta ting effects on shoulder function of the tions associa ted with emotional strain, dissatisfaction,
altered position of the scapulae and glenoid fossae as this apprehension and anxiety'.
pattern evolves. Barlow (1959) sums up the emotion/ muscle connection
Also worth noting in relation to breathing function and thus:
dysfunction are the likely effects on two important muscles,
not included in Garland's description of the dysfunctions Muscle is not only the vehicle of speech and expressive gesture,
resulting from inappropriate breathing patterns, quadratus but has at least a finger in a number of other emotional pies -
lumborum and iliopsoas, both of which merge fibers with for example, breathing regulation, control of excretion, sexual
the diaphragm. functioning and, above all, an influence on the body schema
Since these are both postural muscles, with a propensity through proprioception. Not only are emotional attitudes, say,
to shortening when stressed, the impact of such shortening, of fear and aggression, mirrored immediately in the muscle,
uni- or bilaterally, can be seen to have major implications but also such moods as depression, excitement and evasion
for respiratory function, whether the primary feature of have their characteristic muscular patterns and postures.
such a dysfunction lies in diaphragmatic or muscular A comprehensive review by Linton (2000) of over 900
distress. studies involving back and neck pain concluded that
Among possible stress factors that will result in shorten psychological factors play a significant role, not only in
ing of postural muscles is disuse. When upper chest breath chronic but also in the etiology of acute pain - particu
ing has replaced diaphragmatic breathing as the norm, larly in the process of transition to chronicity. 'Stress, dis
reduced diaphragmatic excursion results and consequent tress or anxiety as well as mood and emotions, cognitive
reduction in activity for those aspects of quadratus l umbo functioning, and pain behavior, all were found to be
rum and psoas which are integral with it. Shortening (of significant in the analysis of 913 potentially relevant
any of these) would likely be a result of this disuse pattern. articles.'
Garland concludes his listing of soma tic changes associ
ated with hyperventilation: 'Physically and physiologically We must not ignore the influence of emotion on muscu
[all of] this runs against a biologically sustainable pattern, loskeletal dysfunction at our (and our patients') peril.
and in a vicious cycle, abnormal function (use) alters nor
mal structure, which disallows return to normal function.'
Garland also s ugges ts tha t counseling (for associa ted SELECTIVE MOTOR UNIT INVOLVEMENT
anxiety or depression, perhaps) and breathing retraining (Waersted et a l 1 992, 1 993)
are far more likely to be successfully initiated if the biome
chanical componen t(s), as outlined, are appropriately The effect of psychogenic influences on muscles may be
treated. more complex than a simplistic 'whole' muscle or regional
Pioneer osteopathic physician Carl McConnell (1962) involvemen t. Researchers at the Na tional Institute of
reminds us of wider implications of respiratory dysfunction. Occupational Health in Oslo, Norway, have demonstrated
4 Causes of musculoskeletal dysfu nction 79
J

that a small number of motor units, particularly muscles, The researchers report tha t similar observa tions have been
may display almost constant, or repeated, activity when noted in a pilot study (Waersted et aI 1992).
influenced psychogenical ly. In their study normal individu The implications of this information are profound since
als performing reaction time tasks were evaluated, creating they suggest tha t emotional stress can selectively involve
a 'time pressure' anxiety. Using the trapezius muscle as the postural fibers of muscles, which shorten over time when
focus of attention, the researchers were able to demonstrate stressed (Janda 1983). The possible 'metabolic crisis' sug
low-amplitude levels of activity (using surface EMC) even gested by this research has strong parallels with the evolu
when the muscle was not being employed. They explain tion of myofascial trigger pOints as suggested by Wolfe &
this phenomenon as follows. Simons (1992), a topic which will be discussed in greater
detail in later chapters.
In spite oflow total activity level ofthe muscle, a small pool of
low-threshold motor units may be under considerable load for
prolonged periods of time. Such a recruitment pattern would
be in agreement with the 'size principle' first proposed by CONC LUSION
Henneman (1957), saying that motor units are recruited
according to their size. Motor units with type I [postural] We have observed in this cha pter evidence of the negative
fibers are predominant among the small, low-threshold units. influence on the biomechanical components of the body, the
If tension-provoking factors [anxiety, for example] are f e r muscles, joints, etc., of overuse, misuse, abuse and disuse,
quently present and the subject, as a result, repeatedly whether of a mechanical (posture) or psychological (depres
recruits the same motor units, the hypothesized overload may sion, anxiety, etc.) na ture. We have also seen the interaction
follow. This can possibly result in a metabolic crisis and the of biomechanics and biochemistry in such processes, with
appearance of type I fibers with abnormally large diameters, breathing dysfunction as a key example of this. In the next
or 'ragged-red' fibers, which are interpreted as a sign of mito chapter we will explore some of the patterns which emerge
chondrial overload. (Edwards 1 988, Lnrsson et a1 1 990) as dysfunction progresses.

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81

Chapter 5

Patterns of dysfunction

We have seen something of the interconnectedness of the


CHAPTER CONTENTS structures of the body in Myers' fascial network model. A s
a consequence o f the imposition o f sustained o r acute
Upper crossed syndrome 82
stresses, adaptation takes place in the musculoskeletal sys
Lower crossed syndrome 82
tem and chain reactions of dysfunction emerge. These can
Layer (stratification) syndrome 83
be extremely useful indicators of the way adaptation has
Chain reaction leading to facial and jaw pain: an
occurred and can often be 'read' by the c1i.n ician in order to
example 84
help establish a therapeutic plan of action.
Patterns from habits of use 84
When we observe, palpate and assess, in the many dif
The big picture and the local event 85
ferent ways that are outlined in this chapter (and the rest of
Janda's 'primary and secondary' responses 85
the book), we are operating in present time. Howevel what
Recognizing dysfunctional patterns 86
is being revealed b y such detective work relates to the com
Excessive muscular tone 86
pound culmination of past mechanical, chemical and
Simple functional tests for assessing excess muscular
emotional adaptations (stresses, strains, micro- and macro
tone 87
traumas, toxicities, deficiencies, fears, anxieties, somatizations
Functional screening sequence 88
and more) all overlaid on the unique, inborn idiosyncratic
Prone hip (leg) extension (PLE) test 89
characteristics of the individual.
Trunk flexion test 90
What is being looked at, touched, tested, pressed, stretched
Hip abduction test 90
and evaluated is in the state it is because of everything that
Scapulohumeral rhythm test 91
has ever happened to it, and our task is to make sense of the
Neck flexion test 92
evidence we can gather, to b uild a picture, to tell a story.
Push-up test 92
The evidence that emerges regarding the relative elasticity
Breathing pattern assessments 92
of skin and fascia, the degree and na ture of shortness,
Seated assessment 92
strength, stamina and firing sequences of muscles, the
Supine assessment 93
changes in range of motion of joints, the presence or other
Side lying assessment 93
wise of periosteal pain points, mechanical interference with
Prone assessment 93
nerves and myofascial trigger pOints, or the status of the indi
Trigger point chains 94
vidual's posture, brea thing and balance - all offer clues as to
the current level of adaptation and compensation. These (and
many other) palpable and assessable changes point us to the
processes that have taken, and are taking place, as the body
adapts to aging, gravity and the stresses of life.
Just as an archaeologist patiently and painstakingly gath
ers shards and slivers, and learns to interpret these frag
ments of evidence from the past in order to construct a
picture of what was, of what has been, so we must put
together a coherent representation of why symptoms are as
they are now, and what needs to be done to assist the indi
vidual toward improvement or recovery.
82 CLINICAL A PPLICATION OF NEU ROMUSCULAR TEC HNIQUES: THE U P PE R BODY

This involves ga thering evidence, and then interpreting Pectoralis major and minor
it in the context of the processes of which the individual is Upper trapezius which all tighten
currently part. How tight, loose, weak, bunched, flaccid, Levator scapulae and shorten
symmetrical, balanced, sensitive or painful the tissues are Sternocleidomastoid
can tell a potent story - but we have to add the words, the while
explana tions. Lower and middle trapezius all weaken
Interpretation of the evidence emerges from the sensations Serra tus anterior and rhomboids
that we perceive with our hands, and to which we add the
As these changes take place they alter the relative posi
descriptors that add color and pattern to the story. The thera
tions of the head, neck and shoulders as follows.
peutic choices that emerge from the patient's symptoms, his
tory and the evidence that tests, palpation and assessment 1. The occiput and C1 and C2 will hyperextend, with the
offer are a crucial part of the therapeutic encounter. head being translated anteriorly. There will be weakness
From the accumulated evidence we need to identify what of the deep neck flexors and increased tone in the suboc
it is tha t the individual is adap ting to, the background to the cipital musculature.
presenting symptoms. Inappropria tely focusing on symp 2. The lower cervicals down to the 4th thoracic vertebra will
toms ra ther than on trying to understand the bigger contex be posturally stressed as a result.
tual picture, and then using this to frame stra tegies tha t 3. Rotation and abduction of the scapulae occur as the
encourage self-regulation, is likely t o retard recovery. increased tone in the upper fixators of the shoulder (upper
Intervention calls for therapeutic choices tha t reduce adap trapezius and levator scapulae, for example) causes them
tive demands and / or enhance adaptive capacity - so allow to become stressed and shorten, inhibiting the lower fixa
ing self-regulation to operate more efficiently, while tors, such as serratus anterior and the lower trapezius.
simultaneously preventing exacerbations and recurrences. 4. As a result the scapula loses its stability and an al tered
When a chain reaction develops, in which some muscles direction of the axis of the glenoid fossa evolves, result
shorten (postural, type I) and others weaken (phasic, type ing in humeral instability that involves additional leva tor
II), predictable patterns involving imbalances emerge. Czech scapulae, upper trapezius and supraspinatus activity to
researcher Vladimi r Janda MD ( 1982, 1 983) describes two of maintain functional efficiency.
these, the upper and lower crossed syndromes, as follows.
These changes lead to cervical segment strain, the evolution
of trigger points in the stressed structures and referred pain
to the chest, shoulders and arms. Pain mimicking angina
UPPER CROSSED SYNDROME (FIG. 5.1)
may be noted, plus a decline in respiratory efficiency.
The solution, according to Janda, is to be able to identify
The upper crossed syndrome, also known as the shoulder
the shortened structures and to release (stretch and relax)
neck or proximal crossed syndrome (Liebenson 2006),
these, followed by reeducation toward more appropriate
involves the following basic imbalance.
function. This key underlying pattern of dysfunction will be
found to relate to a great many of the painful conditions of
the neck, shoulder and arm, all of which will be considered
in later chap ters. \Nha tever other local trea tment these
receive, consideration and reform of patterns, such as the
upper crossed syndrome, must form a basis for long-term
rehabilitation.

INHIBITED TIGHT AND/OR SHORT


LOWER CROSSED SYNDROME (FIG. 5.2)
Deep neck flexors Trapezius and levator scapulae

The lower crossed syndrome, also known as the hip-pelvic


or distal crossed syndrome (Liebenson 2006), involves the
following basic imbalance.

Iliopsoas, rectus femoris


TIGHT AND/OR SHORT INHIBITED TFL, short adductors which all tighten
Pectorals Rhomboids and serratus anterior
Erector spinae group of the trunk and shorten
while
Abdominal and gluteal muscles all weaken

Figure 5.1 Upper crossed syndrome (after Janda). Reproduced with The result of this chain reaction is to tilt the pelvis for
permission from Chaitow (1996). ward on the frontal plane, while flexing the hip joints and
5 Patterns of dysfunction 83

exaggerating lumbar lordosis. LS-Sl will have increased The solution for these common pa tterns is to identify both
likelihood of soft tissue and joint distress, accompanied by the shortened and the weakened structures and to set about
pain and irritation. An additional stress feature commonly normalizing their dysfunctional status. This might involve:
appears in the sagittal plane in which:
deactivating trigger points within them or whi ch might
Quadra tus lumborum shortens be influencing them
while normalizing the short and weak muscles with the objec
Gluteus maximus and medius} weaken tive of restoring balance. This may involve purely soft tis
sue approaches or be combined with osseous adjustment/
When this 'la teral corset' becomes unstable the pelvis is
mobilization .
held in increased elevation and is accentuated when walk
ing. This instability results in LS-Sl stress in the sagittal Such approaches should coincide with reeducation of pos
plane, which leads to lower back pain. The combined ture and body usage, if results are to be other than short term.
stresses described produce instability at the lumbodorsal
j unction, an unstable transition pOint at best.
LAYER (STRATIFICATION) SYNDROME
The piriformis muscles are also commonly involved. In
(FIG. 5.3)
10--20% of individuals, the right piriformis is penetrated
by either the peroneal portion of the sciatic nerve or, rarely,
The layer (stratification) syndrome is a combination of upper
by the whole nerve (the incidence of this is greatly increased
and lower crossed syndromes. According to Janda et al
in individuals of Asian descent) (Kuchera & Goodridge 1997).
Piriformis syndrome can therefore produce direct sciatic pres
Muscle hypotrophy Muscle hypertrophy
sure and pain (but not beyond the knee) (Heinki ng et aI 1997).
Arterial involvement of piriformis shortness can produce
ischemia of the lower ex tremity and, through a relative fix
ation of the sacrum, sacroiliac dysfunction and pain in the
hip. Dural dysfunction is also possible when sacral mechan Cervical erector spinae
Upper trapezius
ics are distorted in this way as the deformations place ten Levator scapulae
sion and torsion on the dural tube.
An almost inevitable consequence of a lower crossed
syndrome pattern is that stresses will translate superiorly, Lower stabilizers
thereby triggering or aggrava ting the upper crossed syn of the scapula
drome pattern outlined above. We can once again see how
the upper and lower body interact with each other, not only Thoracolumbar
functionally but dysfunctionally as well. erector spinae

Lumbosacral
erector spinae

Gluteus
maximus

TIGHT AND/OR SHORT INHIBITED


Hamstrings
Erector spinae Abdominals

INHIBITED TIGHT AND/OR SHORT


Gluteus maximus Iliopsoas

Figure 5.2 Lower crossed syndrome (after Janda). Reproduced with Figure 5.3 Layer (stratification) syndrome. Reproduced with
permission from Chaitow (1996). permission from Juli Et Janda (1987).
84 CLINICAL A P PLICATION OF NEUROMUSCULAR TECHNIQUES: T HE U P PER BODY

(2006), this has a poor prognosis for rehabilitation 'because assessed for the role they might be playing in the person's
of the fixed muscle imbalance patterns at the central nerv pain and restriction condi tions and certainly before these
ous system level'. can be successfully and appropriately treated. Various pro
tocols will be ou tlined in later chap ters that can assist in this
form of functional assessment.

CHAIN REACTION LEADING TO FACIAL AND


JAW PAIN: AN EXAMPLE
PATTERNS FROM HABITS OF USE
In case it is thought that such imbalances are of merely aca
The influences in our da ily lives that relate directly to our
demic interest, a practical example of the negative effects of
habits of use in our work environment, homes and leisure
the chain reactions described above is given by Janda
activities greatly affect our musculoskeletal systems. The
(1986). His premise is that TMJ problems and facial pain can
interaction between our bodies and the objects we are clos
be analyzed in relation to the person's whole posture.
est to (clothes, shoes, chairs, objects that we carry and with
Janda has hypothesized that the muscular pa ttern associ
which we interact) can have profound influences on our
ated with TMJ problems may be considered as locally involv
health, modifying the way we function, for good or ill.
ing hyperactivity and tension in the temporal and masseter
As we go about our daily lives, we position ourselves to
muscles while, because of this hypertonicity, reciprocal inhi
perform our work, to play sport, and even to sleep. These
bition occurs in the suprahyoid, digastric and mylohyoid
situations often involve repetitive and/ or prolonged stresses
muscles. The external pterygoid, in particular, often develops
that may lead to shortened, weakened, fibrotic or in other
spasm.
ways dysfunctional tissues. Consider also that these demands
This imbalance between 'jaw adductors' (mandibular
are often placed on tissues that are already compromised by
eleva tors) and 'jaw openers' (mandibular depressors) alters
previous traumas or habits of use.
the ideal position of the condyle and leads to a consequent
For example, consider the person who has recently
redistribu tion of stress on the joint while contributing to
acquired a job that demands a lot of time spent on the tele
degenerative changes.
phone while simul taneously using their hands on the com
Janda describes a typica l pa ttern of muscular dysfunc
pu ter. The job is set in an open environment where the use
tion of an individual with TMJ problems as i nvolving upper
of a speaker phone compromises privacy, so she tends to
trapezius, levator scapulae, scalenii, sternocleidomastoid,
hold the phone with her shoulder while typing with her
suprahyoid, lateral and medial pterygoid, masseter and
hands. The elevation of the shoulder shortens levator scapula
temporalis muscles, all of which show a tendency to tighten
and upper trapezius while side flexion of the neck affects the
and to develop spasm. He notes tha t while the scalenes are
scalene muscle group. Even with the addition of a shoulder
unpredictable, commonly when overloaded, they will
pad to the phone, the habit of holding the phone wedged in
become atrophied and weak and may also develop spasm,
this manner on a frequent, daily basis will lead to changes
tenderness and trigger points.
in the tissues that are being used. However, the problem can
The postural pa ttern associated with TMJ dysfunction
cascade further.
might therefore involve:
As the tissues become chronically tight and her head
1. hyperextension of the knee joints changes position due to lateral flexion (with mandatory
2. increased anterior tilt of the pelvis rotation) of the cervical vertebrae, her center of gravity is
3. pronounced flexion of the hip joints affected. To remedy this, her body must adapt to the offset
4. hyperlordosis of the lumbar spine head position by counterbalancing, a task that is easily
5. rounded shoulders and winged (rotated and abducted) achieved by a tightening of the contralateral quadratus
scapulae lumborum (or erector spinae or any number of other mus
6. cervical hyperlordosis cles). As this adaptation occurs, a cascade of other changes
7. forward head pOSition may erupt, including tightening of adductors, hamstrings
8. compensatory overactivity of the upper trapezius and and/ or gastrocnemius, and even foot pronation (Joss of
levator scapulae muscles plantar vault integri ty) . This, in turn, can affect gait and the
9. forward head position resulting in opening of the mouth ability to deal with ground force reactions as they travel
and retraction of the mandible. back up through the body with every step taken.
Remedies to problems deriving from this sort of back
This series of changes provokes increased activity of the jaw ground of overuse, misuse and abuse of the body are obvi
adductor (mandibular elevator) and protractor muscles, cre ous, and might involve either completely avoiding, or at
a ting a vicious cycle of dysfunctional activity. Intervertebral least changing, the pattern of use (for example, acquiring a
join t stress in the cervical spine follows. headset for the telephone) or performing activi ties to help
The message which can be drawn from this example is counterbalance the negative effects of the behavior in ques
tha t patterns first need to be identified before they can be tion (stretching, toning, exercising, etc.) .
5 Patterns of dysfunction 85

Treatment of patterns of imbalance that result from trauma, muscle spasm


or from habitually stressful patterns of use, needs to address and a sequence of events which would then include com
the causes of residual pain, as well as a im to improve these pensation and adapta tion responses in many muscles,
patterns of voluntary use, with a focus on rehabilitation followed by the evolution of a variety of possible syn
toward normal proprioceptive function. In Volume 2 of this dromes involving head/ neck, TMJ, shoulder / arm or
textbook, some of the important influences of the close envi others.
ronment and habits of use are discussed and perspectives
Janda's point is that after all the adapta tion that has taken
emerge that will encourage practitioners to use their own
place, treatment of the most obvious cervical restrictions,
bodies more efficien tly and less stressfully, as well as being
where the person might be aware of pain and restriction,
able to advise and guide their recovering patients appropri
would offer limited benefit. He points to the existence of
ately regarding the everyday influences of their close envi
oculopelvic and pelviocular reflexes, which indicate tha t
ronments. Active, dynamic rehabilitation processes tha t
any change in pelvic orienta tion alters the position o f the
reeducate the individual and enhance neurological organi
eyes and vice versa, and to the fact tha t eye position modi
zation may usefully be a ssisted by passive manual meth
fies muscle tone, pa rticularly the suboccipital muscles (look
ods, including basic massage methodology and soft tissue
up and extensors tighten, look down and flexors prepare for
approaches as ou tlined in these textbooks.
activity, etc.). The implica tions of modified eye position due
to altered pelvic position therefore become yet another fac
tor to be considered when unraveling chain reactions of
THE BIG PICT URE AND THE LOCA L EVENT interacti.ng elements (Komendantov 1945). These examples,'
Janda says, 'serve to emphasize that one should not limit
As adaptive changes take place in the musculoskeletal sys consideration to local clinical symptomatology . . . but [that
tem and as decompensa tion progresses toward an inevitably we] should always maintain a general view.'
more compromised degree of function, structural modifica Grieve (1986) echoes this viewpoint. He explains how a
tions become evident. Whole body, regional and local pos patient presenting with pain, loss of functional movement
tural changes, such as those described by Janda (crossed or a ltered pat terns of strength, power or endurance will
syndromes) and epitomized in the case of facial pain out probably either have suffered a major trauma, which has
lined above, commonly result. overwhelmed the physiological limits of relatively healthy
Simultaneously, with gross compensatory changes mani tissues, or will be displayi.ng 'gradual decom pensa tion
festing as structural distortion, local influences are noted in demonstrating slow exhaustion of the tissue's adap tive
the soft tissues and the neural reporting stations situated potential, with or without tra uma' . As this process of
within them, most notably in the proprioceptors and the decompensation occurs, progressive postural adapta tion,
nociceptors. These adaptive modifications include the influenced by time factors and possibly by trauma, leads to
phenomenon of facilitation and the evolution of reflexo exhaustion of the body's adaptive potential and results in
genically active structures in the myofascia (detailed in dysfunction and, ultimately, symptoms.
Chapter 6). Cholewicki & Silfies (2005) remind us of Hooke's law,
which states tha t within the elastic limits of any substance,
the ratio of the stress applied to the strain produced is in
JANDA'S 'PRIMARY AND SECONDARY' rela tion to the force constant. Hooke's law describes the
RESPONSES relation of tension and ex tension w i thin an object's elastic
limits. When we apply a tension on an object, it will be elon
It has become a truism that we need to consider the body as gated in relation to the force constant, i.e. the stiffness of its
a whole; however, local focus still seems to be the dominant spring qua lity. However, if it is subjected to a very large ten
clinical approach. Janda (1988) gives various additional sion, its extension will not be proportionate to the applied
examples of why this is extremely shortsighted. He dis tension. The maximum tension for it to obey Hooke's law is
cusses the events that follow on from the presence of a short called the elastic limit. Beyond that, it will break or fail to
leg, which might well include: fully recoil. This is true for connective tissue, both in trauma
and in therapy
al tered pelvic position
In simple terms, this means tha t tissue capable of defor
scoliosis
mation will absorb or adap t to forces applied to it within its
probable joint dysfunction, particularly at the cervicocra
nial junction
compensatory activity of the small cervicooccipital
muscles
The stress applied to stretch or compress a body is proportional to
modified head position
the strain or change in length thus produced, so long as the limit
later compensation of neck musculature of elasticity of the body is not exceeded.
increased muscle tone
86 CLINICAL A PPLICATION OF NEU ROMUSCULAR TECHNIQUES: THE U P PE R BODY

elastic limits, beyond which it will break down or fail to narmal aI', in same cases, nat at all. Hence the arder in which
compensate (leading to decompensation). Grieve rightly muscles can tract is altered, as is caardinatian. The mast
reminds us that while attention to specific tissues incrimi characteristic feature, hawever, is substitutian, altering the
nated in producing symptoms often gives excellent short entire pattern. This change is particularly evident if the
term results, 'Unless treatment is also focused toward weak muscle is the aganist. If, hawever, the neutralizers
restoring function in asymptomatic tissues responsible for and/ar fixatars are weak, the basic pattern persists but there
the original postural adapta tion and subsequent decom is accessary matian; if the antagonists are weak, the range of
pensation, the symptoms will recur'. matian is increased. (Vasilyeva & Lewit 1996)
An example of Vasilyeva & Lewit's findings, relating specif
ically to a shortened upper trapezius, includes the follow
RECOGNIZING DYSF UNCTIONA L PATTERNS ing observations.
With a short upper trapezius muscle the a ttachments will
Vasilyeva & Lewit (1996) have cataloged observable changes deviate as follows, causing the listed changes.
in m uscle, elevating the art of inspection to a higher level.
The occipital bone will be pulled caudoventrally and
They state:
slightly laterally, causing the head to deviate forward
Because muscular imbalances manifest in individual mus and to the side, with rotation to the opposite side, leading
cles and therefore (primarily) in certain regions, but are fol to craniocervical lordosis.
lowed by compensatory reactions in other areas that restore There will be pull on the spinous processes adding to
balance, it is most important to determine which muscle(s) sidebending and rotation to the opposite side. In com
and which region are primarily affected and where compen pensation, scoliosis will develop at the cervicothoracic
sation is taking place. j unction, to the ipsilateral side, with increased kyphosis.
There will be relative fixation of the cervical and upper
Among the main criteria examined when assessing for pat
thoracic spine with increased mobility at the craniocervi
terns of imbala nce, for example in an extremity joint, are the
cal and cervicothoracic junctions.
following.
The acromion will be pulled craniomedially, leading to
Can the movement be carried out in the desired direction? the clavicle and acromion devia ting craniomedially, pro
Is the movement smooth and of constant speed? ducing compression of the clavicle at the sternal articula
Does the movement follow the shortest path? tion, with compensation involving sidebending at the
Does the movement involve the full range? shoulder girdle toward the opposite side, with rota tion to
the ipsila teral side.
The decision as to which muscles are probably implicated
when abnormal responses are noted is based on the The motor patterns during shoulder abduction, which will
following. be disturbed with a shortened upper trapezius, include the
following.
Dysfunction of agonists and synergists when the direc
tion of movement is abnormal. There will be a shearing between the clavicle and scapula
Neutralizer muscles are implicated if precise motion is at the acromioclavicular joint.
missing. The head and cervical spine w ill move into extension,
If movement is other than smooth, antagonists are ipsilateral flexion and contralateral rotation.
implicated. The shoulder girdle will displace superiorly on tha t side.

Wha t happens if the main culprits in disturbed motor pat Observation may also alert the practitioner to the presence
terns are shortened muscles? of a crossed syndrome - pelvis tilted anteriorly, protruding
abdomen, increased thoracic kyphosis, head thrust for
The shortened muscle is also hyperactive as a rule. Its irrita
ward, rounded shoulders, etc. But which muscles, specifi
tion threshold is lowered and therefore it contracts sooner
cally, among the many involved, are demonstrating relative
than normal, i.e. the order in which muscles contract in the
shortness or weakness or both? Testing is needed and this
normal pattern is altered. If, therefare, the aganist is shart
can involve functional tests (below), as well as a ssessment
ened, the relationship to' the synergists, neutralizers, fixa
of length and strength. A munber of these tests will be
tars and antaganists is aut af balance and the lacal pattern,
detailed in the text a ssociated with particular regions and
i.e. the direction, smoothness, speed and range af matian, is
joints later in the book.
disturbed in a characteristic way. (Vasilyeva & Lewit 1996)
What happens if the main culprits in disturbed motor pat
terns are weak muscles? EXCESSIVE MUSCULAR TONE
The threshold of irritation in the weakened muscle is raised Muscle tone (residual muscle tension) is the continuous,
and therefare, as a rule, the muscle can tracts later than passive partial contraction of muscles. It helps maintain
5 Patterns of dysfunction 87

posture and is often even present during REM sleep. It The limitation of range of motion of a muscle is estimated
depends physiologically on two factors: the basic viscoelastic clinicaUy by slowly extending the muscle until it reaches
properties of the connective tissues associated with the mus a barrier of increasing tension, which could be because of
cle and/ or the degree of activation of the contractile appara increased viscoelastic tension, spastici ty, physiological
tus of the muscle Oanda et a12006, Simons & Mense 1 998). con tracture or fibrosis. vVhen this test shows increased
Janda et al (2006) discuss the importance yet difficulties range of motion (hypermobility) it suggests decreased
of differen tial diagnosis since each condi tion requires a dif muscle tone or laxity of ligamentous and capsular con
ferent type of treatment: nective tissues.
A 'flapping test' for assessing hypo- and hypertonia is
In the former [viscoelastic properties], we speak about muscle
performed by 'grasping the fingertips of the extended
tightness, stiffness, loss of flexibility or extensibility (length)
arms and rhythmically shaking them up and down to see
and in the latter [contractile properties], it is a real increase
how loose or how stiff the muscula ture of each extremity
of muscle contractile activity such as in spasmodic torticol
is'. With progressively more rapid movements, the exam
lis or trismus . . . Clinically, resting muscle tone presents a
iner can estimate the resonant frequency of each limb .
combination of both situations (contractile and viscoelastic
Proximal-distal and bilateral differences are noted.
properties) . . . However, measuring muscle tone objectively
The Wartenberg pendulum test: This simple but extremely
presents a dilemma. Tests of viscoelasticity involve measure
useful test is performed with the relaxed patient sitting
ments of the velocity of motion, viscosity, thixotropy, and
on the edge of the table with legs hanging freely over the
resonant frequency when load is gradually applied. Tests of
edge. The examiner lifts both legs to the horizontal posi
contractile activity are far simpler in tlUlt EMG can be used;
tion (knees straight) and then releases them, observing
however, this is not without inherent difficulties, as in trig
their movement as they swing freely. A normal leg
ger points where only small loci in the muscle show
swings in smoothly decreasing arcs. However, overreac
increased electrical activity. The degree of muscle stiffness
tive reflex activity reduces the number and smoothness
in relaxed subjects can be seen therefore to include both vis
of oscillations of an affected limb, while muscular hypo
coelastic tone and muscular contractile factors.
tonia gradually decreases the amplitude of the arcs.
Regardless of the source, excessive muscular tone is undesir
able since it interferes with normal physiological function Hannon (2006) has revisited this simple test which was ini
ing as well as being wasteful of energy. Yet, it is important to tially developed in the early 1 950s by Wartenberg (1951).
differentiate - through palpa tion of the layers of tissue Hannon suggests tha t this test can be used to evaluate exces
(skin, fascia, fat, muscle fibers, etc.) and inspection of pos sive, Lmnecessary tension in the quadriceps, which offers
ture, patterns of movement and gait analysis - as much as is evidence of what he terms 'underlying "parasitic" muscular
subjectively and objectively possible to determine as the effort' tha t represents a current inability for the individual
cause for the increased tone. to relax the muscles involved. Hannon notes tha t patellar
tension is often seen in the asymptomatic individual, and,
in fact, 'it is rare to find adults able to fully relax the patella
SIMPLE FUI\ICTIONAL TESTS FOR ASSESSING a t will'.
EXCESS MUSCULAR TONE The patient is in a Sitting position with the legs hanging
Simons & Mense (1 998) define resting muscle tone as the vertically.
'elastic and/or viscoelastic stiffness in the absence of con The leg under examination is passively ex tended to 45
, and then released.
tractile activity (motor unit activity and / or contracture) .
Lakie et al (1980) concluded tha t there was no reduction in The pendular movement of the leg is observed and
tone as a resu lt of surgical anesthesia and therefore tha t the documented.
elastic tone of normal resting muscle must be caused by i ts In a relaxed state approximately 10 cycles of elliptical
viscoelastic properties in the a bsence of muscle contractile pendulum swings will occur. 'The classic observa tion is
activity. In clinical practice muscle tone is measurable as the number of cycles accrued before the leg comes to rest.'
stiffness, which is the resistance to passive movement.
This simple test has been applied to the study of aging mus
Studies in 1 998 (Simons & Mense) and 2001 (Mense &
cle responsiveness, cerebral palsy, fibromyalgia, spinal cord
Simons) led the authors to suggest the following simple
injury and vertebral conditions (Fowler et al 2001, Le
methods for evaluating muscle ' tone':
Cavorzin et al 200 1 , Wachter et aI1 996) .
The compliance (compressibility) of a muscle is assessed Hannon notes that even
clinically by pressing a finger into it or by squeezing i t excess muscular effort since tension in the hip rota tors turns
between the fingers to determine how easily i t i s indented the femur either internally or externally. This deviates the
and how 'springy' it is. The less easily it is indented, and shin from the vertical in the frontal plane. The trajectory of
the more it tends to return to i ts original shape, the more the foot during the oscilla tion of the swinging knee, shin pos
stiff (elastic) it is. ture and extraneous effort all offer additional informa tion.
88 CLINICAL A P PLICATION OF NEUROMUSCULAR TEC HNIQUES : THE U P PER BODY

"
I
,
,
, ,
I I

I I
I
,
I
I I
\ I
\ \
\ \
\, ....

A B (i) (ii)

Figure 5.4 A: Wartenberg pendulum test. Sitting, the patient's leg is extended to 45. The leg is released and the pendular swing is observed
and documented. B: Resting shin position. Observation of resting shin posture may identify subtle muscle tension. A slanted shin in the
frontal plane suggests hip rotator tension. A sagittal slant points toward tension in the knee flexors or extensors. C: Extraneous exertion and
passive knee movements. The knee is moved passively to help the patient notice extraneous effort. At fi rst, use only the smallest of
movements. Watch for shudderi ng and stiffness. D: Elliptical versus l inear foot trajectory. In the picture, the shin appears l i ke a swinging
shaft hanging from a hook. If the hook also rolls, as does the femur, the freely moving shin w i l l reflect both the swinging and ro l l i ng
movements. Relaxed pelvic rotators, hamstrings and quadriceps muscles allow the swinging foot to travel an ell iptical path. Tensing the hip
rotators restricts travel to a linear trajectory. Tensing the other muscles reduces the extent of the swing. Reproduced with permission from
Hannon (2006).

Janda has developed a series of assessments - functional A key aspect of Janda's functional assessments relates to
tests - that can be used to show changes that suggest imbal the proposed firing sequence of muscles when particular
ance, via evidence of over- or underactivity. Some of these actions (e.g. hip ex tension, hip abduction) are performed.
are ou tlined below. Jull & Janda (1987) observed that the firing order of the
key muscles for hip/ leg ex tension should be as follows: first
the ipsilateral hamstrings, followed by ipsilateral glu teus
F UNCTIONAL SCREENING SEQ UENCE maximus, and then contrala teral lumbosacral erector
spinae, ipsila teral lumbosacral erector spinae, contralateral
Janda (1996) and Janda et al (2006) have claimed that altered thoracolumbar erector spinae and finally ipsila teral thora
movement patterns can be tested as part of a screening columbar erector spinae.
examina tion for locomotor dysfunction. In general, obser Janda (1982) described the hamstrings and gluteus max
vation a lone is said to be all that is needed to determine imus as prime movers in prone hip extension, with the erec
the al tered movement pattern. However, light palpation tor spinae stabilizing the spine and pelvis.
may also be used if observa tion is difficult due to poor light Based on EMG studies, Vogt & Banzer (1997) disagreed,
ing, a visual problem or if the person is not sufficiently and suggested that the firing pa ttern for prone hip exten
disrobed. sion should be: ipsilateral erector spinae, followed by ipsi
Although some of these tests relate directly to the lower lateral hamstring, contrala teral erector spinae, tensor fascia
back and limb, their relevance to the upper regions of the latae and finally gluteus maximus.
body should be clear, based on the interconnectedness of The usefulness and accuracy of some of these tests has been
body mechanics, as previously discussed. brought into question by research that shows inconsistency
5 Patterns of dysfunction 89

Figure 5.5 Hip extension test as described in


text. Reproduced with permission from Chaitow
(1996).

in some of the purported firing patterns (see description In the test (below) it is suggested that both the movement
below), when groups of asymptomatic individuals were pattern, as well as the timing sequence, should be observed .
tested. The question is also raised as to how accurate palpa
tion methods can be when the difference in firing between
specific muscles may be as little as 30 milliseconds (Lehman PRONE HIP (LEG ) EXTENSION (PLE) TEST
et aI2004). (FIG. 5.5)
The answer to at least some of the objections involves a
Purpose: To assess for the presence of true or false hip exten
weakness in the research in which asymp tomatic individuals
sion, as well as to check for coordinated firing pa tterns dur
are the subjects used in the studies. This factor alone ensures
ing hip extension. Janda did not encourage the palpa tion
that the population being studied fails to match pa tients
approach described below be performed simul taneously
who will be seen clinically - who by definition are unlikely
with the observations, and suggested tha t it interfered with
to be asymptomatic.
normal function. Instead he encouraged observation first,
Lehman et al note that 'In this current study the only con
as described, and suggested tha t ii palpation is carried out
sistent finding between subjects was tha t 13/14 subjects
during the test, this should be after first evalua ting the
fired the gluteus maximus last [on prone leg extension].'
movement pa tterns by observation alone.
In Janda's observation, this finding would be most likely
to occur when gluteus maximus is inhibited, probably due
to excessive tone/ activity in the erector spinae group. Since Observation with palpation
this is a very common clinical presenta tion in symptomatic
The person lies prone and the practitioner stands to the
individuals, it is reasonable to assume tha t many asympto
side at waist level with the cephalad hand spanning the
matic individuals have similar imbalances prior to the onset
lower lumbar musculature and assessing erector spinae
of symptoms. This is acknowledged by the researchers
activi ty bila terally.
who state:
The caudad hand is placed so that the heel lies on the
[We were] unable to identify what is truly an abnormal pat gluteal muscle mass with the fingertips on the hamstrings.
tern of muscular activation. While the participants included The person is asked to raise the leg into extension as the
in this study had no current symptoms they may still have practi tioner assesses the firing sequence.
dysfunctional motor activation patterns, which have not The normal activation sequence is said to be (1) gluteus
presented symptomatically. Future studies should look at maximus, (2) hamstrings, followed by (3) erector spinae
the relationship between activation patterns and the onset of contrala teraL then (4) ipsilatera l. (Note: As discussed
future dysfunction. It should also be noted that the PLE test above, not all researchers or clinicians agree with this
is also used to assess the movement kinematics of patients. sequence. Some believe the hamstrings should fire first,
This paper only investigated muscle onset timing and did or that there should be a simultaneous contraction of
not assess movement kinematics. The PLE test may still be hamstrings and gluteus maxim us.)
a valid test for assessing movement dysfunction, however, If the hamstrings and / or erectors take on the role of
no work has been done to assess this possibility. glu teus as the prime mover, they w ill become shortened
90 CLINICAL A P PLICATION OF NEUROMUSCULAR TECHNIQUES: THE U P PER BODY

(see notes on postural and phasic muscle response to TRUNK FLEXION TEST (FIG. 5.6)
stress and overuse in Chapter 2).
The person is supine with arms extended and reaching
Janda says, 'The poorest pattern occurs when the erector
toward the knees, which are flexed with feet flat on table.
spinae on the ipsilateral side, or even the shoulder girdle
The person is asked to maintain the lumbar spine against
muscles, initiate the movement and activation of gluteus
the table and to slowly lift the head, then the shoulders
maximus is weak and substantially delayed . . . the leg lift
and then the shoulder blades from the table.
is achieved by pelvic forward tilt and hyperlordosis of
Normal function is represented by the ability to raise the
the lumbar spine, which undoubtedly stresses th.is
trunk until the scapulae are clear of the table without the
region' .
feet lifting or the lower back arching.
Abnormal function is indicated when the feet (or a foot)
Kinesthetic aspect of the test lift from the table or the low back arches, before the
scapulae are raised from the table. This indicates psoas
When the hip extension movement is performed there
overactivity and weakness of the abdominals.
should be a sense of the lower limb 'hinging' from the hip
j oint. Note: It may be helpful for the practitioner to slide his hand
If, instead, the hinge seems to occur in the lumbar spine, under the patient's lower back prior to testing to directly
the indication is tha t the lumbar spinal extensors have feel the lifting of the lumbar spine since this movement may
adopted much of the role of gluteus maximus and that not be readily visible on some patients.
these extensors (and probably hamstrings) will have
shortened.
HIP ABDUCTION TEST (FIG. 5.7)
Morris et al (2006) observe tha t the test is positive (i.e. the
Purpose: To screen for the dynamic stability or instability of
pattern is dysfunctional) if:
the lumbopelvic region during hip abduction.
1. significant knee flexion of the ipsilateral leg occurs, sug
The person lies on the side, ideally with head on a cush
gesting overactiva tion of the hamstrings
ion, with the upper leg straight and the lower leg flexed
2. there is delayed or absent ipsila teral gluteus maximus
contraction. Th.is is considered a very important finding
3. the presence of false hip extension is observed. This is
demonstrated when the pivot point (hinge) of the leg
extension during the initial 10 occurs totally or in part a t
the sacroiliac region, instead of totally a t the h i p joint
4. lowering of the flank occurs on either side, suggesting
rotation due to poor lumbopelvic functional stability
5. early contraction takes place at the periscapular muscu
lature, strongly suggesting a chronic functional low back
instability. This is most frequently observed on the con ------ -----
tralateral side. This finding suggests that recruitment of
the upper torso muscula ture has occurred during the hip
extension movement pattern in order to expedite the Figure 5.6 Trunk flexion test. If feet leave the surface or back
process. arches, psoas shortness is indicated. Reproduced with permission
from ehaitow (1996).

Figure 5.7 Hip abduction test which, if normal,


occurs without 'hip hike' (A), hip flexion ( B) or
external rotation (e l . Reproduced with
permission from ehaitow (1996).
5 Patterns of dysfunction 91

at hip and knee, for balance. The uppermost (straight) leg The person is asked to let the arm being tested hang
should rest on the lower leg, the hip of which should be down and to flex the elbow to 90 with the thumb point
flexed to 45 while knee should be flexed to 60. It is ing upward.
important for the patient's upper leg to remain in line The person is asked to slowly abduct the arm toward the
with the torso. horizontal.
The practitioner, who is observing, not palpating, stands A normal abduction will include eleva tion of the shoul
in front of the person and toward the head end of the table. der and/ or rotation or superior movement of the scapula
The person is asked to slowly raise the leg into abduction. only after 60 of abduction.
Normal is represented by pure hip abduction to 45. Note: Abnormal performance of this test occurs if elevation of
The leg should abduct to 20 withou t in ternal or external the shoulder, rotation, superior movement or winging of
rotation or any hip flexion. There should be no ipsilateral the scapula occurs within the first 60 of shoulder abduc
pelvic 'hip hike' (cephalad elevation). A slight initial con tion, indicating levator and / or upper trapezius as being
traction of the lumbar erector spinae or quadratus lum overactive and shortened, while lower and middle trapez
borum may be observed. This is considered to represent a ius and serra tus anterior are inhibited and are therefore
normal isometric stabilizing contraction . weak.
Abnormal is represented by:
1. hip flexion during abduction, indicating tensor fascia
Variation 1
lata (TFL) shortness, and / or
2. the thigh externally rotating during abduction, indi The person performs the abduction of the arm as described
ca ting piriformis shortness, and/ or above and the practitioner observes from behind.
3. 'hip hiking', indicating quadratus lumborum short A 'hinging' should be seen to take place at the shoulder
ness (and probable gluteus medius weakness), and/ or joint, if upper trapezius and levator are normal.
4. posterior pelvic rotation, suggesting short antagonis
tic hip adductors.

Variation 1
Before the test is performed the practitioner (standing
behind the sidelying patient) lightly places the fingertips
of the cephalad hand onto the lateral margin of quadratus
lumborum while also placing the caudad hand so that the
heel is on gluteus medius and the fingertips on TFL.
If quadratus lumborum is overactive (and, by definition,
shortened - see p. 34), it will fire before gluteus and pos
sibly before TFL.
The indica tion would be tha t quadratus (and possibly
TFL) had shortened and tha t gluteus medius was inhib
i ted and weak.
A

Variation 2
When observing the abduction of the hip, there should be
a sense of 'hinging' occurring at the hip and not at waist
level.
If there is a definite sense of the hinge being in the low
back/ waist area the implica tion is the same as in varia
tion 1 - that quadra tus is overactive and shortened, while
glu teus medius is inhibited and weak.
,.

SCAPULOHUMERAL R HYTHM TEST (FIG. 5.8)


This test has direct implications for neck and shoulder
B
dysfunction.
Figure 5.8 Scapulohumeral rhythm test. A : Normal. B: Imbalance
The person is seated and the practitioner stands behind due to elevatio n of the shoulder within first 60 of abduction.
to observe. Reproduced with perm ission from Chaitow ( 1 996).
92 CLINICAL A P P LICATION O F NEUROMUSCULAR TECHNIQUES : THE U PPER BODY

If 'hinging' appears to be occurring at the base of the PUSH - U P TEST


neck, this is an indication of excessive activity in the upper
The person is asked to perform a push-up and /or to lower
fixators of the shoulder and shortness of upper trapezius
himself from a push-up position, as the practitioner
and / or levator scapula is suggested.
observes scapulae behavior.
A normal result will be evidenced by the scapulae pro
Variation 2 tracting (moving toward the spine) without winging or
shifting superiorly as the trunk is lowered .
The person is seated or standing with the practi tioner
If the scapulae wing, shift superiorly or rotate, the indi
standing behind with a fingertip resting on the mid-por
cation is tha t the lower stabilizers of the scapulae are
tion of the upper trapezius muscle of the side to be tested.
weak (serratus anterior, upper and middle trapezius).
The person is asked to take the arm into extension (a
movement which should not involve upper trapezius). In addition to these 'snapshot' pictures of functional imbal
If there is discernible firing of upper trapezius during ance tha t offer strong indica tions of which muscles might
this movement of the arm, upper trapezius is overactive individually be short and/ or weak, a range of tests exists
and, by implication, shortened. for individual muscles. Some of these will be detailed in the
appropriate sections of the therapeutic applications section
of the book.
N ECK FLEXION TEST (FIG. 5.9)
The person is supine wi thout a pillow.
The person is asked to lift the head and place the chin BREAT HING PATTERN ASSESSMENTS
on the chest while raising the head no more than 2 cm
from the table. Motor control is a key component in spinal (and all joint)
A normal result occurs if there is an ability to hold the injury prevention, and loss of motor control involves failure
chin tucked in while flexing the head/ neck. to control joints, commonly because of poor coordination of
Abnormal is represented by the chin poking forward the agonist-antagonist muscle coactivation.
during this movement, which indicates sternocleidomas Three subsystems work together to maintain spinal sta
toid shortness and weak deep neck flexors. bility (Panjabi 1 992):

central nervous subsystem (control)


osteoligamentous subsystem (passive)
muscle subsystem (active).

( There is evidence tha t the effects of breathing pattern disor


( ders, such as hyperventilation, result in a variety of nega
tive influences and interferences, capable of modifying each
of these three subsystems (Chaitow 2004, Hamaoui et al
2002).
The following tests assess the patient's breathing pat
terns. It is suggested that the practi tioner observe several
breathing cycles with each test.
A

SEATED ASSESSMENT (J a n d a 1 9 8 2 )
1. The patient places a hand on the upper abdomen and
another on the upper chest. The practitioner observes the
hands as the pa tient inhales and exhales normally several
"
"
I times. If the upper hand (chest) moves superiorly rather
than anteriorly, and moves significantly more than the
hand on the abdomen, this suggests a dysfunctional
\
'upper chest' pattern of brea thing (see Fig. 14. 1 0, p. 553).
2. The practitioner stands behind and places both hands
gently over the upper trapezius area, fingertips resting
on the superior aspect of the clavicles. As the patient
B ------ inhales the practitioner notes whether the hands move
Figure 5.9 N eck flexion test. A: Normal flexion. B: Abnormal flexion significantly superiorly. If they do, the scalenes are
('chin poking' ) . sugges ting shortness of SCM. Reproduced with overworking, indicating stress and therefore possible
permission from Chaitow ( 1 996). shortening.
------ .----

5 Patterns of dysfunction 93

3. The practi tioner stands or crouches facing the pa tient the lower rib cage, fingers wrapping posteriorly along
who is seated on the edge of the treatment table and the rib shafts. The tissues are then tested for their rota
places the hands on the patient's lower ribs, one on each tional preference, by easing the superficial tissues and
side with fingers wrapping to the posterior surface, and the ribs in a rotational manner, right and then left. Ideally,
notes whether there is lateral excursion of the hands on a symmetrical degree of rota tion should be noted.
inhala tion to evaluate symmetry of movemen t.
4. Standing to the side the practitioner observes the spinal
SID ELYING ASSESSME NT
contours as the patient fully flexes. If there a re obvious
'flat' a reas of the spine (suggesting inability to flex fully), Quadratus lumborum is tested for shortness by direct pal
especially in the thoracic region, this may indicate rib pation (see Volume 2) and/or by use of the functional
restrictions at those levels. assessment described earlier in this chap ter. Quadratus
lumborum is connected to the diaphragm (via a fascial
encasement tha t becomes the lateral arcuate ligament)
SUPI NE ASSESSMENT
(Palastanga et al 2002) as weJ l as to the 12th rib (via d irect
1 . The brea thing pattern is observed. Does the abdomen attachmen t). QL may be involved in breathing dysfunction,
move forward on inhala tion, or does the upper chest particularly when there is reduced lower rib excursion.
inappropriately move first while the abdomen retracts? If
the latter, breathing retraining is called for, as this is a
PRONE ASSESSMENT
paradoxical breathing pattern.
2. Is there a normal observable lateral excursion of lower ribs? 1 . The so-called 'breathing wave' is observed - there should
3. Assessmen t should be performed for shortness of all res be a continuous wave from the base of the spine to the
piratory muscles available in the supine position, includ neck on deep inhalation (Lewit 1 999). If movement starts
ing the following tha t are either involved in respiration above the sacrum (common), or if regions of the spine
or which - if shortened - could interfere with normal res move as a 'block' instead of in a sequential wave-like man
pira tory function: pectoralis major, latissimus dorsi, ster ner, this can be noted as the current representation of a
nomastoid, psoas (since this merges with the diaphragm). dysfunctional pattern, as it involves thoracic spinal move
4. The practitioner stands at waist level while facing the ment. Areas moving en bloc are commonly those areas that
head and places the hands fully extended on each side of were observed not to flex fully in the seated assessmen t.

Figure 5.1 0 I nferior thoracic apert u re and the


dia p h rag m . Reproduced with permission from Gray's
Anatomy for Students (2005).

..--;;;;;ljiiill""'l'l'Wj- Esophageal opening


--->'c---;II<-,I\R-- Costal margin

Lateral arcuate 1r-..II!qj{-- Median arcuate ligament


ligament ----I:;:;:-.::;==:::
.jiiiiO;"-- Medial arcuate ligament
1-1--'!r::;=;--"-- Left crus
Right crus --------1i---....-t -t------ Quadratus lumborum

--'111'---""""''''-- Psoas major


94 CLINICAL APPLICATION OF NEUROMU SCULAR TECHNIQ UES: THE U P P ER BODY

2. The practitioner can now palpate and evaluate for trigger Box 5.2 Trigger point chains (Hong 1 994)
point activity in muscles available in the prone pOSition
tha t are associated with respiration or which - if short When key trigger points were deactivated, Hong noted that
ened - could interfere with normal respiratory function. trigger points in d istant areas, which had previously tested as
active, became inactive.
The findings from these assessments point toward what is
necessary in therapeutic or rehabilita tion terms as part of Deactivated trigger Inactivated associated triggers
breathing retraining (Chaitow et al 2002).
Sternocleidomastoid Tem pora lis, masseter, digastric
Upper tra pezius Tem pora lis, masseter, splenius,
TRIGGER POINT CHAINS (Mense 1 993, Patterson semispinalis, levator scapulae,
1 976, Simons et al 1 999, Trave l l Et Si mons 1 992) rhomboid minor
Sca len ii Deltoid, extensor carpi radia lis,
As compensatory postural patterns emerge, such as Janda's extensor digitorum com munis
crossed syndromes which involve distinctive and (usually) Splenius ca pitis Tem pora lis, sem ispinalis
easily identifiable rearrangements of fascia, muscle and
Supraspinatus Deltoid, extensor carpi radialis
joints, it is inevitable that local, discrete changes should also
evolve within these distressed tissues. Such changes include Infraspinatus Biceps brachii
areas that, because of the particular stresses imposed on Pectoralis minor Flexor carpi rad ial is, flexor carpi
them, have become irrita ted and sensitized. u l na ris, first dorsal interosseous
If particular local condi tions apply (see Chapter 6), these Latissimus dorsi Triceps, flexor carpi u l naris
irritable spots may eventually become hyperreactive, even
Serratus posterior Triceps, latissimus d orsi, extensor
reflexogenically active, and mature into major sources of
su perior digitorum communis, extensor carpi
pain and dysfunc tion. This form of dysfunctional adapta ulnaris, flexor carpi u l naris
tion can occur segmentally (often involving several adjacent
Deep paraspinal Gluteus maximus, medius, m i n imus;
spinal segments) or in soft tissues anywhere in the body (as
muscles (L5-Sl ) piriformis, hamstrings, tibialis,
myofascial trigger points). The activation and perpetuation peroneus longus, soleus,
of myofascial trigger points now becomes a focal point of gastrocnemius
even more adaptational changes. Quadratus l umborum Gl uteus maximus, medius, m i n imus;
Clinical experience has shown tha t trigger point 'chains' piriformis
emerge over time, often contributing to predictable patterns
Piriformis Hamstrings
of pain and dysfunction. Hong (1994), for example, has
shown in his research that deactivation of particular trigger H amstri ngs Peroneus longus, gastrocnemi us,
soleus
points (by means of injection) effectively inactivates remote
triggers (see Box 5.2). In the next chapter the trigger point
phenomenon will be examined in some detail.

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Edi.nb urgh body balance more in chronic low back subjects that in healthy
Chai tow L 2004 Breathing pa ttern disorders, motor control and low subjects? Clinical Biomechanics 1 7:548-550
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Chaitow L, Bradley D, Gilbert C 2002 Multidisciplinary approaches patella (part 1 ) . Journal of Bodywork and Movement Therapies
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Cho l ewick i ) , Silfies S 2005 Clinical biomechanics of the lumbar Heinking K, Jones III J M, Kappler R 1997 Pelvis and sacrum.
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Fowler E, Ho T, Nwigwe A, Dorey F 2001 The effect of quadriceps Hong C-Z 1994 Considerations and recommendations rega rding
femoris muscle strengthening exercises on spastici ty in children myofascial trigger point injection. Journal of Muscu loskeletal
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Gray's anatomy for students 2005 Churchill Livingstone, Janda V 1982 Introduction to functional pathology of the motor sys
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------- --

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Janda V 1986 Extracranial causes of facial pain. Journal of Prosthetic Mense S 1993 Peripheral mechanisms of muscle nociception a n d
Dentistry 56(4) :484-487 local muscle pain. Journal o f Musculoskeletal Pain 1 ( 1 ) : 1 33-170
Janda V 1988 Muscles and cervicogenic pain syndromes. In: Grant Mense S, Simons D 2001 Muscle pain: lmderstanding its nature,
R (ed) Physical thera py in the cervical and thoracic spine. diagnosis, and treatment. Lippincott Williams and Wilkins,
Churchill Livingstone, New York Philadelphia
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Komendantov G 1945 Proprioceptivnije reflexi glaza i golovy u cle tone as related to clinical muscle pain. Pain 75( 1 ) : 1-17
krolikov. Fiziologiceskij Zurnal 31 :62 Simons D, Travell L Simons L 1999 Myofascial pain and dys fLU1c
Kuchera M, Goodridge J 1997 Lower extremity. In: Ward R (ed) tion: the trigger poin t manual, vol l : upper hal f of body, 2nd
FOLU1dations for osteopathic medicine. American Osteopathlc edn. Williams and Wilkins, Bal timore
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Lakie M, Tsementzis S, Walsh E 1980 Anesthesia does not (and can Williams a n d Wilkins, Baltimore
not) reduce muscle tone? Journal of Physiology 30l:32 Vasilyeva L, Lew it K 1996 Diagnosis of m uscular dysfunction b y
Le Cavorzin P, Poudens S, Chagneau F et al 2001 A comprehensive inspection. I n : Liebenson C (ed) Rehabilita tion of the spine.
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Liebenson C 2006 Rehabilitation of the spine, 2nd edn. Lippincott War tenberg R 1951 Pendulousness of the legs as a diagnostic test.
Williams and Wilkins, Baltimore Neurology 1 : 1 8-24
97

Chapter 6

Trigger points

CHAPTER C O N T E N T S Neuromuscular therapy and neuromuscular technique (both


Ischemia and muscle pain 1 0 1 unfortunately abbreviated as NMT) have among their key
Ischemia and trigger point evolution 1 02 aims the removal of sources of pain and dysfunction.
Trigger point connection 1 02 Modern pain research has demonstrated that a feature of all
Microanalysis of trigger poi n t tissues 1 03 chronic pain is the presence (often as a major part of etiology)
Ischemia a n d fibromyalgia synd rome (FMS) 1 03 of localized areas of soft tissue dysfunction that promote pain
FMS and myofascial pai n 1 0 5 and distress in distant structures (Melzack & Wall 1988).
Facilitation - segmental a n d l ocal 105 These are the loci known as trigger points, the focus of enor
Trigger points and organ dysfu nction 1 06 mous research effort and clinical treatment. This chapter has
How to recognize a facilitated spinal area 1 08 as its primary objective the task of surrunarizing current
Local facilitation in muscles 1 08
knowledge and thinking on this topic.
Lowering the n eu ra l threshold 1 09
A great deal of research into the trigger point phenome
Varying viewpoints on trigger poi nts 1 09
Awad's analysis of trigger poi nts 1 09 non - much of it outlined in this chapter - has been con
Nimmo's receptor-tonus techn iques 1 09 ducted worldwide since the first edition of Travell &
I m proved oxygenation and reduced trigger poi n t pain - a n Simons' (1983a) Myofascial Pain and Dysfunction: The Trigger
example 1 1 0 Point Manual, Volume 1: Upper Half of the Body was released
Pa i n-spasm-pa in cycle 1 1 0 by Williams and Wilkins. That book and its companion vol
Fibrotic scar tissue hypothesis 1 1 0 ume for the lower extremities, published in 1992, rapidly
Muscle spindle hypothesis 1 1 0 became the preeminent resource relative to myofascial trig
Radiculopathic model for muscular pain 1 11 ger points and their treatment. Volume 1 was updated in a
Simons' current perspective: an i ntegrated hypothesis 1 1 1 second edition in 1999 (Simons et all to include considerable
Central a n d attachment trigger points 1 1 2
revisions in content and platform.
Primary, key and satellite trigger points 1 1 2
In the second edition of volume 1 of the Trigger Point
Active a n d l a tent trigger points 1 1 3
Essential and spill over target zones 1 1 4 Manual, Simons et al (1999) have built on more recent
Trigger points and j oi n t restriction 1 1 4 research to modify not only the concepts around the theo
Trigger points associated with shoulder restriction 1 1 4 retical basis of trigger point formation but also the most use
Other trigger poi n t sites 1 1 4 ful treatment protocols. Changes in technique application,
Testi ng a n d measuring trigger poi nts 1 1 4 including emphasis on massage and trigger point pressure
Basic skil l requirements 1 1 5 release methods, accompany discussion of injection tech
Needle electromyography 1 1 6 niques, so that appropriate manual methods are now far
U ltrasound 1 1 6 more clearly defined. Suggested new terminology assists in
Surface electromyography 1 1 6 clarifying differences and relationships between central
Algometer use for research and clinical train ing 1 1 7
(CTrP) and attachment (ATrP) trigger points, key and satel
Thermography and trigger points 1 1 7
lite trigger points, active and latent trigger points, and con
Clinical features of myofascial trigger points 1 1 8
Developing skills for TrP pa lpation 1 1 9
tractures, which often result in enthesitis. Many of these
Which method i s more effective? 1 21 definitions have been incorporated in this text to encourage
the development of a common language among practition
ers regarding these mechanisms.
98 C LI N I CA L A P PL I CAT I O N OF N E U R O M U S C U LA R T EC H N I Q U ES: T H E U P P E R B O DY

In their second edition, Simons et al (1999) present an analyzed and in some instances refuted previous research
explanation as to the way they believe myofascial trigger into the area of myofascial trigger points, some of which
points form and why they form where they do. Combining they assert was poorly designed
information from electrophysical and histopathological suggested future research direction and design.
sources, their integrated trigger point hypothesis appears to
Simons et al (1999) present evidence which suggests that
be based solidly on current understanding of physiology
what they term 'central' trigger points (those forming in the
and function. Additionally, the authors have:
belly of the muscle) develop almost directly in the center of
validated their theories using research evidence the muscle's fibers, where the motor endplate innervates it
cited older research (some dating back over 100 years) as at the neuromuscular junction (Fig. 6.1). They postulate the
referring to these same mechanisms (see Box 6.1 for a following.
brief historical summary)

Box 6.1 Historical research into chronic referred muscle pain (Baldry 1993, Cohen Et GibbOns 1998, Simons 1988, 2004, Straus
1991, Van Why 1994)

F Va l l eix 1 841 Treatise on neuralgia. Paris (never substa ntiated) and suggested that pa i n sensations
Noted that when certa i n pa i nfu l points were pal pated they pro emanati n g from nod u l es cou ld be due to nerve pressure (now
d uced shooting pai n to other reg ions (neurolgia). H e also reported d iscounted).
that diet was a precipitating factor in the development of th e Sir William Osler 1 909 Principles and practice of medicine.
painfu l aching symptoms of the back and cervical reg ion. Appleton, New York
Johan Mezger, mid-1 9th century (Haberl ing W 1 93 2 Johan Georg Considered the pa infu l aspects of muscular rheumatism (myalgia)
Mezger of Amsterdam. Founder of modern scientific massage. to i nvolve 'neuralgia of the sensory nerves of the muscles'.
Medical Life) W Tel l i n g 1 91 1 Nodular fibromyositis - an everyday affliction and
Dutch physicia n, developed massage techniques for treating 'nod its identity with so-called muscular rheumatism. Lancet
u l es' and ta ut cord-l i ke bands associated with this condition. 1 :154- 1 58
T I nman 1 858 Remarks on myalgia or muscular pain. British Ca l l ed the condition ' nodular fibromyositis.
Medical Jou rnal 407-408 :866-868 L Llewellyn, A Jones 1 9 1 5 Fibrositis. Rebman, New York
Was able to clearly state that radiating pa i n in these conditions Broadened the use of the word ' fibrositis' to include other condi
(myalgia) was independent of nerve routes. tions including gout.
Uno Helleday 1 876 Nordiskt Medicinkst Arkiv 6 Et 8 (8) A Schmidt 1 9 1 8 Muskelrheumatismus (Myalgiej. Marcus Et
Swedish physician d escribed nod u l es as part of 'chron ic myitis'. Webers Verlag, Bonn
H Strauss 1 898 Kl i n ische Wochenschrift 3 5 :89-91 Book on muscular rheumatism, myalgia.
German physician distinguished between palpable nodules and F Albee 1 927 Myofascitis - a pathological explanation of any
'bands'. apparently dissimilar conditions. American Jou rnal of Surg ery
I Adler 1 900 Muscular rheumatism. Medical Record 57:529-535 3:523-533
Identified cli nical phenomena characteristic of MTrPs as muscular Ca l l ed the condition 'myofascitis.
rheumatism. F Gudzent 1 93 5 Testunt und heilbehondlung von rheumatismus
A Cornelius 1 903 Narben und Nerven. Deutsche M i l i ta ra rztlische und gicht mid specifischen allergen. Deutsche Medizinsche
Zeitschrift 32:657-673 Wochenschrift 61 :901
German physician who demonstrated the pain-i nfl uencing fea German physician noted that chron ic 'muscular rheumatism' may
tures of tender points and n od u l es, i nsisti ng that the rad iating at times be allergic in orig i n and that removal of certai n foods
pathway was not determi ned by the course of nerves. H e a lso from the diet resulted in clinical improvement.
showed that external i nfluences, i ncluding climatic, emotional or M Lange 1 931 Die Muskelharten (Myogelosenj. J F Lehmann's
physical exertion, cou ld exacerbate the a l ready hyperreactive Verlag, Mu nchen
neural structu res associated with these conditions. Cornelius First trigger poi nt manual.
also d iscussed these pain phenomena as being d ue to reflex C H u nter 1 933 Myalgia o f the abdominal wall. Canadian Medical
mechanisms. Association Journal 28:1 57-1 61
A M u l ler 1 9 1 2 Untersuchungsbefund am rheumatische erkronten Described referred pa i n (myalgia) resulting from tender points sit
muskel. Zeitschrift Kl i n ische Medizin 74:34-73 uated i n the abdominal musculature.
German physician who n oted that to identify n od u l es and bands J Edeiken, C Wolferth 1 936 Persistent pain in the shoulder region
req u i red refined palpation skills, aided, he suggested, by l ubricat following myocardial infarction. American Journal of Med i cal
ing the skin. Science 191 : 20 1 -210
Sir William Gowers 1 904 Lumbago: its lessons and analogues. Showed that pressure applied to tender points i n scapula region
British Medical Jou rnal 1 : 1 1 7- 1 21 muscles cou ld reproduce shou lder pa in already bei ng experienced.
Suggested that the word fibrositis be used, believing erroneously This work i nfl u enced Janet Travel l - see bel ow.
that inflammation was a key feature of 'muscular rheumatism'. Sir Thomas Lewis 1 938 Suggestions relating to the study of
Lecture, National Hospital of Nervous Diseases, London. somatic pain. B ritish Medical Jou rnal 1 :321 -325
Ralph Stockman 1 904 Causes, pathology and treatment of chronic A major researcher into the phenomenon of pa i n in general,
rheumatism. Edinburg h Med i ca l Jou rnal 1 5 : 1 07-1 1 6, 223-225 charted severa l patterns of pa in referral and suggested that
Offered support for Gowers' suggestion by reporting finding Kel lgren (see below). who assisted him in these studi es, conti nue
evidence of inflammation i n con nective tissue i n such cases the resea rch.

box continues
6 Trigger points 99

Box 6.1 (continued)

J Kellgren 1938 Observations on referred pain arising from muscle. trial ingestion of allergenic foods or inhalation of house dust
Clinical Science 3 :17 5 -190 extract or particu lar hydrocarbons, with rel ief of symptoms often
Identified (in patients with 'fibrositis' and 'myalgio' ) many of the being achieved by avoidance of a l l ergens. Randolph reports that
features of our current understanding of the trigger point phe severa l of his patients who achieved rel ief by these means had
nomenon, incl ud ing consistent patterns of pain referra l - to dis previously been d iagnosed as having 'psychosomotic rheumatism'.
tant muscles and other structures (teeth, bone, etc.) from pain James Mennel l 1 9 52 The science and art of joint manipulation,
points ('spots') in muscle, l iga ment, tendon, joint and periosteal vol 7. Churchi l l , London
tissue - which could be obliterated by use of novocaine British physician described 'sensitive areas' which referred pain.
injections. Recommended treatment was a choice between manipu lation,
A Reichart 1938 Reflexschmerzen auf grund von myoglosen. heat, pressure and deep friction. He a l so em phasized the impor
Deutsche Medizinische Wochenschrift 64 :823 -824 tance of diet, fluid intake, rest, the possible use of cold and pro
Czech physician who identified and charted patterns of distri bu caine injections as well as suggesting cupping, skin rol l ing,
tion of reflex pain from tender points (nodu les) in particu lar massage and stretching in norma lization of' fibrositic deposits'.
muscles. Janet Travel l (and S Rinzler) 19 52 The myofascial genesis of pain.
M Gutstein 1 938 Diagnosis and treatment of muscular rheuma Postgrad uate Medicine 11 :425-434
tism. British Journal of Physical Medicine 1 :302-321 B u i lding on previous research and fol l owing her own detailed
Refugee Polish physician working in Britain who identified that in studies of the tissues involved, coined the word 'myofascial',
treating muscular rheumatism, manual pressure applied to tender adding it to Steind ler's term to produce 'myofascial trigger points'
(later ca l led 'trigger') points produced both local and referred and fina l ly ' myofascial pain syndrome'. Between 1 942 and 1 993,
symptoms and that these referra l patterns were consistent in Janet Travel l authored four books and more than 1 5 papers on
everyone, if the original point was in the same location. He deac TrPs; however, it was this paper that introduced referra l patterns
tivated these by means of injection. His other papers publ ished for 32 m u scles. Only one paper prior to her 1 983 book had a
between 1 938 and 1 9 51 identified the cond ition with 11 different minor mention of a loca l twitch response.
names, including common rheu matism, idiopathic mya lgia, rheu I Neufeld 1 9 52 Pathogenetic concepts of 'fibrositis' - fibropathic
matic mya lgia, myalgia, muscu lar sciatica, fibrositis, a m uscle dis syndromes. Archives of Physical Medicine 3 3 :363 -369
ease and non-articu lar rheumatism (see below as Gutstein-Good Suggested that the pain of 'fibrosistis-fibropathic syndromes' was
and as Good). due to the brain misinterpreting sensations.
A Steindler 1 940 The interpretation of sciatic radiation and the F Speer 1954 The allergic-tension-fatigue syndrome. Pediatric
syndrome of low back pain. Journal of Bone and Joint Surgery Clinics of North America 1 :1029 -1 037
22:28-34 Called the cond ition the 'allergic-tension-fatigue syndrome' and
American orthopedic surgeon who d emonstrated that novoca ine added to the pain, fatigue and general sym ptoms previously rec
injections into tender points located in the low back and g l uteal ognized (see Randolph above) the observation that edema was a
regions cou l d relieve sciatic pain. H e ca lled these points 'trigger feature, especially involving the eyes.
points'. Janet Travell (see below) was infl uenced by his work and R Gutstein 1 9 5 5 Review of myodysneuria (fibrositis). American
popularized the term 'trigger points'. Practitioner 6 :570-577
M Gutstein-Good 1 940 (sa me person as M Gutstein above) Called the cond ition' myodysneurio'.
Idiopathic myalgia simulating visceral and other diseases. Lancet R Nimmo 1 9 57 Receptors, effectors and tonus: a new approach.
2:3 26 -3 28 Journal of the National Chiropractic Association 27( 1 1 ) :21
Ca lled the cond ition 'idiopathic myalgio'. After many years of research, which paralleled chronologically that
M Good 1 941 (same person as M Gutstein and M Gutstein-Good of Travell, he described his concept of 'receptor-tonus technique',
above) Rheumatic myalgias. The Practitioner 1 46 :1 67 -1 74 involving virtua l ly the same mechanisms as those eventually
Ca lled the cond ition ' rheumatic myalgio'. described by Travell Et Simons (1 983a) but with a more manual
James Cyriax 1 948 Fibrositis. British Medical Journal 2:251 -255 emphasis. 'I have found that a proper degree of pressure, sequential ly
Believed that chronic muscle pain derived from nerve im pinge applied, causes the nervous system to release hypertonic muscle:
ment due to d isc degeneration. 'It [pressure on dura mater] has M Kel ly 1 962 Local injections for rheumatism. Medical Journal of
misled clinicians for decades and has given rise to endless m isd i Austra lia 1 :45 -50
agnosis; for these areas of "fibrositis", "trigger points", or "mya l Austra l ian physician who carried on Kellgren's concepts from the
gic spots", have been regarded as the primary lesion - not the early 1 940s, diagnosing and treating pain (rheumatism) by means
resu lt of pressure on the dura mater' (Cyriax J 1 962 Textbook of of identification of pain points and deactivating these using
orthopaedic medicine, vol 1, 4th edn. Cassell, London). injections.
P Ell man, D Shaw 1 9 50 The chronic 'rheumatic' and his pains . M Yunus et al 1981 Primary fibromyalgia (fibrositis) clinical study
Psychosomatic aspects of chronic non-articular rheumatism. of 50 patients with matched controls. Seminars in Arthritis and
Anna ls of Rheumatic Disease 9 :341 -3 57 Rheumatism 1 1 :1 51 -1 71
Suggested that because there were few physical manifestations First popu larized the word 'fibromyalgio'.
to support the pain cla imed by patients with chronic muscle pain, Janet Travel l , David Simons 1 983 Myofascial pain and dysfunc
their cond ition was essentially psychosomatic (psychogenic tion: the trigger point manual vol 7. Wi l l iams and Wilkins,
rheumatism): 'the patient aches in his l i mbs because he aches in Balti more
his mind'. The definitive work (with vol u me 2, 1 99 2) on the subject of
Theron Randolph 1 9 51 Allergic myalgia. Journal of Mich igan myofascial pain syndrome (MPS).
State Med ical Society 50:487 K Lewit, D Simons 1 984 Myofascial pain: relief by post-isometric
This lead ing American clinical ecologist described the cond ition relaxation. Archives of Physical Medicine and Rehab i l i tation
as allergic myalgia and demonstrated that widespread and 6 5 :4 52-456
severe muscle pain (particularly of the neck region) could be Czech neurologist Karel Lewit described his simple manual treat
reproduced 'at will under experimental circu mstances' following ment of MTrPs, and later emphasized joint dysfunction in MTrPs

box continues
1 00 C L I N I C A L A P P L I C AT I O N O F N E U R O M U S C U L A R T EC H N I QU ES: T H E U P P E R B O DY
[

with suggestions as to joi n t mobilization, and later developed Showed that many 'tender points' in fibromyalgia are i n
va luable concepts of cha ins of MTrPs. rea l ity latent trigger poi nts. He believes t h a t MPS and FMS
David Si mons 1 986 Fibrositis/fibromyalgia: a form of myofascial are d istinctive syndromes but are 'closely related'. States that
trigger points? American Journal of Med icine 81 (Su ppl 3A):93 -98 many people with MPS progress on to develop fibromyalgia.
American physician who collaborated with Travel l in a joint study C-Z Hong 1 994 Electrophysical characteristics af localized twitch
of MPS and who a lso conducted his own studies i nto the con nec responses in responsive taut bands of rabbit skeletal muscle.
tion between myofascial pain syndrome and fibromyalgia syn Journal of Musculoskeletal Pain 2(2) :1 7-43
drome, finding a good deal of overlap. This physiatrist pioneered studi es focusing on identifying taut
M Margoles 1 989 The concept of primary fibromyalgia. Pain bands of MTrPs.
3 6 :391 -39 2 D Simons, J Travel !, L Simons 1999 Myofascial pain and dysfunc
States t h a t most patients w i t h fibromyolgio demonstrate n umer tian: the trigger point manual, vol 1: upper half of body, 2nd edn.
ous active myofascial trigger points. Wi l l iams & Wilki ns, Baltimore
R Bennett 1 990 Myofoscial pain syndromes and the fibromyalgia This second edition, with emphasis on sig nificant research con
syndrome. In: Fricton R, Awad E (eds) Advances in pain research ducted in the 1 5 years since the first edition, altered the founda
a n d therapy. Raven Press, New York tional platform of trigger poi nt theories and trea tment.

Figure 6.1 I ntegrated hypothesis of e n d pla te


dysfu n ction associated with trigger point formation.
SR, sarcop l asm ic reticu l u m . Adapted from Simons et a l
(1999).
Motor nerve terminal

Excess acetylcholine
release

-""'---
Depol arization

;;;
:;
=;=d==-==::=';5d
Cal cium release


=f'=I:::=+=1 '$ Sarcomere
contracture

Compression of vessels

Dysfunctional endplate activity occurs (commonly asso As the endplate keeps producing ACh flow, the actin/
ciated with a strain), which causes acetylcholine (ACh) to myosin filaments slide to a fully shortened position (a
be excessively released at the synapse, often associated weakened state) in the immediate area around the motor
with excess calcium. endplate (at the center of the fiber).
The presence of high calcium levels apparently keeps the As the central sarcomeres shorten, they begin to bunch
calcium-charged gates open and the ACh continues to be and a contracture 'knot' forms.
released, resulting in localized ischemia. This knot is the 'nodule' that is a palpable characteristic
The consequent ischemia involves an oxygen/nutrient of a trigger point (Fig. 6.2).
deficit that, in turn, leads to a local energy crisis and As this process occurs, the remaining sarcomeres of that
inadequate adenosine triphosphate (ATP) production in fiber (those not btffiching) are stretched, thereby creating
the immediate area. the usually palpable taut band that is also a common trig
Without available ATP the local tissue is unable to remove ger point characteristic.
(active transport) the calcium ions that are 'keeping the Attachment trigger points may develop at the attachment
gates open', thereby allowing continued release of Ach. sites of these shortened tissues (periosteal, myotendinous)
Removing the superfluous calcium requires more energy where muscular tension provokes inflammation, fibrosis
than sustaining a contracture, so the contracture remains. and, eventually, deposition of calcium.
The resulting muscle fiber contracture (involuntary,
without motor potentials) is distinctly different from a This model is explored in greater depth later in this chapter,
contraction (voluntary, with motor potentials) and spasm since it represents the most widely held understanding as to
(involuntary, with motor potentials). the etiology of myofascial trigger pOints. Other models exist
The contracture is apparently sustained by the chemistry which attempt to explain the trigger point phenomenon,
at the innervation site, not by action potentials from the including the facilitation concept (below) and the ideas
spinal cord. and methods developed by Raymond Nimmo DC (1981)
6 Trigger poin ts 101

Trigger point complex are released to act on vessels and nerves locally. These
include catec holamines, serotonin, histamine, bradykinin
Taut band Nodule and prostaglandins. Among their effec ts, these substances
A cause vasodilation and vascular permeabili ty, often resu lt
ing in local edema. As edema increases, arterial and venous
vessels are compressed, resulting in a vicious cycle that
further reduces blood supply and sensitizes nociceptors.
Research also shows that when pain receptors are stressed
(mechanically or chemically) and are simultaneously exposed
to elevated levels of adrenaline, their discharge rate increases,
i .e. a greater volume of pain messages is sent to the brain
(Kieschke et al 1988).
\tV-hen the blood supply to a muscle is fully inhibited,
pain is not usually noted until that muscle is asked to con
tract, at which time pain is likely to be noted within 60 sec
B
Contraction onds (Mense et aI2001). This is the phenomenon that occurs
knot
in intermittent claudication. The precise mechanisms are
open to debate but are thought to involve one or more of a
number of processes, including potassium ion build-up, the
lack of oxidation of metabolic products and the release of
Normal algesic substances. Previous concepts of lactate accumula
fibers tion have now been discarded as a maj or factor in ischemic
muscle pain since it is considered to be an ineffec tive activa
tor of muscle nociceptors, although it may have a combined
action with other substances (Mense et aI2001). Further, lac
Figure 6.2 ARB : Tension produced by central trigger point (CTrP) tate (or lactic acid) accumulation following rigorous exer
can result in localized inflammatory response (attachment trigger
cise does not appear to be the cause of delayed onset muscle
point, ATrP). Adapted from Simons et al (1 999).
soreness (12-24 hours) since concentrations rapidly
decrease within 1 hour following cessation of exercise
(Khalsa 2004).
(discussed below) . Before examining these, it will be useful Pain receptors are sensitized when under ischemic condi
to investigate a key element of myofascial trigger point tions (i t is thought) due to the release of algesic substances
development and dysfunction - ischemia. such as bradykinin, a chemical mediator of inflammation.
This has been confirmed by the use of drugs that inhibit
bradykinin release, allowing an active ischemic muscle to
ISCHEMIA AND MUSCLE PAIN remain relatively painless for longer periods of activity
(Oigiesi et aI1975). When ischemia ceases, pain receptor acti
Ischemia can be simply described as a state in which the vation persists for a time and, conceivably, indeed probably,
current blood supply is inadequate for the current physio contributes to sensitization (facilitation) of such structures, a
logical needs of tissue. The causes of ischemia can be patho phenomenon noted in the evolution of myofascial trigger
logic, as in a narrowed artery or thrombus, or anatomic, as points (discussed further below).
in particular hypovascular areas of the body, such as the Although ischemic muscles may remain painless LUltil
region of the supraspinatus tendon 'between the anastomo asked to contract, trigger points in muscle may refer pain
sis of the vascular supply from the humeral tuberosity and even when the muscle is not being actively used. The term
the longitudinally directed vessels arriving from the muscle's 'essential pain zone' describes a referral pattern that is pres
belly' (Tullos & Bennet 1984), or as a result of a sequence of ent in almost every person when a particular trigger point is
events such as occurs in trigger point development outlined active. Some trigger points may also produce a 'spillover
above. Compression of blood vessels or blockage of blood pain zone' beyond the essential zone, or in place of it, where
flow by any means can result in ischemia and excitation of the referral pattern is usually less intense (Simons et aI1999).
nociceptors. These target zones should be examined, and ideally pal
The development of ischemia in muscles can be immedi pated, for changes in tissue 'density', temperature, hydrosis
ate, such as results when trauma occurs, or can be slow and and other characteristics associated w ith satellite trigger
insidious, such as that associated with postural adaptation. point formation (as discussed later in this chapter).
Pain receptors are stimulated (and become sensitized) by Trigger point activity itself may also induce relative
prolonged intense muscular contraction when biological ischemia in the 'target' tissues (Baldry 1993, Simons et aI1999).
substances, known as vasoneuroactive substances (VNS), The mechanisms by which this occurs remain hypothetical
1 02 C LI N I CA L APPLICAT I O N OF N E U RO M U SCULAR T E C H NIQU ES: T H E U P PER B O DY

but may involve a neurologically mediated increase in tone in sidelying sleeping posture, may lead to relative ischemia
in the trigger point's reference zone (target tissues). According under the acromion process (Brewer 1979). These are pre
to Simons et al (1999) these target zones are usually periph cisely the sites most associated with rotator cuff tendinitis,
eral to the trigger point, sometimes central to the trigger calcification and spontaneous rupture (Cailliet 1991), as
point and, more rarely (27%), the trigger point is located well as trigger point activi ty.
within the target zone of referral. This is more than informa Additionally, a number of shoulder and neck muscles,
tional as it translates to a significant clinical application: if including levator scapulae, anterior and middle scalenes, tri
the practitioner is treating only the area of pain and the ceps brachii and trapezius, target the supraspinatus area as
cause is myofascial trigger points, he is 'in the wrong spot' their referred zone and can produce not only pain but also
nearly 75% of the time! autonomic and motor effects, including spasm, vasoconstric
Any appropriate manual treatment, movement or exer tion, weakness, loss of coordination and loss of work toler
cise program that encourages normal circulatory function is ance in the target tissues (Simons et aI1999). Due to weakness
likely to modulate these negative effects and reduce trigger and loss of coordination, the person may adapt by improp
point activity. It is important to note, however, that when erly using these and other muscles with resultant damage to
tissues containing (particularly active) trigger points are the tissues (see patterns of dysfunction, Chapter 5).
exercised prior to the deactivation of the trigger points, the
referred pain is often provoked or increased . Therefore, a
general protocol suggests that manual palpation, examina TRIGGER POINT CONNECTION
tion for and treatment of trigger points, would precede the
Mense (1993) describes the hypothesized evolution of a trig
start of exercise therapy. After treatment of trigger points
ger point, clearly similar to the Simons et al (1999) model.
and elongation of the taut bands housing them, a condi tion
ing program can be implemented to help prevent reactiva A muscle lesion leads to the rupture of the sarcoplasmic
tion. A degree of normal function may return when the soft reticulum and releases calciumfrom the in tracellular stores.
tissue's Circulatory environment is improved and the stress The increased calcium concentration causes sliding of the
producing elements, whether of biomechanicaL biochemi myosin and actin filaments; the result is a local contracture
cal and/ or psychosocial origin, are reduced or removed. (myofilamen t activation without electrical activity) that has
Increased lymphatic flow, which is enhanced by light high oxygen consumption and causes hypoxia. An addi
gliding strokes and other forms of tugging on the skin sur tionalfactor may be the traumatic release of vasoneuroactive
face, such as that created by manual lymph drainage tech substances (for example, bradykinin), which produce local
niques (Chikly 2001 , Wittlinger & Wittlinger 1982), will edema that in turn compresses venules and enhances the
assist in draining the waste materials that accumulate ischemia and hypoxia. Because of the hypoxia-induced drop
within the ischemic tissues, while altering the local cellular in ATP concentrations, the function of the calcium pump in
chemistry and reducing neuroexcitation. Many massage the muscle cell is impaired, and the sarcoplasmic calcium
techniques drain lymphatic wastes; however, some are concentration remains elevated. This perpetuates the con
designed to dynamically induce lymph movement and tracture.
drainage (Chikly 1996, 2001, Wittlinger & Wittlinger 1982) .
Use of these specialized techniques, especially in a system The presence of oxygen deficit at the heart of the trigger
atic protocol that addresses opening the primary pathways point has been confirmed, according to Mense:
of lymph flow in a particular order, may greatly enhance the Measurements of the tissue p02 with microprobes show that
conditions of the in terstitial fluids surrounding the cells. oxygen tension . . . is extremely low. Thus, the pain and
Such movement may also i ncrease the flow of nutrients to tenderness of a trigger point could be due to ischemia
the area, thus improving the cells' physiological status. induced release of bradykinin and other vasoneuroactive
substances which activate and/or sensitize nociceptors.
(Bruckle et a1 1990)
ISCHEMIA AND TRIGGER POINT EVOLUTION
The original 'lesion' could have been the result of any of the
Hypoxia (apoxia) involves tissues being deprived of ade multiple etiological and maintaining factors (overuse, mis
quate oxygen. This can occur in a number of ways, such as use, abuse, disuse) outlined in the overview of stress and
in ischemic tissues where circulation is impaired, possibly the musculoskeletal system in Chapter 4. It could be the
due to a sustained hypertonic state resulting from overuse result of a gross trauma, such as a blow, sudden elongation
or overstrain. The anatomy of a particular region may also (as in whiplash) or laceration, occurring recen tly or even
predispose it to potential ischemia, as described above in years before. It could also be the result of sustained emo
relation to the supraspinatus tendon. Additional sites of rel tional distress, with its influence on somatic structures, or of
ative hypovascularity include the insertion of the infra the effects of hormonal imbalance, specific nu tritional defi
spinatus tendon and the intercapsular aspect of the biceps ciencies, aJlergic (or sensitivity) reactions or increased levels
tendon. Prolonged compression crowding, such as is noted of toxic material in the tissues (see Chapter 4).
6 Trigger points 1 03

Simons describes the trigger point evolu tion as follows. EMG

Visualize a spindle like a strand ofyarn in a knitted sweater . . .


a metabolic crisis takes place which increases the tempera EMG twitch potential

ture locally in the trigger point, shortens a minute part of


the muscle (sarcomere) - like a snag in a sweater - and
reduces the supply of oxygen and nutrients into the trigger
point. During this disturbed episode an influx of calcium
occurs and the muscle spindle does not have enough energy
to pump the calcium outside the cell where it belongs. Thus
a vicious cycle is maintained; the muscle spindle can't
seem to loosen up and the affected m uscle can't relax. ( Wolfe
et (1 1992)
A
MICROANALYSIS OF TRIGGER POINT TISSUES

Shah et al (2003, 2005) have developed a microanalytical


t