Myofascial Induction An Anatomical Approach to the Treatment of Fascial Dysfunction. Volume 2: The Lower Body [1 ed.] 9781913426330, 9781913426347, 9781912085798, 9781912085804, 9781909141902, 9781909141919, 9781913426354, 9781913426361

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of related interest Myofascial Induction™ An anatomical approach to the treatment of fascial dysfunction Volume 1: The Upper Body Andrzej Pilat Forewords by Jan Dommerholt, Robert Schleip and Andry Vleeming ISBN 978 1 91342 633 0 eISBN 978 1 91342 634 7 The Myofascial System in Form and Movement Lauri Nemetz Foreword by David Lesondak ISBN 978 1 91208 579 8 eISBN 978 1 91208 580 4 Mobilizing the Myofascial System A clinical guide to assessment and treatment of myofascial dysfunctions Doreen Killens Forewords by Diane Lee, Thomas W. Myers and BetsyAnn Baron ISBN 978 1 90914 190 2 eISBN 978 1 90914 191 9

Myofascial Induction ™ An anatomical approach to the treatment of fascial dysfunction Volume 2 The Lower Body Andrzej Pilat Forewords Jan Dommerholt Robert Schleip Andry Vleeming

First published in Great Britain in 2023 by Handspring Publishing, an imprint of Jessica Kingsley Publishers An imprint of Hodder & Stoughton Ltd An Hachette UK Company 1 Copyright © Andrzej Pilat 2023 Foreword copyright © Jan Dommerholt 2023 Foreword copyright © Robert Schleip 2023 Foreword copyright © Andry Vleeming 2023 Please see the Permissions and Sources list at the end of the book for copyright acknowledgements. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means without the prior written permission of the publisher, nor be otherwise circulated in any form of binding or cover other than that in which it is published and without a similar condition being imposed on the subsequent purchaser. Disclaimer: Neither the Publisher nor the Author assumes any responsibility for any loss or injury and/or damage to persons or property arising out of or relating 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. A CIP catalogue record for this title is available from the British Library and the Library of Congress ISBN 978 1 91342 635 4 eISBN 978 1 91342 636 1 Jessica Kingsley Publishers’ policy is to use papers that are natural, renewable and recyclable products and made from wood grown in sustainable forests. The logging and manufacturing processes are expected to conform to the environmental regulations of the country of origin. Handspring Publishing Carmelite House 50 Victoria Embankment London EC4Y 0DZ www.handspringpublishing.com

CONTENTS Dedication About the author Foreword by Jan Dommerholt Foreword by Robert Schleip Foreword by Andry Vleeming Preface Online videos Acknowledgments

CHAPTER 1

Connecting and moving forward: Fascia as a multifunctional system Introduction The fascial system and communication between body systems References

CHAPTER 2

Thoracolumbar fascia: The heart of the matter General considerations related to the fascial system of the lower quadrant How load is transferred between the spine, pelvis, arms, and legs Thoracolumbar fascia: The heart of the matter

Conclusion References CHAPTER 3

Lower quadrant assessment Introduction The characteristics of the lower quadrant The assessment process Conclusion References

CHAPTER 4

Pelvic girdle dysfunctions: Lower back and sacroiliac structures; Abdominal area Lower back and sacroiliac structures Introduction: The lower back Anatomical considerations related to the lower back Neurological considerations related to the lower back The pelvic girdle and low back pain The cell–ECM–brain model Introduction: Sacroiliac structures Structure and function of the sacroiliac joint Conclusion Abdominal area Introduction Anatomical considerations related to the abdominal fascial system Biomechanical considerations related to the abdominal fascial system Blood supply to the abdominal fascial system Innervation of the abdominal fascial system Conclusion References

MIT procedures for common pelvic girdle dysfunctions: Lower back and sacroiliac structures; Abdominal area CHAPTER 5

Pelvic girdle dysfunctions: Gluteal structures; Inguinal and pubic structures; Pelvic floor (external) Gluteal structures Introduction Anatomical considerations related to the gluteal structures Biomechanics and the gluteal area Deep gluteal syndrome Conclusion Inguinal and pubic structures Introduction Anatomical considerations related to the inguinal and pubic structures Symphysis pubis dysfunction and groin pain Conclusion Pelvic floor (external) Introduction The pelvic floor, posture, and gravity The pelvic floor system and its supporting structures Endopelvic fascia as a part of the dynamics of the pelvic floor system Pelvic floor dysfunction Conclusion References MIT procedures for common pelvic girdle dysfunctions: Gluteal structures; Inguinal and pubic structures; Pelvic floor (external)

CHAPTER 6

Lower extremity dysfunctions related to the fascial system Introduction Anatomical considerations related to the fascia of the lower limb Thigh structures: Fascia lata Knee structures Lower leg structures: Crural fascia Foot structures Conclusion References MIT procedures for common lower extremity dysfunctions

CHAPTER 7

Fascia and therapeutic movement in translational practice: From the laboratory to the clinic Introduction Human existence as a biological behavior The therapeutic process Conclusion References

Permissions and sources Subject index Author index

DEDICATION In May 2016 I had the opportunity to show a sample chapter of this book to Dr. Leon Chaitow. On reviewing it carefully, he exclaimed: “I want this book!” He also generously agreed to my request to write the book’s foreword. I promised he would be the first to read the book. Sadly, his sudden passing did not allow me to fulfill my promise. I am honored to dedicate the book to this great person, clinician, researcher, writer, lecturer, educator, editor, and visionary. Andrzej Pilat

ABOUT THE AUTHOR

Andrzej Pilat Andrzej Pilat is a physical therapist. Born in Poland, throughout his professional life he has practiced across continents. This has given him the opportunity to be involved in a variety of aspects of physical therapy: health care (a bustling hospital environment; the mystery of an operating room; the adrenaline of intensive care units; and the intimacy of a private practice); teaching (in a university setting, tutoring graduate and undergraduate students); research (decoding the human body’s enigma by dissecting unembalmed cadavers); management (he has been chair of domestic professional associations and international organizations); publishing (he was an editor for the Venezuelan Manual Therapy journal); and information dissemination (he is the author of several papers and books). These experiences have led him to a better understanding of people’s culture, customs, and attitudes towards diseases, thus awakening his interest in

therapeutic approaches and treatments that will adapt as effectively as possible to the individual, as opposed to the disease. In his quest, Andrzej has experienced a fruitful array of different approaches to physical therapy, with a wide range of exercises, modalities, applications (devices), manual applications, and concepts – learned from well-known masters, such as Maitland, Mulligan, McKenzie, Upledger, Barnes, Greenman, and others. The study of different concepts of manual therapy has occupied the last 35 years of his career and he has become intensely interested in fascia in the search for answers to the (always) global response of the body to disease and healing. Andrzej’s experience as a photographer has allowed him to immerse himself in the intimacies of the unembalmed cadaver, capturing in pictures the beauty of the inner body architecture. The pages of this book reflect these experiences by taking the reader on a fascinating journey through the puzzle of the fascia, from a microbiological, anatomical, biomechanical, neuroscientific, and even psychological and philosophical approach. Today Andrzej leads the Myofascial Therapy School, Tupimek, in El Escorial (Madrid), Spain, where he gives instruction in Myofascial Induction Therapy (MIT)™, in collaboration with certified teachers both in Spain and worldwide. Andrzej lectures in specialized workshops and teaches for different master’s programs in local universities and abroad. He has participated in numerous international congresses about fascia, manual therapy, and physical therapy in general. In recent years, his participation in webinars has resulted in a growing international following. Myofascial Induction™: An anatomical approach to the treatment of fascial dysfunction is the result of five years of intense research through a vast amount of scientific evidence about the fascia’s increasing importance to people’s health and illnesses.

FOREWORD by JAN DOMMERHOLT I do not recall when and where I first met Andrzej Pilat, but I suspect it was at either a myofascial pain congress, a fascia congress, or a physiotherapy course or conference somewhere in the world. Often Andrzej’s travels coincided with mine, and every time I attended his lectures several thoughts and associations came to mind. It was clear to me that this man is an innovator in the field of physiotherapy and beyond – someone who follows in the footsteps of other innovators from many different fields, dispelling the many erroneous belief systems so common in our discipline. I have a feeling that already, during his time as a physiotherapy student, young Andrzej would have been questioning his tutors and challenged their teachings and convictions about physiotherapy treatment methods. In a time when the terms evidence-based and evidence-informed physiotherapy had not been invented, Andrzej was probably way ahead of many of his professors in his critical thinking skills and vision for the profession. During our lifetime, physiotherapy has evolved from a tradition-based therapy to an evidence-informed approach. Charles Kettering is quoted as saying: “If you have always done it that way, it is probably wrong” – words that could easily have been uttered by Andrzej Pilat. During a myofascial pain conference in Bangalore, India several years ago, Andrzej and I had numerous opportunities to reflect, share ideas, admire each other’s creative presentation styles, share a beer or two, and ponder about the future of physiotherapy. His attention to detail, his phenomenal dissection videos, animations, and photographs were most impressive, not to mention his good nature and willingness to share his perspective with anyone willing to

listen. Attendees of the congress recognized his brilliant mind, creativity, and tenacity, and our chats were frequently interrupted by requests to take selfies with Andrzej! In a time where many physiotherapists have adopted a mindset that because “pain is in the brain” and “the issues are not in the tissues,” so “hands-on therapies are a thing of the past,” Andrzej continued to defy such developments and instead explored new developments beyond what most of us could ever have imagined. Albert Einstein reportedly stated that: “You can’t solve a problem on the same level that it was created. You have to rise above it to the next level.” That observation is applicable to Pilat at many levels. Myofascial Induction™: An anatomical approach to the treatment of fascial dysfunction is the ultimate proof of the innovative pathway which Andrzej has carved out, often against the contemporary viewpoints of other scientists, social media influencers, and established traditions. At the time I was preparing this foreword, Colleen Kigin, PT, PhD, FAPTA was presenting the 52nd Mary McMillan Lecture as part of the centennial celebration of the American Physical Therapy Association. By pure coincidence the title of her lecture was “Innovation: It’s in our DNA.” Although I am personally not convinced that “the [physical therapy] profession is rich with innovators,” Dr Kigin hit the nail on the head when she summarized, that physical therapy innovators have the ability to connect the dots, accompanied by intense questioning, observing, networking, and experimenting. I have read several older chapters about myofascial induction written by Pilat in other textbooks, but this book goes far beyond anything I have read before or seen during Pilat’s lectures. It was such a pleasure and enrichment to learn about tensegrity, the embryological development of the extracellular matrix, fascial anatomy, pain sciences, allostasis, interoception, and additionally, myofascial induction – all in one book! The many outstanding illustrations, including line drawings, exquisite anatomy photographs, and diagrams complement the text together with links to supporting videos online showing Andrzej at work. While at times, Pilat becomes rather philosophical, he never loses track of educating clinicians and scientists across a wide spectrum in the current knowledge of fascia. I admire and congratulate Andrzej Pilat for

this phenomenal book. It is such an honor to introduce you, the reader, to this outstanding publication. Jan Dommerholt PT, DPT Bethesda Physiocare, Inc. Myopain Seminars Lecturer, Department of Physical Therapy and Rehabilitation Science, University of Maryland Bethesda, MD, USA, September 2021

FOREWORD by ROBERT SCHLEIP Fascia is a connecting (t)issue. While Western conventional medicine underestimated it for centuries as a mere packaging organ, recent advances in assessment methods – such as shear wave ultrasound elastography or harmonic generation microscopy – have triggered an avalanche of new discoveries and insights into the collagenous tissue network that keeps many researchers and clinicians around the world on their toes. Although many aspects remain to be explored, recent publications have shown that this network not only influences muscular force transmission in a significant manner but also constitutes our richest sensory organ. One of the fascinating aspects of the fascial network is its connective nature, which makes it difficult for precision-minded thinkers to describe its clear boundaries and distinctions in a satisfactory manner. While this fact is frustrating to some, it has also piqued the interest of esoteric healing practitioners who wish to project far-reaching hypothetical abilities, such as telepathic intuition or cosmic resonance transmission, into this elusive tissue network. Indeed, among the many different scientific and therapeutic congresses I have attended, I have never seen such a diverse and interdisciplinary audience as at fascia-oriented congresses, ranging from biomechanical engineers, plastic surgeons, meat scientists, matrix biologists, and orthopaedic researchers to osteopaths, yoga teachers, meditation instructors, martial arts gurus, and Reiki practitioners. What does this aspect have to do with the excellent book you are holding in your hands right now? Let me explain after completing the next

two paragraphs. Having been a holistic therapy practitioner and missionary myself for several decades, my personal path has led me more and more to the humble, questioning approach of those scientists who are interested in unraveling the mysteries of the human body in many small and careful steps. When it comes to drawing conclusions about cause-and-effect relationships in the fascia-oriented field I personally tend to side with those researchers who work with a curious “we don’t know” attitude. This approach can be frustrating as it is often less exciting and less charismatic than allowing our wishful thinking to generate broad assumptions and easy explanations about the implications of a perceived fascial phenomenon. On the other hand, I must confess that for therapeutic treatment of myself or my family members, I continue to appreciate the healing attention of therapists who work with a more holistic and intuitive approach. In my experience, their quality of touch, loving presence, and wonderful enthusiasm are priceless components of a healing relationship. These qualities are less often found – at least not with the same depth – among my respected scientific colleagues. Or to put this observation the other way around: When listening to the personal explanations of the best therapists in our field about the healing mechanisms involved in their work, one must often be prepared to hear interpretations that any of my undergraduate Life Science students would easily recognize as premature logical conclusions. If you have already guessed how this situation relates to the author of this book and the brilliant book he has written, you have my collegial applause. Yes, the author, Andrzej Pilat, is indeed a very rare exception to the common disparity described here. I consider him one of the best manual therapists I know, and I do not say that lightly. When I see Andrzej at work, I feel as if I am watching a master artist, like Michelangelo as a painter or like a Butoh dancer in slow motion. But the most impressive aspect for me is his connection with the client: Both seem to be united in a joyful and almost hypnotic process of discovery. Nevertheless, when Andrzej describes his work in terms of suggested fascia changes, I feel like asking all my students to join me in listening to him with eager attention. The way he weaves together various findings and

issues of the latest international research is truly outstanding. The author of this brilliant book has not only been a passionate manual therapist for many decades but has also been actively involved in academic fascia research, including the first Fascia Research Congress (Harvard Medical School Conference Center, Boston, 2007), all subsequent such events, and in several similar congresses which he hosted himself and used to interact personally with the leading scientists in our field. Those of you who have had the pleasure of attending one of the international Fascia Research Congresses know that Andrzej Pilat’s presentations tend to be absolute highlights. After his presentation, he is usually surrounded by a crowd of enthusiastic attendees who want to collaborate with him in one way or another, or to find out how they can get their hands on the fantastic photos and videos of fascia anatomy that he has shown. For many years, his constant response to the latter request has been: “Give me a little more time to finish my book, which will contain all of this and much more.” Here it is, dear friends and companions in the field of fascia research: the long-awaited – and I think truly historic – contribution of Andrzej Pilat to our common field of fascination. Many of the fascial images, based on fresh tissue dissections, are the best presented outside of professional conferences. One cannot help but admire the beauty of the complex architecture of the wonderful connecting tissue called fascia. The book also provides an up-to-date overview of what is currently known about the many functions of this tissue. Finally, this masterpiece in print introduces you to a fascia-oriented manual treatment method that you will surely want to experience yourself after reading the first few chapters. I congratulate the author for this fantastic achievement. Myofascial Induction™: An anatomical approach to the treatment of fascial dysfunction is a milestone contribution to the literature on fascia. Robert Schleip Dr biol.hum., Dipl.Psych. Visiting Professor, IUCS Barcelona, Spain Director, Fascia Research Group, Ulm University, Germany Research Director, European Rolfing Association

Munich, Germany, September 2021

FOREWORD by ANDRY VLEEMING The complexity of fascia and its functions has been well documented, and it is evident that some of its secrets are yet to be unfolded. As this information expands, it is convenient to have a go-to source to help us bring this knowledge together and explore tools useful in applying this information in the clinical setting. Developed over years of dedication and enthusiasm this book delivers exactly that. It is systematically organized to take the reader through the relevant clinical research and literature. It does so in a way that enables us to gain a greater understanding of this three-dimensional sensory organ. Let me explain why… Because it is a continuous matrix fascia is not easy to map. It reaches out to all corners of the body and to every cell. It provides the framework that helps support and envelop muscles, organs, blood vessels and neurons, enabling the body to function as a whole. Its various mechanical properties are intriguing and complex. Addressing this complexity, this book does a wonderful job of bringing us up close and personal to the topographical anatomy. It also helps us explore, through illustration, the anatomical continuity of the fascia and how it relates to other body systems. This is achieved through the use of wonderful photographs and diagrams that help the reader visualize what lies beneath the skin. To start you off in this exploration, the opening chapters provide the reader with an overview of what is currently known in the field. This includes an in-depth description of fascial topographical anatomy, its layers

and architecture. The book then explores embryological development, histological characteristics, neurodynamics, and the role of force transmission relating to the fascia. The later part of the book invites the reader to explore the clinical applications of Myofascial Induction Therapy. This section is neatly categorized into treatment regions – craniofacial, craniocervical, the thorax, upper and lower extremities – with each region providing detailed information regarding clinical assessment and dysfunction. The relevant manual techniques are clearly described in a format that is easy to follow. Evidently much thought has been given to the layout of this book, employing wonderful photography and well-designed diagrams, enabling us to get a deeper understanding of the fascial system. If you wish to expand your knowledge of the anatomical approach to the treatment of fascial dysfunction Myofascial Induction™: An anatomical approach to the treatment of fascial dysfunction will be a very welcome addition to your collection. My warmest congratulations to you, Andrzej Pilat. Professor Andry Vleeming PhD Chairman, Interdisciplinary World Congress on Low Back and Pelvic Girdle Pain Antwerp, Belgium, September 2021

PREFACE The truth of science is always provisional, but still scientific research is the best method to obtain reliable information. In 2003 I published my first book on fascia and Myofascial Induction Therapy: Terapias miofasciales: Inducción miofascial. This was based on the limited scientific information then available and at that time images of fascial anatomy were very scarce. I had to undertake a detailed search for evidence to corroborate the criteria presented in that book. Today, 18 years later, the picture is very different. The problem now is how to make the best selection from the mass of high-quality scientific information on fascia that is available today. This detailed and richly illustrated book distils that information, and puts it into the context of my own extensive study of human tissue, creating a unique textbook and manual on the fascia and on how to manage its dysfunctions. Over the past 15 years I have undertaken many dissections of unembalmed cadavers and this work has allowed me to open up new perspectives in the field of fascia research. Through these anatomical explorations I discovered the harmony, omnipresence, architectural complexity, diversity, and continuity of this amazing fascial system. No less fascinating (although complicated and laborious) was the photographic effort necessary to capture this infinite, diversified, and colorful network. Through macrophotography I discovered the hidden beauty that is the continuum of the endless fascial web. As a result of this detailed research, the extensive approach to fascial anatomy presented in the book (with the support of numerous full-color photographs and videos) encompasses not only the topography of the fascial tissue but also shows its elegance,

structural continuity, and coherence within the chaos. It invites the reader to explore its microstructure and to recognize its essential role and active participation in body movement. Within the contemporary conceptual framework new terminology differentiates between anatomical structure (fascia) and function (fascial system) – a complex biological system responsible for communication (transmission of information) between body components and with the environment. The movement of each human (for example, walking) is personal and almost impossible to duplicate. The uniqueness in the configuration of each individual’s fascial system is part of this process. In order to achieve the desired movement our brain manages its complex neural network, selecting for activation those motor units that enable optimal performance for the task in hand. It is obvious that in this process, the muscles (muscle tissue) are the main engines of movement. However, it should be remembered that none of the muscle fibers acts in isolation. They are fascial structures that transmit dynamic adjustments according to demands. Following this reasoning, the question is: What is the significance of fascia for body movement and what is its relevance in the therapeutic processes? In this context, the book deals with fascia and kinesis, the latter defined in the Merriam-Webster dictionary as “a movement that lacks directional orientation and depends upon the intensity of stimulation.” A human being can choose his movement at will. This attribute is guided by the brain. The brain uses past experiences to anticipate movements. The brain does not see the future, but makes intelligent predictions about what will happen in the immediate future. It is a learning process that involves the senses (exteroception). In this way we perceive the world. In parallel, the same senses are influenced by body condition (interoceptive messages) based on experience, which is personal. The plasticity of the nervous system allows body movement to accommodate to diverse circumstances (for example, facing dangerous situations) based on experience and current information. The nervous system and the fascial system share the principles of plasticity, and adjust movement in an anticipatory and individual way for each person.

This process facilitates the ability to easily recover or adapt to misfortunes or changes (resilience). Myofascial Induction™: An anatomical approach to the treatment of fascial dysfunction describes the properties of the endless and omnipresent fascial network and provides therapeutic solutions for different types of fascial dysfunction. The material is presented in two volumes: Volume 1 analyzes in depth the theoretical aspects related to fascia and focuses on the therapeutic procedures of Myofascial Induction Therapy (MIT™) for the upper body; Volume 2 summarizes and expands on the theoretical aspects and explains the therapeutic procedures of MIT™ for the lower body, where the lower extremities have the function of supporting the weight of the body in the bipedal position and making movement possible through the coordination of their powerful muscles. The chapters of Volume 2 cover the theoretical aspects of fascial system behavior in the lower body segment. The later sections of Chapters 4, 5, and 6 detail the practical applications of Myofascial Induction for the lower body. In the theoretical sections, after defining the fascia as a complex multifunctional biological system, its role of communicator between body systems is discussed in relation to the following issues: human existence as a biological behavior the role of fascia in exteroception, interoception, proprioception, and nociception the influence of fascia on homeostasis the response of fascia in relation to General Adaptation Syndrome the important role of fascia in allostasis and development of allostatic load thoracolumbar fascia as the heart of the matter the role of fascia in pelvic girdle behavior fascial dynamics related to pelvic floor dysfunction

fascia and nerve entrapment syndromes of the lower extremity the complexity of the fascial compartment system. In the practical sections of Chapters 4, 5, and 6, the reader will find a wide range of manual therapeutic procedures which can be selected and used in combination to build up the MIT treatments. These processes are explained in detail and are richly illustrated with diagrams and photographs of their practical application on the body and of hand contacts on samples of dissected tissues. The final chapter summarizes practical aspects of clinical applications, discussing subjects such as: the basic goals of the therapeutic process touch as a therapeutic modality the hand as a therapeutic tool practitioner skills patient’s skills. The introduction to each chapter offers the reader some philosophical background as a reminder that philosophy allows us to relate the strictly scientific with the empirical. Praxis and empiricism are the basis of science. I invite you to join the scientific fascial adventure that allows us to uncover areas of knowledge which may have been forgotten or which are not yet recognized as being related and which might still reveal relevant information. Once discovered, these facts can help us to better understand the kinesis of our body and so help the individual to change their body image and to improve their quality of life. Andrzej Pilat Madrid, December 2022

ONLINE VIDEOS Chapter 4 Video 4.1 Dynamics of the abdominal fascia

Video 4.2 Transverse stroke applied to the psoas

Chapter 5 Video 5.1 Continuity of the gluteal fascia with the thoracolumbar fascia and fascia of the thigh

Video 5.2 Relationship of the sciatic nerve and the piriformis muscle in the subgluteal fold

Chapter 6 Video 6.1 Anatomical continuity of the skin, superficial fascia, and deep fascia in the knee area

Video 6.2 Anatomical structures of the deep fascia of the thigh

Video 6.3 Cross-section of the metatarsal zones

Video 6.4 Longitudinal induction applied to the plantar fascia

Video 6.5 Longitudinal stroke applied to the anterior and lateral compartments of the lower leg

Video 6.6 Deformation of the deep fascia related to movements of the patellofemoral joint

Video 6.7 Anatomical relations of the deep fascia of the thigh and the epimysium of the quadriceps

Video 6.8 Longitudinal stroke applied to the posterior border of the iliotibial band (demonstrated with knee extended)

ACKNOWLEDGMENTS The discovery of the double helix of DNA, whose structural coherence hides in code the morphogenetic and informational potential of life, opened the way to modern biology. It also marked the beginning of the close collaboration between biology, physics, and progressively other disciplines such as computing. The relatively simple interactions between different pairs of nucleotides reveal the almost infinite capacity to store information in the DNA heteropolymer. It is the intimate connection between interaction and information that constitutes the fabric of living matter. Biological complexity is based on specific interactions between molecules. These interactions create complex networks that are balanced by their interconnection. These networks control and regulate the exchange of signals that govern intracellular functions and multicellular behavior throughout the development and functioning of the organism. This fascinating advance of science forced the change of paradigms and integration of scientific streams. The analysis of the behavior of the fascia, as the integrating structure of the body, did not escape these requirements. Thus, the act of writing this book on fascia turned into a long and fascinating scientific adventure. Although not an expert in the aforementioned disciplines, I was fortunate to have the advice and help of friends who made this trip possible and enabled me to finally dock at the destination harbor. My sincere thanks to all listed below for having accompanied me on this long and winding journey. First of all, I would like to thank the editorial team at Handspring Publishing (Mary Law, Andrew Stevenson, Sally Davies, Bruce Hogarth,

Morven Dean, and Hilary Brown) for their dedication, patience, professionalism, and attention to detail in search of editorial perfection. I would like to thank my family for allowing me the long months (years) dedicated to writing the book, especially my wife Yulita, for her unconditional support and her contribution to so many tasks, and also my children Eva, Mártin, and Kamil. Thank you to my friend, architect Michele Testa, for teaching me to select and synthesize the avalanche of scientific information to solve seemingly insoluble problems. I would like to thank the ETM Tupimek team, particularly my son Mártin Pilat, Germán Digerolamo, and Eduardo Castro-Martín for their extensive help, reviews, and critical reading of the manuscript as well as their contributions on issues that I was unaware of. Also, I am grateful to Javier Rodríguez and Jorge Sánchez for their help in preparing the illustrative material and to Rafael García for his help in the search for scientific information. Thank you to the PROMPT team, especially Francesco Testa, Iván Arellano, and Andrea Fiorucci for developing the illustrative material for the book and reflecting my thoughts in the drawings. I am extremely grateful to the late Professor Dr. Horacio Conesa for allowing me to live the adventure of discovering the enigmas of the fascia in anatomical dissections. I would like to thank Dr. Nicolás Barbosa for his art of dissecting fascia during the long hours of anatomical work that we shared. I would also like to thank Professor Dr. Maribel Miguel-Pérez and Dr. Albert Perez-Bellmunt for their critical review of my anatomical interpretations. Thank you to Dr. Ramón Gassó for his analysis and helpful opinions on fascial physiology. I thank the photographer Óscar Ruiz for his art of capturing therapeutic applications in photographic subtlety.

Thank you to Ailén Botta Mazzone for her patience and grace in modeling the applications of therapeutic procedures. I would like to thank Javier Álvarez for introducing me to the world of the analysis of fascia through images and for obtaining the samples for the book. Finally, my special thanks to all who have been part of this adventure.

1 Connecting and moving forward: Fascia as a multifunctional system

KEY POINTS ● The physiological properties of fascial macrostructures in relation to body movement

micro-

and

● The characteristics of movement ● Definition of the internal environment ● The participation of fascia in homeostasis and allostasis behavioral responses ● Correlation of movement with the processes of exteroception, proprioception, and interoception ● Analysis of the nociceptive role of fascia

Introduction The discovery of the double helix of DNA, whose structural coherence conceals the morphogenetic and informational potential of life in code, opened the doors to modern biology. It also marked the beginning of close collaboration between biology, physics, and progressively other disciplines such as computing. The relatively simple interactions between different pairs of nucleotides reveal the almost infinite capacity to store information in the DNA heteropolymer. It is the intimate connection between interaction

and information that constitutes the fabric of living matter. Biological complexity is based on specific interactions between molecules. These interactions create complex networks that are balanced by their interconnection. These networks control and regulate the exchange of signals that govern intracellular functions and multicellular behavior throughout the development and functioning of a living organism such as the human body. Each person is characterized by the individuality of their movements that adapt according to the demands of their body and the environment and to the resources available at a given time. Movement patterns vary from person to person. Equally, the same individual modifies their movement pattern when performing the same task multiple times. These differences in movement patterns are more apparent amongst people suffering from the same dysfunction or disease (e.g., mechanical low back pain). In traditional anatomical and biomechanical research performed on embalmed cadavers, muscles are presented as independent units. This suggests a series of unrelated elements instead of a unique and continuous configuration linking the structures of the body (Pilat et al. 2016). Such an approach makes the analysis of the dissected elements difficult when integrated into a higher level of organization (Huijing 2009). This leads to an understanding of human body movement based on segmental anatomical and biomechanical knowledge. However, a body is more than the sum of its parts and it is so by virtue of the new properties that arise from the relations between parts. The specificity of body behavior comes from the complex integrated functioning of its entirety, and not just from the structural and functional nature of the separate components. In parallel, in the traditional model the concept of “fascia” is related to some anatomical structures such as the tensor fasciae latae, the palmar fascia, the thoracolumbar fascia, and muscle sheaths: In this perspective, muscle forces are transmitted serially, and the torque developed around a joint depends only on the muscle’s torque arm geometrical configuration. Movement patterns are therefore, analyzed through a linear framework of isolated muscle

groups, based on singular muscle attachments and isolated joint actions. (Garofolini & Svanera 2019) Anatomical studies of unembalmed cadavers have provided a new perspective on fascia, which differs from the traditional “fibrous sheet” that “hides” the muscle (Pilat et al. 2016). Without minimizing the importance of treatment protocols, it is worth highlighting the need to customize applications according to the individual patient’s requirements. These processes accentuate the need to understand body movement as a set of synergies that facilitate the exchange of information, communication, and interaction between each other (see Volume 1, Chapter 17). “Motor synergies represent the coordination of neural and physical elements embedded in our bodies in order to optimize the solutions to motor problems” (Garofolini & Svanera 2019). At the base of movement organization there is a (somatic) equilibrium point that exists on the fascia where the neurologicallyand mechanically-generated tensions dynamically balance out. This somatic equilibrium point is at the base of postural control, afferent flow of information to the nervous system about the state of the muscles, and of the coordinative pre-activation of muscular contraction sequences specific for a synergy. (Garofolini & Svanera 2019) The physiological basis of movement is summarized below, justifying the need to focus on systemic reasoning in relation to body movement (see Volume 1, Chapter 2). The objective of this chapter is to argue for the personalization of therapeutic procedures and to justify the inclusion of fascia in this process.

The fascial system and communication between body systems In Volume 1, Chapters 1, 2, and 3, fascia is defined as an omnipresent, highly hydrated, richly innervated, vascularized network with a contractile

capacity – a prodigious complex biological system, which provides mechanoreceptive information to the body, facilitating communication, interaction, adaptation, and protection (Fig. 1.1). From an anatomical and functional perspective fascia is characterized by the continuity of its path, although its morphology changes along its course, adjusting to mechanochemical requirements and the different conditions and situations of each region of the body (see Volume 1, Chapters 2, 3, 6, 7, and 8). Thus, fascia acts as a single functional continuum, a nonfragmentable, complex biological system (Chen et al. 2021).

Figure 1.1 Systemic interrelationships of the fascia as part of connective tissue

Intersystem links The evidence for the anatomical continuity of fascia is discussed in detail in Volume 1, Chapter 3. However, in recent years, research has also provided new and extensive information on the intrinsic continuity and intersystem dynamics of the fascial system.

The internal environment

Effectiveness means achieving goals with an appropriate (optimal) choice and performance of resources in any circumstances, mainly in unexpected, emergent situations (Fig. 1.2). In order to function optimally (be effective) each cell of a multicellular structure (such as the human organism) needs: ● an integumentary tissue (border tissue) that delimits its contents in relation to the external medium through which it exchanges matter and energy ● an internal liquid medium, characterized by optimal physical-chemical parameters that constitute its immediate environment ● an effective communication system that allows it to act in coordination with other cells, so that the organism functions as an integrated whole. At the end of the 19th century, Claude Bernard called this liquid internal medium, which is in continuous dynamic equilibrium with the external medium, the internal environment (in contrast to the external environment with which the organism must maintain a constant exchange of matter and energy). Bernard stated that stability of the internal environment is the essential condition of “free life” (Haldane 1929, Gross 1998). Figure 1.3 shows the relationship of the body’s systems with the internal environment (Batuecas 2018, Vaticón 2018). The main component of the internal environment is the interstitium which is composed of extracellular matrix (ECM) (the substance of the interstitium), ground substance, and cells with specialized functions. The interstitium is a network of fluid-filled cavities that lies under the skin, covers all organs and cells, and acts as a shock absorber to prevent tissues from being torn by the movement of muscles, viscera, and vessels. These cavities are formed from an external structure of collagen and elastin (proteins that give the structure its resistance and elasticity). Benias et al. (2018) found that freezing biopsy tissue before fixation preserved the anatomy of the structure and thus demonstrated that the interstitium is supported by a complex network of thick collagen bundles. The authors state that: “These anatomic structures may be important in… mechanical functioning of many or all tissues and organs,” including the fascia. Recent research by Cenaj et al. (2020) affirms the continuity of

interstitial spaces of the colon and mesenteric fascia within and across organ boundaries, including within perineurium and vascular adventitia traversing organs and the spaces between them “with significant implications for molecular signaling, cell trafficking, and the spread of malignant and infectious disease.” Interstitial fibrosis (a progressive condition that is characterized by fibrous connective tissue replacing normal tissue) is produced by injury, infection, and infiltration of inflammatory cells into the small spaces between tissues. It can create alterations in the ability of tissues to glide over one another and compensatory processes leading to subsequent dysfunction, which can ultimately lead to various pathologies.

Figure 1.2 Systemic properties: the effectiveness of the system

Figure 1.3 Relationship of body systems with the internal environment (Batuecas 2018, Vaticón 2018)

An essential component of the internal environment is the extracellular matrix (ECM) (see Volume 1, Chapter 4) which “is a non-cellular threedimensional macromolecular network composed of collagens, proteoglycans/glycosaminoglycans, elastin, fibronectin, laminins, and several other glycoproteins. Matrix components bind each other as well as cell adhesion receptors, forming a complex network into which cells reside in all tissues and organs” (Theocharis et al. 2016).

Mechanotransduction Cells perceive (sense) their physical environment (the ECM) through the mechanotransduction process, converting mechanical impulses (forces and deformations) into biochemical signals, thus activating various signaling pathways. Mechanotransduction has crucial roles in physiology. “In mammals, embryonic development, touch, pain, proprioception, hearing, adjustment of vascular tone and blood flow, flow sensing in kidney, lung growth and injury, bone and muscle homeostasis as well as metastasis are all regulated by mechanotransduction” (Coste et al. 2010). Adhesion complexes at the cell surface physically (mechanically) link the ECM to the cytoskeleton (which extends from the cell nucleus to the cell membrane) through focal adhesions, comprised of integrins, talin, and vinculin, and connect the ECM to actin filaments. Intracellular forces are then transmitted through the cytoskeletal network (i.e., actin filaments, microtubules, and intermediate filaments). The cytoskeleton is coupled to the nucleus through nesprins (proteins located mainly in the outer membrane of the cell nucleus). Finally, lamins (nuclear proteins which have a structural function and line the inside of the nuclear membrane) bind DNA, thus completing force transmission between the ECM and the interior of the nucleus and reaching the cromatin structure (the complex of genomic DNA and associated proteins in the nucleus of the cell) (Fig. 1.4) (Jaalouk & Lammerding 2009). Recent research on the ECM points to the importance of its interaction with the contractile structures. “Emerging evidence shows that cells are able to sense and store a memory of their past mechanical environment” (Mathur et al. 2020, Chalfie 2009). As already described in Volume 1, Chapter 5, fibroblasts are essential cells in the dynamics of the ECM and are constantly adapting. Their behavior is related to the process of biological memory. Kirk et al. (2021) define biological memory as “the process of a sustained altered cellular state and functions in response to a transient or persistent environmental stimulus.” This process is related to the fibroblasts’ positional, mechanical, inflammatory, and metabolic memory and has implications in body homeostasis and disease (Kirk et al. 2021).

In response, these mechanical signals can adjust cellular and extracellular structure and functions, such as migration, proliferation, adhesion, invasion, differentiation, apoptosis, and gene expression, that are vital for maintaining homeostasis (Jaalouk & Lammerding 2009). Changes in cellular structure and organization, or changes in the cellular environment, can disturb the mechanotransduction process and result in altered cellular function.

Figure 1.4 Mechanotransduction process: force transmission from the extracellular matrix to the cell nucleus structure (see Volume 1, Chapter 8). *Chromatin is a complex of genomic DNA and associated proteins in the nucleus of the cell. After Jaalouk DE & Lammerding J (2009) Mechanotransduction gone awry. Nature Reviews Molecular Cell Biology 10(1):63–73

PIEZOS (and TRPV1) The 2021 Nobel Prize in Medicine was awarded to David Julius and Ardem Patapoutian for the discovery of temperature and touch receptors, which has provided insight into how heat, cold, and mechanical force can initiate the nerve impulses that allow us to perceive and adapt to the world. Julius identified the TRPV1 ion channel as a heat-activated nociceptor in the peripheral nervous terminus, providing insights into the molecular mechanisms of thermoreception (Ernfors et al. 2021). Patapoutian discovered a new class of sensors that react to mechanical stimuli in the skin and internal organs, revealing “crucial missing links” in

understanding the relationship between the senses and the environment. He took a giant step in developing the research of Joseph Erlanger and Herbert Gasser who received the Nobel Prize in Medicine in 1944 for their “discoveries related to the differentiated functions of single somatosensory nerve fibers. These discoveries established important principles for the propagation of action potentials along skin and muscle sensory nerve fibers” (Ernfors et al. 2021). Patapoutian identified the mechanically sensitive piezo ion channels. These channels contain two structurally and genetically similar proteins, PIEZO1 and PIEZO2, which are mechanically activated and mediate touch perception, proprioception, and vascular development. A mechanosensitive ion channel is an ion channel that can sense changes in the mechanical force of the cell membrane and react quickly. It is suggested that piezos consist of two segments – the extracellular and the intramembranous components. When a mechanical force acts on the cell membrane, the extracellular component will drive the intramembranous segment thus opening the orifice for ion flow. This reaction of the ion channel can convert the mechanical signal sensed by the membrane into an electrical signal or a chemical signal (Creative Diagnostics 2021). Each type of receptor has a slightly different use (Fig. 1.5). PIEZO1 is part of the blood pressure monitoring system as well as other internal systems that rely on pressure sensing, such as the respiratory, gastrointestinal, or urinary systems. PIEZO1 receptors are also found in the inner lining of blood vessels and can detect increased blood flow during physical exercise. The PIEZO1 channel also responds to a variety of mechanical force activation and can induce chronic inflammatory diseases in multiple body systems (Fig. 1.6). PIEZO2 is the main mechanical sensor for touch. Proprioception, which is also based on PIEZO2, is the recognition of the body and its segments in three-dimensional space. Piezos are involved in mechanotransduction in several critical processes, including tactile sensation, balance, and cardiovascular regulation (Mahmud et al. 2017). PIEZO1 also plays an important role in regulating CNS processing (Fig. 1.7) and participates in the regulation of the baroreceptor reflex (Fig. 1.8). This discovery was considered a landmark finding in the understanding of the important life activity of mechanical force in mammals. Changes in mechanical forces

(such as osmotic pressure) that maintain life activities can influence cellular dynamics as a result of alterations in piezos, consequently triggering different pathological processes: ● Haliloglu et al. (2016) report that: “Sensory ataxia and proprioception defect with dorsal column involvement together with arthrogryposis, myopathy, scoliosis and progressive respiratory failure may represent a distinct clinical phenotype, and indicate recessive mutations in PIEZO2.” ● Mahmud et al. (2017) report that the dominant mutations in PIEZO2 can cause different forms of distal arthrogryposis. ● García-Mesa et al. (2017) demonstrate the “occurrence of Piezo2 in cutaneous sensory nerve formations that functionally work as slowly adapting (Merkel cells) and rapidly adapting (Meissner’s corpuscles) low-threshold mechanoreceptors and are related to fine and discriminative touch but not to vibration or hard touch.” ● Mikhailov et al. (2019) suggest the involvement of mechanosensitive PIEZO1 in peripheral trigeminal nociception, which provides a new view on mechanotransduction in migraine pathology and suggests novel molecular targets for antimigraine medicine. ● Wang & Hamill (2021) conclude that: “Our proposed, non-synaptic, intrinsic mechanism, where Piezo2 tracks the highly predictable and ‘metronome-like’ intracranial pressure pulses… would have the advantage that a physical force rapidly transmitted throughout the brain also contributes to this synchronization.” ● He et al. (2021) investigated the role of the mechanotransduction of PIEZO1 in hypertrophic scar formation. They observed that PIEZO1 was overexpressed in myofibroblasts from scar tissue. In vitro cyclic mechanical stretching revealed increased PIEZO1 expression in human dermal fibroblasts. The authors state that the involvement of mechanical force is a key regulator in hypertrophic scar formation. ● Shin et al. (2021) suggest that PIEZO2 is widely expressed by neuronal and non-neuronal cells of the peripheral nervous system and by neurons in the spinal cord and brain. They conclude that PIEZO2 is not only involved in the detection of external mechanical stimuli in the skin but

may also serve to detect internal mechanical cues in the nervous system or link to other unexplored intercellular and intracellular signaling pathways in pain circuits. As fascial tissue is the safeguard of body homeostasis, an alteration in mechanotransduction can affect organ development and function and can trigger pathological processes giving rise to inflammatory, autoimmune, and degenerative changes and tumor progression (Jaalouk & Lammerding 2009).

Homeostasis In 1926 the physiologist Walter Cannon coined the term homeostasis, defining it as: “The capacity that living organisms have to maintain constant the characteristics of their internal environment” (Cooper 2008). Batuecas (2018) points out: “Cannon uses the word ‘constant,’ which, if interpreted in a strict sense, means ‘invariable.’ However, the same author, when calling this property ‘homeostasis,’ points out that the prefix ‘homeo’ means ‘similar,’ and not ‘homo’ which means ‘the same.’ Cannon highlights with this clarification his idea that the values that define the composition and other properties of the internal environment can vary, although within narrow margins.” It can be concluded that homeostasis means the maintenance of a stable dynamic state in a system through internal regulatory processes that counteract external disturbances of balance.

Figure 1.5 Expression and function of the newly discovered mechanically sensitive piezoelectric channels in multiple tissues and cells. The human body is permanently exposed to mechanical forces, either passively applied or generated inside cells. Cells can sense whether the mechanical stress of the microenvironment changes and can adapt to altered mechanical demands. Most physiological processes are related to mechanical force, which is also one of the initiating factors of tissue damage and inflammation (Fang et al. 2021, Ernfors et al. 2021, Liu et al. 2022, Kendroud et al. 2021) A Response of TRPV1 thermal sensitive ion channels B Response of PIEZO1 mechanical sensitive ion channels C Response of PIEZO2 mechanical sensitive ion channels

Figure 1.6 The PIEZO1 channel responds to various mechanical force activations and can induce chronic inflammatory diseases in multiple body systems. After Liu et al. (2022) Piezo1 channels as force sensors in mechanical force-related chronic inflammation. Frontiers in Immunology 13:816149

The appropriate fluctuation (feedback) of/between the homeostatic parameters and the consequent optimal performance of body movement depend on the efficient functioning of the three sensory systems exteroception, proprioception, and interoception that make up a coherent and integrated body map (body matrix) (Fig. 1.9).

Exteroception Exteroception can be defined as sensing the outside. The environment plays a critical role in the maintenance of normal cell, tissue, organ, and body features related to movement. The brain learns through the performance of movements. The more an action is repeated, the better the brain anticipates it and sends the correct commands to the rest of the body. The sensory inputs do not trigger motor action, rather they correct the prior estimated probability (prediction error) to create the posterior probability of the final action (prediction remodeling) (Bubic et al. 2010). It should be noted that

the brain does not see the future, rather it uses past experiences to anticipate the probable future. Thus, it makes it easier to face dangerous situations by making intelligent predictions about what could happen in the immediate future even when the attention is elsewhere. The fact that the prediction of events is independent of the state of attention suggests an automatic process. In addition to the visual cortex, this process of anticipating the immediate future involves the hippocampus, which is linked to memory which is also involved in anticipating the future (Ekman et al. 2017).

Figure 1.7 The role of PIEZO1 channels in the regulation of CNS processing. The mechanical behavior of the neural stem cell substrate affects the behavior of PIEZO1 channels. This process leads to neuronal differentiation and the development of neurite morphology and neuron-astrocyte interactions.

After Fang et al. (2021) Structure, kinetic properties and biological function of mechanosensitive Piezo channels. Cell & Bioscience 11(1):13

Proprioception Proprioception, or kinesthesia, is the body’s ability to sense its location, movements, and actions. It is based on a continuous loop of feedback between sensory receptors throughout the body and the nervous system. It is the reason we are able to move freely without consciously thinking about our environment. Interstitial receptors (free nerve endings: Aδ and/or C fibers) and muscle spindles participate in this process. Neurons sense touch, and acceleration, and respond rapidly to specific mechanical signals. Thus, when we move our brain senses the effort, force, and heaviness of our actions and positions through the sensory receptors located on the skin, joints, and muscles and responds accordingly (Proske & Allen 2019, Basmajian & De Luca 1985). Fascia is vital for the proper functioning of the proprioceptive system (Stecco et al. 2007). The presence of mechanoreceptors (Aδ and/or C fibers) (Magerl et al. 2021, Langevin 2021, Fede et al. 2020, Mense 2019, Corey et al. 2011, Tesarz et al. 2011) and muscle spindles (Banks & Barker 2004) embedded in the fascial tissue suggests active participation of the fascia in proprioception, force transmission, and motor control (Mense 2019). The proprioceptive role of the fascial network means that it can update the central nervous system on mechanical tension so that it operates motor units at the right time, rate, and stage of force. According to Mense (2019), the lack of corpuscular proprioceptors in the fascial tissue is not an argument against a proprioceptive function of the fascia.

Figure 1.8 The role of PIEZO1 and PIEZO2 in the regulation of the baroreceptor. The increase in blood pressure causes widening of the aorta and carotid artery and is detected by the abundant PIEZO1 and PIEZO2 channels in the nodose-petrosal-jugular ganglion complex. This complex contains the cell bodies of the aortic baroreceptor neurons that send information via the vagus nerve to the nucleus of the solitary tract in the

medulla (as do the carotid receptors via the glossopharyngeal nerve). The baroreceptor reflex is an integrated reflex that allows changes in blood pressure to be corrected, mainly by varying cardiac output and peripheral resistance to the passage of blood. The force of high blood pressure is transformed into an electronic signal through the activation of PIEZO1 and PIEZO2, which is transmitted to the spinal cardiovascular center. Stimulation of the nucleus of the solitary tract inhibits sympathetic activity toward peripheral blood vessels producing a depressant effect. Consequently, blood pressure and heart rate are reduced. After Fang et al. (2021) Structure, kinetic properties and biological function of mechanosensitive Piezo channels. Cell & Bioscience 11(1):13

Figure 1.9 Movement and the integrated body matrix response – integration of the three senses (exteroception, proprioception, and interoception). Activation of the interoceptive adjustments can lead to an autonomic nervous system response (sympathetic or parasympathetic) or can allow the performance of a habitual action such as drinking a cup of coffee. 1 General rules intended to regulate behavior or thought. 2 Steps in reasoning, moving from a premise to logical consequences.

After Quattrocki E, Friston K (2014) Autism, oxytocin and interoception. Neuroscience and Biobehavioral Reviews 47:410–430

Muscle spindles are present in the vast majority of muscles and are considered the most important proprioceptors (Proske & Gandevia 2012). Banks and Barker (2004) estimate the presence of approximately 50,000 muscle spindles in the entire human body. These fine receptors (embedded in the muscular perimysium and endomysium [Stecco & Stecco 2019]) inform the CNS about the contractile condition of muscles (the length and speed of stretching of the fascicles), muscle force, heaviness, stiffness, viscosity, and stress (Kröger & Watkins 2021, Licup et al. 2015). Motor control, our posture and locomotion are in charge of these receptors. Numerous neuromuscular diseases affect muscle spindle function contributing, among others, to an unsteady gait, frequent falls, and ataxic behavior in affected patients (Kröger & Watkins 2021, Blecher et al. 2017).

Interoception Earlier concepts have usually related interoception to visceral sensations. However, interoception is currently defined as the feeling of the physiological condition of the whole body. As humans, we perceive and feel our bodies in relation to our state of well-being, our energy and stress levels, and our mood and disposition. In order to successfully navigate the world, we must constantly shape and reshape motor outputs to best reflect the demands of the environment. When environmental demands suddenly change the reshaping of motor outputs requires dynamic subsecond changes in action plans to adaptively meet the new constraints of the environment (Brockett at al. 2020). Interoception plays an important role in the perception, anticipation, and generation of pain. Tissue microtrauma, inflammation, and fibrosis can not only change the biomechanics of soft tissues (e.g., increasing their rigidity), but can also profoundly alter the sensory input derived from the affected tissues. Alterations in interoceptive awareness are clinically related to the severity of chronic pain.

Research has identified an afferent neural system in primates and humans that represents all physiological aspects of the physical body. This system constitutes a representation of the material self and could provide a foundation for subjective feelings, emotion, and self-awareness (Fig. 1.10) (Craig 2003) (see Volume 1, Chapter 8 and Fig. 8.6). Interoceptive awareness provides a measure of sympathetic and parasympathetic activity, as well as a potential marker for deficits in self-regulation, and can modulate the exteroceptive representation of the body through interoceptive prediction. In this sense, interoceptive prediction is a reality, as is exteroceptive prediction. Since the brain is a generator of “expectation” affecting the entire body system, all of its subsystems act according to this principle (Barrett & Simmons 2015) (Fig. 1.11).

Collagen network In recent years numerous research papers on the behavior of collagen have been published. This is due to the cooperation between different branches of science, such as molecular biology, chemistry, physics, and computer science. Researchers underline the importance of analyzing the mechanical aspects of collagen and its participation in the mechanotransduction process. Collagen is the main load-bearing component of the fascial tissue. It is a structural scaffold network (see Volume 1, Chapter 5) which establishes the shape and stiffness of tissues and protects them from mechanical failure. It manages the alterations of external loads by modifying (adjusting) its structural alignment through the chemical components that modify the design of its interfaces (cross-links). Each individual collagen bundle is relatively rigid, although its spatial arrangement can provide some resilience, as collagen molecules selfassemble into a fibrous continuous and dynamic dispersed network (“network of networks”), at all levels of their construction and can harden with increasing stress. Individual collagen fibers in regular dense connective tissue, such as those in tendons, can deform by about 20 percent before rupture. By contrast, collagen networks can deform by up to 85 percent before they break (Iqbal et al. 2019, Burla et al. 2020).

Figure 1.10 The spinothalamocortical interoceptive pathway (see Volume 1, Chapter 8 and Fig. 8.6). After Craig AD (2003) How do you feel? Interoception: The sense of the physiological condition of the body. Nature Reviews Neuroscience 3(8):655–666

The design of a distributed collagen network implies that communications are carried out between cross-link points without establishing an intermediary that is in charge of central information management. There is no central server, but each user becomes a server for their own information and transmits it to others (Sharma et al. 2016). Thus, after a deformation of the fascial network reversibility is possible due to the reticular grid-like arrangement of the collagen bundles (Mense 2019). Burla

et al. (2020) report that: “Collagen networks possess a hierarchical structure that can differ at the network level (mesh size), fibril–fibril interaction level (junctions formed either by branching or fibril-fibril crossings), and fibril level (diameter) and molecular level (intrafibrillar cross-linking via telopeptide end regions).”

Figure 1.11 Processing of interoceptive and exteroceptive stimuli by the brain. After Khalsa et al. (2018) Interoception and mental health: A roadmap. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging 3(6):501–513

The connectivity, plasticity (adaptability), breaking strength, and efficiency of networks is controlled by their connectivity (shape and number of cross-links and/or branches) rather than the properties of an isolated fiber (Burla et al. 2019, Koenderink et al. 2009). Optimal configurations are between three or four cross-links of each fiber per

intersection. A higher number of cross-links makes the collagen networks less elastic, thus stimulating the development of their rigidity (Burla et al. 2020). The elasticity of the collagenous network can also be affected by the intrinsic dynamics of the cells. Myosin filaments can actively stimulate actin filaments (anchored in the network by cross-linking) and through them modify the internal tension and behavior of the tension network. Stiffness changes occur in a nonlinear manner and are distributed through cross-links between actin filaments (Koenderink et al. 2009). Alterations in the secretion of collagen by fibroblasts, as a result of mechanical changes (prolonged pathological stress over time) and chemical adjustments (excessive secretion of transforming growth factor beta-1), can also alter fascial dynamics. The process arises due to modifications of the environment (the ECM) of the mechanoreceptors and can alter other processes, such as the transfer of interoceptive and proprioceptive information (Fig. 1.12) (see Volume 1, Chapters 7, 8, and 9). The intrinsic structure of a collagen fibril is complex, facilitating mechanical and electrical (piezoelectric) properties in interaction with other tissue components. This phenomenon allows collagen to modulate the structure of the tissue and therefore its behavior. Collagen can function effectively in a wide variety of tissue configurations providing exceptional mechanical performance and fitting specialized applications. For more information see Volume 1, Chapter 13 and above in this chapter. Collagen structure can be modified as a result of various inputs: ● Hormonal input: Fibroblasts have specific receptors on the plasma membrane for estrogen and relaxin, which could regulate the production of collagen I, collagen III and fibrillin (Fede et al. 2019). ● Chemical input: Aging increases the amount of type I collagen fibers in the extracellular matrix (ECM) of the epimysial fascia and thus increases its stiffness (Pavan et al. 2020). ● Mechanical input: Immobilization and hypomobility produce a pronounced thickening of the muscular connective tissue, which affects the elasticity or stiffness of the muscle (Slimani et al. 2012) and

consequently leads to dynamic changes in joints (Wilke & Tenberg 2020).

Fascial mechanosensitivity Fascia when subjected to deformation has the extraordinary ability to change drastically from a smooth and elastic movement to a state of maximum resistance according to the intensity of the impulse received (Burla et al. 2020). This ability is crucial for biological function: When tissue is elastic cells can move. At the same time, the tissue protecting the cells must not break; therefore, it becomes stiffer when the deformation is excessive (Burla et al. 2019, Burla et al. 2020). After a deformation of the fascia, reversibility is possible due to the lattice-like arrangement of the collagen bundles (Mense 2019, Iqbal et al. 2019). The elasticity and internal stress generated by hyaluronic acid (HA) are crucial in this task (gliding behavior), significantly changing the mechanical response of the composite networks of the fascial system (Stecco et al. 2013, Stecco et al. 2018). HA is the reservoir of water and lubricant in areas of gliding movement, such as joints (synovial fluid), tendons, pleura, pericardium, and the intermuscular spaces. Its participation in scar formation, ovulation, fertilization, transduction, and tumor physiology is relevant (Pratt 2021). Fasciacytes (a form of fibroblasts) are the cells involved in HA synthesis. HA deficiency causes changes in the viscoelasticity of fascial tissue and modifies the activation (irritation) of interstitial receptors. This process can alter innervation patterns (increased receptor density) and can be involved in nociception (Fede et al. 2021b). In recent research Stecco et al. (2022) suggest that accumulation of HA in the ECM can increase fluid viscosity, leading to a lack of gliding between muscle fibers, reduced force transmission, and consequently increased resistance or stiffness during attempted movement. Finally, they suggest that the consequent alteration in the structure and function of the muscle, defined as contracture, is related to the excess of HA from the ECM that was later replaced by collagen, leading to permanent and irreversible thickening of the endomysium and perimysium.

Figure 1.12 Fibroblast–collagen behavior and the changes in fascial dynamics (see Volume 1, Chapter 5). Based on a drawing by Eduardo Castro Martín

Fascia and nociception The network of fasciae is an important part of the musculoskeletal system that is often overlooked. Fascia mobility, especially along shear planes separating muscles, is critical for musculoskeletal function and may play an important, but little studied, role in proprioception. Fasciae, especially the deep epimysium and aponeuroses, have recently been recognized as highly innervated with small diameter fibers that can transmit nociceptive signals, especially in the presence of inflammation. Patients with connective tissue hyper- and hypo-mobility disorders suffer in large number from musculoskeletal pain, and many have abnormal proprioception. The relationships among fascia mobility, proprioception, and myofascial pain are largely unstudied, but a better understanding of these areas

could result in improved care for many patients with musculoskeletal pain. (Langevin 2021) Tissue microtrauma, inflammation, and fibrosis can not only change the biomechanics of soft tissues (e.g., increasing their rigidity), but can also profoundly alter the sensory input derived from the affected tissues. The properties of the fascial mechanoreceptors, Aδ and C fibers, are widely discussed in Volume 1, Chapter 8. Inflammation of direct or neurogenic origin increases the density of nociceptive fibers which may explain pain when fascia is altered (Mense 2019). These fibers are responsible for transmitting nociceptive afferent signals and can project the traumatizing stimulus to the insular cortex instead of the primary somatosensory cortex (which is the projection of proprioceptive sensations). Free nerve endings are capable of bidirectional signaling, and therefore they can contribute to the processes of peripheral and central pain sensitization (Fig. 1.13). Continuous activation of nociceptors can worsen fibrosis and inflammation, causing further tissue stiffness and consequent movement impairment (Strigo & Craig 2016, Ikeda et al. 2003, Koltzenburg 1999). Helene Langevin, the renowned researcher in the field of fascial dynamics, points out in her recent paper (Langevin 2021) that “fascial mobility, proprioception and myofascial pain are three topics that until now have not been covered in the scientific literature, however they have a lot to do with each other. Myofascial pain is an emerging discipline that requires the development of robust tissue biomarkers, to facilitate the development of effective treatments.” Fortunately, in recent years, extensive and interesting research has been published in relation to the nociceptive role of fascia: ● Mense (2019) points out that the fascia nociceptors are the beginning of a nociceptive pathway from the soft tissues to the spinal dorsal horn and probably further to higher centers. ● Fede et al. (2020), in a precise and detailed microscopic study of patients with persistent pain after successful hip joint replacement surgery, shows that the most intensely innervated tissues are (in descending order): the

skin, the superficial fascia, and the muscles. The tendon and the joint capsule were found to be poorly innervated. ● Magerl et al. (2021) point out that “the balance between pain-inhibiting and pain-facilitating mechanisms differs between fascia and muscle, making the fascia a more likely source of hyperalgesia induction.”

Figure 1.13 The nociception process. CGRP – calcitonin gene-related peptide Based on a drawing by Germán Digerolamo

● Weiss and Kalichman (2021), analyzing the contribution of the deep fascia to various painful conditions from histological and experimental studies, report that “different components of the deep fascia, both in humans and animals are richly innervated, with some differences between body segments. These fascial components usually exhibit dense innervation, encompassing amongst others, nociceptive afferents. The application of different types of stimuli, i.e., electrical, mechanical, and

chemical to these fascial components produces long-lasting pain responses. In some cases, the intensity and severity of pain produced by the stimulation of fascia were higher than ones produced by the stimulation of the related muscular tissue.” The authors conclude that “our observations may denote that the deep fascia and its various components could be a source of pain in different pathologies and various pain syndromes.” ● Sinhorim et al. (2021) reviewed the conclusions of 257 articles (of which 10 met the inclusion criteria) based on histological, immunohistochemical, electrophysiological, behavioral, and clinical evidence. The authors report that: “Noxious chemical injection or electrical stimulation into fascia resulted in longer pain duration and higher pain intensities than injections into subcutaneous tissue or muscle.” They conclude that: “Studies showed histological evidence of nociceptive nerve fibers terminating in lower back fascia, suggesting a TLF contribution to LBP.” ● Fede et al. (2021a) in histological research examined the differences in innervation between the aponeurotic and the epimysial fascia. The authors suggest “that the two fasciae have different roles in proprioception and pain perception: the free nerve endings inside thoracolumbar fascia may function as proprioceptors, regulating the tensions coming from associated muscles and having a role in nonspecific low back pain, whereas the epimysial fasciae works to coordinate the actions of the various motor units of the underlying muscle.” ● Vogel et al. (2022) suggest that pain radiation is not simply an effect of increased peripheral input but may afford an individual disposition for the pain radiation response. Substantially higher pain-sensitivity and wider pain areas support fascia as an important contributor to nonspecific low back pain.

Neural code The activity of the neurons of the cerebral cortex represents the sensory information that we acquire from our environment, as well as the

fundamental motor and cognitive functions. We can hypothesize that mechanochemical alterations of the fascial tissue can influence the dynamics of the neural code and the consequent decision-making related to movement. The neural code is the set of combinations of activated neurons that represent in the brain the reaction to a set of stimuli (Li & Tsien 2017). It represents the direct relationship between the activity of neurons, the activity of the muscles, and the behavior of the subject (see Volume 1, Chapter 8). The neural code changes every moment: “it is liquid and constantly flowing” (Yuste 2015). The same set of stimuli can be represented with different neural codes. The neural code affects the functioning of neural networks in relation to learning (Miguel-Tomé 2019). In this way spatial objectives and the exact performance of movement are related to planning and higher level aspects rather than to the details of motor execution. From this brief analysis a question arises about the adaptation of movement in the face of a traumatizing event, particularly when maintained for an extended period of time or repeated over time (stress). Are the prolonged and frequent adjustments available to homeostasis enough to protect the organism?

Plasticity (ability to adapt) Humans, like other vertebrates, have to adapt their physiological condition to environmental changes. To define this process William James introduced the term plasticity, stating that “the laws of Nature are nothing but the immutable habits which the different elementary sorts of matter follow in their actions and reactions upon each other” (James 1890). Although the concept was defined in the field of psychology, it was Santiago Ramón y Cajál (1911) (the father of modern neuroscience) who suggested the anatomical substrate of plasticity at the end of the 19th century. Currently, we have extensive evidence of the capacity for anatomical and functional modification or adaptation of the organism throughout life. Research focuses on the cellular and molecular basis of neural plasticity that is made up of the neuron and glia. Neural plasticity is induced by the experience of a wide range of stimuli, such as environmental pressures, modifications in the internal condition of the organism, or injuries (Nieto-Sampedro 1999,

Nieto-Sampedro & Nieto-Díaz 2005). The glial cells, among which we should highlight the astrocyte, have recently been shown to be involved in many nervous system functions such as neuroregeneration processes (Katiyar et al. 2017). Astrocytes are mechanosensitive cells. They detect mechanical changes through the mechanosensitive ion channel protein PIEZO1. They participate in synaptic activity (plasticity) and in the processing of information in the brain. They also maintain the density of capillaries in the muscles, thus participating in the capacity for physical activity (Velasco-Estevez et al. 2020).

The nervous system and connective tissue (fascia) are characterized by the ability to change over time and the potential for reversibility.

From homeostasis to allostasis (Fig. 1.14) Homeostatic basal conditions (heart and respiratory rate), blood pressure, hormonal levels, and blood glucose level alter depending on the needs that arise (e.g., during activities such as sports training or hard physical work, when facing aggression or danger, or during pregnancy).

Figure 1.14 From homeostasis to allostasis and allostatic load 1 ANS – autonomic nervous system. 2 In our species the fight-or-flight response frequently does not indicate a motor response. However, when it is prolonged over time it becomes successively a stress and then a distress* response. All the phases of stress and distress carry a degree of “allostatic load.” In distress this load can be triggered excessively. 3 Allostasis is not a process that acts in isolation, rather it includes, adapts, and maintains the original homeostasis (stability). Allostasis is thought to enhance the function of homeostatic resources. * Distress is oppressive fear without a precise cause. It is an unpleasant emotion, feeling, thought, condition, or behavior that can affect the way we think, perceive impulses, and act. Its accumulation over time can affect the way we make decisions and our attitudes to health and well-being. People may express distress through sadness, anger, fear, helplessness, and/or despair. They look insecure, depressed, anxious, or overly worried and are easily panicked.

The distinguished physiologist Cannon (1915) concluded that in most cases dangerous and short-term aggression requires an intense motor response which he called fight-or-flight response. This response requires simultaneous participation of the sympathetic division of the autonomic nervous system (ANS) that provides the muscles with a large amount of

energy in a very short time, to always guarantee that the characteristics of the internal environment remain within the limits compatible with life. In addition, this response already has a conscious component based on instinct and experience that involves the limbic system (Batuecas 2018 quoting Cannon). When the response to aggression is prolonged over time, its fundamental protagonist is the hypothalamic–pituitary–adrenal axis. Its characteristics were discovered by Selye (1956) who called it General Adaptation Syndrome or stress response. The stress response is a nonspecific response that is activated against alarm factors (stressors) of a very diverse nature. Stress is characterized by an increase in the amount of cortisol, the main consequences of which are an increase in glucose levels and depression of the immune system. Prolonged stress that leads to high levels of cortisol and catecholamines maintained over time is a nonadaptive response (long-term alarm response or distress) that is associated with functional alterations with undesirable consequences (Selye 1974). This phase is characterized by a considerable functional overload of the cardiocirculatory system, a notable alteration in the endocrine profile (the concentration of hormones increases or decreases inappropriately), immunosuppression, cognitive dysfunctions, and unpleasant mood states (anxiety and/or depression). Taking into account the changing needs of the organism, a new model of physiological regulation termed “allostasis” was proposed (Sterling & Eyer 1988). Allostasis consists of the ability of complex biological systems to preserve their organization not only through reactive responses but also through anticipatory maneuvers (predictive responses). Prediction requires each sensor to adapt its sensitivity to the expected input range (negative or positive sensitization) and also that each effector adapts its response to the expected range of demand (identification of the expected response pattern). Allostatic theory is based on a permanent relationship between the brain and the rest of the body’s components (Sterling & Eyer 1988, McEwen 2000). In this process the key concept is that the brain is capable of predicting the physiological needs of the organism well in advance. Thus, previous experiences and behaviors will mark future actions resulting in a

much more efficient and economical response based on flexible and coordinated physiological control. In this context, the stress response is activated in anticipation of various challenges. Inflammation, pain, and hypomobility are allostatic responses that should conclude when the emergency is resolved. The intensive and recurrent use of allostatic resources creates an allostatic load, which is the state in which normal allostatic processes wear out when physiological systems are no longer able to adapt. The allostatic load generates adverse health consequences associated with alterations of the nervous, endocrine, and immune systems, thereby leading to mortality, morbidity, and also functional and cognitive impairment. Allostatic load is the price that the body pays for being forced to adapt to adverse conditions that should be turned off at the end of stressful circumstances. An excessive allostatic load accumulates resulting in a “distress response” (chronic stress).

Allostasis and the fascial system The allostasis approach fits with the modern concepts of: ● sensory physiology (how cells convert the exteroceptive signals to relay information about stimuli to the nervous system) ● neural computation (behavior of a set of artificial neurons, connected to each other to transmit signals) ● optimal design (the benefit of adapting to the selective stimulus of the environment). The morphofunctional characteristics of the fascia (summarized in this chapter), as well as its integration into the nervous system, allow it to be highly adaptive. When the system operates according to the principles of tensegrity, it can adapt a pre-tension state. Thus, it can maintain the connectivity between its constituent elements, which accordingly allows it to transmit or transfer forces applied to the whole system, and to always react globally to mechanical and chemical stimuli (see Volume 1, Chapter 6). The fascial system is capable of predicting and responding to mechanical events by adjusting its tension availability to functional

requirements. To achieve this goal, it uses prior recognition of a movement pattern (advance control), through chemical resources (release of growth factors) that modulate its tension state. This process also uses an organized “efferent copy” through permanent updating of the nervous system through mechanoreceptors and free nerve endings (see Volume 1, Chapter 8 and above in this chapter). It should be noted that there is a permanent state of synergism (reciprocal action) between the dynamics of the receptors and the tension state of the system. However, it also should be noted that an appropriate request for adjustments (higher tension) can increase its effectiveness, while over-demand or immobility will decrease it. These processes can trigger the progressive onset of dysfunctions that over time can alter movement, affect function, and develop into pathology. As mentioned at the beginning of the chapter, body movement is a process of synergisms which, although following physiological patterns, are simultaneously individualized in a healthy body, and particularly in movement dysfunctions and pathologies.

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2 Thoracolumbar fascia: The heart of the matter

KEY POINTS ● Analysis of the evolution of fascial anatomy and its adaptation to the orthostatic position and bipedal locomotion ● Examination of the anatomical evidence for the continuity of the fascial system ● Thoracolumbar fascia: The heart of the matter

General considerations related to the fascial system of the lower quadrant The bipedal position as an indicator of functionality The bipedal position and locomotion, as a phylogenetic and ontogenetic motor milestone, relates to cultural and cognitive evolution and is an indicator of functionality. The evolution of bipedal locomotion (motor development) has been an exercise in continuous adaptation, a strict selective design delimited by the environment (Niemitz 2010). Environmental tasks, such as the search for food, were associated with four types of challenge (González-Forero & Gardner 2018): ● 60 percent ecological (me versus nature)

● 30 percent ecological cooperative (we against nature) ● 10 percent competitive between groups (us against them) ● 0 percent competitive between individuals (me against you). Interestingly, competition between individuals was relatively unimportant. The findings are intriguing because they suggest that social complexity is more likely to be a consequence rather than a cause of our large brain size, and that human nature is more likely to derive from solving ecological problems and accumulated culture than from social maneuvers. In other words, learning to survive developed our brain more than learning to solve problems caused by others (González-Forero & Gardner 2018). Morphologically, this process dynamizes brain growth and stimulation. The new obstetric challenges caused by moving to bipedalism led to the expansion of the prefrontal cortex, which was crucial for cognitive performance and for the subsequent development of the human brain (Falk et al. 2012). Having a brain capable of understanding that the world works differently in different situations presupposes an adaptive advantage for our ancestors. All these tasks require producing adaptive and complex movements (Thorpe et al. 2007). One example of this process is communication: Speech, gestures, writing, and sign language involve muscle contractions and transmission of impulses. Bipedalism was a fundamental event because the characteristics that are unique to humans developed from it (Lovejoy 1981). However, development of the bipedal position and locomotion is not an easy task in the period when a human begins to walk after birth. Whereas a calf stands up and takes its first steps almost immediately after birth, a child needs more or less a year to do this, and it will be a long time before he or she is able to run. Although as humans we have lost certain motor competencies compared to quadrupeds, evolutionary changes have allowed us to overcome these losses. There are few examples of animals that exhibit as many kinetic abilities as humans (Gibbons 2002). Therefore, it is important to remember

that all processes of memory, sensoriality, and cognition are essential, but only to the extent they promote, suppress, or modify future movements (Nashed et al. 2017, Chan et al. 2016). The fact that humans adapted a bipedal position and locomotion forced the development of a complementary support system for the maintenance of the body’s weight and the optimization of daily activities with a rational use of energy (Willard et al. 2012). The reduction in energy expenditure and the consequent reduction in nutritional needs modified the morphology and thus the function of the upper and lower quadrants of the human body in relation to kinetic tasks. In the upper quadrant, the limbs became shorter and were released from being involved in locomotion. The thumb opposition movement improved and forearm pronation allowed the hand to grasp small objects. Thus, the upper extremities have been able to specialize in purely human functions, such as handling tools, hunting, and developing complex tools and artefacts. This characterization of movement has to be due to the impact of specific factors in the adaptation process (Medina González & Mancilla Solorza 2014). For example, birds can fly and humans cannot, but the human brain invented the airplane and human hands built it; fish can be submerged and swim under water for a long time unlike humans, but the human brain invented the submarine and human hands constructed it; quadrupeds can run quickly and humans cannot, but the human brain imagined the highspeed train and human hands constructed it. In the lower quadrant, the morphology of the human pelvis is explained by the adoption of bipedal locomotion. Nevertheless, the lumbar spine, for example, is not capable on its own of supporting loads received during daily activities (Crisco et al. 1992, Willard et al. 2012). Wood Jones (1944) considers that the topography and dynamics of the fascia of the lower extremity are linked to the fascia’s ectoskeletal function in the upright position of the body. The architectural pattern of the fascial system in the lower quadrant is thereby determined by its weight-bearing function. An example of this might be the fact that the gluteus maximus and tensor fasciae latae muscles insert mainly into the deep fascia rather than on the bone to maximize their mechanical efficiency (Willard et al. 2012).

In order to analyze fascial involvement in the mechanics of the body in relation to the bipedal position and locomotion it is essential to demonstrate the structural and functional continuity of the fascial pathway (Fig. 2.1). The usual anatomical descriptions of fascia, which mostly relate to the precise local topography of individual myofascial units linked to a specific part of the body, are not sufficient. For this reason the focus here will be on the global nature of fascial anatomy and its continuity. Note: The anatomy overview below focuses on the thoracolumbar fascia and its network. Other specific areas of the anatomy of the lower body are discussed in the clinical procedures chapters (see Chapters 4, 5, and 6). For a detailed anatomical analysis, supported by extensive illustrative material from dissections of unembalmed cadavers, the reader is referred to Volume 1, Chapter 3.

How load is transferred between the spine, pelvis, arms, and legs (Vleeming 2021) For most of this century research has focused on where pain is located and how it relates to impaired structures. The tendency to search for quantifiable “physical” impairments within isolated structures prevailed. When the “faulty” structure was identified, predominantly single-modality treatment was used to solve the problem. If this approach failed, patients were eventually classified as having a psychosomatic problem! The practical consequence of this medical approach has been that complex interactive kinematic systems were analyzed and treated as isolated “parts” with the use of increasingly sophisticated technology. This approach neglects the structure and function of the kinematic system as a whole. Subsequently, the treatment of pain and dysfunction became divided amongst several medical specialties, each dealing with different parts of the anatomy. As knowledge of functional anatomy, physiology, biomechanics, and neurology emerged, the questions changed. It was now realized that understanding musculoskeletal problems requires knowledge of how loads are transferred through the body and how

deficiencies in one part of the body can influence the function of the entire system.

Figure 2.1 The consecutive layers of fascial distribution. A Skin. B Langer’s lines. C Superficial fascia with fatty lobules. D Deep fascia. E Aponeurotic fascia (fibrous and dense connective tissue, e.g., fascia of the gluteus medius). F Epimysial fascia (the epimysium of the muscle, e.g., gluteus maximus fascia). G Muscles

With these questions in mind, it becomes of paramount importance to understand the function of the body. Using a simple model consisting of three levers (two legs or two arms and the spine) acting on the pelvis (the basic bony platform), it is not difficult to perceive that this platform, which is capable of extrinsic and intrinsic motion, must be stabilized before the levers (spine, legs or arms) can act on it. A model of biomechanical function leads to biomechanical treatments – a great emotional relief for patients shattered by chronic pain.

Thoracolumbar fascia: The heart of the matter Fascial morphology and dynamics are complex. Research suggests that the fascial structure that is most relevant to the optimum dynamic stabilization of the body is the thoracolumbar fascia (TLF) (Fig. 2.2). Gracovetsky states: the TLF is the most important structure insuring the integrity of the spinal machinery ... the viscoelastic property of its collagen has a direct impact on the way the muscles are used and forces are channeled from the ground to the upper extremities. (Gracovetsky 2008)

Figure 2.2 Thoracolumbar fascia and its attachments to the main muscles of the back

Anatomical considerations relating to the TLF system The structure of the TLF is heterogeneous and consists of layers which make up a dense collagenous network interleaved with loose connective tissue (Fig. 2.3). This architecture facilitates sliding between dense layers, speeds up muscular movement, and therefore supports the dynamics of the spine and its transmission to the extremities and head. The TLF is continuous with the aponeuroses of major trunk muscles which are involved in movement and vertebral control. To achieve the latter requires the unification of the dynamics of an extensive and powerful muscular system (trapezius, latissimus dorsi, gluteus maximus, rhomboid, serrati posterior, internal oblique, external oblique, transversus abdominis, erector spinae complex [multifidus, longissimus, iliocostalis], and quadratus lumborum muscles). The anatomical links between the pelvis and the lower limbs (through the sacrotuberous ligament and biceps femoris muscle), and between the trunk and upper limbs and the head (through the splenius cervicis and trapezius) are through the TLF (Fig. 2.4). Extensive research supports the argument that the TLF participates in the maintenance of the bipedal position, locomotion, and breathing and engages in the flexion and extension of the trunk and force transmission between the upper and lower body quadrants (Gatton et al. 2010, Gracovetsky 2008, Carvalhais et al. 2013, Willard et al. 2012, Chaitow 2004). First, to help understand the anatomy of the TLF, the role of the superficial structures (the skin complex and the superficial fascial system) is explored briefly below (see also Volume 1, Chapter 3).

Figure 2.3 The superficial layer of the deep fascia of the back. Note that the epimysium of the latissimus dorsi and gluteus maximus is a very thin structure. In contrast, the aponeurotic fascia of the gluteus medius is thicker, denser, and more resistant A Trapezius B Epimysial fascia of the latissimus dorsi C Posterior layer of the TLF D Aponeurotic fascia of the gluteus medius E Epimysial fascia of the gluteus maximus

Figure 2.4 Muscular attachments to the superior and deep laminae of the posterior layer of the lumbar fascia. After Barker PJ, Briggs CA, Bogeski G (2004) Tensile transmission across the lumbar fasciae in unembalmed cadavers: Effects of tension to various muscular attachments. Spine (Phila PA 1976) 29(2):129–138

The fascial layers The fascial system of the trunk is a tridimensional assembly of multilayered structures (Fig. 2.5):

● At the surface level, the skin (with the presence of Langer’s lines) is a multilayered, continuous, pre-stressed structure. ● The superficial fascia (with abundant fat content, richly vascularized and innervated) lies directly below the skin and is continuous with it. The superficial fascia does not manifest itself as a clearly defined morphological layer but rather as a tridimensional net of integrated compartments that define the location and morphology of the fat lobes. ● The deep fascia (a fibrous and multilayered structure) is located below the superficial fascia, and connects with the deeper fascial systems (myofascial, neurofascial, viscerofascial, etc.).

The skin The skin is a complex anatomical and functional organ. It remains in a state of continuous pre-tension and participates actively in body movements. “Skin is expected to oscillate during muscle contractions or limb movements” (Yoshitake et al. 2016). This behavior can also be observed during isometric contraction (Yoshitake et al. 2002) and “the activations of motor units induce oscillations in the skin on the muscle caused by muscle deformation” (Yoshitake et al. 2008). Recently, Gómez-Gálvez et al. (2018), while studying the embryonic development of animals, observed that the epithelial cells adopt a novel shape, the “scutoid” (Fig. 2.6). These cells are packed in three dimensions and are in a tightly packed order. Any movement equals a change of shape and consequently leads to energy expenditure. The lateral faces of scutoids can be concave or convex and thus scutoids fit closely together and with no space between them. The authors propose that “scutoids make possible the minimization of the tissue energy and stabilize three-dimensional packing.” They conclude that: “scutoids are one of nature’s solutions to achieve epithelial bending.” Could the scutoid be an extension of the tensegrity model?

Figure 2.5 Stages in the dissection of the thoracolumbar fascia 1 Skin dissection. The skin has been dissected and turned over. Note the vascularization and mechanical continuity of the superficial fascia on the trunk. The blood supply is different in each area – it is abundant in the interscapular and lumbar region and less abundant in the back and gluteal region. Note also the “mirror effect” of vascularization between the skin and superficial fascia areas A Superficial fascia on the dorsal area B Incision line to separate the skin from the superficial fascia C Skin (underside) D Superficial fascia on the lumbar area E Superficial fascia on the gluteal area 2 Superficial fascia dissection. The superficial fascia has been dissected, lifted, and turned over A Superficial fascia (underside) B Deep fascia C Section line 3 Deep fascia dissection. The deep fascia has been dissected, lifted, and turned over A Skin (underside)

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B Superficial fascia (underside) C Deep fascia (underside) D Trapezius E Latissimus dorsi F Thoracolumbar fascia G Gluteus maximus Attachment of the TLF to the large muscles A Trapezius B Superficial fascia (underside) C Deep fascia (underside) D Thoracolumbar fascia E Gluteus maximus

Figure 2.6 A The scutoid – a fascinating new geometrical shape discovered in nature. Both parts of the drawing are scutoids. Although it is difficult to see from this perspective, the surfaces where the two scutoids meet are curved. B Posterior aspect of the proximal right thigh showing closely packed fat lobes embedded in the superficial fascia network. This arrangement resembles the scutoid model (circled area) Figure A is from Gómez-Gálvez P, Vicente-Munuera P, Tagua A, Forja C, Castro AM et al. (2018) Scutoids are a geometrical solution to three-dimensional packing of epithelia. Nature Communications 9(1):2960. Open access. https://creativecommons.org/licenses/by/4.0/.

A network of continuous pre-tensional lines is present in the skin structure. They are called Langer’s lines (Langer 1978) and coincide with the dominant axis of mechanical tension in the skin, creating an

uninterrupted and dynamic network. (Seo et al. 2013, Gibson 1978) (Fig. 2.7) (see Volume 1, Chapter 3).

Figure 2.7 The distribution of Langer’s lines on the trunk and pelvis and their continuation to the limbs

The normal condition of skin tension becomes distorted during pathological processes (e.g., scarring). The misshapen tissue at the surface (epidermis) expands, deforming the underlying structures (Fig. 2.8) (Tsukahara 2012). As a consequence, the skin’s tensional behavior can be altered and affects not only muscle action but also the dynamics of subdermal components, such as the flow of cutaneous nerves, blood, and lymph vessels. Recently, Imagita and Sukezane (2018) investigated the influence of adhesion-related destruction of the fascial structure on dermal and

subcutaneous tissue movement. They prepared “an adhesion model by incising the subcutaneous tissue to anterior tibial muscle and suturing it. After 4 weeks, adhesion was present, restricting dermal movement, and fascial gliding was increased below the site of adhesion during passive articular movement.” They conclude that “such an imbalance in fascial gliding may promote the release of algesic substances, inducing pain, immobility, and arthrogryposis.” The term arthrogryposis is not a specific diagnosis, rather a clinical finding, and it is used in connection with a very heterogeneous group of disorders that include the common feature of multiple joint contractures. When only one joint is affected by a contraction, the condition is not called arthrogryposis (Bamshad et al. 2009). According to Wilke et al. (2020), there is a direct mechanical relationship between the superficial fascia and the dynamics of the skeletal muscles. Compared to resting conditions, restriction of movement of and within the superficial fascia (for example, following scarring) can alter muscle dynamics and vice versa. Consequently, the long-term changes can modify the flexibility of the upper or lower adjacent joints.

Figure 2.8 Fascial entrapment on an area of the back. Note the attachment of the skin and superficial fascia to the deep fascia. Note also the different types of fat deposit in the entrapment area

The superficial fascial anatomical links between the trunk and lower limbs Superficial fascia is located at the subdermal layer. It is firmly attached to the dermis and expands inward until it reaches the deep fascia. Its network supports the arrangement structure of the fatty lobes (Fig. 2.9). The morphology of the superficial fascia varies according to the anatomical area, sex, and age. In the trunk, along its posterior path, after covering the cervical, thoracic, and lumbar areas, it continues to the iliac crest running the length of the entire lower extremity up to the end of the foot. Anteriorly, passing from the cervical segment through the pectoral and abdominal areas to the inguinal area it then becomes the fascia of the thigh and leg, continuing to the dorsum of the foot. This system can be compared to a wetsuit that “intimately” covers the whole body. However, throughout these changes in its path, shape, thickness, and number of fatty lobes, its continuity is always present.

The deep fascial anatomical links between the trunk and lower limbs The deep fascia manifests as a fibrous structure with a continuous path. Beginning at the head it is continuous with the neck, then it covers the pectoral and abdominal area and continues to the iliac crest. In the posterior aspect from the head it continues to cover the back, reaching the iliac crest. From the inguinal region and iliac crest the deep fascia continues up to and including the foot without interruption. Along its course, and associated with its topography, it has different names: gluteal fascia, fascia lata, crural fascia, and fascia of the foot. Throughout its path the deep fascia extends to bones, forms compartments that house muscles and viscera, and marks the course of the vascular and nervous structures (Fig. 2.10).

Conceptual (anatomical) models of the TLF The TLF manifests as a complex system that covers and connects the back muscles and it appears to be the largest aponeurotic body structure (Barker et al. 2004, Barker et al. 2010, Hodges & Cholewicki 2007, Willard et al. 2012). It expands along to the back reaching the sacrum and unfolding laterally joins the abdominal fascial system (Fig. 2.11). With the two fascial

systems (abdominal and thoracolumbar) it forms a kind of dynamic girdle that controls and protects the lumbar spine (Fig. 2.12). Its large area and location allow it to act as a bridge structure between the muscles of the trunk and extremities (Fig. 2.13). Following analysis of the prenatal development and growth of the TLF in macroscopic dissections, Abe et al. (2021) conclude that it is a clear example of the development of “interfascial connections and their topographical relation to muscles.”

Figure 2.9 The superficial fascial system of the lower limb. This specimen is from the unembalmed cadaver of an obese person

Willard et al. (2012) state that “the TLF is a girdling structure consisting of several aponeurotic and fascial layers that separates the paraspinal muscles from the muscles of the posterior abdominal wall.” However, the TLF is not just a passive separator between muscles but rather a complex and dynamic system that is essential for the body’s movement. In the literature there is no unified criteria for the nomenclature relating to the TLF and also there is no consensus on the conceptual (anatomical) model of its morphology and mechanics. The two most accepted models are the two-layered model (Stecco 2015) and the three-layered model (Willard

et al. 2012, Bogduk & Macintosh 1984, Barker et al. 2007). The observations on the dissections of unembalmed cadavers in this book focus on the two-layered model according to Stecco (2015), which states that: “From a functional point of view, the anterior fascia is more closely related to the fascia of the pelvis (iliopsoas fascia) and the abdomen (epimysial fascia of the transversus abdominis muscle), rather than the thoracolumbar fascia.” The two-layered model consists of posterior and anterior layers (Fig. 2.14). The posterior layer covers the paraspinal muscles from behind, and the anterior layer separates the paraspinal muscles from the quadratus lumborum muscle: ● The posterior layer of the TLF (common to both the two-layered and three-layered models) is related to the superficial layer of the deep fascia of the back. It extends over the thoracolumbar area and covers the belly of the paraspinal (multifidus, longissimus, and iliocostalis) muscles. It consists of three collagenous fiber-bundled sublayers: the aponeurosis, the thin epimysium of the latissimus dorsi, and the aponeurosis of the serratus posterior inferior muscle (Fig. 2.15) (Willard et al. 2012). The anatomical connections along its path are as follows:

▶ Cranially, it extends to the trapezius and rhomboid muscles and rises to the nuchal fascia (Fig. 2.16-2, Fig. 2.17). ▶ Caudally it attaches to the posterior superior iliac spine (Fig. 2.16-1) (see also Fig. 2.17, label F), then joins the aponeurosis of the serratus posterior inferior muscle (Fig. 2.15, label G, Fig. 2.16-1), and finally follows the iliac crest up to the origin of the gluteus maximus muscle (Fig. 2.16-1, Fig. 2.15, label J).

▶ Laterally it communicates with the latissimus dorsi (Fig. 2.16.1), external obliques (Fig. 2.16-4), and trapezius (Fig. 2.16-1). ▶ Medially it attaches to the supraspinal ligament and spinous process up to the L4 level (Fig. 2.16-3). ▶ Below the L4 level it attaches to the medial sacral crest (Fig. 2.16-3).

▶ Below the L4–L5 level some fibers cross the midline of the sacrum and

end in the posterior superior iliac spine, the contralateral iliac crest (Fig. 2.16-3, circle), and the long dorsal sacroiliac ligament.

▶ It ends with the complex anchorage at the level of the sacrum. ▶ At the lateral raphe the posterior layer of TLF creates an intersection

that continues with the aponeurosis of the latissimus dorsi (Fig. 2.164), the transversus abdominis muscles, and the iliac crest (Fig. 2.16-5). After sectioning and separating the superficial lamina of the TLF, the mass of the spine extensors (multifidus, longissimus, and iliocostalis muscles) can be observed (Fig. 2.11). This group of muscles is located in the compartment composed of the spinous and transverse processes of the lumbar vertebrae and the superficial and deep sheets of the TLF.

▶ In this layer, note the connection of the latissimus dorsi and the

contralateral gluteus maximus muscles through the TLF (Fig. 2.18).. Carvalhais et al. (2013) demonstrated that manipulation of the tension of the latissimus dorsi muscle modified the passive hip variables, providing evidence of myofascial force transmission in vivo between the gluteus maximus and latissimus dorsi muscles on the opposite side.

● The anterior layer of the TLF separates the paraspinal muscles from the quadratus lumborum muscle (Fig. 2.19) (see also Fig. 2.11). The anatomical connections along its path are as follows:

▶ It attaches to the transverse processes at the lumbar segment. ▶ Cranially it reaches the 12th rib. ▶ Caudally it attaches to the iliolumbar crest and iliolumbar ligament. ▶ It joins the posterior aspect of the aponeurosis of the quadratus

lumborum and continues to the transversus abdominis and through this reaches the fascia of the rectus abdominus (see Fig. 2.12).

▶ Through the fascia of the quadratus lumborum muscle, it reaches the psoas muscle fascia (see Fig. 2.19). ▶ Finally, caudally it also reaches the internal oblique muscle.

Figure 2.10 The multilayered structure of the fascial system. The drawing shows cross-sections of fascial compartments A C5 level B L3 level C Arm D Lower arm E Thigh F Leg G Foot

Figure 2.11 Dissection of the thoracolumbar fascia. Note the continuity of the TLF with the trapezius, latissimus dorsi, and gluteus maximus. Note also the lateral aponeurotic expansion which reaches the serratus posterior inferior and abdominal muscles A Skin B Superficial fascia C Deep fascia D TLF

Figure 2.12 Diagram of the lumbopelvic part of the myofascial complex that surrounds the trunk at the level of L3, which is the anatomical and functional union of the TLF and the abdominal fascial systems

Figure 2.13 The continuity of the deep fascia of the back. The deep fascia is a multilayered structure and extends from the suboccipital area (superior nuchal line) to the lumbopelvic region. All along its pathway, fascia is linked to the limbs. The thoracolumbar fascia is the central structure of unification and interconnection

The presence of the lumbar interfascial triangle (LIFT) is important in relation to the balance of force distribution through the fascial planes related to the TLF (Schuenke et al. 2012, Willard et al. 2012) (see Fig. 2.19). It is the area of intersection of the fascia related to the common extensor mass (multifidus, longissimus, iliocostalis), the abdominal muscles (transversus abdominis, internal obliques, external obliques), serratus posterior inferior muscle, latissimus dorsi and quadratus lumborum muscle. It has been suggested that “this triangle may function in the distribution of laterally mediated tension to balance different viscoelastic moduli, along either the middle or posterior layers of the TLF” (this observation refers to the three-layered model) (Schuenke et al. 2012). It is interesting to observe that at the LIFT level (L3 level) the superficial layer of the deep fascia is continuous with the aponeurosis of the latissimus dorsi muscle and the epimysium of the paravertebral muscles and expands caudally toward the gluteal fascia (through the bonds in the iliac crest) and laterally to the external abdominal oblique muscle. This creates a tough structure which expands at multiple levels with the fibers crisscrossed in different directions (Fig. 2.20). In this way, the mechanical properties of the TLF components “influence the dynamic interaction of muscle groups stabilizing the lumbosacral spine” (Schuenke et al. 2012).

Innervation of the TLF: Role of the TLF in the sensation of pain Most neuroanatomical studies of the lumbar region investigate the innervation of discs, facet joints, and spinal ligaments, however, there was previously very little information available on the innervation of the TLF. Fortunately, recent studies provide valuable information on this subject. Willard et al. (2012) state that the TLF is innervated from both the dorsal and ventral rami, part of the dorsal horn (posterior grey column). The dorsal ramus innervates the posterior to the vertebral septum muscles, and the ventral ramus innervates the muscles anterior to the TLF. Human studies have shown that, as in rats, the TLF is substantially populated with free nerve endings corresponding predominantly to sympathetic fibers (as with muscular innervation) and primarily located in the outer layer of the TLF and in the superficial fascia. Corey et al. (2011) report the presence of the

sensory free nerve endings (nerve fibers) within the collagen matrix of the nonspecialized connective tissues in the low back. These sensory fibers are reactive to antibodies for substance P (meaning that they use substance P as a mediator for nociceptive transmission) and appear to play an important role in the activation of the nociceptive neurons located in the dorsal horn of the medulla. This activation means these mediators have the potential to participate in the pain process (Fede et al. 2020, Langevin 2021, Mense 2019, Schilder et al. 2018, Mense 2016, Corey et al. 2011, Schilder et al. 2014). It has been shown that these free nerve endings, which correspond to unmyelinated C fibers, are involved in neurogenic inflammation meaning they can trigger inflammation in the tissue they innervate (for example, in the synovium of the joints) when nerve damage is present (Wieland et al. 2005). In physiological conditions, the activity of these fibers is orthodromic in nature, meaning they mediate the stimuli that “travel” from the periphery to the medulla. However, in situations when the nerve is affected (neural edema) these fibers can act in an antidromic manner (toward the periphery), causing local inflammation in the innervated tissues, meaning inflammation of neurogenic origin (Kandel et al. 2001, Wieland et al. 2005). It has been shown that this situation increases the density of the nociceptors in the TLF (Mense 2016, 2019). This means that nerve tissue damage can generate a neuroplastic change in the free receptors located in the fascial tissue and generate mechanosensitivity (hypersensitivity to mechanical stimuli) to movement. Wilke et al. (2017) state that the TLF has been proposed as a potential source of chronic pain. Schilder et al. (2016) state that fascia can evoke pain to a higher degree than the underlying muscles. Pain from the underlying muscles should not be completely excluded as a contributor to low back pain. Tesarz et al. (2011) found that the sensory fibers accompanied blood vessels suggesting that at least parts of them are vasomotor fibers. When activated, the fibers may cause ischemic pain. Chou and Shekelle (2010) observed that many fibers – especially in the superficial layer of the TLF – expressed TH (tyrosine hydroxylase), an enzyme characteristic for postganglionic sympathetic fibers (the critical enzyme in the production of dopamine). This finding may explain why patients with low back pain report increased intensities of pain when they are under psychological stress.

Figure 2.14 The two-layered structure of the lumbar fascia

Figure 2.15 The two-layered structure of the thoracolumbar fascia. The posterior layer of the TLF has been sectioned and lifted (H). The mass of the spine extensors has been sectioned and lifted (I) A Superficial fascia (underside) B Thin epimysium of the latissimus dorsi C Deep fascia (underside) D Trapezius E Latissimus dorsi F Anterior (deep) layer of thoracolumbar fascia G Aponeurosis of the serratus posterior inferior muscle H Posterior (superficial) layer of the thoracolumbar fascia (underside) I Back extensor muscles (sectioned) J Iliac crest K Gluteus medius with its aponeurotic fascia L Gluteus maximus M Sacrum

Figure 2.16 Thoracolumbar fascia and its attachments 1 Posterior view of the back GM Gluteus maximus LD Latissimus dorsi SPI Serratus posterior inferior TLF Thoracolumbar fascia Tr Trapezius 2 Lateral view of the neck A Nuchal ligament B Rhomboid aponeurosis 3 Caudal attachments of the TLF Cx Coccyx 4 Muscular attachments of the TLF 5 Close-up of a lateral view of the lumbosacral area A Latissimus dorsi B Thoracolumbar fascia C Sacrum D Gluteus maximus

Figure 2.17 The superficial lamina of the thoracolumbar fascia 1 Image from an unembalmed cadaver dissection 2 Diagram of the superficial lamina of the TLF A Trapezius B Fascia of the latissimus dorsi C Fascia of the external obliques D Fascia of the gluteus medius E Fascia of the gluteus maximus After Vleeming et al. (1995) The posterior layer of the thoracolumbar fascia. Its function in load transfer from spine to legs. Spine (Phila PA 1976) 20(7):753–758

Research into thoracolumbar fascia could help to establish treatment modalities and improve the quality of life for patients with chronic low back pain. Magerl et al. (2021) have investigated “heterotopic somatosensory crosstalk between deep tissue (muscle or fascia) and superficial tissue (skin)” in relation to the temporal and thoracolumbar fasciae. They

conclude that “the balance between pain-inhibiting and pain-facilitating mechanisms differs between fascia and muscle, making the fascia a more likely source of hyperalgesia induction.” Sinhorim et al. (2021), in a scoping review of in vivo and ex vivo studies on the nociceptive role of TLF, point out that: “All the publications confirm the heavily nociceptive nature of the thoracolumbar fascia, implying that it is more sensitive to different kinds of stimulation than the underlying muscle” and suggest that: “Understanding this component of the lower spine is critical for treating patients with chronic lower back pain.” However, they consider that the adjacent muscles cannot be excluded as contributors to LBP.

Figure 2.18

Thoracolumbar fascia as a force transmission structure (Gracovetsky 2001). Transmission of force through the superficial layer from the gluteus maximus to the latissimus dorsi on the opposite side

Figure 2.19 The location of the lumbar interfascial triangle (LIFT). A close-up in the transverse plane at the level of L3

Figure 2.20 Posterolateral aspect of the lumbosacral area Yellow line – iliac crest Red line – L4 level White circle – aponeurotic attachment of the TLF, latissimus dorsi, and abdominal muscles A Latissimus dorsi B Gluteus maximus C Thoracolumbar fascia D Sacrum E Gluteus medius aponeurosis

Willard et al. (2012) summarize all this information stating that: the sensory innervation of the TLF suggests at least three different mechanisms for fascia-based low back pain sensation: (1) microinjuries and resulting irritation of nociceptive nerve endings in the TLF may lead directly to back pain; (2) tissue deformations due to injury, immobility or excessive loading could also impair proprioceptive signaling, which by itself could lead to an increase in pain sensitivity via an activity-dependent sensitization of wide dynamic range neurons; and finally (3) irritation in other tissues innervated by the same spinal segment could lead to increased sensitivity of the TLF, which would then respond with nociceptive signaling, even to gentle stimulation. (Willard et al. 2012)

The data available allow us to ask the question: can we define fascia as a sensitive organ? Although the question sounds daring, the presence of mechanoreceptors suggests an active participation of the fascia in proprioception, transmission of force, and motor control. It can be concluded that (Mense 2016, 2019, Koltzenburg 1999, Tesarz et al. 2011, Ikeda et al. 2003):

Figure 2.21 Thoracolumbar fascia and its muscle attachments A Trapezius B Latissimus dorsi C Thoracolumbar fascia D Gluteus maximus

● There is histological and functional evidence of the existence of nociceptors (free endings) in the TLF. ● Direct inflammation or inflammation of neurogenic origin increases the density of nociceptive fibers, which can explain pain when the fascia is altered, as in the case of nonspecific low back pain. ● Tissue microtrauma, inflammation, and fibrosis can not only change the biomechanics of soft tissues (for example, increasing their rigidity), but they can also profoundly alter the sensory input derived from the affected tissues. ● The continuous activation of nociceptors can worsen fibrosis and inflammation, causing even more tissue rigidity and the consequent alteration of movement. ● Considering that some free nerve endings can function as proprioceptors, the lack of corpuscular proprioceptors in the TLF is not an argument against a possible proprioceptive function of the fascia.

Biomechanical considerations related to the TLF Most research on fascial biomechanics focuses on the TLF. Recent publications analyze in detail the biomechanics and anatomy of the TLF (Willard et al. 2012, Schuenke et al. 2012). It is evidently the largest aponeurosis in the body. Its principal functions are participation in flexion and extension of the trunk (Gatton et al. 2010) and maintenance of body verticality and bipedal locomotion (Gracovetsky 2008, Willard et al. 2012). In the early 1980s, Gracovetsky et al. (1981) asserted that the erect stance is possible because the force generated by the hip extensors is transmitted to the upper extremities through a variety of paths made up of a combination of muscle and ligaments. The two main problems, which overlap in the anatomical and biomechanical analysis, are the transfer of force from the powerful mass of the gluteus maximus to the upper extremity (Gracovetsky 2008) and the difficult maintenance of the physiological curvatures of the spine, particularly cervical and lumbar lordosis. Gracovetsky (2008) asserts “lordosis is the single most important parameter controlling the distribution of forces between fascia and muscles.”

At the superficial layer, through the TLF, the bony and muscular pelvis is interconnected with the hip and gluteal muscles, which provide support to the internal organs and core muscles (Eickmeyer 2017). Finally, crossing the midline, between the gluteus maximus and the contralateral latissimus dorsi muscles, facilitates the TLF's participation in postural and motor control (Fig. 2.21). This connection is expressed in locomotion (rotation of the trunk) (Fig. 2.22) and stabilization of the sacroiliac joints and trunk (Gracovetsky 2008). The superficial layer of the TLF also contributes to trunk extension (Fig. 2.23). In conjunction with the transversus abdominis it creates the hoop tension that stabilizes the lumbopelvic region and allows for correct maintenance of lumbar lordosis (Fig. 2.24). Restoring the control of lordosis should be the first priority in any rehabilitation program. This is true for both lifting and walking (Gracovetsky 2008).

Figure 2.22 Muscle activity across the thoracolumbar fascia during locomotion

Figure 2.23 A Distribution of forces across the thoracolumbar fascia between the gluteus maximus and latissimus dorsi muscles. B In the external lamina of the TLF the collagen fibers are distributed in the shape of a rhombus. When the abdominal muscles (mainly the transversus abdominis) contract (see white arrows) this increases tension in the superficial lamina of the TLF and facilitates lumbar extension

Figure 2.24 The thoracolumbar fascia as a structure of force transmission (Gracovetsky 1981). Red arrows – the abdominal muscles (contraction force mainly from the transversus abdominis). Blue arrows – the resulting tension in the TLF restores lumbar lordosis and helps the body to maintain a vertical position. Both actions provide protection for the vertebral axis and the mechanics of the sacroiliac joints in locomotion

The deep lamina of the gluteal fascia communicates with the underlying muscles including the gluteus medius, piriformis, gemellus superior and inferior, obturator externus, and quadratus femoris (see Chapters 16 and 17). There is a link between the sacrotuberous ligament and the tendon of the long head of the biceps femoris muscle (Fig. 2.25). Gracovetsky (2008) states that: “Longissimus lumborum and iliocostalis lumborum are attached to the lumbar intermuscular apeunorosis [sic] itself part of the sacro tuberous ligament connected to biceps femoris.” The biceps femoris is also connected to the upper thorax by the iliocostalis thoracis. In addition to the

biceps femoris, the gluteus maximus is a major source of power which is transmitted to the arms by the lumbodorsal fascia and latissimus dorsi. The communication and transmission of mechanical impulses was found to be not only from and through the thoracolumbar fascia to the latissimus dorsi muscle but also to the trapezius and through both muscles to the upper extremities (Fig. 2.26).

Conclusion It can be concluded that the TLF is not an independent structure but rather a complex architecture which is structurally and functionally linked to the supporting structures of the pelvic girdle and which is also in charge of transferring forces from the lower limbs to the trunk, upper extremities, and head.

Figure 2.25 The attachments of the deep layer of the TLF along the sacrotuberous ligament A Sacrotuberous ligament B Ischial tuberosity C Tendon of long head of biceps femoris D Muscle belly of long head of biceps femoris E Semitendinosus F Sciatic nerve

G H

Deepest level of the gluteal fascia Gluteus maximus (underside)

Figure 2.26 The deep lamina of the TLF and its attachments. 1 The deep lamina of the TLF and its biomechanical behavior A Gluteus medius fascia B Sacral crest C Sacrotuberous ligament D Sciatic nerve E Ischial tuberosity F Long head of biceps femoris Red oval – posterior superior iliac spine (PSIS) Red arrow – traction from serratus posterior inferior muscle Blue arrow – traction from internal oblique muscle 2 The deep TLF and its attachments. This shows the connections between the paraspinalis and biceps femoris muscles (Gracovetsky 2001) G Paraspinalis muscles H Sacrotuberous ligament I Biceps femoris Part 1: after Vleeming A, Pool-Goudzwaard AL, Stoeckart R, van Wingerden JP, Snijders CJ (1995) The posterior layer of the thoracolumbar fascia. Its function in load transfer from spine to legs. Spine (Phila PA 1976) 20(7):753– 758

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3 Lower quadrant assessment

KEY POINTS ● Principles of clinical reasoning ● Definition of the proper performance of the body ● Definition of dysfunctions of the lower quadrant system ● Establishing reliable ratings criteria for the clinical assessment of myofascial dysfunctions in the lower quadrant ● Importance of the history taking process ● Local versus global assessment ● Analysis of the functional global assessment (myofascial components) ● Stability and mobility ● Dynamic balance and muscle synergy ● Importance of assessing all systems linked to fascia ● Importance of the patient’s appreciation of the assessment process

Voluntary movement is a systemic response toward the fulfillment of a goal (Thelen & Smith 1996).

Introduction Principles of clinical reasoning According to Mark Jones: Clinical reasoning has been defined as a process in which the therapist, interacting with the patient and significant others (e.g. family and other health-care team members), structures meaning, goals and health management strategies based on clinical data, client choices and professional judgment and knowledge. (Higgs and Jones 2000 quoted in Jones & Rivett 2004) Clinical reasoning is an extensive subject and its detailed analysis is beyond the scope of this book. See Figure 3.1 for a summary of the clinical reasoning process. For more detailed information on the assessment process see Volume 1, Chapter 10.

The characteristics of the lower quadrant Human development is related to the orthostatic position. The biped must be able to transfer and manage the loads derived from the action of gravity, the reaction from the ground, and the dynamics of myofascial structures (e.g., muscle contraction) during static and dynamic postures. All forms of bipedal locomotion require a coordinated system of body-weight support and, simultaneously, efficiency in load displacement. Our movements are produced through simple elements (e.g., molecules) that interact in a simple way, following simple rules, and are capable of producing complex behaviors (e.g., locomotion). Nonlinear and self-organizing characteristics are associated with human movement. For this reason, this chapter aims to analyze the assessment of lower quadrant dysfunctions from a systemic viewpoint. Each functional and/or structural alteration in any of the segments of the lower quadrant will

activate adaptive responses. The fascial and nervous systems will take care of this process, although other regions will be involved through compensation behavior. Even a local initial post-traumatic dysfunction can spread to other parts of the same body segment or create a supra- or infraadjacent compensation. With time and repetitive (harmful) use, when the subject moves, a state of sensory-perceptive-motor agnosis will be established and will increase.

Figure 3.1 Clinical reasoning flowchart – practitioner and patient/client perspective. After Jones M, Edwards I, Jenson GM (2019) Clinical reasoning in physiotherapy. In: Higgs J, Jensen GM, Loftus S, Christensen N (Eds.) Clinical Reasoning in the Health Professions. 4th ed. Elsevier, pp. 247–260

A prolonged process of local dysfunction and compensation can involve changes in the CNS as a consequence of its plastic adaptation to changing demands. The severity of the injury, the established compensatory movement patterns, and the recovery prognosis will be linked proportionally to the magnitude and duration of the dysfunction.

Agnosis is an interruption in the ability (of the body’s systems) to recognize previously learned stimuli, leading to difficulties in perception, sensitivity, and recognition of motor patterns.

For these reasons, the purpose of the assessment and any future treatment is to explore the stability and mobility of the whole system, rather than just the stability of individual segments or within individual segments of the lower quadrant. The findings of the different tests should be analyzed together, not separately. Every piece of information must be considered in relation to the whole. Treatment that is limited to the restricted area (where symptoms are present) usually only leads to temporary relief and not to the resolution of the problem. The objective is to restore optimal dynamic stability of the fascial system to allow for a better integration of the central nervous system. The goal is to restore movement synergy. From this point of view, dysfunction is defined as a failure of stability and/or mobility resulting in alteration of the freedom or quality of body movement. The assessment process recommended in this book is not exclusive to MIT and can be used in conjunction with other therapeutic concepts where functional recovery is essential. The focus is on the movement dysfunctions that affect the patient. An exclusive assessment method for the fascial system (to isolate its own dysfunction from those of other tissues) does not currently exist, although the examinations carried out through the different modalities of ultrasound (US) imaging (compression-based US elastography, shear-wave US elastography, B-mode ultrasonography) are promising. The use of US is limited in everyday practice and should be performed by specialized professionals. Therefore, the practitioner is free to

decide which functional tests to use, using the clinical reasoning and assessment processes which focus on the most common dysfunctions linked to the lower quadrant.

The assessment process (Fig. 3.2) The objectives and strategy of the assessment process can be easily incorporated into other therapeutic concepts.

History taking History taking is an important step that should not be overlooked. The history is the story of the illness told by its protagonist. In their own words the patient provides the data that only they can provide and that is relevant to them. This is information that cannot be obtained by other means. The main focus is on quality of life, performance of everyday activities (work, housework, leisure, sports, relationships, quality of sleep), activities such as walking up and down stairs, and movements involving the pelvis and lower extremities. The presence and behavior of pain, restriction of mobility, increased muscle tone and myofascial tensions, dermalgia, myalgia, etc. are recorded. These data are clinical manifestations of abnormal sensitization in a specific receptive area of the nervous system. In this context Chiozza (2007) suggests an interesting interpretation. Illness is something that always happens to someone. The patient feels discomfort consisting of sensations that are attributed to the body; these are called symptoms. There are times when only alterations of the body are perceived, which are considered signs. It may be that a spot on the skin does not create any discomfort to the patient (the symptom is not present), however, it is feasible that this spot is a sign of cancer; the disease is present without the symptoms. The practitioner can recognize and record signs, but symptoms can only be made known from the patient’s story. A symptom is a sensation of the body. A sign is an alteration of the body perceived in the physical world. Recognizing a sign will raise the practitioner's suspicions of a disease. A symptom explained by the patient can allow for the recognition of a disease in the absence of signs.

The use of functional scales is highly recommended. These are questionnaires relating to the patient’s ability to perform everyday tasks. They are a useful tool for monitoring the patient over time and evaluating the effectiveness of an intervention. However, we cannot just rely on numbers (statistics). The practitioner should: ● relate the results of the history taking to the results of the rest of the assessment, comparing the signs with the symptoms ● determine the degree of irritability, severity, and possible nature of the complaint ● identify the presence of alterations in other neuromyofascial structures that share the same levels of innervation as the affected region (a good knowledge of neuroanatomical and myofascial bases of pain is essential) ● compare the initial assessments with the results of complementary tests, if available. Identifying psychological and emotional aspects of the patient’s history, such as anxiety, depression, catastrophism, or kinesiophobia, will help the practitioner to determine potential yellow flags for chronic dysfunctional processes.

Figure 3.2 EE The assessment process algorithm. G – electroencephalogram. MRI – magnetic RO resonance imaging. M – range of movement. TP – trigger point. US – ultrasound

The severity, irritability, and nature of the patient’s complaint need to be identified.

Functional assessment Functional assessment is divided into different parts: global functional assessment, neural tests, viscerofascial tests, circulatory tests, and specific functional tests.

Global functional assessment Stability is the ability to maintain optimal posture and control movements. It can be either static (postural control) or dynamic (motor control). Mobility is a process linked to the elements that contribute to the search for optimal movement. It encompasses the combination of muscle flexibility, joint range of movement, and the synergistic redistribution of energy generated by the muscles, closely associated with the neuromechanics of neuroconnective tissue.

Global functional assessment is divided into two main parts: stability assessment and mobility assessment (Fig. 3.3): ● Stability assessment

▶ static stability ▷ postural control ▷ gravitational load distribution ▷ postural neuroprotection pattern ▶ dynamic stability ▷ motor control ▷ force ▷ resistance

● Mobility assessment

▶ range of movement ▷ internal: local ROM related to each of the segments ▷ external: global ROM related to the external environment

▶ movement synergy ▷ synergistic redistribution of energy generated by the muscles.

Figure 3.3 Global functional assessment flowchart

Stability assessment There is no clear scientific consensus on a specific test or its method of application, and there are many versions of stability tests. The practitioner is at liberty to select any commonly used tests as required, and the choice will be based on their training and the clinical requirements of the case (the category of patient, age, sex, beliefs, etc.). Subsequently, a basic exploration of other systems linked to fascia should be carried out, primarily to rule out associated pathologies and to determine the appropriate course of action, for example, in the presence of pain.

Static stability assessment (Fig. 3.4, Table 3.1)

The static stability assessment shows only a “slice in time.” Its findings are not a reliable reflection of the other hours in the patient’s day.

What does static stability assessment really tell us and how does it relate to the patient’s symptoms? The static posture assessment, particularly from the muscular standpoint, gives you a baseline of info that could save you time in your total assessment but overall will guide you to the regions where you could focus your attention on. It may be your wakeup call that something is not right in a specific region of the body. (Janda 1996) For the practitioner, the analysis of static stability is a useful starting point in the assessment process. However, remember that the body is not symmetrical, and symmetry does not ensure optimal performance of the body in the face of daily tasks. Static stability assessment tests the following: ● Postural control

▶ There

is no commonly agreed definition of correct posture. An individual’s posture is like a fingerprint – it is unique. Each patient needs to be assessed and treated individually with close attention paid to their specific dysfunction and related psychosocial factors.

▶ A postural control test is a simple reassessment tool that can be used to

quickly assess changes in body awareness. It is useful to both the practitioner and the patient, and for the latter it can be a useful didactic tool. Exaggerated asymmetry in static posture is related to a disturbance in the balance of feedback and feedforward actions.

● Gravitational load distribution

▶ This

test allows the practitioner to determine how the patient distributes gravitational load and to identify significant asymmetry (differences, any abnormalities). It guides the practitioner to the areas on which to focus and helps in the subsequent selection of assessment

strategies. This postural behavior shows how the body, through its systems, copes with gravitational load and has adapted to it over time.

▶ It is controversial to assume that joint loading or muscle imbalance issues are causes of the patient’s problem. There are simply too many asymmetries that occur naturally in many people that do not result in painful conditions.

● Postural neuroprotection pattern

▶ The results of static posture assessment should not be ignored. It is

likely that the way patients hold their posture is allied with what their brain feels as discomfort or pain.

▶ Dysfunctions of the fascial system, and the altered chronic state of

sensitization of the peripheral and central nervous systems), can alter the tensional homeostasis of the body permanently in a positive or negative manner by conditioning the subject’s postural attitude and way of moving. The postural pattern is closely related to neural mechanosensitivity, but it can also be related to other types of conditions such as orthopedic disorders (e.g., scoliosis). A chronic mechanosensitive alteration of the lumbar plexus (femoral nerve positive sign) could facilitate the adoption of a pelvic anteversion pattern and/or lumbar hyperlordosis and could lead to a limitation of hip extension. If we apply the same example to the lumbosacral plexus (sciatic nerve positive sign), the characteristic neuroprotective postural stance would involve retroversion and/or anterior pelvic projection, rectification of lordosis, and a tendency to knee flexion.

Figure 3.4 Static stability assessment

Thus, static postural analysis can serve as an indicator, along with the symptoms and other tests, of a scenario of alteration of the neuromyofascial system. The static stability assessment analyzes the distribution of gravitational load. This is a means of finding the areas that require more precise attention and that need to be confirmed using other exploratory tools. The recommended sequence is as follows:

● Assess the patient anteriorly, posteriorly, and laterally. It would also be of interest to view the patient from above to determine how the body is placed spatially (three-dimensionally). Perhaps in the future drone technology will make this possible. ● The patient stands normally in a relaxed position, barefoot, and in underwear (with the patient’s consent) to allow for observation of the anatomical points and lines. ● Observe how the patient deals with their body weight and how the body adapts to the gravitational load over time. ● First, observe the volume symmetry (not the exact geometrical symmetry) of the waist triangles and then check the position of the patient’s hands in relation to the corresponding thighs. ● Finally, note the relationships between the different parts of the body. Do not assume that marked asymmetry is related to specific symptomatology. The static stability assessment is also useful as a point of reference in reassessment.

Dynamic stability assessment (Fig. 3.5, Table 3.2) To understand why we move in a specific way is related to the following question. How does the central nervous system produce purposeful, coordinated movements in its interaction with the rest of the body and with the environment (Latash et al. 2010)? With this in mind, the dynamic stability assessment examines three basic areas: ● Motor control ● Force ● Resistance The theories relating to motor control are covered in detail in Volume 1, Chapter 10. Motor control dysfunctions are manifested by mechanical deficit and/or a feeling of instability, however, mechanical input is not required for this to

happen. Motor impairment can be expressed in three areas:

Figure 3.5 Dynamic stability assessment

● action (muscle tone and muscle strength) ● perception (registration or integration of sensory information) ● cognition (attention, emotions, motivation). The assessment of function should not be based on a single static test – in the same way that a radiographic examination cannot tell us how bones move. An assortment of tests is needed. The findings of individual tests should be analyzed together and not in isolation. Each piece of information has to be examined in relation to the whole.

Table 3.2 contains a summary of the main points of motor control assessment and a brief description of the procedures.

Mobility assessment Mobility assessment – range of movement (Fig. 3.6, Table 3.3) It is logical to assume that a patient’s internal resources are decisive factors in relation to dynamic balance and range of movement (ROM). However, it should be remembered that the body does not move in empty space. Its movement is also closely related to the external environment and its contents. In ROM tests, both internal and external ranges are examined. Internal ROM is defined as the amplitude movement of individual parts of the body and their relationship to other parts. External ROM is the movement of the whole body in relation to external factors, such as the type and quality of the support surface (e.g., rock or sand, rain or snow, high or low temperature). Thus, alterations in ROM (hypo- or hypermobility) are not only related to local events (capsular retractions, muscle shortening) but are also associated with the external environment. The measurement and analysis of ROM should not be limited to quantification. Even if the external ROM is appropriate it may be due to an internal compensatory process, meaning that the deficiency in local amplitude has been corrected (compensated for) by borrowing the range from another inappropriate structure (or structures). ● Range of movement:

▶ internal: local ROM relating to one part of the body ▶ external: global ROM relating to the external environment.

Research shows that when movement is guided by external factors different neural pathways are activated compared to movement guided by internal stimuli, which means that there are separate pathways that guide the two types of impulses. The existence of separate networks of action leads to three considerations:

● Movement distortion can be linked to the inadequacy or failure of internal (structural) factors and/or deficiency in uptake or interpretation of external factors. ● The learning process (recovery of range) requires internal and external stimuli. ● In the therapeutic process the difficulty or impossibility of using one of the reception channels (internal or external) does not prevent the possibility of action but rather suggests promotion of external generation of movement, which may be a helpful strategy (Debaere et al. 2003). Since range is part of performance then performance can never remain constant. To assess the influence of neuroconnective tissue on ROM, the application of neural tension tests is recommended (see Fig. 3.13 and the slump test in Table 3.3). The assessment of mobility and range of movement is summarized in Table 3.3.

Figure 3.6 Mobility assessment – range of movement (ROM)

Mobility assessment – movement synergy (Fig. 3.7, Table 3.4) Muscle activity represents the functional outcome of the nervous system. The assessment of underlying neural strategies, which result in movement and function, is a very complicated task. It cannot be measured directly, especially in persons with motor disorders. Thus, the exploration of muscle activation may reflect the condition of neural mechanisms (Safavynia et al.

2011). The analysis of muscle synergies (flexibility and adaptability) may provide a better understanding of functional deficiency of the nervous system. Research by Overduin et al. (2012) supports that clinical output is related to the neural organization of muscle synergies both at the spinal and cortical levels. Therefore, the assessment of abnormalities in different muscle coordination patterns allows deficiencies in movement planning and execution to be identified. The assessment of mobility and movement synergy is summarized in Table 3.4.

Final observations on global functional assessment This assessment should primarily focus on the whole (bigger) picture, and patterns should be analyzed rather than specific parts of the body. Specific components can be assessed later using the local (specific functional) tests. The tests need to be simple so that they can be easily administered. The static stability and dynamic stability assessments should not be omitted. They can be used to complement the global and local functional tests in the analysis of the presence of pain and its behavior. The interpretation of pain is essential to the assessment process (see Volume 1, Chapters 8 and 10). However, we should bear in mind that pain does not tell the whole story of the patient’s health. The global functional assessment will not disclose an exact picture of the patient’s problem. It is simply a momentary reflection of the patient’s reality. The neurofascial components involved in dysfunction can distort the mechanical analysis. For example, the Thomas test is a maneuver commonly used to assess the shortening of the psoas. However, it can also be used to assess for altered neuromechanics of the femoral nerve which can lead to increased tension in the psoas resulting in loss of hip extension in the neuroprotective response. During the mobility assessment this response can also be associated with loss of adduction and internal coxofemoral rotation. For this reason, assessment of neurofascial components should be the next step.

Figure 3.7 Mobility assessment – movement synergy

Figure 3.8 Neural tests in the algorithm sequence

Neurofascial components (Fig. 3.8) Accurate diagnosis of dysfunctions and pain syndromes of the lower quadrant is difficult due to its complex anatomy and biomechanics. The diagnosis has to be precise. The pain, for example, may be nonspecific (with considerable overlap of its sensory distribution) and difficult to identify, and there may be person-to-person variations. Among the systems involved in dysfunctions of the lower quadrant the importance of the nervous system must be emphasized. Below is a brief analysis of the components of the lumbosacral plexus that can be affected by myofascial dysfunction. Note that neural entrapment can generate neuroprotective and neuroeffector responses with significant consequences for body mechanics.

Lumbosacral plexus and coccygeal plexus The lumbosacral plexus consists of two separate parts (the lumbar plexus and the sacral plexus) which are connected to each other by the lumbosacral trunk. It is also important to include the coccygeal plexus in the assessment in order to complement the analysis of the innervation of the lower quadrant (Fig. 3.9): ● The lumbar plexus consists of the anterior branches of the upper lumbar spinal nerves L1 to L4. It also receives contributions from thoracic spinal nerve 12. The nerve fibers of the lumbar plexus supply the skin and musculature of the lower limbs and external genitals. The lumbar plexus is located in the lumbar region, in front of the transverse processes of the lumbar vertebrae and within the substance of the psoas major (separating

its heads) and close to the quadratus lumborum muscle and the posterior aspect of the kidneys. ● The sacral plexus is formed by the anterior branches of the sacral spinal nerves S1 to S4. It also receives contributions from the lumbar spinal nerves L4 and L5. The nerve fibers of the sacral plexus supply the skin and muscles of the pelvis and lower limbs. The sacral plexus is located on the surface of the posterior pelvic wall, anterior to the piriformis muscle, and behind the ureter and the iliac vessels. ● The coccygeal plexus is formed within the ischiococcygeus from the ventral rami of S4, S5, and Co1. It gives rise to anococcygeal nerves which pierce the ischiococcygeus and the sacrospinous ligament to supply the subcutaneous tissue on the dorsal aspect of the coccyx. The coccygeal plexus supplies the skin in the anococcygeal region and also contributes to the innervation of the ischiococcygeus, sacrospinous ligament, coccygeal ligaments, and periosteum (Woon & Stringer 2014). A knowledge of the distribution of sensitive innervated areas is very useful to the therapeutic process and will help the practitioner to identify referred symptoms (including multifocal symptomatology). The sensory and motor distributions of the branches of the lumbosacral plexus are illustrated in Figure 3.10 (McCrory et al. 2002). The main muscles innervated by the lumbosacral plexus are shown in Figure 3.11.

Nerve entrapment syndrome Nerve entrapment syndrome can be a cause of pain or dysfunction in the lower quadrant (see Volume 1, Chapter 8 for a more detailed discussion of this topic). A knowledge of the nerves that may be involved, their anatomy, motor and sensory functions, and the etiology of their dysfunction helps the practitioner to manage these complex problems. Nerve entrapment may be responsible for several pain syndromes in the lower limb and lumbopelvic segments, for example in the hip, buttock, or groin.

Figure 3.9 The lumbosacral and coccygeal plexuses A Subcostal nerve B Iliohypogastric nerve C Ilioinguinal nerve D Lateral femoral cutaneous nerve E Femoral nerve F Genitofemoral nerve G Obturator nerve H Superior gluteal nerve I Inferior gluteal nerve J Sciatic nerve K Pudendal nerve

Figure 3.12 and Table 3.5 show the locations of the most common entrapments of the lumbosacral plexus and its branches. Tables 3.6 to 3.15 summarize the main aspects of sensory and motor distribution of the components of the lumbosacral plexus, as well as the

most common deficiencies. Potential motor impairment in the regions innervated by specific branches should be considered.

Neural tests When assessing for myofascial dysfunctions it is recommended that neural tests be carried out in order to determine whether or not neural entrapment is involved in the patient’s symptomatology. Figure 3.13 summarizes the basic neural tests related to entrapment of the components of the lumbosacral plexus. How to perform neural tests is not explained in this book, and the reader is referred to the extensive specialized literature on this subject.

Figure 3.10 A Cutaneous sensory innervation of the lower limb. A Ilioinguinal nerve B Iliohypogastric nerve C Posterior rami of sacral and coccygeal nerve D Inferior cluneal nerve E Genitofemoral nerve (femoral branch) E1 Genitofemoral nerve (genital branch) F Lateral femoral cutaneous nerve G Posterior femoral cutaneous nerve

H Obturator nerve I Femoral cutaneous nerve (anterior branch) J Common peroneal nerve K Saphenous nerve L Superficial peroneal nerve M Sural nerve N Tibial nerve O Deep peroneal nerve P Plantar nerve Q Lateral plantar nerve After McCrory P, Bell S, Bradshaw C (2002) Nerve entrapments of the lower leg, ankle and foot in sport. Sports Med 32(6):371–391

Figure 3.10 B 1

2

Innervation of the vulva A Ilioinguinal nerve B Iliohypogastric nerve D Inferior cluneal nerve R Perineal nerve S Pudendal nerve T Medial cluneal nerve U Superior cluneal nerve W Coccygeal plexus Innervation of the sole of the foot K Saphenous nerve M Sural nerve Q Lateral plantar nerve V Medial plantar nerve X Medial calcaneal nerve

Figure 3.11 The main muscles innervated by the lumbosacral plexus

1 Anterior view 1 Obturator nerve 2 Femoral nerve 3 Deep peroneal nerve 4 Superficial peroneal nerve A Psoas B Iliacus C Sartorius D Pectineus muscle E Obturator externus muscle F Adductor brevis G Adductor magnus H Rectus femoris I Adductor longus J Vastus medialis K Gracilis muscle L Vastus lateralis M Vastus intermedius N Tibialis posterior O Extensor digitorum longus P Peroneus longus Q Extensor hallucis longus R Peroneus brevis S Extensor digitorum brevis 2 Posterior view 1 Sciatic nerve 2 Tibial nerve 3 Common peroneal nerve 4 Deep peroneal nerve 5 Superficial peroneal nerve A Biceps femoris (long head) B Semitendinosus C Semimembranosus D Adductor magnus E Biceps femoris (short head) F Plantaris G Gastrocnemius muscle H Popliteus muscle I Soleus J Peroneus longus K Peroneus brevis L Flexor hallucis longus M Flexor digitorum longus N Tibialis posterior

Figure 3.12 The nerves most commonly involved in entrapment of the lumbosacral plexus (see Table 3.5)

1

2

3

Anterior view A Iliohypogastric nerve B Lateral femoral cutaneous nerve C Pudendal nerve D Femoral nerve E Obturator nerve F Saphenous nerve G Common peroneal nerve H Superficial peroneal nerve I Dorsal branch of peroneal nerve Posterior view J Lumbar roots K Posterior cutaneous nerve L Sciatic nerve M Common peroneal nerve N Tibial nerve O Sural nerve The foot P Plantar nerve R Calcaneal nerve

Table 3.5 The most common entrapments of the lumbosacral plexus and their possible causes Anterior view

Dysfunctions

Anterior view

Dysfunctions

Iliohypogastric nerve

Inguinal hernia Implications of abdominal surgery

Saphenous nerve

Knee arthroscopy Tibial periostitis Ankle immobilization (plaster) Sprain of collateral knee ligament Varicose vein surgery

Lateral femoral cutaneous nerve

Lipoplasty Radical changes in weight (diets) Surgery or hip replacement

Pudendal nerve

Prolonged vaginal delivery

Common peroneal

Joint dysfunction of the fibular head

Episiotomy Pelvic trauma Cyclists, taxi drivers (prolonged sitting)

nerve

Ankle immobilization (plaster) Lateral collateral ligament sprain Tendinitis or tendinosis of the peroneals

Femoral nerve

Direct trauma (contact sports such as football or rugby) Renal pathology Pelvic joint dysfunction Hip surgery

Superficial peroneal nerve

Ankle immobilization (plaster) Lateral collateral ligament sprain Malleolus fracture Tendinitis or tendinosis of the peroneals

Obturator nerve

Tendinitis or adductor tendinopathy Pubalgia

Dorsal branch of peroneal nerve

Dysfunction of the ankle or forefoot joints Tendonitis or tendinitis of the tibialis anterior

Red flags: Assessment of neural components ● Cancer ● Unexplained weight loss ● Immunosuppression ● Prolonged use of steroids ● Intravenous drug use ● Urinary tract infection ● Pain that is increased or unrelieved by rest

● Significant trauma related to age ● Bladder or bowel incontinence ● Urinary retention (with overflow incontinence) ● Saddle anesthesia ● Loss of anal sphincter tone ● Major motor weakness in the lower extremities ● Fever ● Vertebral tenderness ● Limited spinal range of motion ● Neurologic findings persisting beyond a month. (Waddell 2004)

Viscerofascial components (Fig. 3.14) Continuity of the visceral fascia Visceral fascia is an essential part of the fascial system. It is a thin, fibrous membrane that envelops organs and glands, binding structures together and also segregating them. The viscera of the abdomen that are linked to the fascia include the stomach, intestines, liver and biliary system, pancreas, spleen, kidneys, ureters, and suprarenal glands. The positions of the abdominal viscera vary slightly with each person and are constantly changing. They depend on gravity, posture, breathing patterns, the amount of abdominal fat, and the digestive process, and they can even be related to the current emotional state of the individual.

Peritoneum The anatomical continuity of the abdominal wall and intra-abdominal structures occurs through the peritoneum (Fig. 3.15). The peritoneum is the serous membrane that lines the interior of the abdominal cavity and provides structure, insulation, lubrication, blood, lymph and nerve supply, and immunity. It is structured in two layers: the outer layer, called parietal peritoneum, is attached to the wall of the abdominal cavity, and the inner layer or visceral peritoneum surrounds some organs of the abdomen. The space between both layers is called the peritoneal cavity and contains a

small amount of lubricating fluid that allows both layers to slide between each other. In men, the peritoneum is completely closed, while in women there is communication between the peritoneal cavity and the outside through the fallopian tube channel. The peritoneum presents a series of folds with different anatomical characteristics – mesos, omentums and ligaments. The peritoneum is divided into two parts, the main cavity and the lesser cavity that is located behind the stomach and the greater omentum. The parietal peritoneum is mechanosensitive, thermosensitive, chemosensitive and nociceptive structure and shares the same autonomic nerve supply as the abdominal wall that it covers. The visceral peritoneum is insensitive.

Evidence of viscerofascial continuity One example of viscerofascial continuity is the renal fascia and its anatomical links. Gray’s Anatomy states:

Figure 3.13 Basic neural tests performed on the lower quadrant to assess for entrapment of lumbosacral plexus components (Butler 1989, Ellis & Hing 2008, Shacklock 2005a, Zamorano 2013)

Figure 3.14 Visceral tests in the algorithm sequence

Figure 3.15 Cross-section of the visceral, myofascial, and aponeurotic girdle at lumbar level Black lines – myofascial structures Red lines – visceral structures Blue lines – aponeurotic structures A Rectus abdominis B Gallbladder C Pancreas D Transversus abdominis E Internal abdominal oblique F External abdominal oblique G Kidney H Serratus posterior inferior I Latissimus dorsi J Quadratus lumborum K Psoas major L Erector spinae and transversospinalis musculature M Peritoneal cavity N Small intestine O Large intestine P Stomach Q Parietal peritoneum R Visceral peritoneum

The kidney and the adipose capsule are enclosed in a sheath of fibrous tissue … and named the renal fascia. … The posterior layer

extends medial ward behind the kidney and blends with the fascia on the quadratus lumborum and psoas major, and through this fascia is attached to the vertebral column. … The renal fascia is connected to the fibrous tunic of the kidney by numerous trabeculæ, which traverse the adipose capsule, and are strongest near the lower end of the organ. … The kidney is held in position partly through the attachment of the renal fascia and partly by the apposition of the neighboring viscera. (Standring 2005) Clinical observation of patients through modern methods of exploration has confirmed the anatomical findings from dissections, for example: ● The continuity of the posterior renal fascia with the quadratus lumborum fascia was observed in a computed tomography study (Lim et al. 1990). ● The relationship between low back pain and urinary infections has been observed (Rivera et al. (2008). ● Changes in breathing patterns in the presence of chronic low back pain were noted (Roussel et al. 2009). ● Cranial–caudal displacement of the kidney during forced respiration in healthy individuals has been observed (Suramo et al. 1984). ● Davies et al. (1994) found that organ displacement following a deep breath can be three times greater than during quiet breathing. ● Tozzi et al. (2011) reported a significant reduced range of kidney mobility in patients with low back pain compared with the range measured in asymptomatic people.

Viscerofascial dysfunctions: Criteria in myofascial induction approaches Fascial dysfunctions and entrapments can create disorder in the visceral fascia and subsequently facilitate the formation of, for example, gastrointestinal dysfunctions. This finding not only suggests the presence of specific pathologies (e.g., visceral) but also disorder in the dynamics of movement between and within the viscera, as well as between the viscerofascial and myofascial structures. The stiffness or decreased mobility

of viscera may encourage the formation of fibrosis. An example of this process is the response of Kupffer cells (stellate macrophages), through the process of mechanotransduction, recognizing an increasing tension in the cellular environment. Liver inflammation, for example, is commonly associated with activation of Kupffer cells (D’Mello & Swain 2011). This process has also been linked with sleep abnormalities, fatigue, and mood disorders (Aouizerat et al. 2009). Through mechanoreceptors the fascial system is in a continuous process of response, adjustment, and feedback (Vaticon 2009): ● somatosomatic ● somatovisceral ● viscerovisceral ● viscerosomatic ● psychovisceral (stress and secretion of cortisol and adrenaline versus slowing peristalsis, increase in hydrochloric acid production, etc.) ● visceropsychic (vagus nerve response, alteration of cognitive behavioral response) Real visceral pain may be minimized or overlooked because it is usually described just as a vague sense of discomfort, malaise, or oppression (Giamberardino 1999). Usually the intensity of pain is not consistent with the extent of internal damage (Vecchiet et al. 1989). It should also be mentioned that symptoms relating to visceral dysfunctions do not only manifest at the specific areas linked to the neuroanatomical organization of the metamere (referred pain). The convergence of visceral and somatic afferent fibers onto the same spinal sensory neurons leads to misinterpretation by higher brain centers (Miller-Keane & O’Toole 2003). Referred hyperalgesia from viscera is frequently accompanied by trophic changes, typically a thickening of the subcutaneous tissue and some degree of local muscle trophy (Fig. 3.16) (Giamberardino et al. 2003, Jänig & Häbler 1995). It can also produce strong autonomic and affective responses (Sikandar & Dickenson 2012).

Visceral dysfunction has the potential to change the body´s overall mechanosensitivity (illness behavior) through the neuroimmunologic mechanisms. One example is the release of cytokines in the brain stimulated by a vagal response related to liver toxicity (Olsen et al. 2011, Bilzer et al. 2006).

Before carrying out an examination of the abdomen, all clothing should be removed from the mammary region to the root of the extremities. The whole area should be examined.

This book does not contain a detailed analysis of viscerofascial anatomy or the clinical approaches for treating viscerofascial structures. These are complex subjects that require extensive analysis. However, in clinical practice the abdominal region is the most examined and treated area of the body, and the practitioner should be aware of the need to identify signs and symptoms relating to the viscerofascial system and also red flags. The practitioner should perform a basic assessment of the abdominal wall (Ferguson 1990), namely: ● a visual examination to look at the shape of the abdomen and to check for skin abnormalities, abdominal masses, and the movement of the abdominal wall with respiration ● palpation to check for crepitus, any abdominal tenderness, and/or the presence of pain and autonomic responses. Figure 3.17 shows the position of the hand during palpation of the abdominal area. Other forms of examination, such as auscultation and percussion, are performed in specialized evaluations relating to the pathology of the abdominal region. The most common visceral dysfunctions and the associated structures are illustrated in Figure 3.18 and summarized in Table 3.16. The anterior abdominal wall is topographically divided into nine areas. Vertically these are delineated by two vertical lines corresponding to the

prolongation of the midclavicular lines which continue up to the midpoint of the inguinal ligament. Horizontally the upper line is tangential to the costal margin and the lower line connects the anterior superior iliac spines. Each of these areas is associated with a particular group of organs. In the presence of visceral dysfunctions, semiological manifestations indicative of particular diseases can be detected in a given area during assessment (Ferguson 1990). The possible manifestations in the different areas of the abdomen are shown in Figure 3.19. To facilitate clinical decision making, it is recommended to use the Rome IV gastrointestinal dysfunctions criteria (Drossman 2017). “The Rome criteria is a system developed to classify the functional gastrointestinal disorders (FGIDs), disorders of the digestive system in which symptoms cannot be explained by the presence of structural or tissue abnormality, based on clinical symptoms” (Drossman 2006) (Fig. 3.20) (see Volume 1, Chapter 10 for a more detailed description of Rome IV).

Figure 3.16 Referred visceral pain

Figure 3.17 Abdominal palpation using the two-handed method

Figure 3.18 The structures most frequently involved in viscerofascial dysfunctions A Cardia B Stomach C Pylorus D Gallbladder E Sphincter of Oddi F Ileocecal valve G McBurney’s point H Ureter I Sigmoid colon

Table 3.16 The main structures associated with viscerofascial dysfunctions Visceral structure

Description

Cardia

The area immediately surrounding the opening from the esophagus into the stomach. The cardiac sphincter helps reduce reflux of stomach contents back up into the esophagus. The orientation of the esophagus as it enters the stomach also provides a natural closure for the cardia as the stomach fills and distends

Sto ma ch

A muscular, J-shaped organ in the abdomen. The stomach stores and digests food through gastric juices and a specialized churning action created by folds on its inside

Pyl oru s

The muscular sphincter (ring of muscle in the tubular gastrointestinal tract) that regulates the movement of digested stomach contents, from the stomach to the duodenum and prevents backflow of duodenal contents into the stomach

Gall bla dde r

A pear-shaped, hollow structure located under the liver and on the right side of the abdomen. Its primary function is to store and concentrate bile, a yellow-brown digestive enzyme produced by the liver. The gallbladder is part of the biliary tract

Sphincter of Oddi

A muscular valve that controls the flow of digestive juices (bile and pancreatic juice) through ducts from the liver and pancreas into the first part of the small intestine (duodenum). Sphincter of Oddi dysfunction describes a situation when the sphincter does not relax at the appropriate time (due to scarring or spasm). The back-up of juices causes episodes of severe abdominal pain

Ileocecal valve

This is located between the ileum (last part of the small intestine) and the cecum (first part of the large intestine). Its function is to allow digested food materials to pass from the small intestine into the large intestine. The ileocecal valve also blocks these waste materials from backing up into the small intestine. It is intended to be a one-way valve, only opening up to allow processed foods to pass through

McBurney ´s point

A point above the anterior superior spine of the ilium, located on a straight line joining that process and the umbilicus, where pressure of the finger elicits tenderness in acute appendicitis

Uret er

A tube about 10 to 12 inches long that carries urine from the kidney to the urinary bladder. The tube has thick walls composed of three coats – fibrous, muscular, and mucus coats which are able to contract. There are two ureters, one attached to each kidney. The upper half of the ureter is located in the abdomen and the lower half is located in the pelvic area

Sigmoid colon

A curved, S-shaped region of the large intestine. It is the final segment of the colon. It transports fecal matter from the descending colon to the rectum and anus

Figure 3.19 Anatomical areas of the anterior abdominal wall and the possible semiological manifestations in each area. Note: the relationship of each area with possible abdominal dysfunctions or pathology is shown here for information only and must not under any circumstances replace the need for specialized assessment performed by a physician

Figure 3.20 Criteria for gastrointestinal disorders (Rome IV)

The relationship of each area with potential abdominal dysfunctions or pathology (shown in Fig. 3.19) is for information only and does not under any circumstances replace the need for specialized assessment performed by a physician.

Red flags: Assessment of viscerofascial components ● Acute gastrointestinal bleeding (e.g., blood in stool, vomiting blood)

● Change in bowel habits (e.g., acute diarrhea, severe constipation) ● Inability to have a bowel movement or pass gas from the rectum ● Inability to swallow (aphagia) ● Jaundice (yellowing of the skin and eyes caused by excess bilirubin [pigment in bile] in the blood) ● Severe abdominal pain or swelling (distention) ● Uncontrolled vomiting ● Unexplained fever (may be caused by infection of the digestive tract) ● Presence of autonomic responses during palpation. (Adapted from Holten et al. 2003)

Lymphatic and superficial circulatory components (Fig. 3.21) The lymphatic system is a network of tissues and organs which helps the body to expel toxins, waste, and other unwanted materials. This extensive system takes care of three major body functions (Cueni & Detmar 2008): ● drainage of excess interstitial fluid (regulation of tissue pressure) and proteins back to the systemic circulation ● regulation of immune responses by both cellular and humoral mechanisms ● absorption of lipids from the digestive system. The lymphatic system can also contribute to the development of diseases such as lymphedema, cancer metastasis, and various inflammatory disorders (Mallick & Bodenham 2003).

Anatomy of the lymphatic system In the human body the lymphatic system is organized in a formation of lymphatic vessels, lymph nodules, and nodes (Fig. 3.22). Humans have approximately 500–600 lymph nodes distributed throughout the body, with

bundles found in the underarms, groin, neck, chest, and abdomen. Lymphatic capillaries merge to form lymph venules and veins that drain via regional lymph nodes into the thoracic duct on the left side or the right lymphatic duct; from there, the lymph flows back into the bloodstream (Fig. 3.23) (Mallick & Bodenham 2003, Hematti & Mehran 2011). ● The thoracic duct (left lymphatic duct) is the largest of the body’s lymphatic ducts. It collects almost all of the lymph that circulates throughout the body. It is located in the mediastinum of the pleural cavity which drains lymph fluid from everywhere except the upper right quarter of the body above the diaphragm and down the midline. ● The lymphatic duct (right thoracic duct) drains lymphatic fluid from the right thoracic cavity, the right arm, and from the right side of the neck and head. This duct is located near the base of the neck and passes along the medial border of the anterior scalene muscle at the side of the neck.

Figure 3.21 Superficial circulatory tests in the algorithm sequence

Figure 3.22 Diagram of the lymphatic system. 1 Anterior view. 2 Posterior view A Lymphatic vessels B Lymph nodules C Lymph nodes

Figure 3.23 Lymphatic drainage areas. The arrows indicate the directions of lymphatic drainage. 1 Anterior view. 2 Posterior view A Area drained by the lymphatic duct B Area drained by the thoracic duct C Location of the lymphatic ducts D Location of the thoracic duct

Lymphatic nodes of the lower quadrant The main lymphatic nodes of the lower quadrant are those of the lower extremities and the abdominal area: ● The popliteal nodes and the inguinal nodes represent the principal node groups of the lower extremities. As they occur in the veins, there are superficial and deep lymphatic flows which follow the superficial and deep venous systems respectively. The main communication between the

surface and deep currents is conducted through the popliteal and inguinal lymph nodes (Latorre et al. 2005). ● The lymphatic system of the abdomen is formed by the lymphatic trunks, the parietal nodes, and the visceral nodes. The lymph proceeding from the entire retroperitoneal plexus is collected by the lumbar trunks, which are the principal origin of the thoracic duct (Latorre et al. 2005).

Biomechanics of the lymphatic nodes In order to provide a continuous outlet for local lymph the presence of intermittent external forces acting on lymphatics is essential. These forces come from the following: ● muscle contractions ● activities of body parts (e.g., breathing patterns) ● arterial pulsations ● external forces acting on the body (Mallick & Bodenham 2003).

Assessment of the lymphatic system of the lower quadrant Due to the fact that the lymphatic system (like other circulatory systems) interacts closely with the fascial system, fascial dysfunctions may affect its proper functioning. For this reason, it is recommended that the practitioner performs a basic assessment of the lymphatic system in the areas affected by fascial dysfunction as outlined below: ● Order of assessment:

▶ Inspection ▷ Abdomen: ascites (fluid collection in the peritoneal cavity) ▷ Lower extremities: color, edema, lesions, hair distribution, varicosities ▶ Palpation of lymph nodes ▷ Location, size, mobility, consistency, delineation, increased

vascularity, shape, tenderness, warmth, erythema. The palpation of

inguinal nodes is shown in Figure 3.24.

▶ Auscultation.

● Symptoms of peripheral vascular–lymphatic dysfunction:

▶ swelling ▶ limb pain ▶ changes in sensation ▶ fatigue.

The arrows on the body outlines in Figure 3.23 indicate the directions of lymphatic drainage.

Red flags ● Persistent swollen lymph node or nodes for more than six weeks ● Lymph node is firm, hard, and red ● Lymph node is more than 2 cm in size ● Lymph node is rapidly increasing in size ● Significant unintentional weight loss, night sweats, or loss of appetite ● Exposure to HIV or hepatitis ● Unexplained fever in a returning traveler.

Figure 3.24 Palpation of inguinal nodes

Conclusion ● The inclusion of the assessments discussed above depends on the competence and experience of the individual practitioner in relation to the patient’s profile and the modalities applied. ● Local functional tests are proposed and discussed in subsequent chapters which focus on clinical dysfunctions that affect different areas of the body. The patient’s expectations, fears, and beliefs influence how the evaluation is conducted. These aspects must be considered for the tests to be interpreted correctly. ● The patient’s appreciation of the process is an essential part of the planning of the treatment.

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4 Pelvic girdle dysfunctions: Lower back and sacroiliac structures; Abdominal area LOWER BACK AND SACROILIAC STRUCTURES KEY POINTS ● Statics and dynamics of the mechanics of the pelvic girdle ● The pelvic girdle and low back pain ● Behavior of the intervertebral disc ● Low back pain and the cell–ECM–brain model ● Structure and function of the sacroiliac joint ● The sacroiliac joint as a multistability system ● The form closure–force closure concept ● Myofascial participation in the behavior of the sacroiliac joint ● Blood supply to the lower back and sacroiliac joint and its relation to fascial dynamics

Introduction: The lower back The influence of gravitational force on the behavior of the human body is discussed in Chapter 6. The statics and dynamics of the mechanics of the pelvic girdle (PG) are also subject to the action of gravitational force. The complexity of bipedal locomotion, force transmission from the lower extremities to the lumbopelvic structures (particularly to the spine), and the behavior of the intervertebral disc (first and foremost its degenerative process) require us to look beyond a purely mechanical analysis and to focus on the neuroprotective and biopsychosocial framework. If we analyze the body as a system we have to look at all levels of its structure and behavior: from molecules (biochemistry), cells (cytology), tissues (histology, anatomy, neurology, biomechanics) to the individual (physiology). Figure 4.1 illustrates two bodies during dynamic stance in relation to the action of gravitational force and postural behavior. A postural pattern can be influenced by structural (static) alterations as well as by neuroprotective and neuroeffector responses. For example, lumbar hyperlordosis, pelvic anteversion, and hip flexion are characteristic in patients with neuromechanical alterations in the lumbar plexus (the tensile load in the reflex areas of the femoral nerve). Retroversion of the pelvis, rectification (body adaptation) in lumbar lordosis, and flexed knee posture (genu flexum) are characteristic of the typical postural pattern seen in imaging that shows altered mechanosensitivity of the lumbosacral plexus. Therefore, along with an analysis of the patient’s signs and symptoms and the performance of specific tests, an analysis of static posture can be used as an indicator of alterations in the neuromyofascial system. Furthermore, mechanical alterations induce biochemical changes in the extracellular matrix (ECM) and alter the cellular functions leading to degeneration. In addition to aging, genetic predisposition, pathoanatomical factors, and nutritional and oxygen supply changes, neurophysiological and physical factors are also involved, all of which need to be examined within a psychological and social framework.

Figure 4.1 Illustration of two types of dynamic stance in relation to the action of gravitational force. The directional arrows from the center toward the periphery “lengthen” the body outline (A). The arrows that point in the opposite direction “shorten” the body outline (B). The two figures are the same size, but the body outline in A appears to be taller

Anatomical considerations related to the lower back The anatomy of the thoracolumbar fascia (TLF) and its relationship with adjacent structures (Fig. 4.2) is discussed extensively in Chapter 2. The importance of the TLF in the biomechanics of the body is emphasized, particularly its role in maintaining the bipedal position, lifting, and locomotion.

When analyzing the deep structures of the lumbar region, it should be noted that the tissues are highly hydrated and characterized by viscoelastic properties (Fig. 4.3). This facilitates the development of adaptability (plasticity) of the fascia. Plasticity means the ability to recover and restructure. This adaptive potential allows the system to recover from disorders or injuries. Changes in the intensity or quality of the hydration (alterations in the behavior of the ECM) can interfere with the optimal functioning of the fascia (see Volume 1, Chapters 5 and 9). The myofascial links of the muscles related to the TLF are described in more detail in Chapter 2. In the current chapter the paravertebral muscle structures are only briefly referred to. The erector spinae muscle is located in the deep posterolateral layer of the back. It is attached to the sacrum, the lumbar spinous processes, and the iliac crest through a common flat tendon. In its lower path it appears as a single muscle, but in the upper lumbar area it divides into three vertical columns of muscles (spinalis, longissimus, iliocostalis). These are covered by and linked to the outer layer of the TLF (Figs. 4.4 & 4.5). The attachments between the TLF and the underlying aponeurosis of the erector spinae and multifidus muscles are relevant to erector spinae activity (Vleeming et al. 2012). Hukins et al. (1990) showed that the TLF restricts the radial expansion of the erector muscles of the spine, increasing by 30 percent the stress generated as a result of its contraction. Due to the fusion of the erector spinae aponeurosis and the deep lamina of the TLF at the level of the sacrum the contraction of these muscles alters the tension of the fascia. These links also compromise the relationship between the erector spinae and gluteus maximus muscles, creating an interdependence between them in relation to the forces exerted on the ilium and the sacrum (Vleeming et al. 2012).

Figure 4.2 Thoracolumbar fascia and its connections. Note the differences in the appearance of the epimysial fascia (B) and the aponeurotic fascia (D) A Trapezius B Epimysial fascia of the latissimus dorsi C Thoracolumbar fascia D Aponeurotic fascia of the gluteus medius E Gluteus maximus (the epimysial fascia has been dissected) Circle – attachment of the gluteal aponeurotic fascia to the deep fascia

As mentioned above, the multifidus is also relevant. The multifidus is a group of small, very strong muscles. They extend along the spine and are made up of two types of fibers (deep and superficial). They are in charge of sacrovertebral and intervertebral movements. Their deep fibers stabilize the lumbar spine and the superficial fibers (in conjunction with the erector spinae muscles) and perform the movement of extension and/or rotation of the spine. The movements in each intervertebral segment are within a very small range and of great precision in the continuous feedback between each vertebra and the fibers of the multifidus. Loss of this precise coordination can alter the intervertebral and sacrovertebral movements, affecting the sacroiliac joints, the pelvic floor structures, the behavior of the disc, and the

dynamics of the zygapophyseal joints that are estimated to carry 16–40 percent of a person’s body weight (Yang & King 1984). Zygapophyseal joint dysfunctions can lead to progressive disc damage (Kumar 2019). Studies have shown that the multifidus muscles are activated before any action is carried out and thus protect the spine from injury (Kumar 2019, Crisco & Panjabi 1991).

Neurological considerations related to the lower back Dysfunctions of the neural components of the lumbar and sacral plexuses are discussed extensively and illustrated in Volume 1, Chapters 10 and 15. Note that neural entrapment can generate neuroprotective and neuroeffector responses with significant consequences for body mechanics. Nerve entrapment syndrome can be a cause of pain and dysfunction. An in-depth knowledge of the nerves that may be involved, their anatomy, motor and sensory functions, and the etiology of their dysfunction will help the practitioner to manage these complex problems. For example, nerve entrapments may be responsible for several pain syndromes in the pelvic girdle and segments of the lower limb, such as pain in the hip, buttock, or groin. A knowledge of the distribution of sensitive areas is very useful in the therapeutic process as it helps with identifying links to referred symptoms (including multifocal symptomatology) (Fig. 4.6). The sensory and motor distribution of the components of the lumbosacral plexus and the most common deficiencies are summarized in Tables 3.6 to 3.15. A potential motor impairment in the region innervated by specific branches should be considered.

Figure 4.3 Lower back area. Note the viscoelastic properties of the thoracolumbar fascia (circled areas). 1 The superficial fascia (B) has been dissected and turned down. The deep fascia is exposed (A). 2 Close-up of the deep fascia. Note the presence of fatty lobes immersed in the highly hydrated fascia. 3 The pressure of the finger deforms the fascia. 4 When the finger is raised, the fascia remains attached to it and is deformed, demonstrating its viscoelastic properties A Superficial fascia B Deep fascia

As previously mentioned, in the assessment of myofascial dysfunctions it is recommended that neural tests be carried out in order to analyze the potential role of neural entrapment in the patient’s symptomatology. The basic neural tests relating to entrapment of the components of the lumbosacral plexus are summarized in Figure 4.7. How to conduct neural tests is not explained in this book. The practitioner should refer to the extensive specialized literature on that topic.

The pelvic girdle and low back pain The treatment of nontraumatic persistent and disabling musculoskeletal pain conditions in the PG represents a great challenge for health care providers. Low back pain (LBP) is now the leading cause of disability worldwide; it affects all age groups and can have a devastating effect on a person’s well-being (Hartvigsen et al. 2018). Since the late 1990s the literature suggests that LBP primarily affects people in high-income countries, and it is commonly associated with modern lifestyle. It is estimated that more than 80 percent of people who live in these countries experience severe LBP at least once in their lifetime (Waddell 2004). However, recent research suggests a significant increase in this condition in middle-income countries and associates the latter with poor health care and an increasingly sedentary lifestyle.

Figure 4.4 Posterior layer of the thoracolumbar fascia 1 Thoracolumbar fascia and back muscles 2 Dissection of the deep fascia A Epimysial fascia of the erector spinae B Deep fascia (dissected and lifted)

3 4

C Spinous process Cross-section at the lumbar level Note the wavy lines of the erector spinae epimysium (circled)

O’Sullivan (2006) classifies LBP into one of two categories: ● Specific LBP

▶ There is primary peripheral pathology with clinical correlation as a mechanism to produce pain (an estimated 10–20 percent of LBP).

● Nonspecific LBP

▶ There is no pathology that causes the pain – it is related to dysfunctions that cause low tolerance of tissues to mechanical load (peripheral sensitization) and predisposition to pain (central sensitization) (an estimated 80–90 percent of LBP).

In the presence of both specific and nonspecific LBP, there is a dysfunction of motor control. Motor control is defined as a coordinated effort of the different groups of muscular components that make up a movement, with sequential recruitment and regulated by the CNS, that guarantees maximum efficiency and stability. Dysfunctions in motor control are categorized as follows: ● Motor control dysfunction

▶ lack of stability or disturbances) ▶ altered or excessive

control during movement (sensorimotor

movements that produce stress in the musculoskeletal structures

● Functional instability

▶ appearance of symptoms in the middle range of movement ▶ diagnosis according to a clinical pattern ▶ inconsistent findings in imaging

● Structural instability

▶ appearance of symptoms in the final ranges of movement ▶ diagnosis through dynamic imaging.

Figure 4.5 Deep back muscles 1 Overview of the back muscles A Trapezius B Scapula C Back extensors

D Spinous process E Latissimus dorsi, dissected and lifted F Thoracolumbar fascia 2 Close-up of the deep back muscles A Semispinalis dorsi B Transversospinales 3 Back muscles A External intercostal muscles B Erector spinae and its attachment to the deep fascia C Iliac crest * Note the thickness of the fascia

It can be concluded that: “LBP is now indeed a global disease” (Ostelo 2018). O’Sullivan et al. (2018) summarize the complexity of the problem in a paper published in The Lancet series on LBP: ● Low back pain (LBP) is a major global challenge, and back-related disability is increasing. ● The majority of LBP is not serious and cannot be linked to a specific structure. ● Most red flags have limited diagnostic accuracy. ● Imaging use is often inappropriate for non-specific LBP. ● Non-pharmacological treatments such as advice and activity should be first-line options in the treatment of non-specific LBP. ● Opioids have small effects, but have substantial risks. ● Psychosocial factors are important contributors to LBP and associated disability. ● A systems approach to LBP involving clinical pathway redesign, changes to payment systems and legislation, and integrated health and workplace strategies is needed. ● Advocate the concept of positive health for LBP—the ability to adapt and to self-manage in the face of social, physical and emotional challenges.

● Need to change widespread misconceptions about the causes, prognosis and effectiveness of different treatments for LBP.

Figure 4.6 Motor and sensory distributions of the lumbosacral plexus. 1 Anterior view. 2 Lateral view. 3 Posterior view A Ilioinguinal nerve B Iliohypogastric nerve C Lateral cutaneous nerve of the thigh D Femoral branch of the genitofemoral nerve E Genital branch of the genitofemoral nerve F Femoral nerve G Obturator nerve H Posterior rami of the sacral and coccygeal nerves I Inferior cluneal nerve J Posterior cutaneous nerve of the thigh K Obturator nerve

Disorders of the PG complex are influenced by multiple interacting factors including genetics, psychological, social, and biophysical factors, comorbidities, and lifestyle (Lewis & O’Sullivan 2018, Hartvigsen et al. 2018, Ostelo 2018) and affect a set of body structures that include the lumbar spine (low back), sacroiliac region, coxofemoral complex, gluteal

structures, abdominal area, inguinal and pubic structures, and pelvic floor components. The spine, for instance, has to mediate between two apparently contradictory mechanical tasks: stability (support of the trunk and protection of the spinal cord) and flexibility (mechanical coordination of the functional units, including intervertebral discs and periarticular structures such as the fascial components) (Panjabi 1992). The key structure in this process is the intervertebral disc which is a complex and dynamic system that modulates spinal mechanics (Erwin 2013).

Behavior of the intervertebral disc Most therapies for pelvic girdle disorders focus on purely mechanical aspects. For example, it is generally considered that the intervertebral disc is the center of spine dysfunction, and its degenerative changes affect the biomechanics of segmental mobility. The expression used by patients and many health care providers is that the disc can slip between the vertebrae and is responsible for the appearance and presence of pain. However, the disc is a fibrocartilage junction (a symphysis) and is a solid, highly organized, and extremely resistant unit of the structure of the spine. It cannot slip.

Figure 4.7 Basic neural tests performed on the lower quadrant (Butler 1989, Ellis & Hing 2008, Shacklock 2005, Zamorano 2013)

There is no clear way of identifying the mechanisms and precise stages of disc tissue damage. The intervertebral disc is the largest nonvascularized organ in the human body and its degeneration is a process basically mediated by cells. It is dependent on the appropriate cellular metabolism and the capacity for correct synthesis of the extracellular matrix (Belavy et al. 2016, Tabares-Neyra & Díaz Quesada 2015, Meisel at al. 2007). The nutrition of the disc’s cells can be compromised by static mechanical loads that mainly compromise the cartilage endplate and this can be the beginning of a degenerative process (Ruiz-Wills at al. 2018). In a healthy spine the cartilage endplate (which is only 1 mm thick) consists of layers of cartilage that form a continuous interface between the disc and vertebral body, and it

can be subject to a process of early and progressive disc degradation. “Damage at the intervertebral disc-vertebra interface associates with back pain and disc herniation” (Berg-Johansen et al. 2017). It is suggested that variability in the thickness of the cartilaginous endplate may be an important factor in the diagnosis of intervertebral disc degeneration (BergJohansen et al. 2018). As already mentioned, the intervertebral disc lacks vascularity and the cartilage endplate is one of the main routes of glucose diffusion for the nutrition of the cells that make up the intervertebral disc. The disc’s survival and its anabolic activity depend on the diffusion of glucose from the peripheral blood vessels to the inside of the disc (Ruiz-Wills et al. 2018). In a recent study Ruiz-Wills et al. (2018) developed a cartilage-endplate model focused on its permeability. In this model, it is considered that the interaction between the diffusion of nutrients and the disc metabolism is highly related to the daily load (periods of rest and moderate physical activity) that the cartilage endplate receives and is a relevant factor in the nutrition of the disc. The authors consider that the peripheral blood vessels surrounding the intervertebral disc which are responsible for its nutrition achieve this by diffusing fixed concentrations of solutes (glucose, oxygen, lactate) that intervene in the nutrition of cells throughout the disc, and they propose a metabolic model (Fig. 4.8). Based on this model, the authors suggest that disc herniation is not always a consequence of the direct degeneration of the nucleus but rather that the degeneration of the cartilage endplate may be responsible for the dehydration of the disc’s nucleus pulposus. The authors conclude that the cartilage endplate usually suffers more severe and early degenerative processes, and according to this evidence it can be considered a potentially important therapeutic target. Figure 4.9 illustrates the disc degeneration sequence in cartilage-endplate degeneration. However, Fields et al. (2018) suggest that “it remains unclear if endplate damage and degeneration (calcification, water loss, etc.) causes physiologic, age-related disc degeneration or results from it.”

Figure 4.8 Nutrition of the intervertebral disc. The supply of nutrients to the nucleus pulposus cells (situated about 6–8 mm from their nearest blood supply) is exclusively dependent on the vertebral capillaries adjacent to the endplate 1 Functional unit of the spine (the intervertebral disc between the two adjacent vertebrae) 2 Nutrition of the intervertebral disc A Nucleus pulposus B Annulus fibrosus C Cartilage endplate D Cartilage E Blood vessels (surrounding the disc and feeding the cartilage endplate)

F Bone (vertebra) After Ruiz-Wills C, Foata B, González-Ballester MÁ, Karppinen J, Noailly J (2018) Theoretical explorations generate new hypotheses about the role of the cartilage endplate in early intervertebral disk degeneration. Frontiers in Physiology 9:1210

Further studies are needed before the aforementioned processes can be defined more precisely. Scientific progress continues to open up new research routes, expanding on analyses that are based mainly on the segmental, biomechanical model and evolving toward the biopsychosocial model in which the neuroscientific and microbiological aspects are important. However, many therapeutic procedures that are primarily based on the long-standing biomechanical model focus on the adjustment or the arrangement of the disc as a solution for the pain experienced by the patient. Another example of the application of the mechanical model is in the analysis of the coupled motion of side bending and rotation in the lumbar spine. It is suggested that one motion cannot be produced without the other. Many approaches to manual therapy incorporate this concept to determine if a consistent pattern exists across the joints. However, after a critical review of the literature, Legaspi and Edmond (2007) concluded that “there is no evidence to support the use of coupled motion principles to evaluate or treat patients with low back pain.”

It has been suggested that the analysis of low back pain dysfunctions based solely on anatomical alterations does not always match the integral function of the low back.

This uncertainty raises the question: Are there nonspinal pain generators involved in LBP?

The hip structures and low back pain It is generally considered that LBP and low back referred pain in the lower extremity are due to changes in the underlying segments of the lumbar spine. This means that the symptoms (pain included) are descending manifestations – their origin is above the region where they present.

However, LBP is a multifactorial dysfunction, and one of the potential contributing factors is the hip joint (Reiman et al. 2009). Anatomical and biomechanical relationships appear to confirm this possibility. The continuity of the fascial system between the lumbar, sacroiliac, and abdominal regions and the thigh structures is obvious (see Volume 1, Chapter 3). Similarly, the shared muscles of the hip and low back (i.e., the psoas, quadratus lumborum, gluteus maximus, piriformis, obturator internus, gluteus medius) connect the bones of the pelvic girdle with the femur. “Contraction of these muscles will affect motion at the spine, pelvis, and hip because of common attachment sites” (Reiman et al. 2009). Research suggests that motor control, adequate range of motion (ROM), and optimal muscle strength may be relevant not only to the correct functioning of the hip but also to the movements of the pelvic girdle. Studies focus on alterations of these movements: “Such alterations are proposed to contribute to low-magnitude loading of the lumbopelvic region and accumulation of tissue stress that, over time, contributes to tissue injury” (Harris-Hayes et al. 2009).

Figure 4.9 Flowchart illustrating how cartilage endplate degradation is related to disc degeneration. Excessive mechanical load facilitates the degradation of the cartilage endplate and generates dehydration of the nucleus pulposus, with the consequent disintegration of the ECM and disc degeneration. After Ruiz-Wills C, Foata B, González-Ballester MÁ, Karppinen J, Noailly J (2018) Theoretical explorations generate new hypotheses about the role of the cartilage endplate in early intervertebral disk degeneration. Frontiers in Physiology 9:1210

Studies on the relationship of hip dysfunction and low back impairment are not conclusive and have focused primarily on athletes. Harris-Hayes et al. (2009) suggest that: “Hip function has been proposed to be related to LBP because of the anatomical proximity of the hip and the lumbopelvic region.” Other researchers (Vad et al. 2004, Wong & Lee 2004) associate LBP with hip and low back ROM deficits. In their investigation into the causes of LBP and its relation to age and gender, Shemshaki et al. (2013) conclude that the rate of involvement of the hip as a source of LBP increases as patients age. Patients with hip osteoarthritis (with presence of pain) and LBP experienced relief from both hip pain and LBP after a total hip replacement (Piazzola et al. 2018). In conclusion, research suggests that the hip joint should be considered as a potential contributor to LBP. However, although clinical prediction rules help to identify the influence of hip impairments in the symptomatology of the lumbar region (Childs et al. 2004, Hicks et al. 2005), they do not provide a protocol for unified therapeutic treatment (Reiman et al. 2009).

Pelvic floor structures and chronic pelvic pain syndrome The pelvic floor is made up of a significant number of structures (see Chapter 5), such as the bones of the pelvic girdle, ligaments, muscles, and fascia, that assume two basic functions: suspension and support. Pelvic floor dysfunction can involve weakness of the fascial system resulting in stress incontinence, fecal incontinence, or pelvic organ prolapse. Aredo et al. (2017) state that chronic pelvic pain syndrome (CPPS) is a common pain condition with psychosocial and somatic symptoms; myofascial comorbidities are frequent. There may be a link between the psychosomatic and myofascial aspects of CPPS. Pharmacological and surgical treatments for CPPS are efficient for the relief of local symptomatology. However, they do not directly target central sensitization or myofascial dysfunction (Klotz et al. 2018). Myofascial pelvic pain is a major component of CPPS and is frequently not properly identified by health care providers (Pastore & Katzman 2012).

In relation to LBP and CPPS, it can be concluded that there is a wide gap “between evidence-based medicine and the management delivered in every day care” (Ostelo 2018). Against this panorama, the narrative needs to change.

The cell–ECM–brain model The cell–ECM–brain model is a new paradigm for understanding body movement. It often highlights the fragile and perhaps oversimplified model that was used in the past. With the old model, it is almost impossible to explain the mechanisms involved in therapeutic processes that use a mechanical approach, particularly in manual therapy. The old paradigms are losing their validity (Bialosky et al. 2017, Coronado & Bialosky 2017, Mintken et al. 2018). The multiple traumatic impacts that our body is subjected to throughout life lead the extracellular matrix to remodel due to its plastic nature. To preserve the desired function, the fascial system produces compensations for movement patterns that are individual to each person. In this order of ideas, the pathomechanical process of the musculoskeletal system, and the related pain and dysfunction, suggests the presence of important anatomical and neurophysiological changes that may also involve fascial structures. Pain and hypersensitivity may be induced by the activation and/or sensitization of peripheral myofascial nociceptors by endogenous substances (Mense & Hoheisel 2016). For instance, histological studies performed on the TLF in humans describe a rich sympathetic innervation and significant presence of peptidergic nerve endings (substance P and calcitonin gene-related peptide), similar to those found in muscle fibers (Corey et al. 2011, Tesarz et al. 2011) (see Volume 1, Chapter 8). Immunoreactivity to substance P, associated with histological modifications such as densification of the extracellular matrix and alteration in the composition of proteoglycans (Stecco et al. 2013), has been reported in tissues with “myofascial dysfunction” (Sanchis-Alfonso & RoselloSastre 2000). Densification of the extracellular matrix may lead to loss of tissue homeostatic equilibrium by initiating remodeling – overexpression of α-actinin and actin cross-linking of fibroblasts and destabilizing of the

tissue architecture (Humphrey et al. 2014). Consequently, a repetitive and/or prolonged nociceptive stimulus of peripheral origin may induce central sensitization and/or altered supraspinal modulation of afferent stimuli; thus, episodic pain may eventually become a chronic disease (Mense & Hoheisel 2016). The role of fascia in the experience of pain is discussed in detail in Volume 1, Chapter 8, particularly in relation to chronic pain. It is suggested that cognitive behavioral, emotional, and social factors have a high influence on pain and disability, as well as on the possible chronicity of the processes. Gerhart et al. (2018) assert that: “Chronic pain is associated with elevated negative emotions, and resources needed to adaptively regulate these emotions can be depleted during prolonged pain.” This homeostatic, biomechanical, and biochemical imbalance could be interpreted as a negative allostatic tissue load (allostatic deregulation) and governed by the principles of the allostatic model, that is, established in a systemic and predictive way. Allostasis can be defined as the stability which organisms acquire through changes (Sterling 2004) (see Volume 1, Chapter 8). Allostatic loading can trigger negative hedonic (connected with feelings of pleasure) assessments of interoceptive afferents and implement aversive and stress responses by the nervous system (neuroimmune response) (Paulus et al. 2009). The neural substrate that represents the pathophysiological condition of myofascial dysfunction is able to predict allostatic load and thus trigger neuroimmunological responses that modify tissue homeostasis, contributing to the allostatic tissue load (Pinho-Ribeiro et al. 2017). Therefore, changes in the fascial system and its innervation may modify the cortical and interoceptive representation of our patients, causing imbalances in the systems of modulation of central responses to peripheral stimuli. In this way, interoceptive allostatic loading, central sensitization, and chronic pain are facilitated (Craig 2003). Considering that “no anatomical structure functions in isolation” (Vleeming et al. 2012) it is logical to conclude that, once again, a systemic view is necessary.

The pathophysiological model for chronic LBP, showing the integration of connective tissue plasticity mechanisms with the mechanisms of the nervous system, is illustrated in Figure 4.10.

Introduction: Sacroiliac structures The bony pelvic girdle is a ring-like structure consisting of two iliac (innominate) bones and the sacrum and coccyx. The sacrum is integrated into the pelvic girdle through two sacroiliac joints. The sacroiliac joint (SIJ) is a passive joint, meaning it is moved or affected according to the position of the body. Although its dynamics depends on muscle contractions there are no specific muscles responsible for this task. No muscles attach directly from the sacrum to the ilium. Force comes from movement in other joints above or below the SIJ that form the kinetic chain (this does not refer to muscular chains but to the three-dimensional system of integrated tensions distributed among different kinds of structures – muscles, tendons, ligaments, joint capsules, discs, aponeuroses, neurovascular bundles – and joined together through the fascial network [the nonspecialized connective tissue]). Force is also directed into the SIJ through gravity. The functions of the SIJ are the transition of force between the spine and the pelvis and the attenuation of the load of the trunk to the lower extremities; the SIJ also facilitates childbirth. The role of the SIJ in dynamic stability is dependent on the large number of muscular and ligamentous structures that surround it. There have been controversies about the relevance of the SIJ in the biomechanics of the lumbar spine and its role in LBP since ancient times. Hippocrates believed that some movement is present in the SIJ only during pregnancy and childbirth and that there was no real mobility in daily activities. Opinions changed from year to year and from researcher to researcher, and they were often contradictory. At present, there is no doubt about the existence of movement in this pair of joints. From the former model that indicated only 1) the movements of nutation and counternutation, 2) the passive stabilizing role of the ligaments, and 3) the role of muscles (separate from the action of ligaments), research has moved

toward a dynamic model of the integral action of the osseous, ligamentous, muscular, and fascial systems (Pilat 1998).

Figure 4.10 Pathophysiological model for chronic low back pain, integrating connective tissue and nervous system mechanisms. After Langevin HM, Sherman KJ (2007) Pathophysiological model for chronic low back pain integrating connective tissue and nervous system mechanisms. Medical Hypotheses 68(1):74–80

Assessment and treatment protocols are equally controversial; there are no unified criteria. Some researchers assert that a high percentage of LBP is

due to the pathology of the SIJ and apply a functional assessment focusing on the symmetry of the movements of the lumbopelvic area. Others believe that an accurate assessment is difficult (almost impossible), and the pain is referred from other structures or is of neuropathic origin (Hammer et al. 2013, Pilat 1998). The dynamic stability of the SIJ is widely discussed in the literature (van Wingerden et al. 2004, 2008, Vleeming et al. 2012). The theory of form closure and force closure, proposed by Snijders et al. (1993) has been updated (Vleeming & Willard 2010, Vleeming at al. 2012) and suggests that the phenomenon of dynamic stabilization of the SIJ differs according to the circumstances. Form closure occurs when the joint is stable and no external force is needed to support it. When the joint is in an unstable condition external forces are necessary to sustain it in dynamic stability. This is known as force closure. The optimal stability of the SIJ is achieved with a combination of both forms. Force closure is the result of changing joint reaction forces generated by tension in ligaments, fasciae, muscles, and ground reaction forces; various muscles are involved in the closure of the SIJ (Vleeming & Willard 2010). Depending on demands and the resources available to the system, it can oscillate between form closure and force closure stabilization. Research provides strong evidence for the stabilizing role of the sacrospinous and sacrotuberous ligaments. Hammer et al. (2019) states that “unilateral ligament injury altered the motion at the pelvis contralaterally.” Pain that manifests around the SIJ can be referred from the trigger points coming from several muscles: the levator ani, coccygeus, gluteus medius, quadratus lumborum, gluteus maximus, multifidi, iliopsoas, longissimus thoracis, iliocostalis thoracis, iliocostalis lumborum, and rectus abdominis. In conclusion, it is considered that dysfunction of the SIJ cannot be treated as an isolated issue.

Structure and function of the sacroiliac joint Structural anatomy of the sacroiliac joint

Researchers disagree on the classification of the SIJ. Some classify it as a synarthrosis and others as a diarthrosis (Bowen & Cassidy 1981). The criteria that tip the balance to the second opinion are: ● the presence of a joint cavity containing synovial fluid ● the existence of adjacent bones with ligamentous support ● the presence of a fibrous joint capsule ● the existence of cartilaginous surfaces. The SIJ engages the segments of the sacrum from S1 to S3 (Vleeming & Stoeckart 2007). The average surface of the sacroiliac joint is 17.5 cm2 (Kapandji 1981) and it has an “L” shape (Porterfield & DeRosa 1991, Sturresson et al. 1989). The significant characteristic of this joint is the irregularity of its surface in the form of ridges and depressions that are modified (morphological changes) throughout life in relation to the movement of the individual during bipedal locomotion (Sgambati et al. 1997). The shape of the joint also limits the articular range of motion (ROM). The SIJ is surrounded by a strong and fibrous joint capsule, that is thinner or almost nonexistent on the posterior aspect of the joint (Bochenek & Reichner 1978). The complex and resistant ligamentous system (according to some researchers it contains the most resistant ligaments of the human body) extends from the joint capsule to reinforce the joint and anchor the bones in their positions allowing for small-range movements and also a spring flexibility capable of absorbing the pressure and force of everyday activities (weight bearing, inertia, rotation, and acceleration/deceleration) and feedback from the ground from the impact of gait, running, and jumping (Weisl 1954, Bernard & Cassidy 1992, Bogduk & Twomey 1992). An average articular movement of about 2 degrees is possible in each direction (Vleeming et al. 2012).

Functional anatomy of the sacroiliac joint Analysis of the bony pelvic girdle suggests an unstable position of the sacrum which, as a result of gravitational force, tends to lean toward anteversion in relation to the iliac bones. In the bipedal position the center

of the gravitational body projects in front of the axis of rotation of the SIJ which may facilitate instability (Fig. 4.11). The mobility of the SIJ is a subject of continuing debate. There is consensus on the main movements of nutation and counternutation. However, several authors also report movements such as tilting, rotation, gliding, and translation (Lavignolle et al. 1983). Nutation refers to anterior– inferior movement of the sacrum while the coccyx moves posteriorly relative to the ilium. Counternutation refers to posterior–superior movement of the sacrum while the coccyx moves anteriorly relative to the ilium. It is suggested that nutation and counternutation are not performed on a fixed axis but rather on one that changes according to age, sex, different interoceptive and exteroceptive impulses, and specific personal characteristics of the locomotor system of the individual (Harrison et al. 1997, Cohen 2005) (Fig. 4.12).

Figure 4.11 Frontal (A) and lateral (B) images of the bony pelvic girdle. Note the unstable position of the sacrum. The arrows indicate the tendency toward anteversion of the sacrum. Red arrows – gravitational force. Blue arrow – destabilization force

According to Kapandji (1981), the position of the sacrum, wedged between the innominate bones, forms the self-locking mechanism of the SIJs. However, study of the SIJ should extend from its topographic anatomy to its functional anatomy, including, in addition to the bones, the dynamic behavior of the ligamentous and muscular systems linked together by the uninterrupted and contractile (Schleip et al. 2019) (intrinsic and extrinsic) fascial network. The stability and simultaneous spring flexibility of SIJ behavior is determined by all of its structures. Thus, the SIJ facilitates transfer of force between the trunk and lower limbs (the three large dynamic levers associated with bipedalism and locomotion) (Fig. 4.13). It can be observed (in a horizontal section of the SIJ) that with ligamentous support the sacrum and SIJ act as a distributor (Fig. 4.14). This behavior not only allows the SIJ to manage the dynamic stability of the pelvic girdle but also allows it to participate in tensional adjustments of other body structures, demonstrating that “no anatomical structure functions in isolation” (Vleeming et al. 2012).

Figure 4.12 Nutation–counternutation movement of the sacrum showing the anchoring role of the ligaments A

Sacrotuberous ligament

B

Sacrospinous ligament

Red arrow – gravitational force Blue arrow – destabilization force (nutation-like movement) Green arrow – counternutation movement

Ligamentous structures and their dynamics There are two types of SIJ ligaments distributed between the anterior and posterior parts of the pelvic girdle: the main (strong) ligaments and the accessory ligaments (Fig. 4.15). The main ligaments are described below:

Figure 4.13 Frontal image of the pelvic girdle. The arrows show the dual mechanical function of the sacroiliac joint: shock absorption for the spine (red arrows) and conversion of torque from the lower extremities into the rest of the body (blue arrows). Both the legs below and the spine above can move in such a way as to direct force into the sacroiliac joint (yellow arrows). Muscles and ligaments that cross the sacroiliac joint influence the transfer of force from above or below

Figure 4.14 Cross-section of the pelvis at the sacroiliac level. Sacroiliac complex as a force distributor. The presence of ligaments around the sacroiliac joint is particularly important as considerable force can be directed into this joint from multiple directions A Ilium B Posterior sacroiliac ligament C Sacrum D Greater sciatic foramen E Sacrospinous ligament F Lesser sciatic foramen G Sacrotuberous ligament H Pubis

Figure 4.15 Sacroiliac ligament system

● Sacroiliac ligaments

▶ Anterior ligament: This reinforces the capsule anteriorly and resists axial translation of the sacrum and separation of the SIJ. ▶ Posterior ligament: This reinforces the capsule posteriorly and tightens during counternutation movements.

● Axial (interosseous) ligament: This is the main connection that keeps the sacrum and the ilium together. It reinforces the inside of the joint and prevents anterior and inferior movement of the sacrum. It is very robust and provides multidirectional stability to the joint. According to classic anatomy texts, this ligament forms the horizontal axis of the rotating movement of the SIJ (Kapandji 1981). ● Short and long posterior sacroiliac ligaments (Vleeming et al. 2012): These connect the posterior superior iliac spine and the iliac crest with the 3rd and 4th segments of the sacrum. They also resist counternutation. The long posterior sacroiliac ligament is the most superficially and dorsally located of the SIJ ligaments and can be easily palpated (Vleeming et al. 1996). ● Anterior sacroiliac ligament: This is the thinnest and most vulnerable of the ligaments. It reinforces the joint capsule. The accessory ligaments are described below: ● Sacrotuberous ligament (STL): This fuses with the posterior sacroiliac ligament. It is connected to the posterior layer of the TLF, the biceps femoris long head (BFlh), and the gluteus maximus and piriformis muscles (Vleeming et al. 1989). It resists nutation of the sacrum during weight bearing and gait. ● Sacrospinous ligament (SSL): The SSL and the STL divide the greater sciatic notch, thus defining the greater sciatic foramen, through which the piriformis muscle passes, and the lesser sciatic foramen, which is the outlet for the internal obturator. The pudendal nerve passes between the two ligaments. Its entrapment is often related to pelvic floor dysfunctions. ● Iliolumbar ligament: This connects the lateral border of the sacrum and the transverse process of L5 with the hip bones (Pool-Goudzwaard et al. 2003), stabilizes the upper part of the SIJ, joining the pelvis with the last two lumbar vertebrae, and limits axial rotation and anterior glide of L5 over the sacrum.

It should be noted that female SIJ ligaments are laxer than in males due to hormonal influences, especially during pregnancy and childbirth.

Behavior of the sacrotuberous ligament and its relation to pelvic girdle dysfunction and pain syndromes The dynamic stability of the SIJ is closely influenced by the STL and SSL (Vleeming et al. 1989, 2012, Cohen et al. 2013). These ligaments counteract the movement of the forward rotation of the sacrum (nutation), which is a consequence of body weight forces (Bogduk & Twomey 1992, Vleeming et al. 1989). They act as anchors stuck in the ischial tuberosity and the spine of the ischium, respectively (see Fig. 4.12). According to some authors, dysfunctions of these ligaments could be related to inflammatory disease (Taurog et al. 2016), pelvic trauma (Cusi et al. 2013), or pelvic incontinence (Doğanay & Aksakal 2013) (all cited in Aldabe et al. 2019). Due to it anatomical location, the STL is more important to body mechanics than the SSL. It is a fan-shaped fibrous band of connective tissue located posteriorly and inferiorly in the pelvis. Through its insertions it anatomically and functionally links the important bony structures: the sacrum, the lumbar spine, and the lower limbs. It runs from the sacrum and the upper coccyx to the tuberosity of the ischial tuberosity. As mentioned above, it is directly attached to the gluteus maximus, BFlh, and piriformis muscles (Fig. 4.16). The cephalic end of the STL joins with the posterior layer of the TLF that further connects with the multifidus and erector spinae muscles (Shafik et al. 2007).

Relationship of the sacrotuberous ligament with the biceps femoris long head The main fascial link is that of the STL with the tendon of the BFlh. It is obvious that both structures are inserted into the ischial tuberosity that is the insertion attachment of the STL and at the same time the origin attachment of the three tendons of the hamstring muscles (BFlh, semitendinosus, and semimembranosus) (Fig. 4.17). The importance of this connection lies in the fact that both structures are not only inserted in the ischial tuberosity, but that there is continuity of fibers between the STL and the BFlh tendon

with no insertion in the periosteum of the ischial tuberosity (Fig. 4.18). This connection (continuity) is critical to the transfer of forces across the SIJ (Vleeming et al. 1989, van Wingerden et al. 1993). Along with the peroneus, tibialis posterior, biceps femoris, STL, TLF, and erector spinae muscles, it reinforces the dynamic stabilization system of the SIJ (the posterior longitudinal path). Researchers report the presence of variations in this continuity. Aldabe et al. (2019) report the following:

Figure 4.16 Sacrotuberous ligament and its attachments 1&2 A Sacrotuberous ligament B Sacrotuberous ligament–piriformis muscle attachment C Piriformis muscle belly D Gluteus maximus, dissected and lifted E Ischial tuberosity F Biceps femoris long head tendon

3

4

G Biceps femoris long head belly H Sciatic nerve Sacrotuberous ligament and gluteus maximus attachments I Sacrotuberous ligament J Sacrotuberous ligament–gluteus maximus muscle attachment K Gluteus maximus muscle belly. The muscle has been dissected and lifted Sacrotuberous ligament and piriformis muscle attachment L Posterior layer of the thoracolumbar fascia M Iliac crest N Gluteus maximus muscle fibers O Sacrotuberous ligament P Sacrotuberous ligament–piriformis muscle attachment Q Sciatic nerve

Figure 4.17 Dorsal aspect of the pelvic girdle 1 Gluteal area. The gluteus maximus and gluteus medius muscles have been removed A Traces of gluteus maximus muscle fibers B Sacrotuberous ligament C Piriformis muscle–sacrotuberous ligament attachment. The thin dorsal fascia of the piriformis is continuous with the sacrotuberous ligament

D E F

2

3

Piriformis muscle Sciatic nerve Ischial tuberosity – the point of contact (and continuation of the fibers) between the sacrotuberous ligament and the tendon of the biceps femoris long head G Traces of the gluteus maximus muscle belly H Tendon of the biceps femoris long head “Bird’s eye view” (from above) of the dorsal part of the pelvic ring I Iliac crest J Gluteus maximus muscle fibers inserted in the iliac crest K Gluteus medius L Sacrotuberous ligament M Traces of gluteus maximus muscle fibers N Gluteus maximus, dissected and lifted O Tendon of the biceps femoris long head Close-up of sciatic tuberosity P Sciatic nerve. Q Tendon of the biceps femoris long head STL Sacrotuberous ligament

Figure 4.18 The attachment of the sacrotuberous ligament (STL) and tendon of the biceps femoris long head (BFlh) to the ischial tuberosity (IT)

● Current evidence suggests that variation exists in the continuity between the STL and BFlh tendon (Vleeming et al. 1989, van Wingerden et al. 1993, both cited in Aldabe et al. 2019). ● “Two studies (Martin, 1968; Philippon et al. 2015) acknowledge that a portion of the STL is confluent with the proximal BFlh or conjoined semitendinosus-BFlh tendon.” ● “… it is intuitive that the superficial, posterior fibers of the BFlh tendon (Sato et al. 2012; van Wingerden et al. 1993) are those more likely to interact with the ligament!”

● The “posterior portion of the BFlh (but not the proximal semitendinosus tendon) was ‘widely connected’ to the STL” (Sato et al. 2012 cited in Aldabe et al. 2019). ● “The seemingly robust connection of the ligament-tendon complex was confirmed histologically, with no separation of the tissues noted” (Sato et al. 2012 cited in Aldabe et al 2019). Gracovetsky (1997), in the analysis of his concept of “a theory of human gait,” explains how the legs interact with the spine in locomotion and affirms the importance of the transmission of forces between the BFlh and STL. The author highlights the force transmission from the BFlh through the STL to the rib cage. In this process the STL structure continues cranially to the posterior superior iliac crest and the lumbar intermuscular aponeurosis. Through its structure it creates links with the longissimus lumborum, iliocostalis lumborum, and multifidus muscles. As these muscles attach to the transverse processes of the vertebrae continuity is established in the transmission of forces between the BFlh and the spine (Fig. 4.19). Although the presence of the ligament–tendon complex of the STL and BFlh is a fact and should be considered when analyzing pelvic girdle dysfunctions, its influence on pelvic girdle dynamics is controversial. Some authors suggest that further investigation is required to confirm the extent of the connection between these two structures and how they relate to biomechanics. Despite this, Hammer et al. (2019), as a result of their morphometric observations, recently concluded that the STL and SSL “significantly contribute to ligament stability of the pelvis” and may be involved in LBP.

Sacrotuberous ligament and gluteus maximus muscle attachment The dynamics of the SIJ is closely associated with the gluteus maximus muscle through its attachment on the posterior surface of the STL. With the support of the sacrotuberous ligament, the gluteus maximus participates in the transfer of load between the lower extremities and the trunk. Through this connection 23.5 percent of the compression forces that the gluteus

maximus generates across the SIJ takes place (Barker et al. 2014). Note the presence of nonspecialized connective tissue in the intermediate planes between the muscles and ligaments (Figs. 4.20 & 4.21). The gluteal fascia is discussed in more detail later in this chapter.

Sacrotuberous ligament and piriformis muscle attachment The piriformis muscle arises from the anterior surface of the sacrum and courses through the greater sciatic foramen before attaching to the uppermost surface of the greater trochanter. In some individuals it merges with the tendons of the obturator internus muscle. The sciatic nerve (superior gluteal nerve [L4, L5, S1]) exits the pelvis through the sciatic notch behind the piriformis muscle (Fig. 4.22). Abnormalities in the piriformis muscle, such as hypertrophy, inflammation, or anatomic variations, result in irritation and entrapment of the sciatic nerve (Yeoman 1928, Mitra et al. 2014). Papadopoulos & Khan (2004) state that 6 percent of sciatic pain may be related to piriformis entrapment. Dalmau-Carolà (2005) reports that myofascial pain syndrome can affect the piriformis. However, potential spontaneous entrapment at the piriformis level is still debated. Smoll (2010) reports an attachment between the piriformis and the STL, and Vleeming et al. (2012) affirm it has been shown that the thin dorsal fascia of the piriformis is continuous with the STL (Figs. 4.22 & 4.23). Dysfunctions of the piriformis and also their relation to the obturator internus in pelvic floor dysfunction is discussed in more detail later in this chapter.

Figure 4.19 Force transmission from the biceps femoris long head toward the upper trunk. The force passes from the BFlh through the sacrotuberous ligament to the aponeurosis of the erector spinae muscles A Multifidus B Iliocostalis thoracis C Longissimus lumborum D Aponeurosis of the erector spinae muscles E Sacrotuberous ligament F Ischial tuberosity G Biceps femoris long head

Sacrotuberous ligament and sacrospinous ligament complex

The STL–SSL complex contributes to pelvic girdle stability. Tensional changes in this complex may be involved in the generation of LBP. Authors report variation in the morphology and anatomy of the STL and SSL (Vleeming et al. 2012). In a recent study, Florian-Rodriguez et al. (2016) conclude that “these ligaments are physically connected at a median distance of 15.5 mm (range 6–36 mm) from the ischial spine.” Hayashi et al. (2013, quoted in Hammer et al. 2019) state that in the embryological process the SSL “develops together with the coccygeus muscle, indicating a close morphological relationship.” Hammer et al. (2019) show that “disruption of the SSL–STL complex causes increased overall pelvis motion and increased bilateral SIJ motion.” The SSL and STL help to distribute the load of the inferior and lateral sacrum, thereby diminishing the load applied indirectly to the SIJ (Hammer et al. 2013). Hammer et al. (2019) observed that the STL–SSL complex participates in SIJ and pubic symphysis stability. Several authors link ligament dysfunctions to pudendal nerve entrapment syndrome. The STL–SSL complex “has functions beyond mechanical stabilization, perhaps as part of neuromuscular feedback loops” (Doğanay & Aksakal 2013, Manning & Arnold 2014). Loukas et al. (2006), after analyzing 100 anatomical samples, observed that 87 percent of specimens exhibited a membranous (falciform) segment, which extends toward the ischioanal fossa. They concluded that these data could have important implications for the understanding of the relationship between the pudendal nerve and the sacrotuberous ligament and its relevance to pudendal nerve entrapment syndrome leading to perineal pain. Hammer et al. (2019), after sectioning the STL and SSL, concluded that instability resulting from partial or complete SSL and STL injury merits consideration in treatment strategies which involve these ligaments as important stabilizers.

Figure 4.20 A Diagram of the relationship of the gluteus maximus with the sacrotuberous ligament. B The relationship of the gluteus maximus with the gluteus medius and thoracolumbar fascia. C Anchoring of the gluteal fascia and its relationship with the sacrotuberous ligament. The gluteus maximus has been dissected and lifted. D The sacrotuberous ligament and its continuity with the tendon of the biceps femoris long head. E Residual fibers of the gluteus maximus on the dorsal aspect of the ligament

Sacrotuberous ligament and posterior layer of thoracolumbar fascia An anatomical and functional analysis of the TLF and its relationship with the adjacent structures (including the STL) is discussed extensively in Chapter 2. Loukas et al. (2008) report a possible connection between the STL and the posterior layer of the TLF. Vleeming et al. (1995) observe that the fibers of the deep layer of the fascia are continuous with the STL. Figures 4.24 and 4.25 show the relationships between the STL and TLF (for more on this see Chapter 2).

Figure 4.21 Gluteal area – relationship of the gluteus maximus and sacrotuberous ligament A Posterior layer of thoracolumbar fascia B Sacrum C Insertion of gluteus maximus into the iliac crest D Iliac crest E Sacrotuberous ligament F Ischial tuberosity G Gluteus medius H Gluteus maximus, dissected and lifted

Figure 4.22 Relationship of the piriformis muscle and sciatic nerve

Long posterior sacroiliac ligament The long posterior sacroiliac ligament is attached to the posterior superior iliac spine and to the largest transverse tubercle of the sacrum between the 3rd and the 4th dorsal sacral foramina (Vleeming et al. 1996). The middle region of the long posterior sacroiliac ligament lies at a confluence of dense connective tissue layers: the erector spinae aponeurosis, the gluteal aponeurosis, and a deep fascial layer (McGrath & Zhang 2005). Authors suggest that “the middle long posterior ligament appears to provide a pathway for the lateral branches of the dorsal sacral rami between the posterior sacral region and the gluteal region.” They provide a morphological basis (histological study) for the proposal that “putative sacroiliac joint pain may be due to an entrapment neuropathy of the lateral branches of the dorsal sacral rami at the long posterior sacroiliac ligament” (McGrath & Zhang 2005). Vleeming at al. (2002) suggest the possible involvement of the long dorsal sacroiliac ligament in peripartum pelvic pain.

Muscle dynamics of the sacroiliac joint

The sacroiliac joints are surrounded by the largest and most powerful muscles of the human body (Bernard & Cassidy 1992). The muscle dynamics are described below:

Figure 4.23 Sacrotuberous ligament and piriformis muscle attachment 1 The gluteal area with the gluteus maximus dissected and lifted A Sacrotuberous ligament B Piriformis muscle belly C Ischial tuberosity D Gluteus maximus, dissected and lifted E Sciatic nerve 2 Close-up Circle – sacrotuberous ligament and piriformis muscle attachment

Figure 4.24 Posterolateral aspect of the lumbosacral area with the gluteus medius and gluteus maximus removed A Trapezius B Latissimus dorsi C Posterior layer of the thoracolumbar fascia D Iliac crest E Gluteus medius muscle fibers F Sacrum (posterior sacroiliac ligaments) G Sacrotuberous ligament

● Erector spinae muscles: During contraction the muscles participate in sacral nutation and thus ligaments are tightened and the SIJ locks. ● Multifidus: Contraction of the muscle facilitates nutation. ● Piriformis: The muscle crosses the SIJ in a perpendicular direction and compresses the joint. ● Transversus abdominis: Contraction of the muscle stabilizes the spine and pelvis. ● Gluteus maximus: The muscle compresses the SIJ through the orientation of its fibers (Fig. 4.26). These fibers blend with the sacrotuberous ligament and thoracolumbar fascia.

● Biceps femoris long head: The muscle tendon crosses over the ischial tuberosity and blends into the sacrotuberous ligament. Contraction of the BFlh increases tension on the sacrotuberous ligament. ● Latissimus dorsi: Via the deep fibers of the thoracolumbar fascia, it attaches to the lower thoracic spinous processes and inserts on the iliac crest. Superficial and oblique caudal fibers blend with the thoracolumbar fascia and then with the contralateral gluteus muscles.

Figure 4.25 Close-up of the posterolateral aspect of the lumbosacral area A Iliac crest B Aponeurotic fascia of the gluteus medius C Gluteus maximus insertion line D Thoracolumbar fascia

E

Gluteus maximus muscle belly

Figure 4.26 The stabilizing muscles and ligament of the sacroiliac joint A Thoracolumbar fascia B Gluteus maximus. Note the orientation of the muscle fibers C Sacrotuberous ligament

None of these muscles acts directly on the sacroiliac joints, nor is it able to perform an active and voluntary movement in them, but through movements in the other joints (those of the lumbar spine, hip, and pubic symphysis), postural modifications, and changes in the body weight of the individual, the aforementioned muscles can develop force that is capable of changing the behavior of the SIJ (Solonen 1957, Korr 1975).

Biomechanics of the sacroiliac joint: A multistability process The range of movement of the SIJ is very limited (2–4 mm). It varies from one individual to another and is dependent on the circumstances of the movement and the age and sex of the individual.

Sacroiliac mobility As mentioned above, during nutation the sacrum rotates in such a way that its promontory moves caudally and anteriorly and the top of the sacrum moves posteriorly. Due to the obliquity of the sacroiliac joints, the iliac wings move closer together and the ischial tuberosities move farther apart simultaneously. This movement is limited by the tension of the sacrotuberous and sacrospinous ligaments and also by the anterosuperior and anteroinferior fascicles of the anterior sacroiliac ligament. During counternutation the opposite movement occurs. The promontory moves cranially and posteriorly, whereas the top of the sacrum moves inferiorly and anteriorly. The iliac wings move farther apart while the ischial tuberosities move closer together. In this situation movement is limited by the tension of the superficial and deep layers of the posterior sacroiliac ligament (Fig. 4.27) (Kapandji 1981). The amount of nutation increases in the standing position, leading the body to adopt a hyperlordotic posture. Counternutation increases in nonloading positions, for example, lying down. In this situation there is a rectification of lumbar lordosis (Sturresson et al. 1989). Movement of the sacrum not only involves the SIJ, but also compromises the lumbosacral and coxofemoral joints. The lowest intervertebral (L5–S1) disc adapts to the plane of the base of the sacrum, leaning forward. This inclination is protected by a strong anterior longitudinal ligament that is fixed at the base of the sacrum reducing the slippage of L5 and consequently the rest of the spine. This stability is reinforced by the action of the iliolumbar ligaments. The resistance of the sacroiliac joints to mechanical load varies depending on the direction of the forces acting on them (the comparisons are with the lumbar segment of the spine). Thus, resistance is greater in

movements of lateral displacement (6 times greater) and in lateral flexion (7 times greater) and is more vulnerable during axial compression (20 times less), and during axial torsion (2 times less). It can be concluded that resistance is lower in movements that involve trunk forward flexion and during the lifting of weights.

Figure 4.27 Nutation–counternutation movement of the sacrum. A Nutation. B. Counternutation.

Reproduced with permission from Black M (2022) Centered: Organizing the Body through Kinesiology, Movement Theory and Pilates Techniques. 2nd edition. London: Handspring Publishing

The behavior of the fibrous complex of the lumbar spine is usually separated from the mechanics of the sacroiliac joints since they act separately. Likewise, the function of the ligament and capsular structures of the sacroiliac joints is limited to passive stabilization, leaving aside the functional interrelation of the ligaments with other soft tissue structures (muscles and fascia). This relationship is essential, for example, in the movement associated with lifting weights when the trunk extensor muscles are unable to counteract the great increase in the moment of force and lift the weight. The aforementioned movement is a combination of the extension of the trunk and the coxofemoral joints. The coxofemoral joint extends through the powerful contraction of the gluteus maximus, gluteus medius, and hamstring muscles. Together they have the ability to lift a heavy weight. The difficulty lies in the transmission of this force toward the extensors of the trunk. The strength of the paravertebral muscles is not sufficient to carry out this transmission. To achieve this they need assistance from the capsules of the apophyseal joints, the posterior ligaments (especially the interspinous, supraspinatus, and sacroiliac ligaments), and the posterior layer of the thoracolumbar fascia. The passive part of this movement is absorbed by the ligaments and capsules; the dynamic part is in charge of the muscles and is transmitted by the TLF. In this way, the entire integrated dynamic system that mobilizes static and dynamic supports acts (Twomey & Taylor 1987). In this task the musculoligamentous network of the SIJ ensures a limited range of motion and, conversely, very high load-bearing strength. How does the system manage to accommodate the two opposing tasks?

Form closure–force closure concept The biomechanical model proposed by Snijders et al. (1993) (Willard et al. 1998, Vleeming & Willard 2010, Vleeming et al. 2012) suggests that an efficient ligamentous complex and competent action of the muscles is indispensable for the proper functioning of the sacroiliac joints. This

biomechanical model also involves the muscles of the trunk and the upper and lower limbs. As mentioned at the beginning of this chapter, the sacrum is integrated into the pelvis as a wedge between the two iliac bones and forms the selflocking mechanism of the SIJs. However, as the axial force increases, the moment of force also increases and the tendency toward counternutation of the sacrum increases. The process is due to the flat shape of the joint surfaces that are mechanically very vulnerable (Snijders et al. 1993) and depends on the degree of trunk inclination and the increase or decrease in SIJ stability. For example, in the seated position forward trunk bending means a stable position of the SIJ, as does a backward tilt. However, in the intermediate position, when the center of gravity is on the ischial tuberosities, the SIJ is unstable. This stability and instability of the SIJ requires the presence of a mechanism capable of acting in two different ways according to the requirements of the movement or position (Greenman 1992). This concept, which was outlined at the beginning of the chapter, is called form closure and force closure (Vleeming et al. 1995) (Fig. 4.28). Form closure occurs when the joint is stable and no external force is needed to support it. When the joint is unstable external forces are necessary to sustain it in equilibrium, i.e., force closure. In this situation, the presence of friction is essential to achieve the objective. Effective stability of the sacrum between the sacroiliac joints involves both form closure and force closure (Snijders et al. 1993). It can be concluded that the passive stability of the SIJ, although apparently ensured by the ligamentous–capsular system, is not enough to guarantee its correct functioning, especially in the tasks associated with activities such as sitting or standing. To achieve the correct level of passive stability, joint action of the ligaments, muscles, and fascia is needed (DonTigny 1993, 1994). Research has shown that nutation is controlled by the tension of the sacrotuberous ligament and counternutation by the tension of the long fasciculi of the posterior sacroiliac ligament. An anatomical link was found between these two ligaments which allows the range of movements of both

to be controlled according to mechanical requirements, thus avoiding excessive tension. This action is of great importance to the joints that bear heavy loads. It should be remembered that approximately 60 percent of the body’s weight is supported on the SIJ. The main muscles that participate in this weight-bearing task are the trunk erector (gluteus maximus), latissimus dorsi, and biceps femoris.

Figure 4.28 The form closure–force closure model

Myofascial participation The mechanism of action is as follows (Vleeming & Willard 2010): The erector of the trunk receives the body weight; its insertion in the sacrum takes it toward nutation, producing tension in the interosseous and the sacrotuberous ligaments. The gluteus maximus, through its location and its connection with the sacrotuberous ligament, compresses the sacroiliac joint. This action produces tension in the thoracolumbar fascia on the contraction side of the gluteus maximus muscle and automatically produces tension in the fascia on the opposite side by the contraction of the latissimus dorsi muscle on the ipsilateral side (Fig. 4.29). Carvalhais et al. (2013) demonstrated that manipulation of the tension of the latissimus dorsi muscle modified the passive hip variables, providing evidence of myofascial force transmission

in vivo between the gluteus maximus and the latissimus dorsi muscle on the opposite side. The biceps femoris long head has the ability, through its contraction, to induce the tension of the sacrotuberous ligament. This action is possible because not all the fibers of its tendon are fixed in the ischial tuberosity, and a great many of them continue its trajectory, integrating into the fibers of the sacrotuberous ligament without inserting in the periosteum (see Fig. 4.18). This behavior of the muscle develops the forces capable of stabilizing the sacroiliac joints in activities that are characterized by instability, for example, during walking. Likewise, in the bipedal position this phenomenon prevents an excess of pressure on the posterior recess of the lumbar disc. In addition, EMG-supported studies have shown the importance of contraction of the oblique abdominal and piriformis muscles in the stabilization of the sacroiliac joints during activities as elementary as sitting in a chair. In forced position the oblique abdominal muscles contract, while the gluteus maximus and the biceps femoris do not respond. When sitting on a soft surface, which offers greater support for the sacroiliac joints, the activity of the abdominal muscles decreases (Richardson et al. 2002). Analyzing the relationship between the pelvic girdle and pelvic floor dysfunction, Beales et al. (2009) proposed a synergistic relationship between the muscles that control pelvic girdle force closure (dynamic stability) in conjunction with breathing, intra-abdominal pressure, and continence (Video 4.1). The researchers applied the active straight leg raise test to two groups of people (the experimental group with postpartum lumbar pain and the control group that was without pain) and in the experimental group recorded alterations in the muscular synergy of the pelvic girdle (similar to straining strategies), increases in intra-abdominal pressure, and depression of the pelvic floor.

Figure 4.29 Connections of the lower limbs to the trunk and upper limbs through the thoracolumbar fascia Blue numbers – connections between the gluteus maximus and latissimus dorsi muscles 1 Latissimus dorsi 2 Gluteus maximus Red numbers – the path of force transmission between the long head of biceps femoris and the erector spinae muscles through the sacrotuberous ligament 3 Erector spinae muscles 4 Sacrotuberous ligament 5 Biceps femoris long head

Innervation of the sacroiliac joint The SIJ is associated with nociception, but in spite of this there are no unified criteria related to the innervation pattern of the SIJ. However, most researchers agree that it is richly innervated by a very complex nervous supply. It is generally considered that the innervation supply of the SIJ comes from the ventral rami of L4 and L5 and the superior gluteal nerve and dorsal rami of L5–S2 (Fig. 4.30). Innervation can vary between individuals, which would explain the variations in referred pain from the SI joint. Examples of the main findings are outlined below:

Figure 4.30 Sacroiliac joint innervation Yellow dots – ventral rami of L4 and L5 Blue dots – dorsal rami of L5–S2

● Ikeda (1991) states that the innervation of the SIJ derives from L2–S2, L4–S2, and L5–S2. However, this has not been verified (Vleeming et al.

2012). ● Murata et al. (2000) state that innervation of the SIJ comes from the sensory neurons in dorsal root ganglions ipsilateral to the joint from L1– S2. The sensory fibers from the L1 and L2 dorsal root ganglions were found to pass through the paravertebral sympathetic trunk. ● The sacroiliac joint receives its innervation from “the ventral rami of L4 and L5, superior gluteal nerve and dorsal rami of L5-S2. The nerve supply to the SI joint varies between individuals and innervation may be almost exclusively derived from the sacral dorsal rami. This may account for the variable patterns of referred pain from the SI joint” (Wong & Kiel 2019). ● Most studies do agree that the nerve supply comes from the ventral rami of L5–S2 and possibly L4. This is because in many individuals sacralization of L5 may lead to SIJ dysfunction (Ikeda 1991). ● In their neuroscientific studies Sakamoto et al. (2001) state that a total of 29 mechanosensitive units were identified in the SIJ: 26 were located in the capsule and 3 adjacent to the muscles (28 nociceptors and 1 proprioceptor). ● Patel et al. (2012) reported successful attenuation of SIJ pain using neurotomy of the L5 dorsal primary ramus and lateral branches of the dorsal sacral rami from S1 to S3 (quoted in Vleeming et al. 2012). ● A histological description of the nerve endings present in the STL has been reported (Sato et al. 2012). ● Varga et al. (2008) examined the occurrence of nerve fibers in the STL and SSL. Their findings showed “the presence of sensory nerve endings (Ruffini-type receptors) in both ligaments. Nerve endings were more concentrated near the ischial tuberosity, particularly in the STL” (quoted in Aldabe et al. 2019). ● The STL and SSL have a proprioceptive role in addition to their mechanical function (Varga et al. 2008). It can be deduced that ligamentous incompetence (excessive laxity) or myofascial dysfunction

in the sacroiliac region can induce compensatory movements and lead to painful conditions (Szadek et al. 2008). ● The innervation of the posterior sacroiliac ligaments is reported to arise from the dorsal sacral rami (Grob et al. 1995). The authors suggest that the innervation is also associated with proprioceptive fibers. For this reason, every surrounding structure could be involved in the sensation of pain. ● Primary afferent Aδ and C nerve fibers consistent with pain generation are identified in the posterior sacroiliac ligaments (Vilensky et al. 2002). ● Florian-Rodriguez et al. (2016) reported that the branches of the S3 and/or S4 nerves could course through the STL or pierce it. ● The structures of the SIJ can be a generator of pain in the posterior sacroiliac region in nonspecific lumbar pain and peripartum pelvic pain.

Blood supply Blood to the sacroiliac joint is supplied by three branches of the internal iliac artery: the superior gluteal artery, lateral sacral artery, and iliolumbar artery.

Assessment The assessment and diagnosis of SIJ dysfunction is challenging. There is a lot of discrepancy and little evidence of the veracity of physical assessment (Murakami et al. 2008). Radiological examinations do not always agree with the physical examination and lead to confusion (Tilvawala et al. 2018). However, on comparing the perpendicular distance from the head of the fibula to the examining table during the Faber test before and after releasing the STL in healthy subjects, Prasertkijkul et al. (2018) observed a decrease in the distance between the head of the fibula and the table. The study demonstrated that releasing the STL could lead to increased range in the Faber test. In low back pain patients who are suspected of having counternutation of the sacrum, releasing the STL may decrease pain. For more on this see Chapter 2 and the MIT procedures at the end of this chapter.

Conclusion The study of the dynamics of the SIJ should include the behavior of the pelvic girdle and all of its components, including fascia in all of its morphological manifestations (Fig. 4.31).

Figure 4.31 The thoracolumbar fascia and its relationships with the sacroiliac joint 1 Deep fascia of the back 2 Posterior aspect of the back GM Gluteus maximus LD Latissimus dorsi SPI Serratus posterior inferior muscle TLF Thoracolumbar fascia Tr Trapezius 3 Outline of the muscles of the posterior layer of the TLF

ABDOMINAL AREA

KEY POINTS ● The abdominal wall as a part of the pelvic girdle ● Anatomical considerations related to the abdominal area ● Distribution of the fascial system in the abdominal area ● Blood supply to the abdominal wall and its relation to fascial dynamics ● Nerve entrapment syndromes related to the abdominal wall

Introduction As mentioned in Chapter 2, the lumbar spine alone is not capable of sustaining the usual loads that it carries daily (Crisco et al. 1992). To stabilize the lumbar vertebrae on the sacral base requires the assistance of a complex myofascial and aponeurotic girdle surrounding the torso (Willard 2007, Willard et al. 2012). The anterolateral component of this girdle is formed by the abdominal fascia structures that are connected laterally to the flat muscles of the abdominal wall.

General considerations related to the abdominal fascial system ● Topographically, the abdominal fascia wall is surrounded by the following boundaries:

▶ superiorly by the cartilages of the 7th–10th ribs and the xiphoid process of the sternum ▶ inferiorly by the inguinal ligaments and the superior margins of the pelvic girdle (iliac crests, pubic crests, and symphysis) ▶ posteriorly by the vertebral column structures.

● The abdominal wall (Fig. 4.32) consists of:

▶ skin ▶ superficial fascia (Camper’s fascia and Scarpa’s fascia) ▶ fat lobes ▶ superficial and deep vascular systems ▶ deep fascia ▶ abdominal muscles and their fascial components (aponeurosis and epimysia) ▶ fascia transversalis ▶ extraperitoneal fat ▶ parietal peritoneum. ● The myofascial system of the abdominal region participates in the dynamics of the pelvic girdle. This participation involves all the previously mentioned components, as well as the visceral and osseous systems (Fig. 4.33). ● The skin and fascia are compliant and deform when under stress. Tension lines in the skin depend on the predominant direction of the collagen fiber bundles in the dermis. They correspond to the direction of Langer’s lines (Kopsch 1908). Langer’s lines are areas of tension in the skin created by the underlying collagen structure and along which the skin is at its maximum tension (Seo et al. 2013, Gibson 1978) (see Volume 1, Chapter 3). Note the distribution of Langer’s lines corresponding to the abdominal wall in Figure 4.33B. ● Components of the circulatory and nervous systems pass through the myofascial structures. ● At deeper levels, links between the myofascial and viscerofascial systems support the activity of the viscera (see Volume 1, Chapter 10).

Figure 4.32 Overview of the layers of the abdominal wall A Skin (cut edge) B Superficial adipose layer of subcutaneous tissue (Camper’s fascia) C Deep membranous layer of subcutaneous tissue (Scarpa’s fascia) D Deep fascia layers (superficial, middle, and deep) E External oblique muscle F Internal oblique muscle G Transversus abdominis muscle H Endoabdominal fascia (transversalis fascia) I Extraperitoneal fat J Parietal peritoneum

Figure 4.33 The anatomical components of the abdominal fascial system. A Skin showing scarring. B Langer´s lines on the skin. C Superficial fascia with fatty lobes. D Innervation of the abdominal area. E Vascularization of the abdominal area. F Deep fascia. G Myofascia. H Lymphatic system of the abdominal area. I Gastrointestinal tract. J Osseous components

Anatomical considerations related to the abdominal fascial system Superficial abdominal fascia The anatomical classification of the abdominal fascia is a good example of the discrepancies that exist in the definitions of fascial nomenclature. Some researchers suggest that the term “superficial fascia” should not be used in relation to the structures located between the skin and the abdominal muscles. Accordingly, they propose that the term “superficial fascia” cannot be considered synonymous with the fascia of Scarpa, Colles, and Camper

(Lancerotto et al. 2011). However, classic anatomy books have retained the older nomenclature, including the term “superficial fascia” (Netter 2011, Standring 2005). In these books the terms Scarpa’s fascia, Colles’ fascia, and the related terms have been retained. The boundaries of the superficial abdominal fascia are not clearly defined in either the cephalic or caudal direction. The superficial abdominal fascia is continuous cranially with the pectoral superficial fascia and caudally with the anterior aspect of the fascia of the thigh, through its links at the level of the inguinal ligaments (crural arch) (Standring 2005) (Fig. 4.34). As discussed in detail in Chapter 3 of Volume 1, the superficial fascia is composed of two layers (superficial and deep layers) and envelops the entire body. However, in the abdominal region, as well as in other areas, the two-layered structure is not clearly defined and most of the subcutaneous fasciae are anchored directly to the deep fascia (Nakajima 2004).

Superficial layer of superficial fascia This layer represents the thick areolar structure that contains a variable amount of fat deposits, often referred to as Camper’s fascia (Standring 2005). There are regional variations in the number, thickness, distribution, and relationships of fat lobes according to factors such as their location and function and also the sex and age of the individual and their overall amount of body fat (Figs. 4.35 & 4.36). The superficial layer lies under the skin and is firmly attached to it through the retinacula cutis (the numerous small fibrous strands that extend through the superficial fascia and attach the deep surface of the dermis to the underlying fascia [see Volume 1, Chapter 3]). It determines the mobility of the skin and superficial fascia over the deep structures. In the male body the superficial layer continues over the penis and the external surface of the spermatic cord to the scrotum. At that level it becomes thin and lacks adipose tissue. Finally, it becomes the superficial perineal aponeurosis. In the female body, it continues from the abdomen to the labia majora and perineum. There is no movement between the skin and the underlying outermost layer of fascia.

Figure 4.34 Superficial abdominal fascia. Note the presence of the retinacula cutis (circled area). There are numerous small fibrous strands that extend through the superficial fascia attaching the deep surface of the dermis to the underlying fascia and determining the mobility of the skin over the deep structures A Anterior superior iliac spine B Superficial veins C Superficial abdominal fascia with adipose lobules D Dissection line E Umbilicus F Skin, dissected and lifted G Pectoral superficial fascia H Xiphoid process

Figure 4.35 The section line of the superficial abdominal fascia. Note the thick areolar structure that surrounds the adipose lobules A Skin B Superficial fascia with adipose lobules C Costal arches (margins)

Figure 4.36 Anterolateral aspect of the lower abdomen and right thigh. Dissection from the cadaver of an obese person. Note the large amount of adipose tissue and the fascial fusion at the level of the crural arch A Deep level of the superficial abdominal fascia B Anterior superior iliac spine C Deep abdominal fascia D Crural arch course (inguinal ligament) E Fascia lata

Deep layer of superficial fascia The deep layer (Scarpa’s fascia) of the superficial fascia is contained by the subcutaneous fascia above and the muscle aponeurosis fascia below. Cranially it is continuous with the fascia of the trunk above and laterally it passes over the crural arch, fusing with the overlying superficial layer. It continues into the thigh, but just below the inguinal ligament it fuses with the fascia lata. In the midline the deep layer is intimately connected to the linea alba and pubic symphysis (Figs. 4.37 & 4.38). The deep layer is more membranous than the superficial layer and contains elastic fibers. The fat lobes are mostly flat. The fascia around the fat is loosely attached to the aponeurosis of the external oblique muscle of the abdomen and is extremely mobile (Markman & Barton 1987). In males it extends over the back of the penis and the spermatic cord to the scrotum. In females it continues toward the labia majora and from there merges with the perineal aponeurosis.

Figure 4.37 Superficial abdominal fascia. The section was made along the linea alba between the pubis and the xiphoid process of the sternum. The skin, along with the superficial fascia, has been dissected and lifted to reveal the deep fascia

A B C

Deep layer of superficial fascia Pubis Deep fascia–muscular aponeurosis

Figure 4.38 Superficial and deep fascia of the abdominal wall. Note the deformation of the fibers of the deep fascia caused by traction of the superficial fascia A Anterior superior iliac spine B Deep abdominal fascia (note its fibrous structure and the irregular density of fibers) C Superficial abdominal fascia D Umbilicus Circle – anchoring of the superficial fascia to the deep fascia

It is worth noting the presence of the components of the circulatory and nervous systems that run through the superficial abdominal fascia structures. In histological sections of Scarpa’s fascia traces of muscular fibers accompanied by fascial envelopes can be observed. Areas of fat with

vessels and nerves just above them can be seen in the membranous Scarpa’s fascia (Fig. 4.39).

Deep abdominal fascia The abdominal wall incorporates four large and paired muscles: the external oblique, internal oblique, rectus abdominis, and transversus abdominis. Its dynamics are closely related to the mechanical behavior of the deep abdominal fascia. The latter is a membranous structure constructed of fibers arranged in different densities and spread over several layers (Fig. 4.40). Ahluwalia et al. (2004) include the epimysium (proprioception) and aponeurosis (force transmission) of the aforementioned muscles in these layers. Cranially deep abdominal fascia is continuous with the pectoral fascia and caudally it merges into the inguinal canal linking to the anterior thigh and becoming the fascia lata (Fig. 4.41) (Gallaudet 1931, Bochenek & Reicher 1997). Anteriorly the deep abdominal fascia branches out toward the oblique abdominal muscles and is firmly inserted into the linea alba (Fig. 4.42). Finally, it continues to the pubis via the insertion of the external oblique muscle. A deep transverse layer of fascia covers the transversus abdominis and subsequently joins the iliac fascia.

Figure 4.39 Scarpa’s fascia. Note the traces of muscle fibers accompanied by fascial envelopes. Areas of fat with vessels and nerves just above them can be seen in the membranous stratum A Superficial layer of superficial fascia (Camper’s fascia) B Neurovascular bundle C Deep layer of superficial fascia (Scarpa’s fascia) D Blood and lymphatic vessels E Deep fascia (myofascia) F Muscle Image courtesy of Ramon Gassó

These fascial connections allow the abdominal muscles to work collectively to facilitate force transmission during movements. The loose connective tissue located between the epimysium of the muscles facilitates gliding between layers, ensuring optimal coordination of movements. In Figure 4.43 morphological differences between the superficial and deep fascia of the abdominal wall and the diversity of fiber orientation in the successive layers can be observed.

Figure 4.40 Deep fascial structures of the abdominal wall

Figure 4.41 Continuity of the deep fascia on the pectoral anterolateral aspect of the abdominal wall and the proximal right area

A B C

Pubis Anterior superior iliac spine Costal arch

Figure 4.42 Structure of the deep abdominal fascia A Pubis B Linea alba C Anterior superior iliac spine D Umbilicus E Costal arch F Pectoral deep fascia G Xiphoid process

Fascial system of the abdominal muscles It is worth noting the importance of the rectus sheath which is formed by the fusion of the aponeuroses and epimysium of the transversus abdominis and the external and internal obliques. When reaching the lateral edge of the

rectus abdominis, this fusion of fibers branches out above and below the muscle, thus creating the sheath. This structure contains the rectus abdominis muscle (Figs. 4.44 & 4.45), which arises from the 5th–7th costal cartilages and the xiphoid process and is located on the anterior abdominal wall. Its fibers have a vertical orientation. Inferiorly the rectus abdominis inserts on the pubic symphysis and pubic crest, merging with the fibers of the ligaments on the anterior aspect of the pubic symphysis. Its left and right sides are vertically separated by the linea alba. It is characterized by its segmental construction with the presence of transverse tendinous intersections that separate eight distinct muscle bellies (Fig. 4.46) and inserts in the anterior layer of the rectus sheath. As mentioned above, the rectus abdominis is surrounded by the aponeuroses of the three remaining large abdominal muscles. The fascia of the external oblique passes over the rectus abdominis. The internal oblique fascia envelops the rectus abdominis (Fig. 4.47). The characteristics of the attachments can vary depending on the location of the insertion:

Figure 4.43 Superficial and deep fascia of the abdominal wall. Note the intrinsic construction of the deep fascia with its multilevel and multidirectional fiber orientation (dashed lines) A Pubis B Skin C Superficial epigastric vein D Abdominal superficial fascia, dissected and lifted E Linea alba F Abdominal superficial fascia G Umbilicus H Abdominal deep fascia (external oblique muscle fascia) I Costal arch J Xiphoid process

Figure 4.44 The left abdominal wall showing the rectus abdominis muscle sheath and its components A Pectoralis major muscle fascia B Linea alba C Rectus abdominis muscle sheath D External oblique muscle fascia E Pubis

Figure 4.45 Abdominal wall – rectus sheath. The deep fascia has been sectioned along the linea alba and lifted A Pubis B Anterior superior iliac spine C Deep abdominal fascia D Tendinous intersection of the rectus abdominis muscle E Rectus abdominis muscle F Costal arch G Xiphoid process

Figure 4.46 The arrangement and orientation of the muscle fibers of the abdominal wall. A Rectus abdominis muscle (wrapped in a composite of the fascia of the external oblique, internal oblique, and transversus abdominis muscles). B External oblique and internal oblique muscles

● The external oblique arises from the posterior aspect of the 5th–12th ribs and attaches to the serratus (through five superior insertions) and latissimus dorsi (through three inferior insertions). Inferiorly its oblique fibers fold onto themselves to participate in the inguinal ligament structure (Fig. 4.48). ● The internal oblique arises from the lowest three ribs. Inferiorly it inserts on the anterior aspect of the iliac crest, the lateral half of the inguinal ligament, and the TLF. The fascia that surrounds the internal oblique is thin and forms part of the rectus sheath. It also participates in the formation of the inguinal ligament and joins with the fascia of the transversus abdominis in the pubis. ● The transversus abdominis (the most internal of the abdominal muscles) arises from the inner side of the 7th–12th costal cartilages, extends to the diaphragm, and continues toward the iliac crest up to the anterior layer of the TLF and the lateral end of the inguinal ligament. ● The umbilicus is an important landmark in the division of the transversus abdominis muscle fibers. Above the umbilicus the transversus abdominis aponeurosis joins the internal oblique aponeurosis to form part of the posterior rectus sheath. Below the umbilicus the transversus aponeurosis only contributes to the anterior rectus sheath (Ahluwalia et al. 2004).

Figure 4.47 Abdominal muscles A Pubis B Inguinal ligament C Internal oblique muscle D Anterior superior iliac spine E Linea alba F Rectus abdominis muscle G Costal arch

Figure 4.48 Abdominal muscles A Pubis B Epimysial fascia of the internal oblique muscle C Linea alba D External oblique muscle, dissected and lifted. Its aponeurosis has been unilaterally detached along the linea alba and lifted E Umbilicus F Tendinous intersection of the rectus abdominis muscle G Rectus abdominis muscle belly H Costal arch

Biomechanical considerations related to the abdominal fascial system ● Skin and fascia are anisotropic materials, meaning that their mechanical behavior is not the same in every direction. It is different depending on how the direction of the loading force relates to the orientation of the collagen fibers in each fascial layer (Chaudhry et al. 2012).

● The skin and abdominal fascia are designed to adapt rapidly in response to the body’s changing requirements, for example, during the digestive process, when there are changes in body weight, and during pregnancy and postpartum recovery. ● The variation in the attachments (Fig. 4.49) suggests that the results of the contraction of certain muscles is not only related to an isolated action but has more to do with the response of an integrated system that acts as a whole.

Figure 4.49 Anatomy of the anterior abdominal wall. Note the differences in the abdominal muscles in relation to the level of attachment A Linea alba B Rectus abdominis muscle C External oblique aponeurosis D Costal cartilage E External oblique muscle F External oblique aponeurosis G Internal oblique aponeurosis H Transversus abdominis aponeurosis I External oblique aponeurosis J Internal oblique aponeurosis K Abdominal aponeurosis

Blood supply to the abdominal fascial system The blood supply to the superficial layers is derived from branches of the femoral artery (which supplies the lower part of the abdomen), the superior epigastric arteries (which supply the peripheral portion of the anterior diaphragm and the superficial muscles of the anterior abdominal wall), and the superficial iliac circumflex artery (which supplies blood to the integument of the groin, the superficial fascia, and the superficial subinguinal lymph nodes) (Fig. 4.50). The inferior epigastric artery (Fig. 4.51) is a major blood vessel that supplies the anterior abdominal wall. It arises from the external iliac artery and subsequently, ascending on the anterior abdominal area, it “pierces the transversalis fascia and enters the rectus sheath ascending posterior to the rectus abdominis muscle” (Joy et al. 2017). Venous drainage into the femoral veins is facilitated via the great saphenous vein, the superficial epigastric vein (Fig. 4.52) (note that the vein is embedded in the superficial fascia), and the thoracoepigastric veins. Video 4.1 demonstrates that that fascial deformation automatically changes the location of the venous structure. It can be concluded that there is an interdependent relationship between the venous system and fascial mechanics.

Figure 4.50 Blood circulation of the abdominal wall Blood supply: A Superior epigastric artery B Anterior intercostal branches C Subcostal artery D Femoral artery Venous drainage: E Thoracoepigastric vein F Superficial epigastric vein G Great saphenous vein

Innervation of the abdominal fascial system

The segmental cutaneous dermatomal innervation pattern of the abdominal wall is illustrated in Figure 4.53 (Lee et al. 2008). The anterior and lateral cutaneous branches of the ventral rami of the 7th–12th intercostal nerves and the ventral rami of the 1st and 2nd lumbar nerves have important sensory and motor functions (Fig. 4.54) (Rudge & Carlstedt 2014). The subcostal nerve originates from the ventral ramus of the last (12th) thoracic nerve. It runs along the lower border of the 12th rib and is included in the lumbar plexus. Subsequently, it passes posteriorly to the kidney and anteriorly extends to the fascia of the quadratus lumborum. It then goes through the transversus abdominis passing between it and the internal oblique. The subcostal nerve then enters the rectus sheath through its front layer. It then becomes subcutaneous halfway between the pubic symphysis and the umbilicus. The subcostal nerve, that is more sensitive to sensory input, supplies parts of the abdominal muscles and gives cutaneous branches to the skin of the lowermost ventrolateral abdominal wall and to the superolateral gluteal region. Pain and motor deficiency can be related to nerve entrapment syndromes. The two nerves which can be involved with the symptomatology of the abdominal area are the iliohypogastric nerve and the ilioinguinal nerve, both of which arise from the lumbosacral plexus and its branches. See Table 4.1 for a summary of the neuroanatomy and dysfunctions associated with each nerve branch.

Figure 4.51 Deep aspect of the abdominal wall A Pubis B Lower epigastric artery. Note its introduction (and perforation) into the muscle epimysium (circle) C Left rectus abdominis muscle, dissected from the linea alba and lifted D External oblique muscle E Internal oblique muscle F Tendinous intersection of the rectus abdominis muscle G Lowest ribs

Figure 4.52 Venous system of the abdominal wall A Anterior superior iliac spine B Pubis C Superficial epigastric vein D Superficial fascia E Umbilicus

Figure 4.53 Dermatomal patterns of the abdominal area

Figure 4.54 Peripheral nerves of the abdominal wall (Ahluwalia et al. 2004) A Iliohypogastric nerve B Ilioinguinal nerve C Iliohypogastric nerve innervation area D Ilioinguinal nerve innervation area

Conclusion An anatomical analysis of the abdominal fascial system evidences its participation in the dynamics of the pelvic girdle, and the system should be analyzed in conjunction with the fascial systems of the TLF and pelvic floor. Table 4.1 Neuroanatomy and dysfunctions of the nerve branches

Peripheral nerve

Nerve roots

Motor innervation

Sensory distribution

Deficiency

Iliohypogastric nerve

T12 L1

Transversus abdominis Internal oblique

Upper buttock Area of suprapubic skin above the inguinal ligament

Hyperesthesia or hypoesthesia of the rectus abdominis Burning or lancinating pain resulting from abdominal surgery and related to scar formation May extend into the genitalia Symptoms similar to trochanteric bursitis May be overlap in sensory supply with the genitofemoral and ilioinguinal nerves

Ilioinguinal nerve

L1

Internal oblique Transversus abdominis

Inguinal ligament Upper medial thigh Lateral scrotum/mons pubis and labia majora

Hypotonia of the lower abdominal wall Hypotonia or paralysis of the internal oblique Hyperesthesia or hypoesthesia of the skin along the inguinal ligament Pain may be localized to the medial groin, labia majora or scrotum, or inner thigh

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MIT procedures for common pelvic girdle dysfunctions: Lower back and sacroiliac structures; Abdominal area

Assessment of the diaphragm

Myofascial induction of the diaphragm: Longitudinal stroke Myofascial induction of the diaphragm: Transverse plane Assessment of the pelvic girdle Pelvic girdle: Transverse plane induction Pelvic girdle: Transverse plane induction at the urogenital level Assessment of the abdominal wall Cross hands induction applied to the abdominal wall Lumbar interfascial triangle (LIFT) Deep-level dissection of the thoracolumbar fascia (TLF) Assessment of the lateral margin of the TLF Lateral margin of the TLF complex, part 1: Transverse stroke Lateral margin of the TLF complex, part 2: Assisted longitudinal stroke Lateral margin of the TLF complex, part 3: Transverse stroke using leverage Lateral margin of the TLF complex, part 4: Direct induction (LIFT area) Lateral margin of the TLF complex, part 5: Direct deep induction (LIFT area) Lateral margin of the TLF complex, part 6: Cross hands induction (LIFT area) Assessment of the TLF Cross hands induction applied to the TLF Assessment of the hip flexors Transverse stroke applied to the psoas Myofascial induction applied to the iliac fossa Assessment of the sacroiliac joints

Longitudinal stroke applied to the sacroiliac region Direct induction applied to the sacroiliac region

5 Pelvic girdle dysfunctions: Gluteal structures; Inguinal and pubic structures; Pelvic floor (external) GLUTEAL STRUCTURES KEY POINTS ● Gluteal structures as part of the pelvic girdle ● Anatomical findings and fascial architecture related to the gluteal area ● Nerve entrapment syndromes related to the gluteal area

Introduction The gluteal fascia is located between the lower end of the trunk and the proximal end of the femur and forms the posterolateral part of the pelvic girdle. The bilateral pronounced shape of the gluteal region (more pronounced in females) is only characteristic of humans and primates. The gluteal region’s shape and size depend on the volume and distribution of the fat layer of the gluteus medius fascia (Sandhofer et al. 2018). The gluteal fascial system forms the anatomical link between the pelvic girdle and lower extremities and therefore, together with the muscles, helps humans to maintain an upright posture while standing and is also essential

to the performance of activities such as walking, running, and climbing. However, it should be noted that the balance of the gluteal structures is unstable, unsafe, and short term (Sandhofer et al. 2018), thus requiring continuous adjustments within the process of dynamic stability. The fascial tissue actively participates in this process.

Anatomical considerations related to the gluteal structures Figure 5.1 shows the consecutive layers of tissues that form the gluteal region.

Skin and superficial fascia The superficial fascia of the gluteal region is very thick, especially in women, and is impregnated with large quantities of fatty lobes. It is one of the main factors that contribute to the prominence of the buttock area (Fig. 5.1A–C).

The skin The skin of the gluteal area is easily deformable and responds rapidly to mechanical stimuli. The tensional changes that affect the dynamics of the skin and the consequent alteration of Langer’s lines (Fig. 5.1B) indicate “that the skin is a main contributor for maintaining the muscle mechanical properties among tissues covering the skeletal muscle” (Yoshitake et al. 2015). As mentioned in Chapter 3 in the description of Langer’s lines, there is no movement between the skin and the superficial layer of the superficial fascia. The skin is not mechanically isolated, nor is it independent from the underlying network. The honeycomb fascia (the superficial layer of the superficial fascia) is attached to the dermis through the fibrils that irregularly emerge from it (Song et al. 2006). These fibrils, called skin ligaments (retinacula cutis), determine the mobility of the skin over the deep structures (Nash et al. 2004) and also provide anchorage of the skin so that it can resist tensile, rotational torque and gravitational forces (Gratzer et al. 2001). The progressive deterioration (effects of the force of gravity, aging, hypomobility) of the muscle–fascia–skin communication network

seems to be responsible for changes to the surface of the skin. One example of this process is gynoid lipodystrophy, popularly called cellulite, which is frequently present in the gluteal and thigh regions, although research related to the pathophysiology of cellulite is inconclusive and often contradictory (Sandhofer et al. 2018).

Figure 5.1 The gluteal area. Note the pronounced gluteal region and marked lumbar lordosis. A Skin. B Langer’s lines. C Superficial fascia. D Deep fascia. E Myofascia. F Skeleton

The skin and subdermal tissue (superficial fascia with fat and neurovascular structures) in the gluteal area may be related to pain perception. Chapter 8 of Volume 1 describes the presence of unmyelinated nociceptive free nerve endings in the subdermal layer that can act as nociceptors (Tesarz et al. 2011, Corey et al. 2011, Mense 2016, 2019). It can be hypothesized that low-intensity mechanical stimuli applied to the subdermal layer will generate a painful response. Fede at al. (2022), following a thorough histological analysis, report the presence of abundant innervation of the superficial fascia. The authors state that autonomous and sensory nerve structures are found mostly around blood vessels and near adipocytes. They also penetrate the connective tissue itself and are found in the middle of fibroadipose tissue. However, it seems that pain sensitivity is not only caused by irritation of the nerve fibers of the skin. Recently, researchers from the Karolinska Institute in Sweden discovered a new sensory organ that can detect painful mechanical damage in the skin. The cells that form the organ are sensitive

to noxious thermal and mechanical stimuli. These are glial cells that through their long expansions form an uninterrupted communication network on the subepidermal border of the skin. In this scenario, glial cells not only support neurons but also participate in the perception of environmental changes and particularly in the identification of mechanical noxious stimuli. It should be noted that “these glial cells, which are intimately associated with unmyelinated nociceptive nerves, are inherently mechanosensitive and transmit nociceptive information to the nerve” (Abdo et al. 2019).

Superficial gluteal fascia After the skin, the next gluteal layer is made up of the superficial fascia which, as previously mentioned, physiologically contains a large amount of fat. Usually, a body mass index (BMI) score of over 30 indicates obesity and is considered harmful to health, increasing the risk of heart attack, stroke, hypertension, diabetes, cancer, arthritis, and other diseases (NIDDK 2017). Research suggests that: “Body fat distribution is an important metabolic and cardiovascular risk factor” (Manolopoulos et al. 2010). Studies confirm that upper body fat (the “apple shape”) is much more dangerous than lower body fat (the “pear shape”) (Manolopoulos et al. 2010). The authors refer to the fact that a high amount of gluteofemoral body fat, as opposed to abdominal fat, fulfills a protective role and is “a determinant of health by the long-term entrapment of excess fatty acids, thus protecting from the adverse effects associated with ectopic fat deposition.” Finally, they claim that “loss of gluteofemoral fat, as observed in Cushing’s syndrome and lipodystrophy is associated with an increased metabolic and cardiovascular risk” (Manolopoulos et al. 2010). The arrangement of the superficial fascia defines the shape, size, and quantity of the fatty lobes and the interrelation between them. Blood supply in the superficial layer of the gluteal region in the middle and lower third is less intense compared to the supply in the lumbar region (Fig. 5.2). This is the reason why the skin in the gluteal region is cold if it remains compressed for a long time, for example when sitting during a long trip.

Structural alterations relating to the superficial gluteal fascia can alter the gliding process in the deeper layers, thus affecting muscle and joint dynamics, as demonstrated by Wilke et al. (2020) and Wilke and Tenberg (2020) in other parts of the body. The authors demonstrate the mechanical interaction between superficial fascia and skeletal muscle and suggest that local alterations of the mechanical properties (muscular tissue in relation to the superficial fascia and vice versa) may modify flexibility in neighboring (superior or inferior) joints. Based on these findings, it is suggested that the use of sliding (stroking) procedures applied to the superficial gluteal fascia would be favorable for functional recovery processes.

Figure 5.2 Superficial fascia of the gluteal region. Notice the difference in vascularization in the lumbar and gluteal regions. Intense vascularization is noticeable in the lumbar region, whereas the gluteal region almost lacks vascularization at the subdermal level A Superficial fascia of the lumbar area B Path of the iliac crest C Superficial fascia of the gluteal area D Skin, dissected and turned over E Line of the dissection of the skin from the superficial fascia

Deep gluteal fascia The deep fascia of the lower quadrant manifests as a continuous, thin and resistant fibrous “stocking” which envelops the underlying structures. Its path is uninterrupted from the abdominal and low back areas to the feet. To its proximal edge are attached the insertions of the abdominal muscles (internal oblique, external oblique, and transversus abdominis), gluteus maximus, and tensor fasciae lata, thus creating mechanical links between the trunk and lower extremities. Along its route the deep fascia has different names (associated with its topography): gluteal fascia, fascia lata, crural fascia, fascia of the foot, and plantar fascia. The morphology of the deep fascia (e.g., thickness, fiber orientation) varies according to the functional requirements of each area. It is thinner around the knee and ankle joints and on the inner aspect of the thigh (Pilat 2017). As mentioned in Chapter 2, the superficial layer of the thoracolumbar fascia (deep fascia of the back) becomes the gluteal fascia from the iliac crest. This complex, continuous, and fibrous tissue extends around the gluteal region, the hip, and the thigh (Fig. 5.3, Video 5.1). Proximally the gluteal fascia is attached to the posterior outer lip of the iliac crest (between the iliac crest and the superior border of the gluteus maximus muscle), sacrum, and coccyx (Fig. 5.4). Distally it is attached to the gluteal tuberosity of the femur and continues laterally as the iliotibial band.

The deep gluteal fascia separates the gluteal muscles from the superficial fascia (Huang et al. 2013) and forms the epimysium of the gluteus maximus, however, it manifests as the aponeurotic fascia in the gluteus medius (see Fig. 5.3). At the proximal edge, it appears as a dense and fibrous structure, covering the anterior two-thirds of the gluteus medius (the posterior third is covered by the gluteus maximus) and the proximal part of

the gluteus maximus (see Figs. 5.3 & 5.4). The presence of loose connective tissue between the two muscles facilitates the sliding process during movement.

Figure 5.3 Deep fascia of the posterolateral aspect of the lumbopelvic and lower extremity region A Lowest ribs B Thoracolumbar fascia C Iliac crest D Gluteus medius fascia. Note the aponeurotic structure E Groove between the gluteus maximus and gluteus medius that facilitates the independence of its contractile dynamics F Sacrum G Gluteus maximus fascia. Note the epimysial structure H Deep fascia of the thigh

Figure 5.4 Thoracolumbar and gluteal fasciae attachments A Line of the iliac crest B Gluteus medius aponeurotic fascia C Groove between the gluteus maximus and gluteus medius D Attachment of the gluteus maximus fascia to the sacrum E Sacrum F Epimysial fascia of the gluteus maximus G Fascia lata

Gluteal fascia compartments At the beginning of this chapter the precarious balance (instability) of the pelvic girdle was discussed. Gluteal myofascial structures are the principal components responsible for optimal efficiency in balance and movement. The large number of muscles related to the behavior of the gluteal fascia are divided into two compartments: ● superficial compartment (function: abduction and extension of the thigh)

▶ gluteus maximus ▶ gluteus medius ▶ gluteus minimus ▶ tensor fasciae latae

● deep compartment (function: lateral rotation of the thigh)

▶ piriformis ▶ superior gemellus ▶ obturator internus ▶ inferior gemellus ▶ quadratus femoris ▶ obturator externus.

From its superior insertion in the iliac crest, the gluteal fascia creates a bifurcation, separating the superficial compartment which forms the fascial layers that enclose the three gluteal muscles: gluteus maximus, gluteus medius, and gluteus minimus (Fig. 5.5). The gluteus maximus, the largest muscle in the human body, is covered in two sheets of gluteal fascia: a superficial sheet and a deep sheet. The superficial sheet, the epimysial gluteal fascia (Fig. 5.6), is thin and firmly attached to the muscle belly. The fatty lobes are so firmly embedded in the fascia that when they are removed with a clamp during dissection the fascia is damaged. This superficial sheet extends intermuscular septa that penetrate the muscle belly creating spaces for their bundles (Fig. 5.7). The deep sheet also extends fibrous septa that compartmentalize the muscle belly (Fig. 5.8). Dissecting the epimysial fascia of the gluteus medius and detaching the gluteus maximus reveals the gluteus medius muscle belly (Fig. 5.9). The deep gluteal fascia stands out for its transverse fibrous structure (Fig. 5.10). In this layer, the presence of the fan-shaped sacrotuberous ligament also stands out. The latter is continuous with the tendon of the long head of the biceps femoris muscle in the sciatic tuberosity (Fig. 5.11). At the deepest level of the gluteal fascia a third sheet is located which covers the surface of the sacrotuberous ligament and also the piriformis, gemellus superior, obturator internus, gemellus inferior, and quadratus femoris muscles (Figs. 5.12 & 5.13).

Biomechanics and the gluteal area

Functions of the gluteus maximus The gluteus maximus is predicted to have considerable (>700 N) capacity for compressive force generation across the sacroiliac joint. Its bony and fibrous attachments may assist in effective load transfer between the lower limbs and trunk (Barker et al. 2004) (Fig. 5.14). The gluteus maximus counteracts and controls the acceleration of the trunk and pelvis in bipedal locomotion and participates in the distribution of body weight. Its activity increases when the trunk participates in the actions of throwing and punching, starting the rotation of the pelvis, and braking as the trunk rotation ends. Additionally, it stabilizes the pelvis during activities such as digging and heavy lifting. Marzke et al. (1988) assign gluteus maximus an important role in “the origin of hominid bipedality.” Carvalhais et al. (2013), in their in vivo electromyographic study, observed the presence of a myofascial force transmission pathway. The force was transmitted from the latissimus dorsi muscle through the TLF and recorded in the gluteus maximus on the opposite side (for more on myofascial force transmission see Volume 1, Chapter 7). The gluteus maximus is highly active during activities such as running, sprinting, and climbing “which supports the idea that human muscle is functionally important for a variety of fast and powerful movements” (Bartlett et al. 2014).

Figure 5.5 Schematic view of the gluteal muscles and their insertion areas. 1 Overview of the three muscles. 2 Insertion areas. 3 Cross-section showing the interrelationship of the gluteal muscles A Gluteus minimus B Gluteus medius C Gluteus maximus D Sacroiliac joint E Iliotibial tract

Likewise, the gluteus maximus plays an important role during weight lifting and returning to the upright position from trunk flexion (Leinonen et al. 2000). Therefore, its weakness could cause errors in the management of forces during this movement that could in turn cause stress on the sacroiliac structures and/or the lumbar spine resulting in low back pain. Conversely, the complementary role of the gluteus maximus in fatigue of the erector muscles of the spine serves as protection for the lower back.

Gluteus medius weakness and gluteal muscle tenderness are common symptoms in people with chronic nonspecific LBP (Cooper et al. 2016). Amabile et al. (2017) evidenced the presence of atrophy in the gluteus maximus in patients with LBP. Gluteus medius and minimus dysfunction can create lateral instability of the pelvis, patellofemoral syndrome, and instability of the ankle (Powers 2010). The gluteal fascia partially serves as the flat tendon of origin of the gluteus medius and forms a portion of the gluteus maximus adjacent to the lower edge of the gluteus medius. Most of the anterior fibers of the gluteal fascia adhere directly to the posterior fibers of the iliotibial tract.

Figure 5.6 Left gluteus maximus fascia 1 Epimysial deep gluteal fascia A Iliac crest B Gluteus maximus fascia with fatty lobes C Line of the transverse section of the gluteal fascia and the gluteus maximus muscle belly D Gluteus maximus fascia (superficial layer) after removal of fatty lobes which are firmly embedded in the fascia. The fascia was damaged when removed with a clamp during dissection 2 Upper third of the gluteus maximus, dissected, lifted, and turned over A Gluteus maximus, dissected, lifted, and turned over B Deep gluteal fascia C Superficial gluteal fascia, dissected, lifted, and turned over

D

Intermuscular septa

Deep gluteal syndrome Irradiated pain in the buttock area, hip, or posterior thigh is generally described as radicular pain, which can be caused by injury to a spinal nerve root (compression by herniated disc, inflammation, foraminal stenosis, or peridural fibrosis). However, the aforementioned symptomatology can also manifest itself as a result of nondiscogenic sciatic nerve entrapment in the subgluteal space (Martin et al. 2015) (Video 5.2). This symptomatology is usually called deep gluteal syndrome. Deep gluteal syndrome manifests itself with sciatic pain accompanied by pain in the buttocks, which is aggravated by sitting (Hopayian & Heathcote 2019). Deep gluteal syndrome involves a conflict of tension and mobility in the subgluteal space (between the middle and deep gluteal fascia), which is related to the gluteus maximus and the posterior surface of the femoral neck.

The subgluteal space extends between the following boundaries (Carro et al. 2016): ● posteriorly to the gluteus maximus ● anteriorly to the posterior border of the femoral neck ● laterally to the linea aspera and the lateral fusion of the middle and deep layers of the gluteal aponeurosis up to the tensor fasciae latae (iliotibial tract) ● medially to the sacrotuberous and falciform fascia ● superiorly to the inferior margin of the sciatic notch

● inferiorly to the origin of the hamstring muscles.

Figure 5.7 Gluteus maximus A Thoracolumbar fascia B Iliac crest C Gluteus medius covered by aponeurotic fascia D Sacrum E Gluteus maximus with the epimysial fascia removed F Intermuscular septa

Figure 5.8 Deep layer of the gluteal fascia A Thoracolumbar fascia B Sacrotuberous ligament C Inferior gluteal nerve (gluteus maximus and hip joint innervation) D Gluteus maximus muscle, dissected, lifted, and turned over

Figure 5.9 Deep layer of the gluteal area A Posterior layer of the thoracolumbar fascia B Sacrum C Gluteus maximus insertion into the iliac crest D Iliac crest E Sacrotuberous ligament F Ischial tuberosity G Gluteus medius H Gluteus maximus, dissected, lifted, and turned over

Figure 5.10 Deep attachments of the gluteal fascia to the thoracolumbar fascia A Latissimus dorsi B Thoracolumbar fascia C Iliac crest D Gluteus maximus muscle attachment E Deep gluteal fascia

Figure 5.11 Deep level of the gluteal myofascial structure A Gluteus maximus, dissected B Sacrotuberous ligament C Gluteus minimus, dissected, lifted, and turned over D Ischial tuberosity E Biceps femoris long head tendon

Figure 5.12 Deepest layer of the gluteal fascia A Sacrotuberous ligament B Sacrotuberous ligament–piriformis muscle attachment C Piriformis muscle belly D Gluteus maximus, dissected and lifted E Sciatic nerve F Ischial tuberosity G Biceps femoris long head tendon H Biceps femoris long head belly

Several muscles are involved in the subgluteal space, particularly the piriformis, as are neurovascular structures such as the superior and inferior gluteal and sciatic nerves and vessels and also the sacrotuberous and sacrospinous ligaments. As a consequence of this, multiple pathologies have been incorporated into deep gluteal syndrome. The etiology of the subgluteal space is related to: “Specific entrapments within the subgluteal space [which] include fibrous bands, piriformis syndrome, obturator internus/gemellus syndrome, quadratus femoris and ischiofemoral pathology, hamstring conditions, gluteal disorders or orthopedic causes” (Carro et al. 2016). The most common syndrome related to deep gluteal syndrome is piriformis syndrome which is the result of

compression of the sciatic nerve through or around the piriformis muscle. Usually the pain manifests along the path of the sciatic nerve, involving the gluteal region and increasing when sitting (Cass 2015). The piriformis is a small muscle that arises from the pedicles of the 2nd–4th sacral segments in the ventrolateral aspect of the sacrum. Its fascial origin is on the capsule of the sacroiliac joint. It passes through the greater sciatic foramen and is inserted into the inner edge of the piriformis fossa of the greater trochanter. The piriformis muscle divides the greater sciatic foramen into two parts: the suprapiriform foramen (which contains the superior gluteal artery, vein and nerve) and the infrapiriform foramen (which contains the inferior gluteal artery, vein, and nerve, sciatic nerve, posterior femoral cutaneous nerve, pudendal nerve, and the nerves to the obturator internus/gemellus superior and quadratus femoris/gemellus inferior) (Hernando et al. 2015). The importance of the piriformis muscle and its fascial connections is due to the proximity of the roots of the 1st–3rd sacral nerves and the superior gluteal nerve that innervates the gluteus medius, gluteus minor, and tensor fasciae lata muscles. The piriformis muscle also connects to the anterior ligament of the sacroiliac joint and the gemelli and obturator internus muscles (McCrory & Bell 1999). The piriformis muscle is separated anteriorly from the retroperitoneal structures and posteriorly from gluteal muscles by the fascial planes (Hernando et al. 2016).

Figure 5.13 Deepest layer of the gluteal fascia 1 Lateral aspect of the left pelvis A Sacrotuberous ligament B Sciatic nerve C Ischial tuberosity Dotted line – iliac crest 2 Deep lateral rotators A Piriformis muscle B Deep lateral rotators of the femur (quadratus femoris, gemellus superior, gemellus inferior, and obturator internus muscles) C Area of connection of the rotator structures, the transition of the sacrotuberous ligament, and the biceps femoris long head tendon

The piriformis muscle is the external rotator of the hip, is an important passive hip stabilizer (Retchford et al. 2013), and acts as a functional stabilizer during hip extension (Morimoto et al. 2018). It also acts “in restricting posterior translation of the femoral head when the joint is flexed due to the shift towards a more posterior position of this muscle with respect to the hip joint in hip flexion” (Carro et al. 2016). Hip flexion, adduction and internal rotation stretch the piriformis muscle and cause narrowing of the space between the inferior border of the piriformis, superior gemellus, and sacrotuberous ligament (Carro et al. 2016).

These anatomical and biomechanical relations between the piriformis muscle and the sciatic nerve can facilitate direct contact between them and may lead to compression of the nerve. The resulting referred pain caused by the myofascial restriction covers a very large area: the lumbosacral region, buttock, posterior aspect of the thigh, groin, and sometimes the foot. Buttock and leg pain becomes worse when sitting, climbing stairs, and/or crossing the legs. During defecation pain is present in the rectum. Sexual dysfunction may also be present. It is important to consider the insertion of the pyramidalis muscle into the sacrotuberous ligament (see Fig. 5.12), which extends from the posterior superior iliac spine and the lower end of the sacrum to the ischial tuberosity. As previously mentioned, this ligament partially serves as an insertion in the tendon of the biceps femoris muscle. Thus, the myofascial restriction may influence the patient’s gait due to the restricted elasticity of the biceps femoris (McCrory & Bell 1999, Carro et al. 2016).

Figure 5.14

Force vectors of the attachments of the gluteus maximus (according to Barker et al. 2004) A Gluteus medius B Ilium C Thoracolumbar fascia D Long dorsal sacroiliac ligament E Sacrum F Sacrotuberous ligament G Coccyx

Cutaneous nerves, vessels, and lymphatics A posterior view of the cutaneous sensory innervation of the gluteal region is illustrated in Figure 5.15: ● The upper anterior part of the gluteal region is supplied by the lateral cutaneous branches of the subcostal and iliohypogastric nerves. ● The upper posterior part is supplied by the posterior rami of spinal nerves L1–L3 and S1–S3. ● The lower anterior part is supplied by branches of the posterior division of the lateral cutaneous nerve of the thigh. ● The lower posterior part is supplied by branches of the posterior cutaneous nerve of the thigh (S1–S3) and the perforating cutaneous nerve.

Figure 5.15 Posterior view of the cutaneous sensory innervation of the buttock, hip, and thigh (according to McCrory & Bell 1999) A Ilioinguinal nerve B Posterior rami of the sacral and coccygeal nerves C lliohypogastric nerve D Inferior cluneal nerve E Posterior cutaneous nerve of the thigh F Lateral cutaneous nerve of the thigh G Obturator nerve

The blood supply of the skin and subcutaneous tissue is derived from perforating branches of the superior and inferior gluteal arteries. The lymph vessels from the gluteal region drain into the lateral group of the superficial inguinal lymph nodes.

Innervation of the gluteal region The gluteal region is supplied by a number of small nerves derived from the 12th thoracic nerve to the 3rd sacral nerve (T12–S3). The superolateral quadrant of the buttock is relatively free of deeper nerves and vessels and is frequently used for intramuscular injections. The main nerves of the sacral plexus either supply or traverse the gluteal region (according to Gardner et al. 1960). The superior gluteal nerve (arising from L4, L5, S1): ● passes above the piriformis and between the gluteus medius and minimus muscles ● supplies the gluteus medius, gluteus minimus, and tensor fasciae latae. The inferior gluteal nerve (arising from L5, S1, S2): ● passes below the piriformis ● supplies the gluteus maximus. The pudendal nerve (arising from S2 to S4): ● “passes deep to the gluteus maximus and continues to the middle of the posterior thigh, where it pierces the fascia, and will ultimately reach the calf” (Gardner et al. 1960). The sciatic nerve (L4–S3): ● runs under the gluteus maximus in its superior path and then halfway along the posterior aspect of the thigh.

Chronic hip, groin, and buttock pain Chronic hip, groin, and buttock pain is a common diagnosis, and its etiology is varied (Fig. 5.16). It could be radicular pain arising from irritation of the upper lumbar nerve roots, referred pain from innervated spinal structures, or chronic regional pain syndrome (McCrory & Bell 1999).

Figure 5.16 Pain distribution in the gluteal, hip, and thigh area A Sacroiliac pain area B Gluteal area pain referred from the lumbosacral plexus C Trochanteric bursitis pain D Ischiogluteal bursitis pain area E Sciatic pain area

Sciatic nerve entrapment Sciatic nerve entrapment can be due to the formation of fibrovascular bands secondary to acute or chronic inflammatory pathology in the subgluteal space and can have different origins (Hernando et al. 2015). Musculotendinous entrapments can be related to:

● obturator internus/gemelli complex ● gluteal compartment syndrome ● intramuscular fibrosis with subsequent retraction of scar tissue ● quadratus femoris and ischiofemoral space pathology ● exercise-induced edema of the quadratus femoris muscle ● ischiofemoral impingement ● enthesopathy of hamstring origin ● primary piriformis syndrome

▶ with an anatomical cause (anatomical variants)

● secondary piriformis syndrome

▶ occurs as a result of a precipitating cause including macrotrauma, microtrauma, ischemic mass, inflammation, or infection.

Fibrous entrapments can be related to: ● fibrovascular bands containing vessels ● formation of fibrovascular bands secondary to acute or chronic inflammatory pathology in the subgluteal space.

Regional approach to nerve entrapment syndromes McCrory and Bell (1999) take a regional approach to nerve entrapment syndromes related to sport. They “note that the often described symptoms are more likely due to compression of structures other then the sciatic nerve,” as outlined below: Lateral Buttock: ● Ilioinguinal nerve ● Iliohypogastric nerve ● Lateral cutaneous nerve of thigh ● T12 root

Lateral Thigh ● Lateral cutaneous nerve of thigh ● Posterior cutaneous nerve of thigh Posterior Buttock ● Posterior rami of the lumbar, sacral and coccygeal nerves ● Iliohypogastric nerve ● Lateral cutaneous nerve of thigh ● Posterior cutaneous nerve of thigh ● T12 root Posterior Thigh ● Lateral cutaneous nerve of thigh ● Posterior cutaneous nerve of thigh ● Inferior medial and lateral cluneal nerves.

Conclusion Dysfunction and chronic pain in the gluteal region are common diagnostic problems due to the complex anatomy of the region. Alterations (dysfunctions) in the fascia that compartmentalizes and at the same time unifies and coordinates the muscular dynamics of this region can influence potential neurological causes of pain (entrapment syndromes). A detailed knowledge of the fascial continuity and interrelations of the fascial structures of the gluteal area will facilitate understanding of this problem.

INGUINAL AND PUBIC STRUCTURES

KEY POINTS ● The inguinal and pubic area in relation to the orthostatic position and bipedal locomotion ● Functional anatomy of the pubic and inguinal area in relation to the most common dysfunctions ● The femoral triangle ● Symphysis pubis dysfunction

Introduction The inguinal area (the groin), which includes the pubis, consists of a threedimensional, complex system of bones, nerves, and myofascia that provides support to and helps maintain the dynamics of the pelvic girdle (Fig. 5.17). It is has been suggested that the kinetics of this complex are the result of the evolutive adaptation to the orthostatic position and the consequent verticalization of the pelvis (see Chapter 2). In a complementary way, this process has influenced the development of the ligamentary supports and also contractile activity during daily actions ranging from bipedal movement to intense increases in intra-abdominal pressure. It should be emphasized that from an anatomical, biomechanical, and neurological perspective the pubic and inguinal areas behave functionally as a unit because it is impossible to conceive the behavior of each part independently of the other. Symphysis pubis dysfunction (SPD) is a group of symptoms that cause discomfort in the pelvic region. Groin pain is a common set of symptoms affecting mainly sportsmen, patients with traumatic pelvic injuries, and pregnant women (Rennie & Lloyd 2017). It commonly begins during pregnancy or sporting activities when the pelvic joints move unevenly and it can be present both at the front and back of the pelvis. SPD and groin pain are sometimes also referred to as pelvic girdle pain. The lack of specificity of the term groin (inguinal area) also leads to much confusion

(Rennie & Lloyd 2017). Because of the complex anatomical arrangements in this region, the diagnosis of chronic pubic, groin, or pelvic girdle pain often remains elusive. No single test is diagnostic. Some authors (Jain et al. 2006), when referring to pregnant or postpartum patients, “stress that the woman’s own description of discomfort is sufficient to diagnose SPD.” Other authors recommend the use of palpation tests (Wellock 2002, Albert et al. 2000, Fry et al. 1997) or diagnostic imaging (Thorborg et al. 2018).

Anatomical considerations related to the inguinal and pubic structures The inguinal region is a bridge area. Here, the abdominal fascia becomes the fascia lata (thigh fascia), and the two types of fascia cover multiple anatomical structures (Fig. 5.18). The pubis (the central structure and a sort of distributor of forces in this area) has numerous muscular and ligamentous attachments that subject it to forces; the pubis resists tensile, shearing, and compressive forces and is able to widen during pregnancy.

Pubis The pubic symphysis is a fibrocartilaginous structure which has very limited movement. Under physiological conditions it reaches displacement of up to 2 mm and 1 mm of rotation (Jain et al. 2006). The mechanical integrity of the pubic symphysis is maintained by the ligaments and myofascial structures that neutralize the shear and tensile stresses to which the pubis is subjected, such as the biomechanical stress generated by intraabdominal pressure. The main pubic ligaments, the superior and inferior pubic ligaments, reinforce the pubic symphysis. The superior pubic ligament is strong and thick. It connects the two pubic bones superiorly, extending laterally as far as the pubic tubercles. The inferior pubic ligament forms an arch spanning the inferior pubic rami. Both ligaments are reinforced by the tendons of the rectus abdominis, abdominal external oblique, gracilis, adductor brevis, adductor longus, adductor magnus, obturator externus, quadratus femoris, pectineus, and psoas minor muscles (Figs. 5.19 & 5.20).

Figure 5.17 The pubic and inguinal area: The three-dimensional, complex system of bones, nerves, and myofascia that provides support to and helps maintain the dynamics of the pelvic girdle. A Bone components. B Fascial components. C Neural components. D Muscular components

Figure 5.18 Continuity of the deep fascia of the abdominal wall and the proximal thigh area A Anterior aspect of the thigh (fascia lata) B Pubis C ASIS D Linea alba E Abdominal deep fascia F Umbilicus G Costal arch

The dynamic stability of the pubis when subjected to forces is crucial to the proper functioning of the whole pelvic girdle and its excessive elasticity can create instability. The innervation of the joint is through the genitofemoral nerve and branches of the iliohypogastric, ilioinguinal, and pudendal nerves (Standring 2005, Becker et al. 2010).

Figure 5.19 Muscles related to dynamic pubic stability A Rectus abdominis B Levator ani C Obturator internus muscle D Gracilis E Adductor longus F Adductor magnus G Adductor brevis H Pectineus I Obturator externus muscle J Quadratus femoris

Linea alba The linea alba (tendinous raphe) extends longitudinally between the xiphoid process and the pubic symphysis and laterally between the medial edges of the rectus abdominis, and it consists of the aponeurosis of the oblique and transversus abdominis muscles (Standring 2005). It inserts inferiorly in the crest of the pubis through a double attachment, which is both superficial and deep. Figure 5.21 shows the fibrous structure of this attachment.

Inguinal ligament The inguinal ligament is a thick band which extends between the anterior superior iliac spine and the pubic tubercle and is part of the deep fascia of the inguinal area. The upper border of the ligament is made up of the distal end of the aponeurosis of the external oblique muscle and caudally it continues as fascia lata (Fig. 5.22). Anatomically the ligament may be considered to be an integral part of the fascia and it is not outside of the fascia (Fig. 5.23). Its main functions are support of the soft tissue in the groin area, anchorage of the external abdominal oblique muscles, and optimization of the performance of the iliopsoas and pectineus muscles in order to maintain the flexibility of the hip region. “The specific force exerted by the oblique abdominal wall muscles during twisting, turning and kicking maneuvers over a period of time, may cause tensioning and cordlike bands within the inguinal ligament” (Rennie & Lloyd 2017). The fascial expansions of the inguinal ligament create spaces, forming the femoral (superficial) and inguinal (deep) rings (Stecco et al. 2013).

Inguinal canal The inguinal canal extends parallel to and above the inguinal ligament following its path and accommodating the neurovascular tract (Fig. 5.24). It covers a short distance (about 4 cm) and extends between the superficial and deep rings. The inguinal canal is formed by the aponeuroses of the transversus abdominis, external abdominal oblique, internal abdominal oblique, crural arch, and transversalis fascia. This is the weak space in the abdominal wall. The canal is the communication path between the structure of the abdominal cavity and the external genitalia (the round ligament of the uterus in women and the spermatic cord in men). Due to the aforementioned anatomical weakness, it is the area where inguinal hernias form (Falvey et al. 2009).

Figure 5.20 Cross-section at the pubic level showing the interrelations of anatomical structures A Vastus lateralis B Tensor fasciae latae C Rectus femoris muscle D Iliacus muscle E Sartorius muscle F Femoral artery G Femoral vein H Gluteus maximus I Anterior pubic ligament J Posterior pubic ligament K Obturator internus muscle L Obturator externus muscle M Pectineus muscle N Ischium O Femur P Bladder Q Rectum R Levator ani S Retropubic fat

Figure 5.21 Abdominal and linea alba insertions in the pubis A Pubis B Linea alba C Deep abdominal fascia. Note the fibrous structure

Femoral triangle In the front part of the thigh the femoral triangle stands out (Fig. 5.25). It is bounded by the inguinal ligament (superior border), sartorius muscle (lateral border), and adductor longus muscle (medial border). Its significance lies in the fact that some of the major neurovascular structures of the lower limb that are embedded in fascial tissue pass through the triangle (Fig. 5.26). These are the: ● femoral nerve, which provides sensory branches to the leg and foot ● femoral artery, which provides the arterial blood supply to the lower limb ● femoral vein, which receives drainage from the great saphenous vein ● femoral canal, which contains about 10 superficial inguinal lymph nodes (Fig. 5.27) and also lymph vessels. The superficial lymph nodes are

located under the deep fascia and drain into the deep inguinal lymph nodes located below the inguinal ligament.

Figure 5.22 Deep abdominal fascia. The dissection line is along the linea alba between the xiphoid process and pubic symphysis. The skin and superficial fasciae have been lifted. Note the continuity of the deep fascia from the pectoral area to the anterior aspect of the thigh A Pubis B Path of the inguinal ligament C Linea alba D ASIS E Deep abdominal fascia F Costal margins G Xiphoid process of the sternum

Figure 5.23 Anterior aspect of the abdominal and inguinal area. On the right the incision is above the inguinal ligament and on the left it is below the ligament A Linea alba B Pubis C Fascia lata D Inguinal ligaments E Inguinal canal F Abdominal external oblique aponeurosis

Figure 5.24 Inguinal ligament area. Note the firm adhesions between the superficial and deep fascia. The area is a protective system for the major neurovascular structures of the lower limb. The skin and superficial fascia have been dissected along the path of the inguinal ligament A ASIS B Line of incision C Superficial fascia D Deep fascia of the thigh E Adhesion between the superficial and deep fascia F Pubis

Figure 5.25 Inguinal area and inguinal triangle A Pubis B ASIS C Navel D Superficial fascia over the inguinal ligament line E Lateral aspect of the thigh F Skin (underside)

Figure 5.26 Inguinal canal structures A Great saphenous vein B Fascia lata C Sartorius D Adductor longus E Femoral artery F Spermatic cord G Femoral nerve H Pubis I Iliopsoas J Inguinal ligament K ASIS L Aponeurosis of the abdominal external oblique M Linea alba N Navel

Figure 5.27 Superficial inguinal lymph nodes A Pubis B Superficial inguinal lymph nodes C ASIS

Symphysis pubis dysfunction and groin pain Clinical aspects of SPD Diagnosis of SPD is based on particular signs and symptoms (RCOG 2015): ● difficulty when walking, especially after standing for a long time ● pain when standing on one leg (e.g., climbing stairs, dressing) ● pain and/or difficulty moving the legs apart ● clicking or grinding in the pelvic area (sometimes audible) ● pain is worse at night when lying on the back ● limited or painful hip movements (e.g., when turning in bed) ● pain referred to the hip, back, or perineum

● knee pain extending down to the ankles and feet ● pain and difficulty during coitus ● occasional urinary incontinence. The most common dysfunctions in the pubic region include adductor longus tendinopathy, inguinal ligament strain, osteitis pubis, and inguinal hernias. Tenderness over the symphysis pubis is common. Palpation in specific points of the groin area is helpful in differential diagnosis. The recommended locations for palpation are shown in Figure 5.28.

Nerve entrapment syndromes related to the inguinal and pubic area Before the therapeutic approach is applied to dysfunctions linked to nerve entrapments, serious neurological diseases should be ruled out, for example (McCrory et al. 2002): ● bladder or bowel dysfunction ● local or global weakness in the lower limbs ● loss of sensation or “pins and needles” ● loss of coordination in the lower limbs ● systemic symptoms (e.g., fever, night sweats, or weight loss) ● night pain or pain when resting ● lower limb or buttock pain that gets worse with exercise

▶ unilateral leg pain and swelling.

Figure 5.28 Palpation area for groin pain

Nerve entrapment syndrome A knowledge of the distribution of sensitive areas is very useful to the therapeutic process. It allows the practitioner to identify links between the referred symptoms (including multifocal symptomatology). Nerve entrapment syndrome can be one of the causes of pain and dysfunction. A comprehensive knowledge of the nerves that may be involved, their

anatomy, their motor and sensory functions, and the etiology of their dysfunction will help the practitioner to manage these complex problems. For example, nerve entrapment could be responsible for several pain syndromes in the lower limb and lumbopelvic segments, such as hip, buttock, or groin pain. The locations of the most common entrapments of the lumbosacral plexus and its branches related to the groin area are shown in Tables 5.1 and 5.2.

Conclusion Dysfunctions of inguinal and pubic structures can affect the dynamics of the entire pelvic girdle. The groinarea is usually forgotten in therapeutic processes that treat, for example, LBP. It is important to remember that the inguinal region is the mechanical link between the abdomen and the thigh and to understand its possible influence on the dynamics of the trunk and lower limb. Applying a therapeutic approach to a single structure will not restore the global dynamics of the region.

PELVIC FLOOR (EXTERNAL) KEY POINTS ● The anatomy and biomechanics of the pelvic floor fascial system in relation to the orthostatic position and bipedal locomotion

● Functional anatomy of the most common dysfunctions related to the pelvic floor ● The pelvic floor as an integral part of the pelvic girdle ● Endopelvic fascia as a dynamic system ● Endopelvic dysfunction ● Therapeutic indications for MIT in dysfunctions of the pelvic floor

Introduction In recent years there has been an increasing amount of research indicating the need to include fascia in the protocols for assessment, treatment, and prevention of pelvic floor dysfunction. Usually, pelvic floor dysfunctions have been associated with dysfunctions in women related to prolapse, incontinence, dysmenorrhea, sexual dysfunctions, or postpartum recovery difficulties. However, recent research expands the range of myofascial pelvic floor dysfunctions to include men, and findings show the usefulness of treatments focused on fascia to the therapeutic process. The research is broadly related to: ● chronic pelvic pain (Pastore & Katzman 2012) ● myofascial pain and pelvic floor dysfunction (Bassaly et al. 2011) ● pelvic girdle joint hypermobility (Hastings et al. 2019) ● endometriosis (Aredo et al. 2017) ● urological dysfunction (FitzGerald at al. 2009) ● interstitial cystitis or painful bladder syndrome (Payne et al. 2010, Hanno et al. 2011) ● chronic interstitial cystitis (Lukban at al. 2001, Howard 2010) ● pelvic organ prolapse (Dixon et al. 2019)

● common urological conditions (Itza et al. 2010) ● prostatitis (Wise & Anderson 2012) ● sexual dysfunction in men (Anderson et al. 2006) ● sexual dysfunction in women (Berghmans 2018) ● voiding dysfunction (Petrikovets et al. 2019) ● constipation (Barros-Nieto et al. 2017) ● a synergistic relationship between the muscles that control the pelvic girdle force closure (dynamic stability) in conjunction with breathing, intra-abdominal pressure and continence (Beales et al. 2009) ● the relationship between the pudendal nerve and the sacrotuberous ligament and its relevance to pudendal nerve entrapment syndrome leading to perineal pain (Loukas et al. 2006) ● cesarean section scar pain treated with fascial scar release techniques (Wasserman et al. 2016) ● thoracolumbar fascia and pelvic pain (Bishop et al. 2016) ● dysfunction of the abdominal muscles in pelvic floor disorders Fan et al. (2020) ● pelvic floor adhesions and fascial treatment (Liedler & Woisetschläger 2019) ● the role of telocytes in calcium metabolism in pregnancy and uterine pathologies (Radu et al. 2017) ● myofascial pain and pelvic floor dysfunction in patients with interstitial cystitis (Origo et al. 2021) ● endometriosis and LBP (Lara-Ramos et al. 2021) ● improvement in the Female Sexual Function Index after myofascial treatment (Frederice et al. 2021). This wide range of evidence demonstrates that it is essential to include the pelvic floor in the assessment of pelvic girdle behavior.

The pelvic floor, posture, and gravity The pelvic floor is a complex three-dimensional neuromyofascial unit that provides support for and helps maintain the dynamics of the pelvic viscera. Its integrity, both anatomical and functional, is key to basic life functions, such as breathing, locomotion, maintaining an upright body position, storage and drainage of urine and fecal material, and also reproductive function (Santoro & Sultan 2016, Rocca Rossetti 2016, Bordoni & Zanier 2013, Butrick 2009). In the evolutionary process the verticalization of the spine has driven the need for morphological adjustments inside and between the pelvic floor structures. The human pelvis, proportionally narrower compared to that of quadrupeds, allowed homo sapiens to travel over longer distances with reduced energy expenditure. However, simultaneously, the dynamics of the pelvic girdle was radically modified, and particularly the dynamics of the pelvic floor. For example, in the female body the uterus and rectum have evolved to the most vertical position possible as opposed to that of quadrupeds (Fig. 5.29). The most complex part of this adaptation was to counteract the negative action of forces resulting from intra-abdominal pressure, together with the negative action of gravitational force. Winckler (1953) states that evolutive adaptation linked to the orthostatic position and consequent verticalization of the pelvis affected mainly the ligament supports of the rectal and intrapelvic urogenital organs. The process that clearly illustrates these difficulties are the demands on the female pelvis during pregnancy. To fulfill these demands, efficient dynamic stability of load transfer by the myofascial system is essential. This stability should include optimal performance of the joints, proper force transmission, and effective support of the pelvic organs to preserve continence and prevent prolapse (Fig. 5.30). Examples of this adaptive process include (Winckler 1953): ● modification of the morphology of the ligamentous structures such as the anterior sacrococcygeal ligament which forms the continuation of the anterior vertebral ligament, and which becomes elastic acting as a hinge in the formation of the anococcygeal ligament (raphe)

● the distal unfolding of the two parts of the levator ani muscle with the consequent placement of the anus and its sphincter complex in front of the anococcygeal ligament (raphe) and the coccyx ● formation of a muscular sling at the level of the anorectal junction by the puborectalis muscle adapting to its essential task of elevating the rectum and defecating (proving the synergy between intra-abdominal pressure and the opening of the anal canal with sphincter relaxation) ● the puborectalis region becoming denser ● the holding in situ of the pelvic viscera by the structures of the endopelvic fascia, myofascia, viscerofascia, and the paths of the neurovascular components of the pelvis.

Figure 5.29 Differences in the arrangement of the endopelvic organs (reproductive system) in relation to the action of gravitational force in the cow (quadruped) and the human adult female (biped) B Bladder R Rectum U Uterus V Vagina

Figure 5.30 Dynamic stability of the pelvic floor A Abdominal pressure (intra-abdominal expulsion force) B Reflex contraction in the face of increased abdominal pressure (retention force)

Consequently, the human pelvis, particularly the pelvic floor, evolved into a dynamic system – a complex of myofascial structures that keeps the pelvic organs in their proper location, limiting their movements, and that is functionally capable of taking part in static posture, mobilization (gait and running), urination and defecation, copulation and fertilization, and gestational development and childbirth. These behaviors (proper locations and functions) of the pelvic organs depend on the dynamic interaction between the pelvic floor muscles and the endopelvic fascia (Sarría et al. 2011). Although contemporary therapeutic practice is based on conceptual models that facilitate the systemic approach, this approach appears to be problematic in relation to the pelvic floor and its dysfunction, and dysfunctions of the pelvic girdle and pelvic floor structures are frequently treated separately. However, a study of the fascial anatomy indicates that both systems should be integrated into the assessment and therapeutic process.

Myofascial components join the viscerofascia (structurally and functionally) to create the most complex functionally integrated system (Fig. 5.31) (Santos et al. 2009, Fernández-de-las-Peñas & Pilat 2012). Analysis of the interaction between the pelvic girdle and pelvic floor structures requires a unified approach.

The pelvic floor system and its supporting structures The term pelvic floor relates to the compound structure which “closes the bony pelvic outlet” (Messelink et al. 2005). As mentioned earlier, the pelvic floor is not an independent structure but rather a three-dimensional complex architecture which structurally and functionally is linked to the supporting structures of the pelvic girdle. The dynamic stability of the pelvic girdle depends on the relationship of the pelvic floor muscles with the pelvic girdle, spine, and hip structures. The bony and muscular pelvis is highly interconnected to the hip and gluteal muscles, which together provide support to the internal organs and core muscles (Eickmeyer 2017). The protection of pelvic organs comes from fascial connections to the bony pelvis and its attached muscles. In their report on “The standardization of terminology of pelvic floor muscle function and dysfunction,” Messelink et al. (2005) state:

Figure 5.31 Cross-section of the pelvis at the L3 level. Note the continuity of the abdominal muscle fascia, psoas muscle, quadratus lumborum, and peritoneum Pe Peritoneum PS Psoas muscle QL Quadratus lumborum TrA Transversus abdominis

The function of the pelvic floor muscles is performed by contraction and relaxation. In its resting state the pelvic floor gives support to the pelvic organs. Whether the support function is normal depends on the anatomical position of the muscles, on the activity of the pelvic floor muscles at rest (active support) and on the integrity of the fascia (passive support). However, recent research leads to the conclusion that the functional integrity of all the components is more due to the dynamics of the fascial

system rather than just its passive structural support. Therefore, each anatomical part of the pelvis and perineum is relevant to the activeness of the whole system. The incompetence of one of the elements will be transmitted to the rest of the components. Any damage to the structural and/or functional interactions of the pelvic girdle and pelvic floor components can potentially cause multifocal dysfunction and/or can be the generator of pain. Pool-Goudzwaard (2003) reported a combination of pelvic girdle pain along with pelvic floor dysfunction, including voiding dysfunction, urinary incontinence, sexual dysfunction, and/or constipation, in 52 percent of the patients studied. Of this 52 percent, 82 percent stated that their symptoms began with either low back or pelvic girdle pain. This interaction in the manifestations of pain and/or dysfunction in the pelvic girdle makes diagnosis and clinical follow-up difficult. The researcher also observed: “certain PLBP [pregnancy-related low back and pelvic pain] patients are characterized by increased activity of the pelvic floor muscles as a mechanism to compensate for compromised pelvic stability.” Therefore, altered load transfer through the pelvis can affect musculoskeletal dynamics creating multiple dysfunctions such as low back or pelvic girdle pain, pelvic adhesions, intestinal and urological disorders, endometriosis, prolapse, impotence, orgasm difficulties, dyspareunia, and nerve injuries (DeLancey 1993, Hodges & Richardson 1996, Hungerford 2003, Mense 2019, Snijders et al. 1993a, 1993b, Vleeming et al. 1995, Lee & Lee 2004a, Lee & Vleeming 2005, Occelli et al 2001, DeLancey 1993 – all cited in Lee 2004; Peters & Carrico 2006, Wurn at al. 2004). Pool-Goudzwaard et al. (2004) state: The ability of pelvic floor muscles to increase stiffness of the pelvic ring is of importance in patients with impairment of pelvic stability. Increased activity of these pelvic floor muscles might compensate for loss of pelvic stability by stiffening the pelvic ring and restoring proper load transfer through the lumbopelvic region.

Bony supports

Of relevance is the bony pelvis as the protective skeleton of the pelvic floor. The pelvic bones (ilium, ischium, pubic rami, sacrum, and coccyx) are linked by the sacroiliac, sacrococcygeal, lumbosacral, and pubic symphysis joints (Fig. 5.32). The dynamics of this assembly is widely discussed in the literature (Pilat 1998, van Wingerden et al. 2004, Willard at al. 2012, Schuenke et al. 2012, Vleeming et al. 2012, Vleeming et al. 2014) and was also discussed in Chapter 2 in relation to the behavior of the sacroiliac joint. As mentioned above, orthostatism, apparently, places the viscera of the lower pelvis in a disadvantageous position, particularly the uterus which tends to adapt a more vertical position compared to the uterus in quadrupeds, thereby increasing the risk of prolapse. However, in the upright position the bony pelvis is oriented vertically, such that compression forces are dispersed to minimize the pressures on the pelvic viscera and muscles and are transmitted to the bones. Barber (2005) states:

Figure 5.32 The bony pelvic girdle A Sacroiliac joints B Sacrum C Coccyx D Pubis

Variations in the orientation and shape of the bony pelvis have been associated with the development of pelvic organ prolapse. … Intraabdominal and gravitational forces are applied perpendicular to the vagina and pelvic floor while the pelvic floor musculature counters those forces with its constant tone by closing. With proper tone of the pelvic floor muscles, stress on the connective tissue attachments is minimized. Leaving aside the secondary question of the variety and range of movements of the pelvic girdle joints, which in fact may vary depending on age, sex, and other circumstances, the main point of interest is the dynamics of force transmission through these joints (Pilat 1998). The theory of dynamic stability proposed by Snijders et al. (1995) has been updated (Vleeming & Willard 2010, Willard et al. 2012). The phenomenon of sacroiliac joint stabilization is known as form closure and force closure. Form closure occurs when the joint is stable, and no external force is needed to support it. In an unstable situation, external forces are necessary to sustain the joint in equilibrium force closure. Optimal dynamic stability of the SIJ is achieved through a combination of both forms. Force closure is the effect of changing joint reaction forces generated by tension in ligaments, fasciae, and muscles and ground reaction forces; various muscles are involved in force closure of the SIJ (Vleeming & Willard 2010). Depending on the demands made on the system and the resources available to it, the SIJ can oscillate between both form and force closure stabilization.

Thoracolumbar fascia: The linking structure The dynamics of the sacroiliac joints are widely linked to the behavior of the TLF and its relation to the muscles (Vleeming & Willard 2010, Vleeming et al. 2012, Willard at al. 2012, Schuenke et al. 2012) (see Chapter 2). The basic characteristics of the TLF and its links with the endopelvic fascia structures are summarized below (Fig. 5.33): ● The TLF is organized to integrate the passive and active elements of the low back. ● The superficial sheet (layer) of the TLF (see Fig. 5.29), through the microstructural disposition of collagen fibers which are arranged in a

rhomboid shape over the lumbopelvic region, links the dynamics of the gluteus maximus and the contralateral latissimus dorsi muscles, managing the counter-rotation movements of both sides of the waist. At the same time, it has a role in multisegmental stability (see below). ● The deep layer of the TLF (see Fig. 5.30) is directly anchored to the pelvis through strong connections on the posterior superior iliac spine and through the sacrotuberous ligaments (STL) on the ischial tuberosity it joins the biceps femoris tendon (long head). The tensional balance at this level contributes to the force closure phenomenon and therefore to the stability of the sacroiliac joints in load transfer. ● The TLF plays an important role in the control of posture through the transfer of loads and the breathing process (Fig. 5.34). ● Numerous studies show the importance of the role of the transversus abdominis in the mechanical efficiency of the TLF and its role in intraabdominal and pelvic pressure related to lumbopelvic stability (see Fig. 5.34). ● The disposition of the layers of the TLF triggers a “hydraulic” amplifying effect on the paraspinal muscles and abdominal contents.

Figure 5.33 Thoracolumbar fascia (TLF) and its connections 1 Superficial layer of the TLF and its continuity with the trapezius, gluteus maximus, and latissimus dorsi muscles A Trapezius B Latissimus dorsi C Gluteus maximus 2 Deep layer of the TLF A TLF B Sacrotuberous ligament C Sciatic tuberosity D Tendon of the long head of biceps femoris muscle E Gluteus maximus, dissected and lifted from the gluteal area F Hamstring muscles G Sciatic nerve

Figure 5.34 Diagram showing the mechanism of internal pressures in the interrelation of the diaphragm, transversus abdominis, and pelvic floor muscles A Diaphragm B Pelvic floor C Transversus abdominis

Supporting muscles The pelvic floor muscles provide mechanical support to the pelvic viscera and act in synergy with the pelvic girdle and trunk muscles to manage the dynamic stability of the pelvis (see Fig. 5.31). The myofascial structures that participate in the statics and dynamics of the pelvic girdle converge on the pelvic floor (Fan et al. 2020). They are

distributed in several layers, connecting the anterior and posterior aspects of the pelvic girdle, the most cranial layer being the peritoneum of the pelvic viscera and the most caudal being the skin of the vulva/scrotum and perineum. The middle layers of the pelvic floor contain predominantly muscular tissue. “Apart from the pure pelvic floor muscles, fibro-muscular and fibrous elements, like the endo-pelvic fascia, are found in this layer” (Messelink at al. 2005). The pelvic floor muscles form a complex constrictor mechanism to the anal canal, vagina, and urethra and their most important functions are maintaining urinary, flatal, and fecal continence and they also contract during sexual activities (Baudino 2016). This muscular complex is usually cataloged according to its different layers as follows (Fig. 5.35): ● The superficial layer (urogenital diaphragm) consists of the following muscles: bulbocavernosus (bulbospongiosus in men), ischiocavernosus, transversus perinei muscles, and external anal sphincter. ● In the deep layer (levator ani muscle) are the puborectalis, pubococcygeus, and iliococcygeus muscles. They form the pelvic diaphragm (the muscular floor of the pelvis) which provides the firm tissue support for the pelvic floor components (Razzak 2018). Based on the results of imaging studies, Baudino (2016) suggests that “the pubococcygeus, iliococcygeus most likely provide the physical support and the puborectalis muscle provides the constrictor function to the anal canal, vagina, and urethra.” The puboanalis muscle elevates the anus and along with the rest of the pubococcygeus and puborectalis fibers keeps the urogenital hiatus closed. The levator ani muscles play an important role in the protection of excess load on the endopelvic fascia so much so that the muscle fiber–fascia interaction is critical. To ensure perineal functional integrity, a perfect balance between the functions (levator ani and tendinous arch) and support (endopelvic fascia) is necessary. While the levator ani with its tonic activity closes the genital hiatus, it is the fascia which stabilizes the organs in their position on the levator ani (Bø et al. 2007).

The muscles most associated with pelvic function or dysfunction are described below:

Figure 5.35 Female pelvic floor muscles 1 Deep pelvic floor muscles A Piriformis B Anococcygeal ligament

2

C Coccygeus D Levator ani: Iliococcygeus muscle Pubococcygeus muscle Puborectalis muscle Superficial pelvic floor muscles A Ischiocavernosus muscle B Bulbocavernosus muscle C Transverse perineal superficial and deep muscles D Pubococcygeus muscle E Iliococcygeus muscle F Levator ani G Gluteus maximus

● The piriformis and obturator internus form the posterolateral pelvic walls. Both muscles are the external rotators of the thigh, as both are also linked to coxofemoral dysfunctions which can affect the dynamics of the lower limb, influencing the position of the foot and affecting gait. However, the reverse action is also feasible when disturbances in the foot complex finally affect the dynamics of the pelvic floor muscles (Bordoni et al. 2021) (Fig. 5.36). ● The abdominal muscles (internal oblique, external oblique, transversus abdominus) act in synergy with the pelvic floor muscles which manage the functional integrity of the pelvis. These are the lumbar multifidi, diaphragm (Bordoni et al. 2016), gluteus maximus (Soljanik et al. 2012), gluteus medius, quadratus lumborum, and thigh adductor muscles. ● The external oblique fascia is one of the tensors of the TLF. A poorquality deep scar (e.g., a C-section scar) can create asymmetry between the pairs of muscles and facilitate adaptive processes, distortion of movements, and pain due to overload of nociceptors (Bishop et al. 2016).

Figure 5.36 Behavior of the obturator internus and piriformis muscles 1 Posterior view of the pelvic floor. Note that the piriformis and obturator internus muscles form the posterolateral pelvic walls. The two muscles are the external rotators of the thigh, and both are also linked to coxofemoral dysfunctions A Sacrum B Piriformis C Obturator internus D Coccyx E Insertion of the obturator internus and piriformis muscles in the greater trochanter 2 Cross-section of the pelvis. The two obturators are linked to the endopelvic fascia, constituting a direct connection between both greater trochanters. Through this, the important connection between locomotion and tensional changes in the pelvic floor is created Gm Gluteus maximus F Femur Oi Obturator internus

The dynamics of the pelvic floor muscles As the intra-abdominal pressure increases, the pelvic floor muscles must contract to maintain the supporting function of the pelvic floor. A contraction of the pelvic floor muscles results in a ventral and cranial movement of the perineum and the upward movement of the pelvic organs together with an anterior movement caused primarily by the vaginal and rectal parts of the levator ani muscle. When the pelvic floor muscles contract, the urethra closes, as do the anus and the vagina. This contraction is important in preventing involuntary loss of urine or rectal contents. In the

female pelvic floor the contraction can also act as a defense mechanism during sexual intercourse. Regarding the control of urinary incontinence, it is worth highlighting the synergism between the detrusor muscle and the pelvic floor muscle complex which prevents the expulsion of urine out of the body through the urethra. The contraction and subsequent relaxation of the pelvic floor muscles results in a reduction in the support given to the urethra, vagina, and anus. Accordingly, the pelvic organs return to their anatomical resting position. The pelvic floor muscles must relax in order to remove the passive continence mechanisms, thereby facilitating normal micturition. The same process is present for relaxation before and during defecation, allowing the anorectal angle to become obtuse and facilitating rectal expulsion (Bø et al. 2007). As the pelvic floor muscles relax or are damaged, the pelvic floor becomes “architecturally” unstructured (Larson et al. 2012). Faced with this imbalance, the fascia temporarily assumes the tasks of loading abdominal pressure and tension. The adaptive nature of the fascia means that if this “temporary” situation (that is maintaining it in continuous stretching) is not resolved, the fascia ends up “adapting” to it, deteriorating its stabilizing function in the future (Morgan et al. 2011). This process facilitates the appearance of prolapse that is directly related to the amount and duration of the force applied.

Endopelvic fascia as a part of the dynamics of the pelvic floor system Fascial support of the endopelvic structures The myofascial structures that participate in the statics and dynamics of the pelvic girdle converge on the pelvic floor (Fan et al. 2020). This continuity (see Chapter 2) facilitates the interaction between the fascial structures of the low back and pelvic girdle and the endopelvic fascia. These structures consist of three layers – the superficial, intermediate, and deep layers: ● The superficial (subdermal) layer (Fig. 5.37) is made up of loose areolar connective tissue composed of cuboid and flat adipose cell lobules and a mix of interwoven collagen and elastin fibers. It is continuous anteriorly with the deep fascia of the abdominal wall. On its caudal path fascia covers the bulbospongiosus, ischiocavernosus, and superficial transverse perineal muscles. It is attached laterally to the ischiopubic rami and fused anteriorly with the suspensory ligament of the clitoris (in the female body). The anterior fascial structures are Scarpa’s fascia, dartos fascia, and Colles’ fascia (superficial fascia layers can sometimes include muscle fibers in the external anal sphincter and dartos fascia in the scrotum). Posteriorly, there is continuity of the fascia through the superficial lumbar fascia, superficial gluteal fascia, and the superficial fascia of the sphincter muscle. The skin ligaments (retinacula cutis) join the adipocyte-rich lobules of the subcutaneous tissue to form a threedimensional network, providing dynamic anchoring of the skin to the underlying tissue. The superficial layer contains the endings of nerves, blood vessels, and lymphatic networks, which originate at deeper layers of the body and travel out to the surface to provide nutrition and sensory innervation to the skin (Roch et al. 2021). ● The middle layer (Fig. 5.38) is formed by the structures of the deep fascia. Anteriorly it begins with the external oblique abdominal fascia, Buck’s fascia, Gallaudet’s fascia, and the deep transverse perineal fascia. Posteriorly it includes the thoracolumbar fascia, gluteal fascia, superficial anococcygeal ligament, and external anal sphincter. The aponeurosis of the external oblique muscle is continuous with the

thoracolumbar fascia (see Chapter 2). It has been observed that through this connection a C-section scar can influence the dynamics of the lumbar spine (Fan et al. 2020). ● The deep layer (Fig. 5.39) consists of the internal oblique fascia and the transversus abdominis fasciae, the psoas fascia and the perineal membrane. Posteriorly it is formed by the presacral fascia, deep anococcygeal ligament, and levator ani fascia.

Figure 5.37 Continuity of the superficial (subdermal) fascial layer related to the pelvic floor. Anteriorly the fascial structures are Scarpa’s fascia, dartos fascia, and Colles’ fascia (superficial fascia layers can sometimes include muscle fibers in the external anal sphincter and dartos fascia in the scrotum). Posteriorly there is continuity of the fascia at the back through the superficial lumbar fascia, superficial gluteal fascia, and superficial fascia of the sphincter muscle

Figure 5.38 Continuity of the middle (deep fascia) fascial layer related to the pelvic floor. Anteriorly the continuity begins with the external oblique abdominal fascia, and then Buck’s fascia, Gallaudet’s fascia, and deep transversus perineal fascia. Posteriorly there is continuity through the thoracolumbar fascia, gluteal fascia, superficial anococcygeal ligament, and external anal sphincter

The endopelvic structures Despite the discrepancies in the nomenclature, most authors agree that the pelvic floor consists of three basic anatomical structures: the perineal membrane, perineal body, and endopelvic fascia.

Perineal membrane The perineal membrane is a complex fibrotic layer (composed of dense connective tissue with a predominance of elastic fibers) that expands over the urogenital triangle, interconnecting with the pelvic floor fascial system. It connects the deep layer of the pelvic floor musculature, coccyx, and anal sphincter. It runs between the lower borders of the ischiopubic rami (the

lateral margins of the triangle). The anterior margin of the perineal membrane fuses with the tendinous arch at the level of its insertion on the pubic bone. The posterior margin is connected medially to the perineal body. The urethra and vagina cross throughout the urogenital hiatus in the perineal membrane to exit at the introitus. The urethral and urethrovaginal sphincters are embedded and interlaced with the perineal membrane. The presence of an appropriate quantity of hyaluronic acid can optimize the mechanics of the urogenital system (Stecco et al. 2011).

Perineal body The perineal body is a kind of a convergence zone for different fascial layers and muscle attachments (Fig. 5.40). It is a fibromuscular structure that is at the junction between the anorectal canal and the posterior vaginal wall or testicles. It is attached to the sides of the ischiopubis rami by the superficial and deep transverse perineal, puborectalis, and pubococcygeus muscles. Studies have shown that the perineal body is in continuity with the peroneal membrane and the retrovaginal fascia (Soga et al. 2007). The puborectal muscle was not found to contribute to the function of the perineal body, as it forms a loop behind the rectum. The perineal body participates in limiting the opening of the urogenital hiatus and has an important anchoring role for the vagina and anorectum (rectovaginal fascia). The pudendal neurovascular trunk provides the vascular and nerve supply to the perineum and the deep and superficial perineal spaces. The presence of smooth muscle fibers, blood vessels, skeletal muscle, collagen and elastin fibers, adipose tissue, and peripheral nerves suggests the active participation of the perineal body in proprioception and nociception.

Figure 5.39 Continuity of the deep (myofascia) fascial layer related to the pelvic floor. Anteriorly there is continuity through the internal oblique fascia, transversus abdominis fascia, iliopsoas fascia, and the perineal membrane. Posteriorly the continuity is through the presacral fascia, deep anococcygeal ligament, and levator ani fascia

Figure 5.40 The perineal body (circle) is the area of convergence of the different fascial layers and muscle attachments

Endopelvic fascia The endopelvic fascia is an integral part of the viscerofascia (fascia pelvis visceralis) that extends as a continuing structure from the uterosacral– cardinal ligament complex to the urogenital diaphragm (and includes the presence of muscle structures such as the obturator internus, levator ani, and piriformis) (Fig. 5.41).

Figure 5.41 Endopelvic muscles embedded in the endopelvic fascia

The expression “endopelvic fascia” is frequently used in clinical language. However, authors assign different names to the same structure, describe different routes along its path, and also disagree on its composition and functions: ● Wu at al. (2017) state “due to its [pelvic floor] complex architecture and poor accessibility, the classical ‘dissectional’ approach has been unable to come up with a satisfactory description, so that many aspects of its anatomy continue to raise debate.” ● Stecco (2014), in her discussion of the nomenclature related to fascia, states “nobody knows exactly what visceral fascia actually is, or if a ligament could be considered part of the visceral fascial system, or another structure.” Although anatomically this (endopelvic fascia) “umbrella” expression is not accepted in the Terminologia Anatomica (FCAT 2011), it will be used in this chapter to avoid confusion with the usual terminology found in the literature. The endopelvic fascia is a thin, superior layer of the pelvic floor. Its anatomical attachments are the pubic bone, perineal membrane and body, superior fascia of the levator ani muscle (tendinous arch), ischial spine and the adjacent anterior margin of the greater sciatic notch. The endopelvic fascia is a network of continuous connective tissue that covers not only the pelvic floor itself but also its lateral walls, the pelvic organs, and their attachments to the pelvis. It envelops and holds the pelvic viscera in their proper anatomical positions and provides support to the bladder, urethra, uterus, vagina, rectum, and anus, so that these organs can maintain appropriate relations with each other to enable adequate functioning. Some researchers (Ramin et al. 2016, Ercoli et al. 2005) suggest that there is continuity of the endopelvic fascia with the abdominal and lumbar fasciae, and that it expands toward the lower back and hips and includes the

fascia of the internal obturator and piriformis muscles. Roch et al. (2021) suggest the possibility of an interaction “between visceral and musculoskeletal kinematics” through the endopelvic fascia. The morphology and composition of the endopelvic fascia vary according to the anatomical region, and its behavior depends largely on the construction of its fibrous components (i.e., its volume, density, and orientation). The dynamics between the endopelvic fascia and the associated organs depends on the anatomical construction and the histological content of the fascia. The behavior of a specific organ is associated with the forces exerted by the adjacent organs (mobility) and the intrinsic movement of each one (motility) (Roch et al. 2021). Functional abnormalities of the pelvic floor may be related to impairment and disruption of muscular and/or fascial origin. The structures that are most vulnerable to architectural deterioration are the endopelvic ligaments.

Endopelvic ligaments What are the structures we call the endopelvic ligaments? As mentioned previously, the endopelvic fascia forms a continuous architecture and provides a stable platform on which the pelvic viscera rest. As a three-dimensional network, it covers all the pelvic organs, surrounding the vagina and part of the uterine cervix. It is composed of loose arrangements of collagen, elastin, and adipose tissue “and is penetrated by blood and lymph vessels and nerves” (Otcenasek et al. 2008). Traditionally, the endopelvic ligaments and their functions have been described as having the same features as the ligaments of the joints, so they are considered to be thick bundles consisting of a dense, regular connective tissue and their suspensory function is emphasized in relation to the intrapelvic organs. However, viewing endopelvic ligaments as cords in isolation has contributed to the misunderstanding of their anatomy and function. In fact, the endopelvic ligaments allow the visceral structures to be relatively mobile while maintaining their proper positioning. De Caro et al. (1998) suggested the absence of true ligaments in the endopelvic fascia. The authors carried out research on plastinated cadavers, analyzing tomographic sections of the pelvis. Their results showed the

presence of a three-dimensional network of icosahedral structures with a larger mesh diameter averaging 1.73 mm in the pelvic periphery and a smaller diameter averaging 1.41 mm close to the pelvic viscera. The authors concluded that: the retroperitoneal connective tissue forms a 3-dimensional network of thin connective laminae that are connected to the visceral adventitia, parietal layer of the pelvic fascia and neurovascular bundles crossing the pelvis. … the retroperitoneal connective tissue constitutes an anatomical structure that, beyond the functional limits of any individual ligament, may have supporting properties. Santos (in Sarría et al. 2011) explained the dynamics of this connective tissue as follows: The icosahedral fascial net described above acts as a functional unifying structure of the pelvic floor, manifesting with a softer contexture along its peripheral path and with greater density along its perivisceral path. Its route creates links between the endopelvic viscera, defining their positioning and interrelation. In the same way, it integrates the path of the neurovascular bundles, associating them with the corresponding viscera. This tensegrity (three-dimensional) network (see Volume 1, Chapter 6) facilitates the development of adaptive reflex mechanisms (in relation to postural changes) and pressure variations related to actions such as coughing, sneezing, fecal and urinary continence, and the emptying reflexes of the urinary bladder or rectal anus. Roch et al. (2021), in their systematic search and review, concluded that the endopelvic fascia is the “continuous unit with various thickenings or condensations that have been named fasciae or ligaments.” Stecco (2015) described the inguinal ligament as being a thickening of the distal part of the fascia of the external oblique muscle as it joins the fascia lata. The ligaments show denser innervation and thereby have the ability to better perceive changes in movement. According to this research, the endopelvic ligaments can be considered to be structurally and functionally integrated elements in the dynamics of the pelvic floor. The most relevant examples of the endopelvic ligaments are the cardinal and the uterosacral ligaments (Figs. 5.42 & 5.43).

Recently, Otcenasek et al. (2008), after analyzing the MRI scans of 15 nulliparous women under the age of 30 with no symptoms of pelvic floor dysfunction and the data from 11 embalmed and 15 unembalmed Caucasian cadavers, constructed a 3D model of womens’ endopelvic fascia concluding: this study avoids the description of artificially isolated parts of the fascia as separate structures due to the dissectability of the tissue. Instead, we emphasize the three-dimensional representation of the whole structure, allowing us to describe the entity as a system rather than describing components of the fascia as single ligaments. The majority of clinical terms can be recognized within this concept. Impairment and disruption of the pelvic floor muscles, fasciae, and ligaments may result in a spectrum of functional abnormalities (even prolapse) often involving multiple fascial compartments due to their shared structural support. As discussed extensively in Volume 1, Chapter 3, the specific names of the fascia are assigned in relation to the structures that the fascia accompanies along its path (e.g., bicipital fascia, fascia pectoralis). A similar naming process has been applied to the endopelvic fascia and its ligaments. Authors usually assign to the fascia the name of the organ which it envelops (e.g., perirectal fascia, pubocervical fascia). In the case of ligaments, names are assigned according to the structures they communicate with (e.g., uterosacral, puborectal, or pubocervical ligaments). However, some authors suggest that these naming conventions are inadequate as they do not acknowledge all the functions of fascia in the determined region (Otcenasek et al. 2008, Ercoli et al. 2005).

Figure 5.42 Ligaments of the pelvic floor A Pubocervical ligaments B Transverse cardinal ligament C Uterosacral ligament

Figure 5.43 A microscopic view of the endopelvic fascia showing the formation of the endofascial ligament. The tensional line of accumulated collagen fibers ultimately assumes the appearance of a ligament. (The image shows this process in a vegetable sponge that has a structure very similar to fascia.)

In conclusion, there is no consensus on definitions and descriptions of the endopelvic ligaments:

● Wang et al. (2010) state that: “The existence and composition of the lateral ligaments of the rectum are still the subjects of anatomical confusion and surgical misconception up to now” and “there are pathways of blood vessels and nerve fibers toward the rectum and lymphatic vessels from the lower rectum toward the iliac lymph nodes.” ● Nano et al. (2000) state that “the lateral ligament of the rectum does not contain important structures.” “At the point of insertion into the endopelvic fascia, the lateral ligaments run close to the urogenital bundle.” ● Cosson et al. (2013) argue that “the pelvic ligaments differ in their biomechanical properties and there is fairly good evidence that the uterosacral ligaments play an important role in the maintenance of pelvic support from a biomechanical point of view.” And they conclude that “all known ‘ligaments’ are necessary to ensure the normal mobility of pelvic organs upon thrusting.” ● Ramanah et al. (2009) suggest that the uterosacral ligament appears to be a condensation of nervous fibers made up of hypogastric and pelvic nerves forming the hypogastric plexus. They concluded: “Histologically, the uterosacral ligament contained connective tissue, nervous fibers, sympathetic nodes, vessels and fatty tissue. No structured ligamentous organization was identified.” ● Cole et al. (2006) determine: “We could not consistently identify normal ligamentous tissue in the uterosacral complexes.” ● Wu et al. (2017) make an interesting observation about the difference between the structure of the pelvic floor in relation to age. They suggest: “The major difference between the young-adult and postmenopausal pelvic floor was the expansion of fat in between the components of the pelvic floor. We hypothesize that accumulation of pelvic fat compromises pelvic-floor cohesion, because the pre-pubertal pelvis contains very little fibrous and adipose tissue, and fat is an excellent lubricant.” The complex functioning of the pelvic floor system, which is capable of participating (concurrently) in several activities, is reflected in the

construction of the uterosacral ligament complex. Otcenasek et al. (2008) describe in detail the insertion of the three parts (vascular, neural, and bony) of the uterosacral ligament in the sacrum: ● The “vascular” part … Visceral branches of the internal iliac vessels (hypogastric artery and vein), which run to the rectum, uterus, vagina, and urinary bladder are surrounded by a sheet of perivascular tissue which creates a compact mass that is connected to the rest of the endopelvic fascia ... ● The “neural” part … The pelvic splanchnic nerves (the “erigent nerves”) proceed from the ventral aspect of the sacral plexus and together with fibers of the inferior hypogastric nerves and fibers from the sympathetic chain, create the neural pelvic plexus (plexus hypogastricus inferior). The perineural connective tissue that arises from the fascia of the piriformis muscle, together with the errigent [sic] nerves, creates the “neural portion” of the uterosacral ligament. ● Sacral bone (true uterosacral ligament): Some fibers insert into the periosteum of the sacral bone, in the vertical line that runs medially from the anterior sacral foramina from S1 to S4. … This insertion is shared with the presacral fascia. These findings allow for new links to be identified, such as the connection of the uterosacral ligament with the piriformis through its insertion in the sacrum. Subsequently, the piriformis shares its insertion in the femur with the obturator internus (both are external thigh rotators linked to coxofemoral dysfunctions). The parts of the uterosacral ligament create a direct link between the endopelvic fascia and the sacroiliac and coxofemoral joints. This is in addition to their connections with the structures of the sacral plexus (particularly the hypogastric plexus) that are distributed over the endopelvic fascia and form the complex fascial skeleton that controls the uterine, vaginal, bladder, and urethral vessels. Again, it is necessary to apply systemic reasoning. To relate the above structures to the theory of tensegrity (Fig. 5.44) (see Volume 1, Chapter 6) the pre-tension alone (i.e., the availability of the

cables to be stretched within the construction) gives the structure its characteristic flexibility, meaning that forces applied to any point of the system are transmitted to all the other constituents, deformations are distributed throughout all the elements, and the whole system reacts as one. A tensegrity structure can be oriented in all directions, regardless of variations in the weight distribution of its elements: It is practically independent of gravity. The ligamentous system of the endopelvic fascia can be compared to this type of construction. While the ligaments maintain a balanced, shared, and symmetric tension, the system acts efficiently. This supports the hypothesis that the connective tissue (endopelvic fascia) is essential and integral to the construction of the female pelvic floor and its proper function.

Pelvic floor dysfunction The multiplicity of dysfunctions of the endopelvic system requires multidisciplinary care by different specialists such as gynecologists, obstetricians, gastroenterologists, colorectal surgeons, urologists, urogynecologists, physical therapists, midwives, psychologists, body workers, yoga, Pilates, Alexander, and Feldenkrais teachers, and other health care professionals.

Figure 5.44 Models demonstrating the tensegrity structures of the pelvic floor. Note that the rigid elements (bones) do not touch directly, but they communicate with each other through the tensile elements (ligaments that are part of the fascia). Reproduced with permission from ArtefactPro

Will pelvic floor dysfunction related to the fascial system be synonymous with pelvic floor pathology? Are we talking about the same process? Pavan et al. (2014) suggest the following definitions: ● Pathology (scar/fibrosis): an excessive deposition of fibrous connective tissue with altered architecture (structure) and function of tissues. ● Dysfunction (densification): increased density of loose connective tissue. The architecture (structure) is generally not altered; the mechanical properties of the fascial tissue are altered (impaired gliding process). Usually, dysfunction is the stage that precedes pathology.

Factors that can affect the optimal behavior of the pelvic floor and trigger the formation of dysfunction Alterations in structural and mechanical conditions

● Impaired force transmission through the pubic symphysis and SI joints. ● Impaired coordination of fascial links between the pelvic girdle and pelvic floor structures. ● Alterations in the tensional equilibrium of the thoracolumbar and endopelvic fasciae (mainly between the endopelvic ligaments). ● Adaptation of the coxofemoral pair (piriformis and obturator internus muscle). ● Loss of optimal gliding movement between the fascial layers (lack of efficient secretion of hyaluronan by fasciacytes). ● Hypomobility or hypermobility:

▶ Immobilization and hypomobility produce a pronounced thickening of

the myofascial tissue, which affects the elasticity/rigidity of the muscle and leads to joint changes (Slimani et al. 2012, Pavan et al. 2020).

Scar formation (e.g., cesarean scar) ● A cesarean scar is one of the main factors in the development of muscle deficits and asymmetries and in the alteration of gliding within and between fascial layers (Wylie et al. 2010). This phenomenon can in turn be the direct or indirect cause of scar pain, abdominal pain, low back pain, or pelvic pain (Fan et al. 2020). ● Muscle asymmetry is due to the poor quality of a deep scar that alters the dynamics of muscle pairs, particularly the external obliques, causing adaptive processes to form over time. These changes are not observable in imaging assessments due to the fact that they affect microscopic structures (Fan et al. 2020). ● A cesarean scar results in the formation of internal adhesions that may cause a number of distressing conditions such as scar overgrowth (keloid), tightened skin (contracture), disturbed bowel movements or bowel obstruction, chronic postsurgical pain or itching, growth of uterine tissue in abnormal locations (endometriosis), impaired circulation and energy flow, and initiation of abnormal signals to the nervous system. All these conditions affect quality of life (Wasserman et al. 2016).

● After a cesarean section endometrial cells may stick to a surgical incision leading to the growth of endometrial tissue outside the uterus, especially in the pelvic cavity (e.g., in the ovaries, behind the uterus, or in the uterine ligaments) or in the urinary bladder, intestine, or rectum. In extreme cases, this buildup of tissue can even reach beyond the pelvic cavity.

Aging ● Aging produces muscle deterioration (decreased strength), hormonal alterations (primarily postmenopausal), and neurological degeneration (gradual denervation) that can lead to pelvic floor dysfunction (Wente & Dolan 2018). ● Swenson et al. (2020) demonstrated that resting levator cavity volume was 80 percent higher among older women, reflecting generalized posterior distension with age.

Immunosenescence Immunosenescence is the gradual decreased capacity of the immune system to respond effectively to infections in the elderly brought on by natural age advancement (Moreau et al. 2017). There is more literature available on the treatment of pelvic floor dysfunction in older women than in men and most of it is concerned with chronic pelvic pain syndrome and chronic prostatitis. There are symptoms related to functional disorders that affect the anorectal area, urinary bladder, reproductive system, and the pelvic floor musculature and its innervation (Breser et al. 2017). These functional disorders cannot be explained by an organic or other specified morphological pathology (Clemens 2008). The key element of this process is the mechanical stress to which the cytoplasm and cell nucleus are subjected within the ECM. There is an increase of stiffness and (age-related) collagen cross-linking in the senescent ECM which leads to progressive immunodeficiency (due to decreased T-cell mobility and eventually T-cell death). It involves a complex process with changes in lymphocytes, which in turn results in a higher incidence and severity of infectious diseases, as well as some types of cancer.

Immunological changes The fascia is sensitive to levels of sex hormones. As an example, the authors Petrofsky & Lee (2015) report that one of the sexual hormones, estrogen, increases elasticity of human connective tissue during the menstrual cycle in women. Changes in elasticity of the plantar fascia during the menstrual cycle can have effects on postural sway and tremor, leading to a potential risk of falling. The fibers that are present in the connective tissue matrix are secreted by fibroblasts and are the main components in the construction of the fascial system (see Volume 1 Chapter 5). Their composition, density, orientation, and proportions can determine the behavior of the fascial structure. The volume and density of certain fibers in a given fascial structure are related to the role it plays in the body: ● Elastin and fibrillin ensure the possibility of rapid temporary deformation. ● Type I collagen ensures tensile strength. ● Type III collagen is distributed in the form of a network of reticular fibers that facilitates resilience. ● Fibroblasts have specific receptors on the plasma membrane for estrogen and relaxin, which could regulate the production of type I collagen, type III collagen and fibrillin. The proportion and behavior of these fibers can be altered as a result of different processes, affecting the way the pelvic floor system conducts itself (Fede et al. 2019): ● An increase in hormonal levels (pregnancy, ovulation cycle) increases the elasticity of the fascial tissue, generating higher levels of type III collagen and a corresponding decrease in type I collagen. ● Estradiol is the most potent natural estrogen. Normal estradiol levels in women vary depending on factors such as age, pregnancy, and the phases of the menstrual cycle. In adult women experiencing regular menstrual cycles (premenopause), normal estradiol levels range from 15 to 350 pg/mL. (The picogram is equal to one trillionth of a gram – 1 pg =

0,000000000001 g). During the menstrual cycle the level can reach 800 pg/mL. During pregnancy, normal estradiol levels can reach 20,000 pg/mL. After the menopause estradiol levels are usually below 10 pg/mL, and fascial tissue becomes enriched in type I collagen. ● The presence of relaxin receptor 1 and estrogen receptor alpha in the deep fascia is lower in the postmenopausal period compared to the premenopausal period (Fede et al. 2019), which would explain why women tend to have more frequent problems (pain) of myofascial origin after menopause (Rollman & Lautenbacher 2001). ● Different effects of hormonal changes on the deep fascia during the menstrual cycle have been observed among users and non-users of hormonal contraceptives. A study of elastography images showed that contraceptive non-users had greater thickness and stiffness of the fascia lata and TLF (Vita et al. 2019). ● Fascial cells respond to the endocannabinoid system by regulating and remodeling the formation of the ECM (Fede et al. 2019).

Alterations in pain perception and proprioception “The extracellular matrix (ECM) plays an active and dynamic role that both reflects and facilitates the functional requirements of a tissue. The mature ECM of the nonpregnant cervix is drastically reorganized during pregnancy to drive changes in tissue mechanics that ensure safe birth” (Nallasamy et al. 2017). The authors demonstrated that during pregnancy, the sexual hormones play important roles to regulate synthesis, processing, assembly, and structural reorganization of both collagen and elastic fibers in the cervix regulating the mechanical function of the tissue. Alterations of the connective tissue can affect the behavior of the fascia and underlying muscle becomes compromised, which is a source of myofascial disorders. Fede at al. (2021a) compared the behavior of two types of fasciae: aponeurosis and epimysium. The authors concluded that: “Two fasciae have different roles in proprioception and pain perception: the free nerve endings inside thoracolumbar fascia may function as proprioceptors, regulating the tensions coming from associated muscles and having a role in nonspecific low back pain, whereas the epymisial [sic] fasciae works to coordinate the

actions of the various motor units of the underlying muscle.” Changes in the connective tissue and collagen expression of the muscle spindle capsule are likely to affect its mechanical properties. Changes in the stiffness of the muscle spindle capsule can affect the transmission of the change in length to the muscle spindles and thus the transduction of sensory information. This change in the structure of the muscle spindle may explain some of the proprioceptive deficits and may have an influence on pain perception during pregnancy and postpartum recovery. Preservation of muscle spindles (embedded in the muscle endomysium, perimysium, and epimysium) and sensitization of proprioception are essential to maintain adequate motor control, as well as stable locomotion and posture (Kröger & Watkins 2021). See also Volume 1, Chapter 8.

Dysfunction process An imbalance in the elements mentioned above can cause the development of pelvic floor dysfunction in which the structural and functional integrity of the pelvic floor components will be compromised, leading to the formation of different pathologies (such as urinary and fecal incontinence, pelvic organ prolapses, sexual disorders, and pain). The dysfunctional mechanism usually begins with progressive pelvic floor muscle weakness which widens the urogenital hiatus, leading to the pelvic floor assuming a more bowl-like configuration. As a consequence of this, the endopelvic fascia becomes the primary mechanism of support for the viscera. Over time, this process can result in modifications of the force vectors applied to the viscera and may lead to pelvic organ dysfunction including prolapse (Barber 2005, Butrick 2009).

Figure 5.45 Sagittal section of the pelvic floor ligaments. The region between the pubourethral ligaments (middle third of the urethra) and the neck of the bladder is called the zone of critical elasticity due to its dynamic behavior, and it is considered fundamental to the mechanism of urination and urinary continence B Bladder P Pubis R Rectum S Sacrum U Uterus

The main load affects the endopelvic ligament system, particularly the zone of critical elasticity, which is prone to prolonged and frequent mechanical loads that lead to irreversible viscoelastic elongations and deterioration of the ligaments (Fig. 5.45). Since the 1960s, in their studies of this process, many authors (including Sarría et al. 2011) highlight the importance of assessing the dynamics (alterations) of the vaginal axis and its relationship with the axis of the uterus. In this process the vagina adopts an angled position with a posteroinferior opening. The axis between the uterus and vagina is posteriorized and sustained in the posterior third of the pelvis. The authors determined that at rest the vaginal axis presents an angulation with value

ranges of between 90 and 100 degrees. The variations in the value of the angle from resting to contraction of the pelvic muscles decreases due to the fascial activity generated by the levator muscles (Sarría et al. 2011) (Fig. 5.46). As outlined above, the functional deterioration of the muscles involved in the dynamics of the pelvic floor reduces the efficiency of load distribution to the bones. Consequently, the load is transmitted instead to the fascial structure (and its ligamentous system) causing the latter to deteriorate with time (changes in viscoelasticity) as it adapts to the mechanical demands resulting from gravitational loading.

Figure 5.46 The relationship between the vaginal axis (red) and the uteral axis (blue) A Uteral axis at rest B Vaginal axis at rest C Uteral axis in uterus with prolapse

As a result of these changes the viscera are no longer optimally positioned, an example of this being the process of prolapse formation. Sarría et al. (2011) observed that during the Valsalva maneuver there is a flattening of the vaginal angle in relation to the rectum, which causes the vagina to rest on the anococcygeal raphe of the pubococcygeal fascicles of the levator muscle and coccyx. Simultaneously, because of its position in relation to the vagina and uterus, there is a displacement of the bladder posteriorly and in the caudal direction. The pressure resulting from this dynamically changes the relationship between the vaginal and uterine angles. In cases of retroverted uterus, the vaginal and uterine axes tend to coincide, facilitating the descent of the uterus through the genital hiatus (Santos et al. 2009, Sarría et al. 2011) (Fig. 5.47). Although the approach proposed in this text does not include therapeutic applications involving intracavitary procedures, it is interesting to study the changes that occur at this level. Innervation of the pelvic floor (Fig. 5.48) posteriorly is through direct efferents from the S2–S4 nerve roots, whereas the anterior pelvis is innervated by the pudendal nerve and its three branches: the dorsal nerve to the clitoris, the perineal branch, and the inferior hemorrhoidal nerve. The identification of free nerve endings that are linked to the nociceptive response (see Volume 1, Chapter 8) (Heppelmann 1995) has led to the recognition of the pathophysiological process of “ligamentary pain” resulting from pressure or traction. Santos et al. (2009), using information from clinical experience, observed the presence of pain patterns (“Santos’ sign”) when applying pressure with the index finger to certain areas during gynecological intracavitary exploration (Fig. 5.49) (Santos et al. 2009, Pilat 2012): ● Painful lateral palpation of the fascial insertions indicates damage to the uterosacral and parametrial ligaments at the level of the dome or in the upper two-thirds of the vagina. ● Painful palpation of the pubocervical fascia at the level of the pubourethral ligaments may produce incontinence (urgency and/or urinary incontinence) or may be indicative of future incontinence.

● Painful palpation in the upper and middle thirds of the posterior vaginal wall can indicate a diagnosis of enterocele or hernia of the pouch of Douglas. These tests are useful in the early diagnosis of endopelvic fascia dysfunction with the presence of hysterocele (uterine prolapse) and dyspareunia (coitalgia). In a study of 800 patients with prolapse (Santos et al. 2009) reported that a positive Santos’ sign (dyspareunia) corresponded with the presence of the above pathologies in more than 40 percent of the patients.

Figure 5.47 Prolapse formation. Note the changes in the shape and location of the uterus. The illustration has been drawn from NMR imaging. Blue line – variation in the position of the uterus axis. Red line – vector for the positional changes of the uterus. Green arrow – vector of the displacement of the uterus axis

Figure 5.48 Innervation of the pelvic floor area. 1 The sacral plexus A Sacroiliac joints B Sacral plexus C Anal canal D Vagina E Urethra F Pubis 2 Cutaneous sensory innervation A Iliohypogastric nerve B Ilioinguinal nerve C Pudendal nerve D Perineal nerve E Coccygeal plexus F Medial cluneal nerve G Inferior cluneal nerve H Superior cluneal nerve

Figure 5.49 Testing for fascial injury of the right uterosacral ligament (Santos’ sign). A clinical finding of pain (Santos’ sign) in the perineal and pelvic structures of tensegrity fascial support can provide an early diagnosis of damage to the support provided by the pelvic fascia and ligament. This damage is associated with urinary incontinence, coital dysfunction, anorgasmia, low back pain, pelvic anteversion that produces verticalization, and endopelvic fascial traction on the pelvic viscera (Sarría et al. 2011). In the illustration the pulp of the index finger is used to apply pressure laterally to the fascial insertions of the upper two-thirds of the vagina. A clinical finding of pain is a positive Santos’ sign. This sign expresses fascial tension infringed by previous damage to the uterosacral and parametrial ligaments at the level of the fundus or the paravaginal ligaments. USL – uterosacral ligaments

Recently, Meister et al. (2019) developed a simple, reproducible assessment of internal and external points to screen for pelvic floor myofascial pain. The authors consider that there is extensive evidence of

the significance of myofascial pain in other pelvic floor symptoms (Bø et al. 2017, Adams et al. 2013, Pastore & Katzman 2012 – all cited in Meister et al. 2019). The authors also affirm the efficacy of pelvic floor physical therapy as a noninvasive treatment option for pelvic floor myofascial pain. In a recent paper Klotz et al. (2020) analyzed the assessment of 187 patients with chronic pelvic pain syndrome. In this study, 56.7 percent (N = 106) were women who had experienced pain for an average duration of 5.71 years. The examination consisted of manual palpation of the external and internal muscles. The muscles of the abdominal wall, back, gluteal region, and thighs were palpated with patients lying in supine position and on their side. Then, internal palpation was performed rectally with the patient lying prone, and in women also inside the vaginal cavity in supine position. The results showed that tender and internal trigger points in the pelvic floor muscles are frequently present in women and men with chronic pelvic pain syndrome, suggesting the need for physiotherapy treatment. However, the equally high prevalence rates of external trigger and tender points in the muscles of the trunk and lower extremities emphasizes the importance of not only treating the pelvic floor muscles; rather, all the muscles connected to the pelvis should be integrated into the therapy. “For internal palpation, the clock scheme was used as orientation, with the symphysis at 12 o’clock and the coccyges at 6 o’clock. These two points were not palpated but were used as reference points for localization of the muscles palpated between them” (Klotz et al. 2020). Santos (1989, Santos et al. 2009) continued his research with the development of the theory of the “urethral-vesico-vaginal hammock,” which is a functional diagnostic procedure, useful in the differential diagnosis of prolapse in relation to incontinence. This reasoning was later also applied by Petros and Ulmsten (1990) in their integral theory of urinary continence. In his analysis of the dynamics of the endopelvic fascia, Santos developed an extensive research process to identify the relevant tender points present in the endopelvic fascia, thus assembling a complete map of functional tensegrity (Santos et al. 2009, after Travell & Simons 1983) (Fig. 5.50).

Several authors point out the usefulness of introducing myofascial procedures into therapeutic protocols for pelvic floor dysfunctions: ● Peters and Carrico (2006) state that pelvic floor therapies should be a first line of treatment for women with chronic pelvic pain related to pelvic floor dysfunction. ● Jarrell (2004) states there is an increasing interest in alternative therapies, particularly in applying the principles of the treatment of myofascial dysfunction to chronic pelvic pain syndrome. ● Díaz-Mohedo et al. (2011) investigated “the role played by the myofascial component in the etiology and clinical manifestation of Chronic Pelvic Pain” and recommended the consideration of a therapeutic approach to the myofascial component in the intervention protocols. ● Lukban et al. (2001) reported a 94 percent improvement associated with urination in patients with chronic interstitial cystitis after the application of direct myofascial release, muscle energy, and stretching exercises. Microscopic changes can also influence the dynamics of the macrostructure and determine the quality of the fascia in this area and its relation to the formation of dysfunctions:

Figure 5.50 The distribution of pelvic floor fascial tender points and their relationship to tensegrity principles (see Volume 1, Chapter 7) (Sarría et al. 2011). 1 Anatomy of the pelvic floor 2 Distribution of pelvic floor myofascial tender points. If intravaginal pressure with the finger (see Fig. 5.50) generates a painful response this indicates the initial phase of dysfunction A Piriformis muscle B Ischiococcygeus muscle C Iliococcygeus muscle D Puborectalis bundle of levator ani muscle E Retropubic insertion of puborectalis and pubococcygeus muscles F Transverse perineal muscle G Ischiococcygeus muscle 3 This illustration shows the dynamic centers of pelvic floor tensional balance (dark blue) and the area and extent of endopelvic trigger points (yellow). According to tensegrity principles, tensional adjustments related to pelvic floor activities are distributed among the dynamic centers. Myofascial dysfunctions of the pelvic floor can affect its functions and stability. The blue arrows indicate the direction of forces in a healthy pelvic floor A Protective buffer: pubococcygeus muscle and anococcygeal ligament (internal view) B Uterosacral ligament C Pouch of Douglas D Parametrial ligaments E Main center: uterine cervix (including uterosacral and parametrial ligaments) F Pubourethral ligaments G Middle center: perineum body H Protective buffer center: pubococcygeus muscle and anococcygeal ligament (external view) Note: The presence of pain in all of the points shown is related to fascial damage

● Kökçü et al. (2002), using histological analysis, compared connective tissue components within the uterine ligaments in women with and without pelvic relaxation. The quantity of collagen, cellularity, and elastic fibers within the connective tissue was evaluated and scored. “The patients with pelvic relaxation had significantly higher scores of collagen and fewer scores of cellularity within the connective tissue samples, compared with the ones without relaxation (p